Intra-abdominal Hypertension and Abdominal Compartment Syndrome in Acute Care Surgery

Organ system

Pathophysiologic effects

Clinical manifestations

Threshold IAP (mmHg)

Cardiovascular

Decreased preload/venous return

Increased afterload

Compression of inferior vena cava

Decreased cardiac output

Increased susceptibility to hypovolemia

Pulmonary

Increased intrathoracic pressure

Cephalad elevation of diaphragm

Extrinsic compression of pulmonary parenchyma

Alveolar atelectasis

Increased airway resistance

Hypoxemia

Hypercarbia

Elevated airway pressures

Increased intrapulmonary shunt

Increased alveolar dead space

Renal

Decreased renal blood flow

Renal vein compression

Renal parenchymal compression

Oliguria

Anuria

Acute renal failure

Gastrointestinal

Decreased mesenteric blood flow

Intestinal ischemia

Bacterial translocation/sepsis

Increased susceptibility to hypovolemia

Increased visceral edema/capillary leak

Metabolic acidosis

Hepatic

Decreased hepatic vein blood flow

Decreased portal vein blood flow

Hepatic dysfunction/failure

Metabolic acidosis

Central nervous system

Increased intrathoracic pressure

Decreased cerebral venous outflow

Increased intracranial pressure

Decreased cerebral perfusion pressure

Abdominal wall

Decreased abdominal wall compliance

Decreased rectus sheath blood flow

Fascial dehiscence

IAP intra-abdominal pressure, IAH intra-abdominal hypertension, ACS abdominal compartment syndrome

Finally, the severity of IAP is less important than the duration of IAH [8]. Prolonged elevations in IAP result in organ dysfunction and failure that can have a significant impact upon the patient morbidity and mortality. Every effort should be made to reduce the period of time that a patient’s IAP exceeds 15 mmHg. The duration of IAH correlates significantly with the increased ICU and hospital length of stay, duration of mechanical ventilation, enteral nutrition intolerance, and mortality. For these reasons, primary fascial closure in the presence of marked visceral edema or abdominal contamination is rarely appropriate and only leads to the need for emergent abdominal decompression, prolonged critical illness, organ dysfunction, and increased healthcare costs.

Prevention of IAH/ACS

When faced with a patient demonstrating risk factors for IAH/ACS, such as intestinal ischemia or abdominal sepsis, the acute care surgeon must decide intra-operatively whether to correct the patient’s pathology through either a single, initial procedure or a staged approach. This decision is based upon the answers to three questions:

1.

Is the patient too ill to tolerate a single procedure/definitive repair?
2.

Can the patient tolerate the postoperative IAH that will accompany primary fascial closure without developing ACS?
3.

Can the source of contamination be safely controlled using a single procedure?

The well-known principles of damage control, as applied to the traumatically injured, are directly applicable to the acute care surgery patient as well. As a result of delayed presentation, under-resuscitation, advanced organ dysfunction/failure, and pre-existing medical comorbidities, some patients are better served by a staged laparotomy approach with the maintenance of an “open abdomen” and temporary abdominal closure until their physiology has improved, and they can tolerate definitive repair. A “single-procedure” approach, in the presence of critical illness, is rarely the correct answer and frequently results in increased morbidity and mortality. The methods for performing such a staged approach are described below.

All patients with intestinal ischemia are at risk for postoperative IAH. Inappropriate primary fascial closure of those patients at significant risk will increase IAP through the mechanisms described in Table 6.1 and result in worsening end-organ dysfunction and failure. This commonly results in a vicious cycle of visceral edema, intestinal malperfusion, and increasing IAP that ultimately culminates in the development of ACS and need for emergent decompressive laparotomy. The keys to avoiding this runaway cascade of progressive shock and organ failure are appropriate end-organ resuscitation (described below) and staged laparotomy in patients at significant risk.

Abdominal sepsis and contamination are significant risk factors for visceral edema and subsequent IAH/ACS. Abdominal contamination initiates a pro-inflammatory cytokine cascade that promotes further visceral edema and elevated IAP. While early primary fascial closure places the patient at risk for IAH/ACS, staged laparotomy and evacuation of cytokine-rich fluid from the abdominal cavity through a temporary abdominal closure help to modulate and downgrade the pro-inflammatory response, improving organ dysfunction and patient survival (Fig. 6.1).

Fig. 6.1

The evolution of IAH/ACS: IAP intra-abdominal pressure; APP abdominal compartment syndrome; IAH intra-abdominal hypertension; ACS abdominal compartment syndrome

Management of IAH/ACS

While surgical decompression is widely and erroneously considered the only treatment for IAH/ACS, non-operative medical management strategies play a vital role in both the prevention and treatment of IAP-induced organ dysfunction and failure (Fig. 6.2) [7]. Appropriate management of IAH/ACS is based upon four general principles:

Fig. 6.2

Medical management of IAH/ACS: IAP intra-abdominal pressure; APP abdominal compartment syndrome; IAH intra-abdominal hypertension; ACS abdominal compartment syndrome