INTRODUCTION
Acute pancreatitis (AP) is an inflammatory process
of the pancreatic parenchyma resulting in glandular
autodigestion initiated by pancreatic enzymes. The pancreas
constitutes 0.1% of the total body weight (BM)
and has 13 times higher protein output than the liver
and reticuloendothelial systems combined (4% BM).
Owing to the fact that pancreas is located in the retroperitoneum
and does not possess a capsule, the inflammatory
process spreads easily and rapidly. At the
onset of AP, parenchymal edema and adiponecrosis
occur (acute edematous pancreatitis). If necrosis spreads
to the parenchyma, accompanied by haemorrhage
and disfunction of the gland, the condition progresses to
the stage of haemorrhagic and necrotising pancreatitis.
Incidence: Documented results vary. In the USA,
the incidence of AP is 19.5, while 8.3 out of 100.000
patients are registered with chronic pancreatitis (1).
Registered cases of AP in 1993 amounted to 215.000,
while in 1998 the number was 183.000. In Germany,
the incidence rate is 17.5 patients in the population of
100.000, while in Finland 73.4:100 000 (2). AP is 3
times more frequent in black people compared to white
people (20.7 versus 5.7 patients in a population of
100.000). AP is also more frequent in men than in
women.
Mortality: The total mortality rate in patients with
mild clinical forms of AP is 15%, while in patients with
severe forms of the disease the mortality rate amounts
up to 30% (3). During the past 20 years, owing to
aggressive intensive care treatment and the introduction
of new therapeutic strategies, the mortality rate in cases
of mild clinical forms has fallen to 5% (3.8-7%), while it
is still high in cases of severe forms, about 20% (15-
25%) (3).
During the first week following the onset of the
disease, most cases of patient death are a result of
multiple organ dysfunction, while in later stages infection
is the main risk factor for a fatal outcome. However,
destruction of the pancreas is the main cause of death.