Contemporary measurement of IAP outside of the laboratory is accomplished by a variety of means. These include direct measurement of IAP by means of an intra-peritoneal catheter, as is done during laparoscopy. Bedside measurement of IAP has been accomplished by transduction of pressures from indwelling femoral vein, rectal, gastric, and urinary bladder catheters. Of these methods, measurement of urinary bladder and gastric pressures are the most common clinical applications [8,9,10,11,12]. In 1984 Kron et al [8] reported a method by which to measure IAP at the bedside with the use of an indwelling Foley catheter Sterile saline (50-100cm³) is injected into the empty bladder through the indwelling Foley catheter. The sterile tubing of the urinary drainage bag is cross-clamped just distal to the culture aspiration port. The end of the drainage bag tubing is connected to the Foley catheter. The clamp is released just enough to allow the tubing proximal to the clamp to flow fluid from the bladder, then reapplied. A 16-gauge needle is then used to Y-connect a manometer or pressure transducer through the culture aspiration port of the tubing of the drainage bag. Finally, the top of the symphysis pubic bone is used as the zero point with the patient supine (Fig. 1).

An alternative bedside technique has been described in which intragastric pressure measurements are taken from an indwelling nasogastric tube. This method has been validated and found to vary within 2.5 cmH₂O of urinary bladder pressures [12]. Of these techniques, measurement of urinary bladder pressure appears to have gained widest clinical acceptance and application [9,13,14].

The terms intra-abdominal hypertension (IAH) and ACS have sometimes been used interchangeably. It is important to recognize the distinction between these entities. IAH exists when IAP exceeds a measured numeric parameter. This parameter has generally been set at between 20 and 25mmHg [10,13]. ACS exists when IAH is accompanied by manifestations of organ dysfunction, with reversal of these pathophysiologic changes upon abdominal decompression [9,10,13,14,15].

The adverse physiologic effects of IAH impact multiple organ systems. These include pulmonary, cardiovascular, renal, splanchnic, musculoskeletal/integumentary (abdominal wall), and central nervous system [9,13,14,15].

Elevated IAP has a direct effect on pulmonary function. Pulmonary compliance suffers with resultant progressive reduction in total lung capacity, functional residual capacity and residual volume [9]. This is manifested clinically by elevated hemidiaphragms on chest radiography. These changes have been demonstrated with IAP above 15mmHg [16]. Respiratory failure secondary to hypoventilation results from progressive elevation in IAP. Pulmonary vascular resistance increases as a result of reduced alveolar oxygen tension and increased intrathoracic pressures. Ultimately, pulmonary organ dysfunction is manifest by hypoxia, hypercapnia and increasing ventilatory pressure. Decompression of the abdominal cavity results in nearly immediate reversal of respiratory failure [9].

Elevated IAP is consistently correlated with reduction in cardiac output. This has been demonstrated with IAP above 20mmHg [17]. Reduction in cardiac output is a result of decreased cardiac venous return from direct compression of the inferior vena cava and portal vein. Increased intrathoracic pressure also results in reduced inferior and superior vena cava flow. Maximal resistance to vena cava blood flow occurs at the diaphragmatic caval hiatus. This is related to the abrupt pressure gradient between the abdominal and chest cavities. Elevated intrathoracic pressure causes cardiac compression and reduction in end-diastolic volume. Elevations in systemic vascular resistance result from the combined effect of arteriolar vasoconstriction and elevated IAP. These derangements result in reduced stroke volume that is only partly compensated for by increases in heart rate and contractility. The Starling curve is thus shifted down and to the right, and cardiac output progressively falls with increasing IAP [9,16,17]. These derangements are exacerbated by concomitant hypovolemia [3].

Increased intrapleural pressures resulting from transmitted intra-abdominal forces produce elevations in measured hemodynamic parameters. including central venous pressure and pulmonary artery wedge pressure (PAWP). Significant hemodynamic changes have been demonstrated with IAP above 20 mmHg [9,16]. Animal models have shown that approximately 20% of IAP is transmitted to the chest cavity from upward bulging of the hemidiaphragms [17]. Accurate prediction of end-diastolic filling pressures by means of equations that subtract a component of pleural pressure from PAWP have not been demonstrated to be consistently reliable, however [16,18]. Recent technologic advances have allowed measurement of right ventricular end-diastolic volumes by means of a rapid thermistor flow-directed pulmonary artery catheter. This technology has been shown to be a more accurate predictor of left ventricular end-diastolic volume and cardiac index than PAWP measurements [18,19]. The cardiovascular environment produced by elevated IAP may be more reliably discerned by reliance on this methodology for hemodynamic measurements.

Graded elevations in IAP are associated with incremental reductions in measured renal plasma flow and glomerular filtration rate. This results in a decline in urine output, beginning with oliguria at IAP of 15-20 mmHg and progressing to anuria at IAP above 30 mmHg [2,9,20]. The mechanism by which renal function is compromised by elevated IAP is multifactorial. Early investigations [2] pointed to elevated renal venous pressure as a means that is sufficient to account for renal insufficiency associated with IAH. Later investigators criticized these studies for failure to establish the effect of direct ureteral compression on renal dysfunction. Subsequent investigations showed no significant difference in renal dysfunction when ureteral stents were used in a subgroup of patients [20].

The adverse renal physiology associated with IAH is pre-renal and renal. Prerenal derangements result from altered cardiovascular function and reduction in cardiac output with decreased renal perfusion. Reduced cardiac output is not solely responsible for renal insufficiency associated with elevated IAP because correction of cardiac indices does not completely reverse impairment in renal function. Renal parenchymal compression produces alterations in renal blood flow secondary to elevated renal vascular resistance. This occurs by compression of renal arterioles and veins. Resistance changes have been measured with graded elevation in IAP. Renal vascular resistance ranges from 500% or greater at 20 mmHg to 1500% or greater at 40 mmHg, and is many times greater than simultaneously measured systemic vascular resistance [20].

The combined effect of prerenal and renal derangements produces progressive reduction in renal plasma flow and glomerular filtration. This results in elevated levels of circulating renin, antidiuretic hormone, and aldosterone, which further elevate renal and systemic vascular resistance. The result is azotemia with renal insufficiency and renal failure that is only partly correctable by improvement in cardiac output [2,9,20].

Splanchnic blood flow abnormalities that result from IAH are not limited to the kidneys. Impaired liver and gut perfusion have also been demonstrated with elevation in IAP. Severe progressive reduction in mesenteric blood flow has been shown with graded elevation in IAP from approximately 70% of baseline at 20 mmHg, to 30% at 40 mmHg. Intestinal mucosal perfusion as measured by laser flow probe has been shown to be impaired at IAP above 10 mmHg, with progressive reductions in flow corresponding to increased measured abnormalities in mesenteric perfusion. Metabolic changes that result from impaired intestinal mucosal perfusion have been shown by tonometry measurements that demonstrate worsening acidosis in mucosal cells with increasing IAH [21]. Similarly, measured abnormalities in intestinal oxygenation have been shown with elevations of IAP above 15mmHg. Impairment in bowel tissue oxygenation occurs without corresponding reductions in subcutaneous tissue oxygenation, indicating the selective effect of IAP on organ perfusion [22]. Not surprisingly, reductions in mesenteric flow have been shown to be greatly exacerbated in the setting of resuscitation after hemorrhagic shock [23].

Impaired bowel perfusion has been linked to abnormalities in normal physiologic gut mucosal barrier function, resulting in a permissive effect on bacterial translocation. This may contribute to later septic complications associated with organ dysfunction and failure [24].

Adverse effects of IAP on hepatic arterial, portal, and microcirculatory blood flow have also been shown with pressures above 20mmHg. A progressive decline in perfusion through these vessels occurs as IAP increases, despite cardiac output and systemic blood pressure being maintained at normal levels. Splanchnic vascular resistance is a major determinant in the regulation of hepatic arterial and portal venous blood flow. Elevated IAP can become the main factor in establishing mesenteric vascular resistance and ultimately abdominal organ perfusion [25]. These abnormalities are amplified in the setting of hypovolemia and hemorrhage, and are only partly correctable by physiologic and resuscitative improvements in cardiac output [21,22,23,24,25].

Although technically not a component of the abdominal cavity itself, the abdominal wall is also adversely impacted by elevations in IAP. Significant abnormalities in rectus muscle blood flow have been documented with progressive elevations in IAP. These perfusion abnormalities are roughly on par with changes in abdominal visceral perfusion with graded increases in IAP. Clinically, this derangement is manifest by complications in abdominal wound healing, including fascial dehiscence, and surgical site infection [26].

Elevations in intracranial pressure (ICP) have been shown in both animal and human models with elevated IAP. These pressure derangements have been shown to be independent of cardiopulmonary function and appear to be primarily related to elevations in central venous and pleural pressures. The exact mechanism of elevated ICP associated with IAH remains to be definitively elucidated, but appears to be a function of impaired cranial venous outflow. Elevated IAP has been demonstrated to coexist with obesity and increased abdominal girth. This is proposed as a chronic form of IAH and has been hypothesized as a mechanism for benign ICP, which is also referred to as pseudotumor cerebri. Abdominal decompression and weight loss via bariatric surgery have been shown to reverse benign ICP associated with IAH [9,27].

The exact incidence of ACS is yet to be established, but it is clearly increased in certain population groups. These include patients with severe blunt and penetrating abdominal trauma, ruptured abdominal aortic aneurysms, retroperitoneal hemorrhage, pneumoperitoneum, neoplasm, pancreatitis, massive ascites, and liver transplantation [14]. Massive fluid resuscitation, accumulation of blood and clot, bowel edema, and forced closure of a non-compliant abdominal wall are common factors among these patients [28]. Additionally, circumferential abdominal burn eschars cause extrinsic compression of the abdominal wall, leading to increases in IAP [9]. Among the trauma population, the group that is especially at risk includes those patients undergoing abbreviated or 'damage control' laparotomy, especially with intra-abdominal packing [9,28]. In one prospective series of 145 patients who were identified as being at risk for development of the ACS [10] the incidence was reported as 14%. The incidence following primary closure after repair of ruptured abdominal aortic aneurysm is reported in one series as 4% [9].

Risk factors for ACS are summarized in Table 1.

The ACS exists when IAH is associated with organ dysfunction that is reversible upon abdominal decompression. The patients at risk have been previously described. Organ dysfunction occurs in multiple systems, as previously mentioned.

Clinical manifestations of organ dysfunction include respiratory failure that is characterized by impaired pulmonary compliance, resulting in elevated airway pressures with progressive hypoxia and hypercapnia. Extremely high driving pressures may be required to maintain minimally sufficient tidal volumes, often with loss of delivered tidal volume by distension of ventilatory tubing. Some authors report pulmonary dysfunction as the earliest manifestation of ACS [14]. Chest radiography may show elevated hemidiaphragms with loss of lung volume [29].

Hemodynamic indicators include elevated heart rate, hypotension, normal or elevated PAWP and central venous pressure, reduced cardiac output and elevated systemic and pulmonary vascular resistance [9,29]. Measurement of right ventricular end-diastolic volume may be a more accurate predictor of a patient's position on the Starling curve [18,19].

Impairment in renal function is manifest by oliguria progressing to anuria with resultant azotemia. Renal insufficiency as a result of IAH is only partly reversible by fluid resuscitation. Renal failure in the absence of pulmonary dysfunction is not likely to be the result of IAH [14,29].

Elevated ICP is an additional clinical manifestation of ACS [29]. Clinical confirmation of IAH requires bedside measurements indicative of IAP. These techniques include transduction of gastric, rectal, and bladder pressures [8,11,12]. A technique for measurement of bladder pressure has been described by Kron et al [8] (discussed above). Experimental and clinical data indicate that IAH is present above an IAP of 20 mmHg [10,13].