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PubMed1992

Preventable complications and death from multiple organ failure among geriatric trauma victims.

We reviewed 374 consecutive trauma patients over age 65 years to determine (1) if the emergency room Trauma Score (TS) could predict mortality, thereby improving ICU triage, and (2) the frequency of preventable complications in patients who died (n = 31). Fifty-two percent of deaths (n = 16) occurred in patients with TS = 15 or 16. Multiple organ failure/sepsis (MOF/S) was the most common cause of death overall (42%) and was also the most frequent cause of death in patients with a TS = 15-16 (63%). Nonsurvivors in the TS = 15-16 subgroup were older (80.9 +/- 2.0 vs. 74.9 +/- 0.5 years, p less than 0.02) and had greater ISSs (15.8 +/- 3.7 vs. 8.0 +/- 0.4, p = 0.001) than survivors. Patients with a TS less than 15 suffered high overall mortality (45%). Preventable complications contributed to mortality in 32% of all deaths and in 62% of MOF/S deaths. Aggressive care to prevent avoidable complications may improve survival in elderly trauma victims.

Age Factors↗
PubMed1999

Limitations of nutrient intake. The effect of stressors: trauma, sepsis and multiple organ failure.

The response to injury includes a diminution in appetite, a decrease in nutrient intake, an acute mobilisation of endogenous energy stores (glucose and fat), but an impaired ability to use them. Lean tissue is broken down to its constituent amino acids, which provide precursors for the synthesis of glucose in the liver (gluconeogenesis). Glucose is used as a source of energy by the brain and red blood cells, as well as by wound tissue. After a discrete injury normal function is normally resumed with a reduced body mass. In very severe injury or sepsis, in those who are physiologically or immunologically impaired or those with a genetic predisposition to the condition, organ failure may develop due to an apparent ongoing inflammatory process. The origin of this process is not always apparent, but loss of integrity of the gastrointestinal tract has been suggested. Apparently adequate nutritional support in the presence of a severe inflammatory stimulus only attenuates the gluconeogenic process, and the breakdown of lean tissue continues. Supply of protein (amino acids) stimulates protein synthesis, but it also stimulates breakdown. Nutrient intake via the enteral route may be limited by gastrointestinal symptoms and via the parenteral route by fluid overload, although this can be circumvented by fluid removal by haemofiltration. It is probable that, if nutritional support in severe trauma/sepsis/multiple organ failure is to be effective, satisfactory pharmacological methods of controlling metabolism will have to be found.

Appetite↗
PubMed1998

Cytokine patterns in patients who undergo hemofiltration for treatment of multiple organ failure.

The excessive uncontrolled activation of inflammatory cells and mediators after trauma or major surgery plays a key role in the development of adult respiratory distress syndrome and multiple organ system failure (MOSF). In the past elevated cytokine levels were shown to influence the outcome of these patients adversely. There are diverging results regarding the removal of circulating cytokines by various methods of hemopurification for clinical improvement of MOSF. Seven patients after trauma or major surgery underwent continuous venovenous hemofiltration (CVVH) for the treatment of severe organ failure of the heart and lungs (Murray score 2.74) but not for renal or liver failure. The cytokine levels were measured at the beginning and 15, 60, 120, and 240 minutes after initiation of CVVH (measure points MP1-5). Clinical improvement during the treatment was monitored, and correlation with cytokine levels was evaluated. Arterially measured tumor necrosis factor alpha rose from 11.14 ng/ml to 17.86 ng/m1 (p < 0.05). Arterial interleukin-6 (IL-6) levels significantly decreased during CVVH from 1284.7 ng/m1 to 557.9 ng/m1; IL-8 levels simultaneously decreased from an initial peak of up to 154.4 ng/m1 at MP3 to 97.3 ng/m1 at MP5. The drop in serum IL-6 and IL-8 levels closely correlated with clinical improvement. After 2 hours of CVVH the hemodynamic situation improved significantly, as revealed by a decrease in catecholamine expenditure, an increase in arterial pressure, and a decrease in pulmonary artery pressure. Moreover, 2 hours after the initiation of CVVH the oxygenation index rose significantly and correlated well with the drop in shunt fraction. The Murray score significantly fell to 1.86. The removal of IL-6 and IL-8 by CVVH after initial stimulation correlates with clinical improvement, which was demonstrated by significantly improved oxygenation and hemodynamics from 2 hours after the initiation of CVVH onward. The elimination of cytokines and several mediators by CVVH may contribute to the cardiopulmonary improvement of critically ill patients. In comparison with the clinical control group (n = 7), which was comparable in terms of MOSF, no intervention led to a similar improvement in cardiorespiratory failure, and overall two of these patients died. Moreover, patients of the control group experienced a significant longer stay at in the intensive care unit.

Adult↗
PubMed1998

Microvascular changes explain the "two-hit" theory of multiple organ failure.

OBJECTIVE: The objective was to determine intestinal microvascular endothelial cell control after sequential hemorrhage and bacteremia. SUMMARY BACKGROUND DATA: Sepsis that follows severe hemorrhagic shock often results in multiple system organ failure (MSOF) and death. The sequential nature of this clinical scenario has led to the idea of a "two-hit" theory for the development of MSOF, the hallmark of which is peripheral vasodilation and acidosis. Acute bacteremia alone results in persistent intestinal vasoconstriction and mucosal hypoperfusion. Little experimental data exist to support the pathogenesis of vascular dysregulation during sequential physiologic insults. We postulate that hemorrhagic shock followed by bacteremia results in altered microvascular endothelial cell control of dilation and blood flow. METHODS: Rats underwent volume hemorrhage and resuscitation. A sham group underwent the vascular cannulation without hemorrhage and resuscitation, and controls had no surgical manipulation. After 24 and 72 hours, the small intestine microcirculation was visualized by in vivo videomicroscopy. Mean arterial pressure, heart rate, arteriolar diameters, and A1 flow by Doppler velocimetry were measured. Endothelial-dependent dilator function was determined by the topical application of acetylcholine (ACh). After 1 hour of Escherichia coil bacteremia, ACh dose responses were again measured. Topical nitroprusside was then applied to assess direct smooth muscle dilation (endothelial-independent dilator function) in all groups. Vascular reactivity to ACh was compared among the groups. RESULTS: Acute bacteremia, with or without prior hemorrhage, caused significant large-caliber A1 arteriolar constriction with a concomitant decrease in blood flow. This constriction was blunted at 24 hours after hemorrhage but was restored to control values by 72 hours. There was a reversal of the response to bacteremia in the premucosal A3 vessels, with a marked dilation both at 24 and 72 hours. The sequence of hemorrhage and E. coli resulted in a progressive enhanced reactivity to the endothelial-dependent stimulus of ACh in the A3 vessels at 24 and 72 hours. Reactivity to endothelial-independent smooth muscle relaxation and subsequent vessel dilation was similar for all groups. CONCLUSIONS: These data indicate that there is altered endothelial control of the intestinal microvasculature after hemorrhage in favor of enhanced dilator mechanisms in premucosal vessels with enhanced constrictor forces in inflow vessels. This enhanced dilator sensitivity is most evident in small premucosal vessels. This experimental finding supports the premise that an initial pathophysiologic stress alters the subsequent microvascular blood flow responses to systemic inflammation. These changes in the intestinal microcirculation are in concert with the "two-hit" theory for MSOF.

Acute Disease↗