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Biomedical subjects

K Katsurada

Publications and source records attributed to K Katsurada.

At least 19 recordsLinked to original sources
PubMed1984

The emergency medical system in Japan.

In Japan, ambulance service was originated by the Osaka Branch Office of the Japan Red Cross in 1931. In 1933 the fire department organ of Yokohama started ambulance service. It was, however, without any legal requirements. Since the early 1960s, Japan has experienced a rapid development of industry and economy, so that traffic accidents have increased, necessitating a nationwide ambulance service system. In October 1961 the Director-General of the Fire Defense Agency organized the Fire Defense Council to study the problem of ambulance service. In response, the Fire Defense Act was amended in 1963, assigning ambulance service responsibilities to Fire Defense organs. During 1982 total ambulance runs numbered 2,125,447, and the total number of transported persons was 2,049,487. Response time is excellent in Japan. More than 50% of persons who called an ambulance could get help within five minutes. First-aid management was given to 56% of total transported persons. Of these, temperature regulation was most often administered, followed by oxygen inhalation, dressing, and hemostasis. Currently, 2,965 (91.1%) municipalities provide ambulance services to 98.3% of the population. The Japanese emergency medical system has serious problems, however, such as an inadequate number of general hospitals and a flood of nonemergent patients. To alleviate such problems, the Ministry of Health and Welfare developed the critical emergency transfer system in 1977.

Ambulances↗
PubMed1983

[Brain death in secondary brain lesion].

The criteria of brain death established by Japanese Society of EEG in 1974, necessitates a prerequisite; be applicable only to "acute destructive, primary gross lesion of brain". Namely, because of insufficient clinical data, secondary brain lesion such as post-anoxia, intoxication, metabolic coma and some kinds of CNS infection were excluded for the object to determine brain death. The criteria published by others also describe that etiology of coma should be clarified, and that careful measures are necessary to diagnose brain death if the cause of coma is unknown. In the present study, it was investigated that whether a clinico-pathological entity of brain death could exist universally regardless of the etiology, and by what means it could be defined clinically. The patients suffering from nondestructive, secondary brain lesions and who showed "brain death-like state" were selected for the study. ("Brain death-like state" requires coma, dilated nonreactive pupis and arrest of respiration concomitantly for more than 6 hours.) And 25 patients were collected, whose underlying diseases were post-anoxia or shock, CO intoxication, Paraquat poisoning, near-drowning or suffocation, hepatic coma, accidental hypothermia and sepsis, with or without the episode of cardiac arrest. Though all the patients died from 1 to 13 days after the insult, clinical signs of brain death-like state were not always irreversible. Isoelectric EEG was obtained on that state in 11 patients and repeated EEG revealed no return on those patients. But another 5 patients showed EEG activity when brain death was strongly suspected clinically.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1977

[Hemodynamic and respiratory function following acute spinal cord injury (author's transl)].

Twenty two cases of the cervical and thoracic cord injury were studied to determine hemodynamic and respiratory function within 7 days from the injury. Most patients showed a tendency of bradycardia and hypotension on admission which were more remarkable in the group of lower cervical cord or the upper thoracic cord lesion than the upper cervical cord group. Such a hypotension and bradycardia tended to recover within 7 days. In cervical cord injury, cardiac output remained unchanged, which indicated that initial hypotension was due to decreased total peripheral resistance. Respiratory rate was slightly increased in most patients, but did'nt show any significant difference among the level of the lesion. PaO2 and PaCO2 were within normal range on admission, however PaO2 decreased gradually in 7 days only in cervical cord injury. Increased pulmonary arterial pressure was confirmed during the above hypoxemic period. It suggests that disturbance of neurological control of pulmonary circulation might play a significant role in the respiratory insufficiency of cervical cord injury.

Adolescent↗
PubMed1975

Haemodynamic defect in patients with severe head injury.

Haemodynamic studies were made in 34 patients with severe head injury. The changes of cardiac output were noteworthy and correlated well with the clinical course and the prognosis of the patients. Marked systemic hypotension at the moment of brain death was mainly caused by the decrease of cardiac output. At this moment, peripheral resistance fell only to normal limits from the raised level. In the patients who survived, the cardiac output increased in proportion to the respiratory insufficiency, that is, the increased A-aDO2 and Qs/Qt. The increase of oxygen consumption was also accompanied by an increased cardiac output, but in the patients with the severest head injury who died, the cardiac output remained low. It failed to respond to increased A-aDO2 and Qs/Qt, and oxygen consumption remained low.

Acute Disease↗
PubMed1975

[Artificial hyperventilation in head injury. I. Spontaneous hyperventilation and assisted ventilation (author's transl)].

The present study was desined to clarify the roles of artificial hyperventilation in management of the patients with cerebral injury. Here reported is the first part of the serial studies and concerned with general informations about hyperventilation. The measurements of PaCO2, minute ventilation volume (VE), dead space (VD), tidal volume (VT), cardiac output (by dye dilution method), oxygen consumption (by Fick' principle) and oxygen equilibrium were performed in the patients suffering from acute, severe head injury. And the effect of assisted ventilation on them were investigated (using pressure-limited respirator). 1. There was a common finding that marked and sustained increase in VE, VA (alveolar ventilation), and decrease in PaCO2 existed during the first week of injury. 97% of both VE and VA were above normal and mean value of PaCO2 was 29-33 mmHg. The syndrome of spontaneous hyperventilation was evidently more prominent in the nonsurvived group of patients. It was noteworthy that increased VE (or VA) was dependent neither on VD or pulmonary dysfunction nor on metabolic acidosis of arterial blood. The relation of VA to base excess in head injury was well contrasted to that of acute CO poisoning. 2. Assisted ventilation resulted in increased VT and decreased respiratory rate, and little change in VE. Consequently, PaCO2 changed only from 33.0 to 29.4 mmHg as a mean of entire series of patients. But when the influence affected by hypoxemic drive was subsided, a significant reduction of PaCO2 was disclosed following assisted ventilation. The assisted ventilation with pure oxygen was also associated with reduced cardiac output (from 6.0l/min to 5.3l/min), though the oxygen consumption changed variedly among the patients. 3. The fact was confirmed that both hypocapnea and alkalosis produced the left-sised shift of oxygen dissociation curve, decrease in P50 (P02 at 50% saturation of oxygen), and in addition, narrowed arterio-mixed venous oxygen difference. The changes of artero-mixed venous oxygen saturation difference which were calculated at 100 mmHg of PaO2 and 40mmHg of mixed venous PO2 were in a linear fashion with those of P50. Apart from the problems on injured brain, the beneficial and non-beneficial effects of hyperventilation were further discussed. The availability and inidcation of artificial hyperventilation should be precisely evaluated later, in a comprehensive manner with the subsequent studies (Part 2 and 3) on cerebral metabolism and intracranial pressure.

Brain Injuries↗