P - ISSN : 2349-6592    |    E - ISSN : 2455-7099
Year : 2019 | Volume : 6 | Issue : 3 | Page : 40 - 44
Source of Funding:None Conflict of Interest:None
Scorpion sting is a major health problem in tropical and subtropical countries.1 A total of 113 species are available in India2; of these Mesobuthus tumulus or Indian Red Scorpion is the most lethal.1 Like many other neglected tropical diseases, due to gross under-reporting, reliable statistics of scorpion envenomation are not available. Even more concerning is the lack of awareness amongst pediatricians regarding the spectrum of manifestations of scorpion envenomation in children and its management in both primary and advanced care settings. We are reporting a series of 3 cases exemplifying the myriad manifestations of scorpion envenomation along with emphasizing the role of prazosin and supportive intensive care monitoring and management. This article also focusses on role of treatment options such as amiodarone and glucose-insulin infusion in management of scorpion envenomation induced myocardial dysfunction, refractory to fi rst line inotropes.
Scorpion sting, PICU, Prazocin
A 2-year-old boy presented 4 hours after a scorpion sting on plantar aspect of right leg. At admission, the child had a heart rate (HR) of 110/min and Grade 2 hypertension with blood pressure (BP) of 144/78 mm Hg. In view of overt features of adrenergic excess, he was started on oral prazosin at a dose of 30 mcg/kg/ dose every 3 hours. For management of pain at sting site, local instillation of 1% lignocaine was done. After 4 doses of prazosin, features of adrenergic storm subsided and child became normotensive. He was, subsequently, discharged after 36 hours of uneventful observation, in a hemodynamically stable condition with only mild edema at sting site. Child was doing well on his follow up visit.
An 8-year-old male child presented with history of witnessed scorpion sting, 4 hours prior to arrival at emergency. The child was restless with profuse diaphoresis. Primary assessment revealed respiratory distress in form of tachypnea, retractions, bilateral crepitation on auscultation and SpO2 of 85% on room air. His perfusion was poor with signs of hypotensive shock manifesting as tachycardia (HR -170/min), weak peripheral and central pulses, cold clammy skin, capillary refi ll time more than 3 seconds and blood pressure of 60/30 mmHg. Though alert, the child was extremely agitated. The child was given 100% oxygen, echocardiography guided fl uid resuscitation and inotropic support in form of dobutamine infusion 10mcg/kg/min, which was further escalated to 20 mcg/kg/min. Prazosin was administered in a dose of 30 mcg/kg/dose every 3 hours through NG tube along with supportive measures as per unit’s protocol. X-ray chest was suggestive of pulmonary edema, while echocardiography revealed decreased cardiac contractility with an ejection fraction of less than 15% though maintaining blood pressure just above 5th percentile for age. Nitroglycerine infusion in a dose of 0.25 mcg/kg/min helped in partial resolution of pulmonary edema. Milrinone infusion was added to address poor cardiac contractility but it triggered fall in BP and had to be discontinued.
In view of lability of patient’s cardiac functions and non-improvement in cardiac contractility on serial echocardiography after 6 days of management, amiodarone infusion was started in a dose of 15 mcg/ kg/min along with insulin infusion in a dose of 0.5 U/kg/hour in 10% dextrose as next line of treatment, based on previous case reports of management of refractory cardiomyopathy in scorpion envenomation. 2 days later, his ejection fraction improved to 35% with further resolution of cardiac failure and pulmonary edema. The child was kept on amiodarone and insulin infusions for 96 hours followed by tapering in view of favorable clinical response. He was discharged after 12 days of PICU stay in stable condition at ejection fraction 40-45% and is doing well on follow up.
A 5 year old boy was brought to emergency, 7 hours after scorpion sting on distal phalanx of left middle fi nger. At admission, child had severe respiratory distress, bilateral crepitations, heart rate of 220/minute, weak pulses and unrecordable BP. His GCS was 8/15 and SpO2 was 66% on room air that improvement only up to 90% on CPAP of 6cm of water so he was intubated and ventilated. After cautious fl uid administration, child was started on dobutamine infusion in a dose of 10 mcg/kg/min which was soon doubled in view of no response. Prazosin was administered in a dose of 30 mcg/ kg/dose every 3 hours. The child, while being resuscitated, suffered from an episode of generalized seizure which was aborted using midazolam with subsequent administration of phenytoin on dose of 20mg/kg.
For no resolution of pulmonary edema and shock adrenaline was added and titrated up to 0.4 mcg/kg/ minute along with milrinone infusion in a dose of 0.75 mcg/kg/minute however child succumbed to a cardiac arrest within 6 hours of PICU admission despite intensive resuscitative efforts.
Scorpion venom is a mixture of toxic neuropeptides along with free aminoacids, serotonin and other enzymes3. These neuropeptides bind to Na+ channels at presynaptic nerve terminals modifying the channels’ kinetic mechanisms to open it whereas K+ channels affecting neuropeptides are pore blocking agents. This results in repetitive fi ring of parasympathetic & sympathetic neurons leading to “autonomic storm”. The complex interaction of sympathetic and parasympathetic stimulation results in typical clinical features in which a transient cholinergic phase follows a prolonged sympathetic hyperexcitation.
Effect on cardiovascular system (CVS)
Indian red scorpion envenomation has prominent CVS manifestations.4 There is transient hypotension in the cholinergic phase in which vomiting and sweating leads to hypovolemia followed by a hyperkinetic phase in which sympathetic hyperexcitation leads to hypertension and tachycardia. Terminally, due to depletion of catecholamines from nerve terminals & simultaneous activation of kinin pathways the patient lapses into a hypokinetic phase of pulmonary edema & shock.
Effect on other systems5
Aberration in clotting mechanisms and Disseminated Intravascular Coagulation (DIC) has been reported.
Seizures, encephalopathy and hemiplegia have been reported mostly as squeal to DIC or less often due to venom itself.
Scorpion venom can lead to hemolysis resulting in renal failure.
Envenomation inhibits insulin secretion. There are reports on scorpion venom induced pancreatitis due to various mechanisms.6
Clinical manifestations are dependent on scorpion species attributes and venom dose/weight ratio7. Severe pain is the fi rst and in about 35% of cases, the only manifestation without any systemic involvement.8 As previously described; the interplay of parasympathetic and sympathetic excitation leads to initial cholinergic symptoms of vomiting, sweating, bradycardia and priapism in males, followed by hypertension, tachycardia, arrhythmia, pulmonary edema, peripheral circulatory failure and shock. Clinical manifestations that suggest a poor prognosis are DIC, respiratory failure and neurological catastrophe such as encephalopathy, hemiplegia and cerebral hemorrhage.4
A consensus classifi cation of clinical consequences of scorpion envenomation divides the manifestations into 3 classes9:
Class I – Local manifestations
Class II – Systemic involvement (non-life threatening)
Class III – Systemic involvement (life threatening)
Details of these manifestations are discussed in Table 1.
Classifi cation of clinical manifestations of scorpion envenomation9
The typical clinical setting and evolution of symptoms in a case of scorpion envenomation is suggestive of diagnosis. Investigations are, therefore, not required for emergency management and are done mainly to establish myocardial involvement and pulmonary edema.
• Typical ECG fi ndings include tented T waves and ST segment elevations in leads I and aVL.
• X-Ray chest may be suggestive of the pulmonary congestion or at times frank pulmonary edema.
• Echocardiography to document the left ventricular systolic dysfunction.
Severe pain needs to be treated with NSAIDS as it will help in allaying the anxiety. In an extremely agitated child, diazepam may be used to sedate the child in order to avoid unnecessary myocardial stress.
Hypovolemia caused by profuse sweating and vomiting needs careful attention. Oral fl uids, where feasible, should be encouraged. If features of peripheral circulatory failure are present, CVP or echocardiography guided fl uid resuscitation is necessary.
Management of pulmonary edema
Pulmonary edema in scorpion envenomation is a result of myocardial dysfunction; hence its management is directed towards maintaining an adequate cardiac output. Dobutamine is used in a dose of 5-15μg/kg/ min along with vasodilators like sodium nitroprusside in a dose of 0.3-5 μg/kg/min or nitroglycerine in a dose of 1-3 μg/kg/min. It is, however, mandatory to rule out hypotension prior to use of vasodilators.
Prazosin is a postsynaptic α1 antagonist. Its effects as a pharmacologic antidote was fi rst reported by Bawaskar.10 It also acts on a cellular level by phosphodiesterase inhibition which leads to cGMP accumulation; thus counteracting the endothelin mediated vasoconstriction by Nitric Oxide induced vasodilation.
The usual dose of prazosin is 30 mcg/kg/dose to be repeated 3 hourly. It is important to ensure that the child is not lifted to sitting or standing position after giving prazosin in order to avoid “fi rst dose phenomenon” of orthostatic hypotension. Therapeutic end points for prazosin administration are warm extremities with easily visible peripheral veins. Prazosin based protocols for management of scorpion sting have led to signifi cant reduction in overall mortality.11
Scorpion antivenom for use against Mesobuthus tumulus is available for clinical use. The peak distribution of scorpion antivenom is achieved in 36 minutes12, the scorpion antivenom is effective only in this time window. It cannot neutralize the venom already bound to receptors and needs to be species specifi c to be effective. Hence, treatment regimens based solely on scorpion antivenom have not been advocated.13
Myocardial damage in scorpion envenomation results from the unregulated sympathetic hyperexcitation. Histopathological studies done in cases of fatal scorpion envenomation have documented coagulative necrosis of myocytes called myocardial contraction bands which are hallmarks of catecholamine cardiotoxicity.14 Presence of acute left ventricular failure precludes the use of beta adrenergic antagonists. In this scenario, the sympatholytic property of amiodarone is utilized as rescue therapy in children suffering from severe left ventricular dysfunction secondary to scorpion envenomation. Santiago et al have described a small series of cases of scorpion envenomation with left ventricular failure managed using intravenous amiodarone.15
Glucose insulin infusion
An alteration of hormonal milieu has been hypothesized in the pathogenesis of scorpion envenomation which is essentially an insulinopenic state due to inhibition of its secretion. The resulting fuel-energy defi cit may account for many of the symptoms and there is experimental evidence of reversal of metabolic and electrocardiographic manifestations of scorpion envenomation by administration of insulin.16 Lack of consistent benefi ts has hindered its inclusion in established protocols; however, as reported in multiple case series, glucose-insulin infusion may be a valuable adjunct in Class III scorpion envenomation with life threatening complications such as pulmonary edema or cardiogenic failure in intensive care settings.17
Scorpion envenomation is associated with signifi cant morbidity in children. Neurological manifestations are poor prognostic indicators.4 Reliable mortality statistics are lacking, however Prazosin based protocols have led to a decrease in mortality.11
Scorpion envenomation is a common pediatric emergency in tropics. The myriad presentations and its severity ranging from mild local symptoms to catastrophic systemic involvement, as exemplifi edin our case series, is dictated by pathophysiologic continuum. Early institution of anti-adrenergic measures in form of prazosin along with intensive supportive treatment aimed at management of shock and pulmonary edema has led to decline in mortality. Second line measures such as amiodarone and insulin infusion should be considered in cases with refractory post-envenomation cardiomyopathy which may lead to a favorable outcome.
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