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Speaker: Dr.M.Kiran KUMAR(P.G.) Moderator and Chair Person: Dr.M. Chandrashekar ( PROFF. & HOD)
3. Left ventricular hypertrophy: causative factors include anaemia, HTN, recurrent volume over load & uraemia Anaesthetic implication : systolic & diastolic dysfunction which contributes to hypotension during fluid removal on haemodialysis 4. Conduction blocks: are frequent due to deposition of calcium in the conducting system Anaesthetic implication : arrhythmias may be precipitated as a result of metabolic abnormalities
5. Pericarditis: due to uraemia Anaesthetic implication : associated with myocardial depression and usually resolves with intensive dialysis FLUID ELECTROLYTE AND ACID-BASE ABNORMALITIES 1. Sodium and water retention : occurs as gfr falls below <10-15ml/min Anaesthetic implication : peripheral and not uncommonly pulmonary edema & HTN
2. Hyperkalemia Anaesthetic implication : can be aggravated by surgical trauma, succinyl choline, hypercarbia, acidosis and hyperglycaemia. It is most important indicator for dialysis 3. Metabolic acidosis: is due to decreased excretion of endogenous acids into the urine Anaesthetic implication :acidosis results in hyperkalemia and HCO3
Haematological abnormalities: Anaemia: synthesis of erythropoietin RBC survival uraemic induced bone marrow depression folate deficiency ,aluminium toxicity Anaesthetic implications:O2 carrying capacity decreased leading to in CO and shifting of O2 dissociation curve to right.
Coagulopathy: Abnormal haemostasis and prolongation of BT due to defect in platelet adhesiveness & activity of platelet factor III and unimpaired prothrombin consumption. Anaesthetic implications: it can be corrected by dialysis .Bleeding from surgical wounds and spontaneous bleeding into GIT, pericardial sac or intracranial vault are of great concern. it also poses a significant risk during insertion of regional blocks.
Impaired leukocyte function: enhanced susceptibility to infection. Anaesthetic implication: need for strict asepsis for all procedures includes IV line infection.
Nervous system
Asterixis, tremor, myoclonus and unusual combination of depressed cerebral function with seizure threshold are all features of severe uraemia. Reversible autonomic dysfunction Sensory involvement in the lower &distal extremities Carpal tunnel syndrome due to Beta-2 microglobin is common
Anaesthetic implication: peripheral neuropathy should be documented before institution of regional nerve blocks and care should be taken.
GIT complications
gastric emptying and reflex oesophagitis . Anaesthetic implication: need for acid aspiration prophylaxis and rapid sequence induction. GLUCOSE CONTROL:is difficult to achieve in diabetics with CRF since there is excretion of glucose by the kidneys as well as the concomitant use of steroids this may lead to hyperglycemia with K+ levels and risk of infection. .
Anaesthetic implication: insulin therapy needs careful management conventional regimes may be inappropriate as a fluid load of 100ml/hr of Dextrose may not be tolerated and addicted and addicted K+ supplementation is also inappropriate. Also such patients have a very high incidence of associated cardiac disease
Albumin levels: are due haemodilution impaired synthesis and loss through diseased nephrons Anaesthetic implication: this leads to altered drug binding with a concomitant change in the potency of the drugs as well as predisposes the patients to pulmonary oedema with accumulation of fluid in the interstitial space.
Bone diseases
Renal osteodystropy & osteomalacia: Hypocalcaemia, Hyperphosphotemia and renal synthesis of 1,25 dihydroxy cholecalciferol leads to 2 hyperparathyroidism which manifests as bone resorption and demineralisation. Anaesthetic implications: care needs to be taken during the positioning of the patients also the action of non-depolarising muscle relaxants may be prolonged in the presence of hypo calcemia.
In view of the above mentioned medical problems and it is essential to optimise the patients condition before taken up for surgery
Anaesthetic management: Principles: o Management of assoc. Medical problems and their anaesthetic implications o Judicious perk operative fluid management o Effect of renal function compromise and drug choice and usage 1.altered protein binding as a result of hypoproteinemia 2.psuedocholinesterase levels 3.electrolyte imbalance and potentiation of toxicity 4.prolongation of NM block with dyselectrolytemia
Specific anaesthetic agents(pharmacokinetics and dynamics in ESRD): 1.TPS : protein bindingfree fraction of the drugs so induction dose should be reduced. 2.Propofol:pharmacokinetics unchanged in CRF. So induction dose remains unchanged and infusion is safe. 3.Ketamine: not much change in pharmacokinetics because of minimal protein binding and <3% of the drug is excreted unchanged by the kidney. 4. Etomidate: larger free fraction is seen only in ESRD as 75%protien bound. 5.Benzodiazepines: extensive protein binding and free fraction in plasma active metabolites may accumulate with more frequent administration
OPIOIDS:
i. Morphine: it is metabolised to morphine -6 -glucuronide in liver, which is a potent analgesic and resp. Depressant. This is excreted by the kidney and can contribute to enhanced effect in renal patients. There fore initial dose and the repeated doses. ii. Pethidine: major metabolite is nor-pethidine and is excreted by via the kidney. It as analgesic and resp. Depressant properties but is not as potent as morphine 6 glucuronide. iii.Fentanyl: it is considered as the pre operative analgesia of choice because of it shorter half life and clearance is not changed much in renal failure its metabolites are also inactive. iv. Alfentanyl: it as a similar pharmacokinetic profileto fentanyl, but as a short half life, there fore can be given as infusion pump. v. Remifentanyl: it undergoes rapid inactivation(elimination half life 5min.)by non specific plasma esterase in the blood independently of renal function. vi.Buprenorphine:mainly metabolised in the liver, as inactive metabolites and does not accumulate in renal failure
acidosis,hypokelamia,hypocalcemia,hypermagnecimia,aminoglycosides and mannitol.Therefore it is important to give the minimum dosage that is required and to use neuromuscular monitoring. a. Succinyl Choline:pseudocholiesterase levels they prolongation of the action, also pre-existing hyperkalemia may be may be aggravated by associated K+ levels. b. Pancuronium: 60% renal excretion, avoided because of their delayed & inappropriate action. c. Rocuronium:Vd & renal clearance. d. Atracurium & cis-atracurium: undergo spontaneous Hoffmann elimination in the blood and are totally independent of renal function for their clearance.Laudonosine,a metabolite of Atracurium and cis-atracurium ,which is known to be cerebral stimulant, is excreted in part through the kidney but is clinically not significant. e. Vecuronium: has 30-40% renal function and produces active metabolite,3 des acetyl vecuronium which is dependent in renal elimination and has 40% NM blocking activity. so, infusions must be avoided.
Neostigmine: renal excretion accounts for 50% of the clearance and thus elimination t1/2 is increased. Inhalational agents: Halothane anaesthesia as been administered to patients of all degrees of renal impairments with complete safety. Isoflurane and desflurane produce negligible levels of inorganic fluoride and are preferred in pts. With renal compromise. Sevoflurane is better avoided, as it produces compound A with use in closed flow systems which may be a contributing factor for nephro toxicity.
Maintenance
Patient may be maintained on either inhalational or short acting opioids such as Fentanyl, alfentanyl along with N2O and suitable MR like Atracurium or cis-atracurium. Titrate the dose of MR with NM monitoring Isoflurane and desflurane are the preferred inhalational agents. Maintain normothermia, normocarbia and normotension. Intra OP volume status should be closely monitored as it is directly related to graft function. Prior to graft insertion target CVP of 10-15cm of H2O has to be maintained Mannitol 0.5-1 gr/kg and furosemide 60-200mg to establish brisk diuresis decreases the incidence of acute tubular necrosis and early anuria. There is no role of renal dose of dopamine during the peri operative period.
monitoring
1. 2. 3. 4. 5. 6. 7. 8. Sp02 NIBP ETCO2 Temperature ECG NM monitoring CVP IBP monitoring may be useful in pts with significant cardiovascular/lung disease/poorly controlled HTN. 9. Pulmonary artery pressure may be indicated in pts with severe cad, LV dysfunction, valvular abnormalities/known pulmonary arterial hypertension
Reversal All renal transplant patients need to be fully reversed and extubated. Reversal is done with Neostigmine and ant cholinergic agent Half-life of Neostigmine is prolonged in pts with ESRD. Post op care: After reversal & extubation pts need to be shifted to post transplant isolated room. Standard monitoring equipment and very close monitoring of fluid balance along with Sr. Electrolytes and serum creatinine is ensured. Any significant decline in urine output should raise suspicion of mechanical obstruction to blood vessels of ureter. Immediate ultrasound Doppler for confirmation and re exploration is warranted.