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
U/A: WBC cast =
pyelonephritis
26
U/A: RBC cast =
acute glomerulonephritis
27
AKI is characterized by:
- deterioration of renal function - hours to days - failure to excrete waste products - failure to maintain fluid & electrolyte homeostasis
28
AKI diagnosis
- 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
29
AKI: s/s
usually absent in early stages ``` generalized malaise fluid overload (dyspnea, edema, HTN) nausea confusion hematuria ``` **Caution: encephalopathy, coma, seizures, death
30
AKI etiology
associated with other systemic disease/clinical conditions/drugs/interventional therapy surgeries that are higher risk for AKI - big CV surgeries - vascular
31
AKI causes: prerenal
hypoperfusion
32
AKI causes: intrarenal
underlying renal causes, ischemia, nephrotoxins
33
AKI causes: postrenal
urinary collecting system obstruction
34
Azotemia
condition marked by abnormally high serum concentrations of nitrogen containing compounds such as BUN & creatinine and is HALLMARK OF AKI, regardless of cause
35
Pre renal azotemia: causes
pre existing CHF, liver dysfunction, septic shock reduced RBF d/t decrease in PP (consider hypotension and vasodilation during anesthesia) hypovolemia & blood loss
36
Early recognition and optimization of prerenal azotemia is important in order to prevent?
ischemia induced acute tubular necrosis & tubular cell injury **rapidly reversible if underlying cause treated**
37
Why are the elderly susceptible to prerenal azotemia?
hypovolemia | renovascular disease
38
Intrinsic azotemia is categorized according to site of injury i.e.....
- glomerulus - renal tubules - ischemia or nephrotoxins (aminoglycosides, contrast dye) - interstitium - renal vasculature
39
What consideration must be given to a surgery that may involve a cross clamping or particular vascular surgeries?
"reperfusion injury" with influx of inflammatory cells/cytokines/oxygen free radicals
40
Postrenal azotemia: treatment option
removal of obstruction percutaneous nephrostomy recovery is inversely r/t duration of obstruction
41
(Patient) risk factors for perioperative renal failure
- pre existing renal dx - advanced age - CHF - PVD - DM - emergency surgery - major surgery (aortic aneurysm repair)
42
(Anesthesia related) Iatrogenic risk factors for perioperative renal failure
- inadequate fluid replacement - hypotension - delayed TX of sepsis - nephrotoxic drugs
43
complications of AKI: neurologic
``` confusion asterixis somnolence seizures polyneuropathy r/t build up of protein and AA ```
44
complications of AKI: CV
``` 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
complications of AKI: heme
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
complications of AKI: metabolic
``` hyperkalemia and metabolic acidosis hyperphosphatemia & hypocalcemia hypoalbuminemia hypermagnesemia uricemia ```
47
complications of AKI: GI
anorexia n/v ileus (buildup of urea?) gastroparesis -- think of periop aspiration risk hypersecretion of gastric acid -- peptic ulceration and GI hemorrhage
48
complications of AKI: infection
respiratory & urinary tracts sites where breaks in normal anatomic barriers have occurred impaired immune response - WBC function impaired
49
Principles that guide anesthetic management
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
Chronic kidney disease defined
estimated GFR < 60 ml/min/1.73m2 for > or = 3 months @GFR < 25 ml/min -- ESRD -- dialysis or rental tx
51
Clinical manifestations of CKD are related to:
- inability to excrete waste - regulate fluid and electrolyte balance - secrete hormones
52
Intrarenal hemodynamic changes likely responsible for progression of CKD
1. glomerular HTN 2. glomerular hyperfiltration & permeability changes 3. glomerulosclerosis
53
Goal and Management of CKD
reduce systemic & glomerular HTN: - ACE inhibitors - ARBs - moderate protein restriction - strict control of BG - hyperlipidema likely - statin therapy advised - smoking cessation
54
Patients with CKD remain relatively asymptomatic until RF is < ____% of normal.
10
55
CKD: 3 stages of adaptation
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
Complications of CKD: uremic syndrome, s/s
``` 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
Complications of CKD: uremic syndrome, TX
dietary protein restriction + dialysis
58
complications of CKD: renal osteodystrophy
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
renal osteodystrophy: tx
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
CKD: anemia
``` normochromic & normotcytic d/t dec erythropoietin excess PTH (replace bone marrow with fibrous tissue) ``` TX: erythropoietin or darbepoietin; avoid blood transfusions; iron
61
complications of CKD: uremic bleeding
increased tendency to bleed & persistent anemia BLEEDING TIME - best correlates with tendency to bleed! hemorrhagic episodes - significant source of morbidity
62
uremic bleeding: TX
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
CKD complications: CV changes
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
CV changes: treatment
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
Management of CKD: BP control
**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
Management of CKD: nutrition
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
Management of CKD: anemia
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
When is dialysis advised for CKD?
GFR 10 ml/min/1.73m2 effective dialysis significantly correlated with survival!
69
Management of Anesthesia: Pre op evaluation
- 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
Management of Anesthesia: Induction considerations
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
Can you induce a pt with CKD with succinylcholine?
Yes if K is <5.5 K release is not exaggerated in pts with CKD But okay to use short onset like roc
72
Management of anesthesia: maintenance considerations with VA
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
Management of anesthesia: maintenance considerations with muscle relaxants
slow excretion of vec and roc --prudent to decrease initial dose and base subsequent doses on TOF cisatracurium independent of renal function!
74
Management of anesthesia: maintenance considerations with opioids
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
Management of anesthesia: maintenance considerations with reversal
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
Management of anesthesia: maintenance considerations with fluid management & u/o
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
Management of anesthesia: maintenance considerations with POSITIONING
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
Management of anesthesia: maintenance considerations with monitoring
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
Management of anesthesia: maintenance considerations with REGIONAL ANESTHESIA
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
Management of anesthesia: POST OPERATIVE CONSIDERATIONS
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
Renal transplant: general anesthesia considerations
``` 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
Renal transplant: regional anesthesia considerations
- 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
Renal transplant: post op complications and associated TX
-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
Renal transplant: additional anesthesia considerations
- 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
AKI management: Treatment Aims
1. limit further renal injury 2. correct fluid/electrolyte/acid base derangements 3. reverse underlying causes of injury (hypovolemia, hypotension, low CO, sepsis) 4. Maintain MAP 65 or > (no evidence supporting outcomes with supraphysiologic values) 5. fluid resuscitation (goal directed therapy) & vasopressor therapy (norepi/vasopressin) 6. diuretics not advised 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