Snakebites
A snakebite with envenomation is a serious medical emergency in which toxins from a venomous snake's modified salivary glands are injected into the body through the bite. Snake venom is a complex biological mixture of dozens of enzymes, polypeptides and protein toxins that can cause rapid skin necrosis, widespread clotting abnormalities, or respiratory paralysis and death. In Vietnam, the common venomous snakes fall into two main families: vipers (Viperidae – green pit vipers, red-tailed pit vipers, Malayan pit vipers), which cause extensive tissue necrosis and coagulopathy; and elapids (Elapidae – cobras, including the monocled cobra, and kraits), which cause muscle paralysis by acting on the neuromuscular junction. Cobras can also cause deep skin necrosis, whereas kraits cause almost no local swelling or necrosis.
At Haute-Derma, the care of snakebite patients focuses on proper first aid with limb immobilization, rapid assessment of local and systemic toxicity so the patient can be transferred for antivenom, and, once the acute phase has passed, surgical debridement of necrotic tissue and laser treatment to restore the appearance of scarred skin.
Pathophysiology
Venom Components and How They Destroy Skin Tissue
- Phospholipase A2 (PLA2): destroys the cell membranes of the epidermis and dermis and releases arachidonic acid, triggering an intense inflammatory reaction with severe swelling and sudden, severe pain at the bite site.
- Metalloproteinases (SVMPs): break down interstitial collagen and damage the basement membrane of small blood vessels, causing leakage, widespread bruising and eventually dry or wet necrosis of all the tissue around the bite.
- Hyaluronidase (the "spreading factor"): breaks down hyaluronic acid in the skin's connective tissue, allowing the venom to penetrate quickly into the deeper subcutaneous tissue and muscle.
Systemic Hemotoxicity and Neurotoxicity
- Hemotoxins: consume fibrinogen and activate or inhibit platelets, leading to disseminated intravascular coagulation (DIC) and uncontrolled bleeding from the bite and from mucous membranes throughout the body.
- Neurotoxins: bind to nicotinic acetylcholine receptors on the postsynaptic membrane (or block acetylcholine release from the presynaptic membrane), blocking neuromuscular transmission and causing progressive muscle paralysis, drooping eyelids and respiratory failure.
Skin and Systemic Signs
Fang Marks and Local Reaction
- Bite marks: venomous snakes usually leave two large, deep fang punctures (about 0.5–1.5 cm apart), sometimes with smaller tooth marks around them. Non-venomous snakes typically leave only a curved row of small, zigzag tooth marks with no distinct fangs.
- Swelling and purpura: right after the bite, the area swells quickly and becomes intensely painful, with bruising and blisters filled with clear or bloody fluid. The swelling advances up the limb very rapidly (it can spread more than 2 cm per hour).
Progressive Skin Necrosis and Systemic Signs
- Skin necrosis: the skin around the bite turns from deep purple to grayish black, then either dries out or becomes foul-smelling and purulent, sloughing off to expose the muscle beneath (very typical of cobra and pit viper bites).
- Systemic symptoms:
- Pit vipers: persistent oozing from the fang marks, bleeding under the skin all over the body, bleeding gums and blood in the urine.
- Kraits: the bite is often almost painless with little swelling, but within 1–4 hours the patient develops drooping eyelids, slurred speech, difficulty swallowing, limb weakness and weak breathing.
Differential Diagnosis by Snake Group
| Pit Vipers (Viperidae) | Cobras (Naja spp.) | Kraits (Bungarus spp.) |
|---|---|---|
| 2 deep fang marks | 2 deep fang marks | 2 small fang marks |
| Rapid, severe swelling; moderate necrosis | Extensive swelling; very deep black necrosis | Almost no swelling or necrosis |
| Very severe (bleeding, fibrinolysis) | Mild or no hemotoxicity | No hemotoxicity |
| None | Delayed neurological paralysis | Rapidly progressive muscle paralysis, drooping eyelids |
First Aid and Emergency Assessment at Haute-Derma
Standard First Aid: Immobilize the Limb
- Have the patient lie still and reassure them. Fully immobilize the bitten limb with a rigid splint and a gentle bandage (as you would for a fracture) to slow the spread of venom through the lymphatic system.
- Keep the bitten limb at or below the level of the heart.
- Never do the following:
- Do not apply a tight tourniquet (it cuts off the blood supply and can lead to necrosis requiring amputation).
- Do not cut the skin, suck out the venom, apply ice, or put leaves or herbal remedies on the bite.
Emergency Triage and Transfer for Antivenom
- Check vital signs (SpO2, blood pressure, respiratory rate). Assess clotting with a bedside 20-minute whole blood clotting test (WBCT20).
- Transfer the patient immediately to a poison control center or general hospital that stocks specific snake antivenom (SAV), the only treatment that effectively neutralizes snake venom.
Debridement and Skin Restoration at Haute-Derma
Surgical Debridement and Cleaning of the Necrotic Ulcer
- Performed once the patient is past the systemic danger phase and clotting tests have returned to normal.
- All clearly demarcated black necrotic skin and muscle is surgically removed, while preserving healthy nerves and blood vessels as much as possible.
- The wound cavity is washed with a dedicated antiseptic solution, and negative pressure wound therapy (VAC) is applied to promote rapid growth of granulation tissue.
Rebuilding Lost Tissue and Improving Scar Appearance
- A serum containing epidermal growth factor (EGF), madecassoside and hyaluronic acid is applied to nourish the granulation tissue in the ulcer bed.
- Once the wound has fully closed, fractional CO2 laser is combined with hyaluronic acid mesotherapy or PRF (platelet-rich fibrin) injections to release tight scar bands, smooth the skin surface and fade post-inflammatory hyperpigmentation (PIH).
