bohomolets 4th year surgery complication of pancreatitis

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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…..

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Page 1: Bohomolets 4th year Surgery Complication of Pancreatitis

O.O.Bogomolets National Medical University

Department of Urology

“Approved”at the Methodist Faculty Surgery

Department # 1 Council“__”_____2008, protocol #_____

Head ofFaculty Surgery Department # 1

Professor _______ M.P.Zakharash

Study Guide for Practical Work for Teachers and Students

Topic: “Complications of pancreatitis”.

Course 4Foreign Students’ Medical FacultyDuration of the lesson – 60 min.

Worked out byAssistant…..

Kyiv2008

Page 2: Bohomolets 4th year Surgery Complication of Pancreatitis

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.

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1. To acquire the skills of psychological contact establishment and creation of

trusting relations between the doctor and the patient.

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

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Circulatory Arrhythmias

Hypovolemia and shock; myocardial infarct

Pericardial effusion, vascular thrombosis

Gastrointestinal Ileus

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.

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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

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.

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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).

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-

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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

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

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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

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

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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

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

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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

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

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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.

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.

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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

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

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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

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

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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

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