Copy of Lecture+ Failure+ +11 08+w+NOTES

8/14/2019 Copy of Lecture+ Failure+ +11 08+w+NOTES

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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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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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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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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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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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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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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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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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Notes

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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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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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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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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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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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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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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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



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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

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