Bile, bile duct and

pancreatic disease
Dr. dr. Shahrul Rahman, Sp.PD, FINASIM

Departemen Ilmu Penyakit Dalam

Fakultas Kedokteran
Universitas Muhammadiyah Sumatera Utara
Cholecystitis
 What is it?
 By definition,
cholecystitis is an
inflammation of the
gallbladder wall and
nearby abdominal
lining.

Abdominal wall

Gallbladder
 Etiology / Pathophysiology
 Can be caused by an obstruction, gallstone or a
tumor.
 90% of all cases caused by gallstones.
 The exact cause of gallstone formation is unknown.

 When there is an obstruction, gallstone or

tumor it prevents bile from leaving the
gallbladder.
 Bile gets trapped and acts as an irritant which causes
cellular infiltration within 3 – 4 days.
 This infiltration causes an
inflammatory process – the
gallbladder becomes enlarged
and edematous.
 Eventually this
occlusion along with bile
stasis causes the mucosal
lining of the gallbladder
to become necrotic.
 Bacterial growth occurs
due to ischemia. Necrotic Gallbladder
  Rupture of the gallbladder becomes a danger, along with spread of
infection of the hepatic duct and liver.
 If the disease is severe and interferes with the blood supply it can cause
the gallbladder to become gangrenous.

Gangrenous
gallbladder Gallstones
 Gallstones . .
 The presence of
gallstones in the
gallbladder is called
cholelithiasis.
 Those who are most at risk.
 These are all adjectives to describe the person most at risk of developing
symptomatic gallstones.
 Fat, Fair, Female, Fertile, Fourty inaccurate, but reminder of the typical patient

FAIR FAT FORTY FEMALE

 Statistics

• About 3 million adults in the U.S. have gallstones

• Elderly, diabetics, obese patients, debilitated

patients  increased incidence of gallstones

• 90% of acute cholecystitis cases due to gallstones

 Background
• Aging is the most significant factor  higher
incidence of acute cholecystitis

• Acute Cholecystitis is the initial presentation

of symptomatic gallstones in 15% - 20% of
patients
 Clinical presentation-I:
 Symptoms:
 fever (70~95%)
 RUQ pain with tenderness (60~100%)
 nausea and vomiting (35~65%)
 abdominal pain (60~90%)
 Physical exam: vary with the severity
 right hypochondrial tenderness
 muscle guarding, rigidity, rebound tenderness
 some degree of fever
 tachycardia
 Murphy’s sign: variable
 Signs and Symptoms.
 Complaints of indigestion after
eating high fat foods.
 Localized pain in the right-upper
quadrant epigastric region.
 Anorexia, nausea, vomiting and
flatulence.

 Increased heart and respiratory rate –

causing patient to become diaphoretic
which in turn makes them think they are
having a heart attack.
Differential Diagnosis of RUQ pain
 Gallstone disease (and its related complications)
 Gastritis/duodenitis
 Peptic ulcer disease/perforated peptic ulcer
 Acute pancreatitis
 Right lower lobe pneumonia
 MI

 If presenting to A&E with RUQ pain all patients should get

 Blood tests
 AXR/E-CXR (to exclude perforation/pneumonia)
 ECG
 Signs and Symptoms.
 Low grade fever.
 Elevated leukocyte count.
 Mild jaundice.
 Stools that contain fat – steatorrhea.
 Clay colored stools caused by a lack of bile in
the intestinal tract.
 Urine may be dark amber- to tea-colored.
 Clinical presentation-II:
 Laboratory finding:
 ALT/AST: mildly raised
 alkaline phosphate: mildly elevated

 bilirubin: variable, may rise to 85 mol/l

 CBC/DC: elevated due to acute inflammation

 Acute Cholecystitis

• RUQ Pain
• Fever
• Leukocytosis

• Severe persistent pain

• +/- Jaundice
• Positive Murphy’s Sign
• Persistent cystic duct obstruction
• Pain lasts > 4 hours
• Usually fatty food ingestion  1 hr before pain
  Biliary Colic
 Acute Cholecystitis

• Distention and inflammation of the gallbladder

• Obstruction of cystic duct  Chemical
irritants in the bile
• Lysolecithin
• Prostaglandins
 Images studies-I
 Ultrasound: the most useful diagnosis tool
 gallbladder wall thickness>4 mm with an increase in its
volume (vesicular hydrop)
 sonographic Murphy’s sign

 biliary sludge in a tender thickened gallbladder but fail

to demostrate stones
 intramural gas, pericholecystic fluid or sloughed mucosa

 no intrahepatic or extrahepatic ducts dilatation

 color doppler scan to r/o ischemia condition

 Acute Cholecystitis

• Thickened gallbladder wall or edema

• Pericholecystic Fluid
• Sonographic Murphy’s Sign
 Management of Acute Cholecystitis
• Supportive care with IVFs, bowel rest, & Abx

• Almost half of patients have positive bile

cultures

• E. Coli is most common organism

• Antibiotic choice: Ampicillin + Aminoglycoside

or 3rd generation cephalosporin
OBSTRUCTIVE
JAUNDICE
 DEFITION OF JAUNDICE
 YELLOW DISCOLOURATION OF SKIN
AND MUCOUS MEMBRANE
Pathophysiologic classification of
Jaundice

 Hemolytic Jaundice

 Hepatic Jaundice

 Obstructive Jaundice(Cholestasis)
Jaundice classification

 predominantly unconjugated
hyperbilirubinaemia

 predominantly conjugated
hyperbilirubinaemia
 TYPES
HAEMOLYSIS

A PREHEPATIC

HEPATIC

POSTHEPATIC

OBSTRUCTIVE
OR SURGICAL
ANATOMY
 BILIRUBIN CYCLE
 BROKEN DOWN RED CELLS ARE
REMOVED BY R.E.S.
 HAEMOGLOBIN SPLITS INTO HAEM
&GLOBIN
 GLOBIN & CELL WALL PROTEIN GO
DOWN
TO AMINOACIDS
 THEY ENTER THE AMINO ACID POOL
 BILIRUBIN CYCLE
CONTINUE
HAEM SPLITS INTO IRON &
BILIRUBIN
[pigments]

IRON STORED AS FERRITIN FOR

REUSE
 BILIRUBIN IS NOT REUSED
[GOES TO THE LIVER]
 COMBINE WITH GLUCOURINC ACID

TO FORM THE CONJUGATED

[ DIRECT ]
BILIRUBIN [ WATER SOLUBLE ]
Van den Bergh reaction [DIRECT]

Alcohol added after van den Gergh [INDIRECT]

URINE IN OBSTRUCTIVE JAUNDICE
TEA COLOUR
CAUSES OF OBSTRUCTIVE
JAUNDICE
 1-STONES
 2-STRICTURES; [BENIGN]
 3-CA. HEAD OF THE PANCREASE
 4-CHOLANGIOCARCINOMA
 5-PERIAMPULLARY TUMOUR
 6-PRESSURE FROM OUTSIDE;L.N.,M.SYN.
 7-CHOLEDOCHAL CYST
 8-PARASITES; FILLING THE LUMEN
 CAUSES IN THE LUNEN
ASCARIS
CLONORCHIASIS PARASITES

HYDATID

PAPILLOMATOSIS

CHOLANGIOCARCINOM
A
STONE IS THE
COMMONEST
 IN THE WALL:STRICTURES

BENIGN STRICTURES

MALIGNANT STRICTURES
 OUTSIDE THE WALL
L.N. ANY MASS OUTSID

Stone in
cystic duct

MIRIZZI SYND

HARTMANN`S POUCH stone

HEAD OF THE PANCREASE

 BENIGN STRICTURES
 1-BILIARY ATRESIA
 2-IATROGENIC
BILIARY SURGERY
GASTRECTOMY
HEPATIC RESECTION
LIVER TRANSPLANT
 3-INFLAMMATORY;CHOLANGITIS , PANCREATITIS,
SCLEROSING
CHOLANANGITIS.
 4-TRAUMA
 5-IDIOPATHIC
 6-RADIOTHERAPY
 BILIARY ATRESIA

NORMAL BILIARY ATRESIA

 THE COMMONEST CAUSE
 STONE SLIPPING INTO THE BILIARY TREE
CHOLANGICARCINOMA
 SCLEROSING CHOLANGITIS
•Associated with U.Colitis in 70% of
cases
•May lead to malignancy
•Unknown aetiology
•Symptoms of cholangitis
•Treatment;Antibiotics
• Or liver transplant

Rosary beads ‫شكل المسبحة‬

 SIGNS
 LOSS OF Wt. IN MALIGNANCY
 TOXIC IN CHOLANGITIS,

[CHARCOT`S TRIAD,;PAIN, FEVER ,JAUNDICE]

 YELLOW DISCOLOURATION OF SKIN,M.M.

 TROISIER`S SIGN. VIRCHOW`S NODE

 TENDER R.U.Q.[IN CHOLANGITIS]

 COURVOISIER` LAW[IN CA.HEAD OF PAN.]

 ABDOMINAL MASS

 ASCITES [IN MALIGNANCY]

 INVESTIGATIONS
 C.B.C. DIFF., ESR.
 L.FT. *S.ALK.P.*
 PROTHROMBIN TIME
 S. AMYLASE
 K.F.T. ELECTRLYTES
 URINE ANALSIS * BILIRUBIN *
 STOOL ANALYSIS,;FAT,BLOOD.
 Obstructive Jaundice
Lab Findings
 Serum Bilirubin
 Feceal urobilinogen (incomplete obstruction)
 Feceal urobilinogen absence (complete
obstruction)
 urobilinogenuria is absent in complete
obstructive jaundice
 bilirubinuria 
 ALP 
 cholesterol 
 MANAGEMENT-1
 CORRECTION OF THE DERENGED
PARAMETRES
 ADMINISTRATION OF VITAMIN K
 ANTIBIOTICS
 MANNITOL PRE, INTRA and
POSTOPERATIVELY TO PREVENT
HEPATO-RENAL SHUTDOWN
 MANAGEMENT-2
 1. STONE-SPHINCTEROTOMY
 2.STONE-EXPLORATION OF C.B.D.
 3.STRICTURE-RESECTION ANASTOMOSIS FOR
SHORT STRICTURES
 4.STRICTURE-STENT FOR SHORT AND LONG
 5.CA.HEAD OF THE PANCREASE
=EARLY-WHIPPLE`S
OPERATION[PANCREATICO-DUODENECTOMY.
=LATE-BYPASS SURGERY[CHOLECYSTO-
JUJENOSTOMY
Pancreatitis
 PANCREATITIS
Pathophysiology :

 Premature activation of zymogens (digestive enzyme

precursors) within the acinar cells, duct system, or
interstitial space. This results in acinar cell damage
and necrosis, edema, and inflammation.
 Digest enzyme activation, impaired microcirculation
and release of cytokines (IL -1,TNF,NO ) contribute
to pancreatic injury and extra pancreatic
complications.
 Inflammatory beyond pancreas leads to local and
systemic complications.
 Acute Pancreatitis
 An acute inflammatory process of the P,may also
involve peripancreatic tissues and/or remote organ
systems.
 Mild and Severe
 Pathology : - Interstitial
- necrotic
 Majority of AP are mild and self-limiting (80%).
 20% of cases are acute severe pancreatitis (ASP),
often complicated by necrosis and infection leading
to multitude complications. -----SIRS.
Causes of Acute Pancreatitis:
 Biliary : Gallstones, microlithiasis, biliary sludge.
 Alcohol
 Anatomic variants (Pancreas divisum, choledochal cyst,etc).
 Mechanical obstructions to flow of pancreatic juice:
- Ampullary : tumors (b/m), stricture/dysf.SOD
- Ductal : stones, strictures, masses/tumors, mucus
(eg.idp mucinous neoplasms), parasites (ascaris).
- Metabolic : Hypercalcemia, Hypertriglyceridemia.
 Drugs.
 Toxins
 Trauma : Blunt and penetrating, Instrumentation
(ERCP,Biopsy P)
 Ischemia : hypotension, arteritis, embolic
 Hypotermia
 Infections
 Venoms (Spider)
 Autoimmune
 Genetic
 Idiopathic.
 Acute Pancreatitis due to Alcohol
 Alcohol abuse :
 Direct citotoxicity.
 Intracellular activation enzyme.
 Effect on sphincter papilla with
pathologic reflux of duodenal contents.
 Increase duct permeability and activation
of pancreatic enzyme.
 Alcohol increase viscosity of pancreatic
secretion rich in Ca and protein witch
block enzyme secretion.
 Acute Pancreatitis due to Gallstone
 Opie 1901 gallstone as cause of pancreatitis,
but 85 – 90 % of stone pass the papilla
spontaneously. However transient obstruction
with temporary impairment of sphincter
induces pancreatitis.

 Considered common bile duct join with

pancreatic duct less than 1 cm from papilla
induces refluks of bile to pancreatic duct.
 Etiology
Drug-induced pancreatitis:
 corticosteroids, estrogen-containing
contraceptives, azathioprine, thiazide
diuretics, and tetracyclines. Pancreatitis
associated with use of estrogens is usually
the result of drug-induced
hypertriglyceridemia.
 Clinical features
 Abdominal pain
 Nausea and vomiting
 Anorexia
 Tachycardia
 Fever
 Ileus
 Abdominal Tenderness
 Grey Turner’s sign
 Cullen’s sign.
Symptoms and signs:
Abdominal pain: The acute attach begins following
a large meal and consist of severe epigastric pain
that radiates through to the back, persistent with
vomiting and retching.
 Whole pancreas  belt  back

 Head right upper abdomenradiates to right

shoulder
 Body epigastric (middle upper abdomen)

 Body and tail left upperleft shoulder

Grey Turner’s Sign
Cullen’s Sign
 ACUTE PANCREATITIS
 Principle diagnosis :

 Clinically : Abdominal pain, nausea, fever, tachikardi

and vomitus.
 Morph. Lesion : Interstitial edematous and
necrotizing. Necrotizing become pancreatic
pseudocyst and pancreatic abscess.

 Recovery of function in 4 – 6 weeks and one half

with pancreatic insufficiency.
 Majority (80%) self limited, 20% are severe.
 Pancreatitis result acinar cell damage and impaired of
ductal permeability

 Inflammatory enhance vasc permeability, edema,

hemorhage.
 Activated kallikrein system and elevated enzyme
production witch in turn to further pancreatic damage.

 Two main etiology : Alcohol abuse and gallstone

( 80 – 90 % ). An other one virus, parasite, trauma
etc.
Diagnosis :
 Diagnosis of AP requires 2 of 3 features :
1. Characteristic abdominal pain.
2. Serum amylase and/or lipase ≥ 3 x unl.
3. Characteristic findings of AP on Abd.USG
and/or CT scan.
 Clinical prognostic scores :
1. Ranson’s Criteria :
2. APACHE II (Acute Phy and Chron.Health
Eval.
3. Hemorrhagic Peritoneal fluid.
4. - Clinical features.
- CRP > 150 mg/L in 72 h---correlate
pancreatic necrosis.
 Imaging classification.
 Laboratory Findings
 Serum amylase concentration: rises from 3-
12h, the peak is 24-48h and 2-5d normal
 Urine rises from 12-24h, slow decrease
 Elevated serum lipase
 Elevated hematocrit due to dehydration
 Low hematocrit due to blood loss
 Laboratory Findings
 Moderate leukocytosis
 In necrotic pancreatitis: sugar>11.1mmol/L,
calcium<2.0mmol/L, PaO2<8.0kPa, increased
BUN, acidosis and even MODS
 Abdominal puncture: bloody ascites,
increased amylase
Differential Diagnosis
 Inferior myocardial infarction/ischemia
 Symptomatic biliary stones,acute cholecystitis,
cholangitis.
 Peptic ulcer disease
 Mesenteric ischemia
 Small bowel obstruction
 Dissecting aortic aneurysm
 Macroamylasemia.
 Consider: MOF, SIRS.
 Management :

 Primary is symptomatic support, causative point such as

hormones inhibit pancreatic secretion so far failed.

 IV line to substitude of fluid in peripancreatic or

retroperitoneal up to 10 L.

 TPN ( amino acid, glucose and lipid ) required in

necrotizing within 72 hr.

 Total 30 – 40 kcal/kg/day with protein 1,5 g/kg.

 Therapy

 Remove offending agent (if possible)

 Supportive !!!
 #1- NPO (until pain free)
 NG suction for patients with ileus or emesis
 TPN may be needed

 #2- Aggressive volume repletion with IVF

 Keep an eye on fluid balance/sequestration and
electrolyte disturbances
Treatment strategies in Severe Acute Pancreatitis
 Resuscitation.
 Assess of severity with the aid scoring system
 Identification and early triage of SAP--ICU/HDU
 Early imaging in patients with SAP
 Identification and Treatment of etiology.
 Early introduction of enteral nutrition.
 Consider Antibiotics.
 Anticipation of complications with appropriate
interventions.
 Chronic Pancreatitis
 Chronic pancreatitis (CP) continued inflammation
with irreversible morphology changes :
fibrosis, ductal abnormality, calcification and
atrophy.

 Clinical features :
1. Epigastric pain, aggravated by meal and
improve by fasting. .
2. Steatorrhea, azotorrhea, diarrhea.
Progressive weight loss due to maldigestion
& Diabetes at advance.
 Pathophysiology :
 Alcohol abuse : Reduce bicarbonate and water
secretion. Increase viscosity, calcification and protein
plug.
 Genetic : Sensitive to alcohol cause of Lithostatin
deficiency as protection of calcification.
 Hyperparathyroid : Damage of acinar cell and intra
ductal stone formation.
 Recurrent exacerbation of acute pancreatitis :
fibrosis via growth factors ( TGFα, TGF ß ).
 Obstructive : Pancreatic divisum, cicatricial stenosis
of amp Vater, neoplasma etc.
 Complications :
- Pseudocyst > 6 weeks,
Obstr intra abd. viscera  ascites, rupture
haemorhage and infected.
- Pancreatic ascites, leakage of pseudocyst,
high amilase fluid.
- Pain due to high circulation lipase triggered
subcutaneus fat necrosis ( Cullen sign )
- Bilier obstruction due to inflammation and
swelling.
- splanchnic and mesenteric venous obstruction.
Etiology : varies with geographic discrepancies.

 Alcohol
 Biliary tract disease
 Hereditary factors
 Autoimmune disease
 Congenital pancreatic anomaly
 Hyperparathyroidism
 Idiopathic
 DIAGNOSE

 Straightforward in calcification in ductal

system ( Radiology, USG and CT scan )
 ERCP reveal dilatation of ductal and more
prominent in more severe case.

 Ductal system may reveal turtous main

containing stones, protein plugs or the
obstruction of common bile duct.
IMAGING
 Radiology : Calcification.
 USG : Pseudocyst, calcification.

 EUS : Cyst, PD dilatation and stone.

 CT scan : Enlargement , irregular contour,

calcification, pseudocyst.
 MRI, similar as CT, but superior in staging

of calcification process. .
 ERCP and MRCP : Invasive to detect and

therapeutic option.
Laboratory :

 Acute — serum amylase elevated.

 Blood glucose.
 CA-19-9 also increased (small). Significant
elevated in coexisting pancreatic cancer .
 Exocrine function test , low sensitivity.
 Management
 Alleviate pain, maintain adequate, reduces symptom :
steatorhea, diarrhea etc.

 Azotorrhea easily to reverse since protease is more

resistent to acid inactivation than lipase.
 Large dose of pancreatic extract, also reduce exocrine
output and relief the pain.
 Prepare enzyme enteric coat to pass gastric barrier.
To make sure concomitant PPI or H2bloker is needed
in overcome detrimental effect of acid.
 Treatment of pain.: Analgesics ( morphin ) etc.

 Intractable & severe pain — CT or EUS -

guided celiac nerve plexus blockage can be
applied.

 If pancreatic duct stricture or calculi----

endoscopic dilatation and stent placement.
 If all above measures ineffective----surgical
treatment.
 CONCLUSION :
ACUTE PANCREATITIS.
 Acute inflammation :

 - mild : oedematous pancreatitis

 - severe : necrotizing pancreatitis

 Mostly with severe pain

 Increased serum amylase and/or lipase

 Complete recovery (80%) or recovery with

sequelae/ transition to CP (20%)
 Chronic Pancreatitis
 Chronic inflammation of the exocrine pancreas
 Fibrosis with destruction of the parenchyma

 Often complicated course

 No recovery, mostly with progressive

functional impairment.