Abdominal Compartment Syndrome

Primary abdominal compartment syndrome

Secondary abdominal compartment syndrome

Severe penetrating abdominal trauma + shock

Severe extra-abdominal bleeding requiring massive resuscitation

Aortic, mesenteric, portal cross-clamping

Extra-abdominal sepsis requiring massive resuscitation

Abdominal sepsis as late complication

56.2 When to Expect ACS in Penetrating Trauma?

ACS, a potentially lethal complication of penetrating injuries, can develop in both abdominal and extra-abdominal penetrating trauma. ACS typically develops in patients who present with severe shock and require urgent hemostasis and fluid resuscitation.

Typical presentations of ACS after penetrating trauma are listed in Table 56.1 and described below:

1.

Penetrating abdominal trauma with shock (Figs. 56.1 and 56.2): This is the classic pattern; patients with major abdominal injuries, especially with abdominal vascular trauma, are at high risk of developing primary ACS. Hemorrhagic shock and subsequent resuscitation is whole-body ischemia-reperfusion injury, which is associated with generalized and localized (intestinal) edema. The venous return from abdominal organs is further compromised by the space-occupying nature of the packs used for hemorrhage control. Open abdomen strategy is a proven approach to prevent ACS, in most of the cases. Fascial closure of the abdomen after damage control surgery (DCS) is not feasible because it can cause ACS, and in any case, a second look is necessary to remove the packs and any potential necrotic tissue and to restore the continuity of the intestinal tract. Urgent need to go to the operating room and the presence of damage control physiology (acidosis, coagulopathy, and hypothermia) are independent predictors of the primary ACS.

Fig. 56.1

Multiple stab wounds requiring damage control surgery, high risk for abdominal compartment syndrome

Fig. 56.2

Isolated stab wound without hemodynamic compromise, suitable for definitive surgery, low risk for abdominal compartment syndrome
2.

Penetrating chest or extremity trauma with shock: This is the classic example of secondary ACS, as there is no abdominal injury or pathology, but the whole-body ischemia-reperfusion injury is present and driving the pathophysiology. The intestinal tract has a significantly lower anti-edema capacity than other vital organs like the brain, lung, or heart. Secondary ACS has the same symptoms (increased airway pressures, decreased urine, and cardiac output) like primary ACS, but secondary ACS is much more elusive since there is no obvious abdominal cause. Massive resuscitation is always present as a major independent predictor. Secondary ACS can be present as early as at the time of the initial surgery on extra-abdominal bleeding sources. Reassessment on the operating table for potential ACS is important, and while a distending non-injured abdomen with high airway pressures could be a clue, measuring the intra-abdominal pressure is always helpful in the differential diagnosis.
3.

After closure of the open abdomen: Premature closure of the open abdomen at the time of the second look laparotomy can result in recurrent ACS. Intraoperative measurement of the IAP during closure and reassessment on the operating table are advisable when the desired level of closure is achieved. It is important to remember that the IAP is most likely to be at its lowest while the patient is on the operating table (anesthetized, paralyzed, flat, and supine), and it will be higher in the intensive care unit (elevation of the head of bed, avoidance of neuromuscular paralysis, nursing). It is hard to measure the IAP at the end of surgery unless there is a femoral line reaching into the inferior vena cava or a urinary catheter is in situ and connected to the OR monitor via a pressure transducer. If there is no IAP measurement available when you close the abdomen, airway pressures as a guide should be discussed with the anesthesiologist.
4.

Late presentation compounded with sepsis: ACS can present in penetrating trauma patients later as a complication of uncontrolled abdominal (primary ACS) or extra-abdominal (secondary ACS) sepsis. Remember that treating the sepsis will also treat the ACS.

56.3 Diagnosis

The presentation of ACS after penetrating trauma with shock is very rapid; most of the cases develop within 12 h of hospital admission representing a second life-threatening insult after the potential exsanguination. In some extreme cases, ACS can develop on the operating table while thoracic or skeletal life-/limb-saving operation is performed. For the prevention of the syndrome, it is essential to be aware of the common scenarios and avoidable situations when ACS could develop (Table 56.2).

Table 56.2

The common scenarios and avoidable scenarios, which could lead to abdominal compartment syndrome in penetrating trauma patients

Prehospital	Delay to definitive care
	Poor control of external hemorrhage
	Uncontrolled crystalloid
	Resuscitation
Emergency department	Delay to hemorrhage control
	Uncontrolled large volume crystalloid resuscitation
	Extensive imaging with uncontrolled resuscitation
	Underestimation of non-cavity bleeders
	Poor control of the environment (hypothermia)
Operating room	Aortic, mesenteric, portal cross-clamping
	Delay to hemorrhage control
	Uncontrolled resuscitation
	Inability to improve hypothermia, acidosis, and coagulopathy
	Tight packing with fascial closure
	Inadequate temporary abdominal closure
	Poor control of abdominal bleeding
	Long surgery
Intensive care unit	Chasing supranormal resuscitation endpoints
	Crystalloid boluses to maintain filling pressures or for Starling curve assessment
	Not measuring IAP
	Inability to recognize rebleeding

The diagnosis of ACS involves the measurement of the IAP. Clinical examination is unreliable in estimating the IAP. The most feasible method is the intravesical route, originally described by Kron and modified by many. The measurement can be done with improvised devices, but today there are several reliable proprietary devices available. Most of these techniques require saline instillation into the bladder before measurement. Historically, the recommended instilled volume was 50 mL and above. However, recent research has shown that there is no need for more than 25 mL of saline through a safe closed system. The limitation of the technique is the intermittent nature and the 5–8 min required to perform each measurement. The IAP can be monitored continuously via a three-way urinary catheter in the most critical patients where the timely recognition of increased IAP is crucial.

The other component of the diagnosis is the organ dysfunction, which is related to the increased IAP. The differentiation of the IAP-related organ dysfunctions can be difficult from the ongoing circulatory, respiratory, and renal dysfunction of an acute penetrating trauma patient. Acute penetrating trauma patients are not necessarily anuric or oliguric when they develop ACS. The urine output has to be judged in the context of the magnitude of the fluid resuscitation (100 mL/h in a patient who is in 10 L positive balance does not necessarily indicate adequate urine output). Young healthy trauma patients are expected to have a hyperdynamic response after major trauma and resuscitation. Close to normal cardiac output in these scenarios can mean compromised circulation. The filling pressures (central venous pressure and pulmonary capillary wedge pressure) can be falsely normal or elevated in patients with increased IAP. Many factors can directly and/or indirectly affect ventilation during the initial phase of shock resuscitation. If no significant lung or intrapleural injury/pathology exists, high airway pressures and low compliance associated with increased IAP can be diagnostic as well.

56.4 Treatment

Recent reports suggest that postinjury ACS, especially in blunt trauma cohorts, is largely preventable with judicious haemostatic resuscitation. The treatment of a compartment syndrome is decompression; in postinjury ACS, this involves a full midline laparotomy. The nonoperative measures, which are more frequently described in acute general surgical and medical literature, are unlikely to be helpful in critically ill penetrating trauma patients where the syndrome is evident within a few hours of ICU admission. In this scenario, there is no time for you to wait and see the potential modest decreases of IAP due to nonoperative measures (positioning, neuromuscular paralysis, evacuation of gastric and intestinal intraluminal contents). These patients are dying. Your immediate efficient action is required. In obvious secondary ACS cases (no intra-abdominal injury), bedside ultrasound-guided drainage of the acutely developed ascites might be a solution, but in most cases not only the peritoneal fluid but rather the intestinal edema which is the main component of the increased IAP. If intra-abdominal injury is excluded, you can even perform decompression in the ICU by using sterile technique (ICU procedure team). In primary ACS cases, usually rebleeding is present, which requires you to perform further formal exploration of the abdomen and control of the hemorrhage preferably after transfer of the patient to the operating room.

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