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
Q

How does MDMA toxicity present?

A
  • 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
Q

How does Lithium toxicity vary with pre-existing use?

A

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
Q

What is the toxicity of Quetiapine?

A
  • 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
Q

What is the toxicity of Bupropion?

A

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
Q

What are the clinical effects of Cinchonism?

A

Quinine/Quinidine overdose

Skin
- Rash, photosensitivity, flushing

CNS
- Blindness, deafness, tinnitus

CVS
- Long QRS, tachyarrhythmias

30
Q

What are the clinical features of ethylene glycol toxicity?

A

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
Q

What are the main features of Nicotine toxicity?

A

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
Q

What are the feature of Iron toxicity?

A

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
Q

What is the toxicity of Des/Venlafaxine?

A

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
Q

What is the toxicity of Colchicine?

A

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
Q

What are the features of Warfarin overdose?

A

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
Q

What are the features of Sulphonylurea overdose?

A

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