Treatment scheme for snakebite poisoning

Treatment scheme for snakebite poisoning:

  1. The proposed treatment principles for intoxications caused by snakebites in the South Pacific and Asian regions were summarized by Dr. D. A. Warrell, and we are relying on his recommendations here.
  2. The general treatment plan is presented in the form of a diagram as depicted in the figure below.
  3. Regarding the use of adrenaline before administering antitoxin, there are discrepancies. Adrenaline is likely best used only to treat potential severe reactions.
  4. If there is a history of prior exposure to antitoxin, allergy to horse serum, severe allergic reactions to other antigens, or asthma, consider preliminary subcutaneous administration of adrenaline, intravenous administration of an antihistamine, and additional intravenous administration of hydrocortisone.
  5. The absence of signs of coagulopathy weakening or even its enhancement 2 hours after antitoxin therapy indicates the presence of venom in the bloodstream and warrants continuation of this therapy.
  6. Antitoxin is not always able to eliminate paralysis caused by neurotoxic venom. It does not prevent early symptoms of paralysis such as ptosis and diplopia, but it may prevent the development of more severe, life-threatening manifestations.
  7. Recommended intravenous doses of antitoxin for Australian snake venom are provided in the table below.
  8. Most snake venoms cause death due to paralysis of the respiratory musculature, acting on neuron membranes in the area of the endplate.
  9. Sutherland described presynaptic and postsynaptic toxins in detail.
  10. Presynaptic snake venoms generally have high molecular weights ranging from 13,000 to 85,000. The most neurotoxic substance known today is botulinum toxin (molecular weight 140,000). Presynaptic toxins (except for bungarotoxin from the Asian krait Bungarus muticinctus and botulinum toxin) cause noticeable ultrastructural changes and paralysis that is difficult to alleviate with antitoxins. Examples include latrotoxin from the spider Latrodectus mactans hasselti (molecular weight 130,000), notexin from tiger snakes (molecular weight 13,500), taipoxin from taipans (molecular weight 45,000), and textilotoxin from the brown recluse spider (molecular weight 88,000).
  11. Postsynaptic snake venoms with smaller molecules block acetylcholine receptors. No ultrastructural changes are observed. Paralysis is easier to alleviate with antitoxin. Examples include venoms from Australian snakes (molecular weight 6,000), alpha-bungarotoxin (molecular weight 7,400), and conotoxins.

Application of antitoxins

v) Application of antitoxins: The decision to administer antitoxin must be final, as trial and error methods are not suitable here. Even if the victim develops severe reactions to the drug, and the bite threatens their life, antitoxin therapy must be continued, possibly using additional medications and reducing the infusion rate. It is highly desirable to administer antitoxin in the intensive care unit in a specially equipped clinic for this procedure. Despite its simplicity, the method of administration has proven its effectiveness in practice. The antitoxin is diluted at a ratio of 1:10 in an appropriate fluid, such as isotonic saline or saline with glucose.

For small children, it is sometimes necessary to dilute it at a ratio of 1:5 due to the risk of fluid overload. An intravenous injection of an antihistamine is administered. A subcutaneous injection of adrenaline (diluted at a ratio of 1:100) is given. The recommended dose is 0.3 ml for adults and 0.1 ml for children. The patient should be warned that the effects of adrenaline, i.e., effects not caused by snake venom, will begin in the next few minutes.

Under certain circumstances, hydrocortisone is administered intravenously (empirical dose: usually starting with 100 mg). It reduces the likelihood of subacute and chronic reactions, such as serum sickness. This is usually recommended for children, those prescribed a large volume of antitoxin (e.g., polyvalent or many vials of monovalent), and those with a history of allergic reactions to horse protein. Antitoxin infusion begins, initially slowly (not exceeding 1 ml/min for 3-5 minutes). The infusion should be completed within 30-40 minutes unless allergic reactions occur. After the procedure, the patient is monitored in the intensive care unit for at least 6 hours.

Ineffectiveness of antitoxin therapy

g) Ineffectiveness of antitoxin therapy: If the antitoxin does not produce the desired reaction, the reasons may include:

  • 1) the use of inadequate monovalent antitoxin; if the snake species cannot be accurately identified, a polyvalent preparation should be used;
  • 2) insufficient amount of the drug administered;
  • 3) the antitoxin has “spoiled,” and its expiration date needs to be checked;
  • 4) an incorrect method of administration was chosen (e.g., intramuscular);
  • 5) too much time has elapsed since the bite, although antitoxin therapy sometimes helps even after 60 hours of venom entry into the body.

Source: MedUniver (https://meduniver–com/Medical/toksikologia/lechenie_ukusa_zmeei.html)