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Running head: Acute Severe Asthma 1 Comprehensive Clinical Case Study Michelle Nissen Managing Common and Acute Health Problems I, NUR 7201 Wright State University, CONH

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Page 1: Comprehensive Clinical Case Study Michelle Nissen Managing

Running head: Acute Severe Asthma 1

Comprehensive Clinical Case Study

Michelle Nissen

Managing Common and Acute Health Problems I, NUR 7201

Wright State University, CONH

Page 2: Comprehensive Clinical Case Study Michelle Nissen Managing

Acute Severe Asthma 2

History and Physical

Source

Patient, reliable source

Patient’s sister, reliable source

Chief Complaint

“I have been wheezing and short of breath for three hours”

History of Present Illness

A.B. presents to the emergency department with increasing shortness of breath and

wheezing. The patient is currently receiving therapy with an albuterol 2.5mg/3mL nebulizer

solution and can only talk in short sentences. Patient states that when she woke up last night with

an asthma attack and she used her rescue inhaler and put on her continuous positive airway

pressure (CPAP) machine and went back to sleep. When she awoke this morning she started

having increasing chest tightness and wheezing and she used her inhaler again. This helped for

about half an hour then the tightness started to come back and she had to use her inhaler again. In

the mean time she took her morning medications which include Prednisone five milligrams (mg)

and Claritin 10 mg. and Symbicort. She used the inhaler three more times without adequate

relief and then her sister drove her to the emergency department.

During initial intervention in the emergency department the patient has received three

doses of albuterol 2.5 mg per nebulizer, two doses of ipratropium 500 mcg. per nebulizer, 80 mg.

methylprednisone intravenously, and two grams of magnesium sulfate intravenously. Now

during examination, the patient reports some relief from therapy with the bronchodilators but is

still wheezing throughout all lung fields, experiencing shortness of breath and chest tightness.

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Acute Severe Asthma 3

The patient reports frequent use of her inhaler of at least once daily and states will wake up at

night with an exacerbation if she forgets to use her CPAP.

Medical History

The patient reports a nine year history of asthma requiring frequent use of rescue inhalers

(at least once a day) for management of symptoms, and night awakenings about two times

weekly. Other medical history includes: sleep apnea and the use of a continuous positive airway

pressure (CPAP) machine at night, morbid obesity, essential hypertension, anxiety, and

depression.

Surgical History

Non-Contributory

Family History

The patient’s mother has a history of depression and her father has a history of kidney

disease and diabetes. A.B. reports that her brother has a history of bipolar disorder, chronic pain,

hepatitis, and liver disease and her sister has a history of asthma and depression. Her maternal

grandmother died two years ago from a stroke and had a history of diabetes and seizures and her

maternal grandfather is alive with a history of diabetes. She has no information concerning her

paternal grandparents.

Social History

A.B. lives in a single story home with her three school age children. She is currently

unemployed due to her asthma and does not get out of the house very often. She reports a

smoking history of three packs daily for nine years, quitting in 2008 when she was diagnosed

with asthma. She denies drinking or illegal drug use and admits to eating whatever she can make

simply and on a low budget with her children. She states she is not currently dating and is not

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Acute Severe Asthma 4

sexually active and does not exercise. She states exercise is too difficult with her asthma and she

is afraid it will cause an attack. She is up to date on her childhood immunizations and reports

that she received the flu and pneumovax shots last fall when she was in the hospital.

Allergies

A.B reports allergies to neurontin, keflex, morphine, and ibuprofen all of which she states

causes her to break out in a rash.

Medications

Table One- Home Medications

Albuterol (Proventil) 2.5mg/3mL nebulizer

solution

Inhale three mL as needed every six hours for

wheezing

Albuterol (Proair HFA) 90mcg/actuation inhalation

aerosol

Inhale two puffs every 4 hours as needed for

wheezing

Budesonide-formoterol (Symbicort)

160-4.5mcg/actuation

Take two puffs two times daily

Loratadine (Claritin) 10mg. Tablet

Take one tablet by mouth daily

Prednisone 5mg. tablet

Take one tablet by mouth daily

Tussionex 8-10mg/5mL oral Take five mL by mouth every 12 hours as needed

for cough

Protonix 40mg tablet

Take one tablet my mouth daily

Benadryl 25mg tablet Take one tablet every six hours as needed

for wheezing

Lisinopril-hydrochlorothiazide (Zestoretic) 20-

25mg tablet

Take one tablet by mouth daily

Review of Systems

General: Denies fever, chills, weight changes, fatigue, malaise

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Acute Severe Asthma 5

Neurological: Denies syncope, seizures, headache, migraines, dizziness, numbness, confusion,

weakness, loss of consciousness, speech difficulties, falling, tremors.

HEENT: Denies vision changes, blurring, double vision, light sensitivity, hearing loss,

tinnitus, pain, discharge, change in taste or smell, sinus pain, runny nose, sore

throat, nose bleeds, hoarseness.

Neck: Denies stiff neck, swollen glands, difficulty swallowing.

Respiratory: Patient complains of wheezing and a dry cough that started about three hours ago.

She states her chest feels tight and she continues to have trouble speaking in full

sentences but has started to have some relief with the nebulizer treatments in the

emergency department. Denies any history of tuberculosis, hemoptysis, or any

sputum production or pain with respiration.

CV: Denies chest pain, palpitations, orthopnea, edema, claudication, hypertension,

difficulty with ambulation prior to asthma attack, any cardiac history, or stress

tests.

GI: Denies nausea, vomiting, diarrhea, constipation, heartburn, difficulty swallowing,

abdominal pain, hematemisis, or changes in stool frequency or consistency.

GU: Denies burning, itching, nocturia, frequency, urgency, hesitancy, urinary

incontinence.

M/S: Denies any joint pain, swelling, aching, restriction on movement, bony

deformities, or redness.

Skin: Denies any new rashes, sores or lesions, itching, pigmentation changes, unusual

hair growth.

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Acute Severe Asthma 6

Psychosocial: States has anxiety, nervousness and irritability during asthma attacks, and a

history of depression due to disease state. Denies any other mood changes,

difficulty concentrating, nervousness, tension, irritability, sleep disturbances, or

suicidal thoughts.

Physical Exam

Vitals: Temperature 99.2*F, Heart Rate: 120 Beats per minute- Sinus Tachycardia,

Respiratory Rate 25 breaths per minute, Blood Pressure 110/61mmHg, Oxygen

saturation 92 percent on four liters nasal cannula.

General: Patient is a well nourished, well developed, 32 year old African American female

in moderate respiratory distress. Patient is alert and oriented to person, place, time

and situation. She appears mildly agitated, with a disheveled appearance. Patient

is able to speak in phrases and is sitting upright leaning forward.

Neurological: All sensation intact, deep tendon reflexes two plus. Primary and cortical sensory

function is intact without deficits. Cranial nerves two through 12 are intact

without deficits.

HEENT: Cranium is normocephalic, atraumatic with appropriate symmetry. No lesions,

parasites, or masses noted. Eyes are equal round and reactive to light and

accommodation. Extraocular movement intact with no nystagmus. Ears are

appropriate shape with no drainage, tenderness or pain with palpations. Nose is

symmetrical, midline with a midline septum and no drainage. Oral mucosa is pink

and dry with no lesions, ulceration or trauma. No visual tonsils or adenopathy.

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Acute Severe Asthma 7

Neck: Neck is supple, without palpable lymphadenopathy or jugular venous distention.

The carotid arteries are two plus, equal without bruits. Trachea is midline and the

patient demonstrates full range of motion with nuchal rigidity.

Respiratory: Audible diffuse wheezes are heard in all lung fields. Breath sounds are decreased

in the bases bilaterally. No crackles or rubs appreciated. Respiratory excursion is

equal, symmetrical, mildly labored with use of accessory muscles and retraction

noted. Capillary refill is normal with no central cyanosis noted.

CV: Heart rate and rhythm regular with S1 and S2 present. No evidence of S3, S4,

clicks, gallops, murmurs or rubs. No evidence of pulses parodoxus. Point of

maximal impulse is not distinguishable due to body habitus. Peripheral pulses are

two plus in upper and lower extremities.

Abdomen: Abdomen is soft, non tender, symmetrical, without scars, lesions, rashes.

Normoactive bowel sounds in all four quadrants without venous hums, frictions

rubs or bruits. Liver, spleen and kidneys non palpable. No rebound tenderness,

guarding or masses noted.

M/S: Full range of motion in all joints without tenderness, deformity, erythema, edema,

ecchymosis, cyanosis, or clubbing. Strength is five of five bilaterally in upper and

lower extremities.

Skin: Skin is warm and dry with no obvious scars, lesion, or rashes.

Laboratory Findings

Table Two: Basic Metabolic Panel

Electrolyte Results Reference Range

Sodium 139 mEq/L 135-148 mEq/L

Potassium 4.7 mEq/L 3.4-5.3 mEq/L

Chloride 103 mEq/L 96-110 mEq/L

Carbon Dioxide 23 mEq/L 19-32 mEq/L

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Acute Severe Asthma 8

Blood urea nitrogen 14 mg/dL 3-29 mg/dL

Creatinine 1.1 mg/dL 0.5-1.2 mg/dL

Calcium 8.2 mg/dL 8.5-10.5 mg/dL

Albumin 3.5 gm/dL 3.5-5.2 gm/dL

Phosphorus 4.0 mg/dL 2.5-4.5 mg/dL

Blood Glucose 140mg/dL 70-100 mg/dL

Glomular Flitration Rate 60mg/dL 60-110 mg/dL

Table Three: Complete Blood Count

Hematology Result Reference Range

Hemoglobin 11.3 gm/dL 12.0-15.6 gm/dL

Hematocrit 34.2 % 35-46 %

White blood cell count 20.6 MILL/L 3.8-10.8MILL/L

Platelet 323 K/mm3 130-400 K/mm3

Table Four: Arterial Blood Gas

Result Reference Range

PH 7.32 7.35-7.45

PC02 48.4 mmHg 35-45 mmHg

P02 86 mmHg 80-100 mmHg

Oxygen Saturation 92% 92-100%

Base Excess -2.1 mmoL/L 0.0-3.0 mmoL/L

HC03 25.3 mEq/L 22-26 mEq/L

Diagnostic Findings:

Chest x-ray: no focal infiltrates. Cardiac silhouette is unremarkable.

Differential Diagnosis

The differential diagnosis for this patient could include vocal cord dysfunction or

paralysis, foreign body aspiration, laryngotrachael mass, tracheal narrowing due to

tracheomalacia or tracheobronchomalacia, chronic obstructive pulmonary disease (COPD),

bronchiectasis, left ventricular failure, pulmonary embolus, allergic bronchopulmonary mycosis,

cystic fibrosis, eosinophilic pneumonia, bronchiolitis obliterans, systemic vasculitis with

pulmonary involvement, emotional laryngeal wheezing, vocal fold dysfunction or episodic

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Acute Severe Asthma 9

laryngeal dyskinesis (Papadakis & McPhee, 2014). Many upper airway disorders such as vocal

cord dysfunction and laryngotrachael mass are differentiated from asthma by the area of

wheezing. These disorders will present with stridor and wheezing localized to the large airways

(Longo et al., 2012). This patient has wheezing throughout the lung fields. A foreign body

aspiration would present with wheezing localized to the specific area blocked by the obstruction

and would show up on x-ray. (Longo et al., 2012). Also, the patient does not have a history of

choking prior to the attack therefore it is unlikely to be a result of foreign body aspiration.

Trachael narrowing by tracheomalacia or tracheobronchomalacia is caused by the

posterior tracheal lumen bulging into the tracheal lumen on expiration. Wheezing is therefore

louder on expiration and would be limited to the upper airways (Leong, Bardin, & Lau, 2013).

This patient is experiencing wheezing throughout the respiratory cycle and is improving with

bronchodilator use making this an unlikely diagnosis. However, this disorder does mimic

asthma and COPD and can be difficult to diagnose. If this patient does not respond to treatment

or continues to have difficult to control asthma referral to a center with the ability to perform

dynamic computed tomography would be warranted for further investigation (Leong, Bardin, &

Lau, 2013). Bronchiectasis is not a likely diagnosis because this is accompanied by a persistent

productive cough with crackles in lower lung fields, both of which are not present in this patient

(Longo et al., 2012). A diagnosis of left ventricular failure is also unlikely as the patient does

not have a cardiac history, is not complaining of chest pain, does not have crackles per

auscultation and has a normal cardiac silhouette per chest x-ray.

Allergic bronchopulmonary mycosis is characterized by an allergic reaction to fungal

antigens colonized in the tracheobronchial tree. Symptoms include infiltrates on x-ray, central

bronchiectasis, and immediate skin reactivity to Aspergillus antigen. Treatment for allergic

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Acute Severe Asthma 10

bronchopulmonary mycosis includes oral corticosteroids which produce a marked improvement

(Papadakis & McPhee, 2014). This patient is currently on chronic steroid therapy for asthma,

therefore it is unlikely this is the cause of this patient’s presentation, however, testing for

reactivity to Aspergillus antigen if not already performed could be recommended to rule out this

disease process. Cystic fibrosis is unlikely in this patient due to the absence of productive cough,

history of pancreatic disorders, and infertility (Papadakis & McPhee, 2014). Eosinophilic

pneumonia presents as an acute illness including fever and purulent sputum, neither of which is

present in this patient (Papadakis & McPhee, 2014).

Bronchiolitis obliterans presents with increasing dyspnea and productive cough that

worsens over several weeks to months (Barker, Bergeron, Rom, & Hertz, 2014). This patient

lacks a productive cough and describes the onset of symptoms as acute in the last three hours.

Systemic vasculitis with pulmonary involvement usually present with systemic symptoms of the

vasculitis such as fever, malaise, joint pain, weight loss and rash. If the vasculitis involves the

small vessels of the lungs presentation may also include alveolar hemorrhage and hemoptysis

(O'Sullivan, 2012). This patient has no history of systemic vasculitis and lacks systemic

symptoms associated with this disease process. Vocal fold dysfunction does not respond to

bronchodilator therapy and therefore would not be an appropriate diagnosis in this patient

(Papadakis & McPhee, 2014). Emotional laryngeal wheezing and episodic laryngeal diskinesia

are also associated with stridor and wheezing contained to the upper airways making these

unlikely in a patient with diffuse wheezing throughout the lung fields (Longo et al., 2012).

COPD is another differential diagnosis, however, this patient is only 33 years old and

COPD does not usually present until the fourth or fifth decade. COPD also presents with either a

productive cough or evidence of hyperinflation per x-ray (Papadakis & McPhee, 2014). Neither

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Acute Severe Asthma 11

of these symptoms is present in this scenario making this diagnosis unlikely. The possibility of

pulmonary embolism also needs to be ruled out. Pulmonary embolism has nonspecific

symptoms such as wheezing, shortness of breath, tachypnea, tachycardia, and pleuretic chest

pain (Fedulle, Fuster, Walsh, & Harrington, 2011). This patient presents with all of these

symptoms except chest pain, therefore obtaining a D-dimer and possibly lower extremity

dopplers to look for deep vein thrombosis would not be inappropriate. The most likely diagnosis

in this patient is acute asthma exacerbation. The diagnosis of acute asthma exacerbation includes

breathlessness, wheezing, cough and chest tightness (Fanta, 2014). This patient is experiencing

all of these symptoms and has a known history of uncontrolled asthma and describes her

symptoms as consistent with other asthma exacerbations. In addition, the patient is responding

to albuterol inhalation treatments which are used to diagnose and evaluate reversibility of airway

obstruction in asthma. A positive response to bronchodilator therapy helps to confirm the

diagnosis of asthma (Papadakis & McPhee, 2014). Further studies including spirometry will aid

in confirming the diagnosis and evaluation of the degree of severity of the exacerbation.

Diagnostic Studies

Patients admitted to the emergency room with asthma symptoms should be quickly

evaluated with a short history and physical and symptoms (Figure1). Treatment should begin as

soon as possible for patient presenting with moderate, severe or life threatening exacerbations.

Further testing should be completed after initial therapy has been completed (Camargo,

Rachelefsky, & Schatz, 2009).

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Acute Severe Asthma 12

Figure 1- Evaluation of Asthma severity in the emergency care setting

The use of additional diagnostic studies indicated in this situation include testing to rule

out the possibility of a pulmonary embolus and testing to evaluate the severity of the asthma

exacerbation and drive further treatment. A d-dimer and lower extremity dopplers should be

obtained to rule out pulmonary embolus. A negative d-dimer has a high sensitivity to rule out PE

and lower extremity deep vein thrombosis is found in 90% of patients with a PE, therefore a

negative finding in both of these studies would make the diagnosis of PE unlikely (Torbicki et

al., 2008). However, if either of these tests returns positive results a computed tomography (CT)

Adapted from: National Asthma Education and Prevention Program, Expert Panel Report 3: Guidelines for the

Diagnosis and Management of Asthma. National Institutes of Health Publication 08-4051. Bethesda, MD,

2007. http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf

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Acute Severe Asthma 13

angiography should be performed. CT angiography has become the method of choice to

diagnose PE and has a specificity and sensitivity of 90 percent for PE.

This patient presents with moderate to severe case of asthma requiring immediate

treatment with albuterol, ipratropium, systemic corticosteroids and the use of magnesium sulfate.

Further testing should be performed to evaluate severity of asthma and drive treatment, including

spirometry to measure peak expiratory flow (PEF) and forced expiratory volume in one second

(FEV1), oxygen saturation, and arterial blood gas analysis (ABG). Peak flow measurement is

the best method of assessing the severity of an asthma attack and is also used to measure

response to treatment (Fanta, 2014). A measurement of PEF and/or FEV1 should be obtained

on arrival to the emergency department or 15 to 20 minutes after initial treatment if the patient is

stable enough to endure testing. In patients admitted to the hospital, once the patient is stable,

testing should be performed daily until discharge (Camargo, Rachelefsky, & Schatz, 2009). In

patients able to tolerate spirometry testing levels of FEV1 and PEF drive the course of treatment

with levels below less than 40 percent of baseline after treatment requiring admission to the

intensive care unit (Papadakis & McPhee, 2014). FEV1 measurements between 40 and 69

percent of predicted are considered moderate exacerbations. Patients with moderate

exacerbations who increase to over 70 percent with treatment are considered to have a good

response and may be sent home or to a regular floor (Camargo et al., 2009). At this point

spirometry has not been performed on this patient therefore the use of symptoms; pulse oximetry

and arterial blood gas analysis is driving treatment.

Continuous pulse oximetry is used to monitor for signs of hypoxia and for titration of

oxygen. Oxygen saturation below 90 percent on room air suggests life threatening asthma and

possible complications such as pneumonia or atelectasis (Fanta, 2014). This patient is requiring

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Acute Severe Asthma 14

four liters of oxygen to maintain an oxygen saturation of 92 percent. This is indicative of a

severe exacerbation. Arterial blood gas analysis is appropriate in patients unable to perform

spirometry or in which there is a possibility of hypoventilation. This patient presents with a BMI

of 40 and would be a risk for Pickwickian Syndrome therefore an ABG was obtained (Fanta,

2014). This patient’s ABG is indicative of a respiratory acidosis with PH of 7.32 and a PC02 of

48.2. In asthma exacerbations the respiratory drive is usually increased causing PC02 to be

decreased. The presence of hypercapnia signals severe narrowing of the airway and possible

impending respiratory failure and the need for mechanical ventilation (Fanta, 2014).

Other laboratory studies are performed to rule out causes or possible complications of the

exacerbation. A complete blood count would be helpful to look for signs of infection. A mild

leukocytosis is expected with an acute exacerbation of asthma but higher counts could signal

pneumonia especially if the patient presents with a fever or purulent sputum (Camargo,

Rachelefsky, & Schatz, 2009). This patient presents with a white count of 20.6mmHg which

points to the possibility of infection. Monitoring of electrolytes would be appropriate in patients

who take diuretics, or who have cardiac disease. The frequent use of short acting beta agonists

can cause a transient increase in potassium, magnesium and phosphate which could cause rhythm

problems in patients with cardiac compromise (US Department of Health and Human Services,

2007).

Measurement of theophylline levels would be appropriate in patients currently taking

theophylline to monitor for toxicity. Chest radiograph is usually not diagnostic in

uncomplicated asthma, however, it is appropriate in patients who have suspected

cardiopulmonary complications such as heart failure or pneumonia or in patients requiring

admission or with an uncertain diagnosis (Fanta, 2014). This patient’s chest x-ray is normal

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Acute Severe Asthma 15

which helps to rule out pneumonia and the possibility of cardiac disease. Electrocardiagram is

also only used in patients with coexisting cardiac disease or COPD to evaluate for signs of

cardiac ischemia (Camargo, Rachelefsky, & Schatz, 2009).

Plan

The course of treatment for asthma exacerbations is based on the history, physical

examination, PEF, FEV1, oxygen saturation, and response to treatment (Figure 2).

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Acute Severe Asthma 16

Figure 2: Management of Asthma Exacerbations

Adapted from: National Asthma Education and Prevention Program, Expert Panel Report 3: Guidelines for

the Diagnosis and Management of Asthma. National Institutes of Health Publication 08-4051. Bethesda,

MD, 2007. Papadakis, M. A., & McPhee, S. J. (2014). Current medical diagnosis and treatment (53 ed.).

New York, NY: McGraw-Hill.

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Acute Severe Asthma 17

This patient is improving per subjective information, however, is continuing to have

symptoms, and has a PC02 over 42mHg therefore the patient will be admitted to the intensive

care unit. The goal of therapy in the hospital is to correct any hypoxia, reversal of airflow

obstruction and reducing the risk of relapse and subsequent attacks (Pollart, Comptom, &

Elward, 2011). Hospital management of these disorders involves the use of inhaled short acting

beta agonists (SABA), inhaled anticholinergics, and systemic glucocorticoids (Fanta, 2014). The

use of inhaled short acting beta agonists is recommended by The National Asthma Education and

Prevention Program report (EPR3) for management of acute asthma exacerbations (Evidence

Category A) (Camargo, Rachelefsky, & Schatz, 2009). Inhaled short acting beta agonists

include albuterol and levalbuterol, bitolterol, pirbuterol, and terbutaline. These agents work by

stimulating the beta 2 receptors and activating the cyclic adenylyl- cyclase AMP-PKA pathway

which results in relaxation of bronchial smooth muscle (Barnes, Brunton, Chabner, &

Knollmann, 2011). Using the inhalation route as compared to systemic administration reduces

the side effects of the medication such as tachycardia and hypertension (Longo et al., 2012). The

most used inhaled beta agonists are albuterol 1.25 to five mg. and levalbuterol 0.63- 1.25mg.

During an acute exacerbation these agents will be given every 20 to 30 minutes for three doses

then every one to four hours as needed or continuously at 10 to 15mg per hour (Camargo,

Rachelefsky, & Schatz, 2009).

Short acting inhaled anticholinergics are recommended by the EPR3 for treatment of

acute asthma only after the use of short acting beta agonists (Evidence Category A) (Camargo,

Rachelefsky, & Schatz, 2009). The short acting inhaled anticholinergic ipratropium works by

preventing cholinergic nerve induced bronchoconstriction. This agent is also administered by

inhalation to reduce side effects (Longo et al., 2012). This medication is administered 250 to

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Acute Severe Asthma 18

500 mcg. per nebulizer three times twenty minutes apart for severe asthma then every six hours

while the patient is in the intensive care unit (Fanta, 2014). Systemic corticosteroids including

hydrocortisone and methylprednisone (intravenous) or prednisone (oral) are recommended by the

EPR3 for the treatment of acute asthma exacerbations (Evidence Category A) (Camargo,

Rachelefsky, & Schatz, 2009). These agents work by switching off the transcription of multiple

activated genes encoded for inflammatory proteins. While it is recommended to give systemic

steroids during an acute attack the mechanisms of action can take up to six hours to have an

effect (Longo et al., 2012). Therefore, recommendations include the use of oral steroids in

patient’s able to tolerate oral medication. In severe cases in which the patient cannot tolerate

oral medication the intravenous route is recommended (Papadakis & McPhee, 2014). Doses

range from 40 to 60 mg per day for oral prednisone and 60 to 80mg every six to 12 hours for

intravenous methylprednisone (Fanta, 2014).

Nonstandard therapies for the treatment of severe acute asthma include the use of

anesthetic agents, parental beta agonists, high dose inhaled corticosteroids, helium oxygen gas

mixtures and leukotriene receptor antagonists. Due to lack of insufficient evidence, these agents

are not currently recommended as first line treatment but in extreme cases when all other

avenues have been explored these agents should be considered (Evidence Category B)

(Camargo, Rachelefsky, & Schatz, 2009). Methylxanthines are no longer recommended for the

treatment of acute asthma. Inhaled beta agonists are more potent and the side effect profile adds

to an increase in adverse affects with their use. These agents are reserved for long term

management in patients who cannot gain control with other medications (Longo et al., 2012).

The EPR3 panel does not recommend the use of antibiotics unless evidence of infection

is present (Camargo, Rachelefsky, & Schatz, 2009). In this case, the patient presents with high

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white blood cell count but no other signs of infection. The patient admits to frequent emergency

room visits for asthma exacerbations with the last visit occurring two weeks ago. A.B. is also

receiving chronic steroid therapy with prednisone. While use of corticosteroids is associated

with an increase in serum white blood cell levels, this patient has been on chronic steroid therapy

and is currently being titrated down, making steroids the unlikely cause of the high white count.

Frequent contact with hospitals and immunosuppression put her at a higher risk for the

possibility of a healthcare associated infection. While her chest x-ray is not indicative of

pneumonia empiric treatment may be indicated due to her increased white count and number of

risk factors for the possibility of pneumonia. Current recommendations for the administration of

antibiotics for healthcare acquired pneumonia recommend the use of either a third or fourth

generation cephalosporin, beta lactam or beta lactamase inhibitor, carbapenen, or a

fluoroquinolone (Rotstein et al., 2008). Initial therapy will include pipercillin-tazobactam 4.5

grams every eight hours intravenously for seven days. Sputum cultures need to be obtained prior

to the start of therapy and results of the cultures should be followed and antibiotics changed or

discontinued based on the results of the cultures.

The guidelines for management of acute asthma also recommend the use of supplemental

oxygen to keep oxygen saturation above 92 percent (Camargo, Rachelefsky, & Schatz, 2009).

This can be accomplished by nasal cannula, facemask, noninvasive positive pressure ventilation

(NIPPV) or intubation and mechanical ventilation. The EPR3 panel recommends the use of

mechanical ventilation for patients who have a cardiac or respiratory arrest, altered mental status,

progressive exhaustion, silent chest, severe hypoxia, failure to reverse respiratory acidosis with

therapy, PH less than 7.2, PC02 increasing by more than five mmHg or over 55mmHg or P02 of

less than 60mmHg. (Evidence Category D) (Camargo, Rachelefsky, & Schatz, 2009). NIPPV

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Acute Severe Asthma 20

should be used in select patients who can tolerate this intervention and are in an area with close

supervision where immediate intubation could be performed if necessary (Evidence Category B)

(Camargo et al., 2009).

This patient has maintained oxygen saturation over 92 percent on four liters by nasal

cannula. She does not meet any other criteria for intubation and mechanical ventilation,

however, has not improved quickly with therapy and has an increased PC02 with respiratory

acidosis. The patient also admits to requiring the use of CPAP at home to sleep and is at a higher

risk for death due to her obesity. A trial of NIPPV should be instituted to reverse the respiratory

acidosis and avoid intubation. Settings for NIPPV are recommended by the EPR3 panel include

starting the expiratory pressure at three cm H2O and increasing it every 15 minutes until a level

of five is achieved, and starting the initial inspiratory pressure at eight cm H2O and increasing by

2cm H20 every 15 minutes to achieve pressure of 15cm H20 (Evidence Category D) (Camargo,

Rachelefsky, & Schatz, 2009).

Spirometry should be performed as soon as the patient can tolerate testing to evaluate

PEF and FEV1 for improvement after initiation of therapy, and 15 to20 minutes post

bronchodilator therapy while the patient continues signs consistent exacerbation. Once therapy

has been effective and the patient’s symptoms are abated spirometry should be performed daily

until discharge (US Department of Health and Human Services, 2007). Other therapies would

include close monitoring of physical findings including the continued use of accessory muscles,

retractions, labored breathing and lung sounds every hour in the intensive care unit. Assessment

of vital signs every hour to include heart rate, blood pressure, and respiratory rate. Assessment

of the patient’s temperature should be performed every four hours to evaluate for signs and

symptoms of infection. Continuous pulse oximetry with parameters to titrate oxygen to keep

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oxygen saturation above 92 percent and orders to notify physician for any required increases in

oxygen. Neurological assessments should be performed every two hours to monitor for any

decrease in mental status or changes in orientation with orders to notify physician of any deficits.

Evaluation of arterial blood gas measurements in one hour post therapy should be performed

with results called to the physician. Further arterial assessments will be based on response to

therapy (Camargo, Rachelefsky, & Schatz, 2009).

The patient also takes several home medications that need to be reviewed. Budesonide is

an inhaled corticosteroid and formoterol is a long acting beta agonist. These agents work to

control asthma and reduce the need for rescue inhalers (Papadakis & McPhee, 2014). These

agents will be continued in the hospital setting to reduce the risk of relapse and the need for short

term beta agonist use. Loratadine is a tricyclic antihistamine that works to prevent symptoms of

rhinitis and urticaria associated with seasonal allergies (Lexi-comp, 2014). This medication has

a drug interaction warning to avoid concomitant use with ipratropium (oral inhalation) and will

be discontinued while the use of ipratropium is required. Prednisone is an oral corticosteroid

recommended for use in long term asthma; however, this patient is currently receiving high dose

intravenous steroids for her acute exacerbation. This medication will be discontinued and will be

reevaluated at discharge.

Tussionex is an antitussive/antihistamine that works to reduce cough due to colds or

allergy. This medication can cause respiratory depression (Lexi-Comp, 2014). The EPR3

recommends avoidance of any medications that can cause sedation in patients with acute asthma

(Camargo, Rachelefsky, & Schatz, 2009). This medication also has a drug interaction with

ipratropium recommending the avoidance of concomitant use (Lexi-Comp, 2014) therefore this

medication will be discontinued and reevaluated at discharge. Protonix is a proton pump

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inhibitor used to reduce the production of acid and reduce symptoms of gastrointestinal reflux

disease. The use of proton pump inhibitors in patients with asthma has been found to produce a

small but significant improvement in morning PEF (Chan, Chiou, Obstein, Tignor, & Whitlock,

2011). This medication does not have any interactions with other medications being

administered and will be continued at 40mg taken orally once daily.

Diphenhydramine is another histamine antagonist that competes for the H1 receptor site

to reduce the symptoms of allergies caused by histamine release (Lexi-Comp, 2014). This

medication also causes respiratory depression and will be discontinued and reevaluated at

discharge. Lisinopril-hydrochlorothiazide is an angiotension converting enzyme combined with

a thiazide diuretic. This medication is used to control hypertension through disruption of the

renin-angiotension system and diuresis (Lexi-Comp, 2014). This patient’s blood pressure has

been stable and laboratory findings are not indicative of any problems with this medication.

However, the use of ACE inhibitors can cause an increase in potassium, and the use of SABAs

can cause a transient increase in potassium which would have to be monitored during treatment

with both of these medications. This medication will be continued at however, daily basic

metabolic panels will be ordered to monitor for increases in potassium, and blood pressure

measurements will be taken hourly to monitor for signs of hypotension.

This patient presents with a blood sugar of 140mg/dL and is going to have high dose

steroid therapy. Therefore, blood sugar should be monitored before every meal and at bedtime

and sliding scale insulin using the following scale (Table 6) should be instituted as necessary to

maintain a target blood sugar between 100mg/dL and 139mg/dL. With a blood sugar of

140mg/dL this patient is considered pre-diabetic and should have a glycated hemoglobin

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(HbA1c) level obtained while in the hospital to assess for the presence of diabetes (The

American Diabetes Association, 2013).

Table 5: Sliding Scale Insulin

Blood Sugar Level Insulin

150-199 mg/dL 1 unit

200-249 mg/dL 2 units

250-299 mg/dL 3 units

300-349 mg/dL 4 units

350-399 mg/dL 5 units

Over 400 mg/dL Notify Physician Adapted from: Effects of subcutaneous insulin protocol, clinical education, and computerized order set on the

quality of inpatient management of hyperglycemia: Results of a clinical trial, Journal of Hospital Medicine, DOI

10.1002/jhm.385, 2009

Laboratory data to assess potassium should be performed in six hours to monitor for

increases in potassium while frequent SABA administration is needed. Complete blood count

should be monitored daily for evaluation of white cell count to monitor for response to antibiotic

therapy. Chest x-ray should be obtained in AM to assess for any signs of pulmonary infiltrate

or other signs of pneumonia that might point to the cause of the high white count. Urinalysis

should be performed to assess for urinary tract infection being the cause of the high white count.

The patient should remain on bed rest with bathroom privileges while requiring NIPPV therapy

but be allowed to get out of bed to chair once symptoms have improved to the point of no longer

needing NIPPV. In the event of respiratory failure intubation with mechanical ventilation would

be the next step. During a severe exacerbation of asthma intubation can be difficult and this

decision needs to be made carefully. If intubation is unattainable the patient could be taken to

the operating room for an emergent criciodotomy and placement of a tracheostomy tube would

be necessary.

Nurse practitioners in Ohio have the authority to prescribe all of the above medications

and therapies (Ohio Board of Nursing, 2014).

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Health Promotion

This patient has a history of very poorly controlled asthma and obesity. She also admits

to not exercising due to fear of an asthma attack. Education prior to discharge should include:

proper inhaler use, asthma self monitoring and self management education, an individualized

action plan, trigger identification with avoidance strategies, and additional follow up planning

(Camargo, Rachelefsky, & Schatz, 2009). This patient would also benefit from education

concerning diet and weight loss. Obesity has been found to increase asthma symptoms and to

affect the patient’s response to medication. Obese patients with asthma have longer stays in the

emergency department and are admitted more often for exacerbations (Moreira et al., 2013).

This patient also has pre-diabetes per laboratory data and high blood pressure. Education on diet

and weight loss could help with all of these disease processes. A.B also states she has a fear of

exercising due to flare ups. Education concerning strategies such as choosing sports with low

minute ventilation, warming up before exercise, wearing a heat exchange mask, and using a short

acting beta agonist or inhaled corticosteroid could help the patient to start an exercise routine that

reduces the risk of an exacerbation caused by exercise (Krafczyk & Asplund, 2011). Other

health promotion activities should include regular visits to primary care for monitoring of blood

sugar, blood pressure, cholesterol screening and vaccinations.

Follow Up

Recommendations by the EPR3 include assessing the patient’s asthma severity score

prior to discharge, education concerning strategies for better control of asthma symptoms,

scheduling a follow up visit with a specialist for any patient with persistent asthma, and for a

plan for follow up teaching to emphasize strategies taught in the hospital performed at this visit

(Camargo, Rachelefsky, & Schatz, 2009). The asthma severity score includes assessment of pre

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exacerbation inhaler use, nighttime awakenings, activity limitations, and oral steroid

requirements. This score should be evaluated prior to discharge to assess the need for treatment

by a specialist (Evidence Category D). Patients with frequent exacerbations requiring

hospitalization that use their rescue inhalers daily are in poor control of their asthma and are at a

higher risk for death. These patients can benefit from care from a specialist who can further

investigate the cause of the frequent exacerbations. Asthma that is considered refractory or

difficult can actually have another reason for the flare-ups. For example, this patient could also

be suffering from some tracheomalacia that is mimicking asthma. Testing using either

bronchoscopy or dynamic computed tomography could be performed on an outpatient basis to

rule out this condition or treat it as appropriate (Leong, Bardin, & Lau, 2013). Follow up for

this appointment with a specialist should occur within one to four weeks of discharge. This

appointment should be made prior to discharge and should include a reminder telephone call on

the day prior to the appointment (Evidence Category B) (Camargo, Rachelefsky, & Schatz,

2009). The patient should be discharged with an inhaled SABA, and inhaled and oral

corticosteroid with enough medication to last until the follow-up appointment (Pollart,

Comptom, & Elward, 2011). Education provided during this visit should mimic the education

provided prior to discharge to reinforce the material already provided and allow for further

assessment of the patient’s understanding and ability to follow the instructions (Camargo et al.,

2009).

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