AN INTERESTING CASE OF PANCREATITIS

Dr.D.Premkumar

Under Prof.P.Vijayraghavan’s unit

A 14years old female patient admitted with Abdominal pain and vomiting for one day.

H/O Abdominal pain-upper abdomen, continuous, sharp radiating to back, no aggravating or relieving factors.

H/O vomiting – indigested food particles, not blood bile stained.

Not passed stools for one day.

No H/O belching, melena,abdominal distension, fever,jaundice, oliguria,hematuria.

No H/O NSAID intake ,passage of worms.

No H/O cough with expectoration, chest pain.

No H/O loss of appetite and loss of weight

Patient was apparently normal till the age of 6yrs.

H/O of recurrent abdominal pain after 6 yrs oa age.

At the age of 10 years Patient was admitted with abdominal pain and vomiting in ICH EGMORE for 10 days. Details not available

Another episode at age 12 years managed in local hospital

Again in DEC 2007 patient had abdominal pain patient was admitted in ICH again and evaluated.The results were as follows-◦ USG abdomen-normal study◦ Sr.amylase-1042◦ CT scan- acute pancreatits◦ MRI – main pancreatic duct normal Edematous pancreas Peripancreatic fluid collection

She was discharged at request with conservative treatment and without a etiological diagnosis.

Patient was relatively symptom free for 2 years.Presently she is admitted with same symptoms

in our hospital.FAMILY HISTORY-her Brother had similar

history 5yrs back.

Patient conscious/oriented/afebrile No pallor/ jaundice/ pedal edema/

xanthomas. PR-90/min BP-100/70 mmhg P/A: no scars, no sinuses, no discoloration, epigastric tenderness+, no guarding no mass, organomegaly CVS- S1,S2. normal RS - NVBS. No added sounds

HB-12.9 TC-6900 DC-P-63% ;L-33% ; E-4% Platelet count-1.2 ESR- 5mm/hr Blood sugar- 116 mg% Blood urea – 30 mg% Sr.creatinine- 1.0 mg% Na+-139 ;K+-3.7

LFT Sr.bilirubin: Total-1.0; direct-0.2 SGOT-50 SGPT-79 SAP-120 Sr.protiens Total-5.9

ALB-3.5 INR-1.1 SERUM AMYLASE-68U/L Serum Calcium-11.2mg%

LIPID PROFILE23/4/09 25/4/09 27/4/09

TG 1650 1320 1343CHL 301 202 251HDL 72LDL 89VLDL 268

USG abdomen : Enlarged edematous pancreas with mixed echogenic

fluid collection around the tail region with ascites(mild)

ECG – WNL

CXR and X ray abdomen erect – NAD

MRCP- NORMAL STUDY

ANA - NEGATIVE

Thyroid function test - NORMAL

Nil per oral Continuous Ryle’s tube aspiration IV FLUIDS Antibiotics Inj tramadol 100 mg IM Inj octreotide 50 microgm s.c tid for 5 days. Proton pump inhibitors

MGE opinion obtained on 24/4/09IMPRESSION: Recurrent pancreatitis with

hypertriglyceridemiaADVICE :family screening.

SGE opinion obtained on 25/4/09IMPRESSION:

Dyslipidemic pancreatitis.

TGL HDL TC LDLFATHER 349 42 199 110MOTHER 139 49 331 120SISTER 70 47 197 90BROTHER 1134 40 561

200

RECURRENT PANCREATITIS HYPERTRIGLYCERIDEMIA FAMILIAL

Common Causes◦ Gallstones (including microlithiasis)◦ Alcohol (acute and chronic alcoholism)◦ Hypertriglyceridemia◦ (ERCP), especially after biliary manometry◦ Trauma (especially blunt abdominal trauma)◦ Postoperative (abdominal and nonabdominal operations)◦ Drugs (azathioprine, 6-mercaptopurine, sulfonamides,

estrogens, tetracycline, valproic acid, anti-HIV medications)◦ Sphincter of Oddi dysfunction

Vascular causes and vasculitis (ischemic-hypoperfusion states after cardiac surgery)

Connective tissue disorders and thrombotic thrombocytopenic purpura (TTP)

Cancer of the pancreas Hypercalcemia Periampullary diverticulum Pancreas divisum Hereditary pancreatitis Cystic fibrosis Renal failure

Infections mumps, coxsackievirus,

cytomegalovirus, echovirus, parasites

Autoimmune (e.g., Sjögren's syndrome)

Occult disease of the biliary tree or pancreatic ducts, especially microlithiasis, sludge

Drugs Hypertriglyceridemia Pancreas divisum Pancreatic cancer Sphincter of Oddi dysfunction Cystic fibrosis Idiopathic

Hypertriglyceridemia (HTG) is reported to cause 1 –4% of acute pancreatitis episodes.

HTG is also implicated in more than half of

gestational pancreatitis cases.

Serum triglyceride (TG) levels above 1,000 mg / dl are usually considered necessary to ascribe causation for Acute Pancreatitis.

1.FAMILIAL

2.SECONDARY Uncontrolled diabetes Hypothyroid Estrogen, tamoxifen , clomiphene , protease

inhibitors , propofol , olanzapine , mirtazapine , and isotretinoin

Alcohol

19-32% of pts have normal amylase levels Time interval since onset of attack: amylase is

the first to return toward normal values, after the 1st hospital day it is the least sensitive

Alcoholic Pancreatitis: related to number of previous attacks (i.e. the parenchyma no longer produces sufficient amounts of enzymes)

Hypertriglyceridemia: hyperlipidemia interferes with the serum assay

Use serial dilution techniques

HTG levels >500 mg / dl may cause a falsely normal amylase level, likely from HTG interference with calorimetric reading of the assay.

Serial dilutions of the serum amylase sample can reduce the TG interference.

S.lipase-more sensitive and specific to acute pancreatitis.

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.

These low density particles are very large and may obstruct capillaries leading to local ischemia and acidemia.

. 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.

PRIMARY HYPERLIPIDAEMIAS1.FAMILIAL CHYLOMICRONEMIA2.APOA-V DEFICIENCY3.FAMILIAL HEPATIC LIPASE DEFICIENCY4.FAMILIAL DYSBETALIPOPROTEINEMIA5. FAMILIAL HYPERTRIGLYCERIDEMA6. FAMILIAL COMBINED HYPERLIPIDEMIA

7. FAMILIAL CHOLESTEROLEMIA-LDLLDL

FHTG relatively common[1in 500] autosomal dominant disorder of unknown etiology.

The major class of lipoprotein elevated- VLDL Type IV hyperlipoproteinemia ( Frederickson) VLDL and chylomicrons- Type V

hyperlipidemia Not associated with atherosclerosis CVD. Treatment-FIBRATES or FISH OIL

Maintenance of TG levels below 500 mg / dl has been seen in multiple case series to expedite clinical improvement.

1.Insulin –lowers TG levels.Insulin activates lipoprotein lipase, an

enzyme that accelerates chylomicron degradation into glycerol and fatty free acids

2.Heparin- also brings down TG

Heparin stimulates the release of endothelial lipoprotein lipase into circulation ,and has been used without insulin to successfully manage HTG.

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

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.

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.

Fibrates Fibrates effectively lower triglyceride

levels by 40 – 60 % and raise HDL-C levels considered first line therapy for primary

HTG Niacin - is not as potential as fibrates but

can lower TG levels by 30 – 50 % 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 %

Hypertriglyceridemia is reported as causative in 1 – 4 % of patients who present with AP.

Secondary causes of HTG to be ruled out. 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.

Amylase level may be found to be normal in the presence of HTG >1000mg/dl.

THANK YOUTHANK YOU