hepatic anesthesia

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anesthetic implications of liver anatomy and physiology.

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Dr. Mohd Saif Khan MD LHMC, New Delhi HEPATIC ANATOMY, PHYSIOLOGY & ANESTHETIC EFFECTS

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HEPATIC ANATOMY GROSS ANATOMY MICROSCOPIC ANATOMY HEPATIC BLOOD FLOW HEPATIC BLOOD FLOW REGULATION INTRINSIC FACTORS EXTRINSIC FACTORS EFFECTS OF ANESTHESIA ON HBF HEPATIC FUNCTIONS ANESTHETIC AGENTS & HEPATIC FUNCTIONS

GROSS ANATOMY:

GROSS ANATOMY Largest internal organ largest gland Wt. :median weight of 1.8 kg in men and 1.4 kg in women. It accounts for about 2% of the total mass of healthy adults and 5% of neonates . Location : Rt. Hypochondrium In the right midaxillary line, the liver spans from the 7th to the 11th ribs. It is covered by peritoneum ( Glisson's capsule) , except for the gallbladder bed, the inferior vena cava (IVC), the bare area, and the porta hepatis .

LOBES vs SEGMENTS OF THE LIVER:

LOBES vs SEGMENTS OF THE LIVER Customary division - into 4 lobes -the right, left, caudate, and quadrate lobes is derived from the topographic anatomy , with the falciform ligament separating the right and left lobes. Functional/segmental division- Divided into 8 segments each receiving a portal pedicle. Couinaud system of division Based on distribution of blood flow via portal pedicles and location of hepatic vein.

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The functional division follows a line ( Cantlie's line) that runs from the medial margin of the gallbladder to the left side of the vena cava. The liver is separated into eight anatomic segments, each with an independent nutrient blood supply and venous and biliary drainage. Appreciation of this segmental anatomy is the basis of anatomic resection of the liver.

Biliary system :

Biliary system BILE CANALICULI RT. & LT. HEPATIC DUCT COMMON BILE DUCT COMMON HEPATIC DUCT CYSTIC DUCT DUODENUM MAIN PANCREATIC DUCT

GALL BLADDER:

GALL BLADDER Concetration and storage of bile Location : inferior surface of liver 7-10 cm long Capacity : 30-50 ml Blood supply: cystic artery Anesthetic interactions with bile formation and storage have not been reported. A ll opioids can potentially cause spasm of the sphincter of Oddi and increase biliary pressure .( fenta causes max spasm).

Vascular supply of liver:

Vascular supply of liver 25% of the cardiac output, Average blood flow between 100 and 130 mL /minute per 100 g. PORTAL VEIN 75% NUTRIENT RICH 5 0 –5 5% OXYGEN HEPATIC ARTERY 25% OXYGEN RICH 45–5 o% OXYGEN MEAN PRESSURE 40-90 mmHg MEAN PRESSURE 5-10 mmHg

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Vascular supply of liver

Venous drainage of liver:

Venous drainage of liver If thrombosis of the major hepatic veins occurs ( Budd- Chiari syndrome ), the caudate veins become the key to drainage of hepatic blood into the IVC. The caudate lobe is usually drained by its own set of veins. In portal hypertension portosystemic shunts dilated. CENTRAL VEINS INTER LOBULAR & SUBLOBULAR VEINS 3 HEPATIC VEINS IVC HEPATIC SINUSOIDS

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LYMPHATIC DRAINAGE SUPERFICIAL DEEP CAVAL HEPATIC COELIAC PARACARDIAL NODES AROUND IVC & HEPATIC NODES

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SYMPATHETIC (T6-T11) From celiac ganglia PARASYMPATHETIC (VAGUS) HEPATIC PLEXUS Stimulation causes ↑Hepatic vascular resistance ↓THBF & blood volume Glycogenolysis Glucose output Nerve supply of liver VAGAL STIMULATION DUE TO SURGERY AROUND GALL BLADDER BED. BRADYCARDIA

MICROSCOPIC ANATOMY:

MICROSCOPIC ANATOMY KIERMAN’S LOBULE Functional unit of liver 50,000–100,000 in number. Each lobule is composed of plates of hepatocytes arranged cylindrically around a centrilobular vein . Liver acinus RAPPAPORT ACINUS Parenchymal mass between 2 centrilobular veins Centre /Axis is formed by PORTAL TRIAD

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3 zones of hepatocytes based on Concentration gradients of oxygen and solutes occur along the sinusoidal spaces. I II III Central vein Portal triad ZONES ZONALITY(zonal relationship ) IN LIVER LOBULE Liver lobule

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ZONE I (PERIPORTAL) O 2 TENSION=250mmHg LEAST SUSCEPTIBLE TO ISCHEMIA ZONE I & II BOTH Chief producer of NH 3 Contain enzymes for urea cycle ↑ No. Of mitochondria ZONALITY(zonal relationship ) IN LIVER LOBULE I II III Central vein Portal triad ZONES

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ZONE III Last to receive blood hence O 2 TENSION= 70mmHg Most susceptible to ischemia Anaerobic metabolism Detoxification & Biotransformation reactions Hence with hypoxic insult to liver Biotransformation of drugs is Amongst the first to be affected . ZONALITY(zonal relationship ) IN LIVER LOBULE

HEPATIC ULTRASTRUCTURE:

HEPATIC ULTRASTRUCTURE HEPATOCYTES are arranged in plates with intervening sinusoids. PITT CELLS : highly mobile lymphocytes KUPFFER CELLS : macrophages attached to endothelium. ITO CELLS : contain fat, store vit . A .

HEPATIC ULTRASTRUCTURE:

SPACE OF DISSE : Around sinusoids. Microvilli of hepatocytes are exposed to this space. SINUSOIDS : specialized capillary system having fenestrated endothelium. ENDOTHELIAL CELLS : fenestrated and highly permeable Allow exchange of molecules b/w hepatocytes and sinusoidal blood. HEPATIC ULTRASTRUCTURE

HEPATIC BLOOD FLOW:

HEPATIC BLOOD FLOW

NORMAL HEPATIC BLOOD FLOW:

NORMAL HEPATIC BLOOD FLOW Total HBF : 1200-1700 ml/min 57.7 ml/100gm/min 25 % of CO The time it takes for red blood cells to traverse from the portal vein to the central vein is approximately 8–9 s, allowing sufficient time for contact with hepatocytes and Kupffer cells.

HEPATIC BLOOD FLOW REGULATION:

HEPATIC BLOOD FLOW REGULATION INTRINSIC FACTORS (regional microvascular ) EXTRINSIC FACTORS (neural and hormonal) VASCULAR AUTOREGULATION HEPATIC ARTERIAL BUFFER RESPONSE

HEPATIC ARTERIAL BUFFER RESPONSE (HABR) :

HEPATIC ARTERIAL BUFFER RESPONSE (HABR) Inter relationship b/w portal venous & hepatic arterial flows. Semi reciprocal relationship. Mediated by adenosine ( arteriolar dilator).

VASCULAR AUTOREGULATION:

VASCULAR AUTOREGULATION Pressure flow relationship in hepatic arterial system It is present when the liver is very active metabolically (postprandial) , but not during the fasted state. Less important mechanism during anesthesia because of fasted state.

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EXTRINSIC FACTORS ↑ HEPATIC BLOOD FLOW Feeding ( hyperosmolarity ) Glucagon β agonists Recumbent position Hepatocellular enzyme induction Acute hepatitis ? hypercapnia ↓ HEPATIC BLOOD FLOW Anesthetic agents Surgical trauma α agonists/ β blockers IPPV/PEEP Vasopressin Hepatic cirrhosis ? hypocapnia

EFFECTS OF ANESTHESIA ON HBF:

EFFECTS OF ANESTHESIA ON HBF INHALATIONAL AGENTS I.V. ANESTHETIC AGENTS VENTILATION CENTRAL NEURAXIAL BLOCKADE HYPOXIA PaCO2 TYPE OF SURGERY

INHALATIONAL AGENTS & HBF:

INHALATIONAL AGENTS & HBF HALOTHANE- max. vasoconstriction in hepatic arteriolar vascular bed, reduces hepatic O2 delivery & hepatic venous O2 saturation. Disrupts HABR. ENFURANE Same effect as halothane but with lesser intensity. ISOFLURANE/SEVOFLURANE Maintains HABR Sevoflurane is also consistently equivalent or superior to isoflurane in maintaining HABF, hepatic O 2 delivery, and O 2 delivery-to-consumption ratios. XENON does not alter HABF.It also does not alter the results of liver function tests.

EFFECTS OF ANESTHESIA ON HBF:

EFFECTS OF ANESTHESIA ON HBF I.V. ANESTHETIC AGENTS- ↓ PV blood flow Total HBF is unchanged. Propofol is the best IV induction agent as it does not disrupt HABR. VENTILATION- Spontaneous- no change IPPV- ↓↓ HBF (↓ C.O.) Positive end-expiratory pressure (PEEP) further accentuates these effects.

EFFECTS OF ANESTHESIA ON HBF:

EFFECTS OF ANESTHESIA ON HBF Central neuraxial blockade Spinal block to T5 level → 23% ↓ HBF HYPOXIA Vasoconstriction in splanchnic & hepatic vasculature ↓ HBF Effect of hypoxia depends on duration, degree & anesthetic used. ↓ MAP ↓ HBF ↓ PV BLOOD FLOW

EFFECTS OF ANESTHESIA ON HBF:

EFFECTS OF ANESTHESIA ON HBF PaCO2 HYPOCAPNIA HYPERCAPNIA VASOCONSTRICTION ↓ HBF VASODIALATION SYMPATHETIC STIMULATION ↓ HBF ↑ HBF EFFECT OF SURGERY Surgical procedures near the liver can reduce hepatic blood flow up to 60%. Probable mechanisms: sympathetic activation, local reflexes, and direct compression of vessels in the portal and hepatic circulations.

HEPATIC FUNCTIONS:

HEPATIC FUNCTIONS

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HEPATIC FUNCTIONS METABOLIC EXCRETORY SYNTHETIC STORAGE OF BLOOD Reservoir function IMMUNITY DETOXIFICATION BILIRUBIN METABOLISM ENDOCRINE BLOOD COAGULATION

METABOLIC FUNCTIONS:

METABOLIC FUNCTIONS Carbohydrate metabolism- glucose buffer function Protein metabolism deamination urea cycle interconversions between nonessential amino acids Lipid metabolism β oxidation of FA→Acetyl CoA→ketone bodies FFA esterified to form TAG. lipoprotein synthesis phospholipids & cholesterol synthesis Glycogenesis Gloconeogenesis Glycogenolysis EUGLYCEMIA SURGICAL STRESS NH3 FORMATION

SYNTHETIC FUNCTIONS:

SYNTHETIC FUNCTIONS PLASMA PROTEINS- Albumin (10-15g/day) Globulins except Ig . CLOTTING FACTORS- all coagulation factors except factor III,IV & VIII. ANTITHROMBIN III, PROTEIN C & S ENZYMES -ALP,SGOT,SGPT PSEUDOCHOLINESTERASE CHOLESTEROL, LIPOPROTEINS ,PHOSPHOLIPIDS ACUTE PHASE REACTANTS

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Albumin Thyroxine -binding globulin α 1 -Antiprotease Transthyretin (thyroid-binding prealbumin ) α -Fetoprotein Transferrin α 2 -Macroglobulin Apolipoprotein B Antithrombin -III Angiotensinogen Ceruloplasmin Proteins, coagulation factors II, VII, IX, X Fibrinogen Antithrombin C, protein C Haptoglobin Insulin like growth factor I Hemopexin Steroid hormone-binding globulin C-reactive protein Proteins Synthesized by the liver

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CLOTTING FACTORS- Rapid turn over(factor VII has shortest half life : 2-6 hr) Hence, best measure of acute hepatic dysfunction. Prothrombin time is the best test The PT, which is normally 11–14 s , measures the activity of fibrinogen, prothrombin, and factors V, VII, and X. ALBUMIN- Slow turn over ( half life : 18-20 days) Hypoalbuminemia is more common in chronic liver disorders such as cirrhosis and usually reflects severe liver damage.

BILE SYNTHESIS:

BILE SYNTHESIS BILE EXCRETION- 600-1200 ml/day CHOLESTEROL BILE ACIDS BILE SALTS ACTIVATION OF LIPASE EMULSIFICATION OF FAT

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BILIRUBIN BILIVERDIN BILIRUBIN GLUCURONIDE EXCRETED IN BILE BILIRUBIN METABOLISM Senescent RBCs Hb Heme Non erythrocytic hemoproteins 75 % 25 % Heme oxygenase Biliverdin reductase UDP Glucoronyl tarnsferase

DETOXIFICATION:

DETOXIFICATION LIPOPHYLIC XENOBIOTICS HYDROPHYLIC METABOLITES DETOXIFICATION PHASE I REACTIONS PHASE II REACTIONS Oxidation, Reduction, Hydrolysis N - Acetylation Mediated by Cyt . P450 Conjugation Reaction Addition of Glucuronic acid,Glycine Sulphate,Methyl gp . INHALATIONAL AGENTS (HALOTHANE ESPECIALLY) COMPETITIVELY INHIBIT CYT P450 & PHASE I REACTION Ethanol, barbiturates, ketamine, and perhaps benzodiazepines (eg, diazepam) are capable of enzyme induction ,

DETOXIFICATION:

DETOXIFICATION Phase III reactions involve specific molecular transporters—known as ATP-binding cassette (ABC) transport proteins. facilitate the excretion of xenobiotics and endogenous compounds. These proteins use ATP hydrolysis to drive molecular transport. Examples: cystic fibrosis transmembrane conductance regulator (CFTR), canalicular copper transporters, and multidrug resistance protein (MDR). MDR-1 (formerly called P-glycoprotein) resides on the canalicular surfaces of hepatocytes and enables biliary excretion of cationic compounds, including anticancer drugs. Dysfunction of ABC transport proteins can disrupt the flow of bile, impair excretion of xenobiotics and endogenous compounds, and induce cholestatic liver injury.

HEPATIC DRUG CLEARANCE:

HEPATIC DRUG CLEARANCE GOVERNED BY- Rate of HBF. Plasma protein binding of drug Hepatic intrinsic clearance. CLEARANCE : Volume of blood from which the drug is completely removed per unit TIME . CLEARANCE = HBF X EXTRACTION RATIO ( Cl ) (Q) (E)

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ER provides a measure of the relative efficiency with which the liver extracts or eliminates a given drug. Amount of drug removed from blood during a single liver transit, expressed as a fraction of 1. CLEARANCE = HBF X EXTRACTION RATIO ( Cl ) (Q) (E)

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HIGH EXTRACTION RATIO LOW EXTRACTION RATIO Propofol Thiopentone Fentanyl , Morphine, Meperidine Diazepam Lignocaine Digitoxin Verapamil Phenytoin Labetalol pancuronium Propanolol Clearance of drugs with high hepatic extraction ratio is more markedly affected by changes in HBF .

Ammonia Metabolism & Excretion:

Ammonia Metabolism & Excretion Ammonia is toxic to the central nervous system (CNS), and freely permeable across the blood–brain barrier HEPATIC ENCEPHALOPATHY

ANESTHETIC AGENTS & LIVER FUNCTIONS:

ANESTHETIC AGENTS & LIVER FUNCTIONS

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BENZODIAZEPINES- Since diazepam & midazolam is metabolized by phase I reaction, hence recovery & elimination times ↑ in Cirrhotics . OXAZEPAM & LORAZEPAM are safe in mild to moderate liver impairment. IV INDUCTION AGENTS- IV agents Change in pharmacokinetics in cirrhotics Thiopentone No change Propofol Prolonged recovery on infusion Etomidate Prolonged elimination

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MUSCLE RLAXANTS - MUSCLE RLAXANTS Action in liver diseases SCh Prolonged Mivacurium Prolonged with infusion Pancuronium / Rocuronium Prolonged Vecuronium Slight ly prolonged Atracurium / Cisatracurium Unchanged(safe)

opioids:

opioids Morphine - prolonged elimination half-life, markedly increased bioavailability of orally administered morphine, decreased plasma protein binding, and potentially exaggerated sedative and respiratory-depressant effects. Mepridine - 50% decrease in clearance and doubling of half life. Fentanyl , sufentanyl , alfentanyl - highly lipid soluble, short acting (because of rapid redistribution to storage sites), almost exclusively metabolized in liver, hence 1 st dose doesn’t affect much but repeated top ups and continuous infusion may build up increase levels in tissues, decrease in elimination and prolonged effect. Remifentanyl - Remifentanyl has an ester linkage that allows for rapid hydrolysis by blood and tissue esterases ; such hydrolysis leads to high clearance, rapid elimination, and recovery.

VOLATILE ANESTHETICS :

VOLATILE ANESTHETICS HALOTHANE- DIRECT EFFECT ↓ HBF IMMUNE MEDIATED INJURY HALOTHANE ASSOCIATED HEPATITIS Ab to TFH MILD, SELF LIMITING HEPATOTOXICITY MASSIVE HEPATIC NECROSIS

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ENFLURANE Cross sensitivity with Halothane. Can cause post operative jaundice in patients previously exposed to Halothane.

Suggested reading:

Suggested reading Miller’s Anesthesia 7 th edition Barasch’s clinical anesthesia 5 th edition Morgan’s Anesthesiology 4 th edition www.medcape.com www.wikipedia.org Campra JL, Reynolds TB: The hepatic circulation .   In: Arias IM, Jakoby WB, Popper H, et al ed. The Liver: Biology and Pathobiology ,  New York: Raven Press; 1988:911. Lautt WW: Mechanism and role of intrinsic regulation of hepatic arterial blood flow: Hepatic arterial buffer response. Am J Physiol 1985; 249:G549.

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