Severe acute pancreatitis is a two-phase systemic disease. The first phase
is a clinical response resulting from systemic effects of proinflammatory m
ediators called SIRS (systemic inflammatory response syndrome), that may le
ad to multiple organ failure and death. The second phase, if the process is
not reversed by natural defences or treatment, may be accompanied by local
complications such as infected pancreatic necrosis.
The severity of the disease must be established early to identify patients
requiring intensive monitoring and support. The clinico-biochemical score (
Ranson score) is about 80% accurate at 48 hours but is not accurate before
this time; the APACHE II system has the sensitivity to predict severe pancr
eatitis in 61% of patients on admission. Although not perfect, the prognost
ic systems of severity remain better than clinical judgement. SIRS followed
by local complications is accompanied by increased energy requirements and
, with the absence of oral intake, a persistently negative nitrogen balance
and mineral and micronutrient deficiencies. Thus, early nutritional suppor
t is indicated. Formerly, total parenteral nutrition was the standard pract
ice for providing exogenous nutrients avoiding pancreatic stimulation. The
use of early enteral feeding has recently been evaluated. Gastric atony and
obstruction of the duodenum by pancreatic oedema or necrosis have been ove
rcome by delivering enteral nutrition to the jejunum, distal to the ligamen
t of Treitz; in this position, regular diets do not stimulate pancreatic se
cretions. The efficacy, tolerance, clinical outcome and cost of enteral nut
rition suggest that this feeding route should be preferred in patients with
severe acute pancreatitis.