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. 2012 Oct 29;2012:bcr-2012-006860. doi: 10.1136/bcr-2012-006860

Secondary spontaneous pneumothorax: a rare complication of pulmonary embolism

Philip Mathieson 1, Ian Reckless 2, Colin Ferrett 3
PMCID: PMC4544206  PMID: 23109413

Abstract

An 85-year-old lady presented with a left middle cerebral artery territory infarct. Several days into her admission she became hypoxic and haemodynamically unstable. A CT pulmonary angiogram showed bilateral pulmonary emboli, right-sided parenchymal cavitation due to infarction and an associated large pneumothorax. She was treated successfully with an intercostal drain and anticoagulation. This case describes the rare phenomenon of secondary spontaneous pneumothorax due to pulmonary infarction from pulmonary embolism. The factors associated with the development of infarcts from pulmonary thromboemboli are poorly understood although a number of predisposing conditions and pathological features have been suggested. Pulmonary infarction occurs in around 10% of cases of pulmonary emboli but the complication of secondary spontaneous pneumothorax would appear to be much less common. One should consider pulmonary embolism as the cause of pneumothorax where there is significant clinical suspicion.

Background

I believe this unusual case of secondary spontaneous pneumothorax could inform and remind clinicians about the potential of pulmonary emboli to cause this complication. There are only a few cases in the literature regarding this diagnosis and the last published case was over 10 years ago.

Case presentation

An 85-year-old lady was admitted with a dense right-sided weakness and mixed dysphasia due to a left middle cerebral artery territory infarct. She was known to have atrial fibrillation but had previously declined warfarin. Her other medical history included hypertension, cerebrovascular disease and ischaemic heart disease. She was a lifelong non-smoker.

The day after admission she was noted to be tachypnoeic and clinical examination revealed mild polyphonic wheeze and fine crepitations bibasally. A chest x-ray (CXR) was suggestive of pulmonary oedema and her diuretics were increased with good effect.

Five days later she acutely deteriorated with hypotension (90/70 mm Hg), tachypnoea (RR 30) and hypoxia (SaO2 89% on room air). Her chest was clinically clear but arterial blood gas analysis showed a pO2 of 7.95 and CO2 of 2.93. A working diagnosis of pulmonary embolism was made and she proceeded to a CT pulmonary angiogram on the same day.

Investigations

The CT pulmonary angiogram demonstrated bilateral pulmonary emboli, and on the right side an area of infarction and cavitation with an associated large pneumothorax involving approximately 70% of the lung (figures 13).

Figure 1.

Figure 1

Arrows demonstrating intraluminal pulmonary arterial emboli.

Figure 2.

Figure 2

Long arrow showing area of infarction and cavitation. Double headed arrow shows large pneumothorax.

Figure 3.

Figure 3

Ultrasound sonography shows consolidation and pleural effusion

Treatment

She had an intercostal drain inserted and was started on low-molecular-weight heparin.

Outcome and follow-up

The drain was removed after 5 days following full re-expansion although her CXRs showed a developing right pleural effusion associated with consolidation in the lower and middle lobes. After a course of antibiotics she had a chest ultrasound scan performed that confirmed consolidation in an anechoic pleural effusion. A pleural aspirate showed an exudate but no empyema. At this stage the patient was clinically improving and she was transferred to another hospital for stroke rehabilitation.

Discussion

Many respiratory disorders have been associated with spontaneous pneumothorax, (eg, emphysema, tuberculosis, lung cancer, Pneumocystis Carinii pneumonia),1 although pulmonary infarction due to pulmonary embolism would appear to be rare, with only a small number of case reports citing this complication. Indeed, the incidence of pneumothorax secondary to pulmonary infarction has never been reported.2

The likely mechanism for pneumothorax in this context is direct alveolar rupture allowing air to enter the pleural space. The development of pneumothorax in the setting of already compromised lung function means secondary spontaneous pneumothorax represents a potentially life-threatening illness that requires immediate intervention. This is in contrast to primary spontaneous pneumothorax that follows a more benign course.

Pulmonary infarction is estimated to occur in only 10% of patients with pulmonary embolism as the dual blood supply from pulmonary and bronchial arteries protects the lung parenchyma. Factors that predispose patients are poorly understood but studies have demonstrated that congestive cardiac failure (presumably leading to impaired circulation to the lung) was significantly associated with the development of infarction. Other groups that appear to be at significantly greater risk include those with distal thromboemboli located in the lower lobe and those with infarcts in contact with the pleura.3 4

Of the reported cases of pneumothorax complicating infarction, the time interval of embolus to pneumothorax may be as long as 5–7 weeks.5 The process of necrosis can be accelerated if infection complicates infarction and results in cavity formation.

Learning points.

  • Pneumothorax is a rare complication of pulmonary embolism.

  • Where there is a suggestive history, clinicians might consider pulmonary embolism as an underlying mechanism for the development of a pneumothorax.

  • The seemingly low incidence would not support routine CT angiography in all patients with a pneumothorax.

Footnotes

Competing interests: None.

Patient consent: Obtained.

References


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