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SURGICAL CONDITIONS OF THE
PANCREAS
OBJECTIVES
1. To have a knowledge of surgical conditions
of the pancreas.
2. To diagnose and treat patients with surgical
conditions of the pancreas.
3. To be able to counsel the patient, the
guardian and/or the family about the
diagnosed surgical problem of the pancreas
Outline
• Introduction
• Congenital abnormalities of the pancreas
• Injuries to the pancreas
• Pancreatitis
• Tumors of the pancreas
introduction
• The name pancreas is derived from the Greek
“pan’’ (all) and “kreas’’( flesh).
-The gland weighs approx. 80gms.
-Is situated retroperitoneally
-It is divided into: head, neck, body and tail
-It overlies the body of the 2nd.lumbar vert. and the aorta.
-It is composed of mainly 2 types of cells (exocrine acinar cells &
endocrine cells known as Islets of Langerhans)
-the exocrine cells secret: cholecystokinin, amylase, lypase, elastase &
chymotrypsine
-the endocrine cells (Islets of Langerhans) secret : glucagon(alpha),
insulin(Beta), somatostatine(Delta) and gastrin(D cells)
Congenital Abnormalities of The
Pancreas
1. Cystic fibrosis (generalized dysfunction of
exocrine glands)
2. Hypoplasia
3. Annular pancreas(failure of complete rotation of
the ventral pancreatic bud during development ,
so that a ring of pancreatic tissue surrounds the
2nd. or the 3rd. part of the duodenum).
4. Ectopic pancreas(sub mucosa of stomach,
duodenum , Gb. hilum of the spleen, in the liver
etc.
5. Cystic disease of the pancreas
Investigations to be done in suspicion of any pancreatic disease
I. To measure pancreatic damage: is achieved by measuring
levels of pancreatic enzymes in body fluids: (amylase,
lypase, trypsin & chymotrypsine)
II. To measure pancreatic function : is achieved by measuring
bicarbonate &enzymes in the pancreatic juice :
1-indirect method of Lundh done by duodenal intubation
2-secretin-pancreozymin test (triple lumen tube)
3-glucose tolerance test
III. To detect morphologic abnormalities of the pancreatic
parenchyma & ducts :(cytology of the pancreatic juice, U/S,
EUS CT-scan, MRI, ERCP ,plain abd. X-ray & CxR
injuries to the pancreas
1. External injuries :
A) Direct blunt trauma
 Blow during automobile/bicycle accident
 Unexpected punch on a relaxed abdomen
The neck of the gland is the most affected.
B) Penetrating injury which usually involves the
stomach, duodenum, colon ,liver or spleen.
2. Iatrogenic injuries :occur in 4 ways
-injury to the tail (splenectomy)
-injury to accessory duct (Santorini)
-fistula (after enucleation of islet cell tumors)
-during sphincterotomy
Clinical presentation
• Hx. Of trauma
• Epigastric pain
• Investigations :
Serum amylase (rises in 90% of the cases)
Abdom. u/s
CT. Scan/MRI
Treatment
• If no overt bleeding OR if bleeding(after
controlling the bleeding):
Drain
NPO
Parenteral support
• If body transection :distal resection
• Repair (usually coarses with high incidence of
fistulization)
Prognosis
• Bleeding from the site of rupture is the most
common cause of death.
 in blunt trauma if there is an associated injury
(duodenum),the mortality rate is 16-28%
In penetrating injury with associated injuries
to the surrounding organs , the mortality is
approximately 50%.
Pancreatic fistulas
Problems:
1. High fluid and electrolytes loss (2 lts./24hrs.)
2. Auto digestion of the pariets
3. Collection of fluid around the gland
TREATMENT
1. If pancreatic duct is intact :conservative Rx.:
 Replace fluid & electrolytes by mouth/iv
 Use somatostatine analogue
 High protein & low carbohydrate diet
 Total Parenteral nutrition
 Zinc oxide cream on the skin
 Percutaneous drainage of the peripancreatic fluid (if
collection)
2. If the duct is totally disrupted :Resection
PANCREATITIS
• Definition : is an inflammation of the gland's
parenchyma.
• Classification : there are 2 useful ways of
classification.
1. According the clinical presentation of the disease
2. According to the etiology of the disease
CLASSIF. According the clinical
presentation
1. Acute pancreatitis
2. Relapsing acute pancreatitis
3. Chronic pancreatitis
The acute and the relapsing acute pancreatitis return to
normal when the primary cause is removed .
The chronic pancreatitis remain with functional/structural
damage even after removal of the primary cause.
CLASSIF.according to the etiology
• Biliary tract disease
• Alcoholism
• Post operation
• Traumatic
• Rare causes (mumps ,hyperparathyroidism ,vascular
diseases, etc. )
• Idiopathic
This classification according to the etiology of the disease
is very important in relating the natural Hx. of the
disease to :
-prognosis
-long term Rx.
-prophylaxis
ACUTE PANCREATITIS
• INCIDENCE :the same in both sex , despite the age
difference(men 30-40yrs.& women 50yrs.)
• Etiology :
 Biliary calculi(50%)
 Alcoholism(25%)
 Post Biliary/gastric surgery
 Trauma (blow to the pancreas)
 Distortion of ampulla of Vater (PUD, ampullary Ca.
 Generalized disorders(hyper calcemia, hyperlypemia,
DM. porphiria)
 Drugs (coticosteroid,ART)
 Viral infections (mumps)
 Auto immune disorders(poly arthritis nudosa)
 After impaired pancreatic blood flow (cardiopulm. by
pass , hypothermia)
Clinical features of acute pancreatitis
• Severe epigastric pain
• Anorexia
• Nausea & vomitings
• By p/e :
 Fever (60%)
 Tachycardia & tachypnea (50%)
 Jaundice (10%)
 Eccymotic discoloration of the flanks (Grey Turner’s sign)
 Eccymotic discoloration of the periumbilical area (Cullen’s
sign)
 Abdominal guarding
Investigations
1. Routine & LFT, RBS, RFT(blood urea),serum calcium
2. Serum amylase
 Elevates in few hrs. & declines after 48hrs.
3. Lipase
 Starts to rise after 48hrs.
4. Plain abd. X-ray
 Sentinel loop (distended loop of SB in the LUQ.)
 Duodenal distention
 Colon cut-off sign (distended transv.colon with collapsed descending
colon)
5. Abd. U/S
6. CT-Scan/MRI
7. MRCP
8. ERCP
9. EUS
10. CxR
Ranosn's criteria to identify high risk patients (severity of the
disease)
The coarse of this disease varies from mild to fulminant
depending on Ranosn’s criteria :
1. Old age (>55yrs.)
2. Rise in blood sugar ( >10mmol)
3. WBC (elevated) (>16,000)
4. LFT (deranged )
5. Blood urea ( >5mg%)
6. Hypocalcaemia (<2mmol)
7. Hct. (low )
8. Spo2 (<60mmHg )
9. Volume of 3rd. Space fluid collection(extra vascular space)
(ascitic fluid, pleural effusion edemas, etc.)
NB: the disease is severe when 3 or more factors are present
Treatment of acute pancreatitis
• Bed rest (admission to ICU)
• NPO
• Iv fluids (aggressive fluid rehydration)
• Frequent monitoring of v/s , diuresis, RFT, LFT blood gases, clotting
factors
• oxygenation
• NG. tube
• Analgesics (pethidine + antispasmodic drug)
• Anticolinergics (to reduce pancreatic secretion):somatostatine,
glucagon,calcitonin,etc.
• Regular RBS dosifications
• Regular serum calcium dosifications
• Antibiotics
• Endoscopic sphincterotomy (if jaundice due to stone)
• Surgery urgently (if does not solve within 7 days, after repeating
U/S & CT-scan to R/O local complications)
• Investigation , identification & Rx. of underlying causes:
 Cholecystectomy within 1 month after the acute phase.( if Gb. stone)
Complications of acute pancreatitis
1. Hypovolemic shock:
 GI fluid loss
 3rd. Space collection
 Retroperitoneal hemorrhage
2. Pulmonary insufficiency due to :
 Retroperitoneal edema
 Elevation of the diaphragm
 Reduced ventilation due to pain
 DIC
3. Infection (3%) : secondary infection of necrotic tissue in pancreatic
bed 1 or 2 weeks after the initial attack).
4. Electrolytes disturbances (hypocalcaemia) 3-30%) :
 Binding of calcium in areas of fat necrosis
 Raised levels of glucagon & calcitonin
 Deficiencies in parathyroid hormone
5. Colonic stricture (scaring of transv. Colon & its meso)
6. Pancreatic pseudo cyst
Prognosis of acute pancreatitis
• Depends on the severity of the disease:
1. Edematous pancreatitis : 3-10% of death
2. Necrotizing pancreatitis : 40-50% of death
3. Totally necrotized : 100% of death
Chronic pancreatitis
Definition : is an incurable, chronic inflammatory
condition that is multifactorial in its etiology, highly
variable in its presentation and a challenge to treat
successfully.
Incidence :
– more frequent in men (4:1)
– Mean age : 40yrs.
Etiology:
Alcohol consumption with high protein and fatty diet
Pancreatic duct obstruction (post- traumatic, pancreatic
Ca. cystic fibrosis, infantile malnourishment, idiopathic
causes)
Stenosis of the ampulla of Vater
Clinical features of chronic pancreatitis
Epigastric pain (93%) with exacerbation by
alcohol intake & referred to the LUQ
(29%),RUQ(44%)&through to the back(56%)
Weight loss (due to loss of appetite and
malabsorpsion
DM.(late)
P/E : is usually non revealing, but there can be:
-jaundice (CBD narrowing)
-tender hard mass (cystic/Ca )
Investigations for ch. pancreatitis
1. Lundh test / secretin-pancreozymine test: abnormal
2. Lactoferrin level in pancreatic juice obtained by ERCP (elevated):
indicating calcifying ch. pancreatitis
3. Stool analysis : steatorrhea in 30% of the cases
4. Plain abdom. X-ray (calcifications in 65%)
5. U/S of the abdomen :enlarged pancreas with cysts & dilated
ducts.
6. CT-scan /MRI :to confirm and R/O other causes of pain in the
retroperitoneal area.
7. ERCP :can demonstrate ductal / papillary stricture & the extent of
the disease if amenable to surgical Rx
8. MRCP
9. EUS
TREATMENT OF CH. PANCREATITIS
 Diet (low in fat & high in protein and carbohydrates)
 No alcohol neither tobacco
 Pancreatic enzyme supplement
 Vit. Supplement (A, D, E, K Vit.B-12) with medium chain
triglycerides
 Strong analgesics
 Splacnic (Celiac) nerve block :CT / EUS guided
 Rx. for DM.(usually insulin)
 SURGEY (based on results of pancreatogram & CT-scan/MRI):
is done when the disease is not controlled by
medical Rx. :
-if head is normal : distal pancreatectomy
-if head is involved : pancreatoduodenectomy
-if the whole gland is affected : total pancreatectomy
Complications of ch. pancreatitis
1. Ch. Pseudo cyst
2. Pancreatic ascites
3. Pancreatic-enteric fistula
4. Pancreatic head ch. Inflammatory mass
5. Splenic and portal vein thrombosis
6. Pancreatic Ca.
Prognosis of ch. pancreatitis
1. Drainage / excision procedures : provide
relief from pain in 75%
2. The quality of life is good if :
– DM. & steatorrhea is controlled
– Abstains from alcohol and / or tabbaco
Pancreatic pseudocyst
Definition :a chronic collection of pancreatic
fluid surrounded by a non epitelized wall of
granulation tissue and fibrosis
Incidence :
-occurs in up to 10% of acute pancreatitis
-occurs in 20-39% of ch. pancreatitis
Clinical features of pancreatic
pseudocyst
• Hx. of pancreatitis
• Palpable epigastic mass
Classification of pancreatic pseudocyst
1. Acute pancr. Pseudocyst :
 Pancreat. duct leak of pancreatic juice surrounded by
a wall of acute granulation tissue without much
fibrosis
 Occurs within 3-4 weeks of the attack
 May resolve spontaneously up to 50% over a coarse of
6 weeks or longer
2. Ch. Pancreatic pseudocyst :
 is a collection of pancreatic juice surrounded by a wall
of ch. granulation tissue and fibrosis
 Usually persists for >6weeks
complications of pancreat. pseudocyst
1. Secondary infection (abscess)
2. Compress adjacent organs / structures
3. Erode into visceral arteries and cause
intracystic hemorrhage/pseodo. aneurisms
4. Perforate and cause
peritonitis/intraperitoneal hemorrhage
Treatment of pancreatic pseudocyst
A. Asymptomatic: is based on expectant Rx.
-may solve spontaneously or
persist w/o complication.
B .Symptomatic (pain, fullness, early satiety or
enlarging ) :
-Percutaneous aspiration(U/S or CT-scan
guided
-Internal drainage
 Endoscopical placement of stents
 Surgical (cystoenterostomy, cystoduodenostomy,
cystogastrostomy, resection of the cyst, distal
pancreatectomy, etc.)
Cancer of the pancreas
are of 2 types :
1. Cancer of the exocrine
2. Cancer of the endocrine
Cancer of the exocrine pancreas
• Incidence :
Affects men and women equally
Occurs more in elderly
About ½ of all patients are>75yrs. old
• Pathology & etiology :
>75% are adenocarcinoma of ductal origin
Some are multicentric in origin
There is slight preponderance of tumor arising in the
head & neck of the gland
Associates with :
tobacco smoking
high protein & fatty diet
ch. pancreatitis
Clinical features of Ca. of the exocrine pancreas
• Nonspecific symptoms such as :
Weight loss
Pain to the right/left of epigastrium
Back pain
Anorexia
Jaundice & pruritus (2/3 of pancr. Head tumor)
• Physical exam. :
Generalized wasting
Hepatomegally (50%)
Courvoisier’s sign :palpable Gb in 30% of the pancr.
head tumor and 50% of the ampullary tumors
Splenomegally (due to Splenic vein thrombosis)
Investigations
1. Routine investigations
2 . Diagnostic investigations :
 LFT (alk. Phosph. Elevated)
 Cytology of the pancreatic juice obtained by ERCP
 Hypotonic duodenogram (inverted 3 sign ,widened
duodenal loop, irregular duodenal mucosa)
 Abdominal U/S (pancr. mass with dilat.of pancr.
duct,GB,CBD &hepatic mets.)
 CT-scan / MRI (pancr. mass , hepatic mets. ,L/nodes
 Duodenoscopy with BIOPSY in cases of ampullary
tumors.
 ERCP & pancreatogram (sharp duct occlusion)
 Transgastric or transduodenal FNAC or Tru-Cut biopsy
under EUS
 Tumor marker CA19-9
Treatment of Ca. of the exocrine
pancreas
More than 80% of the cases are beyond surgical
resection on presentation due to :
-local spread
-paraaortic & mesenteric L/nodes
-hepatic mets.
-advanced age of the patient
Generally , the Rx can be :
1. Palliative
2. Surgical resection
Palliative Rx.
• Is given for about 95% of all cases of
pancreatic Ca.
• Is based on :
– Strong analgesia (opiates) for pain
– Pancreatic supplements for weight loss
– Endoscopic stenting of the CBD through ERCP
– Biliary bypass(80%) :
• Choledochoduodenostomy
• cholecystojejunostomy
Surgical resection
• Is indicated in tumors of <3cms.and mostly
situated near the ampulla, if technically feasible
and in fit patients.
• Is not indicated in tumors of >5cms.and when the
tumors are located in the pancreatic body
• When resection is possible, one of the following
procedures can be done:
1. Pancreatoduodenectomy (Whiplle’s procedure)
2. Regional pancreatectomy (Fortner)
3. Total pancreatectomy
Prognosis of the exocrine pancreatic Ca.
1. Median survival : 6months from the time of
diagnosis
2. Patients with ampullary tumor who undergo
resection :5yrs. (30%)
3. The surgical resection has mortality rate of
8%
Cancer of the endocrine pancreas
• General considerations :
 Comprise 1% of all pancreatic tumors
 Originate from the islets of Langerhans which contain 4
types of cells (alpha ,beta delta & gamma)
 The tumor of the B-cells is more common than the others’
(insulinoma)
 2/3 of the endocrine pancreas’s tumor occur in the body or
tail of the gland.
 1/3 of them are multiple
 Most of them are malignant but have favorable coarse than
the exocrine pancreas tumors
 The cancers of the islets of Langerhans can be associated
with similar lesions in other endocrine glands (specially in
anterior pituitary, parathyroid, and adrenal cortex as
multiple endocrine adenomatosis.
Ca. of the endocrine pancreas
Classification:
I. Functionals :secret peptide products(excess
hormones)that produce clinical
presentations.
1. Insulinoma(Ca. of the Beta cells)
2. Gastrinoma(Ca. of the D cells)
3. Glucogonoma(Ca. of the Alpha cells)
4. Vipoma
5. Somatostatinoma(Ca. of the Delta cells)
II. Nonfunctionals : not associated with excess
hormone levels & are clinically silent.
Insulinoma(Whipple’s triad)
• Coarses with hyperinsulinism and attacks of
hypoglycemia at irregular intervals which
progressively increase in frequency & severity.
• Has 4 stages :
1. Stage I :simulate duodenal ulcer with vague abd.
pain which subsides by carbohydrates.
2. Stage II :coarses with trembling, sweating,
dizziness, blurring of vision & great hunger.
3. Stage III : sluggish mind, unarticulated speech,
uncoordinated movim. diplopia & sometimes
hallucinations.
4. Stage IV :looks like epilepsy / coma
Diagnosis of insulinoma
• Is done by:
1. Clinical features :Whipple’s triad (attacks of
hypoglycemia in fasting state, symptoms relieved by
glucose & glycemia <45mg/100ml.of blood).
2. Investigations :
 FBS
 Dosification of human insulin by
radioimmunoassay (elevated)
 Insulin stimulation & suppression tests
 Endoscopic U/S
 CT-scan /MRI
 Radionuclide scanning
Treatment of insulinoma
• Surgery solves 90% of the problem.
• Extirpation of the tumor aided by palpation or
by intraoperative U/S is done.
• Operative mortality is 2% .
Gastrinoma (Zollinger-Elisson syndrome)
Types : is of 2 types & is suspected in pts. With recurrent
multiple ulceration or when PUD appear in unusual
sites:
1. Type I : is rare & coarses with :
hypergastrinemia
ch. Peptic ulcerations
antral G-cell hyperplasia
2. Type II : coarses with :
intractable peptic ulcerations (often
jejunum)
hypergastrinemia (massive acid
secretion = 500ml/hr.)
diarrhea/steatorrhea
hypokalemia & about ½ are malignant
Investigations for gastrinoma
1. Acid secretion studies
2. Stimulation of circulating gastrin:
 Type I :increased gastrin levels by meat extracts
 Type II : increased gastrin levels by iv calcium 2mg/kg
in 1minute
3. Endoscopic U/S
4. CT-scan /MRI
5. Endoscopy
6. Radionuclide scanning (is done by iv injection of
radioactive somatostatine analogue, because
many of the endocrine pancreas tumors have
somatostatine receptors.)
Treatment of gastrinoma
• Type I :partial gastrectomy to remove the G-
cell bearing area
• Type II :
if tumor is detected : resection
If tumor is not detected :medical Rx. on the
basis of H2 receptor antagonists / PPI.
IF medical Rx. fails : total gastrectomy
49
Glucagonoma(cancer of the Alpha
cells)
• Coarses with DM , dermatitis and
malnourishment.
• Usually is localized in the body or in the tail of
the gland.
• Investigation : CT-scan /MRI
Endoscopic U/S (EUS)
Radionuclide scanning
• Rx. : resection /debulking
VIPOMA :Vasoactive Intestinal Polypeptide(VIP)
secreting neoplasm(WDHA syndrome)
• Coarses with watery diarrhea, hypokalemia and
achlorhydria
• More often, is localized in the body or in the tail
of the gland.
• Investigation :
-CT-scan/MRI
-EUS (Endoscopic U/S)
• Rx. : resection
SOMATOSTATINOMA
• Usually, the somatostatine inhibits pancreatic
and biliary secretions. so :
• Somatostatinoma (cancer of the Delta cells) :
Inhibits secretion of insulin = DM
Inhibits pancreatic exocrine secretion =
steatorrhea
Produces biliary stasis = cholelithiasis
The most common presentations are abdominal pain
(25%), jaundice (25%), and cholelithiasis (19%).
Investigation : dosification of somatostatine level
(>10ng/ml )
Rx. : resection and cholecystectomy
Any question ????
BIBLIOGRAPHY
1. Bailey & Love’s : Short Practice of Surgery
,22nd. edition, 1995.and 25th. edition,2008
2. Schwartz’s Principles of Surgery,8th. edition,
2004.
Thank u very much !!!!

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SURGICAL CONDITIONS OF THE PANCREAS.pptx

  • 1. SURGICAL CONDITIONS OF THE PANCREAS
  • 2. OBJECTIVES 1. To have a knowledge of surgical conditions of the pancreas. 2. To diagnose and treat patients with surgical conditions of the pancreas. 3. To be able to counsel the patient, the guardian and/or the family about the diagnosed surgical problem of the pancreas
  • 3. Outline • Introduction • Congenital abnormalities of the pancreas • Injuries to the pancreas • Pancreatitis • Tumors of the pancreas
  • 4. introduction • The name pancreas is derived from the Greek “pan’’ (all) and “kreas’’( flesh). -The gland weighs approx. 80gms. -Is situated retroperitoneally -It is divided into: head, neck, body and tail -It overlies the body of the 2nd.lumbar vert. and the aorta. -It is composed of mainly 2 types of cells (exocrine acinar cells & endocrine cells known as Islets of Langerhans) -the exocrine cells secret: cholecystokinin, amylase, lypase, elastase & chymotrypsine -the endocrine cells (Islets of Langerhans) secret : glucagon(alpha), insulin(Beta), somatostatine(Delta) and gastrin(D cells)
  • 5. Congenital Abnormalities of The Pancreas 1. Cystic fibrosis (generalized dysfunction of exocrine glands) 2. Hypoplasia 3. Annular pancreas(failure of complete rotation of the ventral pancreatic bud during development , so that a ring of pancreatic tissue surrounds the 2nd. or the 3rd. part of the duodenum). 4. Ectopic pancreas(sub mucosa of stomach, duodenum , Gb. hilum of the spleen, in the liver etc. 5. Cystic disease of the pancreas
  • 6. Investigations to be done in suspicion of any pancreatic disease I. To measure pancreatic damage: is achieved by measuring levels of pancreatic enzymes in body fluids: (amylase, lypase, trypsin & chymotrypsine) II. To measure pancreatic function : is achieved by measuring bicarbonate &enzymes in the pancreatic juice : 1-indirect method of Lundh done by duodenal intubation 2-secretin-pancreozymin test (triple lumen tube) 3-glucose tolerance test III. To detect morphologic abnormalities of the pancreatic parenchyma & ducts :(cytology of the pancreatic juice, U/S, EUS CT-scan, MRI, ERCP ,plain abd. X-ray & CxR
  • 7. injuries to the pancreas 1. External injuries : A) Direct blunt trauma  Blow during automobile/bicycle accident  Unexpected punch on a relaxed abdomen The neck of the gland is the most affected. B) Penetrating injury which usually involves the stomach, duodenum, colon ,liver or spleen. 2. Iatrogenic injuries :occur in 4 ways -injury to the tail (splenectomy) -injury to accessory duct (Santorini) -fistula (after enucleation of islet cell tumors) -during sphincterotomy
  • 8. Clinical presentation • Hx. Of trauma • Epigastric pain • Investigations : Serum amylase (rises in 90% of the cases) Abdom. u/s CT. Scan/MRI
  • 9. Treatment • If no overt bleeding OR if bleeding(after controlling the bleeding): Drain NPO Parenteral support • If body transection :distal resection • Repair (usually coarses with high incidence of fistulization)
  • 10. Prognosis • Bleeding from the site of rupture is the most common cause of death.  in blunt trauma if there is an associated injury (duodenum),the mortality rate is 16-28% In penetrating injury with associated injuries to the surrounding organs , the mortality is approximately 50%.
  • 11. Pancreatic fistulas Problems: 1. High fluid and electrolytes loss (2 lts./24hrs.) 2. Auto digestion of the pariets 3. Collection of fluid around the gland
  • 12. TREATMENT 1. If pancreatic duct is intact :conservative Rx.:  Replace fluid & electrolytes by mouth/iv  Use somatostatine analogue  High protein & low carbohydrate diet  Total Parenteral nutrition  Zinc oxide cream on the skin  Percutaneous drainage of the peripancreatic fluid (if collection) 2. If the duct is totally disrupted :Resection
  • 13. PANCREATITIS • Definition : is an inflammation of the gland's parenchyma. • Classification : there are 2 useful ways of classification. 1. According the clinical presentation of the disease 2. According to the etiology of the disease
  • 14. CLASSIF. According the clinical presentation 1. Acute pancreatitis 2. Relapsing acute pancreatitis 3. Chronic pancreatitis The acute and the relapsing acute pancreatitis return to normal when the primary cause is removed . The chronic pancreatitis remain with functional/structural damage even after removal of the primary cause.
  • 15. CLASSIF.according to the etiology • Biliary tract disease • Alcoholism • Post operation • Traumatic • Rare causes (mumps ,hyperparathyroidism ,vascular diseases, etc. ) • Idiopathic This classification according to the etiology of the disease is very important in relating the natural Hx. of the disease to : -prognosis -long term Rx. -prophylaxis
  • 16. ACUTE PANCREATITIS • INCIDENCE :the same in both sex , despite the age difference(men 30-40yrs.& women 50yrs.) • Etiology :  Biliary calculi(50%)  Alcoholism(25%)  Post Biliary/gastric surgery  Trauma (blow to the pancreas)  Distortion of ampulla of Vater (PUD, ampullary Ca.  Generalized disorders(hyper calcemia, hyperlypemia, DM. porphiria)  Drugs (coticosteroid,ART)  Viral infections (mumps)  Auto immune disorders(poly arthritis nudosa)  After impaired pancreatic blood flow (cardiopulm. by pass , hypothermia)
  • 17. Clinical features of acute pancreatitis • Severe epigastric pain • Anorexia • Nausea & vomitings • By p/e :  Fever (60%)  Tachycardia & tachypnea (50%)  Jaundice (10%)  Eccymotic discoloration of the flanks (Grey Turner’s sign)  Eccymotic discoloration of the periumbilical area (Cullen’s sign)  Abdominal guarding
  • 18. Investigations 1. Routine & LFT, RBS, RFT(blood urea),serum calcium 2. Serum amylase  Elevates in few hrs. & declines after 48hrs. 3. Lipase  Starts to rise after 48hrs. 4. Plain abd. X-ray  Sentinel loop (distended loop of SB in the LUQ.)  Duodenal distention  Colon cut-off sign (distended transv.colon with collapsed descending colon) 5. Abd. U/S 6. CT-Scan/MRI 7. MRCP 8. ERCP 9. EUS 10. CxR
  • 19. Ranosn's criteria to identify high risk patients (severity of the disease) The coarse of this disease varies from mild to fulminant depending on Ranosn’s criteria : 1. Old age (>55yrs.) 2. Rise in blood sugar ( >10mmol) 3. WBC (elevated) (>16,000) 4. LFT (deranged ) 5. Blood urea ( >5mg%) 6. Hypocalcaemia (<2mmol) 7. Hct. (low ) 8. Spo2 (<60mmHg ) 9. Volume of 3rd. Space fluid collection(extra vascular space) (ascitic fluid, pleural effusion edemas, etc.) NB: the disease is severe when 3 or more factors are present
  • 20. Treatment of acute pancreatitis • Bed rest (admission to ICU) • NPO • Iv fluids (aggressive fluid rehydration) • Frequent monitoring of v/s , diuresis, RFT, LFT blood gases, clotting factors • oxygenation • NG. tube • Analgesics (pethidine + antispasmodic drug) • Anticolinergics (to reduce pancreatic secretion):somatostatine, glucagon,calcitonin,etc. • Regular RBS dosifications • Regular serum calcium dosifications • Antibiotics • Endoscopic sphincterotomy (if jaundice due to stone) • Surgery urgently (if does not solve within 7 days, after repeating U/S & CT-scan to R/O local complications) • Investigation , identification & Rx. of underlying causes:  Cholecystectomy within 1 month after the acute phase.( if Gb. stone)
  • 21. Complications of acute pancreatitis 1. Hypovolemic shock:  GI fluid loss  3rd. Space collection  Retroperitoneal hemorrhage 2. Pulmonary insufficiency due to :  Retroperitoneal edema  Elevation of the diaphragm  Reduced ventilation due to pain  DIC 3. Infection (3%) : secondary infection of necrotic tissue in pancreatic bed 1 or 2 weeks after the initial attack). 4. Electrolytes disturbances (hypocalcaemia) 3-30%) :  Binding of calcium in areas of fat necrosis  Raised levels of glucagon & calcitonin  Deficiencies in parathyroid hormone 5. Colonic stricture (scaring of transv. Colon & its meso) 6. Pancreatic pseudo cyst
  • 22. Prognosis of acute pancreatitis • Depends on the severity of the disease: 1. Edematous pancreatitis : 3-10% of death 2. Necrotizing pancreatitis : 40-50% of death 3. Totally necrotized : 100% of death
  • 23. Chronic pancreatitis Definition : is an incurable, chronic inflammatory condition that is multifactorial in its etiology, highly variable in its presentation and a challenge to treat successfully. Incidence : – more frequent in men (4:1) – Mean age : 40yrs. Etiology: Alcohol consumption with high protein and fatty diet Pancreatic duct obstruction (post- traumatic, pancreatic Ca. cystic fibrosis, infantile malnourishment, idiopathic causes) Stenosis of the ampulla of Vater
  • 24. Clinical features of chronic pancreatitis Epigastric pain (93%) with exacerbation by alcohol intake & referred to the LUQ (29%),RUQ(44%)&through to the back(56%) Weight loss (due to loss of appetite and malabsorpsion DM.(late) P/E : is usually non revealing, but there can be: -jaundice (CBD narrowing) -tender hard mass (cystic/Ca )
  • 25. Investigations for ch. pancreatitis 1. Lundh test / secretin-pancreozymine test: abnormal 2. Lactoferrin level in pancreatic juice obtained by ERCP (elevated): indicating calcifying ch. pancreatitis 3. Stool analysis : steatorrhea in 30% of the cases 4. Plain abdom. X-ray (calcifications in 65%) 5. U/S of the abdomen :enlarged pancreas with cysts & dilated ducts. 6. CT-scan /MRI :to confirm and R/O other causes of pain in the retroperitoneal area. 7. ERCP :can demonstrate ductal / papillary stricture & the extent of the disease if amenable to surgical Rx 8. MRCP 9. EUS
  • 26. TREATMENT OF CH. PANCREATITIS  Diet (low in fat & high in protein and carbohydrates)  No alcohol neither tobacco  Pancreatic enzyme supplement  Vit. Supplement (A, D, E, K Vit.B-12) with medium chain triglycerides  Strong analgesics  Splacnic (Celiac) nerve block :CT / EUS guided  Rx. for DM.(usually insulin)  SURGEY (based on results of pancreatogram & CT-scan/MRI): is done when the disease is not controlled by medical Rx. : -if head is normal : distal pancreatectomy -if head is involved : pancreatoduodenectomy -if the whole gland is affected : total pancreatectomy
  • 27. Complications of ch. pancreatitis 1. Ch. Pseudo cyst 2. Pancreatic ascites 3. Pancreatic-enteric fistula 4. Pancreatic head ch. Inflammatory mass 5. Splenic and portal vein thrombosis 6. Pancreatic Ca.
  • 28. Prognosis of ch. pancreatitis 1. Drainage / excision procedures : provide relief from pain in 75% 2. The quality of life is good if : – DM. & steatorrhea is controlled – Abstains from alcohol and / or tabbaco
  • 29. Pancreatic pseudocyst Definition :a chronic collection of pancreatic fluid surrounded by a non epitelized wall of granulation tissue and fibrosis Incidence : -occurs in up to 10% of acute pancreatitis -occurs in 20-39% of ch. pancreatitis
  • 30. Clinical features of pancreatic pseudocyst • Hx. of pancreatitis • Palpable epigastic mass
  • 31. Classification of pancreatic pseudocyst 1. Acute pancr. Pseudocyst :  Pancreat. duct leak of pancreatic juice surrounded by a wall of acute granulation tissue without much fibrosis  Occurs within 3-4 weeks of the attack  May resolve spontaneously up to 50% over a coarse of 6 weeks or longer 2. Ch. Pancreatic pseudocyst :  is a collection of pancreatic juice surrounded by a wall of ch. granulation tissue and fibrosis  Usually persists for >6weeks
  • 32. complications of pancreat. pseudocyst 1. Secondary infection (abscess) 2. Compress adjacent organs / structures 3. Erode into visceral arteries and cause intracystic hemorrhage/pseodo. aneurisms 4. Perforate and cause peritonitis/intraperitoneal hemorrhage
  • 33. Treatment of pancreatic pseudocyst A. Asymptomatic: is based on expectant Rx. -may solve spontaneously or persist w/o complication. B .Symptomatic (pain, fullness, early satiety or enlarging ) : -Percutaneous aspiration(U/S or CT-scan guided -Internal drainage  Endoscopical placement of stents  Surgical (cystoenterostomy, cystoduodenostomy, cystogastrostomy, resection of the cyst, distal pancreatectomy, etc.)
  • 34. Cancer of the pancreas are of 2 types : 1. Cancer of the exocrine 2. Cancer of the endocrine
  • 35. Cancer of the exocrine pancreas • Incidence : Affects men and women equally Occurs more in elderly About ½ of all patients are>75yrs. old • Pathology & etiology : >75% are adenocarcinoma of ductal origin Some are multicentric in origin There is slight preponderance of tumor arising in the head & neck of the gland Associates with : tobacco smoking high protein & fatty diet ch. pancreatitis
  • 36. Clinical features of Ca. of the exocrine pancreas • Nonspecific symptoms such as : Weight loss Pain to the right/left of epigastrium Back pain Anorexia Jaundice & pruritus (2/3 of pancr. Head tumor) • Physical exam. : Generalized wasting Hepatomegally (50%) Courvoisier’s sign :palpable Gb in 30% of the pancr. head tumor and 50% of the ampullary tumors Splenomegally (due to Splenic vein thrombosis)
  • 37. Investigations 1. Routine investigations 2 . Diagnostic investigations :  LFT (alk. Phosph. Elevated)  Cytology of the pancreatic juice obtained by ERCP  Hypotonic duodenogram (inverted 3 sign ,widened duodenal loop, irregular duodenal mucosa)  Abdominal U/S (pancr. mass with dilat.of pancr. duct,GB,CBD &hepatic mets.)  CT-scan / MRI (pancr. mass , hepatic mets. ,L/nodes  Duodenoscopy with BIOPSY in cases of ampullary tumors.  ERCP & pancreatogram (sharp duct occlusion)  Transgastric or transduodenal FNAC or Tru-Cut biopsy under EUS  Tumor marker CA19-9
  • 38. Treatment of Ca. of the exocrine pancreas More than 80% of the cases are beyond surgical resection on presentation due to : -local spread -paraaortic & mesenteric L/nodes -hepatic mets. -advanced age of the patient Generally , the Rx can be : 1. Palliative 2. Surgical resection
  • 39. Palliative Rx. • Is given for about 95% of all cases of pancreatic Ca. • Is based on : – Strong analgesia (opiates) for pain – Pancreatic supplements for weight loss – Endoscopic stenting of the CBD through ERCP – Biliary bypass(80%) : • Choledochoduodenostomy • cholecystojejunostomy
  • 40. Surgical resection • Is indicated in tumors of <3cms.and mostly situated near the ampulla, if technically feasible and in fit patients. • Is not indicated in tumors of >5cms.and when the tumors are located in the pancreatic body • When resection is possible, one of the following procedures can be done: 1. Pancreatoduodenectomy (Whiplle’s procedure) 2. Regional pancreatectomy (Fortner) 3. Total pancreatectomy
  • 41. Prognosis of the exocrine pancreatic Ca. 1. Median survival : 6months from the time of diagnosis 2. Patients with ampullary tumor who undergo resection :5yrs. (30%) 3. The surgical resection has mortality rate of 8%
  • 42. Cancer of the endocrine pancreas • General considerations :  Comprise 1% of all pancreatic tumors  Originate from the islets of Langerhans which contain 4 types of cells (alpha ,beta delta & gamma)  The tumor of the B-cells is more common than the others’ (insulinoma)  2/3 of the endocrine pancreas’s tumor occur in the body or tail of the gland.  1/3 of them are multiple  Most of them are malignant but have favorable coarse than the exocrine pancreas tumors  The cancers of the islets of Langerhans can be associated with similar lesions in other endocrine glands (specially in anterior pituitary, parathyroid, and adrenal cortex as multiple endocrine adenomatosis.
  • 43. Ca. of the endocrine pancreas Classification: I. Functionals :secret peptide products(excess hormones)that produce clinical presentations. 1. Insulinoma(Ca. of the Beta cells) 2. Gastrinoma(Ca. of the D cells) 3. Glucogonoma(Ca. of the Alpha cells) 4. Vipoma 5. Somatostatinoma(Ca. of the Delta cells) II. Nonfunctionals : not associated with excess hormone levels & are clinically silent.
  • 44. Insulinoma(Whipple’s triad) • Coarses with hyperinsulinism and attacks of hypoglycemia at irregular intervals which progressively increase in frequency & severity. • Has 4 stages : 1. Stage I :simulate duodenal ulcer with vague abd. pain which subsides by carbohydrates. 2. Stage II :coarses with trembling, sweating, dizziness, blurring of vision & great hunger. 3. Stage III : sluggish mind, unarticulated speech, uncoordinated movim. diplopia & sometimes hallucinations. 4. Stage IV :looks like epilepsy / coma
  • 45. Diagnosis of insulinoma • Is done by: 1. Clinical features :Whipple’s triad (attacks of hypoglycemia in fasting state, symptoms relieved by glucose & glycemia <45mg/100ml.of blood). 2. Investigations :  FBS  Dosification of human insulin by radioimmunoassay (elevated)  Insulin stimulation & suppression tests  Endoscopic U/S  CT-scan /MRI  Radionuclide scanning
  • 46. Treatment of insulinoma • Surgery solves 90% of the problem. • Extirpation of the tumor aided by palpation or by intraoperative U/S is done. • Operative mortality is 2% .
  • 47. Gastrinoma (Zollinger-Elisson syndrome) Types : is of 2 types & is suspected in pts. With recurrent multiple ulceration or when PUD appear in unusual sites: 1. Type I : is rare & coarses with : hypergastrinemia ch. Peptic ulcerations antral G-cell hyperplasia 2. Type II : coarses with : intractable peptic ulcerations (often jejunum) hypergastrinemia (massive acid secretion = 500ml/hr.) diarrhea/steatorrhea hypokalemia & about ½ are malignant
  • 48. Investigations for gastrinoma 1. Acid secretion studies 2. Stimulation of circulating gastrin:  Type I :increased gastrin levels by meat extracts  Type II : increased gastrin levels by iv calcium 2mg/kg in 1minute 3. Endoscopic U/S 4. CT-scan /MRI 5. Endoscopy 6. Radionuclide scanning (is done by iv injection of radioactive somatostatine analogue, because many of the endocrine pancreas tumors have somatostatine receptors.)
  • 49. Treatment of gastrinoma • Type I :partial gastrectomy to remove the G- cell bearing area • Type II : if tumor is detected : resection If tumor is not detected :medical Rx. on the basis of H2 receptor antagonists / PPI. IF medical Rx. fails : total gastrectomy 49
  • 50. Glucagonoma(cancer of the Alpha cells) • Coarses with DM , dermatitis and malnourishment. • Usually is localized in the body or in the tail of the gland. • Investigation : CT-scan /MRI Endoscopic U/S (EUS) Radionuclide scanning • Rx. : resection /debulking
  • 51. VIPOMA :Vasoactive Intestinal Polypeptide(VIP) secreting neoplasm(WDHA syndrome) • Coarses with watery diarrhea, hypokalemia and achlorhydria • More often, is localized in the body or in the tail of the gland. • Investigation : -CT-scan/MRI -EUS (Endoscopic U/S) • Rx. : resection
  • 52. SOMATOSTATINOMA • Usually, the somatostatine inhibits pancreatic and biliary secretions. so : • Somatostatinoma (cancer of the Delta cells) : Inhibits secretion of insulin = DM Inhibits pancreatic exocrine secretion = steatorrhea Produces biliary stasis = cholelithiasis The most common presentations are abdominal pain (25%), jaundice (25%), and cholelithiasis (19%). Investigation : dosification of somatostatine level (>10ng/ml ) Rx. : resection and cholecystectomy
  • 54. BIBLIOGRAPHY 1. Bailey & Love’s : Short Practice of Surgery ,22nd. edition, 1995.and 25th. edition,2008 2. Schwartz’s Principles of Surgery,8th. edition, 2004.
  • 55. Thank u very much !!!!