Overdoses Flashcards
What differentiates beta blocker and calcium channel blocker overdoses?
- 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
What drug overdoses/toxic exposures will likely present with significant bradycardia?
Beta blockers
CCB’s
Digoxin
Amiodarone
Clonidine
Organophosphates
GHB
What are the features of Acute digoxin toxicity?
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
Who is at risk of chronic digoxin toxicity?
- 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
What are the features of chronic digoxin toxicity?
- 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)
How does arrest management change in acute digoxin toxicity?
- 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
How does salicylate toxicity usually present?
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
What are the typical salicylates in Australia?
Aspirin
Methyl salicylate (1:1.5)
Choline salicylate (1:0.75)
1ml oil of wintergreen = 1400mg Aspirin
What are the effects of TCA overdose at different doses?
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)
What are the ECG changes in TCA overdose?
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
What is the treatment and end points for TCA/Na+ blocker overdose?
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
What are the risk factors for severe toxicity from BB/CCB overdose?
Big dose
Extremes of age
Pre-existing CVS disease
Co-ingestion with -ve inotropes
What is the toxic dose of Ibuprofen?
> 300mg/kg
Causes multiorgan failure
What is different about Mefenamic acid compared to other NSAID’s in overdose?
Causes seizures
Charcoal contraindicated prior to intubation and NG placement due to imminent risk of seizures
What are the clinical effects seen with Theophylline poisoning?
- Hypokalaemia, hyperglycaemia
- Hypotension from B2 mediated vasodilation
- Multidose activated charcoal can be used in bad poisonings
- Age >60 is a marker of severity
What are the indications for Charcoal in Aspirin OD?
- Can be given up to 8hrs post ingestion
- If massive overdose (>300mg/kg) or significant toxicity then intubate prior to giving Charcoal
How does Methotrexate poisoning present and how is it treated?
- 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
How does Baclofen overdose typically present?
- 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
How is Baclofen overdose treated?
- 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
How does cocaine toxicity usually present?
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
What is the treatment for Cocaine OD?
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
How does Valproate overdose present and what is the risk stratification based on?
Simplified
<200mg/kg- Mild sedation
200-1000mg/kg- dose dependent CNS depression
>1000mg/kg- Coma, multiorgan failure, cerebral oedema
What are the metabolic effects of large valproate overdoses?
HAGMA with lactataemia
Hypoglycaemia
Hyperammonaemia
Hypernatraemia
Hypocalcaemia
Which Beta Blockers and Calcium Channel Blockers are the most toxic?
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