A case of Recurrent Pancreatitis

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A case of Recurrent Pancreatitis

  1. 1. <ul><li>AN INTERESTING CASE OF PANCREATITIS </li></ul><ul><li>Dr.D.Premkumar </li></ul><ul><li>Under Prof.P.Vijayraghavan’s unit </li></ul>
  2. 2. <ul><li>A 14years old female patient admitted with Abdominal pain and vomiting for one day. </li></ul><ul><li>H/O Abdominal pain-upper abdomen, continuous, sharp radiating to back, no aggravating or relieving factors. </li></ul><ul><li>H/O vomiting – indigested food particles, </li></ul><ul><li>not blood bile stained. </li></ul>
  3. 3. <ul><li>Not passed stools for one day. </li></ul><ul><li>No H/O belching, melena,abdominal distension, fever,jaundice, oliguria,hematuria. </li></ul><ul><li>No H/O NSAID intake ,passage of worms. </li></ul><ul><li>No H/O cough with expectoration, chest pain. </li></ul><ul><li>No H/O loss of appetite and loss of weight </li></ul>
  4. 4. <ul><li>Patient was apparently normal till the age of 6yrs. </li></ul><ul><li>H/O of recurrent abdominal pain after 6 yrs oa age. </li></ul><ul><li>At the age of 10 years Patient was admitted with abdominal pain and vomiting in ICH EGMORE for 10 days. Details not available </li></ul>
  5. 5. <ul><li>Another episode at age 12 years managed in local hospital </li></ul><ul><li>Again in DEC 2007 patient had abdominal pain patient was admitted in ICH again and evaluated.The results were as follows- </li></ul><ul><ul><li>USG abdomen-normal study </li></ul></ul><ul><ul><li>Sr.amylase-1042 </li></ul></ul><ul><ul><li>CT scan- acute pancreatits </li></ul></ul><ul><ul><li>MRI – main pancreatic duct normal </li></ul></ul><ul><ul><ul><li>Edematous pancreas </li></ul></ul></ul><ul><ul><ul><li>Peripancreatic fluid collection </li></ul></ul></ul>
  6. 6. <ul><li>She was discharged at request with conservative treatment and without a etiological diagnosis. </li></ul><ul><li>Patient was relatively symptom free for 2 years. </li></ul><ul><li>Presently she is admitted with same symptoms in our hospital. </li></ul><ul><li>FAMILY HISTORY-her Brother had similar history 5yrs back. </li></ul>
  7. 7. <ul><li>Patient conscious/oriented/afebrile </li></ul><ul><li>No pallor/ jaundice/ pedal edema/ xanthomas. </li></ul><ul><li>PR-90/min </li></ul><ul><li>BP-100/70 mmhg </li></ul><ul><li>P/A: no scars, no sinuses, no discoloration, </li></ul><ul><li>epigastric tenderness+, no guarding </li></ul><ul><li>no mass, organomegaly </li></ul><ul><li>CVS- S1,S2. normal </li></ul><ul><li>RS - NVBS. No added sounds </li></ul>
  8. 8. <ul><li>HB-12.9 </li></ul><ul><li>TC-6900 </li></ul><ul><li>DC-P-63% ;L-33% ; E-4% </li></ul><ul><li>Platelet count-1.2 </li></ul><ul><li>ESR- 5mm/hr </li></ul><ul><li>Blood sugar- 116 mg% </li></ul><ul><li>Blood urea – 30 mg% </li></ul><ul><li>Sr.creatinine- 1.0 mg% </li></ul><ul><li>Na+-139 ;K+-3.7 </li></ul>
  9. 9. <ul><li>LFT </li></ul><ul><li>Sr.bilirubin: </li></ul><ul><li>Total-1.0; direct-0.2 </li></ul><ul><li>SGOT-50 </li></ul><ul><li>SGPT-79 </li></ul><ul><li>SAP-120 </li></ul><ul><li>Sr.protiens Total-5.9 </li></ul><ul><li> ALB-3.5 </li></ul><ul><li>INR-1.1 </li></ul><ul><li>SERUM AMYLASE -68U/L </li></ul><ul><li>Serum Calcium-11.2mg% </li></ul><ul><li> </li></ul>
  10. 10. <ul><li>LIPID PROFILE </li></ul><ul><li>23/4/09 25/4/09 27/4/09 </li></ul><ul><li>TG 1650 1320 1343 </li></ul><ul><li>CHL 301 202 251 </li></ul><ul><li>HDL 72 </li></ul><ul><li>LDL 89 </li></ul><ul><li>VLDL 268 </li></ul><ul><li>USG abdomen : </li></ul><ul><li>Enlarged edematous pancreas with mixed echogenic fluid collection around the tail region with ascites(mild) </li></ul>
  11. 11. <ul><li>ECG – WNL </li></ul><ul><li>CXR and X ray abdomen erect – NAD </li></ul><ul><li>MRCP- NORMAL STUDY </li></ul><ul><li>ANA - NEGATIVE </li></ul><ul><li>Thyroid function test - NORMAL </li></ul>
  12. 14. <ul><li>Nil per oral </li></ul><ul><li>Continuous Ryle’s tube aspiration </li></ul><ul><li>IV FLUIDS </li></ul><ul><li>Antibiotics </li></ul><ul><li>Inj tramadol 100 mg IM </li></ul><ul><li>Inj octreotide 50 microgm s.c tid for 5 days. </li></ul><ul><li>Proton pump inhibitors </li></ul>
  13. 15. <ul><li>MGE opinion obtained on 24/4/09 </li></ul><ul><li>IMPRESSION: Recurrent pancreatitis with hypertriglyceridemia </li></ul><ul><li>ADVICE :family screening. </li></ul><ul><li>SGE opinion obtained on 25/4/09 </li></ul><ul><li>IMPRESSION: </li></ul><ul><li>Dyslipidemic pancreatitis. </li></ul>
  14. 16. <ul><ul><li>TGL HDL TC LDL </li></ul></ul><ul><ul><li>FATHER 349 42 199 110 </li></ul></ul><ul><ul><li>MOTHER 139 49 331 120 </li></ul></ul><ul><ul><li>SISTER 70 47 197 90 </li></ul></ul><ul><ul><li>BROTHER 1134 40 561 200 </li></ul></ul>
  15. 17. <ul><li>RECURRENT PANCREATITIS </li></ul><ul><li>HYPERTRIGLYCERIDEMIA </li></ul><ul><li>FAMILIAL </li></ul>
  16. 18. <ul><li>Common Causes </li></ul><ul><ul><li>Gallstones (including microlithiasis) </li></ul></ul><ul><ul><li>Alcohol (acute and chronic alcoholism) </li></ul></ul><ul><ul><li>Hypertriglyceridemia </li></ul></ul><ul><ul><li>(ERCP), especially after biliary manometry </li></ul></ul><ul><ul><li>Trauma (especially blunt abdominal trauma) </li></ul></ul><ul><ul><li>Postoperative (abdominal and nonabdominal operations) </li></ul></ul><ul><ul><li>Drugs (azathioprine, 6-mercaptopurine, sulfonamides, estrogens, tetracycline, valproic acid, anti-HIV medications) </li></ul></ul><ul><ul><li>Sphincter of Oddi dysfunction </li></ul></ul>
  17. 19. <ul><li>Vascular causes and vasculitis (ischemic-hypoperfusion states after cardiac surgery) </li></ul><ul><li>Connective tissue disorders and thrombotic thrombocytopenic purpura (TTP) </li></ul><ul><li>Cancer of the pancreas </li></ul><ul><li>Hypercalcemia </li></ul><ul><li>Periampullary diverticulum </li></ul><ul><li>Pancreas divisum </li></ul><ul><li>Hereditary pancreatitis </li></ul><ul><li>Cystic fibrosis </li></ul><ul><li>Renal failure </li></ul>
  18. 20. <ul><li>Infections </li></ul><ul><li>mumps, coxsackievirus, cytomegalovirus, echovirus, </li></ul><ul><li>parasites </li></ul><ul><li>Autoimmune (e.g., Sjögren's syndrome) </li></ul>
  19. 21. <ul><li>Occult disease of the biliary tree or pancreatic ducts, especially microlithiasis, sludge </li></ul><ul><li>Drugs </li></ul><ul><li>Hypertriglyceridemia </li></ul><ul><li>Pancreas divisum </li></ul><ul><li>Pancreatic cancer </li></ul><ul><li>Sphincter of Oddi dysfunction </li></ul><ul><li>Cystic fibrosis </li></ul><ul><li>Idiopathic </li></ul>
  20. 22. <ul><li>Hypertriglyceridemia (HTG) is reported to cause 1 –4% of acute pancreatitis episodes. </li></ul><ul><li>HTG is also implicated in more than half of gestational pancreatitis cases. </li></ul><ul><li>Serum triglyceride (TG) levels above 1,000 mg / dl are usually considered necessary to ascribe causation for Acute Pancreatitis. </li></ul>
  21. 23. <ul><li>1.FAMILIAL </li></ul><ul><li>2.SECONDARY </li></ul><ul><li>Uncontrolled diabetes </li></ul><ul><li>Hypothyroid </li></ul><ul><li>Estrogen, tamoxifen , clomiphene , protease inhibitors , propofol , olanzapine , mirtazapine , and isotretinoin </li></ul><ul><li>Alcohol </li></ul>
  22. 24. <ul><li>19-32% of pts have normal amylase levels </li></ul><ul><li>Time interval since onset of attack: amylase is the first to return toward normal values, after the 1 st hospital day it is the least sensitive </li></ul><ul><li>Alcoholic Pancreatitis: related to number of previous attacks (i.e. the parenchyma no longer produces sufficient amounts of enzymes) </li></ul><ul><li>Hypertriglyceridemia: hyperlipidemia interferes with the serum assay </li></ul><ul><li>Use serial dilution techniques </li></ul>
  23. 25. <ul><li>HTG levels >500 mg / dl may cause a falsely normal amylase level, likely from HTG interference with calorimetric reading of the assay. </li></ul><ul><li>Serial dilutions of the serum amylase sample can reduce the TG interference. </li></ul><ul><li>S.lipase-more sensitive and specific to acute pancreatitis. </li></ul>
  24. 26. <ul><li>The exact mechanism is unclear but it is thought to involve increased concentrations of chylomicrons in the blood. Chylomicrons are usually formed 1-3 hours post-prandially and cleared within 8 hours. However, when triglycerides levels exceed 1,000mg/dL, chylomicrons are almost always present. </li></ul><ul><li>These low density particles are very large and may obstruct capillaries leading to local ischemia and acidemia. </li></ul>
  25. 27. <ul><li>. This local damage can expose triglycerides to pancreatic lipases. The degradation of triglycerides to free fatty acids can lead to cytotoxic injury resulting in further local injury that increases inflammatory mediators and free radicals, eventually manifesting as pancreatitis. </li></ul>
  26. 28. <ul><li>PRIMARY HYPERLIPIDAEMIAS </li></ul><ul><li>1.FAMILIAL CHYLOMICRONEMIA </li></ul><ul><li>2.APOA-V DEFICIENCY </li></ul><ul><li>3.FAMILIAL HEPATIC LIPASE DEFICIENCY </li></ul><ul><li>4.FAMILIAL DYSBETALIPOPROTEINEMIA </li></ul><ul><li>5. FAMILIAL HYPERTRIGLYCERIDEMA </li></ul><ul><li>6. FAMILIAL COMBINED HYPERLIPIDEMIA </li></ul><ul><li>7. FAMILIAL CHOLESTEROLEMIA- LDL </li></ul><ul><li> </li></ul>
  27. 29. <ul><li>FHTG relatively common[1in 500] autosomal dominant disorder of unknown etiology. </li></ul><ul><li>The major class of lipoprotein elevated- VLDL </li></ul><ul><li>Type IV hyperlipoproteinemia ( Frederickson) </li></ul><ul><li>VLDL and chylomicrons- Type V hyperlipidemia </li></ul><ul><li>Not associated with atherosclerosis CVD. </li></ul><ul><li>Treatment-FIBRATES or FISH OIL </li></ul>
  28. 30. <ul><li>Maintenance of TG levels below 500 mg / dl has been seen in multiple case series to expedite clinical improvement. </li></ul><ul><li>1.Insulin –lowers TG levels. </li></ul><ul><li>Insulin activates lipoprotein lipase, an enzyme that accelerates chylomicron degradation into glycerol and fatty free acids </li></ul><ul><li> </li></ul>
  29. 31. <ul><li>2.Heparin- also brings down TG </li></ul><ul><li>Heparin stimulates the release of endothelial lipoprotein lipase into circulation ,and has been used without insulin to successfully manage HTG. </li></ul><ul><li>Despite the success of intravenous (IV) heparin in combination with insulin in HTG management, heparin has come under greater scrutiny. IV heparin does cause an initial rise in circulating lipoprotein lipase levels, but is quickly followed by increased hepatic degradation </li></ul>
  30. 32. <ul><li>Apheresis to lower HTG can be conceptualized as removing a potential trigger for continued damage to the pancreas. However, rigorous data for apheresis with regards to AP complications, length of hospital stay, and mortality are not currently available. </li></ul><ul><li>Apheresis should be started within 48 h of HTGP diagnosis and continued in several sessions until end-of-session serum TG levels are < 500 mg / dl. </li></ul>
  31. 33. <ul><li>Fibrates </li></ul><ul><li>Fibrates effectively lower triglyceride levels by 40 – 60 % and raise HDL-C levels </li></ul><ul><li>considered first line therapy for primary HTG </li></ul><ul><li>Niacin - is not as potential as fibrates but can lower TG levels by 30 – 50 % </li></ul><ul><li>Omega-3 fatty acids studied in a prospective, double-blind, placebo-controlled trial proved capable of lowering high TG (500 – 2,000 mg / dl) by 45 % </li></ul>
  32. 34. <ul><li>Hypertriglyceridemia is reported as causative in 1 – 4 % of patients who present with AP. </li></ul><ul><li>Secondary causes of HTG to be ruled out. </li></ul><ul><li>Bringing down TG level will hasten recovery in addition to usual treatment of acute pancreatitis- bed rest, nil per oral, IV fluids inj. Octreotide, antibiotics. </li></ul><ul><li>Amylase level may be found to be normal in the presence of HTG >1000mg/dl. </li></ul>
  33. 35. <ul><li>THANK YOU </li></ul>

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