RENAL FAILUREBy

MRS. MBA PATIENCE O.B.SC. NURSING ADMIN, B.SC NURSING SCIENCE ,RN, RM, DIP. NSG

ADMIN/PUBLIC ADMIN.

A PAPER PRESENTED AT MANDATORY CONTINUING PROFESSIONAL

DEVELOPMENT PROGRAMME IMO STATE

VENUE: NEWTON HOTEL OWERRIDATE: 7TH -11Th JULY, 2014

INTRODUCTION RENAL FAILURE

Proper function of the renal and urinary systems is essential to life. Dysfunction of the kidneys and lower urinary tract is common and may occur at any age and with varying degrees of severity.

Renal failure is a serious inability of the kidneys to carry out the normal functions of maintaining fluid and electrolyte balance as well as elimination of the end product of metabolism from the body.

Renal failure is present when the excretion of water electrolytes and metabolic waste products is insufficient because of kidney damage that prevent the kidney from maintaining the internal milieu of the body.

There are two types of renal failure:

Acute Renal failure.Chronic Renal Failure.

The former has sudden a onset and is frequently reversible while chronic renal failure develops gradually and can occur as a sequence of an acute episode.

One normal kidney is generally sufficient for maintenance of fluid and electrolyte balance and elimination of metabolic end products.

Therefore renal failure implies bilateral kidney damage. Both acute and chronic renal failure may produce symptoms of uremia which is a toxic state, characterized by a marked accumulation of creatinine, urea and other nitrogeneous wastes in the blood.

OBJECTIVES.At the end of this session, the

participants should be able to understand the following:-The structure and functions of the renal system.Demonstrate adequate knowledge of the concepts, causes, pathophysiology, and clinical manifestations of renal failure.Management of renal failure. Utilize the nursing process approach in the care and finally draw a care plan.

ANATOMY AND PHYSIOLOGY OF RENAL AND URINARY TRACT

SYSTEMAssessment of upper and lower urinary tract function is a part of every health examination and necessitates an understanding of anatomy and physiology of the urinary system as well as of changes in the system on other physiological functions and implementing appropriate nursing care.

ANATOMY OF THE UPPER/LOWER URINARY TRACTS

The renal and urinary tract system include the following:- Kidneys- Ureters- Bladder-Urethra- Physiology of micturition

Figure 1

Renal cortex

Renal column (Bertin)

Calyx (cut edge)

Calyx

Capsule

Figure 2

THE KIDNEYS

The kidneys are a pair of bean

shaped, brownish-red structures located

retroperitonealy (behind and outside the

peritoneal cavity) on the posterior wall of

the abdomen- from the twelft thoracic

vertebra to the third lumbar vertebra in the

adult.

Figure 3

The average kidney weighs 113 to 170g about (4.502) and is 12cm (about 45inces) long and 6cm wide and 2.5cm thick.The right kidney is slightly lower than the left kidney due to the location of the liver.The kidneys are well protected by the ribs, muscles of the abdominal wall by renal fascia made of connective tissue.

The fibrous connective tissue, blood vessels, and lymphatics surrounding each kidney are known as the renal capsule.

The renal parenchyma is divided into two parts:-

The cortex and the medulla. The medulla which is approximately

5cm wide, is the inner portion of the kidney. It contains the loops of henle, vasa recta, and the collecting ducts of the juxtamedullary nephrons.

The collecting ducts from both the

juxta-medullary and the cortical

nephrons connect the renal pyramids,

which are triangular and situated with

the base facing the concave surface of

the kidney (papilla) facing the hilum or

pelvis.

Each kidney contains approximately 8-18 pyramids. The pyramids drain into 4-13 minor calices which drain into 2 to 3 major calices that open directly into the renal pelvis.

The renal pelvis is the beginning of the collecting system, and is composed of structures that are designed to collect and transport urine.Once the urine leaves the renal pelvis its composition or amount of urine does not change.

The cortex which is approximately 1cm wide is located farthest from the centre of the kidney and around the outer most edges. It contains the nephron which is the functional unit of the kidney.

The hilum or pelvis, is the concave portion of the kidney through which a renal artery enters and renal renal vein exit.

The kidneys receive 20% to 25% of the total cardiac output, which means that all of the body’s blood circulates through the kidney 12 times per hour.

The renal artery (arising from the abdominal aorta) divides into smaller and smaller vessels eventually forming the afferent arterioles. Each afferent arteriole branches to form a glomerulus, which is the capillary bed responsible for glomerulus filtration.

Blood leaves the glomerulus through the efferent arteriole and flows back to the inferior vena cava through a network of capillaries and veins.

NEPHRON •Each kidney has 1 million nephrons which usually allows for adequate renal function, even if the opposite kidney is damaged or becomes non functional.•There are two kinds of Nephrons: The cortical and Juxtamedullary cortical Nephrons make up 80-85% of the total number are located in the outermost part of the cortex of the kidney. And the juxtamedullary nephrons make up the remaining 15% to 20% located deeper in the cortex.

•The juxtamedullary nephrons are distinguished by long loops of Henle, which are surrounded by long capillary loops called vasa recta that dip into the medulla of the kidney.The glomerular membrane is composed of three filtering layers:1. The capillary endothelium.2. The basement membrane and 3. The Epithelium.

The glomerular membrane allows filtration of fluid and small molecules yet limits passage of larger molecules, such as blood cells and albumin.

Pressure changes and the permeability of the glomerular membrane of Bowman's capsule facilitate the passage of fluids and various substances from the blood vessels, filling the space within Bowman’s capsule with this filtered solution.

The tubular component of nephron begins in the Bowman's capsule. The filtrate created in the Bowman's capsule travels first into the proximal tube, then the loop of henle, the distal tubules and the cortical or medullary collecting ducts.

• The structural arrangement of the tubule allows the distal to lie in close proximity to where the afferent and efferent arteriole respectively enter and leave the glomerulus.

The distal tubular cells located in this area, known as macula densa, function with the adjacent afferent arteriole and create what is known the juxta glomerular apparatus.The tubular component consists of the Bowman's capsule, the proximal tubule, descending and ascending limbs of the loop of Henle and the cortical and medullary collecting ducts.

This portion of the nephron is responsible for making adjustments in the filtrate based on the bodies needs. Changes are continually made as filtrate travels through the tubules until it enters the collecting system and expelled from the body.

NEPHRONS Figure 4

URETERSThey are long fibromuscular tubes

that connect each kidney to the bladder. These tubes are 24cm and 30cm each. They originate at the lower portion of the renal pelvis and terminate at the trigone of the bladder wall. The left ureter is shouter than the right.

Function - Carries urine to the bladder by peristaltic contraction of the smooth muscle layer.

STRUCTURE•Outer covering of fibrous tissue continuous with the fibrous capsule of the kidney.•A middle muscular layer consisting of interlacing smooth muscle fibres that form a functional unit round the ureter and an additional outer longitudinal layer in lower third.

•An inner layer, the mucosa, composed of transitional epithelium. •The lining of the ureters is made up transitional epithelium called urothelium. The urothelium prevents the reabsorption of urine.

There are three narrowed areas of each ureter: The ureteropelvic junction, the ureteral segment near the sacroiliac junction and the uretero vesical junction.

These three junctions of the ureter have a propensity of obstruction by renal calculi or stricture.

Obstruction of the ureteropelvic junction is the most serious because of its close proximity to the kidney and risk of associated kidney dysfunction.

Functions of the Kidney1. Urine Formation 2. Excretion of waste products3. Regulation of electrolytes 4. Regulation of acid base

balance 5. Control of water balance

6. Control of Blood pressure.7. Renal clearance 8. Regulation of red Blood cell production.9. Synthesis of vit D to active form.10. Secretion of prostaglandins.

BLADDER STRUCTURE

Urinary bladder is a muscular, hollow sac located just behind the pubic bone has the capacity of 300-500ml in adults.Characterized as follows:-Its central, hollow area called the vesicle, which has two inlets ureters and outlet.The bladder contains four layers

a. Outer most layer is the Adventia- made up of connective tissue.

b. Beneath Adventitia is the smooth muscle known as the detrusor.

Beneath the detrusor is submucosal layer of loose connective tissue that serves as an interface between the detrusor and the innermost layer a mucosal lining.

Then the specialized transitional cell epithelium/ membrane that is impermeable to water and prevents reabsorption of urine stored in the bladder.

Bladder neck contains Bundles of involuntary smooth muscular that form a portion of the urethra/sphincter known as internal sphincter. An important sphincteric mechanism helps to maintain continence in the external urinary sphincter at the anterior urethra, the segment most distal from the bladder.

URINE FORMATIONUrine is formed in the nephrons through complex three step process:-•Glomerular filtration•Tubular reabsorption and •Tubular secretion.

NEPHRONS Figure 5

The various substances normally filtered by the glomerulus is reabsorbed by the tubules and excreted in urine, these include; sodium, chloride, bicarbonate, potassium, glucose, urea creatinine and uric acid.

Within the tubule, some of this substances are selectively reabsorbed into the blood. Others are secreted from the blood into the filtrate as it travels down the tubule. Some substances such as glucose, are completely reabsorbed in the tubule and does not appear in urine. Amino-acid and glucose are filtered at the level of the glomerulus and reabsorbed so that neither is excreted in the urine, normally glucose does not appear in urine.

Glucose, appears in urine (glycosuria) if the amount of Glucose in the blood and glome-rular filtrate exceeds the amount that the tubules can reabsorb. Glucose is reabsorbed when the blood glucose level is less than 200mg/dl (11mmol/L).

In diabetes, the blood glucose level exceeds the kidneys reabsorption capacity, and glucose appears in urine. Glycosuria is also common in Pregnancy.

Protein molecules are also generally not found in urine; however, low molecular weight proteins (globulins and albumin) may periodically be excreted in small amounts.

• Transient proteinuria in amounts less than 150mg/dl is considered normal and does not require further evaluation. Persistent proteinuria is suggestive of damage to the glomerular of the kidney.

THE STEPS OF URINE FORMATION 3 STEPS

1. GLOMERULAR FILTRATION 2. TUBULAR-REABSORPTION AND 3. EXCRETION

1.GLOMERULAR FILTRATION•The normal blood flow through the kidneys is about 1,200m/min. as blood flows into the glomerulus from an afferent arteriole, filtration occurs.•The filtered fluid also known as filtrate or utlrafiltrate, then enters the renal tubules. Under normal conditions, about 20% of the blood passing through he glomeruli is filtered into the nephron amounting to about 180L/day of filtrate.

• The filtrate normally consists of water, electrolytes and other small molecules because water and molecules are allowed to pass, whereas larger molecules stay in the blood stream.• Efficient filtration depends on adequate blood flow maintaining a consistent pressure through the glomerulus.

• Many factors can alter this blood flow and pressure including hypotension, decreased aortic pressure in the blood and increased pressure in the renal tubules from an obstruction.

2. TUBULAR REABSORPTION AND TUBULAR SECRETION

The second and third steps of urine formation, occur in the renal tubules. In tubular reabsorption, a substance moves from filtrate back into peritubular capillaries or vasa recta. Of the 180 L (45 gallons) of filtrate that kidneys produce each day, 99% is reabsorbed into the blood stream, resulting in the formation of 1000 to 1500ml of urine each day.

• Although most reabsorption and secretion occurs in the proximal tubule, reabsorption occurs along entire tubule, reabsorption and secretion in the tubule frequently involve passive active transport and the use of energy. Filtrate becomes concentrated in the distal tubule and collecting ducts under hormonal influence and becomes urine, which then enters the renal pelvis and excreted.

PHYSIOLOGY OF MICTURATION

Figure 6

• Micturition (voiding) normally occurs eight times in twenty four (24hrs). It is activated via the micturition reflex arc within the sympathetic & parasympathetic nervous system, which causes a coordinated sequence of events.

• It is initiated when the afferent pelvic nerve, (which originates in S2 to S4) stimulates the bladder to contract resulting in complete relaxation of the striated urethral sphincter and followed by a decrease in urethral pressure, contraction of the detrusor muscle, opening of the vesicle neck and proximal urethra, and flow of urine occurs.

• This coordinated effort by the parasympathetic system is mediated by muscarinic and to a lesser extent cholinergic receptors within the detrusor muscle.• The pressure generated in the bladder during micturition is about 20 to 40cm of H2o in females. It is somewhat more in males age 45 yrs and older due to the cells of the middle lobes of prostrate gland that surround the proximal urethra.

• Any obstruction of the bladder outlet, such as in advanced benign prostatic hyperplasia (BPH), results in high voiding pressure. High voiding pressures make it more difficult to start urine flow and maintain it.

RENAL FAILURE• Acute Renal failure (ARF) is also known as Acute renal Injury, is a rapid loss of kidney function, normally caused by extensive loss of blood as a result of injury or injury from toxic drugs or medications E.g Anti-malaria drugs etc.

• ARF is a reversible clinical syndrome where there is a sudden and almost complete loss of kidney function (decreased GFR) over a period of hours to days with failure to excrete nitrogenous waste products and to maintain fluid and electrolyte homeostasis (Porth, 2005).

• Although ARF is often thought of as a problem seen only in hospitalized patients, it may occur in outpatient setting as well. Some of the factors may be reversible if identified and treated promptly, before kidney is impaired.

This is true of the following conditions that reduce blood flow to the kidney and impair kidney function:-a. Hypovolaemia- shock.b. Hypotensionc. Reduced cardiac Output and Heart failure.d. Obstruction of the kidney, or lower urinary

tract by tumour, blood clot, or kidney stone and

e. Bilateral obstruction of the renal arteries or veins.• If these conditions are treated and corrected before the kidneys are permanently damaged, the increased BUN and creatinine levels, Oliguria and other signs associated with ARF may be reversed.

•CATEGORIES OF RENAL FAILURE •The major categories of ARF are:- pre renal (Hypoperfusion of kidney), •Intra renal (actual damage to kidney tissue)•And post renal (obstruction to urine flow).

Figure 7

•Pre renal ARF, occurs in 60%-70% of cases is the result of impaired blood flow that leads to hypoperfusian of the kidney and a decrease in the GFR common clinical situations are volume depletion states. (haemorrhage or gastiointestinal (GI) Losses), impaired cardiac performance (myocardial infarction, heart failure, or cardiogenic shock) and vasodilatation (sepsis or anaphylasis).

•Intra-renal ARF is the results of actual parenchyma damage to the glomeruli or kidney tubules. Nephrotoxic agents, such as aminoglycosides and radio contrast agents, account for 30% of cases of ACUTE TUBULAR NECROSIS (ATN) and Ischaemia due to decreased renal perfusion accounts for more than 50% cases of ATN.

Characteristics of ATN:- •Intra-tubular Obstruction, tubular back leak/abnormal reabsorption of filtrate and decreased urine flow through the tubule, vasoconstriction and changes process result in a decrease of GFR, progressive azotemia and impaired fluid and electrolyte balance. Conditions such as Burns, crush injuries, infections, and severe blood transfusion reactions can lead to intra renal ARF and ultimately ATN.

•With Burns and crush injuries myoglobin (a protein released from muscle when injury occurs) and haemoglobin are liberated, causing obstruction, renal toxicity, and Ischaemia. Severe transfusion reactions may also cause intra-renal failure; haemoglobin is released through haemolysis, filters through the glomeruli and becomes concentrated in the kidney tubules to such a degree that precipitation of haemoglobin occurs.

•Certain medications especially non-steroidal (NSAIDS) may also predispose a patient to intra renal damage.•The medications interfere with the normal auto regulatory mechanisms of the kidney and may cause hypo perfusion and eventual Ischaema.•Post renal ARF is usually the result of an obstruction some where distal to the kidney. Pressure rises in the kidney tubules and eventually, the GFR decreases.

PATHOPHYSIOLOGY •Renal failure occurs due to decreased blood flow to the kidney leading to renal ischaemia (pre-renal), obstruction of the flow of urine from the kidney itself (lntra-renal). As renal function declines, the end products of protein metabolism which are normally excreted by the kidney in urine accumulate in the blood.

•Uraemia develops and adversely affects every system in the body. The greater the build up of waste products, the more severe the symptoms. These are three well recognized stages of chronic renal disease, reduced renal reserve, renal insufficiency, and End Stage Renal Disease (ESRD).

CLINICAL MANIFESTATION There are four clinical phases of

ARF:-•Initiation•Oliguria•Diuresis •The recovery period.•Initiation period begins with the initial insult and ends when Oliguria develops.

•The Oliguria period is accompanied by an increase in the serum concentration of substances usually excreted by the kidneys (urea, creatinine, uric acid, organic acids and intracellular ions (Potassium & magnesium).•Oliguria < 400 -500ml of urine/day. The body needs about 400mls to remove metabolic waste product from the body.

•In this phase the uraemic symptoms first appear and life threatening conditions such as hyperkalemia develop. •The Diuresis period.Gradual increase in urinary output.Reduction in serum concentration of waste products and ions.Improve urinary output but with marked abnormal renal functions.Uremic symptoms may still be present.Observe closely for dehydration which may increase ureamic symptoms.

PERIOD OF RECOVERY Signals Improvement of renal function.Normal laboratory values.Permanent 1% -3% reduction in the GFR is common.If recovery is not achieved, the following is suggestive of progression to CRF: Lethargy VomitingPersistent nausea.Diarrhoea.

CHRONIC RENAL FAILURE •Chronic renal failure or an end stage Renal failure (ESRD), is a progressive irreversible deterioration in renal function in which the body’s ability to maintain metabolic, fluid and electrolyte imbalance fails resulting in uraemia or azotemia.

•The incidence of ESRD had increased by almost 8% per year of the past 5yrs,•USA – Has had more than 280,000 patients with chronic renal failure.•65% receiving haemodialysis, more than.•28%- 120,000 Have functioning renal transplants, 7%- 24,000 are receiving peritoneal dialysis (United States renal Data system (USRD5) 2004.

CAUSES OF ESRD •Include system diseases, such as •Diabetes mellitus- leading cause.•Hypertension •Chronic glomerulonephritis.•Pylonephrits - inflammation of renal Pelvis.•Lesions - polycystic kidney.

•Vascular Disorders•Medications •Toxic Agents.•Co-morbid conditions that develop during chronic renal insufficiency contribute to the high morbidity & mortality among patients with (ESRD) (Burrows-Hudson; 2005).

•Environmental and occupational agents that have been implicated in CRF include lead, mercury, chromium & cadmium - eg miners mostly. •Dialysis or kidney transplant eventually becomes necessary for patients survival.

Figure 8

CLINICAL MANIFESTATION • Because virtually everybody system is affected by the uraemia of chronic renal failure, patients exhibit a number of signs and symptoms.• The severity of these signs depends in part on the degree of renal impairment, other underlying conditions & age.

Assessing for Signs and Symptoms of Chronic Renal Failure

Figure 9

INVESTIGATIONS•History taking•Urinalysis- specific gravity reduces as against normal of 1.003-1.030.•24hr urine analysis for creatinine clearance.•Blood urea Nitrogen•Renal function test.•Radiological studies.•Uttrasonography•MR I(Magnetic Resonance imaging. )

GOAL OF MANAGEMENT •To maintain kidney function•To maintain Homeostasis •To prevent the development of complication.

PHARMACOLOGIC THERAPY • Complications can be prevented or delayed by administering prescribed phosphate-binding agents, calcium supplements, antihypertensive and cardiac medications eg Diurectics anti seizure medications and erythropoietin. Haematinics and potassium supplements.

CALCIUM PHOSPHOROUS BINDERS:-Hyperphsphatemia and hypocalemia

are treated with medications that bind dietary phosphorous in GIT. E.g calcium carbonate (Os-cal) or calcium acetate are prescribed but there are risk of hypocalcaemia. If calcium is high above 55mg/dl a polymeric phosphate binder such as servelamer hypdrochloride may be used (zonderman & Doyle 2006). All binding agents must be administered with food.

Antacids:- Magnesim antacids are avoided to prevent magnesium toxicity.

Others include:-•Antihypertensive•Anticonvulsants•Erythropoietin.

DIETARY

Low protein- to minimize waste products in the blood.

• Normal diet if patient is on dialysis.•Low salt for ARF

• High protein/low salt in chronic renal failure

A MAN UNDERGOING DIALYSIS

Figure 10

•Dialysis is used to remove fluid and uremic waste products from the body when the kidneys are unable to do so.•In haemodyalysis, machine filters wastes and excess fluids from the blood.•In peritonieal dialysis, you use a two-way catheter to fill the abdominal cavity with dialysis solution that absorbs wastes and excess fluids- then this solution drains out of the body and is replaced with fresh solution.

KIDNEY TRANSPLANT – SURGICAL INTERVENTION

Figure 11

Nursing Management Patient with renal failure require astute

nursing care to avoid complications of reduced renal functions and stresses as well as anxiety of dealing with a life threatening illness.

ASSESSMENT •History of Disease•Fluid status •Potential sources of imbalance

SIGNS OF POSSIBLE COMPLICATIONS

•Physical examination •Urinalysis.

•Obtaining a comprehensive health history, which includes an assessment of risk factors, is the first step in assessing a patient with upper and lower urinary tract dysfunction various diseases or clinical situations.

•Past medical HX•Surgical HX•Family medical Hx.

•Which can place a patient at high risk for urinary tract dysfunction. Data collection about previous health problems or diseases provides the health team with useful informations.

HEALTH HISTORY •Excellent communication skills•Avoid medical jargon•Parity in women- risk factors•Neurological disorders: Diabetic neuropathy, multiple sclerosis, Parkinsons dx etc.•Bladder problems- urinary stasis bladder pressure or kidney infection.

•Nursing Assessment Requires Family History•Other family members with this dx•Members with congenital problems of the kidney ie poly cystic kidneys etc.•Renal tumours, or cancers.

PHYSICAL ASSESSMENT •General observation- signs and symptoms •Palpation (Abdominal)•Auscultation•Chest examination• Assess for clinical findings suggestive of renal disease – genetic syndromes eg seizures, mental retardation & skin involvement.

NURSING DIAGNOSIS •Mr. O.O is a 24yr old undergraduate, admitted into the ward with the history of excessive weakness, poor urine output feeling of fullness in the abdomen and generalized bloating X 2/52. O/E Acutely ill looking young man, with an apprehensive look, facial puffiness, abdominal and lower leg edema, with pitting (+++). There is associated pallor, Nausea, anorexia and vomiting very restless.

•Patient is the 1st child and son of a widow, who lost her husband 10 years ago. Mother is a primary school teacher with 5 children. She narrated that her husband’s people who killed her husband are also after her son. He has been on herbal treatment for a spiritual attack for 6 months prior to the onset of the sickness.•V/s on adm T 390c P 120 R32 Bp 180/120 mmHg •Lab Results – S/E/U/C revealed elevated urea – 200m/ol creatinine – 64.•Weight: 70kg.

•Urinalysis- protein +++, Epith. Cells +++, pus + of HPH.•MED Dx: Acute renal failure.

LIST OF CUES.•24yrs. Undergraduate, 1st son/child,•Excessive weakness, poor urine output, < 400mls/day.•Generalized bloating, facial puffiness, Abdominal + lower leg oedema, Pitting (+++), very restless, pallor (+) anorexia, vomiting.

CLINICAL CHEMISTRY FORM

Figure 12

•Mother believes it is witch hunting from husband’s people.•On herbal Rx for 6 months for spiritual attacks” prior to onset of sickness.•Mother is a primary school teacher with 5 kids, widow.•BP 180/120 mmHg. Urea 200mg/dl. Creatinine 64.

CLUSTERING NURSING DIAGNOSIS

Poor urine output > 400mls/day. Generalized

bloating, facial puffyness, Abdomen/lower legs

oedema, pitting (+++)

Excess fluid vol r/e compromised regulatory

mechanisms AEB generalized oedema.

Anorexia, vomiting, pallor (+), Nausea. Imbalanced Nutrition < body requirement r/t nausea.

Vomiting AEB inadequate caloric intake.

Mother believes it is witch-hunting from husband’s

people on herbal Rx for “spiritual attack” x 6 mths.

Deficient knowledge r/t regiment AEB verbalized

inaccurate information.

1st child and son. Undergraduate. 24 yrs.

Mother a widow. Primary school teacher. Mth 5

children. Husband dead 10yrs ago.

Severe anxiety (R/T unknown out come/previous

experiences of premature death).

Apprehensive look.

NURSING CARE PLANSNO DATE/TIME NSG DX OBJECTIVE NSG ORDERS EVALUATION SIGN1 1/4/13 Excess fluid

vol r/t. compromised regulatory mechanisms AEB generalized oedema. (NANDA)

Fluid balance (NOC) patient will achieve reduction of oedema AEB by urinary output > 30ml/hr within one week of intervention

Fluid MGT (NIC) Weigh the pt daily. Monitor/record i/o,

include all stools, emesis and drainage (if any).

Monitor v/s pulse, resp, BP.

Auscultate breath and heart sounds for signs of fluid overload.

Give iv medications in least amount of fluid possible.

Administer oral and iv fluid as prescribed.

Administer medications eg diuretics as prescribed.

Mr. O.O’s fluid balance was still poor after one weak of intervention AEB persisting generalized oedema and urinary output of < 30ml/hr.

2 Imbalanced Nutrition: less than body requirement r/t nausea/vomiting AEB inadequate caloric intake.

Nutrient intake (NOC) O.O will verbalize and demonstrate selection of foods or meals that will achieve adequate caloric intake to keep pace with disease state within 1-2 wks of adm.

NUTRITION MGT Administer small

frequent feedings as tolerated.

Make meals look appetizing, try to eliminate other procedures at meal time if possible and focus on eating.

Provide frequent oral hygiene.

Offer ice chipls or hard candy if not diabetic.

Consult a dietician. Adjust

potassium/phosphorus restrictions as indicated.

Administer enteral or parenteral feedings as prescribed.

Give prescribed anti emetics.

O.O’s nutrition was fairly managed AEB slight increase in his caloric intake in the last 1 wk.

NOTE: Patients urea and creatinine was so high and due to poverty could not afford Dialysis and patient died after 10 days of management.

3 Deficient knowledge r/t Dx Regiment AEB verbalized inaccurate information

Knowledge: Dx process (NOC) O.O and family will verbalize understanding of ARF and associated RX within 2-3 wks of intervention.

Teaching: DX Process (NIC) Assess knowledge and

understanding of ARF and its RX.

Explain all procedures and tests. Use terms pt/family can understand. Be clear and direct.

Explain the purpose of fluid restrictions.

Discuss need for a reduced protein diet.

Encourage family conference with members of pt’s health care teams as necessary.

O.O and family verbalize understanding or ARF and associated RX.

Severe Anxiety R/t unknown outcome experiences of Premature death.