Renal reduced Flashcards
Major functions of the kidney
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Maintains fluid and inorganinc ion balance
- volume, osmolarity, pH and mineral composition
- Na, K, Ca, Cl-, HCO3, H2O
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Removes metabolic wastes and chemicals from the circualtion
- urea, hormones, medications, toxins
- Gluconeogenesis
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Endocrine function/hormone secretion
- fluid balance = renin, prostaglandins, kinins
- RBC production = erythropoetin
- Bone = active vitamin D (1,25-dihydroxyvitamin D3)
How do the kidneys respond normally to changes in volume status?
Hypovolemia
- SNS stimualtion and angiotensin II → vasoconstriction → ↓GFR and ↑ Na+ reabsorption
- Aldosterone→ ↑ Na+ reabsorption
- ADH(Vasopressin)→ ↑ H2O reabsorption
Hypervolemia→ ↑↓
- ANP (Atrial nateuretic peptide) → ↑ GFR via vasodilation
- ↓ SNS and angio II leads to vasodilation and Na+ excretion
- ↑ capillary hydrostatic pressure discourages Na+ reabsobtion
- ↓ aldosterone = ↓Na reabsorption in distal tubule and coolecting duct
- ↓ADH (Vasopressin) = ↓H2O reabsorbtion at the collecting duct
Normal renal autoregulation and the impact of surgery
Autoregualtion of RBF and GFR occurs between:
- MAP of ≈ 80-200 mmHg
All agents and most anesthetic techniques WILL:
- ↓ GFR
- ↓Urine output
- ↓ Renal Blood Flow
- ↓ Electrolyte excretion
- This will effect all major functions of the kidney
- Indirect and direct stimulation/decreases SNS, circulatory and endocrine
- These effects are reversible at the end of the procedure
Effect of Anesthetics on Normal Renal function
- Surgical stimulation → ADH release→↓ UO
- Baroreceptor response to decreased volume leads to ↑ Aldosterone
-
Autoregualtion may be effected under GA
- Lower limits of autoregulation around 80 mmHg
- Hypotension caused by agents shunts blood away from kidneys
- Decreased RBF → leads to renin release → further renal vasoconstriction and SNS stimulation and FURTHER decreases in RBF
Prostaglandins and the renal system
- Protective against renal ischemia
-
Production of prostagladins stimulated via:
- renal ischemia and hypotension
- Physiologic stress
-
Prostaglandins oppose action of:
- angio II, SNS and ADH to compensate for a ↓ in RBF from physilogic stress
- Thus they INCREASE urine output
- Prostaglandin production dependent on phosphalipase A2 and cyclooxygenase
- Ketoralac inhibits these enzymes significantly and thus poses risk for those with renal insufficiency or at risk for medullary ischemia
Dopamine for renal protection
“Low Dose Dopamine”
1-2 mcg/kg/min → Does NOT decrease the incidence of acute renal failure, dialysis or mortality!!!!
that is old news!
BUT… it does have inotropic effect and diuretic activity!
Impact of spinal and Epidural Anesthesia on renal function
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T4-T10 sympathectomy will:
- ↑ catecholamine release
- ↓ renin release
- ↓ ADH (Vasopressin)
-
GIVE fluid boluses
- this will maintain renal blood flow and GFR and thus maintain renal profusion pressure
Volitile anesthetics and nephrotixicity
Main concern = production of free fluoride ions via metabolism causing tubular injury & loss of concentrating ability → ARF
- Risk = Methoxyflurane > Enflurane > Sevoflurane > Isoflurane > Desflurane > Halothane
- Isoflurane & Desflurane: negligible levels → very low risk
-
Sevoflurane = controversial
- ↑ Free fluoride levels but NO clinical evidence of injury
-
Compound A = sevo degrades with low flow through CO2 absorber
- FDA recommends 2 L gas flow with Sevo
- NO clinical evidence of injury in humans, only RATS
(Eger et al. demonstrated transient changes in renal function has not been reproduced by subsequent studies)
Impact of poitive pressure ventilation on renal system
- The higher the PIP and PEEP the greater the decrease in RBF, GFR and UO
- ↓ Preload, ↓ CO and ↓ Arterial hydrostatic pressure will :
- increase SNS activation of the RAAS →Aldosterone and vasopressin which is
- ↓ Preload, ↓ CO and ↓ Arterial hydrostatic pressure will :
-
Hydration will largely overcome this
- Volume improves venous return, cardiac output and increases arterial pressure and thus increases renal profusion
Periop oliguria
Defintion
Casues
Urine output < 0.5 cc/kg/hour or < 30 cc/hour
- if they are not meeting this…must figure out the problem could be hypotension, dehydration, need lasix?
Causes of periop oliguria
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Prerenal = ↓ renal blood flow
- hypovolemia, ↓ CO
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Intrarenal = Acute tubular necrosis
- renal ischemia from prerenal casue, nephrotoxic drugs, release of hemoglobin or myoglobin (MH/blood products)
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Postrenal = ↓ outflow
- BILATERAL ureter obstruction, bladder rupture
Pre-op eval
HTN? DM, MI, CHF? Meds Dialysis- pre/post weight, how much fluid off, when was last, e-lyte status
Renal failure and effects on the nervous system
- Uremic neuropathy
- Uremic encephelopathy
- distal symmetric mixed motor polyneuropathy
- In ESRD - paresthesias, hyperesthesias in feet and lower estremeties
Renal Labs
- BUN > 50 = indicative of decrease
- Inverse to GFR,
- GFR Not as sensitive as Cr
- Can be abnormal, but GFR ok
- due to- high protein diet, GI bleed, fever, dehydration
- Plasma Creatinine 0.7-1.5 = normal
- 8-17 hour lag after cnange in GFR
- Suggestive of ARF
- 50% increase indicates 50% decrease in GFR
- Cr Clearance < 25 ml/min = moderate disease
- Index of GRF
- Most reliable ESTIMATE of GFR
- (don’t forget about Inulin aka gold standard for calculating GFR)
- < 10 needs dialysis
- Disadvantage - needs 2-24hr urine collection
- Urine spec grav (1.003-1.03)
- Urine osmo (38-140mOsm/L)
Renal failure and infections
- Most common cause of death
- often originates as a pulmonary infection
- use Aseptic technique
Acute Renal failure
definition, diagnosis and types
Sudden deterioration in renal function
- Diagnosed by:
- Serum creatitne ↑ of > 0.5 mg/dL and a 50% ↓ in Cr Cl
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3 categories:
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Prerenal = ↓ RBF, ↓ CO, ↓ blood voume
- CHF, Shock syndromes
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Intrarenal = abnormality in the kidney
- trauma, crush injuries, myoglobin accumulation
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Postrenal = obstruction
- renal calculi
-
Prerenal = ↓ RBF, ↓ CO, ↓ blood voume
High risk patients for ARF following anesthesia
(think of categories →Pre-op conditions)
- # 1 factor = pre-op renal insufficiency
- Pre-op CHF or CAD
- Elderly
- ESLD
(then the Peri-op Events)
- Peri-op cardiac events! (inadequate BP/CO)
- Sepsis/emergency surgeries, Trauma (MODS)
- Hypovolemia
- Nephrotoxic exposure
(then think about the surgery types)
- Surgeries using cardiopulmonary bipass
- Aortic clamping
- Liver or kidney transplant procedures
- Nephrectomy procedures
Anesthesia Care and and Physiologic effects of Acute Renal Failure
- Only go to OR if it is an EMERGENCY
- GOAL = Keep MAP >65
Retention of water, waste products, and electrolytes in the blood and extracellualar fluid
- HTN, CHF and Pulm. Edema (can happen fast!)
- Diluted RBCs (HCT 20-30%)
- GI issues (bleeds, anorexia, nausea and ileus)
- Hyperkalemia (can be fatal)
- Metabolic Acidosis
- Neurological changes (confusion, coma)
- Uremia induce immune supression (Infection)
Goals of the dialysis patient (slide title)
-
AVOID infection and CV events
- 25% annual mortalitity rate for all dialysis patients
- PRESERVE vascular access (for fistula sites)
- AVOID non-dominant arm and upper proption of the dominant arm!
- Remember pre-op dialysis clears many medications!
- low molecular weight drugs (<90% proein bound)
- water solule drugs
Drug dosing in renal failure
- Pharmacy has guideline and formulas
- It is useful to know th Cr Clearance and GFR
-
GFR < 50 mL.min = Reduced doses of drugs excreted unchanged by the kidneys
- If no documented GFR it can be estimated
- significantly ↓ GFR is <10 mL/min
- Oliguric = GFR ≈ 5-15 mL/min
- If no documented GFR it can be estimated
-
Volume of distribution changes!
- no dialysis → water souble durgs will have a larger volume of distribution
- just had dialysis → Vd will be normal
- Half lives = may have to dose farther apart
-
Protein binding is altered
- Acidic drugs = LESS binding and MORE free fraction
- Basic drugs = MORE binding → may need to INCREASE the dose!
Renal Failure
Pre-medication considerations
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Anticholinergics
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Atropine & glycopyrrolate
- Potential for accumulation in multiple doses
- 50% of drug excreted unchanged in urine
-
Scopolamine:
- Usually not given d/t CNS effects
-
Atropine & glycopyrrolate
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Benzodiazepines:
- Use shorter acting & titrate very carefully (avoid diazepam)
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Midazolam
- 60-80% cleared by the kidneys in the form of active metabolite + highly protein bound.
-
GI drugs
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Phenothiazine: Droperidol
- α-blocker → may accentuate hypotension
- Not a problem usually in small doses
-
H2 Blockers:
- Highly dependent on renal excretion
- Metoclopramide will accumulate in renal failure
-
Phenothiazine: Droperidol
Renal Failure
Considerations with Opioids
-
Drug of choice
- Fentanyl: in non-cardiac doses
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Analaougs of Fentanyl
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Sufentanil: DONT USE!
- no change in free fraction but pharmacokinetics unpredictable in renal failure
-
Alfentanil:
- ↓ protein binding, no active metabolite (in theory it is ok, but fentanyl is better)
-
Remifentanil:
- remifentanil acid metabolite (minimally active) no major clinical implications
-
Sufentanil: DONT USE!
-
Opioids with active metabolites
-
Meperidine: NEVER GIVE!
- normeperidine metabolite → toxic
-
Morphine: one dose OK… but avoid repeat dosing
- 6-glucuronide metabolite + highly protein bound →
-
Hydromorphone: one dose OK… but avoid repeat dosing
- hydromorphone-3-glucuronide
-
Meperidine: NEVER GIVE!
Renal failure
Considerations with induction agents
-
Thiopental:
- highly protein bound → free fraction can be 2X normal → causing an exaggerated response
-
Dexmedetomidine:
- highly protein bound
- longer lasting sedation (in recent study)
-
Propofol, Ketamine, Etomidate:
- no major clinical change in their pharmacokinetics
- consider BP drop/CV status to chose proper agent
-
Midazolam:
- 60-80% cleared by kidneys in form of active metabolite + highly protein bound
Renal failure
Considerations for Muscle Relaxants
AVOID!! Know this for boards :)
- D-tubocurarine, metocurine, gallamine
- Pancuronium, pipecuronium, & doxacurium
- Primarily dependent on renal excretion
- 60-90%
- Must monitor neuromuscular function closely
USE CAUTION!!
-
Succinylcholine: → Single dose OK if normal K+
- Gtt problematic→ active metab→ succinylmonocholine
- Remember… sux increases K+ 0.5-1 mEq/L
-
Vecuronium & Rocuronium→ Single dose OK
- 30% renal excretion → may see prolonged effect
BEST CHOICES!!!!
-
Atracurium, cis-atracurium, & mivacurium →
- normal dosing appropriate
- have the most predictable for offset!!
not in slides:
Atra and cis-atra = hoffman elimination (acidosis = longer DOA) mivacurioum = plasma cholinesterases
- mivacurioum = plasma cholinesterases
Renal Failure
Intubation considerations
-
AVOID Succinylcholine
- Unless its an RSI but you MUST know K+ level
- Succs ↑ K+ levels by 0.5-1 mEq/L
- A small dose of a non-depolarizing NMB does NOT alter release of K+ reliably
- USE Lidocaine to blunt stimulus
- May need β-blockers to control HTN
- Delayed gastric emptying (diabetes) & ↑ gastric volume → full stomach = RSI