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).^1,2 They reported a separate series of patients that developed a tense, distended abdomen with elevated pulmonary artery pressures and increased intraabdominal 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 1).

Figure 1 A cycle of ischemia producing intra-abdominal hypertension and the abdominal compartment syndrome.

(Reproduced with permission from Michael Rotondo, MD.)

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

Table 1 Etiology of Abdominal Compartment Syndrome: Who Is at Risk?

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.^3–5

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.^7–12

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 2).

Table 2 Effects of Intra-Abdominal Hypertension on Organ Systems

The classic picture of ACS includes a patient with a tense, distended abdomen and ventilatory insufficiency including hypoxia and hypercarbia, 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 3).

Table 3 Abdominal Compartment Syndrome: Classic Clinical Picture

Figure 2 illustrates a high-risk patient for ACS: tense abdomen, respiratory failure, and progressive oliguria in a multitrauma patient requiring aggressive resuscitation for hemorrhagic shock.

Figure 2 High-risk patient for abdominal compartment syndrome.

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 (Figure 3).

Figure 3 Shock bowel.

The most practical and reliable method of measuring intraabdominal 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 of mercury with the new onset of organ failure. Figure 4 demonstrates the progression of organ dysfunction as intra-abdominal pressure increases over this level. Once defined, ACS mandates immediate decompressive celiotomy (Figure 5).

Figure 4 Progressive organ dysfunction with increasing intra-abdominal hypertension.

Figure 5 Bedside decompressive celiotomy for abdominal compartment syndrome (note massive small bowel edema).

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.

DAMAGE CONTROL

An abbreviated celiotomy and intra-abdominal packing for hemorrhage control in the abdomen was first described by Stone¹³ in 1983. However, the term “damage control” was first coined by Rotondo and Schwab at the University of Pennsylvania in 1993. The current management scheme has been revised to include four stages (Figure 6).^14–16

Figure 6 Algorithm for damage control.

During the initial trauma celiotomy (DC1), it is important to determine each patient’s physiologic reserve in order to make appropriate operative decisions. Physiologic reserve is defined as an individual’s unique ability to tolerate injury. It is a function of several host factors including age, gender, pre-existing disease, genetics, and immunocompetence (Figure 7). As physiologic reserve becomes depleted during hemorrhagic shock, regional and then global malperfusion occur, leading to physiologic exhaustion and subsequent death (Figure 8).¹¹

Figure 7 Host factors define physiologic reserve.

Figure 8 Depletion of physiologic reserve.

Mortality associated with damage control procedures ranges between 25%–60%. Each patient responds and reacts differently to stress and injury, and each individual has a limited amount of compensatory reserve until physiologic exhaustion is reached. Additionally, the extent of injury severity determines the slope leading to physiologic exhaustion (Figure 9).

Figure 9 Physiologic reserve as related to Injury Severity Score (ISS).

Perioperative communication with the anesthesia team enhances survival and reduces complications. This communication includes maintaining the operating room as warm as possible, advising the anesthesia personnel of anticipated blood loss, and avoiding over resuscitation before surgical control of hemorrhage.

During the initial trauma celiotomy, the surgeon must recognize the need for immediate control of major hemorrhage and contamination with maximum replacement of coagulation factors including platelets, fresh frozen plasma, and cryoprecipitate, and in certain circumstances, factor VIIa for microvascular bleeding. Intraoperative monitoring of temperature, arterial blood gases, and volume of resuscitative fluids are important in determining whether a patient is descending down the physiologic curve toward physiologic exhaustion. In addition, for patients suffering hollow viscus injuries, contamination is controlled with linear staples to transect the bowel ends and leave them in discontinuity until a later stage of damage control management.

Table 4 lists clinical parameters that should prompt the surgical team to initiate damage control maneuvers, abort the operation, and return to the ICU for resuscitation and restoration of reserve. Asensio^17,18 recommends instituting damage control early, well before reaching the upper limits of physiologic exhaustion, and describes statistically validated criteria. Using these statistically validated intraoperative predictors of instituting damage control, patients with post-traumatic open abdomen incurred less hypothermia and fewer postoperative complications including intra-abdominal abscess and fistula formation. Patients with early damage control were also subjectively noted to have less bowel edema and were able to undergo definitive abdominal wall closure during their initial hospital stay.

Table 4 Clinical Guidelines to Abort Initial Trauma Celiotomy and Initiate Damage Control Maneuvers

Once a patient fulfills the requirements for DC or is decompressed for signs and symptoms of ACS, the surgeon must commit the patient to the post-traumatic open abdomen and a temporary abdominal closure.

Temporary Abdominal Closure

A TAC is defined as any technique that contains the abdominal viscera during the acute phase of care. Indications for creating a TAC are listed in Table 5.

Table 5 Indications for Temporary Abdominal Closure

Depletion of physiologic reserve Unable to close fascia without undue tension secondary to bowel edema Avoid development of abdominal compartment syndrome after large fluid resuscitation Planned return to operating room Unpacking Re-establish bowel continuity Enteral access Thorough exploration to re-evaluate known injuries and identify missed injuries Associated need for management of extra-abdominal life-threatening injuries (e.g., major pelvic fracture, severe closed head injury)

Historically, a wide variety of techniques for TAC have been used to contain the abdominal viscera during the acute phase of care. However, the “vacuum pack” technique using the method described by Barker et al.¹⁹ best fulfills the first two principles in the management of the post-traumatic open abdomen: protecting the bowel and preserving the fascia.

The bowel and abdominal viscera are protected by placing a perforated, nonadherent material such as a Steri-Drape (isolation bag 50 ′ 50 cm or 1010 large bowel bag 45 ′ 60 cm, 3M Health Care, St. Paul, MN) over the intestines. This is followed by subfascial placement of a moist surgical towel with two large sump drains (Jackson-Pratt, Baxter Health Care Corp., Deerfield, IL) that are brought out through the superior portion of the wound. The entire abdominal defect is then covered with a large adhesive drape (Ioban, 3M Health Care, St. Paul, MN). The sump drains are attached to wall suction to create continuous negative pressure. This technique also counteracts the lateral retraction of the fascial edges and preserves the rectus musculofascial complex for subsequent closure (Figure 10).

Figure 10 Vacuum pack temporary abdominal closure: (A) bowel bag, (B) sterile surgical towel/two large sump drains/large adhesive drape.

Advantages of the Vacuum Pack are listed in Table 6. Using this technique, the period before definitive fascia closure can be safely extended for up to a week after the initial celiotomy.²⁰

Table 6 Advantages of Vacuum Pack Technique

Protects bowel and keeps it below fascia Preserves fascia and prevents loss of domain Readily available, rapidly applied, easily removed Keeps patient dry and maintains sterility Quantitates/qualitates fluid losses Prevents intra-abdominal hypertension/abdominal compartment syndrome Simple, atraumatic, and inexpensive

Three potential stages (Figure 11) follow the placement of the vacuum pack for the post-traumatic open abdomen:

Figure 11 Three potential stages of the post-traumatic abdomen.

Restoration

After the secondary resuscitation in the ICU and correction of physiologic and hemodynamic derangements that occurred during the initial trauma celiotomy or after decompression for ACS, patients with a temporary abdominal closure are returned to the operating room for further evaluation. During this re-exploration, the surgeon must once again make important clinical and technical decisions. All retained perihepatic and intra-abdominal lap pads are carefully removed, preventing dislodgment of clot over liver injuries and avoiding serosal tears from lap pads that are adherent to the bowel. Then a reevaluation of the known injuries and a thorough exploration to identify missed injuries are undertaken. If bowel resection was necessary during the initial damage control celiotomy, establishment of gastrointestinal (GI) continuity is performed and enteral access is established.

It is important to bury suture or staple lines deep within the abdomen and attempt to cover the anastomotic area with omentum. If creation of an ostomy is necessary, the stoma should be placed lateral to the rectus fascia to aid in future plans for colostomy takedown and abdominal wall reconstruction.

Nasoenteric feeding tubes or surgical placed enteral access procedures should be performed during the damage control reoperation stage. Either a nasoenteric feeding tube placed past the ligament of Treitz with nasogastric decompression or an open gastrojejunostomy feeding tube are options for long-term enteral access and supplemental nutrition.

Finally, extensive washout and evacuation of any further hematoma is performed and then a plan on definitive closure is made. If bowel edema is minimal or completely resolved and the fascial edges can be easily approximated without undue tension, then a primary fascial closure can be performed. Radiologic evaluation of the abdominal cavity on all patients must be obtained if the fascia is successfully closed at this stage to ensure that no retained foreign body remains.

If primary fascial closure is not possible because of ongoing physiologic insults or a prolonged inflammatory response with bowel edema and/or contamination, replacement of another vacuum pack is indicated. A good rule of thumb is that if the peak inspiratory pressures rise higher than 10 mm Hg from baseline during fascial approximation, attempts at primary fascial closure should be abandoned, as this can result in abdominal wall necrosis, recurrent abdominal compartment syndrome, serious infectious complications, and even death.

The complication rate associated with the post-traumatic open abdomen is between 25%–50%. The most common complications are listed in Table 8.

Table 8 Complications Associated with Post-Traumatic Open Abdomen

Abdominal	Extra-Abdominal
Wound infection	Ventilator-associated pneumonia
Wound dehiscence	Aspiration pneumonitis
Abdominal wall fasciitis/necrosis	Bloodstream infection
Intra-abdominal abscess/sepsis	Urinary tract infection
Enteroatmospheric fistula	Deep venous thrombosis/pulmonary embolism
	Pressure ulcers (occiput, scapulae, sacrum, heels)
	Multiple organ dysfunction syndrome/multiple organ system failure

Figure 12 describes a recent study on complications after 344 post-traumatic open abdomen patients with TAC. The authors, Miller and colleagues,²¹ reported a 65% success rate on early primary fascial closure. The remaining patients underwent delayed closures by either applying a split thickness skin graft (temporizing skin) to a granulating abdominal wound or using synthetic prosthetic mesh material (prosthetic fascial).

Figure 12 Outcome of 344 open abdomen patients with a temporary abdominal closure.

Primary fascial closure within the first week after the initial celiotomy was associated with a very low complication rate (9%). However, the complication rate increased significantly with three circumstances:

Attempts at closing the fascia primarily under too much tension

Awaiting the formation of granulation tissue before applying a STSG (8 days or more)

Using nonbiologic prosthetic material for closure

Figure 13 compares wound complications versus days to fascial closure. All three circumstances can potentially result in fistula formation, an expensive, labor-intensive, and morbid complication associated with the post-traumatic open abdomen. This occurred in 32 of 276 (8.6%) patients in this study (Figure 14).

Figure 13 Percent of patients with wound complications versus days to fascial closure.

Figure 14 Wound closure complications associated with the post-traumatic open abdomen. ^*p=0.0001 when comparing fistula formation between primary and temporizing groups.

(From Miller et al²¹.)

In reviewing the literature, the incidence of fistula formation in this patient population is between 2%–25%. The etiology of fistulae formation is multifactorial and includes the presence of abdominal infection, bowel ischemia and/or obstruction, exposure of the bowel to atmospheric air for prolonged periods of time (causing desiccation), and the use of packs, dressings, or prosthetic materials that adhere to the serosa of the intestines.^22,23

An enteroatmospheric fistula is defined as a postoperative complication with the open abdomen in which an enterotomy in the GI tract leaks succus or frank stool into the open wound. The absence of overlying soft tissue precludes closure (Figure 15).

Figure 15 Enteroatmospheric fistula.

Protecting the exposed abdominal viscera from injury and desiccation using the vacuum pack, limiting access to the wound to one or two senior surgeons, and early tension-free closure of the fascia are all good preventive measures. However, once a fistula forms, the adjacent viscera must be protected, and the effluent from the fistula controlled. Intubation of the fistula in the middle of the fixed visceral block is not recommended, and in this circumstance, repair of the fistula should not be performed until the patient is infection-free and in a stable physiologic state and has replenished protein and calorie stores. This usually occurs several months later. At that time the fistula can be resected in conjunction with delayed abdominal wall reconstruction.

Because all post-traumatic open abdomens are either colonized or chronically infected, it is now realized that use of synthetic prosthetic material is contraindicated. If the abdomen cannot be closed by the end of the first week, granulation tissue starts to develop, and a “frozen abdomen” is evident by the end of the second week. This creates a hostile environment for early fascial closure and thus necessitates a planned ventral hernia with a delayed reconstruction. A split-thickness skin graft (STSG) is applied over the granulation bed and the patient then requires a 6–12 month recovery period for protein and calorie stores to be replenished before successful abdominal wall reconstruction can be performed (Figure 16). This decision, although life-saving, is very costly and is associated with a loss of productive lifestyle and an inability to return to the workforce.

Figure 16 Mature granulation tissue in an open abdomen, which is then covered with a split-thickness skin graft.

New solution

Because of the high complication rate under these circumstances, an aggressive approach to early fascial closure in the post-traumatic open abdomen is suggested, using a combination of the vacuum pack, vacuum-assisted closure technique (KCI VAC, KCI USA, Inc., San Antonio, TX), and a biologic material, human acellular tissue matrix (Alloderm, LifeCell Corp., Branchburg, NJ) to bridge the gap in the abdominal fascia.

Similar to the vacuum pack, the KCI VAC technique places a perforated, nonadherent plastic drape beneath the anterior abdominal wall to protect the bowel. However, the surgical towel in the middle layer is replaced with a polyurethane sponge cut to size to fit the facial defect. An 18 French suction tube is inserted into the sponge, which is then covered with an adherent occlusive drape, and constant application of negative pressure is obtained with wall suction (Figure 17).

Figure 17 Vacuum-assisted closure—KCI VAC. Note external fixator for damage control orthopedics.

This technique also protects the bowel and preserves the fascia and recaptures loss of abdominal domain. Additional advantages are listed in Table 9.

Table 9 Additional Advantages of KCI VAC

Reduced need for frequent dressing changes Removes excess interstitial fluid Increases vascularity of wound Decreased bacterial counts Improves wound contraction Delays onset of “frozen abdomen”—prevents granulation tissue adhering to fascia Extends window of opportunity for definitive fascial closure

The KCI VAC allows for successful primary fascial closure or closure with the use of Alloderm in most post-traumatic open abdomen patients, even up to 3 weeks after initial damage control procedures or decompressive celiotomy.

Alloderm is a biologic material derived from partial thickness skin of tissue donors treated for removal of all cellular components so that only the native connective tissue matrix remains. Unlike synthetic prosthetic materials, which the body recognizes as foreign, causing encapsulation, Alloderm supports cellular growth and integration with rapid revascularization and transition to the patient’s own tissue. This material serves as a bio-scaffold for the native autologous tissue (Figure 18).

Figure 18 Alloderm with overlying skin flaps for early closure of abdominal fascia.

Alloderm is also tolerant of contamination and can be used for closure in situations where synthetic material is contraindicated (Figure 19). It is best to underlay the Alloderm 4–5 cm lateral to the fascial edges using interrupted 0-prolene sutures and place this biologic material under moderate stretch to prevent future laxity of the abdominal wall.

Figure 19 Alloderm used to bridge fascial gap in contaminated open abdomen wound with KCI VAC placed over the biologic fascial replacement.

Even though long-term results regarding recurrence rates and the development of abdominal wall laxity are not yet available, this method of fascial approximation certainly has significant advantages over the planned ventral hernia method of management with its inherent high risk of wound complications as mentioned previously.^24–30 The combination of using the KCI VAC and placement of Alloderm fulfills the final essential principle with post-traumatic open abdomen: expedite early fascial closure.

Nutritional support for post-traumatic open abdomen

Ironically, after DC surgery, a large abdominal wound defect is created during the period of greatest physiologic stress with ongoing metabolic demands and catabolism. This can cause a tremendous barrier to primary fascial closure, wound healing, and overall rehabilitation. Therefore, close attention to nutritional support and caloric needs is essential to reduce both early and late complications.

During hemorrhagic shock and multitrauma, gut mucosal blood flow is decreased and remains below normal levels despite volume resuscitation. This decreased blood flow is associated with microbe translocation, ischemic bowel, and eventual multiorgan failure.

Basic science research has shown that enteral nutrition augments gut blood flow by locally mediated vasodilation. This enhances absorption of nutrients and preserves gut mucosal integrity and immunologic barrier functions. Additional research has studied the effects of enteral feeding during hemorrhagic shock, showing improved survival with no detrimental gut effects. The reduction in mesenteric blood flow caused by vasopressors is also inhibited and counteracted by the infusion of enteral nutrition. Thus, the gut is the preferred route for nutritional support during critical illness, and the initiation of enteral nutrition within 36 hours of admission or surgery in critically ill patients results in fewer infections and reduced length of stay.

Nutritional support in the open abdomen should be initiated during the restoration phase, after intra-abdominal packing is removed, GI intestinal continuity re-established, and coagulopathy, acidosis, and hypothermia are corrected.

Immune-enhancing diets increase splanchnic blood flow to a greater degree than standard enteral diets. Head-injured and nonseptic critically ill patients have been found to benefit from the use of immune enhancing diets. However, septic patients have a worse outcome with this diet and should be kept on standard formulas.

Although enteral feedings are the preferred route, it is not always possible in severely injured trauma patients with an open abdomen resulting from a prolonged inflammatory response with ongoing bowel wall edema, abdominal distention, high gastric output, and persistent adynamic ileus. In this circumstance, early enteral nutrition should be supplemented with parental nutrition to reach acceptable protein and calorie goals. In addition, enteral nutrition can continue safely during other extra-abdominal operations and procedures.^31,32

Tsuei and colleagues³³ studied nasoenteric feeding in patients with an open abdomen and found it a safe effective method of nutritional support capable of meeting the nutritional goals in most patients. However, there have been no clinical studies to determine the exact percentage of caloric goals required to achieve maintenance of gut integrity and prevent bacterial translocation during the open abdomen. In animal models, over 50% of goal calories were needed to effectively reduce translocation and maintain adequate gut permeability.

Planned Ventral Hernia and Delayed Abdominal Wall Reconstruction

Once the window of opportunity for early fascial closure has passed secondary to an ongoing inflammatory response and bowel edema, a delayed staged closure of the abdominal wall is necessary. Because the open abdomen group remains at high risk for infectious complications, the use of synthetic prosthetic material for reconstruction is also not recommended.

Once the split thickness skin graft can be elevated from the underlying intestines (pinch sign–Figure 20), the inflammatory response has resolved and the underlying granulation tissue dissipated. This usually requires 6–12 months of recovery. Only then can reconstruction be performed safely.

Figure 20 Pinch sign.

The split thickness skin graft is removed and the fascia is mobilized from the surrounding tissue. The skin and subcutaneous tissue are then raised as lateral flaps circumferentially (Figure 21). Options for bridging the fascial gap at this point include the component separation technique and/or closure with Alloderm.

Figure 21 Fascial edges freed from surrounding tissue and skin flaps raised past edge of lateral rectus muscle.

The component separation technique reconstructs the fascial defect with advancement flaps by transecting the external oblique just lateral to its insertion into the rectus sheath and separating it from the internal oblique. The rectus muscle can then be advanced medially and sutured in the midline to close the defect (Figure 22).³⁴

Figure 22 Component separation closure.

This technique can approximate a 10-cm defect without undo tension. Using the modified component separation technique,^35,36 several more centimeters of mobility can be obtained by separating the rectus muscle from the posterior rectus sheath.

The recurrence rate with this method alone is 22%–32%.^37,38 Therefore, complementing or replacing this procedure with the use of Alloderm to bridge the fascial gap is an option.³⁹

CONCLUSION

Damage control techniques and preventive measures to avoid the development of ACS are now the standards of care in the management of traumatic shock (Figure 23). Using a vacuum pack for temporary abdominal closure during the early stages of resuscitation protects the bowel and preserves the fascia.

Figure 23 Algorithm for damage control and open abdomen management.

Complications can then be avoided by not attempting to close the fascia under great tension and maintaining abdominal domain during the recovery phase with the use of the KCI VAC. Multiple attempts at fascial closure can then be safely performed either primarily or with the use of biologic material to bridge the fascial gap during initial hospitalization.

It is no longer acceptable to commit the post-trauma open abdomen patient to a large ventral hernia and delayed reconstruction except for unusual circumstances where a prolonged inflammatory response precludes early fascial approximation.