Ethylene glycol intoxication: Disparate findings of immediate versus delayed presentation

Ethylene glycol is a common household substance responsible for a large number of ingestions in the U.S. each year. In 2001, nearly 5,000 ethylene glycol exposures were reported with more than 1,600 patients requiring medical treatment. There were 16 deaths attributed to ethylene glycol in 2001, second only to ethanol overdose for lethal ingestions. Diagnosis of ethylene glycol ingestion is relatively straight-forward when an individual with a history of exposure is found to have a high anion-gap metabolic acidosis and an elevated osmolar gap. Appropriate treatment can be immediately employed and the diagnosis confirmed by the finding of elevated ethylene glycol levels in the serum. In the absence of exposure history, the differential diagnosis of a high anion-gap metabolic acidosis and an elevated osmolar gap will also lead to consideration of ethylene glycol ingestion. This well-recognized presentation of ethylene glycol toxicity includes findings expected in individuals who present for care soon after their ingestion. A less well-known pattern may be seen in those for whom care is delayed. We present a patient with delayed presentation of ethylene glycol ingestion and review the physiology and biochemistry that underlies this different presentation. Unfortunately, without history or strong laboratory evidence, ethylene glycol ingestion may be easily overlooked in individuals with delayed presentation.     

Clinical features, laboratory findings and imaging appearances of venous diethylene glycol poisoning in patients with liver disease

Background There was a hospital outbreak of venous diethylene glycol poisoning in Guangzhou, China. It is the only massive episode of venous diethylene glycol poisoning in history. Here we report its clinical features, laboratory findings, and imaging appearances. Methods The clinical features of 15 venous diethylene glycol poisoning patients with liver disease were analyzed and summarized. Their laboratory findings and imaging appearances were comparatively analyzed before and after poisoning. Results All poisoned patients presented with oliguric acute renal failure with anuria after a mean of 6 days. Carbon dioxide combination power of 13 patients dropped after a mean of 9 days with valley value on the 10th day, when metabolic acidosis developed. Gastroenteric symptoms or aggravation of gastroenteric symptoms were displayed in 11 patients after a mean of 9 days. Neurological system impairment was observed in 10 patients after a mean of 14 days. Seven patients had low fever after a mean of 6 days. Causes of death of 14 patients included multiple organ dysfunction syndrome, severe lung infection and massive haemorrhage of digestive tract. Blood creatinine and urea nitrogen were abnormal after a mean of 5 days with peak value on the 11th and 14th days, respectively. Serum calcium had no obvious change, and phosphorus was distinctively increased. Liver functions did not change significantly. Poisoned patients had higher white blood cell counts, but lower red blood cell counts and hemoglobin value. Of the 7 patients who exhibited mild moderate or severe patchy consolidation shadowing in the lung, 2 manifested mild or severe gaseous distention and dilation of gastroentedc tract. Conclusions Main features of venous diethylene glycol poisoning in patients with liver disease include oliguric acute renal failure, metabolic acidosis, gastroenteric symptoms or aggravation of gastroenteric symptoms, neurological system impairment and low fever, with a mortality rate of 93.33% in poisoned patients. There is also higher white blood cell counts and anemia, patchy consolidation shadowing in the lung, gaseous distention and dilation of gastroenteric tract, which occurs later than mild patchy consolidation shadowing and earlier than moderate patchy consolidation shadowing in the lung.     

肝病患者静脉二甘醇中毒的临床特点、实验室检查及影像学表现

目的 总结报道肝病患者静脉二甘醇中毒的临床特点、实验室检查及影像学表现.方法 分析总结15例肝病患者静脉二甘醇中毒的临床特点,比较分析中毒前后的实验室检查结果 及影像学表现.结果 中毒病例均出现少尿型急性肾功能衰竭,平均6 d后出现无尿.13例平均9 d后CO2结合力下降,10 d达谷值,代谢性酸中毒.11例平均9 d后出现胃肠道症状或胃肠道症状加重.10例平均14 d后出现神经系统损害.7例平均6 d后出现低热.14例死亡,原因包括多器官功能障碍综合征、肺部严重感染、消化道大出血.血清肌酐、尿素氮平均5 d异常,11、14 d分别达峰值.血清钙无明显变化,血清磷明显升高.肝功能未见明显变化.白细胞增高,红细胞、血红蛋白降低.7例肺部影像学表现为轻度、中度及重度片状实变影,其中2例胃肠道轻度或重度积气、扩张.结论 肝病患者静脉二甘醇中毒的主要特点为少尿型急性肾功能衰竭、代谢性酸中毒、胃肠道症状或胃肠道症状加重、神经系统损害及低热;中毒病死率93.33%;白细胞增高、贫血;肺部片状实变影;胃肠道积气扩张比肺部轻度片状实变影出现晚,比中度片状实变影出现早.     

Ethylene glycol poisoning

Although an uncommon cause of death in Great Britain, ethylene glycol poisoning is potentially serious in that renal and cardiopulmonary failure and central nervous system dysfunction can occur when doses of the order of 100 ml or more are ingested. A case is described in which a child who swallowed approximately 100 ml of ethylene glycol was treated by prolonged peritoneal dialysis. In addition, measures were taken to correct a marked acidosis. Substantial amounts of ethylene glycol were removed by the dialysis fluid and the child made a complete physical and mental recovery.     

Myocarditis complicating ethylene glycol poisoning in the absence of neurological features

The consequences of ethylene glycol intoxication are described in a 42 year old man who presented with a profound metabolic acidosis, cardiogenic shock and renal failure. The clinical and electrocardiographic findings suggested a myocarditis and this was confirmed by endomyocardial biopsy. The striking absence of neurological features in this patient delayed diagnosis, which was not suspected until calcium oxalate crystals were demonstrated at renal biopsy. Retrospective analysis of serum retained at his admission to hospital confirmed toxic levels of ethylene glycol. Following a period of intensive cardio-respiratory support and peritoneal dialysis he made a good recovery with cardiac and renal function returning to normal.     

Acute lindane poisoning with development of muscle necrosis.

A 35-year-old man ingested food contaminated with lindane, an insecticide containing almost pure gamma hexachlorocyclohexane. Grand mal seizures and severe acidemia developed rapidly. The seizures recurred for nearly 2 hours, then ceased. In addition, the patient had muscle weakness and pain, headaches, episodic hypertension, myoglobinuria, acute renal failure and anemia. Pancreatitis developed 13 days after the ingestion of lindane. A muscle biopsy on the 15th day of illness demonstrated widespread necrosis and regeneration of muscle fibres. The patient's condition improved and he was discharged 24 days after the onset of his illness. During the year following the poisoning the patient noted difficulty with recent memory, loss of libido and easy fatigability. One year after lindane ingestion the results of physical examination, including those for muscle power and bulk, were normal.     

Strychnine poisoning as an unusual cause of convulsions

A fatal case of strychnine poisoning is presented. The patient vomited then suffered a series of tonic convulsions which were triggered by tactile stimulation. In between paroxysms he was initially alert. Eventually the patient became comatosed due to anoxia and had a cardiac arrest. He presented with a marked metabolic acidosis and rapidly developed renal failure caused by acute rhabdomyolysis. This clinical picture is classical for strychnine poisoning and the complications which the intoxication produces. Attention is drawn to the fact that survival can even follow the ingestion of very large doses of strychnine providing there is no delay in diagnosis and treatment.     

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.     

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.     

急性百草枯中毒患者的预后因素分析

目的：探讨影响百草枯中毒患者预后的相关因素。方法：收集60例急性百草枯中毒患者的临床资料,均随机接受血液灌流联合血液透析（HP-HD）或血液灌流联合连续性静脉-静脉血液滤过（HP-CVVH）治疗,分析性别、年龄、服毒量、血浆百草枯浓度、服毒至入院时间、百草枯中毒严重指数（SIPP）、APACHEⅡ评分、血清尿素氮、肌酐、丙氨酸转氨酶、天冬氨酸转氨酶、肌酸激酶同工酶、钾、二氧化碳结合力、动脉血pH、动脉血氧分压、动脉二氧化碳分压、白细胞计数等指标与预后的关系。同时评价两种不同血液净化方式的疗效。结果：60例百草枯中毒患者病死率为70%（死亡42例）。存活组和死亡组比较,服毒量[（21.67±15.01）mL vs（86.07±36.49）mL]、血浆百草枯浓度[（6.82±3.58）mg/L vs（12.45±4.67）mg/L]、服毒至入院时间[（3.75±1.04）h vs（9.93±4.25）h]、SIPP[（15.78±8.71）h.mg/L vs（105.54±55.48）h.mg/L]、白细胞计数[（8.84±2.54）×109/L vs（13.42±2.99）×109/L]之间差异具有统计学意义（P〈0.05）。HP-CVVH组病死率低于HP-HD组（62.9%vs 80%）,但差异无统计学意义（P〉0.05）。结论：服毒量、血浆百草枯浓度、服毒至入院时间、SIPP、白细胞计数是影响急性百草枯中毒预后的因素。与HP-HD比较,HP-CVVH不能明显改善百草枯中毒患者的预后。     

急性有机磷农药中毒致肾损害临床分析

目的探讨急性有机磷农药中毒致肾损害患者的发病机制、临床表现和治疗方法,提高抢救成功率。方法收集我院1999年1月。2010年12月收治的急性有机磷农药中毒致肾损害患者的临床资料。回顾患者临床表现特点、综合性治疗措施以及预后。结果共收集急性有机磷农药中毒患者456例,其致肾损害105例,发病率23％,临床表现以蛋白尿（100％）、镜下血尿（93％）为突出表现,部分患者可出现急性肾功能不全（39％）,中毒程度较重的患者可出现1个或多个重要脏器并发症。105例患者治愈97例,治愈率达92．4％,死亡8例,病死率7．6％,死亡的主要原因为多脏器功能衰竭。结论急性有机磷农药中毒致肾损害的预后不仅仅是由肾功能损害程度决定的,它合并其他重要脏器衰竭或严重感染,是导致患者死亡的重要因素,所以,治疗上除尽早、足量使用抗胆碱能药和胆碱脂酶复能剂外,积极采取综合性措施预防和治疗并发症,是提高急性有机磷农药中毒致肾损害患者抢救成功率的重要环节。     

Two fatalities after acute occupational exposure to ethylene dibromide

A worker collapsed while working inside a tank that was later found to contain residues of ethylene dibromide. He died 12 hours later with metabolic acidosis, depression of the CNS, and laboratory evidence of liver damage. A supervisor attempting to rescue the first victim also collapsed inside the tank and died 64 hours later with intractable metabolic acidosis and hepatic and renal failure. The clinical, pathological, and toxicological findings, as well as results of industrial hygiene sampling, are reported. Pathophysiological mechanisms and possible therapeutic interventions are discussed. The cases demonstrate the extreme hazards of exposure to the highly toxic chemical. The importance of protective work practices wherever there is potential exposure to ethylene dibromide is emphasized.     

无创正压通气治疗急性河豚鱼中毒合并呼吸衰竭的疗效观察

目的：探讨无创正压机械通气（NIPPV）治疗急性河豚鱼中毒合并呼吸衰竭的疗效。方法选择21例急性河豚鱼中毒合并呼吸衰竭的患者,观察治疗前后动脉血酸碱度（pH）、动脉氧分压（PaO2）、动脉二氧化碳分压（PaCO2）、动脉血氧饱和度（SaO2）以及呼吸频率（RR）、心率（HR）、血压（BP）和辅助呼吸机动用评分（ARMES）等。结果 NIPPV治疗急性河豚鱼中毒合并呼吸衰竭的患者6 h后pH、PaO2、SaO2、RR、HR、BP、ARMES均明显优于治疗前（P＜0.01）,治疗24 h后可明显降低PaCO2（P＜0.05）。3例患者行有创机械通气治疗,其中2例5 d后顺利脱机,1例经抢救无效死亡。结论急性河豚鱼中毒所致呼吸衰竭具有可逆性、时间性的特点,NIPPV通过提高PaO2、降低PaCO2,迅速缓解呼吸困难、改善呼吸肌疲劳,降低气管插管率和病死率,对于急性河豚鱼中毒合并呼吸衰竭是一种切实有效的治疗措施。     

Multiple organ dysfunction syndrome due to ingestion of fish gall bladder

Objective To investigate changes in renal function, urine N- acetyl- β- D- glucosaminidase enzyme (N- AG), liver function, myocardial enzymes, the pathology of renal damage and the mechanism of acute renal failure (ARF) associated with fish gall bladder poisoning.Methods Eleven patients with acute fish gall bladder poisoning were consecutively admitted to our hospital from September 1997 to October 1999. Renal function, urine N- AG enzyme, liver function, and myocardial enzymes were assayed before and after treatment. One patient consented to a kidney biopsy and the pathology of renal damage was observed under light and electron microscopes.Results All patients had multiple organ dysfunction syndrome (MODS) and 11 patients suffered from ARF. Ten patients had liver dysfunction, ten patients had poisonous myocarditis, and 8 patients had gastrointestinal dysfunction. Renal function, urine N- AG enzyme, liver function, and myocardial enzymes were significantly improved after treatment compared with those of before treatment (P&lt;0.05). Kidney biopsy showed that the main damage site was the proximal renal tubule. All eleven patients recovered and were discharged from the hospital.Conclusions Ingestion of fish gall bladder leads to kidney damage, as well as liver, heart and gastrointestinal tract injury. The mechanism of acute renal function failure is the serious tubular damage, confirming the location of kidney damage. Necrosis of the proximal tubules plays an important role in the development of ARF. Immediate hemodialysis is the most effective treatment.     

血液透析治疗鱼胆中毒致急性肾功能衰竭的临床疗效

目的：观察血液透析滤过及血液灌流治疗鱼胆中毒致急性肾功能衰竭的临床疗效。方法：回顾性分析3例由于鱼胆中毒所致急性肾功能衰竭患者的临床资料,采用血液透析滤过及血液灌流治疗,比较透析治疗前后患者的肾功能、肝功能变化;观察中毒至首次血液透析的时间、服鱼胆量对疗效的影响。结果：经血液透析滤过及血液灌流治疗后,2例患者痊愈出院,至今健康;1例患者死亡。血透治疗后,患者肝、肾功能各项指标较血透前显著下降（P〈0.01）;首次透析的时间越早,疗效愈好（P〈0.01）;服不同数量鱼胆的患者,其血透次数和肾功能恢复的时间差异均无统计学意义（P〉0.05）。结论：及时充分的血液透析滤过及血液灌流治疗鱼胆中毒致急性肾功能衰竭疗效较好。     

Scombroid poisoning. A report of seven cases involving the Western Australian salmon, Arripis truttaceus.

OBJECTIVE: To present the clinical findings of scombroid poisoning due to ingestion of the Western Australian salmon, Arripis truttaceus, occurring in two separate outbreaks involving seven patients. Both outbreaks occurred in March and the fish had been caught in South Australian waters. CLINICAL FEATURES: Onset of symptoms in all patients occurred within half an hour of ingestion of the affected fish. The clinical syndrome included erythema and urticaria of the skin, facial flushing and sweating, palpitations, hot flushes of the body, headache, nausea, vomiting and dizziness. The fish implicated in one outbreak was noted to have a peppery taste. The diagnosis of scombroid poisoning was confirmed by the presence of the clinical syndrome, and by demonstration of high histamine levels in the cooked fish. INTERVENTION AND OUTCOME: Two patients had minor symptoms which had resolved before seeking medical advice. Another two patients had mild symptoms which disappeared after two hours of observation and required no specific treatment. Three patients had evidence of major toxicity which was successfully treated with parenterally administered promethazine. One of the three patients with major toxicity required overnight admission and repeated doses of promethazine to eradicate her symptoms. No patient had symptoms for longer than 12 hours. CONCLUSION: Scombroid poisoning is caused by ingestion of fish which has accumulated scombrotoxin during spoilage. The toxin is heat stable and has been identified as histamine. The clinical presentation closely resembles an acute allergic reaction. This similarity in symptoms may result in the diagnosis of scombroid poisoning being missed by clinicians. Patients with the symptom complex may be incorrectly informed that they are allergic to the fish species. Diagnosis is clinical and can be confirmed by analysis of the histamine content of the fish. Treatment is with antihistamines, however major toxicity may require the same aggressive management as acute anaphylaxis.     

杂合肾脏替代治疗鱼胆中毒合并急性肾损伤患者疗效的研究

目的 本研究旨在观察杂合肾脏替代治疗(hybrid renal replacement therapy,HRRT)在鱼胆中毒致急性肾损伤(AKI)中的应用效果.方法 回顾分析以HRRT方法治疗我科今年收治的8例鱼胆中毒患者,HRRT采用持续缓慢低效血液透析(sustained low-efficiency dialysis,SLED)联合血液灌流(HP)的模式.分别进行3～5次的治疗.观察患者治疗前后相关指标变化.结果 8例患者经HRRT治疗后,相关指标明显改善,肾功能均完全恢复.结论 鱼胆中毒所致严重并发症AKI早期积极采用SLED联合HP治疗能获得满意疗效.     

Acute renal failure following jering ingestion

We report two cases of acute renal failure that followed the ingestion of jering. Features of jering poisoning included clinical presentation of bilateral loin pain, fever, nausea, vomiting, oligo-anuria, haematuria and passage of sandy particles in the urine. Blood urea (40.8 mmol/l; 21.9 mmol/l) and serum creatinine (1249 mumols/l; 693 mumols/l) were markedly elevated. With conservative therapy which included rehydration with normal saline and alkalinisation of the urine with sodium bicarbonate, the acute renal failure resolved.     

Renal tubular acidosis during therapy for diabetic ketoacidosis.

A young woman presented with typical diabetic ketoacidosis. Five hours after insulin had been given hyperchloremic metabolic acidosis developed. This could not be attributed to gastrointestinal loss of bacarbonate, ingestion of HCI or carbonic anhydrase inhibitor, or the administered fluids and electrolytes. The combination of hyperchloremic metabolic acidosis and a urine pH of 5.6 during acidemia prompted specific studies that established the presence of disorders of renal acidification. A transient defect of hydrogen ion secretion in the distal nephron was suggested by the decrease in urine-blood Pco-2 gradient after administration of sodium bicarbonate. Proximal renal tubular acidosis was indicated by the reduced bicarbonate threshold that persisted for approximately 7 weeks.     

连续性静脉静脉血液透析滤过在重型颅脑外伤合并急性肾功能衰竭中的应用研究

目的观察在重型颅脑外伤合并患性肾功能衰竭患者中应用连续性静脉静脉血液透析滤过的治疗方法的效果和有待解决的问题。方法回顾性分析重型颅脑外伤患者41例,按照治疗过程中是否发生急性肾功能衰竭划分为A组（急性肾衰组）23例,B组（对照组）18例,二组患者在性剐、年龄等方面差异无统计学意义。A组患者出现肾衰后停用甘露醇,进行奎天连续性静脉静脉血液透析浇过,B组常规治疗。记录二组患者屈内压、肝肾功、电解质酸碱度变化,1周后APACHEⅢ评分和2周内死亡例数和A组患者肾裹出现时间,连续性静脉静脉血液透析逮过患者滤器使用时间、治疗时间、治疗前后凝血时间改变等数值。结果A组出现肾衰时间为入院后（2．8±1．2）d,行连续性静脉静脉血液透析逢过时间（68±17）h,每个滤器使用时同（23±11）h,患者治疗前后体内凝血时间比较差异无统计擎意义。二组患者的肝功能、酸碱度比较差异无统计学意义（P〉0．05）,肾衰组肾功能指标明显高于B组（P〈0．01）,血钾、血钠平均值有明显差异．A组反而曼接近正常范围。A组患者颅内压平均值明显比B组高,颅内压波动范围却比B组小（P〈0．05）,A组患者1周后APACHEⅢ评分和2周内死亡例数明显大于B组（P〈0．01）。结论在重型颅脑外伤合并患性肾功能衰竭患者中应用连续性静脉静脉血液透析滤过的治疗方法有明显的稳定电解质等内环境指标的作用,但是这些患者颅内压数值和病死率仍然明显增高,治疗中仍然存在很多待解决的问题。