Fatal Pulmonary Barotrauma from a Commercial Flight

CASE REPORT

A 71-yr-old woman was traveling around Australia and New Zealand with her husband. The patient in question had a past medical history of resected meningioma a decade before, very mild asthma on no medications, and a preexisting asymptomatic pulmonary cyst that had been detected on a chest X-ray in 2012. She had been unwell in the 2 wk leading up to the flight with malaise, cough, anorexia, and weight loss.

She had been on a cruise ship for 10 d prior to boarding a 4-h and 20-min flight to Australia from New Zealand, had a 3-d interval, then boarded a 1.15-h domestic flight on a Boeing 737-800. She took her seat opposite her husband on the aisle and, as they took off, she was observed to muffle a cough then to “go to sleep” with her head hanging down a few moments later. She remained without moving until landing 1 h later and, as the flight passengers disembarked, she could not be roused. Unsuccessful attempts were made to rouse her and paramedics were called, the road crew arriving within 12 min. The initial report of the paramedics and consultant retrieval physician was Glasgow Coma Scale 3, deviated gaze to the left,³ trismus, bradycardic and peri-arrest, systolic blood pressure of 60, and no palpable radial pulse. The extrication from on board was difficult and she had to have a supported airway (nasopharyngeal airway) and jaw thrust with supplemental oxygen before being intubated on the runway. She was transported to the local emergency department (Royal Hobart Hospital) and continued to be manually ventilated. The emergency doctors also noted upgoing plantar response and deviated gaze. Differential diagnoses considered at this point were massive pulmonary embolus or catastrophic intracranial hemorrhage.

During her initial assessment, a chest X-ray was performed that showed some opacities in the left hilar region of the lung and air-fluid levels (Fig. 1). Bedside cardiac ultrasound showed a Takotsubo cardiomyopathy and CT scanning showed locules of gas in the cortex of the brain (Fig. 2) (and internal jugular veins) and confirmed a large cavitating lesion in the left lung with air-fluid levels (Fig. 3). She was transferred to the intensive care unit still intubated and the hyperbaric physician was contacted as there was some suggestion of acute barotrauma causing cerebral arterial gas embolism.

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Serial high sensitivity troponin assays were elevated (700+) and discussions were held with the on-call cardiologists, neurosurgeons (because of the history of meningioma), and hyperbaric physicians as well as intensive care unit medical staff and the husband of the patient. Unfortunately, repeat imaging over the next 2 d showed a progression of devastating brain injury with loss of sulcus definition and midline shift, and herniation of cerebellar tonsils. MRI suggested a catastrophic embolic event. She was palliated and extubated as per the wishes of the next of kin and died soon afterward.

DISCUSSION

The differential diagnosis remains either acute pulmonary barotrauma with catastrophic gas emboli to the brain or possible septic emboli, or a combination of both, causing hypoxic brain injury. We also considered barotrauma caused by asthma and gas trapping. Unfortunately, because of the overseas origin of the patient, a postmortem was not completed.

The MRI brain report showed extensive ischemic insult to the brain. The morphology and distribution, in conjunction with foci of susceptibility weighted blooming, are more suggestive of a catastrophic embolic event rather than global hypoxic ischemic encephalopathy. Given the intra-axial gas on CT in the brain and presence of a cavitating lung mass with air crescent sign and surrounding pulmonary hemorrhage, this could be explained by a large air embolus to the systemic circulation (via left heart). A differential of central nervous system septic emboli would also need consideration (particularly given concern for angio-invasive fungal disease in the lung); however, this would not explain the extent of diffusion restriction that was demonstrated.

The timing of onset of symptoms was suspicious for pulmonary barotrauma; the reduction in cabin pressure from 1 ATA at sea level to the equivalent of 0.7 during flight [equivalent to approximately 8000 ft (2438 m) above sea level/560 mmHg] may have allowed any gas locules in the cavitating lesion in the lung to expand and cause extravasation of air into the systemic circulation. This would have caused her pneumocephalus and the air in the internal jugular veins.

Hyperbaric oxygen treatment was not considered in this case due to the prolonged interval since initial insult, the extent of the hypoxic brain injury, and the poor prognostic outcome. Pressurization followed by depressurization may well have caused further extravasation of gas.

Sudden death in an airplane is rare (1 in 10,000 passenger emergencies and 0.31 deaths per million people), although in-flight emergencies are increasing due to the higher numbers undertaking commercial air travel.^4–6 There is very little in the literature regarding pulmonary barotrauma from infective causes in aviation. Pneumothorax and pneumomediastinum from forced Valsalva have been reported in military pilots.⁵

The etiology of this cavitating lesion has not been determined; organisms such as staphylococci have been previously reported, as described in this paper of a fatal air embolism in a child who was ventilated for post-chickenpox staphylococcal pneumonia with pneumatoceles.⁷ The patient in our case had a history of cough and fevers and weight loss, suggesting some sort of infective process. An underlying neoplastic/infiltrative process could not be discounted, nor could mycobacterial infection due to the lack of a postmortem. The pulmonary cyst had been reported in 2012 on a plain chest X-ray, demonstrating a long period of stability.

Death has been reported in airline passengers with rupture of pulmonary bullae and bronchial cysts.^8,9 Structural lung disease is an established risk for hyperbaric treatment due to the risks of gas trapping and expansion injuries.

There are numerous reports of air embolism with infection when mechanically ventilated, but infective causes of barotrauma without invasive ventilation are hard to find in the literature.¹⁰ The Takotsubo cardiomyopathy was presumably a response to the devastating neurological injury.¹¹

This is a rare and unusual presentation and, in this case, with tragic consequences. The case in question describes a 71-yr-old woman with a long history of stable pulmonary cyst who undertook several symptom-free flights before the likely pulmonary cyst rupture during a domestic flight, causing cerebral gas embolism and eventual hypoxic brain injury and death. The cyst may have been weakened by a coexisting lower respiratory infection, but a lack of postmortem details makes this speculation. It is hard to take lessons away from this rare and unfortunate case, but perhaps a suggestion could be made that people with known large pulmonary cysts should not fly with respiratory tract infections. There is a lack of supporting evidence to either support or refute this.