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

• Bungarus sp.
• Naja sp.
• Ophiophagus sp.
• Daboia sp.
• Vipera sp.
• Deinagkistrodon acutus
• Gloydius sp.
• Trimeresurus sp.
• Rhabdophis sp.

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,
• severe headache, shock (refractory arterial hypotension), signs of hypoglycaemia and loss of consciousness (acute pituitary/adrenal insufficiency).

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 syndrome

“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)

Capillary leak syndrome (CLS) 

CLS is unique for Russell's viper envenoming and includes chemosis, periorbital, and facial oedema, bilateral parotid swelling, pleural effusions, ascites, macular oedema, acute angle-closure glaucoma, haemoconcentration, proteinuria, and hypovolaemic shock with low central venous pressure. Patients with CLS are unresponsive to antivenom and are at increased risk of acute kidney injury and death. Symptoms usually appear 12–48 h after the bite Warrell and Williams 2023). 

Local signs & symptoms

• Naja sp., Ophiophagus hannahbites: absence of swelling or only mild local swelling virtually excludes systemic injection of venom (Reid et al. 1963a).

• Crotalids: Local signs of envenoming are on the whole quite mild compared to those of other viperids and in relation to the severity of the systemic envenoming.

• Daboia sp.: D. russelii is an important exception to the rule that a viperid bite can be excluded if local swelling is absent (Warrell 1989). 
  
• Echis sp.: Local swelling may be mild. 
• Bungarus sp.: as a rule absent or vey mild.

also local sign after bites of

• Rhabdophis sp.,
• European viper bites (which stretch into the region).

Compartment syndrome

Even massive swelling, such as occurs in particular following Calloselasma rhodostoma bites, only rarely causes compartment syndrome. The decision to perform a fasciotomy must have a rational basis see (Compartment syndrome). 

Necrosis

Necrosis is often a consequence of cobra and Ophiophagus sp. bites. 

Local effects (eyes)

Venom ophthalmia from Asian species are considered less severe than that from African species. 
Intense local pain; Blepharospasm; Palpebral oedema; Leucorrhoea; photophobia, clouding of vision, temporary blindness
(Chu et al. 2010, Warrell 2023, WHO 2016).

Abdominal pain

Krait bites in particular may be completely unnoticed and unrecognised initially, as these snakes often bite people at night while they are asleep. A krait bite is thus an important differential diagnosis of signs of paralysis (of the cranial nerves, extremities, respiratory musculature).
Abdominal pain is recognized as a characteristic symptom of kraits.

Bleeding and non-clottable blood

Clinically evident signs of a haemostatic defect may be absent. Nonetheless defibrin(ogen)ation may be present to such a degree that the blood is completely incoagulable. For this reason the simple clotting time test should always be performed if a viperid or crotalid bite is suspected.

Incoagulable blood resulting from defibrin(ogen)ation or disseminated intravascular coagulation is a common and important finding in patients systemically envenomed by members of many genera including Daboia, Echis, Vipera, Gloydius, Ovophis, Deinagkistrodon, Protobothrops, Rhabdophis, and Trimeresurus (Warrell 2023).
The haemostatic defects caused by crotalids in the Far East are primarily due to direct activation of fibrinogen ("thrombin-like" activity), while those caused by D. russelii are due to procoagulative venom components.
In the former, clinically evident signs of a haemostatic defect may be absent. Nonetheless defibrin(ogen)ation may be present to such a degree that the blood is completely incoagulable. For this reason the simple clotting time test should always be performed if a viperid or crotalid bite is suspected.
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). 

Acute, delayed and chronic pituitary or adrenal insufficiency and diabetes insipidus

To date, acute pituitary/adrenal insufficiency has been reported in Myanmar, southern India and Sri Lanka. 

Hypopituitarism following Daboia siamensis and Daboia russelii envenoming (Antonypillai et al 2011, Warrell and Williams 2023).

Thrombotic microangiopathy (TMA)

TMA is regularly observed in Daboia sp. bites and includes disseminated intravascular coagulation, microangiopathic haemolytic anaemia. TMA with acute kidney injury is recognised in patients envenomed by Daboia sp. and other species.

Descending paralysis / Respiratory failure

Patients remain conscious even when completley paralyzed. Communication may still be possible by moving fingers on commands. 

• Bungarus sp.
• Naja kaouthia, whereas N. atra does not typically produce considerable neurotoxicity in humans (Mao et al. 2024, Wong et al. 2010).
• Ophiophagus hannah
• Gloydius blomhoffii, G. brevicaudus and some populations of European Vipera (viperid neurotoxicity, clinically indistinguishable from elapid neurotoxicity) (Warrell 2023).

Muscular effects

• Gloydius tsushimaensis: Rhabdomyolysis with a CK value of more than 40,000 IU/L (with renal dysfunction) (Yokoi et al. 2020).
• ?B. niger in China; no reports identified.

Acute kidney injury (AKI) and chronic kidney injury

Acute renal failure is the most common cause of death from Gloydius blomhoffii bites (Sawai 1989).
“Envenoming by many snake species occasionally results in acute kidney injury, but Russell’s vipers are the most dangerous. Acute kidney injury is the major cause of mortality and morbidity among people who have been bitten by these species. 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).
“The risk of progression from acute kidney injury to chronic kidney disease has been seriously underestimated because of inadequate follow-up. However, in India (e.g., Tamil Nadu and Kolkata) and Sri Lanka, where most cases were attributable to D. russelii, progression from acute kidney injury to chronic kidney disease after 1–3 years, often with associated hypertension, ranged from 26% to 49%.” (Warrell and Williams 2023) which may also apply to D. siamensis envenoming in the region.
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).

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

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),
• 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. spitting cobras). Bites on the digits by these species carry a high risk of necrosis."

(Warrell 2023).

Cranial nerve deficits and paralysis of the skeletal musculature including the respiratory musculature and mild or no local swelling

• Elapids
  
  • Bungarus sp.

Cranial nerve deficits and paralysis of the skeletal musculature including the respiratory musculature and substantial local swelling including necrosis

• Elapids
  • (Naja atra) (N. atra does not typically produce considerable neurotoxicity in humans (Mao et al. 2024, Wong et al. 2010)).
  • Naja kaouthia  
  • Ophiophagus hannah
• Crotalids
  • G. blomhoffii (+ possibly bleeding, acute renal failure).

 Incoagulable blood, spontaneous bleeding, local swelling

• Vipers
  • Daboia siamensis
  • (Vipera sp.)

• Crotalids
  • Deinagkistrodon acutus
  • several Trimeresurus sp. 

• Colubrids
  • Rhabdophis sp.

Selection of antivenom

• WHO Snakebite Information and Data Platform: ANTIVENOMS

• For overlapping distribution areas of species:
  Guidelines for the Management of Snakebites, WHO Regional Office SE Asia

• 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.

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

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: Bungarus sp.
• Clinical entries: Naja sp.
• Clinical entries: Ophiophagus sp.
• Clinical entries: Daboia sp.
• Clinical entries: Echis sp.
• Clinical entries:Vipera sp.
• Clinical entries:Deinagkistrodon acutus
• Clinical entries: Gloydius sp.
• Clinical entries: Trimeresurus sp.

• Clinical entries: Rhabdophis sp.

For overlapping distribution areas of species:

• Guidelines for the Management of Snakebites, WHO Regional Office SE Asia

See 'Local treatment' below.

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.

To date, acute pituitary/adrenal insufficiency has been reported in Myanmar, southern India and Sri Lanka. 

Hypopituitarism following Daboia siamensis and Daboia russelii envenoming (Antonypillai et al 2011, Warrell and Williams 2023).

Acute
“In Burma acute pituitary or adrenal insufficiency is frequent enough to justify routine use of intravenous hydrocortisone in all cases of D. siamensis-related shock.” (Warrell and Williams 2023)
See also Antonypillai et al. (2011), Warrell (1989).

Chronic
If patient develops polyuria, particularly after the introduction of steroids: Investigate for diabetes insipidus. Follow-up: for at least 6 months regarding hypopituitarism. Chronic ill health in survivors of the acute episode: Consider the possibility of hypopituitarism (Antonypillai et al. 2011).

• 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).

• Acute renal failure is the most common cause of death from Gloydius blomhoffii bites (Sawai 1989).
• “Envenoming by many snake species occasionally results in acute kidney injury, but Russell’s vipers are the most dangerous. Acute kidney injury is the major cause of mortality and morbidity among people who have been bitten by these species. 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).
• “The risk of progression from acute kidney injury to chronic kidney disease has been seriously underestimated because of inadequate follow-up. However, in India (e.g., Tamil Nadu and Kolkata) and Sri Lanka, where most cases were attributable to D. russelii, progression from acute kidney injury to chronic kidney disease after 1–3 years, often with associated hypertension, ranged from 26% to 49%.” (Warrell and Williams 2023) which may also apply to D. siamensis  envenoming in the region.
• 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).

• Pain control
• Tetanus prophylaxis
• Standard wound care
• Necroses: debridement; split-thickness skin grafting.
• Systemic antibiotics: standard indications

WHO (2010)

For overlapping distribution areas of species:

Guidelines for the Management of Snakebites, WHO Regional Office SE Asia

Bite site

Severe local tissue damage including impairment of function and loss of limbs are complications of a wide range of snakebite on the Indian Subcontinent and Southeast Asia, in particular cobra bites that cause local effects and Calloselasma rhodostoma bites, but are much less frequent if rational first aid and therapeutic measures are applied.

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

Clinical entries: Naja sp. (Asian cobras)

Corneal lesions 

• 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).