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SNAKE BITE
PROF. SUBHASH RANJAN
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INTRODUCTIONIndia estimates approx 2,00,000 bites and 35-
50,000 snake bite deaths/year
No reliable national statistics are available.
Males bitten almost twice as often as females
Majority of the bites being on the lower extremities.
50% of bites by venomous snakes are dry bites, result in negligible envenomation.
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What are Indian FAB FOUR?
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FAB FOUR In India, >200 species of snakes; only 52 are poisonous.
Saw-scaled viper (Echis carinatus) Russell’s viper (Daboia russelii) Common krait (Bungarus caeruleus) Indian cobra (Naja naja)
Neurotoxic 20-30%
1 2 43
Majority of bites 70-80% Hemotoxin / Vasculotoxin
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COMMON INDIAN SNAKES
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COBRA (Naja naja)
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King Cobra (Ophiophagus hannah)
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Saw-scaled Viper (Echis carinatus)
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Green Vine Snake (Ahaetulla nasuta)
Mild Venomous; ASV not required
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Indian Russell's Viper
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Russell’s Viper
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Green Pit Viper
TRPA1/Wasabi Receptor
Infrared Vision
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Indian Green Pit Viper
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Asian Sand Viper (Eristicophis macmahonii)
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Hump Nosed Viper
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Hump Nosed Viper
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Common Indian Krait (Bungarus caeruleus)
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Common Indian Krait (Bungarus caeruleus)
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The Greater Black Krait (Bungarus niger)
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The Greater Black Krait (Bungarus niger)
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Indian Cat Snake Mild Venomous; ASV not required
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Wolf SnakeMild Venomous; ASV not required
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Sea Snake
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Trinket Snake (Elaphe helena monticollaris)
Mild Venomous; ASV not required
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Montane TrinketMild Venomous; ASV not required
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Indian Rat SnakeNon Venomous; ASV not required
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Indian Rock Python
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Variegated Kukri (Oligodon taeniolatus)
Non Venomous; ASV not required
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KEELBACK
http://animalrescuesquadgoa.com/Non%20venemous.html
Non Venomous; ASV not required
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Snake bite
Venomous snakes
Majority (80%) is by non-venomous snakes
About 50% of bites are dry
FACTS
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Is there any medical implication for snake
identification?
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Species: Medical Implications Signs/Symptoms and Potential Treatments
Cobra Krait Russell’s Viper Saw Scaled
Viper Other Vipers
Local pain/ Tissue Damage Yes No Yes Yes Yes
Ptosis/Neurotoxicity Yes Yes Yes! NO No
Coagulation No No Yes Yes Yes
Renal Problems No No Yes NO Yes
Neostigmine & Atropine Yes No? No? NO No
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What is syndromic approach & its significance in Indian
scenario?
Desired when snake is unidentified
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SYNDROMIC APPROACHSyndrome 1Local envenoming (swelling etc) with bleeding/clotting disturbances = Viperidae (all species)
Syndrome 2Local envenoming (swelling etc) with bleeding/clotting disturbances, shock or renal failure = Russell’s viper (and possibly saw-scaled viper – Echis species)With conjunctival oedema (chemosis) and acute pituitary insufficiency = Russell’s viperWith ptosis, external ophthalmoplegia, facial paralysis etc and dark brown urine = Russell’s viper
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SYNDROMIC APPROACHSyndrome 3Local envenoming (swelling etc) with paralysis = cobra or king cobra
Syndrome 4 : Paralysis with minimal or no local envenomingBite on land while sleeping= kraitBite in the sea = sea snake
Syndrome 5 : Paralysis with dark brown urine and renal failure:-Bite on land (with bleeding/clotting disturbance) = Russell’s viperBite in the sea (no bleeding/clotting disturbances) = sea snake
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Composition of Snake Venom
Procoagulant enzymes (Viperidae) Russell’s viper
Haemorrhagins (zinc metalloproteinases)
damage the endothelial lining.
Cytolytic or necrotic toxins
Haemolytic and myolytic phospholipases A2 damage cell membranes, endothelium, skeletal muscle, nerve and red blood cells.
Pre-synaptic neurotoxins (Elapidae and some Viperidae)
Post-synaptic neurotoxins (Elapidae)
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Snake Bite Toxicity Profile ?
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NEUROTOXICITY Starts early- many die before
they reach hospitals Many reverse very well with
ASV if started early Less number of cases
HEMOTOXICITY Starts late hence most of them
reach hospitals Many organ involvement hence
MV is mostly supportive to buy time for organs to recover
More number of cases
70-80%
20-30%
Overlap: Neurohemat
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What is the mode of Neurotoxicity in Krait Bite?
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Krait- Pre-synaptic action
Beta-bungarotoxin- Phospholipases A2
1) Inhibiting the release of Ach from the presynaptic membrane
2) Presynaptic nerve terminals exhibited signs of irreversible physical damage and are devoid of synaptic vesicles
3) ASV & anticholinesterases have no effect
Paralysis lasts several weeks and frequently requires prolonged MV. Recovery is dependent upon regeneration of the terminal axon.
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What is the mode of Neurotoxicity in Cobra Bite?
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Cobra – post-synaptic alpha-neurotoxins “Curare -mimetic toxins’’
Bind specifically to Ach receptors, preventing the interaction between Ach and receptors on postsynaptic membrane.
Prevents the opening of the sodium channel associated with the Ach receptor and results in neuromuscular blockade.
ASV -rapid reversal of paralysis.
Dissociation of the toxin-receptor complex, which leads to a reversal of Paralysis
Anticholinesterases reverse the neuromuscular blockade
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Neuroparalytic Manifestations Study
Ptosis
RSinvolvementBulbar
weakness
N Sharma, S Chauhan, S Faruqi, P Bhat, S Varma, Emerg Med J 2005;22:118–120
Ophthalmoplegia
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Quick Neurological Examination !
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Neurotoxic Envenoming-Examination
Ask the patient to look up and observe whether the
upper lids retract fully.
Test eye movements for evidence of early external
ophthalmoplegia .
Check the size and reaction of the pupils.
The muscles flexing the neck may be paralysed, giving
the “broken neck sign
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Bungarus niger envenoming
20 hr post-bite
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Neurotoxic Envenoming-Examination
Krait can cause fixed, dilated non reactive pupils
simulating brain stem death – however, it can recover
fully
Ask the patient to open their mouth wide and protrude
their tongue; early restriction often due to paralysis of
pterygoid muscles.
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How to identify for bulbar palsy & early resp failure?
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Bulbar & Resp Paralysis Can the patient swallow or are secretions accumulating
in the pharynx- an early sign of bulbar paralysis.
Ask the patient to take deep breaths in and out. “Paradoxical respiration”.
Objective measurement of ventilatory capacity is very useful. Use a peak flow metre, spirometer (FEV1 and FVC)
Ask the patient to blow into the tube of a sphygmomanometer to record the maximum expiratory pressure (mmHg).
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Paradoxical Respiration This is an abnormal pattern of breathing in which the
abdominal wall is sucked in during inspiration (it is usually pushed out).
Paradoxical respiration is due to paralysis of the diaphragm.
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Hematological Side Effects
Venom induces bleeding
Venom induces clotting
Venom induces haemolysis
Haemorrhagin – causes direct endothelial damage by loosening the gap between endothelial cells
Procoagulant factors
Anticoagulant factors
Fibrinonolytic factors
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Snake Venom and the Coagulation Cascade
RVV – Russel’s Viper Venom ECV – Echis
carinatus Venom
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PTT
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PT
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20 min Whole Blood Clotting Test (20-WBCT)
Place a few ml of freshly sampled venous blood in a small glass vessel
Leave undisturbed for 20 minutes at ambient temp & tip the vessel once
If the blood is still unclotted and runs out, the patient has hypofibrinogenaemia/DIC
In the SE Asia, incoagulable blood is diagnostic of a viper bite and rules out an elapid bite
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Local Symptoms & Signs in the Bitten Part
Fang marks Local pain Local bleeding Bruising Lymphangitis Lymph node enlargement Inflammation (swelling, redness, heat) Blistering Local infection, abscess formation Necrosis
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Russell’s Viper Bite
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Venomous Non-venomous
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LOCAL NECROSIS
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What are the systemic manifestations of the
envenomation ?
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Systemic Symptoms & Signs General Nausea, vomiting, malaise, abdominal pain, weakness, drowsiness,
prostration, conjunctival oedema
Cardiovascular (Viperidae) Visual disturbances, dizziness, faintness, collapse, shock, hypotension,
cardiac arrhythmias, pulmonary oedema
Neurological (Elapidae, Russell’s viper) Drowsiness, paraesthesiae, abnormalities of taste and smell, “heavy”
eyelids, ptosis external ophthalmoplegia, paralysis of facial muscles and other muscles
innervated by the cranial nerves, aphonia, difficulty in swallowing secretions,
respiratory and generalised flaccid paralysis
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Systemic Symptoms & Signs
Bleeding & Clotting Disorders Bleeding from recent wounds (including fang marks), venepunctures
and from old partly-healed wounds
Spontaneous systemic bleeding – from gums, epistaxis, bleeding into the tears
haemoptysis, haematemesis, hematochezia or melaena, haematuria, bleeding P/V, bleeding into the skin (petechiae, purpura, ecchymoses) and mucosae (eg conjunctivae)
Intracranial haemorrhage (meningism from SAH, lateralising signs and/or coma from cerebral haemorrhage)
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Systemic Symptoms & Signs Skeletal muscle breakdown (sea snakes, Russell’s viper)
Generalised pain, stiffness and tenderness of muscles, trismus, myoglobinuria hyperkalaemia, cardiac arrest, acute renal failure
Renal (Viperidae, sea snakes) Loin (lower back) pain, haematuria, haemoglobinuria, myoglobinuria, oliguria/anuria, symptoms and signs of uraemia (acidotic breathing, hiccups, nausea, pleuritic chest pain)
Endocrine (acute pituitary/adrenal insufficiency) (Russell’s viper)
Acute phase: shock, hypoglycaemia Chronic phase (months to years after the bite): weakness, loss of
secondary sexual hair, amenorrhoea, testicular atrophy, hypothyroidism etc
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Myoglobinuria after Bungarus niger envenoming
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Pleuropericardial Haemorrhagic Effusion
Manoj Lakhotia et al JIACM 2002; 3(4): 392-4
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Treatment
First AidPrimary/Secondary Care LevelTertiary Care Level
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First AidReassure the victim
Immobilise the bitten limb with a splint or sling
Consider pressure-immobilisation for some elapid bites; AVOID IN COBRA
Avoid any interference with the bite wound as this may introduce infection, increase venom absorption & local bleeding
All rings, watches, constricting clothing should be removed.
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Pressure Immobilization(Elapidae bite)
Developed in 1970 by late Struan Sutherland, Australia
Bandaging entire limb using a long crepe bandage – starting from toe or finger as tightly as for a sprained ankle incorporating a splint.
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Pressure Immobilisation
Pr immobilisation is recommended for bites by neurotoxic elapid snakes, including sea snakes.
Caries risk of sudden envenomation after release – neurotoxic snakes.
Should not be used for viper bites because of the danger of increasing the local effects of the necrotic venom.
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COMPLICATIONS OF ARTERIAL TOURNIQUET
Congestion & swelling Ischaemia & gangrene Damage to peripheral nerves Increased bleeding from bite site
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Tourniquet Gangrene
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INCISION & SUCTION
No!
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TREATMENT
CRYOTHERAPY:No!Increases tendency to necrosis
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TREATMENTHOSPITAL MEASURES FOR ASYMPTOMATIC PTSa) OBSERVATION FOR 24 HOURS
b) MONITOR: PR, RR, BP CBC-TLC ↑, Platelets ↓ Urine output BUN, Creatinine PT, aPTTK, INR CPK (>600 IU/L) Vomiting, diarrhoea Abnormal bleeds Local swelling necrosis ECG Blood gas analysis
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MEDICOLEGAL 39 Code of Criminal Procedure under
Constitution of India Article 21
MLC to be initiated
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Hospital mngt, if tourniquet is a already in place
•Limb is ischemic – remove immediately
•Limb is not ischemic:-1) Snake (unknown) or neurotoxic – Don’tremove until definite treatment (ASV) is initiated
2) Snake is viper – remove the tourniquet
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What is ASV?
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ASV ASV is Ig (usually the enzyme refined F(ab)2 fragment of
IgG) purified from the serum/plasma of a horse/sheep immunised with the venoms of one or more species of snake.
Monovalent/Polyvalent
The ASV in India is a polyvalent type which is active against the commonly found snakes in India including the FAB Four.
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Antivenom
Polyvalent antivenoms from India raised against venom from:•Bungarus caeruleus•Naja naja•Echis carinatus•Daboia russelii
No monovalent vaccine in India
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ASV Average dry weight of venom injected = 63
+/- 7mg by Russell’s Viper or Cobra.
Each vial neutralises venoms of 6 mg Cobra
6 mg Russell's Viper4.5 mg of Krait 4.5 mg of Saw Scaled Viper
Initial dose should be 8-12 vials.
Snake inject same amount of venom into children, dose of ASV is same as adult .
http://cbcreatures.webs.com/snakeantivenom.htm
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What are the indications for ASV use?
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Indications for Antivenom Use Shock
Resp distress /failure
Extensive Local Swelling
Ptosis
Generalized myalgias
Trismus
Mod-to-severe pain with passive movement of extremities
Severe GI Symptoms
Myoglobinuria
Elevated creatine kinase level (>600 IU/l)
Altered level of consciousness
Hyperkalemia
ECG Changes
Leukocytosis.
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Antivenom Reconstitution Freeze-dried (lyophilised) ASV is reconstituted with
10 ml of sterile DW per vial.
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TREATMENT OF SNAKEBITEPROCEDURE OF ADMINISTRATION
Test Dose?No!
Has no predictive value in detecting anaphylactoid or late serum reactions and should not be used.
Not IgE mediated, but complement - activated. May also pre-sensitise the patient, and create greater risk.
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Methods of Administration
IV “push” injection: recons freeze-dried ASV is given by slow iv inj (not more than 2ml/min).
IV infusion: recons freeze - dried ASV is diluted in approx 5-10 ml of isotonic fluid per kg BW (ie 250-500 ml of N/S or 5% Dex in adult pt) and infused at a constant rate over a period of about 1h.
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Antivenom Administration
Adrenaline drawn up in readiness before ASV is administered.
ASV should be given by the IV route whenever possible.
I/M may be given when no i/v access, expeditions with limited med facilities.
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Prophylaxis in High Risk patients
Pre-treated empirically with s/c epinephrine (adrenaline)
IV antihistamines anti-H1 + anti- H2 (Ranitidine)
IV Hydrocortisone 100 mg
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IM Antivenom A maximum of 5-10 ml should be given at each
site by deep IM inj followed by massage to aid absorption
ASV should never be injected into the gluteal region (upper outer quadrant of the buttock) as absorption is exceptionally slow and unreliable and there is always the danger of sciatic N damage by an inexperienced operator.
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Dose
5 vials(50ml)
5-10 vials(50-100ml)
10-20 vials(100-200ml)
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Large vs Small dose
Low dose of snake antivenom is as effective as high dose inpatients with severe neurotoxic snake envenomingAgarwal, Aggarwal, Gupta, et al Emerg Med J 2005;22:397–399.
•High dose group 100ml stat and 100 ml every 6 hrs•Low dose group 100ml stat and 50 ml every 6 hrsUntil recovery of neurological signs
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Timing of ASV
There is no consensus as to the window period of administration of ASV.
Best effects are observed within 4 h of bite .
It has been noted to be effective in symptomatic pts even when administered up to 48 h after bite.
ASV is efficacious even 6-7 days after the bite from vipers
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At the Earliest Sign of a Reaction:
ASV administration must be temporarily suspended
Adrenaline (0.1% solution, 1 in 1,000; 1 mg/ml) is the effective treatment for early anaphylactic and pyrogenic ASV reactions
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Early reaction to ASV Anaphylaxis
Adrenaline (SC or IM) 0.3 to 0.5ml 1:1000 (1mg/ml). Repeated at 5 to 20 min interval if severe.
Adrenaline (IV) - in intractable reaction 2.5 ml iv; 1:10,000 (0.1mg/ml).
Volume resuscitation
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Case scenario……. 34 yr old male shifted from Periph Hosp with H/O snake
bite 6 hrs back has ptosis, respiratory distress, RR 35/mt, BP 120/60, oral secretions present, absent gag and cough reflex shifted to ICU for tertiary care.
On ASV 100ml stat, & 50ml in NS over 6 hrs Oxygen 3l/mt
Patient received in casualty: 2 situations
Patient is comfortable, vitals stable
No ptosis, distress
Patient is dead –what do you think went wrong ?
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What could have been done better ? Bulbar signs-probably aspirated and died Endotracheal intubation could have been placed on T-
piece Ambuing or Transport Ventilator Anticholienesterases Neostigmine with atropine
Patient is dead –what do you think went wrong ?
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Trial of AnticholinesteraseAnticholinesterase (“Tensilon”/Edrophonium) test Record baseline parameters Give atropine IV Give anticholinesterase drug edrophonium chloride
(adults 10 mg, children 0.25 mg/kg body weight) given intravenously over 3 or 4 minutes
Observe
Improvement in ptosis, Respiratory distress, better cough effort, decrease in RR
Tearing, salivation,muscle fasciculation, abdominal cramp,bronchospasm, bradycardia, cardiac arrest
Neostigmine
Positive response
Atropine IV
Negative response
Dose of Neostigmine
Neostigmine 25µg/kg/hr Neostigmine 0.5 mg / 6 hr IV atropine 0.5 mg / 12 hr
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34 yr old male shifted from Periph Hosp with H/O snake bite 6 hrs back has ptosis, respiratory distress, RR 35/mt, BP 120/60, oral secretions present, absent gag and cough reflex shifted to ICU for tertiary care.
On ASV 100ml stat, & 50ml in NS over 6 hrsOxygen 3l/mtRecd neostigmine 0.6mg and 0.6 mg atropine iv
You can have alive but a sicker patient
You can have dead patient
Cobra
Krait
Case scenario…….
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Alive but a sicker patient
Shifted to ICU placed on a Ventilator lot of secretions
Do we continue anticholinesterases ?
Issues to consider
Increased secretions
Increased incidence of VAP ?
We rarely use these drugs once the patient is in the ICU under observation
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Observation of the Response to Antivenom
Cobra bites-Post synaptic
May begin to improve as early as 30 minutes after anti-venom, but usually take several hours.
Krait and sea snakes- Pre synaptic
Depends on the timing of ASV administrationIf delayed may not produce any action or Minimal delayed action
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Repeat Dose
Signs of systemic envenoming may recur within 24-48 hrs Criteria for repeating the initial dose of antivenom Persistence/recurrence of blood incoagulability after 1-2 h Deteriorating neurotoxic or cardiovascular signs after 1-2 h
Continuing absorption- due to improved blood supply following correction of shock, hypovolaemia etc
After elimination of antivenom a redistribution of venom from the tissues into the vascular space.
Causes
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How to Know ASV Dose Administered is Sufficient?
a) Spontaneous systemic bleeding stops in 15-30 min.
b) Blood coagulability is usually restored in 6 hours.
c) Post synaptic neurotoxic envenoming begins to improve in 30 min, but can take several hours.
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How to Know ASV Dose Administered is Sufficient?
d) Presynaptic neurotoxic envenoming usually takes a considerably more time to improve.
e) Active haemolysis & rhabdomyolysis may cease within a few hours & urine returns to its normal colour.
f) In shocked pts, BP may improve in 30 min.
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What is the Max Dose of ASV?
25 – 30 vials
Q. If symptoms persist despite giving max Q. If symptoms persist despite giving max dose, what must be done?dose, what must be done?Ans. Supportive measures & treatment of complications:
Ventilation – Elapid bite Dialysis, transfusions, etc – Viperid bite Fasciotomy, wound surgery, amputation,
etc, as per need.
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Pregnancy and Snake Bite
Pregnant pt is treated the same manner as the nonpregnant .
Spontaneous abortion, bleeding, fetal death & malformations are common.
Lactating mothers can continue lactating
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A 25 yr old male with snake bite has signs of compartment syndrome and the pressure is 60 mmHg, is undergoing surgery, has a Hb of 6 gm%, is hypotensive 100/60, on noradrenalin, acidotic, coagulation profile is normal
Blood is started After 15 mts of surgical time patient develops Dark colored urine BP drops to 80/60 with ARF What are the possibilities ?
Rhabdomyolysis
(Viper Bite)
Treatment Fluids, Mannitol,Alkalinize the urine, Manage electrolytesFasciotomyRRT
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Other Rx
Antibiotics
Hydration
Tetanus prophylaxis
Wound debridement
Fasciotomy for compartment syndrome
Haemodialysis for acute renal failure
Mechanical ventilation
DIC; related mngt
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Criteria for Fasciotomy in Snake-Bitten Limbs
Clinical evidence of an intracompartmental syndrome
Intracompartmental pr >40 mmHg (in adults)
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Disposition (Dry bite)* Viper BiteNo local and systemic envenomationat 8 to 12h by repeated lab tests – ‘Dry Bite’.
* Neurotoxic snakeObservation period 12-24hr.Neurotoxicity can be delayed .
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References N Engl J Med, Vol. 347, No. 5 August 1, 2002
www.nejm.org Page 347-356
WHO Guidelines for the Clinical Management of Snake Bites in the South-East Asia Region
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THANK YOU
Happy Year of the Snake! 新年快乐!