AKI Flashcards
Acute kidney injury: rapid loss of kidney function
- rise in creatinine or reduction of urine output
2. can develop azotermia (increase in nitrogenous waste)
Acute kidney injury: can change in severity
develop over hours to days
Acute kidney injury: can range in how long it occurs and when it occurs
nephrotoxic takes longer to reach than oliguric phase
Acute kidney injury: most common causes
hypotension, hypovolemia, exposure to nephrotoxic agents
What is the most common cause of AKI in the hospital?
pre-renal and ATN (acute tubular necrosis)
What is AKI define by?
A rise in serum creatinine and/or reduction in urine output
What 3 causes is AKI classified into?
- prerenal
- intrarenal
- postrenal
Pre renal AKI is caused by..
External causes —> decreased perfusion of kidneys —> decreased function
Less blood going to kidneys to be filtered and decreased nutrient
Ex: cardiac issue, dehydration, bleeding and burns
How will the body compensate in prerenal AKI?
increase blood flow by increasing blood volume by:
- Angiotensin II
- Aldosterone
- Norepinephrine
- ADH
Prerenal can lead to..
intrarenal
Intrarenal AKI is caused by
direct damage to the kidney tissue –> impaired nephron functioning —> increased waste and H2O and decreased ability to maintain electrolytes
Direct damage can be caused by
prolonged ischemia, nephrotoxins, hemoglobin release from hemolyzed RBIs, myoglobin released from necrotic muscle cells or acute tubular necrosis
Infection, injury
Post renal AKI is caused by
mechanical obstruction of urinary flow and is below the kidneys —> prevention of draining system —> increase pressure and build up of waste —> decrease kidney function
What causes mechanical obstruction?
BPH, prostate cancer, calculi, trauma, external factors, neurological injury
Hydrpnephrosis
bilateral ureter obstruction
If blockage fixed within 48 hours, can usually make a complete recovery
Is post renal AKI common?
no, only about 10% of AKI
What is acute tubular necrosis caused by?
disruption in the basement membrane and patchy destruction of the tubular epithelium
Nephrotoxic agents blood up and plug tubules of kidneys –> tubular epithelial cells slough off and plug tubules –> alters kidney’s ability to filter appropriately
What happens if the basement membrane is not destroyed in ATN?
the epithelium can regenerate and the condition is more reversible
RIFLE
Classificaiton of the stages of AKI. R- risk I- injury F- failure L- loss E- end-stage kidney disease Monitor I/Os closely, serum creatinine and GFR
AKI phases
- Oliguric
- Diuretic
- Recovery
Oliguria
decreased UO of less than 400ml/day
Can occur within 1-7 days of injury
What if the cause of oliguria is ischemia?
oliguria can happen in as fast as 24 hours
Can you determine the type of AKI by what urine is being produced?
Yes
Type of AKI if Anuria
less than 50ml/day
complete bilateral obstruction along urinary tract
Type of AKI if oliguria
prerenal
Type of AKI if nonoliguric
ATN or intrarenal ATN
Oliguric phase
Common symptom: oliguria: less than 400ml/day
50% won’t be oliguric
Longer in the oliguric phase –> poorer prognosis
Lasts 10-14 dyas
Oliguric vs. Nonoliguric
Nonoliguric patients have a higher GFR and/or they reabsorb less in the tubules
Less severe injury with nonoliguric
Diuretics and oliguria
can be used to increase UO but does not shorten the duration of renal failure, decrease retirement for dialysis or improve survival rate and may delay timely initiation of dialysis
Diuretics with established ATN and oliguria
Should not be used as a therapy of ATN. Can be used for a short period of time for volume control but should not postpone dialysis starting
Can use crystalloid if hypovolemic
Oliguric clinical manifestations: Fluid volume
Fluid retention often occurs d/t hypovolemia. Replacing fluids can resolve this
Fluid overload w/ some cases d/t anuria w/ distention of neck veins, pulmonary edema, HF
Oliguric clinical manifestations: Metabolic acidosis
kidneys can’t excrete hydrogen –> acid builds up.
Bicarb is depleted and production is decreased
Oliguric clinical manifestations: Sodium balance
Damaged tubules canot conserve sodium so urine has high sodium and normal to decreased serum sodium.
Be careful when replacing sodium b/c fluid volume expansion
Hyponatermia can cause cerebral edema
Oliguric clinical manifestations: potassium excess
Kidneys can’t excrete potassium.
If AKI is also occurring with a massive trauma, even more potassium is released into extra cellar fluid
Monitor for hyperkalemia by peaked T waves, widening QRS, and ST segment depression
Oliguric clinical manifestations: Hematologic disorder
leukocytosis
Most common cause of death in AKI is infection
Oliguric clinical manifestations: waste product accumulation
Kidneys can’t excrete urea which is the end product of metabolism
Oliguric clinical manifestations: neurologic disorders
nitrogenous waste builds up –> experience fatigue, difficulty concentrating, seizures, stupor, and/or coma
Urine analysis for AKI in oliguric phase
RBC, casts, WBC, specific gravity: 1.010, proteinuria, electrolyte imbalances, osmolarity: 300 (similar to plasma)
Why does it mean when the urine osmolarity looks similar to plasma osmolarity?
there is tubular damage and kidneys are no longer able to concentrate urine
What are casts made of?
mucoproteins of the necrotic renal tubular epithelial cells which slough into tubules
Diuretic phase
- Begins with gradual increase in UO (lasts 1-3 weeks, normalizing of acid-base and electrolyte and waste parameters indicate improvement of renal failure)
- Nephrons still can’t concentrate urine, but kidneys can excrete waste now
What to assess for in the diuretic phase
hypovolemia and hypotension from fluid loss so replace fluids
hyponatremia, hypokalemia and dehydration
Why do you see hyponatremia hypokalemia in the diuretic phase?
because thew nephrons can excrete waste but can’t concentrate it
Recovery phase
begins when GFR increase which allows BUN and creatinine levels to plate/decrease
How long can improve of AKI take?
up to 12 months
What is the recovery phase dictated by?
overall health, severity of AKI, and complications
AKI diagnostics
- History and physical
- UA
- Labs
- Ultrasound
- Renal scan
- CT
- Renal biopsy
History and physical for AKI
Helps to determine the cause of AKI (pre, intra, or post renal) and is the most important
Assess recent s/s, drug treatment
H&P pre renal
history of cardiac disease, dehydration, blood loss
H&P intra renal
nephrotoxic medication, blood transfusion, exposure to contrast media
H&P post renal
history of changes in urinary stream, hematuria, stones, cancer of bladder or prostate
Urinary analysis for AKI
urine sediment containing abundant cells, casts or proteins suggests intrarenal disorders
Labs for AKI
BUN/creatinine and urine sodium levels
Ultrasound for AKI
no nephrotoxic agents needed, done first to rule out obstruction
Renal scan for AKI
loss at renal blood flow and tubular function
CT for AKI
identify lesions, masses, obstructions, vascular abnormalities
Renal biopsy for AKI
best way to confirm an intrarenal cause of AKI
Nurses role to prevent AKI
if patient if at risk for developing AKI like if the patient is dehydrated of receiving nephrotoxic drugs then looks for s/s of AKI
Change in UO or creatinine are late indications and at that point patient can already have a 50% reduction in kidney function
Why are patent with AKI not given an MRI/MRA
because contrast should not be given when someone has an issue with their kidneys
In general contrast dos and donts
No kidney disease
Not with metformin in past 48 hours d/t risk of lactic acidiosis
Give lots of hydration after scans
Contrast induced nephropathy that causes AKI creatinine levels
creatine levels peak around day 4 and return to normal at day 10
AKI professional care
- Prevention/eliminate cause, prevent complications
- Hydration: Maintain intravascular volume and CO
- Manage signs/symptoms while kidneys repair themselves
- Monitor exposure to nephrotoxins
- Diuretic therapy and volume expanders to prevent fluid overload
- Very close monitoring of I&Os
- Watch for hyperkalemia: ECG
AKI nutrition
adequate calories, energy from carbs, increase fats, sodium restricted to prevent edema monitor labs
Why would you start a patient with AKI on renal replacement therapy? (8)
Volume overload, increased potassium, metabolic acidosis, extremely increased BUN, significant change in LOC, cardiac tamponade, pericardia effusion, pericarditis
What is renal replacement therapy (RRT)? Is age a barrier?
peritoneal dialysis, hemodialysis, or continuous renal replacement therapy
Age is not a barrier
Care for hyperkalemia
- Insulin IV
- IV Ca Gluconate (Temporarily blocks K effect on the heart; stabilizes cardiac cells)
- Kayexalate (PO/NG or retention enema)
- IV Sodium Bicarbonate
(Increases pH of the serum and moves K into the cells, lasts about 2 hours) - Dialysis
- Dietary Restriction of Potassium
ACE inhibitors and AKI
- ACE inhibitors can decrease perfusion and cause hyperkalemia so they may need to be reduced or stopped
- ACE inhibitors prevent proteinuria and progression of kidney disease
OVERALL: dosage decrease during and during acute episode put on hold
Infection with AKI
infection is the leading cause of death with AKI
- Monitor for s/s of local and systemic infections
- patients may not have a fever with AKI
Local signs of infection
redness, swelling, pain
systemic sign of infection
fever, leukocytosis
