Compartment Pressures (Abdomen, Extremity) – Measurement

Diagnosis

Identifying at-risk patients and preventing ACS is paramount to achieving optimal patient outcomes. However, ACS occurs across a heterogeneous group of patients; thus identifying at-risk patients will depend on the local patient population and maintaining a high index of suspicion. At-risk patients include, but are not limited to, those with major abdominal or thoracic operations requiring crystalloid fluids greater than 5000 mL/day, trauma or burn patients in severe shock who fail to adequately respond to ongoing volume loading or require a massive transfusion (>10 units of blood in 6 hours), and patients with severe pancreatitis, severe SIRS, or septic shock who require more than 40 mL/kg of crystalloid volume in the first 24 hours. At-risk patients should then have objective intra-abdominal pressure (IAP) measurements as recommended by the Abdominal Compartment Society (WSACS), shown in Figure 61-1-1 .

Relying on physical examination, whether performed by use of simple subjective palpation or objective abdominal girth measurements, has been clearly shown to be nonspecific and poorly correlative with IAP. Therefore patients at risk for ACS, or those who are suspected to have IAH or ACS, should have IAP monitoring performed via the urinary bladder as described by Kron and colleagues and modified by Cheatham ( Figure 61-1-2 ). Briefly, IAP can be assessed via Foley catheter with a pressure-transducer system by instilling 25 mL of sterile saline into the empty bladder and recording the pressure as leveled at the midaxillary line. Today, multiple commercial products are available to aid in performing IAP monitoring. A management algorithm is illustrated in Fig. 61-1-3 .

Abdominal Compartment Syndrome

Generically, a compartment syndrome is a condition in which increased pressure in a confined space adversely effects the circulation and threatens the function and viability of the tissue within the space. This entity can occur in the extremities, orbital globe, intracranial cavity, and abdominal cavity.

The effects of increased intra-abdominal pressure were first described in 1863 by Marey and Burt, who reported the relationship between intrathoracic pressure and elevated intra-abdominal pressure. However, it was not until the 1980s that Kron and Richards coined the term “abdominal compartment syndrome” (ACS). They reported a separate series of patients that developed a tense, distended abdomen with elevated pulmonary artery pressures and increased intra-abdominal pressures postoperatively despite normal mean arterial blood pressure and cardiac performance. All of these patients improved with re-exploration and abdominal decompression.

Intra-abdominal hypertension and the abdominal compartment syndrome are not synonymous. ACS is a late manifestation of uncontrolled intra-abdominal hypertension produced by ongoing ischemia and splanchnic hypoperfusion and the resuscitative measures to counteract the hemorrhagic shock state ( Figure 61-2-1 ).

Table 61-2-1 lists the risk factors associated with ACS. Mortality risk from the fulminant abdominal compartment syndrome has been reported to be as high as 67%.

In addition to the accumulation of blood within the perineal cavity, other factors may contribute to occupying space within the abdominal cavity. This can occur by any shock-induced visceral ischemia and reperfusion edema including major injuries outside the abdominal cavity. Several recent reports have described this “secondary abdominal compartment syndrome,” which occurs most frequently with major pelvic and long bone fractures, and hemorrhagic chest injuries. However, secondary ACS can occur in any setting associated with hemorrhagic shock.

Balough and associates reviewed patients with major torso trauma and found that both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multi­organ failure. Fourteen percent of these patients develop abdominal compartment syndrome, all of which require aggressive resuscitation using crystalloid, blood, and blood products early in their initial management in the emergency department. Therefore, the current emphasis in critical care management of the severely injured patients focuses on identification of predictive factors for the development of ACS and the recognition of intra-abdominal hypertension and treatment before full development of the syndrome.

Intra-abdominal hypertension affects multiple organ systems in a graded fashion. The deleterious consequences appear gradually, and the adverse effects of elevated intra-abdominal pressure occur at lower levels than previously thought and manifest before the development of the fulminant syndrome ( Table 61-2-2 ).

The classic picture of ACS includes a patient with a tense, distended abdomen and ventilatory insufficiency including hypoxia and hypercapnia, as well as increased peak inspiratory pressures. Progressive oliguria occurs despite adequate mean arterial pressure and cardiac output. This is followed by decreased cardiac performance and subsequent cardiovascular collapse unless treatment is instituted immediately ( Table 61-2-3 ).

A high-risk patient for ACS may present with tense abdomen, respiratory failure, and progressive oliguria in a multitrauma patient requiring aggressive resuscitation for hemorrhagic shock.

Common computed tomography findings in this patient population include extraperitoneal hematoma and/or extravasation, intra- and retro-peritoneal edema, and “shock bowel” defined as an intense mucosal enhancement producing a prominent, feather-like appearance to the small intestines.

The most practical and reliable method of measuring intra-abdominal pressures is through the urinary bladder, which acts as a passive conduit. The urinary bladder transmits intra-abdominal pressures without imparting any additional pressures from its own musculature. Fifty to 100 ml of saline is injected into the fully drained bladder. A Foley catheter is clamped distal to the aspiration port and a 16-gauge needle is inserted into this port, which is then attached to a transducer system with the pubic symphysis used as the zero reference point. Commercial kits are available for measuring bladder pressures (AbVisor Intra-abdominal pressure monitor, Wolfe Tory Medical Inc., Salt Lake City, Utah).

The consensus at the World Congress on Abdominal Compartment Syndrome defines this disease entity as persistent bladder pressures over 20 mm Hg with the new onset of organ failure. Organ dysfunction progresses as intra-abdominal pressure increases over this level. Once defined, ACS mandates immediate decompressive celiotomy.

This often rapidly reverses all the adverse affects of increased intra-abdominal pressure and dramatically improves oxygenation and pulmonary compliance, returning peak inspiratory pressures toward normal and promptly reversing the oliguria with a brisk diuresis of resuscitation fluids. Before decompression, all attempts to correct acid–base and electrolyte disturbances including potassium, magnesium, and calcium may avoid cardiac dysrhythmias after decompression. A respiratory therapist should also be immediately available to readjust ventilatory settings to prevent additional pulmonary barotrauma.

Decompression can be performed safely as a bedside procedure in the intensive care unit (ICU). However, with pressures greater the 35 mm Hg, decompression and re-exploration are required in the operating room to identify potential sources of ongoing hemorrhage.

Pathogenesis

The unifying feature that defines all compartment syndromes, regardless of cause or anatomic location, is an increase in intracompartmental pressure (ICP) that impairs tissue perfusion.