To resuscitate extensively burned patients, we have developed a computer-controlled fluid resuscitation (CCFR) system based on the output of urine. The CCFR system consists of an urinemeter, a personal computer and a pair of infusion pumps. This system administers fluid at a rate of infusion calculated by Baxter's formula, and regulates the infusion rate to maintain an adequate urine output. Data are displayed, printed and stored on floppy disk for subsequent analysis. Six extensively burned patients between 32 and 77 years old (average 49.3 years old) were managed with the CCFR system during their initial period of resuscitation. The estimated body surface area burned was 63.5±17.9 (mean±standard deviation)%. The urine output during CCFR was 0.99±0.17ml/kg/hr. The volume infused during the first 24 hours after the burn was 4.04±1.02ml/kg/% burned area. All patients were adequately resuscitated. Detailed data concerning fluid resuscitation were obtained during CCFR therapy. The results suggest that CCFR should be used in the fluid resuscitation of extensively burned patients.

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A 62-year-old woman who had undergone a hemodialysis for chronic renal failure was admitted for unconciousness. A brain CT showed left cerebral infarction. On her 8th hospital day, she suddenly developed a progressive congestive heart failure. An echocardiogram revealed an aortic valve vegetation and blood culture grew methicillin-resistant Staphylococcus aureus (MRSA), confirming the diagnosis of Infective endocarditis. On the 15th day, the patient died of acute heart failure. At autopsy the aortic valve showed a perforation 0.8cm in diameter. It is difficult to treat endocarditis in patients on chronic hemodialysis since such patients have altered host defenses and suppressed immune systems. Vascular access sites are the common source of infections leading to endocarditis and sepsis. Hemodialyzed patients with endocarditis generally fail to respond to medical therapy alone. Once congestive heart failure has occurred due to perforation of a valve leaflet, prompt cardiac valve replacement should be performed at an early stage.

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We report a case of rhabdomyolysis complicated by acute renal failure caused by loss of consciousness after drinking. A 46-year-old man fell asleep in his living room after drinking beer and whisky. Showing no signs of awakening by 10 a.m. the next morning, he was transferred to our emergency center. On admission his consciousness level was II-30 (Japan coma scale), and his temperature was 31.1°C. Laboratory data showed hypoglycemia; mixed acidosis; and elevation of CPK, GOT and LDH. The serum ethanol concentration was 221mg/dl. At the midnight on the first hospital day, swelling of the right hip area develope and it declined to be growing. The patient's consciousness gradually returned, however, he remained oliguric despite treatment with fluid challenge and diuretics. A diagnosis of rhabdomyolysis complicated by acute renal failure was made, and hemodialysis was performed. A triacetate membrane was selected as the dialyzer in order to eliminate serum myoglobin. The acute renal failure improved after hemodialysis 20 times in 38 days. The cause of the rhabdomyolysis is believed to have been pressure necrosis due to immobility for many hours in addition to muscle damage caused by ethanol. Hemodialysis with a triacetate membrane was useful in eliminating myoglobin in acute renal failure caused by rhabdomyolysis.

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This is a report of a 31-year-old male with a ruptured aneurysm of the anterior pancreaticoduodenal artery. The patient developed a sudden upper abdominal pain and consulted us when it became intolerable. No muscular defense or rebound tenderness was present at initial examination. Leucocytosis and mild liver dysfunction were the only abnormal findings on admission. Anemia developed on the second day, which suggested intraperitoneal hemorrhage. CT scans showed a periduodenal hematoma, stenosis of the duodenum and an intraperitoneal hematoma. Celiac angiography showed extravasation from an anterior pancreaticoduodenal artery aneurysm (8mm in diameter). Emergency operation was performed consisting of evacuation of the doudenal intramural, retroperitoneal and intraperitoneal hematomas, resection of the aneurysm and ligation of the gastroduodenal artery. The volume of bleeding was estimated to be 2, 700cc. The postoperative course was uneventful. According to the literature, the prognosis of this disease is poor. If a suitable operation is performed with a precise diagnosis based on CT scanning and angiography, the prognosis can be improved. In dealing with patients who have an acute abdomen with shock, rupture of an aneurysm of the pancreaticoduodenal artery should be considered.

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A case of primary small bowel volvulus presenting with diffuse peritonitis is reported. A 10-year-old female was admitted to our hospital complaining of abdominal pain. On admission muscular guarding and the Blumberg sign were noted in the abdomen. An abdominal X-ray film showed a small bowel gas shadow without a level. Abdominal CT was performed and showed multiple distended small bowel loops with their edematous mesenteric folds converging toward the point of torsion and thickening of the bowel wall. These findings suggested volvulus of the small intestine, and emergency surgery was performed. On laparotomy, massive small bowel necrosis was observed and the root of the mesentery of the small intestine was twisted clockwise approximately 360°. Resection of the necrotic small intestine was performed and the length of the surviving intestine was 2.5m. We made a diagnosis of primary small bowel volvulus because no bands or adhesions were observed in the abdominal cavity. The patient's postoperative course was uneventful, and the patient was discharged on the 22nd day. Primary small bowel volvulus is rare, and diagnosis is very difficult. This case report suggests that CT findings are useful in the diagnosis of primary small bowel volvulus.

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A case of persistent carotid-vertebral anastomosis with occlusion of the right internal carotid artery is reported. This 68-year-old man was admitted to our hospital with left hemiparesis. Physical examination findings on admission were within normal range except for the hemiparesis and his blood pressure was 114 over 70mmHg. Right carotid angiogram revealed an occlusion of the right internal carotid artery and an abnormal vessel connecting the right external carotid artery and right vertebral artery. The vertebral arteries were hypoplastic bilaterally. Thereafter, the patient was transferred to the rehabilitation center and spent 134 days in the hospital. This “abnormal vessel” arises from the right occipital artery which branches from the right external carotid artery at the level between the 2nd and the 3rd vertebrae. It then curves slightly superiorly and joins the third portion of the right vertebral artery. This anastomotic vessel was thought to be “proatlantal artery II” in accordance with Lasjaunias et al. or a “persistent primitive first cervical intersegmental artery” in accordance with Padget. To our knowledge, this is only the 19th case of persistent carotid-vertebral anastomosis reported in the literature.

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After intravenous use and ingestion of approximately 0.05g methamphetamine, an 18-year-old girl was admitted to our emergency room in a state of delirium with a temperature above 41°C. Rhabdomyolysis with myoglobinuria was diagnosed. On the second day, although she had nearly regained full alertness, she developed disseminated intravascular coagulation. On the third day, she became somnolent and delirious again with remarkable elevations in total birilubin, transaminase and other hepatic enzymes. A biopsy of the liver was performed on the 6th hospital day. Microscopically, submassive hepatic cell necrosis was found around the central veins which was accompanied by sparse inflammatory cell infiltration. On the 20th day she was substantially recovered and her hepatic functions had improved. She was transferred from the ICU to the ward. On the 82nd hospital day liver biopsy revealed good regeneration of hepatic cells. The above described hepatic dysfunction and submassive hepatic cell necrosis are considered to be attributable to three primary causes; viral hepatitis, methamphetamine induced allergic hepatitis or direct liver damage by hyperthermia. We were able to rule out viral hepatitis because of her clinical course, viral studies and pathological findings but differentiating between allergic hepatitis and direct hepatotoxicity was not possible with the clinical and laboratory data available in this case.

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