Pneumothorax
A pneumothorax is a collection of air
between the visceral and parietal pleura causing a real rather than potential
pleural space. Recognition and early drainage can be lifesaving. Predisposing
and precipitating factors include necrotizing lung pathology, chest trauma,
ventilator-associated lung injury and cardiothoracic surgery.
Pneumothorax classification
Primary spontaneous pneumothorax
(PSP)
This is caused by rupture of small
apical subpleural air cysts ('blebs') but rarely causes significan
physiological disturbance. Tall young (20-40 years old) men (male/female 5:1)
with no underlying lung disease are usually affected. It is the most common
type of pneumothorax (prevalence 8/105 per year, rising to 200/105 per year in
subjects >1.9 m in height). Following a second primary spontaneous
pneumothorax (PSP), recurrence is likely (>60%). Pleurodesis to fuse
the visceral and parietal pleura using medical (e.g. pleural insertion of
bleomycin or talc) or surgical (e.g. abrasion of the pleural lining) means is
recommended.
Secondary pneumothorax
This is associated with respiratory
diseases that damage lung architecture, most commonly obstructive (e.g.
chronic obstructive pulmonary disease (COPD) and asthma), fibroti or infective (e.g. pneumonia), and
occasionally rare or inherited disorders (e.g. Marfan's and cystic fibrosis)
The incidence of secondary pneumothorax (SP) increases with age and the
severity of the underlying lung disease. These patients usually require
hospital admission as even a small SP in a patient with reduced respiratory
reserve may have more serious implications than a large PSP. ICU patients with
lung disease are at particular risk of SP due to the high pressures
('barotrauma') and alveolar overdistention ('volutrauma') associated with
mechanical ventilation. 'Protective' ventilation strategies using low-pressure,
limited volume ventilation reduce this risk.
Traumatic (iatrogenic) pneumothorax
This follows blunt (e.g. road traffi
accidents) or penetrating (e.g. fractured ribs and stab wounds) chest trauma.
Therapeutic procedures (e.g. line insertion and thoracic surgery) are common
causes of iatrogenic pneumothorax.
Tension pneumothorax
A tension pneumothorax may
complicate PSP or SP but is most common during mechanical ventilation and
following traumatic pneumothorax. It occurs when air accumulates in the pleural
cavity faster than it can be removed. Increased intrathoracic pressure causes
mediastinal shift, compression of functioning lung, inhibition of venous return
and shock due to reduced cardiac output. It is a medical emergency and fatal if
not rapidly relieved by drainage. Detection is a clinical diagnosis; awaiting
chest X-ray (CXR) confirmatio may be life-threatening. Immediate drainage with
a 14G needle in the second intercostal space in the midclavicular line is
essential. A characteristic 'hiss' of escaping gas confirm the diagnosis. A
chest drain is then inserted.
Clinical assessment
Pneumothorax is graded and treated
according to Fig. 35a and Table b. Sudden breathlessness and/or sharp pleuritic
pain suggests a pneumothorax. Most PSPs are small (<30%) and cause
few symptoms other than pain. Clinical signs can be surprisingly difficul to
detect, but in larger pneumothoraxes reduced air entry and hyperresonant
percussion over one hemithorax are characteristic and may be associated with
tachypnoea and cyanosis. Cardiorespiratory compromise may develop remarkably
quickly in a tension pneumothorax and requires immediate drainage.
Occasionally, other pulmonary air leaks may occur (see below). Monitoring reveals
tachycardia, hypotension and desaturation. Blood gases may demonstrate
respiratory failure. CXR confirm the diagnosis (Fig. 35a). Computed
tomography (CT) scan may detect localized pneumothoraxes.
Management
Immediate supportive therapy includes
supplemental oxygen and analgesia. Treatment is dependent on the cause, size
and symptoms.
A tension pneumothorax must be drained
immediately. A small PSP (<30%) is simply observed and spontaneous
reabsorption is confirme on serial outpatient CXR. A PSP >30% may be
aspirated through a 16G needle in the second intercostal space in the
midclavicular line, using a 50 mL syringe connected to a three-way tap and
underwater seal (Fig. 35c). Following overnight observation, successful
aspiration is confirme by lung re-expansion on repeat CXR. Occasionally, intercostal
tube drainage is required for a large PSP with respiratory failure or if
aspiration is unsuccessful.
In general, SP and traumatic
pneumothoraxes always require hospital admission and intercostal chest
drain insertion (Fig. 35d). Multiple intercostal drains may be needed to ensure
adequate lung rexpansion in some patients with multiple loculated
pneumothoraxes. In mechanically ventilated patients, high airway pressures or
large tidal volumes encourage persistent leaks and must be avoided.
Small chest drains (16 G) are nearly
always adequate. Large chest drains are painful and have no significan benefits
A persistent drain leak suggests
development of a bronchopleural fistula (BPF). High f ow, wall suction
with pressures of 5-50 cmH2O, may oppose visceral and parietal
pleura, allowing spontaneous pleurodesis. Physiotherapy and bronchial toilette
are required to maintain airway patency. Early advice on surgical BPF
management is essential. Video-assisted thoracoscopy is as effective as
thoracotomy at correcting BPF but causes less respiratory dysfunction.
Chest drains are removed when CXR
confirm lung expansion and there has been no air leakage through the drain for
more than 24 hours. Drains should not be clamped before removal. Following
adequate analgesia, the drain is pulled out when the patient is in inspiration.
Purse string sutures around the drainage site are then tightly secured.
Air leaks
Pneumomediastinum describes air in the mediastinal-pleural reflection,
outlining the heart and great vessels on CXR. Air may also dissect along
perivascular sheaths into the neck, causing subcutaneous emphysema (SE) or
around the heart with pneumopericardium, which may cause tamponade. Air
leaks follow traumatic damage to the trachea, bronchus and oesophagus or
ventilator-induced barotrauma. SE may cause localized cervical or grotesque
facial and body swelling. It has a characteristic crackling sensation on
palpation. The voice may have a nasal quality, and auscultation over the precordium
may reveal a 'crunch' with each heart beat (Homan's sign). Management includes
good drainage of pneumothorax and 'protective' ventilation strategies (Chapter
42). Failure of spontaneous resolution should prompt investigation, including
bronchoscopy, for problems that decrease chest drain efficiency or undetected
air leaks.
