Clinical Management

The clinical management section is based on analysis of envenoming caused by V. aspis and V. berus and to a small extent by V. ammodytes (see Clinical entries: European vipers.

Documented cases of envenoming due to V. latasti, V. kaznakovi, V. lebetina, V. seonaei and V. ursini are rare or not available. See clinical management: Terrestrial snakes: North Africa, Near and Middle East and biomedical database entries.

The signs and symptoms of envenoming caused by V. ammodytes, V. aspis, V. berus, V. latasti and V. ursini are described as being similar with the exception of V. berus, V. ammodytes and in particular V. aspis in which neurotoxic effects are observed in certain geograpgical areas (Warrell 2010).

Envenoming due to colubrids and the pitviper Gloydius halys in Europe is similarly poorly documented or not at all.

Caution: do not attempt to capture snakes if you are not trained to do so!

Consult

• Which snake species are present in the country where the snake bite took place?

• How does the clinical picture of snakebite envenoming develop? Comparative observations of the various species responsible in the region.

Detailed biological and clinical information on the main culprits in the region

• Vipera sp., European vipers

Comment

Unfortunatelly, tight (arterial) tourniquets are still being applied. They must not be recommended for general use. 

If a pressure bandage / pad but, also, tight (arterial) tourniquets (see comment above) on the affected extremity has been applied,

• they should not be removed until systemic envenoming has been excluded (Ireland et al. 2010, Isbister and Berling 2025)
  or
• after completion of antivenom administration in patients with systemic envenoming (Isbister etal. 2025),
• with gradual removal of a tourniquet to avoid sudden venom influx and respiratory arrest (Pelle et al. 2022).

• Adverse outcomes have been observed in patients with tight pressure bandages left in place for many hours (Little 2023).
• All patients must be observed after removal of the bandage.

Inquire

• time of the bite,
• local pain,
• nausea, vomiting, abdominal pain.

Assess

• state of consciousness.

Measure

• blood pressure/pulse,
• respiratory rate,
• oxygen saturation (pulse oximeter),
• 20WBCT (bedside test), in settings where resources are immediatelly accessible, go directly to 'Laboratory and physical investigations' below,

Observe/investigate

• bite marks,
• extent and intensity of local swelling,
• enlargement and painfulness of regional lymph nodes,
• swelling in the facial region, including the larynx/pharynx (angio-oedema),
• conjunctival oedema,
• clinical signs of a pleural effusion, pulmonary oedema,
• clinical signs of shock,
• bleeding in the region of the swelling,
• bleeding from bite marks and other injuries,
• gingival bleeding,
• blood-stained sputum, vomit ("coffee ground vomitus"), stools (melaena) or urine,
• acute abdomen (intra-abdominal bleeding!),
• focal neurological deficits, meningismus (intracranial bleeding!),
• cranial nerve deficits, such as ptosis, ophthalmoplegia, dysphagia, dysarthria,
• paralysis of the skeletal musculature including the respiratory musculature (→ respiratory insufficiency/respiratory failure),
• myalgia with active and passive movement and upon pressure,
• dark-brown/red urine (differential diagnosis haemoglobinuria)(rhabdomyolysis!),
• flank pain and renal bed sensitive to percussion,

Autopharmacological effects

• Chest X-ray
• cCT

Haematological effects

• Hb, Hct
• Clotting time
• PT/aPTT
• TT
• Fibrinogen
• FSP
• D-dimers
• Platelets

• Blood group/blood sample for cross-matching

Neurological effects

• Blood gas analysis
• Forced expiration test (peak expiratory flow)

Cardiac effects

• Blood pressure, pulse
• ECG

Renal effects

• Urine output (balance, hourly)
• Serum creatinine
• Serum potassium
• Serum bicarbonate.

Varibility of symptoms and degree of envenoming

The symptoms and degree of envenoming depend not only on the amount of venom injected and numerous other variables, but also on the time that has elapsed since the bite. This variable factor must be taken into account when making the following decisions:

• exclusion of envenoming 
• the time interval between clinical examinations
• emergency care (see below) 

The following signs and symptoms are observed following European viper bites and are indicative of a relevant injection of venom: 

• local pain, swelling and skin changes (in particular ecchymoses),
• nausea, vomiting, diarrhoea, abdominal pain,
• arterial hypotension,
• signs of shock (pallor, sweating, tachycardia, arterial hypotension, alterations in consciousness).
• neurological signs and symptoms, in particular cranial nerve deficits (rare and only in certain geographical areas). 

Cardiovascular collapse / arterial hypotension, schock (autopharmacological effects)

One of the major complications following bites from European vipers is a state of acute transient, persistent or recurrent arterial hypotension. Arterial hypotension combined with other signs of an allergic/anaphylactic reaction, such as urticaria, angio-oedema and bronchospasm, generally commence directly following the bite, can, however, be delayed for several hours (Warrell 2005, 2010).

This applies to autopharmacological but also to allergic, IgE-mediated reactions which also can be delayed or biphasic (Stark and Sullivan 1986)

It most often happens pre-hospital and immeditae life support is essential.

Local signs & symptoms

The oedema can take on immense proportions and involve large areas of the trunk, such that it may be a cause of hypovolaemia and arterial hypotension.
Permanent tissue damage is almost always the result of inappropriate first aid and paramedical measures.

Non-clottable blood and bleeding

Systemic bleeding is extremely rare. Significant changes in the haemostatic parameters with or without clinical manifestations are an exception even in cases of severe envenoming.

Descending paralysis / Respiratory failure

Cases of V. aspis bites with signs and symptoms of neurotoxicity have been described for Italy (Antonini et al. 1991, Beer and Putorti 1998, Re et al 1999) and South-Eastern France (de Haro et al 1994, 2002). Mild neurotoxicity has also been described after bites of other European vipers (Warrell 2010).

Myocardial injury

Myocardial damage in association with bites by European vipers has been reported but is extremely rare.

Acute kidney injury (AKI)

Clinically relevant renal dysfunction is rare. If it occurs, it is probably (always) secondary, i.e. primarily a consequence of arterial hypotension.

Patients for whom the initial examination provided no indication for antivenom administration

At least hourly

• state of consciousness,
• heart rate and rhythm,
• arterial blood pressure,
• respiratory rate,
• spontaneous bleeding,
• ptosis,
• local swelling,
• other newly appearing signs and symptoms.

6-hourly (or more frequently if there is cause for suspicion)

• 20WBCT (bedside test), in settings where resources are immediatelly accessible, go directly to 'Laboratory and physical investigations' below,
• urine output.

A complicated course of envenoming requiring antivenom treatment can be excluded if within a 24-hour observation period

• the oedema ceases to increase in extent,
• neither hypotension nor shock have occurred,
• haemostasis is unimpaired,
• there are no cardiac symptoms and no ECG change

Symptomatic emergency medical treatment and antivenom treatment are complementary strategies.

Antivenom must be secured as early as possible while emergency medical teratment is running.

The aim of symptomatic emergency medical treatment is the rapid correction of critical parameters (fluid balance, blood pressure, oxygenation etc.) and the maintenance of vital functions (respiratory, cardiovascular).

Symptomatic measures help bridge the gap until specific treatment (antivenom) can be administered and starts being effective. If no antivenom is available or if the required effect is not achieved with antivenom, the goal is to employ symptomatic measures until such time as the venom naturally starts losing its activity.

The aim of antivenom treatment is neutralisation of the venom. The success of antivenom treatment depends on the quality of the antivenom, the specific properties of those venom components relevant to envenoming and the time point at which antivenom is administered (neurotoxic envenoming).

Systemic Envenoming

"1. Haemostatic abnormalities: spontaneous systemic bleeding (including evidence of internal haemorrhage – ante-partum, intracranial, gastrointestinal etc.), incoagulable blood (20WBCT) or prolonged clotting time, elevated FDP or D-dimer, thrombocytopenia.

2. Cardiovascular abnormalities: hypotension, shock, cardiac arrhythmia, reduced ejection fraction (echocardiogram).

3. Neurotoxicity (paralysis, fasciculations).

4. Black urine indicating generalized rhabdomyolysis or intravascular haemolysis.

5. In patients with definite signs of local envenoming, the following confirm systemic envenoming: neutrophil leucocytosis, elevated serum enzymes such as creatine kinase and aminotransferases, haemoconcentration, uraemia, hypercreatininaemia, oliguria, hypoxaemia and acidosis.

Severe Local Envenoming. 

In the absence of 1–5 above, the development at any stage of rapidly spreading local swelling that involves more than half the bitten limb within 48 hours of the bite, or extensive blistering or bruising, especially in patients showing the abnormalities listed above under (5) and in patients bitten by species known to cause local necrosis (...). Bites on the digits by these species carry a high risk of necrosis."

"To improve the rate of recovery of local swelling after bites by Vipera berus, antivenom has been recommended in adults with swelling that is either extensive (involving more than half the bitten limb within 48 hours of the bite) or rapidly spreading up the forearm (beyond the wrist after bites on the hand) or lower leg (beyond the ankle) 2-4 hours after the bite)."

(Warrell 2023).

Cranial nerve deficits, such as facial diplegia, pharyngo-laryngeal paralysis, bilateral ptosis and external ophthalmoplegia, dysphonia, dysphagia, paraysis of skeletal muscles may be an additional indication given the experince e.g. in Souh-Eastern France (de Harro et al 2002) 

Selection of antivenom

• WHO Snakebite Information and Data Platform: ANTIVENOMS

• World Health Organization(2023). Target product profiles for animal plasma-derived antivenoms: antivenoms for treatment of snakebite envenoming in sub-Saharan Africa

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.

See Antivenom treatment

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.

A sufficiently long follow-up period (at least 24 h) is necessary.

Comprehensive ABCDE approach

ICRC Basic Emergency Care: approach to the acutely ill and injured (SAMPLE and ABCDE approach: first module)

The guidance provided addresses major genus- or species-specific specific snakebite envenoming problems.

Clinical entries: European vipers

See 'Local treatment' below.

Systemic bleeding (Gerrard and Pugh 1982) is the exception even in cases of severe envenoming (Reid 1976).
Clinical features of a bleeding diathesis are unusual, but bleeding from the gums and nose and into the lungs, gastrointestinal and genitourinary tracts, and serosal cavities and retroperitoneally can occur (Warrell 2005).

A decrease in haemoglobin levels has been observed as a consequence of extravasation of erythrocytes in the region of extensive swelling. From Sweden there have been reports of haemolysis following V. berus bites (Persson and Irestedt 1981).

Ecchymoses in the region of the swelling are common and do not represent an indication for antivenom administration.

Cases of V. aspis bites with signs and symptoms of neurotoxicity have been described for Italy (Antonini et al. 1991, Beer and Putorti 1998, Re et al 1999) and South-Eastern France (de Haro et al 1994, 2002). Mild neurotoxicity has also been described after bites of other European vipers (Warrell 2010).

Myocardial damage in association with bites by European vipers has been reported but is extremely rare. There is no conclusive evidence of a primary cardiotoxic effect of the venom in humans. On the other hand, ECG changes (T-wave inversion, tachy and bradyarrhythmias, atrial fibrilation, second degree hardblock) have been observed in patients with European viper bites (Reid 1976, Paersson et al 1981, commented by Warrell 2010).

Increase in serum creatinine, haematuria, proteinuria, oliguria and anuria were observed (Persson and Irestedt 1981). However, clinically relevant impairment of kidney function is rare and probably usually secondary (arterial hypotension).

Necrosis is very rare.

Compartment syndrome

Even extensive swelling of the extremities is not necessarily an indication of compartment syndrome. The decision to perform a fasciotomy must have a rational basis, see Compartment syndrome.