Clinical Management

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?

• Under what circumstances did the snake bite occur, and how did the snake behave?

• 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

• Atractaspis sp., Mole vipers
• Bitis arietans, Puff adder
• Cerastes sp., African desert horned vipers
• Daboia palaestinae, Palestine viper
• Echis sp., Saw scaled vipers
• Naja sp., African cobras

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).

Observe/investigate

• bite marks,
• extent and intensity of local swelling,
• eyes: conjunctivitis, corneal lesions, uveitis (spitting cobras!),
• 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

Local effects

• Split lamp, fluorescein stain (spitting cobras!).

Haematological effects

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

• blood film with 24 hours of the bite (schistocytes > 1% is diagnostic of microangiopathic haemolytic anaemia)
• Free haemoglobin in the plasma and urine
• Haptoglobin

• Blood group/blood sample for cross-matching

Neurological effects

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

Muscular effects

• Myoglobin in the serum/urine,
• Serum creatinine kinase (CK, CPK)
• GOT (AST)
• Serum potassium
• serum phosphate
• serum calcium

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)

Bite marks and dry bites

The fact that a patient has been bitten by a known venomous snake and the presence of bite marks do not automatically allow the conclusion that a clinically relevant injection of venom has taken place. A substantial proportion (up to 50 % are reported) of confirmed bites, including cobra bites, proceed with no detectable symptoms or at the most negligible local signs of envenoming.

Autopharmacological signs & symptoms

The venom of vipers in particular can cause clinical symptoms of autopharmacological venom effects and anaphylaxis in patients within minutes after the bite occuring with Actractaspis engaddensis and A. microlepidota, Bitis arientans, Daboia palaestinae and Macrovipera sp. (Efrati 1979, Leviton et al. 1992, Warrell et al. 1975).
“Acute profound hypotension with or without other features of anaphylaxis is part of the autopharmacological syndrome which may occur within minutes of bites by Daboia species. It may be caused by release of endogenous vasoactive compounds such as nitric oxide, kinins, histamine, serotonin and endothelins” (Warrell 2023).
"Early, repeated, usually transient but sometimes persistent and fatal, syncopal attacks with features of anaphylaxis may develop in patients not previously exposed to venom who have been bitten by some Viperidae, notably also Daboia palaestinae" (Warrell 2023).
Amr et al. (2020) describe “Within 15–20 min after the initial pain of the bite, victims report a sudden sense of weakness, and restlessness, and begin to vomit and sweat. Abdominal pain is associated with diarrhoea which may be watery and blood-stained. There is an anaphylactic syndrome: angioedema affects lips and face, the tongue, which may swell to “several times its normal size”, the glottis (requiring tracheostomy in one case); urticaria; tachycardia; hypotension and shock causing collapse and unconsciousness.”

Local signs & symptoms

Bitesite
The fact that a patient has been bitten by a known venomous snake and the presence of bite marks do not automatically allow the conclusion that a clinically relevant injection of venom has taken place.

On the other hand, local signs, e.g. swelling at the site of the bite, following viperid bites as well as bites of some elapid species (N. nigricollis, N. nubiae, N. katiensis, Walterinnesia aegyptia) are generally an indication that a significant injection of venom has occurred.

With bites from the Cobra species N. haje (and possibly N.arabica, N. melanleuca and N. senegalensis), however, local signs of envenoming may be absent even in cases of severe systemic envenoming (Visser and Chapman 1978, Warrell et al. 1976a).

Atractaspis sp.: as a rule there is generally at least mild local swelling following injection of venom (Warrell et al. 1976c).

Bitis arietans: marked local swelling that often extends to the trunk and causes necrosis (Warrell et al. 1975, Marsh and Whaler 1984).

Causus sp.: local swelling generally appears to occur following injection of venom, but is only marked in a small proportion of cases (Warrell et al. 1976c).

Cerastes cerastes: Local pain, local swelling extending to the entire bitten limb. Local necrosis (Schneemann et al. 2004).

Echis sp.: local swelling always occurs if venom has been injected, but may be only mild (Porath et al. 1992, Warrell et al. 1977).

Daboia palaestinae and Macrovipera lebetina: extensive swelling that may extend to the trunk, necrosis possible but rarely severe as long as the bite is not on the fingers or toes (Efrati 1979, Leviton et al. 1992).

Naja nigricollis: local swelling may be very extensive, possibly involving the trunk, necrosis (Warrell et al. 1976b).

Naja haje: local signs of envenoming usually absent or insignificant (Warrell et al. 1976b, Blaylock et al. 1985, Visser and Chapman 1978).

Walterinnesia aegyptia: local swelling (Yayon et al. 1988).

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.

Eyes (Spitting cobras)
Naja nigricollis, N. katiensis and N. nubiae can cause lesions in the eye. Intense local pain; blepharospasm; palpebral oedema; leucorrhoea; photophobia, clouding of vision, temporary blindness (Chu et al. 2010, Warrell 2023, Warrell and Ormerod 1976; WHO 201a).

Non-clottable blood and bleeding

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 (untreated, i.e. without antivenom treatment, days to weeks).
Most typically caused by bites from carpet vipers (Echis spp.), desert horned vipers (Cerastes cerastes). More uncommonly it may sometimes follow bites by puff adders (B. arietans).

Thrombotic microangiopathy (TMA)

Is observed in the region, e.g. in Echis sp. and Daboia palaestinae envenoming.

Descending paralysis / Respiratory failure

Neurotoxic cobras Naja haje, N. anchietae, N. annulifera, N. melanoleuca.
Walterinnesia sp. ?

Acute kidney injury (AKI)

According to the available data, acute renal failure following a snakebite in North Africa and the Near and Middle East generally appears to be a secondary effect (arterial hypotension, shock, DIC).
For Bitis arietans and Cerastes cerastes venom a primary nephrogenic effect is discussed (Warrell et al. 1975, Schneemann et al. 2004).

Monitoring for signs and symptoms that would indicate systemic envenoming for at least 24h. 

At least hourly

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

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

• 20WBCT (bedside test),
• labortaory-based clotting tests (see above),
• CK, GOT (AST),
• urine output.

The absence of signs of envenoming in the first hours after the bite does not exclude the possibility that a relevant injection of venom has taken place. There may be a long delay before systemic signs of envenoming develop. Moreover, the continued absorption of venom from the region around the site of the bite can lead to renewed symptoms of systemic envenoming even after successful administration of antivenom (e.g correction of the haemostatic defect).

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 (e.g. African spitting cobras). Bites on the digits by these species carry a high risk of necrosis."

(Warrell 2023).

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.

Specific examinations are based on the signs and symptoms as well as laboratory parameters that were used to determine the indications for antivenom administration.

Viperids

• Echis sp., Cerastes cerastes
  • systemic bleeding, 
  • 20WBCT, 
  • labortaory-based clotting tests (see above). 
• Bitis arietans, (Cerastes cerastes)
  • systemic bleeding
  • hypovolaemic/shock parameters
  • platelets.
• Vipera palaestinae, Macrovipera lebetina
  • hypovolaemic/shock parameters.

Elapids

• N. haje, N. melanoleuca, other elapids
  
  • spontaneous breathing,
  • signs of respiratory insufficiency,
  • fist grasp,
  • upward gaze,
  • forced expiration test.

Local envenoming

Evaluation of the efficacy of antivenom with regard to local effects, such as swelling and in particular necrosis, is controversial. However, there is agreement on the fact that the time that normally elapses between the bite and administration of antivenom represents a significant factor that can limit the chances for success of antivenom treatment with regard to local effects.

Haemostasis

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).
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.

Neurotoxic envenoming

Antivenoms may not sufficiently or not at all reverse neurotoxoc envenoming or restore repiratory muscle function only slowly depending on the time when the antivenom is adminstered and the effciuacy of the antivenom.

With these problems in mind, the other two available treatment approaches need to be used concurrently and in a timely manner:

• Acetylcholinesterase inhibitors: see 'Supportive emergency medical treatment', 'Respiratory failure (descending paralysis)',
• 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.

Patients bitten by species of snakes whose venom causes haemostatic defects should be kept in hospital for up to several days after initial treatment, and blood coagulability should continue to be monitored twice daily.

The same considerations apply to patients suffering from elapid bites.

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: Atractaspis sp.

Clinical entries: Bitis arietans

Clinical entries: Cerastes sp.

Clinical entries: Daboia palaestinae

Clinical entries: Echis sp.

Clinical entries: Naja sp. (spitting cobras)

Clinical entries: Naja sp. (neurotoxic cobras)

Guidelines for the Prevention and Clinical Management of snakebite in Africa

A fall in blood pressure is a feature of  envenoming by these species. Sinus tachycardia, orthostatic hypotension, suggests hypovolaemia resulting from extravasation into the tissues of the bitten limb or systemically, external haemorrhage, or generalized increase in capillary permeability (haemoconcentration) (Warrell 2023, Warrell et al. 1975).

Daboia palaestinae
"Early, repeated, usually transient but sometimes persistent and fatal, syncopal attacks with features of anaphylaxis may develop in patients not previously exposed to venom who have been bitten by some Viperidae, notably also Daboia palaestinae" (Warrell 2023).
Adequate intravenous fluid replacement and antivenom administration is important to reverse the development of hypovolaemia as early as possible, which may require large volumes of intravenously administered fluids.

Coagulopathy

• Even severe haemostatic defects that can be detected on laboratory tests may not become clinically evident for a long period, or even not at all.

Bleeding

• Bleeding (gingival bleeding, epistaxis, haematemesis, haematuria, etc., haemorrhagic schock; intracranial) occurs in particular in Echis sp., Cerastes cerastes). More uncommonly it may sometimes follow bites by puff adders (B. arietans).

•  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 and venom-induced coagulation disorders are present, 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).

  Haematuria (especially microhaematuria) is not a reliable sign of a venom-induced haemorrhage in those regions where urinary schistosomiasis (Schistosoma haematobium) is prevalent.

Replacement therapy

Replacement of clotting factors and platelets following antivenom administration to bridge the gap until the antivenom starts being effective, insofar as evident bleeding or the imminent threat of critical bleeding makes this necessary. Also in cases where antivenom is not available or is ineffective and bleeding or the risk of bleeding makes intervention necessary (Warrell 1990b). In all other cases administration of effective antivenom should be a sufficiently effective and quick means of correcting the haemostatic defect. However, it is important to note that replacement of clotting factors and platelets is only effective in the short-term while circulating haemostatically active venom components are still present. Recurrence of venom-induced coagulation abnormalities are an important problem.

• Patients with VICC require blood film with 24 hours of the bite (schistocytes > 1% is diagnostic of microangiopathic haemolytic anaemia); serial creatinine.
• There is limited evidence that antivenom prevents TMA.

• Descending flaccid paralysis classically first involves the eye muscles (ptosis, diplopia and blurred vision), followed by bulbar muscles, respiratory muscle paralysis and limb paralysis.

• Anticholinesterase drugs may produce a rapid, useful improvement in neuromuscular transmission. It is worth trying the ‘Tensilon test’ or “Ice test” in all cases of severe neurotoxic envenoming. This should, however, not delay antivenom treatment or endotracheal intubation (Warrell 2023). 

• Once paralysis is established, it responds only slightly or not at all to antivenom administration.

• Antivenom given early after the bite can prevent neurotoxicity. 

• 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.
• Neurotoxic effects are completely reversible, either in response to antivenom or spontaneously within 1-4 days of mechanical ventilation, ocular muscles within 2–4 days and full recovery of motor function within 3–7 days. (Warrell 2023, WHO 2010a).

• Management of AKI needs to consider the various factors that contribute to acute tubular necrosis
• "Direct venom nephrotoxicity, renal ischaemia secondary to shock, disseminated intravascular coagulation with thrombotic microangiopathy (TMA), haemoglobinuria, myoglobinuria, and hyperkalaemia contribute to acute tubular necrosis.” (Warrell and Williams 2023).
• Renal failure is not a common feature of envenoming in North Africa, Near and Middle East and occurs mainly secondary after prolonged hypotension.
• Management of chronic kidney disease requires availability and access to dialysis and services taking care of complications associated with chronic kidney disease (e.g. arterial hypertension).

Bite site

Spitting cobras
In particular with cobra bites that cause local effects (most importantly, N. nigricollis, N. katiensis, N. nubiae; Clinical entries: Naja sp. (spitting cobras)), the true extent of the necrosis is often only discernible after some time, and thus it is essential that the patient is observed for a sufficiently long period in order to ensure the necessary treatment.

Bitis arietans
“Compartment syndromes may develop, especially involving the anterior tibial compartment after bites on the feet and ankles, leading to ischaemic necrosis of intra-compartmental muscles.” (Amr et al. 2020).

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. 

Eyes

Spitting cobras
see Clinical entries: Naja sp. (African spitting cobras).

Corneal lesions (Naja nigricollis, N. katiensis and N. nubiae)

• Diagnostic
  Slit-lamp or fluorescein examination: corneal erosions.
  Corneal lesions and lesions of the anterior chambers of the eye need to be either definitively excluded or treated systematically in order to avoid damage due to secondary infections.

• Complications
  Permanent opacities and blindness (secondary infection of corneal lesions). Destruction of the eye (panophthalmitis). Hypopyon and anterior uveitis (absorption of venom into the anterior chamber). Facial cranial nerve paralysis (local spread of venom) (Chu et al. (2010); Warrell (2023); Warrell and Ormerod 1976; WHO (2010a)).

• Treatment
  "1) urgent decontamination by copious irrigation
  2) analgesia by vasoconstrictors with weak mydriatic activity (e.g. epinephrine) and limited topical administration of local anaesthetics (e.g. tetracaine)
  3) exclusion of corneal abrasions by fluorescein staining with a slit lamp examination and application of prophylactic topical antibiotics
  4) prevention of posterior synechiae, ciliary spasm and discomfort with topical cycloplegics and 5) antihistamines in case of allergic kerato-conjunctivitis.
  Topical or intravenous antivenom and topical corticosteroids are contraindicated."
  Chu et al. (2010)
  If a corneal lesion cannot be diagnosed because the necessary instruments are not available, the eye should be treated as if a corneal lesion were present (Warrell 1990b).