Kelainan Empedu

dan Pakreas
Oleh :
Yunia Annisa, dr, SpPD,
MKes
1

Pendahuluan
Tujuan :
Mahasiswa mampu memahami dan
menjelaskan serta melakukan diagnosis
dan penatalaksanaan terhadap penyakit
sistim digestive (empedu dan pankreas) :

Kolesistitis
Kolelitiasis
Pankreatitis
Tumor pankreas

Complications of Gallstones

KOLESISTITIS

Acute Cholecystitis
Pathogenesis:
Due to obstruction of cystic duct by
gallstone:
Cystic

duct blockage by gallstone

Obstruction to secretion of bile from gallbladder
Bile becomes concentrated
Chemical inflammation initially
Secondarily infected by organisms released by liver into
bile stream

USS confirms diagnosis (gallstones,

thickened gallbladder wall, pericholecystic fluid)

Acute Cholecystitis
Complications of acute cholecystitis

Empyema of gallbaldder
Gangrene of gallbladder (rare)
Perforation ofgallbaldder (rare)

Treatment

Admit for monitoring

Analgesia
Clear fluids initially, then build up oral intake as cholecystitis
settles
IVF
Antibiotics
95% settle with above management
If do not settle then for CT scan

Empyema percutaneous drainage

Gangrene/perforation with generalised peritonitis emergency
surgery

Obstructive Jaundice
Pathogenesis:
Stone obstructing CBD (bear in mind there are other
causes for obstructive jaundice) danger is progression to
ascending cholangitis.

USS

MRCP

Will confirm gallstones in the gallbladder

CBD dilatation i.e. >8mm (not always!)
May visualise stone in CBD (most often does not)
In cases where suspect stone in CBD but USS indeterminate
E.g.1 obstructive LFTs but USS shows no biliary dilatation
and no stone in CBD
E.g. 2 normal LFTS but USS shows biliary dilatation

ERCP

If confirmed stone in CBD on USS or MRCP proceed to ERCP

which will confirm this (diagnostic) and allow extraction of
stones and sphincterotomy (therepeutic)

Obstructive Jaundice
Treatment
Must unobstruct biliary tree with ERCP
to prevent progression to ascending
cholangitis
Whilst awaiting ERCP monitor for signs
of sepsis suggestive of cholangitis

Ascending Cholangitis
Pathogenesis:
Stone obstructing CBD with infection/pus proximal to the
blockage
Treatment
ABC
Fluid resuscitation (clear fuids and IVF, catheter)
Antibiotics (Augmentin)
HDU/ITU if unwell/septic shock
Pus must be drained* - this is done by decompressing the
biliary tree
Urgent ERCP
Urgent PTC if ERCP unavailable or unsuccesful

Gallstone ileus
Pathogenesis:
Gallstone causing small bowel
obstruction (usually obstructs in
terminal ileum)
Gallstone enters small bowel via
cholecysto-duodenal fistula (not
via CBD)
AXR dilated small bowel loops
May see stone if radio-opaque

Gallstone ileus
Treatment
NBM
Fluid resuscitation + catheter
NG tube
Analgesia
Surgery (will not settle with
conservative management)
enterotomy + removal of stone
Diagnosis of gallstone ileus usually made
at the time of surgery.

KOLELITIASIS

Background
Presence

of gallstones in the
gallbladder.
Spectrum ranges from asymptomatic,
colic, cholangitis, choledocholithiasis,
cholecystitis
Colic is a temporary blockage,
cholecystitis is inflammation from
obstruction of CBD or cystic duct,
cholangitis is infection of the biliary
tree.

Anatomy

Pathophysiology
Three types of stones, cholesterol,
pigment, mixed.
Formation of each types is caused by
crystallization of bile.
Cholesterol stones most common.
Bile consists of lethicin, bile acids,
phospholipids in a fine balance.
Impaired motility can predispose to
stones.

Pathophysiology
Sludge

is crystals without stones. It may

be a first step in stones, or be
independent of it.
Pigment stones (15%) are from calcium
bilirubinate. Diseases that increase RBC
destruction will cause these. Also in
cirrhotic patients, parasitic infections.

Frequency
Affected by race, ethnicity, sex, medical
conditions, fertility.
Every year 1-2% of people develop
them. Hispanics are at increased risk.
Internationally: 20% of women, 14% of
men. Patients over 60 prevalence was
12.9% for men, 22.4% for women.

Morbidity/Mortality
Every

year 1-3% of patients develop

symptoms.
Asymptomatic GS are not associated
with fatalities.
Morbidity and mortality is associated
only with symptomatic stones.

Race
Highest

in fair skinned people of

northern European descent and in
Hispanic populations.
High in Pima Indians (75% of elderly).
In addition Asians with stones are more
likely to have pigmented stones than
other populations.
African descent with Sickle Cell Anemia.

Sex
More

common in women. Etiology may be

secondary to variations in estrogen causing
increased cholesterol secretion, and
progesterone causing bile stasis.
Pregnant women more likely to have
symptoms.
Women with multiple pregnancies at higher
risk
Oral contraceptives, estrogen replacement tx.

Age
It

is uncommon for children to have

gallstones. If they do, its more likely that
they have congenital anomalies, biliary
anomalies, or hemolytic pigment stones.
Incidence of GS increases with age 1-3%
per year.

History
3

clinical stages: asymptomatic,

symptomatic, and with complications
(cholecystitis, cholangitis, CBD stones).
Most (60-80%) are asymptomatic
A history of epigastric pain with
radiation to shoulder may suggest it.
A detailed history of pattern and
characteristics of symptoms as well as
US make the diagnosis.

History
Most

patients develop symptoms before

complications.
Once symptoms occur, severe symptoms
develop in 3-9%, with complications in 1-3%
per year, and a cholecystectomy rate of 3-8%
per year.
Indigestion, bloating, fatty food intolerance
occur in similar frequencies in patients
without gallstones, and are not cured with
cholecystectomy.

History
Best

definition of colic is pain that is

severe in epigastrium or RUQ that last 15 hrs, often waking patient at night.
In classic cases pain is in the RUQ,
however visceral pain and GB wall
distension may be only in the epigastric
area.
Once peritoneum irritated, localizes to
RUQ. Small stones more symptomatic.

Physical
Vital

signs and physical findings in

asymptomatic cholelithiasis are
completely normal.
Fever, tachycardia, hypotension, alert
you to more serious infections, including
cholangitis, cholecystitis.
Murphys sign

Causes
Fair,

fat, female, fertile of course. (4F)

High fat diet
Obesity
Rapid weight loss, Ileal disease
Increases with age, alcoholism.
Diabetics have more complications.
Hemolytics

Differentials
Appendicitis
Cholangitis,

cholelithiasis
Diverticulitis
Gastroenteritis, hepatitis
IBD, MI
Pancreatitis, renal colic, pneumonia

Workup
Labs

with asymptomatic cholelithiasis and

biliary colic should all be normal.
WBC, elevated LFTS may be helpful in
diagnosis of acute cholecystitis, but normal
values do not rule it out.
Study by Singer et al examined utility of labs
with chole diagnosed with HIDA, and showed
no difference in WBC, AST,ALT Bili, and Alk
Phos, in patients diagnosed and those
without.

Workup
Elevated WBC is expected but not reliable.
In retrospective study, only 60% of patients
with cholecytitis had a WBC greater than
11,000. A WBC greater than 15,000 may
indicate perforation or gangrene.
ALT, AST, AP more suggestive of CBD stones
Amylase elevation may be GS pancreatitis.

Imaging Studies
US

and Hida best. Plain x-rays, CT scans

ERCP are adjuncts.
X-rays: 15% stones are radiopaque,
porcelain GB may be seen. Air in biliary
tree, emphysematous GB wall.
CT: for complications, ductal dilatation,
surrounding organs. Misses 20% of GS.
Get if diagnosis uncertain.

CT Scan

Plain Films

Imaging
Ultrasound

is 95% sensitive for stones,

80% specific for cholecystitis. It is 98%
sensitive and specific for simple stones.
Wall thickening (2-4mm) false positives!
Distension
Pericholecystic fluid, sonographic
Murphys.
Dilated CBD(7-8mm).

Ultrasound

Ultrasound

Imaging
Hida scan documents cystic duct patency.
94% sensitive, 85% specific
GB should be visualized in 30 min.
If GB visualized later it may point to
chronic cholecystitis.
CBD obstruction appears as non
visualization of small intestine.
False positives, high bilirubin.

(HIDA scan)
cholescintigraphy or Hepatobiliary
Imino-Diacetic Acid scan,

Imaging
ERCP

is diagnostic and therapeutic.

Provides radiographic and endoscopic
visualization of biliary tree.
Do when CBD dilated and elevated LFTs.
Complications include bleeding,
perforation, pancreatitis, cholangitis.

ERCP

Emergency Department Care

Suspect

GB colic in patients with RUQ

pain of less than 4-6h duration radiating
to back.
Consider acute cholecystits in those
with longer duration of pain, with or
without fever. Elderly and diabetics do
not tolerate delay in diagnosis and can
proceed to sepsis.

Emergency Department Care

After

assessment of ABCs, perform

standard IV, pulse oximetry, EKG, and
monitoring. Send labs while IV placed,
include cultures if febrile.
Primary goal of ED care is diagnosis of
acute cholecystitis with labs, US, and or
Hida. Once diagnosed, hospitalization
usually necessary. Some treated as OP.

Emergency Department Care

Replace

volume with IVF, NPO, +/- NGT.

Administer pain control early. A courtesy
call to surgery may give them time to
examine without narcotics.

Consults
Historically

cholecystits was operated on

emergently which increased mortality.
Surgical consult is appropriate, and
depending on the institution, either
medicine or surgery may admit the
patients for care.
Get GI involved early if suspect CBD
obstruction.

Medications
Anticholinergics

such as Bentyl
(dicyclomine hydrochloride)to decrease
GB and biliary tree tone. (20mg IM q46).
Demerol 25-75mg IV/IM q3
Antiemetics (phenergan, compazine).
Antibiotics (Zosyn 3.375g IV q6) need to
cover Ecoli(39%), Klebsiella(54%),
Enterobacter(34%), enterococci, group
D strep.

Further Inpatient Care

Cholecystectomy

can be performed
after the first 24-48h or after the
inflammation has subsided. Unstable
patients may need more urgent
interventions with ERCP, percutaneous
drainage, or cholecystectomy.
Lap chole very effective with few
complications (4%). 5% convert to open.
In acute setting up to 50% open.

Further Outpatient Care

Afebrile,

normal VS
Minimal pain and tenderness.
No markedly abnormal labs, normal
CBD, no pericholecystic fluid.
No underlying medical problems.
Next day follow-up visit.
Discharge on oral antibiotics, pain meds.

Complications
Cholangitis,

sepsis

Pancreatitis
Perforation

(10%)
GS ileus (mortality 20% as diagnosis
difficult).
Hepatitis
Choledocholithiasis

Prognosis
Uncomplicated

cholecystitis as a low

mortality.
Emphysematous GB mortality is 15%
Perforation of GB occurs in 3-15% with
up to 60% mortality.
Gangrenous GB 25% mortality.

PANKREATITI
S

Function

of the
pancreas is to
release proteolytic
enzymes that
assist in the
breaking down
food products so
that nutrients can
be absorbed.

Etiology and Pathophysiology

Pancreatic Ducts
become obstructed

Hypersecretion of the
exocrine
enzymes of pancreas
These enzymes enter the bile duct,
where they are activated and with
bile back up into the pancreatic
duct

Pancreatitis

Etiology and Pathophysiology

Trypsinogen-

(a proteolytic enzyme)

Normally released into the small intestine, where

it is activated to trypsin

In AP, activated to trypsin in the pancreas

causing autodigestion of pancreas

Progression of Disease
Autodigestion

Acute Inflammation of Pancreas

Necrosis of Pancreas
Digestion of vascular walls
Thrombus and Hemorrhage
Death

Precipitating Factors
Trauma
Use

of alcohol *
Biliary tract disease
Viral or Bacterial disease
Cholelithiasis *
Peptic Ulcer Disease

*most common causes

Clinical Manifestations
Severe

Abdominal pain is predominant symptom

Pain located in LUQ and mid-epigastrium

Commonly radiates to the back
Sudden onset
Severe, deep, piercing, steady
Aggravated by fatty meal or lying recumbent position
Not relieved by vomiting

Clinical
Manifestations
Cyanosis,

Dyspnea
Bowel sounds decreased or absent
Low-grade fever, Leukocytosis
Hypotension, Tachycardia
Jaundice
Flushing
Abnormal lung sounds - Crackles
Discoloration of abdominal wall Turners or
Cullens sign
SIGNS OF SHOCK

Diagnostic Studies
History

and physical examination

Laboratory tests

Serum amylasehallmark test

Serum lipase also elevated
Blood glucose
Serum calcium
Triglycerides

Diagnostic Studies
Flat

plate of abdomen
Abdominal/endoscopic ultrasound
Endoscopic retrograde
cholangiopancreatography (ERCP)
Chest x-ray
CT of pancreas
Magnetic resonance
cholangiopancreatography (MRCP)

Acute Pancreatitis

Can be a medical
emergency associated
with a risk for lifethreatening
complications

Acute Pancreatitis
Pathogenesis
Obstruction of pancreatic outflow

Pancreatic enzymes activated within pancreas

Pancreatic auto-digestion

USS: to confirm gallstones as cause of

pancreatitis
USS not good for visualising pancreas
CT: gold standard for assessing pancreas.
Performed if failing to settle with
conservative management to look for
complications such as pancreatic
necrosis

Acute Pancreatitis
Treatment
Analgesia
Fluid resuscitation
Pancreatic rest clear fluids initially
Identify underlying cause of pancreatitis
95% settle with above conservative
management
5% who do no settle or deteriorate need
CT scan to look for pancreatic necrosis

What do they die of?

Complications
Two

significant local complications

Pseudocyst

Abscess

Complications
Pseudocyst

Cavity surrounding outside of pancreas

filled with necrotic products and liquid
secretions
Abdominal pain
Palpable epigastric mass
Nausea, vomiting, and anorexia
Elevated serum amylase

Complications
Pancreatic

abscess

A large fluid-containing cavity within pancreas

Results from extensive necrosis
Upper abdominal pain
Abdominal mass
High fever
Leukocytosis

Complications
Main

systemic complications are?

Pulmonary
Cardiovascular
Electrolyte

imbalance Hypocalcemia

Goals of Care
Relief

of pain

Prevention

or alleviation of shock

Decrease respiratory failure

of pancreatic secretions

Maintain

Fluid/electrolyte balance

Treatment
1.

Pain management

IV morphine or Dilaudid

Antispasmodic agent
Bentyl
Pro-Banthine

Spasmolytics Nitroglycerine

Positioning sitting up and leaning forward

Why is it important to relieve pain?

Treatment
2. Prevention of Shock hemodynamic
stability
* Administer Blood, Plasma expanders,
Albumin
* LR solution

Treatment
3. Suppress pancreatic enzymes
* NPO
* NG suction
* Antacids, H2 receptor antagonists,
antispasmotics
4. Decrease respiratory distress
* Oxygen; check O2 saturation levels
* Semi-fowlers position, knees flexed,
position changes
* C, DB; incentive spirometer
5. Antibiotics

Treatment
6. Correction of electrolyte imbalance/
hypocalcemia
7.

Maintain Hydration / Nutrition

Treatment
Surgical

therapy if related to gallstones

ERCP
Endoscopic sphincterotomy
Laparoscopic cholecystectomy

Treatment Home Care

Follow up care
Dietary teaching

High-carbohydrate, low-fat diet

Abstinence from alcohol,

Patient/family teaching
* Signs of infection, high blood
glucose, steatorrhea

TUMOR
PANKREAS

2007 Estimated US Cancer Cases*

10th most common cancer Men

766,860

Prostate
29%
Lung & bronchus15%
Colon & rectum 10%
Urinary bladder 7%
Non-Hodgkin
4%
lymphoma
Melanoma of skin
4%
Kidney 4%
Leukemia 3%
Oral cavity 3%
Pancreas
2%
All Other Sites 19%

Women
678,060
26%
15%
11%
6%
4%
4%
4%
3%
3%
3%
21%

Breast
Lung & bronchus
Colon & rectum
Uterine corpus
Non-Hodgkin
lymphoma
Melanoma of skin
Thyroid
Ovary
Kidney
Leukemia
All Other Sites

*Excludes basal and squamous cell skin cancers and in situ carcinomas except urinary bladder.
Source: American Cancer Society, 2007.

2007 Estimated US Cancer Deaths*

4th leading cause of cancer death
Men

Lung & bronchus31%

289,550
Prostate
9%
Colon & rectum 9%
Pancreas
6%
Leukemia 4%
Liver & intrahepatic 4%
bile duct
Esophagus 4%
Urinary bladder 3%
Non-Hodgkin
3%
lymphoma
Kidney 3%
All other sites
24%

ONS=Other nervous system.

Source: American Cancer Society, 2007.

Women
270,100

26%
15%
10%
6%
6%
4%
3%
3%
2%
2%
23%

Lung & bronchus

Breast
Colon & rectum
Pancreas
Ovary
Leukemia
Non-Hodgkin
lymphoma
Uterine corpus
Brain/ONS
Liver & intrahepat
bile duct
All other sites

JP Hoffman ASCO 2006

Poor Survival
AJCC Stage

Median Survival

Resectable (I-II)

14-25months

Locally Advanced (II)

8-15 months

Metastatic (IV)

3-7 months

Risk Factors
Smoking
Age, gender
Obesity
Diet high fat, low fibre
Chronic pancreatitis
Family history BRCA2
-napthylamine

Clinical Presentation

Painless obstructive jaundice (pancreatic head

tumors -2/3)
Abdominal pain
Anorexia, weight loss
Trousseaus sign
Depression
diabetes

Sites of Metastasis
Liver
Peritoneum
Lung
Adrenal
Bone
Rarely

CNS

Pancreatic Epithelial
Malignancies
Malignant

Ductal adenocarcinoma (majority)

Mucinous cystadenocarcinoma
Acinar cell carcinoma
Small cell carcinoma

Uncertain

malignant potential

Mucinous cystadenoma
Solid and cystic papillary neoplams

Ductal Adenocarcinoma
Nuclear atypia
Significant fibrosis

Treatment Approach

Patient Workup
Birphasic

CT
ERCP + stent + /- biopsy
PET scan for possible resection

Surgical Resectability
No

evidence of extra-pancreatic disease

Liver
Retroperitoneum
Peritoneal disease

No

evidence of SMA, hepatic or celiac

encasement (>180 degrees)
Fewer than 20% are surgical candidates

Post Surgical Therapy

No

standard of care for adjuvant therapy

European standard
Chemotherapy alone
US standard
chemoradiotherapy

Treatment Approach

Palliation of Pancreatic Cancer

Pain

management eg nerve block

Obstructive jaundice

Percutaneous drain versus internal stent

Metal versus plastic

Thromboembolism

up to 20%

Depression
Fatigue,

anorexia, weight loss

Complication

History

Examination

Blood tests

Biliary Colic

- Intermittent RUQ/epigastric
pain (minutes/hours) into
back or right shoulder
- N&V

-Tender RUQ
-No peritonism
-Murphys
-Apyrexial, HR and BP (N)

-WCC (N) CRP (N)

- LFT (N)

Acute Cholecystitis

-Constant RUQ pain into

back or right shoulder
-N&V
-Feverish

-Tender RUQ
-Periotnism RUQ
(guarding/rebound)
-Murphys +
-Pyrexia, HR ()

-WCC and CRP ()

-LFT (N or mildly ()

Empyema

-Constant RUQ pain into

back or right shoulder
-N&V
-Feverish

-Tender RUQ
-Peritonism RUQ
-Murphys +
-Pyrexia, HR (), BP ( or )
-More septic than acute
cholecystitis

-WCC and CRP ()

-LFT (N or mildly ()

Obstructive Jaundice

-Yellow discolouration
-Pale stool, dark urine
-painless or assocaited with
mild RUQ pain

-Jaundiced
-Non-tender or minimally
tender RUQ
-No peritonism
-Murphys
-Apyrexial, HR and BP (N)

-WCC and CRP (N)

-LFT: obstructive pattern
bili (), ALP (), GGT (),
ALT/AST ()
-INR ( or )

Ascending Cholangitis

Becks triad
-RUQ pain (constant)
-Jaundice
-Rigors

-Jaundiced
-Tender RUQ
-Peritonism RUQ
-Spiking high pyrexia (38-39)
-HR (), BP ( or )
-Can develop septic shock

-WCC and CRP ()

-LFT : obstructive pattern
bili (), ALP (), GGT (),
ALT/AST ()
-INR ( or )

Acute Pancreatitis

-Severe upper abdominal

pain (constant) into back
-Profuse vomiting

-Tender upper abdomen

-Upper abdominal or
generalised peritonism
-Usually apyrexial, HR (), BP
( or )

-WCC and CRP ()

-LFT: (N) if passed stone or
obstructive pattern ifstone
still in CBD
-Amylase ()
-INR/APTT (N) or () if DIC

Gallstone Ileus

- 4 cardinal features of SBO

-distended tympanic abdomen

-hyperactive/tinkling bowel
sounds

91

Daftar pustaka
Buku

Ajar penyakit Dalam Edisi 6.

Jakarta. Pusat penerbitan Departemen
Ilmu Penyakit Dalam
Harrissons Principles of Internal
medicine, Edisi ke 18. McGraw-Hill

92

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