A secondary hypoxic brain injury is one of the most important determinants of a neurological outcome after a head injury. In the absence of a specific therapy to normalize cerebral blood flow (CBF), some advocators decided that one approach toward preventing cerebral ischemia was to monitor and maintain the cerebral perfusion pressure (CPP). To date, there is no evidence to support which level of CPP is needed to keep an adequate CBF in the management of severe head injuries. Furthermore, some studies suggested that side effects like acute respiratory distress syndrome (ARDS) or a respiratory complication with intentional CPP management therapy affected the patient's outcome. To examine the relationship between CPP and CBF, we analyzed CBF using the Kety-Schmidt N₂O technique, and studied the patient's outcome and respiratory complications. We studied forty patients with severe head injuries (Glasgow Coma Scale<8), who were treated at the Musashino Red Cross Hospital between years 1999 to 2001. We divided the patients into the “high-CPP group (group-H), ” in which CPP was kept above 70mmHg as a threshold of CBF, and the “low-CPP group (group-L), ” in which CPP was kept from 50 to 70mmHg. We analyzed the patients' CBFs and their outcomes, and examined their cardiac indices (CI) and pulmonary arterial diastoric pressures with a thermo-dilution catheter. We also calculated the patients' cerebral vascular resistances (CVR) and compared the results in the two groups. There was no statistical significance concerning CBF, neurological outcomes, pulmonary hemodynamics, or the existence rate of pulmonary complications. The mean CVR in group-H was higher than that of group-L, and we considered that the CBF would be affected by both CVR and CPP. We concluded that the threshold of CPP at 70mmHg is not always appropriate for patients. CPP is affected by certain factors, such as the degree of pressure autoregulation. We should consider both CPP and CVR in the treatments of head injury patients. CPP management is one of the optional therapies that should be chosen with sufficient consideration.

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A case report of histamine (Scombrotoxin) poisoning is presented. Five to ninety minutes after eating cooked swordfish, 30 persons reported feverishness, diarrhea, palpitations, headache, nausea, dyspnea, generalized urticaria, angioedema, and shock. Of these, 13 persons were admitted to Saint Luke's International Hospital. The patients were given intravenous hydration, IV Hl-blocker, and subcutaneous epinephrine as needed. However, 4 patients required continuous administration of epinephrine intravenously for resolution of the anaphylactic shock. These patients required observation in our intensive care unit. On the following day, all the patients were well and ready for discharge from the hospital. There were no symptoms at the time of discharge. Quantitative determination of the plasma concentration of histamine at the time of admission revealed a value of 0.85-43.10ng/ml. Some pieces of the offending tuna were sent for analysis, and 670mg histamine per 100g of the fresh tuna and 750mg histamine per 100g of the cooked tuna were detected. Generally speaking, histamine poisoning is associated with only mild allergic symptoms. However, in this case, some people developed shock and required close observation. This experience suggests that histamine poisoning can be associated with an outbreak of anaphylactic shock and serves as a cautionary example for emergency medical staff.

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