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Snake bite management
Subodh Gyawali
MD Resident, first year
Internal medicine
Snake bite
• Potentially life-threatening disease caused
• by toxins in the bite of a venomous snake.
• by having venom sprayed into the eyes by some species.
• Occupational hazard affecting farmers, plantation workers, herders and
fishermen.
• Neglected tropical disease.
Epidemiology
• Out of more than 3000 species of snakes in the world, some 600 are
venomous and over 200 are considered to be medically important.
• According to the World Health Organization,
• more than 5 million snakebites occur worldwide each year
• approximately 2.5 million envenomations and
• 81,000 to 138,000 deaths
• In Nepal, WHO estimates that 20,000 people are bitten by snakes each year,
resulting in over 1000 deaths
• So far, 89 snake species have been recorded in Nepal .
• Among this great diversity of snakes, we know with certainty of 17 species
of snake that are found in Nepal.
• Not all bites by venomous snakes are accompanied by the injection of
venom.
• Approximately 20% of pit viper bites and higher percentages of other
snakebites (up to 75% for sea snakes) are “dry” bites; i.e., no venom is
released.
• Significant envenomation probably occurs in ~50% of all venomous
snakebites.
Venoms
• Complex chemical mixture of enzymes, polypeptides, non-enzymatic proteins,
nucleotides, and other substances
• Neurotoxins-
• Phospholipase A2 (PLA2) toxins (mostly beta-neurotoxins).
• Postsynaptic neurotoxins (alpha-neurotoxins).
• Hematotoxins- factor V activators, factor X activators, prothrombin activators, and
thrombin-like enzymes or fibrinogenase.
• Cytotoxins- phosphodiesterases, hyaluronidases, peptidases, metalloproteinases etc.
ASK
• Where were you bitten?
• What were you doing/ when were you bitten?
• Did anyone take the picture? What did it look like?
• How the bite occurred and whether there was more than one bite?
• Any signs or symptoms and the timing of onset?
• Initial treatment and first aid that was provided, including timing of first aid
Local effects
• Bite marks:
• Single puncture, dual puncture or marks of multiple tooth marks, only
scratch mark.
• Krait bite may leave no mark at all.
• Site : arm or lower limb , may occur in trunk or other parts also.
Local effects
Cobra
• Swelling and local pain
with or without erythema
or discoloration at the bite
site.
• Blistering, bullae
formation and local
necrosis are also common.
• If it is infected, there may
be abscess formation.
Krait
• Usually do not cause signs
of local envenoming and
can be virtually painless.
Viper
• Swelling, blistering,
bleeding, and necrosis at
the bite site, sometimes
extending to the whole
limb.
• Persistent bleeding from
fang marks, wounds or
any injured parts of the
body.
• Swelling or tenderness of
regional lymph node.
Systemic manifestations
General manifestations
• Nausea,
• Vomiting
• Pain abdomen
• Malaise
• Weakness
• Drowsiness
• Prostration
• Anxiety
• Excessive salivation, etc.
Systemic manifestations
Hematotoxic
• Bleeding may from
venipuncture site, gums,
• Epistaxis
• Hemoptysis
• Melena, rectal bleeding
• Hematuria, bleeding from
vagina
• Subconjunctival
hemorrhage
• Petechiae, purpura,
ecchymosis
Neurotoxic
• Ptosis
• Ophthalmoplegia
• Pupillary dilatation- often
non- responsive to light
• Inability (or limitation) to
open mouth
• Numbness around lips and
mouths
Neurotoxic
• Tongue extrusion- inability
to protrude the tongue
beyond incisors teeth.
• Inability to swallow
• Broken neck sign
• Skeletal muscle weakness.
• Loss of gag reflex
• Paradoxical breathing
• Respiratory failure
LONG TERM COMPLICATIONS (SEQUELAE)
• Chronic ulceration, infection, osteomyelitis or arthritis
• Physical disability
• Chronic kidney disease due to bilateral renal cortical necrosis
• Chronic pan-hypopituitarism may occur in Russell’s viper envenoming
• Sequelae of intracranial bleeding in hematotoxic envenoming
• Delayed psychological morbidity like depression and anxiety, impaired
functioning, post-traumatic stress disorder
Diagnosis
• No investigations available that can
help diagnose the neurotoxic
manifestations
Neurotoxic
Diagnosis
Hematotoxic
•20-minute whole blood clotting test (20WBCT)
•Bleeding time (BT) and clotting time (CT)
•Prothrombin time and International normalization ratio (INR)
•FDP, fibrinogen, d-dimer
•Kidney function test and liver function test
•Complete blood count, blood group
•Urine for RBCs or myoglobin
•Creatine kinase
20 WBCT
• Place 3 ml of freshly sampled venous blood in a small, new, dry, glass tube.
• Leave the tube standing undisturbed for 20 minutes at ambient temperature.
• A positive 20WBCT is a reasonable indication for antivenom administration,
but a negative 20WBCT does not mean that antivenom should be withheld,
especially if other clinical findings of coagulopathy (eg, blood oozing at
puncture sites, bleeding gums, or epistaxis) are present.
SYNDROME FEATURES
SYNDROME 1 Local swelling or other features of local envenoming with paralysis with NO features of
bleeding or clotting disturbances.
COBRA or KING COBRA
SYNDROME 2 Nocturnal bite while sleeping on ground and paralysis with NO/or minimal local sign of
envenoming.
KRAIT
SYNDROME 3 Neurotoxicity with dark brown urine, severe muscle pain, without local swelling, bleeding or
clotting disturbances and with or without renal failure. Bitten on land while sleeping indoors.
KRAIT (B. niger)
SYNDROME 4 Marked swelling (sometime with blisters and necrosis) with incoagulable blood and /or
spontaneous systemic bleeding. RUSSELL’S VIPER (Daboia russelii)
SYNDROME 5 Marked swelling on bitten limb/part often with blisters (sometime with severe pain) without
bleeding or clotting disturbances. PITVIPERS (Ovophis monticola, Trimeresurus sp.: T.
albolabris, and T. popeiorum).
TREATMENT OF SNAKEBITE ENVENOMING
• First aid treatment and transport to the hospital
• Rapid clinical assessment and resuscitation
• Antivenom treatment
• Supportive/ancillary treatment
• Treatment of the bitten part
Recommended first aid treatment
REASSURANCE
• Most are nonvenomous snakes. Many are dry bites.
• Treatable condition.
IMMOBILIZAT
ION
• With a splint or sling.
• Pressure immobilization in case of purely neurotoxic snake bite
• Pressure pad immobilization
• Remove rings, jewelries, tight fittings and clothing
RAPID
TRANSPORT
• To decrease the delay in accessing the emergency care and reduce mortility
CAUTION
• Tight arterial tourniquet must never be recommended
• Delay the release of tight tourniquets if patient has already applied this popular
method of first-aid
• These practices must be discouraged
• Cutting and sucking of bite site.
• Application of snake stone (Jharmauro).
• Application of electric current.
• Application of various chemicals, cow dung etc
Rapid clinical assessment and resuscitation
• Airway
• Breathing
• Circulation
• Disability of the nervous system
• Exposure and environmental control
Antivenom treatment
• Phisalix and Bertrand and Calmette simultaneously, but independently,
presented their observations in the year 1894 on the antitoxic properties of
the serum of rabbits and guinea-pigs immunized against cobra and viper
venoms, respectively.
• The first horse-derived antivenom sera that he prepared were already in
clinical use in 1895 by Haffkine in India and by Lépinay in Viet Nam. The
latter reported the first successful use of antivenin serum therapy in patients
in 1896.
Antivenom in Nepal
• Imported from India and is polyvalent.
• Effective against the four common species of snakes;
• Russell's Viper (Daboia russelii),
• Common Cobra (Naja naja),
• Common Krait (Bungarus caeruleus) and
• Saw Scaled Viper (Echis carinatus).
Indications for administering antivenom
Evidence of Neurotoxicity Ptosis, ophthalmoplegia, broken neck sign, respiratory difficulty, etc.
Evidence of Coagulopathy Evidence of coagulopathy primarily detected by 20 WBCT or visible
spontaneous systemic bleeding, bleeding gums, etc., including
myoglobinuria and hemoglobinuria, deranged PT/INR, etc
Rapid extension of local swelling (more than half of limb) which is not due
to tight tourniquet application.
Evidence of Cardiovascular
Collapse
Shock and hypotension (in case of Russell’s viper bite).
Evidence Of Acute Kidney Injury AKI is an indication for antivenom therapy.
Contradications
• No absolute contraindication to antivenom treatment,
• But patients who have reacted to horse (equine) or sheep (ovine) serum in
the past (for example after treatment with equine anti-tetanus serum, equine
anti-rabies serum or equine or bovine antivenom) and those with a strong
history of atopic diseases (especially severe asthma) are at high risk of severe
reactions and
• Should therefore be given antivenom only if they have signs of systemic
envenoming.
How long after the bite can antivenom be
expected to be effective?
• Antivenom treatment should be given as soon as it is indicated.
• It may reverse systemic envenoming even when this has persisted for several
days or, in the case of haemostatic abnormalities, for two or more weeks.
Route of administration
• Each vial is diluted with 10 ml. of sterile water as supplied with the antivenom.
• Randomized, controlled, double-blind trial in Nepal (Damak & Charali
snakebite treatment centres and Bharatpur Hospital)
• To compare the efficacy of a ten vials initial dose versus a two vials initial
dose of Polyvalent Anti-Snake Venom Serum in the treatment of snake bite
• Result : Similar efficacy and safety of low vs high initial dose regimen of
anti-venom in patients with neurotoxic envenoming in Nepal .Recovery is
faster with high initial dose
Response to treatment
• General symptoms may disappear vary quickly.
• Spontaneous systemic bleeding usually stops within 15-30 min.
• Blood pressure may increase within 30-60 min.
• Neurotoxicity may improve as early as 30 min.
• Blood coagulability is usually restored in 3-9 hrs.
Reasons for failure to respond to antivenom
• Excessive delay in administration of antivenom
• Patient with established respiratory failure.
• If antivenom administered does not contain neutralizing antibodies against
the venom of biting species.
• Insufficient dose of antivenom.
• Inactive or poor quality antivenom.
Prophylactic adrenaline
• Prophylactic adrenaline should be routinely used before initiation of anti-
venom treatment to prevent anti-venom reaction except in older patients
with evidence or suspicion of underlying ischemic heart disease or
cerebrovascular disease.
Antivenom reactions
• within 3 hours of antivenom initiation.
• itching, urticaria, fever, angio-edema, dyspnea, laryngeal edema,
hypotension etc. .
Early
anaphylactic
reactions
• Usually develops 1-2 hrs. after treatment initiation.
• Chills, rigors, fever, fall of blood pressure, febrile convulsion may
develop in children.
Pyrogenic
reaction
• May develop 1- 12 (mean 7) days after treatment.
• Fever, itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy,
proteinuria etc.
Late reaction
(serum
sickness type)
Treatment of Early Anaphylaxis
Reaction/Anaphylaxis
• INTERRUPT antivenom
• IM adrenaline
• IV chlorpheniramine
• IV fluids
• Oxygen
• IV hydrocortisone
• Nebulized salbutamol
IF ANTIVENOM HAS TO BE RESTARTED
• Consider transfer to ICU.
• Continue IV hydrocortisone.
• IV adrenaline infusion will be required and should be started before giving
antivenom.
• Stop infusion 30 minutes after resolution of all symptoms and signs.
Treatment
Pyrogenic reaction
• Do not interrupt antivenom
unless hypotension is present.
• Give injection paracetamol.
• Treat hypotension with rapid
infusion of normal saline.
Serum sickness
• Anti-histaminic Pheniramine
maleate
• If no response to
antihistaminic Prednisolone
SUPPORTIVE/ANCILLARY TREATMENT
• Fluid resuscitation
• Oxygen
• Intubation and ventilation
• Dialysis
• Fasciotomies
When antivenom is not available or not effective
• Neostigmine: 0.5 mg SC/IV/IM (0.02mg/kg). Repeat 4 hourly until
neurotoxicity improves (maximum 10 mg/24hrs)/ Edrophonium
• Atropine: 0.6mg IV / Glycopyrolate
• FFP and cryoprecipitate or whole blood
TREATMENT OF THE BITTEN PART
• Elevation of limb with rest.
• Simple washing with antiseptic solution like chlorhexidine, povidone iodine
etc.
• Broad-spectrum antibiotic if features of infection.
• In case of local necrosis and gangrene: Surgical debridement.
• Tetanus toxoid IM injection should be given. If patient presents with
coagulopathy, it should be postponed until after resolution of coagulopathy.
Recent advances
• A 2016 study by Lewin et al. demonstrated that nanomolar and picomolar
concentrations of varespladib effectively inhibit the phospholipase A2 (PLA2)
activities of selected snake venoms from various continents.
• In 2019, the U.S. Food and Drug Administration (FDA) granted
varespladib orphan drug status for its potential to treat snakebite.
• Other examples of promising small molecule inhibitors include the matrix
metalloproteinase inhibitors batimastat and marimastat. The molecules prolonged
survival, but did not provide full protection.
• In the field of recombinant antivenoms, attention to the use of camelid VHHs (also
known as nanobodies) as therapeutic agents has increased.
ADDovenom: Novel Snakebite Therapy Platform of
Unparalleled Efficacy, Safety and Affordability
• Based on a new disruptive protein-based
nanoscaffold called ADDomer – a megadalton-
sized, thermostable synthetic virus-like particle
with 60 high-affinity binding sites to neutralise
and eliminate venom toxins from the
bloodstream.
PREVENTION OF SNAKEBITE
• Community based education.
• Keep household clean by cutting grasses, bushes, and plants, remove heaps of
rubbish, building materials etc. from near and around house.
• Bamboo, wood piles should be removed from household so that snake cannot hide.
• Close door, windows properly.
• Try to avoid sleeping on floor. If it is unavoidable, then mosquito net should be
used and tucked well under the mattress or sleeping mat. It not only prevents from
krait bite but also from mosquito bite.
• Keep your granary away from the house, it may attract rodents that snakes will hunt
PREVENTION OF SNAKEBITE
• Use high shoes or boots while walking in paddy field, bushes, long grasses.
• In dark, use light or strike the path using stick.
• Never play with snakes, or irritate them even if they are dead. Never provoke them,
they usually do not bite if not irritated or provoked.
• Never insert hands into long grasses, tree holes or mud holes. Take care while
pulling straw.
• Shoes and cloths should be check before wearing, in an area where snakes are
abundant.
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Snake bite management.pptx

  • 1. Snake bite management Subodh Gyawali MD Resident, first year Internal medicine
  • 2. Snake bite • Potentially life-threatening disease caused • by toxins in the bite of a venomous snake. • by having venom sprayed into the eyes by some species. • Occupational hazard affecting farmers, plantation workers, herders and fishermen. • Neglected tropical disease.
  • 3. Epidemiology • Out of more than 3000 species of snakes in the world, some 600 are venomous and over 200 are considered to be medically important. • According to the World Health Organization, • more than 5 million snakebites occur worldwide each year • approximately 2.5 million envenomations and • 81,000 to 138,000 deaths
  • 4. • In Nepal, WHO estimates that 20,000 people are bitten by snakes each year, resulting in over 1000 deaths • So far, 89 snake species have been recorded in Nepal . • Among this great diversity of snakes, we know with certainty of 17 species of snake that are found in Nepal.
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  • 9. • Not all bites by venomous snakes are accompanied by the injection of venom. • Approximately 20% of pit viper bites and higher percentages of other snakebites (up to 75% for sea snakes) are “dry” bites; i.e., no venom is released. • Significant envenomation probably occurs in ~50% of all venomous snakebites.
  • 10. Venoms • Complex chemical mixture of enzymes, polypeptides, non-enzymatic proteins, nucleotides, and other substances • Neurotoxins- • Phospholipase A2 (PLA2) toxins (mostly beta-neurotoxins). • Postsynaptic neurotoxins (alpha-neurotoxins). • Hematotoxins- factor V activators, factor X activators, prothrombin activators, and thrombin-like enzymes or fibrinogenase. • Cytotoxins- phosphodiesterases, hyaluronidases, peptidases, metalloproteinases etc.
  • 11.
  • 12. ASK • Where were you bitten? • What were you doing/ when were you bitten? • Did anyone take the picture? What did it look like? • How the bite occurred and whether there was more than one bite? • Any signs or symptoms and the timing of onset? • Initial treatment and first aid that was provided, including timing of first aid
  • 13. Local effects • Bite marks: • Single puncture, dual puncture or marks of multiple tooth marks, only scratch mark. • Krait bite may leave no mark at all. • Site : arm or lower limb , may occur in trunk or other parts also.
  • 14. Local effects Cobra • Swelling and local pain with or without erythema or discoloration at the bite site. • Blistering, bullae formation and local necrosis are also common. • If it is infected, there may be abscess formation. Krait • Usually do not cause signs of local envenoming and can be virtually painless. Viper • Swelling, blistering, bleeding, and necrosis at the bite site, sometimes extending to the whole limb. • Persistent bleeding from fang marks, wounds or any injured parts of the body. • Swelling or tenderness of regional lymph node.
  • 15. Systemic manifestations General manifestations • Nausea, • Vomiting • Pain abdomen • Malaise • Weakness • Drowsiness • Prostration • Anxiety • Excessive salivation, etc.
  • 16. Systemic manifestations Hematotoxic • Bleeding may from venipuncture site, gums, • Epistaxis • Hemoptysis • Melena, rectal bleeding • Hematuria, bleeding from vagina • Subconjunctival hemorrhage • Petechiae, purpura, ecchymosis Neurotoxic • Ptosis • Ophthalmoplegia • Pupillary dilatation- often non- responsive to light • Inability (or limitation) to open mouth • Numbness around lips and mouths Neurotoxic • Tongue extrusion- inability to protrude the tongue beyond incisors teeth. • Inability to swallow • Broken neck sign • Skeletal muscle weakness. • Loss of gag reflex • Paradoxical breathing • Respiratory failure
  • 17. LONG TERM COMPLICATIONS (SEQUELAE) • Chronic ulceration, infection, osteomyelitis or arthritis • Physical disability • Chronic kidney disease due to bilateral renal cortical necrosis • Chronic pan-hypopituitarism may occur in Russell’s viper envenoming • Sequelae of intracranial bleeding in hematotoxic envenoming • Delayed psychological morbidity like depression and anxiety, impaired functioning, post-traumatic stress disorder
  • 18. Diagnosis • No investigations available that can help diagnose the neurotoxic manifestations Neurotoxic
  • 19. Diagnosis Hematotoxic •20-minute whole blood clotting test (20WBCT) •Bleeding time (BT) and clotting time (CT) •Prothrombin time and International normalization ratio (INR) •FDP, fibrinogen, d-dimer •Kidney function test and liver function test •Complete blood count, blood group •Urine for RBCs or myoglobin •Creatine kinase
  • 20. 20 WBCT • Place 3 ml of freshly sampled venous blood in a small, new, dry, glass tube. • Leave the tube standing undisturbed for 20 minutes at ambient temperature. • A positive 20WBCT is a reasonable indication for antivenom administration, but a negative 20WBCT does not mean that antivenom should be withheld, especially if other clinical findings of coagulopathy (eg, blood oozing at puncture sites, bleeding gums, or epistaxis) are present.
  • 21. SYNDROME FEATURES SYNDROME 1 Local swelling or other features of local envenoming with paralysis with NO features of bleeding or clotting disturbances. COBRA or KING COBRA SYNDROME 2 Nocturnal bite while sleeping on ground and paralysis with NO/or minimal local sign of envenoming. KRAIT SYNDROME 3 Neurotoxicity with dark brown urine, severe muscle pain, without local swelling, bleeding or clotting disturbances and with or without renal failure. Bitten on land while sleeping indoors. KRAIT (B. niger) SYNDROME 4 Marked swelling (sometime with blisters and necrosis) with incoagulable blood and /or spontaneous systemic bleeding. RUSSELL’S VIPER (Daboia russelii) SYNDROME 5 Marked swelling on bitten limb/part often with blisters (sometime with severe pain) without bleeding or clotting disturbances. PITVIPERS (Ovophis monticola, Trimeresurus sp.: T. albolabris, and T. popeiorum).
  • 22. TREATMENT OF SNAKEBITE ENVENOMING • First aid treatment and transport to the hospital • Rapid clinical assessment and resuscitation • Antivenom treatment • Supportive/ancillary treatment • Treatment of the bitten part
  • 23. Recommended first aid treatment REASSURANCE • Most are nonvenomous snakes. Many are dry bites. • Treatable condition. IMMOBILIZAT ION • With a splint or sling. • Pressure immobilization in case of purely neurotoxic snake bite • Pressure pad immobilization • Remove rings, jewelries, tight fittings and clothing RAPID TRANSPORT • To decrease the delay in accessing the emergency care and reduce mortility
  • 24. CAUTION • Tight arterial tourniquet must never be recommended • Delay the release of tight tourniquets if patient has already applied this popular method of first-aid • These practices must be discouraged • Cutting and sucking of bite site. • Application of snake stone (Jharmauro). • Application of electric current. • Application of various chemicals, cow dung etc
  • 25. Rapid clinical assessment and resuscitation • Airway • Breathing • Circulation • Disability of the nervous system • Exposure and environmental control
  • 26. Antivenom treatment • Phisalix and Bertrand and Calmette simultaneously, but independently, presented their observations in the year 1894 on the antitoxic properties of the serum of rabbits and guinea-pigs immunized against cobra and viper venoms, respectively. • The first horse-derived antivenom sera that he prepared were already in clinical use in 1895 by Haffkine in India and by Lépinay in Viet Nam. The latter reported the first successful use of antivenin serum therapy in patients in 1896.
  • 27. Antivenom in Nepal • Imported from India and is polyvalent. • Effective against the four common species of snakes; • Russell's Viper (Daboia russelii), • Common Cobra (Naja naja), • Common Krait (Bungarus caeruleus) and • Saw Scaled Viper (Echis carinatus).
  • 28. Indications for administering antivenom Evidence of Neurotoxicity Ptosis, ophthalmoplegia, broken neck sign, respiratory difficulty, etc. Evidence of Coagulopathy Evidence of coagulopathy primarily detected by 20 WBCT or visible spontaneous systemic bleeding, bleeding gums, etc., including myoglobinuria and hemoglobinuria, deranged PT/INR, etc Rapid extension of local swelling (more than half of limb) which is not due to tight tourniquet application. Evidence of Cardiovascular Collapse Shock and hypotension (in case of Russell’s viper bite). Evidence Of Acute Kidney Injury AKI is an indication for antivenom therapy.
  • 29. Contradications • No absolute contraindication to antivenom treatment, • But patients who have reacted to horse (equine) or sheep (ovine) serum in the past (for example after treatment with equine anti-tetanus serum, equine anti-rabies serum or equine or bovine antivenom) and those with a strong history of atopic diseases (especially severe asthma) are at high risk of severe reactions and • Should therefore be given antivenom only if they have signs of systemic envenoming.
  • 30. How long after the bite can antivenom be expected to be effective? • Antivenom treatment should be given as soon as it is indicated. • It may reverse systemic envenoming even when this has persisted for several days or, in the case of haemostatic abnormalities, for two or more weeks.
  • 31. Route of administration • Each vial is diluted with 10 ml. of sterile water as supplied with the antivenom.
  • 32. • Randomized, controlled, double-blind trial in Nepal (Damak & Charali snakebite treatment centres and Bharatpur Hospital) • To compare the efficacy of a ten vials initial dose versus a two vials initial dose of Polyvalent Anti-Snake Venom Serum in the treatment of snake bite • Result : Similar efficacy and safety of low vs high initial dose regimen of anti-venom in patients with neurotoxic envenoming in Nepal .Recovery is faster with high initial dose
  • 33.
  • 34.
  • 35. Response to treatment • General symptoms may disappear vary quickly. • Spontaneous systemic bleeding usually stops within 15-30 min. • Blood pressure may increase within 30-60 min. • Neurotoxicity may improve as early as 30 min. • Blood coagulability is usually restored in 3-9 hrs.
  • 36. Reasons for failure to respond to antivenom • Excessive delay in administration of antivenom • Patient with established respiratory failure. • If antivenom administered does not contain neutralizing antibodies against the venom of biting species. • Insufficient dose of antivenom. • Inactive or poor quality antivenom.
  • 37. Prophylactic adrenaline • Prophylactic adrenaline should be routinely used before initiation of anti- venom treatment to prevent anti-venom reaction except in older patients with evidence or suspicion of underlying ischemic heart disease or cerebrovascular disease.
  • 38. Antivenom reactions • within 3 hours of antivenom initiation. • itching, urticaria, fever, angio-edema, dyspnea, laryngeal edema, hypotension etc. . Early anaphylactic reactions • Usually develops 1-2 hrs. after treatment initiation. • Chills, rigors, fever, fall of blood pressure, febrile convulsion may develop in children. Pyrogenic reaction • May develop 1- 12 (mean 7) days after treatment. • Fever, itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy, proteinuria etc. Late reaction (serum sickness type)
  • 39. Treatment of Early Anaphylaxis Reaction/Anaphylaxis • INTERRUPT antivenom • IM adrenaline • IV chlorpheniramine • IV fluids • Oxygen • IV hydrocortisone • Nebulized salbutamol
  • 40. IF ANTIVENOM HAS TO BE RESTARTED • Consider transfer to ICU. • Continue IV hydrocortisone. • IV adrenaline infusion will be required and should be started before giving antivenom. • Stop infusion 30 minutes after resolution of all symptoms and signs.
  • 41. Treatment Pyrogenic reaction • Do not interrupt antivenom unless hypotension is present. • Give injection paracetamol. • Treat hypotension with rapid infusion of normal saline. Serum sickness • Anti-histaminic Pheniramine maleate • If no response to antihistaminic Prednisolone
  • 42. SUPPORTIVE/ANCILLARY TREATMENT • Fluid resuscitation • Oxygen • Intubation and ventilation • Dialysis • Fasciotomies
  • 43. When antivenom is not available or not effective • Neostigmine: 0.5 mg SC/IV/IM (0.02mg/kg). Repeat 4 hourly until neurotoxicity improves (maximum 10 mg/24hrs)/ Edrophonium • Atropine: 0.6mg IV / Glycopyrolate • FFP and cryoprecipitate or whole blood
  • 44. TREATMENT OF THE BITTEN PART • Elevation of limb with rest. • Simple washing with antiseptic solution like chlorhexidine, povidone iodine etc. • Broad-spectrum antibiotic if features of infection. • In case of local necrosis and gangrene: Surgical debridement. • Tetanus toxoid IM injection should be given. If patient presents with coagulopathy, it should be postponed until after resolution of coagulopathy.
  • 45. Recent advances • A 2016 study by Lewin et al. demonstrated that nanomolar and picomolar concentrations of varespladib effectively inhibit the phospholipase A2 (PLA2) activities of selected snake venoms from various continents. • In 2019, the U.S. Food and Drug Administration (FDA) granted varespladib orphan drug status for its potential to treat snakebite. • Other examples of promising small molecule inhibitors include the matrix metalloproteinase inhibitors batimastat and marimastat. The molecules prolonged survival, but did not provide full protection. • In the field of recombinant antivenoms, attention to the use of camelid VHHs (also known as nanobodies) as therapeutic agents has increased.
  • 46. ADDovenom: Novel Snakebite Therapy Platform of Unparalleled Efficacy, Safety and Affordability • Based on a new disruptive protein-based nanoscaffold called ADDomer – a megadalton- sized, thermostable synthetic virus-like particle with 60 high-affinity binding sites to neutralise and eliminate venom toxins from the bloodstream.
  • 47. PREVENTION OF SNAKEBITE • Community based education. • Keep household clean by cutting grasses, bushes, and plants, remove heaps of rubbish, building materials etc. from near and around house. • Bamboo, wood piles should be removed from household so that snake cannot hide. • Close door, windows properly. • Try to avoid sleeping on floor. If it is unavoidable, then mosquito net should be used and tucked well under the mattress or sleeping mat. It not only prevents from krait bite but also from mosquito bite. • Keep your granary away from the house, it may attract rodents that snakes will hunt
  • 48. PREVENTION OF SNAKEBITE • Use high shoes or boots while walking in paddy field, bushes, long grasses. • In dark, use light or strike the path using stick. • Never play with snakes, or irritate them even if they are dead. Never provoke them, they usually do not bite if not irritated or provoked. • Never insert hands into long grasses, tree holes or mud holes. Take care while pulling straw. • Shoes and cloths should be check before wearing, in an area where snakes are abundant.

Hinweis der Redaktion

  1. Spiting cobras
  2. The venomous snakes of the world belong to the families Viperidae (subfamily Viperinae: Old World vipers; subfamily Crotalinae: New World and Asian pit vipers), Elapidae (including cobras, coral snakes, sea snakes, kraits, and all Australian venomous snakes), Lamprophiidae (subfamily Atractaspidinae: burrowing asps), and Colubridae (a large family in which most species are nonvenomous Disorders Caused by Venomous Snakebites and Marine Animal Exposures and only a few are dangerously toxic to humans).
  3. Their venom contains toxins which can either inhibit the release of acetylcholine (pre-synaptic toxins) or bind and block its receptor (postsynaptic toxins). Cobra venom is composed mainly of postsynaptic toxins that block muscle-type nicotinic acetylcholine receptors and are responsible for a curare-like paralysis, while krait venoms also contain large quantities of pre-synaptic toxins that inhibit the release of acetylcholine by destroying nerve endings.
  4. Any recent ethanol or recreational drug use that may modify the patient's presentation Pertinent past medical history, such as current medications (especially anticoagulants or beta blockers), any prior snakebites for which antivenom was given, or allergy to animals used in antivenom production.
  5. However, it is not much helpful to diagnose venomous versus non-venomous snakebite. Venomous snake can have single puncture if one tooth is broken or nonvenomous may have distinct two punctures if they have large teeth. n
  6. Degree of swelling, including circumferential measurement at the point of greatest swelling and demarcation of the extent of swelling from the bite site for reference during repeated examinations.
  7. Abdominal pain is particularly common in krait bite. Acute pain abdomen in suspected nocturnal snakebite may be the only initial clue to krait envenoming. patients cannot hold his/her neck straight when sitting up (active or passive) from supine position. This is due to weakness of the flexor muscles of neck. - limb weakness, flaccid paralysis and loss of deep tendon reflexes
  8. and unexplained residual physical disability as reported from Sri Lanka
  9. Complete blood count, blood group etc.: Increased total WBC count indicate systemic envenoming. Hemoconcentration may occur due to systemic bleeding and platelet count may decrease in case of viper envenoming. coagulopathy +ve (non-clotting) 20WBCT or INR >1.2 or patient’s prothrombin time >4-5 seconds longer than laboratory control value] or thrombocytopenia [< 1.0 lakh per microlitre of blood)
  10. Any cloth or bandage may be used for this, as done for fracture limb. Any form of movement causing muscle contraction like walking, undressing will increase absorption and spread of venom by squeezing veins and lymphatics. avoid any interference with the bite wound to prevent infection, increase absorption of venom and increase local bleeding REASSURANCE Most are nonvenomous snakes. Many are dry bites. Treatable condition. IMMOBILIZATION With a splint or sling. Pressure immobilization in case of purely neurotoxic snake bite Pressure pad immobilization Remove rings, jewelries, tight fittings and clothing
  11. This dangerous practice may lead to gangrene, necrosis and loss of the limb. It may also provide patient a false sense of security leading to delay in seeking hospital care. Ideally, the tight tourniquet should only be released when patient is in hospital under medical care and the facilities for resuscitation is ready. Treatment should be started before such release of tight tourniquet.
  12. Torniquet should be released slowly only after resustication and treatment should be started before such release of tight tourniquet.
  13. Prophylactic adrenaline should be routinely used before initiation of antivenom treatment to prevent antivenom reaction except in older patients with evidence or suspicion of underlying ischemic heart disease or cerebrovascular disease.
  14. Clinical trial in Nepal has shown that the mean dose of antivenom required to treat neurotoxic envenoming is 12.5 ± 3.9 vial per patients. However, it may range from as low as five vials to 20 vials, rarely, as high as 30 vials. Do not use more than 20 vials of antivenom. Administration of higher dose antivenom is unlikely to be useful, if the patient has not responded to initial bolus or around 20 vials of antivenom.
  15. In a placebo-controlled trial of 105 Sri Lankan patients who received IV polyvalent antivenom, fewer adverse reactions occurred in those patients who received pretreatment with 0.25 mg subcutaneous epinephrine when compared with placebo (11 versus 43 percent, respectively)
  16. The dose of IV adrenaline infusion is: Add 1 mg of adrenaline to 100 ml normal saline (this contains 1 mg in 100 mL = 1000 mcg in 100 mL = 10 mcg in 1 mL = 10 mcg/mL). If the patient is still hypotensive/has signs of anaphylaxis, start at 0.5-1 mL/kg/h depending on how severe the reaction is. If the patient is normotensive and stable, start at 0.25 mL/kg/h. Titrate up or down according to response and side effects.
  17. : 25 mg twice a day * 3 days Children: 0.25 mg/kg/day in divided doses* 3 days prednisolone: 5 mg, 6 hourly * 7 days Children: 0.7 mg/kg/day in divided doses* 7 days
  18. Based upon small trials, observational studies, and case reports, administration of anticholinesterases (eg, edrophonium (2 mg over 15 to 30 seconds. Then, after 45 seconds, give 8 mg if no response.), where available, or neostigmine 0.02 mg/kg) can identify whether paralysis is due to snakes with purely or predominantly post-synaptic venom effects (eg, cobras, some coral snakes). Observe for improvement in ptosis, upward eye gaze, and respiratory weakness over 30 to 60 minutes. Before attempting administration of edrophonium or neostigmine, intravenous atropine 0.6 mg (0.02 mg/kg in children, maximum 0.6 mg) or glycopyrrolate (0.2 mg per 1 mg neostigmine dose) should be drawn up
  19. Patients with unknown snakebites in regions with neurotoxic snake species may warrant prolonged observation (up to 24 hours post-bite). Snake venoms that cause isolated coagulopathy will usually do so within 12 hours after envenomation. In locations where snakebite can cause systemic myolysis, observation up to 24 hours and pre-discharge measurement of creatine kinase may be warranted. In general, it is wise to observe suspected snakebite patients overnight, rather than discharge them in the evening or at night, as local resources allow.