Cobra Envenomation Medication
- Author: Robert L Norris, MD; Chief Editor: Joe Alcock, MD, MS more...
The definitive therapy for cobra envenomation is antivenom administration, which should be started as soon as possible if evidence of systemic envenoming is present. If specific antivenom is not rapidly available, the patient must be supported using conservative measures alone. Measures include securing the airway and supporting respirations as necessary. Hypotension should be treated initially with intravenous fluids (initially crystalloids but if blood pressure/tissue perfusion fails to improve, then albumin). If hypotension persists after the intravascular volume is replete, vasopressor agents may be necessary.
Evidence supports the trial of cholinesterase-inhibiting drugs, such as edrophonium or neostigmine, as a temporizing measure in a situation of severe cobra venom poisoning with significant neurologic abnormalities until antivenom can be obtained.[13, 14] These temporizing drugs should not, however, delay securing the airway of a victim who is developing respiratory distress or inability to handle secretions.
Antivenom can be started according to the manufacturer's instructions regarding route and dose. Although some manufacturers advise use of an intradermal skin test to predict an acute reaction to antivenom, this procedure is terribly unreliable and only serves to waste precious time. Such recommendations for skin testing should be ignored.
As with any form of bite, update the tetanus status as necessary. Antibiotic prophylaxis is not necessary.
These agents impart passive immunity to the victim against the venom components of the snake(s) for which it is manufactured. The heterologous antibodies bind with venom antigens and block their deleterious effects.
Antivenom (variable, see below)
Several different cobra antivenoms are produced by various countries. They are of variable purity and efficacy. The most appropriate agent for the species involved should be determined and obtained. Given venom variability, antivenom produced in the country of origin of the offending species is preferred. An intradermal skin test for potential acute sensitivity is often recommended by manufacturers before administration. Such skin tests are, however, completely unreliable predictors of anaphylactic/anaphylactoid reactions, and should be omitted. Before administration, intravascular volume should be expanded using crystalloids such as normal saline or Ringer's lactate unless some contraindication (eg, congestive heart failure) is present. Pretreatment with antihistamines (H1 and H2 blockers) can be considered, though their efficacy at preventing adverse reactions to antivenom is unproven. Epinephrine should be immediately available for treatment of an anaphylactoid response to the heterologous serum.
Antihistamines (H1 and H2 blockers) may blunt or prevent an acute allergic reaction when given before the administration of antivenom. If an anaphylactic/anaphylactoid reaction occurs despite pretreatment, further antihistamine dosing may be required. These agents are useful in managing pruritus in cases of delayed serum sickness, which may appear days to weeks following antivenom treatment.
Diphenhydramine can be administered parenterally. It is often the H1 blocker of choice in treating or preventing anaphylactoid reactions. It is also effective orally in treating itching associated with serum sickness. If an acute allergic reaction subsequently occurs, further administration may be required.
Cimetidine is an H2 antagonist coadministered with an H1 antagonist if there is no response to the H1 antagonist alone; it treats itching and flushing in anaphylaxis, pruritus, urticaria, and contact dermatitis.
Useful in treating acute allergic reactions that may occur with antivenom administration and in supporting the blood pressure and tissue perfusion of hypotensive patients with shock unresponsive to IV fluids and antivenom.
With its combined alpha- and beta-adrenergic effects, Epinephrine is the drug of choice for the treatment of an acute anaphylactoid reaction because it halts and reverses the major abnormalities associated with such reactions (eg, hypotension, laryngospasm, bronchospasm, edema, urticaria); it must be available immediately for administration if such a reaction to antivenom occurs.
Dopamine may be required to support blood pressure in the face of hypotension caused by an anaphylactic/anaphylactoid reaction (unresponsive to fluids, epinephrine) or by direct snake venom effects (unresponsive to fluids, antivenom).
Norepinephrine may be used as an alternative to dopamine to support blood pressure in the face of hypotension caused by an anaphylactic/anaphylactoid reaction that is unresponsive to fluids and epinephrine.
Used in management of both acute and delayed allergic phenomena following antivenom administration. Corticosteroids, however, have no primary role in the management of snake venom poisoning.
Steroids ameliorate the delayed effects of anaphylactoid reactions and may limit biphasic anaphylaxis. In severe cases of serum sickness, parenteral steroids may be beneficial to reduce the inflammatory effects of this immune-complex mediated disease.
Prednisone is useful orally in managing mild-to-moderate serum sickness treated on an outpatient basis.
Cholinesterase inhibitors may be effective in temporarily reversing muscle weakness until antivenom can be obtained. Their use might obviate intubation, but airway protection should not be delayed if there is any doubt of the patient's respiratory status or ability to protect the airway.
Edrophonium is a short-acting anticholinesterase agent; it may provide significant improvement in muscle strength (eg, ability to open eyes) within 2 minutes and its effect peaks in 5 minutes. Weakness rapidly returns, however, and can be subsequently treated with a longer-acting agent, such as neostigmine.
Neostigmine is a longer-acting cholinesterase inhibitor that can be used if a trial of edrophonium is effective; it inhibits the destruction of acetylcholine by acetylcholinesterase, which facilitates the transmission of impulses across the myoneural junction.
Consists of administration of immunoglobulin pooled from serum of immunized subjects.
Tetanus immune globulin is used for passive immunization of any person with a wound that might be contaminated with tetanus spores when the person has not previously completed a primary tetanus immunization series.
Toxoids are used to induce active immunity against the respective antigens.
This is a tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine. It promotes active immunity to diphtheria, tetanus, and pertussis by inducing the production of specific neutralizing antibodies and antitoxins. It is indicated for active booster immunization for tetanus, diphtheria, and pertussis prevention for persons aged 10-64 years (Adacel approved for 11-64 y, Boostrix approved for 10-18 y). It is the preferred vaccine for adolescents scheduled for booster.
The immunizing agent of choice for most adults and children older than 7 years is tetanus and diphtheria toxoids. It is necessary to administer booster doses to maintain tetanus immunity throughout life. Pregnant patients should receive only tetanus toxoid, not a diphtheria antigen-containing product. In children and adults, it may be administered into the deltoid or midlateral thigh muscles. In infants, the preferred site of administration is the mid thigh laterally.
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