Pathophysiology of intraabdominal hypertension and abdominal compartment syndrome and relevance to veterinary critical care
Authors: Gardner Alison K. , Schroeder Eric L. 
Published: January 2022

Background

Increased intraabdominal pressure, termed intraabdominal hypertension (IAH), is reported as an independent cause of morbidity and mortality in the human ICU but, until recently, has been rarely described in veterinary species outside of experimental models. Failure to identify severe IAH leads to organ dysfunction, termed abdominal compartment syndrome, and rapidly becomes fatal without therapeutic intervention. Although the veterinary community has been slow to address the concept of IAH and associated comorbidities, recent companion and large animal case series and experimental studies suggest IAH may also be common in veterinary species and correlates well with risk factors and grading systems already described in the human literature.

Pathophysiology

Increasing abdominal pressures exert deleterious local effects through visceral ischemia and reperfusion injury as well as systemic effects on the cardiovascular, pulmonary, renal, and central nervous systems. Even mild grades of IAH increase systemic vascular resistance, impede venous return, increase pulmonary wedge pressure, and decrease pulmonary function. More severe grades cause azotemia, oliguria, decreased coronary blood flow, hypoxia, increased intracranial pressure, and death.

Importance

Many of the common diseases in veterinary patients are associated with IAH, including gastric dilatation–volvulus, colon volvulus, closed pyometra, hemoperitoneum, ascites, uroperitoneum, and hydrops. Monitoring of the veterinary patient is difficult, but several experimental studies validate both the presence of IAH and the ability to monitor abdominal pressures in large and small animal species. Moreover, prompt recognition of IAH and subsequent treatment is feasible in the veterinary ICU.

Key points

Increasing abdominal pressures exert deleterious local effects through visceral ischemia and reperfusion injury as well as systemic effects on the cardiovascular, pulmonary, renal, and central nervous systems.

Increases in central venous pressure, systemic vascular resistance, pulmonary wedge pressure, and a decreased cardiac output by way of both decreased preload and increased afterload have been documented as a result of intraabdominal hypertension (IAH).

Direct diagnosis of IAH is achieved by blind or ultrasound‐guided abdominal needle puncture attached to a water manometer or direct pressure monitoring transducer.

Transvesicular measurement of intraabdominal pressure (IAP) is relatively noninvasive, and many patients that would benefit from rapid diagnosis of IAH and abdominal compartment syndrome already have indwelling bladder catheters.

Recommendations for interventions are based on the assigned grade of IAH (mild, moderate, severe).

Key points

If IAH is strongly suspected or diagnosed, abdominal wall compliance may be improved through judicious use of neuromuscular blockers and sedation.

Decompression, either minimally invasive or surgical, is absolutely recommended for IAPs consistently above 20 mm Hg, especially in the presence of signs attributed to secondary organ dysfunction.