Optimization & perioperative management for patient with renal disease - Venkatesh

8/7/2019 Optimization & perioperative management for patient with renal disease - Venkatesh

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PRESENTATION BY- DR.VENKATESH .MODERATOR - DR.JUI.


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AIMS & OBJECTIVES OF PERIOPERATIVE

MANAGEMENT OF PATIENTS WITH RENAL

DYSFUNCTION.

Proper assessment of the renal status of thepatient & its management.

AKI/CRI/ESRD/Acute on CRI Assessment & management of the multiple

comorbidity .

Prevent AKI in perioperative period.

To formulate an individualized & safe anestheticplan.


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CARDIOVASCULAR SYSTEM CONSIDERATIONS.

Systemic hypertensionSystemic hypertension most common; multipleantihypertensives(3/more); cause/effect; intractable.

Contributes to CHF,CAD,cerebrovascular disease.

Speeds up progressive GFR.Accelerated atherosclerosis,PVD,fluid overload.

Uremic pericarditis/effusion/tamponade.

Causes Na+ & H20 retention; RAA axis activation.

Arrhythmia,conduction blocks dyselectrolytemia.


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Respiratory systemRespiratory system acid base imbalance; pleuraleffusion,pulmonaryedema,pneumonia,pleuritis,interstitial & alveolaredema,muscle wasting.

CNSCNS -- cognitive function, encephalopathy, peripheral

uremic neuropathy, autonomic dysfunction,myoclonuslethargy/confusion,seizures.


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GIGI Uremia induced delayed gastric emptying,adynamicileus,frequent nausea/vomiting,hiccoughs,upper GI

bleed,ascites. EndocrineEndocrine 2 hyperparathyroidism,glucose

intolerance,hypertriglyceridemia.

M

usculoskeletalM

usculoskeletal

muscle wasting & weakness,renalosteodystrophy,periarticular calcification,pathological #.


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HEMATOLOGYHEMATOLOGY --

AnemiaAnemia - erythropoietin,uremicbleeding(GI/epistaxis), RBC survival(frequentdialysis;circulating toxins),bone marrow replacement byfibrous tissue (2 hyperparathyroidism).

Unresponsive to oral iron therapy. Uremic bleedingUremic bleeding - bleeding tendency in presence of

normal laboratory coagulation study & PC (bleedingtime best correlation).

Impaired chemotaxis ,margination & phagocytosis - immunity.

SKINSKIN -- pruritis(cutaneous Ca++

deposition),ecchymosis,hyperpigmentation.


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METABOLIC CONSIDERATIONSMETABOLIC CONSIDERATIONS --

Acid base disturbances High AGMA(failure toexcrete non volatile acids).

Hyperkalemia .

Hypokalemia (net K deficit,dialysis,G

I losses,diuretics). Hyponatremia.

Hypomagnesaemia.

Hyperphosphatemia.

Hypocalcaemia.

Hyperuricemia.

Hypoalbuminaemia.

Aluminium toxicity.


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IMMUNE SYSTEMIMMUNE SYSTEM considered immunocompromised.

Prone for iatrogenic infection.

Uremia causing leucocyte dysfunction.

Dialysis,multiple transfusions HBV,HCV,HIV

infections common.

TB easily missed d/t similar symptoms.


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PREANESTHESIAPREANESTHESIA EVALUATION.EVALUATION.

HISTORYHISTORY

Coexisting comorbidity duration & severity.

Duration,severity & treatment of renal impairment.

Uremic symtoms. Daily fluid intake & urine output.

Effort tolerance.

Active infection.

Previous anesthesia exposure residualcurarisation,drug allergy.

Medications.

Timing & details of last dialysis.


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PHYSICAL EXAMINATIONPHYSICAL EXAMINATION

Pre & post dialysis weight.

Hydration status,edema.

Site & condition of dialysis access. Venous access.

Fever.

Vitals HTN,orthostatic hypotension. Routine physical examination.


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INVESTIGATIONSINVESTIGATIONS Hgb/Hct. TC/DC/PC/BT. Blood sugars.

Urine R/M

; C/S. Coagulation profile. RFT. LFT. SE. ECG/ECHO. CXR. ABG. Screening for HBV,HCV,HIV.


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PREANESTHESIAPREANESTHESIA ADVICE.ADVICE.

Adequate NPO. Antacids & prokinetics.

Dialysis within 24 hours prior Sx.

Post dialysis investigations.

Continuation/stoppage of medications.

Avoidance of sedatives.

Blood/blood products.

High risk consent with standby ICU bed.


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MONITORING.MONITORING.

Basic minimum monitors. NIBP cuff not over an AVF.

ABP,CVP & PAP if large fluid shifts suspected.

Accurate blood loss measurement.

UOP monitoring,ABG & GRBS.

Minimum FiO2 = 0.4

Maintainance of strict fluid balance & UOP ~ 0.5mL/hr.

Patient positioning w.r.t. AVF & frail patients succeptible for# & frequent post operative neuropathy.

IV access difficult,presence of AVF,hemodialysis access.


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?

Regional v/s General anesthesia.?

Regional v/s General anesthesia. Efficacy of local anaesthetic is reduced in acidosis

High incidence of haematoma due altered coagulationprofile.

No comparitive study demonstrating superior renalprotection or improved outcome with GA v/s RA.

Advantage ofAdvantage of neuraxialneuraxial blockadeblockade

sympathetic blockade of T4 T10 segments

suppression of sympathoadrenal stress response &release of catecholamines, renin & AVP.

RBF and GFR are preserved as long as adequate renalperfusion pressure is maintained.


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PHARMACOLOGICAL CONSIDERATIONS INPHARMACOLOGICAL CONSIDERATIONS IN

PERIOPERATIVEPERIOPERATIVE PERIOD.PERIOD.

1. Preservation of RBF and perfusion pressure.2. Avoidance of excessive vasoconstriction.3. Avoidance of nephrotoxic drugs &4. Adjustment of the drug dosages(VD & protein

binding).

Drug depending solely on renal clearance calculated % in drug dosage matching in GFR(creatinine clearanceadjusted dose).

Drugs with less binding (Eg.Phenytoin) normal serumlevels = dangerously high levels of active(unbound)fraction.


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ANESTHETIC AGENTS IN RENAL DISEASE.ANESTHETIC AGENTS IN RENAL DISEASE.

1.1. DIRECT EFFECTSDIRECT EFFECTS Most of agents used in GA notnephrotoxic.

Exception methoxyfluranemethoxyflurane & enfluraneenflurane ( fluoridefluoridehypothesishypothesis).

High output renal insufficiency,unresponsive tovasopressin(Sevoflurane not associated with renalconcentrating defects).

Presents as dilute polyuria,dehydration,hyperosmolarity

& elevated BUN/Sr.Creatinine.

2.2. INDIRECT EFFECTSINDIRECT EFFECTS -- renalvasoconstriction,hypotension,peripheral

vasodilation,low COP.


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Site of metabolism

intrarenal >>extrarenal/hepatic.

Sevoflurane compound A dose dependentnephrotoxin in rats ;Human studies no renalinjury with/without renalimpairment with FGF < 1L.


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ANESTHETIC AGENTS IN RENAL DISEASE.ANESTHETIC AGENTS IN RENAL DISEASE. INDUCTION AGENTS & SEDATIVESINDUCTION AGENTS & SEDATIVES.

1.1. ThiopentoneThiopentone - Free fraction of induction dose almostdoubled in renal failure exaggerated effects substantialreduction in induction dose in uremic patients.

2.2. KetamineKetamine less extensively protein bound thanthiopentone,renal failure minimal influence on freefraction.

Redistribution & hepatic metabolism termination of

action.


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ANESTHETIC AGENTS IN RENAL DISEASEANESTHETIC AGENTS IN RENAL DISEASE..

INDUCTION AGENTS & SEDATIVESINDUCTION AGENTS & SEDATIVES.3.3. PropofolPropofol extensive & rapid hepatic biotransformation

inactive metabolites renal excretion.

Pharmacokinetics unchanged in renal failure,noreports of prolongation of effects in ESRD.

4.4. EtomidateEtomidate 75% protein bound larger free fraction in

ESRD patients - protein binding no alteration ofclinical effects of etomidate induction.


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INDUCTION AGENTS & SEDATIVESINDUCTION AGENTS & SEDATIVES.

5.5. BZDsBZDs extensively protein bound CKD free fraction potentiation of clinical effects.

60 80% of midazolam excreted as its hydroxy

metabolite accumulates in renal failure especially inlong term infusions.

Diazepam & lorazepam also carry a risk of activemetabolite induced sedation on repeated doses.

Alprazolam - protein binding & free fraction CKDpatients more sensitive to sedative effects comparedwith healthy volunteers.


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OPIOIDSOPIOIDS 1.1. MorphineMorphine single dose studies no alteration in

disposition.

y Repeated doses accumulation of6-glucuronidemetabolite potent analgesic,sedative & respiratorydepressant.

y protein binding in ESRD reduction in initial

dosage.

2.2. PethidinePethidine neurotoxic metabolite(normeperidine) irritability,twitching & seizures - not recommended in

patients with poor renal function.


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OPIOIDSOPIOIDS 3.3. HyromorphoneHyromorphone active metabolite(hydromorphone

3 glucuronide) excreted by kidneys accumulation cognitive dysfunction & myoclonus.

4.4. CodeineCodeine potential for prolonged narcosis notrecommended for long term use.

5.5. AlfentanilAlfentanil - protein binding but unchanged

elimination t1/2 & clearance in ESRD;extensivelymetabolized to inactive compounds caution inloading dose but total dose & infusion ratesunchanged.


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OPIOIDSOPIOIDS 4.4. FentanylFentanyl lack of active metabolites,unchanged free

fraction & short redistribution phase opioidopioid ofofchoicechoice.

y Small to moderate doses,titrated to effect welltolerated by uremic patients.

5.5. SufentanilSufentanil free fraction unchanged but variable

pharmacokinetics reported to cause prolongednarcosis in ESRD.


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OPIOIDSOPIOIDS 5.5. RemifentanilRemifentanil rapid metabolism by tissue/blood

esterases weakly active(


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NEUROMUSCULAR BLOCKING AGENTSNEUROMUSCULAR BLOCKING AGENTS --

Most likely group of anesthetic drugs to produceprolonged effects in ESRD.

Sch,atracurium,cis-atracurium & mivacurium minimalrenal excretion of unchanged parent compound.

Coexisting acidosis,electrolyte disturbance & drugtherapy(aminoglycosides,diuretics,immunosuppressants& Mg++ containing antacids) alter pharmacodynamics inpatients with renal disease.


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DRUG % RENALEXCRETION

T1/2 (Hr)Normal/ESRD

Renallyexcreted activemetabolite

Use in ESRD.

d-TC 60 1.4/2.2 - Avoid

Metocurine 45 60 6/11.4 - Avoid

Pancuronium 30 2.3/4-8 + Avoid

Gallamine >85 2.5/6-20 - Avoid

Pipecuronium 37 1.8-2.3/4.4 + Avoid

Doxacurium 30 1.7/3.7 - Avoid

Vecuronium 30 0.9/1.4 + Avoid infusion

Rocuronium 30 1.2-1.6/1.6-1.7 - Variableinfusion

Atracurium &cis-atracurium


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1.1. SchSch Duration of action not significantly prolonged inESRD use justified for RSI provided serum K+ is not

.y Serum K+ to be normalized to extent possible prior Sch

administration.

y Continuous infusion problematic d/t majormetabolite(succinyl monocholine) weakly active &excreted by kidneys.

y Acute,small(~0.5mEq/L) elevations in serum K+ - well

tolerated by chronically hyperkalemic CKD subjects.


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2.2. Long actingLong acting doxacurium,pancuroniumdoxacurium,pancuronium &&pipecuroniumpipecuronium elimination t1/2, plasma clearance

& prolonged duration of action - avoided in ESRD.3.3. AtracuriumAtracurium potential concern of accumulation of

neurotoxic metabolite laudanosine causing seizures inexperimental animals with repeated

dosing/continuous infusion.

4.4. CisCis--atracuriumatracurium greater potency,lower doserequirements lower laudanosine blood

levels(theoretical advantage).


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5.5. VecuroniumVecuronium duration slightly prolonged in renalfailure d/t clearance & elimination t1/2.

y Intubating dose expected to last ~50% longer in ESRD.y Potential for accumulation of 3-desmethyl

vecuronium(active metabolite) in anephric patients oncontinuous infusion prolonged NM blockade.


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6.6. RocuroniumRocuronium similar effects as vecuronium.

7.7. MivacuriumMivacurium slower recovery from bolus dose in

anephric patients d/t low pseudocholinesteraseactivity.

Pharmacokinetics of anticholinesterases affected by

renal failure prolonged duration of action d/t heavyreliance on renal excretion.

Similar effects on excretion ofanticholinergics(atropine/glycopyrrolate) no dosageno dosage

alteration required in reversing patients with CRIalteration required in reversing patients with CRI.


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EFFECTS OF VARIOUS ANESTHETICS ON RENALEFFECTS OF VARIOUS ANESTHETICS ON RENAL

FUNCTION.FUNCTION.


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RISK FACTORS FORRISK FACTORS FOR PERIOPERATIVEPERIOPERATIVE AKIAKI..


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TREATMENT ALGORITHM FOR ACUTE

PERIOPERATIVE OLIGURIA.


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Occurrence of perioperative renal failure depends on

1. The surgery.2. Preoperative and intraoperative haemodynamics.

3. Preoperative renal condition(DM - 10 fold greater riskof renal deterioration in the presence of hypovolemia).

All intravenous and volatile induction agents COP& BP.

High level of neuraxial block upto T4 sympathetictone to the kidneys RBF & GFR.

Mechanical ventilation with positive pressure also RBF.Major surgery extensive third space losses hypovolemia & renal hypoperfusion.


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PATHOGENESIS OFPATHOGENESIS OF PERIOPERATIVEPERIOPERATIVE AKIAKI..


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RENAL PROTECTION INRENAL PROTECTION IN PERIOPERATIVEPERIOPERATIVE PERIOD.PERIOD.

1.1. FLUIDSFLUIDS --

Maintenance of RBF & GFR by adequate hydration prevent further renal injury & preserve renal function.

Hydration effective in prevention of contrast-inducednephropathy & probably the best strategy to preventprogression to frank renal failure.


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2.2. DOPAMINEDOPAMINE RCTs & meta-analyses no prophylactic/therapeutic

effect of dopamine on AKI.

BP/HR improved perfusion pressures UOP

explains the possible benefits of dopamine inpreventing AKI.

3.3. ACETYL CYSTEINEACETYL CYSTEINE

Free radical O2 scavenger ; modulates NO synthesis after

oxidative cell stress. Efficacious in prevention of contrast-induced

nephropathy when given early before the insult.


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4.4. BICARBONATEBICARBONATE

Alkalinization of urine solubility of myoglobin prevents formation of tubular precipitates effective in

Rx of pigmentpigment--induced nephropathyinduced nephropathy(rhabdomyolysis). formation ofnephrotoxic free

radicals(preferentially formed in acidoticenvironments).

formation of free radicals in contrastcontrast--inducedinducednephropathynephropathy as well I/O CIN from 13.7% to 1.7%.


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RENAL PROTECTION INRENAL PROTECTION IN PERIOPERATIVEPERIOPERATIVE PERIOD.PERIOD.5.5. LOOP DIURETICS/MANNITOLLOOP DIURETICS/MANNITOL

Rationale - to flush out casts of necrotic cells that mayobstruct renal tubules.

Loop diuretics also RBF through prostaglandin synthesisandmetabolic workload of the tubules by active sodiumreabsorption.

Diuretics hypovolemia & further exacerbate renal

hypoperfusion imperative to ensure normovolemia beforetheir use.


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Optimization & perioperative management for patient with renal disease - Venkatesh