Snake bites are a common condition caused by animal attacks. Non-venomous snake bites mainly cause local lesions, while venomous snake bites lead to acute systemic poisoning resulting from venoms entering the human body from the wound. Due to the rapid onset and quick development, if there is no prompt and appropriate treatment, snake venoms quickly spreading in the body affects the function of multiple organs in the body, resulting in metabolic disorders, multiple organ failure, and even death.
Venomous snakes contain a variety of different toxic components. The toxic components are composed of enzymes, polypeptides, glycoproteins, and metallic ions, among which there are dozens of toxic proteins. Snake venoms can be divided into hemotoxic venoms, neurotoxin venoms, and cytotoxic venoms.
Snake venom protease acts directly or indirectly on the blood vessel wall, destroys the relevant structures of the blood vessel wall, induces the release of bradykinin, histamine, and serotonin, directly damages capillary endothelial cells, and inhibits platelet aggregation, thus causing bleeding. Snake venom hemolytic factors can directly act on the blood cell membrane, increasing the permeability and fragility. Phospholipase A can hydrolyze lecithin in blood into lysolecithin, resulting in hemolysis. Snake venom procoagulant factors can promote blood coagulation and microcirculation thrombosis, causing disseminated intravascular coagulation (DIC). Thrombin-like enzymes can promote fibrin monomer production and activate the fibrinolytic system, and, under the combined action of snake venom fibrinolytic enzymes, cause defibrinated blood, also known as DIC-like reaction. These hemostatic disorders are known as Venom-induced consumption coagulopathy (VICC).
Neurotoxins are mainly α-neurotoxin (α-NT) and β-neurotoxin (β-NT), acting on acetylcholine receptors in motor end plates (postsynaptic) and motor nerve endings (presynaptic), respectively. α-NT competes for choline receptors, β-NT inhibits the release of acetylcholine and then inhibits its synthesis, all of which can block nerve-muscle conduction and cause neuromuscular flaccid paralysis.
Hyaluronidase in snake venoms can depolymerize hyaluronic acid, dissolve intercellular substances, and increase tissue permeability in local tissues. In addition to local swelling and pain, it also promotes capillary absorption of snake venoms by way of lymphatic vessels and tissues, thus resulting in systemic poisoning symptoms. Proteolytic enzymes can damage blood vessels and tissues, and release a variety of vasoactive substances such as histamine, serotonin, and epinephrine. Cardiotoxins cause cytoclasis and tissue necrosis. In mild patients, local swelling and necrosis of skin and soft tissues occur, whereas in severe patients, massive necrosis in the myofascia and periosteum can occur, resulting in disability of the affected limb. Myocardiopathy and even degeneration and necrosis of myocardial cells may be present.
Signs and Symptoms
Non-venomous snake bites
Two rows of small serrated tooth marks can be seen at the bite site, accompanied by mild pain or bleeding or both. Bleeding and pain can relieve spontaneously within few minutes. There is no obvious local swelling and necrosis. Systemic symptoms are not obvious, and can be manifested by mild dizziness, nausea, palpitations, fatigue. Some patients present systemic allergic manifestations.
Venomous snake bites
Local manifestations are incessant bleeding from the bite wound, swelling of the limbs, subcutaneous hemorrhage, petechiae, hemorrhagic vesicles, vesicles, and severe pain. Systemic presentations include hemorrhage in various parts, such as nasal cavity, gums, urethra, digestive tract, and even intracranial hemorrhage; jaundice, dark brown urine during intravascular hemolysis, and acute renal failure in severe cases. If patients are accompanied by DIC, there may also be shock manifestations such as cold skin, thirst, rapid pulse, and hypotension.
Figure 1 snake bites
Early symptoms are mild, and dizziness, nausea, vomiting, salivation, blurred vision, eyelid ptosis, slurred speech, limb flaccidity, and difficulty in mouthing and swallowing occur in 1 - 4 hours after being bitten. There may be respiratory muscle paralysis, acute respiratory failure, and absence of spontaneous respiration.
There may be limb swelling, ulceration, necrosis, and secondary myocardiopathy, rhabdomyolysis, acute kidney injury, and multiple organ dysfunction syndrome (MODS).
Diagnosis is based on the chief complaints and clinical findings.
The tooth marks of non-venomous snake bites are generally arranged in two rows of arcs or shallow and densely serrated, while the tooth marks of venomous snakes are mostly like “:” and “::”.
Figure 2 tooth marks, left: venomous snakes, right: non-venomous snakes
Patients should immediately get out of the snake bite environment, do not attempt to catch or chase the snake, so as to avoid secondary bites; try to remember the characteristics of the head, body, markings, and colors of the snake, and take photos of the snake if possible; keep calm, avoid panic, and reduce the activity of the injured limb.
Bandage compression fixation can be used for neurotoxic snake bites, but excessive compression should be avoided. Patients should be quickly referred to hospital.
Wounds can be rinsed with lidocaine or procaine injection diluted with saline, and infiltration injections or annular blocking with trypsin or chymotrypsin diluted should be performed.
Snake antivenom immunoglobulins are the only therapeutic products for the treatment of snake-bite envenoming, and the dose depends on the severity. Before treatment with antivenom, a skin test is required, and if the result is positive, desensitization therapy can be used. If necessary, antiallergic drugs can be added to reduce the occurrences of anaphylactic shock.
Debridement and vacuum sealing drainage (VSD) may be required if there is anabrosis.
If there are local necrosis, purulent discharge, and abscess formation, antibiotics should be administered.