Even in cases of severe systemic envenoming the only local signs are redness, mild swelling and paraesthesias. Local pain is a problem, as it can be debilitating.

It is not possible to definitively conclude to what extent there is a haemostatic effect of scorpion venom that is relevant to humans. There is one well-documented case of intracranial bleeding with abnormal coagulation parameters. The cause of the sting in this case was identified as Nebo hierochonticus. In another case with intracranial bleeding, the haemostatic parameters were in the normal range, but it was not possible to identify the species that caused the sting. The intracranial bleeding was explained in the context of the acute arterial hypotension (Rai et al. 1990). Autopsy reports from Trinidad and India contain evidence of bleeding from multiple organs (Reddy et al. 1972, Waterman 1938).

Clinical features and pathophysiology

A considerable number of the signs and symptoms of scorpion envenoming (Mesobuthus tamulus (=Hottentotta tamulus), Leiurus spp., Androctonus spp., Buthus spp., Tityus spp.) are attributed to the fact that scorpion venom is a very potent indirect stimulant of the autonomic nervous system. Their venoms cause release of endogenous catecholamines and acetylcholine. This results in an initial transient cholinergic effects (vomiting, profuse sweating, hypersalivation, priapism, bradycardia, arterial hypotension) which is followed by a longer-lasting adrenergic effects (arterial hypertension, tachycardia, myocardial failure).

Most prominently in Centruroides sp. envenoming, additional neurotoxic effects cause cranial nerve deficits, respiratory distress and  neuromotor hyperactivity. Neurotoxic features of Parabuthus sp. envenoming are ptosis and dysphagia.

The cardiovascular complications have a multi-factorial aetiology:

1. effects of the release of endogenous catecholamines on arterial pressure and impedance,
2. effects of the renin-angiotensin system,
3. effects of catecholamines at the myocardial cellular level (intracellular Ca²⁺ accumulation, increased myocardial oxygen requirements), 
4. reduced myocardial perfusion,
5. direct myocardiotoxic effect (see below "Cardiac effects").

In the majority of patients there are already fully developed haemodynamic disturbances present at the time of hospitalisation, which in practice is 2–3 h after the sting at the earliest (Gueron et al. 1993).

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 appear within a few hours and are followed by T inversion in the precordial or limb leads. QTc >0.40 s. The ECG changes are detectable for a period of several days and then reduce to tented/peaked T waves that can persist for several weeks. The ECG findings are proportional to other findings that reflect the severity of envenoming, namely signs of heart failure and shock (Gueron and Yaron 1970, Gueron et al. 1967).

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. These symptoms appear to play a significant role in the pathogenesis of heart failure following scorpion stings.

CPK, CK-MB: elevated CPK and CK-MB and a CK-MB/CPK ratio of >6% indicate myocardial damage in around half of patients with systemic envenoming. However, the lesions appear to be so small that in most cases neither cardiac insufficiency nor cardiac failure results. They do, however, come into question as the cause of cardiac dysrhythmias (Sofer et al. 1991).

Metabolic complications of envenoming:

Blood sugar: blood sugar is frequently raised.

Serum amylase, plasma immunoreactive cationic trypsin (plasma ICT): acute pancreatitis is a further complication of scorpion envenoming (Bartholomew 1970, Poon-King 1963, Sofer et al. 1991, Waterman 1938). Serum amylase is frequently increased in systemic scorpion envenoming. However, it is neither a sensitive nor a specific sign of acute pancreatitis. In contrast, plasma ICT is both a specific and sensitive parameter for acute pancreatitis and is also increased (Sofer et al. 1991).

Blood gases (respiratory insufficiency): paralysis of the cranial nerves and skeletal musculature together with bronchial hypersecretion lead to respiratory insufficiency and respiratory failure.

Treatment

Recommendations for the treatment of cardiovascular manifestations of scorpion envenoming are not uniform. Various groups of experts in India, Israel, Saudi Arabia, South Africa, Brazil, Mexico and the USA use different drug combinations with or without antivenom.

Treatment of cardiovascular complications

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 (=Hottentotta 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 (=Hottentotta 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 of various expert groups on the treatment of cardiovascular complications

• 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).
• Following scorpion stings in which 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).
• Antivenom is recommended in addition to symptomatic treatment (Curry et al. 1983–84, Freire-Maia and Campos 1987, Dehesa-Davila 1989, Gateau et al. 1992, Ismail 1993).
• Gueron and colleagues question that antivenom can reverse the cardiac pathophysiological effects of scorpion venoms (Gueron et al. 1993, Gueron and Sofer 1994). 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).
• 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. The price, however, is a problem with antivenom plus prazosin being around 10 times as expensive as prazosin alone (Bawaskar and Bawaskar 2011).
• Among critically ill children with neurotoxic effects of Centruroides envenoming, i.v. administration of scorpion-specific F(ab')₂ antivenom resolved the syndrome within 4 hours, reduced the need for concomitant sedation with midazolam, and reduced the levels of circulating anbound venom. Generalizability of these results is limited by the age group studied and the potential for geograhic variation in scorpion venom (Boyer et al 2009).

Renal dysfunction is probably secondary in nature (in association with hypovolaemia and shock) or caused by the effects on the kidneys of the release of endogenous catecholamines.

• Wound care,
• antibiotic treatment.

See Antivenom treatment.