Updated: Aug 6, 2009
Scorpion stings are a major public health problem in many underdeveloped tropical countries. For every person killed by a poisonous snake, 10 are killed by a poisonous scorpion. In Mexico, 1000 deaths from scorpion stings occur per year. In the United States, only 4 deaths in 11 years have occurred as a result of scorpion stings. Furthermore, scorpions can be found outside their normal range of distribution, ie, when they accidentally crawl into luggage, boxes, containers, or shoes and are unwittingly transported home via human travelers.
A scorpion has a flattened elongated body and can easily hide in cracks. It has 4 pairs of legs, a pair of claws, and a segmented tail that has a poisonous spike at the end. Scorpions vary in size from 1-20 cm in length.
Out of 1500 scorpion species, 50 are dangerous to humans. Scorpion stings cause a wide range of conditions, from severe local skin reactions to neurologic, respiratory, and cardiovascular collapse. Envenomation from most scorpions results in a simple, painful, local reaction that can be treated with analgesics, antihistamines, and symptomatic/supportive care. This article focuses on scorpions that generally are considered more dangerous to humans.
Almost all of these lethal scorpions, except the Hemiscorpius species, belong to the scorpion family called the Buthidae. The Buthidae family is characterized by a triangular-shaped sternum, as opposed to the pentagonal-shaped sternum found in the other 5 scorpion families. In addition to the triangular-shaped sternum, poisonous scorpions also tend to have weak-looking pincers, thin bodies, and thick tails, as opposed to the strong heavy pincers, thick bodies, and thin tails seen in nonlethal scorpions. The lethal members of the Buthidae family include the genera of Buthus, Parabuthus, Mesobuthus, Tityus, Leiurus, Androctonus, and Centruroides. These lethal scorpions are found generally in the given distribution:
However, these scorpions may be found outside their natural habitat range of distribution when inadvertently transported with luggage and cargo.
In general, scorpions are not aggressive. They do not hunt for prey; they wait for it. Scorpions are nocturnal creatures; they hunt during the night and hide in crevices and burrows during the day to avoid the light. Thus, accidental human stinging occurs when scorpions are touched while in their hiding places, with most of the stings occurring on the hands and feet.
Scorpions use their pincers to grasp their prey; then, they arch their tail over their body to drive their stinger into the prey to inject their venom, sometimes more than once. The scorpion can voluntarily regulate how much venom to inject with each sting. The striated muscles in the stinger allow regulation of the amount of venom ejected, which is usually 0.1-0.6 mg. If the entire supply of venom is used, several days must elapse before the supply is replenished. Furthermore, scorpions with large venom sacs, such as the Parabuthus species, can even squirt their venom.
The venom glands are located on the tail lateral to the tip of the stinger and are composed of 2 types of tall columnar cells. One type produces the toxins, while the other produces mucus. The potency of the venom varies with the species, with some producing only a mild flu and others producing death within an hour. Generally, the venom is distributed rapidly into the tissue if it is deposited into a venous structure. Venom deposited via the intravenous route can cause symptoms only 4-7 minutes after the injection, with a peak tissue concentration in 30 minutes and an overall toxin elimination half-life of 4.2-13.4 hours through the urine. The more rapidly the venom enters the bloodstream, the higher the venom concentration in the blood and the more rapid the onset of systemic symptoms.
Scorpion venom is a water-soluble, antigenic, heterogenous mixture, as demonstrated on electrophoresis studies. This heterogeneity accounts for the variable patient reactions to the scorpion sting. However, the closer the phylogenetic relationship between the scorpions, the more similar the immunological properties. Furthermore, the various constituents of the venom may act directly or indirectly and individually or synergistically to manifest their effects. In addition, differences in the amino acid sequence of each toxin account for their differences in the function and immunology. Thus, any modifications of the amino acid sequence result in modification of the function and immunology of the toxin.
Scorpion venom may contain multiple toxins and other compounds. The venom is composed of varying concentrations of neurotoxin, cardiotoxin, nephrotoxin, hemolytic toxin, phosphodiesterases, phospholipases, hyaluronidases, glycosaminoglycans, histamine, serotonin, tryptophan, and cytokine releasers. The most important clinical effects of envenomation are neuromuscular, neuroautonomic, or local tissue effects. The primary targets of scorpion venom are voltage-dependent ion channels, of which sodium channels are the best studied. Venom toxins alter these channels, leading to prolonged neuronal activity. Many end-organ effects are secondary to this excessive excitation. Autonomic excitation leads to cardiopulmonary effects observed after some scorpion envenomations. Somatic and cranial nerve hyperactivity results from neuromuscular overstimulation. Additionally, serotonin may be found in scorpion venom and is thought to contribute to the pain associated with scorpion envenomation.
The most potent toxin is the neurotoxin, of which 2 classes exist. Both of these classes are heat-stable, have low molecular weight, and are responsible for causing cell impairment in nerves, muscles, and the heart by altering ion channel permeability.
The long-chain polypeptide neurotoxin causes stabilization of voltage-dependent sodium channels in the open position, leading to continuous, prolonged, repetitive firing of the somatic, sympathetic, and parasympathetic neurons. This repetitive firing results in autonomic and neuromuscular overexcitation symptoms, and it prevents normal nerve impulse transmissions. Furthermore, it results in release of excessive neurotransmitters such as epinephrine, norepinephrine, acetylcholine, glutamate, and aspartate. Meanwhile, the short polypeptide neurotoxin blocks the potassium channels.
The binding of these neurotoxins to the host is reversible, but different neurotoxins have different affinities. The stability of the neurotoxin is due to the 4 disulfide bridges that fold the neurotoxin into a very compact 3-dimensional structure, thus making it resistant to pH and temperature changes. However, reagents that can break the disulfide bridges can inactivate this toxin by causing it to unfold. Also, the antigenicity of this toxin is dependent on the length and number of exposed regions that are sticking out of the 3-dimensional structure.
A total of 13,000 stings have been reported, with the majority being from the nonlethal scorpions. Only 1 of 30 scorpion species found in the United States is dangerous to humans. This lethal scorpion species is the straw-colored Centruroides. Less than 1% of stings from Centruroides are lethal to adults; however, 25% of children younger than 5 years who are stung die if not treated. The epidemiological features of a patient who has been envenomed show a disposition for rural areas (73%), with most of the stings occurring in the summer months between 6:00 pm and 12:00 am (49%) and a second peak from 6:00 am to 12:00 pm (30%). Both of these peaks coincide maximum human activity with maximum scorpion activity. Furthermore, the larger the scorpion population, the larger the incidence rate. Because the offending scorpion is recovered for identification in only 30% of the cases, local knowledge of the type of scorpion populating the area is useful.
In 2006, a total of 16,231 scorpion envenomations were reported to the American Association of Poison Control Centers. However, because of underreporting, this is probably an underestimation of the true number of stings.
Scorpion stings occur in temperate and tropical regions, especially between the latitudes of 50°N and 50°S of the equator. Furthermore, stings predominantly occur during the summer and evening times. In addition, the majority of patients are stung outside their home.
Reliable statistics on scorpion envenomation are not available. Many potentially dangerous scorpions inhabit the underdeveloped or developing world. Consequently, numerous envenomations go unreported, and true incidence is unknown.
A recent 5-year surveillance study in Saudi Arabia found 6465 scorpion sting cases with a mean patient age of 23 years, a male-to-female ratio of 1.9, and a higher incidence of stings in the months of May-October.1
Accurate worldwide data do not exist. The underreporting of scorpion stings is frequent because most envenomations occur in desert and jungle areas that do not have large medical facilities. Furthermore, reporting is not required.
Most deaths occur during the first 24 hours after the sting and are secondary to respiratory or cardiovascular failure.
The highest reported mortality rate is recorded in data from Mexico, with estimates as high as 1000 deaths in 1 year. In the United States, 4 deaths were reported in an 11-year period according to one source.2 However, no deaths were reported to the American Association of Poison Control Centers from 1983 to 1999. Only one death from the Arizona bark scorpion (C sculpturatus) has been reported since 1964.3 Ironically, the highest and lowest mortality estimates are associated with different species within the same genus of scorpion (Centruroides).
Children and elderly persons are at the greatest risk for morbidity and mortality. A smaller child, a lower body weight, and a larger ratio of venom to body weight lead to a more severe reaction. A mortality rate of 20% is reported in untreated babies, 10% in untreated school-aged children, and 1% in untreated adults.
In terms of venom lethality, the venom of Androctonus australis and Leiurus quinquestriatus are the most toxic. C sculpturatus venom is low in toxicity compared with most scorpions of medical importance.
Furthermore, patients in rural areas tend to fare worse than patients in urban areas because of the delay in getting medical help due to a longer travel time to medical centers. Fortunately, better public education, improved control of the scorpion population, increased supportive therapies, and more technologically advanced intensive care units have combined to produce a substantial decrease in mortality from these envenomations.
No racial predilection exists. Any differences in individual reactions to the scorpion sting are a reflection of that individual's genetic composition rather than race.
Females are more susceptible than males to the same amount of scorpion venom because of their lower body weight.
While adults are stung more often than children, children are more likely to develop a more rapid progression and increased severity of symptoms because of their lower body weight. Furthermore, elderly persons are more susceptible to stings because of their decreased physiologic reserves and increased debilitation.
Cerebral infarction, cerebral thrombosis, and acute hypertensive encephalopathy have been described with a variety of Buthidae scorpion envenomations.
The signs of the envenomation are determined by the scorpion species, venom composition, and the victim's physiological reaction to the venom. The signs occur within a few minutes after the sting and usually progress to a maximum severity within 5 hours. The signs last for 24-72 hours and do not have an apparent sequence. Thus, predicting the evolution of signs over time is difficult. Furthermore, a false recovery followed by a total relapse is common.
A person who has been stung by a scorpion usually has 4 signs, with the most common being mydriasis, nystagmus, hypersalivation, dysphagia, and restlessness. The mode of death is usually via respiratory failure secondary to anaphylaxis, bronchoconstriction, bronchorrhea, pharyngeal secretions, and/or diaphragmatic paralysis, even though venom-induced multiorgan failure plays a large role.
Children present with the same symptoms and signs as adults, except their symptoms are more severe and protracted. Furthermore, they may display a restlessness that is out of proportion when compared to any other disease. A child's symptoms have been described as inconsolable crying; uncontrollable jerking of the extremities; and chaotic thrashing, flailing, and writhing combined with contorted facial grimaces. The symptoms mimic a centrally mediated seizure, but the patient is awake and alert the entire time.
The grading of these scorpion envenomations depends on whether or not neurological signs predominate and is as follows:
The causes of scorpion envenomation are primarily accidental. Scorpions are shy creatures and only sting if threatened, cornered, or disturbed (eg, being sat or stepped upon). Curious individuals are at risk because of increased interaction with the scorpion.
| Bites, Insects | Spider Envenomations, Funnel Web |
| Botulism | Spider Envenomations, Redback |
| Caterpillar Envenomations | Spider Envenomations, Tarantula |
| CBRNE - Botulism | Spider Envenomations, Widow |
| Centipede Envenomations | Tetanus |
| Diphtheria | Tetanus |
| Disseminated Intravascular Coagulation | Toxicity, Medication-Induced Dystonic
Reactions |
| Myasthenia Gravis | Toxicity, Organophosphate |
| Pancreatitis | |
| Snake Envenomations, Coral | |
| Snake Envenomations, Rattle |
Myasthenia gravis
Diphtheria
Guillain-Barré syndrome
Neuroleptic overdose
Sympathomimetic overdose
Venomous jellyfish, snake, and lizard envenomation
Seizures
Dystonia
Scorpion envenomation cases vary from those requiring no laboratory tests to scenarios requiring extensive hematologic, electrolyte, and respiratory analysis.
The local sting site shows mixed inflammatory cell infiltrates with eosinophils scattered among collagen bundles in an edematous dermis. Myocardial changes, which are most prominent at the papillary muscle and subendocardial region, include focal myocardial necrosis; myofibril destruction, especially at the I band; fine fatty deposits in the cardiac muscle fibers; interstitial edema; and increased cellularity, mainly lymphocytes and monocytes. Changes resemble interstitial hypoxia-induced myocarditis caused by large doses of catecholamines.
Prehospital Care
Emergency Department Care
Supportive care is the backbone of treatment for systemic symptomatology.
Total >2 = Hospitalization
Medical care
Because the clinical manifestations and severity of the symptoms vary among patients, individualize management of scorpion stings. Furthermore, frequent patient monitoring allows earlier recognition of the life-threatening problems of scorpion envenomation. Treatment generally consists of moving the patient away from the scorpion and stabilizing the patient's airway and vital signs, followed by administration of antivenin and institution of symptomatic and local treatment.
Local poison control centers may assist in management of envenomations.
The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to neutralize the toxin.
Analgesia may be indicated. Exercise caution when using narcotics for a patient with an unsecured airway because respiratory depressive effects may be synergistic with some scorpion venoms. Some recommend against using narcotics to treat scorpion envenomation with signs of systemic toxicity, especially in children. Tetanus prophylaxis is recommended if the patient cannot verify current status. Prophylactic antibiotic therapy is not required. Corticosteroids have not been shown useful in treating venom toxicity. Hypertensive emergencies may require standard antihypertensive therapy. Conversely, hypotension may require fluid resuscitation and/or vasopressors.
Cardiovascular agents can be used to elevate or decrease blood pressure and increase heart rate. Vasopressors and inotropic agents may be necessary in patients who already have been adequately volume resuscitated but remain in shock. Conversely, antihypertensives may be needed in patients with sympathetic-induced hypertension. In particular, the use of the alpha-blocking agent prazosin has been used and recommended. However, all published evidence recommending for or against this agent has come from either retrospective observational or prospective cohort studies. A true randomized controlled trial of this agent has not been published.
At this time, no clear evidence exists as to which agent is most beneficial in specific circumstances. Autonomic instability from scorpion envenomation may lead to rapid, dramatic fluctuations in heart rate and blood pressure. Although many agents have rapid onset, they may also have prolonged effects. Should a hypertensive patient receive a longer-acting agent they may still have medication effects if they develop subsequent hypotension. In any case, agents should be chosen with detailed knowledge of their pharmacology and understanding of the pathophysiology of scorpion venom described above. Ideally, the agents are effective, have rapid onset, can be titrated to effect, have a short half-life if discontinued, and have minimal side effects.
A total of 22 types of scorpion antivenom are listed in the American Zoo and Aquarium Association Antivenom Index. They are available for a number of different species and have varied efficacy. Antivenom use remains controversial. Many researchers report decreased morbidity, mortality, and hospital stay with its use. These researchers and clinicians believe that antivenom therapy cannot be matched by supportive care in severe Buthidae scorpion envenomation. Others suggest that adverse effects (eg, anaphylactic reactions, serum sickness) limit or contraindicate antivenom use.
Until recently, the antivenom for stings by the bark scorpion was manufactured in the Antivenin Production Laboratory of Arizona State University. Its use was controversial. It had been shown to produce rapid resolution of systemic symptoms but not to affect pain or paresthesias. Subsequently, many physicians recommended it in grade III and grade IV envenomations. Adverse effects included immediate and delayed hypersensitivity reactions. Initially, these reactions were rare, but they increased in frequency. This leads some physicians to prefer supportive care only, as they felt that the treatment was potentially worse than the disease. As death was rare if existent, they felt supportive care would yield similar outcomes. Currently, it is no longer being produced. Subsequently, an increased pediatric ICU admission rate of 500% is being reported with scorpion envenomation.
The US Food and Drug Administration has recently given approval for experimental use of a Mexican antivenom (Alarcramyn, manufactured by Instituto Bioclon), which is currently undergoing phase II clinical trials.Scorpion toxins are not good antigens because of small size and poor immunogenicity. They do not induce antibodies that cross-react against toxins of other scorpion species unless a 95% amino acid sequence homology exists between the 2 toxins. Thus, no universal antivenin is available. Instead, 22 types of scorpion antivenin exist.
Furthermore, the neurotoxin component of the scorpion venom tends to be the least immunogenic, resulting in the low efficiency for neurological complications. It usually is prepared from horses because they yield larger quantities. Sheep, goat, or bovine antivenin may be prepared if patient sensitivity to horse serum occurs.
A recent idea was to mix a batch of different scorpion antivenin together to create a universal antivenin, but this exposes the patient to unnecessary antivenin from scorpion species not from the patient's region.
Perform a skin test prior to administering the antivenin. First, dilute 0.1 mL of antivenin in a 1:10 ratio with isotonic sodium chloride solution. Second, administer 0.2 mL intradermally. A positive test result is if a wheal develops within 10 minutes. The skin test has a sensitivity of 96% and a specificity of 68%.
The best result occurs when antivenin is administered as early as possible (preferably within the first 2 h after the sting) and with adequate quantities to neutralize the venom (usually 50-100 times the LD50 amount). A decrease in curative effects occurs with longer sting-serotherapy delay and administration of insufficient amounts of antivenin.
Used to neutralize toxins from scorpions. Produced in Arizona (for use in Arizona only). Not approved by FDA. Use remains controversial, but many physicians recommend it in grade III and IV envenomations. Shown to produce rapid resolution of systemic symptoms but does not affect pain or paresthesias. Results in resolution of symptoms within min to 2 h after administration. Antivenin treatment is based on venom burden, not patient's size. The smaller the victim, the more important it is to administer the full dose because of the venom dose-dependent severity.
Grade I and II: None
Grade III and IV: 1 vial (5 mL) in 50 mL saline IV over 30 min; if severe symptoms still persist after 1 h, repeat once prn
Administer as in adults
None reported
Documented hypersensitivity; may administer in severe envenomation, despite hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Due to presence of horse serum, agents for emergency treatment of anaphylaxis should be available; premedicate with antihistamines or steroids
Prevent the histamine response in sensory nerve endings and blood vessels. They are more effective in preventing histamine response than in reversing it.
An H2 antagonist that, when combined with an H1 type, may be useful in treating itching and flushing in anaphylaxis, pruritus, urticaria, and contact dermatitis that do not respond to H1-receptor antagonists alone. Use in addition to H1 antihistamines. Other H2 antagonists are also available.
Patients with persistent symptoms: 300 mg IV followed by PO administration as outpatient q6h for 2 d or for as long as clinically indicated
25-30 mg/kg/d IV in 6 divided doses
Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Elderly people may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or discontinue treatment if changes in renal function occur
Used for the symptomatic relief of allergic symptoms caused by histamine released in response to allergens.
25-50 mg PO q6-8h prn; not to exceed 400 mg/d
10-50 mg IV/IM q6-8h prn; not to exceed 400 mg/d
12.5-25 mg PO tid/qid or 5 mg/kg/d or 150 mg/m2/d PO divided tid/qid; not to exceed 300 mg/d
5 mg/kg/d or 150 mg/m2/d IV/IM divided qid; not to exceed 300 mg/d
Potentiates effect of CNS depressants; because of alcohol content, do not give syrup dosage form to patient taking medications that can cause disulfiramlike reactions
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction
Wounds resulting from scorpion sting are at risk of Clostridium tetani infection. A booster injection in previously immunized individuals is recommended to prevent this potentially lethal syndrome. Administer tetanus immune globulin (Hyper-Tet) to patients not immunized against C tetani products (eg, persons who have immigrated, elderly individuals).
Used to induce active immunity against tetanus in selected patients. Tetanus and diphtheria toxoids are the immunizing agents of choice for most adults and children >7 y. Booster doses are necessary to maintain tetanus immunity throughout life because tetanus spores are ubiquitous.
In children and adults, administer into the deltoid or midlateral thigh muscles. In infants, preferred site of administration is the mid thigh laterally
Primary immunization: 0.5 mL IM; administer 2 injections 4-8 wk apart and a third dose 6-12 m after the second injection.
Booster dose: 0.5 mL IM q10y
Administer as in adults
Patients receiving immunosuppressants, including corticosteroids or radiation therapy, may remain susceptible despite immunization because of poor immune response; cimetidine may enhance or augment delayed-hypersensitivity responses to skin-test antigens; avoid concurrent use of medication with systemic chloramphenicol because it may impair amnestic response to tetanus toxoid; concurrent use of tetanus immune globulin may delay development of active immunity by several days (interaction is nevertheless clinically insignificant and does not preclude its concurrent use)
Documented hypersensitivity; history of any type of neurological symptoms or signs following administration of this product; FDA recommends that elective tetanus immunization be deferred during any outbreak of poliomyelitis because tetanus toxoid injections are an important cause of provocative poliomyelitis
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not use to treat actual tetanus infections or for immediate prophylaxis of unimmunized individuals (use tetanus antitoxin instead, preferably human tetanus immune globulin); diminished antibody response to active immunization may be observed in patients receiving immunosuppressive therapy; better to defer primary diphtheria immunization until immunosuppressive therapy discontinued; routine immunization of symptomatic and asymptomatic persons with HIV is recommended
These agents induce passive immunity. Administer to patients not immunized against C tetani products (eg, persons who have immigrated, elderly individuals).
Used for passive immunization of any person with a wound that might be contaminated with tetanus spores.
Prophylaxis: 250-500 U IM in opposite extremity to tetanus toxoid lesion
Clinical tetanus: 3000-10,000 U IM
Prophylaxis: 250 U IM in opposite extremity as tetanus toxoid
Clinical tetanus: 3000-10,000 U IM
None reported
Because antibodies in globulin preparation may interfere with immune response to vaccination, do not administer within 3 mo of live-virus immune globulin administration; may be necessary to revaccinate persons who received immune globulin shortly after live-virus vaccination
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Persons with isolated immunoglobulin A (IgA) deficiency have potential for developing antibodies to IgA and may have anaphylactic reactions to subsequent administration of blood products that contain IgA; do not perform skin testing because intradermal injection of concentrated gamma globulin may cause localized area of inflammation and can be misinterpreted, causing the medication to be withheld from a patient not allergic to this material; true allergic responses to human gamma globulin given in prescribed IM manner are extremely rare; do not admix with other medications because usually incompatible
By increasing the action of GABA (inhibitory neurotransmitter), counteract scorpion-induced excessive motor activity and nervous system excitation.
Sedative hypnotic with short onset of effects and relatively long half-life.
By increasing action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.
1-4 mg IV over 2-5 min; may repeat dose in 10-15 min prn
0.05 mg/kg IV over 2-5 min; may repeat dose in 10-15 min prn
Toxicity in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs
Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, Parkinson disease, hypotension, and respiratory depression
Short-acting benzodiazepine that can be administered in continuous infusion for severe nervous system excitation.
0.1 mg/kg IV bolus then 0.1 mg/kg/h; titrate dose upward q5min until symptoms controlled
Administer as in adults
Sedative effects may be antagonized by theophyllines; narcotics and erythromycin may accentuate sedative effects because of decreased clearance
Documented hypersensitivity; preexisting hypotension, narrow-angle glaucoma, and sensitivity to propylene glycol (the diluent)
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, pulmonary disease, renal impairment, and hepatic failure; may require intubation and pressor support
Used to counteract scorpion-induced hyperactivity.
Short-acting barbiturate with sedative and anticonvulsant properties used to produce barbiturate coma for severe CNS hyperexcitation. Requires patient intubation prior to use.
12 mg/kg IV bolus, then 5 mg/kg/h; titrate to symptom abatement or EEG inactivity
Administer as in adults
Concomitant use with alcohol may produce additive CNS effects and death; chloramphenicol may inhibit metabolism; may enhance chloramphenicol metabolism; MAOIs may enhance sedative effects of barbiturates; valproic acid appears to decrease barbiturate metabolism, increasing toxicity; barbiturates can decrease effects of anticoagulants (patients may require dosage adjustments if barbiturates are added to or withdrawn from regimen); decreased contraceptive effect may occur due to induction of microsomal enzymes (alternate form of birth control is suggested); barbiturates may decrease corticosteroid and digitoxin effects through induction of hepatic microsomal enzymes that increase metabolism; barbiturates decrease theophylline levels and may decrease effects; may decrease verapamil bioavailability
Documented hypersensitivity; liver failure; porphyria
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Patient may become tolerant to hypnotic effects; caution in patients with hypovolemic shock, respiratory dysfunction, hypotension, renal dysfunction, congestive heart failure, previous addiction to sedative hypnotics, and congestive heart failure
Tend to be more effective than opiates to control paresthesia and pain at the sting site.
May reduce pain by slowing nerve impulse propagation and reducing action potential, which, in turn, prevents initiation and conduction of nerve impulses.
1.25 mg/kg/dose intralesionally until pain subsides; not to exceed 3-4 mg/kg
Administer as in adults
May enhance effects of CNS depressants; coadministration may increase toxicity of MAOIs, TCAs, beta-blockers, vasopressors, and phenothiazines
Documented hypersensitivity; septicemia, spinal deformities, severe hypertension, and existing neurologic disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Test a dose and monitor for CNS toxicity, cardiovascular toxicity, and signs of unintended intrathecal administration; caution with inflammation or sepsis in region of proposed injection; monitor patient's state of consciousness after each injection; caution in hypertension, cerebral vascular insufficiency, peripheral vascular disease or heart block, hypoxia, hypovolemia, and arteriosclerotic heart disease
Used to counteract the scorpion-induced adrenergic cardiovascular effect.
Blocks beta1-adrenergic, alpha-adrenergic, and beta2-adrenergic receptor sites, decreasing blood pressure.
20 mg IV then 40 mg IV repeated q10-15min until BP controlled or until the maximum accumulative dose of 300 mg is reached
Not established
Suggested: 0.1 mg/kg IV; repeat q15-20min as last resort
Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia resulting from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase blood levels; glutethimide may decrease effects by inducing microsomal enzymes
Documented hypersensitivity; cardiogenic shock, pulmonary edema, bradycardia, atrioventricular block, uncompensated congestive heart failure, reactive airway disease, and severe bradycardia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in impaired hepatic function; discontinue therapy if signs of liver dysfunction occur; in elderly patients, a lower response rate and higher incidence of toxicity may be observed; caution with concomitant beta-blockers; beware of continued hypertension despite decreasing heart rate due to insufficient alpha blockade
Counteracts scorpion-induced adrenergic cardiovascular effects. May improve pulmonary edema through vasodilatory effects.
1 mg PO bid/tid; not to exceed 5 mg/dose
Not established
Acute postural hypotensive reaction from beta-blockers may worsen; indomethacin may decrease antihypertensive activity; verapamil may increase serum levels and may increase patient's sensitivity to prazosin-induced postural hypotension; may decrease antihypertensive effects of clonidine
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal insufficiency and hypotension
Decreases systemic resistance through direct vasodilation of arterioles
10-20 mg IV q4-6h
Not established
MAOIs and beta-blockers may increase toxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May cause hydralazine-induced tachycardia, SLE-type syndrome, and peripheral neuritis
Used to counteract scorpion-induced cholinergic symptoms. Current recommendations are for use in treating symptomatic bradycardias. Traditionally, its use to dry venom-induced, excess, respiratory secretions has been warned against because of its potential adverse cardiopulmonary effects. It may exacerbate pulmonary edema and hypertension and may lead to a subsequent tachycardia. A recent case series has suggested relative efficacy and safety with its use in 5 pediatric patients treated for C sculpturatus sting. However, this should be considered an area in need of further study rather than a change in recommendations.
Used to increase heart rate through vagolytic effects, causing an increase in cardiac output. Also treats bronchorrhea associated with scorpion envenomations. Atropine causes a reversible blockade of muscarinic receptors with subsequent anticholinergic effects. Has been used to reverse vagally induced symptomatic bradycardias, which may be associated with scorpion envenomation. Its use for dry secretions is debated. Will not reverse the somatic or other cranial nerve symptoms.
0.5-1 mg IV q15min until desired effect (Note: for vagolytic cardiac effects, there is a 3-mg limit)
0.01 mg/kg IV q15min until desired effect (Note: For cardiac vagolytic effects, there is a 3-mg limit)
Coadministration with other anticholinergics (eg, pramlintide) has additive effects; pharmacologic effects of atenolol and digoxin may increase; antipsychotic effects of phenothiazines may decrease; TCAs with anticholinergic activity may increase effects
Documented hypersensitivity; thyrotoxicosis, narrow-angle glaucoma, and tachycardia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid in Down syndrome and/or children with brain damage to prevent hyperreactive response; also avoid in patients with coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, and hypertension; cardiac monitoring is mandatory; care must be used to detect marked tachycardia, which may be present with scorpion envenomation; caution in patients with peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in patients with prostatic hypertrophy, prostatism may cause dysuria and may require catheterization; monitor patients for anticholinergic effects (eg, hyperthermia, dilated pupils, dry mucous membrane, tachycardia)
Used to combat hypotension refractory to IV fluid therapy.
Indicated for persistent hypotension not responsive to judicious fluid loading and sodium bicarbonate.
0.05-0.15 mcg/kg/min IV infusion; titrate to effect
0.1-1 mcg/kg/min IV infusion; titrate to effect
Chlorpromazine enhances pressor response by blocking reflex bradycardia caused by norepinephrine
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Administer into a large vein because extravasation may cause severe tissue necrosis; caution in occlusive vascular disease
Sympathomimetic amine with stronger beta than alpha effects. Increases inotropic state with afterload reduction.
5-20 mcg/kg/min IV continuous infusion, titrate to desired response; not to exceed 40 mcg/kg/min
Administer as in adults
Beta-blockers antagonize effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Higher dosages may cause increase in heart rate and exacerbate hypotension
Positive inotropic agent and vasodilator with little chronotropic activity.
50 mcg/kg loading dose IV over 10 min, followed by 0.375-0.75 mcg/kg/min continuous IV infusion
Administer as in adults because has been used in the pediatric ICUs, although safety and efficacy not well established
May precipitate if infused in the same IV line as furosemide
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Slow or stop infusion in patients showing excessive decreases in blood pressure
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scorpion sting, scorpion envenomation, scorpion venom, arthropod sting, insect sting, arachnid sting, venom, antivenom, antivenin, Buthidae, Scorpionidae, Ischnuridae, Buthus, Parabuthus, Mesobuthus, Tityus, Leiurus, Androctonus, Centruroides, Centruroides exilicauda, Centruroides sculpturatus, C sculpturatus, neurotoxin, cardiotoxin, nephrotoxin, toxin, wildlife emergency, envenomation, severe local skin reaction, neurologic collapse, respiratory collapse, cardiovascular collapse, respiratory failure, cardiovascular failure, Buthus, Mesobuthus, Buthotus, Buthus tamulus, Hottentotta, Leiurus, Leiurus quinquestriatus, Leiurus quinquestriatus, Androctonus, Androctonus australis, Hemiscorpius, Hemiscorpius lepturus
David Cheng, MD, Assistant Professor of Emergency Medicine, Associate Emergency Medicine Residency Director, Associate Medical Director of Emergency Services, University of Arkansas Medical Sciences
David Cheng, MD is a member of the following medical societies: American College of Emergency Physicians, American Heart Association, Council of Emergency Medicine Residency Directors, International Society for Mountain Medicine, National Association of EMS Physicians, Society for Academic Emergency Medicine, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.
Judith A Dattaro, MD, FACEP, Assistant Professor of Emergency Medicine in Surgery, Cornell University Medical College; Consulting Staff, Department of Emergency Medicine, Weill-Cornell University Medical Center, New York Presbyterian Hospital
Judith A Dattaro, MD, FACEP is a member of the following medical societies: American Association of Women Emergency Physicians, American College of Emergency Physicians, American Medical Association, Chicago Medical Society, Illinois State Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Ramy Yakobi, MD, MBA, Medical Director of Emergency Department, Beth Israel/Kings Highway Division; Lecturer, Physician Assistant School, Cornell School of Medicine; Lecturer, Pre-hospital Management of Patient, Cornell/New York Presbyterian Hospital; Director of Emergency Department, New York Community Hospital
Ramy Yakobi, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.
Lisa Kirkland, MD, FACP, CNSP, MSHA, Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; ANW Intensivists, Abbott Northwestern Hospital
Lisa Kirkland, MD, FACP, CNSP, MSHA is a member of the following medical societies: American College of Physicians, Society of Critical Care Medicine, and Society of Hospital Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Om Prakash Sharma, MD, FRCP, FCCP, DTM&H, Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California Keck School of Medicine
Om Prakash Sharma, MD, FRCP, FCCP, DTM&H is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Osler Society, American Thoracic Society, New York Academy of Medicine, and Royal Society of Medicine
Disclosure: Keck School of Medicine, USC None None
Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.
Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
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