Abdominal Compartment Syndrome

What is abdominal compartment syndrome?

Abdominal compartment syndrome (ACS) is defined by the presence of organ dysfunction as a result of increased abdominal pressure or intraabdominal hypertension. The increased abdominal pressure reduces blood flow to internal organs, which can lead to multiple system failure and death if not promptly recognized and treated.

Incidence

Very few studies have examined the incidence of ACS outside of trauma patients, among whom it ranges from 1% to 14%, depending on the population and type of trauma studied. The incidence is the highest among critically ill patients.

Risk Factors

The biggest risk factor for developing ACS is critical illness stemming from a wide array of medical and surgical conditions. In particular, any illness that requires a patient to undergo large volume intravenous fluid resuscitation can be associated with ACS; the third-spacing of fluid can lead to increased intraabdominal pressures secondary to tissue edema. Due to large volume fluid resuscitation, ACS is commonly seen in severe burns, trauma, postsurgical patients, and sepsis. Other conditions associated with ACS include intraabdominal and retroperitoneal pathologies such as significant bowel distention, liver transplantation, massive ascites, ruptured abdominal aortic aneurysm with resulting hemoperitoneum, pancreatitis, and abdominal surgery

Causes of Intraabdominal Hypertension and Abdominal Compartment Syndrome

From Vincent JL et al: Textbook of critical care, ed 6, Philadelphia, 2011, Saunders.

Increased Abdominal ContentsDecreased Abdominal Volume
AscitesReduction of large long-standing hernia
HemoperitoneumDirect closure of large, long-standing abdominal wall defect
Abdominal packs
Peritonitis
Retroperitoneal edema (pancreatitis)Retroperitoneal edema (pancreatitis)
Large pelvic, retroperitoneal hematomaLarge pelvic, retroperitoneal hematoma
Intestinal obstruction
Ileus
Gastric distention (esophageal ventilation)
Abdominal aortic aneurysm
Severe constipation
Large abdominal tumor (chronic)
Morbid obesity (chronic)
Pregnancy (chronic)

Independent Predictors of Postinjury Primary and Secondary Abdominal Compartment Syndrome

From Vincent JL et al: Textbook of critical care, ed 6, Philadelphia, 2011, Saunders.

ED ModelICU Model
Independent PredictorsIndependent Predictors
Primary ACSTo OR <75 minTemp ≤34° C
Crystalloids ≥3 LGAPco2 ≥16
Hb ≤8/dl
BD ≥12 mEq/L
Secondary ACSCrystalloids ≥3 LGAPco2 ≥16
No urgent surgeryCrystalloids ≥7.5 L
PRBC ≥3 unitsUO ≤150 ml

ACS, Abdominal compartment syndrome; BD, arterial base deficit; CI, confidence interval; ED, emergency department; GAPco 2 , carbon dioxide gap; Hb, hemoglobin concentration; ICU, intensive care unit; OR, operating room; PRBC, packed red blood cells; Temp, temperature; UO, urine output.

Abdominal compartment syndrome is caused by an increase in intra-abdominal pressure resulting in the dysfunction of multiple organ systems including decreased cardiac output and hypotension, increased thoracic pressure, decreased pulmonary compliance and increased airway pressures leading to impaired ventilation, and decreased visceral perfusion, which in turn may lead to intestinal ischemia, and infarction and oliguric Acute kidney injury.

It is thought that increased renal venous pressure rather than increased intra-parenchymal pressure is the primary cause of Acute kidney injury in the abdominal compartment syndrome.

Common causes of abdominal compartment syndrome include trauma with intra-abdominal hemorrhage, abdominal surgery, retroperitoneal hemorrhage, peritonitis, pancreatitis, massive fluid resuscitation, abdominal banding, repair of large incisional hernia, laparoscopy and pneumoperitoneum, and ileus.

It has been suggested that abdominal compartment syndrome may contribute to as many as 30% of cases of Acute kidney injury in critically ill patients.

Physical Findings & Clinical Presentation

  • •The most striking physical examination finding is often massive abdominal distention.
  • •Difficulty maintaining respiratory support and decreased urine output are also typical hallmarks.
  • •Other common findings include those associated with poor perfusion states and hypotension such as skin mottling, cool extremities, and obtundation. Patients will often have abdominal tenderness, signs of volume overload such as edema and elevated jugular venous pressures, and may present with acute respiratory decompensation.

Etiology

ACS can affect nearly every organ system. High intraabdominal pressures are associated with increased intracranial pressures, which can precipitate cerebral ischemia. Elevated abdominal pressures can cause cardiac compression by decreasing ventricular compliance and contractility as well as impairing inferior vena cava venous return, leading to increased central venous and pulmonary pressures. Due to elevation of the diaphragm, patients will often have reduced tidal volumes and lower chest wall compliance, which can lead to atelectasis, pneumonia, hypoxemia, and hypercarbia. Mechanically ventilated patients will also require increased airway pressures that can lead to barotrauma. In addition, renal vein compression and renal artery vasoconstriction lead to decreased urine output. Reduced mesenteric blood flow can lead to intestinal ischemia and lactic acidosis.

 Diagnosis

Differential Diagnosis

  • •Mesenteric ischemia
  • •Sepsis
  • •Shock
  • •Acute kidney injury
  • •Adult respiratory distress syndrome

Workup

Measurement of intraabdominal pressure is required to make a definitive diagnosis. Bladder pressure is the most common surrogate used to estimate intraabdominal pressures and is measured using a bladder catheter. The most accurate measurements can be obtained with the patient in supine position at end expiration in the absence of abdominal contractions. The threshold abdominal pressure often set for research purposes to define ACS is >20 mm Hg, but patients may have ACS with pressures of >10 mm Hg and above. Oliguria tends to develop at a pressure of 15 mm Hg, and anuria occurs around 30 mm Hg. Intraabdominal pressures can also be estimated using intragastric, intracolonic, and inferior vena cava approaches 

Classification of Abdominal Compartment Syndrome

From Vincent JL et al: Textbook of critical care, ed 6, Philadelphia, 2011, Saunders.

Basis of ClassificationSubcategories
Time frameAcute
Chronic
Relation to peritoneal cavityPrimary
Secondary
EtiologyTrauma
Burn
Postoperative
Pancreatitis
Bowel obstruction
Ileus
Abdominal aortic aneurysm
Oncologic
Gynecologic

Laboratory Tests

Laboratory testing is generally not helpful for the diagnosis of ACS. The presence of lactic acidosis suggests bowel ischemia, which portends a poorer prognosis.

Imaging Studies

Imaging alone has no diagnostic value in ACS, but chest imaging can be helpful to evaluate for diaphragmatic elevation and evidence of pulmonary complications (atelectasis, volume overload, pneumonia, etc.). Abdominal computed tomography imaging will sometimes show renal displacement, inferior vena cava compression, abdominal wall thickening, or bowel injury related to ischemia but should not be relied on to make the diagnosis of ACS.

 Treatment

Supportive care and, when appropriate, surgical abdominal decompression are the mainstays of ACS treatment.

Nonpharmacologic Therapy

  • •Supportive care, often with hemodynamic and ventilatory support, as well as techniques to improve abdominal wall compliance, are the foundations of ACS management.
  • •Severe burns to the abdomen leading to ACS will require surgical escharotomy to improve abdominal wall compliance.
  • •Patients with tense ascites leading to ACS will require large volume paracentesis to decrease intraabdominal pressures.
  • •Patients should be positioned supine if possible as any elevation of the head will increase abdominal pressures.
  • •Rectal and nasogastric decompression is required if ACS is due to massive bowel distention.
  • •Proper sedation and pain control can decrease intraabdominal pressures, and some patients may require ventilatory support and chemical paralysis to maximize abdominal wall relaxation.
  • •Mechanical ventilation is often difficult due to the high pressures that need to be generated to overcome the increased intraabdominal pressures. Often a combination of low tidal volumes, permissive hypercapnia, chemical paralysis, and high positive end-expiratory pressure are required to ensure adequate ventilatory support.
  • •Although there is little data to support its use, the administration of colloid may be superior to crystalloid if the patient requires further volume resuscitation. The administration of intravenous fluids will transiently increase renal blood flow, leading to increased urine output and improved organ perfusion and cardiac output. Vasopressors may also have a role to maintain perfusion pressures, but all of these measures are temporizing and supportive until definitive action through surgical decompression is performed.
  • •The threshold to perform surgical decompression for ACS has yet to be established; however, data suggest that early decompression prior to the development of ACS may lead to better outcomes. If appropriate, consensus dictates that surgical decompression should be performed on all patients with intraabdominal pressure >25 mm Hg; however, some surgeons are more aggressive and will consider decompression with pressures of 15 to 25 mm Hg in the right clinical setting. Surgical decompression by incising vertically through the linea alba can be performed at the bedside in emergent situations and most surgeons will then keep the abdomen open through the use of a temporary abdominal closure device that retains heat/fluid and prevents evisceration until the time is appropriate to attempt to close the abdomen again.

The treatment of abdominal compartment syndrome is abdominal decompression. In patients with massive ascites, paracentesis may be sufficient; however, the definitive therapy most commonly requires surgical decompression, often leaving the abdomen open until inflammation and edema subside.

Acute General Rx

There are no direct pharmacologic agents that treat ACS other than vasopressors, sedatives, pain medications, and paralytics required for supportive care as described above. Despite underlying volume overload, diuretics have no role in therapy. Definitive management is surgical decompression.

Disposition

Close inpatient monitoring, preferably in an intensive care setting, is indicated as mortality can be extremely high (>40%) with ACS.

Referral

Patients with ACS often require admission to an intensive care setting with surgical consultation in case decompression is required.

 Pearls & Considerations

Comments

  • •ACS is seen in critically ill medical and surgical patients, and its diagnosis requires both the presence of intraabdominal hypertension and end organ dysfunction.
  • •ACS is truly a systemic illness that can lead to multisystem organ failure and is therefore associated with a high mortality.
  • •Definitive diagnosis of ACS requires measurement of intraabdominal pressure, which is most frequently estimated using bladder pressure as a surrogate.
  • •Supportive care, including hemodynamic support with colloids, vasopressors, and ventilatory support, is often required, but surgical decompression is the only definitive treatment.
  • •Surgical decompression is indicated for intraabdominal pressures >25 mm Hg; however, precise thresholds have not been established, and earlier decompression may lead to better outcomes.

Sources

  1. Allen R., et al.: Evaluation and management of intraabdominal hypertension. Curr Opin Crit Care 2020; 26: pp. 192-196.
  2. De Laet, et al.: A clinician’s guide to management of intra-abdominal hypertension and abdominal compartment syndrome in critically ill patients. Crit Care 2020; 24: pp. 97.
  3. Maffongelli A., et al.: Abdominal compartment syndrome: diagnostic evaluation and possible treatment. Clin Ter 2020; 171: pp. e156-e160.
  4. Rajasurya V., et al.: Abdominal compartment syndrome: often overlooked conditions in medical intensive care units. World J Gastroenterol 2020; 26: pp. 266-278.
  5. Rogers W.K., et al.: Intraabdominal hypertension, abdominal compartment syndrome and the open abdomen. Chest 2018; 153 (1): pp. 238-259.
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