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Co-exist Test 2 > Renal > Flashcards

Renal Flashcards

1
Q

What is special about blood flow through the kidney?

A

afferent arteriole–> glomerulus–> efferent arteriole

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2
Q

What is GFR?

A
  • Considered the best indicator of renal function
  • based on pt size/gender/weigth/age
  • GFR can be calculated from timed urine volume measurements
  • multiple different formulas exist to calculate
  • ranges
    • normal 90-120mL/min
    • Troubling 60-89mL/min
      • decreases with age
      • maybe normal in elderly
    • abnormal <50 mL/min
      • where we start altering our anesthetics
    • Failure <15 mL/min
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3
Q

What is creatinine clearance?

A
  • Specific test for GFR- most reliable assessment tool for renal function (24 hour urine collection)
  • measures ability of glomeruli to excrete creatinine
  • Normal 95-150 mL/min
  • Mild dysfunction 50-80 mL/min
  • moderate dysfunction <25 mL/min
  • anephric <10mL/min
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4
Q

What does a UA measure?

A
  • Specific gravity
    • measures solutes in urine
    • kidneys ability to excrete concentrate/dilute urine
    • normal 1.003-1.008 (>1.018 indicates reasonable function)
  • Proteinuria
    • >150 mg/day- Can be seent with incrase exercise, HTN, DM
    • >750 mg/day indicates severe glomerular damage
      • more likely to develop AKI
  • Microscope
    • RBC (Bleeding), WBC (infection), casts (disease of nephron) or crystals (metabolism)
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5
Q

What is BUN?

A

Blood urea nitrogen

  • Primary source is liver (protein catabolism)
  • not a reliable indicator of GFR
    • 40-50% passively reabsorbed by renal tubule
    • hypovolemia increases this
    • normal 10-20 mg/dL
    • 20-40 mg/dL: dehydration, high catabolism, decreased GFR
    • >50 mg/dL indicates impairment of renal function
  • increased BUN with normal serum creatinine suggests non renal cause
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6
Q

What is serum creatinine?

A
  • Cretinine is a metabolite of cretine (muscle constitue)
    • generally reliable in healthy patients
  • prodcution and elminiation is relatively constant
  • inversely related to GFR
  • Normal 0.6-1.2 mg/dL
    • lower in elderly/females
  • creatinine levels double for every 50% reduciton in GFR
    • delayed lab
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7
Q

What is BUN: Cr ratio? Normal? Elevater? Low?

A
  • Normal 10:1
    • low tubular flow rates enhanve urea reabsorption but do not affect creatinine handling
  • >15:1
    • volume depletion, CHF, cirrhosis, and nephrotic syndrome
      • increase in nitrogen, decrease in blood flow, decrease in BP (specifically CHF, cirrhosis)
  • <10:1
    • decreased urea input, increased creatinine produciton and volume expansion
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8
Q

What is fractional excretion of sodium?

A
  • Useful in differentiating between prerenal and renal causes of failure
  • >2% or >40 mEq/L
    • ATN/kidney damage
    • inability to conserve sodium- because proximal/distal tubule isn’t reabsorbing Na
    • intrarenal
  • <1 or <20mEq/L
    • increased sodium reabsorption- water follows sodium, less Na in urine because it is reabsorbed
    • normal funcitoning tubules
    • prerenal- hypoperfusion
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9
Q

How can anesthesia effect renal function?

A
  • Effects are complicated and difficult to evaluate
    • type/depht of anesthesia, choice of agent, fluid regimen
  • Indirect or direct effects
    • most are indirect (hypoperfusion)
  • occur with both general and regional anesthesia
    • less pronounced with regional
      • more localized effect
    • with spinals, big sympathomimectomy, vasodilation, drop in BP
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10
Q

Cardiovascular indirect effects on renal system with anesthesia?

A
  • Dose dependent decrease in CO and SVR
  • Decreased sympathetic tone (epidural/spinal)
    • fluid boluses and vasoconstrictors to increase BP
    • DO NOT use dopamine, no changes in outcome
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11
Q

Pulmonary indirect effects on renal with anesthesia?

A
  • Positive pressure ventilation
    • the higher hte PIP and PEEP, the greater decrease in RBF and GFR
      • increase intrathoracic pressure, decrease return SVR, decrease in RA and RVEDP, increase in SNS–> increase NE/Epi–> vasoconstriction–> decrease blood flow to kidneys
    • Increase in SNS activation, RAAS activation, and vasopressin release
    • ensure adequate hydration
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12
Q

Neuro indirect effect on renal system with anesthesia?

A
  • Increased sympathetic tone
    • anxiety, pain, light anesthesia, surgical stimuli
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13
Q

Endocrine indirect effects on renal system around anesthesia?

A
  • Epi, NE, ADH, angiotensin II
    • reduce renal blood flow through vasoconstriction
  • Aldosterone
    • enhances Na reabsorption and water retention
  • Prostaglandins (PGE2)
    • To blanace vasoconstriction and stress
      • in Litchfields online questions, he states prostaglandins vasodilate at kidneys
    • pathway includes phospholipase A2 and cyclooxygenase
      • avoid
        • celebrex, tylenol, toradol
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14
Q

Thiopental renal implications?

A
  • Reduced plasma protein binding
  • increased volume of distribution
  • may undergo some metabolism in kidney
  • decrease initial dose
  • increased sensitivity
  • (not 1st choice of drugs) (BLUE ON PPT)
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15
Q

Etomidate renal implications?

A
  • Highly metabolized to pharmacologically inactive compounds
  • <3% of administered dose found unchanged in urine
  • shorter elimination half life than thipental
  • inhibits 11-b-hydroxylase–> last conversion to cortisl
  • NO change in dosing for renal disease
  • Green on ppt
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16
Q

Ketamine renal implications?

A
  • Biotransformed in the liver
  • Norketamine is active metabolite (1/5 to 1/3 as potent)
    • may contribute to prolonged effects
  • <4% unchanged in urine
  • NO change in intiial dosing
  • May need to reduce subsequent dosing and infusion rate
    • good renal overall!
  • Green on ppt- good to give
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17
Q

Propofol renal implications?

A
  • Clearance exceeds hepatic blood flow (extra hepatic sites)
  • metabolites excreted in urine
  • renal dysfunction does not alter clearance
  • NO change in dosing
    • ​however, vasodilator so need to watch BP
  • Green on ppt
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18
Q

Dexmedetomidine renal implications?

A
  • Sedation and anxiolysis
  • extensive hepatic metabolism (methyl and glucuronide)
  • extensive renal excretion of metabolites
    • active metabolites
  • reduce dosage in patients with renal insufficiency
    • d/t sedation
    • Blue on ppt!
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19
Q

Midazolam renal implications?

A
  • Eliminiation 1/2 time, Vd, and clearance not altered
  • NOchange in bolus dosing; may need to decrease infusion
  • metabolite 1-hydroxymidazolam is about 1/2 as potent as midazolam
  • rapidly conjugated to 1-hydroxymidazolam glucuronide and cleared by kidney
    • may accumulate in kidney failure
  • Blue on ppt!
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20
Q

Diazepam renal implications?

A
  • Highly lipid soluble and extensively protein bound- altered PB, more free drug in renal)
  • renal insufficiency is associated with increased plasma concentrations
  • multiple active metabolites
  • use with caution in renal failure patients
  • prolonged respiratory depression
  • RED ON PPT!! DO NOT GIVE
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21
Q

Methoxyflurane renal implications?

A
  • extensive metabolism- 70% to inorganic fluroid
  • avoid in renal failure patients
  • fluoride-induced nephrotoxicity
    • polyuria, hypernatremia, hyperosmolarity, increased plasma cretine, and inability to concentrate urine
  • <40 umol/L- below toxicity
  • 50-80 umol/L- subclinical toxicity
  • >80umol/L- clinical toxicity
  • >50 umol/L as indicator of toxicity
    • peak values alone not enough for dx of renal problems
  • RED ON PPT!
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22
Q

Halothane renal implications?

A
  • Decreased RBF, GFR, UOP r/t decrease in BP
  • 20% metabolized with metabolites renally excreted
    • trifluroacetic acid and bromide
  • RED ON PPT!
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23
Q

Enflurane renal implications?

A
  • Decreased RBF, GFR, and UOP r/t decrease in BP
  • 2-5% metabolized with metabolites renally excreted
    • fluoride ions
    • renal failure following enflurane has been reported
    • genetics?
  • RED ON PPT!
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24
Q

Isoflurane renal implications?

A
  • Decrease RBF, GFR, UOP
  • Metabolized to trifluoroacetic acid
  • prolonged sedation >24 hours have fluoride ions 15-50 umol/L
  • no renal impairment!
    • GREEN ON PPT
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25
Q

Desflurane renal implications?

A
  • Decreases RBF, GFR, and UOP
  • minimal metabolism
  • no evidence of nephrotoxic effects
  • no renal impairment
    • ​GREEN ON PPT!
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26
Q

Sevoflurane renal implications?

A
  • 3-5% biodegradation
  • inorganic fluroide ions
    • F ions the same or higher than enflurane
    • can be >50 umol/L
  • increased NAG (B-N-acetylglucosaminidase)
    • indicator of acute proximal renal tubular injury
    • BUN and plasma creatinine did not change
      • humans have much more NAG than rats, no damage from sevo in humans
  • CO2 absorbers
    • base -catalyzed degradation
    • vinyl ether compound called compound A
      • renal PCT injury in rates
    • barium hydroxide>soda lime
  • No renal failure notes in low flow or clsoed circuit anesthesia
    • ​most still practice >2 L flow
  • GREEN ON PPT!
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27
Q

Morphine renal implications?

A
  • RED DO NOT GIVE
  • Renal metabolism makes significant contributions morphine metabolism
    • no differencein clearance rates even in pt with cirrhosis
  • M6G (active/75-85%) and M3G (inactive 5-10%)
  • 1-2 % unchanged in urine
  • about 90% excreted by kidneys with the rest via biliary excretion
  • accumulation of metabolites may occur in patients with renal failure
    • prolonged respiratory depression > 7 days reported
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28
Q

Meperidine renal implications?

A
  • RED ON PPT!
  • Hepatic metabolism to normeperidine
  • urinary excretion is principal eliminiation route
  • is pH dependent
    • acidification of urine may speed eliminiation
  • 1/2 life is about 15 hours, up to 35 hours in patients with renal failure
  • normeperidine produces CNS stimulation and toxicity can manifest as myoclonus and seizures
  • in patients receiving meperidine for >3 days- delirium may be observed
    • espeically in the elderly
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29
Q

Fentanyl renal implications?

Sufentanil?

A

all safe renal!!– GREEN ON PPT!

​Fentanyl:

  • metabolized to norfentanyl (minimally active)
  • <10% excreted unchanged in urine
    • detected for 72 hours
  • prolonged respiratory depression in chronic renal failure patients

Sufentail:

  • <1% unchanged
    • n-dealkylation metabolites are considered active
  • maximal renal tubular reabsorption of free drug(why?)
  • metabolites excreted equally between renal/biliary
  • prolonged respiratory depression in chronic renal failure patients
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30
Q

Alfentanil? Remifentanil renal implications?

A

Alfentanil

  • Eliminations 1/2 time and plasma clearance not altered
  • protein binding is reduced and free drug increases
  • <1% excreted unchange

Remifentanil

  • with renal failure
    • no changes in PK and PD
  • In patients on HD
    • reduced clearance and prolonged elimination 1/2l life
    • lower infusion rate required

BOTH GREEN ON PPT!

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31
Q

Hydromorphone renal implications?

A
  • Hepatic metabolite- hydromorphone 3-gluconoride (inactive)
    • potential to accumulate in renal failure- neurotoxic (more theoretical than clinical implications)
  • <1% free hydromorphone excreted in urine
  • caution in renal failure patients
    • Blue on ppt!
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32
Q

Methadone renal implications?

A
  • Metabolite pyrrolidine (inactive)
  • 20-50% excreed as methadone
  • 10-45% in feces
  • safe to use
    • gree on ppt!
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33
Q

Oxycodone renal implications?

A
  • Metabolites noroxycodone (inactive) and oxymorphone (active)
  • prolonged from 2.3 hours- 3.9 hours in patients with renal failure
  • reduce dose and increase interval
    • ​blue on ppt!
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34
Q

Hydrocodone renal implications?

A
  • metabolizes to hydromorphone
    • hydromorphone 3 glucuronide (neurotoxic)
  • decreased clearance in patients with renal disease
  • reduce dose and increase interval
    • blue on ppt!
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35
Q

Succinylcholine renal implications?

A
  • Hyperkalemia
    • 0.5-1 mEq/dL increase in potassium
    • renal failure patients are no more susceptible to exaggerated response to succinylcholine than normal patients
  • infusion problematic
    • succinylmonocholine (metabolite)
      • weaker NMB with longer DOA
  • Green on ppt!
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36
Q

Mivacurium renal implications?

A
  • Metabolized by butyrlcholinesterase
  • longer DOA and slower rate of recovery in patients with CKD
  • Induction dose OK
    • DOA may be increase in 10-15 min
  • Green on ppt!
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37
Q

Atracurium and Cisatracurium renal implications?

A

Atracurium

  • hoffman elimination and ester hydrolysis
  • OK in renal failure patients
  • laudanosine metabolite (30% renal)
    • plasma 1/2 life same in both normal and renal failure patients

Cisatracurium

  • hofmann elmiination (77% of elimination)
  • OK in renal failure patient
  • 16% renally eliminated
  • 4-5x as potent as atracurium, so less laudanosine metabolites

Both green on ppt!

38
Q

Pancuronium renal implications?

A
  • Long acting NM blocking drug
  • 40-60% cleared through the kidneys
    • avoid
  • metabolites are less potent and renally excreted
  • Red on ppt!
39
Q

Vecuronium renal impliactions?

A
  • Metabolized in liver to 3 diff metabolites
  • 3-OH vecuronium has 80% potency of vec
  • approximately 40% excreted uncahnged by kidney
  • single dose fine, but multiple doses/infusions may require adjustment
  • Blue on ppt!
40
Q

Rocuronium renal implications?

A
  • Primarily eliminated by the liver and excreted in the bile
  • NO active metabolites
  • approximately 30% excreted unchanged by the kidney
  • single dose fine, but multiple doses/infusions may require adjustment
    • ​blue on ppt!
41
Q

Cholinesterase inhibitors?

A
  • Neostigmine, pyridostigmine, physostigmine and edrophonium
  • renal excretion accounts for 50-75% of the drugs
  • renal failure decreases plasma clearance as much, if not more than, the long acting neuromuscular blocking drugs
  • Blue on ppt
42
Q

Sugammadex renal implications?

A
  • 75% of dose is eliminated through the urine
  • clearance approaches GFR
  • with substantial renal impairment, clearnace of sugammadex/roc was decreased and elimination 1/2 life was increased
  • dialysis is inconstant in remove suggammadex
  • DO NOT use if creatinine clearance <30 mL/hr
    • ​blue on ppt!
43
Q

Surgical direct effects on kidneys?

A
  • Pneumoperitoneum
    • increased intraabdominal pressure
      • venous compressiona dn decreased CO
      • Renal parenchymal compression
  • bypass
  • aortic cross clamp
  • dissection near renal artery
44
Q

What are indirect effects on renal system from surgery?

A

inflammatory response

45
Q

Acute kidney injury? Occurance? Postop AKI?

A
  • Rapid deterioration of kidney function over hours to days
  • Occurs:
    • all hospitalized- 5%
    • critically ill 8-10%
  • Postop AKI
    • general 1%
    • cardiothoracic and vascular 30%

preoperative AKI increases: hospitalization, mortality, and morbidity

46
Q

Causes of prerenal AKI?

A
  • Absolute decrease ECBV (extracellular blood volume?)
    • hemorrhage
    • volume depletion
  • Relative decrease BV
    • CHF
    • cirrhosis
  • Renal artery
    • stenosis
    • thrombosis/embolism
    • NSAID
    • ACE/ARB
      • blocking enzymes in RAAS, can’t regulate BP as well, kidney more susceptible to hypotension
47
Q

Intrarenal AKI causes?

A
  • ATN
    • ischemic
    • toxic
      • exogenous
        • abx
        • contrast
        • chemo
      • endogenous
        • pigment
        • MM
        • crystals
  • vascular
    • malignant hyertension
    • vasculities
48
Q

Postrenal causes AKI?

A
  • Bladder outlet obstruction
  • bilateral ureteral obstruction
49
Q

Preoperative risk factors for perioperative renal failure?

A
  • Preexisting renal insufficiency
  • advanced age
  • heart disease (CHF, ischemia)
  • smoking
  • DM
  • LIver failure
  • pregnancy-induced hypertension
  • ASA physical status 4 or 5
50
Q

Intraoperative facotrs increase risk for renal failure

A
  • emergency, intraperitoneal, intrathoracic, suprainguinal vascular, transplant surgery
  • aortic cross clamping
  • CPB
  • inotrope use
  • erythrocyte transfusion
51
Q

Postoperative risk factors for perioperative renal failure?

A
  • erythrocyte transfusion
  • vasoconstrictor use
  • diuretic use
  • antidysrhythmic use
  • sepsis
  • nephrotoxins (radiocontrast dyes, NSAID, aminoglycoside antibiotic)
52
Q

Diagnosis/classification of renal injury?

A
  • Increase of serum creatinine of 0.3 mg/dL over 48 hours
  • increase of serum creatinine >50% over 7 days
  • acute drop of UOP to <0.5 mL/kg/hr for >6 hours
  • anuria <100 mL/day- sign of severe injury
53
Q

What are some biomarkers to look at with AKI?

A
  • Neutrophil gelatinase-associated lipocalin (NGAL)
    • induced by renal tubular cells folowing ischemia/reperfusion injury
    • promising
  • Cystatin-C
    • produced by all nucleated cells and is freely filtered, but not absorbed by kidneys
    • maybe used as a measure of GFR; more accurate than creatinine estimates
  • IL- 18
    • synthesized in proximal tubular cells and cells that mediate infalmmatory response
    • indicate more general inflammation than kidney damage
  • kidney injury molecule
    • membrane protein expressed in injured proximal tubular epithelial cells
    • still being defined
  • renal tubular cell enzymes
    • alpha gluthion, s-transferase, N-acetyl-B-D-glucosaminidase

Panel is better–> in general, no single indicator of renal failure

54
Q

AKI phsyiolgical effects?

A
  • Neurological: confusion and somnolence to sz
  • CV: HTN, CHF, pulmonary edema
  • Hematological: anemia and coag
  • metabolic: hyperkalemia, hyperphosphatemia, hypocalcemia, metabolic acidosis
  • GI: N/V, GI bleeding (1/3 of patients)
  • Infection: impaired immune response; respiratory/urinary tracts
55
Q

AKI management?

A
  • No speicifc treatment modalities for AKI
  • Limiting further injury and correcting deragnement
  • correct hypovolemia, hypotension and low CO
    • maintain MAP>65 mmHg
    • Fluids
      • NS/Plasmalyte perferred
        • but NS can bring r/f hyperchloremic metabolic acidosis as well
    • Vasopressors
      • NE vs vasopressin vs phenyl vs dopamine
    • Protection
      • n-acetylcystein or alkalinization of urine
        • can cause anaphylactoid reaction
56
Q

AKI Prognosis?

A
  • Poor - mortality >20%
  • if dialysis required >50%
  • 15% will fully recover
  • 5% will have renal insufficiency and remain stable
  • 5% wille xperience continued renal function deterioration
57
Q

AKI in anesthesia?

A
  • Only lifesaving sx should be undertaken
  • Premed: H2 blocker/PPI/reglan
  • Monitoring
    • intraarterial BP for frequent blood draws
  • Induction
    • RSI with reduced dosages of induction drugs- delayed gastric emptying
    • succinylcholine if K known
  • Maintenance
    • volatile anesthetic vs TIVA
      • propofol has very little impact, just need to watch for hypotension
    • Controlled ventilation
58
Q

Indications for dialysis?

A
  • Fluid overload
  • hyperkalemia
  • severe acidosis
  • metabolic encephalopathy
  • pericarditis
  • coagulopathy
  • refractory GI symptoms
  • drug toxicity
59
Q

Complication of hemodialysis

A
  • Neurological: disequilibrium syndrome (wide fluid shift)
  • Cardiovascular: volume depletion; arrhythmia
  • pulmonary : hypoxemia
  • GI: ascites
  • hematological: anemia, residula anticoagulation
  • metabolic: hypokalemia; large protein loss
  • skeletal: osteomalacia; myopathy
  • infectious: peritonitis
60
Q

What is chronic kidney disease?

A
  • Kidney damage (GFR <60 mL/MIN) for 3 or more months
  • DM &HTN most common cuase
  • mutliple diff stages of CKD
  • GFR <25 mL/min require dialysis or transplant
    • ethnic variations
      • african american, native american and hispanics have higher rates
61
Q

Stages of CKD?

A

adaptation- large renal reserve

  • Stage 1
    • Decrease of >50% of GFR
    • changes in excretion of creatinine and urea
  • Stage 2
    • GFR 10% of normal
    • changes in solutes such as potassium
  • Stage 3
    • variable
    • changes in sodium homeostasis and regulation of ECF
62
Q

Complications of CKD?

A
  • Uremic syndrome
  • renal osteodystrophy
  • anemia
  • uremic bleeding
  • neuro change
  • CV changes
  • altered protein binding of drugs
    • acidic drugs: less binding
63
Q

Treatment of CKD?

A
  • Treat underlying cuase
  • lower BP
  • adequate nutrition and protein restriction
  • treat anemia
  • RRT (renal replacement therapy)
    • hemodialysis
    • peritonela dialysis
64
Q

Preop eval of CKD?

A
  • Goal: preserve renal function and prevent kidney injury
  • renal function- is a continuum: trends in lab values more important
  • stop nephrotoxic drugs: NSAIDS/Aminoglycosids/contrast agent
  • Volume status- dry and wet weights
    • drug admin: bolus vs infusion (based on esimated Vd)
  • Labs:
    • K<5.5 on DOS
    • H/H 10/30
    • Coags DDAVP may be required- helps release von willbrand factor and helpts PLT aggregate
  • HTN therapy- well contorlled; ACE/ARB therapy (hold?)
  • DM management: target glucose 110-150 mg/dL
  • GI: prophylaxis- all drugs renally secreted
65
Q

Monitors/lines needs with CKD

A
  • Minor/moderate: noninvasive monitors OK (not on fistula arm)
  • Complex: aline/cvp/picco/tte or TEE
    • where to place?
      • avoid radial/ulnar/brahcial/axillary
      • use doraslis pedis or femoral
  • Lines
    • peipheral
      • lower arm or dominant hand
      • can dialysis catheter be used or anesthesia?
        • yes, but highly discouraged and proper care is imporant
    • Central
      • maybe dififcult to place
66
Q

Induction of CKD patient?

A
  • Speicfic agent not as important as prevention of severe hypotension
    • multiple cuase
    • smaybe severe
    • treatment: replace volume before induciton
    • small doses or brief infusion of phenylephrine or NE ok
  • RSI
    • can use succinylcholine if K >5.5 and necessary
    • no exaggerated release of K in CKD patients
67
Q

Maintenance in patients with CKD?

A
  • Blanaced technique
    • combo of volatiles, opioids, and MR
    • maintain MAP >65 (>75 mmHg with chronic HTN)
      • NE or phenlephrine
      • risk increases with MAP <60 for 20 min of <50 for 10 min
  • Check position frequently- neuropathy
  • Fluid mgmt
    • 500 mL bag with 60 gtt tubing
    • NS vs 1/2 NS vs LR vs plasmalyte
    • 5% albumin ok
    • blood products for those that require increased oxygen carrying capacity
  • UOP
    • At least 0.5 cc/kg/hr
    • decrease most likely d/t low volume
    • use of diuretics or vasodilators is controversial
68
Q

Emergence in CKD patient?

A
  • Muscle relaxation
    • recurization possible- continue to monitor
  • ECG monitoring
    • electrolyte abnormalities
  • HTN
    • NTG or SNP
    • clevidipine or esmolol
      • both short acting, by esterases?
69
Q

Neuraxial in CKD?

A
  • Coagulopathy and peripheral neuropathy is a concern
    • evaluate coag panel
    • monitor closely
  • Maintain MAP
  • T4-T10 level may improve renal function
70
Q

Regional anesthesia in CKD?

A
  • Doc peripheral neuropathies prior to placement
  • improved surgical conditions
    • max vasodilation (greater blood flow), abolish vasospasm
    • no changes in DOA
71
Q

Preoperative anesthetic consideration of renal endoscopic procedures?

A

Tumor

  • older patients with many diff preexisting conditions
  • CAD, CHF, PVD, COPD and renal impairment

Nephrolithiasis

  • paraplegics and quadriplegics have chance for stones
  • multiple procedures
  • contractions may make positioning difficult
72
Q

Intraoperative considerations for renal endoscopic procedures?

A
  • Topical- not recommended
    • 2% lidocaine jelly with sedation
  • Regional
    • may require a T8 level for procedures involving the ureters
    • does not abolish obturator reflex (external rotation and adduction of thigh)
  • Spinal- Quick onset but will stick around, not good for PACU flor
    • <1 hour 7.5 gm of 0.75% bupi
    • >1 hours 10-12 mg of 0.75% bupi
    • why not lidocaine? (TNS)
  • Epidural
    • 2% lidocaine with epi
    • 15-25 mL
    • takes time to set up
73
Q

Anesthetic consideration for renal endoscopic procedures with GA?

A
  • Monitors: standardized
  • positioning: supine to lithotomy
  • induction: standard
    • ETT vs LMA- need to hold breath to stop stone from moving
    • succinylcholine? if K <5.5, ok
  • Maintenace
    • VA vs TIVA
    • muscle relaxation to obtund the obturator reflex
  • Emergence
    • no specifics
74
Q

Complications of anesthetics with renal endoscopic procedures?

A
  • Decrease BP when lowering legs
  • peroneal nerve injury
  • bladder perforation
    • shoulder pain
  • autonomic hyperreflexia
    • spinal cord injury above T10 (T5 severe manifestations)
    • severs HTN, bradycardia, dysrhythmias and cardiac arrest
    • TXMT: deepen level of anesthesia
    • labetalol 5-10 mg IV
    • SNP 0.5-5 mcg/kg/min
75
Q

ESWL?

A
  • shock waves focused at calculi in kidney or upper 2/3 of ureter
  • 10-20 mm stones or impacted stone
  • 1st gen
    • high energy unit
    • pt immersed in water bath
  • 2nd gen
    • low energy unit
    • uses small water filling coupling device/pad
    • tightly focused sound beam
76
Q

Preop considerations for ESWL?

A
  • 1st gen ESWL- cv/resp changes
  • 2/3gen minimal hemodynamic changes
  • absolute contraindications
    • pregnancy, bleeding disorder, or active UTI
  • Relative
    • presence of abdominal aortic aneurysm or othopedic prosthetic device
    • pt with pacemaker or AICD risk for arrhythmias
      • shock synchornized to 20 mms after R wave (refracotry period)
      • shcok waves can damage the device
77
Q

Intraoperative ESWL considerations?

A
  • Immbolization is very important to limit shock zoen no matter the anesthesia choice
  • General
    • does not decrease the # of shocks required
    • greatest control (espeically ventilation)
    • 1st gen- muscle relaxation for movement
    • 2/3rd gen- limit stone movement
  • Neuraxial
    • T6 level required
    • 1st gen-
      • epidural most common
        • use saline (air can dissipate shcock waves and damage tissue
        • do not use foam tape (dissipate shock wave energy)
      • spinal- less control
    • 2nd gen- spinal (opioids only 50 mcg sufentanil)
  • 2nd/3rd gen
    • TOPICAL- EMLA cream
    • Local infiltration +/- sedation
      • TAP block +/- intercostal block
    • sedation
      • midaz/fent
      • propofol gtt
  • Fluid mgmt
    • liberal admin
    • surgeon may request small doses of furosemide to increase uop and stone removal
78
Q

Postop ESWL considerations?

A
  • Bleeding
    • moderate to severe (self limiting)
  • Perforation or rupture of hollow organs
79
Q

What is a TURP?

A

transurethral resection of prostate

  • Vaporization
    • electocuatery or laser
      • KTP (pvp/greenlight)
      • most common
    • thermocoagulation
      • lase, microwave or radiofrequency
80
Q

Summary of TURP procedure?

A
  • Position: lithotomy or steep trendelenburg
  • special instrumentation: laser or da vinci robot
  • unique consideration; immobility is a must
  • abx: gentamicin 80 mg IV
  • Surgical time <2 hours (longer if using robot)
  • EBL 500 mL (2-5mL/min of resection
  • Postop: irrigation of foley to clear; serum Na concentration
  • morbidity: bleeding or absorption of irrigation fluid
  • pain 1-3
81
Q

Preop consideration of TURPs?

A
  • Patient’s are generally elderklyl with comorbid conditions
  • resp: copd common
  • cv: cad/htn common
  • neuro: cerebrovascular disease
  • renal: renal impairment secondayr to obstruciton
  • endocrine: DM]]
  • heme: if gland >80 grams, need T&C
82
Q

Anesthetic consideraiton for use of neuraxial anesthesia with TURPs?

A
  • Require T9-T10 level
  • 1.6-2 mL of 0.75% bupi
  • 2-3 mL of 0.5% bupi
    • adjuncts: dexmedetomidine or fent
  • Potential for earlier detection of TURP syndrome
  • incidence of post dural puncture headache is very low
83
Q

General anesthesia in TURPs?

A
  • Induction: standard
  • Maintenance: balanced (va/nitrous/opioids)
    • minimal to mod blood loss (if venous sinuses entered)
      • difficult to detect with irrigation fluid
    • irrigation 1.5% glycine, NS, or sorbitol./mannitol mixture (rare)
  • Emergence: minimal pain; changes in BP with lowering legs
    • airway edema with steep trendelenburg
  • Complication: bladder perforation, TURP syndrome, blood loss, or vision problems
84
Q

What is the TURP syndrome physiology?

A
  • Continous irrigation fluid-visibility and wate removal (blood/tissue)
  • incidence: 0.78-1.4% with 25% mortality if severe
  • time frame: 15 min- 24 hours postop
  • resection of prostate opens large venous sinuses and large amt of irrigation fluid can be absorbed
    • 10-30 mL/min
    • 6-8 L in cases that last 2 hours
    • can decrease serum sodium 5-8 mEq/L
    • keep height <60 cm above bed height
      • decreases pressure
  • Various types of fluid used
    • based on type of equipment used
    • 1.2-1.5% glycine (monopolar cautery) - helps prevent electrical current
    • physiological saline (bipolar or lasers)
85
Q

Clinical features of TURP sydnrome?

A
  • Fluid overload- HTN/Bradycardia/pulmonary edema
  • water toxicity- confusion/restlessness/seizure/lethargy
  • hyponatremia- CNS changes/wide QRS/ T wave inversion
  • glycine toxicity- N&V/HA/Transient blindness/loss of light reflex
  • ammonia toxicity- N&V
  • Hemolysis- anemia/clammy skin/hyperkalemia
  • coagulopathy- severe bleeding/DIC
86
Q

Treatment for TURP syndrome?

A
  • Terminante sx ASAP
  • Fluid restriction
  • fursoemide 20 mg IV
  • Eval: chem, CBC, glucose, ABG, obtain 12 lead EKG
  • Start/continue NS infusion
    • Na <120 mEq/L must be treated to goal of 120 mEq/L
    • 3% NS for Na <100 at rate of <100 mL./hr
  • For seizure: midazolam
  • CXR for pulm edema
  • DIC
    • blood products
  • CV collapse- ACLS
87
Q

Preop consideration for scrotal procedures?

A
  • Elderly- metastatic prostate ca accompanied by othe rmed conditions
  • young- tosions
    • emergent operations- needs to occur within 6 hours to prevent irreversible occurence
88
Q

Intraop consideraiton for scrotal procedures

A
  • Sensory level of T10 is required
  • Spinal- same as others
  • epidural - same as others
89
Q

General anesthesia in scrotal procedures?

A

same as before

deeper level of anesthesia are usualyl required to obtund autnomic reflexes that result from intense surgical stim

90
Q

Postop anesthesia consideration for scrotal procedures?

A
  • peroneal nerve injuyr
  • pain
    • toradol
    • ilioinguinal/iliohypogastric nerve block
91
Q

What neuroaxial level is required for:

ESWL?

Endoscopic renal procedures?

TURP?

Scrotal?

A

ESWL= T6 level

Endoscopic= T8

TURP = T9-T10

Scrotal= T10

Co-exist Test 2 (3 decks)

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