20. Differences between it and asthma: the dyspnea is primarily inspiratory, noise occurs on inspiration, does not respond to brochodilators, no hyperinflation on CXR, PFTs show a variable flattening of the inspiratory limb of the flow-volume curve (is the expiratory limb in asthma)
22. Know the clinical manifestations of acute hypercapnea: flushing, agitation, confusion, tachycardia, HA
23. Look for a case where a pediatric patient is being under-ventilated, i.e. giving breaths at too slow a rate while being BVMed
24. Know the potential risks and benefits of administering oxygen to children with chronic respiratory failure
25. The respiratory drive of some of these patients is dependent on hypoxemia, and correcting the hypoxemia could lead to respiratory arrest; goal should be to use the lowest amount of supplemental O2 possible to maintain an SaO2 of 90%
26. Know when to intubate and when to provide oxygen therapy in patients with respiratory failure of various etiologies
27. Failure to respond to O2 administration indicates the need for more aggressive management such as BVM or intubationf there is a process that is affecting their neurologic or neuromuscular processes and interfering with their ability to generate adequate tidal volumes, then earlier intubation would be likely
41. Usually begin with an uncomplicated URI, but the cough lingers for months to years; will see a repetitive coughm cessation during sleep, and a hacky/barky nature to the cough
42. Recognize cough as a major and at times singular manifestation for asthma
45. Best rec is to use saline nasal drops, suctioning
46. Know the initial screening evaluation of chronic cough should include x-ray study if the chest, a sweat test, tuberculin skin test, and PFTs before resorting to other tests
47. Know which conditions that occur in childhood impair the effectiveness of cough: CO, muscle weakness, vocal cord dysfunction, CNS disease, thoracic deformities, pain
49. Know that exercise intolerance may reflect etiologies other than pulmonary disease: anemia, muscle weakness, deconditioning, cardiac disease, psychogenic causes
50. Exercise intolerance = failure to tolerate physical exercise at the level that would be expected for the person’s age and condition
52. Know that exercise intolerance may be a presenting sx of CLD (e.g. asthma, interstitial lung disease) or vocal cord dysfxn
53. Asthma = shortness of breath, chest tightness, cough about 10-15 mins after beginning exertion, nighttime cough
54. Vocal cord dysfxn= paradoxic adduction of vocal cords during inspiration, causing airway obstruction during exercise; also with inspiratory wheezing and throat tightness ; NO night time cough
59. Central sleep apnea is a problem in which they lack the ability to sense hypercapnea
60. Obstructive sleep apnea = a disorder of breathing during sleep characterized by prolonged or partial airway obstruction or intermittent complete obstruction that disrupts normal ventilation during sleep and normal sleep patterns
72. Have to differentiate it from apnea due to positions (neck overflexed), GER with reflex glottic closure and cessation of airflow, and mechanical obstruction of trachea or larynx
88. Anemia of prematurity can contribute to apnea of prematurity when profound (usually if hgb<7), but is a late phenomenon occurring 2-4 weeks after birth
93. Kids who wheeze during infancy continue to wheeze after age 6 about 15% of the time; also about 15% of asthmatics will develop wheezing after age 6
95. Know when to consider foreign body in the ddx of recurrent wheezing
96. Age (older infants and toddlers), abrupt onset of symptoms especially if after eating “danger” foods (popcorn, nuts, hot dog), previously without sx or a long time since any respir probs
97. If the hx strongly suggests FB aspiration, they need prompt rigid bronochoscopy; can’t often see the effects of the FB for up to 24 h after aspirated (air trapping)
98. Contrary to popular belief, the aspiration of a small foreign body, including food, is as common in the left as the right mainstem bronchus in young children because the bifurcation of the trachea remains symmetric until the aortic knob grows larger in later childhood
107. More rare causes include vasculitides (HSP, Wegener’s, Goodpasture’s and SLE), congenital heart or lung defects,vneoplasm, AV malformation, hemangioma, trauma, PE and idiopathic
108. Know the initial management of hemoptysis in children and adolescence
111. After bleeding is controlled a bronchoscopy with BAL is done; look for hemosiderin laden macrophages (are diagnostic for pulm bleeding, don’t usually appear until 3 days after bleed)
112. Management is usually supportive, follow the ABCs of life support, might need embolotx of severe
144. Epiglottitis: appear toxic, have inspiratory stridor, rarely a coughthumb sign; enlarged epiglottis protruding from the anterior wall of the hyopharynx
145. Bacterial tracheitis: toxic appearing, high fever, tachypnea, brassy cough; imaging = subglottic narrowing and a ragged tracheal air column
146. Know the risks of examination in a patient with suspected epiglottitis
153. Recognize that congenital malformations of the lung (e.g. hypoplastic left lung, cystic adenomatoid malformation) may cause respiratory signs and symptoms
155. Intrapulmonary is most common (75-90% of cases); it presents later in life and is usually associated with recurrent unilateral pneumonias, cough, wheezing, fevers
156. Extrapulmonary are far less common and present in early infancy (prior to age 6 months) and in conjunction with other congenital abnormalities
157. Bronchogenic cysts are usually asx and found incidentally on cxr; sometimes present as airway compression or infection
158. Congenital cystic adenomatoid malformation (CCAM) is usually identified on prenatal ultrasound or present in the newborn period with respiratory distress; they may involve the entire lung, they may be associated with other abnormalities; if presenting later may do so with recurrent pneumonia, but would be earlier in life than a pulm sequestration
186. Less common causes include allergic bronchopulmonary aspergillosis, primary ciliary dyskinesia, immunodeficiency and recurrent infections (TB, pertussis, measles); foreign body aspiration can be a cause as well
187. Know that high res CT of the chest is useful to dx it in a child
195. Occurs during inspiration due to collapse of supraglottic structures unable to remain open during times of increased intrathoracic pressure
196. Exacerbated during times of crying or agitation; may be relieved when infant is in prone position
197. Usually resolve spontaneously in the first postnatal year; should also consider other problems like GER that can exacerbate it, and tx those comorbid conditions
205. toxic appearing, high fever, tachypnea, brassy cough; imaging = subglottic narrowing and a ragged tracheal air column
206. Know the clinical course of bacterial tracheitis, including biphasic illness, precipitous worsening, requirement for intubation, and relatively prolonged intubation
207. Often have sx of a croup-like illness for a few days and then a sudden deterioration with spiking fevers, increased hoarseness, toxic appearance, stridor, rtx and decreased O2 sats
220. AgePathogenComments3weeks to 3 monthsC. trachomatisRSVParainfluenzaS. pneumoBordatella pertussisVertical transmissionAfebrileInterstitial infiltrates on cxrBronchiolitis with wheezing most commonOnset usually late fallBronchiolitis or pneumoniaSeen fall through springMajor bacterial cause through childhoodTracheobronchitis with severe paroxysmal cough, no feverPneumonia occasionally seen; usually related to aspiration3 months to age 4 yrsRSV, parainfluenzae, human metapneumovirus, influenza, rhinovirusStrep pneumoMycoplasma pneumoniaMost toddler pneumonia is viralMajor treatable pathogen in this age groupPossible in all agesIncreased incidence in children approaching school age5yrs through adolescenceM pneumoniaC. pneumoniaS pneumoTBMajor treatable cause in school age children and adolescenceAlso an important cause, similar clinical presentation to mycoplasmaStill an important causeComplications, especially empyema, often ensuePrimarily in areas or populations of high TB prevalenceHigher risk at puberty and in pregnancy
221. Know the major acute and chronic complications of pneumonia, including empyema, sepsis, ptx, bronchopleural fistula, and pneumatoceles
222. Necrotizing pna: rare; liquefaction and necrosis of lung tissue due to toxins of highly virulent organisms
223. Lung abscess: usually develop after an aspiration event, frequently involve mouth organisms like streps, anaerobes, gram negative rods
224. Empyema: kids usually present wih persistent fever, decreased appetite, fatigue, chest pain and some degree of respiratory distress; usually requires surgical intervention of some kind (chest tube, VATS)
225. Bronchopleural fistula: development of a connection between the bronchial tree and the pleural space. Is associated with a pretty high morbidity and mortality (30-70%) and requires surgical repair. Usually seen in a very sick kids, if on a vent would likely have an air leak
227. SyndromeTypcal causeAge groupTypical clinical featuresBacterial (suppurative)Pneumococcus, othersAll ages; younger children (<6mos) more commonAbrupt onset, high fever, ill/toxic appearance, more focal findings on exam, chest/abd pain, focal infiltrate if CXR is obtainedAtypical – infancyC. trachomatis<3mostachypnea, mild hypoxemia, lack of fever; wheezing, interstitial infiltrates on CXRAtypical – older childrenMycoplasma>5ygradual onset, low grade fever, diffuse exam findings, diffuse infiltrates if CXR obtainedViralMultiple All ages; 3mos – 5yrs more commonProminent URI sx, low grade or absent fever, diffuse findings/wheezes on exam, possible diffuse interstitial infintrates if CXR obtained
228. Know the lab tests for pneumonia, including x-ray study of the chest, blood cx, CBC, urine antigen detection studies, serology for mycoplasma, sputum cx
230. If being managed inpt the recs are for getting CBC, blood cx, chem panel; sputum cx of possible to test for bacterial pathogens; nasopharyngeal secretions can be tested for viral resp tract pathogens
247. Recurrent pna = more than one radiographically confirmed episode in a year, or more than three episodes in a lifetime, with clinical or radiographic resolution between episodes
248. Ddx includes anatomic lesions, i.e. vascular rings, cysts, pulmonary sequestration; resp tract disorders like CF, GER, aspiration, and immune disorders
257. Know the initial stabilization maneuvers for a newborn infant with DH
258. Know that DH is associated with persistent pulmonary htn, and sybsequent abnormalities including poor growth, tracheomalacia and developmental delay
269. Exudative stage – rapid development of respiratory failure; characterized by profound hypoxemia and atelectasis, sometimes resolves in 3-7 days, but can progress to
270. Inflammatory stage – fibrosing alveolitis and surfactant deficiency; characterized by persistent hypoxemia, decreased lung compliance, and development of pneumothoraces
271. Resolution – may eventually recover normal lung function; final stage consists of resolution of hypoxemia and improved lung compliance;c omplete resolution may take 6-12 months but some develop lifelong restrictive lung disease, lung cysts, or decreased exercise tolerance
299. Must have two mutations on both copies of the CFTR gene in order to be affected
300. For a healthy person whose parents are known carriers, the risk of being a carrier of a mutated CFTR gene is 2/3
301. Of the 4 possible outcomes from that person’s parents, one in four would have two mutated genes, and hence not be “healthy” so they are taken out of the equation on this tricky little scenario (question 2010: 151)
303. Accounts for about 10% of all reported cases of RP during infancy and early childhood
304. RP occurs in about 20% of patients with CF between age 6months and 3 years
305. This was in question 2010: 225, and the scenario was of a child whose weight/height were mismatched, had chronic constipations, and experienced the rectal prolapse after being txed for constipation and passing soft stools – these were supposed the be the CF “red flags”
306. Know the neonatal non-pulmonary manifestations of CF: meconium ileus, meconium peritonitis, prolonged jaundice
307. Mec ileus thick mec obstruction in the distal ileum, usually presents as a small bowel obstruction; consider in newborn with delayed passage of stool and bile stained emesis; abd film may show stacked loops of variably dilated bowel, soap suds bubbly like appearance of the mec (often in the RLQ); distal bowel with paucity of bowel gas
308. Mec peritonitis bowel obstruction leading to perf and spillage of mec into the abd cavity; it often calcifies and forms a “pseudocyst” that can be seen on abd films
313. Know that otitis media, dextrocardia, and/or bronchiectasis may be due to PCD
314. Note that in question 2007:143 the vignette was a boy who had chronic infections, cludding, cough, nasal polyps, rhinorrhea and a “point of maximal impulse displaced t the right” this was supposed to be the clue to dextrocardia and therefore the PCD rather than CF
350. Know that children with severe OSA due to upper airways obstruction are at significant risk for resp distress postoperatively (due to post op airway selling, post op obstructive pulmonary edema)
353. ALTE is an episode that is frightening to the observer and that is characterized by some combination of apnea (centrally or occasionally obstructive), color change (usually cyanotic or pallid but occasionally erythematous or plethoric), marked change in muscle tone (usually marked limpness), choking or gagging
358. Know the ddx of ALTE in infants includes infection, metabolic abnormality, GER, aspiration, cardiac dysrhythmia, seizures, nonaccidental trauma, apnea of infancy