[Traumatic Right Atrial Rupture and Right Ventricular Papillary Muscle Rupture].

A 18-year-old man was driving at 100 km/h on a motorbike and collided with a utility pole. He was taken to our hospital in a state of shock due to an unstable pelvic fracture and cardiac tamponade. Pericardial drainage was carried out, but intrapericardial hemorrhage persisted and the patient underwent emergency thoracotomy and suture of right atrial injury. After hemodynamic condition improved, the patient was transferred to a tertiary care facility. For the pelvic fracture, open reduction and fixation was performed on the 6th day after injury. During recovery, moderate mitral valve regurgitation and severe tricuspid valve regurgitation due to rupture of the right ventricular papillary muscle were diagnosed. The patient's exercise tolerance was too reduced to continue rehabilitation. Thirty-seven days after the injury, mitral and tricuspid valve repair was performed. Four months after the injury, he was discharged without sequelae.

Effect of prostaglandin E1 on ischemia-reperfusion injury during abdominal aortic aneurysm surgery.

OBJECTIVE: Abdominal aortic aneurysm (AAA) surgery subjects the lower extremities to ischemia and reperfusion. Although it is not extensive or prolonged, ischemia of the lower extremities during aortic cross-clamping is gradually and steadily induced. We studied the effects of prostaglandin E1 (PGE1) on ischemia-reperfusion injury of the lower extremities during AAA repair. METHODS: During AAA surgery, two near-infrared spectroscopy probes were positioned on each calf muscle to monitor oxygen metabolism in the lower extremities. We also measured lactate concentration in both iliac veins. RESULTS: Near-infrared spectroscopy signals responded sensitively to aortic cross-clamping and declamping. Lactate increased time-dependently during aortic cross-clamping. The continuous venous administration of PGE1 (20 ng/kg per minute) inhibited the accumulation of lactate during aortic cross-clamping. Declamping of the first iliac artery resulted in a further but transient increase in ipsilateral venous lactate, which may be one component in the mechanism of declamping shock. Prostaglandin E1 eliminated the transient increase in ipsilateral lactate. The administration of PGE1 inhibited the contralateral accumulation of lactate after first declamping, and the lactate level decreased gradually before the second declamping. CONCLUSIONS: Prostaglandin E1 seems to have a protective effect against ischemia-reperfusion injury of the lower extremities during AAA surgery.