Poisonings + OD Flashcards

1
Q

In what time frame can activated charcoal be used?

A

Within 1 hour of ingestion

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2
Q

What dose of salicylates is considered poisoining?

A

> 125mg/kg needs assessment in hospital

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3
Q

Describe the presentation of salicylate poisoning

A
  • Acid base disturbance: met acid (anion gap) + resp alk
  • Electrolyte abnormalities: hypokalaemia
  • CNS disturbance: confusion, seizures, coma

+ increased RR, tachycardia, sweating, warm peripheries, tinnitus

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4
Q

Describe the complications of salicylate poisoning

A
  • Cerebral oedema -> coma
  • Arrhythmias -> heart failure
  • AKI
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5
Q

Describe the A to E in salicylate poisoning

A

A to E

  • A: may be non-patent due if drowsy
  • B: increased RR, ABG: resp alk + met acid (later)
  • C: sweaty, warm, tachycardiac, hypertensive, possible ECG abnormalities. Get IV access and send bloods
  • D: reduced GCS
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6
Q

Describe the important investigations for salicylate poisoning

A
  • Obs
  • ABG
  • Urine: pH
  • Bloods: FBC, U+Es, clotting, glucose, salicylate level (at 2 hours + 4 hours) + paracetamol level
  • ECG
  • CXR
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7
Q

Describe the management of salicylate poisoning

A

Medical:
Senior help, consider ITU/NIPS
1. IV fluids
2. Monitoring: cont cardiac monitor + pulse ox
3. Monitor bloods: glucose, salicylate level, ABG, U+Es
Consider: sodium bicarb (if serum >500mg/L), RRT

Psych:

  • History + risk assessment
  • Liaison psych referral
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8
Q

What dose of paracetamol is considered OD?

A

OD: >75mg/kg

Toxicity is more likely if: >150mg/kg

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9
Q

Describe the presentation of paracetamol OD

A

Often asymptomatic

  • Nausea and vomiting
  • > RUQ
  • > Jaundice and liver dysfunction
  • AKI
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10
Q

What is the most common drug used in OD?

A

Paracetamol

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11
Q

Describe the pathophysiology of paracetamol OD

A

OD results in excessive production of NAPQI (toxic metabolite normally degraded quickly)

  • > overwhelms hepatocyte capacity to metabolise (conjugation with glutathione)
  • > injury + hepatocyte death -> acute liver failure
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12
Q

Describe the investigations for paracetamol OD

A
  • Obs
  • Urine dip
  • Bloods: FBC, U+Es, LFTs, clotting, glucose, VBG/ABG, paracetamol level (after 4 hours only)
  • ECG
  • Abdo USS if symptomatic RUQ
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13
Q

Which patients are at greater risk of toxicity in paracetamol OD?

A

Malnourished:

  • Eating disorders
  • Chronic illness eg. HIV
  • Alcoholics

Drug Hx of enzyme inducers:

  • Anti-epileptics
  • Rifampicin etc
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14
Q

Describe the management of paracetamol OD

A
  • Take history (details of OD, psych, PMH)
  • Examination: for signs of acute liver failure
  • Investigations: bloods, etc
  • Senior help, consider ITU if needed
  • Within 1 hour: act charcoal
  • At 4 hours: take paracetamol level, use chart
  • IV acetylcysteine infusion over 21 hours
  • > monitor glucose. At end of infusion, repeat bloods

+ psych referral, 1-1 care etc

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15
Q

When can a patient with paracetamol OD be discharged?

A

No signs of liver failure
Normal creatinine
NAC stopped
Psych allows

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16
Q

Describe the NAC regimen

A

1st bag: 150mg/kg in 5% dex over 1 hour
2nd bag: 50mg/kg in 500ml 5% dex over 4 hours
3rd bag: 100mg/kg in 1L of 5% dex over 16 hours

17
Q

What are some common side effects of NAC? What is the management?

A

Vomiting common. Can give anti-emetic

Rash. Don’t stop infusion, give chlorphenamine

18
Q

Describe the signs of carbon monoxide poisoning

A

Non-specific

  • Headache
  • Nausea
  • Dizziness
  • Cardiac: MI, arrhythmia, cardiac arrest
  • Neuro: confusion, focal neuro, drowsiness, coma
19
Q

Describe the investigations for carbon monoxide poisoning

A
  • History + examination
  • Bloods: basic bloods (DDx) + VBG/ABG (gold standard), troponins
  • ECG
  • Imaging: CT head, CXR as indicated by symptoms
20
Q

Which key test is elevated in CO poisoning?

A

Carboxyhaemoglobin

21
Q

Describe the management of CO poisoning

A

Medical Mx:

  • Call senior
  • A to E approach
  • High flow oxygen (100% at 15L), consider I+V if low GCS

Extras:

  • Consider non-accidental exposure
  • Ensure other people away from source
  • Discharge to safe place
22
Q

Describe the presentation of TCA OD

A
  • Anticholinergic effects: dilated pupils, blurry vision, tachycardia, hyperthermia, drowsiness, ataxia
  • Seizures, coma
  • Arrhythmia (wide QRS, prolonged QTc), cardiac arrest
23
Q

Describe the treatment of TCA OD

A

Supportive + monitoring

IV sodium bicarb

24
Q

Describe the presentation of benzodiazepine OD

A

Drowsiness, coma

Hypotension, reduced RR

25
Q

Describe the management of benzo OD

A

Supportive + monitoring

Flumazenil IV bolus

26
Q

Describe the presentation of iron poisoning

A

Vomiting, diarrhoea, abdo pain
Metabolic acidosis
Shock, fever, bleeding, jaundice, liver failure

27
Q

Describe the management of iron poisoning

A

IV Desferrioxamine 15mg/kg/hour

*Can also do whole bowel irrigation

28
Q

Describe the presentation of lithium toxicity

A

GI: vomiting, diarrhoea, abdo pain
Neuro: tremor, slurred speech, confusion, ataxia, myoclonus, nystagmus
Cardiac: ECG changes, arrhythmia

29
Q

Describe the management of lithium toxicity

A

Suportive + monitoring (cardiac monitor etc)
IV fluids
Severe: haemodialysis

30
Q

Describe the presentation of digoxin toxicity

A
  • Yellow vision
  • N+V, abdo pain
  • Confusion
  • Arrhythmia, ECG changes: many
31
Q

Describe the management of digoxin toxicity

A

Support + monitor
Correct hypoK
Give antidote: DigiFab

32
Q

Describe the presentation of opioid OD

A
  • Pinpoint pupils
  • Resp depression -> hypoxia, T2RF, cyanosis
  • Bradycardia
  • Drowsiness, coma
33
Q

Describe the management of opioid OD

A

A to E

  • High flow O2, consider assisted ventilation
  • SC/IV naloxone, repeat as needed. Effect lasts 90 mins, need to monitor for re-sedation
  • OOH use intranasal

*Psych liaison/addiction team. Treat withdrawal as needed eg. sedation, methadone

34
Q

Describe the investigations for opioid OD

A

A to E

  • IV access
  • UDS (not urgent or very useful)
  • ECG
  • Bloods: basic (consider DDx/other drugs), ABG
  • CXR
35
Q

Describe the presentation of neuroleptic malignant syndrome

A

Neuro: confusion, agitation, coma
Muscle rigidity
Autonomic: hyperthermia, tachycardia, hypertension

36
Q

Describe the drugs that can cause neuroleptic malignant syndrome

A

Anti-psychotics eg. haloperidol, prochlorperazine

37
Q

Describe the management of neuroleptic malignant syndrome

A
  • History and examination/ A to E
  • IV access and bloods
  • Senior help, consider ITU need
  • Stop drug

Supportive Mx:

  • Cooling: mists, fans, blankets
  • Sedation prn
  • Anti-hypertensives, IV fluids

Monitoring: U+Es, cardiac monitor, etc

38
Q

Describe the effects (presentation + severe complications) of illicit drug OD

A

Cocaine: tachycardia, dilated pupils, sweating, agitation, chest pain
-> vasospasm, MI

Amphetamines eg. metamphetamine, ecstasy/MDMA: increased temp, sweating, tachycardia, dilated pupils, blurry vision, agitation, confusion
-> seizures, stroke, AKI, tachyarrhythmia, ARDS, shock

39
Q

Describe the management of illicit drug OD

A

Cocaine:

  • GTN/nitrates
  • Cooling
  • Sedation: benzos
  • Monitoring
  • **Avoid beta-blockers!!!

Amphetamines:

  • Cooling
  • Anti-hypertensives
  • Sedation: benzos