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Poisonous animals
 
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Clinic

 

Hottentotta tamulus (formerly = Mesobuthus tamulus)

Studies

Bawaskar and Bawaskar 1987: 12 Mesobuthus tamulus (=Hottentotta tamulus) stings. Identification: no criteria given; all had acute pulmonary oedema; time between sting and hospitalisation 1–12 h (mean 4.25 h).
Bawaskar and Bawaskar 1989: 33 Mesobuthus tamulus (=Hottentotta tamulus) stings (identification: no criteria given).
Classification:
Local envenoming:

  • local pain 3/33; time between sting and hospitalisation <1 h.

Systemic envenoming:

  • arterial hypertension 10/33; time between sting and hospitalisation 2–4.3 h (mean 3.1 h).
  • tachycardia 11/33; time between sting and hospitalisation 3 h–11 days (mean 8.3 h).
  • pulmonary oedema 7/33; time between sting and hospitalisation 2.3–20 h (mean 7.2 h).
  • fatal 2/33; time between sting and hospitalisation 44 and 6 h.

Bawaskar and Bawaskar 1992b: 62 Mesobuthus tamulus (=Hottentotta tamulus) stings. Identification: no criteria given.
Classification:
Local envenoming:

  • local pain 18/62.

Systemic envenoming:

  • arterial hypertension 18/62; time between sting and hospitalisation 1.5–65 h (mean 3 h).
  • supraventricular tachycardia 15/62; time between sting and hospitalisation 1–24 h (mean 5.7 h)
  • pulmonary oedema 11/62; time between sting and hospitalisation 2–52 h (mean 11.6 h).
  • fatal 1/62.

Bawaskar and Bawaskar 1994: 163 Mesobuthus tamulus (=Hottentotta tamulus) stings. Identification: no criteria given.
Classification:
Local envenoming:

  • local pain 78/163.

Systemic envenoming:

  • hypertension and bradycardia 42/163; age 6–85 years (mean 30 years); time between sting and hospitalisation 1.5–8 h (mean 2.5 h).
  • hypertension and tachycardia 17/163; age 3–72 years (mean 16 years); time between sting and hospitalisation 1.5–5.5 h (mean 3 h).
  • pulmonary oedema 14/163; time between sting and hospitalisation 4–17 h (mean 11.5 h).
  • hypotension 3/163; age 35, 60, 65 years; time between sting and hospitalisation 1, 4, 6 h.
  • tachycardia 8/163; time between sting and hospitalisation 4–16 h (mean 10 h).
  • fatal 1/163; age 3.5 years; time between sting and hospitalisation 12 h.

Case reports

Karnad et al. 1989: 5 Mesobuthus tamulus (=Hottentotta tamulus) stings. Identification: no criteria given; time between sting and hospitalisation 4–12 h.

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

In patients with only local signs of envenoming: local pain 3/3 (Bawaskar and Bawaskar 1989).

Marked pain radiating out from the site of the sting 18/62. Due to the radiating pain, patients are usually not able to identify the site of the sting. It can be recognised from the localised sweat secretion and a punctate haemorrhagic lesion caused by mechanical injury from the scorpion's sting (Bawaskar and Bawaskar 1992b).

Marked local pain 78/163 (Bawaskar and Bawaskar 1994).

In patients with arterial hypertension as a sign of systemic envenoming: mild local pain 10/10 (Bawaskar and Bawaskar 1989).

In patients with arterial hypertension, supraventricular tachycardia or acute pulmonary oedema as systemic signs of envenoming: mild local pain 44/62 (Bawaskar and Bawaskar 1992b).

Haemostatic effects

Autopsy reports from India contain evidence of bleeding from multiple organs (Reddy et al. 1972).

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. In Hottentotta tamulus envenoming the most notable effect is stimulation of both parts of the autonomic nervous system. This results in transient cholinergic effects (vomiting, profuse sweating, bradycardia, priapism, hypersalivation, arterial hypotension) and longer-lasting adrenergic effects (arterial hypertension, tachycardia, myocardial failure).

Cholinergic effects

Vomiting, profuse sweating, priapism 85/163; onset of symptoms shortly after the sting (Bawaskar and Bawaskar 1994).

Predominantly adrenergic effects

Patients with arterial hypertension: arterial hypertension (120/90–180/140 mmHg); vomiting 10/10, sweating 10/10, priapism, parasternal heave, protodiastolic gallop, apical systolic murmur (mitral regurgitation). 2/10 developed tachycardia, 2/10 pulmonary oedema (Bawaskar and Bawaskar 1989).
Arterial hypertension (130/90–220/140 mmHg); vomiting 18/18, sweating 18/18, hypersalivation 18/18, priapism, parasternal heave 18/18, protodiastolic gallop 18/18, apical systolic murmur (papillary muscle dysfunction: mitral regurgitation) 18/18, facial swelling 18/18; the children were confused, agitated or lethargic. 2/18 developed acute pulmonary oedema (Bawaskar and Bawaskar 1992b).

Patients with arterial hypertension and bradycardia (42/163): arterial hypertension (140/100–210/160 mmHg), heart rate 58–83/min (mean 67/min) (Bawaskar and Bawaskar 1994).

Patients with arterial hypertension and tachycardia (17/163): arterial hypertension (130/104–140/110 mmHg), heart rate 116–180/min (mean 124/min). Systolic murmur, diastolic gallop, pallor, cold extremities 8/17 (Bawaskar and Bawaskar 1994).

Patients with arterial hypotension (3/163): arterial hypotension (90/80, 98/90, 40/– mmHg), heart rate 68, 100, 108/min (Bawaskar and Bawaskar 1994).

Patients with tachycardia: tachycardia (130–215/min); protodiastolic gallop 11/11, apical systolic murmur (mitral regurgitation) 11/11, cold extremities 11/11, 2/11 developed pulmonary oedema (Bawaskar and Bawaskar 1989).
Supraventricular tachycardia (130–180/min, mean 154/min); blood pressure 60/90–110/90 mmHg, vomiting 15/15, sweating 15/15, hypersalivation 15/15, priapism, thready peripheral pulse and cold extremities 15/15 (Bawaskar and Bawaskar 1992b).
Tachycardia (110–160/min, mean 128/min) (Bawaskar and Bawaskar 1994).

Patients with pulmonary oedema: vomiting 12/12, sweating 12/12, orthopnoea 12/12, moist rales over all segments of the lung 12/12, heart rate on average 126/min (80–164/min), mean blood pressure 50–170 mmHg, protosystolic gallop 12/12, apical systolic murmur 8/12, cold, cyanotic extremities 12/12, priapism (Bawaskar and Bawaskar 1987).
Vomiting 11/11, sweating 11/11, hypersalivation 11/11, priapism, tachycardia (83–150/min, mean 125/min), blood pressure 90/70 mmHg – not measurable, clinical signs of severe peripheral vasoconstriction 11/11, massive pulmonary oedema with uncontrollable coughing and bloody-frothy sputum (2/11) (Bawaskar and Bawaskar 1992b).
Pulmonary oedema 14/163, 8 with arterial hypertension, symptoms of shock (Bawaskar and Bawaskar 1994).
Massive pulmonary oedema with uncontrollable coughing and bloody-frothy sputum 2/7 (Bawaskar and Bawaskar 1989).
Pulmonary oedema with normal blood pressure 5/5 (Karnad et al. 1989).

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.

Case fatality rate

2/33. Cause of death: cardiovascular failure 6 and 44 h after the sting (Bawaskar and Bawaskar 1989).

1/163. A 3.5-year-old child was hospitalised in a moribund condition 12 h after the sting (Bawaskar and Bawaskar 1994).

Laboratory and physical investigations

ECG

Patients with arterial hypertension: lowered ST segments in the inferior lateral leads, tented T waves in V2–V6. From the 3rd day after the sting increased QTc interval (0.4–0.5 s) for 3 days and T wave inversion for 3–4 weeks. Initial ventricular bigeminy (3/10) (Bawaskar and Bawaskar 1989).

Patients with tachycardia: hypoxic signs with LAH, Q and ST elevation in I and aVL. These persisted for 24 h (7/11) or 48 h (4/11) (Bawaskar and Bawaskar 1989).

Patients with pulmonary oedema: LAH and widened QRS complexes. Signs of left ventricular hypertrophy (SV1 + RV5 >35 mm); subsequently increased QTc for 3 days and T wave inversion for 4 weeks (Bawaskar and Bawaskar 1989).

Patients with local pain and no systemic signs of envenoming: no ECG changes (Bawaskar and Bawaskar 1989).

Patients who died: hypoxic ECG signs with low voltage, Q and ST elevation in the I and aVL leads. ST depression in II, III and aVF. These patients developed ventricular tachycardia, ventricular fibrillation and suffered cardiac arrest (Bawaskar and Bawaskar 1989).

Treatment (symptomatic)

Arterial hypertension

Patients with arterial hypotension and bradycardia (42/163; see above): single-dose nifedipine 5 mg s.l. plus prazosin (single dose: children 250 µg, adults 500 µg), repeat 6-hourly (18/42). Prazosin alone at the specified dose (24/42) (Bawaskar and Bawaskar 1994).

Patients with pulmonary oedema (14/163; see above): prazosin at the dose specified above, patient in an upright seated position, aminophylline i.v., oxygen (Bawaskar and Bawaskar 1994).

Patients with arterial hypertension and tachycardia (17/163; see above): 8 of these 17 patients developed pulmonary oedema with supraventricular tachycardia, although their blood pressure was well controlled with single-dose nifedipine and prazosin. They required aminophylline i.v. in addition and a further dose of prazosin. All other patients in this group showed clinical improvement with oral prazosin alone (Bawaskar and Bawaskar 1994).

Patients with massive, life-threatening pulmonary oedema (5/163): all 5 patients improved and survived with sodium nitroprusside i.v. (Bawaskar and Bawaskar 1994).

Patients with arterial hypotension and pulmonary oedema: clinical improvement with prazosin alone (Bawaskar and Bawaskar 1994).
Patients with arterial hypotension and tachycardia: clinical improvement with prazosin and oral rehydration (Bawaskar and Bawaskar 1994).

Nifedipine: in 8 patients with arterial hypertension, tachycardia, heart murmurs or imminent heart failure, it was observed that the occurrence of acute pulmonary oedema was temporally related to the administration of nifedipine (Bawaskar and Bawaskar 1994) (comment: in all cases nifedipine was administered s.l.).

All patients who initially had normal blood pressure levels developed arterial hypotension and peripheral circulatory failure 1–4 h after administration of furosemide. CVP was low. Attempts to correct the low CVP with infusion of crystalline fluids resulted in deterioration of the pulmonary oedema. Inotropic substances (dopamine, dobutamine) improved the blood pressure and pulmonary oedema but not the reduced right ventricular preload. If patients with pulmonary oedema who developed arterial hypotension and whose pulmonary oedema deteriorated with intravenous fluids were given captopril (12.5 mg p.o.) along with continued intravenous fluids, the clinical symptoms improved dramatically. Positive inotropic substances were no longer necessary. Captopril administration was continued for 3–4 days (Karnad et al. 1989).


Evaluation and recommendations

According to the results of non-controlled studies and case reports, ACE inhibitors (captopril), postsynaptic alpha-receptor blockade (prazosin) and calcium channel blockers (nifedipine) appear to reduce mortality from Mesobuthus tamulus (H. tamulus) stings from around 30% to approx. 2–3%, as well as reducing morbidity (Bawaskar and Bawaskar 1986, 1987, 1989, 1991, 1992a, b, Karnad et al. 1989). Nifedipine reduces the raised blood pressure and increased myocardial contractility caused by elevated levels of circulating catecholamines. However, it has been noted that patients with arterial hypotension, tachycardia, heart murmurs or imminent heart failure who are given nifedipine develop acute pulmonary oedema that is temporally related to the administration of nifedipine (Bawaskar and Bawaskar 1994) (comment: in all cases nifedipine was administered s.l.!!!). Prazosin reduces preload and left ventricular impedance without raising the heart rate or renin levels. Nifedipine alone will not prevent myocardial damage if the peripheral effects of the venom are not simultaneously neutralised with prazosin. Prazosin also inhibits the suppression of insulin secretion caused by scorpion envenoming (Bawaskar and Bawaskar 1992a, b). Like prazosin, captopril also brings about an economization of cardiac work. In addition, ACE inhibitors inhibit the release of catecholamines from peripheral nerve endings. They also protect the myocardium from catecholamine-induced damage through the binding of free radicals (Karnad et al. 1989).

Diuretics should be used with caution in patients with acute pulmonary oedema following a Mesobuthus tamulus (H. tamulus) sting. Dopamine and dobutamine can potentially contribute to the myocardial damage already caused by endogenous catecholamines (Karnad et al. 1989). Atropine, antihistamines, corticosteroids and digoxin increase cardiopulmonary instability and myocardial oxygen consumption in the presence of high circulating levels of catecholamines (Bawaskar and Bawaskar 1991).

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 1992, Gueron and Sofer 1991, Gueron et al. 1993).

 

Recommendations on the bases of the above evidence for the treatment of systemic Mesobuthus tamulus (H. tamulus) scorpion envenoming: Neutralisation of the peripheral effects of the venom through postsynaptic alpha-receptor blockade with prazosin. Massive, life-threatening pulmonary oedema can be treated by infusion of sodium nitroprusside (Bawaskar and Bawaskar 1992a, b, 1994). ACE inhibitors are an alternative to prazosin (Karnad et al. 1989).

Recent evidence suggests that recovery from Mesobuthus tamulus (=Hottentotta tamulus) stings is hastened and the time in hospital shortened by early administration of scorpion antivenom within 6h of the sting in addition to prazosin compared with prazosin alone in grade 2 scorpion evenoming (definition see below). The price, however, is a problem with antivenom plus prazosin being around 10 times as expensive as prazosin alone (Bawaskar and Bawaskar 2011).

 

Definition grade 2 scorpion envenoming: signs and symptoms of autonomic stormcharacterised by acetylcholine excess or parasympathetic stimulation (vomiting, profuse sweating from all over body, ropey salivation, bradycardia, premature ventricular contraction, hypotension, priapism in men) and sympathetic stimulation (hypertension with blood pressure >140/90, tachycardia with heart rate >120 per minute, cold extremities, transient systolic murmur) (Bawaskar and Bawaskar 2011).

Treatment (specific)

Bawaskar and Bawaskar 2011:  Prospective, open label randomised controlled trial comparing efficacy of scorpion antivenom (F(ab')2 monovalent antivenom, Haffkine Biopharma (Mumbai) plus prazosin (250 μg for children up to 18 years and 500 μg for adults, repeated at intervals of 3h) with prazosin alone (same schedule as above). N=70 patients with grade 2 envenoming (definition see below) due to Mesobuthus tamulus (=Hottentotta tamulus) stings (identification: victim or bystander had seen a red scorpion, had brought in the killed specimen, or recognized the hospital's preserved specimen) admitted to the hospital within 6h of the sting. Primary endpoint: Proportion of patients achieving resolution of the clinical syndrome (sweating, salivation, cool extremities, priapism, hypertension or hypotension, tachycardia) 10 hours after administration of study drugs. Secondary endpoints: Time required for complete resolution of clinical syndrome, prevention of deterioration to higher grade, doses of prazosin required overall and within 10 hours, and adverse events.

 

Conclusions: Recent evidence suggests that recovery from Mesobuthus tamulus (=Hottentotta tamulus) stings is hastened and the time in hospital shortened by early administration of scorpion antivenom within 6h of the sting in addition to prazosin compared with prazosin alone in grade 2 scorpion evenoming (definition see below). The price, however, is a problem with antivenom plus prazosin being around 10 times as expensive as prazosin alone.

 

Definition grade 2 scorpion envenoming: signs and symptoms of autonomic stormcharacterised by acetylcholine excess or parasympathetic stimulation (vomiting, profuse sweating from all over body, ropey salivation, bradycardia, premature ventricular contraction, hypotension, priapism in men) and sympathetic stimulation (hypertension with blood pressure >140/90, tachycardia with heart rate >120 per minute, cold extremities, transient systolic murmur) (Bawaskar and Bawaskar 2011).