1. ANATOMY OF THE PANCREAS
The Pancreas is also called abdominal tiger.
Pancreas is an elongated retroperitoneal organ 15-20cm in
length, it leis against L1-L2 vertebrae, lies posterior to
stomach, separated by lesser sac.
2. PARTS
• It is divided into head, neck body tail
1. Ducts of the pancreas; this is the main duct of the pancreas
It joins the bile duct in the wall of the second part of the
duodenum to form hepato-pancreatic ampulla also called
ampulla of vater (Herring bone pattern).
2. Accessary pancreatic duct (Duct of santorini) It begins in
the head and open the duodenum at minor duodenal papilla
(6-8cm) from the pylorus.
5. FUNCTIONS
1. Exocrine part which secrete pancreatic juice which helps in
digestion of proteins, carbohydrates and fats.
-Acini cells 99%
2. Endocrine part which constituted islets of the pancreas which is
distributed more numerous in the tail of the pancreas.
-B Cells of the islets which secrete insulin
-Alpha Cells secrete glucagon
6. PANCREATITIS
Pancreatitis is the inflammation of the grand parenchyma of
the pancreas.
For clinical purposes, It is useful to divide pancreatitis into
acute, which presents as an emergency, and chronic , which
is a prolonged and frequently lifelong disorder resulting
from the development of fibrosis within pancreas.
10. ACUTE PANCREATITIS
• Acute pancreatitis is defined as the development of the
acute inflammation of normally existing pancreas and is
usually associated with abdominal pain and raised pancreatic
enzymes.
Risk factors
Excessive alcohol consumption
Cigarette smoking and Obesity
Family history of pancreatitis
12. Organisms known to cause infections includes the following:
• Escherisha coli 35%
• Klebsiella 25%
• Enterococcus 28%
• Others;Staphylococci , Pseudomanas aeruginosa , Protues ,
Enterobacter , Anaerobes, Candida (10%)
13. Pathophysiology
• Teological philosophy says nothing but the existence of the almighty is
to be taken as axiomatic, yet the presence of the foprocesses will
always result in pancreatitis.
• The pathophysiology of acute pancreatitis is characterized by a loss of
intracellular and extracellular compartmentation, by an obstruction of
pancreatic secretory transport and by an activation of pancreatic
enzymes. In biliary acute pancreatitis, outflow obstruction with
pancreatic duct hypertension and a toxic effect of bile salts contribute
to disruption of pancreatic ductules, with subsequent loss of
extracellular compartmentation.
14. • Alcohol induces functional alterations of plasma membranes and
alters the balance between proteolytic enzymes and protease
inhibitors, thus triggering enzyme activation, autodigestion and cell
destruction.
• . Once the disease has been initiated, the appearance of interstitial
edema and inflammatory infiltration are the basic features of acute
pancreatitis. The accumulation of polymorphonuclear granulocytes in
pancreatic and extrapancreatic tissue, and the release of leukocyte
enzymes play an essential role in the further progression of the
disease and in the development of systemic complications.
15. • Activation of different cascade systems by proteolytic activity, and
consumption of alpha 2-macroglobulin further characterize the
severe clinical course of acute pancreatitis.
• The two major causes of acute pancreatitis are biliary calculi, which
occur in 50–70% of patients, and alcohol abuse, which accounts for
25% of cases. Gallstone pancreatitis is thought to be triggered by the
passage of gallstones down the common bile duct. If the biliary and
pancreatic ducts join to share a common channel before ending at
the ampulla, then obstruction of this passage may lead to reflux of
bile or activated pancreatic enzymes into the pancreatic duct.
16. • Patients who have small gallstones and a wide cystic duct may be at a
higher risk of passing stones. The proposed mechanisms for alcoholic
pacreatitis include the effects of diet, malnutrition, direct toxicity of
alcohol, concomitant tobacco smoking, hypersecretion, duct
obstruction or reflux, and hyperlipidaemia. The remaining cases may
be due to rare causes or be idiopathic.
17. Clinical features of Acute pancreatitis
Classified as mild, severe and fulminant attacks;
1. Sudden onset of upper abdominal pain , which is referred
to the back and relieved by leaning forward.
2. Vomiting, high fever, tachypnea with cyanosis, severe
illness.
3. Abdominal distension and ascites may be present.
Hiccough when present is refractory
18. Conti….
4. Often milder jaundice due to cholangitis and other biliary
tract obstruction diseases.
5. Feature of shock and dehydration.
6. Oliguria, hypoxia and acidosis.
7. Haematemesis /malena due to duodenal necrosis, gastric
erosion , decreased coagulability /DIC.
8. Neurological derangements due to toxaemia , fat embolism,
hypoxia, ADs, milder psychosis to coma
19. On Examination
1. Tenderness, Guarding, rigidity.
2. Blumberg’s sign, Grey-Turner ‘s sign, Cullen’s sign, Fox sign.
3. Pleural effusion, pulmonary oedema , consolidation.
4. Features of rapid onset of ARDS is seen.
5. Paralytic ileus is common.
6. Chvosteck and Trousseau’s sign
25. Treatment
conservative Rx
• ABC - initiate IV lines
• Rehydration (250-400ml/hr of R/L or N/S, Dextrose saline,
plasma and fresh blood transfusion/ packed cells).
• Pain relievers e.g Pethidine and or others except Morphine.
• Severe haemorrhage episodes; Fresh frozen plasma and
platelet concentration (DIC and
26. Haemorrhage)
• NG aspiration, urinary catheterization to maintain and
monitor urine output 50ml/hr.
• Antibiotics like third generation cephalosporins ; Imipenem ,
Meropenem , Cefuroxime , Ceftriaxone and Cefotaxime.
• Calcium gluconate 10ml IV 8th hourly – hypocalcaemia.
27. • IV Ranitidine 50mg TDS or IV Omeprazole 40mg BD or IV
pantoprazole 80mg BD (stress ulcers and erosive bleeding ).
• Monitor arterial venous pressure line.
• Haemodialysis –Renal failure.
• Somatostatin/Octreotide –reduce pancreatic secretions.
• Steroids in initial phase – shock and respiratory ditress.
28. • Nasojejunal tube placement and feeding.
• Anti-cholinergics, Protease inhibitors and calcitonin.
29. Surgical management
• Laparotomy followed by;
• Percutaneous drainage
• Surgical drainage
• Open surgery is the gold standard for infected pancreatic necrosis.
• Laparotomy-necrosectomy
• Endoscopic necrosectomy
• Endoscopic retrograde cholangiopancreatography associated with
endoscopic sphincterotomy.
• Cholecystectomy
33. CHRONIC PANCREATITIS
• Chronic pancreatitis defined as progressive inflammatory
disease , in which there is irreversible destruction of
pancreatic tissue.
• It is usually progress with severe epigastric pain radiating to
the left shoulder and relieved by leaning forward.
• During the course of disease ,later lone ,there is exocrine and
endocrine pancreatic insufficiency.
34. Aetiology
Alcoholism ; 5-10% of 60 -70 cases of those who develop the
condition with alcohol intake.
Genetic and metabolic factors
Pancreatic duct obstruction resulting from stricture
formation of trauma.
After acute pancreatitis and Hereditory pancreatitis.
Pancreatic carcinoma on the duct and infantile malnutrition.
Pancreatic divisum and annular pancreas. Also Idiopathic
35. Clinical features of chronic pancreatitis
• Pain (epigastric and right subcostal pain with dull and gnawing
character)
• Nausea
• Weight loss ,and
• Others as in acute form type
37. Medical treatment of chronic pancreatitis
Treat the addiction; help the patient to stop alcohol
consumption and tobacco. Involve a dependent counsellor
or psychologist
Alleviate abdominal pain; Eliminate obstructive factors
(duodenum , bile duct , pancreatic duct) ,Escalate analgesia
in a stepwise fashion, for intractable pain , consider CT/EUS
–guided coeliac axis block.
38. Nutritional and pharmacological measures
-Diet ; low in fat and high in protein and carbohydrates
-Pancreatic enzyme with supplementation with meals
- Correct malabsorption of the fat-soluble vitamins and
vitamin B12
-Micronutrient therapy with methionine, vitamin C and E,
Selenium(may reduce pain and slow disease progression).
39. -Steroids (only in autoimmune pancreatitis, for relief of symptoms)
-Medium-chain triglycerides in in [patient with severe fat
malabsorption
- Reduce gastric secretions may help
Treat diabetes mellitus.
Surgical management
Pancreatico-jejunostomy
Necrotectomy
•
40. “Working together is essential for success ;Even freckles would make a
nice tan if they would get together”
41. References
• SRB’S Manual of surgery ,4th Edition. Chapter, 14,page 725.
Sriam Bhat M Ms (GENERAL SURGERY)
Jaypee Brother medical publishers (p) LTD
New Delhi.Panama City. London.phidadelphi (USA)
• Bailey’s and Love’s SHORT PRACTICAL OF SURGERY .26th Edition.
International student’s edition.
• D’Edigio A, Schein M. Surgical strategies in the treatment of
pancreatic necrosis and infection.Br J Surg.
