ABDOMINAL

COMPARTMENT
SYNDROME
(ACS)
PRESENTER: RAJABU A. BAKARI
MMED I - SURGERY.
FACILITATOR: DR RINGO.
OVERVIEW
 Introduction.
 Definition.
 Epidemiology.
 Categories.
 Causes.
 Pathophysiology.
 Signs and symptoms.
 Work-up
 Management.
 Prevention.
 References.
INTRODUCTION

 Refers to organ dysfunction caused by intra-abdominal

hypertension.
 It may be under-recognized because it primarily affects
who are already quite ill.
 Therefore, it is a major cause of morbidity and mortality in
critically ill patient and its early recognition is essential.
Definition

 ACS defined as a pathologic intra-abdominal hypertension

(IAH) develops when IAP is persistently 20 mmHg or
greater, with or without abdominal perfusion pressure less
than 50 mmHg (at least three measurements performed 1 to
3 hours apart); it is associated with failure of one or more
organ systems that was not present previously.
EPIDEMIOLOGY

 According to recent literature, the frequency of abdominal

compartment syndrome in trauma ICU admissions is
anywhere from 5-15% and 1% of general trauma
admissions.
 Abdominal compartment syndrome has been documented
in all age groups. The IAP that leads to morbidity (>20 mm
Hg) appears to be similar in the pediatric population.
TYPES OF ACS
Basically, There are two types :
i. Primary ACS.
ii. Secondary ACS.
Primary ACS

 Develops as a result of pathologic IAH caused by intra-

abdominal pathology.
 Is the most common encountered in victims of multiple
trauma, especially after damage control surgery, and
develops as a result of ileus caused by bowel edema and
contamination, continued bleeding, coagulopathy, packing
used to control bleeding, capillary leak, and massive fluid
resuscitation and transfusion.
COMMON CAUSES OF
PRIMARY ACS
i. Tumor.
ii. Pancreatitis.
iii. Ruptured abdominal aortic aneurysm.
iv. Visceral edema.
v. Abscess
vi. Pneumoperitoneum
vii. Obstructions/ileus.
Secondary ACS

 Develops in absence of intra-abdominal primary pathology,

injury or intervention.
 Is in part iatrogenic and commonly occurs in patients with
shock (any condition) requiring aggressive (extensive) fluid
resuscitation with crystalloids.
 Eg : thermally injured and shock trauma victims, critically
ill hypothermic and septic patients, and patients who have
sustained cardiac arrest.
COMMON CAUSES OF
SECONDARY ACS
i. Acute respiratory distress syndrome.
ii. Major trauma or burns.
iii. Massive fluid resuscitation.
iv. Hypotension.
v. Blood transfusion.
vi. Sepsis.
vii. Coagulopathy
PATHOPHYSIOLOGY

 CENTRAL NERVOUS SYSTEM

- Increased intra-abdominal pressure (IAP) will lead to
increased intracranial pressure and decreased cerebral
perfusion pressure.
 CARDIOVASCULAR
IAP will cause compression of aorta and IVC causing;
i. Decreased venous return to the heart.
ii. Decreased cardiac output
iii. Reduced tissue perfusion.
 GASTROINTESTINAL TRACT
Increased IAP causes compression and congestion of
mesenteric and capillaries resulting in
i. Decreased splanchnic blood flow
ii. Decreased Ph
iii. Decreased gut perfusion leading to ishaemia, necrosis,
cytokines release, bacterial translocation and development
of SIRS further increase IAP.
PATHOPHYSIOLOGY

 RENAL SYSTEM
- Increased IAP leads to decreased renal blood flow and
decreased glomerular filtration.
- oliguria may be observed with IAP of 15 – 20
- An IAP of 30 mmHg leads to anuria.
- Increased of antidiuretic hormone and activation of renin-
angiotensin-aldosterone system.
- Increased water retention.
 PULMONARY
Increased IAP will cause diaphragmatic compression
causing;
i. Increased intra-thoracic pressure
ii. Increased airway pressure
iii. Decreased compliance.
iv. Decreased venous return exacerbating cardiac problem.
CLINICAL PRESENTATION

 It is desirable to recognize IAH early, so it can be treated

before progressing to ACS.

Symptoms:
- Most patients who develops 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
- Other findings may include: hypotension, tachycardia, an
elevated jugular venous pressure, peripheral edema,
abdominal tenderness, or acute pulmonary decompensation.
- There may also be evidence of hypoperfusion, including cool
skin, obtundetion, restlessness or lactic acidosis.
DIAGNOSIS

 A diagnosis of intra-abdominal hypertension cannot

reliably be made by physical examination; therefore, it is
obtained by measuring the intraperitoneal pressure.
 The most common technique is to measure the patient’s
bladder pressure.
How to measure IAP?

 Use of the urinary bladder catheter has

been the gold standard and is the indirect
method used to measure IAP. IAP is
measured in the following ways;
1. Using a regular foley catheter,
disconnect from tubing, directly inject
50ml, clamp, insert needle, and measure
2. Using a three-way foley catheter, inject
saline into one port, and measure the IAP
through the other
 Other measurement kits are commercially available.
 Once measured, the pressure is graded:
1. Grade I (IAP < 12 to 15 cm H₂O).
2. Grade II (IAP <15 to 20 cm H₂O).
3. Grade III (IAP <20 to 25 cm H₂O).
4. Grade IV (IAP > 25 cm H₂O).
Conditions in which the bladder
pressure is unreliable

 i. Bladder rupture.
 Ii. External compression from pelvic packing.
 Iii. Neurogenic bladder. And
 Iv. Adhesive disease.
INDICATIONS FOR IAP
MONITORING
 Post-operative (abdominal surgery) patients.
 Patients with abdominal trauma.
 Ventilated Patients with other organ failure.
 Patients with Abdominal packing
 Patients with signs of ACS:
- oligulia, hypoxia, hypotension, ileus, acidosis, mesenteric
ischemia, elevated ICP
 High cummulative (positive) fluid balance
WORK UPS

 Laboratory studies and abdominal computed tomography

scan are part of workup for abdominal compartment syndrome
 The following Lab studies may be indicated:
- Comprehensive metabolic panel.
- Complete blood cell count.
- Amylase and lipase assessment.
- Arterial blood gases
- PT, aPTT
- Cardiac makers assays.
- Serum lactate levels
MANAGEMENT

 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 compliance
 Nasogastric drainage are simple means for reducing IAP in
patients with bowel distension.
 Hemoperitoneum , ascites, intra-abdominal abscess and
retroperitoneal hematoma occupy space and can elevate
IAP. In some cases, these collections can be evacuated using
percutaneous techniques.
 Abdominal wall compliance can be improved with adequate
pain control and sedation.
HEMODYNAMIC SUPPORT.

 For patient with IAH, limiting the amount of fluid

administration may decrease the risk of developing ACS.
 Some clinicians prefer to administer colloids under this
circumstance instead of crystalloids.
VENTILATORY SUPPORT

 PEEP may reduce ventilation-perfusion mismatch and

improve hypoxemia.
DECOMPRESSIVE
SURGERY
 Surgical decompression remained the mainstay treatment of
ACS.
 With grade III IAH, decompression may be considered
when the abdomen is tense and signs of extreme ventilatory
dysfunction and oliguria develop.
 In grade IV IAH, with signs of ventilator and renal failure,
decompression is indicated.
 In patient with severe head injury and IAP greater than 20
mmHg, even without overt ACS, or intractable intracranial
hypertension without obvious head injury, abdominal
decompression must be considered.
 Decompression (formal laparotomy) is an emergency and is
performed in the operating room.
 Decompression leads to reduction of IAH, severe
hypotension as a result of sudden decrease in systemic
vascular resistance, and abrupt increase in the true tidal
volume delivered to the patient, with washout of the
byproduct of anaerobic metabolism from below the
diaphragm.
 Decompression is performed after adequate preload with
volume has been established. Most patients respond to
decompression and survive.
 When stable, the patient can be returned to operating room
for definitive closure
PREVENTION.

 The prevention of primary ACS entails leaving the

peritoneal cavity open in patients at risk for IAH after high-
risk surgical procedures.
 Patient at high risk for secondary ACS receiving crystalloid
resuscitation must be monitored closely, and IAP must be
measured when patients are given more than 6 liters of
crystalloid in 6-hour period.
 In addition to BP and urine output, monitoring abdominal
perfusion pressure ( abdominal perfusion pressure = MAP –
IAP) by continuously measuring IAP throughout
resuscitation is a helpful indicator of the resuscitation end
point.
 Routine measurement of IAP also must be considered in
critically ill patients because IAH is the leading cause of
chest wall impairment in ARDS.
 Higher index of suspicion is paramount, especially in cases
of secondary ACS, in which the onset is insidious and
manifestations are subtle.
References.

 Sabiston Textbook of surgery 20th edition.

 Schwartzs Principles of Surgery 11th edition.
 Bailey and Love Short Practise of Surgery 28th edition.
 Medscape.
 Uptodate.