By Dr.Tatyana Kravchenko from Surgery Department#1

1. O.O.Bogomolets National Medical University
Department of Urology
“Approved”
at the Methodist Faculty Surgery
Department # 1 Council
“__”_____2008, protocol #_____
Head of
Faculty Surgery Department # 1
Professor _______ M.P.Zakharash
Study Guide for Practical Work for Teachers and Students
Topic: “Complications of pancreatitis”.
Course 4
Foreign Students’ Medical Faculty
Duration of the lesson – 60 min.
Worked out by
Assistant…..
Kyiv
2008

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I. The theme actuality.
Although acute pancreatitis may run a mild self-limiting course, severe pancreatitis
occurs in up to 25% of acute attacks, with a mortality approaching 10%. The majority of
deaths occur within the first week of hospital admission and are caused by local and
systemic complications, including sepsis and respiratory failure. Most clinical studies in
adults cite pancreatic infection as the most common cause of death, accounting for
70-80% of deaths.
II. Startup aims of the study.
To teach students major methods of stone disease diagnosis and treatment.
Student should have knowledge:
1. Definition and prevalence of pancreatitis complications.
2. Clinical manifestations (features) of pancreatitis complications.
3. Pathogenesis of pancreatitis complications
4. Methods of diagnosis.
5. Treatment of pancreatitis complications.
6. Prevention of pancreatitis complications.
Student should be able to:
1. Correctly gather an anamnesis.
2. Compose adequate examination plan for patient with pancreatitis complications .
3. Interpret received results of examinations.
4. Interpret data of x-ray, ultrasound scan, CT, endoscopy.
5. Determine the type of complications basing on investigations’ data.
6. Determine the severity of pancreatitis complications.
7. Compose plan for treatment of patient with pancreatitis complications.
8. Treat patient with complication of pancreatitis.
III. Educative aims of the study.
1. To acquire the skills of psychological contact establishment and creation of
trusting relations between the doctor and the patient.

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2. The development of insight of ecological and socio-economic factors’ influence
on health condition.
3. The formation of deontology concepts and practical skills related to patients with
complication of pancreatitis.
4. The development of responsibility sense for timeliness and completeness of
patient’s investigation, as well as for patient awareness about possible methods
of treatment and adverse effects which are concerned with them.
5. To develop deontology presentations, be able to carry out deontology approach
to the patient
IV. The content of the theme.
Introduction
Severe cases of acute pancreatitis may lead to a number of complications: early
systemic complications of pancreatitis and later complications.
Definitions
Systemic complications of acute pancreatitis are numerous (Table 1) and correlate well
with the severity of the inflammatory process. They may be manifested by shock
(circulatory collapse secondary to sequestration of retroperitoneal fluid or hemorrhage),
respiratory and renal failure and profound metabolic disturbances.
TABLE 1. Systemic complications of pancreatitis
Metabolic Hypocalcemia, hyperglycemia, hypertriglyceridemia,
acidosis
Respiratory Hypoxemia, atelectasis, effusion, pneumonitis
Acute respiratory distress syndrome (ARDS)
Renal Renal artery or vein thrombosis
Renal failure
Circulatory Arrhythmias
Hypovolemia and shock; myocardial infarct
Pericardial effusion, vascular thrombosis
Gastrointestinal Ileus

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Gastrointestinal hemorrhage from stress ulceration; gastric
varices (secondary to splenic vein thrombosis)
Gastrointestinal obstruction
Hepatobiliary Jaundice
Portal vein thrombosis
Neurologic Psychosis or encephalopathy (confusion, delusion and
coma)
Cerebral emboli
Blindness (angiopathic retinopathy with hemorrhage)
Hematologic Anemia
DIC (disseminated intravascular coagulopathy)
Leucocytosis
Dermatologic Painful subcutaneous fat necrosis
The pathogenesis and management of the cardiovascular collapse, respiratory failure,
renal failure, metabolic encephalopathy, gastrointestinal bleeding, and disseminated
intravascular coagulation that complicate severe pancreatitis appear to be identical to
those involved when these processes are superimposed on other disease states that are
characterized by peritonitis and hypovolemia. Cardiovascular collapse is largely caused
by hypovolemia, and its management requires aggressive fluid and electrolyte repletion.
This may necessitate placement of a central venous or Swan-Ganz monitoring catheter.
Changes in hematocrit, filling pressures, and cardiac output can be used to monitor the
adequacy of treatment, but changes in blood pressure, pulse, and urine output do not
accurately and reliably reflect the adequacy of fluid replacement.
The pulmonary manifestations of pancreatitis include atelectasis and acute lung injury.
The latter appears to be similar to the acute lung injury caused by other systemic
processes, including septic shock, ischemia and reperfusion, and massive blood
transfusion. Management includes good pulmonary toilet combined with close
monitoring of pulmonary function. For many patients, intubation and respiratory
support may be required. Renal failure in pancreatitis is usually prerenal and is
associated with a poor prognosis. In severe cases, dialysis, usually hemodialysis, may
be required. Stress-induced gastroduodenal erosions account for most of the

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gastrointestinal bleeding in pancreatitis and prophylaxis with antacids, H2-receptor
antagonists, or proton pump inhibitors may be appropriate. Rarely, massive bleeding
can result from injury to peripancreatic vascular structures, leading to hemorrhage into
the retroperitoneum. The peripancreatic inflammatory process can also cause
thrombosis of major gastrointestinal vessels and result in ischemic lesions involving the
stomach, small intestine, or colon that can cause bleeding. Management of these
complications of pancreatitis is similar to that involved when they occur in the absence
of pancreatitis. Some patients with severe pancreatitis develop disseminated
intravascular coagulation, but it rarely causes bleed-ing, and prophylactic heparinization
is usually not indicated.
In 1992, an international symposium was held to resolve the confusion that had
arisen concerning the terminology used to describe the local complications of
pancreatitis and the value of specific treatments for those complications.[29] The
following definitions were agreed on at that conference:
1. Acute Fluid Collections. These occur during the early stages of severe pancreatitis in
30% to 50% of patients, they lack a wall of granulation or fibrous tissue, and more
than half regress spontaneously. Most are peripancreatic, but some are
intrapancreatic. Those that do not regress may evolve into pseudocysts or involve
areas of necrosis.
2. Pancreatic and Peripancreatic Necrosis. These are areas of nonviable pancreatic or
peripancreatic tissue that may be either sterile or infected. They typically include
areas of fat necrosis, and the necrotic tissue has a puttylike or pastelike consistency.
Some necrotic regions may evolve into pseudocysts, whereas others may be replaced
by fibrous tissue.
3. Pancreatic Pseudocyst. These are collections of pancreatic juice, usually rich in
digestive enzymes, that are enclosed by a nonepithelialized wall composed of fibrous
and granulation tissue (Fig. 55-4). Pseudocysts can be intrapancreatic but are more
commonly extrapancreatic and occupy the lesser peritoneal sac. Pseudocysts are
usually round or oval in shape and are not present before 4 to 6 weeks after the onset
of an attack. Before that time, the fluid collection lacks a defined wall and is usually
either an acute fluid collection or a localized area of necrosis (see earlier).

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Pseudocysts may be colonized by microorganisms, but infection, as evidenced by
the presence of pus, is less common. When pus is present, the infected pseudocyst is
referred to as a pancreatic abscess. Leakage or rupture of a pseudocyst into the
peritoneal cavity results in pancreatic ascites. A pancreaticopleural fistula results
from erosion of a pseudocyst into the pleural space.
4. Pancreatic Abscess and Infected Pancreatic Necrosis. These are circumscribed intra-
abdominal collections of pus, usually in proximity to the pancreas, which contain
little or no necrotic tissue but arise as a consequence of pancreatitis. An infected
pseudocyst is considered a pancreatic abscess. Pancreatic abscess and infected
pancreatic necrosis represent the extremes of a spectrum that includes lesions with
varying amounts of necrosis. Thus, in a pancreatic abscess, there is little necrosis,
and the material has a liquid consistency, whereas in infected pancreatic necrosis,
necrosis predominates, and the material is pastelike or puttylike.
Diagnosis
Contrast-enhanced CT is particularly valuable as a means of quantifying the extent of
pancreatic necrosis (i.e., nonenhancement). The maturation of a pseudocyst can be
followed by both contrast-enhanced CT and endoscopic ultrasound. Management of
local pancreatitis complications is dependent on whether the lesion is sterile or infected
(see later). Occasionally, infection can be diagnosed when plain abdominal films or CT
scans reveal extraintestinal gas bubbles or air either within the area of inflammation or
elsewhere in the retroperitoneum. When the clinical suspicion of infection is high, fine-
needle aspiration of peripancreatic or intrapancreatic fluid for culture and Gram stain
analysis may be particularly helpful.[30] The procedure is most frequently done with
CT guidance, and it is safe when performed by experienced radiologists.
Management of Sterile and Infected Acute Fluid Collections
Sterile acute fluid collections usually resolve spontaneously, and no specific treatment
is indicated. Attempts to drain acute fluid collections, either by using percutaneously
placed drains or by intervening surgically, are discouraged as they are usually
unnecessary, and furthermore, they are likely to lead to infection. Even without

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instrumentation, these fluid collections can become infected, but because they contain
liquid pus with little or no necrotic tissue, they are amenable to transcutaneous catheter
drainage along with antibiotic therapy. It is generally believed that aspirating fluid from
any site near the pancreas yields information that is relevant to all the fluid collections
and that sampling multiple sites is unnecessary.
Management of Sterile and Infected Necrosis
The role of surgical intervention in the management of patients with sterile pancreatic or
peripancreatic necrosis has been the subject of considerable controversy.[31] Opinions
range from those advocating aggressive débridement for patients with sterile necrosis
who fail to rapidly improve on nonoperative treatment to those who claim that surgical
intervention is virtually never indicated when the necrosis is sterile. Those taking the
former position claim that removing the necrotic tissue (i.e., necrosectomy) reduces
morbidity and speeds recovery, whereas those taking the latter position, including me,
base their position on the fact that most people treated nonoperatively will eventually
recover and some who undergo operation may actually be made worse by the operation.
There is, however, a general consensus that patients with infected necrosis require some
form of intervention. Prospective studies have indicated that infection of areas of
necrosis can occur at any time but that it usually occurs during the initial 3 to 4 weeks
of an attack. Although some recent reports have indicated that highly selected patients
might be adequately treated with antibiotics alone,[32] simple antibiotic therapy is
generally considered to be inadequate because the necrotic tissue acts as a foreign body,
making it impossible to sterilize the area with antibiotics alone. Combining antibiotic
therapy with percutaneous catheter drainage may also not be adequate treatment
because the pastelike necrotic tissue does not pass through the small-bore drainage
catheters, and therefore, drainage is usually incomplete. Other methods of removing the
necrotic tissue, either through a transpapillary endoscopic route or using minimally
invasive surgical approaches with an operating nephroscope, have been tried, but
experience with these techniques has been limited and essentially anecdotal. The
conventional approach to managing infected necrosis involves laparotomy and surgical

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débridement of the infected, devitalized tissue. Repeated operations and débridement
may be needed. The timing of the initial débridement appears to be closely related to the
outcome; that is, those undergoing later operations do better and require fewer repeat
operations than those undergoing early operation. Thus, in stable patients, delaying
operative intervention may decrease the overall morbidity of an attack.
The goal of operation in patients with infected necrosis is to remove as much as possible
of the infected, necrotic tissue and to provide drainage for the remaining viable exocrine
tissue. Many different ways of achieving these goals have been described (Box 55-4),
and although each has its advocates, none has been proved super-ior to the others. My
practice is to perform repeat operations, each of which involves débridement and
abdominal wall closure. At the time of the final débridement, drains and a feeding
jejunostomy are placed. For the most part, the repeat laparotomies are performed every
2 to 3 days until no further débridement is possible or necessary.
Management Options for Infected Pancreatic Necrosis
Conventional Approach:
• Débridement with reoperation when clinically indicated or at planned intervals
• Débridement with open or closed packing and reoperation when clinically indicated or
at planned intervals
• Débridement with continuous lavage
Unconventional Approach:
• Antibiotics alone
• Antibiotics with percutaneous drainage
• Antibiotics with endoscopic drainage
• Antibiotics with surgical drainage but not débridement
• Antibiotics with débridement through minimally invasive surgery
Management of Pancreatic Pseudocysts
Most pseudocysts communicate with the pancreatic ductal system and contain a watery
fluid that is rich in pancreatic digestive enzymes. Typically, patients with pseudocysts
have persistent elevations of circulating pancreatic enzymes. Recent reports have shown

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that many pseudocysts eventually resolve without complications and that intervention
is not mandatory in all cases unless the pseudocysts are symptomatic, enlarging, or
associated with complications. The likelihood that a pseudocyst will resolve
spontaneously, however, is dependent on its size. Large pseudocysts (i.e., >6 cm in
diameter) are more likely to become symptomatic either because they are tender or
because of their mass effect on adjacent organs. Those that compress the stomach or
duodenum may cause gastric outlet obstruction with nausea and vomiting. Those that
reduce the capacity of the stomach frequently cause early satiety, whereas those
impinging on the bile duct can cause obstructive jaundice. Pancreatic pseudocysts that
erode into a neighboring vessel can result in formation of a pseudoaneurysm with
hemosuccus pancreaticus and upper gastrointestinal bleeding.
Symptomatic or enlarging pseudocysts can be treated by several methods. Those in the
tail can be treated by excision (i.e., distal pancreatectomy), but excision in the setting of
recent acute inflammation may be hazardous. Most patients who develop symptomatic
pseudocysts are best managed by pseudocyst drainage. In poor surgical risk patients,
percutaneous catheter drainage can be considered, but in my experience, that approach
leads to considerable morbidity because of catheter-induced infection and the
development of a prolonged external pancreatic fistula. Internal drainage can avoid
these problems and seems preferable. Internal drainage can be accomplished either
endoscopically (by transpapillary drainage, cystogastrostomy, or cystoduodenostomy)
or surgically (by cystogastrostomy, cystoduodenostomy, or Roux-en-Y
cystojejunostomy). The approach chosen depends primarily on the locally available
expertise as well as the location of the pseudocyst, but endoscopic drainage may be
preferable in poor surgical risk patients.
Pseudocysts that are directly adjacent to either the stomach or duodenum can be safely
drained endoscopically if there are no intervening vessels. After endoscopic ultrasound
and preliminary aspiration of the cyst fluid to confirm the diagnosis and exclude
intervening vessels, endoscopic drainage is achieved by making an incision into the
pseudocyst through the wall of the stomach or duodenum. To facilitate decompression,
the opening is relatively large, and a pigtail catheter may be placed. Transpapillary
drainage might be more appropriate for patients with pancreatic head pseudocysts

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whose CT and endoscopic ultrasound suggest that incising into the pseudocyst could
be hazardous. At the time of endoscopic retrograde cholangiopancreatography (ERCP),
a stent is passed into the pseudocyst through the papilla of Vater. Unfortunately,
transpapillary drainage, particularly when incomplete, can allow bacteria to enter the
pseudocyst and lead to development of an infected pseudocyst. Another transpapillary
approach involves placing a stent across the duct defect rather than into the cyst through
the defect. By excluding pancreatic juice from the pseudocyst, this bridging intraductal
stent may permit the duct disruption to heal and the pseudocyst to resolve without
drainage. Further experience with this tech-nique will be needed before its ultimate use
can be determined.
Surgical internal drainage of pseudocysts is usually accomplished by creating either a
Roux-en-Y cysto-jejunostomy, a side-to-side cystogastrostomy, or a side-to-side
cystoduodenostomy. The former is usually accomplished by directly anastomosing a
defunctionalized Roux-en-Y limb of jejunum to the opened pseudocyst. Surgical
cystogastrostomy (or cystoduodenostomy) has traditionally been accomplished by
laparotomy and anterior gastrotomy (or lateral duodenotomy). A generous incision is
then made through the posterior wall of the stomach (or medial wall of the duodenum)
into the pseudocyst. Some surgeons now perform cyst-gastrostomy using a laparoscopic
approach.
Management of Pancreatitis-Induced False Aneurysms
Rarely, pancreatic pseudocysts or areas of pancreatic necrosis can erode into pancreatic
or peripancreatic vascular structures. This results in the formation of a false aneurysm
because the vessel communicates with the pseudocyst. That false aneurysm may either
communicate with the ductal system or rupture into the free peritoneal cavity. The
former leads to bleeding into the pancreatic duct (hemosuccus pancreaticus) and
presents as transpapillary upper gastrointestinal bleeding. Rupture into the peritoneal
cavity can lead to hemoperitoneum. Therapeutic angiographic embolization is most
appropriate for the unstable patient, and this approach may also provide definitive
treatment, particularly for those patients whose false aneurysm is in the pancreatic head.

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For those whose false aneurysm is in the tail of the pancreas, subsequent distal
pancreatectomy, after the patient is stabilized, may provide more secure hemostasis.
Management of Pancreatic Ascites and Pancreaticopleural Fistulas
Pancreatic ascites occurs when pancreatic juice gains entry into the peritoneal cavity
either from a pancreatic duct disruption or from a leaking pseudocyst. The diagnosis can
usually be made when high amylase levels are found in the ascitic fluid. The initial
treatment usually is nonoperative and involves attempts to decrease pancreatic secretion
by elimination of enteral feeding, institution of nasogastric drainage, and administration
of the antisecretory hormone somatostatin. Repeat paracentesis may also be helpful.
Roughly 50% to 60% of patients can be expected to respond to this treatment with
resolution of pancreatic ascites within 2 to 3 weeks. Persistent or recurrent ascites can
be treated either endoscopically or surgically. Endoscopic treatment involves
endoscopic pancreatic sphincterotomy with or without placement of a transpapillary
pancreatic duct stent. By reducing the resistance to drainage into the duodenum, and by
bridging the site of duct disruption, this approach is designed to allow the site of
leakage to seal. Surgical treatment of pancreatic ascites, usually preceded by
performance of an ERCP to identify the site of duct disruption, involves either resection
(for leaks in the pancreatic tail) or internal Roux-en-Y drainage (for leaks in the head
and neck region). It seems most appropriate to attempt endoscopic treatment initially
and to reserve surgical treatment for those patients who do not respond to endoscopic
therapy.
The genesis of pancreaticopleural fistula is similar to that of pancreatic ascites, but in
this case, the duct disruption is usually posterior, and the extravasated juice travels in a
cephalad direction through the retroperitoneum to reach the thoracic cavity. Although
the incidence of pancreaticopleural fistula is lower than that of pancreatic ascites, the
management of both is similar.
Management of Pancreaticoenteric Fistulas
Pancreatic pseudocysts or areas of pancreatic necrosis can erode into the small intestine,
duodenum, stomach, bile duct, or splenic flexure of the colon. Occasionally, this results

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in resolution of the pseudocyst, and no further treatment is needed. More often,
however, such an event is accompanied by significant bleeding or signs of sepsis, and
surgical intervention is usually required. Management of these fistulas is determined by
the gastrointestinal organ involved.
Management of Pancreatitis-Induced Splenic Vein Thrombosis and Sinistral
Varices
Because of the close proximity of the splenic vein to the pancreas, splenic vein
thrombosis is not unusual in cases of severe pancreatitis. For the most part, it does not
result in early symptoms, but it may eventually result in the formation of
gastroesophageal varices. Splenectomy provides effective and definitive treatment when
these sinistral varices bleed, but because bleeding occurs in fewer than 10% of these
patients, prophylactic splenectomy is not generally performed.
V. Lesson topic control questions.
Key points:
• Severe cases of acute pancreatitis may lead to a number of complications
• Systemic complications of acute pancreatitis are numerous and correlate well with the
severity of the inflammatory process.
• Diagnosis is not easy and includes Contrast-enhanced CT, endoscopic ultrasound,
plain abdominal films or CT, laboratory tests
• Despite modern treatment options open surgery is still occasionally necessary.
Cases
1. A 50-year-old patient is recovering from an episode of acute pancreatitis. Two weeks
later he complains of persistent epigastric pain. Part of his evaluation is an
ultrasonogram, with reveals a 4-cm cystic structure situated in the lesser sac
posterior to the stomach. Treatment for this time should include:
a) external drainage
b) internal drainage to the stomach

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c) internal drainage to the jejunum
d) resection of the pseudocyst
e) continued observation
2. Five weeks later the patient is still complaining of epigastric pain and the ultrasound
shows a thick-walled cyst arising from the head of the pancreas and measuring 6 cm
in diameter posterior to the stomach wall. Treatment at this point should be:
a) external drainage
b) internal drainage via the stomach
c) internal drainage via the jejunum
d) resection of the pseudocyst
e) continued observation
Answers
1. (e) The patient clinical course and ultrasound finding are consistent with
formation of the pseudocyst. Approximately 40% of pseudocyst may resolve
spontaneously in 4-6 weeks. In the absence of any other sighs of complications,
the patient should undergo continued close observation with serial ultrasounds.
2. (b) The pseudocyst has now persisted for 7 weeks and actually grown.
Definitive treatment is required at this point. External drainage would be indicated
only if the pseudocyst were infected or the cyst walls were not mature enough to
hold suture. Resection should be considered for a pseudocyst located in the tail of
the pancreas. The pseudocyst is adjacent to the stomach, and the simplest form of
drainage would be via cyst gastrostomy.
VII. Supporting materials required for teaching
1. Participation in clinical duties on admission
2. Working in library
VIII. Literature