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Coexisting > Renal > Flashcards

Renal Flashcards

1
Q

What percentage of CO do kidneys receive?

A

20-25%

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2
Q

Autoregulation occurs with MAP between…

A

…50-150 mmHg

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3
Q

Kidney Responsibilities

A
  1. Water conservation
  2. Electrolyte homeostasis
  3. Acid-base balance
  4. Neurohumoral/ hormonal functions
  5. Waste filtration
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4
Q

Precursors to Renal Disease

A
  • DM
  • HTN
  • Family history
  • > 65 y/o
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5
Q

Of the blood that the kidneys receive for CO, where is the majority of it directed?

A

Outer Cortex

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6
Q

What is Glomerular Filtration Rate (GFR)?

A

Measurement of volume filtered through glomerular capillaries and into Bowman’s capsule per unit of time

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7
Q

What is the best measure of renal function?

A

GFR

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8
Q

What do we (mostly) use for GFR measurements?

A
  • Creatinine clearance (most practical & inexpensive)
  • Direct measurement of clearance: Creatinine and Inulin
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9
Q

Normal GFR

A

90 to 140 mL/min/1.73m2

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10
Q

GFR varies with…

A
  • gender
  • body weight
  • age
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11
Q

GFR decreases…

A

…1% per year after age 20 (10% per decade after 30)

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12
Q

When the GFR decreases to ______, we start to see clinical manifestations.

A

GFR < 15 mL/min/1.73m2

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13
Q

% of normal kidney function: Stage 1

A

90% or more

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14
Q

% of normal kidney function: Stage 2

A

60-89%

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15
Q

% of normal kidney function: Stage 3

A

30-59%

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16
Q

% of normal kidney function: Stage 4

A

15-29%

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17
Q

% of normal kidney function: Stage 5

A

< 15%

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18
Q

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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19
Q

Most reliable measure for clinically assessing overall kidney function (GFR)?

A

Creatinine Clearance

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20
Q

Serum Creatinine

A
  • Creatinine is product of muscle metabolism
  • Serum creatinine directly r/t body muscle mass
  • Can be used to reliably estimate GFR in non-critically ill patient
    • ​rate of creatinine production and its Vd can be abnormal in critcally ill pts
  • 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 ↓ from 100 mL/min to 10 mL/min, serum creatinine values do not ↑ for ~ 1 wk
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21
Q

Blood Urea Nitrogen (BUN)

A
  • Directly r/t protein catabolism, inversely r/t GFR
  • Sometimes used, but not ideal
  • Results potentially misleading d/t:
    1. Dietary intake (high or low protein)
    2. Co-existing disease (GI bleeding, febrile illness)
    3. Intravascular fluid volume (dehydration)
    • Can see increase in BUN despite normal GFR in situations above
  • Normal = 10-20 mg/dL
  • Despite extraneous variables: BUN > 50 mg/dL usually reflect ↓GFR/ impaired renal function
    • BUN not elevated in kidney dz until GFR ↓to almost 75% of normal
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22
Q

Renal tubular dysfunction

A

Kidneys do not produce appropriately concentrated urine in presence of a physiologic stimulus for release of ADH

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23
Q

Renal Tubular Function and Integrity: Concentration

A
  • Assessed by measuring urine concentrating ability
  • Urine specific gravity > 1.018 = renal tubules adequately able to concentrate urine
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24
Q

Renal Tubular Function and Integrity: Protein

A
  • Presence of protein may reflect renal tubule damage–why we use this as a measure of renal tubular function
  • Proteinuria- relatively common (5%-10% of adults)
    • Transient: associated w/ fever, CHF, seizures, pancreatitis, exercise
    • Persistent: generally implies renal dz
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25
Q

Patients without renal disease can excrete up to ______ mg of protein per day (greater amounts may be present with exercise).

A

150 mg

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26
Q

What amount of protein in the urine is considered abnormal and indicative of servere glomerular damage?

A

> 750 mg/day

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27
Q

Renal Tubular Function and Integrity:

Fractional Excretion of Sodium (FENA)

A
  • Measure of percentage of filtered Na+ excreted in urine
  • Useful to distinguish hypovolemia and renal injury (differentiate b/t prerenal and renal causes of azotemia)
  • FENA > 2% (or urine Na+ concentration > 40 mEq/L) reflects ↓ ability of renal tubules to conserve Na+ and is consistent w/ tubular dysfunction
  • FENA < 1% (or urine Na+ excretion < 20 mEq/L) occurs when normally functioning tubules are conserving Na+ and is suggestive of prerenal azotemia
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28
Q

Renal Tubular Function and Integrity: Urinalysis

A
  • Useful for renal tubular dysfunction and urinary tract disease
  • Detects presence of:
    • Protein
    • Glucose
    • Acetoacetate
    • Blood
    • Leukocytes
  • Urine pH & solute concentrations (specific gravity) determined
  • Microscopy used to identify cells, casts, microorganisms, crystals
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29
Q

Microhematuria found in U/A may reflect what?

A
  • Glomerulonephritis
  • Renal calculi
  • CA of the GU tract
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30
Q

RBC casts found in U/A may reflect what?

A

Acute glomerulonephritis

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31
Q

WBC casts found in U/A may reflect what?

A

Pyelonephritis

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32
Q

Acute Kidney Injury (AKI) is characterized by…

A
  • Deterioration of renal function- hrs to days
  • Failure to excrete waste products
  • Failure to maintain fluid & electrolyte homeostasis
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33
Q

Diagnosis of AKI

A
  • Increase in serum creatinine > 0.3 mg/ dL in 48 hrs or > 50% increase over 7 days
  • Acute drop in urine: < 0.5 mL/kg/h for > 6 hrs (oliguria)
  • Severe injury: UO < 100 mL/day
  • Diagnostic biomarkers & urinalysis
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34
Q

S&S of AKI

A
  • Generalized malaise
  • Fluid overload
    • dyspnea
    • edema
    • HTN
  • Nausea
  • Confusion
  • Hematuria
  • ** Caution: encephalopathy, coma, seizures, death
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35
Q

AKI Definition: Society of Thoracic Surgeons

A

new dialysis

OR

rise in serum creatinine >2 mg/dL,

50% increase in serum creatinine

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36
Q

AKI Definition: The Acute Dialysis Quality Initiative Group

A

Creatinine rise of:

50% as “risk”

100% “injury”

200% “failure”

(RIFLE criteria)

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37
Q

AKI Definition: Acute Kidney Injury Network

A

1.5X or 0.3 mg/dL creatinine rise w/in 48-hr period

OR

> 6hrs of oliguria (modified RIFLE)

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38
Q

AKI Definition:

Kidney Disease Improving Global Outcomes

(KDIGO)

A

↑ in serum creat at least 0.3 mg/dL w/in 48 hrs

OR

↑ in serum creat 1.5X baseline w/in prior 7 days

OR

UOP < 0.5 mL/kg/h X 6 hrs

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39
Q

KDIGO definiton of AKI

Creatinine Criteria

Stage 1

A

Cr 1.5-1.9X baseline

OR

Cr increase >0.3 mg/dL

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40
Q

KDIGO definiton of AKI

Creatinine Criteria

Stage 2

A

Cr 2-2.9X baseline

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41
Q

KDIGO definiton of AKI

Creatinine Criteria

Stage 3

A

Cr > 3X baseline

OR

Cr > 4 mg/dL

OR

Initiation of Dialysis

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42
Q

KDIGO definiton of AKI

Urine Output Criteria

Stage 1

A

< 0.5 mL/kg/hr X 6-12 hrs

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43
Q

KDIGO definiton of AKI

Urine Output Criteria

Stage 2

A

< 0.5 mL/kg/hr for > 12 hrs

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44
Q

KDIGO definiton of AKI

Urine Output Criteria

Stage 3

A

< 0.3 mL/kg/hr for > 24 hrs

OR

Anuria > 12 hrs

45
Q

AKI Etiology

A
  • 5%-7% of hospitalized patients
  • Associated w/ other systemic disease/ clinical conditions/ drugs/ interventional therapy
46
Q

AKI Causes: Prerenal

A

Hypoperfusion

Hemorrhage, GI fluid loss, Trauma, Surgery, Burns, Cardiogenic shock, Sepsis, Hepatic failure, Aortic or renal artery clamping, Thromboembolism

47
Q

AKI Causes: Intrarenal (intrinsic)

A

Underlying renal causes

Ischemia

Nephrotoxins

Acute glomerulonephritis, Vasculitis, Interstitial nephritis (drug allergy, infiltrative diseases), Acute tubular necrosis, Ischemia, Nephrotoxic drugs (aminoglycosides, nonsteroidal anti-inflammatory drugs), Solvents (carbon tetrachloride, ethylene glycol), Heavy metals (mercury, cisplatin), Radiographic contrast dyes, Myoglobinuria, Intratubular crystals (uric acid, oxalate)

48
Q

AKI Causes: Postrenal

A
  • Urinary collecting system obstruction
  • Nephrolithiasis, BPH, Clot retention, Bladder CA*
49
Q

Azotemia Definition

A

Condition marked by abnormally high serum concentrations of nitrogen-containing compounds such as BUN & creatinine and is hallmark of AKI, regardless of cause.

50
Q

Prerenal Azotemia

A
  • ½ of hospital-acquired cases
    • Pre-existing CHF, liver dysfunction, septic shock
    • Reduced RBF d/t ↓ in PP
    • Hypovolemia & blood loss
  • Rapidly reversible if underlying cause treated
    • Untreated: = ischemia-induced acute tubular necrosis
  • Elderly susceptible: hypovolemia/ renovascular disease
  • Assess volume status, hemodynamics, drug therapy
  • Blood and urine specimens (Refer to Stoelting’s 22.5)
51
Q

What is the hallmark of AKI?

A

Azotemia

52
Q

Intrinsic Azotemia

A
  • Categorized according to site of injury
    • Glomerulus
    • Renal tubules- ischemia or nephrotoxins
    • Interstitium
    • Renal vasculature
  • Ischemic AKI typically reversible, but…
    • Irreversible cortical necrosis occurs if severe or prolonged ischemia
  • Reperfusion: influx of inflammatory cells/ cytokines/ oxygen free radicals
53
Q

Postrenal Azotemia

A
  • Urinary outflow tracts are obstructed (prostatic hyperplasia, prostate/cervical CA)
  • May occur at any level of collecting system
  • Recovery inversely r/t duration of obstruction
  • Treatment: percutaneous nephrostomy
54
Q

Risk Factors for Periop Renal Failure

A
  • Pre-existing renal dx
  • Advanced age
  • CHF
  • PVD
  • DM
  • Emergency surgery
  • Major surgery (aortic aneurysm repair)
55
Q

Iatrogenic Risk Factors for Periop Renal Failure

A
  • Inadequate fluid replacement
  • Hypotension
  • Delayed treatment of sepsis
  • Nephrotoxic drugs
56
Q

Complications of AKI: Neuro

A
  • Confusion
  • Somnolence
  • Asterixis
  • Seizures
  • Polyneuropathy r/t build up of protein & amino acids
57
Q

Complications of AKI: CV

A
  • Systemic HTN
  • CHF
  • Pulmonary edema r/t Na+ & H2O retention
  • Dysrhythmias
  • Uremic pericarditis
    • ​may be asymptomatic or have chest pain and cardiac tamponade
  • LVH
  • Inc CO
  • accelerated CAD, PVD
58
Q

Complications of AKI: Heme

A
  • Anemia (when creat. clearance falls below 30 mL/min)
  • Coagulopathy
  • Hct 20-30% common d/t hemodilution & ↓ erythropoietin
  • ↑ r/f bleeding d/t uremia-induced platelet dysfunction
    • decreased platelet aggregation and adhesiveness
59
Q

Complications of AKI: Metabolic

A
  • Hyperkalemia and metabolic acidosis
  • Hyperphos & hypocalc
  • Hypoalbuminemia
60
Q

Complications of AKI: GI

A
  • Anorexia, N/V
  • Ileus
  • Gastroparesis
  • GI bleeding
61
Q

Complications of AKI: Infection

A
  • Respiratory & urinary tracts and sites where breaks in normal anatomic barriers have occurred
  • Impaired immune response– white cell function are impaired in pts w/ kidney failure
62
Q

Management of AKI

A
  • No specific treatment modalities
  • Treatment aims:
    1. Limit further 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 w/ supraphysiologic values)
    5. Fluid resuscitation (goal-directed therapy) & vasopressor therapy (norepi/vasopressin)
    6. Diuretics not advised
    7. Alkalinization of urine w/ sodium bicarb (rhabdo); reduces incidence of contrast-induced nephropathy
    8. Dialysis- mainstay for severe AKI
63
Q

Indications for Dialysis in Management of AKI

A

Dialysis- mainstay for severe AKI:

  1. Volume overload
  2. Hyperkalemia
  3. Severe metabolic acidosis
  4. Symptomatic uremia
  5. Overdose w/ dialyzable drug – day of surgery/ day before
64
Q

AKI Prognosis

A
  • Hospital acquired AKI is poor
  • Mortality > 20%
  • Dialysis- mortality rates > 50%
  • Full recovery from AKI- 15%
  • Retain a degree of stable renal insufficiency- 5%
  • Continued deterioration throughout life- 5%
65
Q

AKI Management of Anesthesia/Principles that guide anesthetic management

A
  • High M&M
  • Only life-saving surgery
  • Principles that guide anesthetic management:
    1. Maintain adequate systemic BP & CO
    2. Avoid further renal insults – hypovolemia, hypoxia, nephrotoxins
    3. Invasive hemodynamic monitoring – ABGs & Lytes
    4. Consider initiation of post-op dialysis if in stable condition
    5. Caution w/ diuretics
66
Q

Chronic Kidney Disease: Defined

A

Estimated GFR <60 mL/min/1.73m2 for 3 months or more

67
Q

In the US, what is responsible for CKD?

A

DM & HTN responsible for 2/3 of all cases

(also glomerulonephritis, polycystic kidney disease)

68
Q

Clinical manifestations of CKD are due to:

A
  • Inability to:
    • Excrete waste
    • Regulate fluid and electrolyte balance
    • Secrete hormones
69
Q

CKD Incidence and Etiology

A
  • •U.S. Renal Data System of the NIH (2012)-
  • 636,000 individuals with ESRD
  • Prevalence continues- aging population/ increased survival
  • Incidence varies by race & ethnicity (African American, Native Americans, Hispanics)
  • Genetic variables + disparities in healthcare access
70
Q

Diagnosis of CKD

A
  • Diverse signs, non-specific complaints (fatigue, malaise, anorexia)
  • Diagnosis made during routine testing

Serum creatinine level &

urinary sediment analysis

71
Q

Progression of CKD:

Intrarenal hemodynamic changes likely responsible.

A
  • Glomerular HTN
  • Glomerular hyperfiltration & permeability changes
  • Glomerulosclerosis
72
Q

Progression of CKD:

Management

A
  • Reduce systemic & glomerular HTN:
    • ACEI’s & ARBs
    • Moderate protein restriction
    • Control BG
    • Hyperlipidemia - statin therapy advised
    • Smoking cessation
73
Q

Adaptation

A
  • Patients w/ CKD remain relatively asymptomatic until RF is < 10% of normal
  • 3 stages of adaptation:
    1. GFR ↓ w/ ↑ in creat & urea
    2. Serum K ↑ (normal until GFR approaches 10% of normal)
    3. Na+ homeostasis and regulation of ECF (volume overload/ volume depletion)
74
Q

Describe the balance of Na+ in CKD

A

Sodium balance remains fairly intact, but the system can be overwhelmed by abrupt increases or decreases in sodium intake.

Increase Na+ intake = volume overload

Decrease Na+ intake = volume depletion

75
Q

What is uremic syndrome?

A
  • Inability to excrete uremic toxins, secrete, regulate
  • BUN useful clinical indicator of severity & response to therapy
  • Serum creatinine poor clinical indicator
76
Q

S&S of uremic syndrome

A
  • N/V, Anorexia
  • Pruritus
  • Anemia, Fatigue
  • Coagulopathy
77
Q

Treatment of uremic syndrome

A

dietary protein restriction + dialysis

78
Q

Describe renal osteodystrophy

A
  • Secondary hyperparathyroidism & ↓ Vit D production – impairs intestinal absorption of Ca
  • Hypocalcemia stimulates PTH secretion – leads to bone resorption to restore serum Ca concentrations
  • As GFR ↓, phosphate clearance ↓ = ↑ serum phosphate/ ↓ Ca
79
Q

Renal osteodystrophy treatment

A
  • Restrict dietary phosphate
    • oral Ca and Vit D supplements
    • antacids to bind phos in GI tract (avoid mag & aluminum)
      • If medical therapies fail- subtotal parathyroidectomy
80
Q

CKD Complications: Anemia

A
  • Likely responsible for symptoms of fatigue, weakness, low exercise tolerance
  • Normochromic & normocytic d/t decreased erythropoietin
  • Excess parathyroid hormone (by replacing bone marrow with fibrous tissue)
81
Q

Anemia Treatment

A
  • Erythropoietin or darbepoetin
  • Avoid blood transfusions
  • Iron
82
Q

CKD Complications: Uremic Bleeding

A
  • ↑ tendency to bleed & persistent anemia (despite normal platelet count and normal PT/PTT)
  • Bleeding time: best correlates w/ tendency to bleed
  • Hemorrhagic episodes: significant source of morbidity
83
Q

Treatment for uremic bleeding

A
  • Desmopressin: ↑ factor 8-vWF complex (present w/in 2-4 hrs & lasts 6-8 hrs)
  • Conjugated estrogens (onset approx. 6 hrs & lasts 14-21 days)
  • Erythropoietin: enhances platelet aggregation & ↑ platelet counts
84
Q

CKD: Neurologic Changes

A
  • Initial symptoms may be mild
    • impaired abstract thinking, insomnia, irritability
  • As dz progresses- significant changes:
    • seizures, obtundations, uremic encephalopathy, coma
  • Advanced RF:
    • BLE symmetric mixed motor and sensory polyneuropathy & weakness
85
Q

CKD: Neurologic Changes Treatment

A

HD may be helpful

86
Q

CKD: CV Changes

A
  • Systemic HTN- contributes to CHF, CAD, CVD
    • Uncontrolled HTN speeds dz progression
    • Pathogenesis- retention of Na & water + RAAS activation = intravascular volume expansion
  • Dyslipidemias
  • Silent MI
  • Uremic pericarditis
87
Q

CKD: CV Changes Treatment

A
  • Dialysis- d/t hypervolemia & uremic pericarditis
  • Increase dosage of antihypertensives
  • Tamponade- prompt drainage of effusion
88
Q

Management of CKD

A
  • BP control: ACEI & ARBs (1st line), diuretics, Ca channel blockers, aldosterone antagonists
  • Nutrition
    • Protein restriction (0.6 g/kg/day)
    • Phos restriction 600–800 mg/ day
    • Sodium restriction (< 1500-2000 mg/day)
    • Advanced dz- alkali salts
    • Vitamin D
    • Long-term: euglycemia
  • Anemia: Benefits vs risks
    • Erythropoietin (target Hb range 10-11.5 g/ dL)
  • Renal Replacement Therapy
    • Advised when GFR 10 mL/min/1.73 m2
    • Effective dialysis = greater survival
89
Q

Management of Anesthesia: Pre-op

A
  • Preop Eval
    • Renal function stable? –trends in serum creat.
    • Blood volume status before & after dialysis
    • VS
    • BG management
    • BP (ACE-I and ARBs often withheld day of surgery)
    • Serum K should not exceed 5.5 mEq/ L day of surgery
    • Anemia
    • Coagulopathy
    • Gastric aspiration prophylaxis (dose adjustment)
    • Dialysis w/in 24 hrs preceding elective surgery
90
Q

Management of Anesthesia: Induction

A
  • Safe w/ most IV induction drugs – concern is accumulation of active metabolites
  • ESRD pts- respond as if they are hypovolemic
  • Uremia & antihypertensives – result in hypotension
  • Attenuated SNS activity impairs compensatory peripheral vasoconstriction (exaggerated hypotension)
  • Exaggerated CNS effects – uremia induced
  • May induce w/ succinylcholine if K is <5.5
91
Q

Management of Anesthesia: Maintenance

A
  • Balanced approach – VA’s or TIVA, MR’s, opioids
  • VA’s: good control of HTN & decrease dose of MR’s, but depress CO
  • Sevo sometimes avoided (fluoride nephrotoxicity/ compound A), but no evidence of increased risk
  • Muscle relaxants – slow excretion of vec, roc/cisatra independent of renal function
    • ↓ initial dose and base subsequent doses on TOF
  • Opioids:
    • ​morphine & meperidine –> morphine-6-glucoronide & normeperidine (neurotoxic compounds) that rely on renal clearance. Hydromorphone active metabolite (hydromorphone-3-glucoronide) may accumulate in CKD.
92
Q

Management of Anesthesia: Maintenance

Fluid Management & UOP

A
  • May benefit from preop hydration (500 mL) if…
    • Do not require HD or W/out renal dz undergoing surgery w/ high incidence of post-op RF
  • Caution – LR or K-containing fluids
  • UOP – 0.5 mL/kg/h
  • Diuretics not advised in absence of fluid replacement
  • HD dependent – narrow margin of safety
93
Q

Management of Anesthesia: Maintenance

Monitoring

A

Monitoring

  • Avoid:
    • Venipuncture in nondominant arm & upper part of dominant arm
    • Radial and ulnar cannulation (same may be said of brachial and axillary)
  • Considerations:
    • Femoral cannulation: r/f infection
    • DP or PT arteries: inconvenient/difficult to access
    • Arterial pressure & ABG will not be accurate if on same extremity as AV fistula
    • Venous pressure monitoring: may be helpful, CVC access may be difficult
    • TEE
    • Dialysis catheters may be used. Use aseptic techniqu, aspirate heparin, heparin after d/c of use
94
Q

Management of Anesthesia: Maintenance

Associated Concerns

A
  • Positioning – prone to bruising, sloughing/ protect vulnerable nerves
  • Protect fistulas
    • NO BP cuff on arm w/ fistula
    • If possible, maintain intra-op access to arm w/ fistula
95
Q

Management of Anesthesia: Maintenance

Regional Anesthesia

A

Regional Anesthesia

  • Neuraxial may be considered
  • Considerations:
    • Sympathetic block T4-T10- may improve renal function vs platelet dysfunction, residual heparin, Must maintain adequate intravascular fluid volume
    • Brachial plexus block – assess for presence of uremic neuropathies
    • Metabolic acidosis - may decrease seizure threshold in response to LAs
96
Q

Management of Anesthesia: Maintenance–

Reversal

A
  • Reversal – Renal excretion 50% of clearance of neostigmine, prolonged effect
  • “Recurarization” is unlikely
  • Sugammadex: not recommended in low creatinine clearance (< 30 mL/min) or RRT
97
Q

Management of Anesthesia: Post-op

A
  • Skeletal muscle weakness: from residual neuromuscular blockade or… antibiotics, acidosis, electrolyte imbalance
  • Caution w/ parenteral opioids – respiratory depression
  • Avoid NSAIDs
  • Continuous ECG monitoring
  • Supplemental O2
  • Check electrolytes, BUN/creat, HCT
  • Bleeding- uremic coagulopathy
98
Q

Renal Transplantation

A
  • Reserved for pts w/ ESRD on long-term RRT
  • Common causes of ESRD:
    • Systemic HTN
    • DM
    • Glomerulonephritis
  • Cadaver donor – can be preserved for 48 hrs
  • Preop - match HLA antigens and ABO blood groups
  • Immunosuppressive therapy instituted
99
Q

Renal Transplant: Management of Anesthesia

General Anesthesia

A
  • RA and GA successful – GA more common
  • Minimize decrease in CO – promote renal perfusion
  • High-normal BP is required
  • Cisatracurium is often drug of choice
  • CVP is useful
  • Mannitol (osmotic diuretic)
  • Albumin administration is helpful
  • Release of vascular clamps – be aware of hypotension & cv arrest
100
Q

Renal Transplant: Management of Anesthesia

Regional Anesthesia

A
  • Advantages – No ETT & muscle relaxants
    • Advantage negated if need to supplement RA with IV anesthetics
  • BP control may be more difficult
  • Controversial in presence of abnormal coagulation
101
Q

Renal Transplant: Management of Anesthesia

Post-op Complications

A
  • Acute immunologic rejection – almost immediate
  • Delayed signs of graft rejection – fever, local tenderness, decreased UOP
  • Treatment:
    • High dose corticosteroids & antilymphocyte globulin
    • Monoclonal antibodies
    • Tacrolimus
    • Mycophenolate mofetil
    • Dialysis may be required
  • Opportunistic infections
102
Q

Renal Transplant: Management of Anesthesia

Anesthesia Considerations (other)

A

Anesthesia Considerations

  • Often elderly
  • Co-existing CV dz
  • Co-existing DM
  • Consider side effects of immunosuppressant drugs
    • ​HTN, low seizure threshold, anemia, thrombocytopenia
  • Consider drugs excreted by kidneys
    • Avoid drugs that are nephrotoxic or dependent on renal clearance
  • Minimize decreases in RBF
103
Q

Induction agents depend significantly on renal elimination

A

Phenobarbital

Thiopental

104
Q

Muscle relaxants that depend significantly on renal elimination

A

Gallamine

Metocurine

Pancuronium

Vecuronium

105
Q

Cholinesterase inhibitors that depend significantly on renal elimination

A

Edrophonium

Neostigmine

106
Q

Cardiovascular drugs that depend significantly on renal elimination

A

Atropine

Digoxin

Glycopyrrolate

Hydralazine

Milrinone

107
Q

Antimicrobials that depend significantly on renal elimination

A

Aminoglycosides

Cephalosporins

Penicillins

Sulfonamides

Vancomycin

108
Q

Analgesics that depend significantly on renal elimination

A

Codeine

Meperidine

Morphine

109
Q

Target Hb range for CKD

A

10-11.5 g/dL

Coexisting (5 decks)

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