25 Acute Renal Failure CASE STUDY 5 PHARMACOLOGIC Dopamine HcL Lantus (Insuline g

largine) Human regular insulin (Humulin R) Nifedipine (Procardia) Furosemide (La

six) Calcium carbonate (Os-cal) Digoxin (Lanoxin) Sodium polystyrene sulfonate (
Kayexelate) PSYCHOSOCIAL Depression LEGAL ETHICAL Is there an ethical dilemma of
randomizing clients with ARF to a certain dialysis modality? ALTERNATIVE THERAP
Y Prayer PRIORITIZATION Determine risk factors for ARF Assess fluid balance Moni
tor serum potassium levels DELEGATION RN Client education THE DIGESTIVE AND URIN
ARY SYSTEMS Level of difficulty: Moderate Overview: This case involves critical
assessment of the client. The nurse must q uestion the client about decrease in
urinary output; history of hypertension; use of prescribed medicatio ns/herbals
taken independently; history of constipation or diarrhea, anorexia, nausea or vo
miting, and unusual f atigue. The case involves prioritization in a triage situa
tion with other clients experienci ng acute onset of other diseases. The nurse m
ust use critical thinking in triaging clients in order of highest pri ority to a
void or manage complications that could develop. The nurse must be knowledgeable
about s ites of drug metabolism and must constantly monitor for unintended effe
cts of prescribed drug s. GENDER F AGE 60 SETTING Hospital ETHNICITY/CULTURE Bla
ck American PREEXISTING CONDITIONS Hypertension Diabetes mellitus type 2 COEXIST
ING CONDITIONS Diabetes Hypertension LIFESTYLE Housewife

COMMUNICATION Spanish and English DISABILITY Yes SOCIOECONOMIC STATUS Low SPIRIT
UAL/RELIGIOUS Catholic MODERAT E

Client Profile Ms. D is a 60-year-old client who lives in an apartment building

in a comfortable two-bedroom apartment. Her significant others include her paren
ts, who are alive and reside in a nursin g home; and four younger brothers and o
ne sister, all of whom are alive and well and have frequent contact with Ms . D.
Her family history includes both parents having hypertension and a younger brot
her having type I di abetes for five years. Ms. D is 55 and weighs 190 pounds. C
ase Study Ms. D is admitted to the hospital with complaints of increased fatigue
, lethargy , and occasional confusion. After the initial interview, history, and
physical examination by a registered nurse ( RN) and a physician s assistant (P
A), Ms. D is transferred from the triage area to a medical care unit. Vital si g
ns in the emergency department (ED) are: Blood pressure:160/98 Pulse: 78 Respira
tions: 16 Temperature: 98.5 F Ms. D informs the receiving nurse in the medical un
it that she is on lantus (Ins ulin glargine) ten units daily at bedtime, and doe
s fingerstick glucose monitoring every four hours during the day . She admits be
ing anxious because during the past two weeks she has experienced unusual drynes
s of the ski n, which requires scratching. Ms. D decided to come to the hospital
and goes to the ED because she believes sh e will get attention faster. When Ms
. D is asked about the amount of urine voided since she awoke, she informs the r
eceiving nurse and PA that since she has awakened, she has urinated a smaller am
ount within a seven-hour pe riod when compared to other times. However, Ms. D be
lieves the decrease in urinary output is related to her decrease in appetite, in
cluding fluids. Ms. D is currently taking furosemide 40 mg PO daily, captopril 5
0 mg PO two time s per day for high blood pressure, and ibuprofen or naproxen oc
casionally for joint pains. She is also ta king insulin for diabetes and ibuprof
en PRN joint pain prescribed by her primary health care provider. Ms. D a lso re
ports a noted decrease in urinary output and unusual irritation frequently. She
is admitted to the unit an d placed on a cardiac monitor. A peripheral intraveno
us line is inserted, and IV fluid of NaCL 0.45% at 75 mL/hr is initiated. The nu
rse continues with the physical assessment and auscultation of her heart sounds.
There is S3 g allop and bilateral rales over lung fields, especially at the bas
es, and +1 pedal edema at the ankles. Ms. D is plac ed in a semi-Fowler s positi
on, and the nurse assigns a certified nursing assistant to remain with Ms. D, wh
ile she documents her findings. A chest Xray is done and signs of congested hear
t failure are evident. Furosemide 40 mg IV is administered stat. Ms. D is seen b
y a health care provider and a history and physical examination are done, the hi
story and assessment done 26 Part 1 THE DIGESTIVE AND URINARY SYSTEMS

by the nurse are reviewed, and the following diagnostic and laboratory tests are
ordered: X-ray of the kidneys, ureters, and bladder (KUB); renal ultrasonograph
y; and a cystoscopy. Ms. D s labor atory values are: Blood urea nitrogen (BUN):
25 mg/dL Creatinine: 2.8 mg/dL Sodium (Na): 130 mEq/L Potassium (K+): 6.8 mEq/L
Calcium: 8 mg/dL Magnesium: 3 mEq/L Phosphorous: 6 mg/dL Glucose: 118 mg/dL Urin
e specific gravity: 1.002 Urine sodium concentration: 48 mEq/L A consent is sign
ed for a cystoscopy and central venous pressure catheter insert ion. The cathete
r is inserted and an X-ray is negative for malposition of the catheter. Intraven
ous fluid is chang ed to Lactated Ringers at 75 mL/hr, and a foley catheter is i
nserted and attached to a urometer collecting ba g. The results of the diagnosti
c and labs tests are received and reviewed by the health care provider: the KUB
is negative for stones obstructing the renal pelvis, ureters or bladder; the ren
al ultrasonography is negative for urinary obstruction, but the renal calyces an
d collecting ducts are dilated, and tissue perfusion is impaired. The cystoscopy
is negative for obstruction of the lower urinary tract. The medical doctor, the
PA, the RN, an endocrinologi st, and a cardiologist review the results of the d
iagnostic studies. A primary diagnosis of ARF is made, and s econdary diagnosis
of congested heart failure. The health care provider discusses the plan of care,
including he modialysis, with Ms. D. She is transferred to the medical intensiv
e care unit (MICU), an electrocardiogram (EKG ) is done, and the client is place
d on continuous telemetry to monitor for life-threatening arrhythmias. Beca use
of the current elevated serum potassium level, the EKG reveals tall, peaked T wa
ves, widening of the QRS complex, and ST segment depression. Dopamine HcL (Intro
pin) infusion 2 microgram/kg is initiated. Questions and Suggested Answers 1. Di
scuss your understanding of the medical diagnosis of ARF, considering all o f th
e information provided in the case study, and the pathophysiology of ARF. Ms. D
s history of hypertension ha s accelerated the progression of diabetic neuropath
y diabetes mellitus. Hypertension is a leading cause of end -stage renal disease
(ESRD), especially among black Americans. It is also the most common cardiovasc
u lar abnormality, which usually exists pre-end stage renal disease. Common comp
lications of hypertension include peripheral vascular disease and renal failure.
Some degree of renal dysfunction is usually present i n the hypertensive client
, even a person with a minimally elevated blood pressure. Renal dysfunction is t
he direct result of ischemia caused by the narrowed lumen of the intra-renal blo
od vessels. Gradual narrowing of the arteries and arterioles leads to atrophy of
the nephrons, which often leads to renal failure. In congest ed heart failure,
there is decreased tissue perfusion to major organs such as the kidneys, and the
long-

term effects of diuretic therapy such as diuresis, gradually affects the renal s
ystem. A history of diabetes mell itus eventually results in diabetic nephropath
y, a microvascular complication associated with damage to the small bl ood vesse
ls that supply the glomeruli of the kidneys, resulting in the development of ren
al dysfu nction. Ms. D s serum potassium is 6.8 mEq/L on admission. It is the mo
st serious electrolyte associated with ki dney disease, usually a result of decr
eased excretion by the kidneys, the breakdown of cellular protein, bleeding, or
metabolic acidosis. A review of the elevated potassium, serum BUN, and creatinin
e indicates that the kidney function is altered. A normal serum potassium is 3.5
5.0 mEq/L. Even small changes in the leve l can have profound effects on cardia
c muscle. Although potassium can be lost in the gastrointestina l (GI) drainage,
the kidneys excrete almost all the potassium. Therefore, an elevated potassium
level is an i ndicator of altered renal CASE STUDY 5 ACUTE RENAL FAILURE 27

function. A normal BUN level is 5 20 mg/dL in adults, but may be slightly higher
i n the elderly. Although urea diffuses freely into both the extracellular and
intracellular fluid, it is ultimately excreted by the kidneys. Therefore, elevat
ed levels are an indication of altered renal function, unless t he client is deh
ydrated, which would cause the urea to be elevated. A normal serum creatinine le
vel is 0.6 1.3 mg /dL for men and 0.5 1.0 mg/dL for women. Ms. D s creatinine is
2.8 mg/dL. In the absence of disorders affe cting muscle mass, elevated creatin
ine levels indicate decreased renal function. If the urea nitrogen is ele vated
and the creatinine is normal, this finding usually indicates a nonrenal cause fo
r the excessive ure a. However, when both values are elevated in addition to the
other disease entities, renal failure is usually a primary cause. Because the r
enal ultrasonography shows renal calyces, dilated collecting ducts, impaired ti
ssue perfusion, and alteration of the renal labs, there is strong evidence of re
nal failure. Ms. D is in the ol iguric phase of acute renal failure, and the man
ifestations of this phase are changes in urinary output, fluid and el ectrolyte
abnormalities, and uremia (the presence of excessive amounts of urea and other n
itrogenous wast e products in the blood). 2. Discuss some of the common causes o
f ARF. ARF is a clinical syndrome characte rized by a rapid loss of renal functi
on with progressive azotemia, which is the accumulation of nitrogenous was te pr
oducts such as BUN and increasing levels of creatinine. There are three phases o
f acute renal failu re (pre-renal, intra-renal, and post-renal). The pre-renal f
actors that cause ARF are those external to the kidn eys that reduce renal blood
flow, and lead to decreased glomerular perfusion and filtration. A critical fac
t or in the pre-renal phase is decreased circulating volume of the blood, which
may be related to hypovolemia, decreased cardiac output, decreased peripheral va
scular resistance, and vascular obstruction. Intra-renal factors include conditi
ons that cause direct damage to the renal tissue, resulting in impaired nephron
function. Some of these factors include nephrotoxic drugs (e.g. aminoglycoside a
ntibiotics, contrast media). Nep hrotoxins can cause obstruction of intra-renal
structures by crystallization or actual damage to the epithelial cells of the tu
bules. Intra-renal causes may also be related to the release of hemoglobin from
hemolyz ed red blood cells (RBCs) or myoglobin released from necrotic muscle cel
ls. Acute tubular necrosis (ATN) i s a type of intra-renal ARF caused by ischemi
a, nephrotoxins, or pigments, and both nephrotoxic ATN and isch emia are respons
ible for 90% of intra-renal ARF cases. Intra-renal causes account for approximat
ely 35% t o 40% of all causes of ARF. Post-renal causes include mechanical obstr
uction of urinary outflow. The common causes are benign prostatic hyperplasia, p
rostate cancer, calculi, trauma, and extrarenal tumors. However, t he two most c
ommon causes of ARF are prolonged renal ischemia and nephrotoxic drugs. 3. Discu
ss the phases that ARF progresses through. Acute renal failure may progr ess thr
ough four phases. The

initial phase begins at the time of the insult and continues until the signs and
symptoms become apparent, and can last for hours or days. The oliguric phase is
caused by a reduction in t he glomerular filtration rate (GFR), with oliguria b
eing less than 400 mL of urine in 24 hours. This phase usu ally occurs within on
e to seven days of the causative event. If the cause is ischemia, oliguria may o
ccur within 24 hours. Elevated potassium (hyperkalemia) is the leading cause of
death in the oliguric phase of ARF. It is the most critical factor to cause deat
h in this phase because in the oliguric phase there is a reduction in GFR, and p
otassium is eliminated by the kidneys. If the GFR is reduced, potassium accumula
tes. Accumulation of po tassium results in lethal arrhythmias and impairment of
neuromuscular function, including muscle we akness, flaccid paralysis, absence o
f deep tendon reflexes and cardiac conduction abnormalities, and eventu ally fat
ality. In the diuretic phase there is a gradual increase in the daily urine outp
ut to one to t hree liters per day, but it may reach three to five liters or mor
e per day. However, although urine output is in creasing, the nephrons are still
not fully functional. Instead, the high urine volume is caused by osmotic diure
sis from the high urea concentration in the glomerular filtrate and the inabilit
y of the tubules to concentrate the u rine. In this phase, the kidneys have reco
vered their ability to excrete wastes, but not to concentra te the urine. In thi
s phase, hypovolemia and hypotension can occur from the massive fluid losses. Al
though th ere is massive diuresis, uremia may still be severe, which will be ref
lected by low creatinine clearances , elevated serum creatinine and blood urea n
itrogen, and persistent signs and symptoms. In this phase, the c lient is monito
red for hyponatremia, hypokalemia and dehydration. The diuretic phase may last f
or one t o three weeks, and it is at this time that the client s acid-base, elec
trolyte, blood urea nitrogen, and cr eatinine values begin to 28 Part 1 THE DIGE
STIVE AND URINARY SYSTEMS

normalize. The recovery phase, the fourth phase of ARF begins when the GFR incre
ases, which allows the BUN and serum creatinine levels to plateau and then decr
ease. The major improvem ents occur in the first one to two weeks of this phase,
but renal function may take up to 12 months to s tabilize. 4. What are the prim
ary strategies of treatment for ARF? The primary strategies for treating ARF are
to eliminate the cause with prescribed medications such as potassium resins, or
to conduct sh ort-term hemodialysis to remove excess potassium from the body. A
nother strategy is to educate the cli ent about foods and drugs that may cause A
RF, and about being knowledgeable of the early signs and symptom s of ARF and th
e appropriate interventions that should be applied to alleviate these signs and
symptoms. It i s also important to prevent complications such as hyperkalemia by
monitoring serum potassium levels and urin ary output, and reporting and docume
nting the levels. Effectively educate the client with acute renal failure about
foods to avoid that will increase serum potassium levels, prescribed medications
that may cause elevated serum potassium, and the importance of follow-up care w
ith the primary healthcare provider. 5. What are common nursing diagnoses for AR
F? Excess fluid volume R/T renal failure and fluid retention Risk for infection
R/T invasive lines and altered immune responses Imbalanced nutrition: less than
body requirements R/T altered metabolic state an d dietary restrictions Disturbe
d thought process R/T effects of uremic toxins on central nervous system Fatigue
R/T anemia, metabolic acidosis, and uremic toxins Anxiety R/T disease process,
therapeutic interventions, and uncertainty of progn osis Potential complication:
arrhythmias R/T electrolyte imbalances Potential complication: metabolic acidos
is R/T inability to excrete H+, impaired Sodium bicarbonate reabsorption, and de
creased synthesis of ammonia 6. Briefly discuss the types and purpose of hemodia
lysis use to eliminate toxic factors from the blood to prevent fatal complicatio
ns. The kidneys are the primary excretory organs for urea, an e nd product of pr
otein metabolism, and creatinine, an end product of endogenous muscle metabolism
. The best serum indicator of renal failure is creatinine because it is not sign
ificantly altered by other factors. The serum potassium levels increase in renal
failure because the normal ability of the kid neys to excrete 80% to 90% of the
body s potassium is impaired. When potassium levels exceed 6 mEq/L or arrhy thm
ias are identified, treatment must be initiated immediately because hyperkalemia
is one of the most serious complications in ARF. There are two options availabl
e for dialysis. One is hemodialysis (HD) a nd the other is peritoneal dialysis (
PD). HD is the method of choice when rapid changes are requ ired in a short time
, but it is technically more complicated than PD because specialized staff, equi
pment, and vascular access are required. The process of HD requires anticoagulat
ion therapy to prevent blood fr om clotting when blood

contacts the foreign membrane material in the dialysis blood circuit. Other reas
ons why HD is more complicated than PD involve the complications that could occ
ur during or after HD, such as h ypotension from the rapid removal of vascular v
olume (fluid shifting) during HD. If hypotension occurs during HD, the usual tre
atment is to decrease the volume of fluid being removed and infuse 0.9% normal s
aline solution (remembering that those clients with heart failure will require s
lower infusion and less volume of normal saline). Painful muscle cramps may occu
r due to rapid removal of sodium and wate r, or from neuromuscular hypersensitiv
ity. The treatment includes reduction of the ultrainfitration rate and the infus
ion of hypertonic saline solution 3.0% slowly to replace sodium loss, while avoi
ding in travascular volume overload and pulmonary edema. Hepatitis is another co
mplication that may occur with HD. T he preventive measure is to maintain infect
ion control measures as designed by the Centers for Disease Control (CDC), and t
he agency protocol. Sepsis may occur and is often related to infections of vascu
lar access sites. The preventive measure is to use aseptic technique and to moni
tor clients for signs and symptoms of sepsis, such as fever, hypotension, and el
evated WBC count. Disequilibrium syndrome occu rs because of the rapid changes i
n the composition of the extracellular fluid. This results in the shift of fluid
into the brain, causing cerebral edema, and manifestations of confusion and res
tlessness. The treatment consists CASE STUDY 5 ACUTE RENAL FAILURE 29

of slowing or stopping the dialysis and infusing hypertonic saline solution, alb
umin, or mannitol to draw fluid from the brain cells back into the systemic cir
culation. The following are prescribed: Furosemide (Lasix) 40 mg IV q6h 24 hours
Nifedipine (Procardia) 20 mg PO three times per day Lantus (Insulin gargline) 1
0 units SC at bedtime Human regular insulin (Humulin R): Fingerstick sliding sca
le (FSS) q4h PRN for: Glucose less than 100 mg/dL, no insulin coverage; 100 140,
two units SC; 141 180, fo ur units SC; 181 220, six units SC; 221 260, eight un
its SC; 261 300, ten units SC; 301 340, twelve units SC ; greater than 341, call
the MD. Calcium carbonate (Os-cal) 4 g PO with meals Digoxin (Lanoxin) 125 mg P
O every morning Sodium polystyrene sulfonate (Kayexalate) 15 g PO daily for pota
ssium level grea ter than 5 mEq/L Monitor serum creatinine, BUN, serum sodium, p
otassium, glucose, hematocrit and hemoglobin, urine protein, and urine specific
gravity daily. Dietary consultation, strict intake and output, record daily weig
ht 7. Including dopamine HcL, which was administered in the MICU, what are the p
urp oses for the prescribed orders? Dopamine HcL is an inotropic cardiac stimula
nt and vasopressor. With con tinuous intravenous infusion, it enhances renal per
fusion by its direct action on alpha- and beta-adrenergic r eceptors and on spec
ific dopaminergic receptors in mesenteric and renal vascular beds. In the dose p
rescr ibed, it increases cardiac output with minimal increase in myocardial oxyg
en consumption and dilates the renal and mesenteric blood vessels. However, in h
igher doses, it will increase the blood pressure. Furosemide is a l oop diuretic
that enhances the effects of the bolus fluid and increases urinary output by ac
tion on the pro ximal and distal ends of the tubule and the ascending limb of He
nle s loop, blocking reabsorption of sodium and chloride. When these are blocked
, passive reabsorption is prevented and the kidneys eliminate the excess urine.
Nifedipine is a calcium channel-blocking agent that effectively treats the hyper
tension associated with ARF by decreasing peripheral vascular resistance through
vasodilation. Further, it increases tissue perfusion to the kidneys. Insulin gl
argine is a long-acting recombinant human insulin analog that differs from human
insulin in that the amino acid asparagines at position A21 is replaced by glyci
ne and two arginines are added t o the C terminus of the Bchain. (Spratto and Wo
ods, 622). After subcutaneous injection, it forms microprecipitat es that gradua
lly release the insulin for long-acting action. Further, it stimulates periphera
l gl ucose uptake especially in muscle and fat tissue. When administered at bedt
ime, insulin glargine maintains glycemi c levels by achieving blood levels that
are relatively stable, and there is less risk for hypoglycemia or hyperglyc emia
during sleep. Human regular insulin is a rapid acting insulin that lowers and s
tabilizes elevated glucose le vels by increasing peripheral glucose uptake espec
ially by skeletal muscle and fat tissue. Further, it inhibit s the liver from co
nverting glycogen

to glucose. It is the preferred agent for sliding scale use. Calcium carbonate i
s a calcium salt used to increase calcium levels, which simultaneously decrease
s the elevated phosphate levels occ urring in ARF. This results from the inverse
relationship between calcium and phosphate serum levels. Digoxi n is a positive
inotropic cardiac glycoside used to treat tachydysrythmias by slowing and stren
gthening the myocar dial contractions, improving stroke volume and cardiac outpu
t. Sodium polystyrene sulfonate (Kayexa late) is a potassium-removing resin used
to treat the hyperkalemia characteristic of ARF. It increases excreti on of pot
assium through the large intestine. Monitoring of serum creatinine is significan
t in renal failure becaus e the kidneys normally filter out large amounts of cre
atinine on a daily basis. However, when kidney filtration is altered, creatinine
levels rise, requiring immediate interventions. Since creatinine is excreted on
ly by the kidn eys, its elevation is a significant indicator of damage to the ne
phrons. The BUN determines how effectively the kidn eys are clearing waste produ
ct from the blood. Therefore, if the kidneys are not functioning properly, there
wi ll be excess urea in the bloodstream. Serum sodium determines if the client
is retaining sodium, because clients in renal failure retain sodium. Monitoring
serum potassium level is important because potassium level is elevated in renal
failure and 30 Part 1 THE DIGESTIVE AND URINARY SYSTEMS

the increase in serum potassium will result in renal failure if not corrected. E
levated serum potassium also affects the cardiac system and the musculoskeletal
system in a significant manner, which could result in complications if not dete
cted and corrected. Monitoring of serum glucose levels is important b ecause the
diabetic client in acute renal failure may experience changes in insulin requir
ements due to the de crease in glucose levels, and because diuretics adversely a
ffect sodium and potassium levels by enhancing the excretion of urine, which cau
ses an increase in excretion of both electrolytes and the increase of glucose le
vels. Monitoring the hematocrit and hemoglobin levels helps determine if anemia
is present. Hematocrit and hemog lobin are decreased in persons with acute renal
failure probably due to diminished erythropoietin production, w hich would requ
ire intervention to retard the development of anemia. Monitoring urine protein i
s im portant because blood proteins do not pass through the kidneys into the uri
ne because they are too large. When kidney function is altered, protein may pass
into the urine, and protein in the urine may be a sign of permanent kidney dama
ge, or failure. Urine specific gravity helps in the diagnosis of acute renal fai
lure , because the urine specific gravity is usually decreased and fixed, reflec
ting the inability of the tubules to produce a concentrated or diluted urine in
response to changes in plasma osmolarity. Dietary consultation is required by a
registered dietitian to calculate the client s daily dietary requirements. The d
ietitian is then prepared to work wi th the client, the medical doctor, the urol
ogist, and the endocrinologist in developing a diet with specifi c levels of pro
tein, sodium, potassium, and calories to compensate for the hypercatabolic state
. Clients with ARF often have a high rate of metabolism. This hypercatabolic sta
te causes a breakdown of muscle protein, which will lead to increase in azotemia
if aggressive nutritional management is not in place. Strict intake and output
p rovides information on the client s physiological response to fluid and the ki
dney s functioning status. When the kidn eys are not functioning properly, as in
ARF, accurate assessment of intake and output is paramount to ma nagement of fl
uid and electrolyte imbalance. Daily weight determines water retention and the e
ffectiveness of medi cal interventions used to improve the client s state of hea
lth, such as furosemide. 8. What are the most common adverse reactions to the pr
escribed medications? The most common adverse reactions to dopamine HcL are hypo
tension, bradycardia, headache, hypertension, palpitations, tachycardia, vomitin
g, and arrhythmias. The most common adverse reactions to furosemide are h ypokal
emia, hypotension, hyponatremia, hypochloremia, hypomagnesemia, hypovolemia, met
abolic alkalosis, a nd dehydration. The most common adverse effects associated w
ith nifedipine are marked hypotensio n, peripheral and pulmonary edema, tachycar
dia, nausea, diarrhea, dizziness, lightheadedness, and disturbanc es in equilibr
ium. The most common adverse reaction to insulin glargine is hypoglycemia and it
s man ifestations, including

diaphoresis, nausea, nervousness, palpitations, and weakness. The most common ad

verse reaction to human regular insulin is hypoglycemia and its manifestations
as noted above. The most common adverse reaction to calcium carbonate is constip
ation, anorexia, nausea and vomiting, diarrhea, and rebound hyperacidity may occ
ur. The most common adverse effects of digoxin are bradycardia (most common) and
hypotension and those associated with digoxin toxicity (diarrhea, anorexia, nau
sea and vomiting, headache, blurred vision and halo effects, disorientation, res
tlessness, confusion, dysrrythmias, and AV heart block). The most common adverse
effects of sodium polystyrene sulfonate include hypocalcemia, hypokalemi a, hyp
omagnesemia, hypernatremia, constipation, nausea, vomiting, and gastric irritati
on. 9. Discuss the drug-to-drug, drug-to-food/herbal interactions for the prescr
ibed medications. Drug-to-drug interactions may occur with the simultaneous use
of dopamine HcL and phenytoin, which will cause severe bradycardia and hypotensi
on. Halothane and cyclopropane, when used concurrently with dopamine HcL, increa
se the risk of hypertension and ventricular arrhythmias. The simultaneous use wi
th monoamine oxidase (MAO) inhibitors, ergot alkaloids (ergotamine), doxapram, g
uanethidine, guanadre l, and some antidepressants may result in severe hypertens
ion. Dopamine may be antagonized by alpha- or beta -blocking agents. The vasopre
ssor response may be decreased in the presence of tricyclic a ntidepressants, re
quiring higher doses of dopamine (Gahart and Nazareno, 426). There are no clinic
ally sig nificant drug-tofood/ herbal interactions established. With intravenous
furosemide, drug-to-drug inter actions may occur with the simultaneous use of t
hiazide diuretics or corticosteroids and may increase t he risk of hypokalemia.
Furosemide potentiates antihypertensive agents including nitroglycerin and nitro
prusside sodium. CASE STUDY 5 ACUTE RENAL FAILURE 31

Aminoglycosides, cisplatin, and amphotericin B increase the risk of ototoxicity

and amphotericin B also increases the risk of nephrotoxicity. Furosemide may inc
rease the activity of wa rfarin sodium, heparin, streptokinase, beta-blocking ag
ents, lithium (may cause lithium toxicity), and nonpolarizing mu scle relaxants.
The simultaneous use with digoxin or amiodarone may cause dysrrythmias, and inc
rease d risk of cardiotoxicity if used concurrently with pimozide or sparfloxaci
n. When used with insulin or su lfonylureas, dopamine may cause hyperglycemia by
decreasing glucose tolerance. Dopamine effects may be inh ibited by phenytoin,
ACE inhibitors, nonsteroidal anti-inflammatory agents (NSAIDs), probenecid, or s
alic ylates (if used in clients with liver cirrhosis or ascites). (Gahart and Na
zareno, 570). Smoking may increase th e secretion of antidiuretic hormone, decre
asing the diuresis and cardiac output effects of furosemide. There are no clinic
ally significant drug-to-food/herbal interactions with intravenous furosemide es
tablished. Drug-t o-drug interactions are numerous with concurrent use with nife
dipine. Simultaneous use of rifampin, quinupristin/dalfopristin, itroconazole, a
nd diltiazem increases the effects of nifedipine. Barbiturates, n afcillin, cime
tidine, and ranitidine decrease the serum levels of nifedipine. Nifedipine incre
ases the effects of ant icoagulants, cyclosporine, digoxin, diltiazem, magnesium
sulfate, tacolimus, theophylline, an d vincristine with higher risk of toxicity
of these agents. When quinidine is used concurrently with nifedipine , quinidin
e s effects are decreased and there is an increased risk of hypotension, bradyca
rdia, pulmonary edema, atrioventricular block, and ventricular tachycardia. Grap
efruit juice increases nifedipine serum levels and St. John s Wort and melatonin
decrease nifedipine effects. Drug-to-drug interactions with the si multaneous u
se of insulin glargine and other agents either increase or decrease the glucoselowering effec ts of insulin glargine. Those agents that increase the insulin s
effects include ACE inhibitors, dispyramide, fl uoxetine, MAO inhibitors, octreo
tide, phopoxyphene, salicylates, and sulfonamides. Those that decrease its gluco
se-lowering effects are danazol, diuretics, isoniazid, niacin, and somatropine.
Clonidine and lithium sa lts may potentiate or decrease insulin s effects. Altho
ugh drug-to-food/herbal interactions technically may not o ccur, eating foods hi
gh in simple sugars or other carbohydrates will decrease the effectiveness of in
sulin glargine by increasing serum glucose levels, requiring an increase in the
dose of insulin. The only drug-to-d rug interaction associated with regular insu
lin is that the use of oral hypoglycemics will increase the effects of regular i
nsulin and, because this type of insulin is rapid acting, the concurrent use wou
ld greatly increase the risk of hypoglycemia. As with all insulins, the increase
d intake of simple sugars and carbohydrates will require increasing the dose of
regular insulin. Drug-to-herbal interactions may occur with the simultaneous use
of garlic and ginseng, which may potentiate hypoglycemic effects. Drug-to-drug
interactions may occur w

ith the simultaneous use of calcium carbonate and quinidine or amphetamines, inc
reasing the effects of th ese agents. Decreased levels of salicylates, calcium c
hannel blocking agents, ketoconazole, tetracyclines, an d iron salts are seen wi
th concurrent use of calcium carbonate. Drug-to-food/herbal interactions include
increased act ion and adverse effects when used with lily of the valley, pheasa
nt s eye, and squill. Drug-to-dru g interactions may occur with the simultaneous
use of oral diazepam and thiazides, loop diuretics, barbiturate s, CNS depressa
nts, alcohol, SSKIs, cimetidine, and muscle relaxants by potentiating their effe
cts. Fluoxetin e and isoniazid increase the half-life of diazepam, ranitidine de
creases GI absorption of diazepam, and oral contraceptives, valporic acid, disul
firam, isoniazid, and propranolol cause decreased metabolism of diazepam. K ava
increases the action of diazepam. Numerous drug-to-drug interactions are associa
ted with the use of d igoxin. Amiodarone, anticholinergics, atorvastatin, benzod
iazepines, captopril, diltiazem, dipyridamole, erythromycin, esmolol, flecainide
, fluoxetine, hypoglycemic agents, levothyroxine, hydroxychloroquine, ibuprofen,
i ndomethacin, itraconazole, methimazole, nifedipine, propranalol, quinidine, q
uinine, telmisar tan, tetracyclines, tolbutamide, and verapamil increase digoxin
levels, increasing the risk of digoxin toxicity. Albuterol increases digoxin bi
nding to skeletal muscle and amphotericin B increases potassium deplet ion, thus
increasing the risk of digoxin toxicity. The following agents decrease digoxin
effects: amilari de, aminoglycosides, aminosalicylic acid, antacids, cholestyram
ine, colestipol, diopyramide, metoclopramide, spirola ctone, sulfasalazine, and
thyroid. Beta-blocking agents pose an increased risk of complete heart block . P
arenteral calcium preparations cause cardiac dysrrhythmias and large volume gluc
ose infusions increase potassiu m loss and increase the risk of digoxin toxicity
. Chlorthalidone, ethacrynic acid, furosemide, and t hiazides increase potassium
and magnesium loss resulting in an increased risk of digoxin toxicity. Ephedra,
ephedrine, and epinephrine 32 Part 1 THE DIGESTIVE AND URINARY SYSTEMS

increase the chance of cardiac dysrhythmias. Aloe, buckthorn bark/berry, cascara

sagrada bark, German chamaomile flower, ginseng, hawthorn, Iceland moss, Indian
snakeroot, ivy leaf, licorice, marshmallow root, rhubarb root, sarsaparilla roo
t, castor bean oil, may apple root, yellow dock ro ot, oleander, purple foxglove
, squill, and senna pod/leaf must be used with extreme caution because they incr
ea se the effects of digoxin. St. John s Wort decreases digoxin s action. Drug-t
o-drug interactions may occur with the simultaneous use of sodium polystyrene su
lfonate and antacids or laxatives that will decrease the effects of sodium polys
tyrene sulfonate. No clinically significant drug-to-food/herbals have been estab
lished. 10. Discuss the gerontologic considerations of ARF. The older adult is m
ore susc eptible than the younger adult to ARF as the number of functioning neph
rons decrease with age. Impaired functio n of other organ systems (e.g. cardiova
scular disease, impaired pancreas function) can increase the risk of developing
ARF. The aging kidneys are less able to compensate for changes in fluid volume,
solute load, an d cardiac output. The prognosis after an episode of ARF is gener
ally worse in the older adult than in the younge r person. The mortality rate of
ARF is 5% to 25% higher in the older adult than in the younger adult, an d deat
h is usually caused by infection, gastrointestinal hemorrhage, or myocardial inf
arction. 11. Discuss client education for ARF. The client should be taught to av
oid expos ure to nephrotoxins, particularly those in the over-the-counter produc
ts, prevent infection and other major stress ors that can slow healing, and to m
onitor weight, blood pressure, and pulse daily. Also advise the client t o maint
ain dietary restriction as planned with the registered dietitian and the health
care provide r or nurse practitioner. The importance of follow-up care should al
so be discussed. References Black, J.M. and Hawks, J.H. (2005). Medical-Surgical
Nursing: Clinical Managemen t for Positive Outcomes. Philadelphia: W.B. Saunder
s. Broyles, B.E. (2005). Medical-Surgical Nursing Clinical Companion. Durham, NC
: C arolina Academic Press. Cavanaugh, B.M. (2003). Nurse s Manual of Laboratory
Diagnostic Tests. Philadelphi a: F.A. Davis. Corbet, J.V. (2004). Laboratory Te
sts and Diagnostic Procedures with Nursing Dia gnoses (6th ed.). Upper Saddle Ri
ver, NJ: Prentice Hall. Gahart, B.L. and Nazareno, A. R. (2005). 2005 Intravenou
s Medications. St. Louis : Mosby. Heitz, U. and Horne, M.M. (2005). Mosby s Pock
et Guide Series: Fluid, Electrolyte and Acid-Base Balance (5th ed.). St. Louis:
Mosby. Huether, S.E. and McCance, K.L. (2004). Understanding Pathophysiology (3r
d ed.). St. Louis: Mosby. Ignatavicius, D.D. and Workman, M.L. (2006). Medical-S
urgical Nursing across the Health Care Continuum (5th ed.). Philadelphia: W.B. S
aunders. Spratto, G.R. and Woods, A.L. (2005). 2005 Edition: PDR Nurse s Drug Ha
ndbook. Cli fton Park, NY: Thomson Delmar Learning.

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