Fluid Management, Intra-Abdominal Hypertension and the Abdominal Compartment Syndrome: A Narrative Review

Abstract

Background: General pathophysiological mechanisms regarding associations between fluid administration and intra-abdominal hypertension (IAH) are evident, but specific effects of type, amount, and timing of fluids are less clear.

Objectives: This review aims to summarize current knowledge on associations between fluid administration and intra-abdominal pressure (IAP) and fluid management in patients at risk of intra-abdominal hypertension and abdominal compartment syndrome (ACS).

Methods: We performed a structured literature search from 1950 until May 2021 to identify evidence of associations between fluid management and intra-abdominal pressure not limited to any specific study or patient population. Findings were summarized based on the following information: general concepts of fluid management, physiology of fluid movement in patients with intra-abdominal hypertension, and data on associations between fluid administration and IAH.

Results: We identified three randomized controlled trials (RCTs), 38 prospective observational studies, 29 retrospective studies, 18 case reports in adults, two observational studies and 10 case reports in children, and three animal studies that addressed associations between fluid administration and IAH. Associations between fluid resuscitation and IAH were confirmed in most studies. Fluid resuscitation contributes to the development of IAH. However, patients with IAH receive more fluids to manage the effect of IAH on other organ systems, thereby causing a vicious cycle. Timing and approach to de-resuscitation are of utmost importance, but clear indicators to guide this decision-making process are lacking. In selected cases, only surgical decompression of the abdomen can stop deterioration and prevent further morbidity and mortality.

Conclusions: Current evidence confirms an association between fluid resuscitation and secondary IAH, but optimal fluid management strategies for patients with IAH remain controversial.

Keywords: abdominal compartment syndrome; abdominal hypertension; colloids; crystalloids; fluid therapy; hypertonic; maintenance; open abdomen; resuscitation; sepsis.

Figure 1

The four hits of shock. Graph showing the four-hit model of shock with evolution of patients’ cumulative fluid volume status over time during the five distinct phases of resuscitation: Resuscitation (R), Optimization (O), Stabilization (S), and Evacuation (E) (ROSE), followed by a possible risk of Hypoperfusion in case of too aggressive de-resuscitation. On admission patients are hypovolemic, followed by normovolemia after fluid resuscitation (EAFM, early adequate fluid management), and possible fluid overload, again followed by a phase going to normovolemia with late conservative fluid management (LCFM) and late goal directed fluid removal (LGFR) or de-resuscitation. In the case of hypovolemia, O₂ cannot get into the tissue because of convective problems; in the case of hypervolemia, O₂ cannot get into the tissue because of diffusion problems related to interstitial and pulmonary edema, gut edema (ileus and abdominal hypertension). Adapted according to the Open Access CC BY License 4.0 from Malbrain et al., with permission [17].

Figure 2

Flowchart of literature review and selection of included publications.

Figure 3

The vicious cycle of fluid resuscitation, abdominal hypertension and kidney injury. Adapted according to the Open Access CC BY License 4.0 from Malbrain et al., with permission [17]. AKI: acute kidney injury; IAH: intra-abdominal hypertension.

Figure 4

Fluid movement in normal conditions (A) and abdominal hypertension (B). The physiological movement of fluid is determined by the imbalance between hydrostatic and colloid osmotic pressures. It is best described by the revised Starling equation: J_v = L_pA[(P_c − P_i) − σ(II_c − II_i)], where J_v is net fluid filtration, L_p the capillary hydraulic permeability, A the capillary surface area (which is available for fluids and small molecule filtration), σ the capillary reflection coefficient, P_c the capillary hydrostatic pressure, P_i the interstitial hydrostatic pressure, II_c and II_i the capillary and interstitial colloid osmotic pressures, respectively. Generally, P_c dependent on the differences between the arteriole hydrostatic pressure (P_A) and the venule hydrostatic pressure (P_V). This difference strongly corresponds to the hydraulic resistances in arterioles and venule (R_A and R_V, respectively), which was described by the Pappenheimer Soto-Riviera Equation: P_c = (P_v [R_A/R_V] + P_A)/(1 + [R_A/R_V]). According to this equation, every increase in P_A or P_V, as well as an increase in R_A/R_V (e.g., following intra-abdominal hypertension leading to venous congestion) or increase P_c. Under normal physiological conditions, the sub-glycocalyx colloid osmotic pressure strongly corresponds to interstitial pressure and its value ranges between 70% and 90% of the interstitial colloid pressure. Adapted from Levick et al. [133].

Figure 4

Fluid movement in normal conditions (A) and abdominal hypertension (B). The physiological movement of fluid is determined by the imbalance between hydrostatic and colloid osmotic pressures. It is best described by the revised Starling equation: J_v = L_pA[(P_c − P_i) − σ(II_c − II_i)], where J_v is net fluid filtration, L_p the capillary hydraulic permeability, A the capillary surface area (which is available for fluids and small molecule filtration), σ the capillary reflection coefficient, P_c the capillary hydrostatic pressure, P_i the interstitial hydrostatic pressure, II_c and II_i the capillary and interstitial colloid osmotic pressures, respectively. Generally, P_c dependent on the differences between the arteriole hydrostatic pressure (P_A) and the venule hydrostatic pressure (P_V). This difference strongly corresponds to the hydraulic resistances in arterioles and venule (R_A and R_V, respectively), which was described by the Pappenheimer Soto-Riviera Equation: P_c = (P_v [R_A/R_V] + P_A)/(1 + [R_A/R_V]). According to this equation, every increase in P_A or P_V, as well as an increase in R_A/R_V (e.g., following intra-abdominal hypertension leading to venous congestion) or increase P_c. Under normal physiological conditions, the sub-glycocalyx colloid osmotic pressure strongly corresponds to interstitial pressure and its value ranges between 70% and 90% of the interstitial colloid pressure. Adapted from Levick et al. [133].

Figure 5

Potential use of POCUS according to WSACS medical management algorithm.