notes by dr Claudio Italiano
Acute inflammatory process due to inflammatory alteration of the pancreas,
characterized by activation and exit of pancreatic enzymes; it is characterized
by abdominal pain of the epigastrium, of the "belt" type, that is, it radiates
also posteriorly, with increase of the values of the amylases and lipases,
typically pancreatic enzymes.
P.A. edematous, self-limiting
P.A. persistent, in which complications can develop
P.A. necrotic hemorrhagic, fulminating evolution, burdened by a high percentage
of mortality.
The first problem is the stratification of patients, to differentiate mild-moderate forms from severe forms that must be treated with great care. In the US the Ranson criteria are used, ie the patient is framed according to some parameters and this possibility allows first of all to decide in which cases to use invasive maneuvers (ERCP, peritoneal washing, exploratory laparotomies), to select the patient to be subjected to intensive medical therapies and finally to be able to evaluate the results of the therapeutic trials on homogeneous cases.
At the entrance:
- Age'> 55 aa
- Leukocytes> 16,000
- Blood sugar> 200 MG / DL
- LDH> 350U / L
- SGOT> 250 U / L
Within 48 hours:
- Ht decrease> 10%
- Increased azotemia> 5 mg / dl
- Calcemia <8 mg / dl
- PaO2 <60 mmHg - BE> 4 mEq / L (see emogas)
- Estimated liquid loss> 6 L
The prognosis is so correlated with mortality:
<3 signs <1%;
3 - 4 positive signs: 15%;
5 - 6 positive signs up to 100%
Subsequently, other Authors have obtained comparable predictive values by
changing and replacing some parameters.
Currently, the APACHE II system is used (Acute Physiology and Chronic Health
Evaluation) which has the advantage of being immediately applicable (not after
48 hours) and can be repeated during the course of the disease, also achieving
better predictive efficacy.
Another prognostic index able to frame the patient as a critic is that already
described in peritoneal lavage (it should be remembered that this method is
burdened by 0.8% complications). Among the humoral markers an important role is
that of PCR. It has been shown that high levels of PCR on the second day (peak>
300 mg / mL) and / or a persistent rise> 125 mg / mL for the presence of
peripancreatic collections.
Another prognostic index is the one proposed by Balthazar related to the TAC
exam:
A: Normal pancreas: 0 POINTS
B: Increased volume of the pancreas and other adjacent tissues: 1 POINT
C: Inflammatory changes in the pancreas and peripancreatic adipose tissue: 2
POINTS
D: Peripancreatic fluid collection: 3 POINTS
E: two or more peripancreatic fluid collections, gas in the pancreas and
peripancreatic tissues: 4 POINTS
The following points must be added to this score: 0 in the absence of necrosis,
2 with 30% necrosis, 4 with 50% necrosis, 6 with necrosis> 50%.
The scores are summed and the prognosis is as follows: between 7 and 10 points
morbidity of 92% and mortality of 17%; between 0 and 2 points morbidity of 2%
and zero mortality.
It varies according to the cases analyzed: in the USA prevails the intake of
alcohol, while in the European prevailing biliary lithiasis (together are
responsible for 85% of all pancreatitis).
- Biliary lithiasis. In 60% of episodes of P.A. biliary lithiasis is found. The
calculation causes an obstacle to the outflow of the pancreatic secretion due to
obstruction of the terminal choledochus or inversion of the biliary flow that
can flow back into the Wirsung. Sometimes obstructive jaundice may appear.
- Ethanol. The action of alcohol is pathogenic as it causes conditions with
synergistic action: - vagal stimulation: spastic contraction of the sphincter of
Oddi which hinders the outflow of pancreatic secretion
- Increased gastrin
secretion - increased sensitivity of secretion pancreatic receptors - increased
permeability of ductules pancreatic to the enzymes they contain (backscattering
mechanism) - formation of protein aggregates in the ductules and consequent
obstruction of the excretric pathways.
The importance of the incidence of alcohol etiology of P.A. it must not be
underestimated in the anamnesis; in fact it is necessary to investigate
thoroughly the habits related to the alcohol intake by the patient both in the
periods immediately preceding the acute episode, and in previous periods as the
alcoholic insult is responsible for the chronic pancreatitis of alcoholics,
which are however susceptible to exacerbations.
- Idiopathic (about 8-10%)
- Post-operative (biliary tract interventions, ERCP, gastrectomies,
splenectomies, pancreatic biopsies). In these cases, the pathogenesis is due to
peripancreatic edema which hinders the pancreatic circulation
- Hypercalcemia (acute hyperparathyroidism, multiple myeloma). In this case the
pathogenesis is thought to be due either to the activation by Ca ions of
pancreatic enzymes or to the formation of stones
intraduct them.
- Drugs (steroids, thiazides, furosemide)
- Familial hyperlipoproteinemia (I, IV, V)
- Pregnancy (III Trimester)
- Trauma
- Kidney failure
- Immunological factors (lupus, polyarteritis nodosa, vasculitis)
- Pancreas divisum
The pancreas has a very complex activity: through the beta insula and beta cells
it produces insulin, but the exocrine part of the organ produces many of the
enzymes used by the body in the digestion process of complex foods. However,
enzymes are synthesized as inactive precursors and packed into the intracellular
compartment as pro-enzymes. There are still inhibitors of the proteases secreted
by the same pancreatic cells, tissue, whose task is to inject the prostheses if
there was an accidental activation, and plasmatic. The latter are alpha 1
antitrypsin and alpha 2 macroglobulin. Alpha 1 antitrypsin has the task of fast
binding to activated prostheses and to transfer them to alpha 2 macroglobulin.
The latter, with a molecular weight much higher than the first, forms a complex
with the protease that is easily removed from the reticuloendothelial system.
The efficiency of this system is demonstrated by the plasma half-life of this
complex: 10 '. The subtlety of these "protective" systems shows us the need for
a rich pancreatic vascularization whose deficit may be responsible for the
inactivation of one of these mechanisms and an imbalance of the system in favor
of the secretive digestive activity.
Whatever the etiology of P.A. this is expressed first of all by the activation
and the intraparenchymal diffusion of the secreted enzymes.
A central role is certainly played by the trypsin derived from the conversion
into active form of the trypsinogen (this activation can also be carried out by
Ca ions or by a slightly alkaline pH).
Trypsin has in fact its own action as it is able to generate edema, haemorrhage
and necrosis of tissues at high doses, but its peculiarity is to activate, even
if present in small quantities proenzymes such as elastase and phospholipase, as
well as activate complement components (Kinina callicrein system that have a
determining role in alterations of tissue permeability).
This activates a cascade system:
- Trypsinogen, trypsin
- activated phospholipase and elastase
- activation of the complement
- vascular and cellular destruction
- tissue hypoxia and necrosis
- release of trypsin proelastase and phospholipase.
The entity and the "self-activating" mechanism of this phenomenon is such that
the tissue and plasma inhibition systems are insufficient.
- Elastase: It performs its action on the vessel walls causing haemorrhage
- Phospholipase A: Exerts its cytotoxic effect on cell membranes.
- Kallicreine-quinine system: It produces vasodilatation, increased cell
permeability, pain, plays an important role in the genesis of the III space and
therefore in shock.
Each of these injurious actions operates in synergy with the other and the final
result is amplified by the presence of ischemia and possible bacterial
superinfection that often complicate cases of more severe pancreatitis.
There are some theories that want to explain the pathophysiology of parenchymal
damage, even if some of these have only a historical value; are shown below:
- Obstruction - secretion: greater duodenal release of secretin
- Oddi spasm and protein clots of the ducts
Common channel Structure including choledochus + Wirsung: the obstruction of
this structure would allow biliary reflux in the Wirsung with consequent
pancreatic damage (This structure is present only in 5% of cases and therefore
the theory would serve to explain the P.Asolo cases)
Duodenal reflux. Enterochinase would flow back into Wirsung and activate
Tripsinogen (gastroresecated patients)
Backscatter. Alcohol increases the permeability of pancreatic ductules
The anatomical-pathological pictures of acute pancreatitis are variable and
often the boundaries are not so demarcated as to always make possible a sure
framework.
However, the initial picture is characterized by edema and in this case the
clinical form is self-limiting.
The next picture is that of acute hemorrhagic pancreatitis; characteristic of
this picture is the presence of hemorrhagic areas that can evolve into
pseudocysts or may give rise to pancreatic abscesses
A more serious picture is that of cellular necrosis characterized by both
parenchymal and extraparenchymal necrosis areas (above all peritoneal
steatonecrosis, retroperitoneal and at the roots of the months)
The septic evolution of the pancreatitic process is identified in the
anatomopathological picture of ascissualized pancreatitis characterized by
multiple pancreatic abscesses.
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