Post-traumatic thrombotic microangiopathy following pelvic fracture treated with transcatheter arterial embolization: a case report.

BACKGROUND: Thrombotic microangiopathy is caused by various conditions, but few cases secondary to trauma have been reported. We present the rare case of a patient with thrombotic microangiopathy-induced high-impact trauma with hemorrhagic shock. CASE PRESENTATION: An 86-year-old Japanese woman was transferred to our hospital after a traffic accident. A whole-body computed tomography scan revealed pelvic fractures with massive extravasation. She received a blood transfusion and emergency angiographic embolization. On post-traumatic day 1, she showed unexplained severe hemolysis, thrombocytopenia, and renal failure despite her stable condition. Disseminated intravascular coagulation was excluded because her activated partial thromboplastin time and prothrombin time-international normalized ratio were normal. Her fragmented red blood cell concentration was 28.8%. We suspected clinical thrombotic thrombocytopenic purpura and started plasma exchange. She recovered fully after the plasma exchange and was discharged on day 31. We eventually diagnosed thrombotic microangiopathy because her ADAMTS13 activity was not reduced. CONCLUSIONS: It is important to recognize the possibility that thrombotic microangiopathy may occur after severe trauma. In the critical care setting, unexplained thrombocytopenia and hemolytic anemia should be investigated to eliminate the possibility of thrombotic microangiopathy. Early plasma exchange may help to prevent unfortunate outcomes in patients with thrombotic microangiopathy following trauma.

[Tension pneumothorax during hyperbaric oxygen therapy].

The authors present a case of an 86-year-old man who developed tension pneumothorax while receiving hyperbaric oxygen therapy (HBOT) for adhesive intestinal obstruction. The patient experienced general malaise and was admitted to our hospital with abdominal pain due to intestinal obstruction, which was revealed by computed tomography on day 3. He received HBOT from day 5. On day 6, while receiving the 2nd session of HBOT, he experienced severe dyspnea and backache after decompression and developed cardiac arrest soon after he was moved out of the compression chamber. Tension pneumothorax was detected, and he was successfully resuscitated by immediate thoracic drainage. Though tension pneumothorax during HBOT is extremely rare, it is a life-threatening emergency. Therefore, it is essential to detect and manage pneumothorax prior to HBOT.

[Use of high frequency oscillatory ventilation in a patient with fulminant fat embolism syndrome].

We report a case of fulminant fat embolism syndrome treated with high frequency oscillatory ventilation (HFOV). A 77-year-old woman sustained a right tibia and fibula fracture and a left open tibia fracture after a traffic accident. She was conscious and her respiratory condition was normal on admission. However, she suddenly progressed to a coma and was intubated for approximately 2 hours after the accident; she developed critical respiratory failure. We used HFOV and were able to maintain her respiratory status. However, her right heart failure deteriorated and she died 95 hours after the accident. It was difficult for her to survive without percutaneous cardiopulmonary support.

[Lethal myocardial injury associated with hydrogen sulfide poisoning: report of two cases].

We investigated two cases of hydrogen sulfide poisoning in which the patients showed lethal myocardial injury. Both patients had planned to commit suicide by inhaling hydrogen sulfide. In case 1, a 17-year-old man was confused and was brought to our hospital by ambulance. An electrocardiogram (ECG) revealed diffuse elevation of the ST segment on the second hospital day. The patient recovered and was discharged from the hospital on the 15th day. However, he died suddenly on the 18th day. In case 2, a 21-year-old man was found lying on the floor and was admitted to our hospital. ECG showed tall T waves after 5 hr. Tachycardia and tachypnea occurred after 12 hr. After 16 hr, the ECG showed a marked elevation of the ST segment, and the patient developed cardiac arrest. Even though percutaneous cardiopulmonary support was used, he died on the 4th day. It is highly probable that myocardial injury asscociated with hydrogen sulfide poisoning was not caused by systemic hypoxia but by selective myocardial toxicity. These cases demonstrate that delayed presentation of a lethal myocardial injury should be considered while treating cases of hydrogen sulfide poisoning.