Renal system

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