SURGICAL DISEASES OF PANCREAS

ANATOMY AND PHYSIOLOGY

The pancreas is a retroperitoneal organ that lies behind the posterior peritoneal
membrane at the level of the second lumbar vertebra. The pancreas is divided into
three portions: (1) the head, which fits closely into the curve of the duodenum; (2) the
neck, which lies over the superior mesenteric vessels; and (3) the body and tail,
which are closely adherent to the posterior wall of the stomach and the spleen.
Resection of the pancreas at the level of the neck results in a 50% reduction in
pancreatic mass.
The two major components of the exocrine pancreas are the acinar cells and the
ductular network. Together they constitute 80% to 90% of the pancreatic mass. The
acinar cells secrete the enzymes responsible for digestion. Pancreatic enzymes are
synthesized, stored (as zymogen granules), and released by the acinar cells of the
gland, principally in response to cholecystokinin and vagal stimulation. Lipase and
amylase are secreted in active forms, whereas proteolytic enzymes are secreted in
inactive forms and are activated by duodenal enzyme enterokinase. Within the
pancreas are small numbers of cells that are responsible for the secretion of
hormones that control glucose homeostasis. They are called islets of Langerhans and
constitute 2% of the pancreatic mass. Insulin and glucagons, as well as somatostatin,
are produced by the islets of Langerhans. The main pancreatic duct, or duct of
Wirsung, runs the entire length of the pancreas and joins the common bile duct to
empty into the duodenum at the ampulla of Vater. The duct usually is 2 to 3.5 mm in
diameter, contains 20 secondary branches, and lies in the center of the pancreas.
The accessory pancreatic duct, or duct of Santorini, enters the duodenum 2-2,5 cm
proximal to the ampulla of Vater.
The organ weighs 75 to 100 g and is 15 to 20 cm long. The pancreas lies close
to a number of organs, and major vessels.
The pancreas receives its blood supply from a variety of major arterial sources.
In the head of the pancreas, there are arcades in the anterior and posterior surfaces,
which generally collateralize. These arcades arise from branches of the
gastroduodenal and superior mesenteric arteries. The splenic artery supplies the
body and tail of the pancreas. The splenic artery arises from the celiac trunk and
 2

courses along the superior surface of the pancreas to the spleen. About 8 branches
of the splenic artery supply the body and tail of the pancreas.
The venous drainage of the pancreas and duodenum follows the arterial supply.
All venous effluent from the pancreas ultimately drains into the portal vein.
The lymphatic drainage of the pancreas is diffuse and contents superior
mesenteric lymph nodes, peripyloric nodes, pancreaticolienal nodes etc. The
absence of a peritoneal barrier on the posterior surface of the pancreas results in a
direct communication of the intrapancreatic lymphatics with the retroperitoneal
tissues, and this probably contributes to the often involvement of the retroperitoneal
space in the process in acute pancreatitis.
The exocrine and endocrine secretion of the pancreas is regulated by a rich
neural supply that includes sympathetic fibres from the splanchnic nerves,
parasympathetic fibres from the vagus.

CONGENITAL ANOMALIES OF THE PANCREAS

Annular pancreas, in this rare condition, a ring of pancreatic tissue from the
head of the pancreas surrounds the descending duodenum. The abnormality usually
presents in infancy and reveals by vomiting due to duodenal obstruction. There is bile
in the vomiting, if the constriction is distal to the entrance of the common bile duct. X-
ray shows a dilated stomach and proximal duodenum (double bubble sign) and little
air in the rest of the small bowel.
No attempt should be made to resect the obstructing pancreas; because a
pancreatic fistula or acute pancreatitis often develops postoperatively. The obstructed
segment should be passed by a duodenojejunostomy or duodenoduodenostomy.
Heterotopic (aberrant) pancreas (accessory pancreas) is a submucosal
nodule of normal pancreatic tissue, usually found in the stomach, or duodenum, or in
a Meckel’s diverticulum, rare in the gallbladder. The lesions usually are not clinically
significant, although bleeding may occur from mucosal erosion above the heterotopic
pancreatic tissue. In the case of upper GI hemorrhage should be differentiated with
the peptic ulcer bleeding, gastric and duodenal polyps. The diagnosis is established
on the base of endoscopy and contrasted gastrointestinal series. In urgent cases
surgical excision of pathological segment is indicated.
 3

ACUTE PANCREATITIS
Acute pancreatitis is a complex disorder of the exocrine pancreas characterized
by acute acinar cell injury and both regional and systemic inflammatory responses.
Enzymatic self-digestion of the gland is the main concept of acute pancreatitis. It is a
common disease with a broad spectrum of clinical and pathologic findings that
contribute to considerable morbidity and mortality. Conform definition of S.I.Schwartz
– acute pancreatitis is a „non-bacterial inflammation, which initiates by pancreatic
enzymes”.
ETIOLOGY AND PATHOGENESIS
There are several theories concerning origin of acute pancreatitis. However,
majority of them are based on the experimental data, but no one of them explain
completely the pathogenesis of disease.
1) Common channel theory: suggests, that reflux of bile into the pancreatic
ducts might have initiated the process. Flow between the biliary and pancreatic ducts
requires a common channel (30%) connecting these two systems with the
duodenum. As obstacle usually serves gallstone impacted in the ampulla of Vater.
This theory was designed by Lanceraux (1891), and then Opie (1901), and confirmed
experimentally by Claude Bernard in 1856.
2) Vascular theory: Impaired pancreatic blood flow arising from either
anatomic lesions or functional events can induce acute pancreatitis. Examples
include embolization of the pancreaticoduodenal artery after aortography, celiac
artery stenosis, ruptured abdominal aortic aneurysm, and myocardial infarction.
3) Infection theory: The development of acute pancreatitis has been
reported after a variety of bacterial, fungal, parasitic, and viral infections. Infection
may pass into the pancreas by lymphatic, hematogen and enterogenic ways.
Mechanisms include direct cytotoxic effects, coexisting immunosuppression, and
alterations in pancreatic blood flow.
4) Anaphylactic theory: because acute pancreatitis often occurs after
anaphylactic reactions, this theory is appeared. Vasodilatation, increased vascular
resistance are factors, which may cause enzymas delivery from the pancreas.
5) Toxic theory: different toxic agents (such as alcohol) are responsible for
more cases of acute pancreatitis. In experimental studies, acute administration of
alcohol stimulates pancreatic secretion and induces spasm of sphincter Oddi.
 4

The cellular events that lead to acute pancreatitis may be initiated by a variety of
different stimuli, and the process has been considered a final common pathway. The
direct causes of acute pancreatitis are the following – ethanol, large meal, biliary
stones, common bile duct exploration, especially if sphincterotomy was performed,
trauma, and drug-induced (corticosteroids, immunosupressors). In about 15% of
patients have so-called idiopathic pancreatitis, if there is no identifiable cause of the
condition.
The following concepts are favored in the mechanisms of cellular injury: enzyme
activation, increased ductul permeability with diffusion of enzymes into the
interstitium, secretion of enzymes into the interstitium, acinar cell damage due to
detergent substances and ischemia.
The systemic complications of acute pancreatitis seem to develop more as a
result of a disturbance in the balance between activated proteases and their
inhibitors.

PATHOLOGY
Acute pancreatitis is characterized by alterations in acinar cell structure and
function as well as by the development of acute regional and systemic inflammatory
responses. Acute inflammation of the exocrine pancreas has two forms: mild form –
edematous pancreatitis (which includes edematous and hemorrhagic pancreatitis),
and severe form – necrotizing pancreatitis (fat necrosis, and parenchymal necrosis).
The final, and the most severe form is infected necrosis of the pancreas.
Acute edematous pancreatitis is characterized by interstitial edema formation.
The gland becomes enlarged and edematous, with small areas of focal necrosis
involving either the pancreas or areas of adjacent retroperitoneal fat. Hemorrhagic
pancreatitis is characterized by bleeding into the parenchyma and surrounding
retroperitoneal structures In both forms, the peritoneal surface may contain an areas
of fat necrosis. It thought, that hemorrhagic necrosis appears due to influence of
trypsin, elastase and activated kallikrein-kinin system; whereas phospholipase A has
an important role in producing of the fat necrosis.
Although clinical pancreatitis usually is a reversible disease characterized by
acinar cell injury and edema formation, severe pancreatic necrosis develops in 15%
of patients, which can lead to irreversible regional injury or multiorgan system failure.
Histological characteristics of advanced disease include extensive acinar cell
 5

necrosis, interstitial microabscess formation, extensive peripancreatic fat necrosis,

microvascular thrombosis, and local hemorrhage. This group of patients is the
primary source of morbidity and mortality associated with acute pancreatitis.
Necrotic areas in the pancreas can be solitary or multiple, but on the onset of
disease the process almost always is a affected only superficial layer of the organ.

CLASSIFICATION
AP is classified in dependence on the grade of the pathological process in the
pancreas. There are three main forms: 1) Acute edematous (interstitial) pancreatitis;
2) acute necrotizing pancreatitis; 3) suppurative-necrotizing pancreatitis, or infected
necrosis of the pancreas. In accordance to clinical evolution, AP is divided into 1)
mild (reversible, edematous) form (85%), and 2) severe (necrotizing) form (15%).
Three clinical periods of the disease may be distinguished (V.Saveliev, 1997):
First period: hemodynamical disturbances (including pancreatic shock’s appearance)
– first 1-3 days;
Second period: multiorgan system failure – 5-7 days;
Third period: late suppurative complications appearance – 3-4 weeks.

SYMPTOMS
The symptoms of AP are significant variable in dependence on severity of a
case.
Though there may have been slight attacks of pain prior to the main attack, the
acute onset is usually dramatically sudden. The attack frequently begins following a
large fatty meal or excess alcohol consumption.
Pain, Severe epigastric pain develops suddenly, presents in 95-100% of
patients, and may be so violent that patient will cry out. The pain usually radiates in
the left shoulder (Bereznigovski’s sign), in the left loin (Mayo – Robson’s sign), but
mostly radiates like a belt to the back. At early stage the pain is resistant to
analgesics treatment.
The mechanisms of pain is explained by edema and hemorrhage into the
parenchyma of the gland, distention of the pancreatic capsule, releasing of the
vasoactive substances, tissue ischemia, and direct affect on the retroperitoneal
nervous structures by enzymas.
 6

Nausea and vomiting. Reflex vomiting occur in 85-95%. Vomiting is very

persistent, with large amount of material – initially with aliments, then – with biliary
contents. The vomit is never feculent, but hemathemesis may occur.
Intestinal tract disturbances may occur in two contrast forms:
a) Adynamic ileus, which may be generalized, but more often is localized in the first
jejunal loop.
b) Diarrhea is observed in 7% of cases.
In some patients, bluish coloration is present in the face and neck (Mondor’s
sign), in the flank (Grey-Turner’s sign), or periumbilical area (Cullen’s sign).
Occasionally, slight jaundice is observed.
Clinical evidence of pleural effusion may be present, especially on the left
(dyspnea, dullness on chest percussion etc.) Myocardial function is depressed in
severe pancreatitis, because of circulating factors that affect cardiac performance.
The pulse is accelerated, and arterial BP is normal initially, but with tendency to
decrease. In severe cases, the patient may have a shock.
Clinical evidence of encephalopathy is observed in 4% to 20% of patients with
acute pancreatitis. Symptoms may include disorientation, delirium, hallucinations, or
transient acute psychosis.
Temperature is usually normal or slightly elevated in uncomplicated pancreatitis.
In severe, fulminate pancreatitis, fever may be over 38,5˚C.
The abdominal asymmetry due to distention of the transverse colon (Bonde’s
sign) is evident.
Abdominal percussion is painful in the epigastrium (Mandel-Razdolscki’s sign
is slight positive). Occasionally, the liver dullness may disappear (Gobief’s sign),
because of distended large bowel, situated in the upper abdomen. In some patients,
a moveable dullness on the both right and left flanks is observed (Kerven’s sign) –
free fluid in the peritoneal cavity.
Abdominal palpation reveals abdominal tenderness to the epigastrium, above
the pancreas (Körte’s sign), aorta pulsation is absent due to pancreatic edema
(Voskresenski’s sign).
Abdominal auscultation reveals decreased or absent bowel sounds.

DIAGNOSIS
 7

Blood analysis. There is usually a moderate leukocytosis (over 16,000/L), with

shift into the left, lymphopenia. The hematocrit may be elevated as a consequence of
dehydration or low as a result of abdominal blood loss in hemorrhagic pancreatitis.
Elevated C-reactive protein (CRP) may occur in both acute edematous and
necrotizing pancreatitis. Liver function studies show a mild elevation of the serum
bilirubin concentration. The serum amylase concentration rises to more than 2-3
times normal within 6 hours after the onset of an acute episode and remains elevated
for several days.
Urine analysis. Urine amylase excretion is also increased.
X-ray examination. The most frequent findings is isolated dilatation of a segment
of gut (sentinel loop) consisting of jejunum, transverse colon, or duodenum adjacent
to the pancreas. An upper gastrointestinal contrasted series may show a widened
duodenal loop. Chest film may reveal pleural effusion on the left side.
Ultrasound provides an available, rapid, and noninvasive means of imaging the
pancreas that is often helpful. In the case of simple acute pancreatitis, an enlarged
gland is typically seen. The technique is also valuable for assessing and sequentially
evaluating peripancreatic fluid collections or pancreatic pseudocyst. In addition,
ultrasound examination yields information regarding cholelithiasis,
choledocholithiasis, and the status of the intrahepatic and extrahepatic biliary ducts.
Computed tomography (CT) has similar capabilities to ultrasound, although
sensitivity for detecting cholelithiasis is lower. Intraluminal contrast in the duodenum
and small bowel is necessary to optimize CT imaging. CT scan findings may suggest
edematous pancreatitis, areas of necrosis and infected necrosis (fluid and gas, which
are situated in pancreatic or peripancreatic tissue).
The role of ERCP in the diagnostic evaluation of the patient with acute
pancreatitis is severely limited because of the high risk of increasing existing
inflammation. ERCP combined with urgent therapeutic sphincterotomy and gallstone
extraction has been used for patients with impacted ampullary gallstones.
Upper endoscopy presents an indirect data, such as: deformation of the
posterior gastric wall, acute gastroduodenitis, occasionally, multiple ulcerations of the
upper GI tract (with or without hemorrhage).
Laparoscopy reveals direct signs of acute pancreatitis: areas of fat necrosis on
omentum and peritoneum, hemorrhagic fluid, edema of the gastrocolic ligament and
omentum. The indirect signs are: cholestasis, distended gallbladder, and intestinal
 8

paralysis. The amylase concentration is very high in the fluid, obtained from the
peritoneal cavity, during laparoscopy. In additional, laparoscopy may serve as a
curative method, especially in the case of fermentative peritonitis. The simple
laparoscopic drainage of the peritoneal cavity can significantly ameliorate patient’s
status.
Several grading systems have been developed to estimate risks and outcomes
based on the presenting clinical features, and the Ranson criteria are widely adopted.
Pancreatitis-associated morbidity and mortality are directly correlated with the
number of these criteria present. The mortality rate is 2% for 0-2 criteria,15% - for 3-
4, 40% for 5-6, and 100% for 7-8.
RANSON’S CRITERIA OF SEVERITY OF ACUTE PANCREATITIS
On Admission
Age above 55 years
White blood cell count above 16,000/E6L
Glucose level above 200 mg/dL
Lactase dehydrogenase level above 350 IU/L
Serum glutamic-oxaloacetic transaminase value above 250 IU/L

After 48 Hours
Hematocrit decrease of 10%
Blood urea nitrogen level increase of 5 mg/dL
Ca2+ level below 8 mg/dL
PaO2 level below 60 mmHg
Base deficit value above 4 mEq/L
Fluid sequestration greater than 6L

Glasgow (Imrie) parameters. The detection of three or more parameters is a

sign of severe pancreatitis.(p.25)
The APACHE II (Acute Physiology Score and Chronic Health Evaluation)
scoring system for critically ill patients has also been applied. Although not specific
for acute pancreatitis, the APACHE score has some utility by predicting mortality
rates in critically ill patients.
Differential diagnosis should be done with the following conditions: perforated
gastroduodenal ulcer, acute cholecystitis, intestinal obstruction, acute appendicitis,
myocardial infarction, left-side pleuropneumonie etc.

TREATMENT
All patients with acute pancreatitis must be hospitalized. If possible, every
patient should be initially monitored in an intensive care unit. The treatment of acute
 9

pancreatitis, even in severe forms, is initially conservative. There are following goals
of medical therapy:
1) Pain relief;
2) Treatment of clotting disorders;
3) Fluid replacement;
4) Reduction of pancreatic secretion and inhibiting proteases;
5) Eradication of toxemia;
6) Prevention of complications.
Pain relief. Analgesics i.m. and i.v. should be administrated in high doses.
Besides of it, continuous epidural anesthesia (with lidocain), and paranefral blockage
(with Novocain) are largely used.
Treatment of clotting disorders. Heparin (Fraxiparin), low-molecular-weight
dextran, and fibrinolytic therapy have been shown to prevent disseminated
intravascular coagulopathy in acute pancreatitis. Fresh plasma also is indicated in the
event of coagulation disorders.
Fluid replacement. Regional retroperitoneal inflammation and the systemic
microvascular injury contribute to the loss of intravascular plasma volume.
Hypovolemia may be mild or profound to the point of shock. Resuscitation requires
the intravenous administration of large volumes of isotonic crystalloid solution and
correction of acid-base balance (normal saline solution, lactated Ringer’s solution,
isotonic glucose). The initial amount is usually 3L/day intravenously, but under some
circumstances may be considerably more. In severe cases with low serum protein,
the administration of albumin is indicated. In severe hemorrhagic pancreatitis, blood
transfusion is also be required.
Reduction of pancreatic secretion and inhibiting proteases. Oral feeding is
withheld, and a nasogastric tube is inserted to aspirate gastric secretion. Oral feeding
should be resumed only after patient’s improvement, and normalization of serum
amylase. The bag with ice is put on epigastric region, because a local hypothermia
also decreases pancreatic secretion.
Somatostatin and its analogue octreotide inhibit pancreatic enzyme secretion.
Another medications with the same action are: atropine, glucagon, H 2-receptors
antagonists (quamatel).
 10

In order to inhibit proteases in the blood flow, gordox, contrical, aprotinin

(Trasylol) are used empirically. Such therapy should be began as soon as possible,
and in maximal doses.
Eradication of toxemia: a) metoda diurezei forţate; b) peritoneal lavage in some
cases allows to remove toxins from the peritoneal fluid, and prevent its absorption in
the systemic circulation. The technique involves infusion and withdrawing 1-2 L of
lactated Ringer’s solution every hour for 1-3 days. c) Hemodialysis in the event of
acute renal failure. d) plasmoferezei.
Prevention of complications. Antibiotics in the event of necrotizing pancreatitis
are indicated, if possible, according to antibiotic sensitivity test (fine needle aspiration,
blood culture). In the other case, empirical therapy should be indicated: 3 rd generation
cephalosporin with metronidazole.

COMPLICATIONS OF ACUTE PANCREATITIS

Complications of acute pancreatitis can be classified:
1) According to etiology and pathogenesis:
a) Proteases dependent complications;
b) Infectious complications;
c) Hemorrhagic complications;
d) Combined complications.
2) According to localization:
a) Pancreatic and peripancreatic complications;
b) Intraperitoneal complications;
c) Extraabdominal complications.
3) According to time of appearance:
a) Early complications;
b) Late complications.
4) According to pathological findings:
a) Functional complications;
b) Organic complications.
In edematous and necrotizing pancreatitis a common event appears to be
microvascular endothelial cell injury in diverse target organs. Proteases dependent
microvascular lung injury is one such example. This pathologic process is a likely
explanation for the frequent pulmonary symptoms (pleural effusion, pneumonia,
 11

athelectasis), and the occasional adult respiratory distress syndrome in patients with
acute pancreatitis. Other target organs at risk for acute pancreatitis-induced injury are
the liver (hepatitis), kidneys (acute renal failure), heart (myocarditis), and brain
(encephalopathy). However, these are early, have a functional character, and may be
corrected by conservative treatment.
In the period of infected necrosis, complications have an organic character,
these are late, and infection dependent (pancreatic pseudocyst, pancreatic abscess,
peripancreatitis, pancreatic fistula, digestive fistulas, intraperitoneal or GI
hemorrhage). Surgery is almost always indicated.
Pancreatitis-induced peritonitis.
This frequent complication is divided into: a) fermentative peritonitis, b)
suppurative (purulent) peritonitis, and c) pancreatic ascites.
Fermentative peritonitis. Pancreatitis causes an exudate that at first is
retroperitoneal, but soon the peritoneal cavity is involved. It is a chemical peritonitis
initially with a high level of amylase in the exudate. The cause of fermentative
peritonitis is the increased vascular permeability with diffusion of enzymes and toxins
into the peritoneal cavity and retroperitoneal space. According to fluid character it
may be: serous (33%), serous-hemorrhagic (10%), hemorrhagic (44%), and bilious
(13%). Laparoscopy is the method of choice of diagnosis and treatment in severe
fermentative peritonitis. After that pathological fluid is eliminated, peritoneal lavage is
installed.
Suppurative (purulent) peritonitis complicates a course of infected pancreatic
necrosis. It may be induced by purulent peripancreatitis, suppurative omentitis, or
contamination with organisms from the GI tract occurs.
Pancreatic ascites results of compression of the portal vein by enlarged
pancreatic mass. Intraperitoneal fluid accumulates in the very large amount (up to 10-
12 liters). The general status of patients is poor, vomiting and denutrition are
common, abdominal distention and free fluid in peritoneal cavity are evident.
However, this condition is not associated with pain or peritonitis. The ascitic fluid
contains elevated protein (>29g/L) and amylase levels.
Pancreatic abscess.
The common causes of pancreatic abscess are an infected pancreatic
pseudocyst and necrotizing pancreatitis. More often is situated in cephalic part of
pancreas.
 12

The diagnosis is suggested by persistent fever, leukocytosis, and a palpable

abdominal mass. Occasionally, it’s accomplished with symptoms of duodenal
compression (nausea, vomiting, epigastric distention), or common bile duct’s
compression (jaundice). CT scanning or ultrasound facilitates the diagnosis. On
imaging, debris within a cyst is more suggestive of an abscess; percutaneous
aspiration with positive cultures is the definitive preoperative test.
The treatment of choice is wide surgical debridement with removal of all infected
and devitalized tissues, large and effective external drainage, and antibiotics.
Pancreatic pseudocyst
A pancreatic pseudocyst is a fluid-filled cystic structure without a true epithelial
lining that is associated with the pancreas or pancreatic duct. The pseudocyst wall is
composed of displaced adjacent viscera (often stomach, small bowel, or colon) and a
fibrous capsule that has evidence of both acute and chronic inflammation. The
thickness of this fibrous capsule is variable, depending on how long the pseudocyst
has been present. The fluid within the cyst cavity is usually serous in character and
contains pancreatic secretions, including amylase and proteases, as well as albumin
and inflammatory cells. Formation of the pseudocyst begins on 3 rd-4th week, and ends
after 3-6 months.
Pancreatic pseudocyst may be distinguished into: 1) intraparenchymatous and
extraparenchymatous; 2) communicates or non-communicates with the pancreatic
duct; 3) situated in head, body or tail of the gland.
The clinical presentation of a pancreatic pseudocyst is usually that of persistent
epigastric pain or proximal ileus 3-4 weeks after an episode of acute pancreatitis.
Fever, leukocytosis, and a palpable epigastric mass are common, nausea and
vomiting less so. CT scan, ultrasonography, and contrasted x-ray examination of the
upper GI tract are helpful for diagnosis.
Indications for surgical treatment include increasing size, infection,
gastrointestinal tract obstruction, hemorrhage, spontaneous rupture, and failure to
resolve. The operative treatment for pseudocyst depends on the underlying cause of
the cyst as well as the size, location, and maturity of the pseudocyst wall. Operative
drainage can be either external or internal. External drainage is chosen in the
presence of infection or an immature capsule. The disadvantages of external
drainage include the risk of pancreatic fistula formation and a pseudocyst recurrence.
Cystogastrostomy is the simplest and safest alternative if the pseudocyst is adjacent
 13

to the posterior wall of the stomach. Cystojejunostomy using a Roux-en-Y or loop

jejunostomy may also be appropriate. Pancreatic resection is associated with the
lowest recurrence rate (3%), but is limited to pseudocyst occurring in the tail of the
pancreas.
Pancreatic fistula
Pancreatic fistula appears due to pancreatic necrosis, which involves a main
pancreatic duct. Diagnosis includes fistulography and ERCP. Initial management of
pancreatic fistula is conservative: adequate drainage of the fistula channel, closure
with fibrin glue, diet and other measures to decrease pancreatic secretion,
radiotherapy.
If this treatment (which should be done at least 6 months from the time of initial
diagnosis) is failure, surgery is indicated: fistulojejunostomy, or distal pancreatic
resection.
Digestive fistulas
Perforation of the adjacent viscera in acute pancreatitis, such as stomach,
duodenum, and colon, appears in the 3 rd period of disease. Gut fistula occurs due to
nearby suppurative process, vascular thrombosis and affect of the enzymas. Usually,
the diagnosis is clear, but occasionally upper or lower GI endoscopy, and
fistulography are necessary. Overall mortality is up to 50%.
Initial treatment of the digestive fistulas is conservative: total parenteral nutrition,
or enteral feeding through feeding tube, placed beyond of orifice; nasogastric
aspiration and mechanical tamponada of the fistula. Feeding jejunostomy is also
indicated for some cases.
Surgery for digestive fistula consists in segmental resection of the gut. In
fistulas, situated on the colon, right side colostomy should be done.
Suppurative peripancreatitis
Usually necrotizing pancreatitis involves in the process fat tissue of the
retroperitoneal space, including pericolic spaces and paranephrium (peripancreatitis).
In the 3rd period of disease (infected pancreatic necrosis), peripancreatitis becomes
purulent-suppurative of character. Its difficult to distinct “infected necrotizing
pancreatitis” and “suppurative peripancreatitis” before surgery.
After laparotomy the lesser sac, containing pancreas, is opened by transection
of the gastrocolic ligament. The presence of an infected sequestrum mandates to
debride devitalized tissue and to provide external drainage. All peripancreatic spaces
 14

are opened and any necrotic tissue is removed by gentle blunt dissection. Intact
pancreatic tissue should be left. Specific antibiotic coverage is essential and should
be dictated by intraoperative cultures or aspirates from the necrotic tissue.
Cholecystectomy is performed for gallstone disease, and external choledochostomy
or cholecystostomy – if there is a bile duct obstruction. After necrosectomy three
following method of treatment are available: 1) closed lavage via double-lumen
drains, 2) scheduled re-laparotomy after about 24-48 hours, or 3) “open abdomen”
(open packing) with subsequent repeated debridement. Debridement is often
required on multiple occasions, usually at 48- to 72-hour intervals, until a granulating
wound replaces the necrotic tissue. Use of open drainage or marsupialization with
frequent dressing changes has a reported mortality rate of 10% to 15%.
Intraperitoneal and GI hemorrhage
Gastrointestinal bleeding may occur from adjacent inflamed stomach or
duodenum, ruptured pseudocyst, or peptic ulcer. Intraperitoneal bleeding may occur
spontaneously from the celiac or splenic artery or from the spleen, following acute
splenic vein thrombosis.
Management is depended on the source and magnitude of hemorrhage. Acute
bleeding gastroduodenal erosions and ulcers should be treated conservatively, with
hemostatic and anti-secretor therapy, and endoscopic hemostasis. Ruptured
pseudocyst requires urgent surgical hemostasis. One of the major sources of
morbidity and mortality is severe intraperitoneal bleeding, particularly from splenic
artery. In this case the immediate surgical operation with hemostasis is indicated.

CHRONIC PANCREATITIS
Chronic pancreatitis is a disease characterized by progressive and permanent
destruction of the pancreatic exocrine parenchyma associated with fibrosis of the
gland. This condition presents a progressive morphologic and functional
derangement of the pancreas. In chronic pancreatitis, fibrotic destruction of the
exocrine gland is often also accompanied by endocrine dysfunction. Within chronic
pancreatitis, calcifying chronic pancreatitis and obstructive chronic pancreatitis may
be distinguished. The third form, which occasionally is marked, is inflammatory
chronic pancreatitis (N.Angelescu, 2001).
Chronic pancreatitis may be categorized into:
1) Relapsing chronic pancreatitis;
 15

2) Chronic cholecysto-pancreatitis;
3) Obstructive chronic pancreatitis;
4) Pseudotumorous pancreatitis;
5) Calcifying chronic pancreatitis;
6) Pseudocyst.

SYMPTOMS
Pain is the predominant symptom in most patients with chronic pancreatitis (92-
95%). Pain associated with chronic pancreatitis is usually localized to the
epigastrium, with radiation to the back in the region of the upper lumbar vertebrae.
The pain is usually dull rather than sharp and constant rather than intermittent or
colicky. In some patients, pain is accomplished by nausea and vomiting. Weight loss
is the second common sign, and its caused by pain and malabsorption. Postprandial
abdominal pain is common in patients with chronic pancreatitis, and the fear of this
pain can lead to a further reduction in food intake. Malabsorption occurs when loss of
functioning exocrine tissue is advanced, usually greater than 90%. Diarrhea and
steatorrhea is the first clinical signs of malabsorption. About 75% of patients with
calcific pancreatitis and 30% of those with non-calcific pancreatitis have insulin-
dependent diabetes. Jaundice may result from fibrotic biliary obstruction of the lower
portion of the bile duct.

DIAGNOSIS
Abnormal laboratory findings may result from: 1) pancreatic inflammation
(leucocytes, amylase), 2) pancreatic exocrine insufficiency (faecal fat analysis), 3)
diabetes (serum glucose concentration, oral glucose tolerance test), 4) bile duct
obstruction (liver function tests).
Calcifications on the plain abdominal X-ray usually confirm the diagnosis of
chronic pancreatitis. The examination has a sensitivity of 30%.
Barium contrasted examination of the upper GI tract. If duodenal stenosis is
suspected, it may be seen on the films.
Ultrasound is useful in initial evaluation of patients with suspected chronic
pancreatitis. Findings include atrophy of the gland, dilation of the pancreatic duct too
greater than 4 mm, and associated cystic lesions.
 16

CT findings consistent with this diagnosis include glandular atrophy, irregularity

of the pancreatic outline, calcification, and ductal dilation. Small cystic lesions are
well demonstrated by CT. Sensitivity for CT approaches 75% to 90%.
ERCP has become widely recognized as the most sensitive and reliable method
for diagnosing chronic pancreatitis. In severe cases the main pancreatic duct may be
dilated with alternating areas of stenosis. ERCP is also useful in demonstrating
associated anatomic abnormalities, such as common bile duct stenosis or pancreatic
pseudocyst.

TREATMENT
Conservative treatment. The therapy of chronic pancreatitis is aimed at
relieving the pain and at preventing or treating exocrine and endocrine insufficiency.
Patients with chronic pancreatitis should be urgent to discontinue the use of alcohol.
This reduces chronic or episodic pain in more than half of cases.
Diet: low fat diet, frequent small meals, avoidance of foods not individually
tolerated, and diabetes diet in the case of endocrine insufficiency.
The dosage of analgesics is individually adjusted. In the case of a mild pain
spasmolytics (papaverin, plathyphillin, no-spa) are indicated. In moderate and severe
pain the combination of analgesics and antidepressants is administrated.
Pancreatic enzyme supplimentation is administrated in the case of weight loss,
steatorrhea, excessive bowel gas (pancreatine, panzinorm, festal, mezim). B vitamins
should be given in the case of nutritional deficiency due to chronic alcoholism.
Diabetes in these patients usually requires insulin.
Surgical treatment. A pancreatic duct stricture may cause pain. Endoscopic
Wirsungotomy, or pancreatic head stenting may provide improvement. In the case of
calcific pancreatitis, an endoscopic extraction of the pancreatic stones with a basket
may relieve pain and slow the progressive loss of pancreatic function.
Surgical treatment in most cases involves a procedure that 1) facilitates
drainage of the pancreatic duct or 2) resects diseased pancreas. The choice of
operation can usually be made preoperatively based on the findings of a ERCP and
CT scan. Associated bile duct obstruction is common and should be treated by
simultaneous choledochoduodenostomy.
A dilated ductal system reflects obstruction, and when dilatation is present,
procedures to improve ductal drainage usually relieve pain. The usual findings is an
 17

irregular, widely dilated duct (1-2 cm in diameter) with points of stenosis and ductal
calculi. For such patients a longitudinal pancreaticojejunostomy (Puestow procedure)
is indicated. The duct is opened anteriorly from the tail into the head of the gland and
anastomosed side-to-side to a Roux-en-Y segment of proximal jejunum.
Transduodenal open sphincteroplasty and distal (caudal)
pancreaticojejunostomy (Du Val procedure) are other drainage procedures that were
used more often in the past.
Pancreatic resection may be considered when patients have small duct. Distal
pancreatectomy may be performed when pathologic changes are situated to the tail
or body of the pancreas. Immediate pain relief is observed in about 80% of patients
after distal pancreatectomy.
Resection of the pancreatic head by pancreaticoduodenectomy (Whipple
operation) may be performed in selected patients with disease located in the head of
the gland. Indications for pancreaticoduodenectomy include (1) a chronic
inflammatory mass involving the head of the gland, associated with duodenal
stenosis, (2) multiple pseudocyst in the head of the pancreas, and (3) failure of
pancreaticojejunostomy. Pain relief occurs in 70% to 90% of patients.
În pancreatita scleroasă difuză în care tabloul clinic este dominat de durere, iar
permeabilitatea canalului Wirsung este păstrată se pot încerca şi unele operaţii pe
sistemul nervos vegetativ, dintre care cea mai utilizată a fost splanhnico-solarectomia
stângă (secţiunea splanhnicului mare, splanhnicului mic şi ganglionului solar stâng,
operaţia Mallet-Guy). Se mai efectuează neurotomia postganglionară (procedeul
Loşioka-Vacabaiaşi), neurotomia marginală (procedeul Napalkov-Trunin) etc.
Celiac plexus block with alcohol injections provides relief of pain in some
patients.