Abdominal compartment syndrome

Background

Lateral view showing abdominopelvic cavity.

Organ dysfunction caused by intrabdominal hypertension
Increased intrabdominal pressure resulting in decreased organ perfusion, impaired hemodynamics

Pathophysiology

Abdominal perfusion pressure = MAP - intrabdominal pressure
Build up of fluid or blood within the peritoneum or retroperitoneum
- And/or decrease in abdominal wall compliance
Increased pressure within cavity of fixed volume → hypoperfusion of abdominal organs
- Also causes restriction of diaphragmatic excursion and impaired central venous return

Causes

Clinical Features

Most patients are critically ill and unable to communicate
Decreased central venous return
- Increased JVP
- Increased ICP
- Decreased cardiac preload
- Increased cardiac afterload
Increased intrathoracic pressure
- Decreased lung compliance (will cause high peak pressures in vented patients)
- Decreased functional residual capacity
- Worsened V/Q mismatch
Oliguria, renal failure
Bowel ischemia

Differential Diagnosis

Abdominal Trauma

Evaluation

Abdominal compartment syndrome caused by bulimia post vomiting. CT shows dilated stomach with food and air pressed other visceral organs and major abdominal vessels.

A case of abdominal compartment syndrome derived from simple elongated sigmoid colon in an elderly man.. Abdominal CT scan of the patient pre-decompression (a) and post-decompression (b). The arrow shows the inferior vena cava, which was collapsed pre-decompression.

Workup

Physical exam is neither sensitive nor specific

Link to steps on how to measure bladder pressure with arterial line and video.

Obtain bladder pressure
- Normal = <12 mmHg
- Intra-abdominal hypertension (IAH) = 12 - 20 mmHg
- Concern for abdominal compartment syndrome = >20 mmHg (also requires evidence of end-organ damage)

Diagnosis

Abdominal compartment syndrome = IAH >20 mmHg PLUS end-organ damage
Abdominal perfusion pressure <60 mmHg suggests abdominal hypoperfusion^[1]
Note that IVC scanning for volume status is especially unreliable as collapse may not represent volume depletion in the context of high intra-abdominal pressures^[2]

Management

Nonoperative

Often first line approach when no abdominal injury present^[3]

Limit fluid resuscitation
Nasogastric and bladder decompression
Electrolyte repletion
Antibiotics
Pressors with goal MAP 65
CRRT
Percutaneous fluid drainage (remove ascites if present)
Treat pain and adequately sedate
Reverse Trendelenburg
Consider metoclopramide

Operative

Definitive treatment

Laparotomy provides decompression
- High complication rate
- No guidelines for timing of closure

Disposition

Admit

External Links

References

↑ Al-Dorzi HM et al. Intra-abdominal pressure and abdominal perfusion pressure in cirrhotic patients with septic shock. Ann Intensive Care. 2012; 2(Suppl 1): S4.
↑ Bauman Z et al. Inferior vena cava collapsibility loses correlation with internal jugular vein collapsibility during increased thoracic or intra-abdominal pressure. J Ultrasound. 2015 Dec; 18(4): 343–348.
↑ Hunt, L., Frost, S. A., Hillman, K., Newton, P. J. and Davidson, P. M. (2014) ‘Management of intra-abdominal hypertension and abdominal compartment syndrome: a review’, Journal of Trauma Management & Outcomes, 8(1).

Authors:

[1] Al-Dorzi HM et al. Intra-abdominal pressure and abdominal perfusion pressure in cirrhotic patients with septic shock. Ann Intensive Care. 2012; 2(Suppl 1): S4.

[2] Bauman Z et al. Inferior vena cava collapsibility loses correlation with internal jugular vein collapsibility during increased thoracic or intra-abdominal pressure. J Ultrasound. 2015 Dec; 18(4): 343–348.

[3] Hunt, L., Frost, S. A., Hillman, K., Newton, P. J. and Davidson, P. M. (2014) ‘Management of intra-abdominal hypertension and abdominal compartment syndrome: a review’, Journal of Trauma Management & Outcomes, 8(1).

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