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PANCREAS

In this disease of pancreas and types symptoms clinical feature and management

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Shivam Antil
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0% found this document useful (0 votes)
6 views16 pages

PANCREAS

In this disease of pancreas and types symptoms clinical feature and management

Uploaded by

Shivam Antil
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
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PANCREAS

 Reteroperitoneal.

 15-20 CM.

 Head, neck, body, tail.

 Ducts –

• Main – Duct of Wirsung – joins the bile duct in the wall of 2nd part of duodenum to
form hepatopancreatic ampulla (of vater).

• Accessory – Duct of Santorini – opens into duodenum at the minor duodenal papilla
– 6-8 cm from pylorus.

Arterial supply –

1. Pancreatic branches from splenic artery.

2. Superior pancreaticoduodenal artery.

3. Inferior pancreaticoduodenal artery.

Venous drainage – Portal vein.


Functions –

Exocrine –

Digestion of proteins, carbohydrates and fats.

Endocrine –

Islets of pancreas – α cells – glucagon, β cells – insulin.

Serum amylase – normal – 200 to 250 somogyi units.

Pancrease - amylase isoenzyme - P

Salivary gland - amylase isoenzyme - S

 1000 units –(amylase isoenzyme - P) acute pancreatitis.

Amylase level raised -

common in acute pancreatitis, pseudocyst of pancrease, pancreatic trauma etc.

Other conditions -

Salivary gland diseases, mesenteric ischemia, ruptured aortic aneurysm, intestinal obstruction,
ectopic gestation, salpingitis, perforated duodenal ulcer

Serum lipase also increase in acute and chronic pancreatitis.

Pancreatitis -

• Classification –

1. Acute pancreatitis.

2. Acute relapsing pancreatitis.

3. Chronic relapsing pancreatitis.

4. Chronic pancreatitis.

Acute – acute inflammatory reversible changes.

Chronic – chronic continuous morphologically irreversible changes.

Defn – development of acute inflammation in normaly existing pancreas.

MC cause – biliary tract disease.

Pathogenesis – biliary stone induced pancreatic ductal obstruction (MC) and ductal hypertension.

Other causes – duodenal ulcer, crohn’s, duodenal periampullary ulcer/tumour, trauma,


pancreatic duct stricture, pancreatic divisum, ascariasis, Clonorchis sinensis.

Alcohol – direct toxicity, hypersecreation of gastric and pancreatic juices, reflux, plugging of
pancreatic proteins, spasm of sphincter of Oddi etc
Types of acute pancreatitis –

1. Interstitial acute pancreatitis (mortality – <1%).

2. Necrotisitng pancreatitis –
A. Sterile (mortality – 10%).

B. Infected (mortality 30-40 %) – CT guided aspiration and gram staining – if positive –


pancreatic necrosectomy.

Organism –

 Polymicrobial – 60 %.

 E coli (35%), Klebsiella (25%), enterococcus (25%).

C/F –

• Sudden onset, acute abdominal pain, referring to back.

• Severe, agonising, refractory , relieves/ reduced on leaning forward.

• Vomiting, high fever, tachypnoea with cyanosis.

• Tenderness, rebound tenderness, guarding, rigidity, abdominal distension, severe illness.

• Mild jaundice (cholangitis, bile duct disease, obstruction)

• Shock and dehydration.

• Oliguria, hypoxia.

• Grey turner’s sign/ culen’s sign/ Fox sign.

• Haematemesis/ melaena (duodenal necrosis, gastric erosion, DIC).

• Refractory hiccough.

• Ascites, paralytic ileus.

• Pleural effusion, pulmonary edema , ARDS.

• Neurological symptoms – psychosis/ coma.

• Hypovolemia.

• Hypoalbuminaemia.

• Leucocytosis with neutrophilia.

• Thrombocytopenia.

• Hyperglycaemia.

• Hyperbilirubinaemia.

Investigations –

• Serum amylase > 1000 somogyi units.

• Serum lipase.

• Serum trypsin.

• Trypsinogen activation polypeptide, CRP, Phospholipase A2.


• LFT.

• Blood urea, serum creatinine.

• Blood glucose.

• Serum calcium.

• Arterial PO2 and PCO2.

• Total count, PCV, Platelet counts, coagulation profile.

• Peritoneal tap – amylase, lipase and protein levels.

• Plain X-Ray –

• Sentinel loop – dilated proximal bowel loop.

• Colon cut off sign – distension of transverse colon with collapse of descending colon.

• Air – fluid level in duodenum.

• Renal halo sign – edema around the kidney.

• Obliteration of psoas shadow.

• Localised ground glass appearance – in actue hemorrhagic pancreatitis.

• USG abdomen.

• Spiral CT

• CT guided aspiration – stain and culture.

• MRI, MRCP.

• ERCP.

• Chest X-ray – for effusion and ARDS.

• EUS

Treatment of acute pancreatitis –

1. Conservative (70-90%).

2. Surgical (10-30 %).

3. M/M of complications –

1. Local – pseudocyst / abscess / fistula / haemorrhage.

2. Systemic – ARDS, renal failure, MODS.


Surgery –

• Indications –

1. Patient deteriorates on conservative M/M.

2. Pancreatic abscess, infected necrosis.

3. Diagnosis in doubt.

4. Severe nectrotising pancreatitis.

Surgery –

• Open surgery – gold standard.

• Necrosectomy + wide debridement + adequate drainage + cholecystectomy + closure in


layers.

• Open method – laparotomy + necrosectomy + wide debridement + wash + wide packing +


open wound for repeated wash and packing till healthy granulation tissue develops.

• Closed continuous peritoneal lavage / extraperitoneal lavage can be used.

Complications and its management –

1. Acute fluid collection –

• Peripancreatic, rarely intrapancreatic.


• 50% regress spontaneously, rest form pseudocyst.

• CT guided aspiration at one puncture site to confirm absence of abscess.

2. Acute pseudocyst –

• Collection of fluid with pancreatic juice near pancreas with thin fibrin wall and granulation
tissue.

• Forms in 2 weeks – resolves spontaneously .

• Percutanous fluid removal under guidance / endoscope.

Pancreatic pseudocyst –

• Lined by granulation tissue (not true cyst).

• Common in peripancreatic region, in lesser sac

• 4 weeks post attack – chronic entity.

• Usually sterile.

• May rupture – pancreatic ascites.

• Pancreatico - pleural fistula.

4. Pancreatic necrosis –

• Focal/diffuse area of non-viable pancreatic parenchyma with peripancreatic fat


necrosis.

• Initially sterile – eventually infected.

• Paste / putty like material.

• Fate – pseudocyst, abcess , fibrosis.

• CT guided aspiration and culture.

• Repeated laparotomy with debridement and jejunostomy.

5. Pancreatic abscess –

• Collection of pus in lesser sac.

• May slough off pancreatic / splenic vessels – torrential bleed.

• Single / multiple.

• May rupture into viscera, extend into other part of abdomen.

• Features of sepsis, tender palpable mass epigastrium, leucocytosis.

• t/t – antibiotics , percutaneous U/S or CT guided aspiration and drainage , or open drainage.

6. Respiratory complications -

• Severe and life threatening.


• Due to distension of abdomen, diaphragmatic elevation, pleural effusion,
intravascular coagulation in lungs and ARDS.

• ABG done , ventilatory support.

7. Pancreatic pseudoaneurysm –

• Enzymatic (elastase) dilatation of wall and aneurysmal dilatation – splenic vessels (50%),

- gasteroduodenal vessels (15 %),


pancreaticoduodenal arteries (10%)

• May rupture in gut – massive upper GI bleed, in pancreas – haemosuccus pancreatitis.

• CT angiogram.

• Critical care, BT, emergency angiographic embolization, open surgery and ligation – high
mortality.

8. Pancreatic fistula –

• Due to ductal wall disruption and necrosis or after surgical necrosectomy.

• Into bowel , or into skin.

• Low (<200 ml) or high (>200 ml) output.

• Confirmed by biochemical analysis, ERCP, CT fistulogram.

• If persists > 6 months – sphincterotomy + resection of fistula + pancreatic resection +


pancreaticojejunostomy.

Pseudocyst of pancreas

• Localised collection of sequestered pancreatic fluid usully 3 weeks after acute pancreatitis,
recurrent chronic pancreatitis and trauma.

• Usually lesser sac adjacent to stomach.

• 50% of acute pancreatitis leads to pseudocyst, 20-40% resolves spontaneously.

• Types –

• Communicating.

• Non-communicating

• Acute.

• Chronic.

D’ Egidio classification –

• Type I – After acute pancreatitis, Normal duct anatomy, no fistula/communication.

• Type II – after acute on chronic pancreatitis, abnormal duct anatomy, 50 % chances of fistula.

• Type III – after chronic pancreatitis, abnormal anatomy with stricture, always
communicating.
Gross pathology –

• Cyst wall initially thin , matures to thick (formed).

• Lined by fibrin , no endothelium – so pseudocyst.

• Brownish fluid with sludge like necrotic material.

• High amylase levels - > 5000 SI.

• If infected – pancreatic abscess.

C/F –

• Swelling epigastrium,

• hemispherical,

• smooth, soft,

• not moving with respiration, not mobile,

• upper margin diffuse , lower margin – well defined,

• resonant/ impaired resonant,

• transmitted pulsation confirmed by knee-elbow position.

• Infected – tender mass, toxic look , fever with chill and rigor.

• Stomach is stretched towards anterior abdominal wall, ryle’s tube will be felt per abdomen –
BAID TEST.

• D/D –

• Aortic aneurysm.

• Retroperitoneal cyst/tumour.

• Cystadenocarcinoma of pancreas.

• Cyst of liver.

• Mesenteric cyst.

• Hydatid cyst.

Investigation –

• USG abdomen -< 6 cm conservative.

• CT scan.

• MRCP – ductal anatomy.

• ERCP – for communication.

• LFT, serum amylase.

• EUS guided aspiration and analysis of fluid for amylase and CEA. High amylase – pancreatic
pseudocyst, high CEA mucinous neoplasm.
CHRONIC PANCREATITIS

Risk factor classification 2001 –

• Toxic – alcohol/tobacco/dietary/drug.

• Metabolic – hypercalcemia.

• Idiopathic.

• Genetic mutations.

• Autoimmune disease.

• Recurrent ischemia.

• Obstructive – stenosis at papilla, duct stone.

Classification –

1. Based on main duct –

1. Large duct disease.

2. Small duct disease.

2. Staging -
A. No complication, no steatorrhoea, no IDDM.

B. Complication present , but no steatorrhoea, no IDDM.

C. 1. Endocrine function impairment - IDDM.

2. Exocrine functions impaired – steatorrhoea.

3. 1+2+complications.

C/F –

• Pain – persistent , radiates to back, diminishes over years – pancreatic burnt out.

• Exocrine dysfunction – steatorrhea, malabsorption, diarrhoea.

• Endocrine dysfunction – IDDM

• Mild jaundice.

• Mass per abdomen.

• Mallet-guys sign – in right knee-chest position if left hypochondrium is palpated tenderness


can be evoked.

Investigations –

• CT abdomen – may see a pseudocyst, calcification, ductal stones - strictures - dilatation,


fibrosis.

• ERCP

• MRCP

• EUS

• Secretin cholecystokinin test – overnight fasting,

- double lumen tube is placed in duodenum,

- gastric and duodenal juices are aspirated,

- continuous IV secretin 1 u/kg/hr and CCK are infused for 90 minutes.

- Duodenal sample is checked every 10 minutes for volume, HCO3, amylase, lipase, protease.

• LFT.

• Serum trypsinogen.

• Fecal elastase.

T/t –

• Conservative –

 Avoid alcohol.

 Low fat , high protein diet, small frequent meals.

 Pancreatic enzyme supplement.


 Analgesics.

 Sugar control.

 For steatorrhoea – PPI+lipase and low fat ;diet.

Endoscopic therapy –

• Pancreatic duct sphincterotomy.

• Stone extraction.

• Stricture dilatation and stenting.

Surgeries –

• Puestow’s operation – duct opening , removal of all stones, and anastomosis to jejunum.
Spleen removed.

• Whipple’s procedure – if pancreatic head is injured.

CARCINOMA PANCREAS

• Males.

• 80% are metastatic at the time of diagnosis.

• 60-65 years.

• Aetiology –

• Smoking.

• High energy diet rich in fat.

• Chronic pancreatitis.

• Familial pancreatitis.

• Diabetes mellitus.

• Carcinogens like benzidine, DDT.

• Hemochromatosis with pancreatic calcification.

• Chirrhosis, obesity.

• Previous cholecystectomy.

• Peutz jegher syndrome, hereditary nonpolyposis colonic cancer.

• Head and neck.

• Ampullary/ periampullary.

• Body and tail - 30%

Periampullary carcinoma –
 Tumour arising at or near ampulla.

 Adenocarcinoma from head of pancreas (50%)

 Tumour of ampulla of vater (30%)

 Distal bile duct carcinoma (10%)

 Duodenal carcinoma adjacent to ampulla (10%)

Pathology –

Gross –

• Grayish white scirrhous nodular gritty tumour.

• > 3 cm size – nodal and distant spread .

• Hmg, necrosis, induration.

• Dilated pancreatic duct.

Microscopy –

• Malignant cells with variable degree of differentiation, fibrosis, halo around tumour due to

obstruction of the adjacent ducts by tumour leading to chronic pancreatitis in proximity.

• Vascular and lymphatic spread with perineural invasion.

• Colloid, signet cells, squamous, adenosquamous, adenosquamous, anaplastic, sarcomatoid.

Spread –

• Local spread – duodenum, portal vein, superior mesenteric vein, reteroperitoneum,


perineural spread.

• Nodal spread – perihepatic nodes – hard dark greenish nodes.

• Distant spread – liver , lung adrenal, brain, bone.

Clinical features –

• Jaundice and weight loss.

• Cystadenocarcinoma – pain and mass abdomen.

• Jaundice – short duration, severe , progressive, associated with pruritis.

• Back pain – due to involved reteropancreatic nerves, more in night, after food and
recumbency, relieved on leaning forward.

• Diarrhoea, steatorrhoea, acholic stool, tea coloured urine.

• Silvery stool – mixing of undigested fat with metabolised blood oozed from tumor.

• Scratch mark on back.

• Migratory superficial thrombophlebitis – trousseau’s sign.

• Ascites.
• Left supraclavicular lymph node.

• Blumer’s self.

• Palpable gall bladder – non tender, soft, globular , smooth, moves with respiration, moves
horizontally, dull on percussion, - Courvoisier’s law.

• Enlarged liver – hydrohepatosis/ secondaries.

• Splenic vein thrombosis with splenomegaly (10%).

INVESTIGATIONS –

• LFT – high conjugated billirubin (van den Berg’s test), low albumin with altered A;G ratio, PT
is widened, increased serum ALP.

• USG abdomen – GB, liver, CBD > 10 mm dia. , LN status, portal vein, ascites.

• Barium meal shows widened duodenal “C” loop – pad sign, Reverse 3 sign is seen in
carcinoma- periampullary region.

• Spiral CT – portal vein infilteration, retro peritoneal LN, size of the tumour.

• ERCP with pancreatic juice cytology or brush biopsy is useful, MRCP to see biliary tree.

• CA 19-9 – tumour marker, CEA – cystadenocarcinoma.

• Coeliac and superior mesenteric angiogram – tumour invasion.

• Gasteroduodenoscopy – biopsy.

• Endosonography guided FNAC.

• Urine – bile salts (Hay’s test), bile pigments (fouchet’s test), urobilinogen.

• Staging laparoscopy.

• CT angiogram.
M/M –

Preoperative preparation –

1. Hydration.

2. Pre-op glucose.

3. Pre-op mannitol.

4. Inj. Vit. K.

5. ERCP stenting to drain bile.

6. Pre-op antibiotics and TPN.

7. PFT and pulmonary physiotherapy.

T/T –

• 10-20% is operable.

• Criteria for resection –

1. < 3cm.

2. Periampullary tumours.

3. Growth not adherent to portal system.

Operable cases

• Whipple’s operation – removing –

1. Head and neck of pancreas.

2. C-loop of duodenum.

3. 40% of distal stomach.

4. 10 cm proximal jejunum.

5. Lower end of common bile duct.

6. gall bladder.

7. Peripancreatic.

8. Pericholedocal, perihepatic and paraduodenal LN.


Continuity -

A. Pancreaticogasterostomy.

B. Pancreaticojejunostomy.

C. Gasterojejunostomy.

Total pancreatectomy with nodal clearance.

Inoperable cases – to palliate obstructive jaundice, duodenal obstruction and pain.

B. Cholecystectomy with gasterojejunostomy and roux-en-Y choledochojejunostomy.

C. ERCP and stenting to drain bile.

D. Chemotherapy, neo-adjuvant chemotherapy.

E. Enzymes for steatorrhoea, control of diabetes.

Adjuvent therapy –

• Chemotherapy – gemcitabine.

• Radioactive iodine.

• Immunotherapy.

• Neoadjuvent chemoradiotherapy.

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