Severe acute pancreatitis: Clinical course and management

doi:10.3748/wjg.v13.i38.5043

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Oct 14, 2007 (publication date) through Jul 24, 2024

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastroenterol. Oct 14, 2007; 13(38): 5043-5051
Published online Oct 14, 2007. doi: 10.3748/wjg.v13.i38.5043

Table 2 Clinical course of AP/SAP

Clinical		Pathophysiologic process
Early: d 1-10 after HA	Hypovolemia Abdominal pain	Fluid sequestration Liberation of pro- and anti-
ESAP in about 20% of SAP	Dysfunction Pulmonary Renal	inflammatory cytokines Endotoxemia
	Cardiocirculatory	Liberation of vasoactive substances
	Liver	Disturbance of blood coagulation
	Intestine	Translocation of endotoxin and bacteria
Late > 2 wk after HA	Local and systemic	Bacterial translocation
Late > 2 wk after HA	septic complications	CARS
	IN, SPN	Anti-inflammatory reaction Immunosuppression

AP: Acute pancreatitis; SAP: Severe acute pancreatitis; ESAP: Early severe acute pancreatitis; HA: Hospital admission; IN: Infected necrosis; SPN: Sterile pancreatic necrosis; CARS: Compensatory antiinflammatory syndrome.

Citation: Beger HG, Rau BM. Severe acute pancreatitis: Clinical course and management. World J Gastroenterol 2007; 13(38): 5043-5051
URL: https://www.wjgnet.com/1007-9327/full/v13/i38/5043.htm
DOI: https://dx.doi.org/10.3748/wjg.v13.i38.5043