Into the Venomous Abyss: Unveiling Rare Complications Following Scorpion Bites

Introduction

Scorpion envenomation is an important public health hazard in tropical and sub-tropical regions, including India. Out of 1500 species of scorpions worldwide, 50 are dangerous to humans. Among 86 species in India, Mesobuthus tamulus (Indian red scorpion) and Heterometrus swammerdami are of medical importance.¹ Clinical manifestations are varied ranging from simple allergic reaction to severe compromise of cardiac, respiratory and central nervous system (CNS) function. Cardiovascular manifestations are particularly prominent following stings by Indian red scorpion², but neurological complications, of which intracranial haemorrhages and cerebral infarction are common.³

Case 1: A 22-year-old male, suffered a scorpion sting over left anterior chest. Within 2 hours, the patient started having chest pain associated with cold sweating. On admission, the patient complained of breathlessness and palpitation after 2-3 hours of the scorpion bite. He had no prior history of cardiac abnormalities or risk factors. Findings on clinical examination were as follows: Blood pressure 60 mmHg systolic; pulse 128/min, regular and jugular venous pressure was raised; the respiratory rate was 52/min and room air saturation of 75%. Examination of the respiratory system showed bilateral coarse basal rales. Cardiovascular system examination revealed loud s3 at apex, no murmur or pericardial rub. Central nervous examination patient is drowsy. Per abdominal examination was within normal limit. Local examination revealed cold peripheries; swelling and erythema over left anterior chest.

Investigations

Arterial blood gas analysis (ABG) showed pH7.30, pO2=55.4%, pCO2= 38.8%, HCO3= 18.4, Lactates=3.27 and laboratory investigations showed White Blood Cells of 29,230/mm3 with neutrophilia, haemoglobin of 10.5gm/dl, platelet count was 3.75 million/cmm, serum creatinine of 1.2 mg/dl random blood sugar was 136 mg/dL. Trop T was 0.883 ng/ml (0.000-0.014); ProBNP was 35673 pg/ml (0.000-125.0); CPKMB was 26.46 ng/ml (1.39-6.22).

Electrocardiogram (ECG) recorded on admission showed secondary ST-T changes and tachycardia [Figure 1a]. However, subsequent ECG two days later revealed normal sinus rhythm with ST segment elevation with concavity upward in lead II, III, aVF, V2, V3 and T- wave inversion in all precordial and chest leads. Chest radiograph showed bilateral fluffy shadows suggestive of pulmonary oedema [Figure 2a]. Echocardiogram demonstrated severe global hypokinesia of left ventricle(lv) with moderate mitral and tricuspid regurgitation and severe lv dysfunction, with ejection fraction 25%.

Treatment

Patient was initially treated with injection prazocin 30µg/kg/dose and later with intravenous dopamine, noradrenaline, dobutamine, frusemide and corticosteroids with oral aspirin, and nitrates, and noninvasive oxygen therapy in the form of continuous positive airway pressure for type I respiratory failure. Patient was shifted to intensive care unit for further management.

Outcome and follow-up

Patient was kept in Intensive Care Unit (ICU) with oxygen supplementation and regular vitals monitoring and arterial blood gas monitoring. Patient’s blood pressure increased gradually, repeat white blood cell count was 9340 cells/cmm, Troponin T was 0.040 ng/ml (0.000-0.014); NT Pro BNP was 2435 pg/ ml (0.000-125.0); CPKMB was 4.86 ng/ml (1.39-6.22); arterial blood gas analysis: pH 7.45, pCO2 40,pO2 88, sO2 98.0, serum lactate 0.8, serum bicarbonate 25.9. Pulmonary oedema subsided as Serial X-ray chest showed clearing up of the lung fields [Figure2b]. Serial ECG was recorded over the next 5 days, these showed persistence of q wave and T wave inversion in lead I and aVL, v4- v6 [Figure 1b], and echocardiogram demonstrated mild mitral and tricuspid regurgitation and left ventricular ejection fraction 45%. Patient improved in 5-6 days. Patient was discharged and followed-up to 2 years for cardiac dysfunction and later died due to underlying cardiac condition at a local hospital.

Case 2: A 45-year old male, known hypertensive on medical management, presented with history of scorpion sting following which he had headache, vomiting and left sided weakness. After admission to our hospital, he developed ventricular tachycardia (Figure 3a) for which he was given intravenous Amiodarone and Lignocaine. After an hour, the heart rate was 72/min; BP= 180/110 mmhg. He became drowsy with Glasgow coma scale (GCS) = E2V2M3; Pupils- assymetrical reactive to light and left hemiparesis was noted. Patient was intubated in view of poor GCS. His computed tomography (CT) brain revealed Right Frontotemperoparietal Intracerebral hemorhage with ventriculomegaly (Figure 3b).

He was advised craniotomy and evacuation of hemorrhage after neurosurgical consultation. Over the next 12 hours, he again developed sudden onset hypotension with ventricular tachycardia and cardiac arrest. He was revived with cardiac pulmonary resuscitation for 15 min with Cardio-version (200J) subsequently. Post resuscitation, the patient was comatose with Glasgow Coma Scale of 3/15. Pupils were 4 mm equal, fixed and dilated. Two hours later, he went into sudden cardiac arrest and could not be revived.

Discussion

Scorpions have a worldwide distribution and highly toxic species are found in Africa, India, Mexico, North Africa, South America. Toxins of Centroides and Parabuthus species exhibit Neurotoxicity, toxins of Androctonus, Buthus, Mesobuthus exhibit Cardiotoxicity. Most stings cause only pain at bite site; <10% cause systemic toxicity. Cerebrovascular accidents have been reported in around 8% of cases.

Various mechanisms of toxin action

• Release of vasoactive, inflammatory and thrombogenic peptides and amine constituents (histamine, serotonin, bradykinin, leukotrienes, thromboxane), which act on the coronary vasculature and induce coronary artery vasospasm and facilitate platelet aggregation as well as thrombosis.⁴
• Direct cardiotoxicity causing toxic myocarditis by reduction of Na-K-ATPase and adrenergic myocarditis by releasing adrenaline and noradrenaline from neurons, ganglia, and adrenals, thereby increasing myocardial oxygen demand by direct inotropic and chronotropic effect on already compromised myocardial blood supply.⁴
• Scorpion venom inhibits angiotensin converting enzyme, resulting in accumulation of bradykinin, which is implicated in the development of pulmonary edema.⁴

Bahloul et al. examined the histopathology of two fatal myocarditis causes resulting from a scorpion bite, revealed a mixed picture of toxic myocarditis and coagulative myocytolysis, similar to catecholamine-induced cardiomyopathy.⁵ Valdivia et al. reported a series of 32 children with scorpion bite who developed cardiac complications. Among these, 50% exhibited myocarditis, 12.5% had subclinical disease, 63% had observed ECG changes.⁶

Patil SN conducted a retrospective analysis on fatal scorpion stings and its treatment wherein out of 242 patients 141 patients developed cardiotoxicity. Out of them 96 had received prazosin as a first line of treatment. Out of 96, 23 needed dobutamine to treat cardiac complications. Mortality was highest in only prazosin, no dobutamine group and lowest in prazosin, dobutamine group.⁷

Pathophysiology of stroke in scorpion poisoning has been attributed to various mechanisms:

1. Autonomic storm induced sudden surge in blood pressure causing rupture of perforators.

2. Myocarditis induced cardioembolic stroke.

3. Venom induced DIC causing increased platelet aggregation.

4. Venom induced vasculitis caused by endothelial damage.

5. Hypotension induced watershed infarcts.

6. Catecholamine excess induces increased endothelin resulting in vasoconstriction.^8,9

In our first patient findings mimicked acute myocarditis (including clinical symptoms, changes in ECG, elevated cardiac enzymes, regional wall motion abnormality in echocardiogram). Probably, coronary vasospasm associated with above-mentioned sequences (myocarditis, pulmonary edema) has precipitate acute cardiomyopathy in our case. Venom induced vasculitis and autonomic storm could have been the probable cause in our second patient causing a hemorhhagic stroke. There are very few cases of cardio or neurotoxicity due to scorpion bite reported in the literature. Hence, it worth reporting these rare cases.

Learning points

• Scorpion venom can have a potent cardiotoxic and neurotoxic effect though rare but life-threatening.
• Any age group can develop cardiac complication irrespective of previous health conditions.
• A routine serial ECG must be included in the investigation to early detection of any cardiac manifestation and if required cardiac markers and echocardiogram helps in early diagnosis of acute cardiac complications like acute myocardial infarction.
• In initial phases of autonomic storm i.e. accelerated hypertension one can use prazosin but monitor the patient for left ventricular failure. Addition of Dobutamine can be life-saving.
• Scorpion bite-associated stroke may manifest as intracranial bleed or ischaemic infarct.
• Voltage-dependent ionic channels are the target of scorpion venom.
• Case fatality can significantly increase in presence of complications and multisystem involvement.

Acknowledgements: We would like to thank all patients and their families for the trust and faith they have shown on us throughout their treatment. We would also like to thank our head of department and co-author for their continuous support and guidance.

Conflict of interest:

None

Funding support:

None

**Undertaking : This study was conducted by me (Dr V Niranjani) in my PG college i.e Apollo BGS hospital, Mysore.