ACMT Toxicology Visual Pearl – The Fang and the Furious

3. Descending paralysis

Background

The pictured snake is from the genus Acanthophis, commonly known as the death adder, and a member of the Elapidae family of snakes. Common species include Acanthophis antarcticus (“Common Death Adder”), Acanthophis pyrrhus (“Desert Death Adder”), Acanthophis praelongis (“Northern Death Adder”), and several others. [1-3]  They are native to parts of Australia, Papua New Guinea, and other nearby islands. [4-6]  Death adders, like other elapids, possess short, thick hollow fangs by which they deliver the complex mixture of toxins that comprises their venom, which is neurotoxic and causes descending paralysis.[1]  Despite the name “adder,” they are from a different family than other adders, such as the puff adder.

What are the components of Death Adder venom? [3-5]

Death Adder venom is a complex mixture of toxins that have several neurotoxic effects, both at presynaptic and postsynaptic neurons.

• Three-finger toxins (3FTxs) [3, 5]
  • Long-chain alpha-neurotoxins which make up ~60% of the venom.
  • Act as post-synaptic competitive antagonists at nicotinic acetylcholine receptors
  • Leads to reversible neuromuscular blockade, which responds well to early antivenom administration [4]
• Phospholipase A2 (PLA2) neurotoxins [3, 5]
  • The second most abundant component of the venom, comprising up to ~22%
  • Impairs neurotransmitter release by irreversible presynaptic binding of motor nerve terminals, leading to neurotoxicity that is poorly responsive to antivenom [4]

What are the clinical effects of envenomation by Death Adder?

• The toxidrome is predominantly systemic neurotoxicity that presents as a rapidly progressive descending flaccid paralysis. [4]
• Symptoms: diplopia, ptosis, and bulbar weakness, which can progress to upper extremity and intercostal muscle weakness, and, in severe cases, respiratory failure necessitating mechanical ventilation. [4, 7-9]
• Less commonly, myotoxicity and coagulopathy have been reported [10, 11]

What is the management of envenomation by Death Adder?

• Specific Death Adder antivenom is the key to management, and its efficacy is time-dependent. For further information on how to obtain exotic antivenom if applicable, please see:  ACMT Toxicology Visual Pearl: Hiss-teria Averted
• Established neurotoxicity may not be reversed, especially when symptoms are caused by irreversible presynaptic toxin binding. [9]
• Dosing is by vial rather than weight-based, and one vial of death adder antivenom is generally sufficient to bind all circulating venom in all patients, including the pediatric population. [2, 4, 6, 12]
• Respiratory depression may require supplemental oxygenation and mechanical ventilation, with prolonged ventilatory support reported. [4]
• Cholinesterase inhibitors (e.g., neostigmine) can be considered in severe neurotoxicity or if antivenom is not available. [13, 14]

Bedside Pearls

• Acanthopis genus (Death Adder) envenomation is primarily characterized by systemic neurotoxicity presenting as a rapidly progressive descending flaccid paralysis.
• Rapid administration of specific antivenom is the key to successful management.
• In cases of severe neurotoxicity, or when antivenom is unavailable or delayed, cholinesterase inhibitors can be effective in limiting the development and progression of neurotoxic symptoms