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Acanthophis sp.

Case reports

Papua New Guinea

Lalloo et al. 1996: 32 Acanthophis sp. bites.Identiication: immunological 32/32, morphological 1/32. 18/32 had signs of envenoming.

Campbell 1966: 15 "A. antarcticus" bites (according to present criteria not clearly identifiable taxonomically: A. antarcticus, A. praelongus, A. laevis or A. rugosus? → Acanthophis sp.); identification: morphological 8/15; by the patient or his employer 5/15; according to the patient's description and clinical criteria 2/15.

Currie et al. 1988: 1 Acanthophis sp. bite; identification: snake killed by villagers.

Curriet et al. 1990: 2 Acanthophis sp. bites; identification: recognition from photographs 1/1, clinical picture.

Hudson 1988: 1 A. antarcticus bite (according to present criteria not clearly identifiable taxonomically: A. antarcticus, A. praelongus, A. laevis or A. rugosus? → Acanthophis sp.); identification: morphological.

White 1987a, 1992: 12 Acanthophis sp. bites; identification: all victims were snake owners.

Signs & symptoms

Autopharmacological effects

Vomiting 5/18 (Lalloo et al. 1996).

Local effects

Swelling at bite site 0/18, lymph node pain 12/18, tender enlarged lymph nodes 11/18 (Lalloo et al. 1996).

Local pain 5/15, minor local oedema 4/15. Painful enlargement of regional lymph nodes 9/15 (however, this sign not present in one of the patients with the most severe envenoming) (Campbell 1966).

Local pain and minor local swelling in several patients (White 1987a, 1992).

Haematotoxic effects

0/18 incoagulable blood (Lalloo et al. 1996).

Neurological effects

Ptosis 17/18, ophthalmoplegia 10/18, diminished hand grip 5/18, equired intubation 5/18, required ventilation 5/18,  (Lalloo et al. 1996).

Ptosis 3/15, severe generalised paralysis including paralysis of the respiratory musculature and respiratory insufficiency 1/14 and respiratory failure 1/15 (Campbell 1966, Currie et al. 1988, 1990, Hudson 1988).

Ptosis and incomplete ophthalmoplegia 1/12 (White 1987a, 1992).

Case fatality rate/Mortality

In untreated cases 15% (Campbell 1966).



As long as the neurotoxic effects of the venom can be treated adequately, there should be no long-term damage.

Laboratory and physical investigations

1. Haemostasis

No haemostatic defects: 6 patients investigated had normal haemostatic parameters (Campbell 1966).

2. Leucocytes
Leucocytosis (10,000/mm3) in 3/6 patients investigated (Campbell 1966).

The serum of a patient in Papua New Guinea bitten by Acanthophis antarcticus gave positive results for Acanthophis and Notechis scutatus (Notechis scutatus does not occur in Papua New Guinea!) with the  'CSL Venom detection kit' (Currie et al. 1988).

First aid

The compression-immobilisation method is recommended. This type of bandage was removed in one patient, and 3 hours later, i.e. 24 hours after the bite, systemic signs of envenoming appeared (vomiting, ptosis, dysphagia, dysphonia, dyspnoea) (Currie et al. 1988). This shows how important it is to leave a compression-immobilisation bandage in place until all necessary preparations for treatment have been made.

Treatment (symptomatic)

  1. Endotracheal intubation and artificial respiration (Campbell 1966).
  2. Edrophonium (Tensilon®) and long-acting anticholinesterase agents (e.g. neostigmine methylsulphate):
    Following atropine sulphate (0.6 mg) i.v. and neostigmine methylsulphate (2.5 mg) i.v., reversal of the ptosis, dysphagia, dysarthria and dyspnoea within 5 min (Currie et al. 1988).

In one patient with complete bilateral ptosis, dysphagia and signs of paralysis of the extremities and respiratory musculature, all symptoms (with the exception of the bilateral ptosis) abated 2 h after the administration of 2 vials of Death adder antivenom, CSL. Symptoms improved quickly and obviously after 0.6 mg of atropine sulphate and 10 mg of edrophonium chloride, according to objective evaluation criteria (percentage of iris not covered by the upper lid, retraction of the upper lid measured in seconds) (Hudson 1988).

One patient with severe envenoming improved temporarily with atropine/neostigmine, but then had to be intubated and required artificial respiration. Lasting reversal of the signs of envenoming only occurred once a sufficient dose of antivenom had been administered. In contrast, a woman with mild envenoming (mild ptosis and dysarthria) experienced adequate improvement of her symptoms with neostigmine/atropine and did not require antivenom. It can thus be concluded that although neostigmine represents a useful adjuvant treatment in cases of severe envenoming, it is most probably not sufficient on its own to halt the progression of neurological symptoms. In cases of mild envenoming, in contrast, neostigmine treatment may suffice (Currie et al. 1990). 

Treatment (specific)

Death adder antivenom, CSL, Parkville, Australia.

Polyvalent (Australia-New Guinea), CSL, Parkville, Australia.

No controlled clinical studies are available. Details of efficacy of antivenom: Campbell 1966, Currie et al. 1990, Hudson 1988.
Indications for antivenom
Progressive neurotoxic symptoms of envenoming.
Very rapid and complete reversal of neurological symptoms, even when the antivenom was administered a number of hours after the bite (Campbell 1966, Currie et al. 1990, Hudson 1988, Lalloo et al. 1996).



The optimum management of bites by this species may include prompt treatment with both antivenom and anticholinesterase in addition to effective first aid (Lalloo et al. 1996).