Kent R. Olson

Physical assessment and differential diagnosis of the poisoned patient

SummaryThe rapid diagnosis and immediate intervention required in patients with serious drug overdose or poisoning makes toxicological screening of limited value to the emergency department physician. Instead, a careful clinical evaluation using the history, physical examination, and the more readily available laboratory tests may allow a tentative diagnosis and the initiation of life-saving treatment. Laboratory tests should include serum osmolality, electrolytes, glucose, BUN and an estimation of the anion and osmolar gaps. The ECG can also provide useful information.Clinical findings of important include altered blood pressure, pulse, respiration and body temperature, the presence of coma, agitation, delirium or psychosis, and muscular weakness. An ophthalmological examination is also of importance in the acutely poisoned patient. Oral burns or dysphagia may occur following ingestion of any strongly reactive substance, but the absence of oral burns does not preclude the possibility of oesophageal or stomach injury. Odours and skin colour may also contribute to the diagnosis.Comprehensive toxicology screening may not be immediately available, or may be inaccurate, thus adding little to the information obtained during the initial evaluation of the poisoned patient.

Osmolar gap with Minimal Acidosis in Combined Methanol and Methyl Ethyl Ketone Ingestion

Methyl ethyl ketone is a common solvent but data on overdose in humans are scarce. We report a case of co-ingestion of methyl ethyl ketone together with methanol associated with a hyperosmolar coma without anion gap metabolic acidosis. Blood levels of methyl ethyl ketone and its metabolite, 2-butanol, indicated that this solvent did contribute approximately 20 mosm/L to an observed osmolar gap of 99 mosm/L. At the levels detected, methyl ethyl ketone may have inhibited methanol metabolism, contributing to the low serum formate (1.3 mmol/L) and normal anion gap despite a blood methanol of 67 mmol/L.

Massive Naproxen Overdose with Serial Serum Levels

ContextMassive naproxen overdose is not commonly reported. Severe metabolic acidosis and seizure have been described, but the use of renal replacement therapy has not been studied in the context of overdose.Case DetailsA 28-year-old man ingested 70xa0g of naproxen along with an unknown amount of alcohol in a suicidal attempt. On examination in the emergency department 90xa0min later, he was drowsy but had normal vital signs apart from sinus tachycardia. Serum naproxen level 90xa0min after ingestion was 1,580xa0mg/L (therapeutic range 25–75xa0mg/L). He developed metabolic acidosis requiring renal replacement therapy using sustained low efficiency dialysis (SLED) and continuous venovenous hemofiltration (CVVH) and had recurrent seizure activity requiring intubation within 4xa0h from ingestion. He recovered after 48xa0h.DiscussionMassive naproxen overdose can present with serious toxicity including seizures, altered mental status, and metabolic acidosis.ConclusionHemodialysis and renal replacement therapy may correct the acid base disturbance and provide support in cases of renal impairment in context of naproxen overdose, but further studies are needed to determine the extraction of naproxen.

Ventricular Dysrhythmias Associated with Poisoning and Drug Overdose: A 10-Year Review of Statewide Poison Control Center Data from California

BackgroundVentricular dysrhythmias are a serious consequence associated with drug overdose and chemical poisoning. The risk factors for the type of ventricular dysrhythmia and the outcomes by drug class are not well documented.ObjectiveThe aim of this study was to determine the most common drugs and chemicals associated with ventricular dysrhythmias and their outcomes.MethodsWe reviewed all human exposures reported to a statewide poison control system between 2002 and 2011 that had a documented ventricular dysrhythmia. Cases were differentiated into two groups by type of arrhythmia: (1) ventricular fibrillation and/or tachycardia (VT/VF); and (2) torsade de pointes (TdP).ResultsAmong the 300 potential cases identified, 148 cases met the inclusion criteria. Of these, 132 cases (89xa0%) experienced an episode of VT or VF, while the remaining 16 cases (11xa0%) had an episode of TdP. The most commonly involved therapeutic classes of drugs associated with VT/VF were antidepressants (33/132, 25xa0%), stimulants (33/132, 25xa0%), and diphenhydramine (16/132, 12.1xa0%). Those associated with TdP were antidepressants (4/16, 25xa0%), methadone (4/16, 25xa0%), and antiarrhythmics (3/16, 18.75xa0%). Drug exposures with the greatest risk of death in association with VT/VF were antidepressant exposure [odds ratio (OR) 1.71; 95xa0% confidence interval (CI) 0.705–4.181] and antiarrhythmic exposure (OR 1.75; 95xa0% CI 0.304–10.05), but neither association was statistically significant. Drug exposures with a statistically significant risk for TdP included methadone and antiarrhythmic drugs.ConclusionsAntidepressants and stimulants were the most common drugs associated with ventricular dysrhythmias. Patients with suspected poisonings by medications with a high risk of ventricular dysrhythmia warrant prompt ECG monitoring.

Case Files of the California Poison Control System, San Francisco Division: Blue Thunder Ingestion: Methanol, Nitromethane, and Elevated Creatinine

Keywords Nitromethane.Methanol.CreatinineCase PresentationA 41-year-old man with a history of ethanol abuse wasfound on the streets with his clothing saturated with fecalmaterial. In the emergency department (ED), he wasconfused and had an unsteady gait. He was sleepy andslow in responding, although easily arousable. He admittedto being depressed and said that he tried to commit suicideby consuming vodka and “Blue Thunder”, a fuel for radio-controlled racing cars that he had purchased from a hobbyshop the day before presentation. He denied any other drugingestion or previous medical history and was not takingany medications. He did not have any focal neurologicalsymptoms, visual disturbance, gastrointestinal symptomssuch as nausea or vomiting, or chest discomfort.His vital signs were within normal limits: temperature36.4°C, blood pressure 145/87 mm Hg, heart rate 95/min,respiratory rate 16/min and pulse oximetry saturation 97%on room air. His physical examination was unremarkableexcept for an unsteady gait. His cranial nerves, motor, andsensory findings were grossly intact. As he had attemptedto leave the ED several times despite being ataxic, he wasplaced in restraints and sedated with intravenous boluses oflorazepam and admitted for further workup.Computed tomography of his brain did not show anygross abnormalities. Initial laboratory data included: sodium135 mmol/L, potassium 3.8 mmol/L, chloride 97 mmol/L,bicarbonate 21 mmol/L, blood urea nitrogen 7.9 mmol/L(22.0 mg/dL), creatinine 8,270 μmol/L (93.6 mg/dL), andglucose 6.5 mmol/L (117 mg/dL). The anion gap was17 mmol/L. Lactic acid and hepatic enzymes were withinnormal limits. The serum ethanol, acetaminophen, andsalicylate levels were below detection limits. UrinalysiswasnormalwithapHof5.5.Serumsampleswerereferredtoanoutside laboratory for methanol, ethylene glycol, acetone,isopropyl alcohol, and paraldehyde levels. After 4 h ofsupportive treatment including intravenous fluids, repeatlaboratory results were: sodium 134 mmol/L, potassium3.8 mmol/L, chloride 98 mmol/L, bicarbonate 23 mmol/L,blood urea nitrogen 6.9 mmol/L (19.0 mg/dL), and glucose6.5 mmol/L (117 mg/dL).The laboratory had independently decided that nitro-methane was an interfering substance and did not repeat thecreatinine level. The anion gap was now 13 mmol/L and thecalculated osmolality [1] was 282 mmol/kg. Serum osmo-lality determined by freezing point depression was430 mmol/kg (reference range 275-295 mmol/kg). Theosmolar gap was estimated to be 148 mmol/kg.Is this Patient’s Presentation Consistent with MethanolPoisoning?After ingestion, the hepatic enzyme alcohol dehydrogenaseconverts methanol to formaldehyde, which is then con-verted to formic acid by formaldehyde dehydrogenase [2].Although formaldehyde is more toxic than formic acid, it

Symptomatic Exposures Among California Inmates 2011–2013

Prisoners have a high prevalence of substance misuse and abuse, but few studies have examined symptomatic exposures among incarcerated populations. We sought to further characterize the nature of these exposures among this population using the California Poison Control System data. Keyword searches identified inmate cases in 2011–2013 for patients 20+u2009years old exposed to a single substance and taken to hospital from jail, prison, or police custody. Comparisons were made with non-inmate cases during the same period, using similar limitations. Body stuffers and body packers were analyzed as a subgroup. Seven hundred four inmate cases were compared to 106,260 non-inmate cases. Inmates were more likely to be younger, male, and to have engaged in drug misuse or abuse. They most commonly ingested methamphetamine, heroin, acetaminophen, and anticonvulsants. Inmates were more likely to receive activated charcoal (OR 9.87, 8.20–11.88), whole bowel irrigation (OR 44.50, 33.83–58.54), undergo endotracheal intubation (OR 4.09, 2.91–5.73), and to experience a major clinical outcome or death (OR 1.41, 1.05–1.89). When body stuffers and packers were removed, clinical findings were similar, though the odds of a major outcome or death became statistically non-significant. Body stuffers and body packers primarily used methamphetamine and heroin, and compared with other inmates had significantly higher odds of both adverse clinical effects and poor outcome. This large series provides a profile of symptomatic exposures among inmates, a little-studied population. The potential for high morbidity among body stuffers and packers suggests that a high index of suspicion of such ingestions be maintained when evaluating patients prior to incarceration.

Massive Lindane Overdose with Toxicokinetics Analysis

BackgroundLindane is a possible carcinogen with known teratogenicity and immunologic and neurotoxic properties. Despite reports of seizures, coma, and death associated with its use as well as banning of its environmental use by the Environmental Protection Agency (EPA), the US Food and Drug Administration (FDA) still allows treatment with lindane as a second-line scabicide and pediculicide. We present a case of a massive suicidal ingestion of lindane in which the patient survived the ingestion, though he did expire shortly thereafter from an unrelated cause pre-discharge.MethodsPharmacokinetic analysis of serum lindane concentrations was performed with Phoenix® WinNONLIN®. The estimated distribution half-life for lindane was 10.3xa0h, and the terminal half-life was 162.9xa0h, much longer than the previously reported terminal half-life of 25–36xa0h. Because of this long half-life, repeated lindane exposures may lead to accumulation of lindane in the tissues.ResultAfter overdose, toxicity may be delayed and full recovery may be prolonged.