Sympathetic nervous system activation, antivenin administration and cardiovascular manifestations of scorpion envenomation

Abstract

We performed two-dimensional echocardiograms and determined plasma norepinephrine levels on admission and at 24 h after hospitalization, in 16 children with scorpion envenomation. All patients came from areas where scorpions have been identified as Tityus zulianus and received antivenin at the site of the accident or upon admission. Based on the presence or absence of cardiovascular manifestations, patients were divided into two groups. Group A: 10 patients had cardiovascular manifestations of pulmonary edema. Four patients had mild pulmonary edema (Left ventricular ejection fraction: 0.43±0.19) and six had moderate to severe pulmonary edema (Ejection fraction: 0.31±0.09. p=NS, M±SD). Plasma norepinephrine was elevated on admission (1279±824) and decreased at 24 h in seven of eight patients (474±140 pg/ml, p<0.03). Group B: Six patients had no cardiovascular manifestations. These patients had normal chest X-rays and normal echocardiograms. Plasma norepinephrine was not elevated (188±180 pg/ml). Time interval from the accident to antivenin administration was significantly longer in Group A compared to Group B (4.5±3.3 vs 1.2±0.4 h, p<0.03) and correlated directly with the absolute change in plasma norepinephrine (r=0.76, p<001). Consequently, we strongly recommend very early administration of antivenin in the medical management of scorpion envenomation by T. zulianus.

Introduction

Scorpion envenomation is a public health problem in certain countries of Asia (Bawaskar and Bawaskar, 1992), Africa (Abroug et al., 1991, Bergman, 1997) and the American continent (Cupo et al., 1994a, Cupo et al., 1994b, Mazzei de Dàvila et al., 1997). Clinical manifestations and final outcome vary according to the geographical site where the accident occurred. This is probably due, in part, to the predominance of certain species and to the biochemical characteristics of the scorpion venom (Gueron et al., 2000, Fatani et al., 1998).

The mechanisms responsible for the toxic actions of the scorpion venom, on the cardiovascular system, are still the subject of intense controversy and research (Ismail, 1995, Texeira et al., 2001). Most investigators consider that, the cardiovascular manifestations (i.e. pulmonary edema and shock) are secondary to the peripheral vascular and myocardial effects of scorpion envenomation (Gueron et al., 1990, Karnad et al., 1989). A syndrome of systemic inflammatory response to the venom has also been postulated as an explanation for the cardiovascular manifestations (Magalhaes et al., 1999). However, the principal toxic compounds of the venom are single chain polypeptides that interfere with the sodium conductance of mammalian excitable tissues (Gordon et al., 1996). These sodium channel neurotoxins induce the release of norepinephrine and acetylcholine (Freire-Maia, 1995). Although, kinins appear to be involved in the cardiovascular and lethal effects of certain species of scorpions (i.e. Leiurus quinquestriatus) (Bagchi and Deshpande, 1998, Shapira et al., 1998, Fatani et al., 1998), scorpion envenomation is currently considered to resemble the massive outpouring of catecholamines seen in pheochromocytome crises (Gueron et al., 2000).

We have identified, in Mérida–Venezuela, geographical zones in which extremely dangerous scorpions predominate. These scorpions have been identified as Tityus zulianus (Mazzei de Dàvila et al., 1999). Clinical manifestations are mainly cardiovascular and potentially lethal (Mazzei de Dàvila et al., 1997). In order to study the effects of scorpion envenomation on the sympathetic nervous system and on the myocardium of children, who suffered scorpion envenomation in Mèrida, Venezuela; we performed transthoraccic two-dimensional echocardiography and measured systemic venous norepinephrine by high-pressure liquid chromatography. In addition, we have indirectly studied the therapeutic role of antivenin by assessing the relationship between sympathetic nervous system activation and the time interval from the accident to antivenin administration.