It is known that moderate cerebral hypothermia produces excellent neuronal recovery in patients with severe brain injury, but the high incidence of severe systemic infections, DIC and ARDS is a major problem with this treatment. This paper shows how pituitary hypofunction induced by hypothermia leads to an immune crisis. The limited activation of lymphocytes and T-cells with lower growth hormone plays an important role in the occurrence of this immune crisis. The prevention of cerebral ischemia by delivering enough oxygen to maintain the O₂ER at 2-23% and CPP>80mmHg was much more important than ICP management within 15-24 hours of surgery. The major mechanisms of neuroprotection by cerebral hypothermia were the prevention of cortical synaptic excitation, NO-induced radicals, brain swelling and synaptic injury of the dopamine nervous system. Based on these findings, a novel treatment using prolonged cerebral hypothermia was developed. The pharmacological activation of dopamine synapses and replacement of LH after prolonged cerebral hypothermia were very useful in neuronal recovery even in patients in a vegetative state. Clinical results were excellent. Resurts in patients rated 3-6 on the Glasgow coma scale (GCS) were as follows: good recovery (n=35 or 47%), mild disability (n=12 or 16%), severe disability (n=4 or 5%), vegetates state (n=5 or 7%) and death (n=19 or 25%). The low incidences of severe disability and vegetative state are especially worthy of attention.

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Numerous processes that contribute to neuronal death after brain ischemia/hypoxia have been identified. Among these processes, high concentrations of excitotoxic neurotransmitters, in particular glutamate, and accumulation of intracellular Ca²⁺ appear to be major factors. Recently, it has been demonstrated that mild hypothermia (32∼34°C) suppresses these ischemia-induced events, and protects the brain against ischemic/hypoxic injury. In the present article, the use of mild hypothermia in clinical practice, including our own experience and the United States' experience in head injury, is reviewed.
Indications for mild hypothermic therapy include head injury, cerebral infarction, vasospasm following subarachnoid hemorrhage, and ischemic injury associated with cardiopulmonary arrest. Our institution's protocol requires initiation of hypothermia within six hours after the ischemic insult. Maintenance of intravascular volume and peripheral vasodilation must be accomplished before the start of cooling. The target core body temperature is 32∼34°C and the duration is 2 to 10 days, depending upon the cerebral pathophysiology. Temperature reduction is accomplished by body surface cooling, chilled intravenous fluids, and cold gastric lavage. Brain oriented neuro-intensive care is necessary and specific neuromonitoring, such as internal jugular bulb blood temperature and oxygen saturation is useful. Blood and cerebrospinal fluid biochemistry analysis is performed. The timing of rewarming is based on computed tomographic determination of intracranial pressure. Rewarming may be accomplished over several days. Core body temperature in excess of 37°C is carefully avoided. The adverse effects of the mild hypothermia therapy have included cardiac arrhythmias, hypokalemia, hyperglycemia, coagulopathy and immuno-suppression. The management approaches to these adverse effects are described.
In conclusion, mild hypothermia appears to be effective for brain protection resuscitation. Safe and standardized methods for the clinical application of mild hypothermia have been well defined. However, the technique should be applied carefully and, for the immediate future, in conjunction with informed consent.

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It is difficult to manage unstable circulation and prolonged respiratory failure related to SIRS (systemic inflammatory response syndrome) induced by surgical stress after radical esophageal surgery.
Glucocorticoid (methylprednisolone 10mg·kg^-1) was administered to patients immediately after radical esophageal surgery to control excessive reactions induced by surgical stress. The efficacy of glucocorticoid in the steroid group (N=8) and the control group (N=12, no treatment) was compared.
Plasma cytokine (interleukin-6 and 8) levels in the steroid group were significantly lower than those in the control group on the first postoperative day. Half as much fresh frozen plasma was needed to maintein total plasma protein and urine volume in the steroid group over 7 postoperative days. The intubation period of patients in the steroid group was significantly shorter than in the control group. Adverse effects of steroids such as abnormalities in glucose tolerance, infection, or delay in wound healing did not appear.
These results suggest that single postoperative administration of glucocorticoid can prevent excessive release of cytokines induced by surgical stress and can reduce the loss of plasma to the interstitial spaces caused by the hyperpermeability of the systemic capillary vessels.
Glucocorticoid did not shorten the length of admission, but decreased the amount of fresh frozen plasma transfusion, shortened intubation periods, and was very useful for postoperative management in patients with radical esophageal surgery.

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A 16-year-old female who had taken approximately 1g of colchicine developed severe colchicine intoxication that progressed to multiple organ dysfunction syndrome. Three hours post ingestion abdominal pain and numbness of the extremities occurred. During the several hours before seeking medical attention these symptoms worsened progressively, and she was referred to the emergency room of our institution 32 hours post ingestion. Laboratory studies revealed hypoxia, metabolic acidosis, multiple organ dysfunction, and disseminated intravascular coagulation. The patient was transferred to the intensive care unit (ICU) and administered dopamine. Eight hours later, continuous hemodiafiltration was performed due to oliguria. Twenty six hours after admission to the ICU, the patient experienced sudden-onset convulsion and circulatory collapse; cardiac arrest occurred after 28 hours in the ICU. Cardiopulmonary resuscitation for 3 hours did not result in the recovery of spontaneous circulation. The symptoms of colchicine overdose are severe, and treatment is extremely difficult, as illustrated by the case described here.

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Prolonged paralysis of 7 days in a patient who received 360mg of vecuronium infused continuously for 114 hours is reported.
A 63-year old male patient who had no evidence of neurological disorder entered the ICU after cardiac surgery. After cessation of continuous infusion of vecuronium, maximum levels of serum vecuronium and its metabolite, 3-hydroxyvecuronium, were 53.1 and 142.4ng·ml^-1 respectively.
This suggests that the reason for the prolonged paralysis was the protracted period required metabolize and eliminate the vecuronium and its metabolite due to drug-induced liver dysfunction. Hypoproteinemia and the drugs used to treat it (antibiotics, Ca-channel blockers and diuretics) seemed to enhance the paralysis. We recommend the use of a peripheral nerve stimulator when the use of a muscle relaxant is necessary in a critical case setting.

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A 38-year-old female was transfered to our hospital due to hypotension. Echocardiography revealed diffuse severe hypokinesis. Circulatory support with intraaortic balloon pumping (IABP) and percutaneous cardiopulmonary support (PCPS) was initiated for fulminant myocarditis. Severe hypokinesis continued and motion of the valves was not recognized. PCPS was continued for 340 hours, IABP for 415 hours, artificial ventilation for 30 days, and continuous hemodiafiltration for acute renal failure for 40 days. The wall motion of the heart recovered completely as did renal function. The patient was discharged on the 189th day without neurologically consequences. Circulatory support was carried out safely and effectively in a patient with severe hypokinetic heart due to fulminant myocarditis.

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An 18-year-old female was admitted to our ICU for dyspnea. She had bloody sputum, hypoxia and hypoproteinemia with proteinuria. Massive doses of methylprednisolone (750mg·day^-1) were administered for 3 days. She recovered temporarily. Renal biopsy revealed crescentic glomerulonephritis and transbronchial lung biopsy revealed alveolar hemorrhage. The examination of autoantibodies was positive for perinuclear antineutrophil cytoplasmic autoantibodies (P-ANCA). Pulmonary and renal function deteriorated gradually despite the administration of prednisolone (60mg·day^-1). Plasma exchange and hemodialysis were performed and massive doses of methylprednisolone (1g·day^-1) were administered for 3 days. Pulmonary function recovered, but it was necessary to continue hemodialysis. Pulmonary function deteriorated again one month later. P-ANCA tested negative after plasma absorption, but pulmonary function grew worse as abnormalities in blood coagulation progressed. The patient died from hemorrhagic cerebral infarction. We believe this was a case of Wegener's vasculitis with P-ANCA. We administered of massive doses of methylprednisolone, and performed plasma exchange and plasma absorption, but these therapies proved to be ineffective. The levels of P-ANCA, white blood cells and C-reactive protein did not reflect the virulence of the disease in this patient. It is important to investigate the indices that reflect the activity of this disease and the choice of the appropriate therapy for the level of virulence.

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