CHRONIC RENAL FAILURE

INTRODUCTION As a part of my advance practice of nursing clinical posting I was posted in Medical intensive care unit of SGRD 13/08/2012 to 18/08/2012. During this period I came across Mrs. Mary Agnes with the diagnosis chronic Renal Failure. I took this case for nursing Care Study.

BASELINE DATA

Name Age Sex I. P. No D.O.A Marital Status Religion Nationality Education Occupation Personal Address Treating Physician Service/Ward Provisional Diagnosis

: : : : : : : : : : : : : :

Mrs. Mary Agnes 58 years female 211715 07/08/2012 Married Christian Indian 8th Standard Housewife AMRITSAR Dr. SOURAV Medical Intensive Care Unit Chronic Renal Failure Stage V On Hemodialysis

INVESTIGATION

DATE

INVESTIGATION DONE

REPORTED REFERENCE VALUE 10.6mg/dl VALUE 12-16mg/dl

INFERANCE

07/08/2012 07/08/2012 07/08/2012 07/08/2012 07/08/2012 07/08/2012 07/08/2012 08/08/2012 08/08/2012 08/08/2012 08/08/2012 08/08/2012

Haemoglobin Differential count neutrophil lymphocyte Eosinophil Monocyte basophil ESR Random Blood sugar pH Pco2 Po2

Anaemia

90% 8% 1% 1% 0% 97mm/hr 164mg/dl 7.385 35.4 mm/hg 91.9 mmol/L

40-74% 20-40% 1-9% 0-3% 0% 0-9mm/hr 80-120mg/dl 7.34-7.45 35-45mm/hg 75-100mmol/l

Increased Decreased Normal Normal Normal Infection Hyperglycemia Normal Normal Normal

08/08/2012

Hco3

20.7 mmol/L

22-26mmol/L

Normal

08/08/2012

Tco2

18.0 mmol/L

21-27mmol/L

decreased

09/08/2012

Serum creatinine

2.22 mmol/L

0.50.9mmol/L

Increased

09/08/2012 09/08/2012 09/08/2012

sodium potassium choride

131meq/l 2.98meq/l 91.5meq/l

133-145meq/L Normal 3.5-5.3 meq/L 98-106 meq/L Hypokalemia hypocalcemia

DATE: 09/08/2012 ARTERIAL BLOOD GAS ANALYSIS

3

Sl.no 1

PH PCO2

7.385 35.4

M:7.35-7.44 35-45

F:7.35-7.45 32-42mm of Hg

2 3 4 5

PO2 HCO3 TCO2 BEB

91.9 20.7 18.0 -3.6

75-100 22-26 23-27 -24-2.3

75-100 20-24mmol/L 21-25mmol/L -3.3 1.2mmol/L

6 7

SBC %SO2

21.4 96.8%

22-26 95-98%

22-26mmol/L 95-98%

11/08/2008 ECHOCARDIAOGRAPHY IMPRESSION: SMALL PERICARDIAL EFFUSION DIAGNOSIS: CHRONIC RENAL FAILURE STAGE V

MEDICATIONS DRUG DOSAGE FREQUENCY ACTION INDICATION SIDE EFFECTS NURSING CONSIDERATION TAB. Zostrum 1g 1-0-1 Third generation Cephalosporin. Treatment of respiratory tract infections; Intraabdominal infection; Urinary tract infections; Septicemia; Bone
Hypersensitivity reactions, -Monitor PT and INR rash, skin reactions, fever, regularly. eosinophillia, urticaria, & prutitis. slight Hematological decreases in

The

drugs

chemical structure has the methylthiotetrazole

hemoglobin concentration side chain that may cause and hemoglobin level. GI bleeding effects Diarrhea or loose Vitamin Hepatic-mild, transient

disorder. K promptly bleeding

and joint infections; stools, nausea, vomiting, reverses Gynecological infections. disorders.
elevation of SGOT, SGPT, and alkaline phosphates

-Tell patient to report adverse reactions.

concentrations.

Renal effects Transient -Instruct patient to report at I.V. elevation in BUN and discomfort serum creatinine insertion site.

concentration.
5

Tab Amlog

10mg

1-0-0

Antianginal

Chronic stable angina, vasospastic angina, Hypertension.

CNS:Headache, somnolence, fatigue, dizziness,light headedness, parasthesia. CV:Edema, flushing, palpitations. GI:Nausea, abdominal pain. GU:Sexual difficulties. Musculoskeletal: Muscle pain. Respiratory:

*Use

cautiously

in

patients receiving other peripheral vasodilators, especially those with severe aortic stenosis, and in those with heart failure. Because drug

is metabolized by the liver, use cautiously

and in reduced dosage in patient with severe hepatic disease. * ALERT: Monitor

patient carefully. Some patients

especially those with

Dyspnea.

severe

obstructive

coronary artery disease, have developed increased frequency, duration, or severity of angina or acute MI after initiation of calcium channel

blocker therapy or a time of dosage increase. *Monitor blood pressure frequently initiation Because of during therapy.

drug induced has a acute

vasodilation gradual

onset,

hypotension is rare. *Notify prescriber if

signs of heart failure occur, such as swelling of hands and feet or

7

shortness of breath. *Caution continue

*Tell

patient taking

to drug,

even when feeling better. patient sublingual

nitroglycerine may be taken as needed when angina symptoms are acute. If patient continues nitrate

therapy during adjustment

of amlodipine dosage, urge compliance. continued

Tab. Catapress

150mg

1-1-1

Antihypertensive Essential and renal Dry

mouth, -Use patient

cautiously with

in

hypertension, severe drowsiness, cancer pain that is dizziness, unresponsive epidural or to headache, spinal constipation,

severe

coronary insufficiency, recent cerebrovascular MI,

opiate analgesia or impotence, vivid disease. other more dreams, urinary -Drug may be given to dry, lower blood pressure in some

conventional methods retention; of analgesia.

itching, burning rapidly

sensation in the hypertensive eye; fluid or emergencies. -Monitor blood

electrolyte imbalance,

GI pressure and pulse rate Dosage is to

upset, orthostatic frequently. hypotension, weakness, sedation, usually

adjusted

patients blood pressure & tolerance.

pruritis, myalgia, -Elderly patient may be

urticaria, nausea, more insomnia, arrhythmias, agitation.

sensitive

than

younger ones to drugs hypotensive effect. -Observe tolerance therapeutic which may patient to for drugs effects, require

increased dosage -Alert:When stopping therapy in patients receiving both clonidine and a betablocker, gradually withdraw betablocker minimize reactions. -Do not stop drug first the to

adverse

10

before surgery. -Instruct patient to take drug exactly as

prescribed. -Advise patient that

stopping drug abruptly may cause high severe blood

rebound pressure.

Tell him

dosage must be reduced gradually over 2 to 4 days as instructed by prescriber. -Tell patient to take the last immediately bedtime. -Caution patient that dosage before

11

drug

may

cause

drowsiness but that this adverse effect will

usually diminish over 4 to 6 weeks. -Inform patient that

dizziness upon standing up can be minimized by rising slowly from a sitting or lying position and avoiding sudden position change. Tab. Losar 50mg 1-0-0 Antihypertensive Management of hypertension. Headache, dizziness, pain, - Treatment with I.V back pantoprozole should be myalgia, stopped when P.O form tract is warranted. - Drugs can be given without regard to

respiratory disorders,

asthenia/fatigue,

12

first

dose meals.

hypotension; rash, -Instruct patient to take angioedema; disturbances; GI exactly as prescribed & at about the same time Inform

transient elevation everyday.

or liver enzymes; patient that tab. Should taste disturbances be swallowed whole and hypokalemia. and not crushed, split, Predictably cough or chewed. has not as been -Tell patient that a antacids dont affect drug pantaprazole

reported specific

related events in absorption. any of the losartin study trials. Headache, irritability, weakness, - Use cautiously,

if at all, if patient takes cardiac

glycosides or has sarcoidosis or

13

rebound hyperacidity, nausea, constipation, flatulenc

renal or cardiac disease. - Record amount

and consistency of Manage constipation with laxatives or stool softeners. - Monitor calcium levels, especially in patient with mild impairment. Watch for evidence of hypercalcemia (nausea, vomiting, confusion, headache, and renal stools.

14

anorexia. Tab. Calcit 0.25mg 0-1-0 Vitamin derivative D3 Hypocalcaemia in patient under long term dialysis Anorexia, nausea, -Use vomiting, patients cautiously in

receiving

diarrhea, lastitude, cardiac glycosides and polyurea, in those with or

Hypoparathyriodis sweating, m headache,

sarcoidosis thirst, hyperparathyroidism.

Pseudoparathyriod and vertigo. ism -To manage secondary hyperparathyroidis m and resulting metabolic bone disease in predialysis patients (moderate to severe chronic

-Monitor calcium level; multiplied phosphate level, by it

should not exceed 70. during determine level Stop twice and adjustment, calcium weekly. notify if

prescriber

hypocalcaemia occurs, but resume after returns

15

renal failure with creatinine clearance of 15 to 55ml/minute).

to normal. should

Patient receive

adequate daily intake of calcium. Observe for bone

hypocalcaemia, pain, before therapy. -Vitamin intoxication and and

weakness during

D causes

various adverse effects, including headache,

somnolence, weakness, irritability, hypertension, arrhythmias, conjunctivitis, photophobia,

16

rhinorrhea,

nausea,

vomiting, constipation, polydipsia, Pancreatitis, taste, anorexia, nephrocalcinocic, polyuria, nocturia, dry metallic mouth,

weight loss, bone and muscle pain, pruritus, hyperthermia, decrease libido. - Tell patient to report early symptoms of and

vitamin D intoxication. - Instruct patient to adhere calcium to diet and

17

supplementations, and to avoid unapproved OTC drugs and

magnesium containing antacids. -Alert Tell patient that drug mustnt be taken by anyone for whom it was not prescribed. Its the most potent form of vitamin D available.

18

Tab Fefol -Z

0-0-1

Dried Ferrous -Iron deficiency Sulphate

Nausea, epigastric -Use cautiously on long pain, vomiting, term basis. upset may be

constipation, black -GI stools, anorexia.

diarrhea, related to dose. -Between meals doses are preferable. Drug

can be given with some foods, absorption decreased. -Enteric products coated reduce GI although may be

upset but also reduces amount absorbed. -Alert Oral iron may stain stools black. this of iron

Although

19

unabsorbed

iron

is

harmless, it could mask malena. -Monitor hemoglobin, hematocrit, reticulocyte during therapy. -Iron overload uptake may of and count

decrease

technetium 99m and thus interfere with

skeletal imaging. -Tell patient to take tablets preferably with juice or water, but not with milk or antacids. Alert inform patient

that as few as 3 to 4

20

tablets

can

cause

serious iron poisoning in children. -Caution patient not to substitute one iron salt with another because amount of elemental iron vary. -Advise patient to

report constipation and change in stool color or consistency.

21

ANATOMY AND PHYSIOLOGY OF KIDNEYS

One of the most complex, beautifully engineered organs of the human body, the kidneys perform several essential tasks including the excretion of waste products, the maintenance of homeostatic balance in the body and the release of important hormones. To achieve this, human kidneys have a highly developed, superbly refined anatomy and physiology. The urinary system helps maintain homeostasis by regulating water balance and by removing harmful substances from the blood. The blood is filtered by two kidneys, which produce urine, a fluid containing toxic substances and waste products. From each kidney, the urine flows through a tube, the ureter, to the urinary bladder, where it is stored until it is expelled from the body through another tube, the urethra.

Location and Basic Structure of the Kidneys

The kidneys are located near the vertebral column at the small of the back; the left kidney lying a little higher than the right. Each is identical in structure and function. They are bean-shaped, about 10 cm long and 6.5 cm wide. Each kidney comprises an outer cortex and an inner medulla. The kidney is supplied with oxygenated blood via the renal artery and drained of deoxygenated blood by the renal vein. In addition, urine produced by the kidney as part of its excretory function, drains out via narrow tubules and the ureter, in turn connected to the bladder. The kidneys are surrounded by three layers of tissue: The renal fascia is a thin, outer layer of fibrous connective tissue that surrounds each kidney (and the attached adrenal gland) and fastens it to surrounding structures.

22

 The adipose capsule is a middle layer of adipose (fat) tissue that cushions the kidneys. The renal capsule is an inner fibrous membrane that prevents the entrance of infections.

Inside the kidney, three major regions are distinguished, as The renal cortex borders the convex side. The renal medulla lies adjacent to the renal cortex. It consists of striated, coneshaped regions called renal pyramids (medullary pyramids), whose peaks, called renal papillae, face inward. The unstriated regions between the renal pyramids are called renal columns. The renal sinus is a cavity that lies adjacent to the renal medulla. The other side of the renal sinus, bordering the concave surface of the kidney, opens to the outside through the renal hilus. The ureter, nerves, and blood and lymphatic vessels enter the kidney on the concave surface through the renal hilus. The renal sinus houses the renal pelvis, a funnel-shaped structure that merges with the ureter.

Blood and nerve supply

Because the major function of the kidneys is to filter the blood, a rich blood supply is delivered by the large renal arteries. The renal artery for each kidney enters the renal hilus and successively branches into segmental arteries and then into interlobar arteries, which pass between the renal pyramids toward the
23

renal cortex. The interlobar arteries then branch into the arcuate arteries, which curve as they pass along the junction of the renal medulla and cortex. Branches of the arcuate arteries, called interlobular arteries, penetrate the renal cortex, where they again, where they again branch into afferent arterioles, which enter the filtering mechanisms, or glomeruli, of the nephrons.

figure 1. (a) The urinary system, (b) the kidney, (c) cortical nephron, and (d) juxtamedullary nephron of the kidneys.

24

Blood leaving the nephrons exits the kidney through veins that trace the same path, in reverse, as the arteries that delivered the blood. Interlobular, arcuate, interlobar, and segmental veins successively merge and exit as a single renal vein.

Autonomic nerves from the renal plexus follow the renal artery into the kidney through the renal hilus. The nerve fibers follow the branching pattern of the renal artery and serve as vasomotor fibers that regulate blood volume. Sympathetic fibers constrict arterioles (decreasing urine output), while less numerous parasympathetic fibers dilate arterioles (increasing urine output).

The Nephron

The main functional unit of the kidney is the nephron. There are approximately one million nephrons per kidney. The role of nephrons is to make urine by: Filtering blood of small molecules and ions such as water, salt, glucose and other solutes including urea. Large macromolecules like proteins are untouched. Recycling the required quantities of useful solutes which then re-enter the bloodstream. (A process called reabsorption) Allowing surplus or waste molecules/ions to flow from the tubules/ureter as urine.

25

Filtration and Reabsorption in the Kidneys

During progress through the nephron, some solutes like sodium chloride, potassium and glucose are reabsorbed, along with water, back into the bloodstream. This maintains a correct balance of these chemicals within the blood, assisting blood pressure regulation, for example. The filtration and reabsorption of glucose within the kidneys also helps to maintain correct levels of vital blood sugars. When this regulation breaks down very serious health consequences can follow.

Urea and uric acid are nitrogen containing waste products from metabolic processes in the body. These substances are potentially toxic and are partially excreted by the kidneys to maintain good health. Interestingly, of the filtrate which enters each nephron from the blood, only about 1% actually leaves the body as urine because of the various reabsorption mechanisms driven by osmosis, diffusion, and active transport.

26

Tubular Secretion in the Kidneys

Another, less familiar, mechanism for urine production in the kidneys is tubular secretion. Specialized cells move solutes directly from the blood into the tubular fluid. For example, hydrogen and potassium ions are secreted directly into the tubular fluid. This process is coupled or balanced by the re -uptake of sodium ions back into the blood. Tubular secretion of hydrogen ions, augmented by control of bicarbonate levels, is important in maintaining correct blood pH. When the blood is too acidic (acidosis) more hydrogen ions are secreted. If the blood becomes too alkaline (alkalosis),

27

hydrogen secretion is reduced. In maintaining blood pH within normal limits (about 7.357.45)

The Kidney as an Endocrine Gland

In addition to its excretory and homeostatic roles, the kidneys also release two important hormones into the blood. These are: Erythropoietin which acts on bone marrow to increase the production of red blood cells Calcitriol which promotes the absorption of calcium from food in the intestine and acts directly on bones to shift calcium into the bloodstream. Finally the kidney produces the enzyme renin, an important regulator of blood pressure.

28

29

30

INTRODUCTION Renal Failure Renal failure results when the kidneys cannot remove the bodys 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, leading to a disruption in 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 (U.S. Renal Data System, 2001). Chronic renal failure (CRF) is the progressive loss of kidney function. The kidneys attempt to compensate for renal damage by hyper-filtration (excessive straining of the blood) within the remaining functional nephrons (filtering units that consist of a glomerulus and corresponding tubule). Over time, hyper-filtration causes further loss of function. Chronic loss of function causes generalized wasting (shrinking in size) and progressive scarring within all parts of the kidneys. In time, overall scarring obscures the site of the initial damage. Yet, it is not until over 70% of the normal combined function of both kidneys is lost that most patients begin to experience symptoms of kidney failure. Chronic renal failure, or ESRD, is a progressive, irreversible deterioration in renal function in which the bodys 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). The incidence of ESRD has increased by almost 8% per year for the past 5 years, with more than 300,000 patients being treated in the United States
31

(USRDS, 2001). ESRD may be caused by systemic diseases, such as diabetes mellitus (leading cause); hypertension; chronic glomerulonephritis; pyelonephritis; obstruction of the urinary tract; hereditary lesions, as in polycystic kidney disease; vascular disorders; infections; medications; or toxic agents. Autosomal dominant polycystic kidney disease accounts for 8% to 10% of cases of ESRD in the United States and Europe (Perrone, Ruthazer & Terrin, 2001). Comorbid conditions that develop during chronic renal insufficiency contribute to the high morbidity and mortality among patients with ESRD (Kausz et al., 2001). Environmental and occupational agents that have been implicated in chronic renal failure include lead, cadmium, mercury, and chromium. Dialysis or kidney transplantation eventually becomes necessary for patient survival. Dialysis is an effective means of correcting metabolic toxicities at any age, although the mortality rate in infants and young children is greater than adults in the presence of other, nonrenal diseases and in the presence of anuria or oliguria (Wood et al., 2001).

DEFINITION Chronic renal failure, or ESRD, is a progressive, irreversible deterioration in renal function in which the bodys 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). The incidence of ESRD has increased by almost 8% per year for the past 5 years, with more than 300,000 patients being treated in the United States Types Chronic renal failure (CRF) can be classified by the site (location) of primary damage:

Pre-renal CRF Post-renal CRF (obstructive uropathy)

32

Renal CRF

The cause for CRF sometimes can be determined by a detailed medical history, a comprehensive physical examination, and laboratory studies. More often than not, determining the cause of CRF is difficult if not impossible. Even a kidney biopsy may be inconclusive, because all forms of kidney failure eventually progress to diffuse scarring and look the same on kidney biopsy. The most common causes for CRF are diabetes and high blood pressure (hypertension.) Kidney disorders, including chronic renal failure, are common in patients who have multiple myeloma (cancer that begins in a type of white blood cell called plasma cells). Several different factors are related to renal disease associated with multiple myeloma. Myeloma cells produce large numbers of proteins in the urine (called proteinuria). These proteins often form deposits in the kidneys (condition called amyloidosis) and cause kidney failure. In addition, multiple myeloma increases the risk for hypercalcemia (high levels of calcium in the blood) and anemia (low levels of red blood cells) and results in high blood levels of uric acid, which also increase the risk for chronic renal failure. Pre-Renal CRF Some medical conditions cause continuous hypoperfusion (low blood flow) of the kidneys, leading to kidney atrophy (shrinking), loss of nephron function, and chronic renal failure (CRF). These conditions include poor cardiac function, chronic liver failure, and atherosclerosis ("hardening") of the renal arteries. Each of these conditions can induce ischemic nephropathy. Post-Renal CRF Interference with the normal flow of urine can produce backpressure within the kidneys, can damage nephrons, and lead to obstructive uropathy, a disease of the

33

urinary tract. Abnormalities that may hamper urine flow and cause post-renal CRF include the following:

Bladder outlet obstruction due to an enlarged prostate gland or bladder stone

Neurogenic bladder, an overdistended bladder caused by impaired communicator nerve fibers from the bladder to the spinal cord

Kidney stones in both ureters, the tubes that pass urine from each kidney to the bladder

Obstruction of the tubules, the end channels of the renal nephrons Retroperitoneal fibrosis, the formation of fiber like tissue behind the peritoneum, the membrane that lines the abdominal cavity

Vesicoureteral reflux (VUR), the backward flow of urine from the bladder into a ureter

PATHOPHYSIOLOGY

As renal function declines, the end products of protein metabolism (which are normally excreted in urine) accumulate in the blood. Uremia develops and adversely affects every system in the body. The greater the build-up of waste products, the more severe the symptoms. There are three well-recognized stages of chronic renal disease: reduced renal reserve, renal insufficiency, and ESRD. STAGE 1 Reduced renal reserve, characterized by a 40% to 75% loss of nephron function. The patient usually does not have symptoms because the remaining nephrons are able to carry out the normal functions of the kidney. STAGE 2 Renal insufficiency occurs when 75% to 90% of nephron function is lost. At this point, the serum creatinine and blood urea nitrogen rise, the kidney loses its ability to concentrate urine and anemia develops. The patient may report polyuria and nocturia
34

STAGE 3 End-stage renal disease (ESRD), the final stage of chronic renal failure, occurs when there is less than 10% nephron function remaining. All of the normal regulatory, excretory, and hormonal functions of the kidney are severely impaired. ESRD is evidenced by elevated creatinine and blood urea nitrogen levels as well as electrolyte imbalances. Once the patient reaches this point, dialysis is usually indicated. Many of the symptoms of uremia are reversible with dialysis. The rate of decline in renal function and progression of chronic renal failure is related to the underlying disorder, the urinary excretion of protein, and the presence of hypertension. The disease tends to progress more rapidly in patients who excrete significant amounts of protein or have elevated blood pressure than in those without these conditions.

CLINICAL MANIFESTATIONS Chronic renal failure (CRF) usually produces symptoms when renal function which is measured as the glomerular filtration rate (GFR) falls below 30 milliliters per minute (< 30 mL/min). This is approximately 30% of the normal value. When the glomerular filtration rate (GFR) slows to below 30 mL/min, signs of uremia (high blood level of protein by-products, such as urea) may become noticeable. When the GFR falls below 15 mL/min most people become increasingly symptomatic. Uremic symptoms can affect every organ system, most noticeably the following:

Neurological systemcognitive impairment, personality change, asterixis (motor disturbance that affects groups of muscles), seizures (rare)

35

Gastrointestinal systemnausea, vomiting, food distaste (often described as bland, metallic, "like cardboard") Blood-forming systemanemia due to erythropoietin deficiency, easy bruising and bleeding due to abnormal platelets Pulmonary systemfluid in the lungs, with breathing difficulties Cardiovascular system chest pain due to inflammation of the sac surrounding the heart (Pericarditis) and pericardial effusion (fluid accumulation around the heart) Skin generalized itching COMPARISION PICTURE OF THE CLINICAL MANIFESTATIONS BOOK PICTURE Anuria Cognitive Impairment Personality Changes Breathing Difficulty Nausea Bleeding Pericarditis Generalized Itching PATIENT PICTURE Present Present Absent Present Present Absent Absent Absent

36

DIAGNOSTIC EVALUATION Blood tests Creatinine and urea (BUN) in the blood: Blood urea nitrogen and serum creatinine are the most commonly used blood tests to screen for, and monitor renal disease. Creatinine is a breakdown product of normal muscle breakdown. Urea is the waste product of breakdown of protein. The level of these substances rises in the blood as kidney function worsens. Estimated GFR (eGFR): Physician may calculate an estimated GFR using the information from blood work. It is important to be aware of estimated GFR and stage of chronic kidney disease. Physician uses stage of kidney disease to recommend additional testing and suggestions on management. Electrolyte levels and acid-base balance: Kidney dysfunction causes imbalances in electrolytes, especially potassium, phosphorus, and calcium. High potassium (hyperkalemia) is a particular concern. The acid-base balance of the blood is usually disrupted as well. Decreased production of the active form of vitamin D can cause low levels of calcium in the blood. Inability to excrete phosphorus by failing kidneys causes its levels in the blood to rise. Testicular or ovarian hormone levels may also be abnormal. Blood cell counts: Because kidney disease disrupts blood cell production and shortens the survival of red cells, the red blood cell count and haemoglobin may be low (anaemia). Some patients may also have iron deficiency due to blood loss in their gastrointestinal system. Other nutritional deficiencies may also impair the production of red cells.
37

Other tests Ultrasound: Ultrasound is often used in the diagnosis of kidney disease. In general, kidneys are shrunken in size in chronic kidney disease, although they may be normal or even large in size in cases caused by adult polycystic kidney disease, diabetic nephropathy, and amyloidosis. Ultrasound may also be used to diagnose the presence of urinary obstruction, kidney stones and also to assess the blood flow into the kidneys. Biopsy: A sample of the kidney tissue (biopsy) is sometimes required in cases in which the cause of the kidney disease is unclear.

38

MEDICAL MANAGEMENT Once CRF has been diagnosed, the physician attempts to determine the cause and, if possible, plan a specific treatment. Nonspecific treatments are implemented to delay or possibly arrest the progressive loss of kidney function.

Control hypertension (high blood pressure)Target systolic blood pressure (BP) is 120 to 135 mm Hg; target diastolic BP is 70 to 80 mm Hg. Antihypertensive medication from the Angiotensin Converting Enzyme class is preferable because of protective effects on the kidneys. Restrict dietary proteinDietary protein is broken down into amino acids and absorbed from the stomach into the blood. The amino acids are taken from the bloodstream and used to build muscle and perform other essential functions. Excess amino acids are further broken down into carbohydrates and nitrogen-containing waste that is eliminated by the kidneys. Amino acid disposal further burdens the kidneys, and is believed to speed the progression of CRF. This process is like forcing a damaged machine to work harder, causing it to break down sooner than expected. Affected patients must be cautious not to overdo protein restriction, because it can lead to malnutrition and muscle wasting. Moderate protein restriction for a CRF patient is about 0.6 to 0.8 gm/kg/day, which is effectively achieved by following the advice of a dietician. Manage pre-end-stage renal disease (pre-ESRD)Treatment for pre- endstage renal disease (ESRD) should begin once the glomerular filtration rate (GFR) falls below 30 millilitres per minute (< 30 mL/min). Pre-ESRD management includes the identification and treatment of anaemia (low red blood cell count). When the GFR drops below 30 mL/min, anaemia often develops because the kidneys produce an inadequate amount of
39

erythropoietin (EPO). This hormone is made by the kidneys and travels to the bone marrow, where it stimulates red blood cell production. Anaemic patients are candidates for EPO (Procrit) injections to maintain their haematocrit (volume percent of red blood cells in whole blood) between 30% and 36%. Identify and Treat Secondary Hyperparathyroidismwith the loss of kidney function, phosphate accumulates in the blood. Excess phosphate in the blood reduces levels of blood calcium, and low blood calcium levels trigger the parathyroid gland (located in the neck) to release more parathyroid hormone (PTH). Parathyroid hormone (PTH) then dissolves bone tissue to release stored calcium and raise the level of calcium in the blood. This chronic cycle of events is called secondary hyperthyroidism.

The net result of this condition is the development of metabolic bone disease (renal osteodystrophy). These patients are at risk for bone fractures, bone and muscle pain, which can sometimes be accompanied by severe itching, and cardiovascular complications. Severe itching is thought to be in part due to the elevated circulating PTH level itself.

Patients with secondary hyperthyroidism should limit their intake of foods that are high in phosphate (e.g., dairy products, colas). Many patients must take medication with meals that binds the phosphate (phosphate-binders) and prevents it from being absorbed into the blood and allows it to be excreted in the stool (faeces). In general, calcium based salts (e.g., TUMS, Oscal) have been the phosphate-binders prescribed. A new organic based phosphatebinder called renagel has recently become available and, although it is more expensive, it has many advantages over the calcium based phosphate-binders.

40

Most patients also require a potent vitamin D supplement (e.g., calcitrol, hexitrol), which helps to suppress excess Parathyroid hormone (PTH) production. The final metabolic step in the synthesis of vitamin D occurs normally in the kidney and there is often a deficiency of this vitamin in these patients. Cinacalcet hydrochloride (e.g., Sensipar) may be used alone or in combination with Vitamin D supplements or phosphate-binders to treat patients with secondary hyperparathyroidism who are on dialysis. Sensipar tablets should be taken with food and the dosage varies, depending on calcium and phosphate levels in the blood. Side effects include nausea, vomiting, and diarrhoea.

Antiseizure Agents. Neurologic abnormalities may occur, so the patient must be observed for early evidence of slight twitching ,headache, delirium, or seizure activity. If seizures occur, the onset of the seizure is recorded along with the type, duration, and general effect on the patient. The physician is notified immediately. Intravenous diazepam (Valium) or phenytoin (Dilantin) is usually administered to control seizures. The side rails of the bed should be padded to protect the patient.

Erythropoietin. Anaemia associated with chronic renal failure is treated with recombinant human erythropoietin (Epogen). Anaemic patients (hematocrit less than 30%) present with nonspecific symptoms, such as malaise, general fatigability, and decreased activity tolerance. Epogen therapy is initiated to achieve a haematocrit of 33% to 38%, which generally alleviates the symptoms of anaemia. Epogen is administered either intravenously or subcutaneously three times a week. It may take 2 to 6 weeks for the haematocrit to rise; therefore, Epogen is not indicated for patients who need immediate correction of severe anaemia. Adverse effects seen with Epogen therapy include hypertension (especially during early stages of treatment), increased clotting of vascular access sites, seizures, and depletion of body
41

iron stores (Fink et al., 2001) The patient receiving Epogen may experience influenza-like symptoms with initiation of therapy; these tend to subside with repeated doses. Management involves adjustment of heparin to prevent clotting of the dialysis lines during haemodialysis treatments, frequent monitoring of hematocrit, and periodic assessment of serum iron and transferrin levels. Because adequate stores of iron are necessary for an adequate response to erythropoietin, supplementary iron may be prescribed. In addition, the patients blood pressure and serum potassium level are monitored to detect hypertension and rising serum potassium levels, which may occur with therapy and the increasing RBC mass. The occurrence of hypertension requires initiation or adjustment of the patients

antihypertensive therapy. Hypertension that cannot be controlled is a contraindication to recombinant erythropoietin therapy. Patients who have received Epogen have reported decreased levels of fatigue, an increased feeling of well-being, better tolerance of dialysis, higher energy levels, and improved exercise tolerance. Additionally, this therapy has decreased the need for transfusion and its associated risks, including blood borne infectious disease, antibody formation, and iron overload (Fink et al., 2001). OTHER THERAPY: DIALYSIS Hyperkalemia is usually prevented by ensuring adequate dialysis treatments with potassium removal and careful monitoring of all medications, both oral and intravenous, for their potassium content. The patient is placed on a potassiumrestricted diet. Occasionally, Kayexalate, a cation-exchange resin, administered orally, may be needed. The patient with increasing symptoms of chronic renal failure is referred to a dialysis and transplantation center early in the course of progressive renal disease. Dialysis is usually initiated when the patient cannot maintain a reasonable lifestyle with conservative treatment

42

SURGICAL MANAGEMENT Kidney Transplantation Kidney transplantation involves transplanting a kidney from a living donor or human cadaver to a recipient who has ESRD. Kidney transplants from wellmatched living donors who are related to the patient (those with compatible ABO and HLA antigens) are slightly more successful than those from cadaver donors. The success rate increases if kidney transplantation from a living donor is performed before dialysis is initiated (Mange, Joffe & Feldman, 2001). Due to the overwhelming numbers of persons on kidney transplant waiting lists, new techniques for matching nonrelated living donors are being developed (Gridelli & Remuzzi, 2000). COMPLICATIONS Potential complications of chronic renal failure that concern the nurse and that necessitate a collaborative approach to care include the following: Hyperkalemia due to decreased excretion, metabolic acidosis, catabolism, and excessive intake (diet, medications, fluids) Pericarditis, pericardial effusion, and pericardial tamponade due to retention of uremic waste products and inadequate dialysis Hypertension due to sodium and water retention and malfunction of the renin angiotensinaldosterone system Anemia due to decreased erythropoietin production, decreased RBC life span, bleeding in the GI tract from irritating toxins, and blood loss during hemodialysis Bone disease and metastatic calcifications due to retention of phosphorus, low serum calcium levels, abnormal vitamin D metabolism, and elevated aluminum levels.

43

NURSING MANAGEMENT The patient with chronic renal failure requires astute nursing care to avoid the complications of reduced renal function and the stresses and anxieties of dealing with a life-threatening illness. Examples of potential nursing diagnoses for these patients include the following: Excess fluid volume related to decreased urine output, dietary excesses, and retention of sodium and water Imbalanced nutrition: less than body requirements related to anorexia, nausea and vomiting, dietary restrictions, and altered oral mucous membranes Deficient knowledge regarding condition and treatment regimen Activity intolerance related to fatigue, anemia, retention of waste products, and dialysis procedure Low self-esteem related to dependency, role changes, changes in body image, and sexual dysfunction

Nursing care is directed toward assessing fluid status and identifying potential sources of imbalance, implementing a dietary program to ensure proper nutritional intake within the limits of the treatment regimen, and promoting positive feelings by encouraging increased self-care and greater independence. It is extremely important to provide explanations and information to the patient and family concerning ESRD, treatment options, and potential complications. A great deal of emotional support is needed by the patient and family because of the numerous changes experienced.

44

NURSING DIAGNOSIS

1. Excess fluid volume related to decreased urine output, dietary excesses, and retention of sodium and water 1. Assess fluid status: a. Daily weight b. Intake and output balance c. Skin turgor and presence of edema d. Distention of neck veins e. Blood pressure, pulse rate, and rhythm f. Respiratory rate and effort 2. Limit fluid intake to prescribed volume. 3. Identify potential sources of fluid: a. Medications and fluids used to take medications: oral and intravenous b. Foods 4. Explain to patient and family rationale for restriction. 5. Assist patient to cope with the discomforts resulting from fluid restriction. 6. Provide or encourage frequent oral hygiene.

2. Imbalanced nutrition; less than body requirements related to anorexia, nausea, vomiting, dietary restrictions and altered oral mucous membranes. 1. Assess nutritional status: a. Weight changes b. Laboratory values (serum electrolyte, BUN, creatinine, protein, transferrin, and iron levels) 2. Assess patients nutritional dietary patterns: a. Diet history b. Food preferences
45

c. Calorie counts 3. Assess for factors contributing to altered nutritional intake: a. Anorexia, nausea, or vomiting b. Diet unpalatable to patient c. Depression d. Lack of understanding of dietary restrictions e. Stomatitis 4. Provide patients food preferences within dietary restrictions. 5. Promote intake of high biologic value protein foods: eggs, dairy products, meats. 6. Encourage high-calorie, low-protein, low-sodium, and low-potassium snacks between meals. 7. Alter schedule of medications so that they are not given immediately before meals. 8. Explain rationale for dietary restrictions and relationship to kidney disease and increased urea and creatinine levels. 9. Provide written lists of foods allowed and suggestions for improving their taste without use of sodium or potassium. 10. Provide pleasant surroundings at meal-times. 11. Weigh patient daily. 12. Assess for evidence of inadequate protein intake: a. Edema formation b. Delayed healing c. Decreased serum albumin levels

3. Deficient knowledge regarding condition and treatment. 1. Assess understanding of cause of renal failure, consequences of renal failure, and its treatment: a. Cause of patients renal failure b. Meaning of renal failure c. Understanding of renal function
46

d. Relationship of fluid and dietary restrictions to renal failure e. Rationale for treatment (hemodialysis, peritoneal dialysis, transplantation) 2. Provide explanation of renal function and consequences of renal failure at patients level of understanding and guided by patients readiness to learn. 3. Assist patient to identify ways to incorporate changes related to illness and its treatment into lifestyle. 4. Provide oral and written information as appropriate about: a. Renal function and failure b. Fluid and dietary restrictions c. Medications d. Reportable problems, signs, and symptoms e. Follow-up schedule f. Community resources g. Treatment options

4. Activity intolerance related to fatigue, anemia, retention of waste products, and dialysis procedure 1. Assess factors contributing to fatigue: a. Anemia b. Fluid and electrolyte imbalances c. Retention of waste products d. Depression 2. Promote independence in self-care activities as tolerated; assist if fatigued. 3. Encourage alternating activity with rest. 4. Encourage patient to rest after dialysis treatments.

5. Disturbed self-esteem related to dependency, role changes, change in body image, and change in sexual function 1. Assess patients and familys responses and reactions to illness and treatment.
47

2. Assess relationship of patient and significant family members. 3. Assess usual coping patterns of patient and family members. 4. Encourage open discussion of concerns about changes produced by disease and treatment: a. Role changes b. Changes in lifestyle c. Changes in occupation d. Sexual changes e. Dependence on health care team 5. Explore alternate ways of sexual expression other than sexual intercourse. 6. Discuss role of giving and receiving love, warmth, and affection.

PROMOTING HOME AND COMMUNITY-BASED CARE

Teaching Patients Self-Care. The nurse plays an extremely important role in teaching the patient with ESRD. Because of the extensive teaching needed, the home care nurse, dialysis nurse, and nurse in the outpatient setting all provide ongoing education and reinforcement while monitoring the patients progress and compliance with the treatment regimen. A nutritional referral and explanations of nutritional needs are helpful because of the numerous dietary changes required. The patient is taught how to check the vascular access device for patency and how to take precautions, such as avoiding venipuncture and blood pressure measurements on the arm with the access device. Additionally, the patient and family require considerable assistance and support in dealing with the need for dialysis and its long-term implications. For instance, they need to know what problems to report to the health care provider, including the following: Worsening signs and symptoms of renal failure (nausea, vomiting, change in usual urine output [if any], ammonia odor on breath)
48

 Signs and symptoms of hyperkalemia (muscle weakness, diarrhea, abdominal cramps) Signs and symptoms of access problems (clotted fistula or graft, infection) These signs and symptoms of decreasing renal function, in addition to increasing BUN and serum creatinine levels, may indicate a need to alter the dialysis prescription. The dialysis nurses also provide ongoing education and support at each treatment visit.

CONTINUING CARE. The importance of follow-up examinations and treatment is stressed to the patient and family because of changing physical status, renal function, and dialysis requirements. Referral for home care provides the home care nurse with the opportunity to assess the patients environment, emotional status, and the coping strat egies used by the patient and family to deal with the changes in family roles often associated with chronic illness. The home care nurse also assesses the patient for further deterioration of renal function and signs and symptoms of complications resulting from the primary renal disorder, the resulting renal failure, and effects of treatment strategies (eg, dialysis, medications, dietary restrictions). Many patients need ongoing education and reinforcement on the multiple dietary restrictions required, including fluid, sodium, potassium, and protein restriction. Reminders about the need for health promotion activities and Health screening is an important part of nursing care for the patient with renal failure.

GERONTOLOGIC CONSIDERATIONS Changes in kidney function with normal aging increase the susceptibility of elderly patients to kidney dysfunction and renal failure. Because alterations in renal blood flow, glomerular filtration, and renal clearance increase the risk for medicationassociated changes in renal function, precautions are indicated with all medications.

49

This is because of the frequent use of multiple prescriptions and over-the-counter medications by elderly patients. The incidence of systemic diseases, such as atherosclerosis, hypertension, heart failure, diabetes, and cancer, increases with advancing age, predisposing older adults to renal disease associated with these disorders. Therefore, nurses in all settings need to be alert for signs and symptoms of renal dysfunction in elderly patients. With age, the kidney is less able to respond to acute fluid and electrolyte changes. Therefore, acute problems need to be prevented if possible or recognized and treated quickly to avoid kidney damage. When the elderly patient must undergo extensive diagnostic tests, or when new medications (e.g., diuretic agents) are added, precautions must be taken to prevent dehydration, which can compromise marginal renal function and lead to ARF. The elderly patient may develop atypical and nonspecific signs and symptoms of disturbed renal function and fluid and electrolyte imbalances. Recognition of these problems is further hampered by their association with preexisting disorders and the misconception that they are normal changes of aging.

CHRONIC RENAL FAILURE IN OLDER ADULTS Historically, the age of patients developing ESRD steadily rose each year, but it appears to have stabilized since 1993 at a mean age of 60 years. In the past, rapidly progressive glomerulonephritis, membranous glomerulonephritis, and nephronsclerosis were the most common causes of chronic renal failure in the elderly. Today, however, diabetes mellitus and hypertension are the leading causes of chronic renal failure in the elderly (Bakris et al., 2000). Other common causes of chronic renal failure in the elderly population are interstitial nephritis and urinary tract obstruction. The signs and symptoms of renal disease in the elderly are commonly nonspecific. The occurrence of symptoms of other disorders (heart failure, dementia) can mask the symptoms of renal disease and delay or prevent diagnosis and treatment. The patient often develops signs and symptoms of nephrotic syndrome, such as edema and proteinuria. Hemodialysis and peritoneal dialysis have been used effectively in
50

treating elderly patients (Carey et al., 2001). Although there is no specific age limitation for renal transplantation, concomitant disorders (ie, coronary artery disease, peripheral vascular disease) have made it a less common treatment for the elderly The outcome, however, is comparable to that of younger patients. Some elderly patients elect not to participate in these treatment strategies. Conservative management, including nutritional therapy, fluid control, and medications, such as phosphate binders, may be considered in patients who are not suitable for or elect not to participate in dialysis or transplantation.

HEALTH EDUCATION 1. Explain the nature of chronic renal failure. 2. Explain the medical regimen and its rationale, including diet (restricted protein, sodium, and potassium intake), restricted fluid intake, and medications (purposes, dosage, interval, and adverse reactions). 3. Teach the patient self-observational skills (temperature, pulse, respirations, blood pressure, intake, and output and weight) and record keeping. 4. Explain avoidance of infection. 5. Explain personal hygiene, rest, and exercise. 6. Explain when to call the physician. 7. Explain the plan for medical follow-up. 8. Explain renal dialysis and transplantation. The term chronic renal failure applies to the process of continuing significant irreversible reduction in nephron number, and typically corresponds to CKD stages 3 5. The dispiriting term end-stage renal disease represents a stage of CKD where the accumulation of toxins, fluid, and electrolytes normally excreted by the kidneys results in the uremic syndrome. This syndrome leads to death unless the toxins are removed by renal replacement therapy, using dialysis or kidney transplantation

51

REFERENCES SECTION A : ELECTRONIC SOURCES

http://www.ncbi.nlm.nih.gov/pubmed/22822091. Accessed august 24, 2012 http://chronicrenalfailure.medscape.com/Medscape/chronicrenal failure/ClinicalMgmt/CM.v02/public/index.CM.v02.html. Accessed august 23, 2012.

SECTION B: BOOK REFERENCES

Sandra M.N. Lippincott manual of nursing practice. Philadelphia, J B Lippincott Company;2006:760-765 Toni S. Renal Nursing. Philadelphia, Baillere Tindall;1997:383-445 Seidel H. M, Ball W J, Dains J E, benedict G W. guide to physical examination. Baltimore, mosby year book Inc;1991:413-420 Black m j, hawks j h. medical surgical nusing: clinical management for positive outcomes.missouri, Elsevier Inc ;2005: 963-978 Stephen J, Mcphee, Maxine A. Papadakis, Lawrence M. Tierney. Current Medical Diagnosis & Treatment, 47th (2008) Mcgraw-Hill Companies, U.S.A. Tanago A Emil. Smiths General Urology, 17th edition, Lange publications. Mc cauhan Young Satacy. Lewis text book of medical surgical nursing 10 th edition, Page Marilynn E. Doenges, Mary F. Jeffries, Mary Frances Moorhouse Nursing care plans 2nd Edition, F.A. Davis company 1915 Arch street Philadelphia, USA. Page No.556-566. Amy M. Karch Nursing Drug Guide 2002, J.B. Lippincot Company, Philadelphia,USA. Suzane C. Smeltzer, Brenda G. Bare T.B. of Medical Surgical Nursing 9th Edition, Lippincot Publishing Company, Philadelphia, U.S.A
52

NURSING PROCESS

NURSING ASSESSMENT

IDENTIFIED NEEDS AND PROBLEMS OF THE PATIENT Loss of consciousness since 3 days Decreased cardiac output since 3 days Anuria due to decreased renal function since 1 week Generalised edema and ascites due to retention of fluid since 2 days Nutritional impairment due to dietary restrictions

NURSING DIAGNOSIS Ineffective airway clearance related to decreased cough reflex as evidenced by increased secretions in chest Impaired breathing pattern related to loss of consciousness secondary to cardiac and renal dysfunction as evidenced by presence of ventilator support for respiration Impaired cardiac output related to fluid overload secondary to compromised renal function Fluid volume excess related to decreased renal function as evidenced by generalised body edema and ascites Imbalanced nutritional status, less than body requirement related to decreased intake secondary to dietary restrictions to reduce nitrogenous waste products Impaired bladder elimination, anuria, related to renal dysfunction as evidenced by absence of urinary elimination

53

 Impaired family coping related to sudden hospitalization as evidenced by verbalization of relatives Knowledge deficit of family members regarding chronic renal failure and its management High risk for infection related to compromised immune system High risk for injury related to unconscious state

54

HEALTH EDUCATION NATURE OF THE DISEASE:

I explained the nature and progression of chronic renal failure to Mrs. Mary Agnes and her family members, I explained the associated problems and complications she may develop and the reason behind it. I also told them about the home care of the patient after discharge

SIGNS AND SYMPTOMS OF COMPLICATIONS:

I explained to Mrs. Mary Agnes and her family members regarding the importance of monitoring for the signs and symptoms of complications like cardiac problems, anaemia etc. I also taught her and her care givers self- observational skills like monitoring temperature, pulse, respirations, blood pressure, intake and output and proper record keeping.

DIET:

I explained to Mrs. Mary Agnes and her family members renal the diet for chronic renal failure, I explained the importance of fluid and salt restrictions, and to ensure protein and vitamin intake in order to prevent complications, I taught them how to measure intake and output and also proper recording of the dietary status. I explained to them regarding monitoring for edema and neck vein distension in case of fluid overload.

HEMODIALYSIS I explained to Mrs. Mary Agnes and her family members regarding the need for hemodialysis and the regime of hemodialysis, I explained the process of dialysis and the prepeparation for the procedure and after care at home
55

EXERCISE: I explained to Mrs. Mary Agnes and her family members the need fo mild exercise and for monitoring activity tolerance. I taught her breathing and coughing exercises and range of motion exercises. Redemonstration was taken.

MEDICATION: I explained to Mrs. Mary Agnes and her family members regarding the importance of taking medications and the action of each medication, its dose, route, frequency and also the signs of adverse drug reactions

REST AND SLEEP I explained to Mrs. Mary Agnes and her family members to ensure at least 7-8 hours of sleep every day and also rest periods in between. I advised her to avoid strenuous activities

FOLLOW-UP: I explained to Mrs. Mary Agnes and her family members the importance of doing follow-up, I explained the need for doing repeated blood tests especially the blood electrolyte levels in order to monitor for and prevent the complications. PROGNOSIS OF THE PATIENT Date Patient condition

14/08/2012 patient on ventilator support in SIMV mode, GCS score-3/15, on haemodialysis. 15/08/2012 Patient on ventilator support in SIMV mode, GCS improved to 5/15 16/08/2012 Patient is being weaned from ventilator on t-piece, GCS is 8/15 17/08/2012 Patient on nasal oxygen, GCS is 10/15 18/08/2012 Patient discharged on request against medical advice.

56

APPLICATION OF OREMS GENERAL THEORY OF NURSING:

Dorothea Orem's Self-Care Theory: INTRODUCTION: Dorothea Orem (1914-2007) One of foremost nursing theorists. Born 1914 in Baltimore. Earned her diploma at Providence Hospital Washington, DC 1939 BSN Ed., Catholic University of America 1945 MSN Ed., Catholic University of America Involved in nursing practice, nursing service, and nursing education During her professional career, she worked as a staff nurse, private duty nurse, nurse educator and administrator and nurse consultant Received honorary Doctor of Science degree in 1976 Published first formal articulation of her ideas in Nursing: Concepts of Practice in 197, second in 1980,and in 1995.

DEVELOPMENT OF THEORY : 1949-1957 Orem worked for the Division of Hospital and Institutional Services of the Indiana State Board of Health. Her goal was to upgrade the quality of nursing in general hospitals throughout the state. During this time she developed her definition of nursing practice. 1959 Orem subsequently served as acting dean of the school of Nursing and as an assistant professor of nursing education at CUA. She continued to develop her concept of nursing and self care during this time.

57

 Orems Nursing: Concept of Practice was first published in 1971 and subsequently in 1980, 1985, 1991,1995, and 2001

Theory of Self Care :

This theory Includes: Self care - practice of activities that individual initiates and perform on their own behalf in maintaining life ,health and well being Self care agency - is a human ability which is "the ability for engaging in self care" -conditioned by age developmental state, life experience socio cultural orientation health and available resources Therapeutic self care demand - "totality of self care actions to be performed for some duration in order to meet self care requisites by using valid methods and related sets of operations and actions" Self care requisites - action directed towards provision of self care. - 3 categories of self care requisites are: o Universal self care requisites o Developmental self care requisites o Health deviation self care requisites

1. Universal self care requisites Associated with life processes and the maintenance of the integrity of human structure and functioning Common to all , ADL Identifies these requisites as: Maintenance of sufficient intake of air ,water, food Provision of care associated with elimination process Balance between activity and rest, between solitude and social interaction Prevention of hazards to human life well-being and
58

 Promotion of human functioning

2. Developmental self-care requisites Associated with developmental processes/ derived from a condition Or associated with an event E.g.- adjusting to a new job, -adjusting to body changes 3. Health deviation self-care Required in conditions of illness, injury, or disease .these include:- Seeking and securing appropriate medical assistance Being aware of and attending to the effects and results of pathologic conditions Effectively carrying out medically prescribed measures Modifying self concepts in accepting oneself as being in a particular state of health and in specificforms of health care Learning to live with effects of pathologic conditions

59

CONCEPTUAL FRAMEWORK FOR OREMS THEORY

Self care

Self care agency

Therapeutic self care demand

Nursing capablities

60

JUSTIFICATION OF SELECTING THE THEORY

I have selected this theory of Orems general nursing because the main concept of this theory was to develop self-care. With this theory I can identify the client problem and encourage my patient to perform her self-care activities.

SELF CARE

My patient Mrs. Mary Agnes is unable to perform her activities of daily living as she was in ventilator support and was later weaned from the ventilator and put on nasal oxygen. Her condition was explained to her family and family was involved in her care.

SELFCARE AGENCY

These are the people to provide care to the patients who are unable to do self-care activities by themselves because of their disease condition. Here, the self-care agencies are the patient daughter, the staff nurses and me.
SELFCARE REQUISITES

When i met the patient she was unable to perform her self-care activities because of her disease condition. So she needs assistance to do her daily activities. I explained to patient daughter about her needs and activities, how she can help the patient in performance of the self-care activities.
THERAPEUTIC SELFCARE DEMAND

It is the patients need for assistance in daily activities. To meet her demands nursing staff or family members can help her. I assisted the client to meet her demands. I taught about importance personnel hygiene. Encouraged the client to discuss about benefits of self-care.
61

RESEARCH SUPPORT

1. GOLD NANOPARTICLE SENSORS FOR DETECTING CHRONIC KIDNEY DISEASE AND DISEASE PROGRESSION Authors : Ophir Marom; Farid Nakhoul; Ulrike Tisch; Ala Shiban; Zaid Abassi; Hossam Haick Posted: 06/15/2012; Nanomedicine. 2012;7(5):639-650. 2012 Future Medicine Ltd Abstract Aim: To study the feasibility of a novel nanomedical method that utilizes breath testing for identifying chronic kidney disease (CKD) and disease progression. Results: A combination of two to three gold nanoparticles sensors provided good distinction between early-stage CKD and healthy states (accuracy of 79%) and between stage 4 and 5 CKD states (accuracy of 85%). A single sensor provided a distinction between early and advanced CKD (accuracy of 76%). Several substances in the breath were identified and could be associated with CKD-related biochemical processes or with the accumulation of toxins through kidney function loss. Conclusion: Breath testing using gold nanoparticle sensors holds future potential as a cost-effective, fast and reliable diagnostic test for early detection of CKD and monitoring of disease progression. 2. PLANNED EARLY INITIATION OF DIALYSIS IN PATIENTS WITH STAGE V CHRONIC KIDNEY DISEASE IS NOT LINKED TO BETTER SURVIVAL OR CLINICAL OUTCOMES, ACCORDING TO THE RESULTS OF A RANDOMIZED CONTROLLED TRIAL REPORT Authors: Laurie Barclay, MD New England Journal of Medicine. 2010; 363: 609-619, 678-680.

62

The study sample consisted of 828 adults randomly assigned between July 2000 and November 2008. Mean age was 60.4 years, there were 542 men and 286 women, and 355 had diabetes. In the early-start group, median time to the initiation of dialysis was 1.80 months (95% confidence interval [CI], 1.60 - 2.23 months) vs 7.40 months (95% CI, 6.23 8.27 months) in the late-start group. Because they became symptomatic, 75.9% of the patients in the late-start group started dialysis when the estimated GFR was above the target of 7.0 mL/minute. During a median follow-up period of 3.59 years, there were 152 deaths among 404 patients in the early-start group (37.6%) and 155 deaths among 424 patients in the late-start group (36.6%). For early initiation, the hazard ratio of death was 1.04 (95% CI, 0.83 - 1.30; P = .75). Frequency of adverse events, including cardiovascular events, infections, and dialysis complications, also did not differ significantly between the groups. "In this study, planned early initiation of dialysis in patients with stage V chronic kidney disease was not associated with an improvement in survival or clinical outcomes," the study authors write. "The results show that with careful clinical management, dialysis may be delayed until either the GFR drops below 7.0 ml per minute or more traditional clinical indicators for the initiation of dialysis are present." 3. A DOUBLE-BLIND, RANDOMIZED, PARALLEL, PLACEBOCONTROLLED STUDY EXAMINING THE EFFECT OF CROSS-LINKED POLYELECTROLYTE IN HEART FAILURE PATIENTS WITH CHRONIC KIDNEY DISEASE Authors and Disclosures: Maria Rosa Costanzo; J. Thomas Heywood; Barry M. Massie; Julie Iwashita; Lee Henderson; Merab Mamatsashvili; Hamayak Sisakian; Hamlet Hayrapetyan; Philip Sager; Dirk J. van Veldhuisen; Detlef Albrecht Posted: 08/08/2012; Eur J Heart Fail. 2012;14(8):922-930. 2012 Oxford University Press Abstract Aims This double-blind, randomized, parallel, placebo-controlled investigation evaluated the effects of cross-linked polyelectrolyte (CLP) on serum potassium and measures of congestion in patients with heart failure (HF) and chronic kidney disease (CKD). Methods and results The primary endpoint was change in serum potassium over time. Exploratory endpoints included: weight, physician and patient assessment of
63

exertional dyspnoea, effect on N-terminal pro brain natriuretic peptide (NT-proBNP) levels, New York Heart Association (NYHA) classification, 6 min walk test (6MWT), and quality of life by Kansas City Cardiomyopathy Questionnaire (KCCQ). Serum potassium was similar in CLP (n =59) and placebo (n =52) groups throughout the 8week study. Weight loss was greater in the CLP than in the placebo group at Weeks 1 (P =0.014) and 2 (P =0.004), and this trend continued until the end of the study. After 8 weeks, by physician assessment, the percentage of patients experiencing marked or disabling dyspnoea tended to be lower in the CLP than in the placebo group (7.3% vs. 23.9%, P =0.128). Fewer patients in the CLP than in the placebo group had NTproBNP levels >1000 pg/mL at Week 4 (P =0.039) and Week 8 (P =0.065). The proportion of patients improving by at least one NYHA functional class over the study was higher in the CLP than in the placebo group (48.8% vs. 17.4%; P =0.002). Effects on 6MWT at Week 8 (p =0.072) and quality of life (overall KCCQ score) at Week 4 (p =0.005) and 8 (P =0.062) all favoured the CLP cohort. Four treatment-unrelated deaths occurred in the CLP group and none in the placebo group (P =0.056). Conclusion In advanced, symptomatic HF with CKD, CLP is associated with beneficial clinical effects without significant serum potassium changes. Trial registration: NCT01265524.

64

SUMMARY

Chronic renal failure is a life changing disease condition, which alters the entire the health maintenance of the clients life. It is a progressive disorder that can aggravate and even lead to death, if not managed properly, Chronic renal failure (CRF) is the progressive loss of kidney function. The kidneys attempt to compensate for renal damage by hyper-filtration (excessive straining of the blood) within the remaining functional nephrons (filtering units that consist of a glomerulus and corresponding tubule). Over time, hyper-filtration causes further loss of function. Causes can be prerenal, renal and post renal causes. Management includes medical management with antihypertensive and diuretics as the stages process dialysis becomes in evitable, dialysis is a huge burden on the client physically, financially and emotionally. Chronic renal failure (CRF) is the end result of a gradual, progressive loss of kidney function. Causes include chronic infections (glomerulonephritis, pyelonephritis), vascular diseases (hypertension, nephrosclerosis), obstructive processes (renal calculi), polycystic kidney disease, collagen diseases (systemic lupus), nephrotoxic agents (drugs, such as aminoglycosides), and endocrine diseases (diabetes, hyperparathyroidism). This syndrome is generally progressive and produces major changes in all body systems. The final stage of renal dysfunction, end-stage renal disease (ESRD), is demonstrated by a glomerular filtration rate (GFR) of 15%20% of normal or less. Diabetes and hypertension together are responsible for more than 70% of all cases of end-stage kidney disease.

65

CONCLUSION Chronic renal failure, or ESRD, is a progressive, irreversible deterioration in renal function in which the bodys 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). The incidence of ESRD has increased by almost 8% per year for the past 5 years, with more than 300,000 patients being treated in the United States (USRDS, 2001). ESRD may be caused by systemic diseases, such as diabetes mellitus (leading cause); hypertension; chronic glomerulonephritis; pyelonephritis; obstruction of the urinary tract; hereditary lesions, as in polycystic kidney disease; vascular disorders; infections; medications; or toxic agents. Autosomal dominant polycystic kidney disease accounts for 8% to 10% of cases of ESRD in the United States and Europe (Perrone, Ruthazer & Terrin, 2001). Comorbid conditions that develop during chronic renal insufficiency contribute to the high morbidity and mortality among patients with ESRD (Kausz et al., 2001). Environmental and occupational agents that have been implicated in chronic renal failure include lead, cadmium, mercury, and chromium. Dialysis or kidney transplantation eventually becomes necessary for patient survival. Dialysis is an effective means of correcting metabolic toxicities at any age, although the mortality rate in infants and young children is greater than adults in the presence of other, nonrenal diseases and in the presence of anuria or oliguria (Wood et al., 2001). CHRONIC RENAL FAILURE IN OLDER ADULTS Historically, the age of patients developing ESRD steadily rose each year, but it appears to have stabilized since 1993 at a mean age of 60 years. In the past, rapidly progressive glomerulonephritis, membranous glomerulonephritis, and nephrosclerosis were the most common causes of chronic renal failure in the elderly. Today, however, diabetes mellitus and hypertension are the leading causes of chronic renal failure in the elderly (Bakris et al., 2000). Other common causes of chronic renal failure in the elderly population are interstitial nephritis and urinary tract obstruction. The signs and
66

symptoms of renal disease in the elderly are commonly nonspecific. The occurrence of symptoms of other disorders (heart failure, dementia) can mask the symptoms of renal disease and delay or prevent diagnosis and treatment. The patient often develops signs and symptoms of nephrotic syndrome, such as edema and proteinuria. Hemodialysis and peritoneal dialysis have been used effectively in treating elderly patients (Carey et al., 2001). Although there is no specific age limitation for renal transplantation, concomitant disorders (ie, coronary artery disease, peripheral vascular disease) have made it a less common treatment for the elderly.

67

Sl.no Assessment

Nursing diagnosis

Objectives

Nursing interventions

implementation

Evaluation

1.

Subjective data: Nil

Ineffective airway clearance related to decreased cough

Patient will be able to maintain a clear airway

Assess the airway

Auscultated the airway, shows increased secretions

Patient maintained patent airway and was weaned from the ventilator And airway was clear as evidenced by

Objective data: reflex as evidenced auscultation of chest shows increased secretions and crepitus by increased secretions in chest

Provide fowlers position Provide endotracheal suctioning to remove the accumulated secretions

Provided fowlers position Provide endotracheal

suctioning every absence of 2 hourly crepitus on auscultation

68

 Administer nebulization as ordered by physician

Administered nebulization as per doctor order with Duolin 2ml Q2H

Subjective data: NIL

Impaired breathing pattern related to loss of

Patient will be able to maintain normal

Assess the pattern of breathing.

Assessed the pattern of breathing

Patient maintained normal breathing pattern as

Objective data Patient is unconscious and is on ventilator. :

consciousness

secondary to cardiac breathing and renal dysfunction as evidenced by presence of ventilator support for respiration. Provide adequate
69

pattern

Administer oxygen as per the oxygen saturation level.

Administered oxygen as per the saturation level

evidenced by a normal respiratory rate of 20 breaths/minute

Provide adequate

suctioning to ensure proper oxygen saturation. Monitor pulse oxymetry readings at regular intervals 3 Subjective data: NIL Impaired cardiac Patient maintains normal cardiac output. Assess the fluid status of the client

suctioning to ensure proper oxygen saturation Monitored pulse-oxymetry readings at regular intervals .

Assess the cardiac status of the client

Assessed the cardiac status of the client, she is showing decreased heart rate of 60 b/m Assessed fluid status of the client she is

Patient maintained normal cardiac output as evidenced by the normal heart rate of 74

Objective data: output related to on observation and heart rate fluid overload secondary to

is decreased i.e compromised renal 60 b/m. function

70

showing fluid overload as evidenced by generalized pitting edema and ascites Maintain intake output chart Assist in hemodialysis as indicated Monitor for signs of cardiac failure Maintained the intake output chart Assisted in hemodialysis Monitored for signs of cardiac failure

beats/minute

71

Subjective data: NIL

Fluid volume excess Patient will related to decreased be able to maintain normal fluid volume.

Assess the fluid volume status of the patient

Assessed the fluid volume status, patient is having generalized edema and

Patient maintained normal fluid volume as evidenced by the absence of edema and absence of neck vein distension

Objective data: renal function as patient on observation has generalized pitting edema and ascites. evidenced by generalized body edema and ascites

Monitor the intake and output chart

ascites Monitored the intake and output Intake is 50ml/hour Output is nil

Restrict the fluid intake

Restricted fluid intake to 50ml/hour as per physician order

72

 Assess for Skin turgor and presence of edema

Assessed ski n, turgid and edema is present in extremities and ascites is present

Assess for. Distention of neck veins Assess the Blood pressure, pulse rate, and rhythm

Neck veins are distended

Blood pressure is 150/100 mm of Hg, pulse rate is 60b/minute, rhythm is slow. Assisted in

Assist in hemodialysis in order to

73

haemodialysis

eliminate the excess fluid

Subjective data: NIL

Imbalanced nutritional status,

Patient maintains normal nutritional status

Assess the nutritional status of the patient

Laboratory values (serum electrolyte, BUN, creatinine, protein, transferrin, and iron levels were assessed patient is having anaemia, and increased sodium levels Patient is on naso-gastric

Patient maintained normal nutritional status as evidenced by resolution of edema and ascites and normal serum albumin levels

Objective data: less than body Patient is on nasogastric tube feeds of 50ml/hour requirement related to decreased intake secondary to dietary restrictions to reduce nitrogenous waste products

Assess patients

74

nutritional dietary patterns

tube feeding at a rate of 50ml/hr and is being given 1040 Kcal of energy and 52 gms of protein. Intake is 1200ml, output is 870 ml Assessed for the formation of edema, delayed wound healing and serum albumin levels

Monitor the intake and output of the patient Assess for evidence of inadequate protein intake

75