Acute pancreatitis

1. Acute pancreatitis Maen K Abu Househ Tareq F Al Hammouri Mohammad Amir

3. A little anatomy and physiology The pancreas is situated in the retroperitoneum. It is divided into a head, which occupies 30% of the gland by mass, and a body and tail, which together constitute 70%. The head lies within the curve of the duodenum, overlying the body of the second lumbar vertebra and the vena cava. The aorta and the superior mesenteric vessels lie behind the neck of the gland.

4. Cont.. Behind the neck of the pancreas, near its upper border, the superior mesenteric vein joins the splenic vein to form the portal vein. The tip of the pancreatic tail extends up to the splenic hilum. The main pancreatic duct branches into interlobular and intralobular ducts, ductules and, finally, acini. Clusters of endocrine cells, known as islets of Langerhans, are distributed throughout the pancreas. Islet cells consist of differing cell types: 75% are B cells (producing insulin); 20% are A cells (producing glucagon); and the remainder are D cells (producing somatostatin) and a small number of pancreatic polypeptide cells.Clusters of endocrine cells, known as islets of Langerhans, are distributed throughout the pancreas. Islet cells consist of differing cell types: 75% are B cells (producing insulin); 20% are A cells (producing glucagon); and the remainder are D cells (producing somatostatin) and a small number of pancreatic polypeptide cells.

5. Embryogenesis Some problems might occur as for example the malrotation that can occur during the fifth week resulting in an Annular pancreas.

7. Physiology In response to a meal, the pancreas secretes digestive enzymes in an alkaline (pH 8.4) bicarbonate-rich fluid. The proteolytic enzymes are secreated in an inactive form, the maintenance of this is important in preventing pancreatitis. Spontaneous secretion is minimal; the hormone secretin, which is released from the duodenal mucosa, evokes a bicarbonate-rich fluid. Cholecystokinin (CCK) (synonym: pancreozymin) is released from the duodenal mucosa in response to food. CCK is responsible for enzyme release. Vagal stimulation increases the volume of secretion.Spontaneous secretion is minimal; the hormone secretin, which is released from the duodenal mucosa, evokes a bicarbonate-rich fluid. Cholecystokinin (CCK) (synonym: pancreozymin) is released from the duodenal mucosa in response to food. CCK is responsible for enzyme release. Vagal stimulation increases the volume of secretion.

8. Pancreatitis Is inflammation of the gland parenchyma of the pancreas.

9. Classification Classified into: Acute Chronic is defined as a continuing inflammatory disease of the pancreas characterized by irreversible morphological change typically causing pain and/or permanent loss of function. Many patients with chronic pancreatitis have exacerbations, but the condition may be completely painless

10. Acute pancreatitis

11. Classification Mild 80% Mortality rate 1% Severe 20% Mortality rate varies from 20% to 50%.

12. Pathophysiology Due to many causes, pancreatic pro-enzymes will be activated, and not released to the duodenum, so they will return back to the pancreas in the active form and cause autodigestion of the pancreas, which in turn will lead to an acute inflammatory reaction.

13. Incidence Acute pancreatitis accounts for 3% of all cases of abdominal pain. The disease may occur at any age, with a peak in young men and older women.

14. Aetiology The two major causes of acute pancreatitis are biliary calculi, which occur in 50�70% of patients, and alcohol abuse, which accounts for 25% of cases.

15. Gallstone pancreatitis is thought to be triggered by the passage of gallstones down the common bile duct. If the biliary and pancreatic ducts join to share a common channel before ending at the ampulla, then obstruction of this passage may lead to reflux of bile or activated pancreatic enzymes into the pancreatic duct. Patients who have small gallstones and a wide cystic duct may be at a higher risk of passing stones.

16. The proposed mechanisms for alcoholic pancreatitis include the effects of diet, malnutrition, direct toxicity of alcohol, concomitant tobacco smoking, hypersecretion, duct obstruction or reflux, and hyperlipidaemia.

17. Among patients who undergo ERCP, 1�3% develop pancreatitis, probably as a consequence of duct disruption and enzyme extravasation. Patients with sphincter of Oddi dysfunction or a history of recurrent pancreatitis, and those who undergo sphincterotomy or balloon dilatation of the sphincter, carry a higher risk of developing post-ERCP pancreatitis. Patients who have undergone upper abdominal or cardiothoracic surgery may develop acute pancreatitis in the postoperative phase, as may those who have suffered blunt abdominal trauma. Hereditary pancreatitis is a rare familial condition associated with mutations of the cationic trypsinogen gene. Patients have a tendency to suffer acute pancreatitis while in their teens, progress to chronic pancreatitis in the next two decades and have a high risk (possibly up to 40%) of developing pancreatic cancer by the age of 70 years. Occasionally, tumours at the ampulla of Vater may cause acute pancreatitis. It is important to check the serum calcium level, a fasting lipid profile, autoimmune markers and viral titres in patients with so called idiopathic acute pancreatitis. It is equally important to take a detailed drug history and remember the association of corticosteroids, azathioprine, asparaginase and valproic acid with acute pancreatitis. A careful search for the aetiology must be made in all cases, and no more than 20% of cases should fall into the idiopathic categoryAmong patients who undergo ERCP, 1�3% develop pancreatitis, probably as a consequence of duct disruption and enzyme extravasation. Patients with sphincter of Oddi dysfunction or a history of recurrent pancreatitis, and those who undergo sphincterotomy or balloon dilatation of the sphincter, carry a higher risk of developing post-ERCP pancreatitis. Patients who have undergone upper abdominal or cardiothoracic surgery may develop acute pancreatitis in the postoperative phase, as may those who have suffered blunt abdominal trauma. Hereditary pancreatitis is a rare familial condition associated with mutations of the cationic trypsinogen gene. Patients have a tendency to suffer acute pancreatitis while in their teens, progress to chronic pancreatitis in the next two decades and have a high risk (possibly up to 40%) of developing pancreatic cancer by the age of 70 years. Occasionally, tumours at the ampulla of Vater may cause acute pancreatitis. It is important to check the serum calcium level, a fasting lipid profile, autoimmune markers and viral titres in patients with so called idiopathic acute pancreatitis. It is equally important to take a detailed drug history and remember the association of corticosteroids, azathioprine, asparaginase and valproic acid with acute pancreatitis. A careful search for the aetiology must be made in all cases, and no more than 20% of cases should fall into the idiopathic category

19. To learn It is essential to establish the aetiology Investigate thoroughly before labelling it as �idiopathic� After the acute episode resolves, remember further management of the underlying aetiology If the aetiology is gallstones, cholecystectomy is desirable during the same admission

20. Clinical presentation Pain is the cardinal symptom Starts quickly, reaching maximum intensity within minutes rather than hours and persists for hours or even days. The pain is frequently severe, constant and refractory to the usual doses of analgesics. Pain is usually experienced first in the epigastrium but may be localised to either upper quadrant or felt diffusely throughout the abdomen. There is radiation to the back in about 50% of patients, and some patients may gain relief by sitting or leaning forwards.

21. The suddenness of onset may simulate a perforated peptic ulcer, while biliary colic or acute cholecystitis can be mimicked if the pain is maximal in the right upper quadrant. Radiation to the chest can simulate myocardial infarction, pneumonia or pleuritic pain. In fact, acute pancreatitis can mimic most causes of the acute abdomen and should seldom be discounted in differential diagnosis.

22. Nausea, repeated vomiting and retching are usually marked accompaniments. The retching may persist despite the stomach being kept empty by nasogastric aspiration. Hiccoughs can be troublesome and may be due to gastric distension or irritation of the diaphragm.

23. �. On examination Tachycardia, tachypnea, hypotension (shock) and hyperthermia Mild icterus can be caused by biliary obstruction in gallstone pancreatitis, and an acute swinging pyrexia suggests cholangitis. There may be tenderness and gaurding over the epigastric region

24. Abdominal examination may reveal distension due to ileus or, more rarely, ascites with shifting dullness. Grey Turner�s sign Cullen�s sign Fox�s sign Subcutaneous fat necrosis A mass can develop in the epigastrium due to inflammation Chest exam may revile pleural effusion particularly left sided. Pulmonary oedema and pneumonitis can occur too. Cerebral abnormalities due to hypoxia Bleeding into the fascial planes can produce bluish discolouration of the flanks (Grey Turner�s sign) or umbilicus (Cullen�s sign). Neither sign is pathognomonic of acute pancreatitis; Cullen�s sign was first described in association with rupture of an ectopic pregnancy. Subcutaneous fat necrosis may produce small, red, tender nodules on the skin of the legs. (Cullen�s sign). It takes 24-48 hours to appear and predicts a severe attack of acute hemorrhagic pancreatitis. Bleeding into the fascial planes can produce bluish discolouration of the flanks (Grey Turner�s sign) or umbilicus (Cullen�s sign). Neither sign is pathognomonic of acute pancreatitis; Cullen�s sign was first described in association with rupture of an ectopic pregnancy. Subcutaneous fat necrosis may produce small, red, tender nodules on the skin of the legs. (Cullen�s sign). It takes 24-48 hours to appear and predicts a severe attack of acute hemorrhagic pancreatitis.

26. Investigations General: CBC: ? WBC , ? Hct. Serum Electrolytes. Liver function test. Serum Calcium ?. Blood Sugar ? .

27. Investigations Laboratory Tests: Serum Amylase ?. Serum Amylase Isoenzymes (P+S Types). Urinary Amylase (More sensitive). Amylase � Creatinine clearance ratio. Serum Lipase ?. Peritoneal fluid analysis. ** 10 Folds increase in amylase according to the lab normal values>>>Acute pancreatitis. A serum amylase level three to four times above normal is indicative of the disease A normal serum amylase level does not exclude acute pancreatitis, particularly if the patient has presented a few days later. Increases immediately and remain elevated for 3 � 5 days Milder forms associated with higher levels Can be high in: If the serum lipase level can be checked, it provides a slightly more sensitive and specific test than amylase. CT is probably the best single imaging investigation A serum amylase level three to four times above normal is indicative of the disease A normal serum amylase level does not exclude acute pancreatitis, particularly if the patient has presented a few days later. Increases immediately and remain elevated for 3 � 5 days Milder forms associated with higher levels Can be high in: If the serum lipase level can be checked, it provides a slightly more sensitive and specific test than amylase. CT is probably the best single imaging investigation

28. Investigations Radiology: Chest X-Ray. Abdominal X-Ray: Sentinel loop, Gallstones. Barium Meal. Ultrasound & CT scan: Enlarged pancreas, abcsess, fluid collection, hemorrhage, necrosis or pseudocyst. MRI. EUS and MRCP widely available. ERCP Very rarely diagnosis is done using laparotomy.

29. Imaging Plain erect chest and abdominal radiographs Non-diagnostic Generalized or local ileus (sentinel loop) Colon cut-off sign and a renal halo sign Occasionally, calcified gallstones or pancreatic calcification may be seen. chest radiograph: Pleural effusion Diffuse alveolar interstitial shadowing A�sentinel loop�is a�sign�seen on�x-ray�in�gastrointestinal�radiology�that indicates localized�ileus�from nearby inflammation. Simply put, it is the dilatation of a segment of�large�or�small intestine. An isolated distended loop of bowel is seen near the site of injured viscus or inflamed organ. This loop is called a "sentinel loop". It is a feature due to body's efforts to localize traumatic or inflammatory lesions. The local distention of intestinal loop is due to local paralysis and accumulation of gas in the intestinal loop. In acute pancreatitis, the sentinel loop is usually seen in left hypochondrium while in acute appendicitis, the sentinel loop is seen in right iliac fossa. The sentinel loop is seen in right hypochondrium in acute cholecystitis. The colon cutoff sign describes the abrupt termination of gas within the proximal colon at the level of the radiographic splenic flexure, usually with decompression of the distal colon. The sign was originally applied to conventional abdominal radiographs, but similar findings can be seen on computed tomographic (CT). EXPLANATION Inflammatory exudate in acute pancreatitis that extends into the phrenicocolic ligament by directly spreading through the lateral attachment of the transverse mesocolon gives rise to this sign. Infiltration of the phrenicocolic ligament results in functional spasm and/or mechanical narrowing of the splenic flexure at the level where the colon returns to the retroperitoneum. This transition point, or cutoff, is further accentuated by distention of the intraperitoneal transverse colon from the focal adynamic ileus, which is also a result of the underlying inflammatory process. This appearance can mimic a true colonic obstruction. The halo appears as ground-glass attenuation on imaging, due to enhancement of the perirenal fat from the retroperitoneal collection of pancreatic exudates. diffuse alveolar interstitial shadowing in acute respiratory distress syndrome A�sentinel loop�is a�sign�seen on�x-ray�in�gastrointestinal�radiology�that indicates localized�ileus�from nearby inflammation. Simply put, it is the dilatation of a segment of�large�or�small intestine. An isolated distended loop of bowel is seen near the site of injured viscus or inflamed organ. This loop is called a "sentinel loop". It is a feature due to body's efforts to localize traumatic or inflammatory lesions. The local distention of intestinal loop is due to local paralysis and accumulation of gas in the intestinal loop. In acute pancreatitis, the sentinel loop is usually seen in left hypochondrium while in acute appendicitis, the sentinel loop is seen in right iliac fossa. The sentinel loop is seen in right hypochondrium in acute cholecystitis. The colon cutoff sign describes the abrupt termination of gas within the proximal colon at the level of the radiographic splenic flexure, usually with decompression of the distal colon. The sign was originally applied to conventional abdominal radiographs, but similar findings can be seen on computed tomographic (CT). EXPLANATION Inflammatory exudate in acute pancreatitis that extends into the phrenicocolic ligament by directly spreading through the lateral attachment of the transverse mesocolon gives rise to this sign. Infiltration of the phrenicocolic ligament results in functional spasm and/or mechanical narrowing of the splenic flexure at the level where the colon returns to the retroperitoneum. This transition point, or cutoff, is further accentuated by distention of the intraperitoneal transverse colon from the focal adynamic ileus, which is also a result of the underlying inflammatory process. This appearance can mimic a true colonic obstruction. The halo appears as ground-glass attenuation on imaging, due to enhancement of the perirenal fat from the retroperitoneal collection of pancreatic exudates. diffuse alveolar interstitial shadowing in acute respiratory distress syndrome

33. Ultrasound Does not establish a diagnosis of acute pancreatitis Swollen pancreas may be seen Should be performed within 24 hours in all patients to: Detect gallstones as a potential cause Rule out acute cholecystitis as a differential diagnosis And determine whether the common bile duct is dilated.

34. CT Not necessary for all patients, particularly those deemed to have a mild attack on prognostic criteria Useful in: if there is diagnostic uncertainty; in patients with severe acute pancreatitis, to distinguish interstitial from necrotising pancreatitis in patients with organ failure, signs of sepsis or progressive clinical deterioration; when a localised complication is suspected, such as fluid collection, pseudocyst or a pseudoaneurysm.

35. Assessment of severity Interpretation If the score = 3, severe pancreatitis likely. If the score < 3, severe pancreatitis is unlikely Or Score 0 to 2�: 2% mortality Score 3 to 4�: 15% mortality Score 5 to 6�: 40% mortality Score 7 to 8�: 100% mortality Severe pancreatitis is defined by: Ransons = 3 APACHE II�score = 8 Organ failure Substantial pancreatic necrosis (at least 30% glandular necrosis according to contrast-enhanced�CT) APACHE II "Acute Physiology and Chronic Health Evaluation II� severity-of-disease classification system score from 0 to 71 is computed based on several measurements; higher scores correspond to more severe disease and a higher risk of death. Interpretation If the score = 3, severe pancreatitis likely. If the score < 3, severe pancreatitis is unlikely Or Score 0 to 2�: 2% mortality Score 3 to 4�: 15% mortality Score 5 to 6�: 40% mortality Score 7 to 8�: 100% mortality Severe pancreatitis is defined by: Ransons = 3 APACHE II�score = 8 Organ failure Substantial pancreatic necrosis (at least 30% glandular necrosis according to contrast-enhanced�CT) APACHE II "Acute Physiology and Chronic Health Evaluation II� severity-of-disease classification system score from 0 to 71 is computed based on several measurements; higher scores correspond to more severe disease and a higher risk of death.

36. Differential diagnosis Acute cholecystitis. Perforated peptic ulcer. Inferior wall MI. Intestinal obstruction. Mesenteric ischemia. Ruptured abdominal aortic aneurysm.

37. Management of Mild Acute pancreatitis If after initial assessment a patient is considered to have a mild attack of pancreatitis, a conservative approach is indicated intravenous fluid administration frequent but non-invasive observation

38. Management of severe acute pancreatitis Rest the patient (Relief pain): Pethidine 1mg/kg + antispasmodic. Rest the pancreas: NPO . Rest the bowel: NG tube. Resuscitation: IV fluid, electrolytes replacement. Resist enzymatic activity: Protease inhibitors. Resist infection: Antibiotics. Repeated examination. Repeated serum estimations:Ca+2, Mg+2. Respiratory support.

39. Management Urgent ERCP and biliary sphincterotomy within 72 hours improves outcome of severe gallstone pancreatitis. Surgery in case of: Uncertain diagnosis. Infected pancreatic necrosis. Complicated pancreatitis.

40. Causes of death: Hypovolemic shock. Electrolyte disturbances. Sepsis. Renal failure. Respiratory failure.

41. Complications

42. Hemorrhagic pancreatitis Definition: Bleeding into the parenchyma and retroperitoneal structures with extensive pancreatic necrosis. Signs: Abdominal pain Shock Cullen�s sign, Grey turner�s sign & Fox�s sign

43. Acute fluid collection Located in or near the pancreas The fluid is sterile, and most such collections resolve. No intervention is necessary unless a large collection causes symptoms or pressure effects.

44. Sterile and infected pancreatic necrosis Refers to a diffuse or focal area of non-viable parenchyma that is typically associated with peripancreatic fat necrosis. Necrotic areas can be identified by an absence of contrast enhancement on CT. These are sterile to begin with, but can become subsequently infected, probably due to translocation of gut bacteria. Necrotizing pancreatitis accounts for 10% of all pancreatitis but is lethal disease. Sterile necrotic material should not be drained or interfered with.Sterile necrotic material should not be drained or interfered with.

45. Management Laparostomy Pancreatic necrosictomy Peritoneal lavage If the sepsis worsens despite this, then a pancreatic necrosectomy should be considered. This is a challenging operation that carries a high morbidity and mortality, and is best carried out in a specialist unit. The overwhelming majority of patients with peripancreatic sepsis can be successfully treated by conservative means, and necrosectomy should be necessary in a very small proportion of patients. The surgical approach may be through a midline laparotomy, especially if the area involved is around the head of the gland. The duodenocolic and gastrocolic ligaments should be divided and the lesser sac opened. Thorough debridement of the dead tissue around the pancreas should be carried out. If the body and tail of the gland are primarily involved (Fig. 64.25), a retroperitoneal approach though a left flank incision may be more appropriate. The tissues are inevitably friable, and one should be careful not to precipitate excessive bleeding or inadvertently breach the bowel wall. Blunt dissection is preferable to sharp dissection. A feeding jejunostomy may be a useful adjunct to the procedure. If gallstones are the precipitating factor of the pancreatitis, a cholecystectomy should be included. Some prefer a minimally invasive approach to a formal laparotomy. A rigid laparoscope is inserted into the peripancreatic area through a retroperitoneal approach, and vigorous irrigation and suction is combined with a gradual nibbling away of the necrotic debris. Once a necrosectomy has been completed, further necrotic tissue may form. There are several possible ways of dealing with this (listed below), none of which has been proved to be more effective than the others. The last two approaches make greater logistic demands as one is committed to a re-exploration every 48�72 hours. � Closed continuous lavage: Tube drains are left in and the raw area flushed (Beger) (Fig. 64.26). � Closed drainage: The incision is closed, but the cavity is packed with gauze-filled Penrose drains and closed suction drains. The Penrose drains are brought out through the flank and slowly pulled out and removed after 7 days Open packing: The incision is left open, and the cavity is packed with the intention of returning to the operating room at regular intervals and repacking until there is a clean granulating cavity. � Closure and relaparotomy: The incision is closed with drains with the intention of performing a series of planned relaparotomies every 48�72 hours until the raw area granulates (Bradley). If the sepsis worsens despite this, then a pancreatic necrosectomy should be considered. This is a challenging operation that carries a high morbidity and mortality, and is best carried out in a specialist unit. The overwhelming majority of patients with peripancreatic sepsis can be successfully treated by conservative means, and necrosectomy should be necessary in a very small proportion of patients. The surgical approach may be through a midline laparotomy, especially if the area involved is around the head of the gland. The duodenocolic and gastrocolic ligaments should be divided and the lesser sac opened. Thorough debridement of the dead tissue around the pancreas should be carried out. If the body and tail of the gland are primarily involved (Fig. 64.25), a retroperitoneal approach though a left flank incision may be more appropriate. The tissues are inevitably friable, and one should be careful not to precipitate excessive bleeding or inadvertently breach the bowel wall. Blunt dissection is preferable to sharp dissection. A feeding jejunostomy may be a useful adjunct to the procedure. If gallstones are the precipitating factor of the pancreatitis, a cholecystectomy should be included. Some prefer a minimally invasive approach to a formal laparotomy. A rigid laparoscope is inserted into the peripancreatic area through a retroperitoneal approach, and vigorous irrigation and suction is combined with a gradual nibbling away of the necrotic debris. Once a necrosectomy has been completed, further necrotic tissue may form. There are several possible ways of dealing with this (listed below), none of which has been proved to be more effective than the others. The last two approaches make greater logistic demands as one is committed to a re-exploration every 48�72 hours. � Closed continuous lavage: Tube drains are left in and the raw area flushed (Beger) (Fig. 64.26). � Closed drainage: The incision is closed, but the cavity is packed with gauze-filled Penrose drains and closed suction drains. The Penrose drains are brought out through the flank and slowly pulled out and removed after 7 days Open packing: The incision is left open, and the cavity is packed with the intention of returning to the operating room at regular intervals and repacking until there is a clean granulating cavity. � Closure and relaparotomy: The incision is closed with drains with the intention of performing a series of planned relaparotomies every 48�72 hours until the raw area granulates (Bradley).

46. Pancreatic abscess Definition: is a circumscribed collection of pus intra-abdominal resulting from tissue necrosis, liquefaction, and infection. It may be an acute fluid collection or a pseudocyst that has become infected Presentation: Fever Unresolving pancreatitis Epigastric mass

47. is a late complication of acute necrotizing pancreatitis. It is estimated that approximately 3% of the patients suffering from acute pancreatitis will develop an abscess. Abdominal CT scans with needle aspiration to send for culture & Gram stain should be performed. Organisms found Gram �ve (most common) E.coli, pseudomonas, klebsiella Gram +ve Staphylococcus aureas, candida

48. Tx: Antibiotics and percutanous drain placement OR Operative debridement and drain placement. An unremoved infected abscess may lead to sepsis, fistula formation and recurrent pancreatitis.

49. Pseudo cyst Definition: Encapsulated collection of pancreatic fluid by inflammatory fibrosis NOT epithelial cell lining, that's why called �pseudo"cyst. Its incidince is approximately 1 in 10 after alcoholic pancreatitis. Presentation: Epigastric pain Vomiting Mild fever Weight loss Signs Palpable epigastric mass, Tender epigastrium, Ileus

50. Investigations: CBC >> leuckocytosis Amylase >> high Bilirubin>> high if there is obstruction US >> fluid filled mass CT >> fluid filled mass, Multiple cysts ERCP : radiopaque contrast material fills the cyst if there is a communicating pseudocyst

51. DDx : Cystadenocarcinoma,cystadenoma Complications : Infection Bleeding into the cyst Fistula Pancreatic ascitis Gastric outlet obstruction Biliary obstruction SOB

52. Treatment : drainage of the cyst or observation 50% will resolve spontaneously within 6 weeks infection: Percutaneous external drainage & IV antibiotics bleeding: angiogram and embolization

53. Cysts larger than 5cm have a small chance of resolving & a higher chance of complications(bleeding, Infection, rupture). Treatment options are percutanous CT guided aspiration or operative drainage (cystogastrostomy, cystoduodenostomy). A biopsy should be taken during surgical drainage to rule out cystic carcinoma.

54. Chronic pancreatitis Definition: Chronic inflammation of the pancreas region causing destruction of the paranchyma,fibrosis & calsification resulting in loss of endocrine & exocrine functions Two types : 1.Chronic calcific pancreatitis 2.Chronic obstructive pancreatitis 5%

55. Presentation: epigastric and or back pain weight loss steatorrhea as a result of malabsoption (exocrine insufficiency) Diabetes mellitus (endocrine insufficiency

56. Most common cause is Alcohol abuse 70% of cases,in addition to other causes similar to those of acute pancreatitis. D.Dx: PUD,biliary tract diseases,AAA,pancreatic cancer,angina. 2% of patients with chronic pancreatitis will develop pancreatic cancer. Investigations: amylase/lipase>> may be normal due to extensive pancreatic tissue loss. 72 hours fecal fat analysis GTT

57. CT>> highly sensitive for gland enlargemen/atrophy, calcifications,masses,psudocysts. KUB : calcification in the pancreas ERCP>>ductul irregulareties with dilatation & stenosis

58. Treatment Medical: discontinuation of alcohol use. Insulin for type 1 DM. Pancreatic enzymes replacement. Narcotics for pain. Surgical: Surgical treatment is indicated when the pain is severe,prolongd. (Puestow,Duval,Near-total pancreatectomy).

59. Complications of chronic pancreatitis: Insulin dependent DM Steatorrhea Malnutrition Biliary obstruction Splenic vein thrombosis Gastric varices Pancreatic pseudocyst/abscess Narcotics addiction Pancreatic ascites/pleural effusion Splenic artery aneurysm

60. Thank you