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nura 620 anesthesia and coexisting conditions > Renal > Flashcards

Renal Flashcards

1
Q

Precursors of renal disease

A

DM
HTN
Family Hx
> 65 yo

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2
Q

Kidneys receive ______% of CO.

A

20-25%

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3
Q

Kidneys are autoregulated between MAP of _________ mmHg.

A

50-150 mmHg

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4
Q

Kidneys: responsibilities/contributions

A
  • water conservation
  • electrolyte homeostasis
  • acid/base balance
  • neurohormonal functions
  • waste filtration
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5
Q

Normal GFR, variability, and estimated decline

A

90-140 ml/min/1.73m2

varies with gender, body weight, age

decreases 1% per year after the age of 20 (10% per decade after 30)

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6
Q

best measure of renal function

A 
creatinine clearance (most practical & inexpensive)
direct measurement of clearance - creatinine and inulin
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7
Q

What is creatinine clearance

A

most reliable measure for clinically assessing overall kidney function (GFR)

endogenous marker of renal filtration

produced at constant rate

freely filtered - not reabsorbed

normal: ~110-150 ml/min

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8
Q

Pitfall of serum creatinine

A

slow 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 may not increase for about a week

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9
Q

What is serum creatinine?

A

creatinine is a product of muscle metabolism

serum creat directly r/t body muscle mass

can be used to reliably estimate GFR in NON critically ill pt

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10
Q

Normal creatinine

A

men: .8 - 1.3 mg/dl
women: .6 - 1 mg/dl

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11
Q

What is BUN?

A

directly r/t protein catabolism

sometimes used, but not ideal

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12
Q

BUN: results are potentially misleading d/t?

A

dietary intake (high or low protein)

co existing disease (GI bleeding, febrile illness - catabolic illness)

intravascular fluid volume (dehydration)

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13
Q

Despite extraneous variables - BUN > 50 mg/dL (normal 10-20 mg/dL) usually reflect ________ GFR/impaired renal function.

A

DECREASED GFR/impaired renal function

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14
Q

Renal tubular dysfunction

A

established by demonstrating that the kidneys do not produce appropriately concentrated urine in the presence of a physiologic stimulus for the release of ADH

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15
Q

Transient proteinuria

A

relatively common (5%-10% of adults)

associated with fever, CHF, seizures, pancreatitis, exercise

~up to 150 mg protein/day

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16
Q

Persistent proteinuria

A

generally implies renal disease

~>750 mg protein/day

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17
Q

Normal urine specific gravity and use

A

> 1.018 is adequate

measures urine concentrating ability

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18
Q

What is fractional excretion of sodium?

A

measure of percentage of filtered sodium that is excreted in urine

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19
Q

Usefulness of fractional excretion of Na?

A

useful to distinguish hypovolemia and renal injury

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20
Q

FE na > 2% (or urine na concentration > 40 mEq/L) reflects?

A

decreased ability of the renal tubules to conserve sodium

-consistent with TUBULAR DYSFUNCTION

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21
Q

FE NA < 1% (or urine na excretion < 20 mEq/L occurs when?

A

normally functioning tubules are conserving na (more of a reassuring sign)

could be more related to hypovolemia rather than intrarenal injury

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22
Q

U/A: microhematuria can be indicative of?

A
  • renal calculi causing damage
  • cancerous growth
  • glomerulonephritis
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23
Q

Usefulness of a U/A

A

useful for renal tubular dysfunction and urinary tract disease

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24
Q

What values can be obtained from a U/A

A

Detects presence of

  • protein
  • glucose
  • acetoacetate
  • blood
  • leukocytes

urine pH & solute concentrations (specific gravity)

microscopy is used to identify cells, casts, microorganisms, crystals

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25
Q

U/A: WBC cast =

A

pyelonephritis

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26
Q

U/A: RBC cast =

A

acute glomerulonephritis

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27
Q

AKI is characterized by:

A
  • deterioration of renal function - hours to days
  • failure to excrete waste products
  • failure to maintain fluid & electrolyte homeostasis
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28
Q

AKI diagnosis

A
  • serum creatinine increase > .3 mg/dL within 48 hrs or >50% over 7 days
  • acute drop in urine: <0.5mL/kg/hr for > 6 hrs
  • severe injury: UO < 100 ml/day
  • diagnostic biomarkers & U/A
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29
Q

AKI: s/s

A

usually absent in early stages

generalized malaise
fluid overload (dyspnea, edema, HTN)
nausea
confusion
hematuria

**Caution: encephalopathy, coma, seizures, death

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30
Q

AKI etiology

A

associated with other systemic disease/clinical conditions/drugs/interventional therapy

surgeries that are higher risk for AKI

  • big CV surgeries
  • vascular
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31
Q

AKI causes: prerenal

A

hypoperfusion

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32
Q

AKI causes: intrarenal

A

underlying renal causes, ischemia, nephrotoxins

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33
Q

AKI causes: postrenal

A

urinary collecting system obstruction

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34
Q

Azotemia

A

condition marked by abnormally high serum concentrations of nitrogen containing compounds such as BUN & creatinine and is HALLMARK OF AKI, regardless of cause

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35
Q

Pre renal azotemia: causes

A

pre existing CHF, liver dysfunction, septic shock

reduced RBF d/t decrease in PP (consider hypotension and vasodilation during anesthesia)

hypovolemia & blood loss

36
Q

Early recognition and optimization of prerenal azotemia is important in order to prevent?

A

ischemia induced acute tubular necrosis & tubular cell injury

rapidly reversible if underlying cause treated

37
Q

Why are the elderly susceptible to prerenal azotemia?

A

hypovolemia

renovascular disease

38
Q

Intrinsic azotemia is categorized according to site of injury i.e…..

A
  • glomerulus
  • renal tubules - ischemia or nephrotoxins (aminoglycosides, contrast dye)
  • interstitium
  • renal vasculature
39
Q

What consideration must be given to a surgery that may involve a cross clamping or particular vascular surgeries?

A

“reperfusion injury” with influx of inflammatory cells/cytokines/oxygen free radicals

40
Q

Postrenal azotemia: treatment option

A

removal of obstruction

percutaneous nephrostomy

recovery is inversely r/t duration of obstruction

41
Q

(Patient) risk factors for perioperative renal failure

A
  • pre existing renal dx
  • advanced age
  • CHF
  • PVD
  • DM
  • emergency surgery
  • major surgery (aortic aneurysm repair)
42
Q

(Anesthesia related) Iatrogenic risk factors for perioperative renal failure

A
  • inadequate fluid replacement
  • hypotension
  • delayed TX of sepsis
  • nephrotoxic drugs
43
Q

complications of AKI: neurologic

A 
confusion
asterixis
somnolence
seizures
polyneuropathy r/t build up of protein and AA
44
Q

complications of AKI: CV

A 
systemic HTN -- LVH
CHF
pulm edema r/t Na and H2O retention
dysrhythmias, conduction blocks (metabolic derangement)
uremic pericarditis
autonomic neuropathy
Inc CO r/t to maintain O2 delivery (compensation for anemia)
accelerated CAD
45
Q

complications of AKI: heme

A

anemia (hgb 6-8 – dec erythropoietin and dec RBC production and dec in RBC lifespan)
coagulopathy
HCT 20-30% common d/t hemodilution & decreased erythropoietin
increased risk of bleeding d/t uremia induced platelet dysfunction

46
Q

complications of AKI: metabolic

A 
hyperkalemia and metabolic acidosis
hyperphosphatemia & hypocalcemia
hypoalbuminemia
hypermagnesemia
uricemia
47
Q

complications of AKI: GI

A

anorexia
n/v
ileus (buildup of urea?)
gastroparesis – think of periop aspiration risk
hypersecretion of gastric acid – peptic ulceration and GI hemorrhage

48
Q

complications of AKI: infection

A

respiratory & urinary tracts
sites where breaks in normal anatomic barriers have occurred
impaired immune response - WBC function impaired

49
Q

Principles that guide anesthetic management

A

ONLY LIFE SAVING SURGERY WHEN POSSIBLE

  1. maintain adequate systemic BP & CO
  2. avoid further renal insults - hypovolemia, hypoxia, nephrotoxins
  3. invasive hemodynamic monitoring - ABG & lytes
  4. consider initiation of post - op dialysis if in stable condition
  5. caution with diuretics
50
Q

Chronic kidney disease defined

A

estimated GFR < 60 ml/min/1.73m2 for > or = 3 months

@GFR < 25 ml/min – ESRD – dialysis or rental tx

51
Q

Clinical manifestations of CKD are related to:

A
  • inability to excrete waste
  • regulate fluid and electrolyte balance
  • secrete hormones
52
Q

Intrarenal hemodynamic changes likely responsible for progression of CKD

A
  1. glomerular HTN
  2. glomerular hyperfiltration & permeability changes
  3. glomerulosclerosis
53
Q

Goal and Management of CKD

A

reduce systemic & glomerular HTN:

  • ACE inhibitors
  • ARBs
  • moderate protein restriction
  • strict control of BG
  • hyperlipidema likely - statin therapy advised
  • smoking cessation
54
Q

Patients with CKD remain relatively asymptomatic until RF is < ____% of normal.

A

10

55
Q

CKD: 3 stages of adaptation

A
  1. GFR decreases w/ rise in creatinine & urea
  2. serum K increases (normal until GFR approaches 10% of normal)
  3. sodium homeostasis and regulation of ECF (volume overload/volume depletion)
56
Q

Complications of CKD: uremic syndrome, s/s

A 
anorexia
nausea
vomiting
pruritis
anemia
fatigue
coagulopathy
--inability to excrete uremic toxins, secrete, regulate

BUN useful clinical indicator of severity & response to therapy

serum Cr poor clinical indicator

57
Q

Complications of CKD: uremic syndrome, TX

A

dietary protein restriction + dialysis

58
Q

complications of CKD: renal osteodystrophy

A

secondary hyperparathyroidism & dec vit d production – impairs intestinal absorption of ca

hypocalcemia stimulates PTH secretion - leads to bone marrow resorption to restore serum Ca concentrations

as GFR decreases, decrease in phosphate clearance - increase in serum phosphate/decrease in Ca

59
Q

renal osteodystrophy: tx

A

restrict dietary phospate, + oral ca and vit d supplements, antacids (to bind phosphorus in GI tract) (avoid mag & aluminum)

if medical therapies fail - subtotal parathyroidectomy

60
Q

CKD: anemia

A 
normochromic & normotcytic d/t dec erythropoietin
excess PTH (replace bone marrow with fibrous tissue)

TX: erythropoietin or darbepoietin; avoid blood transfusions; iron

61
Q

complications of CKD: uremic bleeding

A

increased tendency to bleed & persistent anemia

BLEEDING TIME - best correlates with tendency to bleed!

hemorrhagic episodes - significant source of morbidity

62
Q

uremic bleeding: TX

A

desmopressin - increases VIII - vWF complex (present within 2 - 4 hours & lasts 6 - 8 hours)

conjugated estrogens (onset approx 6 hours & lasts 14-21 days)

erythropoietin - enhances platelet aggregation & increases platelet counts

63
Q

CKD complications: CV changes

A

systemic HTN: contributes to CHF, CAD, CVD

uncontrolled HTN: speeds progression of disease

pathogenesis: retention of Na and H2O + activation of RAAS = intravascular volume expansion

dyslipidemias

silent MI

uremic pericarditis

64
Q

CV changes: treatment

A

dialysis - d/t hypervolemia & uremic pericarditis (keep in mind that dialysis will not fix HTN if the HTN is not related to hypervolemia)

increase dosage of antihypertensive drugs

tamponade - prompt drainage of effusion

65
Q

Management of CKD: BP control

A

remember that HTN is both a cause and a consequence of CKD - directly correlated with deterioration of renal function

MULTIMODAL DRUG THERAPY

  • ACE inhibitors & ARBs (1st line: especially in patients with proteinuria)
  • diuretics
  • Ca channel blockers
  • aldosterone antagonists
66
Q

Management of CKD: nutrition

A

modest protein restriction (0.6 g/kg daily)

dietary phosphorus restricted (600 - 800 mg/day) - can give phosphorus binders

vitamin D

Advanced disease - alkali salts

Na restriction (<1.5 - 2 g/day) (to prevent volume overload)

long term: euglycemic

67
Q

Management of CKD: anemia

A

benefits vs risks of blood administration and management of anemia intraoperatively

erythropoietin (target hgb 10-11.5 g/dL, but really hard to achieve)

68
Q

When is dialysis advised for CKD?

A

GFR 10 ml/min/1.73m2

effective dialysis significantly correlated with survival!

69
Q

Management of Anesthesia: Pre op evaluation

A
  • is renal function stable? - trends in serum creatinine concentration
  • blood volume status before & after dialysis
  • VS
  • glucose management (parameters may be facility dependent)
  • BP (ACE inhibitors and ARBs often withheld day of surgery)
  • serum K should not exceed 5.5 mEq/L day of surgery (not a hard stop necessarily)
  • anemia (consider surgery type, does the pt need optimization before sx)
  • coagulopathy (consider surgery type, does the pt need optimization before sx)
  • gastric aspiration prophylaxis (dose adjustment)
  • dialysis within 24 hours preceding elective surgery
70
Q

Management of Anesthesia: Induction considerations

A

safely accomplished with most IV induction drugs - concern is accumulation of active metabolites

ESRD - respond to induction agents as if they are hypovolemic/under-resuscitated

uremia & antihypertensives - result in hypotension

Exaggerated CNS effects - uremia induced changes in BBB

attenuated SNS activity impairs compensatory peripheral vasoconstriction (exaggerated hypotension)
–consider with position changes, drug induced myocardial depression, initiation of PPV/Peep, small decreases in blood volume

71
Q

Can you induce a pt with CKD with succinylcholine?

A

Yes if K is <5.5

K release is not exaggerated in pts with CKD

But okay to use short onset like roc

72
Q

Management of anesthesia: maintenance considerations with VA

A

balanced approach

VA: good control of HTN & decrease dose of muscle relaxant
VA: depression of CO potential hazard

sevo sometimes avoided (fluoride nephrotoxicity/compound A), but no evidence that patients with renal disease are at increased risk

73
Q

Management of anesthesia: maintenance considerations with muscle relaxants

A

slow excretion of vec and roc
–prudent to decrease initial dose and base subsequent doses on TOF

cisatracurium independent of renal function!

74
Q

Management of anesthesia: maintenance considerations with opioids

A

morphine & meperidine undergo metabolism to potentially neurotoxic compounds that rely on renal clearance (morphine 6 glucuronide & normeperidine)
hydromorphone also has active metabolite - doesn’t mean that you can’t use, just reduce dose and expect prolongs effect (especially in elderly or other comorbidities)

75
Q

Management of anesthesia: maintenance considerations with reversal

A

renal excretion 50% of clearance of neostigmine, prolonged effect

  • “recurarization” is unlikely because of potentially prolonged effect (so if the patient wakes up kind of weak, consider that its not recurarization, but another issue like metabolic derangement or CNS effect)
  • sugammadex: not recommended in low creatinine clearance (<30 ml/min) or RRT
76
Q

Management of anesthesia: maintenance considerations with fluid management & u/o

A

may benefit from preop hydration (500 ml) if…

  • –do not require HD
  • –w/o renal disease undergoing surgery with high incidence of post op RF

CAUTION - LR or K containing

U/O - 0.5 ml/kg/h

Diuretics in absence of intravascular fluid volume replacement is not advised

HD - dependent - narrow margin of safety

77
Q

Management of anesthesia: maintenance considerations with POSITIONING

A

positioning - prone to bruising, sloughing/protect vulnerable nerves

fistulas must be protected

NO BP cuff on arm with fistula

If possible, maintain intra op access to arm with fistula

78
Q

Management of anesthesia: maintenance considerations with monitoring

A

AVOID venipuncture in nondominant arm & upper part of dominant arm
AVOID radial and ulnar cannulation (same may be said of brachial and axillary)

  • femoral cannulation - risk of infection
  • DP and PT arteries - inconvenient/difficult to access
  • Arterial pressure & ABG will not be accurate if on same extremity of AV fistula
  • venous pressure monitoring - may be helpful, CVC may difficult
  • TEE (for fluid management and overall CV function)
  • Dialysis catheters may be used (THOUGH STRONGLY DISCOURAGED)
    1) asceptic technique
    2) aspirate heparin
    3) heparin after d/c of use
79
Q

Management of anesthesia: maintenance considerations with REGIONAL ANESTHESIA

A

May be considered
Concern for: bleeding, pre existing neuropathies

Considerations:

  • sympathetic block T4-T10 may improve renal function by attenuating catecholamine induced renal vasoconstriction and suppressing surgical stress response
  • BUT pts have platelet dysfunction, increased bleeding times, residual heparin from potential use of dialysis line
  • brachial plexus blockade - assess for presence of uremic neuropathies!!
  • presence of coexisting metabolic acidosis - may decrease seizure threshold in response to LAs
80
Q

Management of anesthesia: POST OPERATIVE CONSIDERATIONS

A

skeletal muscle weakness: from residual NM blockade (unlikely) or….antibiotics, acidosis, electrolyte imbalance (its not that It couldn’t be weakness from inappropriate dosing of NMB, but consider other possibilities as well)

caution w/ parenteral opioids - respiratory depression

avoid NSAIDs - may be more difficult to institute multimodal pain control in this population

continuous ECG monitoring (potential metabolic derangements)

supplemental O2 - don’t tolerate hypoxia well

check electrolytes, BUN, creatinine, HCT, chest xray if concern for pulmonary edema

bleeding - uremic coagulopathy

81
Q

Renal transplant: general anesthesia considerations

A 
RA and GA successful - GA is more common
minimize decrease in CO - promote renal perfusion
high - normal BP is required
cisastracurium is often drug of choice
CVP is useful
Mannitol (osmotic diuretic)
albumin administration is helpful
release of vascular clamps - be aware of hypotension and cardiac arrest
82
Q

Renal transplant: regional anesthesia considerations

A
  • Advantages - No ETT & muscle relaxants
  • Advantage negated if need to supplement RA with IV anesthetics
  • Control of BP may be more difficult
  • Controversial in presence of abnormal coagulation
83
Q

Renal transplant: post op complications and associated TX

A

-acute immunologic rejection - almost IMMEDIATE
only TX: remove the kidney

-delayed signs of graft rejection - fever, local tenderness, deterioration of urine output
TREATMENT:
—high dose corticosteroids & antilymphocyte globulin
—monoclonal antibodies
—tacrolimus
—mycophenolate mofetil
—dialysis may be required

-opportunistic infections may occur

84
Q

Renal transplant: additional anesthesia considerations

A
  • often elderly
  • co existing CV disease
  • co existing DM
  • consider side effects of immunosuppressant drugs - HTN, low seizure threshold, anemia, thrombocytopenia
  • consider drugs that are excreted by kidneys
  • avoid drugs that are nephrotoxic or dependent on renal clearance
  • minimize decreases in RBF
85
Q

AKI management: Treatment Aims

A
  1. limit further renal injury
  2. correct fluid/electrolyte/acid base derangements
  3. reverse underlying causes of injury (hypovolemia, hypotension, low CO, sepsis)
  4. Maintain MAP 65 or > (no evidence supporting outcomes with supraphysiologic values)
  5. fluid resuscitation (goal directed therapy) & vasopressor therapy (norepi/vasopressin)
  6. diuretics not advised
  7. alkalinization of urine with sodium bicarb (rhabdo); reduces incidence of contrast induced nephropathy
  8. dialysis - mainstay for severe AKI; volume overload, hyperkalemia, severe metabolic acidosis, symptomatic uremia, overdose with dialyzable drug - day of surgery/day before

nura 620 anesthesia and coexisting conditions (7 decks)

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