Review of Respiratory Disorders from 2010 ABP Content Specs

2. Stridor

3. Know the ddx of congenital stridor

4. Inspiratory stridor: Laryngomalacia, subglottic stenosis, vocal cord paralysis

5. Expiratory stridor: tracheomalacia or lesions in the airway structures or thoracic cavity

6. Biphasic: vascular rings and slings

7. Know the different etiologies of stridor in children of different ages

8. Birth: choanal atresia, laryngeal web or stenosis, vascular ring, vocal cord paralysis

9. 4-6 weeks: laryngomalacia, tracheomalacia

10. 1-4 years: croup, epiglottitis, foreign body aspiration

11. >5 years: vocal cord dysfunction, exercise, peritonsillar abscess, anaphylaxis

12. Know that endoscopy is the diagnostic tool of choice for laryngeal and vocal cord disorders

13. Laryngomalacia will reveal an omega shaped epiglottis that prolapses during inspiration

14. Paroxysmal vocal cord motion (PVCM)

15. Understand the appropriate approach to the evaluation of congenital stridor

16. Primary evaluation: thorough birth hx, current medical hx, , observation of breathing patterns in different positions, auscultation of the airway

17. Secondary evaluation: can include radiography, spirometry, direct airway visualization (laryngoscopy)

18. Know that vocal cord dysfxn may mimic asthma

19. Also called paroxysmal vocal cord motion (PVCM) or laryngeal dyskinesia

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)

21. Respiratory failure

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

28. Cough

29. Know the ddx of chronic cough in children of different ages

30. Causes of chronic cough in kids with normal CXR:

31. Upper airway cough syndrome (previously post nasal drip syndrome)

32. Expect to find this in a kid over age 3 and with other sx of allergies

33. Asthma

34. GER

35. (usually creates sx during the first few postnatal months and then resolves by age 12 mos)

36. Tracheomalacia

37. Habit-cough syndrome

38. Vocal cord dysfxn

39. Distinguish between clinical manifestations of psychogenic cough and those caused by cough of organic etiology

40. Aka “habit cough syndrome”

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

43. Understand the limited indications for cough suppressants

44. Not better than placebo on several trials

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

48. Exercise intolerance

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

51. Measured by the maximal oxygen consumption test

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

55. Apnea

56. Distinguish between apnea and periodic breathing

57. Apnea is defined as a cessation of respiration for more than 20secs or if for less than 20 secs is associated with cyanosis or bradycardia

58. Know the difference between central and obstructive apnea

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

61. Habitual (nightly) snoring, often with intermittent pauses, gasps or snorts

62. Sleep difficulty

63. Daytime neurobehavioral problems

64. Differentiate among obstructive, central, and mixed sleep-associated apnea

65. Obstructive – see above

66. Central – see above; myelomeningocele, hydrocephalus and Arnold- Chiari can be causes

67. Mixed – combines aspects of OSA and CSA

68. Know the testing procedures to evaluate the presence and degree of obstructive apnea on older children

69. Overnight polysonmnography is the gold standard but isn’t very practical

70. Overnight oximetry or nap time PSG (high specificities but low sensitivities)

71. Know the ddx of central sleep apnea in infancy

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

73. Central apnea can be due to:

74. Infection

75. Prolonged hypoxemia (lung dz, anemia, PDA)

76. Meds / CNS depressants

77. ICH

78. Hydrocephalus

79. Electrolyte abns

80. Hypoglycemia

81. Hypo/hyperthermia

82. Prematurity and immature resp drive

83. Know the tx of idiopathic recurrent apnea in premature infants

84. i.e. apnea of prematurity

85. MUST rule out other treatable causes

86. Treated with caffeine

87. Understand the association between apnea and anemia in premature infants

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

89. Wheezing

90. Differentiate among the dxes responsible for persistent localized wheezes (e.g foreign body, malacia) versus diffuse or migratory wheezes

91. Know the ddx of recurrent wheezing

92. Asthma related causes and non-asthma related causes

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

94. Non-asthma – foreign body, bronchiolitis obliterans, BOOP, bronchiectasis

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

99. Complication= secondary bacterial pneumonia

100. Tachypnea

101. Know that respir rates vary with age and that normal variations occur with sleep, eating and activity in normal children

102. Recognize that tachypnea is a sensitive indicator of respiratory disease

103. Especially lower airway disease and should be looked at in context of other symptoms

104. Hemoptysis

105. Know the ddx of hemoptysis in children

106. Most common etiologies are infection, foreign body and bronchiectasis

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

109. Assess other signs and sx

110. Get a CXR and if dx still not clear get a CT

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

113. Cyanosis

114. Know that cyanosis is not a sensitive indicator of oxyhemoglobin saturation (??)

115. Know the common extrapulmonary causes of cyanosis: R to L shunt, methemoglobinemia

116. The article cited only talks about methemoglobinemia; treat it with methylene blue

117. Know how to validate and quantitate a clinical observation of cyanosis: ABG, oxyhemoglobin sat

118. Clubbing

119. Recognize D/Os commonly associated with digital clubbing

120. Cyanotic heart disease (pulm atresia with unrepaired VSD and collateral pulmonary blood flow), chronic lung disease, biliary cirrhosis, infective endocarditis

121. Upper airway

122. General

123. Croup

124. Distinguish between viral and noninfectious croup

125. Viral/infectious croup

126. Usually parainfluenza

127. Low grade fever, rhinorrhea, mild cough followed 1-3 days later by a harsh, nonproductive “barking” cough and inspiratory stridor

128. Noninfectious/spasmodic croup

129. The cough is similar in that it is barking and nonproductive, but there is no fever, rhinorrhea or other sx of infection; possibly allergic

130. Know the appropriate management of croup

131. Mainstay = cool mist therapy

132. Some evidence that adding steroids to the mist can help decrease inflammation

133. Moderate to severe croup can benefit from heliox and also racemic epi

134. Know the clinical manifestations of laryngotracheobronchitis (croup)

135. See above for infectious croup

136. Epiglottitis

137. Know how to tx a child with it

138. Carefully

139. Don’t examine them invasively, don’t send them to radiology

140. Establish an airway (have anesthesia come ASAP) if looking crumpy

141. Give abx, maybe steroids

142. Differentiate the clinical and radiographic findings of viral croup from those of epiglottitis and bacterial tracheitis

143. Viral croup: cough, runny nose, possible prior low grade fever, don’t appear toxic

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

147. Increased swelling and collapse of airway

148. Lower airway

149. Vascular anomalies

150. Recognize the variable presentation of vascular anomalies affecting the airway

151. Vascular rings and slings; often present with stridor while feeding; biphasic stridor

152. Congenital malformations

153. Recognize that congenital malformations of the lung (e.g. hypoplastic left lung, cystic adenomatoid malformation) may cause respiratory signs and symptoms

154. Pulmonary sequestration:

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

159. Bronchiolitis I think I’m all set with bronchiolitis, thanks.

160. Recognize the clinical manifestations of bronchiolitis

161. Know the indications for hospitalization for a child with bronchiolitis

162. Aspiration syndromes

163. Know how to eval for a suspected foreign body aspiration

164. See prior section

165. Know the long term complications for FB aspiration

166. Bacterial pneumonia os most common complication

167. Can also get atelectasis and bronchiectasis

168. Know the pulmonary complications of GER

169. Wheezing, scarring of vocal cords…

170. Know the possible radiographic manifestations of FB aspiration

171. Lung remains inflated on expiratory films, might see the foreign body, might see atelectasis, air trapping

172. Know that recurrent aspiration can recur with swallowing d/os independent of GER

173. Swallowing dysfunction can be a cause

174. Plan the management of a patient with FB aspiration

175. See above under the wheezing part

176. Understand that hydrocarbon pneumonitis may cause acute and chronic lung disease

177. Hydrocarbons are mineral spirits, gasoline, turpentine, pine oil

178. Acutely can cause aspiration, hypoxemia requiring O2 support, the resp sx usually resolve in 7 days

179. Chronically can cause penumatoceles, pneumothorax, empyema, bacterial pna, respiratory distress syndrome

180. May get proliferative alveolar thickening and that can cause permanent damage to pulm fxn

181. Know that aspiration can occur despite the presence of a tracheostomy

182. Bronchiectasis

183. Know the ddx of it

184. Bronchiectasis abnormal dilatation of the bronchi and bronchioles; may be localized or diffuse and the changes are irreversible

185. Most common cause is CF

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

188. Tracheomalacia

189. Know that it can occur as a complication of chronic mechanical ventilation in children

190. High vent pressures can result in weakening or destruction of tracheal cartilage

191. Know that tracheoesophageal fistula may result in tracheomalacia

192. Can remain problematic despite repair of the fistula

193. Know the clinical manifestations of tracheomalacia and laryngomalacia

194. Laryngomalacia: most common cause of stridor in infants

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

198. Tracheomalacia

199. Occurs during expiration due to collapse trachea during expiratory maneuvers

200. Hallmark = expiratory wheeze

201. Can be isolated or in association with other clinical entities like TEF or trisomy 21; can be acquired due to vents

202. Differentiate between the two – see above

203. Tracheitis

204. Recognize the si/sx of bacterial tracheitis

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

208. Doesn’t respond to the usual txes for croup

209. Know the tx of it

210. Secure an airway; might need a prolonged intubation doe to need to get secrcxretions cleared and also due to degree of edema in the airway

211. Start abx including coverage for staph (nafcillin)

212. Know the microbiology of it

213. Most commonly due to s. aureus

214. Can also be due to parainfluenza, moraxella, nontypable h. flu and oral anaerobes

215. Hemosiderosis

216. Know that it is associated with hemoptysis

217. Parenchymal

218. Pneumonias

219. Know the etiologies of pna in children of different ages

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

226. Know the clinical manifestations of pnas with different etiologies

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

229. Rarely need lab if patient going to be managed as outpt

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

231. Mycoplasma, chlamydophila and legionella can be determined serologically

232. Legionella and pneumococcal infections are detactable with urine antigen testing

233. Know the sequelae of pna and manage appropriately

234. ?

235. Know the methods of prevention and/or control of pna

236. Good hygiene

237. Breastfeeding

238. Immunization with Hib, pertussis and heptavalent pneumococcal vaccines

239. If kid is older than 2 and has risk facrots then needs the 23-valent pneumococcal polysaccharide vaccine

240. Flue shots

241. Know which organisms are likely to cause the pleural and parenchymal complications of pneumonia

242. Usually s. pneumo

243. GAS (strep pyogenes) can cause pneumatoceles

244. S. aureus can cause pneumatoceles, ptx, abscesses, empyema

245. Know that invasive studies (bronch, lung aspiration, open bx) may be indicated in pts with acute pna

246. Know the ddx of recurrent pna

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

249. Know that congenital lesions of the lung may mimic pna

250. Know the significance of pna in a child with NM dz

251. More likely to get aspiration pneumonia

252. Know the tx of pna in a child with NM dz

253. Cover for causes of aspiration pneumonia (ampicillin, ampicillin-sulbactam, clindamycin); probably needs to be admitted

254. Diaphragmatic hernia – covered in GI section

255. Recognize the clinical manifestations of it

256. Know the appropriate therapy

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

259. Know that pulm hypoplasia is associated with DH

260. Trauma

261. Know how to evaluate a child with sx following a chest wall trauma

262. Know how to stabilize a child with respiratory sx following a chest wall trauma

263. Drowning, near drowning, and acute respiratory distress syndrome

264. Know the clinical manifestations of ARDS

265. Tachypnea, decreased lung compliance, worsening hypoxemia leading to respiratory muscle fatigue

266. Disgnostic triad = noncardiogenic pulmonary edema, impaired oxygenation, bilateral pulmonary infiltrates

267. Know the natural hx of ARDS

268. Three stages:

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

272. Know the pulmonary sequelae of ARDS

273. Pulmonary fibrosis

274. Reactive airway disease

275. Severe chronic lung disease (rare)

276. Know that ARDS has multiple etiologies

277. Know that a pt with minimal sx following a near drowning may later develop sx that require hospitalization

278. Know that ARDS may result from a near drowning after a period of initial recovery

279. Know the major causes of death in children with ARDS: sepsis, extrapulmonary multiorgan failure, air leaks

280. Newborn infants

281. Bronchopulmonary dysplasia (chronic lung disease of infants)

282. Recognize that infants with BPD are prone to cor pulmonale and recurrent wheezing with infections

283. Recognize that failure to thrive and severe respiratory infections are common in infants with BPD

284. Recognize that aversive oral motor behavior is associated with BPD, thereby limiting ways to feed such infants

285. Other – not BPD

286. Know the specific radiographic findings in idiopathic neonatal RDS (see below)

287. Differentiate between normal results of a newborn cxr and the radiographic findings that reflect MAS (see below)

288. Differentiate between the normal results of a newborn cxr and the radiographic patterns that reflect pna

289. RDS: underinflation, “ground glass” appearance, air bronchograms

290. TTN: fluid in horizontal fissure, adequate lung expansion with perihilar and central vascular prominence

291. MAS: patchy areas of diffuse atelectasis, focal areas of air trapping, increased lung volumes

292. Pna:

293. Recognize that CLD may result from MAS

294. Asthma

295. CF

296. Know which vitamins are fat soluble and therefore are usually insufficient in children with CF

297. Understand the inheritance of CF

298. Autosomal recessive

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)

302. Know the association of rectal prolapse and CF

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

309. Prolonged jaundice

310. Know the manifestations of CF in infancy: hypoproteinemia, anemia, steatorrhea, recurrent pulmonary sx, hypochloremic alkalosis

311. Know that hemoptysis and ptx can be potentially life threatening complications of CF

312. Primary ciliary dyskinesia (dysmotile cilia syndrome)

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

315. Extrapulmonary

316. Pleural fluid

317. Understand the etiologies of pleural fluid accumulations

318. Transudates = plasma ultrafiltrates that usually result from renal and liver dz or CHF

319. Exudates = inflammatory processes, like pna, malignancy, trauma, systemic inflammatory dz, impaired lymphatic drainage

320. Empyema is a type of exudate and is characterized by the presence of WBCs, a positive gram stain, or frank pus

321. Exudates have LOW pH (b/c of bacterial glucose consumption)LDH will be 2-3x the serum values, and high protein vaues (>3g/dL)

322. 70% of peduatric pleural effusion are parapneumonic effusions

323. Pleural effusions are seen in up to 40% af bacterial pnas, and about 50% of those will progress to empyema

324. Know the characteristics of pleural fluid due to chylothorax

325. Pneumothorax, pneumomediastinum

326. Know the si/sx of ptx

327. Know the appropriate tx for a child with ptx

328. Know that asthma may be associated with either of these

329. Know that ptx is a complication of rescusitation and mechanical ventilation

330. Thoracic deformities

331. Recognize the association between scoliosis and restrictive pulmonary disease

332. Scoliosis can restrict the thoracic cavity, thereby causing a restrictive lung dz

333. Recognize that severe progressive neuromuscular disease of any etiology can produce serious restrictive pulmonary disease

334. Recognize that pectus excavatum is not usually associated with any pulmonary disease or exercise limitation

335. Pulmonary htn and cor pulmonale

336. Know that oxygenation may decrease during normal abnormal sleep, which may cause pulmonary hypertension or exacerbate existing cor pulmonale

337. Know that PHTN is potentially reversible

338. Treatment is aimed at the underlying disease in cases of secondary PH

339. Treatment is sx management and treatment of pulm vasculopathy in idiopathic PH

340. Know the situations in which PHTN and or pulmonale may occur

341. PPHN

342. CHD

343. Lung disease that causes chronic hypoxia (leads to remodeling of the pulmonary vascular wall)

344. Thrombotic or embolic disease

345. Idiopathic

346. Sleep disorders (see prior sections on OSAS, also, its kind of common sense)

347. Know the respiratory and non-respiratory conditions that may cause sleep disorders

348. Understand the sx that reflect poor sleep quality in children

349. Know the appropriate eval of suspected OSA in children

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)

351. SIDS

352. Recognize a child with an ALTE

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

354. Know the appropriate management of a child with ALTE

355. Get a good hx, full PE to assess the severity of the event

356. Article recommends screening for GER, UA and cx, brain neuroimaging, pneumogram, and WBC count

357. Know the risk factors for SIDS- got it.

358. Know the ddx of ALTE in infants includes infection, metabolic abnormality, GER, aspiration, cardiac dysrhythmia, seizures, nonaccidental trauma, apnea of infancy

359. Recognize the limitation of apnea monitors in following infants with ALTEs

360. Diagnostic testing – prior sections pretty much cover this

361. PFTs

362. Know what spirometry measures

363. Oximetry

364. Know the correlation between PaO2 and oxyhemoglobin saturation

365. Understand the value and limitations of pulse ox in caring for children with acute pulmonary dz

366. Blood gas analysis

367. Recognize the limitations of cap blood gas testing

368. Imaging

369. Recognize intrathoracic airway obstruction by x-ray study of the chest

370. Recognize atelectasis by x-ray study of the chest