What Makes Brown Snakes Dangerous?
Brown snakes are mostly found in Australia, and they belong to the family of Elapidae. There are different subspecies under this family, for example- Pseudonaja guttata (speckled brown snake), Pseudonaja textilis (common brown snake or eastern brown snake), etc.
The eastern brown snake has the most powerful bite because of the lethal components found in its venom.
The venom contains the following toxins-
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Presynaptic Neurotoxins - These are responsible for causing paralysis and muscle weakness.
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Postsynaptic Neurotoxins - These are responsible for the rapid action of the venom.
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Procoagulants - This part of the brown snake venom interferes with blood clotting. It causes consumption of the clotting protein (fibrinogen), which in turn leads to defibrination with non-clottable blood. This puts the victim at a major risk of bleeding.
However, the venom does not contain any renal toxins (although renal failure is a common effect of brown snakebite), mycotoxins (that cause myolysis), and neurotoxins.
The potency of snake venom is measured using the LD (lethal dose) 50 scale; the lower the number, the more toxic the bite is. Brown snake has an LD 50 score of .03, while the LD 50 score of a king cobra is 1.09; this makes the former significantly more toxic.
Apart from the powerful bite, the brown snake is considered to be notoriously aggressive, often biting people when stumbled upon or surprised. It can move at a speed of 12 miles per hour which makes it difficult to outrun the reptile in case of an attack.
What Is the Lethal Dose of Brown Snake Venom?
Around 3 mg of brown snake venom is sufficient to kill a normal person. The amount of venom produced by the brown snake depends on the size of the snake; on average, it can produce anywhere between 5 mg to 155 mg per bite.
The king cobra and the black mamba produce far more venom than the brown snake, but the latter is capable of killing more people given the potency of its bite. Despite the potency of its venom, the brown snake does not use it to kill its prey (house mice, birds, lizards, or other snakes) due to its small fangs; rather, it constricts them by using its large body.
What Are the Symptoms of Brown Snake Bite?
The brown snake venom is capable of severe envenomation (systemic poisoning from the bite); it characteristically causes venom-induced consumptive coagulopathy (VICC). The procoagulants present in the venom have the ability to convert prothrombin to thrombin and to significantly deplete coagulation factors (Ⅴ and Ⅶ), protein C, and plasminogen within two hours of the snakebite.
The neurotoxins also present in the venom cause neurological symptoms soon after envenomation; they cause respiratory paralysis by blocking nicotinic acetylcholine receptors at the postsynaptic motor endplate and affect neurotransmitter release at presynaptic motor nerve endings.
After giving a history of being bitten by a brown-colored snake, the patient will complain of neurological symptoms within an hour and coagulopathy symptoms within a few hours; these include-
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Nausea or vomiting.
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Photophobia (extreme sensitivity to light).
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Blurred or double vision.
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Slurred speech.
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Muscle weakness.
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Irritability.
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Altered mental status.
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Dyspnea (difficulty in breathing).
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Epistaxis (bleeding from the nose).
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Gingival bleeding.
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Hematemesis (vomiting of blood).
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Hematochezia (blood in the stool).
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Oliguria (low urine output).
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Dysphagia (difficulty in swallowing).
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Loss of consciousness, collapse, and convulsions.
The physical examination will present characteristic signs of a brown snake bite; they are-
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Fang marks with coagulopathy.
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Little to no edema or erythema.
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Bronchospasm.
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Ptosis (drooping of upper eyelid).
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Trismus (restricted motion of the jaws).
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Cyanosis (bluish discoloration of the skin).
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Paralysis.
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Hypotension.
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Tachycardia (rapid heartbeat) or bradycardia (reduced heartbeat).
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Cardiac arrest.
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Petechiae (red or purple spots on the skin).
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Cerebellar hemorrhage.
What Are the Complications of a Snake Bite?
If the patient is not treated for the above-mentioned symptoms and signs, the following complications will rise from three hours to 12 hours post envenomation-
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Intracranial hemorrhage (bleeding between the brain tissue and skull).
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Respiratory compromise.
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Weakness.
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Bleeding diathesis.
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Anaphylactoid reactions (same as anaphylaxis but without the IgE mediation).
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Serum sickness reaction.
How to Diagnose a Brown Snake Bite?
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In the majority of cases, there is a history of snake bites. History, examination, and laboratory tests focus on whether the patient is envenomed or not and by which snake so that the correct antivenom can be given.
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Laboratory investigations should include a full blood count, coagulation studies including D-dimer (a protein fragment that is made when a blood clot dissolves in the body), and biochemical tests including creatine kinase. A urine analysis is helpful for detecting blood or myoglobin.
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Some literature suggests a snake venom detection kit (VDK), which is useful to identify the type of snake responsible for the envenomation; however, it is not useful to confirm snake envenoming.
How Is Brown Snake Envenomation Treated?
Since most cases have a history of snake bites, treatment does not have to wait till a definitive diagnosis is made. Treatment should start before reaching the hospital and must include basic and advanced life support to ensure an adequate airway.
Prehospital care should also comprise cardiopulmonary resuscitation (CPR) and chemical adjuncts for cardiovascular compromise. Tampering with the bite is not advised as it may cause complications like gangrene, ischemia, bleeding, etc.
An elastic bandage should be placed proximally from the location of the bite to delay the absorption of the neurotoxin, but care should be taken not to obstruct the arterial flow. The bandage is only removed after the antivenom therapy is instituted.
Once the patient is administered in the hospital, treatment is as follows-
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The airway, breathing, and circulation are stabilized.
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Oxygen is administered.
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Intravenous access is established for cardiac monitoring and continuous pulse oximetry.
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A prophylactic tetanus shot is given to prevent wound botulism.
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The patient is premedicated with Antihistamine, which is continued for five days post-antivenom therapy to prevent anaphylaxis.
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Brown snake antivenom, which is made from the plasma of horses immunized with the venom of the said snake, is administered if and when signs and symptoms of envenomation start to appear.
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Initially, larger doses are given if there is severe envenomation; in most cases, the amount of antivenom depends on the victim's size and the extent of envenomation.
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In order to treat nearly 90 % of snake bite victims, on average, five ampules to ten ampules is sufficient.
Conclusion:
Brown snake envenomation is a rare occurrence and is endemic to Australia and New Guinea. Treatment should be started immediately after the snake bite to prevent life-threatening complications. Prompt diagnosis and effective emergency care are necessary to improve the clinical outcome.