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Local venom/poison effects

Definition: Effects that occur locally at the point of entry of the venom/poison and also regionally. They include histological changes to the skin, vessels, nerves and musculature.


Signs and symptoms:

  • In the case of parenteral application of venom (venomous animals):
    • pain,
    • redness, cyanosis,
    • blistering,
    • swelling, compartment syndrome,
    • lymphangiopathy and lymphadenopathy,
    • necrosis.
  • In the case of peroral application of poison (poisonous animals):
    • paraesthesia of the oral mucosa,
    • mucosal irritation,
    • nausea, vomiting, diarrhoea.
  • In the case of venom entering the eye (Spitting cobras and jellyfish):
    • e.g. conjunctivitis, corneal damage.


The mechanisms by which extensive local symptoms of envenoming/poisoning arise, in particular oedema and necrosis, such as are typical with envenoming caused by viperids and crotalids, are complex. Very different factors contribute to the development of such symptoms, and understanding of the biochemical and pathophysiological processes involved is poor.

In contrast to neurological and haemostatic effects, primary therapy has little influence on local effects. Antivenoms only appear to have an effect on local symptoms if they are administered at the same time or shortly after the venom/poison is applied, which in the real-life practice of treating accidents with venomous/poisonous animals is rarely possible. This situation is unsatisfactory, as a large part of the permanent damage caused by envenoming/poisoning is due solely to local effects.

Local effects according to the mode of venom/poison application

Along with the venom/poison composition and the quantity applied, the mode of application also plays a role in the development of local effects.

In the case of peroral consumption of poisonous animals, toxins that are generally systemically active can also cause local functional disturbances of the gastrointestinal tract.

If venom from Spitting cobras or jellyfishes enters the eyes, it can cause conjunctivitis and corneal damage, among other things. These symptoms are probably associated with cytolytic venom components, such as DLF and phospholipases in Spitting cobras or channel-forming cytotoxins in jellyfish.

In the case of parenteral application of venom, the mode of application (s.c, i.m. or i.v) influences the course and range of clinical effects. In accidents with venomous animals, the venom is usually injected subcutaneously. This is also true for snakes with long venom fangs, such as the North American rattlesnakes (Russell 1983). Thus the venom is initially localised in a narrowly confined area of subcutaneous tissue. Hyaluronidases, which occur in insect and reptile venoms (in particular viperids and crotalids), act as "spreading factors". Through depolymerisation of hyaluronic acid, they cause structural loosening of the connective tissue and thus facilitate diffusion of the venom into the tissue. Low-molecular-weight substances, such as neurotoxins from scorpions, elapids and Hydrophiidae, appear to be rapidly transported via the blood circulation, while high-molecular-weight substances, such as coagulation-promoting components from viperid and crotalid venoms, only gradually enter the circulation via the lymphatic system.

During lymphatic transport various venom/poison components can act locally and cause extensive swelling, such as often occurs with viper and pit viper bites.

Myotoxic peptides and myotoxic phospholipases A have been isolated from various snake venoms (North American Crotalus sp., Agkistrodon sp., Bothrops sp. etc.), and these have been shown to cause muscle necrosis following intramuscular administration in animal experiments. No general myolytic activity of these venoms has been demonstrated in humans (possible exception C. horridus), and local muscle necrosis is rare with bites from these snakes, as long as appropriate medical care has been received. If it does occur, it is more likely to be related to indirect effects of the venom, inappropriate medical procedures or contra-indicated first aid methods (tourniquets, incisions) than to the direct effect of local myotoxic components. However, in the rare case of an intramuscular bite, direct myonecrotic activity of such myotoxins is possible (Garfin et al. 1984).

Venom/poison components with direct necrotising effects on skin and muscle

There are very few verified data on venom/poison components that directly cause the development of skin or muscle necrosis extending from the site of application of the venom/poison. "Cardiotoxins" (= cytotoxins, DLF, see also "Autopharmacological venom/poison effects") from the venoms of various cobras (Naja sp.) appear to be responsible for the formation of local soft tissue necrosis in humans. Acting in synergy with phospholipases A, they lead to the destruction of cell membranes.

Dermonecrotic venom fractions have been isolated from various jellyfish, and these lead to cell lysis through the formation of channels in biological membranes. Channel-forming toxins have also been detected in various bacteria, and necrotic effects following envenoming/poisoning may also be associated with bacterial infections.

A toxin with sphingomyelinase D activity was isolated from the venom of Loxosceles reclusa, and it appears to be responsible for the dermonecrotic effects following Loxosceles bites.

The direct, local activity of myotoxins from various snake venoms was discussed above.

Indirect, local oedematogenic and necrotising effects

Muscle and skin necrosis following viperid and crotalid bites are often due to indirect effects of the venom.

Coagulation-promoting venom/poison components, haemorrhagins (see "Haemostatic venom/poison effects") and exogenous or endogenous autacoids (see "Autopharmacological venom/poison effects") can lead to changes in vessel permeability. Ecchymoses, blood-filled blisters and oedema can occur due to extravasation of blood cells or plasma. If the oedema increases in magnitude, the interstitial pressure in the skin and muscle may be raised to such an extent that inadequate blood perfusion results, thus causing muscle and skin necrosis. Localised ischaemia may also be the result of a thrombosis caused by coagulation-promoting venom/poison components.

Another cause of local necrosis that must also be mentioned here is the tourniquet, a commonly used first aid method. Tourniquets inevitably lead to impairment of the blood circulation and ischaemia in the affected limb and thus may alone be responsible for extensive necrosis.

Literature: Gutierrez and Lomonte 1989, Harvey 1990, Mebs and Ownby 1990, Ohsaka 1979, Ownby 1990


Figure 5.2 Local oedematogenic and necrotising effects