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Tension pneumothorax: eyes may be more diagnostic than ears
  1. S Leigh-Smith1,
  2. G Davies2
  1. 1Defence Medical Services, UK
  2. 2Department of Emergency Medicine and Pre-hospital Care, Royal London Hospital, UK
  1. Correspondence to:
 Mr S Leigh-Smith, Flat 3F1, 40 Warrender Park Terrace, Edinburgh EH9 1EB, UK; 
 simonlsuk{at}aol.com

Abstract

A case is presented of unilateral tension pneumothorax in an awake patient who was seen in prehospital care after a significant fall. Because of extrication difficulties it was 40 minutes after the accident when he was first seen and by this stage the tension pneumothorax was well developed. Many features that are taught as “classic” of tension pneumothorax were absent but various other clinical signs were present to aid the diagnosis, and these are reviewed.

  • tension pneumothorax

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A 14 year old boy fell three storeys into a domestic lift shaft. A prehospital care team of emergency physician and paramedic was immediately dispatched, arriving on scene within seven minutes of the accident. There was no access to the patient as the lower lift doors were shut but he could just be seen from the third floor doors. He was standing up, moving around, and talking although confused and agitated. It was 40 minutes after the accident when full patient access was gained at the lower end of the lift shaft. By this stage he was no longer talking and obviously in severe respiratory distress. He was otherwise alert and confused but could just about cooperate with extrication commands. There was no room for a stretcher in the lift shaft. He underwent a rapid extrication in an ambulance chair with a Stifneck collar followed by administration of oxygen.

Examination revealed; a minor occipital contusion but no other external sign of injury, marked agitation, GCS 10 (V1M6E4), moving all four limbs, marked cyanosis, respiratory rate of 30+, warm and well perfused peripheries, heart rate 135, Spo2 unrecordable on 15 litres oxygen with reservoir bag, blood pressure 137/67, central trachea, equal thoracic resonance bilaterally and equal air entry bilaterally but with scattered crepitations.

There was no evidence of flail chest and a provisional diagnosis of unilateral or bilateral tension pneumothorax was made.

Further careful visual inspection in an attempt to lateralise his thoracic injury revealed subtle signs of left sided thoracic hyperexpansion and hypomobility.

Left sided needle thoracocentesis in the 2nd ICS MCL produced a brief hiss of air but with no clinical improvement. Left sided tube thoracostomy was immediately performed after sedation and analgesia with 3 mg midazolam and 20 mg ketamine. This resulted in a large hiss of air that continued for some seconds along with a small haemothorax. Spo2 improved to 90% with thoracostomy and then 95% with tube drainage. He underwent uncomplicated rapid sequence intubation then right sided thoracostomy1 that revealed no tension on that side. Investigation in hospital revealed a ruptured spleen (removed), left pulmonary contusion, stable lumbar fracture, and left pelvic ramus fracture. He had persistent left sided intrapleural air leak, which subsequently settled on conservative management. After two weeks he was discharged home with normal gross cognitive function.

DISCUSSION

Tension pneumothorax is one of six conditions listed as “immediately life threatening thoracic injuries” in ATLS2 teaching. Rapid treatment is required and as such the diagnosis usually relies on clinical signs. Five standard texts list a variety of signs that are variably present to make the diagnosis.2–6 Different emphasis is given to some of these signs in the texts with just two signs (respiratory distress, tachycardia) accepted as being universally present in this disease.

The presence of cyanosis is Fio2 dependent. Gradually developing hypoxia is a consistent feature of developing tension pneumothorax if patients are breathing air. This patient’s Spo2 may have been less than 66% as it has been suggested that this is the highest level at which cyanosis (with a normal haemoglobin) is clinically detectable.7

In a patient who is in severe respiratory distress with tension pneumothorax as a provisional diagnosis it is desirable to be able to lateralise the disease clinically. However, the classically taught tracheal deviation is often absent and at best an inconsistent or late finding.3,8–10 Comparing this case report with the signs listed in these standard texts only one3 gives over-inflation and splayed ribs as signs of the disease. Although not commonly reported ipsilateral hyperinflation and hypomobility have been mentioned in other case reports.10,11 Hyperinflation (along with ipsilateral diaphragmatic depression) has however been noted ipsilaterally in chest radiographs of tension pneumothorax.12 This ipsilateral hyperinflation is a late sign of tension as earlier on there will be hypoexpansion and hypomobility due to collapse of the lung and pain limitation of thoracic movement.

The other commonly taught lateralising signs of hyper-resonance and decreased air entry have been previously noted to be absent even in an advanced state of the disease process.9,13,14 Other authors have commented on the poor reliability in eliciting chest signs by chest physicians15 and doctors in the accident and emergency department16—let alone in prehospital care.

This case report also adds further to the existing evidence base that needle thoracocentesis may be an unreliable treatment for tension pneumothorax.17–24

In conclusion, tension pneumothorax may be a difficult diagnosis to make with variable presentation of signs. Deliberate and careful visual inspection of the chest wall may reveal useful clinical signs. In a supine patient this must be done by getting down to the level of the patient. Careful looking along the line of the thorax may detect subtle differences in thoracic size and mobility.

REFERENCES

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