Pulmonary Agenesis
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1
What is pulmonary agenesis?
Complete absence of lung development.
2
What is bilateral pulmonary agenesis?
Absence of both lungs.
3
Why is bilateral pulmonary agenesis incompatible with life?
Complete absence of both lungs.
4
What condition is bilateral pulmonary agenesis usually associated with?
Anencephaly.
5
Which type of pulmonary agenesis is more common?
Unilateral pulmonary agenesis.
6
What airway abnormality may occur in unilateral pulmonary agenesis?
Absence of the carina with the trachea running directly into a single bronchus.
7
What conditions can cause central airway symptoms in unilateral pulmonary agenesis?
Compression, stenosis, or malacia.
8
What determines the symptoms of unilateral pulmonary agenesis?
Laterality of agenesis.
9
Which side of pulmonary agenesis has a poorer prognosis?
Right lung agenesis.
10
Why does right lung agenesis have a poorer prognosis?
Mediastinal shift distorts the trachea and great vessels.
11
What can severe rightward mediastinal rotation cause?
Compromised blood flow and airway patency.
12
What cardiovascular complication can result from right lung agenesis?
Pulmonary hypertension.
13
What is pulmonary aplasia?
Absence of lung parenchyma with a rudimentary bronchus.
14
What is the most common variant of pulmonary aplasia?
Unilateral pulmonary aplasia.
15
What structures are present in unilateral pulmonary aplasia?
Carina and main-stem bronchial stump.
16
What is absent in pulmonary aplasia?
Distal lung.
17
What distinguishes pulmonary aplasia from agenesis?
Aplasia has a rudimentary bronchus; agenesis has no major airways.
18
What is pulmonary hypoplasia?
Incomplete development of the lungs.
19
What decreases in pulmonary hypoplasia?
Number of alveoli and airway generations.
20
What intrauterine disorders are associated with pulmonary hypoplasia?
Oligohydramnios, thoracic dystrophy, and CPAM.
21
What is the main difference between pulmonary hypoplasia and agenesis?
Hypoplasia involves partial development; agenesis involves no development.
22
What is a bronchogenic cyst?
A congenital cyst from abnormal budding of the tracheal diverticulum.
23
From which embryologic structure does a bronchogenic cyst originate?
Tracheal diverticulum of the foregut.
24
When does bronchogenic cyst development begin?
Before the 16th week of gestation.
25
What is the most common location of a bronchogenic cyst?
Right lung.
26
Where are most bronchogenic cysts located?
Mediastinum (85%).
27
What percentage of bronchogenic cysts are intrapulmonary?
15%.
28
What symptoms may bronchogenic cysts cause?
Respiratory distress, airway compression, and recurrent respiratory infections.
29
Why do bronchogenic cyst manifestations vary?
Depending on the degree of cyst compression.
30
What imaging modalities diagnose bronchogenic cysts?
Chest X-ray, CT scan, and MRI.
31
What imaging is recommended when a bronchogenic cyst is not visible on chest X-ray?
CT scan or MRI.
32
What is the treatment for bronchogenic cysts?
Surgical excision.
33
What does CPAM stand for?
Congenital Pulmonary Airway Malformation.
34
What is CPAM composed of?
Hamartomatous or dysplastic lung tissue mixed with normal lung tissue.
35
What is the incidence of CPAM?
\$1-4\$ per 100,000 births.
36
Why is CPAM difficult to confirm initially?
Chest radiograph and ultrasound may not clearly demonstrate it.
37
What defines macrocystic CPAM on prenatal ultrasound?
Single or multiple cysts larger than 5 mm.
38
What defines microcystic CPAM on prenatal ultrasound?
Echogenic cysts smaller than 5 mm.
39
Who proposed the five pathological types of CPAM?
Stocker.
40
What is CPAM Type 0 formerly called?
Acinar dysplasia.
41
Which anatomical level characterizes CPAM Type 0?
Bronchial.
42
What are the characteristics of CPAM Type 0?
Rare, incompatible with life, and associated with other abnormalities.
43
What do the lungs look like in CPAM Type 0?
Small and firm.
44
What does CPAM Type 0 histology show?
Bronchial-type airways with cartilage, smooth muscle, and glands.
45
What separates the airways in CPAM Type 0?
Abundant mesenchymal tissue.
46
Which CPAM type is the most common?
Type 1.
47
Which CPAM type has the best prognosis?
Type 1.
48
What size are the cysts in CPAM Type 1?
Usually larger than 2 cm.
49
How are CPAM Type 1 cysts typically arranged?
Multiloculated.
50
What type of cyst is CPAM Type 1 considered?
Macrocyst.
51
What is the boundary between CPAM Type 1 and normal lung?
Sharp boundary without a capsule.
52
What epithelium lines CPAM Type 1 cysts?
Pseudostratified ciliated columnar epithelium.
53
What percentage of CPAM Type 1 cases show mucous cell hyperplasia?
35% to 50%.
54
What malignancy is mentioned in association with CPAM Type 1?
Bronchoalveolar carcinoma.
55
Which CPAM type is the second most frequent?
Type 2.
56
What anatomical level characterizes CPAM Type 2?
Bronchiolar.
57
What causes the cystic airspaces in CPAM Type 2?
Overgrowth of dilated bronchiolar structures.
58
What separates the cystic structures in CPAM Type 2?
Alveolar tissue.
59
What are the typical lesions of CPAM Type 2?
Spongelike lesions with multiple small cysts.
60
What congenital defects may accompany CPAM Type 2?
Renal agenesis, cardiovascular problems, diaphragmatic hernia, and syringomyelia.
61
Which CPAM type is uncommon and may cause hypoplasia of remaining lung tissue?
Type 3.
62
What anatomical level characterizes CPAM Type 3?
Bronchiolar/alveolar duct.
63
What do CPAM Type 3 lesions look like?
Solid lesions.
64
Which CPAM type is the only solid type?
Type 3.
65
What histological feature characterizes CPAM Type 3?
Excess bronchiolar structures separated by airspaces resembling late fetal lung.
66
What vascular abnormality occurs in CPAM Type 3?
Absence of pulmonary arteries within the lesion.
67
Which CPAM type is very rare and peripheral?
Type 4.
68
What anatomical level characterizes CPAM Type 4?
Peripheral.
69
What are the characteristics of CPAM Type 4 cysts?
Macrocystic, peripheral, thin-walled, and often multiloculated.
70
What malignancy is associated with CPAM Type 4?
Pleuropulmonary blastoma.
71
What cells typically line CPAM Type 4 cystic spaces?
Alveolar cells.
72
What is the treatment of choice for CPAM?
Surgery.
73
When is surgery indicated for CPAM?
Symptomatic patients and patients with recurrent respiratory infections.
74
Why may asymptomatic CPAM patients undergo surgery?
To prevent malignancy progression and further infections.
75
Why is antenatal surgery for CPAM controversial?
Some CPAMs are asymptomatic.
76
What is pulmonary sequestration?
Isolated lung tissue supplied by systemic arteries.
77
What bronchial connection is absent in pulmonary sequestration?
Connection to the normal bronchial tree.
78
Does pulmonary sequestration participate in gas exchange?
No.
79
What supplies the blood to pulmonary sequestration?
Systemic circulation.
80
Does pulmonary sequestration cause hypoxemia from a right-to-left shunt?
No.
81
Does pulmonary sequestration cause hypoxemia from dead space ventilation?
No.
82
What is the acquired etiology of pulmonary sequestration?
Recurrent respiratory infections causing scarring and collateral systemic circulation.
83
What are the two types of pulmonary sequestration?
Intralobar and extralobar.
84
Which type of pulmonary sequestration is more common?
Intralobar sequestration.
85
Does intralobar sequestration have its own pleura?
No.
86
Where is intralobar sequestration commonly located?
Posterior basal segment of the left lower lobe.
87
What is the pleural relationship of intralobar sequestration?
No pleural separation from the rest of the lobe.
88
What is the arterial supply of intralobar sequestration?
Systemic arteries.
89
What is the venous drainage of intralobar sequestration?
Pulmonary veins.
90
Where is extralobar sequestration commonly located?
Beneath the left lower lobe.
91
Does extralobar sequestration connect to a bronchus?
No.
92
Does extralobar sequestration participate in gas exchange?
No.
93
Does extralobar sequestration have its own pleura?
Yes.
94
What separates extralobar sequestration from normal lung tissue?
Its own pleura and vasculature.
95
What is the arterial supply of extralobar sequestration?
Systemic arteries.
96
What is the venous drainage of extralobar sequestration?
Inferior vena cava.
97
What is the usual age of diagnosis for pulmonary sequestration?
Adolescence.
98
Why is pulmonary sequestration commonly diagnosed during adolescence?
Repeated respiratory tract infections.
99
What is the confirmatory diagnostic test for pulmonary sequestration?
Pulmonary CT angiogram.
100
What finding confirms pulmonary sequestration on CT angiography?
An anomalous systemic vessel.
101
What does pulmonary CT angiography establish?
Systemic blood supply and drainage.
102
What is the treatment of choice for pulmonary sequestration?
Surgical excision.
103
Why is pulmonary sequestration surgically removed?
To prevent recurrent respiratory tract infections.
104
When may surgery for pulmonary sequestration be delayed?
When there are no signs of pulmonary distress.
105
What is an alternative treatment for solid pulmonary sequestration lesions?
Embolization.
106
Do cystic components of pulmonary sequestration respond well to embolization?
No.
107
What is emphysema?
Irreversible distention of air spaces due to disruption of alveolar septa.
108
What structure is disrupted in emphysema?
Alveolar septa.
109
What extent of the lung can emphysema involve?
Part or all of the lung.
110
What is pulmonary overinflation?
Distention of air spaces with or without alveolar rupture, often reversible.
111
What are the two types of secondary overinflation?
Compensatory and obstructive.
112
What causes compensatory overinflation?
Expansion of remaining lung parenchyma after collapse of other portions.
113
What causes obstructive overinflation?
Airway obstruction, sometimes by a pulmonary mass.
114
What is the ball-valve effect?
Air enters during inspiration but cannot escape during expiration.
115
What happens to alveolar air during the ball-valve effect?
Air accumulates in the alveoli.
116
What is the percussion finding in overinflated lungs?
Hyperresonance.
117
What happens to breath sounds in overinflated lungs?
They decrease.
118
What does a unilateral hyperlucent lung look like on X-ray?
Very dark.
119
What causes unilateral hyperlucent lungs?
Localized airway obstruction.
120
What are causes of localized airway obstruction?
Foreign bodies, inflammation, thick mucus, endobronchial tuberculosis, and tumors.
121
What is congenital lobar emphysema?
Localized airway obstruction causing overinflation of one or more lobes.
122
Which lobe is most commonly affected in congenital lobar emphysema?
Left upper lobe.
123
What is the major clinical complication of congenital lobar emphysema?
Severe respiratory distress.
124
Can congenital lobar emphysema be asymptomatic?
Yes, depending on the percentage of affected lung tissue.
125
Can patients with congenital lobar emphysema survive into adulthood?
Yes, especially with a small affected lung area.
126
What causes congenital lobar emphysema?
Congenital bronchial cartilage deficiency, aberrant vessel compression, bronchial stenosis, mucosal flaps, or bronchial kinking.
127
Is congenital lobar emphysema often familial?
Yes.
128
What imaging is requested for asymptomatic congenital lobar emphysema in infants younger than 2 months?
Chest X-ray.
129
How are asymptomatic infants younger than 2 months with congenital lobar emphysema managed?
Observation and monitoring.
130
What diagnostic tests are used for severe congenital lobar emphysema in patients older than 2 months?
CT scan, V/Q scan, and bronchoscopy.
131
How are mild-to-moderate congenital lobar emphysema symptoms managed?
Observe progression of respiratory symptoms.
132
What is the treatment for asymptomatic congenital lobar emphysema?
Conservative management.
133
What is the treatment for congenital lobar emphysema with respiratory distress?
Lobectomy.
134
What does CDH stand for?
Congenital diaphragmatic hernia.
135
What percentage of congenital diaphragmatic hernias are left-sided?
80%.
136
Through which canal does most CDH occur?
Left pleuroperitoneal canal.
137
Is a membranous sac usually present in CDH?
No.
138
Which abdominal organs may herniate into the chest in CDH?
Intestine, stomach, liver, and spleen.
139
When is CDH usually diagnosed?
Antenatally.
140
What are the two common types of congenital diaphragmatic hernia?
Morgagni and Bochdalek hernia.
141
Where is a Morgagni hernia located?
Anterior chest or retrosternal area.
142
Can a Morgagni hernia have a peritoneal sac?
Yes.
143
Where is a Bochdalek hernia located?
Posterior area of the diaphragm.
144
Which side is more common in Bochdalek hernia?
Left.
145
Does Bochdalek hernia usually have a sac?
No.
146
Which CDH type is more common, Morgagni or Bochdalek?
Bochdalek.
147
What are the clinical manifestations of CDH?
Respiratory distress, scaphoid abdomen, and funnel-shaped chest.
148
Why does a newborn with CDH have a scaphoid abdomen?
Abdominal organs herniate into the thorax.
149
What does chest radiography show in CDH?
Contralateral mediastinal shift and cystic lucencies.
150
What do cystic lucencies represent in CDH?
Herniated intestines in the chest.
151
What happens to diaphragm visualization in CDH?
The diaphragm is poorly delineated or not visible.
152
How is CDH treated?
Surgical repair.
153
When should surgical repair of CDH be performed according to recent literature?
After stabilization and optimization of the patient's condition.
154
What pulmonary complication must be monitored in CDH?
Pulmonary arterial hypertension.
155
What is pleural effusion?
Accumulation of fluid in the pleural cavity.
156
Where does pleural fluid primarily originate?
Capillaries of the parietal pleura.
157
What is the normal volume of pleural fluid?
\$10-20\$ mL.
158
What law regulates pleural fluid formation?
Starling's Law.
159
Which pressures determine pleural fluid balance?
Hydrostatic and oncotic pressures.
160
What happens when hydrostatic and oncotic pressures become imbalanced?
Pleural effusion develops.
161
What happens when osmotic pressure increases?
More fluid accumulates.
162
Which pleura has higher hydrostatic pressure?
Parietal pleura.
163
Which pleura is primarily responsible for pleural fluid production?
Parietal pleura.
164
Which structures are primarily responsible for pleural fluid resorption?
Parietal pleural lymphatics.
165
What are pleural stomas responsible for?
Pleural fluid drainage.
166
What is another mechanism of pleural effusion formation?
Increased pleural membrane permeability.
167
What is the most common cause of pleural effusion?
Infection.
168
How does infection cause pleural effusion?
Inflammation increases membrane permeability and draws fluid into the pleural space.
169
What happens to chest expansion in pleural effusion?
Asymmetric expansion with lagging of the affected side.
170
What is the tactile fremitus finding in pleural effusion?
Decreased tactile fremitus.
171
What is the percussion finding in pleural effusion?
Dullness.
172
What is the auscultation finding in pleural effusion?
Decreased breath sounds.
173
What is the most commonly requested diagnostic test for pleural effusion?
Chest radiograph.
174
What radiographic finding suggests pleural effusion?
Opacity in the affected area.
175
Why is the diaphragm poorly delineated in pleural effusion?
Accumulated fluid obscures the diaphragm and meniscus.
176
How can free-flowing pleural fluid be confirmed radiographically?
Lateral decubitus chest radiograph showing fluid layering.
177
What is thoracentesis?
Evacuation of pleural fluid.
178
When is serial thoracentesis performed?
When pleural fluid volume is minimal.
179
When is chest tube thoracostomy indicated for pleural effusion?
Large fluid volumes or expected fluid reaccumulation.
180
When else is chest tube thoracostomy indicated for pleural effusion?
Multiloculated effusion or suspected malignancy.
181
What is the purpose of pleural fluid analysis?
To determine the etiology of pleural effusion.
182
What ratios are assessed in pleural fluid analysis?
Pleural fluid/serum protein and pleural fluid/serum LDH ratios.
183
What is Light's Criteria used for?
Classifying pleural effusion as transudative or exudative.
184
What characterizes a transudative pleural effusion?
Low protein.
185
What characterizes an exudative pleural effusion?
High protein.
186
How many Light's Criteria are needed to classify an effusion?
One criterion is sufficient.
187
What is empyema also called?
Pyothorax.
188
What does the prefix pyo mean?
Pus.
189
What is empyema?
Collection of pus in the pleural space.
190
What is the immediate treatment for empyema?
Chest tube thoracostomy and antimicrobials.
191
What is hemothorax?
Accumulation of blood within the pleural cavity.
192
What is the most common cause of hemothorax?
Trauma.
193
What is another cause of hemothorax?
Iatrogenic injury.
194
How is hemothorax treated?
Chest tube thoracostomy.
195
What is chylothorax?
Accumulation of chyle in the pleural space.
196
What is chyle composed of?
Lipids and proteins.
197
What causes chylothorax?
Leakage from the lymphatic system or thoracic duct.
198
How does chylothorax fluid appear compared with empyema?
Lighter in color.
199
In which postoperative patients is chylothorax commonly seen?
Heart surgery patients.
200
What is the initial treatment for chylothorax?
Chest tube thoracostomy.
201
Why are patients with chylothorax kept NPO?
To reduce chylomicron production.
202
Which medications are used for chylothorax?
Octreotide or somatostatin.
203
What is the treatment for chylothorax unresponsive to conservative management?
Thoracic duct repair.
204
What is pneumothorax?
Accumulation of extrapulmonary air in the pleural space.
205
What causes pneumothorax?
Leakage of air within the lung.
206
What are the two broad etiologies of pneumothorax?
Traumatic/iatrogenic and spontaneous.
207
What causes iatrogenic traumatic pneumothorax?
Interventional procedures and positive-pressure ventilation.
208
What causes non-iatrogenic traumatic pneumothorax?
Penetrating or blunt trauma.
209
What characterizes primary spontaneous pneumothorax?
No specific underlying cause.
210
In which patients is primary spontaneous pneumothorax commonly seen?
Tall patients.
211
What characterizes secondary spontaneous pneumothorax?
An identifiable underlying cause or existing condition.
212
What congenital condition may predispose to secondary spontaneous pneumothorax?
Congenital bullae.
213
What is a closed pneumothorax?
Pleural cavity pressure is less than atmospheric pressure.
214
What is an example associated with closed pneumothorax in the lecture?
Intubation.
215
What is an open pneumothorax?
Pleural cavity pressure equals atmospheric pressure.
216
What is a common cause of open pneumothorax?
Penetrating trauma.
217
What is a tension pneumothorax?
Pleural cavity pressure is greater than atmospheric pressure.
218
In what setting may tension pneumothorax occur?
ICU patients, intubated or non-intubated.
219
What may bagging cause in tension pneumothorax?
Tachycardia.
220
How does the British Thoracic Society assess pneumothorax size?
Interpleural distance at the level of the hilum.
221
What is a small pneumothorax according to the BTS guideline?
Less than 1 cm.
222
What is a moderate pneumothorax according to the BTS guideline?
\$1-2\$ cm.
223
What is a large pneumothorax according to the BTS guideline?
2 cm or more.
224
How does the American College of Chest Physicians assess pneumothorax size?
Distance from apex to cupola.
225
What is a small pneumothorax according to the ACCP guideline?
Less than 3 cm.
226
What is a large pneumothorax according to the ACCP guideline?
Greater than 3 cm.
227
What is the formula for estimating pneumothorax size on chest X-ray?
\$PTX=4.2+[4.7\times(A+B+C)]\$.
228
What does A represent in the pneumothorax size formula?
Maximum interpleural distance at the apex.
229
What does B represent in the pneumothorax size formula?
Distance at the midpoint of the upper half of the lung.
230
What does C represent in the pneumothorax size formula?
Distance at the midpoint of the lower half of the lung.
231
What are the manifestations of a small pneumothorax?
May be asymptomatic, with mild tachycardia and mild dyspnea.
232
What are the manifestations of a large pneumothorax?
Respiratory distress, tachypnea, air hunger, and cyanosis.
233
What oxygen device is used for severe respiratory distress in pneumothorax?
High-concentration oxygen mask or non-rebreather mask.
234
How much oxygen does a non-rebreather mask deliver?
Nearly 100% oxygen.
235
How does a non-rebreather mask prevent rebreathing?
Reservoir bag and one-way valves.
236
What is denitrogenation?
Replacement of lung nitrogen with 100% oxygen.
237
How long is preoxygenation performed for denitrogenation?
3 to 5 minutes.
238
What is the purpose of denitrogenation?
To create an oxygen-rich functional residual capacity before airway intervention.
239
Why is denitrogenation especially important in children?
They consume oxygen faster and have smaller relative lung volumes.
240
What is chest tube thoracostomy?
A procedure to remove pleural air and allow lung re-expansion.
241
What is needle thoracostomy?
Insertion of a needle into the pleural space to decompress tension pneumothorax.
242
Where is needle thoracostomy typically inserted?
Second intercostal space at the midclavicular line.
243
What is subcutaneous emphysema?
Free air entering the subcutaneous tissue.
244
Is subcutaneous emphysema congenital or acquired?
Acquired.
245
What conditions are commonly associated with subcutaneous emphysema?
Pneumothorax and pneumomediastinum.
246
In which patients may subcutaneous emphysema occur?
Patients with chest tubes or after heart or thoracic surgery.
247
What is the usual course of subcutaneous emphysema?
It resolves spontaneously.
248
What is atelectasis?
Collapse of the whole lung or part of the lung.
249
How is atelectasis defined radiologically?
Volume loss.
250
Is the loss of aerated lung in atelectasis reversible?
Yes.
251
How does atelectasis differ from emphysema?
Atelectasis is reversible; emphysema is irreversible.
252
What causes lung volume depletion in atelectasis?
Degassing of the alveoli.
253
What causes atelectasis mechanically?
Imbalance between inward and outward alveolar recoil.
254
What are the three mechanisms of atelectasis?
Contraction, resorption, and compression.
255
What causes contraction atelectasis?
Inhibition or deficiency of surfactant.
256
What is the function of pulmonary surfactant?
Lowers surface tension and prevents alveolar collapse.
257
What neonatal condition is associated with surfactant deficiency?
Respiratory distress syndrome of the newborn.
258
What causes resorption atelectasis?
Imbalance among respiratory gases.
259
Which gases are involved in resorption atelectasis?
Oxygen, hydrogen, nitrogen, and carbon dioxide.
260
What happens to nitrogen during excessive oxygen administration?
Its partial pressure decreases.
261
What is the role of nitrogen in the airway?
It helps keep the airway open.
262
What causes compression atelectasis?
Compression from a pulmonary mass or fluid accumulation.
263
What are causes of external compression atelectasis?
Pleural effusion, pneumothorax, intrathoracic tumors, and diaphragmatic hernia.
264
What can cause complete endobronchial obstruction?
Enlarged lymph nodes, tumors, cardiac enlargement, foreign bodies, mucoid plugs, and broncholithiasis.
265
What are causes of intraluminal bronchial obstruction?
Foreign bodies, asthma, granulomatous tissue, tumors, mucus plugs, and bronchiectasis.
266
What pulmonary infections or conditions may cause intraluminal obstruction?
Pulmonary abscess, chronic bronchitis, acute laryngotracheobronchitis, and plastic bronchitis.
267
What can cause intrabronchiolar obstruction?
Bronchiolitis, interstitial pneumonitis, and asthma.
268
What can cause atelectasis through respiratory compromise or paralysis?
Neuromuscular abnormalities, osseous deformities, restrictive casts, and defective diaphragm movement.
269
What are the consequences of atelectasis?
Impaired gas exchange and lung mechanics, increased pulmonary vascular resistance, and worsening lung injury.
270
How can atelectasis worsen infection?
It may promote bacterial overgrowth.
271
What are the clinical manifestations of atelectasis?
Dyspnea, tachypnea, asymmetric chest movement, and reduced ipsilateral breath sounds.
272
What breath sounds are heard in upper lobe atelectasis?
Bronchial or tubular breath sounds.
273
What is the percussion finding in atelectasis?
Increased dullness.
274
What is the characteristic X-ray finding in atelectasis?
White-out lung.
275
In which direction does the trachea move in atelectasis?
Toward the affected area.
276
Why does the trachea move toward the affected lung in atelectasis?
Volume loss pulls the trachea toward the collapsed lung.
277
How does tracheal position differ between atelectasis and pleural effusion?
Atelectasis pulls the trachea toward the lesion; pleural effusion may push it away.
278
What imaging modalities can diagnose atelectasis?
Chest X-ray, CT scan, and ultrasound.
279
How is atelectasis caused by pleural effusion or pneumothorax treated?
Relieve compression.
280
How is atelectasis caused by a mucus plug treated?
Tracheal or bronchoscopic aspiration, bronchial lavage, or CPAP.
281
How is foreign-body-induced atelectasis treated?
Bronchoscopic examination and foreign body removal.
282
How is asthma-related atelectasis treated?
Bronchodilators and corticosteroids.
283
What additional treatments may be used for asthma-related atelectasis?
Recombinant human deoxyribonuclease or hypertonic saline with or without bronchodilator.
284
How is atelectasis associated with neuromuscular disease managed?
Intermittent positive-pressure breathing and mechanical insufflation-exsufflation.
285
What respiratory support may be used in neuromuscular disease?
Noninvasive bilevel positive pressure.
286
What is the goal of respiratory rehabilitation in neuromuscular disease?
Improve cough reflex.
287
How is cystic fibrosis-related atelectasis managed?
Airway clearance therapies and hypertonic saline with or without bronchodilator.
288
What is pulmonary edema?
Accumulation of fluid in the pulmonary interstitium and alveoli.
289
What are the causes of pulmonary edema due to increased pulmonary capillary pressure?
Cardiogenic and noncardiogenic causes.
290
What is a cardiogenic cause of pulmonary edema?
Left ventricular failure.
291
What are noncardiogenic causes of increased pulmonary capillary pressure?
Pulmonary veno-occlusive disease, pulmonary venous fibrosis, and mediastinal tumors.
292
What are causes of increased pulmonary capillary permeability?
Pneumonia, ARDS, toxins, inflammatory reactions, aspiration, drowning, and radiation.
293
Which inflammatory conditions may cause pulmonary edema?
IRIS and cytokine release syndrome.
294
What therapy may cause cytokine release syndrome-associated pulmonary edema?
CAR-T therapy.
295
Which vasoactive substances can increase pulmonary capillary permeability?
Histamine, leukotrienes, and thromboxanes.
296
What conditions cause diffuse capillary leak syndrome?
Sepsis and systemic inflammatory response syndrome.
297
What immunologic reactions can cause pulmonary edema?
Transfusion reactions.
298
What is a cause of pulmonary edema due to lymphatic insufficiency?
Congenital or acquired lymphatic insufficiency.
299
What causes pulmonary edema due to decreased oncotic pressure?
Hypoalbuminemia.
300
Which diseases may cause hypoalbuminemia-associated pulmonary edema?
Renal disease, hepatic disease, protein-losing states, and malnutrition.
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