Download Running head: CASE STUDY #1 AND #2 CASE STUDY #1 AND #2

Running head: CASE STUDY #1 AND #2
Case Study #1 and #2
Lindsey Moeller
Wright State University College of Nursing & Health
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CASE STUDY #1 AND #2
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Case Study #1
1. What is most likely diagnosis for this patient and what are the criteria for this
diagnosis? What is your rationale?
The most likely diagnosis for this patient is pulmonary artery hypertension (PAP). The
criteria for diagnosis of PAP according to the American College of Cardiology Foundation
(ACCF) and the American Heart Association (AHA) (2009) are a mean pulmonary artery
pressure greater than 25 mmHg, a pulmonary capillary wedge pressure, left atrial pressure or left
ventricular end-diastolic pressure less than or equal to 15 mmHg, and a pulmonary vascular
resistance greater than 3 Wood units (p. 5). Although this patient has no hemodynamic
measurements for diagnosis, she presents with signs and symptoms suggestive of pulmonary
artery hypertension, in addition to her increased risk factors of anorexigen use and smoking. She
has intermittently used Fenfluramine and Phentermine over the past two years for weight loss
increasing her risk for valvular disease and PAH. Multiple studies have shown an association
between the use of Fenjfluramine and Phentermine as little as three months has been associated
with heart valve regurgitation and PAH (Drolet, Simard, & Poivier, 2007; Fleming & Boyd,
2007).
The patient presents with several signs to raise suspicion for PAH. The manifestations of
jugular venous distention with clear lungs, positive hepatojugular reflex, prominent a waves in
the jugular venous pulse, prominent P2 heart sound at the left sternal border, holosystolic
murmur at left sternal boarder that increases with inspiration suggestive of tricuspid
regurgitation, left parasternal heave, ankle edema, and central cyanosis support the diagnosis of
PAH (Moser & Riegel, 2008). These findings are characteristic of right ventricular hypertrophy
(RVH), increased right ventricular and pulmonary pressures, manifested by S4 gallop and loud
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P2 sound. Her symptoms of increasing dyspnea with minimal exertion, fatigue, two episodes of
syncope, occasional chest pressure with activity, peripheral edema, and abdominal fullness also
raise suspicion for PAH.
The EKG revealing right axis deviation, right atrial enlargement, prominent RSR’ in the
precordial leads, anterior ST depression with T wave inversion is characteristic of PAH (Moser
& Riegel, 2008). The chest x-ray is congruent with electrocardiogram (EKG) findings of rightside heart involvement showing clear lung fields, cardiomegaly and an enlarged pulmonary
trunk. The enlarged heart with clear lungs and jugular vein distention on exam alert the
practitioner to think right-sided heart disease.
Each individual physical sign, reported symptom, EKG finding, chest x-ray result are nonspecific to PAH, but when examining holistically in combination with history of smoking and
anorexigen use this leads most likely the diagnosis of PAH. These findings may be present in
other cardiopulmonary diagnoses, but differential diagnosis will be eliminated through further
diagnostic testing and work-up.
2. What diagnostic test should be performed? Explain your rationale.
There are guidelines for diagnostic testing in PAH set forth by the European Society of
Cardiology (2009) and the ACCF/AHA (2009). The goal of testing is to determine the cause of
the PAH, the severity, and guide treatment. Since a chest x-ray and an EKG have already been
completed, a transthoracic echocardiogram (TTE) is the next test to be performed. A TTE
measures size of the right atria and ventricle, estimates pulmonary artery pressure, and overall
function. It also detects any abnormalities in performance of the tricuspid, pulmonic, mitral and
aortic valves. In a standard TTE, the left side of the heart is also examined. Evaluation with a
saline bubble study during a TTE will show the presence of any shunting of blood flow which is
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suspicious for an atrial or ventricular septal defect. The echocardiogram also would help rule out
a congenital heart condition as the cause of the PAH.
A ventilation perfusion scan is needed to determine if the PAH is caused by a chronic
thromboembolic condition and an arterial blood gas to evaluate for hypoxia (Galie et al., 2009;
McLaughlin et al., 2009). If the result of the ventilation perfusion scan is positive, then a high
resolution chest CT angiogram with contrast should be done to evaluate for an acute pulmonary
embolism. The CT of the chest may also show underlying lung disease such as emphysema, lung
nodules or pleural effusions. The arterial blood gives pertinent information about arterial
oxygenation and that specific point in time.
Laboratory studies are also important in ruling out other conditions or causes of PAH. Labs
needed are complete blood count to determine hemoglobin in relationship to oxygenation and a
serum chemistry to optimize electrolytes and assess baseline kidney function (McLMoser &
Riegel, 2008). A b-type natriuretic peptide can be helpful at baseline and to follow the trend
during treatment because it is a predictor of volume overload. Antinuclear antibodies are drawn
and increased levels are seen in connective tissue disorders such as lupus or scleroderma, which
are other causes of PAH. Liver function tests and hepatitis immunology, are needed to assess for
hepatitis and portal hypertension. Thyroid studies that should be included are a thyroid
stimulating hormone level and a Free T4 to evaluate for underlying thyroid disease. Human
immunodeficiency virus infection testing is necessary to eliminate this as a cause as well
(McLaughlin et al., 2009).
In addition to labs, the ACCF and AHA guidelines (2009) recommend baseline pulmonary
function tests (PFT), a six minute walk test, and a right-sided heart catheterization as standard
baseline testing to be performed. The right-sided heart catheterization confirms the diagnosis of
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PAH. The PFT establishes baseline lung function prior to the start of therapy and eliminates
obstructive or restrictive lung disease as the cause of dyspnea. PFT’s are repeated periodically
after initiation of therapy to aid in efficacy of treatment. This patient likely has underlying
obstructive pulmonary disease given her 17 year smoking history. In order to make the definitive
diagnosis of PAH, a right-sided heart catheterization is performed. This is not usually the first
diagnostic test performed because it is the most invasive, but it provides the hemodynamic
measurements to confirm PAH and determines the severity of the disease. Right atrial pressure,
pulmonary artery pressure, pulmonary artery occlusion pressure, peripheral vascular resistance,
cardiac index, and mixed venous oxygen saturation data are collected during the procedure
(Moser & Riegel, 2009). Without these measurements a definitive diagnosis and severity of
PAH could not be made, baseline hemodynamic information would not be obtained and
pharmacological therapy could not be determined.
During the right-sided heart catheterization, a vasoreactivity study using a vasodialator
such as nitric oxide is indicated since the cause of PAH is likey due to anorexigen use (Galie et
al., 2009). This determines whether the patient can tolerate treatment with high dose calcium
channel blockers and predicts if this treatment would be effective. Pharmacological therapy is
determined and initiated after completion of diagnostic testing.
3. What is the appropriate therapy for this patient? Include all types of therapy and
rationale for your choices.
The severity of the PAH determines the first line pharmacologic therapy. This female has
signs and symptoms of severe PAH without even having the hemodynamic measurements from
the right-sided heart cath. Her dyspnea with minimal activity, accentuated S2, parasternal heave,
S4 gallop and increased jugular a waves are physical signs and symptoms associated with severe
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PAH (McLaughlin et al., 2009). According to the World Health Organization and New York
Heart Association classifications of pulmonary hypertension, this patient would be considered
Class IIIa stable or Class IV due to her gradual onset of symptoms including fatigue at rest,
dyspnea with any physical activity, and signs of right ventricular dysfunction (Galie et al., 2009;
McLaughlin et al., 2009). Her treatment will follow a stable Class IIIa approach given her mental
status, blood pressure, and heart rate are stable, without having results of the diagnostic testing to
further determine initial therapy.
First line pharmacological therapies for this patient and the majority of PAH patients are
oxygen, anticoagulation and a diuretic (Galie et al., 2009; McLaughlin et al., 2009; Moser &
Riegel, 2008). Supplemental oxygen is prescribed for hypoxemia and to maintain an oxygen
saturation of 90 percent or greater. Start Coumadin five milligrams (mg) oral once daily every
evening to prevent a pulmonary embolism. International normalized ratio (INR) goal is 1.5-2.5
for a patient with a history of idiopathic PAH or known anorexigen use. INR will be monitored
and dose adjusted to achieve therapeutic INR. Lasix 20 mg oral one tablet twice a day is
prescribed to decrease symptoms of right heart failure and peripheral edema (Lexi-Comp, 2013).
Close monitoring of renal function and hemodynamics is necessary. Dose may need to increased
or decreased according to her response to therapy.
In addition to the standard therapy, a calcium channel blocker may be useful with her
type of PAH. If she has a positive response to the vasoreactive test during the right heart
catheterization, is hemodynamically stable with no right sided heart failure, a calcium channel
blocker is added to her therapy regimen (Galie et al., 2009; McLaughlin et al., 2009; Moser &
Riegel, 2008). This is thought to be most helpful in the earlier stages of PAH. Nifedipine 30 mg
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1 tablet twice a day by mouth is prescribed to reduce peripheral vascular resistance, dilate the
pulmonary artery, and increase oxygen delivery (Lexi-Comp, 2013).
Sildenafil or Tadafil may be used in combination with the Nifedipine for this patient.
These two agents are phosphodiesterase-5 inhibitors which enhance nitric oxide and inhibit the
breakdown of cGMP in the pulmonary circulation promoting vasodilation (Lexi-Comp, 2013).
Sildenafil (Ravatio) 20 mg oral 1 tablet three times a day may be prescribed.
Another drug class of oral medications used to treat PAH is non-selective endothelial
receptor-antagonist. These drugs include bosentan, sitaxsentan and ambrisentan which work by
blocking endothelial receptors and promoting vasodilatation and may improve exercise tolerance
as well as hemodynamics. Bosentan 62.5 mg 1 tablet orally twice a day is the initial dose, after
four weeks increase dose to 125 mg twice a day (Lexi-Comp, 2013).
Prostacyclins may also be added or replace another drug in the treatment regimen, if
disease continues to progress and symptoms do not improve. Illoprost, Treprostinil or
Epoprostenol are examples of prostacyclins’s and their mechanism of action is primarily
vasodialation of the vascular system and has been effective in increasing exercise tolerance
(Moser & Riegel, 2008). A continuous intravenous infusion of Epoprostenol 1-2 ng/kg/minute
may be started, if the other therapies have failed to be therapeutic or may be initiated first if the
patient is unstable with signs of right-sided heart failure (Galie et al., 2009). This infusion is
initiated in the hospital setting through a central venous catheter, with continuous pulmonary and
hemodynamic monitoring. It may be titrated in 2 ng/kg/minute increments every 15 minutes until
a dose is reached in which symptoms of dyspnea, activity intolerance, and syncope improves
(Lexi-Comp, 2013). Usually the dose is between 25-40 ng/kg/minute.
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Combination drug therapy is common when monotherapy as failed to improve symptoms
and quality of life. For advance disease in Class III or IV patients that show no signs of
improvement despite aggressive combination drug therapy, a single or double lung transplant
may be an option (Galie et al., 2009; McLaughlin et al., 2009; Moser & Riegel, 2008). With
continued failure of treatment, a last resort option may be an atrial septostomy. This is for
patients with severe symptoms, refractory to treatment, and recurrent syncope. The atrial
septostomy relieves pressure on the right side of heart and is thought to improve cardiac output.
As previously discussed, this particular patient is initially started on supplemental
oxygen, Lasix, Coumadin, and Nifedipine. She should follow-up in one day to evaluate treatment
response and repeat labs. Monitoring response to therapy and disease progression through labs,
follow-up testing and report of symptoms will determine if and when other drugs such as a PDI5, prostacyclin or endothelial receptor-antagonist should be added.
Preventing infections, increasing activity tolerance, preventing pregnancy and promoting
quality of life are also part of her initial treatment regimen in combination with her medications
(Galie et al., 2009; McLaughlin et al., 2009). At this time she agrees to be immunized with the
influenza and pneumococcal vaccines to further prevent infections that could negatively affect
her respiratory status. She is also advised to discontinue use of her oral contraceptives because of
increased risk of thrombolytic events and begin using another form of contraception. A referral is
made to exercise rehabilitation because she is deconditioned, needs supervision and exercise
recommendations.
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Case Study #2
1. What is your differential diagnosis? Explain.
The differential diagnoses for this patient are renal artery stenosis, acute kidney injury
(AKI), dehydration, dissecting aneurysm, obstructive uropathy, acute tubular necrosis,
rhabdomyolysis, neurogenic bladder, contrast-induced nephropathy, benign prostatic
hypertrophy (BPH), chronic kidney disease, drug induced interstitial nephritis, sepsis, thrombosis
or embolus, endocarditis, and diabetic ketoacidosis (Workeneh & Batuman, 2013). Acute onset
of oliguria is a sign of acute kidney injury which is not a primary disease, but rather a
complication of other disease processes (Marino, p. 579, 2007). These conditions listed can
cause an acute rise in creatinine and decreased urine output. Monitoring, further physical
assessment, and diagnostic testing is needed in order to treat the underlying cause quickly before
irreversible damage occurs to the renal system.
Hypovolemia is the most common cause of decreased urinary output and increased serum
lab values (Needham, 2005). Contrast used during a cardiac catheterization is known to be
nephrotoxic, ace-inhibitors cause vasodilatation decreasing renal perfusion, and aspirin may
cause interstitial nephritis. Sepsis, endocarditis, and thromboembolisms should be considered.
This patient is afebrile, but did undergo an invasive procedure increasing risk for infection. He
also has a known history of hypertension, diabetes and coronary artery disease further increasing
risk for a thromboembolism. Rhabdomyolysis is present when muscle damage occurs and should
be considered given the patients risk of infection, electrolyte abnormalities, and current
decreased activity level (Marino, 2007). Acute tubular necrosis is commonly caused by sepsis,
drug toxicity, radiocontrast dye or rhabdomyolysis. This patient had contrast dye during the
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cardiac catheterization and ace-inhibitors in the past 24 hours that could be the cause of his acute
kidney injury.
An obstruction or stenosis of the urinary tract should be considered as a potential
diagnosis such as renal artery stenosis, BPH, obstruction of urethra, ureter obstruction, and renal
calculi (Needham, 2005; Workeneh & Batuman, 2013). In addition to ruling out obstruction,
diabetic ketoacidosis may be present. The patient is diabetic with dot hemorrhages and hard
exudates on exam, recently had an invasive procedure for worsening angina creating stress on
the body and could lead to uncontrolled glucose levels.
2. What is your next step to diagnose the problem? Explain. Of what value is a
urinalysis and urinary electrolytes?
The next step in diagnosing the problem is obtaining laboratory studies and radiographic
imaging to begin the work-up of the differential diagnosis. A complete blood count (CBC), blood
cultures and adding a serum glucose, phosphorus, calcium, and liver function test (LFT’s) to the
current blood chemistry are ordered (Lewington & Kanagasundaram, 2011). The CBC evaluates
for an elevation in the white blood cell count which could be a sign of an infectious process or
sepsis. The serum glucose is important to follow due to the history of diabetes and to assess for
diabetic ketoacidosis. The calcium and phosphorus can be abnormally high in AKI and are
important to follow treads before and after initiation of therapy. Two sets of peripheral blood
cultures will aid in ruling out a bacterial blood infection as a cause of AKI, even though the
patient is currently afebrile. Liver function test are obtained to evaluate for suspicion of cirrhosis
or a hepatorenal cause of the AKI (Lattanzio & Kopyt, 2011).
A urinalysis with microscope, urine electrolytes, calculated fraction of filtered sodium
(FeNa), urine osmolality, and urine culture are ordered. A urine culture specifically directs the
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provider to sensitive antibiotics for treatment, if bacteria are present in the urine. Urinalyses with
microscopy and urine electrolytes have great significance and add to differentiating between
prerenal, renal, and postrenal causes of acute kidney injury (Lattanzio & Kopty, 2009; Schrier,
2011). Prerenal and renal are the two most common causes of AKI in hospitalized patients. A
few prerenal causes of AKI are dehydration, heart failure, cirrhosis and sepsis. Renal causes are
abnormalities within the kidneys. The urine microscopy usually reveals hyaline casts in prerenal
causes where granular casts are present most often with intrarenal causes of AKI. The amount of
FeNa excreted in the urine is an indicator of the tubular integrity of a functioning nephron. The
FeNa is calculated using urine sodium and serum sodium. Refer to Table 1. below for the lab
characteristics of prerenal and renal.
The urine culture, osmolality, calculated FeNa, urine sodium, and microscope are useful
in guiding diagnosis and treatment, but a basic urinalysis is necessary too. The urinalysis
provides cues to the provider if abnormalities are present with specific gravity, ketones, glucose,
nitrates, blood, white blood cells, protein and leukocytes (Schrier, 2011). Glucose in the urine
may indicate high blood glucose and further evaluation of his diabetes. Presence of blood,
nitrates, white blood cells and leukocytes would certainly increase concern for a urinary tract
infection or an intrarenal cause of AKI.
The lab results discussed above and the physical assessment drive therapy. When urine
electrolytes or urinalysis studies are omitted and treatment is solely based on an acute rise in
serum creatinine, more harm than good could occur (Schrier, 2011). For example, prerenal AKI
is often treated with intravenous fluids and can reverse quickly. Administering large amounts of
intravenous fluids to a patient with intrarenal causes may lead to acute pulmonary edema,
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hypoxia, and respiratory distress. Urine electrolytes, microscope, and culture studies are more
valuable together rather than separate.
In addition to the laboratory studies, this patient needs a renal ultrasound with doppler
and a trans-thoracic echocardiogram (TTE). The renal ultrasound is indicated to assess for renal
artery stenosis, prerenal or postrenal obstruction, calculi, hydronephrosis, blood flow, and kidney
size (Lattanzio & Kopyt, 2011). With his history of hypertension, angina, and diabetes a TTE is
useful in evaluating for heart failure, valve function, hypertrophy, and endocarditis. Heart failure
and endocarditis are known causes of AKI. As diagnostic results become available a more
specific assessment and plan are developed.
3. What are the indications for dialysis in AKI (acute kidney injury)? Be specific.
Initiating dialysis in patients with AKI is individualized; however, once criteria are met,
early initiation is associated with increased survival (Lewington & Kanagasundaram, 2011).
Laboratory studies, past medical history, physical assessment and patient stability are taken into
consideration prior to initiating dialysis. Indications for dialysis are; acidosis uncorrected with
medical management, hyperkalemia >6.5 mmol/L, refractory hypercalcemia, refractory
hypernatremia or hyponatremia, urine output < 0.3 ml/kg in 24hrs, AKI with multiple organ
failure, severe drug toxicity or overdose, hypothermia or hyperthermia, tumor lysis syndrome
with refractory hyperuricaemia, hyperphosphatemia, encephalopathy, blood urea nitrogen > 100
mg/dL, significant bleeding, uremic pericarditis, and refractory volume overload (Brochard et al.,
2010; Lewington & Kanagasundaram, 2011; Needham, 2005). Medical management is usually
attempted first, but when unsuccessful dialysis may be used.
The Acute Dialysis Quality initiative further defines indications for renal replacement
therapy (RRT) as oliguria (<400 mL/24 hours), anuria (<100 mL/24hours), serum pH <7.15
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and/or serum HCO3 <15 mmol/L, PaO2/FiO2 ratio <200 and/or %FO N10%, serum urea >36
mmol/L, and serum potassium >6.0 mmol/L (Bagshaw, p. 270, 2012).
4. Write a set of admitting orders for this patient. Be specific.
Admitting Orders:
Admit to Step-down Telemetry Unit to Cardiology 2 service
Diagnosis: Angina and Acute Kidney Injury
Condition: Stable
Code Status: Full Code
Allergies: NKDA
Vital Signs: Every 2 hour, orthostatic blood pressures x 1 upon admission
Activity: Activity as tolerated, if free of chest pain and SBP >100
Up with assistance to bathroom, up to chair TID with meals
Nursing:
-Admission Height and Weight
-Daily Weights every 0700
-Continuous cardiac monitoring with pulse oximetry
-Place indwelling Foley catheter to straight drain for strict output monitoring
-Monitor Intake and Output every 1 hour
-Accu checks before meals and at HS with carbohydrate counts
-Incentive spirometer every 1 hour x 10 breaths while awake
-Sequential compression devices to bilateral lower extremities at all times while in bed
-Notify primary team if any of the following occur:




increasing shortness of breath
chest pain unrelieved by NTG
Temp <97F or >101.5, HR <50 or >100, SBP <90 or >160, RR <10 or >22, SPO2 <90%
UOP <30ml/hr
Diet: Diabetic carb controlled, 1800 calorie
IV: maintain 2 peripheral 18 gauge intravenous catheters
Medications:
-D/C ACE inhibitor
-D/C ASA
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-Metoprolol 25 mg PO every 12 hours
-Lovenox 30 mg subcutaneous injection daily
-Pepcid 20 mg PO BID
-Regular insulin subcutaneous standard sliding scale + carb counts, 10 CHO’s = give 1 unit
additional insulin
Glucose 150-200, 2 units
201-249, 4 units
250-300, 6 units
301-350, 8 units
>350 call primary team
-Nitroglycerine gtt intravenous continuous, start at 5 mcg/minute, increase by 5 mcg/min every
3-5 minutes to 20 mcg/min. If no relief of chest pain may increase by 10-20 mcg/min to
maximum dose of 400 mcg/min, titrate to relief of chest pain per patient report
Monitor blood pressure and heart rate before and after each titration, maintain HR>50 and MAP
between 70-110 mmHg
-0.9NS @ 150ml/hr intravenous continuous
Labs:
-EKG now and every 6 hours x 2
-Troponin now and every 6 hours x 2
-CPK now and every 8 hours x 3
-CBC with differential on admission
-CBC daily in am
-PT, PTT, INR on admission
-Serum Chem 7 with Magnesium, Calcium, and Phosphorus now and then every 6 hours
-LFT’s on admission
-BNP on admission
-LDL, HDL, triglycerides, and total cholesterol on admission
-HgbA1C on admission
-2 sets Peripheral blood cultures on admission
-Urinalysis with microscope and urine culture on admission
-Urine electrolytes (Na, CL, urea, K), urine osmolality, and urine myoglobin on admission
Special Orders:
-Renal Ultrasound with doppler now- acute rise in creatinine, with decreased UOP over last 24
hours, concern for renal artery stenosis or acute kidney injury versus acute tubular necrosis
-2 D Trans esophageal echocardiogram now- please evaluate for systolic heart failure, valvular
dysfunction and endocarditis. Hx of CAD and Type 2 diabetes, admitted with worsening angina
and hypertension with known S4 gallop, no significant stenosis found on coronary angiography
yesterday, now with AKI.
Nephrology Consult- 54 year old male S/P coronary angiography yesterday for worsening angina
and hypertension. Now showing signs of AKI with Creatinine increasing to 2.9 mg/dL was 1.6
mg/dL on admission, 200 ml UOP in 24 hours, serum BUN 69 mg/dL, and serum K 5.3 mEq/L.
Hx of Type 2 Diabetes, HTN. Urinalysis with microscopy, urine electrolytes, and urine culture
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pending. Renal ultrasound with Doppler flow ordered. Appreciate further recommendations on
diagnostic testing and management.
5. Complete the following chart with specific values present in prerenal and acute
renal failure. Be certain to reference the chart.
Table 1. Lab Values in Acute Renal Failure
Laboratory Test
Prerenal
Acute Renal Failure
FeNa
<1
>1
BUN to creatinine ratio
>20:1
10 to 20:1
Urine specific gravity
>1.020
1.010 to 1.020
Urine osmolality, mOsm per kg
>500
300 to 500
Urine sodium concentration, mEq
<10 (10)
>20 (20)
Hyaline Casts
Granular Casts
perL (mmol per L)
Urine sediment
(Needham, 2005)
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References
Bagshaw, S., Wald, R., Barton, J., Burns, K, Friedrich, J., Housed, A., James, M. Levin, A.
Moist, L., Pannu, N. Stollery, D., & Walsh, M. (2012). Clinical factors associated with
initiation of renal replacement therapy in critically ill patients with acute kidney injury—
A prospective multicenter observational study. Journal of Critical Care, 27, 268-275.
doi: 10.1016/j.jcrc.2011.06.003
Brochard, L., Abroug, F., Brenner, M., Broccard, A., Danner, R., Ferrer, M., Franco, L., Magder,
S., Papazian, L., Pelosi, P., & Polderman, H. (2010). An official
ATS/ERS/ESICM/SCCM/SRLF statement: Prevention and management of acute renal
failure in the ICU patient. American Journal of Respiratory and Critical Care Medicine,
181, 1128-1155. doi:10.1164/rccm.200711-1664ST
Drolet, B., Simard, C., & Poirier, P. (2007). Impact of weight-loss medications on the
cardiovascular system focus on current and future anti-obesity drugs. American Journal
of Cardiovascular Drugs, 7(4), 273-288.
Fleming, R., & Boyd, L. (2007). The longitudinal effects of Fenfiuramine-Phentemnine use.
Angiology, 58, 353-359. doi:10.1177/0003319707302496
Galie, N., Hoeper, M., Humbert, M., Torbicki, A., Vachiery, J., Barbera, J., Beghetti, M., Corris,
P., Gaine, S., Gibbs, J., Gomez-Sanchez, M., Jondeau, G., Klepetko, W., Opitz, C.,
Peacock, A., Rubin, L., Zellweger, M., & Simonneau, G. (2009). ESC Committee for
Practice Guidelines (CPG). Guidelines for the diagnosis and treatment of pulmonary
hypertension: The Task Force for the Diagnosis and Treatment of Pulmonary
Hypertension of the European Society of Cardiology, endorsed by the International
CASE STUDY #1 AND #2
17
Society of Heart and Lung Transplantation. European Heart Journal, 30(20), 2493-2537.
Retrieved from http://guideline.gov/content.aspx?id=15948#Section439
Lattanzio, M., & Kopyt, N. (2009). Acute kidney injury: New concepts in definition, diagnosis,
pathophysiology, and treatment. Journal of American Osteopathic Association, 109(1),
13-19.
Lewington, A., & Kanagasundaram, S. (2011). Clinical practice guideline for acute kidney
injury. The Renal Association; endorsed by the Society for Acute Medicine and the Acute
Intensive Care Society. Retrieved from
http://www.renal.org/clinical/guidelinessection/AcuteKidneyInjury.aspx
Lexi-Comp, Inc. (2013). Lexi-Drugs. Accessed May 20, 2013.
Marino, P. (2007). Oliguria and acute renal failure. The ICU Book, 3rd edition (pp.579-592).
Philadelphia, Pennsylvania: Lippincott Williams & Wilkins.
McLaughlin, V., Archer, S., Badesch, D., Barst, R., Farber, H., Lindner, J., Mathier, M.,
McGoon, M., Park, M., Rosenson, R., Rubin, L., Tapson, V., & Varga, J. (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 in Collaboration with the American College of Chest
Physicians; American Thoracic Society, Inc., and the Pulmonary Hypertension Association.
Journal of the American College of Cardiology, 53(17), 1573-1619. doi:
10.1016/j.jacc.2009.01.004
Moser, D., & Riegel, B. (2008). Pulmonary hypertension and the cardiovascular system. In D.
Lee, Cardiac Nursing: A Companion to Brunwald’s Heart Disease (pp.1335-1346). St.
Louis, Missouri: Saunders Elsevier.
CASE STUDY #1 AND #2
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Needham, E. (2005). Management of acute renal failure. American Family Physician, 72(9),
1739-1746. Retrieved from http://www.aafp.org/afp/2005/1101/p1739.pdf
Schrier, R. (2011). Diagnostic value of urinary sodium, chloride, urea, and flow. Journal of
American Society of Nephrology, 22(9), 1610-1613. doi:10.1681/ASN.2010121289
Workeneh, B., & Batuman, V. (2013). Acute kidney injury. Medscape Reference Drugs,
Diseases & Procedures. Retrieved from http://emedicine.medscape.com/article/243492differential.