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![•Leucocytosis (15,000-20,000/µl)
•Hemoconcentration (hematocrit >44%)
•Azotemia (BUN >22mg/dl)
•Hyperglycemia
•Hypocalcemia
•Hyperbilirubinemia [Serum bilirubin >68µmol/L (>4mg/dl)]
•Increased serum lactate dehydrogenase (LDH> 500U/dl)
•Hypertriglyceridemia
•Hypoxemia (arterial Po2 ≤ 60 mmHg)](https://image.slidesharecdn.com/pancreatitis-150129141139-conversion-gate02/85/Pancreatitis-12-320.jpg)
![Markers of Severity within 24 Hours
SIRS [temperature >38° or <36°C (>100.4° or 96.8°F), Pulse >90,
Tachypnea >24, ↑ WBC >12,000]
• Hemoconcentration (Hct >44%)
• BISAP
• (B) Blood urea nitrogen (BUN) >22 mg%
• (I) Impaired mental status
• (S) SIRS: 2/4 present
• (A) Age >60 years
• (P) Pleural effusion
• Organ Failure
• Cardiovascular: systolic BP <90 mmHg, heart rate >130
• Pulmonary: PaO2 <60 mmHg
• Renal serum creatinine >2.0 mg%
Markers of Severity during Hospitalization
Persistent organ failure
• Pancreatic necrosis
• Hospital-acquired infection
Bedside Index of Severity in Acute Pancreatitis(BISAP)](https://image.slidesharecdn.com/pancreatitis-150129141139-conversion-gate02/85/Pancreatitis-17-320.jpg)
![CT Findings and Grading of Acute Pancreatitis
[CT Severity Index (CTSI)]:
CT severity Index= unenhanced CT score + necrosis score: (maximum = 10; ≥6 = severe disease.)
Grade Findings Score
A Normal pancreas: normal size, sharply defined,
smooth contour, homogeneous enhancement,
retroperitoneal peripancreatic fat without
enhancement
0
B Focal or diffuse enlargement of the pancreas,
contour may show irregularity, enhancement
may be inhomogeneous but there is no
peripancreatic Inflammation
1
C Peripancreatic inflammation with intrinsic pancreatic
abnormalities
2
D Intrapancreatic or extrapancreatic fluid collections 3
E Two or more large collections or gas in the pancreas
or retroperitoneum
4
Necrosis,% Score
0 0
<33% 2
33-50% 4
≥50% 6](https://image.slidesharecdn.com/pancreatitis-150129141139-conversion-gate02/85/Pancreatitis-18-320.jpg)
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Pancreatitis
- 1.
- 2. The Name Game Herophilus(335–280 BC) Rufus of Ephesus I found it! Dude, I named it!!
- 3. He defeated theworld but Pancreatitis defeated him Alexander The Great June 10, 323 BC
- 4. Incidence in US 70hospitalizations/100,000 persons annually. Incidence in India- 1.9 per 1,000 patient years …. And still increasing Acute Pancreatitis
- 5. Etiology: Common Causes Gallstones disease Alcohol(acute &chronic both) Hypertriglyceridemia ERCP, especially after biliary manometry Blunt abdominal trauma Postoperative (abdominal and nonabdominal operations) Drugs (azathioprine, 6-mercaptopurine, sulfonamides, estrogens, tetracycline, valproic acid, anti-HIV medications) Sphincter of Oddi dysfunction Uncommon Causes Vascular causes and vasculitis Connective tissue disorders and thrombotic thrombocytopenic purpura (TTP) Ca. pancreas Hypercalcemia Periampullary diverticulum Pancreas divisum Hereditary pancreatitis Cystic fibrosis Renal failure
- 6. Pathogenesis: Phase I: Intra-pancreaticdigestive enzymes activation & acinar cell injury Phase II: Activation, Chemoattraction, & sequestration of leucocytes & macrophages Phase III: Effects of activated proteolytic enzymes and cytokines, released by the inflammed pancreas, on distant organs.
- 7. Symptoms: Abdominal Pain: •Steady andboring •Epigastric and periumbilical often radiates to the back •More intense on supine position, •May be relieved by sitting with the trunk flexed and knees drawn up.
- 8. Physical examination: Low-grade fever,tachycardia, and hypotension are fairly common. Shock is not unusual. Jaundice (due to edema of the head of the pancreas with compression of the intrapancreatic portion of the common bile duct.) Erythematous skin nodules due to subcutaneous fat necrosis may occur.
- 9. Basilar rales, atelectasis,and pleural effusion, the latter most frequently left sided. Abdominal tenderness and muscle rigidity. Bowel sounds are usually diminished or absent. An enlarged pancreas with walled off necrosis or a pseudocyst.
- 10.
- 11. Investigations: Blood tests Amylaseand lipase Plasma level peak within 24 hours t1/2 of amylase << lipase Sensitivity Specificit y Amylase 67-100 85-98 Lipase 82-100 86-100
- 12. •Leucocytosis (15,000-20,000/µl) •Hemoconcentration (hematocrit>44%) •Azotemia (BUN >22mg/dl) •Hyperglycemia •Hypocalcemia •Hyperbilirubinemia [Serum bilirubin >68µmol/L (>4mg/dl)] •Increased serum lactate dehydrogenase (LDH> 500U/dl) •Hypertriglyceridemia •Hypoxemia (arterial Po2 ≤ 60 mmHg)
- 13. Ultra Sound (US) Littlepart in the diagnosis of the acute pancreatitis Role in biliary pancreatitis Stones in gallbladder Common Bile Duct dilation
- 14. CT Scan Normal-Homogeneous enhancement ofthe whole pancreas Abnormal -Non-visualization of a part of the pancreas Sensitivity of 90-95% Specificity – 100% A dynamic CT scan should be performed in all (predicted) severe cases between 3 and 10 days after admission
- 15.
- 16. Severity of AcutePancreatitis Risk Factors for Severity: • Age >55 years • Obesity, BMI >30 • Co-morbid disease • Altered mental status
- 17. Markers of Severitywithin 24 Hours SIRS [temperature >38° or <36°C (>100.4° or 96.8°F), Pulse >90, Tachypnea >24, ↑ WBC >12,000] • Hemoconcentration (Hct >44%) • BISAP • (B) Blood urea nitrogen (BUN) >22 mg% • (I) Impaired mental status • (S) SIRS: 2/4 present • (A) Age >60 years • (P) Pleural effusion • Organ Failure • Cardiovascular: systolic BP <90 mmHg, heart rate >130 • Pulmonary: PaO2 <60 mmHg • Renal serum creatinine >2.0 mg% Markers of Severity during Hospitalization Persistent organ failure • Pancreatic necrosis • Hospital-acquired infection Bedside Index of Severity in Acute Pancreatitis(BISAP)
- 18. CT Findings andGrading of Acute Pancreatitis [CT Severity Index (CTSI)]: CT severity Index= unenhanced CT score + necrosis score: (maximum = 10; ≥6 = severe disease.) Grade Findings Score A Normal pancreas: normal size, sharply defined, smooth contour, homogeneous enhancement, retroperitoneal peripancreatic fat without enhancement 0 B Focal or diffuse enlargement of the pancreas, contour may show irregularity, enhancement may be inhomogeneous but there is no peripancreatic Inflammation 1 C Peripancreatic inflammation with intrinsic pancreatic abnormalities 2 D Intrapancreatic or extrapancreatic fluid collections 3 E Two or more large collections or gas in the pancreas or retroperitoneum 4 Necrosis,% Score 0 0 <33% 2 33-50% 4 ≥50% 6
- 19. Grading of thedisease: Atlanta criteria (1993) Atlanta Revision (2013) Mild acute pancreatitis Mild acute pancreatitis Absence of organ failure Absence of organ failure Absence of local complications Absence of local complications Severe acute pancreatitis Moderately severe acute pancreatitis 1. Local complications AND / OR 1. Local complications AND / OR 2. Organ failure 2. Transient organ failure ( < 48hrs) GI bleeding ( > 500 cc/24hr) Severe acute pancreatitis Shock – SBP 90 mm Hg Persistent organ failure > 48hrs PaO 2 60 % Creatinine 2 mg/dl
- 20. Management: Acute Pancreatitis Mild AP 80%of cases <5% of mortality Recommended (All Pts.) Admit to general wards Re-feed when pain subsides Not Recommended Antibiotics CT scan Severe AP 20% of cases >95% of mortality Recommended Admit to ICU Antibiotics CT scan on Day 3rd Necrosis Sterile-Observe Infection suspected-FNA Infected necrosis- Necrosectomy
- 21. 1. Aggressive hydration,250 – 500 ml per hour of isotonic crystalloid. Early aggressive intravenous hydration is most beneficial during the first 12 – 24 hrs. •Lactated Ringer’s preferred isotonic crystalloid replacement fluid. 3. Reassessment at frequent intervals within 6hrs of admission and for the next 24–48 hrs. Management:
- 22. Hypertriglyceridemia-associated Pancreatitis: (1) weightloss to ideal weight, (2) a lipid restricted diet, (3) exercise (4) avoidance of alcohol and of drugs that can elevate serum triglycerides (i.e., estrogens, vitamin A, thiazides, & propranolol), (5) control of diabetes.
- 23. THE ROLE OFANTIBIOTICS: 1. Extra-pancreatic infection, i.e. cholangitis, catheter-acquired infections, bacteremia,UTI, RTI, etc. 1. Not recommended for Routine prophylaxis 2. Not recommended in sterile necrosis to prevent infected necrosis 1. Infected necrosis (i) CT-guided fine-needle aspiration (FNA) Gram stain and culture (ii) empiric use of antibiotics after obtaining necessary cultures for infectious agents, without CT FNA. (iii)antibiotics known to penetrate pancreatic necrosis, such as carbapenems, quinolones, and metronidazole. 5. Routine administration of antifungal agents along with prophylactic or therapeutic antibiotics is not recommended.
- 25. 1. ERCP shouldbe done within 24 h of admission in AP with concurrent acute cholangitis. 2. No early need in gallstone pancreatitis lacking laboratory or clinical evidence of ongoing biliary obstruction. 3. In the absence of cholangitis and / or jaundice, MRCP or EUS rather than diagnostic ERCP should be used to screen for choledocholithiasis if highly suspected. 4. Pancreatic duct stents and / or post-procedure rectal nonsteroidal anti-infl ammatory drug (NSAID) suppositories should be utilized to lower the risk of severe post-ERCP pancreatitis in high-risk patients. Roll of ERCP:
- 26. THE ROLE OFSURGERY: 1. Gallstone pancreatitis -cholecystectomy before discharge to prevent recurrence of AP. 2. In necrotizing biliary AP, cholecystectomy is to be deferred until active inflammation subsides and fluid collections resolve or stabilize. 3. No active interventions are required in Asymptomatic pseudocysts and pancreatic and/or extra-pancreatic necrosis. 4. In stable patients with infected necrosis, drainage should be delayed preferably for >4 weeks to allow liquefication &walled-off necrosis. 5. Minimally invasive methods of necrosectomy are preferred to open necrosectomy in symptomatic infected necrosis.
- 27. 1. In mildAP Oral feedings can be started immediately if there is no nausea/vomiting & abdominal pain has resolved. Initiate feeding with a low-fat solid diet. 3. In severe AP, Enteral nutrition is recommended Parenteral nutrition should be avoided, unless the enteral route is not available, not tolerated, or not meeting caloric requirements. 4. Nasogastric and nasojejunal delivery of enteral feeding appear comparable in efficacy and safety. Feeding:
- 28. Complications of AcutePancreatitis: Local complications Necrosis Sterile Infected Walled-off necrosis Pancreatic fluid collections Pancreatic abscess Pancreatic pseudocyst Pain Rupture Hemorrhage Infection GI Obstruction Pancreatic ascites Main pancreatic duct disruption Leaking pseudocyst Involvement of contiguous organs by necrotizing pancreatitis Massive intraperitoneal hemorrhage Thrombosis of blood vessels (splenic vein, portal vein) Bowel infarction Obstructive jaundice
- 29. Systemic complications Pulmonary Pleural effusion,Atelectasis Mediastinal abscess,Pneumonitis Acute respiratory distress syndrome Cardiovascular Hypotension, Hypovolemia Sudden death Nonspecific ST-T changes simulating MI Pericardial effusion Hematologic DIC Gastrointestinal Peptic ulcer disease Erosive gastritis Hemorrhagic pancreatic necrosis with erosion into major blood vessels Portal vein thrombosis, variceal hemorrhage Renal Oliguria,Azotemia,Renal artery and/or renal vein thrombosis Acute tubular necrosis Metabolic Hyperglycemia, Hypertriglyceridemia, Hypocalcemia Encephalopathy, Sudden blindness (Purtscher’s retinopathy) Central nervous system Psychosis Fat emboli Fat necrosis Subcutaneous tissues (erythematous nodules)
- 30. o Early andaccurate diagnosis of acute pancreatitis is crucial. o Early treatment of acute pancreatitis with aggressive IV fluid hydration saves lives and is most beneficial in the first 12-24 hours. o Routine prophylactic antibiotic use is not recommended for acute pancreatitis unless presence of infected necrosis is established clinically or by FNA. o Mild acute pancreatitis due to gallstones warrants cholecystectomy before discharge. Summary:
- 31.
- 32. • “Irreversible” damage •Histological evidence of inflammation, fibrosis, and destruction of exocrine (acinar) & endocrine (islet) tissue. • Can be inferred by clinical evidence of Exocrine (secretory) and endocrine insufficiency. • Obvious structural disease on radiography – Calcifications, multiple beads and strictures • Pain or steatorrhea not necessary. Definations:
- 33. Etiology of CP: IDIOPATHIC ALCOHOL& TOBACCO HEREDITARY
- 34.
- 35. Consequences of ChronicPanc: Pain Steatorrhea Diabetes Biliary obs. B12 def. Cancer
- 36. Chronic Pancreatitis: theSpectrum Damage Starts PAIN “Minimal ∆” “Small Duct” (pos secretin) Structural damage (Pos CT/EUS/ERCP) Steatorrhea “BIG DUCT” CANCER RISK Diabetes Pain may dec 30% 60% 80-90% % Damage
- 37. Make the CorrectDiagnosis • Chronically elevated amylase/lipase do not make CP. • In early CP, imaging and labs may be negative or equivocal • Avoid labelling as CP • Avoid sick role, pyschosocial-economic consequences. • Much acute relapsing pancreatitis is actually early chronic pancreatitis
- 38. Diagnosis of CP: Structural Tests CT MRI/MRCP EUS Function Tests Fecal fat Serum Trypsin Fecal Elastase Glucose/GTT Panc.Polypeptide S-MRCP S-EUS SST E-SST
- 39. Atrophic pancreas, multiple calcifications,stones dilated pancreatic duct Markedly dilated pancreatic duct seen in through the body and tail Gadolinium-enhanced MRI/MRCP- dilated pancreatic duct with multiple filling defects s/o pancreatic duct calculi.
- 40. Pancreatic Function Tests(PFTs): Indirect (often tubeless) Fecal fat Trypsin Glucose/GGT Pancreatic polypeptide Dual Label Schilling test Direct S-MRCP S-EUS e-SST SST (Gold standard functional test) CCK/SST Bentiromide test (historical) Lundh test (Europe)
- 41. Quick and “dirty”PFTs: Trypsin Fecal fat Fecal elastase Fecal chymotrypsin Only stage disease, don’t usually pick up early disease.
- 42. Trypsin: • Rarely donewell • RIA (I131) >>>> ELISA • <20pg/dL, correlates well with pancreatic Steatorrhea • 20-29 Equivocal, often small duct. • >30 Normal • In practice values >80 or so are suggestive of AP • If >150, very specific for AP
- 43. Fecal fat: • Spot –6 or more droplets – Only picks up extensive steatorrhea • 72hr – Must be on 100g fat diet several days before – >7grams/24hrs is steatorrhea – Very nonspecific – Noncompliance high
- 44. Fecal Elastase: Intermediate(100-200) values PROBLEMATIC! 21% of asymptomatic or non-pancreatic control pts. >60yr had fecal elastase <200, 6% <100: CCK and SST correl. better with 72 h FF than FE. False positives if watery stool <100 correlates well with steatorrhea 100-200 borderline >200 normal “Not affected” by porcine enzymes Must use monoclonal ELISA
- 45. E-SST: Probably aboutas good as SST Recent study by Conwell showed CCK still may be more sensitive (not true in past) More cumbersome, takes at least one hour.
- 46. S-EUS: Combined EUSplus SST ` Better coding for SST EUS may add something to SST See pancreatic duct directly and after secretin
- 47. EUS Findings: Foci,Strands, Lobularity (w/w/o honeycombing) Hyperechoic duct walls, Visible side branches, Main PD dilated,Calcific, Cysts Rosemont (GIE June 2009, Catalano, et al) Major criteria: (1) hyperechoic foci with shadowing & main pancreatic duct (PD) calculi & (2) lobularity with honeycombing. Minor criteria: cysts, dilated ducts ≥3.5mm, irregular PD contour, dilated side branches ≥1mm, hyperechoic duct wall, strands, nonshadowing hyperechoic foci, and lobularity with noncontiguous lobules
- 48. EUS: problems: Givesubtle changes in absence of clinical chronic pancreatitis Lots of inter and intraobserver variability Change in “gain” can have big impact Lack of gold standard
- 49.
- 50. New Horizons: Diffusionweighted MRI with secretin EUS elastography MR elastography C14 bicarbonate breath test Secretin-PET
- 51. Diffusion weighted (DWI)MRI with secretin: DWI measures sum of random motions of protons Lower values or delayed peak in chronic pancreatitis, especially with secretin Can also better distinguish AP from CANCER Small insulinomas being detected.
- 52. EUS elastography: Measure oftissue stiffness also uses sound waves to detect reverberations. Good sensitivity But analysis occurs after procedure. Magnetic Resonance Elastography: Better known for liver, but also works for pancreas/spleen.
- 53. Treatment: What are wetreating? Pain –Attacks of acute pancreatitis –Disease flares w/o acute pancreatitis –Chronic pain –Other reasons – Pseudocyst, biliary obstruction, etc. •Exocrine and endocrine insufficiency •Other complications –Gastric outlet obstruction –Pancreatic ascites –Uncommon complications
- 54. Pain: General measures (ALLPATIENTS) –Behavior modification –Control of metabolic factors •Analgesics – Stepwise approach –Non-narcotics (e.g. NSAIDS) –Narcotic •Weaker, mixed agonist-antagonist or partial agonist (e.g. Tramadol) •Stronger narcotic (e.g. morphine, hydrocodone) •Neuromodulating agent (e.g. Pregabalin) •Endoscopic therapy •Surgery •No proven benefit –Oral pancreatic enzyme supplementation –Antioxidants –Celiac plexus block
- 55. Pain in ChronicPancreatitis: Medical management •No inflammatory mass •No pancreatic ductal dilatation, stricture(s) •No peripancreatic complications •Refuses endoscopic therapy/surgery when indicated
- 56. • Pancreatic ductaldilatation and/or stricture(s) •Symptomatic pseudocysts •Biliary stricture (usually temporary) Pain in Chronic Pancreatitis: Endoscopic Therapy (+/- ESWL)
- 57. • Failed endoscopictherapy (usually) –Use as first line in – •Pancreatic ductal stones with heavy stone burden, especially in the body/tail region, usually with pancreatic ductal dilatation and stricture(s) •Inflammatory mass (typically in pancreatic head) •Biliary stricture •Symptomatic pseudocysts (not amenable or after failed endoscopic therapy) Pain in Chronic Pancreatitis: Surgery
- 58. •Resection •Drainage •Combination •Total Pancreatectomy withIslet Auto-Transplantation (TPIAT) Chronic Pancreatitis: Surgery
- 59. Exocrine and EndocrineInsufficiency: •Exocrine Insufficiency –Often undertreated –Timing with meals –Clinical history of steatorrhea seen in severe insufficiency –Fat soluble vitamin deficiencies – 80,000-100,000Units of lipase per meal •Endocrine insufficiency (Type 3c Diabetes) –Often needs Insulin treatment
- 60.
- 61. •Clinical presentation mimicsPancreas cancer •Less common •Pancreatitis, persistent pancreatic mass, scarred or shrunken pancreas, malabsorption •Elevation of serum IgG4 levels •Typical appearance on imaging tests and biopsy •Patients often have involvement of other organs •Absence of pancreatic calcification or cysts •Two forms have been recognized - Type I and II •Excellent response to steroids
- 62. Mayo Clinic criteria: (1)Diagnostic histology; (2) Characteristic findings on CT & pancreatography combined with elevated IgG4 levels; & (3) Response to glucocorticoid therapy, with improvement in pancreatic & extrapancreatic manifestations
- 63. Prednisone : Initial doseof 40 mg/d for four weeks followed by a taper of the daily dosage by 5 mg/week based on monitoring of clinical parameters. Tratment:
- 64. Complications of ChronicPancreatitis: Narcotic addiction Gastrointestinal bleeding Impaired glucose tolerance Jaundice Gastroparesis Cholangitis and/or biliary cirrhosis Cobalamin malabsorption Subcutaneous fat necrosis Nondiabetic retinopathy Bone pain Effusions with high amylase content Pancreatic cancer
- 65. •The spectrum ofrisk factors for CP have broadened •Treatment of pain in CP needs a multidisciplinary approach •Cross sectional imaging helps to assess pancreatic morphology and guides management •An initial conservative approach is reasonable in all patients with painful CP •When appropriate endoscopic therapy/surgery should be considered for pain relief •Autoimmune Pancreatitis is a unique form of CP with excellent response to steroids Take Home Points
Editor's Notes
- #3 Etymologically, the term "pancreas", a modern Latin adaptation of Greek πάγκρεας,[24] [πᾶν ("all", "whole"), and κρέας ("flesh")],[25]originally means sweetbread,[26] although literally meaning all-flesh, presumably because of its fleshy consistency
- #6 The most common cause of AP is gallstones (40– 7 0% ) and alcohol. Clinically evident AP occurs in < 5 % of heavy drinkers. Rare Causes Infections (mumps, coxsackievirus, cytomegalovirus, echovirus, parasites) Autoimmune (e.g., Sjögren’s syndrome)
- #8 Other symptoms: Nausea, vomiting, and abdominal distention Fever.