Running head: DUNBAR CASE STUDIES
Dunbar: Case Study One and Two
Whitney L. Dunbar
Wright State University
Nursing 7201
May 2, 2013
Dr. Kristine Scordo
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DUNBAR CASE STUDIES
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Dunbar: Case Study One and Two
Case Study One
1. What is the most likely diagnoses for this patient and what are the criteria for this
diagnosis? What is your rationale?
The most likely diagnosis for this patient is right-sided heart failure secondary to
pulmonary hypertension (PH). The etiology of secondary PH for this patient is related to the
consumption of the anorectic medications, fenfluramine and phentermine. PH exists once
pulmonary artery pressures escalate to a level that is unsuitable for usual cardiac output. PH
initiates structural deformities mostly in the smaller pulmonary vessels, involving intimal
hyperplasia, medial hypertrophy, adventitial excess, originating thrombosis, different amounts of
inflammation, and plexiform arteriopathy. These alterations may result in additional restriction
of the arterial bed. The limitation of the flow within the pulmonary arterial circulation produces
enhanced pulmonary vascular resistance (PVR) and eventually right-sided heart failure. The
hemodynamic classification of PH consists of a mean pulmonary artery pressure of more than 25
mmHg, a pulmonary capillary wedge pressure, left atrial pressure, or left ventricular enddiastolic pressure less than or equivalent to 15 mmHg, and a PVR more than three Wood units
(American Heart Association (AHA), 2009).
Right-sided heart failure starts developing when the rising of systolic pressure in the right
ventricle reacts to the increase in PVR in order to maintain an adequate cardiac output. Right
ventricle failure happens in PH when the right ventricle myocardium develops ischemia as an
outcome of extreme demands and insufficient right ventricle coronary blood movement (Longo
et al., 2012). Tricuspid and pulmonary valve insufficiency and cor pulmonale are found in
severe cases of PH in addition to right ventricle failure (Papadakis, McPhee, & Rabow, 2013).
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There are various pathogenic pathways that have been linked to the evolution of PH,
comprising of pathways at the molecular and genetic levels and in the smooth muscle,
endothelial cells, and adventitia (AHA, 2009). Secondary PH can occur with various ailments,
involving systemic sclerosis, hepatic cirrhosis and portal hypertension, human
immunodeficiency virus, chronic thromboembolic disease, and the consumption of anorectic
medications (Papadakis et al., 2013).
The criterion for PH includes a history from the patient, physical symptoms the patient
exhibits, and diagnostic tests. Obtaining a history from the patient aids in narrowing down the
differential diagnoses. The patient presents with a complaint of dyspnea for seven months that
started with dyspnea while exercising on her stationary bike and has progressed to dyspnea with
minimal exertion. Patients with PH typically present with dyspnea on exertion initially and
eventually dyspnea at rest with advanced stages of PH. Dyspnea occurs from a decreased
amount of oxygen in the blood either from not enough oxygen existing or due to insufficient gas
exchange. Also, the patient presents with a complaint of fatigue for seven months and two
syncope episodes in the past month. Fatigue and syncope are outcomes from decreased cardiac
output that are associated to elevated pulmonary artery pressure or bradycardia. The patient
complains of occasional substernal chest pressure with excessive exertion. Patients with PH can
present with dull, retrosternal chest pain like angina pectoris (Papadakis et al., 2013). The
patient states she has abdominal fullness and this can be related to right ventricular dysfunction
due to PH (AHA, 2009).
There are various physical findings this patient exhibits for PH. First, the patient appears
to be anxious, in mild distress, and has slightly labored respirations. This can be caused by the
lack of oxygen existing in the blood. Second, the patient exhibits central cyanosis with cyanosis
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of the lips. Central cyanosis is associated with hypoxemia, pulmonary-to-systemic shunt, intrapulmonary shunt, and abnormal ventilation perfusion. Third, the patient has jugular venous
distention and trace edema of the ankles. Patients with moderate to severe PH may exhibit these
signs due to right ventricular dysfunction, tricuspid insufficiency, or both. Fourth, the patient has
a positive hepatojugular reflux (HJR). Patients with PH can have a positive HJR due to high
central venous pressure. Fifth, the patient has a prominent S2 at the second intercostal space at
the left sternal border and a grade III/VI holosystolic murmur at the left sternal border amplified
with inspiration. These two physical findings of patients with PH are a result of tricuspid
insufficiency. Sixth, the patient has a right ventricular S4 and a left parasternal heave. Patients
with PH may exhibit a right ventricular S4 and a left parasternal heave due to the existence of
high right ventricular pressure and hypertrophy. Seventh, the patient has a slightly distended
abdomen and patients with PH can display a distended abdomen due to right ventricular
dysfunction. Eighth, the patient has an elevated jugular vein pressure (JVP) at nine centimeters.
Ninth, the patient exhibits prominent A-waves in the jugular venous pulse due to an increase in
right atrial contraction from PH. The increase in JVP and the A waves in the jugular venous
pulse are related to an excess of right ventricular pressure amongst failure that is linked with a
condensed, less compliant right ventricle (AHA, 2009).
The third criteria for PH includes diagnostic tests. The patient had an electrocardiogram
(ECG) and a chest x-ray performed. The patients’ ECG displays right axis deviation and right
atrial enlargement. The ECG of patients with PH typically shows right axis deviation, right atrial
enlargement, and right ventricular hypertrophy. Right ventricular hypertrophy can display on the
ECG with elevated R-waves, specifically, a R/S ratio greater than one in lead V1. Other criteria
of right ventricular hypertrophy include a deep S-wave in leads V5 or V6 that is greater than
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seven millimeters and has a R-wave less than five millimeters. Usually, there is ST segment
depression and a negative T-wave in the right precordial leads (Ellis, 2012). This patient
exhibits these changes in their ECG. The patients’ chest x-ray presents cardiomegaly with
enlargement of the pulmonary trunk. The chest x-ray of patients with PH usually appears to
have dilated central pulmonary arteries and an enlarged pulmonary outflow tract. In advanced
stages of PH, right ventricular and atrial expansion may be observed. Further diagnostic testing
should be implemented for confirmation of PH (Papadakis et al., 2013).
2. What diagnostic test should be performed? Explain your rationale?
When a history, a physical exam, a risk factor assessment, a chest x-ray, and an ECG are
obtained and there is suspicion for PH, an echocardiogram should then be performed. A Doppler
echocardiogram is noninvasive and can offer an approximation of the right ventricle systolic
pressure, right atrium and ventricle evaluation, left heart disease, valvular heart disease,
congenital heart disease, and recognize any potential cardiac causes of PH. If the right ventricle
systolic pressure is more than 40 mmHg it usually deserves additional evaluation in the patient
with unexplained dyspnea (AHA, 2009). In a systemic review and meta-analysis of 29 studies,
for diagnosing PH, the sensitivity and specificity for echocardiography was 83% and 72%
(Janda, Shahidi, Gin, & Swiston, 2011).
There are many other pivotal tests that can be implemented in order to diagnose a patient
with PH. After an echocardiogram is performed, a ventilation-perfusion (VQ) lung scintigraphy
or a computed tomography pulmonary angiogram (CTPA) is executed in order to rule out
chronic thromboembolic PH in a patient with unexplained dyspnea and suspected PH (AHA,
2009). A retrospective study consisting of 227 patients from a hospital setting were tested for
chronic thromboembolic PH using a VQ scintigraphy or a CTPA. The study supported that the
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VQ scintigraphy had a sensitivity of 96% to 97.4% and a specificity of 90% to 95% compared to
CTPA sensitivity of 51% and a specificity of 99% (Tunariu et al., 2007). If the results of the VQ
scan are normal or low probability then specific tests should be performed in order to rule out
other possible causes of dyspnea. Pulmonary function tests may be implemented to obtain the
patients’ ventilatory function and gas exchange. Overnight oximetry can contribute to the
assessment of a sleep disorder. Human immunodeficiency virus screening is checked for the
human immunodeficiency virus infection. Antinuclear antibody serology is drawn for the
assessment of scleroderma, systemic lupus erythematosus, and rheumatoid arthritis. A liver
function test is drawn to assess for portopulmonary hypertension. A cardiopulmonary exercise
test should be performed to establish a baseline and prognosis (AHA, 2009).
If a patient is believed to have PH after a noninvasive assessment, the patient should have
a right heart catheterization (RHC) completed prior to starting treatment. A RHC is the test
performed to confirm diagnosis of PH and to describe the hemodynamic profile in better detail
and accuracy. The RHC assesses oxygen saturations within the vessels and heart, right atrial
pressure, right ventricular pressure, pulmonary artery pressure, pulmonary arterial wedge
pressure, cardiac output and index, PVR, systemic blood pressure, heart rate, and reaction to
acute vasodilator. However, this patient would not be a candidate for the acute vasodilator test
due to the treatment being long-term calcium channel blockers. Calcium channel blockers
should not be initiated to a patient with right-sided heart failure due to the negative inotropic
effect (AHA, 2009). The sensitivity and specificity for RHC are 93% and 95% for identifying
PH (Roldan, 2012).
3. What is the appropriate therapy for this patient? Include all types of therapy and
rationale for your choices.
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Patients diagnosed with any form of PH can be initiated on a few different medications.
First, fenfluramine and phentermine will be discontinued due to the adverse effects and the
probable cause of the patients PH. Second, the patient may continue her oral contraceptive
medication but she should use dual birth control methods because pregnancy is contraindicated
for patients with PH. Third, patients with PH may be placed of oxygen therapy to maintain
oxygen saturation greater than 92%. A six-minute walk test can be executed for this patient due
to her dyspnea on minimal exertion and will help determine if the patient needs to be placed on
oxygen therapy. Any patient with PH should be educated to let their healthcare provider know
when they are traveling to a high altitude destination or traveling by airplane due to potential
hypoxia pulmonary vasoconstriction. Fourth, this patient may be started on warfarin
anticoagulation due to the patient taking oral contraceptives and having right-sided heart failure.
These are two risk factors for developing a venous thromboembolism. It would be
recommended to start this patient on warfarin 5 mg by mouth (PO) daily to a goal INR of 1.5 to
2.5. After initiating warfarin the patient should return in four days to recheck her INR and adjust
warfarin dosage according to results. Once the INR is at therapeutic level, an INR can be
checked monthly. A prothrombin time and hematocrit should be monitored with the INR. Fifth,
diuretics are used to manage fluid overload from right-sided heart failure. This patient would be
started on furosemide 40 mg PO twice a day. It is suggested to start furosemide for patients with
heart failure and edema between 20 to 80 mg/dose once or twice daily. Doses can increase in
additions of 20 to 40 mg/dose at interims of six to eight hours and can be titrated up to 600
mg/day. The patients weight, intake and output, relief of symptoms, blood pressure, and hearing
should be closely monitored. Serum electrolytes and renal function should be carefully
monitored for hypokalemia and altered kidney function. Sixth, some patients with idiopathic PH
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(IPH) are prescribed digoxin when they have right-sided heart failure, a low cardiac output, and
atrial arrhythmias. Digoxin increases cardiac output and slows down the ventricular rate. This
medication would not be prescribed for this patient at this time since she has secondary PH due
to taking anorectic agents. Before prescribing digoxin the healthcare provider should reevaluate
if there is any improvement of PH once the anorectic medications are discontinued. Also, there
is limited research on digoxin and its benefits on PH (AHA, 2009; Lexi-Comp, Inc., 2013).
Seventh, the patient should receive her vaccinations when they are due because having PH can
place her at a higher risk for becoming critical, for example, if she were to acquire influenza or
pneumonia. A nurse with a certificate to prescribe (CTP) in Ohio may prescribe warfarin per
institutional protocol or it is physician initiated or physician consulted. A nurse in Ohio with a
CTP may prescribe oxygen, furosemide, digoxin, and vaccinations (Ohio Board of Nursing,
2013).
Acute vasodilator testing can be performed during the patients’ RHC and can help guide
the proper PH treatment for the patient. If the result is positive then the patient will be placed on
an oral calcium channel blocker. Since this patient has right-sided heart failure, it would not be
recommended to implement the acute vasodilator test, therefore, would not be placed on an oral
calcium channel blocker. Consequently, this patient would be placed on another medication to
improve her PH (AHA, 2009).
Since the acute vasodilator test would not be performed on this patient, the health care
provider needs to determine if this patient is low risk or high risk based on their clinical
assessment. There are three different classes of drugs that may be used for patients with PH in
addition to the previous stated medications. There is the prostacyclin class that consists of
epoprostenol, treprostinil, and iloprost. Patients with PH lack prostacyclin synthase that results
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in insufficient productions of prostacycline I2, a vasodilator with antiproliferative effects.
Therefore, prostacyclins have become a basis of PH therapy. Also, the endothelian receptor
antagonist (ERAs) class includes bosentan, sitaxsentan, and ambrisentan. These medications
block endothelin-1, a vasoconstrictor and a smooth muscle mitogen that can add to the
progression of PH. In addition, the phosphodiesterase inhibitors (PDE-5) class entails sildenafil
and tadalafil. These medications assist to extend or augment the effects of vasodilating cyclic
nucleotides, cyclic adenosine monophosphate and cyclic guanosine monophosphate. When the
patient is considered low-risk then an oral ERA or a PDE-5 would be the suggested first line of
treatment. If oral treatment were not suitable, a prostacyclin would be considered. An
intravenous (IV) prostacyclin is the advocated first line of treatment for a patient that is
considered high risk that is established from clinical assessment (AHA, 2009).
This patient would be considered high risk due to her presenting signs and symptoms of
right-sided heart failure, dyspnea with minimal exertion, and fatigue at rest. The recommended
medication for patients with severe PH is to initiate IV epoprostenol. Studies have reported
improvements in functional class, exercise intolerance, hemodynamics, and survival of IPH with
IV epoprostenol. For example, a randomized trial of 81 functional class III and IV IPH patients
exhibited substantial progression in the crucial six-minute walk test. The patients treated with
epoprostenol had a 32-meter increase in length compared to a 15-meter reduction with only
conventional therapy. Subordinate results consisted of hemodynamics and quality of life
improvements with epoprostenol. Even though this patient does not have IPH, observational
studies have reported positive outcomes of IV epoprostenol with several forms of secondary PH
and it is the only medication that has exhibited the ability to extend survival. Epoprostenol needs
to be administered through a continuous IV infusion. Educating the patient on sterile technique
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for preparation of epoprostenol, managing the ambulatory infusion pump, and proper care of the
central venous catheter are vital for the patient with PH to learn because an infection or an
infusion interruption can be life-threatening. Typically, it is initiated in the hospital at a dose of
2ng/kg/min. The dose may be changed according to the patients’ symptoms of PH and the side
effects of epoprostenol. Therefore, this patient would be started at 2ng/81.8kg/min. It is thought
that the ideal dose may be found between 25 and 40 ng/kg/min for adult patients. Elevated
cardiac output failure may result from a chronic overdose and the long-term consequences could
be detrimental or unknown. The healthcare provider should educate the patient on the use of
epoprostenol and the common side effects that consist of headache, jaw pain, flushing, nausea,
diarrhea, skin rash, and musculoskeletal pain. The patient should be educated on what signs and
symptoms need to be reported to their healthcare provider immediately (AHA, 2009). A nurse
with a CTP can prescribe Epoprostenol when it is physician initiated or the nurse with a CTP is
within a specialty clinic (Ohio Board of Nursing, 2012). The healthcare provider should review
all medications, necessary laboratory values, if the patient has insurance coverage, and answer all
questions and concerns the patient may have before prescribing a medication. A follow-up
appointment should be scheduled with follow-up laboratory blood work.
There are a few different treatment options for patients with PH who are not effectively
responding to their primary monotherapy. First, patients can be started on a combination therapy
that consists of a prostacyclin with an ERA or a PDE-5. The goal of combination therapy is to
augment efficiency while reducing toxicity. Second, patients who are not responding to
monotherapy could have an atrial septostomy performed. This procedure constructs a right to
left inter-atrial shunt that leads to a reduction in right heart filling pressures, advances right heart
function, and enhances left heart filling. Even though the formed shunt declines systematic
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arterial oxygen saturation, it is projected that the enhanced cardiac output should have the
outcome of a general increase of systemic oxygen supply. Third, a lung transplant is another
option if monotherapy is not effective for a severe PH patient. It can be challenging to figure out
the appropriate timing for lung transplantation. Lung transplants are reserved for patients who
are in end-stage pulmonary disease and continue to have progression of PH despite optimal
medical management (AHA, 2009).
A multidisciplinary management approach for patients with PH is ideal for their
treatment because it can increase the length of their life. The treatment should be individualized.
Therefore, there should be many referrals and consults for this patient with severe PH. There
should be a referral to cardiac rehabilitation because they can provide assistance in improving
her health and well being with her cardiac complications (AHA, 2009). Additional referrals and
consults for this patient include a cardiologist, a pulmonologist, a dietician, a social worker, and
a pharmacist. Also, the healthcare provider should recommend a smoking cessation class for this
patient due to her history of smoking and offer psychiatry if she feels overwhelmed or depressed
about her diagnosis.
Case Study Two
1. What is your differential diagnosis? Explain.
There are many differential diagnoses for this patient that will be discussed. First, acute
kidney injury (AKI) secondary to contrast induced nephropathy can be a diagnosis for this
patient. AKI is described as an increase in serum creatinine by equal or greater than 0.3 mg/dL
within 48 hours, an increase in serum creatinine equal or greater than 1.5 times the patients’
baseline within the previous seven days, or urine output less than 0.5 ml/kg a hour for six hours.
This patients’ serum creatinine has increased to 2.9 mg/dL from 1.6 mg/dL (1.8 times baseline
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within seven days) and currently only has 200 mL of urine over 24 hours (about 8 cc an hour).
Therefore, this patient meets the definition of AKI. Contrast induced nephropathy is described
as an increase in serum creatinine of equal or greater than 0.5 mg/dL or a 25% rise from the
patient’s serum creatinine baseline after 48 hours from a radiological procedure. This patients’
serum creatinine increased by 1.3 mg/d and over 25% from his baseline within 48 hours after
receiving contrast media from the coronary angiography procedure (Kidney Disease Improving
Global Outcomes (KDIGO), 2012).
Second, AKI secondary to hypovolemia due to dehydration may be a diagnosis for this
patient. Typically, intravenous isotonic sodium chloride is given to patients who are at a high
risk for contrast-induced nephropathy prior to their procedure in order to prevent intrarenal
hemodynamic alterations and direct tubule-toxic effects. This patient is at high risk due to his
type two diabetes and coronary artery disease. The patient did not receive any intravenous fluids
besides intravenous nitroglycerin prior to the coronary angiography and this patient may not
have been drinking fluids prior to admission. Hypovolemia is a cause of prerenal failure due to
decreased renal perfusion from reduced intravascular volume. When a patient is undergoing a
procedure where they will be receiving contrast media, hypovolemia enhances the toxic effect
and can lead to AKI. An indication of prerenal failure is a blood urea nitrogen (BUN) to
creatinine ratio of more than 20:1. This patients’ BUN to creatinine ratio is 23.8:1 and indicates
prerenal failure (KDIGO, 2012).
Third, AKI related to acute tubular necrosis is another potential diagnosis for this patient.
Acute tubular necrosis can occur when there is prolonged ischemia to the kidney and causes
necrosis of the proximal tubules of the outer medulla and the proximal convoluted tubules. The
prolonged ischemia is followed by reperfusion. Acute tubular necrosis is expressed by a severe
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increase in plasma BUN and serum creatinine. This elevation can occur from hours to weeks.
This patient potentially could have had ischemia prior, during, or after the coronary angiography
from hypovolemia. The contrast media from the coronary angiography is another cause of
nephrotoxic acute tubular necrosis (KDIGO, 2012).
Fourth, AKI related to acute interstitial nephritis is another possible diagnosis. It entails
interstitial inflammation with edema and potential tubular cell damage. Drugs cause the majority
of cases of acute interstitial nephritis, but it can be caused by an infection, an immunologic
disorder, or an idiopathic condition. Manifestations of acute interstitial nephritis include fever,
rash, arthralgia, and peripheral blood eosinophilia. This patient is afebrile and does not have a
rash or arthralgia, but it may be to soon for these signs and symptoms to appear. Acute
interstitial nephritis should be something to consider if this patient were to develop these signs
and symptoms later (Papadakis et al., 2013).
Fifth, AKI secondary to atheroembolic renal disease (AERD) is another possible
diagnosis for this patient. AERD happens when small elements built up of hardened cholesterol
and fat spread to the small blood vessels of the kidneys. It can then cause a reduction of blood
flow to the tissues and produce swelling and tissue damage that can harm the kidneys. Also, it
can harm the skin, eyes, muscles and bones. It can occur one week after receiving contrast
media. Manifestations include blindness, blue toes, hypertension, decrease in sensation, decrease
or no urine output, drowsiness, swelling in the legs, weight loss, nausea, and dry itchy skin
(Brenner, 2007).
2. What is your next step to diagnose the problem? Explain. Of what value is a urinalysis
and urinary electrolytes?
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The next step to establishing the possible diagnosis of AKI secondary to contrast induced
nephropathy involves the combination of medication review, new laboratory tests, and the
laboratory tests that have already been implemented to help narrow down the differential
diagnoses. The healthcare provider should review what medications the patient has taken in the
last 24 to 48 hours that could possibly cause injury to the kidneys. The patient received contrast
media and angiotensin-converting-enzyme inhibitor in the last 24 to 48 hours that could cause
injury to the kidneys. The laboratory tests that should be ordered are a fractional excretion of
sodium (FeNa), erythrocyte sedimentation rate, urine osmolality, urine specific gravity, urine
sediment, urinalysis, and urine electrolytes. A renal function panel was already drawn and is
another test that allows the healthcare provider to assess kidney function. Also, laboratory tests
can help determine the severity of the renal disease. A treatment plan can be determined with the
proper diagnostic assessment (Longo et al., 2012). A renal ultrasound could be ordered to rule
out AERD if still questioning diagnosis after urine electrolytes, urine analysis, physical
assessment of patient, and a history review of patient (Brenner, 2007).
A urine analysis (UA) can have great value in helping diagnose a kidney disease. It can
offer information comparable to a renal biopsy that is cost-effective and non-invasive. The
collected urine should be assessed within an hour in order to prevent destruction of formed
elements. A UA includes a urine dipstick analysis and a microscopic evaluation if the urine
dipstick has positive results. The urine dipstick includes measuring urinary pH, protein,
hemoglobin, glucose, ketones, bilirubin, nitrates, and leukocyte esterase. Microscopy examines
for crystals, cells, casts, and infecting organisms. For example, if the results displayed
pigmented granular casts and renal tubular epithelial cells alone or in casts, the healthcare
provider would think the patient has acute tubular necrosis. Another example, interstitial
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nephritis usually exhibits white blood cells, white blood cell casts, red blood cells, and a small
amount of protein on the urine dipstick and microscopic examination. In further detail, when
there is more than 150mg of protein being excreted in urine in a 24-hour period, it signifies an
underlying kidney malfunction in an adult. The source is usually glomerular when proteinuria is
more than 1 gram a day to less than 2 grams a day. There are several causes along the nephron
segment that result in less than 1 gram a day of proteinuria (Papadakis et al., 2013).
The measurement of urinary electrolyte concentrations has a vital part in the diagnosis
and treatment plan for different kidney diseases. Typically, sodium, potassium, chloride, and
calcium are the electrolytes that are measured for this test. The normal level for urine sodium is
40 to 220 mEq/L a day but it depends on the patient’s salt and water intake. Urine sodium can
be used as an approximation of the patient’s volume status. Salt-wasting nephropathy and
diuretics are causes for a high urine sodium level. A low urine sodium level can result from
chronic kidney disease, glomerulonephritis, hepatorenal syndrome, kidney injury, or nephrotic
syndrome. The normal results for urine potassium is 25 to 125 mEq/L a day but can vary due to
dietary intake of potassium. An increase in urine potassium may signify acute tubular necrosis,
hypomagnesemia, diabetic acidosis, renal tubular acidosis, and use of non-potassium-sparing
diuretics. A decreased urine potassium level can be caused from adrenal gland insufficiency,
hypoaldosteronism, and medications that include beta-blockers, potassium-sparing diuretics or
nonsteroidal anti-inflammatory drugs. The normal urine chloride level is between 110 to 125
mEq a day and depends on the patient’s salt and fluid intake. An increase in urine chloride can
result from adrenocortical insufficiency, inflammation of the kidney, and production of large
amounts of urine. A low chloride urine level can be caused by Cushing syndrome, salt retention,
and fluid loss. The normal calcium urine level is between 100 to 300 milligrams a day but can
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vary with diet. A high urine calcium level can be caused from chronic kidney disease, leaking of
urine from the kidneys, and loop diuretics. When there are low calcium urine levels, thiazide
diuretics may be the source (Goldman & Schafer, 2012).
3. What are the indications for dialysis in AKI (acute kidney injury)? Be specific.
There are many indications for dialysis when patients have AKI. First, refractory
potassium is an indication for dialysis in AKI. If the potassium level becomes more than 6.5
mmol/L it can cause cardiac conduction abnormalities. Therapeutic measures that stimulate the
intracellular shift of potassium are implemented to decrease the potassium level and when they
are drained, the potassium level can rise. Therefore, the excess of potassium can only be
eradicated with dialysis. Second, metabolic acidosis with a pH less than 7.2 can indicate dialysis
when sodium bicarbonate is no longer effective. Severe metabolic acidosis can injure cardiac
function and intensify hyperkalemia. Salicylates, ethylene glycol, methanol, and metformin are
examples of poisons, drug overdoses, and toxic compounds that can lead to metabolic acidosis
and AKI. Third, dialysis may be started when a patient displays no signs of renal function
recovery with a serum creatinine greater than 12 mg/dL or a BUN level more than 100 mg/dL.
Fourth, progressive uremia is another indication for dialysis with AKI because it can cause
bleeding diathesis, encephalopathy, nausea, vomiting, dehydration, seizures, and pericarditis.
Fifth, pulmonary edema from fluid overload that is resistant to diuretic therapy is another
indication for dialysis with AKI and typically seen in patients with heart failure (Gutierrez &
Morn, 2010; KDIGO, 2012).
4. Write a set of admitting orders for the patient. Be specific.
Admission orders. Admit to Critical Care Medicine, Coronary Intensive Care Unit
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Diagnosis. AKI secondary to contrast induced nephropathy. Secondary diagnosis:
Angina, Hypertension, Type II diabetes mellitus, Diabetic retinopathy, Coronary artery disease
Condition. Serious
Allergies. No known drug allergies
Vital signs. Continuous ECG monitoring; Blood pressure, heart rate, respiratory rate,
oxygen saturation every hour; Temperature every four hours. Call physician if systolic blood
pressure less than 90 or greater than 160, diastolic blood pressure less than 50 or greater than
100, mean arterial pressure less than 60, heart rate less than 50 or greater than 120, respiratory
rate less than eight or greater than 30, temperature less than 97.5°F or more than 101.0°F, any
other sudden changes in vital signs, or urinary output is less than 30 ml for two hours
Activity. Up as tolerated
Nursing. Record admission height and weight; Record daily weights; Accurate intake
and output measured and documented every hour; Insert a foley catheter for accurate intake and
output; Encourage incentive spirometer; Encourage cough and deep breathing; Measure blood
glucose with glucometer before meals and at bedtime; Get a 12 lead ECG stat; If patient
develops chest pain obtain a stat ECG and notify physician
Diet. 1500- calorie diabetic/renal/2g sodium diet; Encourage fluids; 0.8 to 1.0 g/kg per
day of protein intake (KDIGO, 2012)
Intravenous orders. Insert two peripheral IVs; #1. 500 ml 0.9 Normal saline at 999
ml/hr; #2. 1000 ml 0.9 Normal saline at 100ml/hr
Medication orders. Continuous IV nitroglycerin at 5 mcg/min, raise by 5 mcg/min
every three to five minutes to 20 mcg/min, and if there is no response at 20 mcg/min, then titrate
up by 10 to 20 mcg/minute every three to five minutes with a maximum of 400 mcg/min (Lexi-
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Comp, Inc., 2013); Sliding scale regular human insulin subcutaneous injections before meals and
at bedtime with target plasma glucose of 70 to 150 mg/dL; If plasma glucose is less than 70 then
initiate hypoglycemia protocol; 70 to 150 receives no insulin; 151 to 200 receives two units;
201to 250 receives four units; 251 to 300 receives six units; 301 to 350 receives eight units; 351
to 400 receives 10 units; greater than 400 call physician; Hold ACE inhibitor; ASA 81 mg by
mouth daily; Metoprolol 25 mg by mouth twice a day (Hold if heart rate less than 60 or systolic
blood pressure less than 100)
Laboratory orders. Renal function panel every eight hours; Complete blood cell count
daily; Urinalysis daily; MRSA by PCR once; Erythrocyte sedimentation rate once
Special orders. Respiratory therapy to maintain oxygen saturation greater than 92%
with lowest amount of required oxygen; Consult nephrology and cardiology; Nursing
pneumococcal and influenza vaccine screen and administration per local protocol; Physical and
occupational therapy
Thank you,
Whitney Dunbar, ACNP-Student
5. Complete the following chart with the values present in prerenal and acute renal failure.
Be certain to reference the chart.
Table 1
Laboratory Values Present in Prerenal and Acute Renal Failure
Laboratory Test
Prerenal
Acute Renal Failure
FeNa
< 1%
>2%
BUN to creatinine ratio
> 20:1
< 20:1
Urine specific gravity
>1.020
1.010 to 1.020
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Urine osmolality, mOsm per kg
>500
250-350
Urine sodium concentration,
<20
>20
Bland, Hyaline Casts
Granular Casts
mEq per L (mmol per L)
Urine sediment
Note. Normal laboratory values (Gutierrez & Morn, 2010; Papadakis et al., 2013).
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References
American Heart Association. (2009). ACCF/AHA 2009 expert consensus document on
pulmonary hypertension: A report of the american college of cardiology foundation task
force on expert consensus documents and the american heart association: Developed in
collaboration with the american college of chest physicians, american thoracic society,
inc., and the pulmonary hypertension association. Circulation, 119, 2250-2294. doi:
10.1161/CIRCULATIONAHA.109.192230
Brenner, B. (2007). Brenner and rector’s the kidney (8th ed.). Philadelphia, PA: Saunders
Elsevier.
Ellis, K. (2012). EKG plain and simple (3rd ed.). Upper Saddle River, NJ: Prentice Hall Health.
Goldman, L., & Schafer, A. (2012). Goldman’s cecil medicine (24 ed.). Philadelphia, PA:
Saunders Elsevier.
Gutierrez, C., & Morn, C. (2010). Common renal conditions. FP Essentials, 375, 1-44.
Retrieved May 2, 2013, from http://www.aafp.org/fpe/2010/0800/375.pdf.
Janda, S., Shahidi, N., Gin, K., & Swiston, J. (2011). Diagnostic accuracy of echocardiography
for pulmonary hypertension: A systematic review and meta-analysis. Heart, 8, 612-622.
doi: 10.1136/hrt.2010.212084
Kidney Disease Improving Global Outcomes. (2012). KDIGO clinical practice guidelines for
acute kidney injury. Kidney International Supplements, 2, 1-137. Retrieved May 20,
2013, from
http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pd
f
Lexi-Comp, Inc. (2013). Lexi-DrugsTM. Lexi-Comp, Inc. Accessed May 16, 2013.
DUNBAR CASE STUDIES
21
Longo, D., Fauci, A., Kasper, D., Hauser, S., Jameson, L., & Loscalzo, J. (2012). Principles of internal
medicine (18th ed.). New York, NY: McGraw Hill Education.
Ohio Board of Nursing (2012). The formularly developed by the committee on prescriptive
governance. Retrieved May 29, 2013, from
http://www.nursing.ohio.gov/PFS/AdvPractice/Formulary_11-19-12.pdf
Ohio Board of Nursing (2013). The formularly developed by the committee on prescriptive
governance. Retrieved May 29, 2013, from
http://www.nursing.ohio.gov/PDFS/AdvPractice/4-30-13_Formulary.pdf
Papadakis, M., McPhee, S., & Rabow, M. (2013). Current medical diagnosis and treatment (52nd
ed.). New York, NY: McGraw Hill Medical.
Roldan, C. (2012). The ultimate echo guide (2nd ed.). Philadelphia, PA: Lippincott Wiliams
Wilkins.
Tunariu, N., Gibbs, S., Win, Z., Gin-Sing, W., Graham, A., Gishen, P., & Al-Nahhas, A. (2007).
Ventilation-perfusion scintigraphy is more sensitive than multidetector ctpa in detecting
chronic thromboembolic pulmonary disease as a treatable cause of pulmonary
hypertension. Journal of Nuclear Medicine, 48, 680-684. doi:
10.2967/jnumed.106.039438