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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5537_Библиотеки_им_академика_М_И_Перельмана.pdf
and may be more likely to receive higher doses of therapy. Acute bacterial sinus infections can contribute to asthma exacerbations and should be
treated with antibiotics. Although it is debatable whether GERD can
worsen asthma, certainly patients with severe reflux symptoms should be
treated with proton pump inhibitors.
1
Severe allergic rhinitis should be
addressed with intranasal steroids. Patients with known OSAS should
have continuous positive airway pressure (CPAP) continued in the hospital. In some cases, this may lessen nocturnal symptoms.
When to Consult a Specialist
Patients deemed to be at increased risk for mortality or those having a
severe exacerbation should be evaluated by an asthma specialist early in
the hospital course. In addition, patients who do not respond to initial therapy or those who clinically worsen at any time, merit evaluation by an
asthma specialist. It is always better to err on the side of conservative
management when considering a consultation.
Goals for Discharge
The primary goals in inpatient asthma management are to minimize symptoms, improve lung function and in general, return patients toward their
baseline level of functioning. Optimally, asthma symptoms should have
resolved at the time of discharge although in some patients, this will not
be possible. PEF should have returned to ≥ 70% predicted or personal best
prior to considering discharge. To reduce the likelihood of relapse and
readmission, there should be a clearly outlined plan of care, including
pharmacologic management at home and emphasis on the need for regular outpatient follow up with an appropriate physician (i.e. either primary
care provider or an asthma specialist).
Prior to discharge, the patient’s medicines should be converted to an
outpatient regimen. Close observation for 24-hr is recommended after this
adjustment. Discharge therapy should include continuation of oral
systemic steroids to complete the prescribed course, initiation of inhaled
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G. Skloot
corticosteroids in those patients naïve to this therapy prior to admission
(this should be started while the patient is still in the hospital to facilitate
appropriate inhaler use) and continuation of SABA for rescue.
Summary
The clinician should recognize risk factors that increase asthma mortality
and should conduct a focused history and physical examination to quickly
determine the severity of the exacerbation to triage care. Oxygen saturation
and lung function are key objective tests to be done in almost all patients.
The mainstay of therapy includes systemic steroids, SABA and supplemental oxygen. High-risk patients or those who do not respond to therapy as
expected warrant early consultation with an asthma specialist. Readiness for
discharge hinges on return toward normal subjective and objective function.
Discharge planning should focus on both pharmacologic therapy and patient
education. Proper evaluation and management of the patient hospitalized
with an asthma exacerbation should improve outcomes and limit costs.
References
1. National Heart, Lung and Blood Institute. (2007) Expert panel report 3:
Guidelines for the diagnosis and management of asthma: Full report
NIH publication 08-4051.
2. Ginde AA, Espinola JA and Camargo CA. (2008) Improved overall
trends but persistent racial disparities in emergency department visits
for acute asthma, 1993–2005. J Allergy Clin Immunol 122: 313–318.
3. Center for Disease Control and Prevention. (2009) Asthma prevalence
and control characteristics by race/ethnicity — United States, 2002.
Morb Mortal Wkly Rep 53(7): 145–148.
4. Hallstrand TS, Fahy JV. (2002) Practical Management of acute
asthma in adults. Respir Care 47(2): 171–182.
5. Peters SP. (2010) Special considerations in adults for diagnoses that
may coexist with or masquerade as asthma. Ann Allergy Asthma
Immunol 104: 455–460.
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Asthma
6. Lugogo NL, MacIntyre NR. (2008) Life-threatening asthma:
Pathophysiology and management. Resp Care 53(6): 726–735.
7. Shim CS, Williams MH Jr. (1983) Relationship of wheezing to the
severity of obstruction in asthma. Arch Intern Med 143(5): 890–892.
8. Chien JW, Ciufo R, Novak R, et al. (2000) Uncontrolled oxygen
administration and respiratory failure in acute asthma. Chest 117(3):
728–733.
9. Pakhale S, Doucette S, Vandemheen K, et al. (2010) A comparison of
obese and nonobese people with asthma: Exploring an asthma-obesity
interaction. Chest 137: 1316–1323.
10. Sutherland ER, Goleva E, Strand M, et al. (2008) Body mass and glucocorticoid response in asthma. Am J Respir Crit Care Med 178:
682–687.
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Hospital Management of COPD
Exacerbations
Neil Schachter*
Key Pearls
• COPD exacerbations requiring hospitalization account for about 6%
of all episodes but nearly 50% of the costs.
• Five-year survival for patients requiring more than three hospitalizations is less than 40%.
• Comorbidities, particularly cardiovascular events and thromboembolic
disease, are frequent reasons for admission of COPD patients and should
be assessed for all patients hospitalized with a COPD exacerbation.
• Respiratory infection is the most common precipitating event of acute
exacerbations and should be routinely treated.
• Comprehensive discharge planning is required to prevent early
rehospitalization.
Introduction
Prior to the concerted effort on the part of many organizations to recognize important statistics that characterize this syndrome, there was a
notable lack of concern about the incidence or severity of COPD. The
numbers tell us that this is an important disease. Notably, there are an
estimated 12 million Americans with diagnosed COPD, but an equal
number are felt to have early with or undiagnosed disease. COPD is
307
28
Chapter
*Mount Sinai Medicial Center, New York, NY, USA.
currently the third leading cause of death in the US, with over 120,000
deaths/year, 8 years earlier than anticipated. (Centers for Disease
Control (CDC) and Prevention’s National Center for Health Statistics
(NCHS), Deaths: Preliminary Data for 2010. http://www.cdc.gov/nchs/
data/nvsr/nvsr60/nvsr60_04.pdf.) By the late 1990s, the mortality rate
of COPD had risen by nearly 200% (compared to statistics from the
1960s), whereas that of all other major causes of death, including cardiovascular disease, and cancer, had significantly declined. The mortality rate of COPD 10 years after diagnosis remains greater than 50%.
Finally, COPD is the primary cause for about 715,000 hospitalizations/year; it accounts for 16 million office visits annually and is
responsible for direct medical costs of over US$20 billion half annually, about half of which are for hospitalizations.
1–4
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) was
launched in 1998 as a collaboration between government agencies, scientific societies and industry, with a principal goal of producing recommendations for the management of COPD and has established itself as an
authoritative source. Its iteration
3
defined COPD, as follows: “Chronic
obstructive pulmonary disease (COPD), a common, preventable, and
treatable disease, is characterized by persistent airflow limitation that is
usually progressive and associated with enhanced chronic inflammatory
response in the airways and the lungs to noxious particles and gases.
Exacerbations and comorbidities contribute to the overall severity in individual patients.” This concise definition de-emphasizes the prior (but still
useful) concept of COPD as an umbrella term covering a number of clinical and pathologic syndromes, including emphysema (destruction of
alveolar tissue), chronic bronchitis (chronic airway inflammation with
symptoms of cough and phlegm), as well as some forms of asthma (particularly “adult” asthma with an irreversible obstructive component).
Clinical course. COPD is usually a disease of middle age, with the onset
of symptoms in the patient’s 50s or early 60s. In its classic presentation,
it occurs 20 or 30 years after the patient has become addicted to cigarette
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N. Schachter
smoking. Other irritants may be associated with the disease, such as occupational and environmental pollutants. Current smoking is not necessary
for the onset of the disease but there is usually a history of at least 20–30
pack years of smoking. A small but significant subgroup have a hereditary
condition (alpha-1 antitrypsin deficiency) which is associated with an earlier onset of the disease.
Because of the association with cigarette smoking and other pollutants with the development of COPD, comorbidities such as heart disease,
diabetes, osteoporosis and lung cancer occur in a greater-than-expected
number of these patients and frequently result in complications which
contribute to the morbidity and mortality of this disease. An as-yetpoorly-defined predisposition may exist in patients who develop COPD;
it is known as “systemic inflammation” and may contribute to the
progression of the comorbidities as well as COPD itself.
Patients with COPD experience on average an accelerated loss of lung
function which frequently parallels and may in part explain the progression
of symptoms. In addition to this relatively continual progression of the disease, patients with COPD experience acute exacerbations which can accelerate the progression of the disease, leading to early disability and death.
Staging of the disease. Staging of the disease is important for several
aspects of management. Based on spirometry, GOLD guidelines classify
the disease into four stages of severity. Because all stages of the disease
are defined by an obstructive component, the ratio of FEV1/FVC is
required to be less than 0.7. Healthy individuals are able to exhale forcefully more than 70% of their forced vital capacity (FVC: the total amount
of air that a person can forcefully exhale over a period of at least 6 s) in
the first second (FEV1).
• Stage I (mild disease): FEV1 ≥ 80% of predicted
• Stage II (moderate disease): 50% ≤ FEV1 < 80% of predicted
• Stage III (severe disease): 30% ≤ FEV1 < 50% of predicted
• Stage IV (very severe disease): FEV1 < 30% of predicted, or less than
50% of predicted and the patient is suffering form respiratory failure.
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Hospital Management of COPD Exacerbations
Acute Exacerbations
Definition. COPD is characterized by intermittent episodes of deterioration known as acute exacerbations. These are heralded by a worsening of
symptoms beyond the usual day-to-day variation characterized by:
• Increase in dyspnea;
• Increase in cough severity or frequency;
• Increase in sputum volume and/or character.
The typical exacerbation may be accompanied by constitutional
symptoms (e.g. fever) and worsening of spirometric values (FVC and
FEV1). The chest x-ray is usually unchanged unless pneumonia is the precipitating event.
Causes and risk factors. A majority of these episodes, particularly in
patients with mild-to-moderate disease, can be handled in the outpatient
setting. For patients with marginal respiratory reserve, respiratory failure
can complicate the picture and requires hospital management. About 6%
of patients with acute exacerbations will require hospitalization.
5,6
Hospitalization for COPD exacerbation is associated with a poor prognosis. Patients hospitalized on 1–2 occasions have a five-year survival rate
of less than 60% and those with >3 hospitalizations have less than a 40%
survival rate.
Specific indications for hospitalization have been proposed
7
by a joint
position paper of the American Thoracic Society/European Respiratory
Society (see Table 1).
Morbidity/mortality. The decision to hospitalize will depend on a number
of considerations, including:
• The baseline lung function of the patient. Patients with severe or very
severe disease will often be hypoxemic (requiring supplemental oxygen) in their baseline state as a result of reduced mechanical efficiency (obstruction, hyperinflation) and/or gas transport problems
310
N. Schachter
(reduced diffusion and/or V/Q mismatch). Acute exacerbations can
lead to abrupt decompensation resulting in the patient’s usual
supplemental oxygen being unable to keep their saturation at > 90%.
An abrupt change in saturation below the critical level can lead to pulmonary hypertension and cor pulmonale.
• The nature of the precipitating event. As many as two-thirds of acute
exacerbations are attributable to respiratory infections (both bacterial
and viral). Other precipitating factors include airway irritants such as
smoking, pollutants, allergens (in patients with mixed disease
asthma/COPD), as well as aspiration.
• The presence of comorbidities. Patients with COPD are prone to have
comorbidities in a greater proportion than individuals of similar age
and risk factors. In particular, cardiovascular disease, diabetes, lung
cancer and thromboembolic disease (up to 30% of hospitalized
patients) are frequent in this population and may be the precipitating
events in acute exacerbations of COPD.
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Hospital Management of COPD Exacerbations
Table 1. Specific Recommendations for Hospitalization and ICU Admission of the
COPD Patient with Exacerbation
1
Hospitalization
• The presence of high risk comorbid conditions, including pneumonia, cardiac
arrhythmia, congestive heart failure, diabetes mellitus, renal or liver disease
• Inadequate response of symptoms to outpatient management
• Marked increase in dyspnea
• Inability to sleep due to symptoms
• Worsening hypoxemia
• Worsening hypercapnia
• Change in mental status
• Inability of the patient to care for himself or herself (lack of home support)
• Uncertain diagnosis
• Inadequate home care
ICU Admission
• Impending or actual respiratory failure
• Presence of other end organ dysfunctions (e.g. shock and renal, liver or
neurological disturbances)
• Hemodynamic instability
The role of exacerbations in the progression of COPD is clearly documented. Exacerbations in general and those associated with hospitalizations
in particular lead to accelerated loss of lung function, re-exacerbation with
frequent readmissions to hospital and, ultimately, increased mortality.
5–7
Treatment of Acute Exacerbations
The treatment of the hospitalized patient with acute exacerbation involves
identification and treatment of underlying causes of deterioration, reversing bronchoconstriction and inflammation by pharmacologic means,
treating impending or actual respiratory failure with oxygen and/or
assisted ventilation, preventing complications and assuring a smooth transition to posthospital management.
Antibiotics. A majority of COPD exacerbations are felt to be due to respiratory infection. Viruses, including rhinovirus, influenza, parainfluenza,
coronavirus and adenovirus, are the most common isolates. With the
exception of influenza, the isolation of a virus may not imply infection.
Bacterial infections account for up to half of the infections triggering
acute exacerbations. Nontypeable Haemophilus influenzae, Moraxella
catarhallis and Streptococcus pneumoniae are the most commonly
isolated organisms associated with exacerbation. These are frequently
difficult to isolate from sputum, and routine culture and examination of
sputum smear and culture are not recommended. An exception is made for
patients with suspected Pseudomonas infection. Pseudomonas as the
cause of a COPD exacerbation is rare but tends to occur in the most
severely compromised COPD patients, including patients with a prior history of Pseudomonas infection, receiving multiple courses of antibiotics,
or with recent hospitalization for exacerbation. Patients hospitalized for
COPD exacerbation should receive antibiotic therapy. Double blind studies with placebo control indicate that, overall, patients with exacerbations
treated with antibiotics resolve more frequently compared to those receiving placebos. Patients with the most severe exacerbations were the most
312
N. Schachter
likely to experience the beneficial response to a course of antibiotic.
8,9
The
choice of antibiotic depends on the level of suspicion for Pseudomonas.
Patients without risk factors for Pseudomonas should receive a fluoroquinolone (e.g. levofloxacin, moxifloxacin) or a third generation
cephalosporin (e.g. ceftriaxone, cefotaxime). Patients with risk factors for
Pseudomonas should receive either a fluoroquinolone active against
Pseudomonas (e.g. levofloxacin, ciprofloxacin), a fourth generation
cephalosporin (e.g. ceftazidime, cefepime) or an antipseudomonal penicillin (e.g. piperacillin-tazobactam).
Isolation of the influenza virus should be treated with antiviral agents
for which the current strain is susceptible. The antiviral agent zanamivir
is contraindicated in patients with COPD.
Bronchodilators and inhaled corticosteroids. Inhaled beta-2 adrenergic
bronchodilators with or without anticholinergic agents and inhaled corticosteroids are effective treatments for exacerbation of COPD. Short-acting
bronchodilating agents (albuterol and/or ipratropium) are frequently the
preferred agents used in the setting of hospitalized patients with COPD.
They are usually administered by nebulizer either separately or in a combination solution. The latter has an additive effect, due to the separate mechanisms of action by which the agents promote smooth muscle relaxation.
Their effective duration of action is about 4 hr and therefore need to be
administered at regular intervals in order to have sustained bronchodilation.
Use by other routes is usually avoided in the hospital setting. MDIs are difficult to employ in the sick COPD patient, and oral or parenteral administration of these agents has significant cardiovascular toxicity in this setting.
Many patients with severe or very severe COPD are maintained as outpatients on long-acting bronchodilator agents. Salmeterol and formoterol
are two long-acting beta-2 adrenergic agents (LABAs) widely used in the
treatment of COPD. Both drugs have a duration of action of approximately
12 hr. They are generally considered safe and effective for the treatment of
COPD. Formoterol is also available for use as a nebulized solution.
Furthermore, these agents are available in combination with an inhaled
corticosteroid — fluticasone in the case of salmeterol, and budesonide or
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Hospital Management of COPD Exacerbations