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 facial boundaries which may have limited compliance when they become swollen.
Intra-abdominal hypertension is defined as a sustained abdominal pressure above 12 mmHg.
Abdominal compartment syndrome (ACS) is a very serious 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 managed ACS can lend to poor prognosis as ACS is recognized as an independent predictor of mortality. High clinical suspicions with a protocolized monitoring and management should be adapted when treating the critically ill, especially those with large fluid shifts. 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 abdominal compartment syndrome (ACS) are controversial. The dysfunction may be respiratory indicated by high peak airway pressure and inadequate ventilation and oxygenation, decreased urine output caused by falling renal perfusion but is 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 primary and secondary. Primary causes include abdominal blunt or penetrating trauma, hemorrhage, 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 a worse outcome.
ACS can develop in all ICU patients. In an identified series of mixed ICU population, 35% of ventilated patient has found to have 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 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:
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
Any evidence of repeated intra-abdominal hypertension with organ failure is defined as ACS. However, the incidence of organ failure is far greatest with Grade IV IAH. Organs typically affected include the heart, lungs, kidney.
Physiologic cardiac sequelae include decreased cardiac output and increased CVP due to IVC and portal vein compression, increase SVR leads to hypotension. Pulmonary involvement can include decreased thoracic volumes and elevated peak pressures from compression of the diaphragm, decrease in P/F ratio and hypercarbia. Renal compression can lead to decreased GFR and low urine output. Visceral blood flow is also decreased. Neurologic symptoms can include increased ICP from the elevated CVP due to IVC compression contributing to a decrease in cerebral perfusion pressure (CPP).
Abdominal compartment syndrome (ACS) is typically only seen in critically ill patients and will likely be a diagnosis made in the ICU setting, rather than in the ER. Clinical suspicion for abdominal compartment syndrome should be high in patients with penetrating abdominal trauma or surgical patients following large 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 other organ failure, not limited to the abdomen which can make the diagnosis difficult.
While imaging modalities may help in localizing a cause of the elevated abdominal pressure (bleeding, trauma, obstruction, etc.), they are not helpful in making 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 IAH/ACS is present. This can be achieved in many ways including both direct and indirect methods. Direct methods include measurement of abdominal pressure using pressure transducers (e.g. verress needle during laparoscopic surgery) or intraperitoneal catheters (e.g. peritoneal dialysis catheter). Theses methods are highly accurate, however, 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. 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 normal patients. Pressures between 10 to 15 mmHg can be expected following abdominal surgery and in obese patients. Bladder pressures over 25 mmHg are highly suspicious of abdominal compartment syndrome and should be correlated clinically. It is recommended that pressure measurements be trended to show and recognize 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 laying flat.
Surgical decompression remains the mainstay treatment of ACS. However, prevention and early treatment of the potential cause may prevent progression of IAH to ACS. The protocol should be use to try to avoid positive cumulative balance in the those at risk. The enhanced ratio of plasma to packed RBC during resuscitation when treating those with massive hemorrhage. Those patient undergoing initial laboratory at risk for ACS be treated with the prophylactic open abdomen. 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 attempt 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 closed properly after 5-7 days and the compartments 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 inferior portion, 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 ability to wean patients off of vasopressor support. Acute kidney injury can be reversed with less compression of the kidneys and ureters.
Current guildelines which which to be familiar with (as presented by the World Society of the Abdominal Compartment Syndrome) include:
1) Intra-abdominal hypertension (IAH) is defined by a sustained or repeated pathological elevation in IAP of ≥12 mm Hg
2) ACS is defined as a sustained IAP >20 mm Hg 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) Trial of neuromuscular blockade can be used to palliate compressive symptoms in ACS to while awaiting surgical decompression