Organ Failure due to Systemic Injury in Acute Pancreatitis

Role of Intestine in systemic injury:
The small intestine and colon may contribute to bacterial translocation and infected necrosis 
due to its close proximity to the pancreas, and thus to the pathophysiology of systemic 
inflammation. Another role may be played by mesenteric lymph from the GI tract. In an 
experimental study, intravenous administration of mesenteric lymph from rats with intestinal 
ischemia exacerbated pancreatic microcirculatory disturbances and worsened the severity of 
pancreatitis in the recipient rats.
171
Similarly, profound vascular and coagulation changes 
can lead to ischemia of the pancreas
172-174
and bowel
175, 176
. A lower gastric pH which 
correlated with a higher mortality in AP also supported the hypothesis of splanchnic 
ischemia
177
. Additionally, Ischemia-reperfusion can cause oxidative stress
178
. The major 
effect of such perturbations is gut barrier dysfunction with increased intestinal 
permeability
179
, as supported by human studies
180
including a meta-analysis of 18 studies, 
which showed a pooled prevalence of gut barrier dysfunction of 59%
181
. However, parallel 
clinical observations question the gut as being the sole player. These include patients with 
severe ulcerative colitis having a very low prevalence of sepsis
182
despite severe colonic 
ulcers being exposed to fecal matter for long periods. Similarly, while patients with 
fistulizing Crohn’s disease do develop abdominal abscesses, the prevalence of sepsis 
remains low
182
. The translocation hypothesis as being the sole reason for developing 
infected necrosis is further challenged by the fact that bacterial translocation is common 
after dental
183
and endoscopic
184
procedures but is transient. Thus, whether translocation of 
bacteria is the sole reason for infections of (peri) pancreatic necrotic tissue and collections, 
and the sepsis that ensues remains to be determined.