The document discusses pyelonephritis, which is an inflammation of the renal pelvis and parenchyma caused by a bacterial infection. It can be caused by an ascending or hematogenous infection. Symptoms include flank pain, fever, vomiting and frequent urination. Diagnosis involves urine culture and sensitivity as well as imaging tests. Treatment aims to eliminate pathogenic organisms with antibiotics based on culture results and remove any contributing factors to decreased resistance. Mild cases may only require a short course of oral antibiotics while severe cases involving abscesses may require IV antibiotics or even drainage of abscesses.

1. PRESENTED BY : HARPREET KAUR
M.Sc 1st year

3. 1. Regulation of the volume of blood by
excretion or conservation of water.
2. Regulation of the electrolyte content of the blood
by the excretion or conservation of minerals.
3. Regulation of the acid-base balance of the blood
by excretion or conservation of ions
4. Regulation of all of the above in tissue fluid.

4. 1. Kidneys
2. Ureter
3. Bladder
4. Urethra

5. Kidneys
- is to separate urea, mineral salts, toxins
and other waste products from the blood.
- filtering out wastes to be excreted in the urine.
- regulating BP
- regulating an acid-base balance
- stimulating RBC production

6. Ureters
- transports urine from the renal pelvis of the
kidney to which it is attracted, to the bladder.
- pass beneath the urinary bladder, which results
in the bladder compressing the ureters and
hence preventing back-flow of urine when
pressure in the bladder is high during urination.

7. Bladder
- store urine
- expels urine into the urethra (Micturation)
Micturation – involves both voluntary and
involutary muscles.

8. Urethra
- is the passageway through which urine is
discharged from the body

9. Main difference between the urinary system of male
and female is the
“ length of urethra.”

10. 1. Nephrons – functional unit of kidney.
Each kidney is formed of about one
million nephrons.
2. Glomerulus – filters the blood
3. Bowman’s Capsule – is a large double
walled cup. It lies in the renal cortex
4. Tubular Component – necessary
substances are being reabsorbed

11. 1. Loop of Henle – create a concentration gradient
in the medulla of the kidney.
- reabsorb water and important nutrients in the filtrate.
2. Renal Vein – a blood vessel that carries
deoxygenated blood out of the kidneys
3. Renal Artery – supply clean, oxygen-rich blood to
the kidneys
4. Adrenal Gland (Suprarenal Gland) – located on top of
the kidneys and is essential for balancing salt and water
in the body

12. Beginning of the process.
• A process by which the blood courses
through the glomeruli, much of its fluid,
containg both useful chemicals and dissolve
waste materials, soaks out the blood
through membranes where it is filtered and
then flows into Bowman’s capsule.

13. Tubular Reabsorption
• A movement of substances out of the renal
tubules back into the blood capillaries located
around the tubules (peritubular capillaries).

14. • disposing of substances not already in the
filtrate (drugs)
• eliminating undesirable substances that have
been reabsorbed by passive processes (urea
and uric acid)
• ridding the body of excess potassium ions
• controlling pH

15.  is the amount of fluid filtered from the blood into
the capsule each minute. Factors governing the
filtration rate at the capillary beds are:
1.total surface area available for filtration
2.filtration membrane permeability
3.net filtration pressure

16. Kidneys
Arteries and
Veins
Urinary Tract
(ureter)
Urinary
Bladder

17. Hilus
Lobules

18. Nephron
tubule
Kidney
Nephron

19. Renal artery
Hilus
Segmental
arteries
Lobular
arteries

22. Tubular reabsorption
Tubular secretion
Water conservation

23. Urinary Tract
(ureter)
Urinary
Bladder
Urethra

24. • Kidneys performed as the body’s main Excretory
function by filtering the blood and selectively
reabsorbed those materials that are needed to
maintain a stable internal environment.
• Nephrons is the functional unit of the kidneys.
It is composed by a glomerulus which filters the blood
and the tubular component where necessary
substances are reabsorbed into the the blood stream
and the unneeded materials are secreted into the
tubular filtrate for elimination and urine.

25. RENAL DISORDERS

27.  Definition
 Types and description
 Etiology
 Pathophysiology
 Clinical manifestations
 Diagnostic
 Medical management
 Nursing management
 Surgical management
 Nursing management of surgical client

28. Urinary incontinence has been defined by the
international continence society (ICS) as “a condition
in which involuntary loss of urine is a social or
hygienic problem and is objectively demonstrable”.

31.  Stress incontinence
 Urge incontinence
 Overflow incontinence
 Reflex incontinence
 Functional incontinence
 Others
 after trauma and surgery
 Due to prostrate cancer

32.  Urinary incontinence commonly result from many
factors including anatomic defects, physical,
physiological, psychosocial and pharmacological
 Anatomic and physiologic incontinence results
from sphincter weakness or damage, urethral
deformity, altered muscle tone at the
urethrovesical junction (Q-tip test) and detrusor
instability
- Q-tip test is for the urethral hyper mobility of the
urethrovesical junction

33.  Stress incontinence
- Found most commonly in women with relaxed
pelvic floor muscles (from delivery, use of
instrumentation during vaginal delivery or
multiple pregnancies).
- Female urethra atrophy when estrogen
decreases after menopause.
- Prostate surgery for BPH or prostate cancer.
- Repeated straining, urogenital prolapsed and
congenital weakness.

34. - Surgical interventions may cause bladder
neck damage, with possible permanent
incontinence.
- Hypermobile urethrovesical junction.

35. Stress incontinence
Etiology (cough, sneezing, pelvic floor muscle weakness)
Vesical pressure increases
Increased descent
Involuntary urine loss

36.  Major manifestation of urinary incontinence is
involuntarily loss of urine in all types.
1. Stress incontinence
- Leakage in small amounts
- May not be daily

37. - Condition is caused by uncontrolled contraction or
overactivity of detrusor muscle.
- Bladder escapes central inhibition and contracts
reflexively.
- Condition includes CNS disorder (e.g. cerebrovascular
disease , Alzheimer's disease , brain tumor, parkinson’s
disease)
- Bladder disorders (e.g. carcinoma in situ , radiation effect,
cystitis)
- Interference with spinal inhibitory pathways (malignant
growth in spinal cord, spondylosis and the bladder outlet
obstruction)

38. Urge incontinence
Motor disorder
Uninhibited detrusor contraction
Involuntary loss of urine

39. Urinary urgency
Urinary frequency
Periodic leakage in large amount
Nocturnal frequency

40. - Spinal cord lesions above S2 .
- Detrusor hyperreflexia and interference
with pathways coordinating detrusor
contraction and sphincter relaxation.

41. Reflex incontinence
If lesion of spinal cord above S2
Abnormal detrusor contraction
Sphincter relaxation
Involuntarily urine loss

42. - No warning or stress before involuntarily urination
- frequent, moderate volume
- equally during day and night

43. - Elderly often have problem that affect
balance and mobility, there are also some
physical causes

44. Cognitive defect
Functional defect

45. Vesicovaginal or vesicouretheral reflux
Altered continence control

46. - Disorder is caused by bladder or urethral outlet
obstruction ,( or caused by bladder neck
obstruction , urethral stricture ,pelvic organ
prolapse)
- After surgery such as hemorrhoidectomy,
herniorrhaphy, cystoscopy.
- Neurogenic bladder.
- Drugs can also contribute to incontinence,
specially overflow incontinence, examples are :-
opioidus, tranquilizers, sedatives and hypnotic
agents, alcohols, rapid acting diuretics,
antihistamines, atropine, hypotensive agents,
ganglionic blockers

47. Overflow incontinence
If obstruction in bladder outlet
Over distention
Bladder remains full
Urethra constricts
Completed void is not there (urinary retention)
but due to overflow urine leaks involuntarily (but not completely due to
distention and constriction of urethra)

48. OVERFLOW INCONTINENCE
- Feeling of fullness in bladder
- No sphincter control
- Frequent leakage in small amounts
- Palpable and distended bladder
- feeling of incomplete voiding (as in urinary
retention)

49. - Fistula may occur during pregnancy, after
delivery of baby , as a result of
hysterectomy, or invasive cancer of cervix,
or after radiation therapy.
- Incontinence is found as post operative
complication after transurethral, perineal or
retropubic prostatectomy.

50.  Urodynamic examination
- cystometrography
- electromyographic
- urine flow rate (help to identify hypotonic
detrusor or an obstructional or dysfunctional
voiding mechanism)
- Urethral pressure profile (to detect pressure in
urethra in stress incontinence)
- Ultrasonography and catheterization (can detect
the elevated residual urine level)

51. - cystoscopy (for tumors, foreign bodies such a
stones) or structural abnormalities in the bladder
and urethra.
- Q-tip test.
- an excellent diagnostic tool, the bladder diary,
reveals voiding frequency, fluid intake, pattern of
urinary urgency and no. of severity of incontinent
episodes. A seven day diary reveals pattern of
incontinence and may be helpful before a
diagnostic evaluation.

52.  Electrical stimulation
 Medications
#Anticholenergic agents such as
1. Oxybutynin (Ditropan) and Tolterodine (Detrol):-
Anticholenergic agents work by
- increasing volume in the bladder
- inhibits involuntary contractions
- increase the total bladder capacity
- ditropan : antispasmodic action

53. # Tricyclic antidepressants
1. Imipramine (Tofranil) and Amitriptyline (Elavil)
- Increase the bladder ball relaxation and bladder
capacity.
# Pseudoephedrine (Sudafed)
- a very commonly used drug
- stimulates the alpha receptors
- constricts urethra, or the closer mechanism of
urethra
is increased

54. # Vaginal estrogen (for women)
- enriches genitourinary system with
estrogen receptor leads to good blood
supply to vaginal mucosa.
- prevents atrophy of mucosa.
- maintains elasticity of urethra and ability to
close properly.

55.  Monitor fluid intake
 Teach kegal exercises
 Develop a voiding schedule
 Implement biofeedback techniques
 Use behavior modification
 Explore obstructive devices
 Skin care
 Recommend counselling
 Encourage follow up

56. Use of other incontinence products
Disposable pads
Condom systems

57. Stress incontinence
- pelvic floor muscle exercises e.g., kegal
exercises
- weight loss if patient is obese
- cessation of smoking
- topical estrogen products
- external condom catheters or penile
clamps in men

58. - Treatment of underlying cause
- behavioral interventions including bladder
retraining with urge suppression
- decrease in dietary irritants
- bowel regularity
- pelvic floor muscle exercises
- external condom catheters
- Vaginal estrogen creams

59. - Urinary catheterization to decompress
the bladder
- Intra vaginal device such as a pessary to
sport the prolapse
- intermittent catheterization

60. - treatment of underlying cause
- bladder decompression to prevent urethral
reflux and hydronephrosis
- intermittent self catheterization
- diazepam to relax external sphincter as
prescribed

61. Incontinence after trauma and surgery
- External condom catheter
- penile clamp
- placement of artificial implantable
sphincter

62.  Functional incontinence
- Modification of environment or care plan that
facilitate regular, easy access to toilet and
promote patient safety
1. Better lightening
2. Ambulatory assistance
3. Equipment
4. Clothing alterations
5. Timely voiding
6. Different toileting equipment

63. 1. Bladder neck suspension
 Restore the normal urethrovesical junction
or lengthen and support the urethra.
2. Implantation of an artificial urinary sphincter
 Implantation of an artificial urinary sphincter
may help some clients to achieve
continence.
This procedure is usually avoided until all
other treatments have failed.

64.  Maintain adequate urinary drainage
 With bladder suspension, preventing
distention is a priority to help in avoiding
excessive pressure on the healing surgical
site
 Bladder training program is initiated to help
the client to regain detrusor muscle tone.
 Clamp the catheter for lengthening intervals
while urine collects in the bladder, unclamping
it periodically to empty the bladder.

65. If client reports severe pressure,
immediately unclamp the catheter.
If a suprapubic catheter is used, the client
should try to void every two to three hours.
After voiding is attempted, catheter is
drained to measure the residual urine.

66.  Urinary incontinence is uncontrolled leakage
of urine.
 Approximately 17 million people living in the
united states suffer from urinary incontinence.
Among young adults to middle aged women,
prevalence rate is 30% to 40% and it
increases to 30% to 50% in elderly women.
 In contrast urinary incontinence in men tends
to be considerably lower ranging from 1% to
5% in young adult men and increasing 9% to
34% in elderly men

67. Pyelonephritis is the inflammation of renal
pelvis and parenchyma caused by
bacterial infection.

68. Pyelonephritis may
be caused by
either an
ascending or
hematogenous
infection

69.  Infection Primary to:
-calculus
-malignancy
-hydronephrosis
-trauma
 Hematogenous spread
-Bacterial endocarditis
-septicemia
 UTI ( infection carried to kidneys via ascending
route that is travelling up
-vesicouretral reflux
-bladder tumors
-BPH
-strictures
-urinary stones

70. Pyelonephritis may be
 Acute
 Chronic

71. Acute pyelonephritis occurs after bacterial
contamination of urethra or
instrumentation such as catheterization
or cystoscopy.
Starts at renal medulla
spreads to cortex
fibrosis and scarring

72.  Pregnancy
 Calculi
 Chronic Cystitis
 IDDM
 Foreign bodies in UT

73. Bacteria enters renal pelvis
Inflammatory response starts
Increased WBC count
Inflammation of pelvis
Edema and swelling of involved tissue
Spreads to papillae
Reach cortex

74. Develops renal abcess
Perinephric abcess
Emphysematous
pyelonephritis
Not treated
Chronic pelonephritis
Decreased no of functioning
nephrons
Replaced by scar tissue
renal failure
Treatment and decreased
inflamation
Fibrosis and scar
development
Calyces become blunted
with scarring of
interstitial tissue
Fibrosis and altered
tubular reabsorption and
secretion
Decreased renal function

75.  Mild lassitude
 Sudden onset of chills
 Fever
 Vomiting
 Malaise
 Flank pain
 Dysuria

76.  Frequent urination
 Headache
 Symptoms subside after few days except
bacteruria
 Acute pyelonephritis is Characterized by
-enlarged kidneys
-focal parenchymal abcess
-accumulation of polymorphonuclear
leukocytes around and in tubules

77.  Urine culture and sensitivity
 Physical examination
 Studies for calculi
 Cystogram
 IVP
 Retrograde pyelogram
 Cystourethrogram
 Blood culture, WBC count
 X-Ray (KUB)
 MRI/CT Scan
 Cystoscopy, USG, Antibody coated bacteria
test

78. Therapeutic aims
Eliminating the pathogenic organisms
with appropriate antibiotics as identified
by urine culture and sensitivity study
Removing component contributing to
decreased host resistance

79. Mild symptoms
 Short antibiotic course
 Oral antibiotics for 10-14 days
 Fluid intake of 3000ml/day
 Follow up urine cultures
Severe Symptoms
 Hospitalization
 Parenteral antibiotics
 Fluid intake 3000ml/day
 Follow up urine cultures after discharge

80. Dietary alterations e.g for calculi
-Reduce calcium
-Reduce oxalates
for UTI
-acid ash diet

81. Underlying defects to be corrected e.g.
obstruction,
reflux,
calculus

82. Chronic pyelonephritis ( Chronic interstitial
nephritis) is the result of not only acute
pyelonephritis but end result of long
standing UTI with recurrence, relapses of
infections (Slowly ,progressive disease)

83.  Chronic obstruction
 Long standing UTI
 Reflux
 Chronic disorders
 Associated with recurrent acute attacks

84.  H/O acute infection progressing to
chronic renal insufficiency
 No specific symptoms of its own
 Frequently diagnosed incidently when
client shows HTN or its complications
 Chronic PN progresses with other acute
infections

85.  Lab studies shows :
-azotemia
-pyuria
-anemia
-acidosis
-proteinuria
 Renal biopsy
 IVP intravenous pylogram {kind of x ray of urinary
tract}
 USG
 CT scan

86.  Focus is on preventing further renal
damage
Treatment
Appropriate antibiotics
-orally for 2-3 wks
-parenterally for 3-
5days
Control HTN with antihypertensives

87. Nursing Assessment:
 History
-present history
-past history
-family history
-social and personal history
 Physical examination
 Urinalysis
 Blood studies
 Urine culture and sensitivity

88. Clinical problem Nursing
Diagnosis
Nursing
Intervention
Elevated
temperature
Altered comfort
R/T elevated
temperature
-Monitor vital
signs every 2-4
hourly
-Use cooling
blanket
-Antipyretics
-Ensure
adequate
hydration
-Monitor I/O
-Keep dry, avoid
chilling

89. Clinical problem Nursing
Diagnosis
Nursing
Intervention
Flank pain Altered comfort ,
flank pain R/T
inflammation and
tissue trauma
-Palpate abdomen
and flank to
identify painful
area
-Position client
for comfort
-Administer
analgesics as
ordered
-Antibiotic may
control
inflammation and

90. Clinical problem Nursing Diagnosis Nursing
Intervention
Altered urinary
elimination R/T
Frequency,
Dysuria
Frequency,
dysuria
-Explain the client
that why it is
-Give fluids
3000ml/day
-Administer I/V
fluids
-Obtain urine
culture and
sensitivity
-Administer
antibiotics

91. Clinical Problem Nursing Diagnosis Nursing
Intervention
Fluid volume
deficit R/T nausea
and vomiting
Nausea , vomiting -Administer
antiemetics
-Monitor I/O
-Vital signs

92. Potential for
reinfection
Potential for
reinfection R/T
knowledge deficit
regarding
prevention of
recurrence, S/S
-Instruct client about
preventive measures
Fluids 3000ml/day
Medications
Follow up
Hygiene
Empty bladder before
and after intercourse
Void when urge occurs
Avoid bath salts, sprays
Observe for changes

93. Clinical problem Nursing
Diagnosis
Nursing
Intervention
-Force fluids,
3000ml/day
-Medications,
rationale for use,
timings and
method of
administration
-Need for follow
up
- Perineal
Hygiene

94. Clinical Problem Nursing
Diagnosis
Nursing
Intervention
-Empty bladder
before and after
sexual intercourse
-Void when urge
occurs
Avoid bath salts,
sprays for
urination
Observe changes
for recurrence

96.  Acute Kidney Injury (AKI), previously called acute
renal failure (ARF) is the rapid breakdown of renal
(kidney) function that occurs when high levels of uremic
toxins (waste products of the body's metabolism)
accumulate in the blood.
 ARF occurs when the kidneys are unable to excrete
(discharge) the daily load of toxins in the urine.
 Acute renal failure is a syndrome defined by a sudden loss
of renal function over several hours to several days.

97. It is characterized by:
Oliguria
Body water and body fluids disturbances
Electrolyte dearangement

98. India's national CKD registry organized under the
auspices of Indian Society of Nephrology and housed
in Kidney Institute at Nadiad has given data from
45,885 subjects admitted to 166 kidney centers in
India upto January 2010.
ARF affects approximately 1% of patients on
admission to the hospital, 2% to 5% during the
hospital stay, and 4% to 15% after cardiopulmonary
bypass surgery.

99. PRERENAL CAUSES
(55%)
INTRARENAL CAUSES
(40%)
POSTRENAL CAUSES
(5%)

101.  Prerenal causes are those that interfere with renal
perfusion. The kidneys depend on adequate delivery
of blood to be filtered by glomerulus.
Reduced renal blood flow
Lowers the GFR
ARF

102.  Circulatory volume depletion:
Diarrhea, dehydration, vomiting,
hemorrhage, excessive use of
diuretics, burns, glycosuria.
 Decreased cardiac output: Cardiac pump failure,
acute pulmonary embolism, heart failure.
 Decreased peripheral resistance: Spinal anesthesia,
septic shock, anaphylaxis.
 Vascular obstruction: Bilateral renal artery
occlusion.

103. Atherosclerosis
Blood loss
Chronic liver disease
Heart disease

104. Vasoconstriction of
non-essential vascular
beds
Inhibition of salt
loss through
sweat glands
Renal salt and
water retention
Activation of SNS
& Renal-
angiotensin-
aldosterone
system
Hypovolemia

105. It involves parenchymal changes caused by disease
or nephrotoxic substances. Intrinsic ARF accounts
for approximately 40% of the cases of acute renal
failure.
The causes can be classified as follows:
 Vascular disease
◦ Glomerulonephritis (GN) and vasculitis
(inflammation of blood vessels)
◦ Renal artery obstruction (atherosclerosis,
thrombosis)

106. • Renal vein obstruction (thrombosis)
• Low blood platelet and red blood cell counts
 Diseases of tubules and interstitium (space between
parts of tissue)
• Amyloidosis (deposition of proteins in kidney tissues)
• Interstitial nephritis (associated with allergy or
infection)
 Acute tubular necrosis (70%)
• Ischemia (lack of blood flow to an organ)
• Toxins

107. Postrenal ARF is caused by an acute obstruction that
affects the normal flow of urine out of both kidneys.
Blockage/ Obstruction
Causes pressure to build in all of the renal nephrons
(tubular filtering units that produce urine)
Excessive fluid pressure causes the nephrons to shut
down

108.  The degree of renal failure corresponds directly with
the degree of obstruction
 Postrenal ARF is seen most often in elderly men with
enlarged prostate glands that obstruct the normal flow
of urine.

109.  Bladder outlet obstruction due to an enlarged
prostate gland or bladder stone
 Ureteric stones
 Neurogenic bladder (overdistended
bladder caused by inability of the
bladder to empty)
 Tubule obstruction
 Renal injury

111. Based on the amount of urine that is excreted over a
24-hour period, patients with ARF are separated into
two groups:
 Oliguric: patients who excrete less than 400
milliliters per day.
 Nonoliguric: patients who excrete
more than 400 milliliters per day.

112.  Onset or initiating phase: It covers the period
from the precipitating event to the development
of renal manifestations.
 Oliguric-anuric phase: It lasts for 1-8weeks.
Dialysis may be required in this phase.
 Diuretic phase: A gradual or abrupt return to
GFR and leveling of BUN. U/O may be 1000-
2000ml which leads to dehydration.(25% of
deaths occur in this phase)

113.  Recovery phase(3-12months): During this time
the client returns to an activity level similar to that
before the onset of the illness. Mild tubular
abnormalities, glycosuria, decreased concentrating
ability may continue for years and client is at the
risk for fluid and electrolyte imbalance.

114. 1. Decreased blood flow
2. Decreased permeability of glomerular
basement membrane
3. Tubular obstruction
4. Back leak of GF through damaged epithelial
cell tubules

115. Normal auto regulation
In decreased renal blood flow
Nephrons autoregulates Blood flow through
glomerulus and pressure
Efferent arteriole vasoconstriction
Decreases blood flow out of glomerulus
Maintains glomerular pressure sufficient for
filtration

116. renal blood flow
renal perfusion to cortex <90% and medulla <10%
Ratio of hyperperfusion altered
Decreased cortical perfusion
Triggers renin angiotensin system to inc blood flow
rate of perfusion in afferent vessels triggers an
increase renin

117. Renin forms angiotensin II
More reduced blood flow
Increased ischemia
Stimulates prostaglandins synthesis for vasodilation
Compensates Inc blood flow Prolongs hypoperfusion
Decreased prostaglandin inhibition
Renal ischemia
Tubular necrosis
Decreased GFR
Renal failure

119. U/O: 2l/day (dilute with low specific gravity)
Hypertension and tachypnea
Extracellular fluid depletion: (dry mucus
membranes, poor skin turgor, orthostatic
hypotension)
Azotemia

120.  U/O: Less than 400ml/day
 Kidney loses conc. ability

121.  Prerenal failure:
• High specific gravity and osmolarity of urine and there is no
or little proteinuria,
• BUN: Creatinine ratio is significantly elevated b/w 10:1 and
40:1.
 Inrarenal & Postrenal failure:
• Edema, weight gain, hemoptysis, weakness, anemia, HTN,
hematuria.
• Urine has high specific gravity, high Na concentration with
proteinuria.
• Elevated levels of serum creatinine, potassium.

123. • History and Physical examination
• Urinalysis
• Urine culture
• Urine Specific Gravity
Prerenal Failure: Specific Gravity >1.020
Intrarenal Failure: Specific Gravity 1.010 - 1.020
• ECG: to check the effects of hypo and
hyperkalemia.
• X-ray(KUB)

124. - RFT (renal function tests) Serum creatinine, Na, BUN levels.
Criteria for acute renal failure
Serum Creatinine rises >0.3 on 2 contiguous days or
Serum Creatinine rises >0.5 mg/dl or
Serum Creatinine rises >50% above baseline or
Calculated GFR falls >50% below baseline
- Renal biopsy
- Hemogram- Hb, TLC, DLC, Platelet Count
- ABGs- Metabolic Acidosis
- Electrolytes – Na, K, Cal, Mg, Ph, Ca

125.  Urine output
 Blood pressure – Hypertension
 Routine Urine Exam – Presence of sugar,
albumin
 Radiology- Ultrasonography, CT, MRI
 Renal Angiography

127.  A history of chronic symptoms of
fatigue,
weight loss,
anorexia,
pruritis
 Exposure to heavy metals
 Nephrotoxic drug ingestion
 History of trauma
 Blood loss or transfusions
 Evidence of connective tissue disorders or autoimmune
diseases
 Urine output history can be useful.

128. Past medical history
 Hypertension
 Congestive cardiac failure
 Diabetes
 Multiple myeloma
 Chronic infection
 Myeloproliferative disorder

129. Consensus criteria (RIFLE for the diagnosis of ARF
are:
 Risk: serum creatinine increased 1.5 times OR urine
production of <0.5 ml/kg body weight for 6 hours
 Injury: creatinine 2.0 times OR urine production
<0.5 ml/kg for 12 h
 Failure: creatinine 3.0 times or urine output below
0.3 ml/kg for 24 h

130.  Loss: persistent ARF or complete loss of kidney
function for more than four weeks
 End-stage Renal Disease: complete loss of kidney
function for more than three months

131.  Fluid-electrolyte imbalance
• Fluid overload/depletion
• Hyperkalemia
• Hyponatremia
• Hypocalcaemia
• Hypermagnesemia
 Acidosis
 Hematopoietic
• Increased susceptibility to infection
• Anemia
• Platelet dysfunction

133. • Arrhythmia
• Pericardial friction rub
• Hyperkalemia
• Metabolic acidosis
• HTN
• Increased JVP
• Edema
• Increased incidence of
pericarditis
• Apathy
• Defective recent memory
• Dysarthria
• Tremors
• Convulsions
• Coma

134.  Impaired wound healing
 Respiratory
• Altered ABG
• Rales
• Effusions
• Kaussmaul's respirations
 GI complications
• Anorexia
• Nausea
• Vomiting
• Diarrhea
• Constipation
• Stomatitis

136. Objectives
 Preventing and treating effects
 Attaining and maintaining adequate hydration
 Prevention of contributing factors
 Prompt recognition and restoration of optimal
renal function

137. Eliminate the cause
Hemodynamic support
Respiratory support
Fluid management
Electrolyte management
Medication dose adjustment
Dialysis

138. Maintenance of fluid and electrolyte balance on the
basis of output and wt
 Limit Fluid Intake to Urine Output + 300-500 ml/day:
Usually it is calculated on the basis of previous day’s
U/O + an amount of 400ml.
 Monitor weight daily
 Hyponatremia - Proper fluid replacement(limit Na
intake to 2g/day)
 Hyperphosphatemia
• Administration of aluminum hydroxide or other phosphate
binders
• Low phosphorus diet
 Hypocalcemia
• Calcium & Vitamin D supplements

139.  Hypertension
•Fluid and Sodium Restrictions
•Diuretic (Lasix or Mannitol)
•Anti- hypertensive's (Propanolol)
 Hyperkalemia
•Administration of calcium- it antagonizes membrane
actions
•Cation exchange resins (K-bind, Kayexalate)
•Sorbitol – Osmotic cathartic to induce diarrhea to excrete
potassium
•Low potassium diet
•Dextrose-insulin infusion
•Dialysis
•Dietary Potassium intake <50 meq per day

140.  Metabolic Acidosis
•Administration of Sodium bicarbonate, sodium
lactate, and sodium acetate can be given
 Anemia
•Administration of eptoein alfa, folic acid, blood
transfusions
 Infections
•Antibiotic
Nutritional Status
•High Calorie, Low-Protein, Sodium, magnesium,
phosphorus, potassium limited

141.  Hypermagnesemia
 Avoid dark green vegetables and whole grains.
 Treat seizures
• Phenytoin
• Phenobarbitone
 Prevention of pericarditis
• Medications
 steroids
 NSAIDs

142.  Dialysis
• volume overload
• uncontrolled hyperkalemia
• progressive uremia
• Rising BUN/ Cr
• Altered CNS function
• Pericarditis

143.  Oliguria:
• <400cc/24hr 85% will require dialysis
• >400cc/24hr 30-40% will require dialysis
 Mechanical ventilation
 Acute myocardial infarction
 Arrhythmia
 Hypoalbuminemia
 ICU stay
 Multi-system organ failure

144. Access : Veno-venous
 It is a mode of renal replacement therapy for
hemodynamically unstable, fluid overloaded, catabolic
septic patients especially in the critical care /intensive care
unit setting.
 The techniques most commonly used are slow continuous
hemodialysis and hemodiafiltration.
 These patients having various co-morbid conditions are on
mechanical ventilation and various life supporting
modalities which do not merit the dialysis procedure to be
carried out in the routine dialysis set up.

145.  These patients require continuous clearance of waste
produced due to ongoing illnesses and an adequate
potential for infusion of nutritional and inotropic agents
for sustenance of vital parameters.

146.  Presence of marked azotemia
 Fluid overload
 Persistent oliguria
 Hyperkalemia
 Refractory pulmonary edema
 Pericarditis
 Serial rise in blood urea and serum creatinine.
 ARF with cardiovascular instability
 ARF with septicemia
 ARF with septicemia and ARDS.
 ARF with cerebral edema
 Systemic inflammatory response syndrome

147. 1. CRRT by its lower rate of fluid removal can lead to
steady state fluid equilibrium in hemodynamically
unstable, critically ill patients with associated
comorbid conditions eg. M.I, ARDS, septicemia,
bleeding disorders.
2. It provides excellent control of azotemia, electrolytes
and acid base balance.
3. It is efficacious in removing fluid in special
circumstances – post surgery, pulmonary edema;
ARDS etc.

148. 4. CRRT can help in administration of parenteral
nutrition and obligatory I.V medications like pressors
& inotropes by creating an unlimited space by virtue
of continuous ultrafiltration.
5. Hemofiltration modality is effective in lowering
intracranial tension v/s routine intermittent
hemodialysis which can sometimes raise intracranial
tension.
6. Proinflammtory mediators of inflammation are also
shown to have been removed by this modality eg.IL-
1, IL-6, IL-8, TNF-a.

149. This mode of therapy requires regular
monitoring of hemodynamic status and fluid
balance (ultrafiltration rate, replacement fluid);
regular infusion of dialysate; continuous
anticoagulation; ongoing alarms and an
expensive mode of therapy above all.

150. Nursing Assessment
Nursing Diagnosis

151. 1. Fluid volume excess R/T decreased GFR
manifested by edema/weight gain
2. Altered nutrition :less than body requirement
R/T high catabolic state
3. Risk for infection R/T lowered resistance
4. Risk for injury R/T weakness, confusion,
postural hypotension
5. Knowledge deficit about the disease condition

152. Expected outcomes: Patient will be having no fluid
retention as evidenced by no or reduced edema, HR
within limits and stable BP.
Interventions:
-Record I/O, Acid base balance, electrolyte levels
-Measure weight, B.P, Auscultate lungs
-Assess for peripheral edema, decrease in Urine output,
increase in B.P, hyperkalemia
-Assess respiratory rate

153. - -Assess for the need for dialysis
-Inspect skin for breakdown
- Raise extremities
-Treat hyperkalemia by avoiding foods
containing K+, administering kayexalate (Ion
exchange resin)
-Look for S/S of hyperkalemia (muscle weakness,
arrhythmia, flaccidity)

154. Expected outcome: Patient will be having improved
nutrition pattern as evidenced by improved hemoglobin
levels, decreased fatigue and weakness.
Interventions :
- Encourage high carbohydrate, high fat diet
- Restrict potassium and proteins
- Serve in an attractive manner
- Consider likes and dislikes
- Consult dietician

155. Expected outcome: Patient will have reduced chances
of infection as evidenced by normal Hemogram, stable
vital signs.
Interventions:
- Use aseaptic technique during all treatments especially
with invasive lines and catheters
- Relieve pruritis by using superfatted soap and
antipruritic medications
- Maintain pulmonary hygiene

156. Expected outcome: patient will have increased
awareness regarding diet, medication, rest, follow-up.
- Teach the pt and family about:
cause and problems with recurrent failure
Identification of preventable environment or health
factors
prescribed medications
prescribed dietary regimen
Risk for hyperkalemia and reportable S/S
S/S of infection and methods of prevention
Follow-up

158. Chronic kidney disease (CKD) is a
worldwide public health problem. It is
recognized as a common condition that is
associated with an increased risk of
cardiovascular disease and chronic renal
failure (CRF).

159.  Chronic renal failure is a
progressive, irreversible
deterioration in renal
failure in which the body’s
ability to maintain
metabolic and fluid and
electrolyte balance fails,
resulting in uremia or
azotemia ( retention of
urea and other nitrogenous
wastes in the blood).

160. The Kidney Disease Outcomes Quality
Initiative (K/DOQI) of the National Kidney
Foundation (NKF) defines Chronic kidney
disease as either kidney damage or a
decreased Glomerular filtration rate (GFR)
of less than 60 ml/min for 3 or more
months.

161.  Causes of chronic kidney disease include the
following:
 Vascular disease
 Glomerular disease (primary or secondary)
 Tubulointerstitial disease
 Urinary tract obstruction

162. Vascular disease
o Renal artery stenosis
o Atheroemboli
o Hypertensive nephrosclerosis

163.  Renal vein thrombosis primary
Glomerular disease
o Membranous nephropathy
o Immunoglobulin A (IgA)
nephropathy
o Focal and segmental
glomerulosclerosis (FSGS)
o Minimal change disease
o Membranoproliferative
glomerulonephritis

164.  Secondary glomerulus
disease
o Diabetes mellitus
o Systemiclupus erythematus
o Rheumatoid arthritis
o Hepatitis B and C
o Syphilis
o Human immunodeficiency
virus (HIV)
o Parasitic infection

166.  Causes of Tubulointerstitial disease
o Drugs (e.g. allopurinol)
o Infection (viral, bacterial, parasitic)
o Chronic Hypokalemia
o Chronic hypercalcemia
o Polycystic kidneys

167.  Urinary tract obstruction
o Urolithiasis
o Benign prostatic hypertrophy
o Tumours
o Urethral stricture
o Neurogenic bladder

168. Total Glomerular filtration rate decreases (
reduced clearance)
Serum Creatinine and nitrogen level
increase
Nephrons works harder to eliminate
Creatinine and nitrogen

169. Decreased urine concentration results
Urine production increases
Tubules decrease reabsorption of electrolyte
Sodium loss may occur( can result in polyuria)
Renal damage progresses

170. In 2002, K/DOQI published its
classification of the stages of chronic
kidney disease, as follows:
Stage 1 :- Slightly diminished function;
kidney damage with normal or relatively
high GFR (≥90 ml/min). Kidney damage is
defined as pathological abnormalities or
markers of damage, including
abnormalities in blood or urine test or
imaging studies.

171.  Stage 2 :- Mild reduction in GFR (60-89
mL/min) with kidney damage. Kidney
damage is defined as pathological
abnormalities or markers of damage,
including abnormalities in blood or urine
test or imaging studies.

172.  Stage 3 :-
Moderate reduction in GFR (30-59
mL/min).
British guidelines distinguish between
stage 3A (GFR 45-59) and stage 3B (GFR
30-44) for purposes of screening and
referral.
 Stage 4 :- Severe reduction in GFR (15-29
mL/min) Preparation for renal replacement
therapy

173.  Stage 5 :- Established kidney failure (GFR
<15 mL/min, or permanent renal
replacement therapy.

174. Stage 1:- Reduced renal reserve,
Characterized by a 40% to 75% loss of
nephro function.
The patient usually does not have
symptoms because the remaining
nephrons are able to carry out the normal
functions of the kidney.

175. Stage 2:- Renal insufficiency
It occurs when 75% to 90% of nephrons
function is lost.
At this point, the serum Creatinine and
blood urea nitrogen rise, the kidney losses
its ability to concentrate urine and anemia
develops.
The patient may reports polyuria and
nocturia.

176. Stage 3:- End stage renal disease
 The final stage of CRF occurs when there is
less than 10% nephron function remaining.
 All of the normal regulatory, excretory and
hormonal function of the kidney are severely
impaired.
 ESRD is evidenced by elevated by the
Creatinine and blood urea nitrogen levels as
well as electrolyte imbalances.
 Once the patient reaches this point, dialysis is
usually indicated.

177. Neurologic:-
 Weakness and fatigue
 Confusion
 Inability to concentrate
 Disorientation
 Tremors
 Asterixis
 Restless of legs
 Burning of soles of feet
 Behavior changes

178. Integumentory:-
Gray bronze skin color
Dry flaky skin( atrophy of the sweat gland)
Pruritis
Ecchymosis
Purpura
Thin brittle nails
Thinning hairs

179. Cardiovascular:-
Hypertension
Pitting edema ( feet, hands and
sacrum)
Periorbital edema
Engorged neck veins
Pericarditis
Pericardial Effusion
Hyperkalemia
Hyperlipidemia

180. Pulmonary:-
Crackles, thick, tenacious sputum
Depressed cough reflex
Pleuritic pain
Shortness of breath
Tachypnea
Kussmaul type respiration
Uremic pneumonitis

181. Gastrointestinal:-
Ammonia odor to breath
Mouth ulcerations and bleeding
Anorexia, nausea and vomiting
Hiccups
Constipation or diarrhea
Bleeding from gastrointestinal tract

182. Hematologic:-
Anemia
Thrombocytopenia
Reproductive:-
Amenorrhea
Testicular atrophy
Infertility
Decreased libido

183. Musculoskeletal:-
Muscle cramps
Loss of muscle strength
Renal osteodystrophy
Bone pain
Bone fracture
Foot drop

185.  High levels of urea in the blood, which can result
in:
Vomiting and/or diarrhoea which may lead
to dehydration
Nausea Weight loss
Nocturnal urination
 More frequent urination, or in greater
amounts than usual with pale urine, Less
frequent urination, or in smaller amounts
than usual, with dark coloured urine.

186. A build up of phosphates in the blood that
diseased kidneys cannot filter out may
cause:
Itching
Bone damage
Non-union in broken bones
Muscle cramps (caused by low levels of
calcium which can cause hypocalcaemia)

187. A build up of potassium in the blood that
diseased kidneys cannot filter out (called
Hyperkalemia) may cause:
Abnormal heart rhythms
 Muscle paralysis

188.  Failure of kidneys to remove excess fluid may
cause:
Swelling of the legs, ankles, feet, face
and/or hands
Shortness of breath due to extra fluid on
the lungs (may also be caused by
anaemia)

189.  Healthy kidneys produce the hormone
erythropoietin which stimulates the bone
marrow to make oxygen-carrying red blood
cells.
 As the kidneys fail, they produce less
erythropoietin, resulting in decreased
production of red blood cells to replace the
natural breakdown of old red blood cells. As a
result, the blood carries less haemoglobin, a
condition known as anaemia. This can result
in:

190. Feeling tired and/or weak
 Memory problems
Difficulty concentrating Dizziness Low
blood pressure

191. Other symptoms include:
Appetite loss
 A bad taste in the mouth
Difficulty sleeping
Darkening of the skin
Excess protein in the blood

192. Urinalysis:- Decreased GFR can be
detected by obtaining a 24 hours urine
analysis for Creatinine clearance.
As GFR decreases, the Creatinine
clearance value decreases, where as the
serum Creatinine value increase.

193.  Serum Sodium and
Potassium level:- The
kidney is unable to
concentrate or dilute the
urine normally in ESRD.
 Some patient retain
sodium, potassium and
water, increasing the risk
for edema, congestive
heart failure and
hypertension.

194. pH:- With advanced renal disease,
metabolic acidosis occurs because the
kidney is unable to excrete increased
loads of acids.

195. Complete blood Count:- Anemia develops
as a result of inadequate erythropoietin
production, the short life span of RBCs,
nutritional deficiencies and the patient
ability to bleed.
In renal failure, erythropoietin production
decreases and profound anemia results,
producing fatigue, angina and shortness of
breath.

196. Serum calcium and Phosphorus:- With in
the decrease in the GFR, there is an
increase in the serum phosphate level and
a reciprocal or corresponding decrease in
the serum calcium level.

197.  KUB is usually done first to determine
whether there is a problem with the
structure of the renal system.
 An IVP and CT scan can be done to
assess renal structure and function.
 Renal angiography may also be done
to assess the blood supply to and
through the kidneys.
 Renal ultrasonography is useful to
screen for hydronephrosis which may
be not observed in early obstruction.

198.  Renal Biopsy
Percutaneous renal biopsy is performed
most often with ultrasound.

199. The goal of management
is to maintain kidney
function and homeostasis
for as long as possible.
All the factors that
contribute to ESRD and
all factors that are
reversible ( e.g.
obstruction) are identified
and treated.

200.  Antacid:- Hyperphosphatemia and
hypocalcemia are treated with aluminum
based antacids that binds dietary phosphorus
in the gastrointestinal tract.
 Phosphate-Lowering Agents
 Dietary phosphate binders promote the
binding of phosphate, typically with calcium,
to reduce Hyperphosphatemia.
 Calcium acetate
 Calcium carbonate
 Calcitriol

201.  Antihypertensive and cardiovascular agents:-
Hypertension is managed by intravascular
volume control and a variety of
antihypertensive medications.
 Congestive heart failure and pulmonary
edema may also require treatment with fluid
restriction.
 Low sodium diets, diuretics, inotropic agents
such as digitalis or dobutamine and dialysis.

202. Anticonvulsants:- Intravenous diazepam or
phenytoin is usually administered to
control seizures.
Erythropoietin:- Anemia associated with
CRF is treated with recombinant human
erythropoietin ( Epogen).
It is administered subcutaneously three
times a week for the Hematocrit to rise.

203.  Iron Salts
 Ferrous sulphate
 Iron dextran

204. Nutritional therapy:- Careful regulation of
protein intake.
Fluid intake to balance fluid losses.
Sodium intake to balance sodium losses.
Restriction of potassium.
Adequate calorie intake and vitamin
supplementation must be ensured.
The allowed protein must be of high
biologic value.

205.  Dialysis is a process for removing waste and
excess water from the blood, and is primarily used
to provide an artificial replacement for lost kidney
function in people with renal failure.
 Dialysis may be used for those with an acute
disturbance in kidney function (acute kidney injury)
, previously acute renal failure) or for those with
progressive but chronically worsening kidney
function–a state known as chronic kidney disease
stage 5 (previously chronic renal failure or end-
stage kidney disease).

206. The latter form may develop over months
or years, but in contrast to acute kidney
injury is not usually reversible, and dialysis
is regarded as a "holding measure" until a
renal transplant can be performed, or
sometimes as the only supportive measure
in those for whom a transplant would be
inappropriate.

207. It may also be used to treat the
patients with intractable ( not
responsive to treatment) edema,
hepatic coma, Hyperkalemia,
hypercalcemia, hypertension and
uremia.
It is usually initiated when the patient
cannot maintain a reasonable
lifestyle with conservative treatment.

209. A different dialysis technique, continuous
ambulatory peritoneal dialysis (CAPD),
makes use of the fact that the peritoneum
(the lining of the abdominal cavity) is a
differentially permeable membrane. A
plastic bag containing dialysis fluid is
attached to the patient's abdominal cavity..

210.  After about 30 minutes, the fluid is withdrawn
into the bag and discarded. This process is
repeated about three times a day. This type of
dialysis is much more convenient but poses the
threat of peritonitis, should bacteria enter the
body cavity with the dialysis fluid

212. Kidney transplantation, the surgical
implantation of a human kidney from one
person to another , is performed for clients
with irreversible kidney failure.
It involves transplanting a kidney from a
living donor or human cadaver to a
recipient who has ESRD.

213.  Patients with chronic kidney disease should
be educated about the following:
 Importance of compliance with secondary
preventive measures
 Natural disease progression
 Prescribed medications (highlighting their
potential benefits and adverse effects)
 Avoidance of nephrotoxins
 Diet
 Renal replacement modalities, including
peritoneal dialysis, hemodialysis, and
transplantation
 Permanent vascular access options for
hemodialysis

214.  Nursing Diagnosis:- Fluid volume excess
related to decreased urine output, dietary
excesses and retention of sodium and water.
 Intervention:- Assess fluid status.
 Daily weight.
 Intake and output balance.
 Skin turgor and presence of edema.
 Distention of neck veins
 Blood pressure, pulse rate and rhythm
 Respiratory rate and effort

215. Limit fluid intake to prescribed volume.
Identify potential sources of fluid:
Medications and fluids used to take
medications : oral and intravenous
Explain to patient and family rationale for
restriction.
Provide or encourage frequent oral
hygiene.

216. Nursing diagnosis:- Altered nutrition; less
than body requirements related to
anorexia, nausea, vomiting, dietary
restrictions.
Interventions:- Assess nutritional status:
 Weight changes.
 Anthropometric measures
 Laboratory values ( serum electrolyte,
BUN, Creatinine and iron level)

217.  Assess patient’s nutritional dietary pattern.
 Diet history
 Food preferences
 Calorie counts
 Assess for factors contributing to altered
nutritional intake
 Anorexia, nausea and vomiting
 Depression
 Lack of understanding of dietary restrictions

218.  Provide patient’s food preferences with in
dietary restrictions.
 Promote intake of high biologic value protein
foods: eggs, diary products, meats.
 Encourage high-calorie, low protein, low
sodium and low potassium snacks between
meals.
 Alter schedule of medications so that they are
not given immediately before meals.

219. Explain rationale for dietary restrictions
and relationships to kidney disease and
increased urea and Creatinine levels.
Provide written list of foods allowed and
suggestions for improving their taste
without use of sodium and potassium.
Provide pleasant surroundings at meal
times.
Weigh patient daily.

220.  Nursing Diagnosis:- Knowledge deficit
regarding condition and treatment.
 Intervention:- Assess understanding of cause
of renal failure, consequences of renal failure,
and its treatment:
Cause of patient’s renal failure.
 Meaning of renal failure.
 Understanding of renal function.
 Relationship of fluid and dietary restrictions to
renal failure.
 Rationale for treatment.

221. Provide explanation of renal function and
consequences of renal failure at patient’s
level of understanding and guided by
patient’s readiness to learn.
Assist patient to identify ways to
incorporate changes related to illness and
its treatment into lifestyle.
Provide oral and written information as
appropriate about:

222. Renal function and failure.
Fluid and dietary restrictions
Medications
Follow up schedule
Community resources
Treatment options

223. Nursing Diagnosis:- Activity intolerance
related to fatigue, anemia, retention of
waste products and dialysis procedure
Intervention:- Assess factors contributing
to fatigue:
 Anemia
 Fluid and electrolyte imbalances
 Retention of waste products
 Depression

224. Promote independence in self care
activities as tolerated ;assit if fatigued.
Encourage alternating activity with rest.
Encourage patient to rest after dialysis
treatments.

226. Acute tubular necrosis is a kidney disorder
involving damage to the tubule cells of the
kidneys, resulting in Acute Kidney Failure
(AFI).

227. Acute tubular necrosis or (ATN) is a
medical condition involving the death of
tubular cells that form the tubule that
transports urine to the ureters while
reabsorbing 99% of the water (and highly
concentrating the salts and metabolic
byproducts). Tubular cells continually
replace themselves and if the cause of
ATN is removed then recovery is likely.

228. Acute Kidney Injury (AKI) is observed in
about 5% of all hospital admissions and in
up to 30% of patients admitted to the
intensive care unit (ICU). ATN is the most
common cause of AKI in the renal
category, and the second most common
cause of all categories of AKI in
hospitalized patients, with only prerenal
azotemia occurring more frequently.

229. It may be classified as :
Toxic
Ischemic

230. Toxic ATN can be caused by:
Free hemoglobin or Myoglobin
Medication such as antibiotics such as
aminoglycoside
Cytotoxic drugs such as Cisplatin
Intoxication (ethylene glycol)

231. Toxic ATN is characterized by:
Proximal tubular epithelium necrosis due to
a toxic substance.
Necrotic cells fall into the tubule lumen,
obliterating it, and determining acute renal
failure.
Basement membrane is intact, so the
tubular epithelium regeneration is
possible.
Glomeruli are not affected.

232. Ischemic ATN can be caused :
When the kidneys are not sufficiently
perfused for a long period of time
(e.g. renal artery stenosis, shock).
Hypoperfusion can also be caused by
embolism of the renal arteries.
Ischemic ATN specifically causes skip
lesions through the tubules.

233. Blood transfusion reaction.
Injury or trauma that damages the
muscles.
Recent major surgery.
Septic shock or other forms of shock.
Severe low blood pressure (hypotension)
that lasts longer than 30 minutes.

234. Liver disease and kidney damage caused
by diabetes (diabetic nephropathy) may
make a person more susceptible to the
condition.
Exposure to medications that are toxic to
the kidneys (such as Aminoglycoside
antibiotics)
Antifungal agents (such as Amphotericin)
Dye used for X-Ray studies.

235. Causes of ischemic acute tubular necrosis:
Hypovolemic states: hemorrhage, volume
depletion from gastrointestinal (GI) or renal
losses, burns, fluid sequestration.
Low cardiac output states: heart failure
and other diseases of myocardium,
valvulopathy, arrhythmia, pericardial
diseases, tamponade.
Systemic Vasodilation: sepsis,
anaphylaxis.

236. Disseminated intravascular coagulation.
Renal vasoconstriction: cyclosporine,
amphotericin B, norepinephrine,
epinephrine, hypercalcemia
Impaired renal autoregulatory responses:
cyclo oxygenase (COX) inhibitors,
Angiotensin-Converting Enzyme (ACE)
inhibitors, Angiotensin receptor blockers.

237. Causes of Nephrotoxic Acute Tubular
Necrosis:
 Certain drugs like:
 Aminoglycosides.
 Amphotericin B
 Radio contrast media
 Cisplastin
 Cyclosporin
 Pentamide (used to treat Pneumocystic
carnii)

238.  Sulpha drugs
 Acyclovir, Indinavir
Radio contrast media

239. Follows a well defined 3 part sequence of:
Initiation Phase
Maintenance Phase
Recovery Phase

240. Initiation Phase:
Decreased B.P.
Hypoperfusion of Kidneys
Affects kidney’s Ischemia
autoregulatory system

241. Decreased production Cell injury
of Vasodilators
Causes further Cell
death
Vasoconstriction and Ischemia
Loss of function of
nephrons and tubules

242. Characterized by:
Stabilization of GFR at very low rate.
Lasts for 1- 2 weeks.

243. Characterized by:
Regeneration of epithelial cells of tubules.
Sometimes abnormal diuresis, causing salt
and water loss, dehydration.

244. Decreased consciousness
Coma
Delirium or confusion
Drowsy, lethargic, hard to arouse
Oliguria or Anuria
Edema, fluid retention
Nausea, vomiting

245. Symptoms of acute kidney failure may also
be present.
Incresed BUN and serum creatinine levels.
Fractional excretion of sodium and of urea
may be relatively high.
Presence of casts, kidney tubular cells,
and red blood cells in urinalysis.

246. Urine sodium may be high.
Urine specific gravity and osmolarity
decreased indicating dilute urine.

247. The degree of acute kidney injury (AKI) is
determined using the “RIFLE”
R : Risk of renal dysfunction,
 I : Injury to the kidney
 F: Failure
L: Loss of kidney function
E : End-stage renal disease

248. Complete Haemogram:
 Anaemia
Serum Chemistries:
 BUN
 Serum Creatinine
 Hyponatremia
 Hyperkalemia

249.  Hypermagnesemia
 Hypocalcemia
 Hyperphosphatemia
Urinalysis
Ultrasound
CT Scan
MRI
Renal biopsy.

251. In most people, acute tubular necrosis is
reversible. The goal of treatment is to
prevent life-threatening complications of
acute kidney failure.
Treatment focuses on preventing the excess
build-up of fluids and wastes, while
allowing the kidneys to heal. Patents
should be closely monitored for
deterioration of kidney function.

252. Anti Hyperkalemia therapy.
Dialysis.
Anti- oxidants: prevent reperfusion
damage as well as haemodynamics.
Diuretics.
N- Acetylcystine: used for Acetaminophen
toxicity.

253. Correction of oliguria, which may increase
due to the use of diuretics.
Fluid restriction: intake equals to output
considering the sensible loss also.
Restricting the substances normally
removed by Kidney like proteins, sodium,
potassium etc.

254. The duration of symptoms varies. The
decreased urine output phase may last
from a few days to 6 weeks or more. This
is occasionally followed by a period of high
urine output, where the healed and newly
functioning kidneys try to clear the body of
fluid and wastes.

255. One or two days after urine output rises,
symptoms reduce and laboratory values
begin to return to normal.

256. Chronic renal failure
End-stage renal disease
Gastrointestinal loss of blood
Hypertension
Increased risk of infection

257. Altered consciousness related to
accumulation of uremic toxins.
Fluid and electrolyte imbalance related to
sodium and water retention.
Altered nutrition less than body
requirement related to nausea and
vomiting.
 knowledge deficit related to diseased
condition and its management.

259. Glomerulonephritis is a type of kidney
disease that involves the glomeruli.
 During glomerulonephritis, the glomeruli
become inflamed and impair the kidney's
ability to filter urine.

260. The glomeruli are very small, important
structures in the kidneys that supply blood
flow to the small units in the kidneys that
filter urine, called the nephrons.

262. Glomerulonephritis, also known as
glomerular nephritis, abbreviated GN, is
a renal disease characterized by
inflammation of the glomeruli, or small
blood vessels in the kidneys

263. GN is a proliferative immunologic non
bacterial inflammation of the glomerular
structure due to antigen – antibody
reaction.

266. 1 Thin Basement Membrane Disease
2 Non Proliferative GN
 Minimal change GN
 Focal Segmental Glomerulosclerosis (FSGS)
 Membranous glomerulonephritis
3 Proliferative
 IgA nephropathy (Berger's disease)
 Henoch-Schönlein purpura
 Post-infectious
 Membranoproliferative/mesangiocapillary GN
 Rapidly progressive glomerulonephritis

267. it is an autosomal dominant inherited
disease characterised by thin glomerular
basement membranes on electron
microscopy.

268.  This is characterised by low numbers of
cells (lack of hypercellularity) in the
glomeruli. They usually cause nephrotic
syndrome. This includes the following
types:
1. Minimal change GN
2. Focal Segmental Glomerulosclerosis (FSGS)
3. Membranous glomerulonephritis

269.  This form of GN causes 80% of nephrotic
syndrome in children, but only 20% in adults.
There is fusion of podocytes (supportive cells
in the glomerulus).
 Rx: Treatment consists of supportive care for
the massive fluid accumulation in the patients
body (oedema) and as well as steroids to halt
the disease process (typically Prednisone 1
mg/kg).

270.  Only certain foci of glomeruli within the kidney
are affected, and then only a segment of an
individual glomerulus.
 The pathological lesion is sclerosis (fibrosis)
within the glomerulus and hyalinisation of the
feeding arterioles, but no increase in the number
of cells (hence non-proliferative).
Rx: Steroids are often tried but not shown to be
effective. 50% of people with FSGS continue to
have progressive deterioration of kidney
function, ending in renal failure.

271.  MGN is characterized by a thickened glomerular
basement membrane without a hypercellular
glomerulus.
 The basement membrane may completely
surround the granular deposits, forming a "spike
and dome" pattern.
 Prognosis follows the rule of thirds: one-third
remain with MGN indefinitely, one-third remit, and
one-third progress to end-stage renal failure .
 As the glomerulonephritis progresses, the tubules
of the kidney become infected, leading to atrophy
and hyalinisation. The kidney appears to shrink.

272.  This type is characterised by increased
number of cells in the glomerulus
(hypercellular).
 Usually present as a nephritic syndrome and
usually progress to end-stage renal failure
(ESRF) over weeks to years
Types
 IgA nephropathy (Berger's disease)
 Henoch-Schönlein purpura
 Membranoproliferative/mesangiocapillary GN
 Rapidly progressive glomerulonephritis

273.  IgA nephropathy usually presents as macroscopic
haematuria (visibly bloody urine). It occasionally
presents as a nephrotic syndrome.
 It often affects young males within days (24-
48hrs) after an upper respiratory tract or
gastrointestinal infection.
 It shows increased number of mesangial cells
with increased matrix (the 'cement' which holds
everything together).
 Immuno-staining is positive for IgA deposits
within the matrix.
 Prognosis is variable, 20% progress to ESRF.
 ACE inhibitors are the mainstay of treatment

274. HSP is a systemic variant of IgA
nephropathy which causes a small-
vessel vasculitis and associated
glomerulonephritis.

275.  It can occur after essentially any infection,
specially with Streptococcus pyogenes.
 Streptococcal titers in the blood (antistreptolysin
O titers) may support the diagnosis.
 It shows diffuse hypercellularity due to
proliferation of endothelial and mesangial cells,
as well as an influx of neutrophils and monocytes.
 The Bowman space is compressed, in some
cases to the extent that this produces a crescent
formation characteristic of crescentic
glomerulonephritis.
 Treatment is supportive, and the disease
generally resolves in 2-4 weeks.

276. This is primary, or secondary to SLE,
viral hepatitis, hypocomplementemia.
One sees 'hypercellular and
hyperlobular' glomeruli due to
proliferation of both cells and the matrix
within the mesangium.
Presents usually with as a nephrotic
syndrome, with inevitable progression to
ESRF.

277.  Crescentic glomerulonephritis induced by
infective endocarditis
 It is demonstrated circumferential and cellular
crescent formation with interstitial nephritis.
 It has a poor prognosis, with rapid
progression to kidney failure over weeks.
 Steroid therapy is sometimes used
 Any of the above types of GN can be rapidly
progressive.

278.  Additionally two further causes present
as solely RPGN.
1. Goodpasture's syndrome, an
autoimmune disease whereby antibodies
are directed against basal membrane
antigens found in the kidney and lungs. As
well as kidney failure, patient have
hemoptysis (cough up blood).
High dose immunosuppresion is required (IV
Methylprednisolone) and cyclophosphamide,
plus plasmapheresis.

279. 1. Wegener's granulomatosis and polyarteritis.
 There is a lack of immune deposits on staining,
but blood tests are positive for ANCA.
 The majority of glomeruli present "crescents".
Formation of crescents is initiated by passage
of fibrin into the Bowman space as a result of
increased permeability of glomerular basement
membrane.
 Fibrin stimulates the proliferation of parietal
cells of Bowman capsule, and an influx of
monocytes.
 Rapid growing and fibrosis of crescents
compresses the capillary loops and decreases
the Bowman space which leads to renal failure
within weeks or months.

280.  Hereditary: result from a gene on the X chromosome
passed on from carrier mothers who have no features,
or minimal features of the problem,
 Idiopathic
 Infections
• Post streptococcal GN: Beta hemolytic
streptococcal infection, URTI. Called as acute
poststreptococcal glomerulonephritis, or APSGN.
• Bacterial endocarditis
• Viral infections e.g. hep. B,C AIDS
• Fungal and parasitic

281.  Immune disease
• Lupus (SLE)
• Goodpasteur’s syndrome
• IgA nephropathy
 Vasculitis
polyarteritis nodosa
Wegener vasculitis
Henoch-Schönlein purpura
 Conditions causing scarring of glomeruli
• HTN
• Diabetic nephropathy
• Focal segmental GN

282.  dark brown-colored urine
(from blood and protein)
 sore throat
 diminished urine output
 fatigue
 lethargy
 increased breathing effort
 headache
 high blood pressure
 seizures (may occur as a
result of high blood
pressure)
 rash, especially
over the buttocks
and legs
 weight loss
 joint pain
 pale skin color
 fluid accumulation
in the tissues
(edema) in m’ing

283. S/S of Kidney failure
• Lack of appetite
• Nausea
• Vomiting
• Fatigue
• Difficulty in sleeping
• Dry /itchy skin
• Muscle cramps at night

284. Any1or 2 degree infection
Immune response activates
Antibodies formed in response to antigen
Antigen-antibody complex formed
Deposition of immune complex in
glomeruli

285. Soluble circulating complexes lodge in filtration
barrier
Complex bind and activate complement which
enhances migration of WBCs to site
WBCs release proteolytic enzyme from
lysosomes
Damages the glomerular cells
Results in filtration barrier being damaged

286. If Damage Is
Great
Dec. Functional
Surface area
Dec. GFR
Azotemia
Majority glomeruli
affected
Hyalinization
Dilated tubules with
hyalin casts
ESRD
Permeability es
Allows more proteins
to leave the cappilary
lumen and RBC
Proteinuria &
hematuria
Foamy cola coloured
urine

287. Lab studies
CBC
BUN, Creatinine
Urinalysis
-urine dark
-low pH
-sp. Gravity 1.020mOsm/L
-proteinuria
RBC and red cell cast

288.  Imaging studies
• Radiograph(chest)
• CT scan
 Other tests
• Serology
• Anti Nuclear Antobody
• Serum complement
• Renal Biopsy
Streptozyme test
Antistreptolysin O
Cultures of throat and skin lesions
Blood culture

289. Symptomatic management
Sodium and fluid restriction
Bed rest
Protein restriction
Dialysis if needed
Calcium supplements
Plasmapheresis if needed
Manage edema

290. For HTN
 Diuretics
 Angiotensin-converting enzyme (ACE) inhibitors
 Angiotensin II receptor agonists
 Calcium channel blockers
 Beta blockers
For circulatory congestion & pulm edema
• Preload and afterload restriction
• Diuretics
• Nitrates
• Morphine
• Dialysis

291.  Strep or other bacterial infection: antibiotic.
 Lupus or vasculitis. : corticosteroids and immune-
suppressing drugs.
 IgA nephropathy: Fish oil supplements
 Goodpasture's syndrome. Plasmapheresis
Plasmapheresis is a mechanical process that
removes antibodies from your blood by taking
the plasma out of your blood and replacing it
with fluid or donated plasma.

292.  Acute kidney failure. Loss of function in the
filtering part of the nephron may cause waste
products to accumulate rapidly.
 Chronic kidney failure. the kidneys gradually lose
function. usually requires dialysis or a kidney
transplant
 High blood pressure. Damage to your kidneys and
the resultant buildup of wastes in the bloodstream can
raise your blood pressure.
 Nephrotic syndrome. may accompany
glomerulonephritis and other conditions that affect
the filtering ability of the glomeruli.
 UTI
 Fluid overload

293.  Nursing Assessment
 History
• Recent respiratory infection or
skin infection
• Questioned for systemic disorders
• Recent invasive procedure
 Physical examination
 Ascitis
 Pleural effusion
 Urine examination
 Colour
 Amount
 Vital signs

294. Clinical
Problem
Nursing
Diagnosis
Nursing
Intervention
Edema Potential fluid
volume excess
R/T glomerular
damage and
decreased
GFR
-Monitor daily
weight
-Check for
puffiness
-Monitor I/O
-Daily measure
edema parts
-Restrict fluid
intake
-Restrict salt
intake

295. Clinical
Problem
Nursing
Diagnosis
Nursing
Intervention
Infection Potential for
infection R/T
lowered
resistance
-Give hard
candies to
relieve thirst
-Check lung
sounds for
pulmonary
edema
-Check for
Blood in urine
and feaces
-Isolate the pt
-Restrict visits

296. Clinical
Problem
Nursing
Diagnosis
Nursing
Intervention
Anorexia
,increased
proteinuria
Altered
nutrition less
than body
requirement
R/T
proteinuria,
decreased
-Teach client to
avoid
infections
-check WBC
count
-High calorie
diet
-Low protein
diet
-Check urinary
proteins

297. Clinical
Problem
Nursing
Diagnosis
Nursing
Intervention
Fatigue
Appetite and
increased
catabolism
Activity
intolerance
-Consult
dietician
-Manage
nausea and
vomiting with
antiemetics
-Decreased
salt and
potassium diet
-Adequate bed
rest

298. Clinical
Problem
Nursing
Diagnosis
Nursing
Intervention
R/T fatigue -Direct
correlation of
activity and
amount of
hematuria and
proteinuria –
Limit activity
-High caloric
diet

299. Clinical
Problem
Nursing
Diagnosis
Nursing
Intervention
-Encourage
client to talk
about his
fears
-Emotional
support
-ROM
exercises to
prevent
contractures
and joint
trauma

301. The nephrotic syndrome is characterized by
heavy proteinuria (more than 3.5g protein)
and is usually associated with
hypoalbuminemia ,hyperlipidemia and
edema.

302.  The increased
glomerular permeability
found in nephrotic
syndrome is responsible
for massive excretion of
proteins in urine.
 This results in decreased
serum protein and
subsequent edema
formation.

303.  The normal glomerular capillary wall
keeps blood cells and most proteins in
the blood.
 In patients with proteinuria, protein
leaks across the wall into the urine.

304. The barriers in the capillary wall that
keep protein out of the urine are
1. the endothelial cell lining the capillary
lumen
2. the basement membrane
3. epithelial cells (podocyte) normally
has little “feet” (pods) that sit on the
basement membrane and are
connected by a thin membrane.
podocytes appear to be the most
important barrier that prevents protein
from leaking into the urine

308.  Primary glomerular
diseases (Idiopathic)
 Lipoid nephrosis
 Membranous
nephropathy
 Membranoproliferative
glomerulonephritis
 Proliferative
glomerulonephritis
 FSGS
 Minimal change disease-
in children (fusion of foot
processes
 Allergens
 Bee sting
 Poison ivy
 Poison oat
 Insect repellent
 Drugs
 Penicillamine
 Bismuth
 Gold
 Trimethaprime

309.  Collagen- Vascular
diseases
 SLE
 Polyarteritis nodosa
 Metabolic diseases
 DM
 Amyloidosis
 Multiple myeloma
 Infectious diseases
 Quartan malaria
 Bacterial endocarditis
 Schistosomiasis
 Secondary syphilis
 Neoplastic Disorders
 Bronchogenic
carcinoma
 Hodgkin disease
 Colonic cancer

310.  Vascular diseases
 Constrictive Pericarditis
 Renal vein Thrombosis
 Inferior vena cava obstruction
 Congenital Nephrotic Syndrome
 Herodofamilial Nephrotic
syndrome
 Pregnancy

311. Becoz of immunologic, inflammatory or metabolic
abnormality(DM) ,HTN, GN
Increased glomerular basement membrane permability
or glomerulus get damaged
Low mol wt proteins such as albumin and alpha-globulin
are excreted in excess amt
Albumin synthesis and production imbalances
Hypoalbuminemia

312. Decreased plasma oncotic
pressure
Fluid shifts to interstitial space
from intravascular
Compartment
Decreased intravascular vol
Decreased renal blood flow
Decreased GFR
Stimulation of production of
aldosterone and ADH
Excessive sodium and water
retention leading to edema
Urinary loss of
inhibitors of clotting
(antithrombin3)
Thrombosis Stimulates hepatic
lipoprotein
synthesis
Hyperlipidemia
Fat bodies appear
in urine

313.  Proteinuria(>3.5g/day),
 hypoalbuminemia,
 hyperlipidemia
 edema.
A few other characteristics are:
1. Excess fluid in the body.
• Puffiness around the eyes,
(morning)
• Edema over the legs which is
pitting
• pleural effusion.
• pulmonary edema.
• ascites.

314. 2. Hypertension (rarely)
3. foamy urine, due to a lowering of the surface
tension by the severe proteinuria.
4. hematuria or oliguria are uncommon, and
are seen commonly in nephritic syndrome.
5. rash associated with Systemic Lupus
Erythematosus,
6. neuropathy associated with diabetes.

315.  Urine sample shows proteinuria (>3.5 per
1.73 m2 per 24 hour).
 Hypoalbuminemia: albumin level ≤2.5g/dL
(normal=3.5-5g/dL).
 hypercholesterolemia, elevated LDL, usually
with concomitantly elevated VLDL
 Electrolytes, urea and creatinine (EUCs)
 Biopsy of kidney
 Auto-immune markers (ANA, ASOT, C3,
cryoglobulins, serum electrophoresis)

316.  Monitoring and maintaining euvolemia
 monitoring urine output, BP regularly
 fluid restrict to 1L
 diuretics (IV furosemide)
 Monitoring kidney function
 do EUCs daily and calculating GFR
 Prevent and treat any complications
 Albumin infusions are generally not used
because their effect lasts only transiently.
 Prophylactic anticoagulation may be
appropriate in some circumstances.

317.  Immunosupression (corticosteroids, cyclosporin).
 Standard ISKDC regime for first episode:
prednisolone -60 mg/m2/day in 3 divided doses
for 4 weeks followed by 40 mg/m2/day in a single
dose on every alternate day for 4 weeks.
 Frequent relapses treated by: cyclophosphamide
or nitrogen mustard or cyclosporin or levamisole.
 blood glucose control if diabetic.
 Blood pressure control. ACE inhibitors (they have
been shown to decrease protein loss)

318.  Venous thrombosis: due to leak of anti-
thrombin 3, which helps prevent thrombosis.
This often occurs in the renal veins. Treatment
is with oral anticoagulants (not heparin as
heparin acts via anti-thrombin 3 which is lost in
the proteinuria so it will be ineffective.)
 Infection: due to leakage of immunoglobulins,
encapsulated bacteria such as Haemophilus
influenzae and Streptococcus pneumonia can
cause infection.
 Acute renal failure is due to hypovolemia.
 Pulmonary edema

319. Growth retardation:It occurs in cases
of relapses or resistance to therapy.
Causes of growth retardation are protein
deficiency from the loss of protein in
urine, anorexia (reduced protein intake),
and steroid therapy (catabolism).
Vitamin D deficiency
Thyroxin is reduced due to decreased
thyroid binding globulin.
Microcytic hypochromic anaemia

320. Nursing Assessment
 Assess edema
 Check daily wt
 Accurate I/O
 Measure abdominal girth/ extremity size
 Assess skin condition
 Assess for effectiveness of treatment
 Avoid trauma
 Effectiveness of diuretic therapy

321. Clinical Problem Nursing Diagnosis Nursing
Intervention
Retention of
sodium and fluid
Edema
Altered fluid and
electrolyte balance
R/T retention of
sodium and fluid
Impaired skin
integrity R/T edema
-Check daily
weight -
Measure abdominal
girth
-Maintain I/O chart
-Low sodium diet
-Monitor
electrolytes
-Assess for the skin
integrity
-Keep pt dry

322. Clinical Problem Nursing Diagnosis Nursing
Intervention
-Turn the pt
frequently
-Maintain hygiene
-Relieve pressure
from pressure
points
-Use air or water
mattresses
-Provide scrotal
support in men

323. Clinical
Problem
Nursing Diagnosis Nursing
Intervention
Protein loss Altered nutritional
pattern R/T protein
loss
-Assess for S/S of
infection
-Serve small
frequent feedings
-Protein intake 1.0
to 1.5 per kg of
body wt
-Serve food in an
attractive manner
-Ask for the likes
and dislikes of pt

324. Clinical Problem Nursing Diagnosis Nursing
Intervention
Low immunity Potential for
infection R/T
intake of
immunosuppressiv
e drugs
-Maintain hygiene
-Use aseptic
technique
-Avoid exposure
to persons with
known infections
-Avoid invasive
procedures or
maintain strict
asepsis

325. Clinical problem Nursing
Diagnosis
Nursing
Intervention
-Obtain specimen
for culture and
sensitivity when
infection is
suspected
-Administer
antibiotics as
prescribed
-Tell the pt S/S of
infection

326. Clinical Problem Nursing Diagnosis Nursing
Intervention
Edema Altered body
image R/T
puffiness of face
and edema of legs
-Restrict fluids
and sodium
-provide
knowledge
regarding the
causes for edema
-Ventilate his fears
-Remove the
mirrors from the
room to avoid him
to look his face

328.  The normal function of the urinary bladder is
to store and expel urine in a coordinated,
controlled fashion. This coordinated activity
is regulated by the central and peripheral
nervous systems. Neurogenic bladder is a
term applied to a malfunctioning urinary
bladder due to neurologic dysfunction or
insult emanating from internal or external
trauma, disease, or injury.

329. Neurogenic bladder refers to dysfunction
of the urinary bladder due to disease of the
central nervous system or peripheral
nerves involved in the control of
micturition.

330.  Brain lesion
 stroke
 brain tumor
 Parkinson disease
 Hydrocephalus
 cerebral palsy
 Shy-Drager syndrome
 Spinal cord lesion
 motor vehicle and diving accidents
 Multiple sclerosis (MS)
 myelomeningocele
 Sacral cord injury
 Sacral cord tumour

331.  Herniated disc
 Injuries that crush pelvis
 Lumbar laminectomy
 Radical hysterectomy
 Abdominoperineal resection
 Peripheral nerve injury
 Diabetes mellitus
 AIDS
 poliomyelitis
 Guillain-Barré syndrome
 severe herpes in the genitoanal area
 pernicious anemia
 neurosyphilis (tabes dorsalis)

332.  urinary tract infection
 kidney stones - these may be difficult to determine
because you may not be able to feel pain associated
with kidney stones if you have spinal cord
abnormalities. Symptoms of kidney stones include:
 chills
 shivering
 fever
 urinary incontinence
 small urine volume during voiding
 urinary frequency and urgency
 dribbling urine
 loss of sensation of bladder fullness

333.  Lab studies
 Urinalysis and urine culture
 Urine cytology
 Chem 7 profile: Blood urea nitrogen (BUN) and
creatinine
 Other tests
 Voiding diary: A voiding diary is a daily record of the
patient's bladder activity
 Pad test :This is an objective test that documents the
urine loss. Intravesical methylene blue test or oral
Pyridium or Urised may be used. Methylene blue and
Urised turns the urine color blue; Pyridium turns the
urine color orange.
 Diagnostic procedures
 Postvoid residual urine

334.  Uroflow rate :Uroflow rate is volume of urine
voided per unit of time.
 Filling cystometrogram
 filling cystometrogram
 Voiding cystometrogram (pressure-flow study)
 Cystogram
 Electromyography
 Cystoscopy
 Videourodynamics

335. TREATMENT

336.  Stress incontinence may be treated with
surgical and nonsurgical means.
 Urge incontinence may be treated with
behavioral modification or with bladder-
relaxing agents.
 Mixed incontinence may require
medications as well as surgery.
 Overflow incontinence may be treated with
some type of catheter regimen.
 Functional incontinence may be resolved
by treating the underlying cause (eg,
urinary tract infection, constipation) or by
simply changing a few medications.

337.  Absorbent products :Absorbent products
are pads or garments designed to absorb
urine to protect the skin and clothing.
 Urethral occlusive devices :Urethral
occlusive devices are artificial devices that
may be inserted into the urethra or placed
over the urethral meatus to prevent urinary
leakage.
 Catheters
 Indwelling urethral catheters
 suprapubic tubes
 self-intermittent catheterization.

338.  Surgical care for stress incontinence involves
procedures that increase urethral outlet
resistance. Operations that increase urethral
resistance include :
 bladder neck suspension
 periurethral bulking therapy
 sling procedures
 artificial urinary sphincter
 Surgical care for urge incontinence involves
procedures that improve bladder compliance or
bladder capacity.
 sacral neuromodulation
 botulinum toxin injections,
 detrusor myomectomy
 bladder augmentation

339.  Avoidance of dietary stimulants
 avoiding spicy foods like curry, chili
pepper, cayenne pepper, and dry mustard.
 Avoiding citrus fruits like grapefruits and
oranges.
 Avoiding chocolate-containing sweets.
Chocolate snacks
 Avoiding treats contain caffeine

340.  Beverages
 Avoid beverages that contain caffeine
:coffee, tea, hot chocolate, and sodas, milk,
Over-the-counter medicines
 Avoid carbonated beverages
citrus fruits drinks
acidic juices
artificial sweeteners.
 fluid restriction

341.  Pelvic floor exercise
 Vaginal weights : Vaginal weights are
tamponlike special help aids used to
enhance pelvic floor muscle exercises..
 Biofeedback :Biofeedback therapy is a
form of pelvic floor muscle rehabilitation
using an electronic device for individuals
having difficulty identifying levator ani
muscles. These devices allow the patient
to receive immediate visual feedback on
the activity of the pelvic floor muscles.

342.  Electrical stimulation :Electrical stimulation
is a more sophisticated form of biofeedback
used for pelvic floor muscle rehabilitation.
This treatment involves stimulation of levator
ani muscles using painless electric shocks.
 Bladder training: Bladder training generally
consists of self-education, scheduled voiding
with conscious delay of voiding, and positive
reinforcement.

343.  Medications
 Sympathomimetic drugs
 estrogen
 tricyclic agents
 The 3 main categories of drugs used to
treat urge incontinence include :
 anticholinergic drugs
 antispasmodics
 tricyclic antidepressant agents
 When a single drug treatment does not
work, combination therapy, such as
oxybutynin (Ditropan) and imipramine
(Tofranil) may be used.
.

344.  Estrogen derivatives
 Conjugated estrogen
 Anticholinergic drugs
Propantheline bromide (Pro Banthine)
Dicyclomine hydrochloride (Bentyl)
Hyoscyamine sulfate (Levsin/SL, Levsin)
 Antispasmodic drugs
Solifenacin succinate (VESIcare)
Darifenacin (Enablex)
OxybutyninChloride
Tolterodine
Trospium

345.  Tricyclic Antidepressants
Imipramine hydrochloride
Amitriptyline hydrochloride

346.  contact dermatitis
 skin breakdown
 pressure sores and ulcers
 secondary infections
 urinary tract infection.
 bladder infection
 bladder stones
 ascending pyelonephritis
 urethral erosion.
 urethral injury.
 bladder spasms

347. unique to suprapubic catheter
 skin infection
 hematoma
 bowel injury
 problems with catheter reinsertion
Untreated urinary tract infections may lead
to urosepsis and death.

348. Excellent
 Depends on the underlying condition
that has precipitated urinary
incontinence
 Urinary incontinence itself is easily
treated and prevented by properly
trained health care individuals.

350.  The urinary bladder occupies the deep pelvic
cavity and is well protected.
Because the bladder is located within the
bony structures of the pelvis, it is protected
from most external forces. This is the reason
it is rarely traumatized.
 However it can suffer traumas which can
cause extraperitoneal and intraperitoneal
ruptures

351. It is the injury to the urinary bladder caused by
either blunt or penetrating accidents.
The probability of bladder injury varies
according to the degree of bladder distention;
therefore, a full bladder is more likely to
become injured than an empty one.

352. 60 - 85% - Blunt injuries
15 - 40% - Penetrating injury
10 - 29% - Pelvic fractures
0.3% - Caesarean section
30% - Bladder biopsy

353. Penetrating and blunt trauma (main causes of
bladder injury) during accidents.
Iatrogenic causes include surgical
misadventures from gynecologic, urologic, and
orthopedic operations near the urinary bladder.
 Spontaneous or idiopathic bladder injuries
without an obvious underlying pathology
constitute the remainder.

354. Other causes include:
Surgeries of the pelvis or groin (including
hernia repair and abdominal hysterectomy)
Tears, cuts, bruises, and other injuries to the
urethra (most common in men)
 Straddle injuries (direct force accidents that
injure the scrotum area between a man's legs)
Deceleration injury (for example, a motor
vehicle accident that occurs with a full bladder
while wearing seatbelt)

356. ◦ The most common mechanisms of blunt trauma
are road traffic accidents (87%), falls (7%), and
assaults (6%).
 Deceleration injuries usually produce both
bladder trauma (perforation) and pelvic fractures.
◦ Approximately 10% of patients with pelvic fractures also
have significant bladder injuries.

357. ◦ The likelihood of the bladder to sustain injury is
related to its degree of distention at the time of
trauma.
◦ Injury may occur if there is a blow to the pelvis
that is severe enough to break the bones and
cause bone fragments to penetrate the bladder
wall.
◦ Generally the bladder injury in these cases is
associated with other injuries as well, the
commonest being to the spleen and rectum.

358.  The most common cause of penetrating trauma is
gunshot wounds (85%), followed by stabbings
(15%).
 It is also associated with abdominal and/or pelvic
organ injuries.
 Combined penetrating trauma of the rectum and
urinary bladder is rare.
 The combination of penetrating trauma to both
rectum and the urinary system is associated with
high morbidity and mortality.

359.  During prolonged labor or a difficult forceps
delivery, persistent pressure from the fetal head
against the mother's pubis can lead to bladder
necrosis.
• Direct laceration of the urinary bladder is reported
in 0.3% of women undergoing a Caesarean
delivery.
• Previous Caesarean deliveries, and the adhesions
that can remain subsequently, are a risk factor.

360. • Bladder injury may occur during a vaginal or
abdominal hysterectomy.
• Blind dissection in the incorrect tissue plane
between the base of the bladder and the
cervical fascia results in bladder injury.

361. Perforation of the bladder during a bladder
biopsy, cystolitholapaxy, transurethral
resection of the prostate (TURP), or
transurethral resection of a bladder tumor
(TURBT) is common.
Incidence of bladder perforation is reportedly
as high as 36% following bladder biopsy.

362.  Orthopedic pins and screws can
commonly perforate the urinary bladder,
particularly during internal fixation of
pelvic fractures.
 Thermal injuries to the bladder wall may
occur during the setting of cement
substances used to seat arthroplasty
prosthetics.

363. • Alcoholics and those individuals
who chronically drink large
quantities of fluids are susceptible
to this type of injury (bladder over
distension )
Person who holds urine for long
time during over distension.

364. Type I injuries are partial tears of the mucosa.
This is the most common injury pattern of
multisystem trauma patients and is associated
with blunt trauma.
Type II or intraperitoneal bladder ruptures.
This is usually the result of a direct blow to the
distended organ.

365.  Type III or interstitial pattern. This is an intramural or
partial-thickness laceration of the intact serosa. CT
cystography is used to diagnose this. Intramural
contrast is shown within the bladder wall. This
condition is usually the result of blunt trauma.
 Type IV bladder injury is extraperitoneal. It is the
most common bladder rupture. It is subdivided into
simple and complex injuries.

366. Extraperitoneal bladder ruptures
• Traumatic extraperitoneal ruptures are usually
associated with pelvic fractures (89%-100%). The
bladder rupture is most often due to a direct burst
injury or the shearing force of the deforming pelvic
ring.
• These ruptures are usually associated with
fractures of the anterior pubic arch, and they may
occur from a direct laceration of the bladder by the
bony fragments of the osseous pelvis.

367. • The anterolateral aspect of the bladder is
typically perforated by bony spicules.
Forceful disruption of the bony pelvis tear
the wall of the bladder.
• The degree of bladder injury is directly
related to the severity of the fracture.
• The classic cystographic finding is contrast
extravasation around the base of the bladder
confined to the perivesical space

368. • With a more complex injury, the
contrast material extends to the
thigh, penis, perineum, or into the
anterior abdominal wall.
• The bladder may assume a teardrop
shape from compression by a pelvic
hematoma.

369. Classic intraperitoneal bladder ruptures are
described as large horizontal tears in the dome
of the bladder. The dome is the least supported
area and the only portion of the adult bladder
covered by peritoneum.
The mechanism of injury is a sudden large
increase in intravesical pressure in a full
bladder.

370. When full, the bladder's muscle fibers are
widely separated and the entire bladder wall is
relatively thin, offering relatively little
resistance to perforation from sudden large
changes in intra vesical pressure.
Intraperitoneal bladder rupture occurs as the
result of a direct blow to a distended urinary
bladder.

371. This type of injury is common among
patients diagnosed with alcoholism or
those sustaining a seatbelt or steering
wheel injury.
Since urine may continue to drain into
the abdomen, intraperitoneal ruptures
may go undiagnosed from days to weeks.

372. Electrolyte abnormalities (e.g.,
hyperkalemia , hypernatremia, uremia,
acidosis) may occur as urine is reabsorbed
from the peritoneal cavity.
Such patients may appear anuric, and the
diagnosis is established when urinary
ascites are recovered during paracentesis.

373.  Intraperitoneal ruptures demonstrate contrast
extravasation into the peritoneal cavity, often
outlining loops of bowel and pooling under the
diaphragm.
 An intraperitoneal rupture is more common in
children because of the relative intra-
abdominal position of the bladder. The bladder
usually descends into the pelvis by age 20
years.

374. Clinical signs of bladder injury are relatively
nonspecific; however, a triad of symptoms are
often present: GROSS HEMATURIA
SUPRAPUBIC
PAIN OR
TENDERNESS
DIFFICULTY OR
INABILITY TO
VOID

375. Hematuria invariably accompanies all
bladder injuries. Gross hematuria is the
hallmark of a bladder rupture.
More than 98% of bladder ruptures are
associated with gross hematuria, and 10%
are associated with microscopic
hematuria.

376. An abdominal examination may reveal
distention, guarding, or rebound
tenderness.
Absent bowel sounds and signs of
peritoneal irritation indicate a possible
intraperitoneal bladder rupture.
A rectal examination should be performed
to exclude rectal injury.

377.  Shock or hemorrhage (the symptoms include)
Increased heart rate
Pale skin
Sweating
Skin cool to touch
Drowsiness
Lethargy
Decreased alertness
Coma

378.  History of trauma
 Gross hematuria
 Suprapubic pain
 Difficulty to void
 Abdominal tenderness
 Foley’s catheter
 CT scanning
 Cystography

379. It is often the first test performed in patients
with blunt abdominal trauma.
The CT scan of the pelvis provides
information on the status of the pelvic organs
and bony pelvis .
It most sensitive test for bladder perforation

380. The European Association of Urology (EAU)
developed guidelines for the appropriate
management of genito-urinary trauma.
In suspected renal injuries the hemodynamic
situation of the patient is the benchmark for
the diagnostic and therapeutic algorithm.

381. Most extraperitoneal ruptures can be
managed safely with simple catheter
drainage (ie, urethral or Suprapubic).
Leave the catheter in for 7-10 days and
then obtain a cystogram.
All extraperitoneal bladder injuries heal
within 3 weeks

382. Intraperitoneal bladder rupture
Most require surgical exploration, as they do
not heal with catheterization alone. Urine
continues to leak into the abdominal cavity,
resulting in urinary ascites, abdominal
distention, and electrolyte disturbances.
All wounds should be explored and should be
surgically repaired.

383. Extraperitoneal extravasation
Bladders with extensive extraperitoneal
extravasation are often repaired
surgically.
Early surgical intervention in these cases
decreases the length of hospitalization
and potential complications. It also
promotes early recovery.

384.  Hemorrhage
 Pelvic infection
 Peritonitis
 Urge incontinence
 Urinary extravasation
 Wound dehiscence
 Obstructive uropathy

385. The patient should return in 7-10 days for
staple removal and wound check.
The X-ray cystogram should be done 10-14
days after surgery.
If the cystogram finding is normal, the urethral
catheter can be removed.
Advise the patient that they may return to
normal activity 4-6 weeks after surgery.

386. Nursing Assessment
Nursing Diagnosis

387. 1) Hypovolemia related to gross hemorrhage.
2) High risk for infection related to
extravasation of urine and open wounds.
3) Acute pain related to injury of the bladder.
4) Fluid and electrolyte imbalance related to
hemorrhage.
5) Anemia related to gross hematuria.

389.  Hydronephrosis is
distention and
dilation of the renal
pelvis and calyces,
usually caused by
obstruction of the
free flow of urine
from the kidney,
leading to
progressive atrophy
of the kidney

391. The obstruction may be either
partial
complete
and can occur anywhere from the
urethral meatus to the calyces of the
renal pelvis.

392. Intrinsic
obstructions (occur
within the tract)
 blood clots,
 stones,
 sloughed papilla
 tumours of the
kidney, ureter and
bladder.
Extrinsic obstructions
(caused by factors outside of
the urinary tract)
 pelvic or abdominal tumours
 retroperitoneal fibrosis or
neurological deficits.
 Strictures of the ureters
(congenital or acquired),
 neuromuscular dysfunctions
 schistosomiasis which
originate from the wall of
the urinary tract.

393. Urinary Tract Obstruction
Dilation of structure behind obstruction
Backflow of urine
Dilation of kidney pelvis
Pressure on kidney structure Stasis of
urine
Dilation of kidney pressure on Infection
tubules renal calculi
arteries
Ischemia
Tubular damage

394.  It depend upon
whether the
obstruction is
 acute or chronic,
 partial or complete,
 unilateral or bilateral.
 Unilateral
hydronephrosis may
occur without any
symptoms, while acute
obstruction can cause
intense pain.[1]

395. Acute
Hydronephrosis
 Renal colic
 Changes in urinary
output (oliguria, anuria)
 Hematuria
 Palpable bladder
 Hypertension
 Hesitancy
 Urgency
 Incontinence
 Post voiding dribling
 Decreased force of
stream
Chronic
hydronephrosis
 No symptoms
 Intermittent pain
 Elevated RFT

396. An enlarged kidney may be palpable on
examination.
suprapubic tenderness along with a
palpable bladder.
If the obstruction is complete, an
enlarged kidney is often palpable on
examination.

397. Blood (U&E, creatinine)
urine (MSU, pH) tests
Ultrasound
An IVU
Antegrade or retrograde pyelography

398. The choice of imaging depends on the
clinical presentation
(history, symptoms and examination
findings).
In the case of renal colic the initial
investigation is usually an IVU
CT /MRI

399.  Removal of the obstruction
 drainage of urine.
 the specific treatment depends upon where the
obstruction lies, and whether it is acute or
chronic.
 Acute obstruction of the upper urinary tract is
usually treated by the insertion of a
nephrostomy tube.
 Chronic upper urinary tract obstruction is
treated by the insertion of a ureteric stent or a
pyeloplasty.
 Lower urinary tract obstruction is usually
treated by insertion of a urinary catheter or a
suprapubic catheter.

400.  Nursing Assessment
 Nursing Diagnosis
1. Pain R/T by obstruction of urinary
flow
2. Fluid and electrolyte imbalance R/T
renal dysfunction
3. Altered elimination Pattern R/t
incontinence , urgency, dribling

402. Healthy kidneys sends
erythropoietin
To bone marrow to
produce RBCs
Bone Marrow produces
RBCs
RBCs carry oxygen
through the blood
stream
available to the organs
throughout the body
Oxygen is made
Normal Kidney Function

403.  Dialysis is primarily
used to provide an
artificial replacement
for lost kidney function
(renal replacement
therapy) due to renal
failure.

404. In serious kidney disease, kidney function
is impaired or totally lost.
In such a situation, it is by the process of
"Dialysis" that waste products and excess
fluids are removed from the blood.

405.  Acute Indications for Dialysis/Hemofiltration:
• 1) Hyperkalemia
• 2) Metabolic Acidosis
• 3) Fluid overload (which usually manifests as
pulmonary edema)
• 4) Uremic pericarditis, a potentially life threatening
complication of renal failure
• 5) And in patients without renal failure, acute poisoning
with a dialysable drug, such as lithium, or aspirin.

406. Chronic Indications for Dialysis:
• 1) Symptomatic renal failure.
• 2) Low glomerular filtration rate (GFR) of less than
10-15 mls/min)
• 3) Difficulty in medically controlling serum
phosphorus or anaemia when the GFR is very low

407. Dialysis works on the principles of
 Diffusion
 Osmosis of solutes and fluid across a
semipermeable membrane.
 ultrafiltration

409.  Blood flows by one side of a semipermeable
membrane
 and a dialysate or fluid flows by the opposite
side.
 Smaller solutes and fluid pass through the
membrane. The blood flows in one direction and
the dialysate flows in the opposite.

410. The concentrations of undesired solutes
(for example potassium, calcium, and
urea) are high in the blood, but low or
absent in the dialysis solution and constant
replacement of the dialysate ensures that
the concentration of undesired solutes is
kept low on this side of the membrane.

411.  There are two types of dialysis:
1. Hemodialysis
 2. Peritoneal dialysis
Each method has it own advantages and
disadvantages but it is the medical condition &
attitude that will decide which method will suit
you best.

412.  Dialysis using a
filtering process of the
blood by a machine is
called hemodialysis

413.  Hemodialysis utilizes counter current flow, where the
dialysate is flowing in the opposite direction to blood
flow in the extracorporeal circuit.
 Counter-current flow maintains the concentration
gradient across the membrane at a maximum and
increases the efficiency of the dialysis.
 Fluid removal (ultrafiltration) is achieved by altering
the hydrostatic pressure of the dialysate
compartment, causing free water and some
dissolved solutes to move across the membrane
along a created pressure gradient.

414.  The dialysis solution that is used is a sterilized
solution of mineral ions. Urea and other waste
products, and also, potassium and phosphate,
diffuse into the dialysis solution.
 However, concentrations of sodium and chloride
are similar to those of normal plasma to prevent
loss.
 Bicarbonate is added in a higher concentration
than plasma to correct blood acidity. A small
amount of glucose is also commonly used.

416. In general, the larger the body size of an
individual, the more dialysis he will need.
In the North America and UK, 3-4 hour
treatments (sometimes up to 5 hours for
larger patients) given
3 times a week are typical

417.  blood is allowed to flow, a few ounces at a time,
through a special filter that removes wastes and
extra fluids.
 The clean blood is then returned to your body.
 Removing the harmful wastes and extra salt and
fluids helps control blood pressure and keep the
proper balance of chemicals like potassium and
sodium in body.

418. Getting Your Vascular Access Ready
Equipment and Procedures
Dialysis Machine
Dialyzer
Dialysis Solution
Needles

419. One important step before starting hemodialysis is
preparing a vascular access:
 a site on your body from which your blood is
removed and returned.
 A vascular access should be prepared weeks or
months before starting dialysis.
 It will allow easier and more efficient removal
and replacement of your blood with fewer
complications.

420. Three primary methods are used to gain
access to the blood:
an intravenous catheter
an arteriovenous (AV) fistula
or a synthetic graft.

421.  Catheter access sometimes called a CVC
(Central Venous Catheter), consists of
 a plastic catheter with two lumens (or
occasionally two separate catheters)
 It is inserted into a large vein (usually the vena
cava, via the internal jugular vein or the femoral
vein) to allow large flows of blood to be
withdrawn from one lumen, to enter the dialysis
circuit, and to be returned via the other lumen.

422. Non-tunnelled cathetar
Tunnelled catheter

425.  AV (arteriovenous)
fistulas are
recognized as the
preferred access
method.

426.  To create a fistula, a vascular surgeon joins an
artery and a vein together through anastomosis.
 Since this bypasses the capillaries, blood flows
rapidly through the fistula.
 One can feel this by placing one's finger over a
mature fistula. This is called feeling for "thrill" and
produces a distinct 'buzzing' feeling over the
fistula.

428. Fistulas are usually created in the
nondominant arm and may be situated on
the hand (the 'snuffbox' fistula'),
forearm (radiocephalic fistula, in which
the radial artery is anastomosed to the
cephalic vein),
elbow (usually a brachiocephalic fistula,
where the brachial artery is anastomosed
to the cephalic vein).

429. A fistula will take a number of weeks to
mature, on average perhaps 4-6 weeks.
During treatment, two needles are inserted
into the fistula, one to draw blood and one
to return it.

430.  AV (arteriovenous) grafts are much like
fistulas in most respects, except that an
artificial vessel is used to join the artery
and vein.

433. The graft usually is made of a synthetic
material, but sometimes chemically
treated, sterilized veins from animals are
used.
Grafts are inserted when the patient's
native vasculature does not permit a
fistula. They mature faster than fistulas,
and may be ready for use several weeks
after formation (some newer grafts may be
used even sooner).

434. The dialysis machine is about the size of a
dishwasher. This machine has three
main jobs:
1. pump blood and watch flow for safety
2. clean wastes from blood
3. watch blood pressure and the rate of
fluid removal from your body

435. A cylindrical bundle of hollow fibers, whose
walls are composed of semi-permeable
membrane, is anchored at each end into
potting compound (a sort of glue) through
which blood is passed.
 Dialysis solution, the cleansing fluid, is
pumped around these fibers.
The fibers allow wastes and extra fluids to
pass from blood into the solution, which
carries them away.

436.  Blood port at each end of
the cylinder
communicates with each
end of the bundle of
hollow fibers forming
"blood compartment"
1. Two other ports are cut
into the side of the
cylinder. These
communicate with the
space around the hollow
fibers, the "dialysate
compartment."
4 Openings

439. Your dialysis center may use the same
dialyzer more than once for your
treatments.
Reuse is considered safe as long as the
dialyzer is cleaned before each use.
The dialyzer to be labeled with name and
check to see that it has been cleaned,
disinfected, and tested.

440. Dialysis solution, also known as dialysate,
is the fluid in the dialyzer that helps
remove wastes and extra fluid from blood.
 It contains chemicals that make it act like
a sponge.

441. Bicarbonate
Na
K
Ca
Mg
Cl
glucose

442. blood and dialysate flow rates
dialysis solution conductivity
temperature
 pH
analysis of the dialysate for evidence of
blood leakage
presence of air.

445. Most dialysis centers use two needles—
one to carry blood to the dialyzer
and one to return the cleaned blood to
body.

447.  Cramping
 Drops in blood
pressure
 Headaches
 Nausea and vomiting
 Feeling washed out
 Abnormal heart
rhythms
 Infections
 Fatigue
 Chest Pains
 Leg-cramps
 Anemia
 Renal
Osteodystrophy
 Itching
 Sleeping Disorders

448. Patient may experience a syndrome called
"washout".
 The syndrome may begin toward the end of
treatment or minutes following the treatment
last 30 minutes or 12-14 hours
"are too tired, too weak to converse”
symptoms including headaches, nausea and
loss of appetite.
Eating a light meal, rest and quiet help the
patient cope with washout until it has 'worn
away.'

450. 1. Dialysis machine prepared
2. The patient is carefully weighed.
3. Standing and sitting BP are taken.
4. Temperature is taken.
5. Access is set up.
6. Heart rate
7. Breathing rate
8. Chest assessment
9. Examination of venous access
10. Access is set up

452.  The pump and a timer are started.
 Blood taken Out is 200-350ml/min
 half hour BP is taken.
 Most dialysis patients are on moderate to severe
fluid restrictive diets
 During dialysis, occasionally, patients may have low
BP , then Trendelenburg position could be given for
a short time.

453.  Hemodialysis may remove 2-5 kilograms
(5-10 pounds) of fluid
 Fluid to be removed is set according to the
"estimated dry weight."
 Dry weight represents what the patient
should weight without fluid built up

454. The patient is disconnected from the
plumbing - blood lines
Needle wounds are bandaged with gauze,
held for up to 1 hour with direct pressure to
stop bleeding,
Temperature
Standing and sitting BP
Weight to confirm removal of desired
amount of fluid.

455. A patient on dialysis has a prescribed diet
to prevent catabolism and control the level
of serum uremic products that accumulate
between dialysis treatments.
Typically, this daily diet includes
60 grams of protein,
2 grams of sodium,
2 grams of potassium,
1,000 ml of water.

456. water-soluble vitamins
a stool softener
a phosphate binder (to bind calcium with
phosphate in the gastrointestinal tract,
remove it in the stool, and prevent
osteodystrophy).

457. For morning dialysis, arrange an early
breakfast
Give him water-soluble medications after
dialysis
hold antihypertensive medications. Dialysis
lowers blood pressure (BP),
Send I.V medications (such as antibiotics,
calcitriol, and iron compounds) with the
patient.

458. assess site for bleeding and BP before
letting him resume activity.
evaluate serum K level for hyperkalemia.
avoid using access arm for administering I.V.
medications, taking BP, or drawing blood.
 Assess the thrill of the access site each
shift.

459.  If patient has diabetes and ESRD and becomes
hypoglycemic, give him apple juice instead of
orange juice.
 Monitor Intake Output
 Monitor
 bruising,
 eye hemorrhages,
 tarry stools,
 signs of anemia.
 Monitor hematocrit level
 Provide Psychological Support.

462. Dialysis using the natural filtering
membrane of the body called "Peritoneum"
is called Peritoneal Dialysis.

463. With peritoneal dialysis, the network of tiny
blood vessels in abdomen (peritoneal
cavity) is used to filter blood.

464. the peritoneal membrane ,surrounding
intestine, act as a natural semipermeable
membrane and if a formulated dialysis fluid
is instilled around the membrane then
dialysis can occur by diffusion
Excess fluid can also be removed by
osmosis, by altering the concentration of
glucose in the fluid.

465. Diabetes
Hypertension
Glomerulonephritis
Polycystic Kidney Disease
Hypotension

466. Inflammatory Bowel Disease
Intestinal Disease
Multiple Surgical Scars

467.  Can be done at home.
 easy to learn.
 Easy to travel with, bags of solution
 Fluid balance is easier than on hemodialysis
 Excluding kidney transplant, PD is first choice
method in treating chronic kidney failure.

468. Requires a degree of motivation and
attention to cleanliness while performing
exchanges.
Possible complications

470. 3 types
Continuous ambulatory peritoneal dialysis
(CAPD)
Continuous cyclic peritoneal dialysis
(CCPD)
Intermittent peritoneal dialysis (IPD)

471. Continuous ambulatory peritoneal dialysis
common
The dialysate passes from a plastic bag
through a catheter and into the abdomen.
 No machine is necessary.
 After 4 to 6 hours, the solution is drained
back into the bag and replaced with fresh
solution.
The solution is usually changed 4 times a
day.

474.  It uses a machine called a cycler to minimize the need for
manual exchanges.
 It allows dialysis to be done at night while patient sleeps.
 Dialysate is warmed by cycler machine to body temperature
 It fills abdomen while the patient is lying in bed.
 Dwell time can be programmed into the cycler.
 When dwell time completes, the used dialysate is drained and
replaced.
 The cycler is programmed to fill and drain the abdomen
automatically at night.
 It performs several exchanges while the patient sleeps with one
exchange done in the morning before unhooking from the
machine.

475.  Continuous cyclic
peritoneal dialysis is like
CAPD, except that a
machine is used to fill and
drain the dialysate through
the catheter.
 This procedure is
performed nightly, for 10 to
12 hours, during sleep. It
requires the help of a
partner.

476. Intermittent peritoneal dialysis uses a
machine, much like CCPD, to add and
drain the dialysate.
 Each session may last up to 24 hours.
 Intermittent peritoneal dialysis treatments
are usually performed in a hospital for a
total of 36 to 42 hours weekly.

477.  The apparatus consists of two bags
 one empty and one with the fluid,
 bag of dialysis fluid comprises glucose
dissolved in water. It determines the osmotic
gradient,.
 Common strengths of glucose are 0.5%, 1.5%,
2.5% and 4.25%.
 It is connected via flexible tubing to a Y-shaped
fitting.
 The bag is heated to body temperature, to avoid
causing cramping.

479.  Dialysis fluid is instilled via a
peritoneal dialysis catheter, (
Tenckhoff Catheter)
 Catheter is surgically placed
through the wall of the patient's
abdomen as a permanent access
 The catheter is placed 1 inch
below and to the side of the navel.
 2-4 inches of the catheter extends
out of the body.

481. Through catheter, peritoneum is filled with
dialysate sol.
The dialysate absorbs the excess water
and the waste products.
The dialysate remains in the peritoneum for
a certain period of time. This is known as
‘dwell time’. Varies from 20min-8hrs

483. The bag of dialysis fluid is hung from an
IV stand
The tubing attached to the bag of fluid
is uncoiled, and the second (empty) bag
is placed on the floor.
The Y-shaped connector is attached to
the catheter tip;
a protective cap is removed from both
of these before the connection is made

485. Once connected to the system
the patient clamps the tubing connected to
the full bag of dialysis fluid
releases the twist valve located in the tip of
their catheter; this permits fluid to flow out
of the peritoneal cavity.
the effluent (used dialysis fluid) from within
the peritoneum can drain out of the
catheter into the lower, waste bag.
Emptying the abdomen takes 15 min

486. When the abdomen has drained, the
lower drain-bag is clamped off.
The twist valve in the catheter is also
closed.
 The clamp is then removed from the
upper tubing, permitting dialysis fluid to
drain into the abdomen.

487. Once the entire bag of fluid (1500 to 3000
mL) has been introduced to the abdomen,
the patient then cleans their hands again
The Y-connector is detached from the
catheter tip and a new protective cap is
placed on the end of the catheter.
The effluent is inspected after a dialysis
exchange is complete
The effluent is drained into a toilet

489.  Volume to be infused
Number of exchanges / day
Type of PD (manual or automated)
Type of dialysis solution
Glucose is used in dialysate to pull fluid
out of the patient
New molecule (icodextrin) more effective
for fluid removal

490.  INFECTION
 PERITONITIS
 FLUID LEAKS :may occur into surrounding soft tissue,
often the scrotum in males.
 HERNIAS
 ACCUMULATION OF FIBRIN: To break up the fibrin,
Heparin must be injected into the bags of dialysate
(generally 1mL Heparin per liter of dialysate) until the
fibrin clears up.

491.  Infection is the most common problem for people
on PD.
 keep catheter bacteria-free to avoid peritonitis
 Rules :
• Store supplies in a cool, clean, dry place.
• Inspect each bag of solution for signs of contamination
before you use it.
• Find a clean, dry, well-lit space to perform exchanges.
• Wear sterile gloves to perform exchanges.
• Wash your hands every time you need to handle
catheter.
• Clean the exit site with antiseptic every day.

492.  Keep a close watch for any signs of infection and
report them so they can be treated promptly e.g
 Fever
 Nausea or vomiting
 Redness or pain around the catheter
 Unusual color or cloudiness in used dialysis
solution
 A catheter cuff that has been pushed out

494.  Dialysis is a process used to
remove fluid and uremic
waste products from the
body when the kidneys are
unable to do so.
 It may also be used in
treating patients with
intractable (not
unresponsive to treatment)
edema, hepatic coma,
Hyperkalemia, hypertension
and uraemia.

495. Patients with no renal function have been
maintained for a number of years by
dialysis. Successful kidney transplantation
eliminates the need for dialysis.
Although the costs of dialysis are usually
reimbursable, limitations on the patient’s
ability to work resulting from illness and
dialysis usually impose a great financial
burden on patients and family.

496. Method of therapy include:-
Hemodialysis
Continuous renal replacement therapy
(CRRT)
Peritoneal Dialysis

497. Acute dialysis is indicated when there is a
high and rising level of serum potassium,
fluid overload, or impending pulmonary
edema, increasing acidosis, pericarditis
and severe confusion.
It may also be used to remove certain
medications or other toxins from the blood.

498. Chronic or maintenance dialysis is
indicated in CRF, known as ESRD, in the
following instances: the occurrence of
uremic sign and symptoms affecting all
body systems (nausea and vomiting,
severe anorexia, increasing lethargy,
mental confusion), Hyperkalemia, fluid
overload not responsive to diuretics and
fluid restriction, and a general lack of well
being.

499. Hemodialysis: - It is the most commonly
used method of dialysis. It is used for
patients who are acutely ill and require
short-term dialysis (days to weeks) and for
patients with ESRD who require long term
or permanent therapy.
A dialyzer or artificial kidney serves as a
synthetic, semi permeable membrane,
replacing the renal glomeruli and tubules
as the filter for the impaired kidneys.

500. For patients with CRF, hemodialysis
prevents death, although it does not
compensate for loss of the kidney’s
endocrine or metabolic activities.
Patients receiving hemodialysis must
undergo treatment for the rest of their lives
(usually three times a week for at least 3 to
4 hours per treatment) or until they
undergo successful kidney transplantation.

501. The objective of hemodialysis is to
extract toxic nitrogenous substances from
the blood and to remove excess water.
In hemodialysis, the blood, laden with
toxins and nitrogenous wastes, is diverted
from the patient to a machine, a dialyser, in
which the blood is cleansed and then
returned to the patient.

502.  Diffusion: - The toxins and
wastes in the blood are removed
by diffusion; that is, they move
from an area of greater
concentration in the blood to an
area of lesser concentration in the
dialysate.
 The dialysate is a solution
composed of all the important
electrolytes in their ideal
extracellular concentrations.

503. The electrolyte level in the blood can be
brought under control by properly adjusting
the dialysate bath.
The semi permeable membrane impedes
the diffusion of large molecules, such as
red blood cells and proteins.

504. Osmosis: - Excess water is removed from
the blood by osmosis, in which water
moves from an area of higher solutes
concentration (blood) to lower solute
concentration (the dialysate bath).

505.  Ultra filtration: - is defined as water
moving under high pressure to an area
of lower pressure. This process is
much more efficient at water removal
than is osmosis.
 Ultra filtration is accomplished by
applying negative pressure or a
suctioning force to the dialysis
membrane. Because patients with
renal disease usually cannot excrete
water, this force is necessary to
remove fluid to achieve fluid balance.

506.  Dialysers:- Most dialyser or artificial
kidneys are either flat- plate dialysers or
hollow fibre artificial kidneys that contains
thousands of tiny cellophane tubules that
act as semi permeable membranes.
 The blood flows through the tubules while
a solution, the dialysate circulates around
the tubules. The exchange of wastes from
the blood to the dialysate occurs through
the semi permeable membrane of the
tubules.

507.  The concentrations of solutes (for example
potassium, phosphorus, and urea) are
undesirably high in the blood, but low or
absent in the dialysis solution and constant
replacement of the dialysate ensures that the
concentration of undesired solutes is kept low
on this side of the membrane.
 The dialysis solution has levels of minerals
like potassium and calcium that are similar to
their natural concentration in healthy blood

508. For another solute, bicarbonate, dialysis
solution level is set at a slightly higher level
than in normal blood, to encourage
diffusion of bicarbonate into the blood, to
act as a pH buffer to neutralize the
metabolic acidosis that is often present in
these patients.

509. A typical composition would be in mmoL / L
sodium 140.0
potassium 1.0
calcium 1.25
bicarbonate 34.0
magnesium 0.5
chloride 107.5
glucose 5.5

510. Blood can be removed, cleaned and
returned to the body at rates between 200
and 800ml/min;first, however, access to
the patient’s circulation must be
established. Several kinds of access are
available.

511.  Subclavian, internal jugular and femoral
catheter:- Immediate access to the patient’s
circulation for acute hemodialysis is achieved
by inserting a double- lumen or multilumen
catheter into the subclavian, internal jugular,
or femoral vein.
 Although this method of vascular access is
not without risk (e.g. hematoma,
pnemothorax, infection, thrombosis of the
subclavian vein, inadequate flow), it can be
used for several weeks.

512. The catheters are removed when no
longer needed because the patient’s
condition has improved or another type of
access has been established.
Double lumen, cuffed catheter may also be
surgically inserted into the subclavian vein
of patients requiring a central venous
catheter for dialysis over a longer term.

513.  Fistulas: - A more permanent access, known
as fistula, is created surgically ( usually in the
forearm) by joining (anastomosis) an artery to
a vein, either side to side or end to side.
 Needles are inserted into the vessels to
obtain blood flow adequate to pass through
the dialyser. The arterial segment of the
fistula is used for arterial flow and venous
segment for reinfusion of the dialyzed blood.

514. The fistula takes 4 to 6 weeks to mature
before it is ready to use. This gives time for
healing and for venous segment of the
fistula to dilate to accommodate two large-
bore (14 or 16 gauge) needles.
The patient is encouraged to perform
exercise to increase the size of these
vessels (i.e. squeezing a rubber ball for
forearm).

516.  Graft: - An arteriovenous graft can be created
by subcutaneously interposing a biologic,
semi biologic or synthetic graft material
between an artery and vein.
 The most commonly used synthetic graft
material is expanded polyfluoroethylene.
Usually a graft is created when the patient
own blood vessels are not suitable for fistula.
Patients with compromised vascular systems
(e.g. from diabetes) often need to have a graft
to undergo hemodialysis.

517. Grafts are usually
placed in the
forearm, upper
arm, or upper
thigh. Infection and
thrombosis are the
most common
complications of
arteriovenous
grafts.

518. In hemodialysis, the client’s toxin-laden
blood is diverted into a dialyzer, cleaned
and then returned to the client. While the
blood is in the dialyzer, a mechanical
proportioning pump causes dialysis fluid to
flow on the other side of membrane.
Toxins diffuse across the membrane from
the blood to the dialysate.
Strict asepsis must be maintained
throughout the procedure.

519. One of the vital aspect of hemodialysis is
the establishment and maintenance of
adequate blood access. Without it
hemodialysis can not be done.
The major route of access are external
arteriovenous shunts and subclavian
catheters for acute dialysis and internal
arteriovenous fistulae and grafts for
chronic dialysis.

520. The external arteriovenous shunt
requires surgical placement of two rubber
like silicone ( Silastic) cannula into the
forearm or leg.
The two cannula are connected to form a
U shape. Blood flows form the client’s
artery through the shunt into the vein.

521. When the client is to be connected to the
hemodialyzer, a tube leading to the
membrane compartment is connected to
the arterial cannula.
Blood then fills the membrane
compartment and flows back to the client
by way of a tube connected to the venous
cannula.

522. When dialysis is completed, the arterial
cannula is clamped. Once the blood in the
membrane compartment has been
returned to the body, the venous cannula is
clamped and the ends of the two cannula
are reattached to form their U.
This access can be created quickly and
thus is particularly suitable when dialysis
must be started immediately

523. Infection at insertion site.
Accidental dislodgment
Hemorrhage
Skin Erosion

524. The internal arteriovenous fistulas is the
access of clients receiving chronic dialysis.
The fistula is created through a surgical
procedure in which an artery in the arm is
anastomsed to a vein in an end to side,
side to side, side to end or end to end
fashion.
The result is an opening or fistula between
a large artery and a large vein.

525.  The internal arteriovenous graft is used primarily
for chronic dialysis. In this approach , an artificial
graft made of water-repellent fabric is used to
create an artificial vein for blood flow.
 The graft is used in clients who do not have
adequate blood vessels for surgical creation of a
fistula.
 One end of the artificial graft is anastomsed to an
artery, tunneled under the skin and anastomsed to
a vein. The graft can be used 2 weeks after
insertion.
 Complication include clotting, aneurysms and
infection.

526. Hemodialysis as a treatment for CRF must
be continued intermittently for the client’s
lifetime unless successful kidney
transplant is performed.
A typical schedule is 3 to 4 hours of
treatment 3 days per week.

527. The overall effect of hemodialysis are to-
 Clear waste products from the body.
 Restore fluid, electrolyte and acid base
balance.
 Reverse some of the untoward
manifestations of irreversible renal failure.

528. Excess fluid, potassium, urea nitrogen,
and acid ions are lost but only temporarily.
Nutritionally, CHO intolerance is usually
reduced.
Amino acid, protein, glucose and water
soluble vitamins are lost.
Anemia generally worsens because of
blood loss associated with the therapy.

529.  Renal osteodystrophy usually improves with
dialysis.
 Men who have maintenance dialysis often
have low testosterone levels and develop
gynecomastia, which is usually transient.
 The usual effect of hemodialysis on serum
concentration of medications is increased
clearance, which is therapeutic in case of
overdose.
 Dosage schedule are altered to prevent, as
much as possible.

530.  Complication of hemodialysis:-
 Hypotension may occur during the treatment
as fluid is removed. Nausea and vomiting,
diaphoresis, tachycardia, and dizziness are
common signs of hypotension.
 Painful muscle cramping occurs, usually
late in dialysis as fluid and electrolytes rapidly
leaves the extracellular spaces.
 Dysrhythmais may result from electrolyte
and pH changes or from removal of
antiarrhythmic medications during dialysis.

531.  Air embolism is rare but can occur if air
enters the patient’s vascular system.
 Chest pain may occur because of anaemia or
in patients with arteriosclerotic heart disease.
 Dialysis disequilibrium results from cerebral
fluid shifts. Manifestations include headache,
nausea and vomiting, restlessness,
decreased level of consciousness, or
seizures; it is more likely to occur in acute
renal failure or when BUN levels are very
high(exceeding 150 mg/dl).

532. Dialysis disequilibrium syndrome can
occur, particularly during the client’s first
few dialysis episodes.
 Rapid solute removal from the blood
probably causes a relative excess of
solutes interstitially and intracellularly ( an
osmotic gradient).
 The excess causes cerebral edema,
which leads to increased intracranial
pressure.

533. Many dialysis centers avoid this
complication by first time dialyzing
for shorter times at a reduced
blood flow rate.
It is characterized by
 mental confusion
 Deterioration of the level of
consciousness
 Headache and seizures.
 It may last for several days.

535.  Deficient fluid volume or excess fluid
volume related to impaired renal function,
fluid shifts between dialysate and blood and
blood loss during hemodialysis.
 Expected Outcome:- Neither a fluid volume
deficit nor an excess will occur, as evidenced by
the absence of edema or dehydration.
Monitor fluid volume status:-
o Monitor the client’s fluid status by observing
daily weights, orthostatic blood pressure, skin
turgor and mucous membrane moistness and
by meticulous intake and output comparisons.

536. Help the client understand that vomiting,
diarrhea, and working or playing in a hot
environment may cause excessive fluid
loss and must be prevented and
controlled.

537.  Follow fluid restriction:- Fluid restrictions
are difficult for most clients. Offer suggestions
about reducing thirst and moistening lips with
lip balms, frequent oral hygiene.
 Taking ice chips
 If intravenous fluids are used, carefully attend
to them to ensure proper administration rate.
 Water may be restricted so that the client can
drink more nutritious liquids , such as apple
juice, cranberry juice or milk.

538.  Monitor fluid status during
hemodialysis:-
 Carefully monitor the client’s vital
signs including postural B.P.
pulse, weight and intake and
output.
 Watch for hypovolemia and
retention of dialysate.
 If the client is undergoing
hemodialysis, hypotension and
excess fluid removal are risk;
monitor carefully.

539.  Nursing Diagnosis:- Risk of infection
related to venipuncture and connection of
tubing during hemodialysis.
 Expected Outcome:- The client will remain
free of infection, as evidenced by a normal
white cell count, absence of fever.
 Interventions:- Use strict aseptic technique
during venipuncture and when attaching
tubing.
 Assess the site for any redness, inflammation
and itching.

540. Hand washing should be done before
starting the procedure.
Check the WBCs count of the patient to
rule out any infection.
Use disposable tubing for every patient
and proper disposal of the tubing should
be done after the end of the procedure.

541.  Nursing Diagnosis:- Risk for injury related
to trauma to hemodialysis vascular access
site.
 Expected Outcome:- The client will not
experience injury to the vascular access site,
as evidenced by continued patency of the
site.
 Intervention:- Careful attention to the access
site-to prevent infection and clotting.
 A dressing is used to protect cannula and
subclavian catheters from infection.

542.  The access site must also be protected from
trauma that could cause clotting, bleeding or
physical disruption of the site. E.g. Warn the
client against wearing tight sleeves or
carrying purse over the access site.
 The limb that contains the access site should
not be used to take blood pressure or to draw
blood.
 Between dialysis periods, the skin over the
fistula or graft requires only routine care with
soap and water.

543.  The site of the fistula should be carefully
assessed.
 To assess the patency, palpate over the
fistula for a thrill and auscultate for bruit at
regular intervals.
 The client must also learn to assess the
access site for patency.
 Keep the access site clean at all times to
prevent infection.
 Avoid injections, intravenous (IV) needles or
fluids, or taking blood samples in the access
site arm.

544.  Advise patients to avoid wearing jewellery or
tight clothing, sleeping on, or lifting heavy
objects with the access arm.
 Check the temperature and colour of the
fingers and the pulse of the access arm for
adequate circulation.
 Check for signs of infection at the access site.
 Needle insertions for hemodialysis treatments
should be rotated so that one spot is not
repeatedly stuck and weakened.

545. Nursing Diagnosis:- Risk of complications
related to hemodialysis procedure.
 Expected Outcome:- The client will not show
any sign of complication in between the
hemodialysis.
 Intervention:- Technical problem such as
blood leaks, insufficient loss of fluid and
clotting should be avoided by carefully
monitoring during hemodialysis.
 The vital signs should be carefully monitored
during hemodialysis.

546. Rapid solute removal must be avoided.
Air embolism should be avoided while
attaching the tubing.
Continuous observe the patient for
hypotension and dysrhythmais because
this can occur because of removal of
antiarrhythmic medicines.
 Observe the patient for dialysis
equilibrium syndrome.

547. Nursing Diagnosis:- Risk for
compromised family and ineffective
individual coping related to chronic
illness, uncertain future for the client, role
reversal and effects of long term dialysis.
 Expected Outcome:- The client and family
will cope with the chronic illness and future
deterioration, as evidenced by acceptance of
the client’s problems and ability to support the
client.

548. Interventions:-
Involve in decision making:- Assistance for
the client and significant others must begin
before dialysis is started.
Provide Support:- Encourage the client
and significant others to discuss their
feelings and concerns, together and
individually, using therapeutic
communication techniques.

549.  The nurse assist the patient to identify effective
and safe coping strategies to deal with these ever
present problems and fears.
 Referring the patient and family to mental health
provider with specific expertise in care of patients
receiving dialysis may be helpful.
 Counseling and psychotherapy may be needed.
 The nurse need to convey a nonjudgmental
attitude to enable the patient and family to discuss
options and their feelings about these options.

550. Team conferences are helpful for sharing
the information and providing every team
member the opportunity to discuss the
need of the patient and family.

551. PERITONEAL
DIALYSIS

552.  Peritoneal Dialysis is the method of renal replacement
therapy used by approximately 120,000 patients
worldwide.
 Peritoneal dialysis provides approximately 10% of
normal kidney function. It does not reverse chronic
kidney disease or kidney failure.
 Since the introduction of Continuous Ambulatory
Peritoneal Dialysis (CAPD) almost three decades ago,
its popularity has increased greatly, mainly because of
its simplicity, convenience and relatively low cost.

553.  In essence, Peritoneal Dialysis involves the
transport of solutes and water across a
membrane that separates two fluid
containing compartments. These two
compartments are:
 The blood in peritoneal capillaries, which in
renal failure contains excess of urea,
creatinine and other solutes.

554.  The dialysis solution in the peritoneal cavity,
which typically contains sodium, chloride,
lactate or bicarbonate and which is
rendered hyper-osmolar by the inclusion of
high concentration of glucose.

555.  The Peritoneum is a serosal membrane that
lines the peritoneal cavity. It has a surface
area that is thoroughly to be approximately
equal to the body surface area and so
typically ranges from 1 to 2 m2 in an adult.
Divided into two:
 The Visceral Peritoneum, lines the gut and
other viscera.
 The Parietal Peritoneum, lines the walls of
abdominal cavity.

556.  The Visceral Peritoneum accounts for about
80% of the total peritoneal surface area and
receives its blood supply from the superior
mesentric artery, whereas its venous
drainage is via the portal system.
 Total peritoneal blood flow cannot be
measured but has been indirectly estimated
at between 50 and 100 ml per minute.

557.  The main lymphatic drainage of the
peritoneum and of the peritoneal cavity is
via large collecting ducts into the right
lymphatic duct. There is however, additional
drainage via lymphatics in both visceral and
peritoneal peritoneum.

558.  Peritoneal Dialysis involves 3 phases:
 Infusion
 Dwell
 Drain


559.  Infusion :A sterile, dialysis
solution flows into your peritoneal
cavity by gravity via a catheter or
tube that has been surgically
placed into the abdomen. The
filling takes about 10 minutes.
Once the filling is complete, the
catheter is shut so that it does
not leak.

560.  Dwell : The lining of the peritoneal cavity
called the peritoneum acts as a natural filter.
It lets the waste products and excess fluids
in the blood filter through into the dialysis
solution, while holding back important
substances that the body needs. The length
of time varies from 3 - 6 hours. While the
solution is in the body you can move about

561.  Drain : The dialysis solution
containing the wastes is drained
again by gravity from your body
through the catheter into an empty
bag. This takes about 10-20
minutes. A bag containing sterile
dialysis solution replaces the bag
containing waste products. The
whole process is then repeated.
Each of these replacements is
called a ' Bag Exchange'

562.  During the course of Peritoneal Dialysis
dwell, three transport processes occur
simultaneously:
 Diffusion
 Ultra filtration
 Absorption

563.  CAPD solutions are packed in the clear, flexible plastic
bags or less commonly in semi- rigid plastic containers.
 The bags are typically made from polyvinyl chloride
through theoretical concern about phthalic acid
leachates have led to bags of other composition being
developed.
 Some new PD solutions are packed with different
solution components in two (or three) chamber bags,
which are mixed before infusion into the peritoneal
cavity.

564.  For Adult patients, CAPD solutions are
available in the volumes of 1.5, 2.0, 2.25,
2.5 or 3.0, depending on the manufacturer.
 The commonly used bags are routinely
overfilled by 100 ml to allow for flushing.
 The standard volume prescribed has been
2L but 2.5L is also widely used.

565.  Generally, larger volumes are prescribed in
order to increase the solute clearance, but
they may not always be tolerated by smaller
patients because of symptoms induced by
increase in intra- peritoneal hydrostatic
pressure.

566.  The electrolyte concentration of CAPD
solution varies little by manufacturer.
 Solutions contain no potassium and
sodium levels are set at about 132 – 134
mM.
 Higher sodium concentrations would lead to
less diffusive removal of sodium during
dwells.

567.  Low sodium solutions have been proposed
as a means of augmenting sodium removal
but would likely lead to hyponatremia, as
well as requirement for more glucose to
maintain a given osmolarity.
 Up until recently, all commonly marketed
CAPD solutions contained lactate as the
bicarbonate generating base. Now
bicarbonate based PD solutions have
become available in most countries and are
increasingly used.

568.  Both pure bicarbonate solutions and
bicarbonate- lactate mixtures are available.
 The two compartment bag system is used to
keep the bicarbonate separate from the
calcium and magnesium until just before
use.
 Bicarbonate solutions have a normal pH
and so cause less discomfort on infusion
than lactate based solutions.

569.  They are believed to be theoretically more
biocompatible and it is hoped that they will
enhance peritoneal host defenses and
improve peritoneal membrane longevity and
even patient survival.
 To date, however, there is little evidence
that bicarbonate solutions improve long
term patient outcome.

570.  Dextrose (Glucose Monohydrate) is the
osmotic agent commonly used in CAPD
solutions, and preparations containing
1.5%, 2.5% and 4.25% dextrose solutions
are routinely available and are labeled as
such.

571.  Dextrose as an osmotic agent in PD has the
advantage of being familiar, relatively safe
and inexpensive and also a good source of
calories.
 There is concern however that it
predisposes patients to hyperglycemia,
dyslipidemia, obesity and long term
peritoneal membrane damage.

572.  Amino Acid based Solutions: They are used for
nutritional supplementation as they are largely absorbed
by the end of 4- 6 hour dwell.
 They are reasonably effective osmotically (compared to
1.5% dextrose solution) but can only be used once daily
because in larger amounts they tend to cause acidosis
as well as rise in blood urea.
 These side effects may have to be addressed with oral
alkali therapy and more dialysis respectively.

573.  Icodextrin: It is a poly glucose preparation
which is widely available in market.
 It is iso-osmotic solution which induces ultra
filtration by its Oncotic effect

574.  The pH of traditionally lactate based PD
solutions is lowered to about 5.5 to prevent
carmelization of glucose to minimize
generation of GDPs during heat sterilization.
 Lowering pH would further decrease GDP
but would cause infusion pain in patients.

575.  Three types of Peritoneal Dialysis are
present. These are:
 Continuous Ambulatory Peritoneal Dialysis
(CAPD).
 Continuous Cyclic Peritoneal Dialysis
(CCPD).
 Intermittent Peritoneal Dialysis (IPD).

576.  Continuous Ambulatory Peritoneal
Dialysis (CAPD):
 CAPD is the most common type of
peritoneal dialysis.
 It needs no machine.
 It can be done in any clean, well-lit place.
 The dialysate passes from a plastic bag
through the catheter and into abdomen of
the patient.

577.  The dialysate stays in the abdomen with the
catheter sealed.
 After several hours, patient drains the
solution back into the bag.
 Then refill the abdomen with fresh solution
through the same catheter.

578.  Now the cleaning process begins again.
 While the solution is in the body, patient
may fold the empty plastic bag and hide it
under the clothes, around the waist, or in a
pocket.
 Drainage of spent dialysate and inflow of
fresh dialysis solution are performed
manually, using gravity to move fluid into
and out of the peritoneal cavity.

579.  CAPD is a form of self treatment, needs no
machine and no partner.
 The Dwell time for CAPD is 4- 6 hours and
Drain time is usually 30 – 40 minutes and
generally needs 4 sessions a day with a
range of 3- 5 sessions depending upon the
requirement of the individual.

580.  CCPD is like CAPD except that a machine,
which connects patient to catheter,
automatically fills and drains the dialysate
from the abdomen or Peritoneal Cavity.
 The machine does this at night while the
patient sleeps.
 The treatment lasts for 10- 12 hours every
night.

581.  IPD uses the same type of machine as
CCPD to add and drain the dialysate.
 IPD can be done at home, but it’s usually
done in the hospital.
 IPD treatments take longer than CCPD.
 Treatments are done several times a week
for a total of 36- 42 hours per week.

582.  CAPD: Pros
 Can perform treatment alone.
 Can do it at times patient chooses.
 Can do it in many locations.
 No need of a machine.
 Cons
 It disrupts the daily schedule.

583.  CCPD
 Pros
 Can be performed at night, mainly while
patient sleeps.
 Cons
 Needs a machine and help from a partner.

584.  IPD
 Pros
 Health professionals usually perform treatments.
 Cons
 May need to go to a hospital.
 It takes a lot of time.
 Needs a machine.

585.  Complications include:
 Catheter site infections.
 Peritonitis.
 Bleeding at the catheter site.
 Electrolyte imbalance.
 Nausea and Vomiting.
 Respiratory Distress.

586.  Scarring of the lining of abdominal wall.
 Leaks in the lining of abdominal wall.
 Active Inflammatory Bowel Disease
(Crohn’s Disease or Ulcerative Colitis)

587.  May be able to have more salt and fluids.
 May eat more protein.
 May have different and liberal potassium
restrictions.
 Need to cut back on the number of calories
patient eats. This limitation is because the
sugar or dextrose in the dialysate may
induce weight gain.

588.  Fluid and electrolyte imbalance related to
dialysate exchange during Peritoneal
Dialysis.
 Knowledge deficit regarding procedure of
Peritoneal Dialysis, possible complications,
diet.
 Risk for complications like respiratory
distress, nausea and vomiting related to
infusion of large amount of dialysate.

590. Kidney transplantation is a surgical
procedure to remove a healthy, functioning
kidney from a living or brain-dead donor
and implant it into a patient with
nonfunctioning kidneys.

592.  Kidney failure occurs when the kidneys cannot
perform their normal tasks.
 When kidney function is less than 10 per cent,
 the kidneys cannot remove excess water, salt, or
wastes, and the body's tissues begin to swell.
 When wastes accumulate in the blood, people
become seriously ill. Blood pressure starts to rise
and, without medical help, kidney failure is life
threatening.

593. The most common diseases leading to kidney failure
include:
 glomerulonephritis
 diabetes
 polycystic kidney disease
 drug-induced kidney failure
 pylonephritis
 urinary tract obstruction
 high blood pressure

594.  congenital renal obstructive disorders leading to
hydronephrosis, including the following:
• ureteropelvic junction obstruction
• vesicoureteral reflux
• posterior urethral valves
• prune belly syndrome
• megaureter
 congenital nephrotic syndrome
 Alport syndrome
 nephropathic and juvenile cystinosis
 polycystic kidney disease
 nail-patella syndrome
 glomerulonephritis
 Berger disease
 hemolytic uremic syndrome
 Wegener granulomatosis
 Goodpasture syndrome

595. Patients who have chronic renal failure -
e.g. due to causes such as chronic
pyelonephritis, diabetes mellitus,
hypertension, polycystic kidneys, or
connective tissue disorders, are
maintained on dialysis until a suitable
donor kidney becomes available. .

596. Kidneys can be donated for transplant from
either:
 a cadaver (recently deceased donor), or
 a living related donor.
In both cases necessary conditions are that there
is:
 ABO Blood Group compatibility, and
 human leucocyte antigen (HLA) tissue-type
compatibility

597.  transplant surgeons - physicians who specialize
in transplantation and who will be performing the
surgery. The transplant surgeons coordinate all
team members.
 nephrologists - physicians who specialize in
disorders of the kidneys.
 urologists - physicians who specialize in
diagnosis and treatment of disorders of the
genitourinary tract.
 transplant nurse coordinator - a nurse who
organizes all aspects of care provided to your
child before and after the transplant.

598.  social workers -.
 dietitians - professionals who will help your child meet
his/her nutritional needs before and after the transplant.
 physical therapists - professionals who will help your
child become strong and independent with movement
and endurance after the transplantation.
 other team members - several other team members will
evaluate your child before transplantation and provide
follow-up care, as needed. These include, but are not
limited to, the following:
• pharmacists
• anesthesiologists
• hematologists
• infectious disease specialists
• respiratory therapists
• lab technicians
• psychologists

599.  Kidney transplantation involves surgically
attaching a functioning kidney, or graft, from a
brain-dead organ donor (a cadaver transplant) or
from a living donor, to a patient with ESRD.
 Living donors may be related or unrelated to the
patient, but a related donor has a better chance
of having a kidney that is a stronger biological
"match" for the patient.

600.  Nephrectomy
1. Open nephrectomy
2. Laproscopic nephrectomy
3. Modified laproscopic nephrectomy
 Tranplant surgery

601. The surgical procedure to remove a kidney
from a living donor is called a
nephrectomy.

602.  In a traditional, open nephrectomy, the kidney
donor is administered general anesthesia and a
6–10-in (15.2–25.4-cm) incision through several
layers of muscle is made on the side or front of
the abdomen at the costo vertebral angle
 The blood vessels connecting the kidney to the
donor are cut and clamped, and the ureter is
also cut and clamped between the bladder and
kidney.

604. The kidney and an attached section of
ureter are removed from the donor. The
vessels and ureter in the donor are then
tied off and the incision is sutured together
again.
A similar procedure is used to harvest
cadaver kidneys, although both kidneys
are typically removed at once, and blood
and cell samples for tissue typing are also
taken.

605.  Laparoscopic nephrectomy is a form of minimally
invasive surgery using instruments on long,
narrow rods to view, cut, and remove the donor
kidney.
 The surgeon views the kidney and surrounding
tissue with a flexible videoscope.
 The videoscope and surgical instruments are
maneuvered through four small incisions in the
abdomen, and carbon dioxide is pumped into the
abdominal cavity to inflate it for an improved
visualization of the kidney.
 .

606.  Once the kidney is freed, it is secured in a bag
and pulled through a fifth incision, approximately
3 in (7.6 cm) wide, in the front of the abdominal
wall below the navel.
 Although this surgical technique takes slightly
longer than an open nephrectomy, studies have
shown that it promotes a faster recovery time,
shorter hospital stays, and less postoperative
pain for kidney donors

607.  A modified laparoscopic technique called hand-
assisted laparoscopic nephrectomy may also be
used to remove the kidney. In the hand-assisted
surgery, a small incision of 3–5 in (7.6–12.7 cm)
is made in the patient's abdomen.
 The incision allows the surgeon to place his
hand in the abdominal cavity using a special
surgical glove that also maintains a seal for the
inflation of the abdominal cavity with carbon
dioxide.

608. The technique gives the surgeon the
benefit of using his or her hands to feel the
kidney and related structures. The kidney
is then removed through the incision by
hand instead of with a bag.

609. Once removed, kidneys from live donors
and cadavers are placed on ice and
flushed with a cold preservative solution.
The kidney can be preserved in this
solution for 24–48 hours until the
transplant takes place. The sooner the
transplant takes place after harvesting the
kidney, the better the chances are for
proper functioning.

610.  During the transplant operation, the kidney recipient is
typically under general anesthesia and administered
antibiotics to prevent possible infection.
 A catheter is placed in the bladder before surgery begins.
 An incision is made in the flank of the patient, and the
surgeon implants the kidney above the pelvic bone and
below the existing, non-functioning kidney by suturing the
kidney artery and vein to the patient's iliac artery and
vein.

611.  The ureter of the new kidney is attached directly
to the kidney recipient's bladder.
 Once the new kidney is attached, the patient's
existing, diseased kidneys may or may not be
removed, depending on the circumstances
surrounding the kidney failure.
 Barring any complications, the transplant
operation takes about three to four hours.

613. It includes
 blood tests
 diagnostic tests
 psychological and social evaluation of the child (if old
enough) and the family
 Tests are done to gather information
 These tests include those to analyze the general health
of the body, including the child's heart, lung, and kidney
function, the child's nutritional status, and the presence of
infection. Blood tests will help improve the chances that
the donor organ will not be rejected.

614.  Pretransplant tests, as well as giving a clear
picture of the patient's overall health status, help
in identifying potential problems before they
occur. They also help in determining whether
transplantation is truly the best option. This
increases the likelihood of success.
 Physical exam - Gives the doctor an overall
picture of the patient's conditions.

615.  Chest x-ray - Determines the health of the
patient's lungs and lower respiratory tract.
 Complete medical and surgical history -
Determines what additional tests may need to be
done.
 Electrocardiogram (EKG or ECG) - Determines
how well the patient's heart is working and may
reveal heart damage that was previously
unsuspected.
 Ultrasound with Doppler examination -
Determines the quality of the iliac vessels.

616.  Blood tests - The patient's blood count, blood and tissue
type, blood chemistries, and immune system function will all
be checked. In addition, blood tests for certain infectious
diseases will be performed.
 Blood typing - Every person is a blood type A, B, AB or O.
The donor's blood type does not have to be the same as the
recipient's blood type, but it must be "compatible“
 Pulmonary function test - The patient will be asked to
breathe into a tube attached to a measuring device, which will
reveal how well his lungs are working and determine his
blood's capacity to carry oxygen.
 Upper gastrointestinal (GI) series - This will show whether
the patient's esophagus and stomach are disease free.
 Lower GI series - Ensures that the patient is free of intestinal
abnormalities.
 Renal function studies - Urine may be collected from the
patient for 24 hours in order to determine if the kidneys are
working correctly. Blood tests such as serum creatinine are
also performed to measure kidney function.

617.  Tissue typing - This test is done on white blood
cells. White blood cells have special "markers" that
distinguish "tissue type", which are used to find a
matching kidney.
 Panel Reactive Antibody (PRA) - A way of
measuring immune system activity within the body.
PRA is higher when more antibodies are being
made. It is easier to acquire a kidney if a recipient's
immune system is calm or measures 0%. An
immune system may be active from blood
transfusion, pregnancy, a previous transplant or a
current infection.
 Viral testing - Determines if the patient has been
exposed to hepatitis, cytomegalovirus (CMV),
Epstein-Barr (EBV), or acquired immune deficiency
syndrome.
 Mammogram - X-ray of a woman's breast that can
detect signs of breast cancer.

618.  Pap smear - Cells collected from a woman's cervix
that are microscopically analyzed for signs of cancer.
 Echocardiogram - Reveals any abnormalities in the
heart.
 Dental Evaluations - You need to have a dental
check-up before you will be listed for transplant. Your
dentist must tell us that your teeth and gums are
healthy. You will also need to be checked by your
dentist every year while you are waiting for your
transplant.

 Other tests - Any special tests or doctor visits that
might be needed for the transplant workup.

619.  Crossmatch Testing - This test is done when a
donor kidney is available. Your blood is mixed
with the donor's blood. If there is no reaction
(negative crossmatch) it means you are
"compatible" with the donor. If there is a reaction
(positive crossmatch), the kidney will not work for
you because it is "incompatible".
 Other Tests - The transplant doctors will ask for
any special tests they think you will need. For
example, people with diabetes will need more
tests for their heart. Your transplant coordinator
or dialysis doctor can help you make
arrangements for these tests.


620. These tests may include:
 blood chemistries - these may include serum
creatinine, electrolytes (such as sodium and
potassium), cholesterol, and liver function tests.
 clotting studies, such as prothrombin time (PT)
and partial thromboplastin time (PTT) - tests that
measure the time it takes for blood to clot.
 function tests

621. They may include:
 blood type: Each person has a specific blood type:
type A+, A-, B+, B-, AB+, AB-, O+, or O-.
 human leukocyte antigens (HLA) and panel reactive
antibody (PRA): These tests help determine the
likelihood of success of an organ transplant by
checking the genetic types of recipients cells as well
as the antibodies in recipients blood.
 Antibodies in the bloodstream will try to attack
transplanted organs. Therefore, patients who receive a
transplant will take medications that decrease this
immune response. The higher PRA, the more likely
that an organ will be rejected.

622. kidney, liver, and other vital organ viral
studies: These tests determine if your child
has antibodies to viruses that may
increase the likelihood of rejecting the
donor organ, such as cytomegalovirus
(CMV).

623.  renal ultrasound
 kidney biopsy
 intravenous pyelogram (IVP) –
 The transplant team will consider all information
from interviews, patients medical history,
physical examination, and diagnostic tests in
determining whether patients can be a candidate
for kidney transplantation.
 After the evaluation and patient has been
accepted to have a kidney transplant

624. Graft survival is 80% one year after the procedure, and
60% 5 years after the procedure - according to 2001
UK statistics.
The relatively high overall success rate for kidney
transplants can be attributed to the following:
 The vascular connections are relatively simple
 It is possible to accept kidneys from live donors,
which enables very close blood matching between
donors and recipients.
 Partly due to above, there are fewer immuno-
supression-related problems (in which the body's
own immune system react against the new kidney)
than might otherwise be the case.


625.  the patient may receive an enema or a laxative to clean
out his intestines and prevent constipation after surgery.
 Hair from the chest and abdomen will be shaved to
prevent infection,
 and an intravenous (IV) line will be inserted in the arm or
just under the collarbone to give medication and prevent
dehydration.
 The patient will also be given a sedative to help him relax
and feel sleepy before going to the operating room.
 Body wash with betadine scrub
 Vital Signs checked and recorded
 Psychological support

626. The patient will be under general
anesthesia throughout the surgery. Once
asleep, the transplant surgeon will make
an incision on the right or left side of the
lower abdomen just above the groin.

627.  surgical team will then place the donor kidney
into the abdomen
 and connect the kidney's blood vessels to the
recipient's iliac artery and vein.
 The surgeons will then connect the ureter to the
bladder.
 A small drain, called a Jackson Pratt, may be
placed into the abdominal cavity to drain any
excess fluid.

628.  Some pain and discomfort, which medication will
help to relieve.
 The patient will be asked to cough periodically to
keep his lungs clear. If it hurts to cough, the patient
should ask someone to support his abdomen.
 The patient will have an IV line in his arm or neck
under the collarbone, which will be used to give
fluids and medication for the first few days after
surgery.

629.  For several days after surgery, the patient will have a
catheter in his bladder to drain urine. He may feel
uncomfortable, and may feel that he has to urinate
constantly, but it is only temporary.
 During surgery, one drain may be placed in or near
the incision. The drain will be removed 5 to 10 days
after surgery.
 Dialysis may still be needed to help clear excess fluid
and toxins in the body until the kidney recovers from
the procurement process.

631.  The most critical part of kidney transplantation is
preventing rejection of the graft kidney.
 Different transplant centers use different drug
combinations to fight rejection of a
transplanted kidney.
 The drugs work by suppressing your immune
system, which is programmed to reject
anything "foreign," such as a new organ.
 Like any medication, these drugs can have
unpleasant side effects.

632.  Some of the most common immune-suppressing
drugs used in transplantation are described
here.
Cyclosporine: This drug interferes with
communication between the T cells of the
immune system. It is started immediately after
the transplant to suppress your immune system
and continued indefinitely.

633. • Corticosteroids: These drugs block T-cell
communication as well. They are usually given at
high doses for a short period immediately after the
transplant and again if rejection is suspected.
Corticosteroids have many different side effects,
including easy bruising of the skin, osteoporosis,
avascular necrosis (bone death), high blood pressure,
high blood sugar, stomach ulcers, weight gain, acne,
mood swings, and a round face. Because of these side
effects, many transplant centers are trying to reduce
the maintenance dose of the drug as much as possible
or even to replace it with other drugs.

634. • Azathioprine: This drug slows the production of T cells
in the immune system. Azathioprine is usually used for
long-term maintenance of immunosuppression. The
most common side effects of this drug are suppression of
the bone marrow, which produces blood cells, and liver
damage. Many transplant centers are now using a newer
drug called mycophenolate mofetil instead of
azathioprine.
• Newer antirejection drugs include tacrolimus, sirolimus,
and mizoribin, among others. These drugs are now being
used to try to reduce side effects and to replace drugs
after episodes of rejection.
• Other costly and experimental treatments include using
antibodies to attack specific parts of the immune system
to decrease its response.