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TRANSCRIPT
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Renal Failure
NUR 3218
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Renal Failure
Partial or complete impairment of kidney
function
Inability to excrete waste products
Types
Acute renal failure
Chronic renal failure
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Notes
Kidney disease has been on the rise & ESRD hasmore than doubled in the past decade
Due to diabetes, HBP & glomerulonephritis
Acute usually sudden onset, can affect many body
systems can be reversible with aggressive care Loss of about 50% of function
Chronic slower onset, affects all body systems irreversible Loss of about 90-95% of nephron function
Renal insufficiency loss of about 25% function
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Acute Renal Failure
Rapid loss of kidney function
BUN & serum creatinine
Oliguria
Types of ARF Prerenal
Hypovolemia, CO, vascular failure
Intrarenal (Intrinsic)
ATN (acute tubular necrosis), kidney tissuedamage, nephrotoxins
Postrenal
Obstructed urine flow
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Notes
Leads to accumulation of waste products in the body Occurs due to compromised blood flow (shock), toxins, tubular
ischemia, infections & obstructions Prerenal from decreased blood flow or ischemia in the nephrons
conditions that cause decreased CO
Prolonged prerenal (hypoperfusion) can cause further progression of RF Shock (septic, anaphalactic, cardiogenic), decreased CO,HF, Pulm emb,cardiac tamponade
Intrarenal - actual tissue damage from inflammatory or immunologicprocesses OR from prolonged hypoperfusion causes impaired renalfunction ATN, Acute glomerulonephritis, nephrotoxins (NSAIDs, antibiotics),
vasculitis, hepatorenal syndrome Postrenal obstruction of urine flow b/t kidney & urethra
Urethral or bladder cancer, urethral stricture, cervical cancer, Prostateenlargement
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Acute Tubular Necrosis
Intrarenal condition caused by
ischemia, nephrotoxins, or pigments.
ATN (exception of causes from
pigments) results in 90% intrarenal
ARF
Potentially reversible
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Acute Renal Failure
Prerenal & Postrenal can resolve
quickly with treatment of the underlying
cause
Intrarenal (ATN) takes longer to resolvedue to potential tissue damage
If dont recover from ARF, can develop
CRF Clinical course follows 4 phases
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Notes
PREVENTION IS THE KEY!
Often seen in ICUs.
ATNs continue to have 50% mortality rate.
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Clinical Phases
Initiating Phase
Onset, Initial insult to kidney to symptoms
Oliguric (< 400 ml/day)
Most common manifestation of ARF
Metabolic acidosis, mental changes
Fluid overload, sodium depletion, potassium
build-up, low calcium, high phosphate
BUN and creatinine elevations
Variable length
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Notes
See TABLE 47-2 in text and specific descriptions ofmanifestations on pages 1200-1201
Initiating Phase (Onset) gradual accumulation ofnitrogenous wastes, with elevation of serum Ct & BUN
Can last hours or days Oliguric decreased GFR, sudden decrease in the UO
100-400/24 hrs which does not respond to diuretics orfluid challenge Occurs 1-7 days after causative event; depends on cause
Last about 8-15 days Longer the duration, the less chance of recovery
May be drowsy, disoriented or comatose
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Clinical Phases
Diuretic Kidneys begin to excrete urine, but cant concentrate
Occurs 2-6 weeks after initial injury
May last 1-3 weeks
Recovery GFR , BUN & Ct decrease
Outcome based upon overall health, severity of ARF& any complications
Can take up to 12 months
Vulnerable to insult during this time
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Notes
Diuretic gradual increase in GFR, indicates recovery ofdamaged nephrons UO increases, can be 3-5 L/day of dilute urine
Can see hypotension from fluid loss & tachycardia
LOC - will begin to improve
Recovery return to normal level of function or can developCRF if not full recovery
- uremia may still be severe.
ALSO, non-oliguric form of ARF.
No major decrease in urine output so less complicated Still need to observe blood and urine components for waste product
accumulation and changes in electrolyte, acid-base, and fluidbalances.
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Nursing and Collaborative
Management PREVENTION IS KEY!!
Health promotion
Avoid dehydration
Avoid conditions that cause ARF History
Early recognition of renal problems
Autoimmune conditions
Infections Monitor lab values
Awareness of nephrotoxic substances
Drug history
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Notes
TEXT gives long list of causes of ARF
Are numerous clinical conditions that can lead to ARF
Avoid dehydration esp in FL & in the summer for children andolder adults
Infections streptococcal especially
Nephrotoxic NSAIDs, tylenol, antibiotics like amphoteracin B,vancomycin, tetracycline aminiglycosides like gentamicin antineoplastics like cisplatin & methotrexate Other things likepesticides & fungicides & heavy metals & X-ray dyes (especiallyin older adults)
Careful matching of blood products
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Clinical Manifestations of ARF
Azotemia - accumulation of nitrogenous
waste products in the blood
Uremia - syndrome of renal failure as it
affects other body systems
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Notes
AZOTEMIA accumulation of nitrogenous
waste in the blood measured by BUN & Ct
Uremia - urinary, cardiovascular, respiratory,
GI, Hematologic, neurologic, and metabolic
changes (See Table 47-3) in text
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Diagnostic Tests
Serum BUN & creatinine, electrolytes,
anemia
Metabolic acidosis
Creatinine clearance
Urinalysis
Renal ultrasound, CT scan, IVP
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Notes
Acute & Chronic lab values are very similar CT & BUN will gradually increase see metabolic acidosis
Remember Ct is better indicator of renal function b/c not affected byhydration or catabolism
Serum potassium will increase as renal fx declines
Serum phosphorus will be increased Serum calcium decreased Can also see anemia if decreased erythropoietin Creatinine clearance decreased b/c GFR is decreased Urine will have RBCs casts, myoglobin KUB an enlarged kidney may indicate obstruction
IVP especially dangerous with decreased renal function becauseof dye
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Nursing Diagnosis
Excess fluid volume r/t compromised
regulatory mechanisms
Imbalanced nutrition: Less than bodyrequirements r/t dietary restrictions
Ineffective protection r/t abnormal
blood profiles
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Nursing & Collaborative Care
Ensure adequate intravascular volume &adequate cardiac output
Pharmacology
Volume replacement Loop diuretics
Low-dose dopamine
Kayexalate (if hyperkalemia)
Sodium bicarbonate (if metabolic acidosis) Avoid NSAIDs & ace inhibitors
Use nephrotoxic drugs sparingly
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Notes
Maintain renal perfusion!!!
Goals aimed at treating the underlying cause & preservingas much kidney fx as possible
Treatment varies some based on the clinical phase in Volume fluid challenges to increase renal blood flow May or may not be prescribed with diuretics
Low dose dopamine to increase blood flow to the kidney -& increases BP
Some type of invasive monitoring to know fluid & pressurestatus
Ace inhibitors used to help ARF from nephrotoxic ATN
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Nursing & Collaborative Care
Fluid Balance
Assess edema, CHF, & pulmonary
edema
Accurate I & O, daily weights
Restrict fluid if hyponatremic
Problems that occur
Hyperkalemia
Hyponatremia
Metabolic acidosis
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Notes
Careful monitoring of labs and working with dietician
Assess edema, CHF, & pulmonary edema
Provide adequate nutrition w/o placing a stress on the kidney Accurate I & O, daily weights (1 kg = 1000 ml fluid)
If fluid is restricted, it can be calculated as the UO + 600 ml. Restrict fluid if hyponatremic
Problems that occur Hyperkalemia
Hyponatremia may be dilutional with actual high levels of sodium
Metabolic acidosis
Adequate calories, high carb, low Na, low K, low phosphorus, low protein
Know foods that should be avoided High K apricots, artichokes, bananas, etc High Na - bouillon, canned soups, preserved meats, cheeses, olives, pickles, etc High phos dried beans & peas, eggs, fish, organ meats, nuts & seeds
TPN/enteral feedings if unable to tolerate oral
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Nursing & Collaborative Care
Nutrition
Adequate calories to prevent catabolism
Monitor protein intake
Restrict potassium, phosphate, & sodium
Give calcium supplements/phosphate
binding agents
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Notes
Adequate calories from carbs and fats
- calories average 30 35 kcal/kg of body weight
- 30-40% total calories from fat
Protein intake depends upon degree of catabolism
- control nitrogenous waste production - limit starvation ketosis
- about 0.6 2 grams/kg/day
- can add essential Amino Acid supplements
Restrict potassium, phosphate, and sodium
- potassium and sodium depends on plasma levels and symptoms ofedma, hypertension, and CHF
- limit phoshates and give calcium supplements and/or phosphate-binding agents
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Nursing & Collaborative Care
Treat elevated potassium levels
Regular insulin IV
Sodium bicarbonate
Calcium gluconate IV
Dialysis
Kayexalate (sodium polystyrene
sulfonate)
Dietary restriction of potassium
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Notes
See Table 47-5
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Nursing & Collaborative Care
Promote Rest Anemia contributes to fatigue Increase activity/ambulation as condition
improves
Prevent Injury & Infection Electrolyte imbalance & uremia may contribute
to mental confusion Good skin care, measures to relieve pruritus Aseptic technique for all invasive lines
Assist with Patient & Family Coping Mental changes ARF explanations Medications, diet, infections, follow-up care
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Notes
Pruritis occurs because of uremic deposits
in the skin
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Gerontologic Considerations
Older adult more susceptible to ARF
Consider differences in treatment, e.g.
diuretics
Higher mortality rate due to infection, GI
hemorrhage, or MI
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Collaborative Care
Temporary dialysis therapies
Hemodialysis
Special vascular access, Vas-Cath Peritoneal dialysis
Tenkoff catheter
Hemofiltration - CRRT
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Notes
Vascular access preferred site is subclavian vein or jugular overthe femoral b/c infection, mobility & visualization Can be used immediately Special catheter with 2 lumens outflow & inflow
PD abd catheter has to be placed uses the peritoneum as thedialysis membrane Slower process, some pts may not tolerate the large amount of fluid
introduced into the abdomen
Hemofiltration CRRT Continuous renal replacement therapy -procedures that are better tolerated by critically ill pts for removingwaste products, uses a dialysate solution, but is better tolerated,
need to be hospitalized & require intensive are nursing double lumen dialysis catheter inserted in the subclavian or jugular
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Chronic Renal Failure
Presence of kidney damage or glomerular
filtration rate (GFR) less than 60 ml/min for 3
months or longer
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Notes
Normal GFR is 125 ml/min
Measured by Urine Creatinine Clearance
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Chronic Renal Failure
Progressive, irreversible destruction of thenephrons of both kidneys
Occurs over months to years, determined by
severity of symptoms & preservation offunction
Deteriorates to End Stage Renal Disease(ESRD) & will need dialysis or transplant
Uremic syndrome- systemic & labmanifestations of ESRD
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Notes
Disease is usually a slow process occurring over years ofdamage *Diabetes see most in obesity, sedentary, family history, Native
Americans
*Hypertension African Americans likely to have HTN
*Glomerulonephritis
Systemic Diseases Sickle cell
Scleroderma
SLE
Polycystic disease
*Most frequent causes
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Etiology of Chronic Renal Failure
Born with over 2 million nephrons, kidney
failure after 85%-90% lost
African Americans with hypertension Native Americans with diabetes
Incidence increasing
Insurance companies & Medicare now pay
for ESRD treatment
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Notes
Causes are due to many different
diseases
Incidence is on the rise
Greater in persons over 65 & with a risk factor
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Chronic Renal Failure - Terms
Diminished Renal Reserve
Renal function declines
Creatinine clearance declines Ct & BUN normal
Nocturia & polyuria Renal Insufficiency
GFR continues to decline
Ct & BUN begin to elevate
Medical management
End-Stage Renal Disease
Excessive waste build-up
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Notes
CRF Terms often heard NOT Current Stage Guidelines SEETABLE 47-6 for STAGES of Chronic Kidney Disease Diminished renal reserve, but not metabolic wastes in blood a healthy
kidney is able to compensate See more nocturia & polyuria b/c the kidney is less able to concentrate urine
Renal Insufficiency - kidney is now unable to compensate & see waste
accumulate & the kidney beginning to be unable to handle the bodysneeds Elevated uric acid, phosphorus Care is medical management here with medications, managing fluid, BP,
electrolytes, & diet Always progresses to stage III just depends upon how fast the progression is May have this for years
End Stage Renal Disease - excessive build-up of waste products in theblood & kidney can no handle More severe fluid & electrolyte imbalances Without treatment, is fatal
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Clinical Effects of ESRD
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Notes
Can develop slowly over months to years
Urea is the end product of protein metabolism,
so BUN & Ct will elevate
Kidney normally excretes K+, so if functiondeclines, then potassium will accumulate
Bones will demineralize d/t high phos & low ca
stimulates parathyroid hormone, whichreleases Ca
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Clinical Effects of ESRD
Regulatory Functions
Waste product accumulation (BUN, Ct)
Anemia because erythropoietin
Metabolic acidosis
Hyperkalemia Abnormal fluid & sodium balance (HBP)
Hyperuricemia
Hyperphosphatemia, hypocalcemia
Glucose intolerance
Cardiac System HBP LV hypertrophy CHF
Cardiac arrhythmias
Uremic pericarditis
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Notes
Can develop slowly over months to years
Urea is the end product of protein metabolism, so BUN & Creatininewill elevate
Kidney normally excretes potassium, so if function declines, thenpotassium will accumlate
Bones will demineralize due to high phosphorus and low calcium stimulates parathyroid hormone, which releases Ca
Hyperlipidemia occurs causing cardiac problems from impaired fatmetabolism leads to increased triglycerides, increased cholesterol,increased LDL
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Clinical Manifestations
Respiratory System
Dyspnea, tachypnea
Kussmaul's respirations
Uremic pleuritis/lung
GI System
Mucosal ulcerations
Metallic taste in mouth
N, V, D, C,
Anorexia
Weight loss, malnutrition
GI bleeding
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Notes
CRF causes changes to ALL body systems primarily effectsof those things related to fluid volume, electrolyte, acid-base& the build up of nitrogenous waste
RESPIRATORY d/t metabolic acidosis
Kussmaul's esp if severe metabolic acidosis
Can develop uremic lung type of pneumonia due to elevated uricacid
GI excessive ammonia from uremia irritates the GI mucosa& causes ulcerations Ulcerations can place the pt at risk for bleeding from them if they
become severe
Constipation is due to the fluid limitations, activity limitations
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Clinical Manifestations
Cardiovascular
Hypertension, peripheral edema
CHF
Arrhythmias
Cardiomyopathy
Uremic pericarditis
Hematology Anemia
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Notes
CV effects related to excess volume
Arrhythmia electrolyte imbalances
HEME anemia b/c of decreased EPO
production by the kidneys also deficient
in iron
Bleeding from the GI tract
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Clinical Manifestations
Neurological System
as CRF progresses
CNS depression (lethargy, inability to concentrate, declining mental
ability, seizures)
Peripheral neuropathy, paresthesias Cerebral swelling
Integumentary System
skin pigment
Uremic frost
Hair & nails dry & brittle
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NEURO develop a uremic encephalopathy b/c uremic toxinsdamage the axons also is from the build-up of waste products General CNS depression which will continue to progress if untreated Peripheral neuropathy see changes in sensation, may complain of
restless leg syndrome or feeling bugs crawling inside of legs Muscle weaknesses, diminished DTRs
Asterixis can occur SKIN increased pigment due to urochrome being deposited in the
skin, which has a yellowish-grey coloration Just darker in dark skinned clients The uremia causes prurutis May also see uremic frost when urea crystallizes on the skin, see
most when the BUN is very high & pt has refused or dialysis has beenw/d
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Clinical Manifestations
Urinary
Decreased or absent urine output
+ for protein, heme & casts
Musculoskeletal
Muscle weakness, bone pain
Renal osteodystrophy Uremic deposits in the eye
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Notes
URINE unless it is the early stages, their
may be high UO of dilute, unconcentrated
urine esp at night
MS renal osteodystrophy from theabnormalities in calcium & phosphorus
bones become thin & weak & can have
pathological fxs Eye may burn & water from irritation
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Clinical Manifestations
Reproductive System
Infertility, libido
hormone levels, amenorrhea
Psychological Changes
Personality & behavioral changes
Body image alterations
Anxiety, depression, & grief
G i t i C id ti f
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Geriatric Considerations of
Renal Failure
GFR rate declines every 10 years after age 50
Older adults are more likely to have other
chronic conditions that contribute to RF
Have difficulty performing PD & have difficultygetting to HD
appointments
Often need community
resources for assistance
Ch i R l F il
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Chronic Renal Failure
Diagnostic Tests
Serum creatinine, BUN
Urinalysis
24-hour urine
Creatinine clearance (= GFR)
KUB, ultrasound, CT
Renal scan, angiogram
Renal biopsy
Serum electrolytes
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Notes
See Textbook discussion
Causes extreme changes in some blood values
Can also calculate the GFR & CrCl
Other studies would be included to monitor the
effects on the other body systems, there are
just the RF ones
X-rays can be done but of limited value
Nursing Diagnosis for
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Nursing Diagnosis for
Renal Failure
Excess Fluid Volume r/t compromised regulatorymechanism
Activity Intolerance r/t weakness, metabolic
alterations
Imbalanced Nutrition: Less than bodyrequirements r/t restricted diet, anorexia
Impaired skin integrity r/t prurutis of uremia
Ineffective Protection r/t hyperkalemia
Risk for Infection r/t uremic toxins, chronic
disease
Fatigue r/t anemia, disease state
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Notes
Many ND could be included in the list
these relate to the primary problems seen,
but their could be others depending upon
the health status of the individual pt
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Nursing & Collaborative Care
Administer prescribed medications Antihypertensives
ACE or ARB
BB or Ca channel blockers
Antidiabetic agents
Electrolytes to correct imbalances,kayexealate
Phosphate binding agents Erythropoietin
Caution with digixon preparations & otherdrugs with kidney clearance
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Notes
See Text, pp. 1209-1211
Conservative measures are always tried first with dialysis being thelast resort
Aimed at slowing the progression of the CRF & preventing
complications Especially those pts with DM & HBP
Control BP antihypertensive & diuretics Weight loss if obese Therapeutic lifestyle exercise, smoking cessation, avoid alcohol
Beta blockers decrease the incidence of cardiac mortality ACE decrease proteinuria & delay progression of CRF, also ARB,
angio rec inh -
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Notes
Control BS monitor & keep bs under control Hyperkalemia another problem of CRF can give IV glucose & insulin
to move K out of the cell or can give Kayexelate a cation exchangeresin give PO or as a retention enema; dialysis
Phosphate binding tums or Remegel to bind with ph want aluminumfree phosphate binder
EPO to get Hct between 30-35%, very effective in helping to improvefatigue
Drugs to avoid drugs excreted by the kidney are always a concern - &doses may have to be adjusted Includes primarily Dig, antibiotics, & pain meds
Dig adjust dose down
Aminoglycosides, penicillin &tetracycline have to adjusted down NEVER give Demerol b/c liver changes then kidney has to excrete
NEVER give NSAIDs b/c they cause renal vasoconstriction
Avoid or only use in very small amounts as prescribed - Tylenol
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Nursing & Collaborative Care
Nutrition & Fluid Balance
Protein restriction
Sodium restriction
Protein restriction
Avoid salt substitutes, foods high in
potassium
Limit fluid intake
Restrict phosphorus
Comply with dietary restrictions
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Notes
See Table 47-8 in text Protein metabolism is the primary cause of uremia, so
protein should be limited in CKD, 0.6 0.75 g/kg of idealbody weight) (unless on dialysis) but not avoided whencreatinine clearance is 25 ml/min or less. or will developnegative nitrogen balance & lose muscle & becomemalnurished Chronic renal insufficiency 0.6 0.8 g/kg of body weight/day
Dialysis 1.2 1.3 g/kg of ideal body weight/day
50% protein should be high biologic value containing all of the
essential amino acides Evaluated & calculated based upon individual needs & type of
dialysis being used
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Notes
Sodium restriction 2-4 g/day depending onedema and HTN - esp when little or no urineoutput as it will contribute to edema Also BP, weight. & if on dialysis is factored in
Potassium restriction 2-4 g (39 mg = 1 mEq) Fluid will also depend upon the UO & type of
dialysis Phosphorus limited (1000 mg/day) but is
primarily in foods that are high in protein May need calcium supplements, foods with calcium Use calcium or aluminum based antacids
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Nursing & Collaborative Care
Prevent infection & injury
Meticulous skin care
Pruritis
Avoid places/persons with infections
Stool softeners
Activities to lessen bleeding
Monitor for confusion, falls
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Notes
Skin attention to any breaks in skin
vascular access or PD catheter site
Pruritis d/t urate crystal excreted thru the
skin, sometimes uremic frost Avoid soaps, lotions that may be irritating
May need antipuritics, such as Benadryl
Monitor H & H, stools for occult blood,avoid aspirin products
Collaborative Care & Nursing
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Collaborative Care & Nursing
Management of CRF
Promote comfort, rest & sleep
Tend to have a number of chronic complaints, not acute
pain
Cool room temperature at night
Rest periods as needed Fatigue Epogen or Procrit
Promote coping
Noncompliance is an issue, also depression
Social problems, relationships, vocation
Adjustments to dialysis
Implications for the future
Collaborative Care & Nursing
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Collaborative Care & Nursing
Management of CRF
Dialysis is initiated when GFR is less than 10-15ml/min (severe kidney impairment)
Movement of fluid & particles across asemipermeable membrane
Removes waste & toxic material
Sustains body function for both acute & chronicRF
Can also be used to remove drugs & poisonsfrom the body, to correct serious metabolicimbalances
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Notes
Selection of dialysis is based upon a number offactors, lab values + clinical manifestations
Begins when conservative approaches no longerwork
Type of dialysis is determined by the physicianbased upon patient factors Adv & disadv to both
Diet and fluid amounts more difficult before dialysisinitiated; hemodialysis more restrictive than peritoneal