ACS is a poorly appreciated complication of increased IAP. Trauma, surgery, and certain medical conditions can be the culprit. Prolonged, unrelieved elevation of IAP can produce pulmonary compromise, renal impairment, cardiac failure, central nervous dysfunction, shock, and death [1–6].
The adverse physiologic effects of ACS can be divided into systemic and local effects [1–3]. The systemic hemodynamic effects are very complex in nature. Usually, the patient manifests low cardiac output and high systemic vascular resistance in the context of high central venous and pulmonary capillary wedge pressure. Increased IAP reduces venous return and increases intra-thoracic pressure, with impairment of ventricular compliance. In effect, there will be decreased stroke volume and low cardiac output, with compensatory increase in peripheral vascular resistance. Also, there is a reduction in both static and dynamic compliance of the lungs and perfusion of the kidneys, as well as of other retroperitoneal and intraperitoneal organs, except for the adrenals. High intra-thoracic pressure interferes with cerebral venous return, with decreased cerebral perfusion leading to brain dysfunction. On the other hand, local effects of ACS are probably best reflected by wound dehiscence secondary to direct pressure on the wound, as well as interference with local blood supply.
The incidence of ACS varies between 15 and 38% of all surgical patients admitted to intensive care units [2,9]. A high index of suspicion is imperative for optimal outcome. If not recognized and treated in timely manner, ACS can result in multiorgan system failure and death. Animal studies have shown that IAP higher than 20 mmHg results in abdominal compartment syndrome [4,5,8]. The adverse effects are reversible with the relief of pressure, if done at the proper time. Several clinical reports [1–3,6,7,9–16] have emphasized the importance of early recognition of this syndrome.
Traditionally, IAP has been measured indirectly through the urinary bladder using a Foley catheter. This technique was adopted to avoid direct invasive techniques, and was subsequently popularized by Kron et al  in 1984. Those authors measured IAP in 17 postoperative patients using the technique described above under Materials and methods. Ten patients had IAP of 10–15 mmHg. None of them developed renal insufficiency. In contrast, seven patients had IAP of more than 25 mmHg and had a drop in urine output. Three patients were not explored and died of acute renal failure. The other four patients were explored and had a prompt diuresis. However, two of the four succumbed later to sepsis. Kron et al concluded that, in the early postoperative period, IAP higher than 25 mmHg requires re-exploration and decompression of the abdomen.
Iberti et al  in 1987 conducted another study in a canine model. IAP was established by infusing warm saline in 500 cc increments, to total of 5 l. IAPs were measured using a separate transducer through the abdominal wall. Simultaneously, the bladder pressures were measured through a transuretheral catheter after a 5-min equilibration period. As opposed to the technique described by Kron et al , Iberti et al did not prime the Foley catheter with sterile saline. Pressures obtained through the bladder were not significantly different from the abdominal pressures, and therefore those authors concluded that the bladder could be used to measure the actual IAP accurately .
These results could not be reproduced at the range of IAPs generated in our study. We were limited by IAP of 15 mmHg, because it would not be ethical to subject our patients to ACS for the sake of the study. Accepting this limitation, and realizing that abdomen–bladder relationship might or might not differ at higher pressures, we identified the following interesting findings: (1) The urinary bladder had a higher baseline pressure than the abdomen in every patient compared. This may be related to the intrinsic detrusor muscle activity that might have been stimulated by the infused volume, rate of infusion, or even the temperature of the saline used to prime the Foley catheter. (2) On an individual basis, pressures measured across the bladder wall were not similar, but had high positive correlation coefficients. Although the lines generated by the data points were parallel, they were not identical. Also, there was a wide range of interception (-3.2 to -30.5) and a variable regression coefficient (1.0–3.1). This variability might be explained by the first finding, above. (3) Global analysis of the data from all patients showed a weak correlation between pressures measured across the bladder wall. This might be related to the biologic variation between our study subjects with regard to age, sex, weight, height, body mass index, or even history of pregnancy in females.
These findings eliminated our ability to predict IAP using ICP, and raise the question of other as yet unknown variables that may play an important role in determining the relationship between the abdominal cavity and the urinary bladder.