Abdominal compartment syndrome

Dr. Harsoor Sidharameshwar, Head of Department,

Dr. Sapna T.S., Postgraduate,
Bangalore Medical College & Research Institute

Introduction
Abdominal compartment syndrome is a potentially lethal condition caused
by any event that produces intra-abdominal hypertension. The most common
cause is blunt abdominal trauma. Measurement of intra-abdominal pressure
(IAP) has a grade I recommendation and is a priority measure in monitoring
of polytrauma patients in the intensive care unit (ICU). Due to very poor
outcome associated, early decompression, prevention, prediction and
surveillance is prudent.

Intra-abdominal pressure
Intra-abdominal pressure (IAP) is the steady-state pressure within the
abdominal cavity.It is affected by respiratory cycle and position of the
person.

IAP is directly affected by the volume of viscera, space occupying “lesions”

like ascites, blood, fluid, tumors etc. and decreased abdominal wall
compliance as in burn eschars, third-space edema etc.

Normal IAP is approximately 5-7 mmHg in critically ill adults. Critical IAP
that causes end organ dysfunction varies among patients as a result of
difference in physiology and preexisting co-morbidities. IAP needs to be
monitored in all shock resuscitation patients irrespective of the cause like
burns, sepsis, trauma, hypovolemia.

Normal adult 0-5 mmHg

Typical ICU patient 5-7 mmHg

Post-laparotomy patient 10-15 mmHg

Patient with septic shock 15-25 mmHg

Patient with acute abdomen 25-40 mmHg

Intra - abdominal hypertension

IAH is defined as a sustained or repeated pathological elevation in

IAP ≥ 12 mmHg.

IAH is graded as follows

Grade I 12–15 mmHg

Grade II 16–20 mmHg

Grade III 21–25 mmHg
Grade IV > 25 mmHg

Abdominal Perfusion Pressure (APP)

It is analogous to Cerebral Perfusion Pressure, where it determines the

perfusion. It is measured as:

APP = MAP – IAP

Mean Arterial Pressure = MAP

Intra-abdominal Pressure = IAP

Abdominal perfusion pressure is negatively affected when MAP declines or

IAP rises. This parameter is superior to other end points of resuscitation,such
as arterial pH, lactate levels, and base deficits, in predicting survival in IAH
and ACS. Target APPs of more than 60 mm Hg are associated with
improved survival, whereas an APP of less than 50 mm Hg is associated
with increased mortality.

Abdominal Compartment Syndrome

ACS is defined as a sustained IAP > 20mmHg that is associated with new
organ dysfunction/ failure (with or without an APP < 60mmHg).

It is also described as the combination of

 1. IAP greater than 25mmHg.

2. Progressive organ dysfunction. (UO <1ml/kg/h, PaO2/FiO2<150,

Peak airway pressure > 45 cm H2O, or cardiac index <3L/min/m2 ).

3. Improved organ function after decompression.

Classification

ACS can be classified based on the duration of the syndrome, the presence
or absence of intraperitoneal pathology, and the cause of raised IAP.

I. Acute and chronic – examples of chronic ACS are morbid obesity,

pregnancy and chronic constipation.
II. Based on etiology – Trauma, burns, postoperative, pancreatitis, bowel
obstruction, Ileus, abdominal aortic aneurysm, oncological,
gynecological,
III. Relation to peritoneal cavity –
a) Primary IAH or ACS is a condition associated with injury or
disease in the abdominopelvic region that frequently requires
early surgical or interventional radiological intervention.
eg, trauma, ascitis, tumours.

b) Secondary IAH or ACS refers to conditions that do not

originate from the abdominopelvic region.
eg, sepsis, burns, massive resuscitation.

c) Recurrent IAH or ACS refers to the condition in which IAH

or ACS redevelops following previous surgical or medical
treatment of primary or secondary IAH or ACS

Risk factors for intra-abdominal hypertension and abdominal

compartment syndrome

1. Diminished abdominal wall compliance

Abdominal surgery
Major trauma
Major burns
Prone positioning
2. Increased intra-luminal contents
Gastroparesis/gastric distention/ileus
Ileus
Colonic pseudo-obstruction
Volvulus

3. Increased intra-abdominal contents

Acute pancreatitis
Distended abdomen
Hemoperitoneum/pneumoperitoneum or intra-peritoneal fluid
collections
Intra-abdominal infection/abscess
Intra-abdominal or retroperitoneal tumors
Laparoscopy with excessive insufflation pressures
Liver dysfunction/cirrhosis with ascites
Peritoneal dialysis
Capillary leak/fluid resuscitation
Acidosis
Damage control laparotomy
Hypothermia
Increased APACHE-II or SOFA score
Massive fluid resuscitation or positive fluid balance
Polytransfusion

4. Others/miscellaneous
Age
Bacteremia
Coagulopathy
Increased head of bed angle
Massive incisional hernia repair
Mechanical ventilation
Obesity or increased body mass index
PEEP>10
Peritonitis
Pneumonia
Sepsis
Shock or hypotension
Large volume resuscitation (> 5 L/24 hrs), acidosis, hypothermia,
coagulopathy/multiple transfusion, organ dysfunction, Ileus and abdominal
surgery / primary fascial closure are independent risk factors for
debelopment of ACS.

Technique of IAP measurement

IAP can be measured by direct and indirect methods.

Direct measure - Direct measurement is done using an intra-peritoneal

catheter connected to a pressure transducer. During laparoscopic procedures
an automatic electronic insufflator provides continuous monitoring of
pressure.

Indirect measure –
Inferior vena cava pressure - Transfemorally measured pressure in the infra-
diaphragmatic vena cava correlates directly with IAP.

Intra-gastric pressure - IAP can be measured by water manometer via a

nasogastric or gastrostomy tube.

Transgastral technique - A gastric tonometer with a balloon attached is

introduced into the stomach via the oro- or naso-pharynx and used for
measurement.

Rectal route – rarely used.

Urinary bladder pressure – Gold Standard

Safest and most feasibile way to monitor IAP is the intravesical pressure.
1. Expressed in mmHg (1 mmHg = 1.36 cm H2O).
2. Measured at end-expiration.
3. In supine position.
4. Zeroed at the iliac crest in the mid-axillary line.
5. Performed with an instillation volume of 25 mL of saline [1 mL/kg for
children up to 20 kg]
6. Measured 30-60 seconds after instillation to allow for bladder detrusor
muscle relaxation.
7. Measured in absence of active abdominal muscle contractions.
Pathophysiology
Abdominal distention as a consequence of hypovolemic shock and massive
resuscitation are important causes of IAH and, consequently, of ACS in
trauma patients. In states of shock, vasoconstriction mediated by the
sympathetic nervous system forms short circuits characteristic of IAH
pathogenesis and progression to ACS as follows: 1) liberation of cytokines,
2) formation of free oxygen radicals, and 3) decrease in the cellular
production of adenosine triphosphate. In response to the tissue damage
caused by hypoxia, proinflammatory cytokines are liberated. These
molecules promote vasodilation and increase capillary permeability, causing
greater edema. Edema can rapidly ensue as the result of capillary leak,
increasing tissue edema of the intestine, causing IAP elevation.

IAH affects all the organ system. Its clinical features are as follows-

Hypovolemic shock
Systolic hypotension, narrow pulse pressure, lactic acidosis, tachycardia,
Increased core to peripheral temperature gradient, weak pulses, Abnormal
mentation
Acute kidney injury/acute renal failure
Oliguria, increased serum creatinine,
Acute respiratory failure (new or worsened if pre-existing)
Hypoxia and hypercarbia, Increased peak airway pressures (volume
cycled ventilation), Decreased resultant tidal volumes (pressurecycled
ventilation), Decreased release volumes (airway pressure release ventilation)
Acute hepatic failure
Increased liver function tests, Jaundice, coagulopathy

Management

I. Serial monitoring of IAP

In any patient who has 2 or more risk factors or in the presence of new
or progressive organ failure, baseline IAP should be measured. If IAP
> 12mmHg persistently, treatment should be initiated. If not, patient
should be observed for increase in IAP in the event of organ failure.

II Optimization of systemic perfusion and organ function.

III Medical interventions to reduce IAP

IAP should be measured every 4-6 hours/ continously and therapy is

titrated to maintain IAP ≤ 15mmHg and APP ≥ 60mmHg.

1. Improve abdominal wall compliance

Sedation & analgesia
Neuromuscular blockade
Avoid head of bed > 30 degrees
2. Evacuate intra-luminal contents
Nasogastric decompression
Rectal decompression
Gastro-/colo-prokinetic agents
3. Evacuate abdominal fluid collections
Paracentesis
Percutaneous drainage
4. Correct positive fluid balance
Avoid excessive fluid resuscitation
Diuretics
Colloids / hypertonic fluids
Hemodialysis / ultrafiltration
5. Organ Support
Maintain APP > 60 mmHg with vasopressors
Optimize ventilation, alveolar recruitment
Use transmural (tm) airway pressures
Pplattm = Pplat - IAP
Consider using volumetric preload indices

If IAP > 25mmHg (and/or APP < 60mmHg) and new organ dysfunction /
failure is present, it is considered refractory ACS and needs surgical
decompression.

IV. Prompt surgical decompression in refractory IAH.

Surgical abdominal decompression has long been the standard life-saving

intervention. Decompressive laparotomy with temporary abdominal wall
closure reduces IAP and improves systemic perfusion. It should be
undertaken before organ failure is irreversible.
Damage control strategy – It aims at treating the lethal triad of acidosis,
hypothermia and coagulopathy. Laparatomy aims at controlling hemorrhage,
preventing contamination and avoiding further injury. Postoperatively,
consequences like massive intestinal edema, intra-abdominal packing,
retroperitoneal hematoma and tight closure of abdomen by themselves can
cause abdominal compartment syndrome.

Systemic Reperfusion Injury

Rapid decompression of the abdomen results in acute hypovolemia as a
result of the decompression of the mesenteric vascular bed and release of
lactic acid into the blood stream. This is also a sequel of abrupt drop in
central filling pressure and systemic vascular resistance. Supraventricular
arrhythmias and episodes of asystole have also been reported. The factor
responsible for these adverse events is the rapid washout and systemic
circulation of lactic acids, potassium, and other by products of anaerobic
metabolism, from the reperfused viscera and lower extremities.

Concept of open abdomen

Post laparotomy temporary closure of the abdomen is recommended and
staged re-operation for closure is undertaken. Various techniques for
temporary closure are skin approximation, Bogota bag, Vicryl mesh, Dexon
mesh, Open-Steri-Drape, Wittman Patch, Vacuum assisted closure etc.

Definitive surgery for closure of abdomen is undertaken at a later stage.

Most patients will tolerate primary fascial closure within 5–7 days if
decompressed before significant organ failure develops.

The aims of management are to maintain APP ≥ 60mmHg and IAP ≤

12mmHg.

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