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Summary Table

Category	Detail
Risk Factors	Post-operative state (upper abdominal/thoracic surgery), general anesthesia, prolonged bed rest, obesity, smoking, neuromuscular weakness, endobronchial lesion, foreign body aspiration, mucus plugging
Etiology	Airway obstruction (mucus plug, tumor, foreign body), external compression (pleural effusion, pneumothorax), surfactant deficiency, pulmonary fibrosis
Patient Presentation	Post-operative patient with low-grade fever within the first 24 to 48 hours, dyspnea, tachypnea, hypoxia
Classic Physical Exam	Decreased or absent breath sounds over affected area, dullness to percussion, tracheal deviation toward the affected side, decreased chest expansion ipsilaterally
Key Diagnostic Results	CXR: ipsilateral opacification with volume loss signs (elevated hemidiaphragm, mediastinal shift toward affected side, rib crowding). Hypoxemia with elevated $A\text{-}a\ \text{gradient}$
Management	Incentive spirometry, early ambulation, deep breathing exercises, chest physiotherapy; bronchoscopy for refractory mucus plugging
Keywords	"Post-operative day 1 fever," "decreased breath sounds," "tracheal shift toward the lesion," "opacification with volume loss," "incentive spirometry"

1. Pathophysiology

Atelectasis refers to the collapse of previously aerated lung parenchyma, resulting in loss of lung volume and impaired gas exchange. Understanding the mechanism behind each subtype is essential because the vignette will often hint at the underlying cause.

Obstructive (resorptive) atelectasis is the most commonly tested form. When an airway becomes completely blocked (by a mucus plug, aspirated foreign body, or endobronchial tumor), gas trapped distal to the obstruction is gradually absorbed into the pulmonary capillary blood. Since the alveoli cannot be replenished with fresh air, they collapse. This is particularly relevant in the post-operative setting, where general anesthesia suppresses the cough reflex, impairs mucociliary clearance, and reduces tidal volume, all of which promote mucus retention and subsequent airway obstruction.

Compressive atelectasis occurs when an external force pushes on the lung parenchyma from outside, preventing full expansion. Common causes include pleural effusion, pneumothorax, an elevated diaphragm (as in ascites or abdominal distension), and large mediastinal or thoracic masses. In this subtype, the airway itself is patent; the lung simply cannot expand against the compressive force.

Adhesive atelectasis results from surfactant deficiency or dysfunction. Surfactant normally reduces alveolar surface tension, preventing small alveoli from collapsing at end-expiration according to Laplace's law. When surfactant is absent or dysfunctional (as in neonatal respiratory distress syndrome or ARDS), alveoli collapse despite patent airways.

Cicatrization (contraction) atelectasis develops when pulmonary fibrosis or granulomatous disease causes scarring of the lung parenchyma. The fibrotic tissue contracts and pulls the surrounding alveoli inward, reducing their volume.

Relaxation (passive) atelectasis occurs when the normal negative intrapleural pressure is disrupted, as in pneumothorax. Without the negative pressure that keeps the lung expanded against the chest wall, the lung recoils inward.

The physiological consequence of all forms of atelectasis is intrapulmonary shunting: blood continues to perfuse the collapsed, non-ventilated alveoli but cannot participate in gas exchange. This produces ventilation-perfusion (V/Q) mismatch and, in extensive collapse, true right-to-left shunt. The result is hypoxemia with an elevated $A\text{-}a\ \text{gradient}$. A key distinction: mild V/Q mismatch from small areas of atelectasis improves with supplemental oxygen, whereas true shunt from large areas of collapse is refractory to supplemental oxygen.

2. Classification and Clinical Manifestation

By Mechanism

Type	Mechanism	Classic Clinical Scenario
Obstructive (Resorptive)	Complete airway blockage causes distal gas absorption and alveolar collapse	Post-operative mucus plug; endobronchial tumor; foreign body aspiration in children
Compressive	External force compresses lung parenchyma	Large pleural effusion; tension pneumothorax; elevated diaphragm from ascites
Adhesive	Surfactant deficiency increases alveolar surface tension	Neonatal respiratory distress syndrome (RDS); ARDS
Cicatrization (Contraction)	Pulmonary fibrosis/scarring causes parenchymal retraction	Tuberculosis; radiation fibrosis; sarcoidosis
Relaxation (Passive)	Loss of negative intrapleural pressure	Pneumothorax
Replacement	Alveoli are filled and replaced by tumor or other tissue	Bronchoalveolar carcinoma (lepidic-predominant adenocarcinoma)

By Extent

Extent	Description	Clinical Significance
Subsegmental (discoid/plate-like)	Small linear opacities, often at lung bases	Very common post-operatively; usually clinically insignificant
Segmental	Collapse of a bronchopulmonary segment	May cause localized symptoms
Lobar	Entire lobe collapses	Produces noticeable opacification and volume loss on CXR; clinically significant dyspnea
Complete lung	Entire lung collapses ("whiteout")	Medical emergency; severe hypoxemia and hemodynamic compromise

By Severity

Feature	Mild/Subsegmental	Moderate (Segmental/Lobar)	Severe (Complete Lung)
Symptoms	Often asymptomatic	Dyspnea, cough, low-grade fever	Severe dyspnea, tachycardia, hypotension
Breath sounds	Normal or mildly decreased	Decreased over affected region	Absent on affected side
Tracheal deviation	None	May shift toward affected side	Shifts toward affected side
Oxygen requirement	None or minimal	Supplemental oxygen needed	May require mechanical ventilation

Atelectasis is the classic cause of fever on post-operative day 1 to 2 ("Wind"), making it the first consideration when a recently operated patient develops an early, low-grade fever.

The other causes of post-operative fever in sequence are urinary tract infection (day 3), wound infection (day 5 to 7), deep vein thrombosis/pulmonary embolism (day 7 to 10), and drug fever (any day).

3. Diagnostic Workup

Test	Role	Key Findings
Chest X-ray (CXR)	Best initial test	Opacification with volume loss signs: ipsilateral hemidiaphragm elevation, mediastinal/tracheal shift toward affected side, rib crowding, compensatory hyperinflation of adjacent lobes
Arterial Blood Gas (ABG)	Assess gas exchange	Hypoxemia; elevated $A\text{-}a\ \text{gradient}$; respiratory alkalosis initially (due to tachypnea)
CT Chest	Further characterization	Better delineation of the cause (endobronchial lesion, lymphadenopathy, mass); distinguishes atelectasis from consolidation
Bronchoscopy	Both diagnostic and therapeutic	Gold standard for identifying and treating obstructive causes (mucus plug removal, biopsy of endobronchial lesion)
Pulse Oximetry	Screening/monitoring	Decreased $SpO_2$; rapid bedside assessment

The chest X-ray is the best initial test for evaluating atelectasis. The hallmark finding is opacification of the affected lung region combined with signs of volume loss. This distinction is critical on the exam: both atelectasis and pneumonia can produce opacification on CXR, but only atelectasis demonstrates volume loss. The signs of volume loss include elevation of the ipsilateral hemidiaphragm, shift of the mediastinum and trachea toward the collapsed side, crowding of the ribs on the affected side, and compensatory hyperinflation of the remaining lung. In lobar collapse, each lobe produces a characteristic radiographic pattern:

The right upper lobe collapses superiorly and medially, producing a density along the right mediastinal border with elevation of the right hilum. The right middle lobe collapses anteriorly and medially, causing blurring of the right heart border on the PA view (silhouette sign) and a wedge-shaped density on the lateral view. The right lower lobe collapses posteriorly and medially, producing a triangular opacity behind the heart. The left upper lobe collapses anteriorly, creating a veil-like opacity over the left hemithorax without significant mediastinal shift. The left lower lobe collapses posteriorly and medially, producing a triangular retrocardiac density similar to the right lower lobe.

Arterial blood gas analysis reveals hypoxemia with an elevated $A\text{-}a\ \text{gradient}$, confirming intrapulmonary shunting. Early in the course, the patient may demonstrate respiratory alkalosis due to compensatory tachypnea.

CT chest is ordered when the CXR findings are equivocal, when there is concern for an underlying endobronchial lesion or mass causing the obstruction, or when rounded atelectasis needs to be distinguished from a lung malignancy. Rounded atelectasis, which is associated with prior asbestos exposure and pleural thickening, appears as a rounded peripheral opacity with the characteristic "comet tail sign" (curvilinear bronchovascular structures sweeping into the mass).

Bronchoscopy serves as both a diagnostic and therapeutic tool. It is indicated when obstructive atelectasis does not resolve with conservative measures, or when an endobronchial lesion is suspected. It allows direct visualization, mucus plug removal, foreign body extraction, and tissue biopsy if a tumor is identified.

4. Management and Treatment

Setting	Intervention	Details
Prevention (post-operative)	Incentive spirometry	10 maximal inspiratory efforts every 1 to 2 hours while awake; begin immediately post-operatively
	Early ambulation	Mobilize within 6 to 8 hours after surgery when feasible
	Adequate pain control	Epidural analgesia or patient-controlled analgesia for thoracic/upper abdominal surgery to allow deep breathing
Acute treatment	Deep breathing and coughing exercises	Supervised respiratory therapy
	Chest physiotherapy	Percussion, postural drainage, vibration; particularly useful for mucus mobilization
	Suctioning	For intubated patients unable to clear secretions
	Positive pressure ventilation	CPAP or BiPAP to recruit collapsed alveoli; 5 to 10 cmH$_2$O as starting CPAP pressure
	Bronchoscopy	Therapeutic mucus plug removal or foreign body extraction; indicated for refractory atelectasis
Treat underlying cause	Thoracentesis/chest tube	For compressive atelectasis from pleural effusion or pneumothorax
	Tumor management	Surgical resection, radiation, or stenting for endobronchial lesion
	Surfactant replacement	For neonatal RDS (adhesive atelectasis)

Prevention is the most commonly tested management concept for atelectasis. In the post-operative setting, the single most important intervention is incentive spirometry, which encourages sustained maximal inspiration to recruit collapsed alveoli. The patient should perform 10 breaths every 1 to 2 hours while awake, aiming for the highest inspiratory volume possible. This is combined with early ambulation and effective pain control, as inadequate analgesia limits the patient's ability to take deep breaths, perpetuating the cycle of hypoventilation and collapse.

For established atelectasis, chest physiotherapy (percussion, vibration, and postural drainage) helps mobilize secretions and facilitate their clearance. In mechanically ventilated patients, suctioning is used to remove accumulated secretions from the airways.

Positive airway pressure with CPAP or BiPAP provides a pneumatic splint that holds alveoli open and recruits collapsed lung units. This is useful in patients with diffuse atelectasis or those who cannot perform incentive spirometry effectively. Starting pressures are typically 5 to 10 cmH$_2$O for CPAP.

When atelectasis is refractory to conservative measures (persistent lobar collapse despite 24 to 48 hours of respiratory therapy), therapeutic bronchoscopy is the next best step. This allows direct suction of mucus plugs and lavage of the obstructed airway. Bronchoscopy is also indicated urgently when foreign body aspiration is suspected.

For compressive atelectasis, treatment targets the compressing lesion: thoracentesis or chest tube placement for pleural effusion or pneumothorax, paracentesis for tense ascites causing diaphragmatic elevation, or surgical intervention for mediastinal masses.

For adhesive atelectasis in neonates (RDS), the treatment is exogenous surfactant replacement (beractant or poractant alfa) administered via the endotracheal tube, combined with CPAP or mechanical ventilation.

An important point: antibiotics are not indicated for atelectasis itself. Although post-operative atelectasis causes fever, this is not an infectious process. Antibiotics should only be started if there is clinical evidence of superimposed pneumonia (purulent sputum, leukocytosis with left shift, new or worsening infiltrate without volume loss signs).

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Pneumonia	Both produce opacification on CXR and post-operative fever	Pneumonia shows air bronchograms without volume loss; atelectasis shows volume loss signs (mediastinal shift toward lesion, hemidiaphragm elevation). Pneumonia fever is typically later (POD 3 to 5) with productive cough and leukocytosis
Pleural effusion	Both cause opacification and decreased breath sounds on the affected side	Pleural effusion produces a meniscus sign on upright CXR and shifts the mediastinum away from the affected side (opposite to atelectasis). Dullness to percussion is present in both, but effusion demonstrates absent tactile fremitus
Pneumothorax	Both cause decreased breath sounds and dyspnea	Pneumothorax shows hyperlucency (not opacification) on CXR, hyperresonance on percussion (not dullness), and tracheal deviation away from the affected side in tension pneumothorax
Pulmonary embolism	Both occur post-operatively with dyspnea, tachypnea, and hypoxia	PE typically presents later (POD 5 to 10), CXR is often normal or near-normal (Westermark sign, Hampton hump are uncommon), and CT pulmonary angiography reveals intraluminal filling defects. D-dimer is elevated in PE
Endobronchial tumor	Can cause obstructive atelectasis and may be the underlying etiology	Consider when atelectasis is recurrent or non-resolving despite adequate respiratory therapy, especially in a smoker. CT and bronchoscopy with biopsy are essential for evaluation
Mucus plug vs. foreign body	Both cause obstructive atelectasis with identical radiographic findings	Foreign body aspiration has an acute onset, often with a witnessed choking episode, and is more common in children (ages 1 to 3) or elderly with impaired swallowing. Mucus plugging is gradual and associated with post-operative state or chronic lung disease
Rounded atelectasis vs. lung mass	Both appear as rounded opacities on CXR/CT	Rounded atelectasis shows the "comet tail sign" with adjacent pleural thickening and volume loss; lung mass shows no volume loss and may have irregular borders, spiculation, or lymphadenopathy

6. Traps and High-Yield Pearls

The most common trap with atelectasis questions centers on the direction of tracheal and mediastinal shift. Students frequently confuse atelectasis with pleural effusion or tension pneumothorax, all of which produce opacification or abnormality on the same side. The rule is straightforward: atelectasis pulls structures toward the collapsed lung (volume loss), while pleural effusion and tension pneumothorax push structures away (volume gain). If the vignette describes a post-operative patient with tracheal deviation toward the side of the opacity, atelectasis is the answer. If the trachea deviates away, think effusion or tension pneumothorax.

A second common error is treating post-operative day 1 fever with antibiotics. Test-writers present an early post-operative fever with a CXR showing basilar opacities and expect you to recognize atelectasis and choose incentive spirometry, not empiric antibiotics. The presence of fever alone does not equal infection.

Another tested concept is distinguishing atelectasis from pneumonia on imaging. Both cause opacification, but the presence of air bronchograms without volume loss points toward pneumonia (the airways remain patent and visible against the consolidated, fluid-filled alveoli). Atelectasis, by contrast, demonstrates volume loss signs and may lack air bronchograms in the obstructive subtype (because the airway is blocked).

Finally, be aware of the right middle lobe syndrome scenario: recurrent or chronic right middle lobe atelectasis due to the anatomy of the right middle lobe bronchus, which is long, narrow, and surrounded by lymph nodes. When a vignette describes persistent right middle lobe collapse, the test is assessing whether you will order bronchoscopy to evaluate for an underlying obstructing lesion.

The core competency being tested in atelectasis questions is the ability to recognize volume loss on imaging, correctly identify the direction of mediastinal shift, choose appropriate non-pharmacologic interventions (incentive spirometry and early ambulation), and avoid premature antibiotic use for non-infectious post-operative fever.

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