Abdominal Compartment Syndrome

Abdominal Compartment Syndrome (ACS), marked by heightened pressure in the abdominal cavity, poses a severe risk to critically ill patients, often leading to multisystem organ failure. Established in 2004, the World Society of Abdominal Compartment Syndrome (WSACS) standardized ACS definitions and guidelines due to underdiagnosis. Intra-abdominal pressure (IAP) is a critical metric, and ACS is diagnosed when IAP exceeds 20 mm Hg, with organ dysfunction possible before this threshold. Failure to promptly recognize and manage ACS is an independent predictor of mortality. Clinical suspicion, protocolized monitoring, and swift intervention are crucial, emphasizing the potential for reversible organ dysfunction with early identification and intervention.

Abdominal compliance, contingent on the elasticity of the abdominal wall and diaphragm, plays a pivotal role in physiological equilibrium. Elevated intra-abdominal pressure (IAP) disrupts this balance, causing vasculature dysfunction characterized by compromised vasomotor tone and endothelial intercellular junctions. Additionally, IAH prompts increased antidiuretic hormone release, exacerbating volume retention.

The World Society of Abdominal Compartment Syndrome (WSACS) stratifies IAH into four grades:

• Grade I (IAP 12-15 mm Hg):
• Grade II (IAP 16-20 mm Hg):
• Grade III (IAP 21-25 mm Hg):
• Grade IV (IAP >25 mm Hg):

Grades III and IV, with IAP exceeding 20 mm Hg, raise suspicion for ACS. Surgical procedures carrying a high IAH risk include liver transplantation, damage control surgery, and abdominal aneurysm repair.

ACS may stem from primary causes like trauma or secondary factors such as ascites or pregnancy. Chronic IAP elevation occurs in conditions like obesity and cirrhosis, with higher body mass index correlating with baseline IAP increase.

Various factors contribute to IAH and ACS, categorized as:

• Diminished Abdominal Wall Compliance:
  • Abdominal surgery
  • Intra-abdominal adhesions
  • Major trauma
  • Major burns
  • Mechanical ventilation
  • Obesity
• Increased Intraluminal Volume:
  • Gastroparesis
  • Gastric distension
  • Ileus
  • Constipation
  • Toxic megacolon
  • Volvulus
• Increased Extraluminal Abdominal Volume:
  • Hemoperitoneum
  • Pneumoperitoneum
  • Severe pancreatitis
  • Liver failure with ascites
  • Retroperitoneal or intra-abdominal tumors
  • Intra-abdominal abscesses
  • Laparoscopy with excessive insufflation pressures
  • Peritoneal dialysis
• Capillary Leak/Fluid Resuscitation:
  • Damage control surgery
  • Bacteremia
  • Systemic inflammation
  • Coagulopathy
  • Sepsis
  • Massive fluid administration
  • Blood product transfusion

Pathophysiology

Elevated intra-abdominal pressures exert profound effects on various organ systems, precipitating complex pathophysiological changes.

Cardiovascular System: IAH induces compression of the inferior vena cava, impeding venous return and causing lower extremity edema. Reduced venous return diminishes cardiac output, leading to decreased blood and oxygen delivery to peripheral tissues. Additionally, elevated IAP prompts diaphragmatic elevation, increasing intra-thoracic pressures, and directly compressing the heart, ultimately compromising ventricular compliance.

Pulmonary System: Increased intrathoracic pressures restrict pulmonary compliance, reducing tidal volume and functional residual capacity while elevating pulmonary vascular resistance. Rising airway pressures hinder ventilation, causing difficulties in gas exchange. Alveolar atelectasis contributes to increased dead space, resulting in hypoxemia and hypercarbia.

Renal System: IAH compromises renal function by impeding arterial and venous blood flow, diminishing the glomerular filtration rate, and causing acute kidney injury with reduced urine output. Blood diversion from the renal cortex further exacerbates dysfunction. Activation of the renin-angiotensin-aldosterone system increases systemic vascular resistance and water-sodium reabsorption, with oliguria occurring at an IAP of 15 mm Hg and anuria at 30 mm Hg.

Gastrointestinal System: Reduced abdominal compliance under increased IAP leads to diminished splanchnic blood flow, resulting in tissue hypoxia, increased capillary permeability, and edema. This sets the stage for an inflammatory response, aggravates intestinal malperfusion, and heightens the risk of bacterial translocation and infection. Hepatic system impairment ensues, with decreased flow impacting metabolism and clearance, contributing to metabolic acidosis.

Nervous System: Elevated IAP diminishes venous drainage from the brain, escalating intracranial pressure and decreasing cerebral blood flow. Increased PaCO2 further amplifies arterial blood flow to the brain, exacerbating intracranial pressure. This intricate interplay within the nervous system underscores the multifaceted consequences of elevated intra-abdominal pressure in Abdominal Compartment Syndrome.

Evaluation of Abdominal Compartment Syndrome

1. Imaging Modalities:
   • While not standard for ACS diagnosis, imaging can reveal early indicators of intra-abdominal hypertension (IAH), a precursor to ACS.
   • Early signs on imaging include peritoneal-to-abdominal height ratio >0.52, maximal anteroposterior to transverse abdominal diameter ratio >0.8, bowel wall thickening, diaphragm elevation, vena cava narrowing (<3 mm), and significant intra-abdominal fluid.
2. Intra-Abdominal Pressure (IAP) Measurement:
   • Direct Methods:
     • Utilize pressure transducers (e.g., Veress needle during laparoscopic surgery) or intraperitoneal catheters (e.g., peritoneal dialysis catheter).
     • Highly accurate but invasive.
   • Indirect Method (Most Accepted):
     • Measure IAP through intravesicular catheter pressures.
     • Aseptically clamp Foley catheter, connect to a 3-way stopcock adjusted to mid-axillary line at iliac crest for transducer zeroing.
     • Inject 25 cc sterile saline into the bladder.
     • Measure at end-expiration in complete supine position.
     • Normal pressures below 5 mm Hg; 10-15 mm Hg post-surgery and in obese patients; >25 mm Hg highly suspicious of ACS.
     • Trend measurements every 6 hours for potential ACS development.
     • Contraindications include bladder trauma, neurogenic bladder, benign prostatic hypertrophy, and pelvic hematoma.
3. Alternative Screening Methods for IAH:
   • Central Line Placement:
     • Measures inferior vena cava (IVC) pressure.
   • Manometry through Jackson-Pratt Drain:
     • Less common, measures pressure through a drain.
   • Intragastric Pressure Measurement (Nasogastric Tube):
     • Less validated and infrequently used.
4. Considerations:
   • If bladder measurements are unavailable, alternative methods may be considered.
   • Be cautious of potential inaccuracies in measurements due to pelvic fractures, bladder hematomas, peritoneal adhesions, or other contraindications.

This step-by-step evaluation emphasizes the importance of a comprehensive approach, ranging from early imaging indicators to the gold standard of IAP measurement, allowing for timely identification and intervention in cases of Abdominal Compartment Syndrome.

Comprehensive Management

Managing Abdominal Compartment Syndrome (ACS) involves a nuanced approach, considering the etiology of elevated intra-abdominal pressure (IAP), duration of elevation, and the degree of organ dysfunction.

1. Non-Surgical Interventions:
   • Intervention choice and timing depend on factors such as etiology, IAP duration, and organ dysfunction.
   • Nonsurgical measures include nasogastric decompression, rectal tube decompression, endoscopic decompression, and percutaneous drainage for ascites or hematoma.
   • Improving abdominal wall compliance through sedation, neuromuscular blockade, and dressings/eschar release is crucial.
   • WSACS recommendations include optimizing fluid administration, resuscitation with hypertonic products or colloids, and consideration of hemodialysis or ultrafiltration. However, evidence quality is low.
2. Percutaneous Catheter Drainage:
   • Suitable for ACS caused by increased extraluminal abdominal volume (air, fluid, or blood).
   • Less invasive than surgical laparotomy and can be a temporary solution when immediate surgery is not viable.
3. Surgical Decompression:
   • Considered if conservative measures fail, and organ dysfunction persists.
   • Emergent laparotomy provides rapid relief, especially when compromised blood flow or mechanical obstruction contributes to organ dysfunction.
   • After surgical decompression, temporary open abdomen management with negative pressure dressing helps prevent infections, reduces insensible losses, and minimizes fascial retraction.
   • Fascial closure, using mesh or primary techniques, can be attempted in subsequent evaluations.
4. Complications of Surgical Decompression:
   • Fistula formation, protein loss, abdominal wall retraction with hernia development, and wound infections are potential complications.
   • Up to 20% of cases may experience recurrent ACS, either due to ongoing causative factors or inadequate IAP reduction.
5. Debates on Ideal Timing for Surgical Decompression:
   • Despite extensive literature, the ideal timing for surgical intervention remains debated.
   • Early surgery may stress the patient, necessitating consideration of surgery after multiple conservative management attempts.

In summary, ACS management requires a tailored approach balancing non-surgical and surgical interventions based on the patient’s unique circumstances. While surgical decompression is definitive, it poses complications, and the timing should be judiciously determined after exhausting conservative measures. The overarching goal is to alleviate elevated IAP, restore organ function, and optimize patient outcomes.

Prognosis:

Untreated abdominal compartment syndrome (ACS) carries a grave prognosis, and delayed intervention is strongly associated with high mortality rates. Intra-abdominal hypertension (IAH) serves as an independent predictor of mortality, with each grade indicating a progressive worsening of outcomes. Many case series highlight the substantial impact of resulting multiorgan failure, often extending the recovery period to weeks or even months, despite treatment. Patients with ACS frequently experience prolonged dependency on mechanical ventilation, dialysis, and extended hospital stays, underscoring the severity and long-term implications of the condition.

Differential Diagnosis:

The differential diagnosis for ACS encompasses various conditions that share clinical features:

1. Mesenteric Ischemia:
   • Impaired blood supply to the intestines leading to abdominal pain and potential organ damage.
2. Ruptured Abdominal Aortic Aneurysm:
   • Emergency characterized by the tearing of the aorta, causing severe abdominal pain and potential life-threatening bleeding.
3. Toxic Megacolon:
   • A complication of inflammatory bowel disease with severe inflammation and dilation of the colon.
4. Acute Appendicitis:
   • Inflammation of the appendix presenting with localized abdominal pain.
5. Acute Diverticulitis:
   • Inflammation or infection of small pouches in the intestinal wall, often causing abdominal pain and tenderness.

Complications:

1. Renal Failure:
   • Impaired kidney function due to reduced blood flow and increased intra-abdominal pressure.
2. Bowel Ischemia:
   • Reduced blood supply to the intestines leading to tissue damage and potential necrosis.
3. Respiratory Distress or Failure:
   • Elevated intra-abdominal pressure restricting diaphragmatic movement, impacting respiratory function.
4. Increased Cranial Pressure:
   • Diminished venous drainage from the brain, causing elevated intracranial pressure.
5. Cardiac Failure:
   • Reduced venous return and compromised cardiac output due to increased intra-abdominal pressure.
6. Potential Death:
   • If left untreated or if intervention is significantly delayed, ACS can lead to fatal outcomes.

The complications associated with ACS highlight the systemic impact of elevated intra-abdominal pressure on vital organs, emphasizing the critical need for prompt diagnosis and intervention.