Download Nur 4206 Management of patients with renal/urinary disorders

By Linda Self
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Regulation of water excretion
Regulation of electrolyte function
Regulation of acid-base balance—retain
HCO3- and excrete acid in urine
Regulation of blood pressure--RAAS
Regulation of RBCs
Vitamin D synthesis
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Secretion of prostaglandin E and prostacyclin
which cause vasodilation, important in
maintaining renal blood flow
Excretion of waste products-body’s main
excretory organ. Urea, creatinine, phosphates,
uric acid and sulfates. Drug metabolites.
Stimuli for Renin Excretion
Angiotensinogen in liver
Renin release
Angiotensin I
Converting enzyme in lungs
Angiotensin II
Renal autoregulation
Increased BP, increased circulating volume
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Renin—raises BP
Bradykinins—increase blood flow and vascular
permeability
Erythropoietin
ADH
Aldosterone—promotes sodium reabsorption
and potassium excretion
Natriuretic hormones—released from the
cardiac atria and brain.
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Hypertension
Diabetes mellitus
Immobilization
Parkinson’s disease
SLE
Gout
Sickle cell anemia, multiple myeloma
BPH
Pregnancy
SCI
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GFR decreases following 40 years with a yearly
decline of about 1 mL/min
Renal reserve declines
Multiple medications can result in toxic
metabolites
Diminished osmotic stimulation of thirst
Incomplete emptying of bladder
Urinary incontinence
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Sp. Gravity—1.005-1.020
Microscopic examination for protein, RBCs,
ketones, glycosuria, presence of bacteria,
general appearance and odor
Leukocyte esterase—enzyme found in WBCs
Nitrites –bacteria convert nitrates to nitrites
Osmolality—accurate measurement of the
kidney’s ability to concentrate urine. Normal
range is 500-1200 mOsm/kg.
Culture important in ‘Id’ing pathogen
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Albuminuria—albumin in urine not
measurable by dipstick
Normal values in freshly voided sample should
range between 2.0-20 for men and 2.8-28 for
women. Higher levels indicate
microalbuminuria.
Can also be determined by 24h specimen
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Urine osmolality—indication of concentrating
ability, changes seen early in disease processes
Creatinine clearance—tests clearance of
creatinine in one min. Reflects GFR.
Serum creatinine—measures effectiveness of
renal function. 0.6 to 1.2 mg/dL
Urea nitrogen—also indicator of renal function.
7-18 mg/dL. Measures renal excretion of urea
nitirogen, a byproduct of protein metabolism.
Is not always elevated with kidney disease. Not
best indicator of renal function.
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Liver must function properly to produce urea
nitrogen. BUN levels indicate the extent of
renal clearance of this nitrogenous waste
product.
May see elevation of BUN with bleeding into
tissues or from rapid cell destruction from
infection/steroids
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Ratio of BUN to creatinine distinguishes
between renal and non-renal factors causing
elevations
Dehydration can affect the BUN
When blood volume is down, or BP is low,
BUN level rises more rapidly than creatinine
level.
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Volume of fluid filtered from renal glomerular
capillaries into Bowman’s capsule per unit of
time
Generally expressed in ml/minute
Normal GFR generally is 125mL/minute
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Cockcraft-Gault formula
Modification of Diet in Renal Disease Study
Group formula (MDRD)
Schwartz formula
Starling equation
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No common pathologic condition, other than
renal disease, increases the serum creatinine
level
Serum creatinine does not increase until at least
50% of renal function is lost
Is a calculated measure of glomerular filtration
rate. Is best indicator of overall kidney
function.
 Based on 24 hour urine collection
 Midway will obtain serum creatinine. Serum
creatinine levels vary with age, gender and
body muscle mass
 Calculate: (Volume of urine X urine creatinine)
Divided by serume creatinine
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KUB
Ultrasonography
CT
MRI
Nuclear scans
IV urography—IVP. NPO before. Bowel prep.
Nephrotoxic agent. Metformin.
VCUG
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Cystoscopy
Ureteral brush biopsy
Kidney biopsy
Urodynamic tests—cystometrogram. Measures
detrusor muscle function.
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Antigen-antibody complexes form in blood and
become trapped in glomerular capillaries
Induce an inflammatory response
Manifested by proteinuria, hematuria,
decreased GFR and alteration in excretion of
sodium
Acute and chronic glomerulonephritis
Nephrotic syndrome
Antigen (group A strep)
Antigen-antibody product
Deposition of antigen-antibody complex in glomerulus
Increased production of epithelial cells lining the glomerulus
Leukocyte infultration of the glomerulus
Thickening of the glomerular filtration membrane
Scarring and loss of glomerular filtration membrane
Decreased GFR
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Staph, klebsiella, CMV, mono, hep B,
mycoplasma, group A beta-hemolytic strep
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Hematuria
Edema
Azotemia-accumulation of nitrogenous wastes
Urine appearance may be cola colored
Hypertension
Hypoalbuminemia
Hyperlipidemia
Rising BUN and creatinine
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Hypertensive encephalopathy
Heart failure
Rapid decline in renal function can occur to
ESRD
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Treat s/s such as elevated BP
Check GFR by 24h urine for creatinine clearance
ANA
Treat streptococcal infection with antibiotics,
preferably PCN
Corticosteroids
Immunosuppressants
Limit dietary protein, increase CHO
Restrict sodium
May progress to chronic glomerulonephritis, will
treat as in CKD
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Is not a specific glomerular disease
Is a syndrome with a cluster of findings that
include:
Marked increase in protein in urine (especially
albumin)
Hypoalbuminemia
Edema
High serum cholesterol and LDL
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A condition of increased glomerular permeability
Results in massive protein loss
Often linked genetically or r/t
immune/inflammatory process
Caused by chronic glomerulonephritis, diabetes
mellitus with glomerulosclerosis, amyloidosis,
lupus, multiple myeloma and renal vein
thrombosis
Major manifestation is edema
Hallmark is albuminuria exceeding 3.5g/day
Damaged glomerular
cap. membrane
Loss of plasma
protein (albumin)
Stimulates synthesis
of lipoproteins
hyperlipidemia
Damaged glomerular capillary
membrane
Loss of plasma proteins
hypoalbuminemia
Decreased oncotic pressure
Generalized edema>RAAS>sodium
retention>>>>edema
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Massive proteinuria
Hypoalbuminemia
Edema
Lipiduria
Hyperlipidemia
Increased coagulation
Renal insufficiency
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Renal biopsy to determine specific cause
Steroids
Immunosuppressive agents
ACEIs can decrease proteinuria
Cholesterol lowering agents
Heparin to reduce coagulability
Limit sodium intake
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Reversible clinical syndrome whereby there is
sudden and pronounced loss of kidney
function
Occurs over hours to days
Results in kidneys failure to excrete
nitrogenous wastes
Intrarenal actual parenchymal damage
 Prolonged renal ischemia from myoglobinuria
(rhabdo, trauma, burns), hemoglobinuria
(transfusion reaction, hemolytic anemia)
 Nephrotoxic agents like aminoglycosides,
radiopaque contrast, heavy metals, solvents,
NSAIDs, ACEIs, acute glomerulonephritis
Prerenal 60-70% of cases
 Volume depletion as seen in hemorrhage, renal
losses from diuretics, GI losses from vomiting,
diarrhea
 Impaired cardiac output 2ndary to MI, heart
failure, dysrhythmias, cardiogenic shock
 Vasodilation from sepsis, anaphylaxis,
antihypertensive meds
Postrenal
Urinary tract obstruction by calculi, tumors, BPH,
blood clots
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Initiation occurs with the insult
Oliguria with urinary output less than
400ml/24h . rising potassium, BUN, Cr. Not
responsive to fluid challenges.
Diuresis period— gradual increase in urinary
output. Beginning recovery. Renal function
gradually improves
Recovery—may take 3-12 months. May have
permanent reduction in functioning of 1%-3%.
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Prerenal-hypotension, tachycardia, decreased
CO, decreased urinary output, lethargy
intrarenal and postrenal—oliguria or anuria,
hypertension, tachycardia, SOB, orthopnea,
n/v, generalized edema and weight gain,
lethargy, confusion
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Nonoliguric form also exists. Phases are
similar.
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Elevated BUN and creatinine
Sodium retention but may be deceptive due to
water retention
Potassium increased
Phosphorus increased
Calcium decreased
H&H decreased
Sp. Gravity decreased and fixed
Objectives : Restore normal
chemical balance and prevent complications
until restoration of renal function
 Identify and treat underlying cause
 Maintain fluid balance—wts, serial CVP
readings, BP, strict I&O
 May give Mannitol, Lasix or Edecrin
 May need temporary dialysis
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If prerenal, fluid challenges and diuretics to
enhance renal blood flow
Oliguric renal failure, low dose dopamine.
Calcium channel blockers may be used to
prevent influx of calcium into kidney cells,
maintains cell integrity and increase GFR
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Hyperkalemia—closely monitor electrolytes
Kayexalate/Sorbitol—may need Flexiseal
IV dextrose, insulin and calcium may help shift
K+
Cautious administration of any medication that
can be nephrotoxic
Monitor ABGs and acid-base balance
Monitor phosphate levels
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Azotemia and uremia are directly related to the
rate of protein breakdown
Dietary proteins are individualized to each
patient. Is a catabolic state and if insufficient
intake, patient may lose up to 0.5-1 pounds
daily. Encourage high CHO. Protein needs for
non-dialysis patients need 0.6g/kg of body
weight
Dialysis patients will need 1-1.5g/kg
Fluid restriction=urine volume plus 500ml
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Monitor fluid and electrolyte balance
Reduce metabolic demands
Promote pulmonary function
Prevent infection
Provide skin care
Provide support
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Progressive, irreversibe deterioration in renal
function
Causation: #1 diabetes mellitus, hypertension,
glomerulonephritis, pyelonephritis, polycystic
kidney disease, vascular disorders, others
Uremia---collection of nitrogenous wastes
normally excreted by the kidneys. S/S include:
HA, seizures, coma, dry skin, rapid pulse,
elevated BP, scanty urine, labored breathing
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Nephrons hypertrophy and work harder until
70-80% of renal function is lost
Nephrons could only compensate by
decreasing water reabsorption thus:
Hyposthenuria—loss of urine concentrating
ability occurs
Polyuria—increased urine output
Then isosthenuria—fixed osmolality
Gradual decline in urinary output
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GFR greater than or equal to 90mL/min/1.73
m2. Kidney damage w/normal or increased
GFR
GFR = 60-89, mild decrease in GFR
GFR = 30-59, moderate decrease in GFR
GFR = 15-29. severe decrease in GFR
GFR < 15. Kidney failure
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Every body system is affected
CV—hypertension (RAAS), heart failure,
pulmonary edema, pericarditis, MI
Pulm.—crackles, Kussmaul, pleuritic pain
Derm—severe pruritus, uremic frost (urea
crystals)
GI—n/v, anorexia, uremic fetor (ammonia
odor to breath), constipation or diarrhea
Neurologic—LOC changes, confusion, seizures,
agitation, neuropathies, RLS
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Hematologic—anemia, thrombocytopenia
Musculoskeletal—muscle cramps, renal
osteodystrophy, bone pain, bone fractures
Metabolic changes—urea and creatinine,
sodium, potassium, acid-base, calcium and
phosphorus
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Calcium and phosphorus binders—Calcium
carbonate, calcium acetate
Antihypertensives
Antiseizure—valium or dilantin
Erythropoietin
Iron supplements
Diet—CHO and fat, vitamins, restrict protein
Indications:
1. Uremia
2. Persistent hyperkalemia
3. Uncompensated metabolic acidosis
4. Fluid volume excess
5. Uremic encephalopathy
6. Remove toxic substances
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Based on principles of diffusion, osmosis and
ultrafiltration
Diffusion—removal of toxins and wastes.
Move from blood to dialysate.
Osmosis—excess water is removed. Goes from
area of higher solute concentration (blood) to
lower concentration (dialysate)
Ultrafiltration—water moves from high
pressure area to lower pressure. Applied by
negative pressure, more efficient than just by
osmosis
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ASHD
Disturbances of lipids worsened by dialysis
Anemia and fatigue
Gastric ulcers
Renal osteodystrophy
Sleep problems
Hypotension
Muscle cramps
Dysrhythmias
Dialysis equilibrium from cerebral fluid shifts
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Caused by rapid decrease in fluid volume and
blood urea nitrogen levels during HD
Change in urea levels can cause cerebral edema
and increased ICP
Neurologic complications include: HA,
vomiting, restlessness, decreased LOC,
seizures, coma or death
Can be prevented by starting HD for short
periods and low blood flows
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Hemodialysis
In ICUs where patient is too unstable to have
hemodialysis, can have CRRT
Peritoneal dialysis
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More successful if done before dialysis
HLA and ABO compatibility
Donor kidney placed in iliac fossa
Patient must be free from infection
Similar care for patient post-op as any surgery
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Post-op—assess for s/s of rejection such as
oliguria, edema, fever, increasing blood
pressure, weight gain and swelling or
tenderness over transplanted area
Monitor creatinine level, in those on
cyclosporine, may be the only s/s
Monitor WBCs
Monitor urinary output, may need
hemodialysis temporarily (2-3 weeks may
initially have ATN)
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Occurs in types 1 and 2
Severity of diabetic renal disease is related to
extent, duration and effects of atherosclerosis,
htn and neuropathy.
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Microvascular complication of diabetes
First manifestation is persistent albuminuria
Diabetic patients are always considered to be at
risk for renal failure
Avoid nephrotoxic agents and dehydration
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Stage 1—at time of diagnosis of diabetes.
Kidney size and GFR are increased. Blood
sugar control can reverse the changes.
Stage 2, 2-3 years after diagnosis. Basement
membrane changes result in loss of filtration
surface area and scar formation. These changes
are called glomerulosclerosis.
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Stage 3, 7-15 years after diagnosis.
Microalbuminuria is present. GRF may be
normal or increased.
Stage 4, albuminuria is detectable by dipstick.
GRF decreased. BP is increased. Retinopathy is
present.
Stage V, GFR decreases at an average rate of
10ml/min./year
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Cystitis
Ureterovesical reflux
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If bacteriuria, following should have cultures done:
All men
All children
Patients with diabetics
Those with recent instrumentation
Those hospitalized or who live in long term care
Pregnant women
Sexually active
Postmenopausal
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Obstruction
Stones
Diabetes mellitus
Gender
Age—anticholinergics, neuromuscular
conditions, hypoestrogenism
Sexual activity
Alkalotic urine
Vesicoureteral reflux
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Most common organism is E. coli
Other causative organisms are: S. saprophyticus,
K. pneumoniae, Proteus and Enterobacter
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Bactrim, Macrodantin, Cipro,Levaquin
Fluids, avoid urinary irritants
Hygiene
Prevention
Acute pyelonephritis
 Will have fever, chills, leukocytosis, bacteriuria
and pyuria
 CVA tenderness
 US or CT to r/o any obstruction
 Urine C&S
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Tx:
Hydration
Antiemetics
Two week course of antibiotics such as
Bactrim, Cipro, gentamycin w/or w/o
ampicillin, 3rd generation cephalosporin
Pregnant women hospitalized for 2-3 days
f/u culture in two weeks
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Stress incontinence—invol. loss of urine w/
activities that increase intraabdominal pressure
Urge incontinence—unable to suppress signal
from bladder to brain
Overflow incontinence-when bladder is distended,
will have small amount of incont.
Functional incontinence as seen in Alzheimer’s
Reflex incontinence as seen in SCI patients
Mixed-stress and urge
Neurogenic bladder—lesion of ns leads to urinary
incontinence
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May be caused by MS, SCI, HNP, spinal tumor,
spina bifida, diabetes
Spastic—upper motor neuron lesion
Flaccid—lower motor neuron lesion. Fills then
have overflow incontinence
Assess by checking residuals, I&O, UA,
assessing sensory awareness
Tx-urecholine, surgery, intermittent caths, S/P
caths
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Diuretics
CNS depressants which affect LOC
CVAs
Parkinson’s
Depression and altered self-esteem
Inability to ambulate safely
Assistance products cost prohibitive for patient
UTI
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TCAs
Anticholinergics—Sudafed, Detrol, Ditropan
Estrogen in women
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Weight loss in obese
Fluid management
Transvaginal or transrectal electrical
stimulation
Inflatable cuff
Vaginal cone retention exercises
Urinary catheterization
Scheduled toileting
Pelvic muscle exercises
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Presence of calculi in urinary tract
Cause pain as they pass
Nephrolithiasis is formation of stones in the
kidney
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Involves three conditions:
Slow urine flow resulting in supersaturation of
the urine with the particular element
Damage to the lining of the urinary tract
Decreased inhibitor substances in the urine
that would otherwise prevent supersaturation
and crystal aggregation
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Metabolic risk factors such as hyperuricemia,
hyperoxaluria or hypercalcemia
High dietary calcium not contributive unless
metabolic or renal tubular defect exists
Immobilization
Urinary stasis, dehydration and urinary
retention mamy be causative
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Evaluate for bladder obstruction
UA will reveal RBCs, odor, turbidity, WBCs
MRI, KUB, CT
Noncontrast helical CT has highest sensitivity
IV urography will show obstruction
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Analgesia
Avoid NSAIDs if to have lithotripsy (affect
platelets)
Hydration
Urine straining
Lithotripsy (monitor ECG and sedate patient)
Minimally invasive surgical procedures (MIS)
such as stenting, nephrolithotomy
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Antibiotics
Thiazide diuretics for hypercalciuria
Allopurinol and vitamin B6 for oxalate
containing stones
Uric acid stone—allopurinol and alkalinizing
the urine. Sodium bicarbonate or potassium
citrate helpful.
Cystine –captopril and
alphamercaptopropionylglycine w/ hydration
and alkalinazation of urine
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Urothelial
Tx with BCG
Radiation
chemotherapy
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Ureterostomy
Conduits—to intestine and stoma
Sigmoidostomies-divert urine to large intestine
so no stoma
Ileal reservoir—surgically created pouch