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TETANUS

ETIOLOGY – Clostridium tetani


• Anaerobic gram-positive –
• cannot survive heat and
oxygen
• Spore-forming bacteria
• very resistant to heat and the
usual antiseptics. They can
survive autoclaving at 249.8°F
(121°C) for 10–15 minutes;
resistant to phenol and other
chemical agents
• Spores found in soil, animal
feces
https://www.cdc.gov/vaccines/pubs/pinkbook/downloads/tetanus.pdf
• Two exotoxins
• Tetanolysin
• Tetanospasmin
• a neurotoxin
• estimated human lethal dose = 2.5 ng/kg
• The incubation period—3 to 21 days after
infection.
• Most cases occur within 14 days.
PATHOGENESIS
Anaerobic
conditions allow Toxin binds in
germination of central nervous
spores and system
production of toxins

Leads to Interferes with


unopposed muscle neurotransmitter
contraction and release to block
spasm inhibitor impulses

https://www.cdc.gov/vaccines/pubs/pinkbook/downloads/tetanus.pdf
Tetanus Prone Wound
Wounds are considered to be tetanus-prone if they are
sustained either more than 6 hours before surgical treatment of
the wound or at any interval after injury and show one or more
of the following:
1. Puncture wound
2. Significant degree of devitalized tissue
3. Clinical evidence of sepsis
4. Confirmation with soil/manure likely to contain tetanus
organism
5. Burns
6. Frosbite
7. High velocity missile injuries
WHO ATS Recommendation
TIG Admission for Adult and Child
1. 250IU IM
2. Increase to 500IU IM if
 Wound older than 12 hours presence
 Risk of heavy contamination
 Patient more than 90kg
RABIES
• Rabies is an infectious viral disease that is almost always
fatal following the onset of clinical symptoms.
• In up to 99% of cases, domestic dogs are responsible for
rabies virus transmission to humans
• .Yet, rabies can affect both domestic and wild animals.
• Spread to people  bites or scratches, usually via saliva.
SYMPTOMS
• Incubation period -- 2–3 months
• but may vary from 1 week to 1 year,
• dependent on -- location of virus entry and viral load.
• initial symptoms of rabies include
• a fever with pain and unusual or
• unexplained tingling,
• pricking, or
• burning sensation (paraesthesia) at the wound site.
• As the virus spreads to the central nervous
system, progressive and fatal inflammation of the
brain and spinal cord develops.
TYPES OF RABIES
• Furious rabies
• hyperactivity,
• hydrophobia (fear of water)
• aerophobia (fear of drafts or of fresh air) -
sometimes
• Death occurs -- cardio-respiratory arres in 2
days

• Paralytic rabies
• Missdiagnosed  under reporting cases
DIAGNOSIS
Current diagnostic tools are not suitable for
detecting rabies infection before the onset of
clinical disease, and
• unless the rabies-specific signs of hydrophobia or
aerophobia are present, clinical diagnosis may be
difficult.
• Human rabies can be confirmed intra-vitam and
post mortem by various diagnostic techniques
that detect whole viruses, viral antigens, or
nucleic acids in infected tissues (brain, skin,
urine, or saliva).
TRANSMISSION
• People are usually infected following a deep bite or
scratch from an animal with rabies, and transmission to
humans by rabid dogs accounts for 99% of cases.
• Afrika and Asia – 95% rabies death worldwide
• America, Australia, and Western Europe  bats
• Rodents  do not have evidence
• Transmission can also occur when infectious material –
usually saliva – comes into direct contact with human
mucosa or fresh skin wounds.
• Human to human bites  no evidence
• Contracting rabies through consumption of raw meat or
animal-derived tissue has never been confirmed in
humans.
WHO recommendation 2014
• Rabies –
• Pre-Exposure (PrEP)
• Post-Exposure (PEP)
SNAKE BITE
• Venom glands of Elapidae and Viperidae are situated
behind the eye, surrounded by compressor muscles.
• The venom duct opens at the base of the fang,
conducting venom to its tip through a groove or canal.
• In Viperidae, but not Elapidae or Colubridae, fangs are
mounted on a rotatable maxilla, making them erectile.
• In Colubridae, venom secreted by Duvernoy’s
(supralabial) glands tracks down grooves in posterior
maxillary fangs.
• Spitting cobras squeeze venom forward from tips of their
fangs in a fine spray directed towards the eyes of an
aggressor.
Venomous snake in SEA
• Elapidae
• Viperidae
• Colubridae
Elapidae
• relatively long,
• thin,
• usually uniformly-coloured snakes
• large smooth symmetrical scales on the top of the
head.
• cobras (Naja), kraits (Bungarus), death adders,
taipan, black and brown snakes (Acanthophis,
Oxyuranus, Pseudechis, Pseudonaja) and sea-
snakes
Viperidae
• divided into
• typical vipers (Viperinae) and
• pit-vipers (Crotalinae) that have a heat-sensitive loreal
pit organ situated between nostril and eye.
• relatively short,
• thick-bodied,
• short-tailed snakes
• many small rough scales on the top of the head
• characteristic patterns of coloured markings on
their backs.
Colubridae
Among Colubridae, red-necked keelback
(Rhabdophis subminiatus) and yamakagashi
(R. tigrinus) are dangerous.

More than a dozen other species can cause


mild local envenoming (e.g. cat snakes -
Boiga).
EPIDEMIOLOGY SNAKE BITE
• Indonesia: medically important species throughout the
>18 000 islands include
• B. candidus,
• N. sputatrix,
• N. sumatrana,
• C. rhodostoma ,
• T. (T.) albolabris;
• D. siamensis and, in West Papua and Maluku,
Acanthophis laevis.
• Hundreds of bites each year are treated in Sumatra, Java,
East Kalimantan, Sulawesi, Wetar and West Papua.
SNAKE CLASSIFICATION
• CATEGORY 1: Highest Medical Importance
• highly venomous snakes that are common or
widespread and cause numerous snakebites,
resulting in high levels of morbidity, disability or
mortality.
• CATEGORY 2: Secondary Medical Importance
• highly venomous snakes capable of causing
morbidity, disability or death, but for which (a)
exact epidemiological or clinical data are lacking
or (b) are less frequently implicated because of
their behaviour, habitat preferences or occurrence
in areas remote from large human populations.
PATOFISIOLOGI SNAKE VENOM
• Local envenoming
• Hypotension and shock
• Bleeding and blood clotting disturbances
• Procoagulant enzymes activate intravascular coagulation,
producing consumption coagulopathy and incoagulable blood
• Complement Activation
• Neurotoxicity
• Neurotoxic polypeptides and PLA2s  paralysis by blocking
transmission at the neuromuscular junction.
• Patients with paralysis of the bulbar muscles may die of upper
airway obstruction or aspiration, but the most common mode of
death after neurotoxic envenoming is respiratory paralysis.
• Myotoxicity
Recommended first-aid:
• Reassurance,
• Immobilization of the whole patient, especially their bitten
limb,
• Accelerated transport to medical care (summoned by
emergency telephone helpline) ideally in recovery
position.
• Unless neurotoxic elapid bite can be excluded, apply
pressure-pad (simpler, more practicable than
pressurebandage immobilization).
• Never use, recommend or condone tight
(arterial) tourniquets
• In Indonesia, Biofarma produces a
polyvalent antivenom to cover venoms
of neurotoxic Naja sputatix, Bungarus
fasciatus (that rarely, if ever, bites
humans) and Calloselasma rhodostoma,
but, unaccountably, ignores important
species such as Bungarus candidus,
Daboia siamensis, Trimeresurus species
and all the Eastern Indonesian Australasian
Elapidae.
Management
• Primary Survey
• [Danger]
• [Response]
• Airway
• Breathing
• Circulation
• Disability
• Environment
• Secondary survey
History
• 4 INITIAL QUESTIONS
• “Where (in what part of your body) were you bitten?
Point to the place” Observe any local signs – fang
marks, swelling, bruising, persistent bleeding,
prehospital traditional treatment\
• “When were you bitten and what were you doing when
were you bitten?” If the bite was very recent, there may
not have been time for signs of envenoming to
develop. If the patient was bitten at night while asleep, a
krait was probably implicated; if in a paddy field, a cobra
or Russell’s viper; if while tending fruit trees, a green pit
viper; if while swimming or wading in water a cobra
(fresh water) or sea snake (sea or estuary).
• “Where is the snake that bit you?” or “What did it look
like; did anyone take a picture?”
• “How are you feeling now?”
PEMERIKSAAN FISIK
• Examination of the bitten part
• General examination
• Neurotoxic envenoming: Bulbar and respiratory paralysis
• Generalized rhabdomyolysis
• Examination of pregnant women
Ptosis examination
SPECIES DIAGNOSIS
• Photo
• Snake was bought up
• Description
PEMERIKSAAN PENUNJANG
• 20 minute whole blood clotting test
PEMERIKSAAN PENUNJANG
• plasma prothrombin time (PT) or activated partial
thromboplastin time (aPPT) and measurement of
fibrin(ogen) related antigens, also known as fibrin
degradation products (FDP) or fibrin split products (FSP),
by agglutination of sensitized latex particles or of D-dimer
• The International Normalized Ratio (INR)
• Thrombo-elastography (TEG) and thromboelastometry
(TEM, ROTEG, ROTEM)
ANTIVENOM
• is the only specific antidote to snake venom.
• immunoglobulin [usually pepsin-refined F(ab’)2
fragment of whole IgG] purified from the plasma
of a horse, mule or donkey (equine) or sheep
(ovine) that has been immunised with the venoms
of one or more species of snake.
• Types: monospecific and polyspecific
• In Indonesia, Biofarma produces a polyvalent antivenom
to cover venoms of neurotoxic Naja sputatix, Bungarus
fasciatus (that rarely, if ever, bites humans) and
Calloselasma rhodostoma, but, unaccountably, ignores
important species such as Bungarus candidus, Daboia
siamensis, Trimeresurus species and all the Eastern
Indonesian Australasian Elapidae
How long after the bite can antivenom be
expected to be effective?
• as soon as it is indicated
• reverse systemic envenoming even when this has
persisted for several days or, in the case of haemostatic
abnormalities, for two or more weeks.
Antivenom reactions
• A substantial proportion of patients develop reactions,
either early (within a few hours) or late (5 days or more)
after being given antivenom.
• Example:
• Early anaphylactic reactions
• Pyrogenic (endotoxin) reactions:
• usually develop 1-2 hours after treatment
• shaking chills (rigors), fever, vasodilatation and a fall in blood pressure.
• Febrile convulsion
• Late (serum sickness type) reactions:
• develop 1-12 (mean 7) days after treatment
• fever, nausea, vomiting, diarrhoea, itching, recurrent urticaria,
arthralgia, myalgia, lymphadenopathy, periarticular swellings,
mononeuritis multiplex, proteinuria with immune complex nephritis and
rarely encephalopathy.
Contraindications to antivenom:
Prophylaxis of high risk patients
• no absolute contraindication
• patients who have reacted to horse (equine) or sheep
(ovine) serum in the past (for example after treatment with
equine anti-tetanus serum, equine anti-rabies serum or
equine or ovine antivenom)
• those with a strong history of atopic diseases (especially
severe asthma) are at high risk of severe reactions and
should therefore be given antivenom only if they have
signs of systemic envenoming.
Prevention of antivenom reactions
• Subcutaneous epinephrine (adrenaline) *adult dose
0.25mg of 0.1% solution is given just before antivenom
treatment is started (see below), followed by an
intravenous anti-H1antihistamines such as
chlorphenamine.
• The adult dose of epinephrine (adrenaline) is 0.25ml of 0.1%
solution (0.25 mg) by sub-cutaneous injection (children 0.005 ml/kg
body weight of 0.1% solution) (T)
• In asthmatic patients, prophylactic use of an inhaled
adrenergic β2 agonist such as salbutamol may prevent
bronchospasm.
Supply, selection, storage and shelf-life of
antivenom
• SUPPLY
• to determine how much antivenom remains unused 
CALCULATION
• SELECTION
• Polyvalent (polyspecific) antivenoms are preferred
• STORAGE
• Lyophilised antivenoms (shelf life about 5 years) should be stored
at below 25ºC and
• liquid antivenoms (shelf life 2-3 years) should be stored at 2-8 ºC
and not frozen
• Can be used – out of expired date
• liquid antivenoms --vopaque or which contain visible particles should not
be used as precipitation of protein indicates loss of activity and an
increased risk of reactions.
Administration Antivenom
• Freeze-dried (lyophilised) antivenoms are
reconstituted, usually with 10 ml of sterile water
for injection per ampoule.
• Administration
• Intravenous “push” injection:
• slow intravenous injection (not more than 2 ml/minute)
• Intravenous infusion
• freeze-dried or neat liquid antivenom is diluted in
about 5 ml of isotonic fluid per kg body weight (i.e.
about 250 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 30-60 minutes.
Administration Antivenom
Administration
• Intramuscular injection of antivenom
• Large molecules  absorb slowly by lymphatics
• Bioavailability is poor, especially after intragluteal injection
• Hematoma formation
• Isciatic nerve damage
• Can be used when:
• at a peripheral first aid station, before a patient with obvious
envenoming is put in an ambulance for a journey to hospital that
may last several hours (Win-Aung et al., 1996);
• on an expedition exploring a remote area very far from medical
care;
• when intravenous access has proved impossible.
DOSAGE ANTIVENOM
• In practice, the choice of an initial dose of antivenom is
usually empirical
• Some antivenom dosage regimens recommended in
national management guidelines seem illogical, based on
what is known of the pharmacokinetics and
pharmacodynamics of venom-antivenom interactions
Observation after adm. antivenom
Conservative management
• Neurotoxic envenoming with respiratory paralysis:
assisted ventilation assisted for a month; using
anticholinesterase
• Haemostatic abnormalities: strict bed rest to avoid minor
trauma; transfusion coagulation factor or platelet  be
careful of microthrombi
• Shock, myocardial damage: hypovolaemia should be
corrected with colloid/crystalloids, controlled by
observation of the central venous pressure. Ancillary
pressor drugs (dopamine or epinephrine-adrenaline) may
also be needed. Patients with hypotension associated
with bradycardia should be treated with atropine.
Conservative management
• Acute kidney injury: conservative treatment or dialysis
• Dark brown urine (myoglobinuria or haemoglobinuria):
correct hypovolaemia with intravenous fluid, correct
acidosis with a slow intravenous infusion of 50-100 mmol
of sodium bicarbonate.
• Severe local envenoming: local necrosis,
intracompartmental syndromes and even thrombosis of
major vessels  surgical (warning). Prophylactic broad
spectrum antimicrobial treatment – be used.
Anticholinesterase treatment
• Atropine sulphate (0.6 mg for adults; 50 μg/kg for
children) or glycopyrronium is given by intravenous
injection followed by neostigmine bromide or
methylsulphate (Prostigmin) (or distigmine,
pyridostigmine, ambenomium etc. in appropriate doses)
by intramuscular injection 0.02 mg/kg for adults, 0.04
mg/kg for children.
• Short acting edrophonium chloride (Tensilon) is ideal for
this test but is rarely available in the Region. It is given by
slow intravenous injection in an adult dose of 10 mg, or
0.25 mg/kg for children.
• The patient is observed over the next
30-60 minutes (neostigmine) or 10-20
minutes (edrophonium) for signs of
improved neuromuscular transmission.
• Ptosis may disappear (Fig 83) and
ventilatory capacity (peak flow, FEV-1 or
maximum expiratory pressure) may
improve.
• Patients who respond convincingly can be
maintained on neostigmine methylsulphate,
0.5-2.5 mg every 1-3 hours up to 10 mg/24
hours maximum for adults or 0.01-0.04
mg/kg every 2-4 hours for children by
intramuscular, intravenous or subcutaneous
injection together with atropine to block
muscarinic side effects.
• Patients able to swallow tablets may be
maintained on atropine 0.6 mg twice each
day, neostigmine 15 mg four times each day
or pyridostigmine 60 mg four times each
day.
ICE PACK TEST
Treatment of the bitten part
• WOUND MANAGEMENT
• Blisters/bullae/”blebs” – aspiration only if threaten to rupture
• Abscesses – aspirated
• Frank skin necrosis  surgical debridement
• ANTIBIOTIC
• immediate broad spectrum antibiotics (e.g. gentamicin with benzyl
penicillin, amoxycillin or a cephalosporin plus a single dose only of
gentamicin – to avoid the risk of kidney injury- plus metronidazole)
and tetanus prophylaxis.
• Other possible antibiotics include amoxycillin/caluvulenic acid,
piperacillin/tazobactam, ciprofloxacin and third generation
cephalosporin.
Treatment of the bitten part
• Compartmental syndromes and fasciotomy
Discharge assessment
• Implications of having had a snakebite: most patients can be
assured of a full recovery in time.
• Rehabilitation exercises: encourage them to continue until
normal function is restored to the bitten limb.
• Follow-up appointment: encourage the patient to return after an
interval of 1-2 weeks to check on their progress and to allow
further reassurance.
• Late serum sickness-type reactions:warn them of the
symptoms and reassure them that this complication of
antivenom can be treated.
• Reducing the risk of further bites: provide advice, ideally in the
form of a leaflet, explaining the principles of snakebite
prevention to be shared with their families and neighbours.