O Develop Either Into Hepatocytes or Intrahepatic Ductal Cells

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Weight – 1.

7 kg

Posterior surface of liver – bare area – not covered by peritoneum

Peritoneal reflection:

 Right triangular ligament


 Left triangular ligament
 Falciform ligament
 Lesser omentum free margin – contains hilar structure

Liver blood supply

 80 percent – portal vein


 20 percent – hepatic artery
 Right hepatic artery is larger

Hilum structures

 Porta hepatis is the hilum of the liver – situated on the visceral surface of the liver
 W/n free edge of lesser omentum: (hepatoduodenal ligament) hepatic artery, portal vein, bile
duct
 Bile duct laterally, hepatic artery in front and medially, portal vein posteriorly

Segmental anatomy: 8 segments

 Independent functional unit – each has a branch of hepatic artery, branch of portal vein and
branch of bile ducts
 Line b/n gb fossa and middle hepatic vein: cantlie’s line
 Segment V-VIII: right hep artety

Hepatic lobules:

 Functional unit
 Sheets of liver cells, separated by sinusoids – they carry blood to the central vein – then to
central vein
 During passage thru sinusoid, many important interaction takes place b.n blood and hepatocytes

Embryology

 Foregut derivative
 Cell population is bipotential
o Develop either into hepatocytes or intrahepatic ductal cells
 Epithelium of vitelline and umbilical vein: gives rise to liver endothelium – they give rise to
sinusoids
 Septum transversum (mass of mesenchymal connective tissue): supporting CT, hematopoietic
cells, Kupffer cells (all these from mesoderm)

Liver function tests

 Serum bilirubin
 ALP – in cholestatic liver disease of biliary obstruction it increases
o May also increase due to skeletal causes
 AST
 ALT
 Gamma-GT
o Ast, ALT, GGT – acute hepatocellular damage
 Albumin
 PT

Biliruibin, albumin, PT – measurements of liver function

Functions of liver

 Core body temp maintain


 pH balance
 correct lactic acidosis
 clotting factor synthesis
 glucose metabolism – glycolysis and gluconeogenesis
 urea formation
 protein catabolism
 bilirubin formation
 drug and hormone metabolism + excretion
 removal of foreign antigen and gut endotoxin

acute liver failure causes

 viral hepatitis
 drugs
o halothane
o INH
o Rifampicin
o Antidepressants
o NSAID
o Paracetamol overdose
o Valproic acid
o Mushroom poisoning
o Shock
o Multiorgan failure
o Acute budd chiari syndrome
o Wilson’s disease
o Fatty liver of pregnancy

Features of ALP

 Clinical jaundice
 Neurological sign – hep enceph
o Liver flap
o Drowsiness
o Confusion
o Then coma

ALF rx

 Fluid and electrolyte


 Acid base balance
 Blood glucose monitoring
 Nutrition
 Renal function (dialysis – hepatorenal syndrome)
 Ventilation support
 Treat infection
 Monitor and treat cerebral edema
 Liver transplantation in some
o Criteria:

CLD

 Lethargy and weakness may precede clinical jaundice


 Hyperdynamic circulation – high C.O, large pulse volume, low bp, red warm extremity
(vasodilation?)
 Fever – release of cytokine from diseased liver/bacterial infection
 Skin and nail changes
 Endocrine – hypogonadism, gynecomastia
 Hep enceph – flapping temor
 Ascites – late feature
 Muscle wasting – protein catabolism
 Skin bruising – coagulopathy
o Pt with CLD are at greater risk of surgical and anesthetic complications

Imaging of the liver: USG, CT, MRI, ERCP, Direct endoscopic cholangiography EUS, PTC, Angiography,
PET-CT, Laparoscopy

USG
 1st line
 Detection of focal liver lesion
 Assessment of biliary tract dilation
 Differentiate cyst (benign lesion) from malignant lesion such as metastasis – not always easy to
diff
 In fatty person – usg difficult
 Fatty liver makes the quality of USG poor and diagnosis difficult – attenuation of the signal
 Less useful to determine etiology of a lesion

CT scan:

 Spiral ct
 Contrast enhanced ct
o Oral contrast – visualization of stomach and duodenum in relation to liver
o Intravenous contrast – early arterial phase – visualization of early primary small cancer
– there blood supply is preferably arterial
o Venous phase shows: branches of portal vein and drainage via the hepatic veins
o Inflammatory lesion – rim enhancement
o Hemangioma – late venous enhancement
 Measure densitiy og lesions
 For diagnosis and staging
 Can measure local and distant metastasis

MRI

 Superior to CT scan
 Liver specific contrast agent – can identify very small primary HCC focus – normal hepatocytes
will take up contrast, neoplastic cells will not
 Also helpful for liver mets – esp from colorectal cancer
 This can also be employed by MRCP

ERCP

 In obs jaundice – stone removal, biliary drainage


 Assessment of coagulation is necessary

EUS

 Extra hep biliary apparatus


 Porta hepatis and para aortic lymphadenopathy

Angiography
 Only for therapeutic intervention
 Occlusion of AVM can be done
 Therapeutic angiographic embolization of liver tumor – transarterial chemoembolization (TACE)

PET scan – FDG-PET

Laparoscopy: for staging of primary hepatopancreatico biliary system

Liver trauma:

 Second most common organ injured after spleen

Classification of liver trauma:

 Blunt – maybe assoc with splenic or renal injury – more common + higher mortality
o Contusion
o Lacetation
o Avulsion
 Penetrating – assoc with chest/pericardial involvement
o Stab
o Gunshot

Management of liver trauma

 Rescuscitate – ABC
 Assessment: CT chest, abdomen with contrast
 Hemodyn unstable: laparotomy
 Treatment
o Correct coagulopathy
o Suture laceration
o Major vascular injury: resection
o Diffuse parenchymal injury: packing
 Remember associated injuries

Dx of liver injury:

 Liver – well vascularized


 Blood loss – major early complication
 Suspect of liver injury in case of all lower chest and upper abdominal trauma/stab wounds
 FAST (Focused assessment sonography in trauma) – dx of free intraperitoneal fluid in pt with
trauma and hemodyn instability
 Hemodyn stable pt should have contrast ct of chest/abdomen – evidence of parenchymal dmg
Initial mx of liver injuries penetrating trauma :

 ABC (like ATLS)


 2 large bore cannula: periiph venous access
 10 units of blood
 FBC, Urea, electrolytes, clotting test, LFT, RBS, serum amylase , ABG
 Intubation: if inadequate gas exchange
 Chest drain: if pneumo/hemothroaz
 After starting these resuscitation: transfer pt to ot table, continue resusc there
 In case of coagulopathy: FFP, cryoprecipitate
 If pt is hemodyn stable: contrast CT prior to laparotomy

Initial mx in case of blunt trauma:

 Initial resusc and mx as above for penetrating injuries


 Hem unstable: imm laparotomy , stable: ct to further evaluate nature of injury
 Hem stable: conservative mx
 Indication for discontinuation onf conservstive mx
o Hem instaibilty development
o Ongoing blood loss despite correction of underlying coagulopathy
o Development of gen peritonitis (signs)

Surgical approach to liver trauma :

 Incision that allows access to both liver and spleen


 Compress with packs
 Correct coagulopathy
 Placement of atraumatic clamp across foramen of winslow – Pringle maneuver – can also be
done laparoscopically - inflow occlusion facilliates suturing of lacerations and vessels
 Repair hepatic artery injury with 6-0 prolene
 Portal vein injury with 5-0 prolene
 These will help with inflow occlusion
 If bleeding persists still
o Heaptic vein injury
o Or IVC injury
o Dmg to liver parenchyma
 Abdominal packs placed and abdomen closed to facilitate the compression
 In case of crush injury: placing of packs is adequate and they should be removed after 48 hour

Complications of liver trauma

 Shock and hemodynamic instability


 Subcapsular/intrahepatic hematoma
 Catastrophic/torrential hemorrhage internally
 Abscess secondary to infection in area of parenchymal ischemia – esp after penetrating trauma
o Antibiotic
o Aspiration of necrotic tissue under USG guidance, once the necrotic tissue has liquefied
 Biliary fistula
 Late vascular complications
o Hepatic artery aneurysm
o Av fistula
o Arteriobiliary fistula
 Hepatic failure

Long term outcomes:

 Parenchymal regeneration occurs rapidly late complications rare


 Biliary stricture
 Atrophy or stricture of one liver lobe, compensatory hypertrophy of the remaining liver lobes
may occur
 Obs jaundice may occur due to stricture in extrahep biliary apparatus- requires
hepatodochojejunostomy (Roux-en-Y)

Bleeding varices management:

 Acute onset of large volume bleeding


 Lower esop is most common site
 After initial resuc the diagnosis needs to be confirmed
 Admit to ICU
 Venous access
 Resication with blood
 LFT
 Coagulation profile – correct coagulopathy by – FFP
 Avoid hypovolemia – it may increase portal pressure and exacerbate variceal bleeding
 IV vit K + tranexamic acid IV
 Activate major transfusion protocol
 Cirrhosis  hypersplenism  thrombocytopenia  platelet transfusion needed if platelet count
falls below 50 k
 Telipressin – splanchnic vasoconstrictor – to prevent splanchnic vasodilation and potential
hepatorenal syndrome
 Prophylactic antibiotic
 After pt is stable – upper GI endoscopy to confirm dx
 Esophageal balloon tamponae/ through it there are channels that allow gastric/esophageal
aspiration – deflate the balloon after 12 hours to prevent pressure necrosis of the esophagus
 endoscopic
o band ligation – constrictor rubber band at the base of the varix
o scleroth3rapy –
 Intubation maybe needed if there is hepatic coma/encephalopathy

TIPSS (transjugular intrahepatic portosystemic shunts)

 When not responding to drug therapy or band ligation or other modes of endoscopic therapy
 Done with local anesthesia, fluoroscopic guidance
 Catheter  IJV  SVC  RA  IVC  hep vein  lover parenchyma  portal vein
 The tract through liver parenchyma dilated by a balloon catheter  metallic stent is placed
 Complication
o Early
 Perforation of liver capure
 Fatal intraperitoneal hge
 TIPSS occlusion and further variceal haemorrhage – occurs in well compensated
cirrhosis
 Post shunt encephalopathy – it can be reduced by narrowing the lumen of the
shunt if the encephalopathy is severe
o Delayed/long term: stenosis of the shunt – [resent as further variceal hge
 Contraindication: portal vein occlusion

Surgical shunt for varices

 Indication: patient with CTP grade A cirrhosis


 Alternative: long term beta blocker therapy, sclerotherapy
o Beta blocker lower portal pressureby: vasodilation and decreasing cardiac output –
reduces risk of rebleeds
 Shunt classification
o Selective – splenorenal – preserves blood flow to liver – decompresses left side of the
portal circulation that would have given rise to esophageal varices – lower incidence of
hep enceph
o Non selective – portocaval
o Prophylactic shunting doesn’t cause any benefit

Budd chiari syndrome – affects young females – lover acutely congested

Caroli’s disease: congenital dilation of biliary tree

Ascending cholangitis:

 Assoic with obstruction


 Presentation: clinical jaundice, rigor, tender RUQ – charcot’s triad
 USG: dilated bile ducts
 LFT: obstructive picture
 Medical emergency
 Results inmulti organ failure+septicemia
 Rx:
o Rehydration
o 1st line broad spectrum antibiotics
o Urgent endoscopic percutatanoeis drainage of the biliary tree
o Removethe causative – most commoly ductal stones

Pyogenic liver abscess:

 Inmajority etiology unknown


 Cause:
o Biliary stone dss
o Intra abd sepsis
o Appenditcitis
o Diverticular disease
 Presentarion: anorexia, fever, malaise, ruq discomfort
 Common in: diabetic, immunosuppressed, elderly
 Usg/ct: multi-loculated cystic mass
 Confirm: aspiration and cytology
 Rx
o Antibiotics
o Usg guided aspiration
o Caution during the aspiration – avoid development of empyema thoracis

Amebic liver abscess:

 Presentation: dysentery
o Abscess
 Common site of abscess: paracecal, liver
 Dx: isolation of parasite from stool – and microscopy
 Rx
o Conservative: metronidazole tds 7-10 days
o If doesn’t respond – inv further
o Monitor resolution by USG

Hydatid liver disease:

 Echinococcus granulosus
 Presentation:
o Upper abd discomfort
o After minor abdominal trauma – rupture of cyst – acute abdomen
o Active cysts have largenumber of daughter cysts
 Cyst can rupture thru diaphragm – empyema,
 Into biliary tract – obs jaundice
 Dx can be made by ELISA antigen test
 Rx for prevention of progressive enlargement – one course of albendazole/mebendazole
 PAIR
o Intial course of albendazole
o Puncture of cysts image guided
o Aspiration of the contents of the cysts
o Injection of hypertonic saline in cyst cavity
o Re-aspiration
 PAIR attempted only if there is no communication with the biliary tract
 If medical and PAIR fail – consider surgical intervention
 Surgical optionsjoto: liver resection or local excision
 Peroperative durgs praziquantel or albendazole given to prevent abdominal/peritoneal
contamination with hydatid daughters
 Pack peritoneal cavity with hypertonic saline soaked packes
 The reduced cavity maybe packed with greater omentum – omentoplasty
 Rupure of cyst into biliary tract - obstructive jaundice/ascending cholangtisis keno

Liver neoplasm

HCC

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