Transcript Case Study

Renal System
Case Scenario
Case Study
Tia Smith is a 26 year old female patient who is 10 hours post-partum
following an emergency C-section for twins. She was 33.5 weeks
pregnant and had a difficult pregnancy with PIH (pregnancy induced
hypertension) and frequent urinary tract infections. On admission Tia
was diagnosed with HELLP syndrome (hemolysis, elevated liver
enzymes, low platelets) which necessitated immediate delivery of her
babies. During the C-section Tia became hypovolemic resulting from
massive hemorrhaging and required blood products and fluid
replacements. Tia eventually developed hypovolemic shock and
remained unstable for 2 hours. For the past nursing shift Tia has been
hypotensive with blood pressures ranging from 59/37 to 95/52. Tia’s
urinary output has been 2-12cc/hr of brown cloudy foul smelling
urine. During your morning assessment you discover the following:
Case cont’d








VS: T: 37.4
P: 125bpm
R: 33
BP: 96/62
Respiratory: Chest is clear fine crackles heard throughout all lung
fields, there is diminished A/E at the bottom of the R & L lobes
CV: S1, S2 audible with pericardial friction, bounding rapid pulse
Mental Status: drowsy and with assistance will orient slowly to PPT,
pt c/o persistent hiccups
Neurovascular: edema, skin cool & pale, bruises observed
throughout extremities, skin turgor poor, bilateral decreased sensation
in feet
GI: pt c/o N&V
Genitourinary: pt has foley catheter draining brown cloudy foul
smelling urine at 2-12cc/hr
Psychosocial: pt very emotional and crying at times because she
cannot be with her newborn babies and is unable to breastfeed, she is
concerned for their health, and does not understand how this
happened to her
So… What is Tia’s diagnosis?
Acute Renal
Failure
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

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

Incidence of ARF
2-5% of all hospitalized patients
 10-20% are critically ill
 Mortality Rate- 25% increases to 75% if
complicated by other life
threatening conditions

Anatomy of the Kidney
Composition of the Renal System
Figure 26.4 The Structure of the Kidney
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 26.4a, b
Vascular Structure of the Nephron

Renal artery  Segmental artery  Lobar artery 
Interlobar arteries  Arcuate arteries  Small
interlobular arteries  Smaller afferent arteries 
Capillary bed (Glomerulous)  Efferent arteriole 
Peritubular capillaries  Interlobular vein  Arcuate
vein  Renal vein
Nephron
http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html
Figure 26.6 A Representative Nephron
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 26.6
Renal Corpuscle
Initial filtering component of the
nephron.
 Consists of glomerulus (small network
of capillaries enclosed in a Bowman’s
capsule).
 Fluids from blood in the glomerulus is
collected in the Bowman’s capsule to
form ‘glomerulus filtrate.
 This is then further processed along the
nephron to form urine.

Renal Corpuscle
Glomerular Capsule
Not everything can pass through
 What fits through?

Na+, K+, Ca2+, Mg2+, Cl-, S04-, P042 Hc03 and H+
 Nutrients such as monomers
 Wastes (nitrogenous wastes)
 Small hormones
 WATER!!!

Glomerular Capsule
What doesn’t fit through??
 Cells
 Plasma proteins

Glomerular Filtration Rate
(GFR)
The speed with which we pass our blood
through our kidneys and filter it is
proportional to how well we can clean our
blood.
 Speed of filtration is the GFR
 In one minute both kidneys using all their
nephrons can filter 125ml/min=180
liters/day!!
 We have on average 5 liters of blood in our
bodies

Glomerular Filtration Rate
Amount of filtration changes with blood
pressure
 Built in regulatory system

Glomerular Filtration Rate
Pressures
Out of the Blood (into the capsule)
• Blood Pressure=60mm Hg
Into the Blood (Out of the Capsule)
• Osmotic Pressure=32mm Hg
• Capsular hydrostatic pressure=18mm
Hg
Glomerular Filtration Rate

Net pressure on fluids within the renal
corpuscle.

60 mm Hg- (32 mm Hg + 18 mm Hg)= 10 mm Hg

Therefore, in the renal corpuscle, the net
force on fluids is OUT of the blood (into
the capsule) and this is called the
filtration pressure
Specialized Cells of the
Proximal Convoluted Tubule
• Brush boarder cells
• Large surface area allowing for reabsorption of the
filtrate into the blood stream
Key Feature: Highly permeable to water & many
solutes
Specialized Cells of the
Descending Loop of Henle
•Simple squamous epithelial cells that lack
brush boarders
•Small surface area resulting in a decrease in
the amount of filtrate reabsorbed into the blood
stream
Key feature: Highly permeable to water but not
solutes
Ascending Loop of Henle

Similar to those of the PCT except fewer
microvilli
Key feature: Highly permeable to solutes
(particularly sodium chloride), not permeable
to water
Juxtaglomerular
Apparatus
Endocrine structure that secretes the hormones
erythropoietin and renin
Key Feature: Renin triggers angiotensin to turn into
angiotensin I which turns to angiotensin II which
constricts the walls of arteries to increase BP
Erythopoietin stimulates the production of RBC when
kidneys are exposed to low O2 concentrations

Renin-Angiotensin System
Specialized Cells of the Late
Distal Convoluted Tubule
Cuboidal cells that fall into two distinct
regions, principle cells and intercalated
cells
 Key feature (principle cells): Permeable
to water & solutes and regulated by
hormones
 Key feature (intercalated cells):
Involved in the secretion of H ions for
acid/base balance

Specialized Cells of the
Medullary Collecting Duct
Cuboidal cells
 Key feature: Hormonally
regulated permeability to
water and urea

Normal Kidney Function
Summary
Maintain Homeostasis
 How does it do this….

10 Functions of the Kidney’s



Urine Formation: Formed in the nephrons through
a complex three-step process: GF, tubular
reabsorption, and tubular secretion
Excretion of waste products: eliminates the
body’s metabolic waste products (urea, creatinine,
phosphates, sulfates)
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
Kidney Function con’td

Regulation of acid-base balance:
elimination of sulphuric and phosphoric acid
Kidney function cont’d

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
(#particles dissolved/kg urine (glucose & proteins are
osmotically active agents)
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.
Still talking about kidney
function…



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
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)
Kidney function cont’d


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 (PGE & PGI). They
have a vasodilatory effect
Timeline of Events
PIH
HELLP
EMERGEN
CY CSECTION
HYPOVOLE
MIC SHOCK
HEMORRHAGE
HYPOVOLEMIA
ACUTE RENAL FAILURE
HELLP SYNDROME



A syndrome featuring a combination of "H" for hemolysis
(breakage of red blood cells), "EL" for elevated liver enzymes,
and "LP" for low platelet count (an essential blood clotting
element).
PREGNANCY COMPLICATION - occurring in 25% of
pregnancies with toxemia or pre-eclampsia.
Symptoms include






Shortness of breath
H/A
Dimmed vision
Nausea
Dizziness & Fainting
Edema
Pain in the upper abdomen
Effects of HELLP on Mom & Baby

Mothers with HELLP are at increased
risk for:




Liver rupture, DIC, abruptio placentae, and acute
renal failure, stroke, seizure, ARD, pulmonary
edema
1st order of tx is management of blood clotting
issues
Women with a hx of HELLP are considered at risk
for future pregnancies
After delivery, mothers vitals are CLOSELY
monitored to observe for complications
NURSING PROCESS
Acute Renal Failure
Definition:
“Acute Renal Failure is an abrupt
reduction in renal function.”
Acute Renal Failure

Three Stages to Renal Failure
1) Prerenal acute renal failure
 2) Intrarenal acute renal failure
 3) Postrenal acute renal failure

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)
Acute Renal Failure: Classification
Prerenal Acute Renal Failure
60-70% of patients with Acute Renal Failure
are Prerenal.
 GFR declines because of the decrease in
filtration pressure.
 Poor perfusion results from renal
vasoconstriction, hypotension, hypovolemia
 Failure to restore blood volume or blood
pressure may cause acute tubular necrosis or
acute cortical necrosis.

Prerenal acute renal failure
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
respond as if volume depletion has occurred.

Prerenal ARF

Causes include:

Secondary to renal hypoperfusion which occurs in setting of
extracellular fluid loss





Impaired/inadequate cardiac output
Drugs





Diarrhea
Vomiting
Diuretics
NSAIDs
ACE Inhibitors
Hypovolemia
Hemorrhage
Renal vasoconstriction
Intrarenal ARF
May result from: Acute tubular necrosis
(ATN), cortical necrosis, acute
glomerulonephritis, drug allergy, .
 ATN caused by ischemia occurs most
commonly after surgery (40%-50%)
 ATN also caused by sepsis, severe
burns, or trauma
 Can be caused by antibiotics

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
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
Glomerulonephritis


uncommon cause, most associated with CRF
Caused by:


Can be a primary disorder or can occur secondary to systemic
disease
Systemic lupus erythematosus
Intrinsic ARF

Vascular Disease


Can occur on microvascular and macrovascular
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

Acute Interstitial Nephritis


Interstitial disturbance that leads to ARF
Caused by:

Allergic reaction to drugs
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

Postrenal ARF

Causes include:
Bladder tract
obstruction
 Prostatic hypertrophy
 Catheters
 Neurogenic bladder


Postrenal causes are typically reversible
Clinical Manifestations of ARF

Cardiovascular






Respiratory





Dyspnea
Crackles
Tachypnea
Kussmaul’s respirations




Lethargy
Tremors
Memory loss
Confusion
Musculoskeletal


Muscle spasms
Weakness
Genitourinary


Mental Status


Arrhythmias
BP, N, high or low
Anemia
P, rapid, bounding, or N
Pericardial-type chest pain


GI




Oliguria
Anuria
abN urine colour, clarity, smell
Moist tongue & increased saliva
Dry tongue & mucous membranes
N&V
Integumentary





Moist, warm skin & pitting edema
Decreased skin turgor
bruises
Pallor
Thin, brittle hair & nails
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
display LOC normal for patient
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
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
Nursing Care Plan

Interventions

Monitor & document
electrolyte levels q8-12h,
especially:




Rationales

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


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
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
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.
Diagnostic
Testing
Measuring kidney
function
Diagnostic Tools
Urinalysis
 Blood Work
 X-ray
 Urogram (intravenious pyelogram)
 Ultrasound
 Doppler
 Scopes
 Biopsies

The Urinalysis
Also called a routine UA (urinalysis)- gross and microscopic
examination of urine to determine pH, gravity and
substance
Gross Assessment- appearance and odor of the urine
Microscopic Assessment- bacteria, RBC, WBC, crystals, casts.
Normal Findings of Urinalysis:
pH- 4.5-8.0
Gravity-1.001 to 1.030
Protein- Negative
RBC/WBC- Negative
Glucose- Negative
Ketones- Negative
Nitrates- Negative
The Urinalysis

Normal


inorganic material such as NA+, Cl-, Mg+, SO4-, PO4-, and
NH4+ and organic materials such as urea, creatinine, and uric
acid in the urine.
Abnormal

RBCs, WBCs, bacteria protein, glucose, ketones

Urinalysis involves evaluation of color, turbidity, protein,
pH, specific gravity, sediment

Presence of bacteria, RBCs, WBCs, casts or crystals in
the urine sediment may indicate a renal disorder.
Assessing Urine
The first morning void is considered
ideal as it has the greatest
concentration and lowest pH
(maximizing the ability to detect formed
elements).
 A regular void (with appropriate
washing of the genitals) is usually
satisfactory.
 A midstream or catheterized specimen
is more appropriate for culture and
bacteria count.

Assessing Blood
Why assess the blood?
 Electrolyte balance
 Acid-base homeostasis
 Regulates serum concentrations of BUN
and Creatinine
 Produce erythropoietin

BUN, creatinine, creatinine clearance
presentation by students
Normal Blood and Serum Lab Values
Sodium
Potassium
Chloride
BUN
Creatinine
135- 145 mEq/L
3.5- 5.3 mEq/L
98- 106 mEq/L
10- 20mg/dL
60-110 umol/L (Female)
70-120 umol/L (Male)
Phosphorus 0.8- 1.4 mmol/L
Calcium
2.0- 2.6 mmol/L
Magnesium
1.6- 2.6 mg/dL
Hemoglobin 120-140g/L (Female)
140-160g/L (Male)
Lab Tests for Renal Function:
Blood Tests

Blood Urea Nitrogen



Measures the concentration
of urea in the blood
Urea is formed from protein
metabolism and is elevated
when glomerular filtration is
reduced
BUN rises in states of
dehydration and acute
chronic renal failure because
passage through tubules is
slowed

Serum Creatinine Level


Should be a stable value
When creatinine levels rise
and accumulate in the
plasma:
 Double  renal function is
about half of Normal
 Tripled  ~ 75% of RF is
lost
Represents a decrease in GRF
Estimating GFR and Creatinine Clearance
GFR- Filtration rate/min at the glomerulus.
170 x Serum Creatinine concentration^-0.999
X age^-0.176
X 0.762 (if female)
X 1.18 (if race is African)
X blood urea nitrogen concentration^-0.17
X serum albumin concentration^-0.318
= GRF in Adults
Creatinine Clearance- The clearance rate in mL/min of the
waste product creatinine.
0.55 x Length/ Serum Creatinine
INTERVENTION
Medications for ARF
Pharmacologic treatment of ARF has been
attempted on an empirical basis, with varying
success rates. Several promising experimental
therapies in animal models are awaiting
human trials
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.
Medications for ARF continued
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
Medications for ARF continued
Diuretics
Furosemide
(Lasix) only given with severe
fluid overload
Increases
excretion of water by interfering with chloridebinding cotransport system, which, in turn, inhibits sodium
and chloride reabsorption in the thick ascending loop of
Henle and the distal renal tubule
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
Medications for ARF continued

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.
Adult dose: 2-5 mcg/kg/min
Nursing Assessments: Monitor BP during
administration, stop infusion if BP drops 30mm
Hg, Monitor I&O
Medications for ARF continued

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
Nursing assessments: Assess resp. and pulse rate,
rhythm, depth, lung sounds, monitor I&O,
electrolytes, blood pH, PO2, HCO3, monitor urine
pH, and UO during beginning of treatment,
monitor for alkalosis, monitor ABGs and blood
studies
13 have passed and now Tia is
diagnosed with…
Chronic Renal Failure

13 years have passed  Tia is now 39 years of age
and has been experiencing declining renal function
over the past 13 years. Tia has lost 15lbs on her
already small frame, she feels generally ill most of
the time with frequent N&V, she suffers from fatigue,
muscle twitching & cramps decreased sensation in
her hands and feet and generalized puritus. The
Physician has diagnosed Tia with ESRD and has
determined that long term dialysis will be required.
Chronic Renal Failure
ESRF
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
(GFR) of <60 mL/min/1.73 m2 for 3 or more
months

Alterations-Acute Renal Failure
Renal Impairment
50% of Normal
Renal Insufficiency
25% of Normal
Renal Failure
< 20% of renal fcn remains
End stage renal
disease (ESRD)
< 10% of renal fcn remains
GFR- 50mL/Min
Serum Creatinine: less than 2 mg/dL
BUN: High normal
GFR 25-40mL/min
Serum Creatinine: 1.5-3.0 mg/dL
(mildly elevated)
BUN: Mild azotemia
GFR < 25mL/min
Serum Creatinine: > than 3.0 mg/dL
Electrolyte imbalances
GFR < 10 mL/min
Creatinine and BUN: marked increase
Electrolyte imbalances
Acidosis
Statistics

In the U.S. The US Renal Data System (USRDS)

Internationally: The incidence rates of end-
has shown a dramatic increase in patients with CRF
who require chronic dialysis or transplantation. In
1999, there were 340,000 such patients, but, by
2010, this number is projected to reach 651,000.
stage renal disease (ESRD) have increased steadily
internationally since 1989. The United States has the
highest incident rate of ESRD, followed by Japan.
Japan has the highest prevalence per million
population, with the United States taking second
place.
Statistics Cont’d

Mortality /Morbidity:

Race:
CRF is a major cause of
morbidity and mortality, particularly at the later
stages. The 5-year survival rate for a patient
undergoing chronic dialysis is approximately 35%.
This is approximately 25% in patients with diabetes.
The most common cause of death in the dialysis
population is cardiovascular disease.
Affects all races
Chronic Renal Failure
“Slow, progressive, (months to years) irreversible loss of renal
function.”
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 effects
every system in the body.
The greater the buildup of waste products, the more severe the
symptoms.
Approximately 1 million nephrons are present in each kidney,
each contributing to the total GFR. Regardless of the etiology of
renal injury, with progressive destruction of nephrons, the
kidney has an innate ability to maintain GFR by hyperfiltration
and compensatory hypertrophy of the remaining healthy
nephrons.
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 GFR has decreased to 50%, when the renal
reserve has been exhausted. The plasma creatinine value will
double with a 50% reduction in GFR.
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
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
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. ESRD is evidenced by elevated
creatinine and BUN levels as well as
electrolyte imbalances.
 Dialysis is usually indicated at this point.

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.
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.

Glomerulonephritis is the
inflammation and damage of
the filtration system of the
kidney and can cause kidney
failure.
Postinfectious conditions and
Lupus are among the many
causes of glomerulonephritis.
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.

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
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).

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.
Clinical Manifestations
Extracellular volume expansion and totalbody 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).
 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.

Signs and Symptoms


Neurologic
weakness, fatigue,
confusion, disorientation,
tremors, seizures,
restlessness of legs, burning
of soles of feet, behavioral
changes.
Integumentary
Gray-bronze skin colour, dry,
flaky skin, pruritus,
ecchymosis, thin brittle nails,
coarse, thinning hair

Pulmonary
Crackles, thick tenacious
sputum, depressed cough
reflex, pleuritic pain,
shortness of breath,
engorged neck veins,
tachypnea, uremic
pneumonitis, “uremic lung”

Gastrointestinal

Hematologic

Musculoskeletal
Ammonia odour to breath,
metallic taste, mouth
ulcerations and bleeding,
anorexia, N&V, hiccups,
constipation or diarrhea,
bleeding from GI tract.
Anemia, thrombocytopenia
Muscle cramps, loss of muscle
strength, renal
osteodystrophy, bone pain,
bone fractures, foot drop
Nursing Care Plan
Excess fluid volume r/t
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.
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







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
effusion: paradoxical pulse (>
10 mm drop in BP during
inspiration) and signs of shock
d/t compression of the heart by
a large 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





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









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.




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.
Diet





Protein restriction b/c urea, uric acid and organic acidsthe breakdown product of dietary and tissue proteinsaccumulate 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
of immune function.
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.
Nursing Diagnoses

Altered fluid volume (excess) related to
compromised regulatory mechanism
(renal failure) with retention of water as
evidenced by intake greater then output
(oliguria)
Nursing Diagnoses
Risk for Altered cardiac output: decrease
related to fluid overload
Assessments:
-Monitor BP & HR
-Assess color of skin, mucous
membranes and nail beds
-Note occurrence of slow pulse, hypotension,
flushing, nausea/vomiting and depressed
level of consciousness
-Maintain bed rest
Assessments continued

Monitor lab results

Potassium, Calcium, magnesium,
phosphate
Nursing Diagnosis

Altered nutrition: less than body
requirements related to ulcerations of
oral mucousa

Patient Outcomes:

Maintains/regains weight
Altered nutrition continued

Assessments/Interventions
Document dietary intake
 Provide frequent, small feedings
 Offer frequent mouth care if possible with
dilute (25%) acetic acid solution.
 Consult with dietician/nutritional support
team
 Restrict K, Na, and phosphorus intake as
indicated

Nursing Diagnosis

This one is for the family

Potential knowledge deficit related to
unfamiliarity with information resources
as evidenced by questions/request for
information
Knowledge Deficit continued
Review disease process, prognosis, and
precipitating factors
 Discuss dietary plan/restrictions.

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
Adult dose: 20-80 mg PO/IV once; repeat
6-8h prn or dose may be increased by 2040 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

Medications for CRF continued

Phosphate-lowering agents

Calcium acetate (Calphron, PhosLo)



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;
Calcium carbonate (Caltrate, Apo-Cal, Tums)



Combines with dietary phosphorus to form insoluble calcium
phosphate, which is excreted in feces.
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
Phosphate-lowering
agents

Calcitriol (Rocaltrol, Calcijex)


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)


Increases intestinal absorption of calcium for treatment of
hypocalcemia and increases renal tubular resorption of
phosphate
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
Phosphate-lowering
agents

Lanthanum carbonate
(Fosrenal)


for reduction of high
phosphorus levels in
patients with ESRD
Adult dose: Initial: 250-500
mg PO tid pc (chewable
tabs); adjust dose q2-3wk
to target serum
phosphorus level
Maintenance: 500-1000 mg
PO tid pc
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 910mg/dl, assess for hypocalcemia: headache,
N/V, confusion
Medications for CRF continued

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
Medications for CRF continued

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

Medications for CRF continued

Iron Salts


To treat anemia
Ferrous sulfate (Feosol, Feratab, Slow FE)



Adult dose: 100-200mg tid
Iron sucrose (Venofer)



Replaces iron stores need for RBC development
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

Tia’s kidney function continues to
decline and she is forced to begin
dialysis
Dialysis
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
May be used for very sick clients who have suddenly lost kidney
function
May be used for stable clients who have permanently lost
kidney function
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
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

Prescription for Dialysis
A prescription for dialysis is given by a
physician who specializes in the kidney
(nephrologist)
 The MD will set various parameters for
the treatment

Time and duration of the dialysis sessions
 Size of the dialyzer
 Rate of blood flow

Types of Dialysis
1. Hemodialysis
2. Peritoneal Dialysis
Hemodialysis
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
 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

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
 N&V
 Reaction to the dialyzer
 Air embolism

Complications of HD

Because HD requires access to the circulatory
system, clients have a portal of entry for microbes,
which could lead to 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 common)

Anticoagulants also come with their own risk of side effects
and complications
Rare Complication of HD

On the rare occasion, a client may have a
severe anaphylactic reaction







Sneezing
Wheezing
SOB
Back pain
Chest pain
Sudden death
This can be caused by the sterilant in the
dialyzer or the material in the membrane
itself
Hemodialysis ~ The
“Integra”
Three Types of Access for HD
IV catheter
Arteriovenous (AV) fistula
Synthetic graft
The type of access is influenced by factors
such as expected time course of the clients
renal failure and the condition of the clients
vasculature
 Some clients may have multiple accesses,
usually because an AV fistula or a graft is
maturing and an IV catheter is still being
used




IV Catheter
(Central Venous Catheter)


Consists of a plastic catheter with two lumens which is inserted
into a large vein (vena cava via the internal jugular vein) to
allow large flows of blood to be withdrawn from the first lumen
The blood goes into the dialysis circuit, and is returned to the
body via the second lumen



This type of access is used for clients who need rapid access for
immediate dialysis




Non-tunneled
Tunneled
Clients who are likely to recover from ARF
Client with end-stage renal failure
Clients waiting for other sites to mature
This type of access is very popular for clients because it doesn’t
involve needles for each treatment
Complications of an IV
Catheter

Venous Stenosis
This is the abnormal narrowing of the
blood vessel
 Because the catheter is a foreign body in
the vessel, it often provokes an
inflammatory reaction in the vein wall
 This results in scarring and narrowing of
the vein, often to the point where the vein
occludes

AV Fistula



This access is recognized as the preferred access
method
To create a fistula a vascular surgeon joins an artery
and a vein together
Since this bypasses the capillaries, blood flows at a
very high rate through the fistula





This can be felt by placing a finger over a mature fistula
(thrill)
Usually created in the non-dominant hand
It can be situated on the hand, forearm or the elbow
It will take approximately 4-6 weeks to mature
During treatment, 2 needles are inserted, one to
draw blood out of the body and the other to return
blood to the body
Advantages of an AV Fistula
Decreased infection rate
 Increased blood flow rates, therefore a
more effective dialysis treatment
 Decreased incidence of thrombosis

Complications of an AV Fistula

If an AV fistula has a very high flow rate and the
vasculature that supplies the rest of the limb is poor,
than a ‘steal syndrome’ can occur



Blood that enters the limb is drawn into the fistula and
returned to the general circulation without entering the
capillaries of the limb
This results in cool extremities of the limb, cramping pains
and possible tissue damage
Long term complications can be the development of a
bulging in the wall of the vein (aneurysm)


The vessel wall is weakened by the repeated insertion of
needles over time
Can be reduced by careful needling technique
Hemodialysis ~ fistula
AV Graft
This is much like a fistula, except an
artificial vessel is used to join the artery
and the vein
 Grafts are used when client’s own
vasculature does not permit a fistula
 An AV graft will mature much faster
than an AV fistula, and it could be ready
to use within days after formation

Hemodialysis ~ Graft
Complications of an AV Graft

AV grafts are at high risk for narrowing
where the graft is sewn to the vein


As a result clotting or thrombosis may
occur
As a foreign material is being placed in
the body, there is a greater risk of
infection
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 patientcare technician who is monitoring the patient.

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
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.

Temporary Hemodialysis Catheter
Exit site at
surface of the
skin
Inserted in
the jugular
vein
Tip located at
junction of
SVC and right
Atrium
Tunneled Hemodialysis Catheter
Dacron cuff
Catheter tunnel
Exit site
Inserted in
the jugular
vein
Tip located at
junction of
SVC and right
Atrium
Peritoneal Dialysis
Peritoneal Dialysis
Peritoneal Dialysis
Catheter
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
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
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

Disadvantage of PD
Requires a degree of motivation and
attention to cleanliness while
performing PD
 There are a number of complications

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.
This loss of function can manifest as a loss of dialysis
adequacy, or poorer fluid exchange (also known as
ultrafiltration 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
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

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)
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)

Assessments During
Treatment





Ask client how he/she feels
 Dizziness, diaphoretic,
The machines automatically take BP and HR every 30
minutes
 Can program the machines to take it at whatever
interval is necessary (every min, 10 min, 15 min)
Try to recognize a problem before it starts (ex.
Hypovolemic shock)
Assess access site
 Watch trend of BP
 It usually gradually decreases throughout the course of
the treatment, but look for sudden or drastic drops
Assess access site
 Bleeding, swelling, tenderness
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
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
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
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
Responsibilities of Nursing Staff
After Dialysis

A dialysis nurse will give unit leader or primary nurse
a verbal report of treatment




Encourage client to rest




Avoid treatments or physio for a couple of hours if possible
Watch fluid intake


Any complications during treatment
Check BP standing and sitting
Assess access site
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
Does everyone understand
how important we are?
Kidneys
Urine