Envenomation Flashcards
Discuss briefly the clinical effects of Australian alpidae snakes
Brown
- Consumptive coaguloapthy alwasy present- VICC alwasy present with bleeding of gums and persistant haemorrahge at venesection sites or intracerebral bleeding. -INR >3 but usually unrecordable, undetectable fibrinogen and elevated dimer >100
-Parital VICC INR <3 but abnormal with low but detectable fibrinogen
-Recovery of VIC occurs at the 10-20 hour mark
-MAHA + renal failure in 10%
-neurotoxcitiy rare,
- myotoxicity not present
-Early collapse occurs in 33% of cases and arrest in 5%
-Systemic symptoms are often absent (50%)
Thrombotic microangiopahy (10%)
Tiger
- Consumptive coaulopathy always present with significant enveoming but may resolve spontaneously in 24 hours,
- Neurotoxicity develops in about 30% of envenomings and is usually apparent within 1-2 hours of the bite, but is slow in onset and progresses over many hours.
- Myotoxicity uncommon slow onset (20%)
- MAHA
- Systemic symptoms common
- Thrombotic microangiopahy (<5%)
Death adders
- Consumptive coagulopathy not present
- neurotoxicity common - symmetrical descending paralysis usually manifest within 6 hours. Early sings include ptosis, blurred vision, diplopia and difficulty swallowing.
- myotoxicity not present
- systemic symptoms common local bite site pain often present
Black ( Mulga, Collet, Butler)
- Systemic features of headache, abdo pain, Nause D&V are almost universal in envenomation.
- Consumptive coaguloapthy not present, anticoagulant coagulopathy is frequent but clinical features such as bleeding gums are rare. -Minor elevation in ApTT and INR otherwise normal profile
- Acute haemolysis may occur and cause anaemia although is rarely of sufficient magnitude so as to require blood transfusion
- Neurotoxicity not present
- Myotoxicity - common may develop over hours to day may be severe and result in renal failure
BLACK (Red bellied and blue bellied black)
- Local pain + systemic symptoms
- small proportion develop myotoxicity - myalgias and minor CK raise
- Anticoagulant coaguloapthy may occur but is not usually associated with clinically significant bleeding
- Minor but unpleasent long term neuro sequelae may occur such as anosmia and areas of numbness and parasethesia.
Taipan
- May be heralded by collapse within a few minutes
- Consumptive coagulopathy always present with significant envenomation
- Neurotoxicity common
- Myotoxicity rare
- Systemic symtpoms common
- Thrombotic microangiopahy (<5%)
Sea snake -coaguloapthy not present Neurotoxicity present Myotoxicity common Systemic symptoms common
Discuss prehospital care in snake bite
First aid aims to delay lympahtic spread of venom
- Keep patient calm and still
- Avoid tourniquets, ice, cutting, cuking of the bite site or electric shocks
- Apply PIB- broad elasticised pressure bandage over the entire limb, immobilisation of limb, immobilistation of the whole patient
- If bite on torse apply direct pressure immobilise patient
- dont wash site as may need SVDK
- PBI may be left on for hours don’t remove unless
- – fully assessed in an appropriate hospital or antivenom administration has commenced
Discuss transport of a snake bite patient
Patients should be transported to a hospital that
1) has doctors present, able and willing to undertake snakebite managment including definitive treatment of severe envonomation and management of early complications of treatment ie: anaphylaxis
2) Laboratory facilities capable of performing necessary investigations on a 24 hour basis
3) antivenom stocks adequate for definitive treatment of severe envenoming by all snakes indigenous to that geopgraphical area
Discuss resuscitation of snake bite patients
Most patient will not require
Potential life threat associated with australian terrestrial snake envenoing incldue
- cardiac arrest
- sudden collapse (hypertension)
-respiratory failure secondary to paralysis
-seizures
-uncontrolled haemorrhage secondary to severe venom induced consumptive coaguloapthy
Discuss determining whether a patient has been envenomed
Based on history, physical examination and laboratory resutls
History
- Geopgraphical area of bite
- Appearance of snake (usueally only useful for death adders and red bellied black snakes)
- Anatomical site of bite
- Number of strikes
- Use of PBI
- early symptoms (collapse, nausea and vomitnig, bleeding, weakness)
- pre hosptial course
Examination
- Vitals
- Mental state
- Evidence of bite
- lymphadenopathy
- evidence of abnormal bleeding (especiall bite site, gingival sulci)
- evidence fo descending symmetrcial flaccif paralysis (occular, small muscles of the face and bulbar function
- respiratory (peak expiratory flow rate)
Bloods
- Coags (INR and aptt, d-dimer)
- FBC
- CK
- Renal fucntion
Bloods taken initially if nil biochemical or physical signs of envonmation bloods 1 hour post bandage and then 6 and 12 hours post bite if all g can go home
Discuss what type of antivenom to use
Monovalent antivenom is preferable to polyvalent as it is more specific, cheaper and associated with less adverse events
Polyvalent consist of one of each of the monovalent vials – represent a large protein laod and is therefore associated with an increased risk fo anaphylaxis
- indications for polyvalent include clinical or lab evidence of snak envenoming in australia or PNG when the correct monovalent antivenom cannot be identified or is not avialable
- Not requried in Tasmania – tiger antivenom is recommended, or in Victoria (combiantion of brown and tiger)
Use of antivenom is base on
- knowledge of snakes found in the area
- clinical syndrome
- snake identifciation if viable should be performed by professional herpetologits
In many regions particular in the southwest and east one vial each of brown and tiger snake antivenom will cover the clinical important snake particularly if VICC is presnet
Discuss how to administer antivenom and complications of administration
- One vial of relevant snake monvalent antivenom is required to treat both children and adults. It is given by IV infusion diluted 1:10 into normal saline over 15 minutes
- Give as a slow push in arrest or life threatening situations
- the use of repeat or multiple vials is no longer recommended based on invitro and clincial evidence from the australian snakebite project
- premedication for anaphylaxis is not required - but should be ready to treat - should be given in a critical care area
Immediate
1) Anaphylactic reaction
- incidence is approxiamtly 40%
- usually mild and manifested by erythema or urticaria - severe cases manifest with hypotension
- stop infusion
- Give 02, iv fluids and IMI adrenalein 10mic/kg to lateral thigh
- once resolved antivenom infusion cautiously restarted
Delayed
1) Serum sickness
- Benign self limiting complicaiton may occur 5-10 days after antivenom
- manifestation include, fever, rash arthralgia and myalgia
- oral steroids (prednisone 50mg/day) ameliiorate symptoms
- all patient should be warned about this potentional side effects prior to dischareg
Discuss SVDK
SVDK is designed to support the choice of a single monovalent antivenom to use
It is not used to determine whether envenomation has occurred. False positive and -ves occur If the SvDK does not match the clinical picture treat the pitcutre.
If there is doubt about the snake responsible two monovalent antivenoms are superior to polyalent
Cut a key hole in the PBI to access the snake bite for the swab - may be performed on urine as a second line, never on serum or blood
Discuss adjunct therapy
- Wound care
- ADT
- Clotting factor replacement is controversial and the subject of ongoing research. It is reasonable to administer FFP folowwing antivenom administration to patient who have active and potentially life threatening bleeding.
- Products hasten the recovery of INR in some patient but will prolong coaguloatphy in others
Serum sickness after 1 or 2 vials is unlikley
prednisone 1mg/kg up to 50mg for 5 days mare attenuate the severity of the symptoms
Discuss systems effected in envenomation
System -Nausea vomting -Headache 0abdominal pain -diarrhoea -diaphoresis
CNS:
- decending paralysis, ptosis, facial and bulbar involvement -paralysis extraoculur muscles
- repsitorary waekness
CVS
- Sudden collapse
- Cardiac arrest
- Dizziness
- Hypotension
Coagulation
- Local site bleeding or braising
- Haemorrhage (GIT, CNS, Genuri, mucous membranes)
Myotoxicity
- Muscle pain
- tenderness and weakness
- CK and myoglobuinuria
Other
- Renal failure (Microangiopathic haemolytic anaemia)
- Local pain
- swelling
Discuss indications for antivenom administration
Absoulute
- Sudden collapse, cardiac arrest or seizure
- abnormal INR - evidence of VIC
- evidence of paralysis with ptosis and or opthalmoplegia - any neuro features
Relative
- Systemic sx (vomiting, headache, abdominal pain)
- Abnormal aPTT
- CK >1000UL
- Leucotytosis/lymhpopenia
Discuss sea snake envenomation
Most bties are small superficial and relatively painless
Non specific features of envenoming including headache nasuea and vomtign
Systemic envenoming is usually characterised by symmetrical descending flaccid paralysis which usually manifests within 6 hours. Early signs include ptosis blurred vision diplopia and difficulty swallowing. If left untreated it may progress to generalised paralysis resp failure and secondary hypoxic cardiac arrest.
Protentional early life threats that require immediate intervention include
- -rapid onset paralysis with secondary resp failure
- hypotension
Discuss bluebottle envenomation
The toxins are contained within nematocysts on the tentacles and released on contact.
Stings are associated with immediate burning pain typically lasting up to 2 hours and linear or elliptical erythematous welts
Stings are mild self limiting and respond to first aid
- reassure the patient
- placed under a hot shower for 20 minutes - should not be scalding or uncomfortable
- simple analgeisa
DDX
Pain associated with irukandji syndrome is usually delayed severe and generalised. Significant linear dermal markings are not seen
-
Discuss stonefish envenomation
TOXIN: the venom contains pre and post synaptic neurotoxins vascular permeability factors tissue necrosis factors and a vasodilator
Clinical:
- immediate severe pain at the site
- local swelling brusing and puncture makrs - a remnant of the spne may be left in the wound
- systemic envonomation is rare
- CVS signs such as hypotension, bradycardia, collapse pulmonary oedema and cyanosis are rarely reported
Prehospital -
Reassure the patient and give simple oral analgesia such as paracetaol.
-Immerse both limbs in hot water- the unaffected limb is immeresed to ensure the water temperature is tolerable
Hospital
- Continue hot water immersion
- Morphine as needed
- consider regional anaethesia with a long active local
Antivenom
- Used in treatement of severe pain refractory to first air, opiates and regional anaethesia
- give 1 ampule (2000 units) for every two spine puncture wounds (max of 3 ampules) undiluted by IM injection or diluted in 100ml of normal saline IV over 20 minutes
DIscuss box jellyfish (chironex fleckeri) envenomation
TOXIN: still to be identificed – the lethal component appears to affect CA channels.
Clinical
- stings are associated with immediate severe pain, typically lasting up to 8 hours and linear welts which charactersitically occur in crosshatched pattern
- in 25-30% of cases the sting is still adherant
- systemic envenoming is heralded by collapse or sudden death within a few minutes of the sting
- CVS effects includ HTN, hypotension, tachycardia impaired contraction and dysrhythmias
- delayed hypersensitivity reaction occur in at least 50% of patients and manifest as pruritic erythema at the original sting site 7-14 days after the sting
