Compartment syndrome occurs when pressures increase within a fixed cavity of the body, leading to ischemia, muscle damage, and organ dysfunction. These "fixed" spaces are constrained by muscular and fascial boundaries, which may have limited compliance when they become swollen.
Intra-abdominal hypertension is defined as the sustained intra-abdominal pressure (IAP) above 12 mmHg.
Abdominal compartment syndrome (ACS) is a severe illness seen in critically ill patients. ACS results from the progression of steady-state pressure within the abdominal cavity to a repeated pathological elevation of pressure above (> 20mmHg) with associated organ dysfunction. Failure to recognize and immediately manage ACS can lend to poor prognosis as ACS is recognized as an independent predictor of mortality. High clinical suspicions with protocolized monitoring and management should be adapted when treating the critically ill, especially those with significant fluid shifts. This clinical diagnosis should be considered in patients with tense or distended abdomen with associated instability; however, it may also be seen without abdominal distention.
The exact clinical conditions that define ACS are controversial. The dysfunction may present with respiratory concerns such as high peak airway pressure and inadequate ventilation and oxygenation or decreased urine output caused by falling renal perfusion, but these concerns are reversible with intervention.
Abdominal compartment syndrome has medical and conservative management options, and treatment is aimed at identifying and treating the cause of the compartment syndrome. However, patients with clinical deterioration may require emergent surgical decompression.
Abdominal compartment syndrome can be divided and classified into two groups, primary and secondary ACS. Primary ACS causes include abdominal blunt or penetrating trauma, hemorrhage, abdominal aortic aneurysm (AAA) rupture, intestinal obstruction, and retroperitoneal hematoma. Secondary causes include pregnancy, ascites, ileus, burns, intra-abdominal sepsis, and large-volume fluid replacement (> 3 liters). Chronic causes of elevated intra-abdominal pressure include pregnancy, cirrhosis, obesity, intra-abdominal malignancy, and peritoneal dialysis. These are all causes of intra-abdominal hypertension, defined as repeated intra-abdominal pressures > 12 mm Hg. The presence of organ dysfunction in this setting due to compressive symptoms now confirms a diagnosis of abdominal compartment syndrome.
Studies have shown that mortality after ACS caused by AAA rupture neared 47%. The disease can become devastating once other organ systems become involved due to compression, and primary ACS tends to have an increasingly worse outcome.
ACS can develop in all ICU patients. In an identified series of mixed ICU population, 35% of ventilated patients were found to have intra-abdominal hypertension (IAH) or ACS. Risks factors include a plethora of medical conditions but may be classified based on abdominal wall mechanics. Risk factors include those that reduce abdominal compliance, increase intra-abdominal contents, increase luminal contents or third space expansion, and cause a capillary leak. 
With intraperitoneal bleeding, trauma, or abscess, the physiologic response of inflammation and swelling can be held responsible for intra-abdominal hypertension. In the setting of intestinal obstruction, the dilated loops of bowels can cause compressive symptoms within the abdominal cavity. As abdominal pressure increases, the syndrome may begin to involve other organ systems due to further compression.
Intra-abdominal hypertension is graded from I to IV:
Any evidence of continued intra-abdominal hypertension with organ failure is defined as ACS. However, the incidence of organ failure is highest in patients with grade IV IAH. Organs typically affected include the heart, lungs, kidney.
Physiologic cardiac sequelae include decreased cardiac output, and increased central venous pressure (CVP) due to inferior vena cava (IVC) and portal vein compression, increase systemic vascular resistance (SVR) leads to hypotension. Pulmonary involvement can present as decreased thoracic volumes and elevated peak pressures from compression of the diaphragm, a decrease in P/F ratio, and hypercarbia. Renal compression can lead to decreased GFR and low urine output. Visceral blood flow is also reduced. Neurologic symptoms can include increased Intra-cranial pressure (ICP) from the elevated CVP due to IVC compression, contributing to a decrease in cerebral perfusion pressure (CPP).
ACS is typically only seen in critically ill patients and will likely be a diagnosis made in the ICU setting, rather than in the emergency department. Clinical suspicion for abdominal compartment syndrome should be high in patients with penetrating abdominal trauma or surgical patients following extensive abdominal surgery. Patients may present with abdominal pain and distension. However, this is not a sensitive or specific finding. Patients in the ICU setting may present with a wide array of organ failure, not limited to the abdomen, which can make the diagnosis difficult.
The physical exam may reveal an increased abdominal girth, tense abdomen, cyanosis, wheezing, and difficulty breathing.
In abdominal compartment syndrome, the displacement of the diaphragm cephalad leads to compression of the thorax, which causes an increase in work of breathing, ventilation/perfusion inequality, and increases in both peak and plateau pressures.
The tense abdomen also prevents venous return, resulting in elevated intracranial pressure and decreased cerebral perfusion pressure.
While imaging modalities may help in localizing a cause of the elevated abdominal pressure (bleeding, trauma, obstruction), they do not help make the specific diagnosis of abdominal compartment syndrome. The most accurate manner of confirming this diagnosis is from measured abdominal pressures. The IAP should be measured when any known risk intra-abdominal hypertension (IAH) is present. This measurement can be achieved in many ways, including both direct and indirect methods. Direct methods include measurement of abdominal pressure using pressure transducers (e.g., Veress needle during laparoscopic surgery) or intraperitoneal catheters (e.g., peritoneal dialysis catheter). Theses methods are highly accurate; however, they are limited by their invasiveness. The more commonly used method is an indirect measurement such as intravesicular catheter pressures (e.g., Foley catheter), which has become the gold standard due to its widespread availability and limited invasiveness. The trans-bladder technique involves using aseptic clamping the drainage tubing of the Foley then connecting the Foley to a three-way stop tap adjusted to the level of the mid-axillary line at the iliac crest to zero transducers follow by injecting 25cc of sterile saline into the bladder. Measurements should be taken at end-expiration and complete supine position and expressed in mmHg. Bladder pressures below 5mm Hg are expected in healthy patients. Pressures between 10 to 15 mm Hg can be expected following abdominal surgery and in obese patients. Bladder pressures over 25 mm Hg are highly suspicious of abdominal compartment syndrome and should be correlated clinically. It is recommended that pressure measurements be trended to show and recognize the worsening of intra-abdominal hypertension.
Contraindications to using bladder pressures include bladder trauma, neurogenic bladder, BPH, and pelvic hematoma. Bladder pressures may be inaccurate if the patient is not sedated or lying flat.
CT scan may reveal several things such as the collapse of the vena cava, round abdomen, bowel thickening, and or bilateral inguinal herniation. The following grading system is used to categorize abdominal compartment syndrome:
Grade I: 10-15 cm H2O
Grade II: 15-25 cm H2O
Grade III: 25-35 cm H2O
Grade IV, greater than 35 cm H2O
Non-surgical therapeutic options for treatment of intra-abdominal hypertension involves an overall goal to improve the following: abdominal wall compliance with decreased muscle contraction, evacuation of luminal contents by decompression (NG tube), evacuation of abdominal fluid by drainage, and correction of positive fluid balance through goal-directed volume resuscitation.
The primary treatment for ACS is surgical decompression. However, the early use of non-surgical interventions may prevent the progression of IAH to ACS. Early recognition involves supportive care to include keeping patients comfortable with pain well-controlled. Decompressive procedures such as NG tube placement for gastric decompression, rectal tube placement for colonic decompression, and percutaneous drainage of abscesses, ascites, or fluid from the abdominal compartment. The neuromuscular blockade has been described to be used as a brief trial in an attempt to relax the abdominal musculature, leading to a significant decrease in abdominal compartment pressures in the ventilated ICU patient. If conservative and medical management does not resolve the IAH and further organ damage is noted, surgical decompression using emergent laparotomy may be considered. 
After surgical laparotomy for compartment syndrome, the abdominal fascia may be closed using temporary closure devices such as (vacs, meshes, and zippers). The fascia can be appropriately closed after 5-7 days after the compartment pressures and swelling have decreased.
With surgical abdominal decompression, organ dysfunction may also improve rapidly as most organ dysfunction is seen as sequelae from compression. With less tension from the abdomen, the diaphragmatic excursion can increase, leading to improved ventilation and reduction of peak airway pressures. Compression of the IVC and circulatory system are relieved, leading to improved cardiac output and the ability to wean patients off of vasopressor support. Acute kidney injury is reversed with less compression of the renal arteries and ureters.
If left untreated, abdominal compartment syndrome is fatal. Even delayed treatment is associated with very high mortality rates. Predictors of mortality include a history of diabetes and transfusion of a high volume of blood products. Many series reports that even with treatment, multiorgan failure can delay recovery for weeks or months. Prolonged need for mechanical ventilation, dialysis, and more extended hospital stays are common in these patients.
After decompression of the abdomen, many patients still require the following treatments:
To prevent abdominal compartment syndrome, many types of mesh are now available for abdominal closure that avoid tension on the abdominal contents. Some studies indicate that abdominal compartment syndrome is less likely to occur in patients resuscitated with FFP and lactate Ringer's compared to just a pure crystalloid.
Current guidelines with which to be familiar (as presented by the World Society of the Abdominal Compartment Syndrome) include:
1) IAH is diagnosed by sustained or repeated elevation in IAP of 12 mm Hg
2) ACS is diagnosed when the IAP is >20 mm Hg, and is associated with organ dysfunction/failure
3) IAH 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
4) A trial of neuromuscular blockade can be used to alleviate compressive symptoms in ACS to while awaiting surgical decompression
The diagnosis and management of abdominal compartment syndrome require an interprofessional team approach. The condition can present in subtle ways, and the diagnosis can easily be missed. If the abdominal compartment syndrome is not diagnosed or treatment is delayed, the outcome is almost always fatal. Mortality rates of 20 to 70% have been reported in patients with blunt abdominal trauma, even with treatment. The reason for the high mortality is due to the early involvement of multiple organs. Also, the higher the abdominal pressure, the higher the mortality. Other factors associated with mortality include surgery lasting more than 2 hours, developing abdominal compartment syndrome within 48 hours of admission, and an elevated lactic acid level despite treatment. Even those who survive have significant morbidity from residual deficits like renal failure, muscle wasting, respiratory distress, and liver dysfunction.
The Interprofessional Team
The diagnosis usually requires a systemic approach and discussion with the interprofessional team. Once the diagnosis is made, all patients require ICU care with continuous monitoring. A wound care nurse should assess the wound every day for healing and report to the clinician if there are any signs of infection or less than optimal healing. Since most patients are kept NPO, a dietary consult for TPN is necessary. Nurses should ensure that all patients have deep venous thrombosis and pressure sore prophylaxis. In addition, nurses need to weigh the patient daily, measure abdominal girth, assess urine output, and organ perfusion. If urine output declines, the nephrologist should be contacted and involved early in the care. Any deviation from normal parameters should be immediately conveyed to the interprofessional team. Pharmacists evaluate prescribed medications and check for drug-drug interactions. As the patient improves, physical therapy should be ordered to get the patient out of bed and encouraging ambulation.
Those who go on to develop chronic abdominal compartment syndrome need lifelong support and monitoring. The current recommendations focus on the prevention of abdominal compartment syndrome. Various techniques for the closure of the abdomen, and even the fluid used to resuscitate the patient may make a difference in the outcome. 
The outcomes for most patients with abdominal compartment syndrome are poor. Those who are diagnosed and treated promptly do have good outcomes, but the recovery is often prolonged. Patients with multiorgan dysfunction have a long road to recovery, marked by wound breakdown, repeated hospitalization, and difficulty performing even the most basic daily living activities. [Level V]
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