Exam 3 Flashcards
AKI risk factors:
Patient Susceptibility
per KDIGO: dehydration > 60 y.o. female gender black race chronic diseases -heart or respiratory failure -diabetes, cancer, anemia
AKI risk factors:
Exposures
per KDIGO: pharmacologic agents: (contrast media, nephrotoxic drugs [chemotherapy, saids, ACE-I, ARBs, antimicrobials like ahminoglycosides]]) acute infection (sepsis) Critical illness/shock Burns, trauma surgery rhabdomyolysis blood vessel thrombosis intoxications
AKI definition
per KDIGO
increase in SCr by 0.3 mg/dL w/in 48 hours OR
increase in SCr to 1.5 times baseline w/in 7 days OR
urine volume 0.5 mL/kg/h for 6 hrs
staging of AKI
per KDIGO
Stage 1: SCr 1.5 - 1.9 times baseline or >/= 0.3 mg/dL increase OR urine output of /= 12 hrs
Stage 3: SCr 3 times baseline OR increase in SCr to >/= 4.0 mg/dL OR initiation of renal replacement therapy OR in patients /= 24 hrs OR anuria for >/= 12 hours
Functional/Pre-renal Failure presentation
increased SCr
Oliguria (
types of kidney damage causing intrinsic acute renal failure
damage to: renal vasculature glomeruli tubules interstitium
Intrinsic Renal Failure presentation
Oliguric or non-oliguric (urine > 500 mL/day)
dilute appearing urine or discolored urine
casts & cellular debris
urinary RBC or WBC
higher FEna than pre-renal
lower BUN/SCr compared to pre-renal
Drug induced post-renal ARF
acyclovir topiramate methotrexate indinavir trimethoprim/silfamethoxazole anticholinergic medications cocaine
post renal? taca-tim
Post-renal presentation
Increased SCr Urine output will depend on extent of obstruction urine crystals cellular debris variable FENa and BUN/SCr ratio
Goals of therapy for acute renal failure
Minimize insult to kidney
shorten time to renal function recovery
provide supportive measures until kidney function returns
restore renal function to baseline function
General treatment approach for pre-renal, intrinsic and post renal AKI
Pre-renal: -hemodynamic support -volume replacement Intrinsic: -remove cause & supportive care -interstitial damage: remove inciting agent, immunosuppressive therapy (e.g. steroids) Post renal: -remove obstruction
what is the fluid dose for prerenal
250ml - 2L bolus then 75ml-200ml/hour maintenance
Electrolytes we worry about
Hypernatremia (no more than 3g/day of sodium)
Hyperkalemia*** (potassium is 90% renally eliminated - can lead to cardiac arrhythmias, reduce potassium intake)
Magnesium
Phosphorus
How to treat Hyperkalemia
(normal value is 3.3-5 mEq/L)
if serum potassium > 6mmol/L, life threatening
1. determine urgency by ECG & k level
2. reverse neuromuscular and cardiac effects with calcium gluconate 1 g. IV push
3. Shift K+ into ICF:
-regular insulin 0.2 units/kg IV/SQ and glucose 100mL D50W
-sodium bicarbonate 1 amp (44 men) IV push
-Beta 2 agonists
4. Removal of K+ from body:
-sodium polystyrene sulfonate (Kayexalate)(Na+-K+ exchange resin) 30 g po/pr q6-8 hrs x 3-4 doses
-dialysis
Indications for Acute Renal Replacement Therapy (RRT)
A - Acid-base abnormalities E - electrolyte imbalance I - intoxications O - fluid Overload (pulmonary edema) U - Uremia
Risk factors for contrast induced nephropathy
CKD (pre-existing renal dysfunction)
diabetes
heart failure (EF 60 per AHA; > 75 per CIN risk score)
hypotension
intra-aortic balloon pump
anemia
others: dehydration, concurrent nephrotoxins, metabolic syndrome, hypertriglyceridemia, hypertension, etc.
How to manage Edema in CKD
- Dietary sodium restriction:
How to manage Hyperkalemia in CKD
Acute therapy depends on K+ level, rapidity of K+ rise, presence of symptoms/ECG changes Chronic management: -dietary K+ restriction for all patients -treat underlying cause if possible -use diuretics if appropriate -use binders chronically
Acute management of hyperkalemia in patients with CKD
- Dialysis - use when failure to respond to other therapies or patient is already on dialysis
2. IV calcium gluconate, use when K+ >/= 7.0 mmol/L - stabilizes the myocardial cell membrane does not remove K+ only lasts about an hour - Insulin + glucose” shifts K+ extracellular to intracellular - in combo w/calcium gluconate or alone Use when K+ 7.0 mmol/L
- Inhaled beta agonist - shifts, use when K+ >/= 7 mmol/L but no ECG changes, no IV access
- Sodium polystyrene sulfonate oral suspension (Kayexalate): cation-exchange resin (removes K+), 15g/60mL 1-4 times daily
- Patiromer sorbitex calcium powder for oral suspension: potassium binder (removes K+), FDA indicated for tx of hyperkalemia (not for emergency or life-threatening), 8.4-25.5 g diluted in 90 mL water taken once daily w/food, administer other oral meds 6 hrs before after,
SE: constipation, diarrhea, hypomagnesemia, nausea
How to manage metabolic acidosis in CKD
consider treating if bicarb
What are the primary and contributing causes of anemia?
primary: decreased production of EPO in kidneys
contributing causes:
uremic toxins inhibit erythropoiesis
reduced red cell life span
iron deficiency
other nutritional deficiencies (folic acid & vitamin B12)
Blood loss (GI tract)
how do you diagnose anemia in CKD?
Hgb
what are the goals of therapy for anemia?
prevent or reverse signs/symptoms and complications
improve survival
improve QOL
reduce need for red blood cell transfusions
what are the steps of managing anemia?
(KDIGO)
1. replete iron stores if low:
- documented anemia with or without ESA if: % SAT = 30% AND ferritin = 500 AND increase in Hgb concentration or decrease in ESA dose is desired (per KDIGO)
-1-3 month trial of po iron for G3-5 CKD
-IV iron for G5 CKD on dialysis
2. consider ESA (erythropoiesis stimulating agent)
for dialysis: consider when Hgb is b/t 9-10 g/dL to keep it from falling below 9 g/dL
Non-dialysis: Hgb
replete iron stores dose
200 mg/day elemental iron in divided doses (ferrous sulfate 325mg po tid)
IV: Ferumoxytol 510 mg IVP followed by 510 mg IV 3-8 days later - for all kinds of dialysis
ESA therapy
Epoetin-alpha: HD: IV three times per week with dialysis
PD or ND: SQ once weekly or every 2 weeks
Monitoring for ESA therapy
-use lowest ESA dose that reduces the need for red blood cell transfusions (no goal Hgb)
HD and PD: reduce or hold therapy if Hgb > 11 g/dL
ND: reduce dose or hold therapy if Hgb > 10 g/dL
corrected calcium equation
(4.0 - albumin)(0.8) + serum calcium
what is the Ca x PO4 goal?
treatment of hyperphosphatemia
dietary restriction (avoid milk, cheese, eggs, beans, chocolate, beer, carbonated beverages, meats, peanut butter, shell fish, yogurt, ice cream)
start early in G3CKD & reduce intake to 60% of normal
when GFR 7 or corrected calcium > 11
600 mg po w/meals +/- snacks
How to treat low vitamin D in G3-4 CKD
measure 25-OH D levels if PTH is above recommended range
if /= 30 ng/mL, maintenance therapy 1000-2000 D3 daily
watch for hypercalcemia
how to treat SHPT
activated vitamin D (1,25 dihydroxyvitamin D2 or 3)
for G4-5 CKD with persistently high PTH levels and/or hypocalcemia despite normal 25-OH levels
decreases PTH synthesis by direct effect on gland
increases calcium & phosphorous absorption from the gut
don’t use if calcium or phosphorous are above target ranges
Calcitriol PO daily or TIW
IV TIW w/dialysis
Treatment of metabolic acidosis
acetate in TPN
for chronic treatment: NaHCO3 tablets or Shohl’s solution - divided doses for total daily dose of 24-48 mEq
acute treatment: add 3 ampules NaHCO3 to 1000 mL D5W
causes of metabolic alkalosis
chloride responsive: gastric fluid loss diuretics chloride unresponsive: hyperaldosteronism severe hypokalemia iatrogenic alkali administration (acetate in TPN, lactated ringers solution)
Treatment of metabolic alkalosis
- correct underlying cause, correct hypokalemia (20-60 mEq K+ infused over 3 hours)
- volume replacement with NS or chloride replacement
- Acetazolamide (carbonic anhydrase inhibitor)
- PPI or H2RA
- severe cases = IV HCl or arginine HCl
causes of respiratory acidosis
increased pCO2 due to decreased ventilation or ventilation-perfusion abnormalities
treatment of respiratory acidosis
O2 replacement/intubation
replacing HCO3- will worsen hypoventilation by promoting retention of pCO2
respiratory alkalosis causes
decreased pCO2 due to increased ventilation hypoxia nervousness or anxiety or pain pg CNS injury fever asthma severe anemia CHF
what is normal plasma osmolarity
290
Hyponatremia
290) or hypotonic (serum osmolality
acute hyponatremia
0.5 meq/L/Hr unless seizures/coma or extreme breathing difficulties, then 1-2 ml/kg/hr of saline 3% with furosemide if CHF present
too rapid correction causes seizures and pontine myelinolysis
Na+ needed =
(Na+ desired - Na+ observed) X 60% actual weight (kg)
NS is 154 meq/L
saline 3% is 513 meq/L
treatment for hyponatremia, hypovolemia
normal saline at 125-200 ml/hr (1-2L total)
d/c diuretics
treat diarrhea/vomiting
treatment for hyponatremia, isovolemia
free water restriction to 1L/day
demeclocycline (blocks ADH)
vasopressin 2 receptor antagonists
furosemide if diuretic is needed
treatment for hyponatremia, hypervolemia
free water restriction +/- Na restriction
IV meds in hypotonic saline
vasopressin 2 receptor antagonists
furosemide if diuretic is needed
Hypernatremia
> 145 meq/L
etiology of hypernatremia, hypovolemia
chronic renal failure
drugs (loop diuretics, laxatives, mannitol)
glycosuria
etiology of hypernatremia, isovolemia
skin losses (burn, fever) diabetes insipidus
Diabetes insipidus
central = decrease in ADH
nephrogenic = resistance to ADH
central (drugs like ethanol and phenytoin), nephrogenic (drugs, chronic renal failure, hypokalemia, hypercalcemia, sickle cell anemia, autoimmune diseases)
high sodium, high glucose - looks like diabetes because losing water which makes serum sodium serum glucose go high
etiology of hypervolemia and hypernatremia
iatrogenic admin of Na+
mineralocorticoid excess or hyperaldosteronism
treatment for hypernatremia hypovolemia
D5W or half saline water deficit (L) = [(Na+ observed/140) - 1](.6 actual weight kg)
treatment for isovolemia hypernatremia
Nephrogenic: chorpropamide (sensitizes ADH receptor), 200-500 mg/day carbamezapine 400-600 mg/day thiazide 25 mg/day if diuretic is needed D5W central: DDAVP/vasopressin thiazide 25 mg/day D5W
treatment for hypervolemia, hypernatremia
Na+ and fluid restrict
thiazide 25 mg/day if diuretic is needed
IV meds in D5W
treatment for hypokalemia
IV if K = 2.5 meq/L, arrhythmias, muscle spasms, or no enteral route available PO: 20-40 mEq/day IV: KCl vs K2PO4 -40-80 men -administer at rate
treatment for hypophosphatemia
IV if phase = 1.0, arrhythmia, CNS disturbances, respiratory difficulties, or no enteral route available PO: 15-60 mmol/day IV: Kphos vs Naphos - usual 15-60 mmil - administer at rate
treatment for hypomagnesemia
IV if Mg = 1.0, arrhythmias, CNS disturbances or no enteral route available PO: 8-80 mEq/day IV: Magsulfate -2-8 g administer @ rate
treatment for hyperkalemia
determine urgency by ecg, K level, chronicity
reversal of neuromuscular and cardiac effects: administer calcium gluconate 1 g IV push
shifting K+ into ICF:
administer regular insulin 0.2 units/kg IV/SQ and glucose as 100mL D50W
sodium bicarb 1 amp IV push
removal of K+ from body:
sodium polystyrene sulfonate 30 g po/q 6-8 hrs X 3-4 doses
dialysis
treatment for hyperphosphatemia
oral phosphate binder: aluminum hydroxide 30 mL aid, calcium carbonate 4-6 g/day
sucralfate 6-12 g/day
treatment for hypermagnesemia
furosemide 40 mg IV and normal saline
dialysis
