Transcript Pancreas

Pancreas
Tail
Body
Head
Uncinate process
Neck
Pancreas

Exocrine





Acinar cells
Spontaneous secretion is minimal
Secretin – evokes bicarbonate-rich fluid secretion
Cholecystokinin (pancreozymin) – evokes pancreatic enzymes
secretion
Endocrine





Islet cells
B cells – insulin
A cells – glucagon
D cells – somatostatin
Pancreatic polypeptide cells
Pancreatitis

Acute pancreatitis
Mild
 Severe


Chronic pancreatitis
Atlanta Definitions

Acute Pancreatitis


Mild Acute Pancreatitis


Acute inflammatory process of the pancreas, with variable involvement
of other regional tissues or remote organs systems
Pancreatitis associate with minimal organ dysfunction and an uneventful
recovery. The predominant feature is interstitial oedema of the gland
Severe Acute Pancreatitis

It is associate with organ failure and /or local complication such as
necrosis ( with infection) pseudocyst or abscess. Most often this is an
expression of the development of pancreatic necrosis although patients
with oedematous pancreatitis may manifest clinical features of severe
attack
Acute Pancreatitis
Acute pancreatitis

Etiology



Gallstones
ETOH
Iatrogenic


Drugs



Cytomegalovirus, ascariasis, scropion venom, mumps, viral hepatitis
Trauma
Anatomical anomalies


Steroid, furosemide, thiazide diuretics, azathioprine
Infection


ERCP
Pancreatic Divisum
Genetic



Familial pancreatitis
Cystic fibrosis
Alpha-antitrypsin deficiency (risk for ca pancreas)
Pancreatic Divisum




Malunion of the pancreatic ducts from the ventral and
dorsal buds of the pancreas…. Results in complete or
partial separation of the duct systems of Wirsung
(main – dorsal) and Santorini (accessory – ventral)
0.3 – 5.8% endoscopy series
5 - 14% autopsy studies
Prone to pancreatitis due to poor outflow of the
accessory duct system

But majority of the patients with pancreatic divisum don’t
have any association with acute pancreatitsi
Pathogenesis – molecular biology

Premature activation: intracellular zymogens
Nuclear factor (Kappa) B
 Activator Protein 1
 Cytokines, Chemokines


Pathological Calcium influx


Gap junction disruption – ETOH
Neurally mediated inflammation

Substance P
Acute pancreatitis


Symptoms
Acute Vs Chronic



History / X ray / CT scans / Pancreatic duct assessment (ERCP / MRCP)
Etiology factors
Complications









MOF / ARDS / SIRS → ICU
Infective necrosis → Operation
Pseudocyst
Splenic vein / portal vein thrombosis → varices / cirrhosis
Endocrine insufficiency DM, absorption
Chronic pancreatitis
Ductal strictures
Pancreatic Malignant Neoplasm
Cardio / Respiratory / Renal / Vascular complications
Acute pancreatitis





Rapid progressive onset of pain
Upper abdominal pain - T G R, may mimic any acute
abdominal conditions
AXR - sentinel loop, calcification, gallstones
CXR – right pleural effusion (reactive sympathetic effusion) 20%
Cullen sign (Thomas Stephen Cullen – Prof of Gynaecology. John Hopkins
Uni)



Grey turner sign (George Grey Turner – Prof of Surgery. London)
Amylase
Lipase
Multifactorial Scoring System





To predict the prognosis
Positive predictive value 50%
Ranson’s
Glasgow
Apache II

12 routinely measured physiological and biochemical
parameters, couple with a score for age and preexisting health status
Ranson’s Criteria







Biliary
Age >70
WCC >16
Glucose >12
LDH >400
AST >250

BUN >0.7
HCT↓10%
Ca <2.0
BE <-5
Oxygen < 60mmHg
Fluid >6 liters






Non biliary
Age >55
WCC >16
Glucose >11
LDH >350
AST >250
BUN >1.8
HCT ↓ 10%
Ca <2.0
BE <-4
Oxygen <60mmHg
Fluid >6 liters
Glasgow Score





Age >55
WCC > 15
Urea > 16
PaO2 < 60mmHg
Glucose >10




LDH > 600
AST / ALT > 600
Ca < 2
Albumin < 22
Assessment

Apache II scoring system
>9 severe attack
 >6, 95% will have complications


C-reactive protein
36 hours after onset of illness
 >210 mgI-1 first 4 days
 >120 mgI-1 at end of first week



CT severity index / MRI
MOF
CT abdomen of Necrotising Pancreatitis
MOF






Respiratory
Neurocerebral
Cardiovascular
Haematological
Renal
Hepatobiliary / Gastointestinal
Bernard MOF scoring system: This scoring system does not include hepatic index
Management

Etiology factor


Early ERCP
Supportive

Organs specific






Ventilation / haemofiltration /
inotropes
Early Intensive support
Nutrition – early jejunal feeding / TPN
Octreotide / Somatostatin
Anticytokines therapy / Anti-inflammatory
agents
Gut selective Decontamination – prevent
translocation of bacteria : SIRS

Management of
Complications:



Antibiotic
Surgery – infective necrosis
Radiological guided
drainage – intraperitoneal abscess
/collection
Nutrition

Enteral feeding
Jejunostomy feeding
 Nutritional support
 Prevent translocation of GI bacteria


TPN

Only if gut not usable
Surgery

Infective necrosis






Clinical / microbiological confirmation
Uncontrolled sepsis
Secondary complications


Indications
Pseudoaneurysm
Intestinal obstruction
Perforation of bowel (ERCP)
Cholecystectomy
Late complications consider surgery when applicable



Pseudocyst
Pancreatic duct stricture / stenosis
Pancreatic ductal stones
Chronic Pancreatitis

Continuing inflammatory disease of the
pancreas characterized by irreversible
morphological change typically causing pain and
/ or permanent loss of pancreatic function
Chronic Pancreatitis - diagnosis




History / Examination
Radiological
Histopathological
Functional deficits
•Malabsorption
•DM
•Sudan staining of stool
72hrs stool collection with diet containing
100g fat per day, if more than 7g per day
excretion is abnormal
•Faecal trypsin / chymotrypsin
•Lundh test – direct duodenal aspiration
•Secretin-pancreozymin test
•Bentiromide test - Enzyme reaction
X Rays
CT- sensitivity 75-90%; specificity 85100% (pancreatic calcification)
degree of calcification does not correlate
with the degree of exocrine insufficiency
MRCP, ERCP
MRI
Histopathological changes:
Parenchymal fibrosis, ductal stricture,
atrophy of acinar and islet cells
•Calcific pancreatitis - alcohol
fibrosis, calcification, and protein plugging
•Obstructive Pancreatitis - stones/Carcinoma
dilatation, acinar atrophy and fibrosis
•Inflammatory Pancreatitis
autoimmune disease (Idopahtic, Sjogren
syndrome & Sclerosing Cholangitis)
Chronic Pancreatitis
Severity


No agreeable assessment method to determine
the severity of chronic pancreatitis
Based on the level of pancreatic dysfunction and
symptoms


Again clinical history and assessment
Radiological assessment for any ductal
disruption
Chronic Pancreatitis

Cambridge Classification

According to ductal anomaly
Level of disease
Main duct
Side branches
Mild
Normal
<3 affected
Moderate
Mildly affected
>3 affected
Severe
Gross disease
Gross disease
Chronic Pancreatitis: etiology







ETOH 70%
Anatomical – pancreatic divisum, ductal stricture
Genetic – cystic fibrosis,  antitrypsin deficiency
Hypercalcaemia
•Decrease HCO3 and
increase protein production,
Tropical pancreatitis
increase viscosity lead to
stone formation
Nutritional pancreatitis
•Acinar cell damage
•Repeat attack lead to fat
Idiopathic Chronic Pancreatitis
necrosis, with interlobular


Early onset <35 yo – poor prognosis
Late onset >45 yo
fibrosis
•Liver impairment lead to
failure to detoxify toxic
substance causing direct
damage to the pancreas
Chronic Pancreatitis

Clinical features:
Multiple somatic / psychosocial symptoms
 Endocrine / exocrine dysfunction
 Burn out syndrome



Usually 15-20 years after onset of illness
Malignancy
Chronic Pancreatitis
Management

Manage symptoms




Endocrine / exocrine function




Pain control – med / thoracoscopic splanchniectomy
Psychosocial support
ETOH
Pancreatic enzyme replacement : PPI
DM control
Malnutrition
Malignancy - investigate if indicated
Chronic Pancreatitis

Other complicatons
Pseudocyst
 Splenic vein thrombosis


Hypersplenism / GIB – require splenectomy
Mesenteric / Portal vein thrombosis
 Pancreatic ductal deformity / stones
 Pancreatic ascites / pleural effusion

Chronic Pancreatitis
Surgery Indications

For focal disease / ductal anomaly




Bypass: pancreaticojejunostomy (Puestow procedure) duct >7mm
Distal Pancreatectomy
Whipple procedure
For pain



If head is > 3cm in size
Bypass surgery – eg Puestow procedure
For suspected malignancy


Distal
Pancreatectomy
Thoracoscopic splanchniectomy
Frey’s operation – Bypass with resection of pancreatic head


Whipple
Laparoscopy
Laparotomy
Chronic Pancreatitis
Management

Conservative





Symptoms
Malnutrition
Endocrine dysfunction
Education
Psychosocial support


ETOH
Depression

Invasive procedure



ERCP
Surgery
Malignancy
Pseudocyst


Collection of pancreatic juice enclosed in a wall of
fibrous or granulation tissue that arises following an
attack of severe pancreatitis.
Acute fluid collection:


Early in the course of acute pancreatitis and is located in or
near the pancreas. The wall is ill defined.
Pancreatic cystic neoplasm:

Cystic lesion lined by epithelium, can be either benign or
malignant in nature
Pseudocyst



4 to 5 weeks after onset of acute pancreatitis
40-60% Spontaneous resolution 6 weeks
> 6 weeks, risk of complication increase

Intervention
Surgical drainage – Open / Laparoscopic
 Endoscopic drainage

Pseudocyst

Adequate assessment of pancreatic duct
Stricture / stones / morphology
 Communication with cyst


Position of cyst in relation to other organs
Cystojejunostomy
Stomach
Cystogastrostomy
Stenting if communicate with PD
Psuedocyst

Complications



Bleeding
Abscess
Percutaneous Drainage
Suspect Malignancy if atypical history or morphology

Suspect malignancy if







Septum / complex architecture
Solid component
Invasion of surrounding structures / metastatic lesion
Raised tumor marker
Lack of amylase in fluid aspirated from the cyst
Other solid lesions in pancreas
No previous history of pancreatitis / trauma
Carcinoma of pancreas
Pancreatic Carcinoma






Weight loss
Pain
Malnutrition
Jaundice
Anorexia
Pruritus
90%
75%
75%
70%
60%
40%




Courvoisier’s sign
Diabetes mellitus
Ascites
GOO

33%
15%
5%
5%
Gastric outlet obstruction
Carcinoma of Pancreas
Symptom and management depends on the location of the tumor
Head of pancreas usually have better prognosis since their symptoms usually
present earlier then tumor located at the body or tail of pancreas
Usually asymptomatic until late in advance stage
May present earlier with obstructive jaundice, duodenal ulceration etc…
Pancreatic Carcinoma






Etiology uncertain
Cigarette Smoking
Diabetes – long standing
Chronic pancreatitis - Amount of risk ?
Familial predispoistion 5-8%
Coffee / alcohol / organic solvents / petroleum
Pancreatic Neoplasms

Ductal Epithelium







Ductal cell AdenoCa
Giant cell Ca
Adenosquamous Ca
Mucinous Ca
MicroadenoCa
Mucinous CystadenoCa
Acinar cells



Acinar cell Ca
Acinar CystadenoCa
Pancreatoblastoma

Non Epithelial Tissue





Uncertain Histogenesis


Fibrosarcoma
Leiomyosarcoma
Histocytoma
Lymphoma
Papillary cystic neoplasm
NeuroEndocrine tumors





Hypervascular tumor
Gastrinoma
Insulinoma
Vasoactive Intestinal
Polypeptidoma
Glucagonoma
Pancreatic carcinoma


Aim of management
Assess resectability
Curative Mx
 Palliative Mx
•Absence of extrapancreatic disease
•Absence of vascular involvement


Clinical & Radiological Staging
(i) Resectable
 (ii) Non resectable
 (iii) Metastatic disease

Pancreatic carcinoma

Ultrasound abdomen



CT abdomen & thorax
ERCP - 97% will have abnormality





Long irregular stricture
Double duct sign
Brush cytology only 40-50% positive
Endoscopic Ultrasonography
EUS - FNAC


Double duct sign
Negative result does not rule out malignancy
Angiogram


When CT show possible vascular involvement in an otherwise resectable disease
Possible aberrant vascular anomaly
Pancreatic Carcinoma
Type of surgery performed will depends on the location and involvement of the tumor
•Whipple operation
•Pylorus preserving Whipple
•Gastric stasis in early post op period
•Not for bulky tumor – inferior tumor clearance
Distal
pancreatectomy +/- splenectomy
Carcinoma of tail of pancreas invade spleen
Pancreatic carcinoma




Palliative Mx – pain control
ChemoIrradiation
Biliary obstruction
Gastric outlet obstruction
•Endoscopic stenting – plastic / metallic
•Surgical bypass
•Double bypass (gastric + biliary)
•Gastric – gastrojejunostomy
•Biliary –
•Choledochojejunostomy
•Choledochoduodenostomy
Pancreatic carcinoma

High index of clinical suspicion


Little clinical sign, non specific symptoms
Especially differentiating between pseudocyst and cystic
neoplasm



History
Radiological features
Nature / Biochemistry of aspirated content


Amylase, tumor marker, cytology etc…
Tumor marker



CA 19.9 most specific, volume related
CA 125
CEA