Prepared by:-Liberatus Makenge MD4

Henry Edward MD4

Snakebites

• A snakebite is an injury caused by the bite of a snake. It often results in two puncture wounds from the animal's fangs. Sometimes poisoning from the bite may occur.

• The number of snakebites that occur each year may be as high as five million. They result in about 2.5 million poisonings and 20,000 to 125,000 deaths. The frequency of bites varies greatly among different parts of the world. They occur most commonly in Africa, Asia, and Latin America,with rural areas more greatly affected

Epidemiology

• 25% are dry bites• 25-75% of stored venom may be discharged in

a bite• Replenished in 3 to 4 weeks• Extremities are most common bite site• Most common victims:

– Intoxicated males age 15-40yrs.– Snake handlers and collectors.

• In Africa approximately 60% of all bites are caused by vipers alone. In drier regions of the continent, the saw-scaled vipers inflict up to 90% of all bites.

• The puff adder is responsible for the most fatalities overall,

• The black mamba, although responsible for far less snakebite incidents, is the species which has the highest mortality rate in Africa and in the world.

Poisonous snakes

ElapidaeCobra, Black Mamba, Kraits. Neurotoxic

Viperidae (Vipers)

Russell’s Vipers.,Saw scaled Vipers.,Pit Vipers.

Haemotoxic

Hydrophidae

Sea SnakesMyotoxic

Krait Pit Viper

Cobra

Puff Adda

BLACK MAMBA

Biochemical composition of Snake Venoms

• Dried snake venom contains mainly proteins (70-90%) and small amounts of metals, amino acids, peptides, nucleotides, carbohydrates, lipids and biogenic amines

• The protein components include enzymes and non-enzymatic proteins/polypeptides

• The main toxins in the venoms of elapid snakes (cobras, kraits and sea snakes) include: polypeptide postsynaptic neurotoxins, cardiotoxins and phospholipases A that may exhibit presynaptic neurotoxicity or myotoxicity

• The main toxins of crotalid (pit viper) snake venoms, on the other hand, are thrombin-like enzymes, hemorrhagic proteases and platelet-aggregation inducers

Effects of envenomation

• Local effects• Systemic effects:

- Neurotoxic.- Haemotoxic.- Haemotoxic.

Local effectsLocal necrosisIncreased vascular permeabilitySwelling and bruising.Myotoxins and cytotoxinsIschemia/ thrombosisVenom ophthalmia

Pit Viper Venom Poisoning(Viperidae)

• The venom of pit vipers causes local swelling, necrosis and systemic bleeding. Hemorrhage is the outstanding symptom of systemic pit viper poisoning

• Clotting defect usually accompanies hemorrhage. The commonest and earliest hemorrhagic manifestation is hemoptysis, which may be seen as early as 20 minutes after the bite

• Bleeding from the gum is less common and follows later after the bite

• Discoid ecchymoses appear in the skin an hour or so later

• Bleeding into the brain or other vital organ may be fatal.

• In severe cases, loss of blood may lead to hypovolemic shock

• In pit viper bite, the clotting defect is primarily due to thrombocytopenia aggravated by defibrination syndrome

Systemic effects

• Elapid venoms (cobras, kraits and sea snakes) generally exhibit neurotoxicity and cardiotoxicity

• The earliest symptom of systemic elapid poisoning is a feeling of drowsiness or intoxication, which starts from 15 min to 5 hr after cobra bites

• Difficulty in opening the eyes (bilateral ptosis: eyelids may remain completely closed though the patient usually remains conscious until respiratory failure is advanced), speaking, opening the mouth, moving the lips and in swallowing follows within 1 to 4 hrs

• Breathing becomes increasingly difficult. In severe poisoning, respiratory failure sets in rapidly

Neurotoxicity

Neurotoxins block transmission at the NM junctionFlaccid/Respiratory paralysisAnticholinesterase drugsUnphysiologic drowsiness

• The neurotoxic effects are mainly at the postsynaptic level of the neuromuscular junction where the neurotoxins block acetylcholine receptors, thereby producing muscular paralysis and respiratory failure

• The major neurotoxins are usually basic polypeptides

cardiotoxicity

• Cardiotoxicity is caused by polypeptide cardiotoxin that affects both excitable and non-excitable cells, causing irreversible depolarization of the cell membrane and consequently impairing the structure and function of various cells, thus contributing to muscle paralysis and leading to circulatory and respiratory failure and systolic arrest

• Cobra venom also causes extensive local necrosis, which requires treatment

• The local necrosis is presumably caused by the combine action of cardiotoxin and phospholipase A2

• Sea snake venoms contain both polypeptide neurotoxins (homologous to elapid neurotoxins) and myotoxins, which are basic phospholipase A2.

• The venom causes respiratory failure (neurotoxic effect), myonecrosis, myoglobinemia and acute renal failure

Renal failure/rhabdomyolysis

ATN: hypotension/hypovolemia, DIC, direct toxic effect on tubules, hemoglobinuria, myoglobinuria

Generalized rhabdo: Release of myoglobin, muscle enzymes, uric acid, K (presynaptic neurotoxins)

Hypotension/shock

VasodilationDirect action of venom on myocardiumBleeding/hypovolemiaVipers: profound hypotension within minutes (ACE inhibitors)

Haemotoxin effect

• Defibrination syndrome is due mainly to the action of ancrod and partly to the activation of fibrinolysis causing fibrinogenolysis.

• Ancrod is a thrombin-like enzyme that acts directly on fibrinogen, releasing only fibrinopeptide A and fibrin monomers that form microclots.

• The microclots formed are easily lysed by plasmin digestion.

• Thus, ancrod causes continual microcoagulation of fibronogen but the microclots are virtually simultaneously lysed.

• In the presence of sufficient amount of ancrod, the rate of consumption of fibrinogen may exceeed its rate of synthesis in the liver, resulting in defibrination syndrome characterized by non-clotting blood.

• Thrombocytopenia is presumably due to the actions of platelet aggregation inducers.

• Aggregoserpentin, a non-enzymatic protein with molecular weight of 28160 has been purified, it activates platelets through the activation of endogenous phospholipase A2 or C.

• Anti-platelet protease may be also be involved.

• Hemorrhage is presumably due to the action of some metalloproteases that cause damage to vascular endothelium.

• L-amino acid oxidases and platelet aggregation inhibitor may also play a role in the hemorrhagic action of the venom.

Coagulopathy

Procoagulants and anticoagulantsIntravascular coagulation, consumption coagulopahty ThrombocytopeniaBleeding from old and recent wounds, gingiva, epistaxis, hematemesis, melena

http://en.wikipedia.org/wiki/File:Epistaxis1.jpg

DIAGNOSIS OF SNAKE BITE

• FANG MARKS: classically, two puncture wounds separated by a distance varying from 8mm to 4cm, depending on the species involved.

• However a side swipe may produce only a single puncture, while multiple bites could result in numerous fang marks.

Evidence of systemic envenomation

• CT> 10 MINUTES• Bleeding manifestations• Oliguria /haematuria• Hypotension• Ptosis• Circumoral paraesthesia• Aphonia/Dysarthria

Investigations• Blood grouping• Hb, elevated PCV• TC-leucocytosis• Platelet count- thrombocytopenia• Peripheral smear – Haemolysis• BT,CT(20 min)• Prolonged PT ,aPTT• BUN• Serum Electrolytes- hyperkalemia • Urine Routine-haematuria• Metabolic /resp acidosis

General Snakebite Management• Calm and reassure the patient.• Secure and maintain airway• Do not delay treatment for any first aid/treatment measure or

wait for signs of envenomation to occur.• Obtain vital signs including O2 saturation• Oxygen to keep saturation > 90% (method as best tolerated by

patient)• Remove ALL watches, rings, and jewelry (not just from

affected limb)• If bite on extremity, immobilize affected extremity at or below

the level of the heart (make sure any immobilization device and practice does not result in becoming a tourniquet over time due to swelling)

• Mark the proximal edge of any discoloration or swelling in ink and write the time on the line (if signs increase during transport, make new marks with the times)

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ANTIVENOM• Monospecific (monovalent) antivenoms are more

effective and less likely to cause reactions than polyspecific (polyvalent) antivenoms.

• Give I/m Epinephrine or I/v chlorpheniramine if allergic reaction occurs. It rapidly reverses the uncomfortable flushing and itching as well as the more serious problem with breathing and dangerous drop in BP.

• Give monovalent if the species of snake is known. Give polyvalent antivenom if the species is not known. Follow the directions given on the antivenom preparation. The dose for children is the same as for adults.

Anti snake venom (Asv)

How to give asv ?

• Initial dose: 4-6 vials, dependent upon patient response. Treatment should begin within 6 hours of snakebite; monitor for 1 hour following infusion. Repeat with an additional 4-6 vials if control is not achieved with initial dose. Continue to treat with 4-6 vial doses until complete arrest of local manifestations, coagulation tests and systemic signs are normal. Monitor closely.

.Maintenance dose: • Once control is achieved, administer 2 vials

every 6 hours for up to 18 hours. Optimal dosing past 18 hours has not been established; however, treatment may be continued if deemed necessary based on the patient’s condition.

• Administer I.V. over 60 minutes at a rate of 25-50 mL/hour for the first 10 minutes. If no allergic reaction is observed, increase rate to 250 mL/hour. Monitor closely.

Antivenom reactions

OTHER TREATMENT

• Surgical opinion

Seek surgical opinion if there is severe swelling in a limb, if it has palsy or painful or there is local necrosis.

Surgical care will include:-

• Excision of diced tissue from wound• Incision of facial membranes to relieve

pressure in limb compartments if necessary.• Skin grafting, If extensive necrosis.• Tracheotomy (or endotracheal intubation)if

paralysis of muscles involved in swallowing occur.

Monitoring

• Level of consiousness• Pulse, BP, Resp rate,Capillary refill time• Clotting time 1/2hr -1hourly• Urine output• Muscle weakness

Supportive care• Give fluid orally or by NGT tube according to daily requirements.

keep a close record of fluid intake and output.• Provide adequate pain relief• Elevate limb if swollen.• Give anti-tetanus prophylaxis.• Antibiotic treatment is not required unless there is tissue necrosis

at wound site.• Avoid intramuscular injection.• Monitor very closely immediately after admission then hourly for

at least 24hrs.

Initiate immediate supportive care:

Secure & maintain airway Prepare for immediate transport (do not delay transport for any first aid/treatment

measures or wait for signs of envenomation to occur) Calm and reassure the patient Obtain vital signs including O2 saturation O2 to keep saturation >90% (method as best tolerated by patient) Do NOT apply any constricting bands, ice or apply suction to the bite (if

constricting band is in place upon EMS arrival, contact Medical Direction)

Use standing order on patients with complaints of a snake bite or signs/symptoms of envenomation:

Local edema, redness, pain, burning sensation, numbness/tingling, vomiting, weakness and/or hypotension

Remove ALL watches, rings, and jewelry Not just from affected limb

If bite on extremity, immobilize affected extremity at or below the heart level. Make sure any immobilization device and practice does not result in becoming a tourniquet over time due to swelling.

Mark the proximal edge of any discoloration or swelling in ink and write the time on the line. If signs increase during transport, make new marks with the times.

Initiate IV Normal Saline in unaffected extremity to maintain adequate peripheral perfusion:

o 20cc/kg bolus o Reassess patient after each

bolus Contact Medical Direction for any

questions, signs/symptoms of allergic reaction, or deterioration in patient condition.

SNAKE BITE STANDING ORDER

I N C LUSI O N

O R D E R S

Special Notes:

1.) There is no need to bring the snake to the hospital. This practice actually increases the risk of secondary bites and can delay transport. In Arizona all rattle snakes use the same antivenin. There is no antivenin for Arizona coral snakes. 2.) Clinical effects of snakebites range from mild local reactions to life-threatening systemic reactions, depending on the species and size of the snake involved; the location of the bite(s); the volume of venom injected; and the age, size, and health of the victim. Children are more likely to suffer significant morbidity and mortality because they receive a larger envenomation relative to body size.

Remember

• Do NOT use ice or cold packs. It does not slow the enzyme activity. It slows the immune-response.

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• DO NOT use tourniquets or restricting bands. All you do is localize all those digestive enzymes.

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• DO NOT lance, or use cut and suck methods. Snakebite is an IM injection. The venom isn’t going to be sucked out. Cutting increases tissue damage to an area already infiltrated with digestive enzymes.

Thank you!