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MIDDLE EAST JOURNAL OF ANESTHESIOLOGY Department of Anesthesiology American University of Beirut Medical Center P.O. Box 11-0236. Beirut 1107-2020, Lebanon Editorial Executive Board Consultant Editors Editor-In-Chief: Ghassan Kanazi Assem Abdel-Razik (Egypt) Executive Editors Fouad Salim Haddad [email protected] Maurice A. Baroody Bassam Barzangi (Iraq) Izdiyad Bedran (Jordan) Chakib Ayoub Marie Aouad Sahar Siddik-Sayyid Dhafir Al-Khudhairi (Saudi Arabia) Mohammad Seraj (Saudi Arabia) Managing Editor Mohamad El-Khatib [email protected] Abdul-Hamid Samarkandi (Saudi Arabia) Mohamad Takrouri (Saudi Arabia) Founding Editor Bernard Brandstater Bourhan E. Abed (Syria) Mohamed Salah Ben Ammar (Tunis) Ramiz M. Salem (USA) Elizabeth A.M. Frost (USA) Halim Habr (USA) Editors Emeritus Editor-In-Chief Anis Baraka Honorary Editors Nicholas Greene Musa Muallem Webmaster Rabi Moukalled Secretary Alice Demirdjian [email protected] The Middle East Journal of Anesthesiology is a publication of the Department of Anesthesiology of the American University of Beirut, founded in 1966 by Dr. Bernard Brandstater who coined its famous motto: “For some must watch, while some must sleep” (Hamlet-Act. III, Sc. ii). and gave it the symbol of the poppy flower (Papaver somniferum), it being the first cultivated flower in the Middle East which has given unique service to the suffering humanity for thousands of years. The Journal’s cover design depicts The Lebanese Cedar Tree, with’s Lebanon unique geographical location between East and West. Graphic designer Rabi Moukalled The Journal is published three times a year (February, June and October) The volume consists of a two year indexed six issues. The Journal has also an electronic issue accessed at www.aub.edu.lb/meja The Journal is indexed in the Index Medicus and MEDLARS SYSTEM. E-mail: [email protected] Fax: +961 - (0)1-754249 All accepted articles will be subject to a US $ 100.00 (net) fee that should be paid prior to publishing the accepted manuscript Please send dues via: WESTERN UNION To Mrs. Alice Artin Demirjian Secretary, Middle East Journal of Anesthesiology OR TO Credit Libanaise SAL AG: Gefinor.Ras.Beyrouth Swift: CLIBLBBX Name of Beneficent Middle East Journal of Anesthesiology Acc. No. 017.001.190 0005320 00 2 (Please inform Mrs. Demirjian [email protected] - Name and Code of article - Transfer No. and date (WESTERN UNION) - Receipt of transfer to (Credit Libanaise SAL) Personal checks, credit cards and cash, are not acceptable “For some must watch, while some must sleep” (Hamlet-Act. III, Sc. ii) SYMPOSIUM ANNOUNCEMENT 29th Annual Symposium Clinical Update in Anesthesiology, Surgery and Perioperative Medicine January 16-21, 2011 St. Martin, French West Indies BROCHURE, ABSTRACT, POSTER AND PAPERS INFORMATION: (Deadline – October 25, 2010) Helen Philips Mount Sinai Medical Center 1 Gustave L. Levy Place Box 1010, Dept. of Anesthesiology New York, NY 10029-6574 Phone: 212 – 241 – 7467 Fax: 212 – 426 – 2009 Email: [email protected] 134 Kingdom of Saudi Arabia, Riyadh King Abdulaziz Medical City National Guard Health Affairs, DEPARTMENT OF INTENSIVE CARE King Abdul-Aziz Medical City - Riyadh is considered a flagship facility in the Middle East, JCI accredited hospital, providing primary and tertiary healthcare services to the National Guard forces, their dependents and civilian employees. As a Center Of Excellence, it performs all major surgeries-including cardiac surgery, liver transplants and conjoined twin separation. We are currently inviting applications for the following posts: Assistant Consultants ICU – Riyadh Our requirements in terms of academics and experience are as follows: • Arab Board in Intensive Care coupled with 3 years critical care / trauma training within a recognized Gulf Region or Western healthcare facility. The Adult Intensive Care Department in KAMC-Riyadh is a Center of Excellence in the Middle East, run at North American standards, staffed with North American Critical Care Board Certified consultants. It has very strong clinical research in affiliation with international centers to conduct randomized controlled trials. The Department has an outstanding achievement profile leading to an excellent international professional reputation. Working at KAMC ICU provides a great opportunity for professional growth. We in turn can offer a generous tax-free salary, 50 days holidays, and educational support for your children, free flights at start and end of your contract, and of course high quality accommodation. The consultant will do 18 shifts per month with flexible scheduling. If you are interested please e-mail your CV indicating which journal advert you are responding to, along with copies of your certificates to the recruitment office of the NGHA for the attention of Mr. John Quinn at Email: [email protected], or fax# +966-1-2520056. For more information please visit our website at: http://www.ngha.med.sa/English/MedicalCities/AlRiyadh/Centers/Pages/ ICUextended.aspx Middle East Journal of Anesthesiology Vol. 20, No. 4, February 2010 CONTENTS editorials Top 10 Cited Paper 2006-2008: International Journal Of Obstetric Anesthesia .............................................................................................................................. Anis Baraka 481 review articles Update On Anesthesia Considerations For Electroconvulsive Therapy ...............................................................Cody Mayo, Alan Kaye, Erich Conrad, Amir Baluch and Elizabeth Frost Management Of Obstetric Hemorrhage ................................................................ A. Rudra, S. Chatterjee, S. Sengupta, R. Wankhede, B. Nandi, G. Maitra and J. Mitra 493 499 scientific articles Comparing Two Methods Of LMA Insertion: Classic Versus Simplified Airway ........................................................................ M. Haghighi, A. Mohammadzadeh, B. Naderi, A. Seddighinejad and H. Movahedi Pretreatment With Remifentanil Is Associated With Less Succinylcholine-Induced Fasciculation ....................................................................................Karim Nasseri, Mehdi Tayebi Arastheh and Shoaleh Shami Epidural Analgesia During Labor – 0.5% Lidocaine With Fentanyl Versus 0.08% Ropivacaine With Fentanyl ............................................................... Wesam Mousa, R. Al-Metwalli and Maanal Mostafa Occupational Fatigue Of The Anesthesiologist: Illusion Or Real? ...................................................................... Afaf Mansour, Waleed Riad and Ashraf Moussa The Effect Of Addition Of Low Dose Atracurium To Local Anesthetic In Retrobulbar Block For Cataract Surgery ............................................. Mohamad Hossein Eghbal, Hesam Tabei, Shoja Alhagh Taregh and Mohammad Reza Razeghinejad Labor Analgesia In Preeclampsia: Remifentanil Patient Controlled Intravenous Analgesia Versus Epidural Analgesia ................................................................................................ Hala El-Kerdawy, Adel Farouk Spinal Anesthesia For Transurethral Resection: Levobupivacaine With Or Without Fentanyl ................................................... Ozgun Cuvas, Hulya Basar, aydan Yeygel, Esra Turkyilmaz and Mehmet M. Sunay Association Between Factors Predicting And Assessing The Airway And Use Of Intubating Laryngeal Mask Airway ............................................... Chryssoula Staikou, Athanassia Tsaroucha, Anteia Paraskeva and Argyro Fassoulaki Preoperative Oral Dextromethorphan Does Not Reduce Pain Or Morphine Consumption After Open Cholesyctectomy ................................................................................... Hossein Mahmoodzadeh, Ali Movafegh and Nooshin Moosavi Beigi 479 509 515 521 529 535 539 547 553 559 M.E.J. ANESTH 20 (4), 2010 Dexamethasone With Either Granisetron Or Ondansetron For Postoperative Nausea And Vomiting In Laparoscopic Surgery ........................................................... Aliya Dabbous, Samar Jabbour-Khoury, Viviane Nasr, Adib Moussa,, Reine Zbeidy, Nabil Khouzam, Mohamad El-Khatib, Frederic Gerges and Anis Baraka case reports Persistent Postoperative Hypertension Following Posterior Fossa Surgery - A Case Report ................................................................Zulfiqar Ali, Hemanshu Prabhakar and Girija Rath Granular Cell Myoblastoma Of Tongue: A Rare Case Of Unanticipated Difficult Intubation ................................................... Lenin Babu Elakkumanan, Anjolie Chhabra, Somnath Bose and Kiran Sharma Use Of Remifentanil In A Patient With Eisenmenger Syndrome Requiring Urgent Cesarean Section ..................................................................Ates Duman, Gamze Sarkilar, Mürüvvet Dayioglu, Mine Özden and Niyazi Görmüs Combined Spinal Epidural Anesthesia For Cesarean Section In A Pregnant Patient With Rare Intracranial Neoplasm ................................................................... Anjolie Chhabra, Neeraj Kumar, Ashwini Kumar, Neena Singh and B.S. Sharma The Use Of Remifentanil In General Anesthesia For Cesarean Section In a Parturient With Severe Mitral Stenosis And Pulmonary Edema .......................................................................................Shahram Amini and Ninoo Yaghmaei Intravenous Regional Analgesia In A Patient With Glanzmann Thrombastenia .............................................................. Sitki Goksu, Rauf Gul, Onder Ozen, Mehmet Yilmaz, Orhan Buyukbebeci and Unsal Onerl Anesthetic Management Of A 29 Week Pregnant Patient Undergoing Craniotomy For Pituitary Macroadenoma .........................................................Oya Yalcin Cok, Sule Akin, Anis Aribogan, Meltem Acil, Bulent Erdogan and Tayfun Bagis Iatrogenic Postoperative Seizure After Mastoid Surgery - A Case Report ............................................................. Erkalp Kerem, Basaranoglu Gokcen, Kokten Numan, Ilhan Emre, Egeli Unal, Ozdemir Haluk and Saidoglu Leyla Psycho-Mimetic Manifestations Following Use Of Propofol In Day Case Surgery - Two Case Reports ................................................................................... Pragnyadipta Mishra, Pradipta Bhakta and Qutaiba Tawfic Use Of Dexmedetomidine As The Main Anesthetic Agent In patients With LarungoTracheomalacia - Three Case Reports ..................................................Khalid Al-Zaben, Ibraheem Qudaisat, Bassam Al-Barazangi and Izdiad Badran Primary Malignant Melanoma Of The Trachea ..... Mohamad Nattout, Nabil Fuleihan, Omar Sabra, Ibrahim Aburizk, Abdul-Latif Hamdan Tracheal Schwannoma: A Misleading Entity ....................................................... Abdul Latif Hamdan, Roger V. Moukarbel, Ayman Tawil, Mohamad El-Khatib, Ussama Hadi 480 565 571 573 577 581 585 589 593 597 599 603 607 611 Editorial TOP 10 CITED PAPER 2006-2008 International Journal of Obstetric Anesthesia On behalf of the Editorial Board of the Middle East Journal of Anesthesiology (MEJA), I would like to congratulate Drs. A. Zeidan, O. Farhat, H. Maaliki, and Dr. A. Baraka from the Departments of Anesthesiology and Neurosurgery, Sahel General Hospital, and the Department of Anesthesiology of the American University of Beirut, Beirut, Lebanon for ranking their paper entitled “Does postdural puncture headache left untreated lead to subdural hematoma?”* which was published in the “International Journal of Obstetric Anesthesia”, Volume 15, Issue 1, 2006, pages 50-58” among the top 10 cited reports between 2006 and 2008. Also, I sincerely thank the Editorial Board of the International Journal of Obstetric Anesthesia for awarding certificates of recognition to the authors of the paper, and for permitting the MEJA to republish the report. The paper reports a 39-year-old pregnant woman who developed cranial subdural hematoma following spinal anesthesia for Cesarean section using a 26gauge spinal needle with an atraumatic bevel. In addition, the paper reviews the literature on 46 patients who developed a postdural puncture headache complicated by subdural hematoma following spinal or epidural anesthesia. The report concluded that postdural puncture headache left untreated may be complicated by the development of subdural hematoma. Also, patients developing a postdural puncture headache unrelieved by conservative measures, as well as the change from postdural to non-postdural headache, require careful follow-up for early recognition and management of possible subdural hematoma. Anis Baraka, MD,FRCA(Hon) Emeritus Editor-in-Chief MEJA Department of Anesthesiology American University of Beirut * Reprinted with permission from International Journal of Obstetric Anesthesia. 481 M.E.J. ANESTH 20 (4), 2010 482 Anis Baraka TOP 10 CITED PAPER 2006-2008 International Journal of Obstetric anesthesia 483 International Journal of Obstetric Anesthesia (2006) 15, 50–58 � 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.ijoa.2005.07.001 CASE REPORT AND REVIEW Does postdural puncture headache left untreated lead to subdural hematoma? Case report and review of the literature A. Zeidan, O. Farhat, H. Maaliki, A. Baraka Departments of Anesthesiology and Neurosurgery, Sahel General Hospital, and Department of Anesthesiology, American University of Beirut Medical Center, Beirut, Lebanon SUMMARY. The patient was a 39-year-old pregnant woman who was scheduled for cesarean section. Spinal anesthesia was induced using a 26-gauge needle with an atraumatic bevel. Postoperatively, the patient developed cranial subdural hematoma manifesting as severe non-postural headache, associated with right eye tearing, fifth cranial nerve palsy and left hemiparesis. The diagnosis was confirmed by computed tomography scan. The patient was managed by careful neurological follow-up associated with conservative treatment and recovered fully after 12 weeks. Our report reviews the literature on 46 patients who developed a postdural puncture headache complicated by subdural hematoma following spinal or epidural anesthesia. It is possible that postdural puncture headache left untreated may be complicated by the development of subdural hematoma. Patients developing a postdural puncture headache unrelieved by conservative measures, as well as the change from postural to non-postural, require careful follow-up for early diagnosis and management of possible subdural hematoma. � 2005 Elsevier Ltd. All rights reserved. Keywords: Subdural hematoma; Dural puncture; Spinal, epidural; Anesthesia; Parturient INTRODUCTION general anesthesia) was scheduled for elective cesarean section under spinal anesthesia. She had no history of trauma, headache or coagulation abnormalities. Preoperative laboratory blood tests, including platelet count, prothrombin time and activated prothromboplastin time, were normal. The patient received no anticoagulants. Before spinal anesthesia, lactated Ringer’s solution 1500 mL was administered. With the patient in the sitting position, spinal anesthesia was performed at the L3-4 interspace using a 26-gauge needle with an atraumatic bevel (Atraucan�, B-Braun, Germany). Subarachnoid puncture was successful on the first attempt and 0.5% plain bupivacaine 12 mg was administered, which led to a sensory block up to T6. The intraoperative course was uneventful except for a decrease in systolic blood pressure from 143 to 110 mmHg, which was treated with i.v. ephedrine 10 mg; the systolic blood pressure remained >110 mmHg throughout the remainder of the operative period. Three days postoperatively, the patient experienced a mild occipital headache, which was assumed to be a PDPH because it was more intense in the sitting position. Over the next two days, the headache improved rapidly following hydration and bed rest. The patient was discharged on the fifth postoperative day. On postoperative day six, the patient suffered from headache Spinal anesthesia can be followed by postdural puncture headache (PDPH), and even cerebral hemorrhage.1–4 This report describes the occurrence of cerebral subdural hemorrhage in a 39-year-old patient undergoing cesarean section under spinal anesthesia, and reviews the literature of 46 patients who developed subdural hematoma following spinal and epidural anesthesia. CASE REPORT A 39-year-old woman, gravida 5 para 4 (three normal deliveries and one uneventful cesarean section under Accepted June 2005 A. Zeidan MD, Staff anesthesiologist, Sahel General Hospital, O. Farhat MD, Staff neurosurgiologist, Sahel General Hospital, H. Maaliki MD, Staff anesthesiologist, Sahel General Hospital, A. Baraka MD, FRCA, Professor and Chairman, Department of Anesthesiology, American University of Beirut Medical Center; Beirut, Lebanon. Correspondence to: Anis Baraka MD FRCA, Professor & Chairman, Department of Anesthesiology, American University of Beirut Medical Center, Beirut, Lebanon. E-mail: [email protected] 50 M.E.J. ANESTH 20 (4), 2010 484 Anis Baraka Postdural puncture subdural hematoma 51 Fig. 1 Cranial CT scan 30 days after spinal anesthesia showing rightsided subdural hematoma. associated with right eye tearing and fifth nerve palsy. On the 15th day, the patient developed diplopia and severe right orbital pain. On the 30th day she came to the hospital when she developed a mild left hemibody weakness. Neurological examination demonstrated mild upper and lower left limb weakness, non-postural severe headache and right eye pain associated with the disappearance of the diplopia and fifth nerve palsy. A computed tomography (CT) scan on the day of admission to the hospital revealed a 1.8-cm thick chronic cerebral subdural hematoma (>2 weeks old) overlying the right fronto-parietal lobe causing compression of the underlying brain and obliteration of the sulci (Fig. 1). The patient was admitted to the department of neurosurgery and surgical versus conservative management was discussed with the patient. She refused the surgical option, and accordingly close regular follow-up of neurological symptoms (lower left limb weakness, headache, and right eye pain), was chosen. The patient showed a marked clinical improvement. Eleven days later, a follow-up CT scan showed good resolution of the hematoma (Fig. 2). Cerebral angiography through the right femoral artery did not reveal an associated aneurysm or arteriovenous malformation. The patient was discharged on the 12th day and recovered fully 12 weeks after dural puncture. DISCUSSION Postdural puncture headache is the most frequent major complication after spinal anesthesia. In the majority of cases the symptoms subside within a few days when treated with analgesics and bed rest. Intracranial sub- Fig. 2 Cranial CT scan 41 days after spinal anesthesia showing decreasing size of subdural hematoma. dural hematoma is rare, but could be a lethal complication that can occur after epidural or spinal anesthesia, as well as following myelography.1–3 The same mechanism has been postulated for both PDPH and subdural hematoma.4 The leakage of cerebrospinal fluid (CSF) from the dural hole causes reduction in CSF volume, which lowers first the intraspinal pressure, and more dangerously, the intracranial pressure. This alteration in cerebrospinal dynamics results in a caudally-directed movement of the spinal cord and brain, which in turn stretches the pain-sensitive structures, dura, cranial nerves and bridging veins. Cerebral veins empty into dural sinuses that are adherent to the inner table of the skull. These veins form short trunks passing directly from the brain to the dura mater. Between these two points, bridging veins take a straight course with no tortuosity to allow for any possible displacement of the brain. The thinnest parts of the bridging veins’ walls are in the subdural space and the thickest are in the subarachnoid portion. This implies that bridging veins are more fragile in the subdural portion than in the subarachnoid space.5 Anteroposterior acceleration or deceleration and/or traction exerted on the bridging veins, may cause a rupture at their weakest point in the subdural space. Cerebral atrophy and low CSF pressure (low CSF volume) will accentuate this mechanism. Following spinal anesthesia, a dural fistula can remain open for many weeks, and the volume of CSF lost may be over 200 mL per day, which can exceed normal CSF production.6 In these circumstances, the rupture of TOP 10 CITED PAPER 2006-2008 International Journal of Obstetric anesthesia 52 International Journal of Obstetric Anesthesia a subdural vein is certainly conceivable. Research on weakness of the dura and abnormalities of connective tissue, particularly abnormality of fibrillin and elastin, is gaining momentum as one of the etiological factors for delayed healing of a dural tear.7 The incidence of PDPH is reduced following dural puncture using a small needle (26-gauge spinal). In contrast, PDPH occurs in up to 80% of parturients who experience inadvertent dural puncture with a large bore needle.8 Nevertheless, the use of a 26-gauge spinal needle in our patient was complicated by PDPH and subsequent subdural hematoma. Thus, once PDPH develops, it should be treated as such irrespective of needle size. The concurrence of neurological symptoms with PDPH does not mean certainty of the formation of intracranial hemorrhage. Continuous loss of CSF leads to intracranial hypotension. Intracranial hypotension is an increasingly recognized neurologic syndrome characterized by postural headache that occurs or worsens shortly after assuming the upright position and disappears or improves after resuming the recumbent position. Additional symptoms may include neck pain, nausea, emesis, interscapular pain, photophobia, diplopia, dizziness, change in hearing, visual blurring, cranial nerve palsies and radicular upper extremity symptoms.7 The occurrence of subdural hematoma increases the intracranial pressure which can be associated with non-postural headache, convulsions, hemiplegia, disorientation and more serious neurological symptoms. Differentiation between the neurological symptoms of intracranial hypotension and subdural hematoma can be difficult. A change in headache characteristics from postural to non-postural should be a warning sign. CT scan of the skull usually gives the correct diagnosis. However, intracranial hematoma 7–21 days old may have the same radiological density as the brain, so magnetic resonance imaging (MRI) or CT scan with contrast may be more reliable.1 The delayed diagnosis, in many cases, implies that subdural hematoma wasn’t taken into consideration as a complication of spinal anesthesia. In our case, there was a major delay between the onset of symptoms and diagnosis. The patient considered the prolonged postoperative headache as a benign complication of spinal anesthesia and she didn’t consult us until the appearance of the hemiparesis. Our patient developed an intracranial hypotension syndrome (eye tearing and fifth nerve palsy) on the sixth postoperative day. The time of formation of the subdural hematoma, although unknown, was most probably on the second or third week after dural puncture. We concur that intracranial hypotension syndrome might be a prodrome of subdural hematoma after dural puncture. Cerebral atrophy, dehydration, anticoagulant, arteriovenous malformations and excessive CSF leakage (mul- 485 tiple dural puncture, large dural hole) are thought to be contributing factors in the pathogenesis of subdural hematoma. In our patient, the angiography of cerebral vessels revealed no associated aneurysm or arteriovenous abnormalities. Furthermore, our patient received no anticoagulants. Review of the literature disclosed 25 cases of subdural hematoma following spinal anesthesia (Table 1).1,4,9–31 Among these 25 cases, the age of patients ranged between 20 to 88 years. The earliest diagnosis of subdural hematoma was six hours after spinal anesthesia and the latest was 29 weeks. Subdural hematoma after spinal anesthesia occurred most frequently on the left side of the brain (13 cases were left-sided, six rightsided, four bilateral and two were intracerebral). The largest spinal needle used was 19 gauge and the narrowest one was a 27-gauge Whitacre needle. Three cases of multiple puncture were noted. Surgery was performed in 20 of these 25 patients, and was followed by postoperative mortality of four patients. Mortality was not related to the age of the patient or the size of the spinal needle used. Also, review of the literature disclosed 21 cases of subdural hematoma after unintentional dural puncture following epidural anesthesia (Table 2),2,10,12,32–49 the most recent being reported by Kayacan et al.49 Nineteen of these 21 cases were obstetric patients. The earliest diagnosis of subdural hematoma was two days after epidural anesthesia and the latest was 20 weeks. Almost half of the patients developed bilateral subdural hematoma (11 cases were bilateral, six left-sided and four right-sided). Surgery was performed in 15 of these 21 patients and two died. In both groups, (spinal and epidural), the size of the hematoma, severity of symptoms, delayed diagnosis and/or interventions did not apparently affect mortality rate. It is possible that parturients are at high risk of developing post dural puncture headache.50–53 The increased incidence of post-dural puncture headache in parturients may be attributed to numerous factors including peripartum dehydration, which could reduce the production of CSF, postpartum diuresis, abrupt release of intra-abdominal pressure and venacaval compression at delivery, which reduces epidural venous pressures. Maternal bearing-down efforts that could increase CSF leakage through the dural hole could also be a factor, as well as early ambulation, anxiety about delivery and hormonally-induced ligamentous changes.54 In addition, it is widely believed that pregnancy increases the risk of stroke; reports showed that the incidence of intracerebral hemorrhage is increased in the six weeks after delivery.55 Furthermore, there was an association between post-partum hemorrhagic stroke and cesarean delivery.56,57 It seems that venous congestion during pregnancy can make bridging veins more susceptible to M.E.J. ANESTH 20 (4), 2010 67/M 33/F 70/M 63/M 50/M 67/M 67/M 68/M 63/F 68/M 71/M 71/M 31/F 42/M 20/M Newrick12 Miyazaki13 Rudehill14 Jonsson15 Giamundo16 Blake17 Beal18 Macon4 Ortiz19 Van de Kelft20 Baldwin21 Bj�rnhall1 Akpek22 Cantais23 Acharya24 Eggert 29/F 27/F Mantia11 25 37/M Pavlin10 Welch 69/M Age/Sex 9 References 1 day, CT scan: left SDH 1 week, MRI: right SDH 10 days, CT scan: left SDH 14 days; MRI: Bilat. SDH, basal ganglia and thalamus hemorrhage 5 days, CT scan: right SDH 29 weeks, CT scan: Bilat. SDH 30 days; CT scan: right SDH 11 days, CT scan: left SDH 2 weeks; CT scan: left SDH 6 days, CT scan: left SDH 3 weeks, CT scan: left SDH 30 days, CT scan: left SDH On 12th day scan was normal, 29 days by angiography: left SDH 21 days, CT scan: right SDH 26 days, CT scan: left SDH 10 days, CT scan: left SDH 5 days, CT scan: right SDH 6 days, angiography: right SDH 48 days, clinical diagnosis: Bilat. SDH Diagnosis time/PDP/ Methods/ Localization of hematoma Pregnancy? None Anticoagulants Pregnancy? None None Previous dural puncture with 22-G one month ago Anticoagulants Multiple puncture None Multiple puncture attempts None None None Pregnancy? None Pregnancy? Multiple puncture attempts with 22-G None Predisposing factors Table 1. Reported cases of subdural hematoma after spinal anesthesia Removal of retained placenta Appendectomy Achilles tendon repair Cesarean section Cystoscopy TURP Urethral dilatation Vaginal hysterectomy Inguinal herniorraphy TURP TURP Inguinal herniorraphy Inguinal herniorraphy Inguinal herniorraphy Cesarean section Inguinal herniorraphy Normal delivery Perirectal abscess Retropubic prostatectomy Procedure 24-G Sprotte 23-G Quincke 27-G Whitacre 22-G 22-G Quincke 22-G 22-G 22-G 25-G Quincke 22-G Quincke 25-G ? 24-G 22-G 21-G 22-G 26-G 25-G 22-G Needle size for spinal anesthesia Fronto-occipital NPH, photophobia and vomiting Severe NPH, vomiting Severe frontal NPH, vomiting and coma Absent mindedness; drowsiness and right hemiparesis NPH and vomiting Headache, vomiting and personality changes NPH, confusion and dizziness Severe headache, left hemiparesis and photophobia NPH, left orbit pain and left hemicranial pain Coma Right frontal pain, confusion and clumsy gait Severe headache, memory deficit and confusion Right orbit pain, dysphasia and right arm weakness Severe headache, vomiting, confusion and drowsiness Severe headache, vomiting and confusion Disorientation and general hyperreflexia Left hemiplegia and aphasia Coma Frontal headache, diplopia and confusion Warning sign (continued on next page) Medical/recovered Medical/recovered Surgical/death Surgical/recovered Surgical/recovered Surgical/recovered Surgical/recovered Surgical/? Surgical/recovered Surgical/death Surgical/recovered Surgical/recovered Surgical/recovered Surgical/recovered Surgical/recovered Surgical/death Medical/neurological deficit? Surgical/neurological deficit Surgical/death Treatment/Outcome 486 Postdural puncture subdural hematoma 53 Anis Baraka TOP 10 CITED PAPER 2006-2008 International Journal of Obstetric anesthesia Slowinski SDH: subdural hematoma; NPH: non-postural headache; PDP: post-dural puncture. Surgical/recovered Medical/recovered NPH and left hemiparesis Confusion and drowsiness 25-G Quincke 26-G Atraucan Cesarean section Right femoral herniorraphy Brain atrophy Pregnancy? Our case 3 days, CT scan: left SDH 88/F 39/F Tan31 30 days, CT scan: left SDH Surgical/recovered Severe headache, six nerve palsy and diplopia 19-G Tubal ligation None 25 days, CT scan: left SDH 41/F Alilou30 Surgical/recovered NPH,diplopia and bilateral abducent nerve palsy 25-G Quincke Saphenous vein ligation None 6 weeks, MRI: bilat. SDH 38/F Surgical/recovered Severe frontal NPH 22-G Quincke Inguinal herniorrhaphy None 38/M 29 Kelsaka28 40 days, CT scan: left SDH Surgical/recovered NPH and confusion 27-G Whitacre Prostate surgery Cerebral aneurysms 59/M Wells27 2 days, CT scan: left intracranial hemorrhage Surgical/neurological deficit? Severe headache, vomiting and left hemiparesis 24-G Cesarean section Pregnancy? 28/F Sharma26 6 h, CT scan: right intracerebral hematoma Age/Sex References Diagnosis time/PDP/Methods/ Localization of hematoma Predisposing factors Procedure Needle size for spinal anesthesia Warning sign Treatment/Outcome International Journal of Obstetric Anesthesia Table 1. continued 54 487 rupture. Also, sudden increases in venous pressure of these dilated veins by coughing, stressing or abdominal compression during labor and delivery (Valsalva maneuver) can lead to an augmentation of tension, especially at the subdural portion of bridging veins.5 The true incidence of subdural hematoma after dural puncture is unknown. In most cases, non postural headache and vomiting are the warning signs. In addition, changes in headache characteristics (intractable headache associated with retro-orbital and frontal pains) were observed in most cases. Most patients with headaches are probably treated without further investigation. Therefore, the true incidence of subdural hematoma after spinal anesthesia may be greater than the published case reports suggest. Suess et al. found that headache lasting >5 days was the chief complaint in 17 reported cases of intracranial hemorrhage after myelography.3 The management of subdural hematoma is either conservative or surgical. Small hematomas often resolve spontaneously. Early blood patching may decrease the risk of subdural bleeding by preventing a fall in CSF volume and subsequent intracranial hypotension. Reynolds and Salvin recommend that “headache after dural puncture with a large needle should be treated promptly with an epidural blood patch.”58 However, when epidural blood patch is performed in the presence of intracranial hemorrhage, rebound intracranial hypertension and neurological deterioration can result.14,47 The practice of administering a prophylactic epidural blood patch to obstetric patients after inadvertent dural puncture with an epidural needle has been controversial. When a large dural hole is known to exist and a functioning epidural catheter is in place, a prophylactic epidural blood patch through the catheter might be tried. Some authors have suggested that prophylactic epidural blood patch may reduce the incidence of subsequent PDPH to 5%–21%.59–61 However, Scavone et al.62 showed recently that prophylactic epidural blood patch after inadvertent dural puncture in parturients did not decrease the incidence of PDPH to the magnitude predicted; the length and severity of PDPH symptoms, however, were decreased. Loeser et al.63 have shown that therapeutic epidural blood patch is not as effective when performed within the first 24–48 h after dural puncture. Also, Safa-Tisseront et al.64 showed recently that the percentage of failure of epidural blood patch was significantly increased when epidural blood patch was performed within three days after dural puncture. Epidural blood patch essentially has two effects. The immediate effect is simply related to volume replacement by compression of the dura that will restore CSF pressure and relieve the headache. The second latent effect is related to sealing of a dura defect. The time interval between these two effects varies considerably. Beards et al.65 demonstrated no M.E.J. ANESTH 20 (4), 2010 488 11. Mantia A M. Clinical report of the occurrence of an intracerebral hemorrhage following post-lumbar puncture headache. Anesthesiology 1981; 55: 684–685. 12. Newrick P, Read D. Subdural haematoma as a complication of spinal anaesthetic. Br Med J 1982; 285: 341–342. 13. Miyazaki S, Fukushima H, Kamata K, Ishii S. Chronic subdural hematoma after lumbar-subarachnoid analgesia for a cesarean section. Surg Neurol 1983; 19: 459–460. 14. Rudehill A, Gordon E, Rahn T. Subdural haematoma. A rare but life-threatening complication after spinal anaesthesia. Acta Anaesthesiol Scand 1983; 27: 376–377. 15. Jonsson L O, Einarsson P, Olsson G L. Subdural haematoma and spinal anaesthesia. A case report and an incidence study. Anaesthesia 1983; 38: 144–146. 16. Giamundo A, Benvenuti D, Lavano A, D’Andrea F. Chronic subdural haematoma after spinal anaesthesia. Case report. J Neurosurg Sci 1985; 29: 153–155. 17. Blake D W, Donnan G, Jensen D. Intracranial subdural haematoma after spinal anaesthesia. Anaesth Intensive Care 1987; 15: 341–342. 18. Beal J L, Royer J M, Freysz M, Poli L, Wilkening M. Acute intracranial subdural hematoma of arterial origin after spinal anesthesia. Ann Fr Anesth Reanim 1989; 8: 143–145. 19. Ortiz M, Aliaga L, Baturell C, Preciado M J, Aguilar J, Vidal F. Intracranial subdural haematoma - a rare complication after spinal anaesthesia. Eur J Anaesthesiol 1991; 8: 245–248. 20. Van de Kelft E, De la Porte C, Meese G, Adriaensen H. Intracranial subdural hematoma after spinal anesthesia. Acta Anaesthesiol Belg 1991; 42: 177–180. 21. Baldwin L N, Galizia E J. Bilateral subdural haematomas: a rare diagnostic dilemma following spinal anaesthesia. Anaesth Intensive Care 1993; 21: 120–121. 22. Akpek E A, Karaaslan D, Erol E, Caner H, Kayhan Z. Chronic subdural haematoma following caesarean section under spinal anaesthesia. Anaesth Intensive Care 1999; 27: 206–208. 23. Cantais E, Behnamou D, Petit D, Palmier B. Acute subdural hematoma following spinal anesthesia with a very small spinal needle. Anesthesiology 2000; 93: 1354–1356. 24. Acharya R, Chhabra S S, Ratra M, Sehgal A D. Cranial subdural haematoma after spinal anaesthesia. Br J Anaesth 2001; 86: 893–895. 25. Eggert S M, Eggers K A. Subarachnoid haemorrhage following spinal anaesthesia in an obstetric patient. Br J Anaesth 2001; 86: 442–444. 26. Sharma K. Intracerebral hemorrhage after spinal anesthesia. J Neurosurg Anesthesiol 2002; 14: 234–237. 27. Wells J B, Sampson I H. Subarachnoid hemorrhage presenting as post-dural puncture headache: a case report. Mt Sinai J Med 2002; 69: 109–110. 28. Kelsaka E, Sarihasan B, Baris S, Tur A. Subdural hematoma as a late complication of spinal anesthesia. J Neurosurg Anesthesiol 2003; 15: 47–49. 29. Slowinski J, Szydlik W, Sanetra A, Kaminska I, Mrowka R. Bilateral chronic subdural hematomas with neurologic symptoms complicating spinal anesthesia. Reg Anesth Pain Med 2003; 28: 347–350. 30. Alilou M, Halelfadl S, Caidi A, Kabbaj S, Ismaili H, Maazouzi W. Cranial subdural haematoma following spinal anaesthesia. Ann Fr Anesth Reanim 2003; 22: 560–561. 31. Tan S T, Hung C T. Acute-on-chronic subdural haematoma: a rare complication after spinal anaesthesia. Hong Kong Med J 2003; 9: 384–386. 32. Jack T M. Post-partum intracranial subdural haematoma. A possible complication of epidural analgesia. Anaesthesia 1979; 34: 176–180. 33. Edelman J D, Wingard D W. Subdural hematomas after lumbar dural puncture. Anesthesiology 1980; 52: 166–167. 34. Reinhold P, Lindau B, Bohm P. Chronic subdural haematoma following epidural anaesthesia. Anasth Intensivther Notfallmed 1980; 15: 428–431. 35. Deglaire B, Duverger P, Muckensturm B, Maissin F, Desbordes J M. Acute intracranial subdural hematoma after accidental dural Anis Baraka Postdural puncture subdural hematoma 57 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. puncture in epidural anesthesia. Ann Fr Anesth Reanim 1988; 7: 156–158. Scott D B, Hibbard B M. Serious non-fatal complications associated with extradural block in obstetric practice. Br J Anaesth 1990; 64: 537–541. Wyble S W, Bayhi D, Webre D, Viswanathan S. Bilateral subdural hematomas after dural puncture: delayed diagnosis after false negative computed tomography scan without contrast. Reg Anesth 1992; 17: 52–53. Campbell D A, Varma T R. Chronic subdural haematoma following epidural anaesthesia, presenting as puerperal psychosis. Br J Obstet Gynaecol 1993; 100: 782–7844. Thons M, Neveling D, Hatzmann W. Intracerebral subdural hematoma after delivery with peridural catheter anesthesia. Z Geburtshilfe Perinatol 1993; 197: 235–237. Garcia-Sanchez M J, Prieto-Cuellar M, Sanchez-Carrion J M, Galdo-Abadin J R, Martin-Linares J M, Horcajadas-Almansa A. Chronic subdural hematoma secondary to an accidental dural puncture during lumbar epidural anesthesia. Rev Esp Anestesiol Reanim 1996; 43: 327–329. Cohen J E, Godes J, Morales B. Postpartum bilateral subdural hematomas following spinal anesthesia: case report. Surg Neurol 1997; 47: 6–8. Skoldefors E K, Olofsson C I. Intracranial subdural haematoma complicates accidental dural tap during labour. Eur J Obstet Gynecol Reprod Biol 1998; 81: 119–121. Diemunsch P, Balabaud V P, Petiau C, et al. Bilateral subdural hematoma following epidural anesthesia. Can J Anaesth 1998; 45: 328–331. Davies J M, Murphy A, Smith M, O’Sullivan G. Subdural haematoma after dural puncture headache treated by epidural blood patch. Br J Anaesth 2001; 86: 720–723. Ferrari L, De Sevin F, Vigue J P, Granry J C, Preckel M P. Intracranial subdural hematoma after obstetric dural puncture. Ann Fr Anesth Reanim 2001; 20: 563–566. Ezri T, Abouleish E, Lee C, Evron S. Intracranial subdural hematoma following dural puncture in a parturient with HELLP syndrome. Can J Anaesth 2002; 49: 820–823. Kardash K, Morrow F, Beique F. Seizures after epidural blood patch with undiagnosed subdural hematoma. Reg Anesth Pain Med 2002; 27: 433–436. Nolte C H, Lehmann T N. Postpartum headache resulting from bilateral chronic subdural hematoma after dural puncture. Am J Emerg Med 2004; 22: 241–242. Kayacan N, Arici G, Karsli B, Erman M. Acute subdural haematoma after accidental dural puncture during epidural anaesthesia. Int J Obstet Anesth 2004; 13: 47–49. Barash P, Cullen B, Stoelting R. Clinical Anesthesia. 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001: 1152. Angle P, Thompson D, Halpern S, Wilson D B. Second stage pushing correlates with headache after unintentional dural puncture in parturients. Can J Anaesth 1999; 46: 861: 861–866. Vandam L D, Dripps R D. Long-term follow-up of patients who received 10,098 spinal anesthetics; syndrome of decreased intracranial pressure (headache and ocular and auditory difficulties). JAMA 1956; 161: 586–591. Loo C C, Dahlgren G, Irestedt L. Neurological complications in obstetric regional anaesthesia. Int J Obstet Anesth 2000; 9: 99–124. Ravindran R S, Viegas O J, Tasch M D, Cline P J, Deaton R L, Brown T R. Bearing down at the time of delivery and the incidence of spinal headache in parturients. Anesth Analg 1981; 60: 524–526. Sharshar T, Lamy C, Mas J L. Incidence and causes of strokes associated with pregnancy and puerperium. Stroke 1995; 26: 930–936. Witlin A G, Mattar F, Sibai B M. Postpartum stroke: A twenty-year experience. Am J Obstet Gynecol 2000; 183: 83–88. Lanska D J, Kryscio R J. Risk factors for peripartum and postpartum stroke and intracranial venous thrombosis. Stroke 2000; 31: 1274–1282. 36/F 29/F 70/M (?) 15/F 21/F 19/F Reinhold34 Newrick12 Deglaire35 Scott36 Wyble37 Campbell38 Thons39 29/F 23/F Vaughan2 Ferrari45 27 Diemunsch43 39/F 19/F Skoldefors42 Davies44 18/F Cohen41 54/F 27/F Edelman33 Garcia-Sanchez 23/F Pavlin10 40 29/F Age/Sex Jack32 References 9 days, CT scan with contrast: left SDH 16 days, MRI: left SDH 4 days, CT scan: left SDH 30 days, CT scan: bilat SDH 23 days, CT scan: left SDH 42 days, CT scan: bilat SDH 5 months, CT scan: right SDH 26 days, CT scan: right SDH 6 weeks, CT scan: bilat SDH On 17th day CT scan normal; 19 days CT scan: bilat SDH Some weeks? -CT scan: bilat SDH 2 days, CT scan: right SDH. 4 weeks, angiography: bilat SDH 21 days, CT scan: left SDH 40 days, autopsy: bilat SDH 8 days, angiography: bilat SDH 28 days, angiography: bilat SDH Diagnosis time/PDP/Methods/ Localization of hematoma Pregnancy? Pregnancy? Pregnancy? A-V malformations Pregnancy? Pregnancy? Pregnancy? None Pregnancy? Pregnancy? Pregnancy? Pregnancy? Anticoagulants Pregnancy? Pregnancy? Pregnancy? Pregnancy? Pregnancy? Preeclampsia? Predisposing factors Table 2. Reported cases of subdural hematoma after epidural anesthesia Normal delivery Labor and then cesarean section Normal delivery Normal delivery Normal delivery Normal delivery For bilateral saphenectomy Normal delivery Cesarean-section Normal delivery Normal delivery TUR-P Normal delivery Normal delivery Normal delivery Normal delivery Normal delivery Procedure Tuohy 18-G Tuohy 16-G Tuohy ?-G Tuohy needle 18-G. Dural puncture by the catheter? Tuohy 16-G Tuohy ?-G Tuohy ?-G Tuohy ?-G Tuohy 16-G? No obvious dural puncture? Tuohy 17-G Tuohy? -G Tuohy 17-G Tuohy 18-G Tuohy 18-G Tuohy 16-G Crawford 18 -G Tuohy ?-G No obvious dural puncture? Needle and size NPH, nausea and vomiting Severe headache, dysphasia, right arm sensory loss Convulsion and coma NPH, left hemiparesis and aphasia Severe headache and drowsiness NPH; photophobia vomiting and right Babinski’s sign Persistent NPH Persistent headache Persistent headache, blurred vision, vomiting. Suicidal attempts and puerperal psychosis Medical/recovered Surgical/recovered Medical/recovered? Surgical/recovered Surgical/recovered Surgical/recovered Surgical/recovered Surgical/recovered Surgical/recovered Surgical/recovered Surgical/recovered Surgical/death Surgical/permanent visual defect Surgical/recovered Death Surgical/recovered Surgical/recovered Treatment/ Outcome (continued on next page) NPH, blurred vision, vomiting. Then confusion and paresis after blood patch Prolonged severe headache Coma Headache; drowsiness, vision loss and right limb weakness Headache; blurred vision; dysphasia and memory deficit Apnea and cardiac arrest Headache; dysarthria and right vision loss Headache; disorientation and muscle weakness Warning sign TOP 10 CITED PAPER 2006-2008 International Journal of Obstetric anesthesia Postdural puncture subdural hematoma 55 489 M.E.J. ANESTH 20 (4), 2010 490 Anis Baraka Medical/recovered residual dural compression after seven hours after epidural blood patch, indicating that the sustained therapeutic response to blood patches reflects sealing of the thecal tear by clot. Blood could persist for more than 18 h after epidural blood patch.65 Other modalities of treatment for PDPH have been proposed. Ayad et al.66 showed that an epidural catheter left in the subarachnoid space for 24 h after a dural puncture significantly reduced both PDPH and the need of epidural blood patch. The mechanism for subarachnoid catheter prevention of PDPH is speculative. The large-bore intrathecal catheter may act as a barrier to CSF leakage by plugging the dural tear, decreasing the CSF efflux from the subarachnoid space to the epidural compartment. Furthermore, the effect of leaving the catheter in place for 24 h may provoke an inflammatory process that facilitates closure of the dural puncture after catheter removal. Also, Charsley et al.67 showed that the intrathecal injection of normal saline (10 mL) was associated with a significantly reduced incidence of PDPH and a reduced need for epidural blood patch. One explanation for the beneficial effect of intrathecal saline is that the increased CSF pressure may result in approximation of the dura and arachnoid at the puncture site, thus sealing the defect. In conclusion, our patient developed a cranial subdural hematoma following untreated PDPH. Patients developing PDPH unrelieved by conservative measures, as well as the change of PDPH from postural to non-postural, require careful follow-up for early diagnosis and management of possible subdural hematoma. SDH: subdural hematoma; NPH: non-postural headache; PDP: post-dural puncture. Tuohy 18-G 36/F Kayacan49 On 7th day scan was normal; 11 days by MRI: right SDH Pregnancy? Normal delivery Persistent severe headache and convulsion Surgical/recovered Tuohy 17-G 31/F Nolte48 20 days, CT scan: bilat SDH Pregnancy? Normal delivery of twins NPH, vomiting, drowsiness Medical/recovered Tuohy ?-G 33/F Kardash47 3 days, CT scan with contrast: left SDH Pregnancy? Normal delivery Headache, seizure Medical/recovered Severe NPH Tuohy 18-G Labor and then cesarean section Preeclampsia and HELLP syndrome (thrombocytopenia) 4 days, MRI: bilat SDH 19/F Ezri46 References Age/Sex Diagnosis time/PDP/Methods/ Localization of hematoma Predisposing factors Procedure Needle and size Warning sign Treatment/ Outcome International Journal of Obstetric Anesthesia Table 2. continued 56 REFERENCES 1. Bjarnhall M, Ekseth K, Bostrom S, Vegfors M. Intracranial subdural haematoma: a rare complication following spinal anaesthesia. Acta Anaesthesiol Scand 1996; 40: 1249–1251. 2. Vaughan D J, Stirrup C A, Robinson P N. Cranial subdural haematoma associated with dural puncture in labour. Br J Anaesth 2000; 84: 518–520. 3. Suess O, Stendel R, Baur S, Schilling A, Brock M. Intracranial haemorrhage following lumbar myelography: case report and review of the literature. Neuroradiology 2000; 42: 211–214. 4. Macon M E, Armstrong L, Brown E M. 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TOP 10 CITED PAPER 2006-2008 International Journal of Obstetric anesthesia 491 Postdural puncture subdural hematoma 57 11. Mantia A M. Clinical report of the occurrence of an intracerebral hemorrhage following post-lumbar puncture headache. Anesthesiology 1981; 55: 684–685. 12. Newrick P, Read D. Subdural haematoma as a complication of spinal anaesthetic. Br Med J 1982; 285: 341–342. 13. Miyazaki S, Fukushima H, Kamata K, Ishii S. Chronic subdural hematoma after lumbar-subarachnoid analgesia for a cesarean section. Surg Neurol 1983; 19: 459–460. 14. Rudehill A, Gordon E, Rahn T. Subdural haematoma. A rare but life-threatening complication after spinal anaesthesia. Acta Anaesthesiol Scand 1983; 27: 376–377. 15. Jonsson L O, Einarsson P, Olsson G L. Subdural haematoma and spinal anaesthesia. A case report and an incidence study. Anaesthesia 1983; 38: 144–146. 16. Giamundo A, Benvenuti D, Lavano A, D’Andrea F. Chronic subdural haematoma after spinal anaesthesia. Case report. J Neurosurg Sci 1985; 29: 153–155. 17. Blake D W, Donnan G, Jensen D. Intracranial subdural haematoma after spinal anaesthesia. Anaesth Intensive Care 1987; 15: 341–342. 18. Beal J L, Royer J M, Freysz M, Poli L, Wilkening M. Acute intracranial subdural hematoma of arterial origin after spinal anesthesia. Ann Fr Anesth Reanim 1989; 8: 143–145. 19. Ortiz M, Aliaga L, Baturell C, Preciado M J, Aguilar J, Vidal F. Intracranial subdural haematoma - a rare complication after spinal anaesthesia. Eur J Anaesthesiol 1991; 8: 245–248. 20. Van de Kelft E, De la Porte C, Meese G, Adriaensen H. Intracranial subdural hematoma after spinal anesthesia. Acta Anaesthesiol Belg 1991; 42: 177–180. 21. Baldwin L N, Galizia E J. Bilateral subdural haematomas: a rare diagnostic dilemma following spinal anaesthesia. Anaesth Intensive Care 1993; 21: 120–121. 22. Akpek E A, Karaaslan D, Erol E, Caner H, Kayhan Z. Chronic subdural haematoma following caesarean section under spinal anaesthesia. Anaesth Intensive Care 1999; 27: 206–208. 23. Cantais E, Behnamou D, Petit D, Palmier B. Acute subdural hematoma following spinal anesthesia with a very small spinal needle. Anesthesiology 2000; 93: 1354–1356. 24. Acharya R, Chhabra S S, Ratra M, Sehgal A D. Cranial subdural haematoma after spinal anaesthesia. Br J Anaesth 2001; 86: 893–895. 25. Eggert S M, Eggers K A. Subarachnoid haemorrhage following spinal anaesthesia in an obstetric patient. Br J Anaesth 2001; 86: 442–444. 26. Sharma K. Intracerebral hemorrhage after spinal anesthesia. J Neurosurg Anesthesiol 2002; 14: 234–237. 27. Wells J B, Sampson I H. Subarachnoid hemorrhage presenting as post-dural puncture headache: a case report. Mt Sinai J Med 2002; 69: 109–110. 28. Kelsaka E, Sarihasan B, Baris S, Tur A. Subdural hematoma as a late complication of spinal anesthesia. J Neurosurg Anesthesiol 2003; 15: 47–49. 29. Slowinski J, Szydlik W, Sanetra A, Kaminska I, Mrowka R. Bilateral chronic subdural hematomas with neurologic symptoms complicating spinal anesthesia. Reg Anesth Pain Med 2003; 28: 347–350. 30. Alilou M, Halelfadl S, Caidi A, Kabbaj S, Ismaili H, Maazouzi W. Cranial subdural haematoma following spinal anaesthesia. Ann Fr Anesth Reanim 2003; 22: 560–561. 31. Tan S T, Hung C T. Acute-on-chronic subdural haematoma: a rare complication after spinal anaesthesia. Hong Kong Med J 2003; 9: 384–386. 32. Jack T M. Post-partum intracranial subdural haematoma. A possible complication of epidural analgesia. Anaesthesia 1979; 34: 176–180. 33. Edelman J D, Wingard D W. Subdural hematomas after lumbar dural puncture. Anesthesiology 1980; 52: 166–167. 34. Reinhold P, Lindau B, Bohm P. Chronic subdural haematoma following epidural anaesthesia. Anasth Intensivther Notfallmed 1980; 15: 428–431. 35. Deglaire B, Duverger P, Muckensturm B, Maissin F, Desbordes J M. Acute intracranial subdural hematoma after accidental dural 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. puncture in epidural anesthesia. Ann Fr Anesth Reanim 1988; 7: 156–158. Scott D B, Hibbard B M. Serious non-fatal complications associated with extradural block in obstetric practice. Br J Anaesth 1990; 64: 537–541. Wyble S W, Bayhi D, Webre D, Viswanathan S. Bilateral subdural hematomas after dural puncture: delayed diagnosis after false negative computed tomography scan without contrast. Reg Anesth 1992; 17: 52–53. Campbell D A, Varma T R. Chronic subdural haematoma following epidural anaesthesia, presenting as puerperal psychosis. Br J Obstet Gynaecol 1993; 100: 782–7844. Thons M, Neveling D, Hatzmann W. Intracerebral subdural hematoma after delivery with peridural catheter anesthesia. Z Geburtshilfe Perinatol 1993; 197: 235–237. Garcia-Sanchez M J, Prieto-Cuellar M, Sanchez-Carrion J M, Galdo-Abadin J R, Martin-Linares J M, Horcajadas-Almansa A. Chronic subdural hematoma secondary to an accidental dural puncture during lumbar epidural anesthesia. Rev Esp Anestesiol Reanim 1996; 43: 327–329. Cohen J E, Godes J, Morales B. Postpartum bilateral subdural hematomas following spinal anesthesia: case report. Surg Neurol 1997; 47: 6–8. Skoldefors E K, Olofsson C I. Intracranial subdural haematoma complicates accidental dural tap during labour. Eur J Obstet Gynecol Reprod Biol 1998; 81: 119–121. Diemunsch P, Balabaud V P, Petiau C, et al. Bilateral subdural hematoma following epidural anesthesia. Can J Anaesth 1998; 45: 328–331. Davies J M, Murphy A, Smith M, O’Sullivan G. Subdural haematoma after dural puncture headache treated by epidural blood patch. Br J Anaesth 2001; 86: 720–723. Ferrari L, De Sevin F, Vigue J P, Granry J C, Preckel M P. Intracranial subdural hematoma after obstetric dural puncture. Ann Fr Anesth Reanim 2001; 20: 563–566. Ezri T, Abouleish E, Lee C, Evron S. Intracranial subdural hematoma following dural puncture in a parturient with HELLP syndrome. Can J Anaesth 2002; 49: 820–823. Kardash K, Morrow F, Beique F. Seizures after epidural blood patch with undiagnosed subdural hematoma. Reg Anesth Pain Med 2002; 27: 433–436. Nolte C H, Lehmann T N. Postpartum headache resulting from bilateral chronic subdural hematoma after dural puncture. Am J Emerg Med 2004; 22: 241–242. Kayacan N, Arici G, Karsli B, Erman M. Acute subdural haematoma after accidental dural puncture during epidural anaesthesia. Int J Obstet Anesth 2004; 13: 47–49. Barash P, Cullen B, Stoelting R. Clinical Anesthesia. 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2001: 1152. Angle P, Thompson D, Halpern S, Wilson D B. Second stage pushing correlates with headache after unintentional dural puncture in parturients. Can J Anaesth 1999; 46: 861: 861–866. Vandam L D, Dripps R D. Long-term follow-up of patients who received 10,098 spinal anesthetics; syndrome of decreased intracranial pressure (headache and ocular and auditory difficulties). JAMA 1956; 161: 586–591. Loo C C, Dahlgren G, Irestedt L. Neurological complications in obstetric regional anaesthesia. Int J Obstet Anesth 2000; 9: 99–124. Ravindran R S, Viegas O J, Tasch M D, Cline P J, Deaton R L, Brown T R. Bearing down at the time of delivery and the incidence of spinal headache in parturients. Anesth Analg 1981; 60: 524–526. Sharshar T, Lamy C, Mas J L. Incidence and causes of strokes associated with pregnancy and puerperium. Stroke 1995; 26: 930–936. Witlin A G, Mattar F, Sibai B M. Postpartum stroke: A twenty-year experience. Am J Obstet Gynecol 2000; 183: 83–88. Lanska D J, Kryscio R J. Risk factors for peripartum and postpartum stroke and intracranial venous thrombosis. Stroke 2000; 31: 1274–1282. M.E.J. ANESTH 20 (4), 2010 492 58 International Journal of Obstetric Anesthesia 58. Reynolds A F, Salvin L. Postpartum acute subdural hematoma; a probable complication of saddle block analgesia. Neurosurgery 1980; 7: 398–399. 59. Cheek T G, Banner R, Sauter J, Gutsche B B. Prophylactic extradural blood patch is effective. A preliminary communication. Br J Anaesth 1988; 61: 340–342. 60. Colonna-Romano P, Shapiro B E. Unintentional dural puncture and prophylactic epidural blood patch in obstetrics. Anesth Analg 1989; 69: 522–523. 61. Trivedi N S, Eddi D, Shevde K. Headache prevention following accidental dural puncture in obstetric patients. J Clin Anesth 1993; 5: 42–45. 62. Scavone B M, Wong C A, Sullivan J T, Yaghmour E, Sherwani S S, McCarthy R J. Efficacy of a prophylactic epidural blood patch in preventing post dural puncture headache in parturients after inadvertent dural puncture. Anesthesiology 2004; 101: 1422–1427. Anis Baraka 63. Loeser E A, Hill G E, Bennett G M, Sederberg J H. Time versus success rate for epidural blood patch. Anesthesiology 1978; 49: 147–148. 64. Safa-Tisseront V, Thormann F, Malassine P, et al. Effectiveness of epidural blood patch in the management of postdural puncture headache. Anesthesiology 2001; 95: 334–339. 65. Beards S C, Jackson A, Griffiths A G, Horsman E L. Magnetic resonance imaging of extradural blood patches: appearances from 30 min to 18 h. Br J Anaesth 1993; 71: 182–188. 66. Ayad S, Demian Y, Narouze S N, Tetzlaff J E. Subarachnoid catheter placement after wet tap for analgesia in labor: influence on the risk of headache in obstetric patients. Reg Anesth Pain Med 2003; 28: 512–515. 67. Charsley M M, Abram S E. The injection of intrathecal normal saline reduces the severity of postdural puncture headache. Reg Anesth Pain Med 2001; 26: 301–305. review articles UPDATE ON ANESTHESIA CONSIDERATIONS FOR ELECTROCONVULSIVE THERAPY Cody Mayo*, Alan D. Kaye**, Erich Conrad***, Amir Baluch**** and E lizabeth F rost ***** Abstract Depression is diagnosed in 14 million Americans every year, and pharmacotherapy is the standard treatment. However, in approximately 50% of patients, pharmacology intervention does not resolve depression. Electroconvulsive therapy (ECT) has been a mainstay as a treatment option for treatment-resistant major depression since its inception in the 1930s. It has also been shown to be effective in treatment-resistant mania and catatonic schizophrenia. The complication rate of ECT has improved from 50% in the 1960’s to almost anecdotal adverse events, similar to the morbidity and mortality seen in minor surgery and childbirth. Although anesthetic agents are administered briefly, many patients experience significant fluctuations in physiologic parameters. The clinical anesthesiologist must be aware of these changes as well as have an understanding of perioperative pharmacological interventions. ECT is a proven therapy for select psychiatric patients, and appropriate anesthesia is a critical part of successful ECT. Careful review of the patient’s medical history may reveal pertinent anesthetic considerations. Introduction Electroconvulsive therapy has earned an evidence based niche in modern day psychiatry as a treatment for refractory major depression, mania and catatonic schizophrenia1,2. Traditionally, it was reserved primarily for the most gravely disabled patients who had failed numerous treatment options. However, ECT is a popular treatment option, and it is estimated that over 50,000 procedures take place annually3. Depression is diagnosed in 14 million Americans every year, and pharmacotherapy is the standard treatment. However, up to 50% of patients do not respond to the initial round of pharmacologic treatment4. Unfortunately, studies have shown that subsequent medication trials have decreasing rates of successful remission5. A meta analysis has shown ECT to be more effective than single or combination pharmacotherapy in achieving remission of major depression6. Elderly patients are also known to be more refractory to pharmacotherapy, but it is estimated that up to 50% will improve with ECT7. * ** Intern, Department of Internal Medicine, Methodist Hospital, Houston, Texas. Professor and Chairman, Department of Anesthesiology, Louisiana State University Health Science Center, New Orleans, Louisiana. *** Department of Psychiatry, Louisiana State University Health Science Center, New Orleans, Louisiana. **** Department of Anesthesiology, Jackson Memorial Hospital/University of Miami, Miami, Florida. ***** Clinical Professor, Mt. Sinai Department of Anesthesiology, New York, New York. Address Correspondence to: Alan D. Kaye, MD, PhD, DABPM, Professor and Chairman, Department of Anesthesiology, Professor, Department of Pharmacology, Louisiana State University School of Medicine, 1542 Tulane Ave, 6th floorAnesthesia, New Orleans, LA 70112, Tel: (504) 568-2319, Fax: (504) 568-2317, E-mail: [email protected] 493 M.E.J. ANESTH 20 (4), 2010 494 Some patients may notice an improvement in their symptoms after one or two sessions of ECT. However, the current practice in the USA is to administer three treatments weekly for two to four weeks. In Europe treatments are administered twice weekly and remission rates are lower2. The benefits of each individual treatment are theorized to build on one another, and response is usually attained between treatment 6 and 12. Some patients may require further treatment, or begin bi-monthly or monthly maintenance treatment if still symptomatic. To date, the exact mechanism of the effectiveness of ECT is unknown. In the earliest days of ECT, prior to proper anesthetic and paralytic control, injuries such as vertebral fractures and chipped teeth were common in up to 50% of patients1. The challenge for the anesthesiologist involves the complex effects, electrical and chemical, converging on the patient’s central nervous system (CNS) at the time of therapy. The anesthesiologist must find the balance between under-medicating, which risks physical injury from convulsion, and over-sedation, which can raise the seizure threshold, preventing a sufficient therapeutic seizure. The complication rate of ECT has improved from 50% in the 1960’s to almost anecdotal adverse events, similar to the morbidity and mortality seen in minor surgery and childbirth2. Physiologic Changes ECT involves placing electrodes on the head and applying a current of electricity for 2-8 seconds sufficient enough to induce a seizure lasting at least 30 seconds, which is considered to be the minimally effective length of time for a therapeutic seizure8. Typically, electrode placement is either bitemporal or bifrontal9. Most treatment centers begin with right unilateral placement in an effort to reduce the cognitive side effects of treatment. Subjective impairment of memory is the most common disturbing adverse event associated with treatment, which usually fully recovers in the weeks to months following treatment8. Understanding the physiologic changes that occur during the procedure allows the anesthesiologist to anticipate and limit complications. Most ECT morbidity results from adverse cardiovascular events10. As the electrical current is delivered, the parasympathetic Cody Mayo et. al nervous system is stimulated, primarily through direct neuronal stimulation of the hypothalamus to the vagal nerve8 resulting in transient sinus bradycardia, or rarely, asystole. Shortly thereafter, the sympathetic nervous system is stimulated, releasing catecholamines, which usually causes tachycardia, hypertension, and may lead to arrhythmias. ECT exerts several other effects on the central nervous system. When a seizure is induced, the metabolic demands of the brain are increased, doubling blood flow velocity through the middle cerebral artery in order to provide enough oxygen to the brain1. There may also be a significant increase in intracranial pressure if the autoregulatory mechanism is overwhelmed by an increase in peripheral blood pressure. Therefore, the presence of cerebral aneurysms and arteriovenous malformations (AVMs) are relative contraindications for ECT. Other relative contraindications to ECT include conditions associated with increased intracerebral pressure, space-occupying cerebral lesions (tumor), recent intracerebral hemorrhage, pheochromocytoma, and recent myocardial infarction8. Preoperative Management There is little time on the day of ECT to perform a detailed evaluation and, therefore, patients are typically seen in a preanesthetic assessment clinic ahead of time and have received medical clearance. Any preoperative evaluation starts with a directed history and physical. Many of these patients can be quite old including over 90 years of age, with poor dentition and body hygiene, and be very apprehensive. Consent may be difficult to obtain. Preoperative fasting status must be determined as patients often do not comprehend the need for withholding food and drink prior to even a short general anesthetic. Special attention should be paid to cardiovascular health, especially a history of myocardial infarction, congestive heart failure (CHF), hypertension (HTN), aneurysms, and arrhythmias, which should result in additional cardiac evaluation. Any focal signs of CNS pathology should result in further neurological assessment11. Documentation of an airway examination, allergies, and current medications should be included as well as informed written consent. Although bag masking is usually all that is required, airway equipment as indicated should be readily UPDATE ON ANESTHESIA CONSIDERATIONS FOR ELECTROCONVULSIVE THERAPY available. Also, standard ASA monitors for blood pressure, heart rate, temperature, oxygen saturation, and capnography should be used. The seizure is monitored via electroencephalogram (EEG), and a bite block is used to protect the patient’s dentition and tongue. Blood pressure and heart rate modulating agents need to be prepared if needed, typically including labetalol, esmolol, nitroglycerin and/or nicardipine. The risk of arrhythmia, ischemia and hypertension can be diminished with oxygenation and pretreatment with appropriate medication, discussed below. In general, a demand pacemaker should be converted to a non-sensing asynchronous mode with a magnet to disable rate responsiveness at the time of treatment; however, different models and brands each have slightly different considerations. Cardiology consultation should be obtained, if warranted, prior to treatment12. JCAHO requirement of side site documentation applies in all cases. Drug Interactions Usually, the condition requiring ECT is also treated pharmacologically, and potential drug interactions are important. Most psychiatric patients may be taking medications with anticonvulsant properties and these medications should be reduced prior to the procedure as tolerated since they increase the seizure threshold2. Anticonvulsants should be continued only in epileptic patients, and the medication withheld the morning of treatment to prevent inhibition of an adequate seizure. Lithium is a popular agent used in bipolar disorder and as an augmentation agent in treatment of refractory major depression. Lithium has been associated with post-procedure delirium and can prolong the effects of succinylcholine8. Even though benzodiazepines may help reduce anxiety before the procedure, their use increases the seizure threshold2. If they cannot be stopped, an option is to exchange long acting benzodiazepines for short-acting ones. Alternatively flumazenil may be used prior to the procedure and has shown no adverse effects on seizure quality1. Theophylline can significantly lower seizure threshold and prolong seizure duration, and this medication should be minimized or discontinued if possible prior to treatment8. Caffeine augments electroconvulsive seizures13. 495 There are very limited studies regarding interference of ECT from continuation of various psychiatric medications but controversy continues in this area. Intraoperative Considerations Successful ECT anesthesia should meet several requirements according to the American Psychiatric Association14. It should be administered by an anesthesiologist who is responsible for both the anesthesia and the cardiopulmonary management10. In general, the anesthesiologist aims to help provide a procedure with an adequate seizure duration, free of associated side effects and injuries, and a quick recovery. The goal of ECT is to induce a 30-60 seizure2. Therefore, only brief anesthesia is required. However, there are many anesthetic options that may be considered. The anesthetic’s properties, including half-life, recovery time, effects on the CNS, autonomic nervous system and cardiovascular systems and interaction with other drugs must be considered to tailor an appropriate therapeutic plan. Induction Agents Methohexital was for many decades the most commonly used induction agent because it has minimal effect on seizure threshold while providing quick induction and recovery. It is designated as “first choice hypnotic” by the American Psychiatry Association14. Methohexital has a wide therapeutic dose range of 0.5-1mg/kg and is easy to titrate. Thiopental is another barbiturate, but compared to methohexital, results in shorter seizure duration and is associated with increased hemodynamic changes1. Propofol has become a more popular choice, and multiple studies have been conducted comparing it to methohexital. Although propofol causes seizures of a shorter duration, the seizures are still of adequate length to provide full therapeutic benefit1. Propofol has repeatedly been shown to be associated with a milder hemodynamic response than methohexital1,15 Whether the drug provides a faster cognitive recovery is debatable. The most recent study available concluded that propofol is associated with a slightly quicker postictal recovery15. Because propofol can increase the seizure threshold, it should not be used in doses greater than 1mg/kg11, or M.E.J. ANESTH 20 (4), 2010 496 in patients for whom an adequate seizure duration with maximal stimulus is not obtained. Etomidate is another drug that may be considered. It has been repeatedly studied and is known to cause seizures of a longer duration than either propofol or methohexital. Unfortunately, etomidate is associated with increased confusion after ECT and longer recovery time16. However, because etomidate does not increase the seizure threshold, studies have shown its use requires significantly lower electrical currents17. Etomidate has also been associated with both reduced hemodynamic responses but higher rates of nausea. A recent small study comparing etomidate to propofol showed no significant difference in hemodynamic parameters18. Therapeutic doses in ECT range from 0.15-0.3mg/kg1. Volatile anesthetics, in particular sevoflurane, are also being studied for use in ECT. However, it has been concluded that sevoflurane offers no benefit over methohexital, yet is more time consuming to the physician16. One trial compared sevoflurane to thiopental and concluded sevoflurane lead to a quicker recovery with comparable hemodynamic changes19. Muscle Relaxants In addition to IV anesthetics, muscle relaxants are critical in ECT to prevent convulsions thus protecting the patient from musculoskeletal injury. Succinylcholine has been used in ECT since the 1950s and is still the muscle relaxant of choice3. It is contraindicated in patients with closed angle glaucoma, malignant hyperthermia potential, and malignant hyperthermia For ECT, doses up to 1mg/ kg may be used11. The anesthesiologist must be aware of patients with a history of pseudocholinesterase deficiency. When succinylcholine is contraindicated, mivacurium, rocuronium, or cis-atracurium are traditional alternatives (unless the patient has pseudocholinesterase deficiency). These agents are nondepolarizing muscle relaxants with significantly longer half-lives and thus, are not considered superior to succinylcholine in most instances. Attenuation of Hemodynamic Responses To attenuate the immediate parasympathetic discharge, which lasts 10-15 sec, pretreatment with IV Cody Mayo et. al atropine or glycopyrrolate is generally recommended. There is some controversy in the literature about the use of atropine on ever patient and some prefer glycopyrrolate because is causes less cognitive impairment since it does not cross the blood brain barrier16. The subsequent sympathetic discharge, which lasts 5-7 min can be attenuated by a wide variety of drugs including beta blockers, calcium channel blockers, nitrates, and the antiquated ganglion blockers. Typically, the psychiatrist and anesthesiologist communicate as to which agents will be administered during ECT, as there are slight regional variations. For patients with cardiovascular complications, esmolol or labetalol have been shown to be the most effective in controlling heart rate and mean arterial pressure5. Labetalol reduces BP spikes and cardiac dysrhythmias, but may also be associated with a shorter seizure duration. Esmolol is slightly preferred by some because it reduces peak systolic BP a little more than labetalol1. However, it may induce a dose-dependent bradycardia20 Verapamil 0.1mg pre-ECT decreases both heart rate and BP21, while nicardipine has only been proven to lower the BP. Nicardipine has not been proven to lower cerebral blood flow and may cause a baroreceptor induced reflex tachycardia20. Studies have also looked at the effects of adding remifentanil to a sedative hypnotic. Remifentanil appears to have no effect on the seizure duration but is effective in lowering the HR and BP for up to 3 min after the procedure22. Some studies have shown a decrease in seizure duration when remifentanil is added to methohexital, however in these studies, the dose of methohexital was also reduced by 40%. The myocardium has been another area of study. Many studies have failed to show either new ECG changes or troponin isoenzyme elevations after ECT. Twenty-four percent of the patients in these studies had cardiovascular disease, including conduction abnormalities, recent MIs and existing regional wall motion abnormalities23. Another study that used echocardiography to evaluate cardiac function during ECT found no evidence of new regional wall motion abnormalities and recommended beta blockers as the drug of choice to minimize heart rate and function changes24. UPDATE ON ANESTHESIA CONSIDERATIONS FOR ELECTROCONVULSIVE THERAPY In recent years research has attempted to correlate Bispectral index (BIS®) of electroencephalography (EEG) to the duration of and recovery from an ECT induced seizure. Entropy technology, from which several brands are now available with similar bioengineering, assesses the hypnotic state of an anesthetized patient. It may assist in indicating appropriate depth of anesthesia prior to seizure. White et al have shown that BIS® readings just after induction positively correlate to the duration of the seizure25. This potentially allows the clinicians to predict relative sufficiency of the induced seizure; however, limited data is available and more studies are warranted. Postoperative Concerns After the treatment, the awake and hemodynamically stable patient should be monitored for at least 30 minutes, usually by a psychiatric nurse or assistant known to the patient. Mental status should be noted and the patient observed for post-ictal delirium. A short-acting benzodiazepine such as lorazepam may be needed for agitation. Headache and muscle soreness are the most common complaints and may indicate that an increase in succinylcholine may be warranted at the 497 next treatment. Any decrease in pulse oxymetry should be evaluated for possible aspiration. Chest auscultation, X- ray and even blood gas analyses may be indicated. If the patient remains asymptomatic, discharge may still be possible.The patient is allowed to resume normal activity as tolerated and any medications that were held prior to the procedure should be restarted. Patients should not work or drive on the day of treatment. Conclusion ECT is a proven therapy for select psychiatric patients, and appropriate anesthesia is a critical part of successful ECT. The anesthesiologist aims to provide amnesia and musculoskeletal relaxation without increasing the seizure threshold. First line drugs are propofol and succinylcholine. The hemodynamic changes following the electric current are usually the only ones requiring management. In general, beta-blockers control heart rate and BP. However the anesthesiologist is also responsible for managing cardiopulmonary complications that may be present before the procedure as well as those that arise during ECT. Careful review of the patient’s medical history may reveal pertinent anesthetic considerations. M.E.J. ANESTH 20 (4), 2010 498 Cody Mayo et. al References 1. Wagner KJ, Mollenberg O, Rentrop M, Werne CR, Kochs EF: Guide to Anaesthetic Selection for Electroconvulsive Therapy. CNS Drugs; 2005, 19(9):745-758. 2. Taylor SM: Electroconvulsive Therapy: A Review of History, Patient Selection, Technique, and Medication Management Southern Medical Journal; 2007 May, 100(5):494-498. 3. Glass RM: Electroconvulsive therapy: time to bring it out of the shadows. JAMA; 2001, 285:1346–1348. 4. Lisanby SH: Electroconvulsive therapy for depression. N Engl J Med; 2007 Nov 8, 357(19):1939-45. 5. Rush AJ, Trivedi MH, Wisniewski SR, et al: Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report. Am J Psychiatry; 2006, 163:1905-1917. 6. Gabor G, Laszlo T: The efficacy of ECT treatment in depression: a meta-analysis. Psychiatr Hung; 2005, 20(3):195-200. 7. Mittmann N, Herrmann N, Einarson TR, et al: The efficacy, safety and tolerability of antidepressants in late life depression: a metaanalysis. J Affect Disord; 1997, 46(3):191-217. 8. Beyer JL, Weiner RD, Glenn MD: Electroconvulsive Therapy, A Programmed Text. 2nd Ed. Washington, DC: American Psychiatric Press. 1998. 9. Rasmussen KG, Varghese R, Stevens SR, et al. Electrode placement and ictal EEG indices in electroconvulsive therapy. J Neurophys; 2007, 19:453–457. 10.Saito S: Anesthesia Management For Electroconvulsive Therapy: hemodynamic and respiratory management. J Anesth; 2005, 19:142– 149. 11.Folk JW, Kellner CH, Beale MD, Conroy JM and Duc TA: Anesthesia for Electroconvulsive Therapy: A Review. The J of ECT; 2000 June, 16(2):157–170. 12.Rastogi S, Goel Sanjay, Tempe Deepak K, et al: Anaesthetic management of patients with cardiac pacemakers and defibrillators for noncardiac surgery. Annals of Cardiac Anaesthesia; 2005, 8:2132. 13.Francis A, Forchtmann L: Caffeine augmentation of electroconvulsive seizures. Psychopharmacology; 1994, 115:320324. 14.Weiner RD: American Psychiatric Association committee on electroconvulsive therapy. The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging. 2nd ed. Washington, DC: American Psychiatric Press. 2001. 15.Geretsegger C, Nickel M, Judendorfer B, Rochowanski E, Novak E, Aichhorn W: Propofol and methohexital as anesthetic agents for electroconvulsive therapy. J ECT; 2007 Dec, 23(4):239-43. 16.Ding Z, White PF: Anestheisa for electroconvulsive therapy. Anesth Analg; 2002, 94:1351–1364. 17.Avramov MN, Husain MM, White PF: The comparative effects of methohexital, propofol, and etomidate for electroconvulsive therapy. Anesth Analg; 1995, 81(3):596-602. 18.Rosa MA, Rosa MO, Marcolin MA, Fregni F: Cardiovascular effects of anesthesia in ECT: a randomized, double-blind comparison of etomidate, propofol, and thiopental. J ECT; 2007 Mar, 23(1):6-8. 19.Rasmussen KG, L aurila DR, Brady BM, L ewis CL, N iemeyer KD, Sun NM, Marienau ME, Hooten WM, Schroeder DR, Spackman TM: Anesthesia outcomes in a randomized double-blind trial of sevoflurane and thiopental for induction of general anesthesia in electroconvulsive therapy. J ECT; 2007 Dec, 23(4):236-8. 20.Zhang Y, White PF, Thornton L, Perdue L, Downing M: The use of nicardipine for electroconvulsive therapy: a dose-ranging study. Anesth Analg; 2005 Feb, 100(2):378-81. 21.Wajima Z, Yoshikawa T, Ogura A, Imanaga K, Shiga T, Inoue T, Ogawa R: Intravenous verapamil blunts hyperdynamic responses during electroconvulsive therapy without altering seizure activity. Anesth Analg; 2002 Aug, 95(2):400-2. 22.Van Zijl DH, Gordon PC, James MF: The comparative effects of remifentanil or magnesium sulfate versus placebo on attenuating the hemodynamic responses after electroconvulsive therapy. Anesth Analg; 2005 Dec, 101(6):1651-5. 23.O’Connor CJ, Rothenberg DM, Soble JS, Macioch JE, McCarthy R, Neumann A, Tuman KJ: The effect of esmolol pretreatment on the incidence of regional wall motion abnormalities during electroconvulsive therapy. Anesth Analg; 1996 Jan, 82(1):143-7. 24.Kadoi Y, Saito S, Takahashi K, Goto F. Effects of antihypertensive medication on left ventricular function during electroconvulsive therapy: study with transthoracic echocardiography. J Clin Anesth; 2006 Sep, 18(6):441-5. 25.White PF, Rawal S, Recart A, Thornton L, Litle M, Stool L. Can the bispectral index be used to predict seizure time and awakening after electroconvulsive therapy? Anesth Analg; 2003 June, 96(6):1636-9. MANAGEMENT OF OBSTETRIC HEMORRHAGE Amitava Rudra*, Suman Chatterjee**, Saikat Sengupta***, Ravi Wankhede***, Biswajit Nandi****, Gaurab Maitra***, and Jayanta Mitra**** Abstract Major obstetric hemorrhage is an extremely challenging obstetric emergency associated with significant morbidity and mortality. Pharmacological treatment of uterine atony has not altered much in recent years apart from the increasing use of misoprostol, although controversy surrounds its advantages over other uterotonics. Placenta accreta is becoming more common, a sequel to the rising caesarean section rate. Interventional radiology may reduce blood loss in these cases. Uterine compression sutures, intrauterine tamponade balloons and cell salvage have been introduced in the last decade. Keywords: Antepartum hemorrhage, postpartum hemorrhage, uterotonics. Obstetric hemorrhage is the world’s leading cause of maternal mortality1. Postpartum hemorrhage (PPH) accounts for the majority of these deaths1. The global maternal ratio of 402 deaths per 100,000 live births2 obscures the fact that 99% of these deaths occur in the developing world3. In addition, even in many developed countries, it is also the maternal complication for which the highest rate of substandard care is observed4. Furthermore, Zeeman’s5 study of obstetric critical care provision identifies hemorrhage as one of the most frequent reasons for admission to intensive care unit. Major obstetric hemorrhage accounts for 30% of cases6. Obstetric hemorrhage is often sudden, unexpected, and may be associated with coagulopathy. Blood loss can be notoriously difficult to assess in obstetric bleeds. Bleeding may sometimes be concealed and the presence of amniotic fluid makes accurate estimation challenging. Hence, early recognition and treatment are essential to ensure the best outcome. Therefore, it is important to have a thorough knowledge of the pathophysiology, etiology, and management strategies of obstetric hemorrhage. The initial assessment of a patient with an obstetric hemorrhage depends on its causes, but in general (1) Take a detailed medical and obstetric history and examine the patient to find the site and cause of the bleeding; (2) Empty the patient’s bladder; (3) Ensure that there are no retained products of conception or genital tract lacerations (anesthesia may be necessary); (4) Estimate blood loss; and (5) Assess the patient’s hemodynamic status and initiate appropriate resuscitation. Professor of Anesthesiology, K.P.C. Medical College, Kolkata., India. * ** Assistant Professor of Anesthesiology, Medical College & Hospital, Kolkata, India. *** Consultant Anesthesiologist, Apollo Gleneagles Hospital, Kolkata., India. ****Associate Consultant Anesthesiologist, Apollo Gleneagles Hospital, Kolkata., India. Corresponding author: Dr. A. Rudra, 1, Shibnarayan Das Lane, Kolkata.-700006, India. E-mail: [email protected] 499 M.E.J. ANESTH 20 (4), 2010 500 A. Rudra et. al Massive obstetric hemorrhage is variably defined as: blood loss more than 1500 ml, a decrease in hemoglobin more than 4 g/dl; or acute transfusion of more than 4 units; or patient receiving treatment for coagulopathy7. The gravid uterus receives up to 12% of the cardiac output, thus obstetric hemorrhage can be rapidly become life threatening. Classification of Obstetric Hemorrhage Antepartum Hemorrhage (APH) This is bleeding after 24 weeks gestation and before delivery. The causes include: l Placenta previa l Placental abruption l Trauma Mechanism of Hemostasis 8 l Uterine rupture After disruption of vascular integrity, mechanisms of hemostasis include (a) platelet aggregation and plug formation, (b) local vasoconstriction, (c) clot polymerization, and (d) fibrous tissue fortification of the clot. Contraction of the uterus represents the primary mechanism for controlling blood loss at parturition. Endogenous oxytocics effect myometrial contraction after delivery. Underestimation of peripartum hemorrhage is a frequent problem. Visual assessments typically underestimate the true amount of blood loss. Moreover, inadequate intravenous fluid administration is common. Hence, the primary problems were delayed recognition of hypovolemia and inadequate volume resuscitation. Table 1 Staging scheme for assessment of obstetric hemorrhage Primary Postpartum Hemorrhage This is defined as blood loss within 24 hours of delivery, which is > 500 ml following a vaginal delivery and > 1000 ml following a caesarean delivery. The causes include: l Uterine atony l Retained product of conception l Genital tract trauma l Clotting defects l Inverted uterus Secondary Postpartum Hemorrhage This is blood loss more than 24 hours after delivery. The causes include: Finding % Blood loss l Pre-eclampsia/HELLP syndrome None <15% to 20% l Intrauterine sepsis Tachycardia Mild hypotension l Pre-existing coagulopathy 20% to 25% Peripheral vasoconstriction l Incompatible blood transfusion l Retained dead fetus Tachycardia (100 to 120 bpm) Hypotension (SBP 80 to 100 mmHg) 25% to 35% Restlessness Oliguria Tachycardia (>120 bpm) Hypotension (SBP <60 mmHg) >35% Altered consciousness Anuria bpm = beats per minute; SBP = Systolic blood pressure ANTEPARTUM HEMORRHAGE Antepartum hemorrhage is a relatively frequent problem, occurring in 5% to 6% of pregnant women8. Recent evidence suggests that antepartum hemorrhage of unknown origin does produce more premature labor and delivery and subsequently, more fetal and neonatal problems9. Cases with abnormal placentation, usually placenta previa or placental abruption, can result in serious complications for both mother and child. Antepartum hemorrhage can also result in postpartum hemorrhage. MANAGEMENT OF OBSTETRIC HEMORRHAGE 501 The antepartum bleeding secondary to placenta previa or abruption is responsible for perinatal mortality rates as high as 22% and 37%, respectively10. intravascular coagulation in 10% of cases. However, if fetal demise occurs, the incidence is much higher (up to 50%)12. Placenta previa Placenta accreta Placenta previa is abnormally low implantation of the placenta in the uterus. Three types of placenta previa are defined, depending on the relationship between the cervical os (rather than the fetal presenting part itself). Placenta accreta is defined as an abnormally adherent placenta. Placenta accreta vera is defined as adherence to the myometrium without invasion of or passage through uterine muscle. Placenta increta represents invasion of the myometrium. Placenta percreta includes invasion of the uterine serosa or other pelvic structures. Any of these placental implantations can produce a markedly adherent placenta that cannot be removed without tearing the myometrium. 1. Complete previa (37%) - the internal os is completely covered. 2. Partial previa (27%) – the internal os is partially covered. 3. Marginal previa – Part of the internal os is encroached on by the placenta. The incidence varies between 0.5% to 1% of pregnancies, usually in association with prior uterine scarring such as a previous caesarean section, uterine surgery, or a previous placenta previa. Bleeding is caused by tearing of the placenta and its attachment from the decidua. The classic sign of placenta previa include: 1. Painless vaginal bleeding during the second or third trimester. 2. With the first episode of bleeding, contractions typically are absent. 3. Onset of bleeding is not related to any particular event. When the diagnosis of placenta previa suspected, the position of the placenta should be confirmed by ultrasonography11. Abruptio placentae Abruptio placentae is separation of a normally implanted placenta from deciduas basalis after 20 weeks of gestation and prior to delivery (incidence 0.2% to 2%). It is classified as mild, moderate, or severe. Fetal distress occurs because of loss of area for maternal fetal gas exchange. When the separation involves only the placental margin, the escaping blood can appear as vaginal bleeding. Alternatively, large volumes of blood loss (1-2 litres) can remain entirely concealed in the uterus. Chronic bleeding and clotting between the uterus and placenta can cause maternal disseminated The combination of a placenta previa and a previous uterine scar increases the risk significantly. In the general obstetric population, placenta accreta occurs in approximately 1 in 2500 and cannot be reliably diagnosed by ultrasonography. In patients with placenta previa and no previous caesarean sections, the incidence is 5% to 7%. With one previous uterine incision, the incidence of placenta accreta has been reported to be 24% to 31% and with two or more previous uterine incisions, the incidence rises to about 50% 13,14. Ultrasonography and MRI may be useful when abnormal placentation is suspected. However, they both have a poor sensitivity and the diagnosis is often made on opening the abdomen and uterus. Therefore, the anesthesiologist must keep in mind the possibility and be prepared to treat sudden massive blood loss. Uterine rupture Rupture of the gravid uterus can be disastrous to both the mother and fetus. Fortunately, it does not occur often. Uterine rupture can be associated with separation of a previous caesarean section and healed incision (scar) in the uterus, rapid spontaneous delivery, or excessive oxytocin stimulation. Moreover, trauma during attempted forceps delivery also may cause uterine rupture in a patient with an unscarred uterus. Overall, however, more than 80% of uterine ruptures are spontaneous and without an obvious explanation. The rupture of a classic uterine scar increases morbidity and mortality because the anterior uterine wall is highly vascular and also may include the area of placental implantation. Lateral extension of the rupture M.E.J. ANESTH 20 (4), 2010 502 A. Rudra et. al can involve the major uterine vessels and typically is associated with massive bleeding. Therefore, when vaginal birth is planned after a previous caesarean section, it is required that a surgical team, including an obstetrician, anesthesiologist, and nursing staff be available, so that emergency caesarean section can be initiated without delay should uterine rupture occur. POSTPARTUM HEMORRHAGE Bleeding after childbirth (postpartum hemorrhage) is an important cause of maternal mortality, accounting for nearly one quarter of all maternal deaths worldwide. Common causes for postpartum hemorrhage (PPH) include failure of the uterus to contract adequately after birth leading to atonic PPH, tears of the genital tract leading to traumatic PPH and bleeding due to retention of placental tissue. Atonic PPH is the most common cause of PPH and the leading cause of maternal death. Uterine atony Uterine atony is the leading cause of PPH, observed alone in 50% to 60% of cases, it presents as painless continuous bleeding, often developing slowly at the beginning. Blood can be concealed in the uterus and not exteriorized until external compression of the uterine fundus is performed. With up to 15% of maternal cardiac output at term supplying the gravid uterus, an atonic uterus can lose 2 liters of blood in 5 minutes. Atony is associated with “overdistension” of the uterus (multiparity, polyhydramnios, multiple gestation), as well as retained placenta, excessive oxytocin use during labor, and operative intervention. Initial management is medical – fluid resuscitation to restore blood volume; oxygen supplementation (high flows via face mask); bladder emptying, uterine massage, and uterotonics. This may allow avoidance of operative intervention. Among the uterotonics (Table 2) oxytocin is the initial therapy – up to 40 IU/ L infused as rapidly as possible15-18. Oxytocin is a systemic vasodilator, and may aggravate hypotension. Increasing this dose does not offer any benefit. Methylergonovine (Methergine) is a second line agent, though it is often bypassed in favour of the prostaglandin analog, carboprost (Hemabate). Neither methylergonovine nor carboprost should be administered intravenously – both are given intramuscularly. Methylergonovine is administered at a dose of 0.2 mg17; if two subsequent doses do not appropriately increase uterine tone, carboprost (0.25 mg) is administered either intramuscularly or into the myometrium. The total dose of carboprost should not exceed 1.5 mg. Both methylergonovine and carboprost have significant side effects. Methylergonovine is a peripheral vasoconstrictor; rapid intravenous injection can cause acute hypertension and cerebrovascular accident, and has been associated with pulmonary oedema and coronary vasospasm. Carboprost is a synthetic analog of prostaglandin F2α; it is a potent systemic and pulmonary vasoconstrictor, and bronchoconstrictor18. Intravenous administration can be associated with severe bronchospasm, and systemic and pulmonary hypertension, even intramuscular administration should be used with caution in asthma. Retained placenta This is the second most important etiology of postpartum hemorrhage (roughly 20% - 30% of cases), Table 2 Commonly used uterotonics Medication Class Administration Dosing Side effects Comments Oxytocin Neurohypophyseal Infusion Up to 40 IU/l Hypotension with rapid infusion Initial therapy Methylergonovine Ergot alkaloid Intramuscular 0.4 mg IM; repeat once Hypertension Sustained increase in uterine tone Carboprost Prostaglandin Intramuscular 0.25 mg 1M repeat up to 1.0 mg total Systemic & pulmonary hypertension, bronchospasm Never administer intravenously MANAGEMENT OF OBSTETRIC HEMORRHAGE but it must be systematically investigated first, because uterine atony is frequently associated and can be misleading12. It is suggested by the finding of an absent or incomplete delivery of placenta. Hence, uterus will not contract, and arteries of the deciduas basalis will continue to bleed. The degree of hemorrhage is often not severe, but it may be insidious, and visual estimates are inaccurate. The condition usually necessitates manual exploration of the uterus. Genital tract lacerations The most common injuries incurred at child birth are lacerations and hematomas of the perineum, vagina, and cervix. Most injuries have minimal consequence, but some puerperal lacerations and hematomas are associated with significant hemorrhage, either immediate or delayed. Genital tract lacerations should be suspected in all patients who have vaginal bleeding despite a firm, contracted uterus. The cervix and vagina must be inspected carefully in these patients. Retroperitoneal hematomas are dangerous because they can become large and develop insidiously, and treatment often requires exploratory laparotomy, blood transfusion, and possibly hysterectomy. Uterine inversion An atonic uterus and an open cervix allow the uterus to “turn inside out” through the birth canal. Fundal pressure and inappropriate traction on the umbilical cord to hasten placental delivery contribute to uterine inversion. The diagnosis is usually obvious. Clinical features include abdominal pain and often severe hemodynamic instability. Along with that a reflex bradycardia can be immediate by the effect of traction on the ligaments supporting the uterus. Uterine relaxation needed for reduction of the uterus with short-time tocolysis (trinitrite) as first line, using a potent vasopressor intravenously at the same time to counteract hypotension (phenylphrine or adrenaline)12. 503 cause of the bleeding; (b) empty the patient’s bladder; (c) ensure that there are no retained products or genital tract lacerations; (d) estimate blood loss; and (e) assess the patient’s hemodynamic status and initiate appropriate resuscitation. Monitor 1. Monitor ECG, blood pressure and oxygen saturation continuously. 2. Monitor urine output hourly. 3. Consider invasive monitoring if the patient is hemodynamically unstable or repeated venepunture is anticipated. Resuscitate The aim of resuscitation is to restore circulating blood volume and to maintain tissue perfusion: (a) high-flow oxygen (8L/min), (b) head-down tilt and left lateral tilt to avoid aorto-caval compression (if not yet delivered); (c) intravenous access (two 14 or 16 gauge cannula) and take blood for complete blood count, clotting and cross-match; (d) fluids: crystalloids, colloid (avoiding dextrans) and if necessary (not to exceed 3.5 liters prior to blood transfusion), blood; (e) O Rhesus negative blood should be immediately available, type specific cross-match will be time consuming; (f) try to avoid dilutional coagulopathy with emperical administration of clotting products, (g) accept hemoglobin of 8 gm/dl. As hypothermia impairs coagulation and shifting of oxygen dissociation curve to left (impair oxygen release at tissue level), fluids should be warned and the patient kept warm with active warming devices or warmed blankets. Appropriate correction of acidosis and hypocalcaemia is also required. Because timing is the essence, all members of the obstetric team should be familiar with the protocol (Box 1). Stop the Bleeding MANAGEMENT General The initial assessment of the patient with an obstetric hemorrhage depends on its cause, but in general (a) take a detailed medical and obstetrical history and examine the patient to find the site and Pharmacological 1) Oxytocin is the drug of choice for the prevention and treatment of atonic PPH. Five to 10 units are given slowly by intravenous bolus followed by an infusion of 10 units per hour. Vasodilation M.E.J. ANESTH 20 (4), 2010 504 A. Rudra et. al Health Organization takes a different view, concluding that oral misoprostol is more expensive, has more side effects, and, crucially, is less effective than oxytocin20. produced by oxytocin may cause hypotension in cardiac or hemodynamically unstable patients. 2) 3) Ergometrine (0.5 mg intravenously or intramuscularly) is as effective as oxytocin, however, intravenous administration possess undesirable effects. The agent is contraindicated in hypertensives due to its blood pressure raising effects. Prostaglandins: A) Hemabate (250 mcg intramuscularly or intramyometrially) contracts the walls of uterus. However, the agent has potential liability to cause life threatening bronchospasm19. B) Misoprostol can be administered orally, sublingually or rectally. Oral or sublingual prostaglandin may be useful in cases in which injectable uterotonics are not available or practical. However, the World Box 1 Bleeding parturient management Invasive/surgical iliac artery or uterine artery ligation (bleeding unresponsive to oxytocics) There is little in the literature to guide practice when pharmacological treatment fails. However, bimannual compression, uterine balloon tamponade, arterial embolization, uterine compression sutures, and uterine artery or internal iliac artery ligation are commonly practiced procedures. The review by Doumouchtsis et al21 of the conservative management of PPH found no statistical difference between the various methods, and the Cochrane collaboration22 failed to identify any relevant randomized control trials. (1) Bimannual compression l Provide early diagnosis, treat the cause l Follow general principles of resuscitation (airway, breathing, and circulation) l Call for help (2) Uterine balloon tamponade l Begin second large-bore intravenous line l Order blood tests (hemoglobin, coagulation screen, cross-match) l Order blood (hematology consultation?) l Provide crystalloid/colloid (Pentastarch) to maintain isovolaemia l Start high-pressure infusion system It has become a well-recognized alternative method of treatment in the conservative management of PPH in association with local or medical treatment, or in the event of their failure. This therapeutic approach avoids morbidity associated with peripartum hysterectomy and preserve fertility. The reported success rate of uterine artery embolization in the literature is more than 90% 24-27 . In most patients, fertility is preserved and normal menstruation returns almost 100%21. Minor complications such as pain and fever due to inflammation are rare (0% - 10%)27. More severe l Provide air warming blanket l Provide auto transfusion device? l Begin prompt treatment of clotting disorders l Monitor urine output l Consider use of vasopressors In the case of intractable PPH, Doumouchtsis et al21 proposes balloon tamponade as the most straight forward, rapid, and least invasive surgical option. An overall success rate of 84% has been reported 21,23. Various balloon devices have been used, with the Sengstaken–Blakemore esophageal catheter being the most frequently employed21. (3) Uterine arterial embolization l Begin arterial line (serial hemoglobin, coagulation studies) l Begin central venous pressure line (after stabilization) Compression of the uterus between one hand in the vagina and, another on the anterior abdominal wall, thereby reducing the bleeding. MANAGEMENT OF OBSTETRIC HEMORRHAGE 505 other interventions have failed, hysterectomy may be required to control bleeding and save life. The decision, however difficult, should be made sooner rather than later and prior to the development of coagulopathy. complications like pelvic infection, pulmonary embolism, or necrosis of uterus and bladder have been reported but are extremely rare28,29. Transfer to the radiology suite is usually done when vital signs are stable because facilities equipped to handle major bleeding are often much better in the operating room. Placement of arterial catheters and occlusion balloons before delivery is currently the treatment options of choice whenever major haemorrhage is highly suspected. These balloons can be used to reduce blood loss significantly while the patient is prepared to undergo embolization. (4) Uterine compression suture (B-Lynch suture) These are useful for patients with uterine atony who respond to bimannual compression. B-Lynch et al30 first described the compression suture in 1997 and others have since developed the technique using vertical31, transverse32, or multiple square suture33,34 to oppose the anterior and posterior walls of the uterus. Successful subsequent pregnancies have been reported, although evidence of fundal grooves from the sutures has been noted31. Uterine necrosis, intrauterine fibrous bands, abdominal adhesions, and pyometria are other noted complications35. (5) Arterial ligation Although ligation of internal iliac, uterine arteries can reduce pelvic blood flows and pulse pressure (85%) distal to the ligation, it may be ineffective if there are extensive collaterals. It can be useful in cases of uterine atony with a success rate of 84% has been described provided they are implemented quickly21. Bilateral ligation of these arteries does not appear to interfere with subsequent reproduction. (6) Peripartum hysterectomy As a last resort, but decided on quickly when all (7) Adjuncts There are some new techniques that are currently controversial and not universally accepted. These include the use of interventional radiology, methotrexate in placenta accreta, cell salvage as a means of reducing donor blood transfusion, tranexamic acid and factor VIIa to aid coagulation. Anesthesia Anesthetic management – both in choice and technique – should be based on a thorough understanding of the physiology of pregnancy and also on the pathophysiology of the problems. The existence of some of the obstetric risk factors may be known early in pregnancy from history and examination (Table 3). (A) Detection of anemia more than physiologic anemia of pregnancy is important because anemia at delivery increases the likelihood of blood transfusion. (B) Coagulation studies may be required in the presence of congenital (Von Willebrand’s disease) or acquired (DIC, dilutional coagulopathy, heparin) coagulation defects. (C) Imaging investigations are useful in the detection of placental abnormalities, with placenta previa and placenta accrete, the most important identifiable risk factors for massive hemorrhage. (D) Ultrasound studies identify placental location, and their ability to detect placenta accreta. In elective placenta previa cases, Royal College Table 3 Antenatal investigations and associated conditions Investigations Associated conditions Full blood count (including hemoglobin, platelets) Anaemia, thrombocytopenia Clotting screen (including fibrinogen, D-dimers) Abdominal ultrasound MRI Anticoagulants, DIC, Dilutional coagulopathy Placenta previa/accreta/increta/percreta Placenta accreta/increta/percreta M.E.J. ANESTH 20 (4), 2010 506 A. Rudra et. al of Obstetricians and Gynaecologists states that the choice of anesthetic is at the discretion of the anesthesiologist but there is increasing evidence to support the safety of regional anesthesia. If regional anesthesia is used, consideration should be given to a combined spinal epidural technique to allow time for surgery. As general anesthesia may be necessary, the patient should be fully prepared for conversion. For placenta accreta cases, although some centers advocate the use of regional anesthesia, general anesthesia may allow for more control11. During general anesthesia, prolonged induction – delivery and uterine incision – delivery intervals were associated with a higher incidence of low Apgar scores and acidotic babies. On the other hand, with spinal anesthesia in the absence of hypotension, a longer induction – delivery interval did not alter either the Apgar score or the acid-base values of the neonates. However, a uterine incision – delivery interval of more than 180 seconds was associated with a high incidence of low Apgar scores and acidotic infants; thus, might be related to reduced placental circulation. Advantages and disadvantages of regional vs. general anesthesia A. Regional Anesthesia 1. Advantages l Less blood loss. l Awake patient with less chance of aspiration. Moreover, parturient will be able to experience delivery of baby. 2. Disadvantages l Peripheral vasodilation hypotension. may exacerbate l General anesthesia may be necessary for patient’s comfort if a hysterectomy is necessary. B. General anesthesia 1. Advantages l Hemodynamic stability. l Security of the airway from the onset of the surgery. l Comfortable patient. 2. Disadvantages l Chance of difficult intubation, inability to intubate, and possible gastric aspiration. l Unconscious patient. In emergencies, hemodynamic instability and concerns over coagulopathy make general anesthesia the technique of choice. Nevertheless, if a working epidural is in place then cautious top-ups may be appropriate. A high-dependency setting is appropriate for at least half of those with a major obstetric haemorrhage11. The majority who do require intensive care do so only for mechanical ventilation and usually for less than 48 hours. An alternative to blood transfusion in the recovery period is intravenous iron. Ferrous sucrose has an excellent safety profile36. Accurate diagnosis and appropriate management of obstetric hemorrhage can reduce maternal morbidity and mortality. Conclusion Obstetric hemorrhage, a leading cause of maternal as well as fetal morbidity and mortality worldwide, can be masked by early pregnancy related physiologic adaptation and complicated by abnormal placentation, ammiotic fluid emboli and infections etiologies. Obstetric hemorrhage is often sudden, unexpected and may be associated with coagulopathy. Because approximately 600-700 ml blood flows through the placental intervillous spaces each minute, obstetric hemorrhage can rapidly result in severe signs of shock. Imaging technologies like ultrasound and magnetic resonance imaging have allowed earlier identification of the cause and institution of therapy for women at risk of hemorrhage. However, limitations in diagnostic sensitivity and specificity as well as the underestimation of blood loss and inadequate resuscitation remain common problems. Early recognition and treatment are essential to ensure the best outcome from these life threatening conditions. MANAGEMENT OF OBSTETRIC HEMORRHAGE 507 References 1. Lolonde A, Davis BA, Acosta A: Postpartum haemorrhage today: ICM/FIGO initiative 2004-2006. UGO; 2006, 94:243-253. 2. Hill K, Thomas K, Abouzahar C, et al: Estimates of maternal mortality worldwide between 1990 and 2005: an estimate of available data. Lancet; 2007, 370: 1311-1319. 3. Baid T: No woman should die giving life. Lancet; 2007, 370: 12871288. 4. Bouvier-Colle MH, Ould El Joud D, Varnoux N, et al: Evaluation of the quality of care for severe obstetrical haemorrhage in three French regions. BJOG; 2001, 108:898-903. 5. Zeeman G: Obstetrical Critical Care: a blue print for improved outcomes. Crit Care Med; 2006, 34: 208-214. 6. International Federation of Gynecology & Obstetrics. Prevention and treatment of postpartum haemorrhage. New advances for low score settings. ICM/FIGO. Joint Statement; November 2006. 7. Scottish Confidential audit and severe maternal morbidity. SPCERH Publication No. 27, 2006. 8. Mayer DC, Spielman FJ, Bell EA: Antepartum and postpartum hemorrhage. In: Chestnut DH (editor). Obstetric anesthesia. Principles and practice; 3rd edition. Philadelphia: Elsevier Mosby, 2004, pp. 662-82. 9. Chan CC, To WW. Antepartum haemorrhage of unknown origin what is its clinical significance? Acta Obstet Gynecol Scand; 1999, 78:186-190. 10.Nielson EC, Varner MW, Scott IR: The outcome of pregnancies complicated by bleeding during the second trimester. Surg Gynecol Obstet; 1991, 173:371-374. 11.Wise A, Clark V: Strategies to manage major obstetric haemorrhage. Curr Opin Anaesth; 2008, 21:281-287. 12.Mercier FJ, de Veldi MV: Major obstetric hemorrhage. Anesthesiol Cl N Am; 2008, 26:53-66. 13.Chattopadhyay SK, Kharif H, Sheerbani MM: Placenta Previa and accreta after caesarean section. Eur J Obstet Gynecol Reprod Biol; 1993, 52:151-156. 14.Clark SL, Koonings PP, Phelan JP: Placenta accreta and prior caesarean section. Obstet Gynecol; 1985, 66:89-92. 15.Palmer CM: Hemorrhage in Obstetrics. In: Palmer CM, D’Angelo R, Paech MJ (editors). Handbook of Obstetric Anesthesia; 2002, Bios Scientific Publishers Limited, Oxford. pp. 139-152. 16.Stoelting RK: Pharmacology and physiology in anesthesia practice; 1987, J. B. Lippincott Co. Philadelphia, pp. 394-414. 17.Douglas WJ, Ward ME: Current pharmacology and the obstetric anesthesiologist. Int Anesth Clin; 1994, 32:1-10. 18.Drug information for the Health Care Professional, 19th edition, vol. 1, 1999. World Color Book Services, Taunton, MA. pp. 782-784. 19.Harber C, Levy D, Chidambaram S, Macpherson M: Life threatening bronchospasm after intramuscular carboprost for postpartum haemorrhage. BJOG; 2007, 114:366-368. 20.World Health Organisation. WHO recommendations for the prevention of postpartum haemorrhage, 2007. 21.Doumouchtsis S: Papageorghiou A, Arulkumaran S. Systemic review of conservative management of postpartum hemorrhage: what to do when medical treatment fails: Obstetr Gynecol Surv; 2007, 62:540-547. 22.Mousa H, Alfirevic Z: Treatment for primary postpartum hemorrhage. The Cochrane Collaboration; January 2007. 23.Dabelea VG, Schultze PM, Mc Duffie RS: Intrauterine ballon tamponade in the management of postpartum hemorrhage. J Obstet Gynaecol; 2006, 107:38S. 24.Deux JF, Bazot M, Le Blanche A F, et al: Is selective embolization of uterine arteries a safe alternative to hysterectomy in patients with postpartum hemorrhage? A J R; 2001, 177:145-149. 25.Mitty HA, Sterling K M, Alvarez M, et al: Obstetric haemorrhage prophylactic and emergency arterial catheterization and embolotherapy. Radiology; 1993, 188:183-187. 26.Hong TM, Tseng HS, Lee RC, et al: Uterine artery embolization: an effective treatment for intractable obstetric haemorrhage. Clin Radial; 2004, 59:96-101. 27.Soncini E, Pelicelli A, Larini P. et al: Uterine artery embolization in the treatment and prevention of postpartum hemorrhage. Int J Gynaecol Obstet; 2007, 96:181-5. 28.Cottier JP, Fignon A, Tranquart F, et al: Uterine necrosis after arterial embolization for postpartum hemorrhage. Obstet Gynecol; 2002, 100:1074-1077. 29.Porcu G, Roger V, Jacquier A, et al: Uterus and bladder necrosis after uterine artery embolization for postpartum haemorrhage. Br J Obstet Gynecol; 2005, 112:122-123. 30.B-Lynch C, Coker A, Lawal A, et al: The B-Lynch surgical technique for the control of massive postpartum haemorrhage: an alternative to hysterectomy? Five cases reported. BJOG; 1997, 104:372-375. 31.Ghezzi F, Cromi A, Uccella S, et al: The hayman technique: a simple method to treat postpartum haemorrhage. BJOG; 2007, 114:362-365. 32.Ouahba J, Piketty M, Huel C, et al: Uterine compression suture for postpartum bleeding with uterine atony. BJOG; 2007, 114:619-622. 33.Cho J, Jun H, Lee C: Haemostatic suturing technique for uterine bleeding during caesarean delivery. Obstetr Gynecol; 2000, 96:129131. 34.Baskett T: Uterine compression sutures for postpartum haemorrhage. Efficacy, morbidity and subsequent pregnancy. Obstetr Gynecol; 2007, 101:68-71. 35.Ochoa M, Allaire A, Stitley M: Pyometria after haemostatic square suture technique. Obstetr Gynecol; 2002, 99:506-509. 36.Bhandal N, Russell R: Intravenous versus oral iron therapy for postpartum anaemia. BJOG; 2006, 113:1248-1252. M.E.J. ANESTH 20 (4), 2010 508 A. Rudra et. al scientific articles COMPARING TWO METHODS OF LMA INSERTION; CLASSIC VERSUS SIMPLIFIED (AIRWAY) Mohammad Haghighi*, Ali Mohammadzadeh*, Bahran Naderi*, Abbas Seddighinejad* and Homa Movahedi* Abstract Background: The aim of this study is to compare two methods of LMA insertion, "classic" versus "simplified" (AIRWAY), due to factors such as: time to insertion, number of attempts, blood stained LMA, air leak around LMA, and gastric inflation. The word "AIRWAY" refers to the similarity of this method to oropharyngeal airway insertion. Method: One hundred ASA class I and II patients elected for lower limb orthopedic surgery but without any head and face injury or head and neck abnormality, having their tooth intact, were selected and divided to two groups of fifty; classic and simplified. In the classic group, the index finger used as a guide, pushes the back of LMA towards the hard palate, inserting it into the pharynx till a resistance is felt and the LMA is then fixed it its place. In the AIRWAY group, the deflated LMA is entered into the mouth in a 180 degree insideout position compared to the classic method without using fingers and is proceeded until it enters the pharynx (sudden loss of resistance) and then returned 180 degree back to its normal position to be fixed in the right place. The attempt numbers, time to insertion, complications such as laryngospasm, blood stained LMA and gastric inflation is being investigated. Result: Demographic data such as age, sex and ASA class, demonstrate no meaningful statistic difference between the two groups. Successful first attempt in AIRWAY group (86%) had no meaningful statistic difference with the classic group (80%) (p>0.05). The overall success rate in LMA insertion (within two attempts) was 100% and 82% in AIRWAY and classic groups respectively (p>0.05) and 11 patients with failed insertion attempts, were excluded from the study. The time for successful insertion was meaningfully less in the AIRWAY group compared to the classic one (p<0.0001).In the classic group 32% of LMAs became blood stained compared to 16% in the AIRWAY group, which the difference was not meaningful. No other complications such as laryngospasm or oxygen desaturation occurred. Conclusion: Comparison of the whole advantages and disadvantages of both groups, mention that, by putting the LMA insertion time together with the low complication rates, the AIRWAY method can be assumed as a preferred simplified method with few complications for inserting LMA. Keyword: LMA, Facilated method insertion, Airway management From Dept. of Anesth. & Intensive Care Medicine, GUILAN Univ. of Medical Sciences, RASHT, Iran. * Assistant Professor of Anesthesia and Intensive Care. Corresponding author: Dr. Mohammad Haghighi, Department of Anesthesiology and Intensive Care Medicine, Guilan, University of Medical Sciences, Rasht, Iran. Tel: 0098 9113315256, Fax: 0098 1317764118. E-mail: [email protected] 509 M.E.J. ANESTH 20 (4), 2010 510 Introduction LMA has changed to a common alternative way in airway management. This instrument has been used more successfully by inexperienced staff and has given an appropriate way in managing the airway both in controlled and spontaneous breathing methods. Considering the problems of a successful airway management which occurs frequently in unauthorized people (e.g.: residents, health care centers staff) in ERs and trauma centers, LMA works as a supraglottic airway manager which is placed close to the larynx to let spontaneous or controlled ventilations with airway pressures less than 15 mmHg be applied5 even in prone and lateral positions1,2,3,4,6. There are several methods of inserting LMA none of them considered to be the definite one2,3, but all tend to decrease the complications7,8,9,10,11. One of these methods is the classic one, with LMA inflated a little and another method used in paralyzed patients is the triple airway maneuver with the patient's mouth opened, head extended and forward mandibular pressure12. In the standard method of inserting LMA usually the cuff is empty and the first attempt success rate is 672,3,11%90-. A little inflation of the cuff is useful in LMA passing posterior pharyngeal arch and eases the insertion resulting a higher success rate. Here the instrument is positioned midline and while having direct contact with patient's mouth and tongue is preceded forward into the pharyngeal space via some help from operator's hand in contact with the esophagus touching it with LMA's tip2,3,4,7,8. In this study we inserted the LMA with a new approach which is similar to the way an oral airway is inserted and thus is named the AIRWAY method. This method was first practiced as a pilot on 20 cases and demonstrated itself as an easier method with less complications besides not having those problems such as hand entrance into patient's mouth and contact with patient's tooth which can be harmful13,14. Patients and Methods In this study which was performed on the first 6 months of 1386 in Pursina educational hospital, one hundred ASA class I and II parents candidate for limb M. Haghighi et. al orthopedic surgery but without any head and facial injury or head and neck abnormality, having their tooth intact, were selected and divided into two groups of fifty; classic and simplified (airway). Informed contest was achieved from the patients and any patient having any contraindications for LMA insertion was excluded. Insertions were performed randomly by anesthesiologists with at least 100 successful LMA insertions. Two groups of 50; named AIRWAY (facilitated) and CLASSIC were studied. In the classic method, the index finger is used as a guide which by pushing the back of LMA towards the hard palate, slides it into the pharynx up to the point of feeling a resistance. The LMA cuff is then filled with an appropriate volume of air and then fixed in place. In the airway method the LMA without being primarily filled with air, is turned in a 180 degree inside-out position compared to the classic position and is inserted into the patient's mouth without contacting the anesthesiologist's hand till there is a sudden loss of resistance due to pharyngeal entrance, and then is returned 180 degree to the normal position and inserted in the pharynx (Figure 1-6). Induction of anesthesia was done with fentanyl (12-μg/kg), TPN (46-mg/kg), Succynilcholine (0.5mg/ kg). Maintenance was with Halothane and O2/N2O (50%/50%) while the patient breathing spontaneously. All patients received ECG, SpO2 & ETCO2 monitoring while airway management efficacy was supervised by bilateral auscultation, chest wall movement and no resistance in inspiration and expiration and finally confirmed by ETCO2. Insertion ease was considered as the time needed for LMA insertion from the beginning to ventilation confirmation. The number of insertion efforts and complications such as laryngospasm, blood-stained LMA and abdominal distention was also evaluated. Epigastric area auscultation during manual ventilation was done and if insertion failed it was repeated by giving repeated doses of TPN and after the third failure, alternative methods were used for airway management. Airway efficiency and patency and LMA position was checked by a resident who didn't know anything COMPARING TWO METHODS OF LMA INSERTION; CLASSIC VERSUS SIMPLIFIED (AIRWAY) Figire 1 The patient candidate for LMA insertion Figire 4 LMA direction to pharynx Figire 2 Without hand contact Figire 5 The 180˚ rotation of LMA Figire 3 LMA insertion as airway method Figire 6 Total insertion of LMA 511 M.E.J. ANESTH 20 (4), 2010 512 M. Haghighi et. al about the patient's group and air leak was detected by giving 20 CmH2O pressure and divided into grade 1: no leak; grade 2: palpable leak; grade 3: just palpable leak with appropriate ventilation; grade 4: audible leak with inappropriate ventilation and grade 5: complete obstruction with no ventilation. age, weight, and ASA class had also no difference (Table 1). Because the airway method compared to the classic method increases the first attempt success rate from 70% to 95% so with α = 0.05 and power of 90%, the number of patients in each group was calculated as 50. Successful first attempt insertion rate in airway group was 86% compared to classic group as 80% with no meaningful difference (p>0.05). The data collected was analyzed be SPSSver 10 and compared in two groups with unpaired T-Test or MANWITHNYU by case. Again Chi-square test was used to analyze numerical data and p<0.05 was considered as meaningful. Results One hundred patients entering in two groups of 50, the classic group contained 36 male and 14 female and the airway group 41 and 9 respectively with no meaningful difference. Demographic data such as In the classic group 90% of patients had LMA number 4 and 10% number 3 and in the airway group 86% and 14% respectively, which showed no meaningful difference. Eleven patients were excluded from the study because of unsuccessful insertion. The successful insertion time was meaningfully shorter in airway group than classic (p<0.0001). Blood stained LMA rate was 32% in classic and 16% in airway group with no meaningful difference. No laryngospasm or SpO2 decrease occurred. Gastric distention from positive pressure ventilation was meaningfully more in classic than airway group. Air leak was 76% in grades 1 and 2 and 24% in grade 3 of the classic group compared to 88% and 12% in airway group respectively with no meaningful difference (p>0.05). Table 1 Demographic, monitoring and Parameters complication data parameter Classic group Airway group P value Age (years) (mean ± SD) N = 50 30 ± 9.4 N = 50 32 ± 7.9 ns Weight (kg) (mean ± SD) 68 ± 9.6 10.7 ± 70 ns 3614/ 419/ ns ----- ----- 372 ± 51 363 ± 33 4 90%)45( 86%)43( 3 10%)5( 14%)&( sex m/f Use of facilitative method Thiopental Na(mg) size LMA ns ns No .Of attempt( n) ns 1 80%)40( 86%)43( 2 12%)6( 14%)7( 3 8%)4( ----- Time of successful insertion(min) 21.7 ± 4.8 10.6 ± 3.7 6 <0.0001 Blood on LMA (n) (16)32% (8)16% 0.06 Gastric insuffilation (n) (11)22% (5)10% ns Leak around the cuff (n) Grade 1 Grade 2 Grade 3 (20)40% (18)36% (12)42% (22)44% (22)44% (6)12% ns ns ns COMPARING TWO METHODS OF LMA INSERTION; CLASSIC VERSUS SIMPLIFIED (AIRWAY) Discussion Using airway method is shown to be more successful in LMA insertion in terms of time needed compared to classic method. Analyzed data demonstrated less time needed in airway method. The disadvantage of standard method of inserting LMA is that in this form, LMA slides over the tongue and may displace the tongue and epiglottis posteriorly but the alternative methods such as semi-filled or lateral usually make less mechanical insult and easier LMA passage. The results show 80% success rate in the first attempt. In airway method there was a 86% success rate in first attempt and 14% in the second one. Condra et al had 97% and 100% success rates respectively probably due to lower LMA cuff volume which couldn't prevent posterior displacement of the tongue as well. A variety of LMA insertion methods have been discussed. In Dingley et al study in Wales, 30% of invertors used the original method while 34% used the alternative ones like semi-filled for laryngoscopic procedures. Wakeling et al mentioned LMA complete filling for facilitating its insertion and lessening mucosal damage. Dingley's studied about sore throat in 3 groups13 which showed that using insertion aid lowers the complications. Nagai S. et al used the modified method for pediatric LMA insertion15, rotating it 90 degree and after inserting two thirds of it through the larynx them re-rotating it and leading it deeply. 513 Nakayama studied 145 pediatric cases using rotating versus routine method9. The success rate in first and second attempt was 99% versus 751,2,3,4% using semi-filled method simultaneously which changed the rates to 96% and 100% respectively. One of our limitations was blinding the LMA insertion time and the number of attempts. We used another person for recording the results to lessen the bias of time and number of attempts. Airway method insertion facilitates LMA passage towards the larynx and sliding over the tongue. Successful attempts correlates well with complications such as hypoxia, laryngospasm, and trauma, due to the number of attempts (secondary to light anesthesia and mucosal damage). Complications in two groups were not in a meaningful range but further studies with larger groups may give more acceptable results. Gastric distention due to displacement of LMA is appropriate in airway group which can be considered as a success factor. Many methods including low inflation, jaw trust, LMA insertion education, airway axis usage, fiberoptic bronchoscopic insertion and NGT guidance all have advantages and disadvantages3,6,7,8,4,5. Our study doesn't need low inflation, special maneuvers such as jaw trust and aiding instruments. This method is known as a facilitating method for LMA insertion7,8,9,11,10. Overall comparison of success and failure rates in this method including the insertion time, shows that the airway method can be considered as a facilitating method with low complication rates. Further studies with larger groups are needed to clarify the differences between different methods. M.E.J. ANESTH 20 (4), 2010 514 M. Haghighi et. al References 1. Brain AIJ: The laryngeal mask-a new concept in airway management. Br J Anaesth; 1983, 55:801-805. 2. Wakeling HG, Butler PJ, Baxter PJ: The laryngeal mask airway: a comparison between two insertion techniques. Anesth Analg; 1997 Sep, 85(3):687-90. 3. Lopez-Gill M, Brimacombe J, Alvarez M: Safety and efficacy of the laryngeal mask airway. Anesthesia; 1996, 51:969-972. 4. Dingley J, Asai T: Insertion methods of the laryngeal mask airway: a survey of current practice in Wales. Anaesthesia; 1996, 51:596599. 5. Gursoy F, Algren JT, Skjonsby BS: Positive pressure ventilation with laryngeal mask airway. Anesth Analg; 1996, 82:33-38. 6. Dingley J, Baynham P, Swart M, Vaughan RS: Ease of insertion of the laryngeal mask airway by inexperienced personnel when using an introducer. Anesthesia; 1997 Aug, 52(8):756-60. 7. García-Aguado R, Viñoles J, Brimacombe J, Vivo M, LópezEstudillo R, Ayala G: Suction catheter guided insertion of the ProSeal laryngeal mask airway is superior to the digital technique. Can J Anaesth; 2006 Apr, 53(4):398-403. 8. Brimacombe J, Keller C, Judd DV: Gum elastic bougie-guided insertion of the ProSeal laryngeal mask airway is superior to the digital and introducer tool techniques. Anesthesiology; 2004 Jan, 100(1):25-9. 9. Nakayama S, Osaka Y, Yamashita M. The rotational technique with a partially inflated laryngeal mask airway improves the ease of insertion in children. Paediatr Anaesth; 2002 Jun, 12(5):416-9. 10.Hsu YW, Pan MH, Huang CJ, Cheng CR, Wu KH, Wei TT, Chen CT: Comparison of the cuffed oropharyngeal airway and laryngeal mask airway in spontaneous breathing anesthesia. Acta Anaesthesiol Sin; 1998 Dec, 36(4):187-92. 11. Matta BF, Marsh DS, Nevin M: Laryngeal mask airway: a more successful method of insertion; 1995 Mar, 7(2):132-5. 12.Aoyama K, Takenaka I, Sata T and Shigematsu A: The triple airway maneuver for insertion of the laryngeal mask airway in paralyzed patients. Can J Anesth; 1995, 42:1010-1016. 13.Brimacombe J, Holyoake L, Keller C, Brimacombe N, Scully M, Barry J, Talbutt P, Sartain J, McMahon P: Pharyngolaryngeal, neck, and jaw discomfort after anesthesia with the face mask and laryngeal mask airway at high and low cuff volumes in males and females. Anesthesiology; 2000 Jul, 93(1):26-31. 14.Dingley J, Whitehead MJ, Wareham K: A comparative study of the incidence of sore throat with the laryngeal mask airway. Anaesthesia; 1994 Mar, 49(3):251-4. 15.Nagai S, Inagaki Y, Harada T, Watanabe T, Hirosawa J, Ishibe Y: A modified technique for insertion of the laryngeal mask airway in children. Masui; 2000 Dec, 49(12):1367. PRETREATMENT WITH REMIFENTANIL IS ASSOCIATED WITH LESS SUCCINYLCHOLINE-INDUCED FASCICULATION Karim Nasseri**, Mehdi Tayebi Arastheh* and S hoaleh S hami ** Abstract Background: Succinylcholine is a popular muscle relaxant and one of its most common side effects is muscle fasciculation. The purpose of this study was to evaluate the efficacy of remifentanil in preventing succinylcholine-induced fasciculation in patients undergoing general anesthesia. Methods: In a prospective, double blind study, 60 ASA I & II patients were randomly assigned into two groups (30 each) to receive either remifentanil1 µg/kg (Group R), or saline 3 ml (Group S) as a pretreatment agent, one minute before induction of general anesthesia by propofol, fentanyl, and 1.5 mg/kg succinylcholine. The duration and the intensity of fasciculation were assessed using a four-point rating scale. Data were analyzed by Mann-Whitney U-test, Fisher exact test and Student-t-test using SPSS software. Results: In the remifentanil group the duration (p<0.001) and the intensity (p<0.001) of fasciculation were lower compared to the saline group. However the incidence of bradycardia was higher in the remifentanil group in comparison to the group which received normal saline. Conclusions: Our findings indicate that remifentanil can reduce the duration and the intensity of succinylcholine induced fasciculation. However, it induces greater bradycardia. Key words: remifentanil, succinylcholine, propofol, fasciculation. From Departments of Anesthesia and Intensive Care and Faculty of Nursing and Midwifery. * Kurdistan University of Medical Sciences, Sanandaj, Iran. ** Faculty of Nursing and Midwifery. Corresponding author Dr. Karim Nasseri: Be’sat Hospital, Keshavarz St, Sanandaj, Iran. Tel: +989183715405, Fax: +988716664663. E-mail: [email protected]. 515 M.E.J. ANESTH 20 (4), 2010 516 Introduction Succinylcholine survives into its sixth decade (1952 to the present) by distinctive advantages, namely, low cost, fast onset of action, fast recovery, excellent muscular relaxation, and nontoxicity of its metabolites1. However, it has some undesirable side effects, such as fasciculation and postoperative myalgia. Numerous methods have been used to alleviate or attenuate fasciculation2,3. Although these methods were helpful to a certain extent, each one had drawbacks of its own. Remifentanil is a synthetic and esterasemetabolized opioid with a rapid onset, an ultra-short duration of action and a stable, short context-sensitive half time compared with other opioids4,5. Recent studies have suggested that propofol in combination with remifentanil may have muscle relaxant properties and could provide adequate conditions for laryngoscopy and tracheal intubation without using muscle relaxants6,7. We designed a prospective double blind, randomized study to evaluate the effectiveness of remifentanil in preventing fasciculation following succinylcholine injection in patients anesthetized with propofol, fentanyl, and succinylcholine. Methods After approval by our institutional Ethics Committee and procurement of patients’ written informed consent, we studied 60 adult patients, ASA physical status I or II, scheduled for ambulatory urological or gynecological surgery under general anesthesia. This study was carried out in the Be’sat Hospital, Keshavarz St. Sanandaj, Iran. Exclusion criteria included known allergy to the pretreatment agent arrhythmia, hypo-or hypertension, dehydration, hyperkalemia, increased intraocular pressure, increased intracranial pressure, history of malignant hyperthermia, presenting a difficult airway, pregnancy, treatment with any drug known to interact with neuromuscular function, and significant renal, neuromuscular, or hepatic disease. The observer and the patients were unaware of the pretreatment used and patients were randomized using computer-generated random numbers into two groups K. Nasseri et. al (30 each) in accordance to the pretreatment designed: NaCl 0.9% (control), and remifentanil 1µg/kg (study) that were always adjusted to a 3-mL volume. Standard monitoring included ECG, non-invasive oscillometric blood pressure, pulse oximetry, and end-tidal carbon dioxide levels. No agent was given for premedication. The induction regimen was standardized for all patients and consisted of the following: At time 0, injection of fentanyl 1 µg/kg together with the pretreatment designed for each group; 2 min later, anesthesia was induced with propofol 2 mg/kg IV and succinylcholine 1.5 mg/kg. Following succinylcholine, the patient was observed by an observer who was unaware of patient’s group and fasciculation was graded according to a 4-point rating scale8: no fasciculation = 0. mild, fine fasciculation of the eyes, neck, face or fingers without limb movement = 1. moderate fasciculation occurring at more than two sites or obvious limb movement = 2. vigorous or severe, sustained, and widespread fasciculation = 3. Changes in the cardiac rhythm or blood pressure following induction of anesthesia were also recorded. Patients were ventilated via face mask and none of them intubated. Anesthesia was maintained with a mixture of N2O/O2 60%/40% with isoflurane11.3%. Sample-size calculation was performed based on the pilot study, in that, the incidence of fasciculation was 96%, and we aimed at detecting a decrease to less than 50% with remifentanil pretreatment. With a power of 80% and type 1 error of 5%, we calculated that 30 subjects were required per group. Statistical analysis was performed using SPSS 14.0 for Windows. Demographic data were analyzed by using the Mann-Whitney U-test. The incidence and the intensity of fasciculation were analyzed using Fisher’s exact test and Student-t-test. Student’s t-test was used to analyze bradycardia and arrhythmia between the two groups. A value of P <0.05 was considered statistically significant. PRETREATMENT WITH REMIFENTANIL IS ASSOCIATED WITH LESS SUCCINYLCHOLINE-INDUCED FASCICULATION Results Demographic data showed there was no ststistical difference balance Groups R & S (Table 1). Table 1 Demographic data and duration of surgery in Groups R-S Age (years) Group R (n = 30) 31.3 ± 11.7 Group S (n = 30) 37.8 ± 13.7 0.6 Weight (kg) 67.4 ± 10.9 69.4 ± 12 0.5 16:14 7 (2.4) 19:11 8 (3.1) 0.6 0.9 Gender ratio (m/f) Duration of surgery (min) P Group R: Remifentanil. Group S: Saline 0.9% Values are mean ± sd or numbers (gender ratio). The duration and the intensity of muscle fasciculation were significantly reduced by pretreatment with remifentanil as compared to that of saline: (P<0.05) (Table 2). Table 2 The duration and the intensity of muscle fasciculation in Group R & S Pretreatment Group R Group S Differeces (95% (n = 30) (n = 30) CI) Intensity 0(n) 4* 1 1(n) 20* 12 2(n) 5* 10 3(n) 1* 7 Duration(second) 21.4(17.8) 41.9(20.6)* 20.5(10.2-30.9) Group R: Remifentanil. Group S: Saline 0.9% * P<0.05 compared with Group NS. Baseline MAP and HR values were not significantly different between the two groups. However, after induction of anesthesia, MAP decreased significantly in group remifentanil compared to baseline values (P<0.05). The percentage decrease in MAP values from baseline was significantly higher in Group remifentanil than in Group saline (16.6% ± 11.8 vs. 6.3% ± 10.7); (P<0.05). Ephedrine was not used in any patient. Following induction of anesthesia, HR decreased in Group remifentanil compared to baseline (P<0.05); whereas, HR in Group saline did not show significant changes compared to baseline. Also, the percentage change from baseline HR values was significantly higher in Group remifentanil than in Group saline (19.2% ± 9.7 vs. 2.9% ± 12.4). In Group remifentanil, eight patients developed a decrease of HR by more than 517 20% from baseline necessitating the use of atropine, while in Group saline none of the patients required atropine (P<0.05). Discussion Succinylcholine is the relaxant of first choice for endotracheal intubation and for short operative procedures requiring good muscular relaxation. However, its use is associated with considerable fasciculation. Fasciculation have been attributed to a prejunctional depolarizing action of succinylcholine, resulting in repetitive firing of the motor nerve terminals and antidromic discharges that manifest as uncoordinated muscle contractions9. To solve this problem, several preventive methods had been tried including: pre-treatment with a small dose of nondepolarizing muscle relaxant10, Pre-treatment with lignocaine11, diazepam12, magnesium sulphate13, highdose Propofol14, and self-timing of succinylcholineinduced fasciculation15. Few studies have been designed to evaluate the effect of pretreatment with opioids on succinylcholine induced fasciculation, none of them used remifentanil. Lindgren and colleagues designed16 a prospective study to compare the effects of tubocurarine, alcuronium, pancuronium, and fentanyl on muscle fasciculation associated with succinylcholine in 171 children undergoing otolaryngological surgery. They concluded that the most effective pre-treatment was fentanyl (2.0 µg/kg) followed, in order, by alcuronium, fentanyl (1 µg/kg), tubocurarine and pancuronium. In another study with a different design, the same authors evaluated the change in intragastric pressure after the administration of succinylcholine in 32 children pretreated with physiological saline or alfentanil 50 µg/kg. anesthesia was induced with thiopentone 5 mg/kg. They concluded that alfentanil 50 µg/kg effectively inhibits the incidence and the intensity of succinylcholine induced muscle fasciculation, moreover, intragastric pressure remains in control values17. Yli-Hankala and colleagues18 studied the effects of alfentanil on succinylcholine induced muscle fasciculation, in a double blind study in 34 children and M.E.J. ANESTH 20 (4), 2010 518 30 adults. They concluded that alfentanil significantly decreased the intensity of visible fasciculation caused by succinylcholine. In children the duration of muscle fasciculation was shorter in the alfentanil group than in the control group. In adults, the intensity rather than the duration of fasciculation was attenuated by alfentanil. The inhibition of fasciculation caused by alfentanil was demonstrated in children in electromyogram recorded on the biceps muscle. Our results demonstrated the efficacy of 1 µgkg remifentanil in reducing both the incidence and the intensity of fasciculation. All patients of our study received fentanyl as premedication, and propofol as anesthesia inducing agent, so fentanyl and/or propofol could not here influenced the results. The mechanism of the inhibitory action of remifentanil on succinylcholine induced muscle fasciculation is unclear. Remifentanil is a new synthetic μ opioid agonist that is characterized by a rapid onset of action due to a short blood-effect site equilibration half-time and a rapid offset of action due to its high clearance by nonspecific blood and tissue esterases19. On the other hand, Propofol has been shown to decrease muscle tone in a dose-dependent manner in clinical use, and this effect is attributed not only to the central nervous system depression but also to a block in the skeletal muscle sodium channels14. Additionally, the administration of propofol 3.5 mg/ kg may attenuate both the incidence and the intensity K. Nasseri et. al of muscle fasciculation14. All patients in our study received an induction dose of propofol (2 mg kg-1), that did not attenuate fasciculation20,21. Propofol and remifentanil are both shortacting anesthetic agents that complement each other pharmacodynamic profiles (i.e., hypnosis, analgesia and return of consciousness)19. In a report, the pharmacodynamics of remifentanil and its interaction with propofol were investigated. The authors reported that propofol reduces remifentanil requirements to suppress responses to laryngoscopy, intubation, and intra-abdominal surgical stimulation in a synergistic manner19. Remifentanil combined with propofol is therefore a promising combination for preventing succinylcholine induced muscle fasciculation. There are some limitations with this study. First, the study design was observational, and we measure a subjective variable (fasciculation) rather than objective variables (increase in potassium, myoglobin, and CPK).The objective variables are not as easy to measure as fasciculation22. Second: We evaluated only remifentanil; therefore, comparisons to other drugs especially non depolarizing muscle relaxants, cannot be made. In conclusion, we believe that remifentanil 1 µg/kg administered for induction of anesthesia is capable of reducing the incidence and the intensity of succinylcholine-induced fasciculation, however, it can concomitantly induce bradycardia. PRETREATMENT WITH REMIFENTANIL IS ASSOCIATED WITH LESS SUCCINYLCHOLINE-INDUCED FASCICULATION 519 References 1. Chingmuh Lee, Ronald L. Katz: Clinical implications of new neuromuscular concepts and agents: So long., neostigmine! So long, sux!. Journal of Critical Care; 2009,24(1):43-49. 2. Yanez P, Martyn JA: Prolonged d-tubocurarine infusion and/or immobilization cause upregulation of acetylcholine receptors and hyperkalemia to succinylcholine in rats. Anesthesiology;1996, 84(2):384-91. 3. Kopman AF, Klewicka MM, Ghori K, Flores F, Neuman GG: Dose-response and onset/offset characteristics of rapacuronium. Anesthesiology; 2000, 93(4):1017-21. 4. Egan TD: Remifentanil pharmacokinetics and pharmacodynamics.A preliminary appraisal. Clin Pharmacokinet; 1995, 29:80-94. 5. Egan TD, Minto CF, Hermann DJ, Barr J, Muir KT, Shafer SL: Remifentanil versus alfentanil: comparative pharmacokinetics and pharmacodynamics in healty adult male volunteers. Anesthesiology; 1996, 84:821-33. 6. Begec Z, Demirbilek S, Ozturk E, Erdil F, Ersoy MO: Remifentanil and propofol for tracheal intubation without muscle relaxant in children:the effects of ketamine. Eur J Anaestesiol; 2009, 26(3):213-7. 7. Massó E, Sabaté S, Hinojosa M, Vila P, Canet J, Mass E, Langeron O: Lightwand tracheal intubation with and without muscle relaxation. Anesthesiology; 2006, 104(2):249-54. 8. Joshi GP, Hailey A, Cross S, et al: Effects of pretreatment with cisatracurium, rocuronium, and d-tubocurarine on succinylcholineinduced fasciculations and myalgia: a comparison with placebo. J Clin Anesth; 1999, 11:641–5. 9. SF, Wong, F Chung: Succinylcholine-associated postoperative myalgia. Anaesthesia; 2002, 55(2):144-152. 10.Betteli G:Which muscle relaxants should be used in day surgery and when. Curr Opin Anaesthesiol; 2006, 19(6):600-5. 11.Amornyotin S, Santawat U, Rachatamukayanant P, Nilsuwankosit P, Pipatnaraphong H: Can lidocaine reduce succinylcholine-induced myalgia? J Med Assoc Thai; 2002, 85:969-74. 12.Hassani M, Sahraian MA: Lidocaine or diazepam can decrease fasciculation induced by succinylcholine during induction of anesthesia. Middle East J Anesthesiol; 2006, 18(5):929-31. 13.Sakuraba S, Serita R, Kosugi S, Eriksson LI, Lindahl SG, Takeda J: Pretreatment with magnesium sulphate is associated with less succinylcholine-induced fasciculation and subsequent tracheal intubation-induced hemodynamic changes than precurarization with vecuronium during rapid sequence induction. Acta Anaesthiol Belg; 2002, 57(3):253-7. 14.Karamaz A, Kaya S, Turhanoglu S, Ozyilmaz MA: Effects of high-dose propofol on succinylcholine-induced fasciculations and myalgia. Acta Anaesthiol Scnd; 2003, 47(2):180-4. 15.Baraka, A: Self-taming of succinylcholine-induced fasciculations. Anaesthesiology; 1977, 46:292-293. 16.Lindgren L, Saarnivaara L: Effect of competitive myoneural blockade and fentanyl on muscle fasciculation caused by suxamethonium in children. Br J Anaesth;1983, 55(8):747-51. 17.Lindgren L, Saarnivaara L: Increase in intragastric pressure during suxamethonium-induced muscle fasciculations in children: inhibition by alfentanil. Br J Anaesth;1988, 60(2):176-9. 18.Yli-Hankala A, Randell T, Varpula T, Lindgren L: Alfentanil inhibits muscle fasciculations caused by suxamethonium in children and in young adults. Acta Anaesthiol Scnd;1992, 36(6):588-91. 19.Mertens MJ, Olofsen E, Engbers FH, Burm AG, Bovill JG, Vuyk J: Propofol reduces perioperative remifentanil requirements in a synergestic manner. Anesthesiology; 2003, 99:347–59. 20.Manataki AD, Anaoutoglu HM, Tefa LK, Glatzounis GK, Papadopoulos GS: Continuous propofol administration for suxamethonium-induced postoperative myalgia. Anaesthesia; 1999, 54:419-22. 21.Smith I, Ding Y, White PF: Muscle pain after outpatient laparoscopyinfluence of propofol versus thiopental and enflurane. Anesth Analg; 1993, 76:1181-4. 22.Theroux MC, Rose JB, Ivengar S, Katz MS: Succinylcholine pretreatment using gallamine or mivacurium during rapid sequence induction in children: a randomized, controlled study. J Cin Anesth; 2001, 13(4):287-92. M.E.J. ANESTH 20 (4), 2010 520 K. Nasseri et. al EPIDURAL ANALGESIA DURING LABOR-0.5% LIDOCAINE WITH FENTANYL VS 0.08% ROPIVACAINE WITH FENTANYLWesam F. Mousa*, R.R. Al-Metwalli** and M anal M ostafa *** Abstract Background: Although lidocaine is a cheap and globally available local anesthetic, yet it is not a popular drug for labor analgesia. This is claimed to its higher intensity of motor block, possibility of transient neurological symptoms (TNS) and its placental transfer with probable drawbacks on fetal well-being. However, these effects could be concentration dependent and, the evidence linking them to lidocaine is still lacking. This study was designed to evaluate the efficacy and safety of 0.5% epidural lidocaine plus fentanyl during labor. Methods One hundred and twenty healthy full term nulliparous women in early labor with a single fetus presented by the vertex were enrolled in this randomized, double-blind clinical trial. Parturient were assigned to receive epidural analgesia either with lidocaine 0.5% plus fentanyl 2 µg-1mL (LF), or ropivacaine 0.08% plus fentanyl 2 µg-1ml (RF) when their cervix was dilated to 4 centimeters. Analgesia was provided with 20 ml bolus of the study solution and maintained at 10 ml-1h. Upper level of sensory loss to cold, Visual Analogue Pain Score (VAPS), motor block (modified Bromage score), the duration of the first and second stages of labor, numbers of instrumental vaginal and cesarean deliveries, the neonatal apgar score, patient satisfaction and side effects, were recorded. Results There were no significant differences in sensory level, pain scores, duration of the first and second stages of labor, numbers of instrumental and cesarean deliveries, the neonatal apgar scores, patient satisfaction or side effect between groups. Although motor block was significantly high in lidocaine group compared to ropivacaine group (p<0.05), all parturient were moving satisfactorily in bed. Conclusions Dilute epidural lidocaine (0.5%) with fentanyl effectively and safely initiates epidural analgesia clinically indistinguishable from 0.08% epidural ropivacaine with fentanyl. Although it induces significant motor block compared to ropivacaine, it still preserves maternal ability to move satisfactorily in bed. Whether further reduction in lidocaine concentration could trim down the motor block, remains to be investigated. Keywords: Anesthesia: Obstetric Technique: Epidural Drug: Lidocaine. * Assistant Professor of Anesthesia and Intensive Care, Tanta University, Egypt. Consultant Anesthesia and Intensive Care, Qatif Central Hospital, Saudi Arabia. ** Assistant Professor of Anesthesia and Intensive Care, King Faisal University. P.O. Box: 40081, Post Code: 31952, Al-Khobar, Saudi Arabia. *** Assistant Professor of Obstetric and Gynecology, Tanta University, Egypt. Correspondence to: Dr. Wesam Farid Mousa, Qatif Central Hospital. P.O. Box: 18476, Post Code 31911, Al- Qatif, Saudi Arabia. E-mail: [email protected] 521 M.E.J. ANESTH 20 (4), 2010 522 Introduction Lidocaine can be used to provide complete analgesia during labor, yet it has been frequently accused with higher intensity of motor blockade that is frequently linked to bad obstetric and fetal outcome as well as decreased maternal satisfaction. As with other local anesthetics1-3, lowering lidocaine concentration and addition of fentanyl, could minimize the intensity of the motor block while maintaining effective analgesia. Although TNS usually occur after spinal anesthesia, likely with hyperbaric lidocaine4, they are uncommon after epidural anesthesia with different types of local anesthetics5,6. Despite clear evidence of placental transfer of lidocaine at rate of 0.5/0.77, reported effects on the newborn have been subtle and probably not clinically significant. Our purpose of this study is to evaluate the efficacy and safety of 0.5% lidocaine plus fentanyl 2 µg-1ml for epidural analgesia during labor, in comparison to, ropivacaine 0.08% plus fentanyl 2µg-1ml. Methods This prospective, double-blind, randomized study protocol was developed in collaboration with obstetricians. After approval of the local Ethics Committee and patients’ written informed consent, one hundred and twenty parturients were en rolled in this study. Inclusion criteria included: request for analgesia, nulliparity, age18-35 years, body weight <90 kg, ASA physical status I or II, gestational age 37 <weeks, single fetus in cephalic presentation, normal fetal heart rate and cervical dilatation of 3-5 cm. Exclusion criteria included: patients receiving analgesia prior to enrollment, presence of complicated hypertension, diabetes mellitus, neurological disease, recent hemorrhage, preeclampsia, eclampsia, suspicion of fetal malformation or intrauterine growth retardation, fever of more than°38 C or history of allergy to local anesthetics. Parturients were randomized by using a computergenerated randomization table to receive epidural analgesia of either 0.5% lidocaine with fentanyl 2µg1 ml (LF), or 0.08% ropivacaine with fentanyl 2µg-1ml (RF). The LF solution was attained by adding 62.5 ml W. F. Mousa et. al lidocaine 1% (625 mg) and 5 ml of fentanyl (250 µg) to a 57.5 ml of preservative-free 0.9% saline. The while RF solution was attained by adding 20 ml of 0.5% ropivacaine (100 mg) and 5 ml of fentanyl (250 µg) to a 100 ml of preservative-free 0.9% saline. Twenty ml was then removed from the resultant 125 ml of either LF or RF solutions to be given to an anesthesiologist not directly involved in the patient’s care or data collection to initiate epidural analgesia. The remaining 105 ml of each study solution was used for continuous epidural analgesia (10 ml-1 hr). Maternal oxygen saturation (SpO2), heart rate and automated noninvasive blood pressure were monitored throughout labour. Upon request of epidural analgesia, each parturient was preloaded with 500 ml of lactated Ringer>s solution before the initiation of epidural analgesia. A 20-gauge epidural catheter (SIMS Portex LTD, UK) was inserted under aseptic precautions in the lateral position at L3-L4 or L4-L5 interspaces with the loss of resistance to saline technique. The epidural catheter was then secured and the parturient placed in the supine position with left uterine displacement with the head of the bed elevated 20-30 degrees. Labor analgesia was initiated by the blinded anesthesiologist with a total volume of 20 ml of one of the study solutions given as four fractionated boluses (5 ml-each) within 4 minutes to achieve a bilateral block at ≥T 10-sensory level. Once the epidural analgesia is established, continuous infusion of 10 ml per hour of the analgesic solution was delivered to the laboring women to maintain labor analgesia. Further boluses of 5-10 ml of lidocaine 0.5% or ropivacaine 0.08% were given from the allocated randomized syringes for breaking through pain. Each fractionated dose was managed as a test dose (aspirating the catheter to detect accidental intravascular injection while unintended intrathecal administration of the epidural analgesic was recognized by the observation of a rapid onset of profound analgesia similar to that observed with intrathecally administered analgesics). Hypotension (systolic blood pressure below 100 mmHg or a 20% reduction from baseline) was treated with additional left uterine displacement, maternal oxygen administration, IV fluid bolus, or ephedrine as indicated. The visual analogue pain scale (VAPS) [0-100 EPIDURAL ANALGESIA DURING LABOR-0.5% LIDOCAINE WITH FENTANYL VS 0.08% ROPIVACAINE WITH FENTANYL- mm scale: 0 = no pain, 100 = worst pain ever] was measured at the peak of contractions before and 5, 10, 20, 30 min after the administration of the epidural analgesia and then at hourly intervals. Sensory level to cold, a Modified Bromage Score (1 = complete block; unable to move feet or knee, 2 = almost complete block; able to move feet only, 3 = partial block; just able to move knee, 4 = detectable weakness of hip flexion, 5 = no detectable weakness of hip flexion while supine with full flexion of knees) were obtained 30 min after epidural injection and again at hourly intervals. Side effects including nausea/vomiting, pruritis, backache, shivering, urinary retention, and respiratory depression, were reported. The duration of the first and second stages of labor, mode of delivery (spontaneous vaginal, instrumental vaginal vacuum-assisted and cesarean deliveries), and 1, 5-min neonatal apgar scores were recorded in each patient. Parturient satisfaction was assessed immediately after delivery as excellent (score 4), good (score 3), fair (score 2), or poor (score 1). Routine intrapartum monitoring was documented by the obstetrician which included; electronic continuous fetal heart rate monitoring (CFHM), hourly progress of labor, cervical dilation, station, and position of the fetal head, and the degree of caput and molding. The progress of labor is considered abnormal 523 if it is two or more hours beyond the normal rate of progress (defined as 1 cm or more dilation per hour during the active phase of labor). Abnormal progress of labor was managed by artificial rupture of membranes, oxytocin infusion or cesarean delivery according to the obstetrician clinical judgment. Patients are allowed to push when cervical dilation is confirmed and when they have the desire to bear down. If maternal effort was judged to be inadequate by the attending obstetrician, epidural infusion rate was halved or stopped. Prolonged second stage (failure to deliver the fetus after the start of pushing for 1 h) was managed with either ventouse extraction, obstetric forceps or by cesarean delivery. The possibility of Transient Neural Symptoms (TNS) [symmetric pain and/or dysesthesia in the buttocks, lower lumbar region and/or legs] were investigated in all parturients during the first three days after delivery. Statistical analysis was performed using unpaired t test to compare parametric data whereas the Fisher>s exact test was used to compare data expressed as percentages. P<0.05 was considered significant. Results One hundred twenty four women were initially included in the study. Four patients (two in each group) were excluded due to accidental dural puncture. The demographic, labor and delivery characteristics of the parturients were similar in each group (Table1). Table 1 Maternal Demographic Data and Labor Characteristics LF (n = 60) RF (n = 60) p 26 ± 4.92 25 ± 4.39 0.311 Height (cm) 165.6 ± 3.59 166.367 ± 2.16 0.156 Weight (kg) 75.07 ± 2.25 77.13 ± 2.14 1.01 Gestational age (wk) 38.20 ± 1.18 38.28 ± 0.94 0.67 Duration of 1st stage (min) 539.67± 25.61 545.33 ± 26.13 0.23 Duration of 2nd stage (min) 61.33 ± 6.76 63 ± 6.59 0.17 36 (60%) 34 (56.66%) 0.85 56(93.33%) 1(1.66%) 2(3.33%) 1(1.66%) 55(91.66%) 1(1.66%) 3(5%) 1(1.66%) 1.00 1.00 1.00 1.00 Age (yr) Oxytocin use (n) % Mode of delivery (n): Spontaneous vaginal Instrumental vaginal C/S (dystocia) C/S (fetal distress) M.E.J. ANESTH 20 (4), 2010 524 Fig. 1 VAPS at each observation time for the first 30 min. VAPS was maintained at zero level throughout the study as was measured at hourly intervals Visual Analog pain Scale The number of neonates that presented with Apgar scores below 7 at one and five minutes were not significantly different between both groups. None of the neonates needed naloxone or NICU admission. Maternal satisfaction was similar in both groups (Table 2). No significant differences were detected in the incidence of side effects or complications between the two groups (Table 3). Twelve hours postoperatively, three patients (2 in RF group and 1 in LF group) developed TNS that persisted for two days. Lidocaine group Visual Analog pain Scale Ropivacaine group VAPS (mm) VAPSVAPS (mm) (mm) The upper level of sensory loss to cold was similar in both groups after 30 min (Fig. 2). The epidural infusion was maintained at a rate of 10ml l-h in both groups without affecting the maternal effort. No patient in either groups requested supplementary analgesia. Visual Analog pain Scale Lidocaine group Ropivacaine group Lidocaine group Ropivacaine group 40 60 pre5 min 10 min 20 min 30 min 30 50 injection 20 40 Time after injection (min) 10 30 200 pre5 min 10 min 20 min 30 min 10 0 injection pre5 min 10 min 20 min 30 min Time after injection (min) injection Level of sensory block Distribution 50.00% Time after injection (min) Fig. 2 Lidocaine group of the upper level of sensory loss to cold atRopivacaine 30 min group 45.00% 40.00% Level of sensory block 35.00% Lidocaine group 30.00% Level of sensory block Ropivacaine group Lidocaine group 50.00% 25.00% Percent of patients Percent of patients The differences in motor block between groups became noticeable within 60 min of the initiation of epidural analgesia and persisted throughout labor. Patients in LF group developed significantly more motor block (85% of patients had modified Bromage score of 4 and 15% had score of 3) than patients in RF group (85% of patients had modified Bromage score of 5 and 15% had score of 4). No patient in either group developed profound motor block (modified Bromage score of 1 or 2) (Fig. 3). Resolution of the sensory and motor block was complete within 2 hours after delivery and discontinuing the epidural infusion. 100 90 80 70 100 60 90 50 100 80 40 90 70 30 20 80 60 10 70 50 0 Percent of patients Both solutions produced effective analgesia during labor without significant differences in VAPS at any observation time for the first 30 min (Fig. 1). VAPS was then maintained at zero level throughout the study as was measured at hourly intervals. W. F. Mousa et. al 45.00% 20.00% 50.00% 15.00% 40.00% 45.00% 10.00% 35.00% Ropivacaine group 40.00% 5.00% 30.00% 35.00% 0.00% 25.00% 30.00% 20.00% T10 T9 T8 15.00% 5.00% 10.00% 0.00% 5.00% T7 T6 T5 T4 T6 T5 T4 Dermatome T8 T7 T6 T5 T4 Dermatome 25.00% 15.00% 20.00% 10.00% T10 T9 0.00% T10 T9 T8 T7 Motor Block Dermatome Lidocaine group Ropivacaine group 90% 80% 70% 60% The Percent most intense Of 50% Patients 40% Fig. 3 motor block experienced by each patient at any assessment interval throughout Motorlabour Block is presented Lidocaine group 30% Motor Block 90%20% 80%10% Ropivacaine group Lidocaine group 0% Ropivacaine group 70% 90% 60% 80% 50% Percent Of 70% Patients 60% 40% 30% Percent Of 50% Patients 1 2 3 4 5 Modified Bromage Score (1-5) 20% 40% 10% 30% 0% 20% 10% 1 0% 1 2 3 4 Modified Bromage Score (1-5) 2 3 4 Modified Bromage Score (1-5) 5 5 EPIDURAL ANALGESIA DURING LABOR-0.5% LIDOCAINE WITH FENTANYL VS 0.08% ROPIVACAINE WITH FENTANYL- Table 2 Apgar scores and Maternal Satisfaction LF (n = 60) RF (n = 60) p Apgar scores First minute <7 (%) 2(3.33%) 2(3.33%) 1.00 Apgar scores Fifth minute <7 (%) 2(3.33%) 1(1.66%) 1.00 Maternal Satisfaction (%) Excellent (4) Good (3) Fair (2) Poor (1) 42(70%) 18(30%) 0 0 39(65%) 21(35%) 0 0 0.70 0.70 Table 3 Side Effects and Complications LF (n = 60) RF (n = 60) p Hypotension 2(3.33%) 1(1.66%) 1 Nausea/Vomiting 2(0.03%) 1(1.66%) 1 Pruritis 25(42%) 27(45%) 0.85 Backache 5(8%) 4(7%) 1 Shivering 3(5%) 3(5%) 1 Urinary retention 1(1.66%) 0 1 Respiratory depression 0 0 Pain, dysesthesia 1(1.66%) 2(3.33%) 1 Discussion This study showed that continuous epidural 0.5% lidocaine with fentanyl effectively provides labor analgesia comparable to epidural 0.08% ropivacaine with fentanyl without significant adverse maternal or fetal outcomes. Albeit, this low concentration of lidocaine continues to be associated with significant more motor block compared to ropivacaine, parturients were able to ambulate adequately in bed with improved maternal satisfaction. We chose that dilution of ropivacaine/fentanyl for comparison because it became the mainstay of routine painless labour in clinical practice in many centers and it appears to provide a true walking epidural8. In recent years there has been a steady decline in the concentrations of local anesthetics used for epidural analgesia in labor1-3,8. Previous reports9,10 using 525 higher concentrations of continuous epidural lidocaine for labor analgesia concluded that; associated high intensity of motor block was not accompanied with any detrimental effects in terms of obstetric outcomes, duration of the second stage of labor, or the mode of delivery. Our study using low lidocaine concentration (0.5%) confirmed the previously mentioned studies with the advantage of less motor block. In the present study, the use of low concentrations of epidural lidocaine (0.5%) continued to be associated with sufficient motor block that precluded true «walking epidural» (observed in ropivacaine group). Despite the belief that links motor blocking properties of epidurally administered analgesics to prolonged second stage and increased instrumental delivery rate, there are some studies, in which least concentrated doses of local anesthetic were used for epidural labor analgesia, and patients were able to walk, yet, instrumentation delivery rate was increased11-13. Also, Evron et al14 in their prospective, randomized double blinded study showed that the lower intensity of the motor block is not associated with any benefit in terms of obstetric outcomes, duration of the second stage of labor, and obstetric intervention. Moreover, the clinical benefits of an ambulating parturient on the progress of labour and labour outcome, other than improved patient satisfaction, remain controversial15,16. In addition Nafisi10 suggested that a pain free mother can cooperate more fully and can push more effectively and this may neutralize the left over motor blocking effect of lidocaine observed in our study. In our study, neonatal Apgar score values were similar in both lidocaine and ropivacaine groups. Lidocaine is frequently chosen for epidural anesthesia for Cesarean delivery due to its rapid onset when compared to bupivacaine. Epidural injection of large dose of lidocaine during Cesarean section may result in a greater accumulation of the drug in newborn17,18, however, reported effects on newborns are probably not clinically significant because the term fetus is able to biotransform lidocaine by hepatic enzymatic activity7. Our results showed that transient neurologic toxicity (TNS) could occur after continuous epidural analgesia with either lidocaine or ropivacaine with no statistical differences between both groups. Other studies described the occurrence of TNS after epidural M.E.J. ANESTH 20 (4), 2010 526 analgesia during labor with bupivacaine, ropivacaine and lidocaine5,6,19. Recently, Shifman et al5 investigated the incidence of TNS in puerperas after epidural analgesia during labor using either 1% lidocaine or 0.2% ropivacaine infusion compared to control. They concluded that epidural analgesia during labor is not a cause of TNS and the type of a local anesthetic (lidocaine, ropivacaine) does not affect its incidence. The incidence of TNS in our study is lower compared to the previously mentioned study (2% versus 25% for lidocaine and 3% versus 27% for ropivacaine). This lower incidence could be credited to the use of lower local anesthetic concentrations in our study. Local anesthetics were first implicated as potentially neurotoxic drugs after reporting cauda equina syndrome following continuous spinal anesthesia20. The Food and Drug Administration issued a safety alert in May of 199221 warning practitioners about the association of cauda equina syndrome with continuous spinal anesthesia. Later in 1993, Schneider et al22 reported a new syndrome of possible transient neurologic toxicity (currently referred to as TNS) after hyperbaric subarachnoid anesthesia with 5% lidocaine. It was postulated by the authors that the stretching of the cauda equina by the lithotomy position stretched some of the nerve fibers within the cauda equina, rendering them vulnerable to toxic potential of a 5% solution of lidocaine. Wong et al. in 199623 reported the first case of TNS after epidural anesthesia. In that case, the patient received a total of 600 mg of 2% lidocaine (preceded by 45 mg of 1% lidocaine as a test dose) over a period of 20 minutes, to provide a level of T7. In view of the large-dose of local anesthetic injected (645 mg) and the large concentration used, the transdural transfer of lidocaine would have resulted in a fairly large concentration of the anesthetic, probably sufficient to cause TNS by a mechanism similar to that produced by 0.5% lidocaine injected intrathecally, W. F. Mousa et. al especially when administered for surgery performed on patients in the lithotomy position24. It was postulated that continuous infusions of a local anesthetic will result in elevated intrathecal concentrations in the spinal fluid. This factor combined with the fact that most deliveries are performed with the parturient in the lithotomy position, could result in TNS after epidural injections of local anesthetics for delivery25. In our study, we did not give a test dose of high lidocaine concentration with epinephrine as in addition, it might affect our clinical end results, there is increasing evidence that this practice is neither sensitive nor specific to detect either vascular or intrathecally catheter misplacement26,27. Instead, we used the “fractionated bolus” technique that considers every dose administered via the catheter as a test dose to safeguard against the possibility of intrathecal or intravascular catheter migration28. In conclusion, epidural lidocaine (0.5%) with fentanyl effectively and safely initiates epidural analgesia clinically indistinguishable from 0.08% epidural ropivacaine with fentanyl. Although it induces significant motor block compared to ropivacaine, it still preserves maternal ability to move satisfactorily in bed. For our knowledge, this is the first study to use low lidocaine concentration (0.5%) for epidural analgesia. Whether further reduction in lidocaine concentration could trim down the motor block, remains to be investigated. Acknowledgements I wish to thank all members of the Department of Anesthesia in Tanta University Hospital, Qatif Central Hospital and King Fahad University Hospital for their encouragement and help in the clinical work. EPIDURAL ANALGESIA DURING LABOR-0.5% LIDOCAINE WITH FENTANYL VS 0.08% ROPIVACAINE WITH FENTANYL- 527 References 1. Owen MD, D’Angelo R, Gerancher J C, et al: 0.125%ropivacaine is similar to 0.125% bupivacaine for labor analgesia using patientcontrolled epidural infusion. Anesth Analg; 1998, 86:527-531. 2. Campbell DC, Zwack RM, Crone LL, Yip RW: Ambulatory labor epidural analgesia: bupivacaine versus ropivacaine. Anesth Analg; 2000, 90:1384-9. 3. Owen MD, Thomas JA, Smith T, et al: Ropivacaine 0.075% and bupivacaine 0.075% with fentanyl 2µg/mL are equivalent for labor epidural analgesia. Anesth Analg; 2002, 94:179-83. 4. Keld DB, Hein L, Dalgaard M, et al: The incidence of transient neurologic symptoms (TNS) after spinal anaesthesia in patients undergoing surgery in the supine position. Hyperbaric lidocaine 5% versus hyperbaric bupivacaine 0.5%. Acta Anaesthesiologica Scandinavica; 2000, 44:285-290. 5. Shifman EM, Butrv AV, Floka SE, Got IB: Transient neurological symptoms in puerperas after epidural analgesia during labor. Anesteziol Reanimatol; 2007, 6:17-20. 6. James RM, Osama BN, David JB, et al: Transient Neurologic Symptoms After Epidural Analgesia. Anesth Analg; 2000, 90:437. 7. Tucker GT: Pharmacokinetics of local anaesthetics. Br J Anaesth; 1986, 58:717-731. 8. Campbell DC: Labour analgesia: what’s new and PCEA too? Can J Anesth; 2003, 50(90001):R8-8. 9. Chestnut DH, Bates JN, Choi WW: Continuous infusion epidural analgesia with lidocaine: efficacy and influence during the second stage of labor. Obstet Gynecol; 1987, 69:323-7. 10.Nafisi S: Effects of epidural lidocaine analgesia on labor and delivery: A randomized, prospective, controlled trial. BMC. Anesthesiology; 2006, 6:15. 11.Liu E, Sia A: Rates of caesarean section and instrumental vaginal delivery in nulliparous women after low concentran epidural infusions or opioid analgesia :systematic review. BMJ; 2004, 328(7453):1410. 12.Zhang J, Yancey MK, Klebanoff MA, Schwarz J, Schweitzer D: Does epidural analgesia prolong labor and increase risk of cesarean delivery? A natural experiment. Am J Obstet Gynecol; 2001, 185:128-134. 13.Sharma SK, McIntire DD, Wiley J, Leveno KJ: Labor Analgesia and Cesarean Delivery :An Individual Patient Meta-Analysis of Nulliparous Women. Anesthesiology; 2004, 100(1):142-148. 14.Evron S, Glezerman M, Sadan O, Boaz M, Ezri T: Patientcontrolled epidural analgesia for labor pain :effect on labor, Delivery and neonatal outcome of0.125% bupivacaine vs0.2% ropivacaine. International Journal of Obstetric Anesthesia; 2004, 13: 5-10. 15.Bloom SL, McIntire DD, Kelly MA: Lack of effect of walking on labour and delivery. N Engl Med; 1998, 339:76-9. 16.Albers LL, Anderson D, Craigin L: The relationship of ambulation in labor to operative delivery. J Nurse-Midwifery; 1997, 42:4-8. 17.Gaiser RR, Cheek TG, Adams HK, Gutsche BB: Epidural lidocaine for Cesarean delivery of the distressed fetus. Int J Obstet Anesth; 1998, 7:27-31. 18.Price ML, Reynolds F, Morgan BM: Extending epidural blockade for emergency Caesarean section. Int J Obstet Anesth; 1991, 1:1318. 19.Wong CA, Benzon H, Kim C: Bilateral radicular pain after epidural lidocaine. Reg Anesth; 1996, 21:600-1. 20.Rigler ML, Drasner K, Krejcie TC, et al: Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg; 1991, 72:275-81. 21.FDA Safety Alert. Cauda equina syndrome associated with the use of small-bore catheters in continuous spinal anesthesia. Washington DC: Food and Drug Administration, 1992. 22.Schneider M, Ettlin T, Kaufmann M, et al: Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 5% lidocaine. Anesth Analg; 1993, 76:1154-7. 23.Wong CA, Benzon H, Kim C: Bilateral radicular pain after epidural lidocaine. Reg Anesth; 1996, 21:600-1. 24.Pollock JE, Liu SS, Neal JM, Stephenson CA: Dilution of spinal lidocaine does not alter the incidence of transient neurologic symptoms. Anesthesiology; 1999, 90:445-50. 25.Freedman JM, De-Kun L, Drasner K, et al: Transient neurologic symptoms after spinal anesthesia. Anesthesiology; 1998, 89:63341. 26.Norris MC, Ferrenbach D, Dalman H: Does epinephrine improve the diagnostic accuracy of aspirationduring labor epidural analgesia? Anesth Analg; 1999, 88:1073-6. 27.Norris MC, Fogel ST, Dalman H: Labour epidural analgesia without an intravascular “test dose”. Anesthesiology; 1998, 88:1495-1501. 28.Campbell DC: Labour analgesia: what’s new and PCEA too? Can J Anesth; 2003, 50(90001):R8-8. M.E.J. ANESTH 20 (4), 2010 528 W. F. Mousa et. al THE OCCUPATIONAL FATIGUE IN ANESTHESIOLOGISTS: ILLUSION OR REAL? Afaf Mansour*, Waleed Riad** and A shraf M oussa *** Abstract Background: Fatigue is usually reported after lack of sleep or excessive physical or mental effort. Endocrine disorders are also associated with the symptoms of fatigue. Symptoms of fatigue were reported 20% of working population. Anesthesiologists are more exposed to stress at work because of long working hours and high demand of the job. The aim of this study was to evaluate fatigue at work from anesthesiologist’ own perspectives and to identify the possible risk factors associated with fatigue. Methods: Two hundred and ten persons, were participated in this survey, they were 50 anesthesiologists, 60 diabetic patients and 100 employees. Participants were asked to answer two self report Questionnaires: The Multidimensional Fatigue Inventory (MFI-20) and General Health Questionnaire (GHQ-12) which used to assess the degree of fatigue and mental health respectively. Results: Total fatigue score was significant in anesthesiologists compared to both patients (P value = 0.047) and employees (P value < 0.001). All sub-items of fatigue score were higher in anesthesiologists compared to those of employees (P value < 0.001), however only general and mental fatigue were higher in comparison to patients (P value = 0.02). The GHQ score of the anesthesiologists was significantly higher when compared to those of the employees (P value < 0.001) but no difference with patients (P value = 0.090). Physical, mental and total score of fatigue were higher in female anesthesiologist. Conclusion: fatigue and psychological distress are common among anesthesiologists in comparison to patients and ordinary hospital employees. Female anesthesiologists were affected more by fatigue. Keywords: fatigue, anesthesia, psychological distress. * Psychiatry department, College of Medicine, Alexandria University, Egypt. ** Departments of Anesthesia, King Khaled Eye Specialist Hospital, Riyadh Saudi. *** Anesthesia Department, King Faisal, Specialist Hospital and Research Centre, Riyadh, Saudi Arabia. Address for correspondence: Dr Waleed Riad, Department of Anesthesia, King Khaled Eye Specialist Hospital, P.O. Box: 7191, Riyadh 11462, Kingdom of Saudi Arabia. Tel: 966-1-4821234-3215, Fax: 966-1-4821908, E-mail: [email protected] The authors did not receive any form of funding from any institution to carry out this study. 529 M.E.J. ANESTH 20 (4), 2010 530 Introduction Fatigue is an everyday experience that individuals report after inadequate rest or sleep, after exertion physical power, after mental effort or when 1 they lack motivation to initiate activities . Many endocrine disorders, such as diabetes, are associated 2 with the symptoms of fatigue . Previous survey on the working population reported 22% incidence of fatigue 3 symptoms . Persistent fatigue is strongly associated with functional status and can lead to absenteeism and 4 work disability . Anesthesiology is a stressful occupation5 due to the long working hours, demanding interpersonal relations, need for sustained vigilance, fear of litigation, competence, unpredictability of work and 6 production pressure . Long-work-hours including night duties with limited and/or interrupted sleep has 7 been reported to be common in anesthesiologist . Chronic stress and fatigue favor the development of exhaustion with professional dissatisfaction and poor 8 work-performance . Willful efforts to remain awake and alert when one are sleep-deprived and fatigued is highly stressful and frequently unsuccessful in the face 1 of such a potent basic pathophysiological onslaught . Some indirect evidence link fatigue with impaired 9 medical decision making and reduced patient safety . Because of its high prevalence and increasingly acknowledged negative effect on the patient’s well being, fatigue has become an important research variable. Besides being investigated as a symptom or side effect, it has also been studied as a precursor of disease10. The main objective of this study was to explore and understand the phenomenon of fatigue rather than testing a hypothesis. It was important to evaluate fatigue at work from anesthesiologist’ own perspectives and its association with psychological distress, comparing them with fatigue samples of employees and diabetic patients. Identification of possible risk factors underlying fatigue, were also observed. Materials and Methods With the approval of the local Research Committee, a total of 210 persons, aged 20-50 years participated in this survey. They received two A. Mansour et. al questionnaires, MF1-20 and GHQ-12, with a covering letter explaining the purpose and the general outline of the study, describing how the data would be used, and guaranteeing anonymity of responses. The voluntary nature of participation was emphasized. Written consent was obtained from all participants. The target group was fifty ansethiologists (33 males, 17 females, 10% married) working in the same hospital and subjecting to high workload, stress, and irregular sleep. The second group comprised 60 diabetic patients (adisease known to induce fatigue) followed up in the outpatient clinic. The last group comprised one hundred employees with wide range of work profile with no nightshift. Persons with substance abuse, smoking, neurological or psychiatric disorders and very obese persons, were excluded from the study because of the known association between these factors and 6 fatigue . Illiterate persons were also excluded because questionnaires used in this study are self report instruments. It took each participant approximately 20 minutes to fill out all the required informations. The Questionnaires The Multidimensional Fatigue Inventory (MFI11 20) is a multidimensional self report instrument designed to measure five aspects of fatigue: general, physical, reduced motivation, reduced activity and mental fatigue. The sum score of the responses (0, 1, 2, 3 or 4) is designated as total fatigue (TF) ranging from 0 to 80. Each subscale contains 4 items for each dimension. It is a 5 point scale ranging from agreement (yes) to disagreement (no). Higher scores mean a higher degree of fatigue, more concentration problems, reduced motivation, or low level of activity. It is short, does not contain any somatic items, and is designed to provide a complete description of the fatigue experience. It was extensively tested in clinical setting and validated in different population. Subjects are instructed to indicate how they felt in the last month. General Health Questionnaire: (GHQ-12) by Goldberg, was used in the present work to assess 12 different aspects of mental health of the participants . The most important reasons for using the GHQ are 13 brevity, intelligibility, and psychometric properties . THE OCCUPATIONAL FATIGUE IN ANESTHESIOLOGISTS: ILLUSION OR REAL? appropriate. If ANOVA Test was significant, Tukey HSD Multiple Comparisons Test was used to compare different groups. Correlation between groups was done using Pearson Correlation Coefficient. For all tests of significance, a P value of 0.05 was used as the level of significance. Numerical data were expressed as a mean value and standard deviation (SD) while categorical data were expressed as numbers and percentages. Results The sociodemographic characteristics are shown in Table 1. Total score of fatigue was statistically significant in anesthesiologists when compared to scores of both diabetic patients (P = 0.047) and employees (P < 0.001) (Fig. 1). Fig. 1 Total Fatigue Score Questionnaire Data expressed as a mean value while error bars represent (SD), 60 50 40 Score Reliability coefficients for GHQ ranged from 0.7813 0.95 . The GHQ used in this study includes 12 items. Each item has the following 4 answer choices: not at all, no more than usual, more than usual, and much more than usual. This questionnaire has been used as a self-report screening instrument for detecting minor psychiatric disorders in the general population. The traditional scoring method (0, 0, 1, 1) is designed to identify individuals reporting psychological distress to be classified as probable cases of minor psychiatric disorders. Given a possible range of scores ranging from 0 to 12, the threshold for cases classification used in the present study was four or higher. This means that all those participants scoring four or more on the GHQ were considered to have mental problems and 3 therefore may need health care . The present work 14 used the improved scoring system , in which, for the “negative” items only, three responses categories (rather than two) are scored as indicating illness. It appears to represent a useful improvement over the conventional scoring, since it provides a wide range among items in the proportion of “ill” responses. Statistical Analysis The results were analyzed using SPPS version 14 (SPSS Inc., Chicago, IL, USA). Statistical analysis was done using independent sample, two tailed t-test or one-way analysis of variance (ANOVA) whatever 531 30 20 10 0 Table 1 Demographic data Anesthesiologists (n = 50) Anesthesiologists Patients Group Employees Patients (n = 60) Employee (n = 100) 10 (20%) 21(42%) 19 (38%) 7 (11.7%) 14 (23.3%) 39 (65%) 46 (46%) 34 (34%) 20 (20%) Male 33 (66%) 31 (51.7%) 58 (58%) Female 17(34%) 29 (48.3%) 42 (42%) 35 (70%) 15 (30%) 38 (63.3%) 22 (36.7%) 60 (60%) 40 (40%) Education 25 (41.7%) 0 (0%) ‹ 12 years 11 (18.3%) 12-14 years 0 (0%) 17(28.3%) 6 (12%) University 7 (11.7%) Postgraduate 44 (88%) Data expressed as number and percentage. Unmarried = single, divorce or widow. 26 (26%) 7 (7%) 50 (50%) 17 (17%) Age: (years) 20-30 31-40 41-50 Sex Marital status Married Unmarried M.E.J. ANESTH 20 (4), 2010 532 A. Mansour et. al Table 2 Score of Sub-items of fatigue Questionnaire Fatigue Questionnaire General fatigue Physical fatigue Reduced activity Reduced Motivation Mental fatigue Anesthesiologists (n = 50) Patients (n = 60) Employee (n = 100) 10.0 (5.0) 9.2 (5.2) 7.3 (4.7) 5.9 (4.3) 9.6 (5.2) 8.0 (4.7)* 8.1 (4.6) 6.1 (4.0) 4.8 (3.4) 7.5 (4.6)* 5.4 (2.5)* 4.8 (3.0)* 2.8 (2.4)* 2.9 (2.5)* 4.8 (2.4)* Data expressed as a mean value (SD), * P < 0.05 versus anesthesiologists. High degree of fatigue was reported in 78% of anesthesiologists, 73.3% of diabetic patients and 53% of the employees. Subitems scores are presented in Table 2, which show that anesthetic group scored significantly higher on all subscales. Fig. 2 General Health Score Questionnaire Data expressed as a mean value while error bars represent (SD) 10 Score 8 6 4 2 0 Anesthesiologists Patients Group Employees Only general and mental fatigue scores were higher in the anesthetic group in comparison to patients’ scores. (P = 0.02). The GHQ-12 score of the anesthesiologist group was higher (statistically significant) when compared to that of employees (P < 0.001) and with no statistical difference with scores of diabetic patients (P = 0.090) (Fig. 2). Psychiatric distress (as judged by total score on GHQ ≥ 4) was experienced by 84% of the anesthesiologist, in comparison to 78.3% of diabetic patients and 54% of the employees. The impact of fatigue on gender (Table 3) revealed that physical, mental and total score of fatigue were higher in female anesthesiologist (P = 0.002, 0.003 & 0.006 respectively). Male employees showed significant physical, reduced motivation and overall fatigue than scores of women Table 3 Fatigue comparisons between male and female within the three groups Anesthesiologists Diabetic Patients (n = 50) (n = 60) General fatigue Male 8.8 (5.3) Female 12.3 (3.5) Physical fatigue Male 7.7 (5.4) Female 12.0 (3.5)† Reduced activity Male 6.2 (4.8) Female 9.2 (4.0) Reduced Motivation Male 5.0 (4.2) Female 7.5 (4.0) Mental fatigue Male 8.1 (5.2) Female 12.4 (4.2)† Total score Male 36.4 (23.3) Female 53.6 (17.6)† Data expressed as a mean value (SD), * P value < 0.05, † P value < 0.01. Employee (n = 100) 7.9 (4.8) 8.1 (4.6) 5.7 (2.7) 5.1 (2.3) 7.4 (4.6) 8.7 (4.5) 5.9 (2.6)† 3.2 (2.8) 6.1 (4.1) 6.2 (4.0) 3.3 (2.4) 2.2 (2.4) 3.8 (3.0) 5.9 (3.5) 3.5 (2.7)† 2.8 (2.1) 7.3 (4.8) 7.8 4.5) 4.4 (2.4) 5.2 (2.3) 32.7 (19.7) 36.9 (19.5) 23.7 (8.6)* 18.0 (8.4) THE OCCUPATIONAL FATIGUE IN ANESTHESIOLOGISTS: ILLUSION OR REAL? (P = 0.033, 0.008 & 0.005 respectively). No statistical significant differences were observed between women and men suffering from diabetes in all dimensions of fatigue. Correlation between total fatigue score MF1-20 and GHQ-12 was strongly positive in anesthesiologist only (r = 0.93 & P = 0.01). In the employees, moderate positive correlation between marital status and total fatigue score was found (r = 0.37 & P = 0.01). There was no evident correlation between age and fatigue. Discussion The present study showed that fatigue in anesthesiologists was significantly high when compared to that of diabetic patients and employees: The GHQ12 score was significantly high when compared to that of the employees but not to that of diabetic patients. Physical, mental and total score of fatigue were higher in female anesthesiologists. Correlation between total fatigue score and GHQ was strong positive only in anesthesiologists, the employees showed moderate positive correlation between marital status and total fatigue score. Studies on fatigue showed that the prevalence rates varied widely depending on the surveyed population. 3 It was reported to be 22% in working and general 15 Norwegian population , and 38% in a UK community 16 survey . Our study proved that chronically-ill patients perceived more fatigue than healthy employees. King and colleagues attributed the fatigue in diabetic subjects to the occurrence of hypoglycemia at night which could not be explained by the biochemical 17 parameters . Consistent with our results, Huibers et al, found the point prevalence of severe fatigue (59% to 63%) among employees and its course characterized 18 by remission and relapse in time . It had been reported that disturbed sleep and fatigue are much prevalent in shift workers thus giving the former good reasons for 19 quitting the shift work . Parker proved that the reduction in physician performance and vigilance resulted from fatigue and 20 sleep loss . Muller et al observed that occupational fatigue significantly increased at the end of night 21 shift . On the other hand, Kinzl et al found that 12.4% of 22 the studied anesthesiologists reported feeling fatigue . 533 This difference could be attributed to a difference in methodology in use, sample size and culture. The participants who had scored above the cutoff point (≥ 4) on GHQ were more likely to suffer from a mental disorder. Psychiatric distress was experienced by 84% of the anesthetics, 78.3% of the patients and 54% of the employees. Previous studies showed a range between 22 and 46% of the respondents of the UK hospital specialists’ exhibit clinically important 23 level of psychiatric morbidity . This difference could be attributed to different cut-off point used. A strong positive correlation between fatigue and psychological distress was observed only in the studied anesthesiologists. Previous studies have shown that fatigue is associated with psychological distress in a 3,16 way that varies across different populations . Thomas found that in residents, the higher the depression scores 24 the more progressive anger and fatigue . Bültmann et al found 57% of the studied employees reporting both fatigue and psychological distress at the same time while 6% reporting fatigue only without psychological 3 distress . Gender influence showed that female anesthesiologists suffered from fatigue more than male anesthesiologists while the opposite was reported in the employees. This could be explained by traditional responsibilities of women towards home duties and children. This is consistent with Hardy et al who attributed this difference to reduced physical fitness, reproductive or combined occupational and domestic 25 responsibilities . On the contrary, previous studies 4,15,16 . found fatigue more among female employees However, Bültmann and colleagues found fatigue score to be highly similar in men and women employees. These differences in the results could be attributed to different conceptualization and operationalization of 3 fatigue and psychological distress . Only the employees showed moderate positive correlation between marital status and fatigue in the current study. Previous work observed that in both genders, employees who reported living alone had 25 significant higher fatigue scores . Parker et al proved that high level of marital disharmony was found among physicians particularly anesthetists and attributed on 20 fatigue . Others showed no or minor effects of marital 15,25 status on fatigue . M.E.J. ANESTH 20 (4), 2010 534 A. Mansour et. al Conclusion Acknowledgement The present study showed that fatigue was more represented in the anesthesiologists group compared to other studied groups. It showed strong positive association with psychological distress. Gender, more than age or marital status, seems to affect fatigue in the anesthesiologists. The authors wish to thank the participating anesthesiologists, who willingly took the time during busy working days to share their experiences with us. Also, the authors express their appreciation for the cooperation of the personnel of the employee unit and participating diabetic patients. References 1. Jackson SH: The role of stress in anaesthetists’ health and wellbeing. Acta Anesthesiol Scand; 1999, 43:583-602. 2. Whybrow DM: Endocrine and metabolic disorders. In: Kaplan HL, Sadock BJ, ed. Comprehensive Textbook of Psychiatry. Williams & Wilkins: Batimore, 1989, 1209-20. 3. Bültmann U, Kant I, Kasl SV, Beurskens AJ, van den Brandt PA: Fatigue and psychological distress in the working population psychometric, prevalence, and correlates. J Psychosom Res; 2002, 52:445-52. 4. Leone SS, Huibers MJ, Kant I, Van Schayck CP, Bleijenberg G, André Knottnerus J: Long-term predictors of outcome in fatigued employees on sick leave: a 4-year follow-up study. Psychol med; 2006, 36:1293-300. 5. Nyssen AS, Hansez I: Stress and burnout in anesthesia. Curr Opin Anaesthesiol; 2008, 21:406-11. 6. Yamakage M, Hayase T, Satob JI, Namiki A, et al: Work stress in medical anesthesiology trainees. Eur J Anesthiol; 2007, 24:803-16. 7. Murray D, Dodds C: The effect of sleep disruption on performance of anesthetists a pilot study. Anesthesia; 2003, 58:520-5. 8. Martin F, Poyen D, Bouderlique E, et al: Depression and burnout in hospital health care professionals. Int J Occup Environ health; 1997, 3:204-9. 9. Lederer W, Benzer A: Programming errors from patient-controlled analgesia. Can J Anesth; 2003, 50:854-5. 10.Apple SA, Mulder P: Excess fatigue as a precursor of myocardial infarction. Eu Heart J; 1988, 9:758-64. 11.Smets EM, Garsen B, Bonke B, De Haes JC: The multidimensional fatigue inventory (MFI) psychometric qualities of an instrument to assess fatigue. J Psychosom Res; 1995, 39:315-25. 12.Goldberg DP: Manual of the General Health Questionnaire. NFER Publishing, Windsor: England, 1978. 13.Jackson G: The General Health Questionnaire. Occup Med; 2007, 57:79. 14.Duncan-Jones P, Grayson DA, Moran PA: The utility of latent trait models in psychiatric epidemiology. Psychol Med; 1986, 16:391405. 15.Loge JH, Ekeberg O, Kaasa S: Fatigue in the general Norwegian population: normative data and association. J Psychosom Res; 1998, 45:53-65. 16.Pawlikowska T, Chalder T, Hirsch SR, Wallace P, Wright DJ, Wessely SC. Population based study of fatigue and psychological distress. BMJ; 1994, 308:763-6. 17.King P, Kong MF, Parkin H, Macdonald IA, Tattersall RB: Well-being, cerebral function, and physical fatigue after nocturnal hypoglycemia in IDDM. Diabetes care; 1998, 21:341-45. 18.Huibers MJ, Bültmann U, Kasl SV, Kant I, van Amelsvoort LG, van Schayck CP, Swaen GM. Predicting the two-year course of unexplained fatigue and the onset of long-term sickness absence in fatigued employees: results from the Maastricht Cohort Study. J Occup Environ Med; 2004, 46:1041-7. 19.Jansen NW, van Amelsvoort LG, Kristensen TS, van den Brandt PA, Kant IJ: Work schedules and fatigue: a prospective cohort study. Occupa Environ Med; 2003, 60 Suppl, 1:i47-53. 20.Parker JB: The effects of fatigue on physician performance- an underestimated cause of physician impairment and increased patient risk. Can J Anesth; 1987, 34:489-95. 21.Muller R, Carter A, Williamson A: Epidemiological diagnosis of occupational fatigue in a fly-in-fly-out operation of the mineral industry. Ann Occup Hyg; 2008, 52:63-72. 22.Kinzl JF, Traweger C, Trefalt E, Riccabona U, Lederer W: Work stress and gender-dependent coping strategies in anesthesiologists at a university hospital. J Clin Anesth; 2007, 19:334-8. 23.Coomber S, Todd C, Park G, Baxter P, Firth-Cozens J, Shore S: Stress in UK intensive care unit doctors. Br J Anesth; 2002, 89:87381. 24.Thomas NK: Resident burnout. JAMA; 2004, 292:2880-9. 25.Hardy GE, Shapiro DA, Dorrill CS: Fatigue in the workforce in the National Health Service trusts: levels of symptomatology and links with minor psychiatric disorder, demographic, occupational and work role factors. J Psychosom Res; 1997, 43:83-92. THE EFFECT OF ADDITION OF LOW DOSE ATRACURIUM TO LOCAL ANESTHETIC IN RETROBULBAR BLOCK FOR CATARACT SURGERY Mohammad Hossein Eghbal*, Hesam Tabei*, Shoja Alhagh Taregh*, Mohammad Reza Razeghinejad** Abstract Background: Addition of some neuromuscular blockers to local anesthetics proved to be effective in improving the quality of anesthesia in different regional techniques. This study was carried out to determine whether the addition of low-dose atracurium to a local anesthetic has any effect on the onset and duration of akinesia in retrobulbar block. Patients and Methods: This study was conducted on sixty-four unpremedicated, ASA I or II patients scheduled for cataract surgery under local anesthesia. The patients were assigned to one of the two treatment groups in a randomized, double-blind manner. The case group received 2 ml of 2% lidocaine (40 mg) and 0.5 mL atracurium (5 mg). The control group received 2 ml of 2% lidocaine (40 mg) and 0.5 ml 0.9% NaCl. The onset of akinesia (the inability to move the eye in all four directions) was scored as 0 to 2: 0, no akinesia; 1, partial akinesia; and 2, complete akinesia. The onset and duration of akinesia and also adverse effects and complications of each method were recorded throughout the study. Results: In 4 out of 64 patients, complete akinesia was not achieved and statistical analysis was done on 60 others with complete akinesia. With regard to age, sex, weight, and duration of the surgery, there were no significant differences between the case and control groups. The onset of complete akinesia was quicker and duration longer in the case group than in the control group. The onset of complete block was 4.7 ± 1.1minutes in the case group and 6.9 ± 0.96 minutes in the control group (P<0.001). The duration of akinesia was 104.07± 17.6 minutes in the case group and 87.1 ± 16.2 minutes in the control group (P<0.001). Conclusion: This study demonstrated that atracurium had a local action on the extraocular muscles. It shortened the onset period of retrobulbar block, prolonged its duration, and provided excellent surgical conditions without any specific complications. Keywords: Akinesia, Atracurium, Nondepolarizing neuromuscular blockers, Retrobulbar anesthesia. From Shiraz University of Medical Sciences, Shiraz, Iran. * Department of Anesthesiology. ** Department of Ophthalmology. Corresponding author: Mohammad Reza Razeghinejad, MD, Poostchi Ophthalmology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran, Tel/Fax: +98 711 2302830. E-mail:[email protected] The authors have no commercial or proprietary interest on the materials discussed in this manuscript 535 M.E.J. ANESTH 20 (4), 2010 536 Introduction There are different approaches to the delivery of local injection anesthesia for cataract surgery. The two main approaches are retrobulbar and peribulbar. The retrobulbar approach appears to be more commonly practiced. This block can provide adequate anesthesia, akinesia and control of intraocular pressure as well as postoperative analgesia1,2. The most fearful complications with this technic are globe perforation, brain stem anesthesia and retrobulbar hemorrhage, which is the most frequent complication and occurs in 1% of the cases1,3,4. Many believe that the peribulbar block is a safer technique, but to produce akinesia a larger volume of anesthetic solution is required. In addition, development of akinesia takes longer and is more frequently inadequate after peribulbar injections compared with retrobulbar injection1. Some clinical trials have shown that addition of a neuromuscular blocker (e.g., vecuronium or pancronium) to the local anesthetic solution improves the quality of anesthesia in different regional techniques5-7. The beneficial effect of atracurium added to local anesthetics on akinesia in peribulbar block in the cataract surgery has been reported5. The aim of this study was to determine whether the addition of low-dose atracurium to a local anesthetic mixture had any effects on the onset time and duration of akinesia in retrobulbar block in patients who undergoing cataract surgery. Patients and Methods This study was conducted on sixty-four unpremedicated ASA I or II patients undergoing cataract surgery (phacoemulsification and intraocular lens implantation) with local anesthesia8. All patients gave informed consent and the study was approved by the Local Ethics Committee. The patients with a history of abnormal bleeding, allergy to local anesthetics, cardiac, hepatic or renal failure, Parkinsonism, unstable angina, clustropobia, high myopia, and monocularity were excluded. Patients were assigned to one of the two treatment groups in a randomized, double-blind manner. The case M. H. Eghbal et. al group comprised 31 and the control group included 33 patients. The case group received 2 mL of 2% lidocaine (40 mg) and 0.5 mL atracurium (5 mg). The control group received 2 mL of 2% lidocaine (40 mg) and 0.5 mL 0.9% NaCl. Local anesthetic solutions were prepared by a nurse anesthetist. All the blocks were performed by the same experienced ophthalmologist who was unaware of the mixture administered. The onset of akinesia (the inability to move the eye in all four directions) was determined by the ophthalmologist for the first 10 minutes and was scored as 0 to 2:0, no akinesia; 1, partial akinesia; and 2, complete akinesia (Table 1). Table 1 Akinesia scoring system after retrobulbar injection of lidocaine or a mixture of lidocaine and atracurium. 0: more than 2-mm movement in any main direction. 1: 1-mm movement in more than 2 main directions or 2-mm movement in any main direction. 2: 0- to 1-mm movement in 1 or 2 main directions. The onset time of complete akinesia was recorded for each patient. All the patients were monitored by automatic noninvasive blood pressure, heart rate, and pulse oximetry throughout the surgical procedure and during the first postoperative hour. After completion of surgery, an anesthesiologist unaware of group assignment recorded the offset time of akinesia in the recovery unit. The adverse effects and complications were also recorded during the study. Statistical analysis was performed using Student’s t test. The results are expressed as mean and standard deviation (SD). Significance was determined at the P<0.5 level. Results In 4 out of 64 patients, complete akinesia (score 2) was not achieved. These patients were excluded and statistical analysis was performed on 60 other patients who achieved complete akinesia. Regarding age, sex, weight, and duration of the surgery, there were no significant differences between the case and control groups (Table 2). However, there was a significant difference between the case and control groups A THE EFFECT OF ADDITION OF LOW DOSE ATRACURIUM TO LOCAL ANESTHETIC IN RETROBULBAR BLOCK FOR CATARACT SURGERY regarding the time onset and duration of akinesia. The onset time of complete block was 4.7 ± 1.1 minutes in the case group and 6.9 ± 0.96 minutes in the control group. This difference was statistically significant (P<0.001). Duration of akinesia was 104.07 ± 17.6 minutes in the case group and 87.1 ± 16.2 minutes in the control group which was significant (P<0.001). There was no specific complication in both case and control groups. No patient needed supplemental anesthetic agent injection. Table 2 Comparison of the two treatment groups regarding age, sex, weight duration of surgery, time to onset of akinesia and duration of akinesia. Case Control Significance Age (yr) 63.37 62.97 0.8 Sex (F/M) 2218/ 2416/ 0.37 Weight (kg) 68.7 ± 9.9 72.2 ± 11.1 0.1 Duration of surgery (min) 20.4 ± 5.09 21.1 ± 6.1 0.5 4.7 ± 1.1 6.9 ± 0.96 <0.001 104 ± 17.6 87.1 ± 16.2 <0.001 Time to onset of akinesia (min) Duration of akinesia (min) Discussion There is debate over whether the peribulbar approach provides more effective and safer anesthesia for cataract surgery than retrobulbar block. In the retrobulbar approach, a needle is inserted into the intraconal space, a space behind the eye formed by the extraocular muscles that contains the major nerves of the eye and its adnexa. Therefore, it may be associated with potentially serious ocular damages such as scleral perforation, stimulation of the oculocardiac reflex and injection of anesthetic agent into the perioptic meningeal space. However, this route may have the advantage of rapid onset of analgesia and akinesia with the use of relatively smaller volumes of anaesthetic agent1,9. The most popular peribulbar anesthetic technique involves dual injections above and below the globe. In the inferior site the needle is inserted for a distance of 25 mm at a point between the lateral third and medial two thirds of the lower orbital margin and four ml of 537 anesthetic solution is injected outside the muscle cone at the level of globe equator. In the case of upper side, the needle is introduced through the upper lid at about 2 mm medial and inferior to the supraorbital notch and 3 ml of anesthetic solution are deposited10. In addition to conjunctival edema often seen, a higher initial IOP is accompanied because of higher volume of anesthetic agent11. The need for additional injection is higher with peribulbar block in comparison with retrobulbar block1. In order to augment the effect of local anesthetics, Küçü kyavuz et al.5 and and Reah et al.6 studied the effect of neuromuscular blockers on the peribulbar block. Küçü kyavuz et al.5 reported the effect of 8 mL of a lidocaine-bupivacaine mixture, plus0.5 mL (5 mg) atracurium was better than the 8 mL of the same local anesthetic mixture plus 0.5 mL 0.9% NaCl. Time to the onset of akinesia in minutes was 10 ± 3 in the atracurium and 7 ± 2 in the control one. The duration of akinesia in minutes was the same in both groups (192 ± 99 versus 194± 53) which was not statistically significant (p>0.05). Moreover, no side effects related to peribulbar block or drugs were observed in any patient. Reah et al.6 compared the effect of 5 ml of 2% Lignocaine with 1:200000 adrenaline, 5 ml 0.75 bupivacaine and 150 IU hyaluronidase with either 0.9% saline 0.25, or vecuronium bromide 0.25 ml. They concluded that the addition of vecuronium at a dose of 0.5 mg to the local anesthetic mixture improves the quality of akinesia. Although Reah et al.6 and Küçü kyavuz et al.5 studied the effect of neuromuscular blocking agents in peribular block, reporting that the addition of neuromuscular blocking agents to the local anesthetic mixture improves the quality of akinesia, our study is the first to use low-dose atracurium in retrobulbar block. In this study, the onset of complete block was more rapid in the atracurium group compared with the control group. This finding is in concordance with that of the two mentioned studies. But, the total amounts of local anesthetic agent in both of these studies were more than those of our study. However, the need for additional injection is higher with peribulbar block in comparison with retrobulbar block1. Nowadays, topical anesthesia is the more popular M.E.J. ANESTH 20 (4), 2010 538 M. H. Eghbal et. al techique for ophthalmic anesthesia. This contributes to a controversy about the optimal technique for cataract surgery. Though topical anesthesia reduces the risk of complications related to needle and systemic toxicity, yet it has the potential disadvantages of incomplete akinesia12. Induction of complete akinesia is an ideal situation for the beginner surgeons, because complete akinesia is not achievable by topical anesthesia. anesthesia technique has been proved. Though the mechanism is still unclear, the hypothesis is that the neuromuscular blockers probably interfere with muscle spindle activity. The motor unit, the number of muscle fibers innervated by a single motor neuron, is the characteristic features of intraorbital muscles which makes the extra ocular muscles most sensitive to the effect of neuromuscular blocking agents6. A major concern in retroblbar block is the potential for central spreading and inadvertent intrathecal injection. The possibility of central spread is a rare occurrence; Nicoll et al.13 reported the incidence of 0.27%. In our study there was no case of central spread of medication which seems to be related to taking into account the predetermined precautions in retrobulbar injection. Our study demonstrated that atracurium had a local action on the extraocular muscles. It shortened the onset time of retrobulbar block, prolonged the duration of retrobulbar block, and provided excellent surgical conditions without known complications. Shortening the onset time of akinesia leads to saving of the time and cost of operating room. Moreover, increasing the duration of akinesia could enable the surgeon to do other ophthalmic operations which last longer than a routine phacoemulsification surgery. Further studies are required to confirm the local effect of atracurium on akinesia of the globe. The additional effect of low-dose nondepolarizing neuromuscular blocking agents to the local anesthetic solution in improving the quality of anesthesia and provision of motor block during intravenous regional References 1. A lhassan MB, K yari F, E jere HO: Peribulbar versus retrobulbar anaesthesia for cataract surgery. Cochrane Database Syst Rev; 2008, CD004083. 2. D avison JA: Features of a modern retrobulbar anesthetic injection for cataract surgery. J Cataract Refract Surg; 1993, 19:284-9. 3. G unja N, Varshney K: Brainstem anaesthesia after retrobulbar block: a rare cause of coma presenting to the emergency department. Emerg Med Australas; 2006, 18:83-5. 4. A shaye AO, U bah JN, S otumbi PT: Respiratory arrest after retrobulbar anaesthesia. West Afr J Med; 2002, 21:343-4. 5. Kucukyavuz Z, A rici MK: Effects of atracurium added to local anesthetics on akinesia in peribulbar block. Reg Anesth Pain Med; 2002, 27:487-90. 6. R eah G, B odenham AR, B raithwaite P, E smond J, M enage MJ: Peribulbar anaesthesia using a mixture of local anaesthetic and vecuronium. Anaesthesia; 1998, 53:551-4. 7. A bdulla WY, Fadhil NM: A new approach to intravenous regional anesthesia. Anesth Analg; 1992, 75:597-601. 8. M uravchick S: Preoperative assessment of the elderly patient. Anesthesiol Clin North America; 2000, 18:71-89, vi. 9. K umar CM: Orbital regional anesthesia: complications and their prevention. Indian J Ophthalmol; 2006, 54:77-84. 10.W ong DH: Regional anaesthesia for intraocular surgery. Can J Anaesth; 1993, 40:635-57. 11.S anford DK, M inoso Y de C al OE, B elyea DA: Response of intraocular pressure to retrobulbar and peribulbar anesthesia. Ophthalmic Surg Lasers; 1998, 29:815-7. 12.B oezaart A, B erry R, N ell M: Topical anesthesia versus retrobulbar block for cataract surgery: the patients’ perspective. J Clin Anesth; 2000, 12:58-60. 13.N icoll JM, A charya PA, A hlen K, B aguneid S, E dge KR: Central nervous system complications after 6000 retrobulbar blocks. Anesth Analg; 1987, 66:1298-302. LABOR ANALGESIA IN PREECLAMPSIA: REMIFENTANIL PATIENT CONTROLLED INTRAVENOUS ANALGESIA VERSUS EPIDURAL ANALGESIA Hala El-Kerdawy*, Adel Farouk** Abstract Background: Epidural analgesia is considered to be the preferred method of labor analgesia in preeclamptic patients. Systemic opioids are another good effective, easy to administer alternative but may cause maternal and fetal respiratory depression. Remifentanil’s rapid onset and offset of effects, should make it an ideal drug for the intermittent painful contraction during labor. Method: 30 preeclamptic patients were randomly assigned to one of two equal groups; Epidural Group: received epidural analgesia according to a standardized protocol using bupivacaine plus fentanyl. Remifentanil Group: PCA was set up to deliver remlfentanil 0.5 μg/kg as a loading bolus infused over 20 seconds, lockout time of 5 minutes, PCA bolus of 0.25 μg/kg, continuous background infusion of 0.05 μg/kg/min, and maximum dose is 3 mg in 4 hours. Women were advised to start the PCA bolus when they feel the signs of a coming uterine contraction. Results: All women demonstrated a significant decrease in VAS score in the first hour after administration of analgesia (P<0.05). Analgesic quality as regard Visual Analog Pain Scores, sedation score, and post-delivery patient satisfaction in both groups, are comparable (P>0.05). PCA remifentanil infusion until time of delivery produce no observable maternal, fetal or neonatal side effects (P<0.05). Conclusion: PCA intravenous remifentanil is an effective option for pain relief with minimal maternal and neonatal side effects in labor for preeclamptic patients with contraindications to epidural analgesia or requesting opioid analgesia. Keywords: Preeclampsia, PCA remifentanil, epidural, labor analgesia. * Department of Anesthesia, and ** Department of Gynecology and Obstetric, Cairo University, Cairo, Egypt. Corresponding author: Dr. Hala El-Kerdawy, Consultant Anesthetist, Anesthesia Department, Saad Specialist Hospital. P.O. Box: 30353, Al-Khobar 31952, Saudi Arabia. Mobile: 00966502573767. E-mail: [email protected] 539 M.E.J. ANESTH 20 (4), 2010 540 H. Kerdawy et. al Introduction The goal of labor pain relief for pre-eclamptic parturients is to provide the most effective analgesia in order to reduce stimulation of the sympathetic nervous system1,2. Epidural analgesia was proven safe for use in such patients3 and particularly beneficial to the mother and baby as it prevents the exacerbation of hypertension and improve uteroplacental circulation.4 The anesthesiologist concerns with epidurals stem from the episodes of hypotension, predisposition of preeclamptic patients to develop pulmonary edema4, and coagulopathies. The latter interfering with the ability to provide neuraxial anesthesia5; hematoma formation6,7 spinal cord compression and permanent paralysis. Disturbances of platelet counts, platelet function or disseminated intravascular coagulation can also increase the risk for excessive bleeding. Coagulopathy, anesthetists are concerned about epidural. On the other hand systemic opioids are the most common form of labor analgesia worldwide and when administered by the proper delivery system, can also be the second most efficacious form of pain relief2. Intramuscularly administered narcotics is a poor method of drug delivery for labor pain as the relatively slow absorption leads to fluctuating peaks and troughs in serum levels8. This method of administration also is painful and is contraindicated when the patient is thrombocytopenic (<50000-75000 platelets)2. The intravenous administration of narcotics is the best method of administration for labor pain. Ideally, the patient controlled analgesia (PCA) system is available to these women. The particular narcotics used in this system include morphine, fentanyl, meperidine, nalbuphine, and alfentanil9. The ideal agent of choice is a short-acting narcotic that does not accumulate over time and has a large therapeutic/ toxic plasma ratio. Regardless of the narcotic chosen, particular monitoring requirements must be in place to avoid potential maternal and neonatal complications2. Therefore, the minimum requirements of monitoring for the mother during administration consist of an hourly respiratory rate and sedation score used for normal labour. Meperidine the most commonly used for labor pain is associated with a high incidence of maternal nausea and sedation, as well as many adverse fetal and neonatal effects10. The use of intravenous patient controlled analgesia (PCA) with fentanyl has been associated with up to a 44% incidence of moderately depressed neonates with low Apgar scores11. Moreover, fentanyl does not always provide adequate pain relief for the intense pain of the late first stage of labor, most likely due to its slow onset of action12. A search for a new opioid to overcome these problems has led to the introduction of remifentanil for labor analgesia13,14,15. Remifentanil has a unique pharmacokinetic profile, with a potent ultra-short μ opioid receptor agonist action. The metabolism of remifentanil is independent of renal and hepatic function. It has rapid onset (time to peak effect 60 to 80 sec) and offset times, irrespective of the duration of administration16. The drug’s context sensitive half-time is three minutes17. Remifentanil rapidly crosses the placenta but is quickly redistributed and metabolized in the fetus18,19. There have been no reports of associated increases in neonatal respiratory depression or lower Apgar scores with the use of remifentanil prior to delivery. With these properties, remifentanil appears to be the opioid of choice for labor, since it can be appropriately titrated for administration when analgesia is required for either very brief or prolonged periods, without the concern of prolonged recovery. It therefore resembles the description of an ideal systemic analgesic for use during labor. To the best of our knowledge, no trial as yet been carried out, to study the efficacy of using remifentanil patient controlled analgesia for the pain management in preeclamptic patients. This study was planned to compare the use of remifentanil PCA intravenous analgesia to epidural bupivacaine plus fentanyl for labor analgesia in preeclamptic patients. Material and Methods After having patient informed consent, thirty nulliparous preeclamptic parturient were studied. Patients were recruited during early first stage of labor before requesting pain relief were studied. Inclusion criteria consisted of; ≥32 weeks gestation, normal cephalic presentation, <5 cm cervical dilatation, LABOR ANALGESIA IN PREECLAMPSIA: REMIFENTANIL PATIENT CONTROLLED INTRAVENOUS ANALGESIA VERSUS EPIDURAL ANALGESIA clinical diagnosis of preeclampsia. Which required at least one of the following three criteria: 1) Systolic blood pressure greater than or equal to 140 mmHg or diastolic blood pressure greater than or equal to 90 mmHg, with proteinuria of 1 + on dipstick. 541 sited for remifentanil delivery and the Remifentanil hydrochloride concentration used was 50 μg/ml (3 mg diluted to 60 ml of normal saline). 2) Systolic blood pressure greater than or equal to 140 mmHg or diastolic blood pressure greater than or equal to 90 mmHg with proteinuria of 2 + or more on dipstick. The PCA was set to deliver 0.5 μg/kg as a loading bolus infused over 20 seconds, lockout time of 5 minutes, PCA bolus of 0.25 μg/kg, continuous background infusion of 0.05 μg/kg/min, and maximum dose is 3 mg in 4 hours. Women were advised to start the PCA bolus when they feel the signs of a coming uterine contraction. 3) Systolic blood pressure greater than or equal to 160 mmHg or diastolic blood pressure greater than or equal to 110 mmHg with proteinuria of either 2 + on dipstick. Oxygen saturation (SpO2), Heart rate (HR), Blood pressure (Bp), and Respiratory rate (RR) were monitored continuously and recorded every 5 minutes. Exclusion criteria were consisted of; remifentanil allergy, progression to eclampsia, evidence of increased intracranial pressure or focal neurologic deficit, Women with a platelet count of less than 80 × 109/L, or evidence of pulmonary edema, nonreassuring fetal heart rate tracing requiring imminent delivery. Hypotension, (defined as reduction of >25% of baseline level), was treated by either additional intravenous crystalloid or intravenous bolus doses (e.g., 2.5-5.0 mg) of ephedrine. Reductions in blood pressure of less than 25% in the presence of a reassuring fetal heart rate tracing (as determined by the managing obstetrician) were not treated. If the assigned analgesia was inadequate for the patient at any time, an alternative was offered and further study recording were discontinued. After arriving to delivery suit, an 18 G intravenous cannula was established and lactated Ringer’s solution at a rate of 100 ml/hour was given to all parturients. Intravenous magnesium sulfate for seizure prophylaxis from the diagnosis of preeclampsia until 24 hours postpartum was given when instructed by the obstetrician. The standard magnesium sulfate regimen is a 4g intravenous bolus given over 20 minutes, followed by a continuous infusion of 2 g per hour. After proper explanation of both techniques patients were randomly assigned to one of two groups. (15 each) Epidural Group: Following lumbar epidural according to a standardized protocol, on epidural catheter was placed under complete aseptic technique at the L3-L4 or L4-L5 interspaces. A test dose of 3 mL of 0.25% bupivacaine was administered, and epidural analgesia was established with initial bolus of 1015 mL of 0.25% bupivacaine plus 1 μg/kg fentanyl. Analgesia was maintained by continuous infusion of 0.125 bupivacaine plus 2 μg/ml fentanyl at a rate of 10-12 ml per hour aiming to obtain a T-10 sensory level. Remifentanil Group: Patients were first introduced to the proper use of the PCA pump (Grasby 3300). A dedicated intravenous cannula was For hourly pain assessment and a visual analogue pain score (0 marked no pain and 10 marked worst pain) was obtained and recorded at three data points before analgesia, one hour after, and after delivery. Satisfactory analgesia is considered if VAS is ≤ 3. Hourly Sedation score was assessed and recorded at the same data points using a four point scale (1= alert, 2= slightly drowsy, 3= drowsy not responding to gentle stimulation, 4= very drowsy). Overall patient satisfaction were determined within 24 hours of delivery (1: poor, 2: fair, 3: good, 4: excellent). Requirement for pharmacologic interventions to treat hypotension and the incidence of complications were recorded. Continuous cardiotocogram monitoring of fetal heart rate uterine contraction were used and analyzed by the obstetrician. Neonatal data included birth weight, Apgar scores at 1 and 5 minutes, umbilical cord arterial blood gas results, naloxone treatment, neonatal intensive care admission. Any morbidities and mortalities were recorded. M.E.J. ANESTH 20 (4), 2010 542 H. Kerdawy et. al Statistical Analysis Maternal vital signs: Demographic data were analyzed with unpaired Student’s t test. Paired Student’s t test was used to compare values in the same group. One way and two ways ANOVA were used for within and between groups comparisons of Maternal hemodynamics. Maternal visual analog score, and sedation score, between groups were compared using Kruskal-Wallis ANOVA test and Friedman two-way ANOVA for within group analysis. Maternal visual satisfaction score was compared using Mann-Whitney test. Maternal side effects and fetal side effects were analyzed using Chi-squared test. All statistical analysis was performed using Excel and SBSS statistical packages. The two groups were comparable with respect to maternal hemodynamic in the means of; SBP, HR, SpO2, and Respiratory Rate. Data were analyzed at three points before starting analgesia (baseline), 1 hour after starting analgesia, and after delivery (Table 2). Table 2 Changes in the mean Systolic Blood pressure before starting analgesia (baseline), 1 hour after starting analgesia, and after delivery. Values are mean ± SD Baseline After analgesia delivery 95 ± 8.7 97.7 ± 7.6 Mean BP (mmHg) - Epidural group - Remifentanil Results 1 hr after 99.4 ± 13 100.5 ± 6.9 96.2 ± 6.6 99 ± 9 group Mean HR (beat/min) Demographic Data Both groups were matches for Age, Weight, Height, Gestational age, Baseline cervical dilatation, and baseline lab results (P>0.05). Incidence of instrumental delivery and cesarean section was higher in Epidural group compared to the Remifentanil one (P<0.05). (Table 1) Table 1 Demographic Data and Type of delivery (mean ± SD or numbers) Variable 80.6 ± 10.8 - Remifentanil 81.2 ± 11.2 79.2 ± 10.3 80.1 ± 8.4 81 ± 7 79.8 ± 10.4 group Mean SpO2 (%) - Epidural group 98.2 ± 1.4 97.8 ± 1.9 97.3 ± 1.9 - Remifentanil 98.4 ± 1.3 97.5 ± 1.5 97.8 ± 1.5 - Epidural group 18.3 ± 3.4 17.5 ± 3.4 17.2 ± 3.1 - Remifentanil group 18.5 ± 3.4 17.8 ± 2.4 17.5 ± 2.6 group Mean Respiratory rate Epidural Remifentanil Group Group (n = 15) (n = 15) Age (year) 26 ± 8 28 ± 9 Weight (Kg) 79 ± 22 84 ± 37 Height (cm) 163 ± 6 162 ± 7 Gestation (week) 36 ± 4 35 ± 3 Cervical Dilatation (cm) 3.2 ± 1.4 3.4 ± 1.5 Baseline lab. Results = Platelet count (× 109/L) = Serum Creatinine (mg/dL) 175 ± 63 0.8 ± 0.3 178 ± 55 0.8 ± 0.25 8* 3* 4* 10 0 3 Type of delivery = Normal delivery = Instrumental Delivery = Cesarean Section - Epidural group * Significant difference compared to remifentanil group Quality of analgesia Maternal pain score, sedation score, and post delivery satisfaction: Maternal Visual Analog Pain Score (VAPS) and Sedation scores were assessed before starting analgesia (baseline), 1 hour after starting analgesia, and after delivery. There were no inter-group differences in the VAS or sedation scores at the three times measured (P>0.05). Within group analysis revealed significant decreased in VAS after starting the analgesia in both groups (Table 3). In the PCA intravenous Remifentanil group, the patient satisfaction was better than in the epidural group although it is was statistically insignificant. (P>0.05) LABOR ANALGESIA IN PREECLAMPSIA: REMIFENTANIL PATIENT CONTROLLED INTRAVENOUS ANALGESIA VERSUS EPIDURAL ANALGESIA Table 3 Changes in the mean Maternal Visual Analog Pain Scale, mean Sedation score (VAS) at baseline, 1 hour after analgesia, and after delivery and patient satisfaction Values are mean ± SD Epidural Group (n = 15) Remifentanil Group (n = 15) Pain VAS Score = Baseline = 1 hr after = After delivery 8 ± 1.7 2.6 ± 1.5 3 ± 1.4 7.9 ± 1.7 3±1 2.8 ± 1.1 Sedation Score (1-4) = Baseline = 1 hr after = After delivery 1 ± 0.25 1.1 ± 0.35 1.06 ± 0.25 1 1.3 ± 0.48 1.1 ± 0.35 2.8 ± 1 3.1 ± 0.9 Patient Satisfaction Score (1-4) Table 4 The number of maternal side effects in the two groups. Values are number (%) Side Effects 543 Maternal Side effects Nausea, and or vomiting in the epidural group was higher than in remifentanil group but still statistically insignificant (P>0.05). Itching and hypotension that necessitated pharmacological interventions, were statistically significantly higher in epidural group than remifentanil group (P<0.05) Fetal and neonatal outcome Fetal heart rate abnormalities (fetal heart rate deceleration to < 90 beats/min or late deceleration) were recorded one hour after start of analgesia, in both groups (Table 5). Two patients in epidural group developed fetal heart rate abnormalities compared to no patients in remifentanil group. Incidence of mechanical ventilation, naloxone used was statistically significant in epidural group compared with the remifentanil one (P<0.05). There were no differences between the neonates in the two groups as regard the APGAR score measured at the two different times. Also no statistically significant difference between groups as regard seizure or umbilical cord blood gases analysis (P>0.05). Epidural Group (n = 15) Remifentanil Group (n = 15) Nausea 7 (46.6%) 5 (33%) Vomiting 2 (13.3%) 1 (6.6%) Discussion Itching 3 (20%)* 1 (6.6%) 4 (26.6%)* 0 (0%) The chief role of the anesthesiologists is to provide safe labor analgesia20, the choice, however, of the optimum technique in preeclamptic patients is controversial21,22. The results of this study indicate that PCA remifentanil for preeclamptic patients during labor and delivery is associated with a decrease in VAS pain score, acceptable sedation score, and good patient satisfaction that is comparable to the epidural technique. The maternal, fetal, and neonatal side effects in remifentanil group were minimal and rapidly resolved due to short duration of action and lack of accumulation of remifentanil. Hypotension Table 5 Incidence of fetal and neonatal side effects. Value are numbers (%) Epidural Group (n = 15) Remifentanil Group (n = 15) 2 (13.3%) * 0 (0%) 1 (6.6%) 0 (0%) 1 (6.6%) 0 (0%) Naloxone 2 (13.3%)* 0 (0%) Umblical cord gas = Umblical artery pH = Umblical vein pH 7.24 ± 0.09 7.3 ± 0.03 7.23 ± 0.07 7.32 ± 0.03 0 (0%) 0 (0%) 2 (13.3%)* 0 (0%) FHR abnormalities at one hour after analgesia Apgar Score ≤7 = 1-minute = 5-minutes Seizure Mechanical ventilation * Significant difference compared to remifentanil group There were no significant differences in the maternal vital signs (SBP, HR, SpO2), or respiratory rate (RR) between the two groups in the doses used, indicating minimal or no serious side effects on the mother by the use of either epidural bupivacainefentanyl, or intravenous remifentanil. Maternal side effects (Nausea, vomiting, itching, and hypotension), were lower in remifentanil group compared to epidural group but was statistically M.E.J. ANESTH 20 (4), 2010 544 significant in case of itching, hypotension, and the rate of instrumental and cesarean section delivery (P<0.05). Some studies found significantly greater requirements for ephedrine in women with severe preeclampsia who received epidural analgesia4,23. Although, maternal side effects were not observed in our study, but its potential it like any opioid analgesia, a well-trained staff therefore is recommended for close observations. The continuous remifentanil infusion until the time of delivery produced no observable fetal or neonatal side effects compared to the epidural group, (P>0.05). This was indicated by the normal Apgar score, reassuring fetal heart rate tracing, normal umbilical cord gases, the absence of need for naloxone, or mechanical ventilation for the neonates. This is attributable to the assumption that remifentanil crossed the placenta was either rapidly metabolized or redistributed in the neonates causing no adverse effects. Our findings of an absence of any fetal or neonatal adverse effects are consistent with other studies13,14,15,24. Other findings are in contradictory25,26,27 with respect to maternal and neonatal side effects, which can be explained by the various doses used and mode of administrations. The short duration of action and the lack of accumulation of remifentanil resulted in rapid spontaneous resolution of any side effects. Whereas the significant FHR abnormalities in the epidural group is similar to the findings of other study28, comparing normotensive women with epidural analgesia, women with hypertension and epidural analgesia had a three-fold increased risk of ominous fetal heart rate tracings. All women demonstrated a significant decrease in VAS score in the first hour after administration of analgesia (P<0.05), denoting effective analgesia in both groups. Comparison of the analgesic quality of the Visual Analog Pain Scores, sedation score, and postdelivery patient satisfaction between the two groups, H. Kerdawy et. al show comparable analgesic efficacy of both techniques (P>0.05). This suggests that remifentanil may have a true analgesic effect on labor pain, an effect consistent with many previous studies8,24. A variety of doses and delivery systems have been previously8,9,15,29 for the purpose of identifying an efficient and safe approach of remifentanil administration. The concomitant use of a background infusion is controversial30. Some studies recommended the use of a background infusion31, and others argued that remifentanil administration without a background provides safe but incomplete analgesia13. Because of the fact that it is difficult, to coincide the peak effect of remifentanil with each uterine contraction but with the subsequent contraction32, a background infusion was chosen in this study to provide constant baseline analgesia and that only the contraction peaks required treatment with rescue boluses. Our regimen results was compared with similar one31 used resulted in effective analgesia with a rate of conversion to regional analgesia of 5%, which is the lowest reported to date. With the PCA intravenous remifentanil used in this study, the patient benefits from a greater sense of control over her pain management, plus the anxiolytic effect of using narcotic (remifentanil), which is an important psychological effect that contributes to the success of this technique. Remifentanil reduces pain during labor and does not cause immediate or prolonged hazards to mother or fetus. Conclusion PCA intravenous remifentanil is an effective option for pain relief with minimal maternal and neonatal side effects in labor for preeclamptic patients with contraindications to epidural analgesia or requesting opioid analgesia. Further studies in larger population of preeclamptic patients are recommended to ensure the safety of this regimen. LABOR ANALGESIA IN PREECLAMPSIA: REMIFENTANIL PATIENT CONTROLLED INTRAVENOUS ANALGESIA VERSUS EPIDURAL ANALGESIA 545 References 1. Robert AD, Piercy JL, Reed AR: The role of the anaesthetist in the management of the pre-eclamptic patient. Current Opinion in Anaesthesiology; 2007, 20:168-174. 2. Mordani K, Macarthur A: Anesthesia considerations of preeclamptic patients. In Preeclampsia, current perspectives on managements. Philip N. Baker, and John C.P. Kingdom (2nd edition) Parthenon Publishing 2004, 196-199. 3. Moore TR, Key TC, Reisner LS, et al: Evaluation of the use of continuous lumbar epidural anesthesia for hypertensive pregnant women in labor. Am J Obstet Gynecol; 1985, 152:404-12. 4. Head B, John O, Robert D, et al: A randomized trial of intrapartum analgesia in women with severe preeclampsia. Obstet Gynecol; 2002, 99:452-7. 5. Greenwood PA, Lilford RJ: Effect of epidural analgesia on maximum and minimum blood pressures during first stage of labour in primagravidae with mild/moderate gestational hypertension. Br J Obstet Gynaecol; 1986, 93:260-3. 6.Lao TT, Halpern SH, MacDonald D, Huh C: Spinal subdural haematoma in a parturient after attempted epidural anaesthesia. Can J Anaesth; 1993, 40:340-5. 7.Yuen TST, Kua JSW, Tan IKS: Spinal haematoma following epidural anaesthesia in a patient with eclampsia. Anaesthesia; 1999, 54:350-4. 8. Thurlow JA, Laxton CH, Dick A, et al: Remifentanil by patient controlled analgesia compared with intramuscular meperidine for pain relief in labor. Br J Anaesth; 2002, 88:374-378. 9. Evron S, Ezri T: Options for systemic labor analgesia. Current Opinion in Anaesthesiology; 2007, 20:181-185. 10.Rayburn WF, Smith CV, Parriott JE, Woods RE: Randomized comparison of meperidine and fentanyl during labor. Obstet Gynecol; 1989, 74:604-6. 11.Morley-Forster PK, Weberpals J: Neonatal effects of patientcontrolled analgesia using fentanyl in labor. Int J Obstet Anesth; 1998, 7:103-7. 12.Scott JC, Ponganis KV, Stanski DR: EEG quantitation of narcotic effect: the comparative pharmacodynamics of fentanyl and alfentanil. Anesthesiology; 1985, 62:234-41. 13.Blair JM, Hill DA, Fee JP: Patient-controlled analgesia for labour using remifentanil: a feasibility study. Br J Anaesth; 2001, 87:41520. 14.Blair JM, Dobson GT, Hill DA, McCracken GR, Fee JP: Patient controlled analgesia for labour: a comparison of remifentanil with pethidine. Anaesthesia; 2005, 60:22-7. 15.Volikas I, Male D: A comparison of pethidine and remifentanil patient-controlled analgesia in labour. Int J Obstet Anesth; 2001, 10:86-90. 16.Glass PS, Hardman D, Kamiyama Y, et al: Preliminary pharmacokinetics and pharmacodynamics of an ultra-short-acting opioid: remifentanil (GI87084B). Anesth Analg; 1993, 77:1031-40. 17.Kapila A, Glass PS, Jacobs JR, et al: Measured context-sensitive half-times of remifentanil and alfentanil. Anesthesiology; 1995, 83:968-75. 18.Volikas I, Butwick A, Wilkinson C, Pleming A, Nicholson G: Maternal and neonatal side-effects of remifentanil patient-controlled analgesia in labour. Br J Anaesth; 2005, 95:504-9. 19.Kan RE, Hughes SC, Rosen MA, Kessin C, Preston PG, Lobo EP: Intravenous remifentanil: placental transfer, maternal and neonatal effects. Anesthesiology; 1998, 88:1467-74. 20.Pattinson RC (editor): Saving mothers. Third report on confidential enquiries into maternal deaths in South Africa, 2002-2004. Pretoria, South Africa: Department of Health, 2007. 21.Ramanathan J, Coleman P, Sibai B: Anesthetic modification of hemodynamic and neuroendocrine stress responses to cesarean delivery in women with severe preeclampsia. Anesth Analg; 1991,73:772-9. 22.Lindheimer MD, Katz AI: Hypertension in pregnancy. N Engl J Med; 1985, 313:675-80. 23.Wallace DH, Leveno KJ, Cunningham FG, Giesecke AH, Shearer VE, Sidawi JE: Randomized comparison of general and regional anesthesia for cesarean delivery in pregnancies complicated by severe preeclampsia. Obstet Gynecol; 1995, 86:193-9. 24.Volmanen P, Akural EI, Raudaskoski T, Alahuhta S: Remifentanil in obstetric analgesia: a dose-finding study. Anesth Analg; 2002, 94:913–7. 25.Jones R, Pegrum A, Stacey RGW: Patient-controlled analgesia using remifentanil in the parturient with thrombocytopenia: case report. Anaesthesia; 1999, 54:459-65. 26.Thurlow JA, Waterhouse P: Patient-controlled analgesia in labor using remifentanil in two parturients with platelet abnormality. Br J Anaesth; 2000, 84:411-3. 27.Olufolabi AJ, Booth JV, Wakeling HG, et al: A preliminary investigation of remifentanil as a labor analgesic. Anesth Analg; 2000, 91:606-8. 28.Montan S, Ingemarsson I: Intrapartum fetal heart rate patterns in pregnancies complicated by hypertension.AmJ Obstet Gynecol; 1989, 160:283-8. 29.Owen MD, Poss MJ, Dean LS, et al: Prolonged intravenous remifentanil infusion for labor analgesia. Anesth Analg; 2002, 94:918-919. 30.David Hill: Remifentanil in obstetrics. Current Opinion in Anaesthesiology; 2008, 21:270-274. 31.Balki M, Kasodekar S, Dhumne S, et al: Remifentanil patientcontrolled analgesia for labour: optimizing drug delivery regimens. Can J Anaesth; 2007, 54:626-633. 32.David Hill: The use of Remifentanil in Obstetrics. Anesthesiology Clin; 26 (2008), 169-182. M.E.J. ANESTH 20 (4), 2010 546 H. Kerdawy et. al SPINAL ANESTHESIA FOR TRANSURETHRAL RESECTION OPERATIONS: LEVOBUPIVACAINE WITH OR WITHOUT FENTANYL Ozgun Cuvas*, Hulya Basar*, Aydan Yeygel*, Esra Turkyılmaz*, Mehmet Melih Sunay** Abstract Background: The objective of the present study was double fold; to compare the characteristics of spinal blocks produced by 0.5% levobupivacaine with and without fentanyl in transurethral resection and to test the hypothesis that, fentanyl added to levobupivacaine, may be used as an alternative to pure levobupivacaine solution, in spinal anesthesia. Methods: Forty males, aged >60 years, ASA I-III patients scheduled for elective transurethral resection were included in a prospective, randomized, double-blinded study. Following a spinal tap, intrathecal injection in Group L (n = 20), 2.5 mL of 0.5% levobupivacaine and in Group LF (n = 20), 2.2 mL of 0.5% levobupivacaine with fentanyl 15 µg (0.3 mL) was performed. The characteristics of sensory and motor block, hemodynamic data, side effects, patient and surgeon satisfaction were recorded. Patients were observed until the level of sensory block was S1 and the Bromage score was 0. Results: There were no significant differences between the two groups for patient demographic, intraoperative, hemodynamic parameters, side effects and satisfaction. The highest level of sensory block was T9 in the Group L, and T6 in the Group LF (p = 0.001). Duration of motor block was shorter in Group LF than in Group L (291.00 ± 81.08 min in Group L; 213.75 ± 59.49 min in Group LF) (p = 0.001). Conclusion: Both regimes are effective, and the addition of fentanyl to levobupivacaine may offers the advantage of shorter duration of motor block and may be used as an alternative to pure levobupivacaine solution in spinal anesthesia, for transurethral resections. Key Words: Anesthetic technique, anesthesia, spinal; Anesthetics, local, levobupivacaine; Analgesics, opioid, fentanyl. * ** Department of Anesthesiology and Intensive Care Medicine Department of Urology, Ankara Training and Research Hospital, Ulucanlar, Ankara, Turkey. Corresponding Author: Ozgun Cuvas, MD, Specialist, Department of Anesthesiology and Intensive Care Medicine, Ankara Training and Research Hospital, Ulucanlar, Ankara-06340 (Postal code), Turkey. Tel: 0312 595 31 84, GSM: 0542 292 82 98. E-mail: [email protected] 547 M.E.J. ANESTH 20 (4), 2010 548 Introduction Spinal anesthesia is widely used for transurethral resections because it allows early recognition of symptoms caused by overhydration, transurethral resection of prostate (TURP) syndrome, and bladder perforation. Many patients undergoing TURP or TURBT (transurethral resection of bladder tumour) have coexisting pulmonary or cardiac disease1. By reducing the dose of local anesthetic used, side effects can be decreased. However, a low dose of local anesthetic cannot provide an adequate level of sensory block. Levobupivacaine is the S(-)- enantiomer of racemic bupivacaine. Levobupivacaine has similar efficacy but an enhanced safety profile when compared to bupivacaine, a major advantage in regional anesthesia2,3. Intrathecal opioids added to local anesthetics enhance analgesia without intensifying motor and sympathetic block, and make it possible to achieve successful anesthesia in spite of the use of a low dose local anesthetic4-6. Levobupivacaine may be a proper alternative local anesthetic for spinal anesthesia in elderly patients with coexisting systemic disease for TUR operations. By adding fentanyl to levobupivacaine, side effects can be reduced. In this study we aimed to investigate the characteristics and side effects of spinal blocks achieved by levobupivacaine with or without fentanyl, for TURP-BT operations. Methods and Materials After obtaining the approval of the Ethics Committee of our Institution and patients’ informed consent, 40 males, aged >60 years, ASA I-III patients scheduled for elective TURP or TURBT operations were included in a prospective, randomized, doubleblind study. Patients with uncontrolled hypertension, infection at the injection site, disorders of coagulation, history of headache, reluctance to the procedure, neurologic disease or hypersensitivity to amide local anesthetics or fentanyl, were excluded. No premedication was given. Patients were randomly assigned into two equal groups for spinal anesthesia according to numbers inserted in sealed envelopes. After routine monitoring and infusion of O. Cuvas et. al 8 mL.kg-1 of sodium chloride 0.9% solution, baseline hemodynamic values were recorded and then spinal anesthesia was performed with the patient in the left lateral position, using a 25 G Quincke needle at the L3-4 interspace and a midline approach. In Group L (n = 20), 2.5 mL of 0.5% levobupivacaine (Abbott Laboratories, Elverum, Norway) and in Group LF (n = 20), 2.2 mL of 0.5% levobupivacaine with fentanyl citrate 15 µg (0.3 mL) (Abbott Laboratories, North Chicago, USA) were administered via intrathecal injection. Solutions were prepared by another anesthesiologist so that the anesthesiologist performing the block was unaware of which drug was injected. Densities of the solutions were measured at 37°C by refractometry (T2-NE, Atago Co. Ltd, Japan). The densities of the pure levobupivacaine and levobupivacaine plus fentanyl solutions were 1.008 and 1.007, respectively. The direction of the needle aperture was cranial during the injection. After free flow of cerebrospinal fluid was verified, anesthetic solution was given in 15 s without barbotage or aspiration. Immediately after the injection, the patients were placed in the supine position. Heart rate (HR), non-invasive systolic, diastolic and mean arterial blood pressures (SAP, DAP, MAP) and oxygen saturation (SpO2) were recorded every 2.5 min for 15 min after intrathecal injection and every 5 min thereafter. A 30% decrease from baseline SAP or SAP <90 mmHg was treated with incremental iv boluses of ephedrine 5 mg and bradycardia (HR <45) was treated with iv atropine 0.5 mg. Supplementary oxygen 2 L min-1 was given via a nasal cannulae if SpO2 was less than 93% with the patient breathing ambient air. Sensory and motor block were assessed every 2.5 min for 15 min after intrathecal injection and every 5 min thereafter until the sensory block regressed to S1. Anesthesia was considered adequate for surgery if pain sensation as assessed by the pinprick test, was lost at the T10 level. Patients were then placed in the lithotomy position and operation started. The time to achieve sensory block of T10, highest level of sensory block, the time to two-segment SPINAL ANESTHESIA FOR TRANSURETHRAL RESECTION OPERATIONS: LEVOBUPIVACAINE ITH OR WITHOUT FENTANYL regression of sensory block and the time to regression of sensory block to S1, were recorded. Motor block was assessed using the Modified Bromage Scale (0 = no motor block, 1 = inability to raise extended legs, 2 = inability to flex knees, and 3 = inability to flex ankle joints). Onset time of motor block, maximum motor block (Bromage score), duration of motor block (the time from intrathecal injection to the regression of motor block to Bromage score = 0) and duration of complete motor block ( the time from intrathecal injection to the regression of the block to a Bromage score of <3) were recorded also. Complete motor block was defined as a Bromage score of 3. Pain was assessed every 5 min from the beginning of surgery using the 10 score Visual Analog Pain Scale (VAS). In the event a patient complaned of a pain score over three, 1.5 µ. kg-1 iv fentanyl would be administered, and in case of failed spinal block, general anesthesia would be performed. Midazolam would be given intravenously in 0.5 mg increments as indicated for anxiolysis. Volume of glycine used, duration of surgery and patient and surgeon satisfaction were recorded at the end of the operation. Patients were interviewed regarding their opinion of the anesthetic procedure. Likewise, the surgeon was asked to estimate the operating conditions on a scale of excellent, good, fair and poor. Patients were observed until the level of sensory block was S1 and the Bromage score was 0. Adverse effects such as hypotension, bradycardia, nausea, vomiting, shivering, sedation, respiratory depression and pruritus, were recorded. Nausea and vomiting were treated with metoclopramide 10 mg iv. Paracetamol 1 gr iv (Bristol Myers Squibb, Renaudin Laboratories, Itxassou, France) was given during infusion lasting 15 min when the patient complained of pain in the postoperative period. The patients were discharged from the recovery room after the motor block was completely resolved, had stable vital signs, minimal nausea or vomiting and no severe pain or bleeding. Our primary endpoint was the difference in the duration of motor block between the two groups. Other endpoints included were the difference, between the two groups, in the characteristics of sensory block, operating conditions, hemodynamic and side effects. 549 A sample size of 19 patients per group was required to detect a 30 minute difference according to the duration of motor block between two groups with a power of 80% and α = 0.05, based on a pilot study. Twenty patients were included in each group. All of the data were analysed with SPSS 12 (SPSS Inc., Chicago, IL., USA) software. Descriptives were quoted as mean ± SD, median (range), number (incidence) as appropriate. Statistical analyses were performed using Student’s t test (for parametric data) and Mann-Whitney U test (for non-parametric data). The incidences of side effects and satisfactions were analysed using Fisher’s exact test and Chi-Square test. The paired t-test was used to investigate hemodynamic changes over time in each group. Statistical significance was set at the p<0.05 level. Results There were no significant differences between the two groups in demographic data, ASA classification, type and duration of operation or volume of glycine used (p>0.05) (Table 1). Hemodynamic parameters were similar in both groups before and during operation (p>0.05) (Figure 1). Fig. 1 Baseline and lowest blood pressures after spinal anesthesia L = Levobupivacaine; LF = Levobupivacaine plus fentanyl. SAP = Systolic arterial pressure, MAP = Mean arterial pressure, DAP = Diastolic arterial pressure. There were no significant differences between two groups (p>0.05) The highest level of sensory block was T9 (T4-T10) in Group L وand T6 (T3-T10) in Group LF, respectively (p =0.001 ). The time to achieve sensory block of T10, time to two-segment regression of sensory block, time M.E.J. ANESTH 20 (4), 2010 550 O. Cuvas et. al Table 1 Demographic and Perioperative Data Group L (n = 20) Group LF (n = 20) p Age (yr) 70.20 ± 7.33 68.80 ± 5.80 0.674 Weight (kg) 71.15 ± 10.31 71.85 ± 7.23 0.902 Height (cm) 170.20 ± 6.04 171.55 ± 4.23 0.369 2/13/5 3/13/4 0.856 ASA Grade (I/II/III) Type of operation TUR-Prostate/Bladder tumour 12/8 13/7 0.744 Duration of operation (min) 68.00 ± 26.82 74.75 ± 32.50 0.478 Volume of glycine (L) 15.65 ± 10.60 17.00 ± 13.36 0.755 Data are means ± standard deviation or number of patients. L = Levobupivacaine; LF = Levobupivacaine plus fentanyl. to regression of sensory block to S1, onset time of motor block, maximum motor block and duration of complete motor block, were similar in both groups (p>0.05). On the other hand, duration of motor block was shorter in Group LF than Group L (p = 0.001) (Table 2). for surgeon satisfaction and p = 0.165 for patient satisfaction). Table 3 Side Effects in Groups L and LF Group L (n = 20) No patient required supplemental oxygen, analgesia or anxiolysis intraoperatively. There were no significant differences between the two groups with respect to side effects (Table 3) or patient or surgeon satisfaction (p>0.05). Group LF (n = 20) p 1.0 Hypotension 3 (15) 3 (15) 4 (20) 1.0 Bradycardia 3 (15) 1 (5) 1.0 Nausea 2 (10) 0 0 Vomiting 0 0 Shivering Sedation 0 4 (20) 0.106 0 0 Respiratory 0 0 depression Pruritus Data are number of occurrences and incidences (%). L = Levobupivacaine; LF = Levobupivacaine plus fentanyl. The surgeon satisfaction was 35% excellent, 65% good in Group L, 50% excellent, 50% good in Group LF and the patient satisfaction was 35% excellent, 55% good, 10% fair in Group L, 65% excellent, 30% good, 5% fair in Group LF, respectively (p = 0.337 Table 2 Characteristics of Spinal Anesthesia in Two Groups Group L (n = 20) Group LF (n = 20) p Sensory block Time to T 10 (min) 6.50 ± 2.62 6.32 ± 3.50 0.525 Highest level (dermatome) T9 (T4-T10) T6 (T3-T10) 0.001* Time to two segment regression (min) 107.00 ± 52.35 106.00 ± 48.62 0.950 Time to regression to S1 (min) 376.75 ± 80.03 337.25 ± 61.29 0.088 4.00 ± 1.49 3.60 ± 1.07 0.931 19/1 18/2 0.553 291.00 ± 81.08 213.75 ± 59.49 0.001* 145.75 ± 51.79 0.231 Motor block Onset time of Bromage 1 (min) Maximum motor block (n) (Bromage Score 3/2) Duration of motor block (min) Duration of complete motor block (min) 167.00 ± 58.47 Data are means ± standard deviation, median (range) or number of patients. L = Levobupivacaine; LF = Levobupivacaine plus fentanyl. * p<0.05: A significant differences between the two groups. SPINAL ANESTHESIA FOR TRANSURETHRAL RESECTION OPERATIONS: LEVOBUPIVACAINE ITH OR WITHOUT FENTANYL Discussion This study demonstrates that 15 µg fentanyl added to 2.2 mL of 0.5% levobupivacaine provides adequate anesthesia which is similar to that obtained from 2.5 mL of 0.5% levobupivacaine for TURP-BT operations, and the lower-dose of local anesthetic used with fentanyl may offer the advantage of shorter duration of motor block. It has been well documented that a combination of opioids and local anesthetics administered intratechally has a synergistic analgesic effect7-8. The use of racemic bupivacaine with fentanyl in spinal anesthesia for urologic surgery is effective. Kuusniemi et al found that the addition of fentanyl 25 µg to 5 mg of bupivacaine for spinal anesthesia resulted in effective anesthesia with motor block of short duration5. Kararmaz et al compared the intrathecal injection of bupivacaine 4 mg with fentanyl 25 µg and bupivacaine 7.5 mg and found that the sensory block was adequate for surgery in both groups, but the density and duration of motor block were more in the bupivacaine group9. Ben-David et al found that a small dose of fentanyl (10 µg) added to dilute bupivacaine( 3 mL of 0.17% solution) in ambulatory patients undergoing knee arthroscopies intensified and increased the sensory block without increasing the intensity of motor block or prolonging recovery4. Goel et al showed that intrathecal fentanyl 12.5 µg added to bupivacaine 0.17% 5 mg in a total volume of 3 mL produced optimal surgical conditions for minor urological procedures10. Reuben et al suggested that a combination of low dose fentanyl (<20 µg) and bupivacaine produced satisfactory analgesia in elderly patients undergoing lower extremity revascularization procedures, in their study11. Beers et al reported that although a subarachnoid block ≥L1 provided adequate analgesia during TURP operations, the level of sensory block at T10 was necessary to provide adequate analgesia because bladder distension elicited pain under the block levels <T1012. At the time of designing our study there was only one published trial that compared plain solutions of 0.5% levobupivacaine with or without fentanyl, in spinal anesthesia13. Lee et al13 compared the 2.6 mL of 0.5% 551 levobupivacaine and 2.3 mL of 0.5% levobupivacaine with fentanyl 15 µg in spinal anesthesia, but there were no data regarding time to two segment regression, time to S1 regression of sensory block and onset time, duration of motor block or complete motor block. In addition, there was no data about the densities of solutions and rate of injection. Our study was therefore designed to give more details. Although Lee et al found that highest level of sensory block was similar between the two groups, in our study, however the combination of levobupivacaine with fentanyl reached a higher level of sensory block. The resolution of motor block was faster in this combination group than in the levobupivacaine group. Low dose local anesthetic used in levobupivacaine with fentanyl group, offered the advantage of shorter duration of motor block. This result was consistent with the resulting from the other studies which investigated the effects of bupivacaine with or without fentanyl in spinal anesthesia5,9. The clinical significance of a reduced duration of motor block resuting from lowerdose levobupivacaine plus fentanyl would be early ambulation. The duration of sensory block to S1 level, however, was not different between the groups, so the overall block resolution was not different. Our results may be used as a building stone for further doseresponse studies. The duration of injection and baricity of injected solutions may be reasonable factors explaining the differences in the highest level of sensory block between two our study that of Lee’s. We injected the local anesthetic solution in 15 s where as Lee did not suggested this time. In considering our measurements, levobupivacaine plus fentanyl solution is more hypobaric than the pure levobupivacaine solution. No data is given about the densities of solutions in the study of Lee13. Opioids such as fentanyl are hypobaric and when added to a local anesthetic will render the subsequent mixture even more hypobaric14. Parlow et al stated that the addition of opioids to isobaric local anesthetics alters the density of the resulting solutions, as well as the direction and extent of spread in a spinal model15. In Lee et al study, three patients (12%) in levobupivacaine group developed shivering. Hypotension occured in four patients (16%) (one M.E.J. ANESTH 20 (4), 2010 552 in group levobupivacaine and three in group levobupivacaine with fentanyl). No patient had nausea, vomiting or pruritis. In our study, side effects related to the spinal fentanyl (pruritus and vomiting) did not occur similar to the results of Lee et al. Patient satisfaction was good in all cases in the study of Lee et al13. In our study, there were no significant differences between the two groups with respect to side O. Cuvas et. al effects or patient and surgeon satisfaction. In conclusion, both regimes are effective, and fentanyl added to levobupivacaine, in the dosage used in the present study, may offer an advantage of decreased duration of motor block and could be an alternative to the use of pure levobupivacaine solution in spinal anesthesia for transurethral resections. References 1. Mebust WK, Holtgrewe HL, Cockett ATK, Peters PC: Transurethral prostatectomy: immediate and postoperative complications. Cooperative study of 13 participating institutions evaluating 3,885 patients. J Urol; 2002, 167(1):5-9. 2. Mcleod GA, Burke D: Levobupivacaine. Anaesthesia; 2001, 56(4):331-41. 3. Casati A, Baciarello M: Enantiomeric local anesthetics: can ropivacaine and levobupivacaine improve our practice? Curr Drug Therapy; 2006, 1:85-9. 4. Ben-David B, Solomon E, Levin H, Admoni H, Goldik Z: Intrathecal fentanyl with small-dose dilute bupivacaine: better anesthesia without prolonging recovery. Anesth Analg; 1997, 85:560-5. 5. Kuusniemi KS, Pihlajamakin KK, Pitkanen MT, Helenius HY, Kirvela OA: The use of bupivacaine and fentanyl for spinal anesthesia for urologic surgery. Anesth Analg; 2000, 91:1452-6. 6. Ben-David B, Frankel R, Arzumonov T, Marchevsky Y, Volpin G: Minidose bupivacaine-fentanyl spinal anesthesia for surgical repair of hip fracture in the aged. Anesthesiology; 2000, 92(1):6-10. 7. Maves TJ, Gebhart GF: Antinociceptive synergy between intrathecal morphine and lidocaine during visceral and somatic nociception in the rat. Anesthesiology; 1992, 76:91-9. 8. Wang C, Chakrabarti MK, Whitwam JG: Specific enhancement by fentanyl of the effects of intrathecal bupivacaine on nociceptive afferent but not on sympathetic efferent pathways in dogs. Anesthesiology; 1993, 79:766-73. 9. Kararmaz A, Kaya S, Turhanoglu S, Ozyilmaz MA: Lowdose bupivacaine–fentanyl spinal anaesthesia for transurethral prostatectomy. Anaesthesia; 2003, 58:526-30,. 10.Goel S, Bhardwaj N, Grover VK: Intrathecal fentanyl added to intrathecal bupivacaine for day case surgery: a randomized study. Eur J Anaesthesiol; 2003, 20:294-7. 11.Reuben SS, Dunn SM, Duprat KM, O’sullivan P: An intrathecal fentanyl dose-response study in lower extremity revascularization procedures. Anesthesiology; 1994, 81:1371-5. 12.Beers RA, Kane PB, Nsouli I, Krauss D: Does a mid-lumbar block level provide adequate anaesthesia for transurethral prostatectomy? Can J Anaesth; 1994, 41(9):807-12. 13.Lee YY, Muchhal K, Chan CK, Cheung ASP: Levobupivacaine and fentanyl for spinal anaesthesia: a randomized trial. Eur J Anaesthesiol; 2005, 22:899-903. 14.Mcleod GA: Density of spinal anaesthetic solutions of bupivacaine, levobupivacaine, and ropivacaine with and without dextrose. Br J Anaesth; 2004, 92:547-51. 15.Parlow JL, Money P, Chan PSL, Raymond J, Milne B: Addition of opioids alters the density and spread of intrathecal local anesthetics? An in vitro study. Can J Anaesth; 1999, 46(1):66-70. ASSOCIATION BETWEEN FACTORS PREDICTING AND ASSESSING THE AIRWAY AND USE OF INTUBATING LARYNGEAL MASK AIRWAY Chryssoula Staikou*, Athanassia Tsaroucha*, Anteia Paraskeva*, Argyro Fassoulaki* Summary Background and objective: The Intubating Laryngeal Mask Airway FastrachTM (ILMA) has been used with success in difficult intubation cases. The purpose of this study is to evaluate the effect of mouth opening, Mallampati classification, thyromental distance and Cormack-Lehane Grade, on the ease of ILMA use. Methods: Eighty one patients ASA I-II, were assessed preoperatively for mouth opening, Mallampati classification and thyromental distance. After induction with propofol and rocuronium, the first investigator recorded Cormack-Lehane Grade by direct laryngoscopy. Subsequently an appropriate size ILMA was inserted by the second investigator and correct placement was confirmed by adequate ventilation and normal capnogram. A maximum of three ILMA insertion attempts were allowed and the number was recorded. Then blind intubation was attempted and classified as follows, according to Intubation Difficulty Grade (IDG): IDG-1: intubation succeeded: at first attempt requiring no or minor ILMA manipulations. IDG-2: intubation succeeded at second attempt requiring major ILMA manipulations or size change. IDG-3: intubation failed after the second attempt or oesophageal intubation occurred at either attempt. In failure of the technique direct laryngoscopy was the alternative approach. Results: Success rates in insertion of ILMA and in blind intubation were 100% and 92.6% respectively. No difference was found between Cormack-Lehane Grade I-II and II-IV or Mallampati classification and number of ILMA insertion attempts or IDG. There was also no correlation between mouth opening, or thyromental distance and number of ILMA insertion attempts or IDG. It is concluded that easiness of ILMA use is irrelevant to mouth opening, thyromental distance, Mallampati classification or Cormack-Lehane Grade. Key words: Airway devices; Intubation Laryngeal Mask Airway Fastrach, Airway assessment; Mallampati Classification, mouth opening, thyromental distance, Cormack-Lehane Grade. * Anesthesiology Dept., Aretaieio Hospital Univ. of Athens. Athens, Greece. Corresponding author: Anteia Paraskeva, E-mail: [email protected], [email protected], Tel: +30-2107286323. 553 M.E.J. ANESTH 20 (4), 2010 554 Introduction In contradiction to the classic Laryngeal Mask Airway (cLMA), the Intubating Laryngeal Mask Airway FastrachTM (ILMA), can be used for ventilation, allowing blind or fiberoptic intubation through the device. The specific design characteristics of the ILMA permits its insertion with the patient’s head in neutral position, without guidance by the fingers into patient’s mouth and with the practitioner not necessarily positioned behind the patient’s head. Those features render the ILMA a valuable airway device in the operating room as well as in emergency medical units1,2. Although insertion and placement of the classic LMA has not been associated with prediction or assessment of a difficult airway3,4, there is evidence that easiness of ILMA use is inversely related to difficult airway5. Indeed intubation with the ILMA has achieved high success rates in patients with difficult intubation6, or were traditional techniques to intubate have failed7. Nevertheless no study has evaluated a possible association between airway assessment and easiness of ILMA use in general population. In this study we investigated the possible impact of mouth opening, Mallampati classification, thyromental distance and Cormack-Lehane grade, on ILMA insertion and blind intubation. Materials and Methods Following approval of the Hospital Ethics Committee and obtaining patient’s informed consent, 81 adults (13 males, 68 females), ASA I-II, scheduled for surgical procedures under general anesthesia with tracheal intubation were recruited for the study. Exclusion criteria were mouth opening less than 2.5 cm, oropharyngeal pathology and risk of regurgitation. Preoperatively, an anesthesiologist ignorant of the study to be undertaken, assessed mouth opening, Mallampati classification (Class I-IV) and thyromental distance. Mallampati classification was assessed, while the patient was sitting with the mouth wide open and the tongue protruding without phonating8,9. C. Staikou et. al Mouth opening was considered as the width of the interincisor gap at midline (expressed as number of anesthesiologist’s fingers fitting in the gap)10. Thyromental distance was defined as the distance in cm, measured from the thyroid cartilage to inside of the mentum, while the patient was sitting with the head extended and the mouth closed11. In the operating room, standard monitoring, consisted of ECG, pulse oximetry, non-invasive blood pressure measurement, gas analyser and side spirometry (Datex-Ohmeda S/5TM Anesthesia Monitor, Helsinki, Finland). After inserting an 18G venous catheter, Ringer Lactate infusion was started and ranitidine 50 mg and metoclopramide 10 mg IV were given. All patients were preoxygenated for 5 minutes with 100% O2. Anesthesia was induced with propofol 2.5 mg/kg and fentanyl 2 μg/kg and rocuronium 0.6 mg/kg, provided face mask ventilation was feasible. Two staff anesthesiologists participated in the study .The first anesthesiologist by direct laryngoscopy using a Macintosh blade 4 without external maneuver2 evaluated in all patients Cormack-Lehane Grade as: Grade I (full view of the glottis). Grade II (glottis partially exposed). Grade III (only epiglottis seen). Grade IV (epiglottis not seen). At completion of laryngoscopy, face mask ventilation was applied again providing 3-5 inflations of 100% oxygen. Then with the patient’s head in neutral position, a second anesthesiologist, having an experience of more 50 successful ILMA uses and standing behind patient’s head, attempted to insert in all patients, the appropriate size of ILMA (ILMATM, Laryngeal Mask Airway Company, UK): (size 3 if body weight less than 50 kg, size 4 if body weight between 50 and 70 kg and size 5 if body weight more than 70 kg). Correct insertion of ILMA, was confirmed by easy bag ventilation without audible leak (at peak airway pressures up to 20 cm H2O) and by a normal capnogram. A maximum of 3 ILMA insertion attempts was allowed and the number of attempts was recorded. Manual ventilation by face mask with 100% O2 and additional boluses of propofol (20-40 mg) were given A ASSOCIATION BETWEEN FACTORS PREDICTING AND ASSESSING THE AIRWAY AND USE OF INTUBATING LARYNGEAL MASK AIRWAY to maintain an adequate level of anesthesia between ILMA insertion attempts. After successful insertion, blind intubation of the trachea was attempted by the same anesthesiologist, with a wire-reinforced, silicone, cuffed tracheal tube specially designed for the ILMA. A 7, 7 or 7.5 and 7.5 or 8 mm ID tube was used for 3, 4 and 5 size ILMA respectively. Attempts for blind intubation were classified by the Intubation Difficutly Grade (IDG) as follows: IDG-1: successful blind intubation at first attempt without any or after minor manipulation of the ILMA, to optimize the position of the ILMA. IDG-2: successful blind intubation at second attempt after further manipulation of the ILMA (the ILMA was withdrawn a few cm without deflating the cuff and repositioned: “up-down” maneuvre) or size change5 combined with maneuvers to adjust patient’s position for alignment with the glottis (optimizing head-neck position, applying mild laryngeal pressure). ILMA size change and the up-down maneuver according to the depth (measured from the black transverse marker on the tracheal tube) resistance was encountered. If resistance was at less than 1.5 cm or at more than 4 cm a smaller size ILMA used. If resistance was between 2-4 cm a larger size of ILMA was used. If resistance was between 1.5-2 cm an up-down maneuver was performed. IDG-3: unsuccessful second attempt for blind intubation or esophageal intubation at either attempt. Between intubation attempts patients were ventilated via the ILMA with 100% oxygen and additional boluses of propofol (20-40 mg) were given to ensure adequate anesthetic depth. If blind intubation failed, direct laryngoscopy was the alternative approach. Complications such as desaturation (SpO2<90%), regurgitation or aspiration, severe bronchospasm and oropharyngeal or dental trauma, occurring at insertion of the ILMA or at blind intubation, were recorded. 555 distributions, while Mallampati classification, mouth opening, Cormack-Lehane grade, number of insertion attempts and IDG did not follow normality. Chi square test was used for association between Mallampati classification or Cormack-Lehane Grade and insertion attempts and between Mallampati classification or Cormack-Lehane Grade and IDG. To analyze bivariate correlations between BMI, thyromental distance or mouth opening and insertion attempts or IDG, the Spearman non parametric correlation coefficient was used, corrected for the number of possible correlations. Statistical significance was considered when P<0.05 for Chi Square test and when P<0.016 for Spearman correlation coefficient. Results Patient characteristics are shown in Table 1. Table 1 Patients characteristics: Age (yrs), Height (cm), BMI (Kg.m-2) and Thyromental distance (cm). Values are mean (SD). Mallampati, mouth opening (number of fingers), Cormack Lehane Grade, insertion attempts and IDG. Values are median (min-max). Age (yrs) 53(15) Height (cm) 165(7) BMI (Kg.m-2) 26(4) Mallampati 2(1-3) Thyromental distance (cm) 8.5(1) Mouth opening (number of fingers) 3(2-4.5) Cormack-Lehane Grade 1(1-3) Insertion attempts 1(1-2) IDG 1(1-3) The overall rate in successful insertion of ILMA was 100%, (91.4% at first attempt and 8.6% at second attempt). Statistics The overall rate in successful blind intubation with the ILMA was 92.6%. Of the successfully intubated patients sixty three (77.8%) had IDG-1, 10 (12.3%) had IDG-2, and eight (9.9%) patients had IDG-3. Data were analyzed using the SPSS 15.0 statistical program (SPSS INC., Chicago, IL, USA). According to Kolmogorov-Smirnov test, age, height, BMI and thyromental distance followed normal Seventy one patients (71/81) had Cormack –Lehane grade I or II, 10 patients (10/81) had a Cormack-Lehane grade III and no patient had grade IV. The rate in successful blind intubation for patients M.E.J. ANESTH 20 (4), 2010 556 C. Staikou et. al with Cormack Lehane grade III was 70% (7/10), with a 60% success (6/10) at first attempt. Eight of the 81 patients (9.9%) were not intubated with the ILMA at either attempt. Seven of them (7/8) had a Cormack-Lehane grade I or II and were easily intubated under direct laryngoscopy. One patient (1/10) had a Cormack-Lehane grade III and could not be intubated under direct laryngoscopy, despite the use of a gum elastic boogie and the McCoy blade and surgery proceeded with an LMA proseal. There was no difference between Mallampati classification or Cormack-Lehane Grade and insertion attempts or IDG (table 2). No correlation was found between thyromental distance, or mouth opening and insertion attempts or IDG (table 2). Table 2 Insertion attempts and IDG in relation to Mallampati score, mouth opening (number of fingers) thyromental distance (cm) and Cormack-Lehane Grade. Insertion attempts IDG Mouth opening (number of fingers) P= 0.480 r = -0.080 P= 0.219 r = -0.138 Mallampati P= 0.296 X2=2.433 P= 0.698 X2=2.205 Thyromental distance (cm) P = 0.150 r = -0.161 P = 0.214 r = -0.139 Cormack-Lehane grade P = 0.588 X2 = 1.936 P = 0.75 X2 = 5.19 * P<0.05 for Chi Square (level of statistical significance). ** P<0.016 for Spearman coefficient (level of statistical significance) Complications, such as desaturation (SpO2<90%), regurgitation or aspiration, severe brochospasm and oropharyngeal or dental trauma, at insertion of the ILMA or at blind intubation, were not recorded. Disscusion According to our results successful insertion of ILMA and intubation with the device has been accomplished in 100% and 92.6% of patients respectively No relationship was found between factors predicting or assessing difficult airway and easiness of the ILMA use. Brain et al, found that tracheal intubation with the ILMA required fewer adjusting manoeuvers in patients with a predicted or known difficult airway5. The authors suggested that in those cases anterior placement of the larynx favors blind intubation with the ILMA because of its structure. Combes et al, in a recent study showed that airway management with the ILMA was simpler in obese than in lean patients13. Although obesity is related to difficult intubation14,15, Cormack-Lehane Grade was not assessed in those patients and the authors suggested less rotating movement of the ILMA in obese patients because of less pharyngeal space, a fact not considered in the definition of difficult airway. Similarly Ferson et al, in a retrospective study found that in 111 patients with a Cormack-Lehane Grade IV, intubation with the ILMA was achieved in 92% of patients and in 63.6% intubation was successful at first attempt6. Also, Agro et al, in a prospective study recorded correct insertion of ILMA in 95% of the patients studied and intubation at first attempt succeeded in 74% of the patients16. In this study only 6 patients had known or predicted difficult airway. Our results are in accordance with the results of Roblot et al17, who did not detect in women any impact of Cormack-Lehane Grade or of a difficult intubation predicting score (Arne’s score) on ILMA use. Although bedside tests are considered poor predictors of difficult intubation, especially if each of them is used alone18,19, we preferred to investigate separately the difficult intubation predictive factors, such as thyromental distance, mouth opening and Mallampati classification, because a possible correlation between ILMA use with each factor could not be revealed, if it was summated in a multifactorial risk score. Also since we decided to assess directly the airway by Cormack-Lehane Grade we thought that at the same time predicting difficult airway was unnecessary. We decided to make up to two attempts for blind intubation since according to Difficult Airway Society (DAS) guidelines up to 4 intubation attempts are allowed in cases difficult intubation is encountered after induction20. Similarly Frappier et al, studying obese patients (BMI >40) did not find any impact of Cormack-Lehane Grade on the easiness of ILMA use21. We are aware of the difficulty to study prospectively a systematic effect of difficult intubation A ASSOCIATION BETWEEN FACTORS PREDICTING AND ASSESSING THE AIRWAY AND USE OF INTUBATING LARYNGEAL MASK AIRWAY predictive factors and Cormack-Lehane Grade on ILMA use in general population. A limitation of our study is a small number of Cormack-Lehane III or IV grade in general population. Since ILMA appears in the revised ASA guidelines22 and also in DAS guidelines20 as an alternative approach to difficult airway, it is important that further studies will delineate our hypothesis, if 557 ILMA is or is not easier to use in a failed intubation scenario. In conclusion, under the present study design, ILMA use was not associated with mouth opening, Mallampati classification, thyromental distance, or Cormack-Lehane Grade. M.E.J. ANESTH 20 (4), 2010 558 C. Staikou et. al References 1. Burgoyne L, Cyna A: Laryngeal mask vs intubating laryngeal mask: insertion and ventilation by inexperienced resuscitators. Anaesth Intensive Care; 2001, 29:604-608. 2. Combes X, Aaron E, Jabre P, Leroux B, Lefloch AS, Andre JY et al: Introduction of the intubating Laryngeal Mask Airway in a prehospital emergency medical unit. Ann Fr Anesth Reanim; 2006, 25:1025-1029. 3. Brimacombe J, Berry A: Mallampati classification and laryngeal mask insertion. Anaesthesia; 1993, 48:347. 4. Mahiou P, Narchi P, Veyrac P, Germond M, Gory G, Bazin G: Is laryngeal mask easy to use in case of difficult intubation? Anesthesiology; 1992, 77:A1228. 5. Brain AI, Verghese C, Addy EV, Kapila A, Brimacombe J: The intubating laryngeal mask. II: a preliminary clinical report of a new means of intubating the trachea. Br J Anaesth; 1997, 79:704-709. 6. Ferson DZ, Rosenblatt WH, Johansen MJ, Osborn I, Ovassapian A: Use of the intubating LMA-Fastrach™ in 254 patients with difficult to manage airways. Anesthesiology; 2001, 95:1175-1181. 7. Parr MJ, Gregory M, Baskett PJ: The intubating laryngeal mask use in failed and difficult intubation. Anaesthesia; 1998, 53:343348. 8. Samsoon GL, Young JR: Difficult tracheal intubation: a retrospective study. Anaesthesia; 1987, 42:487-490. 9. Mallampati SR, Gatt SP, Gugino LG, Desai SP,Waraksa B, Freiberger D, et al: A clinical sign to predict difficult tracheal intubation: a prospective study. Can Anaesth Soc J; 1985, 32:429434. 10.Aiello G, Metcalf I: Anaesthetic implications of temporomandibular joint disease. Can J Anaesth; 1992, 39:610-616. 11.Lewis M, Keramati S, Benumof JL, Berry CC: What is the best way to determine oropharyngeal classification and mandibular space length to predict difficult laryngoscopy? Anesthesiology; 1994, 81:69-75. 12.Cormack RS, Lehane J. Difficult intubation in obstetrics. Anaesthesia; 1984, 39:1105-1111. 13.Combes X, Sauvat S, Leroux B, Dumerat M, Sherrer E, Motamed C, et al: Intubating laryngeal mask airway in morbidly obese and lean patients. Anesthesiology; 2005, 102:1106-1109. 14.Rose DK, Cohen MM: The airway: Problems and predictions in 18,500 patients. Can J Anesth; 1994, 41:372-383. 15.Wilson ME, Spiegelhalter D, Robertson JA, Lesser P: Predicting difficult incubation. Br J Anaesth; 1988, 61:211-216. 16.Agro F, Brimacombe J, Carassiti M, Marchionni L, Morelli A, Cataldo R: The intubating laryngeal mask (Clinical appraisal of ventilation and blind tracheal intubation in 110 patients). Anaesthesia; 1998, 53:1084-1090. 17.Roblot C, Ferrandiere M, Bierlaire D, Fusciardi J, Mercier C, Laffon M: Impact of Cormack and Lehane’s grade on Intubating Laryngeal Mask Airway Fastrach™ using: a study in gynaecological surgery. Ann Fran Anest Reanim; 2005, 24:487-491. 18.Shiga T, Wajima Z, Inoue T, Sakamoto A: Predicting difficult intubation in apparently normal patients. A meta-analysis of bedside screening test perfomance. Anesthesiology; 2005, 103:429- 437, 2005. 19.Iohom G, Ronayne M, Cunningham AJ: Prediction of difficult tracheal intubation. Eur J Anaesthesiol; 2003, 20:31-36. 20.Henderson JJ, Popat MT, Latto IP, Pearce AC: Difficult airway society quidelines for management of the unanticipated difficult intubation. Anaesthesia; 2004, 59:675-694. 21.Frappier J, Guenoun T, Journois D, Philippe H, Aka E, Cadi P, et al: Airway management using the intubating laryngeal mask airway for the morbidly obese patient. Anesth Analg; 2003, 96:1510-1515. 22.Practice guidelines for management of the difficult airway. An updated report by the American Society of Anesthesiologists Task Force on management of the difficult airway. Anesthesiology; 2003, 98:1269-1277. PREOPERATIVE ORAL DEXTROMETHORPHAN DOES NOT REDUCE PAIN OR MORPHINE CONSUMPTION AFTER OPEN CHOLESYCTECTOMY Hossein Mahmoodzadeh1, Ali Movafegh2 and Nooshin Moosavi Beigi3 Summary Background: Dextromethorphan (DM), the D-isomer of the codeine analogue levorphanol, is a weak, noncompetitive N-Methyl-D-Aspartate (NMDA) receptor antagonist. It has been suggested that NMDA receptor antagonists induce preemptive analgesia when administrated before tissue injury occurs, thus decreasing the subsequent sensation of pain. Method: The study was conducted in the Dr Ali shariati hospital, Tehran University of Medical Sciences, Tehran, Iran. In this seventy two patients scheduled for elective cholesyctectomy between February 2005 and December 2006 were randomized into three equal groups to receive as premedication either oral dextromethorphan 45 mg (Group D45 = 24), dextromethorphan 90 mg (Group D 90 = 24) or placebo (Group C, n = 24), 120 min before surgery. A visual analogue scale (VAS) for pain of each patient measured at arrival in the ward and 6 and 24 hours after surgery, was recorded. Results: The demographic characteristics of patients, ASA physical status class, duration of surgery, and the basal VAS pain score were similar in the two groups. There was no significant difference in the mean of the VAS pain scores measured over time or morphine consumption between three groups. Conclusion: Dextromethorphan, 45 and 90 mg orally administrated 2 h before surgery had no effect on postoperative morphine requirement and pain intensity. Key words: dextromethorphan, postoperative pain, preemptive analgesia. 1 2 3 From the Departments of Surgery 1, 2 and Anesthesiology and Critical Care, Ali Shariati Hospital, Tehran Univ. of Medical Sciences, Tehran, Iran. MD, Assist. Prof. Surgery. MD, Associate Prof. Anesth. & Critical Care. MD, Resident Surgery. Corresponding Author: Ali Movafegh MD, Department of Anesthesiology and Critical Care, Dr Ali Shariati Hospital, North Karegar Street, Tehran 1411713135, Iran. Tel: +98-912-3021389, Fax: +98-21-88026017. E-mail Address: [email protected] 559 M.E.J. ANESTH 20 (4), 2010 560 Introduction Opioids, are frequently administered to patients undergoing major surgery to alleviate postoperative pain. However, they may cause adverse effects such as nausea and vomiting, pruritus, urinary retention and respiratory depression1. As the analgesia and side effects of opioids are dose dependent, a multimodal offset may enhance analgesia while minimizing the side effects1. Dextromethorphan (DM), the D-isomer of the codeine analogue levorphanol, is a weak, noncompetitive N-Methyl-D-Aspartate (NMDA) receptor antagonist that has been used as an antitussive drug for more than 40 years2,3. It has been suggested that NMDA receptor antagonists induce preemptive analgesia when administrated before tissue injury occurs, thus decreasing the subsequent sensation of pain2,3.There is good evidence from basic scientific literature to believe that acute postinjury pain states in humans could be treated usefully with a combination of opioids and NMDA antagonists46-. The purpose of the current study was therefore to determined to find out whether preoperative administration of 45 and 90 mg of oral DM would reduce postoperative pain and opioid consumption as compared to a control group. Method & Materials The study was conducted in the Dr Ali shariati hospital, Tehran University of Medical Sciences, Tehran, Iran. The proposal was approved by the Institutional Ethics Committee and informed written consent was obtained from the patients. Between February 2005 and December 2006 seventy two patients, 25-50 years, ASA I & II scheduled for open cholesyctectomy (midline approach) under general anesthesia, were enrolled in this randomized, double- blinded, and placebo controlled study. Patients who received opioids within 48 h of surgery and sedatives or centrally acting drugs(central nervous system depressants or antidepressants) during the 21 days prior to surgery; those with a history of chronic pain, psychotic disorders or addiction including opioids, those with any contraindication to H. Mahmoodzadeh et. al DM and pregnant or lactating women were excluded from the study. All participants were given full explanations of DM and the visual analog scale for pain (VAS) on the day before surgery. All drugs were given by an anesthesiologist who was not involved in patient observation, thus both the observer and patients were blinded to the group assignment. Patients were randomly assigned into three equal groups (24 each): Patients receiving DM 45 mg (Group 45 DM), (Patients receiving DM 90 mg (Group DM 90, and (Group C) using a computer generated randomization list. All patients in the 3 groups received the designated dose orally 120 min before surgery. Placebo was in similar capsules containing sucrose. On arrival to operating room, all patients were monitored with an electrocardiogram (ECG), noninvasive blood pressure and pulse oximetry. An 18gauge cannula was inserted and lactated ringer solution 7 ml.kg-1 was administered. Anesthesia was induced with 2 mg.kg-1 propofol and 0.3 µg.kg-1 sufentanyl; and endotracheal intubation was facilitated with 0.15 mg.kg-1 cisatracurium. After tracheal intubation, anesthesia was maintained by isoflurane and N2O (50%); 0.05 mg.kg-1 cisatracurium and 0.2 µg.kg-1 sufentanyl were administered half hourly. Ventilation was adjusted to maintain normocapnia (end-tidal carbon dioxide partial pressure 4.7-5.3 kPa). Patients were actively warmed to keep core temperature (esophageal) normothermic. At the beginning of the skin sutures, drugs administration was stopped and neuromuscular block was antagonized by IV administration of 2.5 mg of neostigmine along with 1.25 mg atropine. Patients were considered awake when they opened their eyes on demand or after gentle tactile stimulation; they were later extubated. The severity of postoperative pain was measured and recorded using a 10-cm visual analog scale (VAS), (0 = no pain and 10 = the worst possible pain). Patients were asked to score the pain during coughing or movement at arrival in the ward and 6 and 24 hours after surgery. Patients could request rescue analgesia at any time. Morphine, 0.1 mg/kg-1 was given as rescue analgesia at 8-h intervals. PREOPERATIVE ORAL DEXTROMETHORPHAN DOES NOT REDUCE PAIN OR MORPHINE CONSUMPTION AFTER OPEN CHOLESYCTECTOMY According to the previous studies, a sample size of 24 in each group would be sufficient to detect a difference of 3 scores in the mean of pain score, estimating a power of 80%, and a significance level of 5%. Statistical analysis was performed using SPSS package (SPSS Inc., Chicago, IL, USA), version 11.5. Normality of distribution was checked as needed. For statistical analysis of demographic data and for comparison of groups one way ANOVA, repeated measure analysis of variance, Fishers exact or Chisquare tests where appropriate. Tow tailed P<0.05 was taken as significant. Results Seventy two patients were randomized. Three patients were excluded from the study because the surgical complications (two from C group and one from D45 group). Demographic characteristics of patients, ASA physical status class, and surgery time (min) were similar in the two groups (Table 1). Table 1 Demographic characteristics Group Control (n = 22) Group DM 45 (n = 23) Group DM 90 (n = 24) 48.3 ± 14.5 48.2 ± 14.3 46.2 ± 23.3 Age (yr)* 13/9 13/10 14/10 Sex (F/M) Surgery Time (min)* 98 ± 25.6 104 ± 23.2 112 ± 13.2 10/12 12/11 11/13 ASA class (I/II) 78.3 ± 7.5 80.1 ± 10.4 75.1 ± 8.3 Weight (kg)* * Values are expressed as mean ± SD. ** There are no significant differences among the groups. There were no significant differences in the mean of the morphine consumption (12.39 ± 5.24 mg in DM 45 group and 13.71 ± 4.28 mg in DM 90 group, versus 11.88 ± 5.29 in C group) and the time to first morphine request (3.1 ± 1.7 h in DM 45 group and 3.2 ± 1.9 in DM 90 group, versus 2.9 ± 1.1 in control group) (Table 2). There was no significant difference in the mean of VAS pain scores measured over time between three groups(5.55 ± 1.38, 4.83 ± 2.39, 3.62 ± 2.92 in group C; 4.73 + 2.14, 4.22 + 2.36, 4.00 + 2.50 in group DM 45; and 5.18 ± 2.81, 4.12 ± 2.80, 3.24 ± 2.95 in group DM 90, repeated-measures analysis of variance, betweensubjects effects) (Table 2). 561 Table 2 VAS for pain, morphine consumption and time to first morphine injection in the three groups. Group Control Group DM 45 Group DM 90 3.1 ± 1.7 3.2 ± 1.9 Total Morphine 11.88 ± 5.29 Consumption (mg)* Time to First 2.9 ± 1.1 12.39 ± 5.24 13.71 ± 4.28 Morphine Injection (h)* Visual Analogue Scale for pain* 5.55 ± 1.38 4.73 + 2.14 5.28 ± 2.81 - Arriving Ward 4.83 ± 2.39 4.22 + 2.36 4.12 ± 2.80 -6h - 24 h 3.62 ± 2.92 4.00 + 2.50 3.24 ± 2.95 * Values are expressed as mean ± SD. ** There are no significant differences among the groups. Discussion This study demonstrated that in patient undergoing open cholecystectomy, oral premedication with 45 or 90 mg DM did not decrease post-operative pain intensity or morphine consumption when compared to patients who received placebo. Our findings are not consistent with earlier reports that dextromethorphan reduces pain and analgesic requirement after various surgeries7-10. N-methyl-D-aspartate receptor antagonism inhibits wind up or central hypersensitivity of dorsal horn neurons in response to noxious stimulation2-11. Dextromethorphan, an NMDA receptor antagonist has been shown to reduce secondary hyperalgesia but have no effect on primary hyperalgesia on healthy adult male volunteers2,12,13.Other investigators have been unable to demonstrate that DM, in clinically relevant dose, has any effect on primary or secondary hyperanalgesia14,15. The ability of DM to attenuate pain is controversial. Not all investigators agree that DM reduces opioid consumption or acute pain. Although DM have been used successfully as premedication for postoperative pain and morphine consumption reduction in some investigations6-10, other studies have not corroborated these reports16-19. Ilkjaer et al studied 50 patients undergoing nonmalignant elective abdominal hysterectomy. The study was a double-blinded, randomized designed to compare M.E.J. ANESTH 20 (4), 2010 562 post-operative analgesia requirements and pain scores in patients who received preoperative DM or placebo. DM reduced morphine requirements in this sample and a modest (but non-significant) reduction in pain scores was found. They found that oral dextromethorphan 150 mg reduced PCA morphine consumption immediately (0-4 h) after hysterectomy, without prolonged effects on pain or wound hyperalgesia18. Thematic of the controversy surrounding the role of DM in acute pain management, Wadhaw et al. failed to demonstrate the specific opioid sparing effect expected with DM administration. In this 66 patient experimental sample, the investigators concluded that DM dose not improve acute pain scores even at high doses19. Many surgical procedures were included in both positive and negative studies, and there did not appear to be one specific procedure that yielded more benefit than any other. In the dextromethorphan studies, four negative studies used the oral route, and in two of these trials at smaller doses of drug, there was no direct analgesic effect of the intervention16-19. H. Mahmoodzadeh et. al The NMDA blocking properties of DM are likely less potent compared to ketamine2. It is possible that only subset of individuals will benefit from the NMDA properties of DM. As well it may be that DM should be administered parenterally in a dose of at least 1 mg/kg-1 for maximal preventive effect2. Further investigations are required to determine whether larger doses or repeated doses of oral dextromethorphan attenuate post operative pain. However, undesirable side effects of dextromethorphan, including sedation and ataxia, are common in adults when the dose is increased above that recommended for antitussive therapy and may limit its usefulness17. The power analysis for this study indicated that there were sufficient numbers of patients in each group to detect 25% reduction in morphine use and 30 mm reduction in VAS for pain on moving. In conclusion, dextromethorphan, 45 and 90 mg orally administrated 2 h before surgery had no effect on postoperative morphine requirement and pain intensity. PREOPERATIVE ORAL DEXTROMETHORPHAN DOES NOT REDUCE PAIN OR MORPHINE CONSUMPTION AFTER OPEN CHOLESYCTECTOMY 563 References 1. Movafegh A, Soroush AH, Navi A, Sadeghi M, Esfehani F, Akbarian-Tefaghi N: The effect of intravenous administration of dexamethasone on postoperative pain, nausea, and vomiting after intrathecal injection of meperidine. Anesth Analg; 2007, 104:987-9. 2. McCartney C, Sinha A, Kates JA: qualitative systematic review of the role of N-Methyl-Daspartate receptor antagonists in preventive analgesia. Anesth Analg; 2004, 98:1385-400. 3. Wadhwa A, Clarke D, Goodchild CS, Young D: Large-dose oral dextromethorphan as an adjunct to patient-controlled analgesia with morphine after knee surgery. Anesth Analg; 2001, 92:448-54. 4. Davies SN, Lodge D: Evidence for involvement of N-methylaspartate receptors in ‘wind-up’ of class 2 neurones in the dorsal horn of the rat. Brain Res; 1987, 424:402-6. 5. Chapman V, Dickenson AH: The combination of NMDA antagonism and morphine produces profound antinociception in the rat dorsal horn. Brain Res; 1992, 573:321-3. 6. Advokat C, Rhein FQ: Potentiation of morphine-induced antinociception in acute spinal rats by the NMDA antagonist dextrorphan. Brain Res; 1995, 699:157-60. 7. Yeh CC, Jao SW, Huh BK, Wong CS, Yang CP, With WD, Wu CT: Preincisional dextromethorphan combined with thoracic epidural anesthesia and analgesia improves postoperative pain and bowel function in patients undergoing colonic surgery. Anesth Analg; 2005, 100:1384-9. 8. Weinbroum AA: Dextromethorphan reduces immediate and late postoperative analgesic requirements and improves patients’ subjective scorings after epidural lidocaine and general anesthesia. Anesth Analg; 2002, 94:1547-52. 9. Chai YY, Liu K, Chow LH, Lee TY: The preoperative administration of intravenous dextromethorphan reduces postoperative morphine consumption. Anesth Analg; 1999, 89:748-52. 10.Henderson DJ, Withnington BS, Wilson JA, Morrison LM: Perioperative dextromethorphan reduces postoperative pain after hysterectomy. Anesth Analg; 1999, 89:399-402. 11.Netzer R, Pflimlin P, Trube G: Dextromethorphan blocks N-methylD-aspartate-induced currents and voltage-operated inward currents in cultured cortical neurons. Eur J Pharnacol; 1993, 238:209-16. 12.Price DD, Mao J, Frenk H, Mayar DJ: The N-Metyl-D-aspartate receptor antagonist dextromethorphan selectively reduces temporal summation of second pain in man. Pain; 1994, 59:165-74. 13.Ilkjaer S, Driks J, Brennum J, Werenberg M, Dahi JB: Effect of systemic N-methyl-Daspartate recptor antagonist (dextromethorphan) on primary and secondary hyperalgesia in humans. Br J Anaesth; 1997, 79:600-5. 14.Kinnman E, Nygrads EB, Hansson P: Effects of dextromethorphan in clinical doses on capsaicin-induced ongoing pain and mechanical hypersensitivity. J Pain Symptom Manage; 1997, 14:195-201. 15.Kauppila T, Gronroos M, Petrovaara A: An attempt to attenuate experimental pain in humans by dextromethorphan, an NMDA receptor antagonist. Pharmacol Biochem Behav; 1995, 52:641-4. 16.Fisher K, Coderre TJ, Hagen NA: Targeting the N-methyldaspartate receptor for chronic pain management: preclinical animal studies, recent clinical experience and future research directions. J Pain Symptom Manage; 2000, 20:358-73. 17.Rose JB, Romulo C, Cohen DE, Scheriner MS: Preoperative oral dextromethorphan dose not reduce pain or analgesic consumption in children after adenotonsilectomy. Anesth Analg; 1999, 88:749-53. 18.Ilkjaer S, Bach LF, Nielsen PA, Wernberg M, Dahl JB: Effect of preoperative oral dextromethorphan on immediate and late postoperative pain and hyperalgesia after total abdominal hysterectomy. Pain; 2000, 86:19-24. 19.Wadhwa A, Clarke D, Goodchild CS, Young D: Large-dose oral dextromethorphan as an adjunct to patient-controlled analgesia with morphine after knee surgery. Anesth Analg; 2001,92:448-54. M.E.J. ANESTH 20 (4), 2010 564 H. Mahmoodzadeh et. al DEXAMETHASONE WITH EITHER GRANISETRON OR ONDANSETRON FOR POSTOPERATIVE NAUSEA AND VOMITING IN LAPAROSCOPIC SURGERY Alia S. Dabbous*, Samar I. Jabbour-Khoury**, Viviane G Nasr***, Adib A Moussa***, Reine A Zbeidy***, Nabil E Khouzam***, Mohamad F El-Khatib**, Anis S Baraka**** Abstract In a prospective randomized double-blind study, we compared the effectiveness of dexamethasone 8 mg with either granisetron 1 mg or ondansetron 4 mg in the prevention of postoperative nausea and vomiting in patients undergoing laparoscopic surgery. Hundred ASA I and II patients scheduled for laparoscopic surgery were enrolled in the study and 84 patients completed it. Following induction of anesthesia, group I (n = 42) received granisetron 1 mg and dexamethasone 8 mg, group II (n = 42) received ondansetron 4 mg and dexamethasone 8 mg. Nausea and vomiting episodes, pain scores as well as side effects were recorded during the first hour and subsequently during the first 6 and 24 hours postoperatively. Satisfaction scores were obtained at discharge. There was no statistically significant difference between the 2 groups during the 1st 24 hours following surgery in regards to pain scores, satisfaction and side effects manifestations. At 0-1 hour interval, 100% of patients in group I and 97.6% in group II had no vomiting. Total response (no moderate or severe nausea and no rescue antiemetics) was 83.3% in group I and 80.95% in group II, and metoclopramide was used in 7.1% of patients in both groups. At 1-6 hours interval, 97.6% of patients in group I and 100% in group II had no vomiting. Total response was 92.8% in group I and 90.9% in group II, and metoclopramide was used in 4.76% of patients in group I and 2.38% in group II. At 6-24 hours no vomiting occurred in 97.6% of patients in group I and 100% in group II. Total response was 95.2% in both groups, and metoclopramide was used in 2.38% of patients in both groups. In conclusion, the combination of dexamethasone 8 mg with either granisetron 1 mg or ondansetron 4 mg following induction of anesthesia in patients undergoing laparoscopic surgery showed no statistically significant difference in antiemetic efficacy with minimal side effects and excellent patient satisfaction. Key Words: Postoperative nausea and vomiting, Granisetron, Ondansetron, Dexamethasone, Laparoscopy. * Assistant Professor. ** Professor. *** Resident. ****Professor Emeritus, Department of Anesthesiology, American University of Beirut-Medical Center, Beirut, Lebanon. Address correspondence to: Alia Dabbous, MD, Assistant Professor, Department of Anesthesiology American University of Beirut. P.O. Box: 11-0236, Beirut 1107-2020, Lebanon. E-mail:[email protected] 565 M.E.J. ANESTH 20 (4), 2010 566 Introduction Postoperative nausea and vomiting (PONV) are two of the most common and unpleasant side effects following anesthesia and surgery1. Laparoscopic surgery is associated with a high incidence of nausea and vomiting2,3. In a recent review on postoperative recovery profile after laparoscopic cholecystectomy, PONV was seen in 11% of patients and severe PONV in 2% of patients despite prophylaxis with dexamethasone, ondansetron and the use of total intravenous anesthesia technique4. PONV remains to be a predictor of complicated recovery profile and deserves further attention. The combination of ondansetron plus dexamethasone was more effective in the prevention of postoperative nausea and vomiting than ondansetron alone5. Also, the combination of granisetron 40 µg/kg and dexamethasone 8 mg produced 98% PONV free in patients undergoing laparoscopic cholecystectomy versus 83% PONV free with granisetron alone6. In another study, the same combination produced 95% PONV free versus 83% for granisetron alone7. Although the combination of dexamethasone and 5-hydroxytryptamine type 3 (5HT3) antagonists has been previously described, our report is the first to compare the combination of granisetron 1 mg and dexamethasone 8 mg versus ondansetron 4 mg and dexamethasone 8 mg for PONV prophylaxis in patients undergoing laparoscopic cholecystectomy and herniorraphy. The aim of this study is to compare the effectiveness of granisetron 1 mg and dexamethasone 8 mg (group I) versus ondansetron 4 mg and dexamethasone 8 mg (group II) in the prevention of early and late PONV in patients undergoing laparoscopic cholecystectomy and herniorraphy. Materials and Methods After obtaining our institutional review board (IRB) approval and informed written consents from all human subjects, 100 patients, ASA I or II, scheduled for laparoscopic cholecystectomy or herniorraphy were enrolled in this prospective randomized doubleblinded study. 84 patients completed the study (42 in group I and 42 in group II). Exclusion criteria included: Known allergies or hypersensitivity to the study drugs, history of chronic nausea and vomiting or experienced A. S. Dabbous et. al nausea and vomiting in the past 24 hours prior to anesthesia, had received any antiemetics or any drug with antiemetic properties during the 24 hours before anesthesia, had a body mass index ≥35 kg/m2, aged >70 years, were pregnant or breast feeding or had a condition requiring chronic opioid use. Using a computer generated randomization method; Patients were randomized into 2 groups. Group I received granisetron 1 mg and dexamethasone 8 mg while group II received ondansetron 4 mg and dexamethasone 8 mg. The study medications were prepared by a resident, who was not involved in any other part of the study, and were presented to blinded investigators as identical 2 ml filled syringes. After standard monitoring techniques consisting of EKG, pulse oximetry, and blood pressure, patients received 1 mg of midazolam intravenously as a premedication. General anesthesia was induced with intravenous (IV) propofol 2 mg/kg, lidocaine 1 mg/Kg, fentanyl 2 µg/kg, and muscle relaxation was achieved with rocuronium 0.6 mg/kg to facilitate endotracheal intubation. Maintenance of anesthesia was achieved by sevoflurane, oxygen: air mixture (1:1), additional doses of fentanyl up to 4 µg/kg and rocuronium as needed to keep a train of four ratio <0.7. The study medications dexamethasone and granisetron or dexamethasone and ondansetron were administered immediately after induction of anesthesia in both treatment groups. Neuromuscular blockade was reversed at the end of surgery with IV neostigmine (0.05 mg/kg) and glycopyrrolate (0.01 mg/kg). Patients were transferred to the post anesthesia care unit (PACU) and the PACU team was instructed to assess pain scores according to the visual analogue scale VAS. If pain score >5 the patients were given either paracetamol (Prodafalgan™) 1 g IV drip or demerol 20 mg IV bolus. The time of each vomiting episode and the time and intensity of each nausea episode were collected from the nursing chart upon arrival to PACU, at 1 hour, 6 and 24 hours postoperatively. An episode of vomiting was defined as expulsion of stomach contents with no relief of nausea symptoms. The intensity of each nausea episode was graded as mild (discomfort noticed but no disruption of anticipated normal activity), moderate (discomfort sufficient to reduce or affect anticipated normal activity) or severe (inability to perform anticipated DEXAMETHASONE WITH EITHER GRANISETRON OR ONDANSETRON FOR POSTOPERATIVE NAUSEA AND VOMITING IN LAPAROSCOPIC SURGERY normal activity). The initial rescue medication was metoclopramide 10 mg administered as a single IV bolus dose and was given if the patients vomited, complained of moderate or severe nausea and if they requested the treatment medication. Nausea and vomiting assessments were made up to 30 minutes following rescue medication administration and response was defined as improvement or resolution of PONV symptoms. Adverse events were evaluated and recorded by a resident who was blinded to the study drugs used. Postoperative pain was also followed up at 1, 6 and 24 hours postoperatively. Patient satisfaction was recorded just before discharge. Statistical Analysis All values were reported as means ± standard deviation, or numbers and percentages. Data were analyzed using independent sample t-test and chisquared test. A P value less than 0.05 was considered statistically significant. Results Of the 100 patients initially signing the informed consent, 84 patients (42 in group I, 42 in group II) completed the study. There was no statistically significant difference between the two groups in regards to gender, history of PONV and history of motion sickness, age, weight, type of surgery (laparoscopic cholecystectomy or laparoscopic herniorraphy), duration of surgery, history of prolonged gastric emptying, and smoking history (Table 1). Table 1 Demographic data Granisetron + Ondansetron + Dexamethasone Dexamethasone (n = 42) (n = 42) Age (years) Gender (male/female) Weight (kilograms) 46.5 ± 11.7 47.4 ± 14.2 22/20 20/22 75.8 ± 16.1 77.5 ± 14.1 Type of surgery: Lap cholecystectomy Lap Herniorraphy 31 11 30 12 History of PONV 5 4 History of motion sickness 1 2 History of delayed gastric emptying 4 5 History of smoking Duration of surgery (min) 20 18 61 ± 8.4 62 ± 7.4 567 There was no statistically significant difference between the two groups at the three time intervals (0-1, 1-6, 6-24 h) with respect to total response, number of patients who vomited and the use of antiemetics (metoclopramide) (P>0.05) (Table 2). Table 2 Efficacy outcome Granisetron + Dexamethasone (n = 42) Ondansetron + Dexamethasone (n = 42) No Vomiting 0-1 hr 1-6 hrs 6-24 hrs 42 (100%) 41 (97.6%) 41 (97.6%) 41 (97.6%) 42 (100%) 42 (100%) Total response 0-1 hr 1-6 hrs 6-24 hrs 35 (83.3%) 39 (92.8%) 40 (95.2%) 34 (80.95%) 38 (90.9%) 40 (95.2%) Metoclopramide 0-1 hr 3 (7.1%) 3 (7.1%) 1-6 hrs 2 (4.76%) 1 (2.38%) 6-24 hrs 1 (2.38%) 1 (2.38%) Total response = no moderate nausea, no severe nausea and no rescue antiemetic use. All patients who received metoclopramide once were satisfied and did not receive any other antiemetics. In this randomized double-blind study, granisetron 1 mg plus dexamethasone 8 mg was shown to be as effective as ondansetron 4 mg plus dexamethasone 8 mg; At 0-1 hour, 100% of patients in group I had no vomiting and 97.6% of patients in group II had no vomiting. Total response (i.e. no moderate or severe nausea and no rescue antiemetic use) was present in 83.3% in group I and 80.95% in group II. The percentage of patients who received metoclopramide was 7.1% in both groups at 0-1 hour interval as well. At 1-6 hours interval, 97.6% of patients in group I and 100% in group II had no vomiting. Total response was 92.8% in group I and 90.9% in group II, and metoclopramide was used in 4.76% of patients in group I and 2.38% in group II. At 6-24 hours no vomiting occurred in 97.6% of patients in group I and 100% in group II. Total response was 95.2% in both groups, and metoclopramide was used in 2.38% of patients in both groups. Two out of 42 patients in group I, and 2 out of 42 patients in group II complained of dizziness in the PACU; 3 out of 42 patients in group I and 3 out of 42 patients in group II complained of headache in the PACU; one out of 42 M.E.J. ANESTH 20 (4), 2010 568 patients in group I and 3 out of 42 patients in group II were sedated in the PACU; 38 out of 42 patients in group I and 37 out of 42 patients in group II were satisfied with the antiemetic prophylaxis. Pain scores in group I at 0-1 hour were 5 ±1.1 , at 1-6 hours 4.8 ±0.5 and at 6-24 hours 2 ± 0.4. Pain scores in group II at 0-1 hour were 4.7 ± 0.5, at 1-6 hours 4.4 ± 0.4 and at 6-24 hours 2.3 ± 0.4. There was no significant difference between the two groups concerning the side effects and the pain scores. Discussion Laparoscopic surgery without antiemetics prophylaxis is associated with a high incidence of nausea and vomiting2,3. Studies have shown that substituting propofol for a volatile anesthetic reduces the risk of postoperative nausea and vomiting by about 19%, whereas substituting nitrogen for nitrous oxide reduces the risk by about 12%8. Combining these two anesthetic management strategies (i.e., total intravenous anesthesia) reduces the risk by about as much as any single antiemetic8. A 70 percent reduction in the relative risk of postoperative nausea and vomiting is the best that can be expected, even when total intravenous anesthesia is used in combination with three antiemetics8. Therefore, combination therapy using antiemetics acting at different neuroreceptor sites is more effective than using individual components alone. This is particularly true when dexamethasone is combined with a serotonin receptor antagonist such as granisetron or ondansetron. In this prospective randomized double-blind study, we found no statistically significant difference in the incidence of PONV, during the first 24 hours following surgery, when dexamethasone was combined with either granisetron or ondansetron. Multiple previous studies had shown that combination regimens of antiemetics provide significantly better PONV prophylaxis compared with a single antiemetic therapy. Of note, the combination of dexamethasone and ondansetron was better than ondansetron alone5 also, dexamethasone and granisetron was better than granisetron alone6,7. Furthermore, different combination therapies had been proven to be similar in outcome and efficacy8. Our results confirms the results published by Apfel et al where different antiemetic interventions are A. S. Dabbous et. al found to be similarly effective and different antiemetic combinations are found to be similar in outcome and efficacy8. Another meta-analysis found no statistically significant difference in the incidence of early or overall PONV when a 5-HT3 receptor antagonist was combined with either droperidol or dexamethasone. Both combination regimens provided significantly better PONV prophylaxis compared with 5-HT3 receptor antagonists alone9. Gan et al reported a similar study to ours using different dosages and different timing of administration for abdominal hysterectomy. They also found that both combinations were equally effective in preventing PONV in the first two hours postoperatively10. Our study however extends the observation period to 24 hours postoperatively. Dexamethasone is a glucocorticoid that produces strong antiemetic effect, by an undetermined mechanism. It may act through prostaglandin antagonism, serotonin inhibition in the gut and by releasing endorphins. The prophylactic antiemetic effect of dexamethasone has been documented in laparoscopic surgery11-14. There are no reports of dexamethasone related adverse effects in the doses used for management of PONV although even meta-analyses and systemic reviews may have insufficient power to detect rare complications15,16. When dexamethasone is used alone, late efficacy seems to be most pronounced11. The prophylactic antiemetic effect of ondansetron17 and granisetron18 has been documented in laparoscopic surgery. The 5HT3 receptor antagonists are highly specific and selective for nausea and vomiting1. Members of this group exert their effects by binding to the serotonin 5HT3 receptor in the chemorecptor trigger zone (CTZ) and at vagal afferents in the gastrointestinal tracts1. Granisetron is highly selective in its ability to bind the 5HT3 receptors 1000:1 to other receptors such as (5HT1A, 5HT1B, 5HT1C, 5HT1, 5HT2) or α1 and α2 adrenergic, dopamine D2, histamine H1, benzodiazepine, β adrenergic, and opioid receptors, while the selectivity for ondansetron is only 250-400:119. We did not find any difference between the two groups when we compared early versus late in terms of antiemetic efficacy, total response and side effects. A review of the role of dexamethasone for the prevention of postoperative nausea and vomiting DEXAMETHASONE WITH EITHER GRANISETRON OR ONDANSETRON FOR POSTOPERATIVE NAUSEA AND VOMITING IN LAPAROSCOPIC SURGERY compared to placebo shows that dexamethasone treatment, reduced early PONV by 35%, and late PONV by 50%15. The dose most frequently used was 8 or 10 mg IV. The combination of dexamethasone with ondansetron or granisetron further decreased the risk of PONV11,15. The best prophylaxis available is achieved by combining dexamethasone with 5HT3 receptor antagonist11,15. Our report showed that administration of granisetron 1 mg and dexamethasone 8 mg or ondansetron 4 mg and dexamethasone 8 mg following induction of anesthesia in patients undergoing short 569 laparoscopic operations, prevented PONV in a high percentage of patients with minimal side effects and excellent patient satisfaction. In conclusion, dexamethasone 8 mg in combination with granisetron 1 mg or ondansetron 4 mg was found to prevent nausea and vomiting in a high percentage of patients undergoing laparoscopic cholecystectomy and herniorraphy, with minimal side effects and excellent patient satisfaction. There was no statistically significant difference between the two combinations concerning its efficacy or side effects. M.E.J. ANESTH 20 (4), 2010 570 A. S. Dabbous et. al References 1. Habib AS, Gan TJ: Pharmacotherapy of postoperative nausea and vomiting. Expert Opin Pharmacother; 2003, 4:457-73. 2. Fortier J, Chung F, Su J: Unanticipated admission after ambulatory surgery-a prospective study. Can J Anaesth; 1998, 45:612-9. 3. Gerges FJ, Kanazi GE, Jabbour-Khoury SI: Anesthesia for laparoscopy: a review. J Clin Anesth; 2006 Feb, 18(1):67-78. 4. Jensen K, Kehlet H, Lund CM: Post-operative recovery profile after laparoscopic cholecystectomy: a prospective, observational study of a multimodal anesthetic regime. Acta Anaesthesiol Scand; 2007, 51:464-71. 5. McKenzie R, Tantisira B, Karambelkar DJ, et al: Comparison of ondansetron with ondansetron plus dexamethasone in the prevention of postoperative nausea and vomiting. Anesth Analg; 1994, 79(5):961-4. 6. Fujii Y, Saitoh Y, Tanaka H, Toyooka H: Granisetron/dexamethasone combination for the prevention of postoperative nausea and vomiting after laparoscopic cholecystectomy. Eur J Anaesthesiol; 2000, 17:64-8. 7. Biswas BN, Rudra A: Comparison of granisetron and granisetron plus dexamethasone for the prevention of postoperative nausea and vomiting after laparoscopic cholecystectomy. Acta Anaesthesiol Scand; 2003, 47:79-83. 8. Apfel CC, Korttila K, Abdalla M, et al: A factorial trial of six interventions for the prevention of postoperative nausea and vomiting. N Engl J Med; 2004, 350:2441-51. 9. Habib AS, El-Moalem HE, Gan TJ: The efficacy of the 5-HT3 receptor antagonists combined with droperidol for PONV prophylaxis is similar to their combination with dexamethasone. A meta-analysis of randomized controlled trials. Can J Anaesth; 2004, 51:311-9. 10.Gan T, Coop A, Philip B: A randomized, double blind study of granisetron plus dexamethasone versus ondansetron plus dexamethasone to prevent postoperative nausea and vomiting in patients undergoing abdominal hysterectomy. Anesth Analg; 2005, 101:1323-9. 11.Elhakim M, Nafie M, Mahmoud K, Atef A: Dexamethasone 8mg in combination with ondansetron 4mg appears to be the optimal dose for the prevention of nausea and vomiting after laparoscopic cholecystectomy. Can J Anaesth; 2002, 49:922-6. 12.Bisgaard T, Klarskov B, Kehlet H, Rosenberg J: Preoperative dexamethasone improves surgical outcome after laparoscopic cholecystectomy: a randomized double-blind placebo-controlled trial. Ann Surg; 2003, 238:651-60. 13.Feo CV, Sortini D, Ragazzi R, De Palma M, Liboni A: Randomized clinical trial of the effect of preoperative dexamethasone on nausea and vomiting after laparoscopic cholecystectomy. Br J Surg; 2006, 93:295-9. 14.Waknine Y: Preoperative dexamethasone improves outcome of laparoscopic cholecystectomy. Medscape medical news; 2003. 15.Henzi I, Walder B, Tramer M: Dexamethasone for the prevention of postoperative nausea and vomiting: A quantitative systemic review. Anesth Analg; 2000, 90:186-94. 16.Carlisle JB, Stevenson CA: Drugs for preventing postoperative nausea and vomiting. Cochrane Database Syst Rev; 2006, 19:3:CD004125. 17.Koivuranta MK, Laara E, Ryhanen PT: Antiemetic efficacy of prophylactic ondansetron in laparoscopic cholecystecmoy. A randomized, double-blind, placebo-controlled trial. Anaesthesia; 1996, 51:52-5. 18.Fujii Y, Tanaka H, Toyooka H: Granisetron reduces the incidence and severity of nausea and vomiting after laparoscopic cholecystectomy. Can J Anaesth; 1997, 44:396-400. 19.Blower PR: Granisetron relating pharmacology to clinical efficacy. Support care cancer; 2003, 11:93-100. case reports PERSISTENT POSTOPERATIVE HYPERTENSION FOLLOWING POSTERIOR FOSSA SURGERY - A Case Report- Zulfiqar Ali*, Hemanshu Prabhakar* and G irija P R ath * Abstract We report a case of a 20 month old male child who underwent surgery for posterior fossa tumor. Post operatively the child developed persistent hypertension. No active intervention was done as it could have compromised cerebral perfusion pressure. The possible cause is discussed. Key Words: posterior fossa tumor; postoperative; persistent hypertension; reactionary edema; cerebral perfusion pressure. Introduction Postoperative complications are often reported following surgery in the posterior fossa. These are usually of transient nature. They can be devastating if persistent or continue for a long time. We report a case where the patient developed persistent hypertension in the postoperative period. Case History A 20-months-old male child, weighing 9 kg presented with persistent vomiting for 4 months, associated with decreased visual acuity and delayed milestones. Computed tomography revealed a large posterior fossa tumor, composed of solid and cystic components, arising from the vermion and extending to supratentorial compartment. On admission the child was drowsy, had papilloedema and hydrocephalus for which a medium pressure right ventriculoperitoneal shunt insertion was done. A week later, the child was scheduled for elective midline suboccipital craniectomy and tumor decompression. All routine investigations were within normal limits. Adequate fluids and packed red blood cells were given to replace the blood loss of approximately 700 ml. The resection of the tumor adherent to brain-stem led to multiple episodes of severe bradycadia with heart rate decreasing from 130 to 64 bpm. These episodes were resolved on cessation of the surgical stimulus. After tumor excision, it was observed that patient’s blood pressure gradually increased from systolic 70 mmHg to 135 mmHg and the heart rate decreased from 150 to 110 bpm. Methylprednisolone infusion was started and continued for 24 hours. * Department of Neuroanaesthesiology Neurosciences Center, 7th floor. All India Institute of Medical Sciences, New Delhi, India. Address for Correspondence: Dr. Hemanshu Prabhakar, Department of neuroanesthesiology, Neurosciences Center, 7th floor. All India Institute of Medical Sciences, New Delhi, India-110029. Phone no.: +91-11-26588500-4849/4847, Fax: 91-11-26588663, E-mail: [email protected]. 571 M.E.J. ANESTH 20 (4), 2010 572 At the end of an 8 hours surgery, the blood pressure remained high between systolic 130 to 140 mmHg and heart rate in the range of 100 to 110 bpm. In view of manipulation of brain stem structures, it was decided to electively ventilate the child in the postoperative period with adequate sedation and analgesia. However, the hypertension and relative bradycardia persisted for the next 24 hours. The systolic blood pressure returned gradually to the preoperative values of 70-80 mmHg over next 36 hours. The postoperative course was further complicated by pneumothorax secondary to subclavian venous cannulation on the right side. This was successfully managed by inserting an intercostal drain. Trachea was extubated on the seventh postoperative day. At the time of discharge from ICU, the child had no respiratory problems or any fresh neurological deficits. Discussion Surgery on the posterior fossa is attended by transient complications related to respiratory and cardiovascular systems in the postoperative period1. However, such complications if persistent occur due to brain stem compression, ischemia, or hematoma2. It has been postulated that compression on the pressor centre at the rostral ventrolateral medulla results in stimulation of the sympathetic nervous system, leading Z. Ali et. al to systemic hypertension3. A postoperative computed tomographic scan of our patient did not reveal any hematoma. He developed persistent hypertension postoperatively, possibly due to brain-stem edema as a result of intraoperative manipulation. As the edema subsided over the next 36 to 48 hours the blood pressure normalized. Any effort to reduce the pressure could possibly compromise the cerebral perfusion pressure in the presence of edema. In this situation we believe that the increase in blood pressure was a reactionary phenomenon to maintain an adequate perfusion of the edematous brain stem. No active measures to decrease the blood pressure in the postoperative period were taken, as such measures could have resulted in ischemia and infarction of the vital structures of the brainstem. Since such elevated blood pressure could possibly lead to a deranged autoregulation and cerebral hyperemia, hourly neurological examinations were carried out. Fortunately, our patient recovered without any neurological deficit or respiratory or cardiac complication. In conclusion, we believe that under vigilant monitoring, postoperative hypertensive response following posterior fossa surgery need not be treated aggressively, as this response could be a reactionary response to brain edema. References 1. Artru AA, Cucchiara RF, Messick JM: Cardiorespiratory and cranial-nerve sequelae of surgical procedures involving the posterior fossa. Anesthesiology; 1980, 52:83-86. 2. Smith DS, Osborn I: Posterior fossa: Anesthetic considerations. In: Cottrell JE, Smith DS, eds. Anesthesia and Neurosurgery. St. Louis: Mosby, Inc., 2001, 335-351. 3. Kan P, Couldwell WT: Posterior fossa brain tumors and arterial hypertension. Neurosurg Rev; 2006, 29:265-269. GRANULAR CELL MYOBLASTOMA OF TONGUE: A RARE CAUSE OF UNANTICIPATED DIFFICULT INTUBATION Lenin Babu Elakkumanan*, Anjolie Chhabra*, Somnath Bose* and Kiran Sharma* Implication statement: We discuss the clinical presentation of a patient with granular cell myoblastoma and the management of an unanticipated difficult intubation with this rare condition. Literature review of similar cases of difficult intubations due to supraglottic masses was performed and the various methods of management have been enumerated. Abstract Introduction: Intubation with direct laryngoscopy may be impossible in 0.05%-0.35% patients due to an undetected supraglottic mass despite an apparently normal pre-operative airway assessment. We report a case of granular cell myoblastoma of the tongue, as a cause of an unanticipated impossible intubation. Case report: A 55-year-old ASA III male weighing 75 Kg was taken up for emergency exploratory laparotomy with perforation peritonitis. On preoperative airway examination there was no indication of difficult intubation. After induction of anesthesia (rapid sequence with rocuronium) we performed direct laryngoscopy. There was a mass arising from the base of the tongue because of which no recognizable epiglottis or glottic structure could be identified. Despite repeat laryngoscopy, optimal external manipulation and direct laryngoscopy performed by an ENT surgeon, the airway could not be secured. As no fibreoptic laryngoscope was available, a surgical tracheostomy had to be performed. * Department of Anaesthesiology and Intensive care, All India Institute of Medical Sciences, New Delhi, India-110029. Corresponding author: Dr. Anjolie Chhabra, 13/61, West Punjabi bagh, New Delhi, India-110026. Mobile no: 91-9868397814, 91-9810104383, Fax no: 91-11-26588641. E-mail ID: [email protected] Conflicts of interest: Nil. Sources of fund: Solely from institutional sources. 573 M.E.J. ANESTH 20 (4), 2010 574 Introduction Direct laryngoscopy and intubation may be impossible in 0.05%-0.35% of patients despite an apparently normal pre-operative airway assessment1. Supraglottic masses such as lingual tonsils2, 3, epiglottic cysts4,5 and vallecular cysts6 have been reported to be responsible for inability to visualize the glottis on laryngoscopy. We report a case of granular cell myoblastoma of the tongue which resulted in an unanticipated difficult intubation in a full stomach patient scheduled for an emergency laparotomy. Case Report A 55-year-old ASA grade III male patient, weighing 75 kg was taken up for emergency laparotomy with suspected perforation peritonitis. The patient was a known case of alcoholic liver cirrhosis with prolonged prothrombin time (Pt = 28/control = 13). Other investigations were within normal limits. Airway examination revealed normal mouth opening with a modified Mallampatti class II oropharyngeal view. The thyromental, sternohyoid distances, mandibular length and range of neck movements, were all within normal limits. No external mass or distortion of airway was apparent externally. Rapid sequence induction with cricoid pressure was planned. No adventitious breath sounds could be heard even with the patient taking deep breaths during preoxygenation. Anesthesia was induced with 250 mg IV thiopentone followed by 50 mg of rocuronium. On direct laryngoscopy with size 3 McIntosh blade, a soft friable brownish yellow mass of 2 X 3 cm was seen suspended from the base of the tongue. No identifiable epiglottis, glottic cartilage or chink could be seen. The glottis could not be visualized on second laryngoscopy by an experienced anesthesiologist. There was no difficulty on mask ventilation while maintaining the cricoid pressure, with peak airway pressures of 15 cm of H2O. Repeat attempts at laryngoscopy including the McCoy laryngoscope were unsuccessful despite optimal external laryngeal manipulation. A fibreoptic laryngoscope was not available at that time. An otolaryngologist, present in the operating room, did a direct laryngoscopy with a light L. B. Elakkumanan et. al source, which also did not facilitate the visualization of any part of the epiglottis or glottis. As the patient was full stomach scheduled for an emergency surgery, had a deranged coagulation profile and an unidentifiable mass surgery, prolonged airway or mass manipulation was ruled out. After taking consent from the next of kin, an emergency tracheostomy was performed. Tracheal suctioning showed no evidence of aspiration. Repeat direct laryngoscopy by the otolaryngologist and attempt to circumvent the mass resulted in it accidentally getting sheared off. Minimal bleeding was controlled with packing. The subsequent glottic view was Cormack Lehane grade II. Surgery was uneventful. The chest skiagram done on the first postoperative day was found to be normal. Even on retrospective questioning, the patient denied any symptoms including difficulty in swallowing. Postoperatively, patient developed sepsis and disseminated intravascular coagulopathy. He expired on the 10th post operative day. Discussion Myoblastoma is a rare tumour of unclear etiology and histogenic origin which was first described by Abrikossoff in 19267. It occurs most frequently in subcutaneous tissues, tongue, skin, breasts and skeletal muscles. More than 50% of the lesions are situated in the oral cavity and 35% in the tongue. Most often, it occurs between 20-50 years of age. The incidence is equal in both sexes, and it is more frequently found in the black race. The tumour has a characteristic slow growth and generally in the intraoral tissues it never grows larger than 0.5 cm in diameter intraorally. In extra-oral tissues it never grows larger than 2 cm8. It usually forms a circumscribed painless mass. As the tumor is slow growing and painless with minimal effects on swallowing, breathing and speaking, patients frequently overlook it and diagnosis is usually made during some coincidental illness or on routine otolaryngological examination. In a series of nine cases of pre-epiglotttic cysts, three patients (33%) reported difficulty in swallowing, three (33%) had inspiratory stridor, one had vague symptoms and two patients (20%) had no symptoms at all9. Our patient had no symptom at all, even though GRANULAR CELL MYOBLASTOMA OF TONGUE: A RARE CAUSE OF UNANTICIPATED DIFFICULT INTUBATION the tumor was larger than the usually reported size. All bedside tests to assess ease of intubation could not predict difficult intubation in an asymptomatic patient with a supraglottic mass. Upon reviewing literature on supraglottic masses, especially myoblastomas, we realized that we should have pointedly asked the patient for history of difficulty in swallowing a symptom which could have given a clue about the presence of a supraglottic mass. Routine preoperative indirect laryngoscopy could also have helped in detecting such a mases. In a study carried out to assess efficacy of preoperative tests for detecting difficult intubations Yanamoto et al found out a positive predictive value of 31% for indirect laryngoscopy compared with 5.9% for the Wilson risk sum and 2.2% for the Mallampati test10. Various methods have been used for the management of unanticipated difficult intubation due to supraglottic masses. In a report of six cases of vallecular cyst, Cheng et al successfully managed two cases with right and left paraglossal laryngoscopy.11 Kamble et al successfully intubated the trachea by manipulation of the cyst with a styletted endotracheal tube6. In our patient, we feared that manipulation of the pedunculated friable tumor may cause it to break and slip into the trachea, leading to airway obstruction. As our patient was full stomach, prolonged laryngoscopy and mass manipulation was not done. 575 Aspiration of a preepiglottic and vallecular cyst followed by successful endotracheal intubation has been also been done9,11. The external appearance of the mass in our patient was not suggestive of a cyst, so aspiration was not attempted. Fibreoptic intubation is the most effective technique in an unanticipated difficult intubation. In an anesthetized full stomach patient howerver, this technique may be as difficult as direct laryngoscopy especially in an unprepared emergency at night2. In addition, as advancement of the endotracheal tube over the fibreoptic scope is blind, we feared it could impact on the pedunculated tumour and cause it to shear off and migrate down the tracheobronchial tree. Therefore securing the airway by performing a surgical tracheostomy was considered the safest option in this patient. In conclusion we would like to emphasize that during airway assessment, pointed questions should be asked about any difficulty in swallowing, as one third of patients with painless supraglottic masses may provide such a history. Though various airway management devices, such as laryngeal mask airways, are available to deal with difficult intubation in patients with no anatomical distortion of the airway, none could have been safely used in our patient. Therefore indirect laryngoscopy which has better positive predictive value in the detection of such masses, should be incorporated as routine preoperative airway assessment by anesthesiologists. M.E.J. ANESTH 20 (4), 2010 576 L. B. Elakkumanan et. al References 1. Benumof JL: Management of the difficult adult airway. With special emphasis on awake tracheal intubation. Anesthesiology; 1991, 75:1087-110. 2. Davies S, Ananthanarayan C, Castro C: Asymptomatic lingual tonsillar hypertrophy and difficult airway management: a report of three cases. Can J Anaesth; 2001, 48:1020-4. 3. Ovassapian A, Glassenberg R, Randel GI, Klock A, Mesnick PS, Klafta JM: The unexpected difficult airway and lingual tonsil hyperplasia: a case series and a review of the literature. Anesthesiology; 2002, 97:124-32. 4. Ghabash M, Matta M: An asymptomatic epiglottic mass as a cause of difficult intubation - a case report. Middle East J Anesthesiol; 1994, 12:497-500. 5. Mason DG, Wark KJ: Unexpected difficult intubation. Asymptomatic epiglottic cysts as a cause of upper airway obstruction during anaesthesia. Anaesthesia; 1987, 42:407-10. 6. Kamble VA, Lilly RB, Gross JB: Unanticipated difficult intubation as a result of an asymptomatic vallecular cyst. Anesthesiology; 1999, 98:72-3. 7. Becelli R, Perugini M, Gasparini G, Cassoni A, Fabiani F. Abrikossoff’s tumor. J Craniofac Surg; 2001, 12:78-.81. 8. Filipovic I, Seiwerth S, Manojlović S, Susic M. Granular Myoblastoma: A case presentation and review of literature. Acta Stomatol Croat; 2000, 34:203-205. 9. Keenleyside HB, Greenway RE: Management of pre-epiglottic cysts: a report of nine cases. Can Med Assoc J; 1968, 99:645-9. 10.Yamamoto K, Tsubokawa T, Shibata K, Ohmura S, Nitta S, Kobayashi T. Predicting difficult intubation with indirect laryngoscopy. Anesthesiology; 1997, 86:316-21. 11.Cheng KS, Ng JM, Li HY, Hartigan PM. Vallecular cyst and laryngomalacia in infants: report of six cases and airway management. Anesth Analg; 2002, 95:1248-50. USE OF REMIFENTANIL IN A PATIENT WITH EISENMENGER SYNDROME REQUIRING URGENT CESAREAN SECTION Ates Duman*, Gamze Sarkilar*, Mürüvvet Dayioglu*, Mine Özden** and Niyazi Görmüs** Abstract We describe a case of 41 yr old multigravida at 35 weeks gestation, with a diagnosis of Eisenmenger syndrome, requiring urgent Cesarean section. The parturient had signs and symptoms of respiratory distress due to high pulmonary artery pressure, and the pregnancy was complicated by preeclampsia. A general anesthetic consisting of ketamine and etomidate and an intravenous infusion of remifentanil were used to provide stable anesthesia and analgesia for a successful delivery. The baby was delivered with high Apgar scores. The potential benefits and safety of the use of remifentanil in parturients with high pulmonary artery pressures are discussed. Key Words: Cesarean section; Eisenmenger`s syndrome; remifentanil. Introduction Eisenmenger syndrome occurs when a congenital or surgically created shunt between the left and right sides of the heart causes an increase in pulmonary vascular resistance (PVR) that surpasses systemic vascular resistance (SVR) resulting in a reversal of left to right shunt to right to left shunt or bidirectional shunt. Maternal mortality rate in Eisenmenger syndrome is reported to be 50-65% with Cesarean section1,2. For successful outcome, factors that increase PVR or decrease SVR should be avoided during the anesthetic management. Together with appropriate vasoactive or inotropic drugs, opioids are useful for controlling hemodynamic fluctuations during induction of general anesthesia in cardiac patients. Unfortunately, however, opioids are generally omitted during induction of general anesthesia in patients undergoing Cesarean sections because of risk of neonatal respiratory depression. There are a number of case reports in literature describing the successful use of remifentanil for high-risk cardiac patients undergoing Cesarean delivery3-7. In two recent randomized, controlled, blind studies Draisci et al.8 and Bouattour et al.9 showed that remifentanil (0.5 µg.kg-1min-1) can be used safely during anesthesia induction without subsequent neonatal depression whilst providing stable hemodynamics in healthy elective parturients8,9. Data in the literature are incomplete on the use of remifentanil in parturients with high pulmonary artery pressures such as in Eisenmenger syndrome. In this case report we used remifentanil as a part of induction and maintenance of general anesthesia in a parturient with Eisenmenger syndrome undergoing emergency Cesarean section. Departments of * Anesthesiology and Intensive Care and ** Cardiovascular Surgery, Meram Medical Faculty, Correspondence to author: Dr A. Duman, Selcuk Universitesi, Tip Fakultesi, Anestezi ve Reanimasyon AD, Konya, Turkey, 42080. Tel: +905334362823, Fax: +903322232643. E-mail: [email protected] 577 M.E.J. ANESTH 20 (4), 2010 578 A. Duman et. al of anesthesia. She remained cardiovascularly stable during induction and surgery (Fig. 1). Case Report A 41-year-old female, 35 weeks gestation, recently diagnosed as Eisenmenger syndrome due to atrial septal defect, was admitted to our Cardiac Anesthesia Department for emergency Cesarean section due to fetal distress. She had four prior normal vaginal deliveries. During this pregnancy she was diagnosed with serious cardiac disease and preeclampsia. On admission she was dyspneic and cyanosed with clubbing. The electrocardiogram (ECG) demonstrated sinus tachycardia with right bundle branch block and non specific ST segment and T wave changes. Fig. 1 Hemodynamic data of the parturient during anaesthesia. Figure 1: Hemodynamic data of the parturient during anaesthesia. SAP: systolic artery SAP: systolic pressure (mmHg), DAP: diastolic artery pressure (mmHg), artery DAP: diastolic artery pressure(mmHg), HR: heart rate (beat/min). pressure(mmHg), HR: heart rate (beat/min) Hemodynamic data 170 160 150 140 130 120 110 100 90 80 SAP DAP Re m if e B nt as an e l il i in e nf u In sio tu ba n t io 1s n tm 2n in d m 5t in h m 10 in th m 15 in th m 20 in th m 25 in th m 30 in th m 35 in th m in HR Preoperative echocardiography showed; prominent right-to-left shunt with an estimated systolic pulmonary artery pressure of 114 mmHg, ejection fraction of 48%, moderate mitral regurgitation and moderate to severe tricuspid regurgitation. No premedication was given. On arrival to the theatre, two peripheral venous and one radial artery catheters were inserted. Oxygen saturation (SpO2) on arrival was 79% on room air and 96% after preoxygenation. Her baseline systemic blood pressure was 147/94 mmHg and her heart rate was 92 per min. Baby was delivered 6 min after induction with an Apgar scores at 1st and 5th min of 7 and 9 respectively. After delivery, intravenous oxytocin 20 units was administered over 20 min. Duration of surgery and anesthesia were 27 min and 35 min respectively. Mother was extubated in the theatre and remifentanil was discontinued after extubation. umbilical cord arterial pH was 7.4 (Table 1). Induction agents were administered intravenously using, remifentanil 0.5 µg.kg-1 infused in 60 sec followed by slow boluses of ketamine 75 mg and etomidate 10 mg. Tracheal intubation and intermittent positive pressure ventilation were facilitated with suxamethonium 80 mg. Sevoflurane to an end-tidal concentration of 1.2% and remifentanil 0.2 µg.kg-1min-1 in 100% oxygen were administered for maintenance The mother’s initial blood gas measurement showed hypoxemia. Her arterial oxygen saturation Pediatricians commented on the lack of respiratory depression in view of the opioid given to the mother and no naloxone was given to the baby. The baby was transferred to the neonatal ward for routine care and the mother was moved to the Cardiac Intensive Care for further management. Table 1 Arterial blood gas measurements of the parturient and the newborn Maternal Maternal Maternal Fetal preoperative after intubation after extubation umbilical cord (in room air) (100% oxygen) (100% oxygen) 7.47 7.43 7.39 7.40 PO2 (mmHg) 36 49.5 80.6 36.1 PCO2 (mmHg) 27 25.9 32.8 36.9 SpO2 (%) 74 87 95.6 69.5 HCO3 (mmol/L) 22 20.2 21 22.2 BE (mmol/L) -4 -5 -4 -1.8 Blood gases pH USE OF REMIFENTANIL IN A PATIENT WITH EISENMENGER SYNDROME REQUIRING URGENT CESAREAN SECTION improved after induction and ventilation (Table 1). Postoperative analgesia was managed with intravenous 4 mg morphine and 1 g paracetamol. Regular antibiotic therapy was continued according to microbiological advice. The mother’s stay in the ICU was uneventful. Her postoperative echocardiography showed diminished and persistent right to left shunt with moderate mitral and tricuspid regurgitations. Systolic PAP was 85 mmHg. The mother was discharged to the cardiology ward the following day. Discussion Although there are reports of successful use of remifentanil in Cesarean deliveries for compromised cardiac patients10, our case is the first case report describing the use of remifentanil during general anesthesia for emergency Cesarean section, in a patient with Eisenmenger syndrome. The anesthetic technique of induction and maintenance used was safe for the neonate and the hemodynamically compromised mother. The incidence of congenital heart disease is approximately 1%. About 8% of patients with congenital heart disease and 11% of those with leftto-right intra-cardiac shunting develop Eisenmenger syndrome if untreated11. Eisenmenger syndrome is characterized by elevated pulmonary vascular resistance and rightto-left shunting of blood through a systemic-topulmonary circulation connection. Patients diagnosed with Eisenmenger syndrome in adulthood, have high perioperative mortality rates1,12. Eighteen percent of anatomic defects of Eisenmenger syndrome reported by Weiss et al consisted of isolated atrial septal defects1. Our patient was diagnosed as Eisenmenger syndrome due to isolated atrial septal defect by angiography and echocardiography shortly during the third trimester of her pregnancy. Although no randomized controlled trials comparing the safety of general and regional anesthesia for non-cardiac surgery in exist this group of patients, both techniques have been used successfully in patients Eisenmenger syndrome13,14. If general anesthesia is to be used, the anesthetic technique least likely to decrease the patient’s systemic blood 579 pressure and vascular resistance, should be chosen because such changes increase the magnitude of rightto-left shunting and cyanosis. Many agents used for induction and maintenance of general anesthesia do depress myocardial function and reduce systemic vascular resistance15. Opioids are effective in blunting sympathetic discharges during anesthesia and surgery with minimal or no myocardial depression16,17. We decided to use ketamine together with etomidate in order to preserve peripheral vascular resistance and cause minimal myocardial depression during induction. The main concern with opioids for Caesarean section is placental transfer. Remifentanil, a short acting opioid has similar properties to other semi-synthetic opioids in preventing maternal vasopressor responses. Remifentanil is known to be rapidly metabolized by non-specific plasma esterases, therefore it has a very short context-sensitive half life. Remifentanil has been described to provide safe anesthesia in Eisenmenger syndrome patients undergoing non-cardiac surgery13. Although remifentanil is rapidly metabolized and/or redistributed by the newborn18, it seems not to be devoid of side effects. In a study which compared remifentanil with placebo for general anesthesia in patients undergoing Cesarean delivery, Draisci et al. demonstrated that there were significant differences in the mean Apgar score and umbilical cord pH values, indicating depression in the remifentanil group. The authors stated that neonates of remifentanil treated mothers had a greater need for resuscitation in the first minutes after birth, but no case showed evidence of prolonged insult and damage7. Recently in 2008 Palacio et al19, published the utility and safety of 1 µg.kg remifentanil bolus for hemodynamic control during cesarean section in 12 high-risk patients ineligible for spinal anesthesia. Patients were undergoing surgery because of placenta abruptio, subarachnoid hemorrhage, HELLP syndrome, or preeclampsia. Palacio encountered no cases of neonatal rigidity and there was no need for naloxone. The authors concluded that, because of potential risk of neonatal depression, remifentanil should be used selectively and the means for neonatal resuscitation should be available. the main concern in our case, was to provide a smooth induction and stable hemodynamics for the M.E.J. ANESTH 20 (4), 2010 580 mother. In view of Palacio’s result on and consideration of the risk/benefit ratio, remifentanil was used, provided resuscitation measures for the newborn were available. Earlier case reports on the use of remifentanil for Cesarean section in cardiovascularly compromised parturients report different patient and neonatal outcomes. The remifentanil infusion rate in the case reports varied from 0.2 µg.kg-1min-1 to 2 µg.kg-1min-1 3-6 . Wadsworth et al. used 0.5 µg.kg-1min-1 remifentanil for two high risk cardiac patients. First case was 36 weeks gestation, left ventricular failure due to severe aortic regurgitation with stenosis and the second case was 28 weeks gestation hypertrophic obstructive cardiomyopathy. Both neonates required short term respiratory support after delivery6. In a patient with recurrent aortic coarctation, Manullang et al. started remifentanil infusion at 0.05 to 0.1 µg.kg-1min-1 before induction and increased it to 0.2 µg.kg-1min-1 for A. Duman et. al induction. The patient was hemodynamically stable and the newborn was in excellent condition at delivery3. Likewise, no respiratory depression occurred in the baby when Scott et al. used 2 µg.kg-1min-1 remifentanil in a 38 weeks gestation parturient diagnosed as mixed mitral valve disease2. In our case the baby was born with excellent Apgar scores and umbilical blood gas results, despite continuing remifentanil infusion until clamping of the cord. Results of this and previous cases lead us to consider that remifentanil is effective in controlling hemodynamic fluctuations during induction and maintenance of general anesthesia of parturients with Eisenmenger syndrome and high pulmonary artery pressures. Although previous reports suggest a potential requirement for neonatal resuscitation, remifentanil may be useful in cases when maternal risk exceeds the concern of neonatal respiratory depression. References 1. Weiss BM, Zemp L, Seifert B, Hess OM: Outcome of pulmonary vascular disease in pregnancy: a systematic overview from 1978 through 1996. J Am Coll Cardiol; 1998, 31:1650-7. 2. Makaryus AN, Forouzesh A, Johnson M: Pregnancy in the patient with Eisenmenger’s syndrome. Mt Sinai J Med; 2006, 73:1033-6. 3. Scott H, Bateman C, Price M: The use of remifentanil in general anaesthesia for Caesarean section in a patient with mitral valve disease. Anaesthesia; 1998, 53:695-7. 4. Manullang TR, Chun K, Egan TD: The use of remifentanil for Cesarean section in a parturient with recurrent aortic coarctation. Can J Anaesth; 2000, 47:454-9. 5. Mertens E, Saldien V, Coppejans H, Bettens K, Vercauteren M: Target controlled infusion of remifentanil and propofol for caesarean section in a patient with multivalvular disease and severe pulmonary hypertension. Acta Anaesthesiol Belg; 2001, 52:207-9. 6. McCarroll CP, Paxton LD, Elliot P, Wilson DB: Use of remifentanil in a patient with peripartum cardiomyopathy requiring Caesarean section. Br J Anaesth; 2001, 86:135-8. 7. Wadsworth R, Greer R, MacDonald JMS, Vohra A: The use of remifentanil during general anaesthesia for caesarean delivery in two patients with severe heart dysfunction. Int J Obstet Anesth; 2002, 11:38-43. 8. Draisci G, Valente A, Suppa E, Frassanito L, Pinto R, Meo F, De Sole P, Bossù E, Zanfini BA: Remifentanil for cesarean section under general anesthesia: effects on maternal stress hormone secretion and neonatal well-being: a randomized trial. Int J Obstet Anesth; 2008, 17:130-6. 9. Bouattour L, Amar HB, Bouali Y, Kolsi K, Gargouri A, Khemakhem K, Kallel N, Trabelsi K, Guermazi M, Rekik A, Kuroui A: Maternal and neonatal effects of remifentanil for general anesthesia for Cesarean delivery. Ann Fr Anesth Reanim; 2007, 26:299-304. 10.Bilehjani E, Kianfar AA, Toofan M, Fakhari S: Anesthesia with etomidate and remifentanil for cesarean section in a patient with severe peripartum cardiomyopathy-a case report. Middle East J Anesthesiol; 2008, 19:1141-9. 11.Vongpatanasin W, Brickner ME, Hillis LD, Lange RA: The Eisenmenger Syndrome in Adults. Ann Inter Med; 1998, 128:74555. 12.Oya H, Nagaya N, Uematsu M, Satoh T, Sakamaki F, Kyotani S, Sato N, Nakanishi N, Miyatake K: Poor prognosis and related factors in adults with Eisenmenger syndrome. Am Heart J; 2002, 143:739-44. 13.Kopka A, McMenemin IM, Serpell MG, Quasim I: Anaesthesia for cholecystectomy in two non-parturients with Eisenmenger’s syndrome. Acta Anaesthesiol Scand; 2004, 48:782-6. 14.Ghai B, Mohan V, Khetarpal M, Malhotra N: Epidural anesthesia for cesarean section in a patient with Eisenmenger’s syndrome. Int J Obstet Anesth; 2002, 11:44-7. 15.Jones P, Patel A: Eisenmenger’s syndrome and problems with anaesthesia. Br J Hosp Med; 1995, 54:214. 16.Duman A, Sahin AS, Atalik EK, Öztin Ogun C, Basri Ulusoy H, Durgut K, Ökesli S: The in vitro effects of remifentanil and fentanyl on isolated human right atria and saphenous veins. J Cardiothorac Vasc Anesth; 2003, 17:465-9. 17.Hanouz JL, Yvon A, Guesne G, Eustratiades C, Babatasi G, Rouet R, Ducouret P, Khayat A, Bricard H, Gerard JL: The in vitro effects of remifentanil, sufentanil, fentanyl, and alfentanil on isolated human right atria. Anesth Analg; 2001, 93:543-9. 18.Kan RE, Hughes SC, Rosen MA, Kessin C, Preston PG, Lobo EP: Intravenous remifentanil: placental transfer, maternal and neonatal effects. Anesthesiology; 1998, 88:1467-74. 19.Placio FJ, Ortiz-Gomez JR, Fortnet I, Lopez MA, Morillas P: Remifentanil bolus for cesarean section in high-risk patients: study of 12 cases. Rev Esp Anestesiol Reanim; 2008, 55:86-9. COMBINED SPINAL EPIDURAL ANESTHESIA FOR CESAREAN SECTION IN A PREGNANT PATIENT WITH RARE INTRACRANIAL NEOPLASM Anjolie Chhabra*, Neeraj Kumar*, Ashwini Kumar*, Neena Singh** and B.S. Sharma*** Introduction There are several reports of obstetric emergencies in pregnant patients with malignant intracranial tumors precipitated by worsening of the mother’s neurological status which necessitate an early delivery of the fetus before definite therapy can be administered to the mother1-3. We describe a patient with a sphenoid sinus tumor who developed loss of vision due to rapid tumor progression necessitating an early delivery of her twin fetuses by cesarean section. The patient had co morbidities and requested to be awake during the surgery, she was managed using a combined spinal epidural anesthesia. The advantages of combined spinal epidural anesthesia as compared to a single shot subarachnoid block, epidural block or general anesthesia are discussed in a pregnant patient with decrease in intracranial compliance. Key words: Combined Spinal Epidural, Cesarean section, intracranial neoplasm. Case Report A 30 year old multigravida (G3 P1+0+1+1) at 35 weeks of gestation with twin pregnancy (diamniotic dichorionic) and an intracranial space occupying lesion (ICSOL) was referred to the Neurosurgery Department of our tertiary care hospital from a peripheral health center with total loss of vision in the right eye which had progressed over two weeks. A month prior she had developed ptosis of the left eye, which recovered spontaneously. The patient gave history of bilateral frontal headaches, on and off, for last 4-5 years. The headaches were associated with vomiting and had been increasing in intensity for the last two months. On evaluation she was found to have right second, third, sixth cranial nerve palsy, bilateral disc pallor and no papilledema. * Departments of Anesthesiology, ** Obstetrics and Gynecology, *** Neurosurgery, All India Institute of Medical Sciences, New Delhi, India. Corresponding author: Dr. Neeraj Kumar, Senior Resident, Department of Anaesthesiology, All India Institute of Medical Sciences, New Delhi 110029, India. E-mail: [email protected] 581 M.E.J. ANESTH 20 (4), 2010 582 A. Chhabra et. al Magnetic resonance imaging (MRI) of the head showed a homogeneous, enhancing midline mass of 4.2-3.0 cm size in the spheno – occipital region (clivus), anteriorly obliterating the sphenoid sinus, posteriorly extending up to the pre-pontine cistern and superiorly thinning the bone of the hypophyseal fossa. Bilaterally it was extending in to the cavernous sinus encasing the intracavernous portion of internal carotid artery, more on the left. The optic tracts and chiasma appeared to be normal. The findings were suggestive of a chordoma of the clival region. The ventricular system was normal and no parenchymal hypodensity or midline shift was visible (Fig. 1). of 140/80 mm Hg. Airway examination revealed normal mouth opening, Mallampatti grade III view of the oropharynx and normal neck movements. After discussion with obstetrician and neurosurgeon it was decided to perform cesarean section under combined spinal epidural (CSE) anesthesia for which the patient was willing. Fig. 1 After preloading with 500 ml of Ringer lactate and administering local anesthetic, under strict asepsis a CSE block was performed at lumbar 3rd – 4th interspace in the left lateral position with a needle through needle technique using an 18 G Tuohy and 27G pencil point spinal needle (PortexR CSE set). 1ml of 0.5% heavy bupivacaine and 25 µg of fentanyl was administered intrathecally. The epidural catheter was threaded 5 cm into the epidural space. After ten minutes, the sensory block extended from T8 to T12. 5 ml of 2% lignocaine with 1:200000 adrenaline was then slowly administered into the epidural space. 10 minutes later adequate block was established up to T4 and the obstetricians were allowed to proceed with surgery. The patient was also detected to have pregnancy induced hypertension (PIH) (150/100mmHg right upper limb, supine). Oral methyldopa, 500 mg 8 hourly was started. The serum bilirubin (1.5 mg/dL), liver enzymes (SGOT / SGPT – 92/101 IU) and alkaline phosphatase (792 IU) were raised with negative markers for viral hepatitis, suggestive of intrahepatic cholestasis of pregnancy. The prothrombin time and remaining investigations were normal. An early delivery of the fetuses was planned to enable transphenoidal debulking and biopsy of the tumor at a later stage. On pre anesthetic evaluation the patient was fully conscious with a Glasgow coma scale of 15, anxious about her ailment and keen not to be made unconscious for the cesarean section. She was 150 cm tall, 65 kg with a pulse rate of 80 beats/minute, blood pressure The patient was kept nil per os for solids for 8 hours and allowed sips of water till 3 hours preoperatively. On the morning of surgery metoclopramide, ranitidine and methyldopa were administered. Standard monitoring (EKG, pulse oximetry and noninvasive blood pressure) was started. Seven minutes after skin incision a 2.5 kg female baby (Apgar scores of 8 and 9 at 0 and 5 minutes) and two minutes later a 1.8 kg male baby (Apgar scores of 9 and 10 at 0 and 5 minutes) were delivered. Intraoperatively, the BP increased to 140/105 mmHg at the time of positioning for the cesarean. The blood pressure fell 30 min after the epidural drug administration to 84/50 mmHg, which responded to 6 mg bolus of mephentermine and crystalloids. Surgery lasted for 50 mins, the intraoperative period was uneventful. Sensory block receded to T10 level in 155 min, the motor block wore off in 290 minutes. A single dose of 1.5 mg epidural morphine provided pain relief for the first 48 hours postoperatively. Thereafter the epidural catheter was removed and analgesia provided with oral ibuprofen 500 mg 8 hourly. One week later, the blood pressure had normalized COMBINED SPINAL EPIDURAL ANESTHESIA FOR CESAREAN SECTION IN A PREGNANT PATIENT WITH RARE INTRACRANIAL NEOPLASM and a transphenoidal tumor decompression and biopsy was performed under general anesthesia. Histology reported a giant cell tumor of clivus. After an uneventful recovery the patient was advised radiotherapy on an outpatient basis. Discussion Malignant tumors of the sphenoid are rare and have a distinctive clinical presentation. These tumors are aggressive, locally invasive and produce symptoms due to compression of vessels and nerves in the cavernous sinus or orbital fissure leading to multiple cranial neuropathies, visual loss and headaches. Though the tumors are in proximity to the pituitary gland, gland involvement and endocrinopathies are not commonly reported4. Our patient similarly presented with headaches, third left cranial nerve palsy which resolved spontaneously, palsy of the right 2nd, 3rd, 6th cranial due to direct tumor infiltration into the optic foramen and cavernous sinus rather than an increase in ICP Though there were no features of raised ICP (clinically, on MRI and on fundus examination) in the presence of the large ICSOL, a decrease in intracranial compliance was assumed. As she had a twin pregnancy the obstetricians preferred a cesarean section to a prolonged induction and labor for delivery of the fetuses. General anesthesia is usually chosen for patients with ICSOL and severe neurological obtundation1-3. As this patient also had PIH, intrahepatic cholestasis of pregnancy, the possibility of a difficult intubation and a desire to remain awake during delivery of her babies, a regional anesthesia technique was chosen. We wanted to use a regional anesthesia technique which would cause minimum alteration in the ICP, provide safe, titratable intraoperative anesthesia and postoperative analgesia as well. Though regional anaesthetic techniques have been used, there is only one report of a subarachnoid block being used in a pregnant patient with a glioblastoma for an emergency section due to fetal distress5. There are reports of epidural block for labor analgesia and cesarean section in patients with intracranial tumors6,7. However, Hilt et al8 demonstrated that CSF pressure rises significantly even after 10 ml 583 of bupivacaine administration in the epidural space in patients with reduced intracranial compliance, necessitating slow administration of 5 ml volumes at a time. In one of the reports lumbar epidural was administered to minimize increase in ICP resulting from bearing down efforts, however, the patient continued to have headache and features of raised ICP with uterine contraction even after effective block was established6. The advantage of a combined spinal epidural (CSE) over a single injection subarachnoid block is that a dural puncture can be easily performed with a thin pencil point 26/27 G needle which minimizes the CSF leak. In case CSF seepage persists, the low volume epidural would help in tamponading the CSF leak and enable titration of the block without producing a precipitous fall in blood pressure. In addition administration of large volumes of local anesthetic in the epidural space would be avoided and the epidural catheter would enable us to provide good postoperative analgesia. The chance of an accidental dural puncture with the Tuohy needle is always there, however, the incidence of this happening with the CSE technique is documented to be 1.7% as compared to 4.2% with epidural anesthesia alone9. This may be because with CSE the epidural space can be more accurately localized with the aid of the thin pencil point spinal needle rather than by loss of resistance alone, as is used for epidural block9. The use of low dose i.e. 30 µg/kg of epidural morphine did not cause any nausea, vomiting or pruritis. The epidural route was chosen and dose was reduced to minimize the above side effects. Vigilant monitoring of the patient for worsening headache, localizing neurological signs or deterioration of the level of consciousness was done to ensure no untoward sequelae. The need for absolute asepsis during the CSE was essential as an intracranial infection in this patient would have been disastrous. In conclusion the CSE can be safely used for cesarean section in patients with intracranial space occupying lesion (ICSOL) without severe neurological deficit and in whom general anesthesia may not be preferred. M.E.J. ANESTH 20 (4), 2010 584 A. Chhabra et. al References 1. Chang L, Looi-Lyons L, Bartosik L, Tindal S: Anesthesia for cesarean section in two patients with brain tumours. Can J Anesth; 1999, 46:61-5. 2. Smith IF, Skelton V. An unusual intracranial tumor presenting in pregnancy. Int J Obstet Anesth; 2007, 16:82-5. 3. Bharti N, Kashyap L, Mohan VK: Anesthetic management of a parturient with cerebellopontine-angle meningioma. Int J Obstet Anesth; 2002, 11:219-21. 4. Esposito F, Kelly DF, Vinters HV, DeSalles AA, Sercarz J, Gorgulhos AA: Primary sphenoid sinus neoplasm: a report of four cases with common clinical presentation treated with transsphenoidal surgery and adjuvant therapies. J Neurooncol; 2006, 76:299-306. 5. Atanassoff PG, Weiss BM, Lauper U: Spinal anaesthesia for 6. 7. 8. 9. Caesarean section in a patient with brain neoplasm. Can J Anesth; 1994, 41:163-4. Goroszeniuk T, Howard RS, Wright JT: The management of labour using continuous lumbar epidural analgesia in a patient with a malignant cerebral tumor. Anaesthesia; 1986, 41:1128-29. Finfer S.R: Management of labour and delivery in patients with intracranial neoplasms. Br J Anaesth; 1991, 67:784-7. Hilt H, Gramm HJ, Link J: Changes in intracranial pressure associated with extradural anaesthesia. Br J Anaesth. 1986, 58:676-80. Norris MC, Grieco WM, Borkowski M, Leighton BL, Arkoosh VA, Huffnagle HJ, Huffnagle S: Complications of labor analgesia: epidural versus combined spinal epidural techniques. Anesth Analg; 1994, 79:529-37. THE USE OF REMIFENTANIL IN GENERAL ANESTHESIA FOR CESAREAN SECTION IN A PARTURIENT WITH SEVERE MITRAL STENOSIS AND PULMONARY EDEMA Shahram Amini*, Minoo Yaghmaei** Abstract Valvular heart diseases have adverse effects on hemodynamic condition in the parturients during pregnancy. Cesarean section with an opioid based general anesthesia has been used to alleviate these deleterious effects. We hereby describe the effective application of remifentanil, for cesarean section under general anesthesia, in a 30 yr old primigravida suffering of severe multivalvular heart disease and pulmonary hypertension presenting with pulmonary edema who was in active labor and without neonatal respiratory depression. Key words: general anesthesia, cesarean section, remifentanil, mitral stenosis, pulmonary edema. Introduction Mitral stenosis is the most common valvular heart disease in parturients, with significant effects on the mother and neonate especially during labor. General anesthesia is indicated where regional anesthesia is contraindicated or fails or in case of emergency delivery1. Systemic opioids are used to blunt the hemodynamic responses during endotracheal intubation and hormonal stress response during surgery2-4. However, they are associated with unfavorable effects on the neonate and are therefore avoided until after delivery. Remifentanil might be an excellent choice for cesarean section under general anesthesia5,6. We report the use of remifentanil for general anesthesia in a parturient in active labor with severe multivalvular heart disease requiring emergency cesarean section. * Departments of Anesthesiology, ** Obstetrics and Gynecology, Zahedan University of Medical Sciences, Zahedan, Iran. Corresponding author: Shahram Amini, MD. Ali-ebne Abitaleb Hospital, Department of Anesthesiology, Zahedan, Iran. Tel: 0098 915 141 7235, Fax: 0098 511 8640535. E-mail: [email protected] 585 M.E.J. ANESTH 20 (4), 2010 586 Case Report A 30 years old woman (gravid 1 para 0) with a fetus of 36 weeks gestation, presented to the hospital with severe respiratory distress and active labor. The patient had a history of severe mitral stenosis, mitral regurgitation, tricuspid regurgitation, and pulmonary hypertension. Her vital signs revealed blood pressure 90/52 mmHg, pulse rate 130bpm, and respiratory rate 35. Her SpO2 was 85% on room air. She also had bilateral crackles throughout the lungs, and severe diastolic and systolic murmurs. Following preoxygenation, anesthesia was induced with ketamine 2 mg/ kg, remifentanil 1 µg/ kg, and suxamethonium 1.5 mg/kg to facilitate endotracheal intubation. Cisatracurium 0.1 mg/kg was given after endotracheal intubation with remifentanil infused at 0.1 µg/kg/min until delivery and 0.2-0.4 µg/ kg/min with midazolam 0.1mg/kg for maintenance of anesthesia after delivery. The patient received 100 percent oxygen throughout surgery. Standard monitoring included pulse rate, noninvasive blood pressure, EKG monitoring, respiratory rate, pulse oxymetry, ET CO2 and noninvasive cardiac output monitoring using NICO (Novametrix, Wallingford, CT, USA). The patient’s cardiac index was 1.5 L/min/m2. Dobutamine was administered to improve the cardiac output and compensate any decrease in blood pressure. A live 2950g female infant was delivered 4 minutes after skin incision with Apgar score of 8 and 9 at 1 and 5 minutes, respectively with no evidence of respiratory depression. She was transferred to NICU for postoperative care where she had an uneventful stay. At the end of the surgery, residual neuromuscular block was antagonized with neostigmine and atropine and the mother was transferred to the ICU while intubated. Her stay in the ICU was uneventful, she was extubated at 26 hours and on 3rd day was transferred to the postpartum ward. She was discharged on the fifth day postpartum. Discussion Rheumatic mitral stenosis is the most common clinically significant cardiac abnormality seen in pregnant women worldwide6-8 with increased maternal S. Amini & M. Yaghmaei et. al and neonatal mortality9,10. Stenosis of the mitral valve obstructs left ventricular filling resulting in increased left atrial pressure (LAP) and reduced cardiac output. During pregnancy several hemodynamic changes including increased intravascular volume and increased heart rate exacerbate the cardiovascular aberrations associated with mitral stenosis. During natural labor, cardiac output and blood pressure increase with uterine contractions. Immediately after delivery cardiac filling pressures increase dramatically due to vena caval decompression and return of uterine blood. Critical mitral stenosis occurs when the opening is reduced to 1 cm2. As the disease progresses, chronic elevation of LAP leads to pulmonary hypertension, tricuspid and pulmonary valve incompetence, pulmonary edema, and secondary right heart failure. Vaginal delivery under regional anesthesia, especially epidural anesthesia is the usual approach in patients with valvular hear disease11,12. However, since our patient was in active labor with symptoms of severe heart failure, we decided to use general anesthesia instead in order to reduce the labor associated hemodynamic alteration. Moreover, our patient had also mitral and tricuspid regurgitation, and pulmonary hypertension, all of which make her more vulnerable to adverse effects of labor. We used noninvasive cardiac output monitoring to evaluate the patient’s hemodynamic condition. Remifentanil was used before delivery to attenuate the deleterious effects of endotracheal intubation and surgical pain and to reduce further hemodynamic compromises during surgery. The patient did not show significant hemodynamic changes after induction, before delivery, and throughout the surgery. Remifentanil crosses the placenta like other opioids13,14. It undergoes esterase metabolism and has extremely short duration of action that is independent of the duration of infusion15. Use of remifentanil has been associated with stable hemodynamic variables during general anesthesia in high risk patients16-18. with no significant respiratory depression in the neonate6,19,20. However, some have reported transient neonatal respiratory depression requiring short period of ventilation support21,22, transient neonatal chest wall rigidity23 and severe fetal THE USE OF REMIFENTANIL IN GENERAL ANESTHESIA FOR CESAREAN SECTION IN A PARTURIENT WITH SEVERE MITRAL STENOSIS AND PULMONARY EDEMA bradycardia24. The neonate had no evidence of respiratory depression after delivery probably attributed to the low dose of remifentanil administered and the short incision to delivery time technique used. However, low bolus doses of remifentanil has been associated with respiratory depression13,22. 587 In conclusion, we demonstrated the effective application of remifentanil in general anesthesia in a parturient in active labor with severe multivalvular heart disease, pulmonary hypertension and pulmonary edema requiring cesarean section and without adverse effects on the neonate. M.E.J. ANESTH 20 (4), 2010 588 S. Amini & M. Yaghmaei et. al References 1. Draisci G, Valente A, Suppa E, et al: Remifentanil for cesarean section under genera anesthesia: effects on maternal stress hormone secretion and neonatal well-being: a randomized trial. International J of Obs Anesth; 2008, 17:130-136. 2. Vogl SE, Worda C, Egarter C, et al: Mode of delivery is associated with maternal and fetal endocrine stress response. Brit J Obst Gyn; 2006, 113:441-5. 3. Morishima HO, Pederson H, Finster M, et al: Influence of maternal physiologic stress on the fetus. Am J Obstet Gynecol; 1978, 131:28690. 4. Stanely TH, Webster LR: Anesthetic requirements and cardiovascular effects of fentanyl-oxygen and fentanyl-diazepamoxygen anesthesia in man. Anesth Analg; 1978, 57:411-6. 5. Schuttler J, Albrecht S, Breivik H, et al: A comparison of remifentanil and alfentanil in patients undergoing major abdominal surgery. Anesthesia; 1997, 52:307-17. 6. Desai DJ, Golwala MP, Dhimar AA, Swadia VN: Emergency LSCS in a patient with severe mitral stenosis with pulmonary hypertension with aortic regurgitation (NYHA-III). Indian J Anesth; 2002, 46(6):483-485. 7. Soler-Soler J, Galve E: Worldwide perspective of valve disease. Heart; 2000, 83:721-25. 8. Thorne SA. Pregnancy in heart disease. Heart; 2004, 90:450-56. 9. Desai DK, Adanlawo M, Naidoo DP, Moodley J, Kleinschmidt I: Mitral stenosis in pregnancy: a four year experience at King Edward VIII hospital, Durban, South Africa. Brit J Obstet Gynecol; 2000, 107:953-58. 10.Sawhney H, Aggrawal N, Suri V, et al: Maternal and perinatal outcome in rheumatic heart disease. Int J Gynecol Obstet; 2003, 80:9-14. 11.Kuczkowski KM: Labor anesthesia for the parturient with cardiac disease: what does an obstetrician need to know? Acta Obstet Ansthesol Belg; 2004, 40:201-5. 12.Kuzczkowski KM, Zundert AV: Anesthesia for pregnant women with valvular heart disease: the state of the art. Journal of anesthesia; 2007, 21(2):52-57. 13.Nagan KeeW, Khaw KS, Ma KC, Wong AS, et al: Maternal and neonatal effects of remifentanil at induction of general anesthesia for cesarean delivery: a randomized, double-blind, controlled trial. Anesthesiology; 2006, 104:1014-20. 14.Kan R E, Hughes SC, Rosen MA, Kessin C, Preston PG, Lobo EP: Intravenous remifentanil. Placental transfer, maternal and neonatal effects. Anesthesiology; 1998, 88:1467-74. 15.Egan TD, Lemmens HJM, Fiset P, et al: The pharmacokinetics of the new short-acting opioid remifentanil in healthy adult male volunteers. Anesthesiology; 1993, 79:881-92. 16.More RMLE, Grange CS, Anisworth QP, Grebenik CR: General anesthesia using remifentanil for cesarean section in parturients with critical aortic stenosis: a series of four cases. Inter J Obstet Anesth; 2004, 13:183-7. 17.Bedard JM, Richardson MG, Wissler RN: General anesthesia with remifentanil for cesarean section in a parturient with an acoustic neuroma. Can J Anesth; 1999, 46(6):576-80. 18.Manullang TR, Chun K, Egan TD: The use of remifentanil for cesarean section in a parturient with recurrent aortic coarctation. Can J Anesth; 2000, 47(5): 454-59. 19.Scott H, Bateman C, Price M: The use of remifentanil in general anesthesia for cesarean section in a patient with mitral valve disease. Anesthesia; 1998, 53(7):695-7. 20.Molins EJ, Soria GA, Alcala E, Martinez EC, Sanchez CL: Anesthesia for cesarean delivery in a woman with congenital aortic stenosis. Res Esp Anestesiol; 2004, 51(4):221-5. 21.Mertens E, Saldien V, Coppejans H, Bettens K, Vercauteren M: Target controlled infusion of remifentanil and propofol for cesarean section in a patient with multivalvular disease and severe pulmonary hypertension. Acta Anesthesiol Belg; 2001, 52(2):207-9. 22.Van de Velde M, Teunkens A, Kuypers M, et al: General anesthesia with target controlled infusion of propofol for planned cesarean section: maternal and neonatal effects of a remifentanil-based technique. Int J Obstet Anesth; 2004, 13:153-8. 23.Carvalho B, Mirikitani EJ, Lyell D, Evans DA, Druzin M, Riley ET: Neonatal chest wall rigidity following the use of remifentanil for cesarean delivery in a patient with autoimmune hepatitis and thrombocytopenia. Int J Obstet Anesth; 2004, 13(1):53-56. 24.Imarengiaye C, Littleford J, Davies S, Thaper K, Kingdom J: Goal oriented general anesthesia for cesarean section in a parturient with a large intracranial epidermoid cyst. Can J Anaesth; 2001, 48(9):88489. INTRAVENOUS REGIONAL ANALGESIA IN A PATIENT WITH GLANZMANN THROMBASTENIA Sitki Goksu*, Rauf Gul*, Onder Ozen*, Mehmet Yilmaz**, Orhan Buyukbebeci***, Unsal Oner* Abstract Glanzmann thrombastenia (GT) is a rare condition of an inherited autosomal recessive gene characterized with bleeding tendency. The condition is rarely met in the OR. and therefore it is essential that anesthesiologist be cognizant of the risk involved and be prepared with all necessary precautionary measures. We present a GT case in a 27 year old male with a mass in the anticubital region of right wrist that was successfully excised using the non-invasive intravenous regional analgesia (IVRA). The use of platelet transfusion and the recombinant factor VIIa, are stressed. Key words: Glanzmann thrombastenia, Intravenous regional anesthesia, Recombinant factor VIIa, surgery. Introduction Glanzmann thrombastenia (GT) is a rare condition associated with fatal bleeding. Three hundred such cases have been reported in the literature1. It is a trombocyte aggregation deficiency inherited autosomal recessive, characterized with bleeding tendency because of the deficiency of number or function of glycoprotein IIb/IIIa complex found on thrombocyte membrane2. Bleeding time is significantly increased although platelet count, morphology, prothrombine time (PT) and activated partial thromboplastin time (aPTT) values are normal2,3. Most commonly seen bleeding symptoms in these patients are purpura, epistaxis, gingival bleeding and menorrhagia3. Any surgical or invasive procedures can be high bleeding risk in these patients. Platelet transfusion is the only way to stop bleeding. It is, ironic however, that excess platelet transfusion may also increase the bleeding risk due to alloimmunisation4. We present our experience with intravenous regional anesthesia (IVRA) and share information on Glanzmann thrombastenia (GT). From University of Gaziantep, Faculty of Medicine, Gaziantep, Turkey. * Department of Anesthesiology & Reanimation ** Department of Hematology. *** Department of Orthopedic Surgery. Correspondence to: Rauf Gul, Department of Anaesthesiology and Reanimation, Faculty of Medicine, University of Gaziantep, 27310 Gaziantep, Turkey. Phone: 00 90 342360 60 60, Fax: 90-342-360 22 44. E-mail: [email protected] 589 M.E.J. ANESTH 20 (4), 2010 590 Case Report A 27 years-old and 78 kg male, was admitted for excision of a mass in his right anticubital wrist region. For the previous 22 years, patient had been diagnosed as Glanzmann thrombastenia. Except for thrombastenia, the preanesthetic evaluation was not contributory. Preoperative laboratory findings revealed: Hct 45%, Plt 161000/mm3, PT 16.1 sec, INR 1.29, aPTT 32.6 sec, AST 15 U/L, ALT 11 U/L, Glucose 99 mg/dl, Urea 22 mg/dl, Creatinine 0.82 mg/dl, Factor IX 98% (normal range 60-150%), Factor VIII 99% (normal range 60-150%). Radiological examination showed a 32 × 20 mm solid mass with regular borders in the right wrist anticubital region. A Hematological consultation emphasized that anesthetic and surgical interventions could be highly risky because of the diagnosis of GT and the antibodies formed against platelets in the patient. In the operating room (OR), monitoring consisted of ECG, NIBP and pulse oximetry. An intravenous (iv) line, 20-gauge cannula, was done at his left arm. Nacl 0.9% infusion at 3 ml/kg/hr started. Premedication consisted of Midazolam (Dormicum ® roche) 1 mg. To start the IVRA, a 22-gauge cannula was introduced in dorsum of right hand. Following exanguination of blood from right arm using the Esmarch bandage and double layered tourniquet inflated, 3 mg/kg lidocaine (Aritmal ® Biosel) (0.9% NaC1 solution was added to make up a total volume of 40 mL), was given intravenously. Vital signs remained normal during surgery. 2400 units rFVIIa (NovoSeven ® Novo Nordisk) was given 1 hour before and at the beginning of the operation. Bleeding amount was 100 ml approximately. One apheresis platelet suspension was given during operation. After tourniquet deflation, there was some blood leakage from the incision site. After bleeding stopped, patient was transferred to the service ward without any problems. A total 7200 units rFVIIa was given at 2, 6, and 12 hrs postoperatively. Discussion Life threatening difficult to stop hemorrhages mostly develop secondary to trauma or surgical procedures in Glanzmann thrombastenic (GT) patients. S. Goksu et. al The administration of recombinant activated factor VIIa is safe and effective in such cases. Blood and blood products (platelet rich plasma, platelet concentrates) can also be given4,5. The early diagnosis of GT is most important, because only platelet transfusion can be life saving. Platelet agrometria, thromboelastographic techniques, bleeding time measurements, are the methods for follow up of platelet function. However, the platelet agrometria and thromboelastographic techniques are not commonly used4-7. Anesthesiologists rarely meet GT in the OR. All preparation and precautionary measures must be taken. Without the adequate preparation of patient, all anesthetics carry risk factors. Tracheal intubation for one, can cause intractable bleeding and difficulty in airway management. Nasogastric catheters and other oral interventions, can cause bleeding5. Central and peripheral blocks also have bleeding risk.. It is therefore essential that the advantages and disadvantages of a central block should be weighed carefully before being done. In situations such as the GT, minimally invasive analgesic techniques should be the procedure of choice and an IVRA technique should be highly considered. Literature review revealed that surgery of GT patients has been done both under general anesthesia and local anesthesia2,3,5,8,9. However, no IVRA technique has been reported in such cases. The IVRA technique used in our case is minimally invasive and produces bloodless field of the surgical area. Bleeding risk, however, after tourniquet deflation is a disadvantage. Due to the high pressure produced by the IVRA in the tourniquet region, tissue damage may occur. No serious bleeding or tissue damage was observed during and after operation in our patient. It is probable that having given platelet suspension and rFVIIa preoperatively, may have a salutary effect in the prevention of bleeding.. The rFVIIa transfusion is approved in intractable life threatening bleeding situation. It must also be realized that although platelet transfusion is the only accepted treatment in GT, this platelet transfusion may cause antibody formation against Glicoprotein IIb/IIIa, and this can inactivate INTRAVENOUS REGIONAL ANALGESIA IN A PATIENT WITH GLANZMANN THROMBASTENIA succeeding transfusions4. It can concluded that intravenous regional analgesia (IVRA) provides a good non-invasive 591 analgesic technique in the management of patients with Glanzmann thrombastenia. References 1. Ranjith A, Nandakumar K: Glanzmann thrombasthenia: a rare hematological disorder with oral manifestations: a case report. J Contemp Dent Pract; 2008, 1, 9:107-13. 2. Gunaydın B, Özköse Z, Pezek S: Recombinant Activated Factor VII and Epsilon Aminocaproic Acid treatment of a patient with Glanzmann’s thrombasthenia for nasal polipectomy. J1 Anesth, 2007, 21:106-107. 3. Ryckman JG, Hall S, Serra J: Coronary artery bypass grafting in a patient with Glanzmann’s thrombasthenia. J Card Surg; 2005, 20(6):555-6. 4. Welsby IJ, Monroe DM, Lawson JH, Hoffmann M: Recombinant activated factor VII and the anaesthetist. Anaesthesia; 2005, 60:1203-12. 5. Uzunlar HI, Eroglu A, Senel AC, Bostan H, Erciyes N: A patient with Glanzmann’s thrombasthenia for emergent abdominal surgery. Anesth Analg; 2004, 99:1258-60. 6. Monte S, Lyons G: Peripartum management of a patient with Glanzmann’s thrombasthenia using Thrombelastograph. Br J Anaesth; 2002, 88:734-8. 7. Bellucci S, Caen J: Molecular basis of Glanzmann’s Thrombasthenia and current strategies in treatment. Blood Rev; 2002, 16:193-202. 8. Bay A, Oner AF: Glanzmann thrombasthenia successfully operated for nasal deformation with recombinant factor VIIA. Indian Pediatrics; 2006, 43:1094. 9. Nurden AT: Glanzmann thrombasthenia. Orphanet J Rare Dis; 2006, 6, 1:10. M.E.J. ANESTH 20 (4), 2010 592 Anesthetic Management of 29 Week Pregnant Patient Undergoing Craniotomy for Pituitary Macroadenoma - A Case Report - Oya Yalcin Cok*, Sule Akin*, Anis Aribogan*, Meltem Acil*, Bulent Erdogan**, Tayfun Bagis*** Introduction Intracranial space-occupying lesions are rarely present during pregnancy and these disorders seldom require immediate surgical attention. The most common among them is pituitary tumor of which 15-35% has a chance of enlarging during pregnancy1,2. The decision to proceed with surgical intervention depends on the site, size, and type of the tumor, gestational age and neurological signs as well as the patient’s wishes. In case of surgery, multidisciplinary approach is essential in perioperative period. Maternal alterations during pregnancy may complicate the anesthetic management of patients and increase monitoring requirements for safety of both mother and fetus3. Unfortunately, this may become a challenge to all attending physicians, but especially to the anesthesiologists, as the anesthetic plan must meet the needs of both pregnancy and neurosurgery4. Here, we present 29-week pregnant patient undergoing craniotomy for pituitary adenoma and discuss the features of anesthesia providing maternal and fetal safety. Case Report A 29 year-old parturient (gravida 3, para 1, D/C 1, C/S 1) at 27 weeks of pregnancy was presented with blurred vision and headache. She was admitted to the hospital for differential diagnosis of possible causes such as migraine, infection, hemorrhage and increase in intracranial pressure. Her past medical history was unremarkable. Her physical examination disclosed a decreased visual acuity and radiological examination revealed a suprasellar mass lesion consistent with macroadenoma at magnetic resonance imaging (Fig. 1). From Baskent Univ., Faculty of Medicine, Ankara, Turkey. *Department of Anesthesiology and Reanimation. **Department of Neurosurgery. ***Department of Obstetrics and Gynecology. Corresponding author: Dr Oya Yalcin Cok, Baskent University, Department of Anesthesiology and Reanimation. Adana Research and Education Center, Yuregir Adana/Turkey. Tel: +90 322 3272727-1469, Fax: +90 322 3271274. E-mail: [email protected] 593 M.E.J. ANESTH 20 (4), 2010 594 O. Y. Cok et. al Fig. 1 MR images showing suprasellar mass lesion consistent with macroadenoma (Axial FLAIR and sagittal spin echo T1 weighted images). The mass was heterogeneous and hyperintense, 3 x 2.7 cm, elevating vascular structure anteriorly with compression of optic chiasm. After a multidisciplinary consultation with the neurosurgery, obstetrics and anesthesiology departments, initial decision was to delay the surgery until after delivery. However, two weeks later, a rapid deterioration in patient’s visual acuity was detected and physical examination disclosed a total vision loss in the right eye and hemianopsia in the left eye. She was scheduled for an urgent surgical intervention after reconsultation. The preanesthetic assessment revealed a pregnancy at 29th week and parturient was otherwise healthy. Fetal cardiotocography and ultrasound examination revealed that fetus was well and concordant with its gestational age. Neurosurgeons preferred a craniotomy for emergent approach. Intraoperative monitoring included the routine clinical standards for cranial tumor surgery such as heart rates 5-lead ECG, invasive arterial blood pressure, peripheral O2 saturation, end tidal CO2, central venous pressure acquired by threading a central venous catheter into subclavian vein, body temperature and urine output throughout the anesthesia. Arterial blood gases were checked every twenty minutes. Furthermore, fetal heart rate (FHR) was monitored by cardiotocography prior to operation and throughout the surgery and periodically for 24 hours postoperatively. A senior resident obstetrician was ready for assessment of FHR and an urgent caesarean section (C/S) was planned in case of non-reassuring fetal stress at the same operating theatre where suitable set of surgical instruments were also available. In addition, neonatalogist was informed about the case and neonatal ICU was available as if the C/S had to be performed, the baby would have born preterm. Patient was premedicated with ranitidine 50 mg and metoclopramide 10 mg IV prior to operation. Anesthesia was induced with thiopental 400 mg, fentanyl 100 µg, lidocaine 60 mg and dexamethasone 8 mg intravenously. Intubation was facilitated by vecuronium 8 mg. The trachea was orally intubated, 7.5 mm at first attempt without any difficulty with application of cricoid pressure. A left lateral tilt was accomplished to prevent vena cava compression and reverse trendelenburg to the operating table to decrease intracranial pressure. A heated blanket was placed under the patient to keep normothermia. Anesthesia was maintained with fentanyl infusion 0.5-3 µg kg-1hr-1, 0.6-0.8 MAC isoflurane and 50% O2 in air. Controlled ventilation was with a tidal volume 8 mL kg-1 sustaining an end tidal CO2 values at 30 ± 2 mmHg. Surgery lasted approximately for 5 hours. The maternal heart rate and blood pressure remained within normal limits during operation (Fig. 2A and B). Arterial blood gases were in normal range and normothermia was carefully maintained. Anesthetic Management of 29 Week Pregnant Patient Undergoing Craniotomy for Pituitary Macroadenoma Fig. 2A Maternal and fetal heart rates throughout surgery (Beat/min) Fig. 2B Maternal blood pressure values throughout the surgery (mmHg) At the end of surgery, the neuromuscular blockade was reversed and the patient was extubated fully awake in the operating room and transported to the ICU uneventfully. Left temporal anopsia remained unimproved in her neurological examination at discharge from hospital, which was her main complaint preoperatively. Thereafter, she had C/S at 35th week of her pregnancy because of preterm labor and gave birth to a low birth weight child (1870 grams). Discussion The incidence of brain tumors during pregnancy is rare5,6. However, this rare problem may require urgent surgical interventions as brain tumors tend to enlarge during pregnancy due to fluid retention, increased blood volume and hormonal changes7. Management of intracranial tumors in pregnancy is stressful for everyone involved and it should be individualized for the patient8,9. The patient’s features and own wishes have to be considered while providing safety of two patients, the mother and the fetus9. The anesthetic management of a parturient undergoing a non-obstetric surgery includes close monitorization of maternal hemodynamics and 595 respiratory parameters. Continuous and attentive monitoring is also essential for follow-up of the fetus’ well-being during surgery and anesthesia10. However, necessity of fetal heart rate monitoring is still a controversial issue8,11,12,13,14. The purpose of FHR monitoring is to detect fetal hypoxia and metabolic acidosis, which may result in tissue damage or fetal death15. The baseline FHR is typically between 120160 beat/minute in a healthy fetus beyond 20 weeks. Alterations in the baseline rate and variability should be cautiously interpreted by trained personnel, because normal variability reliably indicates the absence of fetal distress, however vice versa does not. Many factors may mimic fetal stress on fetal heart rate monitoring such as inhalational anesthetics, opioids, barbiturates, parasympatholytics, fetal sleep cycles, hypothermia. The risk of misinterpretation under general anesthesia always exists and may lead to unnecessary surgery9,16. In addition, FHR monitoring requires additional trained personnel in the operating theatre and an emergency plan must be available in case of urgency. We advocate the use of FHR monitoring, whenever feasible, since constant maternal hemodynamics do not assure fetal’s well-being17,18. Managing a pregnant patient during craniotomy requires thorough understanding of physiology and pharmacology during pregnancy and a comprehensive knowledge of neurosurgical anesthesia to support practice3,9,19. The combination of pregnancy and neurosurgery requires rapid but smooth induction as advocated for all pregnant patients beyond 20 weeks of gestation. In pregnancy, functional residual capacity is decreased by 20% and O2 consumption is higher than non-pregnant patients. Hypo-and hypercapnia both reduce uterine blood flow inducing fetal acidosis and myocardial depression. Thereby, we aimed to maintain mild hypocapnia during surgery in order to avoid fetal stress, while avoiding hypoxia and providing normoventilation throughout surgery10. Particular attention should be paid to the positioning of parturient, as there is potential risk of aortacaval compression during surgery. The common practice is either to tilt the operation table 20º left laterally or to place a wedge under patient’s right hip, or both, to avoid a hypotension that will also affect the fetus9. The traditional drugs of neurosurgical anesthesia M.E.J. ANESTH 20 (4), 2010 596 should be reconsidered in a pregnant patient. Opioids are effective and compatible with neurosurgery and obstetrics; where as inhalational anesthetics are favored for uterine relaxation9. Since nitrous oxide should be avoided in the first trimester because of its teratogenicity, its aggravating effect on cerebral vasodilatation when used with potent inhalation agents, is another concern throughout whole neurosurgery. In this case, inhalation anesthetics with opioid supplemetation were preferred for their predictable effects on fetal well-being. Diuretics and hypotensives should be used attentively because of feto-maternal fluid shift and decrease in uteroplacental perfusion9. Steroids are advantageous by reducing cerebral edema and accelerating fetal lung maturation. Teratogenicity O. Y. Cok et. al and adverse effects of drugs are another concern for the well-being of the fetus. We aim to emphasize that a pregnant woman has a risk of every type of neurosurgical pathology, that a non-pregnant woman may face. In addition, pregnancy, itself, may cause neurological disorders to become symptomatic or may aggravate the present symptoms2,7. Anesthetists managing patients with both pregnancy and intracranial neoplasm have to base their practice on theoretical knowledge of obstetrics and neurosurgical anesthesia. However, further fetal safety measures such as fetal heart rate monitoring should be utilized whenever feasible in the presence of the fetus as a second patient during all interventions. References 1. Chandraharan E, Arulkumaran S: Pituitary and adrenal disorders complicating pregnancy. Curr Opin Obstet Gynecol; 2003, 15:101-6. 2. Swensen R, Kirsch W: Brain neoplasms in women: a review. Clin Obstet Gynecol; 2002, 45:904-27. 3. Van De Velde M, De Buck F: Anesthesia for non-obstetric surgery in the pregnant patient. Minerva Anestesiol; 2007, 73:235-40. 4. Smith IF, Skelton V: An unusual intracranial tumour presenting in pregnancy. Int J Obstet Anesth; 2007, 16:82-5. 5. Isla A, Alvarez F, Gonzalez A, García-Grande A, Perez-Alvarez M, García-Blazquez M: Brain tumor and pregnancy. Obstet Gynecol; 1997, 89:19-23. 6. Tewari KS, Cappuccini F, Asrat T, Flamm BL, Carpenter SE, DiSaia PJ, Quilligan EJ: Obstetric emergencies precipitated by malignant brain tumors. Am J Obstet Gynecol; 2000, 182:1215-21. 7. Cirak B, Kiymaz N, Kerman M, Tahta K: Neurosurgical procedures in pregnancy. Acta Cir Bras; 2003, 18:5-9. 8. Balki M, Manninen PH: Craniotomy for suprasellar meningioma in a 28-week pregnant woman without fetal heart rate monitoring. Can J Anaesth; 2004, 51:573-6. 9. Kuczkowski KM: Nonobstetric surgery during pregnancy: What are the risks of anaesthesia? Obstet Gynecol Surv; 2004, 59:52-6. 10.Giannini A, Bricchi M: Posterior fossa surgery in the sitting position in a pregnant patient with cerebellopontine angle meningioma. Br J Anaesth; 1999, 82:941-4. 11.Horrigan TJ, Villarreal R, Weinstein L: Are obstetrical personnel required for intraoperative fetal monitoring during nonobstetric surgery? J Perinatol; 1999, 19:124-6. 12.Macarthur A: Craniotomy for suprasellar meningioma during pregnancy: role of fetal monitoring. Can J Anaesth; 2004, 51:535-8. 13.Rosen MA: Management of anesthesia for the pregnant surgical patient. Anesthesiology; 1999, 91:1159-63. 14.Tuncali B, Aksun M, Katircioglu K, Akkol I, Savaci S: Intraoperative fetal heart rate monitoring during emergency neurosurgery in a parturient. J Anesth; 2006, 20:40-3. 15.Garite TJ: Intrapartum fetal evaluation. In: Gabbe SG, Niebyl JR, Simpson JL, eds. Obstetrics: Normal and problem pregnancies. Philadelphia: Churchill livinstone Elsevier Inc, 2007, 364-395. 16.Immer-Bansi A, Immer FF, Henle S, Spörri S, Petersen-Felix S: Unnecessary emergency caesarean section due to silent CTG during anaesthesia? Br J Anaesth; 2001, 87:791-3. 17.Liu PL, Warren TM, Ostheimer GW, Weiss JB, Liu LM: Foetal monitoring in parturients undergoing surgery unrelated to pregnancy. Can Anaesth Soc J; 1985, 32:525-32. 18.Ong BY, Baron K, Stearns EL, Baron C, Paetkau D, Segstro R: Severe fetal bradycardia in a pregnant surgical patient despite normal oxygenation and blood pressure. Can J Anaesth; 2003, 50:922-5. 19.Littleford J: Effects on the fetus and newborn of maternal analgesia and anesthesia: a review. Can J Anaesth; 2004, 51:586-609. UNEXPECTED POSTOPERATIVE SEIZURE AFTER MASTOID SURGERY - A Case Report - Erkalp Kerem*, Basaranoglu Gokcen*, Kokten Numan**, Ilhan Emre**, Egeli Unal***, Ozdemir Haluk* and Saidoglu Leyla* Postoperative seizures (expected after neurosurgery) are rare events. When they do occur, they are usually attributable to an identifiable drug reaction, a metabolic or neurological event1. We report a case of postoperative seizure in postanesthesia care unit. A 19-yr-old female, 48 kg, was admitted to a hospital for left middle-ear surgery. Her medical history, physical examination and laboratory evaluation were normal. Anesthesia was induced with fentanyl 1 µg/kg, thiopental 5 mg/kg and rocuronium 0.5 mg/kg to produce neuromuscular blockade. Anesthesia was initially maintained with oxygen, nitrous oxide and sevoflurane. Mastoid surgery was completed in 195 minutes after induction. The patient was extubated, but approximately 10 minutes after arrival in recovery she started to generalized tonic clonic convulsion. Oxygen was administered by face mask and thiopental 100 mg was administered intravenously. Blood sugar, electrolytes and body temperature were normal. After ten minutes convulsion episode was repeated. Because of the continuing seizure activity in a patient at risk of pulmonary aspiration and security of air way, her trachea was intubated by using thiopental and succinylcholine and ventilation controlled artificially. The seizures were controlled with midazolam and phenytoin. Computerized tomography (CT) showed left temporal cortical suspected hipodensity (Fig. 1) and the patient was transferred to ICU. From Vakif Gureba Hospital, Istanbul, Turkey. * Department of Anesthesiology. ** Department of Ear, Nose and Throat. *** Department of Radiology. Corresponding author: Kerem Erkalp. Kartaltepe Mah., Bilgehan Cad., no. 64/6, 34040, Bayrampasa/Istanbul, Turkiye. Tel: 0090 532 7879500, Fax: 0090 212 621 75 80. E-mail address: [email protected] 597 M.E.J. ANESTH 20 (4), 2010 598 Fig. 1 Computerized tomography (CT) showed left temporal cortical suspected hipodensity (Early postoperative period) Neurological consultation was conducted and it was thought to be a new epileptogenic focus in left temporal lobe with iatrogenic brain injury. After 3 days, the patient was discharged without neurologic deficit in anticonvulsant therapy with phenytoin 300 mg orally. The magnetic resonance imaging (MRI) scan showed hyperintense signals area in left temporal cortex (Fig. 2). She was sent to the ward after normal physical examination findings. There are numerous anesthetic and nonanesthetic causes of postoperative seizures; local anesthetics, inhalation anesthestics, opioids, drug reaction, hypoxia, hypocarbia, hypoglycemia, hyponatremia, hypocalcaemia, acidosis, pyrexia, psychogenic seizures (pseudoseizures). Postoperative seizures may result from global or focal cerebral ischemia due to hypoperfusion, particulate or air emboli, or metabolic E. Kerem et. al Fig. 2 Magnetic resonance imaging (MRI) scan showed hyperintense signals area in left temporal cortex (3 days after surgery) causes2. Iatrogenic complications can and do occur in ear surgery. Damage occur if a cutting burr is used with excessive pressure directed onto an edge of the bone. The BURR can jump of the bone through the exposed dura into the middle fossa with damage to the arachnoids and surface of temporal lobe itself3. The operating microscope has dramatically reduced the risks of injury, but surgeons still maintained a heightened awareness of these complications, as many injuries are not visually detected at the time of surgery4. We believe that, in our case the seizure may have occurred secondary to damage to the temporal cortex due to iatrogenic brain injury. To our knowledge seizures associated with iatrogenic brain injury is not well documented as a cause of postoperative seizures. References 1. Ng L, Chambers N: Postoperative pseudoepileptic seizures in a known epileptic: complications in recovery. Br J Anaesth; 2003, 91:598-600. 2. Bronster DJ: Neurologic complications of cardiac surgery: current concepts and recent advances. Curr Cardiol Rep; 2006, 8:9-16. 3. Tos M: Manual of middle ear surgery. 1995. volume II. 66. 4. Abbas GM, Jones RO: Measurements of drill-induced temperature change in the facial nerve during mastoid surgery: a cadaveric model using diamond burs. Ann Otol Rhinol Laryngol; 2001 Sep, 110(9):867-70. PSYCHO-MIMETIC MANIFESTATIONS FOLLOWING PROPOFOL IN DAY CARE SURGERY - Case Reports - Pradipta Bhakta,* Pragnyadipta Mishra,** and Q utaiba A mir Tawfic *** Abstract Objectives: Propofol has virtually replaced other agents for induction of anesthesia in the ambulatory setting because of its favorable recovery profile. Psycho-mimetic effects, common after use of ketamine, are not so well known for propofol. We present two case reports where patients had two spectrum of abnormal psychological outbreaks after propofol anesthesia. Case Reports: Two healthy young patients were scheduled for short day care procedures under general anesthesia. In both cases anesthesia was induced with propofol plus fentanyl and maintained with inhalational anesthetic agents. After uneventful completion of surgery, both patients were transferred to recovery room where they manifested unusual psycho-mimetic reactions. The first patient had emotional outburst in the form of crying and the other had violent reaction requiring haloperidol for control. Conclusion: Psycho-mimetic reactions can occur after anesthesia using propofol in the short duration day care procedures, in patients with or without preexisting psychiatric problems, needing antipsychotic medications for control. Key Words: Case report, Emotional outbreak, Propofol anaesthesia, Day Care surgery. * ** *** Dept. of Anesthesia and Intensive Care, Sultan Qaboos University Hospital, Muscat, Oman. Dept. of Pediatric Anesthesiology Cincinnati Children’s Hospital & Medical Centre, Cincinnati, Ohio, USA. Dept. of Anesthesia and Intensive care, Sultan Qaboos University Hospital, Muscat, Oman. Corresponding author: Dr. Pragnyadipta Mishra (MD, DNB), Clinical Fellow, Dept. of Pediatric Anesthesiology, Cincinnati Children’s Hospital & Medical Centre, Cincinnati, Ohio-45229, USA, Tel: +1-513-257-1361. E-mail: [email protected] Financial support: There was no financial support of any kind involved with this study. 599 M.E.J. ANESTH 20 (4), 2010 600 P. Mishra et. al Introduction Propofol has replaced other agents for induction of anesthesia in the ambulatory setting because of smooth, fast and clear headed recovery. Contrastingly, subhypnotic concentration of propofol has been reported to result central nervous system (CNS) adverse effects including perioperative mood alterations. We describe two such incidences where patients developed unusual psycho-mimetic manifestations during recovery from short general anesthesia using propofol as induction agent. Case 1 A 23 year old lady, ASA I, weighing 46 Kg, was scheduled for day care anal sphincterotomy. Sedative pre-medication was withheld. Anesthesia was induced with intravenously fentanyl 100 microgram and propofol 100 mg and maintained with 60% N2O in O2 and isoflurane along with incremental doses of propofol and fentanyl. She was kept on spontaneous ventilation with mask and oropharyngeal airway. Duration of operation was approximately 20 minutes and it was uneventful. Total amount of propofol and fentanyl used were 150mg and 150microgram respectively. She behaved abnormally recovery from anesthesia. There was no response to verbal command even though she was opening her eyes. Shortly after that she started weeping and later cried loudly. She was asked repeatedly whether she was feeling pain, but the answer was always negative. Her emotional outburst was settled after reassurance from us. Later she was shifted to PACU for further monitoring. In PACU, a detail history was taken by a female doctor. It was found that she was under constant stress starting from her marriage. She became pregnant immediately after her marriage and was being abused constantly by her in-laws. Case 2 A 29 years old female patient, ASA I, 50 Kg, diagnosed case of incomplete abortion and was scheduled for emergency suction and evacuation. Premedication was withheld. General anesthesia was induced with intravenous fentanyl 100microgram and propofol 120mg. Size three proseal LMA was inserted and anesthesia was maintained with 60% N2O in O2 and incremental doses of propofol and fentanyl when necessary. Inhalational agent was avoided. Spontaneous ventilation was used. Surgery was completed uneventfully in fifteen minutes. Total dose of propofol used was 180mg. She was shifted to PACU after she became awake and stable. In the PACU she behaved abnormally, struggling and trying to jump out from bed. Initially it was thought because of pain. So, incremental doses of fentanyl were given. But even after additional 100microgram of fentanyl there was no change in behavior. Attempt to resist the patient made her more violent. She started using offensive filthy words and thrashing the nursing staff. At this time haloperidol 2.5mg was given intravenously. After that she gradually became quite. Rest of her stay in the recovery as well as general ward was uneventful. Next morning she became fully awake and co-operative. But she was not able to recollect the previous event. Later, a detail history was taken from the patient as well as relative by the psychiatrist and it revealed that she had a history of claustrophobia and bed wetting till the age of nine years. Discussion Psycho-mimetic and emotional reactions are known side effects of ketamine, but they are not so well known with propofol.1,2 Sub-hypnotic concentrations of propofol can produce CNS adverse effects like postoperative alteration in mood. Patients emerging from propofol anesthesia were more likely to exhibit sensation-seeking tendencies (e.g. adventurous, daring, energetic) and to feel elated and even euphoric.3,4 It may result in dream and hallucination in day care setting.5 Even sexual hallucination and opisthotonos have been reported.6,7 To date, no incidence of emotional or psychological outburst has been reported in literature. Both of our patients behaved normally during pre-anesthetic assessment and did not show any signs or symptoms of psychiatric disorders. The anesthesia technique used was well established for short duration day care procedures and none of the PSYCHO-MIMETIC MANIFESTATIONS FOLLOWING USE OF PROPOFOL IN DAY CARE SURGERY agents used for anesthesia other than propofol could have promoted these psycho-mimetic effects. Thus a probable deduction is that propofol may have caused suppression of inhibitory areas of brain that resulted in outburst of long term emotional stress, which was not revealed earlier (as in 1st case) and expression of some hidden psychological behavior (as in 2nd case). Also the inherent psychogenic effects of propofol (mentioned earlier) may have played a role here. Probable explanation of its occurrence in day care cases is that lack of proper preanesthetic counseling and avoidance 601 of premedication may have resulted in expression of psychological phenomenon in the setting of propofol induced inhibition of higher centers of CNS and its inherent psycho-mimetic effect. Conclusion Emotional and psycho-mimetic reactions may occur after propofol anesthesia especially in day care patients with background history of chronic stress and psychological disorders. References 1. Garfield JM, Garfield FB, Stone JG, et al: A comparison of psychological responses to ketamine and thiopentone-nitrous oxidehalothane anesthesia. Anesthesiology; 1972, 36:329-38. 2. Crossen G, Reves J, Stanley T: Dissociative anesthesia. In Crossen G, Reves J, Stanley T (Eds): Intravenous Anesthesia and Analgesia. Philadelphia, Lea & Fabiger, 1988, p. 99. 3. White PF, Freire AR: Ambulatory (Outpatient) Anesthesia. In Miller RD, ed. Miller’s Anesthesia, 6th ed. Philadelphia, pensylvania: Elsevier Churchill Livingstone, 2005, pp. 2603-4. 4. McDonald NJ, Mannion D, Lee P, et al: Mood elevation and outpatient anaesthesia. A comparison between propofol and thiopentone. Anaesthesia; 1988, 43 (suppl.):68-9. 5. Hocking G: Propofol-an interesting new side effect? Anaesthesia; 1996, 51:101. 6. Nelson V: Hallucination after propofol. Anaesthesia; 1988, 43:170-1. 7. Cameron AE: Opisthotonos again. Anaesthesia; 1987, 42:1124. M.E.J. ANESTH 20 (4), 2010 602 P. Mishra et. al USE OF DEXMEDETOMIDINE AS THE MAIN ANESTHETIC AGENT in PATIENTS WITH LARYNGO-TRACHEOMALACIA - A Case Report- Khaled Al Zaben, Ibraheem Qudaisat, Bassam Al Barazangi and Izdiad Badran Abstract The successful use of Dexmedetomidine as the main anesthetic agent for three pediatric patients with tracheomalacia presenting for different kinds of urgent operations is described. Patients were kept spontaneously breathing without intubation during their whole procedures. Surgical conditions were adequate, and hemodynamic and respiratory profiles were within baseline limits. Introduction Providing general anesthesia to patients with tracheomalacia can be a big challenge to the anesthetist in terms of the type of anesthetic agents used and airway and ventilatory management1. Easy collapsibility of the trachea during coughing and recovery from anesthesia may make extubation of the trachea extremely difficult, leading to prolonged intubation and ventilation in these patients1,2. The avoidance of endotracheal intubation, where practical, may decrease postoperative coughing and the risk of airway collapse on emergence3. Dexmedetomidine is a potent alpha-2-adrenergic agonist, which has analgesic and sedative effects with little effect on ventilation4,5. In the present case report, we describe the use of dexmedetomidine as the primary anesthetic in three pediatric patients who underwent different emergency operations without airway intervention. The same surgeon with whom the anesthesia plan was pre-discussed carried out the three operations. From Department of Anesthesia, Faculty of Medicine, Jordan University, Amman, Jordan. Corresponding author: Dr. Khaled AL ZABEN, Department of Anesthesia, Jordan University Hospital, Amman 11942, Jordan. E-mail: [email protected] 603 M.E.J. ANESTH 20 (4), 2010 604 Case 1 A 5-month-old male infant, (4 kg), known to have seizure disorder, developmental delay, failure to thrive and laryngomalacia was scheduled for repair of irreducible inguinal hernia and insertion of a gastrostomy feeding tube. On preoperative evaluation, the patient had inspiratory stridor, tachypnea, and tachycardia. His SpO2 was 88% on 5 L/min. O2. He had left subclavian central venous line inserted due to difficult peripheral venous access. Upon arrival to the OR, standard monitors were applied. A loading dose of Dexmedetomidine (1 µg/ kg) was then given over 10 minutes followed by a 2 µg/kg/hr infusion. A slow infusion of propofol (50 µg/ kg/min) was also started. After the loading dose of Dexmedetomidine, the surgeon was asked to pinch the skin with forceps to assess the adequacy of sedation before infiltration of local anesthetic solution. A total of 3ml Bupivacaine 0.25% was infiltrated by the surgeon. The patient was kept spontaneously breathing with 3 L/minute O2 flow applied through a simple facemask. During the procedure, the patient’s SpO2 remained around its baseline with an end-tidal CO2 of 45-50mmHg measured through a catheter under the face mask. Heart rate and mean blood pressure were decreased by less than 20% from their baseline and there was no significant drop in the respiratory rate. Surgical conditions were excellent throughout. By the end of the surgery, drug infusions were stopped and patient sent back to pediatric intensive care unit (PICU) where he remained sedated for around one and half hours without the need for additional analgesic medications. Case 2 A 3-year-old female patient (10 kg) known to have bilateral hydronephrosis and laryngomalacia was scheduled for diagnostic cystoscopy. On pre-operative assessment she was tachycardic (115 b/m), BP 100/70 mmHg. She had expiratory stridor with SpO2 of 90% on 3L/min. facemask oxygen. Her attending pediatrician indicated that this was her best condition and nothing else could be done to improve her condition. In the operating theatre, standard ASA monitoring was applied and a new peripheral intravenous line was K. Al Zaben et. al secured, A loading dose of Dexmeditomidine 1 µg/kg was infused over 10 minutes then continued as infusion at 2 µg/kg/hr. Propofol 1% infusion was also started at 50 µg/kg/min. Lignocaine gel was applied in the patient’s urethra by the surgeon for topical anesthesia prior to insertion of the cystoscope. The patient was kept spontaneously breathing through a simple face mask with oxygen flow of 4 liters/min. The procedure was done uneventfully in 15 minutes and the patient had no significant changes in her blood pressure, heart rate, respiratory rate and end tidal CO2. She was transferred to the PACU, where she remained sedated for about 80 minutes and discharged to the ward afterwards. Case 3 A 3-year-old female patient (12 kg) with a history of congenital tracheo-esophageal fistula repaired when she was one day old, presented with a history suggestive of foreign body aspiration. She was known to have recurrent chest infections but her current presentation was associated with more than usual difficulty in breathing and transient attacks of cyanosis. She was brought to theatre as an emergency case for rigid bronchoscopy. Preoperative evaluation revealed that the patient is having severe inspiratory stridor and expiratory wheezes. SpO2 was 85% on 4 L/min oxygen via simple facemask. On arrival to the OR, oxygen treatment was maintained at 4 Lit/min. via simple face mask, standard ASA monitors applied, and her in situ venous access checked. Dexmedetomidine 2 µg/kg was given as a loading dose over 10 minutes and continued as infusion 6 µg /kg/hr, Propofol intravenous infusion was also started at 100 µg/kg/min. Topical anesthesia lignocaine spray up to a total dose 4mg/kg was applied two minutes prior to insertion of the rigid bronchoscope. The procedure, which revealed the presence of laryngo-tracheomalacia, was done smoothly in about 15 minutes, and ended with the recovery of a fragment of a melon seed shell from the patient’s right main bronchus. During the procedure, the patient maintained spontaneous ventilation with SpO2 85-90%, End-tidal CO2 45-50 mmHg. There were no significant changes in her baseline heart rate and blood pressure. By the end of the procedure, the infusions were discontinued and the patient was sent to the PACU where she remained USE OF DEXMEDETOMIDINE AS THE MAIN ANESTHETIC AGENT in PATIENTS WITH LARYNGOTRACHEOMALACIA sedated for about two hours and discharged to the ward afterwards. Discussion The choice of anesthetic option for patients with airway malacia who present for different types of surgeries can be difficult and tricky1. This is especially true for those patients presenting for emergency operations where preparation of patients can be limited. The option of general anesthesia technique for these patients usually requires the use of airway and ventilation support maneuvers such as CPAP or PEEP to prevent intraoperative airway collapse. As postoperative coughing with the risk of airway collapse on emergence will increase with the use of endotracheal intubation6-8, the avoidance of a tracheal tube, provides smoother anesthesia course. Also, reports of Laryngeal mask airway (LMA) use in these patients ranged between success3,9,10 and failure6. Although the use of inhalational technique while maintaining spontaneous respiration is a logical way of general anesthesia in these patients, there had been some case reports of Isoflurane and Enflurane induced tracheomalacia11,12. Precipitation of airway obstruction during sevoflurane general anesthesia in a child with congenital tracheomalacia had also been reported6. The use of Intravenous anesthesia maintenance techniques is yet another option especially in older children1. However, the use of Propofol which is the most commonly used intravenous anesthetic agent for total intravenous anesthesia, was found to be associated with dose-related depression of central respiratory output to upper airway dilator muscles and of upper airway reflexes13. In view of those limitations, we opted to use a Dexmedetomidine-based sedation technique, supplemented with minimal dose Propofol and combined with local anesthetic infiltration/topicalization of the surgical site as necessary. Dexmedetomidine is an α 2-adrenergic agonist which is currently FDA-approved for the short-term (less than 24 hours) sedation of adult ICU patients. It has analgesic and sedative effects with little effect on ventilation4. Literature about its clinical use in pediatric patients is based on case reports and includes 605 sedation during mechanical ventilation, prevention of emergence agitation following general anesthesia with sevoflurane or desflurane, provision of proceduralsedation, and to prevent withdrawal following the prolonged use of opioids and benzodiazepines14. Our aim was to avoid airway maneuvering during anesthesia, meanwhile maintaining adequate spontaneous breathing. In all of the three cases herein presented, this was achieved successfully with adequate intra-and postoperative outcome. Use of dexmedetomidine as the sole anesthetic will require higher doses, (5-10 µg /kg/hr), which might affect the respiratory and hemodynamic profile. This is especially true for upper airway surgery as described by Ramsay and Luterman15. Shukry et al16 in their use of dexmedetomidine as the sole anesthetic in four infants requiring bronchoscopy in a dose of 2-5 µg/kg/hr found out that a bolus dose of propofol was needed for one of the patients. They suggested that infusing a small dose of propofol would decrease the Dexmeditomidine needed to achieve adequate surgical conditions without respiratory and cardiac complications, a combination technique opted in our patients. Although brief in duration, rigid bronchoscopy is an intensely stimulating procedure that requires better control of airway reflexes. Seybold et al19 successfully used Dexmedetomidine (2.5 µg/kg/hr with boluses of 0.25-1 µg /kg) combined with propofol 200-250 µg/kg/min for rigid bronchoscopy in two pediatric patients. In our bronchoscopy case we did not use Dexmedetomidine increments but instead we used a higher loading dose and infusion rate (2 µg /kg and 6 µg/kg/hr respectively), and smaller Propofol dose (100 µg/kg/min). Our plan was based on the fact that respiration is more likely to still be preserved when Dexmedetomidine is used as the primary anesthetic agent than Propofol. In conclusion, we report on three cases of successful use of Dexmedetomidine-based anesthesia in patients with airway malacia who presented for different emergency surgeries. Airway interventions were successfully avoided and surgical conditions were adequate. Further controlled studies are needed to establish the safety and efficacy of Dexmedetomidinebased anesthesia in such patients. M.E.J. ANESTH 20 (4), 2010 606 K. Al Zaben et. al References 1. Austin J, Ali T: Tracheomalacia and bronchomalacia in children, pathophysiology, treatment, assessment and anaesthetic management. Pediatric anaesthesia; 2003, 13:3-11. 2. Suto Y, Tanabe Y: Evaluation of Tracheal collapsibility in Patients with Tracheomalacia Using Dynamic MR Imaging during Coughing. AJR Am J Roentgenol; 1998, 171:393-394. 3. Yamaguchi S, Takanishi T, Matsumoto T, et al: Use of a laryngeal mask in a patient with bronchomalacia. Masui; 1996, 45:348-351. 4. Chad M: Brummett, Dexmedetomidine: A Clinical Review, Seminars in Anesthesia, Perioperative Medicine and Pain; 2006, 25:41-42. 5. Takrouri MS, Seraj M A, Channa AB, el-Dawlatly AA, Thallage A, Riad W, Khalaf M: Dexmeditomidine in intensive care unit: a study of hemodynamic changes. Middle East J Anesthesiology; 2002 Oct, 16(6):587-95. 6. Okuda Y, Sato H, Kitajima T, Asai T: Airway obstruction during general anaesthesia in a child with congenital tracheomalacia, EJA; 2000, 17:642-44. 7. Asai T, Shingu K: Airway obstruction in a child with asymptomatic tracheobronchomalacia. Can J Anaesth; 2001, 48:7, 684-687. 8. Celiker V, Basgul E, Karagoz AH: Anesthesia in BeckwithWiedemann syndrome, Pediatric Anaesthesia; 2004, 14:778-780. 9. Ghelber O, Szmuk P, Alfery DD, Ezri T, Agro F: Use of CobraPLUSTM in a child with tracheomalacia. Acta Anaesthesiol Scand; 2007 Jul, 51(6):782-3. 10.Patrick N, Joseph N, Kim R: Use of the Proseal Laryngeal Mask Airway In An Infant With Repaired H-Type Tracheoesophageal Fistula and Tracheomalacia. Pediatric Anesthesia; 2008, 18:74-76. 11.Katoh H, Saitoh S, Takiguchi M, et al. A case of tracheomalacia during Isoflurane Anesthesia. Anesthesia Analgesia; 1995, 80:1051-3. 12.Yamaya K, Ujike Y, Namiki A: Tracheobronchomalacia occurring under general anesthesia: a case report. Rinsho Masui; 1986, 10:33740. 13.Peter R: Eastwood, Peter R. Platt, Kelly Shepherd, Kathy Maddison, David R. Hillman, Collapsibility of the Upper Airway at Different Concentrations of Propofol Anesthesia. Anesthesiology; 2005, 103:470-7. 14.Joseph D: Tobias, Clinical uses of dexmedetomidine in pediatric anesthesiology and critical care, Seminars in Anesthesia, Perioperative Medicine and Pain; 2006, 25:57-64. 15.Ramsay MA, Luterman DL: Dexmedetomidine as a total intravenous agent. Anesthesiology; 2004, 101:787-790. 16.Shukry M, Kennedy K: Dexmedetomidine as a total intravenous anesthetic in infants. Pediatric Anesthesia; 2007, 17:581-583. 17.Seybold JL, Ramamurthy RJ, Hammer GB: The use of Dexmeditomidine during laryngoscopy, bronchoscopy, and tracheal extubation following tracheal reconstruction. Paediatric Anaesth; 2007 Dec, 17(12):1212-1214. PRIMARY MALIGNANT MELANOMA OF THE TRACHEA Mohamad Nattout, Nabil Fuleihan, Omar Sabra, Ibrahim Aburizk, Abdul-latif Hamdan Abstract Tracheal melanomas represent the rarest type of extracutaneous melanomas. The clinical manifestation is similar to other tracheal tumors and ranges from symptoms of airway obstruction such as dyspnea and stridor to other nonspecific symptoms such as hoarseness, cough and hemoptysis. Bronchoscopy is required to draw the origin of the lesion biopsy is needed to establish histologic diagnosis. Treatment consists of either palliative surgery aiming at restoring the airway or tracheal resection and end to end anastmosis. We would like to present here below a rare case of tracheal melanoma and discuss the various diagnostic and therapeutic means. Key Words: melanoma; airway obstruction; trachea. Introduction Primary tumors arising from the trachea are uncommon. The clinical incidence does not exceed 0.2 per 100,000 people per year and the post-mortem prevalence is about 1 per 15,000 autopsies1. When present it is important to recognize the association of primary tracheal tumors with other head and neck tumors, with the increased risk being estimated as 11 fold2. More than fifty percent of these tumors are malignant and the most frequent histopathologic types are squamous cell carcinoma followed by adenocarcinoma There are only few reports in the literature on primary tracheal melanomas and these represent the rarest type of extracutaneous melanomas3-6. This case report describes the relevant radiologic and clinical features of this uncommon malignancy. * Lecturer. ** Professor. *** Resident. ****Associate Professor, Department of Otolaryngology, American University of Beirut Medical Center. Corresponding author: Abdul-Latif Hamdan, MD, FACS, American University of Beirut, Department of Otolaryngology, P.O. Box: 110236, Tel/Fax: 961-1-746660. E-mail: [email protected] 607 M.E.J. ANESTH 20 (4), 2010 608 Case Presentation A 28 year old male, previously healthy, presented to the American University of Beirut with history of severe upper airway obstruction. He reported history of progressive dyspnea, shortness of breath and hemoptysis of two month duration. Medical history was negative for asthma or chest pain or other systemic illnesses. His physical exam revealed “stridor” and suprasternal retractions. Fiberoptic laryngeal endoscopy did not show any laryngeal abnormalities with normal mobility of the vocal folds. Computerized tomography of the neck and chest revealed a tracheal mass obstructing almost ninety percent of the tracheal lumen (Fig. 1). Magnetic Resonance imaging did not show extension into the mediastinum. PET scan did not show any metastatic lesion or other primary except the tracheal lesion. Patient underwent tracheostomy under local anesthesia followed by bronchoscopy. Bronchoscopy revealed a tracheal mass with a nodular surface arising from the right posterolateral wall at the level of the fifth tracheal ring and extending to the seventh tracheal ring. The lesion was occupying most of the tracheal lumen. Biopsy was taken and sent for histopathological examination. The following immunohistochemical stains were performed: HMB45, S-100, Vimentin and Cytokeratin AE1/AE3. All the results were positive except for cytokeratin AE1/AE3 which was negative. The diagnosis was consistent with a primary malignant melanoma of the trachea (Fig. 2). Fig. 1 Computerized Tomography of the neck showing a tracheal tumor arising from the right posterolateral wall of the trachea and occluding almost all the tracheal lumen M. Nattout et. al Fig. 2 A: H & E stain: Tumor composed of interlacing bundles of spindle cells, with vesicular nuclei containing prominent nucleoli, occasional cytoplasmic melanin is noted. The tumor fills and expands the subepithelial stroma. B: HMB-45 positive cells are seen Discussion Primary tracheal melanoma is extremely uncommon despite the increase in the incidence of malignant melanoma of the skin and the few reports of intratracheal metastasis3. In a retrospective review of 360 primary tracheal tumors, only one patient had tracheal melanoma7. The clinical manifestation of primary tracheal melanomas is similar to other tracheal tumors and ranges from symptoms of airway obstruction such as dyspnea, stridor wheezes and cyanosis, to other nonspecific symptoms such as hoarseness, cough, hemoptysis, weight loss and chest pain. Invasion into adjacent structures may present as a neck mass with the presence of dysphagia and odynophagia.2,5. Tracheal tumors are rarely discovered by chest or neck radiographs especially in the early stages. Not more than 50% are identified based on PRIMARY MALIGNANT MELANOMA OF THE TRACHEA these means as reported by a radiologic and clinical study conducted by Li et al. Barium esophagogram is helpful in detecting esophageal invasion when the mass is arising from the posterior tracheal wall. Computerized tomography is the most important imaging modality with an accuracy that exceeds tomography. It provides a good cross sectional image of the trachea and the endoluminal tumor extent, however it may underestimate the vertical length of the tumor in view of the volume averaging5,6. Bronchoscopy is required to draw the origin of the lesion and to map the extent of the tumor in relation to the vocal folds. Biopsy remains the hallmark to establish histologic diagnosis. There are strict criteria for the microscopic diagnosis of primarily melanoma of the trachea and these include the presence of a solitary tracheal tumor containing melanin histologically in the absence of tumor outside the trachea, junctional changes in the mucosa between melanoma cells and normal lining and invasion beyond the epithelium and submucosa8,9. Immunostains for HMB-45 and S-100 are usually positive in these tumors. These were the findings in our reported case. There were several attempts to explain the 609 oncogenesis of mucosal melanomas in general and to postulate the histogenesis of lower respiratory tract melanomas in specific. Shivas and MacLennan have suggested the term “melanogenic metaplasia”, where mucus-secreting cells are histologically altered into melanin- producing cells. Reid and Metha and Walsh reported that squamous metaplasia is the origin of mucosal melanomas. Others have speculated that melanocytes migrate during embryogenesis to the developing lower respiratory tract or arise from a neuroendocrine cell precursor (Kul-chitsky cell)5-9. Treatment consists of either palliative surgery aiming at restoring the airway by means of laser usage or therapeutic with tracheal resection and end to end anastmosis10. For laser usage, various therapeutic options are available and these include the carbon dioxide CO2 laser, the argon, the neodymium:yttriumaluminum-garnet ( Nd: YAG) and the new argon plasma coagulation (APC) technique under flexible bronchoscopy. Radiation therapy or endobronchial brachytherapy may be added especially in cases of incomplete resection. Chemotherapy is recommended however the prognosis remains poor irrespective of the modality of treatment. References 1. Heffner DK: Diseases of the trachea. In: Barnes L, ed. Surgical Pathology of the Head and Neck, vol. 1. New York: Marcel Dekker Inc, 1985, pp. 487-531. 2. Lefor AT, Bredenberg CE, Kellman RM, Aust JC: Multiple malignancies of the lung and head and neck. Arch Surg; 1986, 121:265-70. 3. Koh HK: Cutaneous melanoma. N Engl J Med; 1991, 3:171-182. 4. Allen AC, Spitz S: Malignant melanoma, a criteria for diagnosis and prognosis. Cancer; 1953, 6:1. 5. Mori K, Cho H, Som M: Primary “flat” melanoma of the trachea. J Pathol; 1977, 121:101-4. 6. Duarte IG, Gal AA, Mansour KA: Primary malignant melanoma of the trachea. Ann Thorac Surg; 1998, 65:559-60. 7. Gaissert HA, Grillo HC, Shadmehr MB, Wright CD, Gokhale M, Wain JC, Mathisen DJ: Uncommon primary tracheal tumors. Ann Thorac Surg; 2006, 82(1):268-723. 8. Colby TV, Koss MN, Travis WD: Tumors of the lower respiratory tract. In: Armed Forces Institute of Pathology. Atlas of tumor pathology, third series, fascicle 13. Armed Forces Institute of Pathology; 1995, pp. 483-7. 9. Jennings TA, Axiotis CA, Kress Y, Carter D: Primary malignant melanoma of the lower respiratory tract. Am J CLin Pathol; 1990, 94:649-55. 10.Capaccio P, Peri A, Fociani P, Ferri A, Ottaviani F: Flexible argon plasma coagulation treatment of obstructive tracheal metastatic melanoma. Am J Otolaryngol; 2002, 23(4):253-255. M.E.J. ANESTH 20 (4), 2010 610 Tracheal Schwannoma: A Misleading Entity Abdul Latif Hamdan*, Roger V. Moukarbel*, Ayman Tawil**, Mohamad El-Khatib***, Ussama Hadi* ABSTRACT Primary tracheal tumors are rare with the majority being malignant. Benign lesions are less frequent with primary tracheal schwannomas accounting for less than 0.5% of tracheal tumors. They are more common in females and their clinical presentation is non-specific. Chronic cough, progressive respiratory distress and even asthma-like conditions prevail as presenting symptoms and signs. Laryngotracheal endoscopy reveals a solitary, well encapsulated mass arising most often from the posterior tracheal wall. The diagnosis of tracheal schwannomas is primarily pathological. Endoscopic excision, sleeve excision or tracheal resection, are all commonly accepted treatment modalities. Proper awarness of these lesions is crucial in the pre-operative work-up of patients presenting with stridor. Key words: Trachea, shwannoma, resection. Introduction Primary tracheal tumors are rare with the majority being malignant. Benign lesions are less frequently encountered and embrace a wide heterogeneous group comprising adenomas, papillomas, fibromas, lipomas, hemangiomas and neurogenic tumors1. Though benign as indolent lesions, their clinical presentation might be malignant. The lack of localizing symptoms often misleads the primary physician and results in a delayed diagnosis. Pre-operative work-up and proper mode of anesthesia delivery is important and may avoid a tracheostomy on these patients unless severe obstruction is present. A case report of a rare, primary tracheal schwannoma is described with emphasis on the pathologic findings and modalities of treatment. Case Report A 68 year old lady diabetic, hypertensive and cardiac presented six weeks status open heart surgery with history of respiratory failure following multiple attempts of extubation. Her history dates back to the time of surgery when difficult intubation was encountered upon induction of anesthesia. Direct laryngoscopy and bronchoscopy done by an outside physician revealed a tracheal mass at the level of the second tracheal ring obstructing the airway. A tracheotomy was done and the patient was sent to us for further evaluation and treatment. Further questioning *Department of Otolaryngology- Head & neck Surgery, American University of Beirut Medical Center. **Department of Pathology & Laboratory Medicine, American University of Beirut Medical Center. ***Department of Aneasthesiology, American University of Beirut Medical Center. Corresponding Author: Abdul-latif Hamdan, MD, FACS, Department of Otolaryngology-Head & Neck Surgery, American University of Beirut Medical Center, P.O. Box: 11-0236, Beirut-Lebanon, Tel: 961 1 350000, ext. 7695, Fax: 961 1 746660. E-mail: [email protected] 611 M.E.J. ANESTH 20 (4), 2010 612 of the family members revealed history of asthma with noisy breathing, exertional dyspnea and decrease in exercise tolerance for which the patient was treated to no avail. A fiberoptic nasopharyngeal laryngoscopy revealed normal vocal cord mobility with the evidence of a high tracheal mass. Magnetic resonance imaging of the neck revealed a 1-2 cm tracheal lesion arising from the posterior tracheal wall with a high signal intensity on a T2 weighted images (Fig. 1). There was no evidence of cartilage invasion or extratracheal spread. Bronchoscopy was done under general anesthesia and showed a soft smooth well rounded 2x2 cm mass located around 3cm below the true vocal cords. Incisional biopsy showed an expanding, well circumscribed submucosal mesenchymal neoplasm arising from the respiratory mucosa and compressing submucosal glands. High power view of the tumor showed neural spindled cells with bland nuclei that focally showed a palisaded arragement forming verocay bodies. Immunohistochemical staining for S-100 protein and vimentin were positive (Fig. 2). The diagnosis was consistent with tracheal shwannoma. Fig. 1 T2 weighted images, coronal cuts taken at level of tracheal narrowing, showing obliteration of the lumen by this high signal mass. Fig. 2 Well circumscribed submucosal mesenchymal neoplasm A. L. Hamdan et. al arising from the respiratory mucosa and compressing submucosal glands. High power view of the tumor showed neural spindled cells with bland nuclei that focally showed a palisaded arragement forming verocay bodies. Patient underwent surgical excision of the tumor with resection of two tracheal rings and primary end to end anastomosis. Patient was extubated directly postoperatively with no complications. Routine fiberoptic endoscopy at 6 months interval for the first year showed no recurrences. Discussion Primary tracheal schwannomas are rare lesions of the trachea, accounting for less than 0.5% of tracheal tumors1. They are more common in females with no age predilection2. Their clinical presentation varies and is usually non-specific. Chronic cough, progressive respiratory distress and even asthma-like conditions prevail as presenting symptoms and signs1,2,3. Poor response to conventional medical treatment prompts the physician to seek further investigation. Unfortunately, an average delay of 10-15 months between onset of symptoms and diagnosis is reported3. Radiological studies can be non specific. Computerized Tomography scan usually shows a well circumscribed enhancing mass within the tracheal lumen1,4 with no specific features. Magnetic Resonnance Imaging of a tracheal shwannoma, similar to other peripheral schwannomas, displays isointensity or hyperintensity on T1-weighted images and hyperintensity on T2-weighted images with heterogeneous enhancement as seen in our case5. Laryngotracheal endoscopy reveals a solitary, well encapsulated mass arising most often from the posterior Tracheal Schwannoma: A Misleading Entity tracheal wall; the lower third of the trachea is the most common site followed by the upper and then the middle thirds1,3. Proper awarness of these lesions is crucial in the pre-operative work-up of patients presenting with stridor. The anesthiology team should be ready to secure the airway by means other than the conventional ones such as endotracheal intubation. Laryngeal mask anesthesia or jet ventilation, delivering oxygenation proximal to the site of the lesion and avoiding direct manipulation of the tracheal lumen are important issues to keep in mind. The diagnosis of tracheal schwannomas is primarily pathological. Grossly, they are well circumscribed and encapsulated; microscopically, neural spindle cells in compact fashion (Antoni A areas) as well as in loose myxoid fashion (Antoni B areas) are demonstrated. Verocay bodies, which are areas of palisading nuclei, are present in Antoni A areas3. No capsular invasion, nuclear pleomorphism or mitoses is present. Immunohistochemical stains for S-100 protein and vimentin are positive4. These were the findings in our case. The differential diagnosis of spindle cell lesions of the larynx and trachea includes spindle cell carcinoma, as well as a variety of benign and malignant mesenchymal lesions. Spindle cell carcinoma can be easily identified by demonstrating 613 a direct relationship of the tumor with the adjacent epithelium and by immunohistochemical staining for cytokeratin. Among the benign mesenchymal lesions is nodular fasciitis which may display mitotic figures, but the latter are not atypical. Malignant lesions include a number of spindle cell sarcomas such as fibrosarcoma, synovial sarcoma, and leiomyosarcoma; however, these are extremely rare in this location and do not arise from the surface epithelium. The rarity of these lesions has led surgeons to practice different surgical techniques but the primary treatment is surgical excision. No standard procedure has been adopted. Endoscopic excision, sleeve excision or tracheal resection, are all commonly accepted treatment modalities. Endoscopic excision using either the cold steel instruments or laser is better suited for pedunculated lesions with no extra-tracheal component1. Tracheal resection with reconstruction has been more advocated for sessile lesions with or without an extra-tracheal component1,2, which was the procedure of choice in our case. The duration of follow up after surgical intervention has not been consistent throughout the literature, mainly because of the rarity of the lesion. References 1. Rusch VW, Schmidt RA: Tracheal schwannoma: management by endoscopic laser resection. Thorax; 1994, 49:85-86. 2. Horovitz AG, Khalil KG, Verani RR, et al: Primary intratracheal neurilemoma. J Thorac Cardiovasc Surg; 1983, 85:313-320. 3. Pang LC: Primary neurilemoma of the trachea. South Med J; 1989, 82:785-787. 4. Dorfman J, Jamison BM, Morin JE: Primary tracheal schwannoma. Ann Thorac Surg; 2000, 69:280-281. 5. Baba Y, Ohkubo K, Seino N, Churei H, Shirahama H, Nakajo M: MR imaging appearances of schwannoma: correlation with pathological findings. Nippon-Igaku-Hoshasen-Gakkai-Zasshi; 1997 Jul, 57(8):499-504. M.E.J. ANESTH 20 (4), 2010 GUIDELINES FOR AUTHORS The Middle East of Anesthesiology publishes original work in the fields of anesthesiology, intensive care, pain, and emergency medicine. This includes clinical or laboratory investigations, review articles, case reports and letters to the Editor. Submission of manuscripts: The Middle East Journal of Anesthesiology accepts electronic submission of manuscripts as an e-mail attachment only. Manuscripts must attachment to: be submitted via email Editor-In-Chief, Department of Anesthesiology, American University of Beirut Medical Center Beirut, Lebanon E-mail: [email protected] Human Subjects Manuscripts describing investigations performed in humans must state that the study was approved by the appropriate Institutional Review Board and written informed consent was obtained from all patients or parents of minors. Language: Articles are published in English. Manuscript Preparation Manuscript format required: Double-spaced lines Wide margins (1.5 inches or 3.8 cm) Page numbers start on title page Word count should reflect text only (excluding abstract, references, figures and tables). Editorial 1500 Abstract 250 (General articles) 100 (Case Reports) Clinical or laboratory investigations: The following structured format is required: 1. Cover Letter 7. Discussion 2. Title page 8. Acknowledgements 3. Abstract 9. References 4. Introduction 10. Tables 5. Methods 11. Figures 6. Results 1. Cover Letter Manuscripts must be accompanied by a cover letter, signed by all authors and stating that: - All authors have contributed intellectually to the manuscript and the manuscript has been read and approved by all the authors. - The manuscript has not been published, simultaneously submitted or accepted for publication elsewhere. 2. Title Page Starts at page 1 and includes: - A concise and informative title (preferably less than 15 words). Authors should include all information in the title that will make electronic retrieval of the article both sensitive and specific. - Authors listing: first name, middle initial and last name with a superscript denoting the academic degrees as footprints. - The name of the department(s) and institutions(s) to which the work should be attributed. - The name, address, telephone, fax numbers and e-mail address of the corresponding author. - Disclose sources of financial support (grants, equipment, drug etc…). - Conflict of interest: disclosure of any financial relationships between authors and commercial interests with a vested interest in the outcome of the study. - A running head, around 40 characters. - Word count of the text only (excluding abstract, acknowledgements, figure legends and references). Review article 4000 Original article 3000 Case Reports 800 3. Abstract Letter to Editor 500 Abstract should follow the title page. It should be structured with background, methods, results and conclusion. M.E.J. ANESTH 20 (4), 2010 It should state, the specific purpose of the research or hypotheses tested by the study, basic procedures, main findings and principal conclusions. Provide separate word count for the abstract. 4. Introduction Provide the nature of the problem and its significance. State the specific purpose or research objectives or hypothesis tested. Provide only directly pertinent references and do not include data or conclusions from the work being reported. 5. Methods A. Selection and description of participants: - Describe selection of participants (including controls) clearly, including eligibility and exclusion criteria. B. Technical information: - Identify the methods, apparatus (give the manufacturer’s name and address in parentheses), and procedure in sufficient detail to allow others to reproduce the results. Give references to established methods. Provide references and brief descriptions for methods that have been published. Identify precisely all drugs and chemicals used, including generic names(s), dose(s) ands routes(s) of administration. C. Statistics-describe statistical methods with enough detail to enable a knowledgeable reader with access to the original date to verify the reported results. Define statistical terms, abbreviations and most symbols. Specify the computer software used. Provide a power analysis for the study. 6. Results Present your results in logical sequence in the text, tables and illustrations, giving the main or most important findings first. Do not repeat all the data in the tables or illustrations in the text: emphasize or summarize only the most important observations. Extra or supplementary materials and technical details can be placed in an appendix. 7. Discussion Emphasize the new and important findings of the study and the conclusions that may be drawn. Do not repeat in details data or other information given in the Introduction or the Results sections. For experimental studies, it is useful to begin the discussion by summarizing briefly the main findings, then explore possible mechanisms or explanations for these findings, compare and contrast the results with other relevant studies. State the limitations of the study, and explore the implications of the findings for future research and for clinical practice. Link the conclusions with the goals of the study, but avoid unjustified statements and conclusions not adequately supported by the data. 8. Acknowledgements They should be brief. Individuals named must be given the opportunity to read the paper and approve their inclusion in the acknowledgments. 9. References - References should be indicated by Arabic numerals in the text in the form of superscript and listed at the end of the paper in the order of their appearance. Please be accurate, giving the names of all authors and initials, the exact title, the correct abbreviation of the journal, year of publication, volume number and page numbers. - The titles of journals should be abbreviated according to the style used in the list of Journals Indexed for MEDLINE. Example: (1) from a journal (2) from a book. 1. SHAWW: AND ROOT B: Brachial plexus anesthesia Comparatives study of agents and techniques. Am. J. Surg.; 1951, 81:407. 2. ROBINSON JS: Modern Trends in Anaesthesia, Evans and Gray Ch. 8, Butterworth Pub. Co., London 1967. 10. Tables Tables capture information concisely and display it efficiently: They also provide information at any desired level of details and precision. Including data in tables rather than text frequently makes it possible to reduce the length of the text. - Type or print each table with double spacing on a separate sheet of paper. - Number tables consecutively in the order of their first citation in the text. - Supply a brief title for each. - Place explanatory matter in footnotes, not in the heading. - Explain all nonstandard abbreviations in footnotes. - Identify statistical measures of variations, such as standard deviation and standard error of the mean. 11. Figures - Figures should be submitted in JPEG or TIFF format with a minimum of 150 DPI in resolution. - Colored data if requested by author is chargeable. - If a figure has been published previously, acknowledge the original source and submit written permission from the copyrights holder to produce the figure. Abbreviations and symbols: - Use only standard abbreviations. - Avoid abbreviations in the title of the manuscript. - The spelled-out abbreviations followed by the abbreviation in parenthesis should be used in first mention.
