Toxinology Flashcards
What is anaphylaxis?
A severe life-threatening systemic hypersensitivity reaction *Note: ‘systemic’ can also called ‘generalised’*
By what mechanism does anaphylaxis cause death?
Upper airway obstruction, severe bronchospasm, or by profound anaphylactic shock
What are the two main types of anaphylaxis?
IgE dependent and IgE independent (also called non-allergic anaphylaxis and anaphylactoid reaction)
What is the key trigger for the majority of antigen-induced immune-mediated anaphylaxis?
IgE dependent activation of mast cells and basophils
True or false: rapid systemic development of anaphylaxis does not occur in persons who have previously been sensitised to the antigen
False - it occurs in those who have.
Describe IgE independent anaphylaxis
- A clinical syndrome with identical symptoms to anaphylaxis and with release of the same inflammatory mediators, but follows non-immunological mechanisms
True or false: IgE independent anaphylaxis may occur on first exposure to an agent and doesn’t require a sensitisation period
List some things that can trigger IgE independent anaphylaxis
- Radiography contrast media
- Opioids
- Muscle relaxants
- Physical factors/exercise/temperature
- IV immunoglobulin
- Transfusion reaction to cellular elements (IgG, IgM)
Anaphylaxis results from the sudden release of mast cell and basophil derived mediators into circulation; name three of these.
- Histamine
- Cytokines
- Chemokines
Synthesis of new mediators results from immunological reaction stimulation or any agent capable of producting a sudden ssytemic regranulation of mast cells or basophils; name three of these mediators.
- Leukotrienes
- Tumour necrosis factor
- Prostaglandin
What is the pathophysiology of IgE dependent anaphylaxis?
- Allergen-specific IgE molecules bind to mast cells and basophils via specialised receptors where they stay ready for a subsequent exposure
- When challenged there is a specific allergen release of mediators and cytokines, causing symptoms of anaphylaxis
What is the pathophysiology of IgE independent anaphylaxis?
Certain allergens/substances can trigger the mast cell cascade directly without involving IgE as the initial mediator; reactions are dose-dependent
What is the effect of mast cell activation and granule release on the GIT, airways, and blood vessels?
Describe the clinical presentation of anaphylaxis
- Rhinitis
- Conjunctival erythema, tearing
- Flushing
- Itching
- Urticaria
- Angioedema
- Dysphagia
- Stridor
- Throat and/or chest tightness
- Dyspnoea/bronchospasm
- Cough
- Wheeze
- Cyanosis
- Palpitations
- Tachy or bradycardia
- ECG changes (T and ST changes)
- Hypotension
- CA
- Vascular headache (typically ‘throbbing’)
- Dizziness/syncope
- Confusion
- N+V+D
- Abdo/pelvic pain
Describe the grading system for systemic hypersensitivity reactions and corresponding symptoms for each one
-
Mild - skin and subcutaneous tissues only
- Generalised erythema, urticaria, periorbital oedema, angioedema
-
Moderate - features suggesting respiratory/cardiovascular/GIT involvement
- Dyspnoea, stridor, wheeze, N+V, diaphoresis, throat/chest tightness, abdo pain
-
Severe - hypoxia, hypotension, neurological compromise
- Cyanosis, SpO2 <92%, hypotension, confusion, syncope, LOC, incontinence
What two conditions can mimick upper airway oedema?
- Dystonic reactions mimicking a swollen tongue
- Acute oesophageal reflux (sudden onset of painful throat that feels like swelling; *acid reflux*)
Describe anaphylaxis mx
- Remove causal agent
- High flow O2 or IPPV
- Adrenaline and salbutamol if indicated
- Consider PIT if result of bite/sting
- IV access, fluid therapy if indicated
- ECG monitoring
Describe adrenaline and its use in rx of anaphylaxis
- Alpha recepter agonist - reverses peripheral vasodilation, reduces angioedema and urticaria
- Beta1 adrenergic stimulation - has positive inotropic and chronotropic effects on cardiac muscle
- Beta2 adrenergic stimulation - leads to bronchodilation and stabilises mast cells by inhibiting histamine activation
True or false: Australian venomous snakes mainly cause systemic toxicity rather than local effects.
True
Discuss pathophysiology of coagulopathy with regard to snake bites
- Many snake venoms contain procoagulant toxins that activate the coagulation cascade
- These cause venom-induced consumptive coagulopathy (VICC)
- Brown snakes, tiger snakes, and taipans can cause significant coagulopathy
Discuss the pathophysiology of neurotoxicity with regard to snake bites
- Paralysis is a classic effect
- Neurotoxicity is due to presynaptic neurotoxins which disrupt neurotransmitter release fom the terminal axon and are associated with cellular damage
- This does not respond to antivenom
- Manifests as progressive descending flaccid paralysis
- First sign is ptosis, following by respiratory muscle paralysis peripheral weakness
Discuss the pathophysiology of myotoxicity with regard to snake bites
- Myotoxins damage skeletal muscles
- Local or generalised muscle pain, tenderness, weakness
- Muscle tissue breakdown causes release of myoglobin into the blood
- Myoglobin can damage the kidneys (rhabdomyolysis); it is associated with myoglobinuria and rapidly increasing creatine kinase
Describe presentation less than one hour following snake bite (varies depending on snake and pt)
- Headache
- N+V
- Abdo pain
- Transient hypotension associated with confusion or loss of consciousness
- Coagulopathy
- Regional lymphadenitis
- Oedema
Describe presentation one to three hours following snake bite
- Paresis/paralysis of cranial nerves e.g. ptosis, double vision
- Ophthalmoplegia, dysphonia, dysphagia, myopathic facies
- Haemorrhage from mucosal surfaces, needle punctures
- Tachycardia, hypotension
- Tachypnoea, shallow tidal volume
Discuss presentation more than three hours following snake bite
- Paresis/paralysis of truncal and limb muscles
- Paresis/paralysis of respiratory muscles (respiratory failure)
- Peripheral circulatory failure (shock), hypoxaemia, cyanosis
- Rhabdomyolysis
- Dark urine (due to myoglobinuria or haemolysis)
Describe the examination of a pt with a snake bite
- Examine patient on exposed areas for bite marks or scratches
- Look for local and regional tender lymphadenopathy
- Perform a neurological assessment looking specifically for ptosis or diplopia or other evidence of muscle weakness
- Examine muscles for tenderness and swelling
- Check for myolysis; dark or red urine indicative of myoglobinuria (positive for “blood” and so may be mistaken for haematuria)
Why is the onset of envenomation syndrome likely to be more rapid in children?
Higher ratio of venom to body mass
Justify the PIT
The PIT impedes lymphatic flow, which is how many venoms gain circulatory access
For what does the ARC recommend the use of PIT?
- All Australian venomous snakes including sea snakes
- Funnel web spider
- Blue-ringed octopus
- Cone shell snail
- Bee, wasp, and ant stings in allergic pts
What does the ARC not recommend the PIT for?
- Other spider bites (PIT funnel web only)
- Jellyfish stings
- Fish stings (stonefish etc)
- Bites or stings from scorpions, centipedes, beetles
Describe phase one of funnel web spider toxicity
- Occurs within minutes of the bite
- Symptoms include:
- Pain at the bite site
- Perioral tingling
- Piloerection (goosebumps)
- Fasciculations (most prominent in the face, tongue and intercostals)
- Fasciculations (may progress to more overt muscle spasm: masseter and laryngeal involvement may constitute a threat to the airway)
- Tachycardia
- Hypertension
- Cardiac arrhythmias
- N+V
- Abdominal pain
- Gastric dilatation
- Diaphoresis
- Pupillary asymmetry
- Lacrimation
- Salivation
- Frank pulmonary oedema
- Altered level of consciousness
Describe phase two of funnel web spider toxicity
Resolution of the overt cholinergic and adrenergic crisis. Untreated pts may have gradual onset of refractory hypotension, apnoea, and CA
What is the key toxin in redback spider bites and its chemical effect?
Alpha-latrotoxin - it acts as a presynaptic neurotoxin that stimulates the release of catecholamines from sympathetic nerves and acetylcholine from motor nerve endings in a syndrome known as latrodectism
What clinical presentation is consistent with redback spider bites?
Local and/or spreading pain which can be generalised or regional, often severe
Increased and/or local sweating
Hypertension
Nausea
malaise
Insominia
Tender and swollen regional lymph nodes
Local piloerection
Which direction should bee stings be scraped off?
Sideways
How does the toxin carried by paralysis ticks induce its effect?
Causes progressive paralysis by interfering with presynaptic transmission in motor nerves; it can also cause a relapsing fever and other reactions
Should you remove a paralysis tick from a pt?
Describe the presentation of a box jellyfish sting
- Severe localized pain
- Wide (0.5 -1cm) erythematous lines (Whip weal with frosted ladder pattern)
- Confusion, agitation
- Pulmonary oedema
- Unconsciousness
- Collapse with respiratory failure and/or cardiac arrest
Describe the typical presentation of Irukandji syndrome
- Severe lower back pain
- Muscle cramps
- Nausea and vomiting
- Restlessness
- Anxiety and “sense of Impending doom”
- Pulmonary oedema
- Hypertension
- Onset usually 5 -120 minutes post envenomation (average 30 minutes)
True or false: vinegar or salt water are to be used for nematocyst (jellyfish sting) removal, not fresh water as it activates them
True
What is the presentation of and indications for box jellyfish antivenom?
- Cardiac arrest
- Decreased LOC
- Cardiac and/or respiratory distress or collapse
- Total surface area affected > than half the surface area of one limb
- Intractable pain unrelieved by pain relief management
- Presentation: ampoules with 20,000 units of antivenom
Describe box jellyfish antivenom administration
-
Adult/Child (Non-cardiac Arrest)
- IVI 20,000 units
- Preferred route
- Administered over 10 minutes
- IMI 60,000 units
- May need multiple injection sites
- IVI 20,000 units
-
Adult/Child (Cardiac Arrest)
- IVI 20,000 units
- Administered over 2 – 5 minutes
- May be repeated up to 60,000 units
- In this setting ensure that basic cares and standard cardiac arrest management have been instigated first
- IVI 20,000 units
- Be aware of potential for anaphylaxis
Describe bluebottle jellyfish sting mx
- Pick off any adherent tentacles with fingers
- Rinse stung area well with seawater to remove invisible stinging cells - vinegar is not recommended
- Place the victim’s stung area in hot water (no hotter than the rescuer can comfortably tolerate)
- If local pain is unrelieved by heat, or if hot water is not available the application of cold packs or wrapped ice may be effective
What is the pathophysiology of blue-ringed octopus contact?
Sting contains tetrodotoxin, which causes motor paralysis due to neuronal sodium channel blockade
What is the presentation of cone shell snail or blue ringed octopus envenomation?
- Painless bite
- Numbness of lips and tongues
- Respiratory difficulty leading to paralysis of respiratory muscles (death can occur within 30 minutes of bite)
What are the divisions of clinical syndromes due to plant toxins?
*Note: dangerous ones are bracketed*
- Gastrointestinal irritants (toxalbumins)
- Cardiac toxins (cardiac glycosodes e.g. frangipani, oleander, and is also carried by some cane toads)
- Proconvulsant plants
- Hallucinogenic plants
- Anticholinergic plants
- Other hallucinogenic plants
- “Stinging” plants
List the types of seafood poisoning
- Tetrodoxtoxin poisoning (sodium channel blocking neurotoxin - pufferfish)
- Paralytic shellfish poisoning (mussels, oysters, clams, pipis, scallops, abalone, rock lobster, crab contaminated by eating dinoflagellate algae**)
- Neurotoxic shellfish (NSP) poisoning (mollusks contaminated with brevetoxins)
- Diarrhetic shellfish poisoning (bivalves)
- Encephalopathic (amnesic) shellfish poisoning (domoic acid)
- Ciguatera toxin poisoning (warm water finfish carrying ciguatera toxin)
- Scombroid poisoning (ingestion of spoiled fish with high histamine levels; also called histamine fish poisoning)
