The course of recovery of cardiac function following heart beat restoration was studied in patients with cardiopulmonary arrest. Among patients treated at our center for cardiopulmonary arrest in the last 5 years, 47 (mean age 61.5 years), in whom the heart beat was restored, were selected as subjects. Those with asynergy of the left ventricle were excluded. Echocardiograms were obtained over time to determine time-sequence changes in the ejection fraction (EF), for the analysis of the relationship between cardiac arrest time and the course of recovery of cardiac function. EF within 1 day after heart beat restoration was 69.2±10.9% in patients with cardiac arrest for less than 5 minutes, 62.1±10.4% in those with arrest for 5 to less than 30 minutes, and 57.9±11.0% in those whose arrest exceeded 30 minutes disclosing that cardiac function was increasingly and significantly suppressed as duration of cardiac arrest increased. As for the course of recovery of EF following heart beat restoration, EF was determined to be 61.1±11.8% within 1 day after restoration, 60.5±9.0% after 2-3 days, and 67.6±9.2% after 7-15 days, indicating that cardiac function could be restored after 3 days. It was also revealed that the longer the cardiac arrest, the poorer the recovery of cardiac function. From these results, it was assumed that several days are required to regain cardiac function after heart beat restoration, and that cardiac function is more suppressed and requires more time for recovery as cardiac arrest is prolonged. These results suggest that the pathophysiological conditions of the stunned myocardium may play some part in alteration of the myocardium after heart beat restoration.

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Purpose: Patients with left main trunk (LMT) infarction include many cases who develop cardiopulmonary arrest (CPA) before arriving at a hospital and those who have already gone into shock before reaching the hospital. Relationships between electrocardiographic (ECG) findings and prognosis have not been elucidated. Thus, the purpose of this study was to analyze acute-phase ECG findings in LMT infarction patients and to clarify the prognosis of this disease. Methods: Of 414 patients with acute myocardial infarction (AMI), including patients with prehospital cardiac arrest who underwent emergency coronary angiography (CAG), 10 who had completely occluded LMT were enrolled in the study. An assessment was made of the relationships between ECG findings on admission (or at the resumption of heart beat) and prognosis. Results: The death rate of the 10 patients was 70% (7/10), and the cause of death was low output syndrome (LOS) in 6 patients and cardiac rupture in 1. The assessment of the relationships between ECG findings on admission (or at heart beat resumption) and prognosis showed that 75% (3/4) of the narrow QRS wave form survived, whereas all patients with wide QRS (6/6) died. V1 conduction with this wide QRS was of the rR' type in 4 patients and of R type in 2. Conclusion: The ECG characteristics of LMT infarction, from the aspect of the QRS wave form, have been reported. Hence, the relationships between ECG findings and prognosis in LMT infarction were assessed. It was demonstrated that patients with the most severe AMI suffered LMT infarction showing a wide QRS. All of these subjects died. This QRS wave form was characterized by V1 conduction exhibiting a pattern of right bundle branch block of the rR' or R type. On the other hand, LMT infarction patients with a narrow QRS had a relatively good prognosis when treatment, such as reperfusion, was effective.

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A 19-year-old woman, status post an uneventful pregnancy and delivery, developed a severe migranous headache and visual loss at 2 hours post partum. Computed tomography demonstrated ischemia and edema in the bilateral parietooccipital cortices. Magnetic resonance imaging (MRI) ruled out cerebral sinus thrombosis. Magnetic resonance imaging angiography (MRA) did not reveal remarkable abnormal findings in the major arteries. Cerebral angiography revealed circulation disorder of the bilateral posterior cerebral arteries in the capillary phase. The patient recovered with conservative therapy. The ischemic lesion associated with eclampsia often affects the parieooccipital cortices and basal ganglia. In such cases, the ischemic lesions are often reversible, and the symptoms resolve quickly, usually within a week. Conservative therapy is warranted when major artery stenosis or venous thrombosis can be excluded. Careful follow-up is essetial, however, as cases in which the vasospasm worsened and the patient died have been reported.

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Two cases of HELLP syndrome are reported. Case 1: A 23-year-old primigravid woman, presented at 35 weeks' gestation with uterine contractions and vaginal bleeding. Her laboratory data showed elevated liver enzymes and low platelet count. She was suspected to have HELLP syndrome, and an emergency cesarean section was performed with delivery of a 2, 090g female infant. After delivery, jaundice and oliguria were noticed and the mother lost conscious due to severe hypoglycemia. A glucose infusion, a large volume of fresh frozen plasma and protease inhibitors were administered intravenously. She regained consciousness quickly and recovered without neurological deficits. Case 2: A 31-year-old woman, para 3, gravida 4, complained of nausea, vomiting and epigastralgia. Her blood pressure was elevated and laboratory data showed elevated liver enzymes, low platelet count and hemolysis. She was diagnosed as having HELLP syndrome and an emergency cesarean section was performed with delivery of a 1, 024g male and a 924g female infant. After delivery, oliguria was noticed and platelet count dropped to as low as 18, 000/mm³. This patient also received a large volume of fresh frozen plasma and protease inhibitors. These two cases showed high levels of maternal plasma endothelin in the first postoperative week and case 2 showed elevated tissue polypeptide antigen. These two mediators may play an important role in this syndrome.

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We present a case of pure puffer fish poisoning who developed prolonged ataxia without persistent muscle weakness. Impaired peripheral nerve conduction was suggested to be the cause of the prolonged ataxia. A 40-year-old male, a licensed puffer fish chef, tasted a piece of puffer fish liver when his stomach was empty. Approximately 20 minutes later he recognized numbness in the fingers and lips, the onset of generalized muscle weakness and paresthesia. He was admitted to our hospital for the management of progressive motor weakness one hour after ingestion. Spontaneous breathing disappeared 90 minutes after ingestion. After six hours of mechanical ventilation, spontaneous breathing resumed. Motor paralysis and paresthesia improved within 20 hours, while dizziness persisted for several days, which was not attributable to alcohol in this case. Neurological examination showed prolonged ataxia; he could not stand on one foot until the third hospital day. Serial peripheral nerve conduction velocity studies revealed decreased conduction velocities. In particular, conduction velocities of the sensory nerve were more seriously impaired and required a longer recovery time as compared to those of the motor nerve. Since tetrodotoxin does not affect the central nervous system, such prolonged ataxia in puffer fish poisoning is presumably attributable to decreased peripheral nerve conduction velocities.

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We report a case of post-traumatic delayed stricture of the small bowel. An 11-year-old girl wearing a 2-point seat belt while riding as a passenger in a car was injured. Her demonstrable injuries were an L3 Chance fracture and contused seat belt scar in the lower abdomen. Symptoms of bowel obstruction began 9 days after the injury but then improved. On the 21st day, symptoms of bowel obstruction worsened rapidly, necessitating surgery. Four annular stricture lesions were revealed. Three were resected and one was treated conservatively. Mesenteric injury was slight. Histological findings were Ul-IV and no ischemic change. The time elapsed from the injury to the appearance of these symptoms was approximately 12 days. Laparotomy is important in considering resection. The main causes of this disease are circulatory disorders and inflammatory adhesions, but in our case the source was an organic change in the curative course of small bowel injury.

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