Theme: Pneumonia. Etiology, pathogenesis, clinical classification, ntreatment: regime organization, aerotherapy,antibacterial therapy, nimmunotherapy and physiotherapy, prophylaxis. Congenital anomalies and nchronicle bronchological diseases. Etiology, pathogenesis, clinical nclassification, treatment, prognosis.
Pneumonia (J18) is the acute non-specific inflammation of the pulmonary ntissue with accompanying infectious toxicosis, the respiratory insufficiency, nthe disordered water-electrolytic balance, and other metabolic disorders with nthe pathologic shifts involving various organs and systems in the child’s body.
According to other concepts, the pneumonias mean the group of the acute nfocal infectious inflammatory diseases of the lungs varying in etiology, npathogenesis, and morphological features with the obligate intra-alveolar ninflammatory exudation.
Most cases of pneumonia are caused by microorganisms, noninfectious causes ninclude aspiration of food or gastric acid, foreign bodies, hydrocarbons, and nlipoid substances, hypersensitivity reactions, and drug- or radiation-induced npneumonitis.
EPIDEMIOLOGY
Incidence of acute pneumonia among the children in Ukraine amounts to 4-20 nper 1000 of children population; among the children of the first year of life: 10-15 cases per 1000 of children population; namong the children aged 1-3 years: 15–20 cases per 1000 of children population. nIncidence of acute pneumonia among the children aged over 5 years: 5-6 cases nper 1000 of children population. Acute pneumonia develops in 1% of the patients nwith the acute respiratory viral infections. The lethality of acute pneumonia nis 1.5-6 causes per 10 000 of children population. The respiratory diseases nmake up to 3 –5 % in the structure of lethality in the children aged below one nyear. 
Pneumonia is na substantial cause of morbidity and mortality in childhood (particularly among nchildren <5 year of age) throughout the world, rivaling diarrhea as a cause nof death in developing countries. With an estimated 146–159 millioew episodes nper year in developing countries, pneumonia is estimated to cause approximately n4 million deaths among children worldwide. Currently, the incidence of ncommunity-acquired pneumonia in developed countries is estimated to be 0.026 nepisodes per child-year compared to 0.280 episodes per child-year in developing ncountries.
ETIOLOGY
Although most cases of pneumonia are caused by microorganisms, nnoninfectious causes include aspiration of food or gastric acid, foreigbodies, hydrocarbons, and lipoid substances, hypersensitivity reactions, and ndrug- or radiation-induced pneumonitis. The cause of pneumonia in an individual npatient is often difficult to determine because direct culture of lung tissue nis invasive and rarely performed. Cultures performed on specimens obtained from nthe upper respiratory tract or “sputum” often do not accurately reflect the ncause of lower respiratory tract infection. With the use of state-of-the-art ndiagnostic testing, a bacterial or viral cause of pneumonia can be identified nin 40-80% of children with community-acquired pneumonia.
Table 1. Causes of Infectious Pneumonia
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Bacterial |
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Common |
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Streptococcus pneumoniae |
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Group B streptococci |
Neonates |
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Group A streptococci |
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Mycoplasma pneumoniae |
Adolescents;summer-fall epidemics |
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Chlamydia pneumoniae |
Adolescents |
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Chlamydia trachomatis |
Infants |
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Mixed anaerobes |
Aspiration pneumonia |
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Gram-negative enteric |
Nosocomial pneumonia |
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Uncommon
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Haemophilus influenzae type B |
Unimmunized |
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Staphylococcus aureus |
Pneumatoceles; infants |
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Moraxella catarrhalis |
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Neisseria meningitides |
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Chlamydia psittaci |
Bird contact |
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Yersinia pestis |
Plague |
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Legionella species |
Exposure to contaminated water; nosocomial |
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Viral |
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Common |
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Respiratory synctial virus (RSV) |
Bronchiolitis |
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Parainfluenza types 1–3 |
Croup |
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Influenza A, B |
High fever; winter months |
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Adenovirus |
Can be severe; often occurs between January and April |
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Uncommon |
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Rhinovirus |
Rhinorrhea |
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Enterovirus |
Neonates |
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Herpes simplex |
Neonates |
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Cytomegalovirus |
Infants, immunosuppressed persons |
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Measles |
Rash, coryza, conjunctivitis |
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Varicella |
Adolescents |
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Fungal |
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Aspergillus species |
Immunosuppressed |
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Mucormycosis |
Immunosuppressed |
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Mycobacterial |
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Mycobacterium tuberculosis |
Developing countries |
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Mycobacterium aviumintracellulare |
Immunosuppressed persons |
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Parasitic |
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Pneumocystis carinii |
Immunosuppressed, steroids |
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Eosiophilic |
Various parasites (e.g., Ascaris Strongyloides species) |
The age of the patient may help to identify possible pathogens ( Table 2 ). n
nTable 2 — Etiologic nAgents Grouped by Age of the Patient
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Age group |
Frequent pathogens (in order of frequency) |
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Neonates (<1 month) |
Group B streptococcus, Escherichia coli, other gram-negative bacilli, Streptococcus pneumoniae, Haemophilus influenzae (type b, nontypable) |
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1–3 month |
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Febrile pneumonia |
Respiratory syncytial virus, other respiratory viruses (parainfluenza viruses, influenza viruses, adenoviruses), S. pneumoniae, H. influenzae (type b, nontypable) |
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Afebrile pneumonia |
Chlamydia trachomatis, Mycoplasma hominis, Ureaplasma urealyticum, cytomegalovirus |
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3–12 month |
Respiratory syncytial virus, other respiratory viruses (parainfluenza viruses, influenza viruses, adenoviruses), S. pneumoniae, H. influenzae (type b, nontypable), C. trachomatis, Mycoplasma pneumoniae, group A streptococcus |
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2–5 years |
Respiratory viruses (parainfluenza viruses, influenza viruses, adenoviruses), S. pneumoniae, H. influenzae (type b, nontypable), M. pneumoniae, Chlamydophila pneumoniae, S. aureus, group A streptococcus |
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5–18 year |
M. pneumoniae, S. pneumoniae, C. pneumoniae, H. influenzae (type b, nontypable), influenza viruses, adenoviruses, other respiratory viruses |
Lower nrespiratory tract viral infections in Ukraine are much more common in the fall nand winter, related to the seasonal epidemics of respiratory viral infectiothat occur each year. The typical pattern of these epidemics usually begins ithe fall when parainfluenza infections appear and most often manifest as croup. nLater in winter, RSV and influenza viruses cause widespread infection, nincluding upper respiratory tract infections, bronchiolitis, and pneumonia. RSV nattacks infants and young children, whereas influenza virus causes disease and nexcess hospitalization for acute respiratory illness in all age groups. The nknowledge of the prevailing viral epidemic may lead to a presumptive initial ndiagnosis.
The routes for infecting the lungs:
1) aerogenous: along the airways ninto the respiratory divisions;
2) hematogenous: through the vessels nof the systemic circulation (septic and intrauterine acute pneumonias);
3) lymphogenous: due to the breach of the barrier function of the lymphoid npharyngeal ring.
Pathogenesis nof acute pneumonia in children.
The lower respiratory tract is normally kept sterile by physiologic defense nmechanisms, including the mucocil iary clearance, the properties of normal nsecretions such as secretory immunoglobulin A (IgA), and clearing of the airway nby coughing. Immunologic defense mechanisms of the lung that limit invasion by npathogenic organisms include macrophages that are present in alveoli and nbronchioles, secretory IgA, and other immunoglobulins.
Viral npneumonia usually results from spread nof infection along the airways, accompanied by direct injury of the respiratory nepithelium, resulting in airway obstruction from swelling, abnormal secretions, nand cellular debris. The small caliber of airways in young infants makes them nparticularly susceptible to severe infection. Atelectasis, interstitial edema, nand ventilation-perfusion mismatch causing significant hypoxemia ofteaccompany airway obstruction. Viral infection of the respiratory tract can also npredispose to secondary bacterial infection by disturbing normal host defense nmechanisms, altering secretions, and modifying the bacterial flora.
Bacterial pneumonia most often occurs when respiratory tract organisms ncolonize the trachea and subsequently gain access to the lungs, but pneumonia nmay also result from direct seeding of lung tissue after bacteremia. Whebacterial infection is established in the lung parenchyma, the pathologic nprocess varies according to the invading organism. M. pneumoniae attaches to the respiratory epithelium, inhibits nciliary action, and leads to cellular destruction and an inflammatory response nin the submucosa. As the infection progresses, sloughed cellular debris, ninflammatory cells, and mucus cause airway obstruction, with spread of infectiooccurring along the bronchial tree, as it does in viral pneumonia.
S. npneumoniae produces local edema that naids in the proliferation of organisms and their spread into adjacent portions nof lung, often resulting in the characteristic focal lobar involvement.
Group A nstreptococcus infection of the nlower respiratory tract results in more diffuse infection with interstitial npneumonia. The pathology includes necrosis of tracheobronchial mucosa; nformation of large amounts of exudate, edema, and local hemorrhage, with nextension into the interalveolar septa; and involvement of lymphatic vessels nand the increased likelihood of pleural involvement.
S. aureus npneumonia manifests in confluent nbronchopneumonia, which is often unilateral and characterized by the presence nof extensive areas of hemorrhagic necrosis and irregular areas of cavitation of nthe lung parenchyma, resulting in pneumatoceles, empyema, or, at times, nbronchopulmonary fistulas.
Recurrent npneumonia is defined as 2 or more nepisodes in a single year or 3 or more episodes ever, with radiographic nclearing between occurrences. An underlying disorder should be considered if a nchild experiences recurrent pneumonia (Table 3).
Table 3. DIFFERENTIAL DIAGNOSIS OF RECURRENT PNEUMONIA
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HEREDITARY DISORDERS |
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DISORDERS OF IMMUNITY |
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DISORDERS OF CILIA |
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Classification
The working classification is used, which was approved by the order of the nMinistry of Health of Ukraine dated January 13th 2005 (Table 4).
Table 4. nClassification of pneumonia
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Origin |
Clinico-roentgenological form |
Localization |
Severity |
Clinical course |
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Community-acquired pneumonia (ambulatory) Nosocomial (hospital-acquired)* Ventilation pneumonia: -early** -late Pneumonia, associated with immunodeficiency Pneumonia of newborn: Congenital pneumonia*** Postnatal (acquired) community-acquired and hospital-acquired |
Bronchopneumonia (pneumonia with confluent foci)
Segmentary pneumonia (mono- and polysegmentary)
Croupous pneumonia (lung fever)
Interstitial pneumonia |
Unilateral pneumonia Bilateral pneumonia Diffuse pneumonia -lung -lobe -segment |
Noncomplicated pneumonia Complicated pneumonia: toxic; purulent: -pulmonary (destruction abscess pleurisy pyopneumothorax) -extrapulmonary (osteomyelitis otitis meningitis pyelonephritis etc.). |
Acute (до(less than 6 weeks)
Prolonged (from 6 weeks to 6 months) |
* which developed i72 hours after the patient has been admitted to hospital or i72 hours after his discharge from hospital
** early – the first n72 hours of artificial lung ventilation, late – 4 and more days of nartificial lung ventilation; *** which developed during the first 72 hours of nlife.
The nclassification distinguishes two groups of pneumonias: primary and secondary. nIn case of primary pneumonia the pathological process develops in the pulmonary ntissue and is classified as fundamental disease; in case of secondary pneumonia n– the pathological process complicates other pulmonary diseases (chronic ones) nor diseases of other organs. The severity of pneumonia (mild, nmoderately-severe, severe) depends on the severity of toxicosis, cardiovascular nchanges and respiratory compromise.
Classification of respiratory compromise (RC). RC I – the dyspnea occurs during considerable physical activity; RC II – nthe dyspnea occurs during insignificant physical activity; RC III – the dyspnea noccurs during rest.
Classification of RC in children of early age
The 1st degree is marked by dyspnea, tachycardia during physical nactivity (for infants – physical activity is breast feeding, cry, nrestlessness). Oxygen partial pressure in the arterial blood is 80–65 mm nof the mercury column.
The 2nd degree is marked by dyspnea, tachycardia at rest, nincreasing considerably during physical activity. Mild labial cyanosis, nacrocyanosis. Blowing of the nose wings, retraction of intercostal spaces at nrespiration. The child is slack, restless. The oxygen partial pressure in the narterial blood is 65–50 mm of the mercury column.
The 3rd degree – dyspnea with breathing rate reaching 80–100 per nminute at rest. General cyanosis of the skin and mucous tunics. The nsupplementary muscles take part in respiration. Hypoxic encephalopathy may ndevelop (impairment of consciousness, convulsions). The oxygen partial pressure nis less than
An example of the diagnosis: Pneumonia, acute course, primary, ncommunity-acquired, bronchopneumonia, right-sided S-10, noncomplicated, of nmoderate severity, RC 0.
Clinical Manifestations
Viral and bacterial pneumonias are often preceded nby several days of symptoms of an upper respiratory tract infection, typically rhinitis nand cough. In viral pneumonia, fever is usually present; temperatures are ngenerally lower than in bacterial pneumonia. Tachypnea is the most consistent nclinical manifestation of pneumonia. Increased work of breathing accompanied by nintercostal, subcostal, and suprasternal retractions, nasal flaring, and use of naccessory muscles is common. Severe infection may be accompanied by cyanosis nand respiratory fatigue, especially in infants. Auscultation of the chest may nreveal crackles and wheezing, but it is often difficult to localize the source nof these adventitious sounds in very young children with hyperresonant chests. nIt is ofteot possible to distinguish viral pneumonia clinically from disease ncaused by Mycoplasma and other bacterial pathogens.
Bacterial pneumonia in adults and older childretypically begins suddenly with a shaking chill followed by a high fever, cough, nand chest pain. Other symptoms that may be seen include drowsiness with nintermittent periods of restlessness; rapid respirations; anxiety; and, noccasionally, delirium. Circumoral cyanosis may be observed. In many children, nsplinting on the affected side to minimize pleuritic pain and improve nventilation is noted; such children may lie on one side with the knees drawn up nto the chest.
Physical findings depend on the stage of npneumonia. Early in the course of illness, diminished breath sounds, scattered ncrackles, and rhonchi are commonly heard over the affected lung field. With the ndevelopment of increasing consolidation or complications of pneumonia such as neffusion, empyema, and pyopneumothorax, dullness on percussion is noted and nbreath sounds may be diminished. A lag in respiratory excursion often occurs othe affected side. Abdominal distention may be prominent because of gastric ndilation from swallowed air or ileus. Abdominal pain is common in lower lobe npneumonia. The liver may seem enlarged because of downward displacement of the ndiaphragm secondary to hyperinflation of the lungs or superimposed congestive nheart failure.
Symptoms described in adults with pneumococcal npneumonia may be noted in older children but are rarely observed in infants and nyoung children, in whom the clinical pattern is considerably more variable. Iinfants, there may be a prodrome of upper respiratory tract infection and ndiminished appetite, leading to the abrupt onset of fever, restlessness, napprehension, and respiratory distress. These infants appear ill, with nrespiratory distress manifested as grunting; nasal flaring; retractions of the supraclavicular, nintercostal, and subcostal areas; tachypnea; tachycardia; air hunger; and oftecyanosis. Results of physical examination may be misleading, particularly iyoung infants, with meager findings disproportionate to the degree of ntachypnea. Some infants with bacterial pneumonia may have associated ngastrointestinal disturbances characterized by vomiting, anorexia, diarrhea, nand abdominal distention secondary to a paralytic ileus. Rapid progression of nsymptoms is characteristic in the most severe cases of bacterial pneumonia.
Criteria of the typical acute pneumonia diagnostics
1. nAnamnestic: dry or moist cough, pain in chest, temperature rise above 38°C, nintoxication. Association with acute respiratory viral infections, overcooling nfactor.
2. nClinical nsyndromes:
– respiratory syndrome with acuter nrespiratory viral infection symptoms, deep cough with mucous or purulent-mucous nsputum discharge or with only dry cough;
– toxicosis nsyndrome of ndifferent degree with possible toxic complication from the inner organs. The ntemperature exceeds 38°C nduring three days and more;
– respiratory ncompromise syndrome: dyspnea exceeding 60 per minute in children under 2 months, 50 per nminute – from 2 months to 1 year, 40 per minute – from 1 year to n5 years old (the data of the WHO). Retracting of the yielding places othe chest without any bronchial obstruction (bronchial obstruction usually nmakes it possible to exclude typical acute pneumonia and accompanies atypical, nnosocomial and viral acute pneumonias).
– bronchopulmonary syndrome with local nphysical changes in the lungs: short percussion sound, dullness, weak nrespiration or bronchial respiration; local, constant fine moist rales, ncrepitation.
3. nParaclinical:
– In bacterial pneumonia cases the leucocytosis exceeds 12.0´109/l, rod-nuclear neutrophils exceed 5%, erythrocyte nsedimentation rate exceeds 20 mm/hour. In cases of mycoplasma, npneumocystic pneumonias these changes are less marked.
– The X-ray study confirms the clinical diagnosis and specifies more exactly nthe form of the pneumonia: homogenous shadows (polysegmentary, lobular, nbrnochopneumonias) are characteristic of bacterial pneumonias; non-homogenous – nof acute pneumonias, initiated by mycoplasma; disseminated processes n(interstitial lesion with alveolar infiltration suggests clamidiosis or npneumocystosis); infiltration with confluent foci is characteristic of npneumonia, complicated by destruction. The X-ray control of non-complicated npneumonia, which as a rule resolves in 2–4 weeks, needs not be done.
Characteristics of clinico-roentgenological forms of acute pneumonia
Bronchopneumonia is the most common form, often occurs in early nage and is as a rule a complication of the viral infection, developing in the nform of tracheobronchitis with its peculiar clinical picture.
The clinical picture of bronchopneumonia may nprogress gradually with slow development of the characteristic symptoms at the nend of the 1st – on the 2nd week of the disease. It may nalso occur suddenly, when the clinical picture allows to diagnose pneumonia nduring the first three days. The child with acute respiratory viral infectioafter a short-term improvement acquires intoxication symptoms. The cough nbecomes moister, the dyspnea occurs during physical activity or at rest, the nrespiration rate does not correspond to the body temperarure. The palpatioshows increased voice trembling in case of the expanded process. The short npercussion sound is observed above the lesion focus. The lung auscultatioreveals hard breath with “bronchial” rales. The respiration above the lesiofocus is weakened or hard (but the bronchophony is increaed), constant fine nmoist rales and crepitation are noticed. The blood test reveals moderate nneutrophilic leucocytosis, the erythrocyte sedimentation rate is high. The nX-ray study shows multifocal infiltrative shadows in one lung.
In children patients of the early age the most nprominent symptoms of bronchopneumonia are RC, intoxication, and local changes nin the lungs are found somewhat later: the process is seldom of a bilateral ncharacter.
Segmentary (polysegmentary) pneumonias n(bronchopneumonias) unlike nfocal bronchopneumonia, involve the tissues of the whole segment, being as a nrule in the subatelectasis or atelectasis state, in the inflammatory process. nThat is why the involution of the pulmonary changes is torpid (with clinical nsymptoms disappearing quickly), bearing the risk of pulmonary fibrosis nformation. The term “segmentary pneumonia” indicates the qualitative difference nof this form from bronchopneumonia, it should not be used to denote the ndistribution of pneumonic process. It most frequently occurs in 3–7 year nold children and schoolchildren and has the most widespread monosegmentary ncharacter (usually on the right side). The disease begins suddenly, with ntemperature reaching high levels, marked intoxication symptoms appearing, rare ncoughing. Stomachaches and pain in chest are often observed. The percussiosound is locally short, the local respiration weakening, increased nbronchophony, crepitation are registered. Segmentary pneumonia is distinguished nby acute inflammatory changes in the peripheral blood. The X-ray picture shows nhomogenous shadows with clear linear borders, corresponding to one or several nsegments, and decrease in the lung root structure on the lesion side. Pleural nlesions are frequent (in 50% of children). Polysegmentary pneumonias are usually nmore severe and more often occur in children of the first and second year.
Croupous pneumonia (lung fever) is relatively rare. It is more characteristic to nchildren of the school age, sometimes to 2–5 year old children, and is nmarked by the lobular lesion (most often – superior and inferior lobe of the nright lung). The disease is most often initiated by pneumococcus and is a nhyperergic allergic reaction with characteristic fibrinous inflammation, which ndevelops in the organism, sensibilized by pneumococcus. In some cases the ndisease can be provoked by overcooling, physical or psychical trauma.
The disease is not preceded by an acute nrespiratory viral infection. It begins with sudden temperature rise up to 39–40°C, chill, headache, pain in the chest or right nrise of the abdomen, acute disturbance of the general state. The cough is nabsent on the first days; sometimes it can be dry and rare. The abdominal nsyndrome is frequent to develop. Croupous pneumonia typically has cyclic ndevelopment.
The blood tests show clearly marked leucocytosis, nneutrophillosis with the shift to the left, the increase in the erythrocyte nsedimentation rate to 20–40 mm/hour. The X-ray also reveal the stage ndynamics: the congestion stage (1st–2nd day) is nmarked by the increase of the vascular pattern prominence and restriction ithe diaphragm mobility; the hepatization stage (2nd–7th nday) is distinguished by homogenous shadows with clear borders, corresponding nto the lobe, with the root and the adjacent pleura being involved into the nprocess; in the resolution stage the infiltration gradually disappears.
This diagnosis has a prognostic value, because nprescribing the antibiotic, affecting the pneumococcus, gives fast clinical neffect.
Interstitial pneumonia is the most rare form and is caused by viruses, nmycoplasma, clamidia, pneumocysts and other fungi. It is usually observed iprematurely born and newborn children, and in the older age – in weakened nchildren – it is associated with dystrophy, anemia, diathesis, immunodeficiency nstates. Interstitial cells lesion can be of a local or diffuse character, of aacute or prolonged form. The clinical picture includes a tetrad of symptoms: ndyspnea, hypoxemia, cough, diffuse interstitial infiltration. Even when the ndisease has a favorable development, the roentgenological changes in the lungs nremain for a long time – 6–8 weeks or more. Such form of pneumonia may end neither by complete recovery or by pulmonary fibrosis formation.
Diagnosing nprimary viral pneumonias.
The viral pneumonia diagnosis is confirmed by the npositive results of the immunofluorescent analysis of the nasopharynx lavage nand by the X-ray picture of the lungs showing non-homogenous pneumonic shadow nwithout clear borders, without any changes in the hemogram, characteristic of nbilateral pneumonia.
The pneumonia, caused by influenza, nappears in the first hours of the disease on the background of the severe state nwith hypethermia and has a type of bronchopneumonia or segmentary pneumonia. nPhysical data are scanty and moderately marked. The patient recovers i2–3 weeks. Parainfluenza, adenovirus, respiratory-syncytial pneumonias are noften accompanied by the obstructive syndrome, focal infiltration of the lung ntissue and tend to have a prolonged course. Parainfluenza pneumonia has the nsymptoms of laryngitis.
Diagnosing n“atypical” pneumonias.
“Atypical” pneumonias are pneumonias, caused by nmycoplasma, clamydia, ligionella, coxiella (Coxiella burnetii – is the nagent of fever Ku). The first two pathogens are most common.
Mycoplasmal pneumonia is caused by the smallest extracellular nmicroorganism – Micoplasma pneumoniae, which in 24 hours after the ninfection attaches to the ciliated epithelium cells, impairing the movement of nthe cilia (unique membranous parasits).
The incubation period lasts for 1–3 weeks. nThe disease is more common to children above 5 years old. The disease nbegins gradually. The leading symptoms are persistent long cough, as the nsymptom of tracheobronchitis, sometimes asymmetric, and high temperature, nwithout the general condition being severe, sometimes pharyngitis, enlargement nof the neck lymph nodes are observed. The physical data do not reveal the clear nborder of the percussion sound dullness, the auscultation most often shows ndiffused fine moist rales. The X-ray picture often identifies bilateral, nasymmetric process, “shaggy” infiltration (usually in the inferior sections), ndenser at the root.
Chlamidia trachomatis pneumonias are connected with Chlamydia trachomatis nin children of the fist months and years of life (3 days – 1.5 years nold) and caused by the infection during the pregnancy. Manifest forms are the nmost common – bronchopneumonia and ophthalmoclamidiosis. If respiratory nclamidiosis develops in the neonatal period, it may be of a severe form with nthe respiration disorder syndrome and even have a lethal outcome. The clamidial ninfection of the lungs often begins gradually with mucous-purulent rhinitis, nmoderately tachypnoea, whooping-cough-like dry cough. The temperature does not nrise as a rule or riser to subfebrile level. The one-third of children has nlymphoadenopathy. The auscultation of the lungs shows diffused crepitation oboth sides, non-abundant heterogenous moist rales. The X-ray strudy of the nlungs shows the picture of diffuse interstitial pneumonia, focal alveolar ninfiltrations are possible.
5–20% of acquired pneumonias are associated with Clamidia npneumoniae, which occurs in children of the school age. Clamidia pneumonia nin most cases begins gradually, and forms a bilateral disseminated process by nthe 2nd week. The attention should be paid to the lack of correspondence nbetween the clinically marked pneumonia and relatively non-severe conditiowith minimal intoxication symptoms. The X-ray picture of the lungs reveals nnumerous microfocal infiltration shadows up to
The blood tests of all patients with “atypical” npneumonia show moderate neutrophil leukocytosis, increased erythrocyte nsedimentation rate, there can be some eosinophilia. The clinical course is nprolonged and has a recurrent character.
The differential diagnosis must be nmade first of all with bronchitis and bronchiolitis. Pneumonias must be ndifferentiated from the respiratory tract obstruction (foreign body, naspiration, larynx malformations, laryngospasm), pleurisy, tuberculosis, lung nlesions associated with helminthiasis. Inferior lobe pneumonias must be ndifferentiated from appendicitis, intestinal obstruction, peritonitis; superior nlobe pneumonias – with meningitis.
Treatment
Bed rest should last for the whole fever period. The ntemperature normalizing, the regime becomes less strict during 2–3 days, nand in 3–4 days the child can go for a walk, gradually increasing its nlength (from 20 minutes).
Indications for admission to a hospital are noted in Table 5.
Table 5
FACTORS nSUGGESTING NEED FOR HOSPITALIZATION OF CHILDREN WITH PNEUMONIA
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The diet must correspond to the child’s age. When the ndisease is in acute period, the food should be mechanically and chemically nlight. The liquid amount is increased by 20% in comparison with the age norms n(fruit drinks, juices, tea with lemon etc.).
The etiotropic therapy of acute pneumonia is given taking into account nthe possible pathogens (viruses, bacteria), age, origin of the pneumonia, nclinical picture.
The primary choice of antibacterial drug in case nof bacterial pneumonia and its changing, when it proves to be ineffective, is nalmost always made empirically. For the antibacterial therapy to be successful nit is important to register the effect of treatment and to change the drug if nthere is no effect.
Complete effect: the temperature falls under 38°C in 24–48 hours in case of non-complicated npneumonia and in 3–4 days in case of complicated pneumonia on the nbackground of general condition and appetite improvement, decrease of dyspnea. Partial neffect: the temperature remains on febrile level after the aforementioned nperiod with toxicosis and dyspnea degree decreasing, appetite improvement and nthe negative roentgenological dynamics (destructive pneumonia, metapneumonic npleurisy) being absent. In this case there is no need to change the antibiotic. nNo effect: the temperature remains ofebrile level, with the general condition aggravating and (or) pathological nchanges in the lungs and pleura increasing.
For the empiric (starting therapy) it is nrecommended to use “protected” penicillin, cephalosporin of the 2nd ngeneration, more rarely (in case of hospital-acquired acute pneumonia of nnewborns) – cephalosporin of the 3rd generation, new macrolides; the nlatter are chosen to treat atypical pneumonias.
If the antibiotic has been chosen adequately and nthe effect has been reached quickly in case of non-complicated typical acute npneumonia it is sufficient to carry out the antibacterial therapy for n6–7 days (3–4 days after the temperature has normalized), in case of natypical pneumonia – 14–21 days. In case of complicated acute pneumonia nthe treatment is long (in case of abscesses formation – 42–56 days). It is nusually considered that parenheral treatment should be continued at least for n2 days after the effect and then to pass to the peroral drug nadministration. In cases of non-complicated pneumonia peroral medications are npreferable from the first days of the disease.
In cases of virus pneumonias syndrome and nantiviral therapy is the most important (antigrippal immunoglobulin, in case of ncytomegalovirus acute pneumonia – specific anticytomegalovirus immunoglobulior gancyclovir, drugs of the interferon group).
The use of nsome antibiotics, taking into account their toxicity, is prohibited to the ncertain age: fluorinequinolons – to 12 years, tetracyclins – to 8 years.
In order to treat pneumonias in patients with immunodeficiency states, if the npneumonia is of a bacterial nature, cephalosporins of the 3rd and 4th ngeneration or vancomycin in combination with aminoglycosides (netimycin, namicocin) are prescribed. In case of pneumocystal pneumonia Co-trimoxasol is nchosen, tinidasol and metronidasol are less active. In case of fungal infectio– antifungal drugs are chosen (fluconasol, amphotericin U).
It is necessary to mention that nantistaphylococcus plasma and antistaphilococcus gamma-globulin must be nincluded in the therapy to treat staphylococcus pneumonia.
The prescription of antifungal and nbiopreparations in combination with short courses of narrow-spectrum nantibiotics is restricted to children of the first month and patients with nimmunosuppression.
Pathogenetic therapy is indicated, taking into consideration the general pathogenetic nmechanisms of the disease development. It includes the usage of: n1) anti-inflammatory drugs (mefenamin acid, erespan etc.), which inhibit nthe inflammatory mediators’ activity; 2) antioxidants and nmembrane-stabilizing drugs (vitamins, especially A, E, dimephosphon essenciale etc. for 7–10 days); n3) the treatment of the respiratory compromise: supporting free nconductivity of the respiratory tract, oxygen therapy with moistened oxygen, nimproving bronchial conductivity by injecting 2.4% aminophylline solution in single ndose 4 mg/kg intravenously by drops; 4) treatment of the toxicosis: ninfusion therapy volume in case of pneumonia must not exceed 30–50 ml/kg nper day, the ratio colloid/crystalloid must be 1:2, ratio of crystalloids – 10% nof glucose solution to 0.9% physiological solution (Ringer solution) – nwhen the child is under 2 months old – 4:1, when the child is under 1 year nold – 3:1, more than 3 years old – 2:1, more – under the diuresis control. nThe speed is 10–15 drops per minute.
Symptomatic therapy includes vasoconstictive drugs to treat rhinitis, drugs to treat cough, among nwhich the “mucolytic” group is the most preferable – “mucolytic drugs with nexpectorant effect” and “expectorant drugs”.
Physiotherapeutic treatment. During the acute period of non-complicated pneumonia the ultra-high nfrequency electric field (5–6 séances, microwave therapy), ninductothermia are prescribed. After that 10–15 séances of namplipulsophoresis with nicotine acid solution, calcium chloride, copper or nmagnesium sulfate are given. In case when the disease is lingering and the npulmonary fibrosis is suspected, inductothermia, diathermia, amplipulsophoresis nwith 3% potassium iodide solution, lidase are recommended. In case of purulent npulmonary complications the treatment by amplipulsophoresis with platiphilliand staphylococcus antiphagin or proteolytic enzymes is given at the certaistage of the therapy.
Therapeutic physical culture is begun after the ntoxicosis disappears and the temperature decreases to subfebrile level. It nincludes breathing gymnastics and chest massage (vibromassage, jar massage). It nis useful to do warm and moist inhalations, inhalations with mucolytics, herbal ndecoctions, physiological solution.
The acute period over, adaptogens (eleuterococcus nextraction, Echinacea, Schizandra) and vitamins C, A, E, of B group are nprescribed for peroral administration.
The primary prevention includes child nhardening from the first months of life, rational diet and care, sufficient nstaying in fresh air. It is necessary to prevent and treat in time chronic ninfection sources, treat diseases, provoking pneumonia (intractranial birth ntrauma, rachitis, anemia, hypotrophy, acute respiratory viral infections etc.). nIn order to contror hospital-acquired pneumonias, it is important to take wide nrange of measures to prevent cross-infection in the in-patient hospital ndepartment.
The secondary prevention includes timely and nadequate treatment of acute pneumonia to reach the complete recovery. The naforementioned generally-strengthening therapy, which makes the inflammatory nsources to dissolve, is continued for not less than 2–4 weeks after the ndischarge from the hospital (interchanging vitamin courses combined with plant nadaptogens).
After pneumonia the child should be under the npediatrician’s observation during 6 months, after pneumonia in the nneonatal period – during 1 year. The pediatrician must examine the child during nthe first three months, and the newborn – twice a month, than every month.
Prognosis. If the ndisease was diagnosed in time and the treatment was adequate, mild and nmoderately-severe forms of bronchopneumonia, segmentary and croupous pneumonia nend in recovery in most cases. In several cases, burdened premorbid background, nvirus or bacterial reinfection, late or insufficient treatment may initiate nlingering or chronic bronchopulmonary process. In case of destructive process nand also in case if any pneumonia has a severe form, the prognosis is very nserious.
Table 6. The choice of antibacterial ntherapy to treat the community-acquired pneumonia depending on the child’s age
|
Form of the pneumonia |
Chosen antibiotics |
Daily dose (mg/kg), way of administration |
Alternative drugs |
Daily dose (mg/kg), way of administration |
|
1–6 months |
||||
|
Typical |
Aminopenicillins Amoxicillin/ Clavulanat Ampicillin/sulbactam |
i/v 30
i/v, i/m 150 |
Cephalosporins II Cefuroxime (zinacef) III generation Cefotaxim (claforan) Ceftriaxone (langocef) Ceftazidim (fortum) |
I/m, i/v 50-100
50-100 20-80 50-100 30-50 |
|
Atypical |
Modern macrolides Azithromycin Roxithromycin Clarithromycin Spiramycin Josamycin, Midecamycin |
p/o 5-10 5-8
150 thousand units 40-50 30-50 (< 12years old) |
Co-trimoxazole |
perorally 20 according to trimethoprim |
|
6 months — 6 years |
||||
|
Typical |
Amoxicillin and/or Modern macrolides |
p/o 50-100 |
Amoxicillin/clavulanat, Cephalosporins II Cefuroxime axetil (zinnat) cefaclor III generation Cefixime (cefepime) Cephalosporins II, III |
p/o, i/m, i/v 30-50 60-120 p/o 30-100 40 6-8 i/m, i/v |
|
6—15 years |
||||
|
Typical |
Modern macrolide |
p/o |
Amoxicillin/clavulanat, Cephalosporins II, III Lincosamides Lincomycin |
p/o, i/m, i/v
i/m, i/v 30 |
|
Atypical: non-complicated |
Modern macrolide |
p/o |
Tetracyclines Doxycycline (to children > 8 years old) |
p/o 5 |
|
Complicated with pleurisy or destruction |
Amoxicillin/clavulanat or Ampicillin/sulbactam Cephalosporins II |
i/m, i/v |
Aminoglycosides Gentamycin, Sisomycin, Tobramycin, Netilmycin Amikacin + Cephalosporins of the II, III, IV generation — Cefepime Lincomycin+Aminoglycoside, Carbopenems Meropenem, Imepenem
Levomycetin succinat |
i/m, i/v 2-4
6-9 i/v 12-15 i/m, i/v 50 (< 6 years old) 2g/day >6 years i/v 20-30 (<12 years) 2g/day, if the mass >50kg i/m, i/v 25-30 (<1year) 50 (>1 year)
|
Table 7. The nchoice of antibacterial therapy to treat the hospital-acquired pneumonia
|
Nosological form |
Chosen drug |
Alternative drug |
|
Pneumonias, which occur in departments of general specialization, without any risk factors |
Amoxicillin/clavulanat Ampicillin/sulbactam Cephalosporins II–III, except Ceftazidim |
Cefepime+Aminoglycoside, Fluorinequinols — Levofloxacin 400 mg/day |
|
Pneumonias, which occur in departments of general specialization, with some risk factors |
Cephalosporins III Cefepime Ceftazidim или Cefoperazone+Aminoglycosides |
Carbopenems, Tetracycline/clavulanat or Aztrionam (i/m,i/v 30-50 mg/kg), Vancomycin (i/v 40 mg/kg of the body mass) |
Complications
Complications of pneumonia are usually the result of direct spread of bacterial ninfection within the thoracic cavity (pleural effusion, empyema, pericarditis) nor bacteremia and hematologic spread. Meningitis, suppurative arthritis, and nosteomyelitis are rare complications of hematologic spread of pneumococcal or nH. influenzae type b infection.
S. aureus, S. pneumoniae, and S. pyogenes are the most common causes of nparapneumonic effusions and of empyema (Table 392-6). The treatment of empyema nis based on the stage (exudative, fibrinopurulent, organizing). Imaging studies nincluding ultrasonography and CT are helpful in determining the stage of nempyema. The mainstays of therapy include antibiotic therapy and drainage with ntube thoracostomy. Additional approaches include the use of intrapleural nfibrinolytic therapy (urokinase, streptokinase, tissue plasminogen activator) nand selected video-assisted thoracoscopy (VATS) to debride or lyse adhesions, nand drain loculated areas of pus. Early diagnosis and intervention, nparticularly with fibrinolysis or VATS, may obviate the need for thoracotomy nand open debridement. Fibrinolysis may be more cost effective than VATS.
Table 8. DIFFERENTIATION OF PLEURAL FLUID
|
|
TRANSUDATE |
EMPYEMA |
|
Appearance |
Clear |
Cloudy or purulent |
|
Cell count (per mm3) |
<1000 |
Often >50,000 (cell count has limited predictive value) |
|
Cell type |
Lymphocytes, monocytes |
Polymorphonuclear leukocytes (neutrophils) |
|
Lactate dehydrogenase |
<200 U/L |
>1000 U/L |
|
Pleural fluid/serum LDH ratio |
<0.6 |
>0.6 |
|
Protei >3g |
Unusual |
Common |
|
Pleural fluid/serum protein ratio |
<0.5 |
>0.5 |
|
Glucose |
Normal |
Low (<40 mg/dL) |
|
pH |
Normal (7.40-7.60) |
<7.10 |
|
Gram stain |
Negative |
Occasionally positive (less than one-third of cases) |
Prognosis
Typically, patients with uncomplicated community-acquired bacterial npneumonia show response to therapy, with improvement in clinical symptoms n(fever, cough, tachypnea, chest pain), within 48-96 hr of initiation of nantibiotics. Radiographic evidence of improvement lags substantially behind nclinical improvement. A number of factors must be considered when a patient ndoes not improve with appropriate antibiotic therapy: (1) complications, such nas empyema; (2) bacterial resistance; (3) nonbacterial etiologies such as nviruses and aspiration of foreign bodies or food; (4) bronchial obstructiofrom endobronchial lesions, foreign body, or mucous plugs; (5) pre-existing ndiseases such as immunodeficiencies, ciliary dyskinesia, cystic fibrosis, npulmonary sequestration, or cystic adenomatoid malformation; and (6) other nnoninfectious causes (including bronchiolitis obliterans, hypersensitivity npneumonitis, eosinophilic pneumonia, aspiration, and Wegener’s granulomatosis). nA repeat chest radiograph is the 1st step in determining the reason for delay nin response to treatment.
Mortality from community-acquired pneumonia in developed nations is rare, nand most children with pneumonia do not experience long-term pulmonary sequelae. nSome data suggest that up to 45% of children have symptoms of asthma 5 yr after nhospitalization for pneumonia; this finding may reflect either undiagnosed nasthma at the time of presentation or a propensity for development of asthma nafter pneumonia
n
<!–[i
Right side focal pneumonia
Right side lobar pneumonia
Lobar pneumonia
Left side focal pneumonia
Destructive pneumonia, Abscess of the lung
Pleurisy
Air trapping and nhyperexpansion from airway obstruction
Congenital pneumonia
Crouposus npneumonia
Polisegmental npneumonia
Bronchopneumonia
Bronchiectasis
Bronchiectasis nis a disease characterized by irreversible abnormal dilatation of the bronchial ntree and likely represents a common end stage of a number of nonspecific and nunrelated antecedent events. Its incidence has been decreasing overall ideveloped countries, but it persists as a problem in developing countries. Iat least 1 series of children with bronchiectasis (not due to cystic fibrosis), nthe male to female ratio was 2 : 1.
PATHOPHYSIOLOGY nAND PATHOGENESIS.
In the developed world, cystic nfibrosis (see Chapter 400 n) is the most common cause of clinically significant bronchiectasis. Other nconditions associated with bronchiectasis include ciliary dyskinesia, immune ndeficiency syndromes, and infection, especially pertussis, measles, and ntuberculosis. Bronchiectasis can also be congenital, as in Williams-Campbell nsyndrome, in which there is an absence of annular bronchial cartilage, and Marnier-Kuhsyndrome (congenital tracheobronchomegaly), in which there is a connective ntissue disorder. Other disease entities associated with bronchiectasis include right nmiddle lobe syndrome (chronic extrinsic compression of right middle lobe nbronchus by hilar lymph nodes) and yellow nail syndrome (pleural neffusion, lymphedema, discolored nails).
Three basic mechanisms are ninvolved in the pathogenesis of bronchiectasis. Obstruction can occur because nof tumor, foreign body, impacted mucus caused by poor mucociliary clearance, nexternal compression, bronchial webs, and atresia. Infections due to Bordetella npertussis, measles, rubella, togavirus, respiratory syncytial virus, and Mycobacterium ntuberculosis induce chronic inflammation, progressive bronchial wall ndamage, and dilatation. Chronic inflammation similarly contributes to the nmechanism by which obstruction leads to bronchiectasis. The mechanism by which nbronchiectasis occurs in congenital forms is likely related to abnormal ncartilage formation. The common thread in the pathogenesis of bronchiectasis is ndifficulty clearing secretions and recurrent infections with a “vicious cycle” nof infection and inflammation resulting in airway injury and remodeling.
Bronchiectasis can present iany combination of three pathologic forms, best defined by high-resolution CT n(HRCT) scan. In cylindrical bronchiectasis, the bronchial outlines are regular, nbut there is diffuse dilatation of the bronchial unit. The bronchial lumen ends nabruptly because of mucous plugging. In varicose bronchiectasis, the degree of ndilatation is greater and local constrictions cause an irregularity of outline nresembling varicose veins. There may also be small sacculations. In saccular n(cystic) bronchiectasis, bronchial dilatation progresses and results in ballooning nof bronchi that end in fluid- or mucus-filled sacs. This is the most severe nform of bronchiectasis. Bronchiectasis lies within a disease spectrum of nchronic pediatric suppurative lung disease. The following definitions have beeproposed: prebronchiectasis (chronic or recurrent endobronchial ninfection with nonspecific HRCT changes); HRCT bronchiectasis (clinical nsymptoms with HRCT evidence of bronchial dilation—may persist, progress, or nimprove and resolve); established bronchiectasis (like the previous but nwith no resolution within 2 yr).
CLINICAL nMANIFESTATIONS.
The most common complaints ipatients with bronchiectasis are cough and copious purulent sputum production. nYounger children may swallow the sputum. Hemoptysis is seen with some frequency. nFever can occur with infectious exacerbations. Anorexia and poor weight gaimay occur as time passes. Physical examination typically reveals crackles nlocalized to the affected area, but wheezing as well as digital clubbing may nalso occur. In severe cases, dyspnea and hypoxemia can occur. Pulmonary nfunction studies may demonstrate an obstructive, restrictive, or mixed pattern. nTypically, impaired diffusion capacity is a late finding.
DIAGNOSIS.
Chest radiographs of patients nwith bronchiectasis tend to be nonspecific. Typical findings can include nincrease in size and loss of definition of bronchovascular markings, crowding nof bronchi, and loss of lung volume. In more severe forms, cystic spaces, noccasionally with air-fluid levels and honeycombing, may occur. Compensatory noverinflation of unaffected lung may be seen. Thin-section HRCT scanning is the ngold standard, because it has excellent sensitivity and specificity. CT nprovides further information on disease location, presence of mediastinal nlesions, and the extent of segmental involvement. The addition of radiolabeled naerosol inhalation to CT scanning can provide further information. The CT nfindings in patients with bronchiectasis typically include cylindrical (“tram nlines,” “signet ring appearance”), varicose (bronchi with “beaded contour”), ncystic (cysts in “strings and clusters”), or mixed forms. The lower lobes are nmost commonly affected.
TREATMENT.
The initial therapy for npatients with bronchiectasis is medical and aims at decreasing airway nobstruction and controlling infection. Chest physiotherapy (postural drainage), nantibiotics, and bronchodilators are essential. Two to 4 wk of parenteral nantibiotics are ofteecessary to manage acute exacerbations adequately. nAntibiotic choice is dictated by the identification and sensitivity of norganisms found on deep throat, sputum (induced or spontaneous), or nbronchoalveolar lavage fluid cultures. Chronic prophylactic oral (macrolide) or nnebulized antibiotics may be beneficial. Any underlying disorder n(immunodeficiency, aspiration) that may be contributing must be addressed. Whelocalized bronchiectasis becomes more severe or resistant to medical nmanagement, segmental or lobar resection may be warranted. Lung transplantatiocan also be performed in patients with bronchiectasis.
Overall, the nprognosis for patients with bronchiectasis has improved considerably in the past nfew decades. Earlier recognition or prevention of predisposing conditions, more npowerful and wide-spectrum antibiotics, and improved surgical outcomes are nlikely reasons.
Pulmonary abscesses are localized areas composed of thick-walled purulent nmaterial formed as a result of lung infection that lead to destruction of lung nparenchyma, cavitation, and central necrosis. Lung abscesses are much less ncommon in children than iadults. A primary lung abscess occurs in a previously healthy patient with no nunderlying medical disorders. A secondary lung abscess occurs in a patient with nunderlying or predisposing conditions.
PATHOLOGY AND PATHOGENESIS.
A number of conditions predispose children to the development of pulmonary nabscesses, including aspiration, pneumonia, cystic fibrosis (see Chapter 400 ), ngastroesophageal reflux (see Chapter 320.1 ), tracheoesophageal fistula (see Chapter 316 ), nimmunodeficiencies, postoperative complications of tonsillectomy and nadenoidectomy, seizures, and a variety of neurologic diseases. In children, naspiration of infected materials or a foreign body is the predominant source of nthe organisms causing abscesses. Initially, a pneumonitis impairs drainage of nfluid or the aspirated material. Inflammatory vascular obstruction occurs, nleading to tissue necrosis, liquefaction, and abscess formation. Abscess caalso occur as a result of pneumonia and hematogenous seeding from another site.
If the aspiration event occurred in the recumbent position, the right and nleft upper lobes and apical segment of the right lower lobes are the dependent nareas most likely to be affected. If the child was upright, the posterior nsegments of the upper lobes are dependent and therefore most likely to be naffected. Primary abscesses are found most often on the right side, whereas nsecondary lung abscesses, particularly in immunocompromised patients, have a npredilection for the left side.
Both anaerobic and aerobic organisms can cause lung abscesses. Commoanaerobic bacteria that can cause a pulmonary abscess include Bacteroides nspp., Fusobacterium spp., and Peptostreptococcus spp. Abscesses ncan be caused by aerobic organisms such as Streptococcus spp., Staphylococcus naureus, Escherichia coli, Klebsiella pneumoniae, and Pseudomonas naeruginosa. All patients with a lung abscess should have aerobic and nanaerobic cultures as part of their work-up. Fungi can also cause lung nabscesses, particularly in immunocompromised patients.
CLINICAL MANIFESTATIONS.
The most common symptoms of pulmonary abscess in the pediatric populatioinclude cough, fever, tachypnea, dyspnea, chest pain, vomiting, sputum nproduction, weight loss, and hemoptysis. Physical examination typically reveals ntachypnea, dyspnea, retractions with accessory muscle use, decreased breath nsounds, and dullness to percussion in the affected area. Crackles and, noccasionally, a prolonged expiratory phase may be heard on lung examination.
DIAGNOSIS.
Diagnosis is most commonly made on chest radiography. Classically, the nchest radiograph shows a parenchymal inflammation with a cavity containing aair-fluid level. A chest CT scan can provide better anatomic definition, nincluding location and size.
An abscess is usually a thick-walled lesion with a low-density center nprogressing to an air-fluid level. Abscesses should be distinguished from npneumatoceles, which often complicate severe bacterial pneumonias and are ncharacterized by thin- and smooth-walled localized air collections with or nwithout an air-fluid level. Pneumatoceles often resolve spontaneously with the ntreatment of the specific cause of the pneumonia.
The determination of the etiologic bacteria in a lung abscess can be very nhelpful in guiding antibiotic choice. Although Gram stain of sputum can provide nan early clue as to the class of bacteria involved, sputum cultures typically nyield mixed bacteria and are therefore not always reliable. Attempts to avoid ncontamination from oral flora include direct lung puncture and percutaneous n(aided by CT guidance), bronchoscopic, and transtracheal aspiration. nBronchoscopic aspiration can be complicated by massive intrabronchial naspiration, and great care should therefore be taken during the procedure. To navoid invasive procedures in previously normal hosts, empiric therapy can be ninitiated in the absence of culturable material.
TREATMENT.
Conservative management is recommended. Most experts advocate a 2–3 wk ncourse of parenteral antibiotics for uncomplicated cases, followed by a course nof oral antibiotics to complete a total of 4–6 wk. Antibiotic choice should be nguided by Gram stain and culture but initially should include aerobic and nanaerobic coverage. Treatment regimens should include a penicillinase-resistant nagent active against S. aureus and anaerobic coverage, typically with nclindamycin or ticarcillin/clavulinic acid. If gram-negative bacteria are nsuspected or isolated, an aminoglycoside should be added.
For severely ill patients or those who fail to improve after 7–10 days of nappropriate antimicrobial therapy, surgical intervention should be considered. nMinimally invasive percutaneous aspiration techniques, often with CT guidance, nare the initial and, often, only intervention. In rare complicated cases, nthoracotomy with lobectomy and/or decortication may be necessary.
Overall, prognosis for children with primary pulmonary abscesses is nexcellent. The presence of aerobic organisms may be a negative prognostic nindicator, particularly in those with secondary lung abscesses. Most childrebecome asymptomatic within 7–10 days, although the fever can persist for as nlong as 3 wk. Radiologic abnormalities usually resolve in 1–3 mo but capersist for years.
Atelectasis
Atelectasis, the incomplete nexpansion or complete collapse of air-bearing tissue, is common in infants and nchildren. Atelectasis results from obstruction of air intake into the alveolar nsacs. Segmental, lobar, or whole lung collapse is associated with the absorptioof air contained in the alveoli, which are no longer ventilated.
PATHOPHYSIOLOGY.
The causes of atelectasis cabe divided into five groups ( Table). Viral infections in young children, nspecifically respiratory syncytial virus (see Chapter 257 ), can cause multiple nareas of atelectasis. Mucous plugs from whatever etiology are a commopredisposing factor to atelectasis. Massive collapse of one or both lungs is nmost often a postoperative complication but occasionally results from other ncauses, such as trauma, asthma, pneumonia, tension pneumothorax (see Chapter n410 ), aspiration of foreign material (see Chapters 384 and 394 ), paralysis, nor after extubation. Massive atelectasis is usually produced by a combinatioof factors, including immobilization or decreased use of the diaphragm and the nrespiratory muscles, obstruction of the bronchial tree, and abolition of the ncough reflex.
nTABLE — Anatomic Causes of Atelectasis
|
CAUSE |
CLINICAL EXAMPLES |
|
External compression on the pulmonary parenchyma |
Pleural effusion, pneumothorax, intrathoracic tumors, diaphragmatic hernia |
|
Endobronchial obstructio completely obstructing the ingress of air |
Enlarged lymph node, tumor, cardiac enlargement, foreign body, mucoid plug, broncholithiasis |
|
Intraluminal obstruction of a bronchus |
Foreign body, granulomatous tissue, tumor, secretions, including mucous plugs, bronchiectasis, pulmonary abscess, asthma, chronic bronchitis, acute laryngotracheobronchitis |
|
Intrabronchiolar obstruction |
Bronchiolitis, interstitial pneumonitis, asthma |
|
Respiratory compromise or paralysis |
Neuromuscular abnormalities, osseous deformities, overly restrictive casts and surgical dressings, defective movement of the diaphragm, or restriction of respiratory effort |
|
|
CLINICAL nMANIFESTATIONS.
Symptoms vary with the cause nand extent of the atelectasis. A small area is likely to be asymptomatic. Whea large area of previously normal lung becomes atelectatic, especially when it ndoes so suddenly, dyspnea accompanied by rapid shallow respirations, ntachycardia, cough, and often cyanosis occurs. If the obstruction is removed, nthe symptoms disappear rapidly. Although it was once believed that atelectasis nalone can cause fever, studies have showo association between atelectasis nand fever. Physical findings include limitation of chest excursion, decreased nbreath sound intensity, and coarse crackles. Breath sounds are decreased or nabsent over extensive atelectatic areas.
Massive pulmonary atelectasis nusually presents with dyspnea, cyanosis, and tachycardia. An affected child is nextremely anxious and, if old enough, complains of chest pain. The chest appears nflat on the affected side, where decreased respiratory excursion, dullness to npercussion, and feeble or absent breath sounds are also noted. Postoperatively, natelectasis usually presents within 24 hr after operation but may not occur for nseveral days.
Acute lobar collapse is a frequent occurrence in patients receiving intensive care. If nundetected, it can lead to impaired gas exchange, secondary infection, and nsubsequent pulmonary fibrosis. Initially, hypoxemia may result from nventilation-perfusion mismatch. In contrast to adult patients in whom the lower nlobes and, in particular, the left lower lobe are most often involved, 90% of ncases in children involve the upper lobes and 63% involve the right upper lobe. nThere is also a high incidence of upper lobe atelectasis and especially right nupper lobe collapse ieonatal intensive care units. This nmay be due to the endotracheal tube moving into the right main stem bronchus nand obstructing or causing inflammation of the bronchus to the right upper nlobe.
DIAGNOSIS.
The diagnosis of atelectasis ncan usually be established by chest radiographic examination. Typical findings ninclude volume loss and displacement of fissures. Atypical presentations ninclude atelectasis presenting as a masslike opacity and atelectasis in aunusual location. Lobar atelectasis may be associated with pneumothorax.
In asthmatic children, chest nradiography demonstrates an abnormality rate of 44%, compared with a thorax nhigh-resolution CT (HRCT) scan abnormality rate of 75%. Children with asthma nand atelectasis have an increased incidence of right middle lobe syndrome, nacute asthma exacerbations, pneumonia, and upper airway infections.
In foreign body aspiration, natelectasis is one of the most common radiographic findings. The site of atelectasis nusually indicates the site of the foreign body. Atelectasis is more common whepatients have a delay in diagnosis of >2 wk duration.
Bronchoscopic examinatioreveals a collapsed main bronchus when the obstruction is at the ntracheobronchial junction and may also disclose the nature of the obstruction.
Massive pulmonary atelectasis nis generally diagnosed by chest radiograph. Typical findings include elevatioof the diaphragm, narrowing of the intercostal spaces, and displacement of the nmediastinal structures and heart toward the affected side..
Treatment depends on the cause nof the collapse. If effusion or pneumothorax is responsible, the external compressiomust first be removed. Often vigorous efforts at cough, deep breathing, and npercussion will facilitate expansion. Aspiration with sterile tracheal ncatheters may facilitate removal of mucous plugs. Continuous npositive airway pressure (CPAP) may improve atelectasis.
Bronchoscopic examination is nimmediately indicated if atelectasis is the result of a foreign body or any nother bronchial obstruction that can be relieved. For bilateral atelectasis, nbronchoscopic aspiration should also be performed immediately. It is also nindicated when an isolated area of atelectasis persists for several weeks. If nno anatomic basis for atelectasis is found and no material can be obtained by nsuctioning, the introduction of a small amount of saline followed by suctioning nallows recovery of bronchial secretions for culture and, possibly, for ncytologic examination. Frequent changes in the child’s position, deep nbreathing, and chest physiotherapy may be beneficial. Oxygen therapy is nindicated when there is dyspnea or desaturation. Intermittent positive pressure nbreathing and incentive spirometry are recommended when atelectasis does not nimprove after chest physiotherapy.
In some conditions, such as nasthma, bronchodilator and corticosteroid treatment may accelerate atelectasis nclearance. Recombinant human DNase (rhDNase), which is approved only for the ntreatment of cystic fibrosis, has been used off label for patients without ncystic fibrosis who have persistent atelectasis. This product reduces the nviscosity of purulent bronchial debris. In patients with acute severe asthma, ndiffuse airway plugging with thick viscous secretions frequently occurs, with nthe resulting atelectasis often refractory to conventional therapy. rhDNase has nbeen used in both nebulized form for nonintubated patients with acute asthma as nwell as intratracheally for atelectasis in intubated asthmatics, with nresolution of atelectasis unresponsive to conventional asthma therapies.
Lobar atelectasis in cystic nfibrosis is discussed in Chapter n400 .
Atelectasis can occur ipatients with neuromuscular diseases. These patients tend to have ineffective ncough and difficulty expelling respiratory tract secretions, which leads to npneumonia and atelectasis. Several devices are available to assist these npatients, including intermittent positive pressure breathing, In-Exsufflator, nand noninvasive bilevel positive pressure ventilation via nasal mask or nfull-face mask. Patients with neuromuscular disease who have undergone surgery nare at substantial risk of postoperative atelectasis and subsequent pneumonia. Migrating natelectasis in the newborn infant is a rare and unique presentation and may nbe secondary to neuromuscular disease.
There is aassociation between the development of lobar collapse and the requirement for nmechanical ventilation. Although lobar collapse is rarely a cause of long-term nmorbidity, its occurrence may necessitate the prolongation of mechanical nventilation or reintubation. In patients who are ventilated, positive nend-expiratory pressure (PEEP) or CPAP is generally indicated.
Bacteria are nthe most common causes of pneumonia, but these infections can also be caused by nother microbial organisms. It is often impossible to identify the specific nculprit. Many bacteria are categorized by the staining procedure used to nvisualize bacteria under a microscope. The stains determine if they are ngram-negative or gram-positive bacteria. This gives the physician an idea of nthe severity of the pneumonia and how to treat it.
Gram-Positive Bacteria. These bacteria appear blue on the stain. The following are common gram-positive bacteria:
The most common cause of pneumonia is the gram-positive bacterium Streptococcus pneumoniae (also called S. pneumoniae or pneumococcal pneumonia ). It was thought to cause 95% of community-acquired nbacterial infection, but research now indicates it is far less, accounting for nabout half of all cases.
>Staphylococcus aureus , the other nmajor gram-positive bacterium responsible for pneumonia, accounts for about 10% nof bacterial cases. It is one of the main causes of pneumonia that occurs ithe hospital (nosocomial pneumonia). It is uncommon in healthy adults but cadevelop about five days after viral influenza, usually in susceptible nindividuals, such as people with weakened immune systems, very young children, nhospitalized patients.
Streptococcus pyogenes or Group A Streptococcus.
Gram-Negative Bacteria. These bacteria stain pink . Gram nnegative bacteria are common infectious agents in hospitalized or nursing home patients, nchildren with cystic fibrosis, and people with chronic lung conditions.
The most common gram-negative species causing pneumonia is Haemophilus.
Klebsiella npneumoniae may be responsible for npneumonia in alcoholics and in other people who are physically debilitated
Pseudomonas naeruginosa is a major cause of pneumonia nthat occurs in the hospital (nosocomial pneumonia).
Moraxella ncatarrhalis is found in everyone’s nasal nand oral passages. Experts have identified this bacteria as a cause of certaipneumonias, particularly in people with lung problems, such as asthma or nemphysema.
Neisseria nmeningitidis is one of the most commocauses of meningitis (central nervous system infection), but the organism has nbeen reported in pneumonia, particularly in epidemics of military recruits.
Other gram-negative bacteria that cause pneumonia include E. coli (a cause iewborns), Proteus (found in several damaged lung ntissue), and Enterobacter.
Atypical nPneumonia
Atypical pneumonias are generally caused by tiny nonbacterial organisms ncalled Mycoplasma or Chlamydia pneumoniae and produce mild nsymptoms with a dry cough. Hospitalizatiois uncommon with pneumonia from these organisms.
<!–[if !supportLists]–>· <!–[endif]–>Mycoplasma pneumoniae ( M. pneumoniae ) is the most commononbacterial pneumonia. The condition is usually mild and is commonly known as nwalking pneumonia. Estimates of its prevalence in community acquired pneumonias nin adults range from 1.9% to 30%. In one nstudy, it accounted for over a third of pneumonia cases in children.
Another small non-bacterial organism, Chlamydia npneumoniae ( C. pneumoniae ), is nnow thought to cause 10% of all community-acquired cases of pneumonia. It is most ncommon in children, where it is usually mild. In one study, it was the cause of n14% of cases in a group of children with pneumonia.
Legionnaire’s disease, first diagnosed in 1976, is caused by the organism Legionella pneumophila, and is acquired nby breathing droplets of contaminated water.
Viruses
Viruses that can cause or lead to pneumonia include influenza, respiratory nsyncytial virus (RSV), herpes simplex virus, varicella-zoster (the cause of nchicken pox), and adenovirus. Outbreaks nusually occur between January and April.
Influenza is associated with pneumonia directly or by altering the mucous nblanket and making a person susceptible to bacterial pneumonia.
Respiratory syncytial virus (RSV) is a major cause of pneumonia in infants and npeople with damaged immune systems. Studies indicate that RSV pneumonia may nalso be more common than previously thought in adults, especially the elderly.
Adenoviruses have been implicated in about 10% of childhood pneumonia.
In adults, herpes simplex virus, adenoviruses, and varicella-zoster (the ncause of chicken pox) are generally causes of pneumonia only in people with nimpaired immune systems.
AspiratioPneumonia and Anaerobic Bacteria.
The mouth harbors a mixture of bacteria that is harmless in its normal nlocation but can cause a serious condition called aspiration pneumonia if it nreaches the lung. This can happen during periods of altered consciousness, noften when a patient is affected by drugs or alcohol, or after head injury or nanesthesia. In such cases, the gag reflex is diminished, allowing these nbacteria to enter the airways to the lung. These organisms are generally ndifferent from the usual microbes that enter the lung by inhalation. Many are noften anaerobic (meaning they can live in the absence of oxygen).
Opportunistic nPneumonia .
Impaired immunity leaves patients vulnerable to serious, evelife-threatening, pneumonias known as opportunistic pneumonias. They are caused nby microbes that are harmless to people with healthy immune systems. Infecting norganisms include the following: Pneumocystis ncarinii, Fungi, such as Mycobacterium navium.Viruses, such as cytomegalovirus (CMV). AIDS is a major risk factor nfor opportunistic pneumonia, as are other conditions including lymphomas, nleukemias, and other cancers. Long-term use of corticosteroids and other nmedications that suppress the immune system increase the susceptibility to nthese pneumonias.
Incubation:The incubation period for npneumonia varies, depending on the type of virus or bacteria causing the ninfection. Some common incubation periods are: respiratory syncytial virus, 4 nto 6 days; influenza, 18 to 72 hours.
Duration:With treatment, most types of nbacterial pneumonia can be cured within 1 to 2 weeks. Viral pneumonia may last nlonger. Mycoplasmal pneumonia may take 4 to 6 weeks to resolve completely.
ACUTE PNEUMONIA
Clinical Presentation
Typical nsymptoms include cough, fever, and sputum production, usually developing over ndays and sometimes accompanied by pleurisy. Physical examination may detect ntachypnea and signs of consolidation, such as crackles with bronchial breath nsounds. This syndrome is commonly caused by bacteria, such as S. pneumoniae nand H. influenzae.
Non-specific clinical features:
ü fever, lethargy, anorexia
ü meningism (especially upper lobe)
ü abdominal pain (especially lower lobe)
ü Respiratory manifestations:
ü tachypnoea, respiratory distress, grunt
ü cyanosis
ü localised auscultatory signs
ü cough absent unless airway involvement
ü associated effusions and pneumatoceles (especially Staph aureus).
Diagnosis
Clinical nfeatures and chest X-ray:
may help ndistinguish viral from bacterial.
Identificatioof responsible organisms:
Viral
ü nasopharyngeal aspirate (immunofluorescence and culture)
ü serology: not useful in babies; nuseful in older children.
ü Bacterial
ü blood culture
ü pleural fluid culture
ü lung aspiration
ü urinary or pleural fluid antigen.
ü Atypical
ü serology/cold agglutinins.
Defining Pneumonia by Locations in the Lung
Pneumonia is sometimes defined in one of two ways according to its ndistribution in the lung:
ü Lobar Pneumonia (occurs in one lobe of the lung).
ü Bronchopneumonia (tends to be patchy).
Defining Pneumonia by Origin of Infection
Pneumonia is often classified into two categories that may help predict the norganisms that are the most likely culprits.
Community-acquired n(pneumonia contracted outside the hospital). Pneumonia in this setting often follows a viral respiratory infection.
Hospital-acquired npneumonia. Pneumonia that is contracted nwithin the hospital is called nosocomial npneumonia. Hospital patients are particularly vulnerable to gram-negative nbacteria and staphylococci, which can be very dangerous.
Disease nProcess Leading to Pneumonia
Infectious agents reach the lungs and cause pneumonia through different nroutes:
Most often, organisms that cause pneumonia enter the lungs after being ninhaled into the airways.
Sometimes the normally harmless bacteria present in the mouth may be naspirated into the lungs, usually if the gag reflex is suppressed.
Pneumonia may also be caused from infections that spread to the lungs nthrough the bloodstream from other organs.
Under normal circumstances, however, the airways that take air in and pass nthrough the upper part of the body have very effective mechanisms that protect nthe lung from infection by bacteria and other microbes.
Bacteria or nother infectious agents that evade the airway defense system are attacked ithe alveolar sacs by defenders from the body’s immune system, particularly nmacrophages, large white blood cells that literally eat foreign particles.
These strong defense systems normally keep the lung sterile. If these ndefenses are weakened or damaged, however, bacteria or other organisms, such as nviruses, fungi, and parasites, can gain the upper hand, producing pneumonia.
nContagiousness:The viruses and bacteria that cause pneumonia are ncontagious and are usually found in fluid from the mouth or nose of an infected nperson. Illness can spread when an infected person coughs or sneezes on a nperson, by sharing drinking glasses and eating utensils, and when a persotouches the used tissues or handkerchiefs of an infected person.
Outlook for nHigh-Risk Individuals
nSeverity varies widely depending on individual factors, including the nfollowing:
Hospitalized Patients. For patients who require hospitalization for npneumonia, the mortality rate is between 10% and 25%. If pneumonia develops ipatients already hospitalized for other conditions, the mortality rates are nhigher. They range from 50% to 70% and are greater in women than in men.
Very Young Children. About 20% of stillborn and very early infant mortality ndeaths are due to pneumonia. Small children who develop pneumonia are at risk nfor developing lung problems in adulthood.
Patients with Impaired Immune Systems. Pneumonia is particularly serious ipeople with impaired immune systems, particularly AIDS patients, in whom npneumonia causes about half of all deaths.
Patients with Serious Medical Conditions. The disease is also very ndangerous in people with diabetes, cirrhosis, sickle cell anemia, multiple nmyeloma, and in those who have had their spleens removed.
Risk nby Organisms
Lower-Risk Organisms. The following organisms usually cause pneumonias that are responsive to ntreatment or mild. S. Pneumonia is nthe most common organism and, although it can cause severe pneumonia, it is nvery responsive to many antibiotics. Mycoplasma nand Chlamydia are common causes of npneumonia in children and young adults. They are generally mild and rarely nrequire hospitalization when they are appropriately treated, although recovery nmay still be prolonged. Severe and life-threatening cases are more likely to noccur in elderly people with other medication conditions.
High-Risk Organisms. The nfollowing are high-risk infecting organisms that pose a particular risk for ndangerous pneumonia:
High-risk gram positive bacteria. Staphylococcus naureus. Poses a higher risk for multiple small abscesses in the lung and nnecrosis (tissue death).
High-risk gram-negative bacteria include the following: Pseudomonas aeruginosa. Klebsiella npneumonia.. Legionella pneumophila . nParticularly virulent and can cause damage throughout the body.
Viral pneumonia is usually very mild but there are exceptions.
Influenza pneumonia can be very serious.
Respiratory syncytial virus (RSV) pneumonia rarely poses a danger for nhealthy young adults. However, between 22,000 and 44,500 children are nhospitalized each year because of pneumonia from RSV and the incidence seems to nbe increasing.
Signs and Symptoms:
Pneumonia is a general term that refers to an infection of the lungs, which ncan be caused by a variety of microorganisms, including nviruses, bacteria, and parasites.
Often pneumonia begins after an upper respiratory tract infection (ainfection of the nose and throat). When this happens, symptoms of pneumonia nbegin after 2 or 3 days of a cold or sore throat.
Symptoms of pneumonia vary, depending on the age of the child and the cause nof the pneumonia. Some common symptoms ninclude: fever ,chills ,cough,unusually rapid breathing ,breathing with grunting or nwheezing sounds,labored breathing that makes a child’s rib muscles retract (when muscles nunder the rib cage or between ribs draw inward with each breath) ,vomiting ,chest pain ,abdominal pain ,decreased activity,loss of appetite (in older nchildren) or poor feeding (in infants),in extreme cases, bluish or gray color of the lips and fingernails.
Sometimes a child’s only symptom is rapid breathing. Sometimes when the npneumonia is in the lower part of the lungs near the abdomen, there may be no nbreathing problems at all, but there may be fever and abdominal pain or vomiting.
Whepneumonia is caused by bacteria, an infected child usually becomes sick nrelatively quickly and experiences the sudden onset of high fever and unusually nrapid breathing. When pneumonia is caused by viruses, symptoms tend to appear nmore gradually and are often less severe than in bacterial pneumonia. Wheezing nmay be more common in viral pneumonia.
Some types of pneumonia cause symptoms that give important clues about nwhich germ is causing the illness. For example, in older children and nadolescents, pneumonia due to Mycoplasma (also called walking pneumonia) nis notorious for causing a sore throat and headache in addition to the usual nsymptoms of pneumonia.
Symptoms of Common Pneumonias
General Symptoms.
The symptoms of bacterial pneumonia develop abruptly and may include chest npain, fever, shaking, chills, shortness of breath, and rapid breathing and nheart beat.
Symptoms of pneumonia indicating a medical emergency include high fever, a nrapid heart rate, low blood pressure, bluish-skin, and mental confusion.
Coughing up sputum containing pus or blood is an indication of serious ninfection.
Severe abdominal pain may accompany pneumonia occurring in the lower lobes nof the lung.
In advanced cases, the patient’s skin may become bluish (cyanotic), nbreathing may become labored and heavy, and the patient may become confused.
Symptoms of Pneumonia Causes by Anaerobic Bacteria
People with pneumonia caused by anaerobic bacteria such as Bacteroides, which can produce nabscesses, often have prolonged fever and productive cough, frequently showing nblood in the sputum, which indicates necrosis (tissue death) in the lung. About na third of these patients experience weight loss.
Symptoms of Atypical Pneumonia
General Symptoms for Atypical Pneumonias. Atypical nonbacterial pneumonia is most commonly caused by Mycoplasma and usually appears ichildren and young adults.
Symptoms progress gradually, often beginning with general flu-like symptoms, nsuch as fatigue, fever, weakness, headache, nasal discharge, sore throat, ear nache, and stomach and intestinal distress.
Vague pain under and around the breast bone may occur, but the severe chest npain associated with typical bacterial pneumonia is uncommon.
Patients may experience a nsevere hacking cough, but it usually does not produce sputum.
Specific Risk Factors for Recurrent Pneumonia iChildren
Certain children have a higher thaormal risk for pneumonia and its nrecurrence. Conditions that predispose infants and small children to pneumonia ninclude the following:
Impaired immune system.
Gastroesophageal reflux disorder.
Inborn lung or heart defects.
Abnormalities in muscle coordination in the mouth and throat.
Asthma.
Certain genetic disorders. They include sickle-cell disease, cystic fibrosis (which causes mucus nabnormalities), and Kartagener’s syndrome (which results in malfunctioning cilia, nthe hair-like cells lining the airways).
HOW nIS PNEUMONIA DIAGNOSED.
In many ncases of mild-to-moderate community-acquired pneumonia, the physician is able nto diagnose and treat pneumonia based solely on a history and physical nexamination. Often, however, a diagnosis is not straightforward, particularly nin hospitalized patients.
Medical nand Personal History
The patient’s history is an important part of the diagnosis of pneumonia. nThe patient should be sure to report any of the following:
<!–[if !supportLists]–>· <!–[endif]–>recent or nchronic respiratory infection, exposure to people with pneumonia or other nrespiratory illnesses (such as viral), history of smoking parents,getting cold , recent travel, and occupational risks.
Physical nExamination
Percussion. The physician will also use a test called percussion, in which he or she ntaps the chest lightly. A dull thud instead of a healthy hollow-drum-like nsound, indicates certain condition that suggest pneumonia, including the nfollowing:
<!–[if !supportLists]–>· <!–[endif]–>Consolidation (a ncondition, in which the lung becomes firm and inelastic).
<!–[if !supportLists]–>· <!–[endif]–>Pleural effusion (fluid nbuild-up in the space between the lungs and the lining around it).
Percussion of the upper margiof the lung
The location of the apex of nthe lung
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Percussion of the lower margiof the lung
Percussion of the lower margiof the lung
Auscultation. The most nimportant diagnostic tool for pneumonia is the stethoscope. Sounds in the chest nthat may indicate pneumonia are the following:
<!–[if !supportLists]–>· <!–[endif]–>Rales (a bubbling or crackling nsound). Rales on one side of the chest and rales heard while the patient is nlying down is strongly suggestive of pneumonia.
nRhonchi (abnormal rumblings nindicating the presence of thick fluid).
Diagnostic nDifficulties in Hospitalized Patients
Diagnosing pneumonia is particularly difficult in hospitalized patients n(called nosocomial pneumonia) for a number of reasons, including the following: n
Many hospitalized patients have similar symptoms, including fever or signs nof lung infiltration on x-rays.
In hospitalized patients, sputum or blood tests often indicate the presence nof bacteria or other organisms, but such agents do not necessarily indicate npneumonia.
For a diagnosis of nosocomial pneumonia, physicians should be sure to rule nout other conditions, using a chest x-ray, two sets of blood cultures, a urine nanalysis for Legionella, lung fluid nsample, and possibly other tests for specific organisms.
Laboratory nTests for Diagnosing Infection and Identifying Bacterial Agents
Although antibiotics are available that can destroy a wide spectrum of norganisms, it would be preferable to use an antibiotic that can target the nspecific microorganism causing the pneumonia. Researchers, then, are looking nfor laboratory tests that would identify the specific organism or virus causing nthe pneumonia. Unfortunately, people harbor many bacteria, and sputum and blood ntests are not always effective in distinguishing between harmless and harmful nmicroscopic agents. In severe cases, physicians particularly need to use ninvasive diagnostic measures to identify the infecting agent.
nUrine nTests. A urine test (NOW) is up to 93% accurate iidentifying S. pneumoniae within 15 nminutes. However, a 2000 study indicated that it is not likely to be useful idiagnosing S. pneumoniae as a cause nof pneumonia in children, since the organism is very common in the noses and nthroats of children. This organism, then, would very likely be picked up by the ntest even if it were not the cause of the pneumonia.
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nSputum Tests. nOnly a sample of sputum coughed from the lungs will yield the infecting organism, nand, even then, tests are not always successful in revealing the culprit. The following steps may be required:
The physician first asks the patient to cough as deeply as possible to nproduce an adequate sputum sample. A shallow cough produces a sample that nusually only contains normal mouth bacteria.
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A patient who is not able to cough sufficiently may be asked to inhale a nsaline spray that helps produce an adequate sputum sample.
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In some cases, a tube will be inserted through the nose down into the lower nrespiratory tract to induce a deeper cough.
Even before sending the sample to the nlaboratory, the physician will check it for the following:
<!–[if !supportLists]–>· n<!–[endif]–>Presence of blood (an indication of infection). Color and consistency. If nthe sputum is opaque and colored yellow, green, or brown, then infection is nlikely. Clear, white, glistening nsputum indicates no infection.
In the laboratory, the sputum sample may be used nas follows:
A Gram’s stain is made, which may reveal the presence of bacteria and nwhether they are gram-negative or positive.
A sputum culture may be performed, in which organisms are grown in the nlaboratory.
Blood Tests. Blood tests may be used for nthe following:
White blood ncell count. High levels indicate infection.
peripheral blood leukocytosis with a prepoderanse of neutrophils electrolyte nlosses may be resulting in dehydration, acidosis, hyponatremia, nhypokalemia, hypoalbuminemia; focal infiltration on X-ray.
Blood ncultures. They may be performed for detecting the specific organism causing the npneumonia, but are not often helpful in distinguishing harmful from harmless norganisms.
Detection of nantibodies to S. pneumoniae. Researchers nare using specialized techniques to detect antibodies to S. pneumoniae (immune factors that target specific foreiginvaders), but it is not clear if they are accurate.
Laboratory nTests for Less Common Organisms
If uncommon organisms, such as Legionella, nMycoplasma, and Chlamydia organisms, are strongly suspected more advanced nlaboratory tests may be used:
Specialized techniques can detect antibodies to the organisms in blood nsamples, but these antibodies, such as those responding to Mycoplasma or Chlamydia , nare not present early enough in the course of pneumonia to permit prompt ndiagnosis and treatment. A test performed on whole blood samples that uses a ntechnique called polymerase chain reaction (PCR) is useful for identifying ncertain atypical strains, including Mycoplasma nand Chlamydia pneumoniae, but it is expensive. A urine ntest can be used to diagnose some cases of Legionnaire’s disease.
Chest X-Rays and Other Imaging Techniques
X-Rays. A chest x-ray is nearly always taken to confirm a diagnosis of pneumonia. It may reveal the following:
White areas in the lung called infiltrates, which indicate infection.
Complications of pneumonia, including pleural effusions (fluid around the nlungs) and abscesses.
Other nImaging Tests.
Computed tomography (CT) scans or MRIs may be obtained in the following ncircumstances:
If x-ray nresults are unclear. When patients do not respond to antibiotics.When patients nhave complications.
Whepatients have other serious health problems.
These more nsophisticated imaging techniques can help detect the presence of tissue damage, nabscesses, and enlarged lymph nodes. They can also detect some tumors that nblock bronchial tubes. No imaging technique can determine the actual organism ncausing the infection.
Invasive Diagnostic Procedures
Invasive diagnostic procedures may be required in the following ncircumstances:
When patients have life-threatening complications.
When patients have failed standard treatments for no known reason.
When AIDS or nother immune problems are present.
Each of the procedures has potential complications and is not used under nordinary conditions.
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nThoracentesis. nIf a physician detects pleural effusion and suspects that empyema (pus) is npresent, thoracentesis is performed:
Fluid in the pleura is withdrawn using a long thieedle inserted betweethe ribs.
The fluid is then tested using blood cell counts, Gram stains, cultures, nand chemical tests.
Complications of this procedure include collapsed lung, bleeding, and nintroduction of infection.
Bronchoscopy. A bronchoscopy employs the following:
The patient is given a local anesthetic, supplementary oxygen, and nsedatives.
The physician inserts a fiberoptic tube into the lower respiratory tract nthrough the nose or mouth.
The tube acts like a telescope into the body, allowing the physician to nview the wind-pipe and major airways for pus, abnormal mucus, or other problems. n
The doctor removes specimens for analysis and can also treat the patient by nremoving any foreign bodies or infected tissue encountered during the process.
Bronchoalveolar lavage (BAL) may be employed. This involves injecting high namounts of saline through the bronchoscope into the lung and then immediately nsuctioning the fluid back, which is then analyzed in the laboratory. Studies nfind BAL to be an effective method for detecting specific infection-causing norganisms in patients with serious pneumonia.
The procedure is usually very safe, but complications can occur. They ninclude allergic reactions to the sedatives or anesthetics, asthma attacks isusceptible patients, and bleeding. Fever may follow the procedure.
Lung nBiopsy. In very severe cases of npneumonia or when the diagnosis is unclear in specific cases, particularly ipatients with damaged immune systems, a lung biopsy may be required. Biopsies can be performed in one of two ways:
A Lung Tap. This procedure typically uses a needle inserted between the nribs to draw fluid out of the lung for analysis. It is known by a number of nnames including lung aspiration, lung puncture, thoracic puncture, ntransthoracic needle aspiration, percutaneous needle aspiration, and needle naspiration. It is a very old procedure that is not done often any more, nparticularly in children, since it is invasive and poses a slight risk for ncollapsed lung. Some experts argue, however, that a lung tap offers a more naccurate solution than other methods for identifying bacteria and the risk it nposes is slight. Given the increase in resistant bacteria, they believe its use nshould be reappraised in young people.
nSurgically (thoracotomy), using general anesthesia and an incision. This is nused for diagnosis only in very severe cases. As with bronchoscopy, the nprocedure can also be used to treat the patient, removing damaging lung tissue nand, in severe cases, removing the entire lobe (lobectomy). (In such cases, nremaining lung tissue re-expands after surgery to compensate for any removed ntissue.)
nDifferential diagnosis
Ruling out nCauses in Children. Important ncauses of coughing in children at different ages include:
Physical abnormalities in infants under 18 months. Sinusitis in children 18 nmonths to six years. Psychologic causes in older children and nadolescents.Tuberculosis.Bronchial asthma. Bronchiectasis (irreversible nwidening of the airways, usually associated with birth defects, chronic sinus nor bronchial infection, or blockage).
Atelectasis (collapse of lung tissue). Congestive heart failure. (If heart nfailure affects the lungs, fluid-build up can occur and cause persistent cough, nshortness of breath, and wheezing. In such cases, symptoms are usually worse at nnight.) Severe allergic reactions, such as to drugs. Children respiratory distress nsyndrome.
Interstitial npulmonary fibrosis .
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Acute athelectasis
Pneumomediastinum from gas trapping and air leak
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Left pneumothorax with depressed diaphragm and minimal mediastinal shift nbecause of noncompliant lungs
This radiograph shows pneumothorax and pulmonary interstitial emphysema othe right side.
THE nGENERAL GUIDELINES FOR TREATING PNEUMONIA
Studies are indicating that many npatients are hospitalized unnecessarily for pneumonia and those that are could nbe released sooner. One study, for example, estimated that one-third of npatients who are now routinely hospitalized for pneumonia could be treated nsafely at home, and another 20% could be released from the hospital with only a nshort period of observation. A number of strategies are being devised to ndetermine when and which patients can be safely discharged.
Categorizing Severity
Ruling out the Least Severe Cases. The procedure for deciding on hospitalization or not starts by ruling out patients nin the lowest risk groups (class 1 and 2), who can be discharged with noutpatient care only. This can often be done with a simple physical nexamination, which can often rule out a severe condition. Patients in low-risk categories have the following characteristics:
No other major illnesses are present.
No serious symptoms are present (eg, altered mental state, rapid pulse or nbreathing rate, very low blood pressure, very high fever).
As examples, the following chioldren with signs of pneumonia should be hospitalized, class 1 categories:
Any infant under a month.
Child with severe psychiatric nconditions.
children with abnormal heart rhythms.
children who are vomiting heavily.
Children who are dehydrated.
Determining nThe Next Levels of Severity. If a patient ncannot be categorized in class I, the next step is to determine which of the nother four higher classes the patient fits. This step involves assigning points nto other findings, including the following:
Laboratory test results.
X-ray findings.
Demographics (ie, boy or girl, nursing home patient).
The essential form of treatment is the use of effective antibiotics. nUnfortunately, many hospital germs are resistant to many of the commonly used nantibiotics. In such cases the mortality rate may be as high as 40 per cent.
As well as intensive antibiotic treatment, good nursing, inhaled oxygen to nraise oxygen blood levels and fluids by transfusion, other supportive measures nmay be essential. Patients who recover from lobar pneumonia often do so suddenly. n
Treatment
Supportive:
ü oxygen to maintain SaO2 95%
ü IV fluids if necessary
ü clinical and radiological monitoring.
ü Antibiotics:
ü should be used if bacterial infection suspected or child unwell
ü young children — ampicillin ± flucloxacillin (Staph suspected)
ü older children — penicillin or ampicillin
ü cefotaxime should be reserved for children who are severely ill, responding npoorly or at risk.
Complications:
Pleural effusion
Early diagnostic and therapeutic aspiration (ideally under ultrasound control) n
Large bore intercostal catheter for large effusions or if fluid n”thick”
Surgical decortication is rarely necessary if early drainage and nappropriate antibiotic therapy is used.
Pneumatoceles
Generally conservative
Drainage for npneumothorax or decompression occasionally needed.
The ntreatments include:
o Give aantibiotic.
o Advise the nmother to give homecare.
o Treatfever.
o nTreatwheezing.
Refer to the nfold-out chart and find the heading, “Treatmentinstructions”. Then look at nthe boxes underneath this heading,and find the box that matches each of the nfour treatments listedabove. Use these boxes when treating a child with a nrespiratoryinfection.
Give aantibiotic
WHO recommends treating pneumonia by giving one of the following antibiotics for 5 days:
– co-trimoxazole
– amoxycillin,(in tablet or syrup form)
– ampicillin, or
– procainepenicillin (by daily intramuscular injection).
You need to learn how to give only the antibiotic(s) used in your health centre. The instructions presented here are nfor giving anoral antibiotic.
If the child ncannot take an oral antibiotic (e.g. if the child is unable to drink or will not wake up), however, you nwill need to give a parenteral antibiotic, such as procaine penicillin. If you are unable to give parenteral antibiotics, refer nthe child as quickly as possible without giving the first dose.
Cautions about giving an antibiotic:
o Do not give co-trimoxazole to a baby with jaundice, or to a npremature baby less than one month old.
o Do not give amoxycillin, ampicillin, procaine penicillin, nbenzathinepenicillin or phenoxymethylpenicillin if the child has a history of breathing problems or anaphylaxis (allergic nreaction) afte rtreatment with penicillin.
Treat nfever
Fever is common in acute respiratory infections. The method of treating fever in a child aged 2 months up to 5 nyears will depend on whether the fever is high or low If the fever is high(39″C nor more):
o The child will feel better and eat better if the fever is lowered with paracetamol.It is harder nfor a child with pneumonia to breathe when he or she has a high fever.
Tell the mother to give the child paracetamol every 6 hours in the appropriate dosage until the child’s ntemperature drops below39″. Give the mother enough paracetamol for 2 days.
If the fever is low(38 39″C):
o Advise the mother to give the child more fluids than usual. Paracetamol is not needed.
Tell the mother to keep the child with any fever(38″C or more) lightly nclothed. She should not overwrap or overdress the child, since this will make him or her uncomfortable and may make the fever worse.
Children aged 2 months up to 5 years should not be given antibiotics if they have fever alone. However, fever is a danger sigin young infants, so young infants with fever should be given a first dose of antibiotic and referred to a hospital. They nshould not be given paracetamol for fever.
Treat nwheezing
Children with a first episode of wheezing
Use a bronchodilator to treat children with a first episode of wheezing. A bronchodilator is a drug that helps children with wheezing to breathe more neasily by opening the air passages of their lungs and relaxing the bronchospasm.
Before giving the bronchodilator, look to see if the child is in respiratory distress. Signs of respiratory distress nare:
– the child is uncomfortable,
– the child is obviously not getting enough air into the lungs,
– the child may have difficulty feeding or talking.
This condition can usually be recognized by simple observation.However, nmost children who wheeze are not in respiratory distress. They are alert and are getting enough air ninto their lungs.
If the child is in respiratory distress, give a rapid-acting bronchodilator and refer the child nimmediately to a hospital. The bronchodilator should be given in rapid-acting form so that the child begins to breathe more easily nbefore he or she is referred. If you are unable to administer a rapid-acting bronchodilator,give nthe first dose of an oral bronchodilator (see below), and refer the child immediately to a hospital.
If the child is not in respiratory distress, give an oral bronchodilator (preferably salbutamol) in the nappropriate and show the mother how to give it.
If the child will be referred for other reasons (e.g. danger signs or chest indrawing), give a single dose of noral salbutamol.If there is no other reason for referral, treat the child based on other signs you see (e.g. fast breathing or nfever) and givethe mother enough salbutamol for 5 days of treatment. Tell her nto give it three ntimes daily.
If a child with recurrent wheezing also has adanger sign, you should nremember that this child needs urgent referral to a hospital.Since the assessment process for recurrent nwheezing requiresadditional time, it may cause an unacceptable delay ireferral.You will learn with clinical experience which children with recurrent wheezing and a danger sign should be nfurther assessed with a rapid-acting bronchodilator, and which should be referred without any further assessment.
However, most children with recurrent wheezing have asthma. They may come often to the health centre with wheezing. nYou will cometo recognize these children and treat them promptly with nabronchodilator.
Drug Category: Analgesic and antipyretic agents n– Used to control fever, myalgias, and arthralgias.
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Drug Name |
Acetaminophen (Tylenol, Aspirin-Free Anacin, Feverall) — Treatment of choice for pain in patients who are unable to take aspirin or NSAIDs. |
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Adult Dose |
625-1000 mg PO q4h |
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Pediatric Dose |
<-15 mg/kg |
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Contraindications |
Documented hypersensitivity; G-6-PD deficiency |
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Interactions |
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity |
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Precautions |
Hepatotoxicity in patients with chronic alcoholism; severe or recurrent pain or high or continued fever may indicate serious illness |
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Drug Name supportLineBreakNewLine |
Ibuprofen (Ibuprin, Advil, Motrin) — Usual treatment of choice for mild-to-moderate pain if no contraindications exist. Inhibits inflammatory reactions and pain, probably by decreasing activity of cyclooxygenase, which inhibits prostaglandi synthesis. |
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Adult Dose |
400-800 mg PO q4-6h |
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Pediatric Dose |
10 mg/kg PO q6-8h |
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Contraindications |
Documented hypersensitivity; peptic ulcer disease; recent GI tract bleeding or perforation; renal insufficiency; high risk of bleeding |
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Interactions |
May increase PT in patients taking anticoagulants; concentrations and, possibly, toxicity are increased by probenecid; may decrease effects of loop diuretics; may increase serum lithium levels; may increase methotrexate toxicity |
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Precautions |
Monitor PT closely i patients on anticoagulants; caution in patients with congestive heart failure, hypertension, and decreased renal or hepatic function<!–[if !supportMisalignedColumns]–> |
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Drug Category: Bronchodilators — Studies have nfound that bronchodilators relieve symptoms of bronchitis, and they have beefound superior to antibiotics in this setting. However, in these trials, npatient numbers were disappointingly small given how commonly acute bronchitis nis diagnosed.
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Drug Name |
Albuterol sulfate (Proventil, Ventolin) — Beta-adrenergic agonist useful in treatment of epinephrine-refractory bronchospasm; relaxes bronchial smooth muscle by acting on beta2-adrenergic receptors and has little effect on cardiac muscle contractility. |
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Adult Dose |
2 puffs aerosol q4-6h or 2-4 mg |
|
Pediatric Dose |
Oral: |
|
Contraindications |
Documented hypersensitivity |
|
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 |
|
Precautions |
Hyperthyroidism, diabetes mellitus, and cardiovascular disorders |
Drug Category: Antibiotics — Studies have nfocused on healthy individuals or patients with chronic obstructive lung ndisease (COLD). Patients with chronic obstructive pulmonary disease (COPD) or nlimited cardiopulmonary reserve, such as patients with asthma, may experience a nvery limited beneficial effect.
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Drug Name supportLineBreakNewLine |
Erythromycin (EES, E-Mycin, Ery-Tab) — Inhibits RNA-dependent protein synthesis, possibly by stimulating the dissociation of peptidyl tRNA from ribosomes, inhibiting bacterial growth. Used for prophylaxis in patients who are allergic to penicilli undergoing dental, oral, or respiratory tract procedures. |
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Adult Dose |
250-500 mg |
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Pediatric Dose |
30-50 mg/kg/d |
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Contraindications |
Documented hypersensitivity; hepatic impairment |
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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 |
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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 |
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Drug Name Support LineBreakNewLine |
Clarithromycin (Biaxin) — Reversibly binds to P site of 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociatio of peptidyl tRNA from ribosomes, inhibiting bacterial growth. |
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Adult Dose |
250-500 mg PO bid |
|
Pediatric Dose |
7.5 mg/kg PO bid |
|
Contraindications |
Documented hypersensitivity; patients taking pimozide, astemizole, cisapride, or terfenadine |
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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 i 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 |
|
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 |
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Drug Name |
Azithromycin (Zithromax) — Treats mild-to-moderately severe infections caused by susceptible strains of microorganisms; indicated for chlamydial and gonorrheal infections of genital tract. |
|
Adult Dose |
500 mg |
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Pediatric Dose |
12 mg/kg/d |
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Contraindications |
Documented hypersensitivity; hypersensitivity to erythromycin; patients taking pimozide; hepatic impairment; prolonged QTc interval; pneumonia; elderly or debilitated patients |
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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 |
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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 |
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Drug Name |
Amoxicillin-clavulanic acid (Augmentin) — Semisynthetic bactericidal beta-lactam antibiotic that inhibits cell wall synthesis. It contains amoxicillin combined with clavulanate, a beta-lactamase inhibitor. |
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Adult Dose |
250-500 mg PO q8h |
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Pediatric Dose |
< mg/kg/d |
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Contraindications |
Documented hypersensitivity; PKU (contains phenylalanine); penicillin allergy |
|
Interactions |
Coadministration with warfarin or heparin increases risk of bleeding |
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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 |
Drug Category: Antivirals — Influenza nvaccinations offer coverage for influenza A and B, thereby providing greater nprotection from bronchitis in the appropriate populations. However, amantadine nand rimantadine can be useful during epidemics of influenza A. Zaminivir, a new nagent now in clinical trials, may be effective for influenza A and B.
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Drug Name |
Amantadine (Symmetrel) — Prevents penetration of virus into host by inhibiting uncoating of influenza A virus. |
|
Adult Dose |
100 mg |
|
Pediatric Dose |
4.4 mg/kg |
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Contraindications |
Documented hypersensitivity |
|
Interactions |
Drugs with anticholinergic or CNS stimulant activity increase amantadine toxicity; concurrent administration of hydrochlorothiazide plus triamterene with amantadine may increase plasma concentrations of amantadine |
|
Precautions |
Do not discontinue abruptly; caution in liver disease, uncontrolled psychosis, eczematoid dermatitis, seizures, and in patients receiving CNS stimulants; reduce dose in renal disease when treating Parkinson disease |
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Drug Name |
Rimantadine (Flumadine) — Inhibits viral replication of influenza A viruses H1N1, H2N2, and H3N2; prevents penetration of virus into host by inhibiting uncoating of influenza A virus. |
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Adult Dose |
200 mg/d |
|
Pediatric Dose |
<10 years: 5 mg/kg/d |
|
Contraindications |
Documented hypersensitivity |
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Interactions |
Levels reduced by acetaminophen or aspirin; plasma levels increased by cimetidine |
|
Precautions |
Renal or hepatic impairment |
Drug Category: Corticosteroids, ninhaled — Corticosteroids are the most potent anti-inflammatory agents. nInhaled forms are topically active, poorly absorbed, and least likely to cause nadverse effects. No study has shown significant toxicity with inhaled steroid nuse in children at doses less than the equivalent of 400 mcg/d of nbeclomethasone. They are used for long-term control of symptoms and for the nsuppression, control, and reversal of inflammation.
Inhaled forms reduce nthe need for systemic corticosteroids. They block late asthmatic response to nallergens; reduce airway hyperresponsiveness; inhibit cytokine production, nadhesion protein activation, and inflammatory cell migration and activation; nand reverse beta2-receptor down-regulation and subsensitivity (in acute nasthmatic episodes with long-term beta2-agonist use).
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Drug Name |
Beclomethasone (Beclovent, Vanceril) — Inhibits bronchoconstriction mechanisms, causes direct smooth muscle relaxation, and may decrease the number and activity of inflammatory cells, which, in turn, decrease airway hyperresponsiveness. |
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Adult Dose |
Low dose: 168-504 mcg/d (42 mcg/inhalation, 4-12 inhalations q24h) |
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Pediatric Dose |
Low dose: 84-336 mcg/d (42 mcg/inhalation, 2-8 inhalations q24h) |
|
Contraindications |
Documented hypersensitivity |
|
Interactions |
None reported |
|
Precautions |
Inhaled corticosteroids ca cause oral 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 |
Drug Category: Oxygen — Decreases the work of nbreathing, hence, delaying the onset of respiratory muscle fatigue, allowing nother therapies to work.
|
Drug Name |
Humidified oxygen — Administered by nasal cannula, mask, head box, or tent to maintai transcutaneous oxygen saturations >92%. Nasal cannula is preferred because it is effective, minimally intrusive, and allows full access to the child. |
|
Pediatric Dose |
Administer humidified oxyge through a regulator or oxygen mixer at rates of 0.25-5 L/min or up to 60%; higher requirements signal severe disease, leading to subspecialty consultation or referral |
|
Contraindications |
None reported |
|
Interactions |
None reported |
|
Precautions |
Inspired oxyge concentrations between 50% and 100% carry a substantial risk of lung damage; children with chronic lung disease or congenital heart disease may worse with oxygen administration; children with these conditions should have cardiopulmonary monitoring while receiving judicious oxygen administration; chronic lung disease may remove the hypercapnic drive and drive ventilatio with relative hypoxia; oxygen administration can lead to hypoventilation or apnea; right-to-left intracardiac shunts produce excessive pulmonary blood flow; oxygen administration can reduce pulmonary resistance and increase pulmonary blood flow, leading to pulmonary edema |
Drug Category: Bronchodilators — Act by ndecreasing muscle tone in both the small and large airways in the lungs, nthereby increasing ventilation.
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Drug Name |
Racemic epinephrine 2.25% (MicroNefrin, S-2) — Stimulates alpha-, beta1, and beta2-adrenergic receptors which results in bronchodilatation, increased peripheral vascular resistance, hypertension, increased chronotropic cardiac activity, and positive inotropic effects. |
|
Adult Dose |
0.5 mL diluted in 3 mL 0.9% NaCl inhaled via nebulizer over 15 min q1-2h |
|
Pediatric Dose |
Administer as in adults |
|
Contraindications |
Hypertension; tachycardia >200 beats per min; hypokalemia; arrhythmias; myocarditis |
|
Interactions |
Increases toxicity of other beta- and alpha-blocking agents; concomitant use of loop diuretics requires very careful electrolyte monitoring |
|
Precautions |
Monitor HR, ECG, BP, and serum potassium |
Drug Category: Immunoglobulins — Specific nimmunoglobulin products with anti-RSV activity have been developed for the nprophylaxis of high-risk patients against RSV infection.
|
Drug Name |
Palivizumab (Synagis) — Humanized monoclonal antibody directed against the F (fusion) protein of RSV. Given monthly through the RSV season, it has been demonstrated to decrease the chances of RSV hospitalization in premature babies who are at increased risk for severe RSV-related illness. |
|
Pediatric Dose |
15 mg/kg/dose IM q mo through RSV season |
|
Contraindications |
Documented hypersensitivity |
|
Interactions |
None reported |
|
Precautions |
Thrombocytopenia or coagulation disorder, as with any IM injection |
Drug Category: Nucleoside nanalogs — Ribavirin (1-beta-D-ribafuranosyl-1,2,4-triazole-3-carboxamide) nis a synthetic nucleoside analog that resembles guanosine and inosine. It nappears to interfere with the expression of messenger RNA and inhibit viral nprotein synthesis. Ribavirin has a broad spectrum of antiviral activity ivitro, inhibiting replication of RSV, influenza, parainfluenza, adenovirus, nmeasles, Lassa fever, and Hantaan viruses.
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Drug Name!supportLineBreakNewLine |
Ribavirin (Virazole) — Appears to be safe but expensive. Efficiency and effectiveness have not bee demonstrated clearly in large, randomized, placebo-controlled trials. Routine use at this time cannot be recommended. In adults, ribavirin can be used for the treatment of other infections, including hepatitis C. |
|
Adult Dose |
Because symptomatic bronchiolitis from RSV rarely is a problem for adults, no specific dosing is recommended |
|
Pediatric Dose |
20 mg/mL solution using continuous aerosol administration for 12-18 h/d for 3-7 d |
|
Contraindications |
Documented hypersensitivity; pregnancy; women who may become pregnant during drug course |
|
Interactions |
Zidovudine effects are decreased when administered concurrently with ribavirin |
|
Precautions |
Caregivers must not be pregnant; fertile women must wear adequate mask protection to reduce aerosol exposure; may produce considerable bronchial irritation, coughing, and wheezing; administration through mechanical ventilators may produce mechanical dysfunction; only experienced practitioners should attempt administration |
