Six patients with acute hepatitis A who developed renal failure were studied in order to elucidate the pathogenesis of their renal dysfunction. The patients were admitted to our hospital on the 4-8th day (average, 5.6 days) since the onset of hepatitis symptoms. On admission, all of the patients were suffering from renal failure (serum creatinine 3.9∼19.0mg/dl, FENa 5.4∼13.9), although their hepatitis was nonfulminant except in one case. Bilirubinemia, uricacidemia and activation of the renin-angiotensin system were common to all patients, but none developed endotoxicemia or DIC. Immune complexes were not detected, and complements did not decrease except in 1 patient. Plasmapheresis was performed in 2 patients and daily hemodialysis in 4. Both hepatic and renal function in all patients recovered within about one month of admission. A kidney biopsy was performed in 5 patients on the 12∼38th hospital day (average, at 24.2 hospital days). Histological findings revealed slight glomerular changes without abnormal thickening of glomerular capillary walls. In contrast, changes were noted in renal tubules. All biopsy specimens demonstrated acute tubular necrosis or its recovery findings. Immunofluorescence study demonstrated no deposits of immunoglobulin, complements or fibrinogen in the biopsied renal tissues. Rapid aggravation and complete recovery of renal function in our patients suggests the clinical course of acute tubular necrosis rather than that of glomerulonephritis induced by immune complexes, Moreover, the results of our histological and immunological studies showed no evidence that immune complexes play a role in the development of renal failure. These results suggest that renal failure complicating hepatitis A infection may be caused by acute tubular necrosis in many cases.

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A survey was conducted regarding 141 persons injured in traffic accidents who were transported to the Critical Care Center of Kurume University in 1992. The number of persons who died as a result of the accidents was 33 (23.4%). The mortality rates in car-car collisons was 18.6%. Eleven subjects (20.8%) had their seat belt fastened. There was no difference between the mortality rate of the injured who had their seat belt fastened (group 1) and those who did not (group 2). AIS and ISS were evaluated in both groups. The results of this evaluation in group 1 revealed, an AIS score of 1.8±1.1 for the head and neck region and of 2.0±0.9 for the chest region. The corresponding AIS scores for the head and neck region and chest area in group 2 were 3.7±1.3, and 3.2±1.2, respectively. The AIS scores for the head and neck and chest were significantly higher in group 2 than in group 1 (p<0.005, p<0.05). The ISS score was also significantly higher in group 2 than in group 1 (25.8±13.4 versus 13.9±10.7) (p<0.01). Thus, the findings demonstrate that both injuries of the head and neck region as well as of the chest were fatal more often when the injured were not restrained by seat belts. We conclude that fastening seat belts is a necessary safety measure.

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Cerebral blood flow (CBF) measurements were obtained in 40 head trauma patients using single photon emission CT using 99m-Tc-exametazime (HMPAO) and N-isopropyl-p-[¹²³I] iodo-amphetamine (IMP). Measurement of CBF by HMPAO in the acute phase enabled immediate detection of brain lesions which could not be detected by CT scan performed immediately after the trauma had occurred. The results did not, however, correlate with patient outcomes. In the subacute and chronic phases, HMPAO demonstrated insufficiency of cerebral blood flow which could not be detected by CT scan or MRI, but did not correlate with outcome. As for measurement of CBF using IMP, early images indicated perfusion abnormalities similar to those suggested by HMPAO. The patients whose delayed images showed reduced ligand accumulation defect areas had more favorable courses than those who showed no such reductions. HMPAO was effective in assessing the patient's condition during the acute phase, but subsequently obtained data must carefully be analyzed. Comparisons between early and delayed images obtained using IMP served as an effective means of determining prognosis.

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A consecutive series of 146 patients presenting with ruptured intracranial aneurysm admitted to the Critical Care Center and to the Department of Neurosurgery over the past 3 years, was classified into two age groups, under 65 and over 65 years of age. These two groups were evaluated on the basis of Hunt and Kosnik's grading, CT findings, treatment, prognosis and the presence or absence of warning sign. The patient's clinical condition at the time of admission varied since this hospital provides both critical and primary care, thereby leading to an increased ratio of elderly patients, severe cases and greater mortality than heretofore reported. It is of primary importance to be aware of the frequency and significance of subarachnoidal hemorrhage from ruptured aneurysm and to recognize any warning sign before a major hemorrhage since such recognition and adequate pre-hospital care would improve the outcome of ruptured aneurysm. Also, not only neurosurgical treatment, but also systemic management, including respiration and circulation, should be provided after admission.

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The clinical significance of the plasma level of polymorphonuclear leukocyte elastase (PMN-E) was evaluated in 112 patients with acute myocardial infarction (AMI). Patients were classified according to Killip's (K·I-IV) and Forrester's hemodynamic (F·I-IV) classifications. The PMN-E values were measured using a solid-phase enzyme-linked immunosorbent assay (ELISA) and were then compared between groups. The results were as follows: 1) The mean peak value of PMN-E in patients without heart failure was 257±86μg/l (29±6hrs after the onset of AMI); 2) The mean peak value of PMN-E in these patients correlated well with the mean peak white blood cell count (r=0.65, p<0.0001), the rehabilitation period (r=0.63, p<0.0001) and the mean left ventricle ejection fraction (r=-0.38, p<0.05); 3)In patients without heart failure (K·I, F·I), the peak values of PMN-E were reached on the second day after AMI, and were lower after the third day; 4) The values of PMN-E in 11 non-survivors remained significantly higher than those in 101 survivors after the third day of AMI (seen at four months' follow-up). The PMN-E values were over 300μg/l in non-survivors, contributing to multiple organ failure. Conclusion: In the acute phase of AMI, measuring plasma PMN-E levels is useful for estimating the severity of the condition and predicting the prognosis of the patient.

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We report a case of delayed cardiac rupture associated with traumatic asphyxia. A 61-year-old man was pinned between a diesel shovel and steel material for 30 minutes, then transferred to our hospital. In our emergency room, he was comatose and showed craniocervical cyanosis and subconjunctival petechial hemorrhage. His hemodynamic state was stable and he had no major injury to the chest or abdomen. Initial chest X-rays, echocardiography and electrocardiography showed no abnormalities apart from right second and third rib fractures. He was treated in the intensive care unit under the diagnosis of traumatic asphyxia. Twenty hours after the trauma his hemodynamic condition gradually worsened. Electrocardiography showed sinus tachycardia and low voltage QRS complex, but echocardiography demonstrated no pericardial effusion. Thirty hours after the trauma he suddenly developed shock with a systolic blood pressure of 50mmHg and tachycardia of 170beats/minute, and repeated echocardiography showed massive pericardial effusion. Pericardiocentesis produced 700ml of pure blood. Cardiac tamponade secondary to cardiac rupture was strongly suggested. Emergent median sternotomy was performed, and a tear in the right ventricle was repaired using pledgeted 2-0 polypropylene sutures. He was discharged without any sequelae after 10 days' hospitalization. This case illustrates the importance of thorough cardiac evaluation in patients with traumatic asphyxia.

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A 18-year-old man was admitted with a complaint of enormous abdominal distension and gasping respiration. The patient's colon was inflated as a result of having compressed air forced through the anus by his fellow worker. Chest and abdominal X-ray and arterial blood gas analysis revealed enormous pneumoperitoneum, hypercapnia and hypoxemia (pH 7.10, PCO₂ 84.9mmHg, PO₂ 33.5mmHg). A large amount of gas (air) was released from the abdomen by puncture on the right upper quadrant, and hypercapnia was rapidly improved. Gastrografln enema revealed rupture of the transverse colon and emergency operation was performed. There was a rupture, 3cm in diameter, in the transverse colon along the tenia coli omentalis. Multiple serosal tears (16 in total) were also found throughout the remaining colon.

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A case of torsade de pointes (Tdp) caused by class Ia antiarrhythmic drugs is reported. The patient was a 73-year-old woman with WPW syndrome and hypothyroidism. She had been treated with disopyramide (450mg/day) for 6 months because of paroxysmal supraventricular tachycardia (PSVT), but it was not controlled. A large amount of procainamide (1, 400mg) was added, which caused marked prolongation of the QT interval (QTc=0.67sec) and Tdp. Sustained ventricular tachycardia and shock developed. On admission, electrocardiogram showed ventricular tachycardia, which was treated by DC shock and drip infusion of lidocain and verapamil. But since PSVT reccured frequently, catheter ablation was performed successfully. Class Ia drugs are effective for PSVT in the WPW syndrome patient, but cause prolongation of the QT interval and Tdp. If ordinary doses of these drugs are not effective, surgical treatment should be considered.

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We report a case of dissecting aneurysm of the vertebral artery with a good outcome. A 63-year-old male was brought to our hospital with no spontaneous respiration and no pulse (i.e., DOA). After cardiopulmonary resuscitation, his vital signs recovered. Computed tomography revealed subarachnoid hemorrhage located mainly in the cerebellopontile angle cistern, and cerebral angiograms showed a dissecting aneurysm of the vertebral artery. Emergency surgery was performed. The patient's postoperative course was almost completely favorable except for hoarseness, and he has returned to society. Since the prognosis of dissecting aneurysm of the vertebral artery is good in certain cases, we think appropriate early and aggressive treatment is important.

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Case 1: A 46-year-old female was admitted with sudden onset of coma. CT scan revealed brain stem and bilateral thalamic infarction. On day 3, all brain stem function was absent, while an EEG showed slow-wave activity in the frontal area. Transcranial Doppler sonography demonstrated antegrade flow in the bilateral middle cerebral arteries. Cardiac arrest occurred on day 5. Case 2: A 59-year-old male was admitted in a comatose state. A CT scan revealed a large cerebellar hematoma. Removal of the hematoma and drainage of lateral ventricle were performed, but the patient never regained brain stem function. On days 13 and 14, his condition satisfied the criteria for brain death proposed by the Japanese Ministry of Health and Welfare, except for the persistent EEG activity. Cerebral blood flow studies showed adequate blood flow in both supra and infra-tentorial regions. EEG activity was also observed on day 19. The patient experienced cardiac arrest on day 30. A state of isolated brain stem death, cessation of brain stem function accompanied by persistent EEG activity, may result from a severe cerebrovascular accident in the posterior cranial fossa. This state is usually transient, leading to total brain death, but it may continue for several days when lateral ventricular drainage is performed.

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This paper reports on a case of acute occlusion of the middle cerebral artery in which successful recanalization was achieved by intraarterial infusion of tPA with marked symptomatic improvement. The patient was a 45-year-old female with a history of mitral valve replacement. She suddenly developed left hemiplegia accompanied by dysarthria during daytime activities. An initial CT scan conducted one hour after the onset showed a small low density area in the right thalamus, which was not considered to have been newly formed after the symptom onset. Carotid angiography taken two and a half hours after the stroke manifested a complete occlusion in the M1 portion of the right middle cerebral artery. Then, a superselective catheter was immediately introduced into the middle cerebral artery and guided to the site of embolism for the intraarterial infusion of tPA (300×10⁴IU). Complete recanalization was noted 60 minutes later. The left hemiplegia and dysarthria diminished and finally disappeared several hours after the tPA infusion. This paper discusses the indications and procedures for intraarterial tPA infusion therapy, selectively reviewing the literature. The importance of combination therapy and correct posttreatment is emphasized.

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