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Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
Bohomolets 4th year Surgery Complication of Pancreatitis
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Bohomolets 4th year Surgery Complication of Pancreatitis

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By Dr.Tatyana Kravchenko from Surgery Department#1

By Dr.Tatyana Kravchenko from Surgery Department#1

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  • 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.ZakharashStudy 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
  • 2. 2I. The theme actuality.Although acute pancreatitis may run a mild self-limiting course, severe pancreatitisoccurs in up to 25% of acute attacks, with a mortality approaching 10%. The majority ofdeaths occur within the first week of hospital admission and are caused by local andsystemic complications, including sepsis and respiratory failure. Most clinical studies inadults cite pancreatic infection as the most common cause of death, accounting for70-80% 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.
  • 3. 3 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 patientIV. The content of the theme. IntroductionSevere cases of acute pancreatitis may lead to a number of complications: earlysystemic complications of pancreatitis and later complications.DefinitionsSystemic complications of acute pancreatitis are numerous (Table 1) and correlate wellwith 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 pancreatitisMetabolic Hypocalcemia, hyperglycemia, hypertriglyceridemia, acidosisRespiratory Hypoxemia, atelectasis, effusion, pneumonitis Acute respiratory distress syndrome (ARDS)Renal Renal artery or vein thrombosis Renal failureCirculatory Arrhythmias Hypovolemia and shock; myocardial infarct Pericardial effusion, vascular thrombosisGastrointestinal Ileus
  • 4. 4 Gastrointestinal hemorrhage from stress ulceration; gastric varices (secondary to splenic vein thrombosis) Gastrointestinal obstructionHepatobiliary Jaundice Portal vein thrombosisNeurologic Psychosis or encephalopathy (confusion, delusion and coma) Cerebral emboli Blindness (angiopathic retinopathy with hemorrhage)Hematologic Anemia DIC (disseminated intravascular coagulopathy) LeucocytosisDermatologic Painful subcutaneous fat necrosisThe pathogenesis and management of the cardiovascular collapse, respiratory failure,renal failure, metabolic encephalopathy, gastrointestinal bleeding, and disseminatedintravascular coagulation that complicate severe pancreatitis appear to be identical tothose involved when these processes are superimposed on other disease states that arecharacterized by peritonitis and hypovolemia. Cardiovascular collapse is largely causedby 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 theadequacy of treatment, but changes in blood pressure, pulse, and urine output do notaccurately 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 systemicprocesses, including septic shock, ischemia and reperfusion, and massive bloodtransfusion. Management includes good pulmonary toilet combined with closemonitoring of pulmonary function. For many patients, intubation and respiratorysupport may be required. Renal failure in pancreatitis is usually prerenal and isassociated with a poor prognosis. In severe cases, dialysis, usually hemodialysis, maybe required. Stress-induced gastroduodenal erosions account for most of the
  • 5. 5gastrointestinal bleeding in pancreatitis and prophylaxis with antacids, H2-receptorantagonists, or proton pump inhibitors may be appropriate. Rarely, massive bleedingcan result from injury to peripancreatic vascular structures, leading to hemorrhage intothe retroperitoneum. The peripancreatic inflammatory process can also causethrombosis of major gastrointestinal vessels and result in ischemic lesions involving thestomach, small intestine, or colon that can cause bleeding. Management of thesecomplications of pancreatitis is similar to that involved when they occur in the absenceof pancreatitis. Some patients with severe pancreatitis develop disseminatedintravascular coagulation, but it rarely causes bleed-ing, and prophylactic heparinizationis usually not indicated. In 1992, an international symposium was held to resolve the confusion that hadarisen concerning the terminology used to describe the local complications ofpancreatitis and the value of specific treatments for those complications.[29] Thefollowing 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).
  • 6. 6 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.DiagnosisContrast-enhanced CT is particularly valuable as a means of quantifying the extent ofpancreatic necrosis (i.e., nonenhancement). The maturation of a pseudocyst can befollowed by both contrast-enhanced CT and endoscopic ultrasound. Management oflocal pancreatitis complications is dependent on whether the lesion is sterile or infected(see later). Occasionally, infection can be diagnosed when plain abdominal films or CTscans reveal extraintestinal gas bubbles or air either within the area of inflammation orelsewhere in the retroperitoneum. When the clinical suspicion of infection is high, fine-needle aspiration of peripancreatic or intrapancreatic fluid for culture and Gram stainanalysis may be particularly helpful.[30] The procedure is most frequently done withCT guidance, and it is safe when performed by experienced radiologists.Management of Sterile and Infected Acute Fluid CollectionsSterile acute fluid collections usually resolve spontaneously, and no specific treatmentis indicated. Attempts to drain acute fluid collections, either by using percutaneouslyplaced drains or by intervening surgically, are discouraged as they are usuallyunnecessary, and furthermore, they are likely to lead to infection. Even without
  • 7. 7instrumentation, these fluid collections can become infected, but because they containliquid pus with little or no necrotic tissue, they are amenable to transcutaneous catheterdrainage along with antibiotic therapy. It is generally believed that aspirating fluid fromany site near the pancreas yields information that is relevant to all the fluid collectionsand that sampling multiple sites is unnecessary.Management of Sterile and Infected NecrosisThe role of surgical intervention in the management of patients with sterile pancreatic orperipancreatic necrosis has been the subject of considerable controversy.[31] Opinionsrange from those advocating aggressive débridement for patients with sterile necrosiswho fail to rapidly improve on nonoperative treatment to those who claim that surgicalintervention is virtually never indicated when the necrosis is sterile. Those taking theformer position claim that removing the necrotic tissue (i.e., necrosectomy) reducesmorbidity and speeds recovery, whereas those taking the latter position, including me,base their position on the fact that most people treated nonoperatively will eventuallyrecover 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 someform of intervention. Prospective studies have indicated that infection of areas ofnecrosis can occur at any time but that it usually occurs during the initial 3 to 4 weeksof an attack. Although some recent reports have indicated that highly selected patientsmight be adequately treated with antibiotics alone,[32] simple antibiotic therapy isgenerally considered to be inadequate because the necrotic tissue acts as a foreign body,making it impossible to sterilize the area with antibiotics alone. Combining antibiotictherapy with percutaneous catheter drainage may also not be adequate treatmentbecause the pastelike necrotic tissue does not pass through the small-bore drainagecatheters, and therefore, drainage is usually incomplete. Other methods of removing thenecrotic tissue, either through a transpapillary endoscopic route or using minimallyinvasive surgical approaches with an operating nephroscope, have been tried, butexperience with these techniques has been limited and essentially anecdotal. Theconventional approach to managing infected necrosis involves laparotomy and surgical
  • 8. 8 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
  • 9. 9that many pseudocysts eventually resolve without complications and that interventionis not mandatory in all cases unless the pseudocysts are symptomatic, enlarging, orassociated with complications. The likelihood that a pseudocyst will resolvespontaneously, however, is dependent on its size. Large pseudocysts (i.e., >6 cm indiameter) are more likely to become symptomatic either because they are tender orbecause of their mass effect on adjacent organs. Those that compress the stomach orduodenum may cause gastric outlet obstruction with nausea and vomiting. Those thatreduce the capacity of the stomach frequently cause early satiety, whereas thoseimpinging on the bile duct can cause obstructive jaundice. Pancreatic pseudocysts thaterode into a neighboring vessel can result in formation of a pseudoaneurysm withhemosuccus pancreaticus and upper gastrointestinal bleeding.Symptomatic or enlarging pseudocysts can be treated by several methods. Those in thetail can be treated by excision (i.e., distal pancreatectomy), but excision in the setting ofrecent acute inflammation may be hazardous. Most patients who develop symptomaticpseudocysts are best managed by pseudocyst drainage. In poor surgical risk patients,percutaneous catheter drainage can be considered, but in my experience, that approachleads to considerable morbidity because of catheter-induced infection and thedevelopment of a prolonged external pancreatic fistula. Internal drainage can avoidthese problems and seems preferable. Internal drainage can be accomplished eitherendoscopically (by transpapillary drainage, cystogastrostomy, or cystoduodenostomy)or surgically (by cystogastrostomy, cystoduodenostomy, or Roux-en-Ycystojejunostomy). The approach chosen depends primarily on the locally availableexpertise as well as the location of the pseudocyst, but endoscopic drainage may bepreferable in poor surgical risk patients.Pseudocysts that are directly adjacent to either the stomach or duodenum can be safelydrained endoscopically if there are no intervening vessels. After endoscopic ultrasoundand preliminary aspiration of the cyst fluid to confirm the diagnosis and excludeintervening vessels, endoscopic drainage is achieved by making an incision into thepseudocyst through the wall of the stomach or duodenum. To facilitate decompression,the opening is relatively large, and a pigtail catheter may be placed. Transpapillarydrainage might be more appropriate for patients with pancreatic head pseudocysts
  • 10. 10whose CT and endoscopic ultrasound suggest that incising into the pseudocyst couldbe 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 thepseudocyst and lead to development of an infected pseudocyst. Another transpapillaryapproach involves placing a stent across the duct defect rather than into the cyst throughthe defect. By excluding pancreatic juice from the pseudocyst, this bridging intraductalstent may permit the duct disruption to heal and the pseudocyst to resolve withoutdrainage. Further experience with this tech-nique will be needed before its ultimate usecan be determined.Surgical internal drainage of pseudocysts is usually accomplished by creating either aRoux-en-Y cysto-jejunostomy, a side-to-side cystogastrostomy, or a side-to-sidecystoduodenostomy. The former is usually accomplished by directly anastomosing adefunctionalized Roux-en-Y limb of jejunum to the opened pseudocyst. Surgicalcystogastrostomy (or cystoduodenostomy) has traditionally been accomplished bylaparotomy and anterior gastrotomy (or lateral duodenotomy). A generous incision isthen 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 laparoscopicapproach.Management of Pancreatitis-Induced False AneurysmsRarely, pancreatic pseudocysts or areas of pancreatic necrosis can erode into pancreaticor peripancreatic vascular structures. This results in the formation of a false aneurysmbecause the vessel communicates with the pseudocyst. That false aneurysm may eithercommunicate with the ductal system or rupture into the free peritoneal cavity. Theformer leads to bleeding into the pancreatic duct (hemosuccus pancreaticus) andpresents as transpapillary upper gastrointestinal bleeding. Rupture into the peritonealcavity can lead to hemoperitoneum. Therapeutic angiographic embolization is mostappropriate for the unstable patient, and this approach may also provide definitivetreatment, particularly for those patients whose false aneurysm is in the pancreatic head.
  • 11. 11For those whose false aneurysm is in the tail of the pancreas, subsequent distalpancreatectomy, after the patient is stabilized, may provide more secure hemostasis.Management of Pancreatic Ascites and Pancreaticopleural FistulasPancreatic ascites occurs when pancreatic juice gains entry into the peritoneal cavityeither from a pancreatic duct disruption or from a leaking pseudocyst. The diagnosis canusually be made when high amylase levels are found in the ascitic fluid. The initialtreatment usually is nonoperative and involves attempts to decrease pancreatic secretionby elimination of enteral feeding, institution of nasogastric drainage, and administrationof the antisecretory hormone somatostatin. Repeat paracentesis may also be helpful.Roughly 50% to 60% of patients can be expected to respond to this treatment withresolution of pancreatic ascites within 2 to 3 weeks. Persistent or recurrent ascites canbe treated either endoscopically or surgically. Endoscopic treatment involvesendoscopic pancreatic sphincterotomy with or without placement of a transpapillarypancreatic duct stent. By reducing the resistance to drainage into the duodenum, and bybridging the site of duct disruption, this approach is designed to allow the site ofleakage to seal. Surgical treatment of pancreatic ascites, usually preceded byperformance 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 headand neck region). It seems most appropriate to attempt endoscopic treatment initiallyand to reserve surgical treatment for those patients who do not respond to endoscopictherapy.The genesis of pancreaticopleural fistula is similar to that of pancreatic ascites, but inthis case, the duct disruption is usually posterior, and the extravasated juice travels in acephalad direction through the retroperitoneum to reach the thoracic cavity. Althoughthe incidence of pancreaticopleural fistula is lower than that of pancreatic ascites, themanagement of both is similar.Management of Pancreaticoenteric FistulasPancreatic 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
  • 12. 12 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
  • 13. 13 c) internal drainage to the jejunum d) resection of the pseudocyst e) continued observation2. 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

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