We consider it extremely important to make some clarifications regarding our study published in June 2016.1 The study reported the case of a woman who attended our department in 2013 due to acute cor pulmonale and coma, which were finally attributed to a retrograde venous air embolism through a peripheral intravenous line (PIV). The mechanism of the embolism was not fully understood but we decided to report it due to its singularity and relevance. Our study said: “Our patient was a 79-year-old woman with no relevant medical history who was admitted due to lower limb cellulitis. While hospitalised, she removed her PIV accidentally when she was getting out of bed; as a result, she experienced a sudden drop in arterial blood pressure, tachypnoea, and a decrease in the level of consciousness.” So expressed, it may be inferred that there was a spontaneous ingress of air into the venous system coinciding with the loss of the PIV. However, detailed analysis of the case and the subsequent events clearly contradicts this idea; the case is currently under investigation as the pulmonary air embolism was allegedly caused intentionally by a nursing assistant at our hospital, who is currently remanded in custody (the case is being treated as attempted murder: the patient survived for reasons outside the intent of the suspect).2
Having reviewed the case, we consider it very unlikely that the “spontaneous ingress” of air through a PIV would cause an air embolism of such magnitude in the patient reported due to a number of reasons, including the following: a) for air to enter the PIV, it must be open; however, peripheral lines or catheters by definition should be used in closed systems (to avoid contamination/infection)3–5; b) if a PIV is open or removed from the venous access, blood leaks from the vein in sufficient quantities that is easily detected by the patient, family members, and/or healthcare staff, whereas no blood was observed around the line when our patient was attended; c) Valsalva manoeuvres infrequently induce such considerable air ingress through a PIV; as specified in our article, significant air flows (≥ 0.2L/min) are needed to cause an air embolism6; and d) the hypothetical spontaneous air ingress through a PIV does not usually cause subcutaneous emphysema. Our patient presented significant subcutaneous emphysema extending to the root of the upper limb where the PIV was inserted. Emphysema was probably caused by a high-pressure injection of air or gas, which was extravasated out of the venous layer and penetrated the subcutaneous cellular tissue (this probably saved the patient's life).7–9
Therefore, it is likely that the ingress of air or gas into the patient's venous system was forced and not spontaneous, and that the forced introduction of air caused the removal of the PIV, rather than the contrary sequence of events.
In short, spontaneous passage of air or gas into the venous system through a PIV or the removal of it does not usually cause a severe systemic air embolism; in such cases, we should consider the possibility that the entry of air may have been forced.
Please cite this article as: León Ruiz M, Benito-León J, García-Soldevilla MÁ, García-Albea Ristol E, Arranz Caso JA. Aclaraciones a «Primer caso descrito de coma desencadenado por embolismo aéreo venoso retrógrado: una situación excepcional pero potencialmente letal». Neurología. 2020;35:516–517.