Abdominal Compartment Syndrome (ACS)
David Ray Velez, MD
The Operative Review of Surgery. 2023; 1:142-149.
Table of Contents
Definitions
Definition 1
- Intraabdominal Pressure (IAP): Steady-State Pressure Concealed within the Abdominal Cavity
- Abdominal Perfusion Pressure (APP) = MAP – IAP
- Normal IAP: 5-7 mmHg in Critically Ill Adults
- Intraabdominal Hypertension (IAH): Sustained IAP ≥ 12 mmHg
- Abdominal Compartment Syndrome (ACS): Sustained IAP > 20 mmHg that is Associated with New Organ Dysfunction/Failure
- Primary ACS: ACS that Originates from Injury or Disease in the Abdominopelvic Region
- Secondary ACS: ACS that Originates from Injury or Disease Outside of the Abdominopelvic Region
- Recurrent ACS: ACS that Recurs After a Previously Treated ACS
- Polycompartment Syndrome: Two or More Anatomical Compartments Have Elevated Compartmental Pressures
- Compartments Include Abdomen, Thorax, Head, and Extremities 2
- The Compliance of Each Compartment is Key to Determining the Transmission of Pressure Between Compartments 2
Chronic Elevation
- IAP May Be Chronically Higher in Those with Ascites, Pregnant, or Obese (7-14 mmHg) 3,4
- Acute Increases in IAP May Be Less Well Tolerated if Superimposed on Chronic IAH 5
Intraabdominal Hypertension Grading 1
- Grade I: IAP 12-15 mmHg
- Grade II: IAP 16-20 mmHg
- Grade III: IAP 21-25 mmHg
- Grade IV: IAP > 25 mmHg
Pediatric Changes 1
- Intraabdominal Hypertension: Sustained IAP > 10 mmHg
- Abdominal Compartment Syndrome: Sustained IAP > 10 mmHg that is Associated with New Organ Dysfunction/Failure
Pathophysiology
Pulmonary Effects 6,7
- Intraabdominal Hypertension Causes Upward Displacement of the Diaphragm
- Upward Displacement of the Diaphragm Causes:
- Increased Intrathoracic Pressure
- Decreased Chest Wall Compliance
- Decreased Functional Residual Capacity (FRC)
- Increased Pulmonary Vascular Resistance
- Compression Atelectasis
- Increased Intrathoracic Pressure Causes:
- Increased Pleural Pressure
- Increased Airway Pressures (Peak, Mean, and Plateau)
- Effects on Gas Exchange:
- Hypercarbia and Hypoxia
- Increased Ventilation-Perfusion Mismatch with Dead-Space Ventilation and Intrapulmonary Shunting
Cardiovascular Effects 6-8
- Intraabdominal Hypertension Causes Increased Intrathoracic Pressure
- Increased Intrathoracic Pressure Causes:
- Decreased Preload Due to Increased Central Venous Pressure (CVP) and Pulmonary Artery Pressure (PAP)
- Increased Left Ventricle Afterload Due to Vascular Resistance
- Increased Right Ventricle Afterload Can Cause Septal Deviation to the Left, Further Decreasing Preload
- Results in Decreased Cardiac Output and High Peripheral Vascular Resistance
Renal Effects 6,9
- Intraabdominal Hypertension Causes:
- Poor Renal Perfusion Due to Decreased Cardiac Output
- Renal Venous Resistance
- Direct Renal Compression with Shunting of Blood from the Cortex to the Medulla
- Activation of the RAAS System Leading to Water and Sodium Retention
- Results in Renal Impairment and Oliguria/Anuria
- *First Clinical Sign of Intraabdominal Hypertension
Gastrointestinal Effects 6-8
- Intraabdominal Hypertension Causes:
- Decreased Cardiac Output
- Increased Splanchnic Vascular Resistance
- Results in Poor Mesenteric Blood Flow
- Risk for Mucosal Ischemia and Perforation
Hepatic Effects 7,8
- Intraabdominal Hypertension Causes:
- Decreased Cardiac Output
- Increased Splanchnic Vascular Resistance
- Results in Decreased Hepatic Artery and Portal Vein Blood Flow
- Results in Decreased Liver Function and Lactate Clearance
Central Nervous System Effects 6,7
- Intraabdominal Hypertension Causes Increased Intrathoracic Pressure
- Increased Intrathoracic Pressure Causes Increased Jugular Venous Pressure and Impairs Cerebral Venous Return
- Results in Increased Intracranial Pressure (ICP) and Decreased Brain Perfusion
Extremity Effects 6
- Intraabdominal Hypertension Causes:
- Increased Central Venous Pressure
- Increased Peripheral Vascular Resistance
- Decreased Cardiac Output
- Results in Decreased Peripheral Perfusion of the Extremities
Effects of Abdominal Compartment Syndrome 7
Risk Factors
Reduced Abdominal Wall Compliance 7,10
- Obesity
- Abdominal Surgery
- Prone Positioning
- Rectus Sheath Hematoma
- Burns with Abdominal Eschar
- Mechanical Ventilation with High PEEP
- Ventilator Dyssynchrony
Increased Intraluminal Contents 7,10
- Gastric Distention
- Gastroparesis
- Ileus
- Small Bowel Obstruction
- Colonic Pseudo-Obstruction
- Volvulus
- Intraabdominal Tumor
- Retroperitoneal Tumor
- Damage Control Laparotomy
- Enteral Feeding
- Pregnancy
Abdominal Cavity Collections 7,10
- Ascites
- Hemoperitoneum
- Pneumoperitoneum
- Major Trauma
- Laparoscopy with Excessive Inflation Pressures
- Peritoneal Dialysis
- Abdominal Inflammation-Peritonitis (Pancreatitis)
- Abdominal Abscess
Capillary Leak and Fluid Resuscitation 7,10
- Acidosis
- Hypothermia
- Coagulopathy
- Massive Transfusion
- Trauma
- Sepsis
- Large Volume Fluid Resuscitation
- Major Burns
- Liver Transplant
Presentation
Symptoms 11
- Most Patients are Critically Ill and Unable to Communicate
- Fatigue and Malaise
- Dyspnea
- Lightheadedness
- Abdominal Pain
- Abdominal Distention
Physical Exam
- Tense and Distended Abdomen
- Abdominal Exam is a Poor Predictor of ACS 12-14
Additional Findings 6-9
- Pulmonary:
- Increased Airway Pressures
- Hypercarbia and Hypoxia
- Difficulty Weaning from the Ventilator
- Cardiovascular:
- Decreased Cardiac Output
- Increased Peripheral Vascular Resistance
- Renal Injury and Oliguria/Anuria
- Intestinal Ischemia and Perforation
- Elevated Intracranial Pressure (ICP)
Diagnosis
Diagnosis
- Definitive Diagnosis is Made by the Measurement of Intraabdominal Pressure (IAP) in the Setting of New Organ Dysfunction/Failure 1
- Requires IAP > 20 mmHg
- Perform with a Low Threshed of Suspicion 15
Measurement of IAP 16
- Intravesical (Bladder Pressure) – Standard Method
- Intragastric
- Intracolonic
- IVC Catheters
Requirements for Accurate Measurement 1
- Measured at End-Expiration
- Measured in the Supine Position
- Ensure that Abdominal Muscle Contractions are Absent (Sedation)
- Transducer Should be Zeroed at the Midaxillary Line
How to Measure Bladder Pressure (Procedure) 17
- Place Foley Catheter and Drain the Bladder
- Clamp Foley Catheter
- Zero Transducer at the Midaxillary Line
- Instill Sterile Saline into the Bladder (Maximum 25 cc) 1
- Insert an 18 Gauge Needle Attached to a Pressure Transducer into the Aspiration Port
- Some Commercially Available Catheters Permit Measurement by a Needle-Less Connection System
- Measure the Pressure at End-Expiration
- Wait for 60 Seconds After Instillation of Fluid to Allow Detrusor Muscle Relaxation
Treatment
Definitive Treatment
- Definitive Treatment is by Decompressive Laparotomy with Temporary Abdominal Closure 1
- Immediate Complications of Decompression:
- Bolus of Lactic Acid, Potassium and Other Anaerobic Byproducts (Induced Arrhythmia)
- Decrease in Preload (Induced Hypotension)
- Respiratory Alkalosis
- May Be Able to Avoid Laparotomy in Select Cases:
- Massive Ascites – Percutaneous Catheter Decompression/Paracentesis 18
- Burn Eschars Causing Mechanical Limitations – Escharotomy 19
Options to Temporize or Prevent Progression of IAH to ACS 20
- Place in the Supine Position and Avoid Elevating the Head of Bed
- Improve Abdominal Wall Compliance:
- Sedation and Analgesia
- Paralysis
- Reduce Intraabdominal Volume:
- Orogastric/Nasogastric Tube Decompression
- Foley Catheter
- Percutaneous Catheter Decompression/Paracentesis
- Low Tidal Volume & High PEEP
- Limit Fluid Administration
Morbidity and Mortality
- Failure to Recognize Can Cause Multisystem Organ Failure and Death
- High Mortality Once ACS Develops (40-100%) 21-25
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