Objective: The aims of the present study were to clarify the clinical significance of elevated plasma cardiac troponin I (cTnI) in patients with severe brain damage and to investigate whether the measurement of plasma cTnI is useful for evaluating cardiac function in those patients. Subjects and Methods: The study population comprised patients with traumatic brain injury who scored 8 or less on the Glasgow Coma Scale (GCS) on admission (TBI group; N=6) and those with intracranial hemorrhage due to cerebrovascular disease (ICH/SAH group; N=12). Procedures at admission included the recording or determination of the patient genders, ages, vital signs, ECGs, PaO₂/FiO2 (P/F) ratios, SIRS, and APACHE II scores. CTnI and CK-MB were measured over time. The upper limit of the normal cTnI level in this study was defined as 0.1ng/ml. There were 4 and 7 deaths in the TBI and ICH/SAH groups, respectively. Results: Fifteen out of 18 (83.3%) patients had peak cTnI>0.1ng/ml. Of the 18 patients, 14 (77.8%) showed a cTnI value of 0.1ng/ml or less at 72 hours after a transient increase (peak cTnI). ST-T changes were observed in the ECGs of 8 patients, but the peak cTnI level did not correlate with age, mean blood pressure, heart rates, APACHE II scores, or GCS on admission. On the other hand, 12 (66.7%) of 18 patients had a P/F ratio<300. Chest x-rays and plain chest CT scans revealed lung edema/gravity-dependent consolidation (L/G) in 7 patients. Cardiac echography revealed a decreased ejection fraction in 3 of 9 patients examined. Four patients (66.7%) in the TBI group and 9 patients (75.0%) in the ICH/SAH group were diagnosed with SIRS on admission. The peak cTnI (p<0.05) was significantly higher in the patients with increased SIRS scores. Discussion and Conclusion: Unlike the cTnI elevation typically seen in myocardial infarction, that observed in our patients with severe brain damage was transient. Moreover, few incidences of the cardiac dysfunction were revealed in the brain damage patients with elevated cTnI. Our results suggest that the evaluation of cardiac dysfunction based on cTnI measurement might be of less clinical significance after severe brain damage. Further, the correlation noted between elevated cTnI and the SIRS score on admission suggested that the systemic inflammatory responses at the onset of brain damage might be involved in the cTnI elevation.

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In this study, we evaluated the incidence and timing of nocturnal hypoxemic episode A (SpO₂ below 90% for at least 10 seconds) and hypoxemic episode B (SpO₂ below 90% for at least 10 seconds + a drop in SpO₂ by more than 4% from the baseline for at least 10 seconds) in 22 patients with acute myocardial infarction during 0-3 nights 0-3 after the onset of infarction by continuously monitoring them with a pulse oxymeter. The risk factors (age, BMI, max-CPK serum level, max-CPK-MB serum level and ejection fraction) of hypoxemic episode B were also investigated. Patient age ranged from 31 to 83 years (mean 62.9 years) and the male: female ratio was 19:3. Nineteen of the patients underwent coronary angiography. Lesions were detected in the LAD in 11 patients, in the LCX in 2 patients, and in the RCA in 7 patients. On night 0, hypoxemic episode A was seen in only 1 patient. On night 1, this phenomenon increased significantly (p<0.05) in incidence. No risk factors were identified. Although there were no major complications, an 83-year-old female fell into a delirium on the night 1, when a large number of hypoxemic episodes occurred. We suspect that there was a relationship between delirium and hypoxemic episodes. These findings suggest that acute myocardial infarction patients possibly face potential dangers for several nights following several the acute stage.

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This report presents useful images of high-density imaging (collimation, 3mm) by multidetector row computed tomography (MDCT) in two patients with blunt hepatic injury, resulting from the use of the multidynamic phase scan method, or dripinfusion cholangiography (DIC). The data were visualized on a workstation (ZioM900, Ziosoft Inc., Tokyo). A liver pseudoaneurysm was identified with MDCT in a 21-year-old male on the 14th day following an injury in a by motorbike accident. The pseudoaneurysm gradually faded out in 3 weeks. In a 24-year-old male, 7 days after a motor accident injury, a huge liver pseudoaneurysm was identified with MDCT. The pseudoaneurysm involved the fistula to the hepatic vein (HV) and HV-portal shunt. In addition, bile leakage from the disinsertion of the left hepatic duct was identified on the 14th day with DIC-MDCT.

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We present a case of delayed, massive, life threatening hemothorax due to laceration of the supradiaphragmaitic inferior vena cava in association with blunt thoracic trauma. A 51-year-old man was involved in a traffic accident. While riding his bicycle, he collided with a car. On arrival at our emergency department his vital signs were stable and chest x-rays revealed no abnormal findings. However, twenty-one hours later he complained of difficulty with breathing and suddenly went into shock. Emergency computed tomography revealed a massive right hemothorax without pneumothorax or rib fracture, and chest tube drainage was performed. Because of rapid blood loss from the drainage tube, we decided to perform an immediate open thoracotomy, during which we found that the supradiaphragmatic inferior vena cava was lacerated. Homeostasis was achieved with by suture ligation of the injured sites. The patient's postoperative course was uneventful. Laceration of the supradiaphragmatic inferior vena cava resulting from blunt trauma is relatively rare, but extremely serious. Several days of observation in hospital may be required for patients with severe blunt thoracic trauma.

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