Renal Flashcards

Question 1

Q

What are some functions of the kidneys?

Answer

A

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

Q

What is the nephron?

Answer

A

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

Q

What controls blood flow through the kidneys?

Answer

A

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

Q

Comparison of blood flow and tissue oxygenation throughout the kidney?

Answer

A

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

Q

What are the anatomic divisions of the nephron?

Answer

A

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

Q

What is GFR? Normal ranges?

Answer

A

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

Q

What are the stages of CKD? Manifestations?

Answer

A

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

Q

What is creatinine clearance?

Answer

A

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

Q

What is creatinine?

Answer

A

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

Q

What is BUN?

Answer

A

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

Q

What is fractional excretion of sodium measuring?

Answer

A

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_Nais 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

Q

What is measured in a urinanalysis?

Answer

A

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

Q

What are biomarkers?

Answer

A

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

Q

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

Answer

A

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

Q

Impact of anesthesia on renal function?

Answer

A

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

Q

Use of thiopental in renal disease?

Answer

A

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

Q

Etomidate use in renal patients?

Answer

A

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

Q

Use of ketamine in renal patients?

Answer

A

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

Q

Propofol use in renal disorders?

Answer

A

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

Q

Precedex use in renal failure?

Answer

A

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

Q

Midazolam use in renal dysfunction?

Answer

A

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

Q

Diazepam use in renal dysfunction?

Answer

A

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

Q

Use of methoxyflurane (historic VA) in renal dysfunction?

Answer

A

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

Q

Halothan use in renal dysfunction?

Answer

A

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

Q

Enflurane use in renal dysfunction?

Answer

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?
- Alkaline degradation products conjugated to thiol products

Question 26

Q

Isoflurane in renal dysfunction?

Answer

A

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

Q

Desflurane use in renal dysfunction?

Answer

A

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

Question 28

Q

Sevo use in renal dysfuntion?

Answer

A

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

Q

Morphine use in renal dysfunction?

Answer

A

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

Q

Meperidine use in renal dysfunction?

Answer

A

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

Q

Hydromorphone and codeine use in renal failure?

Answer

A

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

Q

Fentanyl use in renal patients?

Answer

A

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

Q

Sufentanil use in renal failure?

Answer

A

< 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

Q

Alfentanil use in renal failure?

Answer

A

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

Q

Remifentanil use in renal failure?

Answer

A

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

Q

Hydromorphone use in renal failure

Answer

A

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

Q

Methadone use in renal failure?

Answer

A

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

Question 38

Q

Oxycodone use in renal failure?

Answer

A

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

Q

Hydrocodone use in renal failure?

Answer

A

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

Question 40

Q

Succinylcholine use in renal failure?

Answer

A

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

Q

Mivacurium use in renal failure?

Answer

A

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

Q

Atracurium use in renal failure?

Answer

A

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

Q

Cisatracurium use in renal failure?

Answer

A

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

Q

Pancuronium use in renal failure?

Answer

A

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

Q

Vecuronium use in renal failure?

Answer

A

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

Q

Rocuronium use in renal failure?

Answer

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
- conflicting results

Question 47

Q

Cholinesterase inhibitor use in renal failure?

Answer

A

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

Q

Sugammadex use in ESRD?

Answer

A

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

Q

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

what does preop AKI increase?

Answer

A

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

Q

DIagnosis/Classficiation of AKI?

Answer

A

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

Q

Various etiologies of AKI?

Answer

A

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

Q

Risk factors for AKI development perioperatively?

Iatrogenic risk factors?

Answer

A

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

Q

Neuro and Cardiac AKI Complications?

Answer

A

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

Q

Hematologic complications of AKI?

Answer

A

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

Q

Metabolic complications of AKI?

Answer

A

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

Q

GI effects of AKI complications?

Answer

A

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

Q

Infection complications of AKI?

Answer

A

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

Q

Management of AKI?

Answer

A

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

Treatment aims:

Limit further renal injury
Correct fluid/ electrolyte/ acid-base derangements
Reverse underlying causes of injury (hypovolemia, hypotension, low CO, sepsis)
Maintain MAP 65 or > (no evidence supporting outcomes with supraphysiologic values)
Fluid resuscitation(goal-directed therapy) & vasopressor therapy (norepi/vasopressin)
Diuretics not advised
- attempting to convert oliguric to non-oliguric AKI by using diuretics may increase mortality risk and permeennt risk injjury
Alkalinization of urine with sodium bicarb. (rhabdo); reduces incidence of contrast-induced nephropathy
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

Q

Prognosis of AKI?

Answer

A

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

Q

Anesthetic management with AKI?

Answer

A

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

Q

Premeds consideraiton for AKI? Monitoring needed?

Answer

A

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

Question 62

Q

Induction and maintenance consideration with AKI?

Answer

A

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

Q

What is chronic kidney disease?

Answer

A

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

Q

What are the three stages of renal failure?

Answer

A

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

Answer 65

A

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

Answer 66

A

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

Answer 67

A

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
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
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
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
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
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)
Altered protein binding of drugs
- Acidic drugs: less binding (benzos= increased FF)

Answer 68

A

Treat underlying cause
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
Adequate nutrition and protein restriction- reduce progression renal dx
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
RRT- no specific GFR however if GFR <10, usually dialysis is required
- Hemodialysis
- Peritoneal dialysis

Answer 69

A

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

Answer 70

A

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

Answer 71

A

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

Answer 72

A

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

Answer 73

A

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

Answer 74

A

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

Answer 75

A

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

Answer 76

A

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

Answer 77

A

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

Answer 78

A

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

Answer 79

A

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

Answer 80

A

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

Answer 81

A

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

Answer 82

A

Urethroscopy: inspection of urethra

Cystoscopy: inspection of the bladder

Ureteroscopy: inspection of ureter

Nephroscopy: inspection of intrarenal collecting system

Answer 83

A

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

Answer 84

A

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

Answer 85

A

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

Answer 86

A

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

Answer 87

A

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

Answer 88

A

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

Answer 89

A

Peroneal injury
Bladder perforation
Fever/ bacteremia
Pain is usually mild

Answer 90

A

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

Answer 91

A

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

Answer 92

A

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

Answer 93

A

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

Answer 94

A

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

Answer 95

A

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

Answer 96

A

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

Answer 97

A

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

Answer 98

A

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)

Answer 99

A

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

Answer 100

A

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

Answer 101

A

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

Answer 102

A

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

Answer 103

A

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

Answer 104

A

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

Answer 105

A

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

Answer 106

A

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

Answer 107

A

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

Answer 108

A

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

Answer 109

A

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

Answer 110

A

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

Answer 111

A

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

Answer 112

A

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

Answer 113

A

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

Answer 114

A

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

Answer 115

A

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

Answer 116

A

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)

Answer 117

A

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

Answer 118

A

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

Answer 119

A

Hemorrhage
Thrombus
Hypothermia
Pain
- Maybe severe
- ERAS protocols