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.