HPB

lecture
Tomy Lesmana
Departement of Surgery
Airlangga University – Soetomo General Hospital
What I’m going to talk What you going to do
• The liver diseases • Asking whatever and whenever
• Liver abscess • Read the source books
• Neoplasm
• The biliary-tract diseases
• Stone
• Infection
• Cyst
• The pancreas disease
• Infection
• Neoplasm
Liver Abscess
Liver Abscess
Classification:
• PYOGENIC
• Aerobic:
• E.coli - most common
• Klebsiella pneumonia : associated with gas forming abscess
• Others: Pseudomonas aerogenosa, Morganella morganii, Serratia marsecens, etc.
• Anaerobic:
• Bacteroides fragilis - most common
• Others: Fusobacterium spp., anaerobic Streptococci, Clostridium spp., Actinomyces spp.
• 40% polymicrobial, 40% monomicrobial, 20% culture-negative
• AMEBIC : Entamoeba histolytica
• CANDIDA
• TB (rare)
Risk Factor
Increased risk of developing Liver Abscess
• Diabetes mellitus
• Liver cirrhosis
• Immune-compromised state
• Use of PPI
• Advanced age
• Male gender
 Demographic and clinical
features

S. Lodhi et al. Features distinguishing amoebic from pyogenic

liver abscess: a review of 577 adult cases . Tropical Medicine
and International Health 2004;9(6):718-723
Routes of Infection
1.Biliary tree:
biliary obstruction and bile stasis à bacterial colonization (=ascending suppurative cholangitis)
1. Asia: intrahepatic stone – reccurent pyogenic cholangitis
2. Western: malignant obstruction
Other factor: Caroli disease, biliary Ascaris infection, biliary tract surgery (biliary enteric anastomosis)
2.Portal Vein
• Infection of Gitract à ascending portal vein infection (pyelophlebitis)
• Cause of pyelophlebitis: diverticulitis, appendicitis, pancreatitis, IBD, PID, perforated viscus, omphalitis(newborn), CRC
malignancy
3.Hepatic artery
• Any systemic infection (endocarditis, pneumonia, osteomyelitis, sepsis)
• Reflect an altered immune response (malignancy, AIDS, disorders of granulocyte function)
4.Direc extension of nearby focus of infection
• Cholecystitis, subphrenic abscess, perinephric abscess, intestine perforation
5.Trauma
• Blunt or penetrating
• Iatrogenic necrosis: hepatic artery embolization, RFA
6.Cryptogenic (unknown)
• From undiagnosedbiliary/intestinal pathology
• Should evaluating endoscopy, colonoscopy, ERCP
 Sign and Symptoms
Malaise 89% Jaundice 19%–21%
Chills 69% Ascites 18%–21%
Fever 59%–90% Murphy’s sign 16%
Tachycardia 52% Hepatomegaly 16%–52%
Nausea 43%–68% Guarding 14%
Abdominal pain 39%–84% Respiratory distress 13%
Vomiting 30%–32% Hypotension 13%–30%
Right pleural effusion 28% Diarrhea 11%
Weight loss 26% Anorexia 11%
Mavilia M.G. et al: Evolving nature of hepatic abscess. J Clin Transl Hepatol 2016; 4: 158–168
PLA
• Classic symptoms: fever, jaundice, RUQ abd.pain: 10%
• Taiwan study (n=133)
• Fever : 96%
• Chills : 80%
• Abdominal pain:53%
• Jaundice :20%
• Maise, vomiting
• Dyspnea/cough: diaphragm involvement
• Duration: acute to chronic (months)
• Acute: identifiable abdominal pathology
• Chronic: cryptogenic cause
• Endogenous endophthalmitis (3%): specific to Klebsiella hepatic abscesses
PLA
• Physical Exam
• Fever
• RUQ tenderness :40-70%
• Jaundice :25%, often secondary to underlying biliary disease
• Hepatomegaly : 50%
• Chest abnormality : 25%

• Blood Test
• Leukocytosis :70-90%
• Anemia : common
• ALP elevation (mild) : 80%
• Total bilirubin elevation : 20-50%
• Transaminases elevation : 60%
• Hypoalbuminemia and prothrombin time elevation: reflect chronicity

• Blood cultures positive in 50-60% cases

• Immunosuppressed patients à HIV?
ALA
• Symptoms and Sign • Laboratory test
• Abdominal pain : 92% • Stool cyst/trophozoites :12%
• Fever : 90% • Amoebae in aspirate : 42%
• Abd.tenderness : 78% • ALP>120U/L :76%
• Hepatomegaly : 62% • Enzime Immuno Assays
• Anorexia : 47% IHA = Indirect haemagglutination assay
• Weight loss : 39% • Sensitivity 99%
• Specificity >90%
• Diarrhea : 23%
• Jaundice : 22%
Distinguishing amebic from
pyogenic liver abscess

S. Lodhi et al. Features distinguishing amoebic from pyogenic

liver abscess: a review of 577 adult cases . Tropical Medicine
and International Health 2004;9(6):718-723
 Laboratory and radiographic
features

S. Lodhi et al. Features distinguishing amoebic from pyogenic

liver abscess: a review of 577 adult cases . Tropical Medicine
IHA; Indirect haemagglutination assay

and International Health 2004;9(6):718-723

Chest X-Ray
• Right pleural effusion
• Elevated right diaphragm
• Atelectasis
USG
• As a preeliminary screen
• Sensitivity: 80-95%
• Differentiating cystic from solid lesion
• Diagnosis of gall stone
Abdominal Contras Enhanced CT
Sensitivity: 95-100%

PLA “cluster” appearance

ALA: large, lobulated, well-defined cystic mass
peripheral enhancing rim
Honeycomb app
 MRI

T2-wighted, : hyperintense T1-wighted, : hyperintense Contrast T1-wighted, :

absces cavities absces cavities peripheral rim enhancement

Inable to be used for image-guided diagnosis and therapy

 PYOGENIC HEPATIC ABCESS

Clinical suspicion

Empiric Broadspectrum Antibiotics

Computer topography, diagnostic aspiration

Intraabdominal source?

No Yes

Surgical Drainage Identify

Solitary or few, large Multiple small
and Treat Source
abscesess abscesess

Percutaneous Drainage and Treatment Failure

Antibiotics alone
Antibiotics

Identify and Treat Source

TREATMENT ALGORITHM FOR PATIENTS WITH PYOGENIC HEPATIC ABSCESS

 AMEBIC ABSCESS

Clinical suspicion

Computer Tomography

Indirect hemagglutination assay

Oral Antiamebicidal therapy

No additional Rx for
uncomplicated abscess Large, high risk, Rupture
suspeninfected, or
unresponsive abscess

Percutaneous Drainage Surgical Drainage

TREATMENT ALGORITHM FOR PATIENTS WITH AMEBIC ABSCESS

Antibiotics Treatment – Pyogenic
• Blood and aspiration: aerobic and anaerobic cultures
• Broad spectrum:
• Synthetic penicillin-Aminoglycoside/3rdgen cephalosporin+Meronidazole
• Aminoglycoside toxicity: aztreonam,imipenem
• Penicillin allergy-imipenem
• Duration of treatment must beindividualised
• IV antibiotics for 2 weeks (Schwartz:8 weeks)
• Oral antibiotics for 1 month
• Multiple abscesses can require up to 12 weeks oftherapy
• Both the clinical and radiographic progress of the patient should guide the
length of therapy
Antibiotics Treatment – Amoebic
• Metronidazole 3x750mg orally/i.v. – 4 days
• If response, continue for 10 days
• Followed by luminal agents:
• Iodoquinol 3x650mg – 20 days
• Paramomycin 3x500mg – 10 days
• Diloxanide furoate
• If no response:
• Dihydroemetine 4x1.5mg/Kg i.m. – 5 days +
• Chloroquine phosphate 4x600mg orally – 2 days, then 4x300mg
• If no response to medical treatment: Percutaneous drainage
Invasive Treatment
• Percutaneus aspiration: success rates 69-90%
• Drain placement
• Without drain: need >1 time
Indication
• Deterioration in clinical condition despite adequate
treatment
• Abscess with high risk of rupture
• left liver >5cm

• Surgical drainage (open/laparoscopic)

• Impending rupture
• Inadequate catheter drainage
 Solid Benign Neoplasms
• Cavernous Hemangioma
• Focal Nodular Hyperplasia
• Liver Cell Adenoma
Solid Malignant Neoplasms
Liver Neoplasma • Primary
• HCC
• Hepatoblastoma
• Intrahepatic
cholangiocarcinoma
• Metastasis
• Focal nodular hyperplasia
(FNH)
• hypervascular on arterial
phase
• isodense on venous phase
• has a central scar
• Adenoma is hypovascular
• Hemangioma
• asymmetrical peripheral
enhancement
Hepato Cellular Carcinoma
Diagnosis
Lack of symptoms in early stages

Most common presentation:

• Men 50 to 60 years of age who complain of right upper quadrant
abdominal pain and weight loss and have a palpable mass.
• Hepatic decompensation due to chirrosis
Surveillance
Surveillance
• Patients at Risk
• HBV infection: (>10 to 20 cases/100,000) in South- east Asia and tropical Africa
• HCV infection
• Obese, NAFLD, NASH, chronic alcohol abuse, tobacco smoking
• Cirrhosis
• Not all patients with cirrhosis are at equal risk for HCC, and HCC is not always found in patients with cirrhosis
• 70-90% HCC is Cirrhosis
• Annual conversion rate to HCC is 2-6%
• Grains, peanuts, and food products in tropical and subtropical regions :Aflatoxin, produced by
Aspergillus spp
• Male sex (2-8X female)
• Older age
• Persistent increase in alanine aminotransferase (ALT) level / progressive impairment of liver
function / increased a-fetoprotein (AFP) level
Bruix J, et al. Evidence-Based Diagnosis, Staging, and Treatment of Patients With Hepatocellular Carcinoma. Gastroenterology 2016;150:835–853
2010-2016: 8 HCC guidelines

Yu SJ, A concise review of updated guidelines regarding the management of hepatocellular carcinoma around the world: 2010-2016 2016. Clin Mol Hepatol 2016;22:7-17
Surveillance
• Ultrasonography (US)
• Radiographic methodology of choice for HCC surveillance,
• Sensitivity 94%
• Specificity >90%
± Serum α -fetoprotein (AFP)
• Not recommended for surveylance by AASLD, EASL-EORTC, and ESMO-ESDO
• Normal in up to 35% of small HCC – sensitivity for HCC 60%
• AFP+US: additional detection in 6-8% of cases not previously visualized by US

• Interval:Except NCCN guideline (6-12 months), many guidelines have adopted an interval of 6
months based on available data on mean HCC doubling time
Yu SJ, A concise review of updated guidelines regarding the management of hepatocellular carcinoma around the world: 2010-2016 2016. Clin Mol Hepatol 2016;22:7-17
Diagnosis
2 types of diagnostic algorithms in the 8 guidelines
1. Size-based diagnostic algorithms
• When a nodule is identified, definitive diagnosis will be made with a nodule
diameter of <1 cm, 1-2 cm and >2 cm
• Recommended by 5/8 guidelines (KLCSG-NCC, JSH, EASL-EORTC, AASLD, and
NCCN)
2. Non size-based diagnostic algorithms
• Diagnosed with characteristic findings on dynamic CT or dynamic MRI (i.e.
Hypervascularity in the arterial phase and washout in the portal venous or
delayed phase) regardless of tumor size
• Recommended by 3/8 guidelines (APASL and ESMO-ESDO, and ACG)
Non-invasive diagnosis
• Four-phase multidetector computed tomography (MDCT)
• Contrast-enhanced dynamic MRI using extracellular contrast agents

The diagnostic criteria:

arterial phase hypervascularity and venous or delayed phase wash-out
Pathological diagnosis
• Recommended by all 8 guidelines if imaging diagnosis does not
disclose characteristic features of HCC

• Until now, no outcome studies have been performed to show that

survival is prolonged by a biopsy of indeterminate nodules >1 cm
rather than meticulous follow-up for growth
Therapy Options
• Surgical
• Resection
• OLT / LDLT
• Ablative
• Ethanol injection Milan Criteria
• Acetic acid injection
• Thermal ablation (cryotherapy, radiofrequency ablation, microwave)
• Transarterial
• Embolization
• Chemoembolization
• Radiotherapy
• Combination transarterial and ablative: external beam radiation
• Systemic
• Chemotherapy
• Hormonal
• Immunotherapy
Staging
Biliary Stones & Infection
Terminology
• Biliary stones:
• Cholelithiasis
• Choledocholithiasis
• Primary CBDstone
• Secondary CBD stone
• Hepatolithiasis
• Biliary tract Infection:
• Cholecystitis
• Cholangitis

• Sludge: particles <3mm

• Stone: >3mm
Biliary Stones
• Type:
• Cholesterol
• Pigment
• Black
• Brown
• Mixed
Risk Factors
Cholesterol Pigment
• Westen • Asians
• Advancing age • Rural > Urban
• Female
• Pregnancy • Haemolytic syndromes
• Oral contraceptive
• Biliary infection
• Obesity
• Rapid weight reduction • Ileal disease: Crohn’s / Ileal
• Gall bladder stasis resection
• Inborn error of Bile Salt metabolism • Cystic fibrosis of pancreas
• Hyperlipidemia syndromes
The Natural History of Gallstones

Dooley JS.Gallstones & Benign

Biliary Diseases in Sherlock’s
Diseases of the Liver & Biliary
System, 12th Ed.2011
Complications
• Acute cholecystitis àgall bladder empyema àgall bladder perforation
àgeneralized peritonitis
• Secondary CBD stone àCholangitis / Pancreatitis
• Fistulation to duodenum/colon
• Gallstone ileus
• Mirizzi syndrome
• Gallbladder cancer
 Cholelithiasis: Clinical Manifestation
• Sudden-onset pain in the epigastric/RUQ abdomen
• Severe – episodic persist 1-3 hours
• Radiates to the scapulae or shoulder
• May be nocturnal
• May associated with large fatty meals consumption
• Anorexia, nausea, vomiting
• ± RUQ tendernes
• Lab: normal leucocyte, AST, ALT, serum bilirubin and amilase-lipase
Hartley SE, et al. Evaluation and Management of Gallstone- Related Diseases in Non-Pregnant Adults. Faculty Group Practice. October 2014
Imaging Modalities
• Abdominal radiography (upright and supine) – to exclude other
causes of abdominal pain (eg, intestinal obstruction)
• Ultrasonography – procedure of choice in suspected gallbladder or
biliary disease
• MRI-MRCP – if choledocholithiasis or other biliary obstruction is
suspected
Ultrasonography (USG)
• Sens: 95%
• Spec: 90%
• Hiperechoic with
accoustic shadow
Management
• Medical treatments
• Oral bile salt therapy (ursodeoxycholic acid – UDCA)
• Extracorporeal shockwave lithotripsy (ESWL)?
• Surgical treatments
• Cholecystectomy
• Open cholecystectomy
• Laparoscopic Cholecystectomy
Choledocholithiasis: Clinical Manifestation
• Biliary colic
• Reccurent jaundice
• No fever unless there is cholangitis complication
• Lab:
• Elevated bilirubin (total bilirubin often >2.0 mg/dL)
• Elevated alkali phosphatase
• Amylase/lipase are usually normal unless there is
concomitant pancreatitis
 Diagnosis

Costi R et al . Diagnosis and management of choledocholithiasis.

World J Gastroenterol 2014; 20(37): 13382-13401
USG CBDstone
MRCP
ERCP
 Management Option

Costi R et al . Diagnosis and management of choledocholithiasis.

World J Gastroenterol 2014; 20(37): 13382-13401
Laparoscopic IOC àbile duct exploration
Cholecystitis
Acute Cholangitis
• Diagnostic criteria based on TG13
A. Systemic inflammation
A-1. Fever and/or shaking chills (T>38°C)
A-2. Laboratory data: evidence of inflammation (WBC, <4 or>10)
B. Cholestasis
B-1. Jaundice (total bilirubin ≥ 2)
B-2. Laboratory data: abnormal liver function test (ALP, γGT, AST, ALT)
C. Imaging
C-1. Biliary dilatation
C-2 evidence of etiology on imaging
Suspected diagnosis: one item in A + one item in B or C
Definite diagnosis: one item in A, one item in B and one item in C

1.Kiriyama et al. J Hepatobiliary Pancreat Sci (2013) page 28

Acute Cholangitis
• Charcot's triad : 50-70% of patients with cholangitis
• Fever (chilling): 90% of patients
• Abdominal pain: 70% of patients
• Jaundice: 60% of patients

• Reynolds pentad
• altered mental status 10-20% of the time
• hypotension approximately 30% of the time
Choledochal Cyst
Pancreas Neoplasms
• Benign vs Malignant
• Exocrine vs Endocrine
• Exocrine = Adenocarcinoma: 95%
• Endocrine = Neuroendocrine tumor: 5%
CLINICAL PRESENTATION – Symptoms
• Asthenia :86% • Nausea :51%
• Weight loss :85% • Vomiting :33%
• Anorexia :83% • Steatorrhea :25%
• Abdominal pain :79% • Thrombophlebitis :3%
• Superficial thrombophlebitis
• Dark urine :59% • May be migratory (classic Trousseau’s syndrome)
• Jaundice :56% • Pruritus
• Pale stool
The initial presentation of pancreatic cancer varies according to tumor location
• Head : 60-70%
• Body/tail : 20-25%
• The remainder involve the whole organ
CLINICAL PRESENTATION – Signs
• Jaundice :55% • Courvoisier law:
• Hepatomegaly :39% • Obstructive jaundice
• Palpable gall bladder
• Right upper quadrant mass :15% • Without biliary colic
• Cachexia :13%
• Courvoisier’s sign :13%
• Epigastric mass :9%
• Ascites :5%
• Scratch mark
 Bile duct stone Pancreas head tumor

Icterus Exacerbation / remition Progressive

Pain Colic Dull pain
Gall bladder Contracted Hydrops

74
Laboratory Test
• Serum aminotransferases
• Alkaline phosphatase
• Bilirubin
• Tumor Marker
• CA 19-9
• CEA
Imaging
• Abdominl USG
• Sens >95% in tumor >3cm
• Abdominal CT
• MRCP
• ERCP
• EUS
Treatment
• Resectable
• Head and Neck: Pancreaticoduodenectomy
• Whipple Procedure (1935)
• Traverso-Longmire (1978)
• Body and Tail: Distal Pancreatectomy
• Unresectable
• Surgical
• Bypass Choledochojejunostomy roux en Y
• Bypass Gastrojejunostomy
• Coeliac block
• Non Surgical
• Dainage of the bile: Stent ERCP, PTBD
• Percutaneus coeliac block
• Adjuvant Treatment
• Chemotherapy
• Radiation
CYSTIC TUMOR
• Benign
• Inflammatory (Pseudocyst)
• Serous
• Pre-malignant
• IPMN
• MCN
• Malignant
 Cyst fluid analysis
Cyst type CEA Amylase

Pseudocyst Not elevated In thousands

SCN Not elevated Not elevated
Papyllary tumours Not elevated Not elevated
MCN Elevated (>192nd/ml) Not elevated
IPMN Elevated (>192nd/ml) Elevated
Radiological Features
Cyst Type CT and MRI findings
Pseudocyst Internal debris
Pancreatic necrosis
SCN Often comprised of multiple small fluid-filled cyst
Central scar “sunburst” calcification
Honeycomb appearance
Papillary tumours Solid and cystic
MCN Septated solitary cyst
Calcification of the cyst wall (egshell calcification)
IPMN Dilated-MD/SB pancreatic duct
Intracystic nodules>3mm sugest malignancy
EUS more sensitive in picking mural nodules
Recommended Surgery
• Pseudocyst
• Cystojejunostomy Roux en Y
• True cyst
• Excision - Pancreatectomy
Acute Pancreatitis
ACUTE PANCREATITIS
• CLINICAL DEFINITION
• An acute condition presenting with abdominal pain, usually associated with
raised pancreatic enzymes as a result of pancreatic inflammation (injury to
exocrine parenchym)
• PATHOLOGICAL DEFINITION
• Reversible* pancreatic parenchymal injury associated with inflammation

*if underlying cause cf pancreatitis is removed, heal without any impairment of function or
morphologic loss of gland
*Recurrent attacks with irreversible parenchymal injury leading to impairment of function and
morphologic loss is chronic pancreatitis
 SEVERITY
• Mild acute pancreatitis
• No organ failure, local or systemic complications
• Moderately severe acute pancreatitis
• Organ failure that resolves within 48 h and/or
• Local or systemic complications without persistent organ failure
• Severe acute pancreatitis
• Persistent organ failure > 48 h
TYPES
• Interstitial edematous acute pancreatitis
• Acute inflammation of the pancreatic parenchyma and peri-pancreatic tissues, but
without recognizable tissue necrosis
• Necrotizing acute pancreatitis
• Inflammation associated with pancreatic parenchymal necrosis and/or peri-
pancreatic necrosis
Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis— 2012: revision of the Atlanta classification and
definitions by international consensus. Gut 2013;62:102-11
 PATHOPHYSIOLOGY
Activation of Hageman Activation of clotting and
factor XII complement systems à
thrombosis à splenic
veins thrombosis
Lipase activation à Fatty acids + calcium à
Triglycerides à Glycerol + saponification à
Fatty acids Hypocalcemia
Trypsinogen
Elastase activation à 3rd space sequestration of
↓
Digestion of elastic fibers à blood/fluid à
TRYPSIN
Capillary leak/rupture à hemorrhage + hypovolemic
pseudoaneurism shock
Activation of Membrane damage à
Lysolechitinase (derived necrosis
from bile)
Release inflammatory Systemic complications
mediators into circulation
Diagnostic Criteria
• Most often established by the presence of two of the three following criteria:
1. abdominal pain consistent with the disease (acute onset of a persistent,
severe, epigastric pain often radiating to the back)
2. serum amylase and/or lipase greater than three times the upper limit of
normal
3. characteristic findings from abdominal imaging (CT/MRI)

• CT and/or MRI of the pancreas should be reserved for patients

• in whom the diagnosis is unclear (typical pain with normal enzymes)
• who fail to improve clinically within the first 48-72 h after hospital admission
(e.g., persistent pain, fever, nausea, unable to begin oral feeding)
• to evaluate local complications

Greenberg JA, et al. Clinical practice guideline: management of acute pancreatitis. Can J Surg 2016; 59(2): 128-140
Hematological: Pancreatic Enzymes’ Assays
• Serum Amylase
• ONSET: almost immediately Raised Amylase à may not AP
Normal Amylase à may be AP
• PEAK: within several hours
• 3-4 times upper limit of normal within 24 hrs (90%)
• RETURN to normal in 3-5 days
• normal at time of admission in 20% cases
• Compared with lipase, returns more quickly to normal values.
• Serum Lipase à SERUM INDICATOR OF HIGHEST PROBABILITY OF DISEASE
• more sensitive/specific than amylase
• Remains elevated longer than amylase{12 days)
• Useful in late presentation and if the cause is High TG
The End