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Abdominal Compartment Syndrome

Saggi, Bob H. MD; Sugerman, Harvey J. MD; Ivatury, Rao R. MD; Bloomfield, Geoffrey L. MD

The Journal of Trauma: Injury, Infection, and Critical Care: September 1998 - Volume 45 - Issue 3 - p 597-609
Review Article
Free

The abdominal compartment syndrome (ACS) has tremendous relevance in the practice of surgery and the care of critically ill patients because of the effects of elevated pressure within the confined space of the abdomen on multiple organ systems. The problem of ACS goes well beyond the care of trauma patients, encompassing many diverse disease states and clinical scenarios. The problem can be acute, chronic, or secondary to an acute increase in intraabdominal pressure (IAP) upon a chronically increased IAP state. Recent data suggest that some of the adverse effects of elevated IAP occur at lower levels than previously thought and manifest before the development of a fulminant ACS. The ACS, therefore, should be viewed as the end result of a progressive, unchecked increase in IAP from a myriad of disorders that eventually leads to multiple organ dysfunction.

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BACKGROUND

History

The effects of elevated IAP have been known since the late 19th century, when Marey and Burt highlighted the respiratory effects of elevated IAP. [1] In 1890, Heinricius demonstrated that elevation of IAP to 27 and 46 cm H2 O led to death in feline and porcine models. At that time, respiratory dysfunction was believed to be the cause of death in animal models of elevated IAP. [1] It wasn't until 1911 that Emerson first described the cardiovascular derangements in various animal models of intra-abdominal hypertension (IAH), which became possible after the development of crude ventilatory support. [2] Soon thereafter, in 1913, Wendt first described the association of IAH and renal dysfunction and others corroborated his findings. [3,4] Basic science and clinical observations have since confirmed the effects of elevated IAP on multiple organ systems. [5-8] The term ACS was first used by Kron et al. in the early 1980s to describe the pathophysiology resulting from IAH secondary to aortic aneurysm surgery. [9] Currently, the ACS refers to the cardiovascular, pulmonary, renal, splanchnic, abdominal wall/wound, and intracranial disturbances resulting from elevated IAP regardless of cause. The most recent work by Sugrue et al. and Ivatury et al. should revised the classic definition of ACS to include isolated impairment of gut perfusion, inasmuch as it adversely affects outcome independent of cardiopulmonary or renal dysfunction. [10,11]

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Pathogenesis

Many different causes of acutely elevated IAP exist (Table 1). 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. This is not to say, however, that elevated IAP in these individuals is benign. The morbidity that occurs in these conditions (e.g., central obesity and possibly preeclampsia/eclampsia) is at least in part attributable to the chronically elevated IAP. [13-16]

Table 1

Table 1

The ACS can develop in both nonsurgical and surgical patients, either preoperatively or postoperatively. 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. [15-17] 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 compression caused by burn eschars, [34] pneumatic antishock 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." [37-40]

Although 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 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 positive end-expiratory pressure) 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 IAP increases. [41,43] In critically ill patients, these factors are often additive, leading to or aggravating multiple system organ failure via a series of "vicious cycles" perpetuated by progressive increases in IAP.

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Measurement of Intra-Abdominal Pressure

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 the end-expiratory pressure. [42] IAP may be measured directly 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]

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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). Although animal models show a poor correlation between gastric pressure and directly measured IAP, [48] human studies show an acceptable correlation of gastric pressure to urinary bladder pressure (UBP). [50,51] In one of these studies, [51] however, there were few individual measurements at severely elevated IAP, and the other study [50] was limited to a maximum IAP of 20 mm Hg during laparoscopy. Consequently, there may be a significant discrepancy between gastric pressure and UBP at the higher IAPs associated with fulminant ACS.

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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] It is often impractical, however, as well as invasive and associated with significant risk (i.e., venous thrombosis), and no human studies have validated its use.

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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 polyethylene 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 IAPs up to 70 mm Hg (Figure 1). [48,52,53] Given this high degree of correlation at wide ranges of IAP, the ease of use, and the minimal invasiveness of this technique, it is considered the "gold standard" for indirect clinical measurement of IAP. A small, neurogenic bladder, however, 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. [14] The relationship between sagittal abdominal diameter and an increased UBP is shown in Figure 2. 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 premorbid chronically elevated IAP.

Figure 1

Figure 1

Figure 2

Figure 2

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Pathophysiology of Elevaled IAP

IAH affects multiple organ systems in a graded fashion. To better understand the clinical presentation and management of disorders of IAH, one must understand the physiologic derangements within each organ system separately. Table 2 and Figure 3 summarize the pathophysiology of IAH in each of the systems discussed below.

Table 2

Table 2

Figure 3

Figure 3

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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 greater than 20 mm Hg. 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 mm Hg, decreasing with further increases in IAP. [55-57] This results from increased venous resistance within the abdomen and thorax, leading to 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] At an IAP of 10 to 15 mm Hg, however, 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] Although 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 or ulcers. [14]

Increased thoracic pressure and diaphragmatic elevation are responsible for reductions in ventricular compliance. [56] This, combined with increased systemic afterload, reduces cardiac contractility at IAP greater than 30 mm Hg, 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 yascular 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 (Figure 4). [9,13,18,40,53] If the measured pleural pressure is subtracted from these, however, the "true" (i.e., transarterial or transmural) pressures may actually decrease with IAH (Figure 5). [53] If this is not taken into consideration, the hemodynamic profile can be confused with biventricular failure. The ejection fraction, however, is usually normal to slightly elevated, and the presence of elevated IAP can be assessed by UBP.

Figure 4

Figure 4

Figure 5

Figure 5

The hemodynamic effects of IAH are modified by several factors. Studies report a 17 to 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] whereas volume expansion tends to minimize or even reverse this process. [55] In fact, volume loading before abdominal decompression has been advocated by Morris et al. [22] as a means of controlling the hypotension often seen after 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 stated previously, high positive end-expiratory pressure ventilation tends to produce an exaggerated response. [42]

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Renal Derangements

Oliguria progressing to anuria, and prerenal 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 to 20 mm Hg, whereas increases to 30 mm Hg or greater lead to anuria (Table 2). [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. Decompression and reduction of IAP, however, promptly reverses oliguria, usually inducing a vigorous diuresis of resuscitative fluids. [17,21,22,37,49,68]

The mechanisms of renal derangements with IAH involve reduced absolute and proportional renal arterial flow, increased renal vascular resistance with changes in intrarenal 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 attributable to compression of the renal vein and cortical arterioles [7,32,66,67,69] and 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 of glomerular filtration rate. [4,7,32] The changes in renal and systemic hemodynamics lead to increased circulating levels of antidiuretic hormone, renin, and aldosterone (Figure 6), [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 (Figure 6). [71] Ureteral occlusion with postrenal azotemia can be eliminated as an important causal factor in ACS because placement of ureteral stents has not improved renal function. [15]

Figure 6

Figure 6

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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 mm Hg. [8,72] They found that although mesenteric and intestinal mucosal flow reductions first occurred at IAP of 20 mm Hg, hepatic or portal flow became compromised at only 10 mm Hg. In addition, Rasmussen et al. demonstrated a marked increase in hepatic and portal vascular resistance with increased IAP. [73] An IAP greater than 20 mm Hg impairs intestinal perfusion at the mucosal and submucosal levels, leading to a reduction in tissue oxygen tension, anaerobic cell metabolism, acidosis, and free radical generation. [10,11,74-76] In fact, many investigators have demonstrated that measurement of intramucosal pH (pHi) 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 mm Hg. Prolonged low-grade elevation of IAP is associated with bacterial translocation in rat and murine models. [75,79] 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 multiple system organ failure, sepsis, and increased mortality. [11,80] Furthermore, recent evidence supports a relationship between elevations in IAP greater than 10 mm Hg and sepsis, multiple system organ failure, the need for reoperation, and mortality. [76,81] These are some of the strongest arguments for the routine measurement of UBP in critically ill patients (discussed below). Further increases in IAP may lead to intestinal infarction, which is often present in the ileum and right colon without arterial thrombosis.

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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 noninfectious wound complications (e.g., dehiscence, herniation, necrotizing fascitis) often seen in this patient population.

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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] With volume-cycled ventilation, therefore, 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 the 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 previous 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. [13] Abdominal decompression improves the acute respiratory failure almost immediately. [18,49,53] Similarly, the obesity hypoventilation syndrome is best corrected by surgically induced weight loss with reduction in UBP. [13,14]

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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 (Figure 7). [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 (Figure 7). [86,88-90] Reduction in IAP by surgical decompression [91,92] reverses this derangement. Furthermore, chronic elevation in IAP has been implicated as an important causal 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 7

Figure 7

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CLINICAL CONSIDERATIONS

Despite our knowledge of the adverse effects of elevated IAP since the early part of the century, clinical application of these concepts in the management of critically ill patients is a phenomenon of the last two decades. Richards et al. first described the syndrome of renal failure associated with a "tense abdomen" in modern clinical surgery. [68] Kron et al., however, were the first to correlate increases in UBP greater than 25 mm Hg with postoperative renal failure and a reduction in UBP with treatment by surgical decompression leading to return of normal renal function. [9] In this classic paper, Kron et al. suggest that a UBP greater than 25 mm Hg associated with otherwise unexplained oliguria is an indication for decompression. Since these early reports, numerous investigators have documented the existence of a distinct clinical syndrome involving multiple organ systems and associated with increased IAP, in which decompressive celiotomy improves outcome (Table 3). Anecdotal data suggest that ACS without expedient decompression is uniformly fatal. Surgical decompression, however, is 93% effective at reversing the organ dysfunction described in these series and is associated with an overall survival of 59% (range, 25-71%). These series clearly demonstrate the positive effect of decompressive celiotomy on outcome.

Table 3

Table 3

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Surgical and Related Issues

Although most of the literature details the management of ACS after abdominal trauma, one must keep in mind that ACS can occur in a variety of surgical settings, 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 postoperative 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]

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Incidence

The ACS developed in 21 of 145 patients (14%) who sustained severe abdominal trauma (Injury Severity Score > 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 greater than 20 mm Hg with cardiovascular (DO2 I < 600 mL O2 [center dot]min-1 [center dot]m-2), pulmonary (peak airway pressure > 45 cm H2 O), or renal (urinary output < 0.5 mL[center dot]kg-1 [center dot]h-1) dysfunction. The ACS developed within 27 +/- 4 hours with a UBP of 27 +/- 2.3 mm Hg. Ivatury et al. recently found the incidence of IAH (defined as UBP > 25 cm H2 O or 18 mm Hg) after penetrating abdominal trauma to be greater in patients undergoing primary fascial closure (14 of 27, 52%) than in patients receiving prophylactic mesh closure (9 of 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 gutmucosal acidosis (pHi < 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 at improving mucosal acidosis in approximately 71% of the patients (5 of 7) with demonstrated acidotic pHi and IAH. In a retrospective analysis of 107 patients with staged trauma laparotomy and packing, Morris et al. diagnosed ACS in 16 patients (15%). [22] Finally, Fietsam et al. reported a 4% incidence of ACS with primary closure after repair of ruptured aortic aneurysms. [18] The incidence thus 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 cardiopulmonary or severe renal dysfunction).

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Staged Laparotomy and ACS

The concept of the staged or damage-control celiotomy for abdominal trauma or hemorrhage has been in accepted clinical practice for the last two decades. Key to this concept is that prolonged operative time and protracted or extensive surgical repair only invites the bloody vicious cycle of hypothermia, coagulopathy, and acidosis. Instead, rapid and focused control of surgical bleeding combined with laparotomy gauze pad tamponade and other salvage procedures (e.g., stapled division of bowel without resection, drainage of pancreaticoduodenal and biliary injuries, intravascular shunts) are essential in avoiding this vicious cycle and in patient survival. [22,95,97,98] It is the emergence of this surgical philosophy that has created the patient population in which the ACS is most commonly seen at this time.

Moore eloquently reviewed the topic as practiced at the Denver Health Medical Center, [95] conveniently dividing the process into five stages. Stage I involves the selection of patients for and performance of the abbreviated laparotomy. Stage II entails intraoperative reassessment of patient salvageability, initial rewarming and resuscitation, reexploration for appraisal of hemostasis, and evaluation of abdominal closure technique to avoid excessive tension via UBP measurement. Stage III involves standard resuscitative techniques in the intensive care unit (ICU) combined with surveillance for and management of the ACS, to include decompressive laparotomy. Stage IV involves definitive repair of all temporized injuries. And stage V entails the reconstruction of abdominal wall continuity. The majority of debate in the literature revolves around the management of the patient in the ICU, particularly in relation to the criteria used to plan unpacking. Some authors suggest the complete restoration of physiologic reserve before any attempt at operative intervention, citing "physiologic exhaustion" as prohibitive. [22,97] They suggest an almost mandatory wait of 24 to 36 hours or even longer to allow restoration of clotting and euthermia and reversal of acidosis. Decompression is recommended only for advanced ACS. As detailed previously, however, at this point the adverse effects of IAH are multiple and severe. Morris et al., in their series of 107 patients, diagnosed the ACS only when patients had peak inspiratory pressures exceeding 85 cm H2 O or profound oliguria. With this management scheme, ACS was associated with a treated survival of only 37.5%. [22] When decompression was performed with more liberal, prospective criteria using UBP as a guide, however, Meldrum et al. [96] documented a survival rate of 71% with ACS in a similar patient population. Most of the deaths in patients with ACS are related to sepsis or multiple organ failure. The study by Meldrum et al. combined with the basic science and clinical data on the adverse effects of prolonged IAH on intestinal ischemia, the gut-mucosal barrier, and the incidence of sepsis and multiple organ failure, strongly argue for the early and aggressive management of ACS. [8,11,72-81] Only a prospective, randomized trial can definitively settle this issue. It must be kept in mind that an emergent decompression is aimed at reducing IAP and not at definitive therapy of all traumatic injuries. It should entail a limited laparotomy with judicious removal of selected abdominal packs or even the simple removal of towel clips. Both of these can be done at the bedside in the "nonoptimized" patient and impose very little surgical stress. The decompressive procedure in this scenario serves as a lifesaving procedure bridging the gap between damage control and definitive surgery by reducing IAP and improving organ perfusion and function.

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Abdominal Wall Closure and Reconstruction

Closure of the abdomen after any procedure associated with profound hemorrhage and shock, obligatory massive volume resuscitation, and resultant visceral and retroperitoneal edema represents a balance between the IAP necessary to tamponade bleeding and the IAP that produces fulminant ACS. Primary fascial closure is usually not possible or advisable in this setting because of the excessive IAP that results and because of the high likelihood of reoperation. Instead, the use of alternative means of temporary closure such as towel clips or the silastic "Bogota" bag allow coverage without undue tension. [97] With towel clip closure, standard towel clips are applied 1 to 2 cm from the skin edge and 1 to 2 cm apart for the entire length of the incision and then all are wrapped in a moist towel and covered with a self-adhesive iodized plastic sheet. If excessive tension develops, successive removal of clips can reduce IAP. The Bogota bag can be fashioned from a sterilized 3L Foley irrigation bag cut along its seams, fashioned to the necessary size, and sewn to the fascia with 0-monofilament suture or stapled to the skin. Another option is to apply a "nonsticky" Via-Drape (3M, St. Paul, Minn), which is stapled to the skin. This permits direct observation of the peritoneal cavity and avoids injury to the fascia, which will be used for subsequent wound closure. Many authors advocate the use of UBP to guide closure of the abdomen after such surgical procedures. [95] In this way, the choice between primary fascial and the numerous alternative wound-closure techniques can be made based on objective assessment of IAH and the likelihood of the development of ACS.

The next goal is to restore physiologic reserve to allow definitive repair of injuries and reconstruction of the abdominal wall. Definitive closure can simply involve the removal of towel clips or other temporary covers and primary fascial reapproximation. In some cases, this may require successive approximation (i.e., silo reduction) to overcome fascial retraction or allow for complete resolution of intra-abdominal edema. In some patients, however, severe fascial retraction, necrosis, or loss may preclude primary closure. Alternatives in these situations include granulation over viscera or over absorbable synthetic mesh, with omental cover, if possible, in both cases. Granulation over mesh is preferred unless it is contraindicated (e.g., by severe peritonitis, abscesses, or active gastrointestinal leak). Gradual delayed primary closure of the skin can be attempted, leaving a large ventral hernia to be repaired at a later time. If skin approximation is not feasible, a partial-thickness skin graft can be applied to the granulating bowel. With peritoneal contamination, a skin graft can be applied to the viscera once open packing has eradicated infection and allowed granulation tissue to become well established. In either case, the skin grafts can usually be excised without much difficulty in 6 to 12 months, with another attempt at fascial closure. At this stage, fascial closure often requires lateral fascial relaxing incisions or the use of polypropylene mesh. Measurement of UBP can be used at each stage of abdominal wall reconstruction to assess for IAH, because massive incisional hernioplasty alone has been shown to produce the ACS. [40]

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Surveillance for ACS

Elevations in IAP have been shown to produce a graded physiologic response, as discussed previously, and Moore and Meldrum et al. have advocated the grading of IAH based on measurement of UBP. [95,96] At UBP less than 25 mm Hg (grades I and II), maintenance of adequate intravascular volume or hypervolemic resuscitation may be adequate to preserve organ perfusion. With UBP of 26 to 35 mm Hg (grade III), decompression of some sort is necessary for patient salvage, and with UBP exceeding 35 mm Hg (grade IV), reexploration is mandatory. The modifying effects of morbid obesity (as assessed by sagittal abdominal diameter), 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. In a study involving 42 patients undergoing abdominal aortic surgery, Platell et al. demonstrated that a UBP greater than 18 mm Hg had positive and negative predictive values of 85 and 62%, respectively, for the development of oliguria. [20] Sugrue et al. evaluated 100 patients admitted to the ICU after laparotomy and found a 33% incidence of IAH (UBP > 20 mm Hg) 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 were 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] strongly argue for the routine measurement of UBP in select ICU patients at risk for ACS.

Intestinal ischemia secondary to IAH and its assessment by pHi has been well studied in animal models. [8,74] Sugrue et al. found that those patients with pHi less than 7.32 had an odds ratio of 11.3 for IAH. [10] Ivatury et al. assessed 42 patients with penetrating abdominal trauma by pHi, 11 of whom had IAH. [11] Seven of these 11 patients with IAH had acidotic pHi (7.15 +/- 0.2) without overt evidence of the classic ACS. Improvement in pHi occurred with abdominal decompression in five of these seven patients. Furthermore, the authors noted a significantly higher incidence of multiple organ failure and mortality in patients with IAH (4.6 and 39%, respectively) then in patients without IAH (1.5 and 8.5%, respectively; p = 0.006). The use of gastric tonometery to assess occult intestinal ischemia with IAH may thus be useful. In summary, the combination of UBP measurement and assessment of pHi may prove to be a sensitive indicator of early ACS or IAH when renal and cardiopulmonary function is not significantly deranged. Given the association of UBP greater than 10 mm Hg with sepsis, multiple organ failure, and mortality, [76] the presence of elevated UBP in association with an acidotic pHi 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.

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Scheme for the Management of ACS

Critically ill patients who 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, beginning with IAP-guided temporary abdominal closure and continuing until the likelihood of ACS is remote (e.g., after resolution of visceral edema). If there is any suspicion of IAH at any time thereafter, UBP should be reassessed. When UBP is increased greater than 20 to 25 mm Hg with associated deterioration in cardiovascular (e.g., DO2 I < 600 mL O2 [center dot]min-1 [center dot]m-2), pulmonary (e.g., airway pressure > 45 cm H (2) O, PaCO2 > 50 mm Hg), or renal (e.g., urinary output < 0.5 mL[center dot]kg (-1) [center dot]h-1, azotemia) function, abdominal decompression is indicated. In the presence of intestinal ischemia (e.g., acidotic pHi, dusky bowel examined through a silastic closure) not responding to optimization of oxygen delivery, a UBP of 15 to 20 mm Hg should trigger decompression. Furthermore, if these high-risk patients also have head trauma, ICP monitoring via a ventriculostomy catheter may be helpful. If intracranial hypertension does not respond to standard measures, decompressive laparotomy should be considered if UBP exceeds 15 to 20 mm Hg. [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. Preparation for decompression should entail reversal of clotting deficiency, rewarming, reversal of acidosis, and aggressive volume loading. Although some authors suggest the use of mannitol, sodium bicarbonate, and pressors before formal decompressive laparotomy to combat reperfusion syndrome or sudden decreases in vascular resistance, [21,22] others have not demonstrated these catastrophic consequences of sudden reduction in IAP. [11,96] The discrepancy probably lies in the much more advanced and prolonged state of IAH that existed before decompression in the former reports.

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Pediatric Surgical Issues

The current management of abdominal wall defects (AWD) (i.e., gastroschisis or omphalocele) in pediatric surgical patients had its beginnings in the mid 1960s. [101,102] The experience gained in these techniques led to the principles guiding abdominal wall reconstruction in adult patients. In fact, the concept of estimating IAP to guide closure is much more conclusively supported in pediatric patients 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] Although the rate of complications was higher in the silo reduction group, the mortality, hospital stay, and duration of ileus were insignificantly different in the three treatment groups. This led the authors to conclude that primary closure is possible in most neonates. They recommend, however, 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 and Wei demonstrated a higher rate of ascites leakage, ventral hernia, lower-extremity edema, and oliguria in seven newborns with UBP exceeding 20 mm Hg after repair of AWD. [105] Obstruction of the suprahepatic, subdiaphragmatic vena cava leading to the development of acute Budd-Chiari syndrome has been reported after repair of a giant omphalocele. [108] Yaster et al. demonstrated a 50% incidence of oliguria in eight cases of primary closure of AWD, in which all patients with oliguria had gastric pressures exceeding 22 mm Hg. [109] These and other observations of respiratory, hemodynamic, and renal deterioration after tight closure of AWD support the contention that the ACS exists in children as well. [103-107]

Lacey et al. used UBP as a guide to closure of AWD in a prospective study of 42 newborns. [104] They found that UBP altered patient management (i.e., choice of closure, rate of silo reduction, ventilatory management) in 64% of the patients. More than half of the patients undergoing silo reduction had this option chosen because of a prohibitive increase 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 four cases (10%) of ischemic gut or bowel necrosis with clinically normal IAP, all occurring late, in contrast to a 17% incidence of renal failure and a 33% incidence of early bowel necrosis in historical cohorts from the same institution. Rizzo et al. corroborated the conclusions of Lacey et al. 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 necrotizing enterocolitis (NEC) after repair of AWD has been suggested by several authors. [110-113]

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Issues in Clinical Laparoscopy

The adverse effects of CO2 pneumoperitoneum on renal and splanchnic perfusion and the influence on cardiopulmonary function were reviewed previously. [8,72-76] One must keep in mind that clinical laparoscopy generally requires lower levels of pneumoperitoneum than were used in some of the animal studies. [74] Because laparoscopy uses IAP in the range of 15 mm.Hg, the data on organ function at this IAP should determine our evaluation. The current debate on laparoscopy as it pertains to this review revolves around its use in abdominal trauma, as a potentially harmful procedure in patients with limited cardiopulmonary reserve, and the differential influence of various gases on the effects of elevated IAP.

The major concerns with the use of the pneumoperitoneum of laparoscopy in abdominal trauma are with the presence of concomitant closed head injury, the induction of intestinal ischemia and its sequelae, and its use in the marginally stable patient. Numerous animal studies [86-90] and anecdotal human studies [90-92] have documented a direct relationship between IAP and ICP even at the modest elevations of 10 to 15 mm Hg used in laparoscopy. Given these data and the 40% coincidence of intracranial injury with major blunt abdominal trauma, [114] laparoscopy should be used cautiously in patients with suspected head injury and should be considered a relative, if not absolute, contraindication in patients with known intracranial hypertension. Recent data suggest that alternatives to CO2 distention, such as the use of N2 O or helium pneumoperitoneum and the gasless technique, may attenuate the effects of laparoscopy on ICP. [115,116] Further evaluation of laparoscopy is needed, however, before conclusive recommendations can be made regarding these novel alternatives to CO2 pneumoperitoneum.

The data are convincing that modest elevation of IAP (i.e., 15 mm Hg) is associated with gut mucosal and hepatic ischemia and, perhaps, with bacterial translocation in animal models. [8,72-75] The clinical data, however, are conflicting. Although intestinal ischemia and infarction have been described in anecdotal cases of laparoscopic cholecystectomy, [77,78] these were protracted operations in high-risk patients. In addition, a recent study by Eleftheriadis et al. documented significant intramucosal acidosis and modest hepatic microcirculatory flow impairments with elective laparoscopic cholecystectomy compared with the open procedure. [117] No adverse outcome was observed in any of the eight patients who underwent laparoscopy, however. It is reasonable to assume, therefore, that the modest pneumoperitoneum of most laparoscopic procedures produces no clinically significant ill effects related to intestinal ischemia and is safe in the healthy, noncritically ill patient. Its use in patients with existing multiple organ failure or sepsis, however, is unstudied, but conventional wisdom would advise caution in its use given the possibility of gut ischemia and its potential for a "second hit."

Finally, the use of laparoscopy in the marginally stable patient is pertinent to our review of the adverse effects of IAH. Numerous studies have documented minimal changes in CO, heart rate, stroke volume, arterial pressure, and pulmonary function with IAP at or less than 15 mm Hg with laparoscopy, [116,118,119] and the hemodynamic changes are clinically inconsequential in most patients undergoing laparoscopy. [120] In the patient with potential hypovolemia, pericardial tamponade, acute cardiopulmonary dysfunction (all of which can occur in acutely traumatized patients), or in those with chronic cardiopulmonary disease, however, these slight changes may provoke decompensation. Laparoscopy as a diagnostic or therapeutic modality, therefore, should be used with extreme caution in these individuals. Although it may result in retention of CO2, there is no significant difference in the cardiopulmonary effects of CO2 pneumoperitoneum versus that created by other gases (e.g., argon, helium, N2 O). [116,119,121]

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Future Directions

The clinical and basic science investigation of ACS and IAH still has uncharted territories. The role of chronically elevated IAP in the pathogenesis of the co-morbidities 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, or proteinuria develop, with or without clinical presentation of elevated ICP (i.e., headaches, photophobia, seizures, and coma). The cause of pre-eclampsia/eclampsia is unknown, and treatment is aimed at ameliorating the end-organ effects by optimal supportive care. Because pregnancy is associated with increased IAP (unpublished data), it is reasonable to assume that some of this pathophysiology may be attributed to IAH. Furthermore, the role of IAH in the development of 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 or pHi 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 nonsurgical means of reducing IAP using an externally applied negative abdominal pressure device when celiotomy is not absolutely necessary? Is increased IAP leading to increased ICP and decreased CPP the cause of 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?

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SUMMARY

The ACS is a clinical entity that develops from progressive, acute increases in IAP and affects multiple organ systems in a graded fashion because of differential susceptibilities. The gut is the organ most sensitive to IAH, and it develops evidence of end-organ damage before the development of the classic renal, pulmonary, and cardiovascular signs. Intracranial derangements with ACS are now well described. Treatment involves expedient decompression of the abdomen, without which the syndrome of end-organ damage and reduced oxygen delivery may lead to the development of multiple organ failure and, ultimately, death. Multiple trauma, massive hemorrhage, or protracted operation with massive volume resuscitation are the situations in which the ACS is most frequently encountered. Knowledge of the ACS, however, is also essential for the management of critically ill pediatric patients (especially those with AWD) and in understanding the limitations of laparoscopy. The role of IAH in the pathogenesis of NEC, central obesity co-morbidities, and pre-eclampsia/eclampsia remains to be fully studied.

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