In most cases the cause of autopharmacological reactions is the direct toxin-induced release of biogenic amines. Immediate hypersensitivity reactions (type I) appear to be rare.

Tourniquets can cause local swelling and thus mimic local venom effects.

In Australia and the Pacific Islands, local signs of envenoming, such as local pain and local swelling, are not suitable criteria to establish that an injection of venom has occurred, possibly with systemic effects.

In contrast, painfully enlarged lymph nodes are a common, early sign of the development of systemic effects with Australian elapid bites.

As a rule, Australian elapids cause only negligible local effects such as local pain and local swelling; with Pseudonaja sp. such effects are generally absent. Pseudechis sp. are an exception to this rule, in particular Pseudechis australis. There may be swelling of the affected extremity that can even extend to the trunk.

Even coagulation disorders that are severe according to laboratory tests may only be clinically apparent to a slight degree, or not at all. There is a threat of spontaneous haemorrhage with extensive loss of blood or focal bleeding (e.g. intracranial) as long as the haemostatic defect exists. The risk is even greater if a patient does not receive appropriate treatment at a hospital and is then exposed to trauma, even very minor trauma, for example while working.

Loss of large volumes of blood can occur due to blood oozing from the bite wound or from injuries or due to medical or paramedical intervention.
If antivenom is effective, spontaneous systemic bleeding should cease within 15–30 min, and blood coagulability should be restored within 1–6 h. The clotting time test is a simple means to regulate the antivenom dose. The initial dose should be repeated if the blood is still not coagulable 6 h after the first dose (Warrell 1990b). White (1991) suggests repeating antivenom administration as soon as 1–2 h after the first dose.

If antivenom treatment is not successful, it is necessary to consider the possibility of misidentification of the snake that caused the bite, especially if monospecific antivenoms were used.

The haemostatic defects caused by Australian elapids are primarily a consequence of prothrombin activation, which leads to defibrin(ogen)ation with reactive fibrinolysis. Thrombocytopaenia occurs with variable frequency and severity.

Classification (White 1987b)

Haemostatic defects frequent and severe: Notechis sp., Oxyuranus sp., Pseudonaja sp.
Haemostatic defects frequent but mostly mild: Pseudechis australis.
Clinically relevant haemostatic defect unlikely: Pseudechis porphyriacus.

Once paralysis caused by presynaptically active venom components becomes established, it responds only slightly or not at all to antivenom administration. The venoms of Pseudonaja sp., Notechis sp., Oxyuranus sp. and Tropidechis carinatus contain such venom components. Such paralysis does resolve spontaneously, but very slowly, such that long-term artificial respiration may be necessary. Early administration of antivenom is crucial. Paralysis caused by Australian elapids whose venom has purely postsynaptic effects can be easily reversed with antivenom (Acanthophis sp.). The efficacy of acetylcholinesterase inhibitors has not been established for such cases (Currie et al. 1988, 1990, Hudson 1988).

The edrophonium (Tensilon®) test should be performed immediately in every patient with signs of paralysis, in order, if the result is positive, to make the most of the improvement in neuromuscular transmission that can be achieved through use of a longer-acting acetylcholinesterase inhibitor (neostigmine). In some cases this may avoid the need for artificial respiration.

Endotracheal intubation and artificial respiration:

Endotracheal intubation is certain to prevent any form of aspiration. Manual or mechanical ventilation, even though it may have to be employed over a long period of time, can ensure survival of a patient with neurotoxin-induced respiratory failure.

Classification (White 1987b):

Signs of paralysis frequent and severe: Acanthophis sp., Notechis sp., Oxyuranus sp.; probably also Tropidechis carinatus.

Signs of paralysis infrequent: Pseudonaja sp.

Classification (White 1987b):

Rhabdomyolysis frequent: Notechis sp., Oxyuranus sp., Tropidechis carinatus ?
Rhabdomyolysis frequent and sometimes severe: Pseudechis australis.
Rhabdomyolysis frequent but mostly mild: Pseudechis porphyriacus.

No specific cardiotoxins have been isolated from Australian elapid venoms to date.

Cardiac dysrhythmias and cardiac insufficiency or failure thus appear to be secondary effects (e.g. in the context of hyperkalaemia or shock).

Acute renal failure occurs as a secondary effect in the context of various forms of shock, DIC or rhabdomyolysis. However, several Australian elapids do also appear to possess venom components that cause direct renal damage.

Reports of acute renal failure following Pseudonaja textilis bites suggest primary renal damage caused by the venom (Acott 1988).

The snake that caused the bite is generally not available for identification. In Australia there are 3 aids for indirect identification:

• ELISA test kits, which enable identification at the family level within their sensitivity and specificity limits.
  Since 1981 a capillary ELISA has been available from the Commonwealth Serum Laboratories (CSL) (Chandler and Hurrell 1982, Hurrell and Chandler 1982). However, this sometimes produced false-positive results (Jelinek et al. 1991). An improved ELISA test kit has been available since 1991 (Cox et al. 1992, Sutherland 1992).
• Geographical distribution patterns, which in some cases allow certain species to be excluded.
• Clinical patterns of envenoming, which make it possible to narrow down the cause. 

According to evaluation of the studies and case reports available in the literature, certain effects of envenoming appear to have a strong positive or negative predictive value for identifying the snake that possibly caused the bite at the family level. A prospective study that was carried out in northern Australia supports this theory (Currie et al. 1992b).

It is worth trying to identify the snake that caused the bite at the family level, in order to be able to treat the patient with a monospecific antivenom, as these are available for all the medically important species of snakes in Australia. In comparison to polyspecific antivenoms, smaller doses are sufficient to neutralise the venom. The risk of immediate and delayed reactions (serum sickness) to the antivenom can thus be reduced.

Clinical patterns of envenoming:

Signs of paralysis of the cranial nerves, extremities and respiratory musculature and no haemostatic defects or rhabdomyolysis: Acanthophis sp.

Severe haemostatic defect with spontaneous bleeding, (signs of paralysis) and no rhabdomyolysis: Pseudonaja sp.

Severe rhabdomyolysis with consequent signs of paralysis and only a minor haemostatic defect: Pseudechis australis.

Marked paralysis and a severe haemostatic defect as well as rhabdomyolysis: Notechis sp., Oxyuranus sp.

If the selected antivenom is not effective, 3 possible causes need to be considered:

1. correct identification of the cause, but insufficient dose administered;
2. correct identification of the cause, but inadequate efficacy of the antivenom;
3. incorrect identification of the cause → revision of identification.

Even if the desired effect of antivenom administration, namely normalisation of the parameters relevant to envenoming (findings on physical examinations, physical and laboratory investigations), is achieved quickly, this does not mean that the symptoms of envenoming may not re-occur due to continued absorption of venom from a depot in the region of the bite. The parameters relevant to envenoming should be re-investigated (findings on physical examinations, physical and laboratory investigations) at intervals that correspond to the severity of the envenoming. If respiratory insufficiency is to be expected, the patient should be monitored continuously, especially considering the fact that antivenom does not reverse already established symptoms of envenoming caused by postsynaptically active venom components.

Haemostasis should be monitored every 1 to 2 h during antivenom treatment. If there is no tendency for improvement, a further dose of antivenom should be administered (White 1991).

Patients should be kept in hospital after initial success of antivenom treatment, in order to conclusively exclude a recurrence of the symptoms of envenoming. Haemostasis should continue to be monitored every 6 h.

• Excision of necrotic material,
• surgical debridement under general or regional anaesthesia, 
• skin grafting (split-thickness).

For optimal and uninterrupted regeneration of rhabdomyolysis-damaged musculature, a gradual increase in exercise load during the convalescence phase is important.

See Antivenom treatment.