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IVANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY
DEPARMENT OF SURGERY № :1
TOPIC : ACUTE PANCREATITIS
V E L L A I C H A M Y RA J RA J K U M A R
5 4 + G R O U P , I V C O U R S E
0 6 / 0 7 / 2 0 1 5
• Anatomy• DEFINITION• ETIOLOGY• CLASSIFICATION• PATHOGENESIS• PATHOMORPHOLOGY• SIGNS AND SYMPTOMS • Physical examination• COMPLICATIONS • DIFFERNTIAL DIAGNOSIS• DIAGNOSITIC METHODS• TACTICS OF TREATMENT
KEY TO REMEMBER
The pancreas is situated in the retroperitoneum. It is divided into a head, body and tail. 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. Coming off the side of the pancreatic head and passing to
the left and behind the superior mesenteric vein is the uncinate process of the pancreas.
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 pancreas is a dual-function gland, having features of both endocrine and exocrine glands.
The part of the pancreas with endocrine function is made up of cell clusters called islets of Langerhans. Four main cell types exist in the islets.
α alpha cells secrete glucagon (increase glucose in blood), β beta cells secrete insulin (decrease glucose in blood), Δ delta cells secrete somatostatin (regulates/stops α and β cells) and PP cells, or γ (gamma) cells, secrete pancreatic polypeptide.
The pancreas also functions as an exocrine gland that assists the digestive system.
Exocrine cells make and release pancreatic juice. The juice travels through the pancreatic duct into the duodenum. Enzymes in the pancreatic juice help digest fat, carbohydrates and protein in food.
Pancreatic juice discharges into the duodenum through ducts. It is alkaline as it contains bicarbonate and chloride ions.
The pancreas receives parasympathetic nerve fibers from the posterior vagal trunk via its celiac branch. Sympathetic supply comes from T6-T10 via the thoracic splanchnic nerves and the celiac plexus
Pancreatitis is inflammation of the gland parenchyma of the pancreas.
Acute pancreatitis is defined as an acute condition presenting with abdominal pain and is usually associated with raised pancreatic enzyme levels in the blood or urine as a result of pancreatic inflammation.
Acute pancreatitis may recur.
The two major causes of acute pancreatitis are biliary calculi, which occur in 50–70 per cent of patients, and alcohol abuse, which accounts for 25 per cent of cases.
POSSIBLE CAUSES OF ACUTE PANCREATITIS
Following biliary, upper gastrointestinal or cardiothoracic
Drugs (corticosteroids, azathioprine, asparaginase, valproic
acid, thiazides, oestrogens)
Viral infections (mumps, Coxsackie B)
Idiopathic acute pancreatitis Biliary acute pancreatitis (Gallstone
pancreatitis) Alcohol-induced acute pancreatitis Drug-induced acute pancreatitis
(Azathioprine, Mesalazine, Valproate, Propofol, Enalapril and other ACE inhibitors, Statins)
Other acute pancreatitis Acute pancreatitis, unspecified
CLASSIFICATIONV All-russian convention of surgeons, 1978
Clinico-anatomical forms:• Arching form• Fatty pancreatonecrosis• Hemorrhagic pancreatonecrosis
Prevelence of necrosis:• Local(focus) damage of gland• Subtotal dmage of the gland• Total damage of the gland
Accordng to progress:
• Abortive• progressive
Periods of disease:
• Hemodynamic violations and pancreatogenic shock• Functional insufficiency of parenchymatous organ• Degenerative and suppuration complication
PATHOGENESIS OF ACUTE PANCREATITIS
Impaired blood flow
Acinar cell injury
Interstitial inflammation oedema
Release of intracellular proenzymes and lysosomal hydrolases
Activation of enzymes
Delivery of proenzymes to lysosomal compartment
Intracellular activation of enzymes
Fat necrosis(lipase, phospholipase)
Alcohol, drugstrauma, ischaemia,viruses
Metabolic injury(experimental)Alcohol, duct obstruction
DUCT OBSTRUCTION ACINAR CELL INJURY DEFECTIVE INTRACELLULAR TRANSPORT
• Autodigestion is a currently accepted pathogenic theory; accordingto it, pancreatitis results when proteolytic enzymes (e.g.,trypsinogen, chymotrypsinogen, proelastase, and lipolytic enzymessuch as phospholipase A 2 ) are activated in the pancreas rather thanin the intestinal lumen. A number of factors (e.g., endotoxins,exotoxins, viral infections, ischemia, anoxia, lysosomal calcium,and direct trauma) are believed to facilitate activation of trypsin.Activated proteolytic enzymes, especially trypsin, not only digestpancreatic and peripancreatic tissues but also can activate otherenzymes, such as elastase and phospholipase A 2 .
• Spontaneous activation of trypsin also can occur.
• Activation of pancreatic enzymes in the pathogenesis of acute pancreatitis.
• Theory of “general duct” with the reflux of bile into the ducts of pancreas.
• Theory of blockade of outflow of pancreatic juice with the development of intraductal hypertension and penetration of secret into the interstial tissue.
• Violation of blood flow of pancreatic juice (vasculitis, thrombophelibitis, and embolism).
• Toxic and allergic damage of gland.
•The process of acute inflamation of pancreas passes through the stages of edema,pancreatonecrosis and suppuration
•Edema : Hyperemia, increased in volume, with shallow nodes of necrosis .
•Pancreatonecrosis can be fatty or hemorrhagic character (shows whitish yellow necrosis).
•Dystrophy : its exposed microscopically .
•Necrosis: hemorrhages, thrombosis of vessels and signs of inflammatory.
ACUTE PANCREATITIS; HEMORRHAGE AND NECROSIS
SAPONIFICATION OF FAT
A SURGICAL SPECIMEN OF THE
TRANSVERSE COLON AND
SIGNS AND SYMPTOMS
Main symptoms :
• Upper abdominal pain that radiates into the back. It may be aggravated by eating, especially foods high in fat.
• Swollen and tender abdomen
• Nausea and vomiting (coffee ground appearence)
• Increased heart rate
• Weight loss caused by poor absorption (malabsorption) of food.
• This malabsorption happens because the gland is not releasing enough enzymes to break down food.
• Also, diabetes may develop if the insulin-producing cells of the pancreas are damaged.
• Severe intoxication
CULLEN SIGN – DISCOLOURATION AROUND UMBILICUS
Grey-Turner sign- discolouration in the flanks
• The abdominal is distended, peristaltic sounds inaudible.
• The signs of paresis of stomach and intestine appears early.
• On palpation tenderness in the epigastria area and in right and some times in the left hypochondria also marked.
Early • Shock• Acute cardiac, pulmonary, hepatic
insufficiencyLate • Abscess of pancreas• Subdiaphargmatic, interintestinal
abscesses• Pyogenic abscesses of omentum• Phelgmons of retro peritoneal space.• Erosive bleeding.
Acute peritonitis, cholecystitis
Acute mechanical intestinal
Ranson Score:predicting the severity of acute pancreatitis:At admission age in years > 55 years white blood cell count > 16000 cells/mm3 blood glucose > 11 mmol/L (> 200 mg/dL) serum AST > 250 IU/L serum LDH > 350 IU/L At 48 hours Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit fall > 10% Oxygen (hypoxemia PO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid
hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L
APACHE II score(Acute Physiology And Chronic Health Evaluation):
Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality Score 5 to 6 : 40% mortality Score 7 to 8 : 100%
mortalityHemorrhagic peritoneal fluidObesityIndicators of organ failureHypotension (SBP <90 mmHG) or tachycardia > 130
beat/minPO2 <60 mmHgOliguria (<50 mL/h) or increasing BUN and creatinineSerum calcium < 1.90 mmol/L (<8.0 mg/dL) serum albumin <33 g/L (<3.2.g/dL)>
Balthazar scoringBalthazar GradeBalthazar Grade Appearance on CT CT Grade Points Grade A Normal CT 0 points Grade B Focal or diffuse enlargement of the pancreas 1 point Grade C Pancreatic gland abnormalities and peripancreatic inflammation
2points Grade D Fluid collection in a single location 3 points Grade E Two or more fluid collections and / or gas bubbles in or adjacent to
Necrosis ScoreNecrosis Percentage Points No necrosis 0 points 0 to 30% necrosis 2 points 30 to 50% necrosis 4 points Over 50% necrosis 6 points
The numerical CTSI (Computed Tomography Severity Index) has a maximum of ten points, it is the sum of the Balthazar grade points and pancreatic necrosis grade points
Blood test Urine test Biochemical test (amylase, bilirubin, sugar) Ultrasound CT scan Cholecystocholangiography Endoscopic retrograde cholangiopancreatgraphy Laparoscopy Laprocentesis
A complete blood count (CBC) demonstrates leukocytosis (white blood cell [WBC] count higher than 12,000/µL) with the differential being shifted toward the segmented polymorphonuclear (PMN) cells. Leukocytosis may represent inflammation or infection.
A C-reactive protein (CRP) value can be obtained 24-48 hours after presentation to provide some indication of prognosis. Higher levels have been shown to correlate with a propensity toward organ failure. A CRP value in double figures (ie, ≥ 10 mg/dL) strongly indicates severe pancreatitis. CRP is an acute-phase reactant that is not specific for pancreatitis.
LIVER ENZYMES :
Determine alkaline phosphatase, total bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels to search for evidence of gallstone pancreatitis. An ALT level higher than 150 U/L suggests gallstone pancreatitis and a more fulminant disease course.
Obtain measurements for blood urea nitrogen (BUN), creatinine, and electrolytes; a great disturbance in the electrolyte balance is usually found, secondary to third spacing of fluids. Measure blood glucose level because it may be elevated from B-cell injury in the pancreas.
Measure calcium, cholesterol, and triglyceride levels to search for an etiology of pancreatitis (eg, hypercalcemia or hyperlipidemia) or complications of pancreatitis (eg, hypocalcemia resulting from saponification of fats in the retroperitoneum). However, be aware that baseline serum triglyceride levels can be falsely lowered during an episode of acute pancreatitis.
Elevated serum amylase and lipase levels, in combination with severe abdominal pain, often trigger the initial diagnosis of acute pancreatitis.
Serum lipase rises 4 to 8 hours from the onset of symptoms and normalizes within 7 to 14 days after treatment.
Serum amylase may be normal (in 10% of cases) for cases of acute or chronic pancreatitis (depleted acinar cell mass) and hypertriglyceridemia.
Reasons for false positive elevated serum amylase include salivary gland disease (elevated salivary amylase), bowel obstruction, infarction, cholecystitis, and a perforated ulcer.
If the lipase level is about 2.5 to 3 times that of amylase, it is an indication of pancreatitis due to alcohol.
Decreased serum calcium Glycosuria
Increase in size of pancreas, thickening of walls and presence or absence of calculus of gall bladder and common bile duct.
Inhomogeneous swollen pancreas and dilatated bile duct
Edematous swollen tail and extrapancreatic soft tissue edema
CT scan: Intrapancreatic - diffuse or segmental
enlargement, edema, gas bubbles, pancreatic pseudocysts and phlegmons/abscesses (which present 4 to 6 wks after initial onset)
Peripancreatic / extrapancreatic - irregular pancreatic outline, obliterated peripancreatic fat, retroperitoneal edema, fluid in the lessar sac, fluid in the left anterior pararenal space
Locoregional - Gerota's fascia sign (thickening of inflamed Gerota's fascia, which becomes visible), pancreatic ascites, pleural effusion (seen on basal cuts of the pleural cavity), adynamic ileus, etc.
Axial CT in a patient with acute exudative pancreatitis showing extensive fluid collections surrounding the pancreas.
Endoscopic retrograde cholangiopancreatgraphy
Endoscopic retrograde cholangiopancreatogram of a young woman with gallbladder stones.
Conservative treatment Surgical treatment Diet therapy
Fluid replacement:Aggressive hydration at a rate of 5 to 10 mL/kg per hour of isotonic crystalloid solution (e.g., normal saline or lactated Ringer’s solution) to all patients with acute
Pain control:1. Opioids are safe and
effective at providing pain control in patients with acute pancreatitis.
2. Hydromorphone or fentanyl (Intravenous) may be used for pain relief in acute pancreatitis
1. Antibiotic, antiviral drugs in case of etiology is bacteria or virus.
2. Carbapenems 0.5 gram intravenously every eight hours for two weeks.
Anticholinergic drug(atropine sulphate, methacin)
H2-histamine drug(cimetidine, ranisan, ranitidine)
SURGICAL TREATMENT: Superior-middle
laparotomy Cholecystectomy Pancreatectomy Transduodenal
papillotomy with sphincteroplasty
Indications: 1. Infected pancreatic necrosis
2. Diagnostic uncertainty
Sphincterotomy. Using a small wire on the endoscope, the doctor finds the muscle that surrounds the pancreatic duct or bile ducts and makes a tiny cut to enlarge the duct opening. When a pseudocyst is present, the duct is drained.
Gallstone removal. The endoscope is used to remove pancreatic or bile duct stones with a tiny basket. Gallstone removal is sometimes performed along with a sphincterotomy.
Stent placement. Using the endoscope, the doctor places a tiny piece of plastic or metal that looks like a straw in a narrowed pancreatic or bile duct to keep it open.
Balloon dilatation. Some endoscopes have a small balloon that the doctor uses to dilate, or stretch, a narrowed pancreatic or bile duct. A temporary stent may be placed for a few months to keep the duct open.
People who undergo therapeutic ERCP are at slight risk for complications, including severe pancreatitis, infection, bowel perforation, or bleeding. Complications of ERCP are more common in people with acute or recurrent pancreatitis. A patient who experiences fever, trouble swallowing, or increased throat, chest, or abdominal pain after the procedure should notify a doctor immediately.
1. Diet №:5 ( avoid oily, spicy fatty foods, fast foods )
AVOID FAST FATTY FOODS