Abdominal Compartment Syndrome

Etiology

Abdominal compliance is primarily determined by the elasticity of the abdominal wall and the elasticity of the diaphragm. Increased IAP can cause vasculature dysfunction, including loss of vasomotor tone and compromised endothelial intercellular junctions. IAH also causes increased antidiuretic hormone release, further increasing volume retention.[8]

As IAH is viewed as a physiologic continuum. The World Society of the Abdominal Compartment Syndrome (WSACS) recommended that IAH be divided into 4 grades as follows:

• Grade I: IAP 12 to 15 mm Hg
• Grade II: IAP 16 to 20 mm Hg
• Grade III: IAP 21 to 25 mm Hg
• Grade IV: IAP >25 mm Hg [5]

IAH in the presence of organ dysfunction raises suspicion for ACS. The timing of IAH onset affects the risk of progression to ACS. Acute IAH can occur within hours, especially after trauma. Subacute IAH is more common in cases caused by medical conditions, while chronic IAH develops gradually over months or years. Acute and subacute IAH are more likely to lead to ACS, whereas chronic IAH is usually better tolerated unless there's an additional sudden increase in pressure.[9]

Surgical procedures that carry an especially high risk of developing IAH include liver transplantation, damage control surgery, repair of abdominal aortic aneurysm, and large abdominal hernia repairs.[10] Other etiologies must be considered in addition to surgery as potential causes of ACS, which can be classified as primary or secondary. Primary ACS causes include blunt or penetrating trauma, intra-abdominal hemorrhage, abdominal aortic aneurysm rupture, abdominal adhesions, intestinal obstruction, tumor formation, and retroperitoneal hematoma. Secondary causes do not originate from intra-abdominal disease, including pregnancy, ascites, ileus, intra-abdominal sepsis, and large-volume fluid resuscitation.[11] Intra-abdominal pressures can be chronically elevated in pregnancy, cirrhosis, obesity, intra-abdominal malignancy, and peritoneal dialysis.[6][12][13][14] Those with higher body mass index can be expected to have a higher baseline IAP of 9 to 14 mm Hg due to the restrictive effect of adipose tissue.[15]

The causes of IAH and ACS can be broken down into the following categories:

• Diminished abdominal wall compliance
  • Abdominal surgery, intra-abdominal adhesions, major trauma, major burns, mechanical ventilation,  and obesity
• Increased intraluminal volume
  • Gastroparesis, gastric distension, ileus, constipation, toxic megacolon, and volvulus
• Increased extraluminal abdominal volume
  • Hemoperitoneum, pneumoperitoneum, severe pancreatitis, liver failure with ascites, retroperitoneal or intra-abdominal tumors, intra-abdominal abscesses, laparoscopy with excessive insufflation pressures, and peritoneal dialysis
• Capillary leak/fluid resuscitation
  • Damage control surgery, bacteremia, systemic inflammation, coagulopathy, sepsis, massive fluid administration, and blood product transfusion [16][17][18]

Epidemiology

ACS can develop in all intensive care units (ICUs) and critically ill individuals. The Incidence, Risk Factors, and Outcomes of Intra-abdominal Hypertension in Critically Ill Patients (IROI Study) was a prospective study that revealed 34% of patients had IAH on admission, which increased to 48.9% within 14 days. The development of IAH within the observed period was associated with mortality.[19] In another identified series of mixed ICU populations, 32% of patients were found to have IAH and 4% to have ACS.[20]

Pathophysiology

Elevated IAPs can affect multiple organ systems, including the cardiovascular, respiratory, renal, gastrointestinal, and nervous systems.[21][22]

Cardiovascular System

The cardiovascular system can be affected in multiple ways due to elevated IAP. IAH can cause compression of the inferior vena cava, reducing venous blood return to the heart and causing lower extremity edema. Decreased venous return can also reduce cardiac output, resulting in less blood and oxygen delivery to peripheral tissues. Additionally, the increased IAP causes the diaphragm to move upwards, which raises the intrathoracic pressures and places direct pressure on the heart, ultimately decreasing ventricular compliance.

Pulmonary System

Elevated intrathoracic pressures limit pulmonary compliance, thus decreasing tidal volume and functional residual capacity and increasing pulmonary vascular resistance. Airway pressures increase, and patients can have difficulty ventilating. Alveoli exhibit atelectasis, increasing the dead space. Thus, gas exchange is adversely affected as less oxygen is transported and more carbon dioxide is retained, leading to hypoxemia and hypercarbia. 

Renal System

IAH can compromise the renal system by decreasing renal arterial and venous blood flow, affecting the glomerular filtration rate and ultimately leading to acute kidney injury and a subsequent reduction in urine output. Blood is diverted from the renal cortex, further impairing renal function. The renin-angiotensin-aldosterone system is activated, leading to increased systemic vascular resistance through the action of angiotensin II and increased reabsorption of water and sodium mediated by aldosterone. Study results indicate that oliguria can occur at an IAP of 15 mm Hg and anuria at pressures of 30 mm Hg. 

Gastrointestinal System

Decreased abdominal compliance with increased IAP leads to decreased splanchnic blood flow, causing tissue hypoxia, increased capillary permeability, and edema. Further insult propagates the body's inflammatory response, exacerbates intestinal malperfusion, and increases the risk of bacterial translocation and infection. The hepatic system is also affected as decreased hepatic flow leads to impaired metabolism and clearance, contributing to metabolic acidosis. 

Nervous System 

Elevated IAP also decreases venous drainage from the brain, thereby increasing intracranial pressure and decreasing cerebral blood flow. Increased partial pressure of carbon dioxide in arterial blood, PaCO_2, also causes increased arterial blood flow to the brain, further increasing intracranial pressure.[11][22][23]

History and Physical

ACS is usually only observed in critically ill individuals and is more frequently diagnosed in the ICU than in the emergency department. Physical examination is not a reliable indicator of ACS, even when performed by experienced clinicians, so objective measurements are necessary in any patient with risk factors for IAH.[10][24] If a patient has penetrating abdominal trauma, has received large amounts of fluid resuscitation, or has undergone extensive abdominal surgery, there should be a high clinical suspicion for ACS. Diagnosing ACS can be challenging, as ICU patients may have a range of extra-abdominal organ failures. Patients may also be intubated and unable to communicate their symptoms, so thorough monitoring of IAP, chart review to obtain past medical history, and overall clinical picture are essential for diagnosis.[10]

Evaluation

Imaging modalities are not standard practice for diagnosing ACS. However, imaging can show early indicators of IAH that may ultimately lead to ACS, such as a peritoneal-to-abdominal height ratio greater than 0.52, a maximal anteroposterior to transverse abdominal diameter ratio greater than 0.8, bowel wall thickening, elevation of the diaphragm, narrowing of the vena cava less than 3 mm, and a large amount of intra-abdominal fluid.[10]  The most accurate method to confirm the diagnosis is measuring the IAP. The IAP should be measured anytime there is a known IAH risk. IAP measurement can be achieved using both direct and indirect methods. Direct methods include pressure transducers (eg, the Veress needle during laparoscopic surgery) or intraperitoneal catheters (eg, peritoneal dialysis catheters). These methods are highly accurate but are invasive.

The most widely accepted method of measuring IAP is indirect IAP measurements, which involve intravesicular catheter pressures. This is the most practical approach due to its widespread availability and limited invasiveness.[25] This technique involves aseptic clamping of the Foley catheter and connecting the catheter to a 3-way stopcock, adjusted to the level of the midaxillary line at the iliac crest, to zero the transducer. Next, 25 cc of sterile saline is injected into the bladder. Measurements should be taken at end-expiration with the patient in a complete supine position.[5][15] Bladder pressures below 5 mm Hg are expected in healthy individuals.

Pressures reaching 10 to 15 mm Hg can be expected following abdominal surgery and in obese patients. Bladder pressures exceeding 25 mm Hg highly suggest ACS and should be correlated clinically. Pressure measurements should be trended every 6 hours to identify worsening IAH when there is potential for the development of ACS. Contraindications to using bladder pressures include bladder trauma, neurogenic bladder, benign prostatic hypertrophy, and pelvic hematoma.[26][27] Pelvic fracture, bladder hematoma, and peritoneal adhesions will lead to inaccurate measurements.[24] If bladder measurements are unavailable, alternative screening methods for IAH include the placement of a central line to measure inferior vena cava pressure, manometry through a Jackson-Pratt drain, and measurement of intragastric pressure via a nasogastric tube. These are not well-validated and not commonly used methods.[24]

Treatment / Management

Choosing the appropriate intervention and timing of the intervention is determined by the etiology of the elevated IAP, the duration of increased IAP, and the degree of organ dysfunction. Not every patient with ACS will immediately need surgical decompression, as nonsurgical interventions can decrease intraabdominal volume and ultimately improve IAP. If clinically indicated, intraluminal volume can be reduced with nasogastric decompression, rectal tube decompression, or endoscopic decompression. Percutaneous drainage can reduce extraluminal volume in the case of ascites or hematoma.[5][21][24] Abdominal wall compliance can be improved in patients in the supine position, if possible, with adequate sedation and neuromuscular blockade, removal of constrictive dressings, and eschar release, among other options. Other recommendations made by the WSACS include optimizing fluid administration, resuscitating with hypertonic products or colloids, considering hemodialysis or ultrafiltration, and goal-directed resuscitation.[5] However, the quality of evidence is low and needs to be considered when using conservative measures.[15] (A1)

Percutaneous catheter drainage is a viable option for ACS caused by increased extraluminal abdominal volume. This method is far less invasive than a surgical laparotomy and can also be used temporarily if surgical decompression is not an immediate option. Excess extraluminal abdominal volume is caused by excess air, fluid, or blood in the abdominal cavity.[21] 

If conservative medical management does not lead to improved IAH and further organ damage is noted, surgical decompression using emergent laparotomy should be considered.[2][28] With surgical abdominal decompression, organ dysfunction may also improve rapidly, as most organ dysfunction is seen as a direct sequelae of compromised blood flow or mechanical obstruction.[29][30] After surgical decompression, the abdominal fascia may be left open temporarily. The open wound is often covered by a negative pressure dressing system, which helps minimize the risks of infections and fistulas, decreases insensible losses, and prevents retraction of the fascia. With clinical improvement, the patient can return to the operating room within several days for further evaluation and attempted fascial closure, which can be achieved with mesh or primary closure techniques.[6][10] However, some of these approaches may not be feasible at all facilities due to limited resources.[31](B3)

Although surgical decompression is considered a definitive treatment for ACS, it can be associated with many complications, especially when the abdominal wall is left open. Some complications include fistula formation, protein loss by drainage of peritoneal fluid, abdominal wall retraction with ventral hernia development, and wound infection. In addition, up to 20% of surgical decompression is associated with recurrent ACS, either due to ongoing causative agents or inadequate lowering of IAP.[24]

Despite extensive literature published on ACS, the ideal timing for surgical decompression is debatable. Early pursuit of surgical intervention can exacerbate stress on the patient from the surgery itself. Thus, the consensus within the medical community is to consider surgery when multiple conservative management treatments have not improved the patient's condition.[7]

Differential Diagnosis

The differential diagnosis for ACS includes mesenteric ischemia, ruptured abdominal aortic aneurysm, toxic megacolon, acute appendicitis, and acute diverticulitis.

Prognosis

If left untreated, ACS can be fatal, and delayed treatment is associated with high mortality rates. IAH has been identified as an independent predictor of mortality, with each grade associated with worsening outcomes.[10][20] Many series report that the resulting multiorgan failure can delay recovery for weeks or months, even with treatment. Prolonged need for mechanical ventilation, dialysis, and more extended hospital stays are also common in these patients.

Complications

ACS complications include the following:

• Renal failure
• Bowel ischemia
• Respiratory distress or failure
• Increased cranial pressure
• Cardiac failure
• Potential death