To assess the clinical value of a new fatty acid imaging tracer, ¹²³I-β-methyl iodophenyl pentadecanoic acid (BMIPP), I-BMIPP and thallium-201 (Tl) dual imaging was performed at rest in fifteen patients with mild blunt chest trauma (mean AIS thoracic 1.4±0.51, mean ISS 6.47±3.50, mean RTS 7.69±0.43). All patients were prospectively evaluated on the basis of serial electrocardiograms (ECG) and cardiac enzyme studies (total CPK). Tl and BMIPP dual scintigrams were performed within 10 days following admission. SPECT images were divided into seven segments, and the segmental images were visually scored according to tracer uptake on a 3 (severely decreased tracer uptake) to 0 (normal) scale. Nine patients had scintigraphic defects and were considered to have a myocardial contusion. ECG findings, AIS, ISS, and CPK lesvels failed to distinguish between scintigraphically positive patients and scintigraphically negative patients. Five of the 14 hypoperfused segments on BMIPP imaging, showed normal Tl uptake, one showed lower BMIPP uptake than Tl, and the remaining eight showed similar distribution of both tracers. The mismatch between tracer uptake on BMIPP images and Tl images was thought to reflect impaired myocardial fatty acid metabolism. Thus, mild blunt chest trauma results in a higher frequency of traumatic myocardial injury than previously recognized, and BMIPP is a promising radio-pharmaceutical for evaluating impaired myocardial fatty acid metabolism in patients with myocardial contusion.

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To assess the factors related to respiratory complications in patients with cervical spinal cord injury, we retrospectively studied the 43 patients (40 male, 3 female, mean age: 43 years) with complete quadriplegia after cervical spinal cord injury to characterize those who required respiratory management for more than 2 weeks during their hospital stay. All patients had middle or low cervical (C4-C8) myelopathy, and 6 patients had suffered C4 spinal cord segment injuries. Head injuries (8 cases), thoracic injuries (6 cases) and circulatory shock (12 cases) were also observed in these patients. Emergency spinal surgery was performed in 20 cases, and elective surgery was performed in 12 cases. In 41 patients the paralysis as at the time of injury and 2 patients there was temporary impairment of the lowest normally functioning spinal cord segment after surgery. Eleven (26%) of the 43 patients required long-term artificial ventilation (more than 2 weeks) via tracheotomy. They included 7 patients who underwent spinal surgery and 4 patients who did not. The reasons for the long-term artificial ventilation were: lobar atelectasis (4 cases), hypercapia (4 cases), pneumonia (2 cases), pneumohemothorax (2 cases), pulmonary edema (1 case), and cardiac arrest due to asphyxia caused by sputum (1 case). There were patients with thoracic injury in the long-term ventilation group than in the non-respiratory management group, and based onstep wise multiple regression analysis thoracic injury was the only contributor factor (F value; 6.9) related to artificial ventilation. We conclude that the presence of combined injuries, such as thoracic injury, should be considered as an aggravating factor during long-term respiratory management of patients with complete quadriplegia after middle or low cervical spinal cord injury.

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The arterial ketone body ratio (AKBR) has been employed as a specific indicator of the hepatic mitochondrial redox state, mainly in the field of liver surgery, and recently in the field of critical care medicine as well. In the present study, we investigated both AKBR and total ketone body concentration (KBC) in patients undergoing laparotomy, and evaluated the significance of these values in assessing metabolic function in such patients and in their perioperative care. Thirty-one patients were assessed, and their arterial blood was sampled preoperatively, intraoperatively, and immediately postoperatively. On the whole, the AKBR, decreased during laparotomy and returned to within the normal range immediately after the operation, but in patients in the non-survival group it remained around the critical value. A positive correlation was found between AKBR and base excess immediately postoperatively (r=0.38, p<0.05). The 31 patients were divided into 2 groups: 11 with liver cirrhosis (LC group) and 20 without liver cirrhosis (non-LC group). Patients with preoperative shock in both groups had significantly lower AKBRs, both intra- and postoperatively, than patients without shock. In the LC group, the patients with preoperative shock had higher KBC values than those without shock. In the non-LC group, however, no difference in KBC was detected according to whether the patients experienced preoperative shock. These results suggest the following: 1) When patients have preoperative shock, hepatic mitochondrial function is impaired more severely, and consequently ketogenesis increased more significantly in the LC group than in the non-LC group. 2) In patients free of shock, AKBR remained around the normal range in both groups, and ketogenesis as a metabolic response to impairment was increased in the non-LC group, but remained unchanged or depressed in the LC group. We conclude that the combination of AKBR and KBC is useful in assessing metabolic function in patients undergoing laparotomy and enabling treatment of patients in critical condition.

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The purpose of this study was to determine the changes in oxypurine level and the energy status in rat brain after a lateral fluid-percussion injury which was made by a moderate impact of 4.8-5.6atm from a fluid-percussion device using the University of California, San Francisco, method. The amounts of adenine nucleotide and oxypurines were determined by high-performance liquid chromatography in a rat brain extract obtained at 5, 15, 30 and 60min after the impact. Energy charge and total adenine nucleotide (TAN) were calculated by the following formulae: energy charge=ATP+0.5ADP/ATP+ADP+AMP
TAN=ATP+ADP+AMP
No significant difference between the groups was observed with respect to energy charge and TAN. However, hypoxanthine and xanthine were detected through 30min after fluid-percussion impact, whereas negligible amounts of these compounds were detected in the control (sham) group.

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Four cases of intracranial foreign bodies are reported. The first patient was a 58-year-old male who drove nine nails into his head while drunk. On admission the patient was drowsy, and a plain skull film revealed the nails to be embedded intracranially on both sides of the frontal and temporal regions. Carotid angiography showed no vascular injury. The second patient was a 44-year-old male. The patient had fallen from the third floor of a building under construction, to the ground and a steel rod on the ground had pierced his face. On admission the patient was semi-comatose. The rod had penetrated from the right maxilla to the ipsilateral parietal vertex. The third patient was a 9-year-old boy. He had a fallen while running and his left upper orbit had been penetrated by a wooden chopstick which he had been holding in his hand. On admission the patient wasdrowsy. His left eye was intact but blind, extraocular movement was completely impaired, and there was no sensation in the left upper quadrant of the face. Computed tomography (CT) revealed a fragment of the chopstick extending from the orbit to the middle and posterior cranial fossa through the superior orbital fissure. Carotid and vertebral angiography showed no vascular abnormalities. The fourth patient was a 48-year old male. His head had been penetrated by a nail in a nail-gun accident. On admisson he was fully alert and had no neurological deficits. Only head of the nail was seen beside the occipital midline. CT showed that the tip of the nail was located in the right cerebellar hemisphere and vertebral angiography revealed the nail piercing the right transverse sinus. In all four cases, the foreign bodies were removed by the “open and see” policy. After craniotomy and intradural exploration, the foreign bodies were removed from the injured brain and penetrated major dural sinuses under visual control. The second patient, who had been seriously injured, died of encephalo-meningitis. Good recovery was obtained in the other three cases.

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A 37-year-old pregnant woman at 35 weeks gestation was admitted to the OB-GYN service because of fever and sore throat. During hospitalization, she underwent artificial abortion because of fetal death. Since renal failure developed in addition to fever and sore throat, she was transferred to our hospital. After she receiving parenteral fluids and diuretics, her renal failure improved. Seizures and unconsciousness developed, however, in spite of improvement of renal function. Blood chemistry data showed that the serum calcium and magnesium values decreased to 2.6mEq/l and 1.2mg/dl respectively. The serum calcium did not return to normal even after administration calcium gluconate and magnesium supplementation (MgSO₄; Mg 480mg/day) was initiated which resulted in cessation of seizure activity and return of lucidity. This report emphasizes the role of hypomagnesemia in causing seizures and disturbance of consciousness during pregnancy.

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We report a case of glufosinate poisoning containing metabolic alkalosis in a 63-year-old female patient. The patient had ingested 200ml of Basta^®, 18g of glufosinate, in an attempted suicide. Two and a half hours later, she underwent gastric lavage at another hospital, and was then transferred to our hospital. On admission, the patient was alert and her vital signs were stable. She was treated by forced diuresis and carefully observed. Ten hours after ingestion, she became apneic and lost consciousness and mechanical ventilation was started immediately. Repeated generalized convulsions occurred and were treated with diazepam and midazolam. The next day, the patient developed metabolic alkalosis which progressed to pH 7.745, PCO₂ 27.5mmHg, HCO₃^- 38.2mEq/l, and BE 19.1mEq/l. Acetazolamide i.v. and KCl infusion corrected the electrolyte and acid-base in balances, and the patient was discharged after 13 days of hospitalization. No loss of gastric juice, dehydration, or respiratory acidosis was observed in this patient, and forced diuresis had been stopped 8 hours before the onset of the metabolic alkalosis. Therefore, we hypothesize that the glufosinate itself induced the metabolic alkalosis by a mechanism involving impairment of renal acid-base equilibrium. Metabolic alkalosis should be kept in mind as a possible complication by glufosinate poisoning.

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