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A hemlock water dropwort curry: a case of multiple poisoning

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Abstract

Hemlock water dropwort ( Oenanthe crocata ) is perhaps the most poisonous indigenous plant in Britain.1 It is a member of the Umbellifer family and is found in ditches, damp meadows, in steams, by riverbanks, and in marshes. It is a large, stout plant between three and five feet high that flowers in July. The lower stem is usually thick and joins to clusters of fleshy tubers that gives rise to the popular name “dead man’s fingers”. The entire plant is poisonous. The tubers, stems, and leaves contain oenanthotoxin, a highly unsaturated higher alcohol, which is known to be poisonous and a powerful convulsant.2 The majority of the umbellifer family are harmless. These include species of celery, parsley, parsnip, and carrots. The poisonous members are hemlock ( Conium maculatum ), cowbane ( Cicuta virosa ), and hemlock water dropwort.3 Poisoning by hemlock water droplet is an infrequent event. A number of human fatalities have occurred over the years, although animals are its usual victims. A group of eight young adults who were on holiday in Argyll collected what they thought were water parsnips from a small stream. The roots were cleaned, chopped, and added to a curry. All consumed the curry, but the majority of …

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Water hemlocks (Cicuta spp.) are toxic members of the Apiaceae plant family. The best drug treatment for the convulsions associated with acute water hemlock poisoning in livestock and humans has not been determined experimentally. This work compared the therapeutic actions of benzodiazepines (diazepam) and barbiturates (phenobarbital) on water hemlock poisoning in a goat model. C. maculata tubers were orally dosed to goats. Experimental groups consisted of; control saline; 20 mg/kg phenobarbital; 1.0 mg/kg diazepam; 10 mg/kg diazepam; and 1.0 mg/kg diazepam administered as needed to moderate convulsions by intravenous (i.v.) infusion. Diazepam provided nearly instant control of convulsions. Clinical signs of poisoning were completely controlled for the duration of the experiment in the goats that received the 10 mg/kg diazepam dose. These results suggest that diazepam is effective at managing the clinical signs of water hemlock poisoning in goats. We speculate that diazepam can be used as a potential treatment for water hemlock poisoning in other livestock species and humans.
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In recent years, recorded cases related to forensic botany and, in particular, of plant poisoning have become rare. We report on the medicolegal characteristics of an undetermined sudden death (USD) of a woman in which scene there were remnants of a vegetal peeling. After the autopsy, macroscopic findings reported multiorgan failure and requested the investigation of the cause of death. Postmortem blood was firstly investigated on cyanide toxicity presumptively coming from a yucca-like root; however, found cyanide levels were under normality. Because of the lack of morphological features of the encountered plant remains, a genetic nrDNA ITS2 sequence investigation was followed. The resulting DNA sequence could identify the evidence as the water dropwort (Oenanthe spp.) which contains oenanthotoxin, a potent toxin that may be fatal, similar to the more commonly found in hemlock Conium or cowbane Cicuta species. A liquid chromatography-tandem high resolution mass spectrometry (LC-QTOF MS) was later applied to analyse the vegetal extract and stomach content and successfully confirmed the toxin existence. Medicolegal and analytical findings at the forensic laboratory were described, where both biological and chemical techniques could successfully conjugate, as an interdisciplinary research, and explain premortem symptoms and postmortem findings. Present data can be helpful in future investigation on poisoning cases by conjugated polyacetylenes. The present work tries to emphasize the often undervalued plant evidence in legal medicine diagnosis in the context of an unexplained death.
Article
Background Plant poisonings are uncommon in adults, and rarely fatal. Oenantha crocata is a toxic plant growing in the humid grasslands of North America and Western Europe. Case Report We report here two adults who ingested Oenantha crocata roots, having mistaken them for edible tuberous radish. One developed vomiting and needed only 24 h symptomatic treatment, whereas the other suffered prolonged convulsions, cardiac arrest, and severe metabolic acidosis, leading to a fatal outcome. Why Should an Emergency Physician Be Aware of This? Cases of poisoning with Oenantha crocata are rare and destabilizing. With increased interest in “natural” foods and team building by survival training, medical teams should be aware of the management for such poisoning.
Article
Background: Because in todaychr('39')s societies, not only the nutritional role of plants and fungi is very high, but also the main basis of many drugs are plants and plant products, therefore one of the problems of clinical toxicologists is the toxicity of these products. Objective: This study aimed to define the prevalence, symptoms, complications, effective treatments, type of substance use, the cause of intake, location, gender distribution and age of poisoning with herbs and mushrooms in hospitalized patients of Loghman Hakim Hospital in Tehran. Methods: This is a retrospective study with questionnaire formulation. Patients reviewed from the beginning of 2007 to the end of 2013. Results: of 103 cases of poisoning with plants and mushrooms 64.1% were male, and 35.9% were female. The mean age of patients was 21.59 ± 30.51 years. The most commonly used substance is Datura (34%). On the other hand, sole mushroom ingestion was found in 5.8% of cases. The most significant source of plants and mushrooms was reported from herbal-shops (27.18%). The reason behind intake was either random or euphoria. Four patients were admitted to the intensive care unit, and three patients needed intubation. The mean hospital stay was 1.64 ± 1.28 days. Ninety percent of the treatments were supportive, and 75.7% of the patients recovered without any clinical complications. Conclusion: Poisoning with toxic plants and mushrooms is one of the frequent causes of intoxication that is often accidental. In children poisoning is inadvertent, but youth are more likely wanted to have euphoria. Treatment strategies are supportive and symptomatic.
Chapter
Water hemlock belongs to the family Apiaceae (Umbelliferae). The genus Cicuta includes the species spotted water hemlock (C. maculata), Western water hemlock (C. douglasii), and northern water hemlock also known as European water hemlock (C. virosa), C. bolanderi, C. bulbifera, C. californica, C. curtissii, C. mackenziana, C. occidentalis, and C. vagans (Figs. 1, 2, and 3). The active toxic compound in water hemlock is cicutoxin. The hemlock water dropwort (Oenanthe crocata) belongs to the family Apiaceae (Umbelliferae), genus Oenanthe. It is native to Europe but has been introduced to some parts of the United States. It lacks the chambered root of the Cicuta spp. and produces oenanthotoxin, a constitutional isomer (a compound that has the same molecular formula but a different structural formula) of cicutoxin.
Chapter
Water hemlock belongs to the family Apiaceae (Umbelliferae). The genus Cicuta includes the species spotted water hemlock (C. maculata), Western water hemlock (C. douglasii), and northern water hemlock also known as European water hemlock (C. virosa), C. bolanderi, C. bulbifera, C. californica, C. curtissii, C. mackenziana, C. occidentalis, and C. vagans (Figs. 1, 2, and 3). The active toxic compound in water hemlock is cicutoxin. The hemlock water dropwort (Oenanthe crocata) belongs to the family Apiaceae (Umbelliferae), genus . It is native to Europe but has been introduced to some parts of the United States. It lacks the chambered root of the Cicuta spp. and produces oenanthotoxin, a constitutional isomer (a compound that has the same molecular formula but a different structural formula) of cicutoxin.
Article
We developed a synthetic scheme for the synthesis of naturally occurring (14R)-oenanthotoxin and several analogs. Key-steps of this synthesis were an efficient homo-coupling of alkynes and a chemoenzymatic resolution of racemic oenanthotoxin using novozyme 435 and vinyl acetate. The compounds were screened for their cytotoxic activity using a photometric sulforhodamine B assays and several human tumor cell lines. Oenanthotoxin and many derivatives thereof were cytotoxic to tumor cell lines as well as to non-malignant mouse fibroblasts. The highest activity was determined for human ovarian cancer cells A2780 with EC50=3.8μM. Copyright © 2015 Elsevier Ltd. All rights reserved.
Article
Œnantha crocata is a plant found throughout Western France. The oenanthotoxin is quickly poisonous with an ingested dose of a few milligrams. A 43-year-old man, who ingested a few grams of the root of this plant, started to vomit within 30 minutes and developed status epilepticus, which was seriously aggravated by severe rhabdomyolysis. Recovery came after 4 days in intensive care. Medical care must be delivered swiftly to hope for a positive outcome.
Article
Oenanthotoxin (OETX), a polyacetylenic alcohol from plants of the genus Oenanthe, has recently been identified as potent inhibitor of GABA-evoked currents. However, the effects of OETX on the inhibitory postsynaptic currents (IPSCs), as well as the pharmacological mechanism(s) underlying its effects on GABA(A) receptors, remain unknown. The purpose of this study was to elucidate the mechanism underlying the inhibition of GABAergic currents by OETX. Effects of OETX on GABAergic currents were studied using the patch clamp technique on rat cultured hippocampal neurons. Miniature IPSCs (mIPSCs) were recorded in the whole-cell configuration, while the current responses were elicited by ultrafast GABA applications onto the excised patches. OETX potently inhibited both mIPSCs and current responses, but its effect was much stronger on synaptic currents. Analysis of the effects of OETX on mIPSCs and evoked currents disclosed a complex mechanism: allosteric modulation of both GABA(A) receptor binding and gating properties and a non-competitive, probably open channel block mechanism. In particular, OETX reduced the binding rate and nearly abolished receptor desensitization. A combination of rapid clearance of synaptic GABA and OETX-induced slowing of binding kinetics is proposed to underlie the potent action of OETX on mIPSCs. OETX shows a complex blocking mechanism of GABA(A) receptors, and the impact of this toxin is more potent on mIPSCs than on currents evoked by exogenous GABA. Such effects on GABAergic currents are compatible with the convulsions and epileptic-like activity reported for OETX.
Article
Water hemlock, which encompasses a range of species divided across two genera (Cicuta and Oenanthe), are regarded as being among the most poisonous plants both in North America and in the United Kingdom. Despite their toxicity, the literature consists almost entirely of case reports. The aim of this review is to summarize this literature by covering all aspects of taxonomy and botanical characterization, principal toxins, basic pharmacology including mechanisms of toxicity, and the clinical features, diagnosis, and management of poisoning. MECHANISMS OF TOXICITY: The principal toxins, cicutoxin and oenanthotoxin, belong to a group of C17 conjugated polyacetylenes. They act as (noncompetitive) gamma-aminobutyric acid antagonists in the central nervous system (CNS), resulting in unabated neuronal depolarization that can lead to seizures. Ingestion of even a small amount of plant matter may result in severe intoxication. After ingestion, the patient is most likely to experience CNS stimulatory effects including seizures that, in the absence of aggressive supportive care, can result in death. Other features include nausea, vomiting, diarrhea, tachycardia, mydriasis, rhabdomyolysis, renal failure, coma, respiratory impairment, and cardiac dysrhythmias. Treatment consists mainly of prompt airway management and seizure control, plus decontamination if achieved early and after stabilization. In the event of renal failure, the use of hemodialysis has been employed successfully. The ingestion of water hemlock can lead to serious complications that may be fatal. Prognosis is good, however, if prompt supportive care is provided.
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Liquid chromatography-mass spectrometry (LC-MS) analysis of methanol extracts of Oenanthe crocata roots revealed that oenanthotoxin co-eluted with another major polyalkyne, 2,3-dihydro-oenanthotoxin, using the existing high performance liquid chromatography (HPLC) method (isocratic elution from C18 with aqueous methanol) for investigating Oenanthe poisoning. Positive ES or APCI gave [(M+H)-H(2)O](+) and its methanol adduct as major ion species for oenanthotoxin, whereas 2,3-dihydro-oenanthotoxin formed [M+H](+) and its methanol adduct. The two polyalkynes could be chromatographically resolved on C18 by gradient elution with aqueous acetonitrile. This provides superior analysis for oenanthotoxin using HPLC with photodiode array (PDA) detection alone, but for LC-MS/MS aqueous acetonitrile was less suitable due to poor ionisation and, with APCI, an increase in the relative abundance of a [M-1](+) species, which could confuse compound assignment. HPLC-PDA and LC-MS/MS methods using an aqueous acetonitrile or aqueous methanol mobile phase, respectively, were successful when applied to the analysis of the stomach contents of a pony suspected to have eaten O. crocata. Relevant product ion spectra, by ion trap MS/MS, accurate mass data and complete sets of (1)H and (13)C NMR spectral assignments are given for the two compounds.
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Twelve consecutive patients who developed torsade de pointes (polymorphous ventricular tachycardia with marked QT prolongation, TdP) over a 4 year period were treated with intravenous injections of magnesium sulfate. In nine of the patients a single bolus of 2 g completely abolished the TdP within 1 to 5 min, and in three others complete abolition of the TdP was achieved after a second bolus was given 5 to 15 min later. Nine of the patients also received continuous infusion of MgSO4 (3 to 20 mg/min) for 7 to 48 hr until the QT interval was below 0.50 sec. In nine of the 12 patients the TdP was induced by antiarrhythmic agents. The QT interval preceding TdP ranged from 0.54 to 0.72 sec. After the MgSO4 bolus, which prevented the recurrence of TdP, no significant changes were observed in the QT interval. There were no side effects of this treatment. In eight of the 12 patients potassium levels before the TdP were below 3.5 meq/liter; magnesium levels were available in eight patients before TdP, and were normal in all. Five additional patients with polymorphous ventricular tachycardia but normal QT intervals (non-TdP patients) received two to three boluses of MgSO4. This treatment was ineffective in all, but they responded to conventional antiarrhythmic therapy. Thus, MgSO4 is a very effective and safe treatment for TdP, and its application is rapid and simple. Its use is therefore recommended as the first line of therapy for TdP.
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Increases in extracellular calcium (Ca++) can alter vascular tone, and thus may result in increased blood pressure (Bp) and reduced renal blood flow (RBF). Ca++ can stimulate prostaglandin E2 (PGE2) and/or prostacyclin (PGI2) release in vitro, which may modulate Ca++ vascular effects. However, in man, the effect of Ca++ on PG release is not known. To study this, 14 volunteers received low-dose (2 mg/kg Ca++ gluconate) or high-dose (8 mg/kg) Ca++ infusions. The low-dose Ca++ infusion did not alter systemic or renal hemodynamics, but selectively stimulated PGI2, as reflected by the stable metabolite 6-keto-PGF1 alpha in urine (159 +/- 21-244 +/- 30 ng/g creatinine, P less than 0.02). The same Ca++ infusion given during cyclooxygenase blockade with indomethacin or ibuprofen was not associated with a rise in PGI2 and produced a rise in Bp and fall in RBF. However, sulindac, reported to be a weaker renal PG inhibitor, did not prevent the Ca++ -induced PGI2 stimulation (129 +/- 33-283 +/- 90, P less than 0.02), and RBF was maintained despite similar increases in Bp. The high-dose Ca++ infusion produced an increase in mean Bp without a change in cardiac output, and stimulated urinary 6-keto-PGF1 alpha to values greater than that produced by the 2-mg/kg Ca++ dose (330 +/- 45 vs. 244 +/- 30, P less than 0.05). In contrast, urinary PGE2 levels did not change. A Ca++ blocker, nifedipine, alone had no effect on Bp or urinary 6-keto-PGF1 alpha levels, but completely prevented the Ca++ -induced rise in Bp and 6-keto-PGF1 alpha excretion (158 +/- 30 vs. 182 +/- 38, P greater than 0.2). However, the rise in 6-keto-PGF1 alpha was not altered by the alpha 1 antagonist prazosin (159 +/- 21-258 +/- 23, P less than 0.02), suggesting that calcium entry and not alpha 1 receptor activation mediates Ca++ pressor and PGI2 stimulatory effects. These data indicate a new vascular regulatory system in which PGI2 modulates the systemic and renal vascular actions of calcium in man.
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Histamine poisoning can result from the ingestion of food containing unusually high levels of histamine. Fish are most commonly involved in incidents of histamine poisoning, although cheese has also been implicated on occasion. The historic involvement of tuna and mackerel in histamine poisoning led to the longtime usage of the term, scombroid fish poisoning, to describe this food-borne illness. Histamine poisoning is characterized by a short incubation period, a short duration, and symptoms resembling those associated with allergic reactions. The evidence supporting the role of histamine as the causative agent is compelling. The efficacy of antihistamine therapy, the allergic-like symptomology, and the finding of high levels of histamine in the implicated food suggest strongly that histamine is the causative agent. However, histamine ingested with spoiled fish appears to be much more toxic than histamine ingested in an aqueous solution. The presence of potentiators of histamine toxicity in the spoiled fish may account for this difference in toxicity. Several potentiators including other putrefactive amines such as putrescine and cadaverine have been identified. Pharmacologic potentiators may also exist; aminoguanidine and isoniazid are examples. The mechanism of action of these potentiators appears to be the inhibition of intestinal histamine-metabolizing enzymes. This enzyme inhibition causes a decrease in histamine detoxification in the intestinal mucosa and results in increased intestinal uptake and urinary excretion of unmetabolized histamine.
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A 65 year old woman with gall stones presented with crushing chest pain after an attack of biliary colic. The electrocardiogram showed ST segment elevation in leads I, aVL, and V1-V3 while leads II, III, and aVF showed ST segment depression. Cardiac enzyme activity remained within the normal range. During the next three weeks attacks of epigastric and right hypochondrial pain preceded by crushing chest pain with identical electrocardiogram changes occurred with decreasing frequency. Coronary arteriography showed 60% obstruction of the left anterior descending coronary artery and good left ventricular function. During the next three years the patient complained both of mild abdominal pain, probably biliary colic, and mild effort related angina pectoris without a relation between the two symptoms. It is suggested that the attack of variant angina was triggered by biliary colic through sympathoadrenal discharge causing vasospasm.
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Objective To assess factors that might predict serious necrotizing soft tissue infections following illicit drug injection. Design A retrospective review of a consecutive case series. Setting An urban municipal hospital. Patients Thirty patients presenting with cutaneous abscesses resulting from illicit drug injections during a 5-year period. All cases presented clinically with fluctuance, erythema, or induration but required extensive debridement at the time of incision and drainage. Interventions Operative treatment employed wide incision, routine subfascial examination, and aggressive debridement. Clinical management included broad-spectrum antibiotics, critical care support, and reconstructive procedures. Main Outcome Measures Mortality, extent of debridement, preoperative vital signs and laboratory values, Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, bacteriologic and pathologic test results. Results Postoperatively, all patients were housed in the intensive care unit for 8.4±14.5 days. Six patients died (20%). On arrival at the intensive care unit, systolic blood pressure was 80 mm Hg or less in 2 patients, 1 of whom died. White blood cell count on hospital admission was elevated in 27 of 30 patients (mean, 27.2±15.3×109/L) and 2 patients were identified as having human immunodeficiency virus infection. All patients underwent initial surgery less than 24 hours after admission; following debridement, the average wound size was 276±238 cm2 (range, 15-783 cm2). Five patients required extremity amputation, and all other survivors underwent reconstruction with skin grafts and/or myocutaneous flaps. All but 1 patient were reexamined in the operating room within 12 hours and underwent an average of 3.1±1.6 operative procedures. Of those wound cultures obtained in the operating room, there was no pattern to the bacteriologic isolates. Seventeen patients had mixed isolates and 11 had single organisms. Pathologic findings in 20 patients included panniculitis (3 patients), necrotizing fasciitis (11 patients), myositis (6 patients), and osteomyelitis (1 patient). We failed to identify any clinical factor, including temperature, heart rate, systolic blood pressure, white blood cell count, base deficit, albumin level, PO2, or APACHE II score that could predict mortality or the requirement for extensive debridement. Conclusions Parenteral injections of illicit drugs can produce infections that present with signs of simple cutaneous abscess and yet unpredictably become extensive necrotizing soft tissue infections. Treatment requires a high index of suspicion along with an inquisitive operative approach to avoid missing these potentially serious infections.
Objective: The aim of this prospective study was to evaluate whether early thoracic computed tomography (TCT) is superior to routine chest x-ray (CXR) in the diagnostic work-up of blunt thoracic trauma and whether the additional information influences subsequent therapeutic decisions on the early management of severely injured patients. Patients and methods: In a prospective study of 103 consecutive patients with clinical or radiologic signs of chest trauma (94 multiple injured patients with chest trauma, nine patients with isolated chest trauma), an average Injury Severity Score of 30 and an average Abbreviated Injury Scale thorax score of 3, initial CXR and TCT were compared after initial assessment in our emergency department of a Level I trauma center. Results: In 67 patients (65%) TCT detected major chest trauma complications that have been missed on CXR (lung contusion (n = 33), pneumothorax (n = 27), residual pneumothorax after chest tube placement (n = 7), hemothorax (n = 21), displaced chest tube (n = 5), diaphragmatic rupture (n = 2), myocardial rupture (n = 1)). In 11 patients only minor additional pathologic findings (dystelectasis, small pleural effusion) were visualized on TCT, and in 14 patients CXR and TCT showed the same pathologic results. Eleven patients underwent both CXR and TCT without pathologic fundings. The TCT scan was significantly more effective than routine CXR in detecting lung contusions (p < 0.001), pneumothorax (p < 0.005), and hemothorax (p < 0.05). In 42 patients (41%) the additional TCT findings resulted in a change of therapy: chest tube placement, chest tube correction of pneumothoraces or large hemothoraces (n = 31), change in mode of ventilation and respiratory care (n = 14), influence on the management of fracture stabilization (n = 12), laparotomy in cases of diaphragmatic lacerations (n = 2), bronchoscopy for atelectasis (n = 2), exclusion of aortic rupture (n = 2), endotracheal intubation (n = 1), and pericardiocentesis (n = 1). To evaluate the efficacy of all those therapeutic changes after TCT the rates of respiratory failure, adult respiratory distress syndrome, and mortality in the subgroup of patients with Abbreviated Injury Scale thorax score of > 2 were compared with a historical control group, consisting of 84 patients with multiple trauma and with blunt chest trauma Abbreviated Injury Scale thorax score of > 2, prospectively studied between 1986 and 1992. Age (38 vs. 39 years), average Injury Severity Score (33 vs. 38), and the rate of respiratory failure (36 vs. 56%) were not statistically different between the two groups, but the rates of adult respiratory distress syndrome (8 vs. 20%; p < 0.05) and mortality (10 vs. 21%; p < 0.05) were significantly reduced in the TCT group. Conclusions: TCT is highly sensitive in detecting thoracic injuries after blunt chest trauma and is superior to routine CXR in visualzing lung contusions, pneumothorax, and hemothorax. Early TCT influences therapeutic management in a significant number of patients. We therefore recommend TCT in the initial diagnostic work-up of patients with multiple injuries and with suspected chest trauma because early and exact diagnosis of all thoracic injuries along with sufficient therapeutic consequences may reduce complications and improve outcome of severely injured patients with blunt chest trauma.
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The purpose of this paper was to describe some instances in which there may be loss of electromotive force (emf) from myocardial tissue without biologic death of the tissue. Myocardial tissue which is electrically inactive although viable is considered to be electrically silent. Electrically silent myocardial tissue may, under the proper circumstances, regain electrical activity. The development of areas of electrical silence within the myocardium may be associated with electrocardiographic alterations, particularly pathologic Q waves. Such Q waves disappear after the area of electrical silence recovers. It is important to recognize the fact that loss of cardiac emf is not synonymous with tissue death. Judgment concerning the extent of a myocardial infarction or the significance of pathologic Q waves (or other changes in the QRS complex) in patients with tachycardia, angina pectoris, or electrolyte disturbances should take into consideration the possibility of the presence of electrically silent areas. Furthermore, awareness of the electrocardiographic alterations associated with electrically silent areas of myocardium provides an understanding of some difficult electrocardiographic problems and makes it unnecessary to invoke alterations in rotation, position, or sequence of depolarization to explain electrocardiographic findings which do not correlate with the autopsy data.
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SummaryOBJECTIVES To evaluate an immunofluorescence antibody test (IFAT) for diagnosis of schistosomiasis in nonimmune travellers and immigrants from endemic areas. METHODS 65 patients (48 Danes and 17 immigrants) with schistosomiasis were included. The diagnosis of schistosomiasis was based on the presence of schistosome eggs in faeces, urine, sperm, rectal or bladder biopsies and/or the presence of specific antibodies determined by the serological immunofluorescence antibody test (IFAT). Egg excretion was detected using conventional methods and the IFAT performed on whole S. mansoni schistosomula worms, harvested after 8 weeks from mice. Two patterns of immunofluorescence were observed: Fluorescence in the gut of the schistosome called ‘Gut Associated Antigen, GAA’, and fluorescence of the surface of the schistosomula called ‘Membrane Bound Antigen, MBA’. RESULTS Eggs were found in 44% of the Danish patients and in 76% of immigrants. The diagnosis was based on a positive IFAT in 48% of the patients. In patients from nonendemic areas, the finding of antibodies against GAA was diagnostic while optimal sensitivity in the immigrants was reached by measuring antibodies against both GAA and MBA. CONCLUSION In patients from nonendemic areas GAA is a sensitive marker of acute infection with schistosomiasis. In patients from endemic areas the demonstration of both GAA and MBA is necessary to properly identify long-lasting, nonacute infections. Egg-detection and/or measurement of CAA and CCA remain the methods of choice to monitor treatment as the immunofluorescence assay may remain positive for several years after treatment.
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Summary In a Schistosoma haematobium-endemic village in western Madagascar we evaluated ultrasonography and Eosinophil Cationic Protein (ECP) in urine as means to detect the associated urinary tract pathology. 192 individuals were matched according to age and sex, and grouped into infected persons with bladder and, if present, kidney pathology (n= 96); infected persons without pathology (n= 48) and noninfected persons without pathology (n= 48). The median urinary egg count was significantly higher in individuals with ultrasonographically detectable urinary tract pathology (115 eggs/10 ml urine) than in infected persons without (45 eggs/10 ml of urine). At 136 ng/ml, the median ECP level was significantly higher in the 144 infected individuals than in the 48 noninfected persons (0.35 ng/ml). Egg excretion correlated positively with ECP level. The median ECP level was significantly higher in the group with ultrasonographically detectable urinary tract pathology than in the group without (183 ng/ml vs. 67 ng/ml). The results suggest that minor degrees of pathology, particularly at an early stage of infection with S. haematobium, might be overlooked by ultrasonography despite the presence of marked inflammation, as indicated by markedly increased urinary ECP levels in infected individuals without ultrasonographically detectable urinary tract pathology. ECP may therefore provide important information on the evolution of S. haematobium-associated urinary tract morbidity.
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Emergency physicians often encounter wide-QRS-complex tachyarrhythmias, which pose both a diagnostic and therapeutic challenge. Most such rhythms are the result of ventricular tachycardia (VT) related to coronary artery disease. However, the spectrum of VT is broad, with several distinct clinical entities, some of which are benign in their clinical course. Idiopathic fascicular VT is one such entity. We present two cases of idiopathic fascicular VT and discuss the unique electrocardiographic, electrophysiologic, and electropharmacologic properties that make it an identifiable and treatable arrhythmia in the ED.
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We report four cases of occult pneumothorax in patients who had suffered blunt trauma. In each case supine chest X-rays failed to diagnose an anterior pneumothorax. Subsequent spiral computerised tomography scans of the chest showed anterior pneumothoraces in all cases. In two of the cases anterior pneumothoraces were present in spite of a chest drain having been placed in the pleural cavity. We recommend the insertion of anteriorly positioned chest drains to relieve pneumothoraces in severely injured trauma patients.
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In the United States of America, seafood ranked third on the list of products which caused foodborne disease between 1983 and 1992. Outbreaks connected with fish vectors were caused by scombroid, ciguatoxin, bacteria and unknown agents; in shellfish, unknown agents, paralytic shellfish poisoning, Vibrio spp. and other bacteria, followed by hepatitis A virus, were responsible for the outbreaks. At least ten genera of bacterial pathogens have been implicated in seafood-borne diseases. Over the past twenty-five years, bacterial pathogens associated with faecal contamination have represented only 4% of the shellfish-associated outbreaks, while naturally-occurring bacteria accounted for 20% of shellfish-related illnesses and 99% of the deaths. Most of these indigenous bacteria fall into the family Vibrionaceae which includes the genera Vibrio, Aeromonas and Plesiomonas. In general, Vibrio spp. are not associated with faecal contamination and therefore faecal indicators do not correlate with the presence of Vibrio. Viruses are the most significant cause of shellfish-associated disease: in New York State, for example, 33% and 62% of 196 outbreaks between 1981 and 1992 were caused by Norwalk virus and gastrointestinal viruses (small round structured viruses), respectively. In addition, several illnesses are a result of toxic algal blooms, the growth of naturally occurring bacteria and diatoms causing neurotoxic shellfish poisoning, paralytic shellfish poisoning, diarrhoetic shellfish poisoning, amnesic shellfish poisoning and ciguatera. Current estimates place the annual number of ciguatera cases at 20,000 world-wide. Scombroid poisoning is the most significant cause of illness associated with seafood. Scombrotoxin is of bacterial origin and halophilic Vibrio spp. causing high histamine levels are implicated as the source. Scombroid poisoning is geographically diverse and many species have been implicated, namely: tuna, mahi-mahi, bluefish, sardines, mackerel, amberjack and abalone. Temperature abuse has been cited as a major cause of scombroid poisoning. For routine work, the use of faecal indicators to predict the relative level of faecal contamination should not be disposed of. However, the main source of seafood illness is due to species which are not predicted by these organisms. In order to protect public health, routine surveillance using new pathogen-specific techniques such as polymerase chain reaction should be used. This, in combination with risk assessment methods and hazard analysis and critical control points, will begin to address the need for improvement in the safety of seafood.
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This chapter discusses about histamine toxicity from fish products, often called scombroid poisoning, generally involves the ingestion of scombroid fish from the families Scomberesocidae and Scombridae. Scombroid fish include saury, tuna, bonito, seerfish, butterfly kingfish, and mackerel. The free histidine can, under certain conditions, be decarboxylated by some bacteria to produce high levels of histamine. Scombroid fish poisoning clinically resembles that of histamine poisoning intoxication, although controversy still exists as to whether histamine ingested orally is actually toxic, whether histamine is the sole toxic factor or not. It is generally found at high concentrations in foods causing scombroid poisoning. “Samma sakuraboshi” was incriminated in many of the Japanese histamine and histamine–like fish poisonings. The incriminated fish generally contains histamine levels in excess of 100 mg%. No fish could be obtained for chemical analysis, but the outbreak was presumed to be caused by bacterial degradation of histidine to histamine. It is most likely that the histamine produced by autolysis was because of previous bacterial contamination or unsterile conditions during experimentation, thus enabling histamine production by the contaminating microorganisms. However, the use of ammonia levels as a freshness indicator becomes unreliable when fish are kept at a room temperatures of 20°C. Several studies of bacterial histidine decarboxylase have indicated that the addition of vitamins and coenzymes did not enhance histamine formation. Histamine formation in aerated cultures, achieved by the addition of bubbled gas, was much less than that from anaerobic and aerobic cultures.
Article
The manifestations of scombroid fish poisoning closely resemble those of a histamine reaction and include nausea, abdominal pain, diarrhoea, flushing, headache, rashes, vomiting, palpitations, and pruritus. In severe cases burning of the mouth, dizziness, and respiratory distress have been reported. The onset is rapid - a few minutes to a few hours - and recovery is usually complete four to eight hours later. One death only was reported in three series totalling 1660 cases. The toxins are formed by the action of contaminating bacteria on fish muscle, which in scombroid fish is particularly rich in histidine. Histidine is decarboxylated by bacterial enzymes to histamine at temperatures between 20 and 30°C. Fish with histamine concentrations of 100 mg or more/100 g of flesh are usually toxic. Nevertheless as Aiso (cited by Halstead) has shown that 450 to 500 mg of histamine taken by mouth by human volunteers evoked no response at all, the true nature of scombrotoxin remains unknown, though antihistamines have been shown to give symptomatic relief. The fish referred to in our report may have contained up to 250 mg of histamine. Though few bacteria were found at examination, bacterial growth presumably occurred before and perhaps after the demonstrably inadequate curing. Prevention is a matter of adequate refrigeration or preservation as soon after catching as possible. Though most affected fish appear normal, those showing any putrefactive changes around the gills or tasting sharp or peppery, whether cooked or uncooked, should be discarded. 4 cases are reported.
Article
The roentgenographic finding hepatic--portal venous gas (HPVG) has been reported extensively in the pediatric and radiology literature. The surgical implications and clinical significance have yet to be fully defined. This study reviews the 60 reported cases in the literature and adds four new cases. HPVG appears as a branching radiolucency extending to within 2 cm of the liver capsule. HPVG is associated with necrotic bowel (72%), ulcerative colitis (8%), intra abdominal abscess (6%), small bowel obstruction (3%), and gastric ulcer (3%). Mucosal damage, bowel distention and sepsis predispose to HPVG. The current mortality rate of 75% represents an improvement from previous experience. Analysis of survivors indicates that the finding of HPVG requires urgent surgical exploration except when it is observed in patients with stable ulcerative colitis.
Article
The peroral toxicity of histamine in the guinea-pig is shown to be potentiated by simultaneous administration of cadaverine. Toxic effects are observed with relative cadaverine-histamine levels that are similar to those found in scombrotoxic fish. On the basis of currently available evidence, it seems likely that cadaverine, along with histamine, is of importance in the aetiology of scombroid poisoning.
Article
A prospective and cross-sectional study was carried out in various communities in Kwara State, Nigeria, to access the status and implications of urinary schistosomiasis among schoolchildren. Of 425 pupils examined in nine communities, 193 (45.4%) were infected. Infection rates for boys (44.7%) and girls (47.9%) were not significantly different (p greater than 0.5). Children between 11 and 13 years of age had the highest incidence rates (33.6%). However, the percentage of children (25.9%) excreting at least 1000 eggs per 10 ml of urine sample during their first decade of life was significantly higher (p less than 0.01) than for older pupils. The health implications of schistosomiasis acquired early in life, as in this study, are highlighted in the discussion.
Interleukin-1 (IL-1) has been previously shown to stimulate prostaglandin E2 (PGE2) production by osteoblastic cells. This IL-1 effect has also been shown to be potentiated by parathyroid hormone (PTH), which activates both the calcium and the cAMP signal transduction pathways in osteoblastic cells. In the present study, the role of calcium, calmodulin, and cAMP in potentiating the IL-1 effect was examined. The calcium channel blocker verapamil (100 microM) completely inhibited the IL-1 effect. Similarly, the calmodulin antagonist W-7 (50 microM) inhibited the IL-1-induced stimulation. Conversely, the calcium ionophore A23187 (0.1 microM) potentiated the IL-1 effect. The phosphodiesterase inhibitor isobutyl-methylxanthine (IBMX; 100 microM), which elevates cAMP levels in the cells, had a strong potentiating effect on the IL-1-induced PGE2 production. These results suggest that both the calcium and the cAMP second messenger systems can modulate the IL-1 effect on osteoblastic cells.
Article
The 1-year follow-up data of a multicenter randomized controlled trial of methylprednisolone (30 mg/kg bolus and 5.4 mg/kg/hr for 23 hours) or naloxone (5.4 mg/kg bolus and 4.0 mg/kg/hr for 23 hours) treatment for acute spinal cord injury are reported and compared with placebo results. In patients treated with methylprednisolone within 8 hours of injury, increased recovery of neurological function was seen at 6 weeks and at 6 months and continued to be observed 1 year after injury. For motor function, this difference was statistically significant (p = 0.030), and was found in patients with total sensory and motor loss in the emergency room (p = 0.019) and in those with some preservation of motor and sensory function (p = 0.024). Naloxone-treated patients did not show significantly greater recovery. Patients treated after 8 hours of injury recovered less motor function if receiving methylprednisolone (p = 0.08) or naloxone (p = 0.10) as compared with those given placebo. Complication and mortality rates were similar in either group of treated patients as compared with the placebo group. The authors conclude that treatment with the study dose of methylprednisolone is indicated for acute spinal cord trauma, but only if it can be started within 8 hours of injury.
Article
The highest morbidity worldwide from fish poisoning results from the ingestion of spoiled scombroid fish, such as tuna and mackerel, and its cause is not clear. Histamine could be responsible, because spoiled scombroid fish contain large quantities of histamine. Whether histamine is the causative toxin, however, has remained in question. To address this issue, we investigated whether histamine homeostasis is altered in poisoned people. The urinary excretion of histamine and its metabolite, N-methylhistamine, was measured in three persons who had scombroid-fish poisoning (scombrotoxism) after the ingestion of marlin. We measured 9 alpha, 11 beta-dihydroxy-15-oxo-2,3,18,19-tetranorprost-5-ene-1,20-dioic acid (PGD-M), the principal metabolite of prostaglandin D2, a mast-cell secretory product, to assess whether mast cells had been activated to release histamine. The fish contained high levels of histamine (842 to 2503 mumol per 100 g of tissue). Symptoms of scombrotoxism--flushing and headache--began 10 to 30 minutes after the ingestion of fish. In urine samples collected one to four hours after fish ingestion, the levels of histamine and N-methylhistamine were 9 to 20 times and 15 to 20 times the normal mean, respectively. During the subsequent 24 hours, the levels fell to 4 to 15 times and 4 to 11 times the normal values. Levels of both were normal 14 days later. PGD-M excretion was not increased at any time. Two persons treated with diphenhydramine had prompt amelioration of symptoms. Scombroid-fish poisoning is associated with urinary excretion of histamine in quantities far exceeding those required to produce toxicity. The histamine is most likely derived from the spoiled fish. These results identify histamine as the toxin responsible for scombroid-fish poisoning.
Article
We retrospectively reviewed abdominal CT and plain film findings in 23 proved cases of mesenteric infarction to compare the value of the two techniques. Criteria considered specific for infarction on CT were identified in nine (39%) of 23 patients and comprised pneumatosis in seven patients (30%), mesenteric or portal venous gas in three patients (13%), and focally thick-walled bowel in two patients (9%). Criteria considered specific for bowel infarction on plain films were identified in seven (30%) of 23 patients and comprised focally edematous bowel in six patients (26%) and pneumatosis intestinalis in one patient (4%). Only one patient had specific changes on both CT and plain films, but 15 (65%) of the 23 showed specific changes on at least one study. The results indicate that plain films remain an important tool in patients suspected of mesenteric infarction and can provide information that is complementary to CT. Also, as both studies were nonspecific in eight (35%) of our patients, negative or nonspecific findings should not deter further diagnostic or interventional procedures in patients in whom the clinical suspicion of bowel infarction is high.
Article
Calcium channel blockers are recently developed antihypertensive drugs. In terms of mechanisms of action, their specificity is not so well established as that of angiotensin converting enzyme inhibitors but is better understood than that for diuretics or adrenergic-inhibiting drugs. Calcium channel blockers were originally developed for treatment of angina but were found to lower arterial pressure as well. Three of them are now in wide use in the United States; their therapeutic spectrum in regard to type of hypertension is broad. Sublingual nifedipine has replaced intravenously administered vasodilators as immediate treatment of severe hypertension, and all three drugs, given orally, have been shown to be effective in mild, moderate, and severe hypertension. The three drugs available in this country are verapamil, diltiazem, and nifedipine. Pharmacological studies have shown that verapamil has the most negative chronotropic and inotropic effects of the three, with nifedipine producing the most vasodilation and having the potential for causing reflex tachycardia. Actually in practice, these various pharmacological differences have proved to have less significance than previously thought, and the drugs seem to have about equal antihypertensive effectiveness. Comparisons of calcium entry blockers with other drugs have shown them to be equally effective in whites as propranolol but more effective in blacks. Responsiveness appears to be related, as well, to pretreatment plasma renin activity and age. Thus, the antihypertensive effect is directly related to age and inversely related to plasma renin activity. The side effects mostly relate to vasodilation, reflex tachycardia, palpitations, headache, and edema; they are not frequent, and the drugs are well tolerated.
Article
The immune response was assessed in 13 competitive bodybuilders self-administering anabolic-androgenic steroids and ten competitive bodybuilders not administering these drugs. Laboratory assessment included the number and relative distribution of T-cells, T-helper/inducer cells, T-cytotoxic/suppressor cells, activated T-cells, lymphocyte transformation to the mitogens, pokeweed mitogen (PWM), phytohemagglutinin (PHA), Concanavalin-A (CON-A), Staphylococcus aureus Cowan strain I (SAC), serum immunoglobulins, and natural killer (NK) activity. There were no significant differences in T-cell subsets among steroid users and non-users, but lymphocyte transformation studies revealed that the anabolic-androgenic steroid-using group had enhanced proliferative ability to the B-cell mitogen, SAC, in comparison to non-bodybuilding controls. NK activity was significantly (P less than 0.05) augmented in the anabolic-androgenic steroid users but not in the non-using bodybuilders. Serum immunoglobulin levels, in particular IgA, were significantly (P less than 0.017) lower in the steroid-using group. Four of 13 steroid users and three of eight non-steroid-using bodybuilders had detectable antinuclear antibodies. These studies indicate that 1) anabolic-androgenic steroid use as practiced by contemporary athletes is a potent modulator of immune responsiveness and 2) autoantibodies are prevalent in strength-trained men even in the absence of anabolic steroid use.
Article
At present nitrates remain the initial treatment for relief or prevention of angina in patients with coronary artery disease. In cases where nitrates and beta blockers have been used and are ineffective for managing effort angina, calcium antagonists may be substituted or added to the beta-blocking treatment. When the predominant symptom is rest angina, and there is evidence suggesting coronary artery spasm, nitrates and a calcium antagonist can be effective therapy. In patients with heart block, bradyarrhythmias, heart failure, or hypertension nifedipine may be the drug of choice. In contrast verapamil merits choice when supraventricular tachycardia is present. Diltiazem appears intermediate between nifedipine and verapamil and may be particularly useful when hypotension or other side effects must be avoided.
Article
Hemodynamic stability during wide QRS tachycardia is commonly, albeit erroneously, taken as evidence for a supraventricular mechanism. To determine the magnitude for potential misdiagnosis in applying this notion clinically, we analyzed 20 consecutive cases of regular wide QRS tachycardia in conscious adult patients (mean age, 64 years). The most common heart disease was atherosclerotic (75%), with an associated history of remote myocardial infarction in 73% of the cases. Tachycardia was sustained for a mean of 4.8 hours prior to medical evaluation, with a mean rate of 186 beats per minute and mean systolic blood pressure of 111 mm Hg. A diagnosis of ventricular tachycardia (VT) was established in 17 cases (85%). In the patients with VT, atrioventricular dissociation was recognized on the 12-lead electrocardiogram in 38%, with Wellens' morphological features favoring the diagnosis in 73%. Following conversion to sinus rhythm, electrophysiological testing in 17 patients reproduced the clinical arrhythmia in 94% (with a replication rate of 100% in 15 patients with VT), with at least one additional unsuspected VT morphology induced in 53% of patients with VT. Thus, VT should be considered the most likely cause of regular wide QRS tachycardia in the conscious adult patient, especially with a history of remote myocardial infarction. Recognition of this simple principle and careful examination of the 12-lead electrocardiogram may help to prevent the misapplication of pharmacotherapy in the vast majority of these patients. (JAMA 1989;261:1013-1016)
Article
Despite available criteria, diagnosis of the mechanisms of wide complex tachycardia is often incorrect. We aimed in this study to identify reasons for misdiagnoses and the value and limitations of clinical and surface electrocardiographic criteria. The analyzed data of 150 consecutive patients with wide QRS tachycardia from this study and a literature search of key papers in English since 1960 on clinical and surface electrocardiographic criteria form the basis of this report. The final correct diagnosis was made with intracardiac electrograms. Among the 150 patients, 122 had ventricular tachycardia, 21 had supraventricular tachycardia with aberrant conduction, and 7 had accessory pathway conduction. Only 39 of 122 patients with ventricular tachycardia were correctly diagnosed initially. In others, the diagnoses were supraventricular tachycardia with aberrant conduction (43 of 122) or simply a wide QRS tachycardia (40 of 122). Misdiagnosis in patients with aberrant or accessory pathway conduction was also common. Standard electrocardiographic criteria for ventricular tachycardia had unacceptable sensitivity, poor specificity, or both. Collectively such criteria allowed a correct diagnosis of ventricular tachycardia in 92% of cases. Diagnosis of ventricular tachycardia was also suggested by its association with structural heart disease. Criteria suggestive of ventricular tachycardia included atrioventricular dissociation, positive QRS concordance, axis less than -90 deg to +/- 180 deg, combination of left bundle branch block and right axis, QRS duration of greater than 140 ms with right bundle branch block and greater than 160 ms with left bundle branch block and, a different QRS during tachycardia compared to baseline preexisting bundle branch block. Ventricular tachycardia is the commonest underlying mechanism for wide QRS tachycardia. A correct diagnosis can usually be made from clinical and surface electrocardiographic criteria.
Article
Calcium channel blocking drugs are a chemically heterogenous group, so it might be expected that their effects on vascular smooth muscle, cardiac contractility, and conduction tissue may differ. However, the majority of adverse reactions are predictable from their pharmacological actions and may be conveniently grouped in the following categories: 1) vasodilatation, 2) negative inotropic effects, 3) conduction disturbances, 4) gastrointestinal effects, 5) metabolic effects, and 6) drug interactions. Vasodilatory symptoms, namely, dizziness, headaches, flushing sensation, and palpitation, are more likely with nifedipine. Peripheral edema is also common with nifedipine, but the mechanism is uncertain. For a given degree of vasodilation, the greatest negative inotropic effect is seen with verapamil first, diltiazem second, and nifedipine last. Calcium channel blocking drugs are contraindicated in hypertensive patients with second and third degree heart block, sick sinus syndrome, and severe heart failure. Verapamil and diltiazem have a significant effect on cardiac conduction, whereas nifedipine, in therapeutic doses, does not. Local gastrointestinal symptoms, such as nausea and constipation, are common with verapamil. None of the calcium channel blocking drugs have been reported to adversely affect lipid or protein metabolism. However, nifedipine, verapamil, and diltiazem in high doses may inhibit liberation of insulin. The significance of this finding needs to be explored further in hypertensive diabetics. Serum digoxin levels have been shown to increase after administration of verapamil and nifedipine, but there is no evidence that this change has any clinical relevance.(ABSTRACT TRUNCATED AT 250 WORDS)
If a patient has vision immediately following trauma, with subsequent deterioration of visual acuity and/or field, and the presence of a relative afferent pupillary defect, compression of the optic nerve or its vascular supply is very likely. We currently lack a proven optimal treatment, but in the otherwise healthy patient, we suggest an intravenous (IV) loading dose of methylprednisolone 30 mg/kg, and a second 15-mg/kg dose 2 hours after the initial dose, followed by 15 mg/kg every 6 hours. Optic nerve decompression is indicated in this situation when corticosteroids have only a temporary effect, a diminishing one, or none at all. It may also be indicated when there is evidence of a traumatic optic neuropathy with a fractured or narrowed optic foramen or with dislocated bone fragments that directly impinge on the nerve. Optic nerve sheath decompression is indicated in progressive traumatic optic neuropathy when an enlarged fluid-filled sheath has been demonstrated sonographically.
Article
Electrophysiologic studies were performed in 16 patients 11 to 45 years old (mean 33 years) with idiopathic sustained (lasting more than 5 min) ventricular tachycardia (VT) originating from the left ventricle. Endocardial mapping during VT showed that the earliest site of activation was at the apical inferior portion of the left ventricle in 14 patients whose QRS morphology during VT showed a right bundle branch block pattern and left-axis deviation, but at the apical anterosuperior portion of the left ventricle in two patients whose QRS morphology during VT showed a right bundle branch block and right-axis deviation. Single programmed ventricular stimulation induced VT in 13 patients, and rapid ventricular pacing induced VT in the remaining three patients. Rapid ventricular pacing terminated VT in all patients. The relationship between the coupling interval and the echo interval was inverse in all eight patients with a wide VT inducible zone. Entrainment was recognized in three of six patients. The initiation of VT by constant pacing depended on the number of pacing beats but not the duration of pacing in all four patients tested. Intravenous verapamil terminated the VT in 13 of 14 patients. Long-term oral verapamil was also effective in all five patients who required long-term oral therapy for their symptoms associated with VT. In conclusion (1) idiopathic left ventricular tachycardia has unique electrocardiographic, electrophysiologic, and electropharmacological properties, (2) the electrophysiologic characteristics suggest that the mechanism is reentry, and (3) verapamil is effective in both the short- and long-term treatment of VT.
Article
Differential diagnosis between acute myocardial infarction (AMI) and an acute surgical abdomen can be difficult. Although the electrocardiogram (ECG) is the most valuable immediate tool in this differential diagnosis, it is crucial to be aware of certain limitations of the ECG under these circumstances. This report describes a patient presenting with electrocardiographic changes consistent with a Q-wave AMI, a perforated duodenal ulcer, and no evidence of AMI or significant coronary artery narrowing at necropsy.
Article
We describe accidental Hemlock Water Dropwort poisoning in four adults, who ate Hemlock tubers, mistaking them for celery. The patients described almost certainly survived because they boiled the tubers, inactivating Oenanthotoxin, the active principle.
Article
The May 1986 Mt. Hood climbing disaster presented Portland area hospitals the opportunity to initiate a trial of extracorporeal rewarming using cardiopulmonary bypass in ten severely hypothermic patients (two survivors). The data from this experience as well as others previously reported can yield prognostic indicators of survival in cases of accidental hypothermia. These are demonstrated to include: the presence of underlying medical illness, duration of cold exposure, initial core temperature, mental status, the presence of spontaneous respirations, presenting cardiac rate and rhythm, and arterial oxygen tension. Profound hyperkalemia and markedly elevated serum ammonia levels indicate cell lysis; significant hypofibrinogenemia suggests intravascular thrombosis and each laboratory marker predicts a dire outcome. The treatment of choice for severe accidental hypothermia is felt to be rapid core rewarming on cardiopulmonary bypass.
Article
Severe plant poisoning is relatively uncommon in adults. We report two adults who ingested hemlock water dropwort roots, having mistaken them for wild parsnip. One developed prolonged convulsions, severe metabolic acidosis and respiratory distress requiring mechanical ventilation. The toxin--oenanthotoxin--was detected in the gastric aspirate and measured by high performance liquid chromatography.
Article
Five persons who attended a medical conference developed symptoms suggestive of an intoxication after a common meal. Although the symptoms were recognized as typical of scombroid poisoning, no fish of the Scrombridae family had been served. However, food histories implicated bluefish (Pomatomus saltatrix). The initially frozen bluefish had been improperly handled in storage and thawing. Elevated levels of histamine, putrescine, and cadaverine were detected in uncooked samples. This outbreak emphasizes that scombroid-type poisoning (1) can be caused by nonscombroid fish such as bluefish, (2) is probably more common than currently recognized, and (3) may become even more widespread as fish become a larger part of our diet. Physicians who work in conjunction with public health officials can help prevent additional cases and outbreaks.
Article
The extent and consequence of misdiagnosis of wide complex tachycardia (QRS, 120 ms or more; heart rate, 100 or more beats/min) presenting emergently were assessed. Forty-six consecutive episodes of wide complex tachycardia were reviewed and their tachycardia mechanisms subsequently established. All 8 episodes of supraventricular tachycardia with aberrant conduction were correctly diagnosed, whereas 15 of 38 episodes of ventricular tachycardia (39%) were misdiagnosed as supraventricular tachycardia at the time initial therapy was given. Ventriculoatrial dissociation was evident in 11 (73%) of the electrocardiograms of misdiagnosed ventricular tachycardia. Patients with misdiagnosed episodes had poorer outcomes than those with episodes correctly diagnosed (p = 0.0003). Verapamil was administered to patients in 13 of the 15 episodes of misdiagnosed ventricular tachycardia; hemodynamic deterioration occurred in all 13 episodes. Wide complex tachycardia is often incorrectly diagnosed as supraventricular tachycardia when, in fact, the 12-lead electrocardiogram strongly suggests ventricular tachycardia. Verapamil is commonly administered in these circumstances and is frequently associated with a poor outcome.
Article
Two patients are presented who, under conditions of shock and severe metabolic stress, manifested transient Q waves in their electrocardiograms simulating myocardial infarction. The absence of clinical features and enzyme elevations as well as the transient nature of the electrocardiographic changes deny the likelihood of true infarction. Other clinical situations associated with this phenomenon are briefly reviewed and the concept of electrically silent areas of myocardium, without cell death, is discussed as an explanation.
Article
Extraperitoneal gas may be produced by perforation of the descending duodenum, sigmoid diverticula, or rectum, pancreatic or perirenal infection, or extraperitoneal gas of subdiaphragmatic origin, and displays a characteristic spread and localization depending upon its source. The author describes the anatomy of the extraperitoneal fascial planes and compartments and discusses the basic roentgen features of extraperitoneal gas and its distinction from intraperitoneal collections.