A variety of approaches have been taken to protect the brain from ischemia in the field of intensive care. They are categorized into two strategies; one is non-drug therapy and the other is drug therapy. Eight strategies contained in the study of protection from neurodegeneration are keys to successful brain protection. They include (1) improved operative techniques, (2) control of blood pressure and intracranial pressure (ICP) and maintenance of cerebral perfusion, (3) development of new neuroprotective drugs for brain protection, (4) drug therapy based on therapeutic windows, (5) avoidance of perioperative hyperthermia and/or hyperglycemia, and implementation of postoperative hypothermia to prevent reperfusion injury, (6) utilization of a cerebral protection system in the body (ischemic tolerance phenomena), and (7) monitoring of brain function, search for new biomarkers, and further improvement of brain-oriented intensive care therapy. Finally, under the eighth strategy, it is assumed that neurorestorative approaches are taken in case cerebral dysfunction still remains, and that in the future, in combination with introduction of gene therapy, neural regeneration and functional recovery will be pursued while suppressing the onset of ischemic neuropathy completely or keeping it to a minimum.

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Mediastinitis is caused by various diseases. Especially, descending necrotizing mediastinitis (DNM) is a life-threatening emergency after dental and oropharyngeal infection. Every physician should acknowledge the DNM and, in this article, the DNM is reviewed. The dental and oropharyngeal disease is common in DNM, however, if cervical and chest symptom is apparent, neck and chest CT shoud be conducted immediately for early detection of DNM. Aggressive neck and mediastinal surgical drainage is essential for the patient survival. Postoperative follow-up using CT is useful for detecting the recurrence of abscess.

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Understanding mechanism of gas exchange between atmosphere and blood is one of the important parts of respiratory physiology. We describe the important theories and relevant formulae for respiratory care. Most of the formulae can be derived by ideal gas equation and Dalton's law. The new, easily understanding way to derive alveolar gas equation is also shown.

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Hemofilters for continuous hemodiafiltration (CHDF) have been expected not only long lifetime but also high clearance capacity of low molecular proteins, which may cause multiple organ dysfunction syndrome (MODS). To evaluate commercially available hemofilters for CHDF, 18 critically ill patients with renal failure were randomly assigned to receive one of five commercial hemofilters; Panflo APF-06S (APF, Asahikasei Medical), PS filter C07 (PS, Kuraray Medical), Hemofeel CH-0.6L (Toray Medical), UT filter UT-700S (Nipro), and Hemofeel SH-0.8 (SH, Toray Medical); whose membranes were made of polyacrylonitrile, polysulfone, polymethyl methacrylate, cellulose triacetate, and polysulfone, respectively. Solute clearance and sequential ultrafiltration rate were determined. Clearances of small solutes (urea and creatinine) were not significantly different among these hemofilters and did not decrease throughout 24 hours. Clearances of low molecular proteins (β₂ microglobulin, myoglobin, and interleukin-6) by APF and PS were higher than the others, and scarcely decreased even at 24 hours after. All filters were insufficient to remove α₁ microglobulin, molecular weight of 33 kDa, and no filters leaked albumin. Both APF and SH showed higher ultrafiltration rates and longer lifetime over 24 hours than the others. These results suggest that APF may be the best hemofilter for CHDF in the treatment of critically ill patients with renal failure.

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We report a case of relative adrenal insufficiency associated with cardiopulmonary arrest resulting from a ruptured ectopic pregnancy. A 33-year-old female was transported to our hospital 14 hours after the rupture of an ectopic pregnancy; upon arrival, she immediately experienced cardiopulmonary arrest. Her heart was restarted using cardiopulmonary resuscitation (CPR), and she underwent an urgent operation. Her circulatory dynamics destabilized on the 1st postoperative day. An investigation using a pulmonary artery catheter revealed the cause of the instability to be vasodilatory shock. Hydrocortisone was administered after examination using adrenocorticotropic hormone (ACTH) loading. The initial dose of hydrocortisone was 200 mg·day^-1; this dose was gradually tapered over a period of 16 days, and the patient's circulatory dynamics were stabilized. The results of the ACTH load examination suggested relative adrenal insufficiency. Continuous hemodiafiltration (CHDF) and plasma exchange, etc., were used to treat the patient's multiple organ failure, including the coagulation disorder, disseminated intravascular coagulation (DIC), acute liver failure, acute renal failure, and multiple brain hemorrhages. The patient's condition stabilized, and she was moved to a general ward on the 24th postoperative day. No permanent disabilities other than a slight decrease in intelligence were noted. Relative adrenal insufficiency should be considered as a possible cause of acute circulatory dysfunction resulting from extensive internal injury.

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Vasopressin has been described to restore blood pressure in patients with several shock states. We report the effects of vasopressin treatment in eight patients with severe septic shock unresponsive to norepinephrine. Vasopressin was added by continuous infusion at rate of 0.021 ± 0.008 U·min^-1. In all cases, vasopressin induced sustained improvement in mean arterial pressure with a significant increase in urine output. Vasopressin treatment did not affect platelet counts in blood as well as the plasma transaminase and total bilirubin levels. All patients survived without severe adverse effects. The continuous infusion by a small amount of vasopressin may be effective for norepinephrine-resistant septic shock, which leads to the improvement of hemodynamics valuables with better outcome.

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Colforsin daropate hydrochloride (CDH) stimulates adenylate cyclase resulting in increase of intracellular cyclic adenosine monophosphate (cAMP), and exhibits positive inotropic, vasodilative, and diuretic effects. In adult, CDH ameliorates the condition of cardiac failure, even when catecholamines do not. We present here CDH worked effectively for a pediatric patient with severe cardiac failure, for whom neither catecholamine nor phosphodiesterase III inhibitor worked. An 11-month-old girl was admitted to our unit because of cardiac failure. She had been diagnosed as congenital mitral regurgitation and multiple anomalies. She had an upper respiratory tract infection, and cardiac failure developed. Her trachea was intubated and mechanical ventilation was started. Dopamine (7μg·kg^-1·min^-1), milrinone (0.5μg·kg^-1·min^-1) administration failed to improve hemodynamics. CVP was 22 mmHg, and echocardiography revealed LVEDd of 34.1 mm. Serum brain natriuretic peptide (BNP) level was 13,987 pg·ml^-1. Because of cardiogenic pulmonary edema, oxygenation was poor (P/F ratio 89 mmHg). While CDH was rarely reported for pediatric patients, we started CDH (0.1∼0.16μg·kg^-1·min^-1) resulting in increase of urinary output. Two weeks after CDH administration, general edema disappeared and she lost 1.5 kg of weight. CVP decreased to 7 mmHg, BNP decreased to 351 pg·ml^-1, and P/F ratio increased above 400 mmHg. She was weaned from a ventilator successfully. CDH was administered for 2 months. CDH was useful for pediatric patients with refractory cardiac failure.

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We encountered a patient with ulcerative colitis, in whom central venous catheterization was restricted by aerodermectasia of the neck and chest. By using ultrasound-guidance, central venous catheterization of the distal femoral vein was successfully performed. In patients in whom venous catheterization is limited for some reasons, an ultrasound-guided approach could prove valuable in overcoming these limitations.

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The widespread appearance of early CT signs is a contraindication for thrombolytic therapy. Here, we report a patient with an ischemic cerebral vascular disorder and widespread early CT signs as a result of an embolism in the middle cerebral artery (MCA) trunk. Superselective thrombolytic therapy with urokinase improved the symptoms without causing the formation of sequelae. A 20-year-old woman developed left semiparalysis after suddenly falling at a bank. Widespread early CT signs were observed on brain CT scans obtained 1 hour after onset. MRI revealed an embolism in the right MCA (M2). Superselective thrombolytic therapy was started 2 hours after onset, and complete re-canalization was achieved within 3 hours of the thrombolytic therapy. The patient recovered almost completely, with only a slight persisting numbness in her left hand.

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We experienced 2 cases of significant conjugated hyperbilirubinemia after multiple trauma. Usually, the resorption of massive hematoma and large quantities of transfusions increase the production of unconjugated bilirubin. Conjugated hyperbilirubinemia was mainly caused by 2 factors consisted of an impaired active transport of conjugated bilirubin to intrahepatic duct following hepatic hypoperfusion under the shock, and hyperproduction of bilirubin due to the resorption of massive hematoma. According to the clinical course of the improvement of hyperbilirubinemia, other factors including resorption by fasting, mechanical ventilation with PEEP, decreased intestinal motility and bile excretory impairment caused by the shock, the high dose of catecholamine and the narcotics might be associated with the hyperbilirubinemia. Further study about the effect on the hyperbilirubinemia by sivelestat sodium might be necessary. And, the treatment which took up the conjugated hyperbilirubinemia itself is not necessary.

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We report a case of pheochromocytoma presenting as catecholamine cardiomyopathy and noncardiogenic pulmonary edema successfully treated with afterload reduction. A 34-year-old male was admitted to our hospital with complaints of dyspnea and cold sweating. The blood pressure was 130/100 mmHg and the heart rate was 150 min^-1. The chest X-ray showed pulmonary edema and the echocardiography revealed diffuse left ventricular dysfunction (ejection fraction of 20%) without left atrial or ventricular over distension. He was treated with a continuous infusion of nicardipine and oral bunazocin. He was diagnosed as pheochromocytoma with a marked increase in serum concentrations of catecholamines (adrenaline 52,009 pg·ml^-1, noradrenaline 35,810 pg·ml^-1) and the left adrenal tumor on the abdominal CT scan. Pulmonary edema disappeared on the next day and he was free from dyspnea. The left ventricular contraction was improved, and the ejection fraction increased to 24% on the 2nd day and 58% on the 3rd day. The serum adrenaline and noradrenaline concentrations decreased to 6,140 and 6,669 pg·ml^-1, respectively on the 3rd day. A pheochromocytoma was removed successfully on the 12th day. The serum catecholamine concentrations became normal on the 18th day and he was discharged on the 28th day.

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