Renal

Question 1

What are some functions of the kidneys?

Answer 1

Responsibilities/ contributions:

• Water conservation
• Electrolyte homeostasis
  
  • osmolality
• Acid-base balance
• Neurohumoral/ hormonal functions
  
  • hormones involved with: fluid homeostasis, bone metabolism and hematopoiesis
• Waste filtration
  
  • excretion of end products of metabolism nd drugs

Question 2

What is the nephron?

Answer 2

• fundamental unit of the kidney
  
  • Composed of a vascular network close to a series of tubules with distinct physiologic functions that empty into collecting ducts to form urine.
  • Approximately 1 million nephrons in the normal kidney.
  • Receive about 20% of the cardiac output and are responsible for 7% of total body oxygen consumption
• Nephron Anatomy:
  
  • Bowman’s capsule
  • Proximal convoluted tubule
  • Loop of Henle (ascending/descending)
  • Distal tubule
  • Collecting duct

Question 3

What controls blood flow through the kidneys?

Answer 3

• Autoregulatory mechanisms control renal blood flow within a broad range of pressures to maintain a stable GFR.
• Factors and diseases might disrupt renal autoregulation, leading to ischemia and kidney injury. These include:
  
  • hypertension,
  • kidney disease,
  • major surgery,
• Reduced renal blood flow leads to renal hypoxia, inflammation, and fibrosis, which induce microvascular dysfunction in hemodynamic compromised conditions
• Kidney disease can result from disturbances of within
  
  • vascular,
  • glomerular
  • tubular components.
• Knowledge of these factors is important to anesthesia providers to limit decrements in renal function during the perioperative period.

Question 4

Comparison of blood flow and tissue oxygenation throughout the kidney?

Answer 4

• RBF, O2 delivery, O2 consumption of Cortex > Medulla
• Severe hypoxia can develop
  
  • kidneys receive 20% of total CO but extract relatively little O2
  • medulla** only receives **small fraction of total RBF** and flow rates are **extremely slow
    
    • ​tissue oxygen tension is extremely low and medulla extracts close to 80% of O2 delivered to it
    • ​very mild reduction in flow can cause ischemia and hypoxia in renal medulla
• Thick ascending loop of Henle is vulnerable (this is in the medulla as well)
  
  • very metabolically active
  • vulnerable to ischemia during times of reduced blood flow

Question 5

What are the anatomic divisions of the nephron?

Answer 5

• Bowman’s capsule: participates in filtration of blood; creates urinary space
• Glomerulus: tuft of capillaries; filters plasma to produce glomerular filtrate
• PCT: reabsorption of water, ions, organic nutrients
  
  • system begins with proximal convoluted tubule
  • high-density of mitochondria and extensive surface area of apical and basilar cell membranes mark the renal tubule and high energy requireent
  • 80% of energy is for Na/K ATP ase which maintains the osmotic gradient needed for resorption of filtered boluecules
  • even though high energy demand, tubule system supplied by only 10-15% RBF. This is the key etiology behind acute tubular necrosis after hypotensive events
• LOH (thin & thick): reabsorption of water and sodium & chloride ions
  
  • proximal tubule leads to thinner epithelium of descending thin loop of henle
  • then turn 180 degrees to ascending loop of henle
  • 80% of nephrons begin in cortex and have short loops of henle that only go to outer medulla
  • remaining 20% juxtamedullary nephrons start at corticomedullary junction and have more elongated loops of henle that go to the most distal extent of medulla
• DCT: secretion of ions, acids, drugs, toxins; variable reabsorption of water, sodium ions, calcium ions
  
  • have juxtaglomerular apparatus that comprised of specialized epithelial cells called macula densa
  • essential for maintenance of BP
• CD: variable reabsorption of water. reabsorption or secretion of sodium , potassium, hydrogen and bicarb ions
  
  • empties ultrafiltrate into renal pelvis and then ureters

Question 6

What is GFR? Normal ranges?

Answer 6

GFR: measurement of volume filtered through the glomerular capillaries and into the Bowman’s capsule per unit of time

• Considered best indicator of renal function
  
  • Based on patient size/gender/weight/age
• GFR can be calculated from timed urine volume measurements
• Calculation of creatinine clearance is a less accurate method to evaluate GFR
  
  • Cockcroft-Gault Equation – typically underestimates GFR by 10 - 20%
• Ranges
  
  • Normal: 90 - 140 mL/min
    
    • Decreases with age
      
      • about 10%/decade after age 30
  • Abnormal: < 60 mL/min – start altering anesthesia medications
  • Failure: < 15 mL/min
    
    • a/w uremic symptoms and may require dialysis

Question 7

What are the stages of CKD? Manifestations?

Answer 7

• 5 GROUPS
  
  • Stage 1 GFR >90- kidney damage with normal kidney function
  • Stage 2 GFR 60-89mL/min- kidney damage with mild loss kidney function
  • Stage 3 GFR 30-59mL/min
  • Stage 4 GFR 15-29 mL/min
  • Stage 5 GFR <15 mL/min

Manifestations of reduced GFR not seen until 50% normal

• GFR 30% normal, moderate renal insufficiency ensues
  
  • patients remain asymptomatic withonly biochemical evidence of decline GFR (urea/cr increase)
  • further workup reveals symptoms such as nocturia, anemia, loss of energy, decreased appetite, abnormalities in calcium and phos metabolism
• As GFR decreases further- severe renal insufficiency
  
  • profound clinical manifestation uremia and biochemical abnormlaities (academia, volume overload, neuro, cardiac and respiratory manifestations
• GFR 5-10% need renal replacement therapy

Question 8

What is creatinine clearance?

Answer 8

• Specific test for GFR – most reliable assessment tool for renal FCN (however GFR is best indicator of renal function?!)
• Measures ability of glomeruli to excrete creatinine
  
  • Normal: 95 – 150 ml’s/min
  • Mild dysfunction: 50 – 80 ml’s/min
  • Moderate dysfunction: < 25 ml’s/min
  • Anephric: < 10 ml’s/min

Question 9

What is creatinine?

Answer 9

• Creatinine is product of muscle metabolism
  
  • creatine is product of muscle metabolism that is nonenzymatically converted to creatinine
  • rate of creatinine production, and volume of distribution, may be abnormal in critically ill patients
  • single serum creatinine measurement often not accurately reflect GFR in physiological disequilibrium of AKI
• Serum creatinine directly r/t body muscle mass
  
  • creatinine is generally neither secreted nor reabsorbed in kidney
  • amount that appears in urine in specified time interval refects amount filtered at glomerulus.
• Can be used to reliably estimate GFR in non-critically ill patient
• Normal (reflects differences in skeletal muscle mass):
  
  • Men- 0.8-1.3 mg/dL
  • Women- 0.6-1.0 mg/dL
• Slow to reflect acute changes in renal function
  
  • Ex. if acute injury occurs and GFR decreases from 100 mL/min to 10 mL/min, serum creatinine values do not increase for about a week

Question 10

What is BUN?

Answer 10

Blood Urea Nitrogen

• Primary source is liver (protein catabolism)
  
  • BUNdirectly related to protein catabolism and inversely related to GFR
• Not a reliable indicator of GFR (unless protein catabolism is normal and constant)
  
  • 40-50% passively reabsorbed by renal tubule
  • Hypovolemia increases this
• Influenced by:
  
  • dietary intake
  • coexisting dx
  • intravascular fluid volume

Values:

• Normal 10 -20 mg/dL
• 20 – 40 mg/dL: dehydration, high catabolism, decreased GFR
• > 50 mg/dL indicate impairment of renal function
• Increased BUN with normal serum creatine suggests nonrenal cause
  
  • ​high protein diet
  • GI bleed
  • dehydration
  • febrile illness
• BUN concentrations higher than 50 mg/dL usually indicate decreased GFR

Question 11

What is fractional excretion of sodium measuring?

Answer 11

• Fractional Excretion of Sodium- measure of percentage of filtered sodium that is excreted in urine
  
  • shows renal tubule function
  • FE_Na is a measure of sodium clearance as a percentage of creatine clearance.
  • calculated by simultaneous samples of blood and urine collection
  • FE_Na is measure of % filtered sodium excreted in urine. filtered sodium dvidied by GFR
• Useful to distinguish hypovolemia and renal injury (ie acute tubular necrosis)
• FENA > 2% (or urine sodium concentration > 40 mEq/L) reflects decreased ability of the renal tubules to conserve sodium and is consistent with tubular dysfunction
  
  • ​acute tubular necrosis causes impairment in concentrating ability of nephrons, therefore Na and water will be lost in the urine
• FENA < 1% (or urine sodium excretion < 20 mEq/L occurs when normally functioning tubules are conserving sodium
  
  • ​in dehydration, nephrons are trying to conserve Na and water, therefor less is in the urine

Question 12

What is measured in a urinanalysis?

Answer 12

Urinalysis- index of kidney’s concnetrating ability, specifically renal tubular function

• Specific gravity
  
  • Measures solutes in urine
  • Kidney’s ability to excrete concentrate/dilute urine
  • Normal 1.003 to 1.008 (> 1.018 indicates reasonable function)
    
    • dx of renal tubular dysfunction is established by demonstarting kidneys to not produce adequately concentrated urine
• Proteinuria- common and present in 5-10% of adults
  
  • > 150 mg/day- can be normal
    
    • ​greater amounts can be present after strenuous exercise of standing for several hours
  • > 750 mg/day indicates sever glomerular damage
  • More likely to develop AKI
    
    • transient proteinuria may be associated with fever, CHF, seizure activity, pancreatitis, and heavy exercise
    • persistent proteinuria generally connotes significant renal disease
• Microscope
  
  • RBC (bleeding), WBC (infection), Casts (disease of nephron) or crystals (metabolism)

Question 13

What are biomarkers?

Answer 13

• new techniques that allow direct measurement of GFR at bedside and can provide early detection of AKI
• Vary in anatomical origin, physiological function, and time of release after onset of injury
• Dividide into functional and damage biomarkers
• patients with biomarker positive, creatinine negative “subclinical” AKI have worse prognosis than those without a positive biomarker test

Question 14

Examples of biomarkers given in clase (unsure if she’d test over these?)

Answer 14

• Neutrophil gelatinase-associated lipocalin (NGAL)
  
  • Induced by renal tubular cells following 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 inflammatory 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
  
  • α – gluthione, S – transferase, N-acetyl-β-D-glucosaminidase
• Panel vs. single marker?

Question 15

Impact of anesthesia on renal function?

Answer 15

• all generl anesthetics decrease GFR and intraoperative urine flow d/t decreased CO and BP
• iInjury more common with:
  
  • preexisting renal disease
  • nephrotoxic injury
  • hypovolemia
  • combination of these factors which exacerbate renal dysfunction
    *

Question 16

Use of thiopental in renal disease?

Answer 16

• Reduced plasma protein binding (increased amount of free drug)
  
  • increases free fraction of induction dose (almost doubled)
  • accounts for exaggerated clinical effects seen with thiopental in CKD patients
• Increased volume of distribution
• May undergo some metabolism in the kidneys
• Decrease initial dose

Question 17

Etomidate use in renal patients?

Answer 17

• Highly metabolized to pharmacologically inactive compounds
• < 3% of administered dose found unchanged in urine
• Shorter elimination half life than thiopental
• Inhibits 11 β hydroxylase
• NO change in dosing

Question 18

Use of ketamine in renal patients?

Answer 18

• Biotransformation in the liver
• Norketamine is active metabolite (1/5 to 1/3 as potent)
  
  • further metabolized before excreted by kidney
• May contribute to prolonged effects
• < 4% unchanged in urine
• NO change in initial dosing
  
  • ketamine not highly protein bound, renal function has less influence on free fraction
• May need to reduce subsequent doing and infusion rate

Question 19

Propofol use in renal disorders?

Answer 19

• Clearance exceeds hepatic blood flow (extra hepatic sites)
  
  • undergoes extensive rapid hepatic biotransformation to inactive metabolites which are renally excreted
• Metabolites excreted in urine
• Renal dysfunction does not alter clearance
  
  • no prolongation of effects of propofol in renal dysfunction
• NO change in dosing

Question 20

Precedex use in renal failure?

Answer 20

• Sedation and anxiolysis
• Extensive hepatic metabolism (methyl and glucuronide)
• Extensive renal excretion of metabolites
• Reduce dosage in patients with renal insufficiency
  
  • longer lasting sedative effect in subjects with renal impairment
  • most likely explanation is decreased protein binding of preceded in patients with renal dysfunction

Question 21

Midazolam use in renal dysfunction?

Answer 21

• Elimination ½ time, Vd, and clearance not altered
• NO change in bolus dosing; may need to decrease infusion
  
  • use cautiously in renal impairment
• Metabolite: 1-hydroxymidazolam is about ½ as potent as midazolam
• Rapidly conjugated to 1-hydroxymidazolam glucuronide (60-80%) and cleared by kidney
  
  • May accumulate in kidney failure
• benzos as a group are highly protein bound. CKD increases free fraction of benzos in plasma due to low protein.

Question 22

Diazepam use in renal dysfunction?

Answer 22

• Highly lipid soluble and extensively protein bound
• Renal insufficiency is associated with increased plasma concentrations
• Multiple active metabolites
• Use with caution in renal failure patients

Question 23

Use of methoxyflurane (historic VA) in renal dysfunction?

Answer 23

• Extensive metabolism – 70% to inorganic fluoride
• Avoid in renal failure patients
• Fluoride-induced nephrotoxicity
  
  • Polyuria, hypernatremia, hyperosmolarity, increased plasma creatine, and inability to concentrate urine
  • < 40 μmol/L – below toxicity
  • 50 – 80 μmol/L – subclinical toxicity
  • > 80 μmol/L – clinical toxicity
  • > 50 μmol/L as indicator of toxicity
  • Peak values alone not enough for Dx of renal problems
• The nephrotoxicity of methoxyflurane appears to be due to its metabolism, which results in release of the fluoride ions believed responsible for the renal injury. It has been suggested that renal, not hepatic, metabolism of methoxyflurane may be responsible for generating fluoride ions locally that contribute to nephrotoxicity

Question 24

Halothan use in renal dysfunction?

Answer 24

• Decreased RBF, GFR, and UOP r/t decrease in BP and CO
• 20% metabolized with metabolites renally excreted
  
  • Trifluoroacetic acid and bromide
  • halothane oxidized in liver by isozyme of CYP (2EI) to principal metaoblite, trifluoroacetic acid

Question 25

Enflurane use in renal dysfunction?

Answer 25

• 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?
  • Alkaline degradation products conjugated to thiol products

Question 26

Isoflurane in renal dysfunction?

Answer 26

• Decreases RBF, GFR, and UOP
• Metabolized to trifluoroacetic acid
• Prolonged sedation > 24 hours have fluoride ions 15-50 umol/L
  
  • although serum fluoride levels may rise, nephrotoxicity extremely unlikely, even in the presence of enzyme inducers
  • prolonged sedation (>24 hours at 0.1-0.6% iso) of critically ill patients has resulted in elevated plasma fluoride levels, without evidence of kidney impairment
  • up to 20 MAC hours of isoflurane may lead to fluroide levels >50, without detestable postop kidney dysfunction
• No renal impairment

Question 27

Desflurane use in renal dysfunction?

Answer 27

• Decreases RBF, GFR, and UOP
• Minimal metabolism
• No evidence of nephrotoxic effects
• No renal impairment

Question 28

Sevo use in renal dysfuntion?

Answer 28

• 3-5% biodegradation
• Inorganic fluoride ions
  
  • Fl ions the same or higher than enflurane
  • Can be > 50 μmol/L
    
    • not associated with clinically significant renal dysfunction
• Increased NAG (β – N – acetylglucosaminidase)
  
  • Intracellular indicator of acute proximal renal tubular injury
  • BUN and plasma creatinine did not change
• CO2 absorbers with potassium or sodium hydroxide
  
  • Base-catalyzed degradation
  • Vinyl ether compound called Compound A
    
    • Renal PCT injury in rats
    • increased compound A with increased respiratory gas temperature, low flow anesthesia, dry barium hydroxide absorbent (baralyme)
  • Barium hydroxide > soda lime
    
    • alkali such as barium hydroxide lime or soda lime (but not calcium hydroxide) can degrade sevo
  • No renal failure noted in low flow or closed- circuit anesthesia

Question 29

Morphine use in renal dysfunction?

Answer 29

• Renal metabolism makes significant contributions morphine metabolism
  
  • No difference in clearance rates even in patients with cirrhosis
• 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
  
  • M6G (active/75-85%) and M3G (inactive/5-10%)
  • Prolonged respiratory depression > 7 days reported
• Single-dose studies of morphine in renal failure demonstrate no alteration in disposition. Chronic administration may result in accumulation of metabolites which have potent analgesic and sedative effects
• decrease in PB of morphine in ESRD which mandates reduction in initial dose

Question 30

Meperidine use in renal dysfunction?

Answer 30

• Hepatic metabolism to normeperidine
  
  • neurotoxic, renally excreted metabolite
  • not recommended for use in pt with poor renal function
  • Normeperidine produces CNS stimulation and toxicity can manifest as myoclonus and seizures
• Urinary excretion is principal elimination route
• Is pH dependent
  
  • Acidification of urine may speed elimination
• ½ life is about 15 hours; up to 35 hours in patients with renal failure
• In patients receiving meperidine for > 3 days – delirium maybe observed
  
  • Especially in the elderly

Question 31

Hydromorphone and codeine use in renal failure?

Answer 31

• Hydromorphone is metabolized to hydromorphone-3-glucuronide, which is excreted by the kidneys.
  
  • active metabolite accumulates in patients with renal failure and may cause cognitive dysfunction and myoclonus.
• Codeine also has the potential for causing prolonged narcosis in patients with renal failure and cannot be recommended for long-term use.

Question 32

Fentanyl use in renal patients?

Answer 32

• Metabolized to norfentanyl (minimally active)
• <10% excreted unchanged in urine
  
  • Detected for 72 hours
• Prolonged respiratory depression in chronic renal failure patients
• appears to be a better choice of opioid for use in ESRD because of its
  
  • lack of active metabolites,
  • unchanged free fraction, and
  • short redistribution phase.
• Small-to-moderate doses, titrated to effect, are well tolerated by uremic patients.

Question 33

Sufentanil use in renal failure?

Answer 33

• < 1% unchanged
  
  • N-dealkylation metabolites are considered active (10%)
• Maximal renal tubular reabsorption of free drug
  
  • Due to high lipid solubility
• Metabolites excreted equally between renal/biliary
• Increased plasma concentrations and prolonged respiratory depression has been noted in chronic renal failure patients
  
  • pharmacokinetics are variable, and has been reported to cause prolonged narcosis

Question 34

Alfentanil use in renal failure?

Answer 34

• Elimination ½ time and plasma clearance not altered
• Protein binding is reduced and free drug increases
• < 1% decreased unchanged
• caution in adminsitering a loading dose, but total dose and infusion dose similar to those patients with normal renal function

Question 35

Remifentanil use in renal failure?

Answer 35

• With renal failure
  
  • No changes in PK and PD
• In patients on hemodialysis
  
  • Reduced clearance and prolonged elimination ½ life
  • Lower infusion rate required
• remifentanil rapidly metabolized by blood and tissue esterases to a weak active (about 4,600 times less potent), mu opioid agonist compound that is renally excreted, remifentanil acid.
  
  • ​clearance of remifentanil acid can be reduced in renal failure, but clinical implications of metabolite are limited

Question 36

Hydromorphone use in renal failure

Answer 36

• Hepatic metabolite – hydromorphone 3-gluconoride (Inactive)
  
  • Potential to accumulate with renal failure – neurotoxic
• < 1% free hydromorphone excreted in urine
• Caution in renal failure patients

Question 37

Methadone use in renal failure?

Answer 37

• Metabolite pyrrolidine (inactive)
• 20-50% excreted as methadone
• 10-45% in feces
• Safe to use

Question 38

Oxycodone use in renal failure?

Answer 38

• Metabolites noroxycodone (inactive) and oxymorphone (active)
• Prolonged from 2.3 hours to 3.9 hours in patients with renal failure
• Reduce dose and increase interval

Question 39

Hydrocodone use in renal failure?

Answer 39

• Metabolized to hydromorphone
• Hydromorphone 3 glucuronide (neurotoxic)
• Decreased clearance in patients with renal disease
• Reduce dose and increase interval

Question 40

Succinylcholine use in renal failure?

Answer 40

• Hyperkalemia
  
  • 0.5 -1 mEq/dl increase in potassium
    
    • potassium rise is generally well tolerated in patients with chronically elevated serum potassium levels
    • want K <5.5 if considering succinylcholine admin
  • Renal failure patients are no more susceptible to exaggerated response to succinylcholine than normal patients
  • Infusions problematic
    
    • Succinylmonocholine- weakly active metabolite that is excreted by kidney
    • Weaker neuromuscular blocker with longer duration of action
• Conflicting reports of plasma cholinesterase activity in renal failure

Question 41

Mivacurium use in renal failure?

Answer 41

• Metabolized by butyrylcholinesterase (aka pseudocholinesterase)
  
  • decreased pseudocholinesterase activity in renal failure which can cause slower recovery from bolus dose of mivacurium in anpehric patients
• Longer duration of action and slower rate of recover in patients with CKD
  
  • Decreased amount of butyrylcholinesterase and accumulation of active metabolites
• Induction dose OK
  
  • DOA maybe increase by 10 – 15 minutes

Question 42

Atracurium use in renal failure?

Answer 42

• Hofmann elimination and ester hydrolysis
• OK in renal failure patients
• Laudanosine metabolite (30% renal)
  
  • Plasma ½ life same in both normal and renal failure patients
  • may cause seizures in experimental animals and can accumulate with repeated dosing or continuous infusion
    
    • however, not been realized in ICU patients with renal failure receiving prolonged infusions

Question 43

Cisatracurium use in renal failure?

Answer 43

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

Question 44

Pancuronium use in renal failure?

Answer 44

• Long- acting neuromuscular blocking drug
• metabolized by liver into less active intermediates, the elimination half life still primarily dependent on renal excretion (60-80%)
  
  • ​NM function should be closely monitored if these agents are used in patients with abnormal renal function
• 40-60% cleared through the kidneys
  
  • Avoid
• Metabolites are less potent and renally excreted

Question 45

Vecuronium use in renal failure?

Answer 45

• Metabolized in liver to 3 different metabolites
• 3-OH vecuronium has 80% potency of vecuronium
  
  • can accumulate in anephric patients receiving continuous infusion
• Approximately 30 - 40% excreted unchanged by the kidney
• Single dose fine, but multiple doses/infusions may require adjustment
  
  • DOA of vec prolonged as result of reduced plasma clearance and increased elimination half life
    
    • ​incubating dose lasts 50% longer in patients with ESRD

Question 46

Rocuronium use in renal failure?

Answer 46

• 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
  
  • conflicting results

Question 47

Cholinesterase inhibitor use in renal failure?

Answer 47

• Neostigmine, pyridostigmine, physostigmine, & 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
  
  • prolonged duration of action in ESRD due to heavy reliance on renal excretion
  • anticholinergic agent atropine and glyco, used in conjunction with anticholinesterases, are similarly excreted by kidney
  • no dose alternation of anticholinesterase is required when antagnoizing NMB in patients with reduced renal function

Question 48

Sugammadex use in ESRD?

Answer 48

• 75% of dose is eliminated through the urine
• Clearance approaches GFR
• With substantial renal impairment, clearance of sugammadex/rocuronium complex was decreased and elimination ½ life was increased
  
  • reversal of NMB by sugammadex is still as timely and effective in these patients as in healthy controls
• Dialysis is inconstant in removing suggammadex
• Do not use if creatinine clearance < 30 ml/hr

Question 49

What is acute kidney injury? characterization? occurence? causes?

what does preop AKI increase?

Answer 49

• Characterized by:
  
  • Deterioration of renal function- hours to days
  • Failure to excrete waste products
  • Failure to maintain fluid & electrolyte homeostasis
• Occurs:
  
  • All hospitalized - 5%
  • Critically ill – 8 - 10%
• Postoperative AKI
  
  • General – 1%
  • Cardiothoracic & vascular - 30%
• The causes of AKI are classically divided into
  
  • prerenal,- results from hemodynamic or endocrine factors that impair renal perfusion
  • intrarenal (or intrinsic), and
  • postrenal- from urinary tract obstruction
• Preoperative AKI increases:
  
  • hospitalization,
  • mortality, and
  • morbidity

Question 50

DIagnosis/Classficiation of AKI?

Answer 50

• Classifications:
  
  • RIFLE criteria (Risk- Injury-Failure-Loss-End-Stage)
  • Acute Kidney Injury Network
  • Kidney Disease: Improving Global Outcomes (KDIGO)
    
    • combines both RIFLE and AKIN criteria
• Based on
  
  • 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
• Increased appreciation for AKI since development of KDIGO criteria.
  
  • ​Even mild changes in kidney function seem to be associated with short and longterm adverse outcomes

Question 51

Various etiologies of AKI?

Answer 51

• Prerenal- hypoperfusion
  
  • from stoelting 22.4
    
    • ​hemorrhage
    • GI fluid loss
    • trauma
    • surgery
    • burn
    • cardiogenic shock
    • sepsis
    • hepatic failure
    • aortic/renal artery clamping
    • thromboembolism
• Intrarenal (intrinsic)- underlying renal causes, ischemia, nephrotoxins
  
  • ATN most common @75%
    
    • ​ischemia, nephrotoxic drugs, solvent,s heavy metals, contrast dye
  • acute glomerulonephritis
  • vasculitis
  • interstitial nephritis
• Postrenal- urinary collecting system obstruction
  
  • nephrolithisasis
  • BPH
  • Clot retention
  • bladder carcinoma

Question 52

Risk factors for AKI development perioperatively?

Iatrogenic risk factors?

Answer 52

Risk Factors for Perioperative Renal Failure (Stoelting’s 22.6)

• Pre-existing renal dx
• Advanced age
• CHF
• PVD
• DM
• Emergency surgery
• Major surgery (aortic aneurysm repair)
  
  • cardiac, vascular, major abdominal surgery at increased risk for renal dysfuntion

Iatrogenic Risk Factors

• Inadequate fluid replacement
• Hypotension
• Delayed treatment of sepsis
• Nephrotoxic drugs

Question 53

Neuro and Cardiac AKI Complications?

Answer 53

Neurologic:

• confusion,
• asterixis,
• somnolence,
• seizures,
• polyneuropathy r/t build up of protein & amino acids
• autonomic and peripheral neuropathies

Cardio:

• systemic HTN,
  
  • ​RAAS activation lead to HTN
• CHF,
  
  • increased cardiac demand r/t anemia and HTN makes CKD patients prone to congestive heart failure
• pulmonary edema r/t sodium & water retention;
  
  • increased permeability of alveolar-capillary membrane predispose to pulmonary edema
• dysrhythmias,
  
  • due to deposition of Ca in conduction system
• uremic pericarditis
  
  • may present with CP, cardiac tamponade or may be asymptomatic
• accelerated CAD and PVD
• CO _increases_ in kidney failure to maintain oxygen delivery due to decreased blood-oxygen carrying capacity

Question 54

Hematologic complications of AKI?

Answer 54

• anemia
  
  • Almost always present when CrCl <30 mL/min
  • Generally 6-8 g/dL due to decreased erythropoietin
    
    • ​difficult to maintain >9 even with transfusions
• coagulopathy
• HCT 20-30% common d/t hemodilution & decreased erythropoietin
• increased risk of bleeding d/t uremia-induced platelet dysfunction
  
  • decreased Plt Factor III as well as decreased PLT adhesiveness and aggregation
• wbc function impaired
  
  • ​susceptible to infections

Question 55

Metabolic complications of AKI?

Answer 55

• metabolic acidosis
  
  • failure to excrete nonvolatile acids produce increased anion gap metabolic acidosis
• hyperkalemia
  
  • potentially lethal consequence
  • occurs in pt with CrCl <5 mL/min but also develops rapidly in patients with higher clearances in setting of large potassium loads (trauma, hemolysis, infection, K administration)
• hyperphosphatemia
• hypocalcemia
  
  • r/t resistance of PTH
  • decreased intestinal absorption Ca and hyperphosphatemia-associated calcium deposition into bone
  • symptoms hypocalcemia rarely develop unless pt is alkalotic
• hypoalbuminemia
  
  • d/t anorexia, protein restriction, dialysis
• hypermagnesemia
  
  • usually mild
• hyperuricemia
• Hyponatremia
  
  • d/t water and sodium retnetion

Question 56

GI effects of AKI complications?

Answer 56

• anorexia
• N & V
• ileus
• gastroparesis
  
  • secondary to kidney-disease associated autnomic neuropathy may predispose to perioperative aspiration
• GI bleeding
  
  • hypersecretion gastric acid leads to peptic ulceration and GI hemorrhage in 10-30% patients
• increased incidence hep B and C- associated with hepatic dysfunction

Question 57

Infection complications of AKI?

Answer 57

• respiratory & urinary tracts and sites where breaks in normal anatomic barriers have occurred
• impaired immune response- white cell function are impaired in patients with kidney failure
• LEADING CAUSE OF MORBIDITY AND MORTALITY IN PATIENTS WITH AKI

Question 58

Management of AKI?

Answer 58

• No specific treatment modalities
  
  • ONLY lifesaving surgeries should be undertaken in pt with AKI

Treatment aims:

1. Limit further renal injury
2. Correct fluid/ electrolyte/ acid-base derangements
3. Reverse underlying causes of injury (hypovolemia, hypotension, low CO, sepsis)
4. Maintain MAP 65 or > (no evidence supporting outcomes with supraphysiologic values)
5. Fluid resuscitation(goal-directed therapy) & vasopressor therapy (norepi/vasopressin)
6. Diuretics not advised
   
   • ​attempting to convert oliguric to non-oliguric AKI by using diuretics may increase mortality risk and permeennt risk injjury
7. Alkalinization of urine with sodium bicarb. (rhabdo); reduces incidence of contrast-induced nephropathy
8. Dialysis- mainstay for severe AKI. complete day of surgery/ day before Indicated with:
   
   1. volume overload
   2. hyperkalemia
   3. severe metabolic acidosis
   4. symptomatic uremia
   5. overdose with dialyzable drug

Question 59

Prognosis of AKI?

Answer 59

• Poor – mortality > 20%
  
  • If dialysis required > 50%

Those who die from AKI usually die of failure of other organ systems after prolonged and complex hospital courses

• 15% will fully recover
• 5% will have renal insufficiency and remain stable
• 5% will experience continued renal function deterioration

Question 60

Anesthetic management with AKI?

Answer 60

• ensure adequate organ perfusion and oxidation during anesthesia is key principle
  
  • fluid, blood products, vasopressors, and inotrops are tools to achieve adequate organ perfusion
  • MAP <60 for 11-20 min or <55 for >10 minutes is associated with increased incidence AKI. Avoid hypotension during anesthesia and treat promptly
• KDIGO guidelines propose to implement bundle of preventative measures for patients at high risk AKI:
  
  • maintain volume status and perfusion pressure
  • monitor Cr and urine output
  • discontinue nephrotoxic agents
  • use of alternative to radio contrast agent
  • maintain normoglycemia
  • functional hemodynamic monitoring
• High risk patients should be identified preop
  
  • fluid losses and hypovolemia should b corrected by IV fluids
  • periop ADH and RAAS secretion minimized with adequate hydration before anesthetic induction
• Oliguria signals inadequate systemic perfusion,
  
  • prevention of ARF requires rapid recognition through adequate monitors
  • if renal with questionable cardiac/pulmonary function- may need an arterial line for BP monitoring or CVP/Swan monitoring when appropriate
• Avoid nephrotoxic drugs
  
  • NSAID
  • vanc
  • aminoglycosides
  • diuretics
  • contrast

Question 61

Premeds consideraiton for AKI? Monitoring needed?

Answer 61

• correction of hypovolema
• h2 blocker, PPI, reglan for aspiration preventions
• May need intraarterial BP for frequent blood draws, CVP

Question 62

Induction and maintenance consideration with AKI?

Answer 62

• Induction:
  
  • RSI with reduced dosages of induction drugs
  • Succinylcholine if K+ known
• Maintenance:
  
  • Volatile anesthetics vs. TIVA
  • Controlled ventilation
    
    • Avoid hypoxia and hypercarbia which can result in reduced renal blood flow
    • acidosis also can increase K

Question 63

What is chronic kidney disease?

Answer 63

• Kidney damage (GFR < 60 mL/min) for 3 or more months
  
  • ​slow, progressive, irreversible condition characterized by diminished functioning of nephrons and a decrease in renal blood flow, GFR, tubular function, and reabsorptive capacity
• DM and HTN most common cause (account 2/3 of all cases of CKD)
  
  • other causes:
    
    • glomerulonephritis, pyelonephritis, congenital defects
• Multiple different stages of CKD
• GFR < 25 mL/min require dialysis or transplant
• Ethnic variations
  
  • African American, Native American, & Hispanics have higher rates

Question 64

What are the three stages of renal failure?

Answer 64

• Stages
  
  1. decreased renal reserve
  2. renal insufficiency
  3. end-stage renal failure or uremia
• as number of functioning nephrons decrease, s/s and biochemical abnormalities become more severe
• Intrarenal hemodynamic changes are likely responsible for progression of renal disease
  
  • Glomerular HTN
  • Glomerular hyperfiltration & permeability changes
  • Glomerulosclerosis

Question 65

Management of chronic kidney disease?

Answer 65

Reduce systemic & glomerular HTN:

• ACE inhibitors
• ARBs
• Moderate protein restriction
  
  • in animal models, protein intake can influence progression of renal disease
  • recommended for all renal failure patients to decrease protein
• Strict control of BG
  
  • control BG can delay onset of proteinuria and slow progression nephropathy, neuropathy, and retinopathy
• Hyperlipidemia - statin therapy advised
  
  • hyperlipidemia may accelerate renal diesease
• Smoking cessation
  
  • linked to increased risk of development of kidney disease

Question 66

What are the 3 stages of adaptation to impairment of renal function?

Answer 66

• Adaption: Large Renal reserve; patients w/ CKD remain relatively asymptomatic until RF is < 10% of normal
• Stage 1
  
  • Decrease of > 50% GFR
  • Changes in excretion of creatinine and urea (as GFR decreases, these substances rise)
• Stage 2
  
  • GFR – 10% of normal
  • Changes in solutes such as potassium
    
    • ​serum K concentrations maintained WNL until GFR approaches 10% of normal, then hyperkalmeia manifests
• Stage 3
  
  • Variable
  • Changes in sodium homeostasis and regulation of ECF
    
    • sodium balance usually remains intact despite progressive deterioration in renal function and variation dietary intake
    • system can become overwhelmed by abrupt increases in sodium intake, which results in volume overload. OR decreased sodium intake, resulting in volum depletion

Question 67

Complications of CKD?

Answer 67

1. Uremic syndrome- constellation of s/s that reflect kidney’s progressive inability to perform excretory, secretory and regulatory functions. D/t failure of kidney to excrete number of uremic toxins
   
   • anorexia
   • nausea
   • vomiting
   • pruritus
   • anemia
   • fatigue
   • coagulopathy
2. Renal osteodystrophy- change in bone structure and minerlization with progressive CKD
   
   • ​secondary hyperparathyroidism and decreased Vit D production by kidneys
     
     • impaired intestinal absorption Ca
       
       • ​hypocalcemia stimulates PTH secretion, which leads to bone resorption to restor Ca concentration
   • as GFR decreases, decrease in phosphate clearance increases phosphate in body, thereby also decreasing Ca concentration
3. Anemia
   
   • normochromic and normocytic anemia
   • causes fatigue, weakness, decreased exercise tolerance
   • excess PTH hormone also causes bone marrow to become fibrotic, also contributing to anemia
4. Uremic bleeding
   
   • increased tendency to bleed despite normal PLT, PT, PTT
   • Bleeding time is screening test that best correlates with tendency to bleed
   • hemorrhagic episodes sig source morbidity in pt with CKD
5. Neurological changes
   
   • initially mild symptoms (impaired abstract thinking, insomnia, irritability) progressing to sig changes (sz, obtundation, uremic encephalopathy, coma)
   • adv renal failure a/w distal symmetric mixed motor and sensory polyneuropathy marked by paresthesia and hyperesthesia of LE
6. Cardiovascular changes
   
   • Systemic HTN is most sig risk factor CKD. Increases r/f CHF, CAD, CVA
   • Silent MI, cardiac tamponade and uremic pericarditis (inflammation of visercal and parietal layer of pericardium by accumulation of metabolic toxins)
7. Altered protein binding of drugs
   
   • Acidic drugs: less binding (benzos= increased FF)

Question 68

Treatment of CKD?

Answer 68

1. Treat underlying cause
2. BP control
   
   • BP can cause and be a consequence of CKD.
   • Multimodal drug therapy necessary
   • ACE or ARBs are first-line therapy in pt with proteinuria since both these drugs have shown to slow the rate of CKD progression
   • DIuretics, CCB, and aldosterone antagonists are other agents utilized
3. Adequate nutrition and protein restriction- reduce progression renal dx
4. Treat anemia
   
   • desmopressin can treat uremic bleeding
   • conjugated estrogens improve bleeding time
   • treated with erythropoietin or darbepoetin
   • blood transfusions avoided d/t concern for antigen matching with transplant
   • iron injection to maximize response to erythropoietin
5. RRT- no specific GFR however if GFR <10, usually dialysis is required
   
   • Hemodialysis
   • Peritoneal dialysis

Question 69

Preop eval for patient with CKD?

Answer 69

Preoperative evaluation:

• Goal: Preserve renal function and prevent kidney injury
• Renal function – is a continuum: trends in lab values more important
• Stop nephrotoxic drugs: (NSAIDS/aminoglycosides/contrast agents)
• Volume status – dry and wet weights
  
  • Drug administration: bolus vs. infusion (based on estimated Vd)
• Labs:
  
  • K < 5.5 on DOS
  • H/H: 10/30
  • Coags: DDAVP may be required
• HTN therapy – well controlled; ACE/ARB therapy (hold?)
• DM management – Target glucose 110 – 150 mg/dL
• GI: Prophylaxis- all drugs renally secreted

Question 70

Monitor and line considerations for CKD patients?

Answer 70

Monitors

• Minor/moderate: noninvasive monitors OK (not on fistula arm)
• Complex (Advanced disease): A-line/CVP/PICCO/TTE or TEE
• Where to place?
  
  • Avoid radial/ulnar/brachial/axillary/
  • Use dorsalis pedis or femoral
• TEE can be used for hemodynamic status

Lines

• Peripheral
  
  • Lower arm of dominant hand
    
    • avoid any venipuncture in nondominanrt arm as well as upper part of dominant arm.
    • any arterial line placed in arm with AV fistula will be inaccurate with BP and ABGs.
  • Can dialysis catheter be used for anesthesia?
    
    • Yes, but highly discouraged and proper care is important
    • REmember 1) catheter must be accessed aseptically, 2) heparin must be aspirated and then 3) reinstalled after use.
• Central
  
  • Maybe difficult to place
    
    • esp with pt with tunnleed venous access or temp dialysis catheter.
    • can develop vein stenosis

Question 71

Induction consideratiosn for CKD?

Answer 71

• Specific agent not as important as prevention of severe hypotension
  
  • Multiple causes
    
    • May be severe
  • Variability in response to induction meds d/t changes in VD, protein binding, low pH, dependence on renal excretion for parent drug/metabolite
  • Treatment
    
    • Replace volume before induction
    • Small doses or brief infusion of phenylephrine or norepinephrine OK
  • may need additional hemodynamic monitoring to tightly control hypotension as well as hypertension
    
    • ​autoregulation altered in patients with chronic HTN
  • ​exaggerated CNS effects of anesthetic induction agents may reflect uremia-induced disruption of BBB
  • Attenuated SNS activity impairs compensatory peripheral vasoconstriction
    
    • ​small decreases in BV, use of PPV, abrupt changes in position, or drug induced myocardial depression can result in an exaggerated decrease in systemic BP
• RSI
  
  • Can use succinylcholine if K+ < 5.5 mg/dL and necessary
  • No exaggerated release of K+ in CKD patients

Question 72

What are some considerations for the maintenance phase of anesthesia for a patient with CKD?

Answer 72

• Balanced technique
  
  • Combination of volatiles, opioids, and muscle relaxants
    
    • Sevo may be avoided but no evidence of patients having increased renal dysfunction after sevo.
  • Maintain MAP > 65 mmHg (>75 mmHg with chronic HTN)
    
    • Norepinephrine or phenylephrine
    • Risk increases with MAP < 60 mmHg for 20 min or < 50 mmHg for 10 min
• Check positioning frequently
  
  • prone to bruising and sloughing
  • extra padding needed to protect vulnerable nerves around joints
  • BP cannot be taken on side with fistula
  • avoid having the arm with fistula tucked, so it may be assessed during the procedure
• Fluid management
  
  • Use 500 ml bag with 60 gtt tubing
  • NS vs ½ NS vs LR vs Plasmalyte
    
    • LR generally avoided d/t K
    • 0.9% NS may also cause hyperchloremic acidosis and renal vasoconstriction when used in large amounts
  • 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
    
    • hypovolemia can increase renin, aldosterone and ADH levels which leads to a further decline in UOP
    • Preoperative hydration may be beneficial for those pt with severe renal dysfunction not requiring dialysis and those at high risk of postop renal failure.
    • 500 cc crystaolloid should increase UOP in presence of hypovolemia
  • Use of diuretics or vasodilators (fenoldepam) is controversial
    
    • use of diuretics to prevent AKI not recommneded except for mgmt of severe fluid overload

Question 73

Emergence and postop considerations for CKD?

Answer 73

• Skeletal muscle weakness: from residual neuromuscular blockade or… antibiotics, acidosis, electrolyte imbalance
  
  • Although residual NMB after reversal nondepol. NMB with anticholinesterase is rare, dx should b considered in patients with SKD who manifest signs skeletal muscle weakness during early postop period
  • other explanations (Abx, electrolyte imbalance) should also be considered when muscle weakness persists
• Caution w/ parenteral opioids – respiratory depression
  
  • exaggerated CNS depression and hypoventilation with even small doses
  • select opioids without active metabolites that do not rely on kidneys
• Avoid NSAIDs
  
  • ​NSAIDs best avoided. may also exacerbate HTN, precipitate edema and increase r/f CV complications
• Continuous ECG monitoring
  
  • monitor for hyperkalemia
• Supplemental O2
• Check electrolytes, BUN, creatinine, HCT
• Bleeding- uremic coagulopathy

Question 74

Regional anesthesia in patients with CKD?

Answer 74

• Neuraxial
  
  • Coagulopathy and peripheral neuropathy is a concern
    
    • Evaluate coagulation panel
    • Monitor closely
  • Maintain MAP
  • T4-10 level may improve renal function
    
    • By decreasing catecholamine-induced renal vasoconstriction and supressing surgical stress response
  • PLT dysfunction and effect of residual heparin in pt receiving Hemodialysis must also be considered
  • adequate intravascular fluid volume must be maintained to minimize hypotension
• Regional anesthesia- brachial plexus
  
  • Document peripheral neuropathies prior to placement
    
    • presence of uremic neuropatheis should be evaluated before induction of regional anesthesia
  • Improved surgical conditions
  • Maximum vasodilation (greater blood flow), abolish vasospasm
    
    • RA increases arterial blood flow and venous diameter during operation and early post op, preventing early thrombosis and associated fistula failure
    • associated risks include infection, neuropathy, PTX, and intravascular injectio
  • duration of brachial plexus block may be shortened by 40% in pt with chronic renal failure
    
    • not confirmed in controlled studies
  • co-existing metabolic acidosis may decrease threshold for sz in response to LA

Question 75

Physiologic basis for diuretics?

Answer 75

• Therapy for fluid overload- salt and water restrictions/ diuretic therapy?
  
  • fluid overload due to a variety of conditions (CHF, RF, Hepatic cirrhosis) may be first recognized during preop assessment
  • may require elective sx to be delayed to reduce operative risk
  • first line therapy is restriction Na/H2O but diuretic therapy often indicated
• Grouped according to site and MOA
  
  • Proximal tubule diuretics
  • Osmotic diuretics
  • Loop diuretics
  • Distal convoluted tubule diuretics
  • Distal acting diuretics
  • Dopaminergic agonists
• Na+/K+- ATPase pump – primarily responsible for Na+ out in exchange for K+
  
  • under normal conditions, >1% of Na enters urine
  • Na/K ATPase pump causes net movement of positive charge out of cell, creating electrochemical gradient that causes Na to enter luminal (urine) side of cell
• Renal tubular cells allow Na+ influx

Question 76

Where do carbonic anydrase inhibitors work?

Answer 76

Proximal convoluted tubule

ex- acetazolamide

• Carbonic anhydrase inhibitors are drugs that inhibit carbonic anhydrase
  
  • net effect of these agents is of Na and HCO3, which would otherwise have been reabsorbed, remain in urine and results in alkaline diuresis
  • patient may develop metabolic acidsois when taking these
    
    • compensatory process in tubules accommodate effects of carbonic anhydrase inhibitors, so their long-term use rarely causes a problem
• useful agents in contraction alkalosis from aggressive diuresis with loop diuretics
• Can reduce CO2 and improve PaO2 with little accompanying change in pH
• Uses:
  
  • morning sickness
  • open-angle glaucoma
  • increase respiratory drive in patients with central sleep apnea

Question 77

Where do osmotic diuretics work?

USES? SE?

Answer 77

Proximal convoluted tubule

ex mannitol

• mannitol is freely filtered at glomerulus, but poorly reabsorbed by renal tubule
  
  • causes osmotic diuresis
• water-permeable segments of proximal tubule and loop of henle, fluid reabsorption occurs and filtered mannitol is concentrated
  
  • eventually, oncotic pressure in tubular fluid resists further fluid reabsorption
  • mannitol draws water from cells into plasma and increases RBF
• USES:
  
  • Increase ICP
  • AKI prophylaxis in kidney transplantation
    
    • no evidence to support mannitol is effective for prevention or treatment of AKI nepropathy outside of kidney transplant
• SE**​
  
  • hypochloremia
  • intracellular increase K and H
  • circulatory overload with hemodilution and pulmonary edema
  • hyperkalemic metabolic acidosis
  • CNS depression
  • severe hyponatremia requiring hemodialysis

Question 78

What are loop diuretics?

Answer 78

work on thick ascending limb of Henle loop

• Ex- furosemide, bumetanide, torsemide
• inhibits electroneutral transporter, preventing salt reabsorption from occurring
  
  • allow large salt load to pass to distal convoluted tubule
  • first line therapy for treatment of acute decompensated CHF

Question 79

What are distal convoluted tubule diuretics?

MOA?

Uses

Adverse effects?

Answer 79

• ex- thiazides (HCTZ) and metolazone
• MOA- Block NaCl cotransport mechnism across apical plasma membranes
  
  • distal tubule is relatively water impermeable, net NaCl absorption causes urinary dilution
• Uses
  
  • HTN
  • Volume overload disorders
  • relieve symptoms of edema in pregnancy
• A/E
  
  • electrolyte disturbance
  • volume depletion
  • pancreatitis
  • jaundice
  • diarrhea
  • aplastic anemia

Question 80

What are distal (collecting duct) acting diuretics? eXAMPLES?

MOA?

Answer 80

• K-sparing diuretics and competitive aldosterone antagonists
  
  • Ex- spironolactone, eplerenone
• usually, mineralocorticoid hormone, aldosterone, is released by body in response to angiotensin II or hyperkalemia
  
  • aldosterone stimulates Na reabsortpiona nd K excretion in collecting duct
    
    • inhibition of aldosterone causes mild natriuresis and K retention
• Use
  
  • primarily for K sparing diuresis (in pt with volume overload receiving digitalis or hypokalemic alkalosis)
  • treatment of secondary hyperaldosteronism
    
    • ie cirrhosis, ascites

Question 81

What are dopaminergic agnoists? Role in diuretic therapy?

Answer 81

• Dopamine 1-3 mcg/kg/min is natriuretic owing primarily to a modest increase in GFR and reduction in Na reabsorption mediated by dopamine type 1 receptors
  
  • higher doses, pressor response to dopamine is beneficial in pt with hypotension, but little to no renal effect in critically ill or septic patients
  • “renal dose”: dopamine for treatment of AKI has not been demonstrated to have sig renoprotective properties and may
    
    • worsen splanchnic oxygenation,
    • impair GI function,
    • impair endocrine and immune function,
    • blunt ventilatory drive, and
    • increase risk of postcardiac sx afib
• Fenoldopam is selective Da1 agonist with little cardiac stimulation

Question 82

What are some common transurethral (endoscopic) procedures?

Answer 82

Urethroscopy: inspection of urethra

Cystoscopy: inspection of the bladder

Ureteroscopy: inspection of ureter

Nephroscopy: inspection of intrarenal collecting system

Question 83

Characteristics of patients undergoing transurethral procedures?

age, gender, incidence, etiology, associated conditions?

Answer 83

• Age: All ages
• Male:Female: 1:1
• Incidence: 30 -40% of all urological procedures
• Etiology:
  
  • Hematuria,
  • tumors (bladder/ureteral),
  • stones,
  • strictures
• Associated conditions:
  
  • Prostatic hypertrophy,
  • cystitis,
  • cancer,
  • hemorrhagic cystitis,
  • kidney stones,
  • uretero-pelvic junction obstruction

Question 84

Summary of transurethral procedures?

Answer 84

• Position: Lithotomy
  
  • Contractures may make difficult
• Unique Consideration: Use of x-ray, fluoroscopy, or lasers
  
  • Placement of catheters, stents, or drains
• Antibiotics: Cefazolin, Gentamicin (allergies?)
• Surgical time: 15- 45 minutes
• EBL: none
• Mortality: < 1%
• Morbidity: infection, perforation, retained stones, & nerve injury

Question 85

Preop considerations of transurethral procedures?

Answer 85

• Tumors:
  
  • Older patients with many different pre-existing conditions
  • CAD, CHF, PVD, COPD, and renal impairment
• Nephrolithiasis:
  
  • Paraplegics and quadriplegics have predilection for stones
  • Repeat procedures
  • Contractions & pressure sores may make positioning difficult

Question 86

Anesthetic considerations for regional anesthesia in transurethral procedures?

Answer 86

• Topical
  
  • 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 vs epidural (takes time to set up vs more stable cardiac profile)
    
    • typically these procedures are outpatient and anesthetic should be planned accordingly
    • sacral block required for urethral procedures T9-T10 for procedures with bladder and T8 if involving ureter

Anesthetic choice depends on type and length of procedure. age, coexisting dx, and patient preference

Question 87

General anesthesia considerations for transurethral procedures?

Answer 87

• Monitors: Standardized
• Positioning: Lithotomy
• Induction: Standard
  
  • ETT vs. LMA
  • Succinylcholine?– consider paraplegia/quadriplegia comorbidity
• Maintenance:
  
  • Volatile vs. TIVA
  • Muscle relaxation not essential
  • Long- acting narcotics not necessary- pretty minimal pain, tylenol, oxycodone sufficient
• EBL: minimal
• Emergence:
  
  • No specific considerations

Question 88

Complications of transurethral procedures?

Answer 88

Complications

• Decrease BP when lowering legs
• Peroneal nerve injury
• Pain
  
  • Is Toradol acceptable?- generally always ask surgeon
• Bladder perforation
  
  • Shoulder pain, sudden hypotension and tachycardia
  • hard to discern under general anesthesia
• Autonomic hyperreflexia
  
  • Spinal cord injury above T6
  • Sever HTN, bradycardia, dysrhythmias, and cardiac arrest
  • TX:
    
    • Deepen level of anesthesia
    • Labetalol 5-10 mg IV
    • SNP 0.5 – 5 mcg/kg/min
    • Phentolamine 2-5 mg IV

Question 89

Postop considerations of transuretrhal procedures?

Answer 89

• Peroneal injury
• Bladder perforation
• Fever/ bacteremia
• Pain is usually mild

Question 90

What is ESWL?

Answer 90

Extracorporeal shock wave lithotripsy

• Treatment for disintegration of renal stones in non-lower pole of kidney and upper part ureter
  
  • ​in symptomatic pt with stone burden <20 mm, ESWL is effective treatment, but a/w higher likelihood of repeat procedures
  • successful treatment depends on :
    
    • ​obesity
    • skin-to-stone distance
    • collecting system anatomy
    • stone compostiion
    • stone density/attenuation
• Shock waves focused at calculi in kidney or upper 2/3 of the ureter
  
  • Change in tissue density from body to stone cause a shearing/tearing effect
• 10 – 20 mm stones or impacted stones
• 1st Generation
  
  • High energy unit
  • Patient was immersed in water bath
    
    • Could result in significant CV nad Resp effects
      
      • Painful
• 2nd and 3rd Generation
  
  • Low energy unit
    
    • efficiency decreased, results in higher retreatment rates
  • Uses small water filling coupling device or pad
  • Tightly focused sound beam
  • 28% still report severe pain

Question 91

Position and considerations for ESWL procedures?

Answer 91

• Position:
  
  • 1st Generation: Placed into chair – then into water bath
  • 2nd/3rd Generation: Supine
• Unique Consideration: Movement; Special table; shock waves
  
  • First Generation: ECG must be good quality – R wave used to trigger shock
  • May use atropine/glycopyrrolate to increase HR
  • Supraventricular complexes

Question 92

Preop considerations of ESWL? Relative and absolute contraindications to ESWL?

Answer 92

Preoperative:

• 1st Generation: placed in chair and lowered into a water bath
  
  • CV and Resp changes
• 2nd/3rd : minimal hemodynamic changes

Absolute Contraindication

• Pregnancy
• bleeding disorders
• active UTI

Relative

• Presence of abdominal aortic aneurysm or orthopedic prosthetic device
• Patients w/ pacemaker (place in non-demand mode)
• Patients w/ AICD (turn off/on immediately before & after procedure)
  
  • Shock synchronized to 20 mms after R wave (absolute refractory period)
  • Shock waves can (rare) damage the device
  • Have alternative pacing device available

Question 93

Considerations for general anesthesia for ESWL?

Answer 93

• Typically for pediatric, extremely anxious, & bilateral procedures
• Does not decrease number of shock
• Induction: Standard based on preop findings; LMA vs. ET
• Monitors: Standard
• Maintenance: Light GA +/- muscle relaxant
  
  • HFJV has been used to limit movement
• Fluids: liberal use of fluids
  
  • Surgeon may request Lasix
• Emergence: No special considerations

Question 94

Neuraxial anesthesia considerations for ESWL?

Answer 94

T6 level required

• 1st generation
  
  • Epidural most common (unknown duration of surgery)
    
    • Use saline (air can dissipate shock waves and damage tissue)
    • Do not use foam tape (dissipate shock wave energy)
  • Spinal
    
    • Less control
• 2nd/3rd generation
  
  • Spinal (opioids only: 50 mcg sufentanil)
  • Flank analgesia – EMLA cream (2.5% lidocaine/prilocaine)
  • Dermal analgesia – Prilocaine injection
  • Monitored anesthesia care

Question 95

MAC anesthesia for ESWL?

Answer 95

Multiple different combinations have been used

• Propofol-fentanyl
  
  • Post op respiratory complications noted
• Propofol-remifentanil
  
  • Bolus vs. PCA
  • Lack of post procedure pain control
• Midazolam/ketamine

Question 96

Postoperative considerations for ESWL?

Answer 96

• Obstruction
• Cardiac arrythmias
  
  • Dysrhythmia may occur in 20-59% patient with piezoelectric source of shock waves versus 1.4-9% using electromagnetic lithotripers
  • dysrhythmic episodes do not appear to have any clinical significance
  • may be due to mechanical stress on conduction system from shock waves.
  • artifact and dysrhythmia common generally stops when lithotripsy is stopped
• Bleeding
  
  • hematuria always present at end of procedure from shock wave induced endothelial injury to kidney and ureter
  • adequate hydration necessary to prevent clot retention
• Skin bruising
• Damage to hollow organs
  
  • Especially the lungs
• Flank pain
  
  • painful hematoma may occur

Question 97

What is a TURP procedure?

Answer 97

Transurethral resection of prostate

• “Gold standard” therapy for BPH
  
  • mainstay to alleviate urinary obstructive symptoms r/t BPH
  • BPH describes smooth muscle and epithelial cell proliferation within transition zone of prostate
  • symptoms of BPH reflect bladder outlet obstruction (static) and increased smooth muscle tone (dynamic)
• Can be done as outpatient procedure
• Several techniques:
  
  • M-TURP or B-TURP
    
    • use electrically powered cutting-coagulating metal loop
  • HoLEP
  • Bipolar plasma vaporization or laser-vaporization
  • Aquablation
    
    • minimally invasive water ablation technique, combines image guidance and robotics with high-velocity saline stream for targeted and heat-free removal of prostate tissue
    • ​Advantages: shorter surgery time, minimal to no blood loss and reduced risk of fluid absorption
• Anesthetic implications – comorbidities, anesthetic technique, LOS, patient/surgeon preference

Question 98

Patient population of TURP procedures?

Answer 98

• 40- 90 yr, typically 70s and 80s
• 90% develop BPH; 20% of these need surgical intervention
• Associated conditions:
  
  • COPD
  • Heart disease
  • DM
  • DIC (prostate CA)

Question 99

Details of TURP procedure?

Answer 99

• One of the most common urological operations
• Completed with a resectoscope – monopolar& bipolar w/ continuous irrigant
  
  • resection performed with continuous irrigation with isotonic solution
  • bleeding vessels coagulated with coagulating current
  • foley placed at end
• Operative time < 2 hours– if greater, can cause excessive absorption of irrigating fluid which can cause:
  
  • Dilutional Hyponatremia
  • Confusion
  • Seizures
  • Heart failure
  • This is less of an issue with continuous flow biploar resectoscope where saline is used as irrigant
• KTP laser is now most common approach
  
  • Can be completed on anticoagulated patients & patients with bleeding disorders
  • Must wear protective eyewear
  • minimally invasive technique that allows deep vaporization of prostate tissue with minimal blood loss

Question 100

Summary of TURP procedure?

Answer 100

• Position: Lithotomy or steep trendelenburg
• Special Instrumentation: cystoscope, resectoscope, catheters, electrocautery
• Unique considerations: Immobility is a must
  
  • must be absolutely still because any movement can lead to perforation or injury to external sphincter, which can result in postop incontinence
• Antibiotics: Cefazolin and/ or Gentamicin 80 mg IV (allergies?)
• Surgical time: < 2 hours
• EBL: 500 ml’s (3-5 ml’s/min of resection)
• Postop: Irrigation of Foley to clear; Serum Na+ concentration
• Morbidity: Bleeding (10%), absorption of irrigation fluid (2-5%), perforation (0.5%)
• Pain: 1-3

Question 101

Preop anesthesia consideration for TURP procedure?

Answer 101

• Patients are generally elderly with co-morbid conditions
  
  • may have CAD, CHF, PVD, CVA, COPD, Renal impairment
• Resp: COPD common
  
  • smoking hx, PFT, CXR, ABG
• CV: CAD/HTN common
  
  • EKG
  • Assess exercised tolerance
• Neuro: Cerebrovascular disease; Alzheimer’s Disease
  
  • assess mental status
• Renal: Renal impairment secondary to obstruction
  
  • BUN, Cr, electolytes
• Endocrine: DM
  
  • check BG
• Heme: if gland > 80 grams need T&C
• Preop tests & labs based off H & P

Question 102

Regional anesthesia with TURP procedure?

Answer 102

• Anesthetic technique: GA vs neuraxial
  
  • regional allows eval for TURP syndrome
• Neuraxial anesthesia
  
  • Require T8 - 10 level
    
    • ​T10 provides adequate regional anesthesia for TURP by achieving block that interrupts sensory transmission from prostate and bladder neck
    • in addition, this level eliminates uncomfortable sensation of bladder distention
  • Potential for earlier detection of TURP syndrome
  • Incidence of postdural puncture headache is very low
  • Spinal placement maybe difficult r/t arthritis

Question 103

General anesthesia considerations for TURP procedure?

Potential complications?

Answer 103

• Induction: Standard
• Maintenance: Balanced (volatile/nitrous/opioids)
  
  • Muscle relaxation is not mandatory
  • Minimal to moderate blood loss (if venous sinuses entered)
    
    • Difficult to detect with irrigation fluid
• Emergence: Minimal pain; changes in BP with lowering legs
  
  • Airway edema with steep Trendelenburg
• Complications (intra/post-op):
  
  • Hypothermia,
    
    • body temp decreases 1 degree C per hour of surgery
    • shivering occurs in 16% of pt who receive room-temp irrigation fluids
    • hypothermia does not develop if irrigation solution warmed to body temp
  • bladder perforation,
    
    • 2% TURP procedures resulting in extraperitoneal fluid extravasation
      
      • ​awake pt with neuraxial anesthetic may complain during sx of new-onset pain localized to lower and and back
    • evidence of perforation usually not clear until postop
  • TURP syndrome,
  • blood loss, or
    
    • blood loss 2-4 mL/min but individual bleeding difficult to assess owing to mixing with irrigating fluid
    • serial assessment of Hgb may be necessary with prolonged procedures
  • vision problems,
  • fever/bacteremia/sepsis

Question 104

What is the physiology of TURP syndrome?

Factors that predict increased risk for fluid absorption and TURP syndrome?

Answer 104

• Continuous irrigation fluid- visibility and waste removal (blood/tissue)
  
  • surgoen needs clear view in order to perform procedure
• Incidence: 0.78 – 1.4% with 25% mortality for severe symptoms
• Time frame: 15 minutes (start of case) to 24 hours postop
• Resection of prostate opens large venous sinuses and large amounts of irrigation fluid can be absorbed
  
  • 10-30 ml’s / minute
  • 6-8 L in cases that last 2 hours
  • Can decrease serum sodium 5-8 mEq/L
  • Keep fluid height <60 cm above bed height
    
    • (Stoelting’s < 40 & Apex <30 beginning and < 15 end)
• Various types of fluid used
  
  • Based on type of equipment used
  • 1.2 – 1.5% glycine or sorbitol/mannitol (monopolar cautery)
  • Physiological saline (bipolar or lasers)
• TURP syndrome refers to cluster of symptoms r/t hypervolemic water intoxication
  
  • 1) excessive volume expansion (respiratory distress, CHF, pulmonary edema, HTN, bradycardia, HoTN)
  • 2) Hyponatremia
    
    • mental confusion
    • nausea
• Factors that predict increased irrigation fluid absorption during TURP
  
  1. number and size of open venous sinuses
     
     • greater blood loss implies greater potential for irrigant absorption
  2. surgical disruption of prostatic capsule
  3. longer duration of resection
  4. higher hydrostatic pressure of irrigating fluid
  5. lower venous pressure at irrigant-blood interface

Question 105

Clinical features of TURP syndrome?

Answer 105

Fluid overload – HTN/bradycardia/pulmonary edema

• Water toxicity (hypo-osmolality) - confusion/restlessness/seizures/lethargy
  
  • “Classic triad” noticed in awake patient
    
    • increase in systolic and diastolic pressures, and pulse pressure
    • bradycardia
    • mental status changes
• Hyponatremia:
  
  • <120 mEq/L: restlessness and confusion
  • < 115 mEq/L: somnolence, nausea, decease cardiac contractility, hypotension, Wide QRS, ST elevation and dysrhythmias
  • < 100 mEq/L: Seizures/coma, dysrhythmias, severe hypotension, and pulmonary edema
• Glycine toxicity - N&V/HA/transient blindness/loss of light reflex
• Ammonia toxicity- (conversion from glycine) N&V
• Hemolysis – Anemia/clammy skin/hyperkalemia
• Coagulopathy – Severe bleeding/DIC (<1%)
  
  • Systemic fibrinolysis -
    
    • Prostate releases plasminogen activator – plasmin
    • Absorption of thromboplastin

Early manifestations TURP related to rapid intravascular volume expansion independent of change in serum osmolality and sodium

• initial HTN and bradycardia from acute overload may evolve into LHF, pulmonary edema and cv collapse
• with continued absorption, cerebral edema is consequence of hyponatremia
• rapid change is responsible fo rmost s/s of TURP syndrome

Question 106

Treatment of TURP syndrome?

Answer 106

• Terminate surgery as soon as possible
• Fluid overload
  
  • Ensure adequate oxygenation, ventilation, and circulation
  • Monitoring, fluid restriction, furosemide 20 mg IV
  • Evaluate: Chemistry, CBC, glucose, ABG, and obtain 12 lead EKG
  • Goal: > 120 mEq/
  • Na < 100 mEq/L = 3% NS @ < 100 ml/hr
    
    • traditional rate of sodium correction of 0.5mEq/L/hr is for CHRONIC hyponatremia, not TURP syndrome
    • need hypertonic saline for TURP until Na >120
    • treatment with hypertonic saline is a/w development of demyelinating central nervous lesions (central pontine myelinolysis) d/t rapid increase plasma osmolality
      
      • ​hypertonic saline reserved for pt with severe hyponatremia
      • demyelinating syndomre occurs because of excessive shrinkage of brain cells after rapid hydration with hyperosmolar solution
      • brian cells have extruded important osmoles to compensate for chronic hypotonicity
    • no reports of demyelination after treatment of acute TURP syndrome
• For seizures: midazolam
• Chest x-ray for pulmonary edema
• DIC
  
  • Blood products as required
• CV Collapse
  
  • ACLS

Question 107

What is a radical protastectomy?

Answer 107

• Complete resection of the prostate – typically for adenocarcinoma
  
  • nonmalignant disease of prostate is usually treated by TURP
• Radical: entire prostate, both seminal vesicles and lymph nodes
• Despite being limited to men: 2nd most common cancer
  
  • 99% > 50 years old
  • African American 50% > Caucasian men
• Treatment
  
  • Radiation
    
    • hormonal, cryo, chemo, internal and external radiation therapy
  • High focused ultrasound
  • Watch and wait- low risk groups
    
    • ​identified by tumor aggressiveness and biomarkers
  • Surgical approach
    
    • Typically in younger men
    • elderly patients who may die from other disorders other than prostate Ca are being more frequently advsed to pursue nonsurgical therapy
    • surgical approach may be endoscopic with or without robotic assistance
• one concept is emerging that prostate Ca may exist in both clinically significant and insignificant forms

Question 108

Patient characteristics for prostatectomy?

Answer 108

• Age: 40 -80 yr
• Incidence: 20% will develop BPH; 9% will develop prostate CA
• Etiology: Aging
• Associated conditions: COPD, CAD, HTN, DM & RF

Question 109

Summary of radical prostatectomy?

Answer 109

• Position: Lithotomy; steep Trendelenburg (robotic)
• Incision: low midline; multiple port sites (robotic)
• Unique Considerations: Da Vinci robot system; abdominal insufflation, possible sural nerve graft
• Surgical time: 2-4 hours (experienced surgeon)
• EBL: 500 to 1500 ml’s (less w/ robot)
• Postop care: Catheter care & pain control
• Morbidity: Bleeding, DVT, Infection, PE, impotence, & infection
• Pain: 6-8

Question 110

Preop anesthesia considerations for radical prostatectomy?

Answer 110

• Typically, elderly men with multiple pre-existing medical conditions
  
  • Respiratory: PFTs, CXR, AGB
  • Cardiovascular: ECG, stents?, exercise tolerance
  • Neurologic: increased ICP and increased ocular pressure- neurosurgical consult if intracranial lesion or VP shunts
  • Renal: pneumoperitoneum decreases RBF and oliguria
  • Musculoskeletal: arthritis
  • Endocrine: blood sugars
  • Hematologic: T&C 2-4 units
• Preop evaluation should be directed toward detection and optimization of conditions prior to surgery
• Bowel prep may lead to dehydration
• Moderate blood loss expected:
  
  • < 30 g – no T/C necessary
  • 30 – 80 g – T/C 2 units
  • > 80 g – T/C 4 units

Question 111

Regional anesthesia for radical prostatectomy?

Answer 111

• Regional Technique (spinal/ continuous spinal/ continuous epidural) +/- sedation (open procedure only)
• May reduce blood loss and postoperative complications
  
  • T8- T10 level- depending on incision site
  • Sedation – deep to maintain comfort
    
    • Propofol
    • Dexmedetomidine
    • Benadryl

Question 112

Intraop considerations for radical prostatectomy?

Answer 112

• General Anesthesia (laparoscopic/robotic/open) +/- epidural
• Induction: Standard based on patient conditions
  
  • establish lines prior to patient positioning
  • intraarterial/CVP not routine but may be indicated based on comorbidities
• Monitoring: Standard (a-line & central line based on patient conditions)
• Maintenance: Balanced (volatile/opioid/neuromuscular blocking)
  
  • Pt movement is not tolerated with robotic procedures
  • Indigo carmine to visualize ureter- possibility of reaction
  • refrain from dosing epidural catheters because meds will move cephalad during procedure
• Blood/Fluids: Moderate to large blood loss; large bore IV’s; T/C as needed; goal-directed fluid management
  
  • May need vasopressors
• Emergence: steep trendelenburg- may contribute to airway edema
• Complications: indigo carmine reaction, hemorrhage, hypothermia, VAE, & robot malfunction

Question 113

Positioning considerations in radical prostatectomy?

Answer 113

• will be placed in steep trendelenberg (30-45 degrees head down)
  
  • facilitates pelvic access in lap and robotic prostatectomy
• prevent sliding- patient must be well situated on OR table, within vacuum bean bag and then firmly secured with belt
• arms placed on angled armboards prior to lower end table during lithotomy position to minimize crushed fingers
  
  • arms tucked at side
  • pressure points padded carefully
    
    • additional padding to distribute pressure from shoulder braces, if in use
  • pay attention to radial (At humerus), ulnar (at elbow) and lateral femoral cutaneous (lithotomy leg holders) to minimize axonal injuries
• oral ulceration and conjunctival burns may occur d/t lithotomy related reflux of gastric contents
  
  • preop antacid
  • stomach drainage by OG tube
  • waterproof eye tape

Question 114

Postop anesthesia considerations for radical prostatectomy?

Answer 114

• Hemorrhage
• Airway edema
• DVT
• Hypothermia
• Peroneal nerve injury
• Pain-
  
  • Maybe severe
  • ERAS protocols- epidural, TAP blocks

Question 115

What is a radical nephrectomy?

Answer 115

• Main indication: Renal cell carcinoma – 85 – 90% of solid renal masses
  
  • Men 2x’s > women
  • “triad” S/S
    
    • hematuria
    • flank pain
    • palpable mass
  • sometimes tumors are discovered d/t vena caval involvement
    
    • s/s dilated abdominal veins, variocele, lower extremity edema, pulmonary embolism.
    • a/w more advanced dx and a/w mets and poor prognosis.
  • Cell cancers of upper urothelial tract (ureters, renal pelvis) also treated by radical nephrectomy
• Nephrectomies fall into 3 groups: simple, partial and radical
• Refractory to chemotherapy and radiation
  
  • surgical resection only cure
• Up to 25% of patients, the tumor extends into the renal vein and inferior vena cava
  
  • More common in right sided renal cell carcinoma
  • Can have severe pulmonary congestion
  • High incidence of thrombus

Question 116

Summary of nephrectomy procedures?

Answer 116

• Position: Varies based on surgeon preference, disease stage & location- supine or flank
  
  • Incision: Flank, thoraco-abdominal, or trans-abdominal
    
    • incision may cause PTX
• Unique considerations: Renal artery/vein or IVC involvement. Very large tumors may require CV surgeon and cardiac bypass
• Time: 3- 4 hours
• EBL: 500 – massive
• Morbidity: Prolonged ileus, pneumothorax, vascular injury
• Pain: 8 – 10 (radical) 4 (laparoscopic)

Question 117

Preop consideraitons for nephrectomy?

Answer 117

• May be of any age
  
  • Elderly with multiple pre-existing medical conditions
• Preop evaluation should be directed toward detection and optimization of conditions prior to surgery
  
  • Respiratory: Increased post-op pulmonary complications because of location of incision (nonlaparoscopic)
    
    • If pulm dx- consider post-op respiratory complications
  • Hematologic: polycythemia has been associated with renal cell carcinoma
• Assessment of functional capacity is important
• Those with cavo-atrial disease may require PFT’s and TTE/TEE to look for thrombus
• Some may develop paraneoplastic syndrome
  
  • Hypercalcemia, eosinophilia, increased prolactin, & erythrocytosis
• sig injuries can also occur to colon, duodenum, and liver

Question 118

Inraop considerations with radical nephrectomy?

Answer 118

• General Anesthesia (laparoscopic/robotic/open)
  
  • Regional – Epidural vs TAPS/paravertebral block
    
    • Avoided in those with cavo-atrial involvement
• Induction: Standard based on patient conditions
• Monitoring: Standard, a-line & central line (left sided - before SVC)
  
  • Intra-op TEE (if tumor involvement with atria)
• Maintenance: Balanced (volatile/opioid/neuromuscular blocking)
• Positioning: lateral/Trendelenburg
  
  • Decreased FRC, increased V/Q mismatch, & atelectasis
• Blood/Fluids: Moderate to large blood loss; large bore IV’s; T/C; goal-directed fluid management
• Complications (intra/post-op):
  
  • pneumothorax,
  • hypotension w/ positioning,
  • indigo carmine,
  • methylene blue,
  • post-nephrectomy syndrome,
  • brachial plexus injury

Question 119

Postop concerns for radical nephrectomy?

Answer 119

• Hemorrhage
• Thrombus
• Hypothermia
• Pain
  
  • Maybe severe
  • ERAS protocols