A 24-year-old male experienced cardiac arrest following a generalized seizure shortly after being stopped at a border control. Paramedics administered intranasal midazolam, after which the patient became asystolic and underwent prolonged cardiopulmonary resuscitation. The patient had a history of cocaine abuse. Suspected acute cocaine intoxication prompted the administration of intravenous lipid emulsion (ILE). Shortly thereafter, the rhythm converted to ventricular fibrillation and return of spontaneous circulation occurred 80 min after the arrest. No underlying cause was identified on diagnostic imaging or coronary angiography. Toxicological testing confirmed markedly elevated cocaine levels, consistent with body stuffing. Despite initial stabilization in the intensive care unit (ICU), the patient developed multiorgan failure and progressive cerebral edema leading to malignant intracranial hypertension. The patient died within 24 h of admission. This case highlights the potentially fulminant course of cocaine toxicity and suggests that lipid emulsion therapy may be considered as an early rescue intervention in refractory cocaine-induced cardiac arrest when conventional treatment fails. Ein 24-jähriger Patient erlitt kurz nach einer Grenzkontrolle zunächst einen generalisierten Krampfanfall, gefolgt von einem Herz-Kreislauf-Stillstand mit prolongierter kardiopulmonaler Reanimation. In der Anamnese bestand ein Kokainabusus. Bei Verdacht auf eine akute Kokainintoxikation wurde innerklinisch intravenöse Lipidemulsion (ILE) appliziert. Kurz darauf kam es zu einem Rhythmuswechsel von Asystolie in Kammerflimmern, und nach insgesamt 80 min Reanimationsdauer wurde ein Spontankreislauf wiederhergestellt. In der bildgebenden Diagnostik sowie in der Koronarangiographie ließ sich keine strukturelle Ursache des Kreislaufstillstands nachweisen. Auf der Intensivstation entwickelte der Patient ein Multiorganversagen sowie ein progredientes zerebrales Ödem mit konsekutiver maligner intrakranieller Hypertension. Der Patient verstarb innerhalb von 24 h nach Aufnahme. Die toxikologische Analyse ergab stark erhöhte Kokainspiegel im Blut, vereinbar mit sog. „body stuffing“. Body stuffing ist das akute Verbergen von Drogen im Körper, z. B. durch Schlucken, meist aus Angst vor Entdeckung bei einer Polizeikontrolle. Die Verpackung ist häufig unzureichend, was mit einem hohen Risiko einer schweren Intoxikation verbunden ist. Der vorliegende Fall verdeutlicht den potenziell fulminanten Verlauf einer Kokainintoxikation und legt nahe, dass die Lipidemulsionstherapie bei therapierefraktärem, kokaininduziertem Herz-Kreislauf-Stillstand als frühe Rescue-Therapie in Erwägung gezogen werden kann, wenn konventionelle Maßnahmen versagen.

Acute cocaine intoxication remains a common emergency department presentation, with well-described symptoms including agitation, tachycardia, hypertension, and hyperthermia. Cocaine also has sodium channel antagonist properties, resulting in QRS interval prolongation and ventricular dysrhythmias. Cocaine-induced QRS interval prolongation is typically treated with 8.4% sodium bicarbonate to increase the concentration of sodium at sodium channels and increase pH, thereby decreasing the amount of free drug binding to sodium channels. However, drug shortages, including recent shortages of sodium bicarbonate, have prompted the use of alternative therapies to treat drug toxicities typically treated with sodium bicarbonate. We report the case of a 44-year-old male with a history of cocaine use who presented to the emergency department in cardiac arrest with presumed cocaine toxicity. Because of QRS complex widening noted on telemetry, 3 boluses of sodium bicarbonate were administered but only reduced the duration of the QRS interval from 165 to 130 ms with laboratory evidence of acidemia. To help treat the patient's significant acidemia, 500 mL of 36 mg/mL tromethamine (THAM) was administered over 60 minutes. While THAM is not typically used in the treatment of toxicity due to sodium channel antagonism, it has been used in the treatment of metabolic acidosis in the intensive care unit, acting as a buffer by directly accepting protons. Approximately 35 minutes after administration of THAM, the duration of the QRS complex had decreased to 111 ms and venous blood gas analysis showed an improvement in the pH to the normal range. Following THAM administration, the patient's QRS duration remained below 120 ms for the remainder of their hospitalization. This case illustrates the successful use of THAM in conjunction with sodium bicarbonate for the treatment of severe acidemia and refractory QRS complex widening in presumed cocaine toxicity. While sodium bicarbonate remains the mainstay of therapy for sodium channel blocker toxicity, THAM offers a potentially valuable adjunctive treatment, especially in the context of drug shortages.

Esophageal perforation is a life-threatening condition associated with high morbidity and mortality, particularly when diagnosis or treatment is delayed. Foreign body ingestion is a known cause of esophageal injury and may result in severe complications requiring surgical intervention. We report the clinical course and therapeutic management of a young adult who developed cervical esophageal perforation after deliberate ingestion of multiple foreign bodies associated with acute cocaine intoxication and self-induced emesis. The patient presented with cervical pain, extensive subcutaneous emphysema, and pneumomediastinum and underwent exploratory cervicotomy with primary esophagorrhaphy. The postoperative course was complicated by hemopneumothorax requiring thoracoscopic drainage and subsequent esophageal fistulization, which was successfully managed conservatively. This case highlights the diagnostic challenges, multidisciplinary decision-making, and potential complications associated with esophageal perforation secondary to deliberate foreign body ingestion in high-risk patients.

Medial degeneration of the aortic wall represents a critical substrate for the development of acute aortic syndromes, particularly dissection, in both clinically healthy individuals and those with known cardiovascular disease or syndromic features. Among these alterations, Mucoid Extracellular Matrix Accumulation (MEMA) has emerged as a key histopathological marker of aortic fragility, with implications not only for clinical practice but also for forensic investigations of sudden and unexpected deaths. This study presents two autopsy case reports of 41-year-old and 44-year-old individuals who died from acute aortic dissection with no prior evidence of cardiovascular disease or other macroscopic findings that could explain the death. Detailed histopathological examination revealed mucoid extracellular matrix accumulation and associated medial changes; in one case, acute cocaine intoxication was identified as a plausible hemodynamic trigger acting upon an intrinsically vulnerable aortic wall. Furthermore, a narrative review on MEMA and its role in medial layer alteration was conducted, allowing comparison of our findings with existing literature. These cases highlight the forensic significance of identifying medial degenerative lesions in sudden aortic deaths. Comprehensive autopsy and histopathological assessment (hematoxylin-eosin staining) allow the recognition of MEMA and other medial alterations even in individuals without history of cardiovascular disease, support differentiation between intrinsic structural vulnerability and potential external precipitants, and contribute to a more accurate reconstruction of the mechanisms underlying unexpected aortic fatalities. Systematic evaluation of the aortic wall also improves differentiation between intrinsic aortic pathology and external triggers, contributing to scientific understanding and to forensic accuracy, and may support medico-legal evaluations of potential medical malpractice in appropriate contexts.

We present a rare case of a clinically stable 24-year-old male patient who developed acute central chest pain shortly after intranasal cocaine use. Initial chest imaging revealed pneumomediastinum, a small apical pneumothorax, and pneumopericardium-three uncommon yet potentially serious findings. Remarkably, the patient was hemodynamically stable with unremarkable clinical examination and vital signs. High-resolution computed tomography (CT) of the thorax and abdomen with oral and intravenous contrast effectively excluded esophageal rupture, a critical differential diagnosis requiring surgical intervention. The patient was successfully managed with conservative measures including observation and supportive care. Serial imaging demonstrated progressive improvement, with complete radiological resolution confirmed at follow-up. This case underscores the need for clinicians to consider recreational drug use as a cause of thoracic barotrauma, utilize imaging judiciously to exclude life-threatening conditions, and recognize that conservative management may be appropriate in carefully selected, clinically stable patients.