Journal of the American College of Surgeons Volume 216 issue 1 2013 [doi 10.1016%2Fj.jamcollsurg.2012.09.004] John Alfred Carr -- Abdominal Compartment Syndrome- A Decade of Progress (1).pdf

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Abdominal Compartment Syndrome: A Decade of Progress John Alfred Carr, MD, FCCP, FACS Unlike many disease processes that surgeons treat in which progress is slow, the knowledge, definition, diag- nosis, research, and treatment of abdominal compartment syndrome (ACS) have undergone dramatic improvements during the past decade. Considering that ACS was only well characterized and physiologically defined in the labo- ratory in 1985, and better cli
  Abdominal Compartment Syndrome: A Decadeof Progress  John Alfred Carr,  MD, FCCP, FACS Unlike many disease processes that surgeons treat inwhich progress is slow, the knowledge, definition, diag-nosis, research, and treatment of abdominal compartmentsyndrome (ACS) have undergone dramatic improvementsduring the past decade. Considering that ACS was only well characterized and physiologically defined in the labo-ratory in 1985, and better clinically defined in 1989,rapid progress has occurred in both the diagnosis andtreatment of this relatively young entity. 1,2 In fact, themortality rate has dropped from 60% to between 34%and 37% in just the last 10 years. 3-5  Abdominal compartment syndrome is defined as a sus-tained intra-abdominal pressure (IAP) > 20 mmHg that isassociated with new onset of organ dysfunction orfailure. 6  Although often mistakenly used interchangeably, ACS is a separate and distinct entity from intra-abdominal hypertension (IAH), which is defined as a sus-tained or repeated pathologic elevation of the IAP   12mmHg. 6 Intra-abdominal hypertension does not causeorgan dysfunction, and that is the key difference betweenthe 2 disease processes. Normal or mean IAP withinthe nondiseased abdominal cavity is between 2 and5 mmHg, depending on overall body mass index (BMI), but can run as high as 12 mmHg in the obeseadult 7 (Table 1). This chronic IAH does not produceorgan injury and is purely a result of visceral obesity. Itis also important to realize that normal IAP in thecritically ill, who are almost always fluid overloaded andedematous, runs slightly higher, at 5 to 7 mmHg. 6 Determining intra-abdominal pressure The standardized method of determining IAP is by measuring the bladder pressure transmitted througha Foley catheter. This is correctly performed by clamping the catheter tubing beyond the rubber or plastic dia-phragm that allows needle puncture access into the lumenof the catheter, and then instilling a maximum volume of 25 mL saline into the bladder. 6 Overdistending thebladder with excessive volumes of fluid will increase thebladder pressure and not reflect the true IAP. 8 The IAPshould be measured at end expiration with the patientsupine and relaxed or sedated, with the transducer zeroedat the mid-axillary line. 6 Having the patient slightly upright at > 30 degrees has been clearly shown to produceerroneous results because IAP will increase as the head of the bed is elevated from 10 to 30 to 45 degrees. 9 Once the IAP is measured, the abdominal perfusionpressure (APP) can be calculated. The APP is simply the mean arterial pressure minus the IAP. To maintainadequate perfusion to the viscera, an APP of at least60 mmHg is desired. 6 For example, a critically ill patientwith a mean arterial blood pressure of 80 mmHg and anIAP of 22 mmHg, has an APP of 58 mmHg, which is justbelow the critical level. This is when end-organ dysfunc-tion can begin to occur. Primary, secondary, and tertiary abdominalcompartment syndrome There are 3 different types of ACS: primary, secondary,and tertiary, which is also known as recurrent ACS.Primary ACS refers to ACS that occurs due to a primary intra-abdominal (or intrapelvic) cause, such as a rupturedabdominal aortic aneurysm, abdominal trauma, or retro-peritoneal hemorrhage 10 ; these are the most commoncauses. However, other rare conditions, such as malignantascites, a giant ovarian tumor, a rectus sheath hematoma,and ACS after Roux-en-Y gastric bypass, have also beenreported. 11-13  Almost any pathology that creates a space-occupying or expanding lesion within the abdominal orpelvic cavity can cause ACS.Secondary ACS (also known as extra-abdominalcompartment syndrome) refers to ACS that occurs asa result of massive bowel edema secondary to sepsis, capil-lary leak, conditions requiring massive fluid resuscitation,or burns. 14-16 Secondary ACS occurs most commonly after hemorrhagic shock requiring massive fluid resuscita-tion or severe burn injuries requiring massive fluid infu-sion. Although these situations result in total body anasarca, it is the swelling of the bowel that limits renal CME questions for this article available at DisclosureInformation:Authorshavenothingtodisclose.TimothyJEberlein,Editor-in-Chief, has nothing to disclose. Received July 13, 2012; Revised August 26, 2012; Accepted September 10,2012.From the Department of Surgery, Hurley Medical Center, Flint, MI.Correspondence address: John Alfred Carr, MD, FCCP, FACS, Depart-ment of Surgery, Hurley Medical Center, One Hurley Plaza, 7th Floor, West Tower, Flint, MI 48503. email: 135 ª  2013 by the American College of Surgeons ISSN 1072-7515/12/$36.00Published by Elsevier Inc.  perfusion and ventilation due to increased abdominalpressure. There is also an entity known as recurrent ACS (or tertiary ACS) in which ACS recurs after resolu-tion of an earlier episode of either primary or secondary  ACS. Recurrent ACS is relatively uncommon and tendsto be the result of an overly aggressive attempt at abdom-inal closure in an edematous patient with an openabdomen. Prevalence and pathophysiology The prevalence of ACS is difficult to quantify and varieswith the patient population that is studied and the acuity of those patients. In the general medical or surgical pop-ulation, the incidence has been reported to be around0.5% to 8%, but increases to 6% to 14% in trauma patients, depending on the classification of primary,secondary, or both. 14,17,18 The incidence is even higherin burn patients, occurring in 1% to 20%, depending on severity and percentage burn. 18 The various cascades of molecular and cellular eventsthat ultimately lead to ACS are multifactorial, with exten-sive interplay between the capillary membrane and inter-stitial interface, combined with neutrophil activation andhemodilution. I will now examine some of these modelsat the microvascular level. Regardless of which model isused as the example, the inciting event, whether it betrauma with hemorrhagic shock, sepsis, or burns, alllead to a capillary leak syndrome resulting in the extrav-asation of fluid into the interstitium and massive bowelwall edema. The bowel wall has an enormous capacity to hold fluid, and a patient can easily sequester severalliters of fluid within the bowel wall and mesentery.This edema leads to increased pressure within the abdom-inal cavity, which ultimately leads to decreased renalperfusion, decreased bowel perfusion, and loss of ventilatory capacity. A common cause of IAH and ACS is sepsis requiring massive fluid resuscitation. Clinical and basic scienceresearch has shown that interleukin-6, interleukin-8,and tumor necrosis factor e a  all act directly on the endo-thelial cell of the capillary beds within the bowel wall tocontribute to the capillary leak syndrome and bowel walledema. 19,20 In addition, when the septic source is locatedwithin the abdomen, such as with appendicitis, the peri-toneal fluid itself has been shown to contain elevatedlevels of interleukin-6 and tumor necrosis factor e a ,which in turn prime neutrophils and fuel the inflamma-tory cascade and capillary leak. 21,22 Neutrophil priming  refers to an enhanced and overly exaggerated secondary response to injury that occurs after an initial injury orstimulus. 23 Priming results in the neutrophil expressing certain adhesion molecules on its surface, specifically CD11b and CD18, which allows the neutrophil toadhere to the endothelial cell of the capillary andextravasate into the interstitium. 24,25 Central vasodilation and shunting of blood from theperiphery during sepsis result in hypotension, which isusually managed with a combination of fluid resuscitationand vasopressors. Vigorous fluid resuscitation during a phase of capillary leak alters the normal hydrostaticand oncotic pressures, resulting in the formation of intes-tinal edema because of a net efflux of fluid into the inter-stitium. 26  As the bowel edema worsens and IAP increases,upward pressure on the diaphragm increases centralvenous pressure, creating a pressure gradient againstvenous outflow and causing abdominal venous hyperten-sion. The increased IAP also hinders lymphatic efflux of fluid from the abdomen, which only worsens theprocess. 26  All of these factors combining at oncecontribute to the growing edema within the bowel walland mesentery, and IAP continues to increase. The septicpatient who has been aggressively fluid resuscitated is atobvious risk for ACS. Another common cause of IAH and ACS is abdominaltrauma, leading to hemorrhagic shock requiring massivefluid resuscitation. In this model, the initial traumaticevent leads to direct blood loss from vascular damagewithin the abdominal cavity. Whether the patientrequires surgery to control the blood loss or is managednonoperatively, the patient has lost a considerableamount of blood and requires either blood transfusion Table 1.  Grading System for Intra-Abdominal Hypertension GradeInternalpressure, mmHg Description Normal  < 12 This accounts for the obese1 12 e 152 16 e 20 Unusual to have organ dysfunctionin this range3 21 e 25 Not equivalent to ACS unless organdysfunction occurs4  > 25 With organ dysfunction theterminology changes to ACS  ACS, abdominal compartment syndrome. Abbreviations and Acronyms  ACS  ¼  abdominal compartment syndrome APP  ¼  abdominal perfusion pressureBMI  ¼  body mass index IAH  ¼  intra-abdominal hypertensionIAP  ¼  intra-abdominal pressureICP  ¼  intracranial pressureRVEDVI  ¼  right ventricular end diastolic volume index  136  Carr  Abdominal Compartment Syndrome  J Am Coll Surg   or crystalloid resuscitation to restore their circulating blood volume. Similar to the septic model, a microvas-cular capillary leak syndrome is created in which fluidextravasates from the bloodstream and into the intersti-tium of the bowel wall and mesentery creating edema,but the inciting events are different. After trauma, bloodloss followed by resuscitation or transfusion creates anischemia-reperfusion injury to the bowel, which resultsin increased capillary permeability. 26 The main mediatorsof these events are interleukin-1, interleukin-6,interleukin-18, monocyte chemoattractant protein 1,and tumor necrosis factor e a . 27,28  With ongoing fluidresuscitation, decreased oncotic pressure from crystalloiduse, and increased capillary permeability due to the medi-ators mentioned previously, all combine to cause a rapidinfusion of fluid into the bowel interstitium and createedema leading to increased IAP.The same holds true for massive fluid resuscitationafter burns, but again, the molecular mediators areslightly different. After a large burn, basic science researchhas shown that there are increased systemic levels of vascular endothelial growth factor, interleukin-6, inter-leukin-8, and tumor necrosis factor e a . 29-31  Aftera burn, it is these systemic up-regulators of the inflamma-tory response that create endothelial cell leakage from thecapillary bed and result in a net fluid flux into the inter-stitium of the bowel and all the tissues of the body. Forthis reason, plasma exchange, which decreases thesystemic levels of inflammatory cytokines in the blood-stream, has beneficial effects after a major burn. 32 But just as in the other models, the result is a capillary leak syndrome and bowel edema that increases IAP and leadsto IAH.In summary, regardless of the inciting event, an inflam-matory cascade of events and resuscitation leads toincreased hydrostatic pressure, decreased oncotic pressure,ischemia and reperfusion injury, and increased capillary permeability. This leads to interstitial edema, bowelwall edema, and increased IAP, which then leads toincreased central venous pressure, both of which causemesenteric venous hypertension and decreased lymphaticflux out of the abdomen. 23 The result is progressively swollen and more edematous bowel and IAH or ACS. Risk factors Independent and widely substantiated risk factors fordevelopment of ACS include massive fluid resuscitation,multiple transfusions ( > 10 U packed RBC 24 hours),hypothermia (core temperature  < 33  C), base deficit/acidosis (pH  < 7.2), and BMI  > 30 6,16-18,33,34 (Table 2).High-volume fluid resuscitation sufficient to cause ACShas been defined as  > 3,500 mL given in 24 hours. 35 However, other authors believe the risk of ACS doesnot increase substantially unless  > 5,000 mL are givenwithin 24 hours. 6  Abdominal trauma and abdominalsurgery also increase the risk for ACS, but the associationis weaker. 33-35 The literature also cites many other risk factors, such as peritonitis, sepsis, burns, and pancreatitis,but these are risk factors for ACS only in that they allrequire fluid resuscitation, which is the actual underlying risk factor itself. 6 Abdominal compartment syndrome and multipleorgan failure Once the bowel has become massively swollen and IAP isgreatly increased, organ dysfunction occurs. Comparing trauma patients with similar Injury Severity Scores, theincidence of multi-organ failure in those with andwithout ACS is 32% to 55% vs 8 to 12%, respec-tively. 17,36 In addition, in the same cohort of trauma patients, the mortality rate of those with ACS is 43%to 64% vs 12% to 17% in those without ACS. 17,36 Renal   A well-described presentation in the trauma or septicpatient who has received massive fluid resuscitation isa progressively more swollen and tense abdominal wall,followed by decreasing urine output, despite ongoing fluid infusion. A bladder pressure measurement showing an IAP > 20 mmHg combined with evidence of decreasedrenal perfusion is diagnostic of ACS. The underlying pathological process that induces renal failure fromincreased IAP is increased renal venous resistance andincreased renal arteriolar resistance, which leads toreduced renal arterial flow and decreased glomerularfiltration rate. Rabbit, canine, and rodent studies haveall shown that renal blood flow is reduced when IAP isincreased to  > 20 mmHg. 37-39 Glomerular filtration ratedecreased to  < 25% at a pressure of 20 mmHg anddropped to 7% when the pressure was increased to40 mmHg. 38 Renal vascular resistance increased > 500%, which was 15 times higher than the systemicvascular resistance. 38 Renal dysfunction from increasedIAP is due to direct renal vein compression and corticalarteriolar compression, as confirmed by these animalstudies. 37-39 This was later confirmed in a human study  Table 2.  Independent Risk Factors for AbdominalCompartment Syndrome Massive crystalloid fluid resuscitation ( > 5,000 mL in 24 h)Multiple transfusions ( > 10 U packed RBC in 24 h)Hypothermia (core temperature  < 33  C)Base deficit/acidosis (pH  < 7.2)Body mass index ( > 30) Vol. 216, No. 1, January 2013  Carr  Abdominal Compartment Syndrome  137  showing a significantly increased resistive index in therenal arteries as well. 40 In addition, the increased renal vascular resistance leadsto up-regulation of antidiuretic hormone, aldosterone,renin, and angiotensin. 41-43 This worsens the entireprocess because increased levels of antidiuretic hormoneand aldosterone result in sodium and water retention,which can increase bowel edema, and increased levels of renin and angiotensin increase renal vascular resistanceeven more, and worsen renal perfusion. 41-43 Respiratory  Increased IAP pushes up directly against the diaphragm,limits total lung capacity, and decreases functionalresidual capacity. It also decreases pulmonary and respira-tory system static compliances and increases airway resis-tance, alveolar-arterial oxygen gradient, and respiratory dead space. 44  As the diaphragm is pushed up, compressiveatelectasis of the lower lobes occurs and this impairsoxygenation, increases intrapulmonary shunting, andincreases dead-space perfusion. 45 There is also a globalincrease in intrathoracic pressure, which is transmittedto the smaller airways, creating increased airway pres-sures. 46-48 This reduces chest wall compliance and degreeof recoil after inspiration, creating hypercarbia and venti-latory failure. 46,47  Just like in the abdomen, increasedintrathoracic pressure increases pulmonary vascular resis-tance, which worsens oxygenation. 45-48 Some very interesting research in porcine models hasshown that IAH in the face of acute lung injury or acuterespiratory distress syndrome induces and worsenspulmonary edema. 49,50  With intra-abdominal pressuresbetween 20 and 30 mmHg for several hours, the extravas-cular lung water content increased considerably, by up to30%. 49,50 This is believed to be due to increased intratho-racic pressures impeding pulmonary venous return andincreasing pulmonary vascular resistance.Much of the recent research has focused on the use of increased PEEP to match and overcome the abdominalpressure. In other words, have the PEEP set to matchthe abdominal pressure pushing up from below to avoidlung compression. Interestingly, high levels of PEEP(  12 mmHg) will increase IAP considerably, in bothpatients with and without IAH. 51  A summary of thisresearch shows that with low levels of IAH ( < 13mmHg), adding PEEP to match at the same pressurewill counterbalance the effects of IAH and maintainnormal oxygenation and hemodynamics, and preventatelectasis and loss of lung volume. 52 However, withrising levels in IAP and ACS, a sufficient amount of PEEP necessary to match this pressure in the 18 to 22mmHg range results in a 26% loss of cardiac output,decreased total respiratory compliance, decreased chestwall compliance, and did not improve arterial oxygena-tion. 53  Attempts at matching the IAP with the PEEP isnot recommended because the excessive pressure createdin the chest has detrimental effects on cardiac outputand increases the risk of barotrauma, without any improvement in oxygenation. 53 Cardiac  To understand the effects of IAH and ACS on the heart,only 2 main factors need to be kept in mind: a decreasedvenous return and a greatly increased afterload. This isimportant to understand because increasing venousreturn (increasing the central venous pressure) andreducing afterload will restore the cardiac output in thesepatients.Impairment of venous return from the abdominalcavity to the heart, and specifically from the inferiorvena cava, begins to occur with IAPs   15 mmHg. 54 Once the pressure has reached   20 mmHg, there issubstantial collapse of the mesenteric and renal veins, aswell as the vena cava, which results in a considerabledrop in venous return. 55 Ironically, because of theincreased abdominal pressure pushing on the vena cava and pushing upward against the diaphragm andincreasing the intrathoracic pressure as well, the centralvenous pressure will be falsely elevated. Research ina porcine model showed that an IAP of 30 mmHg willartificially increase the central venous pressure by a factorof 4. 56 The novice clinician might think the patient iseuvolemic when in fact, because of continued volumeloss into the bowel interstitium, the patient is intravascu-larly volume depleted. This is evidenced by the markedimprovement in blood pressure and overall hemody-namics with intravascular volume expansion. 50,57-59 The second factor that decreases cardiac output isthe elevated afterload. The afterload is elevated due toincreased systemic vascular resistance, mostly from theabdominal cavity, and increased intrathoracic pressure. 54-58 Increased abdominal pressure has similar physiologicaleffects as to increased end expiratory pressure in the chestcavity. Just as increased PEEP expands the lungs, whichthen constantly apply direct pressure to the mediastinum,so too does the constant direct pressure against the dia-phragm from the swollen viscera. The direct cardiaccompression and increased intrathoracic pressure trans-mitted upward from the abdominal cavity limit ventric-ular compliance and right ventricular end diastolicvolume. 51-53 In addition, there is direct compression of the arterioles within the mesentery of the bowel and otherviscera that account for a substantial increase in theafterload. 138  Carr  Abdominal Compartment Syndrome  J Am Coll Surg 
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