Scorpion stings are a major public health problem in many underdeveloped

tropical and subtropical countries, especially Sahelian Africa, South India,

the Middle East, Mexico, and South Latin America. [1, 2] The estimated annual
number of scorpion stings is 1.2 million leading to 3250 deaths (0.27%). [3]
For every person killed by a poisonous snake, 10 are killed by a poisonous
scorpion. In Mexico, 1000 deaths from scorpion stings occur per year. In
the United States, only 4 deaths in 11 years have occurred as a result of
scorpion stings. Furthermore, scorpions can be found outside their normal
range of distribution, that is when they crawl into luggage, boxes,
containers, or shoes and are unwittingly transported home via human
travelers.
A scorpion has a flattened elongated body and can easily hide in cracks. It
has 4 pairs of legs, a pair of claws, and a segmented tail that has a
poisonous spike at the end. Scorpions vary in size from 1-20 cm in length.

See Arthropod Envenomation: From Benign Bites to Serious Stings, a

Critical Images slideshow, for help identifying and treating various
envenomations.
Out of 1500 scorpion species, 50 are dangerous to humans. Scorpion
stings cause a wide range of conditions, from severe local skin reactions to
neurologic, respiratory, and cardiovascular collapse. Envenomation from
most scorpions results in a simple, painful, local reaction that can be
treated with analgesics, antihistamines, and symptomatic/supportive care.
This article focuses on scorpions that generally are considered more
dangerous to humans.
Almost all of these lethal scorpions, except the Hemiscorpius species,
belong to the scorpion family called the Buthidae. The Buthidae family is
characterized by a triangular-shaped sternum, as opposed to the
pentagonal-shaped sternum found in the other 5 scorpion families.

In addition to the triangular-shaped sternum, poisonous scorpions also tend

to have weak-looking pincers, thin bodies, and thick tails, as opposed to the
strong heavy pincers, thick bodies, and thin tails seen in nonlethal
scorpions.

The lethal members of the Buthidae family include the genera of Buthus,
Parabuthus, Mesobuthus, Tityus, Leiurus, Androctonus, and Centruroides.
The following lethal scorpions are found generally in the given distribution:
 Buthus - Mediterranean area, from Spain to the Middle East
 Parabuthus - Western and Southern Africa
 Mesobuthus – Throughout Asia
 Parabuthus - Western and southern Africa
  Buthotus (ie, Hottentotta) - Across southern Africa to southeast Asia
 Tityus - Central America, South America, and the Caribbean
 Leiurus - Northern Africa and the Middle East
 Androctonus - Northern Africa to Southeast Asia
 Centruroides - Southern United States, Mexico, Central America, and
the Caribbean (Centruroides exilicauda is found in the Baja California
peninsula of Mexico and Centruroides sculpturatus is found in the state
of Sonora, Mexico and the southwestern United States, primarily
Arizona and small parts of Utah, New Mexico, Nevada, and California.)
The accepted taxonomy of the bark scorpion has changed over time.
Either C exilicauda or C sculpturatus have been accepted at various
times. However, recent evidence from biochemical, genetic, and
physiologic characterization of their venom suggests that they are two
different species as listed above.
However, these scorpions may be found outside their natural habitat range
of distribution when inadvertently transported with luggage and cargo.
In general, scorpions are not aggressive. They are ambush predators, often
hiding and waiting for their prey. Scorpions are nocturnal creatures; they
hunt during the night and hide in crevices and burrows during the day to
avoid the light. Thus, accidental human stinging occurs when scorpions are
touched while in their hiding places, with most of the stings occurring on the
hands and feet.

Patofisiologi

Scorpions use their pincers to grasp their prey; then, they arch their tail
over their body to drive their stinger into the prey to inject their venom,
sometimes more than once. The scorpion can voluntarily regulate how
much venom to inject with each sting. The striated muscles in the stinger
allow regulation of the amount of venom ejected, which is usually 0.1-0.6
mg. If the entire supply of venom is used, several days must elapse before
the supply is replenished. Furthermore, scorpions with large venom sacs,
such as the Parabuthus species, can even squirt their venom.
The venom glands are located on the tail lateral to the tip of the stinger and
are composed of 2 types of tall columnar cells. One type produces the
toxins, while the other produces mucus. The potency of the venom varies
with the species, with some producing only a mild flu and others producing
death within an hour. In addition, there is species variability in venom
volume, flow rate, and duration. [4] Generally, the venom is distributed rapidly
into the tissue if it is deposited into a venous structure. Venom deposited
via the intravenous route can cause symptoms only 4-7 minutes after the
injection, with a peak tissue concentration in 30 minutes and an overall
toxin elimination half-life of 4.2-13.4 hours through the urine. The more
rapidly the venom enters the bloodstream, the higher the venom
concentration in the blood and the more rapid the onset of systemic
symptoms.
Scorpion venom is a water-soluble, antigenic, heterogenous mixture, as
demonstrated on electrophoresis studies. This heterogeneity accounts for
the variable patient reactions to the scorpion sting. However, the closer the
phylogenetic relationship between the scorpions, the more similar the
immunological properties. Furthermore, the various constituents of the
venom may act directly or indirectly and individually or synergistically to
manifest their effects. In addition, differences in the amino acid sequence of
each toxin account for their differences in the function and immunology.
Thus, any modifications of the amino acid sequence result in modification
of the function and immunology of the toxin.
Scorpion venom may contain multiple toxins and other compounds. The
venom is composed of varying concentrations of neurotoxin, cardiotoxin,
nephrotoxin, hemolytic toxin, phosphodiesterases, phospholipases,
hyaluronidases, glycosaminoglycans, histamine, serotonin, tryptophan, and
cytokine releasers. The most important clinical effects of envenomation are
neuromuscular, neuroautonomic, or local tissue effects. The primary
targets of scorpion venom are voltage-dependent ion channels, of which
sodium channels are the best studied. Venom toxins alter these channels,
leading to prolonged neuronal activity. Many end-organ effects are
secondary to this excessive excitation. Autonomic excitation leads to
cardiopulmonary effects observed after some scorpion envenomations.
Somatic and cranial nerve hyperactivity results from neuromuscular
overstimulation. Additionally, serotonin may be found in scorpion venom
and is thought to contribute to the pain associated with scorpion
envenomation.
The most potent toxin is the neurotoxin, of which two classes exist. Both
types of neurotoxin are heat-stable, have low molecular weight, and are
responsible for causing cell impairment in nerves, muscles, and the heart
by altering ion channel permeability.
The long-chain polypeptide neurotoxin causes stabilization of voltage-
dependent sodium channels in the open position, leading to continuous,
prolonged, repetitive firing of the somatic, sympathetic, and
parasympathetic neurons. This repetitive firing results in autonomic and
neuromuscular overexcitation symptoms, and it prevents normal nerve
impulse transmissions. Furthermore, it results in release of excessive
neurotransmitters such as epinephrine, norepinephrine, acetylcholine,
glutamate, and aspartate. Meanwhile, the short polypeptide neurotoxin
blocks the potassium channels.
The binding of these neurotoxins to the host is reversible, but different
neurotoxins have different affinities. The stability of the neurotoxin is due to
the 4 disulfide bridges that fold the neurotoxin into a very compact 3-
dimensional structure, thus making it resistant to pH and temperature
changes. However, reagents that can break the disulfide bridges can
inactivate this toxin by causing it to unfold. Also, the antigenicity of this
toxin is dependent on the length and number of exposed regions that are
sticking out of the 3-dimensional structure.

Etiology

The causes of scorpion envenomation are primarily accidental. Scorpions

are shy creatures and only sting if threatened, cornered, or disturbed (eg,
being sat or stepped upon). Curious individuals are at risk because of
increased interaction with the scorpion.
The median lethal dose 50 (LD50) of various scorpion venoms in mg/kg of
a subcutaneous injection into mice and the territorial distribution are listed
below (unfortunately, humans are much more sensitive than mice):
 Leiurus quinquestriatus (Middle East) - 0.25 mg/kg
 Androctonus crassicauda (Saudi Arabia) - 0.08-0.5 mg/kg
 Centruroides noxius (Mexico) - 0.26 mg/kg
 Androctonus mauritanicus (North Africa) - 0.32 mg/kg
 Centruroides santa maria (Central America) - 0.39 mg/kg
 Tityus serrulatus (Brazil) - 0.43 mg/kg
 Buthus occitanus (North Africa) - 0.9 mg/kg
 Centruroides sculpturatus (Southwest United States) - 1.12 mg/kg
 Mesobuthus eupeus (Iran) - 1.45 mg/kg
Generally, most lethal scorpions have an LD50 below 1.5 mg/kg.
The average yield per scorpion via electrical excitation of the venom gland
for a few species is listed below:
 Tityus species - 0.39-0.62 mg
 L quinquestriatus - 0.62 mg
 Buthus species - 0.38-1.5 mg
 Milking the venom gland produces approximately a 4-fold increase in
yield amount compared to electrical excitation.

Epidemiologi

Frequency
United States
Approximately 16,000 stings have been reported, with the majority being
from the nonlethal scorpions. Only 1 of 30 scorpion species found in the
United States is dangerous to humans. The neurotoxin-bearing and
potentially lethal scorpion species in the United States is the Arizona bark
scorpion in the genus Centruroides. [5] Less than 1% of stings from
Centruroides are lethal to adults; however, 25% of children younger than 5
years who are stung die if not treated. The epidemiological features of a
patient who has been envenomed show a disposition for rural areas (59.6-
73%), with most of the stings occurring in the summer months between
6:00 pm and 12:00 am (49%) and a second peak from 6:00 am to 12:00 pm
(30%). Both of these peaks coincide maximum human activity with
maximum scorpion activity. In addition, nocturnal envenomations are
slightly more common than diurnal, as the scorpion is more active at night.
Furthermore, the larger the scorpion population, the larger the incidence
rate. Because the offending scorpion is recovered for identification in only
30% of the cases, local knowledge of the type of scorpion populating the
area is useful.
The 2016 Annual Report of the American Association of Poison Control
Centers' National Poison Data System (NPDS) reported 13,670 case
mentions for scorpion envenomations, with 22 "major" outcomes and 0
deaths. [6] However, because of underreporting, this is probably an
underestimation of the true number of stings.
International
Scorpion stings occur in temperate and tropical regions, especially between
the latitudes of 50°N and 50°S of the equator. Furthermore, stings
predominantly occur during the summer and evening times. [1] In addition,
the majority of patients are stung outside their home.
Accurate statistics on scorpion envenomation are not available. Many
potentially dangerous scorpions inhabit the underdeveloped or developing
world. Consequently, numerous envenomations go unreported, and true
incidence is unknown. However, it has been estimated that there are 1.2
million scorpion stings per year. [3]
A 5-year surveillance study in Saudi Arabia found 6465 scorpion sting
cases with a mean patient age of 23 years, a male-to-female ratio of 1.9,
and a higher incidence of stings in the months of May through October. [7]
In Khuzestan province of Iran, 12,150 annual cases occurred, with
nocturnal envenomations occurring 60.9% of the time, 39.3% stings
occurring on the hands, and 37.3% stings occurring on the feet. June was
the highest month for stings, at 16%, and February, the lowest at 0.6%. [8]
Race
No racial predilection exists.
Sex
Females may be more susceptible than males to the same amount of
scorpion venom because of their lower body weight.
Age
Adults, especially those of workforce age, are stung more often than
children. However, children are more likely to develop a more rapid
progression of symptoms after a scorpion sting, with increased severity and
higher mortality because of their lower body weight, [9] with a global rate of
10 deaths per 1000 cases in children. [10, 11] Furthermore, elderly persons are
more susceptible to stings because of their decreased physiologic reserves
and increased debilitation.

Mortality/Morbidity
Accurate worldwide data are not available. Scorpion stings are
underreported because many envenomations occur in sparsely populated
areas with little public health and medical infrastructure. Furthermore,
reporting is generally not required.
Most deaths occur during the first 24 hours after the sting and are
secondary to respiratory or cardiovascular failure.
The highest reported mortality rate is recorded in data from Mexico, with
estimates as high as 1000 deaths in 1 year. In the United States, 4 deaths
were reported in an 11-year period according to one source. [12] However, no
deaths were reported to the American Association of Poison Control
Centers from 1983 to 1999. Only one death from the Arizona bark scorpion
(C sculpturatus) has been reported since 1964. [13]
Children and elderly persons are at the greatest risk for morbidity and
mortality. A smaller child, a lower body weight, and a larger ratio of venom
to body weight lead to a more severe reaction. A mortality rate of 20% is
reported in untreated babies, 10% in untreated school-aged children, and
1% in untreated adults, but these rates vary across years and regions.
In terms of venom lethality, the venom of Androctonus australis and Leiurus
quinquestriatus are the most toxic. C sculpturatus venom is low in toxicity
compared with most scorpions of medical importance.
Furthermore, patients in rural areas tend to fare worse than patients in
urban areas because of the delay in getting medical help due to a longer
travel time to medical centers and the lack of advanced medical treatments.
[14]
Fortunately, better public education, improved control of the scorpion
population, increased supportive therapies, more technologically advanced
intensive care units and advances in immunotherapy have combined to
produce a substantial decrease in mortality from these envenomations. [15]

Prognosis
Prognosis is dependent on many factors, including species of scorpion,
patient health, and access to medical care. Most patients recover fully after
scorpion envenomation.
Symptoms generally persist for 10-48 hours. If the victim survives the first
few hours without severe cardiorespiratory or neurologic symptoms, the
prognosis is usually good. Furthermore, surviving the first 24 hours after a
scorpion sting also carries a good prognosis.
A worse prognosis can be expected with the presence of systemic
symptoms such as cardiovascular collapse, respiratory failure, seizures,
and coma. Specifically, the following were associated with poor outcomes:
Glasgow Coma Score less than 8 (odds ratio [OR], 9.87) and pulmonary
edema (OR, 8.46). [16]
In children, the following factors were associated with a higher mortality:
metabolic acidosis, tachypnea, myocarditis, pulmonary edema,
encephalopathy, and priapism.

Patient Education
Educate all patients about methods to avoid scorpions (see Prevention).
Delays in seeking medical treatment are associated with higher likelihood
of mortality in children and adolescents. [

History

For patients presenting with scorpion stings, ascertaining the following is

essential:
 Time of envenomation
 Nature of the incident
 Description of the scorpion: Specimen identification by an entomologist
may be helpful (if the scorpion can be captured safely).
 Local and systemic symptoms: Pain and paresthesias often are
present. Nausea and vomiting are common.
The toxicity, variation, and duration of the symptoms depends on the
following factors:
 Scorpion species
 Scorpion age, size, and nutritional status
 Healthiness of the scorpion's stinging apparatus (telson)
  Number of stings and quantity of venom injected
 Depth of the sting penetration
 Composition of the venom
 Site of envenomation: Closer proximity of the sting to the head and
torso results in quicker venom absorption into the central circulation
and a quicker onset of symptoms.
 Age of the victim, as children are more susceptible to severe clinical
manifestations
 Health of the victim
 Weight of the victim relative to amount of venom
 Presence of comorbidities
 Treatment effectiveness
Nonlethal scorpion species tend to produce local reactions similar to a
hymenopteran sting, while lethal scorpion species tend to produce systemic
symptoms. The duration to progress to systemic symptoms ranges from 5
minutes to 4 hours after the sting. The symptoms generally persist for 10-
48 hours.

Physical Examination

Clinical manifestations range from minor local tenderness to multisystem failure followed by
death. [19]

Local tissue effects vary among species. Minimal local tissue effects are present with
Centruroides envenomation. Significant local tissue reaction rules out C exilicauda
envenomation. Tapping over the injury site (ie, tap test) may cause severe pain after a sting
by C exilicauda.

Tachycardia and other dysrhythmias are caused by autonomic effects primarily, although
direct myocardial toxicity with arrhythmogenic effects has been described.

Hypertension or hypotension may be present.

The patient may have hyperthermia.

Respiratory arrest and loss of protective airway reflexes are common causes of mortality.
Pulmonary edema has been described and may be secondary to cardiogenic causes and to
increased capillary permeability.

Autonomic effects include the following:

 Sympathetic overdrive symptoms predominate, causing tachycardia, hypertension,

hyperthermia, and pulmonary edema.
 Parasympathetic symptoms include hypotension, bradycardia, salivation, lacrimation,
urination, defecation, and gastric emptying.
Cranial nerve effects include the following:

 Classic roving or rotary eye movements, blurred vision, tongue fasciculations, and
loss of pharyngeal muscle control may be observed.
 Difficulty swallowing combined with excessive salivary secretions may lead to
respiratory difficulty.

Somatic effects include the following:

 Restlessness and involuntary muscle jerking that can be mistaken for seizures have
been described.
 Presence of true seizures in Centruroides envenomation is controversial and has not
been proven to occur. Seizures are described in association with other scorpion
envenomations.

Cerebral infarction, cerebral thrombosis, and acute hypertensive encephalopathy have been
described with a variety of Buthidae scorpion envenomations.

The signs of the envenomation are determined by the scorpion species, venom composition,
and the victim's physiological reaction to the venom. The signs occur within a few minutes
after the sting and usually progress to a maximum severity within 5 hours. The signs last for
24-72 hours and do not have an apparent sequence. Thus, predicting the evolution of signs
over time is difficult. Furthermore, a false recovery followed by a total relapse is common.

A person who has been stung by a scorpion usually has four signs, with the most common
being mydriasis, nystagmus, hypersalivation, dysphagia, and restlessness. The mode of death
is usually via respiratory failure secondary to anaphylaxis, bronchoconstriction,
bronchorrhea, pharyngeal secretions, and/or diaphragmatic paralysis, even though venom-
induced multiorgan failure may play a large role. Death can occur from toxicity or from
anaphylaxis. These are two separate things, and many “nonlethal” species can cause
anaphylaxis.

Children present with the same symptoms and signs as adults, except their symptoms are
more severe and protracted. Furthermore, they may display a restlessness that is out of
proportion when compared to any other disease. A child's symptoms have been described as
inconsolable crying; uncontrollable jerking of the extremities; and chaotic thrashing, flailing,
and writhing combined with contorted facial grimaces. The symptoms mimic a centrally
mediated seizure, but the patient is awake and alert the entire time.

The grading of these scorpion envenomations depends on whether or not neurological signs
predominate and is as follows:

Nonneurological predominance is graded as follows [2] :

 Mild - Local signs of erythema, swelling and tenderness (estimated 68.6%)

 Moderate - Ascending local signs or mild systemic signs (estimated 26.8%)
 Severe - Life-threatening systemic signs (estimated 4.6%)

Neurologic predominance is graded as follows:

  Grade I - Local pain or paresthesia at the sting site (83%)
 Grade II - Pain or paresthesia that has traveled from the sting site (9.1%)
 Grade III - Either cranial nerve or somatic neuromuscular dysfunction (4.7%)
 Grade IV - Both cranial nerve and somatic neuromuscular dysfunction (3%)

Local signs

Neurotoxic local effects

Local evidence of a sting may be minimal or absent in as many as 50% of cases of neurotoxic
scorpion stings. In fact, tissue necrosis is rarely found.

A sharp burning pain sensation at the sting site, followed by pruritus, erythema, local tissue
swelling, and ascending hyperesthesia, may be reported. This paresthesia feels like an electric
current, persists for several weeks, and is the last symptom to resolve before the victim
recovers.

The tap test is administered by tapping at the sting site. A positive result is when the
paresthesia worsens with the tapping because the site is hypersensitive to touch and
temperature. In fact, wearing clothing over the area and sudden changes in temperature
exacerbate the symptoms. Tapping over the injury site (ie, tap test) may cause severe pain
after a sting by C exilicauda.

Cytotoxic local effects

A macule or papule appears initially at the sting site, occurring within the first hour of the
sting.

The diameter of the lesion is dependent on the quantity of venom injected.

The lesion progresses to a purpuric plague that will necrose and ulcerate.

Lymphangitis results from the transfer of the venom through the lymphatic vessels.

Nonlethal local effects

Pain, erythema, induration, and wheal may be present.

These are secondary to venom activation of kinins and slow-releasing substances.

Local tissue effects vary among species. Minimal local tissue effects are present with
Centruroides envenomation. Significant local tissue reaction rules out C exilicauda (C
sculpturatus) envenomation.

Neurologic signs

Most of the symptoms are due to either the release of catecholamines from the adrenal glands
(sympathetic nerves) or the release of acetylcholine from postganglionic parasympathetic
neurons. One study by Freire-Maia et al (1974) found that the adrenergic signs occur at a low
venom dose, while cholinergic signs occur at high venom dose concentrations (ie, >40
mcg/100 g in Tityus serrulatus scorpion venom). [20] Furthermore, the adrenergic phase tended
to be more dependent on the venom dose than the cholinergic phase. However, dual
manifestations of the adrenergic and cholinergic signs are possible because of varying organ
system sensitivities to these neurotransmitters.

Central nervous system signs are as follows:

 Thalamus-induced systemic paresthesia occurs in all 4 limbs.

 Patients experience venom-induced cerebral thrombosis strokes.
 The level of consciousness is altered, especially with restlessness, confusion, or
delirium.
 Patients have abnormal behavior.
 Ataxia is also a sign.

Autonomic nervous system signs include predominately sympathetic signs, parasympathetic

signs, or a combination of signs.

Sympathetic signs are as follows:

 Hyperthermia
 Tachypnea
 Tachycardia
 Hypertension
 Arrhythmia
 Hyperkinetic pulmonary edema
 Hyperglycemia
 Diaphoresis
 Piloerection
 Restlessness and apprehension
 Hyperexcitability and convulsions

Parasympathetic signs are as follows:

 Bronchoconstriction
 Bradycardia
 Hypotension
 Salivation, lacrimation, urination, diarrhea, and gastric emesis (SLUDGE)
 Rhinorrhea and bronchorrhea
 Goose pimple skin
 Loss of bowel and bladder control
 Priapism
 Dysphagia
 Miosis
 Generalized weakness

Somatic signs are as follows:

 Rigid spastic muscle of the limbs and torso

 Involuntary muscle spasm, twitching, clonus, and contractures
  Alternating opisthotonos and opisthotonus from inactivation of sodium channels,
leading to increased sodium and calcium uptake
 Increased tendon reflexes, especially prolongation of the relaxation phase
 Piloerection accompanied by goose pimples

Cranial nerve signs are as follows:

 Classic rotary eye movement may result in ptosis, nystagmus, and blurred vision.
 Mydriasis is a sign.
 Patients may have tongue fasciculations.
 Dysphagia, dysarthria, and stridor occur secondary to pharyngeal reflex loss or
muscle spasm.
 Patients may present with excessive salivation and drooling.

Peripheral nervous system signs include intense local burning pain with minimal swelling at
sting site, followed by ascending numbness and tingling, then paralysis and convulsions.

Nonneurologic systemic signs

Cardiovascular signs usually follow a pattern of a hyperdynamic phase followed by a

hypodynamic phase. Hypertension is described as follows:

 Hypotension - Less common and occurs secondary to excess acetylcholine or

catecholamine depletion
 High enough to produce hypertensive encephalopathy
 Lasts a few hours
 Observed as early as within 4 minutes after the sting
 Secondary to catecholamine and renin stimulation

Tachycardia is greater than 130 beats per minute, although bradycardia can be observed.

Transient apical pansystolic murmur is consistent with papillary muscle damage.

Cardiovascular collapse occurs secondary to toxin induced myocarditis biventricular

dysfunction and profuse loss of fluids from sweating, vomiting, diarrhea, and hypersalivation.
Note the following:

 Observed in 7-38% of cardiovascular cases

 Mild envenomation - Vascular effect with vasoconstriction hypertension
 Moderate envenomation - Left ventricular failure hypotension with and without an
elevated pulmonary artery wedge pressure, depending on fluid status of the patient
 Severe envenomation - Biventricular cardiogenic shock
 Cardiac dysfunctions attributed to catecholamine-induced myocarditis and increases
in myocardial metabolism oxygen demand (leading to myocardial ischemia–induced
myocardial hypoperfusion) as well as to the direct effects of the toxin (leading to
myocarditis and myocardial conduction interference) [21]

Respiratory signs are as follows:

 Tachypnea may be present.

  Pulmonary edema with hemoptysis and a normal-sized heart is observed in 7-32% of
respiratory cases. This is secondary to a direct toxin-induced increased pulmonary
vessel permeability effect and is also secondary to catecholamine-induced effects of
hypoxia and intracellular calcium accumulation, which leads to a decrease in left
ventricular compliance with resultant ventricular dilation and diastolic dysfunction.
[22]

 Respiratory failure may occur secondary to diaphragm paralysis, alveolar

hypoventilation, and bronchorrhea.

Allergic signs are as follows:

 Patients may have urticaria.

 Angioedema is reported.
 Patients may present with bronchospasm.
 Anaphylaxis is possible.

Gastrointestinal signs are as follows:

 Patients may present with excessive salivation.

 Dysphagia is possible.
 Nausea and vomiting are reported.
 Gastric hyperdistention occurs secondary to vagal stimulation.
 Increased gastric acid output may lead to gastric ulcers.
 Acute pancreatitis may lead to hyperglycemia.
 Liver glycogenolysis may occur from catecholamine stimulation.
 Toxic hepatitis

Genitourinary signs are as follows:

 Patients have decreased renal plasma flow.

 Toxin-induced acute tubular necrosis renal failure may occur.
 Rhabdomyolysis renal failure may result from venom-induced excessive motor
activity.
 Priapism may occur secondary to cholinergic stimulation. One small study by
Bawaskar (1982) found a positive prognostic correlation to the development of
cardiac manifestations following scorpion stings. [23]

Hematological signs are as follows:

 Platelet aggregation may occur because of catecholamine stimulation.

 Disseminated intravascular coagulation with massive hemorrhage may result from
venom-induced defibrination.

Metabolic signs are as follows:

 Hyperglycemia may occur from catecholamine-induced hepatic glycogenolysis,

pancreatitis, and insulin inhibition.
 Increased lactic acidosis may occur from hypoxia and venom-induced increased
lactase dehydrogenase activity.
  Patients may have an electrolyte imbalance and dehydration from hypersalivation,
vomiting, diaphoresis, and diarrhea.

Pregnancy complication signs include toxin-induced uterine contraction, eclampsia, but the
majority of pregnant females do not experience severe sequela. [24]

Symptoms predictive of hospital admission are as follows:

 Priapism (odds ratio 150.59)

 Vomiting (odds ratio 15.82)
 Systolic blood pressure (SBP) greater than 160 (odds ratio 13.38)
 Temperature greater than 38ºC (odds ratio 3.66)
 Heart rate greater than 100 beats per minute (odds ratio 3.35)

Symptomology of specific scorpion species

See the list below:

 Mesobuthus, Tityus, and Leiurus - Tend to cause severe cardiovascular symptoms

 Centruroides - Tend to cause neurological symptoms
 Hemiscorpius - Tend to cause tissue necrosis

Complications
Complications of scorpion envenomation may include the following:
 Cellulitis and abscess formation at sting site [25]
 Dilated cardiomyopathy [26, 27]
 Ankylosis of small joints if the sting occurs at a joint
 Rhabdomyolysis
 Persistent paresthesia
 Antivenin anaphylaxis and serum sickness [28]
 Iatrogenic, high-dose, sedative-hypnotic respiratory arrest
 Respiratory arrest
 Cardiac arrest
 Shock
 Seizures
 Rhabdomyolysis
 Death
 Defibrination after M tamulus stings
 Hemolysis after H lepturus stings
 Pancreatitis after T trinitatis stings
 Antivenom-associated reactions
 Renal failure
Differential Diagnoses
 Botulism
 Caterpillar Envenomation
 Centipede Envenomation
 Coral Snake Envenomation
 Diphtheria
 Disseminated Intravascular Coagulation
 Emergent Management of Myasthenia Gravis
 Emergent Management of Pancreatitis
 Funnel Web Spider Envenomation
 Insect Bites
 Medication-Induced Dystonic Reactions
 Organophosphate Toxicity
 Rattlesnake Envenomation
 Redback Spider Envenomation
 Tarantula Envenomation
 Tetanus
 Widow Spider Envenomation

Laboratory Studies
Scorpion envenomation cases vary from those requiring no laboratory tests
to scenarios requiring extensive hematologic, electrolyte, and respiratory
analysis.
Obtain a CBC count, as Hemiscorpius lepturus has been shown to cause
severe hemolysis. In addition, marked leukocytosis suggests induction of a
venom-mediated systemic inflammatory response‒like syndrome.
Electrolyte evaluation is warranted in patients with venom-induced
salivation, vomiting, and diarrhea.
Coagulation parameters should be measured for venom-induced
defibrination because, at high concentrations, the venom is an
anticoagulant. Defibrination syndrome has been reported following
Mesobuthus tamulus stings.
Glucose levels should be measured to evaluate for hyperglycemia from
liver and pancreas dysfunction.
Troponin and NT-proBNP elevation suggests myocarditis.
Creatine kinase and urinalysis help evaluate for venom-induced excessive
motor rhabdomyolysis. Renal failure may occur secondary to
hemoglobinuria from hemolysis (after H lepturus sting) or myoglobinuria
from rhabdomyolysis
Obtain amylase/lipase values to assess for pancreatitis, which is common,
from Tityus trinitatis stings.
Patients may have increased aspartate aminotransferase and alanine
aminotransferase levels from venom-induced liver cell destruction.
Increased catecholamine, aldosterone, renin angiotensin, and antidiuretic
hormone levels are detected a few hours after the sting. The increased
levels persist for 6 hours, after which a gradual decline occurs.
Obtain arterial blood gas (ABG) measurements as indicated for respiratory
distress or to determine acid/base status.
Additional laboratory abnormalities that may have research relevance
include interleukin (IL)–1 levels, which have been reported to be elevated.
High levels of IL-6, interferon-gamma, and granulocyte-macrophage
colony-stimulating factor are reported in severe envenomations.
Radiolabeled antibodies or immunoenzymatic assays help quantify the
serum venom level because an association exists between the clinical
signs of envenomation and this level. [29] However, it is rarely used, owing to
cost and because clinical grading is as effective. It is most likely only used
as a research tool.

Imaging Studies
Obtain a chest radiograph in cases of respiratory difficulty. Unilateral
pulmonary edema may be seen on chest x-ray films because of the venom
effect on pulmonary vascular permeability.
Echocardiography is more sensitive than electrocardiography and creatine
kinase assays for assessing myocardial compromise after a scorpion sting.
Findings show a diffuse global biventricular hypokinesis with a decreased
left and right ventricular ejection fraction of approximately 0.14-0.38. This
dysfunction can appear just a few hours after the sting and usually
normalizes within 4-8 days. Serial echocardiography findings show that the
return of left ventricular function to a normal state correlates to clinical
cardiorespiratory improvement.
Color-flow Doppler study findings show mitral incompetence, probably
secondary to venom-induced dilated cardiomyopathy.
Myocardial perfusion scintigraphy can also be used to investigate the
contractility and perfusion of the cardiac tissue. [30]

Other Tests
Arterial blood gas determinations show a decrease in arterial oxygenation
tension and an increase in PCO2 within 15 minutes of the envenomation,
findings consistent with mild metabolic acidosis.
Pulmonary artery catheterization findings may include the following:
 Elevated systemic vascular resistance occurs up to 4 times the normal
level, with elevated mean arterial pressure (MAP) of 203 mm Hg.
 Left ventricular failure produces a MAP of 57-69 mm Hg.
  Biventricular failure produces a MAP of 47 mm Hg.
 Low cardiac index occurs with elevated filling pressures.
Perform serial spirometry measurements to help detect impending venom-
induced diaphragmatic failure.
Electrocardiography, if indicated, should be performed. ECG changes
persist for 10-12 days before normalizing. ECG changes are observed in
63% of children who have been envenomated. Rhythm disturbances are
not dose-dependent but are related to the venom composition. Note the
following:
 First-degree block - 10.2%
 Bundle-branch block - 12.8%
 Ventricular repolarization abnormalities - 15%
 T-wave inversion - 39%
 ST changes - 39%
 QTc prolongation - 53%
 Sinus tachycardia - Most common rhythm
 A possible sequence of ECG changes has been noted. This sequence
starts with bizarre, broad-notched, biphasic, peaked T waves with a
beat-to-beat variation. This bizarre T wave is followed by the
appearance of tiny Q waves and then atrioventricular dissociation with
an accelerated junctional rhythm.

Histologic Findings
The local sting site shows mixed inflammatory cell infiltrates with
eosinophils scattered among collagen bundles in an edematous dermis.
Myocardial changes, which are most prominent at the papillary muscle and
subendocardial region, include focal myocardial necrosis; myofibril
destruction, especially at the I band; fine fatty deposits in the cardiac
muscle fibers; interstitial edema; and increased cellularity, mainly
lymphocytes and monocytes. Changes resemble interstitial hypoxia-
induced myocarditis caused by large doses of catecholamines.

Prehospital Care
Primary assessment of airway, breathing, and circulation takes
precedence.
Few studies have evaluated the utility of most first aid.
The utility of negative pressure extraction devices has not been evaluated
for scorpion stings.
Perform endotracheal intubation and vascular access as needed.
Emergency Department Care
Supportive care in all cases and antivenom in severe cases are used for
the treatment of scorpion envenomation.
Grades of Centruroides envenomation are as follows:
 Grade I - Local pain and/or paresthesias at the site of envenomation
 Grade II - Pain and/or paresthesias remote from the site of the sting, in
addition to local findings
 Grade III - Either cranial nerve/autonomic dysfunction or somatic
skeletal neuromuscular dysfunction, as follows:
o Cranial nerve dysfunction - Blurred vision, roving eye movements,
hypersalivation, tongue fasciculations, dysphagia, dysphonia,
problems with upper airway
o Somatic skeletal neuromuscular dysfunction - Restlessness,
severe involuntary shaking or jerking of the extremities that may
be mistaken for a seizure
 Grade IV - Combined cranial nerve/autonomic dysfunction and somatic
nerve dysfunction
Androctonus australis Hector Hospitalization Score is as follows (total ≥2 =
Hospitalization) [31] :
 Priapism: +3
 Vomiting: +2
 SBP >160: +2
 Corticosteroid PTA: +2
 Temperature >38ºC: +1
 Heart rate >100 bpm: +1
Although grading and scoring systems have been developed, they are
limited due to species specificity and low-degree symptoms that would lead
to hospitalization or therapy.

Medical Care
Because the clinical manifestations and severity of the symptoms vary
among patients, individualize management of scorpion stings. Furthermore,
frequent patient monitoring allows earlier recognition of the life-threatening
problems of scorpion envenomation. Treatment generally consists of
moving the patient away from the scorpion and stabilizing the patient's
airway and vital signs, followed by administration of antivenin and institution
of symptomatic and local treatment.
Local treatment
Use ice bags to reduce pain and to slow the absorption of venom via
vasoconstriction. This is most effective during the first 2 hours following the
sting. Alternatively, hot water immersion has been described as a first aid
treatment for scorpion bites in Australia and in Taiwan. [32, 33] A randomized
controlled trial performed in Taiwan suggests that hot water immersion for
Scolopendra bites is as effective as ice pack treatment in relieving pain.
Immobilize the affected part in a functional position below the level of the
heart to delay venom absorption.
Calm the patient to lower the heart rate and blood pressure, thus limiting
the spread of the venom.
For medical delay secondary to remoteness, consider applying a lymphatic-
venous compression wrap 1 inch proximal to the sting site to reduce
superficial venous and lymphatic flow of the venom but not to stop the
arterial flow. Only remove this wrap when the provider is ready to
administer systemic support. The drawback of this wrap is that it may
intensify the local effects of the venom.
Apply a topical or local anesthetic agent to the wound to decrease
paresthesia; this tends to be more effective than opiates and ice
application. [34]
Administer local wound care.
Administer tetanus prophylaxis.
Administer systemic antibiotics if signs of secondary infection occur.
Administer muscle relaxants for severe muscle spasms (ie,
benzodiazepines.)
Systemic treatment
Systemic treatment is instituted by directing supportive care toward the
organ specifically affected by the venom.
Establish airway, breathing, and circulation (ie, ABCs) to provide adequate
airway, ventilation, and perfusion.
Monitor vital signs (eg, pulse oximetry; heart rate, blood pressure, and
respiratory rate monitor).
Use invasive monitoring for patients who are unstable and hemodynamic.
Administer oxygen.
Administer intravenous fluids to help prevent hypovolemia from vomiting,
diarrhea, sweating, hypersalivation, and insensible water loss from a
tropical environment.
Perform intubation and institute mechanical ventilation with end-tidal
carbon dioxide monitoring for patients in respiratory distress.
For hyperdynamic cardiovascular changes, administration of a combination
of beta-blockers with sympathetic alpha-blockers is most effective in
reversing this venom-induced effect. Avoid using beta-blockers alone
because this leads to an unopposed alpha-adrenergic effect. Also, nitrates
can be used for hypertension and myocardial ischemia.
For hypodynamic cardiac changes, a titrated monitored fluid infusion with
afterload reduction helps reduce mortality. A diuretic may be used for
pulmonary edema in the absence of hypovolemia, but an afterload reducer,
such as prazosin, nifedipine, nitroprusside, hydralazine, or angiotensin-
converting enzyme inhibitors, is better. Inotropic medications, such as
digitalis, have little effect, while dopamine aggravates the myocardial
damage through catecholaminelike actions. Dobutamine may be a better
choice for the inotropic effect. [35] Finally, a pressor such as norepinephrine
can be used as a last resort to correct hypotension refractory to fluid
therapy.
Administer atropine to counter venom-induced parasympathomimetic
effects.
Other treatment
Insulin administration in scorpion envenomation animal experiments has
helped the vital organs to use metabolic substrates more efficiently, thus
preventing venom-induced multiorgan failure, especially cardiopulmonary
failure. Unfortunately, no human studies have been conducted.
Administer barbiturates and/or a benzodiazepine continuous infusion for
severe excessive motor activity. In some cases, be aware that meperidine
and morphine may potentiate the venom. Also, the concurrent use of
barbiturates and narcotics may add to the respiratory depression in patients
who have been envenomated.
The use of steroids to decrease shock and edema is of unproven benefit.
A vaccine preparation was tried in experimental animals but was not
pursued because of the need to prepare different antigens according to
different geographical areas and to different species of scorpions living in
the same area.
Antivenom
Antivenom is the treatment of choice after stabilization and supportive care.
Because of the heterogeneity of venom composition between different
scorpion species, one species' antivenom will have limited effect on
another scorpion species' venom. Thus, correct scorpion species
identification is a prerequisite for proper antivenom treatment.
For newer scorpion antivenom, the exact dosing has not been established
as animal studies treatment amount does not translate into human studies
treatment amount. In addition, the quantity to be used is determined by the
patient’s clinical severity, symptom evolution, and treatment response.
Unfortunately, predicting the patient’s response treatment is difficult, which
makes exact antivenom dosing difficult. Furthermore, underdosing will
result in limited or no effect, while overdosing increases the side effects
and hypersensitivity reactions. Because the new antivenoms are highly
purified immunoglobulin fragments, adverse reaction is less frequent and
tends to be mild.
The antivenom significantly decreases the level of circulating unbound
venom within a few hours. The persistence of symptoms after the
administration of antivenom is due to the inability of the antivenom to
neutralize scorpion toxins already bound to their target receptors. Thus,
symptomatic and supportive treatment is needed with immunotherapy. [35]
General time guidelines for the disappearance of symptoms after
antivenom administration are as follows:
 Centruroides antivenom: Severe neurologic symptoms reverse in 15-
30 min. Mild-to-moderate neurologic symptoms reverse in 45-90 min.
 Non-Centruroides antivenom: In the first hour, local pain abates. In 6-
12 hours, agitation, sweating, and hyperglycemia abate. In 6-24 hours,
cardiorespiratory symptoms abate.
While an anaphylaxis reaction to the antivenom is possible, the patient is at
lower risk for this than with other antivenoms for other poisonous
envenomations if there is a scorpion venom—induced large release of
catecholamines. Also, animal-derived antivenom increases the risk of
hypersensitivity reaction compared to human monoclonal-derived
antivenom. Finally, the larger the dose of antivenom, the greater the
change for serum sickness.
In a prospective, randomized, double-blind study, Boyer et al compared
scorpion-specific F(ab')2 antivenom (Anascorp, Centruroides [scorpion]
immune F(ab)2 intravenous [equine], Instituto Bioclon) (n=8) with placebo
(n=7) in children who developed neurotoxic symptoms following scorpion
envenomation. [36] Neuromotor abnormalities were present in all patients at
baseline, and respiratory distress was present in 20%. Beginning 2 hours
after treatment, symptom resolution differed significantly in the antivenom
group compared with the placebo group. Plasma venom concentrations
were undetectable and cessation of the neurologic syndrome occurred
within 4 hours in 100% of antivenom recipients compared with 1 placebo
recipient (p=0.001).
Thus, the Boyer et al study suggests that scorpion-specific F(ab')2
antivenom successfully treated the clinical syndrome, reducing the need for
concomitant sedation and reducing circulating unbound venom levels for
Centruroides envenomation. [36]
For Mesobuthus tamulu envenomations, horse-derived antivenom has
been developed. Natu et al compared the newer antivenom treatment
versus the traditional prazosin treatment in their open label study of 81
envenomated patients and found that antivenom decreased clinical
recovery time to 4.14 hours +/- 1.6 hours compared to prazosin’s clinical
recovery time of 19.28 hours +/- 5.03 hours. [37]
Natu et al also found that the antivenom plus prazosin combination group
had a recovery time of 3.46 hours +/- 1.1 hours but felt it was comparable
to the antivenom group recovery time and recommended that the
combination therapy be reserved for patients presenting with pulmonary
edema with hypertension.
Bawaskar et al compared antivenom plus prazosin versus prazosin in their
open label trial of 70 patients with only grade 2 envenomations (beginning
of systemic involvement) and found that 91.4% of the combination
treatment group had resolution of their clinical symptoms within the 10-hour
mark compared to 22.9% in the prazosin treatment group. [38] Both the Natu
and the Bawaskar studies suggest the utility of the new Mesobuthus
tamulus antivenom for systemic symptoms envenomations.
Kumar et al found that early (< 4 h) administration of antivenom with
prazosin increases the percentage of children not developing myocardial
dysfunction. [39, 40]
Further inpatient care
Inpatient care is dictated by the severity of the envenomation and consists
of stabilizing the patient, neutralizing the venom, providing supportive
therapies, and preventing complications. Patients with grade III or grade IV
Centruroides stings and other severe Buthidae envenomations should be
admitted to the intensive care unit (ICU) and/or treated with antivenom.
Treat all patients with severe systemic symptoms in an intensive care unit
(ICU) setting because of the unpredictability of the symptomology, the risks
associated with antivenin administration, and the need for airway or blood
pressure support.
Young children do worse than adults. Young children may not recover as
quickly as adults after scorpion envenomation and are more likely to
require observation.
Transfer
Transfer is appropriate if antivenin administration or ICU treatments are not
available at the institution where the patient initially presents.

Activity

Rest and immobilization of the sting site is recommended to prevent rapid absorption of the venom
into the circulation.
Prevention
Protective clothing, such as shoes or gloves, may prevent some scorpion
envenomations. Check shoes, gloves, clothing, and backpacks for
scorpions prior to use.
Keep yards free of debris, which can serve as a place for scorpions to hide.
Make sure windows and doors fit tightly to prevent scorpions from entering
the house.
Avoid walking barefoot, especially at night when scorpions are active.
Use a Wood lamp at night because the cuticle of the Centruroides species
is fluorescent under ultraviolet light.
Methods of biological control of scorpions include introducing chickens,
ducks, and owls to the area.
Methods of chemical control of scorpions include using organophosphates,
pyrethrins, and chlorinated hydrocarbons.
Government monitoring of the scorpion public health problem is warranted.

Long-Term Monitoring
Patients displaying local nonascending reactions to the venom may be
discharged after 6 hours of observation, with close follow-up. If the patient
was treated with a pressure bandage, the symptoms may be delayed and
inpatient observation is warranted. Patients with grade I or grade II
Centruroides envenomations may be discharged. Discharge of patients
with other Buthidae envenomations is more problematic because onset of
systemic symptoms may be delayed up to 24 hours.
If an antivenin is administered, monitor the patient for serum sickness over
next the few weeks.
Inform the patient about the possibility of persistent pain or paresthesia at
the sting site.
Instruct patient regarding progression. Discuss symptoms of delayed serum
sickness with patients treated with antivenom.

Medication Summary
The goals of pharmacotherapy are to reduce morbidity, to prevent
complications, and to neutralize the toxin.
Analgesia may be indicated. Exercise caution when using narcotics for a
patient with an unsecured airway because respiratory depressive effects
may be synergistic with some scorpion venoms. Some recommend against
using narcotics to treat scorpion envenomation with signs of systemic
toxicity, especially in children. Tetanus prophylaxis is recommended if the
patient cannot verify current status. Prophylactic antibiotic therapy is not
required. Corticosteroids have not been shown useful in treating venom
toxicity. Hypertensive emergencies may require standard antihypertensive
therapy. Conversely, hypotension may require fluid resuscitation and/or
vasopressors.
Cardiovascular agents can be used to elevate or decrease blood pressure
and increase heart rate. Vasopressors and inotropic agents may be
necessary in patients who already have been adequately volume
resuscitated but remain in shock. Conversely, antihypertensives may be
needed in patients with sympathetic-induced hypertension. In particular, the
use of the alpha-blocking agent prazosin has been used and
recommended. However, most of the published evidence recommending
for or against this agent has come from either retrospective observational
or prospective cohort studies. Gupta et al compared dobutamine versus
prazosin in children and found mortality in both groups to be equal, but the
prazosin group had a quicker resolution in their pulmonary edema (28 h vs
72 h). [41] For prazosin-resistant cardiotoxic cases, a small retrospective
observational study that found the addition of dobutamine to the prazosin
may be beneficial. [42]
At this time, no clear evidence exists as to which agent is most beneficial in
specific circumstances. Autonomic instability from scorpion envenomation
may lead to rapid, dramatic fluctuations in heart rate and blood pressure.
Although many agents have rapid onset, they may also have prolonged
effects. Should a hypertensive patient receive a longer-acting agent they
may still have medication effects if they develop subsequent hypotension.
In any case, agents should be chosen with detailed knowledge of their
pharmacology and understanding of the pathophysiology of scorpion
venom described above. Ideally, the agents are effective, have rapid onset,
can be titrated to effect, have a short half-life if discontinued, and have
minimal side effects.
A total of 22 types of scorpion antivenom are listed in the American Zoo
and Aquarium Association Antivenom Index. They are available for a
number of different species and have varied efficacy. Antivenom use
remains controversial. Many researchers report decreased morbidity,
mortality, and hospital stay with its use. These researchers and clinicians
believe that antivenom therapy cannot be matched by supportive care in
severe Buthidae scorpion envenomation. Others suggest that adverse
effects (eg, anaphylactic reactions, serum sickness) limit or contraindicate
antivenom use.
Scorpion toxins are not good antigens because of small size and poor
immunogenicity. They do not induce antibodies that cross-react against
toxins of other scorpion species unless a 95% amino acid sequence
homology exists between the 2 toxins. Thus, no universal antivenin is
available.
Furthermore, the neurotoxin component of the scorpion venom tends to be
the least immunogenic, resulting in the low efficiency for neurological
complications. It usually is prepared from horses because they yield larger
quantities. Sheep, goat, or bovine antivenins have been prepared if patient
sensitivity to horse serum occurs.
One idea was to mix a batch of different scorpion antivenin together to
create a universal antivenin, but this exposes the patient to unnecessary
antivenin from scorpion species not from the patient's region.
Skin tests have been performed to test for allergic response with locally
produced antivenins. First, dilute 0.1 mL of antivenin in a 1:10 ratio with
isotonic sodium chloride solution. Second, administer 0.2 mL intradermally.
A positive test result is if a wheal develops within 10 minutes. The skin test
has a sensitivity of 96% and a specificity of 68%.
Until mid 2000, the antivenom for stings by the bark scorpion was
manufactured in the Antivenin Production Laboratory of Arizona State
University. Its use was controversial. It had been shown to produce rapid
resolution of systemic symptoms but not to affect pain or paresthesias.
Subsequently, many physicians recommended it in grade III and grade IV
envenomations. Adverse effects included immediate and delayed
hypersensitivity reactions. Initially, these reactions were rare, but they
increased in frequency. This leads some physicians to prefer supportive
care only, as they felt that the treatment was potentially worse than the
disease. As death was rare if existent, they felt supportive care would yield
similar outcomes. Currently, it is no longer being produced.
The best result occurs when antivenin is administered as early as possible
(preferably within the first 2 h after the sting) and with adequate quantities
to neutralize the venom (usually 50-100 times the LD50 amount). A
decrease in curative effects occurs with longer sting-serotherapy delay and
administration of insufficient amounts of antivenin.
In August 2011, the US Food and Drug Administration approved use of a
Mexican Centruroides antivenom (Anascorp, manufactured by Instituto
Bioclon for Rare Disease Therapeutics, Inc). [43]
Give steroids and antihistamines if serum sickness develops.

Antivenins
Class Summary
These agents are composed of venom-specific F(ab’)2 fragments of
immunoglobulin G (IgG) that bind and neutralize venom toxins, facilitating
redistribution away from target tissues and elimination from the body.
Antivenin, Centruroides (scorpion) (Anascorp)

 View full drug information

This is a Centruroides (scorpion) immune F(ab)2 (equine) injection. it
is antivenom indicated for treatment of clinical signs of scorpion
envenomation. Initiate treatment as soon as possible in patients who
develop clinically important signs of scorpion envenomation, including, but
not limited to, loss of muscle control, roving or abnormal eye movements,
slurred speech, respiratory distress, excessive salivation, frothing at the
mouth, and vomiting.

Antihistamines
Class Summary
Antihistamines prevent the histamine response in sensory nerve endings
and blood vessels. They are more effective in preventing a histamine
response than in reversing it.

Cimetidine (Tagamet)

 View full drug information

Cimetidine is an H2 antagonist that, when combined with an H1 type, may
be useful in treating itching and flushing in anaphylaxis, pruritus, urticaria,
and contact dermatitis that do not respond to H1-receptor antagonists
alone. Use this in addition to H1 antihistamines. Other H2 antagonists are
also available.

Diphenhydramine (Benadryl, Benylin, Bydramine)

 View full drug information

Diphenhydramine is used for the symptomatic relief of allergic symptoms
caused by histamine released in response to allergens.

Toxoids
Class Summary
Wounds resulting from scorpion sting are at risk of Clostridium tetani
infection. A booster injection in previously immunized individuals is
recommended to prevent this potentially lethal syndrome. Administer
tetanus immune globulin (Hyper-Tet) to patients not immunized against C
tetani products (eg, persons who have immigrated, elderly individuals).

Diphtheria-tetanus toxoid (dT)

 View full drug information

Diphtheria-tetanus toxoid is used to induce active immunity against tetanus
in selected patients. Tetanus and diphtheria toxoids are the immunizing
agents of choice for most adults and children older than 7 years. Booster
doses are necessary to maintain tetanus immunity throughout life because
tetanus spores are ubiquitous.
In children and adults, administer it into the deltoid or midlateral thigh
muscles. In infants, the preferred site of administration is the mid thigh
laterally

Immune globulins
Class Summary
These agents induce passive immunity. Administer to patients not
immunized against C tetani products (eg, persons who have immigrated,
elderly individuals).

Tetanus immune globulin (TIG)

 View full drug information

Tetanus immune globulin is used for passive immunization of any person
with a wound that might be contaminated with tetanus spores.

Benzodiazepines
Class Summary
By increasing the action of GABA (inhibitory neurotransmitter),
benzodiazepines counteract scorpion-induced excessive motor activity and
nervous system excitation.

Lorazepam (Ativan)
  View full drug information
Lorazepam is a sedative hypnotic with a short onset of effects and
relatively long half-life. By increasing the action of GABA, which is a major
inhibitory neurotransmitter in the brain, it may depress all levels of the CNS,
including limbic and reticular formation.

Midazolam (Versed)

 View full drug information

Midazolam is a short-acting benzodiazepine that can be administered in
continuous infusion for severe nervous system excitation.

Barbiturates
Class Summary
Barbiturates are used to counteract scorpion-induced hyperactivity.

Pentobarbital (Nembutal)

 View full drug information

Pentobarbital is a short-acting barbiturate with sedative and anticonvulsant
properties. It is used to produce barbiturate coma for severe CNS
hyperexcitation. It requires patient intubation prior to use.

Local anesthetics
Class Summary
These agents tend to be more effective than opiates to control paresthesia
and pain at the sting site.

Bupivacaine (Marcaine)

 View full drug information

Bupivacaine may reduce pain by slowing nerve impulse propagation and
reducing action potential, which, in turn, prevents the initiation and
conduction of nerve impulses.
Adrenergic blocking agents and vasodilators
Class Summary
Adrenergic blocking agents and vasodilators are used to counteract the
scorpion-induced adrenergic cardiovascular effect.

Labetalol (Normodyne, Trandate)

 View full drug information

Labetalol blocks beta1-adrenergic, alpha-adrenergic, and beta2-adrenergic
receptor sites, decreasing blood pressure.

Prazosin (Minipress)

 View full drug information

Prazosin counteracts the scorpion-induced adrenergic cardiovascular
effects. It may improve pulmonary edema through vasodilatory effects.

Hydralazine (Apresoline)

 View full drug information

Hydralazine decreases systemic resistance through direct vasodilation of
arterioles.

Anticholinergics
Class Summary
Anticholinergics are used to counteract scorpion-induced cholinergic
symptoms. Current recommendations are for use in treating symptomatic
bradycardias. Traditionally, its use to dry venom-induced, excess,
respiratory secretions has been warned against because of its potential
adverse cardiopulmonary effects. It may exacerbate pulmonary edema and
hypertension and may lead to a subsequent tachycardia. A recent case
series has suggested relative efficacy and safety with its use in 5 pediatric
patients treated for C sculpturatus sting. However, this should be
considered an area in need of further study rather than a change in
recommendations.
Atropine IV/IM (Atropair)

 View full drug information

Atropine is used to increase the heart rate through vagolytic effects,
causing an increase in cardiac output. It also treats bronchorrhea
associated with scorpion envenomations. Atropine causes a reversible
blockade of muscarinic receptors with subsequent anticholinergic effects. It
has been used to reverse vagally induced symptomatic bradycardias,
which may be associated with scorpion envenomation. Its use for dry
secretions is debated. Atropine will not reverse the somatic or other cranial
nerve symptoms.

Vasopressors/inotropics
Class Summary
Vasopressors/inotropics are used to combat hypotension refractory to
intravenous fluid therapy.

Norepinephrine (Levophed)

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Norepinephrine is indicated for persistent hypotension not responsive to
judicious fluid loading and sodium bicarbonate.

Dobutamine (Dobutrex)

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Dobutamine is a sympathomimetic amine with stronger beta than alpha
effects. It increases the inotropic state with afterload reduction.

Milrinone (Primacor)

 View full drug information

Milrinone is a positive inotropic agent and vasodilator with little chronotropic
activity.