liver gb powerpoint
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LIVERLIVER
Gerardo R. Wenceslao, MD, FPCSGerardo R. Wenceslao, MD, FPCS
Diplomate, Philippine Board of SurgeryDiplomate, Philippine Board of Surgery
Fellow, Philippine College of SurgeonsFellow, Philippine College of Surgeons
AnatomyAnatomy
External Surface of Normal Liver
AnatomyAnatomy 1/501/50thth of total body weight of total body weight Surgically divided into the right and left lobe by a Surgically divided into the right and left lobe by a
line through the IVC and Gallbladder (Cantlie’s line through the IVC and Gallbladder (Cantlie’s line)line)
Right lobe-divided into anterior & posrerior Right lobe-divided into anterior & posrerior sectionsection
Left lobe divided into medial and lateral Left lobe divided into medial and lateral segments by falciform ligament segments by falciform ligament
AnatomyAnatomy
Couinaud ClassificationCouinaud Classification
The Couinaud classificationThe Couinaud classification of liver anatomy divides the of liver anatomy divides the liver into eight functionally liver into eight functionally indepedent segments. indepedent segments. Each segment has its own Each segment has its own vascular inflow, outflow and vascular inflow, outflow and biliary drainage.biliary drainage.In the centre of each In the centre of each segment there is a branch of segment there is a branch of the portal vein, hepatic artery the portal vein, hepatic artery and bile duct.and bile duct.In the periphery of each In the periphery of each segment there is vascular segment there is vascular outflow through the hepatic outflow through the hepatic veinsveins
Right hepatic veinRight hepatic vein divides the right lobe into divides the right lobe into anterior and posterior anterior and posterior segments.segments.Middle hepatic veinMiddle hepatic vein divides the liver into right divides the liver into right and left lobes (or right and left lobes (or right and left hemiliver). This and left hemiliver). This plane runs from the plane runs from the inferior vena cava to the inferior vena cava to the gallbladder fossa.gallbladder fossa.Left hepatic veinLeft hepatic vein divides the left lobe into divides the left lobe into a medial and lateral part a medial and lateral part
AnatomyAnatomy
Segmental liver anatomy. Depicted is segmental liver anatomy as originally described by Couinaud. The right lobe consists of segments 5 through 8, the left lobe of segments 2 through 4, and theleft lateral segment of segments 2 and 3
Hepatic resectionsHepatic resections
Rt. Lobectomy-V.VI, VII VIIIRt. Lobectomy-V.VI, VII VIII Rt. trisegmentectomy-inc segment IVRt. trisegmentectomy-inc segment IV Left lobectomy– II , III, IVLeft lobectomy– II , III, IV Left lateral segmentectomy-II, IIILeft lateral segmentectomy-II, III
Vascular SupplyVascular Supply
Arterial Blood SupplyArterial Blood Supply Hepatic arteryHepatic artery
branch of the celiac axisbranch of the celiac axiscarry fully oxygenated bloodcarry fully oxygenated bloodsupplies 25 % of the 1,500 ml of supplies 25 % of the 1,500 ml of
blood that enter the liverblood that enter the liver
Vascular SupplyVascular Supply
Vascular Supply Con’tVascular Supply Con’t
Venous Blood SupplyVenous Blood Supplyportal veins carries partially portal veins carries partially
oxygenated blood as it drains the oxygenated blood as it drains the entire splanchnic circulationentire splanchnic circulation
comprises 75 % of the liver blood comprises 75 % of the liver blood flowflow
it is formed by the confluence of it is formed by the confluence of the superior mesenteric, inferior the superior mesenteric, inferior mesenteric, splenic with coronary mesenteric, splenic with coronary veinvein
Vascular SupplyVascular Supply
Liver FunctionsLiver Functions
Liver functionLiver function
Energy metabolismEnergy metabolism Glycogenolysis-source of energy during Glycogenolysis-source of energy during
fastingfasting Gluconeogenisis- source of energy after Gluconeogenisis- source of energy after
depletion of glycogen (48hrs)depletion of glycogen (48hrs) Lipolysis-occurs during prolonged fasting-Lipolysis-occurs during prolonged fasting-
formation of ketone from fatty acidsformation of ketone from fatty acids GlycogenisisGlycogenisis
Liver functionsLiver functions
Metabolic functionsMetabolic functions Absorption, metabolism and storage of fat Absorption, metabolism and storage of fat
soluble vitamins- A, D, E and Ksoluble vitamins- A, D, E and K One of the sites for activation of Vit D (25-One of the sites for activation of Vit D (25-
hydroxylation)hydroxylation) Only site for storage of vit AOnly site for storage of vit A
Liver functionLiver function
DetoxificationDetoxification Phase 1-Phase 1- Cytochrome P-450-enzyme w/c facilitatesCytochrome P-450-enzyme w/c facilitates
oxidation,reduction and hydrolysisoxidation,reduction and hydrolysis Phase 2-converts hydrphobic compounds to Phase 2-converts hydrphobic compounds to
hydrophilichydrophilic
Liver functionLiver function
Reticuloendothelial function-clear the Reticuloendothelial function-clear the circulation with particulate matters and circulation with particulate matters and microbes.microbes. Kupffer cells-fixed phagocytic cellsKupffer cells-fixed phagocytic cells
Liver functionsLiver functions
Liver functionLiver function
Synthetic functionSynthetic function Sole source of albumin, alpha globulin and Sole source of albumin, alpha globulin and
transport proteins –transferrin, ferritintransport proteins –transferrin, ferritin Proteins involved in hemostasis-fibrinogen Proteins involved in hemostasis-fibrinogen
(factor 1) and vit K dependent factors-( II, (factor 1) and vit K dependent factors-( II, VII, IX and X)VII, IX and X)
Liver function testsLiver function tests
Clearance functionClearance function Ammonia-converted to Urea via Urea cycleAmmonia-converted to Urea via Urea cycle Indirect bilirubin-taken up from the blood by Indirect bilirubin-taken up from the blood by
the hepatocytesthe hepatocytes
Function Tests Con’t.Function Tests Con’t. . . Excretory FunctionExcretory Function
- patency of the biliary tree is- patency of the biliary tree is
reflected by:reflected by:
a. Direct Bilirubina. Direct Bilirubin
b. Enzymes alkaline phosphatase b. Enzymes alkaline phosphatase
and gamma glutamyl transferaseand gamma glutamyl transferase
(GGT) (GGT)
Function Tests Con’t.Function Tests Con’t.
Extent of injuriesExtent of injuries of the liver is of the liver is reflected by the serum level of reflected by the serum level of enzymesenzymes SGOT (AST)SGOT (AST) SGPT ( ALT)SGPT ( ALT) LDHLDH
Imaging of the Liver:Imaging of the Liver:
- used to define parenchymal - used to define parenchymal
lesions:lesions:
1. 1. Ultrasound Ultrasound
- highest yield in defining - highest yield in defining hepatic hepatic abscesses, cystic lesions abscesses, cystic lesions and and most hemangiomas most hemangiomas
Imaging of the Liver Imaging of the Liver Con’t.Con’t.
2. CT scan2. CT scan
used to evaluate presence of peritoneal lesions, portal used to evaluate presence of peritoneal lesions, portal lymphadenopathy & other remote lesionslymphadenopathy & other remote lesions
dual & triple phase bolus iv contrast helical CT scan-dual & triple phase bolus iv contrast helical CT scan-most accurate;detects lesions that are 1cm in sizemost accurate;detects lesions that are 1cm in size
less accurate in detecting tumors in HCC than for less accurate in detecting tumors in HCC than for metastasis (40-60%-<2cm)metastasis (40-60%-<2cm)
--
Imaging of the liverImaging of the liver
MRI-MRI- Less sensitive at spatial discrimination of Less sensitive at spatial discrimination of
lesions than CT scanlesions than CT scan Less accurate than CT scan in detecting Less accurate than CT scan in detecting
liver metastasisliver metastasis More sensitive for detecting early HCC and More sensitive for detecting early HCC and
in distinguishing it from macroregenerative in distinguishing it from macroregenerative nodulesnodules
Better than CT in detecting cystic lesionsBetter than CT in detecting cystic lesions
Imaging the LiverImaging the Liver
Ultrasound
CT - Scan
MRI
Imaging of the Liver Imaging of the Liver Con’t.Con’t.
4. 4. AngiographyAngiography - determine the arterial supply - determine the arterial supply
and can detect large parenchymal and can detect large parenchymal lesionlesion
5. 5. AngioportographyAngioportography - combines CT scan with contrast- combines CT scan with contrast infusion through a catheter infusion through a catheter placed in the superior placed in the superior mesenteric arterymesenteric artery
Imaging of the LiverImaging of the Liver
CT - Angiography
Imaging of the Liver Imaging of the Liver Con’t.Con’t.
6. 6. Needle BiopsyNeedle Biopsy - provides liver tissue for- provides liver tissue for
histologic studieshistologic studies
Imaging of the LiverImaging of the Liver
Liver Biopsy with CT scan view Liver Biopsy
Needle BiopsyNeedle Biopsy
Trauma
PathologyPathology
A. TraumaA. Trauma 22ndnd most commonly injured organ most commonly injured organ
1. Clinical manifestation1. Clinical manifestation ShockShock Abdominal painAbdominal pain Spasm Spasm RigidityRigidity
2. Diagnostic2. Diagnostic CT scan is most usefulCT scan is most useful May also use ultrasound or peritoneal lavageMay also use ultrasound or peritoneal lavage
Hepatic injuriesHepatic injuries
Grade1-subcapsular , non-expanding Grade1-subcapsular , non-expanding hematoma, <10cm.Capsular tear, non-hematoma, <10cm.Capsular tear, non-bleeding,<1cm parenchymal depthbleeding,<1cm parenchymal depth
Grade 2-subcapsular,non-expanding,10-Grade 2-subcapsular,non-expanding,10-50% surface area;intraparenchymal, non-50% surface area;intraparenchymal, non-expanding,<10cm. Capsular tear,active expanding,<10cm. Capsular tear,active bleedung;1-3cm depth,<10cm in lengthbleedung;1-3cm depth,<10cm in length
Hepatic injuriesHepatic injuries
Grade 3- subcaspular >50% surface Grade 3- subcaspular >50% surface area, or expanding.Ruptured area, or expanding.Ruptured subcapsular hematoma w/ active subcapsular hematoma w/ active bleeding; >10cm intraparenchymal bleeding; >10cm intraparenchymal hematoma or expanding > 3cm depth.hematoma or expanding > 3cm depth.
hepatic injurieshepatic injuries
Grade 4- ruptured intraparencymal Grade 4- ruptured intraparencymal hematoma w/ active bleeding. hematoma w/ active bleeding. Parenchymal disruption 25-75% of Parenchymal disruption 25-75% of hepatic lobe or 1-3 Coiunaud segment in hepatic lobe or 1-3 Coiunaud segment in single lobesingle lobe
Hepatic injuriesHepatic injuries
Grade 5- parenchymal disruption >75% Grade 5- parenchymal disruption >75% of hepatic lobe or > 3 Couinaud’s of hepatic lobe or > 3 Couinaud’s segment in a lobe. Juxtahepatic venous segment in a lobe. Juxtahepatic venous injuries injuries
Grade 6- hepatic avulsionGrade 6- hepatic avulsion
Grade 1 hepatic injuryGrade 1 hepatic injury
Grade 1 hepatic injury in a 21-year-old man with a stabbing injury to the right upper quadrant of the abdomen. Axial, contrast-enhanced computed tomography (CT) scan demonstrates a small, crescent-shaped subcapsular and parenchymal hematoma less than 1 cm thick
Grade 2 Liver InjuryGrade 2 Liver Injury
A 20-year-old man with systemic lupus erythematosus presented with grade 2 liver injury after minor blunt abdominal trauma. Nonenhanced axial CT scan at the level of the hepatic veins shows a subcapsular hematoma 3 cm thick
Grade 3 Liver InjuryGrade 3 Liver Injury
Grade 3 liver injury in a 22-year-old woman after blunt abdominal trauma. Contrast-enhanced axial CT scan through the upper abdomen shows a 4-cm-thick subcapsular hematoma associated with parenchymal hematoma and laceration in segments 6 and 7 of the right lobe of the liver. Free fluid is seen around the spleen and left lobe of the liver consistent with hemoperitoneum
Grade 4 Liver InjuryGrade 4 Liver Injury
Grade 5 Liver InjuryGrade 5 Liver Injury
Grade 5 - Global destruction or devascularization of the liver
Treatment of liver Treatment of liver injuriesinjuries
Non operative:Non operative: Absence of peritoneal signsAbsence of peritoneal signs Precise delineation and grading of injuriesPrecise delineation and grading of injuries No associated peritoneal or retroperitoneal No associated peritoneal or retroperitoneal
injuriesinjuries
Tx of hepatic injuriesTx of hepatic injuries
Operative:Operative: Grade 3-5Grade 3-5
Bimanual compression w/ resuscitationBimanual compression w/ resuscitation Pringle maneuverPringle maneuver Finger fracture w/ repair or ligationFinger fracture w/ repair or ligation Debridement of no n-viable parenchymaDebridement of no n-viable parenchyma Omental packOmental pack Closed suction drainsClosed suction drains
Tx of hepatic injuriesTx of hepatic injuries
Operative:Operative: If + for bleeding after compression or If + for bleeding after compression or
Pringle’s –pack the woundPringle’s –pack the wound Re-explored after 18-36 hrs. packs are Re-explored after 18-36 hrs. packs are
removedremoved If still + for bleeding-retrohepatic IVC,hepatic If still + for bleeding-retrohepatic IVC,hepatic
venous injuryvenous injury vascular isolation and Intraval shuntvascular isolation and Intraval shunt
Tx of liver injuriesTx of liver injuries
Operative:Operative: Hepatic resection:Hepatic resection:
High mortality rateHigh mortality rate Considered for those w/total destruction of liver Considered for those w/total destruction of liver
parenchymaparenchyma Extent of injury precludes perihepatic packingExtent of injury precludes perihepatic packing
TraumaTrauma
4. Complications4. Complicationsa. Recurrent bleedinga. Recurrent bleeding
Inadequate hemostasis or loss of coagulation Inadequate hemostasis or loss of coagulation factors secondary to massive transfusionsfactors secondary to massive transfusions
b. Intra-abdominal sepsis/ abcess formationb. Intra-abdominal sepsis/ abcess formation
c. Hemobiliac. Hemobilia Free communication between blood vessels Free communication between blood vessels
and biliary tree; triad of abdominal pain, GI and biliary tree; triad of abdominal pain, GI bleeding and previous trauma; Jaundice may bleeding and previous trauma; Jaundice may be presentbe present
HemobiliaHemobilia
Endoscopic view of clot being extruded from the duodenalpapilla
Hepatic AbscessHepatic Abscess
PyogenicPyogenicEtiologyEtiology::1. Ascending biliary infection1. Ascending biliary infection
2. Hematogenous spread2. Hematogenous spread
3. Generalized septicemia3. Generalized septicemia
4. Direct extension from intraperitoneal4. Direct extension from intraperitoneal
infectioninfection
Pyogenic Abscess - Con’t.Pyogenic Abscess - Con’t.
Cholangitis 2Cholangitis 2 to Calculi or CA to Calculi or CA
- most frequent cause- most frequent cause General septicemiaGeneral septicemia
- second most frequent cause- second most frequent cause E. coli, Klebsiella, StreptococcusE. coli, Klebsiella, Streptococcus
- most common organisms - most common organisms
isolatedisolated
Pyogenic AbscessPyogenic Abscess
Pyogenic AbscessPyogenic Abscess
Pyogenic liver abcessPyogenic liver abcess
They can be solitary, multiple and They can be solitary, multiple and multilocularmultilocular
Single and multiple abcesess-they occur Single and multiple abcesess-they occur in equal frequencyin equal frequency
Single abcess-usually located in the right Single abcess-usually located in the right lobelobe
Pyogenic Abscess Con’t.Pyogenic Abscess Con’t.
Clinical ManifestationsClinical Manifestations::- - fever (“picket fence”) mostfever (“picket fence”) most
commoncommon
- pain – a late symptom- pain – a late symptom
- hepatomegaly - 30 - 60 %- hepatomegaly - 30 - 60 %
- Hepatic tenderness – 5 %- Hepatic tenderness – 5 %
Pyogenic Abscess Con’t.Pyogenic Abscess Con’t.Diagnostic StudiesDiagnostic Studies::
- leucocytosis- leucocytosis- 5 % anemia- 5 % anemia- elevated alkaline phosphatase- elevated alkaline phosphatase- radiograph – elevation and immobility of - radiograph – elevation and immobility of the right leaf of the diaphragmthe right leaf of the diaphragm- obliteration of the cardio-phrenic angle - obliteration of the cardio-phrenic angle and costophrenic angleand costophrenic angle- air fluid level – abscess formed by gas - air fluid level – abscess formed by gas forming microorganismforming microorganism- CT scan – most accurate 90 %- CT scan – most accurate 90 %
Pyogenic Liver AbscessPyogenic Liver Abscess
Chest X - ray
Pyogenic Liver AbcessPyogenic Liver Abcess
CT – scan
Pyogenic Abscess Con’t.Pyogenic Abscess Con’t.
TreatmentTreatment::- - appropriate antibiotic therapy combined appropriate antibiotic therapy combined
with surgical drainage in the selected caseswith surgical drainage in the selected cases- IV antibiotics are usually administered for 2 - IV antibiotics are usually administered for 2
weeks followed by 1 month of oral weeks followed by 1 month of oral treatmenttreatment
- Hepatic abscess can also be drained - Hepatic abscess can also be drained percutaneously under CT or UTZ controlpercutaneously under CT or UTZ control
- Multiple abscesses – treatment rely heavily - Multiple abscesses – treatment rely heavily on appropriate antibiotic coverageon appropriate antibiotic coverage
Pyogenic Abscess Con’t.Pyogenic Abscess Con’t.
PrognosisPrognosis::
Mortality rate:Mortality rate:- surgical and percutaneous - surgical and percutaneous
drainage 7.5 – 20 %drainage 7.5 – 20 %
- antibiotics alone – 50 %- antibiotics alone – 50 %
Amoebic AbscessAmoebic Abscess
- the most common abscess in - the most common abscess in third world countriesthird world countries
- - EtiologyEtiology due to infection of E. due to infection of E. histolytica which reached the histolytica which reached the portal vein from intestinal portal vein from intestinal amoebiasisamoebiasis
Amebic abcessAmebic abcess
Reach the liver by way of portal venous Reach the liver by way of portal venous system from a focus in the bowel wallsystem from a focus in the bowel wall
They are usually large single abcess They are usually large single abcess affecting the right lobe of the liver (dome affecting the right lobe of the liver (dome or inferior surface)or inferior surface)
Contains reddish brown fluid (anchovy )Contains reddish brown fluid (anchovy ) Outer zone: amebas can usually be seenOuter zone: amebas can usually be seen
Amoebic Abscess Con’t.Amoebic Abscess Con’t.
Multiple large amoebic abscessseen at autopsy
Amoebic Abscess Con’t.Amoebic Abscess Con’t.
Autopsy specimen showing a superior and an inferiorsurface amoebic abscess (Right lobe)
Amoebic Abscess Con’t.Amoebic Abscess Con’t.
Cluster of trophozoites in liver abscess
Microscopic
Amebic abcessAmebic abcess
Clinical manifestation:Clinical manifestation: Fever and pain right lower intercostal space-Fever and pain right lower intercostal space-
the most frequent complaintthe most frequent complaint Left lobe abcess: painful epigastric swellingLeft lobe abcess: painful epigastric swelling 1/3- hx of diarrhea1/3- hx of diarrhea
Amoebic Abscess Con’t.Amoebic Abscess Con’t.
A well demarcated swelling is seen in the epigastriumin a case of a left lobe amoebic liver abscess
Amebic abcessAmebic abcess
Diagnostic studies:Diagnostic studies: Stool exam: + for ameba in only 15%Stool exam: + for ameba in only 15% X-ray: similar to those with Pyogenic abcessX-ray: similar to those with Pyogenic abcess Indirect hemagglutination: + most of the timeIndirect hemagglutination: + most of the time Aspiration of the abcess cavity: Anchovy Aspiration of the abcess cavity: Anchovy
paste- considired pathognomonomic paste- considired pathognomonomic frequently establishes the dxfrequently establishes the dx
Amebic Liver AbscessAmebic Liver Abscess
Chest radiograph demonstrating elevation of the right hemidiaphragm
Abdominal CT scan demonstratinga large abscess in the right hepatic lobe
Amoebic Abscess Con’t.Amoebic Abscess Con’t.
ComplicationsComplications:: - Secondary Infection – the most - Secondary Infection – the most
commoncommon - Rupture of the amoebic abscess – - Rupture of the amoebic abscess –
next most commonnext most common Pleuro pulmonary – the most Pleuro pulmonary – the most
common root of rupturecommon root of rupture Rupture to the pericardial cavity – Rupture to the pericardial cavity –
the most seriousthe most serious
Amoebic Abscess Con’t.Amoebic Abscess Con’t.
Rupture of a left lobe amoebicLiver Abscess into pericardium
Huge pericardial effusion in a patient with a superior amoebic liver abscess
Amoebic Abscess Con’t.Amoebic Abscess Con’t.
TreatmentTreatment:: - Parenteral amoebicidal drugs – - Parenteral amoebicidal drugs –
treatment of choicetreatment of choice - Aspiration of amoebic abscess is - Aspiration of amoebic abscess is
done in cases of:done in cases of: persistence of the manifestation persistence of the manifestation
following a course of amoebicidal following a course of amoebicidal drugsdrugs
if the abscess is large and adjacent if the abscess is large and adjacent to important structureto important structure
BENIGNTUMORS
Benign TumorsBenign TumorsHamartomasHamartomas
- composed of tissues normally present in - composed of tissues normally present in the organ but are arranged in disorderly the organ but are arranged in disorderly fashionfashion
- rarely of clinical significance- rarely of clinical significance- they maybe solitary or multiple- they maybe solitary or multiple- they are encapsulated and cystic- they are encapsulated and cystic- with lesion of clinical significance - with lesion of clinical significance
surgical excision is generally indicatedsurgical excision is generally indicated- deeply located lesion must be lest alone - deeply located lesion must be lest alone
after histologic diagnosisafter histologic diagnosis
HamartomaHamartoma
globular calcifications globular calcifications located predominately located predominately in the right lobe of the in the right lobe of the liver liver
HamartomaHamartoma
Benign Tumors Con’t.Benign Tumors Con’t.HemangiomasHemangiomas
- most common benign hepatic tumor- most common benign hepatic tumor- occur more frequently in female- occur more frequently in female- Usually <5cm, asymptomatic and - Usually <5cm, asymptomatic and
discovered only incidentallydiscovered only incidentally- in infant, large hemangiomas often are - in infant, large hemangiomas often are
associated with high cardiac output associated with high cardiac output failurefailure
- most hepatic hemangiomas doesn’t - most hepatic hemangiomas doesn’t require surgical interventionrequire surgical intervention
- potential for rupture is minimal- potential for rupture is minimal
HemangiomasHemangiomas
HemagiomasHemagiomas
HemangiomaHemangioma
Cavernous Hemangioma of the Liver
HemangiomaHemangioma
Usually identified by US or CT scanUsually identified by US or CT scan
Subglissonian hematoma-dx for small Subglissonian hematoma-dx for small lesions not seen by US or CTscanlesions not seen by US or CTscan
Percutaneous biopsy-contraindicated Percutaneous biopsy-contraindicated because of high risk of bleedingbecause of high risk of bleeding
Hemangiomas Con’t.Hemangiomas Con’t.
Indication for surgical excisionIndication for surgical excision- pain- pain
- mass effect- mass effect
- platelet trapping- platelet trapping
- significant growth- significant growth
- early rupture- early rupture
- resection is the therapy of choice- resection is the therapy of choice
Benign Tumors Con’t. Benign Tumors Con’t. Focal Nodule HyperplasiaFocal Nodule Hyperplasia
- many believe that it is not a neoplasm but a - many believe that it is not a neoplasm but a reaction to injuryreaction to injury
- patient are always almost asymptomatic- patient are always almost asymptomatic
- they are frequently detected during celeotomy - they are frequently detected during celeotomy (explore lap)(explore lap)
- frequently not detected by CT or UTZ because - frequently not detected by CT or UTZ because it is isodense it is isodense
- angiogram – sunburst hypervascular pattern- angiogram – sunburst hypervascular pattern
- typically the outer surface are tan and - typically the outer surface are tan and demonstrate a characteristic central stellate demonstrate a characteristic central stellate scarscar
Focal Nodular Focal Nodular HyperplasiaHyperplasia
Gross
Histopathology
Focal Nodular Focal Nodular HyperplasiaHyperplasia
Focal Nodular Focal Nodular HyperplasiaHyperplasia
They are regarded as possible precursor They are regarded as possible precursor to Fibrolammelar Carcinomato Fibrolammelar Carcinoma
Pain- usual indication for resectionPain- usual indication for resection
Hepatic AdenomaHepatic Adenoma
> 50% used oral contraceptive > 5 years> 50% used oral contraceptive > 5 years Lesions have manifested even after Lesions have manifested even after
discontinuation of the drugsdiscontinuation of the drugs They may also develop during pregnancy, They may also develop during pregnancy,
DM and glycogen storage dse.DM and glycogen storage dse. They are bigger and higher rates of They are bigger and higher rates of
intramural or intraperitoneal bleeding-for intramural or intraperitoneal bleeding-for contraceptive userscontraceptive users
Hepatic adenomaHepatic adenoma
Bleeding may also occur during Bleeding may also occur during pregnancypregnancy
May transform to hepatocellular May transform to hepatocellular Carcinoma ( more frequently with Carcinoma ( more frequently with adenomatosis-> 10 adenomas)adenomatosis-> 10 adenomas)
80% are symptomatic with pain or mass 80% are symptomatic with pain or mass effcecteffcect
30%-spontaneous rupture30%-spontaneous rupture
Hepatocellular AdenomaHepatocellular Adenoma
Large Hepatocellular Adenoma on the parietal surface of the left lobe
Hepatocellular AdenomaHepatocellular Adenoma
Cut surface of Hepatic Adenoma
Hepatocellular AdenomaHepatocellular Adenoma
Benign Tumors Con’t.Benign Tumors Con’t.
TreatmentTreatment::ResectionResection
->4cm-increased risk of spontaneous ->4cm-increased risk of spontaneous rupture and malignant transformationrupture and malignant transformation-non-response to cessation of OCP-non-response to cessation of OCP-cannot stop OCP-cannot stop OCP-those who plans to become pregnant-those who plans to become pregnant
METASTATICNEOPLASM
Metastatic NeoplasmMetastatic Neoplasm - the most common malignant tumors of the liver- the most common malignant tumors of the liver - liver is the second only to lymph node as - liver is the second only to lymph node as
metastatic sitemetastatic site - - Four routes in which neoplasm may reach the Four routes in which neoplasm may reach the
liverliver::1. portal venous1. portal venous2. lymphatic spread2. lymphatic spread3. hepatic arterial3. hepatic arterial4. direct extension4. direct extension
- the growth pattern of metastatic tumor is more - the growth pattern of metastatic tumor is more rapid than the original lesionrapid than the original lesion
Metastatic NeoplasmMetastatic Neoplasm
Liver metastases from Adeno-carcinoma primary in the colon
Metastases to the liver
Metastatic AdenoCAMetastatic AdenoCA
Metastatic NeoplasmMetastatic Neoplasm
Clinical manifestationClinical manifestation::- hepatic pain- hepatic pain
- jaundice- jaundice - ascites- ascites - anorexia- anorexia - hepatic nodularity is apparent - hepatic nodularity is apparent physically in 50 % of casesphysically in 50 % of cases
Metastatic Neoplasm Metastatic Neoplasm
Diagnostic studiesDiagnostic studies::1. 1. Laboratory studiesLaboratory studies
- alkaline phosphatase - alkaline phosphatase in 80 % in 80 %- SGPT - SGPT 2/3 2/3- AFP is negative- AFP is negative- CEA is - CEA is in metastatic colonic in metastatic colonic CACA
Metastatic NeoplasmMetastatic Neoplasm
2. 2. Imaging TechniqueImaging Technique- most reliable method of finding liver metastasis- most reliable method of finding liver metastasis
a) a) CT scanCT scan - particularly enhanced CT with - particularly enhanced CT with
selective selective arterial infusion in the hepatic arterial infusion in the hepatic arteryartery - most sensitive means of defining - most sensitive means of defining
intrahepatic metastasis intrahepatic metastasisb) b) UltrasoundUltrasound
- cheapest and provides also a reasonable - cheapest and provides also a reasonable screening testscreening test
Liver metastasisLiver metastasis
Metastatic NeoplasmMetastatic Neoplasm
TreatmentTreatment:: - depend on the type of primary tumor- depend on the type of primary tumor
1. 1. Surgical resectionSurgical resection – the most effective – the most effective mode of therapymode of therapy
IndicationIndication:: a. control of primary tumor is accomplished or a. control of primary tumor is accomplished or
anticipated anticipated b. no systemic metastasisb. no systemic metastasis
c. patients’ condition will tolerate the c. patients’ condition will tolerate the procedure procedure
d. extent of hepatic involvement is that d. extent of hepatic involvement is that resection resulting to total extirpation is resection resulting to total extirpation is
feasible feasible
Liver ResectionLiver Resection
Metastatic NeoplasmMetastatic Neoplasm
2. 2. ChemotherapyChemotherapy3. 3. RadiationRadiation – poorly tolerated by the – poorly tolerated by the
liver, may be palliative for painful liver, may be palliative for painful liver liver metastasis metastasis
4. 4. Hepatic artery ligationHepatic artery ligation – may cause – may cause shrinkage in tumor size but only shrinkage in tumor size but only
transient transient
5. 5. Cryo ablationCryo ablation – may palliate the – may palliate the symptoms and slow the progression of symptoms and slow the progression of the lesion in unresectable tumors the lesion in unresectable tumors
PRIMARY MALIGNANT
TUMORS
Primary Malignant Primary Malignant TumorsTumors
- most common carcinoma in the - most common carcinoma in the first few years of lifefirst few years of life
- Hepatoblastoma- < 2 years old,more - Hepatoblastoma- < 2 years old,more common in malescommon in males
- Fibrolamellar ca- a variant of - Fibrolamellar ca- a variant of HCC ,equal sex incidence, common in HCC ,equal sex incidence, common in adolescent & adolescent & young adultsyoung adults
Hepatocellular CarcinomaHepatocellular Carcinoma(Hepatoma)(Hepatoma)
IncidenceIncidence- varies geographically highest in - varies geographically highest in
africa and Asia, lowest in westernafrica and Asia, lowest in western worldworld
- men are affected twice as often as- men are affected twice as often as womenwomen
- average age affected is 50 years- average age affected is 50 years- can occur at any age- can occur at any age
Malignant HepatomaMalignant Hepatoma
Imaging TechniqueImaging Technique
CT - Scan Ultrasound
HepatomaHepatoma
Hepatoma Con’t.Hepatoma Con’t.
AssociationsAssociations - tumor shows an association with number - tumor shows an association with number of pre-existing diseases and environmentalof pre-existing diseases and environmental
substancessubstances a. a. Chronic HBV and C infectionChronic HBV and C infection - risk of developing hepatocellular - risk of developing hepatocellular carcinoma is 200 fold for Chronic HBV carcinoma is 200 fold for Chronic HBV
carrierscarriers - risk in male carriers as high as 50 %- risk in male carriers as high as 50 %
Hepatoma Con’t.Hepatoma Con’t.
b. b. CirrhosisCirrhosis regardless of etiology regardless of etiology - present in 60 – 90% of patients- present in 60 – 90% of patients especially macronodular,post especially macronodular,post
necrotic cirrhosis necrotic cirrhosis c. c. HemochromatosisHemochromatosis with iron over- with iron over-
load and cirrhosisload and cirrhosis d. d. SchistosomiasisSchistosomiasis and other and other
parasitic infestationsparasitic infestations
Hepatoma AssociationsHepatoma Associations
HCC in a Cirrhotic Liver
HemochromatosisLiver Schistosomiasis
Hepatoma Con’t. Hepatoma Con’t. e. e. Environmental carcinogensEnvironmental carcinogens - industrial substances (poly-- industrial substances (poly-
chlorinated biphenyls; chlori-chlorinated biphenyls; chlori- nated hydrocarbon solvents; nated hydrocarbon solvents; vinyl chloride and polyvinyl vinyl chloride and polyvinyl chloride and organochloride chloride and organochloride pesticidespesticides
- organic materials (aflatoxins)- organic materials (aflatoxins) - thorotrast, an IV contrast agent- thorotrast, an IV contrast agent
(no longer used)(no longer used)
Hepatoma Con’t.Hepatoma Con’t.
Clinical presentation:Clinical presentation:- weight loss & weakness-80%- weight loss & weakness-80%
- dull aching pain in RUQ- dull aching pain in RUQ- fever- fever- jaundice- jaundice
Hepatoma Con’t.Hepatoma Con’t. - - Physical examinationPhysical examination a. hepatomegaly (88 %)a. hepatomegaly (88 %)
b. weight loss (85 %)b. weight loss (85 %) c. tender abdominal mass (50%)c. tender abdominal mass (50%) d. findings associated with cirrhosis (60 %) d. findings associated with cirrhosis (60 %)
- 10 – 15 % present with acute hemorrhage - 10 – 15 % present with acute hemorrhage into the peritoneal cavity with resultantinto the peritoneal cavity with resultant
shockshock - paraneoplastic syndromes in which tumor- paraneoplastic syndromes in which tumor cells secrete hormone like substance that cells secrete hormone like substance that cause unusual syndrome (Cushing’s cause unusual syndrome (Cushing’s syndrome) also may occursyndrome) also may occur
Hepatoma Con’t.Hepatoma Con’t.DiagnosisDiagnosis::
- Alkaline phosphatase – most consistently altered- Alkaline phosphatase – most consistently altered
- - Alpha-fetoproteinAlpha-fetoprotein elevated in 70 – 90 % of caseselevated in 70 – 90 % of cases
- Imaging studies:- Imaging studies: -CT scan-CT scan
- MRI- MRI -arteriography-arteriography -ultrasound-ultrasound
-Percutaneous needle biopsy-Percutaneous needle biopsy
Primary carcinomaPrimary carcinoma
Surgical excision-curative tx Surgical excision-curative tx Transarterial chemoebolization-using gelatin Transarterial chemoebolization-using gelatin
sponges,iodized oil-improved survival rates, sponges,iodized oil-improved survival rates, decrease tumor sizedecrease tumor size
Percutaneous Ethanol injection-dissapearnce Percutaneous Ethanol injection-dissapearnce of lesions<4.5cmof lesions<4.5cm
CryosurgeryCryosurgery Combined radio and chemotx-converts Combined radio and chemotx-converts
unresctable to resectableunresctable to resectable
Liver ResectionLiver Resection
CryoablationCryoablation
CryoablationCryoablation
Cryoprobe tip is placed into the tumorusing ultrasound guidance
Post cryoablation
Hepatoma Con’t.Hepatoma Con’t.
Surgical treatment con’t.Surgical treatment con’t.
c. if lesions are unresectable, patientsc. if lesions are unresectable, patients
have a mean survival time of have a mean survival time of
4 months4 months
d. attempts to induce tumor necrosisd. attempts to induce tumor necrosis
by hepatic artery ligation have by hepatic artery ligation have
shown poor resultsshown poor results
HepablastomaHepablastoma - most common primary malignant liver - most common primary malignant liver
tumor in childrentumor in children
Clinical presentationClinical presentation::
- presents with abdominal distention, - presents with abdominal distention, failure to thrive, other liver symptoms failure to thrive, other liver symptoms of liver failureof liver failure
- Alpha-fetoprotein is frequently (+) - Alpha-fetoprotein is frequently (+) positivepositive
HepatoblastomaHepatoblastoma
HepatoblastomaHepatoblastoma
HepatoblastomaHepatoblastomaPathologyPathology:: - 80 % are solitary liver masses that - 80 % are solitary liver masses that
microscopically show nests and cords of microscopically show nests and cords of primitive cells, resembling embryonic primitive cells, resembling embryonic hepatocyteshepatocytes
TreatmentTreatment:: - treatment is surgical excision- treatment is surgical excision - inoperable tumors are treated with - inoperable tumors are treated with irradiation or chemotherapy but with poor irradiation or chemotherapy but with poor resultsresults
Angiosarcoma or Malignant Angiosarcoma or Malignant HemangioendotheliomaHemangioendothelioma
- highly malignant liver tumor- highly malignant liver tumor
- composed of irregular spindle cells lining - composed of irregular spindle cells lining the lumina of hepatic vascular spacesthe lumina of hepatic vascular spaces
EtiologyEtiology:: - most cases occurs in men (85 %)- most cases occurs in men (85 %)
- high association with chemical agents - high association with chemical agents especially vinyl chloride, Thorotrast, especially vinyl chloride, Thorotrast, arsenicals and organo-chloride pesticidesarsenicals and organo-chloride pesticides
AngiosarcomaAngiosarcoma
Gross Microscopic
Angiosarcoma Con’t.Angiosarcoma Con’t.Clinical presentationClinical presentation:: - tumor commonly spreads locally to the- tumor commonly spreads locally to the spleen (80 % of cases) and distantly to the spleen (80 % of cases) and distantly to the lungs (60 % of cases)lungs (60 % of cases)
TreatmentTreatment:: - resection when feasible, but patients rarely - resection when feasible, but patients rarely
survive 1 yearsurvive 1 year
Sarcomas other than Sarcomas other than angiosarcomaangiosarcoma::
- rare but highly malignant and frequently - rare but highly malignant and frequently not curablenot curable
Portal HypertensionPortal Hypertension - abnormal elevation in portal venous - abnormal elevation in portal venous
pressure (normal 5 – 6 mm Hg)pressure (normal 5 – 6 mm Hg) - - in pressure stimulates the development of in pressure stimulates the development of
venous collaterals, which attempt to venous collaterals, which attempt to decompress the portal system into the decompress the portal system into the systemic systemsystemic system
- collateral veins are very fragile, they form - collateral veins are very fragile, they form portosystemic connections between the portosystemic connections between the portal system and the inferior vena cava via portal system and the inferior vena cava via azygos systemsazygos systems
- when portal pressure exceeds 20 mm Hg, - when portal pressure exceeds 20 mm Hg, dilated veins or varicesdilated veins or varices are likely to develop are likely to develop
Vascular SupplyVascular Supply
Collateral vesselsCollateral vessels
Hepatopetal flow-intrahepatic vasculature is Hepatopetal flow-intrahepatic vasculature is normal,only the portal vein is obstructednormal,only the portal vein is obstructed
Hepatofugal flow- most common pathway of Hepatofugal flow- most common pathway of collateral circulation.collateral circulation. 1. coronary veins1. coronary veins 2.superior hemorrhoidal veins2.superior hemorrhoidal veins 3. umbilcal & paraumbilical veins3. umbilcal & paraumbilical veins 4. veins of Retzius4. veins of Retzius
Portal Hypertension Portal Hypertension Con’t.Con’t.
EtiologyEtiology::1. 1. Intrahepatic causesIntrahepatic causes – most common – most common
a. a. CirrhosisCirrhosis- causes 85 % of portal hypertension- causes 85 % of portal hypertension- Nutritional cirrhosis secondary to alcohol Nutritional cirrhosis secondary to alcohol
abuse-most common.abuse-most common.- postnecrotic cirrhosis-viral hepatitis. postnecrotic cirrhosis-viral hepatitis. - biliary cirrhosis-biliary cirrhosis-- pathologically, produces:- pathologically, produces: 1) progressive narrowing of sinusoidal 1) progressive narrowing of sinusoidal and post sinusoidal vessels due toand post sinusoidal vessels due to centrilobular collagen deposition centrilobular collagen deposition
Alcoholic HepatitisAlcoholic Hepatitis
Mallory’s bodies
A – low power view demonstrating the cardinal features of steatosis, fibrosis , inflammation and hepa- tocellular injuryB – (Black arrow) Mallory BodiesC – (Open arrow) pericellular fibrosis “chicken wire fibrosis”D – the unit lesion (satellitosis)
Portal Hypertension Portal Hypertension Con’t.Con’t.
Portal Hypertension Portal Hypertension Con’t.Con’t.
2) distortion of the sinusoidal 2) distortion of the sinusoidal anatomy by cirrhotic regenera- anatomy by cirrhotic regenera- tive nodules tive nodules
-- resultant sinusoidal block resultant sinusoidal block increases resistance to portal increases resistance to portal blood flow through the liver and blood flow through the liver and portal pressureportal pressure
Portal Hypertension Portal Hypertension Con’t.Con’t.
b. b. SchistosomiasisSchistosomiasis- portal HPN develops when parasitic - portal HPN develops when parasitic ova in small portal venules cause aova in small portal venules cause a presinusoidal blockpresinusoidal block-no impairemnt of hepatic function until -no impairemnt of hepatic function until
late in the course of the dse.late in the course of the dse.c. occasional causes of portal HPNc. occasional causes of portal HPN
1. Wilson’s disease1. Wilson’s disease2. Hepatic fibrosis2. Hepatic fibrosis3. Hemochromatosis3. Hemochromatosis
SchistosomiasisSchistosomiasis
Granulomas due to schistosomiasis in the liver
Wilson’s DiseaseWilson’s Disease
Hepatic FibrosisHepatic Fibrosis
HemochromatosisHemochromatosis
Portal Hypertension Portal Hypertension Con’t.Con’t.
2. 2. Prehepatic causesPrehepatic causes – rare but are more – rare but are more
common in childrencommon in children
a. portal vein obstruction due to a. portal vein obstruction due to either thrombosis, congenital either thrombosis, congenital atresiaatresia
b. stenosis caused by extrinsic b. stenosis caused by extrinsic
compression (tumors)compression (tumors)
Portal Hypertension Portal Hypertension Con’t.Con’t.
3. 3. Posthepatic causesPosthepatic causes – rare – rare a. a. Budd-Chiari syndromeBudd-Chiari syndrome
- characterized by hepatic vein thrombosis - characterized by hepatic vein thrombosis which causes a postsinusoidal block with which causes a postsinusoidal block with resultant hepatomegaly and ascitesresultant hepatomegaly and ascites
- maybe idiopathic or due to a - maybe idiopathic or due to a hypercoagulable state (tumors, hematologic hypercoagulable state (tumors, hematologic disorders, oral contraceptive use and disorders, oral contraceptive use and trauma)trauma)
- - inferior vena caval websinferior vena caval webs most common most common cause of hepatic vein obstruction in asiacause of hepatic vein obstruction in asia
Budd Chiari SyndromeBudd Chiari Syndrome
Gross
HistopathologyHepatic vein thrombosis
Portal Hypertension Portal Hypertension Con’t.Con’t.
b. b. Constrictive pericarditisConstrictive pericarditis - produces a markedly elevated - produces a markedly elevated
inferior vena cava pressure inferior vena cava pressure resistance to venous outflow resistance to venous outflow
- suspected when calcification of - suspected when calcification of the pericardium is presentthe pericardium is present
Constrictive PericarditisConstrictive Pericarditis
Portal Hypertension Portal Hypertension Con’t.Con’t.
Clinical presentationClinical presentation::1. 1. Encephalopathy & ComaEncephalopathy & Coma
- secondary to portosystemic collaterals and - secondary to portosystemic collaterals and hepatic insufficiencyhepatic insufficiency
- related to elevated serum levels of ammonia - related to elevated serum levels of ammonia
2. 2. Gastrointestinal hemorrhageGastrointestinal hemorrhage- gastro-esophageal varices-50% - gastro-esophageal varices-50% - gastritis-30%gastritis-30%- Duodenal ulcers-9%Duodenal ulcers-9%
Portal Hypertension Portal Hypertension Con’t.Con’t.
Hepatic Encephalopathy Variceal Bleeding
Portal Hypertension Portal Hypertension Con’t.Con’t.
3. 3. MalnutritionMalnutrition- in alcoholic cirrhosis- in alcoholic cirrhosis
4. 4. AscitesAscites - hepatic sinusoidal HPN- hepatic sinusoidal HPN
- hypoalbuminemia- hypoalbuminemia-hyperaldoteronism-hyperaldoteronism
5. 5. Collateral venous developmentCollateral venous development - periumbilical caput medusae or - periumbilical caput medusae or hemorrhoidshemorrhoids
6. 6. SplenomegalySplenomegaly -hypersplenism-hypersplenism
WBC ct< 4000/mm3WBC ct< 4000/mm3platelet ct< 100,000mm3 platelet ct< 100,000mm3
Portal HypertensionPortal Hypertension
Portal Hypertension Portal Hypertension Con’t.Con’t.
Spider angioma
Caput medusae
Ascites
Portal Hypertension Portal Hypertension Con’t.Con’t.
Splenomegaly
Portal hypertension Portal hypertension Con’t.Con’t.
Medical managementMedical management:: Acute variceal hemorrhageAcute variceal hemorrhage
- life threatening- life threatening - principal complication of portal HPN that requires- principal complication of portal HPN that requires
emergency interventionemergency intervention 1. 1. Gastroesophagoscopy Gastroesophagoscopy
- should be performed as soon as possible to find the site - should be performed as soon as possible to find the site of bleeding and deter-mine the presence of of bleeding and deter-mine the presence of
varicesvarices - causes of an UGI hemor-rhage- causes of an UGI hemor-rhage
20 – 50 % 20 – 50 % varices varices 20 – 60 % 20 – 60 % erosive gastritis erosive gastritis 6 – 19 % 6 – 19 % PUD PUD 5 – 18 % 5 – 18 % esophageal tears (Mallory Weiss esophageal tears (Mallory Weiss
syndrome)syndrome) - up to 8 % of patients have 2 bleeding sites- up to 8 % of patients have 2 bleeding sites
Portal Hypertension Portal Hypertension Con’t.Con’t.
3. 3. Measures for controlling acute Measures for controlling acute variceal bleedingvariceal bleeding
a. a. Variceal bandingVariceal banding- treatment of choice - treatment of choice - procedure is perform- procedure is perform
endoscopicallyendoscopically- as effective as sclerotherapy- as effective as sclerotherapy- safer- safer
Variceal BandingVariceal Banding
Variceal BandingVariceal Banding
Portal Hypertension Portal Hypertension Con’t.Con’t. b. b. Injection sclerotherapyInjection sclerotherapy
- currently preferred method- currently preferred method - injection results in thrombosis of the vein- injection results in thrombosis of the vein - the procedure is done endoscopically - the procedure is done endoscopically - controls bleeding temporarily in 80 – 90 % - controls bleeding temporarily in 80 – 90 % - mortality rate of 1 – 3 %- mortality rate of 1 – 3 %
- - complicationcomplication rate of approximately 20 – 40% rate of approximately 20 – 40% 1) esophageal perforation1) esophageal perforation2) fever2) fever3) retrosternal chest pain3) retrosternal chest pain4) pleural effusions4) pleural effusions
Injection SclerotherapyInjection Sclerotherapy
Injection SclerotherapyInjection Sclerotherapy
Portal Hypertension Portal Hypertension Con’t.Con’t.
c. c. PharmacotherapyPharmacotherapy1) 1) Vasopressin/NitroglycerinVasopressin/Nitroglycerin (i) (i) VasopressinVasopressin
- potent vasoconstrictor- potent vasoconstrictor - lowers portal pressure by splanchnic - lowers portal pressure by splanchnic
vasoconstriction vasoconstriction results in diminished results in diminished mesenteric blood flowmesenteric blood flow - useful only for short term hemorrhage control- useful only for short term hemorrhage control - does not improve patient survival rates- does not improve patient survival rates
(ii) (ii) NitroglycerinNitroglycerin - lowers portal pressure independently- lowers portal pressure independently
- helps counteract some of the systemic - helps counteract some of the systemic side side effects of vasopressin (e.g. effects of vasopressin (e.g. myocardial myocardial ischemia, limb ischemia, and ischemia, limb ischemia, and bowel necrosis)bowel necrosis)
Portal Hypertension Portal Hypertension Con’t.Con’t.
2) 2) SomatostatinSomatostatin - causes splanchnic vasoconstriction- causes splanchnic vasoconstriction
and and portal pressure with fewer portal pressure with fewer sideside effectseffects
3) 3) Metoclopramide and Penta-Metoclopramide and Penta- gastringastrin
- constrict the lower esophageal - constrict the lower esophageal sphincter sphincter help control bleeding help control bleeding
Portal Hypertension Portal Hypertension Con’t.Con’t.d.d.Balloon tamponadeBalloon tamponade
- Sengstaken-Blakemore tube is a nasogastric - Sengstaken-Blakemore tube is a nasogastric tube with esophageal and gastric balloons for tube with esophageal and gastric balloons for tamponade of varicestamponade of varices
- tubes control bleeding in up 80 % - tubes control bleeding in up 80 %
- bleeding may resume in approximately 20 – 50 % - bleeding may resume in approximately 20 – 50 % when balloon is deflatedwhen balloon is deflated
- pneumonia due to inability to clear salivary - pneumonia due to inability to clear salivary secretions is common unless proximal suction secretions is common unless proximal suction tube is placed above the esophageal balloontube is placed above the esophageal balloon
- esophageal rupture may result from mechanical - esophageal rupture may result from mechanical disruption or ischemia of the esophagusdisruption or ischemia of the esophagus
- to minimize complications - to minimize complications tube should be tube should be used for a limited time (48 hours)used for a limited time (48 hours)
Balloon TamponadeBalloon Tamponade
Portal Hypertension Portal Hypertension Con’t.Con’t.e. e. Transjugular intrahepatic Transjugular intrahepatic
PortosystemicPortosystemic (TIPS) (TIPS) - newest procedure for controlling variceal - newest procedure for controlling variceal
bleedingbleeding - using angiographic techniques, creation of 8 to - using angiographic techniques, creation of 8 to
12 mm shunt between one of the hepatic veins 12 mm shunt between one of the hepatic veins and branch of portal vein and branch of portal vein stent insertion to stent insertion to maintain patencymaintain patency
- rate of post-operative encephalopathy 10 – 30% - rate of post-operative encephalopathy 10 – 30% (same as the surgical shunts)(same as the surgical shunts)
- - complicationscomplications 1) early rebleeding 2) shunt stenosis 1) early rebleeding 2) shunt stenosis 3) thrombosis3) thrombosis
- very helpful in acute hemorrhage in patients - very helpful in acute hemorrhage in patients with portal HPN, particularly those awaiting with portal HPN, particularly those awaiting liver transplantationliver transplantation
Transjugular Intrahepatic Transjugular Intrahepatic Portosystemic Shunt (TIPS)Portosystemic Shunt (TIPS)
Portal Hypertension Portal Hypertension Con’t.Con’t.
Surgical management of Acute massiveSurgical management of Acute massiveBleeding:Bleeding: - acute massive bleeding that fails to respond - acute massive bleeding that fails to respond
to non-surgical maneuvers requires to non-surgical maneuvers requires emergency surgery, especially hypotension emergency surgery, especially hypotension is presentis present
- possibility of bleeding from sources other - possibility of bleeding from sources other than varices should be eliminated before than varices should be eliminated before any surgical procedureany surgical procedure
Portal Hypertension Portal Hypertension Con’t.Con’t.
The decision to proceed with surgeryThe decision to proceed with surgery - made if bleeding continues despite - made if bleeding continues despite
transfusion of 5 units or more of blood transfusion of 5 units or more of blood within 24 hourswithin 24 hours
- risk of death rises after 10 units of - risk of death rises after 10 units of blood have been transfused blood have been transfused due to due to both sepsis and the worsening of both sepsis and the worsening of cirrhotic coagulopathy from the use of cirrhotic coagulopathy from the use of banked bloodbanked blood
Portal Hypertension Portal Hypertension Con’t.Con’t.
- - surgery is not advisable in surgery is not advisable in presence of pneumoniapresence of pneumoniamoderate or severe moderate or severe
encephalopathyencephalopathyalcoholic hepatitisalcoholic hepatitissevere liver failuresevere liver failure
Portal Hypertension Portal Hypertension Con’t.Con’t.- - Type of surgeryType of surgery::
- may be either surgery to - may be either surgery to decompress the portal decompress the portal
venous venous system or surgery to system or surgery to directly ligatedirectly ligate the bleeding the bleeding varicesvarices
1. 1. Emergency portacaval shuntingEmergency portacaval shunting - very effective, over 95 % stops - very effective, over 95 % stops bleedingbleeding - high operative mortality related to - high operative mortality related to
the Child’s classification of the Child’s classification of the the patient patient
a. a. end to side portacaval shunt or a end to side portacaval shunt or a mesocaval shuntmesocaval shunt
Portasystemic ShuntsPortasystemic Shunts
Portal Hypertension Portal Hypertension Con’t.Con’t.
b. 2/3 of peri-operative deaths isb. 2/3 of peri-operative deaths is due to hepatic failure 2due to hepatic failure 2° to acute° to acute
reduction of portal blood flow reduction of portal blood flow to to the liver after shuntingthe liver after shunting lethal contributing factorslethal contributing factors
- pneumonia- pneumonia - renal failure- renal failure
- delirium tremens- delirium tremens
The Child’s Classification for Determining the Operative The Child’s Classification for Determining the Operative Risk of a Shunting Procedure in a Patient with Portal Risk of a Shunting Procedure in a Patient with Portal
HypertensionHypertension
Serum Bilirubin (mg/dL)Serum Bilirubin (mg/dL) < 2< 2 2 - 32 - 3 > 3> 3
Serum Albumin (g/dL)Serum Albumin (g/dL) > 3.5 > 3.5 3 – 3.53 – 3.5 < 3< 3
Presence of Ascites Presence of Ascites AbsentAbsent Early Early controlledcontrolled
SevereSevere
Presence of EncephalopathyPresence of Encephalopathy Absent Absent minimalminimal SevereSevere
Presence of malnutritionPresence of malnutrition Absent Absent Mild Mild Severe Severe
Operative Mortality RateOperative Mortality Rate 2 %2 % 10 %10 % 50 %50 %
Child GroupCA B
Portal Hypertension Portal Hypertension Con’t.Con’t.
2. 2. Ligation of VaricesLigation of Varices - either directly or by esophageal - either directly or by esophageal transection using a stapling device transection using a stapling device
a. ligation is associated with an a. ligation is associated with an operative mortality rate of up to operative mortality rate of up to 30 %30 %b. bleeding recurs within several b. bleeding recurs within several months in up to 80 % months in up to 80 %
c. in most patients, ligation c. in most patients, ligation probably offers no advantage probably offers no advantage
over shunt procedures over shunt procedures
Ligation of VaricesLigation of Varices
AscitesAscites
formation of hepatic lymphformation of hepatic lymph formation of splanchnic formation of splanchnic
lymphlymph HypoalbuminemiaHypoalbuminemia Salt and water retentionSalt and water retention
HyperaldosteronismHyperaldosteronism Anti-diuretic hormoneAnti-diuretic hormone
AscitesAscites
ASCITES Con’t.ASCITES Con’t.The following examinations must be done onThe following examinations must be done onthe ascitic fluidthe ascitic fluid::
1. culture and leucocytes count 1. culture and leucocytes count - WBC count - WBC count 250/ 250/L L infectious infectious2. LDH level2. LDH level - ratio of > 0.6 LDH in the ascitic fluid to serum - ratio of > 0.6 LDH in the ascitic fluid to serum suggestive of infectious or CAsuggestive of infectious or CA3. Serum amylase3. Serum amylase4. Albumin4. Albumin - ratio of serum to ascitic - ratio of serum to ascitic - > 1.1 - > 1.1 portal hpn portal hpn - < 1.1 - < 1.1 malignant ascites malignant ascites
AscitesAscites
Medical tx:Medical tx: Controls 90% of patientsControls 90% of patients Aim is loss wt. (0.5kg-0.75kg/day) by Aim is loss wt. (0.5kg-0.75kg/day) by
Sodium restriction (2000mg/day) and Sodium restriction (2000mg/day) and diuretics (Spironolactone and Furesemide)diuretics (Spironolactone and Furesemide)
Fluid restriction-not necessary unless w/ Fluid restriction-not necessary unless w/ pronounced hyponatremia (< 120mmol/L)pronounced hyponatremia (< 120mmol/L)
AscitesAscites
Refractory ascitesRefractory ascites Serial therapeutic paracentesis w/ or w/o Serial therapeutic paracentesis w/ or w/o
administration of albuminadministration of albumin Peritoneo venous shunt ( Le Veen shunt)-for Peritoneo venous shunt ( Le Veen shunt)-for
those who cannot undergo repeated those who cannot undergo repeated paracentesis and not candidates for liver paracentesis and not candidates for liver transplanttransplant
Transjugular intrahepatic portosystemic Transjugular intrahepatic portosystemic
ParacentesisParacentesis
Contraindications to Contraindications to peritoneovenous shuntsperitoneovenous shunts History of variceal bleedingHistory of variceal bleeding Uncorrectable coagulopthyUncorrectable coagulopthy Bacterial peritonitisBacterial peritonitis Cardiac failureCardiac failure
Ascites Con’t.Ascites Con’t.
Relative contraindication Relative contraindication a. grossly bloody ascitic fluida. grossly bloody ascitic fluid
b. contain many malignant cellsb. contain many malignant cells
c. high protein concentration c. high protein concentration
(> 4.5 g/dL)(> 4.5 g/dL)
Encephalopathy and Encephalopathy and ComaComa
Due hyperammonemia and ammonia Due hyperammonemia and ammonia intoxicationintoxication
Protein from the intestine are converted Protein from the intestine are converted to ammonia by bacteriato ammonia by bacteria
Ammonia are brought to the liver and Ammonia are brought to the liver and converted to urea ( Kreb’s-Henseleit)converted to urea ( Kreb’s-Henseleit)
Hepatic ComaHepatic Coma
1. Reducing nitrogenous material 1. Reducing nitrogenous material
within GITwithin GIT - dietary protein should be reduced - dietary protein should be reduced
to 50 g/day to 50 g/day
- control of active bleeding- control of active bleeding
- K supplement for patients on - K supplement for patients on thiazide diuretics thiazide diuretics
Hepatic Coma Con’t.Hepatic Coma Con’t. 2. Reducing ammonia production 2. Reducing ammonia production andand ammonia ammonia metabolismmetabolism
a. antibiotics to reduce bacteria within a. antibiotics to reduce bacteria within the the bowel (e.g. kanamycin , bowel (e.g. kanamycin , chlortetracycline) chlortetracycline)
b. Cathartics (Lactulose)b. Cathartics (Lactulose) 1) stimulate bacterial anabolism 1) stimulate bacterial anabolism
2) 2) colonic pH – interfere with colonic pH – interfere with ammonia ammonia transfer across colonic transfer across colonic mucosamucosa
c. Glucose- inhibits ammonia c. Glucose- inhibits ammonia production by bacteriaproduction by bacteria
Hepatic ComaHepatic Coma
Gallbladder
Gallbladder AnatomyGallbladder Anatomy - located on the inferior aspect of the liver - located on the inferior aspect of the liver - marks the division of the liver into its right - marks the division of the liver into its right
and left lobesand left lobes1. 1. Anatomic portionAnatomic portion
a. fundus – most anteriora. fundus – most anteriorb. body – serves as the storage areab. body – serves as the storage areac. infundibulum (Hartmann’s pouch) c. infundibulum (Hartmann’s pouch)
– located between the neck and the – located between the neck and the body (most posterior) body (most posterior)
d. neck – connects with the cystic ductd. neck – connects with the cystic duct
GB Anatomy Con’t.GB Anatomy Con’t.
Gallbladder Anatomy Gallbladder Anatomy Con’t.Con’t.
2. 2. Wall of the gallbladderWall of the gallbladder
- composed of smooth muscle - composed of smooth muscle and fibrous tissueand fibrous tissue
- lumen is lined with high - lumen is lined with high columnar epitheliumcolumnar epithelium
Wall Of GallbladderWall Of Gallbladder
Gallbladder Anatomy Gallbladder Anatomy Con’t.Con’t.3. 3. VasculatureVasculature
a. a. Arterial supplyArterial supply - supplied by cystic artery which is- supplied by cystic artery which is
usually a branch of the rightusually a branch of the right hepatic artery (95 % of the time)hepatic artery (95 % of the time)b. b. Venous returnVenous return - via cystic veins to the portal vein - via cystic veins to the portal vein and small veins that drain and small veins that drain directly into directly into the liverthe liverc. c. Lymphatic drainageLymphatic drainage - - from the gallbladder goes both from the gallbladder goes both to the liver to the liver and to hilar nodesand to hilar nodes
GB VasculatureGB Vasculature
Gallbladder Anatomy Gallbladder Anatomy Con’t.Con’t.
4. 4. InnervationInnervation- from the celiac plexus- from the celiac plexus
> > motor innervationmotor innervation travels via vagal travels via vagal postganglionic fibers from the celiac postganglionic fibers from the celiac
ganglia. Preganglionic sympathetic ganglia. Preganglionic sympathetic level is T8 – T9 > level is T8 – T9 > sensory sensory
innervationinnervation travels from travels from sympathetic fiber coursing to the sympathetic fiber coursing to the celiac plexus through the right celiac plexus through the right posterior root ganglion at levels T8 – T9posterior root ganglion at levels T8 – T95. 5. Valves of HeisterValves of Heister - mucosal folds in the cystic - mucosal folds in the cystic
duct (no valvular function)duct (no valvular function)
PhysiologyPhysiology Concentrates bile by absorption of water Concentrates bile by absorption of water
and sodiumand sodium Stimulus for gallbladder emptying is Stimulus for gallbladder emptying is
cholecystokinin (CCK-PZ) cholecystokinin (CCK-PZ) Truncal vagotomy promotes stasisTruncal vagotomy promotes stasis Composition of bile:Composition of bile:
Water- 90%Water- 90% Electrolytes & organic solutes-10%Electrolytes & organic solutes-10%
Cholesterol – 5 %Cholesterol – 5 % Bile acids – 80 %Bile acids – 80 % Lecithin – 15 %Lecithin – 15 %
Biliary SystemBiliary System
500-1000ml –bile that is produced daily500-1000ml –bile that is produced daily 75% of bile are formed by bile canaliculi75% of bile are formed by bile canaliculi Bilirubin diglucuronide- pigment produced Bilirubin diglucuronide- pigment produced
by breakdown of hemoglobinby breakdown of hemoglobin Functions:Functions:
Absorption of triglycerides, Vits A, D, E, K Absorption of triglycerides, Vits A, D, E, K Pathway for the elimination of bilirubin and Pathway for the elimination of bilirubin and
cholesterolcholesterol
Enterohepatic circulationEnterohepatic circulation
Liver conjugates primary bile acidsLiver conjugates primary bile acids
Bile salts are concentrated in the gallbladder
Deconjugation /formation of secondary bile acid in the ileum and colon
colon ileum
Absorption of deconjugated
bile salts
Absorption of conjugated bile salts
Bile acidsBile acids1 ?? Cholic Acid
(synthesized in liver)
Deoxycholic acid 2 ?(produced in the
intestine)
1chenodeo xycholic Acid
(synthesized in liver)
7 α Dehydroxylation
Bacterial
Lithocholic acid 2 ??(produced in the
intestine)7 α Dehydroxylation
Bacterial
7 Ketolithocholic acid 2 ? (produced in the
intestine)
3 ? Ursodeoxycholic acid
Reduction in the liiver
Enterohepatic circulationEnterohepatic circulation
Both primary and secondary bile acid Both primary and secondary bile acid are reabsorbed and taken back tp the are reabsorbed and taken back tp the liverliver
Primary bile acids-constitutes 60%-90% Primary bile acids-constitutes 60%-90% of bile acid poolof bile acid pool
300-600ml-new bile acids which 300-600ml-new bile acids which approximates fecal lossesapproximates fecal losses
Enteroheaptic circulationEnteroheaptic circulation
Malabsorption of bile acid may result to:Malabsorption of bile acid may result to:
1. Fat malabsorption1. Fat malabsorption
2. Defiency in fat soluble vitamins2. Defiency in fat soluble vitamins
3. choleretic diarrhea3. choleretic diarrhea
4.Gallstone formation4.Gallstone formation
Enterohepatic circulationEnterohepatic circulation
Clinical condittions associated with bile Clinical condittions associated with bile malabsorptionmalabsorption Ileal diseaseIleal disease Ileal resectionIleal resection Small bowel obsructionSmall bowel obsruction Blind-loop syndromeBlind-loop syndrome
Gallbladder Con’t.Gallbladder Con’t.Radiologic diagnosis of biliary tract diseaseRadiologic diagnosis of biliary tract disease::
1. 1. Plain abdominal filmPlain abdominal film - demonstrate the 15 % of gallstones that are - demonstrate the 15 % of gallstones that are
radiopaqueradiopaque2. 2. Real time ultrasonographyReal time ultrasonography - 90 – 95 % accuracy in identifying calculi- 90 – 95 % accuracy in identifying calculi - useful in determining the presence of biliary - useful in determining the presence of biliary ductal dilatation, GB wall thickening and the ductal dilatation, GB wall thickening and the presence of pericholecystic fluidpresence of pericholecystic fluid - can be performed in a jaundiced patient- can be performed in a jaundiced patient - usually the initial test obtained in the work up - usually the initial test obtained in the work up of a of a patient with biliary tract diseasepatient with biliary tract disease
Radiologic Diagnostics Radiologic Diagnostics
Plain Abdominal Film Ultrasound
GB Radiologic Diagnosis GB Radiologic Diagnosis Con’t.Con’t.
3. 3. Oral cholecystography (OCG)Oral cholecystography (OCG) - an alternative method for demonstrating - an alternative method for demonstrating
biliary calculi in patients with equivocal biliary calculi in patients with equivocal GB sonogramGB sonogram
- rarely used today - rarely used today
- identifies abnormalities with a 95 – 98 %- identifies abnormalities with a 95 – 98 %
accuracyaccuracy
- patient must ingest iopanoic acid - patient must ingest iopanoic acid tablets on the evening before the studytablets on the evening before the study
Oral CholecystographyOral Cholecystography
Cholelithiasis OCG
Oral CholecystographyOral Cholecystography
GB Radiologic Diagnosis GB Radiologic Diagnosis Con’t.Con’t.
- chief disadvantages lie on its - chief disadvantages lie on its reliance on: reliance on:
a. absorption of contrast medium from a. absorption of contrast medium from gastrointestinal tract gastrointestinal tract
b. uptake and excretion of contrast medium b. uptake and excretion of contrast medium from the hepatocytes from the hepatocytes
c. concentration of contrast medium in the c. concentration of contrast medium in the gallbladder gallbladder
d. patency of hepatic and cystic ductsd. patency of hepatic and cystic ducts
- cholecystokinin stimulation – used to - cholecystokinin stimulation – used to diagnose GB disease in symptomaticdiagnose GB disease in symptomatic
patients with a normal OCGpatients with a normal OCG
GB Radiologic Diagnosis GB Radiologic Diagnosis Con’t.Con’t.
4. 4. Hepatobiliary iminodiacetic acid Hepatobiliary iminodiacetic acid (HIDA) scan (cholescintigraphy)(HIDA) scan (cholescintigraphy)
- provides images of the liver, - provides images of the liver, biliary tree, and the biliary tree, and the
intestinal intestinal transit of bile transit of bile - useful in diagnosis of acute - useful in diagnosis of acute cholecystitis, choledochal cholecystitis, choledochal cyst, bile leak and CBD cyst, bile leak and CBD obstruction obstruction
CholescintigraphyCholescintigraphy
GB Radiologic Diagnosis GB Radiologic Diagnosis Con’t.Con’t.
5. 5. Endoscopic retrograde Endoscopic retrograde cholangiopancrea- cholangiopancrea- tography (ERCP)tography (ERCP)
- useful in evaluating a patient with biliary tract disease- useful in evaluating a patient with biliary tract disease - both diagnostic and therapeutic- both diagnostic and therapeutic
- permits evaluation of the stomach, duodenum, - permits evaluation of the stomach, duodenum, ampulla ampulla of vater pancretic duct and CBD of vater pancretic duct and CBD - if stones are present within the CBD, endoscopic - if stones are present within the CBD, endoscopic
papillotomy can be performed along with extraction of papillotomy can be performed along with extraction of the stones the stones 90 – 95 % success rate 90 – 95 % success rate
- if stricture is present, a stent can be inserted- if stricture is present, a stent can be inserted - complications:- complications:
a. pancreatitis b. bleeding c. duodenal perforationa. pancreatitis b. bleeding c. duodenal perforation - complication rate is approximately 10 %- complication rate is approximately 10 %
- mortality rate of 1 %- mortality rate of 1 %
ERCPERCP
Normal ERCP
ERCPERCP
ERCPERCP
Papillotomy
ERCPERCP
Plasric Stent in the Ampulla Biliary Stent
GB Radiologic Diagnosis GB Radiologic Diagnosis Con’t.Con’t.6. 6. Percutaneous transhepatic cholangio-Percutaneous transhepatic cholangio- graphy (PTHC)graphy (PTHC) - used in evaluating a jaundiced patient- used in evaluating a jaundiced patient
- can localize site of the obstruction- can localize site of the obstruction - allows the placement of biliary drainage - allows the placement of biliary drainage
catheterscatheters - usually performed when ERCP cannot - usually performed when ERCP cannot be performed or when ERCP cannotbe performed or when ERCP cannot
visualize the proximal biliary systemsvisualize the proximal biliary systems systems because of a near-complete systems because of a near-complete
obstruction 2obstruction 2 to tumor, stone or stricture to tumor, stone or stricture
PTHCPTHC
The contrast material The contrast material administered through administered through a Chiba needle a Chiba needle (Arrows) completely (Arrows) completely fills the intrahepatic fills the intrahepatic bile ducts, extremely bile ducts, extremely dilated because of an dilated because of an obstruction of the obstruction of the common bile ductcommon bile duct
GB Radiologic Diagnosis GB Radiologic Diagnosis Con’t.Con’t.
7. 7. CT and MRICT and MRI - expensive but they delineate dilated- expensive but they delineate dilated
ducts as well as retroperitonealducts as well as retroperitoneal
lymphadenopathy and lesions of thelymphadenopathy and lesions of the
pancreas and liverpancreas and liver
8. 8. Intravenous cholangiographyIntravenous cholangiography - no longer performed- no longer performed
CholangiogramCholangiogram
GallstonesGallstones
Normally a balance of bile salts, lecithin and cholesterol keepgallstones from forming. If there are abnormally high levels of bile salts or, more commonly, cholesterol, stones can form. Symptoms usually occur when the stones block one of the biliary ducts, otherwise benign gallstones may be discovered on x-ray or abdominal CT.
GallstonesGallstones
HMG COA
Mevalonate
Choleterol
Bile Acids
HMG COA reductase
Several intermediate steps
7-alpha hydroxylase (rate limiting step)
Pathogenesis of Cholesterol Pathogenesis of Cholesterol Stone Stone
Types of GallstonesTypes of Gallstones
Cholelithiasis Con’t.Cholelithiasis Con’t. 1. 1. Cholesterol stonesCholesterol stones
- large and smooth- large and smooth
- solubility of cholesterol in bile depends on the - solubility of cholesterol in bile depends on the concentration of bile salts, lecithin, and concentration of bile salts, lecithin, and cholesterol. Lecithin and cholesterol are cholesterol. Lecithin and cholesterol are insoluble in aqueous solution but dissolve in insoluble in aqueous solution but dissolve in bile salt – bile salt – lecithin mecilleslecithin mecilles
- failure of the liver to maintain a micellar liquid - failure of the liver to maintain a micellar liquid can be caused by an increase in the can be caused by an increase in the concentration of cholesterol or a decrease in concentration of cholesterol or a decrease in the concentration of bile salts or lecithin the concentration of bile salts or lecithin either can result in stone formationeither can result in stone formation
Cholesterol StonesCholesterol Stones
Cholesterol stoneCholesterol stone
Pure Cholesterol Stone. Transection reveals a glistening crystalline Radiating palisade
Cholelithiasis Con’t.Cholelithiasis Con’t. - conversely, increasing the biliary - conversely, increasing the biliary
concentration of lecithin and bile concentration of lecithin and bile salts should hinder cholesterol salts should hinder cholesterol formationformation
2. 2. Pure pigment (bilirubin) stonesPure pigment (bilirubin) stones - smooth and are green or black in - smooth and are green or black in
colorcolor - associated with hemolytic - associated with hemolytic
disorders, such as sickle cell disorders, such as sickle cell anemia or spherocytosisanemia or spherocytosis
Pure Pigment (Bilirubin) Pure Pigment (Bilirubin) Stones Stones
Cholelithiasis Con’t.Cholelithiasis Con’t. 3. 3. Calcium bilirubinate stonesCalcium bilirubinate stones
- associated with infection or inflammation of - associated with infection or inflammation of the biliary treethe biliary tree a. infection results in an increase in biliary a. infection results in an increase in biliary
calcium as well as an increase in ß-calcium as well as an increase in ß-glucuronidase (converts conjugated glucuronidase (converts conjugated bilirubin to the unconjugated form)bilirubin to the unconjugated form)
b.calcium binds to the unconjugated bilirubin b.calcium binds to the unconjugated bilirubin and preci-pitates to form calcium bili-and preci-pitates to form calcium bili-rubinate stonesrubinate stones
c.normal bile contains glucaro 1,4 lactone, c.normal bile contains glucaro 1,4 lactone, which inhibits the conversion of conjugated which inhibits the conversion of conjugated to unconjugated bilirubin to unconjugated bilirubin deters calcium deters calcium bilirubinate stone formationbilirubinate stone formation
CholelithiasisCholelithiasis
A B
C
A. Pure Biluribinate Stones B. Cholesterol Gallstones
C. Calcium Carbonate Stone
CholelithiasisCholelithiasis
Pigment Stones
Calcium Carbonate Stones
Mixed Stones
MMercedes Benz Stone
Cholelithiasis Con’t.Cholelithiasis Con’t.
Clinical presentationClinical presentation:: Asymptomatic cholelithiasisAsymptomatic cholelithiasis Chronic cholecystitisChronic cholecystitis Acute cholecystitisAcute cholecystitis Complications of cholecystitisComplications of cholecystitis Choledocholithiasis (CBD stones)Choledocholithiasis (CBD stones)
Cholelithiasis Con’t.Cholelithiasis Con’t.Asymptomatic CholelithiasisAsymptomatic Cholelithiasis - treatment is somewhat controversial- treatment is somewhat controversial - approximately 1 – 4 % develop symptoms - approximately 1 – 4 % develop symptoms
or complications or complications - most patients develop symptoms before - most patients develop symptoms before
developing a severe complications of developing a severe complications of cholelithiasischolelithiasis
- there is little evidence that prophylactic - there is little evidence that prophylactic treatment is justified in the management of treatment is justified in the management of cholelithiasis with the exception of calcified cholelithiasis with the exception of calcified or porcelain GB, which should be removed or porcelain GB, which should be removed because the risk of malignancy exceeds 25 because the risk of malignancy exceeds 25 %%
CholecystitisCholecystitis
- inflammation of the gallbladder- inflammation of the gallbladder
- 85 – 90 % cholecystitis is - 85 – 90 % cholecystitis is caused by calculi, bile stasis caused by calculi, bile stasis and bacteria; pancreatic juice and bacteria; pancreatic juice irritation may play a lesser roleirritation may play a lesser role
CholecystitisCholecystitis
Cholecystitis Con’t.Cholecystitis Con’t.Chronic CholecystitisChronic Cholecystitis Clinical presentationClinical presentation - moderate intermittent pain in the RUQ and - moderate intermittent pain in the RUQ and epigastric regionepigastric region - nausea and vomiting- nausea and vomiting - pain may radiate to the back or right scapular- pain may radiate to the back or right scapular regionregion - symptoms may be associated with eating - symptoms may be associated with eating fatty foodsfatty foods
Chronic CholecystitisChronic Cholecystitis
Chronic CholecystitisChronic Cholecystitis
There are areas of There are areas of fibrosis and fibrosis and mononuclear cell mononuclear cell infiltrationinfiltration
Outpouchings of the Outpouchings of the mucosal epithelium mucosal epithelium through the wall through the wall (Rokitansky-Aschoff (Rokitansky-Aschoff sinuses) are also sinuses) are also notednoted
Cholecystitis Con’t.Cholecystitis Con’t.
DiagnosisDiagnosis:: - laboratory studies are generally - laboratory studies are generally
normalnormal
- UTZ reveals stones- UTZ reveals stones
CholecystitisCholecystitis
Ultrasound
Cholecystitis Con’t.Cholecystitis Con’t.TreatmentTreatment:: - elective cholecystectomy- elective cholecystectomy - approximately 95 % of patients receiving - approximately 95 % of patients receiving
surgery for cholecystitis 2surgery for cholecystitis 2 to cholelithiasis to cholelithiasis are completely relieved of their symptomsare completely relieved of their symptoms
- approximately 5 % retains mild symptoms - approximately 5 % retains mild symptoms that presumably unrelated to the biliary treethat presumably unrelated to the biliary tree
Non-operative treatmentNon-operative treatment - oral bile salts, may be appropriate for - oral bile salts, may be appropriate for
patients with small stones and functioning patients with small stones and functioning GB who are not operative candidates or GB who are not operative candidates or who refuse surgerywho refuse surgery
Acute CholecystitisAcute CholecystitisPathophysiologyPathophysiology:: - most cases are due to impacted stone in the - most cases are due to impacted stone in the
GB neck or the cystic duct with resultant GB neck or the cystic duct with resultant obstructionobstruction - direct pressure from the stone on the mucosa or - direct pressure from the stone on the mucosa or
duct obstruction causes duct obstruction causes ischemia, ulceration, ischemia, ulceration, edema, and impaired venous returnedema, and impaired venous return lead to lead to extensive inflammation in and around the extensive inflammation in and around the gallbladdergallbladder
- 75 % of cases, bacterial infection of the bile - 75 % of cases, bacterial infection of the bile and gallbladder wall occursand gallbladder wall occurs
Acute Cholecystitis Con’t.Acute Cholecystitis Con’t.Clinical presentationClinical presentation:: - greatest incidence is in adults 30 – 80 years old- greatest incidence is in adults 30 – 80 years old
- women are affected more than men- women are affected more than men
- most patients give history consistent with prior - most patients give history consistent with prior chronic cholecystitis except this episode is worse chronic cholecystitis except this episode is worse or lasts longeror lasts longer
- fever, nausea, and vomiting- fever, nausea, and vomiting
- right upper quadrant tenderness with or without - right upper quadrant tenderness with or without rebound tendernessrebound tenderness
- Murphy’s sign are common- Murphy’s sign are common
- Gallbladder may be palpable- Gallbladder may be palpable
Acute Cholecystitis Con’t.Acute Cholecystitis Con’t.
Differential diagnosisDifferential diagnosis::1. perforated or penetrating peptic ulcer1. perforated or penetrating peptic ulcer2. myocardial infarction2. myocardial infarction3. pancreatitis3. pancreatitis4. hiatal hernia4. hiatal hernia5. right lower lobe pneumonia5. right lower lobe pneumonia6. appendicitis6. appendicitis7. hepatitis7. hepatitis8. herpes zoster8. herpes zoster
Acute Cholecystitis Con’t.Acute Cholecystitis Con’t.DiagnosisDiagnosis:: 1. 1. Gallbladder ultrasoundGallbladder ultrasound
- diagnostic study of choice- diagnostic study of choice - if acute cholecystitis needs to be documented - if acute cholecystitis needs to be documented
further, a HIDA may be performedfurther, a HIDA may be performed
2. 2. Other mandatory studies includesOther mandatory studies includes - complete blood count- complete blood count - measurement of serum amylase- measurement of serum amylase - serum bilirubin- serum bilirubin - liver enzymes- liver enzymes - ECG- ECG - CXR- CXR
Acute Cholecystitis Con’t.Acute Cholecystitis Con’t.3. 3. Levels of the following may be elevated inLevels of the following may be elevated in patients with acute cholecystitispatients with acute cholecystitis
- serum alkaline phosphatase in 23% - serum alkaline phosphatase in 23% - bilirubin in 45 %- bilirubin in 45 % - aspartate transaminase in 40 %- aspartate transaminase in 40 % - amylase in 13 %- amylase in 13 %
4.4. Ultrasonography Ultrasonography - may show stones and a thick-walled - may show stones and a thick-walled
edematous gallbladder walledematous gallbladder wall
5. Cholescintigraphy5. Cholescintigraphy - will show any existing failure of the gallbladder- will show any existing failure of the gallbladder
Acute Cholecystitis Con’t.Acute Cholecystitis Con’t.
TreatmentTreatment:: - Cholecystitis should be treated with chole-- Cholecystitis should be treated with chole- cystectomycystectomy - As the bile is usually infected, periope-- As the bile is usually infected, periope- rative antibiotics are neededrative antibiotics are needed - - 2 approaches to the timing of surgery2 approaches to the timing of surgery
immediate surgery; that is, within 72 hours of immediate surgery; that is, within 72 hours of the onset of symptomsthe onset of symptoms
delayed surgery; that is, after recovery from the delayed surgery; that is, after recovery from the acute attack with IV fluids and antibiotics. acute attack with IV fluids and antibiotics. Surgery should be performed approximately 6 Surgery should be performed approximately 6 weeks after the acute inflammation has resolvedweeks after the acute inflammation has resolved
Acute Cholecystitis Con’t.Acute Cholecystitis Con’t. - most surgeons now advocate - most surgeons now advocate early early
surgical interventionsurgical intervention in the treatment in the treatment of acute cholecystitisof acute cholecystitis due to the improved safety of current due to the improved safety of current
techniques, the effective-ness of perioperative techniques, the effective-ness of perioperative antibiotics, and the high risk (at least 50 %) of antibiotics, and the high risk (at least 50 %) of recurrent acute cholecystitis if surgery is recurrent acute cholecystitis if surgery is delayeddelayed
approach is as followsapproach is as follows a. if symptoms began within 72 hours of the time of pre- a. if symptoms began within 72 hours of the time of pre- sentation, laparoscopic cholecystectomy is sentation, laparoscopic cholecystectomy is
performedperformed b. if symptoms began more than 72 hours before the b. if symptoms began more than 72 hours before the
time of presentation and the patient is responding to time of presentation and the patient is responding to medical management (NGT, IV, NPO and antibiotics) medical management (NGT, IV, NPO and antibiotics) then surgery is delayedthen surgery is delayed
c. deterioration or failure to improve on medical c. deterioration or failure to improve on medical management is an indication for surgerymanagement is an indication for surgery
Acalculous CholecystitisAcalculous Cholecystitis
- acute or chronic cholecystitis in - acute or chronic cholecystitis in the absence of stonesthe absence of stones
- acute form occurs as a - acute form occurs as a complication of burns, sepsis, complication of burns, sepsis, trauma, or collagen vascular trauma, or collagen vascular diseasedisease
- chronic condition may also be - chronic condition may also be referred to as a referred to as a biliary dyskinesiabiliary dyskinesia
Acalculous CholecystitisAcalculous Cholecystitis
Acalculous Cholecystitis Acalculous Cholecystitis Con’t.Con’t.
EtiologyEtiology: possible causes include:: possible causes include:1. kinking or fibrosis of the gallbladder1. kinking or fibrosis of the gallbladder2. thrombosis of the cystic artery2. thrombosis of the cystic artery3. sphincter spasm with obstruction of the 3. sphincter spasm with obstruction of the
biliary and pancreatic ductsbiliary and pancreatic ducts4. prolonged fasting4. prolonged fasting5. dehydration5. dehydration6. systemic disease, such as the multi-6. systemic disease, such as the multi-
organ failure associated with traumaorgan failure associated with trauma7. generalized sepsis7. generalized sepsis
Acalculous Cholecystitis Acalculous Cholecystitis Con’t.Con’t.
DiagnosisDiagnosis:: - diagnostic tests used and their results - diagnostic tests used and their results
are similar to those for calculous are similar to those for calculous cholecystitis, except that no stones cholecystitis, except that no stones are seenare seen
- cholescintigram is especially accurate - cholescintigram is especially accurate for cholecystitis when it fails to for cholecystitis when it fails to visualize the gallbladdervisualize the gallbladder
Acalculous Cholecystitis Acalculous Cholecystitis Con’t.Con’t.
TreatmentTreatment:: - cholecystectomy or chole-- cholecystectomy or chole-
cystostomy if the patient is too ill cystostomy if the patient is too ill to tolerate cholecystectomyto tolerate cholecystectomy
Gallstone Complications
Mirizzi’s syndromeMirizzi’s syndrome
Mirizzi’s syndromeMirizzi’s syndrome
Hydrops of the GallbladderHydrops of the Gallbladder
Accumulation of Accumulation of mucoid material mucoid material within the gall-within the gall-bladder with no bladder with no inflammation and inflammation and infectioninfection
Hydrops of the GallbladderHydrops of the Gallbladder
Gallbladder mucocele/hydrops Note the gross wall thickening; this is usually measured on theanterior wall of the gallbladder
Hydrops of the GallbladderHydrops of the Gallbladder
perioperative photograph of a gallbladder shows theinflamed mucosa in a gallbladder; note the stones
perioperative photograph of a gallbladder in a patient withacute cholecystitis shows aninflamed, edematous gallbladderwith areas of erythema and congestion.
Empyema of the GallbladderEmpyema of the Gallbladder
Intraluminal abscess of the Intraluminal abscess of the gallbladdergallbladder Patients is toxic, with fever Patients is toxic, with fever
and leukocytosisand leukocytosis Emergency cholecystectomy Emergency cholecystectomy
is neededis needed
Empyema of the gallbladderEmpyema of the gallbladder
In the fresh state, the lumen contained a number of small, In the fresh state, the lumen contained a number of small, faceted stones and copious brown, purulent fluid.faceted stones and copious brown, purulent fluid.
Emphysematous CholecystitisEmphysematous Cholecystitis
Gas within the gallbladder wall Gas within the gallbladder wall with ischemic necrosiswith ischemic necrosis
Clostridium welchii, E. coli, Clostridium welchii, E. coli, KlebsiellaKlebsiella
Seen primarily in diabeticsSeen primarily in diabetics Emergency cholecystectomy Emergency cholecystectomy
is neededis needed
Emphysematous CholecystitisEmphysematous Cholecystitis
Emphysematous CholecystitisEmphysematous Cholecystitis
CT scan shows gas CT scan shows gas within a thickened within a thickened gallbladder wall gallbladder wall (arrows) containing a (arrows) containing a large gallstone large gallstone (arrowhead)(arrowhead)
Note the perichole-Note the perichole-cystic dissection of cystic dissection of the gas (G)the gas (G)
complicationscomplications
2. 2. Gangrenous cholecystitisGangrenous cholecystitis - results when extensive inflammation causes - results when extensive inflammation causes
thrombosis of the cystic artery and resultant thrombosis of the cystic artery and resultant necrosis of the gallbladdernecrosis of the gallbladder
- bile cultures and appropriate antibiotics are - bile cultures and appropriate antibiotics are essentialessential
3. 3. Perforated cholecystitisPerforated cholecystitis - results from necrosis of the gallbladder wall - results from necrosis of the gallbladder wall
and leakage of bile into the peritoneal cavityand leakage of bile into the peritoneal cavity - peritonitis, or more commonly subhepatic - peritonitis, or more commonly subhepatic
abscessabscess
Gangrenous CholecystitisGangrenous Cholecystitis
Acute Gangrenous Acute Gangrenous CholecystitisCholecystitis
The gallbladder has The gallbladder has been opened to show been opened to show marked purulent marked purulent inflammation and inflammation and necrosisnecrosis
Numerous gallstones are Numerous gallstones are surrounded by thick pussurrounded by thick pus
Gangrenous CholecystitisGangrenous Cholecystitis
complicationscomplications4. 4. Biliary – enteric fistula and gallstonesBiliary – enteric fistula and gallstones ileusileus
- complications of cholelithiasis, cystic - complications of cholelithiasis, cystic duct obstruction, recurrent cholecystitis, duct obstruction, recurrent cholecystitis, adhesions to the surrounding viscera, adhesions to the surrounding viscera, perforation, fistula formation, and pass-perforation, fistula formation, and pass-age of the stone into the bowelage of the stone into the bowel
- - site of fistula with the GBsite of fistula with the GB a) duodenum – most commona) duodenum – most common b) colon and other intra-abdominal b) colon and other intra-abdominal
viscera may be involvedviscera may be involved
Gallstones IleusGallstones Ileus
complicationscomplications
- - site of bowel obstructionsite of bowel obstructiona) terminal ileum - most commona) terminal ileum - most common
(narrowest portion of the small bowel)(narrowest portion of the small bowel) stones smaller than 2 – 3 mm usuallystones smaller than 2 – 3 mm usually
passed per rectumpassed per rectumb) if stone is passed free into the b) if stone is passed free into the peritoneal cavity, extra luminal peritoneal cavity, extra luminal obstruction secondary to inflammation obstruction secondary to inflammation and adhesions can occur anywhereand adhesions can occur anywhere
complicationcomplication
Biliary – enteric Fistula and Gallstones IleusBiliary – enteric Fistula and Gallstones IleusCon’t.Con’t. Clinical presentationClinical presentation - bowel obstruction is a disease of the elderly, & - bowel obstruction is a disease of the elderly, &
concomitant multi-system disease is commonconcomitant multi-system disease is common - presents with symptoms of small bowel - presents with symptoms of small bowel
obstruction (nausea, vomiting, obstipation, pain obstruction (nausea, vomiting, obstipation, pain and distension)and distension)
- about 25 % have symptoms of acute cholecystitis - about 25 % have symptoms of acute cholecystitis immediately preceding the episode of obstructionimmediately preceding the episode of obstruction
- about 70 % have history of cholelithiasis- about 70 % have history of cholelithiasis
complicationscomplications
Biliary - enteric Fistula and Gallstones Biliary - enteric Fistula and Gallstones Ileus Con’t.Ileus Con’t. DiagnosisDiagnosis:: - correct diagnosis is made pre-operatively In fewer - correct diagnosis is made pre-operatively In fewer
than 25 % of casesthan 25 % of cases - diagnosis is suggested by the history and by plain - diagnosis is suggested by the history and by plain
films of the abdomenfilms of the abdomen - may show small bowel obstruction accompanied - may show small bowel obstruction accompanied
by air in the biliary tree, or a radiopaque stone in by air in the biliary tree, or a radiopaque stone in the RLQ (seen in 15 % of cases)the RLQ (seen in 15 % of cases)
Cholecystoenteric FistulaCholecystoenteric Fistula
Detection of Detection of cholecystoenteric cholecystoenteric fistulafistularadiologically. radiologically. AA: : ERCP showing ERCP showing appearanceappearanceof pneumobilia with of pneumobilia with common bile duct common bile duct stonestoneand a fistula and a fistula between collapsed between collapsed gallbladder andgallbladder andtransverse colontransverse colon
Fistula
complicationscomplicationsBiliary – enteric Fistula and Gallstones Biliary – enteric Fistula and Gallstones Ileus Con’t.Ileus Con’t. TreatmentTreatment:: - because these patients are often extremely ill, - because these patients are often extremely ill,
emergency laparotomy may permit only emergency laparotomy may permit only localization of the stone, proximal enterotomy, localization of the stone, proximal enterotomy, stone extraction, and closure of the enterotomystone extraction, and closure of the enterotomy
- whole small bowel, CBD and GB must be palpated - whole small bowel, CBD and GB must be palpated for stones as recurrent gallstones ileus (due to for stones as recurrent gallstones ileus (due to other stones) develops in 5 – 9 % of patientsother stones) develops in 5 – 9 % of patients
- cholecystectomy and closure of the biliary fistula - cholecystectomy and closure of the biliary fistula can be performed either concomitantly or after an can be performed either concomitantly or after an interval, depending on the patient’s conditioninterval, depending on the patient’s condition
Gallstones IleusGallstones Ileus
CholecystectomyCholecystectomy
a. a. either an open cholecystectomy or a either an open cholecystectomy or a laparoscopiclaparoscopic
cholecystectomy cholecystectomy can be performedcan be performed1. 1. open cholecystectomyopen cholecystectomy – involves making a – involves making a right subcostal incision and placing right subcostal incision and placing mechanical abdominal retractormechanical abdominal retractor2. 2. laparoscopic cholecystectomylaparoscopic cholecystectomy – involves – involves placing 10 mm and 15 mm ports through the placing 10 mm and 15 mm ports through the abdominal wall and filling the peritoneal abdominal wall and filling the peritoneal cavity with CO2 gascavity with CO2 gas
CholecystectomyCholecystectomy
CholecystectomyCholecystectomy
treatmenttreatment
Advantages and Contraindications of Advantages and Contraindications of Laparoscopic CholecystectomyLaparoscopic Cholecystectomy
AdvantagesAdvantages Relative ContraindicationsRelative Contraindications CosmeticCosmetic Coagulopathy Coagulopathy Shorter hospital stayShorter hospital stay Cirrhosis, portal HPNCirrhosis, portal HPN Rapid return to Rapid return to PregnancyPregnancy ActivityActivity Generalized peritonitisGeneralized peritonitis
Prior surgery(adhesions)Prior surgery(adhesions)Severe cardiopulmonarySevere cardiopulmonaryDiseaseDisease
cholecystostomycholecystostomy
CholecystostomyCholecystostomy
- an alternative procedure when extensive - an alternative procedure when extensive
inflammation makes cholecystectomyinflammation makes cholecystectomy
too dangerous or a patient is too ill to too dangerous or a patient is too ill to
undergo cholecystectomyundergo cholecystectomy
- GB fundus is opened, bile and stones are- GB fundus is opened, bile and stones are
removed and a tube is placed in the GBremoved and a tube is placed in the GB
for external drainagefor external drainage
- Can be done operatively or percutaneously - Can be done operatively or percutaneously
Postcholecystectomy Postcholecystectomy SyndromeSyndrome
- symptoms that develop after or persist - symptoms that develop after or persist despite cholecystectomydespite cholecystectomy
- cholecystectomy for chronic cholecystitis - cholecystectomy for chronic cholecystitis and cholelithiasis and cholelithiasis postcholecystectomy postcholecystectomy symptoms are usually extrabiliary in origin symptoms are usually extrabiliary in origin and caused by:and caused by:
a. hiatal herniaa. hiatal hernia b. peptic ulcerb. peptic ulcer c. pancreatitisc. pancreatitis d. irritable boweld. irritable bowel e. food intolerancee. food intolerance
Postcholecystectomy Postcholecystectomy Syndrome Con’t.Syndrome Con’t.
- symptoms may be biliary in origin and - symptoms may be biliary in origin and caused by:caused by:
a. a stone in the CBDa. a stone in the CBDb. a stone in the stump of the cystic ductb. a stone in the stump of the cystic ductc. stenosis of the sphincter of Oddic. stenosis of the sphincter of Oddid. biliary strictured. biliary stricture
- evaluation should be directed toward - evaluation should be directed toward identifying these extrabiliary and biliary identifying these extrabiliary and biliary etiologies, and made include ERCP, etiologies, and made include ERCP, esophagogastro-duodenoscopy (EGD), UGI esophagogastro-duodenoscopy (EGD), UGI radiograph, ultrasound, and CT scanradiograph, ultrasound, and CT scan
BILIARY DUCT DISORDERS
CholedocholithiasisCholedocholithiasis
- stones in the common bile duct- stones in the common bile duct - can be single or multiple- can be single or multiple - found in 10 – 20 % of patients who - found in 10 – 20 % of patients who
undergo cholecystectomyundergo cholecystectomy - most stones are formed in the GB and - most stones are formed in the GB and
pass into the ductpass into the duct - primary common duct stones can be - primary common duct stones can be
form in the absence of a gallbladderform in the absence of a gallbladder
Positions Positions where the where the gallstones gallstones may get stuckmay get stuck
CholedocholithiasisCholedocholithiasis
CholedocholithiasisCholedocholithiasis Stones are identified Stones are identified
in the common bile in the common bile ductduct
Choledocholithiasis Choledocholithiasis Con’t.Con’t.
Retained stonesRetained stones - stones that remain after surgery complicate - stones that remain after surgery complicate
up to 5 – 10 % of CBD explorationsup to 5 – 10 % of CBD explorations a. no treatment is necessary for smalla. no treatment is necessary for small stones – usually pass spontaneouslystones – usually pass spontaneously
b. treatment options for large stonesb. treatment options for large stones 1) chemical dissolution – 1) chemical dissolution –
intraductal intraductal administration of administration of methyl-tert-butyl methyl-tert-butyl ether or mono- ether or mono-octanoinoctanoin
2) mechanical extraction – under 2) mechanical extraction – under fluoroscopic guidancefluoroscopic guidance
Choledocholithiasis Choledocholithiasis Con’t.Con’t.
c. Primary or recurrent CBD stonesc. Primary or recurrent CBD stones
- can be treated surgically with a - can be treated surgically with a biliary- enteric connection to allow biliary- enteric connection to allow stones to pass out of the biliary stones to pass out of the biliary tree tree
- 2 most common methods are:- 2 most common methods are: a. Choledochoduodenostomya. Choledochoduodenostomy
b. Choledochojejunostomyb. Choledochojejunostomy - transduodenal sphinctero-- transduodenal sphinctero-
plast or endoscopic plast or endoscopic sphincterotomy - sphincterotomy -
acceptable options acceptable options
Choledocholithiasis Choledocholithiasis Con’t.Con’t.
Clinical presentationClinical presentation - some patients are asymptomatic- some patients are asymptomatic - most patients present with RUQ pain - most patients present with RUQ pain
that radiates to the back and right that radiates to the back and right shouldershoulder
- intermittent obstructive jaundice- intermittent obstructive jaundice - acholic stools- acholic stools - bilirubinuria- bilirubinuria
Choledocholithiasis Choledocholithiasis Con’t.Con’t.
DiagnosisDiagnosis:: - GB is not palpable in contrast to neoplastic - GB is not palpable in contrast to neoplastic
obstruction of the CBDobstruction of the CBD - Diagnostic studies include- Diagnostic studies include
a. ultrasonographya. ultrasonographyb. ERCPb. ERCPc. transhepatic cholangiography orc. transhepatic cholangiography or
radionuclide scanradionuclide scan - Liver function test results are consistent - Liver function test results are consistent
with obstructive jaundice and include with obstructive jaundice and include elevations in bilirubin and alkaline elevations in bilirubin and alkaline phosphatasephosphatase
Choledocholithiasis Choledocholithiasis Con’t.Con’t.
Surgical treatmentSurgical treatment:: InvolvesInvolves
a. cholecystectomya. cholecystectomyb. choledochotomy (opening the b. choledochotomy (opening the common duct) common duct)
c. CBD explorationc. CBD exploration d. stone removald. stone removal e. T tube placemente. T tube placement f. T tube operative cholangio-f. T tube operative cholangio-
graphy graphy
CholangitisCholangitis - infection of the bile ducts- infection of the bile ducts - potentially life-threatening disease that - potentially life-threatening disease that results from concurrent biliary infection results from concurrent biliary infection and obstruction and obstruction - E. coli is the most common offending - E. coli is the most common offending
organismorganism
EtiologyEtiology:: - benign postoperative strictures and CBD stones – - benign postoperative strictures and CBD stones –
60 %60 % - other causes:- other causes:
a. neoplasmsa. neoplasmsb. sclerosing cholangitisb. sclerosing cholangitisc. plugged biliary drainage tubesc. plugged biliary drainage tubesd. biliary contrast studiesd. biliary contrast studies
CholangitisCholangitis
CholangitisCholangitis
Endoscopic finding Histopathology
Cholangitis Con’t.Cholangitis Con’t.Clinical presentationClinical presentation:: Charcot’s triad of fever, jaundice, and Charcot’s triad of fever, jaundice, and
RUQ pain is present in 70 % of casesRUQ pain is present in 70 % of cases In severe cases, hypotension may be In severe cases, hypotension may be
presentpresent
TreatmentTreatment:: antibioticsantibiotics resuscitation with fluids and resuscitation with fluids and
electrolyteselectrolytes relief of obstructionrelief of obstruction
Cholangitis Con’t.Cholangitis Con’t.
PrognosisPrognosis:: - depends on the cause of the - depends on the cause of the
obstructionobstruction
- best prognosis to worst- best prognosis to worst
a. stonesa. stones
b. benign strictureb. benign stricture
c. sclerosing cholangitisc. sclerosing cholangitis
d. neoplasmd. neoplasm
Primary Sclerosing Primary Sclerosing CholangitisCholangitis
- disease of unknown etiology that - disease of unknown etiology that affects the biliary tract resulting in affects the biliary tract resulting in stenosis or obstruction of the ductal stenosis or obstruction of the ductal systemsystem
- progressive obstruction, if not relieved, - progressive obstruction, if not relieved, results in biliary cirrhosis and liver results in biliary cirrhosis and liver failurefailure
Primary Sclerosing Primary Sclerosing CholangitisCholangitis
Primary Sclerosing Primary Sclerosing CholangitisCholangitis
Cholangiography ERCP
PSC Con’t.PSC Con’t.Clinical presentationClinical presentation:: - symptoms and signs includes- symptoms and signs includes
a. RUQ paina. RUQ painb. painless jaundiceb. painless jaundicec. usually without fever or chillsc. usually without fever or chillsd. pruritusd. prurituse. fatiguee. fatiguef. nauseaf. nauseag. symptoms of hepatic failureg. symptoms of hepatic failure
- other inflammatory conditions, particularly - other inflammatory conditions, particularly ulcerative colitis may be presentulcerative colitis may be present
PSC Con’t.PSC Con’t. HistologyHistology:: - bile ducts show edema and areas of inflammation - bile ducts show edema and areas of inflammation
and fibrosisand fibrosis
DiagnosisDiagnosis:: - usually made by ERCP or a transhepatic cholangiogram and - usually made by ERCP or a transhepatic cholangiogram and
occasionally by intraoperative cholangiographyoccasionally by intraoperative cholangiography - - criteria needed to fulfill the diagnosis are:criteria needed to fulfill the diagnosis are:
a. thickening and stenosis of a major portion of the biliarya. thickening and stenosis of a major portion of the biliary ductal systemductal system
b. absence of prior surgery, choledocholithiasis, malignancyb. absence of prior surgery, choledocholithiasis, malignancy or congenital biliary anomaliesor congenital biliary anomaliesc. no evidence of primary liver disease, particularly primary c. no evidence of primary liver disease, particularly primary biliary cirrhosisbiliary cirrhosis
PSC Con’t.PSC Con’t. TreatmentTreatment:: - operative management is dependent on the - operative management is dependent on the
level of bile duct involvement and the level of bile duct involvement and the amount of fibrosis presentamount of fibrosis present
- - restoration of adequate and permanent restoration of adequate and permanent biliary damage is the goal of operative biliary damage is the goal of operative managementmanagement
a. internal biliary drainage – via a. internal biliary drainage – via hepatico- enteric or choledocho- hepatico- enteric or choledocho- enteric anastomosis – the preferred enteric anastomosis – the preferred
method of management successful method of management successful only when the major area of involve- only when the major area of involve- ment is the extrahepatic bile ducts ment is the extrahepatic bile ducts
PSC Con’t.PSC Con’t.b. external biliary drainage – using a T b. external biliary drainage – using a T tube or other percutaneous stent, tube or other percutaneous stent, establishes adequate drainage establishes adequate drainage
c. cholestectomy is performed onlyc. cholestectomy is performed only when GB disease requires itwhen GB disease requires it
Postoperative treatmentPostoperative treatment:: - strongly dependent upon the presence of - strongly dependent upon the presence of
preoperative sepsis and the adequacy of preoperative sepsis and the adequacy of drainagedrainage
- steroids are not beneficial and could - steroids are not beneficial and could potentially complicate the postoperative potentially complicate the postoperative coursecourse
PSC Con’t.PSC Con’t.
PrognosisPrognosis:: - poorly defined at present- poorly defined at present - if the liver parenchyma has been - if the liver parenchyma has been
damaged or if the intrahepatic ducts damaged or if the intrahepatic ducts are significantly involved, only hepatic are significantly involved, only hepatic transplantation offers a real chance of transplantation offers a real chance of longevity, and this procedure is only longevity, and this procedure is only possible when the patient is free of possible when the patient is free of sepsissepsis
Fibrosis of the Sphincter Fibrosis of the Sphincter of Oddiof Oddi
- a disorder of uncertain etiology that - a disorder of uncertain etiology that causes colicky RUQ pain, nausea, causes colicky RUQ pain, nausea, vomiting and frequently recurrent vomiting and frequently recurrent pancreatitispancreatitis
- treatment is by endoscopic papillo- - treatment is by endoscopic papillo- tomy of transduodenal sphictero-tomy of transduodenal sphictero-plastyplasty
NEOPLASM
Benign Tumors of the GBBenign Tumors of the GB - rare- rare - includes:- includes:
a. papillomaa. papillomab. adenomyomab. adenomyomac. fibromac. fibromad. lipomad. lipomae. myomae. myomaf. myxomaf. myxomag. carcinoidg. carcinoid
Carcinoma of the GBCarcinoma of the GB
- accounts for 4 % of all carcinomas- accounts for 4 % of all carcinomas
- most common cancer of the biliary- most common cancer of the biliary
tract tract
- occurs in 1 % of all patients under- - occurs in 1 % of all patients under- going biliary tract surgery going biliary tract surgery
Carcinoma of the GBCarcinoma of the GB
The gallbladder wall The gallbladder wall is infiltrated by firm, is infiltrated by firm, greyish-white tumorgreyish-white tumor
The lumen contains The lumen contains gallstonesgallstones
Carcinoma of the GBCarcinoma of the GB
Note the malignant Note the malignant glands provoking glands provoking fibrous reaction in fibrous reaction in the deeper portion of the deeper portion of the wallthe wall
A – Malignant glandA – Malignant gland
Carcinoma of the GBCarcinoma of the GB
AdenoCA of the AdenoCA of the GallbladderGallbladder
Carcinoma of the GB Carcinoma of the GB
Pathogenesis of Gallbladder Carcinoma associated with Gallstones and Inflammation
Carcinoma of the GB Carcinoma of the GB Con’t.Con’t.
EtiologyEtiology:: - although the cause is not known, 90 % - although the cause is not known, 90 %
of the patients have cholelithiasisof the patients have cholelithiasis - about 80 % of the tumors are adeno-- about 80 % of the tumors are adeno-
carcinomacarcinoma - metastases occur by lymphatic - metastases occur by lymphatic
spread to the pancreatic, duodenal, spread to the pancreatic, duodenal, and chelodochal nodes, and by direct and chelodochal nodes, and by direct extension to the liverextension to the liver
Carcinoma of the GB Con’t.Carcinoma of the GB Con’t.Clinical presentationClinical presentation:: - RUQ pain – most common complaint- RUQ pain – most common complaint - Nausea and vomiting- Nausea and vomiting - Diagnosis is rarely made - Diagnosis is rarely made
preoperativelypreoperatively - Patients with calcification of the wall - Patients with calcification of the wall
of the GB (porcelain GB) that is seen of the GB (porcelain GB) that is seen on plain radiograph of the on plain radiograph of the
- abdomen have a carcinoma of the GB - abdomen have a carcinoma of the GB in approximately ½ of casesin approximately ½ of cases
Porcelain GallbladderPorcelain Gallbladder
Porcelain gallbladderPorcelain gallbladder Cholecystectomy Cholecystectomy
should be performed should be performed as soon after diagnosis as soon after diagnosis as possible because of as possible because of high incidence of high incidence of malignancymalignancy
A – stoneA – stone
B – intramural B – intramural calcificationcalcification
Porcelain GallbladderPorcelain Gallbladder
Note extensive, Note extensive, yellowish intramural yellowish intramural calcification and calcification and stonesstones
Porcelain GallbladderPorcelain Gallbladder
Porcelain GallbladderPorcelain Gallbladder
Carcinoma of the GBCarcinoma of the GB
TreatmentTreatment:: - curable cases are those whose tumor is - curable cases are those whose tumor is
found incidentally at cholecystectomy for found incidentally at cholecystectomy for other reasonsother reasons
- if there is microscopic invasion of the GB - if there is microscopic invasion of the GB cholecystectomy with wedge resection of cholecystectomy with wedge resection of the liver and regional lymphadenectomy the liver and regional lymphadenectomy may improve survivalmay improve survival
PrognosisPrognosis:: - poor- poor - 5 year survival rate ranges from 0 - 10 %- 5 year survival rate ranges from 0 - 10 %
CholangiosarcomaCholangiosarcoma
Gross Microscopic
CholangiosarcomaCholangiosarcoma - tumor that arises from the bile duct - tumor that arises from the bile duct
epitheliumepithelium - represents 5 – 30 % of all primary hepatic - represents 5 – 30 % of all primary hepatic
malignanciesmalignancies
Clinical presentationClinical presentation:: - signs and symptoms includes- signs and symptoms includes
right upper quadrant painright upper quadrant pain jaundicejaundice hepatomegalyhepatomegaly occasionally a palpable massoccasionally a palpable mass
- patients are usually 60 – 70 years of age- patients are usually 60 – 70 years of age
CBD Malignant TumorsCBD Malignant Tumors
- rare and difficult to cure- rare and difficult to cure
Clinical presentationClinical presentation:: - patient usually complains of pruritus, anorexia, - patient usually complains of pruritus, anorexia,
weight loss, and an aching RUQ painweight loss, and an aching RUQ pain - jaundice is usually severe- jaundice is usually severe - - diseases associated with this malignancydiseases associated with this malignancy
a. sclerosing cholangitisa. sclerosing cholangitisb. chronic parasitic infection of the bile b. chronic parasitic infection of the bile
ductsductsc. gallstones (present in 18 – 65 % of cases)c. gallstones (present in 18 – 65 % of cases)d. prior exposure to Thorotrastd. prior exposure to Thorotrast
Malignant Tumors of the Malignant Tumors of the bile ductsbile ducts
DiagnosisDiagnosis:: - made by percutaneous - made by percutaneous
transhepatic cholangiography or transhepatic cholangiography or ERCPERCP
- both procedures are capable of - both procedures are capable of biopsy for pathologic examinationbiopsy for pathologic examination
CholangiocarcinomaCholangiocarcinoma
Peripheral Cholangiocarcinoma Hilar Cholangiocarcinoma(Klatskin tumor)
CBD Malignant TumorsCBD Malignant Tumors- tumor may be located in the distal - tumor may be located in the distal CBD (1/3 of cases), common hepatic CBD (1/3 of cases), common hepatic duct or cystic duct (1/3 of cases), or duct or cystic duct (1/3 of cases), or the right or left hepatic duct when the right or left hepatic duct when
the the confluence of the hepatic ducts is confluence of the hepatic ducts is involved, the tumor is involved, the tumor is Klatskin Klatskin
tumortumor
- tumor initially metastasizes to the - tumor initially metastasizes to the regional regional lymph nodes (16 % of lymph nodes (16 % of cases), spread by direct extension cases), spread by direct extension into the liver (14 %), or metastasizes into the liver (14 %), or metastasizes to the liver (10 %) to the liver (10 %)
CBD Malignant TumorsCBD Malignant Tumors TreatmentTreatment:: - generally surgical, although fewer than 10 % are - generally surgical, although fewer than 10 % are
resectable at the time of the initial diagnosisresectable at the time of the initial diagnosisa. tumors in the distal duct – may be a. tumors in the distal duct – may be
resected resected by pancreaticoduodenectomy by pancreaticoduodenectomy (Whipple (Whipple procedure) with procedure) with biliary and biliary and gastro-intestinal gastro-intestinal reconstruction reconstruction
- more proximal lesions can sometimes be locally - more proximal lesions can sometimes be locally resected with biliary reconstructionresected with biliary reconstruction
- average length of survival after resection is 23 - average length of survival after resection is 23 monthsmonths
- postoperative radiation may improve the life - postoperative radiation may improve the life expectancyexpectancy
Whipple’s Procedure
CBD Malignant TumorsCBD Malignant Tumors b. unresectable lesions should have b. unresectable lesions should have rigid stents placed to provide rigid stents placed to provide palliation of the biliary palliation of the biliary obstructive symptoms obstructive symptoms
- laparotomy with no bypass is - laparotomy with no bypass is
associated with an averageassociated with an average survival time of < 6 months survival time of < 6 months
- with stenting, the average - with stenting, the average time time 19 months 19 months
Stent on the CBDStent on the CBD
Endoscopic View
Radiographic View
Malignant Tumors of the Malignant Tumors of the bile ductsbile ducts
PrognosisPrognosis::
- metastatic spread of the tumor is usually - metastatic spread of the tumor is usually slow and is not responsible for deathslow and is not responsible for death
- usual cause of death is related to the - usual cause of death is related to the following:following:
a. progressive biliary cirrhosis due to a. progressive biliary cirrhosis due to inadequate biliary drainage inadequate biliary drainageb. persistent intrahepatic infection and b. persistent intrahepatic infection and abscess formation abscess formationc. general debilityc. general debilityd. sepsisd. sepsis
Choledochal CystsCholedochal CystsClassificationClassification
a. Type I: fusiform dilatation of the CBDa. Type I: fusiform dilatation of the CBD b. Type II: diverticulum of the CBDb. Type II: diverticulum of the CBD c. Type III: choledochocele involving the c. Type III: choledochocele involving the
intraduodenal portion of the CBD intraduodenal portion of the CBD
d. Type IV: cystic involvement of both d. Type IV: cystic involvement of both intra & extrahepatic bile ductsintra & extrahepatic bile ducts
e. Type V: cystic dse of the intrahepatic ductse. Type V: cystic dse of the intrahepatic ducts( Caroli’s disease)( Caroli’s disease)
Choledochal CystCholedochal Cyst
Choledochal CystCholedochal Cyst
Choledochal CystCholedochal Cyst
Type I (Fusiform) Choledochal Cyst
Choledochal CystCholedochal Cyst
Type II Choledochal Cyst Type III Choledochal Cyst
Choledochal CystCholedochal Cyst
Type IV Choledochal Cyst
Choledochal Cyst Con’t.Choledochal Cyst Con’t.Clinical presentationClinical presentation:: - most common presenting symptom is intermittent - most common presenting symptom is intermittent
jaundicejaundice - classic triad of pain, jaundice, and an abdominal - classic triad of pain, jaundice, and an abdominal
mass occurs in only 30 % of the patientsmass occurs in only 30 % of the patients
DiagnosisDiagnosis::- ultrasonography – best initial investigative study- ultrasonography – best initial investigative study- radionuclide scanning – 2nd best- radionuclide scanning – 2nd best- transhepatic cholangiography and ERCP – can- transhepatic cholangiography and ERCP – can
define the extent of the disease but are not define the extent of the disease but are not necessarynecessary
Choledochal Cyst Con’t.Choledochal Cyst Con’t.TreatmentTreatment:: - due to the risk of malignancy, cyst excision (rather- due to the risk of malignancy, cyst excision (rather than bypass) is the cornerstone of surgerythan bypass) is the cornerstone of surgery - Type I – treated with cholecystectomy, cyst - Type I – treated with cholecystectomy, cyst excision, and Roux- en-Y choledocho- excision, and Roux- en-Y choledocho-
jejunostomy jejunostomy - Type II – treated by excision of the CBD - Type II – treated by excision of the CBD
diverticulum diverticulum - Type III – treated by cyst excision and choledo-- Type III – treated by cyst excision and choledo-
choduodenostomy or by choduodenostomy or by transduodenal transduodenal sphincteroplasty sphincteroplasty
- Type IV & V – complete cyst excision; roux-y - Type IV & V – complete cyst excision; roux-y hepatico-jejenostomyhepatico-jejenostomy
Roux-en Y CholedochojejunostomyRoux-en Y Choledochojejunostomy
Trauma (GB injuries) Trauma (GB injuries) Con’t.Con’t.
Types of injuriesTypes of injuries:: - contusions- contusions
- avulsion- avulsion
- rupture- rupture
- traumatic cholecystitis- traumatic cholecystitis
Trauma (GB Injuries)Trauma (GB Injuries)
Gallbladder injuriesGallbladder injuries:: - uncommon but are seen after - uncommon but are seen after
both penetrating and non-both penetrating and non-penetrating traumapenetrating trauma
- associated visceral injuries are - associated visceral injuries are common and most frequently common and most frequently (72%) involve the liver(72%) involve the liver
Trauma (GB injuries) Trauma (GB injuries) Con’t.Con’t.
Clinical presentationClinical presentation::- Most common symptoms:- Most common symptoms:- RUQ pain- RUQ pain- Right chest pain- Right chest pain- Biliary leakage through a penetrating - Biliary leakage through a penetrating wound and shockwound and shock
DiagnosisDiagnosis::- made at laparotomy- made at laparotomy- peritoneal tap may be negative- peritoneal tap may be negative
Roux-en Y CholedochojejunostomyRoux-en Y Choledochojejunostomy
Portal Hypertension Portal Hypertension Con’t.Con’t.
Effective management of EsophagealEffective management of Esophageal
Varices:Varices:- used when patients are not actively - used when patients are not actively
bleedingbleeding
- the goal is to prevent re-bleeding with its - the goal is to prevent re-bleeding with its
concomitant risk of death concomitant risk of death
1. 1. Pre-operative evaluationPre-operative evaluation
a. a. EndoscopyEndoscopy
- used to prove that the esophageal- used to prove that the esophageal
varices bledvarices bled
Portal Hypertension Portal Hypertension Con’t.Con’t.
c. c. Child’s classificationChild’s classification - used to evaluate the operative risk- used to evaluate the operative risk
d. patient’s portal venous anatomy is d. patient’s portal venous anatomy is
determined, verifying the presence ofdetermined, verifying the presence of
a patient portal vein by the followinga patient portal vein by the following
1) splenic and superior arteriography 1) splenic and superior arteriography followed by delayed venous-phase followed by delayed venous-phase imaging – most accurateimaging – most accurate
The Child’s Classification for Determining the Operative The Child’s Classification for Determining the Operative Risk of a Shunting Procedure in a Patient with Portal Risk of a Shunting Procedure in a Patient with Portal
HypertensionHypertension
Serum Bilirubin (mg/dL)Serum Bilirubin (mg/dL) < 2< 2 2 - 32 - 3 > 3> 3
Serum Albumin (g/dL)Serum Albumin (g/dL) > 3.5 > 3.5 3 – 3.53 – 3.5 < 3< 3
Presence of Ascites Presence of Ascites AbsentAbsent Early Early controlledcontrolled
SevereSevere
Presence of EncephalopathyPresence of Encephalopathy Absent Absent minimalminimal SevereSevere
Presence of malnutritionPresence of malnutrition Absent Absent Mild Mild Severe Severe
Operative Mortality RateOperative Mortality Rate 2 %2 % 10 %10 % 50 %50 %
Child GroupCA B
Portal Hypertension Portal Hypertension Con’t.Con’t.
2) 2) Doppler ultrasoundDoppler ultrasound to identify the to identify the portal vein and its tributaries and portal vein and its tributaries and ascertain patency and ascertain patency and
direction of flowdirection of flow - simple and non- invasive- simple and non- invasive
3. 3. SplenoportographySplenoportography - injection of radio opaque dye into - injection of radio opaque dye into the the spleen followed by imaging of the spleen followed by imaging of the
portal system portal system - reserved for specific visualization of - reserved for specific visualization of
the splenic vein the splenic vein e. The portal venous pressure can be measured indirectly by measuring the wedged hepatic venous pressure
Portal Hypertension Portal Hypertension Con’t.Con’t.
2. 2. Type of non-operative managementType of non-operative management a) TIPS a) TIPS
b) b) Direct occlusion of varicesDirect occlusion of varices 1) Endoscopic variceal banding or sclerosis1) Endoscopic variceal banding or sclerosis
- initially effective in up to 80 – 90 %- initially effective in up to 80 – 90 % - principal initial method of - principal initial method of
managementmanagement for esophageal varicesfor esophageal varices
2) Many patients require re-2) Many patients require re-sclerosis sclerosis procedures procedures 3) Esophageal stricture – a major 3) Esophageal stricture – a major risk of risk of chronic therapy chronic therapy
Transjugular Intrahepatic Transjugular Intrahepatic Portosystemic Shunt (TIPS)Portosystemic Shunt (TIPS)
Anatomy and PhysiologyAnatomy and Physiology
AnatomyAnatomy
Normal Liver
Anatomy:Anatomy:
Cut Surface of Normal Liver
Anatomy:Anatomy:
Microscopic
Liver CirrhosisLiver Cirrhosis
Gallbladder Con’t.Gallbladder Con’t.PhysiologyPhysiology:: bile is produced by the liver and transported via bile is produced by the liver and transported via
extrahepatic ducts to the GB, where it is extrahepatic ducts to the GB, where it is concentrated and released in response to humoral concentrated and released in response to humoral and neural controland neural control
1. 1. Hepatic production of bileHepatic production of bile- under neural and humoral control- under neural and humoral control- vagal and splanchnic stimulation, secretin- vagal and splanchnic stimulation, secretin
theophylline, phenobarbital and steroids theophylline, phenobarbital and steroids →→ increase bile flowincrease bile flow
- approximately 600 ml of bile are produced - approximately 600 ml of bile are produced daily (normal range 250 – 1000 ml/day)daily (normal range 250 – 1000 ml/day)
GB Physiology Con’t.GB Physiology Con’t.2. 2. Composition of bileComposition of bile - electrolyte concentration of bile approximates - electrolyte concentration of bile approximates
that of plasma (Lactated Ringer’s solution – that of plasma (Lactated Ringer’s solution – good replacement fluid for biliary losses)good replacement fluid for biliary losses)
a. electrolytes and watera. electrolytes and waterb. bile pigmentsb. bile pigmentsc. proteinc. proteind. lipids d. lipids
- phospholipids, primarily lecithin- phospholipids, primarily lecithin - cholesterol- cholesterol
- bile acids(bile salts); chenodeoxycholic - bile acids(bile salts); chenodeoxycholic acid & cholic acid conjugated acid & cholic acid conjugated
with taurinewith taurine and glycineand glycine
GB Function Con’t.GB Function Con’t.3. 3. Functions of the gallbladder includeFunctions of the gallbladder include::
a. a. storage of bilestorage of bileb. b. concentration of bileconcentration of bile - absorption of water and electrolytes by the - absorption of water and electrolytes by the GB mucosa results in a 10 fold increased GB mucosa results in a 10 fold increased concentration of lipids, bile salts, and bileconcentration of lipids, bile salts, and bile pigments compared with hepatic bilepigments compared with hepatic bile - secretion of mucus protects the GB mucosa - secretion of mucus protects the GB mucosa
from the irritant effects of bile and from the irritant effects of bile and facilitates facilitates the passage of bile through the the passage of bile through the cystic duct. cystic duct. Mucus secretion represents Mucus secretion represents the the “white bile”“white bile” seen with seen with hydrops of the GBhydrops of the GB, , which results which results from cystic duct obstruction from cystic duct obstruction
GB Physiology Con’t.GB Physiology Con’t.
3. 3. release of bilerelease of bile - the coordinated release of bile - the coordinated release of bile
requires simultaneous contraction of requires simultaneous contraction of
the GB and relaxation of sphincter of the GB and relaxation of sphincter of
OddiOddi
- process is predominantly under - process is predominantly under
humoral control (via cholecystokinin),humoral control (via cholecystokinin),
vagal and splanchnic nerves also playvagal and splanchnic nerves also play
a rolea role
Cholesterol StonesCholesterol Stones
Cholelithiasis Cholelithiasis (Gallstones)(Gallstones)
Types and mode of formationTypes and mode of formation - gallstones form as a result of - gallstones form as a result of
biliary solids precipitating out of biliary solids precipitating out of the solutionthe solution
- 70 % are made up of cholesterol, - 70 % are made up of cholesterol, bilirubin, and calcium with bilirubin, and calcium with cholesterol as the major cholesterol as the major componentcomponent
GB Anatomy Con’t.GB Anatomy Con’t.
AnatomyAnatomy
Choledocholithiasis Choledocholithiasis Con’t.Con’t.- - Operative cholangiographyOperative cholangiography
- decreased the need for CBD exploration but - decreased the need for CBD exploration but increased the proportion of positive explora-increased the proportion of positive explora-tionstions
- the - the only absolute indicationonly absolute indication for CBD for CBD exploration is exploration is palpable stone in CBDpalpable stone in CBD- when any of the following are present, - when any of the following are present, operative cholangiography is performed:operative cholangiography is performed:
a. increased size of the CBDa. increased size of the CBDb. history of jaundiceb. history of jaundicec. small stones in the GB with a large cystic c. small stones in the GB with a large cystic ductductd. a history of cholangitis or pancreatitisd. a history of cholangitis or pancreatitis
Choledocholithiasis Choledocholithiasis Con’t.Con’t. - CBD exploration is not necessary if the - CBD exploration is not necessary if the
operative cholangiogram is of good quality operative cholangiogram is of good quality and demonstrates both:and demonstrates both:
a. no filling defectsa. no filling defects b. free flow of contrast medium intob. free flow of contrast medium into the duodenumthe duodenum
- CBD is indicated if the operative - CBD is indicated if the operative cholangiogram shows either:cholangiogram shows either: a. filling defects within the intrahepatica. filling defects within the intrahepatic
or extrahepatic biliary treeor extrahepatic biliary tree b. obstruction of the flow of bile intob. obstruction of the flow of bile into the duodenumthe duodenum
Choledocholithiasis Choledocholithiasis Con’t.Con’t.
ComplicationsComplications:: - stones that remain after surgery complicate - stones that remain after surgery complicate
up to 5 – 10 % of CBD explorationsup to 5 – 10 % of CBD explorations a. no treatment is necessary for smalla. no treatment is necessary for small stones – usually pass spontaneouslystones – usually pass spontaneously
b. treatment options for large stonesb. treatment options for large stones 1) chemical dissolution – 1) chemical dissolution –
intraductal intraductal administration of administration of methyl-tert-butyl methyl-tert-butyl ether or mono- ether or mono-octanoinoctanoin
2) mechanical extraction – under 2) mechanical extraction – under fluoroscopic guidancefluoroscopic guidance
Choledocholithiasis Choledocholithiasis Con’t.Con’t.
c. Primary or recurrent CBD stonesc. Primary or recurrent CBD stones
- can be treated surgically with a - can be treated surgically with a biliary- enteric connection to allow biliary- enteric connection to allow stones to pass out of the biliary stones to pass out of the biliary tree tree
- 2 most common methods are:- 2 most common methods are: a. Choledochoduodenostomya. Choledochoduodenostomy
b. Choledochojejunostomyb. Choledochojejunostomy - transduodenal sphinctero-- transduodenal sphinctero-
plast or endoscopic plast or endoscopic sphincterotomy - sphincterotomy -
acceptable options acceptable options
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