Rebecca Plevin
Heather L. Evans
Presentation
A 28-year-old man is in a high-speed motorcycle collision with a large truck. He is intubated in the field for loss of consciousness and suspected closed head injury and has one episode of hypotension en route to the hospital. In the emergency room, he is noted to have a right arm laceration, an unstable pelvis, and a large scalp laceration. He immediately undergoes angiographic embolization of his bilateral internal iliac arteries and is transferred to the ICU, where he receives 15 L of crystalloid, 6 units of packed red blood cells, 8 units of FFP, and two 6-packs of platelets. After his blood pressure normalizes, he undergoes CT scan of the head, chest, abdomen, and pelvis, revealing a small subarachnoid hemorrhage and an open book pelvic fracture. There are no intra-abdominal injuries, but the intestines are noted to be edematous. An external fixation device is placed on the pelvis for stability. In the next 24 hours, the patient develops progressive hypoxemic respiratory failure and increasing peak airway pressures, persistent hypotension unresponsive to further fluid resuscitation, oliguria, and rising creatinine. On physical exam, his abdomen is distended and tense to palpation.
Differential Diagnosis
While creating the differential diagnosis of abdominal distention and organ failure following trauma, the clinician must first rule out life-threatening causes of these symptoms. In this patient who is persistently hypotensive despite massive volume resuscitation, the immediate concern is a missed intra-abdominal injury. Blood vessel injury leading to hemoperitoneum or bowel ischemia could cause this patient’s symptoms. Hollow viscus injury and intraperitoneal contamination with bowel contents must also be considered given the patient’s mechanism of injury and current presentation, which could be due to septic causes.
Ileus is common following severe trauma, particularly in the setting of massive fluid resuscitation. It is typically self-limited and improves with time. However, ongoing shock and fluid resuscitation could prolong the duration of an ileus. Other less benign causes of abdominal distention, such as Clostridium difficile colitis, must also be ruled out. This bacterial infection can lead to massive bowel wall edema and ileus, which would explain the patient’s progressive abdominal distention and septic symptoms. C. difficile is less likely in a newly hospitalized patient, but as there is no background information about his prior health and antibiotic history, colitis must remain on the differential to avoid missing a catastrophic complication such as bowel perforation. This infection should be placed higher on the differential if the patient receives antibiotics for sepsis or has a significant leukocytosis, even in the absence of diarrhea.
Bowel obstruction is possible given the patient’s abdominal distention. Physical exam would help elucidate inciting factors such as an abdominal wall hernia or scars suggestive of prior abdominal surgery. In the absence of these factors or other chronic medical conditions, bowel obstruction in a young man is less likely. Abdominal distention is a frequent first sign of Ogilvie’s syndrome (acute colonic pseudoobstruction), but it does not typically present this early in the hospital course.
In addition to abdominal distention, the patient developed rapid multisystem organ failure (MSOF). The clinician must consider a systemic inflammatory response such as transfusion-related acute lung injury (TRALI) or adult respiratory distress syndrome in the differential. In addition to MSOF, each of these conditions can cause ileus due to release of inflammatory mediators and result in abdominal distention.
Workup
The first step in working up this patient is to obtain laboratory studies, specifically a complete blood count to evaluate for a drop in hemoglobin and hematocrit. Significant hematocrit decrease would necessitate surgical exploration of the abdomen to locate a bleeding source. Exploratory laparotomy would also be warranted if the patient showed peritoneal signs, as an unrecognized hollow viscus injury and intraperitoneal contamination would quickly lead to sepsis and death if unrecognized. In the absence of immediate indications for operative intervention, imaging studies would be useful. Plain radiographs of the abdomen to look for free air or ultrasound to look for free fluid are faster than CT scan and do not require the patient to be moved from the ICU. Of course, if he were stable enough, a CT scan would provide important additional information about the patient’s injuries.
In the absence of immediate indicators for surgical intervention, the adequacy of the patient’s resuscitation should be evaluated. Given his MSOF and hypotension, sepsis is within the differential, so the patient must be optimized from a medical standpoint while the clinician searches for an infectious source. Central monitoring must be placed and resuscitation started with resuscitation endpoints according to the Surviving Sepsis Campaign guidelines.
There are a number of possible explanations for the sudden increase in peak airway pressures. Pneumothorax must be ruled out by chest x-ray (CXR), and respiratory therapy should be involved to evaluate for airway obstruction with airway secretions or foreign body. Bronchoscopy should be conducted if foreign body (e.g., a missing tooth) is high on the differential. The patient’s decreased urine output should be investigated by checking the position of the Foley catheter and ruling out catheter obstruction. Obtaining urine electrolytes and calculating the fractional excretion of sodium (FeNa) would be useful to evaluate for acute tubular necrosis.
Presentation Continued
As part of his workup, a central venous catheter was placed and the central venous pressure measured at 15 mm Hg. Peak airway pressures on the ventilator >50 mm Hg, and CXR did not show a pneumothorax or evidence of airway plugging. The patient’s urine output remained <5 mL/h. When he was stable enough for transport, a follow-up CT scan was done and was negative for free air or missed solid organ injuries. However, the CT did show distended, edematous bowel, moderate ascites, and narrowing of the inferior vena cava (IVC). The patient had a Foley catheter placed during his initial trauma workup and bladder pressures were measured. The initial bladder pressure was six, and as the patient’s abdominal distention increased his bladder pressure rose to 18. The bladder pressure was 23 when the patient began exhibiting signs of renal, cardiovascular, and respiratory compromise.
Based on this workup, the patient was surmised to have abdominal compartment syndrome (ACS), but unrecognized injury could not be completely ruled out, as a hollow viscus injury might not show up on CT scan and might cause the patient’s ascites. Diagnostic paracentesis (and possible therapeutic) is one option at this point, but due to the patient’s significant bowel edema, exploratory laparotomy and decompression of the abdomen was deemed the more appropriate next step.
Discussion
ACS is defined as “sustained intra-abdominal pressure (IAP) >20 mm Hg (with or without an abdominal perfusion pressure [APP] <60 mm Hg) that is associated with new organ dysfunction/failure.” Intraabdominal hypertension (IAH) also involves elevated IAP but does not result in organ dysfunction. IAH is defined as a pathologic sustained IAP ≥12 mm Hg. IAH is graded based on the degree of hypertension (Table 1). Risk factors for ACS include massive fluid resuscitation and tissue edema, abdominal surgery, ileus, sepsis, and hemorrhage. ACS is therefore most often found in the most critically ill of ICU patients. The prevalence of IAH and ACS has varied from study to study based on the criteria used to define each condition, but in a multicenter point prevalence study the prevalence of IAH and ACS was found to be 50.5% and 8.2%, respectively.
TABLE 1. Grading System for Intra-Abdominal Hypertension
The different types of ACS are differentiated by their respective causes. Primary ACS occurs after injury or disease of the abdominopelvic organs leads to increased IAP, such as with hemorrhage from a large liver laceration or a ruptured abdominal aortic aneurysm. Secondary ACS results from factors external to the abdominal compartment. ACS following massive fluid resuscitation and resulting bowel edema is a classic example of secondary ACS. IAH can be broken down into hyperacute, acute, subacute, and chronic based on the length of time over which the condition develops (seconds, hours, days, and months to years, respectively). Hyperacute IAH is usually the result of physiologic processes such as sneezing or Valsalva. Chronic IAH occurs in pregnancy, liver failure, ascites, and intra-abdominal tumor. These subtypes, of course, do not always require intervention.
While measurement of IAP is the gold standard for diagnosing ACS, CT scan can provide useful clues to the diagnosis. Intrahepatic IVC narrowing may occur as a result of abdominal pressure preventing adequate filling. Bowel walls may appear thickened secondary to edema and the diaphragms may appear elevated. The patient may have a “round belly sign,” defined as an anteroposterior:transverse ratio >0.8 when measured at the level where the left renal vein crosses the aorta.
ACS is clinically significant because it increases a patient’s risk of developing respiratory, cardiovascular, renal, gastrointestinal, and neurologic dysfunction. These conditions are associated with increased ICU time and morbidity, and IAH/ACS are independent predictors of mortality in ICU patients. IAH and ACS are most frequently diagnosed using modifications of the Kron technique, whereby bladder pressure is measured using a urinary catheter (Table 2). There are several commercially available products for measuring bladder pressures. “Home-made” devices to measure bladder pressure can also be assembled, but it is important to remember that these devices have downsides, including potentially less reliable results, increased risk of urinary tract infection, and increased time required to obtain data.
TABLE 2. The Modified Kron Technique for Measuring Bladder Pressure
It is important to note that there are several factors that may affect IAP. Pregnancy and morbid obesity can cause chronically elevated IAP. In hospitalized patients, sepsis, abdominal surgery, and mechanical ventilation may lead to elevated IAP. In order to be considered diagnostic for ACS, the elevated IAP pressure must be sustained and associated with a new pathologic process in one or more organ systems.
Nonoperative Management
Nonoperative management in the early stages of IAP may prevent further progression to ACS and save the patient from undergoing a decompressive laparotomy (Table 3). There are two main techniques by which IAP can be managed. The first is by decreasing the “mass effect” of intra-abdominal contents on tissue perfusion. By removing unnecessary contents from the abdomen, there is more space for edematous bowel. This allows the bowel to take up more space in the abdominal cavity without increasing abdominal pressure and decreasing tissue perfusion. The second mechanism involves improving abdominal wall compliance to increase abdominal cavity volume. The type of intervention chosen depends on many factors, including the reason for ACS developing, other diagnoses in the differential, and patient comorbidities. For example, if missed injury remains a concern, surgery is appropriate, whereas surgical intervention should be avoided if possible in a patient with severe cirrhosis or other severe medical comorbidities.
TABLE 3. Nonoperative Management of Increased IAH
Surgical Treatment
When medical management of IAH fails and a patient develops ACS, surgical decompression of the abdomen is warranted. The goal is to decrease IAP with the aim of improving perfusion to the affected organs. There is no consensus among experts regarding an IAP value that requires surgical intervention. Rather, surgery is necessary when there is evidence of organ dysfunction despite optimal medical therapy using the methods described above. Delaying decompression leads to further tissue ischemia, organ failure, and increased mortality.
Surgical treatment consists of decompressive laparotomy. If space-occupying lesions are present, they should be evacuated at this time. In the past, the abdomen was often closed primarily, but there has been a shift toward staged closure in order to avoid closing the fascia immediately. Using a temporary abdominal closure (TAC) decreases the risk of ACS recurrence, facilitates a second look into the abdomen if necessary, and is often easier than attempting to close the abdomen when significant bowel edema is present.
Methods of addressing the abdomen following decompressive laparotomy include prosthetic mesh, the Bogota bag, vacuum packing (often used in damage control laparotomy following trauma, see Table 4), and negative pressure systems such as vacuum-assisted closure devices. In addition to decreasing the risk of further ACS and allowing access to the abdomen if needed, vacuum packs and negative pressure devices have the additional benefit of removing abdominal exudate (Figure 1). However, care must be taken with wound vacuums to apply the devices correctly in order to minimize the risk of enterocutaneous fistula formation.
FIGURE 1 • Vacuum-packed abdomen.
TABLE 4. Key Technical Steps to Creating an Abdominal Vacuum Pack
Postoperative Management
Patients are still at risk for ACS after surgical decompression. If the fascia is closed, either by primary approximation or with prosthetic mesh, IAP may again become elevated. Even with vacuum packs or negative pressure system, recurrent ACS is possible, particularly if massive fluid resuscitation continues. It is thought that these systems do not always allow for necessary expansion of intra-abdominal volume during postoperative resuscitation and reactive tissue edema.
Because patients remain at risk for ACS following decompressive laparotomy, postoperative care focuses on decreasing IAP by the same methods described above (see “Nonoperative Management”). Bladder pressures should be monitored postoperatively, and the clinician must remain vigilant for further signs of organ dysfunction that could indicate a repeat episode of ACS. Repeat ACS episodes are an indication for second look and release of the TAC.
Patients who undergo laparotomy for ACS need eventual abdominal closure. However, prolonged hospitalization with an open abdomen/vacuum pack often leads to tissue contraction and loss of domain, which makes it difficult or impossible to close the abdomen in a one-stage procedure. These patients may require mesh to augment fascial closure, skin grafting to achieve complete soft tissue coverage, and finally component separation to maintain long-term abdominal wall integrity. Each step may require months of preparation and recovery. Patients with ACS can undergo treatment from months to years before the abdomen is completely “closed.”
Case Conclusion
The patient is taken to the operating room and undergoes exploratory laparotomy. No intra-abdominal sources of bleeding or other injuries are identified, but the patient’s intestines are boggy and edematous. A vacuum pack is placed intraoperatively and the patient returns to the ICU for hemodynamic monitoring including bladder pressure measurements every 4 hours. He is taken back to the operating room for reapplication of the vacuum pack the following day after his peak pressures and acute renal failure, which had improved slightly the prior day, worsen overnight in conjunction with bladder pressure increase from 21 to 40. His bowel is increasingly edematous, but there is no frank intestinal necrosis. Over the following weeks, the patient’s fascia is partially closed, and he is left with a midline abdominal incisional hernia that is repaired with Vicryl mesh once his bowel edema decreases. He stabilizes hemodynamically, his renal function improves, and he is successfully extubated. He is discharged to a skilled nursing facility with wound vacuum in place over his midline soft tissue defect, which decreases in size over several months. Split-thickness skin grafting is used to cover the remaining exposed subcutaneous tissue, and 1 year later, the patient returns to the operating room for component separation and restoration of abdominal wall integrity.
TAKE HOME POINTS
· ACS affects multiple organ systems; therefore, during evaluation of a patient with increased IAP, it is important to rule out other causes of injury to each affected organ system.
· IAH: sustained pathologic IAP ≥12 mm Hg. ACS: sustained pathologic IAP >20 mm Hg accompanied by new organ dysfunction/failure.
· The modified Kron technique is the gold standard for measuring IAP, whereby the intracystic pressure is measured after injecting 25 mL of saline into the urinary bladder.
· IAH may be treated nonoperatively by evacuating intraluminal contents, increasing abdominal compliance, optimizing fluid status, and optimizing tissue perfusion.
· Surgical decompression is necessary when signs of organ dysfunction emerge despite best nonoperative management. TAC is advocated by many in order to decrease the risk of subsequent ACS episodes and facilitate second looks.
· Bladder pressures should be measured even after decompressive laparotomy because compartment syndrome can occur even with TAC.
· Enterocutaneous fistulae are a known complication of temporary negative pressure dressings.
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