Kwame Nkrumah University of

Science & Technology, Kumasi, Ghana

PHARD 582 CLINICAL TOXICOLOGY

Envenomations J. Parkinson

Wonder Abotsi, PhD

Room C114, Tachie Building
Department of Pharmacology, College of Health Sciences, KNUST
Email: wkmabotsi.pharm@knust.edu.gh
wkm_abotsi@yahoo.com
Envenomations
 Venomous snake bites
 Arthropod bites and stings
 Hymenoptera
 Scorpions
 Spiders
SNAKE BITES
Outline
 Snake bite epidemiology
 Families of venomous snakes
 Clinical effects of venoms
 General management as first aid, early
manifestations, complications
 Prevention of snake bites
References
 WHO (2010), Guidelines for the Prevention and
Clinical Management of Snakebites in Africa
 MOH (2017), Standard Treatment Guidelines, 7th
Edition
 Ford (2001), Clinical Toxicology, 1st edition, WB
Saunders
 Mackessy SP (2010). Handbook of Venoms and
Toxins of Reptiles, CRC Press
Snake Bites
 A snake bite is an injury caused by a bite from a
snake often resulting in puncture wounds inflicted by
the animal’s fangs and sometimes resulting in
envenomation.

 It is a life-threatening medical emergency when

envenomation occurs.
 Snakebite is a neglected tropical disease.
SNAKE BITES - EPIDEMIOLOGY
 No required reporting of cases, so quoted incidence
numbers may be inaccurate
 Globally
 ~5 million snake bites occur each year, resulting in up to
2.5 million envenomings, at least 100 000 deaths and
around 3x as many amputations and other permanent
disabilities.
 Africa
 ~ 1 million snake bites annually with about half needing
treatment
Snake Bites - Epidemiology
 Snakebite predominately affects people living in the tropical
and sub-tropical regions of the world.
 vast majority of deaths occur in sub-Saharan Africa and South-East Asia
 poor rural communities in low- and middle-income countries; health
systems are weakest and medical resources sparse.
 Males are bitten more often than females.
 Agricultural workers and children are the most affected.
 Children often suffer more severe effects than adults, due to
their smaller body mass
 The elderly are also at greater risk of mortality.
 India is estimated to have the highest snakebite mortality in the
world.
Snake Bites - Incidences

 Papua New Guinea has some of the highest

snakebite rates in the world, with the country’s
rural central province recording an annual
incidence of 561.9 cases per 100 000 population

 Snakebites are concentrated in mainly rural areas

and vary considerably by season, with the peak
incidence seen in the rainy and harvesting seasons
Snake Bite Deaths Worldwide
SNAKES
 Most snakebites are innocuous and are delivered by non-
venomous species.
 Worldwide, only about 15% of the more than 3000
species of snakes are considered dangerous to humans.
 375 medically important venomous snakes worldwide
 Snakes belong to Class Reptilia, Order Squamata,
Suborder Serpentes
 Comprised of 11 families
 Venomous snakes are in 5* families
 Viperidae is the largest family followed by Elapidae.
Venomous Snakes - Families
Families of venomous snakes & representative species :
 Colubridae
 Boomslang, Bird snake
 Elapidae
 Cobras, kraits, mambas, coral snakes, most Australian snakes
 Hydrophiidae
 Sea snakes, sea krait
 Viperidae
 Viperinae (True/pitless vipers): vipers, adders, asps
 Crotalidae (pit vipers): rattlesnakes, bushmaster, copperhead
General Anatomic Comparisons of
Venomous Snakes

 Colubridae : rear-
fanged
 Elapidae : front-fanged
(proteroglyphous), fixed
maxilla
 Viperidae: front-fanged
(solenoglyphous), mobile
maxilla
ELAPIDAE
 Elapidae have a pair of short permanently erect
(proteroglyphous) fangs.
 A few species are capable of spraying their venom from
forward-facing holes at the tips of their fangs using pressure,
and this can act as a means of defense.
 Has some of the world's most venomous land snakes based on
the murine LD50 of their venom e.g. the inland taipan.
 Examples:
 Common cobra (Naja naja), king cobra (Ophiophagus hannah)
 Kraits: Common krait (Bangarus caeruleus), banded krait (Bangarus
fasciatus), coral snake, tiger snake, mambas (Dendroaspis sp), death
adder
Short permanently erect fangs of a typical elapid
 Common Cobra (Naja naja)

 Well marked hood

 Single (monocellate) or double spectacle mark
Black-necked spitting
cobra (Naja nigricollis)
Common krait (Bungarus Caeruleus) - key identification feature is PAIRED
white bands.
Dendroaspis angusticeps Dendroaspis polylepis
(green mamba) (black mamba)
VIPERIDAE
 Have a pair of relatively long solenoglyphous fangs
which are normally folded up against the upper jaw;
erected when the snake strikes.
 Two subgroups
 True/pitless vipers (Viperinae)
 Pit vipers (Crotalinae)
 Indentation or "pit" between eye and nostril – heat sensing pit organ,
to detect their warm-blooded prey
 Flat triangular-shaped head
 Vertical pupils
 Curved fangs (usually 2; sometimes 1 to 4)
 Rattlesnakes have "rattle" at end of tail .
Viperidae
 Examples
 True/pitless vipers (Viperinae)
 Russell’s Viper (Daboia russelii)
 African saw-scaled viper (Echis ocellatus)
 African puff adder (Bitis arietans)
 Pit vipers (Crotalinae)
 Rattlesnakes
 Cottonmouth
 Copperhead
Russell’s vipers details of fangs.
 .

Russell’s viper (Daboia russelli)

Key identification feature is the black edged almond or chain

shaped marks on the back
Saw-scaled viper/carpet viper (Echis carinatus)
Saw-scaled viper/carpet viper (Echis ocellatus)
Puff adder (Bitis arietans)
 Key Identification
Feature- large plate
scales on the head
PIT VIPER
Thomas Fatora, Wikimedia Commons

Copperhead 19
Fjguyote, Wikimedia Commons

Cottonmouth (water moccasin) 20

Mark Bratton, Wikimedia Commons

Sidewinder rattlesnake 21
Ryan E. Poplin, Wikimedia Commons

Diamondback rattlesnake 22
Ghana: Key Venomous Snakes
 Most important venomous snakes responsible for
significant mortality and morbidity in Ghana
(WHO Category 1):
 West African Saw-scaled/carpet viper (Echis
ocellatus)
 Puff adders (Bitis arietans)
 Black-necked spitting cobra (Naja nigricollis)
 Senegalese cobra (Naja senegalensis)
 Western green mamba (Dendroaspis viridis)
 Venomous snakes:
identification features

Pit
vipers
Venomous snakes: identification
features
 Non-venomous snakebites tend to
leave a row of several small
puncture wounds from the animal’s
many teeth.
 Venomous snake leaves 1-4
(usually 2) larger fang marks
 a new set of fangs could be coming
in while the old set is still in place
 Venomous bites usually bleed a
lot more
 fangs penetrate more deeply +
venom
 Don't rely too much on fang marks
SNAKE VENOM
SNAKE VENOM
 Venomous snakes are often said to be
poisonous, but poison and venom are not the
same thing.
 Poisons must be ingested, inhaled or absorbed,
while venom must be injected into the body by
mechanical means.
 Venoms are generally not toxic if swallowed, and
must be injected under the skin into the tissues that
are normally protected by skin in order to be toxic.
 Snake venom
 Snake venom is modified saliva usually
delivered through highly specialized teeth,
hollow fangs, directly into the bloodstream
or tissue of the target.
 Prey immobilization
 Assist in or start the digestive process
 Self-defense
 The venom gland is a modified salivary
gland, and is located just behind and below
the eye.
 The size of the venom gland depends on the
size of the snake.
 Venom quantity in a venom gland (i.e. amount
extracted by milking) increases exponentially with
the size of the snake.
Snake venom
 Proteins constitute 90-95% of venom's dry weight and they are
responsible for almost all of its biological effects.
 Synergism: different venoms contain different combinations of
enzymes causing a more potent effect than any of the
individual effects.
 Snake venoms vary in their composition from species to species
but also within a single species:
 throughout the geographical distribution of that species
 at different seasons of the year
 as the snake grows older (ontogenic variation)
Snake venom: Components
Enzymes
 Proteolytic enzymes
 Collagenases
 Hyaluronidase
 Phospholipase
 Lactate dehydrogenase
 Acetylcholinesterase
 Nucleotidases
 L-amino acid oxidase
 Endopeptidases, kininogenase,
factor-X, prothrombin activating
enzyme, etc
Non-enzymes
 Polypeptide toxins e.g
cytotoxins, cardiotoxins,
postsynaptic neurotoxins
(e.g. α-bungarotoxin and α-
Cobratoxin)
 Steroids
 Inorganic elements : zinc,
magnesium
 Histamine, bradykinins,
serotonin
 Aminopolysaccharides
 etc
Functional Classification of
Composition of Snake Venoms
 Neurotoxic
 Mostly Elapidae (cobras, kraits, coral snakes), hydrophiidae
(poisonous sea snakes)
 Cytotoxic
 black-necked spitting cobra (Naja nigricollis), Bothrops
asper, saw-scaled/carpet viper**, etc
 Haemotoxic
 Mostly Viperidae, spitting cobra**
 Myotoxicity
 Mostly Hydrophiidae
**certain snake species are capable of causing combinations of these different toxicities
Neurotoxic venom
 Neurotoxic envenoming is characterised by descending
neuromuscular paralysis, beginning with the eyes (ptosis),
facial muscles and other muscles innervated by the cranial
nerves, before progressing to respiratory and generalised
flaccid paralysis
 Predominant toxins include diverse phospholipases A2 (PLA2)
and three-finger toxin (3FTX) families
 acting on the pre- and/or post-synaptic junction, where they can have a
multitude of actions, from blocking potassium or sodium channels, to
acting as nicotinic or muscarinic receptor antagonists
Cytotoxic venoms
 Cytotoxic envenoming are characterised by painful and
progressive swelling at the bite site, developing into blistering
and bruising, that are sometimes coupled with systemic effects,
which include hypovolaemic shock
 Often, extensive local tissue damage develops characterized
by necrosis of the affected limb and requiring surgical
debridement or amputation if left untreated.
 Predominant toxins
 Hydrolytic enzymes, such as snake venom metalloproteinases (SVMPs)
and PLA2s, and non-enzymatic cytotoxic 3FTXs.
Myotoxic venoms
 Myotoxic envenoming is characterized by negligible
local swelling, increasing generalized muscle pain
and tenderness (myalgia) associated with features of
neurotoxic envenoming and progressive descending
paralysis culminating in paralysis of breathing.
 Rhabdomyolysis and potential for renal failure
 Myotoxic single chain peptides (42–44 amino acid
residues) and myotoxic phospholipases A2
 Cytotoxic venoms

Naja nigricollis

Bothrops asper
Haemotoxic venoms
 Haemotoxicity is one of the most common clinical signs in victims of
snakebite, particularly when viperid snakes are responsible for
envenomings.
 Haemotoxic venoms can have cardiovascular and/or haemostatic effects.
 Cardiovascular effects

 dramatic fall in blood pressure leading to shock

 Haemostatic effects

 Local and systemic haemorrhage

 Overt signs include bleeding from the gums, recently healed wounds, the bite site,
the gastro-intestinal and/or genito-urinary tracts and/or haematemesis and
haemoptysis. Intracranial bleeding☠
 Venom-induced consumption coagulopathy (VICC)
 a disseminated intravascular coagulation (DIC)-like syndrome, characterised by low
or undetectable levels of fibrinogen, resulting in incoagulable blood
Haemotoxic venoms
Haemotoxic venoms
Haemotoxic venoms
Pharmaceutical
Snakebites Envenomation Risk
 Factors determining relative risks of human
envenomation by different snakes :
 Venom toxicity/potency
 In some species: size of the snake
 "Effectiveness" of the bite (at injecting venom)
 Innate aggressiveness of the snake
 Likelihood of human contact
 Not all bites by venomous snakes lead to venom
injection.
 On an average of 50% of occasions, no venom is injected
("dry bite“).
CLINICAL FEATURES
CLINICAL FEATURES

When venom has not been injected:

 Out of fear
 Vasovagal attack, bradycardia, collapse
 Misleading symptoms
 first aid
 traditional treatments.
CLINICAL FEATURES
 Following the immediate pain of the bite-increasing
local pain (burning, bursting, throbbing) at the site of
the bite
 Local swelling that gradually extends proximatelly up
the bitten limb and tender, painful enlargement of the
regional lymph nodes draining the site of the bite
 Bites by kraits, sea snakes may be virtually painless
and may cause negligible local swelling.
 Someone who is sleeping may not even wake up when bitten
by a krait and there may be no detectable fang marks or
signs of local envenoming
Local symptoms and signs in the
bitten part

 Fang marks  Lymph node enlargement

 Local pain  Inflammation (swelling,
 Local bleeding redness, heat)
 Bruising  Blistering
 Lymphangitis  Local infection
 Abscess formation
 Necrosis
 Fang marks Persistent bleeding from
fang marks 40min after
bite of pit viper

Blistering at
site of bite
SYSTEMIC SYMPTOMS & SIGNS

Generalised (systemic) symptoms and signs

 Nausea, vomiting, malaise, abdominal pain,
weakness, drowsiness, prostration

Cardiovascular (Viperidae)
 Dizziness, faintness, collapse, shock, hypotension,
cardiac arrhythmias, pulmonary oedema, cardiac
arrest
SYSTEMIC SYMPTOMS & SIGNS

Bleeding and clotting disorders (Viperidae)

 Bleeding from recent wounds (including fang marks,
venepunctures, etc) and from old partly-healed
wounds.
 Spontaneous systemic bleeding – from gums,
epistaxis, bleeding into the tears, haemoptysis,
haematemesis, rectal bleeding or melaena,
haematuria, vaginal bleeding, bleeding into the skin
(petechiae, purpura, ecchymoses) and mucosae
SYSTEMIC SYMPTOMS & SIGNS

Neurological (Elapidae, Russells’s viper)

 Drowsiness, paraesthesiae, abnormalities of taste and
smell, “heavy” eyelids, ptosis, external
ophthalmoplegia, paralysis of facial muscles, difficulty
in opening mouth and showing tongue and weakness
of other muscles innervated by the cranial nerves,
aphonia, difficullty in swallowing secretions,
respiratory and generalised flaccid paralysis
SYSTEMIC SYMPTOMS & SIGNS

Skeletal muscle breakdown (sea snakes, Russell’s viper)

 Generalised pain, stiffness and tenderness of muscles,
trismus, myoglobinuria hyperkalaemia, cardiac arrest

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 etc)
 Bleeding from
gingival sulci

Broken neck
sign in a
child
envenomed
by krait
CLINICAL ASSESSMENT
History
 Four initial questions for history of the time & circumstances of
the bite and the progression of local & systemic symptoms and
signs:
 “In which part of the body have you been bitten”
 Establish snake bite
 “When were you bitten”
 Assessment of severity of envenoming
 “Where is the snake that bit you” or “what did the snake look like”
 Establish whether snake is venomous (which snake is possible)
 “How are you feeling now?”
 Establish most important effect of envenoming: haemotoxic or
neurotoxic (e.g. dizziness/faintness – hypotension/shock;
breathlessness – incipient respiratory failure)
 Examination
 Tooth marks
 absence of discernible fang marks does not exclude snakebite; pattern
of fang punctures is rarely helpful

 Local signs
 Local swelling & enlargement, tenderness of regional lymph nodes -
often the earliest signs of envenoming ~ within 2h of bite

 Bleeding
 gums (gingival sulci) should be examined thoroughly - usually the first
sites of spontaneous systemic bleeding.
 Persistent bleeding from the fang marks, other recent wounds and
venepuncture sites suggest that the blood is incoagulable.

 Shock
 Neurotoxicity/paralysis
 Earliest symptoms – blurred vision, a feeling of heaviness of the eyelids,
apparent drowsiness. Contracted frontalis muscle.
Monitoring of snake-bitten pts
 Ideally, observed in hospital for at least 24 h after
the bite
 The following should be checked at least once every
hour and action taken if there is any deterioration
 Level of consciousness
 Pulse rate & rhythm
 BP
 Respiratory rate
 Extent of local swelling & tenderness
 New symptoms & signs
Investigations
 Haematology
 FBC
 Neutrophil leukocytosis (> 20x109/l) – severe envenoming
 Thrombocytopenia
 20-minute whole blood clotting test
 leave 2-5 ml of blood in dried test tube. Failure to clot after 20
minutes implies incoagulable blood
 PT (as INR), aPTT
 Biochemistry
 BUE and Creatinine – renal dysfunction/acid-base inbalance
 LFT – increased BIL: breakdown of extravasated blood
 Serum enzymes: CK, AST, etc -- muscle damage
Investigations
 Urine examination (appearance, stick testing
for blood, etc)
 Arterial oxygen saturation – evidence for hypoxaemia/
respiratory failure. Arterial puncture contraindicated!; use non-invasive
finger oximeter.

 ECG
 Chest radiography
MANAGEMENT
First Aid (@ Comm. Level tx)
 Move the victim to safety from the area where they might be
bitten again and remove the snake if it is still attached but not
with your bare hands.
 Reassure the victim. Most bites result in negligible or no
envenoming and, even if the patient is envenomed, there is
usually ample time to transport them to medical care. Deaths
occur in hours after elapid bites, in days after viper bites.
 Remove constricting clothing, rings, bracelets, bands, shoe etc
from the bitten limb.
 Immobilize the whole patient, especially the bitten limb, using
a splint or sling. To minimize absorption and spread of venom
from the site of the bite via veins and lymphatics
 Pressure-immobilization method

Its purpose is
to retard the
movement of
venom from
bite site into
circulation,
thus buying
time for the
patient to
reach
medical
care.
 Pressure-pad immobilisation
1 2

3 1. Applying a pad of any available

material directly over the bite
wound.
2. Securing the pad tightly with an
inelastic bandage around the bitten
limb.
3. Immobilisation – Splinting the bitten
limb to prevent movement at any of
its joints.
First Aid
 Transport the patient as quickly and as passively
as possible to the nearest facility available for
medical care (health clinic, dispensary or hospital).
 Avoid the many harmful and timewasting
traditional first-aid treatments.
 Since species diagnosis is important, the snake
should be taken along to hospital if it happens to
have been killed. However, if the snake is still at
large, do not risk further bites and waste time by
searching for it.
Contraindicated Potentially Harmful Treatments
(Do Nots)
 Tourniquet
 Dangers: ischaemia and gangrene, if applied > 2h; damage to peripheral nerves; increased fibrinolytic
activity; congestion and swelling; increased bleeding; increased local effects of venom; and, immediately
after release, shock, pulmonary embolism or rapidly-evolving life-threatening systemic envenoming.

 Wash, rub, massage or tamper with the bite wound: encourage systemic
absorption of venom from the site, may introduce infection.
 Suction bite site by mouth, vacuum pumps: Only small amount of venom
removable, increases tissue necrosis, uncontrolled bleeding
 Incision of bite site: Only small amount of venom removable, increases risk of
infection and tendon damage
 Cryotherapy (ice packs): increases tissue damage
 Electric shock
 Excision of the bite site “Snake stones”
 Cauterization
 Instillation of chemicals e.g. KMnO4
FIRST AID - summary
 The first aid recommended is based around the mnemonic: "Do it
R.I.G.H.T."
 It consists of:
R. = Reassure the patient. Most snakebites are from non-venomous species.
Only 50% of bites by venomous species actually envenomate the patient
I = Immobilize 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,
they do not work and can be dangerous!
G.H. = Get to Hospital immediately. Traditional remedies have NO PROVEN
benefit in treating snakebite.
T = Tell the doctor of any systemic symptoms such as ptosis that manifest on
the way to hospital.
Treatment of Early Symptoms
Distressing and dangerous effects of envenoming may appear
before the patient reaches a health facility.
 Local pain
 Paracetamol p.o. preferable to aspirin/NSAIDs
 Risk of gastric bleeding in pts with incoagulable blood.
 Opiates for severe pain
 Danger of respiratory depression.
 Vomitting - common early symptom of systemic envenoming.
 Lay the patient in the recovery position (on the left side), head down to
avoid aspiration.
 Persistent vomiting can be treated with chlorpromazine by IM inj (25-50
mg in adults, 1 mg/kg in children) or prochlorperazine (IM dose in
adults is 12.5 mg)
Clinical management (@ hospital):
objectives
 To relieve pain and anxiety
 To support the respiration or circulation if
indicated
 To counteract the spread and effect of the snake
venom
 To prevent secondary infection
Non-pharmacological Treatment
 Bed rest
 Reassure
 Keep warm
 Assess patient's airway, breathing and circulation
(ABC of resuscitation)
 If the snake is identified as non-poisonous or there
is absence of swelling or systemic signs after 6
hours reassure the patient
Pharmacological Treatment
 Mild sedation
 Diazepam, oral, 5-10 mg stat
 Pain relief
 Paracetamol, oral
 Morphine, IV, IM, SC
 Not Aspirin or NSAIDs
 Anti-venom treatment
 Use polyvalent anti-snake serum (ASS).
 Have resuscitation tray ready (adrenaline 1: 1000)
 Test dose-0.2 ml, subcutaneous, to test for anaphylaxis??
 ASS 50-100 ml (5-10 ampoules) depending on severity by IV drip in 0.9%
 N/S or 5% Dextrose over 2-4 hours monitor signs and repeat as required.
Pharmacological Treatment ctd
 Monitor patient and correct:
 Hypovolaemic shock - crystalloids/colloids/blood
 Defects of haemostasis - clotting factors/fresh
frozen Plasma/platelets
 Respiratory distress - O2 /intubate/ventilate.
Antivenoms
 The only specific therapy available for treating snakebite
 Indication
 Presence of symptoms and signs of systemic or severe local
manifestations of envenomation.
Antivenoms: appropriate use
 The most important and urgent decision to be made concerning
any patient bitten by a snake is whether or not to give
antivenom
 As antivenom is scarce, expensive and might have
potentially serious side effects, it should be administered
only if there is threat to life or limb.
 Administration may be associated with acute life-threatening
adverse reactions (anaphylaxis), pyrogenic (feverish) reactions, or
later immune complex disease (serum sickness).
 Antivenom is not always necessary: some patients are bitten by
non-venomous snakes and 10%-50% of those bitten by
venomous snakes are not envenomed.
Antivenoms
 Antivenom consists of polyclonal antibodies that are generated
by hyperimmunising animals (horses, donkeys or sheep) with a
single snake venom (monovalent/monospecific).
 The resulting antibodies are purified from serum or plasma and
formulated into intact IgG or F(ab’)2- or Fab-fragment
therapies.
 The antivenom is then either lyophilized or stored as a liquid
 Lyophilized antivenom has a longer shelf life but is more expensive and
must be redissolved in liquid before use.
 Liquid antivenom in glass ampoules should be stored at 2-8 oC (not
frozen).
Antivenoms: deficiencies
 Venom variation
 The antibodies present in any antivenom are specific
to those venoms that were used for immunization
 Limited cross-efficacy (paraspecificity); often restricted
to the same genus of snakes
 Polyvalent (polyspecific) antivenom – a solution
 .
Polyvalent (polyspecific) antivenom
 Generated by hyperimmunising animals against the venoms of
several snake species
 Pooled venom from many (20-50) individual specimens of each snake species;
individuals should come from different parts of the geographical range and
should include some younger (smaller) specimens
 Advantage
 Neutralizing antibodies against a wider pool of antigens
 Circumvent clinical challenges surrounding identifying the snake that has bitten a
patient required to inform antivenom choice
 Disadvantage
 Antivenom contains fewer specific antibodies to the single snake species that
envenomed the patient, effectively making them more dilute – larger therapeutic
doses are required to effect cure
 A potential increased risk of adverse reactions as larger doses of foreign protein are delivered to human victims
 An increased treatment cost as more vials are required to effect cure
Antivenom use
 Antivenom neutralizes a fixed amount of venom. Since
snakes inject the same amount of venom into adults
and children, the same dose/volume of antivenom must
be administered to children as to adults.
 Antivenom should be given as soon as possible once
signs of systemic or severe local envenoming are
evident
 It is almost never too late to try antivenom treatment for
persistent systemic envenoming; it has proved effective in
reversing coagulopathy 10 days or more after Echis bites.
Contraindication to antivemon
 There is no absolute contraindication to antivenom
when a patient has life-threatening systemic
envenoming.
 However, patients with an atopic history (severe
asthma, hay fever, etc) and those with a history of
previous reactions to equine antisera (e.g. anti-tetanus
serum) have an increased risk of severe reactions.
 pretreatment with subcutaneous adrenaline and intravenous
antihistamine and hydrocortisone is justified to prevent or
diminish the reaction.
Hypersensitivity testing
 Intradermal, sc or intraconjunctival tests with
diluted antivenom are not predictive of early
anaphylactic or late serum sickness type antivenom
reactions and should no longer be used
 The large majority of antivenom reactions are not IgE-
based, Type I hypersensitivity reactions
 Most early anaphylactic reactions to antivenom result
from direct complement activation by aggregates of IgG
or its fragments.
Antivenom: administration
 Antivenom is most effective when given intravenously.
 IM injection is not ideal and not generally recommended as
absorption is very slow.
 Antivenom can be given by IV injection at a rate of about 5
ml/min, or diluted in isotonic fluid and infused over 30-60 min.
 The initial dose of antivenom, however large, may not
completely neutralize the depot of venom at the site of
injection or prevent redistribution of venom from the tissues.
 Patients should therefore be observed for several days even if they
show a good clinical response to the initial dose of antivenom.
Response to antivenom tx
 Neurotoxic signs often change slowly, after several
hours, or unconvincingly.
 antivenom will decrease the time course of muscle paralysis
and recovery but not progression of neurotoxic effects --
patient will not survive without life support.
 In cytotoxic envenoming, administration of antivenom
will not reverse but may limit further tissue damage.
 Cardiovascular effects such as hypotension and sinus
bradycardia may respond within 10-20 min
Response to antivenom tx
 Spontaneous systemic bleeding usually stops within
15-30 min and blood coagulability is restored within
about 6 h if an adequate dose of antivenom has been
given.
 If the blood remains incoagulable 6 h after the first dose,
the dose should be repeated and so on, every 6 h, until
blood coagulability is restored.
 Anti-venom treatment

 Currently (EDL Gh) - West Africa polyvalent anti-snake serum

(EchiTAb-plus-ICP)
 Equine polyspecific antivenom against Echis Ocellatus, Bitis Arietans and
Naja Nigricollis
 It is not effective against neurotoxic elapid venoms.
 It is manufactured as a liquid preparation.
 It has to be stored at 2-8oC.
 The shelf-life of the product is 3 years.
 The initial dose of EchiTAb-Plus-ICP antivenom should be 4 vials of 10 mL.
 Before administration, the product should be visually inspected; in case of
turbidity, it should not be used.
 Antivenom reactions: Early
 Begin 3-60 min after starting IV administration of
antivenom.
 Common symptoms
 Cough, tachycardia, itching (especially of the scalp), urticaria, fever,
nausea, vomiting and headache
 More than 5% of patients with early reactions develop
systemic anaphylaxis: hypotension, bronchospasm and angioedema
 Treatment
 Adrenaline (1 in 1000 IM)
 0.5-1.0 ml for adults, 0.01 mg/kg for children.
 Followed by an IV H1-antagonist e.g.
 chlorphenamine maleate (10 mg for adults, 0.2 mg/kg for children) or
 promethazine (25 mg IM in adults)
Antivenom reactions: pyrogenic
 Result from pyrogen contamination of the antivenom
during manufacture.
 Begin within 1-2 hours after treatment: Initial chill with
cutaneous vasoconstriction, gooseflesh and shivering.
Temp. rises, then intense vasodilatation and hypotension.
 In children, febrile convulsions may occur at the peak of the fever.
 Temperature should be reduced by fanning, tepid sponging
and antipyretic medicines such as paracetamol (15 mg/kg)
given by mouth, suppository or via nasogastric tube.
Antivenom reaction: Late
 Late (serum sickness type) reactions occur 5-24
(average 7) days after treatment.
 Symptoms
 itching, urticaria, fever, arthralgia, periarticular swellings,
proteinuria and sometimes neurological symptoms.
 Treatment
 Antihistamine e.g. CPM (2 mg/6 h adult; 0.25 mg/kg/day in
divided dose for children; x5d)
 Predinisolone: patients who fail to response to antihistamine
within 24 h or severe cases
 Ancillary treatment
 Local envenoming
 Antibiotic prophylaxis –
wound infection
 Amoxicillin/clavulanate
 ATS injection
 Tetanol, IM, 0.5 ml stat

 Debridement of necrotic
tissue
 Late complications e.g
hypertrophic scar, etc
Ancillary treatment
 For Coagulopathy - if not reversed after ASV
therapy
 Fresh frozen plasma
 Cryoprecipitate (fibrinogen, Factor VIII),
 Fresh whole blood,
 Platelet concentrate.
Ancillary treatment
 For Bulbar Paralysis & Resp. Failure
 ASV alone not sufficient
 Tracheotomy, Endotrachial intubation & mechanical
ventilation
 Inj. of neostigmine - 50 to 100 microgram/kg/4hrs as a
continuous infusion
 Glycopyrrolate-0.25 mg can be given before
neostigmine in place of atropine
 Does not cross blood brain barrier
Snake venom ophthalmia

Spitting elapid
species can cause
intense conjunctivitis
and bullous corneal
erosions complicated
by secondary
infection, anterior
uveitis, corneal
opacities and
permanent blindness.
Prevention of snake bites
 In the house, where snakes may enter in search of
food or to find a hiding place for a short time.
 Do not keep livestock, especially chickens, in the house, as
some snakes will come to hunt them
 Store food in rat-proof containers
 Raise beds above floor level and use an insecticide-
impregnated mosquito net, completely tucked in under the
sleeping mat.
Prevention of snake bites
 In the farmyard, compound, or garden, try not to provide
hiding places for snakes.
 Use a light and wear proper shoes when walking outside at night.
 Clear heaps of rubbish, building materials and other refuse from near
the house.
 Do not have tree branches touching the house.
 Keep grass short or ground clear around your house and clear
underneath low bushes so that snakes cannot hide close to the house.
 Keep your granary away from the house (it may attract animals that
snakes will hunt).
 Water sources, reservoirs and ponds may also attract animals of prey.
 Listen to wild and domestic animals: they often warn of a snake nearby.
Prevention of snake bites
 In the bush or countryside, firewood collection at night
is a real danger.
 Watch where you walk. Step on to rocks or logs rather than
straight over them as snakes may be sunning themselves on
the other side.
 Do not put hands into holes, nests or any hiding places
where snakes might be resting.
 Wild animals, especially birds, may warn of snakes nearby.
 Be careful when handling dead or apparently dead snakes:
even an accidental scratch from the fang of a snake's
severed head may inject venom. Some snakes may sham
death as a defensive tactic!
Prevention of snake bites
 Rain may wash snakes and debris to the edges of roads, and
flush some species such as burrowing asps (Atractaspis) out of
their burrows. Pedestrians should be careful when walking on
roads after heavy rain especially after dark.
 Drivers or cyclists should never intentionally run snakes over on
the road.
 The snake may not be instantly killed and may lie injured and pose a
risk to pedestrians and other cyclists. The snake may also be injured and
trapped under the vehicle, from where it will crawl out once the vehicle
has stopped or has been parked in a compound or garage.
ARTHROPOD BITES AND
STINGS
Arthropods (“Bugs”)
 Largest phylum in the animal kingdom
 Insects (Hymenoptera)
 Bees, Hornets, Yellow Jackets, Wasps, Fire Ants
 Most important venomous insect known to humans
 More fatalities result from stings by these insects.
 Terrestrial Invertebrates
 Centipedes/Millipedes
 Ticks
 Spiders
 Scorpions
Hymenoptera (WASPS, BEES, AND ANTS)

 Apids are usually docile, stinging only when provoked.

 Female bee is capable of stinging only once. (Male

bees have no stinger).

 Vespid have ability to perform multiple stings.

 Most of all allergic reaction reported yearly occur from

vespid stings.
Composition of Hymenoptera
Venom
 Vespids (wasps, hornets,  Apids (honeybees)
yellow jackets)  Proteins :
 Proteins :  Phospholipase A
 Phospholipase A  Hyaluronidase
 Hyaluronidase, Antigen 5  Acid phosphatase
 Acid phosphatase  Peptides :
 Peptides :  †Melittin (50% of the venom)
 Mast cell degranulating peptide,  Apamin
kinins  Mast cell degranulating peptide
 Formicids (fire ants)
 Proteins : All venoms contain some amount of
 Phospholipase Biogenic amines (diverse)
 Hyaluronidase
†a membrane-active polpeptide---causes
 Unidentified third protein
pain, destruction of tissues, basophils and
 Alkaloids : mast cells degranulation.
 Piperidiones
Reaction to stings
 Local allergic (most common)—urticaria, etc
 Exaggerated local reaction (entire limb may swell)
 Generalized allergic → anaphylaxis
 Toxic reaction (usually from several stings): mostly GI
symptoms (nausea, vomiting, weakness)
 Delayed: resembles serum sickness
 Local infection : more common from yellow jacket stings than
from other species
 Psychiatric reactions
 Dangerous Local Reactions
 Direct eyeball sting : may cause atrophy of iris, abscess of lens,
perforation of globe
 Mouth/pharyngeal sting : local edema may cause airway obstruction
 Hymenoptera Venom: Reactions
 Anaphylactic Reaction
 Can occur from a single sting or multiple stings.
 May range from mild to fatal and death within minutes.
 There is no correlation between the systemic reaction and
the number of stings.
 Delayed Reaction
 DR appearing 5-14 days after the sting consists of serum
sickness-like signs and symptoms.
 Pts can develop fever, malaise, HA, urticaria, lymphadenopathy,
and polyarthritis.
 believed to be immune complex-mediated.
Treatment: Local reactions
 Remove imbedded stinger (honeybees) by scraping;
not by squeezing (because this may inject more venom)
 Wash the sting site with soap and water to decrease risk of
infection.
 Intermittently apply ice to the site to limit local reaction and
delay absorption of venom
 Antihistamines & analgesic may limit discomfort, pruritis, and
decrease local reaction
 Tetanus prophylaxis
 Topical steroid cream (optional and questionably
effective)
Treatment: Anaphylactic (Severe)
Reactions
 Airway management: high flow O2
 IV access : lactated ringers (LR) bolus if hypotensive
 SQ epinephrine 0.01 mg/kg (0.3 mg in adults) ; IV
epinephrine 0.1 mg if severe shock
 IV diphenhydramine 1 mg/kg (50 mg in adults)
 IV cimetidine 300 mg in adults
 IV steroids (100-250 mg hydrocortisone or
methylprednisolone, etc.)
 Consider IV dopamine or epinephrine drip if hypotensive
despite fluids
 Inhaled beta aerosol if wheezing (orciprenaline 0.3 cc or
salbutamol 2.5 cc in 3 cc NS)
Treatment: Severe hypersensitivity
reactions (cont.)

 Remove stinger
 Ice to sting site
 Tetanus prophylaxis
 Observe at least 4 to 6 hours
 Discharge on at least 3 day course of
diphenhydramine and 3 to 7 days course
of steroids (weaning dose is optional)
 Referral for desensitization to an allergist
 Consider discharge prescription for
epinephrine injection (“Epi-Pen” or “Ana-
Kit”)
Treatment: toxic envenomation
 Supportive care
 IV fluids
 Analgesics
 Antiemetics
 Treatment for hemolytic anemia, hepatic failure,
renal failure, myocardial failure, rhabdomyolysis,
DIC as needed
 Remove stingers attached to the skin
Infections from Insect Stings
 No good studies on infection incidence from
different species
 Infections that do occur are usually due to Strep
 Best rules to follow:
 If sting site red & swollen but mainly pruritic:
 treat with PO antihistamines
 If sting site red & swollen but mainly painful:
 treat with PO antibiotics
 If sting site red & swollen & pruritic & painful:
 treat with both antibiotics & antihistamines
Prevention
 Avoidance of high-risk situations
 Walking barefoot outside
 Wearing brightly colored clothes or perfumes
 Walking in orchards and flower gardens
SCORPION STINGS
 Thousands occur each year but few
are emergencies
 Most scorpions are not venomous
 Most can be managed safely at
home
 Seek urgent care for child or elderly
person
 Grasps prey by pincers and then
stings with tail
 Nocturnal
 Crawl into sleeping bags and
unoccupied clothing
 Scorpions stings

 Injects an excitatory
neurotoxin affecting
autonomic and somatic
nervous systems -minimal
local edema
 Pain, restlessness,
hyperactivity, roving eye
movements, respiratory
distress/failure
 Convulsions, drooling,
hyperthermia,
HTN/tachycardia
Scorpion Stings: First Aid

1. Monitor breathing and be

prepared to give CPR if
needed.
2. Wash area.
3. Put ice or cold pack on
area (observe time limits).
4. Seek urgent medical
attention unless symptoms
very mild.

19-122
Scorpion stings: Management
 Cryotherapy (ice) at sting site and supportive care
 Analgesic (Paracetamol, NSAIDs)/Local anaesthetic
(1% lidocaine infiltration) to relieve pain
 Antivenin if symptoms persist after supportive care
 Tachycardia, Fever, Severe hypertension, Agitation
 Sedative/anticonvulsants for persistent
hyperactivity, convulsions or agitation
 Calcium gluconate 10% 0.1ml/kg for muscle
contractions (used but unproven)