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Scorpion Envenomation Clinical Presentation

  • Author: David Cheng, MD; Chief Editor: Joe Alcock, MD, MS  more...
 
Updated: Apr 22, 2016
 

History

For patients presenting with scorpion stings, ascertaining the following is essential:

  • Time of envenomation
  • Nature of the incident
  • Description of the scorpion: Specimen identification by an entomologist may be helpful (if the scorpion can be captured safely).
  • Local and systemic symptoms: Pain and paresthesias often are present. Nausea and vomiting are common.

The toxicity, variation, and duration of the symptoms depends on the following factors:

  • Scorpion species
  • Scorpion age, size, and nutritional status
  • Healthiness of the scorpion's stinging apparatus (telson)
  • Number of stings and quantity of venom injected
  • Depth of the sting penetration
  • Composition of the venom
  • Site of envenomation: Closer proximity of the sting to the head and torso results in quicker venom absorption into the central circulation and a quicker onset of symptoms.
  • Age of the victim, as children are more susceptible to severe clinical manifestations
  • Health of the victim
  • Weight of the victim relative to amount of venom
  • Presence of comorbidities
  • Treatment effectiveness

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.

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Physical

Clinical manifestations range from minor local tenderness to multisystem failure followed by death.[18]

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 is graded as follows[2] :

  • Mild - Local signs of erythema, swelling and tenderness (estimated 68.6%)
  • Moderate - Ascending local signs or mild systemic signs (estimated 26.8%)
  • Severe - Life-threatening systemic signs (estimated 4.6%)

Neurologic predominance is graded as follows:

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

Local signs

Neurotoxic local effects

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

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

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

Cytotoxic local effects

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

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

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

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

Nonlethal local effects

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

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

Local tissue effects vary among species. Minimal local tissue effects are present with Centruroides envenomation. Significant local tissue reaction rules out C exilicauda 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).[19] Furthermore, the adrenergic phase tended to be more dependent on the venom dose than the cholinergic phase. However, dual manifestations of the adrenergic and cholinergic signs are possible because of varying organ system sensitivities to these neurotransmitters.

Central nervous system signs are as follows:

  • Thalamus-induced systemic paresthesia occurs in all 4 limbs.
  • Patients experience venom-induced cerebral thrombosis strokes.
  • The level of consciousness is altered, especially with restlessness, confusion, or delirium.
  • Patients have abnormal behavior.
  • Ataxia is also a sign.

Autonomic nervous system signs include predominately sympathetic signs, parasympathetic signs, or a combination of signs.

Sympathetic signs are as follows:

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

Parasympathetic signs are as follows:

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

Somatic signs are as follows:

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

Cranial nerve signs are as follows:

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

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

Nonneurologic systemic signs

Cardiovascular signs usually follow a pattern of a hyperdynamic phase followed by a hypodynamic phase. Hypertension is described as follows:

  • Hypotension - Less common and occurs secondary to excess acetylcholine or catecholamine depletion
  • High enough to produce hypertensive encephalopathy
  • Lasts a few hours
  • Observed as early as within 4 minutes after the sting
  • Secondary to catecholamine and renin stimulation

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

Transient apical pansystolic murmur is consistent with papillary muscle damage.

Cardiovascular collapse occurs secondary to toxin induced myocarditis biventricular dysfunction and profuse loss of fluids from sweating, vomiting, diarrhea, and hypersalivation. Note the following:

  • Observed in 7-38% of cardiovascular cases
  • Mild envenomation - Vascular effect with vasoconstriction hypertension
  • Moderate envenomation - Left ventricular failure hypotension with and without an elevated pulmonary artery wedge pressure, depending on fluid status of the patient
  • Severe envenomation - Biventricular cardiogenic shock
  • Cardiac dysfunctions attributed to catecholamine-induced myocarditis and increases in myocardial metabolism oxygen demand (leading to myocardial ischemia–induced myocardial hypoperfusion) as well as to the direct effects of the toxin (leading to myocarditis and myocardial conduction interference) [20]

Respiratory signs are as follows:

  • Tachypnea may be present.
  • Pulmonary edema with hemoptysis and a normal-sized heart is observed in 7-32% of respiratory cases. This is secondary to a direct toxin-induced increased pulmonary vessel permeability effect and is also secondary to catecholamine-induced effects of hypoxia and intracellular calcium accumulation, which leads to a decrease in left ventricular compliance with resultant ventricular dilation and diastolic dysfunction. [21]
  • Respiratory failure may occur secondary to diaphragm paralysis, alveolar hypoventilation, and bronchorrhea.

Allergic signs are as follows:

  • Patients may have urticaria.
  • Angioedema is reported.
  • Patients may present with bronchospasm.
  • Anaphylaxis is possible.

Gastrointestinal signs are as follows:

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

Genitourinary signs are as follows:

  • Patients have decreased renal plasma flow.
  • Toxin-induced acute tubular necrosis renal failure may occur.
  • Rhabdomyolysis renal failure may result from venom-induced excessive motor activity.
  • Priapism may occur secondary to cholinergic stimulation. One small study by Bawaskar (1982) found a positive prognostic correlation to the development of cardiac manifestations following scorpion stings. [22]

Hematological signs are as follows:

  • Platelet aggregation may occur because of catecholamine stimulation.
  • Disseminated intravascular coagulation with massive hemorrhage may result from venom-induced defibrination.

Metabolic signs are as follows:

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

Pregnancy complication signs include toxin-induced uterine contraction, eclampsia, but the majority of pregnant females do not experience severe sequela.[23]

Symptoms predictive of hospital admission are as follows:

  • Priapism (odds ratio 150.59)
  • Vomiting (odds ratio 15.82)
  • Systolic blood pressure (SBP) greater than 160 (odds ratio 13.38)
  • Temperature greater than 38ºC (odds ratio 3.66)
  • Heart rate greater than 100 beats per minute (odds ratio 3.35)

Symptomology of specific scorpion species

See the list below:

  • Mesobuthus, Tityus, and Leiurus - Tend to cause severe cardiovascular symptoms
  • Centruroides - Tend to cause neurological symptoms
  • Hemiscorpius - Tend to cause tissue necrosis
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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.
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Contributor Information and Disclosures
Author

David Cheng, MD Associate Professor of Emergency Medicine, Education Director, Associate Emergency Medicine Residency Director, Case Medical Center

David Cheng, MD is a member of the following medical societies: American College of Emergency Physicians, International Society for Mountain Medicine, Council of Emergency Medicine Residency Directors, American Heart Association, National Association of EMS Physicians, Society for Academic Emergency Medicine, Society of Critical Care Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Sean P Bush, MD, FACEP Professor of Emergency Medicine, The Brody School of Medicine at East Carolina University

Sean P Bush, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, International Society on Toxicology, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Received honoraria from BTG Inc. for speaking and teaching.

Ramy Yakobi, MD, MBA Medical Director, Department of Emergency Medicine, Beth Israel Medical Center

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

Disclosure: Nothing to disclose.

Charles J Gerardo, MD, FACEP Associate Professor, Department of Surgery, Division of Emergency Medicine, Duke University School of Medicine; Vice Chief of Program Development, Division of Emergency Medicine, Duke University Medical Center

Charles J Gerardo, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Council of Emergency Medicine Residency Directors, National Hispanic Medical Association

Disclosure: Received research grant from: BTG International Inc.

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, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Lisa Kirkland, MD, FACP, FCCM, MSHA Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; Vice Chair, Department of Critical Care, ANW Intensivists, Abbott Northwestern Hospital

Lisa Kirkland, MD, FACP, FCCM, MSHA is a member of the following medical societies: American College of Physicians, Society of Hospital Medicine, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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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.
Centruroides species. Note the slender pincers generally characteristic of scorpions from the family Buthidae. Photo by Sean Bush, MD.
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.
 
 
 
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