INTRODUCTION — This topic will discuss the clinical manifestations, diagnosis, and treatment of scorpion envenomations from species from North Africa, the Middle East, Asia, South America, and the Republic of Trinidad and Tobago whose stings cause autonomic dysfunction ("autonomic storm") with cardiotoxicity.
The clinical manifestations, diagnosis, and treatment of scorpion that cause neuromuscular toxicity or skin necrosis in other parts of the world are discussed in detail separately. (See "Scorpion envenomation causing neuromuscular toxicity (United States, Mexico, Central America, and Southern Africa)" and "Scorpion envenomation causing skin necrosis, hemolysis, DIC, and acute kidney injury (Middle East)".)
ENTOMOLOGY — Scorpions belong to the phylum Arthropoda. They 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. Scorpions fluoresce when illuminated by ultraviolet light, as from a black light or a medical Wood's lamp (picture 1). This physical property is used to collect scorpions and for pest control. Additional entomology of scorpions is discussed separately. (See "Scorpion envenomation causing neuromuscular toxicity (United States, Mexico, Central America, and Southern Africa)", section on 'Entomology'.)
Geographical distribution and appearance — Dangerous scorpion species capable of causing autonomic dysfunction or "autonomic storm" and their reported geographical distribution include (table 1):
●Tityus (South America, Republic of Trinidad and Tobago) [1-4]
●Androctonus (North Africa, Middle East, Israel, India, Pakistan, and Southeast Asia) [1,5-9]
●Buthus (Mediterranean Spain, North Africa, Middle East) [1,8,10]
●Leiurus (North Africa, the Middle East, Israel, Lebanon, Turkey, and Iran) [1,7,8,11-14]
●Hottentotta (previously Mesobuthus; Asia, especially India) [1,8,15-17]
The appearance and habitat of specific scorpions most commonly responsible for serious clinical effects after stings are as follows:
●Androctonus australis – A. australis (the "yellow fat-tailed scorpion") can grow up to 10 cm in length [18]. Coloration may vary, but it is typically yellow with darker palpal pincers. It has a thick cauda. This scorpion is found in desert regions, including mountainous terrain in North Africa, the Middle East, and India.
●Androctonus crassicauda – A. crassicauda ("Arabian fat-tailed scorpion") is a black scorpion that grows to 12 cm in length and resides in deserts of the Middle East and North Africa [1].
●Buthus occitanus – B. occitanus (the yellow scorpion) is a yellow or yellow-brown scorpion up to 8 cm in length that predominately lives in desert habitats in North Africa [19]. It has also been found in southwestern Europe (Portugal, Spain, and France) although envenomations from the European form is not associated with serious systemic effects.
●Leiurus quinquestriatus – L. quinquestriatus ("death stalker") is a burrowing yellow scorpion that grows to 8 to 11 cm in length [11]. It resides in the deserts of North Africa and the Middle East (Arabian peninsula, Sinai peninsula, Israel, Lebanon, Turkey, and Iran). It is also imported from Egypt as an exotic species sold in Europe and the United States.
●Hottentotta (previously Mesobuthus or Buthus) tamulus – H. tamulus (the red scorpion) is approximately 9 cm in size and has red coloration. It is the most dangerous scorpion indigenous to India, inhabiting tropical and subtropical lowlands [1,16]. It is also found in Pakistan, Sri Lanka [15], and Nepal.
●Tityus serrulatus – T. serrulatus (Brazilian yellow scorpion) has yellow pincers and cauda with dark brown tips and a dark body (picture 2) [1,3]. It achieves an adult size of 6 to 7 cm. T. serrulatus lives in tropical climates of Brazil.
Venom properties — Among the many constituents of scorpion venom, alpha-toxins produce a significant portion of human toxicity by binding to sodium channels in cell membranes and inhibiting inactivation of the action potential [20-22]. This action, along with synergistic effects by other venom components, causes prolonged depolarization and excessive release of acetylcholine from parasympathetic ganglia and epinephrine and norepinephrine from sympathetic ganglia and adrenal glands. This excessive release of neurotransmitters results in an autonomic storm, thus scorpion envenomation may present with the following clinical findings (see 'Clinical manifestations' below):
●Cholinergic excess manifests as marked bronchorrhea, salivation, bronchospasm, diaphoresis, priapism, lacrimation, vomiting, diarrhea, and bradycardia. These effects generally last only a few hours after a scorpion sting [20].
●Sympathetic stimulation typically persists and results in hypertension, tachycardia, and agitation. Severe envenomation may progress to direct myocardial injury with arrhythmias, myocarditis, pulmonary edema, cardiogenic shock, and multisystem organ failure [20].
The mechanism of cardiotoxicity with acute pulmonary edema after scorpion sting is debated but likely reflects a complex interplay of multiple venom effects including catecholamine-mediated coronary, cardiac microcirculatory and systemic vasoconstriction; catecholamine-induced tachycardia and arrhythmias; and depression of myocardial contractility caused by direct effects of scorpion venom and the pro-inflammatory response to envenomation [3,20,23,24]. These factors combine to cause left ventricular dysfunction and acute pulmonary edema.
In addition to these autonomic effects, scorpion venoms enhance pancreatic exocrine secretion in animal models [25] and in humans, can cause acute pancreatitis, especially after Tityus or Leiurus envenomation, which are primarily located in Brazil and North Africa, respectively [1,26-29].
EPIDEMIOLOGY — Worldwide, approximately 1 to 1.5 million scorpion stings occur annually resulting in up to 3000 deaths (figure 2) [20,21]. Because scorpion envenomation is concentrated in rural areas and many stings and deaths may go unreported, these numbers are probably underestimated. Children younger than 10 years of age and older adults are at greatest risk for severe envenomation after a scorpion sting [3,9,27].
Scorpions with stings capable of causing autonomic dysfunction ("autonomic storm") reside in Asia (eg, India, Pakistan, and Sri Lanka), the Middle East (Turkey, Iran, and Lebanon), Israel, North Africa, South America, and the Republic of Trinidad and Tobago (table 1) (see 'Geographical distribution and appearance' above):
●South America and Republic of Trinidad and Tobago – The Tityus species account for most scorpion envenomations requiring medical care in South American and the Republic of Trinidad and Tobago. Tityus serrulatus is most frequently encountered in Brazil [30], while other species (eg, Tityus trivittatus or T. discrepans) are the predominant envenoming scorpion in other regions [1,28,31,32]. In Brazil, the average incidence of scorpionism is approximately eight cases per 100,000 people with mortality occurring in <1 percent of patients [30]. An increased number of scorpion envenomations happen during the rainy season when scorpions are driven from their burrows and seek shelter near human dwellings. Victims tend to be young adult males living in rural regions.
●North Africa – In northern Africa, Androctonus australis, Androctonus crassicauda, Buthus occitanus, and Leiurus quinquestriatus cause the majority of severe scorpion envenomations [9]. Reports from different regions indicate a predilection for stings during the summer months and rates of scorpion stings up to 20 stings per thousand inhabitants (Tunisia) with significant variation depending upon location [1,9,33-35]. Fatalities are uncommon, occurring in <1 percent of patients. Children are at highest risk for mortality after envenomation [1].
●Middle East – In the Middle East and Israel, A. crassicauda and L. quinquestriatus account for the greatest number of serious envenomations, but mortality is low (<1 percent) [1,36,37]. Hemiscorpius lepturus, although responsible for <20 percent of stings in Iran, is the leading cause of death due to scorpion envenomation in that country with fatalities reported in up to 9 percent of stings [38]. (See "Scorpion envenomation causing skin necrosis, hemolysis, DIC, and acute kidney injury (Middle East)".)
●India – Almost 100 scorpion species are found in India and surrounding regions. Most serious envenomations are caused by Hottentotta (previously Methobuthos or Buthus) tamulus which is commonly known as the red scorpion [1,20,39,40]. H. tamulus envenomations are more common in rural regions of southern coastal India during April through June [39]. Stings often occur on the fingers or toes. The 30 percent case fatality rate reported in the 1960s and 1970s is now 2 to 3 percent [41]. This reduction in mortality is largely attributable to greater access to antihypertensive treatment and intensive care [42,43].
CLINICAL MANIFESTATIONS — Scorpion stings are usually unintentional because scorpions would rather escape humans than attack. Scorpions may hide in crevices of stone houses, roofing, bedding, clothing, and footwear [27]. Stings may occur in humans when they dress, get into bed, or when they are either lean or sit against walls. Scorpions may also fall from the ceilings of thatched roofs onto sleeping victims below. Scorpion stings most commonly occur on an extremity when a human unintentionally steps on a scorpion or reaches under debris, rocks, or into crevices of buildings.
Although specific clinical findings after scorpion envenomation with autonomic dysfunction ("autonomic storm") vary somewhat according to the specific scorpion, clinical manifestations have many similarities across species:
●Local effects – Depending upon the specific scorpion, 66 to 90 percent of stings have signs and symptoms limited to local pain, paresthesias, and skin changes (eg, central puncta with swelling, erythema, and localized piloerection (picture 3)) without systemic effects [3,20,31]. Paresthesias and pain may last for several days [3]. In many patients, the sting site cannot be located.
●Systemic effects – Depending upon scorpion species, systemic effects of autonomic storm become apparent in 10 to 33 percent of patients as early as 30 minutes and typically within four hours of being stung. The combined autonomic effects often produce acute respiratory distress marked by tachypnea, crackles, and hypoxemia, hypertension with tachycardia, and altered mental status [1,3,8,20].
Additional findings include [1,3,8,9,20,32,44,45]:
•Parasympathomimetic effects:
-Bradycardia and bradyarrhythmias (eg, atrioventricular block)
-Copious salivation
-Bronchorrhea
-Wheezing
-Vomiting and diarrhea
-Priapism
•Sympathomimetic effects:
-Delirium
-Dilated pupils
-Sinus tachycardia and tachyarrhythmias (eg, supraventricular or ventricular tachycardia)
-Hyperthermia
-Hypertension
-Diaphoresis
-Vasoconstriction with cold extremities
-Spontaneous ejaculation in men
-In patients with late presentations, cardiogenic shock with hypotension and acute pulmonary edema (tachypnea, crackles, and hypoxemia) indicating left ventricular heart failure
When present, parasympathomimetic toxicity typically abates within the first 24 hours; sympathomimetic effects often persist for 48 hours or longer.
Coma and seizures may occur as a secondary consequence of cardiogenic shock with pulmonary edema and hypoxia, cerebral ischemia, or hyperthermia. Hemorrhagic stroke, presumably caused by acute hypertension or rarely, disseminated intravascular coagulopathy, has also been described [46,47].
Other less common neurologic signs reported with these scorpions include local and diffuse paresthesias, tremors, shivering, hyperirritability, myoclonus, and, less commonly, oculogyric crisis (opsoclonus) [27,46,48,49].
Acute pancreatitis manifested by epigastric pain with radiation to the back, vomiting, abdominal tenderness, and elevation of serum amylase or lipase commonly accompanies systemic toxicity from stings by Tityus and Leiurus species but may also occur with other scorpion envenomations [1,20,26,27]. Findings typically resolve within 24 hours [28].
Grading of severity — Several classification systems have been described for scorpion envenomation with autonomic storm based upon regional species-specific findings or expert opinion [3,8,50]. We favor the system proposed by Isbister and Bawaskar because it directs treatment in addition to identifying severity and is applicable to all species (table 2) [20] (see 'Clinical manifestations' above):
●Grade or Class I – Local effects only
●Grade or Class II – Systemic autonomic effects (parasympathomimetic and/or sympathomimetic)
●Grade or Class III – Evidence of cardiotoxicity including heart failure with acute pulmonary edema or cardiogenic shock with hypotension
●Grade or Class IV – Progressive cardiogenic shock with coma, seizures, or other manifestations of multisystem organ failure such as acute kidney or liver injury
ANCILLARY STUDIES — Clinical manifestations determine the appropriate ancillary studies to perform after scorpion stings associated with significant pain and potential for autonomic storm (table 2):
●Grade or class I – No ancillary studies are needed.
●Grade or class II or higher – Although not required for diagnosis or treatment and frequently unavailable in regions where scorpion stings occur, ancillary studies can help classify the severity of the sting in patients with autonomic dysfunction which more precisely guides supportive therapy [3,8,20]. In addition, these tests can support the diagnosis for infants and children with irritability of unknown cause:
•Complete blood count
•Serum electrolytes
•Serum glucose
•Serum lactate
•Serum calcium and phosphate
•Liver enzymes (aspartate aminotransferase [AST] and alanine aminotransferase [ALT], gamma-glutamyl transpeptidase [GGT])
•Serum lipase or amylase
•Blood urea nitrogen and serum creatinine
•Blood gas (venous or arterial)
•Cardiac troponins (preferred, if available) or other cardiac biomarkers (eg, creatine kinase-MB fraction [CK-MB], plasma brain natriuretic peptide [BNP] or NT-proBNP)
•Urine dipstick
•Electrocardiogram (EKG)
•Chest radiograph
•For patients with findings suggestive of cardiotoxicity (eg, arrhythmias, tachypnea with crackles, EKG changes, and/or pulmonary edema on chest radiograph), echocardiography when available
•For patients with petechiae, purpura, or bleeding, prothrombin time, activated partial thromboplastin time, and fibrinogen
•For patients with focal neurologic signs, computed tomography of the brain when available
In patients with systemic features of scorpion envenomation, laboratory studies frequently demonstrate leukocytosis, hyperglycemia, and lactic acidosis with hypokalemia as a result of catecholamine excess and adrenergic stimulation [3,8,21]. In resource-limited regions, an elevated rapid blood glucose is sometimes used to identify scorpion sting as a likely cause of unexplained irritability in infants and young children [3,8]. Electrolyte disturbances including hyperkalemia and hypocalcemia have also been described [8,27].
The first signs of cardiotoxicity typically occur soon after envenomation and include brady- and tachyarrhythmias, other EKG abnormalities (Q waves, ST-segment elevation or depression, peaked or inverted T waves, U waves, and/or prolonged QTc intervals) or elevation in cardiac biomarkers (troponin [preferred] or CK-MB) [9,44,51-53].
An enlarged heart with pulmonary edema on chest radiograph or elevated liver enzymes due to passive liver failure are important indicators of heart failure. In patients with heart failure, echocardiography typically shows acute, decreased left ventricular systolic function with a reduced ejection fraction [8,53]. More global dysfunction with right-sided failure, dilated cardiac chambers, and mitral regurgitation has also been described [54]. If obtained, BNP or NT-proBNP are typically elevated [3].
Elevated lipase or amylase indicates pancreatitis which is frequently associated with vomiting or abdominal pain and is seen most frequently after stings by Leiurus and Tityus species. (See 'Clinical manifestations' above.)
DIAGNOSIS — The diagnosis of scorpion envenomation relies on evidence of a scorpion sting by history or recovery of the scorpion and clinical findings of scorpion envenomation (local pain and erythema with or without systemic features of autonomic dysfunction ["autonomic storm"] or cardiotoxicity) or suggestive findings in a patient presenting in a region where they are indigenous. Clinicians should have a high suspicion for scorpion envenomation when caring for infants or young children from endemic areas presenting with sudden onset of irritability especially when skin changes and or signs of systemic envenomation are present.
Envenomation should also be suspected in any patient who resides in a region endemic for poisonous scorpions and has severe local pain with skin changes (eg, erythema or piloerection) and paresthesias. Up to one-third of patients may display findings of autonomic storm with parasympathomimetic and sympathomimetic stimulation, cardiotoxicity (eg, arrhythmias, electrocardiogram changes, or elevated cardiac biomarkers) and acute pulmonary edema (table 2). Other supportive laboratory findings include hyperglycemia, leukocytosis, and lactic acidosis. (See 'Clinical manifestations' above and 'Ancillary studies' above.)
DIFFERENTIAL DIAGNOSIS — Conditions with signs or symptoms that may overlap with those of scorpion envenomation include:
●Black widow and other widow spider bites – Black widow spider bites commonly occur in the Southern and Southwestern United States. Other widow spiders are found in the Middle East and South America but are not common in India and other parts of Asia (except Japan), and North Africa (table 3). Widow spider envenomation may produce hypertension, tachycardia, sweating, and other signs of adrenergic excess that has a similar presentation to scorpion envenomation. However, widow spider envenomation does not produce parasympathomimetic effects, pancreatitis, or cardiotoxicity, although the pain of the bite could induce a coronary syndrome in predisposed patients. Unlike scorpions, widow spider bites may also produce a characteristic halo lesion at the bite site (picture 4). (See "Clinical manifestations and diagnosis of widow spider bites", section on 'Physical findings'.)
●Other insect stings – Many insects can cause painful bites or stings with a local reaction and may be difficult to distinguish from local reactions caused by scorpion stings; however, persistent severe pain and paresthesias are unusual after most insect stings. The presence of a central puncta (eg, after mosquito bites or hymenoptera stings), bite marks (eg, centipede), itching, or urticaria can help identify common insect bites and stings. The development of characteristic systemic findings of scorpion envenomation (table 2) also distinguishes scorpion stings from bites or stings by other insects. (See "Insect and other arthropod bites".)
●Medical causes of sympathetic overactivity – Tachycardia and severe hypertension with end-organ damage, including hypertensive encephalopathy or heart failure with pulmonary edema, can be caused by several conditions that may mimic the adrenergic stimulation of scorpion envenomation. However, the lack of a localized pain with a skin reaction or parasympathomimetic features in addition to the following findings can usually distinguish these entities from scorpion envenomation:
•Amphetamine, cocaine, or other sympathomimetic intoxication – Intoxication can often be determined by history or a rapid screen for drugs of abuse. (See "Acute amphetamine and synthetic cathinone ("bath salt") intoxication" and "Cocaine: Acute intoxication".)
•Tyramine reaction in patients receiving monoamine oxidase inhibitor (MAOI) medications – This condition should be suspected in patients on MAOI medications. (See "Evaluation and treatment of hypertensive emergencies in adults", section on 'Sympathetic overactivity resulting in hypertensive emergencies'.)
•Sudden withdrawal from short-acting hypertensive medications (eg, clonidine, propranolol, or other beta blockers) – Withdrawal will typically be identified by history of sudden cessation of antihypertensive medication. (See "Withdrawal syndromes with antihypertensive drug therapy".)
•Pheochromocytoma – Pheochromocytoma does not cause parasympathomimetic effects and may be caused by familial syndromes such as multiple endocrine neoplasia type 2, neurofibromatosis type 1, or von Hippel-Lindau. Imaging (eg, ultrasound or computed tomography of the abdomen) demonstrates an adrenal mass. (See "Clinical presentation and diagnosis of pheochromocytoma".)
●Organophosphate exposure – Exposure to organophosphate compounds can cause cholinergic effects that mimic scorpion envenomation. However, organophosphates also cause muscle fasciculations and paralysis which is not seen with scorpion envenomation. Organophosphate poisoning is very common in rural communities as an accidental exposure or means of committing suicide. (See "Organophosphate and carbamate poisoning".)
●Familial dysautonomia (hereditary sensory and autonomic neuropathy type 3) – Familial dysautonomia is a rare genetic syndrome seen almost exclusively in patients with Ashkenazi Jewish heritage. Autonomic storm is a characteristic of this disease. Patients have a smooth tongue without fungiform papillae. It is diagnosed by genetic testing. (See "Hereditary sensory and autonomic neuropathies", section on 'HSAN3 (Familial dysautonomia)'.)
A victim of severe scorpion envenomation presenting late in the clinical course may appear to have primary heart failure. The cardiotoxicity of scorpion envenomation often fully reverses within a few days, which differentiates it from primary heart failure, although the initial treatment of either condition is the same.
Scorpion envenomation may also cause elevated temperature and hypotension that does not respond to fluid therapy and may bear some resemblance to fluid-refractory septic shock. Acute pancreatitis (when present), a rapidly reversing clinical course, and lack of positive cultures all support scorpion envenomation as the etiology. However, empiric antibiotic therapy may be prudent during initial care of these patients.
MANAGEMENT — Management corresponds to the grade or class of envenomation (table 2).
Local pain and wound care — Patients with scorpion stings should have their pain controlled, the region of erythema and swelling cleaned, and tetanus prophylaxis provided, as needed (table 4) [20,21]. Tourniquets, local incision, or application of potassium permanganate or herbal remedies are associated with local tissue infection and gangrene should be avoided [8].
Evidence for pain management after scorpion stings is limited. Oral nonsteroidal antiinflammatory agents (eg, ibuprofen) or acetaminophen suffice for pain management for many patients [20]. Those who present with more severe pain may benefit from topical anesthetics (eg, topical lidocaine or tetracaine) or regional anesthesia (eg, digital block) using a long-acting agent (eg, bupivacaine) [20,55]. Local anesthetics containing epinephrine should be avoided to prevent exacerbation of adrenergic symptoms in patients whose envenomation progresses. Severe pain may require opioid analgesia (eg, fentanyl or morphine). (See "Clinical use of topical anesthetics in children" and "Digital nerve block", section on 'Digital block procedures'.)
Patients with local effects after a scorpion sting should be observed for up to 24 hours for signs of cholinergic excess and adrenergic stimulation in a setting capable of providing intensive care. This observation should consist of frequent patient assessment with vital signs and, whenever available, continuous cardiorespiratory monitoring with pulse oximetry. Approximately 10 to 33 percent of patients will develop systemic findings of autonomic dysfunction ("autonomic storm") with or without cardiotoxicity [3,20,31]. (See 'Clinical manifestations' above.)
If travel to a facility capable of providing appropriate monitoring and advanced care of scorpion stings will take more than three to four hours, then administration of scorpion antivenom, in consultation with an expert in the management of scorpion envenomation by local species, may be appropriate. (See 'Antivenom' below.)
Systemic toxicity — When managing a suspected scorpion envenomation with Grade II or higher severity (table 2), we encourage consultation with a regional poison control center or local physician with expertise managing scorpion stings. To obtain emergency consultation with a medical toxicologist, in the United States, call 1-800-222-1222, or the nearest international regional poison center. Contact information for regional poison centers around the world is provided separately. (See 'Additional resources' below.)
Antivenom — Evidence is inconsistent regarding the benefit of equine-derived F(ab')2 antivenom for reducing or preventing toxicity by old world scorpion species [3,20,21,56,57]. Evidence supports the use of antivenom to treat systemic toxicity after envenomation by Hottentotta (formerly Mesobuthus), Leiurus, and Tityus species. Available antivenoms are not always adequate, and medical training and assistance in the region may be insufficient. Thus, the decision to administer antivenom to patients with scorpion envenomation and autonomic dysfunction requires careful consideration of the likely scorpion and the risks and benefits of the specific antivenom. Furthermore, timely supportive care or toxicity is critical to good outcomes. (See 'Supportive care' below.)
Patients with Grade II or higher scorpion envenomation also warrant treatment with prazosin. (See 'Prazosin' below.)
Indications — The recommendations for use of scorpion-specific antivenom varies by specific scorpion species:
●Hottentotta (formerly Mesobuthus) species – We recommend that patients stung by Hottentotta (formerly Mesobuthus) species who demonstrate signs of Grade II or higher scorpion envenomation (table 2) receive intravenous (IV) scorpion-specific antivenom (Scorpion Venom Antiserum IP, Haffkine Bio-Pharmaceutical Corporation, Limited, India) [40,57,58]. Antivenom should be given as soon as possible after the sting, ideally within four hours, because it is less effective once the venom is fully absorbed.
Small trials performed in patients with systemic scorpion envenomation treated in India and the United States show that equine-derived F(ab')2 scorpion-specific antivenom significantly shortens the duration of systemic toxicity [57]. For patients with Grade II envenomation after stings by Hottentotta (formerly Mesobuthus) species, it also significantly decreases the amount of medication required to control hypertension and prevents progression to cardiotoxicity [40,57-59]. In one trial, pediatric patients who received antivenom required, on average, a total of two doses of prazosin compared to four doses in patients who received prazosin alone [20,40]. In India, the routine use of antivenom and prazosin combined with improved intensive care measures has been associated with a significant decrease in mortality from 26 percent in 1961 to <1 percent in 2012 [8].
●Tityus and Leiurus species – For patients stung by Tityus or Leiurus species who demonstrate signs of systemic scorpion envenomation, we suggest treatment with IV scorpion-specific antivenom. No trials address the efficacy of these antivenoms. However, small observational studies suggest potential benefit in patients with cardiotoxicity, although evidence for antivenom directed against Leiurus species is inconsistent [60-62].
●Androctonus or Buthus species – Evidence does not support administration of scorpion-specific antivenom to patients with Grade II or higher envenomation after stings by Androctonus or Buthus species given the low likelihood of death and the potential for adverse effects from the antivenom [57,63,64] (see 'Epidemiology' above). Nevertheless, because high quality evidence is lacking, some regional experts still support its use.
Observational studies and one trial of scorpion antivenom for stings by Androctonus and Buthus species have failed to show a benefit of scorpion-specific antivenom over supportive care alone [57]. However, these studies were performed over 10 to 20 years ago and have significant methodologic flaws (eg, lack of blinding, baseline differences in severity of illness prior to antivenom administration between groups, and/or lack of controlling for the time between reported sting and antivenom administration) [57].
Additional treatment for systemic manifestations of scorpion envenomation include prazosin and aggressive supportive care of cardiotoxicity to prevent mortality. (See 'Prazosin' below and 'Supportive care' below.)
Dosing and administration — Clinicians should follow the guidance of experts in their regions and manufacturer instructions when determining the dose of antivenom. The dose of antivenom varies by species and is also based upon the estimated amount of venom delivered during the sting and the severity of envenomation [3,20,21,65]. Antivenom dosing is not based upon the patient's weight and should not be reduced in children. Scorpion antivenom should be given IV.
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 IV infusion of the antivenom (if applicable) and treating symptoms appropriately (table 5 and table 6). (See "Anaphylaxis: Emergency treatment".)
With the exception of antivenoms produced in Iran and Egypt (for which there is limited information), scorpion antivenoms consist of equine-derived F(ab')2 fragments. Compared with previously used whole immunoglobulin scorpion antivenoms, allergic reactions are much less common with the newer antivenoms (<5 percent of patients) and are mild [65,66]. Limited evidence from small trials suggests that the risk of either anaphylaxis or serum sickness after scorpion-specific F(ab')2 equine antivenom is low (estimated as <1 percent) [40,65-67].
All patients receiving antivenom should be informed of the possibility of serum sickness and the symptoms suggestive of serum sickness (eg, fever, rash, arthralgias, and arthritis) and advised to seek medical care if such symptoms occur. (See "Serum sickness and serum sickness-like reactions".)
Prazosin — For patients with Grade II or higher scorpion envenomation (table 2) caused by Hottentotta (formerly Mesobuthus) species, we recommend prazosin in addition to scorpion-specific antivenom rather than antivenom alone. Prazosin has been shown to mitigate excessive catecholamine release and progression to cardiotoxicity (see 'Sympathetic toxicity' below). For patients with Grade II or higher scorpion envenomation caused by Androctonus, Buthus, Leiurus, or Tityus species, we suggest treatment with prazosin. The recommended prazosin dose for scorpion envenomation is 0.5 mg (30 micrograms/kg, maximum dose 0.5 mg in pediatric patients) orally or via gastric tube every three hours until systemic toxicity resolves.
The introduction of prazosin in India as a routine measure in the management of scorpion envenomation in addition to improved intensive care measures and the widespread use of scorpion-specific antivenom has been associated with a significant drop in mortality from 26 percent in 1961 to <1 percent in 2012 [8]. In a retrospective review that compared outcomes of 36 children who did or did not receive prazosin in addition to insulin and glucose therapy (no longer recommended), mortality was significantly lower among those who received prazosin (1 of 16 compared with 7 of 20 patients) [68]. Prazosin has also been associated with marked clinical improvement and recovery in children presenting with advanced signs of pulmonary edema and cardiogenic shock who did not respond to scorpion antivenom [69]. Furthermore, prazosin is an inexpensive medication that can be given by the oral route. Thus, it is relatively easy to store and administer in resource-poor settings.
In other regions, the routine use of prazosin and advancements in supportive care have also been associated with a decrease in mortality but direct evidence of benefit is lacking [21,27,69].
Supportive care — All patients with Grade II or higher scorpion envenomations (table 2) should be admitted to a unit capable of providing intensive supportive care. Clinicians should anticipate the need to treat autonomic dysfunction ("autonomic storm"), cardiotoxicity, and pancreatitis. (See 'Clinical manifestations' above and 'Venom properties' above.)
Autonomic dysfunction (autonomic storm) — Supportive treatment of autonomic stimulation and its complications after scorpion envenomation is provided (table 2) and discussed below.
Parasympathetic toxicity — Soon after scorpion envenomation, patients may require frequent oral suctioning for excessive salivation and administration of oxygen and/or inhaled albuterol to treat bronchorrhea and bronchospasm. Administration of subcutaneous epinephrine for bronchospasm should be avoided because it may enhance sympathetic toxicity.
Atropine may also potentiate sympathomimetic effects after envenomation and should be avoided unless patients develop severe bradycardia (bradycardia with hypotension and/or somnolence) or third degree atrioventricular block [20,21,70].
Vomiting may be treated with antiemetics (eg, metoclopramide or, if no hypocalcemia or prolonged QTc on electrocardiogram [EKG], ondansetron). Fluid losses should be replaced with IV isotonic fluids (eg, normal saline or buffered isotonic solutions such as Ringer’s lactate). The clinician should avoid fluid overload which may exacerbate heart failure in patients with sympathetic toxicity.
Sympathetic toxicity — Prazosin, a post-ganglionic alpha1-adrenergic receptor blocker counteracts excessive catecholamine release and is the primary treatment for sympathetic storm in conjunction with antivenom. Prazosin has also been shown to decrease the risk of progression to cardiotoxicity [40].
Heart failure — Heart failure after scorpion envenomation is caused by excessive circulating catecholamines. The resulting left ventricular dysfunction with reduced ejection fraction can be rapidly reversed with proper treatment. Prazosin, a post-ganglionic alpha1-adrenergic receptor blocker that counteracts excessive catecholamine release and, through its action as a vasodilator, provides treatment for heart failure and acute pulmonary edema is associated with reduced duration of cardiotoxicity when given in conjunction with antivenom [8,20,21,57]. Continuous IV infusion of nitroglycerin and a combination of dobutamine and nitroglycerin have also been used successfully to treat pulmonary edema and decompensated shock in critically ill patients [20,71].
Stabilization of patients also encompasses general treatment of acute decompensated heart failure with reduced left ventricular function/ejection fraction (table 7).
Key interventions include:
●Acute pulmonary edema – Patients with tachypnea and signs of pulmonary edema should receive supplemental oxygen, assisted ventilation (eg, noninvasive or mechanical ventilation) as needed for respiratory failure, and diuretics. (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Supplemental oxygen and assisted ventilation' and "Treatment of acute decompensated heart failure: Specific therapies", section on 'Diuretics'.)
The initiation of noninvasive and mechanical ventilation in children is discussed separately. (See "Noninvasive ventilation for acute and impending respiratory failure in children" and "Initiating mechanical ventilation in children", section on 'Inadequate oxygenation'.)
●Hypotension – Patients who develop persistent cardiogenic shock despite treatment with antivenom and prazosin warrant vasopressor support and afterload reduction. In small case series, dobutamine, at a continuous infusion of 5 to 20 micrograms/kg/minute, has successfully reversed severe heart failure after scorpion envenomation and is most commonly used [20,21,71,72]. (See "Treatment of acute decompensated heart failure: Specific therapies", section on 'Management of hypotensive patients'.)
Patients with refractory heart failure with hypotension and pulmonary edema despite dobutamine therapy may benefit from a carefully titrated nitroglycerin infusion (starting dose: 0.5 micrograms/kg/minute; if no response, increase the infusion by 50 percent every 15 minutes as needed up to a maximum dose of 5 micrograms/kg/minute) [20,71].
Unlike prazosin, other vasodilators, such as hydralazine or nifedipine, cause reflex sympathetic stimulation which may compound excessive catecholamine release after a scorpion sting and should be avoided [20,21].
Tachyarrhythmias — Tachyarrhythmias after scorpion envenomation typically arise from catecholamine-induced myocarditis, myocardial ischemia, or both [20,21]. Electrolyte disturbances (eg, hyperkalemia or hypocalcemia) have also been described [8].
In addition to emergency administration of scorpion-specific antivenom, these arrhythmias should be treated according to the principles of advanced cardiac life support (ACLS) (algorithm 1) and pediatric advanced life support (PALS) (algorithm 2). Although evidence is lacking, amiodarone may have a theoretical advantage over lidocaine for treating patients with ventricular arrhythmias after scorpion stings because of its sympatholytic effects. (See "Advanced cardiac life support (ACLS) in adults", section on 'Management of specific arrhythmias' and "Pediatric advanced life support (PALS)", section on 'Tachycardia algorithm'.)
Clinicians should also assess for hyperkalemia or hypocalcemia and provide emergency therapy if present (table 8). (See "Treatment and prevention of hyperkalemia in adults", section on 'Treatment approach to hyperkalemic emergencies' and "Management of hyperkalemia in children", section on 'Initial emergent therapy'.)
Delirium and other neurologic complications — Benzodiazepines (eg, midazolam or diazepam) can help manage delirium and are also indicated for the initial treatment of seizures in conjunction with appropriate stabilization and treatment of underlying causes such as hypoxemia, hypotension, and hypoglycemia (algorithm 3 and table 9). (See "Management of convulsive status epilepticus in children", section on 'Emergency antiseizure treatment' and "Convulsive status epilepticus in adults: Management", section on 'Emergency antiseizure treatment'.)
Patients with acute stroke should undergo initial stabilization, emergency neuroimaging, and treatment according to whether ischemia or hemorrhage are present. (See "Initial assessment and management of acute stroke".)
Hyperthermia — Sympathetic stimulation and agitation may cause serious hyperthermia. Treatment consists of support of airway, breathing, circulation; treatment of seizures, if present; and rapid cooling as describe separately. (See "Heat stroke in children", section on 'Hospital management' and "Severe nonexertional hyperthermia (classic heat stroke) in adults", section on 'Management'.)
Pancreatitis — Pancreatitis after scorpion envenomation is typically transient, lasting one to two days and responds to supportive care including pain control, no oral intake except medications until pain is resolving, regular monitoring of blood glucose with insulin administration for hyperglycemia, and monitoring of electrolytes and calcium. Fluid replacement should be done carefully in patients with co-existent heart failure. Pancreatic necrosis or pseudocyst are uncommon but should be sought as the etiology of persistent abdominal pain with vomiting. (See "Management of acute pancreatitis", section on 'Initial management'.)
OUTCOME — With timely administration of prazosin, scorpion-specific antivenom, and supportive care, most patients with systemic toxicity fully recover from scorpion envenomation within one to two days [3,8,21,57]. Mortality is <1 percent.
PREVENTION — False ceilings or bed nets below thatched roofs prevent scorpions from falling onto people while they sleep [8]. Reducing small cracks and crevices in homes decreases the risk of human-scorpion interactions. In scorpion-infested areas, clothing, shoes, packages, and bedding should be carefully checked for scorpions. Footwear is recommended. Unnecessary ground cover and debris should be removed in order 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.
ADDITIONAL RESOURCES
Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)
SUMMARY AND RECOMMENDATIONS
●Medically important scorpions – Dangerous scorpion species capable of causing autonomic dysfunction or "autonomic storm" and their reported geographical distribution are provided in the table (table 1). (See 'Geographical distribution and appearance' above.)
●Clinical manifestations – Scorpions may hide in crevices of stone houses, roofing, bedding, clothing, and footwear. Stings may occur in humans when they dress, get into bed, or when they either lean or sit against walls. Scorpions may also fall from the ceilings of thatched roofs onto sleeping victims below. (See 'Clinical manifestations' above.)
Most stings have signs and symptoms limited to local pain, paresthesias, and skin changes (eg, central puncta with swelling, erythema, and localized piloerection (picture 3)) without systemic toxicity. In many patients, the sting site cannot be located. (See 'Clinical manifestations' above.)
Systemic effects include autonomic stimulation ("autonomic storm") with parasympathomimetic and sympathomimetic effects and cardiotoxicity characterized by left-sided heart failure with pulmonary edema, cardiogenic shock, cardiac arrhythmias, and multisystem organ dysfunction. A suggested grading system classifies the severity of envenomation and helps to guide treatment (table 2). (See 'Clinical manifestations' above and 'Grading of severity' above.)
●Ancillary studies – Patients with local effects and no progressive toxicity after a sting (Grade I envenomation) do not require ancillary studies.
When available, ancillary studies can help classify the severity of the sting in patients with Grade II or higher envenomation characterized by systemic effects. Leukocytosis, hyperglycemia, and lactic acidosis with hypokalemia caused by catecholamine excess and adrenergic stimulation are characteristic findings. A complete list of suggested studies for patients with systemic toxicity is provided. (See 'Ancillary studies' above.)
Cardiotoxicity typically becomes evident within hours of envenomation and includes (see 'Ancillary studies' above):
•Brady- and tachyarrhythmias
•Other electrocardiogram (ECG) abnormalities (eg, Q waves, ST-segment elevation or depression, peaked or inverted T waves, U waves, and/or prolonged QTc intervals)
•Elevation in cardiac biomarkers (eg, troponin [preferred] or creatine kinase-MB fraction [CK-MB])
•An enlarged heart with pulmonary edema on chest radiograph
•Elevated liver enzymes due to passive liver failure
•In patients with heart failure, echocardiography typically shows acute, decreased left ventricular systolic function with a reduced ejection fraction
●Diagnosis – The diagnosis of scorpion envenomation is clinical; a confirmed scorpion sting requires corroborating history or recovery of the scorpion combined with clinical findings of scorpion envenomation.
However, clinicians should have a high suspicion for scorpion envenomation when caring for infants or young children from endemic areas presenting with sudden onset of irritability, especially when skin changes and or signs of systemic envenomation are present. Envenomation should also be suspected in any patient who resides in a region endemic for poisonous scorpions and has severe local pain with skin changes and paresthesias, especially when cardiotoxicity with or without acute pulmonary edema occurs. (See 'Diagnosis' above.)
●Management – Management depends upon the severity of envenomation (see 'Management' above):
•Grade I – Patients with local effects after scorpion stings should have their pain controlled, the region of erythema and swelling cleaned, and tetanus prophylaxis provided, as needed (table 4). These patients warrant observation in settings capable of intensive care for up to 24 hours in case of progression to systemic toxicity. (See 'Local pain and wound care' above.)
•Grade II or higher – When managing a suspected scorpion envenomation with autonomic dysfunction (Grade II or higher severity) (table 2), we encourage consultation with a regional poison control center or local physician with expertise managing scorpion stings. (See 'Additional resources' above.)
Treatment recommendations vary according to the confirmed or suspected scorpion:
-Hottentotta [formerly Mesobuthus]) – For patients stung by Hottentotta (formerly Mesobuthus) scorpions with Grade II or higher scorpion envenomation (table 2), we recommend treatment with intravenous (IV) scorpion-specific antivenom (Grade 1B). For these patients, we also recommend prazosin in addition to scorpion-specific antivenom rather than antivenom alone (Grade 1B). (See 'Antivenom' above and 'Prazosin' above.)
-Other species – For patients with Grade II or higher envenomation after stings by Leiurus or Tityus scorpion species, we suggest treatment with IV scorpion-specific antivenom (Grade 2C). Available evidence does not support the use of antivenom for patients with systemic toxicity after stings by Androctonus or Buthus species. (See 'Antivenom' above.)
For patients with Grade II or higher scorpion envenomation caused by Androctonus, Buthus, Leiurus, or Tityus species, we suggest treatment with prazosin (Grade 2C). (See 'Prazosin' above.)
●All patients with Grade II or higher scorpion envenomation should be admitted to a unit capable of providing intensive supportive care. Clinicians should anticipate the need to treat autonomic dysfunction, cardiotoxicity, and pancreatitis. Key interventions are described in the table (table 2) and above. (See 'Supportive care' above.)
