Compartment Syndrome of the Abdominal Cavity
Ajai K. Malhotra
Rao R. Ivatury
Abdominal Compartment Syndrome
Introduction
The association of elevated intra-abdominal pressure (IAP) and organ system dysfunction was described as early as the mid-nineteenth century [1]. However, the acceptance of this association as a distinct nosologic entity—abdominal compartment syndrome (ACS)—happened only in the late twentieth century. Even now, more than 20 years after the phrase was coined by Kron et al. [2], there is disagreement as to whether ACS is a distinct clinicopathologic entity in which the organ system dysfunction is causally related to the elevation in IAP or whether the elevated IAP is merely an epi-phenomenon observed in some critically ill patients, especially those receiving large volume crystalloid resuscitation [3]. The reasons for this are many and include (1) the variability of normal IAP [4], (2) lack of agreement as to the best method of measuring IAP [5], (3) lack of agreement about the level of IAP that is well tolerated and any elevation beyond which leads to pathologic consequences in the form of organ system dysfunction (Fig. 152.1) [6], (4) lack of agreement as to when intervention is necessary—in the prodromal phase to prevent development of organ system dysfunction or only after there is evidence of organ system dysfunction [7], and (5) the ideal intervention. These reasons not withstanding, the sheer volume of literature published about all aspects of this condition over the last two decades has reduced the army of skeptics to a corporal’s guard. The current chapter focuses on the current understanding of ACS and attempts to provide a practical approach to the diagnosis, and management of this potentially devastating condition.
 Figure 152.1. The continuum of normal intra-abdominal pressure to intra-abdominal hypertension (IAH). As the level of IAH increases organ dysfunction appears and the condition is called abdominal compartment syndrome. Note that the boundaries of normal IAP/IAH and IAH/ACS are wavy (grey zone). These boundaries are different in different individuals and also under different physiological state in the same individual. |
The abdominal cavity is a space defined partly by rigid and inflexible structures—pelvis, spine, and coastal arches—and partly by more flexible structures—the musculoaponeurotic abdominal wall and the diaphragm. The total volume that can be accommodated within the confines of the abdomen is limited by these anatomical boundaries. Whenever there is a discrepancy between the available space, defined by the anatomical limits of the abdominal cavity, and the sum total volume of intra-abdominal structures—fluids and intra-abdominal organs—the pressure within the abdominal cavity tends to rise. This situation may arise from any condition that leads to increase in the total volume of structures—accumulation of fluid or swelling of organs—or decreased space—vigorous muscle contraction, loss of domain, etc. Initially the discrepancy is well tolerated by stretching of the flexible boundaries. However, as the limits of this accommodation are reached, even small increments in the intra-abdominal volume lead to large increases in IAP [6]. The elevated IAP affects organ system function in multiple ways. In the initial stages there is a purely mechanical effect best observed in the respiratory system, with embarrassment of ventilation due to elevation of the diaphragm, and in the kidneys where there is a fall in the glomerular filtration pressure affecting renal function. As the IAP continues to rise, there is decreased venous return to the heart affecting cardiac function and resulting in decreased cardiac output (CO). This reduction in CO has profound effects on every cell within the body as it globally decreases tissue perfusion. Finally, there is evidence that the elevated IAP in and of itself acts as a potent pro-inflammatory stimulus augmenting the systemic inflammation already set in motion by (1) the primary process that initiated the elevation of IAP and (2) tissue hypoperfusion caused by the diminished CO.
 Figure 152.2. Effect of increasing intra-abdominal pressure on cardiac output (CO), hepatic artery flow (HA), superior mesenteric artery flow (SMA), and gastrointestinal mucosal flow (mucosa). Note that the splanchnic and mucosal flows start to decrease even at fairly low levels of intra-abdominal hypertension and even when global CO has not been affected. |
Definitions
As already mentioned earlier, there are no uniformly accepted definitions of the terms used in the context of ACS. Often, ACS and elevated IAP are used interchangeably, and the units of pressure measurement vary between mm Hg and cm H2O. At the first World Congress on Abdominal Compartment Syndrome held at Noosa, Australia, in December 2004, attempts were made to develop consensus definitions of these terms and also to standardize the units and methodology used for measuring IAP. The definitions that follow are those that were developed at that conference and are used throughout the chapter. The units used are mm Hg unless otherwise specified. The method used to measure IAP, unless otherwise specified, is by the well-described technique of measuring bladder pressure, where the level of the pubic symphysis is considered 0 mm Hg [8].
Normal IAP: IAP varies between subatmospheric to a mean of 6.5 mm Hg [4]. It is affected by body habitus (chronically elevated in morbid obesity) [4], phase of respiration (higher during inspiration), and body position (elevated in the erect position) [5].
Consensus definition : IAP to be considered normal should be measured in the supine position, at end expiration and should have a value < 10 mm Hg [7].
Elevated IAP—intra-abdominal hypertension (IAH): Brief elevations of IAP are fairly common and seen during sneezing, coughing etc and are of little clinical significance. Even in critically ill patients, brief elevations maybe observed during changes in body positions etc and are likewise clinically unimportant [4]. For IAP to be considered elevated, in a clinically significant fashion the elevation has to be sustained. The value at which IAP is considered elevated is a matter of debate; however, since alterations in physiology maybe observed even at relatively mild elevations to about 12 mm Hg, this value is the one supported by consensus.
Consensus definition : IAH should be defined as peak measured IAP of ≥12 mm Hg on two measurements 1 to 6 hours apart [7].
ACS: The point at which IAH develops into ACS remains controversial. Although it is generally agreed that ACS is the association of IAH, causing one or more organ system dysfunction, how the organ system dysfunction should be identified is not as well defined. When very sensitive and often invasive measures of organ system dysfunction are used, even minor elevations of IAP have been shown to affect function (Fig. 152.2) [9]. Also organ system function maybe affected at a certain IAP in one individual whereas the same level of IAP may not significantly alter organ system function in another individual [4]. Second, the level of IAH that is well tolerated can be different under differing physiologic states even in the same individual. For example, the threshold at which IAH leads to organ system dysfunction is significantly lowered posthemorrhagic shock as compared with baseline conditions [10]. Last, there is evidence that primary ACS (caused by an intra-abdominal pathology—see later) is less well tolerated than secondary ACS [11] (caused by resuscitation in the absence of significant intra-abdominal pathology—see below).
Consensus definition : ACS should be diagnosed in the presence of (1) peak IAP of ≥20 mm Hg on two measurements 1 to 6 hours apart and (2) one or more organ system failure that was not previously present as defined by sequential organ failure assessment (SOFA) score of ≥3 (or an equivalent scoring system) [7].
Types of ACS: Initially ACS was described after intra-abdominal catastrophe—traumatic or inflammatory—and termed primary ACS [2]. More recently, it has been recognized that ACS can also develop in the absence of abdominal injury/pathology. This is usually observed in patients requiring massive volume resuscitation for any form of shock, usually traumatic or septic. It is believed that this form of ACS, termed secondary ACS, is due to leakage of fluid from within the capillaries resulting in massive edema of the intra-abdominal organs causing increased volume [11,12]. At times, the two conditions may coexist as in a patient with an intra-abdominal injury/pathology who during the recovery phase develops pneumonia and sepsis resulting in leaky capillaries. Recurrent ACS may be observed following therapy for either primary or secondary ACS, and this has been called tertiary ACS [13]. Finally, a very early hyperacute form of secondary ACS has been recognized that develops while repair of extra-abdominal injuries is being carried out simultaneous with massive volume resuscitation required for the hemorrhagic shock produced by the extra-abdominal injury [11]. Previously, hyperacute ACS was used to describe physiologic, transient, clinically insignificant elevations of IAP observed during sneezing, coughing, etc [14].
Consensus definitions
Primary ACS: Primary ACS is defined as ACS developing in a person where the proximate cause of the ACS is intra-abdominal/pelvic pathology that usually requires abdominal surgery and/or angio-radiologic intervention. The pathology may be traumatic, and/or inflammatory in nature [7].
Secondary ACS: Secondary ACS is defined as ACS developing due to increased volume of intra-abdominal contents from accumulation of fluid and/or visceral swelling, and where the proximate cause of the increase in volume is not any intra-abdominal/pelvic pathology requiring abdominal surgery and/or angio-radiologic therapy. Secondary ACS is usually observed during massive volume resuscitation for major nonabdomino/pelvic injuries, burns, severe acute pancreatitis, septic shock from a nonabdomino/pelvic infective source, etc [7].
Tertiary ACS: Tertiary ACS solely refers to ACS that develops or persists despite previous attempts to prevent or treat primary or secondary ACS [7].
Hyperacute ACS: The term should be reserved for a very early form of secondary ACS that develops while surgical and/or angio-radiologic control of an injury is being carried out simultaneous with massive volume resuscitation for the shock caused by the same injury [11].
 Figure 152.3. Effect of abdominal compartment syndrome on various body systems. |
Impact of ACS on the Body
ACS has profound and far reaching effects on every major organ system of the body (Fig. 152.3). As mentioned earlier, these effects are related to (i) the mechanical pressure caused by IAH, (ii) the reduced perfusion to the tissues caused by diminished CO, and (iii) ACS amplifying the systemic inflammatory response already in motion due to the primary pathology, its treatment and tissue hypoperfusion.
Cardiovascular Effects
ACS affects each of the three determinants of cardiac function—preload, contractility, and afterload. IAH leads to compression of the inferior vena cava decreasing venous return from the lower half of the body [15]. In addition, elevated IAP raises the diaphragm leading to increased intrathoracic pressure, further impeding venous return to the heart [16]. Paradoxically, the central venous and the pulmonary capillary wedge pressures actually rise leading to a dissociation between the commonly used measures of cardiac filling and true cardiac end diastolic volumes. This increase in the filling pressure is merely the transmission of increased intrathoracic pressure to the measured intravascular pressure and not a true reflection of intravascular volume and cardiac filling [17]. Other techniques that directly measure cardiac end diastolic volumes tend to give a more accurate picture of cardiac filling [18]. The decreased venous return and cardiac filling negatively impact cardiac contractility. In addition, ACS directly leads to a decrease in ventricular compliance further affecting cardiac filling and contractility [15]. The effects of elevated intrathoracic pressures are more prominent on the right ventricle. Normally the right ventricle acts more as a conduit than as a pump. The elevated intrathoracic pressures however lead to an increase in pulmonary vascular resistance due to direct compression of the lung parenchyma leading to an increase in right-sided afterload. To overcome this increased right-sided afterload, the right ventricle has to play a more active role if left ventricular filling is to be maintained [19]. Last, ACS leads to an increase in systemic vascular resistance—left-sided afterload—that initially may cause the mean arterial pressure to rise; however, as the CO continues to fall, the net result is a lowering of systemic blood pressure, further compromising perfusion [20]. The diminution in CO can be partially ameliorated by volume loading [15,16,20]. However, for a sustained improvement in systemic perfusion, the ACS needs to be treated usually by abdominal decompression.
Respiratory Effects
The direct mechanical effect of elevated IAP results in the diaphragm moving cephalad into the chest [21]. This results in a reduction in minute ventilation leading to hypercarbia and
respiratory acidosis. The compressive effect also leads to an increase in pulmonary closing volume and decrease in functional residual capacity and lung compliance [16]. The effect of these later changes is a mismatch between ventilation and perfusion and increased right to left shunting causing hypoxia. Clinically the earliest observed change is an increase in peak airway pressure, or if the patient is on a pressure limited ventilatory mode, a decrease in tidal volume [16]. If the ACS is not treated at this stage, the full effects on the respiratory system are observed with hypoxia, hypercarbia, and respiratory acidosis [16]. The hypoxia caused by the respiratory system effects adds to the tissue hypoxia produced by the diminished tissue perfusion due to the cardiovascular effects of ACS.
respiratory acidosis. The compressive effect also leads to an increase in pulmonary closing volume and decrease in functional residual capacity and lung compliance [16]. The effect of these later changes is a mismatch between ventilation and perfusion and increased right to left shunting causing hypoxia. Clinically the earliest observed change is an increase in peak airway pressure, or if the patient is on a pressure limited ventilatory mode, a decrease in tidal volume [16]. If the ACS is not treated at this stage, the full effects on the respiratory system are observed with hypoxia, hypercarbia, and respiratory acidosis [16]. The hypoxia caused by the respiratory system effects adds to the tissue hypoxia produced by the diminished tissue perfusion due to the cardiovascular effects of ACS.
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