SNAKE AND SCORPION ENVENOMATION - PowerPoint Presentation

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SNAKE AND SCORPION ENVENOMATION

DR MOHD KASHIF ALI

MD,FNB

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SNAKE BITE

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Common varieties of snakes and unique toxicity

include

Elapidae

(cobras, kraits): highly neurotoxic, some species also have cytotoxicity

Viperidae

(rattlesnakes, vipers): local swelling and tissue destruction, intravascular hemolysis, bleeding tendency

Hydrophidae

(sea snakes):

myotoxicity

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VENOM PROPERTIES

Snake venom is a complex mixture of toxins used primarily to immobilize and sometimes initiate digestion of

prey

Composition of venom varies greatly from one species to another. 

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LOCALLY ACTING TOXINS :

enzymes which cause tissue destruction through diverse mechanisms (

eg

, phospholipase A

2

 [PLA

2

],

phosphodiesterases, hyaluronidases, peptidases, metalloproteinases).

Swelling, blistering, ecchymosis, tissue necrosis, and paincommonly seen after snakebites by many, but not all Viperid snakes.Local effects are minimal or absent after bites of many elapid snakes (kraits, some mambas, or death adder)other elapid snakes can cause serious tissue necrosis (eg

, some African and Asian cobras).

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NEUROTOXINS

Neurotoxins generally target the neuromuscular junction (NMJ)

presynaptically

,

postsynaptically

, or at both sites and affect skeletal muscle

.

The site of venom action has significant consequences for the ability to treat the resulting paralysis as follows

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PRESYNAPTIC

based on PLA

2

 and damage the terminal axon at the NMJ, through entry into the cell

.

paralysis is not reversible with

antivenom

or

anticholinesterasekraits and many Australian snakes.

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POSTSYNAPTIC

target the acetylcholine receptor on the muscle endplate, blocking response to acetylcholine, external to the cell. 

This type of paralysis can sometimes be fully reversed with

antivenom

, or the neuromuscular block overcome with anticholinesterases

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MYOTOXIN

Rhabdomyolysis

may

occur

some Australian snakes, sea snakes, some kraits, South American rattlesnakes, Sri Lankan Russell’s

viper

Secondary

hyperkalemia

and acute kidney injury can occur if muscle damage is extensive and may lead to secondary cardiotoxicity.

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HEMOSTASIS TOXIN

interference

with blood clotting, usually by increasing bleeding tendency, with resulting consumptive coagulopathy and

hemorrhage

.

Less commonly, clotting and thrombosis may be promoted (

eg

, Martinique viper venom) and cause deep vein thrombosis, pulmonary emboli, and cerebral infarction

.Targets within the coagulation cascade include factor X, IX, and V activators;

procoagulants that activate factor II (prothrombin); and direct and indirect fibrinogenolytics or fibrinogenases. 

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CARDIOTOXIN

hypotension can arise from direct actions of venom components, such as angiotensin-converting enzyme inhibitors and natriuretic peptides

.

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CLINICAL FEATURES

A high index of suspicion should be maintained in children who suddenly become ill while

unsupervised

outside, particularly in rural areas and in the summer months.

Signs of Snakebite

Signs of snakebite, but not necessarily envenomation, may include puncture marks (usually on limbs) that may be difficult to see; may consist of single, double or multiple puncture marks or scratch marks; may be bleeding or oozing; multiple punctures suggest severe envenomation.

Regional tender lymphadenopathy may be present after bites from both nonvenomous and venomous snakes.

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Features of

Envenomation

Local effects

are progressive limb swelling, blistering and discoloration, bleeding/oozing, and pain.

Nonspecific features

include headache, nausea, vomiting, abdominal pain, collapse, and unconsciousness (may be transient).

Specific features

include

Myolysis: Painful, tender muscles, dark urine

Neurotoxicity: Blurred vision, diplopia, ptosis, dysarthria, dyspnea, respiratory failure, difficulty swallowing or breathing, slurred speech, weakness/paralysis, paraesthesia Coagulopathy: Spontaneous bleeding from mucosal surfaces, and continual bleeding from the bite site or venipunctures.

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Early clues that a patient has severe envenomation:

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

drowsiness or early ptosis/ophthalmoplegia

Early spontaneous systemic bleedingPassage of dark brown urine

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MANAGEMENT

1. FIRST AID

The first aid recommended is based on the mnemonic:

“Do it R.I.G.H.T.”

R

=

R

eassure the patient.

I = Immobilise in the same way as a fractured limb. Children can be carried. Use bandages or cloth to hold the splints, not to block the blood supply or apply pressure. Do not apply any compression in the form of tight ligatures.

G.H. = Get to Hospital immediately.T = Tell the doctor of any systemic symptoms such as ptosis that manifest on the way to hospital.

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Are tourniquets useful?

While

widely used by lay people, adverse effects are frequent, including

Ischemic damage

Ineffective in retarding venom flow.

Potentially increase the necrotic action of the venom

Sudden neurotoxic blockage and clotting when released

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In light of these problems the

Pressure

Immobilisation

Method (PIM)

has been advocated as a reliable technique to inhibit venom flow into the system. PIM

invoIves

tying a crepe bandage around the limb including an integral splint, in the same way as for a sprain

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Incision, suction, electric shocks,

cryotherapy

and washing the wound are contraindicated.

Keep the patient as still and quiet as possible.

Fast the patient, be prepared for vomiting.

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2. IMMEDIATE CLINICAL MANAGEMENT

Assess and maintain airway

100% oxygen if respiratory signs present

Respiratory support as indicated

Establish intravenous access and administer intravenous fluids if required

Maintain pressure

immobilisation

bandage and arrange retrieval to an appropriate hospital

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The bandage should not be removed until patient is fully assessed (clinical history, examination, laboratory tests), stabilized (ABC, IV line in situ, IV fluid resuscitation) and if envenomed, appropriate dose of IV

antivenom

given.

Do not leave pressure

immobilization

bandage in place for long periods of time, especially in an asymptomatic patient.

Remember!

Ideally, compression bandages should not be released until the patient is under medical care in hospital, resuscitation facilities are available and antivenom

treatment has been started.

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Release of a tight tourniquet or compression bandage may result in the dramatic development of severe systemic envenoming.

After removal of pressure

immobilisation

bandage, the patient should be fully re-evaluated within 2 hours (including repeat laboratory testing) or earlier if symptoms

develop

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3. ICU MANAGEMENT

Airway and breathing

Intubate and commence positive pressure ventilation for unstable airway, hypoventilation , hypoxemia

Circulatory failure

Treat shock with isotonic fluids and

pressors

, if required.

Avoid central lines in the presence of coagulopathy.

Ongoing care in the ICUObserve closely for onset and progression of muscle weakness.

Monitor urine output- indwelling catheter as necessary.Serial clinical assessment of respiratory function Check and update tetanus immunisation status (once coagulopathy has resolved).Avoid unnecessary venepunctureIf bandage left in situ, then regular observations for limb circulation should be performed

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LAB INVESTIGATIONS

Laboratory testing in cases of possible snakebite is crucial in diagnosis and is urgent. Frequent repeat testing is almost always required. This is to ensure that delayed envenoming or failure to respond to initial treatment is not missed.

Coagulation studies. If initial tests are normal, repeat testing at least twice, at approximately 2–3 hour intervals, or more urgently if the patient develops clinical evidence suggestive of envenoming.

CBC and blood film for hemolysis.

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Where laboratory testing is not rapidly accessible a whole blood clotting time (WBCT) may be performed.

The

20 Minute Whole Blood Clotting Test (20 WBCT) was adopted as the standard test for coagulopathy.

It

crucially requires a clean, new and dry test tube. A few mL of fresh venous blood is left undisturbed for 20 minutes, and then gently tilted. If the blood is still liquid this is evidence of coagulopathy and confirms that the biting species is

Viperine

.

Cobras or kraits do not cause anti-hemostatic symptoms.

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Myoglobinuria

or a significantly raised CK indicates

myolysis

. In such cases beware associated

hyperkalaemia

that can cause lethal cardiac toxicity.

Abnormally raised

creatinine

or urea indicates renal damage.Hyponatremia can also develop, most likely in response to over vigorous IV fluid replacement.Temporary elevation of LFTs sometimes occurs but is rarely of significance

LDH is elevated in hemolysis.

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ANTI SNAKE VENOM

What is

antivenom

?

Antivenom

is immunoglobulin (usually the enzyme refined Fab2 fragment of

IgG

) purified from the serum of a horse or sheep that has been immunized with the venoms of one or more species of snake.

The polyvalent antivenom neutralises the venoms of 4 most important venomous snakes encountered in India (Indian cobra, Indian krait, Russell’s viper, saw-scaled viper).

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Indications for antivenom

(Guidelines for the Clinical Management of Snake bite in the South-East Asia Region, WHO 2005)

 

Systemic envenomation:

Haemostatic abnormalities: spontaneous systemic bleeding, coagulopathy (20WBCT or other laboratory) or thrombocytopenia (<100 x 109/litre)

Neurotoxic signs: ptosis, external

ophthalmoplegia

, paralysis

etc Cardiovascular abnormalities: hypotension, shock, cardiac arrhythmia, abnormal ECGAcute renal failure: oliguria/anuria (clinical), rising blood creatinine/ urea, haemoglobin-/myoglobinuria, dark brown urine , urine dipsticks, other evidence of intravascular haemolysis or generalised rhabdomyolysis (muscle aches and pains, hyperkalaemia) Supporting laboratory evidence of systemic envenoming

Local envenomation:Local swelling involving more than half of the bitten limb (in the absence of a tourniquet) Swelling after bites on the digits (toes and especially fingers)Rapid extension of swelling (for example beyond the wrist or ankle within a few hours of bites on the hands or feet)Development of an enlarged tender lymph node draining the bitten limb

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How long after the snake bite can ASV be given?

Antivenom

treatment should be given as soon as it is indicated.

It is effective in reversing systemic symptoms even after several days or, in the case of

haemostatic

abnormalities, may even be given after two or more weeks.

However, when there are signs of local envenoming,

without

systemic envenoming, antivenom will be effective only if it can be given within the first few hours after the bite

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Antivenom

administration

Storage temperature 0° to 4° prior to re-constitution. The

antivenom

can be used

upto

2 years from the date of manufacture. It should always be given IV.

Prepare the patient and clinical environment for potential anaphylaxis or

anaphylactoid reaction to antivenom.Reconstitute

antivenom powder with 10 ml of sterile water.Shake well and rotate it between the palms of hands until fully dissolved, and let the vial stand for serum to clear. The initial dose is 8-10 vials for both adults and children.Dilute the antivenom about 1:10

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ASV test doses have been abandoned. They have no predictive value in

anaphylactoid

or late serum reactions and furthermore, may pre-sensitize the patient to the protein

Start infusion very slowly, carefully observing patient for reaction (look for flushing, rash, tachycardia, hypotension, bronchospasm; in younger children warning signs also include nasal, palatal, or ocular

pruritis

, coughing, sneezing, profuse sweating,

faecal

or urinary urgency or incontinence, abdominal pain)

Increase rate aiming to give whole dose over 15 to 20 minutes.Approximately 20% of patients who receive ASV develop a reaction either early (within a few hours) or late (5 days or more) after being given

antivenom.

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Anaphylaxis

This can occur due to the polyvalent

antivenom

.

Some mild reactions resolve with temporary cessation of the

antivenom

infusion and recommencing infusion at a slower rate.

Severe, life-threatening anaphylaxis can evolve very rapidly and so adrenaline should be given at the very first sign of a reaction, even when only a few spots of

urticaria have appeared or at the start of itching, tachycardia or restlessness.

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Antivenom

administration must be temporarily suspended

Lie the patient flat (if not already)

High flow/100% oxygen and support airway/ventilation as required

Rapid infusion of normal saline as required (up to 60mL/kg or more)

Adrenaline IM into the lateral thigh, 0.01mg/kg to maximum of 0.3 mg, can be repeated every 5-10 minutes if the patient’s condition is deteriorating.

Alternatively an IV adrenaline infusion can be used and titrated to effect. Monitor BP every 3–5 minutes (using the arm opposite to the infusion). Beware that as the reaction resolves, adrenaline requirements will fall, the blood pressure will rise unless the infusion rate is reduced.

It is especially vital to prevent hypertensive episodes in severely

coagulopathic

patients as this can cause intracerebral haemorrhage.

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Additional treatment for anaphylaxis:

Hydrocortisone IV 1- 2 mg/kg. This will act only for a few hours, but may prevent recurrent anaphylaxis.

H1 blocker:

chlorpheniramine

maleate IV 0.2 mg/kg

H2 blocker: ranitidine 1 mg/kg

Consider

nebulised

salbutamol for bronchospasm, nebulised adrenaline for upper airway obstruction and IV atropine for severe bradycardia

.

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SUPPORTIVE TREATMENT

Anticholinesterase drugs (neostigmine) have a variable, but potentially very useful effect in patients with neurotoxic envenoming, especially those bitten by

cobras.

Heparin

, corticosteroids, and

antifibrinolytic

agents should not be used.

Secondary

bacterial infection of the bite wound may occur with abscess formation which may require drainage and antibiotics. Prophylactic antibiotics are not justified.Despite the commonly observed findings of extensive limb swelling with risk of compartment syndrome,

fasciotomy seldom indicated. If planned, it should be performed only after coagulation and haemostasis has been corrected

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SYSTEMIC TOXICITY

Snakebite coagulopathy:

Some snakes (viper) may cause a significant coagulopathy as part of envenoming. This is due to potent

procoagulants

in the venom, which in vivo cause consumption of fibrinogen and fibrinolysis i.e.

defibrination

syndrome.

This may occur rapidly following envenoming, within 30 to 60 minutes. Platelets are usually unaffected.

DIC profile should be sent and antivenom therapy should be immediately begun. Once active venom is all neutralized by

antivenom normal homeostasis rapidly rectifies the problem (sometimes within 3 hours).Antivenom therapy can be titrated against the resolution of the coagulopathy, in particular, the fibrinogen level. Antivenom therapy can be stopped when fibrinogen levels are rising. Levels need not be normal before stopping therapy.

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Replacement therapy with clotting factors (e.g. whole blood, FFP, cryoprecipitate) should be avoided except for life-threatening bleeding as it can make the coagulopathy worse if there is still active venom (provides “fuel for the fire”).

Even if enough

antivenom

has been given, many coagulation parameters will remain abnormal for hours or days, especially fibrinogen degradation products.

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SCORPION STINGS AND ENVENOMATION

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INTRODUCTION

India has about a 100 species of scorpions of which two (

Mesobuthus

tumulus-

common red scorpion

;

Palamnaeus

swammerdami- black scorpion) are frequently encountered. These nocturnally active creatures inhabit areas with warm, moist climates.The venom contains neurotoxins that inhibit inactivation of voltage-gated sodium channels. It also blocks the calcium activated potassium channels.

This causes an excessive activation of sympathetic and parasympathetic nervous system and a massive release of catecholamines.

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This

“autonomic storm”

results in tachycardia, increased myocardial oxygen consumption, coronary and systemic vasoconstriction and increased afterload.

Scorpion venom also suppresses secretion of insulin leading to hyperglycemia, hyperkalemia, increased free fatty acids and free radical accumulation.

Most of the deaths due to scorpion sting are attributed to cardiopulmonary complications such as myocarditis and acute pulmonary edema

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CLINICAL FEATURES

Most stings are minor, with the most serious

envenomations

occurring in children

Local effects

Pain, swelling,

ecchymoses

, tissue necrosis

Systemic/neurologic effectsAutonomic storm begins with profuse perspiration, tachypnea, tachycardia, excessive salivation, vomiting, priapism (correlates with cardiac involvement) and then progresses to shock

A wide variety of neurologic symptoms like agitation, rigidity, tremor, twitching, encephalopathy, convulsions, cerebral edema and coma have been described.

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Cardiovascular effects

The autonomic storm results in intense tachycardia, increased cardiac work, excessive afterload, all of which culminates in circulatory failure.

Tachycardia usually persists for few hours and may be an early sign of myocardial injury.

Hypertension usually lasts for 4-6 hours and then cardiogenic shock sets in characterized by hypotension and cold peripheries.

Shock, if untreated may lead to

multiorgan

failure, culminating in death.

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Multiple mechanisms lead to cardiovascular failure.

Myocardial ischemia

Myocarditis with raised CPK-MB

isoenzymes

and cardiac troponin I levels

High vascular resistance in both systemic and pulmonary circulations leading to low cardiac output

Pulmonary edema, either cardiogenic or non cardiogenic

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Other effects

Pancreatitis

Metabolic acidosis, hyperglycemia, hyperkalemia

DIC

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TREATMENT

Local

Clean the wound with antiseptic solution and water

Local instillation of lignocaine, if pain is severe

Immobilize the limb

Cold compresses

Pain relief with oral or parenteral agents.

Narcotics should be avoided because they appear to have a synergistic neurotoxic effect with the venom

.

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Supportive measures

Intubation may be indicated if respiratory failure or inability to handle secretions

Fluids in small aliquots to maintain

euvolemia

Tetanus toxoid, if previously not immunized

Benzodiazepines for seizures

Insulin therapy may be necessary to maintain blood glucose and reverse metabolic abnormalities: insulin has a

cardioprotective

agent in this setting.

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Scorpion antivenin.

The clinical efficacy of the antivenin is questionable as it does not counteract the venom induced autonomic storm and some patients develop significant anaphylaxis.

It is not routine practice to administer

antivenom

therapy. If used, should be administered within 30 min after the sting, which may only rarely be possible.

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Prazosin

Symptomatic patients who present within the first 4-6 hours following scorpion sting (early

envenomation)

may be treated with oral

prazosin

.

Prazosin

is an alpha adrenergic blocker and is a pharmacological antidote to the action of scorpion venom. It antagonizes the effect of catecholamines. It reduces cardiac afterload and hypertension without increasing the heart rate.

CNS sympathetic stimulation is reduced.

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It also causes an increase in insulin secretion and may reverse the metabolic derangements.

It should be administered to all children with autonomic storm. The recommended dose is 30 mcg/kg/dose. The dose can repeated after three hours and then every six hours until clinical features of autonomic storm have subsided.

Generally, more than 4 doses may not be required in children.

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Other options and supportive measures

Agents with combined alpha and beta blocker blockade such as

labeletol

.

Hydralazine and/or

nifedipine

may also reduce hypertension, but do not have the other beneficial effects of

prazosin

. Uncontrollable hypertension may need initiation of vasodilator infusions (sodium nitroprusside, nitroglycerine). These agents mandate invasive arterial monitoring as hypotension may be catastrophic and profound.

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Fluid intake and output should be optimized.

Dobutamine

and other

inodilators

may be used if cardiogenic shock is present.

Child may need

ventilatory

support, either non-invasive or invasive.

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What is not useful and may be dangerous

Hydrocortisone, lytic cocktail, digoxin.

Poor prognostic markers:

Delay in initiation of

prazosin

therapy

Presentation > 24

hrs

after significant envenomation Presence of pulmonary edema,

Presence of arrhythmia or myocardial ischemiaEncephalopathy

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End