( NEUROMUSCULAR REHAB SPECIALIST )
DPT lecturer and clinical incharge ZIHS
Pneumothorax is the presence of air in the pleural space, which can
either occur spontaneously, or result from iatrogenic injury or trauma
to the lung or chest wall. Primary spontaneous pneumothorax
occurs in patients with no history of lung disease. It principally
affects males aged 15–30 in whom smoking, tall stature and the
presence of apical subpleural blebs are additional risk factors.
Secondary pneumothorax affects patients with pre-existing lung
disease, especially COPD, bullous emphysema and asthma. It is
most common in older patients and is associated with the
highest mortality rates.
2. Clinical features
• There is sudden-onset unilateral pleuritic chest pain or breathlessness (those
with underlying chest disease may have severe breathlessness).
• With a small pneumothorax the physical examination may be normal; a larger
pneumothorax (>15% of the hemithorax) results in decreased or absent breath
sounds and a resonant percussion note.
• A tension pneumothorax occurs when a small communication acts as a one-way valve
allowing air to enter the pleural space from the lung during inspiration but not
to escape on expiration; this causes raised intrapleural pressure which leads to
mediastinal displacement, compression of the opposite lung and impaired systemic
venous return and cardiovascular compromise.
CXR shows the sharply defined edge of the deflated lung with complete lack of
lung markings between this and the chest wall. CXR also shows any mediastinal
displacement and gives information regarding the presence or absence of pleural
fluid and underlying pulmonary disease. Care must be taken to differentiate
between a large pre-existing emphysematous bulla and a pneumothorax to avoid
misdirected attempts at aspiration; where doubt exists, CT is useful in distinguishing
bullae from pleural air.
• Primary pneumothorax, where the lung edge is <2 cm from the chest wall and the
patient is not breathless, normally resolves without intervention.
• In young patients presenting with a moderate or large spontaneous primary
pneumothorax an attempt at percutaneous needle aspiration of air should be
made in the first instance, with a 60–80% chance of avoiding the need for a chest drain.
• Patients with chronic lung disease always require a chest tube and inpatient
observation, as even a small pneumothorax may cause respiratory failure.
Intercostal drains should be inserted in the 4th, 5th or 6th intercostal space in
the mid-axillary line, following blunt dissection through to the parietal pleura, or
by using a guidewire and dilator (‘Seldinger’ technique). The tube should be advanced
in an apical direction, connected to an under-water seal or one-way Heimlich valve, and
secured firmly to the chest wall. Clamping of the drain is potentially dangerous and
never indicated. The drain should be removed 24 hrs after the lung has fully
reinflated and bub-bling stopped. Continued bubbling after 5–7 days is an
indication for surgery. Supplemental oxygen is given, as this accelerates the rate at
which air is reabsorbed by the pleura. Patients with a closed pneumothorax should not
fly until the pneumothorax has resolved, as the trapped gas expands at altitude.
Patients should be advised to stop smoking and be informed about the risks of a
recurrent pneumothorax (25% after primary spontaneous pneumothorax).
4. Recurrent spontaneous pneumothorax:
Surgical pleurodesis, with thoracoscopic pleural abrasion or
pleurectomy, is recommended in all patients following a second
pneumothorax (even if ipsilateral), and should be considered following
the first episode of secondary pneumothorax if low respiratory
reserve makes recurrence hazardous. Patients who plan to continue
activities where pneumothorax would be particularly dangerous
(e.g. diving) should also undergo definitive treatment after the first
episode of a primary spontaneous pneumothorax.
5. Pulmonary Embolism
Deep venous thrombosis (DVT) and pulmonary embolism (PE) can be considered
under the heading of venous thromboembolism (VTE). The majority (75%) of PEs
arise from the propagation of lower limb DVT. PE is common, occurring in ∼1% of all
patients admitted to hospital and accounting for ∼5% of in-hospital deaths. Amniotic
fluid, placenta, air, fat, tumour (especially choriocarcinoma) and septic emboli (from
endocarditis affecting the tricuspid/pulmonary valves) are rare.
The varied clinical presentation, non-specific nature of the physical signs and the
lack of sensitive and specific diagnostic tests can make the diagnosis of PE difficult. It is
helpful to consider three questions:
• Is the clinical presentation consistent with PE?
• Does the patient have risk factors for PE?
• Is there any alternative diagnosis that can explain the patient’s
presentation? A recognized risk factor for PE is present in 80–90% of patients.
The clinical features depend largely upon the size of embolism and comorbidity.
CXR: PE may give rise to a variety of non-specific appearances but may be normal. A
normal CXR in an acutely breathless and hypoxaemic patient should raise the
suspicion of PE, as should bilateral changes in a patient with unilateral pleuritic
chest pain. CXR can also exclude alternatives such as heart failure, pneumonia or
ECG: ECG changes in PE are common but usually non-specific. The most common
findings are a sinus tachycardia and anterior T-wave inversion; larger emboli may
cause right heart strain revealed by an S1Q3T3pattern, ST-segment and T-wave
changes, or right bundle branch block. The ECG may also suggest an alternative
diagnosis such as myocardial infarction and pericarditis.
ABG: Typically show a reduced PaO2 and a normal or low PaCO2, but are occasionally
normal. Metabolic acidosis may occur in acute massive PE with cardiovascular
D-dimer: This is a specific degradation product released into the circulation when
cross-linked fi brin undergoes endogenous fibrinolysis. A low D-dimer level has a high
negative predictive value and is a useful screening test. However, a suggestive clinical
picture in a high-risk patient must be investigated further even when the D-dimer level
is normal. Non-specific elevation of the D-dimer is observed in a number of
conditions other than PE, including myocardial infarction, pneumonia and sepsis.
7. CT pulmonary angiography (CTPA): The development of rapid acquisition helical CT
scanners has popularised the use of CTPA. It not only may exclude PE but may also
reveal an alternative diagnosis. Limited resolution may hinder the detection of small
peripheral emboli but further advances in CT are likely to improve this.
Ventilation–perfusion scanning: The sensitivity and specificity of V./Q. scanning
are enhanced by a clinical probability assessment. A normal V./Q. scan virtually
excludes PE, and a low-probability scan in the presence of a low clinical probability
makes PE unlikely. Similarly, the presence of a high-probability scan in a patient
with a high clinical probability almost certainly establishes the diagnosis of PE.
However, V./Q. scanning is of limited value when PE is suspected in patients with
pre-existing cardiopulmonary pathology (e.g. COPD or cardiac failure) because in
these cases 70% of scans are indeterminate.
Doppler USS of the leg veins: This is the investigation of choice in patients
with clinical DVT, but may also be applied to patients in whom PE is suspected,
particularly if there are clinical signs in a limb, as many will have identifiable
proximal thrombus in the leg veins.
8. Echocardiography: This is helpful in the differential diagnosis and assessment of
acute circulatory collapse. Acute dilatation of the right heart is usually present in
massive PE, and thrombus (embolism in transit) may be visible. Alternative diagnoses,
including left ventricular failure, aortic dissection and pericardial tamponade, can
usually be established with confidence.
Pulmonary angiography: This has largely been superseded by CTPA.
• Oxygen should be given to all hypoxaemic patients in a concentration
necessary to restore SpO2 to >90%.
• Hypotension should be treated by giving i.v. fluid or plasma expander; diuretics
and vasodilators should be avoided.
• Opiates may be necessary to relieve pain and distress but should be used with
• Resuscitation by external cardiac massage may be successful in the moribund
patient by dislodging and breaking up a large central embolus
9. Anticoagulation: Should be commenced immediately in patients with a high or
intermediate probability of PE, but can usually be safely withheld from patients with a
low clinical probability pending further investigation. Low molecular weight heparin
administered subcutaneously is as effective as i.v. unfractionated heparin and easier
to administer. The dose is standardised for the weight of the patient and does
not require monitoring by tests of coagulation. Heparin is effective in reducing
mortality in PE by reducing the propagation of clot and the risk of further
emboli. It should be administered for at least 5 days and anticoagulation continued
using oral warfarin. Heparin should not be discontinued until the international
normalised ratio (INR) is >2. The optimum duration of warfarin therapy is not clear.
Current guidelines suggest that patients with an underlying prothrombotic risk or a
history of previous emboli should be anticoagulated for life. Those with a reversible
risk factor require 3 mths of therapy, although 6 wks may be sufficient for some.
Six mths of therapy is currently recommended for idiopathic VTE.
Thrombolytic therapy: Thrombolysis appears to improve outcome when acute
massive PE is accompanied by shock, but it is not clear whether there is any advantage
of thrombolysis over heparin in patients with a normal BP. Patients with PE appear
to have a high risk of intracranial haemorrhage and must be screened carefully for
10. Caval filters: Selected patients with recurrent PE despite adequate anti-coagulation,
or those in whom anticoagulation is contraindicated, may benefit from insertion of
a filter in the inferior vena cava below the origin of the renal vessels.
Patients who develop PE after an operation have the lowest recurrence rate; in other
groups, recurrence rates may be as high as 9%/yr. Echocardiographic evidence of
right ventricular dysfunction identifies patients at risk of developing cardiogenic
shock and an increased risk of death. Persistent pulmonary hypertension and right
ventricular dysfunction 6 wks after PE identify high-risk patients with an increased
likelihood of developing overt right ventricular failure over the next 5 yrs.