Macrophage migration inhibitory factor (MIF) was originally discovered as a soluble factor associated with the mechanism of delayed-type hypersensitivity. Today, MIF is widely accepted as a pluripotent cytokine involved in a broad-spectrum pathological events beyond the immune system. Following the cloning of MIF cDNA, previously unrecognized biological functions of MIF have been revealed. MIF is released as a hormone by the anterior pituitary gland in endotoxin shock, and as a proinflammatory cytokine and glucocorticoid-induced immunomodulator produced in response to a variety of inflammatory stimuli. Based on these findings, it is expected that MIF would be a novel marker which indicates septicemia. Recently, it was found that Toll-like-4 receptor could be regulated by MIF, suggesting its involvement in the innate immunity.

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Lung transplantation has been established as an useful therapy for end-stage lung diseases. The postoperative management of lung transplantation plays an important role on the survival of individual recipient. This review discussed the postoperative management for lung transplantation in ICU. The important points for early postoperative care of lung transplantation are the early detection of acute rejection, the prevention or treatment of infection, the ventilatory support and weaning, the immunosuppression, and the avoidance of reperfusion and ventilator associated lung injury. To achieve these purposes, we should know the preoperative state of recipient and concomitantly understand the physiology of the transplanted lung. Furthermore, the hemodynamic management to prevent lung edema and pulmonary hypertension is important. Recipients with primary pulmonary hypertension need more careful management for remaining hypertention and unstable circulation.

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A 44 year-old man was refered to the ICU for his sudden and severe dyspnea. His physical findings, chest radiograph, and ECG suggested acute pulmonary thromboembolism. Although his trachea was intubated due to severe hypoxemia and rapidly progressing conscious disturbance, it did not improved hypoxemia and, worse than that, induced sudden hypotention and pulmonary arterial congestion. None of medical treatments like inotropes including epinephrine, fluid administration, and mechanical ventilation did not improve his condition and we started emergent percutaneous cardiopulmonary support system (PCPS) to prevent circulatory collapse and probable death. PCPS raised his systolic blood pressure from 70mmHg to 100mmHg. We found hepatosplenomegaly after the beginning of PCPS by palpating his distended abdomen. Emergent pulmonary angiography showed multiple filling defects in the distal pulmonary arteries. Continuous hemodiafiltration (CHDF) was carried out for acute renal failure presenting anuria, hyperkalemia, and metabolic acidosis. Subsequent laboratory findings suggested acute crisis of chronic myelogenic leukemia as his background and we considered that pulmonary thromboembolism had resulted from hyperleukocytosis and hyperthrombocytosis. PCPS was discontinued six hours after the initiation because of gradual occlusion of artificial lung membrane and finally the patient lost his life. Autopsy revealed extensive infiltration of chronic myelocytic leukemic cells in major organs including both lungs. The final diagnosis is pulmonary thromboembolism by blastic crisis of chronic myelocytic leukemia and it is retrospectively non-indicative for PCPS. This case highlights the clinical, radiographic and histolic features of pulmonary leukostasis and reminds us that it is difficult to exclude fatal malignant diseases during resuscitation.

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We experienced intractable atrial or ventricular tachyarrhythmias in two cases of acute myocardial infarction resulted from left main coronary artetry occlusion and reperfusion therapy. Lidocaine, magnesium sulfate, or cardioversion failed to control ventricular tachycardia in the case 1. Disopyramide or cardioversion failed to control atrial flutter also in the case 2 on day 4 after the onset of myocardial infarction. In both cases, intravenous nifekalant followed by cardioversion disappeared arrhythmias. Nifekalant is a pure class III antiarrhythmic drug which prolongs the refractory period of the atrial and ventricular myocardium without negative inotropic action. Our cases showed the efficacy and safety of nifekalant in both atrial and ventricular tachyarrhythmias complicating acute myocardial infarction in left main coronary region with severe heart failure.

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A 49-year-old female who underwent chemotherapy with 5-fluorouracil (5-FU) and cisplatin for uterocervical cancer fell into a coma on the third day of chemotherapy and remained comatose after cessetion of these agents. She was diagnosed as leukoencephalopathy with MRI and electrophysiological examinations, and consequently, anticancer agents were suspected. An anticancer agent, 5-FU often induces leukoencephalopathy usually following more than 2 weeks administration, when its blood concentration reaches toxic level. Co-administered diazepam to prevent emesis and vomiting might confuse the initial symptoms of leukoencephalopathy to develop it to irreversible level. Irreversibility is not usual for 5-FU induced neural injury. Characteristics of this case; i. e., early onset, irreversible neurological damage, and lower blood concentration of suspected drugs suggest that this is a severe and rare example of drug-induced leukoencephalopathy.

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There are few data available on the efficacy and reliability of PEEP valves for a transport ventilator. We evaluated PEEP valves manufactured by Ambu^(R), Inspiron^(R), Smiths Industries^(R), and Vital signs^(R) co. The Smiths Industries^(R) products had the biggest differences between the preset indicators and measured pressures at PEEP 5, 10, 15cmH₂O in comparison with other products. Pressure decrements at PEEP 5, 10, 15cmH₂O were larger in the Inspiron^(R) and the Vital signs^(R) products than in others, and the decrements tended to increase at higher PEEPs. Resistance created by the PEEP valves were negligible. We conclude that pressure monitoring is required for the safe and effective use of commercially available PEEP valves.

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