Toshihisa Sakamoto

Prolonged Hemodynamic Maintenance by the Combined Administration of Vasopressin and Epinephrine in Brain Death: A Clinical Study

The present study attempted long term hemodynamic maintenance in 16 adult brain-dead patients, 14 with head injury and 2 with cerebrovascular accidents. In addition to respiratory and fluid management, 10 were treated with continuous infusion of epinephrine to maintain systolic blood pressure above 90 mm Hg. The remaining 6 patients each received a continuous infusion of synthetic arginine vasopressin (ADH) at a rate of 1 or 2 units/hour (285 +/- 45 microunits/kg/minute) simultaneously with epinephrine. The 10 patients treated with epinephrine alone all succumbed to cardiac arrest within 48 hours of brain death, with a mean survival time of 24.1 +/- 17.2 hours. In the patients who received simultaneous ADH infusion, a minimal dose of epinephrine of no more than 0.5 mg/hr in most instances sufficed to maintain blood pressure. Their mean survival time after brain death was remarkably prolonged to 23.1 +/- 19.1 days. In brain death, ADH plays a critical role in hemodynamic maintenance, and ADH administration permits long term hemodynamic stabilization of brain-death patients, offering increasing opportunities for organ transplantation.

Transcatheter embolization in the treatment of massive bleeding due to maxillofacial injury

Thirty-one cases of massive bleeding due to blunt maxillofacial injuries were treated by several procedures. Blind techniques, such as nasal and/or oral packing or ligation of external carotid artery, failed to achieve hemostasis in 13 of the 18 cases (72.2%) in which they were employed before 1984. Since then, carotid angiography has documented the location of the bleeding in 12 of the 13 cases (92.3%) in which it was employed. Each of the four cases in which extravasation was visualized from the external carotid artery was successfully treated by transcatheter embolization. We conclude that selective, angiographically guided embolization can reliably achieve hemostasis in a high proportion of patients with maxillofacial injury who are in danger of exsanguination from the branches of the external carotid artery.

Computed tomography for diagnosis and assessment of cerebral fat embolism

SummaryA patient with cerebral fat embolism was followed by computed tomography (CT). For the first few days after injury, CT revealed no abnormality. About a week later, multiple low density areas appeared in the white matter of the frontal region. They disappeared within the subsequent 2 weeks while subdural effusions developed in the fronto-parietotemporal regions. As neurologic recovery progressed, the subdural effusions gradually diminished and cerebral atrophy was seen.

Delayed neurotoxicity produced by an organophosphorous compound (Sumithion)

A case of late-onset manifestation of organophosphorous insecticide poisoning is described. The patient was a 70-year-old female who ingested 40ml Sumithion emulsion (50% fenitrothion). At first, no toxic symptoms were apparent. However, 48 h after ingestion certain signs became apparent. An impediment in consciousness was observed. Fasciculation and muscular weakness were noted, while plasma and urinary 4-nitro-3-methylphenol (NMC), the degradation product of Sumithion, reached a maximum. Neither atropine sulfate nor PAM (pyridine 2-aldoxime methiodine) were effective. For 3 weeks the patient required ventilatory support, and consequently her muscle strength and neurological status gradually recovered with falling NMC levels.

Computed tomographic imaging of the brain in after hypoglycemia coma

SummaryA case of severe hypoglycemic coma was studied by sequential Computed Tomographic Imaging (CT) of the brain. The CT 1) was normal in the early stage, 2) subsequently showed a low density area, which was enhanced by the contrast medium, in the cerebral cortex and the boundary zone between the major cerebral arteries, and 3) revealed marked enhancement in the entire cortical region and hypodensity in the periventricular region in the late stage. These CT findings, representing the course of neural cell damage by severe hypoglycemia, are discussed from the pathophysiological viewpoint.