Summary
Highlights
Intra-abdominal pressure is the pressure within the abdominal cavity, a compartment housing organs like the stomach, liver, kidneys, and intestines. This pressure is influenced by the volume of fluids and organs, and elevations can equally transmit throughout, affecting various organs and blood vessels. While known for 150 years, practical application in critical care has increased in recent decades.
Normal IAP is less than 12 mmHg. Sustained pressure above 12 mmHg is considered Intra-Abdominal Hypertension (IAH), graded from 1 (12-15 mmHg) to 4 (>25 mmHg). Abdominal Compartment Syndrome (ACS) occurs when IAP is >20 mmHg with organ dysfunction, often >25 mmHg, carrying a 60-70% mortality. Normal physiological IAP in adults is less than 5 mmHg, with critically ill patients sometimes having 5-7 mmHg, and post-abdominal surgery or obese patients 10-15 mmHg. IAH measurements should be trended to prevent worsening conditions.
Elevated IAP and ACS have serious physiological implications beyond just abdominal organs, leading to significant impairments in cardiac, pulmonary, renal, GI, hepatic, and central nervous system function. Prolonged, untreated IAH results in inadequate perfusion and end-organ failure, highlighting the need for recognition, resuscitation, and prevention of organ dysfunction.
Elevated IAP displaces the diaphragm, increasing intrathoracic pressure, which decreases venous return and cardiac output (detectable even at IAP of 10 mmHg). Compounding factors like positive pressure ventilation and high PEEP worsen this. Afterload (SVR) increases due to compression of aorta, systemic vasculature, and pulmonary vessels. Decreased venous return also arises from IVC compression, potentially leading to peripheral edema and DVT risk. Paradoxical increases in CVP and PAOP due to intrathoracic pressure can also be observed.
Elevated IAP increases intrathoracic pressure, compressing lung tissue and causing pulmonary dysfunction at pressures >15 mmHg. This leads to atelectasis, decreased gas exchange, increased intrapulmonary shunt, decreased CO2 excretion, increased alveolar dead space, and higher peak inspiratory and mean airway pressures. Spontaneous tidal volumes and pulmonary compliance decrease, resulting in hypoxemia and hypercarbia.
Decreased renal blood flow occurs from reduced cardiac output and compression of renal vessels. Increased renal artery and vein pressure shunts blood from the renal cortex, impairing glomerular and tubular function. Oliguria can occur when IAP is >15 mmHg, and anuria when >30 mmHg. Direct renal tissue compression also reduces function. These changes are potentially reversible if IAH/ACS is recognized and treated early.
The GI system is highly sensitive; compression of mesenteric blood flow occurs at IAP >10 mmHg. Mesenteric vein compression leads to venous hypertension and intestinal edema, exacerbated by fluid resuscitation. This swelling further raises IAP, creating a feedback loop. Reduced perfusion causes ischemia, feeding intolerance, metabolic acidosis, increased mortality, and bacterial translocation. In the hepatic system, IAH reduces blood flow to the hepatic artery, vein, and portal vein, impairing microcirculation and reducing lactate clearance. Early changes are noted at IAP >10 mmHg.
Cerebral perfusion is influenced by IAP. Acute, drastic rises in IAP and intrathoracic pressure can significantly increase intracranial pressure (ICP) and reduce cerebral perfusion pressure. Causes include decreased lumbar venous plexus blood flow (increasing CSF pressure), increased pCO2 from pulmonary dysfunction (increasing cerebral blood flow), and decreased cerebral venous outflow (leading to interstitial edema).
Abdominal wall compliance plays a critical role. Visceral edema, enlargement, or free intra-abdominal fluid can reduce compliance, limiting compensation for IAP increases. Decreased compliance allows less room for additional pressure, and increased abdominal wall pressure can impair skin blood flow and wound healing. Abdominal Perfusion Pressure (APP) is calculated as Mean Arterial Pressure (MAP) minus IAP, with a goal of >50-60 mmHg. APP is a strong predictor of visceral perfusion and mortality, better than MAP or IAP alone.
Elevated IAP can be classified into primary and secondary causes. Primary IAH/ACS results from direct abdominopelvic injury or disease (e.g., trauma, surgery, bleeding), often requiring surgical intervention. Secondary IAH results from issues outside the abdominopelvic region (e.g., pregnancy, ascites, large fluid resuscitation, sepsis). Causes also categorize into decreased abdominal wall compliance (trauma, burns, prone positioning), increased intra-abdominal volume from intraluminal contents (gastroparesis, ileus) or intra-abdominal contents (pancreatitis, hemoperitoneum, tumors, peritoneal dialysis), and capillary leak (massive fluid resuscitation, sepsis). Mechanical ventilation can also increase IAP by displacing pressure downwards.