Scorpion Envenom at Ion- [Pri

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eMedicine Specialties > Emergency Medicine > Environmental

Scorpion EnvenomationDavid Cheng, MD, Assistant Professor of Emergency Medicine, Associate Emergency Medicine Residency Director, Associate Medical Director of

Emergency Services, University of Arkansas Medical Sciences

Judith A Dattaro, MD, FACEP, Assistant Professor of Emergency Medicine in Surgery, Cornell University Medical College; Consulting Staff,

Department of Emergency Medicine, Weill-Cornell University Medical Center, New York Presbyterian Hospital; Ramy Yakobi, MD, MBA, Medical

Director of Emergency Department, Beth Israel/Kings Highway Division; Lecturer, Physician Assistant School, Cornell School of Medicine; Lecturer,

Pre-hospital Management of Patient, Cornell/New York Presbyterian Hospital; Director of Emergency Department, New York Community Hospital

Updated: Aug 6, 2009

Introduction

Background

Scorpion stings are a major public health problem in many underdeveloped tropical countries. 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, ie, when they accidentally 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.

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.

Scorpion Envenomation: [Print] - eMedicine Emergency Medicine http://emedicine.medscape.com/article/168230-print

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Scorpions from the family Buthidae (which includes almost all of the potentially lethal scorpions) generally

can be identified by the triangular sternal plate. In other families of scorpions, this feature is more square or

pentagonal. Photo by Sean Bush, MD.

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. These

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


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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 do not hunt for prey; they wait for it. 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.

Pathophysiology

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. 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 2 classes exist. Both of these classes 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


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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.

Frequency

United States

A total of 13,000 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. This lethal scorpion species is the straw-colored Centruroides. 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 (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. 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.

In 2006, a total of 16,231 scorpion envenomations were reported to the American Association of Poison Control Centers. 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. In addition, the majority of patients are stung outside

their home.

Reliable 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.

A recent 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-October.[1 ]

Mortality/Morbidity

Accurate worldwide data do not exist. The underreporting of scorpion stings is frequent because most envenomations occur in desert

and jungle areas that do not have large medical facilities. Furthermore, reporting is 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.[2 ]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.[3 ]Ironically, the highest and lowest mortality estimates are associated with different species within the same

genus of scorpion (Centruroides).

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.

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. Fortunately, better public education, improved control of the scorpion population, increased

supportive therapies, and more technologically advanced intensive care units have combined to produce a substantial decrease in

mortality from these envenomations.


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Race

No racial predilection exists. Any differences in individual reactions to the scorpion sting are a reflection of that individual's genetic

composition rather than race.

Sex

Females are more susceptible than males to the same amount of scorpion venom because of their lower body weight.

Age

While adults are stung more often than children, children are more likely to develop a more rapid progression and increased severity of

symptoms because of their lower body weight. Furthermore, elderly persons are more susceptible to stings because of their

decreased physiologic reserves and increased debilitation.

Clinical

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

Health of the victim

Weight of the victim relative to amount of venom

Presence of comorbidities

Treatment effectiveness

Generally, intrathecal and intravenous routes have immediate effects, while subcutaneous and intramuscular routes take effect

several minutes to hours later.

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

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.


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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 4 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 plays a large role.

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

Mild - Local signs

Moderate - Ascending local signs or mild systemic signs

Severe - Life-threatening systemic signs

Neurologic predominance

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%)


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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 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).[4 ]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

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 - Predominately sympathetic signs, parasympathetic signs, or a combination of signs

Sympathetic signs

Hyperthermia

Tachypnea

Tachycardia

Hypertension

Arrhythmia

Hyperkinetic pulmonary edema

Hyperglycemia

Diaphoresis

Piloerection

Restlessness and apprehension

Hyperexcitability and convulsions

Parasympathetic signs

Bronchoconstriction

Bradycardia

Hypotension

Salivation, lacrimation, urination, diarrhea, and gastric emesis (SLUDGE)

Rhinorrhea and bronchorrhea

Goose pimple skin

Loss of bowel and bladder control


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Priapism

Dysphagia

Miosis

Generalized weakness

Somatic signs

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

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 - 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:

Secondary to catecholamine and renin stimulation

Observed as early as within 4 minutes after the sting

Lasts a few hours

High enough to produce hypertensive encephalopathy

Hypotension - Less common and occurs secondary to excess acetylcholine or catecholamine depletion

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 biventricular dysfunction and profuse loss of fluids from sweating,

vomiting, diarrhea, and hypersalivation.

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 increases in myocardial metabolism oxygen

demand (leading to myocardial ischemia–induced myocardial hypoperfusion) and to the direct effects of

the toxin (leading to myocarditis)

Respiratory signs

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.

Respiratory failure may occur secondary to diaphragm paralysis, alveolar hypoventilation, and bronchorrhea.

Allergic signs

Patients may have urticaria.

Angioedema is reported.

Patients may present with bronchospasm.

Anaphylaxis is possible.

Gastrointestinal signs

Patients may present with excessive salivation.

Dysphagia is possible.


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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

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.[5 ]

Hematological signs

Platelet aggregation may occur because of catecholamine stimulation.

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

Metabolic signs

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 signs - Toxin-induced uterine contraction

Symptoms predictive of hospital admission

Priapism (odds ratio 150.59)

Vomiting (odds ratio 15.82)

Systolic blood pressure (SBP) greater than 160 (odds ratio 13.38)

Temperature greater than 38º C (odds ratio 3.66)

Heart rate greater than 100 beats per minute (odds ratio 3.35)

Symptomology of specific scorpion species

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

Centruroides - Tend to cause neurological symptoms

Hemiscorpius - Tend to cause tissue necrosis

Causes

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.


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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.

Differential Diagnoses

Bites, Insects Spider Envenomations, Funnel Web

Botulism Spider Envenomations, Redback

Caterpillar Envenomations Spider Envenomations, Tarantula

CBRNE - Botulism Spider Envenomations, Widow

Centipede Envenomations Tetanus

Diphtheria Tetanus

Disseminated Intravascular Coagulation Toxicity, Medication-Induced Dystonic Reactions

Myasthenia Gravis Toxicity, Organophosphate

Pancreatitis

Snake Envenomations, Coral

Snake Envenomations, Rattle

Other Problems to Be Considered

Myasthenia gravis

Diphtheria

Guillain-Barré syndrome

Neuroleptic overdose

Sympathomimetic overdose

Venomous jellyfish, snake, and lizard envenomation

Seizures

Dystonia

Workup

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 for leukocytosis and hemolysis in patients with stings from the Hemiscorpius species. Hemiscorpius

lepturus has been shown to cause severe hemolysis.

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.

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.


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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.

Interleukin (IL)–1 levels are elevated in all envenomations.

High levels of IL-6, interferon-gamma, and granulocyte-macrophage colony-stimulating factor are present 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.

Obtain arterial blood gas (ABG) measurements as indicated for respiratory distress or to determine acid/base status.

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 findings are discussed as follows:

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.

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

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.

Sinus tachycardia - Most common rhythm

QTc prolongation - 53%

ST changes - 39%

T-wave inversion - 39%

Ventricular repolarization abnormalities - 15%

Bundle-branch block - 12.8%

First-degree block - 10.2%

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


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then atrioventricular dissociation with an accelerated junctional rhythm.

Procedures

Cerebrospinal fluid pleocytosis is evident on spinal tap studies.

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.

Treatment

Medical Care

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 is the backbone of treatment for systemic symptomatology.

Grades of Centruroides envenomation

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

Cranial nerve dysfunction - Blurred vision, roving eye movements, hypersalivation, tongue fasciculations,

dysphagia, dysphonia, problems with upper airway

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

Priapism: +3

Vomiting: +2

SBP >160: +2

Corticosteroid PTA: +2

Temperature >38ºC: +1

Heart rate >100 bpm: +1

Total ³2 = Hospitalization

Although grading and scoring systems have been developed they are limited due to species specificity and low degree a

symptoms that would lead to hospitalization or therapy.

Medical care


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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 is discussed as follows:

A negative-pressure extraction device (ie, the extractor) may be useful, although the benefit is unproven. The extractor

creates a negative pressure of 1 atm. Apply it to the sting site after incision. Oral extraction is contraindicated.

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.

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.

Administer local wound care and topical antibiotic to the wound.

Administer tetanus prophylaxis.

Administer systemic antibiotics if signs of secondary infection occur.

Administer muscle relaxants for severe muscle spasms (ie, benzodiazepines.)

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 seems to be a better choice for the inotropic effect. 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.

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.

The use of steroids to decrease shock and edema is of unproven benefit.

Antivenin is the treatment of choice after supportive care is established. The quantity to be used is determined by the clinical


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severity of patients and by their evolution over time. Unfortunately, predicting the evolution of symptoms and, thus, the amount of

antivenin that is needed in the future, is difficult.

The antivenin significantly decreases the level of circulating unbound venom within an hour. The persistence of

symptoms after the administration of antivenin is due to the inability of the antivenin to neutralize scorpion toxins already

bound to their target receptors.

Time guidelines for the disappearance of symptoms after antivenin administration are as follows:

Centruroides antivenin: Severe neurologic symptoms reverse in 15-30 min. Mild-to-moderate neurologic

symptoms reverse in 45-90 min.

Non-Centruroides antivenin: 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 antivenin is possible, the patient is at lower risk for this than with other antivenins for

other poisonous envenomations because of the huge release of catecholamines induced by the scorpion venom.

However, the larger the dose of antivenin, the greater the chance 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. 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). In this study, scorpion-specific F(ab')2 antivenom successfully treated the

clinical syndrome, reducing the need for concomitant sedation and reducing circulatingunbound venom levels.[6 ]

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.

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.

Consultations

Local poison control centers may assist in management of envenomations.

Contact the American Association of Poison Control Centers (800-222-1222) to be connected to a local poison control center.

The University of Arizona Poison and Drug Information Center (520-626-6016 from outside Arizona or 800-362-0101 from

Arizona only) has special experience in Centruroides envenomation.

The Antivenom Index, published jointly by the American Association of Poison Control Centers and the American Zoo and

Aquarium Association, lists the locations, amounts, and various types of antivenom stores.

Activity

Rest and immobilization of the sting site is recommended to prevent rapid absorption of the venom into the circulation.

Medication

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


14 of 32 8/14/2010 1:26 AM

prazosin has been used and recommended. However, all published evidence recommending for or against this agent has come from

either retrospective observational or prospective cohort studies. A true randomized controlled trial of this agent has not been published.

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.

Until recently, 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. Subsequently, an increased

pediatric ICU admission rate of 500% is being reported with scorpion envenomation.

The US Food and Drug Administration has recently given approval for experimental use of a Mexican antivenom (Alarcramyn,

manufactured by Instituto Bioclon), which is currently undergoing phase II clinical trials.

Antivenins

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. Instead, 22 types of scorpion antivenin exist.

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 antivenin

may be prepared if patient sensitivity to horse serum occurs.

A recent 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.

Perform a skin test prior to administering the antivenin. 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%.

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.

USA-APL Centruroides scorpion antivenin

Used to neutralize toxins from scorpions. Produced in Arizona (for use in Arizona only). Not approved by FDA. Use remains

controversial, but many physicians recommend it in grade III and IV envenomations. Shown to produce rapid resolution of systemic

symptoms but does not affect pain or paresthesias. Results in resolution of symptoms within min to 2 h after administration. Antivenin

treatment is based on venom burden, not patient's size. The smaller the victim, the more important it is to administer the full dose

because of the venom dose-dependent severity.

Dosing

Adult


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Grade I and II: None

Grade III and IV: 1 vial (5 mL) in 50 mL saline IV over 30 min; if severe symptoms still persist after 1 h, repeat once prn

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; may administer in severe envenomation, despite hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Due to presence of horse serum, agents for emergency treatment of anaphylaxis should be available; premedicate with antihistamines

or steroids

Antihistamines

Prevent the histamine response in sensory nerve endings and blood vessels. They are more effective in preventing histamine

response than in reversing it.

Cimetidine (Tagamet)

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 in addition to H1 antihistamines. Other H2 antagonists

are also available.

Dosing

Adult

Patients with persistent symptoms: 300 mg IV followed by PO administration as outpatient q6h for 2 d or for as long as clinically

indicated

Pediatric

25-30 mg/kg/d IV in 6 divided doses

Interactions

Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol,

metronidazole, procainamide, and lidocaine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy


Precautions

Elderly people may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of

many drugs; adjust dose or discontinue treatment if changes in renal function occur


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Diphenhydramine (Benadryl, Benylin, Bydramine)

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

Dosing

Adult

25-50 mg PO q6-8h prn; not to exceed 400 mg/d

10-50 mg IV/IM q6-8h prn; not to exceed 400 mg/d

Pediatric

12.5-25 mg PO tid/qid or 5 mg/kg/d or 150 mg/m2/d PO divided tid/qid; not to exceed 300 mg/d

5 mg/kg/d or 150 mg/m2/d IV/IM divided qid; not to exceed 300 mg/d

Interactions

Potentiates effect of CNS depressants; because of alcohol content, do not give syrup dosage form to patient taking medications that

can cause disulfiramlike reactions

Contraindications


Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction

Toxoids

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)

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 >7 y. Booster doses are necessary to maintain tetanus immunity throughout life because tetanus

spores are ubiquitous.

In children and adults, administer into the deltoid or midlateral thigh muscles. In infants, preferred site of administration is the mid thigh

laterally

Dosing

Adult

Primary immunization: 0.5 mL IM; administer 2 injections 4-8 wk apart and a third dose 6-12 m after the second injection.

Booster dose: 0.5 mL IM q10y

Pediatric


Interactions

Patients receiving immunosuppressants, including corticosteroids or radiation therapy, may remain susceptible despite immunization

because of poor immune response; cimetidine may enhance or augment delayed-hypersensitivity responses to skin-test antigens;

avoid concurrent use of medication with systemic chloramphenicol because it may impair amnestic response to tetanus toxoid;


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concurrent use of tetanus immune globulin may delay development of active immunity by several days (interaction is nevertheless

clinically insignificant and does not preclude its concurrent use)

Contraindications

Documented hypersensitivity; history of any type of neurological symptoms or signs following administration of this product; FDA

recommends that elective tetanus immunization be deferred during any outbreak of poliomyelitis because tetanus toxoid injections are

an important cause of provocative poliomyelitis

Precautions

Pregnancy


Precautions

Do not use to treat actual tetanus infections or for immediate prophylaxis of unimmunized individuals (use tetanus antitoxin instead,

preferably human tetanus immune globulin); diminished antibody response to active immunization may be observed in patients

receiving immunosuppressive therapy; better to defer primary diphtheria immunization until immunosuppressive therapy discontinued;

routine immunization of symptomatic and asymptomatic persons with HIV is recommended

Immune globulins

These agents induce passive immunity. Administer to patients not immunized against C tetani products (eg, persons who have

immigrated, elderly individuals).

Tetanus immune globulin (Hyper-Tet)

Used for passive immunization of any person with a wound that might be contaminated with tetanus spores.

Dosing

Adult

Prophylaxis: 250-500 U IM in opposite extremity to tetanus toxoid lesion

Clinical tetanus: 3000-10,000 U IM

Pediatric

Prophylaxis: 250 U IM in opposite extremity as tetanus toxoid

Clinical tetanus: 3000-10,000 U IM

Interactions

None reported

Contraindications

Because antibodies in globulin preparation may interfere with immune response to vaccination, do not administer within 3 mo of

live-virus immune globulin administration; may be necessary to revaccinate persons who received immune globulin shortly after

live-virus vaccination

Precautions

Pregnancy


Precautions

Persons with isolated immunoglobulin A (IgA) deficiency have potential for developing antibodies to IgA and may have anaphylactic

reactions to subsequent administration of blood products that contain IgA; do not perform skin testing because intradermal injection of

concentrated gamma globulin may cause localized area of inflammation and can be misinterpreted, causing the medication to be

withheld from a patient not allergic to this material; true allergic responses to human gamma globulin given in prescribed IM manner are

extremely rare; do not admix with other medications because usually incompatible


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Benzodiazepines

By increasing the action of GABA (inhibitory neurotransmitter), counteract scorpion-induced excessive motor activity and nervous

system excitation.

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life.

By increasing action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic

and reticular formation.

Dosing

Adult

1-4 mg IV over 2-5 min; may repeat dose in 10-15 min prn

Pediatric

0.05 mg/kg IV over 2-5 min; may repeat dose in 10-15 min prn

Interactions

Toxicity in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

Contraindications

Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, Parkinson disease, hypotension, and respiratory

depression

Midazolam (Versed)

Short-acting benzodiazepine that can be administered in continuous infusion for severe nervous system excitation.

Dosing

Adult

0.1 mg/kg IV bolus then 0.1 mg/kg/h; titrate dose upward q5min until symptoms controlled

Pediatric


Interactions

Sedative effects may be antagonized by theophyllines; narcotics and erythromycin may accentuate sedative effects because of

decreased clearance

Contraindications

Documented hypersensitivity; preexisting hypotension, narrow-angle glaucoma, and sensitivity to propylene glycol (the diluent)

Precautions

Pregnancy


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Precautions

Caution in congestive heart failure, pulmonary disease, renal impairment, and hepatic failure; may require intubation and pressor

support

Barbiturates

Used to counteract scorpion-induced hyperactivity.

Pentobarbital (Nembutal)

Short-acting barbiturate with sedative and anticonvulsant properties used to produce barbiturate coma for severe CNS hyperexcitation.

Requires patient intubation prior to use.

Dosing

Adult

12 mg/kg IV bolus, then 5 mg/kg/h; titrate to symptom abatement or EEG inactivity

Pediatric


Interactions

Concomitant use with alcohol may produce additive CNS effects and death; chloramphenicol may inhibit metabolism; may enhance

chloramphenicol metabolism; MAOIs may enhance sedative effects of barbiturates; valproic acid appears to decrease barbiturate

metabolism, increasing toxicity; barbiturates can decrease effects of anticoagulants (patients may require dosage adjustments if

barbiturates are added to or withdrawn from regimen); decreased contraceptive effect may occur due to induction of microsomal

enzymes (alternate form of birth control is suggested); barbiturates may decrease corticosteroid and digitoxin effects through induction

of hepatic microsomal enzymes that increase metabolism; barbiturates decrease theophylline levels and may decrease effects; may

decrease verapamil bioavailability

Contraindications

Documented hypersensitivity; liver failure; porphyria

Precautions

Pregnancy


Precautions

Patient may become tolerant to hypnotic effects; caution in patients with hypovolemic shock, respiratory dysfunction, hypotension, renal

dysfunction, congestive heart failure, previous addiction to sedative hypnotics, and congestive heart failure

Local anesthetics

Tend to be more effective than opiates to control paresthesia and pain at the sting site.

Bupivacaine (Marcaine)

May reduce pain by slowing nerve impulse propagation and reducing action potential, which, in turn, prevents initiation and conduction

of nerve impulses.

Dosing

Adult

1.25 mg/kg/dose intralesionally until pain subsides; not to exceed 3-4 mg/kg


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Pediatric


Interactions

May enhance effects of CNS depressants; coadministration may increase toxicity of MAOIs, TCAs, beta-blockers, vasopressors, and

phenothiazines

Contraindications

Documented hypersensitivity; septicemia, spinal deformities, severe hypertension, and existing neurologic disease

Precautions

Pregnancy


Precautions

Test a dose and monitor for CNS toxicity, cardiovascular toxicity, and signs of unintended intrathecal administration; caution with

inflammation or sepsis in region of proposed injection; monitor patient's state of consciousness after each injection; caution in

hypertension, cerebral vascular insufficiency, peripheral vascular disease or heart block, hypoxia, hypovolemia, and arteriosclerotic

heart disease

Adrenergic blocking agents and vasodilators

Used to counteract the scorpion-induced adrenergic cardiovascular effect.

Labetalol (Normodyne, Trandate)

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

Dosing

Adult

20 mg IV then 40 mg IV repeated q10-15min until BP controlled or until the maximum accumulative dose of 300 mg is reached

Pediatric

Not established

Suggested: 0.1 mg/kg IV; repeat q15-20min as last resort

Interactions

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia resulting

from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase blood levels; glutethimide may decrease

effects by inducing microsomal enzymes

Contraindications

Documented hypersensitivity; cardiogenic shock, pulmonary edema, bradycardia, atrioventricular block, uncompensated congestive

heart failure, reactive airway disease, and severe bradycardia

Precautions

Pregnancy


Precautions

Caution in impaired hepatic function; discontinue therapy if signs of liver dysfunction occur; in elderly patients, a lower response rate

and higher incidence of toxicity may be observed; caution with concomitant beta-blockers; beware of continued hypertension despite

decreasing heart rate due to insufficient alpha blockade


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Prazosin (Minipress)

Counteracts scorpion-induced adrenergic cardiovascular effects. May improve pulmonary edema through vasodilatory effects.

Dosing

Adult

1 mg PO bid/tid; not to exceed 5 mg/dose

Pediatric

Not established

Interactions

Acute postural hypotensive reaction from beta-blockers may worsen; indomethacin may decrease antihypertensive activity; verapamil

may increase serum levels and may increase patient's sensitivity to prazosin-induced postural hypotension; may decrease

antihypertensive effects of clonidine

Contraindications


Precautions

Pregnancy


Precautions

Caution in renal insufficiency and hypotension

Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles

Dosing

Adult

10-20 mg IV q4-6h

Pediatric

Not established

Interactions

MAOIs and beta-blockers may increase toxicity

Contraindications


Precautions

Pregnancy


Precautions

May cause hydralazine-induced tachycardia, SLE-type syndrome, and peripheral neuritis

Anticholinergics


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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 (Atropair)

Used to increase heart rate through vagolytic effects, causing an increase in cardiac output. Also treats bronchorrhea associated with

scorpion envenomations. Atropine causes a reversible blockade of muscarinic receptors with subsequent anticholinergic effects. Has

been used to reverse vagally induced symptomatic bradycardias, which may be associated with scorpion envenomation. Its use for dry

secretions is debated. Will not reverse the somatic or other cranial nerve symptoms.

Dosing

Adult

0.5-1 mg IV q15min until desired effect (Note: for vagolytic cardiac effects, there is a 3-mg limit)

Pediatric

0.01 mg/kg IV q15min until desired effect (Note: For cardiac vagolytic effects, there is a 3-mg limit)

Interactions

Coadministration with other anticholinergics (eg, pramlintide) has additive effects; pharmacologic effects of atenolol and digoxin may

increase; antipsychotic effects of phenothiazines may decrease; TCAs with anticholinergic activity may increase effects

Contraindications

Documented hypersensitivity; thyrotoxicosis, narrow-angle glaucoma, and tachycardia

Precautions

Pregnancy


Precautions

Avoid in Down syndrome and/or children with brain damage to prevent hyperreactive response; also avoid in patients with coronary

heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, and hypertension; cardiac monitoring is mandatory; care must

be used to detect marked tachycardia, which may be present with scorpion envenomation; caution in patients with peritonitis, ulcerative

colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in patients with prostatic hypertrophy, prostatism may cause dysuria

and may require catheterization; monitor patients for anticholinergic effects (eg, hyperthermia, dilated pupils, dry mucous membrane,

tachycardia)

Vasopressors/inotropics

Used to combat hypotension refractory to IV fluid therapy.

Norepinephrine (Levophed)

Indicated for persistent hypotension not responsive to judicious fluid loading and sodium bicarbonate.

Dosing

Adult

0.05-0.15 mcg/kg/min IV infusion; titrate to effect

Pediatric

0.1-1 mcg/kg/min IV infusion; titrate to effect


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Interactions

Chlorpromazine enhances pressor response by blocking reflex bradycardia caused by norepinephrine

Contraindications


Precautions

Pregnancy


Precautions

Administer into a large vein because extravasation may cause severe tissue necrosis; caution in occlusive vascular disease

Dobutamine (Dobutrex)

Sympathomimetic amine with stronger beta than alpha effects. Increases inotropic state with afterload reduction.

Dosing

Adult

5-20 mcg/kg/min IV continuous infusion, titrate to desired response; not to exceed 40 mcg/kg/min

Pediatric


Interactions

Beta-blockers antagonize effects

Contraindications


Precautions

Pregnancy


Precautions

Higher dosages may cause increase in heart rate and exacerbate hypotension

Milrinone (Primacor)

Positive inotropic agent and vasodilator with little chronotropic activity.

Dosing

Adult

50 mcg/kg loading dose IV over 10 min, followed by 0.375-0.75 mcg/kg/min continuous IV infusion

Pediatric

Administer as in adults because has been used in the pediatric ICUs, although safety and efficacy not well established

Interactions

May precipitate if infused in the same IV line as furosemide


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Contraindications


Precautions

Pregnancy


Precautions

Slow or stop infusion in patients showing excessive decreases in blood pressure

Follow-up

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.

Further Outpatient Care

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.

Inpatient & Outpatient Medications

Give steroids and antihistamines if serum sickness develops.

Transfer

Transfer is appropriate if antivenin administration or ICU treatments are not available at the institution where the patient initially

presents.

Deterrence/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.


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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.

Complications

Dilated cardiomyopathy

Ankylosis of small joints if the sting occurs at a joint

Rhabdomyolysis

Persistent paresthesia

Antivenin anaphylaxis and serum sickness

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

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.

Patient Education

Educate all patients about methods to avoid scorpions (see Deterrence/Prevention).

Miscellaneous

Medicolegal Pitfalls


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Failure to stabilize the airway and vital signs prior to any specific intervention against the venom

Failure to adequately treat the patient because of underestimation of the envenomation effects

Failure to admit the patient for systemic symptoms

Failure to use ICU monitoring for patients who are severely envenomated

Failure to warn the patient of potential complications and to arrange a follow-up evaluation

Failure to obtain informed consent before antivenin administration

Heavy combination use of barbiturates and narcotics for the hyperdynamic state, leading to concurrent respiratory arrest,

especially in pediatric patients

Some authors caution against narcotic use after certain scorpion envenomations because of possible synergistic effects

on respiration between the narcotics and the venom. The authors recommend adequate treatment of pain with careful

observation for excess sedation.

Likewise, concern exists for respiratory depression associated with benzodiazepine use. However, a retrospective chart

review showed a midazolam drip to be safe and effective in patients with grade III or IV envenomation. This is especially

important in light of the lack of antivenom available for use with C sculpturatus envenomation. The authors recommend

treatment of symptoms with medication as necessary but with close monitoring in the ICU and securing the airway as

needed.

Historically, scorpion envenomations were treated with a "lytic cocktail" of barbiturates and narcotics to decrease the

hyperdynamic state and involuntary muscle activity. However, this combination is no longer recommended because it may

contribute to respiratory depression. This is particularly pertinent for children and patients without a secured airway who exhibit

systemic signs of envenomation.

Atropine has been used to decrease respiratory secretions but, dangerously, may potentiate the sympathetic overdrive

symptoms. However, it should be used in symptomatic bradycardia.

Multimedia

Media file 1: Centruroides species. Note the slender pincers generally characteristic of scorpions from the

family Buthidae. Photo by Sean Bush, MD.

Media file 2: Centruroides limbatus, identified by Scott Stockwell, PhD. A small barb at the base of the stinger

may be helpful in identifying Centruroides or Tityus species, although its presence is variable. Photo by Sean

Bush, MD.


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Media file 3: Scorpions from the family Buthidae (which includes almost all of the potentially lethal scorpions)

generally can be identified by the triangular sternal plate. In other families of scorpions, this feature is more

square or pentagonal. Photo by Sean Bush, MD.

References

Jahan S, Mohammed Al Saigul A, Abdul Rahim Hamed S. Scorpion stings in Qassim, Saudi Arabia--a 5-year surveillance

report. Toxicon. Aug 2007;50(2):302-5. [Medline].

1.

Langley RL, Morrow WE. Deaths resulting from animal attacks in the United States. Wilderness Environ

Med. Feb 1997;8(1):8-16. [Medline].

2.

Boyer L, Heubner K, McNally J, Buchanan P. Death from Centruroides scorpion sting allergy [abstract]. J Toxicol Clin

Toxicol. 2001;39:561-562.

3.

Freire-Maia L, Pinto GI, Franco I. Mechanism of the cardiovascular effects produced by purified scorpion toxin in the rat. J

Pharmacol Exp Ther. Jan 1974;188(1):207-13. [Medline].

4.

Bawaskar HS. Diagnostic cardiac premonitory signs and symptoms of red scorpion sting. Lancet. Mar

6 1982;1(8271):552-4. [Medline].

5.


28 of 32 8/14/2010 1:26 AM

[Best Evidence] Boyer LV, Theodorou AA, Berg RA, et al. Antivenom for critically ill children with neurotoxicity from scorpion

stings. N Engl J Med. May 14 2009;360(20):2090-8. [Medline].

6.

Abroug F, Ayari M, Nouira S, et al. Assessment of left ventricular function in severe scorpion envenomation: combined

hemodynamic and echo-Doppler study. Intensive Care Med. Aug 1995;21(8):629-35. [Medline].

7.

Amaral CF, Dias MB, Campolina D, Proietti FA, de Rezende NA. Children with adrenergic manifestations of envenomation after

Tityus serrulatus scorpion sting are protected from early anaphylactic antivenom

reactions. Toxicon. Feb 1994;32(2):211-5. [Medline].

8.

Amaral CF, Lopes JA, Magalhaes RA, de Rezende NA. Electrocardiographic, enzymatic and echocardiographic evidence of

myocardial damage after Tityus serrulatus scorpion poisoning. Am J Cardiol. Mar 15 1991;67(7):655-7. [Medline].

9.

Amaral CF, Rezende NA. Treatment of scorpion envenoming should include both a potent specific antivenom and support of

vital functions. Toxicon. Aug 2000;38(8):1005-7. [Medline].

10.

Amitai Y, Mines Y, Aker M, Goitein K. Scorpion sting in children. A review of 51 cases. Clin Pediatr

(Phila). Mar 1985;24(3):136-40. [Medline].

11.

Bahloul M, Ben Hamida C, Chtourou K, et al. Evidence of myocardial ischaemia in severe scorpion envenomation. Myocardial

perfusion scintigraphy study. Intensive Care Med. Mar 2004;30(3):461-7. [Medline].

12.

Bawaskar HS, Bawaskar PH. Clinical profile of severe scorpion envenomation in children at rural setting. Indian

Pediatr. Nov 2003;40(11):1072-5. [Medline].

13.

Bawaskar HS, Bawaskar PH. Severe envenoming by the Indian red scorpion Mesobuthus tamulus: the use of prazosin

therapy. QJM. Sep 1996;89(9):701-4. [Medline].

14.

Bergman NJ. Scorpion sting in Zimbabwe. S Afr Med J. Feb 1997;87(2):163-7. [Medline].15.

Bharani AK, Sepaha GC. Myelopathy after scorpion sting. Arch Neurol. Nov 1984;41(11):1130. [Medline].16.

Biswal N, Mathai B, Bhatia BD. Scorpion sting envenomation: complications and management. Indian

Pediatr. Aug 1993;30(8):1055-9. [Medline].

17.

Bond GR. Antivenin administration for Centruroides scorpion sting: risks and benefits. Ann Emerg

Med. Jul 1992;21(7):788-91. [Medline].

18.

Brand A, Keren A, Kerem E, Reifen RM, Branski D. Myocardial damage after a scorpion sting: long-term echocardiographic

follow-up. Pediatr Cardiol. 1988;9(1):59-61. [Medline].

19.

Carbonaro PA, Janniger CK, Schwartz RA. Scorpion sting reactions. Cutis. Mar 1996;57(3):139-41. [Medline].20.

Cupo P, Jurca M, Azeedo-Marques MM, Oliveira JS, Hering SE. Severe scorpion envenomation in Brazil. Clinical, laboratory and

anatomopathological aspects. Rev Inst Med Trop Sao Paulo. Jan-Feb 1994;36(1):67-76. [Medline].

21.

Curry SC, Vance MV, Ryan PJ, Kunkel DB, Northey WT. Envenomation by the scorpion Centruroides sculpturatus. J Toxicol

Clin Toxicol. 1983-1984;21(4-5):417-49. [Medline].

22.

Das S, Nalini P, Ananthakrishnan S, Sethuraman KR, Balachander J, Srinivasan S. Cardiac involvement and scorpion

envenomation in children. J Trop Pediatr. Dec 1995;41(6):338-40. [Medline].

23.

De Rezende NA, Dias MB, Campolina D, Chavez-Olortegui C, Diniz CR, Amaral CF. Efficacy of antivenom therapy for

neutralizing circulating venom antigens in patients stung by Tityus serrulatus scorpions. Am J Trop Med

Hyg. Mar 1995;52(3):277-80. [Medline].

24.

Devi CS, Reddy CN, Devi SL, et al. Defibrination syndrome due to scorpion venom poisoning. Br Med J. Feb

7 1970;1(5692):345-7. [Medline].

25.

el-Amin EO. Issues in management of scorpion sting in children. Toxicon. Jan 1992;30(1):111-5. [Medline].26.


29 of 32 8/14/2010 1:26 AM

Freire-Maia L, Campos JA, Amaral CF. Approaches to the treatment of scorpion

envenoming. Toxicon. Sep 1994;32(9):1009-14. [Medline].

27.

Gateau T, Bloom M, Clark R. Response to specific Centruroides sculpturatus antivenom in 151 cases of scorpion stings. J

Toxicol Clin Toxicol. 1994;32(2):165-71. [Medline].

28.

Ghalim N, El-Hafny B, Sebti F, et al. Scorpion envenomation and serotherapy in Morocco. Am J Trop Med

Hyg. Feb 2000;62(2):277-83. [Medline].

29.

Gibly R, Williams M, Walter FG, McNally J, Conroy C, Berg RA. Continuous intravenous midazolam infusion for Centruroides

exilicauda scorpion envenomation. Ann Emerg Med. Nov 1999;34(5):620-5. [Medline].

30.

Goyffon M, Vachon M, Broglio N. Epidemiological and clinical characteristics of the scorpion envenomation in

Tunisia. Toxicon. 1982;20(1):337-44. [Medline].

31.

Gueron M, Ilia R, Sofer S. The cardiovascular system after scorpion envenomation. A review. J Toxicol Clin

Toxicol. 1992;30(2):245-58. [Medline].

32.

Gueron M, Margulis G, Ilia R, Sofer S. The management of scorpion envenomation

1993. Toxicon. Sep 1993;31(9):1071-83. [Medline].

33.

Gueron M, Weizmann S. Catecholamine excretion in scorpion sting. Isr J Med Sci. Jul-Aug 1969;5(4):855-7. [Medline].34.

Ismail M. The scorpion envenoming syndrome. Toxicon. Jul 1995;33(7):825-58. [Medline].35.

Karnad DR. Haemodynamic patterns in patients with scorpion envenomation. Heart. May 1998;79(5):485-9. [Medline].36.

Kric-Dautovic S, Begovic B. Acute renal insuffiency & toxic hepatitis folowing scorpion sting. Med arh. Feb 2007;61:123-4.37.

Krifi MN, Kharrat H, Zghal K, et al. Development of an ELISA for the detection of scorpion venoms in sera of humans

envenomed by Androctonus australis garzonii (Aag) and Buthus occitanus tunetanus (Bot): correlation with clinical severity of

envenoming in Tunisia. Toxicon. Jun 1998;36(6):887-900. [Medline].

38.

Magalhaes MM, Pereira ME, Amaral CF, et al. Serum levels of cytokines in patients envenomed by Tityus serrulatus scorpion

sting. Toxicon. Aug 1999;37(8):1155-64. [Medline].

39.

Malhotra KK, Mirdehghan CM, Tandon HD. Acute renal failure following scorpion sting. Am J Trop Med

Hyg. May 1978;27(3):623-6. [Medline].

40.

Muller GJ. Scorpionism in South Africa. A report of 42 serious scorpion envenomations. S Afr Med

J. Jun 1993;83(6):405-11. [Medline].

41.

Murthy KR, Hase NK. Scorpion envenoming and the role of insulin. Toxicon. Sep 1994;32(9):1041-4. [Medline].42.

Naqvi R, Naqvi A, Akhtar F, Rizvi A. Acute renal failure developing after a scorpion sting. Br J

Urol. Aug 1998;82(2):295. [Medline].

43.

Nouira S, Boukef R, Nciri N, et al. A clinical score predicting the need for hospitalization in scorpion envenomation. Am J Emerg

Med. May 2007;25(4):414-9. [Medline].

44.

Otero R, Navio E, Cespedes FA, et al. Scorpion envenoming in two regions of Colombia: clinical, epidemiological and

therapeutic aspects. Trans R Soc Trop Med Hyg. Dec 2004;98(12):742-50. [Medline].

45.

Radmanesh M. Androctonus crassicauda sting and its clinical study in Iran. J Trop Med Hyg. Oct 1990;93(5):323-6. [Medline].46.

Radmanesh M. Cutaneous manifestations of the Hemiscorpius lepturus sting: a clinical study. Int J

Dermatol. Jul 1998;37(7):500-7. [Medline].

47.

Rajarajeswari G, Sivaprakasam S, Viswanathan J. Morbidity and mortality pattern in scorpion stings. (A review of 68 cases). J

Indian Med Assoc. Oct 1979;73(7-8):123-6. [Medline].

48.


30 of 32 8/14/2010 1:26 AM

Reddy CR, Suvarnakumari G, Devi CS, Reddy CN. Pathology of scorpion venom poisoning. J Trop Med

Hyg. May 1972;75(5):98-100. [Medline].

49.

Sofer S. Scorpion envenomation. Intensive Care Med. Aug 1995;21(8):626-8. [Medline].50.

Sundararaman T, Olithselvan M, Sethuraman KR, Narayan KA. Scorpion envenomation as a risk factor for development of

dilated cardiomyopathy. J Assoc Physicians India. Nov 1999;47(11):1047-50. [Medline].

51.

Tu A, ed. Handbook of Natural Toxins: Invertebrate Venoms. Vol 2. New York, NY: Marcel Dekker; 1984:513-678.52.

Velasco-Castrejon O, Lara-Aguilera R, Alatorre H. [Clinical and epidemiological aspects of scorpion sting in a hyperendemic

area]. Rev Invest Salud Publica. Apr-Jun 1976;36(2):93-103. [Medline].

53.

Keywords

scorpion sting, scorpion envenomation, scorpion venom, arthropod sting, insect sting, arachnid sting, venom, antivenom, antivenin,

Buthidae, Scorpionidae, Ischnuridae, Buthus, Parabuthus, Mesobuthus, Tityus, Leiurus, Androctonus, Centruroides, Centruroides

exilicauda, Centruroides sculpturatus, C sculpturatus, neurotoxin, cardiotoxin, nephrotoxin, toxin, wildlife emergency, envenomation,

severe local skin reaction, neurologic collapse, respiratory collapse, cardiovascular collapse, respiratory failure, cardiovascular failure,

Buthus, Mesobuthus, Buthotus, Buthus tamulus, Hottentotta, Leiurus, Leiurus quinquestriatus, Leiurus quinquestriatus,

Androctonus, Androctonus australis, Hemiscorpius, Hemiscorpius lepturus

Contributor Information and Disclosures

Author

David Cheng, MD, Assistant Professor of Emergency Medicine, Associate Emergency Medicine Residency Director, Associate

Medical Director of Emergency Services, University of Arkansas Medical Sciences

David Cheng, MD is a member of the following medical societies: American College of Emergency Physicians, American Heart

Association, Council of Emergency Medicine Residency Directors, International Society for Mountain Medicine, National Association of

EMS Physicians, Society for Academic Emergency Medicine, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Judith A Dattaro, MD, FACEP, Assistant Professor of Emergency Medicine in Surgery, Cornell University Medical College;

Consulting Staff, Department of Emergency Medicine, Weill-Cornell University Medical Center, New York Presbyterian Hospital

Judith A Dattaro, MD, FACEP is a member of the following medical societies: American Association of Women Emergency

Physicians, American College of Emergency Physicians, American Medical Association, Chicago Medical Society, Illinois State

Medical Society, and Society for Academic Emergency Medicine


Ramy Yakobi, MD, MBA, Medical Director of Emergency Department, Beth Israel/Kings Highway Division; Lecturer, Physician

Assistant School, Cornell School of Medicine; Lecturer, Pre-hospital Management of Patient, Cornell/New York Presbyterian Hospital;

Director of Emergency Department, New York Community Hospital

Ramy Yakobi, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine and American

College of Emergency Physicians


Medical Editor

Lisa Kirkland, MD, FACP, CNSP, MSHA, Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo

Clinic; ANW Intensivists, Abbott Northwestern Hospital

Lisa Kirkland, MD, FACP, CNSP, MSHA is a member of the following medical societies: American College of Physicians, Society of

Critical Care Medicine, and Society of Hospital Medicine


Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment


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Managing Editor

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H, Professor, Department of Medicine, Division of Pulmonary and Critical Care

Medicine, University of Southern California Keck School of Medicine

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H is a member of the following medical societies: American Academy of Allergy

Asthma and Immunology, American College of Chest Physicians, American College of Physicians, American Federation for Medical

Research, American Osler Society, American Thoracic Society, New York Academy of Medicine, and Royal Society of Medicine

Disclosure: Keck School of Medicine, USC None None

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis

University School of Medicine

Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of

Physicians


Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of

Emergency Medicine, Harvard Medical School

Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for

Academic Emergency Medicine


Further Reading

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