Crit Care Nurse 2006 Broscious 17 27

Sharon K. Broscious and Judith CastagnolaChronic Kidney Disease: Acute Manifestations and Role of Critical Care Nurses

Published online http://www.cconline.org 2006 American Association of Critical-Care Nurses

2006, 26:17-27. Crit Care Nurse

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362-2049. Copyright 2011 by AACN. All rights reserved.Telephone: (800) 899-1712, (949) 362-2050, ext. 532. Fax: (949)The InnoVision Group 101 Columbia, Aliso Viejo, CA 92656.

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http://ccn.aacnjournals.org CRITICALCARENURSE Vol 26, No. 4, AUGUST 2006 17

Sharon K. Broscious is an associateprofessor in the School of Nursing atTroy University, Atlantic Region, inNorfolk, Va.

Judith Castagnola is a facility adminis-trator at DaVita Peninsula Dialysis inNewport News, Va.

Despite the improved diagno-sis and treatment of kidney disease,late diagnosis with resultant perma-nent damage to the kidneys stilloccurs. A work group established bythe National Kidney Foundation, theKidney Disease Outcome QualityInitiative (KDOQI), was asked todevelop clinical practice guidelinesand a uniform classification systemfor chronic kidney disease (CKD).CKD is a public health issue becauseof its increasing incidence and thehigh cost of interventions.1 An addi-tional concern is the increasing inci-dence of kidney disease in AfricanAmericans and Native Americans.2

According to the 2004 reportfrom the US Renal Data System,3 thenumber of patients with CKD receiv-ing therapy in 2002 was 431284.This number is a 4.6% increase overthe number for the year 2001. Theadjusted rate for CKD was 1435cases per million population72%of patients were undergoing dialysis;

the other 122374 had a functioningtransplant. The adjusted rate ofCKD for the white population was1060 cases per million; for the AfricanAmerican population, 4467 cases permillion; and for the Native Americanpopulation, 2569 cases per million.

In 2002, Medicare expenses forCKD treatment increased 11% overthe level in 2001; Medicare expenseswere $17 billion and non-Medicareexpenses were $8.2 billion. Fromthe individual perspective, Medicarecosts per year are approximately$53000, with deductibles and copay-ments bringing the total to $63000per year. Total cost for the entire CKDprogram was approximately $25.2billion at the end of 2002.3

The KDOQI has identified 5 stagesof kidney failure (Table 1) on the basisof glomerular filtration rate (GFR).4

Normal GFR in men is 125 to 150mL/min per 1.73 m2 (1.73 m2 isconsidered the standard normal bodysurface area). Chronic kidney failure

Chronic Kidney DiseaseAcute Manifestationsand Role of CriticalCare Nurses

CoverArticle

Authors

* This article has been designated for CE credit.A closed-book, multiple-choice examination fol-lows this article, which tests your knowledge ofthe following objectives:

1. Identify the expected outcomes of patients with chronic kidney disease (CKD)

2. Describe the pathophysiology of CKD

3. Discuss the impact of CKD in relation to body systems

Sharon K. Broscious, RN, DSN, CCRNJudith Castagnola, RN, MSN

Corresponding author: Sharon K. Broscious, Troy Uni-versity, Atlantic Region, 5425 Robin Hood Rd, Ste B1,Norfolk, VA 23513. (e-mail: [email protected])

To purchase electronic or print reprints, contact TheInnoVision Group, 101 Columbia, Aliso Viejo, CA92656. Phone, (800) 809-2273 or (949) 362-2050(ext 532); fax, (949) 362-2049; e-mail,[email protected].

CEContinuing Education

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is defined by the KDOQI as havingkidney damage lasting for 3 monthsor more or having a GFR less than60 mL/min per 1.73 m2 for 3 monthsor more, with or without kidney dam-age.4 End-stage renal disease (ESRD) isdescribed as the stage of CKD whendamage to the kidneys is permanentand kidney function cannot maintainlife; consequently, patients at this timerequire dialysis or transplantation.5

ESRD is at the far end of the spectrumof progressive renal dysfunction.Healthy People 2010 identifies the 5risk factors for ESRD as diabetesmellitus, hypertension, proteinuria,family history, and increasing age.2

Unfortunately, patients are oftenasymptomatic in the early stages ofkidney failure when renoprotectivestrategies6 that could slow or reversethe process of kidney damage couldbe implemented. Because of the lackof early signs and symptoms andinterventions, patients may come toan acute care facility with signs andsymptoms of newly diagnosed ESRD.What do critical care nurses need toknow about CKD and its treatmentto improve patients outcomes? Athorough assessment of this complexsituation by critical care nurses is

ventricular hypertrophy and ST-Twaves consistent with a strain pattern.A funduscopic examination showedbilateral chronic and new hemor-rhages (cotton wool hemorrhagesand exudates), arteriolar narrowing,and arteriovenous nicking. Labora-tory results are reported in Table 2.J.M. was admitted to the intensivecare unit with a diagnosis of ESRDdue to hypertension with hyperten-sive crisis and metabolic acidosis.

PathophysiologyThe kidneys act as regulators for

many of the bodys functions andcontrol complex processes that main-tain homeostasis (Figure 1). The kid-neys receive approximately 20% to25% of the cardiac output per minute;blood is filtered through the nephrons,the functioning units of the kidneys.Each kidney has approximately 1million nephrons, providing a largereserve of nephrons that enableshomeostasis to be maintained, evenwhen nephrons have been damaged.7

However, when 90% of nephrons arelost, renal function is significantlyimpaired, resulting in ESRD.4,8 Thebest laboratory indicator of kidneyfunction is the estimated GFR. Severalequations are available to estimateGFR. The National Kidney DiseaseEducation Program of the NationalInstitute of Diabetes and Digestiveand Kidney Diseases, the NationalKidney Foundation, and the AmericanSociety of Nephrology have recentlyrecommended the Modification ofDiet in Renal Disease Study equationas the formula to calculate GFR9:

GFR = 186 (serum creatinine[mg/dL])-1.154 (age [years])-0.203

0.742 (if female) 1.210 (ifAfrican-American)

8

essential, because multiple body sys-tems are altered when kidney func-tion is impaired. In this article, we usea case study to review the pathophysi-ological changes that occur when thekidneys fail, resulting in admission tothe critical care unit. The immediateinterventions and the expected out-comes are also presented.

Case StudyJ.M., a 34-year-old African Amer-

ican man, came to the emergencydepartment with a 6-day history ofincreasing swelling in both lowerextremities. A similar swelling hadoccurred once before recently buthad cleared up spontaneously. J.M.said he had no history of headaches,hypertension, nausea, vomiting ordiarrhea, fever and chills, shortnessof breath, chest pain, urinary prob-lems, weight loss, confusion or otherneurological changes, or exposure totoxic substances. He also stated thathe was not taking any medication.On physical examination, his bloodpressure was 222/142 mm Hg, hisheart rate was 110/min with S3 andS4 gallops, and his respiratory ratewas 24/min with bibasilar crackles.Electrocardiography showed left

18 CRITICALCARENURSE Vol 26, No. 4, AUGUST 2006 http://ccn.aacnjournals.org

Table 1 Chronic kidney disease defined by the National Kidney Foundation*

Stage

1

2

3

4

5

Description

Kidney damage with normalor increased GFR

Kidney damage with milddecrease in GFR

Moderate decrease in GFR

Severe decrease in GFR

Kidney failure

Glomerular filtration rate (GFR), mL/minper 1.73 m2

>90

60-89

30-59

15-29

On the basis of this formula, J.M.had a GFR of 3 mL/min per 1.73 m2,meeting the definition of kidney fail-ure. Whatever the underlying causeof CKD, the effects of kidney failureon the bodys homeostatic mecha-nisms are the same. The next sectionprovides a comparison of the nor-mal homeostatic regulations and thealterations assessed in J.M.

Alterations in Regulatory FunctionsBody Water Regulation

Fluid volume is altered when thekidney loses its ability to excretewater because of damaged nephronsand the resultant decreased GFR.Other factors that contribute to the

developmentof fluid vol-ume overloadare protein-uria andincreasedrenin. Protein-uria occurs inresponse todamage of theglomeruli.High bloodpressure cancause scleroticchanges in theglomeruliwith a result-ant loss ofprotein, espe-cially albuminin the urine.10

This damageto the kidneysfrom hyper-tension is alsoknown ashypertensive


Figure 1 Homeostatic functions of the kidney.

Body water regulation

Urine output

Blood pressure

Normalkidney

function inhomeostasis

Electrolyte balance

Sodium

Potassium

Phosphorus

Calcium

MagnesiumAcid-base balance

Metaboliccompensation

Metabolic (endocrine) regulation

Erythropoietin

Renin-angiotensin-aldosterone

Vitamin D

Excretory regulation

Nitrogenous waste products

Drug metabolites and otherwastes

Uric acid

Table 2 J.M.s laboratory results

Laboratory test

Serum urea nitrogen,mmol/L (mg/dL)

Creatinine, mol/L (mg/dL)

Sodium, mmol/L

Potassium, mmol/L

Chloride, mmol/L

Carbon dioxide,mmol/L

Uric acid, mol/L (mg/dL)

Calcium, mmol/L (mg/dL)

Phosphorus,mmol/L (mg/dL)

Hemoglobin, g/L

Hematocrit

Arterial blood gaseson room air

Urinalysis

Alkaline phosphatase, U/L

Admission results

67.47 (189)

1909.4 (21.6)

127

5.8

90

9.9

1142.0 (19.2)

2.05 (8.2)

3.91 (12.1)

83

0.252

pH 7.32PCO2 22.9 mm HgBicarbonate 11.9 mmol/LBase excess -12PO2 45.9 mm Hg

4+ protein2+ hematuria

536

Results after dialysis

66.04 (185)

1865.2 (21.1)

129

3.9

89

12

Not determined

2.35 (9.4)

3.87 (12)

Not determined

Not determined

pH 7.44PCO2 18.1 mm HgBicarbonate 12.5 mmol/LBase excess -9PO2 81.7 mm Hg

Not determinedNot determined

378

Reference intervals

2.9-6.4 (8-18)

53-106 (0.6-1.2)

135-147

3.5-5.0

95-105

23-30

237.9-505.6 (4-8.5)

2.20-2.58 (8.8-10.3)

0.81-1.61 (2.5-5.0)

140-180

0.42-0.52

pH not determinedPCO2 33-44 mm HgBicarbonate 21-28 mmol/LBase excess not determinedPO2 75-100 mm Hg

30-120



nephrosclerosis and may cause dam-age not only to the glomueruli butalso to the arteriolar walls.8 The lossof albumin in the urine contributesto fluid shifting from the intravascu-lar space to the interstitial spacebecause of decreased oncotic pres-sure. As a response to decreasedGFR, aldosterone is released from theadrenal cortex, causing the kidneysto reabsorb sodium and water. Fluidretention in turn results in the devel-opment of respiratory and cardio-vascular clinical manifestations. InJ.M., cardiovascular assessment find-ings included 3+ edema of the lowerextremities, an albumin level of 32g/L, blood pressure of 222/142 mmHg, the presence of S3 and S4 heartsounds, sinus tachycardia (heart rate108-112/min), crackles in the lungs,and a decreased sodium level (dilu-tional hyponatremia).

Acid-Base BalanceMetabolic acidosis is associated

with CKD because the tubules cannotexcrete hydrogen ions (H+), resultingin the use of bicarbonate (HCO3

-)anions to maintain acid-base balance.Two other buffering systems are inplace that assist in compensating forthe acidosis. Hydrogen ions combinewith ammonia produced in the renaltubule cells to form ammonium,which combines with chloride and isexcreted in the urine. This mechanismhelps to remove H+ while generatingHCO3

-. However, because of impairednephron function, excretion of ammo-nium is decreased. The third mecha-nism involved with acid-base balanceresults in H+ combining with phos-phate (one of the bodys bufferingsystems). Metabolic acidosis alsocontributes to a shift of calcium fromthe bone, allowing H+ to enter and

Serum phosphorus and calciumlevels are also altered in CKD. WhenGFR is less than 30 to 50 mL/minper 1.73 m2, phosphorus excretionis impaired.10 Because of the recipro-cal relationship between phosphorusand calcium, this increased retentionof phosphorus results in a decreasein the serum level of calcium. Threeadditional mechanisms can affectcalcium level. Calcium is found in 3forms in the blood: attached to pro-tein, attached to other complexes,and free or ionized. Because somecalcium is bound to protein, totalserum calcium level can decreasewhen albumin level decreases. J.M.had proteinuria. This loss of albumincan contribute to a decreased serumlevel of calcium. CKD also has aneffect on vitamin D synthesis. Thekidneys normally convert inactivevitamin D to its active form: 1,25-dihydroxycholecalciferol.11 Impairedvitamin D synthesis results indecreased absorption of calcium inthe gastrointestinal tract. The thirdmechanism that affects serum levelsof calcium is the endocrine system.When the serum level of calciumdecreases, the parathyroid glandincreases its secretion of parathyroidhormone, causing calcium to bereleased from the bone and compen-sating for the decreased serum levelof calcium.12 Results of J.M.s labora-tory tests showed a calcium level of2.05 mmol/L (8.2 mg/dL) and aphosphorus level of 3.91 mmol/L(12.1 mg/dL), indicating impairedphosphorus excretion and a recip-rocal decrease in calcium level.

Alterations in Excretory Function

In CKD, nitrogenous wasteproducts from protein metabolism

be buffered in the bone.7 Results ofJ.M.s laboratory tests revealed a pHof 7.32, HCO3

- 11.9 mmol/L, baseexcess -12, and serum carbon dioxide9.9 mmol/L, all indicating metabolicacidosis. A decreased arterial PCO2of 22.9 mm Hg results from anincreased respiratory rate as thebody attempts to compensate forthe acidosis by exhaling the respira-tory acid carbon dioxide. The aniongap can be used to determine thecause of the metabolic acidosis. Nor-mally the kidney conserves HCO3

-

and excretes H+. In CKD, when theglomeruli are damaged, metabolicacids such as sulfuric and phosphoricacid are retained, causing a wideningof the anion gap.8 The anion gap iscalculated mathematically:

Anion gap = Na+ (Cl- + HCO3-)

The normal anion gap is approx-imately 12 mmol/L. J.M.s anion gapwas 127 (90 + 11.9) = 25.1 mmol/L,supporting the diagnosis of metabolicacidosis due to kidney failure.

Electrolyte BalanceMultiple electrolyte levels are

altered in patients with CKD. Potas-sium levels may be normal until late inESRD, and elevated potassium levelsare often associated with CKD becauseof the inability of the kidney to excretepotassium as a result of decreasedGFR. In addition, when metabolic aci-dosis is present, potassium ions shiftfrom the intracellular compartment tothe extracellular space in exchange forH+, in an effort to maintain extra-cellular acid-base balance. The kid-neys normally excrete 40 to 60 mmolof potassium daily.11 J.M.s potassiumlevel was 5.8 mmol/L, increasing hisrisk for fatal dysrhythmias.


are retained in the body, resultingin azotemia, as evidenced by theincreased serum levels of urea nitro-gen and creatinine. The tubules,which are permeable to urea, nor-mally reabsorb little urea. However,as GFR decreases, more urea is reab-sorbed. Although elevated serumlevels of urea nitrogen alone can indi-cate other abnormalities, such asdehydration, elevation of serum levelsof both urea nitrogen and creatinineindicates kidney failure. The serumurea nitrogencreatinine ratio (normal10:1 to 20:1) was once used to assesskidney function, but the ratio is notconsidered as an important indicatortoday. J.M.s serum level of urea nitro-gen was 66.05 mmol/L (185 mg/dL),and his serum creatinine level was1909.4 mol/L (21.6 mg/dL), result-ing in a ratio of 9:1. This slightlydecreased ratio could reflect fluidoverload from the CKD or an undi-agnosed liver disease, because J.M.salkaline phosphatase level was alsoelevated.

Proteinuria and hematuria areassociated with glomerulonephritisand result from damage of theglomeruli with the resultant increasedpermeability. Albumin is a sensitiveindicator of CKD related to diabetes,glomerular disease, and hyperten-sion.13 Although J.M. had no historyof kidney disease, he did have hyper-tension, which can damage theglomeruli. Glomerular damage wasevidenced by the 4+ protein and 2+hematuria.

Uric acid is an end product ofpurine metabolism that is filtered inthe glomeruli and secreted into thedistal tubule.10 Impaired glomerularfunction results in decreased excre-tion of uric acid by the kidney andmay result in the development of

gouty arthritis with deposits of uricacid in joints or soft tissue.8 J.M.suric acid level was 1142 mol/L(19.2 mg/dL). This elevated level ofuric acid increased J.M.s risk of goutdeveloping with symptoms such asjoint pain, redness, and swelling,particularly in the great toe.

Alterations in Metabolic/Endocrine Functions

Anemia results from several fac-tors in patients with CKD. The per-itubular capillary endothelium inthe kidneys produces erythropoietin,which is needed to stimulate bonemarrow to release red blood cells. Inaddition, uremia inactivates erythro-poietin. Failure of this mechanismresults in a normochromic, normo-cytic anemia. Uremia can also con-tribute to anemia by shortening thelife span of the red blood cells. Finally,the low hemoglobin level contributesto acidosis, because less hemoglobinis available in the body to buffer acids.Additionally, uremia causes impairedplatelet aggregation, increasing thepotential for bleeding.10 J.M.s hemo-globin level was 83 g/L, his hemat-ocrit was 0.252, and his plateletcounts were adequate. The decreasedhemoglobin level and hematocritcould have caused signs and symp-toms of anemia, and although hisplatelet count was adequate, theplatelets would not function effec-tively, increasing the risk for bleeding.

Renin is released in response tochanges in intravascular pressureor sympathetic stimulation.8 Theresultant stimulation of the renin-angiotensin-aldosterone systemcontributes to the retention of waterand elevated blood pressure.4,14 Reninis an enzyme released from the jux-taglomerular cells in response to

decreases in blood flow to the kidney,changes in tubular fluid composition,or stimulation by the sympatheticnervous system. Renin then acts onangiotensinogen, a plasma protein,and converts it to angiotensin I.Angiotensin I in turn is convertedto angiotensin II by angiotensin-converting enzyme in the lungs.Angiotensin II produces 2 outcomes.The first is a short-acting vasocon-striction. The second action is anincrease in blood pressure throughstimulation of the adrenal cortex,which releases aldosterone, causingsodium reabsorption and concomi-tant water reabsorption by the kid-neys. J.M.s blood pressure was221/142 mm Hg. It was unknownon admission whether J.M. had aprimary hypertension that had ledto kidney failure or if the kidney fail-ure had contributed to the hyperten-sion. The retention of water andproduction of angiotensin certainlycontributed to the hypertension andthe cardiovascular and respiratoryfindings from fluid overload.

Assessment Findings Because the pathophysiological

changes associated with CKD affectevery body system (Figure 2), a thor-ough nursing assessment of patientswith CKD is essential. A systemsapproach to assessment is used here.

CardiovascularHypertension is a result of

increased fluid retention and stim-ulation of the renin-angiotensin-aldosterone system. In addition,hypertension can lead to the devel-opment of CKD. For J.M., it wasunknown whether the hypertensioncontributed to the renal failure orthe renal failure contributed to the

22 CRITICALCARENURSE Vol 26, No. 4, AUGUST 2006 http://ccn.aacnjournals.org by guest on August 11, 2014http://ccn.aacnjournals.org/Downloaded from

hypertension. J.M.s clinical assess-ment revealed left ventricular hyper-trophy and a strain pattern on theelectrocardiogram, indicating long-standing left ventricular failure.Auscultation of heart sounds revealedan S3 (fluid overload) and S4 gallop(decreased compliance and hyper-tension). Funduscopic examinationshowed arteriovenous nicking andcotton wool hemorrhages with exu-dates (hypertensive retinopathy), allindicating significant hypertension.The sinus tachycardia could havebeen a compensatory mechanismfor the decreased PaO2, the anemia,the metabolic acidosis, or the fluidoverload. Uremic pericarditis, anothermanifestation of ESRD, often devel-ops from the accumulation of toxins;

nate carbondioxide in anattempt toreestablishnormal pH.Fluid overloadwith pul-monary con-gestion wasmanifested inJ.M. by crack-les, decreasedPaO2, andincreased res-piratory rate.J.M.s acid-base resultsweredescribed pre-viously. Thefocus of thenursingassessment isbreathsounds, respi-ratory rateand pattern,

and results of arterial blood gasanalysis.

GastrointestinalAnorexia, weight loss, nausea,

and vomiting are frequent findingsin patients with CKD, although J.M.said that he did not have these signsand symptoms. Halitosis, a metallictaste in the mouth, and ulcers in themouth may occur because bacteriain the mouth break down urea intoammonia. Gastrointestinal bleedingfrom altered platelet function andincreased gastric acid secretion fromincreased release of parathyroid hor-mone10 may occur. The focus of thenursing assessment includes inspect-ing oral mucous membranes, moni-toring weight, checking stool for

J.M. did not have this manifestation.Electrolyte imbalances such ashyperkalemia and hypocalcemia canalso lead to dysrhythmias. The focusof the nursing assessment is periph-eral edema, circulatory overload evi-denced by congestive heart failureand pulmonary edema, cardiac dys-rhythmias, hypertension, and elec-trolyte levels.

RespiratoryAn increased respiratory rate may

result from fluid overload, as a com-pensatory mechanism for metabolicacidosis, or from decreased PaO2.Although not identified as Kussmaulrespirations, deep breaths associatedwith metabolic acidosis occur as acompensatory mechanism to elimi-


Figure 2 Clinical manifestations of chronic kidney disease.

Integumentary

Bruises, pruritus, dry skin,skin color changes ashengray to yellowish, dry brittle hair and nails

Clinical manifestations of

chronic kidney disease

Respiratory

Increased respiratory rate,Kussmaul respirations,crackles, decreased PO2

RenalDecreased urine output,

azotemia, proteinuria,hematuria, hyperuricemia

Gastrointestinal

Anorexia, nausea, vomiting, halitosis,metallic taste in mouth,bleeding in gastrointestinal tract

NeurologicalPeripheral neuropathy, restless legs,

change in level of consciousness, lethargy, confusion, encephalopathy, altered motor function

Hematological

Anemia, weakness,fatigue, pallor,lethargy, bleeding dueto impaired plateletaggregation

Musculoskeletal

Renal osteodystrophy, decreasedcalcium, vitamin D impairment,hyperparathyroidism, pathological fractures

ImmuneIncreased risk of infection

Cardiovascular

High blood pressure, increased heart rate,dysrhythmias, electrocardiographic changes,abnormal heart sounds, retinopathy, fluidretention with peripheral edema and/or pulmonary edema


occult blood, and noting breathodor.

NeurologicalCentral nervous system findings

in patients with CKD can rangefrom confusion and difficulty con-centrating to seizures and coma.These findings are described as ure-mic encephalopathy. Impairedthinking processes are sometimesdescribed as BUN [blood ureanitrogen] blunting. The effects ofCKD on the peripheral nervous sys-tem result in peripheral neuropathy,particularly affecting the lowerextremities. The cause of these neu-rological effects is thought to beatrophy and demeylination of thenerves as a result of uremic toxinsand electrolyte imbalances.8,10 Earlyfindings include restless leg syn-drome progressing to pain, sensa-tions of tightness in the legs, andpain in a stocking-like pattern.Finally motor function may beimpaired with resultant changes ingait and fine motor movement.8,10

J.M. had none of these neurologicalsigns or symptoms. The focus of thenursing assessment is mental statusand motor and sensory function.

IntegumentaryPruritus often occurs in patients

with CKD because of the excretionof waste products and phosphate10

through the skin. The skin is oftendry because of decreased activity ofsweat glands and oil glands, and theskin may undergo changes in color,from pallor related to the anemia toa yellow-brown or gray aspect fromurochrome, a urinary pigment.8 Thenails and hair may become brittle.Bruises may also occur because ofimpaired platelet function and

increased capillary fragility. J.M. hadnone of these manifestations. Thefocus of the nursing assessmentincludes inspection of the skin forcolor changes or impaired integrityas a result of scratching of the skinby the patients.

MusculoskeletalRenal osteodystrophy results from

the loss of calcium in the bones andineffective conversion of vitamin Dto allow absorption of calcium. Threebone changes are associated withthis syndrome: (1) osteomalacia dueto inadequate absorption of calciumfrom the gastrointestinal tract, (2)osteitis fibrosa or bone demineral-ization due to increased parathyroidhormone, and (3) osteosclerosis,which is manifested as bands ofincreased and decreased bone densityin the vertebrae.8 J.M. had no indica-tions of skeletal deficiencies, althoughhis calcium level was 2.05 mmol/L(8.2 mg/dL). The focus of the nursingassessment is monitoring calciumand phosphorus levels. Signs andsymptoms of hypocalcemia includeneuromuscular irritability manifestedby paresthesia and tetany, which isassessed by testing for the Chvosteksign and the Trousseau phenomenon,muscle cramps, hypotension, andprolonged QT interval.

HematologicalDecreased erythropoietin levels

result in anemia. J.M.s laboratoryresults showed decreases in hemoglo-bin level and hematocrit. The focusof the nursing assessment is detectionof signs and symptoms of anemia,including pallor, fatigue, shortnessof breath, and tachycardia, and onlaboratory evaluation of hematocritand hemoglobin and iron levels.

ImmunologicalIncreased levels of uremic tox-

ins can lead to impaired immuneand inflammatory responses withresultant defects in granulocytes,impaired B- and T-cell functioning,and impaired phagocytosis.10 Thefocus of the nursing assessment isexamination for signs or symptomsof an impaired inflammatory andinfectious response. Infection is acommon occurrence in patients withCKD that often results in hospital-ization and death.10

RenalIn patients with CKD, urinary

signs and symptoms are related tofluid balance; as GFR decreases, urineoutput decreases. Retention of wasteproducts such as urea nitrogen andcreatinine leads to azotemia, whereasuric acid retention may lead to gout.Proteinuria and hematuria were dis-cussed previously. The focus of thenursing assessment is fluid balance(intake and output, daily weight,edema) and monitoring of labora-tory results.

Current Standards of Care The clinical manifestations due

to the pathophysiological changesof CKD create a need for immediateinterventions and constant monitor-ing. Because J.M.s serum level ofurea nitrogen was 67.47 mmol/L(189 mg/dL) and his creatinine levelwas 1909.4 mol/L (21.6 mg/dL),the immediate clinical action requiredfor J.M., according to the KDOQIclinical action plan for CKD, wasrenal replacement therapy1 startedas soon as possible. After the initialassessment was completed in theemergency department, a nephrolo-gist was consulted and a double-


lumen percutaneous catheter wasinserted. Hemodialysis was selectedas the intervention rather than peri-toneal dialysis because of J.M.s acutecondition.

The mechanics of hemodialysis,with all access types, involves bloodbeing removed from the body by theblood pump of the dialysis machine;the blood then passes through thedialyzer14 (artificial kidney), where itis cleansed by osmosis and diffusion(hemodialysis works by diffusion oflow-molecular-weight solutes acrossa semipermeable membrane). Finally,the blood completes the circuit andreturns to the patients vascular com-partment, the cycle repeats constantlywhile the patient is on dialysis. Thetotal amount of blood outside thebody at any time is approximately200 to 300 mL.

A vascular access for arterial flowand venous return is needed for thedialysis procedure. Of 3 access types,1 is temporary and 2 are permanent(Table 3). The central venous catheteris the least desirable because compli-cations are common, particularlyinfection; however, because of theemergent nature of J.M.s situation,a temporary access was required.The right internal jugular vein is thepreferred site,15 although the femoralvenous or subclavian venous sitesare also used. Using the subclaviansite can cause venous stenosis andthrombosis,16 interfering with anyfuture access for fistulas or grafts;therefore, it should be used only whenthe femoral or jugular sites are notaccessible.

A temporary access is placed in alarge central vein and can be usedfor as long as 3 months. The proce-dure is done by using sterile techniquein an angiography suite, procedure,

tional support, and/or obtainingblood samples. It is important toknow which site will be used, as wellas the size and body type of thepatient, to determine what size andlength catheter is needed. If the jugu-lar or the subclavian site is used,catheters must be longer than if thefemoral site is chosen, because of thepositioning of the catheter. The dial-ysis catheter has a large lumen, 11.5For 12F, which allows a smooth flowof blood throughout the hemodialy-sis procedure.

Additional immediate interven-tions initiated because of J.M.s criti-cal condition included oxygen vianasal cannula at 4L/min, cardiacmonitoring to assess for dysrhyth-mias, insertion of a peripheral intra-venous catheter and an indwellingFoley catheter. After his initial dialy-sis, J.M. was placed on a 1000-mLfluid restriction and a renal diet of

or operating suite; however, becauseof J.M.s critical condition, the pro-cedure was done at the bedside. Theright jugular vein was used, and a20-cmlong catheter was insertedinto the vein and then sutured inplace by using suture wings. Oncethe catheter was in place, whilemaintaining aseptic technique, anurse instilled heparin into eachlumen, per facility protocol, to equalthe total volume of each lumen (thelumen volume is printed on eachlumen of the catheter). A cathetercap was then placed on each lumen,and a dressing was placed over thesite. J.M. was now ready for dialysisafter placement of the catheter hadbeen verified with a chest radiograph.

Several brands and types of dial-ysis catheters are available17; thosecommonly used are double or triplelumen. The triple lumen gives anadded lumen for drug therapy, nutri-


Access type

Arteriovenous fistula: Apermanent access that is created surgically byconnecting an artery to a vein

The forearm is the mostcommon site

Arteriovenous graft: A per-manent access createdsurgically by using a syn-thetic material tunneledunder the skin

One end of graft is con-nected to an artery; theother, to a vein

Catheter: A temporaryaccess in which acatheter is placed into alarge central vein such asthe internal jugular vein

Advantages

Preferred route for dialysis;once matured, has goodblood flow, few problems

It is long lasting and isassociated with fewercomplications than areother accesses

Shorter maturation timethan fistula; site can beused in 3-6 weeks

No maturation time Catheter can be used

immediately after place-ment and is often usedin emergent situations

Disadvantages

Long maturation time (3-4months until it can be usedfor dialysis)

May not enlarge enough toprovide a good blood flowfor dialysis

Higher incidence of thrombo-sis and clotting than witharteriovenous fistula

Higher incidence of stenosisthan with fistula

Involves use of syntheticmaterial, creating thepotential for an allergicresponse

Increased risk of infection incatheter, at exit site, and inbloodstream

Decreased flow rates withcatheter lead to low ureareduction rate

Potential for discomfort atcatheter exit site and devel-opment of poor body image

Table 3 Access sites for hemodialysis


60 g of protein, 2 g potassium, and2 g sodium. Fluid volume intake isbased on 500 mL/day (insensiblefluid loss) plus fluid equal to the urineoutput of the preceding 24 hours.8

Once a patients condition stabi-lizes, after the diagnosis of CKD ismade and initial treatment has begun,the patient is referred to a surgeonfor establishment of a permanentvascular access. The National KidneyFoundation18 recommends the arte-riovenous fistula as the preferred typeof access; this access is associated withfewer complications and provideslonger trouble-free use than does anarteriovenous graft or a catheter. Thecatheter is the access least recom-mended because of the frequentcomplications associated with its use.J.M. had an arteriovenous fistulaplaced 8 days after admission. Nurs-ing assessment after a fistula is placedfocuses on patency of the fistula,determined by palpating a thrill andauscultating a bruit.

Expected OutcomesOn the basis of the KDOQI guide-

lines, the focus of treatment in CKDis specific therapy, dialysis in J.M.scase, and treatment of comorbidconditions.19 Particularly for J.M.,the clinical findings such as hyperten-sion, anemia, calcium and phospho-rus balance, and nutritional statusrequired treatment.

The expected outcomes and nurs-ing considerations for J.M. wouldinclude the following:

Adequate hemodialysis20 isdetermined by measurement of levelsof nitrogenous waste products (serumlevels of urea nitrogen and creatinine)and the urea reduction ratio, in whichthe measurements from before andafter dialysis are entered into a math-

ematical formula. Adequate dialysiswill also result in correction of acid-base imbalance, fluid volume over-load, and electrolyte imbalances(particularly sodium and potas-sium). Results of J.M.s laboratorytests after dialysis are found in Table2. J.M. initially received daily dialy-sis for 3 days. Correction of the fluidimbalance in turn will correctimpaired gas exchange. Nursingimplications include fluid restric-tion, monitoring, and daily weight.The focus of educating patients isteaching about foods that are highin potassium and the importance ofpotassium restriction in preventingcardiac dysrhythmias. Disregardingpotassium restriction can be fatalfor a patient with CKD. Immediatereferral to a dietician is also appro-priate because not only potassiumbut also sodium and phosphorus arerestricted on a renal diet.

Blood pressure within normallimits21 is related to several interven-tions, including adequate hemodial-ysis and fluid restriction. The mostimportant nondrug management forhypertension is fluid removal andrestriction of sodium and fluid in thediet. Education of patients focuses onteaching about foods high in sodiumthat must be avoided and manage-ment of fluid intake. Pharmacologicalintervention includes the use ofangiotensin-converting enzymeinhibitors, which decrease not onlysystemic blood pressure but alsointraglomerular pressure by dilatingthe efferent arteriole.8 Angiotensin-converting enzyme inhibitors mustbe used with caution because a con-comitant increase in serum potassiumlevels may occur. Calcium channelblockers are also effective in decreas-ing blood pressure through systemic

vasodilatation. J.M. was treated withcaptopril (Capoten) and nifedipine(Procardia). For patients on dialysis,antihypertensive medications shouldbe given after hemodialysis to preventhypotension.

Prevention of other cardiovas-cular diseases22 is accomplishedthrough control of hypertension andfluid volume, physical exercise, andprevention of end-organ damage.Cardiovascular disease is the leadingcause of death in patients with ESRD.22

A physician-approved exercise pro-gram for patients with CKD providesthe positive benefits of exercise suchas decreasing blood pressure, choles-terol and triglyceride levels, andinsomnia and the obvious benefit ofmaintaining weight control. Nursinginterventions focus on monitoringweight loss/gain, blood pressure, andperipheral edema and on educatingpatients about diet and exercise.

Target hemoglobin and hemat-ocrit levels can be reached23 throughthe use of iron supplements, multivi-tamins, and epoetin alfa (Epogen),which stimulates production of redblood cells. Nursing interventionsinclude monitoring hemoglobin levelsand hematocrit and assessing patientsfor clinical findings of anemia.

Prevention of bony changes24 isaccomplished through the manage-ment of calcium and phosphoruslevels. In addition to dietary man-agement, phosphate binders (alu-minum hydroxide) or calcium salts(PhosLo) may be used to reach thisoutcome. Because medications arethe primary method of removingphosphorus from the body (dialysisremoves very little), the necessity oftaking the phosphate binder withfood to be effective is a significantaspect of patients education. Moni-


toring calcium and phosphorus levelswould also be part of the nursing role.

Adequate nutrition (based onalbumin level)25 is managed throughdietary regulation. Proteins of highbiological value are essential becausetotal protein intake is restricted.Adequate protein levels result inmaintenance of fluid balance, heal-ing and maintenance of skin integrity,and finally maintenance of immunefunction. Providing dietary educationon appropriate protein foods andserving size is an important activityof nurses and/or dieticians, alongwith monitoring albumin levels.

ConclusionThe significant role of critical

care nurses in providing care topatients with CKD is clear. A thor-ough assessment of all body systemsis essential in evaluating each patient.This assessment will enable the earlydetection of systemic alterationsrelated to CKD and the implementa-tion of appropriate interventions.Education of patients about themanagement of CKD and continuedevaluation of patients outcomes arealso essential so that critical carenurses can determine the effective-ness of interventions.

AcknowledgmentsThe data reported here have been supplied by the USRenal Data System. The interpretation and reporting ofthese data are the responsibility of the author(s) and inno way should be seen as an official policy or interpreta-tion of the US government.

References1. National Kidney Foundation. K/DOQI clini-

cal practice guidelines for chronic kidneydisease: executive summary. Available at:http://www.kidney.org/professionals/kdoqi/guidelines_ckd/p1_exec.htm. AccessedMay 15, 2006.

2. National Institute of Diabetes and Digestiveand Kidney Disease. Healthy People 2010objectives: chronic kidney disease. Availableat: http://www.niddk.nih.gov/fund/divisions/KUH/KidneyHP2010.htm.Accessed May 15, 2006.

3. US Renal Data System. USRDS 2004

21. National Kidney Foundation. K/DOQI clini-cal practice guidelines on hypertension andantihypertensive agents in chronic kidneydisease. Available at: http://www.kidney.org/professionals/kdoqi/guidelines_bp/guide_1.htm. Accessed May 15, 2006.

22. National Kidney Foundation. K/DOQI clini-cal practice guidelines for cardiovasculardisease in dialysis patients. Available at:http://www.kidney.org/professionals/kdoqi/guidelines_cvd/overview.htm. AccessedMay 15, 2006.

23. National Kidney Foundation. K/DOQI clini-cal practice guidelines for anemia of chronickidney disease: update 2000. Available at:http://www.kidney.org/professionals/kdoqi/guidelines_updates/doqiupan_iv.html#11.Accessed May 15, 2006.

24. National Kidney Foundation. K/DOQI clini-cal practice guidelines for bone metabolismand disease in chronic kidney disease. Avail-able at: http://www.kidney.org/professionals/kdoqi/guidelines_bone/index.htm. Accessed May 15, 2006.

25. National Kidney Foundation. K/DOQI clini-cal practice guidelines for nutrition inchronic renal failure. Available at: http://www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html.Accessed May 15, 2006.

Annual Data Report: Atlas of End-StageRenal Disease in the United States, NationalInstitutes of Health, National Institute ofDiabetes and Digestive and Kidney Dis-eases, Bethesda, Md. Available at: http://www.usrds.org/atlas.htm. Accessed May15, 2006.

4. National Kidney Foundation. K/DOQI clini-cal practice guidelines for chronic kidneydisease: evaluation, classification, and strat-ification. Guideline 1: Definition and stagesof chronic kidney disease. Am J Kidney Dis.2002;39(suppl 1):S1-S266. Also available at:http://www.kidney.org/professionals/kdoqi/guidelines_ckd/ex2.htm#ckdex1.Accessed May 15, 2006.

5. Copstead LC, Banasik JL. Pathophysiology:Biological and Behavioral Perspectives. 2nd ed.Philadelphia, Pa: WB Saunders Co; 2000.

6. Ruggenenti P, Schieppati A, Remuzzi G.Progression, remission, regression of chronicrenal disease. Lancet. 2001;357:1601-1608.

7. Heuther SE, McCance KL. UnderstandingPathophysiology. 3rd ed. St Louis, Mo:Mosby; 2004.

8. Price S, Wilson L. Pathophysiology: ClinicalConcepts of Disease Processes. 6th ed. StLouis, Mo: Mosby; 2003.

9. Kidney Learning System. Frequently askedquestions about GFR estimates. Availableat: http://www.kidney.org/professionals/KLS/gfr.cfm. Accessed May 15, 2006.

10. Porth CM. Pathophysiology Concepts ofAltered Health States. 6th ed. Philadelphia,Pa: Lippincott; 2002.

11. Metheny N. Fluid and Electrolyte Balance.4th ed. Philadelphia, Pa: LippincottWilliams & Wilkins; 2000.

12. Wallace M. Anatomy and physiology of thekidney. AORN J. 1998;68:799-780, 803-804,806, 808, 810-811, 813-816, 819-824, 827-828.

13. National Kidney Foundation. K/DOQI clini-cal practice guidelines for chronic kidneydisease: guideline, assessment of protein-uria. Available at: http://www.kidney.org/professionals/kdoqi/guidelines_ckd/p5_lab_g5.htm. Accessed May 15, 2006.

14. Cannon JD. Recognizing chronic renal fail-ure. Nursing. January 2004;34:50-53.

15. Kapoian T, Kaufman J, Nosher J, ShermanRA. Dialysis access and recirculation. In:Henrich WL, Bennet WM, eds. Atlas of Kid-ney Disease. 1999:5.1-5.14. Available at:www.kidneyatlas.org/book5/adk5-05.ccc.QXD.pdf. Accessed May 15, 2006.

16. Trerotola SO. Hemodialysis catheter place-ment and management. Radiology. 2000;215:651-658.

17. Ash SR. The evolution and function of cen-tral venous catheters for dialysis. SeminDial. 2001;14:416-424.

18. National Kidney Foundation. K/DOQI clini-cal practice guidelines for vascular access,2000. Am J Kidney Dis. 2001;37(suppl 1):S137-S181.

19. National Kidney Foundation. K/DOQI clini-cal practice guidelines for chronic kidneydisease: guideline 2. Evaluation and treat-ment. Available at: http://www.kidney.org/professionals/kdoqi/guidelines_ckd/ex2.htm#ckdex2. Accessed May 15, 2006.

20. National Kidney Foundation. K/DOQI clini-cal practice guidelines for hemodialysis ade-quacy: update 2000. Available at: http://www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_uptoc.html#hd.Accessed May 15, 2006.

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CE Test Test ID C064: Chronic Kidney Disease: Acute Manifestations and Role of Critical Care NursesLearning objectives: 1. Identify the expected outcomes of patients with chronic kidney disease (CKD) 2. Describe the pathophysiology of CKD 3. Discuss the impact of CKD in relation to body systems

Program evaluationYes No

Objective 1 was met Objective 2 was met Objective 3 was met Content was relevant to my

nursing practice My expectations were met This method of CE is effective

for this content The level of difficulty of this test was: easy medium difficult

To complete this program, it took me hours/minutes.

Test answers: Mark only one box for your answer to each question. You may photocopy this form.

1. Why is chronic kidney disease (CKD) a public health issue? ?a. Because of increasing incidence and the high cost of interventionsb. Because of increasing cost of insurance premiums and loss of insurance c. Because of limited access to dialysis centers and limited public education of thediseased. Because of limited access to dialysis centers and the high cost of interventions

2. Which of the following are 3 risk factors for end-stage renal diseaseaccording to Healthy People 2010? a. Hypertension, proteinuria, and family history b. Diabetes mellitus, coronary artery disease, and smokingc. Obesity, smoking, and proteinuriad. Increasing age, hypertension, and hypercholesterolemia

3. In relationship to cardiac output, what percentage of blood is f iltered through the nephrons per minute in normal homeostasis? a. 20% to 25%b. 35% to 45%c. 45% to 50%d. 75% to 80%

4. Which of the following best describes the response to decreasedglomerular f iltration rate? a. Cortisol is released from the adrenal medulla, resulting in reabsorption ofsodium and water.b. Aldosterone is released from the adrenal cortex, resulting in excretion ofwater, sodium, and potassium.c. Antidiuretic hormone is released resulting in reabsorption of water, sodium,and potassium.d. Aldosterone is released from the adrenal cortex, resulting in reabsorption ofwater and sodium.

5. Which of the following best illustrates the correct anion gap equation?a. Anion gap = Na+ + (Cl- + HCO3

-)b. Anion gap = Na+ - (Cl- + HCO3

-)c. Anion gap = 6.1 + log (HCO3

- / [0.03 PCO2])d. Anion gap = Cl- + (Na+ / HCO3

-)

6. Which of the following best describes the normal excretion of potassium by the kidneys?a. 20 to 40 mmol dailyb. 40 to 60 mmol dailyc. 30 to 50 mmol daily d. 80 to 100 mmol daily

7. Which of the following best describes the function of the endocrine system in CKD in relationship to hypocalcemia?a. The thyroid gland increases it secretion of thyroid hormone, stimulatingthe release of cortisol into the blood. b. The thyroid gland decreases secretion of thyroid hormone, decreasingthe amount of calcium excreted. c. The parathyroid glands secrete parathyroid hormone, decreasing theamount of calcium released from the bone into the vascular system.d. The parathyroid glands secrete parathyroid hormone, increasing theamount of calcium released from the bone in the vascular system.

8. Which of the following cardiovascular changes do critical carenurses need to monitor during their assessment of the patient withCKD?a. Peripheral edema, cardiac dysrhythmia, and electrolyte levels b. Gastroesophageal reflux disease, pulmonary edema, and hypotensionc. Dehydration, gastrointestinal bleeding, and hypotensiond. Endocarditis, hyperglycemia, and congestive heart failure

9. Which of the following are associated with renal osteodystrophy? a. Osteomalacia, osteitis fibrosa, and osteosclerosisb. Peripheral neuropathy, osteoperiostitis, and osteophlebitisc. Osteomatosis, osteomyelitis, and dysostosisd. Dermatitis, desmosis, and myelolysis

10. As blood completes the circuit during dialysis, approximately how much blood is outside the body at any time? a. 75 to 150 mLb. 100 to 300 mLc. 200 to 300 mLd. 250 to 400 mL

11. The National Kidney Foundation recommends which type ofaccess for permanent vascular access? a. Infusaportb. Ash catheterc. Arteriovenous graftd. Arteriovenous fistula

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Test ID: C064 Form expires: August 1, 2008. Contact hours: 2.0 Fee: $12 Passing score: 8 correct (73%) Category: A Test writer: Todd M. Grivetti, RN, BSN, CCRN

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