Catching Your Breath: Managing COPD Exacerbations
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National Emphysema Foundation - Is Prednisone a Friend or Foe?.Chronic Corticosteroid Use in Patients with COPD | AAFP
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Exacerbations of COPD are associated with a more rapid decline in lung function. Pharmacists can be instrumental in educating patients and can serve as a resource for multidisciplinary teams in the setting of COPD exacerbations.
Chronic obstructive pulmonary disease COPD is an inflammatory disease of the lung characterized by progressive airflow limitation that is not fully reversible. Emphysema is a destruction of the alveolar surfaces that results in the inability to perform efficient gas exchange.
Most patients with COPD have elements of both emphysema and chronic bronchitis. The term COPD is now used more frequently, since it encompasses both conditions. Approximately 12 million people in the United States have been diagnosed with COPD, and it is estimated that another 12 million are undiagnosed.
COPD development is due to environmental exposures and various other factors. Cigarette smoking is the most common risk factor for COPD. In recent years, studies have shown an increase in the prevalence of COPD among women; this increase is due to a rise in the number of women who smoke, changes in occupational trends, and possibly greater susceptibility.
Exacerbations of COPD cause a more rapid decline in lung function and result in increased hospital admissions and mortality, which are associated with a greater financial burden. People with known COPD average 1. This article will highlight the management of acute COPD exacerbations. The GOLD Committee, which was formed inis a multidisciplinary team of healthcare providers and scientists who are working to promote COPD awareness and provide strategies for effective patient care.
This article will discuss some of the GOLD recommendations. This imbalance can cause hyperinflation, hypercapniaor hypoxemia, depending upon the severity of the exacerbation. Exacerbations may be precipitated by several factors. However, in more than one-third of exacerbations, the cause is not identified.
The three cardinal symptoms of COPD exacerbation are increased dyspnea, cough, and purulent sputum production. An exacerbation is acute in nature and is associated with a change in symptoms that is beyond normal day-to-day variation. Patients experiencing exacerbations should receive a thorough medical assessment including medical history, exposure history, clinical signs of severity, comorbidities, and additional laboratory tests.
Laboratory assessments include comparison of pulse oximetry with the patient at rest and during activity if the patient can ambulate, chest radiographs, electrocardiogram, electrolytes, and whole blood count. Spirometry is not recommended during exacerbations because the readings are inaccurate and the task is difficult for patients to perform. Management of exacerbations may occur in the inpatient or outpatient setting, depending upon the severity of the exacerbation and other patient-specific factors and circumstances.
Hospitalization may be indicated for patients who experience frequent exacerbations, have significant comorbid conditions, or cannot be managed easily in the outpatient setting. A worsening of clinical status, including the development of new physical signs or a pronounced increase in symptom intensity, also may warrant hospitalization.
The goals of exacerbation therapy are to decrease symptoms to baseline and prevent subsequent exacerbations. Pharmacologic treatment of exacerbations involves bronchodilators, corticosteroids, and antibiotics.
Short-Acting Bronchodilators: Short-acting beta 2 -agonists e. In a meta-analysis examining improvement of airflow obstruction with use of short-acting bronchodilators, the change in forced expiratory volume in 1 second FEV 1 did not differ significantly between metered-dose inhalers MDIs and nebulizers.
Methylxanthines theophylline and aminophylline are considered second-line IV therapy in patients having an insufficient response to short-acting bronchodilators. Although inhaled long-acting beta-agonists, long-acting anticholinergicsand corticosteroids are the mainstay of COPD maintenance therapy, they are not appropriate for the treatment of COPD exacerbations. High doses of short-acting beta-agonists, short-acting anticholinergicsand systemic corticosteroids are better suited to decreasing acute respiratory symptoms, whereas long-acting agents are indicated for reducing day-to-day symptoms, preventing exacerbations, and limiting disease progression.
If these agents are used concomitantly during an exacerbation, the patient has a higher likelihood of experiencing adverse effects, since the medication classes are very similar.
Corticosteroids: The benefits of systemic corticosteroid use as a component of COPD exacerbation treatment have been well established. However, the optimal dosage and duration have yet to be determined. Systemic corticosteroids have been shown to shorten length of hospital stay, decrease recovery time, improve FEV 1and improve arterial hypoxemia. In the past, the GOLD guidelines suggested the use of prednisolone 30 to 40 mg daily for 10 to 14 days.
In addition, there were no significant differences in mortality, need for mechanical ventilation, short-term adverse effects, recovery of lung function, or improvement of disease-related symptoms. However, patients receiving the shorter course of corticosteroids had a significant reduction in corticosteroid exposure and a shortened length of hospital stay.
At this time, the GOLD guidelines note that nebulized budesonide may be used as an alternative to systemic corticosteroids. Antibiotics: Antibiotic use in the management of exacerbations remains controversial. Antibiotic resistance is an increasing problem worldwide. The choice of the antibiotic should be based on the local pattern of bacterial resistance. Studies support the use of antibiotics when the patient has signs of bacterial infection. The recommended length of treatment is 5 to 10 days.
Titrated oxygen is associated with less acidosis, a lower need for ventilation, and reduced mortality compared with the use of high-flow oxygen during exacerbations.
Ventilatory Support: Some patients may require noninvasive nasal cannula or facial mask or invasive orotracheal tube or tracheostomy ventilatory support in order to maintain proper oxygenation. Criteria for the use of noninvasive ventilation and invasive mechanical ventilation are given in TABLE 2. It may be appropriate to allow a trial of noninvasive methods prior to advancing support, as these modalities are associated with improvement in clinical signs, a decreased need for escalation to invasive mechanical ventilation, and reduced mortality.
Although ventilatory support may seem necessary, it is important to take patient preferences into consideration and to be mindful of the risks. There is not an established optimal length of hospitalization for patients with COPD exacerbations. Prior to discharge, patients should be clinically stable for a minimum of 12 to 24 hours and should need inhaled short-acting beta 2 -agonists no more than every 4 hours.
A plan for effective home management and follow-up should be coordinated and clearly communicated to the patient and his or her caregivers and healthcare providers. It is imperative that discharge planning include medication counseling to ensure patient and caregiver comprehension and proper medication use. Despite efforts to prevent COPD exacerbations, the rate of readmission remains quite high, which has caught the attention of the Joint Commission and the Centers for Medicare and Medicaid Services in recent years.
The frequency and severity of COPD exacerbations have been associated with poor prognosis and increased mortality. Pharmacists can counsel patients about how to prevent future COPD exacerbations, including disease education, smoking cessation, pneumococcal and annual influenza vaccinations, and proper inhaler technique for maintenance therapy.
Chronic obstructive pulmonary disease. National Institutes of Health. Fact sheet: chronic obstructive pulmonary disease COPD. Accessed February 21, World Health Organization.
Chronic obstructive pulmonary disease fact sheet. Accessed February 20, Gender differences in COPD: are women more susceptible to smoking effects than men? COPD and gender differences: an update. Transl Res. Corticosteroid therapy for patients with acute exacerbations of chronic obstructive pulmonary disease: a systematic review.
Arch Intern Med. Respir Med. Prediction of the clinical course of chronic obstructive pulmonary disease, using the new GOLD classification: a study of the general population. Infections and airway inflammation in chronic obstructive pulmonary disease severe exacerbations.
Bronchodilator delivery in acute airflow obstruction. A meta-analysis. Oral corticosteroids in patients admitted to hospital with exacerbations of chronic obstructive pulmonary disease: a prospective randomised controlled trial.
Effect of systemic glucocorticoids on exacerbations of chronic obstructive pulmonary disease. N Engl J Med. Controlled trial of oral prednisone in outpatients with acute COPD exacerbation.
Efficacy of corticosteroid therapy in patients with an acute exacerbation of chronic obstructive pulmonary disease receiving ventilatory support. Association of corticosteroid dose and route of administration with risk of treatment failure in acute exacerbation of chronic obstructive pulmonary disease.
Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. Short-term vs conventional glucocorticoid therapy in acute exacerbations of chronic obstructive pulmonary disease: the REDUCE randomized clinical trial.
Miravitlles M, Anzueto A. Antibiotics for acute and chronic respiratory infections in patients with chronic obstructive pulmonary disease. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial. Gay PC. Complications of noninvasive ventilation in acute care. Respir Care.
Risk factors of hospitalization and readmission of patients with COPD exacerbation—systematic review. Readmissions for Chronic Obstructive Pulmonary Disease, Eisenhower C. Impact of pharmacist-conducted medication reconciliation at discharge on readmissions of elderly patients with COPD. Ann Pharmacother. Can the targeted use of a discharge pharmacist significantly decrease day readmissions? Hosp Pharm. Sehatzadeh S.
Influenza and pneumococcal vaccinations for patients with chronic obstructive pulmonary disease COPD : an evidence-based review.
❾-50%}Maintenance dose of prednisone for copd -
Decreasing transcription transrepression can decrease the production of inflammatory cytokines, chemokines, adhesion molecules, and receptors. Alternatively, increasing transcription transactivation of selected DNA genes can increase inflammatory cytokine production or anti-inflammatory proteins, such as annexin A1 also known as lipocortin.
Prednisone is often prescribed as an oral anti-inflammatory drug for myriad medical diseases and disorders in an attempt to attenuate systemic inflammatory response and restore a dynamic physiological homeostasis in patients—for example, in patients who have significant inflammatory response with sepsis and respiratory failure from community-acquired pneumonia. The common chronic diseases treated with prednisone range from asthma, COPD, and inflammatory bowel disease to rheumatoid arthritis, sarcoidosis, and granulomatosis with polyangiitis.
Prednisone has not cured any of these conditions, but it can induce temporary remission of symptoms and cause adverse effects AEs in patients who try to live normally between exacerbations of their underlying ailment. Prednisone was the 22nd most commonly prescribed drug in the United States in , with more than 25 million prescriptions written. Three stages must occur for successful signal transduction by prednisone and other oral corticosteroids CSs into target tissues and cells: extracellular, cytoplasmic and nuclear Table 1.
Then, in stage 3, the GR activated by prednisolone is able to translocate through nuclear pores and bind to glucocorticoid response elements GREs on glucocorticoid-sensitive DNA genes.
Because mRNA acts as template for protein synthesis or translation, corticosteroids can either stimulate or inhibit the synthesis of specific proteins. Transcription of DNA is tightly regulated by the acetylation of core histones, which keep DNA coiled tightly, forming chromatin, which cannot be transcribed by RNA polymerase. Acetylation of selected core histones allows a portion of DNA to uncoil, permitting transcription by RNA polymerase encoding in mRNA the instructions for ribosomes to synthesize inflammatory proteins eg, cytokines.
Deacetylation of histones causes DNA to coil again and inhibits transcription. Any interruption of signal transduction can foil the therapeutic effects of CSs. CSs can decrease the production of cytokines and decrease activation of key cells, including T lymphocytes, dendritic cells, macrophages, mast cells, basophils, and eosinophils.
CSs decrease leukocyte migration, decrease white blood cell phagocytosis by stabilizing lysosomes, and cause lymphopenia to result in general immunosuppression. CSs, through annexin A1, inhibit phospholipase A2, which reduces production of prostaglandins, leukotrienes, and thromboxanes. The potency of CSs Table 2 5 is measured by the degree of skin blanching or vasoconstriction after topical application to the skin of a human, mouse, rat, or guinea pig.
Understanding why ICSs are failing to control symptoms and prevent exacerbations is at the crux of expert consultation. ICSs remain the most effective first-line daily controller drug therapy, and adherence can reduce the need for prednisone and help prevent death.
But is asthma the correct diagnosis? Is the ICS being delivered by the inhaler effectively into the lungs? Is the patient a responder or a nonresponder to ICSs? OCS therapy has been a pillar primarily in the treatment of severe asthma exacerbations since the s in outpatient practice Table 3. Systemic CSs oral, intravenous, or intramuscular can prevent death from asthma exacerbations and relapse 7 and in acute care settings should be administered in all but the mildest exacerbations in adults and adolescents.
The individualized written asthma action plan should provide access for reporting to clinicians whenever an exacerbation occurs and include clear instructions on when and how to take OCSs at home. Courses lasting 5 to 7 days in adults have been found to be as effective as and day courses, respectively.
GINA reflects the best available evidence at the time the recommendations were prepared. Adherence to guidelines will not ensure successful treatment in every patient. In recent years, studies have shown an increase in the prevalence of COPD among women; this increase is due to a rise in the number of women who smoke, changes in occupational trends, and possibly greater susceptibility. Exacerbations of COPD cause a more rapid decline in lung function and result in increased hospital admissions and mortality, which are associated with a greater financial burden.
People with known COPD average 1. This article will highlight the management of acute COPD exacerbations. The GOLD Committee, which was formed in , is a multidisciplinary team of healthcare providers and scientists who are working to promote COPD awareness and provide strategies for effective patient care. This article will discuss some of the GOLD recommendations.
This imbalance can cause hyperinflation, hypercapnia , or hypoxemia, depending upon the severity of the exacerbation.
Exacerbations may be precipitated by several factors. However, in more than one-third of exacerbations, the cause is not identified.
The three cardinal symptoms of COPD exacerbation are increased dyspnea, cough, and purulent sputum production. An exacerbation is acute in nature and is associated with a change in symptoms that is beyond normal day-to-day variation.
Patients experiencing exacerbations should receive a thorough medical assessment including medical history, exposure history, clinical signs of severity, comorbidities, and additional laboratory tests. Laboratory assessments include comparison of pulse oximetry with the patient at rest and during activity if the patient can ambulate, chest radiographs, electrocardiogram, electrolytes, and whole blood count.
Spirometry is not recommended during exacerbations because the readings are inaccurate and the task is difficult for patients to perform. Management of exacerbations may occur in the inpatient or outpatient setting, depending upon the severity of the exacerbation and other patient-specific factors and circumstances.
Hospitalization may be indicated for patients who experience frequent exacerbations, have significant comorbid conditions, or cannot be managed easily in the outpatient setting. A worsening of clinical status, including the development of new physical signs or a pronounced increase in symptom intensity, also may warrant hospitalization.
The goals of exacerbation therapy are to decrease symptoms to baseline and prevent subsequent exacerbations. Pharmacologic treatment of exacerbations involves bronchodilators, corticosteroids, and antibiotics. Short-Acting Bronchodilators: Short-acting beta 2 -agonists e. In a meta-analysis examining improvement of airflow obstruction with use of short-acting bronchodilators, the change in forced expiratory volume in 1 second FEV 1 did not differ significantly between metered-dose inhalers MDIs and nebulizers.
Methylxanthines theophylline and aminophylline are considered second-line IV therapy in patients having an insufficient response to short-acting bronchodilators.
Although inhaled long-acting beta-agonists, long-acting anticholinergics , and corticosteroids are the mainstay of COPD maintenance therapy, they are not appropriate for the treatment of COPD exacerbations.
High doses of short-acting beta-agonists, short-acting anticholinergics , and systemic corticosteroids are better suited to decreasing acute respiratory symptoms, whereas long-acting agents are indicated for reducing day-to-day symptoms, preventing exacerbations, and limiting disease progression.
If these agents are used concomitantly during an exacerbation, the patient has a higher likelihood of experiencing adverse effects, since the medication classes are very similar. Corticosteroids: The benefits of systemic corticosteroid use as a component of COPD exacerbation treatment have been well established. However, the optimal dosage and duration have yet to be determined. Systemic corticosteroids have been shown to shorten length of hospital stay, decrease recovery time, improve FEV 1 , and improve arterial hypoxemia.
In the past, the GOLD guidelines suggested the use of prednisolone 30 to 40 mg daily for 10 to 14 days. In addition, there were no significant differences in mortality, need for mechanical ventilation, short-term adverse effects, recovery of lung function, or improvement of disease-related symptoms.
However, patients receiving the shorter course of corticosteroids had a significant reduction in corticosteroid exposure and a shortened length of hospital stay. At this time, the GOLD guidelines note that nebulized budesonide may be used as an alternative to systemic corticosteroids. Antibiotics: Antibiotic use in the management of exacerbations remains controversial. Antibiotic resistance is an increasing problem worldwide. The choice of the antibiotic should be based on the local pattern of bacterial resistance.
Inflammation may be present in both asthma and COPD. The strategic use of prednisone can soothe and thus heal the delicate lining layer of these passageways, making them more resistant to bronchospasm. Prednisone has another effect in preserving or even increasing the receptors for inhaled bronchodilators. Thus prednisone is used both to combat inflammation and to enhance the effectiveness of one of the most valuable bronchodilators we have for asthma and COPD.
The downside is well-known. It causes wear and tear on the bones, and in some patients the acceleration of cataract formation and the worsening of glaucoma high pressure in the eyes. The bone problem is much worse in women than men, and it is a particular problem in small-boned, light-skinned women beyond the menopause. On the other hand, large-boned, dark-skinned people have relatively little trouble with prednisone. Men have far less trouble than women, probably because their bones are larger to start with.
The benefits of chronic corticosteroid use in patients with chronic obstructive pulmonary disease COPD are not well-established. Compared with patients who have asthma, patients with COPD have unclear benefits from corticosteroids.
Few randomized trials have been conducted to determine the additional benefit of this therapy in patients with COPD. All had been taking prednisone at a daily dosage of at least 5 mg per day for the preceding six months. Excluded were those with a clinical diagnosis of asthma, a strong family history of atopy or a concomitant major illness. All subjects also received inhaled triamcinolone acetonide.
Patients were randomly assigned to receive their usual maintenance dose of prednisone for six months or to be withdrawn from prednisone at a rate of 5 mg per week. Study results revealed that the number of COPD exacerbations per patient was similar 2. Spirometric results, dyspnea and health-related quality of life indicators did not differ significantly between the two groups. Weight decreased in the demand group by 4. The authors concluded that withdrawal of chronic low-dose systemic steroids did not adversely affect COPD—related outcomes.
Furthermore, steroid-associated complications, such as weight gain, were affected by withdrawal of this agent. It is likely that this change will not adversely affect the management of the disease. Furthermore, patients are likely to experience quality-of-life benefits from discontinuing oral corticosteroid therapy, including reduced body weight.
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In the past, the GOLD guidelines suggested the use of prednisolone 30 to 40 mg daily for 10 to 14 days. However, the most recent update. All had been taking prednisone at a daily dosage of at least 5 mg per receive their usual maintenance dose of prednisone for six months. Inhaled steroids tend to be used as maintenance medications to keep symptoms under control for the long term. Doses are measured in micrograms (mcg). All had been taking prednisone at a daily dosage of at least 5 mg per receive their usual maintenance dose of prednisone for six months. Otherwise, steroid advocates recommend maintenance doses of –15 mg·day−1 for those patients who do show significant clinical benefit 3, mainly in. People with known COPD average 1. Accessed February 21, Physicians believe that between 1, mg per day is necessary to help prevent osteoporosis.The perils of prednisone. But is this approach correct? Is it safe? What have patients taught us about prednisone? In short:. Prednisone is a prodrug.
Prednisone is a glucocorticoid. Prednisone is a mineralocorticoid. But is prednisone a poison? Prednisone and other glucocorticoids regulate the metabolic and inflammatory function of many cells, tissues, and organs by directly modulating DNA transcription. Decreasing transcription transrepression can decrease the production of inflammatory cytokines, chemokines, adhesion molecules, and receptors.
Alternatively, increasing transcription transactivation of selected DNA genes can increase inflammatory cytokine production or anti-inflammatory proteins, such as annexin A1 also known as lipocortin.
Prednisone is often prescribed as an oral anti-inflammatory drug for myriad medical diseases and disorders in an attempt to attenuate systemic inflammatory response and restore a dynamic physiological homeostasis in patients—for example, in patients who have significant inflammatory response with sepsis and respiratory failure from community-acquired pneumonia.
The common chronic diseases treated with prednisone range from asthma, COPD, and inflammatory bowel disease to rheumatoid arthritis, sarcoidosis, and granulomatosis with polyangiitis. Prednisone has not cured any of these conditions, but it can induce temporary remission of symptoms and cause adverse effects AEs in patients who try to live normally between exacerbations of their underlying ailment.
Prednisone was the 22nd most commonly prescribed drug in the United States in , with more than 25 million prescriptions written. Three stages must occur for successful signal transduction by prednisone and other oral corticosteroids CSs into target tissues and cells: extracellular, cytoplasmic and nuclear Table 1.
Then, in stage 3, the GR activated by prednisolone is able to translocate through nuclear pores and bind to glucocorticoid response elements GREs on glucocorticoid-sensitive DNA genes. Because mRNA acts as template for protein synthesis or translation, corticosteroids can either stimulate or inhibit the synthesis of specific proteins.
Transcription of DNA is tightly regulated by the acetylation of core histones, which keep DNA coiled tightly, forming chromatin, which cannot be transcribed by RNA polymerase. Acetylation of selected core histones allows a portion of DNA to uncoil, permitting transcription by RNA polymerase encoding in mRNA the instructions for ribosomes to synthesize inflammatory proteins eg, cytokines.
Deacetylation of histones causes DNA to coil again and inhibits transcription. Any interruption of signal transduction can foil the therapeutic effects of CSs. CSs can decrease the production of cytokines and decrease activation of key cells, including T lymphocytes, dendritic cells, macrophages, mast cells, basophils, and eosinophils.
CSs decrease leukocyte migration, decrease white blood cell phagocytosis by stabilizing lysosomes, and cause lymphopenia to result in general immunosuppression. CSs, through annexin A1, inhibit phospholipase A2, which reduces production of prostaglandins, leukotrienes, and thromboxanes. The potency of CSs Table 2 5 is measured by the degree of skin blanching or vasoconstriction after topical application to the skin of a human, mouse, rat, or guinea pig.
Understanding why ICSs are failing to control symptoms and prevent exacerbations is at the crux of expert consultation. ICSs remain the most effective first-line daily controller drug therapy, and adherence can reduce the need for prednisone and help prevent death.
But is asthma the correct diagnosis? Is the ICS being delivered by the inhaler effectively into the lungs? Is the patient a responder or a nonresponder to ICSs? OCS therapy has been a pillar primarily in the treatment of severe asthma exacerbations since the s in outpatient practice Table 3.
Systemic CSs oral, intravenous, or intramuscular can prevent death from asthma exacerbations and relapse 7 and in acute care settings should be administered in all but the mildest exacerbations in adults and adolescents. The individualized written asthma action plan should provide access for reporting to clinicians whenever an exacerbation occurs and include clear instructions on when and how to take OCSs at home.
Courses lasting 5 to 7 days in adults have been found to be as effective as and day courses, respectively. GINA reflects the best available evidence at the time the recommendations were prepared. Adherence to guidelines will not ensure successful treatment in every patient.
Guidelines should not be setting a standard of care or exclude other evidence-based effective asthma treatments. One of our most important goals in managing asthma is always to reduce and eliminate the need and use of OCSs at every opportunity by improving asthma control within the framework of GINA However, strict adherence to best-practice reports or guidelines may leave a patient with asthma who does not respond to ICSs to require escalating dosages of ICSs and even daily OCSs.
Finally, strict adherence to guidelines may leave patients who have been misdiagnosed with asthma to continue treatment for a disease they do not have.
The risks of complications and danger is never greater than when patients are prescribed daily prednisone or methylprednisolone. A common pitfall is to prescribe prednisone for its therapeutic benefits while distancing concern for AEs and the risk of causing a concurrent condition to occur. Prednisone is an iatrogenic poison whenever clinicians lose awareness of these dangers or when it is prescribed inappropriately or for too long.
It is imperative to realize that even short courses of prednisone 5 to 14 days can be associated with AEs and risks of developing new conditions or exacerbating underlying conditions that require immediate diagnosis and treatment Table 4. Iatrogenic Cushing syndrome is the most common cause of Cushing syndrome. The AEs of prednisone can cause nonspecific signs and symptoms that patients can mistake for ordinary daily aches and pains Table 5. The occurrence of these effects is often associated with dose and duration of therapy.
Serious and often life-threatening complications can occur from even short-term use of prednisone. OCS-sparing attempts should be made early and frequently but only under medical supervision. OCSs should be tapered slowly to avoid triggering adrenal crisis and even death. There are other dangers clinicians must be aware of. Of the more than 1. Within 30 days of drug initiation, there was an increase in rates of sepsis, venous thromboembolism VTE , and fracture, which diminished over the following 31 to 90 days.
Patients taking 4 or more OCS prescriptions within a given year had 1. Having 4 or more OCS prescriptions was linked to significantly greater odds of developing osteoporosis, hypertension, obesity, type 2 diabetes, GERD, peptic ulcer disease, gastrointestinal tract bleeding, bone fractures, and cataracts. For patients requiring prednisone daily or who need a prednisone-sparing strategy, monoclonal antibodies offer hope when repeated attempts at withdrawal of prednisone fail. Although there are no evidence-based guidelines for tapering of OCSs, gradual tapering is frequently a part of treatment protocols to reduce the risk of severe asthma symptoms and acute exacerbations returning.
Time to recovery of endogenous cortisol production in the patient after stopping prednisone can vary considerably. Withdrawal from long-term OCS therapy can result in secondary adrenal insufficiency from adrenal atrophy from hypothalamic-pituitary-adrenal axis suppression after discontinuation of prednisone, particularly if the patient has remained on prednisone at a dosage greater than 7.
If adrenal suppression is suspected, early morning cortisol should be measured when the prednisone dose is reduced to 7. Adrenal suppression often occurs following abrupt discontinuation of prednisone. ICSs may also be absorbed systemically to the degree that they can cause adrenal suppression. Table 6 summarizes a number of pitfalls to avoid when treating patients with prednisone and other OCSs. The benefits of prednisone outweigh the risks when treating severe exacerbations, and the medication can be life-saving.
However, medical treatment for an illness can produce a worse net result than the illness does, notably via AEs. Cardiac arrhythmias, bone fractures, gastrointestinal tract bleeding, mood changes, tuberculosis or fungal pneumonia, sepsis, and venous thromboembolism can be triggered by prednisone but are often considered events separate from asthma and prednisone.
Invasive pulmonary aspergillosis has been associated with the use of high-dose ICSs in a patient with asthma. The report of these complications linked to prednisone should prompt every clinician to assess each patient during the review of systems for underlying heart disease, osteoporosis, GERD, peptic ulcer disease, depression, smoking, cancer, and estrogen replacement. Patient education and regular review of symptoms in the primary care setting are important in early detection of AEs from OCSs or ICSs eg, Cushing syndrome, diabetes, osteoporosis apart from adrenal suppression during withdrawal of prednisone.
Patients certainly need to be more aware this important safety information as they prepare to take prednisone as directed by their asthma action plan. All drugs can be poisons and should be prescribed for their medicinal properties only when appropriate indications exist. The dose and duration of prednisone treatment should be kept short as possible days. All patients should be monitored by email, video visit, or telephone call to assess clinical response.
Take time to confirm the asthma diagnosis and consider add-on maintenance drugs to reduce or eliminate the dosage and need for prednisone.
Patient safety is a contact sport where the patient and clinician must team up to reduce impairment and risks from asthma and drug therapy. Safety never happens by accident.
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