Anesthesia considerations (airway, drugs, fluid, acid-base disorder, electrolyte, dialysis ) and management in CKD

1. ANESTHESIA MANAGEMENT IN
CKD

2. HISTORY
37 yrs old
Secheduled for Angiorhapphy on 19/2/19
He was diagnosed with stage V CKD for 15 years due to HTN
Since then he was on HD
HD frequency – 2 times/week
Last HD- 18/2/19

3. • Medical history- DCM with severe MR and TR
• Drug history- Tab Digoxin, Losartan, lasix, Shelcal, Vit C, FeFa
• Past Surgical history- Kidney Transplant in 2008 under GA
• Past anesthesia history- no complication
• Youngest of the family( monk)

4. HISTORY CONT…
• O/E
• Well built
• Visible carotid pulsation
• Apex at 5th ICS
• Pansystolic murmur heard all precordium
• Abdomen was soft
• Airway examination – Not significant
• Mallampati grade- I

5. HISTORY CONT….
• Investigations:
• 11/2/18(11pm)
• WBC- 5.93
• Hb- 6.8, Hct-22.8
• Plt- 172
• Urea- 120
• Creatinine- 15.4
• K- 5.6

6. HISTORY CONT….
• 2D echo:
• LVEF- 58%
• Moderate MR , AR and TR
• All dilated cardiac chamber
• Moderate PHTN
• ECG

7. CHRONIC KIDNEY DISEASE
• Definition: Kidney damage for >3 months, as defined
by structural/functional abnormalities of the kidney,
with or without decreased GFR, manifest by either:
• 1) pathological abnormalities, or
• 2) markers of kidney damage, including abnormalities
in the composition of blood or urine, or in imaging
tests GFR<60ml/min/1.73m2 for > 3months,with or
without kidney damage

8. STAGES OF CKD
• Stage 1: GFR >= 90 mL/min/1.73 m2
• Normal or elevated GFR
• Stage 2: GFR 60-89 (mild)
• Stage 3: GFR 30-59 (moderate)
• Stage 4: GFR 15-29 (severe; )
• Stage 5: GFR < 15 (ESRD)
• Am J Kidney Dis 2002; 39 (S2): S1-
246

9. GLOMERULOPATHIES
Primary glomerular disease
Focal glomerulosclerosis
Membranoproliferative
glomerulonephritis Membranous
nephropathy
Immunoglobulin A nephropathy
Diabetes mellitus
Amyloidosis
Post-infective glomerulonephritis
systemic lupus erythematosus
Wegener granulomatosis
Tubulointerstitial diseases
Analgesic nephropathy
Reflux nephropathy with
pyelonephritis
Myeloma kidney
Sarcoidosis
TUBULOINTERSTITIAL DISEASES
CAUESES OF CKD

10. HEREDITARY DISEASES
• Polycystic kidney disease
• Alport syndrome
• Medullary cystic disease
• Systemic hypertension
•
Renal vascular disease
•
Obstructive uropathy
•
Human immunodeficiency virus
infection
OTHERS
CAUSES OF CKD

11. COMPLICATIONS OF CKD
1.Uremic syndrome- reflects inability of kidney to perform its
function
2.Renal osteodystrophy
3.Normochromic and normocytic Anemia – decrease
erythropoietin production
4.Uremic bleeding-despite normal Plt count, PT and APPT
5.Neurologic changes- insomnia, irritability, seizure, coma
6.CVS- HTN, CCF, CAD, silent MI, dyslipidemias

12. HEMATOLOGIC
• Normocytic normochromic
• Anemia – nearly always present when creatinine clearance is <30
mL/min
• Usually Hb 6-8 g/dL due:
• Decrease erythropoietin production
• Decrease red cell production
• Decrease red cell survival
• GI bleed
• Hemodilution
• Bone marrow suppression recurrent infection
• Blood loss for lab testing

13. • Increase level of 2,3-DPG- in response to decrease O2 carrying
capacity
• Metabolic acid also favors rightward shift
• Both Plt and WBC functions are impaired – prolong BT and recurrent
infection
• Decrease factor 3 activity
• Decrease Plt adhesive and aggregation
• Recently undergone HD – residual effect from heparin

14. CVS
• CO increases to maintain O2 delivery( decrease blood O2 carrying
capacity)
• Systemic arterial HTN – Na retention and abnormal RAS system
• LVH
CCF and PE – ECF overload(Na), increase cardiac demand( anemia,
HTN), increase permeability of alveolar capillary membrane
• Arrhythmias – conduction blocks ( metabolic abnormalities, deposition of
Ca)
• Uremic pericarditis
• Accelerated PVD and coronary atherosclerosis
• Hypovolemia – 2ry to excessive removal during dialysis

15. PULMONARY
• Increase MV – as compensation for metabolic acidosis
• Hypoxemia(widening alveolar to arterial O2 gradient) –
PE, interstitial oedema
• PE

16. ENDOCRINE
• DM due to peripheral insulin resistance( DM is the
common cause of CKD)
• Insulin metabolism is decreased in patient with renal
failure – high risk of developing hypoglycemia
• Hyperparathyroidism- metabolic bone disease
• Hypertriglyceridemia- abnormal lipid
metabolism(artherosclerosis)

17. GI
• Uremic symptoms - Anorexia, nausea, vomiting, ileus
• GI hemorrhage (10 – 30%)– hypersecretion of gastric content
• Delayed GI emptying – autonomic neuropathy
• Increase of Hep B and C- repeated blood transfusion

18. NEUROLOGICAL
• Uremic encephalopathy:
• Asterixis
• Lethargy
• Confusion
• seizure
• Coma
• Autonomic and periphery neuropathy
• Periphery neuropathy are typically sensory and involves distal lower
extremities

19. • 7) Metabolic:
• hyperkalemia, hyperphosphatemia, hypomagnesemia, hyperuricemia,
hypocalcemia, hypoalbuminemia
• Water and Na retention – hyponatremia and ECF overload
• Increase anion gap metabolic acidosis- failure to excrete nonvolatile
acid products
• hypokalemia usually occurs when creatinine clearance is < 5 mL/min
• Hypermagnesemia is usually mild unless increase intake
• Hypocalcemia – 2ry to resistance to parathyroid home, intestinal
calcium absorption(synthesis of 1,25-dihydrocholecalciferol),
hyperphosphatemia-associated calcium deposition into bone
• Hypoalbuminemia- CKD pt rapidly lose tissue protein , anorexia, protein
restriction, dialysis

20. TREATMENT
• Underlying causes:
1.BP-
• Target : with proteinuria - 130/80mmHg
• Without protienuria- 140/90 mmHg
• Multimodal drugs – ACEI/ARBS(first line with
proteinuria), diuretics, Ca channel blockers,
aldosterone antagonist

21. TREATMENT
• 2. Nutrition:
• Modest protein restriction
• Overly restriction – risk of malnutrition and its
complication
• Daily protein intake - 0.6 g/Kg
• Phosphate 600-800 mg/kg
• Vitamin D supplementation
• Na restriction < 1.5 -2 g/day
• Hb1Ac- <7%

22. TREATMENT
• 3. Anemia
• Erythropoietin in all stages
• Avoid transfusion to prevent sensitization
human leukocyte antigen (HLA) complexes –
future transplant
• Intermittent parenteral iron- maximizes
erythropoietin response
• Target Hb- 10 – 11.5 g/dL

23. MANAGEMENT OF ANESTHESIA
• Preoperative evaluation
• Induction of anesthesia
• Maintenance of anesthesia
• Postoperative management

24. PREOPERATIVE EVALUATION
• CKD patients have complex and overlapping medical
problems:
• loss of renal function,
• Diabetes,
• CVD, HTN,
• Anemia, dyslipidemia,
• Poor nutrition status,
• Neuropathy
• Overall decrease quality of life.

25. PREOP EVALUATION
• The extent of preoperative testing is dependent on pts
comorbid diseases.
• Has high risk of complication and prolong hospital or ICU stay
• Em- surgery- 5* greater risk of death
• ESRD who undergo cardiac surgery- mortality ranges from 10-
20% and concomitant DM and age >60yrs further increases
risk of death
• Cardiac arrhythmias and sepsis common cause in periop
mortality
• Appropriate counselling
• If postop dialysis is imminent- book dialysis

26. PREOP EVALUATION
• CKD pts already on dialysis need to be determine:
• Dialysis adequacy
• Preop dialysis need
• Postop dialysis timing
• Dosage requirement for all medications
• Patients on HD usually require preop dialysis within 24
hrs before surgery to reduce the risk of volume overload,
hyperkaliemia, and excessive bleeding
• Patients on PD who are undergoing abdominal surgery
should be switched to HD until wound healing is
complete.
• PD should be continued for those undergoing non-

27. PREOP EVALUATION
• Kidney transplanted patients:
• Because of complicated interactions and
immunosupressive, a nephrologist with specialized
knowledge of renal transplant should be involved in
preop evaluation dosing and adjustment.

28. PREOP EVALUATION
• S. creatinine, BUN, eGFR:
• detects underlying renal deficiency,
• quantify perioperative risk(esp by eGFR)
• possibility of developing AKI,
• influences the choice of the drugs
• AKI in the setting of CKD:
• need prompt evaluation and identify
precipitating factors.
• If elective procedures –postpone until
resolution of AKI

29. PREOP EVALUATION GOALS
• BP should be controlled
• Antihypertensive continued
• ARBs and ACEI often avoided on the day of
surgery- risk of intraoperative hypotension
• Serum K+ - < 5.5 mEq/L
• Patients maintained on dialysis should
undergo dialysis within 24 hrs preceding
elective surgery- minimize volume overload,
hyperkalemia, uremic bleeding
• Heparin – depending upon surgery

30. GOALS OF PREOPERATIVE
ASSESSMENT
• Blood volume status- weight before and after
dialysis
• Hct of at least 30-35%
• Correct coagulopathy
• Aspiration prophylaxis - H2 blocker dose
adjustment
• Reviewing the drugs to be given- dose
adjustment, drugs to avoid(NSAIDs)
• Blood glucose level

31. DRUGS USED IN ANESTHESIA THAT
SIGNIFICANTLY DEPEND ON RENAL
ELIMINATION
• Induction agents – Phenobarbital, Thiopental
• Muscle relaxant – Metocurine, Pancuronium,
vecuronium
• Cholinesterase inhibitors - Endrophonium,
Neostigmine
• CVS drugs- Atropine,Digoxin, Glycopyrolate,
Hydralazine, Milrinone
• Antimicrobials – Aminoglycosides, Cephalosporins,
Penicillins, Sulfonamides, Vancomycn
• Analgesics – Codeine, Meperidine(Pethidine),
Morphine

32. INDUCTION OF ANESTHESIA
• Ideal anesthesia for CKD- not known
• Determined by pts coexisting disease, surgical approach, and desired
anesthetic goal
• Eg: Pts with nausea, vomiting or GI bleeding – Rapid sequence induction
• Safely accomplished with most IV induction agents
• Dose of agent should be carefully considered
• Eg: reduce dose for critically ill, recently had HD, hypovolemia
• Patients at risk of AKI will need reduced dose:
• Prior to renal excretion agents undergo redistribution and biotransformation
into inactive products
• In hypovolemia, there is diversion of blood to essential organs and crosses
BBB- effects of induction agents may be exacerbated

33. INDUCTION OF ANESTHESIA
• High risk of developing hypotension:
• Exaggerated CNS effect of anesthetic agent – uremia-induced disruption
of BBB
• Antihypertensive
• Attenuated SNS- impairs compensatory peripheral vasoconstriction
• Small decrease in blood volume,
• positive pressure ventilation,
• abrupt changes in body position,
• drug induced myocardial depression can result in exaggerated decrease
in systemic BP

34. INDUCTION OF ANESTHESIA
• Reduced dose for thiopental – increase Vd and reduced protein binding
(75%- 85% protein bound)
• Propofol 1-2 mg/Kg
• Etomidate – 0.2 mg/kg
• If indicated RSI - succinylcholine if K+ <5.5(but has reduced pseudo-
cholinesterase level)
• K+ release is not exaggerated in CKD
• Short acting non-depolarizing is selected
• Eg: Rocuronium 1mg/kg, vec 0.1 mg/kg, cisatra 0.15 mg/kg,
• If hyperkalemic:
• Propofol + Lidocaine without relaxant intubation

35. MAINTENANCE OF ANESTHESIA
• Goal- control HTN with minimal deleterious effect on CO ( In CKD
increase CO is the principal compensatory mechanism for tissue
delivery in anemia)
• Balance anesthesia with volatile, propofol, fentanyl, sufentanyl,
afentanil, remifentanyl.
• Ovoid Meperidine(Pethidine) – accumulation of its metabolite
normeperidine(seizure)
• Can use morphine- but has prolong effect(cleared by dialysis)
• Volatile anesthetics is not dependent on renal function
• Sevoflurane avoided – fluoride nephrotoxicity/ compound
A(theoretical/laboratory risk) if used FGF <2L/min

36. • Methoxyflurane and enflurane are avoided
• Vecuronium and rocuronium – slow excretion(Lynam and
colleague – 99 vs 54 mins)
• Mivacurium –decreases by 10 – 15 mins(reduced level of
pseudocholinesterase level)
• Atracurium and Cisatracurium – clearance is independent of
renal function(Hofmann elimination)
• Laudanosine(principal metabolite of Atracurium and
Cisatracurium) clearance is delayed.
• Neostigmine renal clearance is 50%, edrophonium and
pyridostigmine is 75%.
• Therefore less risk of recurarization

37. VENTILATION
• Controlled ventilation is preferred
• Inadequate spontaneous ventilation – progressive
hypercarbia – respiratory acidosis – severe circulatory
depression – increase in serum K+.
• Respiratory alkalosis – shifts Hb dissociation curve to
left – exacerbate pre-existing hypocalcemia – reduce
CBF

38. VASOPRESSORS AND
ANTIHYPERTENSIVE
• Thiazides >90%, Furosemide > 70% - excreted by the
kidney
• Propranolol – completely metabolized in the liver
• Esmolol – biodegraded by esterase in RBC cytosol
• Calcium channel blockers – extensively metabolized in
the liver
• Hydralazine – 15% excreted unchanged in urine
• If vasopressor is necessary – Phenylepherine is
effective

39. OPIOIDS IN CKD
• Morphine and Meperidine end product morphine-3-
glucoronide and normeperidine respectively accumulates in
CKD
• Normeperidine causes seizures in CKD esp those on
dialysis.
• Hydromorphone end-product hydromorphone-3-glucoronide
accumulates in CKD but may be used safely with proper
monitoring and dose adjustment.
• Afentanil, Fentanyl, Remifantanil and Sufentanil lack active
metabolite
• However, elimination half life of fentanyl is prolonged in CKD

40. FLUID MANAGEMENT
• Goal – maintenance of euvolemia and renal perfusion
• Features of hypovolaemia can be masked by anesthesia and
surgery
• Invasive monitoring may improve assessment but disease
state such as sepsis causes maldistribution of intravascular
volume
• Further intraop blood loss and fluid shift during can
compound these problems.
• General goal:
• UOP- >0.5 mL/kg/h
• MAP- >65-70 mmHg
• CVP – 10-15 mmHg
• Pulmonary wedge pressure – 10 -15 mmHg

41. FLUID MANAGEMENT AND UOP
• Those who don’t require dialysis:
• Proper preop hydration with balanced salt solution
• Caution with K+ containing fluids (eg RL)
• UOP goal – 0.5 mL/Kg/h
• Administration of Mannitol or furosemide in volume depleted further
compromise renal function
• Patient dependent of dialysis:
• Noninvasive surgery– replacement of only insensible water loss ( eg.
0.45% NS)
• Invasive surgery – replaced with balanced salt solutions or colloid
• CVP measurement as a guide

42. CURRENT EVIDENCE
• Balance salt solution preferred
• Plasma lyte/ RL preferred than chloride rich 0.9% saline because of hyperchloremia on
kidney function
• However :
• In hypochloremia and alkalosis – 0.9% preferred over balance crystalloid
• Hyperkalaemia – avoid RL(contains 4 mEq/L K) if have to large volumes
• Glucose solution aggravates uremia
• Blood loss – replace with colloid or PRC
• Hydroxyethyl starch – associated with AKI

43. MONITORING
• Preservation of radial, ulna, brachial and
axillary artery especially on non-dominant
upper arm.
• Right atrial / Pulmonary artery/TEE
monitoring
• CVP – difficult in tunneled venous access/
temporary dialysis line
• IBP – poorly controlled BP

44. ASSOCIATED CONCERNS
• Bruising and sloughing of skin – poor nutrition
• Extra paddings needed
• Protection of AV fistula
• No BP to AV fistula site – risk of thrombosis
• No tucking of fistula arm(if all possible) –
fistula thrill checking periodically throughout
surgery

45. REGIONAL ANESTHESIA
• Theoretically, sympathetic blockade of T4-T10 may improves
renal perfusion
• Brachial plexus block for AV fistula:
• Analgesia
• Abolishes vasospasm
• Vasodilation that facilitates surgery
• Concerns:
• Platelet dysfunction
• Residual heparin
• Volume status
• Uremic neuropathies
• Co-existing metabolic acidosis – decreases threshold for seizure

46. POSTOPERATIVE MANAGEMENT
• Though rare in CKD – monitoring of residual neuromuscular
blockade
• (Consideration - antibiotics, acidosis, electrolyte imbalances)
• Opioids residual effects
• Avoid NSAIDs – exacerbate HTN, precipitate edema, increases
risk of CVS complication)
• Hyperkalaemia
• Recheck of electrolytes, BUN, creatinine, Hct
• Uremic bleeding
• 0.9% traditionally preferred(lacks K+) but may exacerbate
preexisting acidosis

47. POSTOP CARE
• Risk of AKI due to relative hypotension caused by :
• ongoing 3rd space fluid loss,
• pharmacological causes( NSAID, ACEIs, ARBS,)
• Residual effects of anesthesia
• Epidural anesthesia
• Therefore post op fluid therapy is otmost importance
• Guided by clinical examination, monitoring UOP, renal function
and electrolytes
• Studies has shown 80% of patients with post op AKI responds to
fluid therapy alone(”Optimize fluid and defined pressure)

48. THANK YOU