CASE 15464 Published on 13.03.2018

Fatal complication of intrapleural fibrinolysis: massive air embolism

Section

Chest imaging

Case Type

Clinical Cases

Authors

Loretta Calderan, MD, Roberta Antea Pozzi-Mucelli, MD, Rossella Delle Donne, Manuel Gianvalerio Belgrano MD, Maria Assunta Cova, MD

U.C.O. di Radiologia,
Radiologia; Str. di Fiume
447 34149 Trieste, Italy;
Email:roberta.pozzimucelli@gmail.com
Patient

72 years, male

Categories
Area of Interest Head and neck, Thorax, Cardiac ; Imaging Technique CT-Angiography
Clinical History
Patient with left pleuric mesothelioma complicated with empyema, not suitable for surgery, underwent positioning of thoracic drainage. Through drainage, he underwent pleural fibrinolytic therapy. After 10 minutes from administration of therapy, he developed loss of consciousness and after a while appeared cyanotic, with bradycardia and hypotension.
Imaging Findings
Brain CT was performed for suspicion of haemorrhage, but didn't demonstrate any bleeding or signs of acute ischaemic stroke; most prominent finding was a discrete amount of air in the peripheral cerebral vessels (Fig. 1).
Thoracic CT angiography (for suspicion of pulmonary embolism) didn't show signs of thrombi. Mesothelioma was well-recognisable and also the pleural cavity with thoracic drainage in it. The main finding was a large amount of air inside the left heart, ascending aorta and all coronary arteries (Fig. 2-4), compatible with massive air embolism. No fistulas were identified with CT.
The patient was immediately brought into a hyperbaric chamber but died towards the end of treatment.
Autopsy was performed, which demonstrated important cardiac infarct as cause of death. Nevertheless it still wasn't able to confirm a fistula.
Pathologist concluded that the drainage probably created a decubitus fistula with a pulmonary vein and when intrapleural fibrinolysis was performed it “opened” the fistula allowing air to enter a blood vessel.
Discussion
Air embolism is a rare but potentially fatal occurrence, in fact the nonspecific nature of the signs and symptoms, as well as the difficulty in documenting the diagnosis does not allow the true incidence of it to be known; it can occur in either the venous or arterial system depending on where the air enters the systemic circulation. Venous air embolism occurs when air enters the systemic venous system and reaches the lungs via the pulmonary arteries leading to trapping of air bubbles in the pulmonary capillary bed, while systemic arterial embolism, as in our case, is due to the entry of air into pulmonary veins or directly into the arteries of the systemic circulation. The severity of symptoms varies according to the amount of air instilled and the end location of the air bubble; patients may be asymptomatic or, as in our case, may have a cardiovascular collapse. Lethal volumes of air in an acute bolus for humans has been hypothesized to be around 3-5 ml/kg and it is estimated that 300-500 ml of gas introduced at a rate of 100 ml/sec is a fatal dose for humans [1].
Air embolism may result from a number of medical-surgical procedures, as reported in literature, such as placement of an IV-access or an IV infusion [2], CT- guided transthoracic needle biopsy of pulmonary nodules [4] or following diagnostic bronchoscopy [3].
Intrapleural fibrinolysis is an established modality in the management of complicated parapneumonic effusions, empyema and multiloculated malignant effusions, providing symptom relief and palliation [4]. A possible complication described in literature is pleural bleeding [5]; whereas there is none regarding air embolism as a complication of this type of procedure.
Contrast-enhanced CT imaging is the modality of choice in cases of suspected air embolism, as it can perfectly demonstrate air in the cavities of the heart, in the main vessels and filling defects in the coronary arteries. This setting was very evident in our case as our images demonstrate.
The primary therapeutic intervention is now considered to be hyperbaric oxygen treatment, which results in overall reduction in the air bubble size by “crushing” the bubbles in the body. It has also been shown to minimise endothelial damage and end-vessel occlusion and reduce oedema in hypoxic tissues [6]. Nevertheless, treatment may prove futile if the air bolus is larger than 50 ml [1].
Differential Diagnosis List
Massive air embolism
Pulmonary embolism
Brain haemorrhage
Final Diagnosis
Massive air embolism
Case information
URL: https://www.eurorad.org/case/15464
DOI: 10.1594/EURORAD/CASE.15464
ISSN: 1563-4086
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