Surgery II - Pancreas 2014
Surgery II - Pancreas 2014
Surgery II - Pancreas 2014
Pancreas
Exocrine pancreas
Comprises 85% of pancreatic mass
Secretes 500-800 ml/day of colorless, alkaline,
isosmotic juice
Secretion is inhibited by:
Somatostatin
PP
Glucagon
Centroacinar and Intercalated Duct Cells
Secretes water and electrolytes
They contain carbonic anhydrase
Responsible for the formation of
bicarbonate
Bicarbonate (HCO3)
Amount is directly proportional to the rate
of secretion
Chloride
Amount is inversely proportional to the rate
of secretion
Sodium and Potassium- amount is constant
Secretin
Major stimulant for bicarbonate secretion
Released from duodenal mucosa in
response to acidic chyme from the stomach
CCk, gastrin, accetylcholine
Weak stimulants of HCO3
Acinar Cells-Secretes digestive enzymes
CCK-primary stimulant
Carbohydrates
Amylase
Secreted in its active form
Completes the digestive process started by
the salivary amylase
Hydrolyzes starch and glycogen to simple
sugars (glucose, maltose, dextrins)
Acinar Cells
Protein
Proteolytic enzymes-secreted as proenzymes
Endopeptidase
Proelastase Elastase
Chymotrypsinogen chymotrypsin
Trypsinogen trypsin
Exopeptidase
Procarboxypepetidase
Carboxypeptidase
Fat
Lipase-active
Phospholipase A2
Secreted as pro-enzyme
Requires bile for its action
Trypsinogen
Converted to trypsin in the dueodenum by
enterokinease
Also activated by acidic enviroment ( pH <7)
Activates the proenzyme to active form
Mutation of trypsinogen results to premature
intrapancreatic activation---familial pancreatitis
Pancreatic secretory trypsin inhibitor (PSTI) or SPINKI
Inhibits action of trypsin by blocking active site
Ensures activation of digestive enzymes occurs
only within the duodenum
Failed expression of PSTI results familial
pancreatitis
Endocrine Pancreas
They are composed of various cells located in the Islet
of Langerhans
(1 2%)
The primary function is to regulate glucose homeostasis
Beta Cells
70% of Islet cell mass
Located in the central portion if the islet
Hormones produced
Insulin
Inhibit endogenous glucose production
Facilitates glucose transport into the cells
Inhibits
glycogenolysis,
fatty
acid
breakdown and ketone formation
Stimulates protein synthesis
Amylin counterregulates insulin secretion and
function
Pancreastatin
Decrease insulin and somatostatin release
Decrease pancreatic exocrine secretion
Increase glucagon release
Stimulates insulin secretion
Amino acids (arginine, lysine,leucine)
Glucagon
Acute Pancreatitis
Pathogenesis of Pancreatitis
Involves activation of inactive enzymes within the pancreatic
parenchyma
The primary defect-extrusion of zymogen granules are
blocked
Fusion of zymogen granules w/ Lysosomes
Lysosomal enzymes (Cathepsin B) actvitates
trypsinogen to trypsin
Gallstone Obstruction
Acute Pancreatitis
Etiology
Tumors
Should be considered in non-alcoholic
1-2% have pancreatic Ca
Drugs
Thiazide diuretics furosemide, tetracycline.. Etc..
Infections
Mumps,
coxsackie
virus,
Mycoplasma
pneumonia
Hyperlipidemia
Fatty acids
Endothelial injury, sludging of blood cells
Ishemic states
Iatrogenic
Pancreatic biopsy, gastrectomy
Splenectomy
ERCP
Mild pancreatitis
No systemic complications
Low Ransons
Sustained clinical improvement
Severe pancreatitis
High Ransons
Encephalopathy, ARDS
Hct >50% , urine output-< 50 mL/h
Hypotension, fever, peritonitis
Clinical Presentations
Acute pancreatitis may vary from mild abdominal discomfort
to profound shock, hypotension and hypoxemia
May present with epigastric pain radiating to the back with
nausea and vomiting
Discomfort may be relieved by sitting and aggravated by
lying
Findings may vary with severity of inflammatory process
May have mild to moderate abdominal tenderness
In severe cases may have rigid abdomen, epigastric guarding
and rebound tenderness
Severe pancreatic inflammation and necrosis may cause
retroperitoneal hemorrhage which leads to:
Large 3rd space fluid loss
Hemococentration- elevated HCT
Hypovolemia
Pre-renal azotemia
Hypotension
Tachycardia
Blood dissection along different planes
Grey Turners sign
Blood extends to the flank tissues resulting to
flank ecchymosis
Cullens sign
Blood dissects up to the falciform ligament and
create peri-umbilical ecchymosis
Surgical Specimen
A. Stomach
B. Spleen
C. Fat
D. Pancreas
Diagnosis
Serum Markers
1. Serum amylase
Mumps
CBD Stones
Sentinel Loop Sign
Ultrasound
The best way to confirm biliary pancreatitis
Changes from normal anatomy and vascular landmarks;
presence of swelling and loss of tissue plane
For patients
intervention
with
risk
for
surgical
Chronic Pancreatitis
Gross
Histopathology
Etiology
Alcohol
Most common cause worldwide -70%
Risk is dose related (150g/d)
Risk is still present even at low exposure ( 1-20 g/d)
Related also to the duration
Typically after 16-20 years of alcohol
consumption
Directly alters the integrity of the pancreatic ducts acini
Acetydehyde Interferes with the intracellular
transport of digestive enzymes & colocalization with
lyzosomes
o Leads to autodigestion
High protein, low carbohydrate, low volume secretory
output
o Precipitation of protein
Decreased Lithostathine
Other causes
Hyperparathyroidism
ERCP
Treatment
o Restriction of fat to 75 g/day
o Exogenous pancreatic enzyme
Non-enteric
coated
pancreatic
enzyme + prton pump inhibitor
Manifestations:
o Apancreatic Diabetes (typeIII):
Surgical therapy
Can delay progression of chronic pancreatitis
Drainage procedures
Transduodenal sphincteroplasty
Duval procedure
Puestow procedure
Side to side pancreaticojejenostomy
Duct must be 6mm
Pain relief in 75-85%
20% recurrence
Resectional procedures
Distal pancreatectomy Focal inflammation localized to the body
and tail
No ductal dilatation
Resection of 40-80%
With significant risk of recurrence
Complications:
Pseudocyst:
Most common complication of chronic
pancreatitis
Acute pseudocyst-collection of pancreatic juice 34 weeks after acute pancreatitis. Persistence of
the pseudocyst for >6weeks-Chronic pseudocyst
Resolve spontaneously in 50% of cases
over acourse of 6 weeks or longer
>6cm resolves less frequently but may
regress over period of months
May form an abcess if w/ secondary
bacterial infection
Diagnosis
Continued elevation of serum amylase
CT scan is the most helpful examination
Ultrasound
UGIS
ERCP
Distal Pancreatectomy
Resectional procedurtes:
Total pancreatectomy
95% distal pancreatectomy:
Intented for sclerotic (small duct) dse.
Pain relief in 77% nof patients
High risk for brittle diabetes,hypoglycemic
comma and malnutrition
Pseudocyst
Treatment:
Observation:
50-60% resolution rate for asymtomatic patients
Surgery:
Persistence of sypmtoms(pain, inability to
eat,GIT and biliary obstruction
Enlargement
Complications
Infection
Hemorrhage
Rupture
External Drainage-for infected pseudocyst
Internal drainage (best treatment)
Small piece of cyst wall should be excised for
histopathology to rule out malignancy
Cystogastrostomy - most commonly used
Cystojejenostomy - most verastlie; can be used
for those that penetrate the transverse mesocolon,
paracoloic gutter or lesser sac
Cystoduodenostomy
Cystgastrostomy Completes
Anterior Gastrotomy
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Treatment
Duodenum preserving
resection (DPPHR)
Splenic and portal vein thrombosis
Pancreatic-enteric fistula
7.
pancreatic
head
PANCREATIC TUMORS
Adenocarcinoma of the Pancreas
Most are>60 years old
Mutation of K-ras oncogene
Slightly more common in men
2/3-head or uncinate process
Diagnosed earlier because of obstructive jaundice
15%-body
10%-tail
85-90%-unresectable at the time of dx
Risk factors
Family hx
Cigarette smoking
Dietary high in fat low in fiber, fruits and vegetable
Diabetes mellitus
Chronic pancreatitis
Pancreatic CA may arise anywhere in the pancreas, with the
most frequent focus in the head
Pancreatic Carcinoma
A typical Pancreatic Carcinoma patient
Note marked weight loss and jaundice
Clinical Manifestations:
1. Weight loss (most common)
2. Pain (dull and aching epigastric and radiates to the back,
aggravated by eating and lying down) due to obstruction
to the pancreatic duct and perineuralinvasion
3. Progressive jaundice 75 % (cancer of the head of the
pancreas)
4. Anorexia and weakness (50 %)
5. Pruritus
6. Hepatomegaly
Diagnostic examinations
1. Ultrasound
2. CT-scan
o Multidetector ,dynamic,contrast enhanced CT scan
90-95% accuracy in predicting unresectablity
Criteria of unresectability
o Invasion of superior mesenteric
artery
o Invasion of the hepatic artery
o Enlarged
LN
outside
the
boundaries of resection
o Ascites and distant metastasis
3. EUS
o Used when there is high suspicion of pancreatic CA
but no mass seen on CT scan
o Sensitive test for portal and superior mesenteric
vein invasion
o Transluminal biopsy of pancreatic mass
o 80%-accuracy in predicting resectabilty
4. Diagnostic laparoscopy :
o Advocated in patients felt resectable by CT
scan.Improves the accuracy in predicting
resectability by 98%
o Best applied in pt. with large tumors (>4cm)
located on the body and tail
o Pts. with eqiuvocal findings of metastasis or ascites
o Advanced dse. e.g. marked wt loss Ca19-9
(>1000U/mL)
Treatment
o Prior to surgery
Improve nutrition, correct anemia
Preoperative renal function
Adequate hydration
o Whipples Surgery
The only definitive and potentially curative
treatment of periampullary carcinoma. It is
performed for localized cancer of the ampulla,
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Distal Pancreatectomy
ERCP
Pancreatic CA has a fairly characteristic appearance on
ERCP, with pancreatic ductal obstruction, often combined
with bile duct obstruction
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Pancreatic Carcinoma
Choledochojejunostomy
Gastrinoma
Diagnosis:
Serum gastrin > 200pg/ml
Basal acid output> 15mmol/hr
Secretin provocative test-if gastrin is not markedly
elevated.+ if >200pg/ml than the basal level
Octreotide scintigraphy-test of choice for localizing
gastrinoma.
EUS + Octreotide scintigraphy-90% success rate in
localizing gastrinomas
Treatment
Surgical
Pancreatic resection-solitary gastrinoma w/o mets
If w/ MEN 1 syndrome
Total parathyroidectomy
If located in the duodenum
Full thickness excision
On the pancreas w/o involvement of the ducts
enucleation
For inoperable malignant gastrinoma
Chemotherapy
Streptozocin
Doxouribicin
5 FU
Unresectable or Gastrinoma cannot be localized
Proton pump inhibitor
Highly Selective Vagotomy
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HYPERINSULINISM
Insulinomas
Arise from Beta cells
Most common islet cell neoplasm
90% are solitary and benign
10%-malignant
<5% are associated with MEN 1
Mmultiple-they have high recurrence rate
Symptoms
Related to cerebral glucose deprivation
Bizarre behavior
Tremors
Syncope
Seizures
Whipples triad
Fasting hypoglycemia(bld glucose <50mg/dl
Hyperinsulinemia (>20uU/ml)
Relief of symptoms by intravenous glucose
Diagnosis
Fasting hypoglycemia
Hyperinsulinemia (> 20uU/ml)
Insulin/glucose ratio ->0.3
Imaging
EUS- 90% success rate in localizing the tumor
CT scan
Treatment
Most are treated by enucleation
Distal pancreatectomy or whipples
Large tumors ( >2cm)
Close to the main pancreatic duct
Tumor cannot be localized
Medical tx
Diazoxde-inhibits insulin release
Frequent feedings w/ slowly absorbed CHO
Serous Cystadenoma
Benign tumor w/o malignant potential
Commonly seen in elderly female
Spongy w/ multiple small cyst
Mucinous Cystadenoma
Benign but w/ malignant potential
Common in elderly female
Most are located in the body and tail
Ovarian stroma-key path feature
+ stain for mucin
Almost all will evolve into CA if untreated
SPLEEN
Anatomy
Adult spleen weighs between 100 to 250 grams. 7-11cmlength
It is located in the left upper quadrant and protected by the
lower portion of the rib cage
Its position is maintained by several ligaments:
Splenophrenic
Splenorenal
Splenocolic
Gastrosplenic (contains the short gastric vessels)
It is supplied by the Splenic Artery (branch of the celiac
artery); venous drainage course through the splenic vein
Accessory spleens have been reported in 14 to 30 % of
patients usually seen at the hilum of the spleen, gastrosplenic,
splenocolic, gastrocolic, splenorenal ligaments and greater
omentum
Splenosis
Autotransplantation of splenenic fragments after trauma
Capable of performing some reticuloendothelial
function
The pulp is consist of three (3) zones:
Red pulp: 75% of total volume. Comprised of venous
sinuses.Separated
by
reticulum.Contains
macrophages.Serves as filter, removes microrganisms,
cellular debris,antigen-antibody complexes and old
erythrocytes
White pulp-consists of lymphoid follicles
Periarticular lymphatic sheath-T-lymphocytes
B-lymphocytes-lymphoid follicles
Serves the immunologic function of the spleen
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Accessory Spleen
The accessory spleens seen here at the hilum of the normalsized spleen are not uncommon and by themselves have no
significance
Spleen
Open circulation - (90%)
Blood goes first to reticular space and cords
Comes in contact with macrophages
Closed circulation-(10%)
Goes directly to the arteriovenous anastomosis
Host Defense
Opsonins makes organism attractive to phagocytes
Tuftsin enhances the phagocytic activity of
leukocytes
Properdin stimulates the alternative pathway of
complement fixation
Circulating monocytes are converted to fixed
macrophages at the red pulp
Produces immunoglobulin (IgM) and IgG
Release opsonic antibodies from the white pulp
Physical Examination
Normally not palpable
Felt in about 2 % of healthy adults
No significant dullness elicited by percussion over
spleen either anteriorly or laterally
As organ enlarges, dullness is detected at the level
of the 9th ICS in the left anterior axillary line
Ultrasound
CT scan
Plain Radiography
Angiography
Localization and treatment of hemorrhage in
trauma cases
Alternative or adjunct in the treatment of
hematologic disorders (SAE)
Deliver y of therapies in patients with cirrhosis
Nuclear imaging
Tc 99 sulfur colloid
Demonstrates the location and size
Helpful in localizing accessory spleen after
unsuccessful splenectomy for ITP
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Splenic index
Express the volume of spleen in ml.
Determined by multiplying the spleens length,
width and height
Normal SI 120ml-480ml
2. Evaluation of Function
Splenectomy
Diagnostic Studies
CBC serial Hct determination; WBC count frequently
greater than 15,000/ml3
X-ray of the abdomen fractured ribs should arouse
suspicion of injury to the spleen; more specific findings:
o Elevated immobile diaphragm
o Enlarged splenic shadow
o Medial displacement of gastric shadow
o Widening of space between splenic flexures and
preperitoneal fat
CT scan
Angiography
Delayed Rupture
A, preoperative; B, postoperative
RUPTURE OF SPLEEN
Etiology:
Splenic injuries in which there is disruption of the organs
parenchyma, capsule and blood supply
Tranasabdominal or transthoracic penetrating trauma
Non-penetrating trauma spleen is the most frequently
injured organ following blunt abdominal trauma or
lower thoracic cage trauma
Operative trauma 2 % of patients whose operation
involved the viscera in the left upper quadrant of the
abdomen
Spontaneous rupture most often caused by malaria
and infectious mononucleosis
Clinical Manifestations:
Signs and symptoms vary according severity and rapidity of
infra-abdominal hemorrhage and the interval between injury
and examinations
Hypovolemia and tachycardia
Slight reduction in blood pressure
Generalized abdominal pain while of patients complain of
localized left upper quadrant pain
Splenic Injuries
Indications for early laparotomy
Need for transfusion within 24 hrs
Hemodynamic instability
Surgical management of splenic injunry
Splenorraphy
Partial splenectomy
Splenectomy
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Hereditary Spherocytosis
Splenic Injury
Red Blood Cell Disorders
Hereditary spherocytosis
Deficiency in one of the membrane proteins
(spectrin,ankyrin,band3 protein, protein 4.2)
Spherical less deformable shape, they sequestered and
destroyed in the spleen
The
most common of hemolytic anemia which
splenectomy is the primary treatment
In children-delayed until ages of 4-6 years
Congenital Hemolytic Anemia
Red Cell enzyme deficiency
Glucose 6 phosphate deficiency
Enzyme needed to maintain the ratio of reduced
to oxidized glutathione protecting it from
oxidative damage
Pyruvate Kinase deficiency
Most common congenital hemolytic anemia
Enzyme needed for glycolysis
Hemoglobinopthies
Thalassemia
Reduced or absent production of hemoglobin chains
Alpha chains-needed for the production of fetal and
adult Hgb
Beta chains-involved in adult Hgb synthesis
Hypochromia and microcytosis
Unbalanced alpha and b subunits
Cannot release oxygen
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Platelet Disorder
Idiopathic thrombocytopenic purpura
Premature removal of platelets opsonized by
antiplatelet IgG autoantibodies produced by the spleen
Children-70-80%-spontaneous remission
30,000-50,000/cu.mm-easy bruising
10,000-30,000/cu.mm-spontaneous petechiae and
eccymosis
<10,000/cu.mm-internal bleeding
Medical Tx
Prednisone 1mg/kg
Effective in 75% of pt (1-3 weeks)
Goal: platelet ct of > 100,000 /cu mm
Initiated when fall to <20,000-30,000/cu
mm
Only 15%-25% achieve a lasting response
IV IgG
Given when platelet ct remains low after
steroid tx
Given for 2 days
Splenectomy
Provides prompt and permanent response
1week
Failure of medical tx
Platelet count below 10,000/ cu mm
after 8 weeks of therapy
Prolonged use of steroids w/ undesirable
effects (> 10-20mg/d for 3-6 months to
maintain platelet ct of >30,000/cu.mm
Provides permanent response (75-85%) in 1
week
Portal Hypertension
One of the most common findings with portal hypertension is
splenomegaly, as seen here. The spleen is enlarged from the
normal 300 grams or less to between 500 and 1000 gm.
Splenic Cyst
True cyst- lined by squamous epithelium
Primary true cyst
Small (<8cm) asymptomatic. Can be observed.
>8cm
w/
symptoms-partial
splenectomy,unroofing
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Parasitic cyst
Secondary to Echinococcus
Tx. by splenectomy after sterilization by NaCL or
silver nitrate
Pseudocyst
Secondary to trauma
Most are small (<4cm) and undergo spontaneous
resolution
Can be observed safely
Hodgkins Disease
Splenic Abcess
Hematogenous spread-most common cause
Most are solitary and unilocular
Treatment:
Solitary and unilocular--image guided percutaneaous
drainge+antibiotics
Multilocular---splenectomy+ antibiotics
Hodgkin's disease, liver involvement
Sarcoidosis
Non-caseating inflammatory granulomatous lesion
Second organ most commonly affected
Indications for splenectomy
Massive splenomegaly (>1kg)
Thrombocytopenia
Anemia
Compression of adjacent organ
pain
Splenic Tumor
Hemangiomas
Angiosarcoma
Associated with exposure to vinyl chloride or thorium
dioxide
Splenectomy Outcome
Appearance of Howell-Jolly bodies
Increased in platelet count
Increase in WBC count
Consider sepsis if
WBC ct > 15,000/cu.mm after 5 days
Platelet/WBC ratio of < 20
Pulmonary: left lobe atelectasis-the most common
complication
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