Sixty-eight patients who sustained head trauma with mild to moderate disturbance of consciousness were investigated and divided by age into two groups: those 70 or above and those less than 70. The average GCS score was 12.5 in the 21 elderly cases, and 12.8 in the 47 non-elderly cases. In the elderly patients, abnormal findings, including acute subdural hematoma and/or cerebral contusion, were found on the initial CT in 19 cases. The outcomes of the elderly patients were poor, with severe disability in four cases and death in eight cases. The causes of death in the elderly patients were talk and deteriorate in the acute stage in three patients and infectious diseases in the chronic stage in five patients. In elderly patients, cerebral contusion commonly progresses over time into intracerebral hematoma in the acute stage, and the patient lapses into talk and deteriorate with a poor outcome. Therefore, rapid diagnosis of intracerebral hematoma by repeated CT scan in the acute stage and monitoring of the cardiorespiratory system during the chronic stage are the two most important factors in treating elderly patients with head trauma.

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The object of this study was to define the relationship between patient transport time to a neurosurgical center and the incidence of rebleeding after subarachnoid hemorrhage (SAH). The usefulness of sedation for the prevention of rebleeding was also discussed. Thirty-one patients with SAH came to our clinic by ambulance, within 4 hours after the onset, between January 1992 and December 1993. We divided these patients into two groups; an ultraearly (UE) group consisting of 13 patients arriving within one hour after the onset, and early (E) group consisting of 15 patients arriving between one and 4 hours after the onset. Neurological conditions at admission were similarly distributed in the two groups. Outcome was evaluated using the Glasgow coma scale. In the UE group, the number showing good recovery (GR) was 9 and dead (D) 1, while in the E group the respective numbers were 5 and 6. Prognosis in the UE group was thought better than that of the E group. Many UE patients were comatose preoperatively because of an initial drowsy state after the onset and sedation immediately after the diagnosis of SAH. Thus, UE admission reduced the incidence of aneurysmal rebleeding. On the other hand, patients in the E group arrived having already recovered from the initial shock state, such that stressful medical treatments and examinations were performed while the patients' consciousness was clear. The incidence of rebleeding tended to be increased in the E group. It is important to shorten the transport time to neurosurgical centers to improve the outcome of SAH.

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To clarify the clinical picture and hospital mortality of patients with acute pulmonary embolism accompanied by shock, 96 consecutive patients with acute pulmonary embolism admitted to the Hiroo General hospital from Dec. 1980 to Apr. 1995 (51 men and 45 women; mean age 59±12 years) were reviewed. Pulmonary embolism was confirmed by pulmonary angiography, lung perfusion scanning, or autopsy. The patients were subdivided into two groups based on the presence (group A; n=22) or absence (group B; n=74) of shock. Shock was defined simply as hypotension under 70mmHg. The majority of patients in both groups had risk factors for venous thromboembolism. The major presenting manifestations in group A were dyspnea at rest (54%), syncope (23%) and cardiopulmonary arrest (23%), while those in group B were chest pain (43%), dyspnea on exertion (22%) and dyspnea at rest (15%). On 12-lead electrocardiography, complete or incomplete right bundlebranch block, an S_IQ_IIIT_IIIpattern and T wave inversion in leads V₁ to V₃ were observed more often in group A. Two-dimensional echocardiography revealed marked right ventricular dilatation in all group A patients and in 43% of group B patients. All patients with this finding were proven to have massive pulmonary embolism. In 75% of group A patients, severe hypokinesis of the right ventricular free wall was also shown. Eighteen (82%) of the 22 group A patients developed shock within 30 minutes after the onset of symptoms, and two developed shock as a result of recurrence of pulmonary embolism 2 or 3 days after the onset. Sixteen patients (73%) in group A and 41 patients (55%) in group B received thrombolytic therapy. In-hospital mortality was 68% in group A and 0% in group B. Conclusions: 1) The hospital mortality in patients with acute pulmonary embolism accompanied by shock is very high and prophylaxis of venous thromboembolism is urgently needed in patients with recognized risk factors. 2) Two-dimensional echocardiography is a sensitive method of detecting the right ventricular overload in massive pulmonary embolism. Utilization of this technique soon after the onset of symptoms is important for diagnosis and treatment.

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In order to clarify whether nitric oxide (NO) is produced by human monocytes stimulated with interferonγ and lipopolysaccharide (IFNγ+LPS), we examined IFNγ+LPS-stimulated cultured monocytes derived from four healthy volunteers for the expression of inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) by using the reversed transcription method, we also measured and assessed the NO₂ levels in the supernatants of IFNγ+LPS-stimulated cultured monocytes by the Griess method. Furthermore, to clarify how TNFα is involved in the production of NO in monocytes, the expressions of iNOSmRNA and NO₂ was determined by the above procedure after IFNγ+LPS stimulation in the presence of TNFα monoclonal antibody. iNOSmRNA was expressed in the IFNγ+LPS-stimulated monocytes derived from all four volunteers, while its expression was almost totally suppressed after addition of the TNFα monoclonal antibody. Furthermore, the NO₂ level in the supernatants of IFNγ+LPS-stimulated cultured monocytes was significantly higher than in the cells cultured with TNFα monoclonal antibody. These findings suggest that NO is produced by iNOS induced by the stimulation with IFNγ+LPS and that TNFα, probably released from stimulated monocytes, is essential for the expression of iNOSmRNA in human monocytes.

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HLA antibodies have been implicated in the production of transfusion-related acute lung injury (TRALI). A 35-year-old man with hemorrhagic gastric ulcer was given three units of concentrated red cells (CRC) by transfusion. At the end of the third CRC transfusion, the patient developed dyspnea and shock. PaO₂ was 34.1mmHg with oxygen delivered at 3l/min by face mask. Chest X-ray showed diffuse infiltration of both lung fields. The lowest PaO₂/F_IO2 ratio was 138. TRALI was dramatically improved by high PEEP. Therefore, he could be weaned from the ventilator on the fourth hospital day. Serological studies demonstrated the recipient's HLA type to be A (2, 24), B (52, 61) and Cw (-, -), and serum from one of three donors had a high titer (64 times) of HLA antibodies (B52). Cross match of the donor serum and recipient lymphocytes and platelets yielded the following results; lymphocyte toxicity test (LCT) indicated strong positivity, the mixed passive hemagglutination (MPHA) method was positive and the MPHA method with chloroquine was negative. The donor was a multiparous, having delivered three children. We are convinced that this TRALI was caused by anti-HLA antibody in CRC.

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