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European Review for Medical and Pharmacological Sciences 2011; 15: 211-213 Effect of anesthesia in a patient with pre-existing anisocoria P. ACETO, V. PERILLI, F. VITALE, L. SOLLAZZI Department of Anaesthesiology and Intensive Care, Catholic University of the Sacred Heart, Rome (Italy) Abstract. – In this case report, we describe an accentuation of a pre-existing anisocoria shortly after tracheal intubation in a patient undergoing thyroidectomy. A 45-yr-old female patient with unequal pupillary diameter (right 2 mm > than left) and decreased light reflex in the right eye – due to a previous eye trauma – was scheduled for thyroidectomy because of multinodular goiter. Anesthesia was induced with propofol 2,5 mg/kg, fentanyl 3 mcg/kg and cisatracurium 0.15 mcg/kg. Immediately after tracheal intubation, examination of the right eye revealed a markedly dilated pupil (8 mm) which was nonreactive to direct and consensual light reflex. The left pupil was 2 mm, and normally reactive to light. An increase in heart rate was also registered (> 20% of baseline) with spontaneous return to baseline within 2 minutes. The right pupil returned to preoperative size within approximately one hour after awakening. From this case report, it emerges that a preexisting anisocoria may be exacerbated during anesthesia probably due to incomplete abolition of response to painful stimulus, such as tracheal intubation, provided by anesthetic drugs in the affected eye. The main contributing factor for accentuation of anisocoria could be sympathetic dominance in the pupil with pre-existing mechanical interruption in compensatory parasympathetic mechanisms. Key Words: Finding of anisocoria during anaesthesia is a disturbing and unusual sign and may indicate serious neurological conditions. Previous reports have documented unilateral mydriasis occurring as a result of accidental direct or indirect exposure of papillary muscles to mydriatic (alphaadrenergic or anticholinergic) agents before or during surgery3-7. Sometimes, ciliary ganglion may be unintentionally anaesthetized by the spread of local anaesthetics8,9. Other possible causes may be mechanical ones, such as eye trauma during intubation or dislocation of an unstable cervical spine resulting in Horner’s syndrome, or asymmetric impaired venous return from head and neck resulting in anisocoria with concurrent exophthalmos2. In case of hypertension after intubation, an acute intracranial hemorrhagic event (e.g. undiagnosed intracranial aneurysm) should be suspected3. Evidence supporting effects of anaesthetic drugs has been discussed10, but cases of exacerbated pre-existing unilateral mydriasis in patients undergoing general anaesthesia have never been described. In the present case report, we describe an accentuation of a pre-existing anisocoria shortly after tracheal intubation in a patient undergoing thyroidectomy. Anaesthesia, Anisocoria, Sympathetic system. Introduction Pupillary function is controlled by a balance of sympathetic (dilator) and parasympathetic (constrictor) neural pathways. Pharmacologic or mechanical disruption of these pathways may result in anisocoria1,2. A variety of potential causes for anisocoria exists, ranging from normal to life threatening variation1. Case Report An ASA I, 65 kg, 168 cm, 45-yr-old female patient was scheduled for thyroidectomy because of multinodular goiter. When she was 20 years old, she had an eye trauma resulting in the damage of iris sphincter muscle. Preoperative neurologic examination revealed unequal pupillary diameter (right 2 mm > than left) and decreased light reflex in the affected eye with normal visual function. The vital signs and results of laboratory tests were normal. Corresponding Author: Paola Aceto, MD; e-mail: [email protected] 211 P. Aceto, V. Perilli, F. Vitale, L. Sollazzi Patient did not receive anaesthetic premedication. At the patient’s arrival in the operating room, electrocardiogram, peripheral oxygen saturation, non invasive blood pressure, expired carbon dioxide and bispectral index were monitored. Anaesthesia was induced with propofol 2,5 mg/kg and fentanyl 3 mcg/kg. Cisatracurium 0.15 mcg/kg was administered to facilitate tracheal intubation. Immediately after tracheal intubation, examination of the right eye revealed a markedly dilated pupil (8 mm) which was non-reactive to direct and consensual light reflex. The left pupil was 2 mm, and normally reactive to light. Neither eye was oedematous or showed signs of pressure or traumatic injury. We also registered an increase in heart rate (>20% of baseline) with spontaneous return to baseline within 2 minutes. Systemic blood pressure was preserved. We felt that surgery could proceed because of her history of anisocoria. Desflurane in an air-oxygen mixture was used for maintenance of anaesthesia. No supplementary doses of fentanyl or cisatracurium were required. Ventilation was adjusted to maintain normocapnia (end-Tidal partial pressure of carbon dioxide range, 35-40 mmHg). At the end of the procedure, which lasted 50 minutes, neuromuscular blockade was reversed with neostigmine (2.5 mg) and atropine (1 mg). After establishing recover of a spontaneous diaphragmatic breathing with adequate Tidal volume, the tracheal tube was removed. The right pupil returned to preoperative size within approximately one hour after awakening. The 24hr postoperative course was uneventful. Discussion In the present case, we find an exacerbation of preexisting anisocoria in a patient undergoing general anaesthesia. In the first instance, we theorized that this phenomenon was due to the parasympathetic dominance caused by sympathicolysis as a result of concomitant use of propofol and fentanyl. However, the parasympathetic-dominant status would induce a rapid constriction in the normal eye, but much slower constriction in the tonic pupil, resulting in marked differences in the two pupillary diameters. In our patient, we did not find a constric212 tion in the normal eye but only an evident accentuation of anisocoria in the affected eye which appeared immediately after intubation and was associated with a brief increase in heart rate. This reaction is suggestive of a sympathetic dominance due to a disruption of the sympathetic-parasympathetic balance and may reflect an abnormal response to a painful stimulus, such as tracheal intubation, leading to suppose that administered anaesthetic drugs provided unaccomplished sympathicolysis. Sympathetic block induced by thoracic epidural in presence of anaesthetics such as propofol and sevoflurane was previously pointed out to determine anisocoria in a patient without preoperative papillary abnormalities10. The Authors concluded that the parasympatheticdominant status was the main contributing factor for the Adie pupil to appear. In fact, anisocoria associated with an Adie pupil is believed to originate from a peripheral mechanism involving parasympathetic postganglionic fibers, arising by a damaged ciliary ganglion that innervate the iris sphincter muscle, responsible for pupillary constriction. The accentuation of anisocoria in our patient probably resulted from just the opposite process. As a possible proof of sympathetic status dominance, the iris dilator muscle – responsible for pupillary dilation and receiving sympathetic input from the superior cervical sympathetic ganglion via the long ciliary nerve of the trigeminal nerve’s ophthalmic branch – was not or was weakly affected by anaesthetic drugs. The role of painful stimulus, such as tracheal intubation, remains undetermined. It must be taken into account that, when anisocoria occurs in patients under general anaesthesia, the cause can be difficult to diagnose as convergence response and neurological symptoms cannot be confirmed without a wakeup test3. The pilocarpine test, which is effective even in a vegetative state, also appears to be useful to rapidly differentiate neurogenic from phenylephrine-induced mydriasis11. In the patient of this case report, neither phenylephrine or wake-up test were performed because of her known medical history of unilateral dilated pupil due to a lesion of iris sphincter muscle caused by a previous direct eye trauma. In the absence of the patient’s history of anisocoria, we believe that intraoperative wake-up test or the more rapid pilocarpine test would have been indicated. Effect of anesthesia in a patient with pre-existing anisocoria From literature, it emerges that unilateral mydriasis under anaesthesia may reflect alterations in either sympathetic or parasympathetic autonomic tone, triggered by either a disturbance in cranial nerve function or a pharmacological alteration in autonomic nerve transmission. Anisocoria during anaesthesia has previously resulted from accidental direct or indirect eye exposure to phenylephrine4,5, submucosal infiltration with epinephrine6 or lidocaine plus epinephrine 8 or as a result of cocaine spread (nasociliary ganglion block)9. Anisocoria has also been described after airway topical anaesthesia with lidocaine and phenylephrine provided by an oxygen driven face mask nebulizer 3 . Anisocoria may be also caused by impaired ocular blood flow. In a child showing anisocoria during renal transplantation probably due to a retinal hypoperfusion, mydriasis slowly developed on both eyes, but was more pronounced for the left pupil and was associated with concurrent bilateral congiuntival chemosis. Evidence of impaired ocular blood flow was obtained by cranial ultrasound. The pupil size returned to normal with administration of norepinephrine12. Therefore, the assessment of perioperative unilateral mydriasis should always include consideration of accidental exposure of mydriatic agents before or during surgery. As neurologic assessment by physical examination is often difficult under general anaesthesia, in absence of any history of anisocoria or certain causes of anisocoria, the diagnosis of any intracranial pathology to rapidly exclude life-threatening neurologic events requires a cranial computed tomography scan. In conclusion, from this case report, it emerges that a pre-existing anisocoria may be exacerbated probably because of the uncompleted abolition of response to painful stimulus, such as tracheal intubation, provided by anaesthetic drugs in the affected eye. The main contributing factor could be sympathetic dominance in a pupil with pre-existing mechanical interruption in compensatory parasympathetic mechanisms. –––––––––––––––––––– Acknowledgements We would like to acknowledge Jacqueline Melvin for her careful revision of the manuscript language. References 1) T HOMPSON HS, M ILLER NR. Disorder of Pupillary Function, Accommodation, and Lacrimation. In: Miller NR, Newman NJ, eds. Walsh & Hoyt’s, Clinical Neuro-Ophtlalmology. Williams & Wilkins; 1997: pp. 961-1040. 2) MARTIN, TIMOTHY J. Horner's syndrome, PseudoHorner's syndrome, and simple anisocoria. Curr Neurol Neurosci Rep 2007; 7: 397-406. 3) PRIELIPP RC. Unilateral mydriasis after induction of anaesthesia. Can J Anaesth 1994; 41: 140-143. 4) RUBIN MM, SADOFF RS, COZZI GM. Postoperative unilateral mydriasis due to phenylephrine: a case report. J Oral Maxillofac Surg 1990; 48: 621-623. 5) STIRT JA, SHUPTRINE JR, STERNICK CS, KORBON GA. Anisocoria after anaesthesia. Can J Anaesth 1985; 32: 422-424. 6) D'SOUZA MG, HADZIC A, WIDER T. Unilateral mydriasis after nasal reconstruction surgery. Can J Anaesth 2000; 47: 1119-1121. 7) WU SH, HUANG SH, LU IC, LEE SS, CHANG YL, CHU KS. Unilateral fixed dilated pupil during plastic surgery–a case report. Acta Anaesthesiol Taiwan 2007; 45: 175-179. 8) HOLMGREEN WC, BADDOUR HM, TILSON HB. Unilateral mydriasis during general anaesthesia. J Oral Surg 1979; 37: 740-742. 9) STEWART D, SIMPSON GT, NADER ND. Postoperative anisocoria in a patient undergoing endoscopic sinus surgery. Reg Anaesth Pain Med 1999; 24: 467-469. 10) KOBAYASHI M, TAKENAMI T, KIMOTSUKI H, MUKUNO K, HOKA S. Adie syndrome associated with general anaesthesia. Can J Anaesth 2008; 55: 130-131. 11) SITZMAN BT, BOGDONOFF DL, BLECK TP, SPIEKERMANN BF, CHANG CW. Postoperative anisocoria: neurogenic or phenylephrine induced? A rapid diagnostic test. Anesth Analg 1996; 83: 633-635. 12) R EMPF C, H ELMKE K, G OTTSCHALK A, FAROKHZAD F, BURMEISTER MA. Intraoperative anisocoria in a child during renal transplantation. Acta Anaesthesiol Scand 2008; 52: 307-309. 213