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RENAL SYSTEM : ANAESTHETIC
CONSIDERATIONSModerator: Dr. Arvind KharePresented by: Dr. Aji Kumar
Department of Anaesthesia, JLN Medical College, Ajmer
Kidney plays vital role in: ● regulating the volume & composition of body fluids and acid base balance. ● eliminating toxins ● producing hormones like renin, erythropoietin, active vitamin D.
- Each kidney 1 million functional units ( nephrons).
Each nephron consists of – ▪ Renal corpuscle ( Glomerulus, Bowman’s capsule, mesangial cells) ▪ Proximal convoluted tubule ▪ Loop of henle (descending and ascending) ▪ Distal tubule ▪ Collecting tubule ▪ Juxtaglomerular Apparatus.
Introduction
Combined blood flow through both kidneys (20-25% of total cardiac output)
80% of RBF goes to cortical nephrons. 10-15% goes to juxtamedullary nephrons.
CLEARENCE - volume of blood completely cleared of a substance per unit of time.
RENAL PLASMA FLOW = clearence of PAH { [ PAH]u / [PAH]p} x urine flow
RENAL BLOOD FLOW = RPF / (1- haematocrit) Normal RPF = 660 ml/min Normal RPF = 1200 ml/min
Renal circulation
Glomerular Filtration Rate Volume of fluid filtered from the glomerular capillaries
into bowman’s capsule per unit time Normal values - 120 +/- 25 ml/min (male) 95 +/- 20 ml/min (female) Calculated using inulin or creatinine clearence Filtration Fraction = GFR/RPF = ( 20%)
Autoregulation of renal blood flow occurs between MAP of 80 and 180 mm Hg
Acute Renal Failure
“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”.
Staging of Acute Kidney Injury (AKIN)
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
RIFLE criteria for acute kidney injury
Chronic renal failure/CKD is characterized by a progressive and irreversible decline in renal function over the course of at least 3-6 months
CHRONIC RENAL FAILURE
Pre operative evaluation Most patient with ARF requiring surgery are
critically ill Optimal peri operative management dependent
on preoperative dialysis Preoperative dialysis on the day or previous day of
surgery Physical and lab examination to assess cardiac
and pulmonary function Physical signs of fluid overload ,hypovolemia
checked
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 S. urea(15-45 mg/dl) S.Creatinine (0.6-1.3 mg/dl) Creatinine clearence (110-150 ml/min) Serum Electrolytes- HyperKalemia Urinalysis CXR ECG & ECHO ABG- Metabolic acidosis, hypoxemia, Imaging modalities
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
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
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
OpioidsMorphine 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
Inhalation Agents Halothane Inorganic fluoride levels are less No
NeprotoxicityIsoflurane Inorganic fluoride levels are less No
NeprotoxicityDesflurane 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 nephrotoxic
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
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.
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
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.
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
Maintenance Ideal maintenance - control hypertension with
minimal effects on cardiac output,
Controlled ventilation with cuffed endo-tracheal 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 with 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 inlimited or
reduced doses
Drugs contraindicate
dPremeditation Midazolam,
TemazepamDiazepam
Induction Thiopental, Propofol, Etomidate
Ketamine
Maintenance Isoflurane, Desoflurane, Halothane, Propofol
Sevoflurane Enflurane, Methoxyflurane
Muscle Relaxants
Sch, Atracurium, Cisatracurim
Vecuronium, Rocuronium
Pancuronium
Opioids Alfentanil, Remifentanil, Sufentanil
Fentanyl, Morphine
Pethidine
Local Anaesthetic
Bupivacaine, 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