Scorpion envenomation in children is potentially fatal condition. Scorpion
envenoming cause an autonomic storm resulting in a massive release of
catecholamines, angiotensin II, glucagon and cortisol. As a consequance of these
changes, scorpion envenoming result in a syndrome of fuel energy deficits, producing
multi-system-organ failure and death. The objective of the present study was to
determine circulating levels of adrenaline, nor-adrenaline, angiotensin converting
enzyme (ACE), angiotensin II, kallikrein, nitric oxide (NO), aldosterone as well as
Na+, K+ and Ca+2 in scorpion envenomed children. The relationship between these
vasoactive mediators and the severity of scorpion envenomation and the outcome of
envenomed children would be evaluated. The present study included 40 scorpion
envenomed children of both sexes and their age ranged 1-13 years. According to the
severity of envenomation, they were divided into 2 groups, mild and severe. 10
apparently healthy children were considered as control group. All of them were
subjected to complete clinical examination and routine laboratory investigations.
Plasma levels of angiotensin II, adrenaline and nor-adrenaline were determined
using ELISA assay. Serum aldosterone level was determined using RIA method. The
enzyme activities of kallikrein and ACE and NO level were determined using
spectrophotometric assay. Serum levels of Na+ and K+ were determined by flame
photometer and Ca+2 by flame atomic absorption. All of these parameters were
assayed on admission and after 24 hours. All envenomed children showed on
admission significant increase in levels of angiotensin II, adrenaline and noradrenaline,
ACE, NO, aldosterone and Na+ in comparison with healthy control (P <
0.01, P < 0.01, P < 0.01, P < 0.01, P < 0.01, P < 0.01, P < O.00l and P < 0.001)
respectively. On the other hand, kallikrein activity, K+ and Ca+2 levels were
significantly decreased (P < O.05, P < O.00l and P < O.05) respectively. However,
on the second sample (after 24 hours) it was noted that the levels of ACE, angiotensin
II and NO were still higher than those in healthy control (P < O.05, P < O.001 and P
< O.05) respectively, but non significant difference was detected in kallikrein activity
on comparing the second sample with healthy control. In conclusion, these
vasoactive mediators might play an important role in pathogenesis of multi-systemorgan
failure and death that occur with scorpion envenomation