GUIDED BY : DR. C. GADKARI MAMPRESENTED BY : DR. ANURAG GIRI

Located in rt upper quadrant of the abdomen under right lower rib cage and projects for a variable extent into left upper quadrant

Held in place by ligamentous attachment to the diphram, peritonium ,great vessles and upper GI track.

Rt lobe further divided into: 1. CAUDATE POSTERIOR SURFACE

2. QUADRATE INFERIOR SURFACELiver is divided into 8 segments

Largest internal organ and body’s metabolic headquarter

Wt. 1.5kg (2%)of total body weight of adult

Liver receives 25% of cardiac output via dual supply (portal vein and hepatic artery)

Portal vein drains blood from GI track and supply 75% of liver inflow (1L/min)

Hepatic artery supply 25% Due to high O2 contents in hepatic artery each vessel

supply 50% of hepatic O2 Portal vein have low vascular resistance (8-10mm/hg) Hepatic venous pressure is 0 mm/hg

Functional unit Is lobule (1x2mm). 50,000-1,00,000

Lobule consists of plates of hepatocytes located in a radial distribution about a central vein

Efferent blood supply from portal vein and hepatic arterey enters at periphery of lobule

Bile formed in the hepatocytes flows into canaliculi (located between plates of hepatocytes) and drains to the bile duct

The large pores in the endothelium lining are sinusoids lined by two types of cell : typical endothelial cells and large kupffer cells(reticulo endothelial) capable of pagocytizing bacteria and other foreign matter in the blood. Allow plasma and its protein to move into the tissue space surrounding hepatocytes (space of dissc) This fluid drains into the lymphatic system

Microcirculation of liver lobule ZONE 1: PERIPORTEL : Receive O2 rich blood

from portal vein and hepatic artery. ZONE 2: MEDIOLOBULAR : As blood moves

through sinusoid it passes from zone 2 to zone 3. ZONE 3: CENTRILOBULAR : Poor in O2

Sympathetic innervation from T3 to T11 controls resistance in hepatic venules

When injured hepatocytes turns into fibrous tissue blood flow is impeded and causes portal hypertension

When portal venous flow is reduced the hepatic atrery can increase flow by 100% to maintain hepatic O2 supply.This relation between two vesseles is hepatic artrial buffer response

FUNCTION DETAILS ANAESTHETIC RELEVANCE

BLOOD RESERVOIR 10-15% of total blood volume

Anaesthetics supress sympathetic tone

BLOOD COAGULATION Synt of pro and anticlotting.vit K absorption depends on bile excretion. Thrombopoietin modulates platelet production

Coagulopathies lead to increased perioperative bleeding

ENDOCRINE CONTROL Syn & secretes Insuline like growth factor1,angiotensin, Thyroxine binding globulin Converts T4 to T3. inactivates: corticosteroids, aldosteron, estrogen, androgen, insulin, ADH

Perioperative endocrine abnormalities

BILIRUBIN EXCRETION

Absorbs bil irubin from blood,conjugates and excretes.synthesizes haptoglobin and scavenges Hb

Lipid metabolism Fatty acid synthesis, cholesterol and lipoprotein metabolism

Abnormal cellular function, affect pharmacokinetic and dynamics of anaesthetic agents.

Amino acid metabolism Protein and aminoacid metabolism and urea production

Elevated level and encephalopathy

Immunologic modulation Largest reticuloendothelial organ. Filters out toxins, bacteria and debris. Hepatic macrophages,Tcells and Kupffer cells triggers systemic inflammatory response

Immunocompromise susceptible to perioperative infection and sepsis.

Liver can store 1L of blood and release blood in circulation at low blood volume

Liver stores vit.B12 (1yr supply) vit.D (3mnth supply) vit.A (10mnth supply) Iron transported via apoferrin and stored as ferritin

(blood iron buffer

Energy production and storage of nutrients absorbed from GI track

Glucose buffering function : Store glucose as glycogen convert carbohydrate (fructose and glactose) to glucose

Synthesise glucose from amino acid and triglicerides (gluconeogenesis)

Synthesise fat cholesterol phospholipids and lipo proteins

Metabolise fat,convert fatty acid to acetyl coenzyme A (COA) is excellent source of energy

Cholestrol synthesized is converted to bile salt and secreted to bile,rest is distributed to body to form cellular membrane and other vital structure

Protein metabolism synthesize all plasma protein except gama globolins (which are formed in plasma cell)

Forms 15-50gms protein/day Albumin is the major protein synthesized and

responsible for plasma oncotic pressure

Blood clotting factors Synthesize in liver except factor III (tissue

thromboplastin), factor IV (calcium) and factor VIII (von willbrand)

Vit K is required for synthesis of factor II (prothombin),factor VII , IX , X

Produce around 500ml of bile daily and store in gall bladder in concentrated form 35-50ml

The fat in food in the duodeneum causes release of choleystokenin hormone from duodenel mucose that stimulate gall bladder contraction

Bile contains bile salt,bilirubin and cholestrol. It dissolves fat to absorb into GI track and bile salt

returns to liver by portal vein

Liver has unique ability to regenerate It restores itself after injury or partial hepatectomy Hepatocytes growth factor produced by

mesenchymal cells in the liver Other growth factor are epidermal growth factor,

interlukin-6,cytokines ,tumor necrosis factors

Hepatocellular-like viral hepatitis features of liver injury & inflammation predominate

Cholestatic(obstructive)-gall stones,biliary cirrhosis ,features of inhibition of bile flow predominate

Mixed -both feature are presents

Etiologic diagnosis Estimation of disease sevearity (grading) Estimation of disease stage

Family history – jaundice, anaemia, splenectomy, cholecystectomy,gall stones

Occupation in detail Environmental factor – contacts with rats (weils

diseases), exposures to toxins Travel to other countary Alcohol intake Conact with jaundice patients BT, plasma transfusion ,tattoing, dental treatment

Drug history – narcotics, estrogens Indigestion or pain in rt upper quadrant

A patient of liver dysfunction presents with following complaints:

• Pain in abdomen-the rt. quadrant region• Abdominal distension• Pruritus• Anorexia• Nausea and vomiting• Wt. loss • Fever• Fatigue• Haematemesis• Malaena• Dark coloured urine (yellowish discolouration)• White colour stool • Oliguria

Jaundice Hepatomegaly Spider Naevi Splenomegaly Scratch Marks Ascites Palmer Erythema

Dilated Abdominal Veins

Peripheral Oedema Finger Clubbing Testicular Atrophy Bruising Gynaecomastia Confusion/Coma

Jaundice in sclera or in skin Pallar –sign of anaemia(hemolysis) Gynecomastia , testicular atrophy (cirrhosis) Skin exam- ecchymosis due to prothombin

defficiency, purpura due to thrombocytopenia,spidor angiomas found around face neck shoulder forearm

In chronic cholestatic – scratch marks , finger clubbing

Slight deterioration of the intellact &minimal personality changes may suggest hepatocellular disease

Ascitis Dilatation of periumblical veins Size of liver Tender gall bladder (murphy sign) Auscultation – venous hum over dilated collatral

veins radiating from umblicus called caput medusac

Typical battary of blood test used for initial assesment of liver disease

.Serum alanine aminotranferase (ALT) 5-42u/l

.Serum aspartate aminotransferase (AST) 5-40u/l

.Alkaline phosphatase

Children 25-350 u/l Adult males 25-120 u/l Adult females 25-90 u/l

.Direct (conjugated 0-0.2mg/dl)

. Total bilirubin (0.3 -1.0 mg/dl) .Albumin 3.5-5.0 gm/dl .Prothrombin time 11-15 secs .Gamma glutamyl transpeptidase (GTT) male-upto 40u/l female-upto 25u/l .Hepatitis serology to define types of viral hepatitis

.autoimmune markers to diagnose primary biliary cirrhosis (anti mitochondrial antibody AMA)

Selerosing cholongitis(peripheral antineutrophil cytoplasmic antibody P-ANCA)

Autoimmune hepatitis (antinuclear ,smooth muscle, liver kidney microsomal antibody)

Serum bilirubin: Bilirubin is a break down product of the porphyrin ring of heme containing protein found in two fraction1. Conjugated(direct) : water soluble and can be excreted by kidneys. Upto 30% of total bilirubin. Increased due to liver or billiary tree disease.2. Un- conjugated: Insoluble in water and bound to albumin in blood.Increased due to haemolatic disorder

Urine bilirubin: unconjugated bilirubin always bind with albumin so it is not filtered by kidneys only conjugated bilirubin is found in urine

A urine dipstick test is done for urine conjugated bilirubin

Ammonia is produced in the body during protein metabolism liver ditoxifies it and convert to ureaThere is a poor corelation of blood ammonia and hepatic function as striated muscles also detoxifies ammoniaAmmonia can be elevated in severe portal htn

1. Enzymes reflects the damage to hepatocytes: AST is found in liver,cardiac muscle, skeletol

muscle,kidney,brain,lungs,leucocytes and erythrocytes in decreasing order of concentration.

ALT is found primarily in liver These enzymes released in blood in increased

amount when liver cells are damaged resulting increase in permiability of cell membrane.

There is a poor corelation between degree of liver cell damaged and level of enzymes

Level upto 300u/l are non-specific and may be found in any type of liver disorder

Level upto more than 1000u/l are specific and extensive hepatocellular injury may present

In most acute hepatocellular disorder the ALT is higher than or equal to AST

A ratio of AST:ALT 3:1 is suggestive of ALD

The AST/ALT ratio is helpful in distinguishing between alcohol induced hepatitis and viral hepatitis.

Alcohol tends to damage hepatocyte mitochondria thus causing rise in AST usually greater than twice the ALT.

ALT activity is low in patients with alcohol induced liver disease as these have deficiencies of pyridoxal-5- phosphate, a vitamin necessary for the function of ALT.

A decrease in AST/ALT <1 ratio is more consistent with a diagnosis of viral hepatitis.

ALT-cytosol AST- mitochondria and cyotsol LDH- cytosol ALD- canalicular surface GGT-canalicular surface and microsomes 5 NT-canalicular surface

Cytoplasmic damage- increased AST,ALT,LDH Mitochondrial damage-increased AST Cholestatic damage-increased ALP AND GGT

1.SERUM ALBUMIN: exclusively synthesized by hepatocytes,long half life 15-20 days, poor indicator for acute of chronic hepatic dysfunction

Minimal changes seen in viral hepatitis, drug related hepatotoxicity and obstructed jaundice.

Hypo albuminemia is commom in cirrhosis

2. SERUM GLOBULIN: Group of protein made up of gamma globulin(immuno globulin).

Produced by B lymphocytes and alpha and beta globulin produced in hepatocytes

Gama globulin increased in chronic liver disease

Except factor VIII all blood coagulation factors are made in liver hepatocytes

Measurement of clotting factor is accurate measure of hepetic synthetic function

Serum prothrombine time measures factor II,V,VII and X

PT may be increased in vit.K deficiency PT more than 5 secs. Is poor prognostic sign in

hepatic disease

Test Obstructive ParenchymalAST and ALT

Alkaline phosphataseAlbumin NProthrombin time N Bilirubin N N GGT5’ Nucleotidase N

Xray- limited role detects calcified & gas containg lesions

Barium studies of GIT-In suspected cases of portal HTN to determine esophagogastric varices.-enlargement of lt. lobe of liver(due to tumour, abscess or cirrhosis) may displace the barium filled stomach laterally and anteriorly.-tumours of the head of pancreas may produce displacement or irregularity of 2nd part of duodenum.

USG whole abdomen-to know the size and shape of liver and spleen.-in biliary obstruction, to determine the size of bile ducts, presence of gall stones, presence of mass in the head of pancreas.-in detecting mass lesions such as tumours, cysts or liver abscess.

CT- Abdomen & MRI-in diagnosis of mass lesions in liver or pancreas.-in differentiating intrahepatic fluid collections such as cysts, abscesses and haematomas.-to obtain excellent image of pancreas,liver and spleen.

Magnetic resonance cholengiopancreatiography (MRCP) for visualization of billary tree

Endoscopic retrograde cholengiopancreatiography (ERCP)-allows for biopsy,direct visualisation of the ampulla and common bile duct having some therapeutic options like sphincterotomy,stone extraction,placement of nasobillary catheter and biliary stents

Percutaneous transhepatic cholangiography (THC) – Percutaneous injection of contrast into bile duct under fluoroscopic guidance can determine sight and cause of billary obstruction

Paul Ehrich performed first percutaneous liver biopsy in 1883 in Germany.

TYPES 1. Percutaneous liver biopsy a) blind liver biopsy b) guided liver biopsy c) plugged liver biopsy 2. Transvenous(trans jugular liver biopsy) 3. Laproscopic liver biopsy

Acute hepatitis of unknown cause Chronic liver disease a)to define cause b) grading of inflammatory activity c) staging of chronic hepatitis c and chronic hepatitis b d) monitor response to therapy Diagnosis of metabolic liver disorder Diagnosis and grading of alchoholic liver disease

Staging of advanced cases of primary billiary cirrhosis

Investigation of persistant abnormal and unexplained LFT

Investigation of PUO Diagnosis of focal hepatic lesion Histologic monitoring following liver

transplantation

Unco-operative patient Extrahepatic biliary obstruction Bleeding diathesis or abnormal coagulation profile Tense ascites Hydatid cyst of liver Suspected hemangioma or other vascular tumor Amyloidosis

French word jaune means yellow or icterus, yellow discoloration of skin, sclera and mucous membrane

Clinically evident when serum bilirubin>2.0 mg/dl

Main type of bilirubin increased in plasma Unconjugated>85%of total causes are hemolysis,resorption of large

hematoma,ineffective erythopoiesis,physiological jaundice of new born ,

Conjugated >50%of total causes are: hepatitis cirrhosis,

cholestasis,drugs(anabolic steroids, oral contraceptis) ,toxins

Mixed(conjugated+unconjugated) Conjugated bilirubin is 25-50% of total, viral or

alchohlic hepatitis

Hemolytic Hepatocellular Obstructive

Pre-hepatic: Excessive formation of bilirubin exceeding the capacity of the liver to conjugate it for excretion. The type of bilirubin increased is unconjugated.Urobilinogen is increased in urine and feces

Hepatic: Unconjugated, conjugated or both are increased.

Un conjugated: 1)Defective uptake of bilirubin by liver cell from blood (gilbert’s syndrome). 2) Defective conjugation of bilirubin

Conjugated hyperbilirubenemia: 1)Hepatocellular disease : AST and ALT are raised

2) Intrahepatic cholestasis a) Impairment of secretion of bilirubin from

hepatocyte into biliary canaliculi b) Obstruction of bile flow in canaliculi by

swollen hepatocytes. c) Damage to intrahepatic canaliculi 3) Post hepatic jaundice called as obstructive

surgical or extrahepatic cholestatic

Child-Turcotte Pugh classification is a universally used method developed in 1964.

Total score=15(minimum=3) Grades= A,B,C Grade A(score of 5-6)-low risk with 5% mortality. Grade B(score of 7-9)-moderate risk with 10% mortality. Grade C(score of >10)-high risk with >50% mortality.NB: grade C indicates decompensated cirrhosis.

Factor 1 2 31)Ser. bilirubin <2mg/dl 2-3mg/dl >3mg/dl2)Ser.albumin >3.5g/dl 3-3.5g/dl <3gm/dl3)Prothrombin timea)Prolongation in sec. 0-4sec 4-6sec >6sec b)INR <1.7 1.7-2.3 >2.34)Ascites none slight to tense

moderate5)Hepatic encephalopathy none minimal advanced

(grade I/II) (gradeIII/IV)

Model for end stage liver disease(MELD) is another system to assess the severity of liver disease which was developed at Mayo clinic to assess 3 month outcomes of patients undergoing TIPS(transjugular intrahepatic portosystemic shunt procedure).

Calculation is done by MELD Score:=(0.957xlog e[serum creatinine(mg/dl)]+0.378 x log e[total serum bilirubin(mg/dl)]+1.120 x log e[INR]) x10

Minimum for all value=1 Maximum value for creatinine=4

A day prior to surgery, the anaesthetist should meet the patient and relatives and explain about the risk factors of surgery.

Any expected post-operative ventilatory support monitoring and about possible post-operative complications should be explained to patient and relatives.

Consent Availability of appropriate blood and blood

products and suitable post-operative facilities to be checked.

Anti-anxiety medication is prescribed a night prior to surgery in a guarded dose as there is reduced ability of the liver to metabolize the drug.

Patient to be kept NBM a night prior to surgery but during this period IVF(crystalloids) in a rate of 1-2ml/kg/hr is to be given as these patient who are having jaundice and with hepatorenal syndrome are at increase risk of renal damage if they become dehydrated or hypotensive as a result of pre-op fast as these concentrates toxins in the filtrate.

Dextrose containing fluids is a better choice to give when the patient is NBM as these pt. of hepatic dysfunction are more prone for hypoglycemia.(Liver acts as a glucostat i.e. maintains blood sugar level by glycogenesis and stopping glycogenolysis when there is increased blood sugar in blood and viceversa when there is decrease blood sugar).

The pre-operative risk factors associated with increase post-operative mortality includes-

1)Serum albumin <3gm/dl2)Presence of infection3)WBC >10,000 cells/cubic mm4)Treatment with more than 2 antibiotics.5)Prothrombin time >1.5 sec over control.6)Serum bilirubin >50µmol./litre(2.92mg/dl)7)Presence of ascites8)Malnutriion9)Emergency surgery

Regional anaesthesia is preferred in peripheral surgeries if there is no clotting abnormalities.

Guidelines: 1)Prothrombin time not greater than 2.5sec. above the

lab. control2)Platelet count >50,000/mm33)Bleeding time not greater than 12 min. If bleeding/clotting variables are within these

measurements epidural, spinal and regional block anaesthesia can be employed.

For abdominal surgeries/ pt. with obvious coagulopathy, regional anaesthesia is contraindicated.

Premedication-lorazepam(25-50 mck/kg)+ ranitidine

Induction – thiopentone (3-5 mg/kg) Intubation-succinylcholine (1-2 mg/kg) and low

pressure cuffed oral tracheal tube Maintenance-fentanyl 1 mck/kg, isoflurane,O2,

N2O/air,ippv+peep(aim for paco2 3.5-4.6 pka) Drug infusion- atracurium 0.5 mg/kg per hr Venous access – peripheral cannulae Arterial line-central venous line (two) one for

monitoring one for drug infusion Urinary catheter – for urine output