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