Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5537_Библиотеки_им_академика_М_И_Перельмана.pdf
mometasone in the case of formoterol. Tiotropium is a long acting anticholinergic agent that is also often used in the outpatient treatment of
COPD and may be used with LABAs to good effect. Maintenance of hospitalized patients on these longer-acting bronchodilating preparations with
the use of short-acting bronchodilating agents (SABAs) every 4 hr on an
as-needed basis may offer an alternative strategy to nebulized
short-acting bronchodilators every 4 hr.
Methylxanthines (theophylline and aminophylline) can be administered
orally or intravenously. They provide dose-dependent bronchodilation and
can be titrated using serum levels. They may also have anti-inflammatory
properties. Methylxanthines have lost favor in the treatment of airway
obstruction because of their narrow window of the toxic-to-therapeutic
ratio. They may nevertheless play a role in the refractory patient, as they
may offer an alternative means of achieving airway relaxation independently of the beta and cholinergic receptors.
Oral and parenteral glucocorticoids. Concurrent use of glucocorticoid
therapy by the intravenous or oral route is recommended for the initial
treatment of severe exacerbations of COPD requiring hospitalization.
10,11
The exact mechanism of action is unclear; anti-inflammatory effects as
well as resensitization of beta-adrenergic receptors may be involved. A list
of commonly used steroid preparations administered for obstructive disease is shown in Table 2. High doses of steroids as well as prolonged use
have recently been suggested to be no more effective than short term use
with low doses. By contrast, the high dose intravenous route has been
associated with higher rates of complications as well as increased hospital costs. In a retrospective study by Lindenauer,
12
oral doses of pred-
nisone 20–60 mg once daily were as effective as an intravenous regimen.
Oxygen and assisted ventilation. Oxygen therapy is a fundamental part of the
therapy for COPD exacerbations in the hospital. Adequate supplemental
oxygen should be titrated to keep the patient’s oxygenation at adequate levels
(SaO
2
> 90%; PaO2> 60 mmHg). A number of oxygen delivery systems
allow for the accurate titration of oxygen so as not to cause suppression of
314
N. Schachter
the respiratory drive. These systems (preferably high flow Venturi masks)
allow for reliable delivery of oxygen at F
IO2
between 24 and 55%.13Because
of the possible insidious development of hypercapnea, an arterial blood gas
should be performed after the initiation of oxygen therapy in this setting
(usually within an hour of establishing satisfactory oxygenation).
Noninvasive ventilation (NIV) in the setting of impending respiratory
failure can stabilize patients with severe exacerbations and prevent the
need for intubation with mechanical ventilation (Table 3). Initiation of this
therapy requires skilled adjustment of noninvasive equipment and titration of pressures for patient comfort and is usually best accomplished in
conjunction with a respiratory therapist.
Preventing complications. Patients with COPD have an excess of
comorbidities, based on their frequent history of smoking and the possible effects of an as-yet-poorly-characterized chronic inflammatory
state.
14
Cardiovascular disease is particularly common and may be the
cause of morbidity and death in a large fraction of COPD patients admitted for acute exacerbation. Thromboembolic disease is a frequent complication of COPD exacerbation.
15,16
DVT has been documented in 11%
of 196 patients admitted to a respiratory care unit, though most were
315
Hospital Management of COPD Exacerbations
Table 2. Properties of Corticosteroids Commonly Administered to Treat COPD
Relative
Anti- Relative Duration
Inflammatory Mineralocorticoid Routes of of Action
Steroid Strength Strength Administration (Systemic)
Hydrocortisone 1.0 1.0 IV, IM, oral Short
Cortisone 0.8 0.8 IV, IM, oral Short
Prednisone 2.5–3.5 0.8 Oral Intermediate
Methylprednisolone 4.0–5.0 Less than 0.8 IV, IM, oral Intermediate
Triamcinolone 4.0–5.0 0 IV, IM, oral Intermediate
Dexamethasone 20–40 0 IV, IM, oral Long
* Adapted from: Witek TJ, Schachter EN. (1994) Pharmacology and Therapeutics in Respiratory
Care. WB Saunders, Philadelphia, PA.
asymptomatic. The frequency of PE during acute exacerbations of
COPD has been estimated to be as high as 29% and PE accounts for up
to 10% of deaths in COPD patients treated with long term oxygen. The
high prevalence of this complication with acute exacerbations of COPD
warrants the consideration of PE in exacerbations not responding to
standard therapy, and that prophylaxis be routinely administered in these
patients.
316
N. Schachter
Table 3. Indications and Contraindications for NIV and Mechanical Ventilation
3
Selection for NIV
• Moderate-to-severe dyspnea with use of accessory muscles and paradoxical
abdominal motion
• Moderate-to-severe acidosis (pH < 7.35) and/or hypercapnia (PaCO
2
> 45 mmHg)
• Respiratory frequency > 25 breaths/min
Exclusion for NIV
• Respiratory arrest
• CV instability
• Change in mental status, uncooperative
• Aspiration risk
• Viscous or copious secretions
• Recent facial or gastroesophageal surgery
• Craniofacial trauma
• Nasopharyngeal abnormalities
• Burns
• Extreme obesity
Indications for Mechanical Ventilation with Intubation
• NIV failure
• Severe dyspnea, with use of accessory muscles and paradoxical respiration
• Respiratory rate > 35/min
• Life threatening hypoxemia
• Severe acidosis (pH < 7.25) and severe hypercapnia (PaCO
2
> 60 mmHg)
• Respiratory arrest
• Somnolence, impaired mental status
• CV instability
• Other complications (metabolic abnormalities, sepsis, pneumonia, PE,
bacteremia, massive effusion)
Assuring a smooth transition to posthospital management. Patients with
COPD have a high incidence of rehospitalization.
5
The ideal length of
hospitalization for acute exacerbation is not determined but patients
should be stable both clinically and objectively (e.g. adequate gas
exchange and decreased bronchodilator requirements) for at least 24 hr
before discharge is considered. A written action plan with recommendations for the treatment of a repeat exacerbation is required. The care plan
should be based on guidelines developed for the management of stable
outpatient COPD, such as those described in the GOLD guidelines.
Assessment of immunization status (influenza and S. pneumoniae) should
be made before discharge and the patient immunized if indicated.
Smoking cessation, if the patient is a current smoker, needs to be
addressed. The patient should be evaluated for possible pulmonary rehabilitation at the time of discharge. Patients should be taught how to recognize acute exacerbation and given specific instructions on how to
manage exacerbations. The patient’s home situation should be fully
addressed by home care and respiratory services. Home oxygen and
visiting nurse services when needed should be in place, so that upon
arrival at home the patient will not be without adequate resources.
Medical followup should occur within 4–6 weeks.
Phophodiesterase IV inhibitors.
This newly developed class of agents has now been introduced for the
management of COPD patients. Its role is not as yet totally defined but it
is recommended by the GOLD Guidelines for patients with severe or very
severe airway obstruction (GOLD 3 & 4). The expected outcome is to
reduce the frequency and severity of exacerbations, and when taken in
conjuction with long-acting bronchodilators, to modestly improve FEV1.
GI side-effects and sleep disturbance are the most commonly reported
side effects. The available product in the United States, roflumilast, is
given orally 500 mcg once daily.
3,17
317
Hospital Management of COPD Exacerbations
Conclusions
Acute exacerbations of COPD, particularly those requiring hospitalization,
are critical mileposts in the course of this disease. Early and appropriate
management of these events — including treating their underlying cause,
reversing the physiologic consequences (which include bronchospasm,
respiratory failure and cor pulmonale) and limiting the consequences of
comorbidities — is the challenge for the hospital-based physician. No less
important is ensuring that the COPD patient has received all the preventive
strategies prior to discharge and that a smooth transition back to the outpatient environment has been arranged.
References
1. Brown DW, Croft JB, Greenlund KJ, Giles WH. (2010) Trends in
hospitalization with chronic obstructive pulmonary disease —
United States, 1990–2005. COPD 7(1): 59–62.
2. Centers for Disease Control and Prevention. (2008) Deaths from
chronic obstructive pulmonary disease — United States, 2000–2005.
Morbidity and Mortality Weekly Report 57(45): 1229–1232.
3. Global Strategy for Diagnosis, Management and Prevention of COPD
Updated 2011; http://www.goldcopd.com
4. Lenfant C. (2003) Shattuck lecture: clinical research to clinical
practice — lost in translation? N Engl J Med 349(9): 868–874.
5. Chenna PR, Mannino DM. (2010) Outcomes of severe COPD exacerbations requiring hospitalization. Semin Respir Crit Care Med 31(3):
286–294. [Epub 2010, May 21].
6. Soler-Cataluña JJ, Martínez-García MA, Román Sánchez P, et al.
(2005) Severe acute exacerbations and mortality in patients with
chronic obstructive pulmonary disease. Thorax 60(11): 925–931.
7. Celli BR, MacNee W; ATS/ERS Task Force. (2004) Standards for the
diagnosis and treatment of patients with COPD: A summary of the
ATS/ERS position paper. Eur Respir J 23(6): 932–946.
318
N. Schachter
8. Anthonisen NR, Manfreda J, Warren CP, et al. (1987) Antibiotic ther-
apy in exacerbations of chronic obstructive pulmonary disease. Ann
Intern Med 106: 196–204.
9. Rothberg MB, Pekow PS, Lahti M, et al. (2010) Antibiotic therapy
and treatment failure in patients hospitalized for acute exacerbations
of chronic obstructive pulmonary disease. JAMA 303: 2035
10. Davies L, Angus RM, Calverley PM. (1999) Oral corticosteroids in
patients admitted to hospital with exacerbations of chronic obstructive
pulmonary disease: A prospective randomised controlled trial. Lancet
354(9177): 456–460.
11. Niewoehner DE, Erbland ML, Deupree RH, et al. (1999) Effect of
systemic glucocorticoids on exacerbations of chronic obstructive pulmonary disease. Department of Veterans Affairs Cooperative Study
Group. N Engl J Med 340(25): 1941–1947.
12. Lindenauer PK, Pekow PS, Lahti MC, et al. (2010) Association of
corticosteroid dose and route of administration with risk of treatment
failure in acute exacerbation of chronic obstructive pulmonary
disease. JAMA 303(23): 2359–2367.
13. Schachter EN, Littner M, Luddy P, Beck GJ. (1980) Oxygen delivery
systems in clinical practice. Criti Care Med 8: 405–409.
14. Hurst JR, Perera WR, Wilkinson TM, et al. (2006) Systemic and upper
and lower airway inflammation at exacerbation of chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 173(1): 71–78.
15. Ambrosetti M, Ageno W, Spanevello A, et al. (2003) Prevalence and
prevention of venous thromboembolism in patients with acute exacerbations of COPD. Thromb Res 112(4): 203–207.
16. Rizkallah J, Man SF, Sin DD. (2009) Prevalence of pulmonary
embolism in acute exacerbations of COPD: A systematic review and
meta-analysis. Chest 135(3): 786–793.
17. Calverley PM, Rabe KF, Goehring UM et al. (2009) Roflumilast in
symptomatic chronic obstructive pulmonary disease: two randomised
clinical trials. Lancet 29;374(9691): 685–94.
319
Hospital Management of COPD Exacerbations
This page intentionally left blankThis page intentionally left blank
Evaluation and Treatment of Diffuse
Parenchymal Lung Disease
June Kim and Timothy J. Harkin*
Key Pearls
• The American Thoracic Society (ATS) and the European Respiratory
Society (ERS) have revised the classification of interstitial lung
diseases (ILDs) and introduced the term “diffuse parenchymal lung
disease” (DLPD).
• Special testing may be warranted to confirm occupational exposure
(such as demonstration of ferruginous bodies in asbestosis from lung
biopsies or a hypersensitivity panel for serologic evidence of immune
reaction to organic antigens).
• Many patients who are referred to advanced lung disease programs
for idiopathic lung disease are found to have an underlying systemic
rheumatologic disease, such as rheumatoid arthritis, scleroderma, systemic lupus erythematosis, dermatomyositis, polymyositis, Sjogren’s
disease, or sarcoidosis.
• For patients with DPLDs who present with decompensated
pulmonary symptoms, a chest CT angiogram can help rule out pulmonary embolism and identify infection, heart failure, or worsening
of underlying lung disease. Early bronchoscopy should be considered
for the prompt diagnosis and treatment of atypical lung infections.
321
*Mount Sinai School of Medicine, NY, New York, USA.
29
Chapter
• Idiopathic pulmonary fibrosis (IPF) patients must be considered for
early referral for lung transplantation, because there is no effective
treatment and there is a very high risk of death from respiratory failure. Mean survival is approximately three years.
Introduction
Interstitial lung diseases (ILDs) are a heterogeneous group of disorders
characterized by inflammation and/or fibrosis of the pulmonary interstitium, the microscopic space between alveolar epithelium and capillary
endothelium. In 2002, the American Thoracic Society (ATS) and the
European Respiratory Society (ERS) revised the classification of ILDs
and introduced the term “diffuse parenchymal lung disease” (DLPD), and
separated DLPD into four major categories (Fig. 1).
Each category has distinct clinical, radiographic, and pathologic
characteristics, often presenting significant diagnostic challenges. An
evaluation of a patient with DPLD therefore begins with early consultations with expert clinicians, radiologists, and pathologists who are well
versed in these entities to determine the most likely diagnosis.
1,2
322
J. Kim and T. J. Harkin
Fig 1. ATS/ER classification of diffuse parenchymal lung disease.
1
The following is a brief summary of the clinical evaluation of patients
with suspected DPLD and considerations for the diagnosis and management issues for the hospitalist.
Clinical Evaluation
History
An accurate diagnosis is essential to the appropriate management and
prognostication of a DPLD patient. A comprehensive history is a critical
component of this assessment, because at the most advanced stages of
disease, many entities can be radiographically and pathologically indistinguishable from each other.
There are many medical agents that can cause DPLD (see Table 1).
3
Temporally linking exposure to the drug to the development of respiratory
symptoms and radiographic findings is helpful in the diagnosis of drugrelated DPLD. The inciting agent should be promptly discontinued if this
is suspected. A complete updated list of medications that have been implicated in pulmonary disease is available at http://pneumotox.com.
323
Evaluation and Treatment of Diffuse Parenchymal Lung Disease
Table 1. Drugs that Can Cause DPLD
Antibiotics Cephalosporins, minocycline, nitrofurantoin, quinine
Rheumatologic treatments Gold, leflunomide, methotrexate, NSAIDS,
penicillamine, sulfasalazine, infliximab, etanercept
Cardiology Amiodarone, angiotensin-converting enzyme inhibitors,
aspirin, atenolol, statins
Oncology Bleomycin, busulfan, chlorambucil, dasatnib, melphalan,
imatinib, methotrexate, mitomycin C
Immunomodulators Azathioprine, cyclophosphamide, erlotinib, gefitinib,
interferons, rituxumab, sirolimus
Illicit drugs Cocaine, heroin, intravenous talc, methadone
Miscellaneous High concentrations of oxygen, inhaled or aspirated
fat-containing substances (e.g. mineral oil), paraquat,
radiotherapy
Adapted from Ref. 3.