Puffer fish poisoning in Madagascar: four case reports

An outbreak of puffer fish poisoning in a family with four cases of which one was fatal is reported. The outbreak occurred in July 1998 in Nosy Be, an island located at the north-western part of Madagascar. Diagnostic investigation with application of the mouse bioassay suggested poisoning with a tetrodotoxin as the etiology. The amount of the toxin was 16 MU (mouse unit) per gram meal. A continuing surveillance of the seafood intoxications either in the country or in the west Indian Ocean region is needed.     

Variations in symptomatology of ciguatera poisoning

Ciguatera poisoning reports were examined for patterns of symptomatology when different types of fishes were consumed. Consumption of surgeon fish (Ctenochaetus strigosus), amberjack (Seriola dumerili) and jack (Caranx sp.) resulted in different symptom profiles with a number of statistically significant differences in the reported frequencies of specific symptoms. The results support the contention that the large variability in symptoms associated with ciguatera poisoning is caused by several closely related but distinct toxins.     

Severe carbon monoxide poisoning treated by hyperbaric oxygen therapy--a case report

Carbon monoxide (CO) poisoning is an important cause of mortality and late neurological sequelae such as memory loss, personality changes, psychosis, dementia, and so on. The benefits of hyperbaric oxygen (HBO) therapy are still discussed, but the majority of trials recommend it in severe cases with coma and/or hemodynamic instability, irrespective of carboxyhemoglobin (COHb) level, to prevent permanent neurological deficits. We present a 35-yr-old woman who underwent accidental CO poisoning. Although breathing 100% oxygen by mask during transfer to the hospital, she was in deep coma, hypotensive, cyanotic, and hypoxic (arterial pO(2) 7,41 kPa, HbO(2) 87.8%), with serum COHb 26.7% on hospital admission. Orotracheal intubation, mechanical ventilation, iv fluids, dobutamin, and norepinephrine were administered. COHb level decreased to 17.2% within 1 h. To prevent severe neurological sequelae, the patient was transferred as soon as possible to an HBO center 60 km distant to perform HBO therapy twice at 3.0 and once at 2.2 atm within 24 h. After the second HBO session, the patient regained consciousness, and respiratory failure and shock resolved. She was transferred to our hospital and discharged few weeks later with discrete paresis of peripheral nerves, discrete ischemic brain lesions on computed tomography (CT) scan, and moderately abnormal electroencephalogram (EEG) without cognitive disturbances. She was able to resume her daily activities. We conclude that in severe CO poisoning, normobaric oxygen therapy and resuscitation by fluids, inotropic agents, and catecholamines is essential for survival, but additional HBO therapy seems to prevent major neurological sequelae.     

Severe chlorate poisoning: Report of a case

A case of severe sodium chlorate poisoning was observed within 5 h after suicidal ingestion of 150–200 g of the herbicide. Methaemoglobinaemia was the early symptom of the intoxication. Treatment with methylene blue and ascorbic acid could not prevent a massive haemolysis with disseminated intravascular coagulation. Hypercoagulation and hyperfibrinolysis could be treated successfully with exchange transfusions, heparin and fresh plasma. During the first hours, 70 mmol chlorate were excreted before complete renal failure occurred which required haemodialysis for several weeks. Clinical observations and in vitro experiments provide evidence that methylene blue is effective only in the very early stages of chlorate poisoning. Consequently, the following treatment is suggested: gastric lavage, exchange transfusion, bicarbonate infusion, haemodialysis, anticoagulation with heparin and substitution of clotting factors if necessary.Dedicated to Prof. Gustav Adolf Martini on occasion of his sixty-fifth birthdayA preliminary report has been given at the Spring Meeting of the German Pharmacological Society, Mainz, March 1981     

Digoxin poisoning: case report.

Digoxin overdose leading to toxicity causes a variety of symptoms ranging from cardiovascular, gastrointestinal and central nervous system effects. Toxicity occurs at a serum level of 3.0ng/ml. The value of phenytoin sodium in treatment of digoxin toxicity is discussed.     

冰凉花中毒1例

1例42岁女性关节疼痛患者服用冰凉花煎剂(1ml相当2mg冰凉花)200ml,2次/d,共2d。患者出现头晕、心悸、黄视、恶心、呕吐。入院后,心电图监护显示心房扑动,Ⅱ度～Ⅲ度房室传导阻滞。经吸氧及对症治疗,第3天心电图恢复正常。     

Duboisia myoporoides: native antidote against ciguatera poisoning.

The leaves of Duboisia myoporoides collected in New Caledonia and preserved in alcohol up to the time of analysis contained the following alkaloids: nicotine, nornicotine, atropine and scopolamine. Various minor alkaloids reported by other authors in Australian D. myoporoides were not found in the plant material. The analyses were carried out with gas chromatography-mass spectrometry. The different results with New Caledonian and Australian D. myoporoides may be due to a difference in species, as suggested by Vaillant (Etude des teneurs en scopolamine et hyoscyamine des Duboisia myoporoides R. Br. cultivés en conditions artificielles. Thesis, University of Paris, 1972). Different conditions with regard to location, soil and climate do not seem sufficient explanation for the discrepancies. A review of the literature of ciguatera poisoning reveals that the manifestations only partly resemble those of anticholinesterase poisoning. Nevertheless, a mixture of atropine and PAM has been suggested for the treatment of the entity. In this context it is interesting to note that the natives of New Caledonia have already arrived at a powerful mixture of tropane and pyridinum alkaloids as an antidote.     

Organophosphate poisoning in pregnancy: a case report

A 42-year-old pregnant woman (26 weeks of gestation, G(4)P(0+3)) presented at the emergency department with a two-hour history of dizziness, blurred vision and repeated vomiting. These symptoms started during the use of an undiluted insecticide liquid (diazinon 60 EC) while cleaning a small non-aired bathroom. After clinical and laboratory confirmation for organophosphate poisoning (plasma pseudocholinesterase levels 161 U/l), treatment with atropine and pralidoxime was started. She recovered within 7 days and delivered a healthy baby 12 weeks later (Apgar score 9 and 10) by elective cesarean section. The child showed no signs or symptoms of organophospate, atropine or pralidoxime exposure.     

Chronicity of neurological features in ciguatera fish poisoning.

A 43-year-old woman complained of colicky abdominal pain, followed by numbness, myalgias, and muscle weakness in the four limbs after eating a grouper (Epinepheius spp.). She presented to our hospital 36 hours later with increased myalgias, muscle weakness, and malaise. On examination, the muscle power and sensation in her four limbs appeared to be normal. She was given an intravenous infusion of mannitol 20% (200 ml over 1 hour) and an intramuscular injection of diclofenac (75 mg). Her myalgias then improved and she was discharged. She presented to our hospital again 1 week later with poor appetite, malaise, numbness of the four limbs, and increased muscle weakness. On examination, the muscle weakness was more marked in the lower limbs (4+/5) than in the upper limbs (5-/5) and proximally than distally. She also had some difficulty in getting up from a squatting position. She was given another intravenous infusion of mannitol 20% (200 ml over 1 hour), following which there was subjectively slight improvement in her muscle weakness. Herplasma creatine phosphokinase level was normal. Electromyography performed 4 weeks later revealed no abnormalities. When she was reviewed 45 days after the consumption of the grouper, her muscle weakness and malaise had improved considerably. She could then stand up from a squatting position. However, mild impairment of finger grip was still present. Chronicity of neurological features in other reported cases (e.g., chronic fatigue, relapse of symptoms after exposure to ciguateric fish or alcohol, and peripheral neuropathy) may also indicate a lengthy persistence of ciguatoxins in the body.     

Vibrio parahaemolyticus-food poisoning: case report.

Symptoms of food poisoning occurred following the ingestion of raw shellfish purchased in the Auckland area. Vibrio parahaemolyticus was recoverer from the patient. The potential of this and closely related microorganisms to cause illness is reviewed.     

Gallium poisoning: a rare case report

The authors present a case of a college student who suffered acute gallium poisoning as a result of accidental exposure to gallium halide complexes. This is extremely rare and has never been reported in the literature. Acute symptoms after the incident, which initially presented as dermatitis and appeared relatively not life-threatening, rapidly progressed to dangerous episodes of tachycardia, tremors, dyspnea, vertigo, and unexpected black-outs. Had there been effective emergency medical care protocols, diagnostic testing, treatment and antidotes, the latent manifestations of irreversible cardiomyopathy may have been prevented. Given how quickly exposure led to morbidity, this article aims to raise an awareness of the toxic potential of gallium. This has particular relevance for workers involved in the production of semiconductors where there is a potential for accidental exposure to gallium by-products during device processing. It may also have implications for dentists who use gallium alloys to replace mercury containing amalgam. In the absence of threshold limit values and exposure limits for humans, as well as emergency medical guidelines for treatment of poisoning, the case calls on the National Institute for Occupational Safety and Health and the Occupational Safety and Health Administration to establish guidelines and medical management protocols specific for gallium.     

A case report of Nerium oleander poisoning in cattle

Nerium oleander leaves caused the death within 36 hours of 7 of 17 cattle which had access to boughs of the plant. Arrhythmia and auriculo-ventricular block at ECG were found in three cattle surviving on day 4. In one animal which died on day 4, postmortem examination revealed subendocardial and abomasal hemorrhages. Epidermic tissues of the leaves of N oleander were found in the rumen content. Recovery occurred in the three animals with marked cardiac signs.     

Acute selenium poisoning: case report.

A case of self-poisoning with sodium selenate sheep drench, along with blood and urine levels of selenium, is reported. Treatment included gastric lavage, diuresis, vitamin C, and dimercaprol, and the patient recovered without sequelae.     

Intentional paraquat poisoning: case report.

A case of intentional paraquat poisoning is presented. Early treatment was instituted. At four-month follow-up, the patient was well.     

A case of carbon monoxide poisoning with thrombus in the heart: a case report

Carbon monoxide is a nonirritant, odorless, colorless gas, and is lighter than air. It is an end product of the incomplete combustion of hydrocarbons. Its effects are most prominent in organs sensitive to oxygen deprivation, such as the heart, brain, and kidney. Carbon monoxide poisoning becomes more abundant in winter and at cold places. In Turkey, every year we see several deaths due to poisonous gas leaks from coal or wood stoves. Deaths particularly due to hypoxia-related central nervous system damage and ventricular dysrhythmias are observed. On the other hand, an association between thromboembolic accidents and carbon monoxide poisoning has been shown in literature. Thromboembolic accidents in the mesenteric, central nervous system, and extremities are reported. However, no atrial thrombus has been mentioned. In this study, a case of an atrial thrombus associated with carbon monoxide poisoning following a diagnosis of carbon monoxide poisoning and treatment in the emergency room is reported and the literature is revisited.     

Death camas poisoning in sheep: a case report

Approximately 250 sheep were poisoned and died from ingesting death camas (Zygadenus paniculatus) within a 2-day period on a foothill range in southeastern Idaho. Sixty to 70% of the poisoned sheep were 80-90 lb lambs and the rest were mature ewes. Poisonings were confirmed by field investigation, microhistological analysis of plant fragments from rumen contents of dead sheep, clinical signs, gross and microscopic analysis of tissues, and by experimentally feeding death camas collected on the poisoning site to 3 ewes at the Poisonous Plant Research Laboratory at Logan, UT. Clinical signs and gross and microscopic analysis of tissues were similar in ewes from the field investigation to those in ewes experimentally fed death camas. Ataxia, muscular weakness, trembling, incoordination, discharge of frothy saliva from the mouth and nose, vomition, dyspnea, collapse and death were the most common clinical signs. Gross changes included severe pulmonary congestion and subcutaneous hemorrhage. Microscopic lesions were those of severe pulmonary congestion.     

Treatment of ciguatera fish poisoning with amitriptyline and nifedipine

Ciguatera fish poisoning is the most common fish poisoning in the United States. Symptoms involve the gastrointestinal, cardiovascular and neurological systems. No known treatment exists. We explore the therapeutic effect of amitriptyline in two patients and nifedipine in one patient. Amitriptyline demonstrated resolution of most symptoms except for heat/cold reversal in one patient and heat/cold reversal, pruritus and headache in the second patient. We then used nifedipine in the second patient and noted only the resolution of his headaches. We recommend further study of these agents for the treatment of ciguatera fish poisoning.