A Fatal Case of Acute Renal Failure From Envenoming Syndrome After Massive Bee Attack: A Case Report and Literature Review.

Envenoming syndrome is a systemic toxic reaction to the inoculation of large volume of insect venom, typically after a swarm attack from bees. Africanized honey bees are notorious for their aggressive nature, and human deaths resulting from Africanized honey bee attacks are consistently reported. Whereas anaphylaxis is the most common lethal mechanism of injury, delayed deaths can also occur as a consequence of severe venom toxicity with resultant end organ damage. Acute renal failure complicating massive envenomation is a rare but potentially fatal outcome after Africanized honey bee attack and may be heralded by laboratory evidence of rhabdomyolysis.

Fatal combination of mitragynine and quetiapine - a case report with discussion of a potential herb-drug interaction.

Kratom is a plant with dose-dependent mixed stimulant and opioid properties whose pharmacologic characteristics and social impact continue to be described. The main active isolate of kratom is mitragynine, an indole-containing alkaloid with opioid-like effects. Kratom toxicity and kratom-associated fatalities have been described, including those in association with additional drugs. In this paper we describe the case of a 27-year-old man who was found deceased with a toxic blood concentration of quetiapine in conjunction with the qualitative presence of mitragynine. Investigative and autopsy findings suggested perimortem hyperthermia and seizure-like activity. Kratom toxicity and kratom-associated fatalities are being increasingly reported. Experiments with kratom extracts have shown inhibitory effects upon hepatic CYP enzymes, leading to previous speculation of the potential for clinically significant interactions between kratom and a wide array of medications. Herein is described a fatal case of quetiapine toxicity complicated by mitragynine use. The potential ability of mitragynine to alter the pharmacokinetics of a prescription medication via inhibition of its hepatic metabolism is discussed.

Oxalate Nephropathy After Continuous Infusion of High-Dose Vitamin C as an Adjunct to Burn Resuscitation.

Fluid resuscitation is the foundation of management in burn patients and is the topic of considerable research. One adjunct in burn resuscitation is continuous, high-dose vitamin C (ascorbic acid) infusion, which may reduce fluid requirements and thus decrease the risk for over resuscitation. Research in preclinical studies and clinical trials has shown continuous infusions of high-dose vitamin C to be beneficial with decrease in resuscitative volumes and limited adverse effects. However, high-dose and low-dose vitamin C supplementation has been shown to cause secondary calcium oxalate nephropathy, worsen acute kidney injury, and delay renal recovery in non-burn patients. To the best of our knowledge, the authors present the first case series in burn patients in whom calcium oxalate nephropathy has been identified after high-dose vitamin C therapy.

Sickle Cell Trait-Related Exertional Deaths: Observations at Autopsy and Review of the Literature.

Sickle cell trait-related exertional deaths, although rare, are well-accepted in the field of forensic pathology; however, the increased risk of sudden unexpected deaths in persons with sickle cell trait undergoing strenuous physical activity may be an underappreciated acute phenomenon in the clinical realm. Herein, we report two cases of sickle cell trait-related exertional deaths of active duty military members, with a review of the literature including the pathophysiology of sickle cell trait-related deaths and current military screening guidelines.

Multidrug toxicity involving sumatriptan.

A multidrug fatality involving sumatriptan is reported. Sumatriptan is a tryptamine derivative that acts at 5-HT(1B/1D) receptors and is used for the treatment of migraines. The decedent was a 21-year-old white female found dead in bed by her spouse. No signs of physical trauma were observed and a large number of prescription medications were discovered at the scene. Toxicological analysis of the central blood revealed sumatriptan at a concentration of 1.03 mg/L. Following therapeutic dosing guidelines, sumatriptan concentrations do not exceed 0.095 mg/L. Sumatriptan was isolated by solid-phase extraction and analyzed using liquid chromatography-tandem mass spectrometry in multiple reaction monitoring mode. A tissue distribution study was completed with the following concentrations measured: 0.61 mg/L in femoral blood, 0.56 mg/L in iliac blood, 5.01 mg/L in urine, 0.51 mg/kg in liver, 3.66 mg/kg in kidney, 0.09 mg/kg in heart, 0.32 mg/kg in spleen, 0.01 mg/kg in brain, 15.99 mg/kg in lung and 78.54 mg/45 mL in the stomach contents. Carisoprodol, meprobamate, fluoxetine, doxylamine, orphenadrine, dextromethorphan and hydroxyzine were also present in the blood at the following concentrations: 3.35, 2.36, 0.63, 0.19, 0.06, 0.55 and 0.16 mg/L. The medical examiner ruled the cause of death as acute mixed drug toxicity and the manner of death as accident.

A case of fatal iliac vein rupture associated with May-Thurner syndrome.

May-Thurner syndrome results from long-standing compression of the left common iliac vein (LCIV) and is characterized by the formation of intraluminal spurs leading to obstruction of blood flow and deep vein thrombosis (DVT). Increased intraluminal pressures may occur as a consequence of venous obstruction, which when coupled with other factors thought to further weaken venous wall integrity (ie, inflammation or hormonal imbalances) may produce spontaneous (nontraumatic) and potential lethal venous rupture.We report a case of DVT in a woman with previously undiagnosed May-Thurner syndrome and heterozygosity for factor V Leiden mutation on exogenous hormone therapy, with subsequent spontaneous rupture of the LCIV leading to fatal hemoperitoneum. Autopsy revealed fibrous obliteration of the junction between the LCIV and inferior vena cava with associated DVT, transmural venous rupture, and thrombophlebitis.