A 45 YEAR OLD MALE
DIAGNOSED WITH ALCHOLIC
LIVER DISEASE POSTED FOR
ESOPHAGEAL VARICES
BANDING
MODERATOR : DR SHAHBAZ HASNAIN (PROFESSOR)
DR AMRUTA PATIL (SENIOR RESIDENT)
PRESENTOR : DR SPOORTI PUJARI (JUNIOR RESIDENT)

CHIEF COMPLAINTS
• My patient, Mr. Akash 45 year old male, resident od Talegaon, was admitted to Dr. D.Y.Patil
Medical College and Hospital with the chief complains of-
• c/o pain in abdomen since 12 days
• C/o abdominal distension since 12days

HISTORY OF PRESENT ILLNESS
• Patient was apparently alright 2 months back after which he developed generalized
abdominal distension which was gradual in onset and progressive in nature. It was
associated with epigastric discomfort with sense of heaviness.
• H/o three episodes of blood in vomit of 30-40ml in last 1 month
• H/o pruritis since 1 month
• H/o passing of dark coloured stools and altered colour of urine since 1 month.
• H/o jaundice 6 months back for which he was admitted and conservatively managed.

PAST MEDICAL HISTORY
• Admitted for jaundice six months back – conservatively managed
• History of blood transfusion present
• not a known case of diabetes mellitus, hypertension, tuberculosis, asthma, epilepsy
• no history of any previous surgeries

Family history
• Diet – vegetarian
• sleep – disturbed
• appetite – decresed
• habits – chronic alcoholic since 25 years, stopped six months back

General physical examination
• Patient is thin built and mal-nourished, oriented to time place and person
ON EXAMINATION
• general condition-fair
• afebrile
• pulse rate-108 bpm
• BP-110/70 mmhg
• SPO2-99%
• PICKLE: + + - - - +

Head to toe examination:
• alopecia present bilateral
• parotid swelling noted
• dry skin with spider nevi present on neck shoulders and arm
• Palmar erythema present
• no neck swelling
• neck movements normal
• spine normal

Systemic examination
• Per-abdominal examination –
Inspection:
 skin over abdomen appears normal,
 abdominal distension present,
 umbilicus displaced downwards, transversely stretched,
 abdominal thoracic breathing movements
 no visible pulsations no dilated veins,
 no scars ,sinuses, fistula
• Palpation:
No guarding/rigidity/tenderness
Hepatomegaly +
Splenomegaly +
kidneys not palpable or ballotable

• Percussion :
• Shifting dullness and horseshoe shaped dullnes present
• fluid thrill absent
• Auscultation
• Normal peristaltic sounds heard
• No arterial bruit or Venus Hum
• Cardiovascular system examination– S1 S2 present, no murmurs
• respiratory system examination – bilateral air entry equal

• Central nervous system examination:
• patient is conscious, alert and well oriented to time, place, person
• Higher functions intact
• speech normal
• no flapping tremors
• cranial nerves, sensory and motor system examination –normal
• reflexes normal
• Airway examination:
• temporomandibular joint mobility normal
• thyromental distance 7 cm
• Mallampatti class- grade 1
• dentition – lower molar missing, no loose tooth
• neck movements normal

Investigations
• Complete haemogram with ESR
• Liver function tests
• random blood sugar
• blood urea
• serum electrolytes
• bleeding time/clotting time
• PT/APTT/INR
• chest x-ray
• USG abdomen and pelvis
• OGDOSCOPY

Provisional diagnosis
• 45-year-old male patient with complaints of abdominal pain and distension, blood in
vomit ,a known case of alcoholic liver disease is probably a case of liver cirrhosis with
portal hypertension with esophageal varices posted for esophageal variceal banding.

LIVER CIRRHOSIS AND PORTAL
HYPERTENSION

Anatomy
• Largest internal organ –
weighs around 600 to
1800 gms
• traditionally divided into
four lobes,
• couinaud model –
functional segments eight,
based on hepatic vascular
supply and biliary
distribution

Microscopic
anatomy

Blood supply
• 20 to 25% of resting cardiac output 1500
ML per minute
• hepatic artery 25% (SPO2 to 98%)
• portal vein 75% (SPO2 to 60 to 70%)
• oxygen supply 50:50

Functions of
liver
• Metabolic and storage : carbohydrate protein fat
• Detoxification: alcohol, drugs ,ammonia
• Synthetic: bile, heme, coagulation factors, albumin
cholesterol
• immunologic : kupfer cells, NK cells, T and B lymphocytes
• homoeostatic : glucose/ volume homoeostasis ,hormone
synthesis and degradation.

Liver function
tests
• Hepatocyte function – liver enzymes – AST, ALT, LDH, GST
• Detoxification and excretory function – serum bilirubin
(indirect/ direct), serum ammonia, U.bilirubin
• Synthetic function – serum albumin, serum globulin,
coagulation factors –PT/INR
• Cholestasis - Alk phosphatase, GGT

Hepatic dysfunctions and LFTs
Hepatic
dysfunction
s Causes S. Bilirubin Aminotransferas es
Alkaline
Phosphatase
Prehepatic
Hemolysis,
Hematoma
resorption, Bilirubin
overload post blood
transfusion
Increased
unconjugated
Normal Normal
Hepatic /
hepatocellular
Viral, alcoholic, drug
induced, sepsis,
hypoxemia, cirrhosis
Increased
conjugated
Markedly increased
Normal to slightly
increased
Posthepatic /
cholestatic
Biliary tract stones,
stricture, tumour
Increased
conjugated
Normal to slightly
increased
Markedly increased

CIRRHOSIS
• pathological end point of chronic inflammatory liver
disease
• steady or recurrent parenchymal inflammation, necrosis &
and fibrosis
• formation of regenerative nodules
• distortion of normal liver architecture with increased
resistance to intrahepatic blood flow
• portal hypertension

CAUSES

PORTAL
HYPERTENSION
• Chronic increase in portal venous pressure
• HPVG ( Hepatic Venous Pressure Gradient) maintains flow
• HPVG = WHVP-HFVP (wedged-free HVP)
Normal HPVG 1-5mm Hg
Mild PHT - 5-10mm Hg
• >10mmHg clinically significant
• Shunt formation

PORTAL
HYPERTENSION
• 𝜟P = R X Q
• Increased resistance to intrahepatic blood flow (R)
• Peripheral & splanchnic NO & neural, humoral and
endothelial factors like prostaglandins, VIP, glucagon etc →
splanchnic vasodilatation → increased portal inflow (Q)
• exacerbation of PHT
• Formation of collaterals, ascites, splenomegaly

SYSTEMIC
EFFECTS OF
CIRRHOSIS
1. Hematological
2. Coagulation
3. Cardiac
4. Renal
5. Pulmonary
6. CNS
7. Gastrointestinal
8. Hepatocellular Carcinoma

Hematological
• Anemia
• Chronic illness
• Malnutrition
• Blood loss
• Hypersplenism
• Bone marrow depression

Coagulopathy
1. ↓ synthesis of
• procoagulant except tissue thromboplastin (III), calcium
(IV) and
• von Willebrand factor(VIII)
• anticoagulant factors (protein C, S, antithrombin III)
• clearance of activated factors
2. Thrombocytopenia due to
• Splenic sequestration (splenomegaly)
• decreased level of thrombopoietin
• Immunologic mechanism
• direct bone marrow suppression

Coagulopathy
3. Vitamin K deficiency
4. dysfibrinogenemia
5. Fibrinolysis - accelerated fibrinolysis
Need blood component therapy, vitamin K, Tranexemic acid

Cardiac manifestations
• Hyperdynamic circulation
• low stroke volume rate, high cardiac output, low BP
• PAP raised, PVR normal
• systolic dysfunction – impaired contractility
• Diastolic dysfunction – delayed left ventricular filling
• ECG abnormalities - prolonged QT interval
• Ionotropic and Chronotropic response to stress impaired
• underlying coronary artery disease, cardiomyopathy

Renal dysfunction
• Hypovolaemia ≫ renal hypo perfusion with reduced GFR ≫ activation of RAAS (renin
angiotensin aldosterone) and Vasopressin ≫ sodium and water retention
• Precipitated by pre/intraoperative hypovolaemia, diuretics
• Prone to parenchymal renal disease, sepsis
• Coexisting diabetes, immune complex nephropathies, amyloidosis

Hepato-renal syndrome (HRS)
• functional renal failure with no renal pathology in patients with cirrhosis, reversible
• water retention, ascites, edema, azotemia, oliguria, electrolyte imbalance
• Type 1 – rapid onset (1 to 2 weeks), precipitating cause present example : surgical stress,
GI bleeding, SBP, LVP, poor prognosis, survival 2 to 4 weeks
• Type 2 -gradual in onset, progression of RAAS and vasopressin systems, better prognosis,
survival 6 months

MANAGEMENT
• Maintain renal perfusion
• avoid nephrotoxic drugs like NSAIDs, aminoglycosides, ACE inhibitors, ARBs
• elimination of underlying cause
increase renal perfusion with octreotide, Terlipressin or norepinephrine infusions
combined with volume expansion with albumin
 dialysis
 liver transplantation

Pulmonary complications
1. Vascular
Hepato-pulmonary syndrome(HPS)
Porto-pulmonary hypertension(PoPH)
2. Mechanical
Hepatic hydrothorax
Ascites/Pleural effusion

Hepato-pulmonary syndrome (HPS)
• Defined as abnormal alveolar-arterial oxygen gradient (more than or equal to 15mmhg)
while breathing room air in sitting position
• Intrapulmonary vasodilation V:Q mismatch
• Impaired HPV
• clubbing, cyanosis, spider naevi
• Platypnea - shortness of breath which is worse in standing position and relieved by lying
down
• Orthodexia - falling pao2 by 4mmhg or 5% on moving from supine to erect position

HPS contd..
 Severity depends on pao2
• more than 80 MMHG - mild
• 60 to 80 MMHG - moderate
• 50 to 60 MMHG - severe
• less than 15MMHG - very severe
 Diagnosis – “saline bubble test” on Echo
 Management –
oxygen supplementation to maintain SPO2 over 88%
liver transplant

PORTOPULMONARY HYPERTENSION
• Pulmonary artery hypertension in known case of liver disease with portal hypertension
• Cause – pulmonary endothelial smooth-muscle proliferation or thrombus in situ
• Diagnosis – TTE
PAP more than 25MM HG, PVR more 240dynes/s/cm⁵
• Classification
- mild-PAP 25-35mm Hg
- moderate 35-45mm Hg
- severe > 45mm Hg
PAP > 45 mmHg –Absolute Contraindication for Liver transplant
• Management
Phosphodiesterase inhibitors, prostacyclin analogues to reduce PVR

Hepatic Hydrothorax
• Passage of ascitic fluid from peritoneal to pleural space through defects in diaphragm,
usually on right
• Reduced functional residual capacity, Atelectasis, hypoxia
• Diagnosis- chest x-ray, thoracocentesis
• Management- sodium restriction, diuretics, trans-jugular intrahepatic portosystemic shunt
(TIPS)

Hepatic
encephalopathy
• Neuropsychiatric manifestations in patients with significant
liver disease-acute or chronic
• Sign of decompensated liver disease
• Neurotoxins/ammonia produced in the gut reach the brain
due to failure of liver to detoxify them and portosystemic
shunting
• Precipitated by GI bleeding, infection, portosystem shunts,
diuretic overdose, sedatives, high-protein diet.
• MANAGEMENT:
• Elimination of precipitating cause
• restriction of protein intake
• oral lactulose or neomycin/rifaximin
• Protection of airway
• avoid GA, sedatives, opioids

West-Haven Criteria
Grade Description
I
Trivial lack of awareness, shortened attention span,
disordered sleep
II Lethargy, behavioral change, asterixis
III
Somnolence, confusion, gross disorientation, bizarre
behavior
IV Coma

Ascites
Causes
• Hypoalbuminemia>>>decreased oncotic pressure
• Activation of RAAS with sodium water retention
• Increase portal hydrostatic pressure
Classification
mild (detectable only by ultrasound)
moderate (moderate symmetrical abdominal distension)
large – severe abdominal distension

EFFECT
• Diaphragmatic splinting so decreased pulmonary complaince
• Decreases renal perfusion
• Spontaneous bacterial peritonitis (SBP)
• falsely high CVP
• Predisposes to aspiration
• Abdominal wound dehiscence/herniation.

• Treatment
salt restriction
diuretics-spironolactone/frusemide
non-selective beta blockers to reduce portal hypertension
• Refractory ascites
Midodrin for refractory ascites
Large volume paracentesis – albumin 8 g/L
Trans-juglar intrahepatic photosystem actions (TIPS)
Liver transplant

Anesthetic management

Preoperative assessment
• After detailed pre-operative assessment and general physical examination,
following laboratory investigations were sent
1. CBC
2. B. Glucose
3. B. urea, S. Cr
4. Electrolytes- Na, K, Mg, PO4
5. S. bilirubin, Transaminases, S. Albumin
6. PT/INR, S. fibrinogen
7. Chest X ray, USG
8. ECG, ECHO, Stress ECHO
9. PFT/ ABG
10. Viral markers

Aminotransferases in hepatic disease
Liver disease Aminotransferses
NAFLD AST & ALT normal to < 5 X normal AST:ALT < 1
Acute viral hepatitis > 25 X normal
Chronic viral hepatitis Normal to 10 X normal
Alcoholic hepatitis AST & ALT normal to < 8 X normal AST:ALT - 2:1
Shock liver AST & ALT normal to > 50 X normal AST:ALT - 1:1

Child-Pugh Scoring system
Sign of Hepatic
dysfunction
1 1 point 2 points 3 points
Encephalopathy grade None Grade I-II Grade III-IV
Ascites Absent Mild Severe
Bilirubin (mg/dl) <2 2-3 >3
Albumin (gm/dl) > 3.5 2.8-3.5 < 2.8
INR < 1.7 1.7 -2.3 > 2.3
TOTAL SC ORE 3-15
CLASS A
CLASS B
CLASS C
5-6 – MILD RISK
7-9 – MODERATE RISJ
>10 – POOR RISK
2-10% MORTALITY
12-31% MORTALITY
50-82% MORTALITY, CONTRAINDICATION FOR ELECTIVE SURGERY

MELD SCORE

Preoperative optimization
• Nutrition- low protein, high calorie diet
• optimize hydration
• renal status
• encephalopathy
• coagulopathy
• metabolic and electrolyte derangements
• treatment of active infections
• Hypoglycemia
• minimize ascites/hydrothorax

OT PREPARATION
• Universal precautions for Hepatitis B, C
• Aseptic precautions
• Hypothermia- fluid and other warming devices
• Large bore IV access
• 2 suction apparatus
• Emergency cart
• In high risk cases-
• Hemorrhage - rapid infusion systems, blood conservation techniques
• Invasive monitoring
• Blood & blood products
• Inotrope infusions

ANAESTHESIA CONCERNS
• Maintenance of a hepatic blood flow, oxygenation
• altered pharmacology-increase sensitivity, large volume of distribution, increase free
drug, reduce hepatic clearance, active metabolites
• avoid IM injections, nasal intubations, nasal/ esophageal probe/ nasogastric tubes
• maybe on beta blockers for portal hypertension
• hyporesponsive to vasopressors

FACTORS REDUCE HEPATIC BLOOD FLOW
Hypoxia
Hypocarbia
Intravenous agents
Haemorrhage
Mesentric traction
Increased IAP
IPPV/PEEP
Regional anesthesia
Sepsis
Volatile anesthetics

PREMEDICATION
• avoid sedation- encephalopathy
• avoid diazepam, midazolam
• lorazepam/oxazepam safe
• dose reduction of above drugs due to prolonged duration of action

INDUCTION
INTRAVENOUS AGENTS:
• sensitivity to the CNS depressant effect
• thiopentone - decreased binding
• propofol maintains HABR/extrahepatic metabolism/less encephalopathy, normal recover
INHALATIONAL AGENTS
• reduce MAP & CO → ↓HBF
• avoid halothane/enflurane
• HABR preserved with isoflurane, desflurane
• desflurane safest- rapid emergence, less hepatic metabolism, less ↓CO
• N₂O may be avoided-reduce hepatic blood flow

Opioids and Muscle relaxants
• Morphine - free drug increased, action prolonged
• Pethidine/alfentanil/ buprenorphine- elimination reduced
• Fentanyl – large doses accumulate
• Remifentanil safest
• Scoline –RSI (ascites), pseudocholinesterase ↓– prolonged duration —
• Non depolarizing agents
- slower onset of action
- duration prolonged
- Vecuronium/rocuronium- hepatic metabolism
• Atracurium/cisatracurium –safe
• Neostigmine – unaffected

Intraoperative monitoring
• ECG
• SpO2
• NIBP, EtCO2,
• Temperature
• U.O.
• Blood loss
• Arterial pressure monitoring —
CVP
monitoring
• Neuromuscular monitoring
• Biochemical & hematological
monitoring
• glucose
• hematocrit
• electrolytes
• calcium
• ABG
• TEE/ Pulmonary artery
catheterization/ SVV
• TEG/ Thromboelastometry

Postoperative care
• Analgesia
- Avoid epidural catheters
- Regional analgesia- hematoma
- PCA fentanyl
- NSAIDS not recommended
- Acetaminophen up to 2gm/day
- Tramadol- low dose
• ICU care- CTP-B/C
• Signs of decompensation – encephalopathy, jaundice

Role of neuraxial anesthesia
• coagulopathy/ thrombocytopenia
• post hepatic resection coagulopathy
• hypotension and reduction in hepatic blood flow
• non-responsive to catecholamines
• decreased local anaesthetic requirements

VARICES
• Oesophageal varices are dilated
and tortuous veins in the
oesophageal wall, secondary to
increased venous pressure in the
splanchnic venous bed or in the
superior vena cava. They are
prone to rupture and often are
the sources of massive
haemorrhages from the upper
gastro-intestinal tract and
rectum

• Most commonly at lower oesophagus and stomach
• Upper end of anal canal
• Umblical
• Bare area of liver
• Retroperitoneal
• Risk of spontaneous rupture and bleeding- mortality -25-50%

Management of Variceal bleeding
• Gastro-esophageal varices occur in patients with cirrhosis and portal hypertension with an
HVPG of at least 10 to 12 MM HG.
• Medical management
• Prophylaxis:
Preventive management of variceal haemorrhage includes pharmacological and
endoscopic therapy.
Non-selective beta-blockers which are known to decrease cardiac output (beta-1) and
increase splanchnic arteriolar Vasoconstriction (beta-2), reducing portal flow (eg:
propranolol and nadalol).
Vasopressin also has splanchnic vasoconstriction properties and decreases portal venous
collateral flow and portal pressure.
Somatostatin decreases splanchnic flow, but does so indirectly by reducing glucagon,
substance p, and vasoactive intestinal peptide

PREVENTIVE MEASURES CONTD..
• Endoscopic therapy is an effective means of preventing and controlling variceal bleeding.
• Endoscopic variceal band ligation(EVL) can be performed at the bedside and has largely replaced
endoscopic sclerotherapy (ES), which can be associated with fever, chest pain, dysphagia and
perforation.
• Endoscopic variceal band ligation(EVL) can be performed regularly to manage the bleeding in
patients when combined with pharmacological therapy. Per AASLD practice guidelines it can be
repeated every 1 to 2 weeks until obliteration.
• Surveillance Esophago-Gastro-duodenscopy can then follow every 6 to 12 months

Variceal Hemorrhage
• The first line treatment of variceal haemorrhage, in addition to volume resuscitation with
fluid and blood, and replacement of clotting factors and platelets, is pharmacological
therapy with intravenous Vasopressin and nitroglycerin, Terlipressin, somatostatin or
octreotide prior to Esophago-Gastro-duodenoscopy and continued for 3 to 5 days.
• Patient should also be started on antibiotic prophylaxis with ciprofloxacin or ceftriaxone

• EGD should be performed within 12
hours, and EVL performed to control
bleeding. EVL controls bleeding in
approximately 20-80% of patients and
has the same or better results than ES.
• Multiple follow-up sessions are
required to eliminate the varices, and
are generally performed every 1 to 2
weeks until obliteration.
• Re-bleeding is less after EVL compare to
ES and mortality is lower so EVL is
preferred.

ESOPHAGEAL BALLOON TAMPONADE

• Balloon tamponade with Sengstaken-Blackmore or Minnesota tube can be used for
control of variceal haemorrhage in patients who are unresponsive to
pharmacotherapy and EVL.
• These tubes used two balloons- a gastric balloon and a esophageal balloon to
tamponade a submucosal veins.
• Initial control of bleeding is accomplished in 80% of the patients, but to 50% re-
bleed after balloons are deflated.
• However these tubes can be used as a temporary measure while preparing for
emergent TIPS or surgical shunt.
• With Sengstaken-Blackmore tube NG tube is used to aspirate secretions from the
oesophagus above the balloon, other tubes example Minnesota tube have a
proximal esophageal drainage port so that NG tube is not required.

CONSIDERATIONS FOR SPECIAL PROCEDURES
TIPS (Transjugular Intrahepatic Portosystemic Shunt)
• Interventional radiological procedure
• create a shunt between portal vein and systemic circulation(hepatic vein) through the
liver parenchyma
• Indicated in refractory ascites, variceal haemorrhage, reduce gradient
• Contraindications-CHF, severeTR, mod-severe pulmonaryHTn ,sepsis, biliary obstruction
• Complications - vascular injury, dysrhythmias, hemorrhage, trauma, encephalopathy, renal
failure.

ANESTHETIC CONCERNS FOR ENDOSCOPY
• Complete evaluation and optimization
• Remote location
• Access to the patient
• L.A/Sedation/G.A.
• Encephalopathy
• Airway protection
• Ventilation compromised

THANK YOU