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Scorpion envenomation causing neuromuscular toxicity (United States, Mexico, Central America, and
Southern Africa)

Author: Frank LoVecchio, DO, MPH, FACEP


Section Editors: Daniel F Danzl, MD, Stephen J Traub, MD, Michele M Burns, MD, MPH
Deputy Editor: James F Wiley, II, MD, MPH

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2017. | This topic last updated: Mar 01, 2017.

INTRODUCTION — This topic will discuss the clinical manifestations, diagnosis, and management of
envenomation by scorpions whose stings cause neuromuscular toxicity (eg, Centruroides species [indigenous
to the southwestern United States, Mexico, and Central America] and Parabuthus species [inhabiting Western
and Southern Africa]).

The clinical manifestations, diagnosis, and treatment of scorpion envenomations in other parts of the world
that cause autonomic storm, myocardial depression, and pulmonary edema are discussed separately.

ENTOMOLOGY — Scorpions, which are grouped in the phylum Arthropoda, have a lobster-like body shape
with seven sets of paired appendages: the chelicerae, the pedipalps (claws), four sets of legs, and the
pectines (a pair of comb-like structures on the ventral surface) (figure 1). The segmented tail curves upward
dorsally, ending in a terminal bulbous segment called the telson, which contains paired venom glands and the
stinger. In the United States, a subaculear tooth on a small, slender scorpion is specific to Centruroides
exilicauda (sculpturatus), also known as the bark scorpion (picture 1 and picture 2 and picture 3) [1,2].

Envenomation occurs through stinging, not biting. Scorpions clutch prey in their pedipalps (claws) and thrust
the tail overhead to sting. Although envenomations are sometimes reported as bites, true scorpion bites have
not been documented and would be inconsequential if they did occur. Scorpions can sting multiple times,
although the first sting depletes or nearly depletes the telson of venom.

A characteristic physical property of scorpions is that they fluoresce when illuminated by ultraviolet light, as
from a black light or a medical Wood's lamp (picture 4) [3]. This property is used in collecting scorpions for
breeding or venom harvesting and in providing pest control. The fluorescent pigment in scorpion cuticle is
most likely riboflavin.

SCORPION GEOGRAPHY AND APPEARANCE — Scorpions are found on all continents except Antarctica.
Scorpions characteristically live in desert areas, semiarid grasslands, and the tropics.

Estimates vary regarding the number of scorpion species. Researchers report 1400 scorpion species divided
into nine families [4]. Buthidae is the largest and the most dangerous family and, with few exceptions,
contains the only species capable of producing clinically significant envenomations through their neurotoxic
venoms [5]. At least 30 species can inflict potentially fatal stings [4-6].

Dangerous species capable of neuromuscular toxicity after envenomation include Centruroides in the United

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States, Mexico and Central America and Parabuthus in Southern Africa (table 1).

Common scorpions associated with neuromuscular toxicity and their characteristic appearance are as follows:

● Centruroides exilicauda – C. exilicauda, (also called C. sculpturatus or the bark scorpion, due to of its
preference for residing in or near trees) measures 4 to 7 cm long in length and varies in color from yellow
to brown or tan (picture 1 and picture 2 and picture 3 and picture 5). The presence of a subaculear tooth,
a tubercle at the base of the stinger, is specific to C. exilicauda and is helpful in differentiating this highly
neurotoxic scorpion from other species [5,7]. C. exilicauda is found primarily in northern Mexico and the
southwestern United States (eg, Arizona, New Mexico, western Texas, southeastern California, and near
Lake Mead, Nevada).

● Centruroides vittatus – C. vittatus, the striped scorpion, has a black intraocular triangle and black
stripes on the thorax. C. vittatus is found primarily in the Southwest and Texas but also extends into
southern Indiana and Illinois [8].

● Centruroides suffusus – C. suffusus, also known as the Mexican scorpion, is yellow to tan with dark
longitudinal strips on the abdomen and measures 5 to 7.5 cm. C. suffusus is found throughout Mexico
and is considered the most dangerous among the many species found there.

● Parabuthus granulatus – P. granulatus, or the granulated thick-tailed scorpion, is dark yellow to brown
and is large; measuring 6 to 15 cm [9,10]. It has thin pinchers and a thick tail versus more harmless
scorpions that have thick pinchers and thin tails. It is indigenous to South Africa, western Zimbabwe,
Botswana, Namibia, and southern Angola and is found mainly in dry habitats (receiving less than 600 mm
of rain per year). P. granulatus burrows under shrubs, grass tufts, and other objects and in sandy soil.

● Parabuthus transvaalicus – The Transvaal thick-tailed scorpion or dark scorpion, P. transvaalicus, is


dark brown or black and has a length of 6 to 15 cm. It lives in South Africa, southern Zimbabwe, eastern
Mozambique, and eastern Botswana. It has thin pincers and a thick tail. P. transvaalicus can both inject
and spray its kurtoxin venom [10,11]. It is predominately nocturnal and burrows in sandy or gritty soil and
can be found in thatched roofs.

VENOM — Scorpion venoms are complex mixtures containing mucopolysaccharides, hyaluronidase,


phospholipase, acetylcholinesterase, serotonin, histamine, protease inhibitors, histamine releasers, and
neurotoxins.

Neurotoxins are the most important venom constituents in human envenomations [12-14]. In neuronal
membranes, these toxins cause incomplete inactivation of sodium channels during depolarization that result
in a slow inward sodium current. This action causes membrane hyperexcitability, and leads to repetitive
uncontrolled firing of axons [5]. As a consequence, release of neurotransmitters at synapses and the
neuromuscular junction is enhanced [15] and leads to excessive neuromuscular activity and autonomic
dysfunction.

Some scorpion neurotoxins also have effects on calcium-activated potassium channels [16,17], chloride
channels, and L-type calcium channels [18] but these effects do not appear to contribute significantly to
toxicity [19].

The venom of C. exilicauda venom does not cause local tissue destruction [4-6,20].

REGIONAL EPIDEMIOLOGY

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United States — Centruroides exilicauda (sculpturatus) is the culprit in most reported envenomations. Its
sting causes a significant number of systemic reactions, and can be fatal [5,7]. Centruroides vittatus, the
common striped scorpion, is the second-most commonly reported species in envenomations.

From 1931 to 1940, more than 40 deaths were attributed to C. exilicauda envenomation, mostly in young
children and infants. No deaths attributable to the neurotoxicity from scorpion envenomation have been
reported in Arizona since 1968; in 2001, a scorpion-related fatality was reported, but this death was ascribed
to anaphylaxis rather than to direct venom toxicity [21]. Mortality can usually be prevented with appropriate
supportive care; prior fatalities were caused by respiratory failure that was complicated by metabolic acidosis,
hyperthermia, and rhabdomyolysis from excessive muscular activity [21].

Mexico — At least 134 native species are regarded as dangerous. Among the eight members of the
Centruroides genus, C. exilicauda (sculpturatus), C. noxius, and C. suffusus (the Mexican scorpion) are
usually cited as the most dangerous. Most fatal cases occur in the summer months from April through July. In
the 1980s, hundreds of scorpion fatalities occurred nationwide per year, with respiratory failure as the
proximate cause of death; this figure probably underestimates the true total by a factor of two to three [22]. In
Mexico, scorpion deaths outnumber snakebite deaths 10 to 1 [23].

Southern Africa — Scorpions found in southern Africa include the frequently dangerous Buthidae with
characteristic thin pincers and thick tails) and the relatively harmless Scorpionidae, Bothriuridae, and
Ischnuridae (with characteristic thick pincers and thin tails) [24]. Approximately 22 Parabuthus species are
distributed throughout South Africa, Namibia, Botswana, Zimbabwe, and southern Mozambique. Three other
species can produce systemic toxicity after envenomation but are not considered potentially fatal: Parabuthus
mossambicensis, Uroplectes planimanus, and Opistophthalmus glabrifrons. Certain Parabuthus scorpions
(eg, P. transvaalicus) with large venom vesicles are capable of spraying venom when alarmed [24].

Significant neuromuscular toxicity after envenomation is best described after stings by P. granulatus and P.
transvaalicus [10]. In one description of 277 envenomations by P. transvaalicus, 10 percent of patients
developed severe symptoms and five patients died (case fatality rate 0.3 percent) [25]. Children younger than
10 years of age and adults over 50 years of age appear to be at greatest risk.

CLINICAL MANIFESTATIONS — Scorpion stings are usually accidental because scorpions would rather
escape humans than attack. As such, stings most commonly occur on an extremity, when a human
unintentionally steps on a scorpion or reaches under wood or rocks.

The majority of scorpion envenomations cause local or no pain with minimal to no inflammation. However,
approximately 10 to 30 percent of patients stung by scorpions of the species Centruroides or Parabuthus
develop neuromuscular toxicity that can be life-threatening [5,25].

After envenomation, symptoms may begin immediately and typically progress to maximum severity within 5
hours. Infants can reach Grade IV in as quickly as 15 to 30 minutes after being stung [26,27]. The symptoms
abate at a rate that varies with the age of the victim and the grade of envenomation. Symptomatic
improvement typically occurs within 9 to 30 hours without antivenom therapy in patients with Grade III or IV
envenomation [5]. Pain and paresthesias are exceptions and have been known to persist for up to two weeks.

Grading of severity — Findings after Centruroides or Parabuthus scorpion envenomation are categorized
into four degrees of severity (table 2):

● Grade I envenomation – Grade I envenomations produce local pain and paresthesias at the sting site.
Usually, no local inflammation occurs, and the puncture wound is too small to be observed. If no scorpion

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is seen, the diagnosis may require historical or epidemiologic clues or other physical signs.

The "tap test" has been empirically recommended to confirm a C. exilicauda (sculpturatus) sting,
although its reliability has not been rigorously tested. With the patient looking away or otherwise
distracted, gently tapping the sting site will greatly exacerbate the pain, a sign that does not occur with
other scorpion envenomations [1,2,5].

● Grade II envenomation – Grade II envenomations produce local symptoms as well as remote pain and
paresthesias. The more distant symptoms often radiate proximally up the affected extremity but may
occur in even more remote sites (eg, contralateral limbs) or as generalized paresthesias. Children may
present with unexplained agitation or inconsolable crying.

● Grade III envenomation – Grade III envenomations produce either cranial nerve or somatic skeletal
neuromuscular dysfunction which may be accompanied by autonomic dysfunction:

• Cranial nerve dysfunction – Cranial nerve dysfunction can manifest as dysphagia, drooling
abnormal eye movements with blurred vision, slurred speech, and tongue fasciculations. The
combination of bulbar neuromuscular dysfunction and increased oral secretions from
parasympathomimetic effects as described below may cause problems with airway maintenance.

Abnormal eye movements most often are involuntary, conjugate, slow, and roving. Chaotic
multidirectional conjugate saccades resembling opsoclonus and unsustained primary positional
nystagmus may also be seen [28]. Many patients with abnormal eye movements prefer keeping their
eyes closed.

• Somatic skeletal neuromuscular dysfunction – Somatic skeletal neuromuscular dysfunction


typically appears as restlessness, fasciculations, shaking and jerking of the extremities, alternating
opisthotonos (arching of the back), and emprosthotonos (tetanic forward flexion of the body). These
signs can be mistaken for a seizure. However, the abnormal skeletal muscle activity appears more
undulating and writhing than the tonic-clonic movements of generalized seizures. Also, unlike
patients with seizures, victims of scorpion stings often remain awake and alert.

• Autonomic dysfunction – The most frequently described autonomic findings after envenomation
varies somewhat by species:

- Centruroides – Salivation, vomiting, bronchoconstriction, diaphoresis, and tachycardia


- Parabuthus – Salivation, diaphoresis, and urinary retention

● Grade IV envenomation – Grade IV envenomations manifest both cranial nerve dysfunction AND
somatic skeletal neuromuscular dysfunction. On close examination, victims with skeletal muscle
hyperactivity usually also have cranial nerve dysfunction, meeting criteria for Grade IV. In the most
severe cases of Centruroides envenomation, stridor and wheezing can occur.

Hyperthermia up to 40°C (104°F) may occur due to excess mo tor activity. Respiratory failure, pulmonary
edema, metabolic acidosis, sterile cerebrospinal fluid pleocytosis, rhabdomyolysis, coagulopathy,
pancreatitis, and multiple organ failure have all been described, especially in children with severe
envenomation [29]. Pancreatitis, commonly associated with Tityus scorpion envenomation, rarely occurs
with Grade IV Centruroides or Parabuthus envenomation. When pancreatitis does occur, it is typically
transient.

Scorpion venoms generally do not produce coagulopathy or other significant hematologic effects,

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although disseminated intravascular coagulation has been reported [30].

Although adults appear to be envenomed more often, children are more likely to develop severe illness
requiring intensive supportive care [1,5]. In an observational study of 673 patients with C. exilicauda
(sculpturatus) envenomations, over two thirds of stings occurred in adults [1]. However, 26 percent of children
less than six years of age had severe envenomations (Grade III or IV) versus 6 percent of adults over age 20.

Laboratory evaluation — Laboratory evaluation should be performed according to the severity of


envenomation (table 2):

● Grade I to II envenomation – Laboratory studies are not needed.

● Grade III to IV envenomation – The following studies are warranted in patients with severe
envenomations (Grade III to IV):

• Serum electrolytes
• Liver enzymes (aspartate aminotransferase [AST] and alanine aminotransferase [ALT])
• Blood urea nitrogen and serum creatinine
• Serum creatine kinase
• Urinalysis

Additional testing may be needed depending upon the clinical scenario:

• Complete blood count and coagulation studies in patients with petechiae or purpura (see
"Disseminated intravascular coagulation in infants and children" and "Clinical features, diagnosis,
and treatment of disseminated intravascular coagulation in adults")

• Electrocardiogram and cardiac biomarkers if signs of exacerbation of underlying ischemic heart


disease (see "Initial evaluation and management of suspected acute coronary syndrome (myocardial
infarction, unstable angina) in the emergency department")

• Serum lipase and amylase and pancreatic imaging in patients with findings suggesting pancreatitis
(see "Clinical manifestations and diagnosis of acute pancreatitis")

DIAGNOSIS — The diagnosis of Centruroides or Parabuthus scorpion envenomation is based upon the
following findings:

● Recent visit to or residing in an endemic region for the scorpion (see 'Regional epidemiology' above)
● History of a scorpion sting (often not present)
● Characteristic signs of envenomation (table 2) (see 'Clinical manifestations' above)

Supportive laboratory findings in patients with severe envenomation (Grade III or IV (table 2)) include
evidence of rhabdomyolysis and, rarely, pancreatitis.

Young children from endemic areas presenting with unusual neurologic symptoms (such as agitation,
choreiform movement, or abnormal eye movements) may be assumed to have been envenomed without
history of a sting or scorpion. However, the clinician should always consider other possible diagnoses when
evaluating a patient suspected of scorpion envenomation. (See 'Differential diagnosis' below.)

In older patients, a history of scorpion sting is typically present. However, scorpion stings may be confused
with a wide array of other diagnoses as described below. Although geographically confined in the United
States, scorpions have been known to "hitchhike" on passenger baggage or freight and cause stings in

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regions far removed from the Southwest.

DIFFERENTIAL DIAGNOSIS — Conditions with symptoms that may overlap with those of scorpion
envenomation include:

● Spider bite – Bites or stings from other arthropods may present with symptoms similar to scorpion
envenomation. Specifically, black widow envenomation may produce hypertension, tachycardia,
sweating, and other signs of adrenergic excess. However, it does not produce the abnormal eye
movements, fasciculations, or paresthesias, or induce a positive tap test as found with C. exilicauda
(sculpturatus) scorpion stings. In addition, black widow spider bites frequently produce a characteristic
halo lesion at the site, whereas C. exilicauda stings produce no such lesion. (See "Management of widow
spider bites".)

● Tetanus – Generalized tetanus infection may present up to one month after sustaining a tetanus prone
wound. Signs include autonomic symptoms of irritability, restlessness, diaphoresis, and tachycardia.
These findings are accompanied by trismus, dysphagia, opisthotonus, and severe muscle spasms with
an intact mental status. Although similar in many respects to Grade III or IV scorpion envenomation (table
2). The characteristic ocular movements seen (eg, opsoclonus and primary positional nystagmus) in
victims of a scorpion sting help to differentiate these diagnoses. (See "Tetanus", section on 'Clinical
features'.)

● Botulism – Botulism is a rare but potentially life-threatening neuroparalytic syndrome resulting from the
action of a neurotoxin elaborated by the microorganism Clostridium botulinum. Botulism is classically
described as the acute onset of bilateral cranial neuropathies associated with symmetric descending
weakness. The Centers for Disease Control (CDC) has also suggested that the following be considered
as key features of the botulism syndrome:

• Absence of fever
• Symmetric neurologic deficits
• The patient remains responsive
• Normal or slow heart rate and normal blood pressure
• No sensory deficits with the exception of blurred vision

Thus, in contrast to a scorpion sting, botulism does not cause hypersalivation, opsoclonus, fasciculation,
or painful skeletal muscle contractions. (See "Botulism", section on 'Clinical manifestations'.)

● Neuroblastoma – Opsoclonus-myoclonus-syndrome (abnormal eye movements) is a well-known


paraneoplastic syndrome that occurs in 1 to 3 percent of cases of neuroblastoma. Conversely, as many
as 50 percent of children with opsoclonus-myoclonus have an underlying neuroblastoma. The
characteristic symptoms of OMA are rapid, dancing eye movements, rhythmic jerking, and/or ataxia.
Unlike children with severe scorpion envenomation, those with neuroblastoma do not typically
demonstrate hypersalivation, acute onset of cranial nerve deficits, or skeletal muscle effects. (See
"Clinical presentation, diagnosis, and staging evaluation of neuroblastoma", section on 'Opsoclonus
myoclonus'.)

● Toxic exposures – Several poisons have physical findings similar to those of scorpion envenomation:

• Organophosphates – Organophosphate compound and nicotine ingestion can cause excessive


oral secretions and muscle fasciculations. However, organophosphate and nicotine overdose
frequently cause paralysis and true seizures with loss of consciousness, which is not seen with

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scorpion envenomation. (See "Organophosphate and carbamate poisoning".)

• Drugs of abuse and selected pharmaceutical agents – Sympathomimetic agents (eg,


methamphetamines, cocaine), dissociative agents (eg, phencyclidine [PCP]), and anticholinergic
agents (eg, antihistamines, Jimson weed) often cause motor excitability and hyperthermia that is
similar to the skeletal muscle findings seen after a severe scorpion sting. (See "Anticholinergic
poisoning" and "Phencyclidine (PCP) intoxication in children and adolescents" and "Phencyclidine
(PCP) intoxication in adults" and "Methamphetamine: Acute intoxication".)

A case series of 18 inadvertent methamphetamine poisonings among children in central Arizona


included three victims initially misdiagnosed with a scorpion sting and inappropriately treated with
antivenom; one patient had an anaphylactic reaction [31]. However, poisoning with these agents
does not typically cause cranial nerve findings and is usually associated with delirium.

• Strychnine – Strychnine intoxication, tetanus, or dystonic reactions from medicines that antagonize
dopamine receptors (eg, antipsychotic agents) may all present with painful muscle contraction (eg,
opisthotonus), tonic-clonic movements, and a preserved mental status, similar to the clinical picture
of severe scorpion envenomation. A history of an infected wound (tetanus), exposure to a
precipitating agent (dystonic reaction), or strychnine ingestion can facilitate making these alternative
diagnoses. In addition, patients with tetanus and strychnine exposure do not typically have abnormal
eye movements, and patients with dystonia usually respond rapidly to administration of
diphenhydramine or benztropine. (See "Tetanus" and "Strychnine poisoning" and "Treatment of
dystonia".)

● Seizure – Patients with seizures may have muscle movements similar to victims of scorpion
envenomation but usually do not have an intact mental status or the characteristic roving eye
movements that are seen in victims after a scorpion sting.

● Meningitis – Fever, neck stiffness, hypertonia, and cerebrospinal fluid pleocytosis are seen in children
with meningitis and, rarely, in those with severe scorpion envenomation [29]. As with many other
diagnoses, abnormal eye movements are characteristically not seen with meningitis. (See "Bacterial
meningitis in children older than one month: Clinical features and diagnosis", section on 'Clinical
features'.)

● Esophageal or airway foreign body – Excessive oral secretions and respiratory distress from a
scorpion sting may mimic the presentation of an upper airway or esophageal foreign body. However,
paresthesias, skeletal muscle abnormalities, and cranial nerve abnormalities are not seen in patients with
foreign bodies.

● Status asthmaticus – Occasional wheezing may occur following a Centruroides sting and be mistaken
for an asthma exacerbation until systemic symptoms (eg, paresthesias, neurologic abnormalities)
become evident.

MANAGEMENT — The management of scorpion stings is determined by the severity of envenomation (table
2).

Pain without neuromuscular toxicity — Most scorpion stings result in Grade I or II envenomation (table 2)
[1]. Treatment consists of [12]:

● Pain management:

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• Mild to moderate local pain and/or paresthesias (Grade I envenomation): Pain control such as oral
ibuprofen, other nonsteroidal antiinflammatory drug (NSAID), or oral opioid medications

• Severe local or remote pain and/or paresthesias (Grade II envenomation): Regional anesthesia for
extremity stings; short-acting intravenous opioids (eg, fentanyl) if regional anesthesia not feasible or
effective)

● Wound management:

• Cleansing of the sting site


• Tetanus prophylaxis, as needed (table 3)

• These patients should be observed for 4 hours to ensure no further progression of symptoms.
Progression of symptoms in young children may occur rapidly [5,25]. (See 'Clinical manifestations'
above.)

Prior to discharge, patients should tolerate oral intake, have no progression of symptoms, and their pain
should be adequately controlled with oral medications.

Neuromuscular toxicity — When managing a suspected scorpion envenomation with Grade III or IV severity
(table 2), we encourage consultation with a regional poison control center (WHO list of international poison
control centers or, in the United States, call 1-800-2222-1222) or physician with experience managing
scorpion stings.

Antivenom — We suggest that patients with Grade III or IV envenomation (table 2) after Centruroides
scorpion envenomation (skeletal muscle and/or cranial nerve dysfunction) receive intravenous scorpion-
specific antivenom. We also suggest antivenom administration for Grade III or IV envenomation caused by
Parabuthus species. However, as discussed below, evidence is less clear that Parabuthus antivenom is
effective.

A list of major scorpion antivenoms with manufacturer contact information is available here.

Centruroides antivenom (Anascorp, United States; Alacramyn, Mexico) is widely available in Mexico and
Central America. Anascorp is also approved for use in the United States [32]. In the United States, further
information about administering or obtaining scorpion-specific F(ab')2 equine antivenom may be obtained
from the nearest regional poison control center at 1-800-222-1222.

● Dosing and administration – Centruroides scorpion-specific F(ab')2 equine antivenom is given


intravenously in a dose of three vials dissolved in 20 to 50 mL of normal saline infused over 30 minutes.
Subsequent single vial doses of Centruroides antivenom, up to a total of five vials administered at 30
minutes intervals after the initial three vials may be given until resolution of symptoms.

For Parabuthus scorpion-specific F(ab')2 equine antivenom dosing and administration, consult the
manufacturer’s directions (SAIMR Scorpion Venom Antiserum SAVP, South Africa).

It is important for the patient and/or guardian to understand that the vast majority of Centruroides
scorpion envenomations are unlikely to be a fatal; severe envenomations in very small children are likely
the only potential exception. Therefore, antivenom is almost always not life-saving. However, without
antivenom, the patient will likely have a prolonged period of distressing symptoms. Of all available
treatments, current evidence indicates antivenom is likely to be effective and may significantly reduce the
duration of suffering and hospitalization.

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Prior to the administration of antivenom, medications and equipment for the treatment of anaphylaxis
should be immediately available, including IV fluids, epinephrine, and intubation equipment. Whenever
possible, antivenom should be administered in settings capable of emergency or intensive care.

Allergic reactions should be managed by immediately stopping intravenous infusion of the antivenom (if
applicable) and treating symptoms appropriately (table 4 and table 5). (See "Anaphylaxis: Emergency
treatment".)

Although limited evidence suggests that the risk of serum sickness after scorpion-specific F(ab')2 equine
antivenom is low [22,33]. All patients receiving antivenom should be informed of the possibility of serum
sickness and the symptoms suggestive of serum sickness and advised to seek medical care if such
symptoms occur. (See "Serum sickness and serum sickness-like reactions".)

● Efficacy – The evidence for efficacy of scorpion antivenom varies by species and region as follows:

• United States – Centruroides scorpion-specific F(ab')2 equine antivenom has been distributed to
rural hospitals in Arizona by legislative mandate. Previously used Centruroides goat-derived
antivenom was associated with a 3 percent frequency of immediate hypersensitivity reactions and up
to a 60 percent risk of delayed serum sickness and is no longer used [7,33].

Preliminary evidence indicates that intravenous scorpion-specific F(ab')2 equine antivenom markedly
reduces the duration of clinical signs and symptoms in patients with Grade III or IV and appears to
have a lower risk of anaphylaxis. In a blinded trial of scorpion-specific F(ab')2 antivenom (Anascorp)
in 15 children, ages 6 months to 18 years, who were admitted to a pediatric intensive care unit, total
resolution of clinical symptoms occurred within 4 hours of treatment in all eight antivenom recipients
versus one of seven placebo recipients [33]. Plasma venom concentrations were undetectable in all
eight antivenom recipients but in only one placebo recipient 1 hour after treatment. No immediate
hypersensitivity or symptoms of serum sickness occurred in patients receiving the antivenom.

Although Centruroides F(ab)2 antivenom is expensive, its use is probably cost-effective when given
to patients with severe envenomation because the length of intensive care and hospitalization is
significantly shortened.

• Mexico and Central America – In Mexico, scorpion-specific equine antivenom with activity against
several Centruroides species has long been used because of the higher risk of mortality in these
patients and the lower risk of medical complications [22]. In a large observational study of 38,068
adults and children from Mexico, 20,000 received horse serum antivenom with no immediate
hypersensitivity reactions and no deaths [22].

• Southern Africa – Although recommended by regional experts, evidence is lacking to show efficacy
of Parabuthus antivenom [10,24,25]. Victims of scorpion stings in Africa often have delayed
presentation for medical care and, in many cases, postpone medical care while receiving traditional
treatments. This delay makes assessment of the effectiveness of antivenom difficult because it is
less likely to be effective once severe toxicity is established in the patient.

Supportive care — All patients with Grade III or IV scorpion envenomations should be admitted to a unit
capable of providing intensive supportive care.

Key supportive interventions for these patients include:

● Frequent suctioning of oral secretions.

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● Endotracheal intubation in patients with significant difficulties maintaining their airway or with pulmonary
edema accompanied by hypoxemia.

● Close monitoring for and treatment of myocardial ischemia and/or acute decompensated heart failure in
patients at risk.

● Intravenous fentanyl for pain. Fentanyl is preferred if antivenom administration is planned because, unlike
morphine, fentanyl does not cause histamine release.

● If antivenom is not used, intravenous benzodiazepines (lorazepam or continuous midazolam infusion),


titrated to effect, for sedation and to treat muscle spasticity.

Benzodiazepines should be used carefully or avoided if antivenom administration is planned. Antivenom


reverses the excitatory effects of the scorpion venom and children who have received high doses of
long-acting benzodiazepines (eg, lorazepam) may become oversedated, occasionally requiring
intubation. Thus, a short-acting benzodiazepine (eg, midazolam) is preferred for management of excess
muscle activity and anxiety in pediatric patients. Once antivenom is administered, the clinician should
closely monitor respiratory and mental status for signs of oversedation and further dosing with
benzodiazepines should be avoided.

ADDITIONAL RESOURCES — To obtain emergent consultation with a medical toxicologist, call the United
States Poison Control Network at 1-800-222-1222, or access the World Health Organization's list of
international poison centers.

Consultation with medical toxicologists experienced in treating Centruroides and other scorpion
envenomations in the United States can be obtained by calling the Banner Poison Control Center in Phoenix
at 1-602-495-4884 or the Arizona Poison and Drug Information Center in Tucson at 1-520-626-6016.

A list of major scorpion antivenoms with manufacturer contact information is available here.

PREVENTION — Reducing small cracks and crevices in homes decreases the risk of human-scorpion
interactions. In scorpion-infested areas, clothing, shoes, packages, and camping gear should be shaken out
and checked for scorpions. Footwear is recommended. Unnecessary ground cover and debris should be
removed to reduce potential nesting places.

Certain insecticides, including organophosphates, pyrethrins, and several chlorinated hydrocarbons, are
known to kill scorpions. Spraying insecticides around the home can work indirectly by killing other insects in
the area and reducing the scorpions' food supply. A village-wide scorpion eradication program with pyrethroid
insecticides in the state of Morelos, Mexico reduced the incidence of scorpion stings by 17 percent [34].

SUMMARY AND RECOMMENDATIONS

● Dangerous species capable of neuromuscular toxicity after envenomation include Centruroides in the
United States, Mexico and Central America (picture 5) and Parabuthus in Southern Africa (table 1). (See
'Scorpion geography and appearance' above.)

● Scorpion stings are usually accidental because scorpions would rather escape humans than attack.
Stings most commonly occur when a human unintentionally steps on a scorpion or reaches under wood
or rocks. (See 'Clinical manifestations' above.)

● Findings after Centruroides or Parabuthus scorpion envenomation are categorized into four degrees of
severity (table 2). The majority of scorpion envenomations cause local or no pain with minimal to no

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inflammation. When present, symptoms may begin immediately and typically progress to maximum
severity within 5 hours. Up to 30 percent of patients stung by Centruroides or Parabuthus scorpions
develop neuromuscular toxicity. Although adults appear to be envenomed more often, children are more
likely to develop severe illness requiring intensive supportive care (See 'Clinical manifestations' above
and 'Grading of severity' above.)

● Laboratory studies are not needed in patients with mild (Grade I to II) envenomation. At minimum,
patients with severe effects (Grade III to IV) should undergo assessment as follows (see 'Laboratory
evaluation' above):

• Serum electrolytes
• Liver enzymes (aspartate aminotransferase [AST] and alanine aminotransferase [ALT])
• Blood urea nitrogen and serum creatinine
• Serum creatine kinase
• Urinalysis

Additional studies are necessary for patients with findings of acute coronary syndrome, pancreatitis, or
disseminated intravascular coagulopathy.

● The diagnosis of Centruroides or Parabuthus scorpion envenomation is based upon the following
findings (see 'Diagnosis' above):

• Recent visit to or residing in an endemic region for the scorpion (see 'Regional epidemiology' above)
• History of a scorpion sting (often not present)
• Characteristic signs of envenomation (table 2) (see 'Clinical manifestations' above)

● The management of scorpion stings is determined by the severity of envenomation (table 2). Treatment
of Grade I or II neuromuscular scorpion envenomation consists of pain control, wound management with
tetanus prophylaxis (table 3) as needed, and observation for 4 hours to ensure no progression of
symptoms. Prior to discharge, patients should tolerate oral intake, have no progression of symptoms, and
their pain should be adequately controlled with oral medications. (See 'Pain without neuromuscular
toxicity' above.)

● When managing a suspected scorpion envenomation with Grade III or IV severity (table 2), we
encourage consultation with a regional poison control center (WHO list of international poison control
centers or, in the United States, call 1-800-2222-1222) or physician with experience managing scorpion
stings. (See 'Neuromuscular toxicity' above.)

● We suggest that patients with Grade III or IV envenomation (table 2) after Centruroides scorpion
envenomation (skeletal muscle and/or cranial nerve dysfunction) receive intravenous scorpion-specific
antivenom (Grade 2B). We also suggest antivenom administration for Grade III or IV envenomation
caused by Parabuthus species (Grade 2C). A list of major scorpion antivenoms with manufacturer
contact information is available here. (See 'Antivenom' above.)

● All patients with Grade III or IV scorpion envenomations should be admitted to a unit capable of providing
intensive supportive care. Key supportive interventions for these patients include (see 'Supportive care'
above):

• Frequent suctioning of oral secretions.

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• Endotracheal intubation in patients unable to maintain their airway or who develop pulmonary
edema.

• Close monitoring for and treatment of myocardial ischemia and/or acute decompensated heart
failure in patients at risk.

• Intravenous fentanyl for pain. Fentanyl is preferred if antivenom administration is planned because,
unlike morphine, fentanyl does not cause histamine release.

• If antivenom is not used, intravenous benzodiazepines (eg, continuous midazolam infusion), titrated
to effect, for sedation and to treat muscle spasticity. Benzodiazepines should be used carefully or
avoided if antivenom administration is planned.

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Curry SC, Vance MV, Ryan PJ, et al. Envenomation by the scorpion Centruroides sculpturatus. J Toxicol
Clin Toxicol 1983-1984; 21:417.
2. Russell FE. Venomous arthropods. Vet Hum Toxicol 1991; 33:505.
3. Krifi MN, el Ayeb M, Ben Lasfar Z, et al. Improvement and standardization of antivenoms sera. Arch Inst
Pasteur Tunis 1992; 69:253.
4. Hutt MJ, Houghton PJ. A survey from the literature of plants used to treat scorpion stings. J
Ethnopharmacol 1998; 60:97.
5. LoVecchio F, McBride C. Scorpion envenomations in young children in central Arizona. J Toxicol Clin
Toxicol 2003; 41:937.
6. Gambhir IS, Singh DS, Pattnaik DN. Stroke in a young woman. Postgrad Med J 1998; 74:555.
7. LoVecchio F, Welch S, Klemens J, et al. Incidence of immediate and delayed hypersensitivity to
Centruroides antivenom. Ann Emerg Med 1999; 34:615.
8. Stipetic ME, Lugo A, Brown B, et al. A prospective analysis of 558 common striped scorpion
(Centruroides vittatus) envenomations in Texas during 1997 (meeting abstract). J Toxicol Clin Toxicol
1998; 36:461.
9. Larsen N. Parabuthus granulatus (Granulated thick-tailed scorpion). Biodiversity Explore: The web of life
in Southern Africa. http://www.biodiversityexplorer.org/arachnids/scorpions/buthidae/parabuthus_granula
tus.htm (Accessed on November 03, 2016).
10. Műller GJ, Modler H, Wium CA, Veale DJH. Scorpion sting in southern Africa: diagnosis and manageme
nt. CME 2012:30 http://www.cmej.org.za/index.php/cmej/article/view/2545/2580 (Accessed on Novembe
r 03, 2016).
11. Parabuthus transvaalicus (Transvaal thick-tailed scorpion). Biodiversity Explorer: The web of life in south
ern Africa. http://www.biodiversityexplorer.org/arachnids/scorpions/buthidae/parabuthus_transvaalicus.ht
m (Accessed on November 03, 2016).
12. Isbister GK, Bawaskar HS. Scorpion envenomation. N Engl J Med 2014; 371:457.
13. Chippaux JP. Emerging options for the management of scorpion stings. Drug Des Devel Ther 2012;
6:165.

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14. Debont T, Swerts A, Van der Walt JJ, et al. Comparison and characterization of the venoms of three
Parabuthus scorpion species occurring in southern Africa. Toxicon 1998; 36:341.
15. Vatanpour H, Rowan EG, Harvey AL. Effects of scorpion (Buthus tamulus) venom on neuromuscular
transmission in vitro. Toxicon 1993; 31:1373.
16. Garcia ML, Hanner M, Kaczorowski GJ. Scorpion toxins: tools for studying K+ channels. Toxicon 1998;
36:1641.
17. Inceoglu B, Lango J, Jing J, et al. One scorpion, two venoms: prevenom of Parabuthus transvaalicus
acts as an alternative type of venom with distinct mechanism of action. Proc Natl Acad Sci U S A 2003;
100:922.
18. Arie-Saadia G, Sofer S, Zlotkin E, Shainberg A. Effect of Leiurus quinquestriatus hebreus venom on
calcium and deoxyglucose uptake in cultured cardiac cells. Toxicon 1996; 34:435.
19. Quintero-Hernández V, Jiménez-Vargas JM, Gurrola GB, et al. Scorpion venom components that affect
ion-channels function. Toxicon 2013; 76:328.
20. Sofer S. Scorpion envenomation. Intensive Care Med 1995; 21:626.
21. Boyer L, Heubner K, McNally J, Buchanan P. Death from Centruroides scorpion sting allergy. J Toxicol
Clin Toxicol 2001; 39:561.
22. Dehesa-Dávila M, Possani LD. Scorpionism and serotherapy in Mexico. Toxicon 1994; 32:1015.
23. Klauber LM. Rattlesnakes: Their Habits, Life Histories, and Influence on Mankind, University of Californi
a Press, Berkeley 1997. Vol 1, p.838.
24. Müller GJ. Scorpionism in South Africa. A report of 42 serious scorpion envenomations. S Afr Med J
1993; 83:405.
25. Bergman NJ. Clinical description of Parabuthus transvaalicus scorpionism in Zimbabwe. Toxicon 1997;
35:759.
26. Amaral CF, Rezende NA. Both cardiogenic and non-cardiogenic factors are involved in the pathogenesis
of pulmonary oedema after scorpion envenoming. Toxicon 1997; 35:997.
27. Bergman NJ. Scorpion sting in Zimbabwe. S Afr Med J 1997; 87:163.
28. Clark RF, Selden BS, Kunkel DB, Frost MD. Abnormal eye movements encountered following severe
envenomations by Centruroides sculpturatus. Neurology 1991; 41:604.
29. Berg RA, Tarantino MD. Envenomation by the scorpion Centruroides exilicauda (C sculpturatus): severe
and unusual manifestations. Pediatrics 1991; 87:930.
30. Annobil SH. Scorpion stings in children in the Asir Province of Saudi Arabia. J Wilderness Med 1993;
4:241.
31. Kolecki P. Inadvertent methamphetamine poisoning in pediatric patients. Pediatr Emerg Care 1998;
14:385.
32. Approval letter - Anascorp. US Food and Drug Administration. http://www.fda.gov/BiologicsBloodVaccine
s/BloodBloodProducts/ApprovedProducts/LicensedProductsBLAs/FractionatedPlasmaProducts/ucm266
726.htm (Accessed on August 04, 2011).
33. Boyer LV, Theodorou AA, Berg RA, et al. Antivenom for critically ill children with neurotoxicity from
scorpion stings. N Engl J Med 2009; 360:2090.
34. Ramsey JM, Salgado L, Cruz-Celis A, et al. Domestic scorpion control with pyrethroid insecticides in
Mexico. Med Vet Entomol 2002; 16:356.

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Topic 6490 Version 19.0

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GRAPHICS

Scorpion anatomy

The scorpion has a lobster-like body shape with seven sets of paired appendages: the
chelicerae, the pedipalps (claws or pinchers), four sets of legs, and the pectines
(comb-like structures on the ventral surface). The segmented tail curves up dorsally,
ending in the terminal bulbous segment called the telson, which contains paired venom
glands and the aculeus (stinger).

Reproduced with permission from: Harwood-Nuss, A, Wolfson, AB, et al. The Clinical Practice of
Emergency Medicine, Third Edition. Philadelphia: Lippincott Williams & Wilkins, 2001. Copyright
© 2001 Lippincott Williams & Wilkins.

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Centruroides exilicauda

Courtesy of Banner Good Samaritan Medical Center, Department of Medical


Toxicology.

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Centruroides exilicauda (sculpturatus) or bark scorpion

Courtesy of Banner Good Samaritan Medical Center, Department of Medical


Toxicology.

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Centruroides exilicauda (sculpturatus) or bark scorpion

Courtesy of Banner Good Samaritan Medical Center, Department of Medical


Toxicology.

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Scorpion exhibiting fluorescence under ultraviolet light

Courtesy of Banner Good Samaritan Medical Center, Department of Medical


Toxicology.

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Common scorpions by region and potential toxicity*

For assistance in managing a patient with a suspected scorpion envenomation, contact a regional poison control
center (WHO list of international poison control centers or, in the United States, call 1-800-222-1222 ). A list of
major scorpion antivenoms with manufacturer contact information is available here.

RCTs in humans
show antivenom
Clinical
Region Scorpion species reduces duration
manifestations
and severity of
symptoms?

North Africa Androctonus Autonomic storm No


Buthus Myocardial depression

Leiurus Pulmonary edema

Middle East (including Leiurus Autonomic storm No


Turkey, Iran, and Androctonus Cardiac dysfunction
Lebanon) Pulmonary edema
Israel Acute pancreatitis

Asia Hottentotta (Mesobuthus, Autonomic storm Yes


India, Pakistan, and Sri Myocardial depression
Lanka) Pulmonary edema
Androctonus

Hemiscorpius (Iran) Local tissue necrosis, No


rarely hemolysis and
acute kidney injury

South America Tityus Autonomic storm No


Caribbean (Trinidad) Myocardial depression
Pulmonary edema
Acute pancreatitis

Central America, Mexico, Centruroides Autonomic signs Yes


and southwestern United (primarily
States parasympathetic)
Neuromuscular toxicity

Tityus (Central America As above


only)

Southern Africa Parabuthus Autonomic signs No


(primarily
parasympathetic)
Neuromuscular toxicity

Autonomic storm occurs after stings of "Old World" scorpions that inhabit North Africa, the Middle East, Asia, and
South America. It manifests as a combination of:
Parasympathetic signs: Salivation, lacrimation, vomiting, diarrhea, bronchorrhea, bronchospasm,
diaphoresis, bradycardia, hypotension, miosis, and priapism.
Sympathetic signs: Tachycardia, hypertension, agitation, dilated pupils, and hyperthermia.
Cardiac conduction abnormalities arise from the combined autonomic effects and occur in up to half of
patients. They include atrial tachycardia, preventricular contractions, T-wave and ST-T wave changes, and
bundle branch block.
Myocardial depression is caused by the autonomic disturbance and can progress to cardiogenic shock with

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pulmonary edema.
Parasympathetic findings are present for the first few hours after an "Old World" scorpion sting; sympathetic
effects and myocardial depression persist.
Neuromuscular toxicity follows stings by "New World" scorpions that live in Mexico, Central America, Western
and Southern Africa, and parts of the United States. Findings consist of:
Cranial nerve dysfunction with slurred speech, dysphagia, drooling, tongue fasciculations, blurred vision,
and abnormal eye movements (eg, conjugate, roving, slow and involuntary motion with multidirectional
conjugate saccades [similar to opsoclonus] and unsustained primary positional nystagmus).
Somatic skeletal muscle dysfunction appearing as undulating and writhing restlessness, fasciculations,
extremity shaking and jerking, opisthotonos (arching of the back), and emprosthotonos (tetanic forward
body flexion) with preservation of alertness.

RCT: randomized controlled trials.


* Envenomation with systemic effects occur in approximately one-third of stings. All of these scorpion stings are
associated with local pain and paresthesias. Refer to UpToDate topics on scorpion stings for further discussion of clinical
manifestations, diagnosis, and treatment of scorpion stings.

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Centruroides exilicauda (bark scorpion)

Courtesy of Mitchell Ross, MD.

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Scorpion envenomation with neuromuscular toxicity: Grading of severity and


treatment

For assistance in managing a patient with a suspected scorpion envenomation, contact a regional poison control
center (WHO list of international poison control centers, or, in the United States, call 1-800-222-1222). A list of
major scorpion antivenoms with manufacturer contact information is available here.

Grade Clinical findings Treatment

I Localized pain or paresthesias at site Pain management (eg, ibuprofen)


Local wound care
Tetanus prophylaxis

II Local and remote pain or paresthesias As above, regional anesthesia (eg, digital block) for
severe local pain; intravenous opioids (eg,
fentanyl) for severe remote pain

III As above, and: Antivenom, if available*

Cranial nerve dysfunction: Abnormal eye Supportive care:


movements, dysphagia, drooling, and/or slurred Frequent suctioning of oral secretions
speech Endotracheal intubation if airway compromise
OR or pulmonary edema with hypoxemia
Monitor for and treat myocardial ischemia,
Somatic skeletal neuromuscular
heart failure, and rhabdomyolysis ¶
dysfunction: Undulating and writhing
restlessness, fasciculations, extremity shaking Treat pain with intravenous opioids (eg,
and jerking, opisthotonos (arching of the back), fentanyl ∆ )
and emprosthotonos (tetanic forward body If antivenom is not available, treat muscle
flexion) with preservation of alertness. activity and anxiety with short-acting
benzodiazepines (eg, midazolam) ◊
Autonomic dysfunction:
Provide local wound care as above
Centruoides: Salivation, vomiting,
bronchoconstriction, diaphoresis, and
tachycardia most frequent.
Parabuthus: Salivation, vomiting, and
urinary retention most frequent.

IV All above features present

Grading scale and treatment following envenomation with Centruroides species (southwestern United States,
Mexico, and Central America) and Parabuthus species (southern Africa).

* To obtain antivenom in the United States, contact the nearest regional poison control center at 1-800-222-1222.
¶ Refer to UpToDate topics on the recognition and emergency treatment of myocardial infarction, heart failure, and
rhabdomyolysis.
∆ If antivenom administration is planned, fentanyl is preferred because it promotes less antihistamine release than
morphine.
◊ Benzodiazepines should be used carefully or avoided if antivenom administration is planned because antivenom reverses
the excitatory effects of scorpion venom and patients who have received high doses of benzodiazepines may develop
excessive sedation and respiratory compromise.

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Wound management and tetanus prophylaxis

Clean and minor wound All other wounds ¶


Previous doses
of tetanus Tetanus toxoid- Tetanus toxoid-
Human tetanus Human tetanus
toxoid* containing containing
immune globulin immune globulin ◊
vaccine ∆ vaccine ∆

<3 doses or Yes § No Yes § Yes


unknown

≥3 doses Only if last dose No Only if last dose No


given ≥10 years ago given ≥5 years ago ¥

Appropriate tetanus prophylaxis should be administered as soon as possible following a wound but should be given
even to patients who present late for medical attention. This is because the incubation period is quite variable;
most cases occur within 8 days, but the incubation period can be as short as 3 days or as long as 21 days. For
patients who have been vaccinated against tetanus previously but who are not up to date, there is likely to be little
benefit in administering human tetanus immune globulin more than one week or so after the injury. However, for
patients thought to be completely unvaccinated, human tetanus immune globulin should be given up to 21 days
following the injury; Td or Tdap should be given concurrently to such patients.

* Tetanus toxoid may have been administered as diphtheria-tetanus toxoids adsorbed (DT), diphtheria-tetanus-whole cell
pertussis (DTP, DTwP; no longer available in the United States), diphtheria-tetanus-acellular pertussis (DTaP), tetanus-
diphtheria toxoids adsorbed (Td), booster tetanus toxoid-reduced diphtheria toxoid-acellular pertussis (Tdap), or tetanus
toxoid (TT).
¶ Such as, but not limited to, wounds contaminated with dirt, feces, soil, or saliva; puncture wounds; avulsions; wounds
resulting from missiles, crushing, burns, or frostbite.
∆ The preferred vaccine preparation depends upon the age and vaccination history of the patient:
<7 years: DTaP
Underimmunized children ≥7 and <11 years who have not received Tdap previously: Tdap. Children who receive
Tdap between age 7 and 11 years do not require revaccination at age 11 years.
≥11 years: A single dose of Tdap is preferred to Td for all individuals in this age group who have not previously
received Tdap. Pregnant women should receive Tdap during each pregnancy.
Td is preferred to TT for those who received Tdap previously and when Tdap is not available.
◊ 250 units intramuscularly at a different site than tetanus toxoid; intravenous immune globulin should be administered if
human tetanus immune globulin is not available.
§ The vaccine series should be continued through completion as necessary.
¥ Booster doses given more frequently than every five years are not needed and can increase adverse effects.

Data from:
1. Advisory Committee on Immunization Practices. Recommended adult immunization schedule: United States, 2012.
Ann Intern Med 2012; 156:211.
2. Centers for Disease Control and Prevention (CDC). Updated recommendations for use of tetanus toxoid, reduced
diphtheria toxoid and acellular pertussis (Tdap) vaccine from the Advisory Committee on Immunization Practices,
2010. MMWR Morb Mortal Wkly Rep 2011; 60:13.
3. Centers for Disease Control and Prevention. Updated recommendations for use of tetanus toxoid, reduced
diphtheria toxoid, and acellular pertussis (Tdap) vaccine in adults aged 65 years and older — Advisory Committee
on Immunization Practices (ACIP), 2012. MMWR Morb Mortal Wkly Rep 2012; 61:468.
4. Centers for Disease Control and Prevention (CDC). Updated recommendations for use of tetanus toxoid, reduced
diphtheria toxoid, and acellular pertussis vaccine (Tdap) in pregnant women--Advisory Committee on Immunization
Practices (ACIP), 2012. MMWR Morb Mortal Wkly Rep 2013; 62:131.
5. Immunization Action Coalition. Ask the experts: Diseases & vaccines - Diphtheria, tetanus, pertussis.
http://www.immunize.org/askexperts/experts_per.asp#wound (Accessed September 6, 2017.)
Adapted from: American Academy of Pediatrics. Tetanus (lockjaw). In: Red Book: 2015 Report of the Committee on
Infectious Diseases, 30th Edition, Kimberlin DW, Brady MT, Jackson MA, Long SS (Eds), American Academy of Pediatrics,
Elk Grove Village, IL 2015.

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Rapid overview: Emergency management of anaphylaxis in adults

Diagnosis is made clinically:


The most common signs and symptoms are cutaneous (eg, sudden onset of generalized urticaria, angioedema,
flushing, pruritus). However, 10 to 20% of patients have no skin findings.

Danger signs: Rapid progression of symptoms, respiratory distress (eg, stridor, wheezing, dyspnea,
increased work of breathing, persistent cough, cyanosis), vomiting, abdominal pain, hypotension,
dysrhythmia, chest pain, collapse.

Acute management:
The first and most important treatment in anaphylaxis is epinephrine. There are NO absolute contraindications
to epinephrine in the setting of anaphylaxis.

Airway: Immediate intubation if evidence of impending airway obstruction from angioedema. Delay may lead to
complete obstruction. Intubation can be difficult and should be performed by the most experienced clinician
available. Cricothyrotomy may be necessary.

Promptly and simultaneously, give:

IM epinephrine (1 mg/mL preparation): Give epinephrine 0.3 to 0.5 mg intramuscularly, preferably in the
mid-outer thigh. Can repeat every 5 to 15 minutes (or more frequently), as needed. If epinephrine is injected
promptly IM, most patients respond to one, two, or at most, three doses. If symptoms are not responding to
epinephrine injections, prepare IV epinephrine for infusion (see below).

Place patient in recumbent position, if tolerated, and elevate lower extremities.

Oxygen: Give 8 to 10 L/minute via facemask or up to 100% oxygen, as needed.

Normal saline rapid bolus: Treat hypotension with rapid infusion of 1 to 2 liters IV. Repeat, as needed. Massive
fluid shifts with severe loss of intravascular volume can occur.

Albuterol (salbutamol): For bronchospasm resistant to IM epinephrine, give 2.5 to 5 mg in 3 mL saline via
nebulizer. Repeat, as needed.

Adjunctive therapies:

H1 antihistamine*: Consider giving diphenhydramine 25 to 50 mg IV (for relief of urticaria and itching only).

H2 antihistamine*: Consider giving ranitidine 50 mg IV.

Glucocorticoid*: Consider giving methylprednisolone 125 mg IV.

Monitoring: Continuous noninvasive hemodynamic monitoring and pulse oximetry monitoring should be
performed. Urine output should be monitored in patients receiving IV fluid resuscitation for severe hypotension or
shock.

Treatment of refractory symptoms:


Epinephrine infusion ¶ : For patients with inadequate response to IM epinephrine and IV saline, give epinephrine
continuous infusion, beginning at 0.1 mcg/kg/minute by infusion pump ∆ . Titrate the dose continuously
according to blood pressure, cardiac rate and function, and oxygenation.

Vasopressors ¶ : Some patients may require a second vasopressor (in addition to epinephrine). All vasopressors
should be given by infusion pump, with the doses titrated continuously according to blood pressure and cardiac
rate/function and oxygenation monitored by pulse oximetry.

Glucagon: Patients on beta-blockers may not respond to epinephrine and can be given glucagon 1 to 5 mg IV
over 5 minutes, followed by infusion of 5 to 15 mcg/minute. Rapid administration of glucagon can cause vomiting.

Instructions on how to prepare and administer epinephrine for IV continuous infusions are available as separate
tables in UpToDate.

IM: intramuscular; IV: intravenous.


* These medications should not be used as initial or sole treatment.
¶ All patients receiving an infusion of epinephrine and another vasopressor require continuous noninvasive monitoring of

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blood pressure, heart rate and function, and oxygen saturation.


∆ For example, the initial infusion rate for a 70 kg patient would be 7 mcg/minute. This is consistent with the
recommended range for non-weight-based dosing for adults, which is 2 to 10 mcg/minute. Non-weight-based dosing can
be used if the patient's weight is not known and cannot be estimated.

Adapted from: Simons FER. Anaphylaxis. J Allergy Clin Immunol 2010; 125:S161.

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Rapid overview: Emergent management of anaphylaxis in infants and children*

Diagnosis is made clinically:


The most common signs and symptoms are cutaneous (eg, sudden onset of generalized urticaria, angioedema,
flushing, pruritus). However, 10 to 20% of patients have no skin findings.

Danger signs: Rapid progression of symptoms, evidence of respiratory distress (eg, stridor, wheezing,
dyspnea, increased work of breathing, retractions, persistent cough, cyanosis), signs of poor
perfusion, abdominal pain, vomiting, dysrhythmia, hypotension, collapse.

Acute management:
The first and most important therapy in anaphylaxis is epinephrine. There are NO absolute contraindications
to epinephrine in the setting of anaphylaxis.

Airway: Immediate intubation if evidence of impending airway obstruction from angioedema. Delay may lead to
complete obstruction. Intubation can be difficult and should be performed by the most experienced clinician
available. Cricothyrotomy may be necessary.

IM epinephrine (1 mg/mL preparation): Epinephrine 0.01 mg/kg should be injected intramuscularly in the
mid-outer thigh. For large children (>50 kg), the maximum is 0.5 mg per dose. If there is no response or the
response is inadequate, the injection can be repeated in 5 to 15 minutes (or more frequently). If epinephrine is
injected promptly IM, patients respond to one, two, or at most, three injections. If signs of poor perfusion are
present or symptoms are not responding to epinephrine injections, prepare IV epinephrine for infusion (see
below).

Place patient in recumbent position, if tolerated, and elevate lower extremities.

Oxygen: Give 8 to 10 L/minute via facemask or up to 100% oxygen, as needed.

Normal saline rapid bolus: Treat poor perfusion with rapid infusion of 20 mL/kg. Re-evaluate and repeat fluid
boluses (20 mL/kg), as needed. Massive fluid shifts with severe loss of intravascular volume can occur. Monitor
urine output.

Albuterol: For bronchospasm resistant to IM epinephrine, give albuterol 0.15 mg/kg (minimum dose: 2.5 mg) in
3 mL saline inhaled via nebulizer. Repeat, as needed.

H1 antihistamine: Consider giving diphenhydramine 1 mg/kg (max 40 mg) IV.

H2 antihistamine: Consider giving ranitidine 1 mg/kg (max 50 mg) IV.

Glucocorticoid: Consider giving methylprednisolone 1 mg/kg (max 125 mg) IV.

Monitoring: Continuous noninvasive hemodynamic monitoring and pulse oximetry monitoring should be
performed. Urine output should be monitored in patients receiving IV fluid resuscitation for severe hypotension or
shock.

Treatment of refractory symptoms:


Epinephrine infusion ¶ : In patients with inadequate response to IM epinephrine and IV saline, give epinephrine
continuous infusion at 0.1 to 1 mcg/kg/minute, titrated to effect.

Vasopressors ¶: Patients may require large amounts of IV crystalloid to maintain blood pressure. Some patients
may require a second vasopressor (in addition to epinephrine). All vasopressors should be given by infusion
pump, with the doses titrated continuously according to blood pressure and cardiac rate/function monitored
continuously and oxygenation monitored by pulse oximetry.

IM: intramuscular; IV: intravenous.


* A child is defined as a prepubertal patient weighing less than 40 kg.
¶ All patients receiving an infusion of epinephrine and/or another vasopressor require continuous noninvasive monitoring
of blood pressure, heart rate and function, and oxygen saturation. We suggest that pediatric centers provide instructions
for preparation of standard concentrations and also provide charts for established infusion rate for epinephrine and other
vasopressors in infants and children.

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Contributor Disclosures
Frank LoVecchio, DO, MPH, FACEP Nothing to disclose Daniel F Danzl, MD Nothing to
disclose Stephen J Traub, MD Nothing to disclose Michele M Burns, MD, MPH Nothing to disclose James
F Wiley, II, MD, MPH Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.

Conflict of interest policy

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