#TOXINology #cram #tables
> [!Key Points]
> Antidote:: antivenom
See: [Cameron snakebite](x-devonthink-item://10DC3BB1-027C-40D6-BDB3-4AF0C6B160E6?page=896)
[Bear snakebite](bear://x-callback-url/open-note?id=DDC6CB1A-2E43-484A-B0E2-21228425F01E-34582-0000858523D2BE65)
| species | location | neurotoxicity | coagulopathy | cardiac effects | antivenom |
| ------------------------- | --------------------- | -------------------------------- | ------------- | --------------------- | ---------------------- |
| brown | everywhere but Tas | - | severe VICC | syncope/collapse | 2amps brown |
| tiger | Tas and east coast | delayed paralysis | VICC | sometimes early death | 2ams tiger |
| Black (mulga/red-bellied) | everywhere but tas | mild paralysis | anticoagulant | - | 1am CSL black or tiger |
| Death Adder | not VIC or tas | symmetrical descending paralysis | - | - | 1 am death adder |
| Taipan | north and Coober pedy | paralysis 1-2 hours | severe VICC | - | 1 am taipan |
![[Pasted image 20230701121314.png]]
# Snakes
## Brown snake
- sudden arrest from cardiac arrest
- Vicc
## Tiger snake
- vicc
## Red bellied black
- anticoagulant coagulopqthy
# Effects
> [!tip]- General symptoms and signs to review for
> history:
> - witnessed bite vs suspicion
> - ?multiple bites
> - time since bite
> - where
> - first aid?
>
> symptoms:
> - headache
> - diaphoresis
> - nausea/vomiting
> - abdo pain
> - diarrhoea
> - blurred or double vision
> - slurring speach
> - muscle weakness or pain
> - resp distress
> - dark or red urine
> - local pain at bite site
> - LOC
> - seizures
>
> exam:
> - evidence of bite
> - evidence of venom movement (eg swollen or tender draining lymph nodes
> - neurotoxic paralysis (ptosis, ophthalmoplegia, diplopia, dysarthria, limb weakness, resp muscle weakness)
> - coagulopathy (bleeding gumbs, venipuncture site, bite site)
> - muscle damage (tenderness, pain on movement, red/dark urine indicating myoglobinuria)
## Coagulopathy, VICC
> ==coagulopathy is a leading cause of death in human snake bite==
>
> clinical evidence:
> **bleeding** from bite site, cannula, oral cavity, or occult sites (GI, urinary, intracranial)
2 types:
- **procoagulants** (i.e. prothrombin activators): result in ==venom induced consumptive coagulopathy (VICC)==
- defibrination or [[DIC]]-like picture from brown, tiger, and taipan snakes
- activation of clotting pathway by prothrombin activator toxins and consumption of clotting factors (fibrinogen, factor V, and factor VIII) lead to a **consumptive coagulopathy**
- ==coag studies:==
- INR high or unrecordable
- aPTT prolonged
- fibrinogen level is **low** or undetectible
- D-dimer very high
- direct **anticoagulants** -- result in a a "pure" anti-coagulation picture (black snakes)
- this is biochemical abnormality usualy without clinical consequences
- aPTT si moderately abnormal (1.5-2.5 times above lab reference)
- mild elevation of INR <1.3
- D-dimer and fibrinogen levels are normal
**Thrombotic microangiopathy**:
- always associated with VICC
- microagniopathic haemolytic anameia (presence of fragmented red blood cells on blood film, thrombocytopenia, and rising Cr >120, which may lead to acute renal failure
### VICC severity grading
| parameter| severe VICC| less severe VICC|
| --- | ---| ---- |
| fibrinogen| indetectable level| low but detectible <1.5 g/L |
|INR| > 3.0 | <3.0 |
| D-dimer | very high 100-1000x | high >10x cut off, more than 2.5 mg/L |
## Neurotoxicity
- **pre-synaptic inhibitors** -- seen in tiger and taipan venom
- inhibit the release of neurotransmitter → progressive neuromuscular paralysis
- antivenom may prevent paralysis but cannot reverse neuronal damage that has already occured
- damanged neurons may take weeks to recover
- **post-synaptic inhibitors** -- seen in death adder venom
- non-depolarizing competitive block at post-synaptic receptors (like rocuronium)
> generally neurotox pattern shows cranial nerve involvement → paralysis of large limb muscles → paralysis of resp muscles
>
> ==descending flacid paralysis==
> - eye muscle (*ptosis*, ophthalmoplegia, diplopia) -- to proprly test for ptosis, get pt to look upwards for a full minute
> - followed by bulbar muscle paralysis (dysphagia, dysarthria)
> - followed by limb paralysis
> - followed by resp muscle paralysis
## Myotoxicity
cause [[rhabdomyolysis]] which can result in [[hyperkalemia]] in short term and renal failure due ot myoglobunuria in longer term
- can be local or generalised
- clinical features include:
- myalgia
- muscle tenderness
- weakness
- biochemical features:
- elevated CK levels
- CK usually nomral on admission, but rise over next 24-48 hrs (pleak from 1000 in mild cases to >100,000 in severe cases)
- K may be >5 in severe cases
- renal failure
## time course of systemic effects
- usually over 2-3 hours, but great variation; can range from immediate sudden collapse to up to 12 hrs following fite
average time course:
- within first hour
- headache
- nausea and vomiting
- collapse/transient hypotension
- 1-3 hours
- cranial nerve paralysis (fist evidence usually ptosis and diplopia, followed by dysarthria/dysphagia)
- agitation/confusion
- HTN/tachycardia
- \>3 hours
- paralysis of larger limb muscles
- resp paralysis
- cardio collapse
- rhabdo
- renal failure
- coma
# Treatment
## overview
1. pressure bandage
2. baseline bloods
1. if normal and no features of envenomation → remove pressure bandage → re-check bloods at 1 hour, if still normal, SSU and re-check at 6 hours, 12 hours
2. if abnormal or evidence of envenomation → antivenom
3. If patient remains w/o signs of envenomation and bloods normal at 12 hours, pt discharged in daylight
> [!important] absolute indications for antivenom
> sudden collapse
> seizure
> cardiac arrest
> INR > 1.3
> clinical evidence of paralysis, ptosis and/or ophthalmoplegia
>
> relative indications:
> - systemic symptoms
> - leukocytosis CK >1000
> - elevated aPTT
## pressure immobilisation bandage
- apply pressure bandage starting from teh bite site up the entire limb
- immobilise the limb with a splint, keep patient calm and still
- do not remove the pressure bandage until in facility equipped for snakebite management
# Antivenom
**Brown snake antivenom** - brown snake envenomation
**tiger snake antivenom** - tiger snake, copper head, red-bellied black snake
> *administration:* dilute ampule in 100 mL NaCl, infuse over 15-30 min
# indications
- Clinical evidence of systemic envenoming
- Laboratory evidence of coagulopathy
- CK >1000
## allergy to antivenom
- anaphylaxis incidence ~30%
- Usually mild and manifests w/ erythema or urticaria. Severe cases have hypotension
- stop infusion, then re-start at slower rate if small reaction
- hypotension → fluid resus
- hypotension + hypoxia, wheeze, or stridor → adrenaline 0.01 mg/kg to 0.5 mg
## serum sickness
see also [[Rash#serum sickness]]
- occurs in ~1/3 of pts given antivenom
- flu-like sx: fever, myalgia, arthralgias, rash
- generally develops 4-14 days after administration of antivenom
- warn all patients about serum sickness who get antivenom
- tx: Oral steroids (e.g. prednisolone 50 mg/day in adults or 1–2 mg/ kg/day in children for 5 days) ameliorate symptoms.
# Treat coagulopathy
antivenom
==give FFP in addition to antivenom if life threatening bleeding==
# Related Questions
## snake bite
- [x] 85Q: [Snake Bite](x-devonthink-item://834C484F-DDAA-4819-8DF0-84AE5E70DA1D?page=17) -- [Answer](x-devonthink-item://D46998FE-62E2-4A3A-860D-C32C94B86E42?page=7)
## snakebite
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