The Certificate of Death or Inquest Report are two of the most important official documents issued by medical doctors. These have been used to compile statistics on the cause of death in Japan and for assessment of life or accident insurance claims, as well as, for erasure from a family register, and permission for burial of the dead. Generally, the Certificate of Death is issued when a patient under a docto's care dies of a disease, typically in a hospital. An Inquest Report is issued for all other cases. When a Certificate of Death is issued to the bereaved, the characters stating Inquest Report printed at top of the form must be crossed out with double lines. In the case of an Inquest Report, the characters stating Certicate of Death must similarly be crossed out. In cases of unsuccessful cardiopulmonary resuscitation of patients in cardiopulmonary arrest, the time of death must be stated, not as the time of confirmation of death, but as the estimated time of death before arrival at a hospital. The immediate disease or injury which caused the death must be written on the upper line of space (1). Any underlying causal disease or injury directly related to the above disease or injury must also be written in the space below, and so on, for each of the spaces in order. The last disease or injury written as the underlying cause of death is recorded as the cause of death in Japanese statistics. When death is due to an external cause, details regarding the external cause must be written in the spaceprovided. For example, in the case of a traffic accident, it is necessary to distinguish whether the deceased was a pedestrian, a cyclist, a driver or a nondriver riding on a motorcycle or in a car.

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Background: Recently, the therapeutic values of moderate hypothermia (MH), (32-33°C), have been reappraised for protection against severe brain injury. MH appears to increase susceptibility to bacterial infection, the control of which is considered to be a key factor for successful use of this technique. We reported previously that the functions of polymorphonuclear cells and monocytes are impaired under MH. In this study we compared pro-inflammatory cytokine release from peripheral blood mono-nuclear cell (PBMC) at 33°C and 37°C. Methods: PBMCs were harvested from 3 healthy adults. TNF-α, IL-1β and IL-6 concentrations were measured at 1, 2, 3, 6, 12, 24 and 48 hours after the stimulation by S. cerevisiae or lipopolysaccharide (LPS) by ELISA, Results: At 3, 6 and 12 hours after S. cerevisiae stimulation, and at 1 and 2 hours after LPS stimulation, TNF-α release was significantly, lower at MH than at 37°C. However, there was no difference in IL-1β and IL-6 concentrations after the S. cerevisiae stimulation at 33°C and 37°C. Conclusion: These data suggest that decreased TNF-α release might play a major role in masking manifestations of an infectious process during hypothermic therapy.

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Purpose: Serial changes in neuronal nitric oxide synthase (nNOS) staining were examined in the acute phase of the injured brain. In addition the effectiveness of hypothermia, which has been used for brain resuscitation, was analyzed. Injured rats were exposed to moderate hypothermia just after insult and nNOS expression was examined. Materials and Methods: Wistar rats (males, 200g, n=44) received a focal brain injury by the weight-drop head injury method. Twenty rats were maintained at room tempareture and 15 were cooled to 32.0∼33.0°C after the injury. Brains were perfused serially from time 0 to 6 hours after the injury and specimens were immunohistologically stained with polyclonal nNOS antibody (Tranduction Laboratories, USA). Results: Many nNOS-positive neurons were observed in the injured hemisphere, especially in the caudate putamen and the cortex near the injured surface, and were evident for more than 6 hours in the normal temperature group. Some positive neurons were seen in other parts of the brain including the contralateral hemisphere. In the hypothermic group, only a few neurons stained positive with nNOS antibody for up to 2 hours after the injury, but then positive neurons gradually disappeared. Sham rats chilled to 32.0∼33.0°C (n=9) had few positive neurons in the 6-hour study period. Discussion: NO produced in the brain has several functions related to vasodilation, increased permability of vessels and neurotoxicity. nNOS expression increased with the focal brain injury, and this was suppressed by moderate hypothermia. Further study is needed to determine what regulates the long term expression of nNOS. Conclusions: We conclude from this immunohistological study that moderate hypothermia reduces the induction of nNOS production in the injured brain.

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The outcomes of pre-hospital cardiac arrests were examined according to the “Utstein style” in the emergency medical system of northern Osaka prefecture (a 340km² area with a population of 1, 680, 000). The task force consisted of doctors from three medical centers and paramedics from seven dispatch centers situated in the area. A population based and prospective report from out-of-hospital cardiac arrest cases was conducted in cooperation with other hospitals located in this area. The number of resuscitation cases was determined among 784 cardiac arrests during a one year period (Nov. 1996∼Oct. 1997). This number is equivalent to 46.8 cases per 100, 000 population per year. Resuscitation was attempted in 615 of the 784 cases (36.7 attempts per 100, 000 population per year). Cardiac arrest due to cardiac etiology occurred in 308 patients, while 307 cases had a non-cardiac etiology. Cardiac arrests were witnessed byby standers in an estimated 112 of the 308 cardiac etiology cases. The number of cases witnessed by emergency personnel was estimated to be 23. Of the 308 cases, 201 achieved a return of spontaneous circulation, and 163 were admitted to hospital. Although 8 cases survived without any deficits, only one of the 308 cases was recognized as a survivor with full recovery.

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A 68-year-old man who had suffered from interferon encephalopathy was admitted to our hospital due to cardiopulmonary arrest (CPA) resulting from suffocation. Immediately after recovery of spontaneous circulation, a head CT demonstrated no causative lesions in the brain. On the fifth hospital day during hypothermic cerebral resuscitation, the patient manifested dilated fixed pupils. The second head CT revealed marked brain swelling and high density regions on the falx, tent and subarachnoid space. He died on the seventh hospital day, when an autopsy showed an absence of subarachnoid hemorrhage and vascular thrombosis. We discuss here the me chanism of a high density region on the head CT after whole-brain ischemia and emphasize the importance of a head CT examination for CPA patients to evaluate the situation.

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This is a case report of a 22-year-old female whose tracheomalacia, caused by the long term respiratory management with cuffed tubes, was successfully treated with a Dumon stent. The patient was injured in a fall accident and suffered from severe cerebral contusion. She was intubated on admission and underwent tracheostomy on the 4th hospital day. Although we succeeded in treating her head injury, she suddenly became asphyxiated due to granulomas of the trachea where we concluded that the tip of the tracheostomy tube had scraped occasionally. We removed the tracheostomy tube and had to manage her under nasal tracheal intubation. Endoscopic examinations 30 days after re-intubation revealed a near-complete obstruction of the trachea during expiration located approximately 3-4cm above the carina. Endoscopic findings showed a typical crescent type tracheomalacia. Her trachea easily collapsed when the tracheal tube was withdrawn beyond the lesion. A Dumon stent was inserted into the collapsed lesion to avoid asphyxia. This airway management succeeded in preventing her airway collapse and she has been asymptomatic for 6 months. Judging from the lesion, tracheomalacia in this case seems to be associated with the long term management with an inflated cuff of a tracheal tube. The application of a Dumon stent to a focal tracheomalacia provides sufficient relief from airway collapse without the need for operative intervention.

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This paper reports a case of systemic emphysema associated with the use of the Esophageal-tracheal Combitube (ETC) during pre-hospital management of cardiac arrest. A 53-year-old female lost consciousness after serious hematemesis. Cardiopulmonary resuscitation was started and the ETC was inserted by emergency life saving technicians. About 55 minutes after arrival at the emergency room, the patient was declared dead. Computed tomography demonstrated the presence of air in the subcutaneous tissues, mediastinum, thorax, abdomen, hepatic vein, inferior vena cava and right ventricle. An autopsy was not performed, and the source of air leak could not be identified. However, computed tomography revealed that tracheal laceration had caused the air leak to the surrounding tissues. The systemic emphysema and tracheal laceration would not be main factors in the death of the patient presented here. However, the possibility of these complications should be kept in mind.

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Impaired glucose tolerance is a well-known complication of acute pancreatitis. However, transition from acute pancreatitis to insulin-dependent diabetes mellitus (IDDM) is rare. Recently we encountered a case of IDDM due to diabetic ketoacidosis (DKA) subsequent to acute pancreatitis. We report the present case and also discuss several studies on this pathological condition. The patient was a 38-year-old woman who visited a nearby hospital with high fever and epigastric pain. Hematological and X-ray examinations indicated that the patient was suffering from acute pancreatitis. On the sixth hospital day, she was transferred to this hospital due to hyperglycemia, consciousness disorder and metabolic acidosis. Insulin therapy and continuous hemodialysis were effective in the improvement of these symptoms. However, insulin therapy was necessary after the amelioration of the pancreatitis. Although the patient has a family history of diabetes mellitus, she has no past history of this disease and her HbAlc level was within the normal range. Furthermore, her blood glucose level was normal at the onset of the pancreatitis. A diagnosis of IDDM was made because the blood and urinary C-peptide levels measured at the onset of DKA were low, and the β cell functions were suppressed.

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