Acute Renal failure Patho

physiology & anaesthetic

management
Dr Riyas A
Definition
Acute renal failure (ARF) or Acute kidney injury
(AKI) is characterised by deterioration of renal
functions over a period of hours to few days,
resulting in failure of the kidneys to excrete
nitrogenous waste product and to maintain fluid,
electrolytes and acid-base homeostasis.

Harrison's Manual of Medicine,

Diagnostic Criteria's of ARF
Introduced by Acute Kidney Injury Network (AKIN)
1. Rapid time course ( 48 hrs)
2. Reduction in Kidney functions:
a) Rise in S.Creatinine- Absolute in S.Creatinine of
0.3mg/dl ( 26.4 mol/l) or a percentage in
S.Creatinine of 50% (1.5 fold from baseline).

b) Reduction in urine output (documented oliguria of 0.5

ml/kg/hr for more than six hrs).

Harrison's Manual of Medicine,

 Staging System of Acute Kidney Injury
Stage Serum Creatinine criteria Urine output criteria

1 Increase in s.creatinine of 0.3 mg/dl (26.4 Less than 0.5 ml/kg/hr

mol/l) or for more than 6 hours
increase to 150% to 200% (1.5- to 2fold) from
baseline
2 Increase in s.creatinine to more than 200% to Less than 0.5 ml/kg/hr
300% (> 2 to 3 fold) from baseline for more than 12
hours
3 Increase in s.creatinine to more than 300% (> 3 Less than 0.3 ml/kg/hr
fold) from baseline (or s.creatinine of 4 mg/dl [ for 24 hours or anuria
354 mol/l] with an acute increase of at least 0.5 for 12 hours
mg/dl [44 mol/l])
classification
According to urine flow rates

oliguric
non oliguric
Poly uric renal failure

Major problem inability to maintain dynamic

balance b/w dietary intake of essential substance
and production of waste products
 Etiology and Pathophysiology
Divided into three major categories:

1. Prerenal ARF (~55%)- Diseases that cause renal

hypoperfusion, resulting in function without frank
parenchymal damage,

2. Renal or Intrinsic ARF (~40%)- Diseases that directly involve

the renal parenchyma,

3. Postrenal ARF (~5%)- Diseases associated with urinary tract

obstruction.
 Prerenal Azotemia Renal Azotemia (Intrinsic) Postrenal (Obstructive)
Upper urinary tract
Acute hemorrhage Acute glomerulonephritis
obstruction (ureteral)
Gastrointestinal fluid Interstitial nephritis (drugs, Lower urinary tract
loss sepsis) obstruction (bladder outlet)

Trauma and Surgery Acute tubular necrosis

Burns Ischemia
Nephrotoxic drugs
Low output syndrome
(antibiotics)
Solvents (carbon
Renal artery stenosis tetrachloride, ethylene
glycol)
Relative decrease Radiographic contrast dyes
Sepsis Myoglobinuria
Hepatic failure
Allergic reaction
Pre Renal Azotemia
Most common type

Designation for a rise in S.Cr, BUNdue to

inadequate renal plasma flow and hydrostatic
pressure
Intrinsic AKI
Sepsis

Ischemia
ischemia
Post operative AKI

Burns & acute pancreatitis

d/s of micro vasculature leading to ischemia

Nephrotoxin associated AKI

Nephrotoxin
Contrast agents:m/c clinical course ,increase in
s.cr 24-48hrs,peaking with in 3-5 dys, resolving
with in 1 week

Antibiotids

Chemotherapeutic

toxic ingestions

Endogenous toxins
Contrast agents
(1) hypoxia in the renal outer medulla due to
perturbations in renal microcirculation and
occlusion of small vessels;
(2) cytotoxic damage to the tubules directly or via
the generation of oxygen free radicals, especially
since the concentration of the agent within the
tubule is markedly increased; and
(3) transient tubule obstruction with precipitated
contrast material
contrast
Prevention of radiocontrast nephropathy
depends on adequate hydration (e.g., 1 mL/kg
normal saline initiated at least 4 hours before
and continued for 12 hours after radiocontrast
administration)
Elective surgical procedures should be
deferred until the effects of the dye have been
evaluated and treated.
Nonionic, low-, or iso-osmolar radiocontrast
media are less nephrotoxic but are expensive
and offer optimal cost-benefit ratio when used
in high-risk situations only
Prevention of CONTRAST
N acetyl cystein

fendolopam
Antibiotics & chemotherapy
Aminoglycosides andamphotericin B both cause
tubular necrosis

Cisplatin and carboplatin are accumulated by

proximal tubular cells and cause necrosis and
apoptosis
Ifosfamide may cause hemorrhagic cystitis and
tubular toxicity
Antiangiogenesis agents such as bevacizumab,
can cause proteinuria and hypertension via injury
to the glomerular microvasculature (thrombotic
microangiopathy).
Intrinsic AKI
Post renal
Pre operative evaluation
Most patient with ARF requiring surgery are
critically ill
Optimal perioperative management
dependent on preoperative dialysis
Preoperative dialysis on the day or previous
day of surgery
Physial and lab examination depend up on
cardiac and pulmonary function
Physical signs of fluid overload ,hypovolemia
Pre operative evaluation
Pre ,current and post dialysis weight

pre operative red blood cell transfusion

Drug therapy should be carefully reviewed

Investigations & Diagnostic Tools
CBC - Anemia
BUN (10-20 mg/dl)
S.Creatinine (0.6-1.3 mg/dl)
Creatinine clearence (110-150 ml/min)
Serum Electrolytes- HyperK
Urinalysis
CXR
ECG & ECHO
ABG- Metabolic acidosis, hypoxemia,
Imaging modalities
Urinary Indices
Index Pre-renal Causes Renal Causes

Urinary sodium concentration

<20 >40
(mEq/L)
Fractional excretion of sodium (%) <1 >1
Urine osmolarity (mOsm/L) >400 250300
Urine creatinine/plasma
>40 <20
creatinine
Urine/plasma osmolarity >1.5 <1.1
Pre Anaesthetic Optimisation
No specific treatment
Symptomatic and supportive treatment- hypotension,
hypovolemia, low cardiac output state- maintenance of BP
Treat underlying cause
Correct fluids
Diuretics
Electrolytes and acid-base derangements
Mannitol ??- pre ischemic insult, PG-renal vasodilatation,
free radical scavenging, osmotic diuresis
Low dose Dopamine??
N-acetylcysteine- free radical scavenger, (600 mg orally
BD)
Dialysis
Indication for dialysis
Fluid overload
Refractory GI symptoms
Hyperkalemia
Drug toxicity
Severe acidosis

Mb encephalopathy
Pericarditis
Coiagulopathy
 Anaesthetic
Considerations
Anaesthetic Problems & Concerns
Fluid homeostasis -Hypotension, hypovolemia, CHF, HTN,
pulmonary edema, hypoalbuminemia
Electrolyte disturbances - Hyperkalemia, hypocalcemia
Acid-base disturbances - Metabolic acidosis, hypoxemia
Delayed gastric emptying - Aspiration
Arrhythmias, conduction blocks
Neurological complications
Dilutional Anemia
Infections
Effect on drug handling
 Opioids
Morphine Conj. to M-3-G, M-6-G Active metabolite has renal Dose adjustment
, active metabolite, resp elimination, 40% conj required
depresion occurs in kidney
Meperidine Normeperidine, CNS Active metabolite has renal Dose adjustment
(Pethidine) toxicity elimination required
Fentanyl Plasma protein Clearance not altered safe
binding, free drug
Sufentanil Plasma protein Clearance not altered safe
binding, free drug
Alfentanil Initial vol of Clearance not altered safe
distribution, free drug
Remifentanil No change Clearance not altered safe
 Inhalation Agents
Halothane Inorganic fluoride levels are less No Neprotoxicity
Isoflurane Inorganic fluoride levels are less No Neprotoxicity
Desflurane Inorganic fluoride levels are very less, highly No Neprotoxicity
stable & resists degradation by soda-lime & liver

Sevoflurane Inorganic fluoride levels are less but not stable , Compound A is
degraded by soda-lime to compound A & neprotoxic
undergoes liver metabolism

Enflurane Biotranformed to inorganic fluoride levels after Nephrotoxic,after

prolonged use (> 4hrs) prolonged use

Methoxyflurane Biotranformed to high inorganic fluoride levels Highly

nephretoxic
 Intravenous Agents
Thiopentone CNS effect reversed by redistribution & Metabolism unchanged ,
hepatic metabolism, also 80% protein excretion,
bound, albumin in uremia, free drug,
more free un-ionised drug in acidosis Used in dose

Propofol Metabolised by liver No adverse effect

Etomidate Metabolised by liver, partial renal No adverse effect

excretion
Benzodiazepines Metabolised in liver & excreted by Interval or dose
kidney, longer acting BZD accumulate,
duration of action
Local anaesthetics
Dose reduction needed
Respiratory or metabolic acidosis increases the
risks for CNS toxicity from local anesthetics

Elevated PaCO2 enhances cerebral blood flow and

thus the anesthetic is delivered more rapidly to
the brain. In addition, diffusion of carbon dioxide
into neuronal cells decreases intracellular pH,
which facilitates conversion of the base form of
the drugs to the cationic form. The cationic form
does not diffuse well across the nerve membrane,
so ion trapping will occur, which will increase the
apparent CNS toxicity of local anesthetics
Monitoring
All routine monitoring ECG, NIBP, SpO, EtCO, NM
monitoring

Monitoring urinary output and intravascular volume

(desirable urinary output: 0.5 ml/kg/hr)

Intra-arterial, central venous, pulmonary artery

monitoring are often indicated

Intra-arterial blood pressure monitoring in poorly

controlled hypertensive patients
Pre-Medication
Reduced doses of an opioid or BZD,

H2 blocker - Aspiration prophylaxis,

Metoclopramide -10 mg for accelerating gastric

emptying, prevent vomiting, risk of aspiration,

Antihypertensive agents should be continued until the

time of surgery.
Induction
Patients are at increased risk of aspiration: rapid-sequence
induction with cricoid pressure.

Drugs Normal Dosages Altered Dosages

Thiopental 3-5 mg/kg 2-3 mg/kg
Propofol 1-2 mg/kg 1-2 mg/kg
Etomidate 0.2-0.4 mg/kg 0.2-0.4 mg/kg
Succinylcholine 1-2 mg/kg 0.5-1.5 mg/kg
Atracurium 0.6 mg/kg 0.6 mg/kg
Cisatracurium 0.15 mg/kg 0.15 mg/kg
 Maintenance
Ideal maintenance - control hypertension with minimal
effects on cardiac output,

Controlled ventilation with cuffed endo-trachial tube should

be considered for patients with renal failure,

Fluid therapy: D5W, isotonic crystalloids (lactated Ringers?,

NS), colloids, pRBC,

Anaesthesia can be maintained with inhalation agents or

propofol with muscle relaxants NM monitoring.
Reversal
Neuro-muscular blockage is reversed with Neostigmine or
pyridostgmine in combination with anticholenergic.

Neostigmine and pyridostgmine has 50% & 70% renal elimination

respectively.

Glycopyrolate has 80% renal excretion so should be used

cautiously.

Atropine undergoes 25% renal elimination and rest hepatic

metabolism to form metabolite noratropine which has renal
excretion.

Extubation should be done after complete reversal of NM blockage.

Post Operative
Monitoring of fluid overload or hypovolemia titrated fluids,

Residual neuromuscular blockade,

Monitoring of urea and electrolytes,

ECG monitoring for detecting cardiac dysrhythmias.

Continue oxygen supplementation in post operative period,

Analgesia with regional,

Carefully titrated opioids, CNS depression, respiratory depression

naloxone.
 Drugs Drugs safe Drugs safe in Drugs
limited or contraindicated
reduced doses
Premeditation Midazolam, Temazepam Diazepam

Induction Thiopental, Propofol, Ketamine

Ethiomedate

Maintenance Isoflurene, Desoflurne, Sevoflurene Enflurane,

Halothane, Propofol Methoxyflurane

Muscle Relaxants Sch*, Atracurium, Vecuronium, Pancuronium

Cistracurim Rocuronium

Opioids Alfentanil, Remifentanil, Fentanyl, Morphine Pethidine

Sufentanil
Local Anaesthetic Bupivicaine, Lidocaine

Analgesic Paracetamol NSAIDS

summary
Patients presenting for surgery with renal
insufficiency or failure present a significant
challenge for the anesthesiologis
It is imperative that the anesthesiologist not only
understands the management of these complex
patients but also intervenes to prevent further
renal injury during the perioperative period.
Judicious fluid management,the maintenance of
normovolemia, and avoidance of hypotension are
priorities for the successful prevention of further
renal injury
References
Miller RD. Anesthesia. 7th ed. NY: Churchill
Livingstone Inc.; 2010. Anesthesia and the Renal and
Genitourinary Systems, 2105-2134.

G.Edward morgan 4h edition,746-751

Stoeltings Anesthesia & Co-existing Disease, 5th ed.

Renal Disease,358-384.

Harrisons Principles of internal medicine, 18th ed.

Approach to a Patient with Renal Disease and Renal
Failure,2293-2299
Thank
you..