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Abdominal Compartment Syndrome (ACS)

Abdominal Compartment Syndrome (ACS). Dr Emily Lai Princess 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;

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Abdominal Compartment Syndrome (ACS)

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  1. Abdominal Compartment Syndrome (ACS) Dr Emily Lai Princess Margaret Hospital Joint Hospital Surgical Grand Round 17 Apr 2010

  2. 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

  3. 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 neworgan dysfunction/ failure

  4. 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

  5. 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

  6. Classification of ACS • Recurrent (tertiary) • ACS redevelops following previous surgical or medical treatment of primary or secondary ACS • Associated with significant morbidity and mortality

  7. 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

  8. Pathophysiology Physiological 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

  9. 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

  10. 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

  11. 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

  12. 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

  13. 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.

  14. Measurement of IAP • Direct • Catheter in the peritoneum • Indirect • Intravesical pressure (Gold standard) • Stomach pressure • Rectal pressure • Uterine pressure • Inferior vena cava pressure

  15. 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

  16. Management • Medical • Operative

  17. 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

  18. 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/

  19. Bogota bag http://bestpractice.bmj.com/best-practice/monograph/1125/resources/images.html

  20. 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 analysisCritical Care 2006, 10:R51

  21. 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

  22. 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.

  23. References • World Society of the Abdominal Compartment Syndrome www.wsacs.org • Results from the International Conferenceof Experts on Intra-abdominal hypertensionand Abdominal Compartment SyndromeIntensive 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 analysisCritical Care 2006, 10:R51 • Guideline for management of abdominal compartment syndrome (ACS) in trauma patients in PMH ICU

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