Pneumothorax Explained

Pneumothorax

• Pneumothorax is the presence of air or gas in the pleural space, caused by rupture of the visceral and parietal pleura.
• Air separates the visceral and parietal pleurae, destroying negative pressure and disrupting equilibrium between lung and chest wall elastic recoil forces.
• The affected lung part collapses towards the hilum, impairing oxygenation and ventilation.
• It can be categorized as spontaneous or traumatic, with spontaneous further divided into primary and secondary types.

Spontaneous Pneumothorax

• Primary spontaneous pneumothorax unexpectedly occurs in healthy people, typically men aged 20-40.
• It is caused by spontaneous rupture of blebs (blister-like formations) on the visceral pleura.
• Rupture usually occurs in the lung apices during sleep, rest, or exercise.
• The cause of bleb formation is unknown, but there appears to be a genetic component.
• Over 80% of individuals have emphysema-like changes in their lungs despite no smoking history.
• Secondary spontaneous pneumothorax occurs in individuals with respiratory disorders which compromises the integrity of the visceral pleura

Traumatic Pneumothorax

• Traumatic pneumothorax is due to punctures from fractured ribs or knife/bullet wounds.
• It can result from medical intervention complications (iatrogenic), like transthoracic needle aspiration or mechanical ventilation (barotrauma).
• Traumatic pneumothorax frequently involves both visceral and parietal pleura.

Open vs Tension Pneumothorax

• Spontaneous or traumatic pneumothorax can present as either open or tension pneumothorax.
• In open pneumothorax, air drawn into the pleural space during inspiration through the injured area is forced back out during expiration.
• Open pneumothorax usually results in partial lung collapse.
• In tension pneumothorax, the pleural rupture acts as a one-way valve, allowing air in during inspiration but preventing escape during expiration.
• More air increases pressure, pushing against the lung and causing compression atelectasis, severely impacting oxygenation and ventilation.
• Increased pressure may compress/displace mediastinum, heart, great vessels, and trachea (mediastinal shift).
• The pathophysiologic effects of life-threatening tension pneumothorax include sudden pleural pain, tachypnea, and dyspnea.
• Physical exams may reveal absent/decreased breath sounds and hyperresonance to percussion, complicated by severe hypoxemia, tracheal deviation, and hypotension.

Pneumothorax Diagnosis and Treatment

• Diagnosis is confirmed with chest radiographs, ultrasound, or computed tomography (CT).
• Primary spontaneous pneumothorax is managed in an ambulatory setting with a small catheter with a one-way valve ; some may need surgery to prevent recurrence.
• Tension pneumothorax requires immediate hospitalization and treatment with aspiration, usually with thoracostomy (chest) tube attached to water-seal drainage with sunction
• After evacuation and pleural rupture has healed, the chest tube is removed.
• Persistent air leaks may need pleurodesis (talc instillation into the pleural space) or surgery.

Pleural Effusion

• Pleural effusion refers to the presence of fluid in the pleural space.
• Fluid usually comes from blood or lymphatic vessels beneath the pleural space.
• Effusions are divided into five categories based on mechanisms: transudative, exudative, empyema, hemothorax, and chylothorax.

Transudative Effusions

• Transudative pleural effusions are often clear or slightly discolored with few cells and little protein.
• Transudation of fluid into the pleural space occurs because of changes in hemodynamic or oncotic pressures within the pulmonary vessels.
• Common examples include congestive heart failure (increased venous and left atrial pressures push fluid into the pleural space) and hypoproteinemia.
• Hypoproteinemia (seen with liver/kidney disorders) decreases capillary oncotic pressure, promoting water diffusion.

Exudative Effusions and Empyema

• Exudative effusion occurs in response to inflammation, infection, or malignancy, involving inflammatory processes that increase capillary permeability.
• Biochemical mediators of inflammation open tight junctions between capillary endothelial cells, enabling leukocytes and plasma proteins to migrate out.
• Exudative effusions associated with pneumonia are called parapneumonic effusions, which resolve with the treatment of the underlying infection but can progress to empyema.
• Empyema contains infectious microorganisms that develops because of the contaminated lymphatics block leading to an outpouring of contaminated lymphatic fluid into the pleural space.
• Empyema most commonly occurs in older adults and children as a complication of pneumonia, surgery, trauma, or bronchial obstruction from a tumor.
• Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, and anaerobic bacteria are commonly documented infectious organisms.

Hemothorax and Chylothorax

• Hemothorax is the presence of blood in the pleural space, due to trauma, surgery, cancer, PE, or tuberculosis.
• Chylothorax results from a tear in the thoracic duct leading to chyle leakage into the pleural space; it is a rare complication of surgery/malignancies.
• Malignant pleural effusions often relate to lung cancer, breast cancer, and lymphoma, occurring in an estimated one-third of individuals with lung cancer.

Effects and Diagnosis of Pleural Effusion

• Small fluid collections may not affect lung function and remain undetected but removed by lymphatic system once the condition resolves..
• Dyspnea, compression of the lung with impaired ventilation, and pleural pain are common in larger effusions.
• Large effusions can lead to mediastinal shift and cardiovascular complications.
• Physical examination shows decreased breath sounds and dullness to percussion on the affected side with a pleural friction rub over areas of inflamed pleura.
• Diagnosis is confirmed via chest imaging and thoracentesis.
• Chest radiographs may show large amounts of pleural fluid, though smaller or localized fluid collections may require thoracic ultrasound, CT, or MRI.
• Thoracentesis provides symptomatic relief, with examination of the fluid to determine the type of effusion.
• Analysis includes number/type of cells, pH, and presence/absence of microorganisms.
• Medical pleuroscopy and pleural biopsies are indicated in some cases to evaluate unexplained effusions.

Pleural Effusion Treatment

• Management depends on the type and cause of the pleural effusion.
• Transudative effusions are managed by treating the underlying condition.
• Exudative effusions are also managed by treating the underlying condition in addition to drainage through placement of a chest tube if the effusion is large,.
• Management of empyema includes the administration of appropriate antimicrobials and drainage of the pleural space with a chest tube, often combined with intrapleural enzyme therapy.
• Deoxyribonuclease stimulates pleural fluid formation, reduces pleural fluid viscosity, and promotes resolution of systemic inflammation to achieve adequate drainage
• Malignant exudative effusions may require placement of an indwelling pleural catheter and pleurodesis.
• Hemothorax is managed surgically.
• Chylothorax may improve spontaneously or may require radiation (in the case of malignancy) or surgical management.

Restrictive Lung Diseases

• Restrictive lung diseases are characterized by decreased compliance (stiffness) of the lung tissue.
• More effort is needed to expand the lungs during inspiration, which increases the work of breathing
• Individuals with lung restriction have dyspnea, an increased respiratory rate, and a decreased tidal volume.
• Pulmonary function testing reveals a decrease in the FVC.
• Restrictive lung diseases also can cause ·V/Q· mismatch affecting the alveolocapillary membrane which reduces the diffusion of oxygen from the alveoli into the blood resulting in hypoxemia.
• Common restrictive lung diseases in adults are aspiration, atelectasis, bronchiectasis, bronchiolitis, pulmonary fibrosis, inhalation disorders, pneumoconiosis, allergic alveolitis, pulmonary edema, and acute respiratory distress syndrome.

Aspiration

• Aspiration is the passage of fluid and solid particles into the lung.
• It accounts for 5% to 15% of community-acquired pneumonia cases, especially in older individuals.
• An estimated 45% of the population aspirates while sleeping without causing disease.
• Predisposing factors for clinically significant aspiration and aspiration pneumonia include dysphagia, absent cough reflex, altered level of consciousness, endotracheal intubation, being bedridden, neurologic disorders , home oxygen therapy, and feeding through a nasogastric tube.
• The right lung, particularly the right lower lobe, is more susceptible to aspiration than the left lung because the branching angle of the right mainstem bronchus is straighter.

Aspiration Complications & Clinical Manifestations

• Characteristics of the aspirated material interact with host defenses leading to several pulmonary complications, including aspiration pneumonia, pneumonitis, pulmonary abscess, and airway obstruction.
• Aspiration of oral/pharyngeal secretions results in bronchial and alveolar inflammation and aspiration pneumonitis while bronchial damage includes loss of ciliary function and bronchospasm.
• Acidic fluid damages the alveolocapillary membrane, diminishes surfactant production, causes plasma and blood cells to move from capillaries into the alveoli, and causes the lung to become stiff/noncompliant.
• Aspiration may lead to infection of the lung parenchyma resulting in aspiration pneumonia.
• Gram-negative aerobic bacteria are now more common than anaerobes, and aspiration of large food particles has serious consequences resulting in bronchial inflammation and collapse of airways distal to the obstruction.
• Clinical manifestations of acute aspiration include the sudden onset of choking or intractable cough with or without vomiting.
• Aspiration pneumonitis is characterized by dyspnea, tachypnea, and tachycardia, with auscultation revealing crackles and wheezes along with rapid development of hypoxemia.
• Fever and purulent sputum production are common if aspiration pneumonia develops while Chronic aspiration is characterized by recurrent lung infections/chronic cough/persistent wheezing.
• Diagnosis is made by assessing risk factors/symptoms/chest radiographs, while bronchoscopy with bronchoalveolar lavage is indicated in some individuals.

Aspiration Prevention and Treatment

• Preventive measures for individuals at risk include use of a semirecumbent position, surveillance of enteral feeding, use of promotility drugs, and avoidance of excessive sedation.
• Fasting for a minimum of 8 hours before surgery reduces the incidence of aspiration associated with general anesthesia.
• The use of nasogastric tubes is controversial and oral hygiene may reduce the incidence of aspiration pneumonia.
• Speech-language pathologists employ techniques to reduce the risk of aspiration.
• Treatment of aspiration pneumonitis includes supplemental oxygen and suctioning; mechanical ventilation in severe cases.
• Routine administration of corticosteroids or antibiotics is not recommended for mild to moderate aspiration pneumonitis, but antibiotics are indicated if aspiration pneumonia develops.

Atelectasis

• Atelectasis is the collapse of lung tissue that causes ·V/Q· mismatch, leading to hypoxemia.
• There are three types of atelectasis: obstructive, compression, and surfactant impairment.

Obstructive Atelectasis

• Obstructive atelectasis results from obstructed or hypoventilated alveoli as the air is gradually absorbed.
• Mucous plugging or bronchogenic lung carcinoma, and aspiration of a foreign body are common causes.
• A subset occurs due to hypoventilation, especially in individuals who have undergone surgery or who have severe chest/abdominal pain, breathe shallowly, are reluctant to change position, and produce viscous secretions that tend to pool in dependent portions of the lung, forming ‘platelike' lesions.

Compression and Surfactant Impairment Atelectasis

• Compression atelectasis is caused by external pressure exerted by tumor, fluid, or air in the pleural space or by abdominal distention.
• Surfactant impairment atelectasis results from decreased production or inactivation of surfactant, which is necessary to reduce surface tension in the alveoli and prevent lung collapse.
• Surfactant impairment can occur because of premature birth and from any serious lung injury.

Atelectasis Clinical Manifestations & Treatment

• Clinical manifestations of atelectasis include dyspnea, cough, fever, and leukocytosis.
• Treatment includes deep-breathing exercises, frequent position changes, and early ambulation.
• Deep breathing promotes ciliary clearance of secretions/stabilizes alveoli by redistributing surfactant, and promotes collateral ventilation, while bronchoscopy may be needed to remove foreign bodies.

Bronchiectasis

• Bronchiectasis is persistent abnormal dilation of the bronchi usually in conjunction with other respiratory conditions that are associated with chronic bronchial inflammation, such as cystic fibrosis.
• It also can occur due to prolonged atelectasis, aspiration of a foreign body, recurrent pulmonary infections, tuberculosis, or congenital weakness of the bronchial wall.
• Bronchiectasis is associated with systemic disorders and there may be no known cause.
• Several classification schemes for bronchiectasis have been proposed, but have limited clinical utility due to heterogeneity.
• It results from recurrent inflammatory/infectious insults to the bronchial epithelium leading to infiltration of neutrophils and release of neutrophil-derived proteases that destroy the elastic and muscular components of the bronchial walls.
• Chronic infection caused by Pseudomonas aeruginosa is common and is associated with more rapid lung function decline, more sputum production, and increased mortality.

Bronchiectasis Symptoms, Diagnosis, and Treatment

• The primary symptom of bronchiectasis is a chronic productive cough with dyspnea and fatigue as common symptoms.
• Recurrent lower respiratory tract infections lead to expectoration of copious amounts of foul-smelling, purulent sputum.
• Common signs include clubbing of the fingers and hemoptysis with hypoxemia.
• Pulmonary function studies show decreases in the FVC and expiratory flow rates.
• Diagnosis is confirmed using high-resolution CT treated with antibiotics , anti-inflammatory drugs, bronchodilators, mucolytic agents, chest physiotherapy, and supplemental oxygen.
• Removal of the affected portion of the lung may be necessary, and a lung transplant may be needed in advanced disease.

Bronchiolitis

• Bronchiolitis is a diffuse injury of the bronchioles (small airways 2 mm or less) resulting in inflammation and fibrosis that occurs most commonly in children due to vial infection.
• In adults, it most often results from smoking and chronic bronchitis but can occur in association with an upper/lower respiratory tract infection or with interstitial lung diseases.
• There is a fibrotic process causing scarring of the lungs referred to as organizing pneumonia or severe lung injury where scarring and occlusion cause severe respiratory compromise referred to as bronchiolitis obliterans.
• Clinical manifestations include a rapid ventilatory rate, use of accessory muscles, low-grade fever, and a nonproductive cough with wheezing.
• The V/Q mismatch results in hypoxemia, and diagnosis is made by bronchoscopy with biopsy.
• Bronchiolitis is treated with chest physical therapy that includes humidified air administration, deep-breathing exercises, and postural drainage in addition to pharmacologic management includes antibiotics, corticosteroids, and immunosuppressive drugs.
• Careful handling of the lung tissue prior to surgery, tailored management of antirejection drugs, and the use of other medications can improve bronchiolitis obliterans outcomes after lung transplantation.

Pulmonary Fibrosis

• Pulmonary fibrosis is an excessive amount of fibrous or connective tissue in the lung that can be idiopathic or be caused by formation of scar tissue after active pulmonary disease or from autoimmune disorders .
• Fibrosis of the interstitial lung tissue around the alveoli causes decreased oxygen diffusion across the alveolocapillary membrane and hypoxemia.
• Decreased lung compliance leads to increased work of breathing, a decreased tidal volume, and resultant hypoventilation with hypercapnia.
• Diffuse pulmonary fibrosis has a poor prognosis.

Idiopathic Pulmonary Fibrosis

• Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disease of unknown etiology.
• Prevalence is difficult to determine due to inconsistent diagnostic criteria but typically affects older individuals, and men.
• Environmental factors are felt to be a critical component of the risk with gene polymorphisms linked to development.
• The pathogenesis is felt to be multifactorial caused by epithelial damage along with innate and adaptive immune responses involving neutrophils, macrophages, fibrocytes, resulting in the release of inflammatory cytokines and growth factors that initiates scarring and honeycombing to lung parenchyma.
• IPF presents with dyspnea on exertion and dry cough and auscultation reveals fine crackles showing symptoms and signs of comorbid conditions.
• The diagnosis rests on the use of high-resolution CT scans and biopsies with treatment aimed at pulmonary rehabilitation and management with medication.
• Lung transplant is indicated in selected individuals.

Inhalation Disorders - Exposure to Toxic Gases

• Inhalation of gaseous irritants causes significant respiratory dysfunction commonly caused by toxic gasses (smoke, ammonia, hydrogen chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide).
• Injuries in burns can include heat, smoke particles, and toxic gases from household or industrial combustants causing damage to the airway epithelium promoting mucus secretion, inflammation, mucosal edema, ciliary damage, pulmonary edema, and surfactant inactivation.
• Acute toxic inhalation frequently is complicated by acute respiratory distress syndrome and pneumonia with initial symptoms include burning of the eyes/nose/throat, coughing; chest tightness; and dyspnea along with hypoxemia.
• Treatment includes supplemental oxygen, mechanical ventilation, bronchodilators, corticosteroids, and support of the cardiovascular system with most individuals responding quickly.

Prolonged Exposure to supplemental oxygen

• Prolonged exposure to high O2 can result in oxygen toxicity caused by a severe inflammatory response mediated by oxygen free radicals and lipid peroxidation that leads to disruption of surfactant production/edema/fibrosis and a reduction in lung compliance.
• In infants, this can lead to bronchopulmonary dysplasia with treatment aimed at a reduction of the inspired oxygen concentration.

Pneumoconiosis

• Pneumoconiosis represents any change in the lung caused by inorganic dust inhalation that occurs after years of exposure with progressive fibrosis.
• Most common causes are silica and coal inhaled in the workplace resulting in silicosis or coal workers' lung or asbestosis,
• Deposition of these materials in the lungs causes chronic inflammation resulting in pulmonary fibrosis and deterioration.
• Common clinical manifestations include cough, chronic sputum production, dyspnea, decreased lung volumes, and hypoxemia with diagnosis made from occupational history and chest radiography.
• Treatment is usually palliative and focuses on preventing further exposure, decreasing hypoxemia and bronchospasm, and focuses on pulmonary rehabilitation.

Hypersensitivity Pneumonitis

• Hypersensitivity pneumonitis (extrinsic allergic alveolitis) is an inflammatory disease caused by inhalation of organic particles, and is not IgE mediated.
• Pathophysiology is of type III and type IV hypersensitivity with infiltration of T lymphocytes, inflammatory cells, and autoantibodies resulting in tissue damage.
• It can be classified into acute, chronic non-fibrotic, or chronic fibrotic forms
• The acute form results from high-level exposure with the chronic form results from long-term, low-level exposure and the resulting symptoms may not occur until weeks, months, or years of exposure
• Treatment focuses on the removal of the offending agent and uses medication.

Pulmonary Edema

• Pulmonary edema is excess fluid in the lung caused by disrupted protective mechanisms from lymphatic drainage, capillary hydrostatic pressure, capillary oncotic pressure, and capillary permeability.
• The most common cause is left-sided heart disease, where increased filling pressures on the left side of the heart causes a concomitant increase in the pulmonary capillary hydrostatic pressure.
• Fluid moves from the capillary into the interstitial space and alveoli faster than the lymphatic systems ability to remove it.
• Another cause is pulmonary or systemic injury that causes damage to the alveolocapillary membrane resulting in inflammation that allows water, cells, and plasma proteins to leak out of of the capillary into the interstitial spaces.
• Pulmonary edema also can result from obstruction of the lymphatic system from tumors or fibrotic tissue.
• Fluid in the alveoli results in a low V·/Q· ratio and hypoxemia.
• Clinical manifestations include dyspnea, hypoxia, and an increased work of breathing.
• Physical examination may find inspiratory crackles and dullness to percussion over the lung bases In severe cases, pink, frothy sputum is expectorated, hypoxemia worsens, and hypoventilation with hypercapnia May developed.
• Treatment is directed to treat the root cause of the pulmonary edema, increasing cardiac output with diuretics, vasodilators, and drugs that improve heart contractions; removing the offending agent; providing supplements; maintaining adequate circulation; and managing lymphatic blockage
• Mechanical ventilation may be needed if edema significantly impairs ventilation and oxygenation.