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ANESTHESIA PRACTICE 3 > RENAL DISEASE AND UROLOGIC SURGERY > Flashcards

RENAL DISEASE AND UROLOGIC SURGERY Flashcards

1
Q

what are the two functions of the nephron?

A
  • filtration

* secretion

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2
Q

what are the two sites of filtration in the nephron?

A
  • glomeluar membrane

* tubule system

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3
Q

describe secretion in the nephron

A

substances are secreted from the plasma into the tubules

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4
Q

which type of nephron has longer loops of Henle, therefore more area for fluid/electrolyte exchange?

A

medullary nephrons

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5
Q

describe filtration, reabsorption and excretion in the nephron

A

blood enters the glomerulus from the afferent arteriole, is filtered, and filtrate enters tubule system. most of the water and solutes in the filtrate are reabsorbed into the peritubular capillaries. water and solutes not reabsorbed become urine and is excreted

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6
Q

what two things contribute to the high pressures inside the glomerulus?

A
  • renal artery and afferent arteriolar blood pressure

* high resistance to flow from the efferent arteriole

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7
Q

name the three major layers of the glomerular membrane that differentiate it from capillary membranes

A
  • fenestrated endothelial layer
  • basement membrane
  • epithelial cells that line bowman’s capsule (slit-pore)
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8
Q

what factors contribute to glomerular filtration?

A

glomerular filtration pressure is about 60% of MAP

  • directly proportional to efferent arterial tone
  • opposed by plasma oncotic pressure
  • opposed by renal interstitial pressure
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9
Q

how is glucose reabsorbed from the kidneys?

A
  • SGLT2 in the proximal tubules (90%)

* SGLT1 in the distal glomerulus (10%)

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10
Q

what is the major function of the proximal tubule?

A

Na reabsorption

* water moves passively along osmotic gradients

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11
Q

describe Na reabsorption in the proximal tubules

A

ATPase transfers 3Na for 2K in the peritubular capillary.

* net loss of +charge allows absorption of K, Mg, Ca into proximal tubules

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12
Q

describe reabsorption in the loop of henle

A
  • Na and Cl are reabsorbed in excess of water movement

* Na reabsorption is coupled with K and Cl reabsorption (tubular Cl is the rate limiting factor)

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13
Q

how pervious to water is the loop of henle?

A

the loop of henle is impervious to water thus producing dilute urine

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14
Q

what two substances is the distal tubule impervious to?

A

H2O, Na

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15
Q

what is the tonicity of the fluid in the loop of Henle and distal tubule?

A

hypotonic (dilute)

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16
Q

where is the major site of parathyroid hormone and vitamin D Calcium reabsorption, as well as aldosterone mediated Na reabsorption

A

distale tubule

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17
Q

where are principle cells (P cells) and intercalated cells (I cells) located?

A

cortical portion of the collecting tubules

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18
Q

what is the function of P cells?

A
  • secrete K+

* participate in aldosterone mediated Na reabsorption

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19
Q

what is the function of I cells?

A

responsible for acid base regulation (also mediated by aldosterone)

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20
Q

where is the principal site of anti-diuretic hormone, and also has I cells which acidify urine with either H+ or ammonium ions

A

medullary collecting tubule

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21
Q

in what part of the nephron are fluids/ electrolytes not exchanged?

A

ureter

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22
Q

where is the juxtamedulary apparatus located?

A

afferent arteriole

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23
Q

where is renin contained?

A

juxtamedullary apparatus

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24
Q

what 3 factors stimulate renin release?

A
  • sympathetic beta-1 stimulation
  • afferent arteriolar wall pressure – hypotension
  • decreased sodium levels
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25
Q

describe how renin increases renal sodium & fluid retention

A

renin release from kidney converts angiotensinogen to angiotensin I. ACE converts AI to AII. AII increases aldosterone from the adrenal cortex and ADH from the pituitary

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26
Q

how is creatinine produced?

A

metabolism of muscle proportional to muscle mass

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27
Q

what are the normal ranges for creatinine?

A
  • men: 0.8-1.3mg/dl

* women: 0.6-1.0mg/dl

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28
Q

calculate creatinine clearance

A

((140-age) x lean body weight) / (72 x plasma creatinine)

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29
Q

what is the normal range for creatinine clearance?

A

100-200ml/min

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30
Q

what are the values for:

  • mild renal reserve
  • midl renal impairment
  • moderate renal insufficiency
  • renal failure
  • end stage renal failure
A
  • mild renal reserve: 60-100ml/min
  • mild renal impairment: 40-60ml/min
  • moderate renal insufficiency: 25-40ml/min
  • renal failure:
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31
Q

what is the normal range for blood urea nitrogen (BUN)?

A

10-20mg/dl

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32
Q

how do low renal tubule flow rates affect BUN/creatinine ratios?

A

low renal tubule flow rates enhance urea absorption, but do not affect creatinine handling
* B:C > 10:1

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33
Q

in what situations will B:C ratio be greater than 15:1?

A

volume depletion and edematous disorders

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34
Q

urine pH > 7.0 in the presence of systemic acidosis corresponds to what?

A

renal tubular acidosis

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35
Q

how is specific gravity used for urinalysis?

A

corresponds to urine osmolarity or kidney’s ability to concentrate and regulate urine

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36
Q

protein excretion greater than 150mg/dl is a significant sign of what?

A

proteinurea

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37
Q

red cells in urine are a sign of what?

A

bleeding

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38
Q

white cells in urine are a sign of what?

A

infection

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39
Q

what is the downside of urinalysis?

A
  • markers of global kidney function, not focal or generalized injury
  • markers may not be elevated or out of range until up to 48hr after surgery – way after damage is done
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40
Q

what is the new found protein that seems to be a predictor of future kidney disease?

A

SUPAR –soluble urokinase-type plasminogen activator receptor

* analogous to cholesterol and heart disease

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41
Q

define acute glomerular nephritis

A
  • antibody-antigen rxn – glomeruli become inflamed

* can cause total or partial blockage of glomeruli

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42
Q

what secondary complications can occur as a result of acute glomerular nephritis?

A

glomeruli not blocked have increase permeability allowing large amounts of protein leakage

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43
Q

acute glomerular nephritis usually follows what?

A

1-3wk after a beta-streptococci infection

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44
Q

how does the antigen-antibody rxn cause acute glomerular nephritis?

A

ag-ab rxn forms a precipitate that becomes entrapped in the glomeruli membrane

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45
Q

how long does acute glomerular nephritis last/ how is it treated?

A
  • usually subside in 10d to 2wk

* Tx: supportive care

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46
Q

describe polycystic kidney disease

A

autosomal genetic disease that causes cysts on the kidneys

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47
Q

what conditions are associated with polycystic kidney disease?

A
  • aortic aneurysms
  • brain aneurysms
  • cysts in the liver, pancreas, and testes
  • diverticulosis of the colon
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48
Q

how does polycystic kidney disease present?

A
  • high BP
  • chronic renal disease to failure
  • bleeding or ruptured cysts
  • UTIs
    (progressive disease that eventually leads to kidney failure)
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49
Q

describe renal artery stenosis and hypertension

A
  • narrowing of the artery or arteries feeding the kidneys
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50
Q

describe the progression of renal artery stenosis and hypertension

A
  • narrowing of arteries feeding kidneys results in decreased BP at afferent arteriole –> renin release –> systemic HTN & renal atrophy
  • can progress to kidney failure
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51
Q

how is renal artery stenosis treated?

A
  • renal shunt or angioplasty

* BP control with meds

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52
Q

describe diabetic renal nephropathy

A
  • glucose increases past the kidney’s capacity to reabsorb it
  • filtrate becomes more osmotic and excretes more water/dilutes sodium in urine
  • decreased Na triggers macula dense cells to secrete renin, leading to vasoconstriction and decreased blood flow to kidneys
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53
Q

how is diabetic renal nephropathy treated?

A
  • HTN – usually treated with ACE inhibitors

* control blood sugars

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54
Q

describe hepatorenal syndrome

A
  • rapid deterioration of renal function 2º to liver failure
  • decreased liver function –> decreased blood flow to intestines –> decreased blood flow/vessel tone to kidneys –> renin release –> HTN/decreased BF to kidneys
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55
Q

what are the treatment options for hepatorenal syndrome?

A
  • liver transplant
  • supportive care including dialysis
    (kidney fxn can return after liver transplant)
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56
Q

what renal pathology increases cardiac complications and hospital mortality?

A

acute renal failure/acute kidney injury (AKI)

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57
Q

what surgical procedure has the highest incidence of acute kidney injury?

A

cardiac surgery – 30%

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58
Q

describe azotemia

A

rapid deterioration in renal function that results in retention of nitrogenous waste products in the blood

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59
Q

what is the cause of pre-renal azotemia?

A

decrease in renal perfusion such as in hypotension or hypovolemia

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60
Q

what is the cause of renal azotemia?

A

due to intrinsic renal disease, toxicity, renal ischemia

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61
Q

what is the cause of post-renal azotemia?

A

urinary tract infection

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62
Q

most perioperative AKI occurs in response to what?

A

renal ischemia from hypotension or hypovolemia

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63
Q

how does volume loading decrease the incidence of perioperative AKI?

A

volume loading suppresses renin secretion and increases ANP release

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64
Q

what is the best course of action to take to prevent AKI?

A
  • fluids
  • inotropes
  • vasoactive medications
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65
Q

what MAP values are associated with higher incidence of AKI?

A

MAP

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66
Q

what Hgb level is associated with higher incidence of AKI?

A

graded increase in AKI for prep Hgb

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67
Q

describe oliguria

A

decreased urine output

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68
Q

what is the goal of pre-renal treatments of renal dysfunction?

A

improve renal perfusion

  • treat hypovolemia
  • treat or raise blood pressure
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69
Q

what medications can be used to improve renal perfusion?

A
  • to raise BP – pressors

* to increase glomerular filtration/dilation – dopamine, fenoldapam

70
Q

what fluid doubles the incidence of AKI?

A

NS doubles the incidence of AKI as compared to LR

71
Q

describe the clinical approach to oliguria

A
  • discontinue potential nephrotoxins
  • verify oliguria (check foley catheter)
  • review hemodynamics (BP, CVP, PAP)
  • assume oliguria is pre-renal
  • volume expansion is as effective as prophylactic administration of dopamine or diuretics in high-risk pts
  • maximize RBF, renal perfusion pressure
72
Q

why is “renal dose” dopamine controversial?

A
  • no randomized controlled study has demonstrated a decreased incidence of AKI when dopamine is administered to high-risk pts
  • diuretic effect – increased UOP
  • increased GFR/UOP can increase renal O2 demand
73
Q

treatment for oliguria/ increased serum K+

A

diuretics

74
Q

how do most diuretics work?

A

increase urine output by decreasing reabsorption of Na, K, and water

75
Q

name an osmotic diuretic and describe its mechanism of action

A

mannitol (0.25-1mg/kg)

  • filtered at glomerulus, undergoes limited or no reabsorption in the proximal tubule
  • limits passive water reabsorption in proximal tubule
76
Q

how should mannitol be administered? what is the concern?

A
  • mannitol should be given over 20min
  • mannitol is highly osmotic and if administered too quickly can also increase blood osmolarity –> increased intravascular volume – can initiate cardiac failure in pt with poor cardiac fxn
77
Q

what kind of drug is diamox/ what is the dosing?

A
  • diamox (250-500mg) – carbonic anhydrase inhibitor
78
Q

what is the mechanism of action of carbonic anhydrase inhibitors?

A

interfere with Na reabsorption and H+ secretion in proximal tubules

79
Q

what is the mechanism of action of loop diuretics and where do they work?

A

inhibit Na and K reabsorption in the thick ascending limb of the LoH

80
Q

what is the major side effect of loop diuretics?

A

can cause hearing loss with chronic usage

81
Q

name three loop diuretics and dosages

A
  • furosemide/lasix (10-100mg)
  • bumetetanide/bumex (0.5-1mg)
  • ethycrynic acid (50-100mg)
82
Q

name a diuretic that acts in the distal tubule

A

diuril (500mg)

83
Q

what is the mechanism of action of distal tubule diuretics?

A
  • inhibit sodium reabsorption
  • compete for Cl site on luminal Na/Cl carrier protein
  • also augment Ca reabsorption
84
Q

how does aldosterone work?

A
  • aldosterone causes collecting tubule to reabsorb Na and secrete K
  • increase fluid retention
  • decrease UOP
  • increase BP
85
Q

what is the mechanism of action of aldosterone antagonist diuretic?

A
  • inhibit aldosterone mediated Na reabsorption/ K secretion
86
Q

name an aldosterone antagonist diuretic

A

spironalactone

87
Q

what is the mechanism of action of noncompetitive potassium sparing diuretics?

A

inhibit Na reabsorption/ K secretion by decreasing number of open Na channels in luminal membrane

88
Q

name a noncompetitive potassium sparing diuretic

A

triamterene

89
Q

which anesthetic agents should be avoided for pts with impaired renal function?

A
  • methoxyflurane

* enflurane

90
Q

which antibiotics should be avoided for pts with impaired renal function (5)?

A
  • aminoglycosides
  • cephalosporins
  • amphotericin B
  • sulfonamide
  • tetracyclines
  • vancomycin
91
Q

which NSAIDS should be avoided for pts with impaired renal function (5)?

A
  • aspirin
  • ibuprofen
  • naproxen
  • indomethacin
  • ketorolac
92
Q

should contrast media be avoided for pts with impaired renal function?

A

yes

93
Q

name 7 endogenous nephrotoxins to avoid for pts with impaired renal function

A
  • calcium
  • uric acid
  • myoglobin
  • hemoglobin
  • bilirubin
  • oxalate crystals
  • paraproteins
94
Q

which renal pathophysiology can be described as a progressive and irreversible decline in renal function?

A

chronic renal failure

95
Q

what are the metabolic manifestations of renal failure?

A
  • hyperkalemia
  • hypermagnesemia
  • hyperuricemia
    ____
  • hypophosphatemia
  • hypocalcemia
  • hypoalbunemia
96
Q

what are the hematological manifestations of renal failure?

A

anemia – decreased erythropoietin production

  • decreased RBC production
  • decreased RBC survivability
  • hemodilution from water retention
  • decreased white cell and platelet function
97
Q

how is cardiac output affected for pts with renal failure?

A

CO increases to offset decrease in O2 carrying capacity/ increased preload

98
Q

describe how chronic renal failure can lead to LVH and CHF

A
  • increased angiotensin results in arterial hypertension which results in increased SVR –> increased LVH and CHF
99
Q

how does renal failure affect cardiac rhythm?

A

conduction blocks or dysrhythmias due to electrolyte imbalances

100
Q

what vascular manifestations are seen in pts with renal failure?

A

accelerated peripheral vascular disease, including coronary artery disease

101
Q

how does chronic renal failure manifest in the pulmonary system?

A
  • increased minute ventilation due to metabolic acidosis (kidneys not excreting enough acid from the body)
  • pulmonary edema due to increased membrane permeability
  • increased intravascular volume
102
Q

how does chronic renal failure manifest in the endocrine system?

A

abnormal glucose tolerance 2º to peripheral insulin resistance

103
Q

what GI manifestations are common with chronic renal failure?

A
  • anorexia, nausea/vomiting (azotemia)
  • delayed gastric emptying
  • hepatitis
104
Q

what is the treatment for chronic renal failure?

A
  • dialysis

* transplant

105
Q

describe hemodialysis

A
  • just like an artificial kidney – ultrafiltration of fluid across a semi-permeable membrane
  • blood flows by one side of semi-permeable membrane, dialysate flows by opposite side
106
Q

what operative procedures are required for hemodialysis?

A
  • A-V graft/fistula

* vascath/ portacath

107
Q

describe peritoneal dialysis

A
  • wastes and water are removed from the blood inside the body using the peritoneal membrane
  • catheter is inserted into peritoneum
  • dialysate (hypertonic glucose derivative) instilled – 1-3L
  • clamped for a dwell time, and released and drained (pulls toxins and water out)
108
Q

what are the advantages of peritoneal dialysis?

A
  • can be done anywhere
  • less traumatic fluid shifts
  • well tolerated
109
Q

describe intestinal dialysis

A
  • diet is supplemented with soluble fibers (acacia fiber) – digested by bacteria in colon, increases amount of nitrogen eliminated in fecal waste
  • alternatively, ingestion of 1-1.5L non-absorbable solutions of polyethylene glycol or mannitol q4hr
110
Q

describe myoglobinuria

A

severe muscle breakdown such that myoglobin is filtered by kidney and collecting ducts – clogs the system

111
Q

name four causes of myoglobinuria

A
  • severe muscle wasting
  • malignant hyperthermia
  • transfusion reaction
  • anaphylactic reaction
112
Q

how is myoglobinuria treated?

A
  • keep urine flowing
  • fluids
  • diuretics (mannitol)
    • alkalinize the urine with NaHCO3
113
Q

what are the anesthetic considerations for renal pts?

A
  • dialysis? which type? how recently? (anticoags still on board?)
  • recent electrolytes (especially K)
  • recent CBC
  • blood glucose levels
114
Q

what precautions should be taken when placing monitors on renal pts?

A

no monitors on shunt arm

115
Q

what precautions should be taken on induction of renal pts?

A
  • propofol or etomidate (if hemodynamically unstable)

* No SUX unless K+

116
Q

describe pathognomonic hyperkalemic T-waves

A

peaked, “tented”, come to a point, have a very flat ST segment, long QRS

117
Q

how is acute hyperkalemia treated?

A
  • CaCl2
  • NaHCO3
  • glucose and insulin
  • hyperventilation
118
Q

what is the primary concern of maintenance for renal pts?

A
  • drugs will last longer because they may not be metabolized or excreted
  • judicious use of narcotics, benzodiazepams and relaxants
  • cisatracurium has advantages
119
Q

what are the concerns associated with fluid administration?

A
  • judicial use of fluids
  • use fluids with no K such as 0.9NaCl (instead of LR)
  • glucose free fluids due to glucose intolerance
  • Hgb 7-8 ok (chronically anemic)
120
Q

what are the cardiovascular concerns with renal pts?

A
  • prone to heart failure

* usually hypertensive and need to maintain higher Bps to perfuse brain and heart

121
Q

what are the pulmonary concerns with renal pts?

A
  • easily go into PE
  • PEEP
  • may remain intubated
  • usually metabolically acidotic
  • rapid respirations might not always be pain – consider metabolic acidosis compensation or PE
122
Q

post-operatively, what should be considered if pt has low O2 sats?

A

pulmonary edema

123
Q

what is the most commonly performed urologic/nephrologic procedure?

A

cystoscopy

124
Q

what is the patient position for cystoscopy?

A

lithotomy

125
Q

what are the positioning concerns for lithotomy?

A
  • common peroneal nerve injury
  • saphenous nerve injury
  • obturator or femoral nerve damage/ stretch of sciatic nerve with excessive flexion of thigh
  • compartment syndrome in lower extremities (low perfusion rates)
126
Q

what addition to lithotomy position will exacerbate physiologic complications of positioning?

A

trendelenburg

127
Q

are cystoscopies generally long or short procedures?

A

generally short

128
Q

what kind of anesthetic plan is best for cystoscopies?

A

GA preferred due to shortness of case

* overcomes ventilation issues due to body habitus

129
Q

what level spinal anesthetic works well for cystoscopies?

A

T-10 sensory level

130
Q

why would spinal anesthetics be contraindicated for cystoscopies?

A
  • spinal insertion can take longer than cystoscopy

* recovery from spinal might linger and increase release from PACU

131
Q

why not epidural for cystoscopy?

A

by the time it sets in (15-20min), case could have been done

132
Q

what variables would affect whether or not to run cystoscopy as a MAC?

A
  • patient pain level

* patient’s airway and body habitus

133
Q

what does TURP/TURB stand for?

A
  • TURP – trans-urethral resection of prostate

* TURB – trans-urethral resection of bladder

134
Q

describe a TURP

A

surgeon goes in through cystoscope and uses resectascope to resect prostatic tissue

  • requires lots of irrigation
  • large fluid shifts and blood loss
135
Q

what are the disadvantages of using NS/LR for irrigation (TURP)?

A

ionized, so cannot use cautery

136
Q

absorption of irrigation is dependent upon what?

A
  • type of irrigation
  • length of surgery
  • hydrostatic pressure of irrigant – dependent on height of irrigation fluid
137
Q

on average, how much irrigation fluid is absorbed?

A

20ml/min

138
Q

what are the deleterious effects of irrigation absorption/dilution (TURP syndrome)

A
  • cardiovascular collapse and heart failure
  • pulmonary edema
  • hyponatremia – CNS –seizures, confusion, coma
  • cerebral edema 2º to hypoosmolarity
  • anemia due to hemolysis
139
Q

what are the early signs of TURP syndrome in the awake pt?

A
  • restlessness, headace, N/V
  • CONFUSION/SLURRED SPEECH
  • tachypnea
140
Q

what are the later signs of TURP syndrome?

A
  • seizure – non-responsive pt

* tachycardia and hypertension followed by bradycardia and hypotension followed by CV collapse

141
Q

how is TURP syndrome confirmed?

A

STAT serum Na

142
Q

what is the treatment for TURP syndrome?

A
  • removed absorbed water – loop diuretics
  • restrict fluid intake
  • hypertonic saline to correct hyponatremia
  • correct seizures with benzos and phenytoin
  • intubation to protect AW
  • support CV system as needed
143
Q

what causes hypothermia in TURP procedures?

A

large amounts of cold irrigation

144
Q

what is the cause of TURP-related disseminated intravascular coagulopathy?

A

release of thromboplastin from the prostate

145
Q

what is the cause of TURP-related septicemia?

A

prostate is often colonized with bacteria due to its vicinity to the colon

146
Q

describe the anesthetic choices for TURP/TURB

A
  • spinal/epidural (sensory level to T-10) – has advantage of good pain relief and allows for monitoring of mentation
  • GA – acceptable esp when spinal/epidural puncture is contraindicated in pt
147
Q

describe extracorporeal shock wave lithotripsy (ESWL)

A

repetitive high energy shock waves are focused on the kidney stone to help break it up so it can pass down urinary tract

148
Q

what are the two means of lithotripsy?

A
  • YAG laser

* extracoporeal shock wave lithotripsy (ESWL)

149
Q

describe the use of ureteral stents in lithotripsy

A

ureteral stents are placed prior to aid in passage of small stone fragments via cystoscopy

150
Q

describe the contraindications of regional/continuous epidural for ESWL

A
  • air for loss of resistance technique – residual air can dissipate shock waves and injure neural tissue
  • foam tape may dissipate energy of shocks
  • no control over diaphragmatic movement – might move stone in and out of shock zone
151
Q

why GA for ESWL?

A

allows control of excessive diaphragmatic excursions

152
Q

why not MAC for ESWL?

A

no control of diaphragmatic excursions

153
Q

what are the anesthetic considerations for using ESWL?

A
  • shock waves can cause dysrhythmias even if triggered to R wave of ECG
  • patients with pacemakers and AICDs can be damaged by shock waves
154
Q

describe percutaneous nephrolithotomy tubes

A

tube placed through back into kidney to drain urine and large kidney stones

155
Q

what type of anesthetic is used for percutaneous nephrolithotomy tube placement?

A

GA

156
Q

what position is the pt in for percutaneous nephrolithotomy tubes?

A

prone jackknife

157
Q

what position are prostatectomies/ cystectomies performed in?

A

hyperextended supine position – to ain in pelvic dissection and exposure of pelvic lymph nodes
* t-burg often added

158
Q

what are the surgical considerations for prostatectomies/ cystectomies?

A
  • significant blood loss
  • direct arterial blood pressure monitoring
  • good IV access – consider central line
  • might need indigo carmen or methylene blue for visualization of ureters or check for bladder perforations
159
Q

why not regional for prostatectomy/cystectomy?

A
  • pelvic and abdominal pressure
  • large blood loss exacerbating vasodilation of regional
  • pts sedated under regional have a poor tolerance of the positioning
160
Q

if doing A-V fistula under regional/MAC, what is the major concern?

A

never enough local – when tunneling and placing graft under skin, be prepared to bolus propofol

161
Q

why do pts move during MAC for permacath placement?

A
  • airway obstruction
  • saliva/coughing
  • being in one position for a prolonged time
  • pain from lack of local
162
Q

what technique is used for vascath placement?

A

modified seldinger technique

163
Q

what are the positions commonly used for nephrectomy?

A
  • jackknife

* thorocoabdominal

164
Q

what is the anesthetic plan for nephrectomy?

A
  • GA
  • direct arterial pressure monitoring
  • good IV access +/- central venous line
165
Q

what are the specific considerations for nephrectomy?

A
  • potential for extensive blood loss
  • remember adrenal gland is being removed
  • reflex renal vasoconstriction can occur in the non-affected kidney – can cause post op renal failure (consider mannitol prior to dissection)
166
Q

what is the key issue in renal transplants?

A

immunosuppression

167
Q

how is the pt prepped for renal transplant?

A
  • preoperative optimization with dialysis is manditory

* K

168
Q

what are the best choices for muscle relaxation for renal transplants?

A
  • atracurium/cisatracurium – not renaly excreted

* rocuronium – short acting and not dependent on renal secretion

169
Q

special considerations for renal transplant

A
  • heparin for anticoagulation prior to clamping the iliac vessels
  • injection of CCBs into the graft helps prevent reperfusion injury
  • mannitol helps with osmotic diuresis
170
Q

what are the monitoring considerations for renal transplants?

A
  • CVP useful to evaluate preload
  • UOP – good UOP after arterial anastomosis indicates good graft function (assisted with mannitol)
  • volume loading so kidney has a preload to filter
171
Q

what electrolyte abnormalities are associated with renal transplants?

A

hyperkalemia reported with release of arterial vascular clamp – watch ECG (T-waves)

ANESTHESIA PRACTICE 3 (5 decks)

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