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Poisonous animals
 
Cnidarians (Jellyfish, Corals and Anemones)
 
Venomous fish
 
Scorpions
 
Spiders
 
Hymenopterans (Bees, Wasps and Ants)
 
Sea snakes
 
Terrestrial snakes
 
Miscellaneous animals
 
 
 
 
 
 
 
 

Diagnosis & Treatment — Hospital

 

Who requires antivenom?

See Therapy phase General practitioner / health post and Comments.

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

S  Signs & Symptoms
  • Local pain,
  • local redness,
  • swelling.
D  Diagnostics

Clinical.

T  Treatment

Infiltration with a local anaesthetic (xylocaine 1%, max. 0.5 ml, without the addition of a vasoconstrictor), nerve block.

Wound care: see Therapy phase: General practitioner / health post.

C  Comments

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.

Scorpions that cause local effects

In principle all scorpions.
See Biomedical database entries.

Haemostatic effects

S  Signs & Symptoms

Systemic bleeding.

D  Diagnostics
  • Clinical,
  • laboratory parameters: Hb, Hct, clotting time, PT/aPTT, TT, fibrinogen, FSP, (D-dimers), platelets.
T  Treatment
  • Symptomatic.

→ Antivenom.

C  Comments

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).

Scorpions that cause haemostatic effects

Neurological effects

(Autonomic and somatic nervous systems)

S  Signs & Symptoms

Cholinergic:

  • Vomiting,
  • profuse sweating,
  • hypersalivation,
  • increased bronchial secretion,
  • priapism,
  • bradycardia,
  • arterial hypotension;

Adrenergic:

  • tachycardia,
  • arterial hypertension,
  • myocardial failure,
  • hyperglycaemia;

 

Somatic: neuromuscular dysfunction of the cranial nerves and the skeletal musculature (rolling eye movements, dysphagia, dysarthria, muscle fasciculations, motor agitation).

D  Diagnostics
  • Clinical,
  • ECG,
  • chest X-ray,
  • echocardiography,
  • invasive haemodynamic monitoring,
  • blood gases,
  • blood sugar.
T  Treatment

Cardiovascular complications

  • reduction of afterload with vasodilators (prazosin, hydralazine, sodium nitroprusside), calcium channel blockers (nifedipine), ACE inhibitors (captopril). 

In addition:

  • Fluid replacement if arterial hypotension and low central venous pressure are present (however, there is a need for caution as there may be concomitant pulmonary oedema that could deteriorate!).
  • Medications that should be avoided or that are contra-indicated: pethidine, morphine, barbiturates, atropine (see below), calcium, anti-inflammatory drugs, including corticosteroids, cadiac glycosides.
  • To date, beta-blockers have had no proven benefit and is controversial.
  • Diuretics should only be administered if hypovolaemia and shock have been excluded.

 

→ Antivenom (see below and  General practitioner/ health post).

 

Respiratory disturbances due to paralysis of the respiratory musculature, cranial nerve deficits and bronchial hypersecretion.

  • Early endotracheal intubation, suctioning of bronchial secretions and artificial respiration.

 

→ Antivenom (see below and General practitioner/ health post).

 

C  Comments

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).

Scorpions that cause neurological effects

1. Marked cardiovascular effects mediated via the autonomic nervous system and effects on the somatic nervous system

2. Marked cranial nerve deficits and paralysis of the skeletal musculature mediated via the somatic nervous system and effects on the autonomic nervous system

Cardiac effects

The pathogenesis of 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 the subject of controversy (Abroug et al. 1991, 1992, Gueron and Sofer 1992, Gueron et al. 1993).

Renal effects

S  Signs & Symptoms
  • Flank pain,
  • renal bed sensitive to percussion,
  • eyelid oedema.
D  Diagnostics
  • Clinical,
  • laboratory parameters,
  • urine output (balance, hourly),
  • serum creatinine,
  • serum potassium,
  • bicarbonate.
T  Treatment

Prevention and treatment of acute renal failure.

C  Comments

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.

How is the appropriate antivenom chosen?

D  Diagnostics

How are antivenoms administered and complications caused by antivenoms treated?

T  Treatment

Monitoring of the patient
1. After administration of antivenom (assessment of success of antivenom or indication for continued antivenom treatment)

D  Diagnostics

Specific examinations are based on the signs and symptoms as well as laboratory parameters that were used to determine the indications for antivenom administration.

2. If there is no indication for antivenom treatment following the initial investigation

D  Diagnostics

At least hourly from 12 to 24 h after the sting:

Signs and symptoms as described in the Therapy phase: General practitioner / health post: "Is it likely that a clinically relevant injection of venom has taken place?".

Follow-up
1. Wounds

D  Diagnostics
  • Inspection,
  • bacterial smears.
T  Treatment
  • Wound care,
  • antibiotic treatment.

2.  If antivenom was administered: serum sickness

D  Diagnostics
T  Treatment