Advanced concepts in fluid and electrolyte disturbances in high acuity settings (AKI/CKD) Flashcards by Ruby Trella

metabolic and endocrine functions of kidneys

BP regulation
EPO production
insulin degradation
prostaglandin synthesis
vitamin D metabolism
acid/base balance

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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

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definition of AKI

rise in serum Cr of 0.3 mg/dL or more over 48 hrs or >50% in 7 days

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AKI urine output criteria

< 0.5 mL/kg/hour for >6hrs

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3 types of AKI

prerenal
intrarenal
postrenal

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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

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prerenal AKI causes

excessive fluid loss
decreased renal perfusion
vascular obstructions
drugs

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intrarenal AKI

injury caused by direct damage to the kidney tissue, which results in impaired nephron function

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conditions that predispose to intrarenal injury

infection
tumor growth
diabetes
DI
renal vasculitis

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intrarenal AKI causes

prolonged ischemia
nephrotoxins
acute tubular necrosis
endogenous: rhabdomyolysis, TLS, HRS
antimicrobials: aminoglycosides
immunosuppressants: cyclosporin, tacrolimus
chemotherapy
NSAIDs
street drugs
contrast

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acute tubular necrosis

most common intrarenal AKI cause
tissue destruction, causing permanent renal damage

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causes of acute tubular necrosis

decreased perfusion
shock
sepsis
anaphylaxis
contrast

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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

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fractional excretion of sodium (FeNa)

<1 = prerenal
>2 = ATN

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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)

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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