RENAL
FAILURE
KASONGO
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Mr. KASONGO

Introduction
• Kidney failure is abnormal kidney function in
which the kidneys are unable to adequately
excrete the body’s metabolic waste from the
body or perform their regulatory functions.
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• The substances normally eliminated in the
urine accumulate in the body fluids as a result
of impaired renal excretion, affecting endocrine
and metabolic functions as well as resulting in
fluid, electrolyte and acid-base disturbances.
• Renal failure is a systemic disease and is a final
common pathway of many different kidney and
urinary tract diseases. (Smeltzer et.al. 2010)
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Anatomy of the Kidney
http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html
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Nephron
http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html
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Functions Of The Kidney’s
• Urine Formation: Formed in the nephrons
through a complex three-step process:
Glomerular filtrate, tubular reabsorption,
and tubular secretion
• Excretion of waste products: eliminates
the body’s metabolic waste products (urea,
creatinine, phosphates, sulfates)
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• Regulation of electrolytes: volume of
electrolytes excreted per day is exactly equal to
the volume ingested
– Na – allows the kidney to regulate the
volume of body fluids, dependent on
aldosterone (fosters renal reabsorption of
Na)
– K – kidneys are responsible for excreting
more than 90% of total daily intake
• RETENTION OF K IS THE MOST
LIFE-THREATENING EFFECT OF
RENAL FAILURE
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Renin-Angiotensin System
http://en.wikipedia.org/wiki/Image:Renin-angiotensin-aldosterone_system.png
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• Control of water balance: Normal ingestion
of water daily is 1-2L and normally all but
400-500mL is excreted in the urine
– Osmolality: degree of dilution or
concentration of urine
– Specific Gravity: measurement of the
kidney’s ability to concentrate urine (weight
of particles to the weight of distilled water)
– ADH: vasopressin – regulates water
excretion and urine concentration in the
tubule by varying the amount of water
reabsorbed.
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• Control of blood pressure: BP monitored
by the vasa recta.
– Juxtaglomerular cells, afferent arteriole,
distal tubule, efferent arteriole
• Renal clearance: ability to clear solutes
from plasma
– Dependent on rate of filtration across the
glomerulus, amount reabsorbed in the
tubules, amount secreted into the tubules
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–CREATININE
• Regulation of red blood cell production:
Erythropoeitin is released in response to
decreased oxygen tension in renal blood
flow.
• This stimulates the productions of RBCs
(increases amount of hemoglobin available
to carry oxygen)
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• Synthesis of vitamin D to active form:
final conversion of vit D into active form to
maintain Ca balance
• Secretion of prostaglandins: important in
maintaining renal blood flow.
• They have a vasodilatory effect
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Acute Renal Failure
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Definition
• Acute renal failure (ARF) is an abrupt and
sudden reduction in renal function resulting in
the inability to excrete metabolic wastes and
maintain proper fluid & electrolyte balance
• It is usually associated with oliguria (urine
output <30cc/hr or <400cc/day), although
urine output may be normal or increased
• BUN & creatinine values are elevated
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Statistics of ARF
• Frequency: condition develops in 5% of
hospitalized patients and 0.5% patients
require dialysis
– Elderly are at high risk
– Post-op patients
• Mortality: the mortality rate estimates
vary from 25-90%
• Race: no racial predilection is recognized
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Pathophysiology
• ARF may occur in 3 clinical settings:
• As an adaptive response to severe volume
depletion and hypotension, with structurally
and functionally intact nephrons (Prerenal)
• In response to cytotoxic or ischemic insults
to the kidney, with structural and functional
damage (Intrinsic or Intrarenal)
• Obstruction to the passage of urine
(Postrenal)
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Phases of Acute Renal Failure
• Clinical progression of reversible RF occurs in
four phases:
– Initiation phase
• Begins with initial insult and ends when
oliguria develops
– Oliguric phase
• Accompanied by rise in serum
concentrations of substances usually
excreted by kidneys (urea, creatinine,
organic acids, intracellular cations [K+ &
Mg])
• urinary output <400cc/day
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Diuretic phase
• The kidneys begin to recover
• Initially produce hypotonie urine due to
increase in glomerular filtration rate
Recovery phase
• Tubular function restored
• Diuresis subsides and kidney begins to
function normally again
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Aetiology of acute renal failure
Prerenal acute renal failure
• Is the most common cause of ARF occurring
in 60-70% of cases
• It is caused by impaired blood flow as a result
of intravascular depletion, which leads to
decreased effective circulating volume to the
kidneys
• In patients with prerenal ARF, the
parenchymal is undamaged, and the kidneys
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• Causes include:
– Secondary to renal hypoperfusion which
occurs in setting of extracellular fluid loss
• Diarrhea
• Vomiting
• Diuretics
– Impaired/inadequate cardiac output
– Drugs
• NSAIDs
– Hypovolemia
– Hemorrhage
– Renal vasoconstriction
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• Decreased peripheral resistance due to
anaphylaxis, neurologic injury and some
hypertensive drugs. i.e ACE inhibitors
• Decreased renal vascular blood flow due to
bilateral renal vein thrombosis, embolism and
renal artery thrombosis.
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Intrinsic acute renal failure
• Is the result of actual parenchymal damage to
the glomeruli or kidney tubules
• A physiologic hallmark is failure to maximally
concentrate urine
• Is divided into 4 categories:
• Acute tubular disease
• Glomerular disease
• Vascular disease
• Interstitial disease
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Intrinsic ARF
• Acute Tubular Necrosis
– most common type of ARF, a more
ischemic insult to the kidneys, usually
induced by ischemia or toxins
– Caused by:
• Burns, and crush injuries – myoglobin &
hemoglobin are liberated causing renal
toxicity or ischemia
• Drugs – NSAIDs, ACE inhibitors,
aminoglycosides
• Infections
• Nephrotoxic agents – contrast agent
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• Glomerulonephritis
-uncommon cause, most associated with
CRF
-Caused by:
• Can be a primary disorder or can
occur secondary to systemic disease
• Systemic lupus erythematosus
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Intrinsic ARF
• Acute Interstitial Nephritis
-Interstitial disturbance that leads to ARF
-Caused by:
• Allergic reaction to drugs
• Vascular Disease
-Can occur on microvascular and
macrovascular
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– Caused by:
• Microvascular
-Hemolytic anemia
-ARF secondary to small vessel
thrombosis or occlusion
• Macrovascular
-Suspected in elderly
-Renal artery stenosis or thrombosis
-Atheroembolism secondary to atrial
fibrillation and aortic disease
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Postrenal acute renal failure
• Is rare and occurs with urinary tract
obstruction that affects the kidneys
bilaterally
• Pressure rises in the kidney tubules,
eventually the GFR decreases
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Post renal ARF
• Causes include:
– Bladder tract obstruction
– Prostatic hypertrophy
– Catheters
– Urethral strictures.
– Bladder cancer.
– Spinal cord disease. Trauma from the back,
pelvis or perineum.
• Postrenal causes are typically reversible
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Clinical manifestations
• Muscle weakness
• Dysrhythmias
• Pruritus
• Oliguria
• Pitting oedema
• Hypertension
• Pulmonary oedema
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• Metabolic acidosis with kussmal respirations
(hyperventilation) and pulmonary oedema
• Altered mental state
• Anorexia
• Nausea
• Dry skin
• Headache
• Seizure
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Investigations
• BUN and serum creatinine values
• Creatinine clearance which measures the
kidney’s ability to clear the blood of creatinine
and approximate the glomerular filtration rate
• Urinalysis
• Renal ultrasound
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• Renal scan
• Renal biopsy
• Serum electrolyte analysis will show increased
levels of potassium due to decreased GFR and
increased phosphate concentration
• CT scan or MRI retro grade pyelogram
• Haemoglobin levels will be lower due to
reduced erythropoietin production
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Nursing Care Plan
• Fluid volume deficit related to hemorrhage
(hypovolemic shock)
– Priority to restore fluid balance and circulation
• The patient will:
– show stable vital signs
– have adequate urine output >30cc/hr
– have strong peripheral pulses indicating tissue
perfusion
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Nursing Care Plan
• Interventions
– Bleeding reduction, fluid
resuscitation, blood product
administration, IV therapy
– Monitor VS q2h
– Monitor weight daily
– Skin & tongue turgor
– Monitor and document I&O
– Monitor CBC, ABG,
urinalysis, ECG
• Rationales
– Early intervention can prevent
progression of hypovolemia to
hypovolemic shock that may
result in renal damage
– S&S correlate with the
approximate percentage of
volume loss
• Medullary vasomotor center
stimulation via the
baroreceptor reflex
• ADH
– Foley catheter facilitates
monitoring of urine output
– Shock pt hemodynamically
unstable with compromised
compensatory mechanisms,
volume admin may cause fld
overload
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Nursing Care Plan
• Electrolyte imbalance related to decreased
electrolyte excretion, and metabolic acidosis
– Priority to prevent complications of electrolyte
imbalance
• Within 24h of admission and then continuously,
the pt will:
– Maintain serum electrolyte levels within acceptable
limits
– Have normal sinus rhythm
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Nursing Care Plan
• Interventions
– Monitor & document
electrolyte levels q8-12h,
especially:
• K+, P, Ca, Mg
– Monitor ABG
– Monitor ECG especially:
• High tented T waves,
prolonged PR interval or
widened QRS complex
– Limit dietary & drug intake of
potassium
• Rationales
– Kidneys’ ability to regulate
electrolyte excretion &
reabsorption may result in
high K+ & P, low Ca, &
high/low Mg levels.
– ARF causes metabolic
acidosis which may increase
the release of K+ from cells in
exchange for H+ ions
– Electrolyte abN can trigger
arrhythmias & cardiac arrest
– When kidneys cannot excrete
K+, excess intake can increase
serum K+ to dangerous levels
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Nursing Care Plan
• Knowledge deficit of acute renal failure related
to lack of exposure to information on
management of complex condition
– Priority to provide in depth information on acute renal
failure
• Upon discharge the patient will:
– Be able to identify signs and symptoms to report to
nurse or physician
– Commitment to comply with treatments, including
dialysis, dietary modifications, and activity restrictions
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Mr. KASONGO

Nursing Care Plan
• Interventions
– Provide as appropriate
information on the severity of
ARF & dialysis
• Stages of ARF
• Medications including action
and adverse effects
• S&S
• Procedures such as dialysis
including schedule and
adverse effects
• Dietary modifications
including limitations of
proteins (catabolism),
electrolytes and fluids
• Rest and activity restrictions
• Rationales
– The patient and family need
assistance, explanation, and
support during this time.
– Teaching may decrease
anxiety and fear, and enhance
recovery to patient and family
members.
– Continued assessment of the
patient for complications of
ARF and of its precipitating
cause is essential.
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Medications for ARF
Pharmacologic treatment of ARF has been
attempted on an empirical basis, with
varying success rates.
It is critical to adjust (decrease or
discontinue) medication dosages for patient
in acute renal failure. Administering the
average dose to patient in renal failure can
kill a patient.
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Immediate goal is to retain fluid volume deficit
through use of blood products and
crystalloids
• Normal Saline (0.9% Na) - only one that is
compatible with blood transfusions
– Restores fluid loss
– Provides electrolytes resembling those of
plasma
• Packed RBC
– To increase blood volume
– To restore blood to kidneys
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•Diuretics
–Furosemide (Lasix) only given with
severe fluid overload
–Increases excretion of water by interfering
with chloride-binding cotransport system,
which, in turn, inhibits sodium and chloride
reabsorption in the thick ascending loop of
Henle and the distal renal tubule
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–Adult dose: 20-80 mg PO/IV once;
repeat 6-8h prn or dose may be increased
by 20-40 mg no sooner than 6- 8h after
previous dose until desired effect
–Nursing Assessments: Watch for
hypokalemia, assess BP before and during
therapy can cause hypotension
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• Vasodilators
– Dopamine
• In small doses causes selective dilatation of
the renal vasculature, enhancing renal
perfusion.
• Reduces sodium absorption, thereby
decreasing the energy requirement of the
tubules.
• This enhances urine flow, which, in turn,
helps prevent tubular cast obstruction.
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• Adult dose: 2-5 mcg/kg/min
• Nursing Assessments: Monitor blood
pressure during administration.
• Stop infusion if blood pressure drops
30mm Hg
• Monitor input and out put
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Mr. KASONGO

• Alkalinizer
– Sodium Bicarbonate
– Increases plasma bicarbonate, which
buffers Hydrogen ion concentration;
reverses acidosis
– Adult Dose: Initial dose IV bolus 1
mEq/kg, then infuse 2-5 mEq/kg over 4-
8 hr depending on CO2, pH
• Dilute with equal amounts of NS, 2-5
mEq/kg
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• Nursing assessments:
• Assess respirations and pulse rate, rhythm,
depth, lung sounds
• Monitor input and output, electrolytes,
blood pH, HCO3
• Monitor urine pH at the beginning of
treatment and monitor for alkalosis as well
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Mr. KASONGO

• THANK YOU FOR YOUR ATTENTION!
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Mr. KASONGO

Chronic Renal Failure
ESRF
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Mr. KASONGO

Definition
• Also known as End-Stage Renal Failure (ESRF),
is a progressive deterioration in renal function in
which the body’s ability to maintain metabolic
and fluid and electrolyte balance fails, resulting
in uremia (retention of urea and other
nitrogenous wastes in the blood).
• Decreased kidney glomerular filtration rate
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Pathophysiology
• As renal function declines, the end
products of protein metabolism (which
are normally excreted in the urine),
accumulate in the blood.
• Uremia develops and adversely affects
every system in the body.
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• The greater the buildup of waste
products, the more severe the
symptoms.
• Regardless of the etiology of renal
injury, with progressive destruction of
nephrons, the kidney has an innate
ability to maintain glomerular filtration
rate (GFR) by hyperfiltration and
compensatory hypertrophy of the
remaining healthy nephrons.
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• This nephron adaptability allows for
continued normal clearance of plasma
solutes such that substances such as urea and
creatinine start to show significant increases
in plasma levels only after total glomerular
filtrateion rate (GRF) has decreased to 50%,
when the renal reserve has been exhausted.
• The plasma creatinine value will double with
a 50% reduction in GFR.
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Stages of Chronic Renal Disease
• 3 stages in nephron function
• Stage 1: Reduced Renal Reserve
Characterized by a 40%-75% loss of
nephron funtion.
The patient is usually asymptomatic
because the remaining nephrons are
able to carry out normal function of the
kidney
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Stage 2 of Renal Disease
• Stage 2: Renal Insufficiency
Occurs when 75%-90% of nephron
function is lost.
At this point, the serum creatinine and
BUN rise, the kidney loses its ability
to concentrate urine and anemia
develops. The patient may report
polyuria and nocturia
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Stage 3 of Renal Disease
• Stage 3: End-Stage Renal Disease
The final stage, occurs when there is less
than 10% of nephron function
remaining.
All normal regulatory, excretory, and
hormonal functions of the kidneys are
severely impaired.
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ESRD is evidenced by elevated
creatinine and BUN levels as well as
electrolyte imbalances.
Dialysis is usually indicated at this
point.
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Glomular Filtration Rate
• GFR: a Kidney function test in which
results can be determined from amount
of ultrafiltrate formed by plasma
flowing through the glomeruli of the
kidney.
• As glomular filtration decreases, the
serum creatinine and BUN levels
increase.
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Causes
Type 1 and type 2 diabetes mellitus
cause a condition called diabetic
nephropathy, which is the leading cause
of kidney disease in the United States.
High Blood Pressure (hypertension),
if not controlled, can damage the
kidneys over time.
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Glomerulonephritis is the
inflammation and damage of the
filtration system of the kidney and can
cause kidney failure.
Post infectious conditions and Lupus
are among the many causes of
glomerulonephritis.
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More Causes
Polycystic Kidney Disease is an
example of a hereditary cause of
chronic kidney disease wherein both
kidneys have multiple cysts
Use of analgesics such as
acetaminophen (Tylenol) and
ibuprophen regularly over long
durations of time can cause analgesic
nephropathy, another cause of kidney
disease. Certain other medications can
also damage the kidneys.
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Clogging and hardening of the arteries
(atherosclerosis) leading to the kidneys
causes a condition called ischemic
nephropathy, which is another cause of
progressive kidney damage.
Obstruction of the flow of urine such as
by stones, an enlarged prostate, strictures
(narrowings), or cancers may also cause
kidney disease
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Clinical Manifestation
• Patients with CRF stage 3 or lower
(GFR >30 mL/min) generally are
asymptomatic and do not experience
clinically evident disturbances in
water or electrolyte balance or
endocrine/metabolic disturbances.
• Generally, these disturbances
clinically manifest with CRF stages 4
and 5 (GFR <30 mL/min).
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Clinical Manifestations
• Hyperkalemia usually develops when
GFR falls to less than 20-25 mL/min
because of the decreased ability of the
kidneys to excrete potassium.
• Metabolic acidosis because the kidney
cannot excrete increased loads of acid.
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Clinical Manifestations
• Extracellular volume expansion and
total-body volume overload results
from failure of sodium and free water
excretion.
• Anemia principally develops from
decreased renal synthesis of
erythropoietin, the hormone
responsible for bone marrow
stimulation for red blood cell (RBC).
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• Calcium and Phosphorus imbalance
occurs because of a disorder in
metabolism.
• They have a reciprocal relationship in
the body; as one rises, the other
decreases.
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• weakness, fatigue, confusion,
disorientation, tremors, seizures,
restlessness of legs, burning of soles of
feet, behavioral changes.
• Ammonia odour to breath, metallic
taste, mouth ulcerations and bleeding,
anorexia, N&V, hiccups, constipation
or diarrhea, bleeding from GI tract.
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• Crackles, thick tenacious sputum,
depressed cough reflex, pleuritic pain,
shortness of breath, engorged neck
veins, tachypnea, uremic pneumonitis,
“uremic lung
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Nursing Care Plan
 Excess fluid volume related to
decreased urine output, and
retention of sodium and water
Goal is maintenance of ideal body
weight without access fluid
• Nursing Interventions
 Assess fluid Status
 Daily weight
 I & O
 Skin turgour & edema
 Distention of neck veins
 BP, P, R
 Limit fluid intake to prescribed
volume
 Explain to pt and family rationale
for restriction of food
 Provide or encourage frequent oral
care
 Rationale
 Assessment provides baseline and
ongoing database for monitoring
changes and evaluating interventions
 Fluid restriction will determine on the
basis of weight, urine output, and
response of therapy
 Understanding promotes pt and family
cooperation with fluid restrictions
 Oral hygiene minimizes dryness of
oral mucous membranes
 Expected Outcomes
 Demonstrates no rapid weight changes
 Maintains dietary and fluid restrictions
 Exhibits normal skin turgour without
edema
 Normal vitals
 Reports no difficulty breathing or
shortness of breath
 Reports decrease dryness of oral
mucous membranes.
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Nursing Care Plan
 Hyperkalemia, pericarditis,
pericardial effusion and
temponade, hypertension,
anemia, bone disease
• Goal: Patient experiences and
absence of complications
 Nursing Interventions
 Hyperkalemia
 Monitor serum K levels and
notify physician if greater than
5.5 mEq/L.
 Assess patient for muscle
weakness, diarrhea, ECG
changes( tall tented Twaves,
widened QRS).
• Rationale
 Hyperkalemia causes
potentially life-threatening
changes to the body
 Cardiovascular S & S are
characteristic of hyperkalemia
 Expected Outcomes
 Pt has normal K level
 Experiences no muscle
weakness or diarrhea,
 Exhibits normal ECG pattern
 Vital signs are within normal
limits
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• Pericarditis, Pericardial
effusion, tamponade
 Assess for fever, chills,
chest pain and pericardial
friction rub (signs of
pericarditis).
 If pt has pericarditis, ax q
4 hrs
• Extreme hypotension
• Weak of absent peripheral
pulses, altered level of
consciousness, bulging
neck veins.
• Rationale
 About 30-50% of CRF pts develop
pericarditis due to uremia; fever
,chest pain, and pericardial friction
rub are classic signs
 Pericardial effusion is common
following pericarditis. Signs of
effsusion: paradoxical pulse (> 10
mm drop in BPduring inspiration)
and signs of shock d/t compression
of the heart by a lg effusion.
 Cardiac tamponade exists when
the pt is severely compromised
hemodynamically
 Outcomes
 Has strong and equal peripheral
pulse
 Absence of paradoxical pulse
 Absence of pericardial effusion, or
tamponade
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• Hypertension
 Monitor and record blood
pressure
 Administer antihypertensives
as prescribes
 Encourage compliance with
dietary and fluid restriction
therapy
 Teach pt report signs of fluid
overload, vision changes,
headaches, edema, seizures
• Rationale
 Antihypertensives play a key role
in tx of hypertension associated
with CRF.
 Adherence to diet and fluid
restrictions prevents excess fluid
and sodium accumulation
 These are indications of
inadequate control of
hypertension, and need to alter
therapy
 Outcomes
 BP is within normal limits
 No headaches, visual problems or
seizures
 No edema
 Demonstrates compliance with
dietary and fluid restrictions
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• Anemia
 Monitor RBC count, Hg, and
HCT levels
 Administer prescribes meds:
iron and folic acid
 Avoid drawing unnecessary
blood specimens
 Teach pt to prevent bleeding;
avoid vigorous nose blowing
 Administer blood component
therapy
• Rationale
 Provides Ax of degree of
anemia
 RBCs need iron and folic acid
to be produced.
 Anemia is worsened by
drawing numerous specimens
 Blood component therapy may
be needed if pt has symptoms
 Outcomes
 Pt has normal colour without
pallor
 Hematology values are within
acceptable limits
 Experiences not bleeding form
any site.
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• Bone Disease
 Administer the following
meds as prescribed:
phosphate binders,
calcium supplements, vit
D supplements
 Monitor serum lab values
( calcium, phosphorus,
aluminum)
 Assist pt with exercise
program
 Rationale
 CRF causes numerous physiologic
changes affecting calcium,
phosphorus and vit D metabolism.
 Hyperphophatemia, hypocalcemia,
and excess aluminum
accumulation are common
 Bone demineraliztion decreases
with immobility.
 Outcomes
 Serum calcium, phosphorus, and
aluminum levels are within
acceptable ranges.
 Has no bone demineralization
 Discuss importance of maintaining
activity level and exercise
program.
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Diet
• Protein restriction b/c urea, uric acid and
organic acids- the breakdown product of
dietary and tissue proteins- accumulate
rapidly in the blood when there is impaired
renal clearance.
• The allowed protein must be of high
biologic value (diary products, eggs,
meats). These proteins are those that are
complete proteins and supply the essential
amino acids necessary for cell growth and
repair; also maintenance of fluid balance,
healing and skin integrity, and maintenance
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• Fluid restrictions: fluid allowance is
usually 500-600 ml more than the
previous day’s 24 hr output.
• Calories are supplied by carbs and fats
to prevent wasting and malnutrition
• Vitamin supplementation because a
protein restricted diet does provide the
necessary amounts of vitamins and the
pt on dialysis may lose water soluble
vitamins from the blood during
treatment.
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Medications for CRF
• Diuretics Furosemide (Lasix) only
given with severe fluid overload
• Increases excretion of water by
interfering with chloride-binding
cotransport system, which, in turn,
inhibits sodium and chloride
reabsorption in the thick ascending
loop of Henle and the distal renal
tubule
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–Adult dose: 20-80 mg PO/IV once;
repeat 6-8h prn or dose may be
increased by 20-40 mg no sooner than
6-8h after previous dose until desired
effect
–Nursing Assessments: Watch for
hypokalemia, assess BP before and
during therapy can cause hypotension
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Medications for CRF continued
• Phosphate-lowering agents
–Calcium acetate (Calphron)
–Combines with dietary phosphorus to
form insoluble calcium phosphate,
which is excreted in feces.
–Adult dose: 1-2 g PO bid-tid with each
meal; increase to bring serum
phosphate value to 6 mg/dL as long as
hypercalcemia does not develop;
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• Calcium carbonate (Caltrate)
• Successfully normalizes phosphate
concentrations
• Neutralizes gastric acidity, increase
serum Ca
- Adult dose: 1-2 g PO divided bid-
tid; with meals as a phosphorous
binder; between meals as a calcium
supplement
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Phosphate-lowering agents
– Calcitriol (Rocaltrol)
• Increases intestinal absorption of calcium for treatment of
hypocalcemia and increases renal tubular resorption of
phosphate
– Adult dose for hypocalcemia during chronic dialysis:
• 0.25 mcg/day or every other day, may require 0.5-1 mcg/day
PO
– Sevelamer (Renagel)
• Indicated for the reduction of serum phosphorous in patients
with ESRD.
– Adult dose: Initial: 800-1600 mg PO tid with meals
Maintenance: Increase or decrease by 400-800 mg per
meal q2wk to maintain serum phosphorous at 6 mg/dL
or less
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Phosphate-lowering agents
– Doxercalciferol (Hectorol)
• To lower parathyroid hormone levels in patients undergoing
chronic kidney dialysis. Increases serum Ca
– Adult dose: 10 mcg PO 3 times/wk at dialysis;
increase dose by 2.5 mcg/8 wk if iPTH is not lowered
by 50% and fails to reach the target range; not to
exceed 20 mcg/3 times/wk
Alternatively, 4 mcg IV 3 times/wk; may adjust dose
by 1-2 mcg/8 wk to maintain iPTH levels
– Nursing Assessment for all phosphate lowering
agents: Monitor BUN, creatinine, chloride,
electrolytes, urine pH, urinary calcium, mg,
phosphate, urinalysis urinary Ca should be 9-10mg/dl,
assess for hypocalcemia: headache, N/V, confusion
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Medications
• Anemia
– Epoetin alfa (Epogen, Procrit)
• Stimulates RBC production
– Adult dose: 50 -150 U/kg IV/SC 3 times per week,
then adjust dose by 25 U/kg/dose to maintain
appropriate Hct; maintenance 12.5-25 U/kg, titrate to
target Hct,
– Nursing Assessment: Monitor renal studies: urinalysis,
protein, blood, BUN, creatinine; I&O. Monitor blood
studies, Hgb, Hct, RBC, WBC, INR, PTT
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Medications
– Darbepoetin (Aranesp)
• Stimulates erythropoiesis
– Adult dose: 0.45 ug/kg IV/SC as a single
injection, titrate not to exceed a target Hgb of
12 g/dl
– Has a longer half-life than epoetin alfa
– Nursing Assessments: Assess blood studies,
renal studies; assess BP, check for rising BP as
Hct rises
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Medications
• Iron Salts
– To treat anemia
– Ferrous sulfate (Feosol, Feratab, Slow FE)
• Replaces iron stores need for RBC development
– Adult dose: 100-200mg tid
– Iron sucrose (Venofer)
• Used to treat iron deficiency dute to chronic hemodialysis
– Adult dose: IV 5ml (100mg of elemental iron) given
during dialysis, most will need 1000mg of elemental
iron over 10 dialysis
• Nursing Assessments: Monitor blood studies,
Hct, Hgb, total Fe, monthly. Assess bowel
elimination for constipation
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Dialysis
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What is Dialysis?
• Dialysis is a type of renal replacement
therapy which is used to provide artificial
replacement for lost kidney function due to
acute or chronic kidney failure
• It is a life support treatment, it does not
cure acute or chronic renal failure
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• Healthy kidneys remove waste products
(potassium, acid, urea) from the blood and
they also remove excess fluid in the form
of urine
• Dialysis has to duplicate both of these
functions
Dialysis – waste removal
Ultrafiltration – fluid removal
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Principle of Dialysis
• Dialysis works on the principle of diffusion
of solutes along a concentration gradient
across a semipermiable membrane
• Blood passes on one side of the
semipermeable membrane, and a dialysis
fluid is passed on the other side
• By altering the composition of the dialysis
fluid, the concentrations of the undesired
solutes (potassium, urea) in the fluid are
low, but the desired solutes (sodium) are at
their natural concentration found in healthy
blood
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2 Main Types of Dialysis
• Hemodialysis
• Peritoneal Dialysis
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Hemodialysis
Adapted from National Institute of Diabetes and Digestive and Kidney Diseases.
National Institute of Diabetes and Digestive and Kidney Diseases. End-stage renal disease: choosing a treatment that's right for
you. Available at: http://www.niddk.nih.gov/health/kidney/pubs/esrd/esrd.htm. Accessed May 10, 2000.
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What is Hemodialysis (HD)?
• Client’s blood is passed through a
system of tubing (dialysis circuit) via
a machine to a semipermeable
membrane (dialyzer) which has the
dialysis fluid running on the other side
• The cleansed blood is then returned
via the circuit back to the body
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• The dialysis process is very efficient
(much higher than in the natural
kidneys), which allows treatments to
take place intermittently (usually 3
times a week), but fairly large
volumes of fluid must be removed in a
single treatment which can be very
demanding on a client
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Side Effects of HD
• The side effects are proportionate to
the amount of fluid being removed
• Decreased blood pressure
• Fatigue, Chest pains, Leg cramps
• Headaches, Electrolyte imbalance
• Nausea and vomiting
• Reaction to the dialyzer
• Air embolism
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Complications of HD
• Infection
The risk of infection depends on the
type of access used
• Bleeding may also occur at the access
site
• Blood clotting was a serious problem
in the past, but the incidence of this
has decreased with the routine use of
anticoagulants (Heparin is the most
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Rare Complication of HD
• On the rare occasion, a client may have a severe
anaphylactic reaction
Sneezing
Wheezing
Back pain
Chest pain
Sudden death
• This can be caused by the sterilant in the dialyzer
or the material in the membrane itself
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Equipment Needed for HD
• The HD machine performs the function of
pumping the patient's blood and the dialysate
through the dialyzer.
• The newest dialysis machines on the market
are highly computerized and continuously
monitor an array of safety-critical parameters,
including blood and dialysate flow rates, blood
pressure, heart rate, conductivity, pH, etc.
• If any reading is out of normal range, an
audible alarm will sound to alert the patient-
care technician who is monitoring the patient.
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Equipment – Water System
• An extensive water purification system is absolutely
critical for HD
• Since dialysis patients are exposed to vast quantities of
water, which is mixed with the acid bath to form the
dialysate, even trace mineral contaminants or bacterial
endotoxins can filter into the patient's blood.
• Because the damaged kidneys are not able to perform
their intended function of removing impurities, ions that
are introduced into the blood stream via water can build
up to hazardous levels, causing numerous symptoms
including death
• For this reason, water used in HD is purified
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Equipment – The Dialyzer
• The dialyzer, or artificial kidney, is the piece of equipment that
actually filters the blood
• The blood is run through a bundle of very thin capillary-like
tubes, and the dialysate is pumped in a chamber bathing the fibers
• The process mimics the physiology of the glomerulus and the rest
of the nephron
• Dialyzers come in many different sizes. A larger dialyzer will
usually translate to an increased membrane area, and an increase
in the amount of undesired solutes removed from the patient's
blood.
• The nephrologist will prescribe the dialyzer to be used depending
on the patient
• Dialyzers are not shared between patients in the practice of reuse.
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Peritoneal Dialysis
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What is Peritoneal Dialysis (PD)?
• Peritoneal dialysis works by using the
body's peritoneal membrane, which is
inside the abdomen, as a semi-
permeable membrane.
• A specially formulated dialysis fluid
is instilled around the membrane,
using an indwelling catheter, then
dialysis can occur, by diffusion
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• Excess fluid can also be removed by
osmosis, by altering the concentration of
glucose in the fluid.
• Dialysis fluid is instilled via a peritoneal
dialysis catheter, which is placed in the
patient's abdomen, running from the
peritoneum out to the surface, near the
navel
• Peritoneal dialysis is typically done in the
patient's home and workplace, but can be
done almost anywhere
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Advantages of PD
• Can be done at home
• Relatively easy for the client to learn
• Easy to travel with, bags of solution are
easy to take on holiday
• Fluid balance is usually easier when the
client is on PD than if the client is on HD
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Disadvantage of PD
• Requires a degree of motivation and
attention to cleanliness while performing
PD
• There are a number of complications
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Complications of PD
• Peritoneal dialysis requires access to the
peritoneum.
• As this access breaks normal skin barriers,
and as people with renal failure generally
have a slightly suppressed immune system,
infection is a relatively common problem
• Long term peritoneal dialysis can cause
changes in the peritoneal membrane,
causing it to no longer act as a dialysis
membrane as well as it used to.
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• This loss of function can manifest as a loss
of dialysis adequacy, or poorer fluid
exchange (also known as ultra filtration
failure)
• Fluid may leak into surrounding soft tissue,
often the scrotum in males
• Hernias are another problem that can occur
due to the abdominal fluid load
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Nursing Assessments
• Before client is in the unit, look at the nurses
notes from the treatment before
Any problems, will help nurse plan for the
upcoming treatment
• Look at the client
Strength
Gait
Whether client needs assistance
Color
Puffiness
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• Could be caused by excess fluid, too
much to drink, more fluid should be
taken off with each treatment, changes
in voiding pattern (are they voiding
less than they did last month)
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Assessments Con’t
• Shortness of breath
 Could indicate fluid around the lungs
 Ask about SOB at night (does client have to sleep in a sitting
position?)
• Ask the client how they are feeling
 The client is usually the best source of information
 Clients are in 3 times a week, dialysis nurses really get to know their
clients
• Evaluate access
 Bruising, swollen, tender
 Bruit – listen with the stethoscope for a swishing sound of the blood,
listen all the way up the arm
 Thrill – felt with the fingers, tells the nurse if the blood is flowing in
the fistula (client’s are told to feel for this at home when a fistula is
first initiated)
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Nursing Interventions
• If client comes in with shortness of breath, offer
O2 which can be kept on for the full treatment if
necessary
• Comfort
Client’s are sitting in the same chair for up to four
hours
Offer extra pillows, some clients have special back
pillow they leave in the unit
Ensure TV and audio is working properly
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Nursing Interventions Con’t
• If the blood pressure is dropping too
quickly:
Slow or stop fluid removal for a time
period
The machines are constantly being
adjusted throughout the course of the
treatment depending on the BP
If the BP drops suddenly 200-300cc of
normal saline can be given to balance
fluid levels
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• Usually, more fluid will be taken off
at the beginning of the treatment, this
will allow the client to feel better at
the end
• If the client is elderly, fluid removal
starts slowly to ease them into the
treatment
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Responsibilities of Nursing Staff
Prior to Dialysis
• Ensure client is ready to sit for up to four hours
Encourage client to use washroom before
arriving to the unit
Try to avoid laxatives if possible before
treatment
• Ensure client has eaten meal prior to treatment
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Responsibilities of Nursing Staff
After Dialysis
• A dialysis nurse will a verbal report of treatment
Any complications during treatment
Check BP standing and sitting
Assess access site
• Encourage client to rest
Avoid treatments or physio for a couple of
hours if possible
• Watch fluid intake
Be aware if client is on fluid restriction
• Check thrill and bruit
• Do not take a BP on access arm
• Do not take blood from access arm
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Questions?
Thank you for listening.
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