Severe caffeine poisoning treated with intermittent hemodialysis under circulatory support.

Caffeine poisoning can cause fatal ventricular arrhythmias. In this report, we describe a case of severe caffeine poisoning with extraordinarily high blood caffeine levels. Despite developing refractory ventricular fibrillation, the patient was successfully treated with intermittent hemodialysis (IHD) under circulatory support by venoarterial extracorporeal membrane oxygenation (VA-ECMO). A 22-year-old male was transported to our hospital approximately 2.5 h after ingesting 200 highly caffeinated tablets (200 mg/tablet) (40 g caffeine total) in a suicide attempt. On arrival, the patient vomited frequently with a Glasgow Coma Scale score E3V2M5, heart rate 185 beats/min, and a blood pressure of 97/62 mmHg. Shortly after arrival, the patient developed ventricular fibrillation which was refractory either to three electrical defibrillations or antiarrhythmic drugs, resulting in endotracheal intubation for mechanical ventilation and VA-ECMO. Starting from 2 h after arrival, intermittent hemodialysis (IHD) was performed for 11 h, which markedly improved clinical symptoms and circulatory parameters. Serum caffeine level was 454.9 mg/dL upon arrival at the hospital, but it decreased to 55.5 mg/dL by the end of IHD treatment. Renal replacement therapy (RRT) including intermittent hemodiafiltration, continuous hemodiafiltration, and IHD was continued because of rhabdomyolysis with myoglobinuria and secondary caused acute kidney injury. The patient was weaned off VA-ECMO on hospital day 7, extubated on hospital day 18, weaned from RRT on hospital day 46, and was transferred to another hospital for physical rehabilitation on hospital day 113. IHD under circulatory support by VA-ECMO should be considered in severe caffeine poisoning causing potentially fatal arrhythmias.

Penetrating cardiac injury repaired under "intentional cardiac arrest" with adenosine triphosphate.

BACKGROUND: Repairing a cardiac injury with beating heart is sometimes difficult and is associated with increased risks of complications. Here we report a case of cardiac injury repaired with administration of adenosine triphosphate (ATP). CASE PRESENTATION: A 46-year-old man was stabbed in his chest with a knife and transferred to our hospital. He was hemodynamically unstable, and echocardiography showed pericardial effusion. Emergency thoracotomy revealed a full-thickness injury in the right ventricle next to the coronary artery. He went into cardiac arrest and was resuscitated with adrenaline administration. We tried to suture immediately, but it was difficult because of tachycardia. After administering 20 mg of ATP (80 mg in total over 15 min), bradycardia was induced that led to "intentional cardiac arrest" after which suturing was performed. He was discharged on the 13th day without complications. CONCLUSION: Cases of penetrating cardiac injury repaired using ATP are rare. Administration of ATP may be a useful option while repairing cardiac injuries.

Investigation and treatment of pulmonary embolism as a potential etiology may be important to improve post-resuscitation prognosis in non-shockable out-of-hospital cardiopulmonary arrest: report on an analysis of the SOS-KANTO 2012 study.

Background: The prognosis of non-shockable out-of-hospital cardiac arrest is worse than that of shockable out-of-hospital cardiac arrest. We investigated the associations between the etiology and prognosis of non-shockable out-of-hospital cardiac arrest patients who experienced the return of spontaneous circulation after arriving at hospital. Methods and Results: All subjects were extracted from the SOS-KANTO 2012 study population. The subjects were 3,031 adults: (i) who had suffered out-of-hospital cardiac arrest, (ii) for whom there were no pre-hospital data on ventricular fibrillation/pulseless ventricular tachycardia until arrival at hospital, (iii) who experienced the return of spontaneous circulation after arriving at hospital. We compared the patients' prognosis after 1 and 3 months between various etiological and presumed cardiac factors. The proportion of the favorable brain function patients that developed pulmonary embolism or incidental hypothermia was significantly higher than that of the patients with presumed cardiac factors (1 month, P < 0.0001 and P < 0.0001, respectively; 3 months, P = 0.0018 and P < 0.0001, respectively). In multiple logistic regression analysis, pulmonary embolism and incidental hypothermia were found to be significant independent prognostic factors for 1- and 3-month survival and the favorable brain function rate. Conclusions: In patients who suffer non-shockable out-of-hospital cardiac arrest, but who experience the return of spontaneous circulation after arriving at hospital, the investigation and treatment of pulmonary embolism as a potential etiology may be important for improving post-resuscitation prognosis.

Bilateral ureteropelvic disruption following blunt abdominal trauma: case report.

BACKGROUND: Ureteral injury occurs in less than 1% of blunt abdominal trauma cases, partly because the ureters are relatively well protected in the retroperitoneum. Bilateral ureteral injury is extremely rare, with only 10 previously reported cases. Diagnosis may be delayed if ureteric injury is not suspected, and delay of 36 hours or longer has been observed in more than 50% of patients with ureteric injury following abdominal trauma, leading to increased morbidity. CASE PRESENTATION: A 29-year-old man was involved in a highway motor vehicle collision and was ejected from the front passenger seat even though wearing a seatbelt. He was in a preshock state at the scene of the accident. An intravenous line and left thoracic drain were inserted, and he was transported to our hospital by helicopter. Whole-body, contrast-enhanced computed tomography (CT) scan showed left diaphragmatic disruption, splenic injury, and a grade I injury to the left kidney with a retroperitoneal haematoma. He underwent emergency laparotomy. The left diaphragmatic and splenic injuries were repaired. Although a retroperitoneal haematoma was observed, his renal injury was treated conservatively because the haematoma was not expanding. In the intensive care unit, the patient's haemodynamic state was stable, but there was no urinary output for 9 hours after surgery. Anuresis prompted a review of the abdominal x-ray which had been performed after the contrast-enhanced CT. Leakage of contrast material from the ureteropelvic junctions was detected, and review of the repeat CT scan revealed contrast retention in the perirenal retroperitoneum bilaterally. He underwent cystoscopy and bilateral retrograde pyelography, which showed bilateral complete ureteral disruption, preventing placement of ureteral stents. Diagnostic laparotomy revealed complete disruption of the ureteropelvic junctions bilaterally. Double-J ureteral stents were placed bilaterally and ureteropelvic anastomoses were performed. The patient's postoperative progress was satisfactory and he was discharged on the 23rd day. CONCLUSION: Diagnosis of ureteral injury was delayed, although delayed phase contrast-enhanced CT and abdominal x-rays performed after CT revealed the diagnosis early. Prompt detection and early repair prevented permanent renal damage and the necessity for nephrectomy.