Current concept of pathogenesis of severe acute pancreatitis

Table 1 Complications of severe acute pancreatitis and their mechan isms

Complications	Mechanisms
1. Local complication
Intra and retro-peritoneal fluid collections	Bradykinin, TNF-α, PAF increase vascular permeability with fluid exudation
	Hypoalbuminemia
Pseudocyst	Unabsorbed fluid collection for long duration
Pancreatic fistula, transient	Pancreatic duct rupture, communicating with pse udocyst
2. Systemic complications
Hypotension, hypovolemic shock	Increased vascular permeability, profuse exudation into peritoneal cavity
	Hypovolemia
	Hypoalbuminemia
Intestinal ileus, dehydration,	Peritonitis; loss of peristaltic function; large quantity of digestive fluid sequestrated
hypopotassemia	in intestinal lumen; infusion of large volume of crystaloid solution
Hypocalcemia	Formation of calcium soap plaques with fats on peritoneum and mesentery
Renal insufficiency	Hypotension, low blood volume, decrease of renal blood flow
	(PAF further decreases renal blood flow)
Gastric hemorrhage	Acute gastric mucosal bleeding
Jaundice	Pancreatic head edema in mild jaundice, choledocholithiasis in severe jaundice cases
Interstitial lung edema, ARDS	PLA2 destroys structural phospholipid; PAF and TNF-α increase vascular
	permeability; Neutrophils release elastase and free radicals damage type I & II lung
	epithelial cells with disability of producing surfactants, alveolar atrophy and
	interstitial edema
Disseminated intravascular	Shock, hypercoagulable state; microcirculatory stasis; imbalance of thrombo-
coagulation (DIC)	fibrinolytic system; deletion of antithrombin III
Pancreatic encephalopathy	PLA2 damages structural phospholipid of brain cell membrane; PAF increases
	intracerebral vascular permeability with brain edema and demyelinization of grey
	and white matter
Transient blindness	Retinal ischemia; white cell emboli with exudation, incre ased vascular permeability
Infection, bacteremia, sepsis	Gut barrier dysfunction with translocation of gut bacteria and endotoxemia, bacteremia
Infected necrosis	Cellular immunity decreases, sepsis
Pancreatic abscess	Same as above, hemodynamic changes caused by inflammatory cytokines and
	inflammatory mediators
Heart failture	Underlying ischemic heart disease; overloading of circulation by massive infusion or
	too rapid intravenous dripping