REVIEW ARTICLE Scorpion Sting Dr. H.S.Bawaskar Dr. P.H.Bawaskar Abstract: Scorpion envenomation is a public health problem in tropical and subtropical countries, especially in Africa, Middle East, Latin America and India. At times, it poses a significant life-threatening acute time limiting cardiovascular emergency. Irrespective of different species of scorpion, similar cardiovascular effects are reported. Scientists working on this problem are trying to understand the pathophysilogy of severe scorpion sting by various investigations including, neurotransmitter, radioisotope study, echocardiography, haemodynamic pattern and clinical manifestations. Various regimen including vasodilators, antivenin, platelet activating inhibitors, inotropic support, and metabolic rectifier such as insulin and L-carnitine have been tried. Irrespective of the understanding pathophysilogy and its management the fatality remains high in rural areas due to non-approachable medical facilities and faith in village healers which delays the hospitalization. Scorpion envenoming have been underestimated as this problem faced by the world comprises the majority of underdeveloped and developing countries. Moreover, the medical attendee from poor countries may not be aware of western line of treatments of scorpion sting. Introduction 2000-2001. Of these 49% were a mild clinical, 33.8% had moderate Scorpion envenomation is a public health problem, common in and 17% had severe manifestations. Children exhibit more severe certain areas of the world including Middle East, Latin America, manifestations 7. Venezuela reported children with high fatality8. 13 Africa and India 1, 2, 3. Mesobuthus Tamulus (the Indian red scorpion) out of 78 cases died due to scorpion sting as stated in a report from scorpion venom is a potent sodium channel activator . The clinical Mahad region9. In rural hospitals from western Maharashtra, India manifestations of scorpion envenomation appear to be secondary 3,546 scorpion sting cases are reported in one year, of these 542 had 4 to activation of both the sympathetic and parasympathetic nervous system. In 2/3rd of victims, the main clinical manifestations of scorpion sting are local severe excruciating pain only, which radiates along the corresponding dermatomes accompanied with mild edema and local sweating at the site of sting. Systemic manifestations (vomiting, sweating, salivation, cold extremities, priapism hyper or hypotension, brady or tachycardia and ventricular premature beats or at times non-sustained ventricular tachycardia) are not uncommon due to envenoming by the lethal scorpion species Mesobuthius tamulus, Leiurus quinquestriatus, Androctonus mauretanicus, Buthus occitanus, Centruroides, A crassicauda, Tityus zulianus Tityus serrulatus . Similar 1, 3, 4 cardiovascular manifestations have been reported irrespective of systemic involvement10. Similar report from Pondicherry, Andhra Pradesh and Karnataka states of India.10,11,12 Opinions differ regarding correct treatment of scorpion envenomation7. Recently, WHO reported that the truth of scorpion sting envenoming is not known because many cases do not seek medical attention. Moreover, scorpion envenoming accident occurring in villages of tropical and subtropical countries and many countries including India it was not modifiable disease hence the actual statistical data is scarce. Moreover, majority of the victims attend in the village healers or tantriks or quacks remain unregistered. It has been estimated that there are approximately 1 different species of scorpion . Morbidity and mortality due to million stings per year. In Mexico alone 2,50,000 scorpion stings are scorpion sting is related to acute pulmonary edema, cardiogenic reported yearly, in Tunisia 40,000 stings, 1,000 hospital admission shock and multi-organ failure. A study of 434 cases during a ten and 100 deaths are reported each year. There is a high incidence 4 year period at the national guard hospital in Riyadh showed 92% in other parts of north Africa, the Middle East13, India and Latin had local pain, 25.6% had systemic involvement, hypertension in America. In Khuzestan, southwest Iran, scorpion sting is the 5 17%, Tachycardia in 4% . In a study from western Maharashtra, fourth leading cause of death attributed to Hemi scorpion lepturus we have reported 526 cases studied between 1984-1991 of which 14 236 (45%) had hypertension, 27/(5%) had hypertension with in 2005 pulmonary edema, 139 (27%) had pulmonary edema, 96 (27%) sting is an important, yet neglected, health issue in affected parts of demonstrated tachycardia and 28 (5%) died. A report from ministry world 13. Scientists are keen in treating reporting and studying the of health in Colina state of Mexico recorded 13,223 cases in the year snake bite more than scorpion envenoming. However, the clinical 32 . In Brazil, 37,000 scorpion sting and 50 deaths were reported 13 . This incidence indicates that envenoming by scorpion research done in tropical countries is often neglected by health in the class Archnida. They shelter under bark of trees, dry authority is and unfortunately, there is no consensus regarding firewood or cow dung, in a piles of bricks, paddy husk, beddings, management of scorpion sting similar to snakebite (WHO personal loose tiles of hut and at times in the shoe left empty over night communication). and pockets of trousers and shirt, craves of window and doors. Scorpion antivenin is widely used in many countries such as Brazil, Saudi Arabia, Mexico 15, 16, 17, 18, 19 , 20, 21, 22, 13, 24, 25, 26. The acceptance of scorpion antivenin as an effective treatment in scorpion sting is based mainly on its efficacy in experimental studies. Scorpion antivenin is no better than placebo reported from Tunisia 24. The beneficial effects of antivenin in protecting victims against severe scorpion sting is still questionable 27,28,29 Scorpions have been recognized by a sting with severe excruciating pain, long lasting and rarely threat to the life. They are one of the In tropical countries, sparrows usually bring small scorpion along with the dried grass to build up a nest over window in a pucca house. Farmers and farm labors are often stung by scorpion during handling of paddy husk, harvesting grass over bund in the months of September to November3,32. Travelers, while walking barefoot in the desert are more prone to this painful lifethreatening accidents (Fig.1). There are around 1400 species of scorpions, but only 46-50 of these are potential lethal to humans. (Fig.2)32. oldest known terrestrial arthropods. Fossil scorpions found in Paleozoic strata 430 million year old appear very similar to present species30. They survive heat, drought, can withstand freezing condition for weeks, desert conditions and starvation for months and total immersion in water for days. This remarkable power of adaption, make them many a time independent of ecological condition and gives the race an unbroken continuity. They are strictly carnivorous, feeding on insects. Scorpions are viviparous, give birth to the young ones and sometimes the mother tries to eat the young, but more often, the young ones nibble the mother to death (cannibalism)31. Scorpions belong to venomous arthropods Figure 2 The lethal species belong to Androctonus (Morocco and Senegal eastwards to India, Buthus (Mediterranean, Middle East and East Africa), Hottentotta (Northern Africa and Middle East), Leiurus (East Africa and Middle East), parabuthus (Sudan to South Africa), Mesobuthus (India, Southern and Central Asia), Tityus (South America), Centruoides (USA, Mexico, and Central America). Hemiscorpion lepturus (family scorpiodae) a dangerous species seen in Iran. Palmaneus garvimanus a cactoid species scorpion is bigger in size Figure 1 compare to other species and is black in color it causes severe pain with mild sweating 3,33. (Fig.3) Authors: Dr. H.S.Bawaskar & Dr. P.H.Bawaskar Bawaskar Hospital and Research Center, Mahad, Dist. Raigad, Maharashtra, India. e-mail: [email protected] 33 Clinical Manifestations Clinical effects of the envenoming depend upon the species of scorpion and dose of venom injected at the time of sting. The severity of envenoming is related to age, size of scorpion and season of sting. High incidence of pulmonary edema and fatality are seen in the monthes of June, September and October 3, 9, 39. Irrespective of different species with few exception (Iran and Trinidad) the cardiovascular manifestations due to envenoming are similar 1, 3, 6, 17, 24, 40. The early or premonitory clinical manifestations as result of autonomic storm are characterized by vomiting 34%, profuse sweating from all over body 45%, priapismin males 28%, Figure 3 cold extremities 71% and mild tolerable pain which becomes severe, when extremities became warm is a sign of recovery41. Venom On the clinical presentations or course in hospitalized patients are Tail end of scorpion content two telson glands actively secret the venom at the time of sting which is injected in a prey by sharp divided into 1) Severe local pain only, and 2) Systemic involvement. stinger. All scorpion species secrete venom. Venom is a mixture Local Pain of various active substances of these neurotoxins34. Neurotoxins Severe excruciating pain is the only clinical manifestation seen consist of different small size proteins with a sodium and potassium in 35% of cases. 57%, 33%, 11% lower, upper extremities and cations which interfere the neurotransmitter in the victim. Venom other parts of the body is the site of sting respectively. Severe actions on neurotransmitter are rapid and fast. It contains a peptide pain radiates along with corresponding dermatomes. Due to pain neurotoxin that open the Na+ channels (B–toxin). Sodium is intolerable, inconsolable crying of the child, sudden onset is a primarily an extra cellular ion maintaining electric voltage difference diagnostic sign especially in a early darkness when one can not find across the cell membrane. Venom depolarizes the cell membrane the culprit. Children are confused and anxious due to pain. Local and it also inhibits the deactivation of Na+ channels (alpha- edema, urticaria, fasciculation and spasm of underneath muscle toxin). There is a massive release of endogenous catecholamine at the site of sting due persistent stimulation of pain conducting in to circulation due to delayed inactivation of sodium neuronal receptors and liberated serotonin29, 30. Due to pain there is transient channel by venom (4). Thus venom of the Mesobuthus Tamulus bradycardia, transient rise in blood pressure and mild sweating but (the Indian red scorpion), Buthus Martensi (chene’s scorpion) and extremities are warm3. Sudden tap at the site of sting induces severe Leiurus Quinquestriatius (Israel scorpion) causes autonomic storm by pain and sudden withdrawal of the part is diagnostic of scorpion stimulating both sympathetic and parasympathetic nervous system. sting called TAP sign . Charybdotoxine is the another component of the venom inhibits the calcium dependent K+ channels, similarly iberiotoxin isolated Systemic Manifestations from Mesobuthus Tamulus has similar action on K+ channels35,36 . Clinical manifestations depend upon time lapse between sting and The venom of leiurus species includes chlorotoxin which acts on hospitalization or treatment received at periphery32. According Chloride channels. Scorpion venom also contains serotonin which to clinical manifestations, they are divided into three grades of causes local pain at the site of sting. The venom of Tityus species II, III and IV. All cases had initial sign and symptoms suggestive 37, 38 . Venom of of autonomic storm3. Grade II – hypertension or transient Tityus Serrulatus from Trinidad is pancreotoxic responsible for hypotension, tachycardia, bradycardia, and cold extremities development of acute pancreatitis. Hemi scorpion leptirus is the most Grade III – hypertension, hypotension, tachycardia and pulmonary dangerous scorpion of Khuzestan, south west, hot and humid edema or Massive pulmonary edema, respiratory failure. province of Iran13. Venom causes severe local tissue necrosis, renal Grade IV – tachycardia, hypotension, pulmonary edema with warm failure and cardio respiratory arrest13. extremities called warm shock. a kallikrenin inhibitor causes raised bradykinin 34 Hypertension (mean 85) with cold extremities with or without pulmonary edema, 45% of victims with systemic involvement had raised blood 42% cases usually reported 8-26 (mean 150) hours of sting with pressure soon after a sting. Blood pressure ranges between 140/90 marked tachycardia 140-200 (mean 165) with hypotension systolic and 180/130 mm hg. Children look agitated confused and had blood pressure 50-90 mm hg with warm extremities with or without propped up eyes and puffy face39. Hypertension noted in victim pulmonary edema (warm shock)47. Reappearance of local pain at reported 15 minutes to 11 hours after sting. Majority of cases had the site of sting which was mild or absent on arrival suggestive of headache, chest discomfort and perioral parasthesia. recovery.41 Hemiplegia, cerebral edema, disseminated intravascular coagulation, due to scorpion sting have been reported. Fatality is Transient initial hypotension is due to dehydration caused by high, once neurological complications such as coma, convulsions, excessive sweating, salivation and vomiting which is further miosis, mydriasis occurred.48, 51, 52, 53 aggravated by hot climatic condition of tropical and subtropical countries, while post adrenergic hypotension is due to depletion of Abdominal pain, nausea, vomiting are common signs and catecholamine which is due to over stimulated alpha-1 receptors symptoms of scorpion envenomation in older children and adults . 32, 42, 43 also attributed to acute pancreatitis with raised level of plasma immune-active cationic trypsin seen due to envenoming by Tityus Pulmonary Edema Trinitatatis and Leiurus Quinquestritus54 and due to Mesobuthus Tamulus Pulmonary edema occurs in 27-30% cases with respiratory failure. envenoming. Scorpion envenoming rarely causes acute renal failure. Pulmonary edema develops within 30 minutes to maximum 10 However ill-treated, delayed reporting of a case developed and dies hours after sting. 8% cases reported an acute life-threatening due to multi-organs failure 55. massive pulmonary edema. Rapid onset of pulmonary edema within two hours of envenoming is often accompanied with Investigation severe hypertension. Parasternal sustained systolic lift due to Leukocytosis 11000-26000 per/cu.mm, increase in troponin 1 and sudden rise in pulmonary pressure with right ventricular after other cardiac enzymes, raised inteleukin, tumor necrosis factor, load 3,32 . Sudden onset of breathlessness, intractable cough, poor peripheral oxygenation, ice cool extremities, tachycardia with low volume thread pulse, central cyanosis, bilateral moist rattles heard all over chest, with loud summation gallops and transient systolic murmur due to mitral valve incompetence auscultation over precordium. Intractable cough, with massive expectoration of blood platelet activating factor.56, 57 Rennin, angiotension II, and urinary and serum catecholamine levels.58 X-Ray of chest showed typical picture of pulmonary edema with batwing appearance (Fig. 4 and 5). At times unilateral distribution of pulmonary edema with air bronchogram and cardiomegaly.17, 45, 59 mixed froth from mouth and nostril, with central cyanosis, hypo or hypertension and loud death rattles sound heard few feet away from patient suggestive of massive pulmonary edema42. Victims reported late after 6-10 hours and had persistent pulmonary edema or treated by peripheral doctors with excessive intravenous fluids, steroids, antihistamines, and atropine, diuretic. Such victims developed hypotension, tachycardia, air hunger and prolonged poor tissue circulation with accumulation of anoxic metabolites in the circulation resulting in paralysis of capillary sphincter (vasodilatation) and look cadaver pale. Patients are with irritable, disoriented with or without pulmonary edema suggestive of warm shock45, 46, 47. 58% victims who reported within 8 hours of sting had heart rate 110-200 (mean 143) per minute with mean blood pressure 60-113 35 Figure 5: Batwing after 4 hours Figure 7: Electrocardiogram (ECG) - ECG is most easy available tool in rural Figure 8: setting. No single victim with systemic involvement had normal ECG. Sinus bradycardia seen in early hypertensive cases with heart rate 42-60 per minute which persisted for 3-4 hours, ventricular premature contraction, couplets, transient runs of ventricular tachycardia and rarely a fatal lethal ventricular arrhythmia, sinus tachycardia, injury to conducting system in form of left anterior hemiblock (Fig. 6), right bundle branch block, left bundle branch block (Fig. 7), complete heart block, marked tented T waves mimicking like a acute myocardial infarction pattern (Fig. 8), ST elevated with non-Q infarction pattern, PQRST alternans have been reported. Subsequent broad wide base with round top T wave suggestive of delay repolarization with prolonged QTC (450-650 milliseconds) accompanied by asymptomatic bradycardia and hypotension observed 36-48 hours of hospitalization and persisted for next five days. T wave inversion persists for more than four weeks. Despite good clinical condition of the victim, ECG showed marked changes 60, 61, 62, 63, 64, 65. Figure 6: Echocardiography changes showed poor global contractility 12-15 hours after the sting, with low ejection fraction, decreased systolic left ventricular performance, mitral incompetence, abnormal diastolic filling persisted for 5 days to four weeks. Diminished or hypokinetic left ventricular global movement with decreased systolic function was seen in a scintigraphic study. But in the echocardiograph, there was good correlation between clinical improvement and the return of the left ventricular wall motion toward normal 59, 61, 62, 63. Hemodynamics - It is difficult to perform hemodynamic study in severely ill scorpion sting case. Karnad D.R. from India studied hemodynamic pattern in a patient with Mesobuthus Tamulus envenoming from western Maharashtra India, reported that mild envenomation causes severe vasoconstriction and hypertension while predominant left ventricular dysfunction with normal 36 systemic, vascular resistance with pulmonary edema was seen in severe scorpion sting, however, severe hypotension depends upon the fluid balance. Hypotension and shock with warm extremities occurs terminally due to biventricular dysfunction and terminal vasodilatation (warm shock). Similar hemodynamic pattern was reported from Tunisia, Brazil and Israel47, 65, 66, 68, 69. Patho-physiology Delayed inactivation of neuronal sodium channels results in acute autonomic storm. Sudden liberation of endogenous catecholamine resulted in initial transient rise in blood pressure, bradycardia and increased vascular resistance. Alpha-1 receptors stimulation play an important part in the pathogenesis of acute pulmonary edema due to scorpion sting70. Accumulation of calcium in the heart caused by the action of a liberated catecholamine result in increased requirement of oxygen to myocardium with systolic and diastolic dysfunction.64, 70 There is also experimental evidence of impaired coronary perfusion.71 In addition, the coronary circulation is further compromised due to raised level of rennin and angiotensin II.37 There is no significant evidence of direct effects of venom on myocardium72. Reversible cardiomyopathy attributed to catecholamine.68, 73, 74 Pulmonary edema is due to myocardial dysfunction. However, acute lung injury pattern or adult respiratory distress like syndrome attributed to secretory or non-cardiogenic pulmonary edema reported from Brazil.16 Myocardial and lung parenchymal injury is due to raised level of inteleukine6, tumor necrosis factor and kalikrenin and platelets activating factors. A study of Histopathology showed accumulation of fluid in alveoli and contraction band necrosis in the myocardium and hyaline membrane in the lung in a fatal scorpion sting case.75, 76 The pathophysiology, clinical and histological, pattern is similar to that of patient suffering from pheochromocytoma.42, 77 On the basis of pathophysiology the therapeutic effort should be directed against the clinical manifestations of the over stimulated autonomic nervous system and after effects of excessive catecholamine and correction of hypovolemia.44, 6 6, 78, 79, 80 Management Scorpion sting is un-noticed sudden onset of a accident. Majority of victims are healthier before sting. Sudden onset of myocardial injury with normal size heart and liberated free fatty acids and increased myocardial contraction were digoxin is no more beneficial. 47 While excessive diuretics is hazardous.81 Reduction of preload by applying rotating tourniquet to periphery did help in three out of four victims of severe scorpion sting with pulmonary edema.82 Alpha-blocking properties of chlorpromazine, one of the constitutes of lytic cocktail is responsible to reduce the fatality in children, however out of 100 children with severe scorpion sting treated with lytic-cocktail. Of which 22 died, according to a report from Pondicherry, India. Pethidine and antihistamine (promethazine) enhances the venom toxicity should be avoided in scorpion sting.83 Insulin therapy was advocated by Waterman from Trinidad in 1938.84 Inotropic support was needed by patients admitted with scorpion sting in a intensive care unit irrespective of treatment with insulin glucose drip85. Recently, Gupta V from India reported hypoglycemia in 30%, pulmonary edema 40% and fatality 35% in victims of scorpion sting given insulin glucose drip, while in prazosin treated group fatality was 6.2%.86 Negative inotropic effects of calcium channel blocker (nifedipine) and beta-blocker enhances myocardial failure.87 Steroids enhance the necrotizing effects of circulating catecholamine should be avoided in scorpion sting victims88, 89. Antihistamines inhibit calcium dependent potassium channels like that of Scorpion venom action should be avoided.39, 90 In experimental pharmacokinetic studies with radioactively labeled scorpion venom given intravenously, it was observed that the half life of venom distribution and its excretion were 5.6 minutes and 6.4 hours respectively91. Other similar studies using antivenin showed that the half life of distribution was 1-9 hours with the result of these studies it is concluded that antivenin therapy was inefficient because no interaction could occur between scorpion toxin and antitoxin, justified the use of prazosin and dobutamine92. IgG distribution half life was tenfold longer than that of venom which was short (32 min). In comparison to immunoglobulins, venom distributes fast and achieves greater concentration with a shorter time needed to achieve its maximum concentration72. Severe clinical manifestations due to scorpion sting are alleviated in victim if the antivenin is given within one hour after sting93. However, delayed administration of scorpion antivenin did not prevent the pulmonary edema 94. All the ten cases had severe cardiovascular manifestations, irrespective of administration of scorpion antivenin of these 5 recovered with prazosin and four required inotropic support and one died, according to a report from western Maharashtra, India95. The persistence of signs and symptoms of envenoming after neutralization of circulating venom could be explained by the inability of antivenin to neutralize scorpion toxins bound to their receptors on the sodium channel 96 . A number of specific scorpion antivenins are available but their efficacy is uncertain. Ancillary treatment with vasodilators is crucial in severely envenomed patients79. Administration of scorpion antivenin after one hour of sting did not prevent the development of pulmonary edema8, 27 and cerebral edema (Romero NO, Hernandezt JM 2005), cardiac arrest (Dittrich K, Ahmed R, Ahmed QAA 2002). Captopril angiotrensin converting enzyme inhibitor did help to alleviate the diuretic induced pulmonary edema in Scorpion sting81. Though the result of captopril therapy is similar to other 37 vasodilator, the author reported 5 deaths out of 38 studied cases 78 treated in intensive care unit in tertiary care hospital . In a retrospective study of scorpion sting cases, Rajasekhar Detal from cardiology department from Andhra Pradesh, reported that L-carnitin to reverse myocardial dysfunction following scorpion envenomation especially in patients with hypotension and severe LV dysfunction63. Aprotinin was advocated in the treatment of pulmonary edema to inhibit the platelets activating factor97. Recent study by Mangano Detal confirmed that aprotinin is not free from toxicity and can result in acute renal failure, strokes and myocardial infarction98. Moreover it is expensive, not easily available and can cause severe anaphylaxis. Prazosin is post-synaptic alpha blocker. Prazosin reduces preload, left ventricular impendence without a rising heart rate. It reverses the metabolic syndrome evoked due to excessive catecholamine80. Prazosin is a pharmacological and physiological antidote to venom action39, 99. Three victims developed severe pulmonary edema irrespective of 5 ampoules of scorpion antivenin recovered with oral prazosin a recent report from Saudi Arabia45 similar observations are reported from Tunisia100. Morbidity and mortality depend upon time lapsed between sting and administration of prazosin, since the advent of prazosin the fatality is reduced to 1%28. Massive life threatening pulmonary edema due to severe hypertension or delayed reporting of victim to health center or attended doctor failed to administer the prazosin or inadequate dose of prazosin which advocated three hourly intervals or giving excessivee diuretics, IV fluids, atropine, steroids and antihistamines. These cases need to be treated with intravenous nitroglycerine or sodium nitroprusside drip. 7-10% pediatrics cases developed marked tachycardia, hypotension with warm extremities called “warm shock” necessitates dobutamine drip27, 48. Many toxins from scorpion venoms activate sodium channels, thereby enhancing neurotransmitter release. On this basis, Fantail etal in experimental study showed beneficial effects of intravenous lignocaine, a sodium channel blocker101. Seven young patients admitted with history of scorpion sting presented with pulmonary edema was successfully managed with positive pressure ventilation with PEEP, cardiac support with inotropic and fluid balance according to a report from Nepal 102. Thus management strategy for severe scorpion sting depends upon the understanding of patho-physiology and proper diagnosis of clinical manifestations and their rational and timely interventions with appropriate therapeutic agents. 38 Scorpion antivenin is available for clinical use. Scorpion venom is a potent neuronal sodium channel activator resulting in transient cholinergic (vomiting, sweating, salivation, priapism, ventricular ectopic and bradycardia) and prolonged sympathetic (hypertension, tacahycardia, cold extremities, pulmonary edema, hypotension, shock or warm extremities with pulmonary edema and deaths) stimulations. Ongoing cholinergic phenomenon suggestive of free circulating scorpion which can be neutralized by anti-venom. While sympathetic stimulation suggest after effects and fatality is due to sympathetic over activities. We treated 20 cases of severe scorpion sting with scorpion anti-venom 30-50 ml and oral prazosin. We found that if victim reported earlier within 1-2 hours of sting the recovery time in a group treated with scorpion antivenin and prazosin is shorter than the cases treated with prazosin alone. But the cost of one ampoule of scorpion antivenom is more than 350 Rs and at times 100 ml (10 Ampoules) of anti-venom is advocated. While one mg prazosin cost is Rs. 32 for ten tablets. Further work is in progress. References References for review 1-Ismail M (1995). The scorpion envenoming syndrome. Toxicon; 33:825-58. 2. Gueron M, Ilia R and Sofer S (1992). The cardiovascular system after scorpion envenomation: A review. Clinical Tocxicology; 30:245-58. 3. Bawaskar HS. Diagnostic cardiac premonitory sins and symptoms of red scorpion sting lancet 1982; ii: 552-54. 4. Gwee MCE, Nirtthanan S, Khoo H, Gopalkrishnakone P, Kini Mr. Cheah LS. Autonomic effects of some scorpion venoms and toxins. Clinical experimental pharmacology and physiology 2002; 29:795-801. 5. Dittrich K, Power AP and Smith NA. Scorpion sting syndrome – A ten-year experience. http://www.kfshrc.edu.sa/ annals/152/94139ar.html. 6. Gueron M, llia R and Sofer S. The cardiovascuilar system after scorpion envenomation:a review. Clinical toxicology 1992, 30(2), 245-258 7. Chowell G, Diaz-duenas P, Bustos-saldana, Mireles AA and Fet v. Epidemiological and clinical characteristics of scorpionism in Colina, Mexico (2000-2001) toxicon 2006:1-6. 8. Mazzei de Davila CA, Davila DF, Donis JH, de Bellabarba AD, Villarreal V and Barboza JS. Symapothetic nervous system activation, antivenin administration and cardiovascular manifestations of scorpion envenomation. Toxicon 2002; 40:1339-46. 9. Mundle Pm Scorpion sting. BMJ 1961 1042. 10. Bawaskar Hs and Bawaskar PH. Peripheral doctors form backbone for management of acute life threatening medical emergency evoked due to envenoming by Indian Red scorpion: Mesobuthus tamulus. Bombay Hospital journal 1997;39:71014. 11. DAS S, Nalini P, Ananthakrishnan S, Sethuraman KR et al cardiac involvement and scorpion envenomation in children. J. Trop. O Peditr 1995;41:338-40. 27. White J, Warrell DA, Eddlestom M, Currie BJ, Wyte IM and Isbister GK. Clinical Toxicology – Where are we now? Clinical toxicology 2003;41:263-76. 12. Mahadevan S. Scorpion sting. Indian peditr. 2000;37:504-14. 28. Al-asmari AK, Al-seif AA, Hassen MA and Abdulmakssod NA. Role of parzosin on cardiovascular manifestations and pulmonaryedema following severe scorpion sting in Saudi Arabia. Saudi med. j 2008;29:1296-99. 13. WHO. Rabies and envenoming: a neglected public health issue. Report of a consultative meeting WHO Geneva 10th January 2007 Page 1-32. 14. Pipelzadeh MH, Jalali A, Tarz M, Pourabhaa SR and Zaremirakabadi A. An epidemiological and clinical survey of scporpionism Iranian scorpion Hescorpion Leptus. toxicon 2007; 50:984-92. 16. De-Rezende NL, dias MM, Campolina d, Olortegui CC, Diniz CR and Amaral CFS. Efficacy of anti-venom therapy for neutralizing circulating venom antigen in patients stung by tityus serrulatus scorpion. The Amer. J.Trop.Med.hyg. 1995; 52:277080. 16. Amral CFS, De-rezende NV, and Freire-Maia. acute pulmonaryedema after Tityus serrulatus scorpion sting in children. Amer.J.Cardiol 1993;71:242-45. 17. Mahaba HM, Sayed SE. Scorpion sting, is it a health problem in Saudi Arabia? Evaluation of management of 620 cases. Saudi Medical Journal 1996;17:315-21. 18. Ismail M the treatment of the scorpion envenoming syndrome: the Saudi experience with serotherapy. Toxicon 1994;32:1019-26. 19. Ghalim N, El-Hafny B, Sebti F, Heikel J, Lazar N,Moustanir R and Benslimane A. . Scorpion envenomation and serotherapy in Morocco. Am.J. Trop. Med. hyg. 2000;62(2):277-83. 20. El-gawad Abd TA, Ibrahim HMM, El-sahrigy SAF, Sherif HA. Study of cardiac changes in Egyptian children with scorpion envenomation before and after antivenin. J.Medical Sciences. 2006;6:1033-38. 21. Dehesa davila M and Possani LD. Scorpionism and serotherapy in México. Toxicon 1994;32:1015-18. 22. Mazzei de Davila C, Davila DF, Donis DJ et al sympathetic nervous system activation, antivenin administration and cardiovascular manifestations of scorpion envenomation. Toxicon 2002;40:1339-46. 23. Abroug F, Elatrous S ,Nouira S, Hagiuga H, Touzi N, Bouchoucha S. Serotherapy in scorpion envenomation; A randomized controlled trial. Lancet 1999;359:906-9. 24. Sofer S, Shahak E and Gueron M. Scorpion envenomation and antivenin therapy. J. pediatr 1994;124:973-8. 25. Al-asmari AK and Al-saif AA. Scorpion sting syndrome in general hospital in Saudi Arabia. Saudi. Med. J. 2004;25:64-70. 26. Bawaskar HS and Bawaskar PH. Utility of scorpion antivenin Vs Prazosin in the management of severe Mesobuthus tamulus (Indian red scorpion) envenoming at rural setting. J.asso.Pysicians India 2007;55:14-21. 29. Bawaskar HS and Bawaskar Ph. Treatment of cardiovascular manifestations of human scorpion envenoming: Is serotherapy essential? J.Trop.med.and Hyg 1991;94:156-58. 30. Scorpions. Http://www.kingsnake.com/toxinology/old/ archnid/scorpions.html 31. Deoras PJ. A study of scorpions. Probe 1961;1:45-54. 32. Bawaskar Hs and Bawaskar PH. Sting by red scorpions (buthotus tamulus) in Maharashtra state, india : a clinical study. Trans.Rpy.soc.trop.med.hyg 1989;83:858-60. 33. Bawaskar HS and Bawaskar PH. Scorpion sting: Review of 121 cases. Journal wilderness medicine 1991;2:164-74. 34. cruz NAV, Batista CV, zamudio FZ, Bosmans F , Tytgat J and Possani LD. Phaiodotoxin , a b novel structural class of insect –toxin isolated from the venom of the Mexican scorpion Anuroctonus Phaiodactylus. Eur. J. biochem 2004;271:4753-61. 35. Xu CQ, brone B, Wicher D, Bozkurt O etal BMBKTx1, a vovel Ca+ activated K+ channel blocker purified from the Asian scorpion N Buthus martensi Karsch. J. biological chemistry; 2004;279:34562-69. 36. Pedarzani P, D’hoedt D, Doorty KB, Wadsworth JDF, Joseph JS etal Tamapin, a venom peptide from the Indian red scorpion (Mesobuthus tamulus) that target small conductance Ca+ activated K+ channels and afterhyperpolarization current in central neurons. J. Biochemical Chemistry 2002;277:46101-109. 37-43. Sofer S, Gueron M, White RM, Lifshitz M and apte RN. Interleukin-6 release following scorpion sting in children. Toxicon 1996;34:489-92. 39-83. Bawaskar HS and Bawaskar PH. cardiovascular manifestations of severe scorpion sting in India (review of 34 children). Annal trop.Peditr1991;11:381-87. 40. Bawaskar HS and Bawaskar PH. Management of the cardiovascular manifestations of poisoning by the Indian red scorpion (mesobuthus tamulus). British Heart.J 1992; 68:478-80 41. Bawaskar HS and Bawasakar Ph. Prazoain for vasodilator treatment of acute pulmonary edema due to scorpion sting. Annals of Trop. Med.parasitol. 1987;81:719-23. 42. Mcmanus BM, Fleury TA and Roberts WC. Fatal catecholamine crisis in pheochromocytoma: curable cuses of cardiac arrest. Amer. heart J 1881:930-33. 39 43. Kobal SL, Paran E, Jamaili A, Mizrahi S, Siegel RJ and Leor j. Pheochromocytoma: cyclic attacks of hypettension alternating with hypotension. Nature 2008;5:53-57. 60. Gueron M, stern J and Cohen W. severe myocardial damage and heart failure in scorpion sting. Ame. J.cardiol 1967; 19:719-26. 44. Bawaskar HS and Bawaskar PH.(1986). Prazoisn in management of cardiovascular manifestations of scorpion sting. Lancet; ii:51011. N. Electrocardigraphic. enzymatic and echocardiographic evidence 45. Bawaskar HS and Bawaskar PH. Indian red scorpion envenoming. Indian J. Pediatr 1998;65:383-91. 62. Diaz p, Chowell G, Ceja G, Anuria TCD, Lioyd RC and 46. Bawaskar HS and Bawaskar PH. Clinical profile of severe scorpion envenomation in children at rural setting. Indian pediatrics2003;40:1072-81. centruoides limpidus tecomanus scor[pion envenoamtion. Toxicon 47. karnad DR. haemodynamic pattern in patients with scorpion envenomation. Heart 1998;79:485-89. Prolonged atrio-ventricular block following scorpion bite: a case 48. Sira Devi C, Reddy CN, Devi SL, etal . Defibrination syndrome due to scorpion venom poisoning. BMJ1970, I: 345-47. 64. Gueron M and Margulis G and Sofer s. Echocardiographic 49. Bisarya BN, Vasa vada JP, Bhatt A, Nair PNR and Sharma VK. Hemiplegia aand myocarditis following scorpion bite Indian heart J 1977;29:97-100. 61. Amaral CFS, Lopes JG, magalhaes RA and de-rezende of myocardial damage after Tityus serrulatus scorpion poisoning. Amer.j.cardiol 1991; 67:655-57. Chavez Cc. pediatric electrocardiograph abnormalities following 2004; 1-5 63. Sharifkazemi MB, Rezeaian GR, zamirian M and Hashemi SAR. report. IJMS .2003;28:96-97. and radionuclide angiographic observations following scorpion envenomation by Leiurus quinquestriatus. Toxicon 1990;28:1005-9. 65. Poon-king T. Myocarditis from scorpion sting BMJ; 1963:374-77. 50. Kothari UR, Shah SS, Doshi HV and vasa NT. Myocarditis from scorpion sting: a clinical and electrocardiographic study of 50 cases. Indian Heart J 1976;28:88-92. 66. Sofer S Scorpion envenoamtion (editorial) intensive care 51. Jammihal JH, Srinivas HV. Hemiplegia following scorpion sting. Indian Peditr1972;X:337-38. Bouchoucha S. Right ventricular dysfunction following severe 52. Udayakumar N, Jendiran C and Srinivasan AV. Cerebrovascular manifestations in scorpion sting: a case series. Indain J. Med.sci 2006; 60: 243-44. 53. Bahloul m, Rekik N, Chabchoub I, Chaari A etal. Neurological complications secondary to severe scorpion envenomation. Med. Sci. monit. 2005; 11:cr196-202. 54. Sofer S, Shalev H, weizman Z, Shahak E and gueron M. Acute Pamcreatitis in children following envenomation by the yellow scorpion Leiurus quinquestriatus. Toxicon 1991;29:125-28. 55. Krkic. Dautovics S, Begovic B. Acute reanl insufficiency and toxic hepatitis following scorpion sting. Med.Arh 2007;61:123-4. medicine 1995;21:626-28. 67. Nouira S, Abroug F, Haguiga H, Jaafoura M, Boujdaria R and scorpion envenomation. Chest 1995; 108:682-87 68. Kumar s, Hamdani AA, and Shimy NE. scorpion venom cardiomyopathy. Ame. Heart j.1992; 123:725-29. 69. Hearing SE, Jurca M, Vichi FL Azevedo-Marques MM and Cupo P. reversible cardiomypathy in patients withsevere scorpion envenoming by tityus serrulatus: evolution of enzymatic, electrocardiographic and echocardiographic alterations. Ann.trop. paediatr. 1993; 13:173-82 70. Frire –Maia L and campos JA. Pathophysiology and treatment of scorpion poisoning. In natural toxins edited by Ownby C and Odell G. pergamon press 1989; 1-159. 71. Margulis G, sofer s, zalstein E, Zunker E, Zunker R, Ilia R and gueron M. abnormal coronary perfuision in experimental scorpion 56. Meki AR, Mohamed ZM, Mohey EL-deen NM. Significant of assessment of serum cardiac troponin 1 and interleukin-8 in scorpion envenomed children. Toxicon 2003;41:129-37. envenomation. Toxicon 1994; 32: 1675-78 57. Gueron M, Iliaa R , Shahak E and Sofers. rennin and aldosterone levels and hypertension following envenomation in humans by the yellow scorpion Leiurus quinquestriarus. Toxicon;1992;30:765-67 2003; 29:2266-76. 58. Gueron m , Weizman S Catecholamines and myocardial damage in scorpion sting. Amer.heart J. 1968;25:716-17. 59. Rahav G, weiss T. scorpion sting induced pulmonaryedma (scintigraphic evidence of cardiac dysfunction) Chest 1990; 97:1478-80. 40 72. Abroug F, nouria S, Atrous SE et al. A canine study of immunotherapy in scorpion envenomation. Intensive care med 73. Spall HGV, Robert JD, Sawka AM, Swallow CJ and Mak S. Not a broken heart. lancet 2007; 370:628 74. Wittstein IS. Apical-Ballooning syndrome Lancet 2007;370:545-47 75. Benvenuti LA, Dpouetts KV and Cardoso JLC. Myocardial necrosis after envenomation by the scorpion tityus serrulatus. Trans.roy.soc.trop.med.hyg 2002;96:275-76. Reddy CRRM and Suvarnakumar. pathophysilogy of scorpion venom poisoning. J.trop.med.hyg 1972;75:98-100. 92. Ismail M, Shibl AM, Morad AM, Abdullah ME. Pharmacokinetics of 125I-labelled antivenin to the venom from scorpion androctonus amoreuxi.Toxicon 1983;21:47-56. 77. Gueto L, Arriaga J and zinser j. echocardiographic changes in pheochromocytoma. Chest 1979;76:600-01.78- 93. Ghalim N, El-Hafny B, Sebti F, Heikel J, Lazar N, Moustanir 78. Warrell DA. Venomous bites and stings in Saudi Arabia 1993; 14:196-01. Morocco. Am.J.trop. Med.hyg 2000; 62(2):277-83. 79. Krishnan A Sonawane RV and Karnad DR. Captopril in the treatment of cardiovascular manifestations of Indian red scorpion (mesobuthus tamulus) envenomation. J.Assoc.Physicians. India 2007; 55:2226. The Saudi experience with serotherapy. Toxicon 1994;32:1019-26. 80. Bawaskar HS and Bawaskar PH. Role of atropine in management of cardiovascular manifestations of scorpion envenoming in humans. J.Trop.med and Hyg. 19992; 95:30-35. R and Benslimane A. Scorpion envenomation and serotherapy in 94. Ismail M. The treatment of the scorpion envenoming syndrome: 95. Patil SN, Dhavalikar S, Khedekar a. Role of 2D-echocardiography in scorpion sting (2007). http://www.swamisamarth.com 96. Pande R and Deshpande SB. Protecuve effects of aprotinin on respiratory and cardiac abnormalities induced by mesobuthus tamulus venom in adult rat. Tpxicon 2004;44:201-5. 81. Karnad DR, Deo AM, Apte N, Lohe AS, Thatte S and Tilve GH. Captopril for correcting diuretic induced hypotension in pulmonary edema after scorpion sting. BMJ 1989 ;293:1430-1. 97. Mangano DT, Tudor IC and Dietzel C. The risk associated with 82. Bawaskar HS. Scorpion sting and cardiovascular complications. Indian heart J1977.; 29:228. scorpion envenomation. Amer.j.Thearp 2006; 13:285-87. 83. Mahadevan S, chudhury P, Puri RK and Srinivasan S. Scorpion envenomation and the role of lytic cocktail in its management. Indian J. pediatr 1981; 48:757-61. envenoming and the heart (an Indian experience) Toxicon; 84. Waterman JA. Some notes on scorpion poisoning in Trinidad. Trans.roy.soc.trop.med.Hyg 1938. 31:607-24. F. Scorpion sting envem nomation in children in southeast of 85. Murthy KRK (1991). Insulin reverses hemodynamic changes and pulmonary edema in children stung by the Indian red scorpion mesobuthus tamulus concanesis, pocock. Annal.Trop.Med.parasitol 1991.; 85:651-7 101. Fatani AJ, Harvey AL, furman BL and Rowan EG. The 86. Gupta V. Prazosin: a pharmacological antidote for scorpion envenomation.J.trop.Pediatr 2006.; 52:150-1. 102. 97-Bhadani UK, Tripathi M, Sharma S, Pandey R. scorpion 87. Bawaskar HS and Bawaskar PH. severe envenoming by the Indian red scorpion Mesobuthus tamulus; the use of parzosin therapy. QJM 1996; 89:701-4. 88. Raab w. Key position of catecholamines in functional and degenerative cardiovascular pathology. Amer.J.cardiol 1960; 5:571-78. 89. Abroug F, nouira s, haguiga h etal randomized clinical trial of high dose hydrocortisone hemisuccinate in scorpion envenomation. Ann emerg. Med 1997;30;245-58. 90. Rankin AC.Non-sedating antihistamines arrhythmias. Lancey 1997; 350:1115-16. and cardiac 91. 84-Ismail M, Abdullah ME, Morad A, Ageel AM. Pharmacokinetics of 125I-labelled venom from the scorpion androctonus amoreixi (and&sar). Toxicon 1980; 18:301-08. aprotinin in cardiac surgery 2006. New.Eng.j.Med; 354:353-65 98. Koseoglu Z, Koseoglu A. Use of parzosin in the treatment of 99. Bawaskar HS and Bawaskar Ph. Vasodilators: scorpion 32:1031-40. 100. Bosnak M, Ece a, Yolbas L, Bosnak V, Kaplan M and Gurkan Turkey. J.Wildernesss environ, medicine (in Press) effects of lignocaine on actions of the venom from the yellow scorpion”leiurus quinquestriatus’ in vivo and vitro. Toxicon 2000; 38:1767-01. sting envenomation presenting with pulmonary edema in adults: a report of seven cases from Nephal. Indian J.Med.Sci.2000; 60: Search strategy and selection criteria We are studying and treating scorpion sting cases since 1977 till today. We have got a collection of articles from request reprints obtained from authors since 1977, before electronic media. Extensive search made by scorpion sting, pulmonary edema, catecholamine on pub made and Google. Legends for figures Fig-1: Black scorpion (Palmaneus gravimanus) Fig-2: An Indian red scorpion (mesobuthus tamulus) Fig-3: Tented T waves Fig-4: A Left anterior hemiblock and subsequent development of left bundle branch block with PQRST alternnan 41 Fig 4: A recovery of fig 4A case Fig-6A: Pulmonary edema Fig-5: Bat wing appearance of pulmonary edema Fig 6B: Recovery from pulmonary edema Scorpion sting Local pain without systemic involvement is benign. Vomiting, sweating, salivation, priapism in male, cold extremities suggestive of autonomic storm. Needs close monitoring. Hypertension, hypotension, bradycardia, tachycardia, ventricular entopic and acute myocardial infarction like pattern seen in ECG. Pulmonary edema, hypotension and tachycardia with respiratory failure seen within 30 minutes to 10 hours of sting. Massive life threatening pulmonary edema needs rapid intervention. Tachycardia >125 per minute with warm extremities, with or without pulmonary edema with cadaver pallor with convulsions suggestive of poor prognosis. If victim reports within on hour of sting with autonomic storm, if scorpion antivenin is available in dose of 30 to 100 Ml, it is to be administered by intravenous route. After one hour it has negligible action to neutralize the venom. Even after giving antivenin, victim should be closely monitored for possibility of development of pulmonary edema. Oral parzosin 250 microgram in children below 5 year and 500 microgram above five year to be administered, in every three hour interval till extremities are cold. Single dose of 20-30 mg frusemide, aminophylline, oxygen, in addition to parzosin to be given to pulmonary edema case. Intravenous sodium nitroprusside 3-10 microgram/kg/minute or nitroglycerine drip 5 microgram per minute raised to 15 microgram per minute in case of massive pulmonary edema. Dobutamine 5-15 microgram/kg/min in case of warm shock. BiPaP or non-invasive ventilator is useful for refractory pulmonary edema with respiratory failure. Repeat xylocaine for local pain to be avoided, local pain can be well managed with oral NSAID, Diazepam and local cold therapy. Atropine, steroids digoxin, antihistamines and excessive diuretic to be avoided. 42
© Copyright 2024