У детей в большинстве случаев вирусной этиологии, поэтому АБ не требуются. Бактериальная или вирусная инфекция - вывод делать должен врач, на основе анализа крови и посевов, чем наши врачи регулярно пренебрегают и дают АБ либо по настоянию родителей, либо без должных на то оснований.С гнойной ангиной и пневмонией в этом плане проще. Первую видно при осмотре, а вторую - при наличии снимка. Pediatric Bronchitis Patrick L Carolan, MD, Adjunct Associate Professor, Departments of Pediatrics, Family Practice, and Community Health, University of Minnesota Medical School; Medical Director of Minnesota Sudden Infant Death Center; Attending Staff, Department of Emergency Services, Children's Hospitals and Clinics of Minnesota Updated: May 6, 2010 Pathophysiology Acute bronchitis leads to the hacking cough and phlegm production that often follows upper respiratory tract infection. This occurs because of the inflammatory response of the mucous membranes within the lungs' bronchial passages. Viruses, acting alone or together, account for most of these infections.[2,3 ] In children, chronic bronchitis follows either an endogenous response (eg, excessive inflammation) to acute airway injury or continuous exposure to certain noxious environmental agents (eg, allergens or irritants). An airway that undergoes such an insult responds quickly with bronchospasm and cough, followed by inflammation, edema, and mucus production. This helps explain the fact that apparent chronic bronchitis in children is often actually asthma. Mucociliary clearance is an important primary innate defense mechanism that protects the lungs from the harmful effects of inhaled pollutants, allergens, and pathogens.[4 ]Mucociliary dysfunction is a common feature of chronic airway diseases. The mucociliary apparatus consists of 3 functional compartments: the cilia, a protective mucus layer, and an airway surface liquid (ASL) layer, which work together to remove inhaled particles from the lung. Animal study data have identified a critical role for ASL dehydration in the pathogenesis of mucociliary dysfunction and chronic airway disease.[5 ]ASL depletion resulted in reduced mucus clearance and histologic signs of chronic airway disease, including mucous obstruction, goblet cell hyperplasia, and chronic inflammatory cell infiltration. Study animals experienced reduced bacterial clearance and high pulmonary mortality as a result. The role of irritant exposure, particularly cigarette smoke and airborne particulates, in recurrent (wheezy) bronchitis and asthma is becoming clearer. Kreindler et al demonstrated that the ion transport phenotype of normal human bronchial epithelial cells exposed to cigarette smoke extract is similar to that of cystic fibrosis epithelia, in which sodium is absorbed out of proportion to chloride secretion in the setting of increased mucus production.[6 ]These findings suggest that the negative effects of cigarette smoke on mucociliary clearance may be mediated through alterations in ion transport. McConnell et al noted that organic carbon and nitrogen dioxide airborne particulates were associated with the chronic symptoms of bronchitis among children with asthma in southern California.[7 ] A chronic or recurrent insult to the airway epithelium, such as recurrent aspiration or repeated viral infection, may contribute to chronic bronchitis in childhood. Following damage to the airway lining, chronic infection with commonly isolated airway organisms may occur. The most common bacterial pathogen that causes lower respiratory tract infections in children of all age groups is Streptococcus pneumoniae. Nontypeable Haemophilus influenzae and Moraxella catarrhalis may be significant pathogens in preschoolers (age <5 y), whereas Mycoplasma pneumoniae may be significant in school-aged children (ages 6-18 y). Children with tracheostomies are often colonized with an array of flora, including alpha-hemolytic streptococci and gamma-hemolytic streptococci. With acute exacerbations of tracheobronchitis in these patients, pathogenic flora may include Pseudomonas aeruginosa and Staphylococcus aureus (including methicillin-resistant strains), among other pathogens. Children predisposed to oropharyngeal aspiration, particularly those with compromised protective airway mechanisms, may become infected with oral anaerobic strains of streptococci. Etiology Acute bronchitis is generally caused by respiratory infections; approximately 90% are viral in origin, and 10% are bacterial. Chronic bronchitis may be caused by repeated attacks of acute bronchitis, which can weaken and irritate bronchial airways over time, eventually resulting in chronic bronchitis. Industrial pollution is also a common cause; however, the chief culprit is heavy long-term cigarette smoke exposure. Viral infections include the following: * Adenovirus * Influenza * Parainfluenza * Respiratory syncytial virus * Rhinovirus * Human bocavirus[8,9,10 ] * Coxsackievirus * Herpes simplex virus Secondary bacterial infection as part of an acute upper respiratory tract infection is extremely rare in non–smoke-exposed patients without cystic fibrosis or immunodeficiency but may include the following: * S pneumoniae * M catarrhalis * H influenzae (nontypeable) * Chlamydia pneumoniae (Taiwan acute respiratory [TWAR] agent) * Mycoplasma species Air pollutants, such as those that occur with smoking and from second-hand smoke, also cause incident bronchiolitis.[11 ]Tsai et al demonstrated that in utero and postnatal household cigarette smoke exposure is strongly linked to asthma and recurrent bronchitis in children.[12 ] Other causes include the following: * Allergies * Chronic aspiration or gastroesophageal reflux * Fungal infection Plastic bronchitis Plastic bronchitis is an unusual but potentially devastating form of obstructive bronchial disease. The disease is characterized by the development of arborizing, thick, tenacious casts of the tracheobronchial tree that produce airway obstruction. Patients with congenital heart disease who have undergone a Fontan operation are a group at high risk for development of this problem, for unknown reasons. In some cases, plastic bronchitis appears many years after the Fontan procedure is performed.[13 ]Zahorec et al describe cases occurring in the immediate postoperative period following a Fontan procedure. These patients were successfully managed with short periods of high-frequency jet ventilation and vigorous pulmonary toilet.[14 ] Therapies include endoscopic debridement of the airway, vigorous pulmonary toilet, and aerosolized tissue plasminogen activator. Shah et al performed thoracic duct ligation, resulting in complete resolution of the formation of casts in 2 patients with plastic bronchitis refractory to medical management.[15 ]These results suggest that high intrathoracic lymphatic pressures are related to the development of the recurrent bronchial casts seen in this disorder. Overview Acute bronchitis is a clinical syndrome produced by inflammation of the trachea, bronchi, and bronchioles. In children, acute bronchitis usually occurs in association with viral respiratory tract infection. Acute bronchitis is rarely a primary bacterial infection in otherwise healthy children. (See Pathophysiology, as well as Etiology.) Symptoms of acute bronchitis usually include productive cough and sometimes retrosternal pain during deep breathing or coughing. Generally, the clinical course of acute bronchitis is self-limited, with complete healing and full return to function typically seen within 10-14 days following symptom onset. (See Clinical Presentation.) Chronic bronchitis is recurring inflammation and degeneration of the bronchial tubes that may be associated with active infection. Patients with chronic bronchitis have more mucus than normal because of either increased production or decreased clearance. Coughing is the mechanism by which excess secretion is cleared. Chronic bronchitis is often associated with asthma, cystic fibrosis, dyskinetic cilia syndrome, foreign body aspiration, or exposure to an airway irritant. Recurrent tracheobronchitis may occur with tracheostomies or immunodeficiency states. (See Diagnosis.) Defining chronic bronchitis and its prevalence in childhood has been complicated by the significant clinical overlap with asthma and reactive airway disease states. In adults, chronic bronchitis is defined as daily production of sputum for at least 3 months in 2 consecutive years. Some have applied this definition to childhood chronic bronchitis. Others limit the definition to a productive cough that lasts more than 2 weeks despite medical therapy. Chronic bronchitis has also been defined as a complex of symptoms that includes cough that lasts more than 1 month or recurrent productive cough that may be associated with wheezing or crackles on auscultation. Elements of these descriptors are present in the working definitions of asthma, as well.[1 ] Treatment of chronic bronchitis in pediatric patients includes rest, use of antipyretics, adequate hydration, and avoidance of smoke. (See Treatment and Management.) Analgesics and antipyretics target the symptoms of pediatric bronchitis. In chronic cases, bronchodilator therapy should be considered. Oral corticosteroids should be added if cough continues and the history and physical examination findings suggest a wheezy form of bronchitis. (See Medication.) Epidemiology Data collected from the National Ambulatory Care Survey 1991 Summary showed that 2,774,000 office visits by children younger than 15 years resulted in a diagnosis of bronchitis.[16 ]Although the report did not separate diagnoses into acute and chronic bronchitis, the frequency of visits made bronchitis just slightly less common than otitis media and slightly more common than asthma. However, in children, asthma is often underdiagnosed and is frequently misdiagnosed as chronic or recurrent bronchitis. Since 1996, 9-14 million Americans have been diagnosed with chronic bronchitis annually. Bronchitis, both acute and chronic, is prevalent throughout the world and is one of the top 5 reasons for childhood physician visits in countries that track such data. The incidence of bronchitis in British schoolchildren is reported to be 20.7%. Weigl et al noted an overall increase in hospitalization for lower respiratory tract infection (laryngotracheobronchitis, bronchitis, wheezing bronchitis, bronchiolitis, bronchopneumonia, pneumonia) among German children from 1996 to 2000; this is consistent with observations among children from the United States, United Kingdom, and Sweden.[17 ]The incidence rate of bronchitis in children in this German cohort was 28%. Differences in population prevalences have been identified in patients with chronic bronchitis. For example, because of the association of chronic bronchitis with asthma and the concentration of asthma risk factors among inner-city populations, this population group is at higher risk. The incidence of acute bronchitis is equal in males and females. The incidence of chronic bronchitis is difficult to state precisely because of the lack of definitive diagnostic criteria and the considerable overlap with asthma. However, in recent years, the prevalence of chronic bronchitis has been reported to be consistently higher in females than in males. Acute (typically wheezy) bronchitis occurs most commonly in children younger than 2 years, with another peak seen in children aged 9-15 years. Chronic bronchitis affects people of all ages but is more prevalent in persons older than 45 years. Clinical History Acute bronchitis begins as a respiratory tract infection that manifests as the common cold. Symptoms often include coryza, malaise, chills, slight fever, sore throat, and back and muscle pain. The cough in these children is usually accompanied by a nasal discharge. The discharge is watery at first, then after several days becomes thicker and colored or opaque. It then becomes clear again and has a mucoid watery consistency before it spontaneously resolves within 7-10 days. Purulent nasal discharge is common with viral respiratory pathogens and, by itself, does not imply bacterial infection. Initially, the cough is dry and may be harsh or raspy sounding. The cough then loosens and becomes productive. Children younger than 5 years rarely expectorate. In this age group, sputum is usually seen in vomitus (ie, posttussive emesis). Parents frequently note a rattling sound in the chest. Hemoptysis, a burning discomfort in the chest, and dyspnea may be present. Brunton et al noted that adult patients with chronic bronchitis have a history of persistent cough that produces yellow, white, or greenish sputum on most days for at least 3 months of the year and for more than 2 consecutive years.[18 ]Wheezing and reports of breathlessness are also common. Pulmonary function testing in these adult patients reveals irreversible reduction in maximal airflow velocity. Physical Examination Lungs may sound normal. Crackles, rhonchi, or large airway wheezing, if any, tend to be scattered and bilateral. The pharynx may be injected. Bronchitis and Asthma Recurrent episodes of acute or chronic infectious bronchitis are unusual in children and should alert the clinician to the likelihood of asthma. Bronchitis is often repeatedly diagnosed in children in whom asthma has remained undiagnosed for many years. Similarly, a family history of asthma in parents or siblings may be masked within a history of “recurrent bronchitis.” The diagnosis of "asthmatic bronchitis" or "wheezy bronchitis" is simply asthma. Bronchitis and Immunodeficiency Recurrent episodes of acute or chronic bronchitis may be associated with immunodeficiency. Stiehm identifies the 4 most common immunodeficiencies in pediatric patients[19 ]: · Transient hypogammaglobulinemia of infancy (THI) · Immunoglobulin G (IgG) subclass deficiency · Impaired polysaccharide responsiveness (partial antibody deficiency) · Selective IgA deficiency (IgAD) A summary of immunodeficiency registries in 4 countries listed IgAD in 27.5% of the patients, IgG subclass deficiency in 4.8%, and THI in 2.3%. Patients typically have normal cellular immune systems, phagocyte function, and complement levels. All 4 immunodeficiency states are characterized by recurrent bacterial respiratory infections, such as purulent rhinitis, sinusitis, otitis, and bronchitis. Some patients with selective immunodeficiency may benefit from the use of intravenous immunoglobulin (IVIG), and the long-term prognosis is generally excellent. Ozkan studied immunoglobulin A (IgA) and IgG deficiency in children who presented with recurrent sinopulmonary infection[20 ]and found that the overall frequency of antibody defects was 19.1%. IgA deficiency was observed in 9.3%, IgG subclass deficiency was observed in 8.4%, and both IgA and IgG subclass deficiencies were observed in 1.4%. The prevalence of IgA and/or IgG subclass deficiency was 25% in patients with recurrent upper respiratory tract infections, 22% in patients with recurrent pulmonary infections, and 12.3% in patients with recurrent bronchiolitis. Common variable immunodeficiency is the most frequent of the primary hypogammaglobulinemias. In a Finnish study by Kainulainen et al of patients with common variable immunodeficiency receiving immunoglobulin replacement therapy,[21 ]sinopulmonary infections were the most common clinical presentation: 66% had recurrent pneumonia, 60% had recurrent maxillary sinusitis, and 45% had recurrent bronchitis. In the Kainulainen study, the mean interval from the time of onset of symptoms to diagnosis was 8 years. Evidence of chronic lung damage was noted in 17% of patients at the time of diagnosis, highlighting the importance of early recognition in the prevention of chronic pulmonary sequelae. To improve the recognition of common variable immunodeficiency, the authors suggest consideration of this condition in patients with recurrent sinopulmonary infection. In addition to a low serum IgG concentration, measurement of specific antibody production is recommended to establish the diagnosis. Differential Diagnoses Aspergillosis IgA and IgG Subclass Deficiencies Aspiration Syndromes Influenza Asthma Inhalation Injury Atypical Mycobacterial Infection Passive Smoking and Lung Disease Bacterial Tracheitis Pneumonia Bronchiectasis Respiratory Syncytial Virus Infection Bronchiolitis Rhinovirus Infection Bronchogenic Cyst Sinusitis Bronchopulmonary Dysplasia Tracheomalacia Common Variable Immunodeficiency Tuberculosis Cystic Fibrosis Gastroesophageal Reflux Diagnostic Considerations Consider the following in the diagnosis of bronchitis in pediatric patients: * Retained foreign body * Bronchopulmonary allergy * Immunosuppression Chronic bronchitis is often part of an underlying disease process, such as asthma, cystic fibrosis, dyskinetic cilia syndrome, foreign body aspiration, or exposure to an airway irritant. Recurrent tracheobronchitis may also be seen in patients with tracheostomy or with certain forms of immunodeficiency. In all of these patient groups, chronic bronchitis should not be the primary diagnosis, because it does not describe the pathology of the underlying disorder. Workup Approach Considerations For maximal cost-effectiveness, diagnostic laboratory tests for bronchitis should be performed in a stepwise manner. Patients with uncomplicated acute respiratory illness who are cared for in an outpatient setting need little, if any, laboratory evaluation. Testing in Hospitalized Children For hospitalized children, serum C-reactive protein screen, respiratory culture, rapid diagnostic studies, and serum cold agglutinin testing (at the appropriate age) help to classify whether the infection is caused by bacteria, atypical pathogens (eg, Chlamydia pneumoniae, Mycoplasma pneumoniae), or viruses. Obtain a blood or sputum culture if antibiotic therapy is under consideration. For the child admitted to the hospital with a possible chlamydial, mycoplasmal, or viral lower respiratory tract infection for which specific therapy is considered, test nasopharyngeal secretions for these pathogens, using antigen or polymerase chain reaction testing for Chlamydia species and respiratory syncytial, parainfluenza, and influenza viruses or viral culture. Results will guide appropriate antimicrobial selection. For the child who has been intubated, collect a specimen of deep respiratory secretions for Gram stain, chlamydial and viral antigen assays, and bacterial and viral cultures. Asthma Testing A clinical response to daily high-dose oral corticosteroids may be considered as a diagnostic and therapeutic trial to confirm asthma. Evidence of reversible airflow obstruction revealed by pulmonary function testing confirms the diagnosis of asthma. Cystic Fibrosis Testing A negative sweat test result using pilocarpine iontophoresis should exclude cystic fibrosis. Many states are now using CFTR mutational analyses in newborn screening programs. Immunodeficiency Testing For children in whom immunodeficiency is suspected, measurement of total serum immunoglobulins, immunoglobulin G (IgG) subclasses, and specific antibody production is recommended to establish the diagnosis. Chest Radiography Chest films generally appear normal in patients with uncomplicated bronchitis. Abnormal findings are minimal and may include atelectasis, hyperinflation, and peribronchial thickening. Focal consolidation is not usually present. These findings are similar to the radiographic findings in patients with asthma. Radiographic findings may help exclude other diseases or complications, particularly when abnormalities in either vital signs or pulse oximetry findings are present. Pulmonary Function Testing Pulmonary function tests may show airflow obstruction that is reversible with bronchodilators. Bronchial challenge, such as with exercise or with histamine or methacholine exposure, may demonstrate the airway hyperreactivity characteristic of asthma. Bronchoscopy On fiberoptic bronchoscopy, a diagnosis of chronic bronchitis is suggested if the airways appear erythematous and friable. Bronchoalveolar lavage may be useful in establishing an infectious cause. Bronchoalveolar lavage may reveal numerous monocytic or polymorphonuclear inflammatory cells. In children with chronic aspiration of gastric contents, lipids may be present within macrophages. Treatment Consultations Referral to a pediatric pulmonologist may be helpful for patients experiencing persistent or recurrent symptoms and whose histories suggest the possibility of tracheobronchial foreign body aspiration, cystic fibrosis, immunodeficiency, or persistent asthma for which appropriate first-line symptom or controller therapies have failed. Complications Complications are extremely rare and should prompt evaluation for anomalies of the respiratory tract, including immune deficiencies. Complications may include the following: * Bronchiectasis * Bronchopneumonia * Acute respiratory failure Approach Considerations Emergency care for acute bronchitis or exacerbation of chronic bronchitis must focus on ensuring that the child has adequate oxygenation. Outpatient care is appropriate unless bronchitis is complicated by severe underlying disease. General measures include rest, use of antipyretics, adequate hydration, and avoidance of smoke. Proper care of any underlying disorder is of paramount importance. Consideration of asthma and adequate therapy are critical to an early response. Febrile patients should increase oral fluid intake. Instruct the patient to rest until the fever subsides. Resolution of symptoms, normal findings on physical examination, and normal pulmonary function test results indicate the end of the need for acute treatment. Patients in whom asthma is diagnosed will likely require ongoing therapy for that disease. Patients with defined hypogammaglobulinemia may need periodic immunoglobulin replacement treatments. These are best coordinated with the assistance of a pediatric allergy and immunology or pulmonary specialist. Pharmacologic Therapy Acute bronchitis Medical therapy generally targets symptoms and includes use of analgesics and antipyretics. Antitussives and expectorants are often prescribed but have not been demonstrated to be useful. Few data outside of the research laboratory support the efficacy of expectorants. The prototype antitussive, codeine, has been successful in some chronic-cough and induced-cough models, but few clinical data address upper respiratory infections, and the data that are available suggest little benefit. Data show codeine is little or no better than guaifenesin or dextromethorphan. In otherwise healthy individuals, the use of antibiotics has not demonstrated any consistent benefit in relieving symptoms or improving the natural history of acute bronchitis. Placebo-controlled studies using doxycycline, erythromycin, and trimethoprim-sulfamethoxazole have failed to show significant benefit in patients with acute bronchitis. Preliminary studies suggest a possible role for EPs 7630, an herbal drug preparation derived from Pelargonium sidoides roots, in the treatment of pediatric patients (1-18 y) with acute bronchitis outside the strict indication for antibiotics. Kamin et al demonstrated reduced bronchitis severity symptom scores in patients treated with EPs 7630, with good overall tolerability.[22,23 ] Bronchodilators have failed to demonstrate efficacy in some studies of acute bronchitis. Nevertheless, a trial of inhaled albuterol may be worthwhile, as it may provide significant relief of symptoms for some patients. Chronic bronchitis Bronchodilator therapy should be considered and instituted; either a beta-adrenergic agonist, such as albuterol or metaproterenol, or theophylline may be effective. Beta-adrenergic agents are less toxic, have a more rapid onset of action than theophylline, and do not require monitoring of levels. Inhaled corticosteroids may be effective. In the child who continues to cough despite a trial of bronchodilators and in whom the history and physical examination findings suggest a wheezy form of bronchitis, oral corticosteroids should be added. If the response is suboptimal or if fever persists, antibiotic therapy with an agent such as a macrolide or beta-lactamase–resistant antimicrobial may be considered. Antibiotics should not be the primary therapy. They usually do not result in a cure and may delay the start of more appropriate asthma therapies. Medication In acute bronchitis, medical therapy generally targets symptoms and includes use of analgesics and antipyretics. In chronic bronchitis, bronchodilator therapy should be considered and instituted; either a beta-adrenergic agonist, such as albuterol or metaproterenol, or theophylline may be effective. Beta-adrenergic agents are less toxic, have a more rapid onset of action than theophylline, and do not require monitoring of levels. Inhaled corticosteroids may be effective. In the child who continues to cough despite a trial of bronchodilators and in whom the history and physical examination findings suggest a wheezy form of bronchitis, oral corticosteroids should be added. If the response is suboptimal or if fever persists, antibiotic therapy with an agent such as a macrolide or beta-lactamase–resistant antimicrobial may be considered. Antibiotics should not be the primary therapy. They usually do not result in a cure and may delay the start of more appropriate asthma therapies. Analgesic and antipyretic agents These agents are used to control fever, myalgias, and arthralgias. Acetaminophen (Tylenol, Aspirin-Free Anacin, Feverall) This is the treatment of choice for pain in patients who are unable to take aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). Dosing Adult 625-1000 mg PO q4h; not to exceed 4 g/d Pediatric <12 years: 10-15 mg/kg PO q4-6h prn; not to exceed 2.6 g/d ≥ 12 years: 325-650 mg PO q4h; not to exceed 5 doses/d Interactions Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity Contraindications Documented hypersensitivity; G-6-PD deficiency Precautions Pregnancy B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals Precautions Hepatotoxicity in patients with chronic alcoholism; severe or recurrent pain or high or continued fever may indicate serious illness Ibuprofen (Ibuprin, Advil, Motrin) This NSAID is the usual treatment of choice for mild-to-moderate pain if no contraindications exist. Ibuprofen reduces inflammatory reactions and pain, probably by decreasing activity of cyclooxygenase, which inhibits prostaglandin synthesis. Dosing Adult 400-800 mg PO q4-6h; not to exceed 3.2 g/d Pediatric 10 mg/kg PO q6-8h; not to exceed 2.4 g/d Interactions Coadministration with aspirin increases risk of serious NSAID-related side effects; simultaneous administration with low-dose aspirin may decrease aspirin's cardioprotective and stroke-preventive effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, beta-blockers, and diuretic effect of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; may increase phenytoin or lithium serum levels Contraindications Documented hypersensitivity; peptic ulcer disease; recent GI tract bleeding or perforation; renal insufficiency; high risk of bleeding Precautions Pregnancy B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals Precautions Monitor PT closely in patients on anticoagulants; caution in patients with congestive heart failure, hypertension, and decreased renal or hepatic function Corticosteroids, systemic These agents are used for short courses (3-10 d) to gain prompt control of inadequately controlled acute asthmatic episodes. Systemic corticosteroids also are used for long-term prevention of symptoms in severe persistent asthma, as well as for suppression, control, and reversal of inflammation. Frequent and repetitive use of beta2-agonists has been associated with beta2-receptor subsensitivity and down-regulation; these processes are reversed with corticosteroids. Higher-dose corticosteroids have no advantage in severe exacerbations of asthma, and intravenous administration has no advantage over oral therapy, provided that GI tract transit time or absorption is not impaired. The usual regimen is to continue frequent multiple daily dosing until the forced expiratory volume in 1 second (FEV1) or peak expiratory flow (PEF) is 50% of the predicted or personal best values; then, the dose is changed to twice daily. This usually occurs within 48 hours. Prednisolone (Pediapred, Orapred) Prednisolone works by decreasing inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability. Dosing Adult 5-60 mg/d PO Pediatric 1-2 mg/kg PO qd or divided bid; not to exceed 80 mg/d Tapering not necessary with short courses Interactions Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin, may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics Contraindications Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI tract ulceration or bleeding Precautions Pregnancy B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals Precautions Hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur Prednisone (Sterapred) Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocytes and antibody production. Dosing Adult 60 mg PO initial, then 40-60 mg qd for 5-10 d; taper for longer period Pediatric 2 mg/kg PO initial, then 1 mg/kg/d in 1-2 daily doses; not to exceed 60 mg/d for 3-10 d; taper for longer periods Interactions Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics Contraindications Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, and fungal or tubercular skin infections; GI bleeding or ulceration Precautions Pregnancy B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals Precautions Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use Bronchodilators Studies have found that bronchodilators relieve symptoms of bronchitis, and they have been found to be superior to antibiotics in this setting. However, patient numbers in these trials were disappointingly small, given how commonly acute bronchitis is diagnosed. Albuterol sulfate (Proventil, Ventolin) A beta-adrenergic agonist useful in the treatment of epinephrine-refractory bronchospasm, albuterol relaxes bronchial smooth muscle by acting on beta2-adrenergic receptors. It has little effect on cardiac muscle contractility. A ready-to-use solution for nebulization is available as 0.083% (2.5 mg/3 mL).). Dosing Adult MDI: 2 actuations (90 mcg/actuation) inhaled PO q4-6h PO: 2-4 mg PO tid/qid; not to exceed 32 mg/d Pediatric PO: <6 years: 0.3 mg/kg/d PO divided tid; not to exceed 12 mg/d 6-12 years: 6 mg/d PO divided tid; not to exceed 24 mg/d >12 years: Administer as in adults MDI: 1-2 actuations (90 mcg/actuation) inhaled PO q4-6h prn Nebulizer: <1 year: 0.05-0.15 mg/kg/dose q4-6h 1-5 years: 1.25-2.5 mg/dose q4-6h 5-12 years: 2.5 mg/dose q4-6h >12 years: 2.5-5 mg/dose q6h Interactions Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, and sympathomimetic agents Contraindications Documented hypersensitivity Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Hyperthyroidism, diabetes mellitus, and cardiovascular disorders Metaproterenol sulfate Metaproterenol is a beta agonist for bronchospasms that relaxes bronchial smooth muscle by action on beta2 receptors with little effect on cardiac muscle contractility. Dosing Adult MDI: 2 puffs q3-4h Nebulizer: 0.2-0.3 mL of 0.5% inhalation solution diluted to 2.5 mL with isotonic sodium chloride solution, use tid/qid Pediatric <12 years: Not recommended >12 years: Administer as in adults Interactions Decreases effect of beta-receptor blockers; increases toxicity of MAOIs, tricyclic antidepressants, and sympathomimetics Contraindications Documented hypersensitivity; arrhythmia associated with tachycardia Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Caution in hypertension, cardiovascular disease, congestive heart failure, hyperthyroidism, diabetes, and seizures; not recommended for nursing mothers; adverse reactions include tachycardia, headache, nervousness, dizziness, tremor, gastrointestinal upset, hypertension, paradoxical bronchospasm, and cough Theophylline (Theo-24, Uniphyl) Potentiates exogenous catecholamines and stimulates endogenous catecholamine release and diaphragmatic muscular relaxation, which, in turn, stimulates bronchodilation. It partially acts by inhibiting phosphodiesterase, elevating cellular cyclic AMP levels, or antagonizing adenosine receptors in the bronchi, resulting in relaxation of smooth muscle. Dosing Adult Initial: 10 mg/kg/d PO divided q8-12h, adjust dose in 25% increments to maintain serum theophylline level of 5-15 mcg/mL; maximum 800 mg/d Maintenance: 10 mg/kg/d PO qd or divided q12h, adjust dose in 25% increments to maintain serum theophylline level of 5-15 mcg/mL; maximum 800 mg/d Pediatric Children: Initial dose: 10 mg/kg/d PO divided q8-12h, adjust dose in 25% increments to maintain serum theophylline level of 5-15 mcg/mL; not to exceed 16 mg/kg/d Maintenance: 10 mg/kg/d PO qd or divided q12h, adjust dose in 25% increments to maintain serum theophylline level of 5-15 mcg/mL; not to exceed 16 mg/kg/d Adolescents: Administer as in adults Interactions Aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins, phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics may decrease effects of theophylline; theophylline effects may increase with allopurinol, beta-blockers, ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferon Contraindications Documented hypersensitivity; uncontrolled arrhythmias, peptic ulcers, hyperthyroidism, and uncontrolled seizure disorders Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Caution in peptic ulcer, hypertension, tachyarrhythmias, hyperthyroidism, and compromised cardiac function; do not inject IV solution >25 mg/min; patients diagnosed with pulmonary edema or liver dysfunction are at greater risk of toxicity because of reduced drug clearance Antibiotics Studies have focused on healthy individuals or patients with chronic obstructive lung disease. Patients with chronic obstructive pulmonary disease (COPD) or limited cardiopulmonary reserve, such as patients with asthma, may experience a very limited beneficial effect. Antibiotics should not be the primary therapy. They usually do not result in a cure and may delay the start of more appropriate asthma therapies. Erythromycin (EES, E-Mycin, Ery-Tab) Erythromycin inhibits RNA-dependent protein synthesis, possibly by stimulating the dissociation of peptidyl tRNA from ribosomes, inhibiting bacterial growth. This agent is used for prophylaxis in patients who are allergic to penicillin and will be undergoing dental, oral, or respiratory tract procedures. Dosing Adult 250-500 mg PO qid or 333 mg PO tid Pediatric 30-50 mg/kg/d PO divided qid; not to exceed 2 g/d Interactions Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis Contraindications Documented hypersensitivity; hepatic impairment Precautions Pregnancy B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals Precautions Caution in liver disease; estolate preparation may cause cholestatic jaundice; administer pc to avoid adverse GI tract effects; discontinue if nausea, vomiting, malaise, abdominal colic, or fever occur Clarithromycin (Biaxin) Clarithromycin reversibly binds to P site of 50S ribosomal subunit of susceptible organisms. It may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl tRNA from ribosomes, inhibiting bacterial growth. Dosing Adult 250-500 mg PO bid Pediatric 7.5 mg/kg PO bid Interactions May result in toxic clarithromycin levels and death if administered with pimozide; may cause adverse cardiovascular effects, including death, cardiac arrest, ventricular fibrillation, torsade de pointes, and other ventricular effects if taken with astemizole or cisapride; may increase serum digoxin concentrations as a result of effects of gut flora that metabolize digoxin in >10% of patients; may increase plasma levels of disopyramide, causing arrhythmias and increasing QTc intervals; may cause acute ergot toxicity characterized by severe peripheral vasospasm and dysesthesia, necessitating monitoring in patients taking ergot alkaloids May increase risk of severe myopathy or rhabdomyolysis associated with HMG-CoA reductase inhibitors; may increase levels of tacrolimus, increasing risk of adverse effects such as nephrotoxicity; levels may be increased significantly by fluconazole; levels of both clarithromycin and omeprazole may be increased if taken together; antimicrobial effects may be decreased or frequency of adverse GI tract effects may be increased by rifabutin or rifampin; may increase levels of certain benzodiazepines, prolonging CNS-depressant effects; may increase carbamazepine concentrations Contraindications Documented hypersensitivity; patients taking pimozide, astemizole, cisapride, or terfenadine Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Consider pseudomembranous colitis in patients who present with diarrhea; increased risk of secondary infections if therapy is prolonged; monitor coagulation functions if patient is taking anticoagulant Azithromycin (Zithromax) Azithromycin is used to treat mild to moderately severe infections caused by susceptible strains of microorganisms. It is indicated for chlamydial and gonorrheal infections of the genital tract. Dosing Adult 500 mg PO on day 1, then 250 mg PO on days 2-5 Pediatric 10 mg/kg/d PO on day 1, followed by 5 mg/kg on days 2-5; not to exceed adult dose Interactions May increase theophylline and digoxin levels and toxicity; may potentiate anticoagulant effects of warfarin; may increase cyclosporine levels, increasing risk of nephrotoxicity, neurotoxicity, and other toxic effects; peak serum levels, but not absorption, is reduced by antacids containing aluminum or magnesium Contraindications Documented hypersensitivity; hypersensitivity to erythromycin; patients taking pimozide; hepatic impairment; prolonged QTc interval; pneumonia; elderly or debilitated patients Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Use caution in patients with prolonged QTc intervals; may result in bacterial or fungal overgrowth of nonsusceptible organisms, which may lead to secondary infection, especially if therapy is prolonged or repeated; may increase hepatic enzyme levels or cause cholestatic jaundice; use caution in patients with impaired hepatic function Tetracycline (Sumycin) Tetracycline inhibits bacterial protein synthesis by binding with 30S and, possibly, 50S ribosomal subunits of susceptible bacteria. It is used to treat bacterial infections caused by susceptible gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. It is less effective than erythromycin in mycoplasmal, chlamydial, and Bordetella pertussis infections. Dosing Adult 250-500 mg PO qid Pediatric ≤ 8 years: Not recommended >8 years: 25-50 mg/kg/d PO divided qid Interactions Bioavailability may be decreased by antacids containing aluminum, calcium, magnesium, or bismuth subsalicylate; may increase hypoprothrombinemic effects of anticoagulants, necessitating careful monitoring of PT; may decrease pharmacologic effects of PO contraceptives, causing breakthrough bleeding and increased risk of pregnancy Contraindications Documented hypersensitivity to minocycline or tetracycline; severe hepatic dysfunction Precautions Pregnancy D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus Precautions Never administer outdated tetracycline, since degradation products are highly nephrotoxic and can cause Fanconi-like syndrome; photosensitivity reaction may occur after prolonged exposure to sunlight or tanning equipment; decrease doses in renal impairment (consider serum drug level determinations in prolonged therapy); tooth discoloration if used during tooth development (last one half of pregnancy through age 8 y) Doxycycline (Vibramycin) Doxycycline is a broad-spectrum bacteriostatic antibiotic that inhibits protein synthesis. Dosing Adult 100 mg PO bid on day 1, then 100 mg PO qd/bid for at least 6 d Pediatric ≤ 8 years: Not recommended >8 years: <45 kg: 5 mg/kg/d PO/IV divided bid on day 1, followed by 2.5-5 mg/kg/d PO/IV qd or divided bid; not to exceed 200 mg/kg/d ≥ 45 kg: 200 mg/d PO/IV divided bid on day 1, followed by 100-200 mg/kg/d PO/IV qd or divided bid Infuse IV over 1-4 h Interactions May increase PT in patients taking warfarin, necessitating monitoring of PT and dose adjustment if indicated; reduces activity of penicillin; absorption decreased by antacids, bicarbonate, calcium, and iron supplements Contraindications Documented hypersensitivity; severe hepatic dysfunction Precautions Pregnancy D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus Precautions Caution in hepatic or renal disease; may increase cranial pressure; may cause GI tract symptoms, photosensitivity, hemolytic anemia, and hypersensitivity reactions; infuse IV over 1-4 h; avoid exposure to direct sunlight; tooth discoloration if used during tooth development (last one half of pregnancy through age 8 y) Amoxicillin-clavulanic acid (Augmentin) Amoxicillin is a semisynthetic bactericidal beta-lactam antibiotic that inhibits cell wall synthesis. This agent contains amoxicillin combined with clavulanate, a beta-lactamase inhibitor. Dosing Adult 250-500 mg PO q8h Pediatric <3 months: 30 mg/kg/d PO divided q12h ≥ 3 months: 40-80 mg/kg/d PO divided q12h Interactions Coadministration with warfarin or heparin increases risk of bleeding Contraindications Documented hypersensitivity; PKU (contains phenylalanine); penicillin allergy Precautions Pregnancy B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals Precautions Can produce false-positive result on dipstick test for urine glucose; increases risk of rash in patients with mononucleosis or in patients taking allopurinol; diarrhea may occur; adjust dose with renal impairment Antivirals Vaccination is the most important preventive measure for influenza; vaccinations offer coverage for influenza A and B and, thereby, provide greater protection from bronchitis in the appropriate populations. Antiviral drugs represent a second line of defense. Antiviral agents with activity against influenza virus include amantadine, rimantadine, oseltamivir, and zanamivir. Amantadine and rimantadine are not currently recommended by the Centers for Disease Control and Prevention (CDC) for influenza because of widespread resistance among influenza A strains. Oseltamivir (Tamiflu) resistance emerged in the United States during the 2008-2009 influenza season and was found in some strains of H1N1 influenza virus during the 2009-2010 epidemic. For current recommendations on the use of antiviral drugs for influenza, see the CDC information for health care professionals on antiviral drugs for influenza. Oseltamivir (Tamiflu) Oseltamivir inhibits neuraminidase, which is a glycoprotein on the surface of influenza virus that destroys an infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, oseltamivir decreases release of viruses from infected cells and thus viral spread. This agent is effective against influenza A and B, although resistance against influenza A emerged in the United States during the 2008-2009 influenza season. Start within 40 hours of symptom onset. Available in capsules and oral suspension. Dosing Adult Acute illness: 75 mg PO bid for 5 d Prophylaxis: 75 mg PO qd for 10 d Pediatric Acute illness: <1 year: Not indicated ≥ 1 year: ≤ 15 kg: 30 mg PO bid for 5 d >15-23 kg: 45 mg PO bid for 5 d 24-40 kg: 60 mg PO bid for 5 d >40 kg: Administer as in adults Prophylaxis: <1 year: Not indicated ≥ 1 year: ≤ 15 kg: 30 mg PO qd for 10 d >15-23 kg: 45 mg PO qd for 10 d 24-40 kg: 60 mg PO qd for 10 d >40 kg: Administer as in adults Interactions None reported Contraindications Documented hypersensitivity Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Caution in renal impairment, chronic cardiac or respiratory disease, and breastfeeding; do not use in children <1 y (preclinical trials have demonstrated death in young animals, possibly related to immature blood-brain barriers) Zanamivir (Relenza) Zanamivir is an inhibitor of neuraminidase, which is a glycoprotein on the surface of the influenza virus that destroys the infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, release of viruses from infected cells and viral spread are decreased. Zanamivir is effective against both influenza A and B. It is inhaled through the Diskhaler oral inhalation device. Circular foil discs that contain 5-mg blisters of drug are inserted into the supplied inhalation device. Dosing Adult Treatment: 10 mg (2 inhalations, 5 mg/inhalation) inhaled PO q12h for 5 d; initiate within 2 d of symptom onset Prophylaxis: 10 mg (2 inhalations, 5 mg/inhalation) inhaled PO qd for 10 d; initiate within 36 h of exposure Pediatric Treatment: <7 years: Not established ≥ 7 years: Administer as in adults Prophylaxis: <5 years: Not established ≥ 5 years: Administer as in adults Interactions None reported Contraindications Documented hypersensitivity, obstructive airway disease Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Monitor respiratory status; may cause bronchospasm; caution in breastfeeding Corticosteroids, inhaled Corticosteroids are the most potent anti-inflammatory agents. Inhaled forms are topically active, poorly absorbed, and least likely to cause adverse effects. No study has shown significant toxicity with inhaled steroid use in children at doses less than the equivalent of 400 mcg/d of beclomethasone. They are used for long-term control of symptoms and for the suppression, control, and reversal of inflammation. Inhaled forms reduce the need for systemic corticosteroids. They block late asthmatic responses to allergens; reduce airway hyperresponsiveness; inhibit cytokine production, adhesion protein activation, and inflammatory cell migration and activation; and reverse beta2-receptor down-regulation and subsensitivity (in acute asthmatic episodes with long-term beta2-agonist use). Beclomethasone (Qvar) Beclomethasone inhibits bronchoconstriction mechanisms, causes direct smooth muscle relaxation, and may decrease the number and activity of inflammatory cells, which, in turn, decrease airway hyperresponsiveness. It is available in a metered-dose inhaler (MDI) that delivers 40 or 80 mcg/actuation. Dosing Adult MDI: 40-80 mcg inhaled PO bid; may increase dose, not to exceed 320 mcg bid Pediatric MDI: 40 mcg inhaled PO bid; may increase dose, not to exceed 80 mcg bid Interactions None reported Contraindications Documented hypersensitivity Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Inhaled corticosteroids can cause PO thrush and hoarseness (can prevent by rinsing mouth after dosing and by using with MDI spacer); large doses (>800 mcg/d) have adverse systemic effects including growth retardation and HPA inhibition Fluticasone (Flovent HFA, Flovent Diskus) Fluticasone has extremely potent vasoconstrictive and anti-inflammatory activity. It is available in an MDI (44-mcg, 110-mcg, or 220-mcg per actuation) and Diskus powder for inhalation (50-mcg, 100-mcg, or 250-mcg per actuation). Dosing Adult MDI: 88 mcg inhaled PO bid; may increase dose, not to exceed 440 mcg bid Diskus: 100 mcg inhaled PO bid; may increase dose, not to exceed 500 mcg bid Pediatric MDI: 4-11 years: 88 mcg inhaled PO bid >11 years: Administer as in adults Diskus: 4-11 years: 50 mcg inhaled PO bid >11 years: Administer as in adults Interactions Coadministration with barbiturates, phenytoin, and rifampin decreases effects of triamcinolone Contraindications Documented hypersensitivity; fungal, viral, and bacterial skin infections Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Inhaled corticosteroids can cause PO thrush and hoarseness (can prevent by rinsing mouth after dosing and by using with MDI spacer); large doses (>800 mcg/d) have adverse systemic effects, including growth retardation and HPA inhibition; high-dose long-term therapy has been associated with HPA inhibition and may retard growth Budesonide inhaled (Pulmicort Flexhaler, Pulmicort Respules) Budesonide reduces inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators involved in the asthmatic response. It is available as Flexhaler powder for inhalation (90 mcg/actuation [delivers approximately 80 mcg/actuation]) and Respules suspension for inhalation. Dosing Adult Flexhaler: 180-360 mcg (2-4 actuations) inhaled PO bid; not to exceed 720 mcg bid Pediatric Flexhaler: <6 years: Not established 6 years or older: 180 mcg inhaled PO bid (2 actuations bid); not to exceed 360 mcg bid (4 actuations bid) Nebulizer: 0.25 mg/d to 0.5 mg bid; dose and frequency of nebulization depends on whether patient was previously treated with inhaled or PO corticosteroids Interactions None reported Contraindications Documented hypersensitivity Precautions Pregnancy C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus Precautions Inhaled corticosteroids can cause PO thrush and hoarseness (can prevent by rinsing mouth after dosing or using with MDI spacer); large doses have adverse systemic effects, including growth retardation and HPA inhibition; do not mix nebulizer solution with other nebulized medications; administer nebulized solution using tight-fitting mask or mouthpiece; not for treatment of acute attack Источник: http://emedicine.medscape.com/article/1001332-overview
