The European adder, Vipera berus is the only venomous snake native to the UK. It is also found across northern Europe, into the Arctic Circle, and Asia. It is most commonly found on dry, sandy heaths, sand dunes, rocky hillsides, moorlands and woodland edges. In the UK the snake is a protected species and it is illegal to intentionally kill or injure an adder; it is also illegal to sell or transport adders for sale (Wildlife and Countryside Act, 1981).
The European adder grows to about 50–60 cm in length and can vary in colour from pale grey to dark brown in the male and from olive green/yellowish-brown to reddish-brown in the female. It is distinguishable from the two other snakes native to Britain, the grass snake (Natrix natrix) and the rarer smooth snake (Coronella austriaca), by a black-brown dorsal zig-zag patterning and a V-shaped marking on the head (Figure 1). Note, however, that in darker coloured male snakes this patterning may not be obvious. Another distinguishing feature is the eye of the adder that is elliptical with a typical vertical slit as compared with the round shaped eyes of the grass and smooth snakes (Figure 2).
Two adders in their natural habitat showing the characteristic zigzag pattern along their back.
The adder hibernates over winter and emerges in the spring as ambient temperatures rise. From about mid-April the males seek the females for mating. The other reptiles in that it does not lay eggs, but gives birth to live young from late August to early September. These young snakes resemble small versions of the adult snake and are only about the size of an earthworm.
The venom
The adder uses its venom to immobilize its prey including lizards, amphibians, small birds and mammals, waits until they die and then swallows them whole. The venom is a cytotoxic complex mixture of high molecular weight proteins, mainly proteases, peptide hydrolases, hyaluronidase and phospholipases (Siigur et al, 1979; Calderón et al, 1993; Samel et al, 2006). In bite victims hypovolaemia and local oedema result from an increase in vascular permeability. This is due initially to the release of pharmacologically active substances such as histamine, serotonin, bradykinin and prostaglandins, and later due to direct action of venom on heart and blood vessels. In serious cases fluid loss from the capillary bed combined with vasodilatation can cause hypovolaemia and shock. The cardiac effects that occur in some animals bitten by an adder may be due to impaired circulation and poor perfusion of the myocardium, due to coronary spasm and hypovolaemia (Pelander et al, 2010). Renal impairment may be due to hypovolaemic shock.
The bite
The adder is not an aggressive snake and generally only bites when provoked. Bites rarely occur during the winter when the snake is in hibernation but are frequent during the summer months. Almost 70% of adder bites occur from April to July ( Sutton et al, 2011). Dogs are frequently bitten on a limb or on the face, after stepping on or near a snake or sniffing around in undergrowth. Adder envenomation causes significant morbidity but low mortality in dogs. Not all bites result in envenomation as a snake can inflict a dry bite, that is, without injecting any venom into the victim. Death after adder bite is relatively rare and reported mortality in dogs with bites of Vipera berus or V. xanthina palaestinae (a Middle Eastern relative of the European adder) is 3 to 4% (Aroch and Harrus, 1999; Segev et al, 2004; Lervik et al, 2010).
Clinical effects
Local effects
All symptomatic dogs develop local effects (Table 1). This typically manifests as localized painful swelling often occurring within minutes of the bite and in most cases is present within 2 hours. Puncture wounds may be visible at the bite site but local swelling may make it difficult to locate them. The swelling gradually spreads and may become haemorrhagic.
| Local effects |
| Pain, progressive swelling and sometimes local bleeding |
| Systemic effects |
| Mental status changes, shock, coagulopathy, renal, hepatic and cardiac effects |
If the bite is to the snout or head the swelling may affect the dog's ability to eat, drink and thermoregulate. Without antivenom swelling will persist at 24 hours and may increase, lasting several days (Lervik as a result of muscle damage but there is no correlation between the degree of swelling and the CK value (Lervik et al, 2010). Necrosis at the bite site can occur but is rare.
Systemic effects
In addition to local effects systemic effects also occur. These include shock, collapse and hypotension that develop soon after the bite (VPIS case data). Other typical signs include mental status changes varying from lethargy and depression to coma; also, pain, tachycardia, hyperthermia, bruising, pale mucous membranes, hypersalivation, vomiting, panting, tachypnoea and lameness. Respiratory distress, coagulopathy, renal, hepatic and cardiac effects can also occur.
Cardiac effects
Some dogs develop cardiac effects after an adder bite. In two Swedish studies of canine adder bite the incidence of cardiac affects was 11% of 53 dogs (Lervik et al, 2010) and 54% of 24 dogs (Pelander et al, 2010). In this latter study the cardiac troponin concentrations were also measured and it was observed that myocardial damage, as evidenced by raised cardiac troponin concentrations, can occur with or without electrocardiogram (ECG) abnormalities in dogs with adder envenomation (Pelander et al, 2010).
Cardiac effects in dogs with an adder bite include cardiac murmur, atrial premature complexes, idioventricular rhythm, tachycardia or bradycardia, ST segment elevation and premature ventricular complexes. The timing of cardiac effects is very variable. Increase in cardiac troponin concentrations reportedly occurred within 2 hours of a bite in some dogs and within 12 hours in others (Pelander et al, 2010). In another study initial cardiac auscultation was normal in all dogs but 11% had cardiac abnormalities at 24 hours (Lervik et al, 2010).
Renal effects
Renal impairment is not common in dogs after adder bite. In the Swedish study of 53 cases of adder bite none of the dogs developed renal impairment. However, most dogs received intravenous fluids and this may have protected against renal toxicity (Lervik et al, 2010). Renal effects include raised urea and creatinine, hypoproteinaemia and hypoalbuminaemia.
Hepatic effects
Mild or (more rarely) moderate increases in liver enzymes may occur after adder bite. Raised liver enzymes were reported in 65% of 53 cases in the Swedish study (Lervik et al, 2010).
Haematological effects
Coagulopathy is occasionally reported after adder bite with anaemia, thrombocytopenia, leucocytosis, disseminated intravascular coagulation and haematuria.
Prognosis
Death from adder bite is rare in dogs (3–4% of cases) and is usually associated with severe renal impairment (Hume, 2000; Sim, 2000). It can occur after 5–7 days in dogs that receive no treatment (Bratberg and Flesja, 1973). In a recent review of 53 canine cases of adder bite in Sweden, there were no fatal cases (Lervik et al, 2010).
Management of adder bites in dogs
After a bite by an adder the bite site should be left alone; the use of incisions, suction and tourniquets are not recommended as they may introduce infection, aggravate bleeding and restrict circulation.
Any dog with clinical effects should be hospitalized for at least 12 hours. Critical interventions are intravenous fluids and antivenom administration. Intravenous fluids should be given in all cases to ensure adequate hydration. The pulse, blood pressure, respiration and body temperature should be monitored, as should renal and hepatic function in severe cases. If possible the ECG should be checked on admission and at 12 hours and 24 hours after the bite. If there is any evidence of bleeding a coagulation profile should be checked.
Antivenom administration
Administration of specific adder antivenom is the optimum treatment and is expected to reduce morbidity with rapid improvement of swelling and reduce hospitalization time (see Table 2 for indications and dosage). The most commonly used product is European viper antiserum sourced from Croatia (Institute of Immunology, Zagreb), which is approved for veterinary use in the UK by the Veterinary Medicines Directorate (VMD). Also VMD approved is a product from Poland (Biomed) although published data on its use in animals appear scant. Both are relatively inexpensive (Table 3).
| Indications for the administration of antivenom: |
| All dogs with a bite to the facial region, as severe swelling may impair thermoregulation |
| All dogs where the swelling is significant or has spread beyond the next major joint proximal to the bite |
| Any dog with hypotension unresponsive to intravenous (IV) fluid therapy |
| Any dog with evidence of coagulopathy |
| Any dog with any electrocardiogram abnormality |
| When to use: |
| If indicated, as soon as possible after the bite |
| In dogs with only local effects, it can be given up to 24 hours after the bite |
| In dogs with systemic effects it can be given as long as the signs are present |
| Dosage: |
| European adder antivenom (Croatia): a 10 ml ampoule diluted in 2–3 volumes of isotonic (0.9%) saline administered by slow IV injection at a rate not exceeding 2 ml per minute or by IV infusion over 30 minutes. Note the package insert recommends an intramuscular route but IV administration is likely to be more effective |
| There is no authorized product in the UK to treat adder bites in animals, and the human product has to be imported. For more information see the Veterinary Medicines Directorate (VMD) website http://www.vmd.gov.uk |
| Two products are available: the European viper antiserum sourced from Poland (Biomed) and the much more commonly used antivenom from Croatia (Institute of Immunology, Zagreb). Published data on the use of the Polish antivenom in animals are limited. |
| In an emergency the antivenom (from Croatia) is available through the Veterinary Poisons Information Service (VPIS) and Vets Now ToxBox service. Contact the VPIS on 020 7188 0200 to find the location of your nearest ToxBox. (Note the ToxBox also contains other drugs/products that may be required in the treatment of emergency poisoning: activated charcoal, apomorphine, Intralipid®, Parvolex® (acetylcysteine), plasma (fresh/frozen), methocarbamol, vitamin K1 tablets). |
Antivenom needs to be given as soon as possible after a bite for maximum efficacy. The author recommends that practices in adder rich areas hold antivenom. In dogs with only local envenoming (swelling) there is no value in giving antivenom more than 24 hours after the bite. Where there are signs of systemic envenoming (e.g. shock, bleeding, cardiac effects, generalized oedema, etc) it can be used later, even days after the bite (D Warrell, personal communication, 2011).
The dose of antivenom is the same irrespective of the size of the victim as the dose is designed to counteract the venom of one bite. Excessive use of antivenom may result in the development of severe adverse reactions. Clinical improvement should be seen rapidly after administration, but if systemic signs persist a second dose can be given after 1–2 hours.
Adverse reactions to antivenom are very uncommon and are of two types:
Other treatments
Analgesia should be given as required, but opioid analgesics are preferred over non-steroidal anti-inflamatory drugs because of the risk of renal impairment after adder envenomation.
Although frequently used, there is no role for steroids in the treatment of adder bites in dogs (except in rare cases of adverse reactions to antivenom as described above) (D Warrell, personal communication, 2011). Steroids have not been proven to have any benefit in dogs with adder bites. In a study in dogs bitten by V. xanthina palaestinae steroid use was associated with increased mortality (Segev et al, 2004). In a review of 53 dogs bitten by V. berus in Sweden, treatment with steroids had no clear positive or negative effects. There was a slight trend towards more swelling in dogs given steroids (but that may have been because treating veterinarians gave steroids to dogs with severe swelling) (Lervik et al, 2010). The initial swelling observed after adder bite is due to the cytotoxic effect of the venom rather than an inflammatory response. Steroid use may increase the risk of infection and slow and diminish the response to antivenom and so must not be given where antivenom is used.
There are no studies evaluating the effect of antihistamines (e.g. chlorphenamine) on the outcome of adder bite in dogs. They have been used in many cases and are theoretically of benefit as the venom causes a release of endogenous histamine. Antihistamines also have a sedating effect that may be beneficial.
The routine use of an antibiotic in dogs with adder envenomation is not required as infection is not common. In a review of 53 cases of canine adder bite, 19% of dogs received antibiotics but none developed signs of infection (Lervik et al, 2010). A prophylactic broad-spectrum antibiotic should be considered in any dog with widespread necrosis.
In dogs with severe anaemia, coagulopathy or bleeding packed red cells or blood transfusions may be required. There are no studies on the treatment of arrhythmias in dogs after adder bite. The most specific treatment is antivenom administration. If this is not available the arrhythmia should be treated conventionally with an anti-arrhythmic drug and/or inotropic drugs as required.
Conclusions
Adder bites in dogs are common in the summer and although they can cause significant morbidity death is rare. Antivenom is the most specific treatment and is expected to reduce morbidity with rapid improvement of swelling and reduce hospitalization time. Veterinary practices in adder-rich areas should keep stocks or have mechanisms to locate antivenom speedily. Analgesia, antihistamines and intravenous fluids are also commonly used.