Unveiling the Rare Presentation of Acetylsalicylate Overdose: Grand Round.

BACKGROUND: This case report highlights a rare occurrence of aspirin overdose presenting only as severe coagulopathy. CASE PRESENTATION: An 85-year-old woman was admitted to the hospital with multiple lumbar vertebral compression fractures causing severe back pain. The patient had self-medicated with excessive consumption of Bufferin A containing 330 mg of aspirin. On arrival, she showed no typical symptoms of salicylate toxicity, such as nausea, vomiting, hyperventilation, tinnitus, or hearing loss. However, blood work revealed a significant decrease in vitamin K-dependent coagulation factors leading to coagulopathy. The administration of 20-mg menatetrenone (vitamin K) resulted in rapid improvement in coagulation abnormalities. The patient's blood salicylate level was later determined to be 42.7 mg/dL. DISCUSSION: Acute salicylate poisoning is known to cause coagulopathy because of the inhibition of vitamin K-dependent coagulation factors. However, this case is unique because it demonstrates coagulopathy as the sole manifestation of aspirin toxicity without any other symptoms. CONCLUSIONS: This case highlights the importance of considering the possibility of aspirin toxicity in patients with coagulopathy, especially those who are regularly consuming aspirin.

Severe aconite poisoning successfully treated with veno-arterial extracorporeal membrane oxygenation: A case report.

BACKGROUND: Most species of aconite contain highly toxic aconitines, the oral ingestion of which can be fatal, primarily because they cause ventricular arrhythmias. We describe a case of severe aconite poisoning that was successfully treated through veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and in which detailed toxicological analyses of the aconite roots and biological samples were performed using liquid chromatography-tandem mass spectrometry (LC-MS/MS). CASE SUMMARY: A 23-year-old male presented to the emergency room with circulatory collapse and ventricular arrhythmia after ingesting approximately half of a root labeled, "Aconitum japonicum Thunb". Two hours after arrival, VA-ECMO was initiated as circulatory collapse became refractory to antiarrhythmics and vasopressors. Nine hours after arrival, an electrocardiogram revealed a return to sinus rhythm. The patient was weaned off VA-ECMO and the ventilator on hospital days 3 and 5, respectively. On hospital day 15, he was transferred to a psychiatric hospital. The other half of the root and his biological samples were toxicologically analyzed using LC-MS/MS, revealing 244.3 mg/kg of aconitine and 24.7 mg/kg of mesaconitine in the root. Serum on admission contained 1.50 ng/mL of aconitine. Beyond hospital day 2, neither were detected. Urine on admission showed 149.09 ng/mL of aconitine and 3.59 ng/mL of mesaconitine, but these rapidly decreased after hospital day 3. CONCLUSION: The key to saving the life of a patient with severe aconite poisoning is to introduce VA-ECMO as soon as possible.

[Aconite, in 4.50 from Paddington: Continuous Activation of Voltage-Gated Sodium Channel].

Aconite belongs to the genus Aconitum and the Ranunculaceae family, which contains approximately 300 species worldwide. Aconite, the poison mentioned in Agatha Christie's novel 4.50 from Paddington, contains aconitum alkaloids in all parts of the plant, including the roots, stem, leaves, and flowers. Aconitum alkaloids continuously activate voltage-gated sodium channels in the myocardium, central nervous system, and skeletal muscle. Activated sodium channels trigger automaticity and cause pre-excitation of cardiomyocytes, which precipitates various types of ventricular arrhythmias.

Poisoning by abnormally high blood phenobarbital concentration treated with extracorporeal therapy.

Phenobarbital poisoning, which may cause circulatory collapse as well as respiratory arrest in severe cases, has one of the highest mortality rates among acute drug poisonings. A 58-year-old man arrived at the emergency room in a deep coma (Glasgow Coma Scale E1V1M1) after taking an unknown dose of phenobarbital which had been prescribed for his cat's seizures. Venous blood gas analysis revealed hypercapnia (PvCO2: 113.0 mmHg) and a blood phenobarbital concentration of 197.3 µg/mL. Shortly after his arrival, respiratory arrest and circulatory collapse occurred. Mechanical ventilation after intubation, intravenous noradrenaline infusion, and multiple-dose activated charcoal through a nasogastric tube was started. Six hours after arrival, blood phenobarbital concentration was abnormally elevated to 356.8 µg/mL with circulatory collapse requiring an increased dose of intravenous noradrenaline infusion (up to 0.13 µg/kg/min). Continuous renal replacement therapy including high flow continuous hemodialysis was performed until hospital day 5, during which blood phenobarbital concentration decreased to 96.2 µg/mL on hospital day 4, resulting in a sufficient resumption of spontaneous breathing and full improvement of circulatory collapse. A search of the literature revealed that the peak phenobarbital concentration in the present case exceeded those of fatal cases, as well as those of survivors of acute phenobarbital poisoning. However, the patient was successfully treated with continuous renal replacement therapy. Among modalities of extracorporeal treatment, continuous renal replacement therapy could be considered if a patient's circulation is unstable.

Disseminated Varicella zoster infection with abdominal pain and periarterial fat stranding in a patient taking pomalidomide.

BACKGROUND: Disseminated Varicella zoster virus infection (DVI) is a severe infection associated with severe abdominal pain of unknown cause. We report a case in which periarterial (the celiac artery and superior mesenteric artery) fat stranding (PFS) on computed tomography (CT) was the presumed cause of abdominal pain in a patient taking pomalidomide. CASE PRESENTATION: A 62-year-old woman was admitted to our hospital with abdominal pain. Her medical history was multiple myeloma treated with pomalidomide. Computed tomography showed no remarkable findings on admission, but 1 day later, a contrast-enhanced CT showed PFS. A skin eruption appeared on day 4 and we started acyclovir. On day 10, Varicella zoster virus antigen and antibody tests were positive, confirming the diagnosis of DVI. The abdominal pain subsequently improved, together with the PFS, and she was discharged. CONCLUSION: When patients present with severe abdominal pain and PFS, DVI and acyclovir must be considered.