Advanced concepts in fluid and electrolyte disturbances in high acuity settings (AKI/CKD) Flashcards
metabolic and endocrine functions of kidneys
BP regulation
EPO production
insulin degradation
prostaglandin synthesis
vitamin D metabolism
acid/base balance
acute kidney injury
partial or complete impairment of kidney function
abrupt decrease in kidney function
results in an inability to excrete metabolic waste products and water from the body
rapid onset and ranges from a slight deterioration in kidney function to severe impairment
potentially reversible
definition of AKI
rise in serum Cr of 0.3 mg/dL or more over 48 hrs or >50% in 7 days
AKI urine output criteria
< 0.5 mL/kg/hour for >6hrs
3 types of AKI
prerenal
intrarenal
postrenal
prerenal AKI
related to factors that are external to the kidneys
a reduction in systemic circulation reduces BP to the kidneys
can lead to intrarenal disease if impaired perfusion to the kidneys is prolonged
prerenal AKI causes
excessive fluid loss
decreased renal perfusion
vascular obstructions
drugs
intrarenal AKI
injury caused by direct damage to the kidney tissue, which results in impaired nephron function
conditions that predispose to intrarenal injury
infection
tumor growth
diabetes
DI
renal vasculitis
intrarenal AKI causes
prolonged ischemia
nephrotoxins
acute tubular necrosis
endogenous: rhabdomyolysis, TLS, HRS
antimicrobials: aminoglycosides
immunosuppressants: cyclosporin, tacrolimus
chemotherapy
NSAIDs
street drugs
contrast
acute tubular necrosis
most common intrarenal AKI cause
tissue destruction, causing permanent renal damage
causes of acute tubular necrosis
decreased perfusion
shock
sepsis
anaphylaxis
contrast
contrast induced nephropathy
renal vasoconstriction, free radical generation
usually resolves within 1-3 weeks
risk fx: CKD, DM, HF, high contrast doses
tx: supportive care
fractional excretion of sodium (FeNa)
<1 = prerenal
>2 = ATN
postrenal AKI
when the flow of urine is obstructed and urine backs up into the renal pelvis and impairs kidney function
can lead to hydronephrosis (distension and dilation of the kidney)
causes of postrenal AKI
blood clots
tumors
calculi
urethral strictures
neurogenic bladder
BPH
trauma
ureteral obstruction
bladder dysfunction
urethral obstruction
glomerulonephritis
inflammation of glomeruli
acute or chronic
causes of glomerulonephritis
infections
immune diseases
vasculitis
hypertension
diabetic nephropathy
chronic glomerulonephritis
end stage of glomerular inflammatory disease
characterized by proteinuria, hematuria, development of uremia
tx is supportive and symptomatic
lab tests: urine, serum, dx
RIFLE
classification/staging criteria based on GFR, Cr, and UO over time
Risk
Injury
Failure
Loss
ESKD
manifestations of AKI
oliguria
elevated BUN and Cr
uremia
decline in GFR: anuria, oliguria, azotemia
S3, S4
crackles, DOE, weight gain, edema, fluid overload
lab manifestations of inability to excrete waste and maintain homeostasis
increasing BUN
increasing Cr
hyperkalemia
hyponatremia
metabolic acidosis
hyperphosphatemia/hypocalcemia
anemia
hemodilution and inability to excrete
labs and diagnostic testing for the kidneys
BUN and Cr
GFR
urinalysis
ABG
renal US
CT
renal biopsy
prerenal treatments
restore adequate circulation to kidneys:
monitor I/O
sx of FVE
VS
administer crystalloid or colloid fluids
vasopressors
intrarenal treatments
minimize nephrotoxic substances and treat underlying cause:
fluid restriction
dietary restrictions of Na and K
lower K levels with NaHCO3, glucose & insulin, kayexalate
decrease transfusions for anemia
prevent infection: abx but monitor levels
decrease serum Cr
postrenal treatments
treat outlet obstruction:
monitor I/O
pain assessment
monitor lytes during diuresis
IV fluids
AKI collaborative treatment
avoid nephrotoxic drugs (NSAIDs and ACEs, IV contrast)
monitor for drug toxicity
hypovolemia, & d/t blood loss
inflammation
maintain nutritional status
AKI dietary management
provide adequate calories to prevent catabolism:
protein restriction
Na restriction
K restriction
phosphorus restriction
vitamin supplements
fluid restriction
stages of AKI resolution
diuretic stage
recovery stage
diuretic stage
waste products now being filtered but unable to concentrate urine
up to 5L/day of UP
monitor for hypo Na and K, dehydration, hypotension
lasts 1-3 weeks
recovery stage
GF increases causing BUN/Cr to decrease
major improvements in 1-2 weeks
can take up to 1yr for full recovery
AKI NANDAs
fluid volume deficit or excess
imbalanced nutrition
anxiety
chronic kidney disease
progressive and irreversible
5 progressive stages
5 stages of CKD
Stage 1: diminished renal reserve
Stage 2: renal insufficiency
Stage 3: moderate renal failure
Stage 4: severe renal failure
Stage 5: End-stage renal disease (ESRD)
diagnosis of CKD
history
labs
presenting s/s
Cr and BUN
clinical signs of CKD
uremia
anemia
CHF
HTN
dysrhythmias
edema
pericarditis
pulmonary edema
infection
altered glucose control
N/V
fatigue
seizures
delayed wound healing
metabolic acidosis
CKD treatment
dialysis
BP control (K sparing diuretics, ACE inhibitors)
EPO/iron/folic acid/B12
normal/high protein diet (if on dialysis)
low Na/K/Phos
calcium supplements
CKD NANDAs
fluid volume excess
altered fluid and electrolyte imbalance
altered nutrition
infection
bleeding
