Urgent administration of antivenom following proven krait bites in Southeast Asia irrespective of neurotoxic symptoms

Neuromuscular paralysis because of snakebite envenoming is a life-threatening and common clinical syndrome caused by most elapids (family Elapidae) and few species of pit vipers and true vipers (family Viperidae) [1].In Southeast Asia, cobras and kraits are responsible for most cases of neurotoxic envenoming.Two major neurotoxin classes, alpha-neurotoxins (α-NTs) and beta-neurotoxins (β-NTs), target the neuromuscular junction and cause flaccid muscle paralysis [2].Beta-neurotoxins belong to the group I phospholipases A 2 and act at the presynaptic motor nerve terminal.They are the major neurotoxins in krait venom and cause synaptic vesicle depletion with declining acetylcholine release and degeneration of the nerve terminal [3].Phospholipases A 2 have a molecular mass of 13 to 16 kDa which corresponds to 115 to 125 amino acids [2].After subcutaneous injection of venom during the bite, toxins are resorbed from the interstitial space into the blood circulation either directly or through lymphatic vessels and leave the blood circulation to reach and act at the neuromuscular junction [4,5].The small molecular size of neurotoxins facilitates the journey and most victims develop neurotoxic signs within 6 h after the bite [6].Once neurotoxic signs are present and nerve terminals damaged, administration of antivenom will likely be ineffective.Here, we propose the administration of antivenom to all patients with a confirmed krait bite who present within the first 6 h after the bite, regardless of neurotoxic signs, and present arguments for this approach. Frequency of neurotoxic signs and duration of muscle paralysis after krait envenomingFlaccid muscle paralysis of varying degrees is the major clinical symptom caused by β-NTs in krait venom.This becomes life-threatening when respiratory muscles are affected and immediate intubation and mechanical ventilation are necessary to save the victim's life.Krait bite envenoming often leads to prolonged failure of neuromuscular transmission caused by morphological damage to motor neuron endings.Animal studies in rats found full recovery of muscle strength 7 days after β-bungarotoxins were injected into the musculus soleus, without the use of antivenom [3].In a retrospective case series of patients bitten by Bungarus species in Thailand, including 68 bites of Bungarus candidus, 9 of Bungarus fasciatus, and 1 of Bungarus flaviceps, 88.6% of the patients showed neurotoxic signs within the first 8 h after the bite and 76% required mechanical ventilation (Table 1).The median time between bite and antivenom administration was 5 h and the median time on the ventilator was 6 days [6].