Random Toxicology

hrhodes's version from 2015-10-12 04:45


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How do you do HDIT?Correct K, 50mls 50% dextrose, 1U/kg Actrapid, 50mls 50%/hr ans 0.5u/hr actrapid/hr, correct K and titrate Glucose to euglycaemia
Which Bblockers are bad?Propanolol - like TCA as Na blocker, sotolol increased QT, TdP
Rx of BbockersFluids, atropine, isoprenaline, adrenaline, HDIT, NaHCO3 for wide QRS, benzos for seizures, GLUCOSE
Do Bblockers of CCB cause hypoglycaemia?BB = hypo, CCB hyperglycaemia
Which are the bad CCB?Diltazem and Verapamil esp if slow release 10 tablets - be aggressive with decontamination and expect significant sequalae
What dose of Calcium do you use in CCB OD?60mls 10% Ca gluconate, 20mls 10% Ca Chloride
Amlodipine/nifedipine se?Mild tachycardia, no real hypotension


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What clinical features might you expect with acute aspirin OD?GI: Nausea + Vomiting, CNS: tinnitus, vertigo, Agitation, hyperventilation, seizures, coma Other: Hyperthermia, hyper/hypoglycaemia, hypoklaemia
What acid base changes in Aspirin ODResp alkalosis, RAGMA - if acidotic = imminent demise!
What are the indications for urinary alkalinidsation?any symptomatic patient
When would you use HD in salicylates?Often not required if good decontamination and early urinary alkalisation but use if alkalisation not possible, rising levels despite UA, severe toxicity = ALOC, acidaemia and renal failure, very high >7,6mmol/L - lower threshold in elderly
When can aspirin ODs be discharged?any symptomatic pt requires admission, should observe for 6 hours, clinical features must have resolved, salicylate levels <2.2mmol/L
Dose expected to cause symptoms in aspirin OD?150mg/kg - decontaminate, severe =


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In Organophosphate poisoning what symptoms do you get?Cholinergic syndrome: wet, slow, Basha: Bradycardia, bronchorrheoa, bronchospasm, diarrhoea, lacrimation, vomiting, miosis
Atropine is given in what doses and what will it not improve?1.2mg iv, double every 2 mins. end points - Normal HR, secretions dried up, brnchospasm improved. Will not have any effect on tremor and weakness as it is muscurinic and these are nicotinic mediated


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How does cyandide cause toxicity?Cyanide inhibits ATP production at mitochondrial level (oxidative metabolism) high lactate.
What is the most used cyanide kit in Oz?Dicobalt kit is most used in Australia - it has not been shown to be effective
What are the side effects of dicobalt edentate kit?Hypotension, laryngeal oedema, convulsions - therefore should confirm that there is definitely cyanaide fox - lactic acid >10, decreased LOC
What is a better treatment for cyanide tox?5g iv hydroxycobalamin repeated x 3 15minutely, is the better, safer kit (with evidence to show it works) as no formation of methaemogobin (formed by amyl nitrite, sodium nitrite and mopped up by the thiosulphate) this is bad if in house fire and already hypoxic
How does hydroxycobalamin work?turns it into B12 and pee it out
What is another cyanide antidote and when would you use?Sodium Thiosulphate - only for mild cases


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WRT Oxy/diss curve what does left and right shift mean?Left shift = loaded up/held on Hb/won't let go. Right shift = lets it go and be delivered
How do people go with acute CO poisoning?Bad. Most die before getting to hospital. those that get to hospital don't tend to have neuroseqaulae (6% at 12 months) as they were only exposed a small amount - this is different to long term low level accidental exposure
What are the COHb levels useful for?Not much other than confirming diagnosis, they are retrospective as at time of interpreataion the patient will have already cleared, they are ok at predicting symptoms but do not predict outcomes
What tests should you do for CO poisoning?BSL, Para, ECG, HCG, ABG, COHb, FBC< U+E, Trop (high chance of AMI), MMSE
Who should be considered for hyperbaric O2 in CO poisoning?All patients COHb >30%, pregnant woman >15%, comotosed
What are the clearance times for COHb?240mins - RA, 90mins - 100% O2, 23mins - 100% at 3atm - these are not well established in symptomatic patients
What is it important to remember to arrange for the accidental exposures index them so can contact trace and offer neuro follow up in 1-2 months


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How do you evaluate a hydrogen peroxide burn?OGD is best way, absence of oropharygeal burns does not mean there is no other lower down (10-15% have only oesophageal or lower injury)
What are the mechanisms of injury H2O2?1. Direct Gi injury, 2. O2 formation and gas embolus 3. Distend hollow viscera (thus get an AXR and CXR too)
Which is worse acid or alkali?Alkali cause more damage - liquid coagulation, sloughing. Alkaline - oesophageal, acids gastric.
Which household items are bad?Drain and oven cleaners are worse, dishwasher tabs an bleach can cause injury but a lot safer
How should children be managed in ED ?NBM until OGD, can have water if throughout not to be significant or large injury as can dilute acids


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Thyroxine OD is it bad?Typically no major effects, mild symptoms 5-7 days afterwards therefore cardiac monitoring in first few days is not indicated


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How does sulphonylurea toxicity cause its effect?Hyperinsulinaemia that can show up within 8 hours and have a very long period of severe hypoglycaemia
How do you treat?not just glucose, need to give octreatide infusion as soon as become hypoglycaemic (not before), and usually run for 24hrs with 5-10% glucose infusion as well to maintain eugycaemia
How does octreatide work?Supresses insulin formation at Iselt cells
What is the problem of giving intermittent boluses go 50% glucose in these patents?High glucose level stimulates insulin release = worsened hypoglycaemia


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How do organophosphates cause toxicity?Inhibit acetylcholinesterase = increased ACh @ muscurinic and nicotinic receptors = cholinergic syndrome - wet, slow, Basha, they alos cause ageing
What treatment?Atropine 1.2g double every 2mins until improved haemodynamics and secretion production, also pralidoxine
What symptoms with the atropine not effect?nicotinic mediated symptoms - tremor, muscle weakness and fasciculations


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Where is it unsafe to leave a button battery ?(!)Nose, ears, oesophagus
In what time frame can they cause corrosive damage?by as little as 6 hours
What are the consequences of leaving the battery?Local burns, perforation, haemorrhage +/- stricture formation latterly if don't just die
How do they present?sometime assymptomatics. sometimes with oesophageal pain and dysphagia but these symptoms can be dalyed for some days
How do you investigate?Plain CXR and AXR
If they are below diaphragm how do you manage?expectantly, repeat XR in 24 hours to ensure has passed pylorus, post pylorus no more XR needed and the amount of metal should not cause them serious issue for absorbtion
What is a pathognomic sign?Halo sign


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What are the 5 stages of iron toxicity?1. 0-6hrs - direct corrosion GIT-diarrhea, vomiting, fluid losses, 2. 6-12hrs absorption of iron and less symptoms, 3. 12-48hrs - RAGMA, vasodilation, 3rd space losses, hepatorenal failure 4. 2-5days Acute hepatic failure, coagulopathy, hypoglycaemia - death, 5. 2-6 weeks - cirrhosis, GI strictures
How else (and more sensibly) can it be through of?direct GI corrosive effects and systemic effects
What is the dose expected to cause systemic effects? Elemental iron 60mg/kg. 20-60mg/kg is likely to cause just GI symptoms
What tests should you do in suspected iron toxicity?BSL, para, ECG, ABG - May have mixed metabolic RAGMA - Fe, NAGMA (diarrhoea) and alK as vomiting), lactate (B2 cause), AXR (to quantify amount), Serum iron level at 4-6hours -peak absorption - 500mcg/dL suggests systemic tox, falling venous bicarb can be used as a substitute if no iron levels available
4-6hr serum iron level that predicts systemic fox500mcg/dL or 90micromol/L
What is the treatment for Fe toxicity?Fluids and electrolyte replacement, desferroxamine iv until stable and serum levels reduced to 350mcg/dL
What are the indications for desferroxamine?>60mg/kg elemental iron, peak iron serum level >500mcg/dL, signs or symptoms of systemic fox - metabolic acidosis, altered mental state, shock and chronic iron overload
What are endpoints to cease rx? patient stability and serum iron <350mcg/dL. Avoid infusions >24hrs because or risk ARDS
How should desferoxamine be given?full cardiac monitoring, 500mg in 100mls saline, 15mg/kg/hr increased to 40 if severe and reduced if hypotensive. usually takes
Complications of desferroxaminehypotension esp at high dose, Toxic retinopathy, Hypersenstivity reaction, ARDS >24hrs, yersinia infections and other secondary infections
Is pregnancy a contraidication?NOPE


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how does methaemoglobinaemia occur?oxidation of haem moiety fe2 - fe3
Which drugs can cause metHb?Local anaesthetics, nitrates, nitrites, dapsone, sulfa and rifampicin - Recreational amyl nitrate and poppers
population at risk?afroamericans
What effect does methhaemoglobinaemia have on Oxy/diss curve?Shift to left - unable to release O2. methhaemoglobiaema unable to carry O2
Symptoms and signs of methaemaglobinameia?grey blue skin, chocolate brown blood - DOES NOT CHANGE ON EXPOSURE TO AIR, pulse ox 85% (falsely high) due to similar wavelengths of oxyhaem and methhaem, SaO2 on blood gas also falsely high a this is measuring partial pressure dissolved O2 in blood as well as that carried (or in this case not carried) by blood. This difference is known as being an increased oxygen saturation gap
What is needed to accurately measure SpO2?co-oximetry - can differentiate between, oxy-, deoxy-, carboxyl- and meathhaemaglobin
What is the treatment for methaemoglobinaemia?Methylene blue. Some thoughts on using NAC (no proven effect) Hyperbaric O2, exchange transfusion


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What are the differences between acute and chronic lithium toxicity?Acute: GIT symptoms, chronic: Neuro toxicity - ataxia, tremor, hyper/hypotonia, seizures and coma
What classification system is used for chronic Li fox?Hansen-Amdisen 3 grades
What are the causes of chronic Li Toxicity?Impairment of renal Li excretion - dehydration, AKI, Drug interactions-NSAIDS, ACEi, thiazides, toprimate, diabetes insipidus
What disease can Lithium cause?Diabetes insipid us - HyperNa, pee out unconcentrated wee
What are the indications for HD in Li Toxicity?Often only needed in chronic, acute you can just rehydrate and aim UO >1ml/kg/hr. In chronic HD if neuro symptoms and >2.5mmol/L Li
What tests should you do in Li Toxicity?BSL, para, ECG, Li Level (to confirm not predict), TFTs, Urine Na, search for other causes of ALOC
How do you treat?ABCD-seek and treat seizures, Fluids resus and strict balance, HD if neuro symptoms and Li >2.5mmol/L, cease NSAIDs, ACEi, thiazides, toprimate


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What are the safe doses of local anaesthetics?BRLMP Bupivicaine 1-2.5mg/k, robupivicaine 2.5-3mg/kg, Lidocaine 4-6mg/kg, Merpivicaine 4-6, Prilocaine 6-8mg/kg
Which is the most cardiotoxic LA?Bupivicaine 1-2.5mg/kg can cause TCA like ECG die to prolong binding to Na-channel on myocardium
What are the first signs of LA fox?Neurotox- perioral tingle, anxious, tinnitus, dizziness, confusion AND THEN Seizures, coma and CV collapse - dysrhytmia, hypotension, Resp depression
What dose of LA causes MetHb?It is not dose dependent therefore any susceptible individual
How do you treat MetHb?1-2mg/kg Methylene blue
How do you treat LA toxicity?ABCD Cardiotoxic effects: NaHCO3 1-2mEq/kg (100mls), fluids, prolonged CPR, Intralipid 20% 1-2ml/kg
How does Intralipid work?lips sink for lipophylic drugs
Name 3 other drugs Intralipd maybe useful forpropanolol, TCAs, verapamil (and of course LAs)
Adverse effects of intralidimmediate - allergy, anaphylaxis, pulmonary hypertension
What are the benefits of adding Adrenaline to LA injections?Increase duration of action and safe dose due to vasoconstriction - add 1 to safe dose numbers other thing you can add is NaHCO3 for alkaline - less pain, increase efficacy


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Liver centre referralINR, AKI, Acidotic, Low BSL+platelets, encephalopathic or hypotense
When is Rumack-Matthew chart used?Acute ingestion ONLY, 4-15hours
What time frame does NAC have to be used to get 100% efficacy?8hours. (at 4hrs >300mg/L untreated get 90% hepatotoxicity)
How does NAC work?Sulphyhydrl donor
How do you give NAC?IV. Over 20hrs it should be continued longer than 20hrs with continued ALT?AST rise, late presenters and chronic supra therapeutic
What is the incidence of anaphylactoid reactions with NAC?10-50% always restart
List 3 drugs which would increase pt risk in paracetamol OD and describe the mechanism responsible for that increaseInduce Cytochrome p450 - Isoniazid, Rifampicin, Carbamezipine
Name 2 other factors which would put the pt at an increased risk of liver damage from paracetamolChronic alcohol ingestion >50g day, prolonged starvation