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Comprehensive Clinical Case Study Michelle Nissen Managing ...
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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
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.
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
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
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.
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.
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
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
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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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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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).
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
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
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
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).
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.
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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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
Acute Severe Asthma 19
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
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
Acute Severe Asthma 21
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
Acute Severe Asthma 22
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
Acute Severe Asthma 23
(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).
Acute Severe Asthma 24
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
Acute Severe Asthma 25
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).
Acute Severe Asthma 26
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