Increased serum formate in the diagnosis of methanol poisoning

Early diagnosis is essential for successful treatment in methanol poisoning. Methanol detection by gas chromatography is not available in most hospitals. Methanol increases the osmolal gap in serum and its metabolite formate increases the anion gap. The sensitivity of these indirect diagnostic methods is not good at low concentrations of methanol or formate. We therefore studied the usefulness of formate measurement in diagnosing methanol poisoning. In 15 patients poisoned with methanol, serum formate was measured enzymatically on a Cobas Mira analyzer using formate dehydrogenase and nicotinamid adenine dinucleotid. Day-to-day coefficient of variation was 5%, and the upper reference limit was 2 mg/dL (0.4 mmol/L). Methanol was detected in all 15 patients of whom 14 had elevated serum formate concentrations. Anion gap was increased in 11 of 11, and osmolal gap in 11 patients of 15 examined. Metabolic acidosis was present in 12 of 15 patients, but pH was below 7.30 in only 9 of them. Four patients with no symptoms had formate concentrations in the range 2-38 mg/dL (0.5-8.3 mmol/L), indicating that increased serum formate was a sensitive indicator of methanol poisoning. Our results proved formate analyzes to be a simple, sensitive, and specific way of diagnosing methanol poisoning. Confounders are patients admitted early, or concomitant ethanol ingestion, and therefore no acidosis. This problem may, however, be omitted by repeated formate analysis in patients developing metabolic acidosis.     

Formate kinetics in methanol poisoning

OBJECTIVE: The objective is to describe the kinetics of formate, the main toxic metabolite of methanol, in a series of consecutive patients treated in the same intensive care unit for severe methanol poisoning. METHODS: The charts of the patients admitted between 1987 and 2001 were reviewed. Inclusion criteria were: a history of deliberate methanol ingestion, with a blood methanol concentration greater than 20 mg/dL (6.2 mmol/L) or a high anion gap metabolic acidosis. Indications for hemodialysis were: blood methanol concentration >50 mg/dL (15.8 mmol/L), metabolic acidosis (bicarbonate <15 mmol/L, arterial pH <7.30), visual toxicity. Antidotal therapy included ethanol administration in 22 cases, and fomepizole in three cases. Serial blood measurements were obtained for pH, bicarbonate, methanol and formate. Endogenous and hemodialysis elimination half-lives were calculated as t1/2 =0.693/Ke. Fick principle was applied for hemodialysis clearance calculation. RESULTS: The records of 25 methanol poisoned patients were analysed. Among them, 18 patients had sufficient data to allow accurate determinations of formate kinetics. Formate half-life elimination during hemodialysis was 1.80+/-0.78 h, which was statistically different from the values observed before or in the absence of dialysis (6.04+/-3.26 h, P =0.004). The mean hemodialysis formate clearance rate calculated in eight cases was 176+/-43 mL/min. A rebound in plasma formate concentration was observed in three patients after the discontinuation of hemodialysis. CONCLUSIONS: In accordance with previous isolated case reports and in contrast with a recent case series, our data document that hemodiaysis is effective in reducing formate elimination half-life. The impact on clinical outcome is still debatable.     

Formic acid and methanol concentrations in death investigations

Methanol ingestion results in the formation of formic acid, a toxic metabolite that can cause metabolic acidosis. Methanol toxicity is therefore dependent on the amount of methanol ingested, the nature of treatment received, elapsed time since ingestion, and the accumulation of formic acid. Both methanol and formic acid concentrations are determined at this laboratory using headspace gas chromatography. An examination of 12 fatalities attributed to methanol poisoning is presented. Six individuals were found deceased, and their postmortem methanol and formic acid concentrations ranged from 84 to 543 mg/dL and 64 to 110 mg/dL, respectively. In the other six individuals, hospital treatment such as bicarbonate, ethanol infusion, and hemodialysis was administered. Antemortem methanol and formic acid concentrations ranged from 68 to 427 mg/dL and 37 to 91 mg/dL, respectively, whereas corresponding postmortem methanol and formic acid levels ranged from undetectable to 49 mg/dL and undetectable to 48 mg/dL, respectively. Hospital treatment of formic acid toxicity resulted in significantly reduced postmortem methanol and formic acid concentrations. Furthermore, the toxicological relevance of nine methanol-positive cases where postmortem methanol concentrations ranged from 3 to 142 mg/dL, with corresponding formic acid levels of less than 10 mg/dL, is discussed.     

Gas chromatographic analysis of methyl formate and application in methanol poisoning cases

A modified headspace gas chromatographic method for analysis of formate in biological fluids is described. Serum or whole blood specimens were methylated in the presence of concentrated sulfuric acid and sodium propionate (internal standard) dissolved in methanol. Derivatization was performed at 35 degrees C for 30 min before injection (0.5 mL headspace) onto a Hallcomid-Carbowax packed GLC column. Using serum or aqueous standards, the method was linear from 5 to 100 mg/dL. The limit of detection was 2.5 mg/dL. Day-to-day precision was less than 5% (CV) at 54 mg/dL formate. Formate and methanol were analyzed in 3 methanol poisonings, two of which were fatal. Formate analysis is considered important in any patient with suspected methanol poisoning who presents for medical assistance with metabolic acidosis. The extent of ocular toxicity correlates better with formate concentration than with methanol concentration.     

Hyperglycemia Is a Strong Prognostic Factor of Lethality in Methanol Poisoning

Methanol poisoning is seen in the form of isolated episodes, or intentional ingestion and epidemics. Despite its efficient treatment, methanol poisoning has high morbidity and mortality rates. So far, several studies have been performed to identify the prognostic factors in methanol poisoning. Recently, during the treatment of patients with methanol poisoning, we observed that patients’ blood glucose levels were high on presentation to the hospital, particularly in those who expired. Through a literature search, we found that no studies have been performed on blood glucose levels or hyperglycemia in methanol poisoning. Therefore, the present retrospective study was done as a preliminary investigation to understand whether there was a meaningful relationship between methanol poisoning and blood glucose level on presentation, and also if hyperglycemia could be considered as a prognostic factor for mortality. In this retrospective study, a review of the hospital charts was performed for all patients who were treated for methanol poisoning from March 2003 to March 2010 in two hospitals in Tehran, Iran. Those with definitive diagnosis of methanol poisoning, no history of diabetes mellitus, and normal or low body mass index (<25) were included. Patients’ demographic information, clinical manifestations, time elapsed between ingestion and presentation, blood glucose level on presentation (before treatment), results of arterial blood gas analysis, and the clinical outcome were recorded. Statistical analysis was done using SPSS software (version 17, Chicago, Illinois, USA) and application of Mann–Whitney U test, Pearson's chi-square test, Pearson correlation coefficient (r), receiver operating characteristic (ROC) curve, and logistic regression. P values less than 0.05 were considered as the statistically significant levels. Ninety-five patients with methanol poisoning met the inclusion criteria and were included in the study. Of these, 91 (96%) were male and 4 (4%) were female. Mean age was 31.61?±?14.3 years (range, 13 to 75). Among the 95 patients, 68 survived (72%) and 27 expired (28%). Median blood glucose level was 144 mg/dL (range, 75 to 500). There was no significant statistical correlation between blood glucose level and time of treatment, age, pCO₂, or serum bicarbonate concentration, but blood glucose level had a statistically significant correlation with pH (r?=??0.242, P?=?0.02) and base deficit (r?=?0.230, P?=?0.03). The mean blood glucose level was 140?±?55 and 219?±?99 mg/dL in the survivor and non-survivor patients, respectively (P?<?001). Considering the cutoff level of 140 mg/dL for blood glucose and using logistic regression analysis, and adjusting according to the admission data with significant statistical difference in the two study groups, the odds ratio for hyperglycemia as a risk factor for death was 6.5 (95% confidence interval?=?1.59–26.4). Our study showed that blood glucose levels were high in methanol poisoning and even higher in those who died in comparison with the survivors. Therefore, hyperglycemia might be a new prognostic factor in methanol poisoning, but further studies are needed to determine whether controlling hyperglycemia has therapeutic consequences.     

Elevated blood lead levels resulting from the ingestion of air rifle pellets

There have been numerous reports of lead poisoning resulting from the ingestion of foreign bodies. A case involving the ingestion of spent air rifle pellets is described. No clinical symptoms were observed, despite the fact that the young child exhibited elevated blood lead levels as high as 2.7 micromol/L (56 microg/dL). X-rays of the child's abdomen confirmed the ingestion of the pellets. The patient was treated with laxatives, and the pellets were successfully passed over the course of the next few days. Prior to release from the hospital, the child's blood lead level had dropped to 1.7 umol/L (35 microg/dL).     

Massive Ethylene Glycol Ingestion Treated with Fomepizole Alone—A Viable Therapeutic Option

Fomepizole is used to treat and prevent toxicity from ethylene glycol poisoning. Treatment with fomepizole without hemodialysis in massive ethylene glycol ingestion has been rarely reported in the literature; however, published literature and practice guidelines recommend considering dialysis for ethylene glycol levels >50 mg/dL. We report a case of massive ethylene glycol ingestion resulting in the highest serum ethylene glycol concentration in a patient without ethanol co-ingestion who was treated with fomepizole and was not hemodialyzed. A 48-year-old male presented to the emergency department after reportedly ingesting >1liter of antifreeze in an attempt at self-harm. He denied concomitant ethanol consumption. His initial presenting serum ethylene glycol level was 700 mg/dL, with normal renal function, and a metabolic acidosis with a high anion gap. One hour after presentation, he was started on intravenous fomepizole. Treatment with fomepizole continued until the patient's plasma ethylene glycol concentration was 16 mg/dL. His metabolic acidosis quickly resolved, he had no adverse reactions to the treatment, and his renal function remained normal. Ultimately, he was discharged to a psychiatric unit without sequelae. Published literature and practice guidelines suggests considering hemodialysis initiation in patients with an ethylene glycol level >50 mg/dL. This recommendation is anecdotally, rather than evidence, based. With the potential risks inherent in hemodialysis, our case provides evidence that treatment with fomepizole without hemodialysis appears to be a viable alternative option in patients with even extremely high plasma ethylene glycol concentrations as long as their renal function is intact.     

急性乙二醇中毒3例报告及文献回顾

乙二醇为防冻剂的主要成分。乙二醇主要在肝脏内先后代谢为羟乙醛、乙醇醛、乙醇酸及草酸。这些代谢特可导致代谢性酸中毒。典型临床表现通常为3个阶段：第1阶段在摄入后12h内，乙二醇致中枢神经系统抑制；第2阶段在摄入12～24h后，出现代谢性酸中毒和心肺疾病；第3阶段在摄入后24～72h。出现肾小管坏死和肾衰竭。乙二醇致死量为1．4-1．6ml／kg[成人（70kg）约为100m1]。一旦怀疑乙二醇中毒，应尽快测定乙二醇和乙醇酸血浓度明确诊断。中毒治疗原则包括早期及时洗胃，给予乙醇或甲吡唑解毒剂，血液透析，碳酸氢钠vitB6等。大多数乙二醇中毒患者经早期诊断治疗后可恢复正常。本文报告3例急性乙醇中毒，3例患者均为男性（48岁），每人服用防冻液约为150ml。2倒出现头痛有，1例出现上腹不适、兴奋、躁动。3倒患者在摄入乙醇后12～18h出现代谢性酸中毒，24h出现血尿。经洗胃和血液透析，给予法莫替丁40mg，10％葡萄糖酸钙20ml。4％碳酸氢钠静脉注射，38％白酒200ml口服。2倒治愈，1例于摄入乙二醇后29h死亡。     

Percutaneous absorption and distribution of methanol in a homicide

A woman was alleged to have committed suicide by consuming a gasoline additive shortly before jumping from a second floor balcony within her home. She was found dead by police with a multitude of injuries, lying nude in a partially evaporated unknown residue that was later determined to be methanol. Samples collected at autopsy were found to contain methanol in the following concentrations: femoral blood 31.2 mg/dL, pulmonary artery blood 111.0 mg/dL, aortic blood 77.8 mg/dL, vitreous fluid 196.4 mg/dL, brain 22.0 mg/100 g, liver 21.2 mg/100 g, and kidney 25.9 mg/100 g using a headspace gas chromatographic method. Significantly, no methanol was detected in samples recovered from the esophagus, stomach, duodenum, small intestine, bile, or urine. These findings are inconsistent with either recent or delayed oral ingestion of methanol. We concluded that absorption of methanol occurred dermally and through the oral mucosa as she lay dying and saturated in the fuel additive. Based upon the toxicological data and a comprehensive forensic investigation (including documentation and analysis of evidence recovered at the scene and the autopsy), the cause of death was determined to be blunt impact trauma and methanol poisoning.     

Acute Chloroform Ingestion Successfully Treated with Intravenously Administered N-acetylcysteine

Chloroform, a halogenated hydrocarbon, causes central nervous system depression, cardiac arrhythmias, and hepatotoxicity. We describe a case of chloroform ingestion with a confirmatory serum level and resultant hepatotoxicity successfully treated with intravenously administered N-acetylcysteine (NAC). A 19-year-old man attempting suicide ingested approximately 75 mL of chloroform. He was unresponsive and intubated upon arrival. Intravenously administered NAC was started after initial stabilization was complete. His vital signs were normal. Admission laboratory values revealed normal serum electrolytes, AST, ALT, PT, BUN, creatinine, and bilirubin. Serum ethanol level was 15 mg/dL, and aspirin and acetaminophen were undetectable. The patient was extubated but developed liver function abnormalities with a peak AST of 224 IU/L, ALT of 583 IU/L, and bilirubin level reaching 16.3 mg/dL. NAC was continued through hospital day 6. Serum chloroform level obtained on admission was 91 μg/mL. The patient was discharged to psychiatry without known sequelae and normal liver function tests. The average serum chloroform level in fatal cases of inhalational chloroform poisoning was 64 μg/mL, significantly lower than our patient. The toxicity is believed to be similar in both inhalation and ingestion routes of exposure, with mortality predominantly resulting from anoxia secondary to central nervous system depression. Hepatocellular toxicity is thought to result from free radical-induced oxidative damage. Previous reports describe survival after treatment with orally administered NAC, we report the first use of intravenously administered NAC for chloroform ingestion. Acute oral ingestion of chloroform is extremely rare. Our case illustrates that with appropriate supportive care, patients can recover from chloroform ingestion, and intravenously administered NAC may be of benefit in such cases.     

Ethylene glycol ingestion treated only with fomepizole

Introduction

Ethylene glycol is a widely used chemical that is capable of causing significant injury if ingested. Treatment for ethylene glycol poisoning typically includes basic supportive care, alcohol dehydrogenase inhibition, and hemodialysis. Recent data have suggested that hemodialysis may not be necessary for cases of ethylene glycol poisoning that can be treated with fomepizole as blocking therapy before acidosis or renal dysfunction develops.

Case Report

A 33-year-old man presented to the emergency department 1 hour after drinking approximately 1/2 gallon of ethylene glycol antifreeze and an unknown quantity of beer. On arrival he was mildly inebriated but otherwise displayed no other features of ethylene glycol poisoning. Fomepizole therapy was initiated and initial laboratory studies later revealed an osmol gap of 157 mOsm and an ethylene glycol concentration of 706 mg/dL. Nephrology and toxicology services were consulted. Over the next 3 days, fomepizole therapy was continued while the patient’s acid-base status and renal function were closely monitored. No evidence of acid-base abnormalities or renal impairment was ever observed and the patient was discharged to psychiatric care on the fourth hospital day.

Discussion

This report describes the case of a patient who presented soon after a massive ingestion of ethylene glycol with very high serum concentrations. He was successfully treated using fomepizole and basic supportive care. Our patient developed neither renal insufficiency nor metabolic acidosis. His concomitant ethanol consumption, early presentation, and treatment likely contributed to his favorable outcome. This case report underscores the effectiveness of supportive care and fomepizole in the treatment of ethylene glycol poisoning.     

Treatment of severe pediatric ethylene glycol intoxication without hemodialysis

BACKGROUND: There is limited experience treating severe ethylene glycol poisoning in children without hemodialysis. The objective of this study was to describe the clinical course and outcome of severe pediatric ethylene glycol poisoning treated without hemodialysis. METHODS: Patient records were identified retrospectively by hospital discharge diagnosis (ICD-9 code) of ethylene glycol poisoning from 1999 through 2002 at a pediatric medial center. Patients with initial serum ethylene glycol concentrations less than 50 mg/dL or those who received hemodialysis were excluded. RESULTS: Six patients with an age range of 22 months to 14 years were admitted for treatment of ethylene glycol poisoning over a four-year period. Initial serum ethylene glycol concentrations ranged from 62 to 304 mg/dL (mean 174.0 mg/dL). The lowest-measured individual serum bicarbonates ranged from 4 to 17 mEq/L. All patients were initially admitted to intensive care. One patient received ethanol only, two patients received fomepizole only, and three patients received a loading dose of ethanol and then were converted to fomepizole therapy. None of the patients received hemodialysis. Treatment was continued until the serum ethylene glycol was less than 10 mg/dL. Metabolic acidosis resolved with intravenous fluid and supplemental bicarbonate within 24h. All patients had a normal creatinine upon presentation and at discharge. The mean length of stay in intensive care was 21h and on the ward was 33.7h. One episode of hypoglycemia occurred in a 22-month-old. All patients recovered without evidence of renal insufficiency or other major complications at discharge. CONCLUSION: Six pediatric patients with severe ethylene glycol intoxication and normal renal function were successfully treated without hemodialysis.     

Expert opinion: fomepizole may ameliorate the need for hemodialysis in methanol poisoning

Fomepizole is now the antidote of choice in methanol poisoning. The use of fomepizole may also change the indications for hemodialysis in these patients. We have addressed this change in a review of articles on methanol poisonings. Review of the literature (through PubMed) combined with our own experiences from two recent methanol outbreaks in Estonia and Norway. The efficiency of dialysis during fomepizole treatment was reported in only a few reports. One recent study challenged the old indications, suggesting a new approach with delayed or even no hemodialysis. Methanol-poisoned patients on fomepizole treatment may be separated into two categories: 1) The critically ill patient, with severe metabolic acidosis (base deficit >15 mM) and/or visual disturbances should be given buffer, fomepizole and immediate hemodialysis: dialysis removes the toxic anion formate, and assists in correcting the metabolic acidosis, thereby also reducing formate toxicity. The removal of methanol per se is not important in this setting because fomepizole prevents further production of formic acid. 2) The stable patient, with less metabolic acidosis and no visual disturbances, should be given buffer and fomepizole. This treatment allows for the possibility to delay, or even drop, dialysis in this setting, because patients will not develop more clinical features from methanol poisoning when fomepizole and bicarbonate is given in adequate doses. Indications and triage for hemodialysis in methanol poisonings should be modified. Delayed hemodialysis or even no hemodialysis may be an option in selected cases.     

Treatment of methanol and isopropanol poisoning with intravenous fomepizole

CASE REPORT: We report a case of mixed methanol and isopropanol poisoning in a patient who refused dialysis but agreed to treatment with intravenous fomepizole. The patient was asymptomatic on arrival, with initial blood methanol and isopropanol concentrations of 146 mg/dL and 39 mg/dL, respectively. Blood ethanol was undetectable. The patient was treated with fomepizole twice daily intravenously until blood methanol was undetectable. No side effects of therapy, other than transient eosinophilia, were observed. The evolution was uneventful and no metabolites of either alcohol were detected at any time during the hospitalization. The decay of plasma methanol and isopropanol under fomepizole treatment were well described by first-order kinetics. The plasma elimination half-lives of methanol and isopropanol were 47.6 hours and 27.7 hours, respectively. Fomepizole appears to have been effective in blocking the toxic metabolism of both methanol and isopropanol and was associated with a favorable outcome.     

Hyperglycemia in acute aluminum phosphide poisoning as a potential prognostic factor

Aluminum phosphide (AlP) is a solid fumigant widely used in Iran as a grain preservative. When reacted with water or acids, AIP produces phosphine gas, a mitochondrial poison that interferes with oxidative phosphorylation and protein synthesis. Poisoning by AIP is one of the most important causes of fatal chemical toxicity in Iran. There are few studies in the medical literature addressing prognostic factors associated with AlP poisoning. In this prospective study conducted across a 14-month period commencing on 21st March 2006, we enrolled all patients admitted to the ICU of Loghman-Hakim Hospital Poison Center (Tehran, Iran) with AIP poisoning, no history of diabetes mellitus diagnosed before hospitalization, and normal body mass index. We recorded patient-specific demographic information, blood glucose level on presentation (before treatment), arterial blood gas (ABG) analysis, time elapsed between ingestion and presentation, ingested dose, duration of intensive care admission, and outcome data related to each presentation. We enrolled the group of patients who survived the intoxication as a control group and compared their blood glucose levels with those who died because of AlP poisoning. Data were analyzed by Statistical Product and Service Solutions (SPSS) software (Version 12; Chicago, Ilinois, USA) using logistic regression, Pearson correlation coefficient and Student's t-test. P values of 0.05 or less were considered as the statistical significant levels. Forty-five patients (21 women and 24 men) with acute AlP poisoning were included in the study. The mean age was 27.3 +/- 11.5 years (range: 14-62 years). Thirteen patients survived (29%) and 32 expired (71%). AlP poisoning followed deliberate ingestion in all patients. The time elapsed between ingestion and arrival at the hospital was 3.2 +/- 0.4 h. There was no significant difference between survived and non-survived groups according to age, gender, and time to treatment. However, the difference between mean blood glucose levels in survived (143.4 +/- 13.7 mg/dL) and non-survived (222.6 +/- 20 mg/dL) cases was statistically significant (P = 0.021). There was no significant correlation between blood glucose level and time to treatment, age, gender, pH, HCO3 concentration, and ingested dose. Twenty-three (71.9%) of non-survived and four (30.8%) of survived patients had a blood glucose level greater than 140 mg/dL. After adjusting according to age, gender, ingested dose, pH and HCO3 concentration The odds ratio for hyperglycemia as a risk factor for death was 5.7 (CI of 1.4-23.4). In our study, patients who succumbed to AIP poisoning had significantly higher mean blood glucose levels than those who survived. This correlation of hyperglycemic effect and mortality suggests that it may be useful in guiding risk assessment and treatment of AIP poisoning. Management of hyperglycemia may have a useful role in treatment of these patients by allowing increased entrance of glucose into cells and reducing oxygen consumption.     

What are the adverse effects of ethanol used as an antidote in the treatment of suspected methanol poisoning in children?

BACKGROUND: Ethanol used as an antidote is said to have various adverse effects, particularly in children. The rate of these adverse effects is not known. METHODS: Twenty-one-year retrospective chart review (1980-2000) from suspected methanol poisoning patients treated with ethanol in two large pediatric tertiary care centers. RESULTS: A total of 60 children (median age of 24 months) received ethanol for suspected methanol poisoning: 39 orally and 21 intravenously. Median initial methanol level was 4.16 mmol/L (13.3 mg/dL) (range 0 to 87.5 mmol/L or 0 to 280 mg/dL). Median duration of ethanol treatment was 16 hours (range 1.5 to 72 hours). None [0% (95% CI 0-5%)] of the 60 patients developed symptomatic hypoglycemia. Of the 50 patients that had a glucose level measured, none [(0% [95% CI 0-6%)] had a serum glucose concentration < 2.78 mmol/L (< 50 mg/dL). Eight patients [16% (95% CI 8-30%)] had at least one serum glucose concentration between 2.78-3.61 mmol/L (50-65 mg/dL), but none of those had symptoms compatible with hypoglycemia. A total of 42 patients [84% (95% CI 70-92%)] had all their serum glucose concentrations > 3.61mmol/L (> 65 mg/dL). There was no identifiable difference in the glucose intake between the serum glucose concentration groups. Six out of the 60 patients [10% (95% CI 4-21%)] were described as more drowsy after ethanol but none was comatose or needed intubation. No child showed signs of hypothermia [0/40 (95% CI 0-8%)] (rectal temperature < 35 degrees C), hepatotoxicity (0/12) (AST or ALT > 100 U/L) or even thrombophlebitis (0/21). None of the 22 patients with toxic levels of methanol (> or = 26.2 mmol/L- > or = 20 mg/dL) died or had ethanol-induced morbidity despite wide variation in ethanol levels. CONCLUSION: The rate of clinically important adverse effects related to ethanol used as an antidote to treat methanol poisoning in children was either absent or low in a tertiary care pediatric hospital setting. There was no morbidity or mortality associated with ethanol when it was used despite wide variation in ethanol levels. These results suggest that with appropriate monitoring and intravenous glucose intake in a controlled environment such as a pediatric intensive care unit, ethanol therapy does not carry as many risks as currently believed.     

Toxicity following unintentional DDT ingestion

INTRODUCTION: Dichlorodiphenyltrichloroethane (DDT) ingestion is an uncommon cause of poisoning worldwide. To date, no cases of renal impairment after oral intake of DDT in humans have been reported. We describe the clinical course and management of two patients presenting after DDT ingestion, one of whom developed acute oliguric renal failure. CASE REPORT: A father and son mistook DDT powder for flour while preparing fish for a meal, and after eating they developed symptoms compatible with acute organochlorine insecticide poisoning. Both were intubated endotracheally due to recurrent convulsions and loss of consciousness followed by admission to the intensive care unit. Both cases developed severe metabolic acidosis. Acute oliguric renal failure (ARF) was diagnosed in the son in the second day, with a blood urea nitrogen level of 47 mg/dl and creatinine 6.4 mg/dl. Urinalysis disclosed abundant RBCs on the third day. Vigorous fluid resuscitation and strict monitoring helped reverse its clinical course by the tenth day. Both patients recovered within two weeks and were discharged without sequelae. CONCLUSION: Clinicians should not overlook the possibility of DDT poisoning in the differential diagnosis of acute renal failure and seizures. More strict measures should be taken to prohibit misidentification of DDT and similar products, particularly in the developing world.     

Full Recovery from a Potentially Lethal Dose of Mercuric Chloride

Introduction

Mercuric chloride poisoning is rare yet potentially life-threatening. We report a case of poisoning with a potentially significant amount of mercuric chloride which responded to aggressive management.

Case Report

A 19-year-old female presented to the Emergency Department with nausea, abdominal discomfort, vomiting of blood-stained fluid, and diarrhea following suicidal ingestion of 2–4 g of mercuric chloride powder. An abdominal radiograph showed radio-opaque material within the gastric antrum and the patient’s initial blood mercury concentration was 17.9 μmol/L (or 3.58 mg/L) at 3 h post-ingestion. Given the potential toxicity of inorganic mercury, the patient was admitted to the intensive care unit and chelation with dimercaprol was undertaken. Further clinical effects included mild hemodynamic instability, acidosis, hypokalemia, leukocytosis, and fever. The patient’s symptoms began to improve 48 h after admission and resolved fully within a week.

Discussion

Mercuric chloride has an estimated human fatal dose of between 1 and 4 g. Despite a reported ingestion of a potentially lethal dose and a high blood concentration, this patient experienced mild to moderate poisoning only and she responded to early and appropriate intervention. Mercuric chloride can produce a range of toxic effects including corrosive injury, severe gastrointestinal disturbances, acute renal failure, circulatory collapse, and eventual death. Treatment includes close observation and aggressive supportive care along with chelation, preferably with 2,3-dimercapto-1-propane sulfonate or 2,3-meso-dimercaptosuccinic acid.     

Polyuria, Acidosis, and Coma Following Massive Ibuprofen Ingestion

Ibuprofen was the first over-the-counter nonsteroidal anti-inflammatory drug available in the United States. Despite being a common agent of ingestion, significant toxicity in overdose is rare. We report a case of a massive ibuprofen ingestion who developed polyuria, acidosis, and coma but survived, despite having a serum ibuprofen concentration greater than previous fatal cases. A 19-year-old man ingested 90 g (1,200 mg/kg) ibuprofen. He was initially awake and alert, but his level of consciousness deteriorated over several hours. Seven hours following the ingestion, he was intubated and mechanically ventilated secondary to loss of airway reflexes. He developed a lactic acidosis and polyuria, which lasted for nearly 24 h. His serum creatinine peaked at 1.12 mg/dL. An ibuprofen level drawn 7 h postingestion was 739.2 mg/L (therapeutic 5–49 mg/L). We describe a case of a massive ibuprofen overdose characterized by metabolic acidosis, coma, and a state of high urine output who survived with aggressive supportive care. This case is unique in several ways. First, ibuprofen levels this high have only rarely been described. Second, polyuria is very poorly described following ibuprofen ingestions.     

American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning

EPIDEMIOLOGY: Almost all cases of acute methanol toxicity result from ingestion, though rarely cases of poisoning have followed inhalation or dermal absorption. The absorption of methanol following oral administration is rapid and peak methanol concentrations occur within 30-60minutes. MECHANISMS OF TOXICITY: Methanol has a relatively low toxicity and metabolism is responsible for the transformation of methanol to its toxic metabolites. Methanol is oxidized by alcohol dehydrogenase to formaldehyde. The oxidation of formaldehyde to formic acid is facilitated by formaldehyde dehydrogenase. Formic acid is converted by 10-formyl tetrahydrofolate synthetase to carbon dioxide and water. In cases of methanol poisoning, formic acid accumulates and there is a direct correlation between the formic acid concentration and increased morbidity and mortality. The acidosis observed in methanol poisoning appears to be caused directly or indirectly by formic acid production. Formic acid has also been shown to inhibit cytochrome oxidase and is the prime cause of ocular toxicity, though acidosis can increase toxicity further by enabling greater diffusion of formic acid into cells. FEATURES: Methanol poisoning typically induces nausea, vomiting, abdominal pain, and mild central nervous system depression. There is then a latent period lasting approximately 12-24 hours, depending, in part, on the methanol dose ingested, following which an uncompensated metabolic acidosis develops and visualfunction becomes impaired, ranging from blurred vision and altered visual fields to complete blindness. MANAGEMENT: For the patient presenting with ophthalmologic abnormalities or significant acidosis, the acidosis should be corrected with intravenous sodium bicarbonate, the further generation of toxic metabolite should be blocked by the administration of fomepizole or ethanol and formic acid metabolism should be enhanced by the administration of intravenous folinic acid. Hemodialysis may also be required to correct severe metabolic abnormalities and to enhance methanol and formate elimination. For the methanol poisoned patient without evidence of clinical toxicity, the first priority is to inhibit methanol metabolism with intravenous ethanol orfomepizole. Although there are no clinical outcome data confirming the superiority of either of these antidotes over the other, there are significant disadvantages associated with ethanol. These include complex dosing, difficulties with maintaining therapeutic concentrations, the need for more comprehensive clinical and laboratory monitoring, and more adverse effects. Thus fomepizole is very attractive, however, it has a relatively high acquisition cost. CONCLUSION: The management of methanol poisoning includes standard supportive care, the correction of metabolic acidosis, the administration of folinic acid, the provision of an antidote to inhibit the metabolism of methanol to formate, and selective hemodialysis to correct severe metabolic abnormalities and to enhance methanol and formate elimination. Although both ethanol and fomepizole are effective, fomepizole is the preferred antidote for methanol poisoning.