Overdoses Flashcards

1
Q

What differentiates beta blocker and calcium channel blocker overdoses?

A
  • BB = hypoglycaemia
  • CCB = hyperglycaemia
  • BB get hyperkalaemia
  • CCB get more pronounced lactic acidosis
  • BB can get QT prolongation and TdP (sotalol)
  • BB can get seizures and Na+ channel toxicity (propranolol, the most dangerous)
  • CCB more pronounced vasodilation
  • BB can cause bronchospasm, both can cause pulmonary oedema
  • Both should receive charcoal, CCBs can also get whole bowel irrigation (WBI)
  • Calcium is useful as an inotrope in both but is the antidote in CCB
  • BB get bronchospasm, CCB not
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2
Q

What drug overdoses/toxic exposures will likely present with significant bradycardia?

A

Beta blockers
CCB’s
Digoxin
Amiodarone
Clonidine
Organophosphates
GHB

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3
Q

What are the features of Acute digoxin toxicity?

A

Ingestion >10mg or 30mcg/kg have severe toxicity
- Get CVS (brady/tachy arrhythmias, arrest), GI (abdo pain, upset) and CNS (confusion, coma) effects
- Hyperkalaemia is a sign of serious toxicity, still treated with
-Serum levels not accurate within 6hrs of ingestion
- Acute serum levels >15nmols/L associated with severe toxicity

Specific Arrhythmias
- Bidirectional VT
- AFluttter with high grade AV block
- AFib with high grade block/regularised AF
- Slow AF + junctional tachycardia (less specific)
- Down sloping ST segment (reverse tick, salvador dali sign)

A top differential for tox ingestion with K+ > than expected for acidosis

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4
Q

Who is at risk of chronic digoxin toxicity?

A
  • Usually not an overdose but precipitated but dysequilibrium ie hypovolaemia, infection, renal failure etc
    Risk factors: Elderly, CKD, poor cardiac function, on medications that can impair renal function
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5
Q

What are the features of chronic digoxin toxicity?

A
  • Visual changes including yellow haloes around lights
  • confusion/lethargy
  • Brady/tachydysrhythmias
  • abdo pain, N/V, diarrhoea

Same indications for digibind as acute with same dosing, except lower serum digoxin level + symptoms needed (>2nmol/L)

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6
Q

How does arrest management change in acute digoxin toxicity?

A
  • Electricity often doesnt work whilst digoxin levels high, consider taking out of algorithm until digibind in
  • Consider Lignocaine 100mg for tachydysrhythmias
  • Consider 2mls/kg of sodium bicarbonate for hyperkalaemia
  • Adrenaline and salbutamol may help with hyperkalaemia but can worsen dysrhythmias caused by digoxin
  • Consider MgS04 10-20mmols for tachydysrrhythmias
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7
Q

How does salicylate toxicity usually present?

A

GI
- abdo pain, N/V, haemorrhagic gastritis
CNS
- delerium, agitiations, tinnitus, seizures, coma
Metabolic
-primary resp alkalosis followed by metabolic acidosis
- Hypoglycaemia (relative or absolute), often need to aim for higher BSL as brain levels lower
- Hyperthermia

100-300mg/kg = GI, tinnitus
300-500mg/kg = HAGMA, multi organ failure
>500mg/kg = cerebral oedema, death

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8
Q

What are the typical salicylates in Australia?

A

Aspirin
Methyl salicylate (1:1.5)
Choline salicylate (1:0.75)
1ml oil of wintergreen = 1400mg Aspirin

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9
Q

What are the effects of TCA overdose at different doses?

A

5-10mg/kg (mild)
- tachy, confused, agitated

10-20mg (moderate)
- significant anticholinergic features, delerium and reduced GCS

> 20mg (severe)
- Seizures, coma, hypotension, arrhytmias, death

Acidosis worsens TCA overdose due to alpha receptor antagonism (worsens hypotension) and greater Na+ channel blockade (worsens arrhytmias/ECG)

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10
Q

What are the ECG changes in TCA overdose?

A

R wave in AVR >3mm or >0.7 amplitude of S wave (most specific)
Sinus tach
QRS and QT prolongation
QRS >110msec increased risk of seizures
QRS >160msec increased risk of VT/VF

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11
Q

What is the treatment and end points for TCA/Na+ blocker overdose?

A

Sodium bicarbonate
1-2mls/kg bolus with Q5min repeat

Indicated for seizures, arrhythmias, QRS >120msec and peri-intubation to prevent/treat CVS collapse

End point is reversal of above and aiming pH 7.50-7.55

Other treatments
Lidocaine 100mg IV for resistant arrhythmias despite pH 7.55
3% saline for resistant cardiac toxicity

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12
Q

What are the risk factors for severe toxicity from BB/CCB overdose?

A

Big dose
Extremes of age
Pre-existing CVS disease
Co-ingestion with -ve inotropes

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13
Q

What is the toxic dose of Ibuprofen?

A

> 300mg/kg
Causes multiorgan failure

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14
Q

What is different about Mefenamic acid compared to other NSAID’s in overdose?

A

Causes seizures
Charcoal contraindicated prior to intubation and NG placement due to imminent risk of seizures

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15
Q

What are the clinical effects seen with Theophylline poisoning?

A
  • Hypokalaemia, hyperglycaemia
  • Hypotension from B2 mediated vasodilation
  • Multidose activated charcoal can be used in bad poisonings
  • Age >60 is a marker of severity
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16
Q

What are the indications for Charcoal in Aspirin OD?

A
  • Can be given up to 8hrs post ingestion
  • If massive overdose (>300mg/kg) or significant toxicity then intubate prior to giving Charcoal
17
Q

How does Methotrexate poisoning present and how is it treated?

A
  • Acute ingestions are almost always benign
  • Repeat supratherapeutic overdoses can be life threatening with multi-organ failure and bone marrow suppression
  • Charcoal can be considered within 2hrs of acute ingestion
  • Antidote is Folinic acid (not folic acid) which is the activated form
18
Q

How does Baclofen overdose typically present?

A
  • Baclofen is a GABAa inhibitor but in overdose loses selectivity and can inhibit the inhibitors, leading to paradoxical seizures
  • CNS depression and Delerium
  • Loss of brainstem reflexes to the point of mimicking brain death
  • > 200mg in adults is a toxic dose
  • 1x 25mg tablet in a small child can be lethal
  • Variable CVS effects in including hypotension, AV blocks, bradycardia, paradoxical tachycardia
19
Q

How is Baclofen overdose treated?

A
  • If toxic dose then early intubation and sedation
  • Charcoal via NG post intubation
  • Benzos for seizures
  • IV fluids/pressors for hypotension
  • Coma lasts apporx 48hrs
20
Q

How does cocaine toxicity usually present?

A

Sympathomimetic and Na+ channel blocker activity (particularly fast Na+ channels)

CNS- paranoid delerium, rigidity, myoclonic jerks, seizures
Cerebral oedema, SAH

CVS- Tachycardia, HTN, prolonged QT and QRS, malignant arrhytmias
Vasospastic AMI, APO, dissection

Other- Rhabdo, hyperthermia, tachypnoea, resp complications

21
Q

What is the treatment for Cocaine OD?

A

AVOID B-blockers
- Unopposed Alpha

Hypertension
- Benzos, GTN/SNP
- Consider Phentolamine 1mg IV with repeat if refractory

VT
- Sodibic 50-100mmol + hyperventilation aiming pH 7.50-55
- If refractory give IV Lignocaine

Chest pain
- Aspirin, GTN, Calcium channel blockers
- May need angiography

Seizures
- Benzos and SodiBic

Hyperthermia
- Benzos, cool fluids, may need aggressive cooling techniques

22
Q

How does Valproate overdose present and what is the risk stratification based on?

A

Simplified
<200mg/kg- Mild sedation
200-1000mg/kg- dose dependent CNS depression
>1000mg/kg- Coma, multiorgan failure, cerebral oedema

23
Q

What are the metabolic effects of large valproate overdoses?

A

HAGMA with lactataemia
Hypoglycaemia
Hyperammonaemia
Hypernatraemia
Hypocalcaemia

24
Q

Which Beta Blockers and Calcium Channel Blockers are the most toxic?

A

BB’s
- Sotalol (K+ blocker)
- Propranolol (Na+ blocker)

CCB’s
- Verapamil (SR forumlations readily form a Bezoar, indication for WBI)
- Diltiazem (Potent vasodilator with some -ve inotrope effects)
- Other CCBs cause vasodilation but not significant -ve inotropy, so often get compensatory tachycardia

25
How does MDMA toxicity present?
- Mixed amphetamine and serotonin like syndrome - Bruxism (teeth grinding) is very common - Hyponatraemia can occur due to mixed direct SIADH from MDMA activity and excessive water intake - Hepatotoxicity can occur, more common with chronic use
26
How does Lithium toxicity vary with pre-existing use?
Acute and not on lithium - Direct GI irritation causing N/V, diarrhoea and pain - Rare to have neuro complications, need renal impairment, dehydration or hyponatraemia Acute and on lithium - The most dangerous form - GI symptoms as above - Much higher risk of neuro toxicity - increased tremor, hyperreflexia, ataxia, AMS, seizures, coma - Dysrhythmias Chronic overdose - No GI symptoms but high risk of neuro symptoms - SILENT syndrome, nephrogenic DI, electrolyte abnormalities, prolonged QT, bradycardya - More likely complications during treatment
27
What is the toxicity of Quetiapine?
- The leading cause of overdose related intubation in Australia - Seizures in 5% - Tachycardia (anticholinergic) but hypotension (alpha antagonism) - >3gm is severe toxicity - peak 6hrs for IR, 24hrs for SR - Watch for urinary retention Adrenaline is relatively contraindicated, alpha antagonism of quetiapine can lead to Adrenaline causing mainly beta effects, leading to worsened tachycardia and vasodilation
28
What is the toxicity of Bupropion?
Basics - Mix of SNRI, SDRI and anticholinergic activity - Typically prescribed for nicotine withdrawal, depression and ADHD - IR formulations take 6hrs to peak and SR 24hrs, leads to delayed toxicity Neurotoxicity - delerium, seizures, coma - sympathetic stimulation (mimics amphetamines) - Can be a brain death mimic - Non-epileptic myoclonic jerks Cardiac toxicity - prolonged QT/QRS from K+ channel blockade - direct myocardial depression, leads to severe LV failure, bradycardia and collapse
29
What are the clinical effects of Cinchonism?
Quinine/Quinidine overdose Skin - Rash, photosensitivity, flushing CNS - Blindness, deafness, tinnitus CVS - Long QRS, tachyarrhythmias
30
What are the clinical features of ethylene glycol toxicity?
Stage 1 (1-12 hrs) - Ethanol like symptoms - Euphoria, ataxia, slurred speech, reduced GCS Stage 2 (6-24hrs) - HAGMA, tachypnoea, tachycardia, hypertension, coma Stage 3 (24-72hrs) - Worsening acidosis - ARF, hypocalcaemia - Seizures, coma, death Diagnosis - Calcium oxalate crystaluria - Measure serum and blood gas lactate, some VBG analysers interpret EG as lactate, thus there will be a large lactate gap - increased OG, HAGMA Electrolytes - Hypocalcaemia is pathognomonic - Also get hyperkalaemia, hypomagnesaemia and hypoglycaemia Treatment - Fomepizole/Ethanol - Dialysis - Sodi bic and hyperventilation to combat acidosis - IV Pyridoxine 50mg - Thiamine IV 300mg Long term - Cranial and peripheral neuropathies
31
What are the main features of Nicotine toxicity?
Early (0-1hrs) - N/V/D, abdo pain - Fasciculations, seziures - High Hr and BP (nicotinic) - Bronchorrhoea/constriction Late (1-4hrs) - Bradycardia, hypotension (muscarinic) - Paralysis, coma - Hypoventilation/apnoea Toxic doses oral - <0.5mg/kg = minor - 0.5 - 5 = mod-severe - >5mg/kg = lethal - lethal toxicity at 1mg/kg if mucosal or IV Treatment - Wash skin/remove clothes - Atropine IV - Supportive care
32
What are the feature of Iron toxicity?
Toxicity - <60mg/kg = minor GI - 60-120mg/kg = systemic toxicity - >120mg/kg = lethal - Strongest Fe tabs have 105mg/pill Timeline - 0-6hrs = GI irritation, may be severe with significant fluid losses/bleeding - 6-12 pseudo-improvement - 12-48hrs = HAGMA, vasodilatory shock, hepatorenal failure - Chronic = GI strictures/cirrhosis Treatment - AXR to assess for amount - WBI +/- endoscopy - Desferrioxamine Discharge - If asymptomatic at 6hrs (IR) or 12hrs for SR - asymptomatic and Fe <60umol/L - Gastro F/U considered
33
What is the toxicity of Des/Venlafaxine?
Toxicity - >5gm is severe - >8gm is life threatening - Delayed up to 16hrs with SR - >2gm ingestion need to be monitored for >16h-24hrs Clinical - Seizures - Serotonin toxicity - Cardiac depression (>8gm) - QT/QRS prolongation - tachycardia, HTN, mydriasis, sweating, delirium Decontamination - AC if within 4hrs - Consider WBI with >8gm ingestions Treatment - Benzos for seizures - If >8gm then early intubation even if asymptomatic currently - Inotropes for LV support
34
What is the toxicity of Colchicine?
Toxicity - 0.1-0.5mg/kg = potentially severe toxicity, GI symptoms - 0.5-0.8mg/kg = 10% Mortality - >0/8mg/kg= Highly likely death from multiorgan failure Clinical - 2-24hrs = N/V/D, leukocytosis, fluid shifts and loss - 2-7 days = Multiorgan failure and pancytopaenia - >7 days = rebound leukocytosis, alopecia and possible recovery Treatment - Immediate AC followed by MDAC - Supportive measures - Consider early intubation for non-compliant or vomiting patients to facilitate NG and MDAC
35
What are the features of Warfarin overdose?
Toxicity - >0.5mg/kg in those not on warfarin Clinical - Delayed bleeding 24-48hrs - INR >5 = high risk of haemorrhage Decontamination - AC +/- MDAC with large ingestions Treatment - Haemorrhage = Vit K, FFP, Prothrombinex VF - No haemorrhage but INR >2 = 10mg PO vitamin K (250mcg/kg) for 7 days with repeat INR's - No haemorrhage but INR <2 = repeat INR at 25 and 48hrs
36
What are the features of Sulphonylurea overdose?
Toxicity - 1 tab in children - Children/non-diabetics more vulnerable - Hypoglycaemia can last days - Can occur at therapeutic doses in the elderly/renal impairment Management - Oral complex carbohydrates - Octreotide SC/IV, 50mcg bolus then 25mcg/hr - IV dextrose only if hypoglycaemic, hyperglycaemia will stimulate further insulin release Disposition - Needs at least 18hrs monitoring - Need to be euglycaemic for at least 12hrs post octerotide/glucose infusion ceasing - Don't discharge overnight