Preoperative diagnosis of obturator hernia by computed tomography in six patients.

Obturator hernia is a rare condition, and the prognosis of patients with this condition is poor. A retrospective study was performed on six patients with obturator hernia between 1993 and 1998. They had been diagnosed preoperatively by computed tomography (CT). The initial CT scan of the abdomen, including the pelvic area, revealed an incarcerated bowel in the obturator foramen of all six patients. All patients underwent laparotomy on the day of admission. Resection of the small bowel was performed in three patients, and release of the small bowel was performed in the remaining three patients. There were no perioperative deaths. In elderly women who have evidence by abdominal plain X-ray studies of small bowel obstruction, we recommend performing CT scan of the abdomen, including CT scan of the pelvic area, for detection of obturator hernia.

[Diffusion-weighted imaging of brain death: study of apparent diffusion coefficient].

DWI(Diffusion-weighted images) of the brain has been revealed to be useful in diagnosis of several clinical conditions. However, little is known about DWI with regard to brain death. We had opportunities to study patients with brain death. Case 1. A 34-year-old woman experienced cardiopulmonary arrest due to severe ventricular fibrillation, and resuscitated after about 120 minutes. After brain death, DWI showed high signals in the cerebral cortex, putamen, thalamus, brain stem and cerebellum, and ADC(apparent diffusion coefficient) values were 30-40% lower than those of normal volunteers. Case 2. A 45-year-old woman experienced cardiopulmonary arrest due to pontine hemorrhage, and was resuscitated after about 20 minutes. Before brain death, DWI showed high signals in the cerebral cortex, putamen, thalamus, brain stem and cerebellum, and ADC values were the same as those of normal volunteers. After brain death, DWI showed more clearly defined in these areas, but ADC values were 30-40% lower than the first values. DWI and ADC mapping shows areas corresponding to edema of a cytotoxic nature and to ischemic tissue. The characteristic views of high signals in the whole area of the brain were present, and an objective evaluation was possible with DWI after the brain death diagnosis by measuring ADC values.

[Neuromonitoring of acute internal carotid artery occlusion].

We experienced a patient with acute thrombosis of the unilateral internal carotid artery. We monitored the brain tissue temperature and intracranial pressure not only in both hemispheres simultaneously but also continuously throughout the process of brain death. The patient was a 73-year-old male who presented to our emergency room with right hemiparesis and aphasia. On admission to our department, no specific pathological findings were identified by brain CT. However a following investigation with left carotid arteriogram demonstrated a complete occlusion of the left internal carotid artery. Probes to monitor intraparenchymal temperature (Tip) and intracranial pressure(ICP) were inserted surgically into the bilateral hemispheres, and these two parameters were monitored continuously until the patient's death. Initially, Tip in the infarcted hemisphere was lower than that in the intact hemisphere, and the left hemisphere's ICP was significantly higher than that of the right one. When the ICP in the left hemisphere exceeded 40 mmHg, bilateral ICPs became equal. Brain herniation was confirmed when the ICP became progressively elevated thereafter. Subsequently the bilateral Tips became equal and lower than the bladder temperature following the brain herniation. In this case, we successfully monitored two parameters while the patient was in the process of brain death; i.e., brain ischemia, complete loss of brain circulation and subsequent decrease in the brain tissue temperature.

Intravenous detergent poisoning.

CASE REPORT: In the literature regarding surfactant poisoning, the route of exposure has almost always been oral. We report a case in which about 40 mL of bath detergent for home use was self-injected. The primary pathophysiologic effects were relative hypovolemia and cardiac dysfunction. The patient experienced frequent ventricular tachycardia, acute renal failure, rhabdomyolysis, hemolysis, and coagulation dysfunction. Intensive care included the administration of antiarrythmial agents and hemodialysis. The patient survived and was discharged from our hospital without sequelae.

[Sepsis due to Salmonella Oranienburg--a case report].

A previously healthy 15-year-old female was admitted to our hospital complaining of nausea and vomiting. She did not complain of diarrhea. A physical examination revealed a lower right quadrant abdominal tenderness without rebound or spontaneous pain and a knocking pain of the costovertebral angle. A high fever, knocking pain of costovertebral angle, and urinary findings including Gram's stain, lead us to suspect a urinary tract infection, cefotiam was administered intravenously. Spiking fever with shaking chills continued for three days, and three sets of blood cultures were positive for Salmonella Oranienburg, but her urine culture was negative. Her history was taken again, revealing an intake of a processed squid product. The product was confirmed by the local public health center to be Salmonella Oranienburg. Finally food poisoning by Salmonella Oranienburg with sepsis was diagnosed. With cefotiam she became better and was discharged from the hospital on the 10th hospital day. During admission to the hospital she did not experience any diarrhea, and her stool culture was negative. Epidemics of Salmonella Oranienburg food poisoning are relatively rare in the literature. In Japan, one has arisen as a result of contamination of a processed squid product in March 1999. However, there have been no cases without so-called gastroenteritic symptoms (abdominal pain and diarrhea) who were previously healthy and developed sepsis caused by Salmonella Oranienburg, reported in Japan. Even in previously healthy patients, with an epidemic situation of non-typhoidal salmonellosis, salmonella sepsis must be ruled out. Among such cases, those who present with spiking fever and shaking chills should be given antibiotic therapy after taking appropriate cultures.

[A case of hypertensive intracerebral hemorrhage associated with ipsilateral internal carotid artery occlusion].

We report a case of intracerebral hemorrhage associated with ipsilateral internal carotid artery occlusion. The patient was a 54-year-old man, who developed a small cerebral hemorrhage in the left internal capsule. He was admitted with mild right hemiparesis to out hospital. Left carotid angiography showed an occlusion at the origin of the internal carotid artery. Right cerebral angiography revealed the slow filling of cerebral arteries of left hemisphere by the cross flow. He was treated conservatively. Two days after admission, the neurological examination revealed no notable abnormalities. The etiology of hemorrhage of this case is presumed as the arterial necrosis due to hypertension. There has been no report on the intracerebral hemorrhage associated with ipsilateral internal carotid artery occlusion. Our case suggests that the volume and enlargement of cerebral hemorrhage may be influenced by cerebral perfusion pressure.

Severe respiratory distress following sodium oleate ingestion.

CASE REPORT: Oleic acid and oleate are pulmonary toxins used to create laboratory models of acute respiratory distress syndrome, but there is little information on human toxicity. We report the intentional ingestion of 50 mL sodium oleate 20% by a 22-year-old woman with no symptoms for the first 2 days after ingestion. Her respiratory status deteriorated rapidly on day 3 progressing to acute respiratory distress syndrome (PaO2/FIO2 < 100 mm Hg) on day 4. Treatment with high-dose steroids and intensive respiratory support including high-frequency jet ventilation were associated with gradual but complete recovery by day 39. The delayed onset of symptoms suggested that the lung injury was due to the systemic circulation of oleate to the lungs rather than to direct aspiration. In oral poisoning by sodium oleate, the lung is the first and most lethally affected target organ in humans. This case demonstrates that ingestion of a relatively small amount of sodium oleate can cause delayed, progressively severe, lung injury.

The Tokyo subway sarin attack: disaster management, Part 1: Community emergency response.

The Tokyo subway sarin attack was the second documented incident of nerve gas poisoning in Japan. Prior to the Tokyo subway sarin attack, there had never been such a large-scale disaster caused by nerve gas in peacetime history. This article provides details related to how the community emergency medical services (EMS) system responded from the viewpoint of disaster management, the problems encountered, and how they were addressed. The authors' assessment was that if EMTs, under Japanese law, had been allowed to maintain an airway with an endotracheal tube or use a laryngeal mask airway without physician oversight, more patients might have been saved during this chemical exposure disaster. Given current legal restrictions, advanced airway control at the scene will require that doctors become more actively involved in out-of-hospital treatment. Other recommendations are: 1) that integration and cooperation of concerned organizations be established through disaster drills; 2) that poison information centers act as regional mediators of all toxicologic information; 3) that a real-time, multidirectional communication system be established; 4) that multiple channels of communication be available for disaster care; 5) that public organizations have access to mobile decontamination facilities; and 6) that respiratory protection and chemical-resistant suits with gloves and boots be available for out-of-hospital providers during chemical disasters.

The Tokyo subway sarin attack: disaster management, Part 2: Hospital response.

The Tokyo subway sarin attack was the second documented incident of nerve gas poisoning in Japan. The authors report how St. Luke's Hospital dealt with this disaster from the viewpoint of disaster management. Recommendations derived from the experience include the following: Each hospital in Japan should prepare an emergent decontamination area and have available chemical-resistant suits and masks. Ventilation in the ED and main treatment areas should be well planned at the time a hospital is designed. Hospital disaster planning must include guidance in mass casualties, an emergency staff call-up system, and an efficient emergency medical chart system. Hospitals should establish an information network during routine practice so that it can be called upon at the time of a disaster. The long-term effects of sarin should be monitored, with such investigation ideally organized and integrated by the Japanese government.

The Tokyo subway sarin attack: disaster management, Part 3: National and international responses.

The authors report the national and international responses to the disaster produced by the Tokyo subway sarin attack. From a worldwide historical perspective, there had never been such a large-scale disaster caused by nerve gas during peacetime. Therefore, this event should be studied from various viewpoints in cooperation with members of the international community. To this end, the Japanese government should help coordinate a large-scale and detailed investigation of the Tokyo subway sarin attack, including the long-term effects of sarin. The authors also recommend that the Japanese Self Defense Forces should be used more effectively in large-scale disasters. The system of direct control of disaster management by the Japanese government could be useful in a large-scale disaster.

[Early treatment for body fluid shifts and circulatory derangement in patients with extensive burns].

The initial postburn period is characterized by body fluid shifts and circulatory derangement, or so-called burn shock. The fluid shifts are mainly due to a marked increase in capillary permeability. This loss of capillary integrity is so great that colloid including albumin, readily disperse into the extravascular space. This is limited to the burned area when of 30% or less of the body surface area (BSA) is involved, but is found throughout the entire body when more than 30% of the BSA is involved. The tremendous fluid shifts from the intravascular to the extravascular space result in edema formation and hemoconcentration. Along with the reduction in intravascular volume, there is a rapid reduction in cardiac output which gradually returns to the normal level 24 to 48 hours after burn injury. Therefore fluid resuscitation should be initiated immediately after injury. Currently a number of methods for achieving adequate volume replacement are available. In this paper we review fluid resuscitation methods for patients with extensive burns and also introduce recent topics on new regimens for resuscitation.

Effects of hypertonic saline and dextran 70 on cardiac contractility after hemorrhagic shock.

OBJECTIVE: The effects of a bolus of 7.5% NaCl-6% dextran 70 (HSD) on cardiac contractility were evaluated in anesthetized sheep with hemorrhagic shock. BACKGROUND: HSD has been shown to be effective at resuscitation in cases of hypovolemia caused by hemorrhage. Common hemodynamic findings after the injection of HSD in hemorrhagic shock are the restoration of cardiac output, increased blood pressure, and improvement of peripheral circulation. Some mechanisms by which HSD maintains circulation in hemorrhagic shock have been proposed: rapid shift of fluid from intracellular to extracellular space, improved peripheral perfusion, and increased cardiac contractility. Conflicting data exist, however, regarding the positive effect of HSD on cardiac contractility after hemorrhagic shock. METHODS: Hemorrhagic shock was induced by shedding mean blood volume of 31.4 mL/kg, and mean blood pressure was maintained at 50 mm Hg for 30 minutes. The HSD group (n = 6) received HSD (4 mL/kg), and the saline group (n = 6) received normal saline (40 mL/kg) after shock. Cardiac functions were measured in both groups using the left ventricular end-systolic pressure-volume relationship and preload recruitable stroke work during the experimental period: before shock, immediately after the resuscitation, and 2 hours after resuscitation. RESULTS: Hemodynamic parameters in both groups demonstrated similar changes throughout the experimental period without significant difference between the two groups. Not only the slopes of end-systolic pressure-volume relationship and preload recruitable stroke work but also their placements did not result in any significant differences between the groups. CONCLUSION: HSD seems to be an effective resuscitation fluid after hemorrhagic shock because the volume required to maintain circulation is smaller than that of normal saline. Our data, however, show that HSD does not enhance cardiac contractility after hemorrhagic shock.

[Cardiac contractile dysfunction in response to surgical stress including trauma, hemorrhage, and infection].

Shock and multiple organ failure are complications of primary conditions such as trauma, hemorrhage and infection. Ample evidence of cardiac contractile dysfunction has been obtained in both septic patients and experimental animal models of endotoxin shock. Recent advance in molecular biology and immunology has improved our understanding of the pathogenesis of septic shock, and thus, it is now believed that the host's inflammatory response to infection contributes to the development of septic shock. In addition, effects of toxic host mediators including cytokines, kinins, eicosanoids, platelet-activating factor, and nitric oxide, which are produced by activated cells, on cardiovascular system have been examined. The possible involvement of the nitric oxide pathway, not only as a marker for cytokine-induced effects on myocyte gene expression, but also as a mediator for cytokine-induced contractile dysfunction, was explored. According to this hypothesis, trauma and hemorrhage, both of which lead to host's inflammatory response, is also considered to induce contractile dysfunction. In this paper we reviewed the influences of various shock states on cardiac contractility. Hemorrhagic and burn shocks possibly depress cardiac contractility as well as septic and endotoxin shocks. Therefore, it is necessary to improve contractile depression in the diseased states to meet oxygen demand of each patient under monitoring patient's circulatory and metabolic conditions.

Non-ischemic myocardial fibrosis after long-term asbestos exposure.

To determine whether or not myocardial fibrosis in the left ventricle increases after exposure to asbestos fiber, we studied myocardial fibrosis in 42 autopsied hearts; 17 of asbestosis (AS) and 18 of chronic pulmonary disease (CP) without pneumoconiosis. Seven patients with extracardiopulmonary disease were used as a control group (CONT). The extent of myocardial fibrosis in the left ventricle was significantly greater in the AS group compared to the other groups (AS 3.6 +/- 1.3% vs. CP 2.4 +/- 1.0% vs. CONT 1.6 +/- 0.8%). There was a significant difference in the appearance ratio of focal fibrosis between the asbestosis group and the other groups. Focal fibrosis was observed in none of 7 control patients, in 3 of 18 patients with chronic pulmonary disease and in 9 of 17 patients with asbestosis. We concluded that characteristic myocardial fibrosis was observed in humans after long-term asbestos exposure.

Effects of hypertonic saline and dextran 70 on cardiac functions after burns.

The effects of hypertonic saline-dextran (HSD) on cardiac contractility and hemodynamics after burns were studied in anesthetized animals with full-thickness 50% total body surface area burns that were resuscitated with HSD or lactated Ringer solution (LR) alone. No significant difference in cardiac contractility during 6 h postburn was observed between the two groups, as assessed by the end-systolic pressure-volume relationship and the stroke work-end-diastolic volume relationship. An additional bolus of HSD at 6 h postburn caused no significant changes in the end-systolic pressure-volume relationship and stroke work-end-diastolic volume relationship in the burned and sham-burned animals, both of which were resuscitated with HSD. Ten minutes of hemodynamic changes following HSD infusion at 30 min postburn revealed a sudden increase in stroke volume with biphasic responses in left ventricular systolic pressure, which first decreased, then increased, and finally returned to the pre-HSD value. End-diastolic volume was maintained at approximately 110% of the pre-HSD value during this period. We concluded that HSD does not enhance cardiac contractility after severe burns but does produce direct effects on postburn circulation to reduce afterload and augment preload, resulting in a short-lived increase in cardiac output.

Myocardial salvage: its assessment and prediction by the analysis of serial myocardial contrast echocardiograms in patients with acute myocardial infarction.

It has been difficult to assess myocardial salvage in patients with coronary reflow because of the lack of appropriate methods of determining the risk area and assessing effects of coronary reflow in patients, myocardial contrast echocardiography was performed in 28 patients with acute myocardial infarction before reperfusion, immediately after reperfusion, and in the chronic stage with the right and left coronary arterial injection of sonicated ioxaglate. Contrast-deficit and contrast-filled areas before reperfusion were defined as the risk area and noninfarct area, respectively. If the ratio of peak subtracted gray level in the risk area to that in the noninfarct area was < 0.4, the risk area was taken as a contrast defect. Contrast defect was observed even after reperfusion in 8 (29%) patients, and the defect was consistently observed in the chronic stage in all of them. Contrast defect disappeared after reperfusion in the other 20 patients but reappeared in 4 (20%) of them in the chronic stage despite the patent infarct-related vessel. Left ventricular function recovery of the risk area in the chronic stage as assessed with regional wall motion and wall thickness was better in the patients without contrast defect after reperfusion than in patients with persistent or reappeared contrast defect. In conclusion, (1) myocardial salvage is improbable in patients with contrast defect immediately after reperfusion, (2) contrast enhancement immediately after reperfusion does not necessarily imply myocardial salvage in the chronic stage, and (3) myocardial echocardiography in the chronic stage may provide clinically useful information about myocardial salvage in patients with myocardial infarction.

[Nontraumatic acute subdural hematoma caused by the rupture of transdural anastomotic vessels in moyamoya disease].

A case of nontraumatic acute subdural hematoma caused by the rupture of transdural anastomotic vessels in a patient with Moyamoya disease is reported. The patient was a 55-year-old woman who was admitted to our hospital in a comatose state. A diagnosis of acute subdural hematoma associated with Moyamoya disease was made on the basis of CT and angiographic findings. No lesions suggestive of trauma, such as cerebral contusion, could be detected during surgery. Although total evacuation of the hematoma was performed, she developed the apallic syndrome and did not recover consciousness. Judging from the angiographic and operative findings, it appears that subarachnoid hemorrhage occurred first and stretched the transdural anastomotic vessels which supplied the collateral circulation. This led to tearing of some of the vessels, and their proximal ends were consequently exposed in the subdural space. The surgical treatment of acute subdural hematoma associated with Moyamoya disease requires the closest attention to avoid damage to the collateral circulation. Although we carefully arrested the bleeding without using a coagulator in order to spare the collateral vessels, the transdural anastomosis was no longer visible on postoperative angiograms. Our experience suggests that hematoma irrigation with trephination therapy, which may minimize the damage to the collateral circulation, may be the most appropriate treatment for acute subdural hematoma associated with Moyamoya disease. Furthermore, cerebral revascularization should be performed for the treatment of the circulatory disturbance intercepted by the hematoma itself or by operative manipulation.

Effect of aggressive haemoperfusion on the clinical course of patients with paraquat poisoning.

The effect of aggressive haemoperfusion; i.e. haemoperfusion of 10 h or more during the first 24 h after ingestion, on the clinical course of paraquat poisoning was studied. Among 40 patients admitted within 15 h after ingestion of paraquat with an SIPP of less than 100 (h x micrograms ml-1), 21 received aggressive haemoperfusion and 19 received conventional haemoperfusion; i.e. haemoperfusion of less than 10 h during the same period. Survival rates of patients with severity between an SIPP of 100 and Proudfoot's curve in the two groups were compared by the log-rank test. Aggressive haemoperfusion did not improve the outcome but did improve the survival rates; that is, the number of patients surviving at particular points in time (P < 0.05). The length of haemoperfusion for the aggressive haemoperfusion group was longer than that for the conventional group on the first day (P < 0.001), but the difference was insignificant during the following two days. Neither the time from ingestion to haemoperfusion, urine volume from the first to third day, nor initial plasma-paraquat concentrations and SIPP were significant between groups. These findings imply that aggressive haemoperfusion reduces the severity of paraquat poisoning and elongates survival time. We, therefore, propose that the efficacy of more aggressive haemoperfusion, such as the 'continuous haemoperfusion' proposed by Okonek et al., should be further studied.