Approach to SCORPION ENVENOMATION in pediatrics.pptx

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1. SCORPION ENVENOMATION

2. INTRODUCTION Scorpions are primarily seen in tropical and subtropical regions with hot and dry temperatures. Around 25 species are poisonous Majority of stings are reported at night , as during day they hide in cracks of buildings. Scorpion sting is common and life threatening and time limiting medical emergency seen mainly in rural areas Higher in sourthern states like tamil nadu , Puducherry , Maharashtra, and Karnataka along with fewer northern states like Madhya Pradesh and West Bengal. The pediatric age group has reported mortality rates of 7.07 per 10,00,000 in infants and 3.78 per 10,00,000 in children between 1 and 4 years of age. The mortality of scorpion sting among the pediatric age group in the preprazosin era was up to 30 %; however, post introduction of prazosin , the mortality had reduced to <1–3%.

3. ETIOPATHOGENESIS Though there are multiple species of scorpions seen in India, Hottentotta tamulus , (previously known as Mesobuthus tamulus ) ( Indian red scorpion, most poisonous ) is the most common species to cause significant clinical manifestations and toxicity. Stings from this scorpion present predominantly with autonomic hyperstimulation (autonomic storm), pulmonary edema, and cardiac effects. The other common scorpion found in India is Palamnaeus swammerdami (black scorpion ).

4. Scorpion venom is a complex compound with various toxins of which the most clinically relevant compound is scorpion alpha toxin. This alpha toxin binds to voltage-gated sodium channels and prevents them from inactivation causing hyperpolarization and persistent autonomic excitation (autonomic storm). The autonomic storm starts as an initial transient cholinergic storm (parasympathetic excess phase) followed by a prolonged adrenergic storm (sympathetic excess phase) with an overlap of symptoms while transition. Myocardial dysfunction sets in due to vasospasm and increased myocardial demand during the adrenergic storm. The entire course usually settles in within 48 hours post scorpion sting.

5. CLINICAL FEATURES

6. Scorpion envenomation by certain species can cause neuromuscular manifestations like muscle jerks, fasciculations , paralysis, abnormal oculomotor movements, visual disturbances, and vasospasm leading to stroke, dysphagia , and dysphonia . Rarely neurological manifestations may be severe enough to cause respiratory compromise. Other rare manifestations like skin necrosis, hemolysis , disseminated intravascular coagulation, and renal failure are also reported in the literature.

7. EVALUATION A thorough clinical assessment (history and examination) along with a 12-lead electrocardiography (ECG) and chest X-ray would suffice for optimal management of scorpion envenomation in most settings. In the setting of a tertiary care pediatric intensive care unit (PICU), availability of bedside echocardiography (ECHO) may be used as an additional tool in evaluating cardiac function. In critically ill children requiring PICU, additional investigations like hemogram , renal function test, and electrolytes will aid in providing optimal care. In ECG, features like low voltage, wide QRS complex, peaked T waves, hemiblock , and ST-segment elevation/depression are reported. The more prominent the ECG changes (especially early in the course), the worse the myocarditis and the prognosis.

8. DIFFERENTIALS Following are the close differentials to scorpion envenomation : Unexplained sudden-onset cardiogenic shock/congestive cardiac failure (CCF) secondary to various causes like viral myocarditis Cholinergic toxidrome secondary to poisonings Intoxication with stimulants like cocaine and amphetamines Pheochromocytoma Black widow spider bites

9. EMERGENCY CARE Initial assessment and stabilization should be as per pediatric advanced life support (PALS) guidelines. Symptom-specific management of scorpion sting is classified into five groups based on physiological hemodynamic patterns as given below. 1. Asymptomatic children : Require close monitoring of vitals for 24 hours 2. In children with local pain and no systemic features : Administer oral paracetamol (15 mg/kg). Avoid lignocaine injections and steroids.

10. 3)In children with evidence of autonomic storm and/or features of myocarditis with no evidence of CCF : Start them on oral prazosin and consider repeating every 6 hourly till resolution of autonomic storm (return of warm extremities is a useful sign at bedside). Ensure adequate oral intake and if oral intake is poor, start them of full-maintenance intravenous fluids in the initial 6 hours (during autonomic storm, fluid deficit is more common due to diaphoresis, profuse sweating, vomiting, and poor oral intake) and subsequently fluid intake can be adjusted based on bedside assessment of urine output and intravascular volume status.

11. In children with features of myocarditis and CCF : Classify them into early CCF [tachycardia, tachypnea , basal crepitations , elevated jugular venous pulse (JVP), etc., with normal blood pressure (BP) and no hypoxia ] late CCF (early CCF features plus pulmonary edema as evidenced by marked work of breathing, worsening hypoxia not improving with supplemental oxygen, pink frothy sputum, coarse crepitations over lung fields.

12. Management of children with early CCF: ƒ Start on dobutamine infusion at 4–6 µg/kg/min and titrate up to 10–15 µg/kg/min. Target normal peripheral perfusion and decrease in heart rate rather than normalization of BP as it may not increase to 50th centile with dobutamine . Accept 5th centile BP if perfusion is adequate. ƒ ƒ Avoid furosemide in the initial 12 hours, until the intravascular volume deficit caused by profuse sweating, vomiting, etc. is corrected. ƒ It is preferable not to use inotropes with longer half-life (e.g., milrinone and levosimendan ) as first-line agents, as the clinical status can rapidly change over time. ƒ Avoid adrenaline and noradrenaline infusions unless hypotension is refractive to dobutamine and optimization of intravascular volume. ƒ Avoid opioids like morphine early in the course. ƒ Be cautious with oral prazosin , if a child is on dobutamine infusion and has a BP on the lower side of normal (close to 5th centile ).

13. Management of children with late CCF (pulmonary edema and cardiogenic shock): Provide noninvasive ventilation (NIV), and if not improving within 1 hour, intubate and mechanically ventilate with adequate positive end-expiratory pressure (PEEP) (to improve lung compliance and to decrease left ventricular afterload ). For sedation and analgesia, use drugs like ketamine with least impact on hemodynamics along with short-acting paralytic agents peri -intubation. ƒ Continue dobutamine at maximum tolerated dose (maximum 15 µg/kg/min). ƒ If pulmonary edema and hypoxia persist even after positive-pressure ventilation, start intravenous sodium nitroprusside (SNP) infusion at 0.5–1 µg/kg/min and titrate up to achieve improvement in oxygenation parameters and lung compliance (maximum up to 5 µg/kg/ min). Avoid SNP if hypotensive (BP close to 5 th percentile) ƒ In children who are hypotensive with poor perfusion, the preferred vasodilator for pulmonary edema is intravenous nitroglycerine infusion (1–5 µg/kg/min) Avoid oral prazosin if a child is on intravenous vasodilators. ƒ Adrenaline infusion can be tried as a desperate measure in a child with refractive hypotension and poor perfusion.

14. In both early and late phases of CCF, all the supportive measures should be continued for at least 24 hours before attempting withdrawal. Taper and stop the vasodilator first, followed by dobutamine . Rarely children may present with atypical features like central nervous system (CNS) manifestations with seizures/encephalopathy. In this scenario, management is purely supportive. Benzodiazepines are the first-line agents for controlling seizures followed by phenobarbitone or levetiracetam . Avoid phenytoin as the risk of cardiac arrhythmias is high.

15. SPECIFIC MANAGEMENT

16. KEY LEARNING POINTS In scorpion sting envenomation , the autonomic storm predominates in the initial 4–6 hours, which is often followed by myocarditis by 8–12 hours with some overlap in between 6 and 12 hours phase . Diuretics should be avoided in the initial 12 hours, even if there is pulmonary edema, as the intravascular volume is likely to be low. In the initial autonomic storm phase, prazosin and adequate fluids are the mainstay of therapy. Prazosin can be given even if BPs are borderline, provided the intravascular volume is preserved . In myocarditis , prazosin is still continued, but it acts mainly as a vasodilator (decreases afterload ) and aids in the management of cardiac failure. If the child is already on inotropes , then easily titratable vasodilators like nitroglycerin (NTG) and SNP (short acting agents) are preferred over prazosin . Morphine should be avoided (when given for initial pain), as it increases the chance of arrhythmia . Bedside ECG recording, available in all settings, is a very good indicator of the severity of myocardial injury and useful for prognosis. Inotropes should be tapered based on the trends of clinical assessment of perfusion rather than actual BP or serial ECHO