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Scorpion Envenomation

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
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; 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
Contributor Information and Disclosures

Updated: Nov 8, 2007

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.

Scorpions from the family Buthidae (which include...

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.

Scorpions from the family Buthidae (which include...

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
  • 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 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.51 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 1964.52 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.

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.
  • 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%) 
  • 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).2 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
        • 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.
      • 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.3
    • 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.
  • 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.

More on Scorpion Envenomation

Overview: Scorpion Envenomation
Differential Diagnoses & Workup: Scorpion Envenomation
Treatment & Medication: Scorpion Envenomation
Follow-up: Scorpion Envenomation
Multimedia: Scorpion Envenomation
References

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Further Reading

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
Disclosure: Nothing to disclose.

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
Disclosure: Nothing to disclose.

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
Disclosure: Nothing to disclose.

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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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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
Disclosure: Nothing to disclose.

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
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