Dr. H. Bawaskar, a physician known for his extensive research in snake bites discusses the diagnosis of different types of snake bites and the corresponding management for each. Here he covers Indian Krait and Cobra bites.

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Snake-bite poisoning is an occupational hazard and a common accident reported among farmers, villagers, labourers, hunters, trekkers, snake rescuers, migrating population like shepherds, scientists working with snakes for milking, and persons who take care of snakes in snake parks are more prone for snake bite accidents. It is a common accident reported in tropical and subtropical countries.

Snake bites evoke a time-limiting, life-threatening emergency. More than 20,00,000 snake bite incidences are reported in India and of these >46,900 people die each year, which means that every hour 5 patients lose their lives to snake bites*. This is just a tip of the iceberg as a majority of the times, victims die at home by being attended to by a Mantrik or on the way to a hospital, and the cases remain unreported. Lack of knowledge, improper training regarding early reorganisation of venomous snake bites and rapid intervention may add to mortality and morbidity.

Irrespective of high fatality, snake bites remain totally neglected in rural India though they are recognized in the type A category of neglected tropical diseases by WHO. It is a surprise to note, and snakebite poisoning is seldom mentioned as a priority for health research in a developing country like India.

Availability of snake-venom antigen detection kits (ELISA), mono-specific or antivenom producers in India should be encouraged to prepare anti-venom from venom obtained from snakes caught from relevant areas of the country. Recently, the high incidence of snake bites was attributed to electric load shading for more than 12 hours in rural areas. The government should provide all facilities including anti-snake venom (ASV), life support gadgets like ventilators and emergency treatment rather than giving compensation to the relatives of patients who die from snake bites.

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India's poisonous snakes

Of more than the 3,000 known species of snakes, only about 300 are venomous and there are about 216 species of snakes identifiable in India, of which 52 are known to be poisonous. The major families of poisonous snakes in India are:

• Elapid which includes common cobra (Naja naja), king cobra and common krait (Bungarus caerulus, banded krait, sind krait)
• Viperidae includes Russell’s viper, Echis carinatus (saw-scaled or carpet viper) and pit viper
• Hydrophidae (sea snakes)

Venom secretion in all venomous snakes appears to vary in seasons more in warmer months with high morbidity and fatality. The darker the snake, the more venom it secretes.

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Krait venom

Krait venom is ten times more lethal than the cobra, victim report too late due to delayed clinical manifestations.

Krait Bungarus caeruleus

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Krait is nocturnal in habit. Its fangs are small size like that of a 24-size needle. It injects the venom deep into the skin. Though the venom is of small molecular size, it is absorbed slowly as skin has poor circulation and reflexes are blunted during sleep. Beta bungarotoxin in the krait venom bears similarity to botulinum toxin. Common Indian Krait venom contains both presynaptic beta bungarotoxin and alfa bungarotoxin.

1. Mode of action: The toxins initially release acetylcholine at the nerve endings at the neuromuscular junction and then damage it subsequently preventing the release of acetylcholine and receptors are damaged and destroyed, the cause of resistance to anti-cholinesterase.
2. Symptoms: Initial release of acetylcholine results in autonomic nerve stimulation, in addition, to release of cholecystokinin explained by acute abdominal pain, vomiting, staring look, blurring of vision, gooseflesh, salivation, hypertension, pulmonary oedema.

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Clinical manifestations of Common Krait bite

The common krait is regarded as the most dangerous species of venomous snake in the Indian subcontinent. Most bites occur during the cooler months of June to December, when snakes may, during the course of their hunting activity, linger on a person’s bedding to take advantage of the warmth. 

Krait bite patterns

Patients	Total	Percentage
Male	79	56
Female	62	34
Approximate Time of Bite	Total	Percentage
6 pm to 12 am	34	24.11
12 am to 5 am	106	75.17
Day bite	1
Activity at the Time of Bite	Total	Percentage
Sleep	140	99.29
Activity	1
Snake seen, killed and brought to the hospital	42	29.78
Saw the snake and confirmed by specimen and photographs	19	13..47
Site of Bite	Total	Percentage
Lower extremities	43	30.49
Upper extremities	32	22.69
Other parts	28 (neck- 7, abdomen- 2, axial- 5, back- 6, chest- 3, ear- 5)	19.85
No history of bite	38	26.95

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Krait bite symptoms

Signs & Symptoms	Total	Percentage
Pain in abdomen	120	85.10
Chest pain	102	72.34
Tenderness over abdominal and other muscles	121	85.81
Vomiting	59	41.84
Difficulty in deglutition	110	78
Sweating	24	17.02
Bilateral ptosis	126	89.36
Blurred vision	72	51.06
Suffocation	86	60.99
Ophthalmoplegia	100	70.92
Pooling of saliva	52	38.87
Hypertension	23	16.31
Hypotension	5	3.58
Bradycardia	6	4.25
Tachycardia	3	2.12
Pulmonary oedema	4	2.83
Quadriplegia	42	29.78
Neck drop	47	33.33
Respiratory depression	50	35.46

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Because of negligible or absent local manifestations, envenomation is neglected and falsely initially attributed to ant or rat bite or no bite at all.

The venom stimulates the autonomic nervous system within 20 to 30 minutes of the bite.

1. The victim wakes up to transient abdominal colicky pain, vomiting (once or twice), and chest pain. Relatives and even an inexperienced doctor could neglect these vital symptoms by attributing them to indigestion or acidity or an acute attack of appendicitis and minimum T wave inversion due to hypoxia.
2. Such a victim is then referred and admitted to the intensive coronary care unit. The tissues having a high concentration of acetylcholine receptors are affected earlier. The sphincter pupillae, elevator palpebral superior, neck muscles, bulbar, limbs, and at last the diaphragm and intercostal muscles are affected.

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Clinical effects are seen within 30 minutes or sometimes too late in around 18 hours.

1. Quadriplegia with aphasia and dilated pupils may be diagnosed as brain death or locked in syndrome [pseudo coma] or GB syndrome. The patient can communicate by flicker venom-induced paralysis of pupillary muscle resulting in non-reacting pupils, but this is not the sign of irreversible brain damage.
2. After recovery, few patients have signs and symptoms of peripheral neuropathy.
3. Many times, patients succumb to iatrogenic respiratory infection or adult respiratory distress syndrome.

At times, krait-bite victims even bring the killed snake but do not develop any clinical manifestations, local fangs marks without urticaria, indicated bite without envenoming or “dry bite”.

An inexperienced treating doctor may diagnose a krait bite envenoming even if a patient brings a specimen of wolf snake. To confirm or identify the venomous krait it is best to look at the tail which is covered by white bands till its end. This feature is absent in wolf snake (picture below), a non-venomous species which apparently looks like krait.

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Management of Krait bite

In krait bite there is a destruction of receptors, thus neurological manifestations may persist for weeks till there is a regeneration of receptors. At this stage administration of ASV is merely a waste.

Ventilation may be required if:

• Pooling of saliva in the victim is noticed
• Is unable to lift the neck from the pillow
• There is a reduction in SpO₂ saturation
• Respiratory failure is noticed
• Abdominal-thoracic respiration occurs

If suffocation and signs of cerebral hypoxia occur:

• At the periphery, one can do entro tracheal intubation
• If this is not possible a laryngeal mask can be put directly over the larynx and ambu bag ventilation can be started

The last to recover is ptosis and the proximal muscles of lower limbs.

Anticholine esterase inhibitor (AChI)

Indian common krait venom contains both pre- and post-synaptic blockers. Whether the victim responds to AChI or not can be confirmed by placing an ice-filled glove finger over the eyelids. Hypothermia sensitizes the AChl receptors of acetylcholine. If there is a slight improvement in ptosis one can try AChI. 

Severe uncontrolled hypertension

In krait bite, this is attributed to the blocked presynaptic receptors and unblocked post-synaptic receptors which release epinephrine into circulation. At times the victim may land up with acute myocardial failure with pulmonary oedema and need intravenous nitroglycerine drip and BIPAP ventilation. Severe hypertension with tachycardia and pulmonary oedema recover with nitroglycerine drip and non-invasive ventilation.

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Cobra bite 

Cobra venom is of smaller molecular size and rapidly absorbed into the circulation. The venom reversibly attaches to postsynaptic receptors. Absorption is further accelerated by the threat of death and liberated catecholamine and running can kill the victim within 8 minutes.

1. Mode of action: Cobra venom binds specifically to the acetylcholine receptors, preventing the interaction between acetylcholine and receptors on postsynaptic membrane, thereby resulting in a neuromuscular blockade.
2. Treatment: Administering appropriate antivenom ( in India polyvalent antivenom against krait, cobra, Russell’s viper and Echis) accelerates the dissociation of the toxin-receptor complexes and reverses paralysis.

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3. Cardiotoxin content of cobra venom has a direct action on skeletal, cardiac, smooth muscles, nerves and neuromuscular junction causing paralysis, circulatory, respiratory failure, cardiac arrhythmias, heart block and systolic cardiac arrest because of venom release causing calcium ions to move from the surface membrane to the myocardium.

Cobra bite tends to occur during the daytime when transportation is more readily available.

1. Soon after the bite, the victim experiences severe pain at the bite site having fang marks. Fang marks are covered with blood clots. There is a rapid progression of swelling from the bitten part to the rest of the limb. Victims bitten by the hooded cobra may die of cardiac lethal ventricular arrhythmias or cardiogenic shock due to massive myocardial infarction.
2. The skin at and around the bite site becomes ecchymosed.
3. The victim subsequently develops tense blebs and massive damage of skin and subcutaneous tissue due to myocytolysis and huge non-healing ulcers.
4. Later, the victim may develop stress-induced or ballooning cardiomyopathy as a result of massive liberation of endogenous catecholamine into circulation. This phenomenon, however, could be absent in children. 

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Management of cobra bite 

Local tissue damage requiring plastic surgery skin grafting

A majority of the victims recover within 24 hours and may require not more than 5-6 doses of AChI. In our experience, a victim declared as dead by a peripheral doctor only based on the absence of respiration and non-reacting pupils was recovered with artificial ventilation, CPR, and AChI.

*Source: Snakebite envenoming. Prevalance of snakebite envenoming.

In the upcoming articles, Dr. H Bawaskar discusses the treatment and management of victims reporting with Russell's viper and sea snake bites. 

The writer, Dr. Himmatrao Bawaskar is a renowned Indian physician with publications in The Lancet. He has done extensive research in scorpion sting- diagnosis and treatment protocol.

Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.

The author did not accept any payment for the article.