​Kembara Xtra - Medicine - Atelectasis

​Kembara Xtra - Medicine - Atelectasis 
BASICS DESCRIPTION
The incomplete expansion of lung tissue as a result of collapse or closure is known as atelectasis. Impaired airway mucus clearance results from the reduction of lung capacity and function.
Generally classified as:
- Obstructive: blockage of the airway
- Nonobstructive: lack of contact between parietal and visceral pleurae, lung tissue replacement by scarring or infiltrative illness, surfactant malfunction, and parenchymal compression
The rate of collapse, the volume of lung affected, and the presence of underlying lung disease and/or comorbidities in the patient all influence the symptoms. Hypoxemia may be brought on by decreased respiratory gas exchange.

EPIDEMIOLOGY The average age is 60 years, but anyone can get it.
No preference exists for race or financial status; male = female.
Incidence

Asbestos workers might develop rounded atelectasis in up to 65-70% of cases.
Depending on the collateral ventilation and the number of lobes involved, lobar atelectasis varies.
Prevalence
Up to 90% of patients may experience postoperative atelectasis, particularly following significant cardiovascular or gastrointestinal (GI) surgeries.

PATHOPHYSIOLOGY AND ETIOLOGY
The most prevalent type of atelectasis is obstructive (resorptive), which is brought on by intrinsic airway obstruction. It can be brought on by airway wall abnormality (such as congenital deformity and emphysema) or luminal obstruction (such as a foreign body, mucus plug, asthma, cystic fibrosis, trauma, or mass lesion).
– A full collapse of the alveolar tissue results from the fast resorption of alveolar air into the deoxygenated venous system distal to the obstruction.
- FiO2 fraction of inspired oxygen The 79% ambient nitrogen in the atmosphere dissociates from the alveoli more slowly than the quick O2 dissociation distal to the barrier. By maintaining positive pressure inside the alveoli, this prevents collapse.
However, with increased FiO2, the nitrogen content is reduced, allowing atelectasis to develop quickly at the commencement of blockage.
– Age, underlying lung disease, and FiO2 are only a few of the patient-related factors that can affect the health and functionality of the collateral ventilatory systems (pores of Kohn, canals of Lambert, and fenestrations of Boren) in each lobe.
- The fenestra of Boren increase in emphysema patients as a compensatory mechanism, which can delay atelectasis despite an obstructive lesion or bulk.
Nonobstructive atelectasis - Pleural membrane separation of the visceral and parietal layers causes passive atelectasis, which occurs after a pleural effusion or pneumothorax.
Space-occupying lesions, cardiomegaly, abscess, or severe lymphadenopathy can all cause compression atelectasis.
Alveoli are compressed by increased chest wall pressure, which reduces functional residual capacity (FRC) or resting lung volume.
- Adhesive atelectasis caused by radiation, smoke inhalation, acute respiratory distress syndrome (ARDS), or uremia. Alveoli collapse and elevated surface tension are results of the underlying surfactant failure.
– Cicatrization, which is pleural or parenchymal scarring, is a common complication of toxic or radiation exposure, granulomatous illness (such as sarcoidosis), and drug-induced fibrosis (such as amiodarone and cyclophosphamide).
- Replacement atelectasis: full lobar collapse brought on by the appearance of a diffuse tumor (bronchioalveolar cell cancer).
As a result of their severe pleural illness, people who were exposed to asbestos often develop rounded atelectasis.
The rest
- Hypoxia brought on by a pulmonary embolus
- Muscular weakness: a side effect of anesthesia or neuromuscular illnesses affecting the breathing muscles
Child Safety Considerations
Children have a higher risk of getting atelectasis because their compensatory and collateral ventilation systems are less developed.

RISK FACTORS include prolonged bed rest and critical care, as well as general anesthesia (including postoperative epidural anesthesia and long-acting muscle relaxants).
A significant blood transfusion of four units
Insertion of a nasogastric tube Hypothermia
High plateau pressure (>30 cm H2O) and tidal volume (Vt >10 mL/kg) during mechanical breathing Risk factors for postoperative atelectasis in patients:
- Age between 60 and 6 years.
- COPD, a condition that affects the lungs.
- Obstructive snoring
- CHF, or congestive heart failure
Alcoholism and smoking
Thoracic hypertension
- Hemoglobin 10 g/dL - BMI >27 kg/m2 (poor evidence) - Albumin 3.5 g/dL
- Functional dependency in activities of daily living (ADLs) of ASA class II+
- Cardiothoracic, vascular, upper GI, neurosurgical, oromaxillofacial, and ENT surgical procedures
Right middle lobe syndrome (Brock syndrome): wedge-shaped density extending inferiorly and anteriorly from the hilum; sometimes a precursor to more significant postoperative pulmonary problems. Most commonly observed on lateral chest radiography; no universally accepted clinical description

DURATIONAL PREVENTION
Early mobilization, deep breathing practices, coughing, and regular body position changes
In patients undergoing elective heart surgery, preoperative physical therapy decreased the incidence of atelectasis, pneumonia, and length of stay (LOS). Other postoperative pulmonary problems or mortality, however, remained unchanged. Before conclusions on the effectiveness of incentive spirometry (IS) and chest physiotherapy can be made, significant RCTs are also required.
Postoperative pulmonary problems, including as pneumonia and respiratory failure, are linked to mechanical ventilation settings without positive end-expiratory pressure (PEEP), plateau pressures, and high Vt (Vt >10 mL/kg):
Utilize low Vt and plateau pressures with adequate PEEP to reduce ventilator-induced damage.
Continuous positive airway pressure (CPAP) during anesthesia induction and reversal of anesthesia-induced atelectasis after intubation by a recruitment maneuver may reduce postoperative pulmonary complications. - Ensure lower FiO2 during anesthetic induction and intraoperatively to prevent nitrogen washout.

CONDITIONS OFTEN Associated with
Trauma, respiratory syncytial virus (RSV), bronchiolitis, pulmonary edema, pulmonary embolism, pneumonia, pleural effusion, pneumothorax, obstructive lung diseases (COPD and asthma), bronchial stenosis, pulmonic valve disease, and pulmonary hypertension, as well as neuromuscular conditions like muscular dystrophy, spinal muscular atrophy, spinal cord injury, and Guillain-Barré syndrome

History includes smoking, COPD, pulmonary insufficiency, exposure to radiation, asbestos, or other air pollutants, as well as tachypnea and sudden-onset dyspnea, nonproductive coughing, and pleuritic pain on the afflicted side.

PHYSICAL EXAMINATION - Signs of cyanosis or hypoxia - Diminished chest expansion - Tracheal or precordial impulse displacement toward the affected side; dullness to percussion - Bronchial breathing in patent airway - Wheezing or absent breath sounds in obstructed airway

DETECTION & INTERPRETATION OF DIAGNOSIS

Initial examinations (lab, imaging)
If an infection is suspected, a viral panel, respiratory Gram stain, and culture are recommended.
Despite hypoxemia, PaCO2 levels are often normal or low, according to ABG.
Lateral, PA, and chest x-ray (CXR)
- Raised diaphragm, displaced hilum, mediastinal shift to the side of the atelectatic lung, volume loss in the ipsilateral hemithorax
- Ribs crowded together and the border of the diaphragm or heart silhouetted
- Compensatory hyperinflation of the unaffected lung and compensatory hyperlucency of the remaining lobes of the damaged lung
- The Lobar Collapse
Obstructive atelectasis is indicated by wedge-shaped densities. Discoid (subsegmental or plate) is indicated by small, linear bands (Fleischner lines), which are frequently found at lung bases. Direct symptoms of atelectasis include fissure displacement and opacification of the collapsed lobe. The inverted "S sign of Golden," which denotes neoplastic displacement of the minor fissure, may be observed in right upper lobe collapse.
- Air bronchograms: Compressive atelectasis may be indicated by pleural fluid or air.
- Adhesive atelectasis may first manifest as a diffuse reticular granular pattern, which in more severe cases can develop into a pulmonary edema pattern and bilateral opacification.
Complete atelectasis of the entire lung: opacification of the entire hemithorax and a shift of the mediastinum to atelectatic lung. Pleural-based round density: round atelectasis

Tests in the Future & Special Considerations
To visualize the airway and mediastinal structures and determine the etiology of atelectasis in cases where the cause is unclear, a chest CT or MRI may be indicated.
Pulmonary function tests (PFTs) can be used to diagnose diseases that are obstructive or restrictive as well as low respiratory muscle pressures.
A potent indicator of a higher risk for postoperative pulmonary problems, including atelectasis, is hypoalbuminemia (albumin 3.5 g/L).
Other/Diagnostic Procedures
Flexible fiber-optic bronchoscopy may be an option in situations that are undiagnosed or unresponsive.

GENERAL MEASURES/TREATY
Define and address the underlying cause.
Lay on the unaffected side, promote frequent coughing, deep breathing exercises, and early mobility as part of PEEP for prevention after surgery or general anesthesia.
Despite a lack of proof, IS is frequently administered while awake to prevent postoperative pulmonary problems following coronary artery bypass grafting (CABG).
If you have hypoxemia or severe respiratory distress, you should mechanically ventilate.
Lower plateau pressures (30 mm Hg) and lower Vt (6 mL/kg) are associated with a lower mortality rate. In surfactant-impaired lung regions, PEEP of 15 to 20 mL may be required to maintain arterial O2 saturation.

First Line: MEDICATION
 
Asthma inhalers and steroids should be used, as should effective analgesics to allow deep inspiration and coughing. Mucolytics, such as saline and N-acetylcysteine, can be considered to promote airway clearance. Pharmacotherapy should address the underlying etiology.

Child Safety Considerations
Dornase alfa, a medication used to treat cystic fibrosis in children, may be useful in removing mucus blockage.
In the inpatient context, chest physiotherapy, which includes percussion, drainage, deep insufflation, and saline lavage, is the most often used treatment.
In order to improve mucus clearance in patients with cystic fibrosis and neuromuscular dysfunction, additional physically stimulating modalities (mechanical insufflation-exsufflation, intrapulmonary percussive ventilation, intermittent positive pressure breathing) may be helpful.
Continuous distending pressure has the potential to lessen lung damage in preterm newborns with RDS and has shown some promise in the treatment of such infants. Bronchoscopy in obstructive atelectasis is still debatable. However, bronchoscopy may be helpful if there is a mucus plug or cast present.
Next Line
Numerous studies have shown the effectiveness of fiber-optic bronchoscopy in improving airway clearance, however there is disagreement over how well it works to treat atelectasis. It might be helpful for people who have tried chest physiotherapy unsuccessfully or who have contraindications to it (such as chest wall injuries).

SURGICAL AND OTHER PROCEDURE
Resection of the underlying disease with appropriate surgery (tumor, severe lymphadenopathy)
ALERT
It is more likely coincidental than causal that postoperative atelectasis and fever are related.


CONSIDERATIONS FOR ADMISSION, THE INPATIENT, AND NURSING

Make sure there is enough humidification and oxygenation (you may start with 100% FiO2 and taper). To prevent nitrogen washout, which can expedite atelectasis, increase FiO2 cautiously if obstructive atelectasis is suspected.

CONTINUING CARE AFTERCARE RECOMMENDATIONS

patient observation
Depending on the underlying cause and coexisting comorbidities, monitoring frequency and effectiveness will differ.
Outpatient surveillance may be necessary in cases of atelectasis associated with infection or asthma that are not problematic.


EDUCATION OF PATIENTS
 
Increase mobility as much as possible while promoting regular coughing and deep breathing exercises. If your symptoms worsen or you have shortness of breath, seek additional therapy or visit the ED.

Postoperative atelectasis often resolves spontaneously within 24 hours, but it might last for days.
Treatment of the underlying disease or cancer is necessary for the endobronchial blockage causing lobar atelectasis to resolve.
Only resectable etiologies (such as tumors) or severe cases of atelectasis that result in bronchiectasis and persistent infections warrant surgical intervention.

Acute atelectasis complications include hypoxemia, respiratory failure, and postobstructive drowning of the lung. Chronic atelectasis complications include bronchiectasis, pleural effusion, and empyema.