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  2. 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
  3. 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.
  4. 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
  5. Family history • Diet – vegetarian • sleep – disturbed • appetite – decresed • habits – chronic alcoholic since 25 years, stopped six months back
  6. 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: + + - - - +
  7. 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
  8. 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
  9. • 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
  10. • 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
  11. 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
  12. 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.
  14. 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
  15. Microscopic anatomy
  16. 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
  17. 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.
  18. 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
  19. 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
  20. 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
  21. CAUSES
  22. 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
  23. 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
  24. SYSTEMIC EFFECTS OF CIRRHOSIS 1. Hematological 2. Coagulation 3. Cardiac 4. Renal 5. Pulmonary 6. CNS 7. Gastrointestinal 8. Hepatocellular Carcinoma
  25. Hematological • Anemia • Chronic illness • Malnutrition • Blood loss • Hypersplenism • Bone marrow depression
  26. 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
  27. Coagulopathy 3. Vitamin K deficiency 4. dysfibrinogenemia 5. Fibrinolysis - accelerated fibrinolysis Need blood component therapy, vitamin K, Tranexemic acid
  28. 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
  29. 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
  30. 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
  31. 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
  32. Pulmonary complications 1. Vascular Hepato-pulmonary syndrome(HPS) Porto-pulmonary hypertension(PoPH) 2. Mechanical Hepatic hydrothorax Ascites/Pleural effusion
  33. 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
  34. 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
  35. 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
  36. 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)
  37. 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
  38. 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
  39. 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
  40. EFFECT • Diaphragmatic splinting so decreased pulmonary complaince • Decreases renal perfusion • Spontaneous bacterial peritonitis (SBP) • falsely high CVP • Predisposes to aspiration • Abdominal wound dehiscence/herniation.
  41. • 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
  42. Anesthetic management
  43. 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
  44. 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
  45. 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
  47. 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
  48. 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
  49. 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
  50. FACTORS REDUCE HEPATIC BLOOD FLOW Hypoxia Hypocarbia Intravenous agents Haemorrhage Mesentric traction Increased IAP IPPV/PEEP Regional anesthesia Sepsis Volatile anesthetics
  51. PREMEDICATION • avoid sedation- encephalopathy • avoid diazepam, midazolam • lorazepam/oxazepam safe • dose reduction of above drugs due to prolonged duration of action
  52. 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
  53. 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
  54. 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
  55. 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
  56. 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
  57. 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
  58. • 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%
  59. 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
  60. 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
  61. 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
  62. • 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.
  64. • 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.
  65. 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.
  66. ANESTHETIC CONCERNS FOR ENDOSCOPY • Complete evaluation and optimization • Remote location • Access to the patient • L.A/Sedation/G.A. • Encephalopathy • Airway protection • Ventilation compromised