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Year : 2019  |  Volume : 5  |  Issue : 2  |  Page : 47-56

Abdominal Compartment Syndrome: A Comprehensive Pathophysiological Review

1 Department of Surgery, Maulana Azad Medical College, New Delhi, India
2 Department of Surgery, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
3 Department of Transfusion Medicine, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India

Date of Web Publication20-Aug-2019

Correspondence Address:
Dr. Lovenish Bains
Department of Surgery, Maulana Azad Medical College, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mamcjms.mamcjms_32_19

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With growing knowledge and advances in surgery and critical care, we are witnessing new concepts and understanding in spectrum of disease pathology. Abdominal compartment syndrome (ACS) or intraabdominal hypertension (IAH) is one such intriguing entity that has rapidly caught attention of all surgeons and intensivists. Lately, lot of researches are showing the correlation of ACS-IAH with worse outcomes and even mortality in sick patients. IAH has been found to be an important contributor to early organ dysfunction among patients with trauma and sepsis that can cause significant impairment of renal, gastrointestinal, hepatic, cardiac, pulmonary, and central nervous system function. The pathology is even more significant in cases of abdominal surgery or trauma. ACS-IAH is commonly seen in severely sick patients, with prevalence reaching to as high as 50%. There is an increasing awareness of IAH as evidenced by increasing number of studies in the literature. Although there is lot of documented evidence around the topic of ACS-IAH, measuring and managing it still does not figure in most of protocols and practice guidelines in India. The authors believe that a thorough understanding about IAH will enable medical professional in reducing surgical mortality and morbidity. Hence, there was a need to review literature for the latest concept and evidence especially in the area of ACS-IAH, in context of our country India, where there is dearth of knowledge in this subject and its implications. The present review is set to present the current understanding of IAH from pathophysiological and clinical point of view with future insights.

Keywords: Abdominal compartment syndrome (ACS), intraabdominal hypertension (IAH), intraabdominal pressure (IAP), mortality, organ dysfunction

How to cite this article:
Bains L, Lal P, Mishra A, Gupta A, Gautam KK, Kaur D. Abdominal Compartment Syndrome: A Comprehensive Pathophysiological Review. MAMC J Med Sci 2019;5:47-56

How to cite this URL:
Bains L, Lal P, Mishra A, Gupta A, Gautam KK, Kaur D. Abdominal Compartment Syndrome: A Comprehensive Pathophysiological Review. MAMC J Med Sci [serial online] 2019 [cited 2022 Jan 28];5:47-56. Available from: https://www.mamcjms.in/text.asp?2019/5/2/47/264782

  Background Top

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 concept of intraabdominal hypertension (IAH) was proposed in the late 1800s, forgotten after World War I, and rediscovered near the end of the 20th century.[1] It has received tremendous attention from the last 2 decades. In 2004, a group of international physicians and surgeons across the globe formed the World Society of the Abdominal Compartment Syndrome (WSACS).[2] IAH has a prevalence of at least 50% in the critically ill population.[3] Despite it being identified as an independent risk factor for death,[4] most members of the critical care team do not assess for IAH and are unaware of the consequences of untreated IAH. The consequences include ACS, multisystem organ failure, and death. The problem of ACS goes well beyond the care of surgical patients, encompassing many diverse disease states and clinical scenarios. Therefore, the ACS should be viewed as the end result of a progressive, unchecked rise in IAP from a myriad of disorders that eventually leads to multiple-organ dysfunction.

  Incidence/Prevalence Top

IAH was found to occur in 32.1% of intensive care unit (ICU) patients, and ACS was reported in up to 4.2% of patients requiring critical care.[5] Vidal et al.[1] studied the incidence of IAP in 83 critically ill patients in a single ICU and found that 31% of the patients had IAH at the time of admission to the unit, and the condition developed in another 33% after admission. Also, patients with IAH were more sick and had a higher mortality rate (53% vs. 27%; P = 0.02) as compared to patients without IAH.[6] Reintam et al.[3] performed a study to identify the differences in incidence, course, and outcome of primary and secondary IAH and to determine if IAH is an independent risk factor for death. They found that development of IAH is an independent risk factor for death and further concluded that compared with primary IAH, secondary IAH does not occur as often, has a different development course, and has worse outcomes.[3] A review of studies indicates that IAH has a prevalence of 17% to 83% and ACS incidence is 14% to 56% in critically ill population involving trauma, burns, pancreatitis, aortic aneurysm surgery, liver transplant, and others.[7] These studies indicate that IAH occurs frequently and may worsen patients’ outcome.

  Historical Perspectives Top

The effects of elevated IAP have been known since the late 19th century when Marey and Burt highlighted the respiratory effects of elevated IAP. In 1890, Heinricius demonstrated that elevation of IAP to 27 and 46 cm H2O led to death in feline and porcine models.[8] Emerson[1] in 1911 experimented in dogs and proved that increased IAP may cause death due to cardiac failure. He was actually the scientist who built the foundations of the clinical and experimental research on IAP in the 20th century.[9] Wendt in 1913 first described the association of IAH and renal dysfunction and Bradley corroborated his findings.[10] Basic science and clinical observations have since confirmed the effects of elevated IAP on multiple organ systems. The term ACS was first used by Kron et al.[11] in the early 1980s to describe the pathophysiology resulting from IAH secondary to aortic aneurysm surgery.[11] It became a new clinical entity in the 1980s in emergency surgery patients and ACS terminology is said to be introduced by Fietsam et al. in 1989.[12] WSACS was formed in December 2004, in Noosa, Queensland, Australia, and was attended by 160 multidisciplinary critical care physicians and nurses from around the world; in 2006, they came out with the first standardized consensus definitions regarding IAP and ACS based upon the current understanding of the pathophysiology surrounding these two syndromes.[13] WSACS over a period of time backed by evidence from studies have formulated definitions, standardized measurement methodology, and provided management guidelines.[14] Using Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system for clinical practice guidelines, the WSACS released updated definitions and recommendations in 2013.[15]

  Definitions (WSACS) Top

There was an era of indistinct and variable definitions of IAH/ACS with variable methods of measurement of intraabdominal pressure (IAP) until the WSACS has standardized measurement methodology.[14],[15],[16] Previously Burch/Meldrum classification was widely used that has been now replaced by WSACS grading classification of elevated IAP.[15],[16],[17]

IAH is a sustained or repeated pathological elevation of IAP of 12 mmHg or greater. IAH is graded as follows [[Table 1]]:
Table 1 Grading of intraabdominal pressure

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Abdominal perfusion pressure (APP) − APP is a measure of the relative adequacy of abdominal blood flow. APP is calculated by subtracting the IAP from the mean arterial pressure (MAP): MAP − IAP = APP.

Abdominal compartment syndrome (ACS) − ACS is a sustained IAP greater than 20 mmHg (with or without an APP <60 mmHg) associated with new organ dysfunction or failure.

Salient definitions from the WSACS[14],[15],[16]

  1. IAP is the steady-state pressure concealed within the abdominal cavity.
  2. The reference standard for intermittent IAP measurements is via the bladder with a maximal instillation volume of 25 mL of sterile saline.
  3. IAP should be expressed in mmHg and measured at end expiration in the supine position after ensuring that abdominal muscle contractions are absent and with the transducer zeroed at the level of the midaxillary line.
  4. IAP is approximately 5 to 7 mmHg in critically ill adults.
  5. IAH is defined by a sustained or repeated pathological elevation in IAP greater than or equal to 12 mmHg.
  6. Primary IAH or ACS is a condition associated with injury or disease in the abdominopelvic region that frequently requires early surgical or interventional radiological intervention.
  7. Secondary IAH or ACS refers to conditions that do not originate from the abdominopelvic region.
  8. Recurrent IAH or ACS refers to the condition in which IAH or ACS redevelops following previous surgical or medical treatment of primary or secondary IAH or ACS.
  9. APP = MAP − IAP.
  10. Abdominal compliance is a measure of the ease of abdominal expansion, which is determined by the elasticity of the abdominal wall and diaphragm. It should be expressed as the change in intraabdominal volume per change in IAP.

  Etiology of elevated IAP Top

The ACS can develop in both nonsurgical and surgical patients[18] [[Table 2]]. Primary ACS is due to injury or disease in the abdominopelvic region, which can be intraluminal or extraluminal causes. Extraluminal causes could be any pathology causing intraabdominal collections outside the bowel lumens, for example, abdominal trauma, hemorrhage, edema, bowel distention, mesenteric venous obstruction, abdominal packs, tense ascites, peritonitis, and tumor.[13],[19],[20] IAH/ACS can also develop due to intraluminal pathology like intestinal obstruction, gastroparesis, pseudocolonic obstruction, pseudomembranous colitis, and others. Increases in retroperitoneal volume from pancreatitis, hemorrhage, or edema can lead to the ACS, which is most often reported after pelvic trauma, and elective or emergent aortic surgery.[27],[28] Extrinsic compression of the abdomen can also lead to increases in IAP. Examples of this include burn eschars, pneumatic antishock garments, tight abdominal closures, and repair of abdominal wall defects or large incisional hernias secondary to a “loss of the right of domain.”[21],[22],[23],[24]
Table 2 Causes of elevated intraabdominal pressure[28]

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Secondary ACS refers to conditions that do not originate in the abdomen or pelvis (e.g., fluid resuscitation, sepsis, burns, and renal dialysis). The ACS develops with acute and rapid (i.e., in hours) elevation in IAP. Chronic increases in intraabdominal 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.” The gradual increase compensates the various organ systems for the changes in IAP. Consequently, the acute deterioration seen with ACS does not occur in these patients.

The causes for IAH leading to ACS is multifactorial in critically ill patients.[26],[27],[28] 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. 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.[25] 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. 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.[26],[28] Thus, in critically ill patients, these factors are often additive, leading to or aggravating multisystem organ failure via a series of “vicious cycles” perpetuated by progressive increases in IAP.

  Pathological effect on organs Top


The abdomen can be considered a compartment with inflexible components such as spine, pelvis, and costal arch whereas pliable components are diaphragm and abdominal wall. The abdominal compartment contains solid organs, hollow organs, fluid, gas, solids, and adipose tissue like stomach, large and small intestine, omentum, liver, spleen, pancreas, gall bladder, kidneys, adrenal glands, ureters, bladder, and, in females, the uterus. Major blood vessels abdominal aorta with its branches and inferior vena cava course through this compartment. Whenever a condition increases the IAP, not only the gut but all major body systems can be affected, and the effects can lead to multisystem organ failure and death [[Figure 1]]. The various adverse effects of IAH and ACS on organ systems are as follows.
Figure 1 Effects of increasing intraabdominal pressure (IAP) on organ function.

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Gastrointestinal function

The mesenteric arterial, hepatic arterial, intestinal mucosal, hepatic microcirculatory, and portal venous blood flow all have been shown to be reduced with IAH.[27] Increased IAP results in an increase in vascular resistance and decreased cardiac output with resultant decrease in gut perfusion and ultimately tissue ischemia. 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.[28] Patients with IAH are also at high risk for stress ulcers because of the loss of the mucosal barrier.[29] An IAP of up to 20 mmHg can decrease mesenteric perfusion by 40%, and pressures up to 40 mmHg can decrease mesenteric perfusion by 70%.[30] The correction of IAH can lead to ischemia reperfusion injury and send inflammatory cytokines to other organs, setting the ground work for multisystem organ failure.[29] Distention of the abdominal wall by IAH leads to decreased compliance of the wall, further compounding the IAH. The vascular liver is extremely susceptible to IAH, even low pressure as 10 mm can decrease hepatic perfusion.[29],[31],[32]

Cardiac function

The elevation in IAP leads to a reduction in cardiac output that is most consistently seen at an IAP > 20 mmHg. The components of cardiac output (i.e., preload, afterload, and contractility) are all adversely affected by increased IAH.[32] The diminished cardiac output 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 these lead to a reduced stroke volume with a compensatory increase in heart rate.[31] Increased thoracic pressure and diaphragmatic elevation are responsible for reducing ventricular compliance.[33] This combined with increased systemic afterload reduces cardiac contractility at IAP over 30 mmHg, shifting the Starling curve to the right and downward.[34] There can be falsely elevated central venous pressures and pulmonary artery wedge pressures because of the effects of IAH. These elevations may lead clinicians to surmise that a patient is volume loaded or overloaded.[31] The increased workload increases myocardial oxygen demand. The systemic vascular resistance increases due to compensatory measures of the sympathetic nervous system to maintain arterial pressure. In addition, the direct compression of the abdominal aorta, due to IAH, further increases systemic vascular resistance and the workload on the left ventricle.[31],[35]

Respiratory function

The diaphragm is pushed upward with the distension of abdomen with intestinal gas, fluid, or edematous organs, impinging on the thoracic cavity. Approximately, 50% of the IAP is dispersed across the diaphragm and affects respiration and ventilation.[34] Pulmonary dysfunction may be one of the earliest signs of ACS.[36] The lungs cannot expand fully, respiratory excursion is limited, and with reduced chest wall compliance decreases the inhaled tidal volume that leads to arterial hypoxemia and hypercarbia. Compression atelectasis may be frequent. Increased peak inspiratory pressure in mechanically ventilated patients can also cause alveolar barotrauma.

Renal function

Kidney is affected by IAH by two ways: by direct compression of renal vessels and by increased renal vasoconstriction caused by renin-angiotensin induced by the decrease in preload. The mechanisms of renal derangements with IAH involves reduced absolute and proportional renal arterial flow, increased renal vascular resistance with changes in intrarenal regional blood flow, and reduced glomerular filtration.[37] The changes in renal and systemic hemodynamics lead to increased circulating levels of antidiuretic hormone, renin, and aldosterone, which further increase renal vascular resistance and produce sodium and water retention.[38] Oliguria is one of the first manifestations of IAH. Oliguria can be seen at IAP of 15 to 20 mmHg, whereas increases to 30 mmHg or above leading to anuria.[39] The renal impairment, as indicated by an elevated serum level of creatinine, may not appear until 2 to 3 days after the incident of IAH.[40] IAH is also an independent cause of renal dysfunction. Kirkpatrick et al.[41] found that in the porcine model, the renal artery resistive index correlated strongly and linearly with the severity of IAH. The peak systolic velocity linearly increased, and the peak diastolic velocity linearly decreased with increasing IAP. Renal Doppler ultrasound is a potential noninvasive screening tool for the renal effects of IAH.[41]


Elevated intracranial pressure and reduced cerebral perfusion pressure have been described with acute changes in IAP in animal models and in human studies.[42] An Increase in IAP forces the diaphragm up decreasing intrathoracic space, increasing the intrathoracic pressure that puts pressure on jugular veins and decreases the drainage of cerebrospinal fluid and blood, leading to increased intracranial pressure.[43]

Peripheral perfusion

Increased IAP is said to increase femoral venous pressure, increase peripheral vascular resistance, and reduce femoral artery blood flow by up to 60%; which increases the likelihood of deep vein thrombosis. Venous return has been shown to be impaired at an IAP as low as 15 mmHg, decreasing with further increases in IAP. This occurs from increased venous resistance within the abdomen and thorax resulting in reduced caval and retroperitoneal venous flow.[36]

IAH can affect almost all body systems, hence it has been proposed as the initial fall of the dominoes on the pathway of multisystem organ failure.[44]

  Clinical Examination Top

Abdominal pain is a common presentation but its history varies depending on the cause of ACS. ACS is usually suggested by an increased abdominal girth. It is a matter of utmost concern if the change is acute and the abdomen is tense and tender. The first signs of IAH like difficult breathing or decreased urine output must be paid attention to. Physical examination was found to be neither sensitive nor specific for the diagnosis of IAH/ACS with a sensitivity of 56%, specificity of 87%, negative predictive value of 94%, positive predictive value of 35%, and accuracy of 84%.[45]

  Radiological Examination Top

Imaging studies such as chest X-ray, ultrasound abdomen, and computed tomography scan are not useful to diagnose IAH/ACS efficiently but can give some clue to the possibility, such as elevated diaphragm, basal atelectasis, inferior vena caval compression, infiltration of the retro peritoneum that is out of proportion to peritoneal disease, massive abdominal distension, direct renal compression or displacement, or bilateral inguinal herniation.[46] Ultrasound (point-of-care ultrasound or POCUS) was comparable to abdominal X-ray, but shown to be superior in determining the gastric content (fluid vs. solid). Furthermore, POCUS allowed faster determination of correct naso gastric tube (NGT) positioning in the stomach, avoiding bedside radiation exposure. It can be used as adjunct tool in both diagnosis and treatment during the course of IAH.[47]

  Measurement of IAP Top

In the past, urinary bladder, stomach, inferior vena cava, uterus, and rectum have been utilized in measurement of IAP.[48] However, most conditions causing increased IAP may preclude them for use. Stomach is contraindicated in gastric laceration repair, ileus or bowel obstruction with large volume gastric aspirate, and partial or total gastric resection; IAP measurement through inferior vena cava is associated with thrombosis, venous thromboembolism, venous or arterial laceration, femoral nerve injury, hematoma formation, pseudoaneurysm formation, and central line-associated bloodstream infections. Rectal and uterine pressure techniques have not been validated and have no clinical implications in the ICU setting.[49]

Kron et al. were the first to measure intravesical pressure using manometer.[12] Later, Cheatham and Safcsak[49] revised this technique by creating a closed system, which was safer and unlikely to introduce bladder infection.[49] WSACS has standardized intravesical (urinary bladder) pressure measurement as the gold standard for measurement of IAH/ACS.[15] This method uses an indwelling urinary catheter, a pressure transducer, and a syringe or similar device, capable of infusing fluid. This technique is reliable, relatively noninvasive, and elementary process.[50],[51] The pressure is measured at end expiration in the supine position after ensuring that abdominal muscle contractions are absent. Waiting for 30 s may help to relax the bladder. The transducer should be zeroed at the level of the midaxillary line and the amount of saline to be instilled is 25 mL as standardized by WSACS. The manometer technique is similar to the method of measuring central venous pressure with a fluid column. With a urinary catheter in place, the only equipment needed is a centimeter ruler. This technique is called the U-tube technique and is a modification of a technique first developed by an emergency department nurse.[45] The clinical validation with the U-tube technique is poor, and the method is recommended primarily for screening. Commercial kits include the AbViser AutoValve (ConvaTec), Bard IAP monitoring device (Bard), and FoleyManometer (Holtech device).

  Management Top

The definitive management of IAH/ACS is surgical decompression, but supportive medical therapy should be attempted before resorting to this. The mission of the WSACS is as follows − now, the Abdominal Compartment Society has always been to promote research, foster education, and improve the survival of patients with IAH/ACS. WSACS has provided algorithm for management of IAH/ACS [Figure 2] and [Figure 3]. Nowadays, the trend is more toward less-invasive and less-morbid therapies such as abdominal wall escharotomy in burns or percutaneous drainage of intraabdominal collections.[52],[53] Experienced clinicians have recognized that if there is no ongoing ischemia or shock requiring aggressive resuscitation, and mild–moderate IAH after abdominal wall reconstruction (AWR) may be permissive and mitigated by spontaneous postoperative accommodation in intraabdominal compliance.[54],[55] In 2017, the incidence of overt ACS was significantly lower than previous decades due to better understanding hemostatic or balanced blood component resuscitation strategies that limit the use of crystalloid fluids.[56] Aggressive fluid resuscitation, especially with crystalloids is more likely to lead to IAH than primary causes like trauma and abdominal sepsis.[57] As these patients are hemodynamically unstable initially, they receive large amounts of crystalloids; the fluid goes into the third space leading to intravascular volume depletion, hypotension, and acidosis with resultant bowel edema and development or aggravation of ACS. Renal dysfunction caused by ACS furthermore aggravates the fluid overload, by impairing diuresis. The WSACS recommends pharmaceutic diuresis in the initial phase and, if needed, hemofiltration should be installed early in the management.[16] Many of IAH/ACS patients will need ventilator support and should have a lung protective strategy like low tidal volume, pressure limitation, permissive hypercapnia, use of positive end-expiratory pressure, and use of muscle relaxants in indicated patients.[45]
Figure 2 Algorithm 1: intraabdominal pressure (IAP)/abdominal compartment syndrome (ACS) medical management (WSACS). WSACS, World Society of the Abdominal Compartment Syndrome.

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Figure 3 Algorithm 2: intraabdominal pressure (IAP)/abdominal compartment syndrome (ACS) management (WSACS). WSACS, World Society of the Abdominal Compartment Syndrome.

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Principles of supportive care are as follows[16],[58],[59],[60],[61],[62]:
  1. Evacuate intraluminal contents: nasogastric and rectal drainage.
  2. Drain extraluminal collections: evacuate hemoperitoneum, ascites, intraabdominal abscess, and retroperitoneal hematoma.
  3. Improve abdominal wall compliance: supine position, adequate analgesia, sedation, and sometimes muscle paralysis.
  4. Optimization of fluid administration: early goal-directed fluid resuscitation.
  5. Optimization of systemic and regional perfusion

A recent systematic review and meta-analysis on effect of decompressive laparotomy on organ function in 286 patients with ACS has been published recently.[63] The baseline mean IAP was 31.7 mmHg and ranged from 23 to 43.4 mmHg that improved to an average of 13.5 mmHg, varying between 11 and 17 mmHg after the decompression. The mortality rate was reported in 11 of 12 studies and ranged from 22.2% to 71.4% in the individual studies; overall, mortality was 49.7%. There was a trend toward a statistically significant correlation between time to decompression and mortality in patients with grades III and IV IAH.

  Recent Insights Top

  1. Procalcitonin (PCT) and C-reactive protein: The correlation of PCT values with IAH grades is quite significant whereas the CRP results remain high in IAH but without significant difference between the different grades of IAH.[64]
  2. Mitochondrial Ca2+ uptake 1-related oxidation/antioxidation disequilibrium is strongly involved in IAH-induced damage to intestinal barriers.[65]
  3. Melanocortin 4 (MC4 receptor) agonist counteracts the intestinal inflammatory response, ameliorating intestinal injury in experimental secondary IAH by MC4 receptor-triggered activation of the cholinergic antiinflammatory pathway. This may represent a promising strategy for the treatment of IAH in the future.[66]
  4. Intestinal fatty acid-binding protein (I-FABP) is excreted in urine and blood specifically from damaged intestinal epithelial cells. Claudin-3 is a specific protein that is excreted in urine following disruption of intercellular tight junctions. I-Fabulous study aims to investigate if I-FABP and Claudin-3 can be used as a diagnostic tool for identifying patients at risk for IAP-related complications.[67]
  5. Melatonin when given prior to decompression reduces the levels of glutathione, malondialdehyde levels, and myeloperoxidase activity in rats with ACS. This indicates its protective effect on oxidative stress during reperfusion and may be a reperfusion injury-limiting agent.[68]
  6. New medical treatment options that are still experimental include tissue plasminogen activator (tPa), theophylline, and octreotide.
    1. tPa was evaluated for retroperitoneal hematoma. The mean IAP was 23.5 mmHg before decompression (range 12−35), and when tPa was given, IAP dropped to a mean of 16 mmHg (range 10−28.5) after 24 h of administration.[69]
    2. Theophylline improved renal function, splanchnic perfusion, and cardiac contractility possibly by counteracting adenosine binding to adenosine receptors.[70]
    3. Octreotide, a synthetic somatostatin analogue, by decreasing myeloperoxidase (MPO) activity and malondialdehyde levels and thereby increasing levels of glutathione if given before decompression of IAP, has been shown to improve the reperfusion-induced oxidative damage in rats with ACS.[71]

All the novel medical options for management of IAH/ACS apart from standard medical management-like evacuation of intraluminal and extraluminal contents, improvement of abdominal wall compliance, are still in experimental stage and not recommended for routine use.

  Conclusion Top

IAH/ACS is not a problem of the abdomen but rather a systemic problem affecting various body systems adversely with deleterious consequences. Addressing this important pathology in a timely manner is crucial for the better outcome of critically ill patients. The problem of IAH/ACS should be always kept in mind and prevention, rather than recognition or cure is far more important posttrauma patients. Mainstay of the management in IAH/ACS is still surgical decompression but less-invasive therapies (drainage, diuresis, and paralytics) must be implemented first. Judicious selection and optimized timing of the intervention may result in better clinical outcomes in the future. More studies are needed are needed for insights into management.

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Conflicts of interest

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