Since 1992, ELSTs (emergency life-saving technicians) as ambulance personnel, who were trained for some kinds of advanced life support, have been treating out-of-hospital cardiac arrest in Japan. This study was performed to determine the nationwide results of prehospital resuscitation, especially those performed by ELSTs. All cases of out-of-hospital cardiac arrest including those due to trauma during 6 months in 1994 were reviewed. There were 31, 206 cases of attempted CPR by ambulance personnel. The incidence of restored circulation on arrival at the hospital, and survival rate after 7 days and after 1 month, were 11.4%, 4.4% and 2.6% for overall CPR. The outcome of those witnessed and given by bystander CPR was significantly better than that of non-witnessed or without bystander CPR. The survival rate for victims treated by ELSTs was higher than that treated by basic ambulance personnel (EMTs), with a statistically significant difference. The 1 month survival rate of patients, who were witnessed, and resuscitated initially by bystanders and then by ELSTs, reached as high as 8.9%.

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To determine the role of soluble cellular adhesion molecules in the development of multiple organ failure (MOF), serum levels of the soluble type intercellular adhesion molecule-1 (sICAM-1) and the endothelial-leukocyte adhesion molecule-1 (sELAM-1) were measured in 25 patients in the Intensive Care Unit in the Gunma University Hospital. MOF was defined as the failure of two or more organs. The patients were divided into four groups according to the presence or absence of MOF and the systemic inflammatory response syndrome (SIRS): group 1, SIRS (-)/MOF (-); group 2, SIRS (-)/MOF (+); group 3, SIRS (+)/MOF (-) and group 4, SIRS (+)/MOF (+). There were no differences in the serum levels of sICAM-1 and sELAM-1 in group 1, group 2 and group 3. However, the serum levels of both sICAM-1 and sELAM-1 were significantly elevated in group 4. The serum levels of the two molecules tended to increase with the number of dysfunctioning organs. These data suggest that the development of organ dysfunction in a patient with SIRS and MOF (group 4) is associated with the interaction between circulating leukocytes and vascular endothelial cells. The serum levels of sICAM-1 were significantly higher in patients with hyperbilirubinemia, ARDS, CNS disorder and DIC. The serum levels of sELAM-1 were significantly higher in patients with renal failure and DIC. The precise mechanism that caused these difference is not clear. Further investigations are required to clarify the role of sICAM-1 and sELAM-1.

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The first purpose of this study is to clarify the duration of“the Golden Time”for operation after traumatic intestinal perforation from the analysis of postoperative water redistribution. Another purpose is to evaluate the influence of colloid administration on postoperative water redistribution in patients with traumatic intestinal perforation. The post-operative water redistributions of 26 cases with traumatic perforation of the small intestine were analysed using two parameters. The first parameter is the time between operation and beginning of the diuresis period (T2-T1). The second parameter is the estimated amount of water, termed“Lost Water (LW)”, that moves out of the intravascular space to the extravascular space during the oliguric period, but never returns to the intravascular space even after the diuretic period. Cases were divided into two groups according to the interval between the injury and the operation. When the point of discrimination was set at 6hrs after the injury, the differences in both parameters (T2-T1 and LW/h) between the two groups were significant (p<0.05). This meant that the Golden Time after traumatic intestinal perforation is presumably 6hrs from the viewpoint of water redistribution. There was also a significant difference in the duration of time that PEEP was necessary, and in maximum FIO₂ between the two groups. The administration of colloids had no significant influence on T2-T1, but reduced LW/h significantly. The prolongation of T2-T1 may be considered to result from over-secretion of antidiuretic hormone (ADH). The infusion of colloids increases the serum osmotic pressure of intravascular fluid which promotes greater secretion of ADH and may result in prolongation of T2-T1. On the other hand, increased plasma osmotic pressure may inhibit the displacement of water from the intra-to the extravascular space and promote the displacement from the extra-to the intravascular space, resulting in a decrease in“Lost Water”.

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In recent years, the significance of leukocyte-endothelial interaction in the development of organ dysfunction during sepsis has become well established. Adhesion molecules, especially the integrin family residing on the leukocyte surface and intercellular adhesion molecule-1 on the endothelial surface, play important roles in this interaction. Recent studies have revealed that the circulating levels of soluble type intercellular adhesion molecule-1 (SICAM-1) rises along with increased expression of ICAM-1 on the endothelial surface. This study was undertaken to investigate the relationship between circulating levels of soluble (sICAM-1) and the onset of organ failure in septic patients. Among 53 patients with sepsis, 40 developed organ dysfunction while 13 did not. Among the 40 septic patients with organ dysfunction, 15 died of multiple organ failure and the others survived. In these septic patients, we measured sICAM-1, interleukin-6 (IL-6), polymorphonuclear leukocyte elastase (PMN-E), thrombomodulin (TM) and endothelin-1 (ET-1). The data presenting a maximum sICAM-1 level in the cases with sepsis alone were compared to the levels in septic patients with or dysfunction on the day of organ dysfunction onset. The relationships between sICAM-1 and IL-6, sICAM-1 and PMN-E, sICAM-1 and TM, and sICAM-1 and ET-1, from the same samples, were also examined. The mean levels of sICAM-1 on the day of organ dysfunction onset were significantly higher (1, 040.3±495.7ng/m) than the maximum level of sICAM-1 in septic patients without organ dysfunction (440.2±232.7ng/ml) (p<0.001). Furthermore, the sICAM-1 levels tended to increase gradually, from the onset of sepsis, until the development of organ dysfunction. There was no correlation between sICAM-1 and IL-6, or between sICAM-1 and PMN-E. In contrast, a positive correlation was recognized between sICAM-1 and the vascular endothelial damage markers such as TM and sICAM-1 (p<0.01). From these results, we speculated that sICAM-1 levels, which increase reflecting endothelial damage, may serve as an indicator of septic organ dysfunction. In conclusion, circulating levels of sICAM-1, which reflect vascular endothelial damage, increase in sepsis with organ dysfunction. Furthermore, the sICAM-1 level may serve as an indicator of the severity of sepsis and thereby facilitate estimating the onset of organ dysfunction.

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