The emergency medical service that is closely related to the citizens' life has changed with the changes in society and in disease structure. It is of deep significance to summarize now the developmental process of its system and the progress in emergency medicine after war from our day's point of view. The postwar system of emergency medical services in Japan started from the Fire Services Act promulgated [enacted] in 1948 which assigned the duty to transport sick and wounded persons to medical institutions on the ambulance team of the fire defense organization. It can be said that, however, the full-dress system went into action in 1964 by the establishment of notification system of emergency medical institutions [emergency hospitals]. And, in the setting of changes and motorization of Japanese society, it was started to organize emergency medical centers in 1967, which has been substantiated by successive measures to organize clinics [medical offices] for holiday/night consultation and to arrange the system for the primary-, secondary- and tertiary emergency medical services. Moreover, the “Evaluation Committee of Emergency Medical Services System” founded in 1989 has been making efforts to perfect the systems, such as establishment of system of qualified acute lifesaving men for repletion of pre-hospital cares. Concerning the emergency medicine, on the other hand, Japanese Association for Acute Medicine was founded in 1973 aiming at scientific development in this domain. And thereafter, many universities have created the chair of acute medicine, which is increasing in number. In 1997, Japanese Society for Emergency Medicine was also founded for further scientific enrichment. Now, at the beginning of a new century, however, the structure and systems of the emergency medical services of our country has a number of problems awaiting solution: to readjust the systems so as to cope with diversification of social environment, to organize emergency medical institutions based on medical service scheme, to substantiate pre-hospital care, to perfect countermeasures against disaster including turning out and transportation by helicopter, expression of consultation departments, etc.

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In Japan, approximately 70, 000 people die suddenly from unknown causes every year. However, only about 10% of these causes undergo a postmortem examinations. This situation has hindered medical professinals from determining the cause of death in many cases and from formulating measures for the prevention and acute-phase treatment of fatal diseases. Japan's official death statistics were considerably influenced by a 1995 revision to the guidlines for preparing death certificates. These revisions were the first to be made in half a century. As a result, the incidence of heart disease has dropped, while that of cerebral vascular disease has risen. In particular, the incidence of “acute heart failure” is decreasing, while that of myocardial infarction is increasing. These revisions also pose new problems in evaluating the actual causes of sudden deaths. Sudden death is defined as death which occurs a short time after the onset of symptoms and for which clinical course and examination findings are scarce. In these situations, autopsies can be used to clarify the cause of death. However, number of autopsies performed in Japan is decreasing. This study attempts to probe the causes of sudden death using autopsy findings. Information from autopsies performed on patients who had died from cardiac arrest in our outpatient clinic within 24 hours of the onset of their symptoms was included in the study. Patients who lived outside of the Saku area were excluded from the study. The autopsies were performed by both clinicians and pathologists. Fifty-five cases of sudden death were investigated by autopsy. This number accounts for 25.3% of the total number of suden deaths. The main cause of death in the autopsied cases was myocardial infarction, accounting for 34.5%. Cardiovascular diseases, including myocardial infarction, aortic aneurysm, pulmonary thromboembolism and cardiomyopathy, accounted for 65.5% of the deaths. Myocardial infarction thus appears to be the main cause of sudden death. However, an autopsy is required to determine the exact cause of death in cases of sudden death.

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To clarify the significant relationship between hematoma enlargement and enhanced CT in acute phase of hypertensive intracerebral hematoma, 29 patients were studied in whom CT could be performed on admission 3 and 6 hours after onset. They were classified into two groups, one with hematoma enlargement (14 cases) and the other without hematoma enlargement (15 cases). The following admission data affecting enlargement were analyzed: Glasgow Coma Scale, mean blood pressure, blood laboratory findings, and CT findings. The group with hematoma enlargement showed significant increases at 6 hours after onset. Extravasation rate in the initial CT was significantly high in the group with hematoma enlargement. These results suggest that admission CT, including contrast enhancement study, and CT at 6 hours after onset are useful for detecting enlargement in hypertensive intracerebral hematoma patients.

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Case: An 11-month-old boy bruised his head and experienced convulsions, followed by a coma with decerebrate rigidity. Initial CT scans showed an acute interhemispheric subdural hematoma and diffuse brain swelling. On day 2, he developed dilated pupils, absent light reflex, and sudden hypotension. Dopamine (DOA) and antidiuretic hormone (ADH) were administered to maintain his circulation. CT scans on day 3 revealed brain tamponade. The patient was diagnosed as brain dead on day 15. The patient was thereafter maintained under mechanical ventilation. DOA and ADH requirements decreased gradually, resulting in shift from DOA to docarpamine on day 146 and in the cessation of ADH administration on day 245. On day 139, autolysed brain parenchyma was discharged through the anterior fontanel and necrotic skin, resulting in the appearance of pneumocephalus on CT scans on day 299. Repeated EEGs, ABRs, dynamic CTs and intracranial Power Dopplers supported the diagnosis of brain death. Nevertheless, the patient's height increased consistently from 74cm on day 1 to 82cm on day 253. The secretion of thyroid stimulating hormone was detected until day 252. The boy developed septic renal failure and died on Day 326. Discussion and Conclusion: Although brain death in adults is usually followed by early cardiac arrest, the infant in this case was sustained in a state of brain death for over 300 days using ordinary intensive care. An analysis of endocrinological function and growth records may help to clarify the mechanism of the patient's sustained heart beat.

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Pathological rupture of the spleen is a recognized but rare complication of malarial infection. This is a case report of a 59-year-old male patient with a pathological rupture of the spleen caused by Plasmodium falciparum infection. The patient first became febrile at 40°C 7 days after returning from Kenya. He was admitted to ourhospital with dysfunction of the renal, liver, and coagulation systems. Examination of a peripheral blood smear and DNA analysis of the blood sample using alle-specific PCR demonstrated a severe malarial parasitemia with P. falciparum alone. He was treated immediately with quinine, which completely removed the parasites by the 3rd day of admission. Nevertheless, repeated ultrasonography revealed a rapidly enlarging spleen, and he suddenly fell into hemorrhagic shock due to rupture of the spleen on the 4th hospital day. The spleen with a tear was removed because of uncontrolled bleeding. Histopathological examination revealed features of atrophy of the lymphoid follicles, dilated sinusoidal space, and prominent erythrophagocytosis. He recovered from severe malaria and was discharged without any disability. It is important to anticipate that malaria can be a primary cause of pathological rupture of the spleen, and we should also pay attention to rapid hyperplasia of the spleen, even after parasitemia has disappeared.

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Two cases of cerebellar hemorrhage resulting from ruptured arteriovenous malformations (AVM) in children are reported. The patients were admitted to our clinic in a comatose state, and CT scans revealed the presence of a cerebellar hemorrhage. The hematoma was partially enhanced using a contrast medium, and arteriovenous malformations were observed in both cases. The intracranial pressure was elevated in both cases, so a cerebral angiography was not performed. The patients were immediately admitted to surgery, and the hematomas and arteriovenous malformations were removed. In both cases, a one-stage operation was performed. One patient was able to return to school after 90 days, and recovered completely, with no neurological deficits. The second patient required rehabilitation for 300 days after the operation and retained right VII-X cranial nerve palsies. Surgery during childhood for cerebellar hemorrhages resulting from arteriovenous malformations has been discussed in the literature. Some authors have recommended that a two-stage operation be performed for patients in a comatose state, such as ours. However, emergency one-stage operations are required in extremely critical cases, such as those of the two patients reported here.

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