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Running head: COMPREHENSIVE CASE 1

Comprehensive Clinical Case Study

Laura Langenhop

Wright State University

COMPREHENSIVE CASE 2

Comprehensive Clinical Case Study

Patient Information

R.D. is a 21 year-old Caucasian male

Source

Patient

Chief Complaint

Diarrhea, vomiting, chest pain, and shortness of breath for three days

History of Present Illness

R. D. is a 21 year-old male seen on hospital day 1 by the cardiac critical care service.

R.D. presented today with vomiting, diarrhea, chest pain, myalgia, and shortness of breath that

began three days ago. The patient stated he was eating pizza and afterwards became sick,

believing the symptoms to be related to the food ingested. Since then, the patient has continued

to experience myalgia, shortness of breath, and chest pain. The chest pain is pleuritic in nature

and worse on palpation of the anterior wall. The patient has rated the chest pain as a 5/10. The

patient has not tried any over-the-counter medications to alleviate the pain. Taking in deep

breaths makes the chest pain worse according to the patient. The patient is also a known

intravenous drug user (IDU) and he reported having emergency services called to his home two

weeks ago following a heroin overdose. According to previous records, the patient required two

doses of Narcan at the time of the overdose by an emergency medical technician (EMT). In the

emergency room, the patient had a bedside abdominal ultrasound that revealed no evidence of

gallstones or hepatomegaly. There was splenomegaly found on the ultrasound. Upon his arrival

to the ICU, the patient was given Phenylephrine for hypotension, along with a 500 mL Lactated

Ringer (LR) intravenous bolus. The patient had two peripheral blood cultures drawn and was


started on prophylactic antibiotics. The patient was ordered a transthoracic echocardiogram that

revealed evidence of vegetation on the tricuspid valve, the right atrium, raising concern for the

possibility of an infected automatic implanted cardiac defibrillator (AICD) and pacemaker.

Medical History

Hypertrophic Obstructive Cardiomyopathy (HOCM)

Depression

Surgical History

Pacemaker/AICD implantation in 2010

Inner ear surgery: Tube to right inner ear in 2000

Family History

Father: N/A (not present)

Mother: Alive. The mother has no current medical issues

Siblings: None

Social History

Cigarettes: 0.5 packs daily over the last three years

Recreational Drugs: Patient uses marijuana daily. The patient also uses heroin on occasion. The

patient states that the heroin used two weeks ago was the first in six months.

Allergies

No known drug allergies

Home Medications

Seroquel 400 mg by mouth at bedtime

Mirtazapine 15 mg by mouth at bedtime

Verapamil 20 mg by mouth BID


Oxycodone-Acetaminophen 5-325 mg one tablet by mouth Q6 hours PRN

Current Medications

Phenylephrine gtt infusing @ 100 mcg/min

Lactated Ringers infusing @ 125 mL/hr

Vancomycin intravenous 1 gram Q8 hours

Heparin subcutaneous 5,000 units Q8 hours

Pantoprazole 40 mg by mouth daily

Potassium chloride intravenous supplementation per replacement protocol

Magnesium sulfate intravenous supplementation per replacement protocol

Seroquel 400 mg by mouth

Review of Systems (ROS)

(At time of Admission)

General: The patient reports fatigue, malaise and fever. The patient denies experiencing

chills, night-sweats, or sleep disturbances.

Neurological: Patient denies dizziness, syncope, or headache. Patient denies confusion, speech

problems, visual changes, or memory loss.

HEENT: Patient denies visual changes, a sore throat, a cough, hearing loss, problems with

speech, or nasal drainage.

Neck: Patient denies lymphadenopathy or tenderness of the neck.

Respiratory: Patient presents with dyspnea reported as pleuritic and worse on inspiration.

Patient denies hemoptysis, wheezing, or orthopnea. Patient denies any sputum

production.


CV: Patient complains of pleuritic chest pain as described above. Patient denies

palpitations, syncope, or tachycardia.

Abdomen: Patient complains of experiencing nausea, vomiting, and diarrhea over the last

couple of days. Patient denies having a difficult time eating, chewing, drinking,

or swallowing. The patient states he has lost weight unintentionally due to the

vomiting and diarrhea of the last several days.

GU: Patient denies change in urinary frequency, urgency, or dysuria.

M/S: Patient denies joint pain, joint swelling, or muscle pain. The patient denies

problems with ambulating or problems with fine motor skills.

Skin: Patient denies ecchymosis, lesions, or trauma to the skin.

Psychosocial: The patient does have a history of depression and takes medication at home.

Currently, the patient feels anxious.

Physical Exam

Vital Signs:

Temperature 102.5 degrees

Blood Pressure 78/54 on arrival to the CVICU and 107/64 via arterial line (on

Phenylephrine)

RR 32

HR 100 bpm

SpO2 100%

General: This is a 21 year-old Caucasian male resting in bed in NAD.

Neurological: Patient is able to follow commands. Patient has intact cranial nerves II-VII.


HEENT: The patient’s skull is normocephalic and a-traumatic. There are no masses or

lesions palpated. The patient’s sclera are white. Conjunctiva are pink. PERRL

@ 3mm. The patient is without nystagmus, hemorrhages, or exudates. Tympanic

membranes are pearly grey bilaterally without erythema. Nasal mucosa is pink

and moist and septum is midline. Oral mucosa is pink, moist, and without

erythema.

Neck: The patient’s trachea is midline. The patient is without lymphadenopathy. The

neck is supple. JVD notes at 8 cm H20 on examination.

CV: Patient presents with a normal heart rate and regular rhythm. The patient has an

S1 and S2. An S3 is heard at the second intercostal space right sternal border. An

S4 is heard at the fifth intercostal space mid-clavicular line. The patient is

positive for Carvello’s sign. Brisk carotid upstrokes without bruits are noted.

The PMI is located at the fifth intercostal space eight centimeters lateral to the

mid-sternal line.

Respiratory: Patient presents with equal air entry. Lung expansion is equal. Patient presents

with noted tachypnea. Patient is without retractions, wheezing, or rhonchi.

Patient presents with rales in bilateral lower lobes. There is dullness to percussion

to both lower lobes of the lung fields. Patient is negative for tactile fremitus.

Abdomen: The abdomen is soft and non-distended. Bowel sounds are active throughout all

quadrants. The patient is negative for mass upon light, moderate, and deep

palpation. The patient is negative for costo-vertebral tenderness. The patient is

negative for hepatomegaly or splenomegaly on physical examination.


G/U: The patient is voiding clear/yellow urine from a Foley catheter. There is no

penile discharge.

M/S: The patient has full range of motion in all extremities with 2+ reflexes and is

symmetric.

Extremities: Peripheral pulses are 2+ and normal. No pedal edema is present. No clubbing or

cyanosis is noted. The patient’s capillary refill is less than three seconds.

Skin: Skin is warm and dry. Coloration is normal for ethnicity. Nails are without

cyanosis or clubbing.

Laboratory Findings:

Table 1: Complete White Blood Cell count and Renal Panel

Complete Blood Cell

Count(CBC)

Results Normal Values

Renal Panel Results Normal Values

WBC 15 3.8-10.8 K cells/mL

Sodium 133 135-146 mmol/L

RBC 4.68 3.8-5.1 M cells/mL

Potassium 3.8 3.5-5.3 mmol/L

Hemoglobin 13.7 11.7-15.5g/dL

Chloride 101 98-110 mmol/L

Hematocrit 38.4 35-40% CO2 21 21-23 mmol/L

MCV 82.1 80-100 fL BUN 14 7-25 mg/dL

MCH 29.2 27-33pg/cell

Creatinine 0.77 0.5-1.2 mg/dL

MCHC 34.2 32-36 g/dL Glucose 100 65-99 mg/dL

RDW 12.8 11-15% Calcium 8.5 8.6-10.2 mg/dL

Platelet 63 140-400 K/uL Phosphorous 1.6 2.5-4.5 mg/dL

MPV 12.3 7.5-11.5 fL Magnesium 1.6 1.5-2.5 mg/dL

Anion Gap 11 8-16 mEg/L


Albumin 3.7 g/dL 3.6-5.1 g/dL

Table 1 normal diagnostic values adapted from (Gomella, 2007) Clinician’s pocket reference 11th

edition. Garden Grove, CA: McGraw Hill

Table 2. Arterial Blood Gas and Coagulation studies

Arterial Blood Gas Results Normal Values

Coagulation Results Normal Values

pH 7.46 7.35-7.45 PT 13.9 12-13 seconds

pCO2 34 35-45 INR 1.1 0.8-1.2

pO2 78 80-100 mmHg

PTT 27.1 30-50 seconds

HCO3 24 22-26 mmol/L

Fibrinogen 455mg/dL

120-360 mg/dL

CO2 Content 23 23-27 mmol/L

BNP 2840 <100

Base Excess -3 -2 to 2 Lactic Acid 1.6 0.5-2.2

Carboxyhemoglobin

0.2 Unknown AST 31 U/L 0-35 U/L

Methoglobin 0.1 0-1.5 % ALT 39 U/L 0-35 U/L

Reduced Hemoglobin

1 0-5 % CRP 27.2 <0.3

% Hemoglobin 96 95-98 % Troponin 1 0.21 0-0.1 ng/mL

CK 36 mU/L 25-145 mU/L

Total Bilirubin

2.2 mg/dL 0.3-1.1 mg/dL

Direct Bilirubin

1.2 mg/dL <0.2 mg/dL

Indirect Bilirubin

0.7 mg/dL <0.8 mg/dL

Table 2 normal diagnostic values adapted from (Gomella, 2007) Clinician’s pocket reference 11th

edition. Garden Grove, CA: McGraw Hill


Diagnostic Findings

Initial blood cultures drawn peripherally revealed gram-positive rods with a final culture

noted as methicillin resistant staphylococcus aureus (MRSA). The chest radiograph completed

on admission to the CVICU determined the patient as having bilateral airspace disease with

noted pulmonary edema in the bilateral lower lobes. A computed tomography (CT) scan of the

chest revealed mild pulmonary congestion without pleural effusion or pneumothorax. The

cardiomediastinal silhouette was unchanged from a previous exam in 2011. There were no other

abnormalities seen. An EKG on admission revealed the patient to be in normal sinus rhythm

without ST-elevation. The EKG also revealed that the patient has left ventricular hypertrophy

and Q-waves of <40 ms in leads V5, V6, AVL, and lead one.

On admission to the CVICU, the patient had a transthoracic echocardiogram (TTE). The

aortic valve was without sign of vegetation, but did have trivial regurgitation. The mitral valve

was without vegetation, but there did appear to be a ruptured chordae that moved vigorously as

related to the systolic motion of the mitral apparatus. The left atrium was without thrombus.

The right atrium revealed large highly mobile vegetation from the superior vena cava (SVC) and

right atrium (RA) junction that extended to the right atrial cavity. The tricuspid valve showed

evidence of vegetation and thickness to the anterior leaflet. There was moderate tricuspid valve

insufficiency seen on the echocardiogram. The pulmonic valve was without vegetation or

concern for valve dysfunction.

Differential Diagnosis

The differential diagnoses for this patient are endocarditis related to IDU, a pulmonary

embolism, cholecystitis, pneumonia, and myocardial infarction. The first differential diagnosis

is infective endocarditis due to IDU. Infective endocarditis is infection of endovascular


structures of the heart (Nishimura et al., 2014). The populations in which endocarditis can be

seen are the elderly, IDU’s, patients with prosthetic valves, and patients with congenital

anomalies (Nishimura et al., 2014). The most common organisms associated with infective

endocarditis are staphylococcus and streptococci (Nishimura et al., 2014).

The patient is febrile, has growth of MRSA on blood cultures, has vegetation on the

tricuspid valve and RA, and has a recent history of IDU. The patient’s C-reactive protein (CRP)

and fibrinogen are also elevated leading to the finding of an inflammatory response (Baynes &

Dominiczak, 2014). All findings listed are major and minor criteria of the Duke Criteria

(Baddour et al., 2005). The Duke Criteria was created in 1994 to classify patients with probable

infected endocarditis. Bacteremia with a known organism and echocardiography are two major

criteria in diagnosing infective endocarditis (Baddour et al., 2005). The patient’s fever, chest

pain, and history of IDU are minor criteria for diagnosing infective endocarditis (Baddour et al.,

2005).

The major risk factor for this patient in acquiring endocarditis is his known IDU.

Seventy percent of patients with endocarditis related to IDU show growth of MRSA on their

blood cultures (Nishimura et al., 2014). In a patient with endocarditis related to IDU, the classic

valve involved is the tricuspid valve. The pulmonic valve is usually not involved due to a lower

pressure gradient (Nishimura et al., 2014). The left sided heart valves (i.e. mitral and aortic) are

involved 40% of the time. In this specific case, only the tricuspid valve and RA show

vegetation. Normally, valve endothelium is immune to circulating bacteria. When endothelium

is disrupted, there is exposure of the underlying matrix proteins, tissue factor, platelets, and fibrin

(Habib et al., 2009). The exposure allows for bacteria to colonize causing infective endocarditis

(Habib et al., 2009).


The second differential diagnosis is pulmonary embolism (PE). The diagnosis of PE

alone is unlikely primarily because the patient presented with a fever and vegetation was found

on the echocardiogram. Suspicion of a PE is based upon the patient’s symptoms of chest pain,

shortness of breath, and young age (Saha & Rao, 2014). Since the patient is likely to have

infective endocarditis involving the tricuspid valve due to IDU, the ACNP should remain

concerned for risk of septic emboli (Baddour et al., 2005). Septic embolization can occur prior

to the start of anti-microbial therapy and can pose a risk during the first month of therapy

(Baddour et al., 2005). To rule out the diagnosis of a septic PE, the ACNP must order a

computed tomography (CT) scan (Saha & Rao, 2014).

The third differential diagnosis is acute cholecystitis. Cholecystitis is sudden

inflammation of the gallbladder (Welch, Chukwumah, Bowens, Arnell, & Ferri, 2011). This

inflammation can cause epigastric pain, sometimes described as chest pain. The patient’s first

symptoms were nausea and vomiting. Leukocytosis and a fever are typically present in a patient

with choleycystitis (Welch et al., 2011). Patients may have either calculous (with gallstones) or

acalculous (without stones) cholecystitis (Welch et al., 2011). The patient stated that he was

eating a pizza before his symptoms began, which poses the possibility of a gastrointestinal

problem. The patient however has a negative abdominal ultrasound and no history of having gall

bladder problem. The patient does not have abdominal pain specific to the right upper quadrant

and does not have a positive Murphy’s sign. These findings along with the TEE report suggest

another etiology (Welch et al., 2011).

The next differential diagnosis is pneumonia. Symptomology of pneumonia includes

chest pain, shortness of breath, and fever (Godara, Hirbe, Nassif, Otepka, & Rosenstock, 2014).

Due to the patient’s age and onset of symptoms, the pneumonia would be considered atypical.


Atypical pneumonia is of the mycoplasma, chlamydia, and legionella species. Other signs and

symptoms for pneumonia are a productive cough, coarse chest crackles, and bronchial breath

sounds (Godara et al., 2014). Though the patient has chest pain, shortness of breath, and fever,

he does not have sputum production and his chest radiograph was negative for atelectasis. Also,

the patient’s chest pain and shortness of breath most likely are related to HOCM and to the

patient’s probable endocarditis (Godara et al., 2014).

The last differential diagnosis would be a non-ST segment elevated myocardial

infarction. A myocardial infarction results from lack of blood and oxygen supply in the

myocardium (Chyu & Shah, 2014). The lack of blood supply and increase in oxygen demand are

a result of a ruptured atherosclerotic plaque. This patient’s risk factors for developing an MI

include his history of IDU, his daily cigarette smoking, and his history of HOCM. The patient

has no other typical risk factors such s coronary artery disease, obesity, and hypertension (Chyu

& Shah, 2014). Patients typically report chest pain that can radiate, shortness of breath, and

diaphoresis. Chest pain usually lasts 15-30 minutes, but may last longer (Chyu & Shah, 2014).

If the patient does not have chest pain on physical examination, the assessment may be

completely normal. In the presence of chest pain, the patient may have an S3 or S4 heart tone,

rales noted from left ventricular failure, and the patient may be visibly short of breath (Chyu &

Shah, 2014).

Electrocardiogram (ECG) findings in a patient with a myocardial infarction reveal T-

wave inversion or depression, ST changes, and may possibly show left ventricular hypertrophy.

Patients with a NSTEMI will also have elevated cardiac biomarkers (i.e. Troponin, CKMB,

BNP, CRP) without the presence of Q-waves on the EKG (Chyu & Shah, 2014). The patient in

this case has a mildly elevated Troponin, a normal CKMB, and an elevated BNP, Fibrinogen,


and CRP. The patient does have Q-waves <40 ms in the septal leads, but the most likely

rationale for this finding is the patient’s septal hypertrophy related to HOCM (Baddour et al.,

2005). Though one cannot fully exclude unstable angina, it is most unlikely. However the

patient’s increased inflammatory markers are related to infective endocarditis and the physical

examination findings are related to his existing HOCM diagnosis. The patient should have serial

Troponin-1 levels drawn to exclude the diagnosis of a NSTEMI (Chyu & Shah, 2014).

Diagnostic Tests and Rationale

CT of Chest

A computed tomography (CT) scan of the chest is a key diagnostic test in the health

management of this patient. A chest CT will not diagnose infective endocarditis as blood

cultures, echocardiography, and symptoms will. A CT scan will, however, help in diagnosing

any septic emboli that have traveled in the lungs. The patient presented to the hospital with chest

pain and shortness of breath. When a patient has shortness of breath in conjunction with

infective endocarditis, it is recommended to gather a chest CT to rule-out emboli (Baddour et al.,

2005). A spiral CT scan is completed during a single held breath in order to eliminate artifact.

A spiral CT has prominent vascular opacification (Saha & Rao, 2014). A better visualization is

seen with the use of intravenous contrast, though in some patients this may not be possible due to

renal function. The chest CT has a sensitivity of 83% and specificity of 96% with a positive

predictive value of 96% (Saha & Rao, 2014).

CT of the Abdomen

As noted, a CT of the abdomen or chest would not diagnose infective endocarditis in

patients. However, a CT is used to rule out embolization due to the vegetation found on the

echocardiogram. Patients with suspected infective endocarditis are also at risk for a splenic


infarction or abscess (Baddour et al., 2005). The infarction and abscess formation are related to

septic embolization of bacteria traveling to the spleen. The majority of splenic infarction and

abscess formations originates from left sided endocarditis. Though splenomegaly is typically

seen in 30% of the cases, splenomegaly may not be present. A CT of the abdomen has a 90-95%

sensitivity and specificity for diagnosing a splenic infarction and abscess (Baddour et al., 2005).

Transthoracic Echocardiogram (TTE) & Trans-esophageal Echocardiogram (TEE)

With a patient suspected of having infective endocarditis, the ACNP has to visually

assess an echocardiogram. When suspicion of infective endocarditis remains low, a TTE is

typically completed first. However, when the TTE is negative for signs of endocarditis, but

suspicion remains high, a TEE is recommended (Baddour et al., 2005). The American College of

Cardiology recommends a TEE for viewing vegetation and valve abnormalities as opposed to a

transthoracic echocardiogram (Baddour et al., 2005). There are three findings on an

echocardiogram that suggest infective endocarditis: valvular vegetation, abscess, and dehiscence

(Gersch et al., 2011). The TTE has a sensitivity of 40-63% whereas a TEE has a sensitivity of

90-100% (Gersch et al., 2011). False negatives may appear in the presence of vegetation too

small to see on the echocardiogram. False positives can occur when there are valvular

abnormalities suspected from endocarditis (Baddour et al. 2005). It is a Class one, Level A

recommendation that patients with an original positive transthoracic echocardiogram have a

trans-esophageal echocardiogram if suspicion for infective endocarditis and cardiac compromise

remains high (Baddour et al., 2005).

Aerobic and Anaerobic Blood Cultures

In diagnosing a patient with infected endocarditis, one of the most substantial tests is the

blood culture. Prior to starting antibiotic therapy for this patient, three sets of blood cultures


should be obtained (Owens and Fowler, 2012). To avoid contamination, two separate sites

should be used with peripheral draws recommended. Serial draws during antibiotic therapy are

recommended in order to detect the eradication of the organism. Up to 50% of blood cultures are

falsely positive in results while five percent report as falsely negative (Owens & Fowler 2012).

The false-positive blood cultures can depend on the virulence of the organism. Growth of

MRSA is always significant, where growth of coagulase negative staphylococci is typically

considered contaminated (Owens & Fowler, 2012).

Culture negative infective endocarditis is seen in 2.5-30% of patients with infective

endocarditis (Gersh et al., 2011). Organisms that may cause culture negative endocarditis

include Brucella species, Coxiella Burnetii, Bartonella species, Tropheryma Whipplei,

Mycoplasma species, and Legionella species (Gersh et al., 2011). In patients with suspected

endocarditis and negative blood cultures, the need for additional microbiology, such as growth of

uncommon microbials on a chocolate agar plate, may be warranted (Gersh et al., 2011).

Treatment of patients should not be delayed even when blood cultures remain negative (Baddour

et al., 2005).

Abdominal Ultrasound

The patient presented to the emergency department with a three-day history of nausea,

vomiting, and diarrhea. The patient also had chest pain, fever, and slightly elevated bilirubin

levels associated with the nausea and vomiting. Along with the TTE, the patient also should

have an abdominal ultrasound to rule out gall bladder disease (Carey, Arnell, Lee, & Scherger,

2011). The initial test of choice for ruling out gall bladder disease is the abdominal ultrasound

(Carey et al., 2011). The abdominal ultrasound has a sensitivity of 95% and a specificity of 90%

in detecting biliary sludge and gallstones (Carey et al., 2011). False positives occur from artifact


from distended bowel loops and calcium bile salt precipitates (Carey et al., 2011). False

negatives occur from gallstones that are too small to see on an ultrasound (Carey et al. 2011).

The patient did have normal liver function tests, but 10-15% of patients may have

choledocholithiasis in the absence of elevated liver enzymes (Carey et al., 2011). For this

reason, an abdominal ultrasound should be ordered.

Prioritized Plan

Treating a patient with infective endocarditis begins with treating the underlying cause.

The blood cultures drawn on admission revealed MRSA growth. Vancomycin is the medication

of choice in treatment of infective endocarditis with positive MRSA growth and is considered a

Level 1B recommendation (Baddour et al., 2005). The dosage recommended for the treatment of

infective endocarditis is 30mg/kg divided into two to three doses per day (Baddour et al., 2005).

In the state of Ohio the acute care nurse practitioner (ACNP) with a certificate to prescribe (CTP)

is able to prescribe Vancomycin per institutional standards (Ohio Board of Nursing, 2014).

The patient required insertion of a right intra-jugular line for monitoring central venous

pressure (CVP) and fluid status. The goal CVP for a patient with sepsis is between 8-12 mmHg

(Dellinger et al., 2012). The patient was started on a lactated ringer infusion at 125 mL/hr versus

normal saline to prevent hyperchloremic acidosis (Dellinger et al., 2012). The ACNP is careful

to monitor fluid status in this specific patient due to the fact that he has an increased risk of

becoming volume overloaded secondary to HOCM and the left ventricle’s inability to eject blood

from the outflow tract (Baddour et al. 2005). The patient initially presented with hypotension

most likely related to sepsis given the patient’s bacterial growth, temperature, tachycardia, and

known source of infection (Dellinger et al. 2012). The patient was started on a Phenylephrine

infusion, the vasopressor of choice for a hypotensive patient with HOCM who does not respond


to fluid resuscitation (Gersh et al., 2011). Phenylephrine is an alpha agonist producing systemic

vasoconstriction (Marino, 2014). By increasing afterload in a patient with HOCM, the coronary

arteries can be perfused. The goal mean arterial pressure for this patient is > 60 mmHg

(Baddour et al., 2005). In the state of Ohio, the ACNP with a CTP can prescribe Phenylephrine

(Ohio Board of Nursing, 2014).

The patient was ordered repeat blood work to monitor renal function and to trend the

complete blood cell count. The patient was also ordered mixed venous saturation every twelve

hours to view tissue oxygenation with a goal greater than 65% (Dellinger et al., 2012). A Foley

catheter was also placed to record and monitor urine output. The goal urine output for this

patient would be 0.5mL/kg/hr (Dellinger et al., 2012).

The AICD was shown on the CT scan of the chest to have a pocket of fluid, most likely

an abscess, surrounding the AICD wires. The patient was taken to the operating room to have

the AICD removed. The removal of the AICD eliminates one source of infection. In the

operating room, the patient received three liters of LR. On admittance back to the CVICU

following the operating room, the patient developed increased shortness of breath and agitation.

The patient was placed on a 15-liter non-rebreather mask for decreased oxygen saturations. An

arterial blood gas was performed and results include a pH of 7.50, PCO2 20, HCO3 21, PO2 66,

SpO2 of 84, and a lactate of 5.5. The chest radiograph revealed pulmonary edema. The patient

was intubated due to respiratory failure likely to flash pulmonary edema. The patient was also

febrile on admittance from the OR at 102.8 degrees Fahrenheit.

The patient was placed on pressure support ventilation with a PEEP of 6 and a pressure

support of 10. The patient was given 40 mg intravenous furosemide for flash pulmonary edema

per guideline recommendation (Hunt et al., 2009). A Fentanyl infusion was initiated for


discomfort related to the AICD extraction at a rate of 50 mcg/hr with an as needed Fentanyl

order for 50 mcg every two hours for increased agitation and sedation. The patient was also

placed on a Propofol infusion with titration orders 10-100 mcg/kg/min for a RASS of negative

two. The patient had a nasogastric tube placed for oral medication administration.

Acetaminophen was given for the patient’s fever. The Phenylephrine infusion will continue to

maintain a MAP greater than 60 mmHg. The patient was changed to a Normosol infusion at 100

mL/hr to maintain hemodynamic stability in light of the patient’s sepsis etiology and increased

lactate. In the state of Ohio, the ACNP with a CTP can prescribe Normosol, Fentanyl, and

Propofol per institutional standards (Ohio Board of Nursing, 2014).

The patient will remain on deep vein thrombosis (DVT) prophylaxis with 5,000 units of

Heparin administered subcutaneously every eight hours. The patient was started on peptic ulcer

prophylaxis with intravenous pantoprazole 40 mg daily. The patient will continue with the

intravenous Vancomycin for MRSA coverage and receive 650 mg of Acetaminophen via the NG

tube for the patient’s fever. In the state of Ohio, the ACNP with a CTP may prescribe Heparin,

Pantoprazole, lactated ringers, Acetaminophen and Phenylephrine (Ohio Board of Nursing).

Follow-up

The completion of antibiotic therapy depends on negative blood cultures results. Blood

cultures should be drawn every two to four days until negative. For this patient, once negative

blood cultures result, it is recommended continuing with four weeks of Vancomycin therapy

(Habib et al., 2009). Patients who have a diagnosis of infective endocarditis remain at a high risk

for relapse. It is a Class IIb, Level C recommendation to have a repeat transthoracic

echocardiogram following completion of treatment (Baddour et al., 2005).


Another issue that can occur during therapy is a fever that will not subside. Typically, a

patient can normalize the fever within five to ten days of treatment (Habib et al., 2009). A

persistent fever during therapy can mean inadequate antibiotics, resistance to antibiotics, infected

central lines, and spread of infection. In the event of a persistent fever, intravenous lines should

be changed and the patient should be re-cultured to look for new growth (Habib et al., 2009). An

echocardiogram should also be obtained in order to assess the patient’s valves and look for new

growth or abscesses (Habib et al., 2009). Finally, serial ECG’s should be performed in order to

assess conduction changes that can occur perivalvular abscesses (Baddour et al., 2005).

Patients with infective endocarditis may need valvular surgery depending on the course

of treatment and the function of the affected valve. In light of anti-microbial therapy, valvular

surgery may be warranted in the presence of heart failure caused by valvular insufficiency.

When there is valvular dehiscence, rupture, fistula, or perforation, or when there is a perivalvular

abscess seen on echocardiogram, there is Level B evidence for the replacement or repair of the

valve (Baddour et al., 2005). Valvular surgery is also recommended when persistent fever

occurs for more than a week within the use of a proper antibiotic regimen and when all other

rationale for fever has been excluded (Habib et al., 2009).

A patient’s systemic embolization is another concern for the ACNP. A patient, who has a

vegetation of greater than 10 mm in diameter, more commonly on the mitral valve, has an

increased risk for embolization. The decision to repair the affected valve is related to the

likelihood of system embolization (Baddour et al., 2005). The patient is also at risk for multi-

organ system failure (Thuny, Grisoli, Collart, Habib, & Raoult, 2012). The ACNP needs to

follow daily laboratory work including a complete blood cell count, renal function, and arterial

blood gas (ABG). The ACNP should perform daily assessments on this patient and remain in


close communication with the nurses on any changes in the patient’s neurological, renal,

pulmonary, or cardiac status (Thuny et al., 2012).

Once he is stable, extubated, and can be managed in an outpatient setting, there is

consideration on how to deliver antibiotics to this patient who has a history of IDU. It is

recommended that a patient who is stable receive antibiotics via a peripherally inserted central

catheter (PICC) line (Baddour et al., 2005). Because this patient has a history of IDU, he cannot

go home because he poses a risk of injecting recreational medications into the PICC line. The

ACNP will need to work with the unit social worker or case manager to see if the patient can

either qualify for a short-term nursing facility or can enter into a drug and alcohol treatment

facility (Baddour et al., 2005; Godara et al., 2014). If there is a chance the patient can be

managed with an oral antibiotic, then the ACNP can attempt to send the patient home with a

responsible caregiver (Baddour et al., 2005).

Health Promotion Activities

It is very important to promote health and wellbeing to the patient. While the patient

remains intubated and sedated, the ACNP should promote health and wellbeing by ordering VAP

prevention including elevating the head of the bed 30 degrees and ordering mouth care to be

performed every four hours (Isakow & Kollef, 2012). The patient will be placed on peptic ulcer

prophylaxis while intubated and without enteral nutrition. Finally, the patient is ordered

subcutaneous Heparin and sequential compression devices to promote deep vein thrombosis

prophylaxis (Isakow & Kollef, 2012).

The ACNP will wean the ventilator setting as the patient tolerates. As fluid from the

pulmonary edema is removed from his lung, the patient’s lung compliance will increase, making

it easier to wean the ventilator and extubate him (Isakow & Kollef, 2012). Once extubated, the


patient will work with physical and occupational therapy to prevent deconditioning (Isakow &

Kollef, 2012).

Nutrition is also an important factor in the health of this patient. While the patient is

intubated, the patient should have a nasogastric tube placed in order to initiate trophic feeds. The

goal for this patient is to receive low dose feeding with 500 kcal per day following 48 hours of

the sepsis diagnosis (Dellinger et al., 2012). The low dose feeding will help with gut motility

and wound healing. The feeds will then be advanced as tolerated. The patient is a young

individual and the goal is to be extubated once the pulmonary edema subsides. Once the patient

is extubated, the patient should be able to have a normal diet and able to swallow appropriately

with protein supplementation as needed (Dellinger et al., 2012).

Currently the patient smokes cigarettes daily. It is important this patient receives

adequate smoking cessation education (National Guideline Clearinghouse [NGH], 2008). The

patient can be given options and explanations on how to quit cigarette usage. Cessation of

smoking is crucial for this patient, not just for this disease, but also to prevent other co-

morbidities in the future (NGH, 2008). Smoking is attributed to cancer, heart disease, and

pulmonary diseases such as emphysema and chronic obstructive pulmonary disease (NGH,

2008). It is the responsibility of the ACNP to educate the patient on the risks of smoking as well

as the benefits for quitting.

This patient has a history of IDU. When considering health promotion for this individual,

the ACNP begins with the root of the issue. The patient is a recreational heroin user who

recently suffered a heroin overdose. Admittance to an inpatient drug and alcohol rehabilitation

center is a valid suggestion (Baddour et al., 2005). Since the patient is at an increased risk for

acquiring endocarditis in the future, offering the patient an outlet to cease IDU activity is crucial.


Also, the patient is at an increased risk for death if he continues using heroin on a recreational

basis Godara et al., 2014). A thorough conversation with the patient and his support system

should be completed in order to promote future health (Baddour et al., 2005).

As noted, the patient is at risk for a reoccurrence of endocarditis. Serial echocardiograms

up to twelve months following the diagnosis are recommended in order to assess valve function

(Thuny et al., 2012). Education is necessary for patients regarding signs and symptoms of

recurrent endocarditis including fever, chest pain, shortness of breath, and malaise. Patients

should be educated on the importance of good oral hygiene in prevention of endocarditis (Thuny

et al., 2012). In patients with a history of endocarditis, all dental and cardiac procedures require

antibiotic prophylaxis in order to prevent infective endocarditis (Baddour et al., 2005). In

patients with infective endocarditis, teaching good hygiene and offering behavioral education

may decrease the risk of endocarditis and are paramount in disease prevention and in promoting

wellbeing (Baddour et al., 2005; Thuny et al., 2012).


References

Baddour, L. M., Wilson, W. R., Bayer, A. S., Fowler, V. G., Bolger, A. F., Levinson, M. E., ...

Taubert, K. A. (2005). Infective Endocarditis. Circulation, 111, 3167-3184.

http://dx.doi.org/10.1161/_CIRCULATIONAHA.105.165563

Baynes, J. W., & Dominiczak, M. H. (2014). Blood and plasma proteins. In Medical

Biochemistry (4th ed.). Retrieved from https://www-clinicalkey-

com.ezproxy.libraries.wright.edu:8443/#!/ContentPlayerCtrl/doPlayContent/3-s2.0-

B978145574580700004X/{%22scope%22:%22all%22,%22query%22:%22C-reactive

%20protein%22}

Carey, W., Arnell, T., Lee, L., & Scherger, J. (2011, November 19). Cholelithiasis and

choledocholithiasis. First consult. Retrieved from https://www-clinicalkey-


1014767/{%22scope%22:%22all%22,%22query%22:%22Ultrasonography%20of

%20abdomen%22}

Chyu, K. Y., & Shah, P. K. (2014). Unstable angina/non-ST elevation myocardial infarction. In

M. H. Crawford (Ed.), Current diagnosis & treatment cardiology (4th ed.). Retrieved

from http://accessmedicine.mhmedical.com.ezproxy.libraries.wright.edu:2048/

content.aspx?bookid=715&sectionid=48214538&Resultclick=2

Dellinger, R. P., Levy, M. M., Rhodes, A., Annane, D., Gerlach, H., Opal, S. M., ... Moreno, R.

(2012). Surviving Sepsis Campaign: International guidelines for management of severe

sepsis and septic shock: 2012. Retrieved from Surviving Sepsis Campaign:

http://www.sccm.org/Documents/SSC-Guidelines.pdf


Gersh, B. J., Phil, D., Maron, B. J., Bonow, R. O., Dearani, J. A., Fifer, M. A., ... Yancy, C. W.

(2011). 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic

cardiomyopathy. Journal of American College of Cardiology, 58(25), e212-e260.

http://dx.doi.org/10.1016/j.jacc.2011.06.011

Godara, H., Hirbe, A., Nassif, M., Otepka, H., & Rosenstock, A. (2014). The Washington

manual of medical therapies (34th ed.). Philadelphia, PA: Lippincott Williams &

Wilkins.

Gomella, L. G. (2007). Clinician’s pocket reference (11th ed.). Garden Grove, CA: McGraw

Hill.

Habib, G., Tornos, P., Thuny, F., Pendergrast, B., Vilacosta, I., Moreillon, P., ... Zamarono, J.

(2009). Guidelines on the prevention, diagnosis, and treatment of infective endocarditis

of the European society of cardiology. European Heart Jouranl, 30, 2369-2413.

http://dx.doi.org/10.1093/eurheartj/ehp285

Hunt, S. A., Abraham, W. T., Chin, M. H., Feldman, A. M., Francis, G. S., Ganiats, T. G., ...

Yancy, C. W. (2009). 2009 focused update incorporated into the ACC/AHA 2005

guidelines for the diagnosis and management of heart failure in adults: A report of the

american college of cardiology foundation/American heart association task force on

practice guidelines . Circulation, 119, e391-e479.

http://dx.doi.org/10.1161/CIRCULATIONAHA.109.192065

Kollef, M., & Isakow, W. (2012). The Washington manual of critical care (2nd ed.).

Philadelphia, PA: Lippincott Williams & Wilkins.

Marino, P. L. (2014). The ICU book (4th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.


National Guideline Clearinghouse. (2008). Smoking cessation services in primary care,

pharmacies, local authorities and workplaces, particularly for manual working groups,

pregnant women and hard to reach communities. Retrieved from https://www-

clinicalkey-com.ezproxy.libraries.wright.edu:8443/#!/ContentPlayerCtrl/doPlayContent/

31-s2.0-12286/{%22scope%22:%22all%22,%22query%22:%22smoking%20cessation

%22}

Nishimura, R. A., Otto, C. M., Bonow, R. O., Carabello, B. A., Erwin, J. P., Guyton, R. A., ...

Thomas, J. D. (2014, March 3). 2014 ACC/AHA guideline for the management of

patients with valvular heart disease: a report of the American college of

cardiology/America heart association task force on practice guidelines. Circulation, 129,

2440-2492. http://dx.doi.org/10.1161/CIR.0000000000000031

Ohio Board of Nursing (2014). The formulary developed by the Committee on Prescriptive

Governance. Retrieved form

http://www.nursing.ohio.gov/PDFS/AdvPractice/Formulary_May-19-2014.pdf

Owens, T. A., & Fowler, V. G. (2012). Infective endocarditis. In S. C. McKean, J. J. Ross, D. D.

Dressler, D. J. Brotman, & J. S. Ginsberg (Eds.), Principles of practice and hospital

medicine). Retrieved from

http://accessmedicine.mhmedical.com.ezproxy.libraries.wright.edu:2048/content.aspx?

bookid=496&sectionid=41304184&jumpsectionID=41319227&Resultclick=2

Saha, S. A., & Rao, R. K. (2014). Pulmonary embolic disease. In M. H. Crawford (Ed.), Current

diagnosis & treatment cardiology (4th ed.). Retrieved from

http://accessmedicine.mhmedical.com.ezproxy.libraries.wright.edu:2048/content.aspx?

bookid=715&sectionid=48214563&jumpsectionID=48217987&Resultclick=2


Thuny, F., Grisoli, D., Collart, F., Habib, G., & Raoult, D. (2012, February 7). Management of

infective endocarditis: challenges and perspectives. Lancet, 379, 965-975.

http://dx.doi.org/10.1016/S0140-6736(11)60755-1

Welch, J. P., Chukwumah, C. V., Bowens, N., Arnell, T., & Ferri, F. F. (2011, August 31). Acute

cholecystitis. First Consult. Retrieved from https://www-clinicalkey-


1016248/{%22scope%22:%22all%22,%22query%22:%22Cholecystitis%22}