acute renal failure patho physiology & anaesthetic management
TRANSCRIPT
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Dr Riyas A
Acute Renal failure Patho
physiology & anaesthetic
management
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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,
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Diagnostic Criteria's of ARFIntroduced 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 μmol/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,
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Staging System of Acute Kidney InjuryStage Serum Creatinine criteria Urine output criteria
1 Increase in s.creatinine of ≥0.3 mg/dl (≥26.4 μmol/l) orincrease to ≥150% to 200% (1.5- to 2fold) from baseline
Less than 0.5 ml/kg/hr for more than 6 hours
2 Increase in s.creatinine to more than 200% to 300% (> 2 to 3 fold) from baseline
Less than 0.5 ml/kg/hr for more than 12 hours
3 Increase in s.creatinine to more than 300% (> 3 fold) from baseline (or s.creatinine of ≥4 mg/dl [≥354 μmol/l] with an acute increase of at least 0.5 mg/dl [44 μmol/l])
Less than 0.3 ml/kg/hr for 24 hours or anuriafor 12 hours
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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
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Etiology and PathophysiologyDivided 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.
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Prerenal Azotemia Renal Azotemia (Intrinsic) Postrenal (Obstructive)
Acute hemorrhage Acute glomerulonephritis Upper urinary tract obstruction (ureteral)
Gastrointestinal fluid loss
Interstitial nephritis (drugs, sepsis)
Lower urinary tract obstruction (bladder outlet)
Trauma and Surgery Acute tubular necrosis
Burns Ischemia
Low output syndrome Nephrotoxic drugs (antibiotics)
Renal artery stenosisSolvents (carbon tetrachloride, ethylene glycol)
Relative decrease Radiographic contrast dyesSepsis MyoglobinuriaHepatic failureAllergic reaction
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Pre Renal Azotemia
Most common type
Designation for a rise in S.Cr, BUNdue to
inadequate renal plasma flow and hydrostatic
pressure
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Intrinsic AKI
Sepsis
Ischemia
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ischemia
Post operative AKI
Burns & acute pancreatitis
d/s of micro vasculature leading to ischemia
Nephrotoxin associated AKI
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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
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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
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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 radiocontrastadministration)
Elective surgical procedures should be deferred until the effects of the dye have been evaluated and treated.
Nonionic, low-, or iso-osmolar radiocontrastmedia are less nephrotoxic but are expensive and offer optimal cost-benefit ratio when used in high-risk situations only
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Prevention of CONTRAST
N acetyl cystein
fendolopam
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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).
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Intrinsic AKI
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Post renal
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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
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Pre operative evaluation
Pre ,current and post dialysis weight
pre operative red blood cell transfusion
Drug therapy should be carefully reviewed
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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
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Urinary IndicesIndex Pre-renal Causes Renal Causes
Urinary sodium concentration (mEq/L) <20 >40
Fractional excretion of sodium (%) <1 >1
Urine osmolarity (mOsm/L) >400 250–300Urine creatinine/plasma creatinine >40 <20
Urine/plasma osmolarity >1.5 <1.1
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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
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Indication for dialysis
Fluid overload
Refractory GI symptoms
Hyperkalemia
Drug toxicity
Severe acidosis
Mb encephalopathy
Pericarditis
Coiagulopathy
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AnaestheticConsiderations
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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
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OpioidsMorphine Conj. to M-3-G, M-6-G
, active metabolite, respdepresion
Active metabolite has renal elimination, 40% conj occurs in kidney
Dose adjustment required
Meperidine(Pethidine)
Normeperidine, CNS toxicity
Active metabolite has renal elimination
Dose adjustment required
Fentanyl ↓ Plasma protein binding,↑ free drug
Clearance not altered safe
Sufentanil ↓ Plasma protein binding,↑ free drug
Clearance not altered safe
Alfentanil ↓ Initial vol of distribution,↑ free drug
Clearance not altered safe
Remifentanil No change Clearance not altered safe
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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 stable & resists degradation by soda-lime & liver
No Neprotoxicity
Sevoflurane Inorganic fluoride levels are less but not stable , degraded by soda-lime to compound A & undergoes liver metabolism
Compound A is neprotoxic
Enflurane Biotranformed to inorganic fluoride levels after prolonged use (> 4hrs)
Nephrotoxic,afterprolonged use
Methoxyflurane Biotranformed to high inorganic fluoride levels Highly nephretoxic
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Intravenous AgentsThiopentone CNS effect reversed by redistribution &
hepatic metabolism, also 80% protein bound, ↓albumin in uremia, ↑ free drug, more free un-ionised drug in acidosis
Metabolism unchanged ,↓ excretion,
Used in ↓ dose
Propofol Metabolised by liver No adverse effect
Etomidate Metabolised by liver, partial renal excretion
No adverse effect
Benzodiazepines Metabolised in liver & excreted by kidney, longer acting BZD accumulate, ↑duration of action
↑ Interval or ↓ dose
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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
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Monitoring• All routine monitoring – ECG, NIBP, SpO₂, EtCO₂, 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
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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.
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InductionPatients are at increased risk of aspiration: rapid-sequence
induction with cricoid pressure.
Drugs Normal Dosages Altered DosagesThiopental 3-5 mg/kg 2-3 mg/kgPropofol 1-2 mg/kg 1-2 mg/kgEtomidate 0.2-0.4 mg/kg 0.2-0.4 mg/kgSuccinylcholine 1-2 mg/kg 0.5-1.5 mg/kgAtracurium 0.6 mg/kg 0.6 mg/kgCisatracurium 0.15 mg/kg 0.15 mg/kg
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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 Ringer’s?, NS), colloids, pRBC,
Anaesthesia can be maintained with inhalation agents or propofol with muscle relaxants ↓NM monitoring.
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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.
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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.
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Drugs Drugs safe Drugs safe inlimited or
reduced doses
Drugs contraindicated
Premeditation Midazolam, Temazepam Diazepam
Induction Thiopental, Propofol, Ethiomedate
Ketamine
Maintenance Isoflurene, Desoflurne, Halothane, Propofol
Sevoflurene Enflurane, Methoxyflurane
Muscle Relaxants Sch*, Atracurium, Cistracurim
Vecuronium, Rocuronium
Pancuronium
Opioids Alfentanil, Remifentanil, Sufentanil
Fentanyl, Morphine Pethidine
Local Anaesthetic Bupivicaine, Lidocaine
Analgesic Paracetamol NSAIDS
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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
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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
• Stoelting’s Anesthesia & Co-existing Disease, 5th ed. Renal Disease,358-384.
• Harrison’s Principles of internal medicine, 18th ed. Approach to a Patient with Renal Disease and Renal Failure,2293-2299
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Thank you..