Abdominal Compartment
Syndrome (ACS)
Dr Emily LaiPrincess Margaret Hospital
Joint Hospital Surgical Grand Round 17 Apr 2010
World Congress on Abdominal Compartment Syndrome 2004
• Intra-abdominal pressure (IAP): – steady-state pressure concealed within the
abdominal cavity; – increases with inspiration and decreases with
expiration– affected by the volume of solid organs and the
intestines, space-occupying lesions, and the extensibility of the abdominal wall
• Abdominal perfusion pressure = MAP – IAP
World Congress on Abdominal Compartment Syndrome 2004• Normal IAP ~ 5-7mmHg • Intra-abdominal hypertension (IAH)
– Sustained or repeated pathological elevation in IAP >= 12mmHg
• Abdominal compartment syndrome (ACS)– a sustained IAP > 20mmHg that is associated with a
new organ dysfunction/ failure
Classification of ACS
• Primary
– Associated with injury or disease in the abdominopelvic region or a condition that develops after abdominal surgery
– Frequently requires early surgical and radiological intervention
– e.g. # pelvis, massive retroperitoneal haematoma, ruptured AAA, ileus, post-liver transplantation
Classification of ACS
• Secondary (medical or extra-abdominal)
– Include conditions that do not originate from the abdomen
– e.g. major burns, sepsis or other condition requiring massive fluid resuscitation
Classification of ACS
• Recurrent (tertiary)
– ACS redevelops following previous surgical or medical treatment of primary or secondary ACS
– Associated with significant morbidity and mortality
Causes of ACS
• Intraperitoneal or retroperitoneal haematoma– Trauma, # pelvis, ruptured AAA…
• Sepsis– Intra-abdominal sepsis, pancreatitis, major burns…
• Excessive fluid resuscitation > 5L within 24 hours• Pneumoperitoneum• Ileus/ intestinal obstruction• Iatrogenic
– Post incisional hernia repair, post abdominal packing…
** Patient with ascites, large abdominal tumors, pregnancy and morbid obesity have lower thresholds to develop ACS
PathophysiologyPhysiological Insult/ critical illness
(e.g. Haemorrhage, sepsis)
Systemic inflammatory response
Capillary endothelial damage
Interstitial edema (including bowel wall and mesentery)
Fluid accumulates, stretching the abdominal wall until it becomes less compliant
Intra-abdominal pressure increases
Multisystem effects of ACS
• Cardiovascular
– Compression of IVC diminishes venous return to the heart (preload)
– Increased afterload due to raised systemic vascular resistance and raised intra-thoracic pressure
– Reduces cardiac output– Venous stasis in the legs
Multisystem effects of ACS
• Respiratory– Diaphragm is forced into the thorax, reducing
the intra-thoracic volume, increasing the intra-thoracic pressure and compressing lung parenchyma
– Hypoventilation and VQ mismatch causing hypoxia and respiratory acidosis
– Compensatory increase in positive end expiratory pressure may further impede venous return and raised jugular pressure, which can result in raised ICP and cerebral edema
Multisystem effects of ACS
• Renal
– Reduction in GFR and renal plasma flow, with increase in renal vascular resistance
– Leads to oliguric renal failure
– Raised ADH, renin and aldosterone leads to retention of sodium and water
Multisystem effects of ACS
• Gastrointestinal– marked reduction in hepatic, splanchnic and
mesenteric blood flow when IAP > 15– Mucosal ischemia and translocation of bacteria
or inflammatory mediators into the circulation– Provokes systemic inflammatory response,
prolonged ileus or leads to anastomotic dehiscence post-operatively
• Central nervous system– Raised intracranial pressure
Symptoms/ signs
• No characteristic clinical signs are indicative of ACS
• Clinical judgment fails to detect significant IAH over 40% of the time
– Kirkpatrick, A.W., et al., Is clinical examination an accurate indicator of raised intra-abdominal pressure in critically injured patients? Can J Surg, 2000. 43(3): p. 207-11.
– Sugrue, M., et al., Clinical examination is an inaccurate predictor of intraabdominal pressure. World J Surg, 2002. 26(12): p. 1428-31.
Measurement of IAP
• Direct – Catheter in the peritoneum
• Indirect– Intravesical pressure (Gold standard)– Stomach pressure– Rectal pressure– Uterine pressure– Inferior vena cava pressure
Bladder Technique
• Foley catheter tubing clamped • 50ml saline instilled into the bladder • A 16G needle inserted via the
aspiration port proximal to the clamp and attached to a pressure transducer/ manometer
• The level of pubic symphysis is used as zero
• Measured at end-expiration and in supine position
• Contraindication: patient with suspected or confirmed bladder trauma
Management
• Medical
• Operative
Medical Management
• Close monitoring in ICU• Sedation and paralysis • Optimization of ventilation and oxygenation• Optimal fluid resuscitation • Administration of inotropes • Gastric suctioning • Correction of coagulopathy • Correction of hypothermia • CVVH for aggressive correction of metabolic acidosis
associated with acute renal failure despite medical therapy
Operative Treatment
• Decompressive laparotomy– immediate
improvement of haemodynamic status
– Variety of techniques• e.g. Bogota bag,
Wittmann patch, vacuum-pack closure
• Temporary abdominal closure
http://www.mdconsult.com/
Bogota bag
http://bestpractice.bmj.com/best-practice/monograph/1125/resources/images.html
Decompressive laparotomy (DL)
• Detailed effects of DL on organ function are only rarely reported.
• IAP threshold levels for DL reported in the literature vary considerable.
• DL decreases IAP to < 20 mmHg in most studies
• A positive effect on organ function is reported in most studies, but the effect is inconsistent, and the duration of this effect is not clear.
• Reported mortality after DL for ACS is high.
Jan J De Waele et al. Decompressive laparotomy for abdominal compartment syndrome – a critical analysis Critical Care 2006, 10:R51
Decompression-reperfusion Syndrome
• Haemodynamic instability
• Release of lactic acid, potassium and adenosine that accumulate during anaerobic metabolism
• Result in arrhythmias, metabolic acidosis and cardiac depression
Conclusion
• Abdominal compartment syndrome is fatal
• Early recognition of patients at risk, frequent monitoring of IAP, and early initiation of treatment are important in preventing irreversible multiorgan failure.
References
• World Society of the Abdominal Compartment Syndrome www.wsacs.org
• Results from the International Conference of Experts on Intra-abdominal hypertension and Abdominal Compartment Syndrome Intensive Care Med (2006) 32:1722–1732
• Narendra Nath Basu, Simon Cottam Abdominal Compartment Syndrome Surgery 2006 260-262
• Scheppach et al. Abdominal Compartment syndrome Best practice & Research Clinical Gastroenterology 23 (2009) 25-33
• Kirkpatrick, A.W., et al., Is clinical examination an accurate indicator of raised intra-abdominal pressure in critically injured patients? Can J Surg, 2000. 43(3): p. 207-11.
• Sugrue, M., et al., Clinical examination is an inaccurate predictor of intraabdominal pressure. World J Surg, 2002. 26(12): p. 1428-31.
• Jan J De Waele et al. Decompressive laparotomy for abdominal compartment syndrome – a critical analysis Critical Care 2006, 10:R51
• Guideline for management of abdominal compartment syndrome (ACS) in trauma patients in PMH ICU