The document discusses the liver, cirrhosis, and portal hypertension. It begins by describing the anatomy and functional units of the liver, including the portal triads and zones. It then discusses cirrhosis and portal hypertension in more detail. Cirrhosis is defined as scarring of the liver from long-term damage that blocks blood flow and can lead to hepatic failure and portal hypertension. The document lists various etiologies of cirrhosis including infections, liver disorders, bile duct blockages, drugs/toxins, and discusses some specific conditions in more detail. It concludes by describing the clinical features and complications of cirrhosis and portal hypertension.

6. I, caudate lobe; II-IV theI, caudate lobe; II-IV the
left-; V-VIII the rightleft-; V-VIII the right
hemiliver

8. Functional unit:Functional unit: acinusacinus
PT:PT: PV, arteriole, bilePV, arteriole, bile
ductuleductule
Zone 1Zone 1 is well O2; moreis well O2; more
resistant than zone 3.resistant than zone 3.
SinusoidsSinusoids lack BM; havelack BM; have
fenestrated endoth. Bilefenestrated endoth. Bile
canaliculi join to formcanaliculi join to form
bile ductulesbile ductules
BM: basement membrane
THV: terminal hepatic venule
PT: Portal triad

10. Cirrhosis & PortalCirrhosis & Portal
HypertensionHypertension

11. Cirrhosis: OverviewCirrhosis: Overview
 L. processes nutrients & filter blood; controls BGL &L. processes nutrients & filter blood; controls BGL &
cholesterol, & makes coagulantscholesterol, & makes coagulants
 It can regenerate: large portion can be removed. But if theIt can regenerate: large portion can be removed. But if the
damage is chr., repair fails & scars:damage is chr., repair fails & scars: cirrhosiscirrhosis
 It cannot be reversedIt cannot be reversed
 Goal: stop progress, by Rx underlying causeGoal: stop progress, by Rx underlying cause
 Cirrhosis have serious complications like PH &Cirrhosis have serious complications like PH &
hepatopulmonary syn. It can also increase risk of HCChepatopulmonary syn. It can also increase risk of HCC
 In children d. of biliary tract & inherited d. are the mostIn children d. of biliary tract & inherited d. are the most
common. Adults: alcoholcommon. Adults: alcohol

12. DefinitionDefinition
Chr. liver d.:Chr. liver d.: progressive damage & regen. ofprogressive damage & regen. of
liver parenchyma lastingliver parenchyma lasting >6mo.>6mo. It canIt can lead tolead to cirrhosis.cirrhosis.
Causes:Causes: inf., metabolic, genetic, drugs,., metabolic, genetic, drugs, idiopathic,idiopathic,
structural d., HCC & AIDstructural d., HCC & AID
Cirrhosis:Cirrhosis: scarring of Liver from injury/long-term d.scarring of Liver from injury/long-term d.
blocking BF:blocking BF: HC failure &HC failure & Portal HTNPortal HTN
Chr. Hepatitis:Chr. Hepatitis: chr. inflam. inchr. inflam. in
liver leading to cirrhosisliver leading to cirrhosis
& liver failure; persistent& liver failure; persistent
for a period of 6mofor a period of 6mo
BF: blood flow. D: disorder/diseaseBF: blood flow. D: disorder/disease

14. At the end we will learnAt the end we will learn
 >100 liver diseases>100 liver diseases
 CLD is rare in children (1/5000)CLD is rare in children (1/5000)
 CLD may beCLD may be idiopathicidiopathic
 Most CLD are preventableMost CLD are preventable
 Commonest c/of PH is cirrhosisCommonest c/of PH is cirrhosis
 Commonest c/of HCC is HBVCommonest c/of HCC is HBV
 HCV is curableHCV is curable
CLD: chr. liver d. PH: portal HTN. HCC: HC CaCLD: chr. liver d. PH: portal HTN. HCC: HC Ca

15. Etiology of Cirrhosis/CLD & PHEtiology of Cirrhosis/CLD & PH
InfectionsInfections
Liver disorders:Liver disorders:
Bile ductal blockages:Bile ductal blockages:
Drugs & toxins:Drugs & toxins:

16. Liver disorders:Liver disorders:
– Autoimmune hepatitis:Autoimmune hepatitis:
– Chr.Chr. alcoholismalcoholism
– Hereditary:Hereditary:
 HemochromatosisHemochromatosis
 αα1-antitrypsin deficiency1-antitrypsin deficiency
 GSDGSD
 GalactosemiaGalactosemia
 Cystic FibrosisCystic Fibrosis
 Fructose intoleranceFructose intolerance
 TyrosinemiaTyrosinemia
 Wilson DWilson D
– Indian childhood cirrhosisIndian childhood cirrhosis

17. Autoimmune Liver DiseasesAutoimmune Liver Diseases
By autoantibodies; rare in children:By autoantibodies; rare in children: 2% of LD in2% of LD in
specialized pediatric L. centersspecialized pediatric L. centers
Broad clinical spectrum.Broad clinical spectrum. Quickly responds to steroidsQuickly responds to steroids
& immunosuppressants& immunosuppressants
CommonCommon SS:SS: tiredness & unwellness, anorexia, schooltiredness & unwellness, anorexia, school
deterioration.deterioration. HSM, abnormal LFT,HSM, abnormal LFT, autoantibodiesautoantibodies,,
characteristic livercharacteristic liver biopsybiopsy
DxDx is often byis often by exclusionexclusion. Anti-sm Ab, anti-liver kidney. Anti-sm Ab, anti-liver kidney
microsome type 1 Ab, ANA. Biopsy may be necessarymicrosome type 1 Ab, ANA. Biopsy may be necessary forfor
type & severity of L. damagetype & severity of L. damage
2 types:2 types: AIH & AI sclerosing cholangitisAIH & AI sclerosing cholangitis

18. Inherited liver diseasesInherited liver diseases
2 common are2 common are haemochromatosis & alpha-1 antitrypsin d.haemochromatosis & alpha-1 antitrypsin d.
Haemochromatosis:Haemochromatosis: excess Fe is absorbed & deposited.excess Fe is absorbed & deposited.
The commonest is hereditary. 2y HC occurs inThe commonest is hereditary. 2y HC occurs in
hemolytic a. Genetic HC affects M x5. As Fhemolytic a. Genetic HC affects M x5. As F
menstruate, are unlikelymenstruate, are unlikely to show SS till >10y afterto show SS till >10y after
MP.MP. More in N EuropeMore in N Europe
SS:SS: HM, joint p, fatigue, wt loss, darkening of skinHM, joint p, fatigue, wt loss, darkening of skin
("bronzing“), AP, loss of libido. DM & heart d. may("bronzing“), AP, loss of libido. DM & heart d. may
dev.; also cirrhosis, HCC, testicular atrophy. Blood Fedev.; also cirrhosis, HCC, testicular atrophy. Blood Fe isis
confirmatory. HC DNAconfirmatory. HC DNA test is done for screeningtest is done for screening

19. Rx.Rx. of haemochromatosisof haemochromatosis
Goal:Goal: remove excess Fe. Fe is removed by phlebotomy: ½Lremove excess Fe. Fe is removed by phlebotomy: ½L
blood is removed/w for 2-3y until Fe is reduced; thenblood is removed/w for 2-3y until Fe is reduced; then
less frequentlyless frequently
 Avoid dietary Fe, most commonly offal, fortified BFAvoid dietary Fe, most commonly offal, fortified BF
cereals, Fe medicinescereals, Fe medicines
 LimitLimit vitamin Cvitamin C
 No alcoholNo alcohol
 If HC has caused cirrhosis, the riskIf HC has caused cirrhosis, the risk
of HCC is higherof HCC is higher
Screening/6moScreening/6mo

20. Alpha-1 antitrypsin d.Alpha-1 antitrypsin d.
an imp. liver protein A1AT,an imp. liver protein A1AT, is lacking/low. Pts. canis lacking/low. Pts. can
make it;make it; but, the disease prevents entrance to blood & itbut, the disease prevents entrance to blood & it
accumulates in liveraccumulates in liver
 A1ATA1AT protects lungs from damage.protects lungs from damage. The lungs becomeThe lungs become
damaged: SoBdamaged: SoB
 1% COPD have it. Risk of cirrhosis is high1% COPD have it. Risk of cirrhosis is high
SS:SS: first symptoms appear usually in lungs: COPD:first symptoms appear usually in lungs: COPD: SoB/SoB/
wheezing, unexplained wt loss & barrel-shaped chestwheezing, unexplained wt loss & barrel-shaped chest AsAs
it progresses, SS of cirrhosis may appearit progresses, SS of cirrhosis may appear
 A1AT in blood will confirmA1AT in blood will confirm

21. Rx.:Rx.: No cure. Replacement has been triedNo cure. Replacement has been tried
 Rx COPD & cirrhosis: ABT, inhaled medications. DiureticsRx COPD & cirrhosis: ABT, inhaled medications. Diuretics
& other measures to reduce edema& other measures to reduce edema
 No alcohol, smokingNo alcohol, smoking
 Healthy dietHealthy diet
 Flu & pneumonia vax.Flu & pneumonia vax.
 Treat inf.Treat inf. asapasap. Occasionally the lungs or liver deteriorate. Occasionally the lungs or liver deteriorate
despite Rx. Lung/liver transplant may be neededdespite Rx. Lung/liver transplant may be needed
 With appropriate Rx A1AT is usually not fatal. But,With appropriate Rx A1AT is usually not fatal. But,
complications a/with them can be fatalcomplications a/with them can be fatal
 It is v. imp. that people with inherited LD do all they canIt is v. imp. that people with inherited LD do all they can
to stay healthyto stay healthy

22. Wilson DWilson D
 AR; 1/30,000; typically in 2AR; 1/30,000; typically in 2ndnd
D (neurological 3D (neurological 3rdrd
D)D)
 Mutations in ATP7B Cu translocase, a protein mainlyMutations in ATP7B Cu translocase, a protein mainly
expressed by the hepatocyte to regulate Cu. ATP7Bexpressed by the hepatocyte to regulate Cu. ATP7B
synthesize ceruloplasmin. Cu accumulates within L. Thesynthesize ceruloplasmin. Cu accumulates within L. The
severity of L damage: asymptomatic - cirrhosis. 2/3severity of L damage: asymptomatic - cirrhosis. 2/3rdrd
showshow
hemolysis., coagulopathy, & renal failure. 6% WD have ac.hemolysis., coagulopathy, & renal failure. 6% WD have ac.
LD. KF rings are seen in 50%. 50% show psychiatric-LD. KF rings are seen in 50%. 50% show psychiatric-
psychotic SS. Rx can now effectively treat & gene therapy ispsychotic SS. Rx can now effectively treat & gene therapy is
effective in animal modelseffective in animal models
 Low S. ceruloplasmin & high urine Cu help to perform theLow S. ceruloplasmin & high urine Cu help to perform the
Dx in most cases, some false negatives are describedDx in most cases, some false negatives are described
 Severe mutations (nonsense, frameshift) are a/with theSevere mutations (nonsense, frameshift) are a/with the
most severe d, while missense mutations (60%) show amost severe d, while missense mutations (60%) show a
variable severity & outcome. Liver biopsy is now used invariable severity & outcome. Liver biopsy is now used in
cases with ambiguous biochemical parameters & tocases with ambiguous biochemical parameters & to

23. Bile ductal blockagesBile ductal blockages
– Cong.: biliary atresiaCong.: biliary atresia
– Sclerosing cholangitis
– Gallbladder surgeryGallbladder surgery

24. Drugs & toxinsDrugs & toxins
– Paracetamol. arsenic, INHParacetamol. arsenic, INH
– MethotrexateMethotrexate
– Excess vitamin A, ironExcess vitamin A, iron
– Afla toxinAfla toxin
InfectionsInfections
– Hepatitis B, C, DHepatitis B, C, D
– Schistosomiasis, brucellosisSchistosomiasis, brucellosis
– Echinococcosis, advanced or cong. syphilisEchinococcosis, advanced or cong. syphilis

25. Indian Childhood CirrhosisIndian Childhood Cirrhosis
a CLD of children (1–3y) due to deposition of Cu in liver.a CLD of children (1–3y) due to deposition of Cu in liver. It isIt is
a non-Wilsonian Cu overload by ingested Cu occurs ina non-Wilsonian Cu overload by ingested Cu occurs in
genetically susceptible infantsgenetically susceptible infants
 It had a v. high CFR before but has eventually becomeIt had a v. high CFR before but has eventually become
preventable, treatablepreventable, treatable
 Now rareNow rare
CLD: chr liver d. CFR: case fatality rateCLD: chr liver d. CFR: case fatality rate

26. The commonestThe commonest surgicalsurgical c/of cirrhosis inc/of cirrhosis in
childhood is biliary atresiachildhood is biliary atresia
The commonestThe commonest medicalmedical causes arecauses are
– infectionsinfections
– alpha-1- antitrypsin Dalpha-1- antitrypsin D
– metabolic LDmetabolic LD

27. C.F. of C.L.D/CirrhosisC.F. of C.L.D/Cirrhosis
Often asymptomatic in early!Often asymptomatic in early! Start with L. failure.Start with L. failure.
Severity depends on damageSeverity depends on damage
– Early:Early: fatigue, weakness, AN, AP,fatigue, weakness, AN, AP, wt. losswt. loss
– Later:Later: jaundice,jaundice, dark urinedark urine, itching, edema, ascites,, itching, edema, ascites,
poor healing, drug toxicity, testicular atrophy, poorpoor healing, drug toxicity, testicular atrophy, poor
hair,hair, hepatic facies,hepatic facies, easy bruising; esophageal,easy bruising; esophageal,
stomach & anal varices;stomach & anal varices;
kidney failure, gall stoneskidney failure, gall stones
A small number getA small number get liver cancerliver cancer

28. CF have 2 componentsCF have 2 components
SS of Hepatocellular failureSS of Hepatocellular failure
– pallor, edema,pallor, edema, fatigue,fatigue, jaundice,jaundice, itchy skin, dark urine,itchy skin, dark urine,
ANVANV,, wt. loss, palmar erythemawt. loss, palmar erythema
– AP & swelling, pale stool, hepatic facies, spider nevi,AP & swelling, pale stool, hepatic facies, spider nevi,
pigmentationpigmentation
– testicular atrophy, poor hair, gynecomazia, poor libidotesticular atrophy, poor hair, gynecomazia, poor libido
SS of Portal HypertensionSS of Portal Hypertension
– ascites, distended vein (caput medusa), splenomegaly,ascites, distended vein (caput medusa), splenomegaly,
varices at PS junctions: hematemesis,varices at PS junctions: hematemesis, bloody/tar-bloody/tar-
colored stoolcolored stool

29.  Muehrcke nailsMuehrcke nails
 Terry nailsTerry nails

31. Kayser–Fleischer ringKayser–Fleischer ring
at limbus: depositionat limbus: deposition
of Cu in Descemet m.:of Cu in Descemet m.:
characteristic in mostcharacteristic in most
neuro-Wilson & 50% ofneuro-Wilson & 50% of
hepatic WDhepatic WD
Arcus senilis

32. XanthomatosisXanthomatosis

33. Mechanism of Ascites in CirrhosisMechanism of Ascites in Cirrhosis
 Portal hypertension:Portal hypertension: commonestcommonest
 Hepatic arterial vasodilatationHepatic arterial vasodilatation
 HypoalbuminemiaHypoalbuminemia
 2y hyperaldosteronism2y hyperaldosteronism
 Raised ADHRaised ADH

34. Complications of CirrhosisComplications of Cirrhosis
 Palmar erythemaPalmar erythema
 HypogonadismHypogonadism
 Darkening of skinDarkening of skin
 GynecomaziaGynecomazia
 HypersplenismHypersplenism
 Spider neviSpider nevi
 Caput medusaCaput medusa
 Ascites, edemaAscites, edema
 Varices: hgeVarices: hge
 ItchingItching
 Abdominal infx.Abdominal infx.
 EencephalopathyEencephalopathy
 Raised drug toxicityRaised drug toxicity
 Liver cancerLiver cancer

37. Spider naevi (arterial
spider, vascular spider,
naevus araneus, naevus
arachnoidius, spider
angioma

38. DiagnosisDiagnosis
 LFTLFT
 CT, USG, laparoscopyCT, USG, laparoscopy
 BiopsyBiopsy
 Others:Others:
– FibroscanFibroscan
– Measuring the amount of caffeine in the salivaMeasuring the amount of caffeine in the saliva
– Measuring the pressure within the liver veinMeasuring the pressure within the liver vein
– Ascitic fluid analysisAscitic fluid analysis

39. TreatmentTreatment
Nothing cures scarNothing cures scar
Goals:Goals:
– Rx underlying causesRx underlying causes
– Preventing further damagePreventing further damage
– Rx symptoms & complicationsRx symptoms & complications
 Fight inf. Vax. flu, pneumonia, hepatitisFight inf. Vax. flu, pneumonia, hepatitis
 Cut down absorption of wastes/toxinsCut down absorption of wastes/toxins
 FEB. Salt restrictionFEB. Salt restriction
 HemostasisHemostasis

40.  Liver transplant SOSLiver transplant SOS
 No hepatotoxic drugsNo hepatotoxic drugs
 No alcoholNo alcohol
 Diet: extra calories & a generous protein to helpDiet: extra calories & a generous protein to help
liver regenerateliver regenerate
 If cirrhosis is advanced limit proteinIf cirrhosis is advanced limit protein

41. PORTAL HYPERTENSIONPORTAL HYPERTENSION
 Portal vein:Portal vein: SV with SMV: carries 70% of liver blood.SV with SMV: carries 70% of liver blood.
Ends in sinusoidsEnds in sinusoids
 Double capillariesDouble capillaries
 Raised pressure in PV >Raised pressure in PV >11mmHg11mmHg or a splenic pulpor a splenic pulp
pressure of >16mmHg. Clinically this is not measuredpressure of >16mmHg. Clinically this is not measured
directly until a TIPS is decideddirectly until a TIPS is decided
SV: splenic vein. SMV: superior mesenteric vein. PH: portal hypertensionSV: splenic vein. SMV: superior mesenteric vein. PH: portal hypertension
TIPS: transjugular intrahepatic portosystemic shuntTIPS: transjugular intrahepatic portosystemic shunt

43. PH:PH: splenomegalysplenomegaly && porto-systemic shunts at:porto-systemic shunts at:
 Lower end ofLower end of eophaguseophagus via GE veins:via GE veins: hemat./malenahemat./malena
 AnalAnal veins:veins: hemorrhoidshemorrhoids
 UmbilicalUmbilical veins:veins: caput medusacaput medusa
 Abdominal wall & retroperitoneum:Abdominal wall & retroperitoneum: distended veinsdistended veins
GE: gastroesophagealGE: gastroesophageal

45. Eesophageal varicesEesophageal varices
• Gastroesophageal junction to 15cm upGastroesophageal junction to 15cm up
• Slow oozing or sudden severe hgeSlow oozing or sudden severe hge
Gastric varicesGastric varices
Extension of esophageal varices or varices inExtension of esophageal varices or varices in
fundus & upper body. Can occur alonefundus & upper body. Can occur alone
Rectal varices:Rectal varices: hemorrhoidshemorrhoids

47. Gastric varicesGastric varices
Rectal varicesRectal varices

48. Aetiology of Portal HTNAetiology of Portal HTN
• IntrahepaticIntrahepatic:: 80%80%
• CirrhosisCirrhosis is the commonest; scar tissue blocks BF &is the commonest; scar tissue blocks BF &
slows liver functionsslows liver functions
•Schistosomiasis, cong. hepatic fibrosis, etc.Schistosomiasis, cong. hepatic fibrosis, etc.
• PrehepaticPrehepatic:: 20%20%
•PV thrombosis:PV thrombosis:
• extension of obliterative process of umb. veinextension of obliterative process of umb. vein
• omphalitis (in newborn)omphalitis (in newborn)
• PosthepaticPosthepatic (rare): cons. pericarditis, tricuspid(rare): cons. pericarditis, tricuspid
incompetence,incompetence, Budd-Chiari syn.Budd-Chiari syn. (occlusion of HV)(occlusion of HV)

49.  Cong. hepatic fibrosis:Cong. hepatic fibrosis: hematemesis, normal LFTs,hematemesis, normal LFTs,
hepatomegaly. May have polycystic disease & otherhepatomegaly. May have polycystic disease & other
renal D. Etiology is unknownrenal D. Etiology is unknown
 Hepato-portal sclerosis:Hepato-portal sclerosis: thickening of intrahepatic PVthickening of intrahepatic PV
obstructs BF: leads to collateral veins in porta hepatisobstructs BF: leads to collateral veins in porta hepatis
 Suprahepatic obstructionSuprahepatic obstruction c/by a web in the IVC orc/by a web in the IVC or
Budd-Chiari syn. Extremely rare. CF may mimicBudd-Chiari syn. Extremely rare. CF may mimic
constrictive pericarditis. DD by echo-, venographyconstrictive pericarditis. DD by echo-, venography

50. CF of portal hypertensionCF of portal hypertension
may not always be specificmay not always be specific
 Splenomegaly (hypersplenism: pancytopenia)Splenomegaly (hypersplenism: pancytopenia)
 Caput medusaCaput medusa
 Hematemesis, melena or PR bleedHematemesis, melena or PR bleed
 AscitesAscites
 Encephalopathy: poor liver function & diversion of bloodEncephalopathy: poor liver function & diversion of blood
away from liveraway from liver

51. DD of uncommon CLDDD of uncommon CLD
ConditionsConditions PresentationPresentation
Budd-Chiari SynBudd-Chiari Syn AscitesAscites
Primary sclerosingPrimary sclerosing
Cholangitis (PSC)Cholangitis (PSC)
Abnormal LFT/jaundiceAbnormal LFT/jaundice
Primary bil. cirrhosis (PBC)Primary bil. cirrhosis (PBC) Abnormal LFT, malaise,Abnormal LFT, malaise,
lethargy, itchinglethargy, itching
Caroli diseaseCaroli disease Abdominal pain/sepsisAbdominal pain/sepsis
Simple liver cystSimple liver cyst Pain/coincidental findingsPain/coincidental findings
Polycystic liver diseasePolycystic liver disease Pain/hepatomegalyPain/hepatomegaly

52. Diagnosis:Diagnosis: by detecting CLD, encephalopathy, ascites,by detecting CLD, encephalopathy, ascites,
varices.varices. Investigations:Investigations: esophagoscopy, Ba-swallow,esophagoscopy, Ba-swallow,
USG, celiac axis angiogramUSG, celiac axis angiogram
PV Thrombosis:PV Thrombosis: Dx is difficultDx is difficult
may present within 5y age as hematemesis with onlymay present within 5y age as hematemesis with only
splenomegaly & low plateletsplenomegaly & low platelet
• H/of umbilical V cannulation & abdo. sepsis (40%), orH/of umbilical V cannulation & abdo. sepsis (40%), or
trauma/pancreatitis. PVT is mainly congenital. LFTs intrauma/pancreatitis. PVT is mainly congenital. LFTs in thesethese
are normal. USG may confirm PVT: collateral veinsare normal. USG may confirm PVT: collateral veins in thein the
porta hepatis replacing the PVporta hepatis replacing the PV

53. TreatmentTreatment
Esophageal variceal bleeding:Esophageal variceal bleeding:
By the time pt. reaches ERBy the time pt. reaches ER
- 1/31/3rdrd
– stopped bleeding– stopped bleeding
- 1/31/3rdrd
– still oozing– still oozing
- 1/31/3rdrd
– still bleeding heavily– still bleeding heavily
Initial measures: ICUInitial measures: ICU
- BT: up to 10 unitsBT: up to 10 units
- LFT: coagulation profileLFT: coagulation profile
- If <50,000, platelet transfusion- If <50,000, platelet transfusion
- Endoscopic evaluation & treatment- Endoscopic evaluation & treatment

54. • Encephalopathy: may need ventilatorEncephalopathy: may need ventilator
• Bronchial aspiration – a frequent complicationBronchial aspiration – a frequent complication
• If profuse bleed prohibits endoscopy:If profuse bleed prohibits endoscopy:
• Insert Sengstaken – Blakemore tube & tamponade;Insert Sengstaken – Blakemore tube & tamponade;
deflate after 12h to avoid pressure necrosisdeflate after 12h to avoid pressure necrosis

56. Endoscopic sclerotherapyEndoscopic sclerotherapy
- Ethanolamine oleate- Ethanolamine oleate
- Sodium tetradesyl sulphate- Sodium tetradesyl sulphate
- 5% phenol in Almond oil- 5% phenol in Almond oil
- Butyl cyanoacrylate- Butyl cyanoacrylate

57. DrugsDrugs
• I/V Vasopressin. SE: Abdo. crampsI/V Vasopressin. SE: Abdo. cramps
• I/V Octreotide (Somatostatin analogue): EquallyI/V Octreotide (Somatostatin analogue): Equally
effective, safeeffective, safe
TIPSSTIPSS (transjugular intrahepatic portosystemic stent)(transjugular intrahepatic portosystemic stent)
revolutionized the Rx. Main Rx for drugrevolutionized the Rx. Main Rx for drug
resistant cases or in endoscopic Rx failureresistant cases or in endoscopic Rx failure

58. Surgical shuntSurgical shunt
(Replaced by TIPSS & liver transplant)(Replaced by TIPSS & liver transplant)
Surgical shunts:Surgical shunts:
• splenorenalsplenorenal
• portocavalportocaval
SE: encephalopathy (40%)SE: encephalopathy (40%)
No benefit for pts. who have no bleedingNo benefit for pts. who have no bleeding

59. C.I.C.I. of Liver transplantof Liver transplant
• Age >65 yAge >65 y
• H/o IHD, HF, Chr. Respiratory diseaseH/o IHD, HF, Chr. Respiratory disease
• Previous Surgical shunts (relative C.I.)Previous Surgical shunts (relative C.I.)

60. Rx of Ascites of CLDRx of Ascites of CLD
• Salt restrictionSalt restriction
• DiureticsDiuretics
• ParacentesisParacentesis
• Peritoneovenous shuntingPeritoneovenous shunting
• TIPSSTIPSS
• Liver transplantLiver transplant

61. MCQMCQ
 Hepatitis A & E are common c/of CLDHepatitis A & E are common c/of CLD
 Vaccines for HBV protects against HDVVaccines for HBV protects against HDV
 Haemorrhoids in cirrhosis are due to HC failureHaemorrhoids in cirrhosis are due to HC failure
 Palmer erythema is normal in pregnancyPalmer erythema is normal in pregnancy
 Commonest c/of PHT is cirrhosisCommonest c/of PHT is cirrhosis

62. MCQMCQ
 Commonest surgical c/of cirrhosis in children isCommonest surgical c/of cirrhosis in children is
biliary atresiabiliary atresia
 Edema in CLD starts in legsEdema in CLD starts in legs
 CLD may be idiopathicCLD may be idiopathic
 Autoimmune LD have good prognosisAutoimmune LD have good prognosis
 A1AT protects lungsA1AT protects lungs
 Aflatoxin can cause cirrhosisAflatoxin can cause cirrhosis

66. Next lecture:Next lecture:
UTI in ChildrenUTI in Children

67. THANK YOU