Abdominal compartment syndrome (ACS)
Damage control laparotomy
Early goal-directed therapy
1. Description of the problem
What every clinician needs to know
Abdominal compartment syndrome (ACS) occurs when intra-abdominal pressure (IAP) is greater than 20 mm Hg, causing multiple organ failure. ACS is preceded by intra-abdominal hypertension (IAP greater than 12 mmHg). It relates to space that is occupied by blood, clot, ascites, intraluminal gas or visceral edema in a fascial space that is only poorly distensible. The standard of care is to decompress the peritoneal space, which may be accomplished by a variety of techniques depending on the etiology of the ACS.
Clinical features are generally related to the effects of the space-occupying lesion on diverse organ systems. Physical examination is rather poor at determining which patient does or does not have the ACS. Instead, at-risk patients should be regularly monitored for changes in IAH, generally as intravesical pressure. Most commonly, clinicians identify an increase in peak airway pressures on volume cycled ventilation (VCV), decreased resultant tidal volume in pressure controlled ventilation (PCV), decreased release volumes on airway pressure release ventilation (ARPV), oliguria, or decreased mean arterial pressure.
Key management points
Monitor at-risk patients, including those with retroperitoneal processes and large volume resuscitation for extra-abdominal disease.
Ensure accurate measurement of IAP in a sedated patient.
Treat readily correctable causes, including gaseous distention; neuromuscular blockade is not a substitute for decompression of the peritoneal space.
Evaluate for ascites that may be percutaneously drained.
If unable to manage as above, then emergent abdominal decompression is warranted.
If the OR is not immediately available, or the patient is unstable, bedside decompression should be undertaken without delay.
Early diagnosis and therapy enhances outcome.
2. Emergency Management
Emergency management steps
Once the diagnosis is made, immediate management addresses support of effective circulating volume. Plasma volume expansion (PVE) coupled with vasopressor support is appropriate. AVOID pure alpha agonists as these only create vasoconstriction and decrease end-organ flow to already relatively poorly perfused organs. Recall that the ACS reduces cardiac output (CO) by impeding venous return (VR) from excessive IAP. Thus, PVE is the most efficacious initial step in management, but may require myocardial contractility support as well since many patients have sepsis as their principal diagnosis.
The next step consists of emergency decompression of the excessive IAP. Here, emergency management is dichotomous and is based upon the etiology of the IAP. One group of patients may be successfully managed with percutaneous drainage of massive ascites. A bedside ultrasound will readily identify fluid and should be applied in those with burns and patients with extra-abdominal disease. A Focused Assessment by Sonography for Trauma (FAST) examination that is used in the ED for the initial evaluation of injured patients will suffice as organ-based imaging is not required. One need only identify the presence or absence of large volume intraperitoneal fluid. A note of caution: the FAST will only identify fluid and will not determine its nature. Blood and ascites have the same appearance on FAST. Thus, percutaneous drainage is appropriate only for those WITHOUT injury.
If a large volume of fluid is noted, emergency management may proceed by performing a standard paracentesis, inserting a standard triple-lumen catheter for drainage, or placing a temporary peritoneal dialysis catheter for drainage. Ultrasound guidance may be helpful during catheter placement to help avoid iatrogenic injury to underlying viscera.
Virtually all other patients should NOT undergo percutaneous drainage as their ACS will generally stem from intraperitoneal blood/clot, visceral edema, or retroperitoneal hemorrhage, and requires that the peritoneal envelope be physically enlarged. Many of these patients will be post-op and require relaparotomy with subsequent open abdomen management; immediate reclosure is inappropriate. Special note should be made that these patients will certainly develop a reperfusion-associated visceral edema after decompression and their incision should be midline and from just below the xiphoid to just above the symphysis pubis. An unusual subset of patients will have ACS from colonic gaseous distention and may be safely and effectively managed by emergency colonoscopic decompression.
Initial or relaparotomy may be safely performed in the OR as well as the ICU. ICU decompression may be performed with deep sedation using propofol and fentanyl; neuromuscular blockade is not required. However, appropriate equipment to open the abdomen (including lighting, cautery and surgical instruments) and pack and provide simple suture ligation of bleeding vessels is required. Occasionally, the patient may be too unstable to move to the OR until after the peritoneal space is initially decompressed in the ICU. Of note, such procedures may be performed in both surgical AND medical ICUs.
Many methods of temporary abdominal closure are available and may be applied with equal efficacy, including the homemade “VAC pack,” the proprietary KCI VAC device, the Bogota bag, and others. Special note is made that a patient may develop the ACS even with an open abdomen. Such patients generally develop either massive visceral edema or post-op hemorrhage.
Measuring bladder pressure has been demonstrated to correlate well with intra-abdominal pressure (IAP). Progressive increases in IAP have been shown to lead to the ACS. ACS results in decreased perfusion to the kidneys and the gut, while decreasing cardiac output and impeding respiratory excursion. The ACS confers increased mortality and morbidity risk to patients with increased IAP. Recognition of a developing ACS allows providers early intervention prior to the onset of complications from the ACS.
All SICU patients at risk for intra-abdominal HTN.
Risk identifiers for increased IAP
Damage control laparotomy.
Intra-abdominal procedure in conjunction with (a) Large volume resuscitation (>10 liters crystalloid equivalent); or (b) coagulopathy requiring correction with the massive transfusion protocol; or (c) large volume blood component therapy (PRBC greater than 10 U, or FFP greater than 8 U).
Severe sepsis or septic shock.
Open body cavity.
Sepsis, severe sepsis, or septic shock.
Cirrhosis or liver failure with ascites.
Mechanical ventilation with PEEP greater than 10 cm H2O pressure (intrinsic or extrinsic).
Intra-abdominal hypertension: IAP>12 mmHg.
Abdominal compartment syndrome: a clinical syndrome resulting from increased IAP manifested as increased peak airway pressure, oliguria, metabolic acidosis, decreased cardiac performance (mean arterial pressure, cardiac output, SvO2), decreased abdominal perfusion pressure, and decreased mentation. The ACS is commonly associated with IAP>20 mmHg but may occur at lower pressures as well based on individual patient characteristics, including the abdominal perfusion pressure.
Abdominal perfusion pressure (APP): Mean arterial pressure (MAP) – intra-abdominal pressure (IAP); Normal APP>60 mmHg.
On admission to the SICU, patients will be evaluated by the bedside nurse and the physician team for risk identifiers for increased IAP.
Patients who are identified at risk will be monitored by bladder pressure measurements to determine IAP according to the following schedule: (a) on arrival to the SICU; (b) every 2 hours for the first 8 hours; (c) every 4 hours for the next 8 hours; (d) every 8 hours for the next 24 hours; and (e) subsequent frequency of measurement will be determined by the physician team if IAP is greater than 12 mmHg @ 24 hours.
Notify the physician team of all IAPs greater than 12 mmHg and abdominal perfusion pressures less than 60 mmHg.
These values will be recorded on the nursing flowsheet.
Intravesical pressure is the gold standard for measuring IAP. There are several devices that may be used to measure this pressure, including a bedside manometer, an arterial line set-up attached via a stopcock, and commercially available devices. The key features are (a) to ensure that the patient is adequately sedated to remove the effects of intra-abdominal muscular tension on the measurement; and (b) not using more than 25 cc of volume to distend the bladder; and (3) aligning the transducer axis with the level of the bladder. A normal IAP is less than 12 mmHg.
Abdominal perfusion pressure is a supplementary measure to assess the potential impact of intra-abdominal HTN (IAP greater than 12 mmHg) on visceral perfusion and is calculated as MAP – IAP = APP; normal APP is >60 mmHg. APP is useful in those patients with IAP>20 mmHg in whom there is no readily identifiable and attributable organ failure.
Establishing the ACS requires coupling an IAP>20 mmHg with an attributable organ failure. Generally, the pulmonary, renal, and cardiovascular systems are most rapidly compromised. However, enteral alimentation intolerance may also serve as an attributable organ failure supporting peritoneal space decompression in the setting of IAH.
Figures 1-4 depict the initial appearance at bedside decompression for ACS, the 1st washout after thoracic compartment syndrome decompression, tertiary peritonitis, and enteroatmospheric fistulae. (Figure 1) (Figure 2) (Figure 3) (Figure 4)
Diagnosis may be confounded by the setting in which patients are at risk for developing intra-abdominal HTN and the ACS. Generally, patients at risk share several common features, including the potential for indirect acute lung injury, acute tubular necrosis, and acute kidney injury/acute renal failure, as well as sepsis/severe sepsis/septic shock leading to myocardial depression and systemic hypotension.
Such patients are also at risk for relative adrenal insufficiency, further confounding the clinician’s surety that the hemodynamics and organ dysfunction are truly related to the intra-abdominal HTN. Generally, the rapidity of the development of increased IAP provides a strong clue that the abnormalities are related to the rising pressure; the more rapid the rate of rise, the greater the likelihood that there is a causal relationship. The corollary to that statement is that one must be monitoring the IAP to detect its rate of rise.
Intravesical pressure is directly measured but is only a reflection (albeit tightly coupled) of intraperitoneal pressure. Therefore, IAP is subject to a host of influences that may falsely elevate its level; as a rule, IAP is not artificially lowered by any influences. Generally, muscular activity, large bladder-distending volumes, concomitant urinary retentions from a dysfunctional catheter, and transducer positioning failure influence the measurement of IAP.
Regardless of the etiology, intra-abdominal HTN coupled with an attributable organ failure should prompt therapy. In fact, understanding the precise etiology is not necessary prior to providing surgical decompression in an unstable patient. Despite the fact that ascites may be managed with percutaneous drainage, proceeding with surgical decompression is equally efficacious. The etiology of the intra-abdominal HTN will be readily apparent at the time of operation and may require further operative intervention (i.e. subtotal colectomy for toxic megacolon from C. difficile colitis or from colonic ischemia).
The ideal confirmatory test is also the ideal therapy: laparotomy. Upon decompression, the viscera generally explode out of the abdomen, often accompanied by blood, clot, or ascites. Once decompressed, airway pressures decrease, MAP increases, and urine output may increase. However, once AKI or ARF is established abdominal decompression will not reverse the renal abnormalities; recovery depends on factors other than relief of intra-abdominal HTN.
4. Specific Treatment
Specific therapy as noted above relates to abdominal decompression, with the gold standard being decompressive laparotomy. Select cases of ACS due to rapidly identified ascites may be managed by percutaneous drainage of the ascites. Rare cases of ACS from gaseous distention of the colon (i.e. post-colonoscopy, Ogilvie’s syndrome) may be managed by colonoscopic decompression.
There are no specific medications to use for ACS.
There are no refractory cases of ACS. All peritoneal spaces may be decompressed. Even patients with dense adhesions may have their peritoneal spaces decompressed with meticulous dissection.
5. Disease monitoring, follow-up and disposition
Expected response to treatment
The expected response to decompression is the prompt normalization of IAP and reversal of untoward hemodynamics and pulmonary mechanics. Large volume PVE needs and pressor support may not abate in the face of reperfusion injury in multiple organ systems, as well as the ongoing fluid, salt, and protein loss via the open abdomen. Prognosis is generally related to the underlying disease process that led to the intra-abdominal HTN and ACS, and not the open abdomen. However, patients with prolonged open abdomen management are at increased risk of developing the difficult-to-manage complication of enteroatmospheric fistula (EAF).
Management of EAF is complex but generally relies on bowel rest, nutritional support with total parenteral nutrition, scrupulous wound care, EAF isolation using negative pressure wound therapy techniques, and ultimate resection, reanastomosis, and immediate coverage with vascularized tissue. These patients generally have rather prolonged inpatient courses, measured in months, with multiple readmissions for the management of catheter-related infection and catheter-related sepsis prior to definitive repair.
An incorrect diagnosis should be suspected when upon abdominal decompression there is no blood, clot, or ascites; the viscera are not edematous; and the intestines do not spontaneously sit above the level of the skin. This situation is quite rare.
Follow-up is not different from standard ICU care with the exception that the patient should undergo regular (every 48-72 hours) abdominal washouts to reduce the bacterial burden of the peritoneal space and to limit the adhesions between the viscera and the posterior aspect of the anterior abdominal wall. Limiting adhesions in this way preserves the ability of the abdominal wall to move and be repositioned in anticipation of ultimate closure.
The underpinnings of this syndrome from a pathophysiologic perspective are straightforward and are familiar to clinicians in multiple settings including extremity or thoracic compartment syndrome, as well as intracranial hypertension as explained by the Monroe-Kellie doctrine. In essence, all compartment syndromes have dysregulation of the normal pressure/volume relationships for that tightly bounded compartment.
It does not matter if the boundary is bone or fascia, it matters that there is too much volume in the compartment relative to the compartment’s ability to stretch, distend, or accommodate. In the abdomen, there are multiple elements that can increase in size and therefore serve as a space-occupying lesion in either the peritoneal space or the retroperitoneum. Blood, clot, ascites, edematous viscera, gas, as well as lap pads left during a damage-control procedure, can all lead to an intolerable increase in IAP.
As the pressure climbs within the abdomen, the venous return is progressively compromised, the diaphragms are displaced cranially, and these untoward side effects give rise to the early clinical expressions of impending ACS. The clinician identifies these events as hypotension, hypoxemia, hypercarbia, oliguria, and reduced pulmonary compliance. As the IAP continues to climb, progressive organ failure from a decrease in the net flow across the organ system from a reduced MAP and a higher venous outflow pressure lead to multi-system organ failure and, if unrelieved, death.
Currently unexplored is the concept of organ-specific compartment syndrome. Certain organs such as the kidney reside in a tightly bounded fascial compartment, Gerota’s capsule. Blunt injury that does not disrupt the capsule but does injure the kidney may create unacceptable pressures within the capsule and lead to an organ-specific compartment syndrome. At present, we do not have the ability to readily and reliably measure these pressures, nor are there criteria nor recommendations as to when to (if ever) decompress injured kidneys.
Similar arguments may be advanced for the liver with large subcapsular hematomas. The spleen is a different situation, as one can readily survive without a spleen, or with only part of the spleen, without other interventions besides a polyvalent vaccine. Renal or hepatic loss may be addressed with extracorporeal techniques such as dialysis or solid organ transplantation. Thus, it may be more appropriate to investigate whether it is appropriate to decompress these organs or not.
The epidemiology is in flux with regard to ACS. In part, the epidemiology depends on the vigor with which one investigates the presence or absence of intra-abdominal HTN. If one does not measure IAP, then the ACS generally will not be recognized and one’s epidemiology will be nil. As recognition of the importance of IAP, intra-abdominal HTN, and ACS becomes more prevalent, it is likely that there will be a relatively substantial increase in the recorded incidence.
Prognosis depends less upon having had an ACS and more upon the underlying cause that led to the compartment syndrome. Clearly if the syndrome is related to colonic insufflation during colonoscopic biopsy as an outpatient, the prognosis is superb. If, on the other hand, the ACS is related to visceral edema and hemorrhage from a Grade V liver laceration in the setting of traumatic brain injury with a large subdural hematoma with midline shift, pelvic and extremity fractures, and severe pulmonary contusions related to a flail chest and sternal fracture in an 82-year-old on aspirin and therapeutic warfarin, the prognosis is rather grim.
Generally, the ACS leads to an open abdomen approach for management, and prognosis is indeed negatively affected if the patient develops an EAF or tertiary peritonitis (a reflection of the failure of host defense). In general, outcome is related to the presence of organ failure with increasing mortality corresponding to increasing numbers of failed organs.
A special note is made of those with pre-existing hepatic failure and the ACS leading to an open abdomen. This patient population has a nearly uniformly dismal prognosis related to coagulopathy, severe protein-calorie malnutrition, impaired host defense, and ongoing protein, salt, and water losses via their open abdomen in generally massive ascites.
Special considerations for nursing and allied health professionals.
I would suggest addressing issues with pressure ulceration, turning with an open abdomen, adjustment of ventilator settings with on open anterior abdominal wall, explaining the increased work of breathing due to the loss of the zone of apposition with respect to weaning, and how to address protein loss via the open abdomen with respect to the nutritional prescription.
What's the evidence?
Ball, CG, Kirkpatrick, AW, McBeth, P. “The secondary abdominal compartment syndrome: not just another posttraumatic complication”. Can J Surg. vol. 51. 2008. pp. 399-405. (An evidence-based review of secondary ACS and its management.)
Balogh, Z, McKinley, BA, Holcomb, JB. “Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure”. J Trauma. vol. 54. 2003. pp. 848-59. (This study demonstrates the predictability of ACS on ICU admission and highlights the need for early and close monitoring of high-risk patients.)
Cheatham, ML, Malbrain, MLNG, Kirkpatrick, A. “Results from the conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. Part II: recommendations”. Intensive Care Med. vol. 33. 2007. pp. 951-62. (An evidence-based review of the current consensus recommendations for intra-abdominal HTN and ACS.)
Cheatham, ML, Safcsak, K. “Long-term impact of abdominal decompression: a prospective comparative analysis”. J Am Coll Surg. vol. 207. 2008. pp. 573-9. (Abdominal decompression does not negatively affect long-term physical or mental health perception, quality of life, or ability to resume employment.)
Daugherty, EL, Hongyan, L, Taichman, D. “Abdominal compartment syndrome is common in medical intensive care unit patients receiving large-volume resuscitation”. J Intensive Care Med. vol. 22. 2007. pp. 294-9. (A prospective cohort study of MICU patients and the incidence of ACS in patients receiving high-volume resuscitation.)
Maerz, L, Kaplan, LJ. “Abdominal compartment syndrome”. Crit Care Med. vol. 36. 2008. pp. S212-5. (A review of the pathophysiology, diagnosis, and therapy of intra-abdominal HTN/ACS.)
Malbrain, MLNG, Cheatham, ML, Kirkpatrick, A. “Results from the conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. Part I: definitions”. Intensive Care Med. vol. 32. 2006. pp. 1722-32. (Review of the current consensus definitions of intra-abdominal HTN and ACS.)
Malbrain, ML, Chiumello, D, Pelosi, P. “Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study”. Crit Care Med. vol. 33. 2005. pp. 315-22. (This study is a multi-center, international description of intra-abdominal HTN in the critically ill and its relationship to outcomes.)
Scalea, TM, Bochicchio, GV, Habashi, N. “Increased intra-abdominal, intrathoracic, and intracranial pressure after severe brain injury: multiple compartment syndrome”. J Trauma. vol. 62. 2007. pp. 647-656. (Intra-abdominal hypertension increases intracranial pressures, and IAP should be followed closely in patients with traumatic brain injury.)
Gracias, VH, Braslow, B, Johnson, J. “Abdominal compartment syndrome in the open abdomen”. Arch Surg. vol. 137. 2000. pp. 1298-1300. (Incidence of ACS in patients with an open abdomen.)
Madigan, MC, Kemp, CD, Johnson, JC, Cotton, BA. “Secondary abdominal compartment syndrome after severe extremity injury: are early, aggressive fluid resuscitation strategies to blame”. J Trauma. vol. 64. 2008. pp. 280-5. (Aggressive fluid resuscitation increases the likelihood of developing secondary ACS in trauma patients.)
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- Abdominal compartment syndrome (ACS)
- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
- 4. Specific Treatment
- 5. Disease monitoring, follow-up and disposition
- Special considerations for nursing and allied health professionals.
- What's the evidence?