Pancreatitis PDF
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Manipal University College Malaysia
Prof Naga
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Summary
This document is a presentation on pancreatitis. It covers various aspects of the condition, including causes, such as gallstones and alcohol, along with the classification of different types of pancreatitis, such as acute, chronic, and recurrent acute. It also discusses the clinical features, complications, investigation methods (including imaging), and management strategies. The presentation further delves into prognostic markers, and presents the diagnostic criteria and systems, such as Ranson's criteria, and the BISAP score. The material also touches upon the different potential complications of this condition.
Full Transcript
Pancreatiti s Prof Naga Acute pancreatitis: interstitial oedematous (90 to 95%) and necrotizing types Recurrent acute pancreatitis Classific Chronic pancreatitis ation Chronic relapsing pancreatitis Acute and...
Pancreatiti s Prof Naga Acute pancreatitis: interstitial oedematous (90 to 95%) and necrotizing types Recurrent acute pancreatitis Classific Chronic pancreatitis ation Chronic relapsing pancreatitis Acute and recurrent acute pancreatitis are associated with a full recovery. Chronic pancreatitis is associated with inflammation and fibrosis Causes of acute pancreatitis Mechanical obstruction: Autoimmune: Sjogren Gallstones syndrome, autoimmune thyroiditis, sclerosing Toxic effect: alcohol cholangitis. Metabolic: Hyperlipidaemia, Iatrogenic: Post-ERCP, Surgery Hyperparathyroidism Ischemia Drugs: Azathioprine, corticosteroids, Trauma Idiopathic Infections: Mumps, Coxsackie Gallstones and alcohol are the leading causes of acute pancreatitis. Pancreas divisum- affects 7% of the population. Sphincter of Oddi dysfunction, Genetic causes: Cystic fibrosis. Anatomic/ Hereditary pancreatitis- protease serine 1 Genetic (PRSS1) also called (cationic trypsinogen). A mutation in PRSS1 gene renders causes trypsinogen resistant to autolysis, leading to activation in the pancreas. Serine protease inhibitor Kazal type 1 (SPINK1) codes for trypsin inhibitor, Mutation here leads to activation within pancreas. Acute pancreatitis presents with central or epigastric abdominal pain, radiating to the back or in between the shoulder blades. The pain may be mild or severe; and is associated with nausea and vomiting. In severe acute pancreatitis, the patient may be Clinical in shock. Several systems for assessing the severity of features the attack: The Ransom system for patients with alcohol- related pancreatitis. The APACHE II score is also helpful SIRS and multi-organ failure (especially if developing after 48 hours) are markers of severity. Examination may reveal shock, with abdominal tenderness and guarding. There may be bruising in the flanks Cont’d (Grey-Turner sign) and around umbilicus (Cullen’s sign). Jaundice and respiratory failure are features of severe inflammation. Local: pseudocysts, abscesses, ascites, GI bleed, ileus, portal vein thrombosis. Systemic: shock, respiratory failure, AKI, hypocalcaemia, hyperglycaemia, DIC and fat necrosis Complicati Early: cardiac failure, renal failure, ons respiratory failure, DIC and venous thrombosis Late: pseudocyst, abscess, diabetes, fistula, ascites and stricture, FBC may reveal evidence of complications such as DIC Biochemistry: Serum or urine amylase- raised and confirms the diagnosis. Serum amylase 5 times the normal Investiga upper limit is highly suggestive of acute pancreatitis. tion Serum pancreatic lipase may be increased but is less specific. Biochemical profile may reveal features of complications like hypocalcaemia, hyperglycaemia, hypalbuminaemia, or uraemia. Contrast-enhanced CT or MRI remains the gold standard for diagnosis. It is best done 48 hours after admission. Ultrasound is helpful at presentation; and can help diagnose a biliary cause. Diagnosti Ultrasound: To identify gallstones as a possible c imaging cause Diagnose vascular complications like thrombosis Identify areas of necrosis and other possible aetiologies of an acute abdomen. CXR: Pleural effusion, usually left-sided Elevation of hemidiaphragm Basal atelectasis Cont’d Acute pulmonary oedema. AXR: Localised ileus of small intestine (sentinel loop) Spasm of descending colon (colon cut- off sign) Largely supportive. Nutrition is important- enteral rather than parenteral nutrition is preferred. Adequate fluid balance is essential. ABG must be measured. Managemen Prophylactic antibiotics not indicated t unless severe necrotizing pancreatitis. Adequate analgesia but opiates should be avoided- increase the tone of sphincter of Oddi. Little evidence that early ERCP and sphincterotomy is helpful. Pseudocysts: require no treatment if small. Large and recurrent collections need drainage or surgical excision. Pancreatic abscess formation: suggested by fever, neutrophil leucocytosis and deterioration about 1-2 weeks after initial presentation. Managemen Intensive treatment with antibiotics and either t- cont’d surgical or percutaneous drainage is required. Necrotizing pancreatitis: Necrosectomy is usually required and can be done laparoscopically, video-assisted retroperitoneal debridement (VARD), minimal access retroperitoneal pancreatic necrosectomy (MARPN) or endoscopic transgastric route. Prognosis varies with the severity of attack. Markers of severe acute pancreatitis: Age > 55 years. WBC > 16× 109/L. Prognosis Hypocalcaemia (calcium < 2.2 mmol/L) Renal impairment ( urea increase by > 2 mmol/L Hypoxaemia ( < 8 kPa ) Acidosis (base deficit > 4 mmol/L) Within 48 hours of admission Glasgow Age > 55 years system to Glucose > 10 mmol/L WBC > 15×109/L predict LDH > 600 i.u/L severity Transaminases > 100 i.u/L of Hypocalcaemia < 2 mmol/L pancraeti Blood urea > 16 mmol/L tis Low arterial PaO2 < 8 kPa Serum albumin < 32 g/L Chronic pancreatitis is an inflammatory condition that results in irreversible morphological change and impairment of exocrine and endocrine function. Age usually > 40 years M>F 2 patterns seen: Chronic A chronic relapsing course with recurring acute pancreati pancreatitis and a stepwise deterioration OR A truly chronic gradual deterioration leading to pancreatic tis insufficiency. Risk factors include alcohol abuse, ductal obstruction (stones, trauma, pseudocysts, tumours), SLE , cystic fibrosis. Recognised associations: hypercalcaemia, hyperlipidaemia, congenital pancreatic malformations. Patients may present with an acute episode of pancreatitis or an insidious onset of persistent or recurrent episodes of abdominal pain and weight loss. Late complications include impaired Clinical glucose tolerance, diabetes mellitus, features malabsorption (steatorrhea), profound weight loss and oedema due to hypalbuminaemia. Predisposes to pancreatic cysts, pseudocysts, and pancreatic carcinoma. Ascites and jaundice may occur. Serum amylase fluctuates but may be moderately raised on testing. Plain AXR may show calcification of the pancreas. Ultrasound and CT scan demonstrates Investiga cysts, calcification and enlarged ducts. tions ERCP may show scarring of the ductal system and even stones in the pancreatic duct. MRCP (magnetic resonance cholangiopancreatography ) is increasingly being used. Precipitating factors especially alcohol needs to removed. Adequate analgesia is required. Steatorrhea best managed with enzyme supplements. Blood sugar control with insulin Managemen Thoracoscopic splanchnicectomy in refractory pain not due to duct dilatation. t Surgery may be indicated: Sphincterotomy or sphincteroplasty, partial pancreatectomy, or opening the pancreatic duct and anastomosing with duodenum or jejunum. Total pancreatectomy with replacement of enzymes and insulin. Quit smoking 10 years ago. https://www.bmj.com/co ntent/384/bmj-2023- 070920 Pathways of pain, inflammatio n and fibrosis response in chronic pancreatiti s. A 46-year-old man presents with 2-day history of nausea and upper abdominal pain. The pain was described as gnawing, constant, radiating to the back and associated with reduced appetite. The pain is not made worse by movement, Clinical coughing or breathing and improves with Vignette sitting or leaning forward. He was on vacation over the weekend and consumed up to 3 bottles of whisky and > 10 beers a day. PMH: hypertension, dyslipidaemia. On hydrochlorothiazide, simvastatin and ibuprofen for joint pains on and off. On examination: BP 140/90 mmHg, PR 110 bpm, RR 12/min, afebrile. No cutaneous stigmata of liver disease, tattoos or needle tracts. Epigastric tenderness but no guarding or rebound tenderness. Cont’d Liver and spleen not enlarged. Bowel sounds are present and normal. PR normal. Lab tests: WBC 13,500/ mm3 AST 105 U/L, ALT 48 U/L , ALP 90 U/L and total bilirubin 0.8 mg/dL. Rest of the blood tests within normal limits. The differential diagnosis includes all of Q 1 the following except: (relate A) Gastric ulcer to the B) Alcoholic hepatitis C) Acute pancreatitis clinical D) GERD vignette) E) Acute cholecystitis. The next best test to perform to make a Q 2 diagnosis is: (relate A) ERCP to B) Abdominal ultrasound C) Serum amylase and lipase levels clinical D) OGDS vignette) E) MRI imaging A 40-year-old man with history of HPT, dyslipidaemia and previous cholecystectomy presents with his third episode of acute pancreatitis. Which of the following the LEAST likely cause of acute pancreatitis? Q 3. A) Hydrochlrothiazide B) Hypertriglyceridemia C) Hypercholesterolemia D) Idiopathic E) Pancreas divisum A 65-year-old man is in the hospital for the last 5 days with acute pancreatitis. He is febrile (38.90C), WBC 17500/ mm3 and serum creatinine 150 µmol/L. What is the next step in management? Q 4 A) Start on iv antibiotics B) Start on clear liquid diet C) Perform EUS D) CT scan of abdomen E) MRI imaging of abdomen Enteral nutrition is more beneficial than parenteral nutrition in acute pancreatitis. The benefits of enteral nutrition include all of the following except: A) Does not stimulate pancreatic Q 5 secretion B) Shortens the length of hospitalization. C) Lowers the rate of infection D) Is less expensive E) Maintains intestinal integrity. In which of the following patients with acute pancreatitis should antibiotics be started? A) A patient with fever 38 degrees B) A patient with WBC count 12500/mm3 C) A patient with persistent abdominal Q 6 pain on day 3 of hospitalization. D) A patient with a large pseudocyst on CT scan E) A patient with > 30% necrosis on CT scan Q 7 A 40-year-old man with alcoholic chronic pancreatitis would like to know if his life expectancy is shortened by his condition. Which of the following is the best response? A) His life expectancy is unchanged by the diagnosis B) His life expectancy will be normal if he abstains from alcohol C) If he abstains from both alcohol and tobacco, his life expectancy will be normal D) His life expectancy is reduced but abstaining from alcohol will decrease mortality Q 8 A 27-year-old lady presents with 3-month history of epigastric pain, nausea and steatorrhea. Abdominal image showed pancreatic calcification and dilated pancreatic ducts consistent with chronic pancreatitis. The patient moved to the USA from south India 4 months ago. What is the likely aetiology of her condition? A) Hereditary pancreatitis B) Alcoholic chronic pancreatitis C) Gallstones D) SLE E) Tropical pancreatitis