Transcript renal ppt ck pt 2

Management of Patients with
alterations in the Renal system
C. Cummings RN, EdD
Renal Anatomy
Anatomy
• System includes the kidneys and entire urinary
tract
• 2 kidneys located behind the peritoneum, on
either side of the spine
• Weighs about 8 oz and the left if longer and
narrower than the right
Kidney
 Renal capsule- fibrous tissue
 Renal cortex- outer tissue
 Medulla-inner tissue with
“fans”
 Pyramids-12-18/kidney
 Papilla-end of the pyramid
 Calyx-collects the urine at
the end of the papilla
 Renal pelvis- calices form it
and leads to ureter
Renal blood flow
• Kidneys receive 20-25% of the total cardiac
output
• Blood flow is 600-1300 ml/min
• Renal artery comes off of the abdominal aorta
• Exits off the renal vein and into the IVC
Nephrons
• Functioning unit of the
kidney
• Urine is formed from
blood
• 1 million nephrons
• Blood comes from the
afferent arterioles,
enters the glomerulus
• Leaves by efferent
arterioles
Nephron parts
• Bowman’s capsule
surrounds the
glomerulus
• Proximal convoluted
tubule
• Loop of Henle
• Distal convoluted tubule
• Collecting ducts
Renin-angiotensin system
• Renin is produced by the macula densa cells
note changes in the distal convoluted tubules
• Based on decreased BP, bld volume and bld NA
levels
• Renin changes angiotensinogen into
angiotensin I, ACE changes it to angiotensin II
Angiotensin II
• Leads to 4 main outcomes:
– Increased Na concentration (aldosterone from adrenal
cortex)
– Increased serum Na level by tubular reabsorption of Na in
ascending loop of Henle (constricts afferent arteriole to
decrease GFR, if bld volume is low)
– Allows fluid to be removed and increases Na concentration
in the bld, if blood volume if normal (constricts efferent
arteriole to increase GFR)
– Enhances reabsorption of Na from DCT
Renal regulatory functions
• Glomerular filtration- water,
electrolytes, Cr, urea N and
glucose are filtered
• Blood, albuminis too large
• Forms 180 L of filtrate/day
or GFR=125ml/min
• Regulated by constricting
and dilating the afferent
arteriole
• When SBP goes below
70mm Hg, GFR stops (MAP
of 60)
Tubular reabsorption and Secretion
 Reabsorption
– Most of the water and
electrolytes are reabsorbed,
65% of filtrate to keep urine
output at 1-3 L
– Most of water reabsorption is
in the PCT, some is in DCT
– DCT is affected by ADH and
aldosterone
– ADH enhances water
reabsorption by increasing
membrane permeability
– Aldosterone reabsorbs Na
 Solute Reabsorption
– 50% of urea, no creatinine
– Most Na, Cl is reabsorbed in
the PCT, some in the collecting
ducts by aldosterone
– K is reabsorbed in the PCT and
the ascending loop of Henle
– Bicarb, Ca and Phosphate are
in the PCT
– Glucose is reabsorbed up to
220mg/dl > will be excreted
 Tubular secretion is
substance need to be
excreted, such as K and H
Renal hormones
• Renin= RAAS (renin-angiotensin-aldosterone system)
• Prostaglandins- PGE and PGI, regulate filtration and
vascular resistance
• Bradykinins-dilates the afferent arteriole and
increase capillary membrane permeability
• Erythropoetin-released when there is decreased
oxygen, triggers RBC production in the bone marrow
• Vitamin D activation- converted to its active form in
the kidney
Renal Assessment
• Personal history- what questions should we
ask?
• What about diet, why is that important?
• What is a normal urine output?
• What types of medical conditions can affect
the kidneys?
Renal Assessment
Inspection- note any swelling or discoloration
in the flank region, costovertebral angle is 12th
rib and vertebrae
Auscultate for what?
How do you palpate the kidneys?, not be
done is suspect pheochromocytoma, what is
that?
Percuss what? Only the kidneys or bladder
too?
Diagnostic tests
• Blood
– Creatinine- end product of
muscle and protein
metabolism (0.6-1.2)
– BUN- excretion of urea N
from protein metab, liver
failure, trauma will elevate
(10-20 mg/dl
– Ratio BUN/CR is 12-20:1,
dehydration can cause BUN to
be elevated, but not CR
– Decreased ratio will occur
with FVE
• Urine
– Urinalysis for inspection,
odor, cloudiness, pH, specific
gravity
– What is a normal S.G.?
– What things would be
abnormal in the urine?
– How high is the bacterial
count in order to be treated?
Diagnostic tests
• IVP- intravenous pyelogram,
now called IV urography
• Given a contrast dye, should
not give if pt has renal
insufficiency
• Shows the size, shape and
location of kidneys
• Patency of calices, pelves
and ureters
• Detects obstructions and
masses
Diagnostic Tests
• CT of the kidney
• Renal Arteriogram
Diagnostic
• Renal Biopsy
– Check blood counts
before procedure, may
need to transfuse
– Given procedural
sedation
– Monitor the site for
bleeding 24 hours after,
bruising on flank, H&H
– Bedrest for 6 hours
– Will have hematuria
Cystoscopy
• Visualize the bladder
and any abnormalities
Urinary Tract Infections
• UTI’s are the most prevalent nosocomial infections,
costing 1.6 billion/yr
• How can they be prevented in the hospital?
• What is the recommended length of time a catheter
should remain in, in the acute care setting?
• What factors may contribute to a UTI?
• Which organisms are most commonly the cause of
UTI’s?
Urinary Tract Infections
• Cystitis- inflammation of the bladder,
interstitial cystitis, unknown etiology
• Can lead to urosepsis, has a high mortality and
prolonged hospitalization
• Incidence is greater in women than men and
increases by 50% in women over 80
Case Study- UTI
• 24 y.o. sexually active female, who arrives in
the ED, complaining of frequency, urgency and
dysuria. She has difficulty initiating a stream.
This has been occurring for the past 3 days,
but not she feels weak and has noticed some
blood in her urine
Case Study
• What type of questions may you ask this
patient?
• What type of urine sample would you get?
• The urine comes back with > 100,000 c./ml
• Should this be treated? What is the most
common antibiotic that is given for an
uncomplicated 3 day course?
Case Study
• What nursing diagnoses would be appropriate
for this patient?
• What patient education should be done?
• Include diet and prevention therapy
Urinary Incontinence
• Incontinenceinvoluntary loss of urine
• Not a normal result of
aging
• In the elderly, can be
caused by:
– Medications, disease,
depression, unable to
walk or get to the BR
Types of incontinence
• Stress- most common, occurs during coughing,
sneezing, jogging or lifting, weakening of the bladder
neck can occur with childbirth, can’t tighten the
urethra enough to overcome the urge to void
• Urge- when they feel the “urge” to go, they can not
hold it until they find a BR, called overactive bladder,
can be caused by CVA, parkinson’s disease, MS, UTI,
BPH, artificial sweeteners, caffeine, alcohol, diruetics,
nicotine
Incontinence
• Overflow- when the detrusor muscle fails to
contract, the bladder becomes overdistended, leaks
out to prevent rupture, may be urethral obstruction,
diabetic neuropathy, pelvic surgery
• Reflex- abnormal detrusor contractions r/t
neurologic problems- CVA, spinal cord lesions, MS
• Functional- loss of cognitive function in patients with
dementia
Incontinence
• 85% of all cases are women
• Contributing factors are:
– Medications- diuretics, opioids
– Diseases- CVA, arthritis, parkinson’s
– Psychological disturbances
• Physical examination
– Assess for bladder fullness- bladder scan,
cystocele, note detrusor muscle
Incontinence- Interventions
Exercise- kegel’s strengthen pelvic floor
Weight reduction, decrease fluids at night
Drug therapy- estrogen, antispasmodicsditropan, probanthine, bentyl, detrol,
antidepressants- tricyclics- anticholinergics
and alpha-adrenergics, so decrease urination
Vaginal cone- weighted cones to tighten
muscles, pessary to hold bladder up in cases
of cystocele
Incontinence- Surgery
• Vaginal or retropubic
surgery
• Elevates the urethra,
repairs cystocele
• Postop- monitor
voiding, may have SP
catheter, PVR should be
less than 50ml, monitor
for bleeding
Incontinence education
• What type of education should be provided
for bladder training?
• How can you get the family to help?
• If the patient does need to straight cath or
have a foley at home, what things should they
monitor for?
Renal Calculi- Urolithiasis
• Nephrolithiasis- stones in the kidney
• Ureterolithiasis- stones in the ureter
• 75% of the stones contain Ca- Ca oxalate or Ca
phosphate
• 15% struvite, 8% uric acid and 3% cystine
• 90% of patient have a metabolic risk factor for
the stones
• Incidence is higher in men
Renal calculi
• Formation is from
– Slow urine flow from the
element, such as Ca
– Damage to the lining of
the tract
– Decreased inhibitor
substances in the urine
that would dissolve
Renal Calculi Risk Factors
• Hypercalcemia– Increased intake or renal
failure
– Hyperparathyroidism
– Immobilization
• Hyperoxaluria– genetic trait that
overproduces
– Excess intake from spinach,
rhubarb, coca, beets, wheat
germ, pecans, okra, chocolate
• Hyperuricemia– Gout with purine metabolism
disorder
– Increased purines from
cancers and thiazide diuretics
• Struvite– Magnesium ammonium
phosphate and carbonate,
urea splitting bacteria causes
• Cystinuria– Genetic defect of amino acids
Renal Calculi
• Symptoms:
– Renal colic- what is that?
– Oliguria vs anuria, what
is the difference?
• What is the
predominant nursing
diagnosis?
• Interventions:
– Drug therapy:
• Pain relief, what should
be used?
• Besides opioids, what
medication may be
helpful?
– Lithotripsy• Shock wave therapy to
break up stones
• Monitor ECG, bleeding
after
• Strain the urine for stone
collection
Surgical interventions
• Nephrolithotomy and
ureterolithotomy
– Endoscope or lithotriptor to
grasp and extract the stone
– Nephrostomy tube is left in
place
– Keep the nephrostomy site
sterile and never irrigate with
more than 10 ml
– May be performed as an open
procedure if the stone is too
large
Patient education
• How can the patient prevent getting more
stones?
• What foods should be avoided if the patient
has a calcium oxalate stone? A calcium
phosphate stone? A struvite stone? A uric acid
stone?
• How much fluid should the patient take in per
day?
Renal Disorders
Polycystic kidney disease- genetic disorder,
cysts develop on the kidney, most patients are
hypertensive, RAAS is activated
As the patient ages, kidney is more damaged
Controlled by monitoring the BP and using
ACE inhibitors, control the cell proliferation of
PKD, follow a low NA diet
Control for pain, many need a transplant
Polycystic kidney
PKD
Glomerulonephritis
• Third leading cause of ESRD
• Disorders that cause are often autoimmune, such as:
– Lupus, Goodpasture’s syndrome, Wegener’s
granulomatosis, amyloidosis, diabetes, HIV, hepatitis C,
cirrhosis, sickle cell disease, endocarditis
• Infectious processes also cause, such as:
– Beta-hemolytic streptococcus, Staph bacteremia, syphilis,
pneumococcal mycoplasma or klebsiella, CMV,
histoplasmosis, varicella, toxoplasmosis
Glomerulonephritis
• An infection may
precipitate
• Symptoms occur 10
days
• 75% of patients have
edema of face, hands,
eyelids
• Fluid overload and
circulatory congestion
Glomerulonephritis
• Urine is smoky or
reddish brown with
hematuria and oliguria
• HTN with wt. gain
• Fatigue, anorexia, N&V
• What kind of labs would
be done?
• What lab would be
done to assess for a
strep infection?
• What type of 24 hour
urine would be done?
Case Study- Nephrotic Syndrome
8 y.o. presents to the
hospital with swelling of
the face and hands. He
has the sickle cell trait.
His mother has noted a
marked decrease in his
urine output and it
looks dark brown. He
complains of feeling
tired and not wanting to
eat.
Case Study
• What process occurs with Nephrotic
syndrome?
• What would you expect to see in his urine?
What about his lab values?
• His mother asks if this condition can be cured,
what would you say?
• What type of treatment may be prescribed?
Medications and therapy
Benign Prostatic Hypertrophy
• Prostate become
hyperplastic and enlarges
with age
• Prostate extends upward
into the bladder and
inward, narrowing the
urethral channel
• Obstructs urine flow,
overflow incontinence
• Bladder becomes irritable
and leads to urgency and
frequency, muscles enlarge
and can lead to
hydroureters and
hydronephrosis
BPH
• Symptoms:
– Nocturia
– Frequency, urgency
– Reduced stream and
force
– Incomplete emptying
and dribbling
– Hematuria in elderly
males
• Assessment:
– Digital rectal exam
– Urinalysis
– PSA level, what is this
for?
• What nursing diagnoses
would be appropriate?
BPH
Medications:
– Shrink- Proscar,
finasteride, lowers DHT,
may take 6 months to
lower, major side effect is
ED and decreased libido
– Alpha-adrenergic
blockers- Hytrin, Cardura,
Flomax, constricts the
prostrate and reduces
pressure
Avoid medications that
may cause urinary
retention, such as
anticholinergics,
antihistamines and
decongestants
Don’t take in a large
amounts of fluid, avoid
alcohol and diuretics,
that can cause
overdistention
BPH Surgery
• TURP- transurethral
resection of the prostate
• Can only remove pieces of
the prostrate in chip form
• Suprapubic, Retropubic and
Perineal prostatectomydone when the prostate is
large or the bladder also
needs to be explored
BPH surgery
• Postop:
– Assess incision site if
applicable for bleeding
– Continuous Bladder irrigation
(CBI) done 24 hours post
surgery
– Monitor for FVE, running total
of I & O
– Bleeding is to be expected,
but urine should not be
“frank” blood, may have clots,
monitor H&H
– May have bladder spasms,
ditropan or B&O supp.
Renal Failure
• Renal failure is the loss of function r/t nephron
damage. In CRF, 90-95% of the nephrons are
lost before failure is obvious
• ARF, only 50% decrease in nephrons can cause
failure, ARF is a sudden onset and may last < 3
mo, good prognosis
• Most common causes of CRF are:
– Diabetes (43%), HTN (25%), glomerulonephritis
(8%)
Acute Renal failure- ARF
• Types of ARF:
– Prerenal azotemia- correct by
increasing BP, giving volume,
improve C.O., prolonged
damage can lead to intrarenal
failure
– Intrarenal- ATN- infections,
drugs, NSAID’s,
aminoglycosides, tumors,
glomerulonephritis
Phases of ARF
• Onset:
– Hours to days, precipitating event until oliguria,
BUN and Cr increase
• Oliguric:
– Urine output of 100-400ml/day, does not respond
to diuretics or fluid challenges, BUN and CR
increase, K, Magnesium and Phosphate increase,
Na is retained, but masked with fluid, dilutional,
lasts 8-15 days
Phases of ARF
• Diuretic:
– Urine output increases rapidly, can be 10L/day of
dilute urine, electrolyte losses occur, BUN
decreases last, 2-6 weeks, until BUN falls, renal
tubular function returns
• Recovery:
– Functions at lower level, may take up to 12
months to return to normal
• In critically ill patients, 50-80% mortality rate
for those who develop ATN
Case Study for ARF
25 y.o. male admitted to the ICU post MVA, he
had multiple fractures, ruptured spleen and
significant blood loss. He has been in the ICU
for 24 hours and is ventilated. He has
received blood transfusions and maintenance
IV fluids, but his blood pressure continues to
drop and is presently 80/44, his urine output
has only been 100 ml for the past 12 hours.
What do you expect is occurring?
Case Study for ARF
• What type of ARF is the patient experiencing?
What phase is he in?
• What can be done to initially correct this
problem?
• What nursing interventions should be done to
monitor for patient improvement?
• The MD says that the patient has prerenal
azotemia, what does that mean?
Case Study- ARF
• If the patient is in the
oliguric phase, what
would the lab values
be?
•
•
•
•
•
•
•
•
•
CR –
Bun –
Na –
K–
PhosphorusCa –
Magnesium –
BicarbonatepH-
Case Study- ARF
• Because of the
disruption in
electrolytes, what
symptoms may the
patient experience?
• Besides electrolytes,
what other labs should
the RN monitor?
•
•
•
•
•
KNaPhosphateCaH-
Case Study- ARF
• What are the main
Nursing diagnoses for
this patient?
• What medications may
be given to this patient?
• Besides replacements,
what other meds would
be needed?
• What should his diet
include?
• How much protein can
he take in?
• How much fluid?
Case Study- ARF
• The patient remains oliguric and has persistent
hyperkalemia, FVE and metabolic acidosis, the MD
decides that he must begin dialysis to remove the
end-products
• CRRT is ordered, what does this mean? Why is this
done instead of Hemodialysis?
• What type of catheter would be inserted? Where is
the cath inserted?
• Why not have a renal fistula done?
Case Study- ARF
• Prisma machine used for
CRRT
• Can do hemofiltration, uses
a double venous access,
one catheter is arterial and
one venous return
• Changes in fluid removal
can be set for every 30-60
minutes and so they don’t
remove as much as regular
hemodialysis
• Set blood flow at 150ml/hr,
dialysate rate at 1L/hr
Case Study- ARF
• After 5 days on CRRT, the patient’s kidneys
begin to improve and his urine output is
>30ml/hr, his BP has stabilized and he is off of
all vasopressors. He is being transferred to
the floor.
• What types of things should be still be careful
of? What agents may be nephrotoxic to him?
Chronic Renal Failure
• Progressive, irreversible
kidney disease
• Kidney function does not
recover, ESRD
• Have azotemia (increased
nitrogen wastes), uremia
(azotemia with symptoms),
uremic syndrome (clinical
and labs r/t ESRD)
Chronic Renal Failure
• Stages of CRF:
– Stage 1: Diminished Renal Reserve- renal function
is reduced, but no accumulation of wastes, can’t
concentrate urinepolyuria and nocturia
– Stage 2: Renal Insufficiency- wastes accumulate,
no response to diuretics, oliguria and edema
develop, decreased GFR
– Stage 3: ESRD- excessive wastes, BUN and CR, H,
treatment is dialysis
Chronic Renal Failure
Metabolic changes:
–
–
–
–
BUN, CR elevated
Na elevated in later stages, may appear nl or low at first
K elevated, up to 7 or 8 mEq/L, can cause cardiac arrest
H is elevated metabolic acidosis, lungs try to blow off
Kussmaul’s respirations
– Ca is low, phosphorus is elevated stimulation of PTH,
which causes Ca to be released form bone renal
osteodystrophy, lack of vitamin D also makes it worse
Chronic Renal Failure
• Cardiac changes:
– Hypertension- most have because of what?
– Hyperlipidemia- changes fat metabolism elevated trigylcerides,
cholesterol and LDL
– Heart failure- resulting from increased cardiac workload r/t volume,
HTN and CAD
– Uremic pericarditis- pericardial sac becomes inflammed with toxins
pericardial effusion, tamponade and death
• Hematologic:
– Anemia occurs because of decreased erythropoetin and RBC’s
• GI changes:
– Ammonia from urea breakdown causes halitosis and stomatitis
– Anorexia, N & V occurs, PUD may occur
Chronic Renal Failure
• Clinical Signs:
– Neurologic
• Lethargy, seizures, coma
from uremia
– Cardiovascular
• Tachycardia, increased BP,
elevated CVP, peripheral
edema
– Respiratory
• Tachypnea, kussmaul’s
• Clinical Signs:
– Hematologic
• Anemia, bleeding, fatigue
– GI
• Abdominal pain, anorexia,
foul breath
– Urinary
• Oliguria, proteinuria,
hematuria, amount depends
on dialysis
– Skin
• Yellowish tint, pruitus,
uremic frost, purpura and
ecchymosis
Chronic Renal Failure
• What are the common
nursing diagnoses for
the patient with CRF?
Chronic Renal Failure- Interventions
• Diet therapy:
– Increase calories, but restrict Protein, Fluid, K, Na,
Phosphorus, why restrict protein? If the patient is
on peritoneal dialysis, protein may be increased
– Take vitamins and minerals- return vitamin D, Ca,
folic acid
Chronic Renal Failure- Interventions
• Drug therapy– Diuretics- only if FVE that is not on dialysis
– Biologic response modifiers- procrit
– Phosphate binders- amphojel, alternagel, renagel,
tums, oscal
– Stool softeners- colace, miralax
– Vitamins- folic acid, ferrous sulfate
– Antihypertensives- ACE, Ca channel and betas may
be used
Renal Replacement Therapies
• Hemodialysis
– Better clearance
– Short time for treatment
– Have to leave home
3x/wk
– Can cause disequilibrium
syndrome, muscle
cramps, hemorrhage
– Restricted diet
• Peritoneal dialysis
– Easy access
– Fewer hemodynamic
complications
– Infections and adhesions
can occur
– Less effective
– Protein loss and
peritonitis
– Uses intra-abdominal
catheter
Hemodialysis
• Used in patients with:
–
–
–
–
–
–
Fluid overload
Pericarditis
Uncontrolled HTN
Uremic signs
Worsening anemia
Irreversible renal failure
when other therapies
are not possible
Hemodialysis
• Process:
– Diffusion of molecules
with the use of dialysate
solution, high in
electrolytes, water
– Waste products move
from the blood through
the filters
semipermeable
membrane into the
outflow resevoir
– Water is also removed
by osmosis as it follows
the solutes
Hemodialysis
• Hemo filter- over 1
million fine hairs, act as
nephrons
• Venous access
• AV shunt- only short
term
• Can become dislodged,
or bleed
Hemodialysis
• Venous access
• AV fistula or graft- artery
and vein anastomosed, as it
matures, blood flow
increases and it enlarges
• Do not take BP or blood
draws from that arm
• Assess pulses
• Palpate for thrill and listen
for bruits
• No lifting of heavy objects
Hemodialysis Care
• Weigh the patient before and after, know the “dry
wt”
• Measure BP, HR and Respirations
• Watch for orthostatic hypotension
• Watch for disequilibrium syndrome- after HD is
completed, change in fluid and urea headache,
N&V, change in LOC, cerebral edema, seizures,
slowing down the fluid removal can prevent it
• Bleeding can occur, from heparinization of the lines
and low blood counts
• Infectious diseases, such as hepatitis C and HIV
through blood transmission
Peritoneal dialysis
• Silastic Catheter is
inserted in the
abdominal cavity
• Dialysate is inserted,
dwells for 3-4 hours,
allowing fluid to mix
with dialysate
• Effluent or outflow is
then opened and waste
products and water are
removed
Peritoneal dialysis
• Process is by diffusion and osmosis of products
• Dialysate has water and electrolytes, also glucose in
2.5, 5 or 10%, determines the amount of diffusion
• Heparin and antibiotics may be added to dialysate
• Can be done either throughout the day with a Y-set
or at night with an automatic cycler
Peritoneal dialysis
Complications
– Peritonitiscontamination of
catheter, cloudy outflow,
fever, abdominal pain and
cramping
– Pain
– Poor outflow and
leakage- can be caused by
constipation, fibrin clots
in the catheter
Tenckhoff, peritoneal
catheter
Renal Transplantation
• Selection:
– Free from medical
problems, such as
cancer, heart disease
and diabetes ( should be
under control)
– Age is 2-70
– Use living and cadaver
donors
Renal Transplantation
• Postoperative Care
– Monitor urine output, should return to normal in
48 hours, color may be pink with some clots
– Complications:
• Rejection
– Hyperacute- within 48 hours, fever, pain and increased BP
– Acute- 1 wk to 2 yrs, most common, oliguria, fever, enlarged
kidney, elevated BUN, Cr
– Chronic- months to years, gradual increase in BUN, Cr, fluid
retention, fatigue
Renal Transplantation
• Complications
– ATN- may have occurred due to damage to
transplanted kidney
– Thrombosis- renal artery or vein 2-3 days post
– Renal artery stenosis- may lead to hypertension,
can often be repaired with a stent
– Infections- on immunosuppressives for life
• Cyclosporine, prednisone, imuran
Renal Transplant Surgery
http://Kidney transplant surgery