Should dobutamine be used in severe scorpion envenomation

To the Editor:

We are grateful to Dr Madias for his interest in our work and overall positive appreciation. He rightly points out to striking similarities between takotsubo syndrome and scorpion cardiomyopathy—a fact that has been seldom alluded to heretofore. Yet, the fundamental role of the stimulation of the autonomic nervous system (sympathetic and parasympathetic) following scorpion envenomation has usually been highlighted in the pathophysiology of envenomation.¹ However, the relevance of the sudden release of high circulating catecholamine levels to the disease severity (in particular relating to cardiovascular consequences) has rarely been advocated. Indeed, the prevailing opinion so far ascribed to scorpion toxin itself the majority of the pathophysiological consequences of scorpion envenomation. The toxin is thought to have direct effects on target organs.² Besides, the therapeutic approach consisting in antagonization of catecholamines effects has rarely been explored, in comparison to the huge research seeking scorpion toxin antagonization whether in circulation or already linked to its receptors. These divergent approaches have generated an ongoing controversy between scientists supporting or opposing the thesis of the “toxin” or “mediators” pathways in scorpion disease.

Hopefully, takotsubo syndrome with its characteristic cardiomyopathy pattern induced by catecholamine outpouring triggered by toxin effects on the autonomic nervous system is able to reconcile all these views and may provide a common consensual pathophysiological scheme.

Dr Madias rightly raises concerns about the use of dobutamine as a bridge therapy to recovery in scorpion envenomated patients presenting with acute heart failure. In particular, he seems to fear a potential extrapolation to takotsubo myocardiopathy, and reluctant to a concept by which a catecholaminergic-induced cardiomyopathy could be treated by catecholamines (or dobutamine) infusion. It is usually recommended that the bridge therapy to recovery in takotsubo cardiomyopathy should be administration of β-blockers having a potential blockage of α-receptors as well. In the most severe cases, transient extracorporeal circulatory support is advocated.³ Nevertheless, our own experience with dobutamine administration to enhance LV an RV performance (not only contractility, but also cardiac output and arterial pressure) provides evidence on the drug effectiveness regarding both physiologic effects and patient-centered outcomes and has become largely recommended in severe scorpion envenomation.⁴ In addition, the example of the treatment of the catecholaminergic cardiomyopathy related to pheochromocytoma by dobutamine or dopamine is also instructive.⁵ In this connection, the animal model of scorpion envenomation which is highly reproducible could also serve as a simple model to takotsubo cardiomyopathy. It may represent an opportunity to explore some pathophysiologic and therapeutic aspects of takotsubo syndrome. We hope that a new era of collaboration between northern and southern scientists is slightly open. This can also offer a spotlight to a disease (scorpion envenomation) that suffered international neglect for decades.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.