Abstract
BackgroundIntra-abdominal hypertension and abdominal compartment syndrome contribute significantly to increased morbidity and mortality in critically ill patients. This study describes pathophysiologic effects of the acutely elevated intra-abdominal pressure on microvascular fluid exchange and microcirculation. The resulting changes could contribute to development of organ dysfunction or failure.Methods16 pigs were randomly allocated to a control-group (C-group) or an interventional group (P-group). After 60 min of stabilization, intra-abdominal pressure of the P-group animals was elevated to 15 mmHg by Helium insufflation and after 120 min to a level of 30 mmHg for two more hours. The C-group animals were observed without insufflation of gas. Laboratory and hemodynamic parameters, plasma volume, plasma colloid osmotic pressure, total tissue water content, tissue perfusion, markers of inflammation and cerebral energy metabolism were measured and net fluid balance and fluid extravasation rates calculated. Analysis of variance for repeated measurements with post-tests were used to evaluate the results with respect to differences within or between the groups.ResultsIn the C-group hematocrit, net fluid balance, plasma volume and the fluid extravasation rate remained essentially unchanged throughout the study as opposed to the increase in hematocrit (P < 0.001), fluid extravasation rate (P < 0.05) and decrease in plasma volume (P < 0.001) of the P-group. Hemodynamic parameters remained stable or were slightly elevated in the C-group while the P-group demonstrated an increase in femoral venous pressure (P < 0.001), right atrial pressure (P < 0.001), pulmonary capillary wedge pressure (P < 0.01) and mean pulmonary arterial pressure (P < 0.001). The protein mass decreased in both study groups but was significantly lower in the P-group as compared with the C-group, after 240 min of intervention. The increased intra-abdominal pressure was associated with elevated intracranial pressure and reduced tissue perfusion of the pancreas and the gastric- and intestinal mucosa.ConclusionElevation of intra-abdominal pressure has an immediate impact on microvascular fluid extravasation leading to plasma volume contraction, reduced cardiac output and deranged perfusion of abdominal organs.
Highlights
Intra-abdominal hypertension and abdominal compartment syndrome contribute significantly to increased morbidity and mortality in critically ill patients
Mean arterial pressure (MAP) remained essentially stable with no between-group differences during the study
Results as means with SD in parentheses; Control group: C-group; Intervention group: P-group; *:P
Summary
Intra-abdominal hypertension and abdominal compartment syndrome contribute significantly to increased morbidity and mortality in critically ill patients. Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are known to affect morbidity and mortality in the critically ill patient [1,2]. Depending on the patient populations, the incidence of IAH has been reported in the range of 32-50% [2,3,4]. The occurrence of ACS varies among specific groups of patients, with an incidence found to be around 4% in a general medical-surgical population [2,5]. The underlying pathophysiological mechanisms are not fully understood, but are frequently related to an increase in the intra-abdominal volume resulting in a shift to the steeper part of the abdominal pressure-volume curve. A reduction in abdominal wall compliance could lead to the same result. The condition may follow massive fluid resuscitation, as in sepsis or burn injuries, leading to increased extravasation of fluid from the vascular to the interstitial space and edema formation [8]
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