Presentation

Classic and critical presentations

• Neurological
  
  
  
  • Increased IAP has been shown to decrease cerebral perfusion pressure by decreased cardiac output (CO) and hypotension, as well as via increased thoracic pressure with functional obstruction of cerebral venous outflow.
  
  
• Cardiovascular
  
  
  
  • Increased IAP directly compresses the vena cava, decreasing venous return and cardiac output (CO), which increases systemic venous congestion and edema. The diaphragm bulges upward, displacing the heart and compromising diastolic filling, which further decreases CO.
  
  
• Respiratory
  
  
  
  • The cephalad displacement of the diaphragm also decreases pulmonary compliance, leading to segmental alveolar collapse and subsequent ventilation/perfusion mismatches. In patients on ventilators (majority of patients), an increase in peak airway pressures and peak inspiratory pressures will be observed in addition to increased difficulty in ventilating overall. The increase in thoracic pressure artificially increases central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP), compromising the value of these markers for guiding resuscitation.
  
  
• Renal
  
  
  
  • Direct compression of the kidneys combined with decreased vascular inflow and outflow can create oliguria and compromise renal function even in the setting of maintained hemodynamics.
  
  
• Gastrointestinal
  
  
  
  • Direct compression within the abdominal cavity decreases splanchnic blood flow leading to bowel ischemia and necrosis. This also contributes to the formation of bowel edema, which in turn increases IAP.
  
  
• Musculoskeletal
  
  
  
  • Musculoskeletal dysfunction, both within the abdominal wall and in the extremities, is also observed as a result of decreased CO, global ischemia, and reperfusion injury.

Diagnosis and evaluation

• The most efficient way to recognize and treat ACS is by recognizing and correcting predisposing factors before ACS occurs.
  
• In the closed abdomen, the gold standard approach to measuring IAP uses a urinary bladder catheter (“bladder pressures”) with the patient in full supine position.
  
  
  
  • Normal IAP ranges from 0 to 5 mmHg, with IAP after uncomplicated surgical procedures ranging between 3 and 15 mmHg.
    
  • A maximum of 20–25 mL of sterile saline is injected into the catheter, which is then clamped and connected to a transducing device.
    
  • The pubic symphysis is used as the zeroing point on a supine patient.
    
  • Time should be allowed for the detrusor muscle of the bladder to accommodate the volume before the pressure is measured.
    
  • IAP should be measured at end expiration.
  
  
• IAP may be artificially elevated by abdominal wall contraction (such as in an awake patient or in situations of inadequate analgesia), body habitus (obesity), or patient positioning (raising the head of the bed). In intubated patients, pharmacological paralysis may enhance the accuracy of IAP measurements as well as provide therapeutic benefit.

Critical management

• Early recognition of risk factors and delaying definitive abdominal wall closure remains the best therapy for ACS. In cases in which the abdominal wall is already closed or the decompression is inadequate, timely intervention can be life-saving.
  
• Any patient suspected of having ACS should have frequent measurements of IAP.
  
• The definitive treatment for a patient with ACS is decompressive laparotomy.
  
• There is some evidence to support the use of percutaneous decompression using a diagnostic peritoneal lavage catheter as an alternative treatment prior to decompressive laparotomy.
  
• There is no standard consensus on when to intervene. The decision is made based on clinical judgment, presence of end-organ failure, and serial measurements of IAP.
  
• Aggressive fluid resuscitation to maintain hemodynamics may overcome some of the deleterious effects of increased IAP; however, others have recommended conservative resuscitation to avoid excess third-spacing, bowel edema, and subsequent worsening of IAP. In trauma patients and other select groups, consider the use of blood products and colloids over crystalloids.
  
• CVP and PCWP are unreliable in the setting of increased IAP. Determination of right ventricular end-diastolic volume with pulmonary artery catheters has been suggested as a surrogate endpoint, as has maintenance of abdominal perfusion pressure (mean arterial pressure − IAP) above 50 mmHg, but neither has been tested in prospective, randomized clinical trials.
  
• If the underlying insult causing ACS is expected to resolve within a relatively short time period, temporizing measures other than surgical decompression can be adopted. Liberal analgesia and sedation as well as pharmacological paralysis are adjunct measures that may decrease abdominal wall tension. Paracentesis and renal replacement therapy can be used in appropriately selected patients to normalize fluid balance.
  
• When the decision to surgically decompress is made, resuscitation to a euvolemic status is imperative, as surgical decompression results in the following:
  
  
  
  • Decreased systemic vascular resistance
    
  • Increased respiratory tidal volumes
    
  • Washout of byproducts of anaerobic metabolism, releasing acid, potassium, and other potentially arrhythmogenic byproducts into the circulation.
  
  
• Remember that ACS can occur even in the already decompressed abdomen – either due to an incision that is too small or due to an abdominal closure system that is too tight.

References

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