Bluefish-associated scombroid poisoning. An example of the expanding spectrum of food poisoning from seafood

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.     

Was it something she ate? Case report and discussion of scombroid poisoning

WE REPORT THE CASE OF A 51-YEAR OLD WOMAN who developed headache, nausea, palpitations, tachycardia and hypertension 30 minutes after eating a tuna fish salad. Elevated histamine levels in the salad helped to confirm a suspected diagnosis of scombroid poisoning. The signs, symptoms, pathophysiology and management of poisoning from spoiled scombroid fish are discussed.     

Drug overdose--reducing the load.

OBJECTIVE: To review available information about various methods for reducing gastrointestinal absorption of a poison or drug. DATA SOURCES: Articles on overdose and accidental poisoning generated by the Australian Medlars Service and concentrating on the period between 1985 and 1990 were surveyed. Earlier studies were included if relevant. STUDY SELECTION AND DATA EXTRACTION: English language articles with an emphasis on studies using objective methods to measure individual and comparative efficacy of gastrointestinal decontamination techniques were selected. A total of 65 articles were reviewed. DATA SYNTHESIS: Gastric emptying procedures (gastric lavage or emesis caused by syrup of ipecac) are only effective if performed within one hour of drug ingestion. Gastric lavage is superior to syrup of ipecac. Oral administration of activated charcoal is more effective than either gastric emptying procedure, and is recommended for most cases of poisoning. Cathartics (sorbitol) can be used with activated charcoal. Whole bowel lavage with polyethylene glycol is indicated in selected cases of potentially lethal overdose where the toxic substance cannot be absorbed by charcoal and has passed the pylorus. CONCLUSIONS: Children--syrup of ipecac can be given at home to children older than 12 months. Most children who reach hospital can be treated by charcoal alone. ADULTS--Most patients are managed with supportive care and, in the absence of contraindications, a single dose of activated charcoal if seen within four hours of ingestion of the poison or drug. Gastric lavage is used if the patient presents within one hour of ingestion and has clinical features of toxicity.     

Delayed cyanide poisoning following acetonitrile ingestion.

Acetonitrile (methyl cyanide) is a common industrial organic solvent but is a rare cause of poisoning. We report the first recorded UK case. Acetonitrile is slowly converted to cyanide, resulting in delayed toxicity. We describe a case of deliberate self-poisoning by a 39-year-old woman resulting in cyanide poisoning 11 hours later which was successfully treated by repeated boluses of sodium nitrite and thiosulphate. The half-life of conversion of acetonitrile was 40 hours and harmful blood cyanide levels persisted for over 24 hours after ingestion. Departments treating or advising in cases of poisoning need to be aware of the delayed toxicity of acetonitrile. Monitoring in an intensive care unit of cases of acetonitrile poisoning should continue for 24-48 hours.     

The clinical features of migraine as a manifestation of allergic disease.

Patients with a clinical history of migraine were evaluated psychiatrically, and by electroencephalography. They were challenged with food antigens by skin-prick test, and abdominal symptoms were evaluated following oral ingestion of food allergens. A significant correlation was found between challenge with specific food allergens and the development of migraine headaches, the appearance of abdominal symptoms and the occurrence of positive skin reactions. Psychiatric abnormalities and EEG alterations were associated with the occurrence of headaches and allergic clinical features. It is suggested that the clinical features of migraine can be explained as a result of release of chemical mediators following antigen-antibody reactions in the brain and other tissues where specific antibodies are localized. The continuous ingestion of the responsible food allergens would account for the raised tissue concentrations of noradrenaline, histamine and other mediators to which the clinical features of migraine are attributed.     

Ciguatoxin-induced food poisoning in a community. Implications for disease surveillance and medical practice in Jamaica

This article highlights an outbreak of food poisoning, the result of ingestion of Ciguatoxin-infected fish in a community. The case presentations of the patients involved are used to illustrate the clinical aspects of Ciguatoxin poisoning. The public health aspects of this incident and their relevance to disease surveillance are then discussed. Information of significance to general medical practice in relation to this particular type of fish poisoning, the effect of which could prove fatal in some cases, is also discussed.     

Ciguatera in Australia. Occurrence, clinical features, pathophysiology and management

Ciguatera is a type of food poisoning that results from eating certain tropical fish which have become toxic. It is common in Australia: 175 outbreaks, which involved 527 people, were reported in Queensland between 1965 and 1984. It seems restricted to certain areas around the Australian coastline. Most reports have involved the narrow-barred Spanish mackerel, Scomberomorus commersoni, most of which were caught in southern Queensland waters. Up to 2100 cases may have occurred in north Queensland between 1965 and 1984, which were not recorded by the writers. The symptoms of ciguatera in Australia are similar to those reported elsewhere in the South Pacific. Ciguatoxin acts by increasing the permeability of excitable membranes to sodium ions. This type of membrane is found throughout the body in nerve tissue as well as in heart and skeletal muscle. The treatment of ciguatera remains symptomatic and supportive only. Major advances in treatment for ciguatera and detection of ciguatoxin await the means of producing additional ciguatoxin.     

苏眉鱼中毒的急救护理

目的 提高对苏眉鱼类中毒的认识,避免和防范大规模中毒事件的发生。方法 分析34例苏眉鱼中毒患者的临床资料,总结临床急诊抢救护理经验,并追踪调查半年内患者的情况。结果 苏眉鱼中毒多在2～10小时发病,以急性胃肠炎表现为主,多伴有较长时间温度感觉倒错,部分惠者遗留有不同程度的神经系统症状及性欲减退。34例中毒惠者l8例治愈,l6例好转。结论 苏眉鱼中毒是一种严重的中毒,医务人员和卫生行政部门应高度重视。     

Features of Ciguatera Fish Poisoning Cases in Hong Kong 2004-2007

Ohjective To review the clinical features and laboratory investigations of ciguatera patients in Hong Kong between 2004 and 2007 in order to show the timely sampling of implicated fish from ciguatera victims and application of validated mouse bioassay for confirming suspected clinical cases of ciguatera. Methods Diagnosis of the ciguatera victims was based on history of coral fish consumption and clinical presentations stated in official guidelines for clinical diagnosis of ciguatera fish poisoning in Hong Kong. Food remnants of coral fish samples were collected swiftly from ciguatera victims between 2004 and 2007 for ciguatoxins （CTXs） analysis. Results Major clinical symptoms in ciguatera patients included gastrointestinal and neurological effects including limb numbness and diarrhoea, which developed at 0.5 to 15 hours after consumption of fish. In most cases, neurological symptoms were more common than gastrointestinal symptoms. A broad range of attack rate （10%-100%） was observed in each ciguatera outbreak. Validated mouse bioassay on ether extracts of the food remnant samples confirmed that all were CTXs-positive （〈0.5 - 4.3 MU/20 mg ether extract） and directly linked to the corresponding ciguatera cases. Conclusion Consistency between clinical and laboratory analysis for ciguatera poisoning illustrates the application of laboratory mouse bioassay in a timely fashion for confirming ciguatera poisoning cases and implementing effective public health measures. With further improvement in laboratory techniques, features of ciguatera fish poisoning cases can be better defined, Further studies are needed to determine the risk of each class of CTXs （Pacific-, Indian- and Caribbean-CTXs） in Hong Kong.     

Quinine poisoning in children

The accidental ingestion of quinine by children causes significant morbidity and mortality. We have reviewed quinine poisoning as presented in the medical literature and our experience of paediatric quinine poisoning during the period from January 1975 to September 1986. The clinical features that were seen in our patients were similar to those that are described in larger series. In our series, 13 children were identified, of whom 11 children were aged one to two years. Ten children either remained asymptomatic or made a complete recovery. Two children had a persisting major deficit and one died. Once ingestion of quinine has occurred, absorption should be prevented by the emptying of the stomach with ipecacuanha or gastric lavage promptly and then by the administration of activated charcoal. Once toxicity develops, supportive therapy should be given, but there is no specific therapy to reduce toxicity or to enhance elimination. Physicians who prescribe quinine should be aware of the potential dangers to small children.     

Clinical and epidemiological aspects of methylmercury poisoning.

An opportunity to study the effects of methylmercury poisoning in humans was provided by the large outbreak in Iraq in 1971-2. In adults, poisoning resulted from the ingestion of home-made bread prepared from methylmercury-treated seed grain and there was a highly significant correlation between the amount of bread ingested and blood mercury levels. Poisoning in infants resulted either from prior exposure in utero or from suckling or both. Blood mercury levels were higher in infants and children than in adults. There was no increased incidence of congenital defects. Symptoms and signs of poisoning and histopathological changes were mainly confined to the CNS. Symptoms developed, on average, 1-2 months after exposure. In children there was mental retardation with delayed onset of speech and impaired motor, sensory and autonomic function. Severely affected children were blind and deaf. In adults, the clinical picture could be classified as 1, mild (mainly of sensory symptoms) 2, moderate (sensory symptoms accompanied by cerebellar signs) and 3, severe (gross ataxia with marked visual and hearing loss which, in some cases, progressed to akinetic mutism followed by coma). Grades 1 and 2 carried a better prognosis thant grade 3. Interference with transmission at the myoneural junction was found in 14% of patients studied. There was no evidence of peripheral nerve involvement per se and sensory symptoms may be of central origin. The clinical differences between the Iraqi and Japanese outbreaks may be a result, in part at least, of the severe, prolonged and continuous exposure which occurred in the latter outbreak. Improvement was observed among the mild and moderate group. Treatment with chelating agents, thiol resin, haemodialysis and exchange transfusion lowered blood mercury concentrations but produced no convincing clinical benefit. To be effective, treatment may need to be instituted soon after exposure.     

Ethylene glycol poisoning

Seven men with ethylene glycol poisoning were treated at our institution during a ten-year period. Six patients survived. Ethylene glycol levels on admission did not directly correlate with the severity of metabolic abnormalities or subsequent complications. The timing of the patients' admissions altered the clinical picture and results of therapy. Patients who came to our facility later than 12 to 24 hours after ingestion had established renal failure and required prolonged hospitalization. We were able to prevent renal failure in the one patient started on dialysis less than 23 hours after ingestion. Our patients exhibited the metabolic, CNS, cardiopulmonary and renal manifestations of ethylene glycol poisoning.     

Ciguatera update

Ciguatera fish poisoning is probably more important than any other form of seafood poisoning. Its epidemiology is complex and it is impossible to predict outbreaks. Toxic fish (which look, taste and smell normal) contain ciguatoxins derived from microalgae via the food chain. The toxins are not destroyed by cooking and, if consumed in sufficient dose, can cause symptoms persisting for weeks, months or years. The incidence of ciguatera is expected to increase in association with global warming and widespread bleaching and death of coral.     

523例变态反应性皮肤病患者过敏原检测结果分析

目的：探讨变态反应性皮肤病患者常见过敏原的分布特征。方法：对本院皮肤科门诊523例变态反应性皮肤病患者按荨麻疹组（322例）和皮炎、湿疹组（201例）进行分类;应用德国MORA-SUPER生物共振治疗仪对患者进行吸入、食入、其他变应原检测,进行相关统计学分析。结果：过敏原阳性率荨麻疹组为87.89%,皮炎、湿疹组为83.08%;从过敏原分布特征来看,以多种、多组物质过敏的患者为多;皮炎、湿疹组内少年组与中老年组之间阳性率差异较大。荨麻疹组前十位过敏原是：螨和昆虫（占54.97%）、霉菌（占49.38%）、海鲜类（占31.37%）、组胺（占20.50%）、酵母（占14.91%）、食用防腐剂（占14.29%）、抗氧化剂（占13.66%）、蛋黄（占12.11%）、甜味剂（占9.01%）、香料和药草（占7.45%）;皮炎、湿疹组前十位过敏原是：螨和昆虫（占55.22%）、霉菌（占36.82%）、海鲜类（占31.84）、重金属（占15.92%）、抗氧化剂（占13.43%）、组胺（占12.44%）、食用防腐剂（占11.44%）、酵母（占8.46%）、谷类（占7.96%）、蛋黄（占7.46%）、广泛环境毒素（占7.46%）。结论：变态反应性皮肤病患者的过敏原分布具有一定特征,可为本地区过敏性疾病的预防和i台疗提供一定依据。     

Histamine poisoning associated with eating tuna burgers

Context  Histamine poisoning occurs when persons ingest fish in which bacteria have converted histidine to histamine, a process that usually can be controlled by storage at low temperatures. From 1994 to 1997, North Carolina averaged 2 cases annually; however, from July 1998 to February 1999, a total of 22 cases of histamine fish poisoning were reported. Objectives  To examine the increase in histamine case reports, identify risk factors for poisoning, and develop recommendations for prevention. Design and Setting  Case series evaluated in North Carolina from July 1998 to February 1999. Subjects  Reported case-patients with 2 of the following symptoms within 2 hours of eating tuna: rash, facial flushing, vomiting, diarrhea, dyspnea, a tight feeling in the throat, headache, or a metallic or peppery taste in the mouth. Results  Twenty cases occurred during 5 outbreaks, and there were 2 single occurrences. Of the 22 persons affected, 19 (86%) sought emergency medical care. All case-patients ate tuna: 18 ate tuna burgers, 2 ate salad containing tuna, and 2 ate filets. Tuna samples (available from 3 outbreaks) had histamine levels above the Food and Drug Administration regulatory level of 50 ppm (levels were between 213 and 3245 ppm). In 19 cases, the tuna used to prepare burgers or salads was frozen and thawed more than once before serving. Violations of recommended temperature controls were identified in 2 of the 5 restaurants, accounting for 14 (64%) cases. Conclusions  Tuna burgers, a relatively new menu item in restaurants, were associated with an increase in histamine poisoning cases in North Carolina. Tuna ground for burgers can be susceptible to both temperature fluctuations and bacterial contamination.      

Dettol poisoning and the need for airway intervention

OBJECTIVES. To (1) characterise the clinical features of Dettol poisoning on a territory-wide basis, (2) assess the need for airway intervention after such poisoning and its time frame after ingestion, and (3) identify predictors for such an intervention. DESIGN. Case series. SETTING. Sixteen accident and emergency departments in Hong Kong. PATIENTS. Patients with Dettol ingestion who presented within 48 hours of ingestion from July 2005 to June 2009, derived from the database of the Hong Kong Poison Information Centre. RESULTS. In all, 213 patient records were identified, of which 36 were excluded based on pre-defined criteria and 177 were analysed. Among the latter, the median age was 32 (range, 2-95) years and the male-to-female ratio was 1:2.7 (48:129). Intentional ingestion constituted the majority (95%) of cases. The most common symptoms were related to the local irritative/corrosive effects on the aero-digestive tract, such as gastro-intestinal upset and localised throat pain. Airway intervention was required in 14 (8%) patients. All interventions were performed within 12 hours of Dettol ingestion and three cases involved re-intubation after extubation. Univariate analysis showed that a Glasgow Coma Scale score of <8, older age, a larger amount ingested, lip swelling, lung crackles, and wheezing were all associated with airway intervention. In the multivariate analysis using forward stepwise logistic regression, only coma (Glasgow Coma Scale score of <8) remained statistically significant. CONCLUSIONS. Delayed airway obstruction (>12 hours after Dettol ingestion) is unlikely. For those who are intubated, careful assessment of airway adequacy before extubation is strongly recommended to avoid extubation failure and subsequent re-intubation. Patients in coma (Glasgow Coma Scale score of <8) should prompt airway intervention.     

118例重症监护室急性中毒患儿临床分析

目的 分析重症监护室(ICU)急性中毒住院患儿的临床特点,为急性中毒患儿的预防和救治提供依据。方法 对笔者医院2005年1月~2014年12月118例0~14岁因急性中毒收住ICU患儿的病案进行回顾性统计分析。结果 118例急性中毒患儿占同期该科室住院病例2.56%,占意外伤害9.2%,男孩多于女孩,男女性别比为1.74:1,以幼儿期(32.2%)和学龄期(39.8%)为主。误服为首要的中毒原因,95.8%的患儿为经口摄入有毒物质,主要为药物中毒,不同种类有毒物质中毒其转归不同,药物中毒治愈率较高。治愈52例(44.0%),好转56例(47.5%),放弃治疗10例(8.5%)。结论 急性中毒对儿童生命具有极大的威胁,预防是重要措施。     

依地酸钙钠对驱铅治疗的评价和探 讨

目的研究探讨依地酸钙钠对驱铅治疗的临床作用机制。方法该院于2006年8月-2012年8月接收并诊断铅中毒患者共计350例，对其采用依地酸钙钠进行驱铅治疗方案，研究探讨其临床作用机制，观察治疗不良反应，统计数据并进行分析和评价。结果350例铅中毒患者在治疗之后贫血症状明显改善，体内血红蛋白的含量均增加，平均增加（19±13．5）g／L，有1例患者在用药之后出现过敏反应，其余患者的其他症状消失，基本恢复正常，总有效率为98．28％。结论依地酸钙钠对驱铅治疗的临床作用效果明显，不良反应轻且易控制，因此依地酸钙钠治疗铅中毒在临床上值得进一步研究与探讨。     

Bupropion poisoning: a case series

OBJECTIVE: To investigate the toxicity of bupropion hydrochloride in deliberate self-poisoning in adults and accidental ingestion by children. DESIGN AND SETTING: Prospective study of cases identified from calls to the New South Wales Poisons Information Centre (NSW PIC), with follow-up through hospital medical records. PARTICIPANTS: Patients with bupropion poisoning managed in hospital, about whom the NSW PIC was contacted for advice, from 1 November 2000 to 31 July 2001 (59 adults and 10 children). MAIN OUTCOME MEASURES: Clinical effects, adverse outcomes (including seizures and death) and treatment. RESULTS: 45 of the 59 adults were followed up (76%), 19 of whom had taken bupropion alone. Major clinical effects of bupropion included sinus tachycardia (83%), hypertension (56%), seizures (37%), gastrointestinal symptoms (37%) and agitation (32%). Seizures were dose-dependent, with those having seizures ingesting a significantly higher median dose (P = 0.02). All seizures were brief and self-limiting. 29 patients received decontamination therapy. 10 patients required pharmacological sedation, 10 were admitted to intensive care and six were intubated. None died. Eight of 10 accidental ingestions by children were followed up (80%); one child had symptoms (vomiting and hallucinations). CONCLUSIONS: Bupropion overdose caused significant clinical effects in adults, but few in children.     

Scombroid fish poisoning illness and coronary artery vasospasm

We present an interesting case of a young man with coronary artery vasospasm complicating scombroid fish poisoning illness. The initial presentation included tachycardia and significant hypotension. A 12-lead ECG showed sinus tachycardia with marked widespread ST segment depression and ST elevation in aVR. Symptoms subsequently improved with intravenous fluid rehydration, antihistamines, and glyceral trinitrate. The underlying pathogenesis and treatment of this rarely described manifestation of the fish poisoning illness is discussed.