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Pharyngitis followed by hypoxia and sepsis: Lemierre syndrome
320
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 4 • April 2001
2. Coates W, Jehle D, Cottington E: Trauma and full moon: A waning theory. Ann Emerg Med 1989;18:763-5 3. Nijsten MW, Willemsen SE: Accidents a matter of chance? Ned Tijdschr Geneeskd 1991 ;135:2421-4 4. Laverty WH, Kelly IW: Cyclical calendar and lunar patterns in automobile property accidents and injury accidents. Percept Mot Skills 1998;86:299-302 5. Morris RW: Circadian and circa annual rhythms of emergency room drug-overdose admissions. Prog Clin Biol Res 1987;227:451-7 6. Bfichthold-Stfiubli: Lexikon des deutschen Aberglaubens, Berlin, 1920 7. Unterreitmeier H: German astrology in the late middle ages. Archiv for Kulturgeschichte 1983;65:21-41
ATTRIBUTION OF CAUSALITY IN ADVERSE DRUG REACTIONS To the Editor:--We are concerned that the cardiopulmonary arrest in the patient described by Johri and colleagues could be certainly attributed to haloperidol, as proposed by the authors. 1 The temporal association with the last dose of haloperidol was interpreted as supporting the suspect that the 2 events were directly linked, but there is no much more than this in favor of the hypothesis. The previous medical history is almost vague and rhabdomyolysis or malignant hyperthermia is a more likely explanation than acute cardiac toxicity for the serious reactions to neuroleptic agents that occurred in the past. The case record does not convincingly rule out the possibility that the administration of haloperidol fortuitously coincided with the reported event so as to produce an apparent cause-effect relationship. Alternative explanations have not been sought. The patient was given diphenhydramine in addition to haloperidol. If a life-threatening arrythmia was the cause of the cardiopulmonary arrest it is important to remind that also first-generation Hi-blockers, including diphenhydramine, are potential triggers of malignant arrythmias. 2 4 However, the corrected QT interval measured after successful cardiopulmonary resuscitation was normal and this finding is not fully consistent with cardiac toxicity by either haloperidol or diphenhydramine. This patient probably had an increased risk of cardiopulmonary arrest and sudden death irrespectively of the exposure to neuroleptic agents or other drugs. The finding of cardiomegaly and bibasilar atelectasis on the chest radiograph performed at admission, before haloperidol or diphenhydramine was given, suggests indeed an underlying heart disease that was not previously recognized. These discrepancies are relevant, although the article merits consideration as it raises the important matter of causality attribution when reporting adverse drug reactions in the field of emergency medicine. Numerous schemes for classification of causality have been proposed and are used in different countries. 5 All of them emphasize that causality can be attributed only when there is a plausible time relation to administration of the suspected agent and the adverse reaction cannot be explained by concurrent diseases or other drugs or chemicals. This is not the case of the patient described by Johri and colleagues. We have assessed the likelihood that the event reported in the article was indeed drug-related using the Naranjo Adverse Drug Reaction Probability Scale, a validated and simple method for estimating the probability of adverse drug reactions. 6 We calculated a probability score 3 for haloperidol and 1 for diphenydramine, with scores > 9 indicating the event as highly probable, 5 to 8 probable, 1 to 4 possible, and 0 doubtful. The likelihood of a causal relation with haloperidol or diphenhydramine was very low for either drug, with a slightly higher but not significant probability score favoring haloperidol. The conclusions reached in the article appear there-
Copyright @ 2001 by W.B. Saunders Company 0735-6757/01/1904-0019535.00/0 doi:l 0.1053/ajem.2001.24466
fore to be incorrect as objective evidence for a proper attribution of causality to haloperidol is very scant. Johri and colleagues do not prove other than a temporal association between administration of haloperidol, and diphenhydramine as well, and the cardiopulmonary arrest experienced by the patient. Interpretation of causal relation needs to be rigorously adjusted for the presence of potential confounding factors. If we analyze data using objective and quantitative tools for estimating the cause and effect relation, we can reasonably infer that many other similar reports are flawed by a substantial methodological inconsistency. Stringent criteria should be used and great caution advised for meaningful conclusions to be drawn when attributing to a specific agent causality of adverse effects, particularly in case reports of single patients. GIUSEPPE FAMULARO,MD PHD
Department of Medical Sciences San Camillo Hospital Rome, Italy CLAUOIODE S]MONE,MD Department of Experimental Medicine University of L. Aquila, Aquila, Italy
References 1. Johri J, Rashid H, Daniel PJ, et al: Cardiopulmonary arrest secondary to haloperidol. Am J Emerg Med 2000;18:839 2. Zareba W, Moss AJ, Rosero SZ, et al: Electrocardiographic findings in patients with diphenydramine overdose. Am J Cardiol 1997;80:1168-1173 3. Wang WX, Ebert SN, Liu XK, et al: "Conventional" antihistamines slow cardiac repolarization in isolated perfused (Langendorff) feline hearts. J Cardiovasc Pharmacol 1998;32:123-128 4. Staffa JA, Jones JK, Gable CB, et al: Risk of selected serious cardiac events among new users of antihistamines. Clin Ther 1995; 17:1062-1077 5. Edwards IR, Aronson JK: Adverse drug reactions: definitions, diagnosis, and management. Lancet 2000;356:1255-1259 6. Naranjo CA, Busto U, Sellers EM, et al: A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981 ;30:239-245
PHARYNGITIS FOLLOWED BY HYPOXIA AND SEPSIS: LEMIERRE SYNDROME To the Editor:--Symptoms of pharyngitis are a frequent presenting complaint of emergency department (ED) patients. The majority of these cases are caused by viral pathogens. Thus, it is generally accepted that antibiotics are not warranted in most adult patients with sore throats. On the other hand, complications of withholding antibiotics, although infrequent, can lead to lifethreatening consequences. Lemierre syndrome is an anaerobic oropharyngeal infection that occurs in previously healthy patients, usually caused by Fusobacterium necroforum. The incidence of Fusobacterium infection declined dramatically in the 1950s with the emergence of penicillin. 1 Over time the organism has become increasingly resistant to penicillin, therefore clindamycin is now the therapeutic drug of choice? Today the mortality rate remains at about 15%. 3 We report a recent patient that we treated at our institution who presented with Lemierre syndrome. Five days before his ED visit, this previously healthy 20-yearold college student complained of dysphagia and odynophagia. Initially, the patient went to the infirmary at his college. He was advised to rest, increase liquids, and take nonsteroidal antiinflam-
Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1904-0020535.00/0 doi:l 0.1053/ajem.2001.24507
• CORRESPONDENCE
321
FIGURE 1. Chest CT showing multiple bilateral cavitary lesions suggestive of abscesses.
matory drags (NSAIDs). Over the next several days, the patient developed myalgia, vague abdominal pain, and anorexia. He denied having a fever, but experienced "shaking chills." The patient then began having moderate difficulty breathing, secondary to severe pleuritic chest pain. This provoked his visit to the ED. He denied HIV risk factors, alcohol, and illegal drug use. Physical examination was remarkable for a young, well-built, toxic appearing man in moderate respiratory distress. His vital signs were: blood pressure 107/48 mmHg, heart rate 118 beats/ min, respiratory rate 32 breaths/min, temperature 36.5°C (orally), and room air pulse oxygen saturation of 89%. The patient had icteric pupils, dry mucus membranes, erythematous inflamed tonsils without exudates, and anterior cervical lymphadenopathy, greater on the right. The chest examination revealed scattered tales bilaterally and point tenderness over the left lower anterior chest wall. His laboratory results were notable for a white blood cell count of 4.600/ram 3 with 24% bands, platelet count of 94,000/ mm 3, bilirubin of 3.8 mg/dl, LDH of 1,552 IU/L, D-dimer > 4.0 mcg/mL. The patient's chest x-ray film revealed a small right middle lobe infiltrate. A spiral chest computed tomography (CT) scan revealed multiple bilateral scattered "nodular consolidations" and small effusions. Echocardiogram was negative for vegetation. Blood cultures were obtained. The patient was admitted and started on heparin and azithromycin. During the ensuing days the patient's condition worsened. His antibiotics were changed multiple times. On the forth hospital day his blood cultures came back positive for gram-negative bacillus. Repeat chest CT showed multiple bilateral cavitary lesions (Fig 1). The right side of his neck became swollen. A neck CT was negative for abscess and thrombosis. The patient's condition continued to deteriorate and he was transferred to the medical intensive care unit. His neck swelling worsened and dentistry was consulted. Dentistry stated no apparent odontologic infection was seen. On the fifth hospital day his blood cultures isolated Fusobacterium necrophorum. On hospital day 7 a repeat neck CT showed thrombosis of his right internal jugular vein (Figs 2, 3). The patient's fever and hypoxia persisted and vascular surgery was consulted. He was taken to the operating room the following morning. The surgeons reported a "dense inflammatory process involving the entire carotid sheath. The jugular vein could not safely be dissected, and, therefore it was ligated at the neck." After surgery the patient's fever resolved. He was discharged on hospital day 14, but treated with IV clindamycin for an additional 2 weeks. The patient suffered no long-term sequela. The incidence of Lemierre syndrome was significantly higher in the preantibiotic era. The first known case may well be that of a "postanginal septicemia" reported in 1900 by Courmont and
FIGURE 2. CT of neck with contrast showing thrombosis of the right internal jugular vein. Cadde. 4 It was not until 1936 that Lemierre published a case series of 20 young patients with this disease. 5 Lemierre's syndrome is an anaerobic septicemia. It usually begins with an acute pharyngitis, followed by thrombosis of the internal jugular vein. From this point metastatic infection throughout the body occurs, most commonly affecting the lungs and joints. The majority of cases are caused by Fusobacterium necroforum, an anaerobic gram-negative normal inhabitant of the oral mucosa. An enhanced CT of the neck is the study of choice to show internal jugular thrombosis. 1 It is interesting to note that our patient's initial neck CT was negative. Likewise, after 10 days of
FIGURE 3. CT of neck with contrast showing thrombosis just above the right jugular vein bifurcation.
322
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 4 • April 2001
antibiotics he remained ill and required surgery, an intervention that is rarely necessary today. Complications of pharyngitis, such as retropharyngeal abscess, peritonsillar abscess, Lemierre syndrome, fasciitis, rheumatic fever, and glomerulonephritis, although rare, can be life threatening. The clinician managing a patient with an apparently uncomplicated pharyngitis should consider these diseases and warn the patient to be aware of symptoms suggesting a more serious infection. Patients with sore throats, who become more ill following conservative treatment, should be considered for antibiotic therapy and have a more extensive work-up performed.
ing. A MEDLINE search showed no current articles mentioning this side effect, and according to Searle, "A thorough review of the literature has failed to reveal the clinical characterization of this pigment." The manufacturers report that this side effect usually manifests in cases of overdose or hepatic insufficiency and is likely attributable to a minor metabolite that is of no significance to the patient. The dark brown urine discoloration caused by metronidazole is an uncommon side effect occurring largely in cases of overdose or liver failure and may be mistaken for bilirubin, blood, myoglobin, or hemoglobin, but is apparently of little clinical significance. GLENNK. GEETrNGMD MCP/Hahnemann University Department of Emergency Medicine
FREDERICKW. FIESSELER,DO
PETZRB. RICHMAN,MD Department of Emergency Medicine Morristown Memorial Hospital Morristown, NJ
JAMESR. ROBERTSMD Chair, Mercy Hospital of Philadelphia Department of Emergency Medicbw Philadelphia. PA
RENeE L. RIOGS,BA Lake Erie College of Osteopathic Medicine Erie, PA
References 1. Sinave cP, Hardy GJ, Fardy PW: The Lemierre syndrome: Suppurative thrombophlebitis of the internal jugular vein secondary to oropharyngeal infection. Medicine 1989;68:85-94 2. Henry S, DeMaria A, McCabe WR: Bacteremia due to fusobacterium species. Am J Med 1983;75:225-231 3. Barker J, Winer-Muram HT, Grey SW: Lemierre syndrome. South Med J 1996;89:1021-1023 4. Courmont P, Cade A: Sur une septicao-pyohemie de I'homme simulant la peste et causee par un streptobacille anaerobie. Aarchives de Med Exp et d'Anat Pathol 1900; No. 4 5. Lemierre A: On certain septicemias due to anaerobic organisms. Lancet 1936;1:701-703
URINE DISCOLORATION SECONDARY TO METRONIDAZOLE To the Editor:--We would like to report an unusual side effect and interesting case of urine discoloration secondary to metronidazole overdose that may be unfamiliar to many clinicians. Two hours before presenting to the ED, a 25-year-old woman took between 15 and 20 tablets of 500mg metronidazole in a suicide attempt. The metronidazole had been prescribed a week before to treat a urinary tract infection. She denied any coingestants and complained only of mild nausea, several episodes of vomiting, and dark urine. We obtained a clean catch urine sample, which was dark brown in color and clear. Urinalysis showed a positive dipstick analysis (Multistix 10SG by Bayer) for protein, bilirubin, leukocytes, nitrites, and ketones, but was negative for blood. Microscopic examination showed 5 to 10 white blood cells, 0 red blood cells, and 2+ bacteria. There was no evidence of liver disease or hyperbilirubinemia. She remained asymptomatic during her 4 hour ED stay and was discharged with a prescription of trimethoprim/sulfamethoxazole for her urinary infection. Many substances have been reported to discolor urine, but metronidazole is only rarely mentioned. Review of Goldfrank's Toxicology showed no evidence of this side effect. 1 The Physician's Desk Reference (PDR) mentions this phenomenon, but states that, "Although the pigment has not been positively identified, it is almost certainly a metabolite of metronidazole and seems to have no clinical significance. ''2 The PDR showed dark urine as a side effect of metronidazole in 1 in 100,000 users of the medication, a number that G.D. Searle & Co. states was drawn from Food and Drug Administration and corporate adverse event report-
Copyright @ 2001 by W.B. Saunders Company 0735-6757/01/1904-0021 $35.00/0
doi:10.1053/ajem.2001.24509
References 1. Goldfranck LR, Flomenbaum NE, Lewin NA, et al: Goldfrank's
Toxicologic Emergencies (ed 5) East Norwalk, CT, 1994 2. Physicians' Desk Reference (ed 54) Medical Economics Data Production Co, Montvale, NJ, 2000, p 2918
ANTERIOR DISLOCATION OF THE HUMERAL HEAD FROM BUNGLE JUMPING To the Editor:--Bungee jumping is a new sport that has become popular world-wide over the past decade. It originated on Pentecost Island of the South Pacific, where vines were tied to the ankles of jumpers, who then dove off wooden platforms to prove the passage from childhood to adulthood. A healthy 20-year-old man, with no previous history of musculoskeletal injury, did a bungee jump from a height of 50 meters. There was neither equipment failure nor any bodily contact with the ground and platform during the jump. During the ascent on the first rebound, he felt severe pain over his right shoulder, and he could not lift his right arm anymore after bungee jumping. He was sent to our E.D. several hours later with right shoulder deformity and tenderness. The vital signs were stable and there were no neurologic symptoms or signs. The remainder of the physical examination was noncontributory. Plain radiographs of the right shoulder showed anterior dislocation of the right humeral head with hill sachs deformity around greater tuberosity of the right humeral head (Fig 1). After administering a short-acting phenobarbital sedation, the closed reduction was performed smoothly (Fig 2), then the patient was discharged with a nonsteroidal anti-inflammatory drug and muscle relaxant. One month after the injury, the range of motion in the fight shoulder was within normal limits and the tenderness had already subsided. Bungee jumping involves leaping off from heights of up to 50 to 140 meters with an elastic cord attached either to the lower limb or around the waist, then falling until the rope reaches the elastic limit, then rebounding a significant distance upward. The serum level of catecholamine and stress hormone in people during bungee jumping appears normal, 1 however, a marked central betaendorphin release during bungee jumping was reported in 1994, 2 perhaps explaining feelings of exhilaration many days after jumping.
Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1904-0023535.00/0 doi:l 0.1053/ajem.2001.24454
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 4 • April 2001
2. Coates W, Jehle D, Cottington E: Trauma and full moon: A waning theory. Ann Emerg Med 1989;18:763-5 3. Nijsten MW, Willemsen SE: Accidents a matter of chance? Ned Tijdschr Geneeskd 1991 ;135:2421-4 4. Laverty WH, Kelly IW: Cyclical calendar and lunar patterns in automobile property accidents and injury accidents. Percept Mot Skills 1998;86:299-302 5. Morris RW: Circadian and circa annual rhythms of emergency room drug-overdose admissions. Prog Clin Biol Res 1987;227:451-7 6. Bfichthold-Stfiubli: Lexikon des deutschen Aberglaubens, Berlin, 1920 7. Unterreitmeier H: German astrology in the late middle ages. Archiv for Kulturgeschichte 1983;65:21-41
ATTRIBUTION OF CAUSALITY IN ADVERSE DRUG REACTIONS To the Editor:--We are concerned that the cardiopulmonary arrest in the patient described by Johri and colleagues could be certainly attributed to haloperidol, as proposed by the authors. 1 The temporal association with the last dose of haloperidol was interpreted as supporting the suspect that the 2 events were directly linked, but there is no much more than this in favor of the hypothesis. The previous medical history is almost vague and rhabdomyolysis or malignant hyperthermia is a more likely explanation than acute cardiac toxicity for the serious reactions to neuroleptic agents that occurred in the past. The case record does not convincingly rule out the possibility that the administration of haloperidol fortuitously coincided with the reported event so as to produce an apparent cause-effect relationship. Alternative explanations have not been sought. The patient was given diphenhydramine in addition to haloperidol. If a life-threatening arrythmia was the cause of the cardiopulmonary arrest it is important to remind that also first-generation Hi-blockers, including diphenhydramine, are potential triggers of malignant arrythmias. 2 4 However, the corrected QT interval measured after successful cardiopulmonary resuscitation was normal and this finding is not fully consistent with cardiac toxicity by either haloperidol or diphenhydramine. This patient probably had an increased risk of cardiopulmonary arrest and sudden death irrespectively of the exposure to neuroleptic agents or other drugs. The finding of cardiomegaly and bibasilar atelectasis on the chest radiograph performed at admission, before haloperidol or diphenhydramine was given, suggests indeed an underlying heart disease that was not previously recognized. These discrepancies are relevant, although the article merits consideration as it raises the important matter of causality attribution when reporting adverse drug reactions in the field of emergency medicine. Numerous schemes for classification of causality have been proposed and are used in different countries. 5 All of them emphasize that causality can be attributed only when there is a plausible time relation to administration of the suspected agent and the adverse reaction cannot be explained by concurrent diseases or other drugs or chemicals. This is not the case of the patient described by Johri and colleagues. We have assessed the likelihood that the event reported in the article was indeed drug-related using the Naranjo Adverse Drug Reaction Probability Scale, a validated and simple method for estimating the probability of adverse drug reactions. 6 We calculated a probability score 3 for haloperidol and 1 for diphenydramine, with scores > 9 indicating the event as highly probable, 5 to 8 probable, 1 to 4 possible, and 0 doubtful. The likelihood of a causal relation with haloperidol or diphenhydramine was very low for either drug, with a slightly higher but not significant probability score favoring haloperidol. The conclusions reached in the article appear there-
Copyright @ 2001 by W.B. Saunders Company 0735-6757/01/1904-0019535.00/0 doi:l 0.1053/ajem.2001.24466
fore to be incorrect as objective evidence for a proper attribution of causality to haloperidol is very scant. Johri and colleagues do not prove other than a temporal association between administration of haloperidol, and diphenhydramine as well, and the cardiopulmonary arrest experienced by the patient. Interpretation of causal relation needs to be rigorously adjusted for the presence of potential confounding factors. If we analyze data using objective and quantitative tools for estimating the cause and effect relation, we can reasonably infer that many other similar reports are flawed by a substantial methodological inconsistency. Stringent criteria should be used and great caution advised for meaningful conclusions to be drawn when attributing to a specific agent causality of adverse effects, particularly in case reports of single patients. GIUSEPPE FAMULARO,MD PHD
Department of Medical Sciences San Camillo Hospital Rome, Italy CLAUOIODE S]MONE,MD Department of Experimental Medicine University of L. Aquila, Aquila, Italy
References 1. Johri J, Rashid H, Daniel PJ, et al: Cardiopulmonary arrest secondary to haloperidol. Am J Emerg Med 2000;18:839 2. Zareba W, Moss AJ, Rosero SZ, et al: Electrocardiographic findings in patients with diphenydramine overdose. Am J Cardiol 1997;80:1168-1173 3. Wang WX, Ebert SN, Liu XK, et al: "Conventional" antihistamines slow cardiac repolarization in isolated perfused (Langendorff) feline hearts. J Cardiovasc Pharmacol 1998;32:123-128 4. Staffa JA, Jones JK, Gable CB, et al: Risk of selected serious cardiac events among new users of antihistamines. Clin Ther 1995; 17:1062-1077 5. Edwards IR, Aronson JK: Adverse drug reactions: definitions, diagnosis, and management. Lancet 2000;356:1255-1259 6. Naranjo CA, Busto U, Sellers EM, et al: A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981 ;30:239-245
PHARYNGITIS FOLLOWED BY HYPOXIA AND SEPSIS: LEMIERRE SYNDROME To the Editor:--Symptoms of pharyngitis are a frequent presenting complaint of emergency department (ED) patients. The majority of these cases are caused by viral pathogens. Thus, it is generally accepted that antibiotics are not warranted in most adult patients with sore throats. On the other hand, complications of withholding antibiotics, although infrequent, can lead to lifethreatening consequences. Lemierre syndrome is an anaerobic oropharyngeal infection that occurs in previously healthy patients, usually caused by Fusobacterium necroforum. The incidence of Fusobacterium infection declined dramatically in the 1950s with the emergence of penicillin. 1 Over time the organism has become increasingly resistant to penicillin, therefore clindamycin is now the therapeutic drug of choice? Today the mortality rate remains at about 15%. 3 We report a recent patient that we treated at our institution who presented with Lemierre syndrome. Five days before his ED visit, this previously healthy 20-yearold college student complained of dysphagia and odynophagia. Initially, the patient went to the infirmary at his college. He was advised to rest, increase liquids, and take nonsteroidal antiinflam-
Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1904-0020535.00/0 doi:l 0.1053/ajem.2001.24507
• CORRESPONDENCE
321
FIGURE 1. Chest CT showing multiple bilateral cavitary lesions suggestive of abscesses.
matory drags (NSAIDs). Over the next several days, the patient developed myalgia, vague abdominal pain, and anorexia. He denied having a fever, but experienced "shaking chills." The patient then began having moderate difficulty breathing, secondary to severe pleuritic chest pain. This provoked his visit to the ED. He denied HIV risk factors, alcohol, and illegal drug use. Physical examination was remarkable for a young, well-built, toxic appearing man in moderate respiratory distress. His vital signs were: blood pressure 107/48 mmHg, heart rate 118 beats/ min, respiratory rate 32 breaths/min, temperature 36.5°C (orally), and room air pulse oxygen saturation of 89%. The patient had icteric pupils, dry mucus membranes, erythematous inflamed tonsils without exudates, and anterior cervical lymphadenopathy, greater on the right. The chest examination revealed scattered tales bilaterally and point tenderness over the left lower anterior chest wall. His laboratory results were notable for a white blood cell count of 4.600/ram 3 with 24% bands, platelet count of 94,000/ mm 3, bilirubin of 3.8 mg/dl, LDH of 1,552 IU/L, D-dimer > 4.0 mcg/mL. The patient's chest x-ray film revealed a small right middle lobe infiltrate. A spiral chest computed tomography (CT) scan revealed multiple bilateral scattered "nodular consolidations" and small effusions. Echocardiogram was negative for vegetation. Blood cultures were obtained. The patient was admitted and started on heparin and azithromycin. During the ensuing days the patient's condition worsened. His antibiotics were changed multiple times. On the forth hospital day his blood cultures came back positive for gram-negative bacillus. Repeat chest CT showed multiple bilateral cavitary lesions (Fig 1). The right side of his neck became swollen. A neck CT was negative for abscess and thrombosis. The patient's condition continued to deteriorate and he was transferred to the medical intensive care unit. His neck swelling worsened and dentistry was consulted. Dentistry stated no apparent odontologic infection was seen. On the fifth hospital day his blood cultures isolated Fusobacterium necrophorum. On hospital day 7 a repeat neck CT showed thrombosis of his right internal jugular vein (Figs 2, 3). The patient's fever and hypoxia persisted and vascular surgery was consulted. He was taken to the operating room the following morning. The surgeons reported a "dense inflammatory process involving the entire carotid sheath. The jugular vein could not safely be dissected, and, therefore it was ligated at the neck." After surgery the patient's fever resolved. He was discharged on hospital day 14, but treated with IV clindamycin for an additional 2 weeks. The patient suffered no long-term sequela. The incidence of Lemierre syndrome was significantly higher in the preantibiotic era. The first known case may well be that of a "postanginal septicemia" reported in 1900 by Courmont and
FIGURE 2. CT of neck with contrast showing thrombosis of the right internal jugular vein. Cadde. 4 It was not until 1936 that Lemierre published a case series of 20 young patients with this disease. 5 Lemierre's syndrome is an anaerobic septicemia. It usually begins with an acute pharyngitis, followed by thrombosis of the internal jugular vein. From this point metastatic infection throughout the body occurs, most commonly affecting the lungs and joints. The majority of cases are caused by Fusobacterium necroforum, an anaerobic gram-negative normal inhabitant of the oral mucosa. An enhanced CT of the neck is the study of choice to show internal jugular thrombosis. 1 It is interesting to note that our patient's initial neck CT was negative. Likewise, after 10 days of
FIGURE 3. CT of neck with contrast showing thrombosis just above the right jugular vein bifurcation.
322
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 4 • April 2001
antibiotics he remained ill and required surgery, an intervention that is rarely necessary today. Complications of pharyngitis, such as retropharyngeal abscess, peritonsillar abscess, Lemierre syndrome, fasciitis, rheumatic fever, and glomerulonephritis, although rare, can be life threatening. The clinician managing a patient with an apparently uncomplicated pharyngitis should consider these diseases and warn the patient to be aware of symptoms suggesting a more serious infection. Patients with sore throats, who become more ill following conservative treatment, should be considered for antibiotic therapy and have a more extensive work-up performed.
ing. A MEDLINE search showed no current articles mentioning this side effect, and according to Searle, "A thorough review of the literature has failed to reveal the clinical characterization of this pigment." The manufacturers report that this side effect usually manifests in cases of overdose or hepatic insufficiency and is likely attributable to a minor metabolite that is of no significance to the patient. The dark brown urine discoloration caused by metronidazole is an uncommon side effect occurring largely in cases of overdose or liver failure and may be mistaken for bilirubin, blood, myoglobin, or hemoglobin, but is apparently of little clinical significance. GLENNK. GEETrNGMD MCP/Hahnemann University Department of Emergency Medicine
FREDERICKW. FIESSELER,DO
PETZRB. RICHMAN,MD Department of Emergency Medicine Morristown Memorial Hospital Morristown, NJ
JAMESR. ROBERTSMD Chair, Mercy Hospital of Philadelphia Department of Emergency Medicbw Philadelphia. PA
RENeE L. RIOGS,BA Lake Erie College of Osteopathic Medicine Erie, PA
References 1. Sinave cP, Hardy GJ, Fardy PW: The Lemierre syndrome: Suppurative thrombophlebitis of the internal jugular vein secondary to oropharyngeal infection. Medicine 1989;68:85-94 2. Henry S, DeMaria A, McCabe WR: Bacteremia due to fusobacterium species. Am J Med 1983;75:225-231 3. Barker J, Winer-Muram HT, Grey SW: Lemierre syndrome. South Med J 1996;89:1021-1023 4. Courmont P, Cade A: Sur une septicao-pyohemie de I'homme simulant la peste et causee par un streptobacille anaerobie. Aarchives de Med Exp et d'Anat Pathol 1900; No. 4 5. Lemierre A: On certain septicemias due to anaerobic organisms. Lancet 1936;1:701-703
URINE DISCOLORATION SECONDARY TO METRONIDAZOLE To the Editor:--We would like to report an unusual side effect and interesting case of urine discoloration secondary to metronidazole overdose that may be unfamiliar to many clinicians. Two hours before presenting to the ED, a 25-year-old woman took between 15 and 20 tablets of 500mg metronidazole in a suicide attempt. The metronidazole had been prescribed a week before to treat a urinary tract infection. She denied any coingestants and complained only of mild nausea, several episodes of vomiting, and dark urine. We obtained a clean catch urine sample, which was dark brown in color and clear. Urinalysis showed a positive dipstick analysis (Multistix 10SG by Bayer) for protein, bilirubin, leukocytes, nitrites, and ketones, but was negative for blood. Microscopic examination showed 5 to 10 white blood cells, 0 red blood cells, and 2+ bacteria. There was no evidence of liver disease or hyperbilirubinemia. She remained asymptomatic during her 4 hour ED stay and was discharged with a prescription of trimethoprim/sulfamethoxazole for her urinary infection. Many substances have been reported to discolor urine, but metronidazole is only rarely mentioned. Review of Goldfrank's Toxicology showed no evidence of this side effect. 1 The Physician's Desk Reference (PDR) mentions this phenomenon, but states that, "Although the pigment has not been positively identified, it is almost certainly a metabolite of metronidazole and seems to have no clinical significance. ''2 The PDR showed dark urine as a side effect of metronidazole in 1 in 100,000 users of the medication, a number that G.D. Searle & Co. states was drawn from Food and Drug Administration and corporate adverse event report-
Copyright @ 2001 by W.B. Saunders Company 0735-6757/01/1904-0021 $35.00/0
doi:10.1053/ajem.2001.24509
References 1. Goldfranck LR, Flomenbaum NE, Lewin NA, et al: Goldfrank's
Toxicologic Emergencies (ed 5) East Norwalk, CT, 1994 2. Physicians' Desk Reference (ed 54) Medical Economics Data Production Co, Montvale, NJ, 2000, p 2918
ANTERIOR DISLOCATION OF THE HUMERAL HEAD FROM BUNGLE JUMPING To the Editor:--Bungee jumping is a new sport that has become popular world-wide over the past decade. It originated on Pentecost Island of the South Pacific, where vines were tied to the ankles of jumpers, who then dove off wooden platforms to prove the passage from childhood to adulthood. A healthy 20-year-old man, with no previous history of musculoskeletal injury, did a bungee jump from a height of 50 meters. There was neither equipment failure nor any bodily contact with the ground and platform during the jump. During the ascent on the first rebound, he felt severe pain over his right shoulder, and he could not lift his right arm anymore after bungee jumping. He was sent to our E.D. several hours later with right shoulder deformity and tenderness. The vital signs were stable and there were no neurologic symptoms or signs. The remainder of the physical examination was noncontributory. Plain radiographs of the right shoulder showed anterior dislocation of the right humeral head with hill sachs deformity around greater tuberosity of the right humeral head (Fig 1). After administering a short-acting phenobarbital sedation, the closed reduction was performed smoothly (Fig 2), then the patient was discharged with a nonsteroidal anti-inflammatory drug and muscle relaxant. One month after the injury, the range of motion in the fight shoulder was within normal limits and the tenderness had already subsided. Bungee jumping involves leaping off from heights of up to 50 to 140 meters with an elastic cord attached either to the lower limb or around the waist, then falling until the rope reaches the elastic limit, then rebounding a significant distance upward. The serum level of catecholamine and stress hormone in people during bungee jumping appears normal, 1 however, a marked central betaendorphin release during bungee jumping was reported in 1994, 2 perhaps explaining feelings of exhilaration many days after jumping.
Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1904-0023535.00/0 doi:l 0.1053/ajem.2001.24454