Abdominal Compartment Syndrome: Pearls & Pitfalls

Author: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX) and Michael Gottlieb, MD (EM Attending Physician, Rush Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)


You are caring for a 28-year-old male transferred to your trauma center with severe abdominal and pelvic trauma after an MVC. The patient was found to have a grade IV hepatic laceration and open book pelvic fracture. He was given 3 units of pRBCs and 3 units of FFP before transfer, which stabilized him for transfer. His current vital signs are HR 112 bpm, BP 108/58 mm Hg, RR 26, oxygen saturation 90% on room air, and oral temperature 96F. On your exam, the patient is in distress, and his abdomen is significantly distended and tense to palpation.

What is abdominal compartment syndrome?

Abdominal compartment syndrome (ACS) is defined by sustained intra-abdominal pressure (IAP) > 20 mm Hg with associated organ injury. The condition was first described in 1863, but not significantly discussed until the 1990s (1-3). Intra-abdominal hypertension (IAH), or elevated pressures within the abdomen in the absence of end organ injury, has been associated with increased mortality and lengths of stay, but just because the patient has IAH does not mean he/she has ACS. Approximately 3-13% of patients will develop ACS in the setting of IAH (4-7).

ACS possesses a large number of associated risk factors, but all of these are related to 4 components: diminished abdominal wall compliance, increased intraluminal contents, increased abdominal contents, or capillary leak/fluid resuscitation (7-9).

Unfortunately, ACS is associated with a mortality ranging from 25-100% (1-5, 7). However, it is often missed in the ED. While one of our primary roles is to resuscitate and manage acute life-threatening conditions, we are finding ourselves boarding critical patients in the ED. With this increased boarding, emergency clinicians must recognize, diagnose, and manage ACS.

What is the underlying pathophysiology?

The abdomen is a compartment defined by the abdominal wall anteriorly and posteriorly, the diaphragm superiorly, and the pelvic floor inferiorly. A normal intra-abdominal pressure ranges from 2-5 mm Hg, which can increase to 7 mm Hg in critically ill patients (8-10). However, other conditions can also increase this baseline level, such as obesity (7-16 mm Hg at baseline) and pregnancy (up to 14 mm Hg) (11-13).

ACS is just like any other form of compartment syndrome, with decreased tissue perfusion and oxygenation resulting from elevated pressure within a fixed space (8,14). ACS increases bowel edema and intestinal ischemia, allowing for bacterial translocation. However, ACS does not just affect the abdominal organs (1,3,4,15-18). Other systems affected include the renal, CNS, cardiovascular, pulmonary, and biliary systems.

There are three categories of ACS, based on the cause and duration (1,2).

  1. Primary: Intrinsic etiology resulting from an intra-abdominal injury or disease
  2. Secondary: Extrinsic etiology that does not come from the abdominopelvic region (sepsis, fluid resuscitation, burns)
  3. Recurrent: ACS redevelops following a prior episode of either primary or secondary ACS.

What can you find on history and exam?

You cannot diagnose what you do not consider. Most patients with ACS will be critically ill, with many intubated or with poor mental status. Thus, keep this condition in mind in patients who are critically ill with the risk factors from Table 1. Other risks factors include prior abdominal surgeries or known intra-abdominal adhesions (1,2,19), which reduce abdomen’s ability to compensate for increased pressures. Patients who are awake may have worsening pain, distension, and difficulty breathing (10,20). Orthopnea may be present (10,20). Worsening or refractory hypotension with new organ failure are major clues to ACS. Oliguria and renal dysfunction are two of the earliest findings in ACS (21,22).

Exam in ACS possesses major limitations and cannot exclude the diagnosis with a sensitivity of 40-60%, though specificity for several findings range from 80% to 94% (16,17). Increased abdominal distension, elevated abdominal wall tension, and absence of bowel soundsare associated with diagnosis (23,24). While it seems measuring the amount of abdominal distension would work, literature suggests this is not a reliable predictor (23-25). Diffuse edema, increasing abdominal tension with palpation, and frequent high-pressure alarms on a ventilated patient suggest the disease (10,20).

What role do labs and imaging play?

Labs play an important role in ACS, as organ dysfunction is a key part of the diagnosis. CBC, renal and liver function, VBG (pH and lactate), electrolytes, and urinalysis are recommended. Severe organ dysfunction may be represented by increased creatinine, troponin, liver function tests, or lactate, as well as reduced glomerular filtration rate (1,2,24,26,27). Metabolic acidosis is present in severe ACS with elevated lactate. D-lactate is a produce of intestinal bacterial metabolism and may be an early detector of intestinal ischemia, but this test may not be obtainable.  Intestinal fatty acid binding protein (I-FABP) and interleukins have also been evaluated but are not ready for primetime (20,28-30).

Just like your exam, imaging may demonstrate findings associated with ACS, but normal imaging cannot exclude the diagnosis. Abdominal x-ray may reveal free air or intestinal dilation, and chest x-ray may show pleural effusions, diaphragm elevation, and atelectasis (1,2,31-33). CT of the abdomen/pelvis can reveal many findings suggesting ACS: increased intestinal AP diameter, IVC collapse, diaphragm elevation, pneumoperitoneum, renal vessel compression, thickened bowel wall, and inguinal hernias bilaterally (32-34). Narrowed vasculature and organ compression on CT strongly suggest ACS. There are several other findings on CT cited in the literature concerning ACS: the round belly sign (RBS) is an increased ratio of anteroposterior to transverse diameter of more than 0.80, and the peritoneal-to-abdominal height ratio (PAR) is the ratio of the anteroposterior peritoneal compartment diameter (distance from linea alba to posterior part of duodenum) and anteroposterior abdomen diameter (distance from linea alba to posterior fascia) measured along the midline. A PAR > 0.52 suggests IAH, while values < 0.45 possess a 100% negative predictive value (1,2,32-36). Other values of CT include evaluating for the underlying etiology of ACS.

What about intra-abdominal pressure? When should you measure IAP, and how is it measured?

While history, exam, labs, and imaging have roles in the diagnosis of ACS, measuring IAP is imperative.  Measure IAP in any critically ill patient with a risk factor for ACS and new/worsening organ failure (1,2,10,20). You can measure IAP through direct or indirect measurement. Direct measurement includes placing a catheter into the peritoneal cavity, while indirect measurements are obtained through the bladder, rectum, stomach, or vagina. In the ED, bladder pressures are the easiest and most reliable means of assessing IAP (1,3,4,7,37-39). However, obtaining bladder pressures is contraindicated in those with traumatic bladder injury, pelvic packing, or history of cystectomy (37).

Intermittent IAP assessment every 4-6 hours is recommended by the World Society of the Abdominal Compartment Syndrome (37,40). Assessing more frequently than 4 hours is not recommended. In the ED, a single measurement in a patient with risk factors is recommended (10,20,37). However, if the patient remains in the ED for longer than 4 hours, you may need to obtain a repeat measurement. There are means of continuous measurement, but data suggest that continuous and intermittent assessments are equally reliable. Plus, continuous assessment needs a 3-way catheter for measurement (3,7,37).

To measure bladder pressures, you need the following: Foley catheter kit, Kelly forceps, 60-mL syringe with sterile saline, 3-way stopcock, arterial line pressure transducing tubing, 1 Liter of intravenous fluids, and a pressure bag (1,3,37-43).

Make sure the patient is placed supine and relaxed. Coughing and inadequate sedation can increase bladder pressure. While most patients with ACS will be mechanically ventilated, you can measure IAP in awake, spontaneously breathing patients, but just ensure these patients are provided appropriate analgesia. Obtain the pressure at end-expiration with an appropriately placed Foley catheter (1,2,27,37,39)). Zero the pressure transducer at the level of the bladder in the mid-axillary line. Be sure to install a maximum of 25 mL of warm saline (cold saline will increase the pressures) (3,37,43,44). Once you have placed 25 mL into the bladder, wait 30 seconds to allow the detrusor muscle to relax.  Another measurement technique includes urine drainage manometry with 50 mL of sterile saline and the Foley catheter tubing as the device for measurement. The catheter tube is placed perpendicular at the pubic symphysis level, with a ruler to measure the fluid height. Use a ruler to obtain pressure readings, which conversion of cm H20 into mm Hg by multiplying by 0.74 (45-49).

What are pitfalls in IAP measurement?

Obesity, pelvic pathology, and radiation cystitis can elevate IAP (1,2,20,31,37).Falsely low readings may occur with a leak in the transducer system. IAH is defined by values > 12 mm Hg. Keep in mind there are several grades of IAH and ACS (1,2,20,31,37,48,49).

Remember, diagnosis includes IAP > 20 mm Hg with organ dysfunction. However, patients at risk for ACS are critically ill and may have several contributors to organ failure (7,9,37-39). This is one of those classic “chicken or the egg” situations, as some patients may have organ dysfunction from the primary illness or injury (1,2,9,20,37).  Timing of injury can assist. ACS is likely when IAP > 20 mm Hg with organ dysfunction that occurs in a time-dependent association (1,2,9,20,37). Patients with oliguria and IAP > 20 mm Hg likely have ACS as well (21,22,50).

Ok, you have diagnosed ACS. What’s the management?

Management targets improving end-organ perfusion and reducing elevated IAH. The WSACS management algorithm includes evacuating intraluminal contents and intraabdominal space-occupying lesions, improving compliance of the abdominal wall, optimizing intravascular fluid therapy, and increasing systemic perfusion (20,37,41).

Abdominal perfusion pressure (APP) is calculated by mean arterial pressure (MAP) minus IAP (37,51,52). APP is an assessment of the intra-abdominal organs and is a better predictor of survival than IAP or MAP alone (37,51,52). While a goal APP > 60 mm Hg is generally recommended, there is no evidence-based goal for a specific APP (9,22,37). Optimize APP first by ensuring adequate intravascular volume, but avoid hypervolemia (41,53).  Fluid administration should be minimal, as third spacing increases IAH (1-3,37,54,55). In hypotensive patients, early vasopressor and inotropic support may be needed (1-3,9,37,53-55). Norepinephrine and dobutamine possess the greatest literature support for use in ACS (56-59).

Treat pain and agitation, as these increase IAP (1,2,9,37,41). Though many will be intubated, mechanical ventilation should be avoided if possible, as this converts negative-pressure system to positive pressure, increasing IAP (41,60). In the mechanically ventilated patient, target as low PEEP and plateau pressures as oxygen saturation allows (9,37,41,60). Paralysis can also be used while awaiting adequate decompression (61-63). However, prolonged paralysis does not appear to result in persistent reduction in IAP (61-63).

Abdominal compartment decompression is essential, with reducing intraluminal and intra-abdominal contents. Ileus and luminal distension are common due to intestinal ischemia (10,20,37,41). Metoclopramide and erythromycin (prokinetic agents) can reduce intraluminal contents. NG or OG tube placement can also reduce gastric contents and pressure, and with stimulant laxatives, neostigmine, rectal tube drainage, and/or colonoscopy can reduce colonic distension (37,41). Ascites, blood, abscess, and free air can increase IAP, and if any of these are present, they should be removed (10,20,37,41). Therapeutic paracentesis is recommended if ascites is present, and percutaneous drainage may be used to remove extraluminal air (64-66). Thoracic decompression is recommended for pleural effusion or pneumothorax, and escharotomy is recommended for patients with severe burns that are causing increased IAP (37,41).

Patients may fail to respond to the above measures, necessitating surgical decompression via laparotomy. This is the definitive intervention, reducing IAP and improving patient hemodynamic status and end-organ prefusion (37,41,67-69). Surgical decompression improves patient mortality, and the earlier the intervention, the better (improved survival and reduced morbidity with earlier decompression) (70).

Disposition and Prognosis

Most patients with ACS require ICU level care (1,2,9,37). Just keep in mind repeat assessments in patients who are boarding may be needed. Prognosis primarily depends on rapid diagnosis and early management. Patients with older age, comorbidities, greater volume received in resuscitation, and major organ dysfunction have higher mortality rates (10,20,37,71-73).

Key Points

  • ACS is a potentially deadly condition caused by increased pressure within the abdominal compartment.
  • ACS is defined by IAP > 20 mm Hg with organ dysfunction.
  • Four underlying causes contribute: decreased abdominal wall compliance, increased intraluminal contents, increased abdominal contents, or capillary leak/fluid resuscitation.
  • History and physical examination may suggest the diagnosis, but they should not be used to exclude ACS. Labs and imaging can also assist in diagnosis.
  • The gold standard for diagnosis is intra-abdominal pressure measurement, typically through a Foley catheter.
  • Management includes increasing abdominal wall compliance, evacuating gastrointestinal contents, avoiding excessive fluid resuscitation, draining intraperitoneal contents, and decompressive laparotomy in select cases. Patients typically require admission to a critical care unit.

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