Pathophysiology of pulmonary complications of acute pancreatitis

Table 1 Complications of acute pancreatitis

I Pancreatic

1 Necrosis-sterile vs infected

2 Pseudocyst-infection/rupture/hemorrhage

3 Abscess

II Local-extrapancreatic

1 Involvement of contiguous organs (intraperitoneal hemorrhage, GI bleeding, thrombosis of splenic vein, bowel infarction)

2 Pancreatic ascites

3 Obstructive jaundice

III Systemic

1 Pulmonary

a Early arterial hypoxia

b Atelectasis, pneumonia, pleural effusion, mediastinal abscess

c ARDS

2 Cardiac: shock, pericardial effusion, EKG changes, arrhythmias

3 Hematologic: DIC, TTP/HUS

4 Gastrointestinal: GI bleeding (portal-splenic vein thrombosis, colonic infarction)

5 Renal: azotemia, oliguria

6 Metabolic: hypocalcemia, hyperglycemia, hypertriglyceridemia, acidosis, elevation of free fatty acids

7 CNS: psychosis, pancreatic encephalopathy, Purtscher’s retinopathy

8 Peripheral: fat necrosis (skin and bones), arthritis

9 Miscelaneous: rhabdomyolysis

Table 2 Pathogenic players in respiratory insufficiency

1 Phospholipase A2

2 Trypsin inhibitor

3 FFA/Lipoprotein lipase

4 Complement activation (C5a)

5 MIF

6 IL-6, IL-8, IL-1β

7 NO

8 TNF-α

9 fMet-Leu-Phe (a bacterial wall product)

10 ICAM-1

11 β-2-integrin (CD11b/CD18)

12 Trypsin

13 NF-κB

14 Substance P

Table 3 Pro-inflammatory cytokines

IL-1β -major inflammatory mediator, major activator of macrophages and enhances B and T cell activation

IL-6 -acute phase reactant, stimulates B cell differentiation

IL-8 -stimulates the upregulation of adhesion molecules, chemotactic factor for neutrophils and lymphocytes

TNF-α -recruitment of inflammatory cells, regulation of cytokine production, and promotion of pancreatic acinar cell death by apoptosis

IL-10 is an anti-inflammatory cytokine by inhibiting macrophages releasing inflammator mediators.