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Running head: CASE STUDY #1 AND #2 1

Case Study #1 and #2

Lindsey Moeller

Wright State University College of Nursing & Health

CASE STUDY #1 AND #2 2

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


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 right-

side 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 non-

specific 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


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


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


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


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.


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 PDI-

5, 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.


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


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


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,


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


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-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 reportMonitor 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


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

perL (mmol per L)

<10 (10) >20 (20)

Urine sediment Hyaline Casts Granular Casts

(Needham, 2005)


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