1. GUIDED BY : DR. C. GADKARI MAM
PRESENTED BY : DR. ANURAG GIRI
2.
3. 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 SURFACE
Liver is divided into 8 segments
4. Largest internal organ and body’s metabolic
headquarter
Wt. 1.5kg (2%)of total body weight of adult
5.
6. 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
7.
8. 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
9. 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
10.
11. 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
12. 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
13. 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
14. BILIRUBIN
EXCRETION
Absorbs bilirubin
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
Immunocompromise
susceptible to
perioperative infection
and sepsis.
15. 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
16. 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
17. 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
18. 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
19. 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
20. Bile contains bile salt,bilirubin and cholestrol.
It dissolves fat to absorb into GI track and bile salt
returns to liver by portal vein
21.
22. 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
23. 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
24. Etiologic diagnosis
Estimation of disease sevearity (grading)
Estimation of disease stage
25. 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
26. Drug history – narcotics, estrogens
Indigestion or pain in rt upper quadrant
27. 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
29. 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
30. Slight deterioration of the intellact &minimal
personality changes may suggest hepatocellular
disease
31. 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
32. 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
33. .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
35. Serum bilirubin: Bilirubin is a break down product of
the porphyrin ring of heme containing protein found in
two fraction
1. 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
36. 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
37. Ammonia is produced in the body during protein
metabolism liver ditoxifies it and convert to urea
There is a poor corelation of blood ammonia and
hepatic function as striated muscles also detoxifies
ammonia
Ammonia can be elevated in severe portal htn
38. 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.
39. 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
40. 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.
42. Cytoplasmic damage- increased AST,ALT,LDH
Mitochondrial damage-increased AST
Cholestatic damage-increased ALP AND GGT
43. 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
44. 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
45. 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
47. 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.
48. 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
49. 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
50. Percutaneous transhepatic cholangiography
(THC) – Percutaneous injection of contrast into
bile duct under fluoroscopic guidance can
determine sight and cause of billary obstruction
51. 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
52. 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
53. 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
54. 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
55. French word jaune means yellow or icterus, yellow
discoloration of skin, sclera and mucous
membrane
Clinically evident when serum bilirubin>2.0 mg/dl
56. 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
59. 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
60. 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
61.
62. 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.
63. Factor 1 2 3
1)Ser. bilirubin <2mg/dl 2-3mg/dl >3mg/dl
2)Ser.albumin >3.5g/dl 3-3.5g/dl <3gm/dl
3)Prothrombin time
a)Prolongation in sec. 0-4sec 4-6sec >6sec
b)INR <1.7 1.7-2.3 >2.3
4)Ascites none slight to tense
moderate
5)Hepatic
encephalopathy none minimal advanced
(grade I/II) (gradeIII/IV)
64. 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
65. 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.
66. 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.
67. 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).
68. The pre-operative risk factors associated with
increase post-operative mortality includes-
1)Serum albumin <3gm/dl
2)Presence of infection
3)WBC >10,000 cells/cubic mm
4)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 ascites
8)Malnutriion
9)Emergency surgery
69. 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. control
2)Platelet count >50,000/mm3
3)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.
70. 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
