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SCORPIONS, ANDROCTONUS SPECIES

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Scorpions are members of the order Scorpionida, and are the most primitive and oldest members of the terrestrial arachnids.

Specific Substances

    1) Androctonus species
    2) A. aeneas
    3) A. amoreuxi
    4) A. australis
    5) A. crassicauda
    6) ANDROCTONUS SPECIES SCORPIONS

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) DESCRIPTION: Scorpions of the genus Androctonus are commonly referred to as fat-tailed scorpions. Androctonus species are native to North Africa. They are found throughout the semi-arid and arid regions of Africa and the Middle East.
    B) TOXICOLOGY: Androctonus australis venom have at least 5 distinct toxins which bind sodium channels and also prolong the axonal action potential by slowing down the inactivation process of these channels. There may also be effects on potassium channels. Other effects observed in animals, injected with the venom included rapid and significant increases of norepinephrine, epinephrine, neuropeptide Y, endothelin 1, and atrial natriuretic peptide (ANP).
    C) EPIDEMIOLOGY: In areas where Androctonus scorpions are endemic, envenomations have been reported. These scorpions can be kept as pets or in zoos worldwide, so although highly unusual and very rare, envenomations could occur outside the geographic area where these scorpions normally live.
    D) WITH POISONING/EXPOSURE
    1) ENVENOMATIONS: Although A. australis, A. amoreuxi, A. aeneas and A. crassicauda are all potentially dangerous North African species. A. australis is responsible for about 80% of the accidents and 95% of the deaths; pulmonary edema may develop.
    2) CLINICAL EFFECTS: Symptoms are a result of depolarization of nerves and muscles as a consequence of effects in sodium and potassium ion channels.
    3) SPECIES OF CLINICAL CONCERN: A. australis envenomation can produce hypertension, diaphoresis, fever, shivering, vomiting, priapism, cardiogenic shock, pulmonary edema, and an altered level of consciousness. A. crassicauda envenomations may cause pain, tachycardia, tachypnea, agitation, irritability, seizures, coma, salivation, diaphoresis, vomiting, hypotension, leukocytosis, hyponatremia, elevated serum amylase, elevated creatine phosphokinase and elevated lactate dehydrogenase.
    4) TYPICAL SYMPTOMS: Most patients develop local pain only. Ten to 20 percent of patients who present to the hospital will develop systemic effects after envenomation. In general, about 3% of all patients stung by Androctonus scorpions develop systemic effects.

Laboratory Monitoring

    A) Patients who develop only local pain may not need any laboratory studies.
    B) Monitor vital signs. In symptomatic patients obtain an ECG and initiate continuous cardiac monitoring.
    C) Patients that develop systemic symptoms may require labs that may include a basic metabolic panel, creatinine phosphokinase, and arterial blood gases.
    D) Obtain a chest x-ray and begin continuous pulse oximetry in patients with evidence of pulmonary edema.

Treatment Overview

    0.4.7) BITES/STINGS
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Management of mild to moderate toxicity may require only symptomatic treatment and good local wound care (eg, update tetanus vaccination as needed, cleaning of the site of the sting). Patients with local pain only can be treated with analgesics as needed. Ice can be used to reduce pain at the site of envenomation on a temporary basis and local anesthetics have also been used at the site of envenomation and pain. Patients who develop nausea and vomiting can be treated with antiemetics and fluid hydration as needed. Hyperthermia can be treated with external cooling and antipyretics.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) The mainstay of treatment for severe toxicity is supportive care. Seizures are rare, initially treat with benzodiazepines, barbiturates as needed. Pulmonary edema is the leading cause of death in these patients, and can be treated with mechanical ventilation with PEEP and dobutamine (a dobutamine infusion has been shown to be effective in treating cardiogenic shock and pulmonary edema from an Androctonus envenomation). Ischemic priapism can be treated with therapeutic aspiration followed by local injections of sympathomimetics as needed.
    C) DECONTAMINATION
    1) PREHOSPITAL: There is no role for ipecac or activated charcoal for scorpion stings. Local wound care is reasonable but will not directly treat the envenomation.
    2) HOSPITAL: There is no role for the use of activated charcoal, whole bowel irrigation, or gastric lavage for scorpion stings.
    D) AIRWAY MANAGEMENT
    1) Pulmonary edema may develop in severe cases of scorpion stings and may necessitate early intubation if respiratory status worsens quickly. Manage airway aggressively and administer oxygen as needed. Excessive secretions and respiratory distress are common with most species.
    E) ANTIDOTE
    1) Antivenoms have been developed against the scorpion venom. However, studies have shown that the efficacy of these antivenoms has shown mixed results.
    F) ENHANCED ELIMINATION
    1) There is no evidence for the use of dialysis, hemoperfusion, urinary alkalinization or multiple dose charcoal.
    G) PATIENT DISPOSITION
    1) OBSERVATION CRITERIA: Patients with symptoms that are worsening or systemic symptoms should be sent to a healthcare facility for observation and observed for 4 to 6 hours or until they are clearly improving. Criteria for discharge include patients who are medically stable and clearly improving.
    2) ADMISSION CRITERIA: Any patients with worsening symptoms or systemic symptoms that are worrisome (eg, abnormal vital signs) should be admitted to the hospital, and may necessitate an ICU admission if they develop severe symptoms such as pulmonary edema requiring vasopressor and/or intubation. Patients should not be discharged until they are clearly improving and medically stable.
    3) CONSULT CRITERIA: Depending on the severity of symptoms, an intensivist consultation may be needed for patients who develop pulmonary edema and require ICU care. A toxicologist or poison center may be involved at any time for advice and help to facilitate access to antivenoms.
    H) PITFALLS
    1) One potential pitfall may be the lack of recognition of the potential severity of symptoms. Another is that these scorpions may be kept as pets in areas where they are not endemic, and thus stings may potentially occur worldwide.
    I) TOXICOKINETICS
    1) The absorption of Androctonus australis venom is rapid in humans. The venom concentration in blood peaked within 30 minutes in a series of envenomated patients. The mean elimination half-life of Androctonus australis venom in a case series of patients with grade II envenomations was about 2 hours.
    J) PREDISPOSING CONDITIONS
    1) Extremes of age, especially small children, may be more sensitive to the effects of scorpion venom, especially since the dose of scorpion venom per body weight may be far higher for small children compared to adults. Older adults with multiple co-morbidities may be more sensitive to systemic effects of scorpion venom.
    K) DIFFERENTIAL DIAGNOSIS
    1) Envenomations from other arthropods (eg, spiders, insects, other scorpion genera) may have similar features of Androctonus stings.

Range Of Toxicity

    A) TOXICITY: A single sting can be fatal, although death is less common with current management including use of intensive care facilities for patients with pulmonary edema and the use of antivenom.

Vital Signs

    3.3.3) TEMPERATURE
    A) HYPERTHERMIA
    1) Hyperthermia is an important sign in stings from A. australis (Goyffon et al, 1982).
    2) INCIDENCE: In a series of 600 patients, most of whom sustained A. australis envenomation, 37 (6%) developed fever (Abroug et al, 1997).
    3) INCIDENCE: In a series of 825 patients with Androctonus australis or Buthus occitanus stings, 32 (3.9%) developed fever (Abroug et al, 1999).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: In a series of 51 patients with Androctonus crassicauda envenomation, one infant developed shock (Ismail, 1994).
    b) INCIDENCE: In a series of 600 patients, most of whom sustained A. australis envenomation, 4 (0.7%) developed cardiogenic shock (Abroug et al, 1997) Two of these patients died.
    c) In another series of 172 patients, 70% of whom were stung by A australis, 10 (6%) developed hypotension (Hammoudi-Triki et al, 2004).
    d) INCIDENCE: In a series of 825 patients with Androctonus australis or Buthus occitanus stings, 9 (1.1%) developed cardiogenic shock (Abroug et al, 1999).
    B) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) In a series of 51 patients with Androctonus crassicauda envenomation, mild hypertension developed in most children under age 11 and a few adults (Ismail, 1994).
    b) INCIDENCE: In a series of 600 patients, most of whom sustained A. australis envenomation, 28 (5%) developed hypertension (Abroug et al, 1997).
    c) INCIDENCE: In a series of 825 patients with Androctonus australis or Buthus occitanus stings, 94 (11.4%) developed hypertension (Abroug et al, 1999).
    C) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) In a series of 51 patients with Androctonus crassicauda envenomation, 3 developed tachycardia (Ismail, 1994).
    b) In another series of 172 patients, 70% of whom were stung by A australis, 14 (8%) developed tachycardia (Hammoudi-Triki et al, 2004).
    D) HEART FAILURE
    1) WITH POISONING/EXPOSURE
    a) In a series of 5 adults with pulmonary edema after Androctonus envenomation, all had tachycardia, decreased stroke volume and increased pulmonary capillary wedge pressure secondary to left ventricular dysfunction (Abroug et al, 1991).
    b) In a series of 9 adults with pulmonary edema after A. australis envenomation, all demonstrated hypokineses of the left ventricle with depressed left ventricular systolic function (mean ejection fraction 26%) (Abroug et al, 1995).
    E) BRADYCARDIA
    1) WITH POISONING/EXPOSURE
    a) In a series of 51 patients with Androctonus crassicauda envenomation, one developed bradycardia (Ismail, 1994).
    b) In another series of 172 patients, 70% of whom were stung by A australis, 10 (6%) developed bradycardia (Hammoudi-Triki et al, 2004).
    c) A 54-year-old woman stung by an A. crassicauda scorpion developed bradycardia (40 beats/minute) 12 hours later which resolved by 24 hours (Blum et al, 1992).
    F) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Two women stung by A. crassicauda scorpions developed ST and T wave changes which resolved within 24 hours (Blum et al, 1992).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DYSRHYTHMIAS
    a) The venom of Androctonus amoreuxi was studied in animals. Researchers found that the arrhythmias and infarcts occurred at a time when the tissue concentration of the venom in the heart was very low, suggesting these cardiac abnormalities might be a result of indirect factors (Ismail & Abd-Elsalam, 1988).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) PULMONARY EDEMA
    1) WITH POISONING/EXPOSURE
    a) SUMMARY
    1) In Tunisia, the Androctonus australis and Buthus occitanus scorpions are likely to produce severe envenomation. Pulmonary edema is the most severe respiratory effect of envenomation and can be the leading cause of death. Although the exact mechanism is unknown, the development of acute left ventricular failure has been associated with severe envenomation including pulmonary edema. Clinical manifestations usually associated with pulmonary edema include: young age, tachypnea, diaphoresis from excess catecholamine release and from sympathic and parasympathic nervous system stimulation, agitation which may be associated with seizures and coma. In addition, pulmonary edema is often preceded by high blood pressure that may lead to the neurologic effects observed (Bahloul et al, 2013).
    2) CASE REPORT: A 65-year-old woman developed immediate pain in her left calf and left flank following a presumed bite and was initially treated with hydrocortisone and IV promethazine for the unknown bite. However, 3.5 hours later she developed severe agitation and slurred speech and was brought to an Emergency Department. Upon physical examination, erythema and swelling were detected on the left calf along with 2 macules on her left flank. Despite treatment with an IV antihistamine and hydrocortisone, the patient became severely agitated and required IV midazolam. She suddenly became drowsy with weak radial pulses and fine crackles in all lung fields requiring immediate intubation. Chest x-ray showed evidence of pulmonary edema. About this time, it was confirmed that the patient had been stung by an Androcotonus Crassicauda (the scorpion had been found on the patient's bed clothes) and was treated with 10 mL of polyvalent scorpion antivenom. Within 30 minutes, the patient's skin became warmer and sweating decreased; however, agitation and tachycardia were still present. She gradually improved and over the next 5 hours the patient was successfully extubated and was discharged 1 day later with no symptoms (Aghabiklooei et al, 2014).
    b) ONSET
    1) Pulmonary edema occurs with A. australis stings; in one study the mean onset time was 9.6+/-5.2 hours. All 5 patients seen had increased pulmonary capillary wedge pressure (Abroug et al, 1991).
    c) INCIDENCE
    1) In a series of 600 patients, most of whom sustained A. australis envenomation, 12 (2%) developed pulmonary edema (Abroug et al, 1997). Two of these patients died.
    2) In a series of 825 patients with Androctonus australis or Buthus occitanus stings, 6 (0.7%) developed pulmonary edema (Abroug et al, 1999).
    3) In a series of 8 adults with pulmonary edema after A. australis envenomation, all had decreased right ventricular ejection fraction (mean 24%) and cardiac index (mean 2.44 liters/minute/meter(2)) and increased pulmonary artery occlusion pressure (mean 23 mmHg) (Nouira et al, 1995). The right ventricular dysfunction was not associated with an increase in pulmonary vascular resistance, and appeared to be secondary to left ventricular dysfunction.
    d) RISK FACTORS
    1) In a retrospective study of patients with severe scorpion sting admitted to an intensive care unit of a hospital in Tunisia, multivariate analysis indicated that the following factors were associated with pulmonary edema (PE): age less than 5 years, sweating, agitation, leukocytes great than 25,000 and a plasma protein concentration of 72 g/L or more. A respiratory rate greater than or equal to 30 breaths/minute along with sweating and agitation was associated with the presence of PE in 84% of cases. A plasma protein concentration of 72 g/L or greater had a sensitivity of 78% and a specificity of 88% to predict the presence of pulmonary edema. In addition, the presence of a plasma protein concentration of 72 g/L or greater along with an increased respiratory rate (greater than 30 breaths/minute), agitation, sweating and hyperglycemia was present in 95% of PE cases. The authors suggested that these simple parameters along with laboratory analysis and chest x-ray may be useful criteria in identifying patients at risk for potential myocardial dysfunction. Study limitations included the lack of scorpion identification and the exclusion of patients with only local effects (Bouaziz et al, 2006).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) PSYCHOMOTOR AGITATION
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: In a series of 51 patients with Androctonus crassicauda envenomation, 10 (20%) developed restlessness, irritability or agitation (Ismail, 1994).
    b) Agitation has been associated with A. australis envenomations (Nouira et al, 2007).
    c) CASE REPORT: A 65-year-old woman developed immediate pain in her left calf and left flank following a presumed bite and was initially treated with hydrocortisone and IV promethazine for the unknown bite. However, 3.5 hours later she developed severe agitation and slurred speech and was brought to an Emergency Department. Upon physical examination, erythema and swelling were detected on the left calf along with 2 macules on her left flank. Despite treatment with an IV antihistamine and hydrocortisone, the patient became severely agitated and required IV midazolam. She suddenly became drowsy with weak radial pulses and fine crackles in all lung fields requiring immediate intubation. Chest x-ray showed evidence of pulmonary edema. About this time, it was confirmed that the patient had been stung by an Androcotonus Crassicauda (the scorpion had been found on the patient's bed clothes) and was treated with 10 mL of polyvalent scorpion antivenom. Within 30 minutes, the patient's skin became warmer and sweating decreased; however, agitation and tachycardia were still present. She gradually improved and over 5 hours the patient was successfully extubated and was discharged 1 day later with no symptoms (Aghabiklooei et al, 2014).
    B) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: In a series of 51 patients with Androctonus crassicauda envenomation, 3 (6%) developed lethargy, drowsiness or coma (Ismail, 1994).
    b) INCIDENCE: In a series of 600 patients, most of whom sustained A. australis envenomation, 2 developed an altered level of consciousness (Glasgow coma score < 10) (Abroug et al, 1997).
    c) INCIDENCE: In a series of 825 patients with Androctonus australis or Buthus occitanus stings, 2 (0.2%) developed an altered level of consciousness (GCS < 10) (Abroug et al, 1999).
    C) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) In a series of 51 patients with Androctonus crassicauda envenomation 2 (4%) developed seizures (Ismail, 1994).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) In a series of 51 patients with Androctonus crassicauda envenomation 3 developed vomiting (Ismail, 1994).
    b) INCIDENCE: In a series of 600 patients, most of whom sustained A. australis envenomation, 7 (1%) developed vomiting (Abroug et al, 1997). In another large case series (n=1303), 52 patients (4%) reported vomiting following A. australis envenomation. Abdominal pain and diarrhea were also reported following envenomation (Nouira et al, 2007).
    c) INCIDENCE: In a series of 825 patients with Androctonus australis or Buthus occitanus stings, 17 (2.1%) developed vomiting (Abroug et al, 1999).
    B) EXCESSIVE SALIVATION
    1) WITH POISONING/EXPOSURE
    a) In a series of 51 patients with Androctonus crassicauda envenomation, one developed profuse salivation (Ismail, 1994).
    C) PANCREATITIS
    1) WITH POISONING/EXPOSURE
    a) In a series of 51 patients with Androctonus crassicauda envenomation 2 developed elevated serum amylase levels (Ismail, 1994).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) PRIAPISM
    1) WITH POISONING/EXPOSURE
    a) In a series of 51 patients with Androctonus crassicauda envenomation 1 developed priapism (Ismail, 1994).
    b) INCIDENCE: In a series of 600 patients, most of whom sustained A. australis envenomation, 7 (1%) developed priapism (Abroug et al, 1997). In another large case series of patients who sustained an envenomation (n=1303) , incidence rates were similar (1.8%), but priapism was the most common adverse effect associated with hospitalization (Nouira et al, 2007).
    c) INCIDENCE: In a series of 825 patients with Androctonus australis or Buthus occitanus stings, 16 (1.9%) developed priapism (Abroug et al, 1999).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) In a series of 51 patients with Androctonus crassicauda envenomation 9 developed leukocytosis (Ismail, 1994).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    1) WITH POISONING/EXPOSURE
    a) In a series of 51 patients with Androctonus crassicauda envenomation 2 developed profuse sweating (Ismail, 1994).
    b) INCIDENCE: In a series of 600 patients, most of whom sustained A. australis envenomation, 54 (9%) developed profuse sweating (Abroug et al, 1997).
    c) In another series of 172 patients, 70% of whom were stung by A australis, 16 (9%) developed excessive sweating (Hammoudi-Triki et al, 2004).
    d) INCIDENCE: In a series of 825 patients with Androctonus australis or Buthus occitanus stings, 70 (8.5%) developed profuse diaphoresis (Abroug et al, 1999).
    B) ERUPTION
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: In a series of 51 patients with androctonus crassicauda envenomation, generalized erythema developed in 20% to 25% of children under the age of 5 years (Ismail, 1994).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: In a series of 51 patients with Androctonus crassicauda envenomation, 3 (6%) developed mild rhabdomyolysis (elevated CPK and/or LDH) (Ismail, 1994).
    B) PAIN
    1) WITH POISONING/EXPOSURE
    a) Local pain at the site of the sting occurs in virtually all envenomated patients. Local pain is the only manifestation in most patients; 10% to 20% of patients who present to the hospital go on to develop systemic manifestations as well (Abroug et al, 1999; Aloufy et al, 2000; Hammoudi-Triki et al, 2004). The incidence of systemic effects among all patients stung by Androctonus scorpions is probably closer to 3% (Elatrous et al, 1999).
    b) In a large case series of patients with A. australis envenomations, localized pain was reported in over 90% of patients (Nouira et al, 2007).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: In a series of 51 patients with Androctonus crassicauda envenomation, 5 (10%) developed hyperglycemia (Ismail, 1994).

Summary Of Exposure

    A) DESCRIPTION: Scorpions of the genus Androctonus are commonly referred to as fat-tailed scorpions. Androctonus species are native to North Africa. They are found throughout the semi-arid and arid regions of Africa and the Middle East.
    B) TOXICOLOGY: Androctonus australis venom have at least 5 distinct toxins which bind sodium channels and also prolong the axonal action potential by slowing down the inactivation process of these channels. There may also be effects on potassium channels. Other effects observed in animals, injected with the venom included rapid and significant increases of norepinephrine, epinephrine, neuropeptide Y, endothelin 1, and atrial natriuretic peptide (ANP).
    C) EPIDEMIOLOGY: In areas where Androctonus scorpions are endemic, envenomations have been reported. These scorpions can be kept as pets or in zoos worldwide, so although highly unusual and very rare, envenomations could occur outside the geographic area where these scorpions normally live.
    D) WITH POISONING/EXPOSURE
    1) ENVENOMATIONS: Although A. australis, A. amoreuxi, A. aeneas and A. crassicauda are all potentially dangerous North African species. A. australis is responsible for about 80% of the accidents and 95% of the deaths; pulmonary edema may develop.
    2) CLINICAL EFFECTS: Symptoms are a result of depolarization of nerves and muscles as a consequence of effects in sodium and potassium ion channels.
    3) SPECIES OF CLINICAL CONCERN: A. australis envenomation can produce hypertension, diaphoresis, fever, shivering, vomiting, priapism, cardiogenic shock, pulmonary edema, and an altered level of consciousness. A. crassicauda envenomations may cause pain, tachycardia, tachypnea, agitation, irritability, seizures, coma, salivation, diaphoresis, vomiting, hypotension, leukocytosis, hyponatremia, elevated serum amylase, elevated creatine phosphokinase and elevated lactate dehydrogenase.
    4) TYPICAL SYMPTOMS: Most patients develop local pain only. Ten to 20 percent of patients who present to the hospital will develop systemic effects after envenomation. In general, about 3% of all patients stung by Androctonus scorpions develop systemic effects.

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Patients who develop only local pain may not need any laboratory studies.
    B) Monitor vital signs. In symptomatic patients obtain an ECG and initiate continuous cardiac monitoring.
    C) Patients that develop systemic symptoms may require labs that may include a basic metabolic panel, creatinine phosphokinase, and arterial blood gases.
    D) Obtain a chest x-ray and begin continuous pulse oximetry in patients with evidence of pulmonary edema.
    4.1.2) SERUM/BLOOD
    A) BASIC METABOLIC PANEL
    1) Patients that develop systemic symptoms may require labs that may include a basic metabolic panel, creatinine phosphokinase, and arterial blood gases.
    B) ACID/BASE
    1) Obtain arterial blood gases and/or pulse oximetry in patients with evidence of pulmonary edema.
    4.1.4) OTHER
    A) OTHER
    1) ECG
    a) Obtain an ECG and institute continuous cardiac monitoring in symptomatic patients.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Obtain a chest radiograph in patients with evidence of pulmonary edema.

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.6) DISPOSITION/BITE-STING EXPOSURE
    6.3.6.1) ADMISSION CRITERIA/BITE-STING
    A) SUMMARY
    1) Any patients with worsening symptoms or systemic symptoms that are worrisome (eg, abnormal vital signs) should be admitted to the hospital, and may necessitate an ICU admission if they develop severe symptoms such as pulmonary edema requiring vasopressor and/or intubation. Patients should not be discharged until they are clearly improving and medically stable.
    B) PROSPECTIVE STUDY TO PREDICT NEED FOR HOSPITALIZATION
    1) Nouira et al (2007) prospectively derived (using 868 consecutive patients older than 10 years) and then validated (using 435 consecutive patients older than 10 years) a scoring system to predict the need for hospitalization after Androctonus australis sting. Patients with life threatening symptoms on ED presentation (hypotension, clinical signs of shock, respiratory failure or distress, CNS depression (GCS 13 or lower) and those 10 years old or younger were excluded. The following clinical manifestations were found to correlate with the need for admission and were assigned points on the scale (range for the scale 0 to 12 points):
    1) Priapism: Rating: +3 (OR 150.59; 95% CI 54.2-257.12)
    2) Vomiting: Rating: +2 (OR 15.82; 95% CI 5.5-25.49)
    3) Systolic blood pressure of greater than 160 mmHg: Rating: +2 (OR 13.38; 95% CI 5.75-21.12)
    4) Corticosteroids administration before arrival to ED: Rating: +2 (OR 10.06; 95% CI 3.8-19.16)
    5) Time delay to ED arrival of greater than 30 minutes: Rating: +1 (OR 3.71; 95% CI 1.53-9.01)
    6) Temperature greater than 38 degrees Celsius: Rating: +1 (OR 3.66; 95% CI 1.75-7.63)
    7) Heart rate greater than 100 beats per minute: Rating: +1 (OR 3.35; 95% CI 1.38-8.13)
    a) A mean score of 3.8 +/- 1.5 was recorded for hospitalized patients as compared to 1.0 +/- 0.3 in nonhospitalized patients (p < .001). Sensitivity of the tool was 89.2% using a cutoff value of 2 (108 patients among 121 required hospitalization). Negative predictive value was 97.1% (identified 438 patients among 451 did not require hospitalization). During the initial clinical evaluation, the authors concluded that a cutoff value of 2 provided both good sensitivity and negative predictive value. A score of less than 2 generally indicated that a patient could be safely discharged.
    b) The study was designed to be independent of any biologic markers due to a possible delay or lack of availability in rural health care settings. It was also designed to have broader application because not all victims may undergo biologic assessment during initial examination (Nouira et al, 2007).
    6.3.6.3) CONSULT CRITERIA/BITE-STING
    A) Depending on the severity of symptoms, an intensivist consultation may be needed for patients who develop pulmonary edema and require ICU care. A toxicologist or poison center may be involved at any time for advice and help to facilitate access to antivenoms.
    6.3.6.5) OBSERVATION CRITERIA/BITE-STING
    A) Patients with symptoms that are worsening or systemic symptoms should be sent to a healthcare facility for observation and observed for 4 to 6 hours or until they are clearly improving. Criteria for discharge include patients who are medically stable and clearly improving.

Monitoring

    A) Patients who develop only local pain may not need any laboratory studies.
    B) Monitor vital signs. In symptomatic patients obtain an ECG and initiate continuous cardiac monitoring.
    C) Patients that develop systemic symptoms may require labs that may include a basic metabolic panel, creatinine phosphokinase, and arterial blood gases.
    D) Obtain a chest x-ray and begin continuous pulse oximetry in patients with evidence of pulmonary edema.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) There is no role for ipecac or activated charcoal for scorpion stings. Local wound care is reasonable but will not directly treat systemic effects of an envenomation.

Summary

    A) TOXICITY: A single sting can be fatal, although death is less common with current management including use of intensive care facilities for patients with pulmonary edema and the use of antivenom.

Minimum Lethal Exposure

    A) SUMMARY
    1) A single sting can be fatal, although death is less common with current management including use of intensive care facilities for patients with pulmonary edema and the use of antivenom (El-Amin et al, 1994).

Toxicologic Mechanism

    A) ANDROCTONUS AUSTRALIS venom consists of a single chain of 60 to 70 amino acids and four disulfide bridges (Rochat et al, 1970) Martin & Rochat, 1986). There are actually 5 distinct toxins in this venom with a high affinity for specific binding sites on the sodium channel of excitable membranes. A prolongation of the axonal action potential is created by slowing down the inactivation process of the sodium channel (Jover et al, 1978; Rochat et al, 1979). The percent of toxin found in this venom is quite low, being about 3% of the total venom weight (Martin et al, 1987).
    B) According to a canine study, involving nine dogs who were intravenously administered scorpion venom (Androctonus australis hector), the hemodynamic changes observed, including transient increases in the mean arterial pressure (MAP), the pulmonary artery occlusion pressure (PAOP), and the decline in cardiac output, were associated with a rapid and significant increase in norepinephrine, epinephrine, neuropeptide Y, endothelin 1, and atrial natriuretic peptide (ANP). In particular, the increase in MAP was directly related to the rapid 28-fold increase of norepinephrine levels and appeared to be less significantly associated with serum toxin levels. There also appeared to be a significant direct relationship between the increase in PAOP and ANP plasma levels, suggesting that measurement of ANP plasma levels may be useful as an early biomarker of cardiac dysfunction following scorpion envenomation (Nouira et al, 2005).

General Bibliography

    1) AMA Department of DrugsAMA Department of Drugs: AMA Evaluations Subscription, American Medical Association, Chicago, IL, 1992.
    2) Abroug F, Ayari M, & Nouira S: Assessment of left ventricular function in severe scorpion envenomation: combined hemodynamic anc echo-Doppler study. Intensive Care Med 1995; 21:629-635.
    3) Abroug F, Boujdaria R, & Belghith M: Cardiac dysfunction and pulmonary edema following scorpion envenomation. Chest 1991; 100:1057-1059.
    4) Abroug F, ElAtrous A, & Nouira S: Serotherapy in scorpion envenomation: a randomized controlled trial. Lancet 1999; 354:906-909.
    5) Abroug F, Nouira S, & Haguiga H: High-dose hydrocortisone hemisuccinate in scorpion envenomation. Ann Emerg Med 1997; 30:23-27.
    6) Aghabiklooei A, Zamani N, & Hassanian-Moghaddam H: Getting stung by black scorpion Androctonus crassicauda: a case report. Hum Exp Toxicol 2014; 33(10):1081-1084.
    7) Aksel G, Guler S, Dogan NO, et al: A randomized trial comparing intravenous paracetamol, topical lidocaine, and ice application for treatment of pain associated with scorpion stings. Hum Exp Toxicol 2015; 34(6):662-667.
    8) Aloufy A, Taitelman U, & Tamir A: Evaluation of scorpion stings in Israel (abstract). J Toxicol Clin Toxicol 2000; 38:511.
    9) Amr ZS, AMR SS, & El-Oran RM: Scorpion stings in Jordan. Ann Tropical Med & Parasitology 1994; 88:99-101.
    10) Bahloul M, Chaari A, Dammak H, et al: Impact of hydrocortisone hemisuccinate use on outcome of severe scorpion-envenomed adult patients. Am J Ther 2014; 21(6):e181-e188.
    11) Bahloul M, Chaari A, Dammak H, et al: Pulmonary edema following scorpion envenomation: mechanisms, clinical manifestations, diagnosis and treatment. Int J Cardiol 2013; 162(2):86-91.
    12) Belghith M, Boussarsar M, & Haguiga H: Efficacy of serotherapy in scorpion sting: a matched-pair study. Clin Toxicol 1999; 37:51-57.
    13) Blum A, Lubezki A, & Sclarovsky S: Black scorpion envenomation: two cases and review of the literature. Clin Cardiol 1992; 15:377-378.
    14) Bouaziz M, Bahloul M, & et al: Factors associated with pulmonary edema in severe scorpion sting patients--a multivariate analysis of 428 cases. Clin Toxicol (Phila) 2006; 44(3):293-300.
    15) Boyer DM: Antivenom Index, Department of Herpetology, San Diego Zoo, San Diego, CA, 1999.
    16) Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 2012; 17(1):3-23.
    17) Burdett T, McIntosh H, & Murphy K: Antivenom for scorpion sting (letter). Lancet 2000; 355:66-67.
    18) Chamberlain JM, Altieri MA, & Futterman C: A prospective, randomized study comparing intramuscular midazolam with intravenous diazepam for the treatment of seizures in children. Ped Emerg Care 1997; 13:92-94.
    19) Chin RF , Neville BG , Peckham C , et al: Treatment of community-onset, childhood convulsive status epilepticus: a prospective, population-based study. Lancet Neurol 2008; 7(8):696-703.
    20) Choonara IA & Rane A: Therapeutic drug monitoring of anticonvulsants state of the art. Clin Pharmacokinet 1990; 18:318-328.
    21) El Ayeb M & Rochat H: Polymorphism and quantitative variations of toxins in the venom of the scorpion Androctonus australis Hector. Toxicon 1985; 25:755-760.
    22) El-Amin EO, Sultan OM, & Al-Magamci MS: Serotherapy in the management of scorpion sting in children in Saudi-Arabia. Ann Tropical Pediatrics 1994; 14:21-24.
    23) Elatrous S, Nouira S, & Bebes-Ouanes L: Dobutamine in severe scorpion envenomation. Effects on standard hemodynamics, right ventricular performance, and tissue oxygenation. CHEST 1999; 116:748-753.
    24) Gateau T, Bloom M, & Clark R: Response to specific centruroides sculpturatus antivenom in 151 cases of scorpion stings. Clinic Tox 1994; 32(2):165-171.
    25) Goyffon M, Vachon M, & Broglio N: Epidemiological and clinical characteristics of the scorpion envenomation in Tunisia. Toxicon 1982; 20:337-344.
    26) Guieu R, Kopeyan C, & Sampeiri F: Use of dantrolene in experimental scorpion envenomation by Androctonus Australis Hector. Arch Toxicol 1995; 69:575-577.
    27) Hammoudi-Triki D, Ferquel E, Robbe-Vincent A, et al: Epidemiological data, clinical admission gradation and biological quantification by ELISA of scorpion envenomations in Algeria: effect of immunotherapy. Trans Royal Soc Trop Med Hygiene 2004; 98:240-250.
    28) Hegenbarth MA & American Academy of Pediatrics Committee on Drugs: Preparing for pediatric emergencies: drugs to consider. Pediatrics 2008; 121(2):433-443.
    29) Hvidberg EF & Dam M: Clinical pharmacokinetics of anticonvulsants. Clin Pharmacokinet 1976; 1:161.
    30) Ismail M & Abd-Elsalam MA: Are the toxicological effects of scorpion envenomation related to tissue venom concentration?. Toxicon 1988; 26:233-256.
    31) Ismail M, Abd-Elsalam MA, & Morad AM: Do changes in body temperature following envenomization by the scorpion Leiurus quinquestriatus influence the course of toxicity?. Toxicon 1990; 20:1265-1284.
    32) Ismail M, Abdullah ME, & Morad AM: Pharmacokinetics of (125)I-labelled venom from the scorpion Androctonus amoreuxi (Aud and Sav). Toxicon 1980a; 18:301.
    33) Ismail M: The treatment of the scorpion envenoming syndrome: the Saudi experience with serotherapy. Toxicon 1994; 32:1019-1026.
    34) Ismail M: Treatment of the scorpion envenoming syndrome: 12-years experience with serotherapy. Int J Antimicrobial Agents 2004; 21:170-174.
    35) Jover E, Martin-Moutot N, & Couraud F: Scorpion toxin: specific binding to rat brain synaptosomes. Biochem Biophys Res Comm 1978; 85:377.
    36) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    37) Lieberman P, Nicklas R, Randolph C, et al: Anaphylaxis-a practice parameter update 2015. Ann Allergy Asthma Immunol 2015; 115(5):341-384.
    38) Lieberman P, Nicklas RA, Oppenheimer J, et al: The diagnosis and management of anaphylaxis practice parameter: 2010 update. J Allergy Clin Immunol 2010; 126(3):477-480.
    39) Loddenkemper T & Goodkin HP: Treatment of Pediatric Status Epilepticus. Curr Treat Options Neurol 2011; Epub:Epub.
    40) Manno EM: New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003; 78(4):508-518.
    41) Martin MF, Rochat H, & Marchot P: Use of high performance liquid chromatography to demonstrate quantitative variation in components of venom from the scorpion Androctonus australis Hector. Toxicon 1987; 25:569-573.
    42) Montague DK, Jarow J, Broderick GA, et al: American Urological Association guideline on the management of priapism. J Urol 2003; 170(4 Pt 1):1318-1324.
    43) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    44) Nouira S, Abroug F, & Haguiga H: Rignt ventricular dysfunction following severe scorpion envenomation. Chest 1995; 108:682-687.
    45) Nouira S, Boukef R, Nciri N, et al: A clinical score predicting the need for hospitalization in scorpion envenomation. Am J Emerg Med 2007; 25(4):414-419.
    46) Nouira S, Elatrous S, Besbes L, et al: Neurohormonal activation in severe scorpion envenomation: correlation with hemodynamics and circulating toxin. Toxicol Appl Pharmacol 2005; 208:111-116.
    47) Nowak RM & Macias CG : Anaphylaxis on the other front line: perspectives from the emergency department. Am J Med 2014; 127(1 Suppl):S34-S44.
    48) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    49) Pomeranz A, Amitai P, & Braunstein I: Scorpion sting: successful treatment with nonhomologus antivenin. Isr J Med Sci 1984; 20:451-452.
    50) Product Information: diazepam IM, IV injection, diazepam IM, IV injection. Hospira, Inc (per Manufacturer), Lake Forest, IL, 2008.
    51) Product Information: diphenhydramine HCl intravenous injection solution, intramuscular injection solution, diphenhydramine HCl intravenous injection solution, intramuscular injection solution. Hospira, Inc. (per DailyMed), Lake Forest, IL, 2013.
    52) Product Information: dobutamine HCl 5% dextrose intravenous injection, dobutamine HCl 5% dextrose intravenous injection. Baxter Healthcare Corporation (per DailyMed), Deerfield, IL, 2012.
    53) Product Information: lorazepam IM, IV injection, lorazepam IM, IV injection. Akorn, Inc, Lake Forest, IL, 2008.
    54) Rachesky IJ, Banner W Jr, & Dansky J: Treatments for Centruroides exilicauda envenomation. Am J Dis Child 1984; 138:1136-1139.
    55) Rimsza ME, Zimmerman DR, & Bergeson PS: Scorpion envenomation. Pediatrics 1980; 66:298-301.
    56) Rochat H, Bernard P, & Couraud F: Scorpion toxins: chemistry and mode of action. In: Ceccareli BE & Clementi F (Eds): Advances in Cytopharmacology, 3, Raven Press, New York, NY, 1979, pp 325.
    57) Rochat H, Rochat C, & Miranda F: The amino acid sequence of neurotoxin I of Androctonus australis Hector. Eur J Biochem 1970; 17:262.
    58) Scott R, Besag FMC, & Neville BGR: Buccal midazolam and rectal diazepam for treatment of prolonged seizures in childhood and adolescence: a randomized trial. Lancet 1999; 353:623-626.
    59) Sofer S, Shahak E, & Gueron M: Scorpion envenomation and antivenom therapy. J Pediatr 1994; 124:973-8.
    60) Sreenath TG, Gupta P, Sharma KK, et al: Lorazepam versus diazepam-phenytoin combination in the treatment of convulsive status epilepticus in children: A randomized controlled trial. Eur J Paediatr Neurol 2009; Epub:Epub.
    61) Trestrail JH III: Scorpion envenomation in Michigan: three cases of toxic encounters with poisonous stow-aways. Vet Hum Toxicol 1981; 23:8-11.
    62) Vanden Hoek,TL; Morrison LJ; Shuster M; et al: Part 12: Cardiac Arrest in Special Situations 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. American Heart Association. Dallas, TX. 2010. Available from URL: http://circ.ahajournals.org/cgi/reprint/122/18_suppl_3/S829. As accessed 2010-10-21.