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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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S1 with prominent split S2, no S3, no murmurs. Examination of the abdomen is normal,
and examination of extremities shows no thigh swelling or edema.
Differential Diagnosis
CCS NOTE
Only patients who are hypoxemic should receive supplemental oxygen and get a chest
x-ray. Pulse oximetry is part of vital signs. ABG should not be done as a routine lab but
should be ordered if the results will aid in diagnosis or change your clinical
management.
Setting: emergency department
Initial Diagnostic Plan Results
pH 7.36; PCO2 44 mm Hg; PO2 60 mm Hg
(results do not mean intubation is needed, but
rather that patient is decompensating and
requires immediate, more aggressive therapy,
i.e., non-invasive positive pressure ventilation
and critical care evaluation for possible ICU
Asthma exacerbation1.
Secondary pneumothorax from underlying asthma2.
Pulmonary embolism from a lower extremity DVT above the knee3.
Congestive heart failure from a viral cardiomyopathy4.
Community-acquired pneumonia5.
Arterial blood gas
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admission)
Normal heart size; no acute cardio-pulmonary
process, no pneumothorax
100 L/min (baseline 400-500 L/min)
Negative
Gram stain negative and no growth
Assessment
The patient has a history of asthma and a recent upper respiratory infection, and she now
presents with wheezing, acute shortness of breath, and a markedly diminished peak flow. The
presence of diffuse wheezing on examination with a peak expiratory flow significantly below
the patient’s baseline suggests a severe asthma attack. The history of rhinitis and nasal polyps
with recent use of cold medication raises the question of an exacerbation associated with
aspirin sensitivity.
In a young patient presenting with shortness of breath with an underlying pulmonary disease
such as asthma, a secondary pneumothorax needs to be considered. The chest x-ray (especially
an expiratory film) in this case would aid in the diagnosis.
Further Treatment Plan
PA and lateral chest x-ray
Peak flow (not usually performed during an
exacerbation and mainly helpful if patient’s
baseline peak flow is known)
Influenza nasal swab
Sputum culture and Gram stain
Nebulizer treatment with short-acting beta-agonist-2 agonists (first-line bronchodilator)
and can add nebulized short acting anti-cholinergics
1.
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Diagnostic Plan
Look for a precipitating cause. Viral infection is the most common. Bacterial pneumonia is not
likely here given the negative chest x-ray. If in doubt, consider getting sputum culture with
Gram stain and blood cultures before starting antibiotics.
Discussion
Asthma is a disease characterized by inflammatory hyperreactivity of the respiratory tree to
various stimuli, resulting in reversible airway obstruction. The combination of mucosal
inflammation, bronchial musculature constriction, and excessive secretion of viscous mucus-
causing mucous plugs produces bronchial obstruction. The bronchial hyper-reactivity occurs in
an episodic pattern with interspersed normal airway tone.
Asthma can occur at any age but is usually seen in the young, 80% of whom “outgrow” the
condition by adulthood.
Etiology. Intrinsic (idiosyncratic) asthma occurs in 50% of asthmatics who are nonallergic. A
bronchial reaction occurs secondary to nonimmunologic stimuli, such as infection, irritating
inhalant, cold air, exercise, and emotional upset. The attacks are severe, and prognosis is less
favorable.
Extrinsic (allergic) asthma (20% of cases ) results from sensitization and is precipitated by
allergens. Specific immunoglobulins (IgE class) are produced, and the total serum IgE
concentration is elevated. There is a positive family history of allergic disease. Other
symptoms include allergic rhinitis, urticaria, and eczema. Prognosis is good.
Supplemental oxygen if the patient is hypoxemic and consider non-invasive positive
pressure ventilation if there is an increased work of breathing
2.
IV glucocorticoids (e.g. methylprednisolone)3.
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Many patients have features of both types (intrinsic and extrinsic components).
Signs and symptoms of asthma. In a mild attack, slight tachypnea, tachycardia, prolonged
expirations, and mild, diffuse wheezing is seen. In a severe attack, the use of accessory muscles
of respiration, diminished breath sounds, loud wheezing and intercostal retraction are seen.
Poor prognostic factors include fatigue, diaphoresis, pulsus paradoxus (>20 mm Hg), inaudible
breath sounds, decreased wheezing, cyanosis, and bradycardia.
Variants of Asthma
In the acute phase, ABG abnormalities are as follows: decrease in PaCO2, increase in pH,
and normal/low PaO2. In severe asthma/status asthmaticus, there is a decreased PaO2,
Respiratory infection is the most common stimuli to cause an asthma exacerbation; studies
have documented that viruses (e.g., respiratory syncytial, corona, rhino and influenza,
depending on patient age and time of year) are the major cause.
Pharmacologic stimuli are important in some cases; the most common etiologic agents
associated with asthma exacerbation are aspirin, NSAIDs, coloring agents such as
tartrazine, and beta-antagonists.
The typical aspirin sensitivity affecting adults (10%) is nasal polyposis syndrome, which
usually starts with perennial vasomotor rhinitis; later, asthma appears that occurs with
minimal ingestion of aspirin. There is significant cross-reactivity between aspirin and other
NSAIDs (ibuprofen, naproxen). Patients can be desensitized by daily administration of
aspirin (cross-tolerance also develops to other NSAIDs). The mechanism by which aspirin
and similar drugs cause asthma seems to be chronic overexcretion of leukotrienes, which
activate the mast cells; this is why leukotriene synthesis inhibitors and antagonists are
considered to be effective.
Cough variant asthma
Exercise-induced bronchoconstriction
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increased PaCO2, and decreased pH (bicarbonate level usually is normal in acute phase but
becomes elevated in chronic). A normal PCO2 may indicate respiratory muscle fatigue in an
acute asthmatic patient.
Chest x-ray findings are nonspecific in an asthmatic attack. Chest x-ray may help to rule out
acute bacterial infection and pneumothorax.
Asthma is a clinical diagnosis based on the history and physical examination. PFTs in a poorly
controlled asthmatic can show an obstructive pattern with a significant bronchodilator response
defined as a 12% improvement in the FEV1 or FVC and/or increase of 200 ml post-
bronchodilator challenge. PFTs may also be normal in a well-controlled asthmatic. A
provocative challenge may be performed with methacholine, cold air or exercise, which
typically shows a decrease in FEV1 and /or FVC of at least 20%.
Treatment of Asthma
Essential components of asthma management are routine monitoring of symptoms and lung
function, patient education, control of trigger factors, and pharmacologic. The goals of
treatment are to reduce impairment from symptoms, minimize hospitalizations and loss of lung
function, and minimize adverse effects from asthma medications. Effective asthma management
requires a preventative approach, with regularly scheduled visits during which symptoms are
assessed, pulmonary function is monitored, medications are adjusted, and ongoing education is
performed. Patients with poor perception of increasing asthma symptoms may also benefit from
assessment of their peak expiratory flow rate at home.
Pharmacologic therapy varies according to asthma severity and asthma control. Asthma control
is based on the current level of symptoms, FEV
1
or PEFR values, and number of exacerbations
requiring oral glucocorticoids per year. A stepwise approach to therapy is recommended, in
which the dose of medication, number of medications, and/or frequency of administration are
increased as necessary and decreased when possible. At each return visit, the patient’s asthma
control is evaluated. If the asthma is not well-controlled, therapy should be “stepped-up.” If the
185
asthma is well-controlled, therapy can be continued or possibly “stepped-down” to minimize
medication side effects.
Basic Science Correlate
Physiology of airflow obstruction limitation in asthma is a result of a narrowing of the
airway lumen, causing variable reductions in airflow is a pathognomonic feature of
asthma. The mechanisms causing airflow limitation include contraction of airway
smooth muscle, thickening of the airway wall due to inflammation and edema, and
plugging of airways with mucus. The main component of the rapid changes in airflow
limitation is the smooth muscle, and is the basis for beta-agonist therapy that directly
relaxes smooth muscle. Bronchoconstriction may be due to direct effects of contractile
agonists released from inflammatory cells such as leukotrienes and histamine, which
are potent bronchoconstrictors released by mast cells and eosinophils.
For mild intermittent asthma, recommend a short-acting inhaled beta-2-selective
adrenergic agonist. Recommend use as-needed for relief of acute symptoms as well as for
prevention of symptoms caused by exercise or trigger exposure, as opposed to regularly
scheduled administration.
For mild persistent asthma, recommend inhaled glucocorticoids as initial long-term
controller therapy, along with short-acting inhaled beta-2 agonists as needed.
For moderate persistent asthma, it is very reasonable to add a long acting beta-2 agonist
to the inhaled glucocorticoid.
For severe persistent asthma, there are many choices, both pharmacologic and non-
pharmacologic; consider risk versus benefit to the patient and side effect profile of the
desired therapy (leukotriene modifiers, systemic corticosteroids).
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Airway inflammation also plays a critical role in airflow obstruction. This
inflammation occurs throughout the tracheobronchial tree with varying degrees of
obstruction dependent upon the diameter of the airway. Usually obstruction in large
airways leads to airflow limitation with decreased flow rates. Conversely, obstruction
in small airways leads to airway closure, air trapping with an increase in residual
volume seen on PFTs (increased TLC, RV and FRC), and in many cases dynamic
hyperinflation. Clinically the patient complains of chest tightness, and the discomfort of
an asthma attack may be due to air trapping and breathing at higher lung volumes to
maintain airway patency and sustain adequate ventilation.
Studies of bronchial thermoplasty, a technique that applies radiofrequency waves to the
airways during bronchoscopy to decrease large airway smooth muscle mass (ASM
mass), provide another line of evidence supporting a central role for airway smooth
muscle in large airways in the pathogenesis of asthma. Preliminary evidence suggests
that reducing ASM mass by this technique improves asthma control.
Bronchial hyperresponsiveness (BHR) is another defining feature of asthma and is a
manifestation of reversible airflow obstruction due to smooth muscle contraction. BHR
represents an exaggerated constrictor response to a variety of physical, chemical, or
environmental stimuli. BHR can be quantitated by the dose response to pharmacologic
agents such as methacholine or histamine, causing a 20% fall in FEV1 or FVC. While
BHR is not specific for asthma, patients with asthma typically demonstrate BHR to
much lower doses of these agents than normal or allergic individuals. While airway
smooth muscle is clearly involved in bronchial hyperresponsiveness, the precise
mechanism that causes airway smooth muscle to become hyperresponsive is not known.
Final Diagnosis
Asthma exacerbation
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Case 2
Chief Complaint
Chronic cough
History and Physical Examination
A 28-year-old woman comes to the clinic for evaluation of intermittent cough over the last
few months. She recently started running several times a week and has noticed that the
cough is much worse after she returns. She has noted occasional wheezing as well,
particularly on very cold days. She is a nonsmoker and is otherwise healthy.
She is a well developed, well nourished woman in no acute distress. Her temperature is
36.7 C (98.0 F), BP 108/70 mm Hg, pulse 64/min, and respirations 18/min. Physical
examination is unremarkable.
Differential Diagnosis
Initial Management
Setting: outpatient
Exercise-induced asthma/exercise-induced bronchoconstriction1.
Gastroesophageal reflux2.
Postnasal drip (upper airway cough)3.
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Initial Diagnostic Plan Results
FEV1 108% of predicted, FVC 111% of
predicted, FEV1/FVC 93%. TLC and DLCO
within normal limits; flow volume loop is normal
Significant drop in both the FVC and FEV1
>20% with administration of methacholine
Assessment
This clinical presentation of exercise-induced cough is a common variant of asthma. Symptoms
are often worse after exercise is completed. The normal PFTs (performed at rest) do not rule
out this diagnosis. A methacholine challenge test should be performed to confirm this
diagnosis. However, the clinical scenario is probably adequate, and the patient may be
empirically treated.
Other common noninfectious causes of cough include allergic rhinitis, postnasal drip, and
gastroesophageal reflux disease. However, there is no evidence to support these other causes
in this patient.
Treatment Plan
Discussion
The term “exercise-induced asthma” is often used to describe episodic bronchoconstriction
following exercise in asthmatic patients. This terminology can be misleading since exercise is
not an independent risk factor for asthma, but can be categorized as a bronchoconstriction in
patients with underlying asthma. In the pulmonary literature there is some research which
Pulmonary function tests
Methacholine challenge test
Inhaled beta agonists before exercise, such as albuterol
1.
Cromolyn is sometimes used as an alternative
2.
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