In the field of emergency medicine, it is not rare for patients to suffer brain death despite aggressive measures. With the establishment of the Organ Transplant Law in 1997, donations of organs such as heart, lungs, liver, pancreas, and small intestine from brain-dead patients became possible. However, as of today, organ donation remains rare, despite the large numbers of patients who await organ transplantation. Donation requires a family offer or an approach to a family about organ donation options by those caring for the patient. But, even if the patient expresses an interest in organ donation, the wills of the patient or the family cannot be honored unless the critical care physician approaches the family about organ donation options. During the period from January 2004 to November 2005, 13 patients who suffered from severe brain damage survived for 24 hours or more after admission to the ICU, and were evaluated for clinical brain death. Then we approached the families of all 13 patients about organ donation options, the families of 12 patients expressed an interest in organ donation, and the families of 9 patients met with a donor coordinator. The families of all 9 patients agreed to donate organs and tissues, resulting in organ and tissue donations involving 17 kidneys, 1 pancreas (simultaneous donation of pancreas and kidney), 4 heart valves/aorta, 12 eyes, and 4 skin donations. At the terminal stages of critical care, there is a high degree of interest in organ donation among families of brain-dead patients, and blood relatives especially tended to agree to organ donation. Through the involvement of a donor coordinator, donations of organs and tissues were achieved for about 70% of the patients. It is concluded that critical care physicians and neurosurgeons approaching families about organ donation options can lead to increases in organ donations.

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Clinical analysis was conducted for 26 patients who were transferred and admitted for emergency treatment of anaphylaxis in a secondary healthcare setting in Toho University Omori Medical Center during the two years between September 2003 and August 2005. Possible triggering factors for anaphylaxis were foods in 12 patients, drugs in 11 patients, and other factors (bee sting and rat and hamster bites) in three patients. The foods included fish for seven patients; meat, soba or buckwheat noodles, and citrus fruits for one patient each; and other foods for two patients. Five of the patients tested had positive results for a specific radioallergosorbent test (RAST). Drugs were all oral agents including non-steroidal anti-inflammatory drugs (NSAID) in eight patients and antibiotics in three patients. The results from a drug lymphocyte stimulation test (DLST) were positive for only two of the patients. All patients experienced cutaneous and respiratory symptoms. Seven patients experienced symptoms of disturbance of consciousness, and nine patients experienced symptoms of shock, either drug-induced (five patients) or food-induced (four patients). No significant difference was observed between the two groups. Nineteen of the 26 patients had a history of allergies. Although the rate is significantly higher than the general population, the patients experiencing symptoms of shock included three cases of drug-induced shock without a history of allergies. This reaffirms the importance of paying special attention to drug-induced anaphylactoid reactions that may cause sudden symptoms of shock in a patient without a history of allergies. Thirteen patients were treated with epinephrine (0.5±0.4mg) and 24 patients with corticosteroids. The outcome was good for all patients, and no biphasic anaphylaxis was observed. Although corticosteroids are not a first-line agent, they may play a role in the prevention of biphasic anaphylaxis.

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This is a case of reversible posterior leukoencephalopathy syndrome that was caused by malignant hypertension. A 47-year-old man was admitted to our hospital because of somnolence. He had no neurological focal signs except anisocoria on admission. His blood pressure was 260/170mmHg, and he had bilateral retinal hemorrhage. Plain brain computed tomography (CT) and flair magnetic resonance imaging (MRI) on admission showed diffuse edema in the white matter of bilateral parieto-occipital lesion. By contrast, no abnormalities were found on diffusion weighted MRI. He was diagnosed as hypertensive encephalopathy, and treated with vasodilating agents. He became alert two weeks after admission, and the abnormal findings on CT and MRI disappeared two months after admission. The biopsy findings of the kidney showed proliferative arteriosclerosis compatible with malignant hypertension. Thus, we concluded that he developed a reversible posterior leukoencephalopathy due to malignant hypertension. Combilation of diffusion weighted MRI and Flair MRI could make it possible to distinguish cytotoxic edema from vasogenic edema. Vasogenic edema is reversible and has good prognosis. Diffusion weighted MRI on admission may help early diagnosis of vasogenic edema, and be useful for decision making in an emergency department.

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