Living donor liver transplantation has evolved rapidly in Japan due to the scarcity of cadaveric organ sources and is reaching the 10th anniversary of clinical application. Its application began in small children, but has now been extended to larger children and even adults, and graft-size mismatching is being overcome by the safe use of right-lobe grafts. Virus-related cirrhosis and hepatic malignancies are now being included in its indication as in western countries. There remain, however, several unsolved problems including the timing of transplantation and preoperative management, perioperative latent infections, biliary complications in chronic phase, refractory rejection, posttransplant lymphoma, and recurrent original diseases. Some of these problems are closely related with the predestinate use of small-for-size grafts in living donor liver transplantation. The further development of transplant hepatologists and transplant systems including all related fields, consolidation of economical support by public insurance, and above all, a constant mutual support system with cadaveric transplant program are important tasks to be dealt with in Japan.

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Reperfusion therapy has been a major therapeutic strategy to reduce infarct size, preserve left ventricular function and improve survival in patients with acute myocardial infarction. However, it is sometimes underused or done at less than optimal timing. Decreasing the time interval between symptom onset and hospital admission or between bystander cardio-pulmonary resuscitation in out-of-hospital cardio-pulmonary arrest and transport to a well-experienced hospital for emergent cardiology is necessary to treat all eligible patients including those with coronary thrombolysis or angioplasty, with reperfusion therapy as soon as possible. Adjunctive therapies to protect infarct-related myocardium from ischemic or reperfusion injury, and to prevent left ventricular remodeling and reocclusion of the infarct-related artery should be developed for the improvement of both short-and long-term prognosis.

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To determine whether inhaled nitric oxide (NO) at a concentration of 20 parts per million (ppm) attenuates or enhances oxygen-induced lung injury, the effect of inhaled NO on the formation of 8-hydroxydeoxyguanosine (8-OHdG), a marker for oxidative DNA damage, was studied in rat lungs. Forty male Wister rats were divided into three groups; 20 rats in the control group, 10 rats in the oxygen group, and 10 rats in the oxygen-NO group were exposed either to room air, 100% oxygen, or oxygen with 20ppm NO for 48 hours. Their lungs were removed and homogenized. DNA was extracted to measure 8-OHdG/dG×10⁵. In the control group, 8-OHdG/dG×10⁵ was 1.02±0.35. Exposure to either 100% oxygen or oxygen with 20ppm NO caused significant increase in 8-OHdG/dG×10⁵ from 1.02±0.35 to 1.77±0.74 (P<0.01) or to 1.37±0.55 (P<0.05), respectively. Although statistically not significant (P=0.09), the magnitude of increase in 8-OHdG/dG×10⁵ was lower in the oxygen-NO group than that in the oxygen group. These results suggest that inhalation of NO does not enhance the oxidative injury of DNA in rat lungs.

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There are no reports on pressure spreading during pressure support ventilation (PSV) in the lung. We studied changes in alveolar pressure during PSV.
Six mature mongrel dogs were anesthetized with pentobarbital 25mg·kg^-1 and intubated with a Univent tracheal tube (I. D. 8.5mm, Fuji Systems, Japan). They were ventilated on continuous positive pressure ventilation (CPPV) mode with the EVITA2 ventilator (Dräger, Germany). Anesthesia was maintained by infusion of pentobarbital 2-3mg·kg^-1·hr^-1. Alveolar pressure was measured from a capsule which was glued to the surface of the lung in the intercostal space in the right lateral position using the “closed-chest capsule technique” (Bates, 1989). Tracheal pressure was measured from the occlusion catheter of the Univent-tube. Pressure support (PS) levels were set at 5 and 10cmH₂O, PEEP 5cmH₂O, and O₂ concentration 0.21. The rising time of PS was set at about 0.5sec. Pressure-time curves of the circuit of ventilator, trachea and alveoli were recorded on a polygraph simultaneously. Tidal volume, respiratory rate, minute volume and duty ratio were measured with a respiratory monitor (OMR-8101, Nihon Kohden, Japan). P_0.1 was measured with EVITA2. During CPPV, the pressure difference between the trachea and alveoli was very small and the time phases of inspiration and expiration were consistent with each other. The velocity of inspiratory and expiratory pressure changes was slower in the trachea and alveoli than in the circuit. Mean compliance and mean resistance of the respiratory system were 19.0 ml·cmH₂O^-1 and 16.3cmH₂O·l^-1·sec^-1 respectively. During PSV, the pressure difference between the trachea and alveoli was very small, as with CPPV. The pressure waveform of the circuit plateaued during inspiration, but the tracheal and alveolar pressures never showed a plateau. In conclusion, in normal mongrel dogs, the influence of resistance in the lung was negligible on pressure spreading during CPPV and PSV.

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We report on a patient with acute respiratory distress syndrome (ARDS) whose PaO₂ had deteriorated during nitric oxide (NO) inhalation while pulmonary arterial pressure decreased. A 70-year-old man developed septic shock and ARDS due to bacterial pneumonia. Noradrenaline and dopamine were intravenously administered for circulatory support, with administration of antibiotics, steroid and urinastatin. During 10ppm NO inhalation, mean pulmonary arterial pressure decreased from 23 to 20mmHg and PaO₂ decreased from 54.8 (F_IO₂=1.0) to 49.2 (F_IO₂=0.96)mmHg. Mean arterial pressure increased, with the cardiac index, pulmonary artery wedge pressure and pulmonary capillary pressure remaining unchanged. PaO₂ increased following discontinuation of NO. Our findings suggest that inhalation of NO may occasionally induce deterioration of oxygenation in patients with septic ARDS while decreasing pulmonary arterial pressure.

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We applied extracorporeal lung assist (ECLA) with a heparin-bonded (Carmeda BioActive Surface^TM) bypass circuit to a full-term newborn male, weighing 3, 324g, suffering from severe respiratory failure due to meconium aspiration syndrome. Veno-arterial ECLA with a minimax plus^TM oxygenator via the right internal jugular vein and the right common carotid artery was initiated 55 hours after birth. Heparin was administered as a bolus of 100IU·kg^-1 prior to cannulation, and continued at 3 to 15IU·kg^-1·min^-1 to maintain an activated coagulation time (ACT) of 120-160 seconds. The oxygenator was changed once during the treatment because of plasma leakage. The patient was weaned from ECLA 89 hours and 25 minutes after initiation. He was weaned from the ventilator 7 days after the termination of ECLA and discharged on the 53rd hospital day. The amount of heparin required for anticoagulation was reduced with the use of a heparin-bonded circuit. However, the disadvantage of a heparin-bonded membrane oxygenator is plasma leakage which results in impairment of gas exchange.

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We treated six patients suffering from toxic epidermal necrolysis between 1986 and 1995. All patients were managed on a floating burn bed in an isolated room of an intensive care unit. The etiology of toxic epidermal necrolysis was unknown in three cases. Steroid therapy was continued in the intensive care unit for the first and second patients, but was discontinued on ICU admission for the four subsequent patients. The first patient died of Pseudomonas aeruginosa sepsis, but the remaining five patients survived. Blistered skin and mucosal lesions healed in all patients. Organ dysfunction was found to have developed two weeks after the onset of disease in two patients as evaluated by an organ dysfunction score. Prevention of infection appears to be important in the management of patients with toxic epidermal necrolysis. In the first patient treated, steroid therapy appeared to be harmful. A randomized, control study is needed to determine the effect of steroid therapy on the prognosis of patients with toxic epidermal necrolysis.

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We report the case of a 3 year-old girl with a history of anaphylactic shock due to latex, who was successfully managed during the perioperative period. She underwent three operations for meningocele and exstrophy of the cloaca uneventfully. During central venous catheterization prior to the start of the fourth operation, an unexpected shock occurred and the operation was canceled. The shock was diagnosed as being caused by latex allergy. The diagnosis was established using the IgE-RAST latex test and skin prick tests. The operation was re-scheduled after recovery. To determine how to cope with latex allergy during the perioperative period, conferences were held among the medical staff, including surgeons, anesthesiologists, pediatricians, operating nurses, ward nurses, and ICU nurses. We determined whether surgical, anesthetic, and nursing implements ordinarily used contain natural latex material. All of the implements and devices containing latex such as surgical gloves, anesthetic circuits, and infusion routes were replaced with non-latex substitutes. Indispensable latex implements were wrapped to prevent direct contact with the patient's skin. Four months later, using latex-free procedures, the operation was performed uneventfully. In conclusion, avoiding latex exposure is possible in perioperative management of patients with latex allergy. In order to avoid latex exposure in such patients, communication and cooperation among medical staff members is essential. Continuing care instruction for patients' families is advised.

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Polymyxin B (PLB) is a cationic antibiotic which stoichiometrically neutralizes the lipid A moiety of endotoxin. We evaluated the safety and effectiveness of PLB administration in preoperative patients in a randomized controlled and open clinical trial. Twelve thousand five hundred units of PLB were given intravenously every 6 hours to the patients of hepatectomy or esophagectomy from the beginning of the operation and was continued until postoperative day 5. Postoperative laboratory data, plasma endotoxin, serum interleukin (IL)-6 and IL-8, parameters of systemic inflammatory response syndrome (SIRS) score, acute physiology and chronic health evaluation (APACHE) II score, multiple organ failure (MOF) score, length of ICU and hospital stay, morbidity, and mortality were evaluated. No adverse effects of PLB administration were detected. The plasma endotoxin levels on postoperative days (POD) 0 and 1 in the PLB groups were 8.2±2.3pg·ml^-1 and 5.5±2.1, whereas those of the control group were 21.7±11.3 and 8.2±4.5. Serum IL-6 and IL-8 during the five postoperative days in patients with PLB were lower than those of control patients. However, the difference was not significant. Maximum levels of laboratory data (white blood cell counts, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, total bilirubin, C-reactive protein) within 2 weeks after the operation, length of high body temperature, the number of the positive parameters of SIRS definitions, and length of SIRS in the PLB group tended to be lower than those of control group, but no significance was noted between the groups. PLB administration significantly lowered MOF score (4.0±0.7 in control group vs 2.4±0.2 in PLB group, P=0.045) and hospital stay (53.3±8.9 days in control group vs 30.8±3.3 in PLB group, P=0.027). It also lowered the initial 24-hour APACHE II score (22.3±3.2 vs 13.4±4.9), and the number of dysfunctioned organs (2.3±0.4 organs vs 1.6±0.4) and ICU stay (4.0±1.4 days vs 1.2±0.6, P=0.055). Preoperative PLB administration reduced both postoperative MOF score and length of hospital stay, and may be useful in preventing MOF.

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