A 62-year-old female patient presents with fever, cough, and an infiltrate on her chest radiograph. She receives intravenous fluids and antibiotics, but her symptoms worsen, eventually requiring intubation for respiratory decompensation and vasopressors for presumed septic shock. The intensive care unit is full, so the patient remains in the emergency department. During this time, her condition worsens, and she develops new renal and hepatic injury. You wonder if there is something you may be missing. Could this patient have abdominal compartment syndrome? If so, how do you test for it, and what are the next steps in management?

Discussion

Abdominal compartment syndrome (ACS) is a disease that can lead to significant morbidity and mortality.^1–3 However, it is not often considered in the emergency department. With high rates of ED boarding in many areas, it is essential for the ED clinician to be aware of this disease and monitor for it.

ACS is similar to limb compartment syndrome in that there is excessive pressure within a closed space (ie, the abdominal compartment), resulting in damage to the surrounding structures. This exists as part of a continuum beginning with elevated intra-abdominal pressure (IAP) and ending with organ dysfunction (see Table 1). There are numerous causes of ACS, but they mainly fall into four general categories: reduced abdominal wall compliance (eg, abdominal surgery, obesity), increased abdominal contents (eg, large-volume ascites, hemoperitoneum), increased intraluminal contents (eg, ileus, gastroparesis), or capillary leak (eg, sepsis, pancreatitis).^4,5

Table 1: Grading of Intra-Abdominal Hypertension and Abdominal Compartment Syndrome

IAH, intra-abdominal hypertension; IAP, intra-abdominal pressure

Obtaining a relevant history may prove challenging because most patients with ACS are critically ill, and many are intubated. For patients who can provide a history, worsening abdominal pain, abdominal distension, or difficulty breathing (particularly when supine) may be reported.^6,7 The physical examination is also limited in these patients; studies demonstrate a sensitivity of 40–60 percent and a specificity of 80–94 percent for ACS diagnosis.^8,9 Abdominal distension and the absence of bowel sounds are associated with ACS, but their absence cannot exclude it.⁵ Therefore, clinicians should remember this condition for critically ill patients with worsening or refractory hypotensio and those with new organ failure.

Laboratory studies may demonstrate evidence of severe organ dysfunction, including elevations in lactate, creatinine, and liver markers.¹⁰ If obtained, a computed tomography scan of the abdomen and pelvis may demonstrate an increased anteroposterior diameter, inferior vena cava collapse, diaphragm elevation, renal vessel compression, thickened bowel wall, pneumoperitoneum, or inguinal hernias bilaterally.^11–13 However, neither the history and physical examination nor advanced imaging is sufficient to exclude the diagnosis. Therefore, clinicians who are concerned about ACS should measure the IAP (see Table 2).

Table 2: Measuring IAP in Suspected ACS

IAP, intra-abdominal pressure; ACS, abdominal compartment syndrome;
Adapted from Gottlieb et al.⁵

FIGURE 1A

FIGURE 1B

FIGURE 1C
PHOTOS: Michael Gottlieb and Brit Long

Although multiple methods of IAP measurement have been proposed, intravesicular measurement generally preferred. As the name suggests, this measurement is obtained by placing a Foley catheter into the bladder. When measuring IAP, the patient should be supine and relaxed to avoid artificially increasing the IAP measurements.^5,10 Ensure the patient’s pain is adequately controlled and measure the pressure at end-expiration.¹⁴ Clinicians should use warm saline to avoid detrusor muscle spasm, and no more than 25 mL of fluid should be instilled to avoid false elevations of IAP.¹⁴ ACS is defined as an IAP >20 mm Hg with evidence of organ dysfunction.¹⁴

Treatment of ACS focuses on improving end-organ perfusion by reducing IAP. This includes four main steps: 1) evacuating intraluminal and intraperitoneal contents, 2) improving abdominal wall compliance, 3) optimizing intravascular fluid therapy, and 4) early surgical consultation for possible surgical decompression.

Ileus and luminal distension are common in patients with ACS.^15,16 Nasogastric or orogastric tubes can reduce gastric distension, while prokinetc agents (eg, metoclopramide, erythromycin) may help reduce intraluminal contents.^14,17 Extraluminal pathologies (eg, ascites, hemoperitoneum, pneumoperitoneum) may also require drainage, which can be performed percutaneously or through operative drainage.^18–20

Adequate analgesia and sedation should be provided because pain and sedation can further increase IAP. If the patient is intubated, clinicians should aim for as low positive end-expiratory pressure and plateau pressures as the oxygen saturation allows.^10,16 Paralysis can also be used as a temporary bridge for refractory cases while awaiting surgical decompression.^21–23

Clinicians should avoid excessive fluid administration because third spacing will worsen existing ACS.^10,16 If patients are hypotensive or septic, early vasopressor and inotropic therapy may be preferable in these patients; norepinephrine and dobutamine have the best literature support in treating ACS-associated hypotension.^24–27

In cases that are refractory to the above interventions, surgical decompression may be warranted. Therefore, it is important to consult a surgeon early in the management of suspected ACS patients.

Case Resolution

You suspect ACS and assess the IAP using a Foley catheter. The IAP is 25 mm Hg, and a repeat creatinine level is significantly elevated. You place an orogastric tube, administer metoclopramide, ensure the patient is adequately sedated, and consult a surgeon for possible operative management. The patient is taken to the operating room for surgical decompression. 

Dr. Gottlieb is associate professor, ultrasound division director, and ultrasound fellowship director in the department of emergency medicine at Rush University Medical Center in Chicago.

Dr. Long is an emergency physician in the San Antonio Uniformed Services Health Education Consortium at Fort Sam Houston, Texas.

References

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