NOTES Chronic Renal Failure cmj
Module #13: Nursing Care of the Individual with Genitourinary Disorders:
Chronic Renal Failure
Chronic Renal Failure & ESRD (click here)
& Transplant (see Online tutorial in Module)
A. Etiology/Pathophysiology (general)
1.
2.
Normal physiology-( ref to ARF-A & P)
Progressive renal tissue destruction and loss of function
a. Progresses over years without being recognized until kidneys unable
to excrete metabolic wastes and electrolytes: End-stage Renal
Disease (ESRD)
b. Incidence increasing- especially in older adults; higher in African
Americans , Native Americans; large Hispanic population requires
dialysis here in local area; 300,000 patients with ESRD, incidence
increased almost 8% per year for past 5 years
c. Chronic renal failure- diffuse bilateral disease of kidneys with
progressive destruction and scarring; loss of function precedes lab
abnormalities- renal size usually decreased
d. *Diabetes-leading cause of ESRD; then HTN; also
glomerulonephritis, cystic disorders, developmental disorders,
infectious disease (HIV), neoplasms, obstructive disorders,
autoimmune disorders such a s *lupus, *scleroderma; hepatorenal
failure, drug toxicity such as recreational heroin, crack cocaine,
*NSAIDs
e. Stages of renal failure See Table 27.8 p. 776 (*recognize this/
have new classification-PPT slides includes)
1)
Stage I: Reduced or decreased renal reserve
a)
Unaffected nephrons compensate for lost nephrons
b)
GFR about 50% normal & 50% nephron los
c)
BUN and creatinine essentially normal (some
sources say creatinine doubled here-still without
symptoms)
d)
*patient is asymptomatic. (Important to have
baseline serum creatinine; varies for male and
female; gradual decline with aging; **makes drugs
more toxic due to inability to excrete drugs)
2) Stage II: Renal Insufficiency
a)
75% nephron loss
b)
GFR falls to 20-50% of normal with decreased
solute clearance
c)
Decreased hormone production including activated
vit D; have reduced serum calcium; decreased
erythropoietin with reduced RBC’s and anemia; etc
d)
Elevated BUN and creatinine, mild azotemia,
decreased ability to concentrate urine; may have
nocturia and fixed urine specific gravity
e)
*Require nephrologists consult at this stage
RNSG 2432  257
f)
3)
4)
Insult to kidneys-precipitate onset renal failure
(infections, dehydration, exposure to nephrotoxins,
urinary tract obstructions, certain drugs)
g) Require *BP meds; erythropoietin injections,
dietary control; use of phosphate binders can
delay onset ESRD. (*may have polyuria with
low, fixed specific gravity…wastes not
cleared; azotemia, anemia, HTN)
Stage III-IV: Renal Failure/ESRD
a)
GFR falls to less than 15-20% normal function
b)
Less than 5% GFR always considered ESRD:
dialysis or transplant required or death occurs
c)
As 90% or more nephrons destroyed = ESRD,
BUN, and creatinine clearance decreases,
serum creatine increases, urine specific
gravity fixed at 1.010 (if urine produced at all)
d)
Have *UREMIA; “urine in the blood”-uremic toxins
(1) Loss of erythropoietin>chronic anemia
(lowered H & H); fatigue
(2) Fluid and sodium retention, hyperkalemia,
hypermagnesemia, hyperphosphatemia
and hypocalcemia; metabolic acidosis due
to impaired hydrogen ion excretion
*As renal function declines; and end products of protein
metabolism (which are typically excreted in urine)
accumulate in blood)…all body systems adversely
affected
B. Manifestations (all body systems affected!) See text page 777 (* review
carefully; “why” each body system affected); early manifestations: nausea,
apathy, weakness, fatigue; progress to frequent vomiting, increasing weakness,
lethargy, confusion
1.
2.
Nervous system
a. Mood swings; impaired judgment, inability to concentrate and
perform simple math functions; psychotic symptoms
b. Tremors, twitching, convulsions
c. Peripheral neuropathy; “restless legs”, foot drop, sensations
crawling, prickling
d. High levels of uremic (from elevated BUN) toxins may cause axonal
damage; demyelization of nerve fibers; dialysis may not reverse
motor neuropathy; should slow general CNS symptoms; anemia
also decreases cognition; need at least 33% to function
normally
e. *Neurologic changes attributed to increased nitrogenous waste
products, electrolyte imbalances, metabolic acidosis and axonal
atrophy and demyelination of nerve fibers
Skin
a. Pale, grayish-bronze color due to absorption and retention or urinary
pigments that normally give characteristic color to urine; color pale
due to anemia
b. Dry scaly; severe itching; pruritus due to dry skin plus calciumphosphate deposition in skin and sensory neuropathy
258  RNSG 2432
c. Bruises easily; platelet abnormalities
d. Hair dry, brittle and may fall out.
e. Uremic frost; urea crystallizes on skin; see only if BUN
extremely high
3.
Eyes
a. Visual blurring and occasional blindness (“Uremic red eye” from
irritation due to calcium-phosphate deposits in the eye)
4.
Fluid and electrolyte effects
a. Urine less concentrated (unable to concentrate; have “fixed
urine specific gravity” (*need to understand this); proteinuria and
hematuria (lost through the glomerulus)
b. Sodium and water retention; if large amounts body water
retained, have dilutional hyponatremia; lead to CHF, HTN, edema;
may have normal or low sodium levels; *sodium intake must be
individually determined, generally restricted to 2 g per 24
hours.
Tent shaped “T”
c. *Hyperkalemia; muscle weakness, paresthesia, *EKG changes
(fatal arrhythmias at 7-8 mEg/L; need to lower when reaches 6
mMEq/L; due to decreased excretion by kidneys, breakdown of
cellular protein, bleeding and metabolic acidosis and food);
hyperkalemia due to decreased excretion by the kidneys,
breakdown of cellular protein, bleeding and metabolic acidosis; also
from food, dietary supplements, drugs and IV infusions! (Why does
hyperkalemia develop; what are the dangers and how manged-see
text p. 105 +*)
d. *Hyperphosphatemia, hypocalcemia, hypermagnesia (*kidneys
unable to eliminate Mg) Note slide-how does kidney function affect
the bone and calcium balance? How is parathyroid hormone
effected? See text p. 108+
RNSG 2432  259
1)
2)
3)
Calcium and phosphorous> reciprocal relationship;
one rises, other decreases
a)
Decreased kidney filtration leads to increase
in serum phosphate level with reciprocal
decrease in serum calcium level
Renal failure, active vit D lacking; unable to absorb
calcium from GI tract; low serum Ca stimulates PTH >
resorption of calcium and phosphate from bone;
excess phosphate binds with calcium leading to formation of
insoluble metastatic calcification deposited throughout the
body; develop renal osteodystrophy
a)
Osteomalacia: lack of mineralization of newly
formed bones
b)
Osteitis fibrosa; calcium absorbed from bones,
replaced by fibrous tissues
c)
Osteoporosis
d)
Bones fragile, break easily; bone tenderness and
pain
Magnesium; primarily excreted by kidneys; generally no
problem unless client ingests magnesium; Avoid
magnesium containing products as milk of magnesium,
magnesium citrate, etc.
e. Metabolic acidosis
1)
260  RNSG 2432
Impaired kidneys unable to excrete acid load (mostly from
ammonia) and from defective reabsorption/regeneration of
bicarbonate; Kussmaul respiration, uncommon in chronic
renal, reduces severity of acidosis > increases carbon
dioxide excretion. *How does Kussmaul breathing do this?
(text p. 125)
5.
GI effects
a. All parts affected-inflammation of mucosa due to excessive urea
b. Mucosal ulcerations due to inc. ammonia produced by bacterial
breakdown of urea; uremic fetor
c. Anorexia, nausea, vomiting, hiccups
d. GI bleeding due to GI irritation, platelet defect; diarrhea from
hyperkalemia
6.
Hematologic
a. Anemia typically normocytic, normochromic –dec. erythropoietin;
nutritional deficiencies, dec. RBC lifespan
b. Iron deficient
c. Bleeding tendencies -impaired platelet function
d. Impaired immune system
1)
WBC decline-changes in leukocyte function and altered
immune response; diminished inflammatory response
2)
Cellular and humoral immune responses suppressed
7.
Cardiovascular effects
a. Systemic HTN, usually present prior to ESRD, worsens with sodium
retention and inc. extracellular fluid
b. Inc. risk for MI, atherosclerotic vascular disease, elevated
triglyceride levels
c. CHF > pulmonary edema; peripheral edema; arrhythmias from
electrolyte imbalances
d. Pericarditis: metabolic toxins irritate pericardial sac
8.
Endocrine
a. Elevated uric acid levels; risk for gout
b. Resistance to insulin glucose intolerance
c. High triglyceride and elevated HDL resulting in accelerated
atherosclerotic process
d. *Caution in dosing diabetic who are uremic; insulin is normally
excreted by kidneys
e. Menstrual irregularities; reduced testosterone levels
f. Hypothyroidism
g. Gonadal dysfunction
C. Therapeutic Interventions/Collaborative Care/Diagnostic Tests (review
ARF notes; Text p. 749-751 & Table 27-1)
Diagnostic Test/Assessment (*know normal values)
1.
Identify CRF (chronic renal failure; monitor renal function by following level
or metabolic wastes and electrolytes
a. Urinalysis: fixed specific gravity 1.010 (low); excess protein,
blood cells, cellular casts
b. Urine culture; identify infection
c. BUN and serum creatinine; evaluate kidney function
1)
Mild azotemia: BUN 20-50 mg/dl
2)
Severe renal impairment BUN > 100 mg/dl
RNSG 2432  261
3)
4)
Uremic symptoms > BUN 200mg/dl
*Creatinine levels >4 mg/dl = serious renal
impairment (**better indicator than BUN of renal
function); elevated BUN –responsible for
neurological symptoms (Need to understand this!)
d. **Creatinine clearance: reflects GFR and renal function (most
accurate; need 24 hour urine collection (see text p. 750)
e. *Serum electrolytes: monitored throughout course of CRF
f. CBC: moderately severe anemia with hematocrit 20-30%; low
hemoglobin; reduced RBC’s and platelets
g. Renal ultrasonography: CRF; dec. renal size (see text p. 750
h. Kidney biopsy: diagnose underlying disease process; differentiate
acute from chronic (review care of client with renal biopsy, p. 750)
D. Management CRF and ESRD (Death if no treatment with ESRD; attempt to
delay onset ESRD) See also text p. 786-787 Nursing Care Plan; client with ESRD.
Following interventions apply to both (typically…and similar to ARF)
Medications *(refer also to p. 750-751; 766-767; 779)
1.
General effects of CRF on medication effects
a. *Increased half-life and inc. plasma levels of meds excreted
by kidneys; monitor carefully
b. *Dosage may change when in renal failure; do not give
demerol to patients on dialysis (toxic); digitalis excreted
largely by kidney*
c. Dec. drug absorption if phosphate-binding agents administered
concurrently
d. *Low plasma protein levels > lead to toxicity when protein-bound
drugs are given
e. *Avoid nephrotoxic drugs (Aminoglycosides, penicillin in high
doses, carefully monitor vancomycin due to toxic accumulation);
Amphoteracin B very nephrotoxic ; also contrast-media induced
nephrotoxicity
f. *If on dialysis; many drugs removed by dialysis; varies with
hemodialysis and peritoneal dialysis: CHECK before giving
g. Typically do NOT give antihypertensive drugs before hemodialysis
(BP may drop); give after dialysis. (work closely with co-nurse &
dialysis nurse on this!)
2.
Diuretic (furosemide, other loop diuretics -reduce edema; dec. blood
pressure, lower potassium)
Antihypertensive medications: ACE inhibitors preferred
Sodium bicarbonate or calcium carbonate- correct mild acidosis
*Oral phosphorus binding agents (calcium carbonate, calcium acetate;
Phoslo, aluminum hydroxide)- lower phosphate levels and normalize calcium
levels
a. Give with meal to act as binding agent
b. Give between meals to act as calcium supplement (when calcium
agent used)
3.
4.
5.
262  RNSG 2432
6.
Aluminum hydroxide (potential for aluminum toxicity) for “acute”
treatment of hyperphosphatemia; long term use of aluminum is
associated with neurologic symptoms and osteomalacia ; better to
use calcium based products for phosphate binding!
7.
Vit D supplements-improve calcium absorption (activated vit D3)
8.
Meds to correct anemia
a. Erythropoietin by injection (Epogen or Procrit….stimulate
production RBCs)
b. Folic acid, iron supplement to combat anemia (Don’t give iron with
phosphate binders, calcium); require multiple vitamin supplements
9.
Antacids to treat gastric irritation
a. No magnesium based- magnesium toxicity
10. Medications to combat dangerous high potassium levels (*know
these…see AFR. Text p. 106 & 107 & 765!)
a. Intravenous bicarbonate, insulin glucose
b. Sodium polystyrene sulfonate (Kayexalate)
How and why do these medications work?
Dietary and fluid management (Why can these work?)
1.
*Early in CRF: diet modification-slow kidney failure avoid uremic
symptoms (usual guidelines)
a. Restrict proteins (40gm/day) of high biologic value
b. Increase carbohydrate intake (35kcal/kg/day)
c. Limit fluid to 1-2 L per day; limit sodium to 2 g/day (usual
guideline is 500-600 ml more than previous’ day’s 24 urine output)
d. Restrict potassium to (60-70 mEg/day; no salt substitutes);
avoid bananas, prunes, raisins, orange juice, tomatoes, deep green
and yellow vegetables
e. Restrict phosphorus food (especially milk, ice cream, cheese; also
meat, eggs, dairy products) to 1000 mg/day
*When renal function at approx 5-10% = ESRD…following options must be
selected___________________________________________________________
Renal Replacement Therapies; used when medications and dietary modifications
no longer effective
1.
2.
3.
4.
Hemodialysis: establish vascular access (create AV fistula) months
Peritoneal Dialysis: can be initiated when indicated; training of patient
and/or family required
Transplantation
Death
Dialysis: manages ESRD; does not cure it*
Hemodialysis
1.
Hemodialysis See text p. 767 fig 27-5; also text. P. 768 Nursing Care of
the Client Undergoing Hemodialysis
a. *Uses principles- diffusion and ultrafiltration to remove
electrolytes, waste products and excess water (soluble substances
and water) from the body through a semi-permeable membrane
RNSG 2432  263
(*What is diffusion? What is ultrafiltration? P.767-768-know these
definitions)
b. Dialysis: diffusion of solute molecules across semipermealble
membrane from high to low solute concentration
1) Used to remove excess fluid and metabolic wastes produced in
renal failure
2) Dialysate: dialysis solution ; separated from blood by
semipermeble membrane
3) Hemodialysis: blood passes through semipermealble
membrane filter outside of body
4) Peritoneal dialysis: uses peritoneum surrounding abdominal
cavity as dialyzing meembrane; typically used for chronic
renal failure.
c. Hemodialysis
1) Do 3-4 times a week; takes 3-4 hours at a time
2) Early animal experiments in 1913; first dialysis in 1940; 2 0f
17 patients survived; experimental until 1950’s due to lack of
intermittent blood access (only acute renal failure only)
3) 1960-Dr. Scribner developed Schribner shunt; initially “Death
Panels” to determine who could dialyze! 1970 congress under
Medicare gave access to all for dialysis; 300,000 now on
dialysis!
d. *Continuous renal replacement therapy (CRRT): used for
clients with acute (or chronic) renal failure who cannot tolerate
hemodialysis and rapid fluid removal (see text p. 768, 769 and Table
27-6 (CAVH, CAVHD, CVVHD)
1) Blood continuous circulated through highly porous hemofilter
from artery to vein or vein to vein; better for less stable
clients
264  RNSG 2432
2.
Hemodialysis process
(*understand principles of operation)
Diffusion takes
places here
a. Blood removed from patient into extracorporeal circuit (flow at about
350-500 ml/min)
b. Diffusion and ultrfiltration occurs in dialyzer (long plastic cartridge
containing thousands of parallel hollow tubes or fibers which are
semi-permeable membrane made of cellulose-based or other
synthetic materials. Blood pumped into the top of cartridgedispersed into all of the fibers)
c. “Cleaned” blood returned to patient
RNSG 2432  265
Locate the
dialyzer!
d. *Glucose, electrolytes, water can pass through but larger molecules
(protein, red blood cells) are blocked from passing through the semipermeable membrane
e. Substances can be added to dialysate to diffuse into the blood of the
client (i.e. additional K if level is low)
3.
Vascular access (the other critical component of hemodialysis!)
a. Acute or temporary access gained by inserting double lumen
catheter into subclavian, jugular or femoral vein (temporary)
1)
Blood drawn from proximal portion of catheter and
returned to circulation through distal end of catheter
2)
Allow for immediate use; no needle sticks; likely to have
poor blood flow; clot easily and become infected
266  RNSG 2432
b. May have “Permanent” central line catheters such as Quinton,
Permacaths and newest ones as Lifesite Ports (not often used
locally)- provide access into IJ, femoral, subclavian; tunneled
1)
Also for immediate use; no needle sticks; good for
patients without any other access
2)
Lifesite Port; good blood flows, implanted under skin and
tunneled into internal jugular (IJ)
3)
Note: typically central line access sites -more prone to
complications (infections, clotting, etc)
a. Require high dosages heparin to maintain flow; risk
for bleeding (heparin kept in line)
b. Only dialysis nurses/tech access these sites!!
c. *Arteriovenous (AV) fistula (click here for direct link)-long term
access for dialysis (Text 769, Fig 27-7)
1)
Surgical anastomosis of artery and vein in non-dominant
arm, usually radial artery and cephalic vein preferred (also
called primary AV fistula)
RNSG 2432  267
Site for cannulationdialysis of AV fistuals
a)
b)
c)
d)
Time needed to “mature”; may take even 3-6 months
Palpable pulsation (thrill) and bruit on auscultation
Less prone to clotting and infections
Require “good” vessels for placement
d. * Dialysis access using a “graft” (typically also called a
fistula, but a synthetic material used -graft
“Internal Graft: insertion of internal graft; used
when an artery is surgically connected to a vein
with a short piece of special tubing placed under
the skin. Needles can be inserted in this graft…”
1)
268  RNSG 2432
Surgical insertion of grafting material (Gortex) to
connect vein and artery
a) Used in clients with poor blood flow etc
b) Can use usually within 7-14 days
c) More prone to complications than “primary” AV fistula
(infections, clotting, poor blood flow)
*Note: “primary fistula” and “fistula made with with
graft” material serve same purpose…management
slightly different! Need to understand difference!!l
e. Assess functional fistula/graft for complications (regardless
if primary AV fistula or graft)
a) Thrombosis: (clotted off); check for palpable thrill,
audible bruit
b) Infection: check for redness, drainage; more
common in AV fistula; requires removal of fistula
Graft material used in this photo; listen
for bruit, feel for thrill; no BP’s on this
arms, no restrictive bands!
1)
4.
Prevent complications with fistulas/grafts (*know
this!)
a) Identify presence of functional fistula/graft
b) No BP’s or venipunctures done at fistula/graft site
c) No constricting bands above AV fistula/graft and
keep elevated especially post surgical insertion
d) Recognize complication of “steal syndrome” with AV
fistula/graft (decreased blood supply distal to affected
site); report and MD treat.
Complications of hemodialysis (*important to understand these!)
a. Fluid and electrolyte related
1)
Hypotension, most common- related to changes in
osmolality, rapid removal from vascular department,
vasodilation
2)
Usual- hold Bp meds prior to dialysis
b. Cardiovascular (arrhythmias)
c. Bleeding- platelet function and use of heparin during dialysis;
potential needle separation during dialysis
1)
“Central line” catheters contain 10,000 u Heparin; NEVER
for “regular” IV access without specific
training/instructions
d. Neurologic: seizures (*know why this happens!)
1)
Disequilibrium syndrome especially with initial dialysis
a) Urea, sodium and other solutes removed more rapidly
from blood than from cerebrospinal fluid and brain
b) Creates a high osmotic gradient in the brain; causes
shift of fluid into the brain and cerebral edema; causes
nausea, vomiting, confusion, headaches, twitching and
seizures
RNSG 2432  269
e. *Infection: local or systemic
1)
Staphylococcus aureus septicemia-infected vascular
access; high rates of hepatitis B and C, CMV, HIV
5.
Dietary & other considerations related to hemodialysis
(*understand why needed!) (p. 768; 784-788)
a. Fluid restriction ( usual - 1000 cc/24 hours or 500-600 in 24 hours
plus previous 24 hours urine output; weigh before and after dialysis;
1 kg = 2.2 lb; 1000 g = 1 kg = 1000 cc/l liter fluid
b. **Should not gain more than 1-2 lb between dialysis. How
many Kg does this =?
How much fluid does this equal?
c. Continued phosphorous, potassium, sodium restrictions
(slightly more liberalized than prior to starting dialysis)
d. Protein- to amount necessary for nitrogen balance; if too high
difficult to dialyze waste products; too low, decreased albumin,
increased death rate
e. Calories to maintain or reach ideal weight
f. **Medications: generally hold medications (especially BP)
prior to hemodialysis; medications dialyze “out” during
dialysis; BP medications may cause the BP to drop (already
falls during dialysis!) Check before giving medications prior to
dialysis.
g. Invasive procedures (wound care, injections, etc, should not
be done during or immediately after dialysis, have to bleeding
risk due to use of hearin during dialysis.
h. Assess for patency of fistula (palpable thrill and audible bruit)
i. Never use these access sites or fistula for “regular IV
administration of drugs….unless especially instructed to do
so!
Peritoneal dialysis See text p. 770 fig 27-8
270  RNSG 2432
“Manual” method of
peritoneal
dialysis-no “cycler” used
1.
Peritoneal dialysis: peritoneal membrane used as dialyzing membrane
(semi-permeable membrane)
a. Warmed sterile dialysate instilled into peritoneal cavity via
catheter inserted into peritoneal cavity
b. Metabolic waste products and excessive electrolytes diffuse into
dialysate while it remains in abdomen
c. Water diffusion controlled by glucose (dextrose) concentration
in the dialysate which acts as an “osmotic” agent
**What is osmosis?
d. Amount of solution removed determined by glucose
concentration of the dialysate! **Need to understand this
concept!!
e. Excess fluid/solutes removed more gradually; less risk for unstable
client
f. Fluid drained by gravity into sterile bag at set interval-removing
waste products/ excess fluid
1)
“Clear” solution ‘fills” abdomen
2)
“Yellow” urine appearing fluid drains out (looks like urine,
should be clear)
g. Terminology:
1)
Dwell time: time that dialysate fluid remains in peritoneal
cavity (depends upon types)
2)
Fill: fluid infused into peritoneal cavity (usually takes 10-15
minutes)
3)
Drain: time fluid drains from peritoneal cavity by gravity
flow (usually takes 20-30 minutes)
RNSG 2432  271
2.
Types of Peritoneal dialysis
a. CAPD: most common, continuous ambulatory peritoneal dialysis;
exchanges 4-5 times a day; treatments-ongoing 24 hours a day; 7
days a week; 2 liters solution in peritoneal cavity except during
drain time; independent treatment
b. CCPD: continuous cycler peritoneal dialysis; uses delivery devise
(cycler) during nighttime hours and continuous dwell during day
The cycler — automatically fills
and drains abdomen, usually at
night during sleep — can be
programmed to deliver specified
volumes dialysis solution on
specified schedule
3.
Complications
a. *Infection: peritonitis (dialysate return looks cloudy; abdominal
tenderness), tunnel infections, catheter exit site infections; priority
problem!
b. Hypervolemia: hypertension, pulmonary edema
c. Hypovolemia: hypotension
d. Hyperglycemia: glucose concentrations high for osmosis for fluid
loss; can add insulin to solution; obesity and malnutrition (early
satiety due to glucose)
272  RNSG 2432
e. *Hypokalemia: loss of potassium and protein through
peritoneal membrane
1) diet liberalized; can have more protein
f. Ineffective clearing wastes; gradual
4.
Comparison Peritoneal and Hemodialysis (Know this!)
Peritoneal
Hemodialysis
No vascular access & heparin (except
placement peritonal catheter)
No rapid fluctuation of in extracellular
fluid; continuous process
Diet liberalized; more protein, personal
adjustment of fluid intake by increasing
amount of dextrose in dialysate
(osmosis to cause loss of fluid) *still
should control Na, Mg, Phosphorous
intake & fluid…
May require less insulin; add insulin to
dialysate
Potential increased risk for infection
(peritonitis)
Requires vascular access and heparin
Slower process; less effective in waste
elimination
Increased serum triglycerides
Altered body image; weight gain
(increased glucose (dextrose intake)
Rapid fluid/electrolyte shift; done only
3-4 times a week; 3-5 hours
Diet more restrictive; only means to
control fluids is by dialysis 3-4 times
week and personal regulation fluid
intake
Onset of dialysis may allow control of
diabetes to improve
Still at risk for infection; blood borne
due to dialysis and vascular access
(Hepatitis, HIV)
Rapid improvement in fluid and electrole
status
Improved control of serum triglycerides
Minimal body image change
Clotting of access site
Kidney Transplant
1.
2.
3.
4.
5.
6.
7.
Kidney Transplant (See text p. 783, Nursing Care of the Client Having a
Kidney Transplant) *important to read & PDS on Liver Transplant
Treatment choice for ESRD; limited by availability of kidneys; improves
survival and quality of life for ESRD client; 90-95% 1 year survival rate
(reverses many of pathophysiological changes of ESRD); may last 25 years;
subject to chronic rejection
a. Requires life long medications
b. Multiple side effects from medications
c. Increased risk of tumors
d. *Increased risk of infection
e. Major surgery
Organ donors: majority from cadavers; transplants living donors increasing
Close match between blood and tissue type desired; HLA are compared
What is HLA? (text p. 233 to recall)
Living donors- good physical health; nephrectomy major surgery; remaining
kidney must be healthy
Cadaver donors; meet criteria for brain death, age varies, free of systemic
disease, malignancy or infection including HIV, hepatitis B, C (See Organ
Donation PPT program)
Kidney removed- preserved by hypothermia
RNSG 2432  273
a. Transplant within 24-72 hours (time extended)
b. Use technique: continuous hypothermic pulsatile perfusion, and
transplant up to 3 days
c. Donor kidney placed in lower abdominal cavity, renal artery, vein,
and ureter are anastomosed; extraperitoneally in iliac fossa (right
preferred); do not remove “old” kidney unless extremely large
(polycystic or infection source)
8.
Care of the recipient - major surgery; general anesthesia
a. Pre-op:
1)
2)
3)
b. Post-op
1)
2)
274  RNSG 2432
Answer questions/concerns
Remain on dialyisis as ordered
Administer immunosuppressive drugs before surgery
Careful assessment of renal function (fluid and electrolyte
balance)
Maintain urinary catheter patency; hourly I&O; keep urine
at 100 cc/hr; monitor for ATN (acute tubular necrosis
3)
4)
5)
6)
c. *Teach
1)
2)
3)
4)
Monitor for BUN, creatinine and creatinine clearance, daily
weights, all labs
Monitor vital signs and hemodynamic pressure
Replace fluids based on urine utput of precious 30-60
minutes (like treating ARF); diuretics as ordered
Monitor for complications:
a) hemorrhage
b) ureteral anastamosis failure (urine leak into
periotoneal cavity); dec. urine output with
abdominal tenderness/swelling
c) renal artery thrombosis; abrupt onset HTN and
d) dec. GFR
e) infection due to immunosuppression
Prevention infection due to immunosuppression
(lead to kidney loss); major complication: handwashing,
avoid crowds, kids
Monitor daily weights; vital signs for inc. temperature;
gain in weight (rejection, loss kidney function)
Avoid crowds, ills persons, crowds, especially first 3
months
Signs of rejections (know them):
a) Inc. weight
b) Pain and/tenderness over transplant site
c) Dec. urine output
d) Fever >100 degrees
e) Progressive azotemia; protenuria, HTN (chronic
f) Rejection > renal failure
d. Monitor for rejection see text p. 246 Table 9-3
1)
Hyperacute
a) Pre-formed antibodies to donor antigen
b) function ceases within 24 hours (no treatment;
remove kidney)
2)
Acute
a) cell-mediated mmune response to HLA antigens
b) occurs days to months after transplant
c) have signs of inflammation; impaired organ
function
d) 50% experience- differentiate between rejection
and medication (cyclosporine) toxicity
e) treat with steroids, monoclonial or polyclonal
antibodies such as OKT3 or HTG
3)
Chronic rejection
a) gradual deterioration of organ function
b) starts 4 months to years after transplant
c) no effective treatment; return to dialysis or retransplant
d) *Involves humoral and cellular immune response
9.
Responses to transplant & other facts
a. Rejection of a first kidney “may not” jeopardize the second.
RNSG 2432  275
b.
c.
d.
e.
f.
g.
h.
10.
Depression occurs with rejection.
The longer a person goes without rejection, the better the prognosis.
Leading causes of death are infection, CVA, and MI.
Living related donor survival for 1 year is 95%.
Living related donor kidney survival for 3 years is 65%.
Cadaveric donor survival for 1 year 78%.
Cadaveric donor kidney survival for 3 years is 45%.
Immunosuppressive medication See also text p. 248-9 Medication
Administration & required PDS
a. Prednisone (prevent infiltration of T lymphocytes) cornerstone
drug: side effects: cushnoid changes; avascular necrosis, GI
disturbances, diabetes, infection, risk of tumor
b. Cytoxic Agents
1)
Azathioprine (Imuran); prevents rapid growing
lymphocytes: side effects: bone marrow toxicity,
hepatotoxicity, hair loss, infection, risk of tumor
2)
Cylosporin (Neoral, Sandimmune); interferes with
production of interleukin 2 which is needed for growth and
activation of T lymphocytes; side effects: *nephrotoxicity,
HTN, heptotoxicity, gingical hyperplasia, infection
3)
Cellcept (Mycophenolate); Cyclophosphamide (Cytoxan);
newer drugs used instead of Imuran due to decreased
toxicity.
c. Monoclonal antibody (OKT3 or Orthoclone); used to treat
rejection or induce immunosuppression; decreases CD3 cells within 1
hour; side effects: *anaphylaxis, fever/chills, pulmonary edema, risk
of infection and tumors (treat prior to administration; reaction
increases chance of success)
d. Antilymphocyte Globulins: contain antilymphocyte antibodies
produced by immunizing horses, etc with human lymphocytes to
stimulate production of antibodies; administered to client, binds to
peripheral lymphocytes and mononuclear cells, removes them from
circulation (must skin test for sensitivity to horse serum prior to use)
1)
Antithymocyte globulin (ATG (ATGAM)
2)
Antilymphocyte globulin
Nursing Care/Collaborative Care (CRF, ESRD & Transplant)
1.
2.
Determine stage of renal failure; provide appropriate instruction; critical to
caution about drugs, dehydration, etc that may compromise already
impaired renal function
Nursing diagnoses
CRF/ESRD/management with dialysis
a. Fluid volume excess rt inability of kidneys to excrete fluid,
inadequate dialysis, and excessive fluid intake as manifested by
edema, HTN, bounding pulse, weight gain, SOB, pulmonary edema
b. Impaired tissue perfusion: renal* text p. 784
276  RNSG 2432
c. Impaired skin integrity rt decrease in oil and sweat gland activity,
hyperphosphatemia, deposition of calcium-phosphate precipitates,
capillary fragility, excess fluid and neuropathy as manifested by
itching, bruising, dry skin, edema, excoriation
d. Imbalanced Nutrition: less than body requirements rt restricted
intake of nutrients, especially protein, nausea, vomiting, anorexia
and stomatitis as manifested by loss of appetite and weight and
decreased albumin levels
e. Risk for Infection rt suppressed immune system, access sites, and
malnutrition secondary to dialysis and uremia
f. Risk for injury (fracture rt alteration in the absorption of calcium and
excretion of phosphate, altered vitamin d metabolism
g. Disturbed body image
Kidney transplant (in addition to immediate post-op concerns)
a. *Ineffective protection rt effects of medications that
compromise immune system, loss of tissue integrity
b. *Risk for impaired tissue integrity (graft rejection) rt presence of
foreign body
c. Risk for infection rt compromised immune system
3.
Nursing Care of Client Undergoing Hemodialysis (see text p. 768)
a. Note importance of pre-post weights
b. Identify medications to be held with dialysis (medication will dialyze
out; no BP medications prior to dialysis due to BP fall during dialysis;
need for supplement with water soluble vitamins (give after
dialysis); antibiotics typically after dialysis
c. *Fluid intake restricted unless patient has urine output.
d. *Assess vascular access; protect access site
e. Assess for complications related to hemodialysis
f. Provide for teaching (diet/fluid restrictions/cautions related to
access)
4.
Nursing Care of Client Undergoing Peritoneal Dialysis (see text p.
771)
a. Differentiate between hemodialysis and peritoneal dialysis (food and
fluid restrictions, compare advantages/disadvantages of each
method
b. Instruct in strict aseptic technique in managing peritoneal dialysis
c. Instruct regarding signs and symptoms of infection
d. Instruct how to manage problems during instillation of dialysate
solution
5.
Nursing Care of Client Having a Kidney Transplant (see text p. 783)
a. Review pre-post-operative care (p. 256a)
b. Monitor for signs symptoms of rejection
c. Teaching
1)
Avoid crowds; immune suppressed
2)
Medication compliance; medication information!
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278  RNSG 2432