pulmonology Flashcards
epiglottitis
-MC associated with Haemophilus influenzae; streptococcal species in immunized patients
-Sudden onset of high fever, dysphagia, drooling, muffled voice, inspiratory retractions, cyanosis, and soft stridor
-Pts sit in “sniffing dog” position (neck hyperextended, chin stretched forward)
-Progression to total airway obstruction may occur and result in respiratory arrest
-Definitive dx: Direct inspection of epiglottis (OR during intubation) > cherry-red and swollen epiglottis
-Imaging: Lateral neck radiograph > “thumbprint” sign caused by swollen epiglottis
-Treatment:
-Endotracheal intubation to establish airway
-Blood and epiglottis cultures performed
-IV antibiotics (ceftriaxone or equivalent cephalosporin) x 2-3 days, followed by PO abx x 10 days
-Extubation within 1-2 days, when reduction in size of epiglottis is evident
laryngomalacia
-Congenital disorder in which the cartilaginous support for the supraglottic structures is underdeveloped
-Manifests as inspiratory stridor in infants, usually within the first 6 weeks of life -> Stridor worse with supine positioning, increased crying, URIs, and feeding
-Typically, benign and resolves by 2 years of age
-Treatment:
-Mild (no stridor at rest, no retractions): Treatment usually not needed
-Severe (stridor at rest, retractions, OSA, increased work of breathing, feeding difficulties, FTT): Laryngoscopy > surgical supraglottoplasty (remove excess tissue)
croup
-MCC is parainfluenza virus serotypes; children 6 months – 5 years in fall and early winter
-Edema in the subglottic space accounts for predominant signs of upper airway obstruction (inflammation of entire airway is typically present)
-Prodrome of URT symptoms, followed by barking cough, laryngitis, and stridor
-Mild: Stridor only with agitation
-Worsening obstruction: Stridor at rest, retractions, air hunger, cyanosis, hypoxemia
-Imaging: Not indicated (possible in atypical presentations to rule out other causes)
croup tx
-Mild croup: Supportive, hydration; with or w/o dexamethasone
-expose child to cold moist air
-Dexamethasone: 0.15-0.6 mg/kg PO/IV x 1 dose
-Alternative/adjuvant therapy: Prednisolone (1 mg/kg) QD x 3 days and/or inhaled budesonide
-Severe/stridor at rest: Nebulized racemic epinephrine (diluted in sterile saline!)
-give dexamethasone too (prevents rebound)
-Sx resolution within 3-4 hours of glucocorticoids/nebulized epinephrine -> safely discharged without fear of rebound
-If recurrent doses of nebulized epinephrine treatments required > admission for observation, supportive care, and repeat steroid dosing/neb treatments as needed
-Impending respiratory failure > intubation with endotracheal tube, with extubation within 2-3 days
asthma
-Chronic airway inflammation with hx of respiratory symptoms such as wheeze, SOB, chest tightness, and cough
-Vary over time and in intensity, along with variable expiratory limitation
-MC chronic ds of childhood (6.2 million children in U.S.)
-M > F, black children > Hispanic and non-Hispanic white children, low socioeconomic status
-Up to 80% of kids develop sx prior to 5 years of age
-Approx 40% of infants/young children who have wheezing with viral infections in first few years of life will have continuing asthma through childhood
-Strongest predisposing factor is atopy (personal or familial)
-Sensitization to inhalant allergens increases over time
-Principal allergens: Perennial (dust mite, animal dander, cockroach, soil mold)
-Triggers (besides allergens): Tobacco smoke exposure, exercise, cold air, pollutants, chemical odors, and rapid changes in barometric pressure
-Shedding of airway epithelium, edema, mucus plug formation, mast cell activation, and collagen deposition beneath basement membrane
-Inflammatory cell infiltrates > bronchial hyperresponsiveness, airflow limitation, disease chronicity
-Airway wall remodeling/irreversible changes
asthma sx
-Dx based largely on judgment and assessment, activity limitation, and quality of life
-Wheezing is most characteristic sign -> Also, “chest congestion,” prolonged cough, exercise intolerance, dyspnea, and recurrent bronchitis/PNA
-Auscultation: Prolonged expiratory phase with wheezing
-Increased severity: High-pitched wheeze with diminished breath sounds
-Severe obstruction: No wheeze because of poor air movement
-Flaring of nostrils, intercostal and suprasternal retractions, use of accessory muscles
-Cyanosis of lips/nail beds with underlying hypoxia
-Tachycardia/pulsus paradoxus
-Agitation/lethargy may be signs of impending respiratory failure
asthma: lab findings: Airflow assessment
-Spirometry
-FEV1 (forced expiratory volume in 1 second) and FEV1/FVC (forced vital capacity – volume exhaled in 1 breath) – Diminished
-Emphasis placed on documenting excessive variability in lung function
-Following treatment administration, + exercise challenge test, + bronchoprovocation test, variation in lung function between visits
-PEFR monitoring: Children with moderate to severe asthma, history of severe exacerbations, or poor perception of airflow limitation/worsening condition
-Body box plethysmography to determine lung volume measurements
-RV, FRC, and TLC usually increased in asthma (air trapping/hyperinflation), VC is decreased
-Infants sedated with compression techniques/forced oscillation
asthma: lab findings: bronchial hyperresponisveness
-To stimuli such as inhaled pharmacologic agents (histamine, methacholine, and mannitol) or physical stimuli (exercise/cold)
-Mannitol bronchoprovocation approved by FDA
-Simulates airway responses to specific physiologic situations by creating an osmotic effect within the airway, subsequently resulting in an inflammatory response
-Typically note a 15-20% drop in FEV1 (depending on agent/stimulus)
other findings in asthma
-Pulsus paradoxus
-Early findings: Hypoxemia, normal PaCO2, respiratory alkalosis
-Later findings:
-< 91% and respiratory acidosis indicative of significant obstruction
-With metabolic acidosis > impending respiratory failure
-Hypercapnia once FEV1 < 20% predicted value
-PaO2 < 60 mmHg, PaCO2 > 60 mmHg/rising > 5 mmHg/hour: Relative indications for mechanical ventilation in a child with status asthmaticus
-Imaging: Not indicated
asthma assessment
-Severity directs level of initial therapy
-2 general categories: Intermittent and persistent (mild, moderate, severe)
-Most accurate in pts not receiving controller therapy
-Already on therapy -> classified according to level of med requirement to maintain control
-Control refers to degree to which symptoms, ongoing functional impairments, and risk of adverse events minimized/goals of therapy met
-Performed at every visit
-Categorized as “well-controlled,” “not well-controlled,” and “very poorly controlled”
asthma: assessment (risk)/step of therapy
asthma: control assessment (impairment)
asthma: control assessment (risk)/recommended action
asthma: stepwise management approach
asthma: pharm therapy
-Long-term controller medications and quick-relief medications (SABAs)
-Long-term: Anti-inflammatory agents (inhaled corticosteroids, leukotriene modifiers), long-acting bronchodilators (and LAMAs), and biologics
-Inhaled corticosteroids (ICS)
-Most potent inhaled anti-inflammatory agents
-Low-dose ICS can provide adequate control, but some patients may need higher doses (step up) due to variable responsiveness -> Greater risks for systemic adverse effects with higher doses
-Early intervention can improve control and prevent exacerbations, but do not prevent development of persistent asthma/alter course
-Delivered in different devices – MDI, dry powder inhaler (DPI), and nebulized aerosol suspensions
-ICS + LABA (salmeterol, formoterol, and vilanterol)
-LABAs are beta-agonists
-Latest guidelines > preference of ICS-LABA as maintenance therapy (Step 3 and above)
-Formoterol tends to be the preferred add-on LABA
-Quick onset of action
-Found to reduce exacerbations and provide control at relatively low-maintenance ICS dose requirement
-Leukotriene antagonists (montelukast, zafirlukast)
-Monotherapy or add-on therapy (alternate/in addition to LABA)
-Long-acting muscarinic antagonists (tiotropium)
-Approved for QD maintenance (6 years and older) as an add-on to ICS-LABA
-Can be added to an ICS as independent adjunct only if LABA cannot be used in certain individuals (unable to tolerate/use drug/device or have contraindications to LABA)
asthma: pharm therapy: biologics and theophylline
-Biologics (omalizumab, mepolizumab, dupilumab)
-Moderate-severe asthma, symptoms inadequately controlled with medium-high dose ICS
-Effective at reducing exacerbations, improving lung function and symptom control, and decreasing oral corticosteroid use
-Theophylline, PO corticosteroids rarely utilized
asthma: pharm therapy: SABAs
-Quick relief medications: SABAs (albuterol, levalbuterol, pirbuterol, terbutaline)
-Nebulizer, MDI, DPI
-Better to use PRN versus regularly
-Anticholinergics (ipratropium), systemic corticosteroids (prednisone, prednisolone, methylprednisolone) as supplements
asthma: monitoring
-Regular follow-up visits are important to assess degree of control and consider appropriate adjustments in therapy
-At each step, patients should be instructed to avoid/control exposure to allergens, irritants, or other factors that contribute to asthma severity
-Consider referral to specialist:
-< 5 years: Moderate, persistent; Step 3 or 4 care; considered for Step 2
-> 5 years: Step 4 or higher; considered for Step 3
-Considered for allergen immunotherapy or biologic consideration
asthma: exercise-induced bronchospasm
-Occurs minutes after vigorous activity, peaks 5-10 minutes after stopping, resolves over 20-30 minutes
-Tx prior to physical activity or exercise usually effective (if only manifestation despite being otherwise “well-controlled”)
-SABAs, LTRAs, cromolyn, or nedocromil
-SABA + cromolyn or nedocromil even more effective
-Salmeterol and formoterol may block bronchospasm up to 12 hours; montelukast up to 24 hours
-Promote extended warm-up period
asthma: acute exacerbation
-Home
-SABA, 2-6 puffs from MDI, every 20 minutes, up to 3 times; or via nebulizer
-Improvement > continue every 3-4 hours x 1-2 days
-Failed completion of improvement > SABA + PO corticosteroid
-Marked distress > ED or 911 for assistance
-Office/ED
-PFTs (when feasible), pulse oximetry -> Maintain oxygen > 90%
-FEV1 or PEFR > 40%: SABA (nebulizer or inhaler) x 3 doses in first hour; with or without PO corticosteroids
-FEV1 or PEFR < 40%: High-dose SABA + ipratropium bromide q 20 minutes x 3 doses; supplemental oxygen PRN; corticosteroids
-Impending/ongoing respiratory arrest > intubated/ventilated with 100% oxygen, IV corticosteroids, ICU admission
-ICU admission: FEV1 or PEFR < 25%, less than 10% improvement after treatment/values that fluctuate widely
asthma: acute exacerbation: pt discharge
-Sustained response of bronchodilator therapy of at least 1 hour or greater than 70% of predicted/personal best and oxygen saturation > 90% in room air
-Action plan given, reviewed
-Inhaled SABA and PO corticosteroid x 3-10 days
-F/U and specialist recommendations provided
bronchiolitis/respiratory syncytial virus
-Ds of small bronchioles with increased mucus production and occasional bronchospasm, sometimes leading to airway obstruction
-MC in infants and young children; potentially life-threatening -> Leading cause of hospitalization of infants
-MCC is respiratory syncytial virus (RSV), though other viruses may cause
-Extremely contagious via contact with infected respiratory secretions
-Incubation of 4-6 days
-Presents as a progressive respiratory illness similar to common cold (rhinorrhea and cough)
-Young infants may not have a prodrome – apnea may be first sign!
-Progresses over 3-7 days to noisy, raspy breathing with audible wheezing
-EDUCATE THE PARENT IT WILL GET WORSE BEFORE IT GETS BETTER
-Bronchiolar obstruction: Prolonged expiratory phase, nasal flaring, intercostal retractions, suprasternal retractions, air trapping
-Auscultation: Diffuse wheezes and crackles
-More severe disease: Grunting, cyanosis
bronchiolitis/respiratory syncytial virus dx and tx
-Laboratory/Imaging Studies
-Pulse oximetry - 90-91%
-Rapid viral diagnosis of NP secretions via PCR (not necessary for diagnosis)
-CXR: Lung hyperinflation/flattened or depressed diaphragms, areas of increased density
-Treatment
-Supportive therapy: Respiratory monitoring, fever control, hydration, upper airway suctioning, supplemental oxygen
-Hospitalization: Respiratory distress, hypoxemia, apnea, inability to tolerate oral feeding, high-risk children
-Abx, bronchodilators, corticosteroids, chest physiotherapy, and hypertonic saline seldom effective
bronchiolitis/respiratory syncytial virus: complications and prevention
-Complications/Prognosis
-Most hospitalized children show improvement in 2-5 days with supportive treatment alone
-Tachypnea, hypoxia > rapid progression to respiratory failure > assisted ventilation
-Incidence of asthma higher in children hospitalized for bronchiolitis as infants
-Mortality rate highest among infants with pre-existing cardiopulmonary or immunologic impairment
-Prevention:
-Monthly injections of palivizumab (RSV-specific monoclonal antibody), just before onset of RSV season (December through March in U.S.)
-Indicated for infants with prematurity (< 29 weeks gestation), chronic lung disease of prematurity, hemodynamically significant cyanotic and acyanotic congenital heart disease in first year of life
influenza
-MC A/H1N1, A/H2N2, and B; isolated avian and swine outbreaks
-Infection rates in children > adults – initiate community outbreaks
-Incubation period is 2-7 days, spread via respiratory droplets
-Sudden onset high fever, severe myalgia, headache, and chills -> Overshadow coryza, pharyngitis, and cough
-Fever, diarrhea, vomiting, and abdominal pain are common in young children
-Infants may develop a sepsis-like illness and apnea
-Acute illness lasts 2-5 days, viral shedding may persist for several weeks in children
-Testing: PCR has highest specificity and sensitivity (nearly 100%)
influenza tx, complications, prevention
-Treatment
-Supportive care, management of pulmonary complications (bacterial superinfection)
-Antivirals: Useful if within 48 hours of symptom onset (oseltamivir) x 5 days
-Discuss side effects with parents!
-Complications/Sequelae
-LRT symptoms MC in children < 5 years
-Hospitalizations MC in children < 2 years
-Secondary bacterial infections (lungs, ears, sinuses)
-Encephalitis, myositis
-Prevention
-Trivalent and quadrivalent vaccines (IIV or LAIV) recommended for all individuals 6 months and older
-Prophylaxis with oseltamivir used in select cases of children > 3 months; inhaled zanamivir in children > 5 years
pertussis (whooping cough)
-Caused by Bordetella pertussis (only infects humans, transmitted via coughing)
-Incubation period 7-10 days, patients most contagious during the first 2 weeks of cough
-Peaks among those less than 6 months of age (too young for complete immunization + most likely to have severe complications)
-Catarrhal stage: 1-2 weeks
-Non-specific signs (low-grade fever, nasal congestion)
-Paroxysmal stage: 3-4 weeks duration
-Coughing occurs in paroxysms during expiration (to dislodge plugs of necrotic bronchial epithelial tissues and thick mucus)
-Forceful inhalation against narrowed glottis that follows = “whoop”
-Convalescent stage: 1-2 weeks
-Gradual resolution of symptoms
pertussis (whooping cough): dx and tx
-Dx:
-Isolation of B. pertussis or detection of nucleic acids (PCR)
-Culture from NP swabs or aspirates
-Lymphocytosis present in 75-85% of infants and young children, but not diagnostic
-Radiograph: Segmental lung atelectasis, perihilar infiltrates
-Treatment
-Macrolides (azithromycin, clarithromycin, erythromycin)!
-Complications/Prognosis:
-MC is PNA (primary or secondary)
-Other complications: Atelectasis, free air (from paroxysms), epistaxis, hernias, retinal/subconjunctival hemorrhage, OM, sinusitis
viral pneumonia
-Common cause of CAP in children < 2 years
-MCC: Human rhinovirus, adenovirus, parainfluenza, influenza, coronavirus, and human metapneumovirus
-URI commonly precedes onset of lower respiratory disease
-Wheezing/stridor may be more prominent than in bacterial PNA
-Cough, respiratory distress, rales, decreased breath sounds more non-specific
-Dx:
-Fluorescent antibody, ELISA, and/or PCR only if it will change management, for high-risk patients, or for epidemiology/infection control
-Imaging not indicated in B/L, symmetrical findings on exam, no significant distress, no temperature
-Findings non-specific: Hyperinflation, peribronchial cuffing, increased interstitial markings, and subsegmental atelectasis
-Tx:
-supportive; no evidence to support use of antibiotics
bacterial pneumonia
-CAP is MCC of childhood mortality worldwide
-MCC of bacterial PNA in children of all ages is Streptococcus pneumoniae
-Usually follows a lower respiratory tract infection
-Compromised pulmonary defense systems increase risk of PNA
-Abnormal mucociliary clearance, impaired cough function, immunocompromised state, aspiration of oral secretions, or intake and malnutrition
-Hallmarks: Fever, tachypnea, and cough
-Respiratory distress and hypoxemia are signs of more severe disease
-Auscultation: Focal crackles or decreased breath sounds in setting of consolidation/effusion
bacterial pneumonia: labs and tx
-Dx:
-CXR: Indicated for those hospitalized or to assess for complications
-Lab studies only for hospitalized patients
-Blood cultures, inflammatory markers, CBC (for complications)
-Sputum cultures
-Tx:
-< 4 weeks of age: Ampicillin + aminoglycoside
-4-12 weeks of age: Hospital admission, IV ampicillin x 7-10 days -> Similar for 3-6 months
-> 6 months of age: High-dose amoxicillin (divided into 2 or 3 doses, daily) x 7 days
-Additional therapy: Oxygen, hydration/electrolyte supplementation, and nutrition
mycoplasma pneumonia
-MC in children > 5 years of age, long incubation (2-3 weeks), onset of symptoms is slow
Clinical Manifestations
-Fever, headache, cough, chest pain, malaise
-Cough dry at onset, sputum production later
-Sore throat, OM, OE, and bullous myringitis may occur
-Rales, decreased breath sounds, or dullness to percussion may be present
-Diagnosis
-PCR is gold standard for diagnosis
-CXR: Interstitial or bronchopneumonic infiltrates
-Treatment: Macrolide x 5-10 days, supportive measures
cystic fibrosis
-Autosomal recessive
-chronic sinopulmonary infections, malabsorption, and nutritional abnormalities
-Defect in gene that encodes epithelial chloride channel called the CF transmembrane conductance regulator (CFTR) protein
-Alters salt and water movement across cell membrane -> abnormally thick secretions in various organs
-One of MC lethal genetic ds in U.S. (1:3000 Caucasian, 1:9,200 Hispanic)
-Most develop obstructive lung ds assoc with chronic infection and progressive loss of pulmonary function
cystic fibrosis sx
-Approx 15% of newborns with CF are born with meconium ileus
-Severe intestinal obstruction resulting from inspissation (high viscosity) of tenacious (adherent) meconium in terminal ileum
-Virtually diagnostic -> further testing always indicated regardless of screening results
-FTT due to malabsorption from exocrine pancreatic insufficiency (failure of pancreas to produce sufficient enzymes to digest fats and protein)
-Failure to gain wt despite good appetite
-Frequent, bulky, foul-smelling, oily stools
-Hypoproteinemia, anemia, deficiency of fat-soluble vitamins (ADEK)
-Severe dehydration and hypochloremic alkalosis, bronchiectasis, nasal polyps, chronic sinusitis, rectal prolapse, or unexplained pancreatitis or cirrhosis
-Respiratory symptoms: Productive cough, wheezing, recurrent PNA, progressive obstructive airway disease, exercise intolerance, dyspnea, or hemoptysis
-Infections with S. aureus and H. influenzae (first few months), then P. aeruginosa
-Chronic infection -> airflow obstruction and progressive airway/lung destruction -> bronchiectasis and lung function decline
-Pulmonary exacerbations: Increased cough and sputum production, decreased exercise tolerance, malaise, wt loss, and decrease in measures of lung function -> tx -> Abx and augmented airway clearance
cystic fibrosis dx and tx
-Diagnosis
-All states in U.S. perform newborn screening for CF ->
Measure immunoreactive trypsin (IRT), a pancreatic enzyme
most with CF have an elevated IRT
-+ screen -> confirmation via sweat testing and/or mutation analysis
-Sweat chloride concentration > 60 mmol/L following an abnormal newborn screen or when obtained for clinical symptoms or family history of CF
-Genotyping that reveals two disease-causing CFTR mutations
-Treatment (multidisciplinary by accredited CF foundation)
-GI: Pancreatic enzyme supplementation, high calorie/protein/fat diet, daily multivitamins (ADEK), salt supplementation
-Respiratory: Airway clearance therapy and aggressive abx use
-Inhaled hypertonic saline, inhaled abx (tobramycin, aztreonam), PO azithromycin, bronchodilators, anti-inflammatories
-Protein-rescue therapies (CFTR modulators – 4 currently FDA-approved)
-Directly target underlying defects in CFTR
-Approval in younger age ranges > life expectancy to increase (median 40 years of age)
foreign body aspiration
-Significant cause of death each year
-6mo–3yo at highest risk
-Typically lodges in supraglottic airway (protective mechanisms -> laryngospasm), smaller objects (coins) my pass glottis and obstruct trachea
-Acute onset, inability to vocalize/cough (complete obstruction) and cyanosis with marked distress
-Progressive cyanosis -> LOC -> seizures -> bradycardia -> cardiopulmonary arrest
-Drooling, stridor, ability to vocalize (partial obstruction)
-Lower respiratory tract: Asymmetrical physical findings – decreased breath sounds, localized wheezing, recurrent PNA in one location (chronic cough is suspicious as well)
-Diagnosis: Gold-standard is rigid or flexible bronchoscopy (rigid is standard for removal)
-Treatment
-Prevention is key! ->Counsel parents on age-specific, safe foods and toys
-Upper airway obstruction:
-Partial: Cough reflex to remove FB
-Complete: BLS/PALS guidelines!
-Never blind sweeps
-Open airway with jaw thrust – FB visualized > remove
-If becomes unresponsive > CPR (chest compressions may help to dislodge FB)
-Lower airway FB:
-Rigid bronchoscopy under general anesthesia
-Followed by B-adrenergic neb treatments + chest physiotherapy
-Complications: Failure to identify FB > bronchiectasis, lung abscess
test
know if pt is well controlled or not - should we step up?
-place a dx (severity of asthma)
