Ethylene glycol poisoning following ingestion of brake fluid

A 32-year old male, with a history of depression and previous suicide attempts, was brought to hospital comatose after ingestion of brake fluid. He developed severe metabolic acidosis with an increased anion gap, hypotension, seizures and mild renal impairment. He required intensive care treatment for ventilatory and inotropic support. The clinical features, diagnosis and treatment of this unusual poison are discussed.     

Treatment of methanol poisoning with ethanol and hemodialysis.

Twelve cases of methanol poisoning are reviewed. The clinical presentation and biochemical features are described and the results of treatment with alkali, ethanol and dialysis reported. The outcome of methanol poisoning appears to be related more to the interval between the time of ingestion and the start of therapy and to the degree of acidosis than to the initial serum methanol level. Therefore, early and aggressive treatment with bicarbonate and ethanol and subsequent institution of hemodialysis are strongly recommended whenever methanol can be detected in the blood, especially when metabolic acidosis of the anion-gap type is present, when mental or visual disturbances are present, or when more than 30 ml of absolute methanol has been consumed.     

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.     

Cerebral depression due to propylene glycol in a patient with chronic epilepsy--the value of the plasma osmolal gap in diagnosis

A case of propylene glycol poisoning is described in a 39 year old woman which resulted in her admission to hospital in status epilepticus. She had had a long-standing history of uncontrollable epilepsy. The diagnosis of propylene glycol poisoning resulted directly from the finding of a high plasma osmolal gap on admission. This finding would have been missed if later samples only had been analysed. Plasma osmolality and the osmolal gap should be considered first line investigations in patients presenting with metabolic acidosis and cerebral signs and symptoms. Since her discharge from hospital a year ago the patient has had no further seizures.     

An unusual cause of severe metabolic acidosis

A 50-year-old man was transferred to the intensive care unit with high anion gap metabolic acidosis. Investigations suggested a diagnosis of pyroglutamic acidaemia. Factors contributing to the acidosis were medications (paracetamol and flucloxacillin), sepsis and renal failure. The acidosis resolved with supportive therapy and withdrawal of the drugs. It is important to recognise this treatable aetiology of metabolic acidosis.     

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.     

Salicylate poisoning in children: report of three cases

To raise clinicians' awareness of chronic (therapeutic) salicylate poisoning as a common cause of admission in paediatric patients presenting to hospital with respiratory distress (a clinical manifestation of metabolic acidosis) and a history of 'over the counter' treatment with salicylate (Aspirin). We present two complex cases and provide a review of the literature on pathogenesis, clinical presentation and management of salicylate poisoning. A complete history of the illness, including questions on drug use, is vital in assessing the cause of metabolic acidosis in children. Due to the limited options available in managing such patients in many developing countries, emphasis should be placed on prevention of poisoning by educating the community and health care providers.     

Fatal xylenol self-poisoning

A case of fatal xylenol ingestion by a long-stay mental hospital patient is described. The clinical course was similar to that observed in other phenolic poisonings with active bowel sounds, nausea and vomiting, severe metabolic acidosis, hypotension and cardiac and renal failure. The formulation of xylenol ingested contains alcohol which would facilitate absorption; due to the dangers of such poisonings care must be exercised as to access and exposure to xylenol sterilising agents.     

高乳酸血症与代谢性酸中毒的相互关系

目的 观察重症患者的高乳酸血症与代谢性酸中毒的相关性,以提供更为准确的反映组织灌注的指标.方法 回顾了2009年8月至2010年4月,9个月间所有重症医学科(ICU)患者的血气分析结果.入选标准为患者同时抽取的一份动脉血标本同时送检血气分析、血清电解质、血清白蛋白检查,其中血气分析结果中乳酸升高,满足高乳酸血症标准(Lac≥2 mmol/L)的结果.结果 在这一乳酸升高(Lac≥2)的人群中用传统方法判断代酸,代酸发生率33.9%,用Stewart's方法判断代酸,代酸发生率为56.0%.但该组人群血清pH值不具有典型酸血症的特点(7.42±0.07),存活组中乳酸占代酸的百分比为(33.6±17.9)%,死亡组中乳酸占代酸的百分比为(42.1±18.5)%,P=0.008;存活组中SIG占代酸百分比为(28.6±23.5)%,死亡组中SIG占代酸的百分比(44.9±23.0)%,P=0.000.结论 在ICU乳酸升高的人群中,乳酸并不是引起代酸的主要成分,乳酸和SIG共同组成代酸的主要组分,但乳酸占代酸的百分比和SIG占代酸的百分比升高可能提示预后不佳,这两个指标也许能为临床提供更准确的反映组织灌注的信息.

Abstract：

Objective To investigate the acid-base abnormalities of the patients with hyperlactatemia and explore the relationship of hyperlactatemia and metabolic acidosis so as to seek a more precise index of reflecting organ perfusion. Methods From August 2009 to April 2010, all consecutive patients admitted into intensive care unit received an analysis of blood gas. Those individuals with arterial lactate ≥2 mmol/L were selected. Results In the group of hyperlactatemic patients, the occurrence of metabolic acidosis as judged by the traditional method was less than that by the Stewart's method (33.9% vs 56. 0% ). No typical acidemia was found. And all components of metabolic acidosis were calculated. Lactate and SIG (strong ion gap ) contributed a certain percentage to metabolic acidosis in the survivor and nonsurvivor groups [(33.6±17.9)% vs (28.6 ±23.5)%, (42.1 ±18.5)% vs (44.9 ±23.0)%].Conclusion Among the hyperlactatemic patients (Lac ≥ 2 ), lactate and unmeasured anions account for most instances of acidosis. These two indicators may offer a more accurate reflection of tissue perfusion.     

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.     

Lactic acidosis and ketoacidosis: biochemical and clinical implications.

A case of lactic acidosis presented the opportunity for review of the association between lactic acidosis and ketoacidosis. The diagnosis of lactic acidosis or the combination of lactic acidosis and ketoacidosis is established clinically by the detection of a metabolic acidosis of the "unmeasured anion gap" type in the absence of significant renal failure, poison intake or a strongly positive clinical test for ketones. Before treatment can be planned the biochemical basis of lactic acidosis and ketoacidosis must be understood -- especially the fact that lactic acidosis is not a single disease entity but has many possible causes. Among important considerations is the relation between the blood concentrations of bicarbonate and organic acid anions. After recovery from metabolic acidosis of the unmeasured anion gap type, metabolic alkalosis is common. Decreased bicarbonate excretion plays an important role in the pathogenesis of the latter and may be the result of potassium or chloride loss, or both. The deficits, if present, should be corrected with appropriate therapy.     

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.     

Hyperkalaemic quadriparesis secondary to chronic diclofenac treatment

A 76 year old woman presented with a quadriparesis associated with hyperkalaemia. She had a 10 month history of treatment with oral diclofenac sodium. On admission she had hyperkalaemic metabolic acidosis with a normal anion gap and mild renal impairment. Her weakness resolved after withdrawal of diclofenac and medical correction of her hyperkalaemia. Non-steroidal anti-inflammatory drugs are known to cause hyperkalaemic acidosis and should be used with caution, especially in the presence of renal impairment.     

慢性肺心病复合型酸碱失衡血乳酸、丙酮酸水平的研究

本文对104例次慢性肺心病并发碱酸失衡患者进行血气分析,测定血钾,钠,氯和乳酸、丙酮酸含量以及阴离子空隙(AG)。结果血乳酸含量>2mmol/L 者62例(59.6%),>5mmol/L 者9例(8.6%)。丙酮酸含量>0.14者35例(33.7%)。L/P比值>21者37例(35.6%)。其中,呼酸合并代酸和呼酸合并代碱,代酸两组的 AG 值>20mmol/L,血乳酸含量均值5mmol/L,提示肺心病合并复合型酸碱失衡者,除应用预计值代偿公式和 AG 值外,测定血乳酸、丙酮酸含量是判断代酸的一项重要指标。     

Severe metabolic acidosis complicating massive ibuprofen overdose.

We report the progress of a patient who presented following the ingestion of ibuprofen in overdose. He survived despite developing an extremely severe metabolic acidosis.     

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.     

Wilson's disease with hepatic presentation in childhood

Diagnosis of Wilson's disease with hepatic presentation in childhood using clinical and common laboratory parameters is still challenging and is often missed or delayed. The aim of the study was to document the clinical and laboratory parameters of hepatic presentation of Wilson's disease in children. The study was conducted at a tertiary-care hospital in a developing country. Clinical and common laboratory parameters were recorded in 32 Wilson's disease children with hepatic presentation. The diagnosis was based on positive family history, Kayser-Fleischer ring, low serum ceruloplasmin level, elevated basal urinary copper excretion and favorable response to therapy with D-penicillamine. Mean age+/-SD at presentation was 9+/-2.97 years and 21 (65.6%) were boys. Chronic liver disease (21; 65.6%) followed by fulminant hepatic failure 1(6; 18.8%) were the commonest presentation. In the whole group, Kayser-Fleischer ring was found in 21 (65.6%), low serum ceruloplasmin in 16 (50%) and elevated basal urinary copper excretion in all 32 (100%) children. Diagnosis of Wilson's disease was made at presentation on the basis of i) Kayser-Fleischer ring, low serum ceruloplasmin, elevated basal urinary copper excretion and favorable response to D-penicillamine therapy in 11 (34.4%), ii) Kayser-Fleischer ring, elevated basal urinary copper excretion and favorable response to D-penicillamine therapy in 10 (31.2%), iii) elevated basal urinary copper excretion and favorable response to D-penicillamine therapy in 6 (18.8%) and iv) low ceruloplasmin, elevated basal urinary copper excretion and favorable response to D-penicillamine therapy in 5 (15.6%) children. Wilson's disease can not be excluded in children presenting with hepatic involvement using the commonly practiced clinical and laboratory parameters. A combination of various clinical and laboratory parameters were used for the diagnosis of Wilson's disease in the studied children with hepatic presentation.     

D-lactic acidosis secondary to short bowel syndrome

A 12 year old boy presented with 11 episodes of weakness, ataxia, nausea, slurred speech, dehydration, and sometimes severe lethargy bordering on coma. A year previously the boy had small intestinal resections leaving 20 cm of small bowel remaining. D-lactic acidosis was diagnosed on the basis of a D-lactate level of 5.23 mmol/l. The clinical presentation of the disease is recurrent episodes of unusual neurological manifestations and severe metabolic acidosis. The diagnosis is dependent on the presentations and the plasma D-lactate level. Development of the syndrome seems to be the effect of the accumulation of D-lactic acid.     

慢性肺心病并发复合性酸碱失衡及微机诊断(附310例分析)

310例住院肺心病患者复合性酸碱失衡638例次,以文献中普遍采用的Emmett和Narins分类方法为基础,将肺心病并发复合性酸碱失衡进一步分类,其中二重型9种,三重型7种,四重型2种,计18种。这是一种新的较为合理细致的分类方法,并根据文献中使用的单纯性酸碱失衡代偿预计公式进一步推导出电子计算机诊断复合性酸碱失衡的18个预计公式。经873例次血生化,血气分析,诊断与临床符合率97%。     

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.