Inhaled nitric oxide (NO) therapy is becoming an indispensable measure in neonatal intensive care to rescue critically ill neonates with hypoxemic respiratory failure. Inhaled NO improves oxygenation and reduces pulmonary hypertension, but it also may have the following beneficial effects: (1) decreasing pulmonary capillary pressure; (2) inhibiting pulmonary microvascular leaks; (3) inhibiting pulmonary leukocyte aggregation and adhesion; (4) inhibiting pulmonary platelet aggregation and adhesion; and (5) inhibiting hypertensive pulmonary vascular changes. Inhaled NO therapy has been receiving much attention as a preventive measure for acute respiratory distress syndrome and pulmonary hypertensive diseases. The indices for improvement of oxygenation and the measures for augmentation of oxygenation during inhaled NO are beginning to be described, but no device for inhaled NO therapy exists which can be used easily and safely by anyone. Aerosolized prostaglandin therapy has not yet been established either. Neither therapy should be performed without obtaining informed consent and institutional approval.

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Reperfusion therapy for acute myocardial infarction (AMI) has reduced early mortality, however the incidence of cardiac rupture following AMI has not significantly decreased. Cardiac rupture is a catastrophic complications and there are few reports of patients who have successfully recovered. The percutaneous cardiopulmonary support system (PCPS) is useful in maintaining circulation during circulatory collapse. Surgical interventions using PCPS were performed in eleven patients with cardiac rupture. Attempts at surgical repair were possible in six patients when PCPS was used as the circulatory assist deveice. On the other hand, when PCPS was used as a circulatory assistance device, but none survived. PCPS was used in five patients as both a circulatory assistance device and for surgical support at low temperature (20°C). Two of these five patients survived and were uneventfully discharged. This new strategy of using hypothermic percutaneous cardiopulmonary support bypass should prove to be useful for successful repair of post-infarction rupture.

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We studied the mechanism of severe mitral regurgitation (MR) secondary to acute myocardial infarction and the prognosis of patients who underwent surgical mitral repair. The subjects were nine patients (2 men and 7 women) ranging in age from 58 to 78 years (mean, 73), who underwent immediately surgical treatment for acute MR. The site of infarction was inferior in eight patients and anterior in one. Severe congestive heart failure, shock or hypotension existed in all patients. The mechanism of MR was accurately diagnosed with two-dimensional and Doppler echocardiography in five patients with leaflet prolapse, and ruptured papillary muscle in four patients with restricted motion of the posterior leaflet and central regurgitation. Mitral valvuloplasty was attempted in six patients (two with ruptured papillary muscle and four with papillary muscle dysfunction. Three patients underwent mitral valve replacement on the 4.2 (mean) hospital day. Death occurred in one patient who had already developed severe multiple organ failure by admission. One patient with mitral valve replacement underwent reoperation for late thrombosis of the artificial valve. No cardiac events occurred over the long term in patients with mitral valvuloplasty. We concluded that mitral valvuloplasty, when technically feasible, is the procedure of choice for acute ischemic MR because valve-related events are less than valve replacement.

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About 600 residents and rescue staff were exposed to what was found to be sarin vapor in the city of Matsumoto on June 27, 1994. Fifty-six patients were admitted to hospitals for symptoms of some kind of gas poisoning. We examined the clinical and laboratory findings of 264 patients who were treated at six hospitals. The presence of extremely low cholinesterase values in blood plasma suggested at first that the toxication was caused by an organic phosphorus chemical. But there were many aspects that could not be explained by hitherto-known organic phosphorus toxication. We exchanged information to establish the nature of the substance responsible and to facilitate treatment. The Nagano Prefecture Public Health and Pollution Research Institute reported on July 3 that they found “sarin” and its degraded substances from the air and water at the presumed site of emission of the toxic substance. This paper is based on the report which we submitted to the “Hospital Liaison and Review Committee on the Matsumoto Toxic Gas Poisoning”.
Almost all patients admitted to hospitals had severe miosis and tachycardia followed by bradycardia. Recovery to normal red blood cell cholinesterase activity was gradual reaching normal levels during the 3 month period after exposure to the toxic substance. Visual acuity and visual area improved after several weeks. The relationship between subjective symptoms and blood plasma cholinesterase values was examined. Those with such subjective symptoms as headache, fatigue, feverish feeling, visual field abnormalities, poor vision and abnormal subjective sensations had significantly low blood plasma cholinesterase values in the acute phase. Pseudocholinesterase values (ChE%), expressed as a percentage taking the normal minimum value to be 100%, were decreased in 53 of 222 patients (23.9%) examined within 5 days of exposure. A correlation was found between the degree of decline of ChE% and pupil diameter (P<0.01). Creatine kinese (CK%), expressed as a percentage taking the normal maximum value to be 100%, was correlated with ChE% examined within 5 days of exposure.

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A 31-year-old man was admitted to the ICU with a diagnosis of primary pulmonary hypertension and severe hypoxemia caused by hemoptysis. Examinations revealed 112/56mmHg of systemic artery pressure, 113/54mmHg of pulmonary artery pressure and a PaO₂/F_IO₂ ratio of 87. Continuous intravenous infusion of PGE₁ and dopamine worsened the pulmonary hypertension. Continuous intravenous infusion of PGE₁ and amrinone improved pulmonary hypertension (75/53mmHg; vs. systemic artery pressure 110/70mmHg) and raised the PaO₂/ F_IO₂ ratio to 300.
The patient died of massive hemoptysis several days later, however amrinone may be an effective agent for treating primary pulmonary hypertension.

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We report a case of influenza A (H3N2) infection followed by multiple organ failure (MOF). The patient, a 16-year-old female who had been found to have an ECG abnormality, was admitted to our ICU for acute respiratory, cardiac and renal failure. On examination, it was established that the MOF resulted from rhabdomyolysis, viral pneumonia and viral myocarditis. She was immediately treated with artificial respiration, blood purification and catecholamines. In the treatment of MOF, continuous hemofiltration (CHF) was effective for the maintenance of proper water balance and electrolytes, and the removal of myoglobin. Although the fatal complications of influenza are very rare, early recognition and prompt treatment are important to prevent serious complications as shown in the case of a young adult with chronic heart disease.

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