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Atelectasis: Causes, Consequences, Comorbidities, Pathophysiology,

Prevention, and Treatment
Article · February 2021

DOI: 10.31080/ecprm.2021.10.00791
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Cronicon O P EN A C C ESS EC PULMONOLOGY AND RESPIRATORY MEDICINE
Review Article
Atelectasis: Causes, Consequences,

Comorbidities, Pathophysiology, Prevention, and Treatment
Nicholas A Kerna1,2*, Uzoamaka Nwokorie3, Abdullah Hafid4, Kevin D Pruitt5, Fernand Jean-Baptiste6, Mary Ann
Christy Ortigas7, Wail Taha Mohammed Taha8, Joseph Anderson II9, and Priya John10
1
SMC–Medical Research, Thailand
2
First InterHealth Group, Thailand
3
University of Washington, USA
4
Academy of Integrative Health and Medicine (AIHM), USA
5
Kemet Medical Consultants, USA
6
Department of Biological Sciences, Florida Atlantic University, USA
7
University of Nevada, Las Vegas, USA
8
School of Medicine, Al Fashir University, Sudan
9
International Institute of Original Medicine, USA
10
Fettle Path, USA
*Corresponding Author: Nicholas A Kerna, (mailing address) POB47 Phatphong, Suriwongse Road, Bangkok, Thailand 10500.
Contact: [email protected].
Received: January 11, 2021; Published: February 27, 2021
DOI: 10.31080/ecprm.2021.10.00791
Abstract
Impeded compliance in the respiratory system and diminished oxygenation are signs of atelectasis. Although not thoroughly
explained, several mechanisms resulting in atelectasis are commonly held: compression, alveolar gas resorption, and surfactant
impairment. Various and diverse factors precipitate atelectasis, such as introducing FiO2, obesity of the patient, general and
intubated anesthesia, chronic obstructive pulmonary disease (COPD), the patient’s age, surgery, and type of surgery. Atelectasis
results in compliance reduction, oxygenation deterioration, and exacerbation of lung impairment. Comorbidities of atelectasis
include cardiomyopathy, type 2 diabetes, hypertension, and stroke.
Many patients who undergo a surgical procedure with general anesthesia experience atelectasis. Hence, it is critical to identify the
underlying etiology and mechanism of atelectasis, applying a specific therapeutic approach and eliminating or reducing perioperative
complications in the lungs and alveoli. Atelectasis’ prevention and treatment range from spontaneous ventilation, preoxygenation,
CPAP or PEEP, and recruitment maneuvers. Properly applied recruitment maneuvers improve respiratory mechanisms and gaseous
transfer in patients who manifest atelectasis under general anesthesia. Nevertheless, more studies regarding the administration
and verifying the effectiveness of such procedures on oxygenation and lung parameters would further confirm, to a greater or lesser
degree, their beneficial and uniform contribution to the improved prognoses of impaired patients.
Keywords: Alveoli; COPD; General Anesthesia; Intubation; Lung Impairment; Respiratory
Abbreviations
ARDS: Acute Respiratory Distress Syndrome; COPD: Chronic Obstructive Pulmonary Disease; CPAP: Continuous Positive Airway
Pressure; T: Computed Tomography; EIT: Electric Impedance Tomography; FiO2: Fraction of Inspired Oxygen; MRI: Magnetic Resonance
Imaging; PEEP: Positive End Expiratory Pressure; QoL: Quality of Life
Introduction
Atelectasis is a significant clinical condition which is frequently an antecedent of or a contributor to other postoperative pulmonary
complications that are generally complicated. Atelectasis involves alveolar collapse, which is reversible. Atelectasis occurs from an
obstruction in the airway that serves affected alveoli involved in respiratory gas exchange [1].
Citation: Kerna NA, Nwokorie U, Hafid A, Pruitt KD, Jean-Baptiste F, Ortigas MAC, Taha WTM, Anderson II J, John P. “Atelectasis: Causes,
Consequences, Comorbidities, Pathophysiology, Prevention, and Treatment”. EC Pulmonology and Respiratory Medicine 10.3 (2021): 92-
104.
Atelectasis: Causes, Consequences, Comorbidities, Pathophysiology, Prevention, and Treatment
93
Historical perspective
For several decades, surgeons and anesthesiologists have recognized that patients with otherwise healthy lungs can experience
significant respiratory compromise after the administration of general anesthetics [2].
Atelectasis’ symptoms include diminished compliance in the respiratory system and accompanied by reduced oxygenation. Atelectasis
was initially presumed to be a cause of impaired oxygenation during general anesthesia. Bendixen., et al. (1963) hypothesized that
ventilating patients spontaneously, deprived of deep episodic breathing, might result in advanced atelectasis complicated by augmented
shunting and reduced pulmonary compliance. However, these changes were reversible by hyperinflating the lungs [3].
Due to conventional radiology limitations at that time, it had been problematic to confirm this hypothesis until the advent of enhanced
imaging technologies. More contemporary and useful images techniques include computed tomography (CT), magnetic resonance imaging
(MRI), electric impedance tomography (EIT), ultrasonography, and—the most current procedure—intravital microscopy for diagnosing
atelectasis [4,5]. The use of these newer imaging procedures has revealed that about 90% of patients who undergo general anesthesia
develop atelectasis and in some cases, resulting in aveolar damage. Severe atelectasis can lead to respiratory failure and death [2,5,6].
The following summarizes the causes, consequences, comorbidities, pathophysiology, prevention, and treatment of atelectasis, and
calls for further research into the effectiveness of specific treatment procedures.
Discussion
Causes and pathophysiology of atelectasis
The degree of susceptibility for the attack of atelectasis is the greatest for patients under anesthesia. Although the precise mechanisms
underlying atelectasis remain unsettled, three mechanisms contributing to intraoperative atelectasis are recognized worldwide [7]. These
mechanisms are compression, alveolar gas resorption, and surfactant impairment [8].
Compression
The distinctive effect of general anesthesia on alveoli is mechanical compression. Compression atelectasis occurs when the thorax’s
pleural pressure exceeds intrapulmonary pressure, leaving the alveoli unable to persist in an open state [9,10]. When a patient under
anesthesia is placed in a supine position, heightened pleural pressure is encountered due to various organs’ weight against the diaphragm,
contributing to compression atelectasis [11].
The diaphragm equilibrates pressure between the lungs and abdomen [12]. A change in blood pressure can increase intrapleural
pressure, further adversely affecting patients with specific commorbidities [11–13].
Alveolar gas resorption
Aveolar gas resorption is affected by two processes. The first process involves oxygen tension during oxygen supplementation. Under
normal conditions, the lungs’ low-ventilation regions compared to perfused regions exibit decreased alveolar oxygen tension when the
amount of inspired oxygen is low. During general anesthesia, when the inspired oxygen’s fraction is enhanced with supplemental oxygen,
a proportionate increase in the partial pressure of arterial oxygen occurs. Consequently, gaseous exchange between the alveolus and
the capillary is enhanced. Besides, the alveolar nitrogen tension decreases as the aveolar volume is reduced due to nitrogen loss and a
corresponding increase in oxygen absorption [14].
Consequences, Comorbidities, Pathophysiology, Prevention, and Treatment”. EC Pulmonology and Respiratory Medicine 10.3 (2021):
92-104.
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The second process is triggered by an overall collapse of small airways. Under this scenario, gas pockets form, which become trapped
in alveoli distal to the obstruction. These gas pockets progressively collapse as oxygen uptake proceeds according to the diffusion gradient
[9].
Surfactant impairment
Pulmonary surfactant, a surface-active phospholipid, decreases the surface tension of the alveoli. Its presence enhances stability of
alveoli, preventing alveolar collapse. Anesthesia adversely affects surfactant, hindering its stabilizing properties. The repetitive opening
and closing of alveoli during general anesthesia (with mechanical ventilation) results in diminished levels of surfactant, leading to
increased surface tension and a significant reduction in or loss of functional residual capacity [15].
Causes of atelectasis
Fraction of inspired oxygen (FiO2)
During mechanical ventilation, the introduction of high FiO2 contributes to the development of atelectasis, impairing respiratory
gaseous exchange [16,17].
Ventilation parameters and tidal volume
The setting of ventilation parameters and tidal volume is especially critical in acute respiratory distress syndrome (ARDS) patients.
These patients express low tidal volumes. Positive end-expiratory pressure should be maintained (being mindful of existing pulmonary
lesions) [18].
Obesity in the patient
A slight association has been observed between of atelectasis and body mass index [19]. However, a low residual functional capacity
and more significant abdominal pressure are observed in obese patients [20]. Together, these factors contribute to alveolar collapse. The
prevalence of atelectasis is more significant in the obese group than the non-obese group of patients undergoing surgery [21].
Anesthesia
Atelectasis may be observed in a patient after the initiation of general anesthesia [22]. Anesthetics cause respiratory depression and
impairment of the neurological control of the respiratory muscles [23].
Chronic obstructive pulmonary disease (COPD)
COPD patients develop mild atelectasis and slight shunt. Moreover, a worsening of the V/Q ratio is encountered [22].
The preventive mechanism for atelectasis in COPD patients has not been wholly explained [24]. Hyperinsufflation circumvents
compressive alveolar collapse, reducing the drop in residual functional capacity, although promoting absorption atelectasis [22]. Also,
equilibrium can be augmented by the slight flexible recoil of the thoracic wall and lung, decreasing lung volume [24].
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Age of the patient
A patient’s age is not the most crucial factor contributing to atelectasis. However, children are prone to atelectasis owing to lower
residual capacity. Greater pliability of the thoracic cage (rib cage) and related paradoxical movements of the diaphragm also predispose
children to atelectasis [25]. The application of 5 cm H2O effectively twarts atelectasis in this population [24.25].
With an increase in age, the incidence of premature closure of the small airways ensues with a corresponding rise in regions of low
ventilation perfusion ratios. This scenario discourages compression atelectasis, but may promote absorption atelectasis [26].
Surgery and the type of surgery
Regardless of the type of surgery, atelectasis is predominant during the intial phase of anesthesia [27]. Surgical trauma can trigger
reflexes in the phrenic nerve, affecting the respiratory muscles. These surgically-induced reflex-disruptions result in respiratory
impairment, causing constriction. These factors combined produce hypoventilation and a concomitant decrease in residual function
capacity, contributing to atelectasis [28].
In laparocscopic procedures, pneumoperithoneum insufflation pressure is factorial in promoting or discouraging atatelectasis [29].
In thoracic surgery, lung compression is accompanied by secretion-excess and airway reactivity. In cardiac surgery (pulmonary
bypass), shunt and hypoxiemia develop with atelectasis—facilitated by increased capillary permeability and aveolar edema, resulting in
increased lung weight and extravascular pulmonary fluid [30].
Consequences of atelectasis
Compliance reduction
Compliance reduction results from diminished lung volume, impairing pulmonary function [31].
Oxygenation deterioration
During surgery under general anesthesia, the shunt’s persistence corresponds to the degree of atelectasis [32]. Small airway closures
and atelectasis contribute significantly to hypoxemia in patients undergoing surgery, resulting in hypovolemia, anemia, hypoventilation,
and disturbances in the ventilation-perfusion ratio [31,32].
Aggravation of lung impairment
As the alveoli open and close repetitively, pulmonary damage occurs in the atelectatic region and throughout the lungs. The amount
of lung tissue affected by atelectasis is inversely proportional to the amount of lung tissue that needs to adapt to the tidal volume applied
[18,33].
Postoperative infections
In the experimental setting (as opposed to the clinical setting), a correlation between respiratory infection progression and
perioperative atelectasis has been established [34]. Atelectasis interferes with antibiotic agents’ absorption and perfusion into the lungs,
disrupting the precise and efficacious drug concentrations needed to effectively control pathogens, resulting in persisent infection or
delayed recovery [35].
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Comorbidities and sequelae of atelectasis
Comorbidities of atelectasis include cardiomyopathy, diabetes mellitus (Type-II), hypertension, and stroke [20,25].
Prevention and treatment of atelectasis
Preparations should be made in the prevention of or rapid response to atelectasis during any phase of the perioperative period, bearing
in mind that the intial introduction of the anesthesia is the most vulnerable period.
Spontaneous ventilation
Spontaneous ventilation contributes to lung conscription, compensating for the loss of diaphragmatic tone and a reduced gradient of
arterial aveolar oxygen [27,33].
Preoxygenation
Preoxygenation (using a FiO2 less than 1 before inducing anesthesia) is reached as the patient inhales gas with FiO2 equal to 1. Such
levels of oxygen concentration and denitrogenation induce atelectasis [16,17,36].
Continuous positive airway pressure (CPAP) or positive end-expiratory pressure (PEEP)
The application of CPAP at 5–6 cm H2O during anesthetic initiation prior to orotracheal intubation, inhibits intraoperative atelectasis
by restoring oxygenation, increasing oxygen reserves, and restoring lung volume in dead spaces [36]. Pressure of about 10 cm of H2O is
needed by obese patients [37]. Lung overdistension may appear at PEEP H2O levels over 10 cm to 15 cm, which is avoided at lower levels
[36,38].
Optimum ventilation parameters
Low tidal volume with moderate to high PEEP is more potent in and in keeping with collapse avoidance than high tidal volume and low
PEEP [39]. When ventilating one lung, 8 ml/kg tidal volume, a PEEP of 4–10 cm H2O, and 35 cm H2O of plateau pressure-assisted level
reduce the occurrence of atelectasis post-surgically [40].
Recruitment maneuvers
Recruitment maneuvers are applied once atelectasis is confirmed. The maneuvers’ aim is to provide a constant increase of
transpulmonary pressure, reversing the collapse of aveoli [41]. Recruitments stimulate surfactant release, reinstate alveolar stability, and
lessen any damage caused by mechanical ventilation.
The efficacy of the maneuvers is subject to various factors, such as ventilator adjustments, the patient’s pulmonary condition, and
the patient’s threshold in amplified thoracic pressure [41]. The maneuvers typically take place laterally and until maximum results are
achieved [39,42]. Hence, recruitment maneuvers should be chosen to match the patient’s particular state and status.
The transpulmonary pressure necessary for distention is dependent on pleural pressure. Consequently, transpulmonary pressure
must be higher than pleural pressure in cases of compliance-reduction in the thoracic cage [39]. Higher pressures of up to 60–70 cm H2O
are required for patients experiencing acute respiratory distress syndrome due to more significant surfactant impairment and alveolar
edema [43,44].
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The pressure required to avoid alveolar collapse is comparatively lower than that required to inflate the alveolus. The pulmonary
components are stabilized and re-occlusion is avoided when PEEP is applied after recruitment. Also, when recruitments are applied
devoid of PEEP, a transitory effect is observed. Hence, after re-occlusion, PEEP is employed to avoid the reoccurrence of atelectasis.
Optimum PEEP accomplishes alveolar opening while avoiding hyper-distension of ventilated areas [32,42,44].
The recruitments are generally applied to patients experiencing impairment in gaseous exchange while under anesthesia—when a
high fraction of inspired oxygen is applied or due to a low PEEP [32,45].
There are several parameters for evaluating the efficacy of the recruitment maneuvers, such as the increase in the ratio of the partial
pressure of oxygen to the fraction of inspired oxygen, the decrease in alveolar-capillary gradient for oxygen tension, the outcome of
lungcompliance and end-expiratory lung volume. The combination of an increase in residual functional capacity and dead space reduction
generates maximum effect in normalizing the aveoli while avoiding lung hyperdistension [2,40].
Recruitment maneuvers have been shown to diminish the shunt or atelectasis in various conditions and surgical procedures. Claxton.,
et al. (2003) reported on the success of one-lung ventilation—in patients after cardiopulmonary bypass and in a bariatric surgery group
of patients—in avoiding shunt and atelectasis [31].
Frequently after recruitment, a transitory reduction in oxygenation is seen. This reduction occurs due to the hemodynamic worsening
and the blood flow shunt to highly insufflated regions [45]. Experiemental models have demonstrated that specific recruitment maneuvers
can have lethal results in cases of pheumonmia and sepsis [4].
Moreover, recruitment maneuvers are contraindicated for intracranial hypertensive patients as they are prone to barotrauma. These
patients must also be monitored precisely as high transpulmonary pressure, such as those observed in particular intensive recruitment
maneuvers, has been associated with the breakdown of the alveolocapillary barrier—causing the release of cytokines into the interstitial
pulmonary edema and blood [45].
Types of recruitment maneuvers
Two types of recruitment maneuvers can be applied to non-pulmonary disease patients undergoing anesthesia and surgery. The first
is the vital capacity maneuver, which provides comprehensive lung distension that is not pathological, ameliorating atelectasis that might
occur after cardiopulmonary bypass or induction [44].
The second maneuver is applied during pressure-regulated ventilation. This procedure involves an incremental increase in inspiratory
pressure and positive end-expiratory pressure for every two to three respiratory cycles. This procedure maintains a sustained differential
pressure of 20 cm to 25 cm H2O until a peak inspiratory pressure of 40 cm H2O and a PEEP of 20 cm H2O is attained. This state is regulated
for about a minute, followed by a decrease until an optimum PEEP is achieved [30]. This maneuver seems related to low hemodynamic
decline compared to its vital capacity complement. Levels are reached at respiratory frequencies of 10 to 12 cycles per minute and
inspiration- expiration ratios from 1:1 to 1:1.5 [32].
Special considerations in children
Compared to adults—children have smaller aveolar diameter, airways, and a flexible ribcage. Nevertheless during anesthesia, the
atelectasis is dispersed in children similar to adults. However, the inspiratory pressure required for children is less. than adults [4].
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Efficacy of non-invasive mechanical ventilation
CPAP at approximately 10 cm H2O can reestablish RFC, diminishing atelectasis and hypoxemia by improving intrathoracic pressure
and reducing respiratory exertion. The use of CPAP in patients who experience hypoxemia after abdominal surgery reduces the frequency
of atelectasis, the requirements for reintubation, and the frequency of respiratory infections. The use of non-invasive ventilation with
pressure-assistance seems to reduce the occurrence of atelectasis, regarding the application of continuous positive pressure [46].
Application of analgesia
Appropriate analgesia provides a reduction of atelectasis owing to an upsurge in lung volume and vital capacity. It also improves
diaphragm activity indexes [40,41]. Local epidural methods, in combination with local anesthetics, may be advantageous. Experimental
data regarding these methods are inconclusive: 1) outcomes are inconsistent concerning how pulmonary complications are cleared; 2)
how a specific type of analgesia could hinder abdominal and intercostal muscles that assist ventilation. Systemic opiates can raise the
pressure produced by the abdominal muscles, decreasing lung volume, while epidural analgesia can cause the condition [47].
Atelectasis secondary to pleural effusion (caused by pneumonia and or pleurisy)
One of the most significant risk factors for atelectasis is pleural effusion [48], an extreme buildup of fluid in the pleural space. Pleural
effusion occurs due to an imbalance in the production and removal of fluids. Although pleural fluid may not indicate a specific disease, it
impies a causal pathology—pleural effusions accompany several lung, pleural. and systemic disorders [49].
Mechanism of atelectasis secondary to pleural effusion
Probable mechanisms of pleural fluid buildup are as follows:
• Interstitial fluid in the lungs secondary to increased pulmonary capillary pressure (as in heart failure or penetrability as in
pneumonia).
• Reduced intrapleural pressure.
• Diminished oncotic plasma pressure (as in hypoalbuminemia).
• Pleural membrane penetrability and lymphatic flow obstruction (as in pleural malignancy or infection).
• Diaphragmatic disorders (as in hepatic hydrothorax).
• Rupture of the thoracic duct (as in chylothorax).
Although several diseases cause pleural effusion, pneumonia is recognized as the foremost cause in adults and children [50]. Extensive
pleural effusions may not only give rise to compressive atelectasis but may also cause complete lung collapse, accompanied by a
contralateral shift of the mediastinum [51].
Signs and symptoms of atelectasis secondary to pleural effusion
Pleural effusion interrupts the respiratory mechanism of atelectasis patients, which can progress to restrictive respiratory failure.
Respiratory parameters include total lung capacity, forced vital capacity, and functional capacity. A disparity in ventricular diastolic col-
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lapse and ventilation-perfusion may arise, depending on the degree of atelectasis caused by effusion. Consequently, the most commonly
observed symptoms are mild, nonproductive cough and dyspnea [52].
Diagnosis of atelectasis secondary to pleural effusion
The following diagnostic application of bronchoscopy is recommended in suspected atelectasis, central lung lesion, or massive pleural
effusion [52]. Doyle and Lawler (1984) described seven criteria for diagnosing the rounded atelectasis [53] (Table 1).
1. A rounded, peripheral lung form that is never surrounded entirely by the lung
2. A form that is considerably dense at its periphery
3. A form that creates an acute angle with the pleurae
4. Thickening of adjacent pleurae
5. Bronchi and vessels uniting in the direction of the mass
6. A blurred centrally focused edge
7. The existence of an air bronchogram
Table 1: Seven criteria for diagnosing the rounded atelectasis, adapted from Doyle and Lawler (1984) [53].
Radiologic diagnosis—chiefly the chest radiograph—is employed when signs and symptoms are suspected of having been caused
by pleural effusion (as in atelectasis consequent to pleural effusion). Generally, the bilateral decubitus chest radiograph is performed to
evaluate the underlying atelectasis [52]. Cytological analysis of pleural fluid is also utilized in diagnosing atelectasis resultant to pleural
effusion [54].
Treatment of atelectasis secondary to pleural effusion
The selection of conservative treatment is based primarily on the specific cause and etiology, fluid drainage, and pleurodesis.
Surgical intervention is employed for more severe or life-threatening cases. Specific treatment aimed at the primary cause resolves most
transudative effusions, including atelectasis.
Pleurodesis is the most suitable treatment choice for repeated accumulative effusions. This procedure entails inserting a chest tube
and introducing sclerosing chemical agents into the pleural cavity, creating bonds between the chest wall’s outer and inner surfaces, to
avoid air or fluid accumulation in the pleural cavity. This method is the most efficacious and minimally invasive procedure available to
resolve pleural effusion [55].
The drainage process is accomplished by intercostal tubes or pigtail catheters, allowing the patient to remain ambulatory [56]. The
urosac applied as a chest drainage bag has been shown to be safe, effective, and economical in several studies [57]. The surgical management
of atelectasis secondary to a pleural effusion includes pleuropneumonectomy, decortication, window operation, pleurectomy, closure of
bronchopleural fistula with or without grafting, thoracostomy and thoracoplasty, and fenestration [58].
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Consequences of untreated atelectasis (or failed atelectasis treatment) secondary to pleural effusion
Patient presentation of pleural effusion accompanied by atelectasis is frequently observed in emergency departments and intensive
care units. The determination of the extent of the pleural effusion and the degree of atelectasis is essential. Large-area pleural effusion
poses a risk of compressive atelectasis, collapsing a lung (with a mediastinum contralateral shift) [51].
Atelectasis can arise as a complication in the perioperative period, contributing to morbidity and mortality and the progression of
pneumonia and acute respiratory failure [59].
The pleural effusion diagnosis is challenging as the pleura is an inner cavity, lacking direct access. Several noninvasive diagnostic
procedures are limited for definitive diagnosis. Treatment choice is based on any underlying disease, disease distribution in the pleural
cavity, and the physician’s experience. Delays or setbacks in a timely and accurate diagnosis can result in significant adverse consequences,
including diminishing the patient’s quality of life (QoL) [60].
Conclusion
Diminished compliance in the respiratory system and reduced oxygenation are hallmarks of atelectasis. Although not entirely
understood, several mechanisms resulting in atelectasis are generally accepted: compression, alveolar gas resorption, and surfactant
impairment. Numerous and varied factors contribute to or directly cause atelectasis, such as introducing FiO2, obesity in the patient,
general anesthesia, COPD, the patient’s age, surgery, and type of surgery. Atelectasis results in compliance reduction, oxygenation
deterioration, and aggravation of lung impairment. Comorbidities of atelectasis include cardiomyopathy, type 2 diabetes, hypertension,
and stroke.
Many patients who undergo a surgical procedure under general anesthesia experience atelectasis. Thus, it is vital to recognize the
underlying causes and mechanisms of atelectasis in order to select and apply a specific therapeutic approach, eliminating or minimizing
perioperative complications in the lungs and alveoli. The prevention and treatment of atelectasis range from spontaneous ventilation,
preoxygenation, CPAP or PEEP, and recruitment maneuvers. Appropriately applied recruitment maneuvers enhance respiratory
echanisms and gaseous exchange in patients who develop atelectasis under general anesthesia. Nevertheless, further studies regarding
the application and overall efficacy of such procedures on oxygenation and lung parameters would help confirm, to a greater or lesser
degree, their beneficial and consistent contribution to the improved prognoses of affected patients.
Conflict of Interest Statement
The authors declare that this paper was written in the absence of any commercial or financial relationship that could be construed as
a potential conflict of interest.
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Atelectasis: Causes, Consequences, Comorbidities, Pathophysiology,

Article · February 2021

Mary Ann Christy Rubin Ortigas Uzoamaka Nwokorie

USAT-Harvard Dataverse Project View project

Doctor of Philosophy (PhD) in Biomedical Science – Dissertation View project

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Atelectasis: Causes, Consequences,

Keywords: Alveoli; COPD; General Anesthesia; Intubation; Lung Impairment; Respiratory

Causes and pathophysiology of atelectasis

Alveolar gas resorption

Fraction of inspired oxygen (FiO2)

Ventilation parameters and tidal volume

Obesity in the patient

Chronic obstructive pulmonary disease (COPD)

Age of the patient

Surgery and the type of surgery

Aggravation of lung impairment

Comorbidities and sequelae of atelectasis

Prevention and treatment of atelectasis

Continuous positive airway pressure (CPAP) or positive end-expiratory pressure (PEEP)

Optimum ventilation parameters

Types of recruitment maneuvers

Special considerations in children

Efficacy of non-invasive mechanical ventilation

Atelectasis secondary to pleural effusion (caused by pneumonia and or pleurisy)

Mechanism of atelectasis secondary to pleural effusion

Probable mechanisms of pleural fluid buildup are as follows:

• Reduced intrapleural pressure.

• Diminished oncotic plasma pressure (as in hypoalbuminemia).

• Diaphragmatic disorders (as in hepatic hydrothorax).

• Rupture of the thoracic duct (as in chylothorax).

Signs and symptoms of atelectasis secondary to pleural effusion

Diagnosis of atelectasis secondary to pleural effusion

Treatment of atelectasis secondary to pleural effusion

Conflict of Interest Statement

Volume 10 Issue 3 March 2021

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