Alleged breaches of "standards of medical care" in a patient overdose death possibly related to chronic opioid analgesic therapy, application of the controlled substances model guidelines: case report.

OBJECTIVES: The objectives of this medicolegal case report are the following: 1) to present details of a chronic pain patient (CPP) who was placed on chronic opioid analgesic therapy (COAT), and subsequently overdosed on multiple drugs, some of which were not prescribed by his COAT physician; 2) to present both the plaintiff's and defendant's (the COAT prescriber) expert witnesses' opinions as to the allegation that COAT prescribing was the cause of death; and 3) based on these opinions, to develop some recommendations on how pain physicians can utilize the use of Controlled Substances Model Guidelines in order to protect the patient and themselves from such an occurrence. METHODS: This is a case report of a CPP treated by a pain physician. RESULTS: Differences between the plaintiff's and defendant's expert's opinions are explained utilizing the Controlled Substances Model Guidelines. CONCLUSIONS: Some CPPs may withhold information critical to their COAT treatment. Application of the Controlled Substances Model Guidelines and the newer Federation of State Medical Boards' policy on opioid prescribing can be helpful in improving patient care and may be helpful in protecting the physician medicolegally.

[Possibilities for toxicologic evidence in adipocere formation and postmortem interval of several years]. / Toxikologische Nachweismöglichkeiten bei Fettwachsumwandlung und mehrjähriger Liegezeit.

It is reported on a 31-year-old man, whose dead body was found together with numerous packets of poisons and medicaments in a forest after a post-mortem period of nearly 3 years. Despite advanced skeletization and complete transformation of the still existing residual soft tissues to adipocere, highly toxic concentrations of two heavy metals (cadmium: 0.30 mg/kg; thallium: 0.91 mg/kg) and minor levels of three organic substances (phenobarbitone: 0.32 mg/kg; nordazepam: 0.14 mg/kg; salicylic acid: 0.04 mg/kg) were detected in adipoceratous samples. Even if it is not possible to derive similar blood levels from post-mortem values, the cause and manner of death (suicidal intoxication) could be clarified with the necessary degree of certainty. Few comparable literature reports either deal with exhumations or non-toxic concentrations of substances in morphologically better preserved adipoceratous bodies. Our case demonstrates that toxicological analyses may contribute to the clarification of the cause of death even if advanced adipocere formation with a longer post-mortem interval is present.

Diagnostic performance of the EMIT-tox benzodiazepine immunoassay, FPIA serum benzodiazepine immunoassay, and radioreceptor assay in suspected acute poisoning.

We evaluated the diagnostic performance of the EMIT-tox serum benzodiazepine assay adapted to a Hitachi 717 analyzer (EMIT), the Abbott ADx serum benzodiazepine fluorescence polarization immunoassay (FPIA), and a radioreceptor assay (RRA) in 113 patients with suspected acute poisoning. The reference method was high-performance liquid chromatography with ultraviolet detection after solid-phase extraction. For the discrimination between negative and positive samples, the areas under the receiver-operating characteristic (ROC) curves were 0.976, 0.991, and 0.991 for EMIT (cutoff, 50-ng/mL diazepam), FPIA (cutoff, 12-ng/mL nordiazepam), and RRA (cutoff, 50-ng/mL diazepam), respectively. For the discrimination between non-toxic and toxic concentrations, the areas under the ROC curves were 0.896, 0.893, and 0.933, respectively. EMIT (with the cutoff lowered to 50 ng/mL), FPIA, and RRA can be reliably used to screen for the presence of benzodiazepines in serum, but in many cases they cannot discriminate between toxic and nontoxic concentrations.

Abnormal ventricular repolarization mimicking myocardial infarction after heterocyclic antidepressant overdose.

In 2 young adult women who experienced acute heterocyclic antidepressant intoxication, we found a quite unusual electrocardiographic pattern characterized by abnormal ST-tract elevation in the right precordial leads associated with a marked QRS widening (right bundle branch block and left anterior fascicular block type). Because serum electrolyte imbalance and acute myocardial ischemic events were excluded, the mechanism by which antidepressant overdose may produce such elevation of the ST tract remains unclear.

Effect of ethanol ingestion on outcome of drug overdose.

It was traditionally assumed that ethanol, as part of an intentional drug overdose, will increase morbidity and mortality. The authors prospectively studied the effect of ethanol on the outcome of intentional drug overdose in 468 adults, 196 of whom required hospital admission. Ethanol was detected in significantly fewer patients who required admission. Ethanol ingestion was not related to coma, impaired vital signs or mortality. Indeed, the duration of coma was significantly shorter in patients in whom ethanol was detected, but this group had a lesser incidence of multiple drug and nonbarbiturate hypnotic ingestion and a greater incidence of chronic ethanol use. Thus, it seems that ethanol is not associated with a worse clinical course if the drug overdose patient reaches medical care before an irreversible event.

Benzodiazepine overdosage: plasma concentrations and clinical outcome.

Plasma concentrations and their relation to clinical outcome were evaluated in 21 patients who reached emergency treatment facilities following acute overdosage with benzodiazepine derivatives. Diazepam was implicated in 18 of the 21 cases, with plasma diazepam levels ranging from 585-8,635 ng/ml. In four cases of overdosage with diazepam alone, patients were minimally sedated and were discharged within 24 h, despite diazepam doses as high as 750 mg and plasma levels as high as 4,792 ng/ml. However, concurrent ingestion of diazepam together with other central depressant drugs (such as ethanol, barbiturates, analgesics, or tricyclic antidepressants) produced serious intoxication in 5 of the remaining 14 patients, regardless of the diazepam dosage or plasma concentration. Thus the severity of poisoning following benzodiazepine overdosage is determined largely by co-ingestion of other central depressants rather than the amount of benzodiazepine ingested or its concentration in plasma.