No to hattatsu. Brain and development
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In the management of severe pediatric brain injury, attention has previously been paid to brain edema, ICP elevation and low cerebral perfusion pressure (CPP). However, in the acute stage within 3-6 hours after trauma, brain hypoxia and hyperglycemia associated with diffuse brain injury are often observed. We have pointed out brain thermo-pooling (elevation of brain tissue temperature) and brain hypoxia caused by defective release of oxygen from hemoglobin (due to decrease in red blood cell enzyme (DPG)) as a new mechanism of brain injury. ⋯ Another problem is immune crisis associated with secondary pulmonary infections. To prevent them, early enteral nutrition and replacement of L-arginine were most useful, as well as preconditioning for rewarming as follows: serum albumin > 3.0 g/dl; lymphocyte > 1500/mm3; T-H (CD4) lymphocytes > 55%; serum glucose, 120-140 mg/dl; vitamin A > 50 mg/dl; Hb > 12 g/dl and 2,3 DPG, 10-15 mumol/gHb; O2 ER, 23-25% and AT-III, > 100%. The clinical benefit of this therapy is still controversial.
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Trauma victims are directly transferred to a level I trauma center bypassing local hospitals. First, airways and cervical stability are secured. Intracranial hematoma should be promptly evacuated. ⋯ The goal of intracranial pressure (ICP) management is to maintain the ICP at less than 15 mmHg and to maintain minimum cerebral perfusion pressure at 45-55 mmHg. External ventricular drainage provides direct control of the ICP by allowing intermittent drainage of the CSF (5-10 ml/hour). Mannitol is effective but hyperventilation is not recommended.