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Poisonous animals
 
Cnidarians (Jellyfish, Corals and Anemones)
 
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Scorpions
 
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Clinic

 

Tityus spp.

Studies

Brazil

Amaral et al. 1991: 5 T. serrulatus stings in children between 3 and 9 years. Identification: scorpions available for identification. Time between sting and antivenom administration 0.5–13 h; time between sting and admission to an intensive care unit 2–32 h, all patients survived.

Amaral et al. 1992: 6 T. serrulatus stings in children between 2 and 9 years; 3 of the children are the same as 3 of those reported by Amaral et al. 1991, above. Identification: scorpions available for identification. Time between sting and antivenom administration 0.5–13 h; time between sting and admission to an intensive care unit 3–32 h, 2 children died.

Campos et al. 1980: 40 scorpion stings in children. Identification: T. serrulatus according to statements of the patients or their relatives; only cases of severe envenoming were included in this retrospective study. A total of 1,173 stings were recorded at the Toxicological Centre of the Joao XXIII Hospital, Belo Horizonte, Brazil, from January 1972 to December 1978; 323 were children <12 years. In adults the course of envenoming was always benign; all cases of severe envenoming involved children (the reported cases are included in the larger study population of Freire-Maia and Campos 1989, see below).

Freire-Maia and Campos 1989: 168 scorpion stings in children. Identification: Tityus sp., mostly T. serrulatus; however, identification criteria not specified. Only severe cases were included in this retrospective study. A total of 3,860 stings were recorded at the Toxicological Centre of the Joao XXIII Hospital, Belo Horizonte, Brazil, from January 1972 to December 1987; 1,038 were children <14 years. In adults the symptoms normally consisted of local pain. All cases of severe envenoming and all fatalities occurred in children.

Hering et al. 1993: 2 T. serrulatus stings in patients between 4 and 18 years. Identification: scorpions available for identification. Time between sting and hospitalisation 15 min–6.5 h. All patients received antivenom immediately after hospitalisation. No patient died.


Trinidad
Bartholomew 1970: 30 scorpion stings. Identification: stings attributed to T. trinitatis. 6 of the patients brought in the scorpion that had caused the sting.
Poon-King 1963: 45 scorpion stings. Identification: stings attributed to T. trinitatis. However, none of the patients brought in the scorpion that had caused the sting and only one patient saw the scorpion by which he/she had been stung.

Case reports

Brazil
Nishioka et al. 1992. Identification: T. serrulatus; 1 case.

Trinidad
Waterman 1938.

Signs & symptoms

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 (Freire-Maia and Campos 1989).

Local effects

Local pain 5/5 (Amaral et al. 1991); 40/40 (Campos et al. 1980); 168/168 (Freire-Maia and Campos 1989); 12/12 (Hering et al. 1993); 45/45 (Poon-King 1963). In contrast to Leiurus quinquestriatus envenoming, local pain is recorded in 100% of cases following Tityus spp. stings.

Neurological effects (autonomic 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. Both parts of the autonomic nervous system are stimulated. This results in transient cholinergic effects (vomiting, profuse sweating, bradycardia, hypersalivation, arterial hypotension) and longer-lasting adrenergic effects (arterial hypertension, tachycardia, myocardial failure). In contrast to Leiurus quinquestriatus envenoming, priapism is very rarely recorded following Tityus spp. stings (Freire-Maia and Campos 1987, 1989).

Vomiting 5/5, hyperthermia 2/5, restlessness 3/5, sweating 3/5, tachypnoea 5/5, tachycardia 5/5, arterial hypertension 0/5, pulmonary oedema 3/5 (Amaral et al. 1991).
Tachycardia 38/40, vomiting 37/40, fever 25/40, tachypnoea 14/40, sweating 13/40, dyspnoea 10/40, cardiac insufficiency 10/40, arterial hypertension 7/40, pulmonary oedema 6/40, dehydration 6/40, hypersalivation 6/40, restlessness 5/40, cerebral seizures 5/40, clinical signs of shock 3/40, cardiac arrest 3/40, bradycardia 2/40, bradypnoea 2/40, diarrhoea 2/40, abdominal pain 1/40, coma 1/40 (Campos et al. 1980).

Vomiting 144/168, tachycardia 126/168, tachypnoea 94/168, sweating 79/168, restlessness 54/168, drowsiness 42/168, cardiac arrhythmias (excluding tachycardia/bradycardia) 30/168, hyperthermia 29/168, dyspnoea 26/168, cardiac insufficiency 25/168, pulmonary oedema 20/168, bradycardia 17/168, arterial hypertension 12/168, confusion 10/168, cardiac arrest 8/168, cerebral seizures 8/168, shock 5/168. In contrast to Leiurus quinquestriatus envenoming, priapism is only recorded in 1% of cases following Tityus spp. stings (Freire-Maia and Campos 1989).

Nausea/vomiting 12/12, hypersalivation 11/12, sweating 12/12, abdominal pain 5/12, tachypnoea and dyspnoea 12/12, tachycardia 12/12, alternating tachycardia and bradycardia 4/12 (persisting for 48–96 h), arterial hypertension 8/12 (spontaneous normalisation within 2 h), cardiac arrhythmias 8/12, pulmonary oedema 7/12 [for 12 h after the sting; in 3 patients the pulmonary oedema occurred 1–3 h after the sting; see also "Treatment (symptomatic)"], precordial pain 1/12, agitation 12/12, tremor 6/12, priapism 1/12 (Hering et al. 1993).
Hypersalivation 45/45, vomiting 42/45, epigastric pain 32/45, pain in the abdomen upon palpation 28/45, tachypnoea 22/45, fever 18/42, sweating14/45, tachycardia 17/45, bradycardia 8/45, extrasystoles 11/45, sleepiness 13/45, restlessness 9/45, shock 9/45 (Poon-King 1963).
Fasciculations and hypaesthesia of the left side of the face (facial sting) (Nishioka et al. 1992).

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"). Direct toxic effects of components of scorpion venom are also possible. The pulmonary oedema that occurs with severe envenoming is interpreted as cardiogenic, but also as being attributable to non-cardiogenic factors, such as increased pulmonary vascular permeability (Amaral et al. 1991, 1992, Freire-Maia and Campos 1987, 1989).

Case fatality rate

11/3,860 adults and children; all fatalities were children who were hospitalised more than 3 h after the sting (Freire-Maia and Campos 1989).

Laboratory and physical investigations

1. ECG

Sinus tachycardia 5/5, ventricular extrasystoles 1/5, myocardial infarction-like ECG pattern 3/5 (Amaral et al. 1991).

Sinus tachycardia 32/40, prominent U waves 16/40, T wave inversion and ST elevation or depression 10/40, LAH 1/40, ventricular ectopic beats 1/40, complete AV block 1/40, sinus node arrest 1/40, sinus bradycardia 1/40, wandering pacemaker 1/40 (Campos et al. 1980).

Sinus tachycardia 12/12, first-degree AV block 5/12, ventricular extrasystoles 8/12, pathological Q waves7/12, ST elevation/depression 10/12, T wave changes 12/12, increased QTc 8/12, U waves 6/12 (Hering et al. 1993).
ECG changes (T wave inversion, ST segment elevation/depression, increased QTc, conduction disturbance) 34/45. Normalisation within 3–6 days (Poon-King 1963).


2. Echocardiography, colour Doppler

Echocardiography: reduced left ventricular systolic function, poor mobility of the interventricular septum, reduced mobility of the posterior wall of the left ventricle or reduced left ventricular fractional shortening or a combination of these findings (5/5). 4/5 children were followed up after 8–20 days and all had improved with regard to left ventricular systolic function. Echocardiography was more sensitive for detecting myocardial damage following a scorpion sting than electrocardiography or creatine kinase (Amaral et al. 1991).

Colour Doppler: mitral regurgitation 3/5. At follow-up after 8–20 days this had disappeared (Amaral et al. 1991).

Reduced left ventricular systolic function: in most of the 12 patients diffuse left ventricular hypokinesis, reduced eject fraction and reduced left ventricular fractional shortening were recorded. In some of the 12 patients segmental left ventricular hypokinesis, in particular of the interventricular septum. Mild transient mitral regurgitation 9/12. In 8 patients the changes detectable on echocardiography normalised within 1 week, and in 2 patients within 2 weeks (Hering et al. 1993).


3. CK-MB, CPK, SGOT
CK-MB (normal <10 U/l): measured in 2/5 children and found to be increased (16.5 and 38 U/l). CK (normal 10–80 U/l): increased in 2/5 children (120 and 213 U/l) (Amaral et al. 1991).
Increased CK with a maximum within 24 h after the sting 12/12;  increased CK-MB fraction 9/12 (Hering et al. 1993).

4. Chest X-ray

Signs of pulmonary oedema 3/5 (Amaral et al. 1991).

Cardiothoracic ratio >0.5 2/6. Signs of pulmonary oedema, mainly unilateral 4/6, bilateral 2/6, peripheral 6/6, air bronchogram 3/6 (Amaral et al. 1992).

5. Blood sugar, glycosuria
Increased (125–246 mg/dl) 4/5 (Amaral et al. 1991).
Blood sugar levels determined in 20 patients: mean 153 ± 19 mg% (65–400 mg%); >120 mg% 12/20 (Campos et al. 1980).
Increased blood sugar and glycosuria 12/12 (Hering et al. 1993).
Increased blood sugar  6/45, glycosuria 19/45 (Poon-King 1963).

6. Serum amylase
Neither sensitive nor specific as a parameter for acute pancreatitis.
Increased (162–364 U/dl; normal 60–160 U/dl) 3/5 (Amaral et al. 1991).
Determined in 8 patients: mean 211 ± 38 U (60–360 U) (Campos et al. 1980).
Increased serum amylase 12/12 (Hering et al. 1993).
Increased serum amylase 29/45 (Poon-King 1963).
Increased serum amylase 24/30 (Bartholomew 1970).

7. Plasma immunoreactive cationic trypsin
A sensitive and specific parameter for acute pancreatitis.

8. Potassium
Hypokalaemia 12/12 (Hering et al. 1993).

9. Leucocytes
Increased (12,900–31,980/mm³) 5/5 (Amaral et al. 1991).
Determined in 10 patients: mean 20,080 ± 3,602/mm³ (10,400–44,400/mm³) (Campos et al. 1980).
Leucocytosis 12/12 (Hering et al. 1993).

Treatment (symptomatic)

1. Local pain
Dipyrone, a pyrazolone derivative, 40 mg/kg BW/day i.v., local infiltration of lidocaine without the addition of adrenaline (Freire-Maia et al. 1994).

2. Vomiting
Metoclopramide 0.5–1.0 mg/kg BW i.v. initially, followed by 2–3 oral doses per day (Freire-Maia et al. 1994).

3. Hyperthermia
Dipyrone 40 mg/kg BW/day i.v. and/or physical measures (Freire-Maia et al. 1994).

4. Cardiac arrhythmias

Atropine is not recommended (see "Diagnosis & treatment: Hospital"). However, if there is severe bradycardia caused by sinus arrest or complete AV block, atropine 10–20 µg i.v. is recommended as an emergency measure.

Beta-blockers are not recommended. In many cases the arrhythmias disappear after correction of the hypoxia and/or acid-base balance or electrolyte disturbances. Ventricular tachycardia without haemodynamic defects (e.g. arterial hypotension or shock) lidocaine 1 mg/kg BW i.v., maximum of 3 doses at an interval of 5 min. Ventricular tachycardia with arterial hypotension or shock, electric cardioversion (Freire-Maia et al. 1994).


5. Heart failure and pulmonary oedema

If the patient is not dehydrated, treatment of pulmonary oedema with oxygen and furosemide i.v. (1 mg/kg BW every 8 h). If this treatment is not effective, intubation and artificial respiration (Freire-Maia et al. 1994).


6. Arterial hypertension
Phenoxybenzamine, prazosin or nifedipine (Freire-Maia et al. 1994).

7. Circulatory failure
Dobutamine and/or dopamine 2.5–20 µg/kg BW/min i.v. (Freire-Maia et al. 1994).
Intravenous fluids, dopamine, dobutamine (Amaral et al. 1991, 1992).

8. Further contra-indicated medications
Barbiturates, benzodiazepines (Freire-Maia et al. 1994).

Treatment (specific)

Antivenom

  • Scorpion antivenom (Butantan Institute, São Paulo, Brazil), 20–40 ml i.v. in all children with signs of severe envenoming immediately after hospitalisation and observation in an intensive care unit (Freire-Maia and Campos 1989).
  • Scorpion antivenom (Butantan Institute, São Paulo, Brazil), 5–10 vials i.v. (Hering et al. 1993).
  • Scorpion antivenom (FUNED, Belo Horizonte, Minas Gerais, Brazil), 40 ml i.v. (Amaral et al. 1991, 1992).
  • Scorpion antivenom (FUNED, Belo Horizonte, Minas Gerais, Brazil), 20 ml i.v. immediately after hospitalisation (Freire-Maia et al. 1994).
  • Scorpion Fab2 fragment antivenom (Fundacao Ezequiel Dias, Belo Horizonte, Barzil) (Rezende et al. 1995).

 

Rezende et al. 1995: Study to assess the kinetics of envenoming and antivenom (circulating venom and antivenom concentraions) in correlation with the clinical course of 18 severely envenomned patients stung by Tityus serrulatus scorpions (Indentification: scorpions captured and identified at the time of admission). Clinical inclusion criteria: in addition to local pain, at least one of the following features: vomiting, psychomotor agitation, prostration, profuse sweating, tachypnea, sinus tachycardia, arterial hypertension or hypotension, sinus bradycardia, cardiac failure or arrhythmias, shock, pulmonary edema, leucocytosis, hyperglycemia or serum amylase > 160 mU/ml. Antivenom treatment: 5-30 ml (1-6 ampules) of scorpion Fab2 fragment antivenom.

Results: Increased levels of circulating venom antigens were detected before, but no longer 1h after antivenom treatment. Vomiting and local pain decreased within the same period, hyperglycemia after 12h, cardio-respiratory manifestations after 6-24h. All patients recovered completely.

Note: The persistence of critical features of the scorpion envenoming syndrome point to the inability of antivenom to neutralize venom already bound to receptors and pathophysiological process already triggerd by the first wave of venom before the antivenom has been administered necessitating simultaneous symptomatic treatment. Early administration of antivenom is crucial to be effective.

 

Rezende et al. 1999: Study to compare the levels of circulating venom in patients with local vs systemic Tityus serrulatus scorpion envenoming. Study design as above (Rezende et al. 1995).

Results: Patients with systemic envenoming had significantly higher circulating venom concentrations than patients with local envenoming.

 

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

Freire-Maia and Campos argue in favour of the use of antivenom and symptomatic measures for the treatment of scorpion envenoming and refer to the low mortality in the investigated patient groups. In discussions regarding the importance of antivenom in the treatment of scorpion stings, the issue of the low efficacy of commercially available antivenoms is brought up time and again. This is countered by the argument that the appropriate response should be to improve the antivenoms (Campos et al. 1980, Freire-Maia and Campos 1987, 1989, Freire-Maia et al. 1994).

Clear improvement after antivenom administration 12/12. The course of envenoming in these patients was monitored closely (see above) (Hering et al. 1993).

The persistence of critical features of the scorpion envenoming syndrome point to the inability of antivenom to neutralize venom already bound to receptors and pathophysiological process already triggerd by the first wave of venom before the antivenom has been administered necessitating simultaneous symtomatic treatment. Early administartion of antivenom is crucial to be effective (Rezende et al. 1995).