Abdominal compartment syndrome

Abdominal compartment syndrome
Classification and external resources
eMedicine article/829008

Abdominal compartment syndrome occurs when the abdomen becomes subject to increased pressure. Specific cause of abdominal compartment syndrome is not known, although some causes can be sepsis and severe abdominal trauma. Increasing pressure reduces blood flow to abdominal organs and impairs pulmonary, cardiovascular, renal, and gastro-intestinal (GI) function, causing multiple organ dysfunction syndrome and death.[1]

Pathophysiology

Abdominal compartment syndrome occurs when tissue fluid within the peritoneal and retroperitoneal space (either edema, retroperitoneal blood or free fluid in the abdomen) accumulates in such large volumes that the abdominal wall compliance threshold is crossed and the abdomen can no longer stretch. Once the abdominal wall can no longer expand, any further fluid leaking into the tissue results in fairly rapid rises in the pressure within the closed space. Initially this increase in pressure does not cause organ failure but does prevent organs from working properly - this is called intra-abdominal hypertension and is defined as a pressure over 12 mm Hg in adults. However, if the pressure continues to rise over 20 mm Hg and organs begin to fail, the syndrome has now progressed to the end stage of the highly fatal process termed abdominal compartment syndrome. These pressure measurements are relative. Small children get into trouble and develop compartment syndromes at much lower pressures while young previously healthy athletic individuals may tolerate an abdominal pressure of 20 mm Hg very well. The underlying cause of the disease process is capillary permeability caused by the systemic inflammatory response syndrome (SIRS) that occurs in every critically ill patient. SIRS leads to leakage of fluid out of the capillary beds into the interstitial space in the entire body with a profound amount of this fluid leaking into the gut wall, mesentery and retroperitoneal tissue. (For a much more extensive discussion on the topic and physiology visit the Wikipedia section discussing intra-abdominal hypertension.)

Abdominal compartment syndrome follows a destructive pathway similar to compartment syndrome of the extremities. When increased compression occurs in such a hollow space organs will begin to collapse under the pressure. As the pressure increases and reaches a point where the abdomen can no longer be distended it starts to affect the cardiovascular and pulmonary systems. When abdominal compartment syndrome reaches this point without surgery and help of a silo the patient will most likely die. There is a high mortality rate associated with abdominal compartment syndrome.[1][3][4]

Treatment

Non-operative medical management

There are now multiple papers noting that early intervention using medical management for intra-abdominal hypertension can prevent abdominal compartment syndrome from occurring and can result in reduced costs of care. All of these papers suggest early detection of elevated intraabdominal pressure via bladder pressure monitoring and introduction of a treatment protocol are required for optimal results.[5][6][7][8][9] A very nice review of medical management for IAH / ACS was published by Dr. Mike Cheatham in 2009 and Dr. De Keulenaer in 2011.[10][11] Furthermore, visiting the website of the World Society of Abdominal compartment syndrome allows one to download assessment and management algorithms free of charge.[12] More detailed information on medical management for this syndrome can be found on the intraabdominal hypertension page

Finally, the diagrams and algorithm provided here are useful items to assist in evaluation and management of these complex patients.

Treatment algorithm for IAH/ ACS

Operative decompression

Surgical decompression can be achieved by opening the abdominal wall and abdominal fascia anterior in order to physically create more space for the abdominal viscera. Once opened, the fascia can be bridged for support and to prevent loss of domain by a variety of medical devices (Bogota bag, artificial bur, and vacuum devices using negative pressure wound therapy [13]).

References

  1. ↑ 1.0 1.1 http://findarticles.com/p/articles/mi_qa3689/is_200401/ai_n9346109/
  2. ↑ [J Intensive Care Med 2000;15:201-220]
  3. ↑ http://emedicine.medscape.com/article/829008-overview
  4. ↑ http://www.abdominalcompartmentsyndrome.com/
  5. ↑ Cheatham ML, Safcsak K. Is the evolving management of intra-abdominal hypertension and abdominal compartment syndrome improving survival? Critical care medicine 2010;38:402-7.
  6. ↑ Kimball EJ, Mone M, Hansen H, et al. A prospective evaluation of the protocolized management of intra-abdominal hypertension and the abdominal compartment syndrome. Acta Clinica Belgica 2009;64:272 - Abstract 110.
  7. ↑ Sun ZX, Huang HR, Zhou H. Indwelling catheter and conservative measures in the treatment of abdominal compartment syndrome in fulminant acute pancreatitis. World J Gastroenterol 2006;12:5068-70.
  8. ↑ Oda S, Hirasawa H, Shiga H, et al. Management of Intra-abdominal Hypertension in Patients With Severe Acute Pancreatitis With Continuous Hemodiafiltration Using a Polymethyl Methacrylate Membrane Hemofilter. Ther Apher Dial 2005;9:355-61.
  9. ↑ Ennis JL, Chung KK, Renz EM, et al. Joint Theater Trauma System implementation of burn resuscitation guidelines improves outcomes in severely burned military casualties. The Journal of trauma 2008;64:S146-51.
  10. ↑ Cheatham ML. Nonoperative management of intraabdominal hypertension and abdominal compartment syndrome. World J Surg 2009;33:1116-22.
  11. ↑ De Keulenaer BL, De Waele JJ, Malbrain ML. Nonoperative management of intra-abdominal hypertension and abdominal compartment syndrome: evolving concepts. The American surgeon 2011;77 Suppl 1:S34-41.
  12. ↑ WSACS.org
  13. ↑ Fitzgerald JEF, Gupta S, Masterson S, Sigurdsson HH. Laparostomy Management using the ABThera™ Open Abdomen Negative Pressure Therapy System in a Grade IV Open Abdomen Secondary to Acute Pancreatitis. International Wound Journal 2012. PMID 22487377

External links