SNAKE BITE MANAGEMENT

PRESENTER : Dr.Harini
MODERATOR : Dr.Sanjay
 INTRODUCTION

Snakes are distributed through out most of earth`s surface except arctic
antarctic and many islands
 In India more than 200 species have been identified but only 52 are poisonous
Common krait ( Bungarus cerulus) ,Indian cobra ( Naja naja) , russell`s viper
(Daboia russelii ), saw scaled viper ( Echis carinatus ) are the most poisonous
 ELAPIDAE

VIPERIDAE

HYDROPHIDAE
SNAKE VENOM
More than 90% of snake venom is protein
Toxic component is classified into 4 categories :

Enzymes

Polypeptides

Glycoproteins

Compounds of low molecular weight

SNAKE VENOM
Phospholipase A2 (lecithinase) :
Present in the venom of all families of poisonous snakes

It inhibits electron transfer at cytochrome c level and renders mitochondrial

bound enzymes soluble

Damages mitochondria, red blood cells, leucocytes, platelets, peripheral

nerve endings, skeletal muscle, vascular endothelium, and other membranes
Hyaluronidase
Promotes the spread of venom through tissues and proteolytic enzymes are
responsible for the local edema,blistering and necrosis

Acetylcholinesterase
Found in most elapid venoms, it does not contribute to their
neurotoxicity
Zinc metalloproteinase haemorrhagins: Damage vascular endothelium,
causing bleeding.

Procoagulant enzymes: serine proteases and other procoagulant enzymes

that are thrombin-like or activate factor X, prothrombin and other clotting factors.
These enzymes stimulate blood clotting with formation of fibrin in the blood
stream.
Paradoxically, this process results in incoagulable blood because most
of the fibrin clot is broken down immediately by the body’s own plasmin
fibrinolytic system and, sometimes within 30 minutes of the bite, the levels
of clotting factors are so depleted (“consumption coagulopathy”) that the
blood will not clot.
 Some venoms contain multiple anti-haemostatic factors
 Russell’s viper venom contains toxins that activate
factors V, X, IX and XIII, fibrinolysis, protein C, platelet aggregation,
anticoagulation and haemorrhage
Alpha neurotoxins bind to acetylcholine receptors at motor end plate

Beta neurotoxins first cause release of acetylcholine at the nerve endings at

the myoneural junction and then damage the endings ,preventing further
release of transmitter leading to flaccid paralysis

Polypeptides are rapidly absorbed into the systemic circulation and cause
systemic toxicity in vessel rich organs as well as pre and post synaptic
membranes
CONSEQUENCES OF SNAKE-BITE
Victims of snake-bite may suffer any or all of the following:

(1) Local envenoming confined to the part of the body that has been bitten

(2) Systemic envenoming involving organs and tissues away from the part of
the body that has been bitten.

(3) Effects of anxiety prompted by the frightening experience of being bitten

(4) Effects of first-aid and other pre-hospital treatments that may cause
misleading clinical features.
DEATH FROM SNAKE BITE
SYMPTOMS AND SIGNS OF SNAKE BITE
Anxious people may over-breathe so that they develop pins and needles of the extremities,
stiffness or tetany of their hands and feet and dizziness.

Vasovagal shock after the bite or suspected bite-faintness and collapse with profound
slowing of the heart.

Highly agitated and irrational and may develop a wide range of misleading symptoms.

 Blood pressure and pulse rate may increase and there may be sweating and trembling

Constricting bands or tourniquets may cause pain, swelling and congestion that suggest
local envenoming.

Ingested herbal remedies may cause vomiting.

LOCAL SYMPTOMS AND SIGNS IN THE BITTEN PART

Fang marks
Local pain
Local bleeding
Bruising
Lymphangitis (raised red lines tracking up the bitten limb)
Lymph node enlargement
Inflammation (swelling, redness, heat)
Blistering
Local infection, abscess formation
Necrosis
NEUROPARALYTIC POISON

Symptoms – 2Ps 5Ds

Ptosis Dyspnea
Paralysis Dysphonia
Dysarthria
Diplopia
Dysphagia
Typical symptoms within 30 min– 6 hours in case of Cobra bite

● Krait and the hump- nosed pit viper are known for delayed appearance of
symptoms which can develop after 6–12 hours

● Ptosis in Krait bite have been recorded as late as 36 hours after

hospitalization
CHRONOLOGICAL ORDER OF APPEARANCE OF SYMPTOMS

1 .Furrowing of forehead and Ptosis (drooping of eyelids)

2. Diplopia (double vision)
3. Dysarthria (speech difficulty)
4. Dysphonia (pitch of voice becomes less)
5. Dyspnoea (breathlessness)
6. Dysphagia (Inability to swallow)
7. Intercostal and skeletal muscles occurs in descending manner.
OTHER SIGNS
1. Impending respiratory failure
2. Absent deep tendon reflexes
3. Head lag
4. Stridor
5. Ataxia
6. Hypertension and Tachycardia may be present due to hypoxia
HOW TO IDENTIFY IMPENDING RESPIRATORY FAILURE?

Bedside lung function test in adults

i. Single Breath Count – number of digits counted in one exhalation –
normal >30
ii. Breath Holding Time – breath held in inspiration – normal > 45 sec
iii. Ability to complete One sentence in One breath.
VASCULOTOXIC (HEAMOTOXIC OR BLEEDING)
Local manifestations :
Local swelling
 Bleeding
 Blistering
 Necrosis.
 Pain at bite site
 Severe swelling
 Compartment syndrome.
 Tender enlargement of local draining lymph node
SYSTEMIC PRESENTATIONS

● Gingival bleeding ● Subconjunctival hemorrhages

● Epistaxis ● Continuous bleeding from the
● Ecchymotic patches bite site
● Vomiting ● Bleeding from pre-existing
● Hematemesis conditions(haemorrhoids,
● Hemoptysis bleeding from freshly healed
wounds)
I. ACUTE KIDNEY INJURY (AKI)
• Declining or no urine output, deteriorating blood chemistry - serum
creatinine, urea or potassium.

• Russell’s viper frequently cause acute kidney injury.

• Bilateral renal angle tenderness, albuminuria, hematuria,hemoglobinuria,

myoglobinuria followed by oliguria and anuria with AKI
II . IDIOPATHIC SYSTEMIC CAPILLARY LEAK SYNDROME
(ISCLS)

• Hypotension-Severe

• Hypoalbuminemia

• Hemoconcentration without albuminuria

• Profound derangement of the vascular endothelium resulting in leakage of

plasma and proteins into the interstitial compartment

• Parotid swelling, conjunctival chemosis, myalgia, thirst and systemic

hypotension observed in patients indicate capillary leak syndrome.
EARLY LAB AND RADIOLOGICAL MARKERS OF ISCLS

 Increased HCT

 Leukocytosis

 Pleural effusion[cxr]
III . PROGRESSIVE PAINFUL SWELLING[PPS]
● Local venom toxicity
● Russel’s viper bite, Saw scaled viper bite and Cobra bite
● Local necrosis which often has a rancid smell
● Limb is swollen and the skin is taut and shiny
● Blistering with reddish black fluid at and around the bite site
● Skip lesions around main lesion
● Ecchymoses due to venom action destroying blood vessel wall
● Compartment syndrome
● Regional tender enlarged lymphadenopathy
SEA SNAKE POISON
● Muscle aches ● Compartment syndrome

● Muscle swelling ● Cardiac arrhythmias

● Involuntary contractions of ● Hyperkalaemia

muscles.
● Acute kidney injury due to
● Passage of dark brown urine.
myoglobinuria

● Subtle neuroparalytic signs

OCCULT BITE
● Krait bite victims often present in the early morning with paralysis with no local
signs with no bite marks.

● Snakebite victim gets up in the morning with severe epigastric/umbilical pain

with vomiting persisting for 3– 4 hours and followed by typical neuroparalytic
symptoms within next 4- 6 hours.

● There is no history of snakebite

Unexplained respiratory distress in children in the presence of ptosis or sudden

onset of acute flaccid paralysis in a child is highly suspicious symptom in endemic
areas particularly of Krait bite envenomation

● Patients may present with throat, chest or joint pain.

MANAGEMENT OF SNAKE BITE
First aid treatment
Transport to hospital
Rapid clinical assessment and resuscitation
Detailed clinical assessment and species diagnosis
Investigations/laboratory tests
Antivenom treatment
Observing the response to antivenom
Deciding whether further dose of antivenom are needed
Supportive/ancillary treatment
Treatment of the bitten part
Rehabilitation
Treatment of chronic complications
SNAKE BITE : FIRST AID
Evidence of snake bite :
● Fang puncture marks
● Bleeding
● Swelling of the bitten part
● Check history of snakebite
● Look for obvious evidence of a bite
● Krait bite no local marks may be seen
● Reassure the patient as around 70% of all snake bites are from non-
venomous species
● Immobilize the limb by applying splint extending to the entire length of
the limb, immobilizing all of the joints of the limb
e.g. spade, piece of wood or tree branch, rolled up newspapers etc
● Do NOT block the blood supply
● Don't apply pressure
● Recovery position (prone, on the left side)
● Protect airway to minimize the risk of aspiration of vomitus
● Nil by mouth till victim reaches a medical health facility
● Shift the victim to the nearest health facility (PHC or hospital) immediately.
● Arrange transport of the patient to medical care as quickly, safely and
passively as possible
● Victim must not run or drive himself to reach a Healthfacility
● Remove shoes, rings, watches, jewelry and tight clothing from the bitten
area
● Leave the blisters undisturbed.
● Inform the doctor if progress of swelling, ptosis or new symptoms that
manifest on the way to hospital
● Do not attempt to kill or catch the snake as this may be dangerous
● Traditional remedies have NO PROVEN benefit in treating snakebite
● Do not use alternative medical/herbal therapy
● Do not wash the wound
● Do not interfere with the bite wound (Incisions, suction, rubbing,
tattooing, vigorous cleaning, massage, application of herbs or
chemicals, cryotherapy, cautery)
● Do NOT apply or inject anti snake venom (ASV) locally.
● Do not tie tourniquets as it may cause gangrenous limbs.
● Elastocrepe bandage may be applied by qualified medical
personnel only
● The bandage should be wrapped over the bitten area as well
as the entire limb with the limb placed in a splint
RAPID PRIMARY CLINICAL ASSESSMENT AND RESUSCITATION

Airway
Breathing (respiratory movements)
Circulation (arterial pulse)
Disability of the nervous system (level of consciousness)
Exposure and environmental control (protect from cold, risk of drowning etc.)
DETAILED CLINICAL ASSESSMENT AND SPECIES DIAGNOSIS

history of the circumstances of the bite and the progression of

local and systemic symptoms and signs is very important.
Four useful initial questions :
•“In what part of your body have you been bitten?”
•“When and under what circumstances were you bitten?”
•“Where is the snake that bit you?”
•“How are you feeling now?”
EXAMINATION OF BITTEN PART :

The extent of swelling

Lymph nodes draining the limb should be palpated
Intracompartmental pressure should be measured
Blood flow and patency of arteries and veins assessed
Signs of necrosis
VASCULOTOXIC NEUROTOXIC

Bleeding from multiple Respiratory paralysis

orifices with Hypotension
tachypnoea or bradypnoea
Reduced urine output
or paradoxical respiration
Obtunded mentation (drowsy,
obtunded mentation
confused)
peripheral skeletal muscle
 cold extremities paralysis
Pregnant women

Fetal distress
Vaginal bleeding
Threatened abortion

Lactating mothers

Continue lactation
Clinical situations in which snake-bite victims might
require urgent resuscitation:
Profound hypotension and shock
Terminal respiratory failure
Sudden deterioration or rapid development of severe systemic envenoming
following the release of a tight tourniquet or compression bandage
Cardiac arrest precipitated by hyperkalaemia resulting from skeletal muscle
breakdown (rhabdomyolysis) after bites by sea snakes, certain kraits and
Russell’s vipers
Early clues that a patient has severe envenoming:
 Snake identified as a very dangerous one.
 Rapid early extension of local swelling from the site of the bite.
 Early tender enlargement of local lymph nodes, indicating spread of venom
in the lymphatic system.
 Early systemic symptoms: collapse (hypotension, shock), nausea, vomiting,
diarrhoea, severe headache, “heaviness” of the eyelids, inappropriate
(pathological) drowsiness or early ptosis/ophthalmoplegia.
 Early spontaneous systemic bleeding.
 Passage of dark brown/black urine.
IDENTIFICATION
OF SNAKE
IDENTIFICATION
● Many cases the biting snake is not seen, and very often its description by
the victim is often misleading

● Identification of the type of snake should not hold the treatment.

● At times the bite mark might not be visible (e.g., in the case of Krait)

● Clinical manifestations of the patient may not correlate with the species of
snake brought as evidence
● Examine carefully the snake, if brought, and identified if possible.

● Discourage bringing the killed snake into the emergency department.

● Identification of the species even if killed should be carried out carefully,

since crotalids can envenomate even when dead.
POISONOUS SNAKES
● All poisonous snakes are generally brightly coloured

● Venomous snakes have a very distinctive head,looks like hand or

triangular and side portion is wide.

● Cobra group of snakes are Highly Venomous

● Venomous snakes has heat sensitive pit

● All sea snakes are Highly Poisonous

NON POISONOUS
● Non Poisonous Snakes are not brightly coloured
● Non Poisonous Snake head is usually narrow and elongated
● Usually Non-venomous snake do not have Fangs but few snakes do have
fangs
● Pythons are Non Venomous but equipped with rows of teeth
LABORATORY TESTS
OTHER TESTS
Hematocrit Arterial blood gas
Platelet count pH
WBC count Desaturation
Blood film Urine examination
Plasma/ serum ECG
Biochemical abnormalities

Warning: Arterial puncture is contraindicated in patients with haemostatic

abnormalities (Viperidae and some Australasian Elapidae)

ANTI SNAKE VENOM THERAPY
ANTI SNAKE VENOM THERAPY
Antivenom is immunoglobulin purified from the plasma of a horse, mule or
donkey or sheep that has been immunized with the venoms of one or more
species of snake
“Specific” antivenom, implies that the antivenom has been raised against the
venom of the snake
Monovalent (monospecific) antivenom
Polyvalent (polyspecific) antivenom
 ASV is indicated - signs and symptoms of envenomation with or
without evidence of laboratory tests, administer FULL dose without
any delay.
 Do NOT wait for any test report
 History of Bite; known or unknown, if there is spontaneous abnormal
bleeding beyond 20 minutes from time of bite, start ASV, Do NOT wait
for 20 WBCT report
 No absolute contraindications to ASV
 Do not routinely administer ASV to any patient claiming to have bitten
by a snake
 Do not delay or withhold ASV on the grounds of anaphylactic
reaction to a deserving case
 Do NOT give incomplete dose.
Lyophilised antivenom (heat stable; to be stored at cool temperature;
shelf life 3-5 years)

Liquid antivenom (heat labile; ready to use; requires reliable cold

chain [2-8 degree C and NOT frozen] with a refrigeration shelf life of 2
years but costlier)

Use depending on the availability before expiry date.

ADMINISTRATION OF ANTIVENOM
Epinephrine should be always ready before antivenom is administered
Antivenom should be given by IV route whenever possible
2 methods :
1) Intravenous “push” injection: Reconstituted freeze-dried antivenom
or liquid antivenom is given by slow intravenous injection
(not more than 2 ml/minute).
2) Intravenous infusion: Reconstituted freeze-dried or liquid antivenom is
diluted in approximately 5-10 ml of isotonic fluid per kg body weight
(i.e. 250-500 ml of isotonic saline or 5% dextrose in the case of an adult
patient) and is infused at a constant rate over a period of about 1 hour.
ANTI SNAKE VENOM DOSE
ANTI SNAKE VENOM DOSE

Reconstitute ASV supplied in dry

powder form by diluting in 10 ml of
distilled water/ normal saline
● Mixing is done by swirling only
● Do not shake vigorously
● Caution: Do not use, if reconstituted
solution is opaque to any extent
 ASV INFUSION AND DOSAGE PREPARATION
Each vial of ASV be dissolved in  Volume of infusion is reduced
10 ml of distilled water according to the body size and
 Then added to an infusion medium
the state of hydration of the
such as normal saline (10 vials of
patient
AVS dissolved in 100 ml of
 Oliguric patients restrict fluids
distilled water and added to 400ml
and use infusion pump to give
of normal saline)
full dose of ASV over 30 minute
DOSE OF ASV FOR NEUROPARALYTIC SNAKEBITE

ASV 10 vials stat as infusion over 30 minutes

2nd dose of 10 vials after 1 hour if no improvement within 1st hour.

DOSE OF ASV FOR VASCULOTOXIC SNAKE BITE

Two regimens
1. Low dose infusion therapy
2. High dose intermittent bolus therapy
LOW DOSE INFUSION
THERAPY
10 vials for Russel’s viper
6 vials for Saw scaled viper
Stat, as infusion over 30
minutes
 2 vials every 6 hours as
infusion in 100 ml of normal
saline
Continue till clotting time
normalizes or for 3 days
whichever is earlier.
HIGH DOSE INTERMITTENT
BOLUS THERAPY
10 vials of polyvalent ASV stat
over 30 minutes as infusion
Followed by 6 vials 6 hourly as
bolus therapy till clotting time
normalizes and/or local swelling
subsides
HOW MUCH VENOM ..??
HOW MUCH ASV …??
Range of venom injected is 5 mg-147 mg

 Dose range is between 10 and 30 vials

 Each vial neutralizes 6 mg of Russell’s Viper venom

 Depending on the patient condition, additional vials can be considered

Capillary leak syndrome require higher dose of ASV

 Early recognition and effective treatment like infusion of fresh frozen

plasma and reduction of hemoconcentration has a key role to reduce mortality

MONITORING OF PATIENTS AND
PRECAUTIONS DURING ASV
ADMINISTRATION
 Give ASV only by the IV route, and slowly
 Intervene immediately at the first sign of any reaction
 Observe all patients carefully every 5 min for first 30 min
 Then at 15 min for 2 hours for manifestation of a reaction
 STOP infusion at the earliest sign of an adverse reaction
 Rate of infusion can be increased gradually in the absence of a reaction
until the full starting dose has been administered
 Administration over a period of ~1 hour
PROPHYLACTIC EPINEPHRINE

 Adults 0.25 mg of 0.1% solution by subcutaneous

injection

Children 0.005 mg/kg body weight of 0.1% solution

ASV ADMINISTRATION
NEVER give ASV by IM route
2N
Never inject the ASV locally at the bite site
Maintain all aseptic precautions
before starting ASV to prevent any
pyrogenic reactions 3M
Maintain a strict intake output chart
 Monitor colour of urine to detect
acutekidney injury early
ASV - REPEAT DOSES
● Repeat clotting test every 6 hours until
coagulation is restored
● Repeat ASV every 6 h until coagulation is restored
● Patients who continue to bleed briskly
repeat ASV within 1-2 hours
REPEAT DOSES IN NEUROTOXIC ENVENOMATION
Initial dose of ASV 10 vials stat as infusion
 2nd dose of 10 vials if no improvement within 1st hour
Repeat 2nd dose may be required even after 2-3 hours if relapse of signs
of neurotoxicity (may be due to delayed absorption)

Maximum dose is 20 vials

PERSISTING COAGULOPATHY IN SPITE OF LARGE DOSES ASV

1.Fresh frozen plasma (FFP)

2. Cryoprecipitate (fibrinogen, factor
VIII)
3. Fresh whole blood- when FFP and
cryoprecipitate are not available
 LATE ARRIVED VICTIMS : ASV DOSE PROTOCOL
1 .Late after the bite
2. After several days
3. With acute kidney injury

• Determine current venom activity

• If YES , administer ASV.
• Bleeding- viper envenomation
• If NO coagulopathy is evident
• Perform 20WBCT
NO ASV
• Determine if any coagulopathy is
• Treat kidney injury
present
• Treat any other complications
OBSERVATION OF THE RESPONSE TO ANTIVENOM

General: The patient feels better. Nausea, headache and generalized aches and
pains may disappear very quickly.
Spontaneous systemic bleeding (e.g. from the gums): This usually stops within
15-30 min
Blood coagulability (as measured by 20WBCT): This is usually restored in 3-9 hr

In shocked patients: Blood pressure may increase within the first 30-60 minutes
and arrhythmias such as sinus bradycardia may resolve.
Neurotoxic envenoming of the post-synaptic type (cobra bites) may begin to
improve as early as 30 minutes after antivenom, but usually takes
several hours.
Envenoming with presynaptic toxins (kraits and sea snakes) will not respond
in this way.
Active haemolysis and rhabdomyolysis may cease within a few hours and
the urine returns to its normal colour.
ASV REACTIONS
MANAGEMENT PROTOCOLS
20%-60% patients treated with ASV
develop either early or late mild
reactions

 NO ASV TEST DOSE MUST BE ADMINISTERED

 SKIN/CONJUNCTIVAL HYPERSENSITIVITY
TESTING DOES NOT RELIABLY PREDICT EARLY
OR LATE ANTI SNAKE VENOM REACTIONS AND
IS NOT RECOMMENDED.
 ASV REACTIONS

EARLY ANAPHYLACTIC REACTIONS

PYROGENIC REACTIONS

LATE REACTIONS ( SERUM SICKNESS LIKE)

EARLY ANAPHYLACTIC REACTIONS

Within 10–180 min of start of Few patients may have

therapy severe life-threatening
Characterized by itching, anaphylaxis
urticaria, dry cough,  Hypotension
nausea and vomiting,  Bronchospasm
abdominal colic, diarrhoea,  Angio- oedema
tachycardia, and fever
PYROGENIC REACTIONS

Develops 1–2 h after treatment Caused by contamination of

Symptoms the ASV with pyrogens during
the manufacturing process
● Chills
● Rigors
● Fever
● Hypotension
LATE (SERUM SICKNESS–TYPE) REACTIONS

Develop 1–12 (mean 7) days after treatment

Fever
Recurrent urticarial
Nausea Immune complex
Arthralgia
Vomiting nephritis
Myalgia
Diarrhoea Encephalopathy
lymphadenopathy
Itching
PREMEDICATION BEFORE ASV
Prophylactic adrenaline is recommended before ASV
Adult : adrenaline (epinephrine) is 0.25 mg of 0.1% solution
by subcutaneous injection
Children: 0.005 mg/kg body weight of 0.1% solution
TREATMENT OF EARLY REACTION
Stop ASV temporarily
● Oxygen
● Start fresh IV Normal Saline infusion with a new IV set
● Epinephrine (adrenaline) (1 in 1,000 solution, 0.5 mg (i e 0.5 ml) in adults
IM over deltoid or over thigh
● Epinephrine : Children 0.01 mg/kg body weight) for early anaphylactic and
pyrogenic ASV reactions
● Chlorpheniramine maleate (adult dose 10 mg, in children 0.2 mg/kg) IV
● Hydrocortisone can be given but it is unlikely to act for several hours
Once the patient has recovered
● Re-start ASV slowly for 10-15 minutes
● Keeping the patient under close observation
● Then resume normal drip rate
HIGH RISK PATIENTS

1. History of hypersensitivity Give ASV only if they

2. Previous Exposure to
animal serum such as equine
ASV,
tetanus-immune globulin
or rabies-immune globulin
3. Severe atopic conditions
have signs of systemic
envenoming
Premedication
● Inj. Hydrocortisone 200 mg
● Chlorpheniramine
maleate 22.75 mg
TREATMENT OF LATE REACTIONS [SERUM SICKNESS]

Inj. Chlorpheniramine 2 mg in adults

● Children (0.25 mg/kg/day) 6 hourly for 5 days.
● Patients who fail to respond within 24–48 hrs
Prednisolone
● 5 mg 6 hourly in adults
● 0.7 mg/kg/day in children
● 5 days course
DESENSITIZATION PREMEDICATION
PROCEDURE
Only in case of severe 1. Inj. Hydrocortisone 100 mg I.V.
anaphylaxis reaction to ASV 2. Inj. Adrenaline 0.5 ml sc/im
with shock 3. Inj.Promethazine
● Generalised anasarca after
injection of very few ml of ASV
usually less than 5 ml of diluted
ASV
● Change the batch of ASV
STEPS
OF INSTRUCTIONS TOTAL SOLUTION DILUTION
DILUTION VOLUME
1 Dilute 1 ml of ASV in a 10 A
vial in 9 ml of 0.9% Nacl
2 1 ml of solution A+9 ml of 10 B 1:10
Normal Saline
3 1 ml of solution B + 9 ml 10 C 1:100
of Normal Saline

4 1 ml of solution C + 9 ml 10 D 1:1000
of Normal Saline

5 1 ml of solution D + 9 ml 10 E 1:10,000
of Saline
Inject 0.1 ml of solution E I.V

Watch for Anaphylaxis for 15 mts

after dilution
&
Preparation
No Reaction
of
Solution E,
Inject another 0.1 ml of Solution E I.V Follow the
Injection
Watch for Anaphylaxis for 15 mtss
Protocol

No Reaction
 Inject entire solution E I.V

Watch for Anaphylaxis for 15 mts

After dilution
&Preparation
No Reaction Of SolutionE,
Follow the
Injection
After solution E is injected continue the
same process as follows for other
Protocol
solutions is the following sequence:
● Solution D followed by
● Solution C
● Solution B
● Solution A
● Then full dose.
ATROPINE AND NEOSTIGMINE
ATROPINE: NEOSTIGMINE (AN) DOSE SCHEDULE

ADULTS
● Atropine 0.6 mg followed by
Neostigmine (1.5mg) IV stat
● Repeat dose of Neostigmine
0.5mg with Atropine every 30
minutes for 5 doses
CHILDREN
● Inj. Atropine 0.05 mg/kg
Followed by inj. Neostigmine
0.04 mg/kg intravenous
● Repeat dose of NS 0.01Mg/kg
every 30 minutes for 5 doses
ATROPINE: NEOSTIGMINE (AN) DOSE SCHEDULE

● Tapering dose at 1 hour, 2 hour, 6 hours and 12 hour.

● Majority of patients improve within first 5 doses
● Observe the patient closely
● An observation for 1 hour to determine if the neostigmine is effective
● After 30 minutes, the improvement should be visible by an improvement in
ptosis.
WHEN TO STOP….??
1. Complete recovery from neuroparalysis.
2. Side effects in the form of fasciculations or bradycardia
3. No improvement after 3 Doses
Improvement by atropine neostigmine indicates Cobra bite
No improvement after 3 doses of Atropine Neostigmine
● Probable Krait bite
● Krait affects Presynaptic fibres where calcium ion acts as
neurotransmitter
Inj. Calcium gluconate 10ml IV slowly over 5-10 min every 6 hourly
● Continue till neuroparalysis recovers which may last for 5-7 days
● Children 1-2 ml/kg (1:1 dilution)
OTHER MANAGEMENTS IN SNAKE BITE
● Mechanical ventilation
● Volume Replacement
● Forced alkaline Diuresis(FAD)
● Management of Hyperkalemia
● Management of Severe
Acidosis
● Dialysis
● Management of shock
and Myocardial damage
● Management of Local
severe envenoming
SNAKE BITE :INDICATION OF DIALYSIS
● Blood urea >130 mg/dl (27 mmol/L) (BUN 100 mg/dl)

● Sr. Creatinine > 4 mg/dl (500 μmol/L)

● Daily rise in blood urea 30 mg/dl (BUN > 15)

● Sr. Creatinine > 1 mg/dl

● Sr. Potassium > 1 mEq/L

● Fall in bicarbonate >2 mmol/L

● Fluid overload leading to Pulmonary oedema

● Hyperkalaemia (>7 mmol/l or Hyperkalaemic ECG changes- tall peaked

T waves, prolonged P-R interval, absent P wave, wide QRS complexes)

● Unresponsive to conservative management.

● Uremic complications – Encephalopathy, Pericarditis.

REFERENCES
WORLD HEALTH ORGANIZATION GUIDELINES FOR MANAGEMENT OF SNAKE BITES
EMERGENCY TREATMENT OF A SNAKE BITE
J Emerg Trauma Shock 2008 Jul –Dec ;1(2):97-105