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. 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. Surgical decompression remains the mainstay treatment of ACS. However, prevention and early treatment of the potential cause may prevent progression of IAH to ACS.[1, 2, 3, 4, 5, 6, 7, 8]
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. This has led to a better understanding of the relationship between IAH and abdominal compartment syndrome.
The World Society of the Abdominal Compartment Syndrome has published the following definitions and recommendations[3] :
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:
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. (See Treatment and Medication.)
For patient education information, see the Digestive Disorders Center as well as Aortic Aneurysm, Abdominal Pain in Adults, Pancreatitis, Chronic Kidney Disease, Sepsis (Blood Infection), and Cirrhosis.
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.[9] 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.
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.
Causes of primary (ie, acute) abdominal compartment syndrome include the following:
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.[12]
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:
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.[15]
Secondary ACS in patients with lower extremity vascular injuries from penetrating injury or blunt trauma was associated with a 60% mortality in one study.[16]
Causes of chronic abdominal compartment syndrome include the following:
According to recent literature, the frequency of abdominal compartment syndrome in trauma ICU admissions is anywhere from 5-15% and 1% of general trauma admissions. 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.
Abdominal compartment syndrome has been documented in all age groups. The IAP that leads to morbidity (>25 mm Hg) appears to be similar in the pediatric population.
If left untreated, abdominal compartment syndrome is almost uniformly fatal.[1, 17] Eddy and colleagues documented a mortality of 68% for patients with documented abdominal compartment syndrome.[18] Most of the population was male (70%), and most had experienced blunt trauma (80%). In the subsequent literature, mortality rates have ranged from 25-75%.
The high mortality in 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.[19]
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.[12]
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.[15]
A 5-year retrospective study at 3 level 1 trauma centers in Chicago identified the following prognostic factors in trauma patients with ACS[20] :
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.[10, 11, 12, 13, 16, 21, 22]
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:
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:
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:
Abdominal compartment syndrome itself can involve almost any organ system, as described in the following:
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.[23]
The following lab studies may be indicated:
Abdominal CT scanning can reveal many subtle findings. Pickhardt et al found the following in patients with abdominal compartment syndrome[24] :
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.
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.[34] 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.[23, 25, 26, 7]
In an excellent group of articles, Burch et al developed a grading system.[27] 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:
End-organ damage has been observed with IAP as low as 10 cm H2 O, and multiple studies have found damage at values ranging from 20-40 cm H2 O. 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.[25] The APP is equal to the mean arterial pressure minus the IAP.
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 over-resuscitated patient is much more likely to develop abdominal compartment syndrome, and often the prehospital setting is where this begins.[21]
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.[28] A group in Taiwan has used laparoscopic decompression successfully in blunt abdominal trauma patients who have an IAP of 25-35 cm H2 O.[29]
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.[30, 2]
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.[31]
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 the following:
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.
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.
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.
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.
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.[32]
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.[33]
Hecker et al described 5 treatment columns for intra-abdominal hypertension/acute compartment syndrome[1] :
If conservative therapy fails, emergency laparotomy is the most effective therapeutic approach to achieve abdominal decompression.[14, 1, 28, 29, 2, 5, 7]
The World Society of the Abdominal Compartment Syndrome has published the following definitions and recommendations[3] :
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.
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.
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.
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.