INTRODUCTION

Renal failure results when the kidneys cannot remove the body’s metabolic wastes or perform
their regulatory functions. The substances normally eliminated in the urine accumulate in the
body fluids as a result of impaired renal excretion, affecting endocrine and metabolic
functions as well as fluid, electrolyte and acid base disturbances. Renal failure is a systemic
disease and is a final common pathway of many different kidney and urinary tract diseases.
Each year the number of deaths from irreversible renal failure increases.

TOPIC

END STAGE RENAL DISEASE

DEFINITION

End-stage renal failure, also known as end-stage renal disease (ESRD), is the final,
permanent stage of chronic kidney disease, where kidney function has declined to the point
that the kidneys can no longer function on their own. A patient with end-stage renal failure
must receive dialysis or kidney transplantation in order to survive for more than a few weeks.

STAGES OF CHRONIC KIDNEY DISEASE: The stages of ESRD is classified based on

the glomerular filtration rate. According to the National Kidney Foundation ( United States)
the normal GFR range is 90 to 120 ml / min / 1.73 metre square.

Below shows the five stages of CKD and GFR for each stage:

 Stage 1 with normal or high GFR (GFR > 90 mL/min)

 Stage 2 Mild CKD (GFR = 60-89 mL/min)

 Stage 3A Moderate CKD (GFR = 45-59 mL/min)

 Stage 3B Moderate CKD (GFR = 30-44 mL/min)

 Stage 4 Severe CKD (GFR = 15-29 mL/min)

 Stage 5 End Stage CKD (GFR <15 mL/min)

ETIOLOGY
Diabetes is a leading and the most common cause of Chronic Kidney Disease. It is the
primary cause.

The secondary cause is hypertension, which is followed by:

 Glomerulonephritis
 Pyelonephritis
 Polycystic kidney disease

Heriditary and congenital disorders

 Alport syndrome
 Nephrophthisis
 Polycystic kidneys

Auto immune diseases

 Lupus
 IgA nephropathy

Obstructive uropathy

 Bilateral calculi
 Bilateral Pelviureteric Junction Obstruction Stenosis
 Posterior urethral valves

Renal cancers

MISCELLANEOUS CAUSES

 Renal vein thrombosis

 Renal cortical necrosis
 Renal tuberculosis
 Reflux nephropathy
PATHOPHYSIOLOGY
1. Damage of nephron result in hypertrophy and hyperplasia of remaining
nephron, leading to decreased function of nephron to excrete effectively.
2. Due to low renal perfusion renin-angiotensin system is activated and secretion
of aldosterone cause sodium and water retension. This leads to hypertension,
increased vascular volume, edema and heart failure.
3. There is potassium imbalance ( Hyperkalemia) due decreased renal excretion
of potassium, rapid administration of potassium and movement of potassium
from ICF compartment to ECF compartment. This occurs due to acidosis
when hydrogen ions enter the cells to buffer the pH of the ECF, the potassium
moves out of the cell.
4. As the nephrons fail to excrete effectively, the ends products of protein
metabolism ( normally excreted in urine) accumulate in blood. As a result the
blood urea nitrogen (BUN) and creatinine increase and uremia develops.
Uremia adversely affects every system in the body and results in skin
disorders, gastro-intestinal manifestations, neurologic manifestations, sexual
dysfunction and may also cause pericarditis. Uremia also contribute to blood
coagulopathies.
5. Disturbance in erythropoietin synthesis occurs and result in anaemia. Mild
hemolysis and bleeding ( coagulopathies due to uremia) also cause anaemia.
6. The kidneys fail to regulate the acid base balance due to decreased excretion
of metabolically produced acid and loss of bicarbonate ( HCO3). So there is
accumulation of non-volatile acids and cause metabolic acidosis.
7. Due to decreased GFR, there is decreased phosphate elimination and increase
in serum phosphate level ( hyperphosphatemia). This result in decreased
serum calcium level ( hypocalcemia). As a compensatory mechanism there is a
increased secretion of parathormone from parathyroid gland which causes
calcium resorption and calcium leaves bone and finally bone changes and
bone diseases like osteomalacia occurs.
8. The kidneys are responsible for the final conversion of the inactive Vit- D to
its active form i .e.1, 25 Dihydroxycholecalciferol. But in renal failure this
process is disturbed and thus causes renal rickets and osteodystrophy.
 9. Therefore overall renal failure leads to metabolic, endocrinal disturbances and
disturbances of internal homeostasis equilibrium.

PATHOPHYSIOLOGY OF CHRONIC KIDNEY DISEASE

SODIUM
POTASSIUM ELIMINATION ERYTHROPOIET ACID BASE ACTIVATION PHOSPHATE
AND
BALANCE OF IN BALANCE OF VITAMIN D ELIMINATIONN
WATER
BALANCE NITROGENOUS PRODUCTION
WASTE

HYPER
TENSI HYPERKALEMIA ANAEMIA SKELETAL
ON BUFFERING
HYPOCALCEMIA
COAGULOPATHIES
INCREASED EDEMA
VASCULAR
VOLUME BLEEDING ACIDOSIS
HYPERPARATHY
UREMIA
ROIDISM

HEART PERICA
FAILURE RDITIS

SEXUAL
IMPAIRED SKIN GASTROINT NEUROLOGIC DYSFU
IMMUNE DISORDERS ESTINAL MANIFESTATI NCTION OSTEODYSTROPHIES
FUNCTION MANIFESTA ONS
CLINICAL MANIFESTATION

The clinical manifestation are a result of retained substances including urea, creatinine,
electrolytes, hormones,and many other substances. Uremia is a syndrome that incorporates all
sign and symptoms seen in various systems throughout the body.

Ocular symptoms

 Hypertensive retinopathy

Neurologic

 Weakness and fatigue

 Headache
 Sleep disturbances
 Inability to concentrate
 Disorientation
 Tremors
 Confusion’
 Seizures
 Asterixis-hand flapping tremor
 Burning soles of feet
 Behaviour changes

Psychologic

 Denial
 Anxiety
 Depression
 Psychosis

Cardiovascular

 Hypertension
 Pitting edema ( feet, hands, sacrum)
 Periorbital edema
 Engorged neck veins
 Atherosclerotic heart disease
 Myocardiopathy
 Pericarditis
 Pericardial effusion
 Heart failure

Pulmonary

 Thick, tenacious sputum

  Crackles
 Depressed cough reflex
 Shortness of breath
 Tachypnea
 Kussmaul type respirations ( very deep respirations )
 Uremic pnemonitis
 Pulmonary edema

Gastrointestinal

 Ammonia odour to breath “uremic fetor”

 Metallic taste
 Anorexia, nausea and vomiting
 Mouth ulcerations and bleeding
 Hiccups
 Gastritis
 Peptic ulcer
 Constipation or diarrhoea
 Bleeding from gastro-intestinal tract
 Stomatitis

Hematologic

 Anaemia
 Thrombocytopenia
 Bleeding

Metabolic

 Carbohydrate intolerance
 Hyperlipidemia
 Nutritional deficiencies
 Gout

Reproductive

 Amenorrhea
 Decreased libido
 Sexual dysfunction
 Infertility/ azoospermia
 Testicular atrophy

Endocrine

 Hyperparathyroidism
 Thyroid abnormalities
Musculoskeletal

 Muscle cramps
 Loss of muscle strength
 Renal osteodystrophy
 Bone pain
 Bone fractures
 Foot drop

LABORATORY VALUES IN CHRONIC RENAL FAILURE

Specific gravity of urine: The specific gravity of urine remains low and fixed and is similar
to that of glomerular filtrate i.e. about 1.010. Normal specific gravity of urine is 1.020 to
1.030

Blood urea nitrogen: Serum creatinine and BUN increases. Serum creatinine is more
sensitive indicator of renal function than blood urea nitrogen, as BUN is affected not only by
renal disease but also by protein intake.

Elevated triglyceride: Hyperinsulinemia stimulates hepatic production of triglycerides.

Almost all patient with uremia develop hyperlipidemia, with elevated very low density
lipoproteins, normal or decreased low density lipoproteins (LDLs) and decreased high density
lipoproteins

Hyperkalemia: Hyperkalemia is due to decreased excretion of potassium from the kidneys

and excessive intake of potassium in diet, medicatios and fluids. When serum potassium level
reaches 7-8 m mol/ litre fatal dysrhythmias can occur. Normal K value is 3.5-5.5 m mol/ litre

Sodium: It may be normal or low in CRF. Normal Na value is 2.5-5.5 mg/dl

Hyperphosphatemia and hypocalcemia: Usually the phosphate level is raised and blood
calcium level decreases as calcium and phosphorus are inversely related. The normal range of
calcium is 4.5-5.5 m Eq/litre. Normal range of phosphate is 2.8 – 4.5 m Eq /litre.

Magnesium: Magnesium is primarily excreted by kidneys and hyper magnesemia is not a

problem. Normal range is from 1.3 – 2.1 m Eq / litre.

Decreased RBC count: The RBC count decreases due to inadequate erythropoietin
production and shortened life span of RBCs.

Plasma bicarbonate: The average adult produces 80-90 m Eq/ litre of acid per day. This acid
is normally buffered by bicarbonate. In renal failure plasma bicarbonate level, which is an
indirect measure of acidosis, usually falls to a new steady state of around 16-20 mEq / litre

Parathormone: Decreased serum calcium level causes increased secretion of parathormone

from parathyroid glands.
OTHER DIAGNOSTIC EVALUATION

Arterial blood gas analysis: ABG levels show low blood Ph. Low carbon dioxide and low
bicarbonate.

ECG changes: There is tall tented T waves and widened QRS which indicate hyperkalemia.

MEDICAL MANAGEMENT

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

Medical management is accomplished primarily with medication and diet therapy, although
dialysis may be needed to decrease the level of uremic waste imbalance.

Treatment is aimed to prevent complications which are as follows:

 HYPERKALEMIA: Hyperkalemia may provoke life threatening dysrhythmias. It is

prevented by ensuring adequate dialysis treatments with potassium removal and
careful monitoring of medications and fluids for their K- content. Sodium
polystyrene sulphonate ( Kayexalate) a cation- exchange resin, may be needed for
acute hyperkalemia.

 HYPERPHOSPHATEMIA AND HYPOCALCEMIA: It may cause renal osteodystrophy.

Phosphate intake is generally restricted to less than 100 mg / day, but dietary control
alone is usually inadequate. Calcium based phosphate binders such as calcium
carbonate ( os-cal) or calcium phosphate are prescribed which help to bind
phosphate in bowel and is then excreted in stool but there is a risk of hypercalcemia.
If calcium is high or the calcium phosphorus product exceed 55 mg/dl, a polymeric
phosphate binder such as sevelamer (Renagel) may be prescribed.

 Hypocalcemia is often a problem. Then serum phosphate level is lowered and

supplemental calcium is provided along with active form of vitamin D.

 HYPERTENSION: Treatment of hypertension includes:

1. Weight loss ( if obese )
2. Therapeutic lifestyle changes
3. Diet recommendations
4. Administration of antihypertensive drugs
5. It is recommended that target BP be less than 130/80 mm of Hg
 HEART FAILURE AND PULMONARY EDEMA: These conditions require low sodium
diets, diuretic agents, inotropic agents such as digoxin or dobutamine and dialysis.
  ANEMIA: The most important cause of anemia is decreased production of
erythropoietin due to the decrease in the number of functioning renal tubular cells.
Blood transfusions should be avoided unless the patient experiences an acute blood
loss or has symptomatic anaemia. Erythropoietin is administered intravenously or
subcutaneously three times a week in ESRD and it may take 2 to 6 weeks for the
hematocrit to increase. Supplemental iron, vitamin B 12 and folic acid are usually
administered as well.
 DYSLIPIDEMIA: Recommendations for patients with ESRD include a goal of low LDLs
below 100 mg/ dl ( 2.6 m mol/ litre) and maintaining a triglyceride level below 200
mg/dl (2.25 m mol/litre)
 NEUROLOGIC ABNORMALITIES: Neurologic disorders may occur so the patient must
be observed for early evidence of slight twitching, headache, delirium or seizure
activity. IV Diazepam or phenytoin is usually administered to control seizures. The
side rails of the bed should be raised and padded to protect the patient.

DIETARY MANAGEMENT
Dietary intervention is necessary with the deterioration of renal function and includes
careful regulation of protein intake (0.6 to 1.2 g/kg/day), fluid intake to balance fluid losses,
sodium intake to balance sodium losses, and some restriction of potassium. At the same
time, adequate caloric intake (36 K Cal/kg/day) and vitamin supplementation must be
ensured. Protein is restricted because urea, uric acid, and organic acids- the break down
products of dietary and tissue protein –accumulate rapidly in the blood when there is
impaired renal clearance. The allowed protein must be of high biological value ( dairy
products, eggs, meats).High biologic value protein are complete proteins and supply
essential amino acids for growth and repair. High calorie diet is adviced to prevent wasting.
Vitamin supplementation is necessary because protein restricted diet does not provide the
necessary complement of vitamins. Vit C recommended is 100 mg/day. Ca recommended
intake is 1000 – 1500 mg/kg/day.

Usually the fluid allowance per day is 500 ml to 600 ml more than the previous day’s 24
hour urine output.

Some foods with high potassium contents should be avoided eg. Oranges, bananas, melons,
tomatoes, prunes, deep green and yellow vegetables ,beans and legumes.

Foods containing high phosphorus content like yogurt, milk, cheese should be avoided.

RENAL REPLACEMENT THERAPIES

The main renal replacement therapies include the various types of dialysis and kidney
transplantation.
DIALYSIS Types of dialysis include hemodialysis and peritoneal dialysis .Dialysis is technique
in which substances move from the blood through a semi-permeable membrance into a
dialysis solution (dialysate) and to remove the waste products in renal failure.

Dialysis is begun when the patient’s uremia can no longer be adequately managed
.Generally dialysis is initiated when GFR or creatine clearance is less than 15ml/min. But this
criterion can vary in different clinical situation and the physician will determine when to
start dialysis based on the patients clinical status.

SURGICAL MANAGEMENT

A Patient with ESRD finally needs the treatment with kidney transplantation .During the past
40 years more than 400000 kidney transplantations have been performed world wide.

Kidney transplantation involves transplanting a kidney from a living donor or

deceased donor to a recipient who has no renal function. Transplantation from well
matched living donors who are related to patient (those with compatible ABO and human
leukocyte antigen) is slightly more successful than from cadaver donors.

For the donor kidney laboratory studies include 24 hour urine study for creatinine
clearance and total protein ,CBC and electrolyte profiles .Hepatitis B and C ,HIV and
cytomegalovirus are done to assess for the presence of any transmissible diseases.

The donor patient has to undergo ECG and chest X ray , renal ultrasound and renal
arteriogram or three dimensional CT are done to ensure that the blood vessels supplying
each kidney are adequate and there are no anomalies and to determine which kidney will
be removed.

Kidneys are removed and can be preserved up to 72 hours but most transplant
surgeons prefer to transplant kidneys before 24 hours of removal.

PREOPERATIVE MANAGEMENT

A complete physical examination is performed to detect any conditions that would cause
complications after transplantation.

The patient is evaluated for any infections including gingival (gum) disease and dental
carries

Diagnostic tests includes

i) Tissue typing

ii) Blood typing

iii) Antibody screening

iv) Study of lower urinary tract to assess bladder neck function and to detect urethral reflux,

If routine dialysis has been established hemodialysis is often performed the day before
transplantation to optimize the patients physical status.

A psychological evaluation is conducted to assess the patients ability to adjust to the

transplant copying styles, social history ,social support available and financial resources.

PREOPERATIVE NURSING MANAGEMENT

Patient teaching should address to post operative pulmonary hygiene ,pain management
options, dietary restrictions ,IV and arterial lines ,tubes and early ambulation .Patient may
be concerned about the donor and anxious about the outcome of surgery.

Helping the patients to deal with these concerns is part of the nurse’s role.

POST OPERATIVE MEDICAL MANAGEMENT

The goal of care is to maintain homeostasis until the transplanted kidney is functioning well.

After a kidney transplantation rejection and failure can occur within 24hours within 3 to 14
days or after many years .Since the body’s immune response views the transplanted kidney
as foreign it continually works to reject it to overcome or minimise the body’s defense
mechanism immunosuppressive agents are administered.

POST OPERATIVE NURSING MANAGEMENT

Nursing management includes:

1)Assessing the patient for transplant rejection by monitoring blood pressure ,weight
,assessing oliguria and edema ,fever ,swelling or tenderness over the transplanted kidney or
graft.

2) Preventing infection by maintaining aspetic technique during procedures such as

dressings, catheterization etc .Patient must be protected from exposure to infection by
hospital staff ,visitors and others patients with active infection .Attention to hand hygiene
and use of mask is important.

3) Monitoring urinary function

4) Addressing psychological concerns

5) Monitoring and managing potential complications e.g. gastro intestinal ulceration and
corticosteroid induced bleeding, fungal colonization e.g. GI tract and urinary bladder
secondary to corticosteroid and antibiotic therapy.

6) Teaching patients self care and

7) Continuing care

COLLABORATIVE CARE

Collaborative care for Chronic Renal Failure comprises of the following

1. Drug Therapy

2. Nutritional therapy

3. Dialysis and

4. Surgical intervention i.e kidney transplantation

5. Home and community based care

The patients must be provided with ongoing education. The patient must be taught how
to check the vascular access device for patency and appropriate precautions such as
avoiding venipuncture and blood pressure measurements.

The patients and family need to know what problems to report to the health care provider
,These include the following

1) Worsening signs and symptoms of renal failure (nausea vomiting ,change in usual urine
output ,ammonia odour on breath.)

2) signs and symptoms of hyperkalemia(muscle weakness,diarrhoea,abdominal cramps)

3) signs and symptoms of access problems (clotted fistula or graft ,infection)

NURSING ASSESSMENT

HISTORY TAKING
The nurse should obtain a complete history of existing renal disease in family .History of
diabetes mellitus, hypertension ,drug history ,diet history educational status and
occupational history. History of past illness and treatments ,dialysis etc.

PHYSICAL EXAMINATION

Nurse must perform thorough physical examination including vital signs, cardiovascular
,pulmonary ,GI, neurologic ,dermatologic and muscutoskeletal systems.

DATA ANALYSIS

Laboratory values (serum electrolyte, BUN, creatinine, protein, transferrin and iron
levels)must be assessed.

Blood glucose levels ,RBC count ,ECG changes ,bold pressure and weight recordings must be
assessed.

NURSING DIAGNOSIS

1)Excess fluid volume related to decreased urine output ,dietary excesses and retention of
sodium and water.

GOAL-Maintenance of ideal body weight without excess fluid

NURSING INTERVENTION RATIONALE

1.Assess fluid status by: Assessment provides baseline and ongoing

a)Daily weight checking database for monitoring changes and
b)Intake and output balance evaluating interventions.
c)Observing distension of neck veins
d)Monitoring blood pressure ,pulse rate
and rhythmn
e)Respiratory rate and effort

2.Limit fluid intake to prescribed volume To prevent fluid overload.

3. Explain to patient and family rationale Understanding promotes patient and

for fluid restriction. family cooperation with fluid restriction.

4.Administer diuretics as prescribed

2)Imbalance nutrition less than body requirements related to anorexia ,nausea and
vomiting ,dietary restrictions and altered oral mucous membranes

GOAL: Maintenance of adequate nutritional intake.

NURSING INTERVENTION RATIONALE

1.Assess nutritional status by monitoring Gives baseline data for monitoring changes
weight changes and laboratory values. and evaluating effectiveness of intervention.

2.Assess the patients diet history and food Past and present dietary patterns are
preferences . considered in planning meals.

3.Assess for anorexia, nausea ,vomiting, To promote adequate dietary intake by

depression, stomatitis and lack of elimination of problems related to feeding.
understanding of dietary restrictions.

4.Provide patients food preferences within Increased dietary intake is encouraged.

dietary restrictions.
Complete proteins are provided for positive
5.Promote intake of high biologic value nitrogen balance needed growth and
protein foods, eggs, dairy products, meat. healing.

6.Encourage high calorie ,low protein, low Reduce source of restricted foods and
sodium and low potassium snacks between proteins and provides calories for energy
meals ,sparing protein for tissue growth and
healing.

7.Provide pleasant surroundings at meal Unpleasant factors that contribute to

times patients anorexia are eliminated.
3)Activity intolerance related to fatigue ,anemia, retention of waste products and dialysis
procedure.

GOAL-Participation in activity within tolerance.

NURSING INTERVENTION RATIONALE

1)Assess factors contributing to activity Indicates factors contributing to severity of
intolerance fatigue
a)fatigue b) anemia c)fluid and electrolyte
imbalances d)Retention of waste products
e)Depression
2)Promote independence in self care Promotes improved self esteem
activities as tolerated assist if fatigued
3)Encourage alternating activity with rest Promotes activity and exercise within limits
4)Encourage patient to rest after dialysis and adequate rest.
treatments

4)Impaired skin integrity related to uremic frost and changes in oil and sweat glands

GOAL-Skin will remain intact and patient will feel comfortable

NURSING INTERVENTIONS

1.Keep the skin clean while relieving itching and dryness .Use soap such as basis soup

2.Add bath oil to bath water to maintain moisture and softness

3.Apply prescribed ointments or creams to relieve itching

4.Keep the patients nail short and trimmed to prevent excoriation

5.Keep hair clean and moisturised.

6.Administer prescribed antihistamines for relief of itching.

5)Constipation related to fluid restrictions and ingestion of phosphate binding agents

GOAL-Patient will be relieved of constipation

NURSING INTERVENTIONS

1.Be aware that phosphate binders cause constipation that cannot be managed with usual
interventions.

2.Encourage high fiber diet, bearing in mind the potassium content of some fruits and
vegetables .

3.Use stool softners as prescribed and use of commercial fiber supplements may be done.

4.Avoid laxatives and cathartics that cause electrolyte toxicities (compound containing
magnesium or phosphorous.

5.Increase activity of the client as tolerated.

6)Risk of injury while ambulating related to potential fractures and muscle cramps due to
calcium deficiency

GOAL-Patient will be ensured a safe level of activity.

NURSING INTERVENTION

1)Inspect patients gait,range of motion and muscle strength .

2)Monitor serum calcium and phosphate levels watch for hypocalcemia or hypercalcemia
and treat if needed.

3)Administer analgesics as ordered and provide massage for severe muscle cramps.

4)Monitor x rays and bone scan results for fractures bone demineralization and joint
deposits.

5)Calcium supplements to be given between meals to increase serum calcium.

6)Vit D supplemented to increase absorption and utilization of calcium.

7)Increase activity as tolerated avoid immobilisation because it increases bone

demineralization.

7)Knowledge deficit regarding conditions and treatment.

GOAL-Increased knowledge about condition and related treatment.

NURSING INTERVENTION

1.Provide explanation of renal function and consequences of renal failure at patients level of
understanding and guided by patients readiness to learn.

2.Provide oral and written information as appropriate about

a)Renal function and failure.

b)Fluid and dietary restrictions

c)Medications

d)Reportable problems sign and symptoms

e)Follow up schedule

f)Community resources and

g)Treatment options

POTENTIAL NURSING PROBLEMS

1.Hyperkalemia due to decreased excretion ,metabolism, acidosis, catabolism and excessive

intake(diet, medications ,fluids)

2. Pericarditis pericardial effusion and pericardial tamponade due to retention of uremic

waste products and inadequate dialysis.

3.Hypertension due to sodium and water retention and malfunction of the renin angiotensin
aldosterone system.

4.Anemia due to decreased erythropoietin production, decreased RBC lifespan ,bleeding in

the GI tract from irritating toxins and ulcer formation and blood loss during hemodialysis.

5.Bone disease and metastatic and vascular calcifications due to retention of phosphorous
low serum calcium levels ,abnormal vit D metabolism and elevated aluminium levels.

PROGNOSIS
The prognosis of the ESRD depends upon the conservative management provided to the
patient including dialysis and the availability and success of kidney transplantation.

Kidney transplantation was first done in 1954 in Boston between identical twins .Kidney
transplantation is extremely successful with 1 year graft of about 90% for deceased donor
transplants and 95% for live donor transplants.

A patient has already sustained enough kidney damage when he had moved into the fifth
stage of CKD therefore appropriate conservative therapy with renal transplantation can

prolong the life .Otherwise the outcome of the disease is seen usually poor.

BIBLIOGRAPHY

1)Suzzane C Smeltzer etal ;Brunner and Suddharths Text Book of medical surgical
Nursing ;Wolters Kluwer Publication ;Fourth Indian Reprint 2012.Pg no 1325 to 1333 ,Pg no
1351 to 1354

2)Chintamani,Lewis Medical Surgical Nursing .Elsevier Reprint ,2011,Pg No 1207 to 1215 .Pg
no 1223-1226

3)Prof PV Ramachandran ,etal ;Lippincott Manual of Nursing Practice;9 th Edition;Wolters

Kluwen India Pvt Ltd Ch21;pg no 804 to 806

4)Anne Waugh .Allison Grant;Ross and Wilson Anatomy and Physiology in Health and Illness
Elsevier reprint 2005;Ch13pg no 354