Kinetic analysis was used to study the time course of plasma cholinesterase (ChE) and erythrocyte acethylcholinesterase (RBC AChE) activities in 17 patients after intentional/accidental ingestion of organophosphorus pesticides. There was almost no plasma ChE until abrupt increases occurred from the 0 to 12th day after the ingestion. This initial null phase continued for more than 7 days only in cases seriously poisoned with fenitrothion, but it lasted less than 3 days even in life-threatening intoxication with other compounds. For RBC AChE, the null phase in the patients was from 3 to 6 days longer than it was for plasma ChE. The recovery of both enzymes increased exponentially and approached asymptotes, to which a simple one-compartment model was successfully fitted. The half-life for this recovery period, the mean of which was 11.3 days for plasma ChE and 26.7 days for RBC AChE, was related neither to the severity of clinical symptomes nor to the chemical structure of the pesticides. The data obtained were not sufficient to determine with more complicated models the supplementary effects of reactivation and aging on the phosphorylated enzymes. These results indicate that (1) newly formed enzyme/erythrocyte is a leading factor in the recovery, (2) the half-life of recovery is not a good indicator of the clinical course, and (3) dynamics of enzyme inhibition are different among compounds.

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The purpose of this study was to determine the significance of coronary artery spasm in emergency room patients with transient loss of consciousness. Thirty-two consecutive patients with transient loss of consciouness admitted to our emergency room were studied. Conventional neurologic and non-invasive cardiovascular tests were performed for 29 patients and the cause was established in 14 patients (a cardiovascular cause in 2 patients and a non-cardiovascular cause in 12). Three patients were not examined. The coronary spasm provocation test was carried out by intracoronary injection of methyl ergonovine in 11 patients in whom the cause of the unconsciousness was not determined despite conventional evaluation. The provocation test was not done in 4 other patients with unconsciousness of undetermined cause because of other medical problems or advanced age. Coronary spasm with an ischemic electrocardiographic change was induced in 4 of the 11 patients (36%). One patient developed a pre-syncopal state due to profound hypotension during the coronary spasm. Chest pain before syncope occurred in only one of the 4 patients with coronary spasm. Prodromal symptoms could not differentiate the coronary spasm from other causes of syncope. Coronary spasm was the cause of the transient loss of consciousness in 13% of the consecutive emergency room patients. These results suggest that the coronary spasm provocation test is useful for evaluating patients with unexplained transient loss of consciousness.

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A newly developed method of radioreceptor assay has made it possible to determine the concentration of active metabolites of diazepam in urine. Hence we evaluated the effect of fluid administration on urinary excretion of the active metabolites of diazepam in rabbits subject to acute diazepam poisoning. Animals, weighing 3.1kg on average, received diazepam in doses of 15mg/kg of body weight intravenously and an hour later they started to receive saline at a rate of 50ml/kg/hr for three hours. Blood was taken and urine was collected every hour for 7 hours. The serum concentrations of diazepam and desmethyldiazepam were determined by high performance liquid chromatography. The urinary concentration of active metabolites of diazepam was determined by radioreceptor assay. The serum concentration of diazepam and desmethyldiazepam was 1, 519.2±542.7ng/ml before saline administration. Saline administration significantly increased the serum elimination rate constant of diazepam. It was calculated to be 0.452±0.090/hr in rabbits receiving saline and was 0.200±0.031/hr in rabbits not receiving saline. The urinary excretion of active metabolites of diazepam in the first seven hours was 528.9±404.7μg as diazepam equivalent in rabbits receiving saline. It was 51.6±33.3μg in rabbits not receiving saline (p<0.01). Thus saline diuresis significantly enhanced urinary excretion of the active metabolites of diazepam. The urine volume was 270.6±117.4ml in seven hours in rabbits receiving saline, and 70.7±32.7ml in rabbits not receiving saline. Saline administration did not increase creatinine clearance but it did increase the fractional excretion of the active metabolites of diazepam. A significant positive correlation was found between the urinary excretion of the active metabolites of diazepam and the urinary excretion of sodium or urine volume. These findings indicate that with saline administration, the active metabolites of diazepam may escape being reabsorbed in the renal tubule in the same way as sodium does.

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We studied the relationships between mechanisms of injuries and characteristics of injuries in severe traffic trauma. First we evaluated the injury severity score (ISS) in all of the traffic injury victims transported by ambulance to our Trauma Center. Of 286 cases, we selected for this study 222 cases with ISS≥16 (mortality rate 33.3%). Many of excluded 64 cases with ISS≥15 were unconscious due to drinking on admission; ambulance attendants might misjudge their iujury severity. The 222 cases were divided into 3 groups according to the mechanism of injury; car passengers (n=46), two-wheeled vehicle passengers (n=108), and pedestrians (n=68). In addition, 87 free-fall injury victims with ISS≥16 were studied as a control. In each group we examined the patterns of injuries with abbreviated injury scale (AIS)≥3 and causes of death. The highest incidence (above 60%) of head injury was similar among the groups. There was a significantly high incidence of abdominal injury in car passengers (39.1%) and pelvic injury in pedestrians (39.7%). The major causes of death were similar among the groups; they were severe head injury or massive hemorrhage. However, the major lethal hemorrhage region was different among the groups; it was the abdomen in car passengers, and the pelvis in pedestrians. A high incidence of severe hepatic injury in car passengers and severe pelvic fracture in pedestrians may be related to massive hemorrhage. Presence of unconsciousness in blunt injury victims may be the major factor leading ambulance attendants to select them for transport to the Trauma Center. Unconsciousness on admission would prevent rapid identification of the bleeding regions, which should be given preference in treatment. The study revealed that the risk region of massive hemorrhage may be peculiar to the mechanism of injury. This study should be of use in the initial treatment of severe traffic injury victims.

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A number of intracranial aneurysms complicating polycystic kidney disease (PKD) have been reported; however they include only 29 domestic cases. Cerebral hemorrhage with PKD is also not rare. PKD is considered a hereditary malformation with autosomal dominant transmission. Recently we had two cases of intracranial hemorrhage that were coincidentally associated PKD. One patient had an aneurysmal subarachnoid hemorrhage. In the other case, although no aneurysm was detected by four-vessel angiography, the patient had three cerebral hemorrhages. The third hemorrhage resulted in death in spite of successful control of the blood pressure. The coexistence of intracranial hemorrhage and PKD could be due to blood vessel fragility caused by collagen disease and connective tissue diseases. Furthermore hypertension due to PKD could become an accepted risk factor for arteriolar changes besides those congenital disorders of the blood vessels. Adequate treatment of hypertension as well as detecting cerebrovascular disorders could be the most beneficial medical approach for patients with PKD.

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A 22-year-old man sustained burn injuries over the face, bilateral upper extremities and the upper chest wall (35% as burned surface area) during toluene sniffing in a closed space. Facial burns and singed nasal hair were observed on admission. He was conscious and complained of dyspnea. Bronchoscopy revealed soot and a pale mucosa of the trachea and the bronchi as well. On the 3rd day after the injury, the PaCO₂ level had increased. Repeated suctioning and irrigation were necessary to remove a tenacious secretion mixed with soot, coagula, and tissue debris. On the 10th day, under bronchoscopic visualization, congestion of the tracheal wall, and denuded cartilage were observed in some places, and bronchial lumens distal to the carina were partially obstructed by tissue debris. It became more difficult for the patient to eliminate carbon dioxide (PaCO₂ 60∼70mmHg), while the oxygenation property of the lungs was still maintained (PaO₂/F_IO₂ 200∼400). The peak inspiratory pressure was as high as 60∼70cmH₂O. Pulmonary infection made adequate ventilation more difficult. Ultimately, pneumothorax due to barotrauma occurred and the patient died because of respiratory insufficiency accompanying pyothorax. This single case is worth reporting because the pulmonary parenchyma was spared burn injury evidenced by the maintenance of oxygenation, while the major bronchi and proximal bronchioli sustained severe burn injuries, ultimately leading to bronchial obstruction with difficulty in CO₂ elimination.

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Recently, we applied digital subtraction angiography in peripheral veins (ivDSA) in 2 cases of severe electrical injury of the extremities in early stages. In these early stages, occlusion, tapering, wall irregularities, and stenosis could be seen in the main arteries. Also, we found collateral blood vessels from the main artery and arterial network defect that could not be clearly depicted with the usual angiograms. Tissues in the defective portions of the collateral blood vessels and arterial network were necrotic. IvDSA also revealed aneurysm formation which was histopathologically confirmed as a pseudoaneurysm from the torn elastic fibers of the tunica media. In a non-invasive manner and without special maneuvering, ivDSA can be performed frequently to examine blood vessel lesions and blood flow impairment in severe electrical injury of the extremities. This method is useful especially for estimating necrotic lesions from an early stage and investigating aneurysm formation.

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