Scorpion Sting REVIEW ARTICLE Dr. H.S.Bawaskar Dr. P.H.Bawaskar

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