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Am J Emerg Med 2003 Jan;21(1):51-4
Chiayi Veteans Hospital, the dagger Emergency Department, Veterans General Hospital-Taipei, National Yang-Ming University, Taipei, Taiwan, R.O.C.
Tetrodotoxin (TTX) poisoning, although uncommon, is frequently seen in Taiwan, Japan, and Southeast Asia. It is rare but significant in the United States as well. Only three cases have been reported in the EM literature. We report an outbreak of six cases of TTX poisoning from eating puffer fish. On April 17, 2001, an outbreak of TTX poisoning occurred among Mainland Chinese fishermen who shared puffer fish on their boat in the Taiwan Strait. All six cases were middle-aged men (aged 32-49 yr). Onset of symptoms began approximately 2 to 3 hours after ingestion; symptoms included orolingual numbness, acroparesthesia, and breathlessness. As a result of delayed transportation and initial resuscitation, one patient presented in full cardiac arrest, with recovery of spontaneous circulation after successful cardiopulmonary resuscitation. With the exception of this patient, the initial acid-base abnormalities were inconsistent with severity of illness and mild hypercapnia was common (4 out of 5). The patient who presented in full arrest died 1 day after admission as a result of intractable bradycardia (complete atrioventricular block), a finding rarely mentioned in the literature, despite intravenous atropine and dopamine infusion. The remaining patients survived without significant sequelae and were discharged after short-term observation and supportive care, although some had neurologic and cardiopulmonary manifestations (muscle weakness, hypotension, hypoxemia, and hypercapnia). Some mildly hypoventilated patients recovered well without endotracheal intubation and ventilatory support. Favorable outcomes in most patients can be obtained if aggressive supportive treatment is provided in time. Thus, appropriate prehospital and ED ventilatory support (the implementation of a bag-valve mask or endotracheal intubation with good ventilatory support) is mandatory for those patients with respiratory failure. Most patients experience onset of symptoms within 6 hours of ingestion, but a few have a delayed onset up to 20 hours. Therefore, for those TTX-intoxicated patients without immediate prominent respiratory insufficiency, at least 24 hours of intensive monitoring of their respiratory state is necessary because of the different susceptibility and unpredictability of an individual course. Copyright 2003, Elsevier Science (USA). All rights reserved.)
PMID: 12563582, UI: 22449933
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Am J Emerg Med 2003 Jan;21(1):32-4
Department of Emergency Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
The study objective was to describe the morbidity of patients presenting with heroin overdose (HOD)-induced noncardiogenic pulmonary edema (NCPE) at an urban ED. A retrospective chart review of patients presenting between 1996 and 1999 with the diagnosis of HOD was conducted. Using a standardized data abstraction form, information on prehospital care, ED care, demographics, and cointoxications was collected. One hundred twenty-five charts (78%) were available for review. Of these, 13 (10%) were diagnosed with NCPE and all were male. In the field, NCPE patients had an average relative risk of 6, a Glasgow Coma Scale of 4, and all needed naloxone. The average admitted duration of use was 2.9 years for those who developed NCPE compared with 13.2 years for those who did not. Five (42%) NCPE patients tested positive for cocaine use and 7 (58%) tested positive for alcohol. In this cohort, the NCPE patients were male and less experienced users with initial low relative risk and Glasgow Coma Scale which demanded prehospital naloxone use. (Am J Emerg Med 2003;21:32-34. Copyright 2003, Elsevier Science (USA). All rights reserved.)
PMID: 12563576, UI: 22449927
Ann Pharmacother 2002 Sep;36(9):1481-2; author reply 1482-3
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PMID: 12196075, UI: 22183775
Ann Pharmacother 2002 Sep;36(9):1399-402
Division of Pediatric Nephrology, University of Virginia, Charlottesville, VA 22908, USA.
OBJECTIVE: To report a young man on phenytoin who developed acute neurologic symptoms after isradipine was introduced to his treatment regimen and discuss the possible causes of this drug interaction. CASE SUMMARY: A 21-year-old white man, with propionic acidemia and seizures treated with phenytoin and carbamazepine, was started on isradipine for essential hypertension. Soon thereafter, he developed acute and severe lethargy, ataxia, dysarthria, and weakness that resolved once isradipine was withheld. Phenytoin concentrations were within normal limits or elevated, despite sequential reductions of phenytoin dosage, during concomitant isradipine administration. DISCUSSION: Isradipine is a known inhibitor of the CYP450 isoenzyme family. Although the daily dose of phenytoin was decreased significantly, phenytoin blood concentrations remained high, suggesting a pharmacokinetic interaction. Previously, the patient had never had neurologic symptoms associated with increased phenytoin concentrations. This also indicates a likely pharmacodynamic interaction between phenytoin and the calcium-channel blocker. Both phenytoin and isradipine have been shown to bind to calcium channels and to inhibit calcium entry into the cells. Binding of isradipine to the brain has been described in humans and animals, and calcium-channel blockers have been shown to cause potentiation of anticonvulsant action of phenytoin. CONCLUSIONS: Acute pharmacokinetic and pharmacodynamic interactions between phenytoin and isradipine were probably responsible for the lethargy, dysarthria, ataxia, and weakness our patient developed. The combination of phenytoin and calcium-channel blockers should be used with caution.
PMID: 12196060, UI: 22183760
Ann Pharmacother 2002 Sep;36(9):1387-90
Department of Psychiatry, Taipei Medical University--Wan Fang Hospital and Taipei Medical University, Taipei, Taiwan.
OBJECTIVE: To report 2 cases of metoclopramide-induced supersensitivity psychosis. CASE SUMMARIES: A 74-year-old Taiwanese man was treated with metoclopramide 5 mg 4 times daily for 6 months. A second patient, a 65-year-old Taiwanese man, was treated with metoclopramide 5 mg 4 times daily for 3 months. After discontinuation of metoclopramide, both patients developed hallucinatory experiences and delusions. DISCUSSION: This is the first report of metoclopramide-induced supersensitivity psychosis. Chronic administration of a dopamine antagonist (e.g., metoclopramide) might induce dopamine receptor supersensitivity. It is hypothesized that exacerbation or occurrence of psychotic symptoms following neuroleptic withdrawal results from mesolimbic dopamine supersensitivity. CONCLUSIONS: The complications of long-term metoclopramide therapy should be seriously considered when the treatment regimens are being planned. Clinicians should attempt to treat patients with the lowest effective dosage of medication for the briefest therapeutic period to minimize the risks of adverse reactions.
PMID: 12196057, UI: 22183757
Ann Pharmacother 2002 Sep;36(9):1380-2
Department of Internal Medicine, San Camillo Hospital, Rome, Italy. gfamularo@uni.net
OBJECTIVE: To report a patient with lung cancer and idiopathic myelofibrosis with myeloid metaplasia who developed purpura and acute renal failure while receiving levofloxacin, and review the existing literature on quinolone nephrotoxicity. CASE SUMMARY: A 73-year-old white man, with a medical history of non-small-cell lung cancer and idiopathic myelofibrosis with myeloid metaplasia, was prescribed levofloxacin because of a lower urinary tract infection. Three days later, he presented with palpable purpura and erythematous skin lesions over the lower limbs and trunk, with a markedly reduced urinary output. Serum creatinine and urea nitrogen were 6.4 and 190 mg/dL, respectively. Levofloxacin was discontinued, and prednisone, furosemide, and intravenous fluids were given. The patient fully recovered over the ensuing 4 weeks. CONCLUSIONS: Nephrotoxicity associated with levofloxacin is uncommon. Allergic interstitial nephritis or vasculitis is believed to be the underlying pathologic process. Definitive diagnosis requires performance of renal biopsy, although this is not always feasible. In this case, a return of renal function to normal, with the disappearance of purpura following the discontinuation of levofloxacin and corticosteroid treatment, supports the presumptive diagnosis of a hypersensitivity reaction to levofloxacin.
PMID: 12196055, UI: 22183755
Gastroenterol Clin Biol 2002 Oct;26(10):939-40
PMID: 12434106, UI: 22321250
Hum Exp Toxicol 2002 Mar;21(3):137-45
Centre Anti-Poisons, Hjpital Salvator, Marseille, France.
Vipera aspis aspis (V.a.a.) is the most dangerous poisonous snake in South-Eastern France. The clinical symptoms observed after V.a.a. envenomations involve mostly local signs (pain, edema) associated in the more severe cases with systemic symptoms (gastro-intestinal and cardiovascular manifestations). Since 1992, several unusual cases of moderate and severe 'neurotoxic' envenomations by V.a.a. snakes have been reported in a very localized area in South-Eastern France. Most of the human patients mainly suffered neurological signs owing to cephalic muscle paralysis. Drowsiness and dyspnea were observed for the most severe cases. Envenomed animals suffered respiratory distress and paralysis. The local signs were never as severe as observed after envenomations by vipers in other French regions. Human patients with moderate or severe clinical features received two intravenous injections of Viperfav antivenom, the first dose inducing the decrease of the neurological signs and the second reducing significantly the edema. Neurotoxic components immunologically cross-reacting with toxins from V. ammodytes ammodytes venom from Eastern Europe were detected in the blood of all patients suffering neurological symptoms after a V.a.a. bite. The protective efficacy of various antivenoms was evaluated in mice. The existence of geographical variations in the composition of V.a.a. venom emphasizes on the use of polyvalent antivenom in the treatment of viper envenomations in France.
PMID: 12102539, UI: 22096852
Lancet 2003 Feb 1;361(9355):429-30
Department of Hepatology Rigshospitalet, University Hospital, DK-2100, Copenhagen, Denmark
[Medline record in process]
PMID: 12573400, UI: 22462364
Lancet 2003 Feb 1;361(9355):429
Department of Clinical Toxicology and Pharmacology, Newcastle Mater Misericordiae Hospital, Locked Bag 7, NSW 2310, Hunter Region Mail Centre, Australia
PMID: 12573399, UI: 22462363
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N Engl J Med 2003 Feb 6;348(6):557-60; author reply 557-60
PMID: 12572578, UI: 22459791
PMID: 12572577, UI: 22459790
PMID: 12572576, UI: 22459789
PMID: 12572575, UI: 22459788
PMID: 12571266, UI: 22459261
N Engl J Med 2003 Jan 30;348(5):474-6; author reply 474-6
PMID: 12557870, UI: 22445048
N Engl J Med 2003 Jan 30;348(5):473-4; author reply 473-4
PMID: 12556553, UI: 22444746