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Abdominal Compartment Syndrome

2001; Lippincott Williams & Wilkins; Volume: 39; Issue: 1 Linguagem: Inglês

10.1097/00004311-200101000-00008

1537-1913

Rubén Peralta, Horacio Hojman,

Muscle and Compartmental Disorders

Introduction Abdominal compartment syndrome (ACS) is defined as a condition in which increased pressure is confined to the abdomen and is associated with a clinical picture involving hemodynamic, respiratory, and renal dysfunction. ACS occurs secondary to accumulation of fluid or gas, or both, in the abdominal cavity. It can have many different causes, including intra-abdominal bleeding after blunt and penetrating abdominal trauma, after abdominal packing for uncontrollable bleeding, and after aggressive fluid resuscitation with resultant bowel edema, 1–4 retroperitoneal edema 5 or bleeding, 6–8 pancreatitis, 9 ascites, 10 or liver transplantation. 11 A compartment syndrome develops when an expandable tissue is surrounded by a less compliant, more rigid tissue. The classic description is that of muscular edema developing in an extremity. The muscle is surrounded by a more rigid, less distensible fascia. The muscular swelling, contained by the fascia, causes elevation of tissue pressure inside the compartment. Compartmental hypertension causes decreased tissue perfusion secondary to capillary and venular collapse, followed by anaerobic metabolism, acidosis, and eventually tissue necrosis. The abdominal cavity can act as a compartment. When the volume of intra-abdominal contents suddenly increases, the more rigid muscular fascia of the abdominal wall and sometimes even the skin limit expansion. The level at which the increased intra-abdominal pressure (IAP) can be called ACS is controversial. Oliguria, hypercapnia, and high inspiratory airway pressures during mechanical ventilation are considered to be late manifestations of ACS. 2 Because IAP can be measured in millimeters of mercury or centimeters of water, a word of caution is needed when evaluating different studies. Whereas some authors use millimeters of mercury, 12–17 others use centimeters of water. 3,10,18,19 Although these units can be easily converted (1 mm Hg = 1.36 cm H2O), their varied use adds a small amount of confusion for comparative purposes. Historical Perspective For more than a century, the medical literature has documented that elevation of IAP can produce serious pathological derangements. 20 More recent studies 21–24 delineated the respiratory, hemodynamic, and renal compromise caused by increased IAP. The medical and particularly the surgical community largely ignored these reports. In the last two decades, a large number of experimental and clinical studies demonstrated that increased IAP, resulting in ACS, is a common and clinically significant entity in critically ill patients. 3,5,18,25,26 Incidence The exact incidence of ACS is difficult to estimate. The number varies in different trauma series from 5.5%15 to 35%. 27 Many factors, including the nature of the patient population, acute versus chronic processes, and the level of IAP considered to be ACS, can account for this variability. Etiology The classic scenario is the patient who has undergone trauma surgery as a result of intra-abdominal hemorrhage, 1–4 particularly after damage control laparotomy. 2 The concept of damage control laparotomy 28–32 or abbreviated laparotomy for trauma entails a quick laparotomy, with expeditious control of bleeding and bowel spillage. These critically ill patients have a very limited physiological reserve and cannot tolerate prolonged surgical procedures. They are usually hypothermic, acidotic, and coagulopathic. After achieving temporary control, the surgical procedure is interrupted and the patient is quickly transferred to the surgical intensive care unit (ICU) for rewarming and correction of coagulopathy. 33,34 After hypothermia, coagulopathy, and acidosis are corrected in the ICU, the patient returns to the operating room for completion of the procedure. During the period when the patient is in the ICU, some degree of intra-abdominal hemorrhage is expected to continue, and the patient is at risk for ACS. The abdominal packing that is purposely left in the abdomen to achieve hemostasis is an additional contributing factor to the development of ACS. 12,15 Shelly and associates 11 described three patients in whom ACS developed as a result of intra-abdominal bleeding after liver transplantation. As early as 1988, Savino and colleagues 10 noted the effect of elevated IAP in critically ill cirrhotic patients with ascites. Other causes that have been described include retroperitoneal edema after aortic surgery 5,35 and retroperitoneal bleeding (Fig. 1). 6 ACS has also been described after other types of abdominal surgery, such as gynecological 7 and urinary tract surgical procedures, 36 and with abdominal distention caused by megacolon 37 or fecal impaction 38 (Fig. 2).Fig. 1.: Axial computed tomography scan showing the irregular contour of the abdominal aortic aneurysm and the dissection of blood into the right perinephric and posterior pararenal space (arrow).Fig. 2.: Radiograph of kidney, ureter, and bladder shows an abnormally dilated rectosigmoid colon, partially filled with feces with a proximal colon of normal size. Note that the superior extent of the dilated sigmoid colon is reaching up to the left hemidiaphragm.More recently, attention has been drawn toward the development of ACS in patients involved in multiple trauma who do not have any intra-abdominal injury. 8 These patients experience abdominal compartment syndrome secondary to massive bowel edema and ascites. The mechanism involved is still subject to speculation but is believed to be caused by shock with associated bowel hypoperfusion. The correction of the hypovolemia is followed by secondary reperfusion injury, capillary leak, and tissue swelling. This reperfusion injury is probably in part responsible for the increased abdominal pressure as described in “classic” ACS. ACS has also been described after burns, probably secondary to reperfusion injury of the bowel, as described previously. 16,17 In a 2000 report, Ivy and coworkers 39 found a 20% incidence of ACS in 10 patients with greater than 20% body surface area burns. The authors used an IAP of 25 mm Hg to define intra-abdominal hypertension, but defined ACS only when laparotomy was needed because of high peak inspiratory pressures during mechanical ventilation. A more detailed analysis of the results showed that 90% of the patients in this group had an IAP of at least 15 mm Hg. As is discussed later, this degree of IAP can cause many physiological problems. Pathophysiology Bowel Dysfunction Significant organ dysfunction can occur with relatively low IAP. 40–42 Caldwell and Ricotta 43 demonstrated a significant decrease in blood flow to intra-abdominal organs of dogs after increasing IAP to 20 and 40 mm Hg. Significantly, they found increased blood flow to the adrenal gland. Diebel and others 25 reported similar results in a rodent model. This decrease in splanchnic blood flow occurred despite maintaining mean arterial pressure with intravenous fluid administration. Bongard and colleagues 44 reported the presence of mucosal ischemia, even with the relatively low IAP of 15 mm Hg. Eleftheriadis and associates 45 confirmed splanchnic ischemia with tissue acidosis by measuring hepatic blood flow and intramural gastric pH in patients undergoing laparoscopic cholecystectomy. After discontinuing the pneumoperitoneum, hepatic blood flow significantly increased and intramural gastric pH returned to normal. Even bowel necrosis has been described with the moderately increased IAP of laparoscopic cholecystectomy. 40–42 Sugrue and others, 46 in a prospective study, confirmed the presence of mucosal ischemia in trauma patients undergoing laparotomy closure. Such bowel ischemia may be at least in part responsible for the increased rate of anastomotic breakdown reported in trauma patients with abdominal compartment syndrome. 47 Decreased tissue perfusion with subsequent mucosal ischemia can lead to bacterial translocation. 48–50 Hemorrhage, when associated with increased IAP as low as 10 mm Hg, has been reported to increase bacterial translocation. 51 It remains unclear whether the bacterial translocation is a contributing factor to the multisystem organ failure seen in humans. Increased Intracranial Pressure A particular concern in patients with head injury and elevated IAP is worsening of intracranial pressure (ICP) with the associated decrease in cerebral perfusion pressure (CPP). Bloomfield 1 and Ertel 15 and their associates described three patients with multiple trauma and concomitant head injury in whom abdominal decompression and release of the ACS resulted in a dramatic decrease in ICP (Fig. 3). Pneumoperitoneum has been described as causing elevation of the ICP in humans. 52,53 Although it is questionable whether this increase in ICP is associated with decreased CCP in normal patients, 54 this is a particular concern in head injury patients undergoing any type of diagnostic laparoscopy. Josephs and coworkers 55 described the effect of pneumoperitoneum on ICP and CPP on pigs. They found a significant increase in ICP with pneumoperitoneum that was independent of changes in partial pressure of arterial carbon dioxide (PaCO2) and pH. Other authors reported similar findings. 56–58 Although there are descriptions of elevated ICP with pneumoperitoneum using carbon dioxide, 59 the experiments adjusted the mechanical ventilator to minimize changes in PaCO2. Rosenthal and others 57 did not find a decrease in CPP because mean arterial pressure (MAP) increased in their study. Contrary to this, in a very similar experiment, Bloomfield and associates 58 reported a significant decrease in CPP when MAP changed only minimally. The effect of increased IAP on ICP appears to be mediated mechanically by diaphragmatic elevation, reduced chest wall compliance, and increased central venous pressure (CVP).Fig. 3.: Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) kinetics compared with bladder pressure during Day 1 of admission in a multiple-trauma patient with combined abdominal and head trauma in whom abdominal compartment syndrome is developing. ICU—intensive care unit. From Ertel W, Oberholzer A, Platz A, et al. Incidence and clinical pattern of the abdominal compartment syndrome after “damage-control” laparotomy in 311 patients with severe abdominal and/or pelvic trauma. Crit Care Med 2000;28:1747–1753. 15 Used with permission.Respiratory Compromise In the classic descriptions of ACS, 2,3,15,18,60–64 the lungs of patients with increased abdominal pressure were often mechanically ventilated. ACS usually presented with high peak inspiratory pressures and very low respiratory system compliance. Chest radiographs in these patients typically show clear but small lung fields and elevated hemidiaphragms. Compression of alveoli produces alveolar hypoventilation, with increased dead space ventilation and hypercarbia. Atelectasis develops easily in such patients, producing areas of ventilation-perfusion mismatch and associated hypoxemia. The atelectasis associated with ACS increases the incidence of nosocomial pneumonia. Positive end-expiratory pressure (PEEP) is required to maintain oxygenation, 1 further complicating the hemodynamic monitoring. Previous hemorrhage may worsen the severity of the pulmonary dysfunction associated with increased IAP. 65 Hemodynamic Changes Kashtan and colleagues 23 demonstrated in canine experiments that increased IAP decreases cardiac output. These changes were more marked in hypovolemic dogs compared with euvolemic dogs. Several mechanisms have been proposed, among them diminished venous return, increased vascular resistance, and changes in the position of the heart secondary to elevation of the diaphragm. The tense abdomen obstructs venous return to the heart by compressing the inferior vena cava (IVC), 66,67 decreasing cardiac output. Iwase and others 68 reported that the pressure in the IVC correlated with IAP during the pneumoperitoneum induced for laparoscopic cholecystectomy. Rosenthal and associates, 57 in a swine model, demonstrated that progressively increasing IAP narrows the lVC at the level of the diaphragm. Narrowing of the IVC and increased abdominal pressure can decrease venous return and contribute to the development of venous hypertension and lower extremity edema. 69,70 It is unclear whether the decreased venous return from the lower extremities places such patients at increased risk for deep vein thrombosis and pulmonary embolism. Increased IAP is transmitted to the chest cavity, where it causes a spurious increase in the measurement of CVP and pulmonary artery occlusion pressure (PAOP), 15,23 similar to that observed when intrathoracic pressure is increased by the application of PEEP (Table 1). These increased values can be particularly problematic, considering that such patients have a diminished venous return and may be hypovolemic. Subtracting the intrathoracic pressure, measured with an esophageal balloon, can help to determine transmural values for CVP and PAOP. The use of the right ventricular end-diastolic volume measurements has been suggested as a better method to guide the resuscitation. 71,72Table 1: Changes in Physiological Variables After Decompressive Laparotomy in Patients with Abdominal Compartment SyndromeSystemic vascular resistance may also be elevated with increased IAP. The mechanism responsible for the increased SVR is unclear but is likely related to mechanical compression of capillary beds. 10–12,23,24 Renal Dysfunction Oliguria often occurs, despite adequate blood pressure and cardiac output, when IAP is increased. Abdominal decompression usually results in immediate diuresis (Fig. 4). 12,15,18,73–75 The cause of the decrease in urine output is multifactorial. In 1982 Harman and others 24 described the effect of artificially elevated IAP on renal function in dogs. They noted a marked decrease in the glomerular filtration rate (GFR) and cardiac output. The decrease in GFR persisted after correction of the reduced cardiac output by volume expansion. The decreased GFR was attributed to direct compression of the renal parenchyma. Blood flow to the intra-abdominal organs, including the kidneys, 13,24,43 is reduced when IAP is increased. Barnes and colleagues 76 demonstrated a greater reduction in blood flow to the kidneys compared with other intra-abdominal organs during intra-abdominal hypertension. The increased IAP can also directly compress intra-abdominal veins, including the renal veins. Stenting of the ureters does not prevent the development of oliguria. 24 The elevated renal venous pressure, together with decreased renal blood flow, is likely responsible for the decreased GFR that occurs when IAP is increased (Fig. 5). 62,77Fig. 4.: Typical kinetics of different physiological variables during Day 1 admission in a multiple-trauma patient in whom abdominal compartment syndrome is developing. CVP = central venous pressure; PAP = peak airway pressure; VT = tidal volume; ICU = intensive care unit. From Ertel W, Oberholzer A, Platz A, et al. Incidence and clinical pattern of the abdominal compartment syndrome after “damage-control” laparotomy in 311 patients with severe abdominal and/or pelvic trauma. Crit Care Med 2000;28:1747–1753. 15 Used with permission.Figure 4: ContinuedFigure 4: ContinuedFig. 5.: Renal Doppler examination demonstrated absent arterial flow signal in the left kidney.The increased IAP seems to be an independent marker of renal dysfunction. 46,78 In a prospective study, Sugrue et al 78 reported that elevated abdominal pressure was a separate determinant in postoperative renal failure, only secondary to hypotension, sepsis, and age above 60, in surgical patients admitted to the ICU after abdominal surgery. Miscellaneous Diebel and associates 25 described a significant reduction of the abdominal wall flow with increased IAP in a porcine model. This effect might help explain the high incidence of wound complications seen in trauma patients with ACS. 27 Maxwell and coworkers, 8 reporting on six patients in whom secondary ACS developed, noted that two experienced compartment syndrome of the extremities, requiring fasciotomy. It is significant that, although extremity compartment syndrome is usually associated with orthopedic or vascular injuries, in one case there was no associated injury to explain its development. The authors speculated that a global mechanism of ischemia and reperfusion might explain these findings. Diagnosis Physical exam alone is unreliable for the diagnosis of ACS. Although ACS can occur with normal abdominal exam, it is our experience that these patients always present with a very tense abdomen. A nondistended but tense abdomen is relatively common. Because of the difficulty of clinical assessment of IAP, a more objective method is necessary for the determination of increased IAP. Measurement of Intra-Abdominal Pressure The intra-abdominal pressure can be measured directly or indirectly. Direct measurements use a transducer placed into the abdomen or connected to a catheter located in the abdomen. Although this method is used during laparoscopic surgery, it is impractical in the ICU setting. Measuring bladder pressure is an indirect, yet very accurate, method of measuring intra-abdominal pressure. 75,79,80 This method involves infusing of 50 to 100 mL of sterile saline into an empty bladder via a Foley catheter, clamping the Foley distal to the aspiration port and then attaching a pressure transducer via the aspiration port. The wall of the urinary bladder acts as a passive diaphragm when the bladder volume is between 50 and 100 mL. The zero reference point is the top of the symphysis pubis with the patient supine. Because the bladder is acting as a passive transducer, anything that might limit its wall motility can affect the reading. Fortunately, the most common cited 81 contraindications for the use of bladder pressure, mainly neurogenic or contracted bladder, are uncommon in clinical practice. Although experience is somewhat limited, pelvic fractures with associated hematoma have not been associated with inaccurate readings of bladder pressure. This technique is now commonly used to measure IAP in the ICU setting. When there are concerns that the bladder pressure might not be accurate, alternative methods to measure IAP must be sought. Other indirect methods include the introduction of a central venous catheter into the IVC 22,68 and the measurement of intragastric pressure via a nasogastric tube. 82 Computed Tomography Findings Although ideally the diagnosis of ACS should be made on basis of the clinical picture and confirmed by measurements of bladder pressure or equivalent, sometimes patients with intra-abdominal disease undergo computed tomography (CT) scans (Figs. 6, 7, and 8). Pickhardt and others 9 described the CT findings in four patients with confirmed ACS. They measured the anteroposterior and transverse abdominal diameters at the level where the left renal vein crosses the aorta. They reported that the anteroposterior to transverse abdominal ratio was increased (round belly sign) in patients with ACS. The ACS patients had a ratio of 0.85 compared with 0.70 in controls. Other CT findings included extrinsic compression of the IVC with associated venous distention below the level of compression, compression of the kidneys, and abnormal bowel wall thickening with enhancement by intravenous contrast.Fig. 6.: Axial computed tomography scan showing a large liver hematoma involving the right lobe of the liver, with extension through the liver capsule and a large hemoperitoneum.Fig. 7.: Axial computed tomography scan showing a high-density collection surrounding a loop of small bowel (open arrow) along with extraluminal air in the mesentery (arrow). Also note the hemopneumoperitoneum.Fig. 8.: Axial computed tomography scan reveals a large loculated fluid collection in the upper abdomen with an air-fluid level (arrow).Treatment The treatment for intra-abdominal hypertension should be directed toward prevention, avoiding closure of the abdominal wall under tension and liberally using a mesh closure when elevated abdominal pressure is expected postoperatively (Fig. 9). 3,83 In 1948, Gross proposed a two-stage repair of omphaloceles to avoid the consequences of increased IAP as a result of an abdominal cavity too small for the bowel loops. 84 Mayberry and coworkers 27 reported that ACS could be effectively prevented in severely injured trauma patients undergoing celiotomy. They documented a 0% incidence of postoperative ACS among 47 patients with mesh closure of the abdominal wall, compared with 33% among 26 patients who underwent primary fascial closure. The two groups were otherwise similar in injury severity score and demographics.Fig. 9.: Temporary closure with a silo sewn to the skin. Note the visible loops of bowel.In a 1999 retrospective review, Ciresi and colleagues 83 reported their 3-year experience with the use of mesh closure after abdominal trauma or ruptured abdominal aortic aneurysm repair. They found that a mesh closure appeared to reduce the incidence of ACS and facilitated secondary closure of the abdominal wall. Mesh closure of the abdominal wall also reduced the incidence of abdominal abscesses, necrotizing fasciitis, and enteral fistula. 5,33,83 Once the syndrome develops, the treatment for intra-abdominal hypertension and compartment syndrome is decompression via a laparotomy. Regrettably, there is no consensus as to when to intervene. Some authors 2 proposed that an IAP of 20 to 25 mm Hg warrants intervention, particularly when associated with clinical signs of increased IAP. 8 Others recommended intervention between 25 to 35 mm Hg. 12,60 It should be recalled, however, that significant organ hypoperfusion, mucosal ischemia, and bacterial translocation can occur with an IAP as low as 10 mm Hg. In a retrospective study, Maxwell and colleagues 8 presented a series of six patients with secondary ACS. The authors reported that early decompression was associated with increased survival. The average time for decompressive laparotomy was 3 hours in the survivors compared with 25 hours in patients who died. Because hypervolemia can partially compensate for the deleterious effects of increased IAP on venous return and cardiac output, 23 patients with ACS should be aggressively fluid resuscitated, preferably while monitoring cardiac output and right ventricular end-diastolic volume. 18,71,72 Meldrum and coworkers 12 proposed a grading system for selective management of patients with increased IAP. Grade 1 patients, with bladder pressures between 10 and 15 mm Hg, are treated conservatively. Grade 2 patients, with bladder pressure between 16 and 25 mm Hg, are treated with aggressive fluid resuscitation to maintain cardiac output. Grade 3 patients, with bladder pressure in the 26-to 35-mm Hg range, require abdominal decompression that can be done at the bedside. Grade 4 patients, with bladder pressures >35 mm Hg, are suspected to have ongoing intra-abdominal injury and should undergo formal exploratory laparotomy in the operating room. At Massachusetts General Hospital, we have used neuromuscular blocking agents in an attempt to reduce the IAP, especially when “spontaneous” resolution of the cause is expected (i.e., an overly resuscitated cirrhotic patient or a patient with secondary ACS). This practice has been described by others. 39 Intra-abdominal hypertension decreased an average of 10 mm Hg after complete neuromuscular blockade. A “reperfusion syndrome” consisting of severe hypotension, coagulopathy, and even asystole 85 has been associated with abdominal decompression and has been attributed to the sudden washout of by-products of anaerobic metabolism. 11,37 Its incidence has been reported to be 12–25%, although it appears to be lower in modern series, probably reflecting an increased awareness of this problem with early intervention. Treatment includes volume expansion to maintain cardiac filling. Some authors 11 suggest the empiric use of inotropic support and correction of acid-base balance with sodium bicarbonate. 8 Decreasing ventilatory support and PEEP after decompression also improves venous return and cardiac output.