Snake Bite Presented by : Abdulaziz Alshaikh Supervised by: Dr.Adel Altamimi

O Snake bite is a well-known occupational hazard amongst farmers, plantation workers, and other outdoor workers and results in much morbidity and mortality throughout the world. O It account for approximately 125,000 deaths annually worldwide. O Out of the available yearly statistics, the United States alone had 50,000 cases of bites, of which 7000 were by venomous snakes. Interestingly, of those 7,000 snakebite victims, 1,200 did not seek medical attention and yet they fully recovered. In all, there were 15 fatalities and thus the chance of survival is 499 out of 500.

O To a large extent the manifestation of snakebite depends upon the species of snake, and therefore identification of the type of snake is important. At times the bite mark might not be visible (e.g., in the case of krait). The killed snake brought as evidence helps in identification of snake, in which case species- specific monovalent Anti snake venom (ASV) can be administered. O The three major families of venomous snakes are the Elapidae, the Viperidae, and the Hydrophidae

O Elapidae (cobra, king cobra, krait, and coral snake): These snakes have heads that are of about the same width as their necks. The head is covered with large scales but lack laureal shields. Their pupils are round and they are oviparous. These snakes have grooved fangs that are short, fixed, and covered by mucous membrane. They, therefore, cannot bite through clothes and usually deliver only a sublethal dose.

COBRA

King Cobra

Krait Snake

O Viperidae (vipers): The head of a viper is triangular, wider than the neck, and has laureal shields. They have vertically elliptical pupils and are ovi-viviparous. Their fangs are long, movable, and canalized like hypodermic needles. They are further subdivided into pit viper and pitless viper subfamilies. The Crotalinae (pit vipers) have a special sense organ, the pit organ, to detect their warm- blooded prey. This is situated between the nostril and the eye. The rattlesnake belongs to the pit viper subfamily, while the Russell's viper and the saw-scaled viper belong to the pitless viper subfamily.

Russell’s viper

Crotalidae

O Snake venom

O The normal function of snake venom is to immobilize the prey and to assist in digestion. O Phospholipase A2 is present in the venom of all families of poisonous snakes and is the enzyme that has been most widely studied. Phospholipase A2 inhibits electron transfer at cytochrome C level and renders mitochondrial- bound enzymes soluble. It damages red blood cells, leukocytes, platelets, skeletal muscle, vascular endothelium, peripheral nerve endings, and the myoneural junction

O Hyaluronidase helps spread of venom through tissues, and proteolytic enzymes are responsible for the local edema, blistering, and necrosis O α - Neurotoxins bind to acetylcholine receptors at the motor end-plate, whereas β - neurotoxins first cause release of acetylcholine at the nerve endings at the myoneural junction and then damage the endings, preventing further release of transmitter.[3] All this leads to a flaccid paralysis of the victim3

O Management

FIELD MANAGEMENT Initial first aid of envenomation is directed at reducing the spread of venom and expediting transfer to an appropriate medical center. General principles : O The patient should be removed from the snake's territory, kept warm and at rest, and be reassured. O The injured part of the body should be immobilized in a functional position below the level of the heart. O The wound should be cleansed, except in areas in which a venom detection kit is used (ie, Australia). O Withhold alcohol and drugs that may confound clinical assessment. O Attempt to identify the snake, without endangering the patient or rescuer. A digital photo taken at a safe distance may be useful. Snake parts should not be handled directly. The bite reflex may remain intact in recently killed snakes, possibly being able to inflict a bite. O Transport the patient to the nearest medical facility as quickly as possible.

Pressure immobilization : O The pressure immobilization technique to delay systemic absorption of snake venom has widespread use in Australia, where elapid toxin primarily causes neurotoxicity without tissue necrosis and where there may be significant delays in transfer to medical facilities. O However, the value of pressure immobilization against venoms is unproven. Some venoms, such as cobra and viper venom, primarily produce local necrosis; in this setting, localization of toxin may worsen the syndrome. Other potential problems with this technique include the availability of suitable materials and difficulty in determining the appropriate pressure to apply. If the compression bandage is too loose, it will fail to work, and if too tight, it may obstruct arterial flow.

Hospital treatment O When the patient reaches the emergency department, evaluation should begin with the assessment of the airway, breathing, circulatory status, and consciousness. O Urgent resuscitation will be needed in those in shock (cardiovascular toxicity), those with respiratory failure (neurotoxin), and in those who have had cardiac arrest (due to hypoxia, cardiac toxicity, or hyperkalemia from rhabdomyolysis). O A significant proportion of snake bites do not result in envenomation; thus, patients without clinical features of local or systemic envenomation should be closely observed before discharge from medical attention.

O Some people who are bitten by snakes may develop quite striking symptoms and signs, even when no venom has been injected. O Anxious people may hyperventilate so that they develop pins-and-needles sensation in the extremities, spasm of their hands and feet, and dizziness. O The first clinical indications of systemic envenomation are often nonspecific symptoms such as nausea, vomiting, abdominal pain, and headache. O The effects of snake venom can be divided into distinct syndromes, which may vary in severity depending upon the species of snake

O Evaluation of the bite:

Physical examination: O Clues for severe snake envenomation should be sought. They consist of the following: O Snake identified is a very venomous one O Rapid early extension of local swelling from the site of the bite O Early tender enlargement of local lymph nodes, indicating spread of venom in the lymphatic system O Early systemic symptoms O Early spontaneous systemic bleeding (especially bleeding from the gums) O Passage of dark brown urine

Neurotoxicity : O Venoms of the elapids of the Australia-Pacific region are associated with severe neurotoxicity. Neurotoxicity is characterized initially by ptosis, diplopia, and bulbar palsy with onset between 1 to 10 hours following envenomation. Symptoms can later progress to dysarthria and more generalized weakness. As a result, frequent, serial observations for ptosis, diplopia, and impaired swallowing function are of paramount importance. Ventilatory support may be required for airway protection or respiratory paralysis.

Coagulopathy: O Venom may be either a procoagulant or an anticoagulant, but both produce similar coagulation disorders rapidly. Signs of overt bleeding should be sought following a snake bite. Low-grade bleeding from gums and epistaxis are common. O It is not possible to correct coagulation defects without sufficient antivenom; as a result, persisting bleeding should prompt the administration of additional antivenom. O Clotting factor replacement with whole blood or fresh frozen plasma is only indicated in cases of life-threatening hemorrhage after the use of antivenom

The 20-min whole blood clotting test (20 WBCT): O The 20 WBCT is a simple bedside test of coagulopathy to diagnose viper envenomation and rule out elapid bite. It requires a new clean, dry test tube made up of simple glass that has not been washed with any detergent. A few milliliters of fresh venous blood is drawn and left undisturbed in the test tube for 20 min; the tube is then tilted gently. If the blood is still liquid after 20 min, it is evidence of coagulopathy and confirms that the patient has been bitten by a viper. Cobras or kraits do not cause antihemostatic symptoms.

Hypotension and shock : O Hypotension and shock may result from a snake bite. The mechanisms for these findings include: vasodilation, a direct action of venom on the myocardium, and/or hypovolemia due to bleeding. Following a snake bite, assessment of fluid status clinically, or where available, with central monitoring is important.

Rhabdomyolysis : O The presence of muscle pain, weakness, and dark urine is suggestive that massive rhabdomyolysis has occurred. Creatine kinase and electrolytes, particularly hyperkalemia, should be followed serially, and the presence of myoglobinuria should be documented. Urine dipstick tests for the presence of blood detect both myoglobin and hemoglobin (as well as hematuria) and positive results are suggestive of significant rhabdomyolysis. O Plasma volume expansion with intravenous isotonic saline should be given as soon as possible.

Renal failure O Renal failure following a snake bite may be multifactorial resulting from hypotension, rhabdomyolysis and/or disseminated intravascular coagulation. O In a prospective observational study of 100 patients envenomed with Crotalus durissus, 29 patients developed acute renal failure (ARF) due to rhabdomyolysis. O Independent risk factors for ARF included age less than 12 years. a delay in antivenom therapy of >2 hours and a creatinine kinase at admission >2000 U/L. O In contrast, diuresis at admission >90 mL per hour was protective.

Cobra spit ophthalmia : O The venom of the spitting cobras (Naja spp.) found in Asia and Africa can cause corneal damage if introduced into the eye. Acutely, the eye should be irrigated with copious quantities of water or saline. Slit lamp examination and fluorescein staining should be performed to confirm corneal ulceration; topical antibiotic ointment should be applied if this is present. The instillation of diluted antivenom is not recommended

O Anti–snake venom

O Anti–snake venom (ASV) are immunoglobulins prepared by immunizing horses with the venom of poisonous snakes and subsequently extracting and purifying the horses' serum. O They are the only effective antidote for snake venom. O Antivenoms may be species specific (monovalent/monospecific) or may be effective against several species (polyvalent/polyspecific)

Indications for ASV: O The use of antivenom depends upon availability and the risk-benefit ratio; thus, this is a clinical decision, which must be made for each patient on an individual basis. O Any decision to use antivenom must take into account the association of most antivenoms with a high incidence of allergic reactions. Antivenoms are generally indicated when: O There is evidence of systemic envenomation (neurotoxicity, coagulopathy, rhabdomyolysis, persistent hypotension, and/or renal failure). O There is severe local envenomation, manifested by local tissue destruction.

Dose of ASV:

ASV administration: O ASV can be administered either by slow intravenous injection at a rate of 2 ml/min or by intravenous infusion (antivenom diluted in 5–10 ml per kilogram body weight of normal saline or D 5 W and infused over 1 h). O All patients should be strictly observed for an hour for development of any anaphylactic reaction. O Epinephrine should always be kept ready before administration of antivenom. O ASV sensitivity testing is no longer recommended as a lack of response does not predict the large majority of early (anaphylactic) or late (serum sickness type) reactions.

Adverse reactions: O Early anaphylactic reactions occurs within 10–180 min of start of therapy and is characterized by itching, urticaria, dry cough, nausea and vomiting, abdominal colic, diarrhea, tachycardia, and fever. Some patients may develop severe life-threatening anaphylaxis characterized by hypotension, bronchospasm, and angioedema. O When the patient shows signs of a reaction, antivenom administration must be temporarily stopped and adrenaline (1 in 1000) given intramuscularly in an initial dose of 0.5 mg in adults or 0.01 mg/kg body weight in children. O The dose can be repeated every 5–10 min if necessary.

O Late (serum sickness–type) reactions develop 1–12 (mean 7) days after treatment. Clinical features include fever, nausea, vomiting, diarrhea, itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy, immune complex nephritis and, rarely, encephalopathy. O Late (serum sickness–type) reactions usually respond to a 5-day course of oral antihistamine. O Patients who fail to respond within 24–48 h should be given a 5-day course of prednisolone.

Failure to respond: O Failure of response to antivenom may be due to the wrong monovalent antivenom, insufficient antivenom, inactive antivenom or an excessive delay in administration after envenomation. O Expired antivenom, sometimes used by veterinarians, may retain its potency for some time following its use-by date. O The risk-benefit ratio may still support its use if no "in date" antivenom is available.

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