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year 4 CDM 2 > Overdose > Flashcards

Overdose Flashcards

1
Q

Other specific antidotes

A
  • Opiates: Naloxone (specific antagonist)
  • Benzodiazepines: Flumazenil (specific antagonist) can cause seizures so not used as often
  • Ethylene glycol, methanol: Ethanol, Fomepizole (alcohol dehydrogenase inhibitors)
  • Dapsone: Methylene blue (reducing agents) turns haemoglobin back to normal state
  • Organophosphates: Pralidoxime (Cholinesterase reactivators)
  • Digoxin: Digibind (antibody fragments)
  • Snake bites: Zagreb antivenom
  • Paracetamol poisoning: Acetylcysteine, Methionine (Glutathione repleters)
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2
Q

Benzodiazepines MoA

A

Work by enhancing the effects of the inhibitory neurotransmitter GABA, particularly at the GABAa receptor by increasing the frequency of chloride channels. Causes sedation, anti-anxiety, anti-seizure, and generalized muscle relaxant effects. Used for sedation and as hypnotics

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3
Q

Features of Benzodiazepine overdose and withdrawal

A

Features of Benzodiazepine overdose: drowsiness, ataxia, dysarthria, hypotension, bradycardia, respiratory depression and coma.

Benzodiazepine withdrawal symptoms: insomnia, irritability, anxiety, tremor, loss of appetite, tinnitus, perspiration

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4
Q

Features of Benzodiazepine overdose management

A
  • Airway, breathing and circulation
  • Oral activated charcoal
  • Monitor vital signs
  • 12 Lead ECG
  • Supportive care
  • Antidote - flumazenil (not often used, supportive care often adequate)
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5
Q

Flumazenil

A
  • Has a shorter half life the benzos and repeated administration may be required
  • Bolus administration is IV over 15s, may have to give further doses
  • Contraindicated in TCA overdose, receiving benzos for seizure control or raised intracranial pressure. Increases seizure risk. Best to avoid if you don’t know what’s been co-ingested
  • Can be used in iatrogenic overdose or in patients with chronic respiratory disease to avoid intubation and ventilation
  • Reverses effects of Benzos in minutes
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6
Q

When to use Flumazenil and contraindications

A
  • Used in severe OD with marked respiratory impairment of consciousness or respiratory distress
  • Contraindications: Benzodiazepine dependent, mixed TCA OD, history of epilepsy
  • When given monitor with ECG
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7
Q

Timings of iron overdose

A

Uncommon, may be serious especially in children

Timings of iron overdose
- Early (0-6hrs): N+V, abdo pain, diarrhoea (bloody), massive GI fluid loss
- Delayed (2-72 hours): black offensive stools, drowsiness/coma, fits, circulatory collapse
- Late (2-4 days): acute liver necrosis (hepatocellular necrosis), renal failure
- Very late (2-5 weeks): Gastric strictures

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8
Q

Investigations into iron overdose

A
  • History - establish amount of elemental iron taken (differs between ferrous sulphate and ferrous fumerate), serious overdose >10mg/kg
  • Iron concentration: After at least 4 hours, Repeat after 2-3 hours
  • Blood count: raised WCC
  • U&E’s
  • Bicarbonate - monitor daily to check for metabolic acidosis
  • Glucose [usually see hyperglycaemia]
  • Clotting - monitor daily
  • LFT’s
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9
Q

Treatment of iron overdose

A
  • Gastric decontamination (Gastric lavage): if large OD and presenting early
  • Activated charcoal is ineffective
  • Desferrioxamine
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10
Q

Desferrioxamine

A
  • Chelates iron and reduces toxicity
  • Chelate iron ( forms ferrioxamine) is water soluble and excreted in urine (red discolouration)
  • Can cause adverse effects, e.g. hypotension and pulmonary oedema
  • Contraindicated in renal failure
  • Used for patients with severe toxicity: Fits, coma, circulatory collapse. GI symptoms, leucocytosis, or hyperglycaemia and high iron concentration (>3 mg/l)
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11
Q

Supportive care for iron overdose

A
  • Hypotension - I.V fluids
  • Vomiting - Antiemetics
  • Fits - Diazepam / Lorazepam
  • Acidosis - Correct with bicarbonate
  • Renal failure - Dialysis
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12
Q

Examples of opiates/opioids

A
  • Heroin
  • Morphine
  • Methadone
  • Dihydrocodeine
  • Codeine
  • Pethidine
  • Dipipanone
  • Dextropropoxyphene
  • Tramadol
  • Buprenorphine
  • Opiates are naturally derived from the poppy plant whilst opioids are synthetic
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13
Q

Illegal Opiates effects and administration

A

Opiates administration: Oral, smoked, IV, inhaled

Opiates effects:
- CNS and respiratory depression: coma
- ‘Pin-point’ pupils
- Hypotension, tachycardia
- Hallucinations
- Rhabdomyolysis
- Non-cardiac pulmonary oedema

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14
Q

Opiate overdose management

A
  • Airway management if reduced GCS or respiratory rate
  • Breathing: Consider Opioid receptor antagonist (Naloxone), Ventilation
  • Circulation
  • Disability – reduced GCS. Consider Opioid receptor antagonist (Naloxone)
  • Hepatitis B,C and HIV precautions (IV users)
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15
Q

Naloxone

A
  • Used in suspected opiate intoxification for diagnosis and treatment
  • Diagnosis: if responds to naloxone confirms opioid toxicity
  • Indications: Reduced respiratory rate (<10/min), Reduced conscious level (<10/15)
  • Adults: 400 micrograms up to 2.0mg or more, in children titrate up from 0.1mg
  • Repeat as necessary or use a continuous infusion- 2/3 of initial dose required to rouse patients by IV infusion per hour, then titrate down
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16
Q

Investigations of opioid toxicity

A
  • FBC
  • U+E
  • CK (?rhabdomyolysis)
  • ABG: mixed acidosis
  • urine drug screen
  • CXR (?pulmonary oedema)
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17
Q

Naloxone risks

A
  • Dose of naloxone should be titrated up gradually to reduce risk of sudden withdrawal symptoms
  • Can cause acute withdrawal syndrome in long term uses: muscle aches, diarrhoea, palpitations, rhinorrhoea, yawning, irritability, nausea, fever, tremor, cramps
  • Unmasking of pain if taken for pain
  • Hypertension
  • Behavioural disturbances (high doses)
  • Rarely fits, arrhythmias, pulmonary oedema
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18
Q

Naloxone half life

A
  • Naloxone has a half-life of 1hr which is less than many opioids (check for re sedation after this time)
  • Self-discharge during alert phase with subsequent coma / death
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19
Q

Patients at risk of hepatotoxicity following a paracetamol overdose

A
  • patients taking liver enzyme-inducing drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s Wort)
  • malnourished patients (e.g. anorexia nervosa) or patients who have not eaten for a few days
  • Chronic alcohol use
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20
Q

Mechanism of paracetamol overdose

A
  • the usual paracetamol metabolism pathways (Para-glucuronide and Para-sulphate via bile) are rapidly saturated
  • the other pathways via CYP 2E1 and CYP 3A4 generate toxic NAPQI
  • the body can detoxify a small amount of NAPQI with endogenous glutathione but this gets rapidly saturated causing Hepatocellular injury
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21
Q

Paracetamol overdose presentation early and epidemiology

A

Almost half of overdoses presenting to hospital include paracetamol

Presentation of paracetamol overdose early: abdo pain, N/V, altered clotting (non-specific)

22
Q

Presentation of Paracetamol overdose delayed

A
  • Hepatic necrosis: takes 2-3 days. Get jaundice, RUQ pain, encephalopathy, coagulopathy, Fulminant hepatic failure, death (3-6 days after overdose)
  • Renal failure (acute tubular necrosis): less common 2-7 days after poisoning, oliguria, loin pain, AKI
  • Others: Hypoglycaemic, Metabolic acidosis
23
Q

Paracetamol overdose investigations

A
  • Paracetamol level (4 hours after overdose): best early predictor of prognosis, indicates antidotes
  • Clotting: PT or INR- increased due to reduced clotting factor production
  • U&E’s
  • ABG: metabolic acidosis
  • LFT’s: elevated
24
Q

Paracetamol overdose: poor prognostic features

A
  • PT or INR rising after day 3
  • PT >100 s at any time
  • Bilirubin > 70 micromol/l
  • Metabolic acidosis
  • Encephalopathy [III or IV]
  • Raised Lactate: not resolved after fluid resus
  • Creatinine > 300 micromol/L
25
Q

Paracetamol overdose treatment

A
  • Activated charcoal: within 1 hour
  • supportive therapy: vitamin K, fluids, dialysis, glucose infusions
  • consider liver transplant
  • N-acetylcysteine (IV)
  • Antidote second line N-acetylcysteine: Methionine (oral)
26
Q

N-acetylcysteine

A
  • Mechanism: glutathione precursor (allows detoxification of NAPQI by providing glutathione)
  • Should be given within 8hrs of ingestion ideally but can be effective up to 24hr- but given at any time after severe poisoning
  • Indicated if serum paracetamol is above treatment line after 4hrs
  • Given in 3 IV infusions over 21 hours (the first over 1hr) mix with 5% glucose
  • Effectiveness decreases with time
  • Benefit in patients with fulminant hepatic failure
27
Q

When to give N-acetylcysteine

A
  • the plasma paracetamol concentration is on or above the treatment line regardless of risk factors for hepatotoxicity
  • there is astaggered overdose or there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration;
  • patients who present 8-24 hoursafter an acute overdose of more than 150 mg/kg of paracetamol
  • patients who present > 24 hoursif they are clearly jaundiced or have hepatic tenderness, their ALT is above the upper limit of normal
28
Q

Side effects of N-acetylcysteine

A
  • Vomiting (give IV antiemetic)
  • coagulopathy
  • anaphylactoid reaction due to dose related histamine release, resulting in urticaria, wheeze, itch and hypotension (stop infusion, give antihistamine then restart). Not true allergic reactions
29
Q

When is liver transplant indicated for paracetamol overdose

A
  • pH below 7.3 after 24hrs
  • INR above 6.5, creatinine above 300 and grade 3 or 4 HE
30
Q

Supportive treatment for paracetamol overdose

A
  • Vitamin K
  • Fresh frozen plasma (for active bleeding only)
  • Hepatic intensive care: Fluid balance, Inotropic support, Intracranial pressure monitoring in HE
  • Dialysis for renal failure
  • Orthotopic liver transplantation
30
Q

Mechanism of salicyclate poisoning

A
  • uncouples oxidative phosphorylation, causing metabolic acidosis
  • also stimulates CNS respiratory centre causing increased RR and respiratory alkalosis
31
Q

When should plasma salicyclate be measured in peak overdose

A

Every 2hrs until levels peak (can take up to 6hrs

31
Q

Aspirin overdose symptoms and signs

A

Dizziness, Sweating, Tinnitus, Vomiting, Vasodilation, Hyperventilation, Hypertension, Agitation, Delirium, Coma (especially children)

32
Q

Aspirin overdose clinical features

A
  • Metabolic acidosis: Salicylic acid uncouples oxidative phosphorylation causing anaerobic metabolism
  • Respiratory alkalosis: direct CNS ‘receptor centre’ stimulation initially before becoming metabolic acidosis
  • Hypoglycaemia
  • Hypokalaemia
33
Q

Aspirin overdose investigations

A
  • Plasma salicylate concentration
  • Urea,electrolytes,bicarbonate
  • Blood glucose
  • Arterial blood gases
34
Q

Aspirin overdose treatment

A
  • Gastric decontamination: 50g activated charcoal within 1 hour. Gastric lavage and activated charcoal if very large overdose (rarely used)
  • Sodium bicarbonate: prevention of CNS penetration
  • MDAC (Multiple dose activated charcoal), Urinary alkalisation (sodium bicarbonate): enhanced elimination
  • Haemodialysis
35
Q

Aspirin overdose: Haemodialysis

A
  • Highly effective at removing salicylate, also corrects metabolic abnormalities
  • Consider if pH <7.3, salicylate level >700mg/l (600 mg/l in children), patients in renal failure
36
Q

Supportive medication for aspirin overdose

A
  • Airway
  • I.V fluids
  • Ventilation
  • Glucose for hypoglycaemia
  • KCl for hypokalaemia
37
Q

Indications for Haemodialysis in salicyclate overdose

A

serum concentration > 700mg/L
metabolic acidosis resistant to treatment
acute renal failure
pulmonary oedema
seizures
coma

38
Q

Aspirin overdose ABG

A

A mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis.

39
Q

TCA overdose ECG changes

A
  • sinus tachycardia
  • widening of QRS
  • prolongation of QT interval

Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias

40
Q

Clinical features of a TCA overdose

A
  • Anticholinergic effects (presenting features): hot dry skin, dilated pupils, tachycardia, urinary retention, agitation, delirium, fits, coma, hypertonia, hyperreflexia
  • Sodium channel blocking effects: Cardiac Arrhythmias, conduction block, prolonged QRS and QT interval
  • Alpha adrenoceptor antagonism: Hypotension and vasodilation
  • Not very common but very fatal
41
Q

TCA overdose: investigations

A
  • Urea & electrolytes
  • Blood glucose
  • Arterial blood gases: metabolic acidosis due to tissue hypoxia
  • ECG: wide QRS, long QT, long PR
  • QRS duration >160ms (4 small squares) = very high risk of arrhythmia. >120ms (3 small squares) = requires specific urgent action
  • Constant cardiovascular monitoring: CCU or ITU if large overdose or initial ECG abnormal
42
Q

TCA overdose treatment

A
  • Gastric decontamination: activated charcoal within 1 hour
  • Multiple doses of activated charcoal: every two hours can enhance elimination of some tricyclics (amitryptiline, nortryptiline)
  • IV bicarbonate: first line for hypotension or arrhythmias
43
Q

How to correct Arrhythmias in TCA overdose

A
  • More likely if pH < 7.4 (metabolic acidosis)
  • Give Sodium Bicarbonate for: Acidosis, Wide QRS complex [>120ms], Arrhythmias (ventricular tachycardia), Hypotension not responding to fluids, cardiac arrest
  • Correct K+ if hypokalaemia
  • If bicarbonate fails and the patient is haemodynamically unstable consider DC cardioversion or overdrive pacing
  • Don’t use anti-arrhythmics or dialysis
44
Q

What to do in TCA overdose if bicarb fails

A
  • DC cardioversion
  • lidocaine
  • MgSO4
  • do not use anti-arrhythmic
45
Q

TCA overdose: fits

A
  • Use Diazepam or Lorazepam
  • If fails consider paralysis and mechanical ventilation
46
Q

Newer antidepressants

A
  • SSRIs (specific serotonin reuptake inhibitors): citalopram, escitalopram , fluoxetine, paroxetine ,sertraline
  • SNRI (serotonin noradrenergic reuptake inhibitors): Venlafaxine
  • NaSSA (noradrenergic and specific serotonergic antidepressant): Mirtazapine
  • NaRI (selective noradrenaline reuptake inhibitor): Reboxetine
  • RIMA (reversible inhibitor of monoamine oxidase A): moclobemide
47
Q

Serotonin syndrome

A
  • Caused by excess MAOI, SSRI’s (with ST Johns Wort and Tramadol), ectasy and amphetamines
  • Cognitive-behavioural changes: agitation, confusion, hallucinations, coma,
  • Neuromuscular dysfunction: tremor, teeth grinding, myoclonus, hyperreflexia
  • Autonomic dysfunction: tachycardia, fever, hyper or hypotension, flushing, diarrhoea
  • Others: Vomiting, seizures, hyperpyrexia, rhabdomyolysis, renal failure, coagulopathies
48
Q

Management of Serotonin syndrome

A
  • supportive including IV fluids
  • benzodiazepines
  • more severe cases are managed using serotonin antagonists such ascyproheptadineand chlorpromazine

year 4 CDM 2 (39 decks)

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