Upper airway obstruction as a result of massive subcutaneous emphysema following accidental removal of an intercostal drain

D. J. Williams*, S. I. Jaggar and C. J. Morgan

Department of Anaesthetics, Royal Brompton Hospital, Sydney Street, London SW6 6NP, UK

* Corresponding author: Department of Anaesthetics, Morriston Hospital, Morriston, Swansea SA6 6NL, UKE-mail: davidjwilliams{at}doctors.org.uk

Accepted for publication October 26, 2004.


    Abstract
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 Abstract
 Case history
 Discussion
 References
 
A case is described of extensive subcutaneous emphysema with rapid and life-threatening airway obstruction. The incident followed inadvertent removal of a chest drain in a patient with a persistent air leak from an iatrogenic pneumothorax. The pneumothorax had developed during pacemaker insertion.

Keywords: complications, upper airway emergency ; complications, upper airway obstruction ; complications, subcutaneous emphysema ; complications, pneumothorax ; complications, pneumomediastinum ; equipment, chest drain ; equipment, chest tube drainage ; equipment, pacemaker


    Case history
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 Abstract
 Case history
 Discussion
 References
 
A 68-yr-old female patient (BMI 32) was admitted for elective insertion of a permanent pacemaker (PPM) for complete heart block. She had severe chronic obstructive pulmonary disease (COPD) managed with home nebulizers and intermittent oral steroids. Other past medical history included chronic myeloid leukaemia (currently in remission), ischaemic heart disease, and hypertension. She was allergic to penicillin, which caused a rash.

On admission, she gave a history of exertional dyspnoea, orthopnoea, and chest pain on walking 10 m. On examination, she had pitting ankle oedema and a palpable 4-cm liver edge. Heart sounds were inaudible and jugular venous pulsation could not be seen. There was diffuse bilateral wheeze on auscultation of the chest. Arterial blood gases on oxygen 24% were: 88%, 6.33 kPa, 7.88 kPa, H+ 44 mmol litre–1.

A PPM was inserted via the left subclavian vein using midazolam sedation and local anaesthesia with lidocaine. The PPM functioned correctly; however, the procedure was technically difficult and resulted in an iatrogenic pneumothorax occupying 30% of the left chest. This was immediately recognized during the procedure and confirmed on chest X-ray. A left intercostal drain (ICD) was therefore inserted under local anaesthesia and connected to 5 cm suction via an underwater seal, resulting in re-expansion of the lung.

Five days later, the underwater seal was still bubbling, but the ICD was accidentally removed by nursing staff. Within minutes, the patient developed gross and rapidly progressive surgical emphysema extending from the groin to the neck, face and hands (Figs 1 and 2), with a hoarse voice, respiratory distress, and stridor (ventilatory frequency 30 bpm, heart rate 110 beats min–1, blood pressure 130/80 mm Hg). On auscultation, bilateral breath sounds were present. Oxygen was administered via face mask, the anaesthetic team was called, and the patient was transferred immediately to the operating theatre. The surgical team was also called, and preparations made for emergency tracheostomy if necessary.



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Fig 1 Facial appearance showing severe subcutaneous emphysema (reproduced with the patient's permission).

 


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Fig 2 Chest X-ray obtained on the ward before contacting the anaesthetic team.

 
Following pre-oxygenation, anaesthesia was induced by spontaneous inhalation of sevoflurane in oxygen. Laryngoscopy revealed a Cormack-Lehane grade 2 view of the larynx, which was grossly narrowed and oedematous. Succinylcholine 100 mg was administered, and the trachea was successfully intubated using a size 6 mm tracheal tube over a gum elastic bougie. Haemodynamic stability and arterial oxygen saturations of more than 90% were maintained throughout. Positive pressure ventilation was then commenced. Vecuronium 8 mg was given, and a left apical intercostal drain was inserted and connected to an underwater seal. An audible hiss was heard on incision of the skin before the pleura was opened. The underwater seal bubbled vigorously but did not result in rapid resolution of the subcutaneous emphysema or changes in haemodynamic or respiratory function.

The patient was sedated with propofol and transferred to the intensive care unit (ICU). A CT scan revealed persisting large left and smaller right pneumothoraces, with gross subcutaneous emphysema of the chest wall (Fig. 3). Despite these findings, the PPM continued to function normally. A further ICD was inserted under local anaesthesia to facilitate drainage of the left pneumothorax, and a nasogastric tube was inserted to facilitate feeding.



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Fig 3 CT scan of thorax showing residual bilateral pneumothoraces and massive subcutaneous emphysema of chest wall.

 
The size 6 mm tracheal tube was too small to facilitate weaning from ventilation and bronchial toilet. It was therefore electively exchanged for a size 8 mm tracheal tube 3 days after initial intubation. Persistent swelling of the larynx was noted. However, there was no obstruction to intubation on this occasion.

Weaning was prolonged as a result of the persistent air leak, surgical emphysema, COPD, and body habitus. Formal tracheostomy was therefore performed 7 days after admission to ICU. The chest drains stopped bubbling and were removed 20 days after insertion. Artificial ventilation was discontinued, and the patient was discharged home on a reducing dose of oral steroids 10 days later. On review in the outpatient clinic a month after discharge, she remained well and the surgical emphysema had completely resolved.


    Discussion
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 Abstract
 Case history
 Discussion
 References
 
Subcutaneous emphysema is relatively common in anaesthetic and surgical practice, and is usually a self-limiting condition. Involvement of the hypopharynx sufficient to cause airway obstruction is rare,13 but may be rapidly fatal.1 An acute rise in intra-alveolar pressure may cause extravasation of air under pressure into the perivascular interstitial tissues, which then dissects between soft tissue planes, causing swelling and tissue compression. In this patient, air probably also tracked from the pleural cavity to the subcutaneous tissues via the drain site. The resulting subcutaneous emphysema may spread widely to involve the face, arms, thorax, and abdomen causing disfigurement. Other possible consequences depend on the site involved:

  1. Hypopharynx. Compression of the upper airway can occur causing acute obstruction.13 Jugular venous compression may occur leading to impaired cardiac output (by reduced venous return) and raised intracranial pressure.4 5
  2. Chest wall. Involvement leading to restriction of ventilation,4 68 or pacemaker malfunction9 may occur.
  3. Mediastinum. Reduction in cardiac output by compression of the heart and great vessels may occur.4 10

In addition, subcutaneous emphysema may be associated with tension pneumothorax,11 and tension pneumopericardium,3 causing respiratory failure and reduction in cardiac output.

It is notable that this patient developed gross, life threatening, tension subcutaneous emphysema before positive pressure ventilation was commenced. A possible cause of this development could have been a pressure gradient between the alveoli and subcutaneous tissues arising from alveolar air-trapping secondary to COPD. The patient had no history of angioedema or recent changes in medication to suggest an allergic cause for the rapid, generalized tissue swelling.

Dissection of air into the soft tissues of the neck in this condition can cause sore throat, dysphagia, dysphonia, stridor and dyspnoea, and may resemble the symptoms of epiglottitis.3 If the patient's condition permits, plain chest and lateral soft-tissue X-rays of the neck may aid diagnosis. Fibre-optic nasopharyngeal laryngoscopy may aid assessment of airway obstruction.3 However, these investigations should not delay definitive management. In the great majority of patients, subcutaneous emphysema resolves spontaneously over several days. High-flow oxygen therapy speeds resolution by facilitating resorption of nitrogen from the distended tissues and pneumomediastinum.3 12 Restriction of ventilation from subcutaneous emphysema of the chest wall may be relieved by incision,8 or by insertion of large-bore subcutaneous drains connected to an underwater seal or suction.6 13 14

Symptoms suggestive of airway obstruction require immediate intervention. Tracheal intubation and emergency tracheostomy (if the former is unsuccessful) may both be extremely difficult, and should be performed by an experienced anaesthetist and surgeon in the operating theatre with immediate access to additional staff and equipment. The anaesthetic technique depends on the patient's clinical condition and the judgement of the anaesthetist, but may include inhalation or i.v. induction, awake fibre-optic intubation, or awake tracheostomy under local anaesthesia.

Clinically significant pneumothorax requires ICD insertion, and pneumopericardium requires decompression using a pericardial needle.3 Release of air from tension subcutaneous emphysema may mimic the release of a tension pneumothorax, with an audible hiss on insertion of the ICD, and bubbling of the underwater seal drain.15 A chest X-ray should be performed following insertion to confirm correct placement.

An ICD that is still bubbling should never be clamped or removed, as this may convert a simple pneumothorax into a tension pneumothorax. Some institutions routinely clamp ICDs during transfer from the operating table on the grounds that this will prevent disruption or possible reflux of the underwater seal into the pleural cavity if the drainage bottle is lifted during this process. However, provided that the drainage bottle is kept 1 m below the level of the patient, reflux should not occur and the seal should remain intact. Alternatively, substitution of the underwater seal for a Heimlich valve may provide a safe and effective system for transfer.


    References
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