To study the characteristics of lesions in the upper gastrointestinal (GI) tract following paraquat poisoning, the upper GI tracts in 37 autopsy cases of paraquat poisoning were histopathologically examined. Lesions which developed in less than twelve days after paraquat ingestion were characterized by coagulation necrosis of the epithelia and erosion, followed by granulation tissue. The lesions were probably due to the corrosive effects of paraquat on the epithelia. Lesions which appeared more than twelve days after ingestion were characterized by infections with herpes virus, cytomegalovirus or Candida. These infectious lesions were observed only in patients administered steroids for over five days to prevent pulmonary fibrosis. On the other hand, in 2 patients who survived more than twelve days after ingestion, no infectious lesions of the upper GI tract were observed. One of these patients had undergone no steroid therapy and the other had steroid therapy lasting three days. We suggest that lesions of the upper GI tract in paraquat poisoning are modified and aggravated by long-duration steroid therapy.

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Hematological influences related to transfer by helicopter are practically unknown to practitioners. This study was undertaken to elucidate the effects of transfers by helicopter on the blood coagulation-fibrinolysis system in humans. Ten healthy men who agreed to the experiment were exposed to 30 minutes of flight at 600 meters altitude in a Kawasaki BK-117 helicopter. Blood samples were collected 4 times for each subject (before, during and after flight), from the antecubital vein in which a plastic catheter had been placed before flight. These samples were centrifuged immediately after flight and the sera were stored in a freezer until analysis. Prothrombin time (PT), activated partial thromboplastin time (aPTT), von Willebrand antigens, antithrombin-III activities (AT-III), fibrinogen levels (Fbg), plasminogen activities (Plg), alpha2-plasmin inhibitor activities (alpha2-PI) and FDP levels (FDP) were determined and total protein and colloid osmotic pressure (COP) were also measured in the same samples. During and following flight, PT showed no specific change but aPTT was slightly shortened, von Willebrand antigen levels were increased, AT-III, Fbg, Plg, and alpha2-PI were all decreased slightly and FDP was increased slightly. Protein and COP were also decreased, but these changes were all within normal values. These results suggest that flight by helicopter acts as a kind of stress and the blood coagulation-fibrinolysis system might be stimulated by such stress.

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The end-tidal carbon dioxide concentration (ETCO₂) has been demonstrated to be a useful indicator of effectiveness of external cardiac massage and restoration of spontaneous circulation (ROSC) in animal models. It hes also been reported that ETCO₂ might be a prognostic indicator of success in CPR. In human models, however, consistent results have not been obtained concerning effectiveness as an indicator of success in CPR. Therefore, we prospectively measured ETCO₂ in 50 patients in out-of-hospital cardiac arrests during CPR. Nineteen patients who were successfully resuscitated had higher average ETCO₂ values one minute after the initiation of ETCO₂ recording in the emergency care unit (first ETCO₂) than did 31 non-resuscitated patients. However this result shows that ETCO₂ is not specific enough to be an indicator of success in CPR, because values varied widely in both groups. In 16 non-cardiogenic patients (with cerebral or respiratory factors), the first ETCO₂ of the 7 resuscitated patients was significantly higher than that of the 9 non-resuscitated patients. The first ETCO₂ of all 7 resuscitated patients was higher than 0.8%, and patients with a first ETCO₂ lower than 0.8% were not resuscitated. This indicates that ETCO₂ may be an indicator of CPR success in non-cardiogenic patients. Our findings suggest that differences in etiology of cardiac arrest may be one of the reasons for controversy as to whether ETCO₂ can be an indicator of CPR success.

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The science of resuscitation has made remarkable strides and the resuscitation success rate after brief cardiopulmonary arrest under optimum conditions now approaches 75%. However, the success rates for cardiovascular and cerebral resuscitation remain very low. Recently, in animal experiments, it has been reported that CPB (cardiopulmonary bypass) can effect reperfusion and assist reliably in circulation, thereby enhancing survival and cerebral recovery rates after prolonged cardiac arrest. In 1988, we started trials of resuscitation of patients dead on arrival (DOA), using stand-by CPB. Up to this time we have attempted resuscitation of 7 patients in this trial.
(1) CPB apparatus
We have placed the CPB apparatus for DOA patients in the emergency room. The reservoir and circuit are primed beforehand with lactated Ringer's solution for emergency use. We call this method the “Stand-By CPB System”.
(2) Indications for CPB in DOA patients
When a DOA patient is admitted to our department, we first attempt resuscitation using standard advanced life support methods. However, if this proves ineffective and the patient fulfils all the criteria for CPB, i.e. witnessed cardiac arrest, endogenous etiology other than brain disease, age under 60 years and patient not resuscitated after more than 20min of SECPR (standard external cardiopulmonary resuscitation), we then consider resuscitation of the patient using CPB.
(3) Method of CPB in DOA patients
We use the femoral vein and artery as cannulation sites. Until restoration of spontanous circulation, CPB flow is regulated at 50-60ml/kg/min. During CPB, efforts are made to control the activated clotting time (ACT), blood temperature and blood pressure. We include a continuous hemofiltration filter in the circuit for dehydration.
(4) Clinical cases
Over the past 2 years, stand-by CPB has been instituted in 7 patients in our department. Patient age ranged from 21yrs to 60yrs (mean, 37.4yrs). The diseases causing cardiopulmonary arrest were acute myocardial infarction in 4 cases, severe asthma in one case, idiopathic cardiomyopathy in one case, and hyperkalemia due to chronic renal failure in one case. Upon admission, ECG patterns were either ventricular fibrillation or standstill. The time from cardiac arrest to the time of admission ranged from 15min to 30min, and the time from admission to the start of CPB ranged from 19min to 55min.
(5) Patient outcome
In these 5 patients, neurological status was improved including restoration of spontaneous breathing, appearance of auditory brainstem response, and appearance of response to pain. In 5 patients, spontaneous circulation was restored. Only three of these patients, however, were successfully weaned from CPB, and of these, one patient died from LOS (low output syndrome) 11hrs after weaning. In total, two patients were revived by the resuscitation, and one of them recovered without any neurological damage in spite of a 40-min cardiac arrest.
Although some problems still remain, we believe there are many advantages of CPB in DOA patients. With the use of CPB, cerebral reperfusion can be optimized, blood temperature and pressure can be controlled promptly, and various agents can be delivered safely and accurately for the prevention or amelioration of reoxygenation injury.

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Soluble barium salts, commonly used in industrial fields, are highly toxic. Hypokalemia, arrhythmia and weakness are the common signs of barium salt poisoning and the lethal dose is thought to be about 1.0g. A 21-year-old man complained of vomiting, diarrhea and a tingling sensation after the accidental ingestion of barium chloride. Hypokalemia (3.2mEq/l) and electrocardiogram abnormality (giant U-wave) were also observed. The patient ingested only about 0.1g of barium chloride, but plasma barium concentration was 8.5μM (measured by ICP-AES; inductively coupled plasma emission spectroscopy). Other laboratory findings were normal. Magnesium sulphate was given orally (40g) for antagonistic action against that of barium and therapeutically 40mEq of potassium was infused intravenously over 6 hours. Potassium excretion into urine was 30.6mEq over 24 hours. At 45 hours after admission, plasma potassium had recovered to 4.3mEq/l. Electrocardiogram normalized within 3 hours, and gastrointestinal and neurological signs were absent by the next morning.The mechanism of cardiac toxicity in barium chloride poisoning has not yet been clearly defined. Although some of the ECG changes may be associated with hypokalemia, a Ca channel blocking mechanism could also be responsible.

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The case of a 62-year-old male with acute development of a traumatic intracerebellar hematoma, which was identified on serial CT scans, is reported. The patient fell and struck his occiput when he was involved in a traffic accident on June 25, 1988. He complained of headache and vomited, and was transferred to this hospital within one hour after the accident. On admission, he was alert and well oriented. Plain skull roentgenogram showed a right occipital linear fracture. The initial CT scan showed a small high density area in the right cerebellar hemisphere suggesting a hematoma, associated with hemorrhage in the IVth ventricle and subarachnoid space. Gradually, the patient became drowsy and began vomiting frequently. CT scan performed 3 hours after injury revealed an increased volume of hematoma in the right cerebellar hemisphere with slight shift of the IVth ventricle to the opposite side. Emergency posterior fossa craniectomy was then performed 5 hours following injury and the hematoma was totally evacuated with debridement of the contused cerebellar hemisphere. The postoperative course was uneventful. At follow-up examination 4 months later the patient was found to be leading a normal life without any neurological deficit. Traumatic acute intracerebellar hematomas, unassociated with subdural or epidural hematoma of the posterior fossa, are relatively rare. Early diagnosis and management should be made so as not to result in fatal brain stem injury.

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Three cases of bilateral epidural hematomas were found in a total of 153 cases of epidural hematoma over a period of 8 years among 2, 482 cases of head injury which required admission. In all cases, CT scan within 6 hours of head injury revealed simultaneous bilaterally-coexisting epidural hematomas. In two cases, skull x-ray films showed bilateral linear skull fractures. Under the skull fractures, acute bilateral epidural hematomas were demonstrated by CT scan. The origin of hematoma was thought to be related to the fractures. In one of the latter cases, skull x-ray films showed a linear skull fracture in the left fronto-parietal area and bilateral epidural hematomas were demonstrated by CT scan. A hematoma on the right side was thought to be the result of dural stripping caused by negative pressure at the site opposite the site of impact. In two of the three cases, hematomas were removed bilaterally. All patients were discharged without any major neurological deficit.

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