Hypoperfusion, Shock S t a t e s , an d A b d o m i n a l Compartment S y n d ro m e (A C S )

Koen Ameloot, MDa,1, Carl Gillebert, Manu L.N.G. Malbrain, MD, PhDa,b,*
KEYWORDS  Shock  Abdominal compartment syndrome  Hypoperfusion
MD
a,1

, Nele Desie,

MD

DEFINITIONS

Intra-abdominal pressure (IAP) varies from individual to individual and is influenced by body mass index, body position (head of bed elevation), and the severity of a patients critical illness.1,2 In general, normal adult IAP is considered 5 mm Hg to 7 mm Hg. Intra-abdominal hypertension (IAH) has been defined by the World Society of the Abdominal Compartment Syndrome (WSACS) (www.wsacs.org) as sustained increased IAP greater than or equal to 12 mm Hg and abdominal compartment syndrome (ACS) as IAP greater than or equal to 20 mm Hg with new organ dysfunction or failure.1,2 Given the marked variation in IAP values that may be measured in critically ill patients and given that in some patients even a slight elevation of IAP can cause end-organ hypoperfusion, it is unlikely that a single threshold value of IAP is universally applicable to all critically ill patients. IAP in excess of 25 mm Hg, a level of IAH commonly associated with significant organ dysfunction, is generally accepted to suggest the need for abdominal decompression.1,3
EPIDEMIOLOGY OF IAH/ACS

A multicenter epidemiologic study reported IAH (defined as mean IAP !12 mm Hg) present in 32% of critically ill medical and surgical ICU patients and ACS present in
M.L.N.G.M. is member of the medical advisory board of Pulsion Medical Systems, a monitoring company. The other authors have nothing to disclose. No funding support. a Intensive Care Unit, Ziekenhuis Netwerk Antwerpen, Campus Stuivenberg/Erasmus, Lange Beeldekensstraat 267, B-2060 Antwerpen 6, Belgium b High Care Burn Unit, Ziekenhuis Netwerk Antwerpen, Campus Stuivenberg/Erasmus, Lange Beeldekensstraat 267, B-2060 Antwerpen 6, Belgium 1 Drs Ameloot and Gillebert equally contributed to this work. * Corresponding author. Intensive Care Unit, Ziekenhuis Netwerk Antwerpen, Campus Stuivenberg/Erasmus, Lange Beeldekensstraat 267, B-2060 Antwerpen 6, Belgium. E-mail address: Manu.Malbrain@zna.be Surg Clin N Am 92 (2012) 207220 doi:10.1016/j.suc.2012.01.009 surgical.theclinics.com 0039-6109/12/$ see front matter 2012 Elsevier Inc. All rights reserved.

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4%.4 The prevalence of elevated IAP in patients developing organ failure suggests that IAH may be a key factor in the development of multiple system organ failure, a major cause of ICU mortality.5

MEASUREMENT OF IAP

IAH is difficult to detect by clinical examination alone. Assessment of IAP, most commonly using the surrogate measurement of intravesicular or bladder pressure, has been identified as essential to accurate diagnosis and treatment of patients with IAH or ACS.68 According to the WSACS consensus guidelines, IAP should be measured at end expiration in the complete supine position after ensuring that abdominal muscle contractions are absent and with the transducer zeroed at the level of the midaxillary line at the iliac crest after an instillation volume of maximal 20 mL to 25 mL.1 Alternatively, IAP can be measured continuously via a balloon-tipped nasogastric tube (CiMON, Pulsion Medical Systems, Munich, Germany).9 Given the high prevalence of IAH in critically ill patients, the importance of routine measurement of IAP cannot be overemphasized.

PHYSIOLOGY

The organ dysfunctions that characterize IAH and ACS may be related to either direct compressive effects, such as occur with IAP-induced pulmonary or renal failure, or more commonly may be related to inadequate end-organ perfusion as a result of decreased abdominal perfusion pressure (APP) due to decreased cardiac output (CO) and increased IAP (Fig. 1).

IAP

Vascular Compression

Diaphragm Elevation

Organ Compression

Cardiac Compression Inferior Vena Cava Flow CVP Venous stasis DVT PE Cardiac Preload P EDV

Pleural + intrathoracic pressure

Renin Aldosterone

PAOP Systemic Afterload

Cardiac Contractility

Legend: APP abdominal perfusion pressure CO cardiac output CVP central venous pressure DVT deep vein thrombosis EDV end diastolic volume IAP intra-abdominal pressure MAP mean arterial pressure PAOP pulmonary artery occlusion pressure PE pulmonary embolism P transmural pressure

MAP

CO

APP

Fig. 1. Cardiovascular effects of IAH. DVT, deep vein thrombosis; EDV, end-diastolic volume; PE, pulmonary embolism; Ptm, transmural pressure.

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Cardiovascular Implications of IAH Decreased cardiac output in IAH/ACS

Cardiac function may be distilled into 3 essential components: preload, afterload, and contractility. Elevated IAP has a negative impact on all 3 of these interrelated components.
Decreased preload

It has been demonstrated that IAP of only 10 mm Hg can significantly reduce inferior vena cava (IVC) blood flow and cardiac preload.1016 Reduced venous return has the immediate effect of decreasing CO through decreased stroke volume by the FrankStarling relation. In patients with IAH, multiple mechanisms are responsible for the reduced cardiac preload. First, as originally described by Coombs,17 intrathoracic pressure (ITP) is increased as a result from a cephalad movement of the diaphragm due to increased IAP. This decreases blood flow through the IVC and limits blood return from below the diaphragm in a pressure-dependent manner.10,12,17 Reducing ITP by limiting peak and mean airway pressures through pressure-limiting ventilatory strategies or institution of neuromuscular blockade to increase chest wall compliance improves venous return and cardiac function in this patient population.1,18,19 Second, when IAP rises, this cephalad deviation of the diaphragm narrows the inferior vena cava as it passes through the diaphragm.20 Finally, the concept of abdominal vascular zones analogous to the pulmonary vascular zone conditions described by West should be emphasized. According to this concept, increased IAP increases venous return when the transmural IVC pressure (defined as IVC pressure minus IAP) at the thoracic inlet significantly exceeds the critical closing transmural pressure (zone 3 abdomen). This is most often the case in hypervolemic patients with high IVC pressure. In zone 3 conditions, the abdominal venous compartment functions as a capacitor. By contrast, when the transmural IVC pressure at the thoracic inlet is below the critical closure transmural pressure (zone 2 abdomen), venous return is significantly decreased. This is most often the case in hypovolemic patients and by extension most noncardiogenic shock patients. In zone 2 conditions, the abdominal venous compartment functions as a collapsible starling transistor.21 This model illustrates why hypovolemia (especially in combination with positive pressure ventilation and positive end-expiratory pressure [PEEP]) predisposes patients to lower CO in response to elevated IAP than does normovolemia.21
Decreased contractility

Diaphragmatic elevation and increased ITP can also have marked effects on cardiac contractility. Traditionally, the right ventricle has been considered solely a conduit for delivering blood to the lungs and left ventricle. Compression of the pulmonary parenchyma increases pulmonary artery pressure and pulmonary vascular resistance while simultaneously reducing left ventricular preload. As right ventricular afterload increases, the right side of the heart must play a more active role in maintaining CO.22 In response to worsening right ventricular afterload, the thin-walled right ventricle dilates with decrease in RVEF and increase in ventricular wall tension and myocardial oxygen demand. This increased oxygen requirement, coinciding with an increase in right ventricular work requirement, places the myocardium at risk for subendocardial ischemia and further reductions in right ventricular contractility. Also, the interventricular septum may bulge into the left ventricular chamber impeding left ventricular function with further decreases in CO. Right ventricular dysfunction can become severe in the presence of marked IAH leading to significant reductions in left ventricular contractility as a result of this ventricular interdependence.22,23 Reduced left ventricular output may contribute to the development of systemic hypotension, worsening right coronary artery blood flow,

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ischemia, and right ventricular contractility. This decrease in contractility results in a rightward and downward shift on the Frank-Starling curve (Fig. 2). Although initially responsive to fluid loading and inotropic support at lower levels of IAH, the reduced biventricular contractility of advanced IAH/ACS can effectively be treated only by abdominal decompression.
Increased afterload

Elevated IAP can cause increased systemic vascular resistance in 2 ways: first, through direct compressive effects on the aorta and systemic vasculature, and second, more commonly, as compensation for the reduced venous return and falling stroke volume (as stated above supra). As a result of this physiologic compensation, mean arterial pressure (MAP) typically remains stable in the early stages of IAH/ACS despite reductions in venous return and CO. These increases in afterload may be poorly tolerated by patients with marginal cardiac contractility or inadequate intravascular volume.2427 Preload augmentation through volume administration seems to ameliorate, at least partially, the injurious effects of IAH-induced increases in afterload. It has also been proposed that the use of a moderate PEEP might efficiently reduce the increase in ventricular afterload.1012,18
Effects of IAH on Pulmonary Function

The interactions between the abdominal and the thoracic compartments pose a specific challenge for clinicians. The abdominal and thoracic compartments are linked through the diaphragm and, on average, 50% of the increase in IAP is transmitted to the thoracic compartment, increasing ITP.2830 IAH causes an increase in alveolar pressures, dead space, and shunt fraction and a decrease in tranpulmonary pressures, functional residual capacity and static compliance of the chest wall, resulting in hypoxemia and hypercapnia.31 These effects already take place at IAP of 15 mm Hg and are accentuated by the presence of hypovolemia.32 In postoperative patients, the presence of capillary leak, positive fluid balance, and raised IAP put patients at exponential risk for lung edema. In a porcine model, for example,

Fig. 2. IAH creates a rightward and downward shift of the Frank-Starling curve, so that for the same change in preload (DP) only a small change in stroke volume (DSV) can be observed.

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the application of IAP of 15 mm Hg after oleic acidinduced lung injury resulted in a greater than 2-fold increase in pulmonary edema, as measured by extravascular lung water (EVLW).33
Effects of IAH on End-Organ Perfusion Neurologic

A close relationship between IAP and intracranial pressure (ICP) has been observed in several animal and human studies.34 As a result of IAH, cerebral perfusion pressure, defined as MAP minus ICP, decreases. The increased ITP in IAH (described previously) causes a functional obstruction of cerebral venous outflow. This, in combination with reduced systemic blood pressure as a result of the effect of IAH on cardiac function, causes a decrease in cerebral perfusion pressure. As a result, laparoscopic procedures should be performed with caution in patients with recent head injury.3537
Kidney

After emergency abdominal surgery, IAH occurs in 33% to 41% of patients and is associated with acute kidney injury and mortality.38,39 Elevated IAP significantly decreases renal venous and arterial blood flow, leading to renal dysfunction and failure. Oliguria develops at IAP of 15 mm Hg and anuria at 30 mm Hg in the presence of normovolemia and at lower levels of IAP in patients with hypovolemia.4042 Kidney perfusion pressure can be defined as MAP minus IAP.43 Therefore, in theory, decreased kidney function can be prevented either by decreasing IAP or increasing MAP. Ulyatt44 suggested that filtration gradient (FG) is a more appropriate parameter to explain acute kidney injury associated with IAH. The FG can be calculated as glomerular filtration pressure minus proximal tubular pressure, which in conditions of IAH can be simplified as FG 5 MAP (2 IAP). Thus, changes in IAP have a greater impact on renal function and urine production than do changes in MAP. It is not surprising, therefore, that decreased renal function, as evidenced by development of oliguria, is one of the first visible signs of IAH. Also, in patients admitted with advanced systolic heart failure, IAH on admission (in this study defined as IAP >8 mm Hg) was associated with increased creatinine and after treatment with diuretics or renal replacement therapy both IAP and creatinine decreased.45,46 This finding was confirmed in a small case series were patients with refractory ascites due to heart failure were successfully treated by large fluid paracentesis with significant improvement in renal function.47
Gastrointestinal

Virtually all intra-abdominal and retroperitoneal organs demonstrate a decrease in blood flow in the presence of IAH.12 It seems that through worsening the mesenteric perfusion, IAH and ACS may serve as the second hit in the 2-hit model for the causation of multiple organ dysfunction syndrome, by triggering a vicious cycle from gut hypoperfusion leading to intestinal edema, ischemia, and bacterial translocation.2 In the presence of hypovolemia or hemorrhage, these negative effects of increased IAP are augmented.
Hepatic

Experimental data have demonstrated a decrease in hepatic arterial blood flow, caused by extrinsic compression, with IAP of only 10 mm Hg.48,49 Changes in portal venous blood flow were only seen with IAP of 20 mm Hg. In another study, a strict association between IAH and liver dysfunction was not found although a correlation between the degree of IAH and the degree of hyperbilirubinemia existed.50 Recent studies also show an inverse relation between IAP and the plasma disappearance rate of indocyanine green.51,52

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CLINICAL PRACTICE Cardiopulmonary Monitoring in Patients with IAH Do not use intracardiac filling pressures to assess fluid responsiveness

According to the Frank-Starling principle, ventricular preload is defined as myocardial muscle fiber length at end diastole. Ideally, the appropriate clinical correlate is left ventricular end-diastolic volume (LVEDV). Because LVEDV cannot be easily measured, pressure-based parameters (baroindicators), such as left ventricular end-diastolic pressure, left atrial pressure (LAP), and pulmonary artery occlusion pressure (PAOP), have long been used clinically as surrogate estimates of intravascular volume. Although likely valid in normal healthy individuals, the multiple assumptions necessary to use PAOP and central venous pressure (CVP) as estimates of left ventricular preload status and right ventricular preload status, respectively, are not necessarily true in critically ill patients with IAH/ACS.16 These patients commonly demonstrate multiple significant aberrations in cardiac function that can interfere with the accuracy of PAOP and CVP measurements as estimates of intravascular volume (Fig. 3). First, both PAOP and CVP are measured relative to atmospheric pressure and are the sum of intravascular pressure and ITP. As a result, in patients with IAH/ACS, cephalad elevation of the diaphragm and secondary elevated ITP, PAOP, and CVP also tend to be erroneously elevated despite decreased LVEDV due to decreased venous return.11,13,15,23,24,53 Transmural PAOP (PAOPtm) (ie, measured PAOP minus pleural pressure) has been identified as decreasing with rising ITP, correctly reflecting the inherent decreased venous return and cardiac preload. Other studies found that 20% to 80% of IAP, or, on average, 50%, is transmitted to the thorax.28 As a rule of thumb, a quick estimate of transmural filling pressures can be obtained by subtracting half the IAP from the measured filling pressure (eg, PAOPtm5 PAOP IAP/2).54 Alternatively, the index of transmission can be calculated, although this might be a bit complicated for bedside use. This can be done by looking at changes in IAP (DIAP) (eg, by means of a Velcro belt) versus changes in CVP (DCVP). The index of transmission can then be calculated as DCVP divided by DIAP. It has not been shown that real measurement of pleural pressure by an esophageal catheter improves the ability of PAOP alone to predict volume recruitable increases in CO.16,54 Second, ventricular compliance is dynamically changing from beat to beat in critically ill patients, resulting in a variable relationship between pressure and volume.55

Changing ventricular compliance

Mitral valve disease

Catheter position

Preload

LVEDV

LVEDP

LAP

PAOP

Altered ventricular geometry

Elevated intrathoracic or intra-abdominal

Fig. 3. The PAOP assumption: why intracardiac filling pressures do not accurately estimate preload status. LVEDP, left ventricular end-diastolic pressure; LAP, left atrial pressure. (Adapted from Cheatham ML. Right ventricular end-diastolic volume measurements in the resuscitation of trauma victims. Int J Intens Care 2000;7:16576; with permission.)

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As a result, changes in intravascular pressure no longer reflect changes in intravascular volume, further reducing the accuracy of intracardiac filling pressures, such as PAOP and CVP, as estimates of preload status. In general, the presence of IAH causes a flattening and rightward shift of the ventricular compliance curve.20 Third, patients with IAH-induced pulmonary hypertension or acute lung injury demonstrate increased pulmonary vascular resistance and are at significant risk for tricuspid valve regurgitation. Finally, in patients with IAH/ACS, proper placement of the pulmonary artery catheter (PAC) tip in West lung zone 3 may be difficult. Compression of the pulmonary parenchyma as a result of elevated IAP can markedly alter the normal progression of alveolar distention. The use of PEEP to restore alveolar volume, oxygenation, and ventilation increases the relative size of West zone 1 at the expense of zones 2 and 3.16 Hemodynamic monitoring can only improve patient care and outcome when clinicians thoroughly understand both the appropriate use as well as the potential measurement errors associated with the use of parameters, such as PAOP and CVP. Resuscitation to absolute PAOP and CVP in patients with IAH/ACS should be avoided because such a practice can lead to under-resuscitation, inappropriate administration of diuretics, and inappropriate end-organ perfusion.
Use volumetric monitoring to assess fluid status Continuous right ventricular end-diastolic volume obtained with PAC The new gener-

ation of PACs allows continuous determination of CO, right ventricular ejection fraction (RVEF), and right ventricular end-diastolic volume index (RVEDVI) (Vigilance monitor, Edwards Lifesciences, Irvine, CA, USA).22,24,5659 Continuous CO monitoring provides a beat-to-beat assessment of patient response to therapeutic interventions. RVEF is used to calculate the RVEDVI using the equation, RVEDVI 5 SVI/RVEF, where SVI indicates stroke volume index. Independent of the effects of changing ventricular compliance and increased ITP or IAP, RVEDVI has been reported in several studies as an accurate indicator of preload recruitable increases in cardiac index (CI) in a variety of patient populations, including hemorrhagic, cardiogenic, and septic shock. Moreover, it has been shown that RVEDVI goal-directed fluid resuscitation leads to a reduction of hard clinical endpoints, such as multiple organ failure and death.24 Many studies report that at high levels of PEEP, RVEDVI consistently maintained a highly significant correlation with CI, whereas PAOP and CVP frequently exhibited inverse correlations with CI.22,58 Although some investigators have raised concern that mathematical coupling, the interdependence of 2 variables when one is used to calculate the other, may explain the significant correlation between RVEDVI and CI, 3 separate studies have confirmed the validity of RVEDVI as a predictor of preload recruitable increases in CI.60,61
Intermittent global end-diastolic volume obtained with PiCCO Pulse contour analysis

uses a dedicated PiCCO thermistor-tipped arterial catheter (Pulsion Medical Systems, Munich, Germany) to continuously analyze patient heart rate and arterial pressure waveform. By calculating the change in pressure over time from end diastole to end systole and making several assumptions regarding the elastic and mechanical properties of the arterial tree, continuous beat-to-beat SVI can be estimated and CI calculated. This technology can also be used to measure stroke volume variation (SVV), the variation in beat-to-beat stroke volume during a single respiratory cycle, and pulse pressure variation (PPV), which have been suggested as valuable predictors of fluid responsiveness.62 Due to the unique mechanical characteristics of each patients arterial tree, initial calibration of the monitoring system using the transpulmonary

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thermodilution technique and the Stewart-Hamilton equation greatly improves the accuracy of the stroke volumes subsequently calculated. Pulse contour analysis has several advantages over traditional intermittent thermodilution PAC monitoring. First, it is less invasive, only requiring an arterial catheter and a central venous catheter. Second, it provides an estimate of global end-diastolic volume (GEDV) and global ejection fraction as opposed to RVEDV and RVEF. Third, PiCCO allows calculation of EVLW index (EVLWI) as surrogate predictor of capillary leak.
Fluid Resuscitation in Patients with IAH/ACS Use volumetric measurements

As discussed previously, volumetric measurements should be used because only GEDVI index (GEDVI) and RVEDVI correctly reflect ventricular filling in IAH/ACS because traditional intracardiac filling pressures (PAOP and CVP) tend to be erroneously elevated despite intravascular fluid depletion in patients with IAH/ACS.63
Use continuous hemodynamic monitoring

Cardiac contractility in critically ill patients changes dynamically from beat to beat and can be described as a series of ventricular function curves.55 Each curve has an associated ejection fraction and associated optimal LVEDV. Resuscitation to this plateau LVEDV is widely believed to optimize patient intravascular volume, cardiac function, and end-organ perfusion. As a result of this constantly changing ventricular compliance there cannot be a single value of RVEDVI or GEDVI that can be considered the goal of fluid resuscitation in every patient with IAH/ACS. Each patient must, therefore, be resuscitated to the LVEDV that optimizes the circulation at that specific moment of time. Because this optimal volume varies in response to a patients improving or deteriorating cardiac status, the true value of continuous hemodynamic monitoring becomes clear.
Use abdominal perfusion pressure as resuscitation target

APP is defined as MAP minus IAP.64 Because patients with IAH/ACS have end-organ hypoperfusion due to the combination of reduced MAP and increased IAP with secondary increased end-organ pressure, it seems reasonable to use APP in stead of MAP in combination with arterial lactate and urinary output as primary resuscitation targets. APP has been demonstrated to exceed the clinical prediction of IAP alone in 2 clinical trials. In a retrospective trial of surgical/trauma patients, Cheatham and colleagues64 reported that APP greater than 50 mm Hg optimized survival. Moreover APP was superior to MAP, arterial pH, lactate, and base deficit and hourly urinary output as predictor of patient outcome. Cheatham16 reported, in a mixed surgical/ medical population, that failure to maintain APP greater than 60 mm Hg by day 3 discriminated between survivors and nonsurvivors. As a resuscitation endpoint, APP has yet to be subjected to a prospective, randomized clinical trial.
Use pulse pressure variation as predictor of fluid responsiveness

Target APP values should be achieved through a balance of judicious fluid resuscitation to reach optimal LVEDV and through application of appropriate vasopressive and/ or inotropic medications. Indiscriminate fluid administration should be avoided because it places patients at risk for secondary ACS and because it increases EVLWI in patients with capillary leak. Because in patients with IAH/ACS the increased IAP prevents venous return from the legs and the mesenteric veins, the classical passive leg-raising test may be false negative.65,66 The Trendelenburg position has a beneficial effect on IAP and results in a more pronounced venous return from the legs and mesenteric veins but has the disadvantage of increased risk of ventilator-associated

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pneumonia and increased ICP. SVV and definitely PPV are better predictors of fluid responsiveness in patients with IAH/ACS than classical passive leg raising. Increased IAP results in concomitant increased ITP, however, and thus increased SVV and PPV also. This means that the classical 10% to 12% SVV/PPV cutoff cannot be used. A 20% to 25% SVV/PVV cutoff has been proposed to determine fluid responsiveness in patients with ACS. Moreover, PPV has been demonstrated superior to SVV for predicting fluid responsiveness in the patients.6769
Mechanical Ventilation in Patients with IAH/ACS Recruitment and PEEP setting

Compression of the pulmonary parenchyma as a result of elevated IAP and cephalad deviation of the diaphragm reduces functional residual capacity of the lungs.31 Therefore, higher opening pressures are needed to recruit the lungs (40 1 IAP/2). PEEP should be set equal to IAP to counteract IAP to counteract the deleterious effects on respiratory function caused by IAP while at the same time avoiding overinflation of already well-aerated lung regions.31 Moreover, the increased left ventricle afterload induced by increased IAP may be counteracted by moderate PEEP, as reported in a recent French echocardiographic study.70
Use transmural plateau pressures

IAH decreases total respiratory system compliance by a decrease in chest wall compliance whereas lung compliance remains unchanged.31 Because tidal volume equals compliance (plateau pressure [Pplat] PEEP), this reduced compliance together with increased PEEP reduces tidal volumes during pressure-controlled ventilation. During lung-protective ventilation, inspiratory pressure can be safely elevated if transmural Pplat (Pplattm 5 Pplat IAP/2) is not higher then 35 cm H2O.2
Monitor extravascular lung water

EVLWI should be monitored because patients with IAH/ACS are at increased risk for pulmonary edema and patients with primary ACS often develop a secondary acute respiratory distress syndrome.31,33 The PAOP criterion in acute respiratory distress syndrome consensus definition is futile in patients with IAH/ACS because PAOP is erroneously elevated.
Use of neuromuscular blockers

Consideration of neuromuscular blockers should balance the potentially beneficial effects on abdominal muscle tone, resulting in decreased IAP and improved APP against the potentially detrimental effect on respiratory muscles and lung mechanics, resulting in atelectasis and superinfection.54
Treatment of ACS

Immediate abdominal decompression should be considered in any patient who demonstrates evidence of ACS. In surgical patients, this is best achieved by either performing a decompressive laparotomy or revising a patients temporary abdominal closure if the abdomen is already open.71 The decompressive laparotomy can be performed either in the operating room or at a patients bedside in the ICU based on current hemodynamic stability. Such a procedure should not be feared or delayed because rapid decompression after the diagnosis of ACS dramatically improves cardiac function and results in improved organ perfusion and survival. Once a patients abdomen in open, both IAP and APP should continue to be monitored. In patients with an open abdomen, inability to maintain adequate APP is an indication to decompress the patients abdomen further through either a larger

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laparatomy or placement of a looser, more compliant temporary abdominal closure. In medical patients whose IAH is secondary to accumulation of ascites or resuscitation fluid, paracentesis should be considered a viable alternative to open abdominal decompression. Leaving the paracentesis catheter in place until a patients condition stabilizes allows ongoing drainage of peritoneal fluid, continued reduction in IAP, and a reduced incidence of recurrent ACS. In medical patients with IAH without ACS, ileus should be corrected and diuretics or renal replacement therapy in combination with albumin considered. Patients whose IAH is secondary to retroperitoneal hemorrhage, visceral edema, or ileus are best served by open abdominal decompression because paracentesis is not effective in reducing the severity of IAH or restoring end-organ perfusion. The timing of closing a patients abdomen after decompression should be guided by measurements of IAP and APP.
SUMMARY

IAH and ACS have been increasingly recognized as causes of significant morbidity and mortality in critically ill patients. Cardiovascular dysfunction, as a result of elevations in ITP and IAP, plays a major role in the systemic organ dysfunction and failure that characterizes IAH/ACS. Aggressive hemodynamic monitoring and optimization of both systemic and regional perfusion are essential to improve patient outcome. Traditional measures of intravascular volume, such as PAOP and CVP, are erroneous in patients with IAH and reliance on such measurements may lead to inappropriate fluid resuscitation and administration of diuretics, leading to end-organ hypoperfusion. Volumetric estimates of preload recruitable increases in CO, such as RVEDVI and GEDVI, should be used in such patients with changing ventricular compliance and elevated ITP and IAP. Clinicians must be aware of the interactions between IAP, ITP, PEEP, and intracardiac filling pressures to correctly resuscitate these patients. Patients should be resuscitated to maintain APP of 50 mm Hg to 60 mm Hg through judicious fluid resuscitation and application of vasopressive/inotropic agents. When adequate APP cannot be maintained or a patient demonstrates evidence of ACS, strong consideration should be given to performing abdominal decompression to relieve severe IAH and restore adequate cardiovascular function.
REFERENCES

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