Acute renal failure patho physiology & anaesthetic management


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Acute renal failure patho physiology & anaesthetic management

  1. 1. Dr Riyas A Acute Renal failure Patho physiology & anaesthetic management
  2. 2. 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,
  3. 3. 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 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,
  4. 4. 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 μmol/l) or increase 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 anuria for 12 hours
  5. 5. 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
  6. 6. 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.
  7. 7. 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 stenosis Solvents (carbon tetrachloride, ethylene glycol) Relative decrease Radiographic contrast dyes Sepsis Myoglobinuria Hepatic failure Allergic reaction
  8. 8. Pre Renal Azotemia  Most common type  Designation for a rise in S.Cr, BUNdue to inadequate renal plasma flow and hydrostatic pressure
  9. 9. Intrinsic AKI  Sepsis  Ischemia
  10. 10. ischemia  Post operative AKI  Burns & acute pancreatitis  d/s of micro vasculature leading to ischemia  Nephrotoxin associated AKI
  11. 11. Nephrotoxin  Contrast agents:m/c clinical course ,increase in 24-48hrs,peaking with in 3-5 dys, resolving with in 1 week  Antibiotids  Chemotherapeutic  toxic ingestions  Endogenous toxins
  12. 12. 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
  13. 13. 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
  14. 14. Prevention of CONTRAST  N acetyl cystein  fendolopam
  15. 15. 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).
  16. 16. Intrinsic AKI
  17. 17. Post renal
  18. 18. 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
  19. 19. Pre operative evaluation  Pre ,current and post dialysis weight  pre operative red blood cell transfusion  Drug therapy should be carefully reviewed
  20. 20. 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
  21. 21. Urinary Indices Index Pre-renal Causes Renal Causes Urinary sodium concentration (mEq/L) <20 >40 Fractional excretion of sodium (%) <1 >1 Urine osmolarity (mOsm/L) >400 250–300 Urine creatinine/plasma creatinine >40 <20 Urine/plasma osmolarity >1.5 <1.1
  22. 22. 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
  23. 23. Indication for dialysis  Fluid overload  Refractory GI symptoms  Hyperkalemia  Drug toxicity  Severe acidosis  Mb encephalopathy  Pericarditis  Coiagulopathy
  24. 24. Anaesthetic Considerations
  25. 25. 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
  26. 26. Opioids Morphine Conj. to M-3-G, M-6-G , active metabolite, resp depresion 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
  27. 27. 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,after prolonged use Methoxyflurane Biotranformed to high inorganic fluoride levels Highly nephretoxic
  28. 28. Intravenous Agents Thiopentone 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
  29. 29. 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
  30. 30. 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
  31. 31. 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.
  32. 32. 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
  33. 33. 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.
  34. 34. 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.
  35. 35. 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.
  36. 36. Drugs Drugs safe Drugs safe in limited 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
  37. 37. 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
  38. 38. 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
  39. 39. Thank you..