ABDOMINAL COMPARTMENT SYNDROME

ByMahmoud Zaghloul Raslan, MD

Surgical Consultant, MGH, Madina

Introduction● Abdominal compartment syndrome

refers to organ dysfunction caused by intraabdominal hypertension (IAH).

● It may be under-recognized because: - it primarily affects patients who are already quite ill - organ dysfunction may be incorrectly ascribed to progression of the primary illness.

● Since treatment can improve organ dysfunction, it is important that the diagnosis be considered in the appropriate clinical situation without any delay

Definitions● Intraabdominal hypertension

(IAH) and abdominal compartment syndrome (ACS) are distinct clinical entities and should not be used interchangeably.

● Intraabdominal pressure (IAP) : It is the steady state pressure concealed

within the abdominal cavity. For most critically ill patients, an IAP of 5 to 7 mmHg is considered normal.

● Patients with increased abdominal girth that developed slowly e.g. the mobidly obese and pregnant individuals may have chronically higher baseline IAP (as high as 10 to 15 mmHg) without adverse sequelae

Abdominal perfusion pressure (APP): ● It is calculated as the mean arterial pressure (MAP) minus the IAP

APP = MAP - IAP.

● Elevated IAP reduces blood flow to the abdominal viscera

● Abdominal perfusion pressure (APP) was found to be better than other resuscitation endpoints e.g. hourly urinary output for predicting the outcomes.

● A target APP of at least 60 mmHg is correlated with improved survival from IAH and ACS.

● Intraabdominal hypertension (IAH) It is defined as a sustained IAP of ≥12 mmHg.

● Intraabdominal hypertension (IAH) can be further graded as follows: - Grade I = IAP 12 to 15 mmHg - Grade II = IAP 16 to 20 mmHg - Grade III = IAP 21 to 25 mmHg - Grade IV = IAP >25 mmHg.

● Hyperacute IAH : - Elevation of the IAP lasting only seconds. - It is due to laughing, coughing, straining, sneezing, defecation, or physical activity. IAH with ACS due to gastric over-distention following endoscopy has been described.

● Acute IAH: - Elevation of the IAP that develops over hours. - It is usually the result of trauma or intraabdominal hemorrhage and can lead to the rapid development of ACS.

● Subacute IAH :- Elevation of the IAP that develops over days. - It is most common in medical patients and can also lead to ACS.

● Chronic IAH:- Elevation of IAP that develops over months (pregnancy) or years (morbid obesity). - It does not cause ACS, but does place the individual at higher risk for ACS if they develop superimposed acute or subacute IAH.

● Abdominal compartment syndrome (ACS): - It is defined as a sustained IAP >20 mmHg (with or without APP <60 mmHg) that is associated with new organ dysfunction.

● For clinical purposes, ACS is better defined as IAH-induced new organ dysfunction without a strict IAP threshold, because no IAP can predictably diagnose ACS in all patients.

● Patients with an IAP < 10 mmHg generally do not have ACS, while patients with an IAP > 25 mmHg usually have ACS.

● Patients with an IAP 10-25 mmHg may or may not have ACS, depending upon individual variables such as blood pressure and abdominal wall compliance.

● Higher systemic blood pressure may maintain abdominal organ perfusion when IAP is increased, since the abdominal perfusion pressure (APP) is the difference between the mean arterial pressure and the IAP.

● Abdominal wall compliance initially minimizes the extent to which an increasing abdominal girth can elevate IAP .

- When a critical abdominal girth is reached, abdominal wall compliance decreases abruptly. Further increases in abdominal girth beyond this critical level result in a rapid rise of IAP and ACS if untreated.

- Increased abdominal wall compliance due to chronic increased abdominal girth (e.g. pregnancy, cirrhosis with ascites, morbid obesity) may protect against ACS .

Epidemiology● The incidence of IAH is less

well characterized.- The incidence of ACS

in trauma patients varies considerably.

- It ranges from 1 to 14 percent in different studies.

● ACS was considered present if there was:

- persistent IAH- progressive organ dysfunction despite resuscitation and - improvement following

decompression

Etiology & risk factors● ACS can be classified as:

- Primary ACS is due to injury or disease in the abdominopelvic region (e.g. abdominal trauma, hemoperitoneum, pancreatitis); intervention (surgical or radiologic) of the primary condition is often needed.

- Secondary ACS refers to conditions that do not originate in the abdomen or pelvis (e.g. fluid resuscitation, sepsis, burns).

- Recurrent ACS defines a condition in which ACS develops again following previous surgical or medical treatment of primary or secondary ACS

● ACS generally occurs in patients who are critically ill due to any of a wide variety of medical and surgical conditions. Some of these include:-Trauma : Injured patients in shock who require aggressive fluid resuscitation are at risk for ACS.

- Burns: Patients with severe burns (>30 percent total body surface area) with or without concomitant trauma are also at risk for ACS. Importantly, ACS must be distinguished from other intraabdominal problems that occur in these critically ill patients (eg, necrotizing enterocolitis, ischemic bowel).

- Liver transplantation: IAH (IAP >25 mmHg) was found following liver transplantation in 32% patients.

- Abdominal conditions : Massive ascites, bowel distension, abdominal surgery, or intraperitoneal bleeding can increase intraabdominal pressure.

- Retroperitoneal conditions: Retroperitoneal pathologies, such as ruptured abdominal aortic aneurysm, pelvic fracture with bleeding, and pancreatitis, can lead to ACS.

- Medical illness: Conditions that require extensive fluid resuscitation (e.g. sepsis) and are associated with third spacing of fluids and tissue edema can increase IAP.

- Post-surgical patients: Patients undergoing operations in which they are given large volume resuscitation, particularly with crystalloid in the face of hemorrhagic or septic shock, are at risk for ACS.

Physiologic consequences

● IAH can impaire the function of nearly every organ system, thereby causing ACS .

Clinical presentation● It is desirable to recognize IAH early, so it

can be treated before progressing to ACS.

● Symptoms: - Most patients who develop ACS are

critically ill and unable to communicate.

- The rare patient who is able to convey symptoms may complain of malaise, weakness, lightheadedness, dyspnea, abdominal bloating, or abdominal pain.

● Physical signs: - Nearly all patients with ACS have

a tensely distended abdomen. Despite this, physical examination of the abdomen is a poor predictor of ACS.

- Progressive oliguria and increased ventilatory requirements are also common in patients with ACS.

- Other findings may include hypotension, tachycardia, an elevated jugular venous pressure, jugular venous distension, peripheral edema, abdominal tenderness, or acute pulmonary decompensation.

- There may also be evidence of hypoperfusion, including cool skin, obtundation, restlessness, or lactic acidosis

● Imaging findings: - Imaging is not helpful in the diagnosis of

ACS.

- CXR may show decreased lung volumes, atelectasis, or elevated hemidiaphragms.

- Computed tomography (CT) may demonstrate tense infiltration of the retroperitoneum that is out of proportion to peritoneal disease, extrinsic compression of the inferior vena cava, massive abdominal distention, direct renal compression or displacement, bowel wall thickening, or bilateral inguinal herniation

Diagnostic evaluation● Definitive diagnosis of ACS

requires measurement of the IAP.

● This is particularly true for patients who have trauma, liver transplantation, bowel obstruction, pancreatitis, or peritonitis because these conditions are known to be associated with ACS.

● Measurement of intraabdominal pressure: - IAP can be measured indirectly using intragastric, intracolonic, intravesical (bladder), or inferior vena cava catheters.

● Measurement of bladder (ie, intravesical) pressure is the standard method to screen for IAH and ACS. It is simple, minimally invasive, and accurate.

Indications for IAP monitoring● Postoperative (abdom. Surgery) pts● Pts with abdominal trauma● Ventilated pts with other Organ

Failure● Pts with signs of ACS:

Oliguria, hypoxia, hypotension, acidosis, mesenteric ischemia, ileus, elevated ICP.

● Pts with high cumulative fluid balance● Pts with abdominal packing

Management approach● Management of IAH and ACS

consists of supportive care and, when needed, abdominal decompression.

● Some exceptions include escharotomy release to relieve mechanical limitations due to burn eschars and percutaneous catheter decompression to relieve tense ascites.

● Supportive care: - Goals:

- Reduction of intraabdominal volume.

- Measures to improve abdominal wall compliance .

● Nasogastric and rectal drainage are a simple means for reducing IAP in patients with bowel distension.

● Hemoperitoneum, ascites, intraabdominal abscess and retroperitoneal hematoma occupy space and can elevate IAP. In some cases, these collections can be evacuated using percutaneous techniques.

● Patient should be placed in a supine position.

● Abdominal wall compliance can be improved with adequate pain control and sedation.

● Ventilatory support:- High peak and mean airway pressures can be problematic. Tidal volume reduction, a pressure-limited mode, and/or permissive hypercapnia may be necessary.

● Positive end-expiratory pressure (PEEP) may reduce ventilation-perfusion mismatch and improve hypoxemia.

● Hemodynamic support:

- For patients with IAH, limiting the amount of fluid administration may decrease the risk of developing ACS.

- Some clinicians prefer to use colloids under this circumstance instead of crystalloids.

● There is no role for diuretic therapy in the resuscitation of patients with acute ACS.

● The only appropriate management is to open the abdomen.

Surgical decompression● SURGICAL DECOMPRESSION: - There is general agreement that

surgical decompression is indicated for ACS.

- Decompressing the abdomen prior to the development of ACS is becoming increasingly common and may improve survival.

● Various approaches include:- Surgical decompression for all patients whose IAP is greater than 25 mmHg.

- Many clinicians suggest surgical decompression at a lower IAP (e.g. 15 to 25 mmHg.

● Surgical decompression is considered when the IAP is 20 mmHg or greater, regardless of signs of ACS..

● Most surgeons perform decompression and then maintain an open abdomen using temporary abdominal wall closure.

● Surgical decompression can be performed in the operating room if the patient is medically stable for transfer or at the bedside in the intensive care unit.

Morbidity and mortality● MORBIDITY AND MORTALITY:

- Failure to recognize IAH prior to the development of ACS causes tissue hypoperfusion, which may lead to multisystem organ failure, and potentially death.

- Although the development of IAH alone is not a predictor of multiorgan failure, mortality for patients who have progressed to ACS range from 40 to 100%.

Open abdomen● INTRODUCTION:

- Refers to a defect in the abdominal wall that exposes the abdominal viscera.

● Damage control surgery associated with trauma and ACS is the most frequent reason for open abdomen.

● Etiology: - The most common circumstances

that result in open abdomen include the following:

1. Damage control surgery:- It is an operative strategy that is used to manage immediately life-threatening conditions by delaying definitive management of less severe

2. Abdominal compartment syndrome (ACS):

-Increased volume in the abdomen is typically the result of an increase in interstitial fluid as is seen with large volume resuscitation, but space occupying fluid (blood or ascites) in the peritoneum or retroperitoneum can also contribute.

3. Septic abdomen: - Bowel perforation with severe contamination of the peritoneal cavity can result in recurrent intra-abdominal sepsis.

- Under this circumstance, it may be desirable to leave the abdominal wall open and use negative-pressure wound therapy to remove residual or reaccumulated fluid or pus.

4. Refractory intracranial hypertension :- A more controversial indication for open abdomen is refractory intracranial hypertension associated with traumatic brain injury.

● Complications of open abdomen:

Related to fluid efflux from the abdomen, exposure of the bowel, and abdominal muscle retraction.

- Fluid loss: - A significant amount of fluid can be lost through an open abdomen.

- Protein loss: – The fluid that is secreted by the peritoneum is rich in protein with about 2 grams of protein lost from the abdomen for each liter of fluid removed.

- Fistula formation: – With open abdomen, the bowel is frequently manipulated and is at risk for injury.

- Loss of domain: - With open abdomen from a midline

abdominal incision, the musculature of the abdominal wall retracts the fascia laterally.

- The use of a negative pressure wound system helps to counteract the lateral forces on the abdominal wall and may allow primary closure of the fascia and skin .

● Temporary closure techniques: - In some patients, delayed primary

closure of the abdominal fascia is possible once edema subsides. However, if closure is premature, ACS can recur.

● ABDOMINAL CLOSURE — Each time the patient is returned to the operating room, the abdomen is assessed for potential closure.

● Fascial closure:

1. Primary fascial closure: - Associated with the lowest rate of complications following management of the open abdomen.

- Because of the high hernia rate, biologic mesh reinforcement during primary fascial closure is frequently used.

2. Functional closure:

- Functional closure refers to the bridging of a residual fascial defect with a biologic mesh (in-lay technique).

- Once the biologic mesh is placed, the skin is closed over surgical drains placed into the subcutaneous space.

3. Planned ventral hernia: - If primary fascial closure or

functional closure cannot be achieved.

- Skin-only closure: A skin-only closure approximates the skin over the fascial defect leaving a ventral hernia.

- Split-thickness skin graft:

- If the skin cannot be approximated, the viscera within the wound are allowed to adhere to each other and to the abdominal wall. Once the abdominal contents have “solidified” and there is a healthy bed of granulation tissue overlying the bowel, a split-thickness skin graft can be placed.

Summary and recommendations● Increased IAP is called intraabdominal

hypertension (IAH). Abdominal compartment syndrome (ACS) refers to organ dysfunction caused by intraabdominal hypertension.

● ACS can impair the function of nearly every organ system.

● Diagnosis of ACS requires that IAP be measured. Symptoms, physical signs, and imaging findings are insufficient to diagnose ACS.

● Management initially consists of careful observation and supportive care. In some cases abdominal compartment decompression is required.

● We suggest that surgical decompression is not delayed until the development of ACS (Grade 2C).

● Following surgical decompression, an open abdomen is maintained using a variety of temporary abdominal closure techniques.

● Following temporary abdominal closure, the patient is monitored in ICU.

- Abdominal dressings associated with the closure (adhesive dressings, gauze, negative pressure systems) are changed, as needed, and the abdominal contents inspected every two to three days.

● We suggest the use of a negative pressure system (towel or sponge based) to control and quantify fluid loss (Grade 2C).

● Once the indication for the open abdomen has resolved, the abdomen is closed, preferably with a primary fascial closure. If primary fascial closure cannot be achieved, functional closure can be performed.

● If the gap between the fascia is deemed to be too large for a functional closure, primary skin closure can be performed, or skin grafts placed once a layer of granulation tissue has developed.

● The message is:

- Be ACS-minded.- Decompress early.- Apply TAC techniques.- Definitive abdominal closure as early as possible.

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