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Cc 13 renal
Critical Care (408)
Loma Linda University
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Renal System Acute Kidney Injury AKI Diagnostics RIFLE criteria multinational group of nephrologists 3 categories of severity of injury R – risk (septic, shock, etc.) I – injury F - failure 2 categories for outcomes L – loss (kidney function loss) E – end-stage kidney disease
AKIN criteria (creatinine) serum creatinine ↑ by 0/dL over 48 hrs.
> 50% ↑ in creatinine level
UOP: < 0/kg/hr / 6hours
labs drawn at least twice over 48hrs to watch for creatinine variation
kidneys: paired organs | protected by ribs approx. 12cm long, 6cm wide, 2 thick main functional unit of urinary system renal cortex: outer layer renal medulla: inner layer nephron: functional unit of kidney 180L of filtrate per day concentrates to 1-2L of urine glomerular filtration rate (GFR): amount of filtrate formed in nephrons | assess kidney function normal GFR = approx. 125mL/min CKD = GFR <60mL/min for 3+ months renal failure = GFR <15mL/min highly vascular up to 20% of CO Functions waste removal, prostaglandin SYNTHESIS blood pressure (BP) regulation thru RAAS RBC (erythrocyte) production vitamin D activation acid/base | fluid | electrolyte balance
spectrum of acute onset kidney disorders sudden decline of GFR (within 48hrs or less) fluid retention retention of waste products normally filtered out at worst acute renal failure degree of injury measured by UOP creatinine GFR (amount of filtrate produced by nephrons) UOP not always reliable d/t diuretic treatment (Lasix, etc.) kidneys injured creatinine not excreted thru urine creatinine goes to blood stream other signs/symptoms unbalanced I/O not explained by other factors weight gain & edema (d/t fluid retention) crackles in lungs (d/t fluid retention) PRErenal azotemia (low GFR, low UO)
INTRArenal POSTrenal
impaired renal BF hypoperfusion < GFR & UOP azotemia (↑ nitrogenous waste [BUN, creat] in blood) = AKI/ARF if caught early it can be fixed example prolonged hypotension low blood volume/ low CO dehydration clots, infection (sepsis)
actual kidney/nephron damage harder to fix than pre-renal may hear it called ATN acute tubular necrosis example: rhabdomyolysis- endotox trauma (blunt or penetrating) (contrast) nephrotoxic drugs (vancomycin)
√ vanco levels to assess kidney
urine outflow obstruction if cannot relieve put in nephrostomy tubes urine can’t leave kidneys less common cause in ICU example cancer/tumors compressing the ureters/urethra kidney stones urinary stasis
AKI - Prognosis depends on cause depends on how quickly TX is started depends on how sick the patient is ↑ length of stay ↑ mortality (15-60%) → CKF & permanent dialysis
functions AKI – Systemic Effects acid base imbalance metabolic acidosis | hyperkalemia gastrointestinal electrolyte imbalance altered motility neuromuscular electrolyte imbalance neuromuscular issues integumentary edema stretched, weak skin tissue uremic crystals (uremic frost) d/t urea needs to be excreted but it’s not excreting thru urine
endocrine kidney damage renin (RAAS), erythropoietin not secreted renin not secreted impaired BP erythropoietin not secreted anemia no prostaglandin release to regulate renal blood flow skeletal impaired Ca absorption weak bones, impaired blood clotting
cardiovascular excess fluid edema & HTN renin not secreted impaired BP regulation electrolyte (K) imbalance arrhythmias could go to cardiac arrest hematopoietic no erythropoietin anemia respiratory fluid overload crackles & dyspnea (SOB) rapid respirations acid/ base imbalance Lab Normal Values
AKI/Renal Failure Values
Nursing Management
Medical Management
Patient Education BUN 5 – 20 mg /dL
↑: >20 Prevention Assessment be aware of risk factors strict I/O daily weight daily labs hemodynamic monitoring Interventions medication administration promptly notify MD
Prevention Fluids replace early pre-renal AKI restriction: prevent complications removal: dialysis if kidney not functioning Medications d/c or reorder w/ renal dosing diuretics phosphorus binder (pt. can eat remove phosphorus) electrolyte replace or removal
Prevention Risk factors Nutrition ↓ K diet ↓ PO (phosphate) diet fluid restriction Medications timing MoA
Creat 0 – 1.
mg /dL
↑: >1 – d/t unable to eliminate Creat BUN: Cr 10:1 varies based on type Creat Clearan ce
110 –
120
mg / mi n
↓: < 50mg/min
Albumin 3 – 5
g/ dL
↓ – moves extravascular edema pH 7 – 7.
↓: <7
metabolic acidosis K (>4)
3 –
4.
mE q/L
↑: kidneys unable to secrete potassium Na 135 – 145
mE q/L
↓: usually relative/dilute hyponatremia Ca 8 – 10.
mg /dL
↓: phosphorus ↑
Phos (>4)
2 –
4.
mg /dL
↑: kidneys unable to secrete phosphorus Mg (>2)
1 –
2.
mE q/L
↑: kidneys unable to secrete magnesium Hct 40- 50%
↓: fluid retention & anemia of kidney dz
filter to increase pressure across membrane large amounts of fluid can be removed 5-20 ml/min, 7-30 l/24h AKI SXS: Secondary to toxic metabolites: fatigue, malaise, nausea, vomiting, pruritis, mental status changes, oliguria, anuria, fluid overload resulting in dyspnea and orthopnea
catheter implanted into abdomen dialysate instilled into peritoneal cavity dwell time drains by gravity risk for peritonitis d/t access to peritoneal cavity high temp abdominal tenderness cloudy fluid in drainage bag
too long too short blood clot acid/base imbalance
disconnectio n in circuit air embolus cardiac arrest
AKI phases: (4) 1. Onset – kidney injury occurs a. Hours to days; from significant blood loss, burns, fluid loss, diabetes insipidus. Renal blood flow: 25% of normal, tissue 25%, UO < 0 mL/kg/hour 2. Oliguric – UO decreases from renal tube damage a. 8-14 days; dec glomerular filtration, urine formation, renal clearance, UO <400mL/day, maybe as low as 100, increase in azotemia, dialysis initiation (BUN and Cr*), electrolyte disturbances, acidosis, fluid overload *the longer this stage is, the poorer the prognosis 3. Diuretic – kidneys heal/UO increases, but tubule scarring/damage occur. Begins when UO is >400 mL/day. BUN begins to fall a. 7-14 days; when cause of AKI is renal tubule scarring and edema, increased GFR, daily UO >400 mL, possible electrolyte depletion (osmotically high BUN) 4. Recovery – tubular edema resolves, renal function improves a. Several mos-1 year; decreased edema, normalization of fluid/electrolyte balance, return of GFR to 70% or 80% of normal b from when BUN STABLE AND UO NORMAL to the day pt. returns to normal activity
AKI and EKG Peaked t waves (k > 5) Prolonged PR interval Widening QRS complex Loss of P wave “sine wave” Asystole (k > 8)
Treatment: CALCIUM (gluconate or chloride) reduces risk of v-fib caused by hyperkalemia. INSULIN administered w/glucose
to facilitate uptake of K into cell Filtration: convection Dialysis: diffusion
Cc 13 renal
Course: Critical Care (408)
University: Loma Linda University
