Pneumothorax

Overview of Classification

• Pneumothorax is categorised by aetiology into spontaneous, traumatic, and iatrogenic types.
• A physiological classification also exists: simple, communicating, tension, and catamenial pneumothoraces.
• Risk factors and triggers vary depending on the underlying pathophysiology and clinical context.

Primary Spontaneous Pneumothorax (PSP)

• Occurs in individuals with no known clinical lung disease.
• Commonly affects tall, thin males under 40 years of age.
• Cigarette smoking is the most significant risk factor, increasing the risk 22-fold in men and 9-fold in women.
• Subpleural blebs or bullae rupture, leading to air leakage into the pleural space.
• High-resolution imaging has revealed many cases previously considered idiopathic actually have subclinical lung changes.
• Cannabis use and vaping are emerging contributors due to airway inflammation and structural damage.
• Familial clustering is observed; associated genetic conditions include Birt-Hogg-Dubé syndrome, Marfan syndrome, Ehlers-Danlos syndrome, and homocystinuria.

Secondary Spontaneous Pneumothorax (SSP)

• Occurs in patients with underlying lung disease.
• COPD is the leading cause, accounting for up to 80% of SSP cases in UK studies.
• Other associated diseases include severe asthma, cystic fibrosis, tuberculosis, interstitial lung diseases, pulmonary malignancies, lymphangioleiomyomatosis, and Langerhans cell histiocytosis.
• In cystic fibrosis, the risk increases with age and disease severity; infection with Pseudomonas or Burkholderia species is also contributory.
• HIV-positive individuals may develop SSP from Pneumocystis jirovecii pneumonia (PCP), often with bilateral involvement.
• Symptoms in SSP are generally more severe due to compromised lung reserve.

Catamenial Pneumothorax

• A rare form seen in women aged 30–50, occurring within 72 hours before or after menstruation.
• Usually affects the right lung.
• Thought to arise from pleural endometriosis, with diaphragmatic fenestrations or haematogenous spread of endometrial cells as likely mechanisms.
• Often underdiagnosed and may mimic PSP on initial presentation.

Traumatic Pneumothorax

• Results from blunt or penetrating trauma that disrupts the parietal or visceral pleura.
• Blunt causes include rib fractures and crush injuries; penetrating trauma includes stab or gunshot wounds.
• May be complicated by haemothorax, pulmonary contusion, or diaphragmatic rupture.
• Occult pneumothorax may not be visible on chest radiograph but is detectable on CT imaging.

Iatrogenic Pneumothorax

• Caused by medical procedures breaching the pleura.
• Common interventions include central venous catheterisation (especially subclavian), thoracentesis, transbronchial or CT-guided biopsy, and positive-pressure ventilation.
• Risk is increased in patients with lung disease or inexperience by the operator.
• The routine use of ultrasound in thoracentesis reduces the incidence significantly.
• Mechanical ventilation with high pressures or PEEP is a frequent cause of barotrauma-induced pneumothorax.
• Cases have also resulted from misdirected nasogastric tubes, bronchoscopy, and cardiopulmonary resuscitation.

Tension Pneumothorax

• Occurs when air enters the pleural space but cannot exit, leading to rising intrathoracic pressure.
• Causes mediastinal shift, compression of the contralateral lung, and reduced venous return to the heart.
• Rapidly leads to haemodynamic compromise and death if untreated.
• May complicate any pneumothorax type, especially under mechanical ventilation.
• Risk factors include high ventilator pressures, obstructed chest drains, chest trauma, bullous lung disease, and occlusive dressings over open chest wounds.

Pneumothorax ex Vacuo

• Occurs when a lung fails to re-expand following pleural drainage or lobar collapse.
• Associated with malignancy, mucous plugging, or pleural fibrosis.
• Develops due to extreme negative pressure in the pleural cavity.
• May not require drainage and should be distinguished from other pneumothorax types.

Other Risk Factors and Associations

• Barotrauma due to scuba diving or air travel can precipitate pneumothorax in individuals with bullous lung disease or cysts.
• Hyperbaric oxygen therapy and non-invasive ventilation (NIV) have also been implicated in susceptible patients.
• A history of prior pneumothorax increases the risk of recurrence—rates are up to 30% in PSP and even higher in SSP.
• Recurrence is more likely in smokers, patients with structural lung abnormalities, and those with underlying chronic lung diseases.

Normal pleural pressure dynamics

• In a healthy respiratory cycle, the intrapleural pressure remains negative relative to both alveolar and atmospheric pressures. This pressure gradient keeps the lungs expanded and closely apposed to the chest wall.
• If a communication forms between the alveolar space or the external environment and the pleural cavity, gas flows into the pleural space, following the pressure gradient.
• The lung then collapses partially or completely, depending on the size and persistence of the air leak, leading to a reduction in vital capacity and arterial oxygenation.

Primary Spontaneous Pneumothorax (PSP)

• PSP is generally associated with rupture of apical blebs or bullae in individuals without overt pulmonary disease.
• These patients typically have subclinical abnormalities seen on CT or thoracoscopy. In one study, ipsilateral emphysematous-like changes (ELCs) were found in 89% and contralateral in 80% of PSP cases, compared with only 20% in controls.
• The condition tends to occur in tall, thin, young individuals, likely due to increased negative pleural pressures in the lung apices, which subject alveolar structures to greater mechanical stress.
• Fluorescein-enhanced autofluorescence thoracoscopy (FEAT) can detect sites of leakage not seen on conventional thoracoscopy.

Inflammatory and oxidative stress mechanisms

• Chronic inflammation and oxidative stress are thought to contribute to PSP.
• Bronchoalveolar lavage (BAL) studies have demonstrated increased inflammatory cell counts in small airways.
• Oxidative markers such as plasma malondialdehyde are elevated, while antioxidant enzyme levels like erythrocyte superoxide dismutase are reduced in PSP patients.
• The presence of ELCs may be driven by enzymatic degradation of lung tissue by neutrophil-derived proteases and an imbalance in antioxidant defences.

Genetic and familial influences

• Up to 10% of PSP cases report a positive family history.
• Familial cases have been linked to mutations in the FLCN gene, as seen in Birt-Hogg-Dubé (BHD) syndrome, an autosomal dominant disorder associated with pulmonary cysts, skin lesions, renal tumours, and spontaneous pneumothorax in around 22% of patients.
• Other genetic conditions implicated include Marfan syndrome and homocystinuria.

Secondary Spontaneous Pneumothorax (SSP)

• SSP occurs in the context of underlying parenchymal lung disease.
• The pathophysiology involves rupture of structurally abnormal lung regions such as emphysematous bullae, necrotic cavities, or cysts.
• Diseases associated with SSP include COPD, asthma, tuberculosis, cystic fibrosis, bronchogenic carcinoma, interstitial lung diseases (e.g. idiopathic pulmonary fibrosis, sarcoidosis), connective tissue diseases (e.g. rheumatoid arthritis), Langerhans cell histiocytosis, and lymphangioleiomyomatosis.
• HIV/AIDS patients, particularly those with Pneumocystis jirovecii pneumonia (PCP), have a high incidence of pneumothorax, often with bilateral involvement. PCP-related SSP has declined due to HAART and TMP-SMX prophylaxis.
• Cystic fibrosis patients have a reported SSP incidence up to 18.9%, with high recurrence rates and associations with Pseudomonas, Burkholderia, and ABPA.

Catamenial pneumothorax

• Occurs in premenopausal women and is temporally related to menstruation.
• Most commonly affects the right lung and is associated with thoracic endometriosis.
• Proposed mechanisms include passage of air through diaphragmatic fenestrations, prostaglandin-induced vasoconstriction and bronchiolar disruption, migration of endometrial tissue, and haematogenous spread.
• In one case series, 52% of lesions were localised to the visceral pleura, while 39% involved the diaphragm.

Tension pneumothorax

• Results from a one-way valve mechanism where air enters the pleural space during inspiration but cannot exit.
• As air accumulates, intrathoracic pressure rises, causing ipsilateral lung collapse and mediastinal shift toward the opposite side.
• This compromises venous return to the right atrium by compressing the vena cava and atria, leading to hypotension, hypoxaemia, and cardiovascular collapse.
• Common causes include trauma, mechanical ventilation with high PEEP, fibreoptic bronchoscopy, and invasive procedures like tracheostomy or thoracostomy.
• Infants, especially with meconium aspiration, are particularly vulnerable.
• Any penetrating injury or failed occlusion of an open pneumothorax can lead to this progression.
• Tension pneumothorax must be suspected in any ventilated ICU patient with sudden haemodynamic or respiratory deterioration.

Iatrogenic pneumothorax

• Occurs secondary to medical procedures that breach pleural integrity.
• Common causes include transthoracic needle aspiration biopsy (32–37% incidence), transbronchial biopsy, thoracentesis, central venous catheter placement (especially subclavian), intercostal nerve block, CPR, positive-pressure ventilation, and tracheostomy.
• Therapeutic thoracentesis carries a pneumothorax risk of up to 30% when performed by inexperienced clinicians.
• Use of bedside ultrasound during thoracentesis significantly reduces risk.
• Nasogastric tube misplacement and inadvertent right mainstem bronchus intubation are additional contributors.

Traumatic pneumothorax

• Caused by blunt or penetrating thoracic injury.
• Rib fractures can directly lacerate the pleura or lung parenchyma.
• High-risk occupations (e.g. diving, aviation) increase susceptibility due to barotrauma.
• Complications include hemopneumothorax and bronchopleural fistula formation.
• Tension physiology may develop when a traumatic defect functions as a one-way valve.

Pneumomediastinum and subcutaneous emphysema

• Arises when alveolar rupture allows air to dissect through peribronchial and perivascular connective tissue into the mediastinum.
• May result from intense intrathoracic pressure changes (e.g. Valsalva, vomiting, parturition), asthma, mechanical ventilation, or direct trauma to the oesophagus or airways.
• Air can track from the mediastinum into the neck, retroperitoneum, and subcutaneous tissues, producing widespread emphysema.
• If mediastinal pressure rises sufficiently, rupture of the mediastinal pleura can result in secondary pneumothorax in up to 18% of cases.

Overview

• The true incidence of pneumothorax is likely underestimated due to asymptomatic cases and underreporting of mild symptoms.
• Epidemiological patterns vary depending on pneumothorax type, age group, sex, comorbidities, and smoking status.
• Both spontaneous and non-spontaneous pneumothoraces show distinct distributions in the population.

Primary Spontaneous Pneumothorax (PSP)

• Most commonly affects tall, thin males in their early twenties, with a peak incidence between ages 20–30.
• Rarely occurs in individuals older than 40 years.
• Age-adjusted incidence is 7.4–18 per 100,000 men and 1.2–6 per 100,000 women annually.
• In England and Wales, the overall annual presentation rate is 24 per 100,000 men and 10 per 100,000 women.
• Male-to-female incidence ratio is approximately 6.2:1.
• Smoking is the strongest risk factor, increasing PSP risk by 22 times in men and 9–10 times in women compared to non-smokers.
• Lifetime risk in male smokers is around 12%, compared with 0.1% in non-smokers.
• Risk increases proportionally with the number of cigarettes smoked per day, reaching a 102-fold increase in heavy male smokers.
• Recurrence rate is 20% to 60% within three years after the initial episode.

Secondary Spontaneous Pneumothorax (SSP)

• Typically affects older individuals, with peak incidence between 60 and 65 years of age.
• Age-adjusted incidence is 6.3 per 100,000 men and 2.0 per 100,000 women annually.
• Male-to-female ratio is approximately 3.2:1.
• COPD is the most common underlying cause, with a reported incidence of 26 per 100,000 persons.
• SSP accounts for 50% to 70% of spontaneous pneumothoraces in COPD patients.
• Bacterial pneumonia is implicated in around 11% of SSP cases.
• Pneumocystis jirovecii pneumonia (PCP) is responsible for pneumothorax in 5% to 10% of affected individuals, particularly those with HIV/AIDS.

Iatrogenic Pneumothorax

• Increasingly observed due to the rise in invasive procedures in critical care.
• Common causes include CVC placement, thoracentesis, lung biopsy, and mechanical ventilation.
• Incidence ranges from 5 to 7 per 10,000 hospital admissions (excluding post-thoracic surgery cases).
• Although uncommon, it may cause significant morbidity or even mortality.
• Routine use of ultrasound for thoracentesis reduces the risk significantly.

Traumatic Pneumothorax

• More common than spontaneous forms in emergency and hospital settings.
• Caused by both blunt and penetrating trauma.
• Pneumothorax affects 1–2% of all neonates and up to 19% of neonates with respiratory distress syndrome.
• Associated with high-risk occupations such as diving and aviation.
• Complications include haemothorax and bronchopleural fistula.

Tension Pneumothorax

• Occurs in 1–2% of idiopathic spontaneous pneumothorax cases.
• Historically associated with tuberculosis, which accounted for a 1.4% pneumothorax incidence in TB patients.
• Prehospital needle decompression is performed in 10–30% of trauma cases transported to level-1 trauma centres, though not all have confirmed tension pneumothorax.
• Tension pneumothorax may be present in up to 5% of fatal combat-related thoracic injuries.
• In ICU settings, true incidence is unknown but underreported.
• In the Australian Incident Monitoring Study (AIMS), 17 of 2,000 adverse events involved pneumothorax, and four were diagnosed as tension pneumothorax.

Catamenial Pneumothorax

• Rare subtype predominantly affecting women aged 30–50.
• Typically occurs within 1–3 days after the onset of menstruation.
• Closely associated with thoracic endometriosis, though pelvic disease does not predict thoracic involvement.
• May be under-recognised and misdiagnosed as PSP on initial presentation.

Pneumomediastinum

• Most often seen in young, otherwise healthy individuals aged 20–40.
• Slight male predominance.
• Estimated incidence is 1 per 10,000 hospital admissions.
• Often triggered by intense intrathoracic pressure events (e.g., Valsalva manoeuvre, vomiting, parturition, or asthma exacerbation).

Primary Spontaneous Pneumothorax (PSP)

• Often occurs in otherwise healthy young adults, most commonly tall, thin males in their early 20s.
• Prior to rupture of a subpleural bleb, patients are typically asymptomatic.
• The most common presenting symptoms are sudden-onset pleuritic chest pain and dyspnoea.
• Chest pain is often described as sharp or stabbing, may radiate to the ipsilateral shoulder, and is aggravated by deep inspiration.
• Symptoms frequently begin while the patient is at rest rather than during exertion or Valsalva manoeuvres, despite popular association with increased intrathoracic pressure.
• Mild cases may be well tolerated and show spontaneous symptom improvement over 24 hours, even without resolution of the air accumulation.
• Episodes can take up to 12 weeks to resolve fully if untreated.
• Anxiety and non-specific symptoms like fatigue or malaise are less frequently reported.
• A prior history of pneumothorax is important to elicit due to recurrence risk (15%–40%), with up to 15% of recurrences occurring on the contralateral side.

Secondary Spontaneous Pneumothorax (SSP)

• More common in older adults, typically with underlying lung disease, most notably COPD and cystic fibrosis.
• Dyspnoea tends to be more pronounced than in PSP due to reduced pulmonary reserve.
• Chest pain may persist longer and is often more severe.
• Cystic fibrosis has one of the highest recurrence rates of all underlying conditions (up to 90%).
• Associated conditions include emphysema, pulmonary infections, and interstitial lung disease.
• Unlike PSP, SSP can occur during exertion or secondary to increased intrathoracic pressure from coughing or airway obstruction.
• Risk factors such as smoking, male sex, tall stature, and age over 55 years should be explored.

Iatrogenic Pneumothorax

• Symptoms mimic those of spontaneous pneumothorax and vary depending on age, baseline lung function, and pneumothorax size.
• Common procedures leading to pneumothorax include CVC placement, thoracentesis, lung biopsy, mechanical ventilation, and cardiopulmonary resuscitation.
• History should include recent hospitalisation or intervention involving the thorax, neck, abdomen, or central venous access.

Tension Pneumothorax

• Presents more dramatically than simple pneumothorax, but clinical features may be subtle or misleading, particularly in the critically ill.
• Typical symptoms include sudden-onset pleuritic chest pain (90%) and severe dyspnoea (80%).
• Less common symptoms include anxiety, fatigue, and epigastric pain.
• High-risk scenarios include patients on mechanical ventilation (especially with elevated airway pressures), or with chest trauma.
• Clinicians should maintain high suspicion for tension pneumothorax when a patient experiences acute cardiorespiratory compromise, especially if airway pressures increase or ventilation becomes difficult.

Catamenial Pneumothorax

• Should be considered in women aged 30–50 presenting with recurrent right-sided pneumothorax that coincides with menstruation (typically within 48–72 hours of onset).
• History may reveal prior endometriosis, though this is not always present.

Pneumomediastinum

• Symptoms overlap with pneumothorax but may include distinctive complaints.
• Common historical features include sudden-onset substernal chest pain (67%), persistent cough (42%), sore throat (25%), and dysphagia, dyspnoea, nausea, or vomiting (8%).
• Pain may radiate to the neck, back, or shoulders and worsen with deep breathing, coughing, or lying supine.
• Common triggers include asthma exacerbation, forceful vomiting, childbirth, seizures, Valsalva manoeuvre, or recent endoscopic procedures.
• A history of oesophageal instrumentation or trauma raises concern for oesophageal rupture, which carries high mortality.
• Although traumatic pneumomediastinum is observed in up to 6% of patients with chest trauma, it rarely indicates severe injury.

General Clinical Appearance

• Presentation ranges from completely asymptomatic to severe respiratory distress depending on the size of the pneumothorax, underlying lung pathology, and whether it is under tension.
• Diaphoresis, cyanosis, splinting of the chest wall, and altered mental status may be observed in severe cases.
• Patients with large pneumothoraces or tension pneumothorax may demonstrate decreased alertness or even reduced consciousness.

Respiratory Examination

• Respiratory distress is common in all significant pneumothoraces and may progress to arrest in tension cases.
• Tachypnoea is frequently observed; bradypnoea may occur as a preterminal event.
• Asymmetric chest wall movement may be visible, particularly in large pneumothoraces.
• Tracheal deviation towards the contralateral side may occur in tension pneumothorax but is an unreliable and late finding.
• Breath sounds are typically reduced or absent over the affected hemithorax, but may remain audible even in large pneumothoraces.
• Hyperresonance on percussion may be present, but this is a rare and inconsistent finding.
• Decreased tactile fremitus and adventitious sounds such as crackles or wheezing may be noted.
• Subcutaneous emphysema may be present in pneumomediastinum or after traumatic/iatrogenic pneumothorax.
• The Hamman sign, a crunching sound synchronous with the heartbeat, may be heard in pneumomediastinum, though it is uncommon.

Cardiovascular Examination

• Tachycardia is the most common cardiovascular sign in all forms of pneumothorax.
• Hypotension is a hallmark of tension pneumothorax but may occur late and inconsistently.
• Jugular venous distension may be seen in tension pneumothorax unless masked by profound hypotension.
• Pulsus paradoxus can occur but is not specific.
• Cardiac apical displacement is rare and not commonly identified clinically.

Tension Pneumothorax (Specific Features)

• Marked respiratory distress, chest pain, tachycardia, and hypoxaemia are near-universal findings.
• Auscultation reveals reduced or absent air entry on the affected side.
• Tracheal deviation, though classically described, may be absent or delayed in onset.
• Patients may show signs of shock, including hypotension, weak pulses, and reduced consciousness.
• In mechanically ventilated patients, tension pneumothorax can present as increased airway pressures and sudden drop in oxygen saturation and cardiac output.
• On volume-controlled ventilation, rising peak and plateau pressures may be observed.
• On pressure-controlled ventilation, sudden drops in delivered tidal volume can be a clue.
• Barotrauma-induced pneumothorax typically progresses rapidly in ventilated patients and may lead to pulseless electrical activity (PEA) or asystole if untreated.

Pneumomediastinum (Distinctive Signs)

• May present with subcutaneous emphysema, particularly in the neck or anterior chest wall.
• Hamman sign (precordial crunching synchronous with the heartbeat) is a classical, though inconsistently present, finding.
• Breath sounds may remain normal; there is often no respiratory distress unless associated with underlying lung disease or oesophageal rupture.
• Abdominal distension may occur if intrathoracic pressure is transmitted caudally through diaphragmatic fenestrations.

Spontaneous and Iatrogenic Pneumothorax

• Examination findings are similar for both types and depend largely on the size of the pneumothorax and the patient's lung reserve.
• Tachycardia is usually the earliest and most consistent sign.
• Tachypnoea and hypoxia may also be present, especially in secondary spontaneous pneumothorax.
• Auscultatory findings such as diminished air entry are often subtle and may be missed, particularly in early or small pneumothoraces.

Initial Investigations

• Chest x-ray is the first-line imaging modality in stable patients who can sit upright.
• A postero-anterior (PA) erect inspiratory film is recommended to identify pneumothorax and assess its size and associated features.
• A visible pleural line with absence of peripheral lung markings confirms the diagnosis.
• In supine patients, the deep sulcus sign (an abnormally lucent costophrenic angle) may be the only clue to pneumothorax.
• Chest x-rays also help detect other signs such as subcutaneous emphysema, mediastinal shift, and associated pleural effusion.
• Baseline blood tests including a full blood count and clotting screen are required prior to interventions like chest drain insertion.
• Coagulopathy (INR ≥1.5 or platelets ≤50 x 10⁹/L) should be corrected before invasive procedures in non-urgent cases.

Chest Ultrasound

• Chest ultrasound is increasingly used in emergency and intensive care settings due to its portability and speed.
• It is especially valuable in trauma patients who cannot be mobilised for x-ray.
• Key findings in pneumothorax include absence of lung sliding, absence of comet-tail artefacts, presence of a lung point (where sliding and non-sliding pleura meet), and the barcode (stratosphere) sign on M-mode.
• Ultrasound has higher sensitivity than supine chest x-rays, particularly in detecting small or occult pneumothoraces.
• Operator skill significantly affects diagnostic accuracy, and ultrasound cannot distinguish pneumothorax from bullae or blebs in COPD.
• It is not suitable for monitoring resolution over extended periods due to decreasing accuracy beyond 24 hours after chest drain placement.

CT Chest

• CT is the most sensitive modality for diagnosing pneumothorax and differentiating it from mimics like bullous lung disease.
• It is useful for assessing pneumothorax in trauma, occult pneumothorax, or when chest x-ray and clinical findings are discordant.
• CT can visualise lung blebs and bullae, confirm pneumothorax in patients on mechanical ventilation, and evaluate associated parenchymal disease in SSP.
• In patients with suspected tension pneumothorax who are stable and under continuous monitoring, CT may help guide management, though imaging should never delay emergency decompression.
• CT can also detect pneumomediastinum and distinguish it from pneumothorax when both are suspected.

Arterial Blood Gas (ABG)

• ABG is considered when oxygen saturations fall below 92% on room air or when respiratory distress persists.
• It helps evaluate the severity of gas exchange impairment, particularly in SSP and ventilated patients.
• Respiratory alkalosis is the most common abnormality in PSP, while respiratory acidosis may occur in SSP or in patients with significant comorbidities.
• ABG findings should not delay emergency treatment in patients with suspected tension pneumothorax.

Tension Pneumothorax

• This is a clinical diagnosis requiring immediate decompression and should not be delayed for imaging confirmation.
• Classic signs include hypotension, hypoxia, tracheal deviation, absent breath sounds on the affected side, and jugular venous distension.
• Imaging may show mediastinal shift, increased thoracic volume on the affected side, widened intercostal spaces, and diaphragmatic depression.
• In mechanically ventilated patients, tension pneumothorax can present as increased peak pressures and haemodynamic collapse.
• Chest x-ray is helpful in selected stable patients but not required for diagnosis.

Pneumomediastinum

• Often detected on lateral chest x-ray as air outlining the heart or great vessels.
• Mediastinal air may be seen retrosternally, especially on lateral films, and remains fixed unlike pneumothorax air which migrates with posture.
• CT chest is superior in detecting small or occult pneumomediastinum and should be considered in patients with suspected oesophageal rupture or barotrauma.
• Radiographic signs include the "ring around the artery" sign and lucency around the pulmonary artery or aortic arch.

Other Investigations

• Lateral decubitus films may help detect small pneumothoraces not evident on supine AP views.
• Transillumination in neonates may assist in rapid diagnosis by revealing increased light transmission on the affected side.
• Contrast-enhanced oesophagography is indicated in suspected oesophageal rupture, especially after vomiting or instrumentation.
• Bronchoscopy is not routinely used for diagnosis but may be relevant in trauma or when tracheobronchial injury is suspected.

Pneumothorax Size Estimation

• Radiographic estimation is essential to guide management decisions.
• The British Thoracic Society defines a large pneumothorax as a rim >2 cm between the lung edge and chest wall on a PA film.
• The American College of Chest Physicians uses a >3 cm distance from lung apex to cupola.
• Volumetric estimation using CT is more accurate but often unnecessary unless precise quantification is required.

Pneumonia

• Typically presents with fever, productive cough, and pleuritic chest pain.
• Physical examination may reveal bronchial breath sounds, crepitations, and dullness to percussion.
• Chest x-ray shows consolidation, which helps differentiate it from pneumothorax.

Acute Asthma Exacerbation

• Features include expiratory wheeze, chest tightness, and dyspnoea.
• Symptoms are relieved by bronchodilators.
• May mimic or coexist with pneumothorax, particularly in severe attacks.

Chronic Obstructive Pulmonary Disease (COPD)

• Presents with chronic cough, sputum production, and dyspnoea.
• Acute exacerbation may resemble pneumothorax; bullous changes may be radiographically indistinguishable.
• CT chest is often needed to differentiate between bullae and pneumothorax.

Pulmonary Embolism (PE)

• Presents with sudden-onset chest pain and dyspnoea.
• Risk factors include immobility, malignancy, recent surgery, or thrombophilia.
• V/Q scan or CT pulmonary angiogram confirms diagnosis.

Tuberculosis

• May cause pneumothorax due to rupture of a tuberculous cavity.
• Associated with chronic cough, weight loss, night sweats, and haemoptysis.
• Chest x-ray may show cavitation or infiltrates.

Lung Abscess and Pulmonary Empyema

• Present with fever, foul-smelling sputum, and systemic toxicity.
• Radiologically show cavitating lesions or fluid collections.
• Differentiated by response to antibiotics and imaging findings.

Bronchopleural Fistula

• Persistent air leak following pneumothorax or pulmonary surgery.
• Characterised by dyspnoea, subcutaneous emphysema, and continued bubbling in chest drains.
• Confirmed by imaging and clinical course.

Fibrosing Lung Disease (e.g. Idiopathic Pulmonary Fibrosis)

• Progressive dyspnoea and dry cough.
• Physical findings include inspiratory crackles and clubbing.
• CT reveals reticular opacities and honeycombing.

Acute Coronary Syndrome (ACS)

• Substernal chest pressure with possible radiation to arm, neck, or jaw.
• Associated symptoms include diaphoresis, nausea, and dyspnoea.
• ECG changes and elevated troponins support diagnosis.

Pericarditis

• Sharp chest pain relieved by sitting forward and worsened by inspiration or lying flat.
• Pericardial friction rub may be auscultated.
• ECG shows diffuse ST elevation and PR depression.

Myocarditis

• May present with chest pain, fatigue, arrhythmia, or heart failure signs.
• Often preceded by viral illness.
• Diagnosis aided by ECG, cardiac biomarkers, and MRI.

Aortic Dissection

• Sudden severe tearing chest or back pain.
• May have pulse deficits, mediastinal widening on chest x-ray, and differing arm pressures.
• Confirmed by CT angiography.

Pleurodynia

• Viral myositis of the chest wall.
• Causes sharp pain with movement or breathing.
• Often self-limiting; diagnosis is clinical.

Costochondritis

• Localised chest wall pain, reproducible on palpation.
• No systemic features or radiographic abnormalities.
• Differentiated by tenderness and lack of pleuritic features.

Diaphragmatic Injury

• May follow blunt or penetrating trauma.
• Presents with respiratory distress, bowel sounds in chest, or paradoxical movement.
• CT or MRI required for confirmation.

Gastro-Oesophageal Reflux Disease (GORD)

• Burning chest discomfort often postprandial and worse when supine.
• Associated with regurgitation and sour taste.
• Diagnosis often clinical or by trial of acid suppression.

Oesophageal Spasm

• Mimics angina with substernal pain and dysphagia.
• Pain is episodic and may respond to nitrates.
• Manometry and contrast studies help confirm.

Mallory-Weiss Tear

• Haematemesis following forceful vomiting or retching.
• Pain is not typically pleuritic.
• Diagnosed by endoscopy.

Boerhaave Syndrome (Oesophageal Perforation)

• Sudden severe retrosternal pain after vomiting or straining.
• Rapid onset of shock, fever, and subcutaneous emphysema.
• Confirmed by contrast oesophagram or CT showing mediastinal air.

Mediastinitis

• Severe chest pain, fever, and systemic toxicity.
• Often due to oesophageal rupture or postoperative complication.
• Imaging shows widened mediastinum and air-fluid levels.

Anxiety or Panic Attack

• Sudden onset of chest tightness, palpitations, and dyspnoea.
• Often associated with paresthesia, tremor, and fear of dying.
• Diagnosis of exclusion; physical examination and imaging are normal.

Giant Bullae

• Can mimic pneumothorax both clinically and radiographically.
• Defined as bullae occupying ≥1/3 of the hemithorax.
• CT scan is essential to distinguish from pneumothorax and avoid inappropriate chest drainage.

Pleural Effusion

• Dyspnoea and chest discomfort relieved as fluid accumulates.
• Decreased breath sounds and dullness to percussion.
• Chest x-ray shows meniscus sign; ultrasound or CT may identify underlying cause.

Pneumomediastinum

• May present with chest pain, subcutaneous emphysema, and Hamman’s sign (precordial crunch).
• Often due to barotrauma, oesophageal rupture, or severe coughing.
• Best seen on lateral chest x-ray or CT scan.

Tension Pneumothorax

• Must be distinguished from other causes of sudden haemodynamic collapse.
• Clinical features include absent breath sounds, tracheal deviation, hypotension, and distended neck veins.
• Imaging is not required for diagnosis and should not delay decompression in unstable patients.

Emergency Management of Tension Pneumothorax

• Initiate immediate high-flow oxygen and activate a cardiac arrest call for any patient with suspected tension pneumothorax.
• Do not delay decompression for imaging. Needle decompression should be performed using a standard large-bore safety cannula, preferably in the 4th or 5th intercostal space, mid-axillary line.
• Avoid using blood-control (closed system) cannulas.
• In trauma-induced tension pneumothorax, open thoracostomy is preferred if expertise is available.
• Following decompression, insert a chest drain without delay if trained to do so; otherwise, seek senior support.
• The Advanced Trauma Life Support (ATLS) guidelines now favour the mid-axillary approach (4th–5th intercostal space) over the mid-clavicular site.

General Principles of Pneumothorax Management

• Determine management approach based on pneumothorax type (primary, secondary, traumatic), clinical stability, and patient priorities.
• Refer admitted patients to a respiratory team within 24 hours.
• Size of pneumothorax alone is no longer an indication for invasive intervention, but it may influence procedural safety.
• Asymptomatic or minimally symptomatic patients can be managed conservatively with outpatient follow-up every 2–4 days.
• Ambulatory management with a Heimlich valve or similar device may be considered if local expertise exists.
• Symptomatic patients or those with large PSPs may benefit from needle aspiration or tube drainage.
• High-risk patients with SSP, bilateral pneumothorax, haemodynamic instability, or age >50 with significant smoking history should be admitted for inpatient care.

Oxygen Therapy

• In non-hypercapnic patients requiring admission but without chest drain, target oxygen saturations close to 100%.
• For all other patients, aim for 94–98% (or 88–92% if at risk of type II respiratory failure).
• Once radiological resolution is confirmed, supplemental oxygen is usually not required unless there is concurrent lung disease.

Chest Drain Insertion and Management

• Use a small-bore drain (≤14F) in stable, non-ventilated patients with spontaneous pneumothorax.
• Ensure proper positioning (45–60° sitting angle, ipsilateral arm raised), and apply aseptic technique using the Seldinger method.
• Avoid early application of suction to reduce risk of re-expansion pulmonary oedema.
• Confirm drain position and lung re-expansion via chest x-ray.
• Do not remove the chest drain until bubbling and swinging have ceased and the lung is fully re-expanded.

Surgical Considerations

• Early surgical consultation is warranted for persistent air leak (>5–7 days), failure of lung re-expansion, bilateral or recurrent pneumothorax, and haemothorax.
• Patients with high-risk occupations (e.g., divers, pilots), spontaneous haemothorax, or those who are pregnant should also be referred.
• Surgical pleurodesis (via pleural abrasion, talc poudrage, or partial pleurectomy) and bullectomy are the main strategies to prevent recurrence.
• Video-assisted thoracoscopic surgery (VATS) is preferred for most cases due to lower morbidity, though thoracotomy may offer slightly lower recurrence rates in selected high-risk populations.
• Autologous blood pleurodesis or endobronchial therapies are alternatives for patients unfit for surgery.

Special Populations and Cases

• Catamenial pneumothorax: Managed with surgical pleurodesis and hormonal therapy to suppress ovulation.
• Pneumothorax ex vacuo: Avoid drainage unless symptomatic; treat underlying bronchial obstruction.
• HIV/AIDS: Insert a chest drain early and treat coexistent Pneumocystis jirovecii pneumonia.
• Cystic fibrosis: High recurrence rates; definitive interventions like pleurectomy or pleurodesis are often needed.

Discharge Planning

• Provide all patients with verbal and written safety-net advice regarding recurrence, air travel, and activity.
• Most patients should have outpatient follow-up within 2–4 weeks.
• Patients must be advised to avoid diving indefinitely unless they undergo a definitive surgical intervention.
• Air travel is only permitted after complete radiological resolution.
• Smoking cessation must be addressed, as continued smoking increases recurrence risk fourfold.

Prevention of Recurrence

• Consider surgical pleurodesis in patients with recurrent episodes, those with poor access to emergency care, or in high-risk occupations.
• Talc pleurodesis, minocycline, or doxycycline may be used as sclerosing agents when surgery is not feasible.
• Medical thoracoscopy offers a less invasive alternative, particularly in patients unfit for general anaesthesia.
• Supraclavicular subclavian vein access is preferred over infraclavicular to reduce risk of iatrogenic pneumothorax.
• Pre-emptive chest drain insertion may be considered in patients requiring positive-pressure ventilation with an existing pneumothorax.

Primary Spontaneous Pneumothorax (PSP)

• The overall prognosis is good, particularly for small pneumothoraces in otherwise healthy individuals.
• Many small PSPs resolve spontaneously with conservative management.
• However, recurrence is common. Between 30% and 50% of patients experience an ipsilateral recurrence.
• If left untreated after a first recurrence, the likelihood of further recurrences increases significantly—62% after a third episode and up to 83% following a fourth.
• Contralateral pneumothoraces may also occur in up to 10% of cases.
• Surgical intervention substantially reduces recurrence. Video-assisted thoracoscopic surgery (VATS) with stapling of blebs and mechanical pleural abrasion, or thoracoscopic talc poudrage, both have recurrence rates of approximately 5%.
• Chemical pleurodesis via chest tube, used when VATS is unavailable or declined, has a higher failure rate (~25%).
• Alternative approaches, such as autologous blood patch pleurodesis and endobronchial valve placement, have also shown some efficacy, particularly in patients unfit for surgery.

Secondary Spontaneous Pneumothorax (SSP)

• SSP carries a poorer prognosis due to the underlying lung pathology, such as COPD or cystic fibrosis.
• These patients are at greater risk for both ipsilateral and contralateral recurrences, especially when the disease is bilateral.
• Management decisions in SSP are often dictated by patient stability, degree of respiratory compromise, and available local resources.
• Persistent air leaks are more frequent and may necessitate early surgical referral, pleurodesis, or use of endobronchial interventions.
• Mortality and morbidity are significantly increased in SSP compared to PSP, particularly in older patients and those with advanced lung disease.

Misdiagnosis and Delayed Recognition

• Failure to promptly identify pneumothorax can lead to serious outcomes, particularly if it progresses to a tension pneumothorax.
• Contributing factors include incomplete history, inadequate examination, lack of imaging, or misinterpretation of radiographic findings.
• Delayed diagnosis increases the risk of:
  • Conversion to tension pneumothorax
  • Hypoxaemic respiratory failure
  • Haemodynamic shock
  • Respiratory or cardiac arrest

Procedure-Related Complications

• Iatrogenic harm may arise from emergency interventions such as needle decompression or chest drain placement.
• Potential procedural complications include:
  • Lung laceration or failure of the lung to re-expand
  • Intercostal vessel or internal mammary artery injury leading to haemothorax
  • Persistent air leak or bronchopleural fistula
  • Infection at the insertion site or pleural space (empyema)
  • Injury to the intercostal neurovascular bundle
  • Chest tube-induced arrhythmias

Re-expansion Pulmonary Oedema

• A rare but potentially life-threatening complication following rapid reinflation of a collapsed lung, especially if the pneumothorax has been present for over 72 hours.
• Oedema typically affects the ipsilateral lung but may also involve the contralateral lung.
• Clinical manifestations may include hypoxaemia, hypotension, and respiratory distress requiring mechanical ventilation.
• The exact mechanism is unclear, but likely involves mechanical stress on pulmonary capillaries and reperfusion injury with reactive oxygen species.
• To minimise risk, clinicians often initiate drainage with a water-seal system before applying suction. If full re-expansion is not achieved, gentle low-pressure suction may then be applied.

Talc Pleurodesis-Associated Acute Respiratory Distress Syndrome (ARDS)

• Rarely, systemic inflammatory responses to talc instillation can precipitate ARDS.
• Risk is associated with non-calibrated or small-particle talc.
• Use of size-calibrated talc at appropriate dosages has been shown to significantly reduce this risk, making the procedure generally safe.

Pneumomediastinum

• Air from a pneumothorax can track into the mediastinum, presenting as radiolucent streaks around mediastinal structures on imaging.
• A pathognomonic finding is Hamman’s crunch—a precordial, crunching sound synchronous with the heartbeat, best heard in the left lateral decubitus position.
• While often self-limiting, this complication may require monitoring to exclude associated oesophageal rupture or other serious pathology.

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