Respiratory Disorders - Pediatrics

Asthma Symptoms (ppt)

Coughing Wheezing Chest tightness Shortness of Breath **Need to know what led up to these symptoms & why it's important to treat the underlying process (even when stable). Otherwise they will only treat the obvious... Give comparisons they can relate to (IE: dental hygiene)

The Common Cold

Description and Epidemiology: Young children have on average 6-10 URIs/year. Viruses cause most with 50% resulting from infection by the more than 100 serotypes of rhinoviruses. Parainfluenza viruses, respiratory syncytial virus, coronavirus, and human metapneumovirus are also common agents Other agents: adenovirus, enterovirus, influenza viruses, reoviruses, and human bocavirus. Daycare and preschool attendance assoc w/ increased number of common colds in young children and their spread to school-age children in the family. The acquisition of a virus occurs via inoculation of the nose and possibly the conjunctiva. spread through direct inhalation of virus from a sneeze, nasal blowing, or inoculation via fingers from nasal secretions or fomites. Mental stress, lack of sleep, high basal levels of catecholamines, infrequent exercise, smoking, and low vitamin C intake are risk factors for colds in adults Pathophysiology increase in the number of polymorphonuclear leukocytes (PMN) in the nasal submucosa and epithelium. presence of PMN, rather than bacterial colonization, changes the color of nasal mucus, with green mucus due to PMN enzymatic activity and yellow mucus being caused by the simple presence of PMN With rhinovirus there is an increase in bradykinins and albumin in the nasal secretions, but no increase in histamines. Rhinovirus and coronaviruses do not cause destruction of the nasal epithelium, but adenovirus and influenza have a significant destructive effect on the respiratory epithelium. Clinical Findings nasal congestion, cough, rhinorrhea, fever, and pharyngitis History • Gradual onset • *Prominent nasal symptoms of rhinorrhea* (key finding) • Sore throat and dysphagia • Mild cough • Low-grade fever • After a variable period of 1-3 days, nasal secretions are thicker and more purulent, leading to nasal excoriation. Physical Examination • Conjunctiva: Mild injection • Nose: Red nasal mucosa with secretions of varying colors depending on the degree of nasal mucosa destruction and PMN activity • Throat: Mild erythema • Lymph: Anterior cervical lymphadenopathy with freely movable nodes less than 2 cm • Chest: Clear to auscultation and without adventitious sounds Diagnostic Tests throat culture not done if child has predominantly nasal symptoms but complains of throat irritation if in doubt, a rapid strep test followed by a culture if negative should be done. Differential Diagnosis allergic rhinitis, rhinosinusitis, and adenoiditis can be assoc w/ pharyngitis or, when tonsillar involvement is significant, tonsillopharyngitis (tonsillitis). When tonsillar involvement is minor, the term nasopharyngitis is used. the common cold (viral URI) sx: malaise, sneezing, watery nasal discharge, mild sore throat, may have a fever, not ill appearing duration: 0-10 days etiology: adenovirus, rhinovirus, RSV, parainfluenza, enterovirus mgmt: no abx, symptompatic Rx (saline nose drops, increased fluids, for infants: bulb-syringe the nose before meals and bedtime, for older children: humidifier comments: if lasts longer than 10-14 days, consider other diagnosis (rhino sinusitis) acute rhino sinusitis sx: persistent nasal symptoms for more than 10 days with URI, nasal drainage - purulent or declared, cough. acute presentation with high fever, purulent rhinitis duration: 10-30 days etiology: Streptococcus pneumoniae, Moraella catarrhalis, nontypeable Haemophilus influenzae mgmt: amoxicillin, erythromycin; trimethoprim-sulfamethoxazole or amoxicillin-clavulanic acid duration of tx: 10 days comments: by 7 days should be asymptomatic; change abx 48-72 hours after start of treatment if no response subacute rhinosinusitis sx: same as acute rhino sinusitis but persistent for at least 30 days duration: 30-84 days etiology: same as acute, may be beta-lactamase producing mgmt: amoxicillin-clavulanic acid comments: initial acute infection did not clear, need to switch abx chronic/recurrent rhinosinusitis: sx: malaise, easy fatiguability, unilateral or bilateral nasal discharge, postnasal discharge, nasal obstruction if middle turbinate significantly obstructed duration: recurrent >10 to <28 days but sx free for at least 10 days in between bouts chronic >84 days etiology: same as subacute, plus alpha-hemolytic streptococci and Staphylococcus aureus mgmt: amoxicillin-clavulanic, azithromycin, staph coverage duration of tx: 3-6 weeks comments: may need endoscopic sinus surgery chronic rhino sinusitis does not response to prolonged medical management; investigate differential diagnoses or underlying issues (allergic rhinitis) Management supportive care only use of decongestants, antihistamines, and cough medication not indicated for children <4 years old used with caution in children <6 years old. should receive symptomatic relief for fever, pain, and nasal congestion using normal saline and an antipyretic. Fluid intake should be encouraged. Complications self-limiting but can be complicated by otitis media, rhinosinusitis, or tonsillitis.

Nonbacterial and Bacterial Pneumonia

a lower respiratory tract infection with consolidation of the alveolar spaces involving the airways and parenchyma of the lung. can be lobar, interstitial, or bronchopneumonial. Lobar pneumonia: alveolar space that results in consolidation; "typical" pneumonia. Atypical pneumonia describes patterns of consolidation that are not localized. interstitial pneumonia: cellular infiltrates attack the interstitium, which makes up the walls of the alveoli, the alveolar sacs and ducts, and the bronchioles; this type of pneumonia is typical of acute viral infections, but may also be a chronic process. Nonbacterial pneumonia is the most common pulmonary infection in children and adolescents Aside from viruses, this category includes atypical bacterial pneumonia caused by M. pneumoniae, C. pneumoniae, and Chlamydia trachomatis. Respiratory viruses account for 40% of acquired pneumonia Pneumonitis: lung inflammation that may or may not be associated with consolidation. Bacterial pneumonia occurs as a primary infection caused by organisms that spread from the nasopharynx, or as a secondary complication of a viral pneumonia S. pneumoniae is the leading cause of bacterial pneumonia in all age groups except newborns S. pneumoniae causes a lobar pneumonia S. aureus presents with empyema, abscess, and pneumatocele formation Lobar and interstitial pneumonia and bronchiolar and bronchial inflammation can coexist in a child . Description Primary bacterial is less common in childhood than secondary bacterial infection after a viral infection. Viral often involves both the conducting airways and the alveoli. common problem in young children and can result in serious illness in a young infant. The onset of viral is gradual over a 1- to 2-day period of coryza, respiratory congestion, fever, cough, and increasing fretfulness Viral infection affects the lung defenses by altering normal secretions, inhibiting phagocytosis, modifying the normal bacterial flora, and disrupting the epithelial layer. many childhood viruses set the stage for secondary bacterial infection. Children with immunologic problems or chronic illnesses are prone to primary bacterial pneumonia and experience recurrent pneumonias or fail to clear the initial infection completely. Differentiating bacterial from viral pneumonia is important in infants <6 months. Mycoplasma pneumonia, or primary atypical pneumonia, is the most common cause of pneumonia in children >5 years through the young adult years. usually mild and self-limited. Chlamydia pneumonia: transmission of C. trachomatis from the infected genital tract of the mother to the infant. not apparent until the infant is 2 to 19 weeks old. Epidemiology 90% of childhood bacterial pneumonia is caused by S. pneumoniae Pneumococcal pneumonia occurs most commonly in late winter and early spring, after the cycle of viral URIs. Asymptomatic carriers play a more important role in dissemination of disease than do sick contacts. Children <4 years old suffer the highest attack rate. Pneumonia caused by community-acquired MRSA worrisome occurrence especially with influenza infection. S. aureus presents with chills, high and prolonged fever, dyspnea, and pleuritic chest pain M. pneumoniae, an organism without a cell wall, is transmitted from one symptomatic patient to another by droplet spread. incubation period: 2 to 3 weeks, asymptomatic carriage after infection can last for weeks. prenatal screening -> incidence of C. trachomatis infection of the newborn has decreased should be considered in a mother with inadequate or no prenatal care. 50% of infants born to infected mothers acquire this infection, but only 5% to 20% of these infants develop C. trachomatis pneumonia with a typical onset between 1 and 3 months of age. Clinical Findings in Infants and Young Children neonates may have respiratory manifestations without a fever, or fever only with subtle or no physical findings suggestive of pneumonia. History • Initial history of a mild URI for a few days—similar for both bacterial and viral. • *Abrupt high fever with temperatures greater than 103.3° F (39.6° C), chills, cough, and dyspnea suggest bacterial pneumonia.* • restlessness, shaking chills, apprehension, shortness of breath, malaise, and pleuritic chest pain. Irritation of the pleura causes chest pain in children with pneumonia. • History of group B streptococcal or C. trachomatis infection in the mother • Prenatal drug use or lack of prenatal care is a risk factor for serious bacterial infection (SBI) in the neonate. • *Slower onset of respiratory symptoms, cough, wheezing, or stridor with less prominent fever suggests viral pneumonia.* • Bacterial pneumonia is less likely in a wheezing child • With C. trachomatis, the infant is typically afebrile; prior, concurrent, or no history of inclusion conjunctivitis reported. Physical Examination • Nasal flaring, grunting, retractions • Tachypnea generally greater than 60 breaths per minute in infants less than 2 months old, greater than 50 breaths per minute in children 2 to 11 months old, or greater than 40 breaths per minute at rest in children 1 to 5 years old (may be the only clue), tachycardia, air hunger, cyanosis are significant findings • Fine crackles, dullness, diminished breath sounds In bacterial pneumonia: • Splinting the affected side to minimize pleuritic pain or lying on the side in a fetal position helps compensate for decreased air exchange and improves ventilation. • Tachypnea and retractions • Progression to delirium, circumoral cyanosis, and posturing • Other findings can include: Presence of a pleural effusion and signs of congestive heart failure Abdominal distention, downward displacement of the liver or spleen • Nuchal rigidity without meningeal infection from involvement of the right upper lobe • Decreased peripheral perfusion and capillary refill • Lethargy In viral pneumonia • Wheezing • Downward displacement of the liver or spleen In primary atypical bacterial pneumonia (C. trachomatis): • repetitive, staccato cough with tachypnea, cervical adenopathy, crackles, and rarely wheezing • Conjunctivitis Clinical Findings in Children and Adolescents History • Sick contacts at home • Travel history • Inadequate immunization coverage • FB aspiration • Asthma • Environmental exposure • Initial history of URI • History of a *sudden onset of shaking chills, followed by a high fever, cough, chest pain; these symptoms are associated with bacterial pneumonia* • *A prodrome of chills, headache, sore throat, gastrointestinal symptoms, and malaise is often associated with atypical bacterial pneumonia.* Physical Examination • Elevated respiratory rate, accessory muscle use, wheezes or adventitious sounds such as crackles, retractions, tachypnea, decreased tactile and vocal fremitus, diminished breath sounds • Dullness plus fine and crackling rales on the affected side In bacterial pneumonia: • Changes in level of consciousness • Dry, hacking, productive cough (with rust-colored or bloody sputum if expectorated) In primary atypical bacterial pneumonia (M. pneumoniae and C. pneumoniae): • URI symptoms, low-grade fever (temperature less than 102.2° F [39° C]) • Dry cough with scant sputum • Rhinorrhea is not commonly reported nor found • Typically hear minimal changes or harsh breath sounds and rhonchi on auscultation Diagnostic Tests *A chest x-ray should not be routinely performed in children with pneumonia* use of a chest x-ray in a child <5 with a fever greater than 104° F (40° C) and without features of bronchiolitis. Radiographic evidence of pneumonia: abscesses, lobar infiltrates, effusions, or cavities. no other chest x-ray findings are helpful in differentiating bacterial from viral pneumonia Direct fluorescent antibody (DFA) testing of nasopharyngeal washings may help determine the viral agent, but is generally reserved for children needing hospital admission. The WBC count is normal or mildly elevated with a predominance of lymphocytes in viral pneumonia. Infants and children with significant lower respiratory symptoms may require hospitalization and more extensive diagnostic testing. usual findings in a bacterial pneumonia: • WBC count is elevated (greater than 20,000/mm3) with predominant neutrophils. • Arterial blood gases are consistent with hypoxia. • The organism may be found by culture of nasopharyngeal scrapings (not always accurate), tracheal aspirates, blood (10% to 20% of cases are positive), or lung tap fluid. • Radiographs: lobar or segmental consolidation or a round pneumonia with pleural effusion in up to 30% of children. Frontal and lateral films are needed for adequate visualization. Staphylococcal pneumonia involves the right lobe 65% of the time. Pneumatoceles are common in staphylococcal pneumonia • Blood, urine, and CSF cultures should also be obtained in infants <2 months as part of a septic workup. Blood cultures should also be done in older children who are hospitalized and suspected to have bacterial pneumonia Differential Diagnosis bronchiolitis, congestive heart failure, acute bronchiectasis, FB aspiration, pulmonary abscess, parasitic pneumonia, and endotracheal tuberculosis. appendicitis. meningitis. Management Most healthy older children can be managed as outpatients. Neonates must always be admitted to the hospital if diagnosed with pneumonia regardless of infecting pathogen. Young infants may also need hospitalization unless C. trachomatis is suspected. All children require supportive care with antipyretics, hydration, and rest. Antibiotics reserved for suspected bacterial infection only. Serious infections may require hospitalization for respiratory therapy including humidified oxygen, pulmonary therapy, and/or intubation. Criteria for Hospital Admission for Pneumonia: • Tachypnea: >60 breaths/min in infants <2 months; >50 breaths/min in children 2 to 11 months old; or >40 breaths/min at rest in children 1 to 5 years old • Grunting, dyspnea or apnea • Severe respiratory distress • Oxygen saturation less than 92% with the need for supplemental oxygen (pulse oximetry reading or arterial blood gas) • Toxic appearance • Failure to respond to appropriate oral antibiotic • Neonate to 3 months old • Poor oral intake with signs of dehydration • Pulmonary complications noted on radiographs—abscess, empyema, pneumatocele • Social issues at home that indicate parent or caretaker cannot appropriately monitor and/or care for the child • Outpatient antibiotic treatment (5 to 10 days' duration of therapy): Oral antibiotics are considered safe for most children with pneumonia 1-4 months old: May need to admit unless chlamydia suspected: Treat chlamydia with oral azithromycin for 5 days or erythromycin base or ethylsuccinate for 14 days 4 months to 4 years old: Amoxicillin 80 to 100 mg/kg/day, divided every 6 to 8 hours for 10 days Five years and older: Azithromycin 12 mg/kg/day once a day for 5 days (maximum dose 500 mg), amoxicillin 80 to 100 mg/kg/day divided twice a day or three times a day for 10 days or amoxicillin with clavulanic acid with 80 to 90 mg amoxicillin dosage and use the 7:1 dosage form or Augmentin ES 600 mg/5 mL for 10 days. If chlamydia pneumonia or mycoplasma pneumonia is suspected, azithromycin is an appropriate choice. Erythromycin, azithromycin, or clarithromycin is the recommended treatment if M. pneumoniae or C. pneumoniae is suspected. • Inpatient treatment: Neonate: Ampicillin and cefotaxime, ceftriaxone, or gentamicin 1 month to 5 years old: Cefuroxime and add vancomycin if rapid progression of illness Five years and older: Cefotaxime and azithromycin and add vancomycin if rapid progression of illness • The recommended treatment for S. aureus pneumonia is nafcillin, cephazolin, clindamycin (for MRSA) with vancomycin as an alternative. Prognosis By the 2-3 day of treatment, auscultation should reveal a change in respiratory sounds as the infection begins to consolidate. Increased fremitus, tubular breath sounds, and the disappearance of crackles may be noted. Most children have an uneventful recovery inform parents that their child's cough can last for several weeks. Routine rechecks with chest x-rays are not recommended because radiographic findings may take 6 to 8 days to normalize. If pneumonia recurs or persists for >1 month, the child needs further evaluation for underlying disease. Complications Empyema is common in staphylococcal and GABHS infections. Scarring of the airways and lung tissue can cause dilated bronchi, which results in bronchiectasis. Lung abscess can result if the pneumonia causes necrosis of the lung tissue. M. pneumoniae can spread to the blood, CNS, heart, skin, or joints. A child with sickle cell disease and pneumonia caused by M. pneumoniae has more severe pulmonary disease than the average child does. Children with recurrent pneumonias should be referred for further pulmonary evaluation. Prevention Identify and treat pregnant women with C. trachomatis. Universal vaccination against influenza, HIB, and pneumococcal infection is essential. For high-risk neonates monthly injections of humanized monoclonal RSV antibody are essential

Differentiating Various Forms of Pneumonia in Infants, Young Children, and Adolescents a. bacterial pneumonia b. viral pneumonia c. mycoplasma pneumoniae and Chlamydophila pneumoniae d. d. Chlamydia trachomatis

a. common age: all ages onset: acute; gradual clinical findings: depends on age; starts with URI, cough, dyspnea, tachypnea, rales, decreased breath sounds, grunting, retractions, toxic look; potential progression to severe respiratory distress fever: acute onset of fever (>/= 102.2) CBC: WBCs often elevated >15000/microliter organism: 90% caused by Streptococcus pneumoniae Radiographic findings: lobar consolidation Tx: Depends on bacteria and age of child; amoxicillin, penicillin, methicillin, cefuroxime, gentamicin, vancomycin b. common age: all ages onset: acute; gradual clinical findings: depend on age; cough, coryza, hoarseness, crackles, wheezing, stridor fever: present cbc: normal or slight elevation of WBC organism: RSV, parainfluenza, influenza (types A and B) radiographic findings: transient lobar infiltrates treatment: supportive care c. common age: >5 years old onset: slow clinical findings: persistent cough, malaise, headache fever: >102.2 cbc: normal organism: M. pneumoniae, C. pneumoniae Radiographic findings: varies, interstitial infiltrates treatment: erythromycin/clarithromycin d. common age: 2-19 weeks old (typically 1-3 months old) onset: gradual clinical findings: tachypnea, staccato cough, crackles, wheezing rare, 50% have signs or history of conjunctivitis fever: afebrile cbc: eosinophilia in 75% of cases organism: chlamydia trachomatis radiographic findings: hyperinflation, infiltrates tx: erythromycin Neonatal: Common: Cytomegalovirus •Group B streptococci • Gram-negative enteric bacteria • Listeria • Chlamydia trachomatis Uncommon organisms • Streptococcus pneumoniae • Group D streptococcus • Anaerobes Infants Most common • Respiratory syncytial virus • Parainfluenza • Influenza • Adenoviruses • Metapneumovirus Less common • S. pneumoniae • Haemophilus influenzae • Mycoplasma pneumoniae • Mycobacterium tuberculosis • Bordetella pertussis • Pneumocystis jiroveci Preschool children Most common • Respiratory syncytial virus • Parainfluenza • Influenza • Adenoviruses • Metapneumovirus Less common • S. pneumoniae • H. influenzae • M. pneumoniae • M. tuberculosis • C. pneumoniae School-age Respiratory viruses as above in preschool • M. pneumoniae • C. pneumoniae S. pneumoniae • M. tuberculosis

Differentiating Common Respiratory Diseases That Can Cause Stridor or Similar Signs a. acute laryngotracheitis: b. epiglottitis: c, laryngotracheobronchitis: d. diptheria e. foreign body

a. peak age: 3-36 months old onset: gradual, acute onset at night common findings: URI, seal-bark cough, mild to moderate dyspnea, symptoms worse at night respiratory efforts: rate generally <50 fever: common - low grade CBC: generally normal organisms: usually viral: parainfluenza, adenovirus, RSV specific lab tests: none radiographic view with findings: lateral or AP of neck/subglottic narrowing tx: humidification, corticosteroids in selected cases intubation: rare prevention: none b. peak age: 1-5 years onset: rapid common findings: sore throat, dysphagia, anxiety with inspiratory distress without significant stridor, drooling, muffled speech, looks toxic, tripod position respiratory effort: marked distress fever: high (101.8-104) CBC: high, left shift organism: usually Haemophilus influenzae type B (HIB) specific lab test: none radiographic view with findings: lateral of neck/thumb sign tx: hospitalization, cephalosporin, corticosteroids intubation: usually necessary prevention: immunization - HIB c. peak age: 3-36 months old onset: acute common findings: hoarseness with barking cough, inspiratory stridor and toxic presentation with purulent sputum resp efforts: marked distress fever: high 102.2 CBC: high, left shift organisms: usually staphylococcus aureus specific lab tests: none radiographic view with findings: lateral of neck/subglottic narrowing treatment: hospitalization, staphylococcus coverage intubation: frequently necessary prevention: none d. peak age: any age/unimmunized onset: gradual over 1-2 days common findings: membranous nasopharyngitis, obstructive laryngotracheitis with local infection presenting as sore throat, nasal discharge, hoarseness respiratory efforts: minor to significant signs and symptoms of obstruction fever: low grade CBC; normal to slight leukocytosis, decreased thrombocyte count Organism: Corynebacterium diptheriae Specific lab tests: positive culture radiographic view with findings: signs of obstruction in severe cases tx: hospitalization, erythromycin/penicillin, antitoxin intubation: may be necessary prevention: immunization - DTaP e. peak age: toddlers onset: acute sx or gradual onset common findings: coughing and/or choking episode, dyspnea, wheezing, cyanosis, signs and sx of secondary infection respiratory efforts: minor to significant distress fever: normal to low grade CBC: normal unless secondary infection specific labs: none radiographic view with findings: may see localized hyperinflation, mediastinal shift, atelectasis tx: FB removal, treatment of secondary infection or bronchospasm intubation: endoscopy to remove FB prevention: education on child proofing home and monitoring child

Asthma Medications (ppt) a. Quick relievers: Bronchodilators/short acting Beta 2 agonists b. Reliever tx: Oral Steroids c. Controller: Anti-inflammatory medicatons d. controller: Inhaled Steroids e. controller: Leukotriene agonist f. controller: Combination medications

a. relieve symptoms by relaxing muscles around airways Taken as needed Dilates the bronchi and bronchioles, decreasing resistance in the respiratory airway and increasing airflow to the lungs. Most common examples Albuterol (Proventil, Ventolin, ProAir) - available as HFA MDI and in several nebulizer forms pirbuterol (Maxair) - available as breath actuated brand name MDI Levalbuterol (Xopenex) - available as HFA MDI or liquid for nebulization (.31mg, .63mg, 1.25mg) Ipratropium (anticholinergic) Most effective medication for relief of acute bronchospasm (more so than anticholinergics) Effective as a pre exercise medication More than one canister per month suggests inadequate asthma control Regularly scheduled use is not generally recommended May lower effectiveness and increase side effects May increase airway hyper-responsiveness Using >2 canisters per month-risk factor for death b. Reduce airway inflammation & mucus production Examples Prednisone Prelone/Pediapred (prednisilone) Review Side Effects, parenting tips Category: Quick reliever, Rescue medication Use: Acute asthma exacerbations OR Severe persistent asthma ( not common for children) Many parents prefer treating a child's exacerbations with oral steroids instead of using daily controller therapy such as ICS REASONS THAT HAVE BEEN GIVEN BY PARENTS: >Parents say its easier to give a week of oral medication than every day, >Fear of giving their child daily "steroids", however the dosing of course of oral steroids used to treat exacerbations is at a much higher dosage than the total of dose of inhaled steroids used over time mg = mcg1.0 = 1000 Examples of ICS dose: 44mcg, usually BID x 10months= 52,800 mcg/yr Examples of OCS dose: 30mg/day x 5 days =150mg (150,000mcg)/yr Recurrent exacerbations & need for OCS is a red flag for RISK assessment: c. -help reduce swelling in airways -taken daily **LABA can be added in combination Reduces the swelling and mucus in the airways Taken everyday, even when well, as the health care provider ordered (ex: like brushing your teeth) These medicines DO NOT stop an asthma attack once it starts. follow your action plan when an asthma attack starts! d. Gold standard for treating all levels of persistent asthma EX: Flovent, Qvar, Pulmicort Goal standard therapy for any level Approved dosing recommendations 12mth & up Review prescribing information safety data for "off label" information Monitor response, control & adjust dosing Inhalation technique assessment needed Ensure correct devices are used EX: MDI/AC, Neb Side effects: hoarseness and oral thrush Always rinse your mouth with water and spit it out after taking this medication Barriers: fear of using steroids, device training, Council/educate family Inhaled steroids are the best medicine to treat asthma. They help by reducing the swelling and inflammation in your airways. Using these medicines can help you use your rescue medicine less often. Side effects can happen if you don't use a spacer or rinse your mouth (thrush - a fungal infection in your mouth or a hoarse voice) e. Alternative or additive therapy EX: Singulair (Montelukast) Approved 6mths & older for asthma Oral forms= granules, tablet form, chewable vs. swallow tab Generic form reportedly "bitter taste" Side effects: headache, nausea, post marketing: Neuropsychiatric events(bad dreams, mood/behavior changes including suicidal tendencies) reducing the swelling and inflammation in your airways. help you use your rescue medicine less often. comes in a pill and can be used with other medicines. Sometimes it can give you a headache, an upset stomach or bad dreams. f. ICS + LABA EX: Advair, Symbicort, Dullera Two medicines in one device: Inhaled steroid Long acting bronchodilator Always rinse your mouth with water and spit it out after taking this medicine Side effects: hoarseness, oral thrush, headache, monitor for cardiac symptoms Be careful that the medicine does not get wet.

Acute Spasmodic Croup

recurrent episodes of acute LTB. etiologic agents are similar to those in laryngotracheitis occurs in families with a history of croup. presents with minimal coryza and acute onset of nighttime croup in a well child or a child with very mild cold symptoms. no fever, no pharyngitis, and a normal epiglottis. usually milder and of short duration, but symptoms may be recurrent. treatment plan is the same as indicated for acute LTB. tends to respond to exposure to cool air.

Patho Involved in Airway Disease

two major types of airway obstruction are complete and partial. complete obstruction: neither airflow nor drainage of secretions occurs. leads to lobar atelectasis after the residual gas diffuses into the pulmonary circulation. partial airway obstruction: airflow and secretion drainage occur but are impaired. two separate classifications. bypass valve obstruction: narrowing of the lumen; a wheeze may be produced. resistance to flow is increased, air can still flow in during inspiration and out during expiration. check-valve or ball- valve obstruction: air entry is possible, but during expiration the lumen is completely occluded so that escape of air is impossible. Bronchial FBs and emphysema result in overinflation of lung airways. occurs above the level of the secondary bronchi interferes more with inspiration than expiration. complete and above the bifurcation of the trachea, asphyxia and death can result Partial obstruction: severe dyspnea, stridor (a harsh high-pitched inspiratory sound), and subcostal retractions. Coughing removes nonfixed, high airway obstruction. Poor inspiratory airflow limits the coughing effectiveness. The sound produced by coughing may indicate the level of airway obstruction and assists in making a diagnosis. Obstructions next to the larynx: cough that sounds croupy or barking. Obstructions in the trachea or major bronchi: brassy sound. Lower airway obstructions: peripheral lesions, diffuse in location, involve bronchioles smaller than 3 mm. usual mechanism of narrowing is spasm, accumulation of secretions, edema of the mucous membrane, extrinsic compression, or any combination of these factors. Complete airway obstruction -> atelectasis. A large % of lung volume needs to be involved before symptoms become apparent; small atelectatic changes do not produce obvious clinical manifestations. primary clinical manifestation of lower airway obstruction - expiration. Wheezing is the principal sound patients make if the obstruction allows enough air to pass through the narrowed lumen. Chest excursion diminishes, and the expiratory phase prolongs. Increased airway resistance during exhalation results in overinflation of the lungs, increases the anteroposterior diameter of the chest. Chronic overinflation -> "barrel chest" typical of a patient with chronic lung disease (cystic fibrosis (CF) or emphysema). accumulation of fluids and inflammation in the lower airways usually results in a repetitive hacking, ineffectual cough. percussing an overinflated chest elicits hyperresonance. as obstruction increases - body attempts to compensate by using accessory muscles to assist in breathing. Dyspnea can result and may include orthopnea and exercise intolerance. Cyanosis appears as the oxygen saturation drops below 85% and is an ominous sign. Mild obstruction - reduced respiratory rate and increased tidal volume severe obstruction - increased respiratory rate, increased retractions with the use of accessory muscles, anxiety, and cyanosis. Fine crackles or rales - short, crackling sounds heard during inspiration. caused by airways suddenly opening after having been previously closed. The gas pressure between the compartments equalizes and creates the crackling sound. Fluid accumulation in the airways may also result in crackles. Crackles or rales are not cleared by coughing. Restrictive disease is less common in pediatric patients and is characterized by decreased lung compliance with relatively normal flow rates. neuromuscular weakness, lobar pneumonia, pleural effusion or masses, severe pectus excavatum, or abdominal distention. rapid respiratory rate and decreased tidal volume/capacity

Diagnostic Tests

• Monitoring oxygenation by pulse oximetry and blood gases Blood gas studies assess possible respiratory collapse, used in acute care settings. A rising Paco2 is an ominous sign. • chronic or complicated rhinosinusitis imaging in acute rhinosinusitis controversial because uncomplicated URIs can cause abnormalities of the paranasal sinuses radiographs, ultrasonography, magnetic resonance imaging (MRI), and computed tomography (CT) of the sinuses, soft tissues of the neck, and chest. Abnormalities of the nasal mucosa such as thickening may reflect inflammation. Chest radiographs: posteroanterior and lateral positions, lesions may only be seen in one of the two views. Fluoroscopy: evaluation of stridor and abnormal movement of the diaphragm. Contrast studies (barium esophagogram): recurrent pneumonia, persistent cough, tracheal ring, or suspected fistulas. bronchograms (useful in delineating the smaller airways), pulmonary arteriograms (evaluation of the pulmonary vasculature), and radionuclide studies (evaluation of the pulmonary capillary bed). • sweat testing, cultures and blood work • Endoscopy (bronchoscopy and laryngoscopy), bronchoalveolar lavage, percutaneous tap, lung biopsy, and microbiology studies Children who have unusual signs and symptoms that require such procedures should be referred to medical specialists.

Respiratory System: History

• mnemonic PQRST: P = Promoting, preventing, precipitating, palliating factors • Contacts. family members or close contacts (daycare, school) ill with similar signs/symptoms? • Prevention - using any medications to prevent colds (zinc lozenges echinacea and vitamin C are touted in the press as prevention measures, but may have negative side effects in children and adolescents) • Progression. respiratory signs/symptoms increasing in severity, lessening, or same? Is child easily fatigued, less active, having trouble sleeping, or working harder to breathe? • Treatment. over-the-counter or prescription drugs used? other treatment modalities used, folk cures, complementary therapies, or home remedies? Q = Quality or quantity • how severe - symptoms? interfering with school attendance or play? child's ability to sleep and eat? R = Region or radiation • chest pain? S = Severity, setting, simultaneous symptoms or similar illnesses in the past • Key signs and symptoms. daytime or nighttime cough, fever, vomiting, malaise, rhinorrhea, sore throat, lesions in the mouth, retractions, cyanosis, dyspnea, or increased respiratory effort? • Associated symptoms. decrease in appetite or feeding? Any rashes, headaches, or abdominal pain? • Similar illnesses in the past. history of respiratory tract infections, allergies, or asthma? How many? (croup, pneumonia, rhinosinusitis, streptococcal tonsillopharyngitis, frequent colds)? T = Temporal factors • When begin? • onset acute or insidious or proceeded by the common cold? • How long has it lasted? has it changed over time? • Family history. family history of allergies or asthma? family history of immunodeficiency, ear-nose-throat, or respiratory problems? family -genetic diseases such as CF or alpha 1-antitrypsin deficiency? • Review of systems Note any infections, constitutional diseases, or congenital problems that might have a respiratory component. • Environment anyone in family or in daycare setting smoke? Does the child live or attend school in an urban or industrial area subject to air pollution (e.g., near a major highway, industrial plant, or bus terminal)? Key Characteristics of Cough, Common Causes, and Questions to Ask in a Pediatric History Age factor - Infants have a weak, nonproductive cough. Quality - Staccato-like (Chlamydia trachomatis in infants); barking or brassy (croup, tracheomalacia, habit cough); paroxysmal or inspiratory whoop (pertussis or parapertussis); honking (psychogenic). wet or dry? Duration Acute (most infectious, <2 weeks) subacute cough - 2-4 weeks recurrent (assoc w/ allergies and asthma) chronic >4-8 weeks (CF, asthma). continuous or intermittent? Productivity Mucus producing or nonproductive? Timing During the day, night (assoc w/ asthma), or both? Effect on parent and child Are parents frustrated with the cough? Is it causing them to lose sleep and work time? Are they concerned that the child may have something serious? Associated symptoms Fever—may indicate bacterial infection (pneumonia) Rhinorrhea, sneezing, wheezing, atopic dermatitis—assoc w/ asthma and allergic rhinitis Malaise, sneezing, watery nasal discharge, mild sore throat, no or low fever, not ill appearing—typical of URI Tachypnea—pneumonia or bronchiolitis in infants (infants may not have a cough) Exposure to infection or travel Has the child been out of the country (tuberculosis)? Is there a member of the household being treated for "bronchitis" or another cough illness? Causes Congenital anomalies: Tracheoesophageal fistula, vascular ring, laryngeal cleft, vocal cord paralysis, pulmonary malformations, tracheobronchomalacia, congenital heart disease Infectious agent: Viral (RSV, adenovirus, parainfluenza, HIV, metapneumovirus, human bocavirus), bacterial (tuberculosis, pertussis, Streptococcus pneumoniae), fungal, and atypical bacteria (Chlamydia and Mycoplasma) Allergic condition: Allergic rhinitis, asthma Other: FB aspiration, gastroesophageal reflux, psychogenic cough, environmental triggers (air pollution, tobacco smoke, wood smoke, glue sniffing, volatile chemicals), CF, drug induced, tumor, congestive heart failure

Asthma Education (ppt)

2007 NAEEP evidence based guidelines - National Asthma Education and Prevention Program (NAEPP) Coordinating Committee, an Expert Panel was convened by the National Heart, Lung, and Blood Institute (NHLBI) to update the asthma guidelines. The Expert Panel recommends that patients be educated at multiple points of care where health professionals and health educators may interact with patients who have asthma From 2007 NAEEP: Asthma self-management education is essential to provide patients with the skills necessary to control asthma and improve outcomes . Asthma self-management education should be integrated into all aspects of asthma care, and it requires repetition and reinforcement. It should: — Begin at the time of diagnosis and continue through follow-up care (Evidence B). — Involve all members of the health care team (Evidence B). — Introduce the key educational messages by the principal clinician, and negotiate agreements about the goals of treatment, specific medications, and the actions patients will take to reach the agreed-upon goals to control asthma (Evidence B). — Reinforce and expand key messages (e.g., the patient's level of asthma control, inhaler techniques, self-monitoring, and use of a written asthma action plan) by all members of the health care team (Evidence B). — Occur at all points of care where health professionals interact with patients who have asthma, including clinics, medical offices, EDs and hospitals, pharmacies, homes, and community sites (e.g., schools, community centers) KEY EDUCATIONAL MESSAGES: TEACH AND REINFORCE AT EVERY OPPORTUNITY Basic Facts About Asthma The contrast between airways of a person who has and a person who does not have asthma; the role of inflammation. What happens to the airways during an asthma attack. Role of Medications: Understanding the Difference Between: Long-term control medications: prevent symptoms, often by reducing inflammation. Must be taken daily. Do not expect them to give quick relief. Quick-relief medications: SABAs relax airway muscles to provide prompt relief of symptoms. Do not expect them to provide long-term asthma control. Using SABA >2 days a week indicates the need for starting or increasing long term control medications. Patient Skills Taking medications correctly — Inhaler technique (demonstrate to the patient and have the patient return the demonstration). — Use of devices, as prescribed (e.g., valved holding chamber (VHC) or spacer, nebulizer). Identifying and avoiding environmental exposures that worsen the patient's asthma; e.g., allergens, irritants, tobacco smoke. Self-monitoring —Assess level of asthma control. — Monitor symptoms and, if prescribed, PEF measures. —Recognize early signs and symptoms of worsening asthma. Using a written asthma action plan to know when and how to: —Take daily actions to control asthma. —Adjust medication in response to signs of worsening asthma. Seeking medical care as appropriate. Educate patient, families & health care staff, providers & community workers use technology FREE Online Asthma Games/videos, etc: Quest for the Code™ http://www.starlight.org/asthma/ "Lungtropolis" ALA.org "A"is for Asthma Sesame Street video for young children http://www.sesamestreet.org/parents/topicsandactivities/toolkits/asthma

Asthma: Children vs Adults (ppt)

Children present with symptoms of cough ± noisy or rapid breathing, usually before 5 years of age Adults: Present with symptoms of cough, shortness of breath, chest pain, wheezing, often intermittent or nocturnal Please note that this is a generalization - some kids will present with wheeze, for example

Asthma misdiagnosis (ppt)

Children: chronic/wheezy bronchitis, recurrent croup, recurrent upper respiratory infection, recurrent pneumonia Adults: recurrent bronchitis

Periodic Assessmentand Monitoring - Asthma (ppt)

Clinical assessments every 1 to 6 months, based on asthma severity and patient/family ability to manage asthma Asthma symptoms and severity change, requiring adjustments in therapy Revise AAP

Case #2 (ppt)

Derrick is a 14 yo male with long standing unstable asthma. This is his first visit & he states "none of the medicines work..I have about 4 different kinds....even my asthma puffer isn't helping me when I need it" What might be the problems to consider, what might you change for him?

Anti-IgE Therapy/Immunomodulator: Omalizumab (ppt)

-XOLAIR -multicenter, randomized, DBPCT, phase III -reduces asthma exacerbations, ED visits and hospitalization rates -Adjunctive tx in poorly controlled asthmatics and pt in need of IT but unable to tolerate due to severity of asthma Qualifying for tx: Documented allergy to perennial allergen Serum total IgE 30-700 asthma ages 12+ Subcutaneous injection 150mg/1.2mL following reconstitution with 1.4mL sterile water for injection 150-375 mg SC q 2-4 weeks depending on body weight and pretreatment serum IgE level Do not adminster more than 150mg per injeciton site Monitor for anaphylaxis for 2 hours following at least the first 3 injections

Asthma Predictive Index (ppt)

1 Major Criterion Parental history of asthma Physician-diagnosed atopic dermatitis Allergic sensitization to≥1 aeroallergen* (*House dust mite, cockroach, dog, cat, mold, grass, tree, and weed.) OR 2 Minor Criteria Wheezing unrelated to colds Blood eosinophils ≥4% Allergic sensitization tomilk, eggs, or peanuts Key point: Physicians know the challenge of making a diagnosis of asthma in preschool children who wheeze. The modified Asthma Predictive Index (mAPI) is a tool that provides clinical indicators to define the risk of asthma in children who wheeze. These children may be considered for the diagnosis of asthma and as candidates for long-term controller medication The Asthma Predictive Index (API) was originally developed by Castro-Rodríguez et al, based on data from the TCRS1 A stringent index requires frequent wheezing (score of ≥3 on a scale from 1 "very rarely" to 5 "on most days") in the first 3 years of life plus 1 of 2 major criteria or 2 of 3 minor criteria A loose index for the prediction of asthma requires any wheezing during the first 3 years of life plus 1 of 2 major criteria, or 2 of 3 minor criteria Children with a positive loose index were up to 5.5 times more likely to have active asthma between 6 and 13 years of age, compared with children with a negative loose index. Children with a positive stringent index were up to 9.8 times more likely to have active asthma between 6 and 13 years of age, compared with those with a negative stringent index1 More than 95% of children with a negative stringent index never had active asthma between 6 and 13 years of age The PEAK criteria for an mAPI were later adapted from the TCRS's original version and are more specific A positive index requires a frequency of >3 episodes of wheezing with at least 1 physician-diagnosed episode plus 1 of 3 major criteria or 2 of 3 minor criteria

Factors that Exacerbate Asthma (ppt)

Allergens Respiratory infections Exercise and hyperventilation Weather changes Sulfur dioxide Food, additives, drugs Specific things a child may react to which can cause an asthma episode asthma trigger control plan: Ask parents to identify child's triggers Ask parents what steps the child's doctor suggests to avoid triggers Develop a plan to eliminate or avoid most significant triggers Discuss effort with parents @ each visit Offer resources EPA ,ALA, AAAAI, AAFA,CDC,NIH etc Online For kids: http://pbskids.org/arthur/games/lungdefender/asthma.html

A Family Guide to Asthma (ppt)

Asthma coalition of long island - www.asthmacoalitionoflongisland.com Tobacco action coalition: www.breathefreely.org For help trying to quit smoking: Call 1-866-NY-QUITS - smoking is the largest contributor to lung disease and other serious disease. Talk with your provider about ways to stop smoking Asthma coalition of long island - misison is to reduce the burdens of asthma by assisting every child with asthma to achieve optimal control and by improving the quality of life for children, their families and the community Things to ask your doctor or nurse: May I have an asthma action plan which tells me what to do when I am feeling well or feeling bad from asthma? What medicine should I have in school for treating asthma attacks? Should I see an asthma specialist? What triggers my asthma? How do I take my medicine? What problems can I have with my medicine? How do I get a spacer, peak flow meter or nebulizer? When should I get my flu shot? When should I have a breathing test? How do I know if my asthma is in control? What happens ? What is asthma? What is an airway? What are asthma triggers and how can you avoid them? Dust - use a pillow and mattress covers, wash sheets and blankets weekly in hot water, REMOVE rugs, vacuum with a HEPA filter, no stuffed toys in the bedroom Cockroaces - take garbage out EVERY DAY, keep food areas clean and dry Mold - air out wet places, use dehumidifiers in damp places, fix leaks, stay away from wet leaves Animal dander - no pets in the bedroom, avoid feathers in pillows, comforters and clothes Smoke OR irritants - no smoking home or car, DO NOT use a wood-burning stove, kerosene heater, or fireplace, stay away from strong odors and sprays Did you know secondhand smoke makes asthma WORSE. Children who live with smokers are more likely to have asthma, pneumonia, bronchitis, and ear infections Kinds of Asthma Medicines: Rescure medicine: albuterol, proventil, pro-air, zopenex, or ventolin Use during asthma epsiodes before you exercise Helps to relax airway muscles Controller Medicine Advair, flovent, pulmicort, singulair, symbicort Take daily Reduces airway swelling Ways to make your school asthma friendly: Your school nurse has learned about School Nurse asthma Management -TEACHERS and STAFF learned about asthma -steps have been taken to REDUCE asthma trigers in the classrooms -students with asthma have taken part in Open Airways for Schools -School buses DO NOT run their engines while waiting for students -There is a Tobacco Free Schools Policy Need help making your school asthma friendly? Call the Asthma Coalition of Long Island

Population Disparities in Asthma (ppt)

Current asthma prevalence is higher among Children than adults Females than males Asthma morbidity and mortality is higher among African Americans than Caucasians Low-income populations, minorities, and children living in inner cities experience more ED visits, hospitalizations, and deaths due to asthma than the general population. affects all age groups, most often starts in childhood, affecting more boys than girls. by adulthood, more women than men have asthma. African Americans are more likely than Caucasians to be hospitalized for an asthma attack and to die from asthma. Extrinsic factors associated with high prevalence, morbidity, and mortality include poverty, urban air quality, indoor allergens, and inadequate disease management Number of Long Island Children With Asthma  Ages 0-18* Nassau County ....... 28,408 Suffolk County ........ 33,752 Total 62,160 *Total Population under 18: 671,400 Based on CDC US rate of: 9.3% On average, 3 children in a classroom of 30 are likely to have asthma

Pectus Deformity

Description Pectus excavatum, or funnel chest, - most common congenital deformity of the anterior chest wall and results in sternal concavity Midline narrowing of the thoracic cavity and restriction in chest wall movement are characteristic with an increase in the effect during childhood and adolescence. -> decreased filling of the right heart chamber, lowering cardiac output and a decreased exercise tolerance. Pectus carinatum is much less common. It also progresses during puberty. there is a bowing out of the sternum (also called "pigeon chest"). cosmetically unattractive, fewer complaints about shortness of breath, chest pain, or dyspnea. can lead to psychological distress for the child. Epidemiology if upper airway obstruction -> higher incidence of pectus excavatum many children with this defect are identified at birth or within the first year of life and have no underlying pulmonary problem. The cause in these instances is unknown. Chest wall deformities are found in 66% of patients with Marfan syndrome Clinical Findings History depression (excavatum) or bowing out (carinatum) of the sternum. Fatigue, shortness of breath, decreased exercise tolerance, or chest pain Depression - changes in self-image. Physical Examination • Posterior depression of the sternum and costal cartilage (in pectus excavatum) • Anterior bowing of the sternum (carinatum) Diagnostic Tests • Chest radiography • Exercise testing if substantial pectus excavatum deformity is present • Other cardiac (echocardiogram) and pulmonary function studies as suggested by the degree of excavatum deformity and symptomatology Management If excavatum is the result of pulmonary disease, early treatment of the underlying pulmonary problem occasionally resolves the skeletal deformity. Surgical repair depends on the severity of the defect, demonstration of a decrease in pulmonary function, progression of the defect on serial radiographs, or wish for cosmetic repair. If male with an associated scoliosis or has severe pectus carinatum or excavatum, evaluate for Marfan syndrome. Surgery for children with pectus carinatum is usually for cosmetic purposes. Complications Pectus excavatum can also affect cardiac and pulmonary function.

Viral Pharyngitis, Tonsillitis, and Tonsillopharyngitis

Description Pharyngitis: an inflammation of the mucosa lining the structures of the throat including the tonsils, pharynx, uvula, soft palate, and nasopharynx. generally acute and involves an inflammatory response including erythema, exudate, or ulceration. etiology include a number of viruses and bacteria. If nasal symptoms, it is called nasopharyngitis if no nasal symptoms, the disease is called pharyngitis or tonsillopharyngitis. Most caused by viruses Adenovirus - most common cause of nasopharyngitis Other viruses include Epstein-Barr virus (EBV), herpes simplex virus (HSV), cytomegalovirus (CMV), enterovirus, influenza virus, parainfluenza, and human immunodeficiency virus (HIV). viral organisms generally present with upper nasal symptoms. Epidemiology Adenoviruses are more likely to cause pharyngitis as a prominent symptom. Other viruses (e.g., rhinovirus) are associated with pharyngitis as a minor symptom and rhinorrhea or cough as predominant features. The enterovirus (coxsackievirus, echovirus), herpesvirus, and EBV are also common. occur year-round, but peak seasonally. hoarseness, cough, coryza, conjunctivitis, diarrhea, enanthems (rash (small spots) on the mucous membranes), and exanthems (rash on body) are classic features of a viral infection often spread to siblings and classmates via close contact Clinical Findings History • Pain • Myalgia and arthralgia • Fever • Sore throat and dysphagia Physical Examination • Reactive lymphadenopathy • EBV - exudate on the tonsils, soft palate petechiae, and diffuse adenopathy. • Adenovirus - follicular pattern on the pharynx • Enterovirus - vesicles or ulcers on the tonsillar pillars and posterior fauces; coryza, vomiting, or diarrhea may be present. • Herpesvirus - ulcers anteriorly and marked adenopathy. • Parainfluenza and respiratory syncytial virus (RSV) - lower respiratory tract disease (e.g., croup, pneumonia, and bronchiolitis) with stridor, rales, or wheezing. • Influenza - more systemic complaints. Diagnostic Tests If in doubt, a rapid strep test or a culture should be done. If infectious mononucleosis is suspected in a child, a CBC can identify lymphocytosis and atypical lymphocytes. heterophile antibody testing can be helpful in school- age children and adolescents but may yield a false negative in preschool and younger children and during the first weeks of infection. Epstein-Barr antibody titers to early antigen, EBV IgM, EBV IgG, as well as long-term antibodies (Epstein-Barr nuclear antigen [EBNA]) need to be done to confirm the diagnosis if the results of the tests are not diagnostic. Management only supportive care is needed, including fever and sore throat pain relief with acetaminophen or ibuprofen. Fluid intake should be encouraged.

Foreign Body Aspiration a. Laryngeal Foreign Body b. Tracheal Foreign Body c. Bronchial Foreign Body

Description The cough reflex protects the lower airways, and most aspirated material is immediately expelled with coughing. Onset of a sudden episode of coughing without a prodrome or signs of respiratory infection -> this. Epidemiology Objects that are either too large to be eliminated by the mucociliary system or cannot be expelled by coughing eventually lead to some form of respiratory symptomatology. a large FB occluding the upper airway can cause suffocation. A small object in the lower respiratory tree may airway can cause suffocation. may not produce symptoms for days to weeks. Obstruction results from either the FB itself or edema associated with its presence. Hot dogs are one of the most common causes of fatal aspiration. Toddlers common but can occur in all ages. a. Clinical Findings History rapid onset of hoarseness and the development of a chronic croupy cough with aphonia are reported. Be suspicious of a prior FB aspiration in children with cough, unilateral wheezing, and recurrent pneumonia. Physical Examination hemoptysis, dyspnea, wheezing, and cyanosis. Diagnostic Tests expiratory or lateral decubitus chest radiographs should be ordered. most FBs are not radiopaque, radiographs may not be useful in the diagnosis. if a chest radiograph does not reveal an FB but shows local emphysema—an area that does not inflate or deflate—suspect FB aspiration If the history suggests FB aspiration, bronchoscopy must be undertaken. Direct laryngoscopy might reveal the presence of foreign matter. b. brassy cough, hoarseness, dyspnea, and possibly cyanosis. *homophonic wheeze and the audible slap and palpable thud sound* produced by the momentary expiratory effect of the FB at the subglottic level. c. similar to those seen in either tracheal or laryngeal FB aspiration. Blood-streaked sputum may be expectorated. metallic object - "metallic taste" in their mouths. If object is nonobstructive and nonirritating, few or no initial symptoms may be seen. A small object can act as a bypass valve, and homophonic wheezes can be heard; emphysema or atelectasis can develop as the result of a large obstruction caused by a bronchial FB. limited chest expansion, decreased vocal fremitus, atelectasis, or emphysema-like changes with resulting hyporesonance or hyperresonance. Diminished breath sounds Crackles, rhonchi, and wheezes can be present if air movement is adequate. Most objects are aspirated into the right lung. history may reveal forgotten episode of choking. Clinical Findings History initial episode of coughing, gagging, and choking some objects are inhaled with no choking (e.g., a spear of grass). Hemoptysis rarely occurs as an early symptom, but on rare occasions does occur as an initial symptom months or years after the aspiration event took place. Physical Examination If acute episode is missed or not appreciated, a latent period of mild "wheezing" or cough may be seen. Lobar pneumonia, intractable wheezing, and status asthmaticus can develop. Diagnostic Tests Inspiratory and forced expiratory chest radiographs and chest fluoroscopy are useful in identifying radiolucent FBs Management referred to a pulmonary specialist for bronchoscopy. If object is removed via bronchoscopy before permanent damage occurs, recovery is usually complete. Secondary lung infections and bronchospasms should be treated as suggested Complications If FB is vegetable matter, vegetal or arachidic bronchitis can occur - sepsis-like fever, dyspnea, and cough. If material has been there for a long time, suppuration can occur.

Nasal Foreign Body

Description Young children can be noted immediately by the parent or lie undetected until classic symptoms appear. Clinical Findings History A persistent or recurrent unilateral purulent nasal discharge is reported. Foul odor, epistaxis, nasal obstruction, and mouth breathing are less commonly reported symptoms Young children will often deny inserting a foreign body. Physical Examination *The classic symptom of a nasal foreign body is unilateral, purulent, foul- smelling nasal discharge.* If the foreign body is embedded in granulation tissue or mucosa, it may take on the appearance of a nasal mass. Differential Diagnosis Nasal polyps, purulent rhinitis, adenoiditis, rhinosinusitis, and nasal tumors Management • Removal of the nasal FB, depending on its location, its composition, and the skill of the practitioner. Alligator forceps, suction with narrow tips, and cotton-tipped applicators with collodion with or without topical vasoconstrictor drugs (to reduce swelling) can be used. Other techniques include using a hook or curette to roll the object out. A 5-French catheter with a balloon can be advanced past the FB; inflate the balloon before removing the catheter and (it is hoped) the object with it. • Good lighting (use a headlight) is essential, as is immobilization of the young child via papoose board. • Elevation of the child's head and suctioning of blood and secretions • Otolaryngology referral is merited for young children who cannot cooperate or when the FB is extremely difficult or dangerous to remove, such as paper clips or staples. FB can be forced deeper into the nose if the practitioner is inexperienced at nasal FB removal.

Cystic Fibrosis

Description a multisystem genetic disorder manifested by chronic obstructive pulmonary disease (COPD), gastrointestinal disturbances, and exocrine dysfunction. life expectancy: 37.4 years Epidemiology 1 in 3000 Caucasian births. 1 in 15,000 to 20,000 African-American, 1 in 4000 to 10,000 Hispanic, and 1 in 350,000 Japanese births autosomal recessive genetic disorder involves mutation of the CF transmembrane conductance regulator protein (CFTR), which is expressed in epithelial cells and blood cells. The gene is on chromosome 7, but more than 1500 CFTR mutations have been identified CFTR functions in sodium transport through the epithelial sodium channel, regulates the ATP channels, and is involved in bicarbonate chloride exchange. The CFTR gene defect causes defective ion transport, airway surface liquid depletion, and defective mucociliary clearance The CFTR mutations can be grouped into five classes. Understanding the type of mutation helps direct the type of therapy and has taken on new importance in targeted CF treatment. The most common defect, found in 66% of cases, is a deletion of phenylalanine in position 508 (D508) Polymorphism in non-CFTR genes may explain the difference in the manifestations of the genetic change within different families. mucus obstruction that results causes inflammation and infection. failure to conduct ions across the epithelial cell membranes leads to problems in the lungs, biliary tree, pancreas, intestines, vas deferens, and sweat glands. This results in mucus thickening and target organ damage in the lungs and exocrine glands. In the lung, there is airway depletion, which leads to ciliary collapse and decreased mucociliary transport. the mucous obstruction causes chronic inflammation and infection, and bacterial colonization in trapped mucous secretions Clinical Findings multisystemic progressive illness with varying levels of severity. • Pulmonary. major cause of severe chronic lung disease in children. The lungs are normal at birth but become inflamed with chronic airway infection within a short time following birth. The respiratory epithelium exhibits marked impermeability to chloride and excessive sodium reabsorption. Mucus is viscous, and dehydration of the airway secretions occurs leading to dysfunctional mucociliary transport, airway obstruction, and chronic infections. chronic, dry, frequent cough and sputum production to respiratory failure. Bronchitis, bronchiolitis, bronchiectasis, and pneumonia occur frequently. Bronchospasm resembling acute or chronic asthma may be present. The airways become colonized with S. aureus, H. influenzae, and P. aeruginosa. Burkholderia cepacia is a slower-growing organism found in children with CF. Infection is found in infancy. Pulmonary disease becomes progressive and leads to cor pulmonale, respiratory failure, and death by adulthood. recurrent acute rhinosinusitis, nasal polyps, and allergic bronchopulmonary aspergillosis (ABPA) which starts by childhood and continues into adulthood. Digital clubbing is common. • Gastrointestinal tract and nutrition. During infancy, meconium ileus, pancreatic insufficiency, and rectal prolapse can be manifestations. Meconium ileus develops in up to 15% of newborns born with CF. A meconium ileus syndrome equivalent can also develop in older patients, with desiccated fecal material causing gastrointestinal obstruction. 85% percent of affected children have failure to thrive because of pancreatic enzyme insufficiency. Edema with hypoproteinemia may also be present. thick fat-laden stools (steatorrhea), poor muscle mass, and delayed maturation. Infants with CF who are fed soy-based formulas do very poorly, and severe hypoproteinemia and anasarca quickly result. During childhood, intussusception, hepatitic steatosis, biliary fibrosis, and rectal prolapse can occur. Clinically apparent cirrhosis occurs in 15% of patients with subsequent risk of portal hypertension. Adenocarcinoma of the digestive tract can occur. volvulus, duodenal inflammation, gastroesophageal reflux, bile reflux, fibrosing colonopathy, and poor fat absorption that leads to vitamin A, K, E, and D deficiencies with resulting anemia, neuropathy, night blindness, osteoporosis, and bleeding disorders. • Hepatobiliary tract. Biliary cirrhosis occurs in 2% to 3% of children, jaundice, ascites, hematemesis from esophageal varices, and splenomegaly. Hepatic steatosis. Adolescent patients - biliary colic and cholelithiasis. • Endocrine. Recurrent acute pancreatitis. Cystic fibrosis-related diabetes mellitus (CFRD) with relative insulin deficiency develops as the patient ages due to autolysis of the pancreas as the pancreas body becomes fatty. need annual blood glucose screening because by adulthood up to 30% of patients develop CFRD • Musculoskeletal. Vitamin D deficiency -> osteoporosis when bone reabsorption exceeds bone formation. • Reproductive. delayed sexual development. vas deferens is nonfunctional and atrophied due to CFTR dysfunction, leading to azoospermia and male sterility. incidence of inguinal hernia, hydrocele, and undescended testes is also high. Females - secondary amenorrhea, cervicitis, and decreased fertility. A pregnancy is usually carried to term if pulmonary function is not severely compromised. • Sweat glands. Excessive salt loss can lead to hypochloremic alkalosis, especially in warm weather or after gastroenteritis. often taste salty because of elevated amounts of sodium chloride (NaCl) lost in endogenous sweat. Dehydration and heat exhaustion are concerns. Clinical Manifestations of Cystic Fibrosis: From Neonatal Period to Adolescence Neonatal period: Meconium ileus, Prolonged jaundice, Intestinal atresia Infancy: Cough Colonization with bacteria in mucus Bacterial pneumonia Failure to thrive Hypoproteinemia Abdominal distention Cholestasis Rectal prolapse Steatorrhea Distal intestinal obstruction syndrome (DIOS) Hemolytic anemia Childhood Polyps Steatorrhea Rectal prolapse DIOS Idiopathic pancreatitis Liver disease Adolescence Allergic bronchopulmonary aspergillosis Chronic pansinusitis Nasal polyposis Bronchiectasis Hemoptysis Idiopathic pancreatitis Osteoporosis Diagnostic Tests Patients must have one or more of the clinical features: chronic sinopulmonary disease, gastrointestinal and nutritional abnormalities, salt loss syndrome, chronic metabolic alkalosis or male urogenital abnormalities resulting in obstructive azoospermia one or more laboratory findings that indicate a CFTR abnormality must be present. The results of the sweat test are determined differently depending on age. • The concentration of sweat chloride is greater than 60 mmol/L. • The concentration of sweat chloride is in the intermediate range of 30 to 59 mmol/L for infants <6 months or in the range of 40 to 59 mmol/L for older individuals. • The child has two disease-causing CFTR mutations Sodium chloride concentration goes up with age but a concentration greater than 66 mmol/L is still a diagnostic level. A result of greater than 60 mEq/L of chloride on two specimens is in the diagnostic range for CF. Children with hypoproteinemia may elicit false- negative sweat test results. The second test is genetic analysis for the CFTR mutation. a test that looks for the 40 most common disease-causing mutations that occur in 90% of the CF population is done first. Full sequence analysis will detect most mutations. Prenatal diagnosis has >90% sensitivity for detecting a CF gene mutation on the long arm of chromosome 7. Newborn screening looks for immunoreactive trypsin (IRT) in the blood spot taken at birth. A very high IRT needs to be repeated in 1-3 weeks; when there is an elevation, a DNA analysis looking for CFTR mutation is done. If patient does not meet the classic criteria, nasal transepithelial potential difference (NPD) can be measured. Glycosylated hemoglobin levels may be elevated in older children because of impaired pancreatic functioning. Pulmonary function tests are used to follow the clinical course. Management complicated treatment regimens and should be monitored by a multidisciplinary team at a CF-accredited center. Pulmonary, nutritional, physical, and pharmacologic (antibiotic and antiinflammatory) therapy and psychological counseling must be individualized for each child at each stage of the illness. Home-based maintenance therapy for pulmonary and nutritional interventions is critical. With pulmonary exacerbations, hospital stays for at least 2 weeks for aggressive pulmonary and antibiotic therapy. Oral antibiotics are used to clear colonization and infection. dornase alfa and inhaled tobramycin have the strongest evidence for use in patients with moderate to severe disease with P. aeruginosa and in mild disease. • Inhaled dornase alfa (recombinant human deoxyribonuclease): Daily dornase selectively cleaves the DNA and reduces the mucus viscosity, which improves airway clearance. • Inhaled tobramycin: 300 mg twice a day in 28-day on-off cycles. Tobramycin is an aminoglycoside that results in bacterial death by inhibiting bacterial protein synthesis by binding to 30S and 50S ribosomal units. • Inhaled hypertonic saline: Use at 4 mL twice a day. It works by drawing water into airways. • Chronic administration of azithromycin: Effective for both its antibiotic and antiinflammatory properties by lowering cytokine production • Ibuprofen: Reduction of inflammation but should begin use before inflammation starts • Inhaled β-agonist Lung transplantation is a viable therapy for selected patients who have terminal lung disease

Diphtheria

Description a rare infection in the U.S. with only five cases reported annually. causes a membranous obstruction of the upper airway, including the trachea. produces a toxin leading to a peripheral neuropathy, myocarditis, and acute tubular necrosis Local infection is associated with a low-grade fever, and gradual onset of symptoms over 1-2 days. can also present as otic, conjunctival, and cutaneous infections. Epidemiology Humans are the only reservoir, and the organism is spread by respiratory droplets as well as contact with skin lesions. fomites can act as a vehicle of transmission, and raw milk and milk products can transmit C. diphtheriae. The bacterium is a gram-positive rod with four biotypes (mitis, intermedius, belfanti, and gravis) that can be toxigenic or nontoxigenic caused by the toxigenic strain of C. diphtheriae or C. ulcerans. The toxigenic strains produce two exotoxins —enzymatically active A domain and binding B domain. The binding B domain promotes entry of A into the cell. Asymptomatic carriers can transmit the organism. The incubation period averages from 2 to 7 days but occasionally can be longer incidence is greater in the fall and the winter but skin infections are more common in the summer. Endemic areas include Africa, Latin America, Asia, and the Middle East. Fully immunized individuals can carry the bacteria asymptomatically and may present with a mild sore throat Clinical Findings mild or asymptomatic in partially or fully immunized individuals and severe if unimmunized. Primary Infection • Low-grade fever • Grayish, adherent pseudomembrane found in either the nasopharynx, pharynx, or trachea • Sore throat, serosanguineous or seropurulent nasal discharge, hoarseness, cough • Cutaneous lesions (nonhealing ulcers with dirty gray membrane or colonization of preexisting dermatoses) infected with diphtheria (seen less often) Toxin Production The ability of a strain of C. diphtheriae to produce toxin is related to bacteriophage infection of the bacterium, not to colony type. • Toxin production is more lethal than the primary infection and can induce the following: Myocarditis and electrocardiographic changes Respiratory compromise Cranial nerve and local neuropathies Peripheral neuritis Diagnostic Tests positive culture of C. diphtheriae. Specimens should be obtained from the nose, throat, any skin lesions, and either beneath the membrane or from a portion of the membrane. a special culture medium is needed, the lab needs to be notified if C. diphtheriae is suspected. Toxigenicity tests are performed if C. diphtheriae is confirmed Culture results take 8 to 48 hours treatment begins when diphtheria is suspected. Do not wait for laboratory confirmation. Results of the CBC may be normal or show a slight leukocytosis and thrombocytopenia. Differential Diagnosis Acute streptococcal pharyngitis and infectious mononucleosis nasal FB or purulent rhinosinusitis epiglottitis, laryngeal diphtheria and viral croup Management require hospitalization. • Antitoxin administration (hyperimmune equine antiserum). A single dose needs to be administered if there is a high index of suspicion prior to a positive culture result Allergic reaction to the serum occurs in 5% to 20%, so a scratch test should be performed prior to administration. Intravenous immunoglobulin has not been approved for use. • Antimicrobial therapy. Erythromycin given orally or parenterally for 14 days or penicillin G for 14 days either IM or IV or penicillin G procaine IM for 14 days. • Supportive care for respiratory, cardiac, and neurologic complications as appropriate • Standard and droplet precautions until two cultures are negative • Immunization after recovery because disease does not necessarily confer immunity • Monitoring and antimicrobial prophylaxis of contacts regardless of immunization status Prevention Universal immunization against diphtheria with regular booster injections is the only effective method of control. Infection can occur in immunized or partially immunized children, but in these individuals the disease severity is greatly diminished. Disease generally occurs in nonimmunized children; the frequency of severe life-threatening complications in this group is high.

Pertussis

Description caused by a gram-negative bacillus, Bordetella pertussis, produces pertussis toxin, adenylate cyclase toxin, dermonecrotic toxin, fimbriae, filamentous hemagglutinin, pertactin, and autotransporters. cause significant damage to host immune function and cause local tissue damage in the respiratory tract. classic cough lasts 6 to 10 weeks, but in 50% of adolescents can last longer than 10 weeks whooping cough because of the high-pitched inspiratory whoop following spasms of coughing. not limited to the very young because it occurs in 72% to 100% of adolescent cases with post-tussive vomiting noted in 50% to 70% of adolescent cases The cough is an attempt to dislodge plugs of necrotic bronchial epithelial tissue and thick mucus. If this disease occurs in unvaccinated infants <1 year old, it is often associated with pneumonia, seizures, and encephalopathy. in older children and vaccinated children is complicated by syncope, sleep disturbances, rib fracture, incontinence, and pneumonia Outbreaks of still occur despite the availability of an effective vaccine. Older children and adults can be the vector because their symptoms are not severe. Transmission occurs via aerosolized droplets; children are most contagious during the catarrhal stage and the first 2 weeks after the cough onset Stages of Pertussis Catarrhal: 1-2 weeks • Upper respiratory infection similar to common cold • Mild cough, coryza, sneezing, and low-grade fever (to 101° F [38.3° C]) Paroxysmal: 2 to 4 weeks • Fever is absent or minimal • Persistent staccato, paroxysmal cough ending with an inspiratory whoop • Vomiting at the end of paroxysmal coughing and whoop • Cyanosis, sweating, prostration, and exhaustion after coughing Convalescent: 3 weeks to 6 months • Symptoms wane over a 6-month period • Waning of paroxysmal coughing episodes Epidemiology either a primary disease or reinfection. six species of Bordetella. most common: B. pertussis and B. parapertussis (B. parapertussis causes a mild pertussis-like illness). B. bronchiseptica infrequently causes respiratory infection and B. holmesii causes bacteremia. The last three bacteria are not affected by the vaccine. Transmission of these gram-negative pleomorphic bacilli is by aerosol droplet from coughing or from close contact with infected individuals. Contaminated droplets are inhaled and adhere to the ciliated epithelium of the nasopharynx. incubation period: 6-21 days. occur in adults, who act as a reservoir for the bacteria. usual source of B. pertussis infection in infants is an unrecognized infection in an adult family member with a cough. The highest incidence of mortality occurs in infants <1 month old Clinical Findings Manifestations vary by age group, stage of disease, immunization status, and the presence of transplacentally acquired antibodies classic illness and an asymptomatic infection (in patients who are vaccinated or as a primary illness in those who are not vaccinated) Specific findings in infants <6 months old are generally severe, particularly in neonates, and include: • Apnea (common) often with seizures caused by hypoxemia • No inspiratory whoop • Severe pneumonia and pulmonary hypertension, which are common Findings in older children include: • Persistent, irritating, nonproductive cough that may last for months; resembles a prolonged bronchitic illness • May have severe paroxysms of coughing but generally no whooping sound • Low-grade fever Diagnostic Tests *culturing for B. pertussis is considered the gold standard (it is 100% specific)*, difficult - requires collection from the nasopharynx with a calcium alginate fiber-tipped swab and immediate placement into a special transport medium (Regan-Lowe). Culture can be negative if the person has been ill for >3 weeks, has previously been vaccinated, or if antibiotics have been started. The organism is found most frequently during the catarrhal or early paroxysmal stage. Polymerase chain reaction (PCR) is increasingly popular due to its improved sensitivity and rapid result. PCR testing is done using a Dacron swab or nasal wash from the nasopharynx. However, the U.S. Food and Drug Administration (FDA) has not licensed any PCR tests for this purpose. Commercial tests for elevated immunoglobulins to pertussis toxins are available; however, the FDA has not licensed any for diagnostic use. An elevated IgG to pertussis toxin 3 to 4 weeks after cough can be suggestive of a pertussis infection, but it is not definitive. IgA and IgM analyses lack sensitivity. Leukocytosis (20,000 to 50,000/mm3) with 70% to 80% lymphocytes (lymphocytosis) is a common finding in infants and young children, but is rare in adolescents Differential Diagnosis classic form - the diagnosis is clear due to the paroxysmal cough. the cause can be B. parapertussis as well as B. pertussis. marked lymphocytosis in a child with a persistent cough illness points to B. pertussis. C. pneumoniae, adenoviruses, bocaviruses, and other viral agents can present in a similar fashion. Gastroesophageal reflux, cystic fibrosis, asthma, and foreign bodies Management • *Treatment with antimicrobial agents in the macrolide class is the treatment of choice.* • *pyloric stenosis when erythromycin is used in infants <1 month, azithromycin is the drug of choice.* • Antibiotic treatment choices include: Azithromycin at 10 mg/kg in a single dose for 5 days is given to infants from 0 to 6 months of age. Azithromycin in infants older than 6 months of age (5-day treatment: a single dose of 10 mg/kg/day [maximum of 500 mg] on day 1, then a single dose of 5 mg/kg/day [maximum of 250 mg] on days 2 to 5). Clarithromycin for children >1 month (15 mg/kg/day in two divided doses for 7 days with a maximum dose of 1 g/day). Erythromycin is used in all age groups except for infants < 1 month; for infants and children (40 to 50 mg/kg/day in four divided doses for 14 days with a maximum dose of 2 g/day) and adults (500 mg every six hours for 14 days). • Antimicrobial therapy given in the paroxysmal stage does not alter the course of pertussis, but does limit the spreading of the organism • Corticosteroids should not be used. Care of Exposed Children Recommendations regarding isolation and prophylactic measures for exposed children and adults include the following: • Immunization coverage with diphtheria-tetanus-acellular pertussis (DTaP) or Tdap depending on age group. • Chemoprophylaxis with *erythromycin* (40 to 50 mg/kg/day [maximum, 2 g/day] orally in four divided doses for 14 days) is the *drug of choice for all household and close contacts*, including children in daycare, staff and playmates, irrespective of their immunization status; azithromycin or clarithromycin is better tolerated by adolescents. Start as soon after exposure as possible. An alternate approach that can be used with only adults is to follow closely and treat with macrolides with the first appearance of respiratory signs or symptoms. • Close monitoring of respiratory symptoms for 20 days after last contact with an infected individual Complications Secondary bacterial pneumonia, seizures, epistaxis, subconjunctival hemorrhage, encephalopathy, and death can occur. Activation of tuberculosis Prevention The recommended guidelines for the initial series of DTaP vaccines and booster doses should be followed. just one DTaP immunization can reduce the severity of symptoms in an infant Only children with valid contraindications to receiving pertussis vaccine should be excluded from receiving the vaccine. Immunity following either natural pertussis infection or illness or vaccination is not long lasting. Immunity wanes over time, and the vaccine does not confer active immunity. Pertussis in older children, adolescents, and adults is a mild, often unrecognized disease that if transmitted to an unimmunized infant can result in life-threatening illness. Universal immunization of children younger than 7 years old and adolescents is crucial to control this disease.

Croup (Laryngotracheitis and Spasmodic Croup)

Description causes disease in children <6 years old involves swelling and erythema of the lateral walls of the trachea below the vocal cords in an area called the subglottis rapid, acute, upper airway obstruction of varying degrees at the larynx, harsh, barking cough and inspiratory stridor. viral agents are the cause of most bacterial croup, also called bacterial tracheitis, laryngotracheobronchitis, or laryngotracheobronchopneumonitis, presents with inflammatory cell infiltration of the tracheal walls but also ulceration, pseudomembranes, and microabscesses, results in thick pus within the trachea and lower airways. Epidemiology Parainfluenza type 1 - most common viral agent responsible for fall outbreaks. Other causative agents: other parainfluenza types, influenza, human coronavirus HL-63, metapneumovirus, adenoviruses, and rhinovirus. Parainfluenza type 3 is associated with severe croup. most common in children 6-36 months old (60% are <24 months) and occurs most often in the cold season of the year. incubation period is 3 to 6 days Males > females. Recurrent croup and recurrent laryngitis can develop in children until 6 years old. A positive family history noted in a small % of children in whom croup develops. lasts approximately 5 days. With growth, the child's laryngeal tracheal airway is less vulnerable to the effects of viral infections and less susceptible to obstruction. Clinical Findings depend on the infectious agent responsible and the extent of the upper airway involvement. History • URI prodromal symptoms (rhinorrhea, conjunctivitis, or both) are sometimes present before stridor. • Fever within the first 24 hours • Intermittent stridor—mild to moderate. Classically, this presents as a barky cough. • Gradual onset of symptoms (2 to 3 days) • Symptoms worse at night • May or may not have sore throat • Improvement within a few days for most children with viral croup Physical Examination • Slight dyspnea, tachypnea, and retractions • Mild, brassy, or barking cough (harsh sounding) • Stridor—a high-pitched, harsh sound from turbulent airflow that is generally inspiratory, but may be biphasic • Temperature is typically low grade, but may be elevated to 104° F (40° C). • If visualized on examination of the mouth, the epiglottis will appear normal. • Substernal and chest wall retraction in severe cases • Prolonged inspiration • Wheezing and rales may be heard if there is additional lower airway involvement. Diagnostic Tests Radiography of the soft tissues of the neck and chest displays a classic pattern of subglottic narrowing ("steeple sign") on posteroanterior views, but is usually not done unless there is a question about the diagnosis. Microbiology cultures of the pharynx can be helpful in selected cases that have atypical presentations with severe fever, toxic presentations, and severe inspiratory stridor. Differential Diagnosis acute epiglottitis; acute spasmodic croup (no signs of infection); FB aspiration; retropharyngeal abscess; extrinsic compression from tumors, trauma, or congenital malformations; angioedema (anaphylaxis) or early asthmatic attack; laryngotracheobronchitis or laryngotracheobronchopneumonitis, infectious mononucleosis; and psychogenic stridor Management aim of therapy is to provide adequate respiratory exchange. • Humidified air. A Cochrane review showed no evidence that inhalation of humidified air improved the outcome in croup scores in children with mild to moderate croup. no evidence that the use of steam or cold humidification is harmful. cold air can be helpful. Often a ride in a car at night with the windows down accomplishes the same result. Occasionally vomiting relieves the bronchospasm. • Nebulized epinephrine. short-term benefit of about 2 hours. decrease the need for intubation requires close cardiorespiratory monitoring and should not be used in most primary care settings. • Corticosteroids. decrease inflammation and cell damage without prolonging the viral shedding duration. improve the patient's condition can be administered PO, IM, or by nebulizer. Recommended steroids include IM or oral dexamethasone (0.6 mg/kg orally) and nebulized budesonide with mild or moderate croup in an outpatient setting. dexamethasone at 0.6 mg/kg is more effective than prednisone and nebulized budesonide IM dexamethasone can be used in a vomiting child. Otherwise, PO should be used because the rate of oral absorption = IM therapy limited to 1 to 2 days to avoid immunosuppression and the possibility of secondary bacterial tracheitis. one dose of dexamethasone has been shown to reduce inflammatory edema and to prevent destruction of ciliated epithelium Antibiotics are not indicated. • Cold medications: not indicated, their use has not been shown to be helpful • Bronchodilators: If bronchospasm is also suspected, the use of bronchodilators in the usual doses prescribed for relief of asthma may be advantageous. • Oxygen: Blow-by oxygen is used if the oxygen saturation falls below 92% • Other modalities: In severe croup a helium-oxygen mixture known as heliox can be used. Indications for Hospitalization respiratory rates between 70 and 90, distress, exhibiting stridor at rest temperature higher than 102.2° F (39° C) - carefully evaluated; hospitalization may be necessary if other worrisome symptoms are present. Racemic epinephrine by aerosol - typically leads to rebound swelling several hours later. Corticosteroids - (dexamethasone 0.5 to 2 mg/kg/dose every 8 hours IV), and IV hydration may be necessary Complications Increasing obstruction of the airways causes continuous stridor, nasal flaring, and suprasternal, infrasternal, and intercostal retractions. air hunger and restlessness occur and are quickly followed by hypoxia, weakness, decreased air exchange, decreased stridor, increased pulse rate, and eventual death from hypoventilation. Anything that taxes the child's respiratory efforts, such as crying or feeding, causes more respiratory distress. Examination of the nasopharynx with a tongue depressor may result in sudden respiratory compromise. Severely ill children should be evaluated for acute epiglottitis. Viral pneumonia complicates about 1% to 2% of croup cases.

Bronchitis

Description classified as acute or chronic. Acute - febrile, cough illness lasting < 3 weeks with rhonchi and referred breath sounds associated with inflammation of the large airways including the trachea and the large- and medium-sized bronchi. associated destruction of the ciliated epithelium by the causative agent. associated with pharyngitis as well as rhinitis. Chronic - productive cough lasting for more than 3 months, usually a symptom of another chronic disorder (e.g., allergies, asthma, CF, cigarette smoking). involves conducting airways with complete amounts of bronchial tube cartilage. Epidemiology usually preceded by a viral URI. weakened tissue can succumb to a secondary bacterial infection. common viral agents: influenzavirus, RSV, adenovirus, and parainfluenza virus. Other viral agents: rhinovirus, enterovirus, human metapneumovirus, human bocavirus, and the newer human coronavirus. S. pneumoniae, B. pertussis, and H. influenzae are the most commonly cultured bacterial organisms. M. pneumoniae and C. pneumoniae are also causative agents. Pseudomonas aeruginosa is the common agent in children with CF. incidence peaks in midwinter and declines by midsummer with an increase in the fall. Male > females during the first 6 months of life. Clinical Findings course divided into three phases: a prodrome in which fever and URI symptoms predominate, a 6-day period of marked tracheobronchial symptoms with malaise and fever, and a recovery period lasting 1 to 2 weeks with cough and expectoration History • A dry, hacking, unproductive cough that begins a few days after the onset of rhinitis and fever • Complaints of low substernal discomfort or burning chest pain aggravated by coughing • Initially the cough is dry, harsh, and sometimes brassy in younger children. as it progresses, cough becomes productive, and because younger children swallow the sputum, vomiting and gagging can occur. Physical Examination • Variable rhinitis • Low-grade or no fever • Signs of nasopharyngeal infection and conjunctivitis • Coarse breath sounds, rhonchi, and coarse, changing rales Diagnostic Tests. Chest x-ray is not routinely done unless pneumonia is suspected. Differential Diagnosis Pertussis - cough lasting 2 to 3 weeks because it is found in 10% of patients with chronic cough. recurrent acute bronchitis - evaluated for underlying pathologic conditions. Respiratory tract anomalies, FB aspiration, bronchiectasis, immunodeficiency, allergy, rhinosinusitis, anatomic problems such as gastroesophageal reflux and tracheoesophageal fistulas, tonsillitis, exposure to air pollutants, adenoiditis, and CF Check for tobacco or marijuana use in teenagers. In chronic bronchitis, primary ciliary dyskinesia, cystic fibrosis, foreign body, congenital anomalies, reflux, aspiration, asthma, allergies, autoimmune diseases, immune deficiency, and bacteria pathogens such as B. pertussis, M. pneumoniae, and C. pneumoniae should be considered Management acute bronchitis, no specific therapy is known, and most patients require none. Care is primarily supportive. • Analgesia: For pain • Hydration: Intake of fluids to avoid dehydration • Antiviral/antibiotics: If influenza A is the likely etiologic agent, and there is underlying pulmonary diseases, antiviral therapy should be used. most cases of acute bronchitis are from viral sources, antibiotics are not indicated. If M. pneumoniae or C. pneumoniae is suspected, macrolides can be used. • Cough suppressants: no evidence to support the use. Antihistamines should not be used because of their excessive drying effect; these agents tend to prolong the symptoms. • Bronchodilators: no evidence to support the use of inhaled β- agonists unless there is obstruction and wheezing at the onset of illness . A chest x-ray should be considered if there is evidence of a complex bacterial illness. Mucus generally thins in 5 to 10 days, and the cough decreases. For chronic bronchitis, treatment depends on underlying cause. Bronchodilators, cromolyn sodium, corticosteroids, and anticholinergic agents are used for the treatment of chronic cough associated with asthma or underlying chronic lung disease. If reflux is the cause, underlying treatment of the reflux is indicated. Avoidance of tobacco smoke, dust exposure, and air pollution is important. Antibiotics are used for chronic bronchitis if there is a strong likelihood of developing an underlying bacterial infection Complications malaise continues for another week or so after the cough lessens. In undernourished or chronically ill children, otitis, rhinosinusitis, and pneumonia are common.

Bronchiolitis

Description infectious asthma, asthmatic bronchitis, wheezy bronchitis or virus-induced asthma. characterized by signs of a URI. obstruction of the lower respiratory tract as a result of acute inflammation, edema, and necrosis of the epithelial cells of the small bronchioles. results in bronchospasm and increased mucus production. communicable disease found primarily in infancy. infant seen with wheezing for the very first time the leading cause of hospitalizations for infants. presents with cough, fever, coryza, tachypnea, expiratory wheezing, air trapping, and inspiratory crackles. mild cases - symptoms last for 1 to 3 days. severe cases - cyanosis, air hunger, retractions, and nasal flaring with symptoms of severe respiratory distress within a few hours may be seen. Apnea can occur and may require mechanical ventilation Epidemiology a viral illness, caused by RSV Parainfluenza virus (types 1 through 3), adenovirus, M. pneumoniae, influenza virus, adenovirus, human metapneumovirus, rhinovirus, enterovirus, and herpes simplex cause remainder of cases. Adenovirus and RSV cause long-term complications. incubation period for RSV: 4 to 6 days; late fall -early spring; no outbreaks in summer illness begins with URI symptoms: cough, cold, coryza, and rhinorrhea; progresses over 3-7 days with symptoms of audible wheezing and noisy, raspy breathing >80% of the cases occur in infants <1 year of age with a male-to-female ratio of 1.5:1 spread by close contact with infected respiratory secretions or fomites. most frequent mode of transmission is hand carriage of contaminated secretion. The source of infection is an older family member with a "mild" URI. Older children and adults have larger airways and tolerate the swelling associated with this infection better than infants do. Most cases resolve completely, but recurrence of infection is common, and symptoms tend to be mild. Risk factors for severe RSV disease are high levels of RSV in the nasopharynx, genetically smaller airways, family history of asthma, airway reactivity, premature birth, chronic lung disease, and immunodeficiency. Environmental risk factors include crowding, passive smoking, and absence of breastfeeding. RSV-specific IgE, eosinophils, and chemokines may play a role in the pathogenesis Clinical Findings History • Initial presentation of URI symptoms (cough, coryza, and rhinorrhea) lasting for 3 to 7 days • Gradual development of respiratory distress marked by noisy, raspy breathing with audible wheezing • Low-grade to moderate fever up to 102° F (38.9° C) • Decrease in appetite • No prodrome in some infants; rather they have apnea as the initial symptom Physical Examination • Coryza • Mild conjunctivitis in 33% (Welliver, 2010) • Pharyngitis • Otitis media in up to 15% (Welliver, 2010) • Heterophonous wheezing • Crackles may be heard throughout the breathing cycle • High respiratory rate (approximately 40 to 80 breaths per minute) • Varying signs of respiratory distress and pulmonary involvement (e.g., nasal flaring, grunting, retractions, cyanosis, prolonged expiration) • Abdominal distention • Palpable liver and spleen, pushed down by hyperinflated lungs Diagnostic Tests chest radiographs in previously healthy infants with mild RSV bronchiolitis is not indicated. Evidence-based guidelines - strongly against routine chest radiography severe illness, a chest x-ray may be ordered to rule out pneumonia, but its use must be weighed against the dangers of radiation exposure. even with severe illness the x-ray can be clear with a flattened diaphragm and an increase in anteroposterior diameter. Areas of atelectasis can appear like a pneumonitis, but true pneumonia is uncommon. Early bacterial pneumonia can be difficult to detect and cannot be ruled out by radiographs. Virologic testing is weakly recommended in the guidelines. *Enzyme-linked immunosorbent assays or fluorescent antibody techniques to look for RSV are the diagnostic procedures of choice in most laboratories.* Viral culture of nasal washings can be done in severe cases to confirm RSV, parainfluenza viruses, influenza viruses, and adenoviruses. PCR - helpful in deciding about isolation of cohorts with the same infection in the hospital setting. Hematologic testing - not recommended. If a CBC is done for another reason, a mild leukocytosis may be seen with 12,000 to 16,000/mm3. Routine laboratory tests are usually not required to confirm the diagnosis because they lack specificity. Differential Diagnosis mild afebrile cases, bronchial asthma can be confused with bronchiolitis. foreign body, circulatory failure, congenital heart disease irritants, gastroesophageal reflux, metabolic causes, allergic pneumonitis, vascular rings, lung cysts, and lobar emphysema Management Most infants with mild signs of respiratory distress can be treated as outpatients. • Supportive care consists of adequate hydration and use of antipyretics. • Transcutaneous oxygen saturation monitoring is strongly recommended. • Fluid intake is strongly recommended to prevent dehydration. • The following are strongly *not* recommended: β-agonist Adrenaline Antibiotics (unless indicated for another problem) Inhaled or oral corticosteroids Physiotherapy Viral therapy (ribavirin) Antileukotriene therapy Humidification or steam Parents need to understand: • The management of rhinitis (use of saline drops and suctioning of nares) • Indications for the use of antipyretics • Signs of increasing respiratory distress or dehydration that call for hospitalization • Guidelines for feeding an infant with signs of mild respiratory distress (amount of fluid needed per 24 hours; smaller, more frequent feedings; monitoring of the respiratory rate; and guarding against vomiting) Infants <2 months old and older infants with signs of severe respiratory distress should be hospitalized. Signs suggesting increasing respiratory distress: • Progressive stridor or stridor at rest • Apnea • Increasing respiratory rate (sleeping rate of greater than 50 to 60 breaths per minute) • Restlessness, pallor, or cyanosis • Hypoxia recorded by either blood gas (Po2 less than 60 mm Hg) or pulse oximetry (less than 92% on room air) • Rising Pco2 (recorded by blood gas) • Inability to tolerate oral feedings • Depressed sensorium • Presence of chronic cardiovascular or immunodeficiency disease • Parent unable to manage at home for any reason In-hospital management focuses on supportive care and includes suctioning of upper airways, which is critical; humidified supplemental oxygen; and elevation of the child to a sitting position at a 30- to 40-degree angle. infant's neck should be extended to 30 to 40 degrees. IV fluids needed because respiratory distress interferes with nursing or bottle feeding. subsets of infants who demonstrate significant bronchodilator responsiveness. all infants (especially those with a family history of asthma or atopy) with significant wheezing should be given a one-time trial of an aerosolized beta 2-adrenergic treatment. If after an initial one-time trial there is no improvement, additional use of bronchodilators should be abandoned Occasionally a hospitalized child is not able to be quickly weaned back to room air. Home management of these patients requiring oxygen is extremely difficult and should be undertaken only by someone with excellent pulmonary skills and in consultation with a pediatrician or pediatric pulmonologist. The child should have an O2 saturation study before discharge to help determine the O2 requirements at rest, feeding, play, and sleep. A pneumogram to rule out apnea may also be indicated. Strict outpatient follow-up is mandatory for as long as the child is receiving home O2. Complications The first 48-72 hours after the onset of cough are the most critical. Apneic spells are common in infants. The child is ill-appearing and toxic, but gradually improves. fatality rate: 1% to 2%. Prolonged apnea, uncompensated respiratory acidosis, and profound dehydration secondary to loss of water from tachypnea and an inability to drink are the factors leading to death can cause minor pulmonary function problems and a tendency for bronchial hyperreactivity that lasts for years. associated with the development of asthma Recurrent episodes of wheezing can be seen during childhood in patients with a history of bronchiolitis. This persists into adolescence in 10% of the children still wheezing. Prevention Palivizumab is an RSV-specific monoclonal antibody used to provide some protection from severe RSV infection for high-risk infants. Educate caregivers about decreasing exposure to and transmission of RSV, especially those with high-risk infants. Advice should include limiting exposure to childcare centers, if possible; handwashing; avoiding tobacco smoke exposure; and scheduling RSV prophylaxis vaccination, when indicated.

Rhinosinusitis

Description inflammation and secondary infection of the paranasal sinuses and the adjacent nasal mucosa Three symptoms were required for the diagnosis of acute rhinosinusitis—purulent nasal discharge, nasal obstruction, and facial pain, pressure, or fullness lasting between 10 days and 4 weeks. 5% to 10% of URI are complicated by rhinosinusitis Common causes include: viral infection; allergic and nonallergic rhinitis; anatomic problems such as abnormality of the ostiomeatal complex or septal deviation; cigarette smoking; swimming and diving; high-elevation climbing; and dental infections can have three clinical presentations: • Persistence of URI symptoms for longer than 10 days and less than 30 days without improvement • Severe symptoms with a high fever and purulent rhinitis at the onset and lasting at least 3 to 4 days • Biphasic illness in which there is worsening on day 6 or 7 of a common cold in which the patient develops an increase in respiratory symptoms, nasal congestion, or a new onset or recurrence of a fever. The maxillary and anterior ethmoid sinuses are most frequently involved in children because they are present at birth, but only the ethmoidal sinuses are pneumatized. The frontal sinuses begin their development at 7 years old with complete development at adolescence. The three key elements that keep the sinuses patent include ostia patency, normally functioning cilia, and quality of secretions. Inflammation and edema of the mucous membranes lining the sinuses cause obstruction and set up an ideal situation for bacteria to invade the sinus cavities. conditions predispose children to chronic sinus infection: allergies, nasal deformities, CF, nasal polyps, and HIV infection. divided into acute or chronic, in which symptoms persist for 12 weeks. Risk factors for the development of chronic rhinosinusitis: anatomic blockage; irritant and allergen exposure; defects in mucociliary function; immunodeficiency; and chronic infection with bacteria, viruses, or fungi. a persistent swelling of the sinonasal mucosa impairs sinus drainage. Chronic can be divided further into three distinct syndromes—without polyps, with polyps, and allergic fungal Patients with chronic rhinosinusitis who develop new symptoms of rhinosinusitis, are referred to as having acute-on- chronic rhinosinusitis. Thick, yellow discharge is a common and normal finding with a URI. cautious to not overdiagnose rhinosinusitis and subsequently indiscriminately use antibiotics Epidemiology The various sinuses develop, aerate, and become clinically important at different times during childhood. Ethmoiditis can occur >6 months old, in contrast to frontal rhinosinusitis, which is first seen around 10 years old. The common bacterial organisms responsible for superinfections are S. pneumoniae, nontypeable H. influenzae, Moraxella catarrhalis, and, less often, S. aureus, other streptococci, and anaerobes. Anaerobic bacteria are prominent in chronic rhinosinusitis and include Prevotella spp., Porphyromonas spp., Fusobacterium nucleatum, and Peptostreptococcus spp. Anaerobic and staphylococcal agents are implicated in chronic rhinosinusitis. Recent data from middle ear bacteria indicate that H. influenzae is slightly more prominent as a pathogen with a slight decrease in S. pneumoniae as the prominent pathogen The presence of antibiotic-resistant organisms is associated with prior antibiotic therapy. Cases of recurrent and chronic rhinosinusitis are often caused by recurrent viral URIs associated with daycare attendance, smoking in the home, older siblings at home who reinfect the child, or certain predisposing conditions, such as allergies, nasal polyps, immunodeficiency disorders, or CF— predispose to infections with Aspergillus and Zygomycetes. Clinical Findings in Acute Rhinosinusitis two cardinal symptoms be present: • Purulent rhinorrhea • Either facial pressure or nasal obstruction Other s&s include: • Headache, fever, fatigue, maxillary dental pain, cough, decreased ability to smell (hyposmia), no smell, and ear pressure or fullness Additional key issues: • Cough worse at night because sinus drainage down the pharyngeal wall can induce cough and vomiting • Periorbital cellulitis—a sign of ethmoid sinusitis in children • Occasionally malodorous breath or ears feel full; more than half of all patients with sinusitis also have abnormal middle ear findings Diagnostic Tests radiographs are usually not needed. If symptoms of orbital, intracranial, or soft-tissue abscess, radiographic imaging should be done Facial swelling, acute rhinosinusitis unresponsive to 48 hours of antibiotics, a child with a toxic appearance, chronic or recurrent rhinosinusitis, and chronic unresponsive asthma are also indications for imaging studies, including sinus radiographs, ultrasonograms, or CT scanning. CT is the accepted imaging study for acute or chronic rhinosinusitis Coronal sections show lesions in the ostiomeatal complex and axial images can delineate orbital complications the AAP recommends its use only in children >6 years who are undergoing operative procedures Nasal cultures are difficult to obtain because they must be taken from the middle ostium in the middle meatus Transillumination is subjective and difficult to perform in children. Differential Diagnosis Viral URI, allergic rhinitis, and other causes of headache are the differential diagnoses. may exacerbate asthma. Management Symptomatic pain relief with acetaminophen or ibuprofen has been shown to be helpful 60%-80% of acute rhinosinusitis episodes resolve without antibiotics in about 4 weeks, antimicrobial therapy increases the speed of resolution and reduces the amount of mucosal damage Antibiotics should be prescribed for a course of 10 days or, if the child is responding slowly but not symptom-free, an additional 7 days. Most children show dramatic improvement in 3-4 days (fever and nasal discharge abating). Failure to improve in 48 hours suggests a resistant organism or complications. The course of therapy may be up to 21 days in acute and up to 6 weeks in chronic *In uncomplicated acute in children, first-line treatment should be amoxicillin because it is efficacious, safe, and inexpensive* • Amoxicillin (80 to 90 mg/kg/day), amoxicillin-clavulanate, cefpodoxime, proxetil, or cefuroxime axetil as initial therapy if the child has not taken antibiotics in the past 4 to 6 weeks. The AAP has also recommended amoxicillin 40 to 45 mg/kg/day, but this treatment should not be given if there are high rates of resistance If allergic to amoxicillin—azithromycin, clarithromycin, erythromycin, or trimethoprim/sulfamethoxazole (TMP-SMX) (failure rates are up to 38% with TMP-SMX) • Children at risk for resistant bacterial infections (antibiotic therapy within prior 1 - 3 months, daycare attendance, <2 years old, failure to respond within 72 hours) should receive high-dose amoxicillin-clavulanate (80 to 90 mg/kg/day amoxicillin and 6.4 mg/kg/day clavulanate). The management of chronic - Referral to an otolaryngologist is often needed. Additional management considerations include the following: • Decongestants. if used by patient, limited to 5 days to avoid rebound edema (rhinitis medicamentosa) In older children - may be used if there is significant nasal obstruction • Topical corticosteroids. intranasal steroids may decrease symptoms in patients with uncomplicated sinusitis • Antihistamine. Antihistamines and intranasal steroids may have a role in recurrent or chronic rhinosinusitis if allergic manifestations are present • Saline irrigation. The use of buffered isotonic saline into the nasal cavity by squeeze bottle or neti pot (in late childhood and adolescence) may be helpful in allergic rhinitis, recurrent acute sinusitis, and chronic sinusitis. can be used by patients to help thin secretions and is recommended by some allergists. • Children with complications or signs of invasive infection should be referred to the appropriate medical specialist. Surgical drainage by an otolaryngologist, treatment of allergies and control of allergic rhinitis by an allergist, or both may be necessary. • Comfort measures: acetaminophen, ibuprofen, or codeine for severe pain. A humidifier helps relieve the drying of mucous membranes associated with mouth breathing. Increase oral fluid intake. • Diving is contraindicated • Prevention includes good allergy management, relief of nasal airway obstruction, and attention to persistent nasal discharge Complications Chronic or recurrent rhinosinusitis may result in referral to an otolaryngologist or allergist. Orbital cellulitis secondary to ethmoiditis is a serious, life-threatening complication that is a medical emergency - swelling and erythema of the eyelids, proptosis, decreased extraocular movements, and altered vision. Intracranial complications, such as cavernous sinus thrombosis, subdural empyema, and brain abscess, can also occur. Chronic rhinosinusitis is also associated with intractable wheezing in children with asthma

Bacterial Tracheitis (Laryngotracheobronchitis and Laryngotracheobronchopneumonitis)

Description and Epidemiology acute potentially dangerous bacterial infection of the upper airway that does not involve the epiglottis. inflammatory process involving the larynx, trachea and bronchi with adherent or semiadherent mucopurulent membranes within the trachea. can occur at any age, typically 3- to 10-year-old child. usually follows a viral respiratory infection (generally parainfluenza virus type 1). typically has had a prior croup episode or influenza virus and then becomes secondarily infected with S. aureus, the most common organism cultured, group A streptococci, H. influenzae, or M. catarrhalis Clinical Findings History starts with a URI including croup over a period of 2 to 7 days. A secondary bacterial infection occurs, and then suddenly the child becomes markedly worse. Physical Examination Copious purulent sputum - older children. extent of lower respiratory tract involvement is not realized due to the upper airway obstruction from infection. Inspiratory stridor, rales, wheezing, an increased respiratory rate, and air trapping. The child looks toxic. Diagnostic Tests WBC count is elevated. Leukocytosis with a left shift is noted. differentiated from epiglottitis by its slower clinical course and a normal-appearing epiglottis on examination. The "classic" features of acute epiglottitis are absent (e.g., no thumb sign on a lateral neck film). pulmonary infiltrates and air trapping are seen on chest x-ray. Management • The usual treatments for croup are ineffective, and hospitalization is necessary. • Intubation or tracheostomy is usually necessary to bypass the swelling that develops at the level of the cricoid cartilage and to manage the copious purulent secretions. • Antibiotics that cover staphylococcus are administered. • Oxygen and airway support are necessary. • Most patients become afebrile in 48 to 72 hours if the condition is promptly recognized and treated. The child is weaned from the artificial airway and usually does well.

Epiglottitis

Epidemiology (supraglottitis), inflammation of the epiglottis, the aryepiglottic folds, and the ventricular bands at the base of the epiglottis. causative organism: Haemophilus influenzae type B (HIB). occurs in children 1-5 years old with 25% of cases in children <2 years old. 4-10x higher in Navajo Native Americans and Alaskan Eskimos Since HIB vaccine, drastic decline in # of children with infections caused by this organism; The following organisms have been implicated as causes of supraglottitis: S. pneumoniae, S. aureus, H. parainfluenzae, group A, B, C and G streptococcus, and Bacillus spp. Clinical Findings History abrupt onset of fever, severe sore throat, dyspnea, inspiratory distress without stridor, and drooling. acutely ill and toxic. Physical Examination • Inspiratory and sometimes expiratory stridor • Drooling, aphonia (muffled voice), and high fever • Rapidly progressive respiratory obstruction and prostration • Flaring of the ala nasi and retraction of the supraclavicular, intercostal, and subcostal spaces • Child assumes a position of hyperextension of the neck *No attempt should be made to examine the posterior pharynx because stimulation of the area can induce spasm and obstruction of the epiglottis and lead to respiratory arrest.* older children: • Complaints of sore throat and dysphagia • Stridor, irritability, restlessness, and brassy cough (uncommon) • Airway obstruction follows within 2 to 24 hours. The child sits up with arms back, trunk forward, neck hyperextended, and chin thrust forward (tripod position). • A rare, unusual finding is that of just a hoarse cough and a cherry-red epiglottis. Diagnostic Tests Blood cultures If possibility of this is thought to be remote in a patient with croup, a lateral neck radiograph may be obtained before the physical examination is undertaken. Absence of the "thumb" sign on the radiograph rules out the condition. A health care professional capable of supporting the airway and skilled in intubation must accompany the child to the radiology department and back. Management The time from the onset of symptoms until death may be only a matter of hours. *a pediatric otolaryngologic emergency because of the risk of sudden airway obstruction.* The goal of therapy is to establish an airway and appropriately start antimicrobials. If epiglottitis is suspected, do not examine the throat. Do not place the child in the supine position, and immediately transport the child to the hospital via emergency medical services. The child should be examined in the operating room by an otolaryngologist or an emergency department physician skilled in performing an emergency tracheostomy. An airway must be established, either a nasotracheal airway or a tracheostomy. The diagnosis is confirmed in the OR by depressing the tongue to view the swollen cherry-red epiglottis. An expert in establishing an airway needs to be present because there is a risk of reflex laryngospasm, with acute and complete airway obstruction. • Establish an airway, preferably by nasotracheal intubation • Administer IV broad-spectrum antibiotics to cover H. influenzae. • Administer oxygen and respiratory support. rarely lasts more than 48 to 72 hours. idiopathic pulmonary edema can follow (in up to 9% of patients) after the establishment of an airway due to the changes in pulmonary microvascular pressure subsequent to relieving the obstruction. As improvement occurs, the child can be extubated, but antibiotic therapy should be continued for 10 days. Untreated or undertreated patients have a significant mortality rate. If H. influenzae is identified as the causative agent, rifampin prophylaxis (20 mg/kg in a single dose [maximum, 600 mg] for 4 days) should be given to all household contacts of the patient whose household has: • At least one child younger than 4 years old who is unimmunized or incompletely immunized • Children less than 12 months old who have not received the primary series of HIB vaccine • Immunocompromised children if there are two cases of invasive HIB disease in a daycare center or nursery within 60 days, all members of the nursery need to receive prophylaxis Prevention Routine immunization against HIB Handwashing

Recurrent Epistaxis

Epidemiology incidence of 30% in children from 0 to 5 years, 56% in school-age children 6 to 10 years, 64% in adolescents higher living in dry climates or during the winter months when artificial heating is used. often benign and typically related to mechanical trauma to the area (e.g., nose picking), generally self-limiting. Other factors -> mucosal irritation that result in bleeding include coagulopathies, allergies, neoplasms (e.g., rhabdomyosarcoma), polyps, hemangiomas, chronic rhinitis, URI, FB, chronic use of topical nasal sprays containing corticosteroids or antihistamine decongestants, and viral or bacterial infections of nasal tissue. adolescents - use of recreational drugs such as cocaine. > 95% of cases the anterior portion of the nasal septum, called Kiesselbach area, is the usual site of involvement. blood supply comes from the external carotid through the external maxillary artery. Posterior nosebleeds more common in older adult patients. A coagulopathy, generally von Willebrand disease or platelet aggregation disorders, can manifest as recurrent epistaxis, but a careful history will reveal easy bruising. Clinical Findings History • Recent nasal trauma including nose-picking • Allergies or a recent URI • Unexpected bruising or bleeding from other sites • Frequent nosebleeds (unilateral or bilateral) • Tarry stools (the result of swallowed blood) always question about a family history of excessive bleeding episodes or bleeding disorders. topical nasal medication use, or in the case of the teen, cocaine or other inhaled recreational drugs Physical Examination Nares visualization may include fresh clots, old clots, and/or raw, red skin. The nasal mucosa on the medial surface of the anterior septum may be dry, cracked, excoriated, or scabbed. The bilateral epistaxis, blood in the oropharynx, and difficult to control bleeding suggest posterior bleeding Diagnostic Tests A baseline hematocrit may be indicated in severe or chronic epistaxis -> iron deficiency anemia secondary to the bleeding. Unless the history -> coagulopathy or the nosebleeds are recurrent and refractory to treatment, coagulation studies are not indicated Differential Diagnosis A bleeding disorder or nasal tumor - epistaxis that is severe, prolonged, and recurrent. Red flags for other disorders include epistaxis in a child < 2 years old, evidence of bleeding at other sites, or bleeding that lasts >20 minutes If these abnormalities occur and a coagulopathy is suspected, order a CBC, platelet count, prothrombin time (PT), activated partial thromboplastin time (aPTT), and ristocetin cofactor. If epistaxis is associated with a traumatic injury, evaluate for the presence of a nasal fracture and/or septal hematoma. Management • Have the child sit upright and lean forward to prevent swallowing the blood. • Apply direct pressure at the nasal ala (pinch the nares together at the bony structure) for 5 minutes; 15 minutes if there is still bleeding. Have the parent watch the time • Packing and topical vasoconstrictor drugs are occasionally needed. • Use a bedside humidifier to moisten the air in dry climates or in winter with forced-air heating. Normal saline nose sprays are also effective. Apply topical antibiotic to the site of the septal scab for 5 to 7 days to keep moist, reduce itching, and assist healing. • Topical agents such as Nosebleeds QR are hydrophilic polymers that form an artificial scab when they come into contact with blood. These can be applied via a swab to Kiesselbach plexus. Local applications of a solution of oxymetazoline or Neo-Synephrine (0.25 1%) can also be used • Silver nitrate sticks can be used to cauterize exposed vessels if bleeding persists; however, the site must be easily accessible, visible, and not bleeding briskly. It has a high failure rate and is associated with nasal septum atrophy. •Nasal packing with absorbable oxycellulose material if bleeding continues or the site cannot be localized; if packing is used, prescribe oral antibiotics to reduce the risk of secondary rhinosinusitis and toxic shock syndrome. • Treat the underlying cause of the problem (e.g., trauma from nose- picking; dry air; topical nasal sprays). • Teach parents to leave alone blood scabs because removal may precipitate further bleeding. Prevention instructions on a good nasal regimen to keep the nasal mucosa moist. vaporizer use and normal saline nose drops or sprays or the application of petroleum jelly to the anterior nasal cavity daily If the child uses nasal corticosteroids, make sure the child directs the spray laterally rather than toward the septum. This reduces epistaxis related to nasal spray

Patient and Parent Education

Frequent handwashing and avoiding touching eyes and nose can help prevent the spread of infection. educated about assessment and management of changes in the child's condition. Fluid: Give guidelines on type, amount, and frequency of fluids child should take. Humidification: For laryngotracheobronchitis, take the child out into the cold night air or open a freezer door. In dry climates, humidifiers help in common colds; instruct about cleaning of nebulizers and humidifiers Bulb syringe: Instruct to use the bulb syringe gently and intermittently for suctioning the nares. Normal saline nose drops or spray: Use before feedings and when mucus is thick or crusted. Follow by suctioning nares with bulb syringe. Other educational issues to cover: • Indications for immediate reevaluation of child: Signs & symptoms of respiratory distress toxic appearance, malaise, feeding difficulty, etc • when to expect improvement in the child's symptoms and, if symptoms do not improve as expected, what to do next • Clear instructions about medications—how much to give, when to give, side effects to watch for, how long to give, and the necessity of completing the course of antibiotics • Infection control information if needed—handwashing and disposal of infected secretions • Care of nebulizers and humidifiers—to prevent the growth of organisms, nebulizers and humidifiers should be cleaned daily with soapy water, rinsed thoroughly, soaked for one half hour in a solution of one part vinegar to two or three parts distilled water, and then air-dried. • Instructions on next return visit

Risk Factors for Death from Asthma (ppt)

History of severe exacerbations Prior intubation for asthma Prior admission to Intensive Care Unit 2 or more hospital admissions in the past year 3 or more emergency room visits in the past year Hospital or emergency room visit past month Use of >2 canisters per month of inhaled short-acting beta2-agonist Chronic use of systemic corticosteroids Poor perception of airflow obstruction or its severity Co-morbid conditions (other diseases) Serious psychiatric disease or psychosocial problems Low socioeconomic status and urban residence Illicit drug use Sensitivity to alternaria-mold Lack of written asthma action plan

Risk Factors for Asthma (ppt)

Host factors: predispose individuals to, or protect them from, developing asthma Genetic - Atopy - Airway hyperresponsiveness Gender Obesity Environmental factors: influence susceptibility to development of asthma in predisposed individuals, precipitate asthma exacerbations, and/or cause symptoms to persist Indoor allergens Outdoor allergens Occupational sensitizers Tobacco smoke Air Pollution Respiratory Infections Diet Low-income, urban residents Some minorities History of atopy History of Low birth weight, prematurity Frequent respiratory infections, trends seen with RSV and incidence of developing asthma w/ future viral infections Family history of asthma Living environment with exposure to second-hand smoke before and/or after birth Family history of allergies and/or asthma

Inhaled Medication Delivery (ppt)

Metered dose inhaler (MDI) Dry powder inhaler (DPI) Nebulizer Assessing your patients technique for inhalation therapy, obtain teach back (return demo, verbal ) http://www.youtube.com/watch?v=zG2DVoRP86g spacers and holding chambers: Improves airway deposition Decreases oral-pharyngeal deposition & side effects Passive or active breathing techniques Can be used with or without a mask help the medicine get into the lungs where it needs to be to work in the airways. If you don't use a spacer the medicine stays in your mouth and throat, which doesn't help your asthma. you can get a sore throat, hoarse voice or fungal infection. Spacers can be used with or without a mask so even young children can use the metered dose inhaler/MDI or asthma pump. If you use an MDI and do not have a spacer, ask your health care provider how to get one. Using an MDI: Before handling your medicine, wash your hands with soap and water. Remember to prime it if it hasn't been used before, or not used in 2 weeks or dropped! Remove the cap from the inhaler - make sure opening is clean Hold the inhaler with the mouthpiece at the bottom Shake the inhaler for 5 seconds Tilt your head back a little and breathe out Make sure that your lips make a tight seal around the mouthpiece Press down on the MDI so that the medicine comes out as you start to breathe in Breathe in slowly and steadily for 3-5 seconds Remove the inhaler from your mouth Hold your breath for 10 seconds Breathe out slowly Using an MDI with spacer: Before handling your medicine, wash your hands with soap and water. Remember to prime it if it hasn't been used before, or not used in 2 weeks or dropped! Shake the MDI and take the cap off. put inhaler into spacer Sit up or stand and breathe out normally. breath out all the air in your lungs put spacer in your mouth and close lips tightly around mouthpiece. Spray one puff of medicine into spacer. Start to take a slow deep breath 3-5 seconds. if you hear a whistle, breath slower, but keep taking a deep breath. do not breath through your nose. take the spacer out of your mouth and hold your breath. count to 10 slowly. breath out slowly, like cooling soup on a spoon Wait 1 minute and repeat. using the MDI with a spacer and a mask. Before handling your medicine, wash your hands with soap and water. Remember to prime it if it hasn't been used before, or not used in 2 weeks or dropped! Shake the MDI and take the cap off. Attach the MDI to the spacer. Sit up tall or stand. Place the mask over the nose and mouth. Press down on the MDI. breathe in and out 6 times slowly. Don't worry about breathing into the spacer, the medicine can only go out through the spacer. Remove the mask from the face. Wait one minute and repeat. Diskus demonstration: Before handling your medicine, wash your hands with soap and water. While holding the diskus in one hand, place the thumb of the other hand on the grip and push it away so you can see the lever underneath. Push the lever away until you hear and/or feel a click. Breathe out, then put your lips tightly around the mouthpiece, hold the diskus like a hamburger, and breathe in hard and fast. Take the diskus out of your mouth, hold your breath while you count to 10 slowly. Breathe out slowly through your nose. Close the diskus. Remember, rinse your mouth with water and spit it out! Don't get the diskus wet. Jet Nebulizer/Reusable Nebulizer Decreases total nebulizer time Decreases loss of medication Reusable nebulizer kit lasts up to 6mths Disposable Nebulizer Kit: Limited use -throw away Continued use (> 1wk) & washing causes leakage, ineffective delivery Properly fitted mask Use for infants, young child, those who can not use mouthpiece

Case #5 (ppt)

Mr & Mrs Worry are concerned about the inhaled steroids that your prescribing for their 2 yo son. He is already on Singulair/albuterol, and used 2 courses of oral steroids in 3 months. They ask "what about his growth, don't steroids cause cancer, aren't steroids dangerous to use" What counseling/education can you offer them? What if you don't spend the time & just give a prescription?

Case #3 (ppt)

Mrs. Purr has 2 children with asthma. She has just found out that they are VERY allergic to cats. Of course she has 3 cats in the home (all in home prior to her children) The mother looks upset by the news & the one daughter is crying.. How do you handle this situation?

Case #1 (ppt)

Ms. Denial is here with her daughter Katie, a 20 month old toddler. Katie has had 4 asthmatic episodes this winter, 2 required ER visits with oral steroid therapy. She was prescribed last visit ( 6 weeks ago) nebulized steroids BID, albuterol nebs prn. Today Katie presents with mild-moderate wheezing/coughing & her clothes smell of cigarette smoke. Her mom states "she doesn't sit still for her treatments, and my mom said all that medicine is dangerous for a little girl" What could be a reason she isn't responding to therapy, what are your choices, what steps need to be taken.

Asthma Action Plans (ppt)

NAEEP 2007 guidelines-. Per the expert panel recommendations: Clinicians provide all patients with a written asthma action plan that includes instructions for (1) daily management, and (2) recognizing and handling worsening asthma, including self-adjustment of medications in response to acute symptoms or changes in PEF measures. Written asthma action plans are particularly recommended for patients who have moderate or severe persistent asthma, a history of severe exacerbations, or poorly controlled asthma In a large, scientific review of 36 RCTs involving 6,090 adults who had asthma, asthma self-management—accompanied by regular review of medications and asthma control by a medical practitioner—improved health outcomes significantly more than usual care The Green Zone - peak flow 80-100% No cough, wheeze, chest tightness, or shortness of breath during the day or night. Take your long term control medicine each day. The Yellow Zone - Peak flow 50-80%. Cough, wheeze, chest tightness, or shortness of breath. Waking at night due to asthma. Can do some, but not all, usual activities. Take your long term control medicine and add your quick relief medicine. The Red Zone - Peak flow 50% or less. Very short of breath. Quick relief medicine has not helped. Cannot do usual activities. Symptoms are the same or get worse after 24 hours in the yellow zone. Take long term control and quick relief medicines and CALL YOUR DOCTOR.

Spirometry (ppt)

Patient blows into spirometer. The device measures and records maximum air flow, lung volume, and other parameters which are important in understanding the individuals pulmonary lung function. Effort FEV1

Rules of Two (ppt)

Patients are candidates for maintenance therapy if . They are using a quick-relief inhaler more than 2 times per week They awaken at night due to asthma symptoms more than 2 times per month They refill a quick-relief inhaler prescription more than 2 times per year

Morbidity and Mortality asthma (ppt)

Pediatric high risk populations are Infants & adolescents Infants: Anatomical/physiological differences: Narrow airway diameter, smaller lung capacity Immature cartilage = "floppy" airway, easy to occlude Immature intercostal muscles=diaphragmatic breathing Greater metabolic rate= higher oxygen consumption increased frequency of viral respiratory infections, dependence on others to recognize symptoms, avoidance of exposure to asthma causing inhalants/triggers, & timing of initiating treatment Teens: thought process (denial, illogical thinking) behavior (non-adherence to treatments, independence through experimentation) exposure to asthma causing inhalants/triggers (peer acceptance) lack of adult supervision of asthma management @ home/school Parents of teens need to help them establish healthy habits, take on responsibilities and grow strong and confident. other contributors: Age Comorbidities Under treatment Poor follow-up Inappropriate therapy Under diagnosis or missed diagnosis Limited patient education Low income, urban areas Some minorities

Goals of Asthma Therapy (ppt)

Provide optimal pharmacotherapy with minimal or no adverse medication effects Meet patient's & families expectations of and satisfaction with asthma care #1: Manage uncontrolled asthma so that it becomes controlled Sleep: prevent chronic coughing, asthma symptoms, and asthma exacerbations during the day and night Learn: eliminate missed school days Play: maintain normal activity levels

Addressing Comorbidities Asthma (ppt)

Rhinitis Sinusitis Allergies Eustachian tube dysfunction and otitis media Enlarged adenoids Postnasal drip Gastroesophageal reflux

Assessing and Monitoring AsthmaSeverity and Asthma Control(ppt)

Severity: the intrinsic intensity of the disease process. Severity is measured most easily and directly in a patient not receiving long-term-control therapy. Control: the degree to which the manifestations of asthma (symptoms, functional impairments, and risks of untoward events) are minimized and the goals of therapy are met. Responsiveness: the ease with which asthma control is achieved by therapy. Impairment: frequency and intensity of symptoms and functional limitations the patient is experiencing or has recently experienced Risk: the likelihood of either asthma exacerbations, progressive decline in lung function (or, for children, reduced lung growth), or risk of adverse effects from medication Stepwise approach is intended to assist, not replace, clinical judgment Assign to the most severe step in which any feature occurs Any level of severity of chronic asthma can be life-threatening Asthma specialist consultation recommended for moderate or severe persistent asthma; consider for all persistent asthma Questions completed by child age 4-11 years How is your asthma today? How much of a problem is your asthma when you run, exercise or play sports? Do you cough because of your asthma? Do you wake up during the night because of your asthma?

What are 'Early Warning Signs'? (ppt)

Some of the more common early warning signs before an asthma attack are: A cough (even a little cough is something to treat!), A Wheeze (even a little bit!), A 'funny feeling' in the chest, Some trouble breathing. Others: Chest tightness Itchy eyes a few hours before an attack Tired or not sleeping well the day before Stuffy nose Cranky (may start the day before) Headache Feeling nervous (the day before) Pale complexion

Stepwise Asthma Therapy (ppt)

Step 1: SABA PRN Step 2: Preferred: Low dose ICS. Alt: Cromolyn or Montelukast Step 3: Preferred: Medium dose ICS Step 4: Preferred Medium dose ICS + LABA or montelukast Stap 5: Preferred: High dose IcS + Laba or montelukast Step 6: Preferred: High dose ICS + Laba OR montelukast, oral systemic corticosteroids Consult with asthma specialist if step 4 care or higher is required. Consider consultation at step 3. Reliever therapy -> cough (mucus production) and bronchospasm (bronchial hyperresponsiveness) Environmental controls -> virus allergens and smoke Controller therapy - mucosal airway inflammation

Case #4 (ppt)

Taylor is a 4 yo girl who comes to your office hugging a large stuffed bear. Her asthma is not in good control despite inhaled steroid therapy & further testing shows she is very allergic to Dust mites. Her father gulps & asks"do we have to get rid of ALL her stuffed toys?' as you go to answer the little girls eyes well up with tears... What are the options, what might need to be revised in her plan....

What is Asthma?(ppt)

The Definition-hasn't changed a chronic inflammatory respiratory disease Characteristics: Airway obstruction that may or may not be reversible, either spontaneously or with medication Airway inflammation caused by many cellular components Increased airway hyper-responsiveness Many cells and cellular elements play a role mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness. chest tightness and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial hyper-responsiveness to a variety of stimuli. With asthma, what we see is the tip of the iceberg, the symptoms. At the base of the iceberg is the airway inflammation. This inflammation underlies the bronchial hyper responsiveness of asthma, the air flow obstruction, and the culmination of the inflammatory process is the tip of the iceberg, the symptoms. *Active inflammation of the airways can be present for 6 to 8 weeks following a severe respiratory infection. *Airflow obstruction results from bronchoconstriction, bronchial edema, mucus hypersecretion, and inflammatory cell recruitment including eosinophils, a key inflammatory cell. a life-long disease affecting the bronchial tubes/airways that carry air to the lungs. breathing is sometimes difficult because: Swelling of the lining in the airways (inflammation) Extra mucus in the airways Tightening of the muscles around the airways (muscle spasm) not contagious. It cannot be cured, but it can be controlled with daily medications. anyone with asthma can have an acute (sudden) attack of symptoms. Even if child has no symptoms, children with asthma almost always have some inflammation/swelling in the airways. always a chance that an attack could occur. the severity of asthma can change over the years. There may be months or years when your child needs daily medications for asthma, and there may be periods of time when your child doesn't need these daily medications. air enters the respiratory system from the nose and mouth and travels through the bronchial tubes. in an asthmatic person, the muscles of the bronchial tubes tighten and thicken, and the air passages become inflamed and mucus-filled, making it difficult for air to move in a non-asthmatic person, the muscle around the bronchial tubes are relaxed and the tissue thin, allowing for easy airflow

Six Priority Messages for Asthma (ppt)

The Guidelines are more than 400 pages - the NAEPP decided to condense it into a usable tool for providers - called the Guidelines Implementation Panel Report: six priority messages emerge. Use inhaled corticosteroids Use a writtten asthma action plan Assess asthma severity Assess and monitor asthma control Schedule periodic asthma visits Control environmental exposures 2007 NAEEP -Four Components of Asthma Care Component 1: Assessing and Monitoring Asthma Severity and Asthma Control Component 2: Education for a Partnership in Care Component 3: Control of Environmental Factors and Comorbid Conditions That Affect Asthma Component 4: Medications

Acute Bacterial Pharyngitis and Tonsillitis

The common bacterial etiology includes Streptococcus pyogenes (group A streptococcus), Corynebacterium diphtheriae, Arcanobacterium haemolyticum, Neisseria gonorrhoeae, group C and group G streptococci, and Mycoplasma pneumoniae. Epidemiology The most common bacterial cause of pharyngitis and tonsillitis in children and adolescents is GABHS, which accounts for about 15% to 30% of infections in children with acute sore throat and fever. Group C and group G streptococci can cause pharyngitis, but antibiotic treatment does not prevent its only nonsuppurative complication, glomerulonephritis Arcanobacterium haemolyticum is more common in adolescents but is difficult to culture because the organism grows slowly. Neisseria gonorrhoeae (GC) - cause of adolescent pharyngitis if patient engages in oral sex. Mycoplasma pneumoniae and Chlamydophila pneumoniae are assoc w/ cough along with pharyngitis. C. diphtheriae - extremely rare cause of pharyngitis in the United States. If the throat culture is positive for Staphylococcus aureus, Streptococcus pneumoniae or Haemophilus influenzae, treatment is not needed as these represent normal flora Clinical Findings History GABHS infection: • Most commonly found in 5-15 year-old children; infrequent in children younger than 2 years old • Abrupt onset without nasal symptoms • Constitutional symptoms such as arthralgia, myalgia, headache • Moderate to high fever, malaise, prominent sore throat, dysphagia • Nausea, abdominal discomfort, vomiting, • Presentation in late winter or early spring • N. gonorrhoeae (GC) has no distinctive finding on examination from other pharyngitis. • Lack of a cough or nasal symptoms, along with an exudative, erythematous pharyngitis with a follicular pattern and typical historical findings point to GABHS. • A. haemolyticum causes an exudative pharyngitis with marked erythema and a pruritic, fine, scarlatiniform rash Physical Examination • Petechiae on soft palate and pharynx, swollen beefy-red uvula, red enlarged tonsillopharyngeal tissue • *Tonsillopharyngeal exudate that is yellow, blood-tinged* (frequently) • Tender and enlarged anterior cervical lymph nodes • Bad breath • Stigmata of scarlet fever may be seen—scarlatiniform rash, strawberry tongue, circumoral pallor • Variable presentation; may have mild pharyngeal erythema without tonsillar exudate or cervical adenopathy Diagnostic Tests A rapid strep test (rapid antigen detection test [RADT]) has a high specificity but variable sensitivity; a positive test indicates that a symptomatic person has strep infection and should be treated a negative test does not mean that streptococcal infection is not present It is important not to do a strep test unless the patient has signs and symptoms, since a positive rapid strep test or a positive throat culture can identify a carrier state. The most common tests used to document past GABHS infection: antibody titer to various streptococcal enzymes such as antistreptolysin O (ASO) or anti-deoxyribonuclease B tests (anti-DNase B). The ASO titer rises 1 week postinfection and peaks 3-6 weeks after infection. The DNase B test rises 1-2 weeks after infection, peaks 6-8 weeks following infection, and remains elevated for months even in the face of a mild infection with GABHS. As a result, these tests should not be used to diagnosis GABHS infection in a patient. Management Suppurative complications: otitis media, rhinosinusitis, peritonsillar abscess, mastoiditis, cervical adenoiditis, and meningitis nonsuppurative complications: acute rheumatic fever, acute glomerulonephritis, and poststreptococcal reactive arthritis. antibiotics do not prevent the development of acute glomerulonephritis. If the rapid strep test result is positive, antibiotics should be started immediately. The drug of choice for the treatment of GABHS is penicillin, for children not allergic to it, because of its cost, narrow spectrum of antimicrobial activity, and infrequent adverse reactions • Antimicrobial therapy (based on clinical need)—one of the following Penicillins • Phenoxymethyl penicillin (penicillin V potassium) orally for 10 days: for children less than 60 pounds (27 kg), 250 mg 2 or 3 times a day for 10 days; for children more than 60 pounds, adolescents, or adults, the dose is 500 mg 2 or 3 times a day for 10 days • Amoxicillin suspension often used with young children - more palatable (efficacy seems equal to penicillin). must be taken for 10 days. Amoxicillin at 50 mg/kg once a day to a maximum of 1 g can be used orally for 10 days • Benzathine penicillin G intramuscular (IM) (600,000 units as a single dose if less than 60 pounds [27 kg]; 1.2 million units as a single dose for larger children and adults). If allergic to beta-lactams: • A 10-day course of a narrow-spectrum (first-generation), PO cephalosporin is acceptable, if the child is allergic to penicillin. in up to 5% of penicillin-allergic patients, there is a crossover allergy to cephalosporin. Patients with a type I allergic reaction should not be treated with a first-generation cephalosporin • Clindamycin at 20 mg/kg/day divided in 3 doses for children older than 3 years. • Azithromycin at 12 mg/kg once a day to a maximum of 500 mg. It should be noted that macrolide resistance is as high as 5% to 8% in some parts of the U.S. • Clarithromycin at 15 mg/kg/day divided in 2 doses (maximum 250 mg twice a day) If evidence of penicillin resistance is present, a beta-lactamase- resistant antibiotic can be used, such as amoxicillin-clavulanate or dicloxacillin. • Supportive care—antipyretics, fluids, rest. • Repeat culture is not generally needed except in situations in which it is necessary to ensure eradication of the organism. • Continued symptoms of streptococcal pharyngitis and a positive culture for streptococcus may represent an actual treatment failure or a new infection with a different serologic type of streptococcus. Noncompliance with pharm tx can explain treatment failure, and in these instances, an injection of benzathine penicillin is recommended. For a compliant patient with recurrence, narrow-spectrum cephalosporins, clindamycin, or amoxicillin-clavulanic acid or a combination of penicillin with rifampin are reasonable alternatives • If clinical relapse occurs, a 2nd course of antibiotic is indicated If recurrent infection is a problem, culturing of the family for the chronic carrier state is advised. • Fomites such as bathroom cups, toothbrushes, or orthodontic devices may harbor GABHS and should be cleaned or discarded. • Children can return to school when they are afebrile and have been taking antibiotics for at least 24 hours. Complications Major nonsuppurative late complications caused by GABHS are rheumatic fever, poststreptococcal reactive arthritis, and acute glomerulonephritis. Suppurative complications: cervical adenitis, rhinosinusitis, otitis media, pneumonia, mastoiditis, and retropharyngeal or peritonsillar abscess. Recurrent GABHS tonsillopharyngitis can also be a problem. Sydenham chorea is linked to GABHS infection. the onset or worsening of other neuropsychiatric disorders (obsessive-compulsive disorder, Tourette syndrome, or tic disorder) has been associated with streptococcal infection, PANDAS (pediatric autoimmune neuropsychiatric disorders)

Pathogenesis of Asthma (ppt)

The inflammatory process of asthma causes airway changes, and results in asthma symptoms Viruses, allergens, smoke -> mucosal airway inflammation > bronchial hyperresponsiveness -> bronchospasm and > mucus production -> cough Allergens, sensitizers, viruses, air pollutants -> inflammation: chronic eosinophilic bronchitis -> airway responsiveness -> both lead to symptoms cough, chest tightness, wheeze, dyspnea. Triggers allergens exercse cold air, SO2, particulates allergen -> macrophage/dendritic cell -> th2 cell macrophage <-> eoisinophil allergen -> mast cell -> eosinophil mast cell -> neutrophil mucus hypersecretion, hyperplastia vasodilation new vessels (angiogenesis) mucus plug nerve activation plastma leak edema airway smooth muscle epithelial shedding bronchoconstriction hypertrophy/hyperplasia subepithelial fibrosis sensory nerve activation cholinergic reflex

Indications for Tonsillectomy and Adenoidectomy

Tonsillectomy beneficial in children who are severely affected with recurrent tonsillitis may be helpful in the syndrome of periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis and in obstructive sleep apnea. consider whether a wait-and-see approach is the best strategy to determine if growth and time will negate the need for surgery Cold steel tonsillectomy is associated with less pain and bleeding postoperatively than the traditional method of diathermy Adenoidectomy can also be considered if appropriate medical treatment fails to correct obstructive adenoidal hypertrophy, recurrent or chronic otitis media (after tympanostomy tube placement has been tried), and chronic unresponsive rhinosinusitis. sleep obstructive apnea: tx of choicse is tonsilloadenoidectomy Children with behavioral problems including ADHD may have obstructive sleep apnea as the cause of their ADHD behaviors. Significant morbidity and mortality rates are associated with tonsillectomy including complications such as anesthesia problems, hemorrhage, and infection Approximately 6% of children <3 years experience respiratory complications following tonsillectomy. The morbidity and mortality rates connected with adenoidectomy are not as high

Defense Systems in Children

Young infants and children cannot effectively expectorate mucus, so they swallow it. Cough reflex loss causes aspiration and pneumonia. Temporary breathing cessation, reflex shallow breathing, laryngospasm, and bronchospasm -compensatory efforts aimed at stopping foreign matter from further entry into the lower respiratory tract. Recurrent respiratory infections -> investigation for immunodeficiencies, primary ciliary dyskinesia or cystic fibrosis. mnemonic SPUR determine which children need further workup: S = severe infection P = persistent infection and poor recovery U = unusual organisms R = recurrent infection Immunodeficiencies considered if child has eight or more new ear infections in a year, two or more serious sinus infections, persistent oral candidiasis, 2 or more months on antibiotics without improvement, and/or the need for intravenous (IV) antibiotics to clear infections. if there is recurrent pneumonia, failure to thrive, a family history of immunodeficiency, or two or more deep skin infections

Intro to Respiratory Disorders

a child with a lower respiratory tract disorder such as asthma or bacterial pneumonia - a potentially life-threatening illness that demands prompt attention. ask key questions about the history of the respiratory symptoms; do a systematic and complete examination of the upper and lower airways, including the sinuses; and, if indicated, order specific laboratory tests and radiographic examinations can determine an accurate diagnosis and develop a successful treatment plan in most cases. When children have complicated problems, they can be referred with baseline information to the appropriate medical specialist for additional studies and treatment.

Basic Respiratory Management Strategies a. general b. medication

a. Fluid - Hydration is important to keep mucous membranes and secretions moist. Intake of fluids should be encouraged and parents of young children should be given guidelines regarding the type, amount, and frequency of fluids and feedings that their child should take. • Oxygen administration - help relieve hypoxemia in most children who have acute respiratory distress. Depression of the respiratory drive is possible with supplemental o2 if CNS chemoreceptors are blunted by hypercapnia. at risk are those with issues related to chronic hypercapnia, tend to have chronic severe respiratory diseases such as CF and bronchopulmonary dysplasia. acute situations, administer o2 using an appropriately sized mask or a high-flow O2 source held near the child's face if a mask frightens the child. The safe, acceptable range of O2 saturation is 92% to 95%; higher levels may lead to oxygen toxicity Children seen in primary care settings who require supplemental oxygen should be transported to an acute care hospital setting via emergency medical services for evaluation and stabilization. • Humidification. laryngotracheobronchitis (LTB), taking the child out into the cold night air or opening a freezer door may be beneficial. no evidence for the use of steam or humidification in croup A cold-mist vaporizer helps provide moisture to the nares and oropharynx during a common cold, but the vaporizer must be cleaned daily so that it will not become a source of infection. • Bulb syringe. infants are obligate nose breathers, parents should be instructed in use of the nasal bulb syringe to relieve obstruction of the infant's nares with mucus. Use the bulb syringe gently and intermittently because improper use can cause irritation, inflammation, and respiratory obstruction from tissue damage. Providing parents with written instruction on suctioning the infant's nose with a bulb syringe is advantageous. • Normal saline nose drops, nasal rinses, or spray. Use before feedings and when mucus is thick or crusted. Follow by suctioning the nares with a bulb syringe. Saline nasal rinses are helpful for older children and adolescents. b. • Decongestants and antihistamines should not be used in children <4 years of age use caution in prescribing in children younger <6 years. • Expectorants. Water is one of the most effective expectorants. Do not use in children <4 years • Cough medication. Cough suppressant medications should be prescribed judiciously because coughing is a protective mechanism to clear secretions. the only cough medication recommended is honey, provided the child was > 1 year old - may be the result of a placebo effect

Current Classification of Asthma SeverityNHLBI (NIH) guidelines for children a. 5-11 years b. 0-4 years (ppt)

a. Step 1: intermittent, days with sx </=2/week, nights with sx/nighttime awakenings </=2/month, PEF or FEV1 >/=80%, no interference with normal activity, normal FEV1 in between exacerbations, FEV/FVC >85%, SABA use </=2 days a week Step 2: Mild Persistent. Days with sx > 2 days/week, not daily. Nights with sx 1-4/month, PEF or FEV1 >/=80%, SABA use > 2 days/week not daily, minor limitation in normal activity, FEV/FVC >80% Step 3: Moderate Persistent. Days with sx - daily. Nights with sx: >3/month, or > 1x/week, but not every night. PEF or FEV1 >60%-<80%, SABA use daily, some limitation with normal activity, fEV/FVC 75-80% Step 4: Severe Persistent. Days with sx - continual throughout the day, nights with sx frequent multiple times/week, often 7x/week, PEF or FEV1 </=60%, SABA use several times per day, normal activity extremely limited, fEV/FVC <75% Exacerbations requiring oral systemic corticosteroids: 0-1/year intermittent. >/=2 in 1 year of the rest type b. Well controlled: symptoms </= 2 days/week, nighttime awakening <= 1x/month, no interference with normal activity. SABA <= 2days/week. Exacerbations requiring oral systemic corticosteroids: 0-1 year Not Well controlled: symptoms > 2 days/week, nighttime awakening >1x/month, some limitation with normal activity. SABA >2days/week. Exacerbations requiring oral systemic corticosteroids: 2-3 year Very poorly controlled: symptoms throughout day, nighttime awakening > 1x/week, normal activity extremely limited. SABA sev times a day. Exacerbations requiring oral systemic corticosteroids: >3year Persistent Asthma in Children Need controller therapy Lung function measures (if able) should also be used to assess asthma control

Respiratory System: Physical Exam

anxiety level, respiratory rate and rhythm, use of accessory muscles, color, breath sounds, grunting, and pulse oximetry results. • Measurement of vital signs and observation of general appearance: elevated RR - key indicator of lower respiratory involvement. level of anxiety, nasal flaring, and position of comfort -> respiratory distress. Changes in skin color - subtle or obvious depending on level of deoxygenation. Grunting - small airway disease. • Inspection of: Nose: rhinorrhea—clear, mucoid, mucopurulent; FBs, erosion, polyps, lesions, bleeding; septal position; and color of the mucous membrane. Throat, pharynx, and tonsils: lesions, vesicles, exudate, enlargement of any structure, or other abnormalities. epiglottitis - do not inspect the mouth or attempt to elicit a gag reflex. Chest: depth, ease, symmetry, and rhythm of respiration. use of accessory muscles and the presence of retractions noted. prolonged expiratory phase is assoc w/ respiratory obstruction in the lower airways. • Palpation or percussion (or both) of: Paranasal and frontal sinus: Palpate for signs of sinus tenderness, very insensitive physical assessment finding. Chest: Percuss - dullness or hyperresonance caused by consolidation, fluid, or air trapping. • Auscultation of the chest: Upper tract: noisy breathing, snoring, stridor, rhonchi and referred breath sounds Lower tract: fine crackles or rales, rhonchi, rattles, and polyphonic and monophonic wheezing

key indicators for considering a diagnosis of asthma (ppt)

consider dx of asthma and performing spirometry if any of these indicators are present. not diagnostic by themselves, but the presence of multiple key indicators increases the probability of a diagnosis of asthma. Spirometry is needed to establish a diagnosis of asthma. -Wheezing - high-pitches whistling sounds when breathing out - especially in children. (Lack of wheezing and a normal chest examination do not exclude asthma.) -History of: -cough, worse at night -recurrent wheeze -recurrent difficulty in breathing -recurrent chest tightness symptoms occur or worsen is presence of: -exercise -viral infeciton -animals with fur or hair -house-dust mites (in mattresses, pillows, upholstered furniture, carpets) -mold -smoke (tobacco, wood) -pollen -changes in weather -strong emotional expression (laughing or crying hard) -airborne chemicals or dusts -menstural cycles -symptoms occur or worsen at night, awakening the patient In addition to clinical assessment , Consider diagnostic w/u basic lab test such as CBC to check eosinophil , allergy testing & IgE level if pt is atopic baseline spirometry. Other testing as indicated for assessing other contributing factors or comorbidities.

Asthma Guidelines (ppt)

developed during the past 17 years to increase the awareness of asthma among health professionals, to improve asthma management, to evaluate published reports on asthma and to promote international collaboration in asthma research. The first international guidelines were formulated by the National Heart Lung and Blood Institute (NHLBI) in the USA in 1991 In the USA there are two published evidence based guidelines for the diagnosis and management of asthma that are utilized most often by the medical community: NHLBI Expert Panel report: (2007)EPR3 of the National Asthma Education Programme (NAEPP), & Global Initiative (GINA). NHLBI Guidelines for the Diagnosis and Management of Asthmafocus on four components of asthma care: measures to assess and monitor asthma, patient education, control of environmental factors and other conditions that can worsen asthma, and medications 1991 - the National Heart, Lung, and Blood Institute released guidelines for the diagnosis and management of asthma. 1997 - guidelines updated by the National Asthma Education and Prevention Program's (NAEPP) expert panel. 2002 - An update of selected topics was released by the NAEPP. designed to provide "clinical practice guidelines for the diagnosis and management of asthma." recognizes that the value of clinical practice guidelines depends on their basis in high-quality and current evidence, but that such research may not be ongoing or available for all areas of asthma management. concluded that identifying selected questions warranting intensive review and possible update would be an efficient approach for revising practice guidelines. presents information on medications, monitoring, and prevention. focuses on medication and prevention specifically as they relate to children with asthma. 2007: new guidance for selecting treatment based on a patient's individual needs and level of asthma control and the importance of teaching patients skills to self-monitor and manage asthma and to use a written asthma action plan There are National, State, & Global agencies/ organizations that are actively monitoring, reporting, and researching many aspects of Asthma Some Examples to be familiar with & are good resources: ALA (American Lung Association) CDC (Centers for Disease Control) DOH (Dept of Health), NHBLI( National Heart, Blood & Lung Institute), EPA (United States Environmental Protection Agency), NIEHS (National Institute of Environmental Health Sciences) GINA (Global Initiative for Asthma) WHO ( World Health Organization) FDA (Food & Drug Administration) NAAE(National Association of Asthma Educators) ATS( American Thoracic Society) ACAAI (American College of Asthma, Allergy, Immunology), AAAAI (American Association Of Asthma, Allergy & Immunology), CHEST (American College of Chest Physicians), AAFA ( Asthma & Allergy Foundation of America), AANMA (Allergy & Asthma Network Mothers of Asthmatics) NIH: https://www.nhlbi.nih.gov/sites/default/files/media/docs/asthgdln_1.pdf

Development of Upper Respiratory Tract

maxillary sinuses - second trimester of gestation not fully pneumatized until a child is about 4 years old. Ethmoid sinuses - fourth month of gestation and form the thin lateral walls of the orbit of the eye. pneumatized at birth and can be visualized on plain radiographs when the child is 1 to 2 years old. sphenoid sinuses - first 2 years of life but remain rudimentary until age 6 when they become visible on radiographs. permanent size, but not shape, by age 12 years. the nasal cavity and paranasal sinuses reach adult proportion by age 12 The sinuses become clinically significant sites of infection as follows: • Maxillary and ethmoid sinuses - late infancy • Sphenoid sinuses - third and fourth years of life • Frontal sinuses - sixth to tenth years of life In children <2 to 3 years old, the cricoid ring is the narrowest part of the airway; in older children and adults, the glottis is narrowest. trachea and airways - infant and young child more compliant Hyperextension of the neck can constrict the airway of infants. changes in intrapleural pressure lead to greater changes in an infant's or young child's airways, thereby causing an increased risk of airway collapse. increased chest wall compliance in young infants makes them more vulnerable to adverse events, and their respiratory muscles cannot effectively handle sustained, intense respiratory workload that occurs during severe pulmonary illnesses

Development of the Lower Respiratory Tract

right mainstem bronchus is shorter and wider than the left bronchus. It forms a smaller angle away from the trachea. explains why foreign bodies usually lodge in the right mainstem bronchus. Although the body surface and the number of respiratory airways and alveoli increase 10-fold from birth to adult life, the tissue available for gas exchange increases approximately 20-fold. The newborn's chest is cylindrically shaped and has relatively horizontal ribs, which limits the infant's ability to expand his or her chest. there is greater transverse growth in the lower part of the chest wall, the shape of the chest changes during the first few years of life. results in the ribs being positioned lower anteriorly than posteriorly. The change in positioning of the ribs adds rigidity to the thorax of older children. Primitive airways - fourth week of gestation. sixteenth week of gestation - the number of bronchial branches equals that in adults. Subsequent growth continues by increasing the length of the respiratory tract. sixteenth to twenty-sixth weeks of gestation, vascularization of the future respiratory portion of the lung occurs. Cartilage, glands, and muscles of the airways and type II alveolar cells - week 28. Type II cells allow the fetus to produce a phospholipid called surfactant. The airways continue to grow, and terminal sac formation occurs. week 36 - the terminal sacs divide, and alveoli are formed. 50 million primitive alveoli - birth. After birth the alveolar ducts branch off the third respiratory bronchioles. Alveoli continue to form and number 100 to 200 million in older children and 200 to 600 million in adolescents. The alveolar sacs continue to increase in size. The adult lung contains approximately 300 million alveoli. present at birth - cartilage, mucus glands, goblet cells, and ciliated cells of the conducting airways. Smooth muscle is also present; therefore, even very young infants can have bronchospasm. Airway resistance is higher in newborns and young children. The airways of young infants and children are easily obstructed by inflammation, FBs, or mucous. The maximal inspiratory pressure generated by an infant is equal to that of an adult. the chest wall and supporting structures are softer and more flexible, so chest wall retraction is greatest in young infants. The chest wall of a newborn is highly compliant.

Asthma: Epidemiology (ppt)

third leading cause of preventable hospitalizations in the United States* TAKE HOME MESSAGE Most hospitalizations for asthma can be prevented USA Asthma Prevalence 2001-09 The proportion of persons of all ages with asthma in the United States increased from 7.3% (20.3 million persons) to 8.2% (24.6 million persons). A rising trend in asthma prevalence was observed across all demographic groups studied. Asthma is common, deadly, disruptive, and expensive. 1 in 11 children have asthma black children are 2x more likely to have asthma than white children 1 in 5 children with asthma went to ER for asthma related care in 2009 in 2009 479000 asthma related hospitalizations 1.9 million asthma related ED visits 8.9 million asthma related doctor visits 9 people die from asthma every day Black Americas are 2-3 times more likely to die from asthma than any other racial or ethnic group 1 in 2 children with asthma report missing at least 1 day of school each year because of asthma 3 in 5 people with asthma limit their physical activity nearly 1 in 3 adults with asthma report missing at least 1 day of work each year because of asthma asthma costs our nation $56 billion per year 1 in 4 back adults can't afford their asthma medications 1 in 5 hispanic adults can't affort their asthma meds Asthma Surveillance http://www.cdc.gov/asthma/asthmadata.htm A rising trend in asthma prevalence was observed across all demographic groups studied.