RENAL FAILURE

Melissa Greer, Ylise Dobson,

Megan Stacey, Melissa Terpstra,

& Emily Peterson

The Radical Renal Team

Dr. McCurly

The Radical Renal Team

The Nurses

McTall & McShorty

The Radical Renal Team

The Nurses

McSmall & McGiant

Case Study

Tia Smith is a 26 year old female patient who is 10 hours post-partum following an emergency C-section for twins. She was 33.5 weeks pregnant and had a difficult pregnancy with PIH (pregnancy induced hypertension) and frequent urinary tract infections. On admission Tia was diagnosed with HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) which necessitated immediate delivery of her babies. During the C-section Tia became hypovolemic resulting from massive hemorrhaging and required blood products and fluid replacements. Tia eventually developed hypovolemic shock and remained unstable for 2 hours. For the past nursing shift Tia has been hypotensive with blood pressures ranging from 59/47 to 95/52. Tia’s urinary output has been 2-12cc/hr of brown cloudy foul smelling urine. During your morning assessment

you discover the following:

Case cont’d

• VS: T: 37.4 P: 125bpm R: 33 BP: 96/62

•  Respiratory: Chest is clear fine crackles heard throughout all lung fields, there is diminished A/E at the bottom of the R & L lobes

•  CV: S1, S2 audible with pericardial friction, bounding rapid pulse•  Mental Status: drowsy and with assistance will orient slowly to PPT, pt c/o

persistent hiccups•  Neurovascular: edema, skin cool & pale, bruises observed throughout

extremities, skin turgor poor, bilateral decreased sensation in feet•  GI: pt c/o N&V•  Genitourinary: pt has foley catheter draining brown cloudy foul smelling urine

at 2-12cc/hr•  Psychosocial: pt very emotional and crying at times because she cannot be with

her newborn babies and is unable to breastfeed, she is concerned for their health, and does not understand how this happened to her

So… What is Tia’s diagnosis?

Acute Renal Failure Acute Renal Failure

Anatomy of the Kidney

http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html

Nephron

http://www.venofer.com/VenoferHCP/Venofer_kidneyFunction.html

10 Functions of the Kidney’s• Urine Formation: Formed in the nephrons through a complex

three-step process: GF, tubular reabsorption, and tubular secretion

• Excretion of waste products: eliminates the body’s metabolic waste products (urea, creatinine, phosphates, sulfates)

• Regulation of electrolytes: volume of electrolytes excreted per day is exactly equal to the volume ingested – Na – allows the kidney to regulate the volume of body fluids, dependent

on aldosterone (fosters renal reabsorption of Na)– K – kidneys are responsible for excreting more than 90% of total daily

intake• RETENTION OF K IS THE MOST LIFE-THREATENING EFFECT RETENTION OF K IS THE MOST LIFE-THREATENING EFFECT

OF RENAL FAILUREOF RENAL FAILURE

Renin-Angiotensin System

http://en.wikipedia.org/wiki/Image:Renin-angiotensin-aldosterone_system.png

Kidney Function con’td

• Regulation of acid-base balance: elimination of sulphuric and phosphoric acid

Kidney function cont’d

• Control of water balance: Normal ingestion of water daily is 1-2L and normally all but 400-500mL is excreted in the urine– Osmolality: degree of dilution or concentration of urine

(#particles dissolved/kg urine (glucose & proteins are osmotically active agents)

– Specific Gravity: measurement of the kidney’s ability to concentrate urine (weight of particles to the weight of distilled water)

– ADH: vasopressin – regulates water excretion and urine concentration in the tubule by varying the amount of water reabsorbed.

Still talking about kidney function…

• Control of blood pressure: BP monitored by the vasa recta. – Juxtaglomerular cells, afferent arteriole, distal tubule, efferent

arteriole http://www.wisc-online.com/objects/AP2204/AP2204.swf

• Renal clearance: ability to clear solutes from plasma– Dependent on… rate of filtration across the glomerulus,

amount reabsorbed in the tubules, amount secreted into the tubules

– CREATININECREATININE• Regulation of red blood cell production: Erythropoeitin is

released in response to decreased oxygen tension in renal blood flow. This stimulates the productions of RBCs (increases amount of hemoglobin available to carry oxygen)

Kidney function cont’d

• Synthesis of vitamin D to active form: final conversion of vit D into active form to maintain Ca balance

• Secretion of prostaglandins: important in maintaining renal blood flow (PGE & PGI). They have a vasodilatory effect

Timeline of Events

PIH HELLP EMERGENCY C-SECTION HEMORRHAGE

HYPOVOLEMIAHYPOVOLEMIC SHOCK

ACUTE RENAL FAILUREACUTE RENAL FAILURE

HELLP SYNDROME

• A syndrome featuring a combination of "H" for hemolysis (breakage of red blood cells), "EL" for elevated liver enzymes, and "LP" for low platelet count (an essential blood clotting element).

• PREGNANCY COMPLICATION - occurring in 25% of pregnancies with toxemia or pre-eclampsia.

• Symptoms include-– Shortness of breath– H/A– Dimmed vision– Nausea– Dizziness & Fainting– Edema– Pain in the upper abdomen

Effects of HELLP on Mom & Baby

• Mothers with HELLP are at increased risk for:– Liver rupture, DIC, abruptio placentae, and acute acute

renal failurerenal failure, stroke, seizure, ARD, pulmonary edema

– 1st order of tx is management of blood clotting issues

– Women with a hx of HELLP are considered at risk for future pregnancies

– After delivery, mothers vitals are CLOSELY monitored to observe for complications

Acute Renal Failure

Definition

• Acute renal failure (ARF) is an abrupt and sudden reduction in renal function resulting in the inability to excrete metabolic wastes and maintain proper fluid & electrolyte balance

• It is usually associated with oliguria (urine output <30cc/hr or <400cc/day), although urine output may be normal or increased

• BUN & creatinine values are elevated

Statistics of ARF

• Frequency: condition develops in 5% of hospitalized patients and 0.5% patients require dialysis– Elderly are at high risk– Post-op patients

• Mortality: the mortality rate estimates vary from 25-90%

• Race: no racial predilection is recognized

Pathophysiology

• ARF may occur in 3 clinical settings:– As an adaptive response to severe volume

depletion and hypotension, with structurally and functionally intact nephrons (Prerenal)

– In response to cytotoxic or ischemic insults to the kidney, with structural and functional damage (Intrinsic or Intrarenal)

– Obstruction to the passage of urine (Postrenal)

Phases of Acute Renal Failure

• Clinical progression of reversible RF occurs in four phases:– Initiation phase

• Begins with initial insult and ends when oliguria develops– Oliguric phase

• Accompanied by rise in serum concentrations of substances usually excreted by kidneys (urea, creatinine, ua, organic acids, intracellular cations [K+ & Mg])

• urinary output <400cc/day• May last 1-3 weeks

– Diuretic phase• The kidneys begin to recover• Initially produce hypotonie urine d/t increase in GFR

– Recovery phase• Tubular function restored• Diuresis subsides and kidney begins to function normally again

Prerenal acute renal failure

• Is the most common cause of ARF occurring in 60-70% of cases

• It is caused by impaired blood flow as a result of intravascular depletion, which leads to decreased effective circulating volume to the kidneys

• In patients with prerenal ARF, the parenchymal is undamaged, and the kidneys respond as if volume depletion has occurred.

Prerenal ARF

• Causes include:– Secondary to renal hypoperfusion which occurs in setting of

extracellular fluid loss• Diarrhea• Vomiting • Diuretics

– Impaired/inadequate cardiac output– Drugs

• NSAIDs• ACE Inhibitors

– Hypovolemia– Hemorrhage– Renal vasoconstriction

Intrinsic acute renal failure

• Is the result of actual parenchymal damage to the glomeruli or kidney tubules

• A physiologic hallmark is failure to maximally concentrate urine

• Is divided into 4 categories:– Acute tubular disease – Glomerular disease– Vascular disease– Interstitial disease

Intrinsic ARF

• Acute Tubular Necrosis – most common type of ARF, a more ischemic insult to the

kidneys, usually induced by ischemia or toxins– Caused by:

• Burns, and crush injuries – myoglobin & hemoglobin are liberated causing renal toxicity or ischemia

• Drugs – NSAIDs, ACE inhibitors, aminoglycosides• Infections• Nephrotoxic agents – contrast agent

• Glomerulonephritis – uncommon cause, most associated with CRF– Caused by:

• Can be a primary disorder or can occur secondary to systemic disease

• Systemic lupus erythematosus

Intrinsic ARF

• Acute Interstitial Nephritis – Interstitial disturbance that leads to ARF– Caused by:

• Allergic reaction to drugs

• Vascular Disease – Can occur on microvascular and macrovascular– Caused by:

• Microvascular – Hemolytic anemia– ARF secondary to small vessel thrombosis or occlusion

• Macrovascular– Suspected in elderly– Renal artery stenosis or thrombosis– Atheroembolism secondary to atrial fibrillation and aortic disease

Postrenal acute renal failure

• Is rare and occurs with urinary tract obstruction that affects the kidneys bilaterally

• Pressure rises in the kidney tubules, eventually the GFR decreases

Postrenal ARF

• Causes include:– Bladder tract obstruction– Prostatic hypertrophy– Catheters– Neurogenic bladder

• Postrenal causes are typically reversible

Assessment

• History– Observe for disorder that predisposes pt to ARF– Ask questions about recent illness, infections, or

injuries– Medication history– Urinary patterns– History of GI problems

• Psychosocial– Anxious– Family members

Clinical Manifestations of ARF• Cardiovascular

– Arrhythmias– BP, N, high or low– Anemia– P, rapid, bounding, or N– Pericardial-type chest pain

• Respiratory– Dyspnea– Crackles– Tachypnea– Kussmaul’s respirations

• Mental Status– Lethargy– Tremors– Memory loss– Confusion

• Musculoskeletal– Muscle spasms– Weakness

• Genitourinary– Oliguria– Anuria– abN urine colour, clarity, smell

• GI– Moist tongue & increased saliva – Dry tongue & mucous membranes– N&V

• Integumentary– Moist, warm skin & pitting edema– Decreased skin turgor– bruises– Pallor– Thin, brittle hair & nails

Nursing Care Plan

• Fluid volume deficit related to hemorrhage (hypovolemic shock)– Priority to restore fluid balance and circulation

• The patient will: – show stable vital signs

– have adequate urine output >30cc/hr

– have strong peripheral pulses indicating tissue perfusion

– display LOC normal for patient

Nursing Care Plan

• Interventions– Bleeding reduction, fluid

resuscitation, blood product administration, IV therapy

– Monitor VS q2h– Monitor weight daily– Skin & tongue turgor– Monitor and document I&O– Monitor CBC, ABG,

urinalysis, ECG

• Rationales– Early intervention can prevent

progression of hypovolemia to hypovolemic shock that may result in renal damage

– S&S correlate with the approximate percentage of volume loss

• Medullary vasomotor center stimulation via the baroreceptor reflex

• ADH– Foley catheter facilitates

monitoring of urine output– Shock pt hemodynamically

unstable with compromised compensatory mechanisms, volume admin may cause fld overload

Nursing Care Plan

• Electrolyte imbalance related to decreased electrolyte excretion, and metabolic acidosis– Priority to prevent complications of electrolyte

imbalance

• Within 24h of admission and then continuously, the pt will:– Maintain serum electrolyte levels within acceptable

limits

– Have normal sinus rhythm

Nursing Care Plan

• Interventions– Monitor & document

electrolyte levels q8-12h, especially:

• K+, P, Ca, Mg

– Monitor ABG– Monitor ECG especially:

• High tented T waves, prolonged PR interval or widened QRS complex

– Limit dietary & drug intake of potassium

• Rationales– Kidneys’ ability to regulate

electrolyte excretion & reabsorption may result in high K+ & P, low Ca, & high/low Mg levels.

– ARF causes metabolic acidosis which may increase the release of K+ from cells in exchange for H+ ions

– Electrolyte abN can trigger arrhythmias & cardiac arrest

– When kidneys cannot excrete K+, excess intake can increase serum K+ to dangerous levels

Nursing Care Plan

• Knowledge deficit of acute renal failure related to lack of exposure to information on management of complex condition– Priority to provide in depth information on acute renal

failure

• Upon discharge the patient will:– Be able to identify signs and symptoms to report to

nurse or physician– Commitment to comply with treatments, including

dialysis, dietary modifications, and activity restrictions

Nursing Care Plan

• Interventions– Provide as appropriate

information on the severity of ARF & dialysis

• Stages of ARF• Medications including action

and adverse effects• S&S• Procedures such as dialysis

including schedule and adverse effects

• Dietary modifications including limitations of proteins (catabolism), electrolytes and fluids

• Rest and activity restrictions

• Rationales– The patient and family need

assistance, explanation, and support during this time.

– Teaching may decrease anxiety and fear, and enhance recovery to patient and family members.

– Continued assessment of the patient for complications of ARF and of its precipitating cause is essential.

Acute Renal Failure

LAB VALUES

Medications for ARF

Pharmacologic treatment of ARF has been attempted on an empirical basis, with varying success rates. Several promising experimental therapies in animal models are awaiting human trials

It is critical to adjust (decrease or discontinue) medication dosages for patient in acute renal failure. Administering the average dose to patient in renal failure can kill a patient.

Medications for ARF continued

Immediate goal is to retain fluid volume deficit through use of blood products and crystalloids

• Normal Saline (0.9% Na) – only one that is compatible with blood transfusions– Restores fluid loss

– Provides electrolytes resembling those of plasma

• Packed RBC

– To increase blood volume

– To restore blood to kidneys

Medications for ARF continued

•Diuretics –Furosemide (Lasix) only given with severe fluid overload

•Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the thick ascending loop of Henle and the distal renal tubule

–Adult dose: 20-80 mg PO/IV once; repeat 6-8h prn or dose may be increased by 20-40 mg no sooner than 6- 8h after previous dose until desired effect

–Nursing Assessments: Watch for hypokalemia, assess BP before and during therapy can cause hypotension

Medications for ARF continued

• Vasodilators – Dopamine

• In small doses causes selective dilatation of the renal vasculature, enhancing renal perfusion.

• Reduces sodium absorption, thereby decreasing the energy requirement of the tubules. This enhances urine flow, which, in turn, helps prevent tubular cast obstruction.

– Adult dose: 2-5 mcg/kg/min

– Nursing Assessments: Monitor BP during administration, stop infusion if BP drops 30mm Hg, Monitor I&O

Medications for ARF continued

• Alkalinizer– Sodium Bicarbonate– Increases plasma bicarbonate, which buffers Hydrogen ion

concentration; reverses acidosis– Adult Dose: Initial dose IV bolus 1 mEq/kg, then infuse 2-5

mEq/kg over 4-8 hr depending on CO2, pH• Dilute with equal amounts of NS, 2-5 mEq/kg

– Nursing assessments: Assess resp. and pulse rate, rhythm, depth, lung sounds, monitor I&O, electrolytes, blood pH, PO2, HCO3, monitor urine pH, and UO during beginning of treatment, monitor for alkalosis, monitor ABGs and blood studies

13 have passed and now Tia is diagnosed with…

Chronic Renal Failure• 13 years have passed Tia is now 39 years of age and

has been experiencing declining renal function over the past 13 years. Tia has lost 15lbs on her already small frame, she feels generally ill most of the time with frequent N&V, she suffers from fatigue, muscle twitching & cramps decreased sensation in her hands and feet and generalized puritus. The Physician has diagnosed Tia with ESRD and has determined that long term dialysis will be required.

Chronic Renal FailureChronic Renal Failure

ESRFESRF

Definition

• Also known as End-Stage Renal Failure (ESRF), is a progressive deterioration in renal function in which the body’s ability to maintain metabolic and fluid and electrolyte balance fails, resulting in uremia (retention of urea and other nitrogenous wastes in the blood).

• decreased kidney glomerular filtration rate (GFR) of <60 mL/min/1.73 m2 for 3 or more months

Statistics

• In the U.S. The US Renal Data System (USRDS) has shown a dramatic increase in patients with CRF who require chronic dialysis or transplantation. In 1999, there were 340,000 such patients, but, by 2010, this number is projected to reach 651,000.

• Internationally: The incidence rates of end-stage renal disease (ESRD) have increased steadily internationally since 1989. The United States has the highest incident rate of ESRD, followed by Japan. Japan has the highest prevalence per million population, with the United States taking second place.

Statistics Cont’d

• Mortality /Morbidity: CRF is a major cause of morbidity and mortality, particularly at the later stages. The 5-year survival rate for a patient undergoing chronic dialysis is approximately 35%. This is approximately 25% in patients with diabetes. The most common cause of death in the dialysis population is cardiovascular disease.

• Race: Affects all races

Pathophysiology

• As renal function declines, the end products of protein metabolism (which are normally excreted in the urine), accumulate in the blood. Uremia develops and adversely effects every system in the body.

• The greater the buildup of waste products, the more severe the symptoms.

• Approximately 1 million nephrons are present in each kidney, each contributing to the total GFR. Regardless of the etiology of renal injury, with progressive destruction of nephrons, the kidney has an innate ability to maintain GFR by hyperfiltration and compensatory hypertrophy of the remaining healthy nephrons.

• This nephron adaptability allows for continued normal clearance of plasma solutes such that substances such as urea and creatinine start to show significant increases in plasma levels only after total GFR has decreased to 50%, when the renal reserve has been exhausted. The plasma creatinine value will double with a 50% reduction in GFR.

Stages of Chronic Renal Disease

• 3 stages in nephron function

• Stage 1: Reduced Renal Reserve Characterized by a 40%-75% loss of nephron

funtion. The patient is usually asymptomatic because the remaining nephrons are able to carry out normal function of the kidney

Stage 2 of Renal Disease

• Stage 2: Renal Insufficiency Occurs when 75%-90% of nephron function is

lost. At this point, the serum creatinine and BUN rise, the kidney loses its ability to concentrate urine and anemia develops. The patient may report polyuria and nocturia

Stage 3 of Renal Disease

• Stage 3: End-Stage Renal Disease The final stage, occurs when there is less than

10% of nephron function remaining. All normal regulatory, excretory, and hormonal functions of the kidneys are severely impaired. ESRD is evidenced by elevated creatinine and BUN levels as well as electrolyte imbalances.

Dialysis is usually indicated at this point.

Glomular Filtration Rate

• GFR: a Kidney function test in which results can be determined from amount of ultrafiltrate formed by plasma flowing through the glomeruli of the kidney.

• As glomular filtration decreases, the serum creatinine and BUN levels increase.

Causes Type 1 and type 2 diabetes mellitus

cause a condition called diabetic nephropathy, which is the leading cause of kidney disease in the United States.  

High Blood Pressure (hypertension), if not controlled, can damage the kidneys over time.

Glomerulonephritis is the inflammation and damage of the filtration system of the kidney and can cause kidney failure. Postinfectious conditions and Lupus are among the many causes of glomerulonephritis.

More Causes Polycystic Kidney Disease is an example of a hereditary cause of chronic

kidney disease wherein both kidneys have multiple cysts 

Use of analgesics such as acetaminophen (Tylenol) and ibuprophen regularly over long durations of time can cause analgesic nephropathy, another cause of kidney disease. Certain other medications can also damage the kidneys.

Clogging and hardening of the arteries (atherosclerosis) leading to the kidneys causes a condition called ischemic nephropathy, which is another cause  of progressive kidney damage.

Obstruction of the flow of urine such as by stones, an enlarged prostate, strictures (narrowings), or cancers may also cause kidney disease

Clinical Manifestation

• Patients with CRF stage 3 or lower (GFR >30 mL/min) generally are asymptomatic and do not experience clinically evident disturbances in water or electrolyte balance or endocrine/metabolic disturbances.

• Generally, these disturbances clinically manifest with CRF stages 4 and 5 (GFR <30 mL/min).

Clinical Manifestations

• Hyperkalemia usually develops when GFR falls to less than 20-25 mL/min because of the decreased ability of the kidneys to excrete potassium.

• Metabolic acidosis because the kidney cannot excrete increased loads of acid.

Clinical Manifestations

• Extracellular volume expansion and total-body volume overload results from failure of sodium and free water excretion.

• Anemia principally develops from decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC).

• Calcium and Phosphorus imbalance occurs because of a disorder in metabolism. They have a reciprocal relationship in the body; as one rises, the other decreases.

Signs and Symptoms

• Neurologicweakness, fatigue, confusion, disorientation, tremors, seizures, restlessness of legs, burning of soles of feet, behavioral changes.

• IntegumentaryGray-bronze skin colour, dry, flaky

skin, pruritus, ecchymosis, thin brittle nails, coarse, thinning hair

• PulmonaryCrackles, thick tenacious sputum,

depressed cough reflex, pleuritic pain, shortness of breath, engorged neck veins, tachypnea, uremic pneumonitis, “uremic lung”

• GastrointestinalAmmonia odour to breath,

metallic taste, mouth ulcerations and bleeding, anorexia, N&V, hiccups, constipation or diarrhea, bleeding from GI tract.

• HematologicAnemia, thrombocytopenia• MusculoskeletalMuscle cramps, loss of muscle

strength, renal osteodystrophy, bone pain, bone fractures, foot drop

Nursing Care Plan Excess fluid volume r/t decreased

urine output, and retention of sodium and water

Goal is maintenance of ideal body weight without access fluid

• Nursing Interventions Assess fluid Status Daily weight I & O Skin turgour & edema Distention of neck veins BP, P, R Limit fluid intake to prescribed

volume Explain to pt and family rationale for

restriction of food Provide or encourage frequent oral

care

Rationale Assessment provides baseline and ongoing

database for monitoring changes and evaluating interventions

Fluid restriction will determine on the basis of weight, urine output, and response of therapy

Understanding promotes pt and family cooperation with fluid restrictions

Oral hygiene minimizes dryness of oral mucous membranes

Expected Outcomes Demonstrates no rapid weight changes Maintains dietary and fluid restrictions Exhibits normal skin turgour without edema Normal vitals Reports no difficulty breathing or shortness

of breath Reports decrease dryness of oral mucous

membranes.

Nursing Care Plan

Hyperkalemia, pericarditis, pericardial effusion and temponade, hypertension, anemia, bone disease

• Goal: Patient experiences and absence of complications

Nursing Interventions Hyperkalemia Monitor serum K levels and

notify physician if greater than 5.5 mEq/L.

Assess patient for muscle weakness, diarrhea, ECG changes( tall tented Twaves, widened QRS).

• Rationale Hyperkalemia causes

potentially life-threatening changes to the body

Cardiovascular S & S are characteristic of hyperkalemia

Expected Outcomes Pt has normal K level Experiences no muscle

weakness or diarrhea, Exhibits normal ECG pattern Vital signs are within normal

limits

• Pericarditis, Pericardial effusion, tamponade

Assess for fever, chills, chest pain and pericardial friction rub (signs of pericarditis).

If pt has pericarditis, ax q 4 hrs

• Extreme hypotension• Weak of absent

peripheral pulses, altered level of consciousness, bulging neck veins.

• Rationale About 30-50% of CRF pts develop

pericarditis due to uremia; fever ,chest pain, and pericardial friction rub are classic signs

Pericardial effusion is common following pericarditis. Signs of effsusion: paradoxical pulse (> 10 mm drop in BPduring inspiration) and signs of shock d/t compression of the heart by a lg effusion.

Cardiac tamponade exists when the pt is severely compromised hemodynamically

Outcomes Has strong and equal peripheral pulse Absence of paradoxical pulse Absence of pericardial effusion, or

tamponade

• Hypertension Monitor and record blood

pressure Administer antihypertensives

as prescribes Encourage compliance with

dietary and fluid restriction therapy

Teach pt report signs of fluid overload, vision changes, headaches, edema, seizures

• Rationale Antihypertensives play a key role in

tx of hypertension associated with CRF.

Adherence to diet and fluid restrictions prevents excess fluid and sodium accumulation

These are indications of inadequate control of hypertension, and need to alter therapy

Outcomes BP is within normal limits No headaches, visual problems or

seizures No edema Demonstrates compliance with

dietary and fluid restrictions

• Anemia Monitor RBC count, Hg, and

HCT levels Administer prescribes meds:

iron and folic acid Avoid drawing unnecessary

blood specimens Teach pt to prevent bleeding;

avoid vigorous nose blowing Administer blood component

therapy

• Rationale Provides Ax of degree of anemia RBCs need iron and folic acid to

be produced. Anemia is worsened by drawing

numerous specimens Blood component therapy may

be needed if pt has symptoms Outcomes Pt has normal colour without

pallor Hematology values are within

acceptable limits Experiences not bleeding form

any site.

• Bone Disease Administer the following

meds as prescribed: phosphate binders, calcium supplements, vit D supplements

Monitor serum lab values ( calcium, phosphorus, aluminum)

Assist pt with exercise program

Rationale CRF causes numerous physiologic

changes affecting calcium, phosphorus and vit D metabolism.

Hyperphophatemia, hypocalcemia, and excess aluminum accumulation are common

Bone demineraliztion decreases with immobility.

Outcomes Serum calcium, phosphorus, and

aluminum levels are within acceptable ranges.

Has no bone demineralization Discuss importance of maintaining

activity level and exercise program.

Diet

• Protein restriction b/c urea, uric acid and organic acids- the breakdown product of dietary and tissue proteins- accumulate rapidly in the blood when there is impaired renal clearance.

• The allowed protein must be of high biologic value (diary products, eggs, meats). These proteins are those that are complete proteins and supply the essential amino acids necessary for cell growth and repair; also maintenance of fluid balance, healing and skin integrity, and maintenance of immune function.

• Fluid restrictions: fluid allowance is usually 500-600 ml more than the previous day’s 24 hr output.

• Calories are supplied by carbs and fats to prevent wasting and malnutrition

• Vitamin supplementation because a protein restricted diet does provide the necessary amounts of vitamins and the pt on dialysis may lose water soluble vitamins from the blood during treatment.

Chronic Renal Failure

LAB VALUES

Medications for CRF• Diuretics

– Furosemide (Lasix) only given with severe fluid overload

• Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the thick ascending loop of Henle and the distal renal tubule

– Adult dose: 20-80 mg PO/IV once; repeat 6-8h prn or dose may be increased by 20-40 mg no sooner than 6-8h after previous dose until desired effect

– Nursing Assessments: Watch for hypokalemia, assess BP before and during therapy can cause hypotension

Medications for CRF continued

• Phosphate-lowering agents – Calcium acetate (Calphron, PhosLo)

• Combines with dietary phosphorus to form insoluble calcium phosphate, which is excreted in feces.

– Adult dose: 1-2 g PO bid-tid with each meal; increase to bring serum phosphate value to 6 mg/dL as long as hypercalcemia does not develop;

– Calcium carbonate (Caltrate, Apo-Cal, Tums) • Successfully normalizes phosphate concentrations• Neutralizes gastric acidity, increase serum Ca

– Adult dose: 1-2 g PO divided bid-tid; with meals as a phosphorous binder; between meals as a calcium supplement

Phosphate-lowering agents

– Calcitriol (Rocaltrol, Calcijex) • Increases intestinal absorption of calcium for treatment of

hypocalcemia and increases renal tubular resorption of phosphate

– Adult dose for hypocalcemia during chronic dialysis:• 0.25 mcg/day or every other day, may require 0.5-1 mcg/day

PO

– Sevelamer (Renagel)• Indicated for the reduction of serum phosphorous in patients

with ESRD.

– Adult dose: Initial: 800-1600 mg PO tid with mealsMaintenance: Increase or decrease by 400-800 mg per meal q2wk to maintain serum phosphorous at 6 mg/dL or less

Phosphate-lowering agents

• Lanthanum carbonate (Fosrenal) – for reduction of high

phosphorus levels in patients with ESRD

– Adult dose: Initial: 250-500 mg PO tid pc (chewable tabs); adjust dose q2-3wk to target serum phosphorus levelMaintenance: 500-1000 mg PO tid pc

Phosphate-lowering agents– Doxercalciferol (Hectorol)

• To lower parathyroid hormone levels in patients undergoing chronic kidney dialysis. Increases serum Ca

– Adult dose: 10 mcg PO 3 times/wk at dialysis; increase dose by 2.5 mcg/8 wk if iPTH is not lowered by 50% and fails to reach the target range; not to exceed 20 mcg/3 times/wkAlternatively, 4 mcg IV 3 times/wk; may adjust dose by 1-2 mcg/8 wk to maintain iPTH levels

– Nursing Assessment for all phosphate lowering agents: Monitor BUN, creatinine, chloride, electrolytes, urine pH, urinary calcium, mg, phosphate, urinalysis urinary Ca should be 9-10mg/dl, assess for hypocalcemia: headache, N/V, confusion

Medications for CRF continued

• Anemia– Epoetin alfa (Epogen, Procrit)

• Stimulates RBC production

– Adult dose: 50 -150 U/kg IV/SC 3 times per week, then adjust dose by 25 U/kg/dose to maintain appropriate Hct; maintenance 12.5-25 U/kg, titrate to target Hct,

– Nursing Assessment: Monitor renal studies: urinalysis, protein, blood, BUN, creatinine; I&O. Monitor blood studies, Hgb, Hct, RBC, WBC, INR, PTT

Medications for CRF continued

– Darbepoetin (Aranesp)• Stimulates erythropoiesis

– Adult dose: 0.45 ug/kg IV/SC as a single injection, titrate not to exceed a target Hgb of 12 g/dl

– Has a longer half-life than epoetin alfa– Nursing Assessments: Assess blood studies,

renal studies; assess BP, check for rising BP as Hct rises

Medications for CRF continued

• Iron Salts– To treat anemia– Ferrous sulfate (Feosol, Feratab, Slow FE)

• Replaces iron stores need for RBC development– Adult dose: 100-200mg tid– Iron sucrose (Venofer)

• Used to treat iron deficiency dute to chronic hemodialysis– Adult dose: IV 5ml (100mg of elemental iron) given

during dialysis, most will need 1000mg of elemental iron over 10 dialysis

• Nursing Assessments: Monitor blood studies, Hct, Hgb, total Fe, monthly. Assess bowel elimination for constipation

Dialysis

What is Dialysis?

• Dialysis is a type of renal replacement therapy which is used to provide artificial replacement for lost kidney function due to acute or chronic kidney failure

• It is a life support treatment, it does not cure acute or chronic renal failure• May be used for very sick clients who have suddenly lost kidney function • May be used for stable clients who have permanently lost kidney function• Healthy kidneys remove waste products (potassium, acid, urea) from the

blood and they also remove excess fluid in the form of urine• Dialysis has to duplicate both of these functions

Dialysis – waste removal Ultrafiltration – fluid removal

Principle of Dialysis

• Dialysis works on the principle of diffusion of solutes along a concentration gradient across a semipermiable membrane

• Blood passes on one side of the semipermeable membrane, and a dialysis fluid is passed on the other side

• By altering the composition of the dialysis fluid, the concentrations of the undesired solutes (potassium, urea) in the fluid are low, but the desired solutes (sodium) are at their natural concentration found in healthy blood

Prescription for Dialysis

• A prescription for dialysis is given by a physician who specializes in the kidney (nephrologist)

• The MD will set various parameters for the treatmentTime and duration of the dialysis sessionsSize of the dialyzerRate of blood flow

2 Main Types of Dialysis

• Hemodialysis

• Peritoneal Dialysis

Hemodialysis

Adapted from National Institute of Diabetes and Digestive and Kidney Diseases.

National Institute of Diabetes and Digestive and Kidney Diseases. End-stage renal disease: choosing a treatment that's right for you. Available at: http://www.niddk.nih.gov/health/kidney/pubs/esrd/esrd.htm. Accessed May 10, 2000.

What is Hemodialysis (HD)?

• Client’s blood is passed through a system of tubing (dialysis circuit) via a machine to a semipermeable membrane (dialyzer) which has the dialysis fluid running on the other side

• The cleansed blood is then returned via the circuit back to the body

• The dialysis process is very efficient (much higher than in the natural kidneys), which allows treatments to take place intermittently (usually 3 times a week), but fairly large volumes of fluid must be removed in a single treatment which can be very demanding on a client

Side Effects of HD

• The side effects are proportionate to the amount of fluid being removed

• Decreased blood pressure• Fatigue• Chest pains• Leg cramps• Headaches• Electrolyte imbalance• N&V• Reaction to the dialyzer • Air embolism

Complications of HD

• Because HD requires access to the circulatory system, clients have a portal of entry for microbes, which could lead to infection The risk of infection depends on the type of access used

• Bleeding may also occur at the access site• Blood clotting was a serious problem in the past, but the

incidence of this has decreased with the routine use of anticoagulants (Heparin is the most common) Anticoagulants also come with their own risk of side effects and

complications

Rare Complication of HD

• On the rare occasion, a client may have a severe anaphylactic reactionSneezingWheezingSOBBack painChest painSudden death

• This can be caused by the sterilant in the dialyzer or the material in the membrane itself

Three Types of Access for HD

• IV catheter• Arteriovenous (AV) fistula• Synthetic graft• The type of access is influenced by factors such

as expected time course of the clients renal failure and the condition of the clients vasculature

• Some clients may have multiple accesses, usually because an AV fistula or a graft is maturing and an IV catheter is still being used

IV Catheter (Central Venous Catheter)

• Consists of a plastic catheter with two lumens which is inserted into a large vein (vena cava via the internal jugular vein) to allow large flows of blood to be withdrawn from the first lumen

• The blood goes into the dialysis circuit, and is returned to the body via the second lumen Non-tunneled Tunneled

• This type of access is used for clients who need rapid access for immediate dialysis Clients who are likely to recover from ARF Client with end-stage renal failure Clients waiting for other sites to mature

• This type of access is very popular for clients because it doesn’t involve needles for each treatment

Complications of an IV Catheter

• Venous StenosisThis is the abnormal narrowing of the blood

vesselBecause the catheter is a foreign body in the

vessel, it often provokes an inflammatory reaction in the vein wall

This results in scarring and narrowing of the vein, often to the point where the vein occludes

AV Fistula

• This access is recognized as the preferred access method• To create a fistula a vascular surgeon joins an artery and

a vein together• Since this bypasses the capillaries, blood flows at a very

high rate through the fistula This can be felt by placing a finger over a mature fistula (thrill)

• Usually created in the non-dominant hand• It can be situated on the hand, forearm or the elbow• It will take approximately 4-6 weeks to mature• During treatment, 2 needles are inserted, one to draw

blood out of the body and the other to return blood to the body

Advantages of an AV Fistula

• Decreased infection rate

• Increased blood flow rates, therefore a more effective dialysis treatment

• Decreased incidence of thrombosis

Complications of an AV Fistula

• If an AV fistula has a very high flow rate and the vasculature that supplies the rest of the limb is poor, than a ‘steal syndrome’ can occur Blood that enters the limb is drawn into the fistula and returned

to the general circulation without entering the capillaries of the limb

This results in cool extremities of the limb, cramping pains and possible tissue damage

• Long term complications can be the development of a bulging in the wall of the vein (aneurysm) The vessel wall is weakened by the repeated insertion of needles

over time Can be reduced by careful needling technique

AV Graft

• This is much like a fistula, except an artificial vessel is used to join the artery and the vein

• Grafts are used when client’s own vasculature does not permit a fistula

• An AV graft will mature much faster than an AV fistula, and it could be ready to use within days after formation

Complications of an AV Graft

• AV grafts are at high risk for narrowing where the graft is sewn to the veinAs a result clotting or thrombosis may occur

• As a foreign material is being placed in the body, there is a greater risk of infection

Equipment Needed for HD

• The HD machine performs the function of pumping the patient's blood and the dialysate through the dialyzer.

• The newest dialysis machines on the market are highly computerized and continuously monitor an array of safety-critical parameters, including blood and dialysate flow rates, blood pressure, heart rate, conductivity, pH, etc.

• If any reading is out of normal range, an audible alarm will sound to alert the patient-care technician who is monitoring the patient.

Equipment – Water System

• An extensive water purification system is absolutely critical for HD

• Since dialysis patients are exposed to vast quantities of water, which is mixed with the acid bath to form the dialysate, even trace mineral contaminants or bacterial endotoxins can filter into the patient's blood.

• Because the damaged kidneys are not able to perform their intended function of removing impurities, ions that are introduced into the blood stream via water can build up to hazardous levels, causing numerous symptoms including death

• For this reason, water used in HD is purified

Equipment – The Dialyzer

• The dialyzer, or artificial kidney, is the piece of equipment that actually filters the blood

• The blood is run through a bundle of very thin capillary-like tubes, and the dialysate is pumped in a chamber bathing the fibers

• The process mimics the physiology of the glomerulus and the rest of the nephron

• Dialyzers come in many different sizes. A larger dialyzer will usually translate to an increased membrane area, and an increase in the amount of undesired solutes removed from the patient's blood.

• The nephrologist will prescribe the dialyzer to be used depending on the patient

• Dialyzers are not shared between patients in the practice of reuse.

Peritoneal Dialysis

What is Peritoneal Dialysis (PD)?

• Peritoneal dialysis works by using the body's peritoneal membrane, which is inside the abdomen, as a semi-permeable membrane.

• A specially formulated dialysis fluid is instilled around the membrane, using an indwelling catheter, then dialysis can occur, by diffusion

• Excess fluid can also be removed by osmosis, by altering the concentration of glucose in the fluid.

• Dialysis fluid is instilled via a peritoneal dialysis catheter, which is placed in the patient's abdomen, running from the peritoneum out to the surface, near the navel

• Peritoneal dialysis is typically done in the patient's home and workplace, but can be done almost anywhere

Advantages of PD

• Can be done at home

• Relatively easy for the client to learn

• Easy to travel with, bags of solution are easy to take on holiday

• Fluid balance is usually easier when the client is on PD than if the client is on HD

Disadvantage of PD

• Requires a degree of motivation and attention to cleanliness while performing PD

• There are a number of complications

Complications of PD

• Peritoneal dialysis requires access to the peritoneum. As this access breaks normal skin barriers, and as people with renal failure generally have a slightly suppressed immune system, infection is a relatively common problem

• Long term peritoneal dialysis can cause changes in the peritoneal membrane, causing it to no longer act as a dialysis membrane as well as it used to.

• This loss of function can manifest as a loss of dialysis adequacy, or poorer fluid exchange (also known as ultrafiltration failure)

• Fluid may leak into surrounding soft tissue, often the scrotum in males

• Hernias are another problem that can occur due to the abdominal fluid load

Nursing Assessments

• Before client is in the unit, look at the nurses notes from the treatment before Any problems, will help nurse plan for the upcoming treatment

• Look at the client Strength Gait Whether client needs assistance Color Puffiness

Could be caused by excess fluid, too much to drink, more fluid should be taken off with each treatment, changes in voiding pattern (are they voiding less than they did last month)

Assessments Con’t

• Shortness of breath Could indicate fluid around the lungs Ask about SOB at night (does client have to sleep in a sitting

position?)• Ask the client how they are feeling

The client is usually the best source of information Clients are in 3 times a week, dialysis nurses really get to know their

clients• Evaluate access

Bruising, swollen, tender Bruit – listen with the stethoscope for a swishing sound of the blood,

listen all the way up the arm Thrill – felt with the fingers, tells the nurse if the blood is flowing in

the fistula (client’s are told to feel for this at home when a fistula is first initiated)

Assessments During Treatment

• Ask client how he/she feels Dizziness, diaphoretic,

• The machines automatically take BP and HR every 30 minutes Can program the machines to take it at whatever interval is

necessary (every min, 10 min, 15 min)• Try to recognize a problem before it starts (ex. Hypovolemic

shock)• Assess access site

Watch trend of BP It usually gradually decreases throughout the course of the

treatment, but look for sudden or drastic drops• Assess access site

Bleeding, swelling, tenderness

Nursing Interventions

• If client comes in with shortness of breath, offer O2 which can be kept on for the full treatment if necessary

• ComfortClient’s are sitting in the same chair for up to four

hoursOffer extra pillows, some clients have special back

pillow they leave in the unitEnsure TV and audio is working properly

Nursing Interventions Con’t

• If the blood pressure is dropping too quickly:Slow or stop fluid removal for a time periodThe machines are constantly being adjusted throughout

the course of the treatment depending on the BP If the BP drops suddenly 200-300cc of normal saline can

be given to balance fluid levels• Usually, more fluid will be taken off at the beginning of the

treatment, this will allow the client to feel better at the end• If the client is elderly, fluid removal starts slowly to ease

them into the treatment

Responsibilities of Nursing StaffPrior to Dialysis

• Ensure client is ready to sit for up to four hoursEncourage client to use washroom before

arriving to the unitTry to avoid laxatives if possible before

treatment

• Ensure client has eaten meal prior to treatment

Responsibilities of Nursing StaffAfter Dialysis

• A dialysis nurse will give unit leader or primary nurse a verbal report of treatment Any complications during treatment Check BP standing and sitting Assess access site

• Encourage client to rest Avoid treatments or physio for a couple of hours if possible

• Watch fluid intake Be aware if client is on fluid restriction

• Check thrill and bruit• Do not take a BP on access arm• Do not take blood from access arm

Questions?Questions?

Thank you for listening.Thank you for listening.