With one exception, systemic signs of envenoming following cnidarian stings occur more or less immediately after the sting. Carukia barnesi causes the so-called "Irukandji syndrome", which manifests itself after a delay of a number of hours after an initially harmless local reaction.

Independent of the aetiology, common to all serious cnidarian stings is the possibility that a critical, life-threatening situation may arise within a very short time following the sting. As such there are limits to the formal medical care of such accidents. One strategy to solve this problem is to train paramedics in the initial treatment of cnidarian stings. In principle any cnidarian sting can lead to severe anaphylactic reactions if the patient is already sensitised (Togias et al. 1985). It can be difficult or even impossible to distinguish between anaphylactic shock and toxin-related cardiopulmonary failure (Chironex fleckeri, Pysalia sp.). According to observations to date, however, the severe cases of envenoming with Chironex fleckeri stings appear to have all been toxin-related.

In cases of toxin-related envenoming with respiratory and cardiovascular disturbances, it is important to determine the causative species insofar as different types of envenoming have now been classified, in which relatively well-proven treatment schemes can be applied:

• Chironex fleckeri stings (see below),
• Physalia sp. stings (see below),
• Carukia barnesi stings (see below).

Cnidarian venoms are (thermo-)labile. At body temperature they lose their activity. Thus even if specific treatment, e.g. antivenom, fails, the patient may still be rescued with sustained resuscitation efforts.

With regard to aetiology, these are primarily IgE-mediated anaphylactic reactions (type I hypersensitivity), i.e. the patient must have already been sensitised.

Skin lesions that appear immediately following the sting are toxin-induced, in contrast to delayed or recurrent lesions (see below) (Burnett and Calton 1987, Fisher 1987, Kingston and Southcott 1960, Letot et al. 1990, Strutton and Lumley 1988).

To date there have only been a few cases of regional vascular insufficiency described (Abu-Nema et al. 1988, Adiga 1984, Drury et al. 1980, Williamson et al. 1988). Neither the pathogenic mechanism nor the optimal treatment have been clarified.

Possible pathogenic mechanisms include direct vascular effects, direct neurogenic effects, stimulation of the sympathetic reflex arc or a combination of these mechanisms (Williamson et al. 1988).

To date only a few such isolated cases have been described (Filling-Katz 1984, Laing and Harrison 1991, Peel and Kandler 1990). In all cases there was complete recovery, although this did take as long as up to 10 months (Peel and Kandler 1990).

Most stings affecting the eyes described to date were painful injuries with conjunctival congestion, chemosis, corneal oedema and mild iridocyclitis that resolved on their own or with local treatment within 48 h. However, there have also been reports of iritis, chronic unilateral glaucoma, mydriasis, accommodation disturbances, peripheral anterior synechia, iris depigmentation and blurred vision (Glasser et al. 1992, 1993, Mitchell 1962, Rapoza et al. 1986, Wong and Matoba 1985).

Cnidarian venoms are (thermo-)labile. It is assumed that they lose their activity within 15–20 min after absorption into the tissue or the blood circulation. Thus even if pharmacological /antivenom treatment fail, treatment success may still be possible if there are optimal resuscitation conditions. The patient's condition may deteriorate again after a temporary improvement of the circulatory condition due to renewed mobilisation of venom from the periphery (Williamson et al. 1984b).

In order to be effective, narcotic analgesics must be given at a dose that is only possible if the conditions required for the treatment of respiratory depression are present (Beadnell et al. 1992).

See the Comments above on "Chironex fleckeri/Chiropsalmus quadrigatus stings". There is no antivenom available for Physalia sp.

Symptoms of envenoming that are reminiscent of a mild form of "Irukandji syndrome" have been observed following "Morbakka" (Tamoya virulenta), Tamoya sp. and Gonionemus oshoro stings (Fenner 1991, Otsuru et al. 1974). Stomolophus sp. stings are also said to cause an "Irukandji-like" syndrome (Mingliang and Shide 1990) and possibly other species.

The evdence base for treating  "Irukandji syndrome" is anecdotal. It was developed in Australia and employed for the treatment of a number of patients (Bailey et al 2003, Fenner and Hadok 2002, Fenner et al. 1986a, 1986b, 1988, Martin and Audley 1990).

Wound care.

As with keloids from other causes this is not a rewarding condition to treat.

Topical hydroquinone 1.8% (Burnett and Calton 1987a, Kokelj and Burnett 1990).

No proven treatment available.

There are numerous case reports and some studies on delayed and recurrent skin symptoms following jellyfish stings (Auerbach and Hays 1987, Burnett and Calton 1985, Burnett et al. 1987a, Letot et al. 1990, Mansson et al. 1985, Matusow 1980, Ohtaki et al. 1986, 1990, O'Reilly et al 2001, Piérard et al. 1990, Reed et al. 1984).

Recurrent skin symptoms following jellyfish stings can present a differential diagnostic problem, in particular if they appear after a long delay and if the patient does not remember the sting or the doctor failed to enquire about it.

With regard to aetiology, it is assumed that this is a type IV hypersensitivity reaction. Two different histological forms have been observed:

• contact dermatitis-like skin reactions (Ohtaki et al. 1990),
• skin reactions of a granulomatous nature (Reed et al. 1984).

Auerbach and Hays (1987) observed erythema nodosum with arthralgia and fever following a Physalia physalis sting.

Immunological investigations suggest that it is possible for sensitisation to cnidarians to occur (Burnett and Calton 1987). A case study suggests the same (Togias et al. 1985). On the basis of these observations it is assumed that in patients who develop marked allergic reactions, e.g. angio-oedema, following a cnidarian sting there is a risk of a severe anaphylactic reaction following a further sting. There is cross-reactivity between different cnidarian species (Russo et al. 1983).

This risk can be assessed by detection of specific IgE antibodies and skin tests.