IAH has been established as an independent risk factor for development of organ failure and mortality. A high index of suspicion is crucial to early recognition and prompt treatment in order to avoid the consequences. McNelis et al [14] noted daily fluid balance and peak airway pressure trends in general surgical patients as independent predictors for the subsequent development of ACS [4, 9, 11].

There are four different mechanisms of IAH:

Sustained IAH will, through direct or indirect pathophysiological mechanisms, have adverse effects on virtually every organ system, as outlined below [12, 15–17].

As patients with developing IAH are initially asymptomatic, early clinical monitoring of high-risk patients, with standardized measurement of IAP, may prevent development of ACS.

Risk factors for IAH/ACS include undergoing a damage control laparotomy , massive transfusion (> 10 U PRBC in 24 h), or massive fluid resuscitation (> 5 L in 24 h) and presence of hemoperitoneum, extensive burns, acute pancreatitis, ascites, and large incisional hernia repair with loss of domain, large intra-abdominal fluid collections, or abscesses .

Once ACS develops, patients may have a tense and distended abdomen on physical examination. High peak airway pressures with hypercapnea, hypoxia, oliguria, and cardiovascular dysfunction with hypotension may also be present and should raise the index suspicion and prompt rapid therapy [1–3].

Physical examination is notoriously unreliable and correlates poorly with levels of IAP. Currently, the measurement of bladder pressure is the gold standard. It is an indirect method, which has been proven to be reliable at a minimal cost. First described in 1984 and validated in animal studies in 1987, the technique utilizes a Foley catheter with a pressure transducer system by injecting 25 mL of sterile normal saline into the empty bladder and recording the measured pressure at the midaxillary line (Fig. 3.1).