Abdominal Compartment Syndrome

Practice Essentials

Although compartment syndrome is well recognized to occur in the extremities, it also occurs in the abdomen and, some believe, in the intracranial cavity. Compartment syndrome occurs when a fixed compartment, defined by myofascial elements or bone, becomes subject to increased pressure, leading to ischemia and organ dysfunction. The exact clinical conditions that define abdominal compartment syndrome (ACS) are controversial; however, organ dysfunction caused by intra-abdominal hypertension (IAH) is considered to be abdominal compartment syndrome. Intra-abdominal hypertension is defined as sustainedIAP above 12 mm Hg, and  ACS results from repeated elevation of pressure above 20 mm Hg with associated organ dysfunction.^{[1, 2, 3, 4, 5]}

Organ dysfunction may be respiratory insufficiency secondary to compromised tidal volumes, decreased urine output caused by falling renal perfusion, or any organ dysfunction caused by increased abdominal compartment pressure. Surgical decompression remains the mainstay treatment of ACS.^[6] However, prevention and early treatment of the potential cause may prevent progression of IAH to ACS.^{[7, 1, 2, 8, 9, 10, 3, 11]}

The frequency of abdominal compartment syndrome in trauma ICU admissions is anywhere from 5 to 15% and 1% of general trauma admissions. Abdominal compartment syndrome has been documented in all age groups. The intra-abdominal pressure (IAP) that leads to morbidity (>20 mm Hg) appears to be similar in the pediatric population.^{[12, 13]}  The incidence of IAH/ACS in the pediatric population is 12.7 to 20%.^{[14, 15, 16]}

In a retrospective study, by Bozer et al, of 2887 children (< 18 yr) in 49 children’s hospitals wth ACS, overall mortality was 48.87%, with mortality in patients aged zero to 30 days being 58.61%.^[17]

Abdominal compartment syndrome was recognized clinically in the 19th century when Marey and Burt observed its association with declines in respiratory function. In the early 20th century, Emerson's animal experiments demonstrated mortality associated with abdominal compartment syndrome. Initially, cardiorespiratory compromise was thought to be the cause; however, renal failure was hypothesized by Wendt and was later studied by Thorington and Schmidt. Kron and Iberti developed a simple method of accurately measuring intra-abdominal pressure. This has led to a better understanding of the relationship between IAH and abdominal compartment syndrome.^{[18, 19, 20, 21, 22, 23]}

WSACS guidelines

The World Society of the Abdominal Compartment Syndrome has published the following definitions and recommendations^{[2, 16, 24]} :

• Intra-abdominal pressure (IAP) is approximately 5-7 mm Hg in critically ill adults.
• Intra-abdominal hypertension is defined by a sustained or repeated pathological elevation in IAP of ≥12 mm Hg.
• ACS is defined as a sustained IAP >20 mm Hg associated with organ dysfunction/failure.
• IAH is graded as follows: Grade I: IAP 12-15 mm Hg;  Grade II: IAP 16-20 mm Hg; Grade III: IAP 21-25 mm Hg; Grade IV: IAP >25 mm Hg.
• Patients should be screened for IAH/ACS risk factors upon ICU admission and in the presence of new or progressive organ failure.
• APP should be maintained above 50-60 mm Hg in patients with IAH/ACS [Abdominal perfusion pressure (APP) = mean arterial pressure (MAP) – IAP].
• Fluid resuscitation volume should be carefully monitored to avoid overresuscitation in patients at risk for IAH/ACS.
• Hypertonic crystalloid and colloid-based resuscitation should be considered in patients with IAH to decrease the progression to secondary ACS.
• Surgical decompression should be performed in patients with ACS that is refractory to other treatment options.
• Presumptive decompression should be considered at the time of laparotomy in patients who demonstrate multiple risk factors for IAH/ACS.
• Recommend that studies of IAH or ACS adopt the transbladder technique as a standard IAP measurement technique
• Suggest brief trials of neuromuscular blockade as temporizing measure in treatment of IAH.

Three categories

As the diagnosis of abdominal compartment syndrome became easier to establish, it was observed to occur as a consequence of a variety of primary clinical events. Abdominal compartment syndrome can be divided into the following 3 categories:

• Primary or acute abdominal compartment syndrome occurs when intra-abdominal pathology is directly and proximally responsible for the compartment syndrome
• Secondary abdominal compartment syndrome occurs when no visible intra-abdominal injury is present but injuries outside the abdomen cause fluid accumulation^[25]
• Chronic abdominal compartment syndrome occurs in the presence of cirrhosis and ascites or related disease states, often in the later stages of the disease

In the ED and ICU

In the emergency department and intensive care unit, abdominal compartment syndrome is recognized with growing frequency as the cause of morbidity such as metabolic acidosis, decreased urine output, and decreased cardiac output. The cause of these events might easily be mistaken for other pathologic events such as hypovolemia if the clinician is not alert to the morbidity associated with abdominal compartment syndrome.

Therapy should include fluid resuscitation and transfusion if needed. Pharmacologic therapy is less effective than mechanical drainage. Paracentesis may be a superior alternative to decompressive laparotomy in this patient population.

• References

Pathophysiology

Organ dysfunction with abdominal compartment syndrome is a product of the effects of IAH on multiple organ systems. Abdominal compartment syndrome follows a destructive pathway similar to compartment syndrome of the extremity.

Problems begin at the organ level with direct compression; hollow systems such as the intestinal tract and portal-caval system collapse under high pressure. Immediate effects such as thrombosis or bowel wall edema are followed by translocation of bacterial products, leading to additional fluid accumulation, which further increases intra-abdominal pressure.

At the cellular level, oxygen delivery is impaired, leading to ischemia and anaerobic metabolism. Vasoactive substances such as histamine and serotonin increase endothelial permeability; further capillary leakage impairs red cell transport; and ischemia worsens.

Simon et al demonstrated a significantly lowered threshold for injury from IAH in pigs after hemorrhage and fluid resuscitation.^[26] Oxygen delivery may play an important role.

Although the abdominal cavity (ie, the peritoneal and, to a lesser extent, retroperitoneal cavities) is much more distensible than an extremity, it reaches an endpoint at which the pressure rises dramatically. This is less apparent in chronic cases because the fascia and skin slowly stretch and thus tolerate greater fluid accumulation.

As pressure rises, abdominal compartment syndrome impairs not only visceral organs but also the cardiovascular and the pulmonary systems; it may also cause a decrease in cerebral perfusion pressure. Therefore, abdominal compartment syndrome should be recognized as a possible cause of decompensation in any critically injured patient.

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Etiology

Abdominal compartment syndrome occurs when the IAP is too high, similar to compartment syndrome in an extremity. The 3 types of abdominal compartment syndrome (primary, secondary, and chronic) have different and sometimes overlapping causes.

Primary ACS

Causes of primary (ie, acute) abdominal compartment syndrome include the following:

• Penetrating trauma
• Intraperitoneal hemorrhage
• Pancreatitis^[27]
• External compressing forces, such as debris from a motor vehicle collision or after a large structure explosion
• Pelvic fracture
• Rupture of abdominal aortic aneurysm^[28]
• Perforated peptic ulcer

In one review and meta-analysis of studies of patients who developed ACS after repair of ruptured abdominal aortic aneurysms, mortality was found to be 47%. Treatment included open decompression in 86 patients; percutaneous drainage in 18 (catheter only in 5; combined with tissue plasminogen activator infusion in 13); and conservative measures in 5.^[29]

Secondary ACS

Secondary abdominal compartment syndrome may occur in patients without an intra-abdominal injury, when fluid accumulates in volumes sufficient to cause IAH. Causes include the following:

• Large-volume resuscitation: The literature shows significantly increased risk with infusions greater than 3 L
• Large areas of full-thickness burns^[30] : Hobson et al demonstrated abdominal compartment syndrome within 24 hours in burn patients who had received an average of 237 mL/kg over a 12-hour period^[31]
• Penetrating or blunt trauma without identifiable injury
• Postoperative
• Packing and primary fascial closure, which increases incidence
• Sepsis

A retrospective study reported on risk factors directly associated with mortality in patients with both intra-abdominal hypertension and ACS. Polytransfusion was a strong predictor of mortality, along with a reported history of diabetes and the total amount of blood products used.^[32]

Secondary ACS in patients with lower extremity vascular injuries from penetrating injury or blunt trauma was associated with a 60% mortality in one study.^[33]

Chronic

Causes of chronic abdominal compartment syndrome include the following:

• Peritoneal dialysis
• Morbid obesity
• Cirrhosis
• Meigs syndrome
• Intra-abdominal mass

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Prognosis

If left untreated, abdominal compartment syndrome is almost uniformly fatal.^{[7, 34, 35]} Eddy and colleagues noted a mortality of 68% for patients with documented abdominal compartment syndrome.^[36] Most of the population was male (70%), and most had experienced blunt trauma (80%). In the subsequent literature, mortality rates have ranged from 25 to 75%.

The high mortality associated with abdominal compartment syndrome, even with treatment, reflects the fact that the condition affects multiple organ systems. Furthermore, abdominal compartment syndrome is often a sequela to severe injuries that independently carry a high morbidity and high mortality. Malbrain et al demonstrated that, by itself, elevation of abdominal pressure correlates with increased mortality before the actual development of abdominal compartment syndrome.^[37]

In a meta-analysis by Karkos et al, mortality was 47% in patients in whom ACS developed after repair of a ruptured abdominal aortic aneurysm.^[29]

A retrospective study reported on risk factors directly associated with mortality in patients with both intra-abdominal hypertension and ACS. Polytransfusion was a strong predictor of mortality, along with a reported history of diabetes and the total amount of blood products used.^[32]

A 5-year retrospective study at 3 level 1 trauma centers in Chicago identified the following prognostic factors in trauma patients with ACS^[38] :

• The 30-day mortality was strongly associated with an initial intra-abdominal pressure >20 mm Hg and moderately associated with blunt injury mechanism.
• Lactic acid level >5 mmol/L on admission was moderately associated with increased blood transfusion requirements and with acute renal failure during hospitalization.
• Developing ACS within 48 hr of admission was moderately associated with increased length of stay in the ICU, more ventilator days, and longer hospital stay.
• Initial operative intervention lasting more than 2 hr was moderately associated with risk of developing multiorgan failure.
• Hemoglobin level < 10 g/dL on admission, ongoing mechanical ventilation, and ICU stay >7 days were moderately associated with a disposition to long-term support facility.

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History

The history varies depending on the cause of abdominal compartment syndrome, but abdominal pain is commonly present. Abdominal pain may precede the development of abdominal compartment syndrome and may be directly related to a precipitating event, such as blunt abdominal trauma or pancreatitis.^{[27, 28, 29, 30, 33, 39, 40]}

Syncope or weakness may be a sign of hypovolemia. Although abdominal pain and distention are commonly present, patients may not experience abdominal pain. Difficulty breathing or decreased urine output may be the first signs of intra-abdominal hypertension (IAH).

Furthermore, patients who develop abdominal compartment syndrome may be unable to communicate, because they are often intubated and critically ill.

Signs and symptoms can include the following:

• Increase in abdominal girth
• Difficulty breathing
• Decreased urine output
• Syncope
• Melena
• Nonsteroidal anti-inflammatory drug (NSAID) use
• Alcohol abuse
• Nausea and vomiting
• History of pancreatitis

Abdominal compartment syndrome may be obscured in patients with critical injuries. Failure to consider abdominal compartment syndrome prevents diagnosis and treatment. Many disease processes can contribute to abdominal compartment syndrome. Consider IAH and document intra-abdominal pressures in any of the following patients:

• Intubated patients who have high peak and plateau pressures and are difficult to ventilate
• Patients who have GI bleeding or pancreatitis and are not responding to intravenous (IV) fluids, blood products, and pressors
• Patients who have severe burns or sepsis with decreasing urine output and are not responding to IV fluids and pressors
• Any patient with contradictory Swann-Ganz readings

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Physical Examination

Compartment syndrome in the abdomen is usually suggested by an increased abdominal girth. If this change is acute, the abdomen is tense and tender. Although this may be difficult to recognize in patients with morbid obesity, other patients often have an abdomen clearly out of proportion to their body habitus. This may be easier to visualize with the patient standing or sitting upright.

In addition to distended abdomen, other secondary effects of abdominal compartment syndrome are as follows:

• Wheezes, rales, increased respiratory rate
• Cyanosis
• Wan appearance

Complications

Abdominal compartment syndrome itself can involve almost any organ system, as described in the following:

• Renal failure: This is not prevented by intraureteral stents, which suggests direct compression of renal parenchyma and decreased renal perfusion as causes
• Respiratory distress and failure: Initial signs of abdominal compartment syndrome include elevated peak airway pressures in intubated patients with decreased tidal volumes
• Bowel ischemia
• Increased intracranial pressure (ICP): Decompressive laparotomy has been shown to reduce intractable elevated ICP in patients with IAH
• Failing cardiac output and refractory shock: Abdominal compartment syndrome factitiously elevates central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) in patients who are hypovolemic or euvolemic

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Lab and Imaging Studies

Laboratory studies and abdominal computed tomography scan are part of the workup for abdominal compartment syndrome. Measure intra-abdominal pressure (IAP) if abdominal compartment syndrome is suspected. IAP can be easily monitored by measuring bladder pressure.^[41]

The following lab studies may be indicated:

• Comprehensive metabolic panel (CMP)
• Complete blood cell count (CBC)
• Amylase and lipase assessment
• Prothrombin time (PT), activated partial thromboplastin time (aPTT) if the patient is heparinized
• Cardiac marker assays
• Urinalysis and urine drug screen
• Measurement of serum lactate levels (at many institutions, the sample must be kept on ice)
• Arterial blood gas (ABG): This is a quick way to measure the pH, lactate, and base deficit

Abdominal CT scanning can reveal many subtle findings. Pickhardt et al found the following in patients with abdominal compartment syndrome^[42] :

• Round-belly sign: Abdominal distention with an increased ratio of anteroposterior-to-transverse abdominal diameter (ratio >0.80)
• Collapse of the vena cava
• Bowel wall thickening with enhancement
• Bilateral inguinal herniation

Plain abdominal radiographic studies are often useless in identifying abdominal compartment syndrome, although they may show evidence of free air or bowel obstruction. Abdominal ultrasonography may reveal an aortic aneurysm, particularly with large aneurysms, but bowel gas or obesity makes performing the study difficult.

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Intra-abdominal Pressure Measurement

IAP can be easily monitored by measuring bladder pressure. Measurement of intraluminal bladder pressure consists of instilling about 25 mL of saline into the urinary bladder through the Foley catheter. The recommended volume is 25 mL, but studies have demonstrated similar measurements using only 10 mL.^[43] The tubing of the collecting bag is clamped, and a needle is inserted into the specimen-collecting port of the tubing proximal to the clamp and is attached to a manometer. Bladder pressure (measured in mm H₂O) is the height at which the level of the saline column stabilizes with the symphysis pubis as the zero point.^{[41, 44, 45, 3]}

Grading

In an excellent group of articles, Burch et al developed a grading system.^[46] Patients with higher-grade abdominal compartment syndrome have end-organ damage, which is evidenced by splenic hypercarbia and elevated lactate levels, even if they appear clinically stable. The following grading system has become accepted if IAH is present:

• Grade I: 10-15 cm H₂ O
• Grade II: 15-25 cm H₂ O
• Grade III: 25-35 cm H₂ O
• Grade IV: >35 cm H₂ O

End-organ damage has been observed with IAP as low as 10 cm H₂O, and multiple studies have found damage at values ranging from 20 to 40 cm H₂O. Disparity exists because abdominal compartment syndrome never occurs as an isolated event.

Cheatham et al found abdominal perfusion pressure (APP) to be a much better predictor of end-organ injury than lactate, pH, urine output, or base deficit.^[44] The APP is equal to the mean arterial pressure minus the IAP.

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Approach Considerations

If abdominal compartment syndrome is suspected, the focus of prehospital care is to immediately transport the patient to the emergency department. Remove any constricting garments. Do not place anything on the patient's abdomen (eg, external defibrillators, bundles of blankets, oxygen tanks).

Avoid overly aggressive fluid resuscitation, especially in extremity injuries. The overresuscitated patient is much more likely to develop abdominal compartment syndrome, and often the prehospital setting is where this begins.^[39]

In the emergency department, the first priority of the ED physician is to consider the diagnosis in any patient with the appropriate mechanisms of injury or pathology. Abdominal compartment syndrome will be missed unless it is in the differential diagnosis.

Therapy should include fluid resuscitation and transfusion if needed, as well as surgical consultation. A comprehensive, evidence-based approach to the management of abdominal compartment syndrome that includes early use of an open abdomen has been shown to reduce mortality.^[47] A group in Taiwan (Chen et al) used laparoscopic decompression successfully in blunt abdominal trauma patients who had an IAP of 25-35 cm H₂ O.^[48]

The World Society of the Abdominal Compartment Syndrome has noted that that correct fluid therapy and perfusional support during resuscitation form the cornerstone of medical management in patients with abdominal hypertension.^{[49, 1]}

Pharmacologic therapy is less effective than mechanical drainage. Pressors have a role but may not be equally effective in treating abdominal compartment syndrome. Dobutamine was shown to be superior to dopamine in restoring intestinal mucosal perfusion in a porcine model.^[50]

Inpatient care in acute abdominal compartment syndrome is directed by critical care physicians and surgeons. If an ICU patient experiences decompensation, abdominal compartment syndrome should be reexamined as a potential cause.

IAH may be an ongoing process in any patient with pathology producing intra-abdominal fluid loss. Repeat or continuous IAP measurement is indicated. The abdomen should be clear of any heavy objects.

Consultations may be indicated with a general surgeon, orthopedic surgeon, obstetrician/gynecologist, and vascular surgeon.

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Reperfusion Syndrome

Secondary effects of abdominal compartment syndrome occur immediately after evacuation. Many cases of hypotension and even asystole have been observed. Theories to explain these effects include washout of products of anaerobic metabolism (eg, lactic acid), which may be directly tissue toxic, and suddenly decreased systemic vascular resistance (SVR). Volume resuscitation immediately before decompression has been shown to significantly decrease these events.

Adding mannitol and sodium carbonate (NaCO₃) to the IV fluid bolus may decrease the toxicity of reperfusion syndromes.

Further Outpatient Care

Outpatient care is directed at the primary etiology of abdominal compartment syndrome. Chronic abdominal compartment syndrome requires lifelong medications and lifestyle changes, which may include the following.

• Diuretics
• Fluid restriction
• Weight loss
• Avoidance of alcohol

Transfer

Consider transfer of any patient who requires services not available at the current facility. Patients with abdominal compartment syndrome frequently require admission to the ICU. Any patient with documented abdominal compartment syndrome requires an emergent surgical consultation. Surgical services of multiple disciplines may be consulted. If a surgeon is not immediately available, the patient must be transferred.

Transfer is indicated for any patient meeting local trauma center guidelines.

Deterrence/Prevention

Preventing abdominal compartment syndrome is much more effective than treating it. The literature is replete with recommendations directed primarily at postsurgical care regarding prevention of abdominal compartment syndrome.

Primary fascial closure has been prospectively demonstrated to significantly increase the incidence of abdominal compartment syndrome after laparotomy, specifically in patients who have undergone damage-control surgery. Various types of surgical mesh are helpful to decrease the incidence of abdominal compartment syndrome.

Prevention is also focused on earlier treatment of IAH. Many authors now recommend managing IAH before full abdominal compartment syndrome develops. This can only be accomplished by proactive IAP measurement and monitoring.

Controlled, randomized studies have highlighted the possibility of preventing abdominal compartment syndrome by avoiding pure crystalloid resuscitation in trauma and burn patients. O'Mara et al demonstrated a significantly lower IAP in burn patients resuscitated with a colloid combination of fresh frozen plasma and lactated Ringer solution versus lactated Ringer solution alone, given by the Parkland formula.^[51]

At a large Japanese burn center, Oda et al demonstrated hypertonic lactated saline could be used in smaller volumes to maintain adequate urine output and significantly reduce the rate of abdominal compartment syndrome and associated morbidity.^[52]

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Medical Care

Hecker et al described 5 treatment columns for intra-abdominal hypertension/acute compartment syndrome^[7] :

• Intraluminal evacuation
• Intra-abdominal evacuation
• Improvement of abdominal wall compliance
• Fluid management
• Improved organ perfusion

If conservative therapy fails, emergency laparotomy is the most effective therapeutic approach to achieve abdominal decompression.^{[31, 7, 47, 48, 1, 9, 3]}

Multiple reports document the efficacy of paracentesis in burn patients who develop abdominal compartment syndrome. Although not prospectively validated, it appears to be a superior alternative to decompressive laparotomy in this patient population. It may be performed quickly at bedside and avoids potential complications associated with larger incisions. Paracentesis is also extremely useful in patients with chronic abdominal compartment syndrome from large-volume ascites.

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Surgical Care

Laparotomy decompression

Laparotomy is usually performed when the IAP reaches 25-36 mm Hg in cases of acute pancreatitis.^{[6, 48, 53]}  The incidence of ACS resulting from severe acute pancreatitis has been reported to be 4-27%, with a mortality of 50-75% in patients with severe acute pancreatitis who develop ACS.^[54]  

In cases of a ruptured abdominal aortic aneurysm, there is greater urgency for decompression laparotomy because of the possibility of continuous hemorrhage.^{[6, 48, 53]}  The reported incidence of ACS following open repair of ruptured abdominal aortic aneurysm is 4 to 20%, with increased morbidity and mortality associated with delayed treatment.^{[55, 56]} ​

Recommendations vary regarding whether surgical treatment should be delayed in patients with severe burns.^{[6, 48, 53]}  In severely burned patients, the prevalence of ACS is estimated to be 4.1-17%.^{[57, 58]}

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Guidelines Summary

WSACS guidelines

The World Society of the Abdominal Compartment Syndrome has published the following definitions and recommendations^{[2, 16, 24]} :

• IAH is graded as follows: Grade I: IAP 12-15 mm Hg; Grade II: IAP 16-20 mm Hg; Grade III: IAP 21-25 mm Hg; Grade IV: IAP >25 mm Hg.
• Patients should be screened for IAH/ACS risk factors upon ICU admission and in the presence of new or progressive organ failure.
• APP should be maintained above 50-60 mm Hg in patients with IAH/ACS [Abdominal perfusion pressure (APP) = mean arterial pressure (MAP) – IAP].
• Fluid resuscitation volume should be carefully monitored to avoid overresuscitation in patients at risk for IAH/ACS.
• Hypertonic crystalloid and colloid-based resuscitation should be considered in patients with IAH to decrease the progression to secondary ACS.
• Surgical decompression should be performed in patients with ACS that is refractory to other treatment options.
• Presumptive decompression should be considered at the time of laparotomy in patients who demonstrate multiple risk factors for IAH/ACS.

• References

Medication Summary

The goal of pharmacotherapy is to reduce intra-abdominal pressure. Diuretics are used for this purpose. However, pharmacologic therapy is less effective than mechanical drainage.

• References

Furosemide (Lasix)

• Dosing, Interactions, etc.

Clinical Context:  Furosemide increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. The dose must be individualized. Depending on response, administer at increments of 20-40 mg no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate with 1-mg/kg/dose increments until satisfactory effect is achieved.

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Spironolactone (Aldactone)

• Dosing, Interactions, etc.

Clinical Context:  This agent is used for management of edema resulting from excessive aldosterone excretion. It competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.

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Amiloride

• Dosing, Interactions, etc.

Clinical Context:  Amiloride is a pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. It is a potassium-conserving (antikaliuretic) drug that, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity.

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Class Summary

Diuretics decrease plasma volume and edema through diuresis.

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