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Leiurus quinquestriatus

With scorpion stings, identification of the scorpion that caused the sting is particularly difficult. The majority of victims are small children. If the scorpion is not brought in for identification, then identification on the basis of the patient's description is highly questionable. If the scorpion is available for identification, it is possible in most cases to achieve a conclusive result if identification is performed by an expert. Clinical data from the literature cannot be related to a conclusively identified species in many cases. The clinical information available comes from stings caused by various scorpion species, and it may be that the individual specimens were reliably identified, identified according to unclear criteria or not identified at all. Indirect criteria, such as a course of envenoming considered typical for a particular species of scorpion, and geographical criteria are often used to aid in identification. Because of these factors, the following species are also discussed in this section:

  • Nebo hierochonticus
  • Androctonus crassicauda
  • Scorpio maurus
  • Compsobuthus werneri
  • Buthotus judaicus.



Gueron and Yaron 1970: 34 L. quinquestriatus stings. Identification: "identified as yellow scorpions"; no criteria given.

Classification according to systemic signs of envenoming:

  • arterial hypertension 14/34; time between sting and hospitalisation <3 h.
  • shock but without prior arterial hypertension 9/34; time between sting and hospitalisation <3 h.
  • cardiac insufficiency or pulmonary oedema 11/34; time between sting and hospitalisation <3 h.

Sofer and Gueron 1988: 61 L. quinquestriatus stings in children. Identification: "identification of the scorpions" (criteria not given) 7/9; "typical clinical picture" 2/9.

Classification according to the course of envenoming:

  • Uncomplicated course. These children improved rapidly and were able to leave the intensive care unit within 24 h, 52/61.
  • Complicated course 9/61.
    • Respiratory failure 5/9.
    • Severe cardiorespiratory impairment 4/9.

Sofer et al. 1991: 32 scorpion stings in children. Identification: L. quinquestriatus 25/32, Buthotus judaicus 1/32; "typical clinical picture" 6/32.


  • Asymptomatic 5/32.
  • Systemic envenoming 27/32.

Saudi Arabia

Annobil 1993b: 47 scorpion stings in children. Identification of scorpions brought in by the patients: L. quinquestriatus (possibly L. jordanensis?) 18/47, Nebo hierochonticus 2/47, Androctonus crassicauda 1/47, Scorpio maurus 1/47, Compsobuthus werneri 1/4, not identified 24/47. Prospective study.


  • Severe local pain without systemic signs of envenoming 31/47: L. quinquestriatus 12/31, Scorpio maurus 1/31, Compsobuthus werneri 1/31.
  • Severe local pain and mild systemic signs of envenoming, such as vomiting, hypersalivation and sweating 11/47: L. quinquestriatus 4/11, Androctonus crassicauda 1/11.
  • Severe systemic signs of envenoming, such as pulmonary oedema with or without central nervous signs and symptoms, such as restlessness, cerebral seizures, priapism and coma with or without generalised symptoms of paralysis 5/47: L. quinquestriatus 2/5, Nebo hierochonticus 2/5.

Amitai et al. 1985: 51 scorpion stings in children. Identification: L. quinquestriatus (possibly L. jordanensis?) 32/51, Buthus judaicus 2/51, not identified 17/51; identification criteria not given; it is noted that in the region in which the patients were stung, L. quinquestriatus is the most important species medically.


  • Mild to moderately severe envenoming (mild signs and symptoms of systemic envenoming or only local signs of envenoming, such as local erythema or local swelling) 36/51.
  • Severe systemic envenoming (one or more of the following signs and symptoms: coma, cerebral seizures, cardiac arrhythmia, pulmonary oedema) 15/51.

El-Amin 1992: 96 scorpion stings in children. Identification: on the basis of descriptions by the parents and the scorpions brought in for identification, the following distribution was determined: Leiurus sp. 54/96, Androctonus sp. 23/96, not identified 19/96.

Signs & symptoms

Autopharmacological effects

Experimental and clinical observations suggest that the major systemic effects of envenoming are caused by endogenous catecholamines and acetylcholine, which are released in response to scorpion venom. As these are transmitters in the sympathetic, parasympathetic and somatic nervous systems, the resulting clinical symptoms of envenoming are dealt with in the section "Neurological effects".

However, scorpion venoms are also believed to lead to other indirect effects that are caused by the release of autopharmacologically active substances (such as kinins, prostaglandins and slow-reacting substances). The pathophysiological effects of these substances overlap to a great extent. This makes it difficult to be certain about aetiology. In particular with regard to pulmonary oedema, there has been discussion concerning the effects of mediators on vascular permeability, which might constitute a non-cardiac component of the pulmonary oedema. Peripheral blood pressure regulation is also responsive to a variety of different mediators that might be released.

Local effects

Local pain, sometimes severe 20/47. Local swelling 9/47, local redness and swelling 8/47, local redness 7/47 (Annobil 1993b).
Local pain 87/96 (El-Amin 1992).

Neurological effects (autonomic and somatic nervous system)

Experimental and clinical observations suggest that the major systemic effects of envenoming are caused by endogenous catecholamines and acetylcholine, which are released in response to scorpion venom. In Leiurus quinquestriatus envenoming the most notable effect is stimulation of both parts of the autonomic nervous system. This results in initial transient cholinergic effects (vomiting, profuse sweating, bradycardia, priapism, hypersalivation, arterial hypotension), followed by longer-lasting adrenergic effects (arterial hypertension, tachycardia, myocardial failure).

The cardiovascular impairments that are of primary significance in cases of complicated, life-threatening envenoming have multi-factorial causes:

  1. Effects of endogenously released catecholamines on arterial pressure and impedance;
  2. Effects of the renin-angiotensin system;
  3. Effects of catecholamines at the cellular level in the myocardium (intracellular Ca2+ accumulation), increased myocardial oxygen requirements;
  4. Reduced myocardial perfusion;
  5. Direct cardiomyotoxic effect (see below "Cardiac effects").

The majority of patients have fully developed haemodynamic defects at the time of hospitalisation, generally 2–3 h after the sting at the earliest. Pathological findings can be seen on echocardiography (Gueron et al. 1993).

Functional neurological changes are commonly observed in small children and only rarely in adults and older children (Gueron et al. 1993).

These can be explained in part within the context of hypertensive encephalopathy (Sofer and Gueron 1990).

Anxiety and restlessness 12/47, vomiting 10/47, sweating 7/47, hypersalivation 7/47, drowsiness 4/47, priapism 4/47, peripheral cyanosis 4/47, increased bronchial secretion 3/47, arterial hypotension (<60 mmHg) 2/47 (Annobil 1993b).

Tachycardia 30/51, sweating 20/51, priapism 18/40 male children, vomiting 19/51, hypersalivation 16/51, arterial hypotension 16/51, fever (>37.8°C) 11/51, pupil changes: either constricted with a predominantly parasympathetic effect of the venom or dilated with a predominantly sympathetic effect 9/51, coma 7/51, arrhythmia 5/51, pulmonary oedema 5/51, cerebral seizures 5/51. The severity of envenoming varied significantly depending on the time that had elapsed since the sting. In children who showed severe signs of envenoming, 2.46 ± 1.16 h had elapsed since the sting, and in children who showed mild to moderately severe signs of envenoming, 1.31 ± 1.13 h had elapsed (Amitai et al. 1985).

Vomiting 28/96, sweating 25/96, hypersalivation 15/96, fever 9/96, cerebral seizures 3/96, irritability 87/96, cold extremities 58/96, tachycardia 49/96, tachypnoea 35/96, clinical signs of shock 15/96, arterial hypertension 14/96, priapism 13/96, pulmonary oedema 11/96, arterial hypotension 7/96, bradycardia 4/96, lethargy 4/96 (El-Amin 1992).

Cardiovascular signs and symptoms, including tachycardia and bradycardia 27/27. Arterial hypertension 21/27. Abdominal symptoms including vomiting, hypersalivation, sweating and priapism (common signs and symptoms in 27 children with systemic envenoming). Bradypnoea requiring artificial respiration 4/27. Heart failure and pulmonary oedema 1/27 (Sofer et al. 1991).

Arterial hypertension with a systolic arterial blood pressure of 150–230 mmHg and diastolic arterial blood pressure of 100–130 mmHg (14/34); usually accompanied by profuse sweating, excessive tachycardia and restlessness. These symptoms generally persisted for several hours. In 5 of 14 patients the systolic blood pressure plummeted to shock levels of <80 mmHg, accompanied by peripheral circulatory failure (Gueron and Yaron 1970).
Shock in the absence of prior arterial hypertension 9/34, 3 of these 9 patients had cardiogenic shock, 2 died (Gueron and Yaron 1970).

Congestive heart failure or pulmonary oedema 11/34; ventricular protosystolic gallop rhythm 5/11, 1 of these 5 had an apical systolic murmur and 5/5 had raised blood pressure as well as an ECG pattern corresponding to that of an early myocardial infarct (see below) (Gueron and Yaron 1970).
Respiratory failure or severe cardiorespiratory impairment 9/61; of these 9, 4 suffered cardiogenic shock, 3 had severe arterial hypertension and 1 had a severe airway obstruction; all were lethargic, confused, agitated or had clearly reduced consciousness. 7 children recovered completely, 1 child died, 1 survived with permanent damage, including aphasia. The pathogenesis of the respiratory failure following scorpion stings is considered multi-factorial; however, the significance of a central nervous effect of endogenously released catecholamines is emphasised (Sofer and Gueron 1988).

Cardiac effects

The pathogenesis of the myocardial damage has not been conclusively resolved. The myocardial and vascular effects of endogenous catecholamines, release of which is elicited by scorpion venom, are one – and probably the most vital – component (see above "Neurological effects"). However, it is possible that there are direct cardiotoxic effects of components of scorpion venom, but this is controversial (Abroug et al. 1991, 1992, Gueron and Sofer 1992, Gueron et al. 1993).


Permanent damage, including aphasia 1/61 (Sofer and Gueron 1988).

Duration of hospitalisation: 8–24 h 31/47, 2–3 days 11/47, 5–8 days 5/47  (Annobil 1993b).

Case fatality rate

Mortality is high within the first 24 hours after the sting, mostly affects children and is associated with heart failure (Gueron and Yaron 1970).

9/34: age 9 months–9 years; 6 of these 9 died with clinical signs of pulmonary oedema, 3 died suddenly and unexpectedly (Gueron and Yaron 1970).
1/61 died from shock (Sofer and Gueron 1988).
2/61 (Amitai et al. 1985).
2/96 (El-Amin 1992).

1/47; cause: Nebo hierochonticus; cause of death pulmonary oedema and heart failure (Annobil 1993b).

With the use of systematic treatment aimed at neutralising the over-stimulation of the autonomic nervous system, no patient died in the 5 years between 1993 and 1998 at the Soroka Medical Center. None of these patients received antivenom (Gueron et al. 1993).

Of 2,500 cases evaluated in a study in Saudi Arabia, in which patients received antivenom and symptomatic treatment according to a standardised protocol, only one fatality occurred. This was a 12-year-old boy who received only 2 vials of antivenom 2.5 h after being stung by an unidentified scorpion. Thus the mortality rate in that study was 0.04%; other mortality rates reported in the literature lay between 4 and 6.5% (Ismail 1993).

Laboratory and physical investigations

1. ECG

ECG pattern corresponding to that of an early myocardial infarction: initially tented/peaked T waves, accompanied by ST segment depression in the precordial leads. Subsequently additional ST segment changes (depression or elevation) and appearance of a Q wave in the limb leads. These ECG changes appeared within a few hours and were followed by T inversion in the precordial or limb leads. QTc >0.40 s. The ECG changes were detectable for a period of several days and then reduced to tented/peaked T waves that could persist for several weeks. The ECG findings were proportional to other findings that reflected the severity of envenoming, namely signs of heart failure and shock (Gueron and Yaron 1970, Gueron et al. 1967).

2. Echocardiography and scintigraphy

Study: Gueron et al. 1990: 7 L. quinquestriatus stings in children; identification: criteria not given. The time interval between the sting and hospitalisation was 30 min–4 h; severe arterial hypertension 5/7, one of these children developed respiratory failure; arterial hypotension and pulmonary oedema 1/7; all had indications of myocardial damage, as assessed by enzyme profiles.

Results of echocardiography and scintigraphy: poor global contractility 12–15 h after the sting, with lowered ejection fraction. Systolic myocardial dysfunction, reduced left ventricular compliance and increased left ventricular impedance appear to play a significant role in the pathogenesis of heart failure following scorpion stings. The myocardial damage is attributed to the action of endogenously released catecholamines.


SGOT and CPK are not specific for myocardial damage. Elevated levels could result from skeletal muscle damage caused by the sting; in contrast, elevated CK-MB and CK-MB/CPK ratio are very specific for myocardial damage, such as ischaemia and necrosis.

Elevated SGOT (>35 U/l) at the time of hospitalisation in 25 of the 27 symptomatic children and in 5 of the 5 asymptomatic children. Elevated CPK (>200 U/l) at the time of hospitalisation in 15 of the 27 symptomatic children and in 1 of the 5 asymptomatic children. Elevated CK-MB (>16 U/l) at the time of hospitalisation in 27 of the 27 symptomatic children and in 3 of the 5 asymptomatic children.

13 children fulfilled the enzymatic criteria for myocardial damage with elevated CPK, elevated CK-MB and a CK-MB/CPK ratio of >6%. The only child who suffered heart failure in this study was among these 13 children, as were 5 of the 6 children with ECG changes. None of the asymptomatic children fulfilled the above-mentioned criteria. From this study, it is apparent that roughly half of the children with signs of systemic envenoming develop myocardial damage. However, the lesions are so small that in most cases neither cardiac insufficiency nor cardiac failure results. They do, however, come into question as the cause of bradycardias, tachycardias and other cardiac dysrhythmias. Children with only local signs of envenoming do not develop myocardial damage. There is no direct relationship between the severity of the clinical signs and symptoms and the myocardial damage (enzyme profile in serum) (see above "Signs and symptoms") (Sofer et al. 1991).

4. Catecholamine metabolites in urine

Catecholamine metabolites in urine were investigated in 12 patients with systemic envenoming following scorpion stings: increased vanillylmandelic acid 7/12, increased total free epinephrine and norepinephrine 8/12 (Gueron and Yaron 1970).

5. Blood sugar

Blood sugar levels were investigated in 16 patients: >95 mg% 11/16 (Gueron and Yaron 1970).

6. Serum amylase

Neither sensitive nor specific as a parameter for acute pancreatitis. Serum amylase was investigated in 16 patients with moderately severe abdominal pain: increased 14/16 (Gueron and Yaron 1970).

7. Plasma immunoreactive cationic trypsin

A sensitive and specific parameter for acute pancreatitis.

Study: Sofer et al. 1991: 15 scorpion stings. Identification: L. quinquestriatus 14/15; Buthotus judaicus 1/15; criteria not given. All patients reached hospital within <3 h.

13/14 patients with L. quinquestriatus stings had increased plasma immunoreactive cationic trypsin, i.e. acute pancreatitis is a common complication of envenoming with this scorpion species. Abdominal pain and vomiting may possibly be explained by this finding, as well as the agitation in small children. This form of pancreatitis is generally self-limiting within 24 h.

8. Leucocytes
>15,000/mm³ 14/28, >20,000/mm³ 6/28 (Amitai et al. 1985).

Treatment (symptomatic)

1. Monitoring of patients

If possible, all patients with systemic envenoming should be observed in an intensive care unit.

2. Pain

Local pain: infiltration of the area around the sting with 1% xylocaine (maximum 0.5 ml) (Ismail 1993).

3. Arterial hypertension
Study: Sofer and Gueron 1990: 23 scorpion stings in children. Identification: not specified; patients came from an area in which L. quinquestriatus is the cause of most stings.

The 23 children who were included in the study had arterial hypertension, 21 of them already at the time of hospitalisation. 2 developed arterial hypertension after hospitalisation. Furthermore, they had typical signs of systemic envenoming following a scorpion sting, including dysfunction of the central nervous system (anxiety, drowsiness, agitation), vomiting, hypersalivation, sweating, cardiac dysrhythmias (bradycardia or tachycardia). Central nervous system dysfunction is interpreted as an expression of hypertensive encephalopathy.

Treatment: hydralazine 0.2 mg/kg BW i.v. or nifedipine 0.5 mg/kg BW s.l. or a combination of both or repeated doses of nifedipine.

In all 8 patients who received this treatment normal blood pressure levels were achieved within 5 h, and simultaneously there was normalisation of the agitation, irritability, state of consciousness and respiration.

Conclusion and recommendations: in all patients with scorpion stings in whom the clinical picture is dominated by pulmonary oedema, severe arterial hypertension or hypertensive encephalopathy, the use of vasodilators (hydralazine, nifedipine) for afterload reduction is the treatment of choice (Sofer and Gueron 1990, Gueron and Sofer 1990).

Post-synaptic alpha-receptor blockade (prazosin) in combination with nifedipine (Bawaskar and Bawaskar 1992; see Hottentotta tamulus) and captopril (Karnad et al. 1989) have also been used with success.

4. Pulmonary oedema
See 3. above.

5. Hypovolaemia

Sweating, vomiting, diarrhoea and fever caused by scorpion envenoming, together with fluid loss from high ambient temperatures, can lead to hypovolaemia. Fluid replacement is essential (Gueron et al. 1993).

However, hypovolaemia is frequently concurrent with pulmonary oedema. The use of loop diuretics without fluid replacement in these cases is very dangerous (Karnad et al. 1989; see Hottentotta tamulus).

6. Bradycardia

In some patients the parasympathetic effects dominate at the beginning of the course of envenoming. If atropine is administered at this time point, there may be a sudden occurrence of pulmonary oedema, shock or worsening of the arterial hypertension. In the phase during which transient cholinergic effects occur (bradycardia, vomiting, sweating, priapism), atropine should be avoided. Atropine is only indicated if there is severe symptomatic bradycardia with or without arterial hypotension, provided that there is no concurrent hypovolaemia (Bawaskar and Bawaskar 1992b,c, Gueron and Sofer 1991, Gueron et al. 1993).

7. Respiratory failure
Artificial respiration (Sofer and Gueron 1988).

8. Cerebral seizures

Diazepam i.v., administered slowly under close observation (Ismail 1993).

9. Contra-indicated medications and medications to be avoided
Pethidine, morphine, barbiturates, beta-blockers, calcium, anti-inflammatory drugs, including corticosteroids, atropine (see above) (Ismail 1993, Gueron et al. 1993).

Treatment (specific)

A national, multi-centre study on the impact of antivenom in the treatment of scorpion stings was carried out in Saudi Arabia some time ago. Until that time there were no controlled, clinical efficacy studies. Assessment of the importance of antivenom in the treatment of scorpion stings is very controversial (Gueron et al. 1993, Ismail 1993).

A big problem is the time interval between the sting and the start of treatment. Scorpion venom acts indirectly via the release of endogenous substances, in particular catecholamines and acetylcholine. If this release has already occurred, the resulting effects of envenoming cannot be neutralised by antivenom. The symptoms of envenoming must then be controlled by substances that, for example, antagonise the effects of catecholamines and by other measures such as artificial respiration (see above; Gueron et al. 1993, Gueron and Sofer 1994). However, antivenom may still have an impact during this phase of envenoming, as scorpion venom has a very long elimination half-life and complete absorption of the venom from the subcutaneous region where it was injected takes 7–8 h (Ismail 1993, Ismail and Abd-Elsalam 1988, Ismail et al. 1990, 1992).


Ismail 1993, 1994: around 18,000 scorpion stings were recorded over a period of 9 months from 18 health regions in Saudi Arabia. The patients were treated according to a standardised protocol (identification: Leiurus quinquestriatus and Androctonus crassicauda, 80–90% of the stings; identification criteria not given).

Antivenom: all patients with a confirmed or suspected scorpion sting with systemic signs of envenoming received antivenom.

Dose: minimum 5 vials i.v., in 20–50 ml NaCl, which was repeated if needed up to a maximum dose of 20 vials.

Additional symptomatic treatment:

  • All patients with systemic envenoming were observed in an intensive care unit.
  • Local pain: infiltration of the area around the sting with 1% xylocaine (maximum 0.5 ml).
  • Sedation and anti-emetic treatment: chlorpromazine 0.5–1 mg/kg BW i.m., repeat as needed, or promethazine 0.5–1 mg/kg BW, repeat 6-hourly as needed.
  • Cerebral seizures: diazepam i.v., administered slowly under close observation.
  • Arterial hypertension: hydralazine or nifedipine. 
  • Pulmonary oedema: oxygen, furosemide and fluid restriction; CVP. 
  • Immediate endotracheal intubation and artificial respiration if it becomes necessary.
  • Shock: 0.5 N saline solution (CVP 8–12 cmH2O), maintenance of blood pressure adequate for organ perfusion.

Contra-indicated medications: pethidine, morphine, barbiturates, beta-blockers.

Assessment of the value of antivenom in the treatment of scorpion envenoming

Gueron and colleagues question that antivenom can reverse the cardiac pathophysiological effects of scorpion venoms. Antivenom may be administered to patients to reverese neurotoxic effects, but should be closely observed for cardiorespiratory complications and treated appropriately (Gueron, Ilia and Margulis 2000, Sofer, Bawaskar and Gueron 2009). They point out that with systematic treatment aimed at neutralising the over-stimulation of the autonomic nervous system, no patient had died in the previous 5 years at the Soroka Medical Center. None of these patients received antivenom (Gueron et al. 1993, Gueron and Sofer 1994).


Ismail argues against excluding antivenom from the treatment of scorpion stings and advocates a combination of symptomatic and specific forms of treatment. Preliminary results from the study described above are cited as an argument in favour of antivenom administration. To date, 2,500 cases have been evaluated. Among them there was only one fatality, a 12-year-old boy who received only 2 vials of antivenom 2.5 h after being stung by an unidentified scorpion. Thus the mortality rate in that study was 0.04%; other mortality rates reported in the literature lay between 4 and 6.5%. The incidence of pulmonary oedema, arterial hypertension, arterial hypotension, cardiac arrhythmias and neurological signs and symptoms was low after administration of antivenom. The duration of hospitalisation was shortened. Most patients were free of symptoms within 1–2 days. Ismail's preliminary evaluation of the study results is as follows: the high efficacy of antivenom treatment in this study is probably attributable to the high antivenom doses that were used and the i.v. method of administration. Commercial scorpion antivenoms generally have a very low antibody titre, so that the commonly recommended dose of 1 vial s.c., i.m. or i.v. is completely ineffective. Subcutaneous and intramuscular methods of administration are anyway not suitable for rapidly establishing efficient levels of medication (Ismail 1993, 1994).