eMedicine Specialties > Emergency Medicine > Trauma & Orthopedics

Compartment Syndrome, Abdominal

Author: Richard Paula, MD, Director of Research, Assistant Professor of Emergency Medicine, University of South Florida
Contributor Information and Disclosures

Updated: Feb 23, 2009

Introduction

Background

Compartment syndrome occurs when a fixed compartment, defined by myofascial elements or bone, becomes subject to increased pressure, leading to ischemia and organ dysfunction. Well recognized to occur in the extremities, it also occurs in the abdomen, and some believe, in the intracranial cavity. 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. The 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.

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. More recently, Kron and Iberti developed a simple method of accurately measuring intra-abdominal pressure, leading to a better understanding of the relationship between IAH and abdominal compartment syndrome.

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, which are explained in greater detail in Causes:

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

In the emergency department and ICU, 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 alerted to the morbidity associated with abdominal compartment syndrome.

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, further increasing 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.

Although the abdominal cavity (ie, peritoneal and, to a lesser extent, retroperitoneal cavities) are much more distensible than an extremity, they reach 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.

Frequency

United States

According to recent literature, frequency in trauma ICU admissions is anywhere from 5-15% and is 1% of general trauma admissions.

International

Much of the recent literature on abdominal compartment syndrome has originated from outside the United States, where frequency and morbidity appear to be the same.

Mortality/Morbidity

The morbidity of abdominal compartment syndrome is attributed to its effects on multiple organ systems. Because of this, abdominal compartment syndrome has a high mortality rate even with treatment. Furthermore, abdominal compartment syndrome is often a sequela to severe injuries that independently carry high morbidity and mortality rates.

• In the early 1990s, Eddy and Morris documented an ACS mortality rate of 68%, this has been reflected in the subsequent literature, with similar mortality rates of 25-75%.
• Malbrain et al recently demonstrated there is also a correlation with merely elevated abdominal pressures and mortality prior to the actual development of abdominal compartment syndrome.¹

Race

Nothing has been published indicating a racial or gender difference in the incidence or mortality of abdominal compartment syndrome.

Age

Abdominal compartment syndrome has been documented in all age groups. The intra-abdominal pressure (IAP) that leads to morbidity (>25 mm Hg) appears to be similar in the pediatric population.

Clinical

History

The history varies depending upon the cause of abdominal compartment syndrome (ACS), but abdominal pain is commonly present. Abdominal pain may precede the development of abdominal compartment syndrome and be directly related to a precipitating event, such as blunt abdominal trauma or pancreatitis.

Syncope or weakness may be a sign of hypovolemia. Although abdominal pain and distension are commonly present, patients may not experience abdominal pain; difficulty breathing or decreased urine output may be the first signs of IAH.

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

• 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

Physical

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. Look for the secondary effects of abdominal compartment syndrome.

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

Causes

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

• Primary (ie, acute)
  • Penetrating trauma
  • Intraperitoneal hemorrhage
  • Pancreatitis
  • External compressing forces, such as debris from a motor vehicle collision or after a large structure explosion
  • Pelvic fracture
  • Rupture of abdominal aortic aneurysm
  • Perforated peptic ulcer
• Secondary: Secondary ACS may occur in patients without an intra-abdominal injury, when fluid accumulates in volumes sufficient to cause IAH.
  • Large-volume resuscitation: The literature shows significantly increased risk when more than 3 L are infused.
  • Large areas of full-thickness burns: In 2002, 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.²
  • Penetrating or blunt trauma without identifiable injury
  • Postoperative
  • Packing and primary fascial closure, which increases incidence
  • Sepsis
• Chronic
  • Peritoneal dialysis
  • Morbid obesity
  • Cirrhosis
  • Meigs syndrome

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