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SCORPION STING: CURRENT MANAGEMENT
Dr. Himmatrao Bawaskar
Bawaskar Hospital and Research center, Mahad, Dist-Raigad, Maharashtra, India 402301

Summary


Acute time limiting life threatening refractory pulmonary edema even at times fatal is more painful than severe local intolerable pain what layman even including medical personals knew about scorpion envenoming. We are studying severe scorpion sting cases since 1976. Envenoming by Mesobuthus tamulus (an Indian red scorpion) result in autonomic storm, characterized by vomiting, profuse sweating, cold extremities and life threatening cardiovascular effects. We observed hypertension in 39%, pulmonary edema 29% and severe local pain at the site of sting without systemic effects in 24% cases. Fatality is 0.9% in adults and 7% in children. Prazosin a postsynaptic alpha-1 blocker antagonizes the venom action and act as physiological and pharmacological antidote. Since the advent of prazosin the fatality is reduced to <1% which was more than >40% during pre-prazosin era (1961-83). Cardiovascular morbidity and mortality depends upon the age of victim, season of sting, content of telson (a poisonous glands situated at the terminal segment of tail of scorpion attached with sharp curved stinger) at the time of sting and time lapse between sting and administration of prazosin.

Introduction


Nearly 1000 species of scorpions belonging to six families have been mentioned, but only some species belonging to the family Buthidae, produces neurotoxin venom that is potent lethal toxic to human victims. Of 86 species found in India Mesobuthus tamulus (an Indian red scorpion) and Palmaneus Garvimanus black scorpion (vernacular language called Ingali) often seen all over keral state are the common ones. Mesobuthus tamulus, is the most lethal species flourished all over western Maharashtra, Anantpur and Karnool districts of Andhra Pradesh, Chennai, Pondicherry and Madurai in Tamil Nadu, Bellary in Karnataka, part of Gujarat, Patna area from Bihar. Recently few deaths have been reported from rest of Maharashtra because of change in environmental temperature, routine use of pesticides, and chemical manures by farmers, result in change in venom as a part of acclimatization. Farmers, farm laborers are more prone to get stung by scorpion during handling debris, paddy husk in the months of October- September. Bare feet walking young children in early darkness are at high risk of getting stung, simple wearing of slippers do not protect from sting. Scorpions often fall from loose tiles of huts in beds. Scorpion takes shelter in clothes (shirt shelves, trouser pockets), bedding and shoes.

Culprits


Palmaneus Garvimanus (Big black scorpion)
It inflicts severe excruciating painful sting, mild swelling, sweating, and local fasciculation at the site of sting, transient bradycardia due to pain. No systemic involvement.

Mesobuthus tamulus (An Indian red scorpion)
It has red color claws, tails and legs with body cover with khaki color of size 2.5-4 inches long. Similar lethal scorpion a species capable of inflicting fatal sting are reported from north Africa, the Middle East, south Africa, Brazil, Trinidad, Mexico and Turkey. Despite of zoological differences among various species, the clinical presentation following envenomation is quite identical.

Venom


Scorpion venom contains polypeptides, free amino acids, serotonin, hyaluronidase and various enzymes, which act on trypsinogen. It is the polypeptide, which is neurotoxic. P substance stimulates the cutaneous pain fibers. The mesobuthus tamulus venom is sodium channel activator and causes delay closing of sodium channels resulting in autonomic storm. The toxic content of venom causes inhibition of calcium dependent potassium channels.

Clinical manifestations


Clinical features can be divided in to two groups

  • Severe local pain at the site of sting radiating along with corresponding dermatomes without systemic involvement.
  • Mild local pain or at times absent but present with severe systemic involvement


Local pain or benign sting
Sting by less poisonous scorpion species like Palmaneus Garvimanus (black scorpion) or scorpion with empty venom glands called telson are characterized by sudden onset of severe excruciating pain at the site of sting. Local sweating, swelling and fasciculation are seen over the part of sting. Due to severe pain victim tries to move the affected part of body (site of sting) just to find comfortable position but eventually fails. Subsequently pain radiates along the involved dermatomes. Simple taping over the stung part induces severe pain and withdrawal. Local swelling is often increased by repeated local injections. Many times patient apply a tight tourniquet near the sting site or apply some herbal remedies or even burn the part of sting due to intolerable local pain. Because of severe pain patient is anxious, mild sweating or transient raised blood pressure with bradycardia can be noted, but there are no cold extremities or peripheral vasoconstriction or signs and symptoms suggestive of autonomic storm.

Systemic manifestations
The red scorpion venom is a potent sodium channels activator. Sting injects the venom in skin deep and stimulates the autonomic nervous system resulting in sudden pouring of catecholamines in to circulation. Both sympathetic and parasympathetic twigs are stimulated. But body is not at all prepared for such sudden accident as a result it responds randomly. Autonomic storm is characterized by initial parasympathetic stimulation clinically detected in form of vomiting once or twice, profuse sweating from all over the body, sweat literally flows for 7-17 hours (skin diarrhea), hyper-salivation for 2-12 hours, priapism for 6-18 hours, mydriasis, bradycardia (42-60 beats per minute), hypotension, transient ventricular premature beats with bigeminy pattern. Sympathetic stimulation is characterized by propped eyes, puffy and anxious face, oculo-gyric crisis, chest discomfort, perioral parasthesias at times tingling and numbness (parasthesia) all over body and cool extremities. Skin over hand and feet, palm and sole look like a washer-man hand i.e. fine wrinkles and cold. These changes occur simultaneously with parasympathetic stimulation but persist for long duration. Para-sternal systolic lift, transient systolic murmur of mitral regurgitation due to papillary muscle dysfunction due to coronary spasm is seen. Mild cases have little symptoms with cool extremities without severe sweating. The clinical manifestations at times are apparently diverse irrespective of similar pathology. Another clinically interesting finding observed is that on arrival patients with these symptoms and signs have tolerable mild or at times absent local pain, but start getting severe intolerable pain as soon as there is improvement in peripheral circulation, warming of cool extremities, accompanied with clinical improvement.

Hypertension


Patients can have raised blood pressure up to 210/160 mm hg with sinus bradycardia within 1-4 hours of sting. Children and occasionally adults with severe hypertension tend to be confused, agitated, at times have generalized convulsions, transient hemiplegia and oculogyric crisis. Bilateral extensor planter response, severe headaches, propped up eyes and puffy face are important diagnostic signs in children suggestive of hypertensive crisis. It is difficult to measure accurate blood pressure with routine sphygmomanometer in confused agitated child. Victim at times develops massive life threatening pulmonary edema with froth in mouth and nostril and intractable cough with hypertension.

Pulmonary edema


This is a common cause of fatality in scorpion sting victims, if not intervened in time .It occurs 4-36 hours after sting. Even sudden development of pulmonary edema in a hospitalized patient has been reported necessitating a close vigilance and monitoring of these victims. Clinically pulmonary edema can be suspected when respiratory rate is >24 per minute, orthopnea, intractable cough, low volume fast thready pulse, summation gallops, systolic murmur and basal moist rales which may be auscultated over the dependent part or at times all over chest. 12% victims if remain untreated or reported too late after sting or at periphery if they received atropine, excessive steroids, antihistamine, digoxin and intravenous fluid or massive doses of furosemide develop acute dyspnea, cyanosis, bring copious massive blood stained froth in mouth and nostril. Moist bubbling rales with tracheal death rattles are heard all over chest. At times this patient has marked tachycardia with hypotension.

Tachycardia


In hospitalized children recovering from vasoconstriction usually after 12-18 hours develop marked tachycardia (heart rare 110-240 per Minute) with warm extremities. Such child has air hunger, delirium, may throw convulsive movement, moist basal rales in chest, summation gallops with murmur in the heart. After 20-30 hours in a case recovering from autonomic storm, he develops warm extremities, bradycardia (heart rate 50-60 per minute), split second heart sound with hypotension (70-90 Mm hg) with prolonged QTC (500-650 Msec.) with no complaints. This is result of depletion of tissue catecholamines due to autonomic storm, usually it takes 72-96 hours for recovery.

Other features are pain in abdomen which may be due irritation of worm (round worm infestation is common in villagers) by scorpion venom, in addition to smooth muscle contraction due to acetylcholine excess. Hyperglycemia, raised serum amylase suggestive of acute pancreatitis is transient and reversible. Hemiplegia, aphasia, cerebral infarction and subdural hematoma due to disseminated intra-vascular coagulation have been reported. Acute renal failure has also been reported. Persistent or prolonged hypoxia due to low output state, marked tachycardia, respiratory failure due to pulmonary secretion and edema may result in irreversible cerebral anoxic injury with subsequent persistent cerebral insufficiency and low intelligence rest of life.

Fatality


Victim can die suddenly due to lethal ventricular arrhythmias, which occur within 15-30 minutes of sting. Many cases died due persistent pulmonary edema, tachycardia, hypotension and convulsion and brought to hospital in moribund, comatose condition, pin point pupils with massive pulmonary edema.

Investigations


Total leucocytes count is raised to 14000-21000 resulting in liberation of inteleukin-6 cytokines and tumor necrosis factor alpha. Cardiac enzymes are raised. Serum amylase must be investigated in all cases with upper abdominal pain with vomiting and tachycardia. Serum potassium is raised in early hypertensive phase. In a few cases there is reduction in serum calcium level. If facilities are available serum insulin detection is helpful for further research. Chest X-ray shows bilateral batwing, patchy or interstitial pulmonary edema. At times secondary respiratory infection in form of pneumonitis is often seen in a hospitalized patient recovering from pulmonary edema. On 4th day, mild cardiomegaly is seen in a case recovering from pulmonary edema.

Electrocardiography changes


Hyper-acute tented T waves, bradycardia, first degree heart block, transient ventricular and atrial ectopics, runs of ventricular VPC’s can be observed and detected if case is monitored by cardio scope. PQRST or T waves alternans, acute myocardial infarction like pattern, sinus tachycardia with ST segments depression, left anterior hemi-block, bundle branch block are also seen. Many times left bundle branch block with marked tachycardia is confused for ventricular tachycardia. In such a situation the bundle branch block is tachycardia dependent. Complete heart block, low voltage, widened QRS complexes with tachycardia carries poor prognosis. Prolonged QTc interval (0.50-0.60 seconds) with broad base and round top T waves with bradycardia with hypotension are seen 12-24 hours after sting in a hospitalized patient. Most early changes in ECG such as left axis deviation, Tented T waves and ST segment elevation in lead I and AVL should be closely monitored for possibility of development of acute pulmonary edema.

Pathophysiology


The clinical manifestations, pathological lesions and electrocardiographic changes are due to sudden massive liberation of catecholamines in to circulation similar to pheochromocytoma. Cool extremities with severe vasoconstriction (like Raynaud’s phenomenon), dilated pupils, cold extremities, inhibition of insulin secretion, hyperglycemia, acute myocardial infarction like pattern (spasm of pericardial coronary vessels), pulmonary edema are due to alpha-1 receptors stimulation due to catecholamine excess. Scorpion venom increases the membrane permeability to sodium by opening the voltage sensitive sodium channels, which is accompanied with calcium entry, and blockade of calcium activated potassium channels resulting in relative hyperkalemia. Hyperkalemia further induces the release of catecholamines. Stimulation of alpha-receptors causes potassium efflux from the liver. Hyperkalemia, hypocalcaemia can explain the electrocardiographic changes-tall T waves, prolonged QTc and ST segment changes. Initial short lasting hypotension is due to hypovolaemia, peripheral cholinergic and central vagus stimulation. Delayed long lasting hypotension occurs as result of vasodilatation and depleted catecholamines. Pulmonary edema in scorpion sting is of homodynamic origin and is related to severe impairment of left ventricular systolic function. Local pain is due to sodium channel activation and stimulated of C fibers with local liberated prostaglandins.

Management


No sting should be taken as benign unless observed for 24 hours irrespective of species of scorpion involved.

Local pain

Cut at the sting site and tourniquet is not advisable.
Mild, tolerable pain can be abolished by application cold or ice packs over the site of sting. Severe excruciating pain is transiently relieved by local anesthesia xylocaine without adrenaline. Repeated injections of local anesthesia are often required for pain relief. It is observed that the reappearance of pain after initial local xylocaine is much severe than what was before the first injection. This is because of rapid tolerance to xylocaine and repeated injection stimulates the inflammation and in an inflamed tissue the action of xylocaine is blunted. Hence simultaneously oral diazepam and NSAID with first initial dose of xylocaine can give prolonged relief of pain. However injection of emetine hydrochloride exactly at the site of sting gives prolonged relief from pain, but it is not available and moreover it is cardiotoxic and one need to be careful while injecting because sting is often over the thick skin of sole and many times while injecting it the drug may suddenly be flushed back due to dislodged needle and piston from syringe and enter in the eyes of a person injecting it. Being severe tissue irritant, it causes corneal edema and irritating injury to cornea (author himself suffered of this).

Correction of dehydration

Dehydration due to vomiting, excessive salivation, and profuse sweating should be corrected by continuous vigorous oral rehydration solution. This helps to correct initial hypotension and shock. Intravenous crystalloid solution or hydration by nasal tube may be necessary in a confused, agitated child. Fluid replacement must be corrected since hypovolemia is one of the proposed mechanisms of shock syndrome in scorpion sting. Electrolytes imbalance should be corrected. Calcium can be replaced by encouraging excessive milk consumption. Grape juice may be avoided as it may enhance the prolonged the QTC interval

Scorpion antivenin

Scorpion antivenin is available in India. Though it is specific antidote to venom action but in case of mesobuthus tamulus sting antivenin, it does not prevent or reverse the cardiovascular morbidity and mortality. Moreover it is not free from anaphylaxis. The half-life time of antivenin is longer than venom. In animals no beneficial effects of antivenin are observed if it is injected more than 15 minutes after injecting the venom. It does not counteract the venom induced autonomic storm. In our series, mesobuthus antivenin did alleviate the cardiovascular morbidity and mortality. 21 severe scorpion sting cases aging 3-56 (average22) years were reported within 30 minutes to 21 hours (average 3.5) after sting. All of them had clinical manifestations suggestive of autonomic storm. They received scorpion antivenin by intravenous route and were closely observed for clinical outcome. Out of these, 12 had persistent raised blood pressure, 8 developed pulmonary edema, of which 2 had massive life threatening pulmonary edema, 1 had hypotension with tachycardia and 2 died. Recently it has been reported that scorpion antivenin is no better than placebo. Venom is poor antigen hence it is difficult to prepared potent antivenin. Scorpion venom acts indirectly by releasing auto-pharmacological substance in to circulation.

Prazosin

Alpha-receptors play vital role in the pathogenesis of cardiac failure and pulmonary edema due to scorpion sting. Prazosin is a selective alpha –1 adrenergic receptor blocker. It dilates veins and arterioles, there by reducing pre-load and left ventricular impedance without rise in heart rate and renin secretion. It also inhibits sympathetic outflow in central nervous system. It is phospo-diesterase inhibitor and as a result of this action it enhances cGMP accumulation, which is one of the mediator of nitric oxide synthesis. It enhances insulin secretion, which is inhibited by venom action. Thus its pharmacological properties can antagonize the haemodynamic, hormonal and metabolic effects of scorpion venom action. It can be administered by oral route. Prazosin is simple, scientific pharmacological and physiological antidote to scorpion venom actions; moreover it is free from anaphylaxis.

Prazosin should be given in a dose of 125-250 microgram in children and 500 microgram in adults and should be repeated three hourly until there are signs of clinical improvement in tissue perfusion such as warming of extremities, increase in urine output, appearance of severe local pain at the site of sting which was absent or tolerable on arrival, disappearance of parasthesias, reduction or improvement in heart rate and pulmonary edema, reduction in hypertension or improvement in blood pressure in case of hypotension without hypovolemia, reduction or disappearance of murmur and earliest most important subjective feeling of better. This is because the drug has 1000 times affinity towards the activated alpha-1 receptors. Then dose is to be repeated six hourly till extremities became dry and warm. If the initial dose has been vomited (one should see the vomit carefully), it should be repeated. In a confused, agitated, non-cooperative child, prazosin should be administered by nasal tube after giving intravenous diazepam

Prazosin is life saving drug hence attending doctor himself should administer the drug to the hospitalized patient and he should clinically confirmed by noting the signs and symptoms that drug is absorbed in circulation and started acting.

First dose phenomenon is rare or avoided by administering minimum initial dose of prazosin. However due care should be taken to avoid postural fall in blood pressure. Children should not be lifted. Postural hypotension should be treated by giving head low position and intravenous fluid.

Pulmonary edema


Is a life threatening time limiting emergency often fatal and needs rapid intervention. Patient should be given propped up position, intravenous aminophylline 5mg/kg diluted in dextrose given as a slow bolus to counter the associated bronchospasm. If available isosorbide buccal spray is useful or powder of nitroglycerine should be rubbed on gum and intravenous furosemide 10-20 mg should be given to reduce the preload and pulmonary congestion. In a case of massive pulmonary edema (blood stained froth from nostrils and mouth), intravenous sodium nitroprusside (SNP) drip 3-5 microgram per kg per minute can be started and dose should be raised continuously according to patient’s response and blood pressure. Blood pressure should be closely monitored and maintained at the level of systolic 80-90 mm hg. SNP has to be prepared from fresh powder every four hours; the bottle and saline set should be protected from light. At times a severe case may required 15-36 hours of SNP drip to clear pulmonary edema. Patient should be given oral or injectable cynacobalamine to avoid cyanide toxicity whenever SNP is given for long time. Before starting SNP, IV furosemide is given to avoid sudden fall of intra-ocular pressure and ocular bleed due to SNP drip. IV nitroglycerine can be used 5-8 microgram per minute if SNP is not available. In case of shock or hypotension early administration of dobutamine 5-15 microgram per kg per minute along with SNP drip may be life saving. In children, after 20-24 hours of sting, marked tachycardia (130 and above), warm extremities, pulmonary edema or air hunger respond to IV dobutamine drip, which may be required for 48 hours.

Other therapies


DIC, sub-dural hematoma and hemiplegia, hypoxic brain damage with generalized brain edema are known to occur and should be treated with fresh blood transfusion and decongestive treatment. If the victim becomes delirious or comatose, hyperbaric oxygen might help. Non-cardiac pulmonary or secretary pulmonary edema or adult respiratory distress syndrome is rare due to mesobuthus tamulus envenomation but may necessitate tracheal intubations and hyperventilation. Captopril, lytic cocktail, insulin glucose –potassium drip, L-carnitine have been reported with limited benefits in the management of scorpion sting

Management of cardiac arrhythmias


Initial bradycardia often accompanied with ventricular premature contraction at times ventricular bigeminy pattern with excessive profuse sweating, salivation and priapism is transient and self-limiting provided dehydration and electrolytes imbalance are corrected. Runs of ventricular premature contraction or R on T phenomenon and ventricular tachycardia respond to intravenous lidocaine. Mexiletine is a drug of choice for ventricular premature contraction occurring with gallop because it does not alter the QTC interval, which is already increased due to scorpion envenoming. Intravenous amiodarone should be used with caution in presence of impending myocardial failure or pulmonary edema which may precipitate massive pulmonary edema, marked bradycardia and cardiac arrest, resuscitation trolley should be ready or it should be administered in intensive care unit.

Atropine, steroids, antihistamines, beta-blockers, calcium channel blockers, excessive diuretics, Adrenaline and narcotics should be avoided. They do more harm than good in scorpion envenoming.

Prevention


Scorpions are killed by organophosphorus pesticides. A false ceiling of plastic sheet should be put under the roof of hutto prevent scorpion failing in bed from loose tiles of roof particularly in early June with heavy rain. Shoes, clothes should be checked before wearing. Shoes should be packed with paper so as to prevent the entry of scorpion during night. Hand gloves made of thick rubber (electrician gloves) should be worn while harvesting and handling fire woods, dry cow dung, lifting dry paddy and Jawar husk and sugar cane husk. Simple slippers do not protect. Children should not be allowed to go out side in early darkness without shoes. One should not put hand blindly in craves, doors or storage material during night hours or one should keep distance from mud house wall or one should not backrest to mud wall.
At the time of opening of school benches and rooms should be washed and cleaned.
In endemic areas where high fatality have been reported, the doctors should be aware of severe clinical manifestations or should be trained how to diagnosed and manage the severe scorpion sting.


References


  1. Bawaskar HS Scorpion sting and literature review (monogram) Popular Prakashan mumbai
  2. Bawaskar HS Diagnostic cardiac premonitory signs and symptoms of red scorpion sting Lancet 1982;II: 552-54.
  3. Bawaskar HS and Bawaskar PH. Prazosin in the management of cardiovascular manifestations of scorpion sting Lancet 1986;II: 510-11.
  4. Bawaskar HS and Bawaskar PH. Stings by scorpions (Buthotus tamulus) in Maharashtra state, India: a clinical study. Transaction of Roy.Soc.Trop.med.hyg. 1989,83:858-60.Bawaskar HS and Bawaskar PH.Management of the cardiovascular manifestations of poisoning by Indian red scorpion. British heart Journal 1992; 68:478-80.
  5. Bawaskar HS and Bawaskar PH. Prazosin therapy and scorpion envenomation. JAPI 2000;48:1175-80.
  6. Abroug F, Eiatrous S, Nouria S, et al. Serotherapy in scorpion envenomation : a randomized controlled trial. Lancet 1999;354:906-09.
  7. Mahadevan S. Scorpion sting( personal practice) . Indian pediatric 2000;37:504-13.
  8. Bawaskar HS and Bawaskar PH. Clinical profile of severe scorpion envenomation in children at rural setting. Indian pediatrics 2003;40:1072-75.

Last updated on 01-02-2006

How to cite this url

Bawaskar H.Scorpion Sting Current Management.Pediatric Oncall [serial online] 2006 [cited 2006 February 1];3. Available from:
http://www.pediatriconcall.com/fordoctor/diseasesandcondition/
PEDIATRIC_ANAESTHESIA/scorpion_sting.asp
 
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