Etiology

Many different causes of acutely elevated IAP pressure exist (table I). The ACS develops with acute and rapid (i.e., in hours) elevation in IAP. Chronic increases in intra-abdominal volume, as in morbidly obese patients, lead to a slower increase in IAP as the abdominal wall accommodates and becomes more compliant with time, the phenomenon of ‘stress-relaxation’(12). With this gradual increase, the various organ systems are able to compensate for the changes in IAP. Consequently, the acute deterioration seen with ACS does not occur in these patients. However, this is not to say that elevated IAP in these individuals is benign. The morbidity that occurs in these conditions (e.g., central obesity, and possibly pre-eclampsia/eclampsia) is at least in part due to the chronically elevated IAP (13–16).

Table I

Etiologies of elevated intra-abdominal pressure.

The ACS can develop in both non-surgical and surgical patients. Increases in retroperitoneal volume from pancreatitis, hemorrhage, or edema can lead to the ACS (17–20). This is most often reported after pelvic trauma (17), and elective or emergent aortic surgery (18–20). Increased intraperitoneal volume conditions are the most common source of elevated IAP. These include intraperitoneal hemorrhage, edema, bowel distention, mesenteric venous obstruction, abdominal packs, tense ascites, peritonitis, and tumor (21–28). Laparoscopy with CO₂-pneumoperitoneum also can have adverse effects on cardiopulmonary and renal function (29–33). Extrinsic compression of the abdomen can also lead to increases in IAP. Examples of this include burn eschars (34), pneumatic anti-shock garments (35, 36), tight abdominal closures (22, 23, 25), and repair of abdominal wall defects or large incisional hernias secondary to a “loss of the right of domain” (37–39, 40).

Though artificially categorized for clarity, in most critically ill patients IAH leading to ACS is multifactorial. Massive volume resuscitation for any reason (massive burns, severe pancreatitis, hemorrhagic shock, etc.) can lead to increased IAP, particularly in the postoperative period or in a patient with sepsis (41). This probably results from the effects of ‘capillary leak’, shock with ischemia-reperfusion injury and the release of vasoactive substances and oxygen-derived free radicals all combined with massive increases in total extracellular volume. These increase retroperitoneal and intraperitoneal visceral and vascular volume, leading to elevated IAP (41). Poor pulmonary compliance from acute lung dysfunction (requiring maximal positive pressure ventilation and high PEEP) can exacerbate existing elevations in IAP as the increased intrathoracic pressure is transmitted to the abdominal cavity (12, 42). The circulatory effects of increased IAP, combined with extracellular hypervolemia from massive volume resuscitation, may lead to abdominal wall edema and ischemia, reducing abdominal wall compliance and further accentuating the increase in IAP (41, 43). Thus, in critically ill patients, these factors are often additive, leading to or aggravating multi-system organ failure via a series of ‘vicious cycles’ perpetuated by progressive increases in IAP.

Measurement of intra-abdominal pressure

The key to recognizing ACS in a critically ill patient is the demonstration of elevated IAP. The pressure within the abdominal cavity is normally atmospheric or subatmospheric (i.e., negative) in a spontaneously breathing animal (2, 44–47), but mechanical ventilation produces a positive IAP near end-expiratory pressure with PEEP (42). IAP may be directly measured with an intraperitoneal catheter attached to a manometer or transducer (2, 43–47). The CO₂-insufflators for laparoscopy are used to increase and automatically measure IAP directly.

Indirect methods of estimating IAP are used clinically because direct measurements are not feasible or practical. These techniques include rectal, gastric, inferior vena caval and urinary bladder pressure measurement. Only the last three correlate with directly measured IAP in animal models (48).

Gastric pressure

IAP can be estimated by measuring pressure in the stomach. A nasogastric or gastrostomy tube can be used after instilling 50 to 100 ml of saline into the stomach (49, 50). Alternatively, an intragastric balloon filled with air can be used (51). A water manometer or a pressure transducer is attached to either of these and the midaxillary line is considered ‘zero’ (i.e., atmospheric pressure). While animal models show a poor correlation between gastric pressure and directly measured IAP (48), human studies show an acceptable correlation of gastric pressure with urinary bladder pressure (UBP) (50, 51). However, in one of these studies (Collee et al.) there were few individual measurements at severely elevated IAP, and the other study (Sugrue et al.) was limited to a maximum IAP of 20 mmHg during laparoscopy. Consequently, there may be a significant discrepancy between gastric pressure and UBP at the higher IAP's associated with fulminant ACS.

Inferior vena caval pressure

A femoral vein catheter can be used to measure pressure within the inferior vena cava. This correlates well with IAP measured directly and UBP in various animal models (48). However, this is often impractical, invasive, associated with significant risk (i.e., venous thrombosis), and no human studies have validated its use.

Urinary bladder pressure

This technique was first described by Kron et al. and involves placing a Foley catheter in the urinary bladder (9). The bladder is drained and then filled with 50 to 100 ml of sterile saline. The drainage tubing is clamped just beyond the aspiration port, and a 16-gauge needle connected to PE tubing is inserted into the port, or alternatively, a ‘three-way’ Foley catheter can be used with an adapter for the connection. The tubing can then be attached to a water manometer or pressure transducer, using the symphysis pubis as the zero reference point. This technique has been validated in animal studies showing a high degree of correlation with directly measured IAP (r = +0.85–0.98, p < 0.001) over a wide range of IAP up to 70 mmHg (fig. 1) (48, 52–53). Given this high degree of correlation at wide ranges of IAP, the ease of use, and minimal invasiveness of this technique, it is considered the ‘gold standard’ for indirect clinical measurement of IAP. However, a small, neurogenic bladder or intraperitoneal adhesions may make UBP unreliable at estimating IAP (17). Furthermore, a chronic increase in IAP secondary to central obesity, pregnancy or ascites may suggest an ACS when in fact none exists. The relationship between sagittal abdominal diameter (SAD) and an increased UBP has been previously described (14). This can be used as an approximation of the expected UBP in an obese patient to determine if there may be an acute increase in IAP above the predicated chronically increased IAP. This may be useful in the management of critically ill patients who have pre-morbid chronically elevated IAP.

Figure 1

Correlation between urinary bladder pressure and directly measured intra-abdominal pressure. A high degree of correlation has been shown between these two parameters in numerous animal models. Here the correlation in a porcine model of raised IAP is depicted. (more...)

Cardiovascular derangements

Classically, elevation in IAP leads to a reduction in cardiac output (CO) (2, 5, 7, 8, 21, 26, 29–32, 42, 49, 53–58). This effect is most consistently seen at an IAP > 20 mmHg. The diminished CO results from decreased inferior vena caval flow secondary to direct compression of the inferior vena cava and portal vein as well as from an increased thoracic pressure, which decreases both inferior and superior vena caval flow. The increased thoracic pressure also leads to cardiac compression with decreased ventricular end-diastolic volumes. Markedly increased systemic afterload is also seen with IAH. All of these lead to a reduced stroke volume with a compensatory increase in heart rate.

Venous return has been shown to be impaired at an IAP as low as 15 mmHg, decreasing with further increases in IAP (55–57). This occurs from increased venous resistance within the abdomen and thorax resulting in reduced caval and retroperitoneal venous flow (55). Maximal resistance to caval flow occurs at the suprahepatic, subdiaphragmatic inferior vena cava where the high-pressure zone of the abdomen meets the lower pressure zone of the thorax (59). However, at an IAP of 10–15 mmHg, venous return may actually be enhanced by the mobilization of blood from capacitance vessels within the abdomen (58). This may account for the slight increase in CO with small increases in IAP (54, 55). With IAH the ‘high pressure zone’ of the abdomen impairs lower-extremity venous outflow (60, 61). While there is no proven association between IAH and deep venous thrombosis, the use of intermittent pneumatic compression devices for prophylaxis has been shown to improve the reduced venous outflow during laparoscopy when this is evaluated by duplex imaging (62). Furthermore, markedly obese patients are at high risk for deep venous thrombosis and venous stasis bronze edema and/or ulcers (14).

Increased thoracic pressure and diaphragmatic elevation are responsible for reducing ventricular compliance (56). This combined with increased systemic afterload reduces cardiac contractility at IAP over 30 mmHg, shifting the Starling curve to the right and downward (55). At lower pressures this decrease in contractility is not seen and the changes in CO are related to decreased preload and increased afterload (63). The increase in systemic vascular resistance is secondary to the reduction in CO and direct arteriolar compression within the abdomen. Diaphragmatic elevation markedly elevates pleural pressure in animal models (12, 53, 64). This increase is transmitted to the heart and central veins, leading to spuriously elevated central venous pressure, pulmonary artery pressure, and pulmonary artery occlusion (‘wedge’) pressure combined with a reduced CO (fig. 2) (9, 13, 18, 40, 53). However, if the measured pleural pressure is subtracted from these, the ‘true’ (i.e., transarterial or transmural) pressures may actually decrease with IAH (53). If this is not taken into consideration the hemodynamic profile can be confused with biventricular failure. However, the ejection fraction is usually normal to slightly elevated and the presence of elevated IAP can be assessed by UBP. Also, improvement in CO with a saline fluid bolus may be therapeutic and clarify the situation.

Figure 2

Effects of increased intra-abdominal pressure on cardiac index (CI), pulmonary artery occlusion pressure (PAOP), and pleural pressure (PP). Increased PAOP (‘wedge’ pressure) with reduced CI characterizes the acute abdominal compartment (more...)

The hemodynamic effects of IAH are modified by several factors. Studies report a 17–53% decline in CO depending on volume status and anesthetic use. Hypovolemia (55, 57, 65) and inhalational anesthetics (57) tend to exacerbate the reduction in CO with increased IAP and their effects are additive (57), while volume expansion tends to minimize or even reverse this process (55). In fact, volume loading prior to abdominal decompression has been advocated by Morris et al. as a means of controlling hypotension often seen following an acute reduction in systemic vascular resistance caused by the dramatic reduction in IAP or from an ischemia-reperfusion phenomenon after abdominal decompression. Additionally, as previously stated, high PEEP ventilation tends to produce an exaggerated response (42).

Renal derangements

Oliguria progressing to anuria, and pre-renal azotemia unresponsive to volume expansion, characterize the renal dysfunction of ACS (4, 7, 20, 28, 32, 49, 66, 67). Oliguria can be seen at IAP of 15–20 mmHg, while increases to 30 mmHg or above lead to anuria (table II) (7, 20, 32, 49). Volume expansion to a normal CO (7, 17, 21, 37, 49) and the use of dopaminergic agonists or loop diuretics (9, 18) may be ineffective in these patients. However, decompression and reduction in IAP promptly reverses oliguria, usually inducing a vigorous diuresis (17, 21, 22, 37, 49, 68).

The mechanisms of renal derangements with IAH involves reduced absolute and proportional renal arterial flow, increased renal vascular resistance with changes in intra-renal regional blood flow, reduced glomerular filtration, and increased tubular sodium and water retention (4, 7, 32, 64). These effects are the result of a combination of factors. Cardiac output is reduced by the mechanisms described above. The failure of volume expansion to an acceptable CO to reverse the oliguria is probably due to compression of the renal veins and cortical arterioles (7, 32, 66, 67, 69) and to direct parenchymal compression (7, 17, 69). These changes produce increased renal vascular resistance and reduced renal blood flow independent of changes in CO, and may also result in corticomedullary shunting of renal plasma flow, reducing effective renal plasma flow. These all result in a reduction in glomerular filtration rate (4, 7, 32). The changes in renal and systemic hemodynamics lead to increased circulating levels of antidiuretic hormone, renin, and aldosterone (70, 71), which further increase renal vascular resistance and produce sodium and water retention. Renin and aldosterone levels decrease partially with volume expansion and further by abdominal decompression (71). Ureteral occlusion with post-renal azotemia can be eliminated as an important etiologic factor in ACS because placement of ureteral stents has not improved renal function (15).

Abdominal visceral abnormalities

Mesenteric arterial, hepatic arterial, intestinal mucosal, hepatic microcirculatory, and portal venous blood flow all have been shown to be reduced with IAH (8, 72, 73). Diebel et al. maintained a normal CO and systemic pressure through a range of IAP from 10 to 40 mmHg (8, 72). They found that while mesenteric and intestinal mucosal flow reductions first occurred at IAP of 20 mmHg, hepatic/portal flow became compromised at only 10 mmHg. In addition, Rasmussen et al. demonstrated a marked increase in hepatic and portal vascular resistance with increased IAP (73). An IAP above 20 mmHg impairs intestinal perfusion at the mucosal and submucosal level leading to a reduction in tissue oxygen tension, anaerobic cell metabolism, acidosis, and free radical generation (10, 11, 74–76). In fact, many recent investigators have demonstrated that intra-mucosal pH (pH_i) measured with gastric tonometery is a sensitive clinical indicator of gut ischemia in the ACS (10, 11, 76).

Intestinal ischemia and infarction has been described during prolonged laparoscopy despite apparently normal hemodynamics and renal function (77, 78). Perhaps more common is the low-grade ischemia seen at IAP of 15 mmHg. Prolonged low-grade elevation of IAP is associated with bacterial translocation in rat and murine models (75, 79). Thus, despite normal systemic hemodynamics, profound splanchnic ischemia can be ongoing with IAH. Very few of the overt manifestations of ACS are evident at this point to alert one to developing IAH. It has been suggested that such ischemia is associated with an increased incidence of multi-system organ failure, sepsis and increased mortality (11, 80). Furthermore, recent evidence supports a relationship between elevations in IAP above 10 mmHg and sepsis, multi-system organ failure, need for reoperation and mortality (76, 81). These are some of the strongest arguments for the routine measurement of UBP in critically ill patients. Further increases in IAP may lead to intestinal infarction, often present in the ileum and right colon without arterial thrombosis.

Abdominal wall abnormalities

Increased IAP has been shown to reduce abdominal wall blood flow by the direct, compressive effects of IAH under conditions of stable systemic perfusion, leading to local ischemia and edema (43). This can decrease abdominal wall compliance and exacerbate IAH (41). Abdominal wall muscle and fascial ischemia may contribute to infectious and non-infectious wound complications (e.g., dehiscence, herniation, necrotizing fasciitis) often seen in this patient population.

Pulmonary dysfunction

With an acute elevation in IAP, respiratory failure characterized by high ventilatory pressures, hypoxia and hypercarbia eventually develops (18, 49, 53, 54). Diaphragmatic elevation leads to a reduction in static and dynamic pulmonary compliance (12, 64, 82, 83) and can be readily demonstrated by chest radiographs (49). Therefore, with volume-cycled ventilation peak inspiratory pressures increase. The increase in IAP also reduces total lung capacity, functional residual capacity and residual volume (12). These lead to ventilation-perfusion abnormalities and hypoventilation producing hypoxia and hypercarbia, respectively (49, 52, 53, 84). Pulmonary vascular resistance increases from the combined effects of reduced alveolar oxygen tension and increased thoracic pressure (52). Recent work in a porcine model by Simon et al. has demonstrated that prior hemorrhage and volume resuscitation exacerbate the cardiopulmonary sequelae of IAH (85). Chronic elevation of IAP, as in central obesity, also produces these derangements in the form of obesity hypoventilation syndrome (OHS) (13). Abdominal decompression improves the acute respiratory failure almost immediately (18, 53, 49). Similarly, the OHS is best corrected by surgically induced weight loss with reduction in UBP (13, 14).

Intracranial derangements

Elevated intracranial pressure (ICP) and reduced cerebral perfusion pressure (CPP) have been described with acute changes in IAP in animal models (86–90) and in human studies (91–92). In animal models the changes in ICP and CPP are independent of changes in pulmonary or cardiovascular function and appear to be the direct result of elevated intrathoracic and central venous pressures with impairment of cerebral venous outflow (86, 88–90). This has been demonstrated by ablation of the direct effect of elevated IAP on ICP after median sternotomy, pericardiotomy, and bilateral pleurotomy (fig. 3) (89). Reduction in IAP by surgical decompression (91, 92) reverses this derangement. Furthermore, chronic elevation in IAP has been implicated as an important etiologic factor in the development of benign intracranial hypertension, or pseudotumor cerebri, in the morbidly obese (93, 94). Weight loss by bariatric surgery is associated with improvements in cerebrospinal fluid pressure and symptoms (93, 94).

Figure 3

The role of intrathoracic pressure in mediating intracranial disturbances in acute abdominal compartment syndrome. Performing a sternotomy, pericardiotomy, and bilateral pleurotomies prevents the increase in intracranial pressure (ICP) seen with progressive (more...)

Incidence

While most of the literature details the management of ACS following abdominal trauma (95–98), one must keep in mind that ACS can occur in a variety of settings, but particularly those associated with major, life-threatening hemorrhage and shock, massive volume resuscitation, prolonged operation and coagulopathy. Surgery for hemorrhagic pancreatitis, repair of leaking or ruptured abdominal and thoracoabdominal aneurysms, and liver transplantation have all been complicated by the development of post-operative ACS (9, 18, 21, 49, 68). The ‘bloody vicious cycle’ of hypothermia, profound coagulopathy, and persistent acidosis is a frequent prelude to the development of ACS (95).

The ACS developed in 21 (14%) of 145 patients sustaining severe abdominal trauma (Injury Severity Score, ISS > 15) in a study by Meldrum et al. (96). In this prospective study 60% of ACS patients suffered blunt trauma, all had abbreviated damage control' laparotomies, and 67% required abdominal packing during this initial operation. Liver injuries were the most common source of hemorrhage (57%), but multiple injuries were the rule with splenic, renal, and hollow viscus injuries frequently seen. The ACS was defined as the presence of a UBP of > 20 mmHg with cardiovascular (DO₂I < 600 ml O₂/min/m²), pulmonary (peak airway pressure > 45 cmH₂O), and/or renal (UOP < 0.5 ml/kg/hr) dysfunction. The ACS developed within 27 ± 4 hours with a UBP of 27 ± 2.3 mmHg. Ivatury et al. recently found the incidence of IAH (defined as UBP > 25 cmH₂O or 18 mmHg) following penetrating abdominal trauma to be greater in those patients undergoing primary fascial closure (14/27, 52%) than with those receiving prophylactic mesh closure (9/43, 24%; p = 0.007) (11). None of these patients developed the fulminant ACS at this IAP and intervention was based on the elevated UBP in conjunction with gut-mucosal acidosis (pH_i < 7.15). They also noted a higher mortality and incidence of multiple organ dysfunction syndrome in patients with IAH and those with primary fascial closure. Bedside or operative decompression was effective in improving mucosal acidosis in approximately 71% (5/7) of the patients with demonstrated acidotic pH_i and IAH. In a retrospective analysis of 107 patients with staged trauma laparotomy and packing, Morris diagnosed ACS in 16 patients (15%) (22). Finally, Fietsam et al. reported a 4% incidence of ACS with primary closure following repair of ruptured aortic aneurysms (18). Thus, the incidence varies with the clinical setting and the definition of ACS. When defined in its most contemporary fashion (i.e., IAH that adversely affects any organ system), the incidence is somewhat greater than with the more classic definition (i.e., IAH with severe cardiopulmonary or renal dysfunction).

Diagnosis and surveillance for ACS

Moore and Meldrum et al. have advocated the grading of IAH based on UBP measurement (95, 96). At UBP less than 25 mmHg (grades I–II), maintenance of adequate intravascular volume or hypervolemic resuscitation may be adequate to preserve organ perfusion. With UBP of 26–35 mmHg (grade III) decompression of some sort is necessary for patient salvage, and with UBP exceeding 35 mmHg (grade IV) re-exploration is mandatory. The modifying effects of morbid obesity (as assessed by SAD), hemorrhage, hypovolemia, and anesthetics must be taken into account when interpreting UBP measurement in relation to clinical presentation.

Two recent prospective studies analyzed the use of routine UBP measurement in predicting ACS-related renal dysfunction. Platell et al. demonstrated that a UBP greater than 18 mmHg had a positive and negative predictive value of 85% and 62%, respectively, for the development oliguria in a study involving 42 patients undergoing abdominal aortic surgery (20). Sugrue et al. evaluated 100 patients admitted to the ICU following laparotomy and found a 33% incidence of IAH (UBP > 20 mmHg) and a 33% incidence of renal impairment (99). Furthermore, 69% of the patients with renal impairment had IAH. The odds ratios for renal impairment and death in patients with IAH in this study was 12.4 and 11.2, respectively. These studies, combined with the improved results in the management of ACS with the prospective use of UBP demonstrated by Meldrum et al. (96, 100), strongly argue for the routine measurement of UBP in ICU patients at risk for ACS.

Intestinal ischemia secondary to IAH and its assessment by intra-mucosal pH (pH_i) has been well studied in animal models (8, 74). Sugrue et al. found that those patients with pH_i < 7.32 had an odds ratio of 11.3 for IAH (10). Ivatury et al. assessed 42 patients with penetrating abdominal trauma by pH_i, 11 of whom had IAH (11). Seven of these 11 patients with IAH had acidotic pH_i (7.15 ± 0.2), without overt evidence of the classic ACS. Improvement in pH_i occurred with abdominal decompression in five of these seven patients. Furthermore, they noted a significantly higher incidence of multiple organ failure and mortality in patients with IAH (4.6% and 39%) then in those without IAH (1.5% and 8.5%, p = 0.006). Thus, the use of gastric tonometery to assess occult intestinal ischemia with IAH may be useful. In summary, the combination of UBP measurement and assessment of pH_i may prove to be sensitive indicators of early ACS or IAH, when renal and cardiopulmonary function is not significantly deranged. Given the association of UBP > 10 mmHg with sepsis, multiple organ failure, and mortality (76), the presence of elevated UBP in association with an acidotic pH_i may prove to be an indication for early decompression. The improvement in intestinal perfusion might yield a decreased mortality from multiple organ failure, the most common cause of late death from ACS.

Pediatric critical care

The literature on ACS in pediatric patients is limited to the management of abdominal wall defects (AWD), with some allusion to an association of IAH in the etiology of necrotizing enterocolitis (NEC). The current management of AWD (i.e., gastroschisis or omphalocele) in pediatric surgical patients had its beginnings in the mid-1960's (101, 102). The experience gained in these techniques led to the principles guiding abdominal wall reconstruction following trauma in adult patients. In fact, the concept of estimating IAP to guide closure is much more conclusively supported in the pediatric literature than in adults (103–106). Swartz et al. demonstrated that primary closure (52%), skin flap coverage (10%), and silo reduction (38%) were equally effective in a retrospective study of 106 patients with gastroschisis (107). While the rate of complications was higher in the silo reduction group, the mortality, hospital stay, and duration of ileus were insignificantly different between the three treatment groups. This led the authors to conclude that primary closure is possible in most neonates. However, they recommend that the “degree of visceroabdominal disproportion” and the physiologic response of the newborn to closure must guide the surgeon in the choice of repair. It is the desire to objectively assess this disproportion, and the recognition that deleterious increases in IAP produce a syndrome of IAH similar to that seen in adults, that has stimulated investigators to use IAP as a guide to closure of AWD. Chin et al. demonstrated a higher rate of ascites leakage, ventral hernia, lower extremity edema, and oliguria in 7 newborns with UBP exceeding 20 mmHg following repair of AWD (105). Obstruction of the suprahepatic, subdiaphragmatic vena cava leading to the development of acute Budd-Chiari syndrome has been reported following repair of a giant omphalocele (108). Yaster et al. demonstrated a 50% incidence of oliguria in 8 cases of primary closure of AWD, in which all those with oliguria had gastric pressures exceeding 22 mmHg (109). These and other observations of respiratory, hemodynamic, and renal deterioration following tight closure of AWD supports the contention that the ACS exists in children as well (103–112).

Lacey et al. used UBP as a guide to closure of AWD in a prospective study of 42 newborns (104). He found UBP altered patient management (i.e., choice of closure, rate of silo reduction, ventilatory management) in 64% of the patients. Over half of the patients undergoing silo reduction had this option chosen because of a prohibitive rise in UBP after initial attempts at primary closure. This was despite the fact that a primary closure was mechanically possible and within the realm of ‘visceroabdominal proportion’. This highlights the high degree of subjectivity associated with the assessment of abdominal wall closure by gross appearance alone. There was no case of renal failure or oliguria and only 4 (10%) cases of ischemic gut or bowel necrosis with clinically normal IAP, all occurring late, in contrast to a 17% incidence of renal failure and 33% incidence of early bowel necrosis in historical cohorts from the same institution. Rizzo et al. corroborated Lacey's conclusions in a retrospective study of 32 patients with AWD managed by UBP and showed a trend toward shorter stay and reduced hospital cost (106). Finally, the role of elevated IAP in the development of early NEC following repair of AWD has been suggested by several authors (113).

Schema for management of ACS

Critically ill patients that are at risk for the development of IAH and ACS should be identified based on what has been reviewed thus far (100). These patients should have frequent determinations of UBP performed. This can begin in the operating room with IAP-guided temporary abdominal closure or in the ICU in postoperative or non-surgical patients. Monitoring of UBP should continue until the likelihood of ACS is remote (e.g., after resolution of visceral edema). If there is any suspicion of IAH at any point thereafter, UBP should be reassessed. A surgical consultant should be involved in all patients in whom an ACS is suspected or likely to occur. A decompressive laparotomy requires patient preparation, and proper planning is more likely to lead to an optimally timed and executed decompression. When UBP is increased above 20–25 mmHg with associated deterioration in cardiovascular (e.g., DO₂I < 600 ml O₂/min/m²), pulmonary (e.g., airway pressure > 45 cmH₂O, P_aCO₂ > 50 mmHg), and/or renal (e.g., UOP < 0.5 ml/kg/hr, azotemia) function, abdominal decompression is indicated. In the presence of intestinal ischemia (e.g., acidotic pH_i, dusky bowel examined through a silastic closure), not responding to optimization of oxygen delivery, a UBP of 15–20 mmHg should trigger decompression. Furthermore, if these high-risk patients also have head trauma, ICP monitoring via a ventriculosotomy catheter maybe helpful. If intracranial hypertension does not respond to standard measures, decompressive laparotomy should be considered if UBP exceeds 15–20 mmHg (92).

Abdominal decompression should be guided by UBP and clinical response and can range from bedside removal of towel clips to formal decompressive celiotomy, if necessary. The key to treating a medical patient with ACS is not resuscitation of oxygen delivery. As previously stated, organ hypoperfusion and progression to multiple organ failure occurs despite normal oxygen delivery and consumption. Similar to an extremity compartment syndrome, the treatment of ACS mandates a reduction of IAP even if hemodynamics are acceptable. Like a fasciotomy, the laparotomy must be performed expediently. Otherwise, multiple organ failure becomes the limiting factor in patient survival. Preparation for decompression should entail reversal of clotting deficiency, rewarming, reversal of acidosis, and aggressive volume loading. While some authors suggest the use of mannitol, sodium bicarbonate, and pressors prior to formal decompressive laparotomy to combat reperfusion syndrome or sudden decreases in vascular resistance (21, 22), others have not demonstrated these catastrophic consequences of a sudden reduction in IAP (11, 96). The discrepancy probably lies in the much more advanced and prolonged state of IAH that existed prior to decompression in the former reports, again arguing for timely decompression.

Future directions

The clinical and basic science investigation of ACS and IAH still has uncharted territories. The role of chronically elevated IAP in the etiology of the comorbidities of morbid obesity still warrants further evaluation, particularly in relation to pseudotumor cerebri and hypertension (14, 16, 93, 94). In up to 8% of pregnancies hypertension, renal dysfunction, proteinuria, with or without clinical presentation of elevated ICP (i.e., headaches, photophobia, seizures and coma) develops. The etiology of pre-eclampsia/eclampsia is unknown and treatment is aimed at ameliorating the end-organ effects by optimal supportive care. Since pregnancy is associated with increased IAP (unpublished data), it's reasonable to assume that some of this pathophysiology may be attributed to IAH. Furthermore, the role of IAH on the development of neonatal necrotizing enterocolitis (NEC) needs further assessment.

In addition to new concepts, a better understanding of current issues is needed. For example, is early decompression guided by UBP and/or pH_i beneficial in reducing morbidity and mortality from ACS compared with intervention at a more advanced stage of multiple organ dysfunction? What is the role, if any, of non-surgical means of reducing IAP using an externally applied negative abdominal pressure device when celiotomy is not absolutely necessary? Is increased IAP leading to an increased ICP and decreased CPP the cause for cerebral ischemia and the high frequency of obtundation in critically ill patients? Is UBP a predictor of intestinal ischemia in the pediatric population as it is for oliguria?