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Snake Bite PPT Lecture

Undergraduate medicine lecture

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Dr.P.Natarajan
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71 views18 pages

Snake Bite PPT Lecture

Undergraduate medicine lecture

Uploaded by

Dr.P.Natarajan
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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SNAKE BITE ENVENOMATION

Dr. P. Natarajan
Etiology
1. 216 species of snakes in India; 52 are venomous

2. The major families of poisonous snakes in India:


1. Elapidae (Cobra Naja naja, king cobra and kraits)
2. viperidae (Russell’s viper, Echis carinatus or saw scaled viper or carpet
viper and pit viper) and
3. hydropidae (sea snake).

3. Leading cause of premature death of young earning member of the family

4. In india 35,000-50,000 lives are lost per year


1. The venom is viscous and comes out in small quantity in winter

2. This explains the high fatality rate seen during summer and August, September and
October months due to high environmental temperature.

3. It contains enzyme proteins hydrolase’s, hyaluronidase, l-amino acid oxidase, phospho


mono-and diesterases, 5’nucleotidase, DNAase, phospholipase A2, peptidase and
NAD-nucleosides.

4. Phospholipase A2 destroys mitochondria, red blood cells, leucocytes, platelets,


peripheral nerve endings, skeletal muscle, vascular endothelium and other
membranes, & produces presynaptic neurotoxic activity
Cobra and Krait venom
1. Cobra venom is rich in postsynaptic neurotoxins

2. Cobra venom bind specially to acetyl choline receptors and produce


neuromuscular blockade

3. Cardiotoxin contents of cobra venom are extremely lethal to myocardium.

4. Kobra venom is very quick in action; krait venom action is slow & results in a
visit to the local traditional healer.

5. Krait venom is ten times more lethal than cobra but the victim reports too late
due to its delayed action
Viper venom
1. Viper venom causes coagulation and release of bradykinin responsible
for sudden hypotension and anaphylaxis.

2. Viper venoms interfere with blood clotting.

3. Microangiopathic haemolysis associated with disseminated


intravascular coagulation, acute renal failure and hypotension can
occur.
Pathogenesis
1. Snake venom is a mixture of polypeptides, proteolytic enzymes, and toxins,
which are species specific.

2. Elapidae and the Hydrophidae: neurotoxic and has a curare-like effect by


blocking neurotransmission at the neuromuscular junction. Death due to
respiratory depression.

3. Crotalidae: cytolytic, causing tissue necrosis, vascular leak, and coagulopathies.

4. Pit viper: hemorrhagic shock, adult respiratory distress syndrome, and renal
failure
Clinical Manifestations:
Local
1. Many bites result in only little or no venom injected - “dry bite”

2. Pit viper bites usually occur on the extremities; pain and swelling occur
at the site within minutes.

3. As the venom moves proximally, edema and ecchymosis advance and,


in severe cases, bulla formation and tissue necrosis ensue.

4. Absorption is accelerated by threat of death and liberated


catecholamine and running.
Systemic
1. Systemic symptoms include nausea, vomiting, diaphoresis,
weakness, tingling around the face, and muscle fasciculations.

2. Rarely, patients may present in shock with generalized edema or


cardiac arrhythmias.

3. Complex clotting abnormalities often occur


Systemic manifestation

1. Blurring of vision due to paralysis of ciliary muscles of eyes and loss of


accommodation.

2. Pupils are at times dilated and not reacting to light.

3. Bulbar palsy include difficulty in deglutition, nasal twang in voice due to


palatal palsy, broken neck sign i.e. Unable to lift the neck from pillow.

4. Suffocation, partial or total opthalmoplegia and ptosis also may occur.

5. The victim may suddenly lapse into an acute respiratory paralysis and
shock.
“Locked in” syndrome
1. Few cases develop quadriplegia with total opthalmoplegia and dilated
pupils.

2. The patient appears brain dead or comatose, but such victims recover
totally within 3-4 days if treated properly by maintaining oxygen
saturation with proper ventilator support

3. This phenomenon is due to blocked postsynaptic acetyl choline


receptors including the sphincter pupillary muscle which are rich in
acetyl choline receptors.
Treatment
1. The first task is to determine if the bite was by a poisonous snake and if
envenomation occurred.

2. If the snake has been killed, it should be brought to the emergency


department for identification.

3. More than 80% of snakebites are by nonpoisonous snakes; these bites


cause minimal pain and no swelling and require only local wound care.
Management

1. The victim should not be allowed to walk or run.

2. The bitten part should be kept below the heart level

3. No local incision must be made, sucking, application of ice or


any chemical must be avoided

4. surface venom can be removed by clean cloth or tissue paper

5. Reassure the victim


Local measures

1. Decrease lymphatic flow by Immobilization of the extremity, pressure at


the site of envenomation, and a proximal tourniquet

2. The tourniquet should be loose enough to insert a finger and allow arterial
blood flow, because ischemia may exacerbates local tissue damage.

3. applying ice or using excision and suction cause more tissue damage than
benefit and should be avoided.
Resuscitation
1. On arrival at the emergency department, insert a large-bore
intravenous line

2. Collect blood for baseline laboratory studies

3. Record baseline vital signs

4. Measure and record circumference of the bitten extremity

5. Demarcate of ecchymosis and swelling and moniitor progression

6. Clean the wound and give tetanus toxoid


Anti-snake venom

1. Dry powder in the ampoule of ASV is dissolved by adding 10 ml


of distilled water as diluent

2. Some precipitate remains at bottom it should be discarded

3. A skin test dose need not be given as there is no guarantee that


non sensitive victim will not develop reaction or otherwise.

4. 0.3 ml of adrenaline can be given subcutaneously as prophylaxis


against anaphylaxis
1. The initial dose is 8-10 vials for both adults and children.

2. 100 (10 vials) ml of ASV to be added to 200 ml of normal saline and


given by intravenous route over 30-50 minutes

3. Hypotension and bradycardia are treated with atropine orisoprenaline


drip.

4. In case of shock, without cardiac block dopamine drip may be needed

5. endo tracheal intubations and ventilator support

6. Neostigmine – 0.5 ml neostigmine every 30 minutes till recovery


occurs.
Lab
1. Type and crossmatch blood; coagulopathy may make later typing
impossible.

2. Complete blood cell and platelet counts;

3. Prothrombin and partial thromboplastin times;

4. Fibrinogen and fibrin degradation products;

5. Blood urea nitrogen, creatinine, and creatine phosphokinase levels.

6. These studies need to be repeated at intervals, depending on the severity


of envenomation.
Prognosis
1. Despite the potential for mortality and severe morbidity with
poisonous snakebites, both can be minimized by early and
judicious use of appropriate antivenin.

2. Even extremities with marked tissue necrosis will return to full


function with the resolution of swelling, and only rarely is
delayed skin grafting required.

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