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Transcript
Jieli Li 12/29/05 Chief Complaint Pain and difficulty on swallowing HPI 54 y/o AAM with hx of syphillis, htn, OSA and Langerhans Cell Sarcoma with spinal cord compression s/p steroids and XRT now c/o pain and difficulty upon swallowing. Pt was originally admitted on 11/18 to MICU for spinal chord compression, treated with decadron (11/18 to 12/05) and transferred to GMED on 11/22, now has completed 2 full wks of palliative XRT (11/23-12/7) to the area of T9-12 on TCU. HPI cont. Pt noticed that “food was getting stuck”, soon after that he developed a burning/spasm-like pain in his throat when swallowing. Liquid or solid food makes no difference to him. Pt was started on viscous lidocaine without much improvement. + constipation, denies diarrhea, hematochezia, melena, hematemesis, SOB. Per pt he was tested at outside facility for HIV within the last 6 months and was negative. He reports hx of syphillis > 10 yrs ago s/p treatment. PMH Langerhans Cell Sarcoma with spinal compression s/p decadron and palliative XRT Syphillis Htn Erectile Dysfunction OSA Medications Omeprazole 20 po bid Lidocaine viscous 20 q3 prn swish and spit Dilaudid 2mg q3 prn Cyclobenzaprine 10 tid prn back spasms Albuterol 2 puffs qid Es-Maalox prn Docusate Senna 2 tabs qhs prn History cont. All: SH: Codeine dizziness Denies hx of etoh, tobacco and illicit drug use FH: NC Physical Exam VS: 97.6, 109/61, 83, 18, 7/10 pain Gen: NAD, AAO x 4, slim AAM sitting in bed, speaks with a faint voice Skin: no rash HEENT: PERRLA, o/p clear, no oral ulcers/lesions, no thrush, no erythema of posterior pharynx or uvula Neck: supple, no LAD Heart: rrr, s1s2, no murmurs Physical Exam cont. Lungs: cta bilaterally, no wheezes Abd: soft, mild epigastric tenderness, nondistended, na bs, no HSM Ext: no edema/cellulitis/clubbing Neuro: CN II-XII grossly intact, sensory and motor function intact, DTR 2/2 Laboratory 12.5 2.3 116 36.2 MCV 92 69% neutrophils, 15% lymphs, 14% monos, 1% eosinophils Anion gap panel normal, Cr 1.0 EGD (12/14/05) There are multiple ulcers in the distal esophagus with a large linear line of ulcers tracking up the mid esophagus. Bx and brushing done. The stomach and duodenum were normal. Follow up ID was consulted to decide whether emperic antiviral tx is advisable while awaiting bx/viral cx results to return Ddx included XRT-induced esophagitis, HSV and CMV. Time course and location of the ulcers were suspicious for radiation induced ulcers. Since pt’s pain symptoms were already improving on its own without any specific tx by the time of the ID consultation, no empiric antiviral tx was recommended. Pt’s symptoms resolved on its own 1.5 wks later. Bx results came back negative for HSV and CMV. Overview Odynophagia = painful swallowing Suggests disruption of the esophageal mucosa Any inflammatory process involving the mucosa of the oropharynx or esophagus or its muscle may cause odynophagia Odynophagia is a common symptom of pill-induced esophagitis or infection of the esophagus A muscle spasm may also lead to muscle pain odynophagia Differential Dx of Odynophagia Pill esophagitis Infection Crohn’s involvement of the esophagus (uncommon) Reflux esophagitis (usually not acute) Caustic ingestion Radiation esophagitis Ulcerated neoplasm (usually not acute) Differential Dx of Odynophagia in AIDS patients Candidiasis Herpes simplex CMV Idiopathic HIV ulcers GERD Pill-induced Differential Dx of Dysphagia Extrinsic pressure on the esophagus Thyromegaly, left atrial enlargement Aortic arch aneurysm Zenker’s diverticulum Cervical lymphadenopathy Anomalous right subclavian artery Cephalad extension of gastric cancer Intrinsic narrowing of the esophageal lumen Esophageal tumors Esophageal strictures Disorders of esophageal motility Achalasia Esophageal spasm scleroderma Infectious Esophagitis Bacteria rarely cause primary esophageal infection, although secondary involvement by direct extension from the lung is possible Two most common forms of infectious esophagitis: Candida HSV Other viruses and fungi can cause esophagitis, but usually associated with immunosuppression CMV HIV Candida Esophagitis The most common form of infectious esophagitis Predisposing conditions: DM Abx therapy Immunocompromise Alcoholism Malnutrition Advanced age Occasionally seen in otherwise healthy individuals Presentation usually involves odynophagia, dysphagia, chest pain or upper GI bleeding Diagnosis of Candida Esophagitis Esophagogram EGD Irregular granular or even cobblestone or “shaggy” appearance 25% will have a normal barium esophagogram Required to make the diagnosis Small raised whitish plaques Underlying mucosa is erythematous and friable Biopsy or brush cytology Pseudohyphae Candidiasis on EGD Complications of Esophageal Candidiasis Ulceration and hemorrhage Mycetoma (fungus ball) Formed by necrotic mucosal debris Causes obstruction Strictures Perforation Fistulas Tracheobronchial Aortoesophageal Treatment of Esophageal Candidiasis Oral nystatin Ketoconazole or fluconazole for more extensive involvement or if pt is immunocompromized Amphotericin B if evidence of systemic spread Herpes Simplex Esophagitis Second most common form of infectious esophagitis Presentation is similar to candida esophagitis Esophageal symptoms may be preceded by viral URI type symptoms Herpetic mouth or skin lesions may also develop Usually found in immunocompromized pts, but also sporadically seen in healthy young adults Diagnosis of Herpes Esophagitis Esophagogram Multiple, small, superficial ulcers in the upper or mid esophagus Severe herpes esophagitis may produce extensive ulceration and plaque formation, mimicking the appearance of Candida esophagitis EGD with biopsy and brush cytology are required to confirm the diagnosis Brush cytology Epithelial cells at the edge of the ulcers are characterized by multinucleation, ground-glass nuclei and pathognomonic eosinophilic “Cowdry’s Type A” intranuclear inclusion bodies Herpes Esophagitis on EGD Cowdry A Intranuclear Inclusion Body in a herpetic ulcer Treatment of Herpes Esophagitis Self-limiting disease in immunocompetent individuals, so symptomatic tx only Viscous Xylocaine and PPI In severely immunocompromised pts IV acyclovir CMV Esophagitis Asymptomatic CMV infection is common worldwide The first clinical case of CMV esophagitis was reported in 1985 Unlike herpes esophagitis, CMV esophagitis almost never occurs in immunocompetent patients Vast majority of affected individuals are found to have AIDS Evidence of CMV infection may be present in other organs such as the retina, liver, and colon Occasionally, odynophagia may become so severe pt develop sitophobia (fear of eating) and require TPN Diagnosisof CMV Esophagitis Esophagogram Typically shows 1 or more giant and relatively flat ulcers, sometimes with associated satellite ulcers EGD with biopsy and brush cytology are required to confirm the diagnosis Brush Biopsy Infected cells contain eccentrically placed intranuclear inclusion bodies with surrounding halos mainly found near the base of the ulcers CMV Esophagitis under Microscopy Treatment of CMV Esophagitis Antiviral agents Ganciclovir Bone marrow toxicity Foscarnet Renal toxicity HIV Esophagitis Believed to be caused by HIV Electron microscopy confirm presence of HIVlike viral particles in these lesions Most pts are found to have chronic AIDS with CD4 counts < 100 HIV esophagitis can form giant esophaageal ulcers indistinguishable from CMV esophagitis Account for 40% of all esophageal ulcers in AIDS pts HIV Esophagitis continued. Diagnosis EGD and biopsy are again required to distinguish it from CMV esophagitis Treatment Oral steroids Esophagitis Associated with Immune-Mediated Disease Crohn’s disease Behçet’s syndrome Pemphigoid Pemphigus Epidermolysis bullosa Sarcoidosis Eosinophilic gastroenteritis Chronic graft-versus-host disease after bone marrow transplantation Generalized epithelial desquamation of the upper and middle esophagus, sometimes with ring-like narrowings A nonspecific esophageal motor disorder may also develop resulting in superimposed reflux esophagitis Acid/Alkali Ingestion Acid ingestion Superficial coagulation necrosis and eschar formation immediate chest pain and odynophagia Oral burns may produce local pain and drooling Respiratory symptoms (stridor, dyspnea and hoarseness) if the airway is contaminated Alkali ingestion Tends to be more injurious to the esophageal mucosa Liquefaction necrosis Thermal burns Acid/Alkali Ingestion cont. Symptoms alone do not permit accurate prediction of the presence or absence of esophageal injury Early diagnostic endoscopy should be considered (but not if there is evidence of esophageal perforation) Adequate airway is imperitive NPO and IVF Empiric tx involves abx and corticosteroids, but no good evidence documenting the efficacy Survivors tend to develop strictures because of collagen deposition during healing. Often requires repeated esophgeal dilation Lye-Induced Injury Lye-induced injury increases the risk of squamous cell cancer of esophagus Typically there is a 30- to 50-year lag time Any pt with previous lye inury and new esophageal symptoms should be promptly investigated However periodic endoscopic surveillance is not indicated Pill-Induced Esophagitis Common culprits Antibiotics NSAIDS Tetracyclines (particularly doxycycline) Highest number of reported cases is with ASA Others KCl Quinidine preparations Iron compounds alendronate Pill-Induced Esophagitis cont. Pts typically take meds with small amount of water and then immediately go to bed, then wake up hrs later with severe retrosternal CP and odynophagia Typical lesion shows a small punched out ulcer in a limited area that was conceivably in contact with a high concentration of medication released from a dissolving pill Usually ulceration is superficial and heals in weeks; Rarely, can see deep esophageal ulcer with perforation Late stricture formation may occur Pts with esophageal motility disorders are particularly prone Radiation-Induced Esophagitis Seen in up to 80% of pts receiving XRT to the chest Use of cytotoxic chemo has an additive effect Typically chest pain, dysphagia and odynophagia occur shortly after the initiation of therapy Late stricture formation is a common complication Usually self-limited, treatment is symptomatic