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AMERICAN JOURNAL OF EMERGENCY MEDICINE. Volume 18, Number 5 • September 2000

diflunisal. Knowledge of this interference is important when salicylate toxicity or diflunisal overdose is suspected. PAULA. Szucs, MD

Department of Emergency Medicine Morristown Memorial Hospital Morristown, NJ RICHARD D. SHIH, MD

Department of Emergency Medicine Morristown Memorial Hospital Morristown, NJ New Jersey Poison Center Newark Beth Israel Medical Center Newark, NJ STEVEN M. MARCUS, MD

K. LEFF P.DELGADO

New Jersey Poison Center Newark Beth Israel Medical Center Newark, NJ

References 1. Litovitz TL, Smilkstein M, Felberg L, et al: 1996 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 1997;15:447-500 2. Almond G, Clark RF: Nonsteroidal Anti-inflammatory Agents, in Tintinalli JE, Ruiz E, Krome RL (eds): Emergency Medicine: A Comprehensive Study Guide. New York, NY McGraw-Hili, 1996, pp 792-796 3. Tocco DJ, Breault Go, Zacchei AG, et al: Physiological disposition and metabolism of 5-(2',4'-difluorophenyl) salicylic acid, a new salicylate. Drug Metab Dispos 1975;3:453-466 4. Sarma L, Wang SH, DeliaFera S: Diflunisal significantly interferes with salicylate measurements by FPIA-TDx® and UV-VIS aca method. Clin Chem 1985;31:1922-1923 5. Dalrymple RW, Stearns FM: Diflunisal interferes with determination of salicylate by the Trinder, Abbott TDx® and Dupont aca® method. Clin Chem 1986;32:230 6. Duffens KR, Smilkstein MJ, Bessen HA, et al: Falsely elevated salicylate levels due to diflunisal overdose. J Emerg Med 1987;5:499503V

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AROUSED TO ATRIAL FIBRILLATION? To the Editor:-Viagra (sildenafil), a phosphodiesterase inhibitor used for erectile dysfunction,I,2 is associated with profound hypotension and myocardial ischemia when combined with nitrates. 3 Because affected patients tend to have cardiovascular disease and use multiple medications, it is difficult to define the exact cause for their adverse events. The sexual activity, sildenafil, drug interactions, or the patient's underlying cardiovascular disease can all be implicated. We describe a young healthy patient who developed atrial fibrillation while taking sildenafil for his impotence. A 35-year-old man presented to the hospital, complaining of persistent palpitations that began I hour after ingesting a single 100 mg tablet of sildenafil. The patient interrupted coitus because he felt lightheaded and had palpitations which were followed by a brief syncopal episode. He denied other symptoms or the use of ethanol, recreational drugs including inhaled nitrites, or prescription medicines. His medical history was only significant for erectile dysfunction, and he had used sildenafil previously without complication. Physical examination revealed an alert, anxious male whose vital

signs were normal except for an irregular heart rate ranging between 130 to 140 beats/minute. The cardiac examination revealed an irregularly irregular rhythm without any murmurs. The remainder of his physical examination was normal. An electrocardiogram showed atrial fibrillation at a rate of 114 beats/minute and was without ST segment or T wave abnormalities. Chest radiograph and routine laboratories including complete blood count, electrolytes, liver function tests, coagulation studies, urine toxicology, and cardiac enzymes revealed no abnormalities. Echocardiogram showed only mild tricuspid regurgitation. While in the emergency department, the patient was treated with diltiazem, 25 mg by intravenous bolus and was maintained on a continuous infusion for rate control. He failed chemical conversion twice with intravenous ibutilide, but converted spontaneously 2 days later. His follow-up examination was normal. The temporal relationship between the ingestion of sildenafil and new onset atrial fibrillation in a patient with no known risk factors for atrial fibrillation suggests that sildenafil was causally related to the arrhythmia. We can only assume that the atrial fibrillation occurred during intercourse when the patient developed palpitations and an eventual syncopal episode. We postulate that sildenafil may have caused profound hypotension leading to syncope and reflex tachycardia through catecholamine excess. There have been reports of sildenafil associated myocardial infarction4 and other cardiovascular events. However, we believe that this is the first documented report of sildenafil-associated atrial fibrillation. IN-HE! HAHN, MD ROBERT S. HOFFMAN, MD

New York City Poison Center New York, NY

References 1, Pfizer, Viagra (sildenafil citrate) drug insert, 1998 revised 2, Goldstein I, Lue TF, Padma-Nathan H, et al: Oral sildenafil in the treatment of erectile dysfunction. N Engl J Med 1998;338:1397-404 3. Summary of Reports of Death in Viagra Users Received from Marketing (late March) through mid-November 1998, accessed November 1998, http:www.fda.gov/cder/foi/labeI/1998/ViagralabeI2.pdf 4. Feenstra J, van Drie-Pierik RJHM, Lacle CF, et al: Acute myocardial infarction associated with sildenafil. Lancet 1998;352:957958

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ANAPHYLAXIS FROM INTRAVENOUS THIAMINE-LONG FORGOTTEN? To the Editor:-Anaphylactic reactions to administration of thiamine hydrochloride, although very uncommon can be life threatening. Routine administration of thiamine is commonly practiced by emergency physicians and internists alike while dealing with chronic alcoholics, malnourished and other patients at risk for thiamine deficiency. 1 We present this case of anaphylaxis to intravenous administration of thiamine, a reminder that despite its enormous safety profile, an assumption that thiamine is completely innocuous cannot be made. A 51-year-old woman with history of diabetes mellitus, chronic alcoholism and anxiety disorder was found by the EMS in an acute confusional state. Her home medications included insulin and lorazepam. The family mentioned an allergy to penicillin. Vital signs were: pulse rate 100 beats/min, blood pressure 118/70 mmHg, respiratory rate 20 breaths/min. Twenty-five g of 50% dextrose and 100 mg of thiamine hydrochloride were administered by the EMS intravenously. On arrival at the hospital 20 minutes

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later, she was found to be deeply cyanosed with shallow labored breathing at 28 breathslmin, blood pressure was 1661128 mmHg, pulse rate 118 beatslmin with reduced air entry on chest examination. She was immediately started on mechanical ventilation for impending respiratory arrest. Laboratory values were remarkable for respiratory and metabolic acidosis and serum alcohol level of 124 mg/dL. The next morning the patient was communicative and oriented. She was successfully extubated, vital signs and blood gas that followed were normal. Two and a half hours later, the routine infusion of thiamine hydrochloride was started through a cubital vein. Within moments the patient complained of shortness of breath, warmth and tightness of throat. Heart rate was 145 beatslmin, blood pressure 83/40 mmHg, air entry was diminished, oxygen saturation dropped to 70% with the development of central cyanosis requiring reintubation and resuscitation. She was successfully extubated the next day and discharged 2 days later with an advice to avoid thiamine. When asked if she had had a similar experience before, the patient reported of a similar episode of "intolerance to alcohol" a few months earlier. Review of old records revealed that indeed the patient had visited the ED 5 months earlier after a binge of alcohol. She had complained of nausea and abdominal pain after an intramuscular dose of thiamine. Aggressive fluid resuscitation had been performed for persistent hypotension that developed (blood pressure of 86/44 mmHg). Thiamine hydrochloride is routinely administered to patients with suspected Wernicke's encephalopathy or malnourished states like malabsorbtion, beri-beri, cancer, acquired immunodeficiency syndrome, and chronic alcohol abuse. 1 Systemic reactions to parenteral thiamine are rare but deaths have been reported. 2 Two major types of adverse effects occur. The first, mimics hyperthyroidism in patients on chronic thiamine therapy and resolves on discontinuation of the drug. 1.3 The other are anaphylactic reactions which can be life threatening,1.5 usually occur after multiple parenteral dosages and are IgE-mediated. 4 Most cases of anaphylaxis to thiamine were reported when the vitamin was first introduced for routine use 6 decades ago. Testing patients for sensitivity before administration seems impractical given the rarity of this complication, however physicians need to be aware of this entity to ensure prompt recognition and treatment of this condition. 5 Indiscriminate use of thiamine should also be avoided. SHILPA JOHRI, MD SMITHA SHETTY, MD ANITA SONI, MD SURESH KUMAR, MD

Department of Medicine Lincoln Medical Center Bronx, NY

References 1. Stephen JM, Grant R, Yeh CS: Anaphylaxis from administration of intravenous thiamine. Am J Em Med Jan 1992;10:61-63 2. Leung R, Puy R, Czarny D: Thiamine anaphylaxis. Med J Aus Sep 1993; 159:355 3. Van Haecke P, Ramaekers D, Vanderwegen L, et al: Thiamine induced anaphylactic shock. Am J Em Med May 1995; 13:371-2 4. Fernandez M, Barcelo M, Munoz C: Anaphylaxis to thiamine (Vitamin B1). Allergy Sep 1997;52:958-59 5. Wrenn KD, Siovis CM: Is intravenous thiamine safe? Am J Em Med 1992;10:165

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NOT JUST ANOTHER CASE OF HEMOPTYSIS To the Editor:-The pathogenesis of aortic pseudoaneurysms is unclear and probably multifactorial, stemming from a variety of mechanisms including infection, trauma, and surgical procedures. History and physical examination are often unrevealing. The appearance of a pseudoaneurysm is usually an unsuspected finding on a routine chest radiograph. The picture can be subtle or confusing and may be mistaken for more common disease processes, such as hilar adenopathy, pneumonia, atherosclerotic aneurysm, or neoplasia. Aortic pseudoaneurysms are prone to rupture after the original insult which results in an almost universally fatal occurrence once recognized. It should be repaired surgically soon after diagnosis. We present a case and discuss the diagnosis and treatment for the purpose of increasing its awareness among the medical community. Its incidence will surely increase as more surgical procedures involving the coronary arteries, aortic valve, and thoracic aorta are performed than previously. A 76-year-old man presented to the emergency department (ED) with a chief complaint of intermittent hemoptysis, fever, shortness of breath, and generalized weakness over a course of 3 days. The hemoptysis was described by his wife as bright red, "as if it was from an artery." The patient admitted to a 25 Ib weight loss over the past 2 months and denied any history of nightsweats or risk factors for retroviral disease. He had been a heavy cigarette smoker for many years but stopped 30 years prior. Past medical history include diet-controlled diabetes mellitus and benign prostatic hypertrophy. No history of trauma was ellicited from the patient. Physical examination revealed a cachetic-looking man, alert and oriented, and in no cardiorespiratory distress. Vital signs were: temperature (oral), 98.6 F; pulse, 114 beatslmin, respiration, 18 breathslmin, blood pressure, 128/69 mmHg, and room air pulse oximetry of 97%. Pertinents on physical examination include crepitus and rhonchi left lung field greater than right, no cervical or supraclavicular lymphadenopathy. There were no abnormalities of his skin or extremities. Rectal examination was negative for occult blood. Electrocardiogram showed a sinus tachycardia of 114 beatslmin with no ischemia nor conduction defects. The chest radiograph was remarkable for a large mass in the left upper lung field (Figure 1). Laboratory data revealed a white blood cell count of 32,500 with a 80% neutrophils, hemaglobin 9.4, hematocrit 29.6, platelets 464,000. Chemistry, including liver function, and coagulation profile were normal. First sputum smear revealed mixed gram-positive/negative organisms with epithelial cells and no acid fast bacteria. Subsequent sputum smears were the same. The patient was admitted to the hospital with a diagnosis of left upper lung mass most probably caused by malignancy and associated postobstructive pneumonia. He was started on intravenous cefuroxime and erythromycin. The following day, he underwent bronchoscopy which revealed severe metaplasia from the biopsy and complete extrinsic compression of the posterior apical segment of the left upper lobe. Transesophageal echocardiography was performed that showed a large descending thoracic aortic aneurysm with evidence of pseudoaneurysm formation starting at 25cm level and extending down to the 35cm level. The pseudoaneurysm measured approximately 7.5cm in the widest dimension with evidence of layered thrombus around the margins. Subsequently, a computerized tomography of the chest was performed that revealed a large leaking aortic pseudoaneurym involving the distal aortic arch and proximal descending aorta (Figure 2). The patient was transferred to the Cardiothoracic Surgery Unit of our parent hospital where he underwent surgery to repair the lesion. Intraoperatively, there was significant amount of purulent drainage exuding from the lung and the large pseudoaneurym. The lesion was repaired without incident. However, during his postoperative