Specific Considerations (Murray 2.1-2.7) Flashcards
Describe the first aid for snake bites.
Pressure 15cm bandage to whole limb with immobilisation. Transport to a hospital with (a) doctors able to manage, (b) antivenom on site, (c) 24/7 laboratory on site
What is the minimum duration of observation for suspected snake bite victims?
12 hours - serial exams, serial bloods
Describe the hospital management steps for a snake envenomation.
(1) Resuscitation, (2) Determine if envenomation actually occurred, (3) Assessement over 12 hours: hx, exam, labs, (4) Determine type of antivenom required (indigenous snakes, lab features, clinical picture, CSL SVDK), (5) Give antivenom, (6) Adjuvant/supportive treatment
In what snake envenomation is neurotoxicity rare/not present?
Black and brown snake bites, sea snakes and tiger snakes
In what snake envenomation is neurotoxicity common?
Death adders, taipan
With what snake envenomations is myotoxicity common?
Black and sea snakes
With what snake envenomations is venom-induced consumptive coagulopathy present?
Brown, tiger snakes and taipans
Describe the clinical picture with a brown snake envenomation.
Always has coagulopathy, no neuro- or myotoxicity. Patients have early collapse (33%) or cardiac arrest (5%). Systemic symptoms are frequently abscent (50%). There may be thrombotic microangiopathy (10%).
Describe the clinical picture with tiger snake envenomation.
Patients always have (self-resolving) coagulopathy, uncommonly neuro- and myotoxicity but systemic symptoms are common and thrombotic microangiopathy occurs in <5%
Describe the clinical presentation with death adder envenomation.
No coagulopathy but commonly neurotoxicity without myotoxicity. Some local bite site pain and commonly have systemic symptoms.
How do patients with black snake envenomation present?
Mild anticoagulant effects, no neurotoxicity but myotoxicity is common resulting in renal failure over hours/days. B
What can be said about the coagulation profile in patients with black snake envenomation?
Raised APTT and INR but fibrinogen remains normal, mild anticoagulant effect only. Severe pain + swelling at bite site + commonly have systemic symptoms.
What are the two painful snake envenomations?
Death adders, black snake
What is the clinical presentation anticipated with a taipan snake envenomation?
Significant coagulopathy with common neurotoxicity that is rapid in onset. No myotoxicity and uncommonly thrombotic microangiopathy (5%). Systemic symptoms common.
How do sea snake envenomations present typically?
No coagulopathy, no neurotoxicity but commonly myotoxicity developing over minutes to hours. Systemic symptoms common.
When can the pressure bandage immobilisation be removed?
Not until: the patient has been fully assessed and initial labs are back + antivenom administration has been commenced
Describe the labs to send for a patient who is thought to have been envenomated.
Coags (INR, APTT both required + if possible d-dimer + fibrinogen). FBE, UEC, CK, urinalysis (blood/myoglobin), LDH.
How do you do an early assessment of myotoxicity?
Descending symmetrical flaccid paralysis (ocular, small muscles of face/bulbar function) affected first
What blood test cannot be used to diagnose envenomation?
D-dimer; very high false positive + negative rates
When should patients post-suspected envenomation not be discharged?
At night, subtle delayed neurotoxicity might not be detected
What type of antivenom is used typically in South-West and South-East Australia?
One vial of brown snake and one vial of tiger snake monovalent antivenom
What type of antivenom is preferred?
Monovalent antivenom; less likely to cause anaphylaxis due to smaller protein load
What is the rate of anaphylaxis to snake venom?
1% for monovalent and 5% for polyvalent
In what time frame is a response predicted with antivenom administration?
It may take 10-20 hours for coags to start to normalise but 24-36 horus for them to return to normal
What condition is possible after administration of antivenom?
Serum sickness; it is unlikely after administration of 1-2 vials of monovalent antivenom. Can give 50 mg/day (1 mg/kg/day) of prednisolone for 5/7 to attenuate the severity.
On what tissue samples can a SVDK be done?
On urine or skin (bite site) but never the serum or blood.
What is the most common clinical presentation of acute mushroom toxicity?
A GI illness - vomiting/diarrhoea
What is the most common cause of mushroom death worldwide?
From Amanita phalloides (deathcap), cyclopeptide hepatotoxic poisoning
What can be said about accidental mushroom ingestion in children?
It is usually benign
When should you consider cyclopeptide hepatotoxic poisoning?
When GI symptoms develop >6 hours post-ingestion of mushrooms (esp in Canberra and Melbourne)
What are some antidotes to consider with acute mushroom toxicity?
NAC, silibinin 5 mg/kg IV + infusion for up to 3 days, benzylpenicillin 600 mg/kg/day IV instead of silibinin. For monomethylhydrazine poisoning pyridoxine can be given.
Discuss aconite poisoning.
Found in some herbal Chinese medicines, binds voltage-dependent sodium channels. Similar to LA toxicity.
What are belladonna alkaloids? How does this manifest?
Atropine, scopolamine, hyoscyamine. Competitive blockade of central + peripheral ACh muscarinic receptors leading to the anticholinergic syndrome.
How does foxglove toxicity present?
Digoxin-like effects on cardiac conduction and Na-K ATPase
What is coniine? In what is this found? What does it cause?
Coniine is an alkaloid in poison hemlock, structurally related to nicotine - nicotinic effects + NMB with respi failure
What three plant toxins require attention to fluid/electrolyte balance?
Colchicine, aconite and ricin poisoning
Can you use serum digoxin levels in cardiac glycoside poisoning?
No, does not accurately reflect
List 10 broad toxicological causes of coma.
Alcohol, antipsychotics, anticonvulsants, antidepressants, antihistamines, antimalarials, baclofen, beta-adrenergic (propranolol), centrally-acting alpha-2 agonists (clonidine), cholinergic agents (donepezil, nicotine), hydrocarbons (essential oils), LAs, mushrooms, NSAIDs, opioids, sedative-hypnotic agents. Secondary effects of cerebral oedema, hypoglycaemia, hypotension, hypoxaemia, neuroleptic malignant syndrome, seizures, serotonin syndrome
Describe in the potentially poisoned patient, coma may be the result of what?
(1) Direct toxic effect on the CNS, (2) Secondary effect of poisoning on the CNS (hypoxaemia, hypoglycaemia, hyponatraemia, hypotension, seizures, cerebral oedema), alternative non-toxicological diagnoses (neurotrauma, SOL, infection)
List the complications of reduced GCS.
Pulmonary aspiration, rhabdomyolysis, acute renal failure, compartment syndrome, pressure areas, hypoxic brain injury
What investigations would you consider for a patient with reduced GCS in ED?
Screening Tests: 12-lead ECG, BSL, serum paracetamol level. Detect ingestions requiring interventions: ABG, anion gap, lactate, osmolality/osmolar gap, specific drug levels. To detect and assess complications: ABG, UEC, LFTs, CK, CXR. To exclude/confirm differentials: ABG, UEC, LFTs, CT brain, LP, blood/urine cultures, EEG
What toxic ingestions must be excluded in all patients with coma and metabolic acidosis?
Toxic ETOH + salicylate poisoning
What two toxic ingestions may have very large fluid losses?
Iron or colchicine intoxication
In what drug intoxication may APO readily occur when trying to resuscitate hypotension?
CCB
What are the most common causes of toxic seizures in Australasia?
Venlafaxine, bupropion, tramadol, amphetamines
List 10 toxicological causes for seizures.
(1) Anticonvulsants (carbamazapine), (2) Antidepressants (venlafaxine, TCAs), (3) Antidysrhythmic agents (quinidine), (4) Antihistamines, (5) Antimalarials (chloroquine, quinine), (6) Antipsychotics (atypicals, olanzapine), (7) Baclofen, (8) Isoniazid, (9) OHG (insuli, sulfonylureas), (10) LAs (lignocaine), (11) Nicotine, (12) NSAIDs, (13) Opioids, (14) Salicylates, (15) Sympathomimetic drugs, (16) Amphetamines (cocaine, cannabinoids, theophylline), (17) Withdrawal syndromes (ETOH, benzos, barbiturates, zopiclone)
List 5 the withdrawal syndromes of 5 drugs that can cause seizures.
Alcohol, barbiturates, benzodiazepines, zopiclone, zolpidem, gamma-hydroxybutyrate
With what poisonings does a seizure indicate rapidly required care?
Chloroquine, propranolol, salicylates, theophylline, TCAs
Suggest the dose of barbiturate as a second line agent in the management of toxic seizures.
Phenobarbitone 100-300 mg slow IV (children 10-20 mg/kg slow IV) or thiopentone 3-5 mg/kg if ventilated.
What is the dose of pyridoxine in the management of isoniazid-induced seizures.
Gram-for-gram dose of pyridoxine to match suspected isoniazid dose up to 5 grams IV (children 70 mg/kg not exceeding 5 grams)
What are the key diagnostic features of delirium?
(1) Attention disturbance, (2) Change in cognition not pre-existing, (3) Short onset period, (4) Fluctuating, (5) Direct evidence of aetiology
List 8 toxicological causes of agitation and delirium.
Alcohol, anticholinergic syndrome, antidepressants, atypical antipsychotics, baclofen, benzos and other sedative/hypnotics, cannabis, hallucinogenic agents (ketamine, DMT, 2C-I), neuroleptic malignant syndrome, nicotine, salicylates, serotonin syndrome, sympathomimetic syndrome, synthetic cannabinoids, synthetic cathinones, theophylline, withdrawal syndromes
List complications of agitation of the poisoned patient.
Aspiration pneumonia, DVT/PE, fluid or electrolyte or acid/base disturbances, dehydration, hypoventilation/hypoxia, hyperthermia, physical injuries, rhabdomyolysis
List the conditions that would mimic toxicological delirium (ie ddx for delirium).
Acid-base disturbances, behavioural disturbance, CNS infection, dementia, electrolyte disturbances (hypoNa), endocrine emergencies (thyroid storm), head injury, hypoglycaemia, hypoxia, organ failure, psychosis, seizures, stroke, trauma (SDH), withdrawal syndromes
At what threshold temperature does a patient with delirium require intervention?
39.5 degrees or higher
What is the intervention required for anticholinergic syndrome?
Physostigmine
What is the intervention required for neurolepetic malignant syndrome?
Bromocriptine
What is the intervention required for salicylate poisoning?
Urinary alkalinisation, haemodialysis
What is the intervention required for serotonin syndrome?
Cyproheptadine, neuromuscular paralysis + intubation + ventilation
What is the intervention required for theophylline?
Multi-dose activated charcoal, haemodialysis
Describe what drugs (and in what sequence) are indicated in the management of toxin-induced delirium.
IV diazepam 5 mg should be given every 2-5 minutes until gentle sedation, second line: haloperidol/droperidol. Associated with extrapyramidal and anticholinergic effects. Olanzapine may be a suitable alternative in these instances.
In what conditions should sedation with droperidol/haloperidol be avoided?
If anticholinergic syndrome is suspected OR if a patient has acute extrapyramidal (akathisia, dystonia) symptoms. Avoid droperidol in patients with known prolonged QT syndrome and who are suspected to have significant electrolyte disturbances
A patient has had 15 mg of diazepam with no effect and has an possible dystonia and worsening agitation. What is another agent that can be considered?
Olanzapine, has fewer extrapyramidal effects than haloperidol/droperidol
What should you never forget to do in patients with anticholinergic syndrome?
Urinary retention requires an IDC
