CHRONIC RENAL

FAILURE
Moderator
Dr Vasudeva Upadhyaya, St. Johns Medical College Bangalore
Dr Ravi Bhat, SDM Dharwad

Presenter
Dr Tobu Varghese , Dr Anoop Sebastian
St. Johns Medical College, Bangalore

(Duration - 45 mins)
 Case scenario
"A 60 yr old male patient with Diabetes mellitus with
Creatinine levels of 5 mg%, and on regular dialysis 2
times a week since the past 2 yrs, with ulcer on Right foot
and b/l lower limb swelling possibly DM foot scheduled
for wound debridement.
 What is CRF? ESRD?
• As Per NKF KDOQI (kidney disease outcome and quality
initiative )

• CKD is defined as
• GFR less than 60ml/min/1.73m2 for more than 3 months, with or
without evidence of kidney disease

• Evidence of kidney damage for more than 3 months based on

abnormalities on pathologic specimen, imaging or laboratory tests( Ex-
proteinuria) irrespective of GFR
ESRD
 How do you estimate GFR?
• COCKCROFT - GAULT Equation

GFR (ml/min)= (140-age)x weight in kg

serum creatinine x72
females, multiply by 0.85
From creatinine clearance
GFR=Ucr x V
Pcr
Ucr- urine creatinine
Pcr- plasma creatinine
V- urine flow rate ( ml/min)
 Causes of CRF

• Diabetic Glomerulosclerosis
• Glomerular Diseases
• Primary- focal and segmental glomerulosclerosis, membranoproliferative glomerulonephritis,
membranous nephropathy, Ig A Nephropathy,
• Secondary- post infectious glomerulonephritis, amyloidosis, collagen vascular diseases, HIV associated
membranous nephropathy/ glomerulonephritis, diabetic nephropathy, lupus nephropathy,
• Vascular diseases - hypertensive nephrosclerosis, microangiopathies, renal artery stenosis
• Tubulointerstitial diseases - drug induced, analgesic, reflux induced, chronic pyelonephritis, heavy metals
• Obstructive diseases - nephrolithiasis, retro peritoneal fibrosis/ tumours, prostatic diseases/ congenital
• Cystic diseases and Hereditary- polycystic kidney disease , medullary cystic disease, Alport’s syndrome
• Diseases in renal transplant recipients - rejection, drug toxicity, recurrence of diseases
 Pathophysiological changes/
systemic manifestions of CRF

• Inability of kidney to perform two duties-

• Regulations volume and composition of

extracellular fluid

• Excrete waste products

 CVS
• Increased risk of myocardial infarction compliance
• Heart failure, • Myocardial fibrosis and calcification
• Diastolic causes conduction defects resulting in
dysfunction ,
2nd and 3rd degree blocks
• Arrhythmias,
• Increased incidence of permanent pacing
• Accelerated atherosclerosis, • Hypovolemia and calcium channel
• Deranged lipoprotein metabolism, blockers leads to complete heart block
• Vascular calcifications, • Hypertension- maybe pathology of renal
• Stenotic atherosclerotic lesions, failure or from renal parenchymal or
vascular disease
• Pericarditis,

• Uraemia cardiomyopathy,
• Valvular heart disease.
• Pulmonary edema due to reduced LV
RS
• Hyperventilation secondary to metabolic acidosis
• Volume overload leads to pulmonary congestion
• Hypoxia
• Pleural effusion
CNS
• Lethargy
• Depression
• Uraemic Encephalopathy
• Peripheral and autonomic neuropathy
IMMUNOLOGICAL
• Weakened immunity results in inhibition of cell mediated and humoral
immunity
• Susceptible to infection and poor wound healing

HEMATOLOGICAL
• Anaemia
• Increased 2,3 DPG
• Platelet count normal but quality affected (uraemic thrombasthenia/ uraemic
thrombocytopathy)
• Coagulation parameters deranged
Endocrine changes
• secondary hyperparathyroidism

• hypothermia

MUSCULOSKELETAL

• Muscle weakness

• Renal osteodystrophy

• periarticular calcification

• hyper pigmentation

• pruritis

• ecchymosis
Metabolic acidosis:
• Due to reduction in ammonia synthesis and Reduced ability to excrete hydrogen ions (acid load)
• Results in altered volume of distribution and drug efficacy.

Fluid and electrolytes:

• Develop fluid overload and edema.
• Infusion of large volumes of saline will also result in hyperchloraemic metabolic acidosis.
• Hyperkalaemia is common with the onset of Stage 5 CKD. Excessive exogenous potassium,
transcellular potassium shifts, Acidaemia, insulin deficiency, hypertonicity, and acute beta-
adrenergic receptor block can aggravate hyperkalaemia and should be avoided.
• Hypo/hypernatraemia, hypocalcaemia, hypermagnesaemia and hyperphosphataemia are the other
electrolyte abnormalities that may be present in patients with CKD.
 TREATMENT OF HYPERKALEMIA

• Basic and advanced life support measures as required

• Continuous cardiac monitoring and large bore IV access

• Cardiac membrane stabilisation using calcium chloride or calcium gluconate

• Promote intracellular shift of serum potassium using an infusion of insulin and dextrose whilst
monitoring plasma glucose concentrations

• Excretion of excess potassium (method depends on intrinsic renal function): options include
diuretic therapy to promote renal excretion, oral/rectal cation exchange resins and renal
replacement therapy using dialysis or haemofiltration.
Cardio renal syndrome

Medical management

• Diuretics,

• ACEI, ARB, renin inhibitors,

aldosterone inhibitors

• Nesiritide which is an analogue

of brain natriuretic peptide
(BNP)

• Vasopressin antagonists,
Adenosine antagonists

• Ultrafiltration
 Anaemia - CKD
Causes of anemia in CKD ( Hb less than 12gm/dl)

• Relative EPO deficiency.

• Shortened RBC survival

• Bone marrow suppression.

• Other substrate deficiencies(B12 and folic acid)

• Iron deficiency.

• Blood loss

Blood transfusion-

because of risk of allosensitisation and graft rejection , not advocated unless severe anaemia
decompensated patient.
 Dialysis-benefits and
disadvantages
Haemodialysis and peritoneal dialysis are renal replacement therapies used
• to remove metabolic waste material and
• fluid from the circulation
• to normalise fluid volume and electrolyte concentrations.

Disadvantages of dialysis include:

• Fluid depletion and redistribution to extravascular spaces resulting in depletion of intravascular volume

• Electrolyte disturbance, especially hypokalaemia

• Residual anticoagulation from heparinisation of the haemodialysis circuit.

• Dialysis Disequilibrium Syndrome

• Dialysis Dementia

• Dialysis Hypersensitivity

Dialysis is therefore usually scheduled within 12–24hours preceding surgery.

A post-dialysis measurement of serum electrolytes is required before surgery as dialysis induced electrolyte disturbance can
predispose to intraoperative cardiac dysrhythmias.
 Common surgical interventions
in CKD

• Access for hemodialysis

• AV Fistula

• CAPD catheter

• Renal Transplant
 Pharmacological considerations of
anaesthetic drugs
• gastric absorption

• volume of distribution

• protein binding

• acidosis

• excretion
 Induction Agents and Sedatives

• Thiopental has an increased volume of distribution and reduced plasma protein binding , brain is
exposed to a higher free drug concentration so dose should be reduced.

• Propofol pharmacokinetics is unaltered in established renal failure.

• Renal failure appears to have minimal influence on ketamine action but may worsen hypertension
and cardiac function.

• Clinical effects of an etomidate- anaesthetic induction are not altered in patients with CKD. not
recommended -adrenal insufficiency.

• The benzodiazepines are extensively protein bound. CRF increases the free fraction of
benzodiazepines in plasma, which may potentiate their clinical effect.

• CKD patients are more sensitive to sedative effects of alprazolam than normal persons.

• Dexmedetomidine has longer-lasting sedative effect may be due to less protein binding.
 Inhalation agents

• Nitrous oxide induces mild to moderate reductions in RBF and GFR,

primarily because of its effects on the central circulation.

• Desflurane and isoflurane are safe to use in patients with CKD.

• Sevoflurane can be used avoiding low flow technique (compound A

may cause nephrotoxicity).

• Methoxyflurane / enflurane anaesthesia results in elevated serum

inorganic fluoride levels and hence avoided.
 Analgesics
• Opioids -no direct toxic effects on kidney. but antidiuretic effect may cause urinary retention.

• Morphine and its metabolite ,morphine 6 glucuronide are excreted by kidneys, so prolonged
duration of action.

• Pethidine is avoided in CKD patients, as excretion of its metabolite norpethidine, which is a

convulsant, is dependent on kidneys.

• Fentanyl and its analogues (remifentanil,sufentanil and alfentanil) are safe in patients with
CKD.

• Oxycodone and its metabolites accumulate in renal failure. The dose should be reduced and
dose interval increased.

• Tramadol and metabolite excreted unchanged in the urine. CKD patients may be more prone
for convulsions with tramadol as uraemia is associated with a lowered seizure threshold.

• Prolonged use of acetaminophen is associated with analgesic nephropathy, but occasional or

moderate (including perioperative) use is safe.
 NSAIDS

• The adverse effects of the non-steroidal anti- inflammatory drugs (NSAIDs) are likely to
outweigh any potential benefit in the preoperative period.

• They exacerbate hypertension and precipitate oedema, hyponatraemia, and hyperkalaemia.

• Increased risk of gastrointestinal bleeding, which may be aggravated by the combined effects of
uraemic thrombasthenia and drug-induced platelet inhibition.

• increased risk of cardiovascular complications.

• Nephrotoxic agents that precipitate an acute decrease in GFR and may also cause acute
interstitial nephritis.

• The renal effects of the COX-2 inhibitors are similar to those of the non-selective NSAIDs.
 Neuromuscular blocking and
reversal agents:
• Succinylcholine, atracurium, cis-atracurium, and mivacurium appear to have minimal renal excretion of the
unchanged parent compound.

• In general, the initial dose for neuromuscular block is larger in patients with CKD than in normal subjects.

• But, with the exception of atracurium and cis-atracurium, the dose required for maintaining the block is
reduced.

• To prevent postoperative residual curarization (PORC), the anaesthetist should avoid using long-acting NMBA,
or agents which are excreted in part in the urine, and also make routine use of neuromuscular monitoring.

• Succinylcholine use can be justified as part of a rapid-sequence intubation technique. Atracurium and Cis-
atracurium do not dependent upon renal or hepatic function for its elimination and are safe in patients with
CKD.

• Vecuronium and rocuronium are partially excreted in the urine and may have a prolonged duration of action.

• Pancuronium is 80% excreted by kidneys and should be avoided.

 Pharmacological considerations of
anaesthetic drugs

• The pharmacokinetics of clinically available

anticholinesterases(Neostigmine) and anticholinergic agents
(atropine / glycopyrrolate) used in conjunction, are similarly
excreted by the kidney and have a prolonged duration of
action in CKD.

• Sugammadex may prove useful in preventing PORC when

patients have received an aminosteroid NMBA.
 Management
• Pre-op evaluation

• Optimisation

• Consent

• Investigations

• Conduct of Anaesthesia

• Post op Monitoring
 Pre-op Evaluation

• H/o-Renal failure, duration of rx, daily I/O, Protein intake, dialysis frequency, co
morbidities and rx h/o for the same, exercise tolerance, GERD, treatment h/o,
complications of CKD and dialysis related complications

• Explain about complications of sx, Need for post op dialysis/ Icu care, blood
transfusion.

• Examination- Anemia, Pedal edema, JVP, BP(sitting and standing), Murmurs,

pericardial rub, Crepitations, s/o uremic encephalopathy, Raised ICP symptoms

• Investigations : CBC,S.electrolytes,BUN &S.creat, LFT, coagulation profile (BT,CT,

PT,INR,aPTT), chest Xray, ECG,Echo, ABG,Blood grouping and cross matching
 Pre-op
• NPO orders

• Informed high risk consent

• Preop sedation- Better avoided.Reduce BZD dose.(Midaz safe)

• Anti aspiration prophylaxis- 30ml Na citrate, Ranitidine,ondansetron.

• Continue all drugs especially anti HTN drugs, morning dose of OHA/Insulin
according to institutional protocol,

• Preop dialysis within 24 hrs of surgery (Avoid hepain HD)

• Blood to be arranged( leucodeplted blood) if required

 Anaesthesia goals

• minimising further injury

• preservation of RBF and perfusion pressure

• suppression of stress responses to surgical stimulation

and post operative pain

• avoidance and curtailment of nephrotoxic insults

 concerns - regional anaesthesia
• Risk vs benefit analysis

• Check- BT, Plt count, PT, INR, aPTT

• Risk-

1. Plt dysfunction common- chance of hematoma

2. Uremic encephalopathy- Uncooperative patient,Raised ICP

3. Hemodynamically unstable pts(Need adequate intravascular volume)

4. Heparin administered during HD-hematoma

5. Risk of nerve damage

• Benefits-

• If T4-T10 level blockade – Good renal perfusion(Decreased catecholamine induced

vasoconstriction), Reduced surgical response,
 concerns- general anaesthesia

• Pharmacological considerations of anaesthetic drugs

• Prone for aspiration/ difficult airway

• Iv induction with thio/propofol/etomidate(Given slowly in titrated doses

with dose adjustment)

• Blunt laryngoscopic response( fenta 5mcg/kg or esmolol 0.5mg/kg)

• RSI with Sch (if S.k+ normal) or rocuronium

• Controlled ventilation preferred to avoid hypercarbia,resp acidosis. Adequate PEEP and
maintain hemodynamic stability.

• Fluids-Crystalloids- 0.45NS or RL(according to new studies)

• Colloids – Starch containing colloids avoided.Albumin given

• Blood transfusion- Use leucodepleted blood, Fresh blood,Washout RBC blood

• Forced air warmers and fluid warmers, care of AV fistula, Care of pressure points while
positioning
 intra- op monitoring

• ECG, NBP, Etco2, Temp, Neuromuscular Monitoring, Spo2, U/0(if non

oliguric)

• ABP-Normally not recommended unless-Major sx,IHD pts,Hemodynamically

unstable pts,Pts in CCF.

• CVP monitoring-If major sx involving major fluid shifts(12-14cm

• Use of PA catheter- debatable .Now a days TEE/TTE has replaced

• ABG
assess volume status in patients with
ESRD

• Pre and post dialysis weight(>2kg signifies vol

depletion).

• Clinical examination

• CVP monitoring
 fluid management strategy
• Based on patients I/O daily
• Asses volume status
• Asses blood loss and transfuse based on transfusion trigger
• Crystalloids- 0.45%NS or RL
• Colloids- Starch avoided.
• Blood transfusion- Leucodepleted blood, washed out rbc,
fresh blood
 intra-op renal protection

1. Maintain RBF and Renal perfusion pressure

• Correct hypovolemia, restore circulatory volume

• Vasopressors and Inotropes to maintain MAP 65-75mm Hg

2. Intravascular volume expansion

• Crystalloids , Albumin

3. Avoid nephrotoxic drugs

4. Renoprotective drugs – Dopamine, Fenoldopam, Diuretics( judicious use)

 predictors for renal failure

• Pre op : Old age, IHD, Smoker, T2 DM, Liver d/s, Prev Kidney d/s, Gest HTN, ASA
3,4 ,

• Intra op : Emergency Sx , Major abdomen sx, Vascular sx, Cardiac sx, transplant sx,
CPB , intra op use of inotropes, massive blood loss and blood transfusion

• Post op : transfusion, Diuretics, Use of vasoconstrictors, antiarrhythmic drugs, Sepsis,

Nephrotoxic drugs
 plan for this case

• neuraxial block (spinal)

• Regional - Ankle Block

• General Anaesthesia
THANK YOU