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Spider Envenomation, Redback: Treatment & Medication

Author: Rebecca L Rubin, MD, Clinical Assistant Instructor and Resident Physician, Department of Emergency Medicine, State University of New York Downstate/Kings County Hospital Center
Coauthor(s): Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Contributor Information and Disclosures

Updated: Sep 23, 2009

Treatment

Prehospital Care

  • Pressure immobilization of the bitten limb is not recommended due to the slow and non–life-threatening progression of symptoms. Pressure dressings may also exacerbate pain in the affected area.
  • Ice packs to the bite site and simple oral analgesia may be helpful.
  • Do not administer antivenom in the field due to the risk of a severe allergic reaction.
  • Collection of the spider may aid its proper identification at the emergency department.

Emergency Department Care

  • In patients with severe symptoms and signs of envenomation, treatment with redback spider antivenom should be considered. The benefit of treatment with antivenom should be weighed against the risk of its possible complications, including but not limited to, anaphylaxis and serum sickness.

Consultations

  • The local poison control center may be consulted for spider identification and management of severe envenomations.
  • A surgeon may be consulted if compartment syndrome is suspected.

Medication

Most cases of redback spider envenomation are mild and can be managed symptomatically using common oral analgesics and sedatives.

Redback spider antivenom provides specific treatment in severe cases of envenomation.

Ensure that the patient's tetanus status is up to date.

Antivenom

Redback spider antivenom is the primary treatment of severe latrodectism. Before the introduction of the antivenom in 1995, 14 deaths due to redback spider envenomation were documented in Australia. The antivenom consists of equine IgE fragments raised against aLTX. Each ampule contains 500 units of neutralizing capacity against the Australian redback spider venom, with an average volume of 1-1.5 mL per ampule. The antivenom is usually administered by intramuscular injection. Indications for use of antivenom include severe headache, vomiting, abdominal pain, hypertension, arthralgia, or myalgia. Severe pain at the envenomation site is not considered an indication for antivenom administration.1

Increasing concerns exist about the possible ineffectiveness of the IM route of administration of the redback antivenom. A recent study showed no significant difference in relief of symptoms or patient outcome between IV and IM administration of antivenom.9

The risk of allergic reaction to the antivenom is 0.5% and is higher in patients with a history of horse allergy or prior exposure to equine immunoglobulin. Before using the antivenom, ensure the ability to manage hypersensitivity reaction and check for availability of the appropriate resuscitation/intubation equipment. The risk of serum sickness after exposure to the antivenom is 1.4%.

Possible contraindications to antivenom use include current beta-blocker therapy, as this may reduce the patient's responsiveness to resuscitative therapy in the event of anaphylaxis.1


Redback spider antivenom

Produced by Commonwealth Serum Laboratories Ltd, Australia.

Adult

500 Units IM
Same dose, diluted in 100-150 mL of crystalloid, may be administered as IV infusion over 15-30 min in presence of severe stings and symptoms; additional dose of antivenom should be considered if patient does not respond to first dose within 60 min; diagnosis of redback spider envenomation should be reconsidered if no improvement is observed after second dose of antivenom

IV dose of antivenom may be warranted in confirmed cases of redback envenomation, where no response is observed after administering 2 IM doses of antivenom

Pediatric

Administer as in adults

Documented hypersensitivity to horse serum

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with documented allergy to horse serum (be prepared to treat anaphylaxis with IV fluids, diphenhydramine, and epinephrine)

Analgesics

Patients may experience severe pain at the bite site, and pain control is essential to quality patient care.


Acetaminophen with codeine (Tylenol With Codeine, Capital and Codeine)

Combines analgesic effects of a centrally acting opium-derived alkaloid (codeine) and a peripherally acting nonopioid analgesic (acetaminophen). Indicated for treatment of mild to moderate pain.

Adult

1-2 tab Tylenol #2 (15 mg codeine phosphate plus 300 mg acetaminophen), Tylenol #3 (30 mg codeine phosphate plus 300 mg acetaminophen), or 1 tab Tylenol #4 (60 mg codeine phosphate plus 300 mg acetaminophen) PO q4-6h prn, not to exceed 360 mg codeine and 4 g acetaminophen/24h

Pediatric

Based on codeine: 0.5-1 mg/kg/dose PO q4-6h
Based on acetaminophen: 10-15 mg/kg/dose PO q4h; not to exceed 75 mg/kg/d or 2.6 g/d
<3 years: Not established
3-6 years: 5 mL (1 tsp) PO qid prn
7-12 years: 10 mL (2 tsp) PO qid prn
>12 years: Administer as in adults

Multiple drug interactions exist; please refer to Micromedex for a complete list of drug interactions; toxicity of codeine increases with CNS depressants, tricyclic antidepressants, MAO inhibitors, neuromuscular blockers, CNS depressants, phenothiazines, and narcotic analgesics
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity of acetaminophen

Documented hypersensitivity to drug or related products

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypersensitivity to drug or tablet components, respiratory depression, paralytic ileus, G6PD deficiency, CNS depression, acute abdomen, head injury, increased ICP, impaired liver function, hypothyroidism, adrenal insufficiency, biliary disease, GU/GI obstruction, alcohol and drug abuse history; caution in patients dependent on opiates since this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction; hepatotoxicity with acetaminophen possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products and combined use with these products may result in cumulative acetaminophen doses and exceed recommended maximum dose


Morphine sulfate, injectable (Duramorph, Infumorph, Astramorph).

DOC for narcotic analgesia because of its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Morphine sulfate administered IV may be dosed in a number of ways and commonly is titrated to the desired effect.

Adult

2-10 mg IV administered over 4-5 min or 5-20 mg IM/SC q4-6h prn

Pediatric

0.1-0.2 mg/kg IV/IM/SC q2-4h (not to exceed 15 mg/dose)

May cause severe respiratory depression when used with other CNS depressants; phenothiazines may antagonize the analgesic effects of opiates

Documented hypersensitivity to morphine; asthma, hypotension, respiratory depression, upper airway obstruction, paralytic ileus

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Concurrent administration of other opioid analgesics or CNS depressants, alcohol consumption, circulatory shock, head injury or increased intracranial pressure, respiratory compromise, atrial flutter and other supraventricular tachycardias, elderly and debilitated patients

Benzodiazepines

Patients may experience significant restlessness and anxiety, which may require the use of sedatives for symptomatic control.


Lorazepam (Ativan)

A sedative hypnotic in the benzodiazepine class that has a short onset of effect and relatively long half-life.

Adult

1-2 mg IV/IM (not to exceed 10 mg/d)

Pediatric

0.05-0.1 mg/kg IV/IM (not to exceed 4 mg)

CNS toxicity increases when concurrently used with other CNS depressants

Documented hypersensitivity; narrow-angle glaucoma; untreated open-angle glaucoma; severe respiratory depression

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Concurrent use of other CNS depressants, respiratory depression, elderly/debilitated patients, depressed patients


Diazepam (Valium)

Modulates postsynaptic effects of GABA-A transmission, resulting in an increase in presynaptic inhibition. Appears to act on part of the limbic system, the thalamus, and hypothalamus, to induce a calming effect. Also has been found to be an effective adjunct for the relief of skeletal muscle spasm caused by upper motor neuron disorders.
Rapidly distributes to other body fat stores. Twenty minutes after initial IV infusion, serum concentration drops to 20% of CIndividualize dosage and increase cautiously to avoid adverse effects.

Adult

2-10 mg IM/IV q3-4h prn (not to exceed 30 mg/8 h)

Pediatric

0.04-0.2 mg/kg IV/IM q2-4h prn (not to exceed 0.6 mg/kg/8 h)

CNS toxicity increases when concurrently used with other CNS depressants

Documented hypersensitivity; acute narrow-angle glaucoma; untreated open-angle glaucoma; hypotension; severe respiratory depression

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Concurrent use of other CNS depressants, respiratory depression, elderly/debilitated patients, hepatic insufficiency, depressed patients


Midazolam (Versed)

Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access.

Adult

0.01-0.05 mg/kg (usually 0.5-4 mg, up to 10 mg) IV slowly over several min; may repeat q10-15min until adequate response achieved

Pediatric

<32 weeks: 0.5 mcg/kg/min IV infusion
>32 weeks: 1 mcg/kg/min IV infusion
Children: 0.05-0.2 mg/kg IV over 2-3 min, followed by 1-2 mcg/kg/min continuous infusion

Sedative effects may be antagonized by theophyllines; narcotics, cimetidine, ethanol, and erythromycin may accentuate sedative effects because of decreased clearance; reduce dose of thiopental by 15% when using together

Documented hypersensitivity; preexisting hypotension; narrow-angle glaucoma; sensitivity to propylene glycol (diluent)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, pulmonary disease, renal impairment, hepatic failure, neuromuscular disease, hypotension, and in elderly patients; monitor for respiratory depression with high or repeated doses; consider lower dosages in patients with organic brain syndrome and patients who may have inhibition of benzodiazepine metabolism and clearance (eg, using nicotine, taking cimetidine)

Immunizations

Tetanus immunization should be administered following a redback spider bite. A booster vaccination is recommended in previously immunized individuals.


Diphtheria-tetanus toxoid vaccine (Adacel, Boostrix, Decavac)

Manufactured by first culturing Clostridium tetani and then detoxifying the toxin with formaldehyde. This toxoid commonly is combined with diphtheria toxoid, and both serve to induce production of serum antibodies to toxins produced by the bacteria.
Used to induce active immunity against tetanus in selected patients. Immunizing agent of choice for most adults and children >7 y are tetanus and diphtheria toxoids. Necessary to administer booster doses to maintain tetanus immunity throughout life.
Pregnant patients should receive only tetanus toxoid, not a product containing diphtheria antigen.
In children and adults, may administer into deltoid or midlateral thigh muscles. In infants, preferred site of administration is the mid thigh laterally.

Adult

0.50 mL IM in extremity other than the one that bears the lesion

Pediatric

Administer as in adults

Chloramphenicol may impair the amnestic response to tetanus toxoid; patients receiving concurrent immunosuppressants may remain susceptible despite immunization; concurrent use of tetanus immunoglobulin may delay development of active immunity by several days

Documented hypersensitivity to vaccine's components; presence of febrile illness or acute infection; poliomyelitis outbreak

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Arthus-type hypersensitivity reaction or fever following a prior dose of vaccine, immunosuppression, latex sensitivity, thrombocytopenia, coagulation disorders

More on Spider Envenomation, Redback

Overview: Spider Envenomation, Redback
Differential Diagnoses & Workup: Spider Envenomation, Redback
Treatment & Medication: Spider Envenomation, Redback
Follow-up: Spider Envenomation, Redback
Multimedia: Spider Envenomation, Redback
References

References

  1. White J. CSL Antivenom Handbook. 2nd ed. 2001. Available at http://www.toxinology.com/generic_static_files/cslb_index.html.

  2. Nimorakiotakis B, Winkel KD. Spider bite--the redback spider and its relatives. Aust Fam Physician. Mar 2004;33(3):153-7. [Medline][Full Text].

  3. Graudins A. Widow spider envenomation: Lactrodectism. In: Dart RC, ed. Medical Toxicology. 3rd ed. Lippincott Williams & Wilkins; 2003:1592-1595/248. [Full Text].

  4. Nicholson GM, Graudins A. Spiders of medical importance in the Asia-Pacific: atracotoxin, latrotoxin and related spider neurotoxins. Clin Exp Pharmacol Physiol. Sep 2002;29(9):785-94. [Medline].

  5. Ushkaryov YA, Volynski KE, Ashton AC. The multiple actions of black widow spider toxins and their selective use in neurosecretion studies. Toxicon. Apr 2004;43(5):527-42. [Medline].

  6. Australian Museum. Available at http://australianmuseum.net.au/Redback-Spiders.

  7. Mollison L, Liew D, McDermott R, Hatch F. Red-back spider envenomation in the red centre of Australia. Med J Aust. Dec 5-19 1994;161(11-12):701, 704-5. [Medline].

  8. Isbister GK, Gray MR. Latrodectism: a prospective cohort study of bites by formally identified redback spiders. Med J Aust. Oct 20 2003;179(8):455; author 455-6. [Medline].

  9. Isbister GK, Brown SG, Miller M, Tankel A, Macdonald E, Stokes B, et al. A randomised controlled trial of intramuscular vs. intravenous antivenom for latrodectism--the RAVE study. QJM. Jul 2008;101(7):557-65. [Medline].

  10. Hahn IH, Lewin N. Chapter 115: Arthropods. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS, eds. Goldfrank's Toxicologic Emergencies. 8th ed. New York, NY: McGraw-Hill; 2006.

  11. Isbister GK. Failure of intramuscular antivenom in Red-back spider envenoming. Emerg Med (Fremantle). Dec 2002;14(4):436-9. [Medline].

  12. Isbister GK, Sibbritt D. Developing a decision tree algorithm for the diagnosis of suspected spider bites. Emerg Med Australas. Apr 2004;16(2):161-6. [Medline].

Further Reading

Keywords

spider bite, redback spider, spider envenomation, Jockey spider, latrodectism, latrotoxin, aLTX, neurotoxin, redback spider bite, spider bite treatment

Contributor Information and Disclosures

Author

Rebecca L Rubin, MD, Clinical Assistant Instructor and Resident Physician, Department of Emergency Medicine, State University of New York Downstate/Kings County Hospital Center
Rebecca L Rubin, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Emergency Medicine Residents Association
Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Robert L Norris, MD, Associate Professor, Department of Surgery; Chief, Division of Emergency Medicine, Stanford University Medical Center
Robert L Norris, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, California Medical Association, International Society of Toxinology, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Matthew M Rice, MD, JD, FACEP, Senior Vice President, Chief Medical Officer, Northwest Emergency Physicians; Assistant Clinical Professor of Medicine, University of Washington at Seattle
Matthew M Rice, MD, JD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Washington State Medical Association
Disclosure: Team Health  Salary Employment

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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