Practice nursing
care for Clients
with Renal
Disorders
Renal problems: infectious disorders
The
urinary system is normally one in which a sterile body fluid (urine) is excreted. The unobstructed and complete passage of urine from
the renal and urinary systems is critical to the sterility of the urinary tract. When a structural
abnormality (either congenital or acquired) is present, the potential for
degenerative changes from infection is dramatically increased. Urinary tract infection (UTI) usually refers to infections in this sterile system. Pyelonephritis is a bacterial infection within
the kidney and renal pelvis—theupper urinary tract. Infections within
the lower urinary tract are described in Chapter.
Pyelonephritis
OVERVIEW
With improved diagnostic techniques and
a better understanding of the inflammatory response, pyelonephritis has come to refer to active microorganisms or the
effects of kidney infections. Acute pyelonephritis is the condition resulting
from an active bacterial infection, whereas chronic pyelonephritis results from repeated or continued upper urinary tract infections or infectious sequelae.
Chronic pyelonephritis is usually associated with an anatomic urinary tract anomaly, urinary obstruction or, most commonly,vesi-coureteral reflux.
The vesicoureteral junction is the point at which
the ureter joins the bladder. Reflux refers to
the reverse (e.g., backward,
upward, ascending) flow of urine toward the renal pelvis and kidney.
Pathophysiology
In pyelonephritis,
microorganisms usually ascend from the lower urinary tract into the renal
pelvis. Infection from organisms carried in the
blood (hematogenous) may occur, but mey occur with much
less frequency. Bacteria activate the in-matoryresponse, and
local edema results.
Acute pyelonephritis involves acute interstitial inflammation,
tubular cell necrosis, and a tendency for abscess formation. Abscesses,
pockets of localized infection, can appear in the capsule, cortex, or medulla. The pattern of infection within the kidney
is not uniform; normal tissue and tubules can lie next to infected areas. Fibrosis or scar
tissue develops as the inflammatory process subsides. The calices become blunted, and scars develop in
the interstitial tissue.
Vesicoureteral and intrarenal reflux of infected urine are the
major mechanisms responsible for chronic pyelonephritis. Some papillae in the kidney do not close with increased in-tracaliceal pressure, causing intrarenal reflux. Refluxing papillae are most often located
in the upper and lower poles of the kidney and therefore are more susceptible
to chronic pyelonephritis.
Inflammation, fibrosis, and deformity of the renal pelvis and calices are
evident. Repeated or continuous infectious produce additional scar tissue.
Vascular, glomeru-lar,
and tubular changes within the scars can occur. Filtration, reabsorption,
and secretion are eventually impaired, and renal function is diminished (Figure 71-3).
Etiology
Single episodes of acute pyelonephritis may result from the entry of bacteria associated with pregnancy,
obstruction, or reflux.Chronic pyelonephritis is usually associated with
structural abnormalities and/or obstruction
with reflux. Vesicoureteral reflux or obstruction leading to chronic pyelonephritis is
often due to stones, obstruction, or neurogenic impairment
involving the voiding mechanism. Reflux is more common in
children, who as adults often have scarring associated with chronic pyelonephritis. Clients who develop chronic pyelonephritis without
having reflux as a child are usually adults with a history of spinal cord injury, bladder tumor, prostatic hypertrophy, or urinary tract stones.
Acute or chronic pyelonephritis is more likely to occur in clients who have undergone manipulation of the urinary tract (e.g., placement of a urinary catheter), those who have diabetes mellitus
or chronic renal calculi, or those who overuse analgesics. In clients with
diabetes mellitus, the development and progression of bladder atony increase the tendency to develop pyelonephritis.
In clients with chronic stone disease, j calculi provide a site for ongoing
infection and resultant renal scarring. Nonsteroidal anti-inflammatory
drug (NSAID) use has been associated with papillary necrosis, which then per- \ mits reflux.
The most common pyelonephritis-causing
organism is Escherichia coli. Enterococcus faecalis is typical in hospitalized clients. Both
are organisms of the gastrointestinal tract. Non-£. coli organisms
such as Proteus mirabilis, Klebsiella and Pseudomonasaeruginosa and the more antibiotic-resistant organisms are also causes of pyelonephritis in hospitalized clients. When the
infection is bloodborne,
common infecting organisms include Staphylococcus aureus and the Candida and Salmonella species.
Theories of
noninfectious or idiopathic causes of intrarenal scarring
and the eventual outcome of pyelonephritis include an
antibody reaction, cell-mediated immunity against the bacterial antigens, or an autoimmune reaction.
Incidence/Prevalence
The exact
incidence and prevalence of pyelonephritis are
not known; this diagnosis is not separately reported from all urinary tract infections. Acute urinary conditions of the kidneys or urinary tract, nephritic syndrome, urethral stricture, and cystitis account for more than 7 million new cases annually in noninstutionalized Americans (NIDDK National Kidney and Urologic Diseases Information Clearinghouse, 1999). Women overall have more cases of pyelonephritis. After age 65, rates for men increase greatly because of the increased incidence of prostatitis.
COLLABORATIVE MANAGEMENT
Assessment
HISTORY
The nurse asks
about a history of urinary tract infections (UTIs), diabetes mellitus, stone disease, and other structural
or functional abnormalities of the genitourinary tract. The nurse attempts to
determine whether the UTIs were
associated with pregnancy and asks the
client about any previous experiences with pyelonephritis or
similar symptoms. Recurrences are
common and may lead to a deterioration of renal function.
PHYSICAL ASSESSMENT/CLINICAL MAN IFESTATIONS
The nurse asks the
client about specific symptoms associated with acute pyelonephritis. Chronic pyelonephritis has a less dramatic clinical presentation; signs and
symptoms are usually related to the infection or renal function. The nurse asks the client to describe any vague or nonspecific urinary. The nurse advises the client to complete all prescribed antibiotic
regimens and instructs the client to report any side effects
or unusual symptoms to the prescribing health team member
rather than suspend the regimen. The client and family are referred for
nutritional counseling as needed, because many clients have special nutritional
requirements, such as those caused by diabetes mellitus or pregnancy.
HOME CARE MANAGEMENT
If no surgery is
performed, the client may need assistance with
self-care, nutrition, and medication administration at home.
If surgical intervention is necessary, the client may require help with
incision care, self-care, and transportation for follow-up medical appointments.
HEALTH CARE
RESOURCES
The client may also
briefly need a community health nurse to help administer
medications or nutrition at home. Housekeeping
services may also be helpful while the client is regaining strength.
• Evaluation: Outcomes
The nurse
evaluates the care of the client with pyelonephritis on the basis of the identified nursing
diagnoses and collaborative problems. Expected
outcomes may include that the client will:
• Demonstrate
methods of enhancing comfort
• Report that pain is controlled
• Express satisfaction with pain control
• Describe the role of antibiotics and self-administration of medications
• Explain and offer techniques to ensure adequate nutrition and hydration
• Describe the plan for posttreatment follow-up,
including knowledge of recurrent symptoms
• Modify the prescribed regimen as directed by a health care professional
CRITICAL THINKING CHALLENGE
Your client
is prescribed IV ciprofloxacin (Cipro) for pyelonephritis. She is also prescribed 25 mg meperidine every 3 hours prnfor her pain. Radiographic studies are deferred at this
time because of her pregnancy. A urine culture indicates that the infecting organism is £ coli, and
the sensitivity of the bacteria to ciprofloxacin is confirmed. After 3 days
her pain is absent, her fever is resolved, and her urinary
symptoms are clearing. She is to be discharged today and is to
continue taking her antibiotic orally at
home. A follow-up medical visit is scheduled in 7 days.
• What discharge planning and health care teaching are indicated at this
time?
Renal Abscess
OVERVIEW
An abscess is a
collection of fluid and cells caused by an inflammatory response to bacteria. An abscess may occur within the renal parenchyma (renal abscess), in the renal and Gerota's fascia (perinephric abscess), or in the flank. An abscess is suspected when fever and symptoms are not
relieved promptly by antibiotic therapy.
COLLABORATIVE MANAGEMENT
A renal or perirenal abscess is readily diagnosed via sonogra-phy or a computed tomography (CT) scan. Arteriography andradionuclide
scintillation methods (e.g., gallium scan) also may
be useful for diagnosis. Symptoms of renal abscess include fever, flank pain, and general malaise. Local
fl edema and erythema may
be observed.
Drainage
by surgical incision or needle aspiration is often necessary. Appropriate
broad-spectrum antibiotics are "also prescribed.
Renal Tuberculosis
OVERVIEW
The genitourinary
tract is the most common extrapulmonary site of tuberculosis. Approximately 10% of new cases
of tuberculosis are extrapulmonary (Tolkoff-Rubin, Cotran, & Rubin, 2000). Tuberculosis of the kidney is
sometimes called granulomatousnephritis. After Mycobacterium
tuberculosis invades the kidneys,
usually by a bloodborne route, an inflammatory response is activated and forms scar
tissue (granuloma) that replaces normal kidney tissue.
COLLABORATIVE MANAGEMENT
Clients may
experience urinary frequency, dysuria, hematuria and/or proteinuria, flank pain or renal colic secondary to the passage of clots or stones, pyuria, and hypertension. Skin test (e.g., purified protein derivative [PPD]) or chest x-ray film evidence
of tuberculosis may or may not be present.
Clients with current or previous
pulmonary tuberculosis who show signs of unexplained fever, hematuria,
and sterile pyuria are at high risk for renal tuberculosis. The
diagnosis is made through a urine culture of three clean-catch,
first-morning specimens. Other genitourinary
sites for tuberculosis include the prostate, epididymis, ureters,
testes, bladder, and seminal vesicles.
Antitubercular therapy is the primary treatment. Recommendations include a 2-month course of rifampin, isoniazid, andpyrazinamide followed by 4 months of rifampin and isoniazid. Three to six more months of rifampin and isoniazid may
be recommended for men who may be harboring the organism in the prostate (Tolkoff-Rubin, Cotran, & Rubin, 2000).
Complications
include the loss of renal function, nephro-lithiasis, obstructive uropathy,
and bacterial superinfection of the urinary tract. Surgical excision of diseased
tissue may be indicated to preserve renal function.
CONGENITAL DISORDERS
Renal disorders interfere with the ability of the kidney to filter wastes
and to balance fluid and solutes. The kidneys work in an integrated way with so many other
organ systems; therefore a
renal disorder can significantly affect systemic health
and lead to life-threatening outcomes. Renal disorders can be categorized as congenital, obstructive, infectious, glomerular, and degenerative. Renal tumors and renal trauma are also described in this chapter.
Polycystic Kidney Disease
OVERVIEW
Polycystic kidney
disease (PKD) is one of the most common inherited disorders and affects 250,000 to 500,000 people in theUnited
States. It can be inherited as either an autosomal dominant
trait or, less commonly, as an autosomal recessive trait. People who
inherit the recessive form of PKD usually die in early childhood. The 5% to 10% incidence
of PKD in clients with no family history occurs as a result of a spontaneous genetic mutation. PKD is more common in
Caucasians than in people of other races.
Pathophysiology
Fluid-filled cysts
in the epithelial cells of the nephron characterize PKD. In the dominant form only 5% to 10% of nephronsmay be involved until the fourth decade of life, whereas
in the autosomal recessive form nearly 100% of nephrons are involved at birth. Cysts develop as a result of kidney cell proliferation, altered secretion, and abnormal cell matrix biology (Avner, et al., 1999; Calvet& Grantham, 2001).
Cysts can develop anywhere in the nephron.
Over time, small cysts become progressively larger (up to a
few centimeters in diameter) and
more widely distributed; the glomerular and
tubular membranes are damaged. As the cysts become filled
with fluid, thenephron functions of filtration, reabsorp-tion, and secretion become less effective.
The kidney tissue is
eventually replaced by nonfunctioning cysts, which look like a cluster of grapes (Figure).
The kidneys are grossly enlarged; each cystic kidney may enlarge to two or three times its normal size, becoming as large as a football. Other abdominal organs are displaced, and the client has considerable discomfort. The fluid-filled cysts are also prone to
infection, rapture, and bleeding.
More than 60% of
clients with PKD have high blood pressure. The
cause of hypertension in this disorder is thought to be related to renal ischemia from the enlarging cysts. As the vessels are compressed and renal blood flow decreases, the renin-angiotensinsystem
is activated, raising blood pressure. Control of hypertension is a top priority because proper
treatment can interrupt the vasoconstriction that leads to renal ischemia.
Cysts may also occur in other tissues,
such as the liver, blood vessels of the brain, and cardiac blood vessels. Cysts may
alter liver function or result in spontaneous rapture of vascular cysts (berry
aneurysms) in the brain,
causing sudden death. For reasons as yet unknown, kidney stones occur in 8% to 36% of the
clients with PKD. Heart valve abnormalities (e.g., mitral valve prolapse),
left ventricular hypertrophy, and colonic diverticuli also
are more prevalent in clients with PKD.
Etiology
PKD has at least
two inherited forms. Men and women have an equal chance of inheriting the disease because the
gene responsible for PKD is not located
on the sex chromosomes. The offspring of parents who have PKD have a 50% probability
of inheriting the gene that causes the autosomal dominant
form of the disease.
Manifestations of autosomal dominant polycystic kidney disease (ADPKD) usually do not appear until the fourth decade of life. Half of the affected people develop renal failure by age 50 years. ADPKD-1 is the most severe form
both in disease progression and in mortality. ADPKD-2 involves a slower rate
of cystic formation and growth, resulting in a delayed
progression to renal failure and other complications.
At present,
there is no way to prevent PKD, although early detection and management of
hypertension may slow the progression of renal impairment. Genetic counseling
and evaluation may be useful for adults
who have one parent or both parents with PKD. For those whose clinical symptoms do
not appear until after the childbearing years, offspring can be included in genetic counseling sessions.
COLLABORATIVE
MANAGEMENT
Assessment
HISTORY
The
nurse explores the family history of a client with suspected or actual PKD and asks whether either parent was known to have PKD or whether there is any family history of kidney disease.
The age at which signs and symptoms developed in the parent and any related complications may have prognostic
significance. The client is asked about constipation, abdominal discomfort, a change in urine color or frequency, high blood
pressure, headaches, and a family history of sudden death from a stroke.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
Chart 71-1 lists
key features of PKD. Pain is the presenting symptom in 20% to 30% of clients and islioted in at least 60%. The nurse inspects the abdomen. A protruding and distended abdomen is common as the cystic kidneys swell and push the abdominal contents forward. Polycystic kidneys are easily palpated because of their increased size. The nurse
proceeds with gentle abdominal palpation because the cystic kidneys and nearby tissues may be tender, and palpation is uncomfortable.
The client also may have flank
pain as a dull ache or as sharp and intermittent discomfort. Dull and aching
pain is caused by increased kidney size with distention or from infection
within the cyst. Sharp, intermittent pain occurs in response to a ruptured
cyst or the presence of a stone. When a cyst ruptures, the client may notice bright red or
cola-colored urine. The
nurse suspects infection if the urine is cloudy or
foul smelling or if there is dysuria (pain
on urination).
Nocturia (the need to urinate excessively at night) may be an early disease sign and occurs because of decreased renal concentrating
ability. As renal function further declines, the client experiences increasing
hypertension, edema, and ure-micsymptoms such as anorexia, nausea, vomiting, pruritus, and fatigue. Because berry aneurysms often occur in clients with PKD, a
severe headache with or without neurologic or
vision alterations deserves particular attention.
PSYCHOSOCIAL ASSESSMENT
As an inherited
disorder, PKD may cause complex psychoso-cial responses. The client often has
had direct experience with the effects and consequences of the disease in other
close family members.
He or she may have had a parent who died or other close relatives who required dialysis or
transplantation. While obtaining the family history, the nurse listens carefully for spoken and unspoken feelings of anger, resentment, hostility, futility, sadness, or anxiety;
such feelings may need further exploration. The focus may be one or
both parents or the process of
diagnosis and treatment. Feelings of guilt and concern for the client's own children
may further complicate the adjustment.
DIAGNOSTIC ASSESSMENT
Urinalysis usually reveals proteinuria (protein in the urine) once the glomerali are involved. Hematuria may be gross ormicroscopic. Bacteria in the urine suggest an
infection, usually in the cysts. A urine sample for culture and sensitivity
testing is obtained when there is clinical or laboratory evidence of
infection. As kidney function deteriorates, serum creatinine and blood urea nitrogen (BUN)
levels rise. With worsening kidney function, the 24-hour creatinine clearance decreases. Renal handling of sodium may cause either sodium losses or sodium retention.
Diagnostic studies include renal sonography,
computed tomography (CT), and magnetic
resonance imaging (MRI).
Small cysts are
detectable by sonography,
CT, or MRI. Renal sonography provides
diagnostic evidence of PKD, with minimal risk in
most cases.
Interventions
Common nursing
diagnoses for the client with polycystic kidney disease (PKD) include Acute Pain, Chronic Pain, and Constipation.
Common collaborative problems include Potential for Infection, Hypertension, Stone Formation, or Renal Failure. Chart
71-2 lists some NIC interventions for clients with renal disorders. (See Chapter 70 for
information on renal infections and stone formation. See Chapter 72 for care of
the client with renal failure.)
PAIN
PAIN MANAGEMENT; ANALGESIC
ADMINISTRATION.
Comfort
strategies include pharmacologic, physical, and inte-grative approaches. A combination may be most effective. Non-steroidal anti-inflammatory agents (NSAIDs)
are used cautiously because of their tendency
to adversely affect renal function. Aspirin-containing compounds are avoided to prevent an increased potential for bleeding.
If cyst
infection is the cause of discomfort, the physician orders a
lipid-soluble antibiotic such as trimethoprim/ sulfamethoxazole(Bactrim, Septra, Trimpex) or ciprofloxacin (Cipro), which penetrate the cyst wall.
Monitoring serum cre-atinine levels is necessary because antibiotic therapy can be nephrotoxic.
Applying dry heat to the abdomen or flank may promote comfort when renal cysts are infected.
When pain is severe or debilitating, cysts can be decompressed with percutaneous needle aspiration and drainage.
The nurse
teaches the client methods of enhancing relaxation and promoting comfort via
deep breathing, guided imagery, or other
relaxation strategies. The overall goal is client self-management.
CONSTIPATION
BOWEL MANAGEMENT. The nurse also teaches the client how to prevent constipation. The teaching plan covers adequate fluid intake, the role of increased dietary fiber when fluid intake is more than 2500 mL/24 hr, and the need for regular exercise to achieve regular bowel elimination.
The nurse explains that pressure on the large intestine may further impede
peristalsis as the polycystic kidneys increase in size. Consequently, the
client should know that these recommendations for bowel management might
change, particularly if renal failure also develops. The nurse also advises
about the appropriate use of stool softeners and bulk agents, including the careful use of
laxatives, to prevent complications related to chronic constipation.
HYPERTENSION AND RENAL FAILURE
TEACHING: DISEASE
PROCESS; TEACHING: PRESCRIBED MEDICATION. Blood pressure control is necessary to minimize cardiovascular
complications and slow the progression of renal dysfunction. Nursing
interventions include education to promote
self-management and understanding (see Chapter 36
for more information on hypertension). When renal impairment is evident through
a decreased concentrating ability (e.g., nocturia, low urine specific gravity), the nurse
encourages the client to drink at least
Medications for blood pressure
control include antihyper-tensive agents and diuretics.
Antihypertensive agents include angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, beta
blockers, and vasodilators (see Chart 36-2). ACE inhibitors show
promise in controlling the epithelial-proliferative aspects
of PKD and in reducing mi-croalbuminuria (Torra, 1999). If PKD
progresses to chronic renal failure or end-stage renal disease,
treatment approaches are similar to those in Chapter 72.
The nurse teaches
the client, family, or significant other how to measure and record blood
pressure. The nurse also helps the client establish a schedule for
self-administering medications, monitoring daily weights, and keeping blood pressure records (Chart 71-3). The potential side effects of the medications
are explained. The nurse makes written materials,
such as medication teaching cards and booklets, available.
A low-sodium diet
is often prescribed to control the hypertension that usually accompanies PKD.
However, some clients may experience salt wasting and do not require
a sodium-restricted diet. As the disease progresses, the physician may limit the client's protein intake to slow the development
of renal failure. The nurse assists the client, family, or significant other in
understanding the recommended diet plan and
clarifies its rationale. The nurse works closely with the dietitian to foster the
client's understanding. The nurse may also
initiate a referral for nutritional counseling.
Health Care Resources
The Polycystic Kidney Research
Foundation conducts research and provides
education about PKD. Many publications are available on request; there is a fee for some
materials. Chapters of the National Kidney Foundation (NKF) and
the American Association of Kidney Patients (AAKP) may also provide resources for client information and support.
OBSTRUCTIVE DISORDERS
Hydronephrosis, Hydroureter,
and Urethral Stricture
OVERVIEW
Hydronephrosis and hydroureter are disorders usually associated with
the obstruction of urine outflow. Urethral strictures also obstruct outflow. Prompt recognition and treatment are crucial to
prevent permanent renal damage.
In hydronephrosis, the kidney becomes enlarged as urine accumulates
in the pelvis and kidney tissue. Because the capacity of the renal pelvis is normally 5 to 8 mL,
obstructions within it or at the ureteropelvic junction
(UPJ) quickly result in renal pelvic distention. Kidney medullary pressure
increases as the volume of urine increases. Over
time, sometimes in only a matter of hours,
the blood vessels and renal tubules can be damaged extensively.
In clients with hydroureter, the pathophysiologic effects are similar but
the obstruction is lower in the urinary tract. The ureter is most likely to become obstructed
where the iliac vessels
cross or at the ureterovesical entry.
Dilation of the ureter above the point of obstruction results in enlargement
as urine continues to accumulate.
In a client with a urethral stricture, the obstruction is very low in the urinary tract; this causes bladder distention to occur beforehydroureter and hydronephrosis. The problems and kidney damage are similar
without prompt treatment.
A urinary obstruction can cause
structural damage when pressure builds up directly on tissue. Tubular
filtrate pressure also increases within the nephron as
drainage through the collecting system is impaired. With this added pressure, glomeru-lar filtration decreases or ceases, and renal failure results. Nitrogenous waste products (urea, creatinine,
and uric acid) and electrolytes (sodium, potassium, chloride, and phosphorus) are retained in the serum, and renal regulation of acid-base balance is impaired.
Disorders that can
cause hydronephrosis or hydroureter include
tumors, stones, trauma, congenital structural defects, and
retroperitoneal fibrosis. Early treatment of the causes can prevent hydronephrosis and hydroureter and thus prevent permanent renal
damage. The specific time needed to prevent permanent damage varies and depends on the client's underlying renal status. Permanent damage
may occur in less than 48 hours in some clients and after several weeks in
other clients.
COLLABORATIVE MANAGEMENT
Assessment
The nurse obtains a
history from the client, focusing on known renal or urologic disorders. A history of
childhood urinary tract problems may signal the
presence of previously unidentified structural defects. The nurse inquires
about the client's pattern of urination, especially its amount, frequency, color,
clarity, and odor. The client is asked about recent flank or abdominal pain.
Chills, fever, and malaise may be present with a
urinary tract infection (UTI).
The nurse inspects
each flank to identify asymmetry, which may occur with a renal mass, and gently palpates the client's abdomen to
identify any areas of tenderness. The urinary bladder is also palpated and percussed to
detect distention. Gentle pressure on the abdomen may cause urine leakage, which reflects a full urinary bladder and possible obstruction of the bladder/urethral junction.
Urinalysis may show
bacteria or white blood cells if infection is present. When urinary tract obstruction is prolonged, microscopic examination may reveal tubular epithelial
cells. The chemical analysis of serum is normal unless decreased glomerularfiltration has occurred; serum creatinine and
blood urea nitrogen (BUN) levels increase with a decreased glomerular filtration rate (GFR). Serum electrolyte levels may
also be altered and indicate hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis (bicarbonate deficit).
Intravenous urography reveals ureteral or renal pelvis dilation. Urinary
outflow obstruction may be revealed by sonog-raphy (renalechography)
or computed tomography (CT).
Interventions
FLUID MONITORING; URINARY RETENTION CARE; INFECTION PROTECTION. Urinary retention and potentialfor
infection are the primary problems. Failure to treat the cause
of urinary obstruction may lead to infection and renal failure. Surgery is
usually required to remove or reduce the cause of the obstruction.
DEGENERATIVE DISORDERS
Degenerative disorders that cause
changes in renal function are usually associated with the damage or effects
caused by amultisystem disorder. Many of these degenerative disorders result from changes in kidney
blood vessels.
Nephrosclerosis
OVERVIEW
Nephrosclerosis is a problem of changes in the nephron blood vessels. Vessel walls thicken, and the vessel
lumen narrows. As a result, renal blood flow is decreased and kidney tissue is
chronically hypoxic. Ischemia and fibrosis develop over time.
Nephrosclerosis is
associated with all types of hypertension, atherosclerosis, and a history of
diabetes mellitus. The more severe the hypertension, the greater the risk for extensive kidney damage. Nephrosclerosis is rarely seen when blood pressure is consistently below 160/110 mm Hg.
The changes associated with hypertension may be reversible or within may progress to end-stage renal disease (ESRD) months or years.
Hypertension is the second
leading cause of ESRD. Approximately 30% of
clients requiring lifesaving renal replacement therapy (e.g., dialysis or
transplantation) have hypertension as the cause of their renal failure
(NIDDK).
CULTURAL CONSIDERATIONS
Hypertension is more common in African Americans, and the risks of ESRD from hypertension are also greater for African Americans (Bakris et al., 2000). Between the ages of 25 and 45 years, the ratio of African Americans to Caucasians at risk for ESRD from hypertension is nearly 20:1 (Richardson & Piepho,
2000). These findings do not suggest that ESRD fromnephrosclerosis does not occur in Caucasians but
rather that affected Caucasians are likely to be older.
COLLABORATIVE MANAGEMENT
Treatment aims to control high blood pressure and
preserve renal function. Although many antihypertensive drags may lower blood pressure, the client's response is important in ensuring
long-term adherence to the prescribed therapy. Factors promoting adherence
include regimen simplicity (e.g., once-a-day dosing), low cost, and minimal side effects. Lack of basic knowledge or misinformation about hypertension
poses additional challenges to nurses and all health care
providers working with hypertensive clients. When evidence of renal disease occurs, adherence to
therapy is even more important for preserving health.
Many medications can control high blood
pressure (see Chart 36-2); more than one agent may be
necessary. Angiotensin-converting enzyme (ACE) inhibitors are particularly useful in reducing hypertension and
preserving renal function. Diuretics can maintain fluid and
electrolyte balance in the presence of renal insufficiency. Caution
is required to prevent hyperkalemia when
potassium-sparing diuretics (e.g., triamterene or spironolactone) or combination agents containing a potassium-sparing diuretic are used for
clients with known renal disease.
Renovascular Disease
OVERVIEW
Pathologic processes
affecting the renal arteries may result in severe lumen narrowing and drastically reduced blood
flow to the renal parenchyma. Uncorrected renovascular disease, such as renal artery stenosis or thrombosis,
causes ischemia and atrophy of renal tissue.
Renovascular disease is suspected with a sudden onset of hypertension, particularly in clients older than 50 years. Clients with high blood pressure but with a negative family history for hypertension may also be considered potential candidates for
renal arterystenosis (RAS).
RAS from
atherosclerosis or fibromuscular hyperplasia
(increased amount of tissue) is the primary cause of renovascular disease. Other causes include
thrombosis and renal aneurysms.
Atherosclerotic
changes in the renal artery are often associated with sclerosis in the aorta and other major vessels. Changes in the renal artery are close to where the renal artery and aorta meet. Fibrotic changes
of the vessel wall occur throughout the length of the renal artery.
COLLABORATIVE MANAGEMENT
Assessment
Key features of renovascular disease are listed in Chart 71-8. The
onset of hypertension is usually after age 40 to 50 years, and the family
history is often negative for hypertension. Diagnosis is made by renal arteriography; measurement of renal vein renin levels provides additional evidence
but may not be confirmatory. A renal arteriogram visualizes the renal vascu-lature and offers critical information for invasive
treatment. The comparison of renal vein renin levels may reveal which kidney is producing more renin.
Interventions
Visualization of the type of
defect, extent of narrowing, and surrounding vasculature is critical to decide
treatment intervention. The client's overall condition and the size of the atrophied kidney further influence decisions about
intervention. RAS may be treated by drugs to control high blood pressure and by percutaneous transluminal balloon
angioplasty or by surgical bypass procedures to restore the renal blood supply. Drugs may control high blood pressure but may not
lead to long-term preservation of kidney function. In young and middle-aged
adults, a lifetime of treatment with multiple agents for high blood pressure may make treatment
difficult and the outcomes uncertain.
KEY FEATURES of Renovascular Disease
· Significant, difficult to control btood pressure
· Elevated serum creatinine
· Decreased creatinine clearance
Balloon
angioplasty is considered less risky and requires much less time for recovery than does renal
artery bypass surgery (see Chapter 36). Renal
artery bypass surgery is a major procedure and involves at least 2 months for
convalescence. A bypass may be performed for either one or both renal
arteries. The surgeon inserts a synthetic graft that redirects blood flow from the abdominal aorta into the renal artery, beyond the area of stenosis. Increasingly, splenorenal bypass
procedures can also restore renal blood flow. Technically, the
process is similar
to other arterial bypass procedures (see Chapter 36).
For clients
with RAS, the diagnostic and treatment alternatives present tremendous
decisional conflict. Clients often experience a deterioration of renal
function, as noted by elevated serum creatinine levels and decreased creatinine clearance. These clients are at
increased risk for acute renal failure from the administration of nephrotoxic agents such as ra-diopaque contrast media and from possible intraoperative hy-potensive episodes. However, no treatment probably means that
dialysis is inevitable.
Diabetic Nephropathy
OVERVIEW
Diabetes mellitus
is the leading cause of end-stage renal disease (ESRD) among Caucasians in the
Immunologic
response mechanisms have also been implicated in glomerular basement membrane thickening and other changes in clients with diabetic renal disease. Investigations continue to explore if defects are the result of genetic or metabolic disturbances.
COLLABORATIVE MANAGEMENT
Diabetic nephropathy
is a microvascular complication of diabetes
defined by persistent albuminuria (as
shown by dipstick or a urinary albumin excretion rate above 0.3 g/dL), without evidence
of other renal disease. A diagnosis of renal disease in
clients with diabetes mellitus is made on the basis of the history and clinical
examination. Diabetic renal disease is progressive (Table 71-4).Structural and functional changes occur in the
kidneys of diabetic clients. Initially, kidney size is
slightly increased and glomerularfiltration rates (GFR) are higher than normal. A
radioimmunoassay of urine detects the microlevels of
albumin associated withalbuminuria. Progressive
renal damage occurs before
dipstick procedures can detect protein in the urine. For most clients, proteinuria(albuminuria) indicates the need for a renal biopsy for further
diagnosis. For the client with diabetes, observed microvascular changes in the retinacorrelate well with the renal microvascular changes. Examination of the retina
showing capillary leakage, fibrosis, and the typical changes of diabetic retinopathy
eliminates the need for a risky renal biopsy.
As with nephrotic syndrome, proteinuria may be mild, moderate, or severe. Clients with diabetes mellitus are always considered to be at risk for renal failure. If possible, nephrotoxic agents (e.g., radiopaque contrast
media or aminoglycosides)
and fluid volume deficit are avoided. Clients with worsening renal function may begin to have frequent hypoglycemic episodes and a decreased need for insulin or oral antihyperglycemic agents. The nurse explains to the client that the kidneys metabolize and excrete insulin. When renal function deteriorates, the insulin is
available for a longer time and thus less of it is needed. Unfortunately, many clients believe this means their
diabetes mellitus is improving. The result is accelerated progression to
ESRD. (See Chapter 65 for more information on diabetic nephropathy.)
Care of the client with chronic
renal insufficiency is thought to be more effective when a multidisciplinary case
managementapproach is used. Research has
not demonstrated a clear advantage to such an
approach (see the Evidence-Based Practice forNursing box
above).
TUMORS
Cysts and Benign Tumors
OVERVIEW
Benign urinary
tract growths include cysts and tumors of the renal
parenchyma or urinary bladder. Because malignant growths
may occur within cystic structures, a thorough evaluation is essential. A simple renal cyst grows out of renal parenchymal tissue, usually the cortical tissue. The cyst is filled with
fluid and can cause local tissue destruction as it enlarges. Many cysts
cause no symptoms and are discovered accidentally during fluoro-scopic examination or autopsy.
Although the exact
cause is unknown, cysts are usually considered a structural defect that occurs prenatally.
The etiology and incidence of benign tumors is also unknown. Thus far there are no recognized methods of prevention.
COLLABORATIVE MANAGEMENT
Diagnosis of a
simple renal cyst involves IV urography, sonography, and computed tomography (CT). If the cyst appears
to be filled with fluid at urographic examination,
a sonography is generally recommended; if the cyst
appears denser, a CT scan is needed.
Treatment
may consist of percutaneous aspiration
of a fluid-filled cyst or surgical exploration with the potential for total or
subtotalnephrectomy.
Renal Cell Carcinoma
OVERVIEW
Renal cell
carcinoma is also referred to as adenocarcinoma of the kidney. As with other malignancies, the healthy tissue of the kidney is replaced and displaced by cancer cells. Although the exact mechanism is not known, the tumor cells are thought to originate in the proximal convoluted tubules of the nephron.
Systemic effects occurring with
the cancer are called paraneoplastic syndromes and include anemia, erythrocy-tosis,hypercalcemia, liver dysfunction with elevated liver enzymes,
hormonal effects, increased sedimentation rate, and hypertension.
Anemia and erythrocytosis may appear contradictory: There is some blood loss from hematuria, but the amount lost is not sufficient to cause anemia. Erythrocytosis may
be caused by erythropoietin production in the tumor cells. Hypertension
may result from increased renin.
Parathyroid hormone
produced by tumor cells may be the cause of hypercalcemia; other hormone alterations include increasedrenin levels
(causing hypertension) and increased human chorionic gonadotropin (hCG) levels, which are accompanied by decreased libido and changes in secondary sex characteristics. The cause of the increased sedimentation rate and changes in liver function studies is not known.
Renal tumors are
categorized into four stages (Table 71-5). Complications include metastasis and urinary tract
obstruction. Metastasis usually occurs via the blood or lymph to the adrenal gland,
liver, lungs, long bones, or the other kidney. When the tumor surrounds a ureter, hydroureter and urinary tract obstruction may
result.
The exact cause of
renal cell carcinoma is unknown, but links to tobacco use and exposure to
chemicals such as lead, phosphate, and cadmium have been observed. Other
studies suggest the possibility of hereditary influences.
Renal malignancies
account for approximately 2% of reported
cancers, with about 28,800 new cases and 11,300 deaths annually in the
COLLABORATIVE MANAGEMENT
Assessment
HISTORY
The nurse asks the
client for specific information, including age, known risk factors (e.g.,
smoking or environmental exposures), history of weight loss, changes in urine
color, abdominal or flank discomfort, and
fever. The cause of fever is unknown, butpyrogens produced
by the tumor cells have been implicated.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
Presentations of
renal carcinoma are seen only in 5% to 10% of clients and include flank pain, gross hematuria,
and a palpable renal mass. The nurse asks about
the nature of the flank or abdominal discomfort; clients typically describe
the pain as dull and aching. The pain may be more intense if
bleeding into the tumor occurs. The nurse inspects the flank, noting asymmetry or
obvious protrusions. An abdominal mass may be
detected through gentle palpation. A renal bruit may be heard
on auscultation.
Hematuria is a late common sign. Blood in the urine
may be grossly observable as bright red flecks or clots, or the urine may appear smoky or cola colored. Without gross hematuria, microscopic
examination may or may not reveal red cells.
The skin is
inspected for pallor, darkening of the nipples and breast enlargement (in men). Other findings may include muscle wasting, weakness, generally poor nutritional status, and weight loss.
All tend to occur late in the disease.
DIAGNOSTIC ASSESSMENT
Urinalysis may
reveal red blood cells. Hematologic studies
reveal decreased hemoglobin and hematocrit values, hypercalcemia, increased erythrocyte sedimentation rate, and increased levels of adrenocorticotropic hormone,
human chorionic gonadotropin(hCG), cortisol, renin, and
parathyroid hormone.
Renal masses may be
detected by surgical exploration, IV urogram with nephrograms, or sonography. The mass and surrounding structures may be further delineated by CT with contrast or
magnetic resonance imaging (MRI). Staging or determining the extent of tumor
spread is best accomplished with renal arteriography and
renal venography.
Interventions
Interventions
focus on controlling the cancer and preventing metastasis.
NONSURGICAL MANAGEMENT. Chemotherapy with a variety of agents has had limited effectiveness. The Food and Drug Administration (FDA) has approved expanded clinical trials for the study of interleukin-2 (IL-2), a biologic response modifier (see Chapters 20 and 25). Interferon (INF) and tumor necrosis
factor (TNF) are also being used investigation-ally. Studies withlymphokine-activated killer
(LAK) cells and
tumor-infiltrating lymphocytes (TIL) are in the clinical trial
stage.
SURGICAL MANAGEMENT. Renal cell carcinoma is usually treated surgically by nephrectomy (kidney
removal) when pain, bleeding, or tumor spread cannot be controlled otherwise.
PREOPERATIVE CARE. The client is
instructed about surgical routines (see Chapters 17, 18, and 19).
The nurse explains the probable site
of incision and the postoperative dressings, drains, or other equipment needed and reassures the client about pain relief. Preoperative care includes administering blood and fluids to achieve hemodynamic stabilization.
OPERATIVE PROCEDURE. The client is placed in the lateral position with the operative kidney uppermost; after positioning the arms and legs, the client's trunk area
is flexed to increase exposure of the kidney area. Removal of the
eleventh or twelfth rib is needed to provide better access to the kidney. The
surgeon removes the entire kidney, renal artery and vein, and surroundingGerota's fascia
after ligation of the ureter. The
adrenal gland is left intact. A drain may be placed in the wound before closure.
When a radical nephrectomy is performed, the periaortic lymph nodes are also removed, the
surgical approach may betransthoracic (as discussed in the previous
paragraph), lumbar, or transabdominal depending
on the size and location of the lesion.Radiation therapy may follow a radical nephrectomy. Studies are ongoing to identify the effectiveness of adjuvant therapy (e.g., chemotherapy).
POSTOPERATIVE CARE. Refer to Chapter
19 for postoperative care. Assessment of
urologic and renal function is essential to determine function in the remaining
kidney.
Monitoring. The nurse observes
the client's abdomen for distention from bleeding and symptoms of adrenal
insufficiency. The nurse observes the bed linens under the supine client, because bleeding may be present. Hemorrhage or adrenal
insufficiency may be accompanied by hypotension, a decrease in urine output, and an altered level of
consciousness.
A decrease in blood pressure is
one of the earliest signs of both hemorrhage and adrenal insufficiency; in clients
with hypotension, urine output also decreases immediately. Large water
and sodium losses in the urine occur in clients with adrenal insufficiency; consequently, a large urine
output is followed by hypotension and subsequent oliguria (<400 mL/24 hr or less than 25 mL/hr). The physician may prescribe IV replacement of fluids and the administration of
packed red blood cells.
The second
kidney is expected to provide adequate renal function. The nurse assesses urine
output hourly for the first 24 hours postoperatively; a urine flow of 30 to 50 mL/hr is acceptable. Flow rates of less than 25 to 30 mL/hr
suggest a decrease in renal perfusion.
Initially, the postoperative hemoglobin level, hematocrit values, and white blood cell count may
be measured every 6 to 12 hours.
The nurse monitors the
client's temperature, pulse rate, and respiratory rate at least every 4 hours; careful
measurement and recording of fluid intake and output
are critical. The client is weighed daily.
The client may be in
a special care unit for 24 to 48 hours postoperatively for monitoring of bleeding and/or adrenal insufficiency.
A drain placed near the site of incision removes residual fluid. Because of the
discomfort associated with lung expansion, the client is susceptible to atelectasis.
Fever, chills, thick sputum, or decreased breath sounds suggest pneumonia.
Pain
Management. After surgery, opioid analgesics (e.g., meperidine [Demerol], hydromorphone [Dilaudid], and morphine
sulfate [Statex*^]) are given parenterally.
The incision site, in which the major muscle groups associated
with breathing and movement are
involved, necessitates the liberal use of analgesic agents. These medications may be
required for 3 to 5 days for pain management. Oral analgesic agents
may be considered when the client is
permitted to eat and drink.
Prevention of Complications. One or more
antibiotics may be prescribed for intraoperative and
postoperative prophylaxis. These agents are usually given as single-dose prescriptions. The need for additional antibiotics is
based on clinical and laboratory evidence of
infection. Steroid replacements may be necessary in adrenal insufficiency.
RENAL TRAUMA
OVERVIEW
Trauma to one or both kidneys is
always a concern in penetrating wounds or
blunt injuries to the back, flank, or abdomen. Injury to the kidney can be minor, major, or pedicle. Strategies
to prevent trauma are reviewed in Chart.
Minor injuries include contusions, small lacerations, and disruption of the
integrity of the parenchyma and the calyx (forniceal disruption). In a person with a contusion, one or both
kidneys sustained a bruise because of the major impact. Small blood vessels may be damaged, causing some hematuria. One
or more small lacerations may result in small, localized hematomas.
There may also be a small hematoma at the site of forniceal disruption.
Common causes include falls, contact
sports, and blows to the back and torso.
Major injuries
involve lacerations to the cortex, medulla, or one of the segmental branches of the renal
artery or vein. Deepparenchymal injuries may extend throughout the
kidney and result in hematomas contained
within or disrupting the capsule. Otherparenchymal injuries involve the cortex and cause shattering of tissue, resulting in either an intact or a disrupted capsule.
A major injury is most likely to follow a penetrating abdominal, flank,
or back wound (such as seen with gunshot wounds, knife wounds, or motor vehicle accidents).
Bleeding is extensive, and surgical exploration is often required. Because of the hemorrhage,hypoperfusion of renal parenchyma can produce
short-term or long-term renin-induced hypertension
Pedicle injuries involve a laceration or disruption of the renal artery and/or renal vein. Hemorrhage is extensive and rapid, and death may ensue quickly unless diagnosis and intervention
are prompt.
COLLABORATIVE MANAGEMENT
Assessment
The nurse
obtains a history of the client's usual health status and the events surrounding the trauma from the client, a witness, or emergency personnel. Critical assessment information includes
a history of renal or urologic disease, surgical intervention, or systemic health problems (e.g., diabetes mel-litus or hypertension).
Ureteral and/or renal
pelvic injury may cause diffuse abdominal pain, local collections of urine,
and infection. The nurse asks the client about pain, specifically flank or abdominal pain, and solicits a description: Is the pain
dull? Sharp? Constant? Intermittent?Aggravated
by coughing?
The nurse
measures the client's blood pressure and apical and peripheral pulse rates, respiratory rate, and temperature. The right and left flanks are inspected to determine asymmetry or penetrating injuries of the lower thorax or back. Similarly, the nurse inspects the abdomen for ecchymoses, percusses the abdomen for distention, and observes for penetrating wounds. The urethra is inspected for gross bleeding.
Urinalysis commonly
reveals hemoglobin or red blood cells from the rupture of small or large renal blood vessels. Microscopic
examination of the urine may also show red blood cell casts, which suggest tubular damage. Hemoglobin and hematocrit values decrease with blood loss; the
white blood cell count
is elevated with inflammation or infection.
Fluoroscopic procedures include
IV urography,
renal arte-riography, and computed tomography (CT). A urogram reveals the number of kidneys and the
integrity and patency of the collecting system. Renal sonography is an alternative diagnostic procedure to a urogram that
avoids radiopaque contrast media exposure to clients
with elevated serum creatinine levels.
Renal arteriography reveals
the number of kidneys and, more specifically, the blood supply to each. In
clients with pedicle injuries, the contrast media used in arteriography extravasates from the ruptured vessels, and the renal parenchyma is not visualized. The CT scan shows the location of the injury and vascular and
tissue integrity. Intracapsular and extracapsular hematomas are readily observable on the CT
scan.
Interventions
Nursing diagnoses for
the client with renal trauma include Ineffective (Renal) Tissue Perfusion, Anxiety, Pain, Impaired Urinary Elimination, Post-Trauma Syndrome, and Risk for Infection. Interventions include medications for vascular support, fluids to restore
fluid volume, and surgery when indicated.
NONSURGICAL MANAGEMENT
DRUG THERAPY. Prescribed IV dopamine (Revimine4*1, others) supports renal perfusion. Coagulation factors such as vitaminÊ and platelets are assessed and
administered as needed.
FLUID THERAPY. Fluid administration to restore circulating blood volume is critical for renal tissue
perfusion. Crystalloidsolutions
replace water and some electrolytes and include 0.9% sodium
chloride (NSS), 5% dextrose in 0.45% sodium chloride, and Ringer's solution. When
significant bleeding has occurred, whole blood or packed red cell replacement restores the oxygen-carrying capacity of
hemoglobin. Plasma volume expanders, such as dextran or albumin, help re-establish plasma oncotic pressure
and minimize fluid shift from the intravascular to the interstitial
fluid space.
During fluid
resuscitation or restoration, the nurse administers fluid at the prescribed rate and monitors the client for hemodynamicinstability.
The nurse also monitors vital signs as often as every 5 to 15 minutes and
measures and records urine output hourly. Urine output should be greater than 25 to 30 mL/hr.
SURGICAL MANAGEMENT. Surgical interventions may include nephrectomy and
partial nephrectomy.
For clients with major vascular tearing, the kidney may be surgically removed,
repaired through revascularization techniques, and then reimplanted.
The repair of kidney tissue outside the client
is called bench surgery. Autotransplantation is transplantation of one's own kidney.
Community-Based Care
The nurse
instructs the client, family, or significant other about the effects of the injury and how to assess for infection or other
complications, such as the onset of bleeding or urinary retention. The client is instructed to observe the pattern and frequency of urination and to note whether the color, clarity,
and amount appear normal. The nurse also instructs the client
to seek medical attention if these characteristics change significantly and if a feeling of bladder distention or inadequate
bladder emptying occurs, which suggests an obstruction. Chills, fever, lethargy, and/or cloudy,
foul-smelling urine may
suggest a urinary tract infection. The nurse warns the client
not to ignore these symptoms and to seek medical care promptly if they occur.
ACUTE
AND CHRONIC RENAL FAILURE
Acute and chronic renal failure have become
increasingly niore common in the
The functions of the kidney are
excretion of waste, water and salt
regulation, maintenance of acid balance, and hormone secretion. When renal
function deteriorates gradually, as occurs with most causes of chronic renal
failure, 90% to 95% of the nephrons must
be destroyed before significant renal failure is evident. The client may have
many years of decreased renal reserve and chronic renal insufficiency
before the uremia of end-stage renal failure develops. During this time of decreased renal reserve and chronic renal insufficiency, the client is at increased risk for acute
renal failure because of the
diminished availability of functioning nephrons.
When renal deterioration is
sudden, the capacity of the functioning nephrons is exceeded more quickly, and renal
failure may develop with the loss of only 50% of functioning nephrons. Acute renal failure and chronic renal failure are compared in Table 72-1. Acute renal failure affects many body systems; chronic renal failure affects every body system. The abnormalities are primarily related to the effects of the
following:
· Fluid volume excess
· Electrolyte and acid-base abnormalities
· Accumulated nitrogenous wastes
· Hormonal inadequacies
When renal function decreases to the point where the
kidneys can no longer meet the body's homeostatic
demands, renal replacement therapy is required to prevent death from potentially life-threatening consequences.
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ACUTE
RENAL FAILURE
OVERVIEW
Acute renal failure (ARF) is a rapid decrease in renal function, leading to
the accumulation of metabolic waste in the body. ARF can result from conditions that cause
inadequate kidney perfusion (prerenal failure); damage to the glomeruli, interstitium, or tubules (intrarenal failure); or obstruction (postrenal failure) (Kelly, 1997). ARF in clients with chronic renal insufficiency (CRI) may result in end-stage renal disease (ESRD) or may resolve to nearly the pre-ARF level of renal function. Many factors contribute to renal
insults resulting in ARF, but the acute syndrome may be reversible.
Pathophysiology
The pathophysiologic process of ARF is related to the cause
of the sudden decrease in kidney function and the involved site orsites of the kidney. Hypoperfusion, toxins, tubular ischemia, infections, and
obstruction have different effects on the renal system. Any of these processes can result in a decreased glomerular filtration rate
(GFR), alterations in renal tubular cell membrane integrity, and tubular lumen
obstruction.
With acute hypoperfusion, autoregulatory responses (i.e., renal vasoconstriction, activation of renin-angiotensin-aldosterone, and release of antidiuretic hormone
[ADH]) increase blood volume and improve
renal perfusion. However, these compensatory mechanisms cause urine volume to
fall, resulting in oliguria (urine
output less than 400 mL/day). Tubular cell injury is more likely to occur from the increasing ischemia related to hypoperfusion. Toxins can cause vasocon-strictive responses in the kidney, leading to reduced renal blood flow and renal ischemia.
Interstitial inflammatory
changes resulting from infection, drugs, or infiltrating tumors result in immune-mediated changes in renal tissue. With extensive tubular damage, sloughing of tubular cells and other formed elements (e.g., red blood cell [RBC]
casts) may obstruct the tubular lumen and prevent the formation or outflow of urine.
Obstruction anywhere within the genitourinary tract eventually results in full or partial obstruction to the
formation and outflow of urine.
When intratubular pressure exceeds glomerular hydrostatic pressure, glomerular filtration ceases. This process causes a progressive elevation of the serum blood urea nitrogen (BUN)
and creatinine levels. When the BUN rises faster than the serum creatinine level,
the cause is usually related to protein catabolism or volume depletion. When
both the BUN and creatinine levels rise and the ratio between the
two remains constant, renal failure is present.
TYPES OF ACUTE RENAL FAILURE
Several
syndromes describe the types of ARF. These include prerenal azotemia, intrarenal (intrinsic) ARF, and postrenal azotemia. Table 72-2
summarizes the pathologic changes and causes of ARF.
Prerenal azotemia can be reversed by
establishing normal intravascular volume, increasing blood pressure and
cardiac output. Prolonged, untreated hypoperfusion can
lead to severe ischemic injury and intrarenal failure.
The term intrarenal ARF is often shortened to just ARF in the clinical setting. Other
terms include acute tubular
necrosis (ATN)and lower nephron nephrosis. Infections (bacteria, viral, fungal, or endotoxin),
drugs (especially aminogly-coside antibiotics
andnonsteroidal anti-inflammatory
drugs [NSAIDs]), and infiltrating tumors (e.g., lymphomas or leukemias)
can cause acute interstitial nephritis. Inflammation of the glomeruli (glomerulonephritis) or of the small vessels of the kidneys
(vasculitis) or a major obstruction to blood flow can
also cause intrarenal ARF.
Postrenal azotemia develops from
obstruction to the outflow of formed urine anywhere within the genitourinary
tract.
IPHASES
OF ACUTE RENAL FAILURE
When a client's renal function has been compromised,
the phases of ARF begin (Table 72-3). Increasing numbers of clients
have anonoliguric form of ARF. The description of the phases
of this form of ARF are similar to those described in Table 72-3 except for the references to
urine output. In addition, the
treatment of these clients is less complicated because renal replacement therapy is rarely needed. Interventions to restore
circulating volume, improve cardiac output, or reestablish blood pressure may prevent progression
of the phases when renal hypoperfusion is present.
Etiology
Many types of renal insults can
lead to reduced renal function. Severe hypotension from excessive blood loss or dehydrationresults in hypoperfusion of
blood to the kidneys and can lead to prerenal ARF.
Cardiac disease or heart failure also results in
decreased renal perfusion. The client may be oliguric, or even anuric (less
than 100 mL/24 hr), if the dehydration or renal blood flow obstruction is severe. The following are other conditions that precipitate ARF:
· Nephrotoxic agents (antibiotics, NSAIDs) (Table 72-4)
· Disseminated intravascular
coagulation (DIC)
· Obstruction by
thrombosis or stenosis
· Uric acid crystals
or other obstructing precipitates
· Acute hemolytic
transfusion reactions
· Complications of
infection (e.g., endotoxins or
sepsis)
· Acute glomerulonephritis
· Vasculitis
· Severe hypertension
· Hepatorenal syndrome of cirrhosis
Incidence/Prevalence
ARF affects
20% of all critically ill clients and carries a 50% to 80% mortality rate
(Stark, 1998). Eighty percent of ARF episodes are due to ATN and exacerbations
of CRI. Volume depletion leading to prerenal azotemia is
the most common cause
of acute renal deterioration and is reversible in most cases
with prompt intervention.
For clients
surviving the precipitating event, the opportunity for return of renal
function is good. Complications during the course of ARF can vastly increase
mortality. Bloodstream infections associated with
central and peripheral lines and the pulmonary system are most often involved
in complications. However, the highest
mortality occurs with trauma (70%) and surgery. ARF caused bynephrotoxic substances is associated with
the lowest rates (10% to 26%) of recovery. The prognosis for ARF caused by obstruction or glomerulonephritis is much better.
COLLABORATIVE MANAGEMENT
Prevention
Nurses have an essential role in
the prevention of acute renal failure (ARF). The nurse notes the signs of impending
renaldysfunction through careful physical assessment and close monitoring
of laboratory values. Prompt recognition and correction ofextrarenal problems
usually restore renal function before tissue damage can occur. Careful physical
assessment is required to evaluate the client's fluid status.
Intake and output records and body
weights can assist in identifying trends in
fluid balance. If vascular volume is depleted, decreased urine
output, postural hypotension, and tachycardia will be present. Prompt fluid
resuscitation for clients in the prerenal stage
can prevent intrarenal problems that can lead to renal tissue
damage and renal failure.
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The nurse also
monitors laboratory values for any changes that reflect compromised renal
function. Decreased urine specific gravity
indicates a loss of urine-concentrating ability and is the earliest sign of renal tubular damage. Other laboratory values
that are helpful in monitoring renal function include serum creatinine,
urine and serum electrolytes, and blood urea nitrogen (BUN).
The nurse is
aware of nephrotoxic substances that the client may ingest
or be exposed to (see Table 72-4). The nurse questions orders for potentially nephrotoxic drags, and the ordered dose is validated before the client receives the drag. Antibiotics are the most likely drag group to have nephrotoxic side effects. NSAIDs may
cause or potentiate the risk for ARF. Combinations of drags can cause synergistic reactions, further increasing the risk for ARF. If a client must receive a potentially nephrotoxic drag, the nurse monitors laboratory
values, including BUN, creatinine, and drag peak and trough levels, closely for indications of actual or potential renal dysfunction.
Assessment
HISTORY
The accurate
diagnosis of ARF, including its type and its cause, largely depends on a detailed history. The history must includequestions relating to the potential causes of ARF. The
client is asked about exposure to nephrotoxins, recent surgery or trauma, transfusion, or other factors that might lead to renal ischemia. A medication history is also important, since treatment with certain anti-infectives, aminoglycoside antibiotics, angiotensin-converting enzyme
(ACE) inhibitors, and NSAIDs can cause prerenal failure.
Exposure to radiographic contrast medium can precipitate ARF, especially in older
clients with reduced renal reserve. In some
situations, ARF must be differentiated from chronic
renal insufficiency (CRI). In these cases, the nurse asks about known renal diseases; systemic
diseases, such as diabetes mellitus and systemic lupus erythematosus and other connective tissue diseases; and chronic
hypertension.
To identify possible acute glomerulonephritis,
questions about acute illnesses such as influenza, colds, gastroenteritis, and sore
throats or pharyngitis,
as well as the presence of cocoa-colored urine (hematuria),
are included.
Reversible prerenal azotemia may be suspected after hypotension, hemorrhage or shock, burns, congestive heart failure (CHF), or any situation in which the client
experiences in-travascular volume depletion. Phosphorus-containing bowel preparations and being allowed nothing by mouth (NPO) pre-operatively, in conjunction with the fluid losses of
most surgical procedures, are sufficient to cause prerenal azotemia in many clients (Orias, Mahnensmith,
& Perazella,
1999).
Postrenal azotemia can be identified
by focusing on any history of obstructive disease processes that
would be manifested as difficulty in starting the urine stream, changes in the amount or appearance of the urine, narrowing of the urine stream, nocturia,
urgency, or symptoms of renal calculi. The
nurse also notes any history of malignant carcinoma that may cause bilateral obstruction.
Because of the widely varied
causes and the potentially reversible nature of
the illness, the nurse obtains or validates a detailed history when ARF is
suspected. In clients with postrenal azotemia, the nurse monitors for oliguria or intermittent anuria,
symptoms of uremia, and lethargy.
The nurse reports changes in the character of the urine
stream or difficulty starting urination.
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
The clinical
manifestations of ARF are related to azotemia, as well to as the underlying cause (Chart). Signs
and symptoms ofprerenal azotemia are hypotension, tachycardia, decreased
urine output, decreased cardiac output, decreased central venous pressure
(CVP), and lethargy. The general clinical appearance of a client with prerenal azotemia is similar to that of a client with heart failure or dehydration, depending
on the cause of the renal compromise.
Intrarenal (intrinsic) ARF usually involves damage to the glomeruli, interstitium,
or tubules. Classic manifestations include oliguriaor anuria (absence of urine), edema,
hypertension, tachycardia, shortness of
breath, jugular venous disten-tion, elevated CVP, weight gain, rales or crackles, anorexia, nausea, vomiting, and lethargy or varying levels of consciousness.
Clinical manifestations of electrolyte abnormalities, such as electrocardiographic (ECG) changes, may also be present.
LABORATORY ASSESSMENT
The numerous
alterations in laboratory values in the client with ARF are similar to those occurring in chronic renal failure (CRF). The nurse can expect to find
rising BUN andcreatinine levels, and abnormalities in serum electrolytes. Table 72-5 shows the effects of renal failure on electrolyte values. Clients with ARF,
however, typically do not experience the anemia associated
with CRF un; less there is hemorrhagic blood loss. However,uremic hemolysis secondary to severe azotemia can develop and may be the cause of anemia in the early phase of ARF.
In the early phases of ARF,
urinalysis and microscopic examination of urine may provide diagnostic
information. Urine sodium
levels are often less than 10 to 20 mEq/L in clients with prerenal azotemia. In prerenal azotemia, the urine is often concentrated, with a
specific gravity greater than 1.020. The presence of urine sediment (red blood cells [RBCs], RBC casts, tubular cells), myoglobin,
or hemoglobin; a urinary sodium level lower than 40 mEq/L; and a
specific gravity of 1.010 are indicative of intrarenal failure. Inpostrenal failure, urinary sodium levels may be normal to 40 mEq/L, with a specific gravity of 1.000 to 1.010.
RADIOGRAPHIC ASSESSMENT
X-ray studies help to determine
the cause of ARF. A flat-plate x-ray film of the abdomen is obtained to determine the size of the kidneys. In the absence of underlying renal disease, normal-size kidneys are expected. Enlarged kidneys, possibly due to obstruction, may result from hydronephrosis. This x-ray finding may also illustrate obstructing calculi in the renal pelvis, ureters, or bladder.
Renal ultrasonography is a noninvasive procedure using high-energy sound waves. It is useful in the diagnosis of urinary tract obstruction. Dilation of the renal calyces
and collecting ducts, as well as calculi, can be detected.
Computed tomography
(CT) scans without contrast dye can be obtained to identify obstruction or tumors.
Contrast media are usually avoided to prevent further renal damage. A sonogram is
generally preferred to the intravenous pyelogram (IVP)
to determine kidney size and the patency of
the ureters.
Aortorenal angiography may be used to
examine renal blood vessels and blood flow. The procedure involves
the necessary risk of using contrast media but can
reveal any occlusion of major renal vessels by
thrombus, embolus, or stenosis. Cystoscopy or retrograde pyelography may
be indicated to identify possible obstructive lesions in the urinary tract.
OTHER DIAGNOSTIC ASSESSMENT
Renal biopsy
may be performed if the primary cause is uncertain, an immunologic disease is suspected, or the reversibility
of the renal failure needs to be determined after ARF
has persisted for an extended period. The nurse assists with many of the diagnostic studies, prepares the client before the test, and provides follow-up care. The nurse must be aware of all test results and understand how they may affect the treatment regimen. (See Chapter 69 for a detailed discussion of renal diagnostic tests.)
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Interventions
The primary nursing diagnosis
and collaborative problems for the client with acute renal failure (ARF) are
Excess Fluid Volume, Potential for Pulmonary
Edema, and Potential for Electrolyte Imbalances.
The client with ARF may pass from the oliguric phase (in which fluid and electrolytes are retained) to the diuretic phase. If the client moves to the diuretic phase, hypovolemia and electrolyteloss are the primary problems. As
a result, the client in the diuretic phase of ARF needs a plan of care that focuses on fluid and electrolyte replacement and monitoring.
These examples of output
variation reflect the continually changing
nature of ARF and the need for the plan of care to be
constantly updated to reflect the client's movement through the stages of the disease process. Drug therapy, diet therapy,
and renal replacement therapy (peritoneal dialysis [PD], hemodialysis [HD], or hemofiltration)
are commonly employed in the management of ARF.
DRUG THERAPY. Clients with
ARF receive numerous medications. As kidney function changes, the physician often modifies drug
doses. The nurse is knowledgeable about the site of drug metabolism and is especially careful
when administering medications. The nurse constantly monitors for possible side effects and
interactions of the drags the client with ARF is receiving. Diuretics may be used to increase urine output.
In clients
with prerenal azotemia,
fluid challenges and diuretics are often
used to promote renal perfusion. In clients without signs and symptoms of fluid volume excess, 500
to 1000 mL of normal saline may be infused over a
1-hour period. In prerenal azotemia, the client should respond to the fluid
challenge by producing urine soon after the initial bolus. Diuretics such as furosemide (Lasix) may also be ordered in conjunction with a fluid bolus. If oliguric renal
failure is diagnosed, the fluid challenges and diuretics are discontinued. The physician may prescribe low-dose (1 to 3 |xg/kg) dopamine in a continuous infusion to
enhance renal perfusion and/or increase blood pressure (Zellner, 1999) (Chart 72-4). These clients
often require central venous pressure (CVP) monitoring or measurement of pulmonary arterial pressure
by means of a Swan-Ganz catheter for a more exact evaluation
of their hemodynamicstatus.
They also require constant nursing supervision
for assessment of the response to fluid and drug administration. The nurse carefully monitors for
signs of possible fluid overload.
Calcium
channel blockers may be used to treat ARF resulting from nephrotoxic acute
tubular necrosis (ATN) by preventing the influx
of calcium into the kidney cells, thereby maintaining cell integrity and
improving the glomerular filtration rate (GFR).
DIET THERAPY. Clients who have ARF often have a
high rate of catabolism. The exact mechanism for this state is not well understood. Increases in catabolism may be related to the stress of a critical illness, causing an increase in levels of circulatingcatecholamines, cortisol, and glucagon, all of which stimulate catabolism. The rate of catabolism is
correlated with the severity of uremia and azotemia. This hypercatabolic state causes the breakdown of muscle for protein, which leads to an increase in azotemiaand an even more elevated
serum blood urea nitrogen (BUN) level.
If the client
with ARF has an adequate dietary intake (see Imbalanced Nutrition: Less Than Body Requirements [Chronic
Renal Failure]), nutritional support may not be
necessary. The health care provider may order a consultation with a dietitian, who will calculate the client's caloric requirements. In
conjunction with the dietitian, the health care provider will order a diet with
specific levels of protein and sodium and the amount of fluids
required. If the client does not require dialysis, 0.6 g/kg of body
weight or 40 g/day of protein is ordered. For clients
needing dialysis, the
protein level needed will range from 1 to 1.5 g/kg. The amount of dietary
sodium ranges from 60 to 90 mEq. In the presence of hyperkalemia, dietary potassium is restricted to 60
to 70 mEq.
The amount of fluid permitted is generally calculated to equal the urine volume plus 500 mL. The
nurse continually assesses oral intake to make certain that sufficient
calories are consumed.
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BEST
PRACTICE/or
Administering Renal-Dose Dopamine
Take an
accurate weight because the dose is ordered according to the client's weight.
Know the hospital's policy regarding who is
responsible for calculating the rate of infusion (i.e., physician, pharmacist, or
nurse). Renal-dose dopamine is 1 to 5 //.g/kg body wt/min but is converted to mL/min for an IV infusion. Before hanging the dopamine infusion, double-check the amount of dopamine added to the solution, the total volume of solution (usually 250 mL), and the
calculation mil-liliters per minute.
Do not hang the dopamine infusion until all questions about the
calculation are clarified. If dopamine is to be infused into a peripheral vein,
be sure that the line is intact and secured. Once the infusion is started, check the client's blood pressure and pulse per hospital policy or the physician's orders,
usually at least every 2 hours. Notify the physician of changes in vital signs per
policy or the physician's orders.
Monitor the IV site frequently for clinical manifestations
of infiltration.
If
infiltration occurs, stop the infusion but do not discontinue the IV catheter. Prepare for phentolamine (Regitine, Rogitine*) administration through the IV catheter and subcutaneously into the infiltrated tissue.
Many clients
with ARF are too ill or too anorexic to eat sufficient food. For these clients,
some form of nutritional support (e.g., total parenteral nutrition
[TPN] or hyperalimen-tation)
must be initiated to avoid catabolism. The goals of nutritional support in ARF
are to provide sufficient nutrients to maintain or improve nutritional status, to preserve
lean body mass, to restore or maintain fluid balance, and to preserve renal
function.
If TPN is
administered, the solutions may be formulated to meet the client's specific needs. Because kidney function is unstable in
ARF, the nurse constantly monitors the serum electrolyte concentrations and
facilitates revisions in the hy-peralimentation solution as needed. In addition
to TPN, intravenous (IV) fat emulsion (Intralipid)
infusions provide a non-protein source of
calories. In uremicclients,
fat emulsions can be used in place of glucose to avoid the problems
associated with excessive sugars.
DIALYSIS THERAPIES. Hemodialysis (HD) and peritoneal dialysis (PD) may be implemented for clients with ARF if necessary. Until recently, intermittent hemodialysis (IHD) has been the most common treatment of ARF. The following are indications for dialysis in ARF:
• Uremia
• Persistent hyperkalemia
• Uncompensated metabolic acidosis
• Fluid volume excess unresponsive to diuretics
• Uremic pericarditis
• Uremic encephalopathy
Immediate
vascular access for HD in clients with ARF is established by placement of a dual- or triple-lumen catheter specifically designed for HD. For HD that is expected to be necessary for several weeks, the catheter is usually placed into the subclavian or internal jugular vein. If only
one or two treatments are expected to be necessary, as for removal of drugs or toxins by hemoperfusion,
a femoral site may be selected. Longer use of the femoral site is generally discouraged because
of positioning limitations (i.e., required
immobility) and other potential complications, such as hematomas and infection. Repeated can-nulation of
the femoral site also increases the risk for hematoma formation and makes repeated use of the vein
impossible.
The subclavian vein is often preferred over femoral
vein cannulation because the catheter can be left
in place between dialysis treatments. This placement is also a disadvantage, however, because the longer the
catheter is left in place, the greater
is the chance for infection. The subclavian dialysis catheter
(Figure 72-1) is inserted at the bedside. A physician performs the sterile
procedure, and then the catheter is covered with a sterile dressing. Catheter placement is checked by chest x-ray examination before its use.
HD catheters
have two lumens separating the outflow and inflow extensions of the catheter. Consequently, the continuous outflow
of blood to be dialyzed is separated from the dialyzed blood returned through the inflow port and lumen. A triple-lumen catheter for HD is now available. The third
lumen provides a port for drawing venous blood or administering medication and fluid without interruption of the dialysis lumens.
PD may also
be used in the treatment of ARF, but its use may be limited in the critically
ill, since mechanically ventilated clients may not
be able to tolerate the accompanying abdominal distention, and since its use requires an intact, unin-fected abdominal cavity (Giuliano & Pysznik). PD
uses the peritoneum as
a semipermeable membrane for which dialysate is infused through a catheter implanted in the
peritoneum. A more complete discussion of PD is provided later in this chapter
under Chronic Renal Failure).
CONTINUOUS RENAL REPLACEMENT THERAPIES.
Currently,
continuous renal replacement therapies (CRRTs) have become the standard treatment for ARF. Renal replacement therapies in the form of hemofiltration may be better tolerated
than HD for clients who are critically ill, since rapid shifts
of fluids and electrolytes associated with HD are avoided (Giuliano & Pysznik).
Continuous arteriovenous hemofiltration (CAVH) and continuous arteriovenous hemodialysis and
filtration (CAVHD) provide additional renal replacement therapies for clients with ARF.
These procedures share some similarities with HD, but their use and
indications are specific and limited.
CAVH is indicated for clients who
are fluid volume overloaded, resistant to diuretics, and hemodynamically unstable. The implementation of CAVH requires the placement of both arterial and venous catheters to provide adequate filtration sociated with the pump, but most pumps are
equipped with alarms that detect air. These systems also require the
use of anticoagulants, but at lower doses than needed for AV systems. These
procedures are performed in a critical care unit, and clients require
continuous nursing care.
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POSTHOSPITAL CARE. The posthospital care
for a client with ARF varies widely, depending on the status of the disease when the client is discharged. The course of ARF varies, with recovery lasting up to several months. If the renal
failure is resolving, follow-up care is often
provided by a nephrologist or by the family physician in consultation with the nephrologist.
On occasion, however, ARF results in permanent renal damage and the need for chronic dialysis or even transplantation. In these cases, theposthospital care may be as extensive and multifaceted as it is for any other client with chronic renal
failure (CRF) (see Community-Based Care [Chronic Renal Failure]).
If the ARF is
in the process of resolving, the follow-up care may involve a variety of
services. Frequent medical visits arenecessary, as are routine
laboratory blood and urine tests to monitor renal function. Consultation with a
dietitian may be needed to modify the client's diet according to the degree of
renal function and ongoing nutritional requirements. Clients continuing dialysis after discharge must be taught to limit foods high in potassium and sodium and to observe protein restrictions.
In addition, education concerning the need for limited fluid intake may be
necessary.
Some clients
may need some form of temporary dialysis until
their kidneys can metabolize fluid and waste products independently.
The dialysis begun while the client was hospitalized may be continued
at an outpatient dialysis center for as long as necessary. Teaching concerning the
type of dialysis, care of vascular
access sites, dietary restrictions, fluid restrictions, and prevention of complications is ongoing throughout the recovery phase. Depending on their level of independence and family support, some clients may
also need home care nursing or social work assistance.
CAVH removes large amounts of plasma water and solutes on a
continuous basis. When large volumes of plasma water are removed, electrolytes are also removed. Electrolytes are replaced through prescribed amounts of IV electrolyte solution. The most significant disadvantage of arteriovenous (AV) filtration is the risk of bleeding associated with anticoagulants used to prevent membrane clotting (Craig, 1998).
A double-lumen
dialysis catheter inserted into a large vein (subclavian,
jugular) provides access for CAVHD. CAVHD uses adialysate (a solution composed of water,
glucose, sodium chloride, potassium, magnesium, calcium, and bicarbonate) delivery system to remove nitrogenous or other waste products in
addition to fluid in clients with limited cardiac output,
those with significant hypotension, or those who have been unresponsive to
diuretic therapy. The conventional form of HD would not be tolerated, and PD
would probably be inadequate for
the fluid removal required.
Continuous venovenous hemofiltration (CVVH) is often considered
to be the treatment of choice for critically ill clients. CVVH requires only a double-lumen venous catheter for access
and is powered by a pump, making the rate of filtration more reliable than
that of the mean arterial pressure (Giuliano & Pysznik).
CHRONIC
RENAL FAILURE
OVERVIEW
In contrast to the ability of the
kidneys to regain function following acute renal failure (ARF), chronic renal
failure (CRF) represents a clinical syndrome of progressive,
irreversible kidney injury. When kidney function is inadequate for sustaining life, CRF is referred to as end-stage renal disease (ESRD). Terms
associated with renal failure include azotemia (accumulation of nitrogenous waste products in the bloodstream), uremia (azotemia with clinical symptoms), uremic syndrome (the diverse systemic
clinical and laboratory manifestations associated with ESRD), and renal replacement therapy (hemodialysis [HD], peritoneal dialysis [PD], renal
transplantation; necessary to sustain life in clients with renal failure). ARF
and CRF are compared in Table.
Pathophysiology
STAGES OF RENAL FAILURE
The kidneys
tend to fail in an organized fashion. The client's progression toward ESRD usually begins with a gradual decrease in renal function of 30% to 50% (Table).
Initially, there is a diminished
renal reserve. A 24-hour
urine specimen for monitoringcreatinine clearance is necessary to detect that renal reserve is less than normal. In this stage, reduced renal function
occurs without any measurable accumulation of metabolic wastes in the serum because of the ability
of the unaffected nephrons to compensate for the decreased
functioning of the diseased nephrons. Renal damage is accompanied by an elevation in the systemic blood pressure, resulting in an increase in the pressure within the glomerular apparatus
and the remaining unaffected nephrons. Eventually, the unaffected nephrons may be damaged by long-term exposure to this increased
pressure, leading to the progressive renal damage characteristic of CRF.
However, under stressful conditions, such as infection, fluid overload, or
dehydration, renal function at this stage can appear compromised.
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In the next
stage, renal insufficiency, metabolic wastes begin to accumulate in the blood because the healthier
kidney tissue can no longer compensate for the loss of nonfunction-ing nephrons. Levels of blood urea nitrogen (BUN), serum creatinine, uric acid, and phosphorus are increasingly elevated in relation to the degree of renal function loss. Careful nursing and medical management of fluid volume, blood
pressure, electrolytes, dietary intake, and medication administration may slow the progression of renal failure.
Many clients
ultimately progress to end-stage
renal disease (ESRD). Excessive amounts of nitrogenous wastes, such as urea andcreatinine, accumulate in the blood, and the kidneys cannot maintain homeostasis. Initially,
severe fluid overload and
electrolyte and acid-base imbalances occur. Without renal replacement therapy, fatal complications are likely.
PATHOLOGIC ALTERATIONS
Renal
dysfunction causes multiple pathologic situations, including disruptions in
the glomerular filtration rate (GFR), abnormalities
of urine production and water excretion, electrolyte imbalances, and metabolic abnormalities. The kidneys can maintain an effective GFR until 70% to 80% of renal function is
lost. Homeostasis is maintained until late in the course of renal failure. When
less than 20% of the nephrons are
functional, the GFR is altered despite hypertrophy of the remaining nephrons.
This alteration occurs because the hy-pertrophied nephrons can maintain the excretion of
solutes or waste products only by decreasing water reabsorption.
As a result, hyposthenuria (the
loss of urine concentrating ability) and polyuria (increased urine output) occur.
Both hyposthenuriaand polyuria are early signs of CRF and, if the
problem is untreated at this stage, can cause severe dehydration.
As the
disease progresses, the ability
to dilute the urine is increasingly diminished, resulting in urine with a fixed osmo-lality(isosthenuria). As renal function
continues to diminish, the concentration of urea is increased in the blood, and
urine output decreases. When renal function deteriorates to this level, the client is at risk for fluid overload because of loss of adequate urine output.
METABOLIC
ALTERATIONS
UREA AND CREATININE. Renal failure also causes disturbances in urea and creatinine excretion. Creatinine is derived fromcreatine and phosphocreatine, which are present in skeletal muscle. The normal rate of creatinine excretion
depends on muscle mass, physical activity, and
diet. Without major alterations in the diet or
physical activity, the serum creatinine level remains relatively
constant. Creatinine is partially excreted by the renal tubules, and a decrease in renal function leads to a buildup of serum creatinine. Urea is the primary product of protein metabolism and is excreted by the kidneys. The BUN level normally varies directly with protein intake.
An important
method for accurately estimating the GFR is to
monitor the creatinine clearance of the kidneys. As renal
function andglomerular filtration diminish, creatinine clearance decreases and the serum creatinine level
rises (see Chapter 69).
SODIUM. In addition to
decreased BUN and creatinine excretion, alterations in sodium excretion are
common. Early in chronic renal failure (CRF), the client is
particularly susceptible to hyponatremia (sodium depletion) because, although a diminishing number of nephrons are reabsorbing sodium at their maximal ability, there is an obligatory loss of sodium in urine production. Thus thepolyuria often seen in early renal failure also causes
sodium depletion.
In the later
stages of renal failure, the capacity of the kidneys to excrete sodium
diminishes as urine production decreases. As a result, sodium retention can
occur with only modest increases in dietary sodium intake and can lead to severe fluid and electrolyte imbalances. Sodium retention manifests as hypertension and edema. Despite the sodium
retention, the concurrent retention of water results in an apparently normal serum sodium level; di-lutional hyponatremia is likely, since fluid volume excess
develops (see Table).
POTASSIUM. The kidney is the
primary organ responsible for potassium excretion. Any increase in potassium
load during the later
stages of renal disease can lead to hyper-kalemia (excessive potassium retention). Normal serum
potassium levels of 3.5 to 5mEq/L are
maintained until the 24-hour urine output falls below 500 mL with a decreased GFR. When hyperkalemia develops, serum levels are quickly
elevated and may be 7 to 8 mEq/L or higher. Severe electrocardiographic (ECG) changes result from this elevation,
increasing the risk of fatal dysrhythmias. Other factors contributing to hyperkalemia in renal failure include ingestion of potassium
in medications, failure to restrict
potassium in the diet, excessive tissue
breakdown secondary to the hypercatabolic state,
bloodtransfusions, and excessive bleeding or hemorrhage.
ACID-BASE BALANCE. In the early stages
of renal disease, loss of functioning nephrons causes little change in blood pH because the remaining nephrons increase
their rate of acid excretion. As the loss of nephrons continues,
the kidneys cannot compensate and acid excretion is restricted; a bicarbonate deficit or metabolic acidosis results (see Chapter).
Many factors
contribute to metabolic acidosis in renal failure. First, the kidney becomes
unable to excrete excessive hydrogen ions. Normally, renal tubular cells
secrete hydrogen ions into the tubular lumen for excretion, but
ammonia and bicarbonate are required
in order for excretion to take place. In clients with renal failure, the kidney's ability
to produce ammonia is decreased,
and the normal reabsorption of
filtered bicarbonate does not occur.
This process leads to a buildup of hydrogen ions for which the supply of
bicarbonate and other buffering bases is inadequate. As a result, there is a
base (bicarbonate) deficit in an environment with excess acid. In the presence
of hyperkalemia,
renal ammonium production and excretion are inhibited further.
As renal
failure advances and acid retention increases, respiratory compensation is
essential for maintenance of a blood pH compatible with life. The respiratory
system compensates for the decreased pH by increasing the rate and depth of breathing to
excrete carbon dioxide through the lungs. This pattern
of breathing, called Kussmaul respiration, is
increasingly apparent when
worsening renal failure results in respiratory alkalosis. Serum bicarbonate
measures the extent of
metabolic acidosis (bicarbonate deficit). Individuals with CRF
usually require treatment with alkali replacement to counteract acidosis.
CALCIUM AND PHOSPHATE. A complex, balanced reciprocal relationship between calcium and phosphate is influenced by
vitamin D (see Chapter). Vitamin D facilitates calcium absorption in the
intestines, and the kidney produces 1,25-dihydroxycholecalciferol, a hormone needed to create active
vitamin D.
In renal failure, phosphate
retention and a deficiency of active
vitamin D contribute to the disruption in calcium and phosphate
balance and metabolism. Normally, excessive dietary phosphate is excreted by the kidneys in the urine.
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HYPERTENSION. Approximately 80% to 90% of clients with CRF have hypertension. Hypertension may be either the cause or the result of CRF. The elevation in blood pressure
results from fluid and sodium overload and the malfunction of the renin-angiotensin-aldosterone system. The retention of sodium and water in renal disease causes circulatory overload, which leads to an elevated blood pressure. The kidneys respond to a decrease in renal blood flow or low serum sodium
levels by trying to improve the renal blood flow. The release of renin further
stimulates the production of angiotensin and aldosterone. Angiotensin causesvasocon-striction and an elevation in blood pressure. Aldosterone,
a mineralocorticoid released by the adrenal glands,
stimulates the distal convoluted tubule to reabsorb sodium and water. Consequently,
plasma volume is expanded, and the blood pressure is elevated. As a result of this malfunction of the renin-angiotensin-aldosterone system, the blood pressure is elevated either by vasoconstriction or by volume expansion. The kidneys do not recognize the increase in blood pressure and
continue to producerenin. The result is severe
hypertension that is difficult to treat and that ultimately worsens renal function.
Many clients with CRF also have cardiomyopathy and
left ventricular hypertrophy as a consequence of prolonged
hypertension.
HYPERLIPIDEMIA. CRF is associated
with alterations in the metabolism of lipoproteins. Increased triglyceride, total
cholesterol, and low-density lipoprotein levels are seen with a corresponding reduction in high-density lipoprotein levels. CRF
renders individuals at increased risk for coronary artery disease and acute cardiac events.
CONGESTIVE
HEART FAILURE. Many clients with renal failure have some form of myocardial dysfunction. CRF causes
an increased workload on the heart because of anemia, hypertension, and fluid overload. Left ventricular hypertrophy and CHF are common manifestations of late end-stage renal disease
(ESRD). Uremia itself may cause uremic cardiomyopathy, the uremic toxin
effect on the myocardium. CHF is also common in these clients because of the
presence of hypertension and coronary artery
disease. Cardiac disease is the leading cause of death in clients with ESRD
(U.S. Renal Data Systems, 1999).
UREMIC PERICARDITIS. Pericarditis also occurs in clients with CRF. If it is not treated effectively, this inflammation of the pericardium can lead to pericardial effusion, cardiac tamponade,
and death. The pericardial sac becomes inflamed and irritated byuremic toxins or infection. Signs and
symptoms include localized, severe chest pain, an increased pulse rate, a low-grade fever, and an intermittent and transient pericardial friction rub that can be heard on auscultation.
As the pericarditis continues and the pericardial effusion worsens, dysrhythmias may
develop; heart tones become softer and less audible, the blood pressure decreases, and the client
may experience shortness of breath. Progressive
pericardial effusion results in cardiac tamponade, a
medical and surgical emergency in which pulse pressure diminishes and bradycardia or asystole results.Treatment of pericardial tamponade involves removal of pericardial fluid by placement of a
needle, catheter, or drainage tube into the pericardium or pericardiectomy with pericardial drainage. The
incidence of uremic pericarditis has diminished with the initiation of early, aggressive
dialysis.
iHEMATOLOGIC ALTERATIONS
Anemia is the
primary hematologic abnormality in clients with CRF. Normochromic, normocytic anemia
is a common manifestation of CRF and contributes to the client's symptoms. The causes include a decreased erythropoietin level with resulting decreased red blood cell (RBC) production, decreased RBC survival time resulting from uremia, iron and folic
acid deficiencies, and impaired platelet function as a result of uremic toxins.
GASTROINTESTINAL ALTERATIONS
Uremia can
affect all levels of the gastrointestinal (GI) system. The normal flora of the
oral cavity is altered in uremia. The mouth normally contains the enzyme urease,
which hy-drolyzes urea. The ammonia generated from this reaction contributes to uremichalitosis and may also cause uremic stomatitis (mouth inflammation).
Anorexia, nausea,
vomiting, and hiccups are relatively common in clients with uremia. The specific cause of these symptoms
is uncertain but may be related to increased nitrogenous waste levels (i.e.,
blood urea nitrogen [BUN] and creatinine levels) and metabolic acidosis.
Peptic ulcer disease is also
common in clients with uremia; however, the exact cause is unclear. Uremic colitis
with profound watery diarrhea or constipation may also be present in clients
with uremia. Ulcerations may occur in the stomach or small or large intestine,
causing erosion of blood vessels. The blood loss caused by these erosions may result in melena or, in more serious cases, may progress to hemorrhagic shock from severe GI bleeding.
Etiology
The etiology
of CRF is complex (Table). There are more than 100 different disease processes that can result in progressive
loss of renal function (see also Chapter 71). However,
diabetes and hypertension are the most common causes of CRF.
Incidence/Prevalence
The number of
clients with CRF is continually increasing. The 1999 U.S. Renal Data Systems
annual report suggests that more than 307,000 people in the
glomerulonephritis (11%).
There is a higher incidence of ESRD in men than in women (U.S. Renal Data Systems).
The greatest increase in ESRD is in those 65 years of age and older. More than
221,000 people were estimated to be receiving renal replacement therapy in the
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COLLABORATIVE MANAGEMENT
Assessment
HISTORY
When
taking a history from a client with suspected chronic renal failure (CRF), the
nurse focuses on the signs and symptoms of CRF. The client's age and gender are
noted. The nurse obtains accurate weight and height measurements and inquires
about usual weight and recent weight gain or loss. Weight gain may indicate
cardiovascular overload and fluid retention caused by poorly functioning
kidneys. Weight loss may be the result of anorexia associated with the uremic syndrome. The nurse also obtains a complete history of known renal or urologic disorders, long-term health problems, medication use, and current health conditions. The client is asked about knowledge of any existing renal disease or family history of renal disease,
which might indicate a hereditary disorder. A history of kidney infection or renal calculi
could imply past kidney damage. It is important to explore long-term healthproblems
because illnesses such as hypertension, diabetes, systemic
lupus erythematosus,
arthritis, cancer, and tuberculosis can contribute to decreased renal
function.
The nurse
documents use of both prescription and over-the-counter medications because
many medications are potentiallynephrotoxic and can cause renal damage.
The nurse
examines the client's dietary or nutritional habits and discusses any present GI problems. A change
in the taste of foods often
accompanies renal failure. Clients may note that sweet foods are not as appealing or that
certain foods, especially meats, leave a metallic taste
in the mouth. The client
is asked specifically about a history of GI problems, such as nausea, vomiting,
anorexia, hiccups, diarrhea, or constipation. Any of these manifestations can
be the result of the
buildup of nitrogenous or other metabolic wastes that the
body cannot excrete because of renal malfunction.
The nurse questions the client
about his or her current energy level and any
recent injuries or bleeding. Changes in the client's daily routine are explored
as a possible result of physical fatigue.
Weakness, drowsiness, and shortness of breath are typical and suggest impending pulmonary edema
or neurologic degeneration. The nurse asks
specifically about abnormal bruising or bleeding, which may be the result of hematologic changes associated with uremia.
The nurse
discusses the client's urinary elimination in detail, including frequency of urination, appearance of the urine,
and any difficulty starting or controlling urination. This information
can help identify existing urologic disorders that may influence the preservation of existing renal function.
PHYSICAL
ASSESSMENT/CLINICAL MANIFESTATIONS
Chronic renal
failure (CRF) results in many multisystem manifestations
(Chart). Clinical manifestations of CRF or uremia are associated with changes
in fluid volume and chemical composition. The specific causes of many
of these manifestations are not known.
NEUROLOGIC
MANIFESTATIONS. Neurologic manifestations of the uremic syndrome of CRF are numerous (see Chart) and vary widely, depending on nitrogenous waste products, acid-base imbalances, and electrolyte imbalances. The nurse observes for neurologic signs,
ranging from lethargy to seizures or coma, indicating uremic encephalopathy. In addition, the
nurse assesses for sensory changes that generally appear in a glove and stocking distribution over the lower extremities and examines for weakness in the upper or lower extremities (i.e., uremic neuropathy).
If untreated, uremic encephalopathy progresses to seizures and coma. Dialysis is the treatment of choice for neurologicdisturbances associated with CRF. The manifestations of uremic encephalopathy resolve with the initiation of
dialysis. However, improvement in uremic neuropathy is limited if the neuropathy is severe and motor function is already impaired.
CARDIOVASCULAR MANIFESTATIONS. The clinical manifestations of CRF and
uremia lead to specific cardiovascular
abnormalities of fluid volume excess, hypertension, congestive heart failure
(CHF), uremic pericarditis,
and cardiac dysrhythmiasassociated with hyperkalemia. The nurse assesses for signs of a diminished ability to excrete salt and water. The resulting circulatory fluid overload, if untreated, can lead to CHF, pulmonary edema, peripheral edema, and hypertension.
The nurse
assesses heart rate and rhythm, listening for extra
beats (particularly an S3), irregular patterns, or a pericardial friction rub. Unless a hemodialysis (HD) vascular access has been previously created, blood pressure is measured in each arm. The nurse assesses the jugular veins for distention and assesses for the presence of pedal, pretibial, presacral, and peri-orbital edema.
Shortness of breath with exertion and paroxysmal nocturnal dyspnea (PND)
suggest fluid volume excess.
RESPIRATORY MANIFESTATIONS. Respiratory manifestations of CRF vary widely among clients (e.g., breath that smells like urine [uremic fetor or uremic halitosis], deep sighing, yawning, shortness of
breath). The nurse notes the rhythm, rate, and depth of breathing. Tachypnea (increased
rate of breathing) and hyperpnea (increased
depth of breathing) are respiratory compensation mechanisms for worsening
metabolic acidosis.
With severe
metabolic acidosis, the nurse may observe extreme hyperventilation or Kussmaul respiration. A few clients have hilarpneumonitis,
or uremic lung. In these clients, the nurse
assesses for thick sputum, minimal coughing, an increased respiratory rate, and an elevated temperature. A pleu-ral friction rub may be heard with a
stethoscope. Clients often have pleuritic pain
with breathing. The nurse auscultates the
lungs for crackles, which indicate fluid volume overload.
HEMATOLOGIC
MANIFESTATIONS. Hematologic abnormalities include anemia and abnormal bleeding.
The nurse notes indicators of anemia, including fatigue, pallor, lethargy, weakness, shortness of breath, and dizziness. The presence of abnormal bleeding is assessed by observing for bruising, petechiae, purpura, ecchymoses (confluent braises), mucous membrane
bleeding in the nose or gums, abnormal vaginal bleeding, or gastrointestinal
(GI) bleeding (often demonstrated
by black tarry stools [melena]).
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GASTROINTESTINAL MANIFESTATIONS. The nurse assesses for a foul odor to the breath, mouth ulceration, or mouth inflammation and notes any vomiting. Abdominal pain or cramping may be associated with uremic colitis. Stools may test positive for blood.
URINARY
MANIFESTATIONS. The
urinary findings in renal failure reflect the kidneys' decreasing
functioning. At first, changes occur in the amount, frequency, and appearance
of the urine. Many etiologic features of chronic renal disease result inproteinuria;
some cause hematuria.
The quantity
and composition of the urine change as renal function deteriorates. With the
onset of end-stage renal disease (ESRD), the urine may become more dilute and clearer,
reflecting a diminished glomerular filtration
rate (GFR). The nurse must be aware that the actual urine output in a client with CRF varies with the amount of remaining
renal function. The client with ESRD usually hasoligu-ria,
but some clients will remain relatively nonoliguric, producing
INTEGUMENTARY MANIFESTATIONS. There are several dermatologic manifestations of CRF. In clients with uremia, deposition of urochrome pigment
in the skin results in a yellowish coloration. Some African Americans report a darkening of the skin. The anemia of CRF causes a sallowness to the quality of the color, which some people describe as a faded suntan. This is most noticeable in lighter-skinned clients.
Skin oils and turgor are decreased in clients with uremia.
One of the most uncomfortable problems of uremia is severe pruritus(itching). The nurse also assesses
for bruises (ecchymoses), purple patches (purpura), and occasionally, drug-induced rashes.
Uremic frost, a layer of urea crystals
from evaporated perspiration, may appear on the face, eyebrows, axilla, and
groin in clients with advanced uremic syndrome.
PSYCHOSOCIAL ASSESSMENT
CRF and its treatment disrupt more
aspects of a client's life than almost any other illness. Nurses are in a
unique position to
evaluate the client with newly diagnosed renal failure and to assist with these
adjustments.
Psychosocial assessment and
support are part of the nurse's
role from the time that CRF is first diagnosed. Initially, the nurse asks about the client's understanding of the diagnosis and its implications
for treatment regimens (e.g., diet, medication, and dialysis). The nurse
assesses for any signs of anxiety and for the coping mechanisms
used by the client or family members. Some of the psychosocial aspects altered by CRF include family relations, social activity, work patterns, body image, and sexual activity. Thechronicity of ESRD, the variety of treatment options, and the
uncertainties surrounding the course of the disease and its treatment necessitate an ongoing psychosocial assessment.
LABORATORY ASSESSMENT
CRF results in
serious abnormalities in many laboratory values (see Chart). The following blood values are routinelymonitored in clients with CRF: creatinine,
blood urea nitrogen (BUN), sodium, potassium, calcium, phosphate,
bicarbonate, hemoglobin, and hematocrit.
Initially, a
urinalysis is performed, and a 24-hour urine specimen for creatinine and
urea clearance is obtained. In the early stages of renal insufficiency, urinalysis can
reveal key indicators of kidney function. Urinalysis may show excessive protein, glucose, red blood cells (RBCs), white
blood cells (WBCs), and decreased or
fixed specific gravity. Urine osmo-lality is usually decreased. A 24-hourcreatinine clearance
is calculated after serum and urinary creatinine levels
are collected and quantified. These data, along with information on body weight and height, are used to calculate renal creatinine clearance. As renal failure progresses, the urine output may decrease dramatically.
Trends in
renal function and progressive deterioration are typically monitored by
measurements of the serum creatinine and
BUN levels. Serum creatinine levels
may increase gradually over a period of years, reaching levels of 15 to 30 mg/dL or
more, depending on the client's muscle mass. Urea nitrogen levels are directly related to dietary protein intake. Without
dietary protein restriction, BUN levels are typically 10 to 20 times the value of the serum creatinine level.
As dietary protein is increasingly restricted in an attempt
to slow the rate of
progression of renal failure, BUN levels remain elevated but
less than the 10:1 to 20:1 ratio of nonprotein-restricted clients. Other factors affect the
level of BUN, and the nurse must consider these for a complete assessment.
Chapter 69 describes the factors influencing BUN levels, as well as the interpretation of serum creatinine and creatinine clearance.
RADIOGRAPHIC
ASSESSMENT
X-ray findings in clients with CRF
are few. Bone radiographs of the metacarpals and phalanges of the hand
can reveal the presence of renal osteodystrophy. With established ESRD,
the kidneys are atrophic and may be 8 to
CRITICAL THINKING CHALLENGEYou are gathering the initial history for a 67-year-old African-American client admitted to your unit with suspected CRF. The client tells you that he has a history of diabetes, gout, and
peptic ulcer disease. He also states that he has noted a 7-pound weight gain over the last 4 weeks.
• What other questions should you ask this client regarding his symptoms?
• What risk factors for the development of CRF are noted in his past medical
history?
• What cardiac and respiratory manifestations may you findon physical examination of this client?
Analysis
The client
with chronic renal failure (CRF) has usually experienced a progressive degeneration of renal function and is often hospitalized for evaluation and modification of the treatment plan. The focus of care is to control or manage symptoms and prevent complications.
COMMON NURSING
DIAGNOSES AND COLLABORATIVE PROBLEMS
The
following are priority nursing diagnoses for clients with CRF:
1. Imbalanced Nutrition: Less Than Body Requirements related to nausea
and vomiting, decreased appetite, effects
of a catabolic state, decreased level of consciousness, altered taste
sensations, or dietary restrictions
2. Excess Fluid Volume related to compromised regulatory mechanisms
(inability of the kidneys to maintain body fluid balance)
3. Decreased Cardiac Output related to reduction in stroke volume as a result
of electrical malfunction (dysrhythmias) and mechanical
malfunction (increased preload [volume excess] and increased afterload [increased peripheral vascular
resistance])
4. Risk for Infection related to inadequate primary defenses
(broken skin), chronic disease, or malnutrition
5. Risk for Injury related to internal biochemical risk
factors associated with renal failure (increased
susceptibility to bleeding, falls, and pathologic fractures) and
external risk factors, such as drugs
6. Fatigue related to altered metabolic energy
production, imbalance between oxygen supply and demand, and anemia
7. Anxiety related to threat to or change in health status, socioeconomic status, relationships, role functioning,
support systems, or self-concept; situational
crisis; threat of death; lack of knowledge (procedures, diagnostic
tests, disease process, renal replacement therapy); loss of control; feelings of failure; or disrupted family life
8. The primary collaborative problem is Potential for Pulmonary Edema.
ADDITIONAL NURSING
DIAGNOSES AND COLLABORATIVE PROBLEMS
In addition
to the common nursing diagnoses and collaborative problems, clients with CRF may have one or more of thefollowing:
· Diarrhea related
to chemical or electrolyte imbalances, ear, anxiety, or side effects of medications
· Impaired
Oral Mucous Membrane related to parotid gland changes, limited fluid intake, malnutrition, and elevated levels ofuremic toxins
· Impaired Skin Integrity related to altered chemical balance and uremic toxins
· Social Isolation related to illness or alterations in physical
appearance
· Interrupted Family Processes related to situational crisis, educed
income, unemployment, or effects of chronicillness
· Sexual Dysfunction related to altered body function (decreased libido
and/or impotence) from disease and/or effects of
medications, depression, or disturbance in self-esteem or body image
· Disturbed Thought Processes related to irritation, centralnervous system
(CNS) depression, side effects of medications,
sleep deprivation, or clinical depression
· Deficient Knowledge (disease process, care regimen,and follow-up care)
related to lack of informational resources and magnitude of the care issues
· Potential for Sepsis
· Potential for Malnutrition
· Potential for
Electrolyte Imbalances
· Potential for Metabolic Acidosis
· Potential for
Gastrointestinal (GI) Bleeding
Planning and Implementation
The Concept
Map on p. 1683 addresses assessment and nursing care issues
related to clients who have renal failure that has progressed to end-stage
renal disease (ESRD).
IMBALANCED NUTRITION: LESS THAN BODY REQUIREMENTS
PLANNING: EXPECTED OUTCOMES. The client with
CRF is expected to attain and maintain the following:
• Adequate nutritional status
• Ideal
body weight for age, height, and body build
• Laboratory values within safe levels
INTERVENTIONS.
The nutritional requirements and
dietary restrictions for the client with renal failure vary according to the degree of decrease in renal function and the type of dialysis performed, if any (Table).
NUTRITION THERAPY. The purpose of nutrition therapy is the administration of food and fluids to support the metabolicprocesses of a client who is malnourished or at high risk of becoming malnourished. Clients begun on hemodialysis (HD) have an increase in catabolism and subsequent decrease
in intake that often results in a loss of lean body mass. NIC interventions for nutrition therapy are summarized in Chart.
The client is referred to a
registered dietitian for dietary teaching and planning. The nurse in collaboration with the dietitian instructs
the client about alterations in the diet that are necessary as a result of CRF.
Dietary alterations include control of protein
intake; limitation of fluid intake; restriction of potassium, sodium, and phosphorus intake; administration of appropriate vitamin and mineral supplements; and provision of adequate
calories to meet metabolic demand.
If adequate
calories are not supplied, the body will use tissue protein for energy, which leads to a negative nitrogen balance and malnutrition. The dietitian assists in determining the number
of calories and types of nutrients needed to meet nutritional requirements.
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PROTEIN RESTRICTION. There is some evidence to suggest that early implementation of a protein-restricted diet prevents some of the symptoms associated with CRF and may preserve kidney function. Dietary protein is restricted on the basis of the degree of renal
insufficiency and the severity of the symptoms in accordance with the belief that
the accumulation of waste products
from protein metabolism is the priàãó cause of
uremia. However, recently the value of a low-protein diet has been debated.
Malnutrition is often seen in clients undergoing maintenance HD, and at least
one study suggests that a low-protein diet may not be necessary
in renal failure. Some studies indicate that a prescription of
In clinical
practice the glomerular filtration rate (GFR) is often used as an indicator of renal function and can be a guide to safe levels of protein consumption. A client with a severely reduced GFR who is not undergoing dialysis is usually permitted 0.55 to
The client receiving dialysis
requires more protein because of protein loss through dialysis. HD clients have
their protein requirements individually tailored according to their postdial-ysis,
or "dry," weight. Typically, HD clients are allowed protein in the amount of 1 to 1.5 g/kg/day; peritoneal dialysis (PD) clients are
allowed 1.2 to 1.5 g/kg/day because protein is lost with each exchange (Levine). Three fourths
of the protein should be
of high biologic value, such as milk, meat, or eggs. If protein intake is inadequate, a
negative nitrogen balance develops and causes muscle wasting. Serum albumin
and blood urea nitrogen (BUN) levels are used to monitor the adequacy of
protein intake. Decreases in serum albumin levels indicate inadequate protein intake
and malnutrition. Excessive protein
intake can dramatically increase BUN levels in clients with renal failure.
SODIUM RESTRICTION. The nurse monitors fluid and sodium intake. In
clients with little or no urine output, fluid and sodium retention can cause edema,
hypertension, and congestive heart failure (CHF). Most clients with
renal failure retain sodium; a few cannot conserve sodium.
The client's
status in terms of fluid and sodium retention can be estimated by monitoring body weight and blood pressure. Innondialyzed uremic clients, sodium is limited to 1 to
POTASSIUM RESTRICTION. The nurse monitors
potassium intake because hyperkalemia can cause dangerous cardiacdysrhythmias. Cardiac rhythm is monitored for the tall, peaked T waves characteristic of hyperkalemia;
the serum potassium level is also documented. The client with advanced CRF is
instructed to limit potassium intake to 60 to 70 mEq/day. The labels of seasoning agents are carefully inspected for sodium and
potassium content. Clients are instructed to avoid salt substitute agents, many of which are composed of potassium chloride, if oliguria is present. Clients receiving PD or
who are producing urine may not need dietary potassium restrictions.
PHOSPHORUS RESTRICTION. Control of phosphate
levels is begun early in renal failure to avoid osteodystrophy.
The nurse monitors serum phosphate levels, and the physician may order dietary
phosphorus restrictions and medications to assist with phosphate control. Phosphate binders must be taken at mealtime. Most clients with kidney disease already restrict their
protein intake, and because high-protein foods are high in phosphorus, their phosphorus consumption is also reduced.
Chapter 11 lists foods high in potassium, sodium, and phosphorus.
VITAMIN SUPPLEMENTATION. Most clients with
renal failure require daily vitamin and mineral supplementation. Low-protein diets are usually deficient in vitamins, and water-soluble vitamins are removed from the blood during dialysis. In addition, anemia is a chronic problem in clients with renal failure
because of the limited iron content of low-protein diets and decreased
erythropoietin production by the kidneys. Thus
supplemental iron is needed. Calcium and vitamin D supplements
may also be required, depending on the client's serum levels and bone status.
INDIVIDUAUZATION OF THE DIET. Clients undergoing PD
require a slightly different diet from those undergoing HD. Because protein is lost with the dialysate in
PD, a major nutritional problem for these clients is replacing
lost protein. In many
cases, 1.2 to
The nurse plays a vital role in
managing the client's diet. In collaboration with the dietitian, the nurse
provides teaching and performs ongoing assessments of the client's comprehension
of and compliance with dietary regimens. Written examples of the prescribed
diet can be given to the client and family. The nurse and dietitian can help clients adapt the diet to their
budget, ethnic background, and food preferences to maximize caloric intake within
the diet's restrictions.
EXCESS FLUID VOLUME
PLANNING: EXPECTED
OUTCOMES. The
client with chronic renal
failure (CRF) is expected to:
• Achieve
and maintain an acceptable fluid balance
• Minimize the risk of complications from fluid imbalances
INTERVENTIONS.
Management of the client with CRF
includes drug therapy, diet therapy, fluid restriction, and dialysis. Diet therapy is discussed under Imbalanced
Nutrition: Less Than Body Requirements.
FLUID MANAGEMENT. The purpose of fluid management is the promotion of fluid balance and the
prevention of complications resulting from
abnormal or undesired fluid levels. The nurse
monitors the client's intake and output and hydration status. In addition, the
nurse assesses for signs and symptoms
indicative of fluid volume excess, such as
crackles in the bases of the lungs, edema, and distended neck veins.
DRUG THERAPY. Diuretics are prescribed for clients with renal insufficiency when needed for treatment of fluid retention or to help control blood pressure. The diuresis produced from these drugs is useful
in treating fluid overload in clients who still have some urine output. Diuretics are seldom used in clients
with end-stage renal disease (ESRD) after dialysis has been initiated because, as kidney
function diminishes, these drugs
can have harmful side effects, including nephrotoxic and ototoxic effects.
The nurse uses
daily weight measurements and intake and output records as important sources of
assessment data. Daily weight gain generally indicates fluid retention rather
than true body weight gain. The nurse estimates the amount of fluid retained:
FLUID
RESTRICTION. The amount of fluid restriction ordered
is discussed under Sodium Restriction, p. 1684. The nurse
considers all forms of intake, including oral, intravenous, and fluid or medication administration
through gastrointestinal (GI) tubes, when calculating fluid intake. The nurse
assists the client in distributing fluid intake by mouth over a 24-hour period.
The client's response to fluid restriction is monitored, and the health care
provider is notified if signs and symptoms of fluid volume excess persist
or worsen.
DECREASED
CARDIAC OUTPUT
PLANNING: EXPECTED OUTCOMES. The client with
CRF is expected to attain and maintain normal sinus rhythm,
adequate cardiac output, and blood pressure in expected ranges.
INTERVENTIONS. Many clients with long-standing hypertension have
renal insufficiency, and some progress to CRF and ESRD. Therefore the control of
hypertension is an essential factor in preserving renal function. To control hypertension,
the physician may order calcium channel block-ers, angiotensin-converting
enzyme (ACE) inhibitors, alpha-adrenergic and
beta-adrenergic blockers, and vasodilators. Recent studies have documented the effectiveness of ACE inhibitors, as compared with otherantihypertensives,
in slowing the progression of renal failure (Levine, 1997). More inforation on the
specific medications can be found in Chapter 36. Indications vary, depending on the client, and
these drags are used carefully to avoid hyperkalemia and hypotension. Various combinations and doses
may be tried until blood pressure control is adequate and side effects are
minimized. Calcium channel blockers seem to improve the GFR and renal blood flow.
The client and
family or significant others are instructed to measure blood pressure. The
nurse evaluates the client's ability to measure and record blood pressure
accurately using the client's own equipment. The nurse periodically
rechecks measurement accuracy. In addition to accurate measurement of blood
pressure, the client and family must understand the relationship of
blood pressure control and regulation to diet and medication therapy. The nurse further
instructs the client to measure weight daily and to bring records of
blood pressure measurements and
weights for discussion with the physician,
nurse, or dietitian.
The nurse
assesses and monitors, on an ongoing basis, for signs and symptoms of decreased cardiac output, heart failure, congestive heart failure (CHF), and dysrhythmias.
These topics are
discussed in Chapters.
RISK FOR INFECTION
PLANNING: EXPECTED OUTCOMES. The client with CRF
is expected to remain free of infection.
INTERVENTIONS. The nurse or assistive nursing personnel provides
meticulous care to any areas where skin integrity has been broken (incisions, site of drains, puncture sites, cracked or excoriated skin, pressure sores) and provides good
basic preventive skin care. For clients undergoing dialysis,
the nurse also inspects the vascular access site or PD catheter
insertion site. These areas are assessed on an ongoing basis for redness, swelling, pain, and drainage. Vital signs are monitored for any signs or
symptoms of infection.
RISK FOB INJURY
PLANNING:
EXPECTED OUTCOMES. The client with chronic renal failure (CRF) is expected to remain free of injury (will not fall or experience injury from a fall and will not experience pathologic fractures, bleeding, or toxic effects of medications
administered in the presence of CRF).
INTERVENTIONS. Managing drag therapy
in clients with CRF is a complex and ongoing clinical problem.
Many over-the-counter drags contain ingredients that may affect renal function. Therefore it is important to obtain a detailed drag history. The nurse must be aware of the use of each drag,
its side effects, and the site of metabolism. The nurse, in conjunction with
the physician and pharmacist, monitors the client closely for drag-related complications and adjusts dosages accordingly.
Certain
medications must be avoided, and the dosages of others must be adjusted
according to the degree of remaining renal
function. As the client's renal function decreases,
repeated dosage adjustments are necessary.
The nurse assesses for side effects and signs of drug toxicity and
notifies the physician as appropriate.
A number of medications are
routinely administered to clients with renal failure. The nurse giving these medications
understands the rationale for administration and the nursing interventions for each drag. Many
clients have some degree of cardiac disease and may
require cardiotonic drags, such as digoxin.
Clients with decreased renal function are particularly susceptible to digoxin toxicity because the drug is excreted by the kidneys. The
nurse caring for clients
with CRF who are receiving any digitalis derivative, including digoxin,
monitors for signs of toxicity, such as nausea, vomiting, anorexia, visual disturbances, restlessness, headache,
fatigue, confusion, cardiac irregularities (particularly bradycardia [pulse rate, 50 to 60 beats/min] and
tachycardia [pulse rate, 100 beats/min]),
and serum drag levels above therapeutic range. In addition, serum
levels of potassium are monitored
closely in any client receiving cardiotonic medications.
Drags to
control an excessively high phosphate level include phosphate-binding
compounds. Calcium acetate, calcium
carbonate, and aluminum hydroxide are used as phosphate-binding agents in
clients with renal failure. These drags treat the metabolic complications that
if untreated may lead to renal osteodystrophy and
related injuries. To prevent further
complications, the nurse stresses the importance of these
and all medications.
Hypercalcemia (excessively high serum calcium levels) is a possible complication for clients taking calcium-containing compounds to control
phosphate excess. Hypophosphatemia (low serum phosphoras levels)
is also a possible outcome of phosphate binding but is typically also associated
with phosphate depletion in clients who are not eating adequately but are
continuing to take phosphate-binding medications. In clients taking aluminum-based
phosphate binders for prolonged periods,
retention and deposition of aluminum may cause bone disease or neurologic manifestations that may not be reversible. The nurse monitors the client for evidence of muscle weakness, anorexia,
malaise, tremors, or bone pain.
Clients with
renal disease should avoid antacid compounds containing magnesium. Clients with renal failure
cannot excrete magnesium and thus should avoid additional intake.
In addition
to the drugs used to treat renal failure, the use of other medications requires
special consideration. These medications include antibiotics, opioids, antihypertensives,
diuretics, insulin, and heparin.
Many
antibiotics are safe for clients with renal failure, but those excreted
primarily by the kidneys require dose modification. To prevent complications of bloodstream infections from oral cavity bacteria, prophylactic antibiotic treatment is routinely given to clients with CRF before any dental procedures. The
antibiotic and protocol used vary with the client's needs and the
physician's preference.
The nurse
administers opioid analgesics cautiously in clients with renal failure because the effects often last much longer than in people with healthy kidneys. Clients with uremia are
particularly sensitive to the respiratory depressant effects of these drags. Because opioids are metabolized by the liver and not the kidneys, the dose recommendations are often the same regardless of the level of renal function. The nurse monitors these clients closely after opioid administration
and evaluates the need
for additional administration on the basis of the client's reaction to the drag.
As renal
disease progresses, the client with diabetes melli-tus often requires modification of
an insulin or oral antidia-betic drag dose because of decreased
insulin metabolism by ailing kidneys. Frequent blood glucose determinations
are obtained to evaluate
the client's insulin or oral agent needs. Urine glucose measurements are less accurate when
renal disease is present.
Because of poor
platelet function and capillary fragility in renal failure, heparin and other anticoagulants are used cautiously.
FATIGUE
HI PLANNING: EXPECTED OUTCOMES. The client with chronic renal failure (CRF) is expected to
conserve energy by balancing activity and
rest in order to be able to perform self-care and
activities of daily living.
INTERVENTIONS. All clients with renal dysfunction are given some type of vitamin and mineral supplement. Because of diet restrictions and vitamin losses
associated with both peritoneal dialysis (PD) and hemodialysis (HD), water-soluble vitamins
must be replaced. The nurse avoids giving the client these vitamin supplements before HD
treatment because they will be dialyzed out of the body and the client will receive no benefit.
The anemic
client with CRF is treated with recombinant erythropoietin (erythropoietin alfa [Epogen, Procrit]). The goal of
erythropoietin therapy is to achieve a hematocrit of 30%
to 35%. For erythropoietin to stimulate bone marrow to produce red blood cells (RBCs), clients must
have adequate iron stores. In addition, chronic administration
of erythropoietin can deplete iron
stores, necessitating iron supplementation.
Many who receive epoetin alfa report
improved appetite and sexual function along with decreased fatigue;
in some clients, hypertension associated with a rise in hematocrit has been
reported. The improved appetite may challenge clients in
their attempts to maintain dietary protein, potassium, and fluid restrictions and
necessitates additional education.
ANXIETY
PLANNING: EXPECTED OUTCOMES. The client with CRF
is expected to eliminate or reduce feelings of apprehension and tension from an unidentified source as evidenced by:
Seeking
information to reduce anxiety
• Using effective coping strategies
• Reporting an absence of physical manifestations of nxiety
INTERVENTIONS. The nurse has the most frequent contact with the client with CRF when the client is
hospitalized or undergoing in-center
dialysis treatments. Thus nurses perform an ongoing assessment of the client's
anxiety level to determine the level of nursing intervention required. The nurse observes the client's behavior for physical cues indicating
anxiety (e.g., an anxious facial expression or gestures and an increased pulse rate). In addition, the nurse evaluates the support
systems, as evidenced by the involvement of family and friends with
the client's care.
Unfamiliar
settings and situations, and lack of knowledge about treatments
and tests can increase the client's anxiety level. The nurse explains all procedures, tests,
and treatments. The client's knowledge deficits concerning normal renal function and renal failure are identified. Evaluating
the client's current knowledge avoids needless repetition
during teaching sessions. The nurse provides instruction
appropriate to the client's needs and ability to understand. By
explaining the disease process, the nurse enhances the client's
acceptance and decreases anxiety.
The nurse
provides continuity of care, whenever possible, to establish a consistent
nurse-client relationship to decrease anxiety
and promote discussions of client and family concerns. As the nurse-client relationship develops, the client is encouraged to discuss current problems or concerns. A multi-disciplinary
team of professionals participates to provide support and counseling for the client and family,
often over many years of treatment.
The nurse
encourages the client to ask questions and discuss fears about
the diagnosis of renal failure. An open atmosphere
that allows for discussion can decrease anxiety level. Nurses also facilitate discussions with family members or
significant others concerning the prognosis and the potential impact on
the client's lifestyle.
POTENTIAL FOR PULMONARY EDEMA
PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to remain free of pulmonary edema. A secondary outcome is to maintain optimal fluid volume balance through dialysis and pharmacologic measures, thus preventing the onset of pulmonary edema.
INTERVENTIONS. In the client with CRF, pulmonary edema can result from either of two distinct
mechanisms: left-sided heart failure or microvascular injury. In left-sided heart failure,
the heart is unable to adequately eject blood from the left ventricle,
leading to an increase in hydrostatic pressure. The
increased pressure allows fluid to cross the capillaries into the pulmonary interstitium. Pulmonary edema can also occur from injury to the vascular endothelium or alveolar epithelial
cells secondary to uremia. Fluids then leak into the interstitial space and ultimately into the alveoli.
The nurse assesses the client for
early signs of pulmonary edema, such as restlessness, heightened anxiety,
tachycardia, dyspnea, and crackles that begin at the base of the lungs. As pulmonary congestion worsens, the level of fluid in the lungs rises. Auscultation will reveal increased rales,
decreased air exchange,
and dullness to percussion at the upper limits of fluid
collection. The client may expectorate frothy, blood-tinged sputum. With
further cardiac and respiratory compromise, the client can become
diaphoretic and cyanotic.
The client who
develops pulmonary edema is often admitted to the intensive care unit for aggressive treatment, which includes
continuous cardiac monitoring. The client is placed in a high Fowler's position and given oxygen to maximize lung expansion and improve gas exchange. Drug therapy with renal failure and pulmonary edema is difficult at best because of the potential adverse effects of drugs on the kidneys. Treatment of pulmonary edema involves the administration of potent loop diuretics, such asfurosemide (Lasix). Furosemide dosing usually begins at 40 mg,
administered intravenously over a 1- to 2-minute period. This dose may be repeated in 30 minutes if no response is elicited. For clients already receiving
maintenance doses of furosemide, an IV dose equivalent to the oral maintenance dose is given; it is doubled in 30 minutes if no
response is seen (Johnson & Lalonde, 1997). Renalimpairment multiplies the risk of ototoxicity with
the use of furosemide;
thus IV doses are given cautiously.
Morphine
sulfate 1 to 2 mg administered intravenously is usually prescribed to reduce
myocardial oxygen demand by reducing ventricular preload and to provide vasodilation and sedation. The dose is adjusted to achieve the desired
response, but the potential for respiratory depression exists.
Therefore the nurse monitors the client's respiratory rate and blood pressure
closely. To further decrease hydrostatic pressure, a continuous infusion pump
may administer a vasodilator, such as nitroglycerin. Vital signs are monitored
vigilantly, since these drugs in combination may result in severe hypotension.
Nursing
interventions include Foley catheter placement and frequent assessment of urine
output to gauge the effectiveness of diuretic therapy. Diuresis usually
begins within 5 minutes of administration of IV furosemide. Urine output is measured every 15 to 30 minutes during the acute episode and every hour
thereafter until the client is stabilized. In addition, the nurse assesses breath and heart sounds for improvement in
crackles and for the presence of an S3, indicating fluid
overload.
The nurse
monitors serum chemistry results for electrolyte imbalances and reports abnormalities to the appropriate health care provider so that correction of imbalances can be initiated.
Continuous cardiac monitoring is initiated to identify potentialdysrhythmias. Oxygen saturation levels are monitored by pulse oximetry and arterial blood gas values. The
oxygen delivery system is adjusted to maintain adequate oxygen saturation levels. The nurse monitors the client for deterioration,
manifested as increasing pulmonary congestion and hypoxemia. It may be necessary to intubate the client and mechanically ventilate the lungs at this point to prevent death.
Clients with
CRF are at increased risk for developing pulmonary
edema, since they may present with precipitating fluid volume overload and existing cardiac compromise secondary to hypertension and volume overload. Such
clients are less likely to respond quickly to treatment and are more likely to
develop adverse effects from pharmacologic agents as a result of renal
impairment. Occasionally, ultrafiltration may
be used to further reduce fluid volume.
Renal Replacement Therapies
Renal
replacement therapy is required only when the clinical and laboratory
manifestations of renal failure present complications that are potentially life threatening or that pose continuing discomfort to the client. When the client can
no longer be managed with conservative therapies, such as diet, medication, and
fluid restriction, dialysis is indicated. Transplantation may be discussed at any time.
HEMODiALYSiS
Hemodialysis (HD) is one of several renal replacement therapies used for the treatment of renal failure (Table 72-9). Dialysis removes excess fluids and waste products and restores chemical and electrolyte balance. HD involves the
extracorporeal (outside of the body) passage of the client's blood through a semipermeable membrane that serves as an
artificial kidney.
CLIENT SELECTION. Any client may be considered for HD therapy. Initiation of renal replacement therapy depends on the symptoms of the client, not on the creatinine clearance. Dialysis is initiated
immediately for clients who exhibit the following: fluid overload refractory to
diuretics, presence
of pericarditis,
uncontrolled hypertension, neurologic manifestations, and development of bleeding
diathesis. More commonly, dialysis is started when clients have
signs of symptom progression, such as nausea and vomiting,
decreased attention span, decreased
cognition, worsening anemia, and pruritus (Levine,
1997).
The duration
of survival after HD depends on the client's age, the cause of renal failure,
and the presence of other diseases, such as coronary artery disease,
hypertension, or diabetes. The following are general guideline requirements
for appropriate client selection:
· Presence
of fatal, irreversible renal failure when other therapies are unacceptable or ineffective
· Absence of illnesses that would prevent or seriously complicate HD
· Expectation of
rehabilitation
· The client's
acceptance of the regimen
DIALYSIS SETTINGS. Clients may
receive HD treatments in any of several
settings, depending on specific needs. They may be dialyzed in an acute care
(hospital-based) center if they have recently begun treatment or have complicating conditions that require close nursing or medical supervision. Stable
clients with chronic renal failure (CRF) may be he-modialyzed in a freestanding HD center in the community hen they no longer require
intensive supervision. Stable clients may participate in complete or partial
self-care in an outpatient center or with in-home HD.
In-home HD
offers the least disruptive form of therapy and allows for the most adaptation of the regimen to the client's lifestyle. Unfortunately, many clients cannot participate in in-home dialysis because they lack a reliable and
consistent partner to administer the therapy and manage the dialysis
machine. For some clients and partners,
the responsibilities of in-home dialysis are extremely stressful, so that
this option is less desirable. In addition, a water treatment
system must be installed in the home to provide a safe, clean
water supply for the dialysis process.
Regardless of
the setting for therapy, the client needs ongoing nursing support and intervention to maintain this complex and lifesaving treatment.
PROCEDURE. The principles of
HD are based on the passive transfer of toxins, which is accomplished by diffusion. Diffusionis the movement of molecules from an area of higher
concentration to an area of lower concentration. The rate
of diffusion is affected by numerous factors. Diffusion during dialysis occurs more rapidly when the membrane pores are large, there is a large surface area of membrane, the temperature of the solutions is higher, and there is a greater difference in the solute concentrations. Molecules that are too large,
such as RBCs and plasma proteins, cannot pass
through the membrane.
When HD is
initiated, blood and dialysate flow
in opposite directions from their respective sides of an enclosed semiper-meablemembrane. The dialysate is
a balanced mix of electrolytes and water
that closely resembles human plasma. On the other side of the membrane is the
client's blood, which contains metabolic waste products, excess water,
and excess electrolytes. During HD, the waste products move from the blood into the dialysate because
of the difference in their concentrations (diffusion). Excess water is also
removed from the blood into the dialysate (osmosis).
Electrolytes can move in either
direction, as needed, and take some fluid with them. Potassium and sodium
typically move out of the plasma into the dialysate, whereas bicarbonate and calcium move from the dialysate into the plasma. This process continues as the
blood and the dialysate are
circulated past the membrane for a presetlength of time. Water volume may be removed from the plasma by applying positive or negative pressure to the system.
The components of an HD system
include a dialyzer, dialysate, vascular access routes, and an HD machine. The artificial kidney,or dialyzer (Figure 72-3), has four components: a blood compartment, a dialysate compartment, a semi-permeable membrane, and an enclosed structure to
support the membrane.
Dialysate is made from clear
water and chemicals and is free of any metabolic waste products or drugs.
Because bacteria and other microorganisms are too large to pass through the
membrane, dialysate does not need to be sterile. The water
used in dialysate must meet specific standards, and
water treatment systems are used to ensure a safe water
supply. The dialysate composition may be altered according
to the client's needs for treatment of electrolyte imbalances. During HD, the dialysate is warmed to approximately 100° F (37.
8° C) to increase the efficiency of diffusion and to prevent a decrease in
blood temperature.
An essential function of an HD machine is the
monitoring for potential problems, including the following:
· Changes in dialysate temperature
· Presence of air in
the blood tubing
· A blood leak in
the dialysate compartment
· Changes in the pressure or composition within the blood and the dialysate compartments
If any of
these problems are detected, an alarm alerts the nurse. The monitoring systems protect the client from life-threatening
complications that can result if these technical problems
are not corrected.
All models of HD machines
function, in principle, as illustrated in Figure 72-4. Figure 72-5 shows one
type of machine. The duration and frequency of HD treatments depend on the amount of metabolic waste to be cleared, the clearance capacity of thedialyzer, and the amount of fluid to be removed. Most dialyzers provide sufficient clearance to limit the
total number of hours of dialysis to about 12 hours a week. This time is usually divided into
three 4-hour treatments a week. For clients with less muscle or more
ongoing urine production, two 5- to 6-hour treatments a week may be adequate. If the client gains large amounts of fluid weight, a longer treatment time may be needed to remove the fluid without hypotension or severe side effects.
ANTICOAGULATION. To prevent blood clots from forming within the dialyzer membrane
and the blood tubing, anticoagulation with heparin is necessary during HD
treatments. Heparin, a short-acting anticoagulant,
inhibits the tendency of blood to clot when it
comes in contact with foreign surfaces. There is considerable variability among clients intheir anticoagulation response and elimination of heparin.
The heparin dose must
be adjusted on the basis of each client's need. Clients receiving erythropoietin may need
more heparin. Heparin remains active in the body for 4 to 6
hours after administration, making the client at risk for
hemorrhage during and immediately after
HD treatments. The client must avoid any invasive procedures during that time.
Thus the nurse monitors closely for any signs of bleeding
or hemorrhage. Clotting tendencies can be monitored during HD with a
bedside machine (such as the Hemochron), by whole-blood clotting times (Lee-White clotting test), or by activated partial thromboplastin times (aPTT) during and
after HD. Protamine sulfate is given as an antidote
to neutralize heparin's anticoagulant
activity when necessary.
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VASCULAR
ACCESS. For hemodialysis (HD) to be performed, a vascular access route is required (Table 72-10). Dialysis
treatments necessitate the easy availability of a large amount of blood flow—at least 250 to 300 mL/min, usually
for a period of 3 to 4 hours. Normally, the body cannot provide this type of
circulatory access without surgical revision of blood vessels.
LONG-TERM VASCULAR ACCESS. An internal access is preferred for most clients undergoing long-term HD
(see Table 72-10). There are two common choices: an internal arte-riovenous (AV) fistula or an AV graft (Figure 72-6). AV fistulas are formed by connecting (anastomosis) an
artery to a vein. The most commonly used vessels are the radial or
brachial artery and the cephalic vein of the nondominant arm. This process increases the blood flow through the vein to 250 to 400 mL/min, the amount required for
dialysis to be effective.
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Some time is
necessary for an AV fistula to develop, and the amount of time required for the fistula to "mature"
varies. Primary AV fistulas may not be suitable for use for as long as 4 months.
Therefore vascular access must be planned accordingly. As the fistula matures,
the increased pressure of the arterial blood flow into
the vein causes the vessel walls to thicken. This thickening increases their strength and suitability for repeated cannulation.
To obtain
access to a fistula, the nurse cannulates it
or inserts two needles, one toward the venous blood
flow and one toward the arterial blood flow. This procedure allows the HD
machine to draw the blood out through the arterial needle and return it through
the venous needle. The client may require a temporary vascular access (AV shunt
or HD catheter) for HD treatments
until the fistula is ready for use.
AV grafts are used when the AV fistula does not develop or when complications of the AV fistula limit continued use. Thepolytetrafluoroethylene (PTFE) graft is a synthetic material (Gore-Tex). This type of graft is commonly used in older clients undergoing HD.
PRECAUTIONS. Several precautions must be observed to ensure the functioning of an
internal AV fistula or AV graft. First, the nurse assesses for adequate
circulation in the fistula or graft, as well as in the distal portion of the
extremity. The nurse then checks for a bruit or a thrill by auscultation or palpation
over the access site. Repeated compression can result in
the loss of the vascular access; therefore the nurse avoids taking the blood pressure in the arm with the vascular access unless absolutely necessary. The AV fistula or graft is not used for administration of IV fluids; venipuncture is
avoided anywhere in the arm used for HD access. Chart 72-9 lists best practices for care of the
client with an HD access.
COMPLICATIONS. Complications can occur regardless of the type of access. The most common problems
include thrombosis or stenosis, infection, aneurysm formation, ischemia, and
high-output heart failure.
Thrombosis, or
clotting, is the most frequent complication. Some clients are more susceptible to clotting than are
others and may be given anticoagulants. Surgical declotting or revision of stenotic areas is typically performed in the surgical
suite with the use of local anesthesia.
Most
infections that occur in clients undergoing long-term HD involve the vascular
access. The most common organism causing infection is Staphylococcus aureus, which can be introduced by punctures for dialysis access. The nurse
limits the incidence of infections by using careful sterile
technique before needle cannulation (Table
72-11).
Aneurysms can
form in any internal fistula and are caused by repeated needle punctures at the
same site. Aneurysms that appear to be increasing in size may cause loss of the
fistula's function and require surgical repair.
Ischemia
occurs in a few clients with vascular access when the formation of the fistula causes a decrease in arterial blood flow to areas distal to the fistula. Ischemic symptoms (steal syndrome) vary from cold or numb fingers to gangrene. If the collateral
circulation is inadequate, the existing fistula may need
to be ligated and a new fistula created in another
area for circulation to be preserved in the extremity.
The shunting
of blood directly from the arterial system to the venous system, through the fistula, can cause high-output heart failure in
clients with a limited cardiac reserve (see Chapter 35). This complication
occurs rarely, but if it does, the fistula may need to be revised to decrease the
blood flow from the arterial supply.
TEMPORARY
VASCULAR ACCESS. The first type of vascular
access developed was the external arteriovenous (AV) shunt(Figure 72-7; see also Table 72-10), but it is rarely
used today. To create a shunt, the
surgeon places a piece of sil-icone rubber (Silastic) tubing into an artery and a
second piece into an adjacent vein. The tubings are connected
externally to provide a readily available vascular access. The arterial limb is used to obtain the blood for passage
through the artificial kidney (dialyzer membrane), and the venous limb is used to return the blood to the client's body after each pass through
the dialyzer.
Temporary
vascular access with special catheters has replaced the use of the AV shunt for most clients requiring immediate HD. A catheter designed for HD may be inserted into the subclavian,
internal jugular, or femoral vein if no permanent vascular access is available for use (see Dialysis Therapies, pp. 1674 and 1675). The lumens of these devices are considerably smaller
than the permanent accesses, and the duration of each dialysis session is increased (usually requires 4 to 8 hours).
POSTDIALYSIS
NURSING CARE. The
nurse closely monitors the client immediately after dialysis and
for several hours afterward for any side effects from the
treatment. The more common
clinical manifestations of complications include
hypotension, headache, nausea, malaise, vomiting, dizziness, and muscle cramps.
The nurse obtains vital signs
and weight for comparison with predialysis measurements. Blood pressure and
weight are expected to be reduced as a result of fluid removal. Excessive
hypotension may require rehydration with
IV fluids, such as normal saline. The client's temperature may also be elevated,
because the dialysis machine warms the blood slightly. If the temperature is elevated excessively,
sepsis is suspected and a blood sample is obtained, as ordered, for culture and sensitivity determinations.
The heparinization required for hemodialysis (HD) increases the clotting time and thus the risk for excessive bleeding. All invasive procedures must therefore
be avoided for 4 to 6 hours after dialysis, and the nurse continually
monitors the client
for signs ofhemorrhage during dialysis and for 1 hour after
dialysis (Chart
72-10).
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COMPLICATIONS. A variety of fluid-related and infectious
complications can occur from HD. The most common
complications include disequilibrium syndrome and acquisition of viral
infections.
Dialysis disequilibrium syndrome may develop during HD or
after HD has been completed. The cause is unknown but may
be due to the rapid decrease in blood urea nitrogen (BUN) levels during HD. These changes in urea levels can cause cerebral edema, which leads
to increased intracranial pressure. Neurologic complications
can result (headache, nausea, vomiting, restlessness, decreased level of
consciousness, seizures, coma, or
death).
Early
recognition by the nurse of the signs of the syndrome and appropriate treatment
with anticonvulsant medications andbarbiturates
may prevent a life-threatening situation. Dialysis disequilibrium syndrome may be avoided, or minimized, by introducing HD for short periods initially with low blood flows so that
rapid changes in plasma composition are avoided.
Infectious diseases transmitted by blood transfusion are another serious
complication associated with long-term HD. Two of the most serious blood-transmitted infections are hepatitis and human immunodeficiency virus (HIV).
Hepatitis infection in clients with chronic renal failure (CRF) has decreased in recent years, paralleling the
decrease in blood transfusion requirement for these clients because of the availability of erythropoietin therapy. Yet, because of the blood access and the risk of microscopic exposure, hepatitis continues to be a problem for clients undergoing HD. The hepatitis  virus can be transmitted through the use of contaminated needles or
instruments, by entry of contaminated blood through open wounds in the skin or
mucous membranes, or through transfusion of blood contaminated with the
virus.
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The incubation period for acute
hepatitis is 6 weeks to 6 months. Thus the nurse continually monitors the client undergoing HD
who is receiving frequent transfusions for signs of hepatitis virus infection
(see Chapter 59).
HIV is a bloodborne and body fluid-borne virus with some potential threat to clients undergoing HD. Fortunately, the risks
of HIV transmission are minimized by the consistent practice
of standard precautions (blood and body fluids), routine screening of donated
blood for HIV, and decreased numbers of blood transfusions for clients with
end-stage renal disease (ESRD).
Despite this progress, however, an unknown number
of clients may have already been infected with the HIV
virus. Clients who have been undergoing HD and who received frequent transfusions during the early to mid-1980s are at risk for acquired immunodeficiency syndrome (AIDS) (see also
Chapter).
PERITONEAL DIALYSIS
Peritoneal dialysis (PD) takes
place within the peritoneal cavity. PD is slower
than hemodialysis (HD), however, and more time is needed for
the same effect to be obtained.
CLIENT SELECTION. Most clients with chronic renal failure (CRF) can select either HD or PD. For clients who arehemodynamically unstable and for those who cannot tolerate systemic anticoagulation, PD is less hazardous than HD. The lack of vascular access due to inadequate vessels may
eliminate HD as an option. In addition, some clients with a new arteriovenous (AV) fistula receive PD while waiting for the access to mature for HD. PD is also often the treatment of
choice in the older adult and pediatric populations because it offers more flexibility if the client's status changes frequently.
In some relatively rare
situations, PD cannot be performed, usually because of peritoneal adhesions or
intra-abdominal surgery in the peritoneal cavity. In these cases, the peritoneal
membrane's surface area has been reduced too much to allow for adequate dialysis exchange. In other cases, peritoneal membrane fibrosis may occur after repeated infections, which decreases membrane permeability despite adequate surface area.
PROCEDURE. The surgical insertion of a siliconized rubber (Silastic) catheter into the abdominal cavity
is required to allow the infusion of dialyzing fluid (dialysate)
(Figure). According to the physician's order,
1 to
PROCESS. PD occurs through
diffusion and osmosis across the semipermeable peritoneal
membrane and adjacent capillaries. The peritoneal membrane is large and
porous. It allows solutes, which carry fluid with them, to move
by an osmotic gradient from an area of
higher concentration in the body (blood) to an area of lower concentration in the
dialyzing fluid.
The peritoneal cavity is rich in
capillaries and provides a ready access to the blood supply. The fluid and
waste products dialyzed from the client move through the blood vessel walls, the interstitial tissues, and the peritoneal membrane and are
removed when the dialyzing fluid is drained from the body.
The efficiency of PD can be affected by numerous situations,
such as changes in the peritoneal membrane's permeability caused by infection or irritation, and changes in the capillary blood flow resulting from vasoconstriction, vascular disease, or decreased perfusion of the
peritoneum. Excess water removal (ultrafiltration)
in HD is accomplished by
use of hydrostatic positive pressure ortransmembrane negative
pressure on the dialysis machine. In PD, the amount of water removed from the client depends on
the
concentration
of the dialysate.
Increasing the glucose concentration of the dialysate makes
the solution increasingly more hypertonic. The more hypertonic the solution, the greater the osmotic pressure for ultrafiltration and
thus the greater
the amount of fluid removed from the client during an exchange. The physician orders the dialysate concentration on the basis of the client's fluid status.
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MEDICATION ADDITIVES. Heparin may be added to the dialysate to prevent fibrin clot formation in
the catheter or
tubing; this intraperitoneal (IP) heparin administration is necessary
only after new catheter placement or with the occurrence of peritonitis. There is no systemic absorption of heparin with IP administration,
so clotting studies are not needed.
Other agents that may be
administered by the IP route include potassium chloride and antibiotics.
Commercially prepared dialysatedoes not contain potassium chloride. Some clients
will need potassium chloride added to the dialysate so that the dialysate does
not excessively deplete potassium from the plasma. Oral potassium supplements may be
prescribed in selected clients. The physician may order IP administration of antibiotics (e.g., gentamicin, vancomycin, cephalosporins) when
peritonitis is present or suspected. The combination of potassium chloride and antibiotics in the same bag of dialysate is not recommended, because chemical interactions may limit effectiveness.
TYPES
OF PERITONEAL DIALYSIS. Many types of PD are available, including continuous ambulatory PD, multiple-bag
continuous ambulatory PD, automated PD, intermittent PD, and continuous-cycle PD. The selection of the type depends on
the client's ability and lifestyle.
CONTINUOUS AMBULATORY PERITONEAL DIALYSIS.
In continuous ambulatory
peritoneal dialysis (CAPD), the client performs self-dialysis by infusing four 2-L exchanges of dialysateinto the peritoneal
cavity, where the dialysate remains for 4 to 8 hours, 7 days a week. During the dwell period, the client can choose a continuous connect system or a disconnect system.
With the continuous connect system (straight transfer set), the dialysate bag is usually attached to the
catheter by 48-inch (122-cm) tubing; the empty bag and tubing are folded and worn beneath the clothing until they are used for outflow. After
draining, the client removes the bag and connects a new bag to repeat the
process.
With the disconnect system (Y-transfer set), the client removes the connecting tubing and empty dialysate bag after inflow and attaches a
protective cap to the PD catheter junction. The disconnect system eliminates the need to wear the tubing and bag but
requires opening the system two extra times with each exchange. This opening of the system increases the potential for
contamination and infection.
With CAPD treatment, no machine is
necessary, and client
independence is encouraged. Theoretically, no partner is
required. However, many home training programs suggest that a partner be trained in
CAPD as a support for the client should illness or temporary disability occur.
Devices to assist in the safe, uncontaminated connection of the
tubing spike with the dialysate bag are increasingly in use. These devices
can be considered for clients with impaired vision, limited manual
dexterity, or decreased upper extremity strength. CAPD offers the advantage of constant removal of fluid and wastes and more nearly
resembles renal function than does HD. Some clients continue to perform their
own exchanges while hospitalized.
MULTIPLE-BAG
CONTINUOUS AMBULATORY PERITONEAL DIALYSIS. For those who are unable to perform self-CAPD in the acute care setting, a multiple-bag CAPD
(MB-CAPD) system allows continuation of CAPD. With
MB-CAPD, a manifold of tubing connected to the dialysate and
hanging on a portable pole is attached to the PD catheter by
connecting tubing (see Figure 72-8). The nurse inflows the dialysate at the prescribed time, allows the dwell,
and initiates the outflow for each exchange. The MB-CAPD system permits mobility for the ambulatory client
and provides for continuous PD.
AUTOMATED
PERITONEAL DIALYSIS. An automated cycling
machine that provides for dialysate inflow,
dwell, and outflow
according to preset times and volumes may be used. A warming chamber for dialysate is part of the machine.
Automated peritoneal dialysis (APD) may be used in the
acute care setting, the outpatient dialysis center, or the client's home. The
functions are performed in response to machine programming that can be
individualized for the client's specific needs. A typical prescription calls
for 30-minute exchanges (10/10/10 for inflow, dwell, and outflow) for a
period of 8 to 10 hours. The machines have numerous safety
monitors and alarms and are relatively simple to learn to use.
APD has several distinct
advantages. It permits the performance of in-home
dialysis while the client sleeps, allowing him or her to be dialysis free during waking hours. Also, because the number of connections and disconnections are fewer with APD, the incidence of peritonitis has been reduced.
Finally, APD provides a means by which increased volumes of dialysis solution
can be administered to clients who require higher clearances (Levine, 1997).
INTERMITTENT
PERITONEAL DIALYSIS. Intermittent peritoneal
dialysis (IPD) combines the principles of an osmotic pressure gradient and true dialysis. The client usually requires exchanges of
CONTINUOUS-CYCLE
PERITONEAL DIALYSIS. Continuous-cycle peritoneal dialysis (CCPD) also uses an
automated cycling machine. Exchanges occur at night while the client sleeps.
The final exchange of the night is left to dwell through the day and is drained the next evening as the process is
repeated. CCPD offers the advantage of 24-hour dialysis, as in CAPD, but the
sterile catheter system is less often violated.
COMPLICATIONS. Complications are
possible with PD, but many can be treated or prevented with careful nursing
care.
PERITONITIS. The major complication of PD is peritonitis. The most common cause of peritonitis is contamination of the connection site during an exchange. This
infection of the peritoneum is manifested by cloudy dialysate outflow (effluent), fever, rebound abdominal tenderness,
abdominal pain, general malaise, nausea, and vomiting.
When peritonitis is suspected, the nurse sends a specimen of the dialysate outflow for culture and sensitivity
study, Gram stain, and cell count to identify the infecting organism so that an appropriate antibiotic can be ordered. Procedures for routine or periodic culturing of PD effluent vary with institutional practice. In today's era of cost containment, routine
practices are less likely to be the norm. Cloudy or opaque effluent is the earliest sign of peritonitis. Thus nursing observations
are key to the detection and identification of peritonitis. The best treatment of peritonitis is prevention. The nurse must maintain meticulous sterile
technique when caring for the PD catheter and when hooking up or clamping off dialysate bags
(Chart 72-11).
PAIN. Pain during the inflow of dialysate is common during the first few exchanges because of peritoneal irritation; however, it disappears after a week or two. Cold dialysate aggravates discomfort. Thus the dialysate bags
should be warmed before instillation by use of a heating pad to
wrap the bag or by use of the warming chamber of the automated cycling machine. Microwave
ovens are not recommended for the warming of dialysate because
of their unpredictable warming patterns and temperatures.
EXIT SITE AND TUNNEL INFECTIONS. The normal exit site from a PD catheter should be clean, dry, and without pain or evidence of inflammation. Exit site infections (ESIs)
are associated with all types of PD catheters. Such infections can be
difficult to treat and can become chronic. Exit site and tunnel infections cause increased
morbidity, since they can lead to peritonitis, catheter failure, and
hospitalization. Dialysate leakage and pulling or twisting of the catheter can predispose the client to ESIs. A Gram stain and culture should be performed when
exit sites have purulent drainage.
Tunnel infections occur in the path of the catheter
from the skin to the cuff.
Signs of infection include redness, tenderness,
and pain. ESIs are treated with antimicrobials;
however, deep cuff infections usually require catheter
removal.
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INSUFFICIENT FLOW OF THE
DIALYSATE. Constipation is the primary
cause of inflow or outflow problems. To prevent constipation, the physician orders a
bowel preparation before placing the PD catheter.
Because outflow drainage is by
gravity, the nurse ensures that the drainage bag is lower than the client's
abdomen. The nurse inspects the connection tubing and PD system for kinking or twisting and rechecks to make sure that clamps are open. If
inflow or outflow drainage is still inadequate, the nurse attempts to stimulate inflow or outflow by repositioning the client. Turning the client to the other side or making sure that he or she is in good body alignment may help. Having the client in a supine low-Fowler's position seems to minimize the buildup of intra-abdominal pressure. Increased intra-ab-dominal pressure
that occurs in the sitting or standing position,
or with coughing, contributes to leakage at the PD catheter site.
Fibrin clot formation may occur
after PD catheter placement or with the onset of peritonitis. Careful milking
of the tubing may dislodge the fibrin clot and facilitate inflow and outflow.
Radiographic examination is needed to identify PD catheter migration out of the pelvic area. If migration has occurred, the physician repositions the PD catheter.
DIALYSATE LEAKAGE. When dialysis is initiated, small volumes of dialysate are
used. It may take clients 1 to 2 weeks to tolerate a full 2-L exchange without leakage around
the catheter site. Leakage tends to occur most often in obese or diabetic
clients, older adults, and those on long-term steroid therapy (Levine,
1997). Dialysate leakage presents as clear fluid
emitting from the catheter exit site. During this time, clients may require hemodialysis (HD) support.
OTHER COMPLICATIONS. The PD effluent (outflow drainage) is expected to be relatively clear and light
yellow. The nurse notes any change in the color of the outflow. With the initial exchanges, the outflow may be bloody. The physician may
order several in-and-out exchanges of unwarmed dialysis solution in an effort to clear the dialysate of blood. In these cases, the client's hematocrit, pulse, and blood pressure are closely
monitored. If the drainage return is brown, a bowel perforation must be suspected. Similarly, if the outflow is the same color as urine and has the same glucose concentration,
a possible bladder perforation should be investigated. If the drainage is
cloudy or opaque, an infection is suspected.
NURSING CARE
DURING PERITONEAL DIALYSIS. In the hospital
setting, peritoneal dialysis (PD) is routinely
initiated and monitored by the nursing staff. Before the treatment, the nurse evaluates baseline vital signs, including blood pressure, apical and
radial pulse rates, temperature, quality of respirations, and breath sounds. The
client is weighed, always on the same scale, before
beginning the procedure and at least every 24 hours while receiving treatment. Baseline laboratory value determinations, such as electrolyte and glucose levels, are also essential and are repeated at least daily during the PD treatment.
During PD, the
nurse continually monitors the client. Vital signs are taken regularly and recorded on a flow
sheet. For the first few exchanges, the nurse records the vital signs every 15 minutes. The nurse
also performs an ongoing assessment of the client for signs of respiratory distress,
pain, or discomfort. The abdominal dressing around the catheter exit
site is checked frequently for wetness. The nurse monitors
dwell time and initiates outflow. The physician orders
dwell time according to the client's needs for fluid removal
and electrolyte balance.
For hourly exchanges, dwell time
usually ranges from 20 to 40 minutes. Glucose absorption may occur in
some clients, and blood glucose assessment is necessary. The
outflow should be a
continuous stream after the clamp is completely open.
The total amount of outflow is recorded accurately after each exchange.
Accurate inflow and outflow records are maintained when hourly PD exchanges are
done. When outflow is less than
inflow, the difference is equal to the amount absorbed or retained by the client during
dialysis and should be
counted as intake. For clients performing self-CAPD, or when
the MB-CAPD system is used, a daily weight is used to monitor fluid status. A visual
inspection of the outflow bag and daily weights may be sufficient to note the
adequacy of the return.
RENAL TRANSPLANTATION
Dialysis and
transplantation are life-sustaining treatments for end-stage renal disease
(ESRD); transplantation is not considered a "cure." It is
up to each client, in consultation with nephrology personnel, to determine which type of
therapy is best suited to that client's physical condition and lifestyle. In
2001, 13,290 kidney transplants were performed. Currently, more than 48,000 people are awaiting renal transplantation in the
CANDIDATES. Candidates for
transplantation must be free of medical problems that might increase the
risks associated with the
procedure. The usual age range for clients undergoing transplantation is 2 to 70 years of age. In clients older than 70 years of age, the risk of complications increases, but clients older than 70 years of age are considered on an individual
basis. A thorough body systems assessment of the client
is performed before the client is considered for transplantation (see the Legal/Ethical Issues in Health
Care box at right). The process of transplantation can place
a life-threatening stress on the cardiac system in clients with advanced,
uncorrectable cardiac disease. Thus these clients are usually excluded from
consideration for transplantation. Contraindications for transplantation
include metastatic malignant neoplasms, chronic infection, severe cardiovascular disease
unresponsive to treatment, and severe psychosocial problems such as chemical dependency (Bartucci, 1999). In
addition, longstanding disease of
the pulmonary system increases the risk of morbidity and mortality owing to respiratory
tract infections after transplantation. Clients with diseases of the gastrointestinal
(GI) system may require treatment before consideration for transplantation. Such problems as peptic
ulcer and diverticulosis can be severely aggravated by the
large doses of steroids used after transplantation.
The urinary system must be
completely evaluated to ensure its ability
to manage normal urine flow. Many clients with
ESRD have not used their lower urinary tract for extended periods, and ureteral or
bladder abnormalities may require
surgical correction before renal transplantation.
Metabolic
diseases, such as diabetes mellitus, gout, and hyperparathyroidism, cause even
greater risks. These clients can still accept a renal transplant, but careful observation and
management are necessary to limit complications. Other conditions that may
complicate transplantation include malignant neoplasm and inflammatory disease. Clients with a
recent history of a malignant tumor are
usually treated with dialysis because of the shortage of donor organs, the
possibility that the cancer
could attack the transplanted kidney, and the limited life
expectancy of these clients. In addition, the immunosup-pressive agents
used after transplantation increase the risk for cancer recurrence. If more
than 2 to 5 years have passed since eradication of the cancer, the client can be
considered for a transplant.
Other
complicating conditions are considered on an individual basis, depending on the client's current health status. Renaltransplantation can be considered for most of those with ESRD and may
prove to be the optimal therapy for many people (see the Evidence-Based Practice for Nursing box on
p. 1698).
DONORS. The sources of donor
kidneys are living donors,
non-heart-beating donors (NHBDs), and cadaveric donors. The available kidneys are
matched on the basis of immunologic similarity between the donor and the
recipient. Living donors
are most often blood relatives, but in recent years, unrelated donors have been used. NHBDs are persons declared dead by cardiopulmonary criteria. Kidneys from NHBDs are harvested immediately after death in cases
where clients have previously given consent for organ
donation and no longer seek active treatment or by in situ preservation in which a cool preservation solution is infused via a catheter inserted into the abdominal aorta after death is declared. Cadaveric donors are usually individuals who
suffered irreversible brain injury,
typically as a result of trauma. This type of donor must be maintained on a ventilator and
have sufficient cardiovascular
functioning in order for the kidneys to remain transplantable (Bartucci, 1999).
The size of the kidney is seldom
a problem in adults. Pe-diatric cadaveric kidneys hypertrophy to
accommodate adult needs within a few months.
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Organs from living related donors (LRDs)
provide the highest rates of renal graft survival (90%).
Donors are usually at least 18 years old because of legal
requirements and are seldom older than
65 years of age. General physical criteria for donors include the following:
· Absence of systemic disease and infection
· No history of
cancer
· Absence of hypertension and renal disease
· Adequate
renal function as evidenced by diagnostic studies
In addition, LRDs must
express a clear understanding of the associated surgery and a willingness to give
up a kidney. Some transplant centers also require a psychiatric evaluation to
determine the motivation of the donor.
Because of
advances in immunosuppressant therapy and medical management, the United
Network of Organ Sharing (UNOS) reported 1-year renal transplant graft survival
to be 90% for all
centers in the
PREOPERATIVE CARE. Many issues must be
decided before transplantation. Some issues are related to client health and others to the actual transplant procedure. The Clinical Pathway on pp. 1848-1851 highlights care needs for the client undergoing renal transplantation.
IMMUNOLOGIC STUDIES. The major barrier to successful renal transplantation after a suitable donor kidney is available is the body's ability to identify and reject
tissue that is not its own. This immunologic process attacks the
transplanted kidney and renders it nonfunctional. For immunologic contraindications
to be overcome, in-depth tissue typing is done on all candidates for
transplantation. These studies include simple ABO blood group typing for
compatible blood transfusions and human leukocyte antigen (HLA) studies, as
well as other tests. The HLAs have
become the principal histo-compatibility system
used to match transplant recipients with compatible donors. The more similar the antigens of the donor are to those of the recipient, the more likely it is that the transplant will be successful and immunologic rejection will be avoided. Research is ongoing in immunology, and new information in
this area could increase the success rate of organ transplantations
in the future (see Chapter 20).
SURGICAL TEAM. The surgical
team is a group of specialists trained in
transplantation procedures. The team includes operating room nurses
(circulating and scrub nurses), clinical nurse specialists, and preoperative
nurses, as well as transplant surgeons, anesthesiologists, and nephrologists. The role of the preoperative nurse includes the following:
· Teaching about the procedure and postoperative care
· In-depth client assessment
· Coordination of
diagnostic tests
· Development and implementation of treatment plans
The transplant recipient usually requires dialysis
within 24 hours of the surgery. In addition, the recipient often receives a blood transfusion before surgery. Current research favors donor-specific transfusions, in which blood from the kidney
donor is transfused into the recipient. This procedure has resulted in increased
graft survival, especially of organs from LRDs.
OPERATIVE PROCEDURES. The donor nephrec-tomy procedure varies depending on
whether the donor is an NHBD,cadaveric donor, or living donor. The NHBD or cadaveric donor nephrectomy is conducted as a sterile autopsy in
the operating room. All arterial and venous vessels and as long a piece of ureter as possible are carefully preserved.
After removal, the kidneys are preserved until time for implantation
into the recipient. The technique for kidney removal from
living donors requires greater surgical care and is a delicate procedure lasting 3 to 4 hours. A flank
incision is used, and care is taken to avoid scarring. Donors
usually experience more pain than do recipients. They also need
special nursing care and support for the psychologic adjustment
to loss of a body part.
The
transplantation surgery usually takes 4 to 5 hours. The transplanted kidney is
usually placed in the right anterior iliac fossa(Figure 72-9) instead of the usual
anatomic position. This placement allows easier anastomosis of the ureter and the renal artery and vein, and it also allows for assessment by
palpation. The recipient's own nonfunctioning kidneys are not usually removed unless chronic infection in one or both kidneys would
compromise overall recovery. The client is then taken to the postanesthesia unit and then, when stable, to a designated surgical unit in the transplant center or to a critical care unit.
POSTOPERATIVE CARE. Postoperative care of the kidney transplant recipient requires
that nurses be knowledgeable about the expected clinical findings and
potential complications unique to this population. Nursing care includes
ongoing physical assessment with an emphasis on evaluation
of renal function. The transplant recipient requires particularly close attention because the immunosuppressive drug therapy to prevent tissue rejection causes impaired healing and an increased susceptibility to infection.
Careful uro-logic
management is essential to graft success. These clients always have a large
indwelling (Foley) catheter for accuratemeasurements of urine output and decompression of the bladder and to prevent stretch on suture and anastomosis sites on the bladder. An abrupt
decrease in urine output is significant, since it can herald the onset of
complications such as rejection, acute tubular necrosis (ATN),
thrombosis, or obstruction. The urine
color is carefully monitored (usually hourly). The urine is initially pink and bloody, but it gradually returns to normal over a period of several days to several weeks, depending on renal function. A continuous bladder irrigation is occasionally prescribed to
decrease the formation of blood clots, which could increase pressure in the bladder
and jeopardize the graft. Routine catheter care is performed to minimize
contamination of the catheter; the nurse adheres to the agency's policy. The
catheter is removed as soon as possible to avoid infection, usually 3 to 7 days
postoperatively. The nurse is also responsible for obtaining daily urine tests,
including urinalysis, glucose
determinations, tests for the presence
of acetone, culture, and specific gravity measurement.
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During the
postoperative period, the function of the transplanted kidney (renal graft)
can result in either oliguria or diuresis. Oliguriamay
occur as a result of ischemia and ATN, rejection, or other complications. To increase urine
output, the physician may order diuretics and osmotic agents, such
as mannitol.
The nurse and the physician carefully monitor the client's fluid
status because fluid overload can cause hypertension,
congestive heart failure (CHF), and pulmonary edema. Daily weight measurement, frequent blood
pressure readings, and careful intake and output
measurements are required to
evaluate fluid status.
Instead of oliguria,
the client may have diuresis, especially with a transplanted kidney from a living related donor
(LRD). The nurse carefully monitors fluid intake and output and observes
for electrolyte imbalances, such as hypokalemia and hyponatremia.Hypovolemia from
excessive diuresis may cause hypotensive episodes.
The nurse strives to prevent this situation because decreased blood pressure
also decreases the oxygen and blood supply to the new kidney, which
can threaten graft survival.
COMPLICATIONS. Unfortunately,
numerous potential complications are associated with transplantation
surgery.
REJECTION. The most common and the most
threatening complication of renal transplantation is rejection.
Rejection is the leading cause of graft loss. A reaction occurs between the
antigens in the transplanted kidney and the antibodies and cy-totoxic T-cells
in the recipient's blood. These immunologic substances treat the new kidney as a foreign invader and cause tissue destruction, thrombosis, and eventual necrosis of the kidney. The three types of rejection are hyperacute,
acute, and chronic. Acute rejection is the most common type in the transplant client. It is treated with increased
immunosuppressive therapy and can be reversible. Rejection can be diagnosed by
clinical manifestations, a renal scan, and renal biopsy. Table 72-12 summarizes the characteristics of the three types of rejection;
Chapter 20 discusses their pathophysiology and
treatment.
ACUTE TUBULAR
NECROSIS. Prolonged preservation of cadaveric kidneys before transplantation can
result in isch-emicdamage that is manifested as acute tubular necrosis (ATN). These clients usually need to be dialyzed until urine output becomes sufficient and the blood urea nitrogen (BUN) and creatinine normalize. Because ATN is often
difficult to distinguish from acute rejection, clients need to undergo weekly biopsies to assess the need for further immunosup-pression if rejection is occurring.
THROMBOSIS. Thrombosis
may occur during the first 2 to 3 days following transplantation. A sudden decrease in urine production or output may signal impaired perfusion resulting from
thrombosis. Ultrasound examination of the kidney will reveal decreased or absent blood supply, and emergency surgery is required to prevent further ischemic damage or loss of the
graft (Bartucci, 1999).
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RENAL ARTERY
STENOSIS. Stenosis of the renal artery is detected by identification of hypertension, a bruit over the arteryanastomosis site, and decreased renal function.
The involved artery must be surgically resected and the kidney anastomosed to
another artery. Clients with vascular complications nearly always require surgical intervention. Other vascular problems include
vascular leakage or thrombosis, both of which require an emergency transplant nephrectomy.
OTHER COMPLICATIONS. Other complications may involve the
wound or genitourinary tract. Wound complications, such ashematomas, abscesses, and lymphoceles,
can become a medium for infection and can place external pressure on the new
kidney. Infection is a significant cause of morbidity and mortality in the
transplant recipient. Prevention of infection is paramount. Strict aseptic
technique and handwashing must be rigorously enforced. Because of immunosuppression, transplant recipients may not present with
typical signs of infection. Low-grade fevers, mental status changes, and vague complaints of discomfort may be present before sepsis. Nurses play a pivotal role in the early detection of infection.
Genitourinary
tract complications include ureteral leakage, fistula, or obstruction; calculus formation; bladder neck con-tracture; scrotal swelling; and graft rupture.
Surgical intervention may be required.
IMMUNOSUPPRESSIVE DRUG THERAPY. The success of renal transplantation depends on changing the client's immunologic response so that the new kidney is not rejected
as a foreign organ. The nurse administers and is aware of the immunosuppressive drugs that protect the transplanted organ. These drugs include corticosteroids, antilym-phocyte preparations, monoclonal antibodies, and cy-closporine (Cyclosporin A). Chapter 20 discusses the mechanisms of action for these agents and the associated client responses. Clients who must take immunosuppressant medications
are vulnerable to infection secondary tomyelo-suppression. Clients are at risk for developing a
number of fatal viral, fungal, bacterial, or protozoal infections (Giuliano & Sims, 1999).
Community-Based Care
HOME CARE MANAGEMENT
Because of the complex nature of
chronic renal failure (CRF), its
progressive course, and multiple treatment modalities, a case
manager may be useful in the planning, coordination, and evaluation of care. As the renal disease progresses, the client is seen by a physician or nurse practitioner regularly and may have frequent hospitalizations. The nurse, in conjunction
with the dietitian and social worker, evaluates the home
environment and determines special equipment needs before discharge. Once the
client is discharged, home care nurses may direct care and monitor progress Chart
72-12 provides a focused assessment guideline for the client after renal
transplantation.
The nurse provides ongoing
health teaching about the diet in renal disease and the pathophysiologic process
of renal disease. As CRF approaches end-stage
renal disease (ESRD), one of
the following courses of treatment is chosen: he-modialysis (HD), peritoneal dialysis (PD), or
transplantation. For each form of treatment, the client must learn the relevant information and procedures and consider his or her personal lifestyle,
support systems, and methods of coping. Decision making about the treatment modality, or even
whether to pursue treatment, is very difficult for many clients and their families. Nurses provide information and emotional support
to assist clients with these
decisions.
Treatment with HD necessitates a
working knowledge of the
dialysis machine and the care of the client's vascular access. If the client chooses in-home HD, the home
care nurse makes preparations for installation of the appropriate equipment, including a water treatment system.
Regardless of whether the treatment is provided at home or in a
center, the nurse provides ongoing physical assessment and
health teaching to promote maximal independence at home.
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The client receiving PD needs
extensive training in the procedure. The client also needs assistance in
obtaining equipment and the numerous supplies involved. Home care nurses perform physical assessments, monitor vital signs, assess compliance with drug and diet regimens, and
carefully monitor for
signs and symptoms of peritonitis.
The nurse plays a vital role in the
long-term care of the client with a renal transplant. This client is
usually discharged 3 to 4 weeks after surgery. Meticulous
maintenance of prescribed immunosuppressive drug therapy is essential for the
survival of the renal graft. Thus the nurse facilitates acceptance and understanding of this regimen as a part
of daily life. The nurse also carefully monitors for signs of
graft rejection and for complications, such as infection.
HEALTH TEACHING
Health teaching is a primary
function of nurses caring for clients with any form of renal disease. The home care nurse
collaborates with other members of the health care team, especially the dietitian, pharmacist, and physician, to instruct clients and family members or significant others in all aspects of diet therapy, necessary drag therapy, and associated renal pathologic changes. Clients and family members are taught to report signs and
symptoms of complications, such as fluid overload and infection. When a client
requires a more advanced form of therapy, such as dialysis or transplantation, the
teaching focuses on the chosen therapeutic intervention.
HD is the most
complex form of therapy for the client and family to understand. Even if clients receive HD in a
dialysis center instead of at home, they are usually expected to have some knowledge of
the HD machine. The client or a family member or other caregiver must be taught to care
for the vascular access and to report signs of infection and stenosis.
The client who plans to have in-home HD will need a
partner. Both the client and
the partner must be completely educated in the entire process of HD and must be able to
perform it independently before the
client is discharged from the HD center or hospital HD unit.
PD involves
extensive health teaching. This instruction can be given to the client alone or
to the client and a family member or other
caregiver if the client cannot perform the procedure. The nurse emphasizes sterile technique because peritonitis is the most common complication of PD performed at
home. The nurse instructs clients to report the signs and symptoms associated with peritonitis. They should report the
presence of cloudy effluent and abdominal pain, especially when accompanied by rebound tenderness. Clients are taught that
cloudy effluent needs to be analyzed
promptly. A specimen is sent by the home care nurse for culture and sensitivity, cell
count, and Gram
stain to identify the causative organism. Clients are taught
that peritonitis is treated with antimicrobial therapy, usually given by the intraperitoneal (IP) route. To prevent peritonitis, they are taught how breaks in aseptic
technique can occur, resulting in peritonitis. In addition, to
eradicate the infection, nurses must educate clients about the importance
of completing the antibiotic regimen. Nurses need to teach that
repeated episodes of peritonitis can result in diminished ultrafiltrationcapability,
which may necessitate transfer to HD.
The client
receiving a renal transplant also needs extensive health teaching. The nurse provides instruction about drug regimens,
home monitoring, immunosuppression, signs and symptoms of
rejection, infection, and prescribed changes in the
diet and activity level.
PSYCHOSOCIAL PREPARATION
The nurse provides psychologic support for the client and family
or significant others. The nurse facilitates the client's adjustment to the
diagnosis of renal failure and eventual acceptance of the treatment regimens.
For many clients, the reduction
of uremic symptoms in the initial weeks and
months of dialysis treatment creates a sense of euphoria and well-being (the "honeymoon"
period). They feel better physically, their mood may be happy and hopeful, and they tend to
overlook the inconvenience and discomfort of frequent dialysis treatments. The nurse
realizes that this mood is temporary and uses the time to initiate health care teaching. The nurse stresses that although the client's uremic symptoms have diminished, the client will not return completely to the previous state of well-being. The
client and the family may have looked on dialysis as a cure
instead of a required lifelong treatment. Many clients enter a phase of discouragement and
disillusionment sometime during the
first year of treatment; this may last a few months to a year or longer. The
difficulties of incorporating
dialysis into daily life are staggering, and clients often become disappointed and depressed as the problems become apparent. During this time, they may struggle against the idea of having to be permanently dependent on a disruptive therapy. The fear of rejection by health staff and family members or significant others reinforces feelings of
helplessness and dependence. Some people retreat into complete or partial denial
of the disease and the need for treatment. They may deny the need for dialysis
or may not comply with medication administration and dietary restrictions.
Nurses who work with these clients need to monitor any maladaptive behaviors
that may contribute to non-compliance and suggest psychiatric referrals. Nurses
and family members should focus on
the positive aspects of the treatments.
The nurse continues health care education with clients as active participants and decision makers.
Most clients
with chronic renal failure (CRF) eventually enter a phase of acceptance or, at least, resolution. The prospect of a chronic illness may be devastating for some people, and each person reacts differently. To make this long-term adaptation, the client must adjust to continuous change, but specific
concerns depend on the current physical status and particular treatment method.
After clients
have accepted or become resigned to the chronicity of
their disease, they usually attempt to return to their previous activities.
Resuming the previous level of activity,
however, may not be possible. The nurse and other health care professionals can help clients to establish realistic goals that allow them to lead active, productive lives.
HEALTH CARE RESOURCES
Professionals from various
disciplines are valuable resources for the client with renal failure. Home care nurses
are often required
to monitor the client's status and evaluate maintenance of the prescribed treatment regimen (HD or PD). A client with advanced renal
failure may need the assistance of a home care aide in performing the activities of
daily living. Social services personnel are usually involved
because of the complex process of applying for financial aid to
pay for the required medical care (see the Cost of Care box
above). To increase the functional
capacity of the client, a physical therapist may be beneficial. Consultation with a dietitian will assist the client and family members in understanding the special dietary needs. A psychiatric evaluation may be needed to assist with depressive symptoms and maladjustment.
Clergy and pastoral care specialists offer spiritual
support.
Clients with
CRF are routinely observed by a physician, usually a nephrologist. Such organizations as the National Kidney Foundation (NKF), the American Kidney Fund, and
the National Association of Patients on Hemodialysis and
Transplantation (NAPHT) may be helpful to clients and
families.
Evaluation: Outcomes
The nurse
evaluates the care of the client with chronic renal failure (CRF) on the basis of the identified nursing diagnoses and collaborative problems. The expected
outcomes are that the client will:
· Achieve and maintain appropriate fluid volume
· Maintain serum electrolyte levels in expected ranges
· Maintain heart rate and blood pressure in expected ranges
· Comply with the
prescribed dietary regimen
· Maintain an adequate nutritional status
· Seek information to
reduce anxiety
· Use effective coping strategies
· Report an absence of physical manifestations of anxiety
