Poor Man's Methadone: A Case Report of Loperamide Toxicity.

Loperamide, a common over-the-counter antidiarrheal drug and opioid derivative, is formulated to act upon intestinal opioid receptors. However, at high doses, loperamide crosses the blood-brain barrier and reaches central opioid receptors in the brain, leading to central opiate effects including euphoria and respiratory depression. We report the case of a young man found dead in his residence with a known history of drug abuse. At autopsy, the only significant findings were a distended bladder and bloody oral purge. Drug screening found nontoxic levels of alprazolam, fluoxetine, and marijuana metabolites. Liquid chromatography time-of-flight mass spectrometry found an unusual set of split isotope peaks consistent with chlorine. On the basis of autopsy and toxicological findings, loperamide toxicity was suspected because of its opioid properties and molecular formula containing chlorine. A sample of loperamide was analyzed by liquid chromatography time-of-flight mass spectrometry, resulting in a matching mass and retention time to the decedent's sample. Subsequently, quantitative testing detected 63 ng/mL of loperamide or more than 6 times of therapeutic peak concentration. Cause of death was determined as "toxic effects of loperamide with fluoxetine and alprazolam." Because of its opioid effects and easy accessibility, loperamide is known as "poor man's methadone" and may go undetected at medical and forensic drug screening.

Pathological findings in 2 cases of fatal 25I-NBOMe toxicity.

The research compound 25I-NBOMe, also known as CIMBI-5 or INBMeO, was created in academic laboratories as a potent serotonin 2A receptor agonist. Because of its high affinity and ambiguous legal status, recreational drug enthusiasts have used this compound as a powerful alternative to other hallucinogenic drugs such as lysergic acid diethylamide. We report 2 deaths after 25I-NBOMe ingestion by decedents who attended separate "rave" parties. The first case involved a 21-year-old male who admitted taking "acid" to his friend. A sudden violent rage caused him to flail about, and he subsequently became unresponsive. The postmortem examination revealed numerous external injuries that were consistent with physical aggression. The second case involved a 15-year-old female who was socializing outside a rave party, became ill, and rapidly deteriorated as her friend transported her to the hospital. The postmortem assessment was similar to the first case in that external contusions featured prominently. Comprehensive toxicology screens in both cases revealed only evidence of marijuana use. A deeper analysis using time-of-flight mass spectrometry revealed the presence of 25I-NBOMe, which was further confirmed by tandem-mass spectrometry. The behavior and injuries in these cases reveal a consistent pattern preceding fatal 25I-NBOMe toxicity.

Postmortem findings in eight cases of influenza A/H1N1.

In March and early April 2009, cases of a new swine-origin influenza A (H1N1) virus were diagnosed in Mexico and the United States. Influenza virus presents as a respiratory infection with high morbidity and mortality. We describe the postmortem findings of eight confirmed cases of influenza A/H1N1 in a medical examiner setting. The eight cases falling under the jurisdiction of the Harris County Medical Examiner (Houston, TX, USA) with confirmed influenza A/H1N1 infection between June and September 2009 were included in this study. All cases were males between 6 months and 54 years of age. All adult patients had a body mass index from 31 to 49.8 kg/m(2). Five cases had comorbid conditions including one case with sleep apnea and mental retardation, three cases with chronic ethanolism, and one case with thymoma, sarcoidosis, and myasthenia gravis. The remaining three cases had no pre-existing medical conditions. All patients presented with severe flu-like symptoms; yet, only five were febrile. Rapid influenza diagnostic tests were performed in three cases by primary-care physicians, two of which were negative. None of the patients received antiviral medication. The average disease duration time was 8.2 days (3-14 days). A wide range of histopathological findings including tracheitis, necrotizing bronchiolitis, alveolitis, intra-alveolar hemorrhage, and hyaline membranes, both in a focal and in a diffuse distribution, were identified. Influenza A/H1N1 viral infection presents with a wide range of histological findings in a diffuse or focal distribution; most consistently with tracheitis, necrotizing bronchiolitis, and alveolitis with extensive alveolar hemorrhage. These histopathological findings at autopsy along with a clinical history of flu-like symptoms should raise suspicion for influenza A/H1N1 infection, and postmortem analysis by the reverse transcription-polymerase chain reaction (RT-PCR) is recommended for an accurate diagnosis.

Death resulting from ruptured cerebral artery aneurysm: 219 cases.

To characterize the demographics of ruptured cerebral artery aneurysm as a cause of death and to examine the effect of improved diagnostic and therapeutic techniques on the incidence of sudden death associated with the condition, the authors reviewed 219 autopsies performed at the Dallas County Medical Examiner's Office between 1977 and 1997 in which the cause of death was ruptured cerebral artery aneurysm. Ruptured cerebral artery aneurysms accounted for 1.5% of 15,033 natural deaths and 0.4% of all deaths (45,492) followed by autopsy during this period. The majority (56%) of cases occurred in females, with Caucasian females composing the largest group (38%). Seventy-seven percent of cases occurred in individuals between the ages of 31 and 70 years, with the highest concentration in the 41- to 50-year decade (29%). The most common location for ruptured aneurysms was the middle cerebral artery distribution (39%). Multiple aneurysms occurred in 22 (9.1%) cases. Other factors, such as medical history, coexisting disease, symptoms, activity at onset of symptoms, survival time, and toxicology results are also presented. Compared with literature reports before 1980, when ruptured cerebral artery aneurysms were reported as the cause of death in approximately 4% to 5% of sudden natural deaths, the results of this study suggest that despite improved diagnostic and therapeutic techniques during the past two decades, morbidity and mortality from ruptured aneurysms remain a significant health problem.