The data on plasma endotoxin levels suggests endotoxins are significant in human disease. In this review, we first introduce a recently discovered receptor protein (toll-like receptor, TLR) for LPS, then we review our data on endotoxin levels in different diseases. Endotoxin was measured by an endotoxic-specific limulus test (Endospecy). Plasma was treated using the New PCA method, which we established. The main results described in this review are as follows: 1) Plasma endotoxin levels were significantly high only in SIRS with suspected gram-negative infection, 2) plasma endotoxin levels in gastrointestinal perforation were unexpectedly low, 3) a clinical study, performed in Japan, of anti-endotoxin murine monoclonal antibody (E5) indicated that E5 administration reduced the severity of sepsis even in patients with nonbacteremia and nonendotoxemia, and 4) the severity of sepsis was correlated with the plasma level of inflammatory cytokines, but not with endotoxemia.
It was suggested that the entry of endotoxin into the circulation is controlled by an unknown mechanism, and that endotoxin mainly plays a role in the local region of infection to produce cytokines.

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Intravascular volume optimization is crucial to reduce the mortality, morbidity and length of hospital stay in critically ill patients. However, routine clinical variables do not consistently indicate the intravascular volume state adequately. Dilution volumetry is the standard method to evaluate various fluid volumes, even though associated technical difficulties make this method inconvenient in the intensive care unit. Plasma volume determined by the indocyanine green (ICG) dilution method (PV-ICG) has been demonstrated to be safe and equally accurate independently of its disappearance rate from plasma as compared with the radio-iodine labelled serum albumin method. Measurement of blood volume utilizing ICG and pulse dye-densitometry has also been introduced recently without requiring repeated blood samplings. The glucose dilution method has also been proposed as an indicator of the central extracellular fluid volume state without obvious modification of glucose metabolism. Although intravenously administered glucose distributes rapidly into the extravascular compartment, the initial distribution volume of glucose (IDVG) rather than the PV-ICG has been found to correlate linearly with cardiac output in critically ill patients, suggesting that the IDVG rather than the PV-ICG affects cardiac preload. Overestimation of the PV-ICG can occur during the presence of the generalized capillary protein leakage in various pathologic conditions such as burns, sepsis and trauma, since ICG binds to plasma proteins. As the IDVG consistently indicates central extracellular fluid volume regardless of the presence or the absence of leakage, this overestimation can be assessed by the PV-ICG/IDVG ratio, with a higher ratio indicating overestimation. Other non-radioactive tracers have been introduced recently, such as carbon monoxide, hydroxyethyl starch and sodium fluorescein. Although there may be some methodological flaws or complexities in any type of dilution volumetry, it can be used routinely as a clinically relevant variable in the fluid management of critically ill patients.

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The exact mechanism of acute respiratory distress syndrome (ARDS) has not been elucidated, although there is ample evidence for the involvement of recurrent aspiration in the development of ARDS. This study aimed to know the distribution of chronic aspiration which may be involved in childhood acute lung injury.
We analyzed the incidence, the mortality and the etiology of ARDS in our Pediatric Intensive Care Unit (PICU). There were 15 ARDS patients of 570 cases who were admitted to our PICU. Chronic aspiration was suspected to be the primarily involved in 3 cases of ARDS. In these cases, the classical risk factors of ARDS were not present and mild respiratory infection triggered the development of ARDS. Establishment of a long-term treatment plan is needed in childhood ARDS with chronic aspiration because of the possible recurrence of ARDS.

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Patients in the intensive care unit (ICU) are under unusual psychological stress and suffer from the so-called ICU syndrome. Between January 1, 1994 and March 15, 1997, we observed 698 patients for 4 days each from the time of admission to the ICU of our university hospital. We classified the patients' behavior into 23 types, and categorized them as 5 individual sensory-perceptual actions: insomnia, purposeful movement, emotional behavior, delirium and irritation. Of the 23 behaviors, “cooperative during examination”, “voluntary movement”, “getting nervous”, “saying or writing nonsense words”, “crying” and “getting angry” were highly related to self-induced accidents (for example, pulling out their own tubes). Using Quantification Formula II, we quantified 6 of the 23 behaviors as variables, and developed a risk scoring system to prevent or reduce such self-induced accidents in the ICU.
The use of the riskscoring system reduced the frequency of restraints and the incidence of self-induced accidents in our ICU. Objective scoring of definite factors selected from the classified actions of patients was effective in preventing self-induced accidents in our ICU.

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We report a case of Kasabach-Merritt syndrome with giant hemangioma on the neck, which caused airway obstruction. A 2-month-old girl, who had been diagnosed with Kasabach-Merritt syndrome, had a giant hemangioma on her neck, thrombocytopenia, and coagulopathy. She was suffering from airway obstruction and she admitted to the ICU for airway management. Steroid therapy was not effective so in addition to the administration of interferon-α-2a, emergency embolization therapy was performed under general anesthesia. The therapy reduced the size of the hemangioma and the airway obstruction resolved. The patient was extubated uneventfully a few hours after the operation. Her platelet count began to increase after six days with no recurrence of the tumor. We suggest that early embolization therapy with pharmacotherapy is effective for cases with airway obstruction caused by a rapidly spreading tumor.

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A 41-year-old woman was admitted to our ICU because of consciousness disturbance and muscle weakness in her extremities. Hyperosmolar nonketotic diabetic coma was diagnosed on the basis of laboratory data obtained on admission, i. e., hyperglycemia (297mg·dl^-1), hypernatremia (185mEq·l^-1), and negative ketone bodies in urine. Serum osmolality was 388mOsm·kg^-1. Plasma myoglobin levels on the 5th hospital day were 240, 000ng·ml^-1 indicating the development of rhabdomyolysis.
The patient was treated with massive fluid replacement and intravenous administration of diuretics and insulin, for the duration of her consciousness disturbance which persisted for more than 4 weeks. The diagnosis of central pontine myelinolysis (CPM) was made by magnetic resonance imaging (MRI) scans of the brain on the 34th hospital day. The patient gradually recovered her motor function until she regained independent activity of daily life after 3 months. We concluded that CPM and rhabdomyolysis could have be caused by a hyperosmolar state related to hypernatremia and hyperglycemia.

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We report here the successful medical management of subacute cardiac rupture (SCR) following acute myocardial infarction (AMI). Four female cases, 77.8±9.5 (mean±SD) years of age, presented with AMI. The infarct site was anterior in two cases, and inferior in the other two cases. The infarct-related arteries were recanalized successfully by primary percutaneous transluminal coronary angioplasty (PICA) in three cases, but emergency coronary angiography was not performed in the other case. After 18.1±16.1 hours from AMI and 3.2±4.0 hours from admission, SCR appeared as cardiac tamponade. Surgical procedures were rejected and/or not indicated in all four cases. Pericardiocentesis was immediately performed and yielded a pericardial effusion of pure blood. Pericardial drainage was performed, reversing the state of shock in each case, but the amount of pericardial effusion drained was limited to the minimum quantity(20-130ml) which was required to stabilize their circulation. Percutaneous intrapericardial coagulation factor infusion therapy (PICFIT) was subsequently performed, followed by strict bed rest and blood pressure control. The coagulation factor preparations used were thrombin solution in one case and fibrinogen-thrombin-factor XIII preparation in three cases. Intra-aortic counterpulsation was used in one case and artificial ventilation in two cases. The pericardial drainage tubes were removed at 12.3±5.4 hospital days. These therapeutic strategies resulted in the survival and successful discharge of all four cases. The mean hospital stay was 84 days. On discharge, pseudoaneurysm of the left ventricle was not seen nor was diastolic left ventricular function restricted in any case. Two to four years have passed since discharge, and all four patients are still alive with sufficient quality of life. Their clinical courses after discharge were uneventful and the symptoms and signs suggesting constrictive pericarditis were never seen. The efficacy of three treatment modalities (surgery, PICFIT, and conservative management) are discussed regarding 16 cases of SCR. Of all l6 cases of SCR, 7 were treated by surgery, 4by PICFIT, and 5 by conservative management. Eleven cases (6 by surgery, 4 by PICFIT, 1 by conservative management) survived. The surgery and PICFIT groups had more survivors than the conservative group, and this difference was statistically significant (P<0.025). Thus, some cases of SCR after AMI may benefit from PICFIT even when surgical procedures are not undertaken.

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A 69-year old woman was admitted because of nausea and vomiting. On admission she was slightly depressed. Then she gradually became delirious, and leresis, paranoia and confusion developed. On the 52nd hospital day, sudden generalized seizure developed and she was transfered to the ICU. Physical examination revealed a comatose state (JCS III-200), conjugate deviation to the right, right hemiparesis, exophthalmos and struma. Laboratory data confirmed hyperthyroidism, and she was diagnosed as having a thyroid crisis. In addition to the administration of Lugol's solution and thiamazole, she was treated with epidural block in order to restrain sympathetic hyperactivity. After 3 days she recovered from the coma and the hemiparesis.

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A 32-year-old male had been inhaling thinner for over 5 days and was transmitted to our institution due to loss of consciousness. He was in shock and showed an increase in anion gap, severe metabolic acidosis, renal dysfunction, and a high level of serum hippuric acid (177ml·dl^-1) on admission. Thinner mainly consists of toluene that metabolizes to hippuric acid. We performed continuous hemodiafiltration on the patient to eliminate hippuric acid, a metabolite of toluene as his serum level of hippuric acid increased gradually up to 210ml·dl^-1. It was reduced to 2ml·dl^-1 following continuous hemodiafiltration. There is no special treatment for toluene poisoning that will show improvement only through fluid infusion in patients with normal renal function. However, in patients with poor renal function, an accumulation of hippuric acid may not only further metabolic acidosis, but also further damage renal function.
The case presented suggests that the induction of continuous hemodiafiltration for patients who present with acute thinner poisoning complicated by acute renal dysfunction is effective in the removal of accumulated hippuric acid, lowering extended metabolic acidosis and in ultimate recovery from deteriorated renal function.

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