Pneumothorax

Introduction

Pneumothorax is a build up of air in the pleural space; it is usually bilateral unless the mediastinum is intact. Air accumulation causes the normally sub-atmospheric pressure within the pleural space to be lost breaking the surface tension of the pleural fluid and hence atelectasis of the lungs. Loss of negative pressure within the thorax can lead to decreased venous return to the heart. There are three main types of pneumothorax – closed, open and tension.

A closed pneumothorax is caused by air leakage from the pulmonary parenchyma or airways. Inspiration causes pleural pressure to drop which leads to more air being drawn into the pleural space and further compression of the lungs.

An open pneumothorax is rare and occurs when the pleural pressure exceeds atmospheric pressure and hence lung atelectasis occurs.

Tension pneumothorax is a rapidly fatal condition caused by a connection between the pleural space and the outside or the pleural space and the lung creating a one way valve that causes air to be drawn in on inspiration but closes on expiration leading to increasing pressure within the pleural space. Collapse of the lungs and great veins follows.

Causes of pneumothorax can largely be divided into traumatic or spontaneous (idiopathic).

Traumatic pneumothorax due to a trauma is the most common cause and largely seen following road traffic accidents. Most are closed. Rupture of the large airways following external trauma leads to increased pressure in the pleural space. Shearing forces can cause pulmonary bleb formation, which following rupture, causes a pneumothorax. An open pneumothorax occurs following penetrating injuries to the thorax. Diaphragmatic hernias can also result in pneumothorax due to loss of pleural pressure.

Iatrogenic pneumothorax can occur following thoracocentesis, bronchoscopy, biopsies, jugular venipuncture or intubation causing tracheal trauma.

Spontaneous (idiopathic) pneumothorax is classified as primary or secondary depending on the presence of underlying pulmonary disease. Primary have no evidence of underlying pulmonary disease and result from rupture of pulmonary blebs or bullae. Pulmonary blebs are subpleural, thin walled and most commonly found in the apices of the lungs whereas bullae are within the pleura, lined by fibrous pulmonary tissue and emphysematous lung. Blebs are often smaller than bullae.

Secondary spontaneous pneumothorax is more common than primary and can be caused by a wide range of pulmonary diseases. Possible causes include: abscesses (often following necrosis of tumours), emphysema, cysts, neoplasia, pneumonia, pulmonary parasites (e.g. Dirofilaria immitis infection), migrating foreign body, and feline asthma. It can also be seen as a consequence of chronic granulomatous infection (e.g. mycotic granuloma) or chronic airway obstruction leading to overpressurisation of abnormal lungs.

Signalment

Primary spontaneous pneumothorax is most common in large deep chested middle aged dogs. Blebs and bullae are most often found in dogs.

Siberian Huskies seem to be predisposed to spontaneous pneumothorax.

Clinical Signs

There will often be a history of trauma or underlying respiratory disease and the animal should be carefully examined for any other signs of trauma including shock, rib fractures and concurrent thoracic injuries. Spontaneous pneumothorax may be followed by a history of recent exercise.

Generally acutely dyspnoeic and have a shallow rapid pattern of respiration, often accompanied by orthopnoea (breathing easily only in a standing position) and abdominal breathing. If it is caused by trauma, other injuries will often exacerbate the respiratory compromise. If a tension pneumothorax is present, the patient will often appear barrel chested due to the increasing pressure within the thoracic cavity. An open pneumothorax can cause a range of clinical signs from mild to severe due to the communication with the exterior. Subcutaneous emphysema will be present if a concurrent pneumomediastinum exists. Decreased lung sounds will be present dorsally on auscultation, and if percussed, the chest is resonant.

Cyanosis will be present if the animal is hypoxaemic due to impaired gas exchange from pulmonary atelectasis and ventilation perfusion mismatch. High intrathoracic pressures may cause reduced venous return and hence signs of decreased cardiac output e.g. pale mucous membranes and tachycardia, especially in cases of tension pneumothorax.

Diagnosis

Thoracocentesis should be performed prior to radiographs being taken in order to stabilise the animal as this can be both diagnostic and therapeutic.

Radiographs will show elevation of the heart (due to the collapse of lung lobes), lung collapse and hence movement away from the chest wall. A radiolucent area of free air where no vascular structures are present is diagnostic; this is usually most often found in the caudal thorax. The most sensitive view for diagnosis is lateral recumbency though this view is often impossible to take in a dyspnoeic animal. In these cases, a dorso-ventral view is often best. Blebs and bullae tend to be difficult to identify radiographically and may be an incidental finding. The radiographs should be carefully examined for any pulmonary pathology.

Bronchoscopy may be necessary if there is evidence of tracheal or large airway trauma.

Treatment

Supplemental oxygen will usually be required, as is analgesia as decreasing pain will lead to improved respiration.

If the pneumothorax is small in volume (e.g. from a ruptured bullae) then rest may be all that is required if the animal is non-dyspnoeic. Small volumes will be reabsorbed over a few days and so long as they don’t reoccur no action is needed.

If the animal is in respiratory distress, thoracocentesis will be necessary followed by rest. Some cases can be managed by intermittent thoracocentesis, however if air is rapidly accumulating, the pneumothorax redevelops over a short period, or negative pressure is not reached at the end of aspiration then a thoracostomy tube is usually required. If thoracocentesis is required more than three times over a space of hours then a chest drain may be required. Cats frequently get reexpansion pulmonary oedema following thoracocentesis.

When necessary, a thoracostomy tube is placed in the dorsal thorax at the level of ribs 7-8 or 8-9 directed cranioventrally into the pleural space and secured in place with a purse string suture. Radiographs should be taken after to ensure correct positioning. Continuous suction can then be used if air is rapidly accumulating.

If there is a large volume of pleural air or a pulmonary lesion has been identified, surgical exploration is required to identify the source. A thoracostomy tube should be placed in all patients during surgery. If the source of the leak is not obvious during surgery, then it can be identified by filling the pleural space with saline and looking for air bubbles. If an open pneumothorax is present then the wound should be covered and dressed to avoid further contamination before performing thoracocentesis. If a thoracostomy tube is required this should be placed on the same side of the thorax.

A chest tube should be placed prior to ventilation, and positive pressure ventilation should be avoided if a closed pneumothorax is present.

The effectiveness of treatment will be evident in a reduction in the signs of dyspnoea and can be confirmed by radiography.

Prognosis

The prognosis depends on the underlying cause. If the pneumothorax is traumatic in origin then the prognosis is good provided there is no other substantial thoracic trauma. Prognosis for primary spontaneous pneumothorax is usually good. If it is secondary and the underlying disease is focal and can be surgically resected then prognosis is good, if the disease is diffuse then prognosis is poor.

Cats treated for spontaneous pneumothorax non surgically appear to have a better prognosis than dogs

References

Tilley, Larry P. , Smith Jr, Francis W.K. (2007), Blackwell’s Five-Minute Veterinary Consult: Canine and Feline (Fourth Edition) Blackwell Publishing

Ettinger, Stephen J., Feldman, Edward C. (2005), Textbook of Veterinary Internal Medicine (Sixth Edition) Elsevier Saunders

Ettinger, Stephen J. (2001), Pocket Companion to Textbook of Veterinary Internal Medicine (Third Edition) Saunders

Nelson, Richard W., Couto, C. Guillermo (2005), Manual of Small Animal Internal Medicine (Second Edition) Mosby