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Scorpion Bite causing Acute Severe Myocarditis: A Rare Complication

TARACHAND SAINI*, SHAILENDAR GUPTA**, MANIRAM KUMHAR

ABSTRaCT
Scorpion bites are common in India as well as in other countries. Usually, these bites are harmless but sometime have serious clinical sequelae, including death. We report herein a case of scorpion bite that presented with acute severe myocarditis - a rare complication.

Keywords: Scorpion bite, severe myocarditis, pulmonary edema

here are about 1,500 species of scorpions worldwide, out of these 50 are dangerous to human. Among 86 species in India, Mesobuthus tamulus and Palamnaeus swammerdami are of medical importance.1 Almost all lethal scorpions except Hemiscorpius species, belong to the scorpion family called Buthidae. The lethal member of Buthidae include genera Buthus, Parabuthus, Mesobuthus, Tityus, Leiurus, Androctonus and Centruroides. Scorpions live in warm dry regions throughout India. They commonly inhabit the crevices of dwellings, underground burrows, under logs or debris, paddy husk, sugarcane fields, coconut and banana plantations. Their distribution is more in regions with abundant red soil.2 They hunt during night and hide in crevices and burrow during the day to avoid light. Scorpion stings increase dramatically in summer months and lower in winter. Scorpion stings causes a wide range of manifestation, from local skin reaction to neurological, respiratory

and cardiovascular collapse. Cardiovascular effect are particularly prominent after stings by Indian red scorpion (M. tamulus).3 CASE REPORT An 18-year-old girl was stung by a scorpion on the distal phalanx of the left index finger and presented with intense pain and swelling on the local site. She admitted with heart rate 140 beats/minute, and blood pressure 70/40 mmHg. Symptomatic treatment was given. But the patients condition continued to worsen, and she developed severe respiratory distress. Because of respiratory failure, she was immediately intubated and admitted to the intensive care unit. Bilateral basal rales were heard on auscultation, and cardiovascular examination revealed a loud S3 gallop at the apex. Laboratory results were as follows: Hemoglobin was 12.6 g/dl, white blood cell count was 24,380 cells/mm3, platelet count was 1,80,000 cells/mm3 and urine microscopy showed hematuria. Blood urea 71 mg/dl (17-43 mg/dl), serum creatinine 1.6 mg/dl (0.5-1.1 mg/ dl), aspartate transaminase 93 U/l (5-38 U/l), alanine transaminase 30 U/l (5-41 U/l), creatine kinase (CK) 743 U/l (26-190 U/l), CK-MB 52 U/l (0-24 U/l), Trop-I 0.02 ng/ml (0.00-0.04 ng/ml). An electrocardiogram (ECG) revealed sinus tachycardia and ST-T wave changes. Chest X-ray demonstrated bilateral fluffy shadows indicative of pulmonary edema (Fig. 1). Echocardiography reveal hypokinesia of the basal two-third of the interventricular septum with reduced ejection fraction (Fig. 2).

*2nd Year Resident **3rd Year Resident Associate Professor Dept. of Medicine, Jawaharlal Nehru Medical College, Ajmer Address for correspondence Dr Tarachand Saini 20, Gaurav Enclave, Near City Palace, Civil Line, Ajmer, Rajasthan E-mail: drtcsaini20@gmail.com

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dependent sodium channels in the open state leading to continuous, prolonged, repetitive firing of the somatic, sympathetic, and parasympathetic neurons results in autonomic and neuromuscular overexcitation symptoms due to release of excessive neurotransmitters such as epinephrine, norepinephrine, acetylcholine glutamate and aspartate. Meanwhile, the short polypeptide neurotoxin blocks the potassium channels. Scorpion bites usually have a good prognosis. However, occasionally potentially fatal complications such as myocarditis, pulmonary edema and shock occur.4 Among these, myocarditis and resultant pulmonary edema are important causes of death.5 Three possible mechanisms might explain cardiac dysfunction, including adrenergic myocarditis, toxics myocarditis and myocardial ischemia. a-receptor stimulation by toxins play a major role in development of tachycardia, myocardial dysfunction and pulmonary edema.6 Unopposed a-receptors stimulation lead to suppression of insulin secretion, hyerglycemia, hyperkalemia, free fatty acid and free radical accumulation that are injurious to myocardium. Bahloul et al4 examined the histopathology of two fatal myocarditis cases resulting from a scorpion bite. The pathologic conditions revealed a mixed picture of toxic myocarditis and coagulative myocytolysis, similar to catecholamine-induced cardiotoxicity.4 Myocardial ischemia is not only due to the release of catecholamines but also due to effect of cytokines and/or neuropeptide Y on coronary vessels. Cardiac damage might be enhanced by the depressive effect of cytokines upon myocardial cells. Hyperglycemia may also contribute to myocardial injury.7 Valdivia et al8 reported a series of 32 children with scorpion bites who developed cardiac complications. Among these, 50% exhibited myocarditis, 12.5% had subclinical disease, and 63% had observable ECG changes. We observed both ECG changes and myocarditis in this case. CONClUSION We report here the case of an 18-year-old girl who developed life-threatening, acute toxic myocarditis and pulmonary edema, after a scorpion bite. Aggressive medical treatment with inotropic agents, diuretics and parenteral corticosteroids resulted in rapid clinical resolution.

Figure 1. Chest X-ray showing bilateral fluffy shadows.

Figure 2. Echocardiography.

In accordance with these symptoms and findings, a diagnosis of acute heart failure with pulmonary edema was made. Dopamine, dobutamine, diuretics and steroids were given. With treatment, patients status improved. Repeat chest X-ray was clear within 24 hours of initiating this treatment. DISCUSSION Scorpion venom may contain multiple toxin-like neurotoxin, cardiotoxin, nephrotoxin and hemolytic toxin. The primary targets of scorpion venom are voltage-dependent ion channels. The long-chain polypeptide neurotoxin causes stabilization of voltage-

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REFERENCES
1. Erfati P. Epidemiology, symptomatology and treatment of buthinae stings. In: Arthpod Venoms. Handbook of Experimental Pharmacology. Bettini S (Ed.), SpringerVerlag: New York 1978:p.312-5. Bawaskar HS. Personal communication. 1998. Bawaskar HS, Bawaskar PH. Indian red scorpion envenoming. Indian J Pediatr 1998;65(3):383-91. Bahloul M, Kallel H, Rekik N, Ben Hamida C, Chelly H, Bouaziz M. Cardiovascular dysfunction following severe scorpion envenomation. Mechanisms and physiopathology. Presse Med 2005;34(2 Pt 1):115-20. 5. Gueron M, Yaron R. Cardiovascular manifestations of severe scorpion sting. Clinicopathologic correlations. Chest 1970;57(2):156-62. Bawaskar HS, Bawaskar PH. Management of the cardiovascular manifestations of poisoning by the Indian red scorpion (Mesobuthus tamulus). Br Heart J 1992;68(5):478-80. Garg AK, Pimparkar AB, Abraham P, Chikhalikar AA. Myocarditis and pulmonary edema following scorpion bite. (A case report). J Postgrad Med 1983;29(1):46-8. Valdivia HH, Kirby MS, Lederer WJ, Coronado R. Scorpion toxins targeted against the sarcoplasmic reticulum Ca(2+)release channel of skeletal and cardiac muscle. Proc Natl Acad Sci U S A 1992;89(24):12185-9.

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Vitiligo Management Guidelines Released

The most effective management for vitiligo includes phototherapy and combination therapy, according to updated guidelines from the writing group of the Vitiligo European Task Force (VETF), which were accepted for publication and published online August 3 in the British Journal of Dermatology. The European Academy of Dermatology and Venereology and the Union Europenne des Mdecins Spcialistes collaborated with the VETF in developing the new evidence- and expert-based guidelines for vitiligo. The reviewers recommend the following principles of management for segmental vitiligo or limited nonsegmental vitiligo (involving <2-3% of body surface): First-line treatment should be to avoid triggering factors and to use local agents such as corticosteroids or calcineurin inhibitors.

First-line management is to avoid triggering or aggravating factors and to stabilize the patient with NB-UVB therapy for at least three months. Patients who respond to NB-UVB should continue this treatment for nine months or more. An additional consideration is to combine localized UVB therapy with systemic or topical therapies. Second-line treatment for patients with rapidly progressive disease or lack of stabilization with NB-UVB is systemic corticosteroids, 3- to 4-month minipulse therapy or immunosuppressants. Third-line treatment is to graft areas failing to respond to previous treatment, particularly those areas with high cosmetic effect. The Koebner phenomenon, or new development of vitiligo in a previously unaffected area of skin undergoing traumatic injury, may limit graft persistence, Grafts are relatively contraindicated on the dorsum of the hands and similar areas. Fourth-line treatment for widespread (covering >50% of body surface), refractory or highly visible vitiligo is depigmentation using hydroquinone monobenzylether or 4-methoxyphenol alone or in combination with Q switch ruby laser.
(Source: Medscape)

Second-line treatment should be localized narrow-band ultraviolet B (NB-UVB) radiation (311 nm), preferably with the excimer monochromatic lamp or laser. Third-line treatment for patients left with cosmetically unsatisfactory repigmentation on visible areas after first- or second-line therapy is to consider use of surgical techniques.

The reviewers recommend the following principles of management for nonsegmental vitiligo:

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