Abdominal compartment syndrome - NYSORA

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Abdominal compartment syndrome

Learning objectives 

  • Difference between intra-abdominal pressure (IAP) and abdominal compartment syndrome (ACS)
  • Recognize ACS and the pathophysiological consequences of ACS
  • Management of ACS

Definition and mechanisms

  • Normal intra-abdominal pressure (IAP) ranges between 0-5 mmHg while in critically-ill patients, an IAP of 5-7 mmHg is considered normal
  • Intra-abdominal hypertension is defined as a sustained intra-abdominal pressure (IAP) ≥12 mmHg
  • Abdominal compartment syndrome (ACS) is defined as IAP rises > 20 mmHg thereby leading to new organ dysfunction 
  • Abdominal perfusion pressure (APP) is calculated as the mean arterial pressure (MAP) minus the IAP
  • A critically ill patient with high mortality & morbidity

Signs and symptoms

  • Malaise
  • Weakness
  • Dyspnea
  • Abdominal bloating
  • Abdominal pain
  • Hypoxia
  • Hypercabia
  • Oliguria

Etiology

Acute ACS

  • Primary: due to injury or disease in the abdominopelvic region (e.g., pancreatitis, abdominal trauma)
  • Secondary: does not originate in the abdomen or pelvis (e.g., fluid resuscitation, sepsis, burns)

Chronic ACS

  • In association with peritoneal dialysis or chronic ascites 

Artificially raised IAP

  • External compression, for example, prolonged prone positioning for spinal surgery with insufficient provision for abdominal movement

Risk factors

Diminished abdominal wall complianceAcute respiratory failure, especially with elevated intrathoracic pressure
Abdominal surgery with subjectively tight primary closure
Major trauma/burns
Prone positioning, head of bed elevated > 30°
High BMI, central obesity
Increased intra-luminal contentsGastroparesis
Ileus
Colonic pseudo-obstruction
Increased abdominal contentsHemoperitoneum/pneumoperitoneum
Ascites/liver dysfunction
Capillary leak/fluid resuscitationMetabolic acidosis ( pH < 7.2)
Hypotension
Perioperative hypothermia
Polytransfusion (>10 units of blood/24 h)
Coagulopathy (platelets < 55 000 mm-3, prothrombin time > 15 s, partial thromboplastin time > 2 times normal, or international standardized ratio >1.5)
Massive fluid resuscitation (> 5 litre/24 h)
Pancreatitis
Oliguria
Sepsis
Trauma
Burns
Damage control laparotomy

Pathophysiological effects of raised IAP

Central nervous systemIncreased intra-cranial pressure

Cardiovascular systemIncreased systemic vascular resistance
Pulmonary vascular resistance
Decreased venous return with concomitant venous congestion
Gastrointestinal and hepatic systemDecreased coeliac, mesenteric, hepatic and hepatic portal blood flow
Increased oedema, bacterial translocation and liver dysfunction
Renal systemIncreased renal tubular pressure and urinary obstruction
Decreased renal blood flow and urine output
Respiratory systemIncreased ventilation-perfusion mismatch, ventilatory pressure, basal atelectasis and PaCO2
Decreased chest wall and pulmonary compliance and PaO2

Diagnosis

  • Indirect measurement of IAP using intragastric, intracolonic, intravesical (bladder), or inferior vena cava catheters

Management

  • Patients with two or more risk factors should have IAP monitoring 
  • Treatment:
    • Regimens lowering IAP
    • Open the abdominal wound and perform a temporary closure of the abdominal wall with mesh or a plastic bag (Bogota bag)
    • Regiments aiming at organ support
  • Keep abdominal perfusion pressure (APP) (systemic blood pressure – intra-abdominal pressure) > 60mmHg

abdominal compartment syndrome, ACS, IAP, APP

Keep in mind

  • Consequences of decompression:
    • Sudden ↓ cardiac output & SVR
    • Reperfusion: risk of systemic acidosis & hyperkalemia
    • Possible fatal arrhythmia & arrest
    • Sudden change in respiratory compliance (avoid overventilation)
  • Avoid bradycardia (preload is compromised & CO may be heart rate dependent)
  • Maintain high preload particularly once decompressed

Suggested reading

  • Neil Berry, Simon Fletcher, Abdominal compartment syndrome, Continuing Education in Anaesthesia Critical Care & Pain, Volume 12, Issue 3, June 2012, Pages 110–117.
  • Mullens W, Abrahams Z, Skouri HN, et al. Elevated intra-abdominal pressure in acute decompensated heart failure: a potential contributor to worsening renal function? J Am Coll Cardiol. 2008;51(3):300-306.

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