Abdominal Compartment Syndrome, Open Abdomen, Enterocutaneous Fistulae
James F. Whelan
Michel B. Aboutanos
Rao R. Ivatury
I. Abdominal Compartement Syndrome (ACS)
Introduction
Abdominal compartment syndrome (ACS) is a clinical condition in which intra-abdominal hypertension (IAH) leads to impaired end-organ perfusion. If left untreated or unrecognized, this hypoperfusion will lead to gut ischemia, renal insufficiency, and multiple organ dysfunction syndrome. IAH also causes elevation of the diaphragm with resultant respiratory embarrassment and decreased cardiac return to the heart leading to decreased cardiac output and further deterioration in end-organ perfusion. Onset can be insidious or fulminant; clinicians must be astute in making the diagnosis. Mortality of ACS ranges from 42% to 68% after detection and treatment and 100% in those not undergoing decompression. Reduced rates of morbidity and mortality depend on early and aggressive detection and management.
Clinical scenarios
The most common inciting event in the development of ACS is major abdominal trauma. ACS has also been reported after ruptured abdominal aortic aneurysm repair, intraperitoneal hemorrhage, pancreatitis, ileus, intestinal obstruction, post-operative bowel edema, pneumoperitoneum (e.g., secondary to barotrauma), septic shock, overzealous resuscitation, neoplasm, and liver transplantation.
Classification
Two types of ACS have now been described, primary and secondary. The following are the definitions from a consensus conference of the World Society of Abdominal Compartment Syndrome (WSACS):
Primary ACS is caused by a condition associated with injury or disease in the abdominopelvic region that frequently requires surgical or interventional radiologic intervention, or a condition that develops following abdominal surgery such as abdominal organ injuries requiring surgical repair or damage control surgery. Visceral edema from third space losses and ongoing bleeding (surgical and disseminated intravascular coagulopathy) are important factors in the development of primary ACS.
Secondary ACS is caused by conditions that do not originate from the abdomen such as sepsis with associated capillary leak, major burns, major soft tissue and skeletal trauma, or other conditions requiring massive fluid resuscitation. The chief mechanism appears to be fluid sequestration within the viscera due to reperfusion injury and increased capillary permeability. Any patient undergoing massive resuscitation (>10L crystalloid or >10 units of packed red blood cells [PRBCs]) is at risk for the development of IAH and ACS.
Recurrent ACS is a condition in which ACS develops following prophylactic or therapeutic surgical or medical treatment of primary or secondary ACS (e.g., persistence of ACS after decompressive laparotomy) or development of a new ACS episode following definitive closure of the abdominal wall after the previous utilization of a temporary abdominal wall closure.
Clinical manifestations
Diagnosis of ACS should be considered in any trauma or ICU patient with oliguria and abdominal distension or any patient requiring massive resuscitation. Physical examination will not always reveal a distended firm abdomen and is not a reliable
marker for IAH or the development of ACS. Liberal use of bladder pressure measurements is recommended.
Pulmonary effects occur via elevation of the diaphragm, which results in decreased thoracic compliance and elevated peak airway pressures (>40 to 60 cm H2O). The end results are hypoxia, hypercapnia, and respiratory acidosis.
Cardiac manifestations occur due to elevated thoracic pressure, which causes falsely elevated filling pressures (central venous pressure [CVP] and pulmonary capillary wedge pressure [PCWP]), decreased venous return to the heart, and decreased cardiac compliance. The end result is low cardiac output and decreased end-organ perfusion.
Renal effects result from direct parenchymal and caval compression, and decreased cardiac output causing decreased renal blood flow, depressed glomerular filtration rate (GFR) and oliguria.
Gastrointestinal (GI) effects occur from hypoperfusion of the splanchnic beds (direct compression and decreased cardiac output) leading to bacterial translocation and increased septic complications.
Diagnosis
Intra-abdominal pressure (IAP) measurements are essential to the diagnosis of IAH and ACS.
Bladder pressure measurement is the standard for estimation of IAP and can be performed at the bedside with the use of the arterial line pressure transducer.
Technique:
Cross-clamp the Foley catheter drainage tubing just distal to the aspiration port.
Inject 50 to 100 cc of sterile saline into the bladder with a catheter-tipped syringe via the Foley catheter and reconnect to the drainage tubing.
Connect a 16 gauge needle to the arterial line pressure tubing; flush and insert into the aspiration port.
Zero the system at the symphysis pubis while the patient is supine.
IAH is defined by a sustained increase in IAP of 12 mm Hg or more, recorded by a minimum of three standardized measurements conducted 4 to 6 hours apart, with or without a low abdominal perfusion pressure (APP) <60 mm Hg.
Key Definition: APP = MAP (mean arterial pressure) − IAP (intra-abdominal pressure)
ACS is defined as a sustained increase in IAP of 15 to 20 mm Hg or more with or without APP <60 mm Hg and single or multiple organ dysfunction or failure.
Treatment
The current state-of-the-art management of IAH/ACS according to WSACS recommendations is based upon four general principles:
Serial monitoring of IAP. The critical IAP that leads to IAH and ACS varies from patient to patient. The current recommendation is to serially measure APP and to maintain it above 50 to 60 mm Hg in patients with IAH/ACS.
Optimization of systemic perfusion and organ function should be achieved via judicious and balanced fluid resuscitation.
Institution of specific medical procedures to reduce IAP
Non-operative medical management strategies currently play a vital role in both the reduction of IAP and the prevention of organ dysfunction due to IAH. The medical management of IAP may include:
Improvement in abdominal wall compliance via body positioning (such as limiting head elevation to <20 mm Hg), sedation and analgesia to decrease thoracoabdominal muscle tone, and brief use of neuromuscular blockade mainly for mild (12 to 15 mm Hg) to moderate (16 to 20 mm Hg) IAH.
Evacuate intraluminal contents via nasogastric/colonic decompression and the use of prokinetic motility agents.
Evacuate abdominal fluid collections via percutaneous decompression. This is most useful for increased IAH and secondary ACS where elevated IAP is mainly due to fluid sequestration within the viscera.
Correcting positive fluid balance which may include restrictive/judicial fluid resuscitation, diuresis, or continuous venovenous hemofiltration/ultrafiltration.Related posts:
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