There are more than 2,700 species of snakes in the world, with more than 200 species distributed in China, under 9 families and 62 genera, including nearly 57 species of venomous snakes, including golden-ringed snakes, silver-ringed snakes, sea snakes, bamboo leaf green, branded iron head, viper, five-step snakes, cobras, king cobras, pit vipers and more than 10 species. The number of people bitten by venomous snakes worldwide is more than 300,000 each year, with a mortality rate of about 10%. People who have more chances of being bitten by poisonous snakes are farmers, field workers and workers engaged in poisonous snake breeding. Understanding the poisoning mechanism and clinical characteristics of venomous snake bites is of great clinical significance to improve the treatment of venomous snake bites and reduce the mortality rate of venomous snake bites. The venom secreted by the venomous glands in the head of venomous snakes is called snake venom (venom). The toxic components of snake venom are mainly peptides and proteins with enzymatic activity. Snake venom can have a wide range of effects on the body’s nervous system, blood system, muscle tissue, circulatory system, urinary system, endocrine system, digestive system and other organs. After absorption, snake venom is distributed to all tissues of the body, with the kidney being the most abundant and the brain the least. Snake venom is mainly decomposed in the liver and excreted by the kidneys, and the amount of snake venom in the body is extremely small after 72 hours. According to the different toxicological effects of snake venom, our country is still generally divided into three categories of neurotoxic, blood circulation venom and mixed venom for decades, which is not conducive to clinical diagnosis and treatment. According to the initiative of the International Society of Toxins and the research results of scholars from various countries, the toxins that can be isolated, know the molecular weight and structure, and have a clear and clinically relevant mechanism of poisoning are neurotoxin, blood toxin and cytotoxin. 1.1 Neurotoxin mechanism of action Neurotoxins are mainly β-neurotoxin (β-NT) and α-neurotoxin (α-NT), which act on neurosynapses and endplates respectively. β-NT inhibits acetylcholine release and α-NT competes for choline receptors, both of which can block normal nerve conduction and cause neuromuscular bradykinesia. The early clinical manifestations are eyelid drooping and dysphagia, followed by respiratory failure and even respiratory arrest due to respiratory muscle paralysis. Silver ring snake toxin is the most typical neurotoxin. 1.2 Mechanism of action of hematotoxins There are many types of hematotoxins, which act on various parts of the blood system. Snake venom protease acts directly and indirectly on the vessel wall, destroying the relevant structures of the vessel wall, inducing the release of bradykinin, histamine and 5-hydroxytryptamine, damaging capillary endothelial cells and inhibiting platelet aggregation, which can cause bleeding. The direct hemolytic factor of snake venom acts on the blood cell membrane to increase its permeability and fragility. Phospholipase A can hydrolyze lecithin in the blood and become hemolytic lecithin, producing hemolytic effects. Procoagulant factors of snake venom (e.g. factor X and V activators of viper subspecies venom) cause blood clots and microcirculatory thrombosis, resulting in disseminated intravascular coagulation (DIC). The thrombin-like enzyme in viper subfamily venom can both promote fibrin monomer production and activate the fibrinolytic system, so it has a dual role (low-dose pro-coagulation, high-dose anticoagulation); the combined effect of fibrinolytic enzymes in snake venom causes defibrinemia, also called class DIC, some domestic scholars disagree with this name, that is, DIC, in fact, the two are very different in molecular hematology. dic or class dic The common clinical manifestations of DIC are bleeding, subcutaneous bleeding, epistaxis, gingival bleeding in mild cases, and in severe cases, it can cause blood loss of coagulation, wound bleeding, hematuria, gastrointestinal bleeding, and even cerebral hemorrhage. those with DIC are often accompanied by shock, microcirculatory disorders, circulatory failure and acute renal failure, etc. 1.3 Cytotoxic mechanism of action Snake venom hyaluronidase causes local tissue hyaluronic acid depolymerization, interstitial lysis and tissue permeability increase, which can cause local swelling, pain and other symptoms, and make the snake venom toxin more easily absorbed into the blood circulation through lymphatic vessels and capillaries, resulting in systemic toxicity symptoms. Snake venom protein hydrolase can damage blood vessels and tissues, while releasing histamine, 5-hydroxytryptamine, adrenaline and other vasoactive substances. Cardiotoxin (or called membrane toxin, myotoxin, cobra amine, etc.) causes cell destruction and tissue necrosis, which can cause local swelling and skin necrosis in mild cases, and localized necrosis in heavy cases, reaching deep into the muscle periosteum and crippling the affected limbs, and can also directly cause myocardial damage and even myocardial cell degeneration and necrosis. 1.4 Other mechanisms Snake venom can cause allergic reactions when it enters the body as a heterogeneous allogeneic protein. Viruses, bacteria and other pathogenic microorganisms can enter the body through fangs and wounds to cause infection and aggravate local swelling and systemic symptoms. Under the action of various snake toxins, immune cells release inflammatory mediators causing systemic inflammatory response syndrome (SIRS) and even multiple organ dysfunction syndrome (MODS). The clinical manifestations of venomous snake bite include local manifestations of the wound and systemic symptoms of poisoning, and the severity of the symptoms of poisoning is closely related to the type of venomous snake, the amount of venom excreted, the virulence, the amount of venom absorbed, the site of the bite, the route of poisoning, and the time of consultation. 2.1 Local manifestations The bite of a venomous snake can be seen locally as two large “…” shaped fangs. shaped fangs bite marks (larger than the general non-toxic tooth marks); there are also “::” shaped, in addition to the fangs marks, there are also traces of secondary fangs, the latter indicating a deeper snake bite. The larger the venomous snake, the wider the distance between the teeth. There are two rows of neat and uniformly deep tooth marks that are mostly non-venomous snake bites. The local symptoms of neurotoxicity are not obvious, with no redness, swelling, or pain or slight pain and swelling at first, with numbness occurring soon after. Blood poisoning is painful and swollen locally. In mild cases, blood flows from the tooth marks or wounds and is difficult to coagulate, and in severe cases, it can cause the wounds to bleed. The local manifestations of cytotoxic effects include severe pain, redness, swelling, blistering, necrosis and ulceration. 2.2 Manifestations of neurotoxin poisoning: weakness of limbs, difficulty in swallowing, slurred speech, diplopia, drooping eyelids, shallow and slow breathing, suffocation, loss of pupillary reflexes to light and pooling reflexes, coma, respiratory paralysis, cessation of spontaneous breathing, and cardiac arrest. It is seen in the bite of poisonous snakes such as silver-ringed snakes and golden-ringed snakes. 2.3 Manifestations of hematotoxic poisoning Subcutaneous hemorrhagic purpura, epistaxis, gingival bleeding, and even large subcutaneous hemorrhagic bruises. Hematuria, tarry stools, and even cerebral hemorrhage. In addition to systemic bleeding when combined with DIC, there are cold skin flushing, thirst, rapid pulse, decreased blood pressure, shock, jaundice in case of intravascular hemolysis, soy sauce-like urine, and acute renal failure in severe cases. DIC-like syndrome may show prolonged coagulation time, prolonged APTT, PT, TT, decreased Fg, positive “3 P” test and FDP, decreased α2-PI activity, but not significant decrease in AT-III activity and platelets, significant decrease and positive D-dimer. DIC-like syndrome can be seen in bites of bamboo leaf green, branded iron head, five-step snake and red-necked snake. Viper and pit viper bites are often combined with DIC and even MODS. 2.4 Manifestations of cytotoxic poisoning Local swelling may extend to the affected limb or even the trunk, and necrosis and ulceration may disable the affected limb; generalized pain and SIRS may occur, and myocardial damage may lead to cardiac insufficiency, as in the case of cobra bites. Transverse muscle damage can appear as myoglobinuria combined with renal insufficiency, such as sea snake bites. 2.5 The manifestation of mixed toxin poisoning, such as king cobra bite with neurotoxin poisoning as the main manifestation, accompanied by cytotoxic poisoning; five-step snake bite with hematotoxin and cytotoxic poisoning as the main manifestation; pit viper, sea snake bite that is neurotoxin and hematotoxic poisoning as the main manifestation. 3, the diagnosis of snake bite has been confirmed as a kind of snake bite or has been captured to bite people, the diagnosis of snake bite is not difficult. However, most snake bite victims cannot see the snake’s appearance, so it is difficult to accurately determine what kind of snake bite. Immunological methods such as enzyme-linked immunosorbent assay (ELISA) can be used to determine specific snake venom antigens in body fluids such as wound exudate, serum, and cerebrospinal fluid to assist in the diagnosis, but they are not commonly used in clinical practice. Clinically, the identification of venomous snake and non-venomous snake bites is mainly based on dental marks, wound condition, and systemic symptoms. In addition, venomous snake bites need to be differentiated from centipede bites and bee stings. In order to assess the condition of venomous snake bites and guide treatment, the correct diagnosis of venomous snake bites should be made based on the clinical characteristics of the toxins contained in various venomous snakes, such as the local condition of the wound, neurotoxic symptoms, blood toxic symptoms, and cytotoxic symptoms, and to determine the light, heavy (dysfunctional phase), and critical (dysfunctional phase) types. 4 .Treatment of venomous snake bite If a snake bite cannot be ruled out with certainty, it should be observed and treated as a venomous snake bite. After being bitten by a venomous snake, on-site first aid is important, and various measures should be taken to rapidly expel the snake venom and prevent its absorption and spread. Upon arrival at the hospital, comprehensive measures should continue to be taken for treatment. Treatment principles: immediate elimination and destruction of local venom in the wound, discharge of absorbed toxin, use of antivenom as soon as possible after clarifying the type of snake, and treatment of various comorbidities.