Discussion
The Kounis syndrome was first describe in 1991 and, as has been described, it consists in a vasospasm due to allergic reaction. In these cases, treatment with adrenaline is controversial because of the eventual worsening of ischemia, vasospasm and increase in the QT segment. However, in our case it was necessary considering the situation of cardiorespiratory arrest. Vasodilator agents should be contemplated as specific treatment. In our case, intracoronary nitroglycerin was administered (4).
In our case, the most probable trigger of the Kounis syndrome was the intravenous administration of amiodarone. To diagnose anaphylaxis, in addition to pruritus and skin lesions after the drug administration, determination of serum tryptase during the acute phase with subsequent normalization is useful (figure 2). Mast cells are the main inflammatory cells in the allergic reaction. Its degranulation produces the release of inflammatory and vasoactive molecules. Tryptase determination is the main marker of mast cell activity with a 73% sensitivity and 98% specificity (5).
Some drugs have been associated with Kounis syndrome but as far as we know from published evidence, this is the first case with amiodarone. However, there are some cases of anaphylactic shock with intravenous amiodarone in patients who already take it orally, especially in cases of allergy to iodine (6).
The use of VA-ECMO has been previously described in the setting of anaphylactic shock, with few cases being described. This case supports the usefulness of ECMO in refractory shock requiring circulatory support (7).
Another remarkable point to highlight in this case is the usefulness of NO in refractory hypoxemia in a patient with VA-ECMO once initial treatment has failed (deep sedation, pharmacological relaxation and optimized ventilation). In our case it was effective and prevented further aggressive treatments such as pronation or conversion to VAV-ECMO. NO would act as a pulmonary vasodilator, reducing the reflex vasoconstriction that occurs due to hypoxia, improving the pulmonary ventilation/perfusion ratio. And although studies have not shown a reduction in mortality, they have shown a significant improvement of refractory hypoxemia. (8) (9).
Therefore, it is an interesting case, since on one hand, it shows an infrequent cause of cardiorespiratory arrest such as coronary vasospasm due to anaphylactic shock. And on the other hand, it highlights the usefulness of circulatory support with ECMO in the scenario of cardiorespiratory arrest.