Tox Flashcards
Approach to overdose/toxic syndromes
1) resus and management of life threatening feature
2) identify drug and quantity
3) limit absorption/enhance removal
4) Antidotes
5) supportive care
Investigations in poisoning
Urinalysis
Biochemistry —> renal and hepatic impairments
ABG
Anion gap (10-14) Elevated in ethanol, methanol, EG, metformin, cyanide, salicylate
Osmolar gap (2Na+K+urea+glucose). <10 Ethanol, methanol and EG
ECG - TCA
Plasma drug levels
Ways to limit absorption/force elimination
Induced emesis - NO
Gastric lovage - only within 1 hour. Do not do in corrosive agents
ACtivated charcoal - porous, large SA, binds DOES NOT BIND - heavy metals, cyanide, alcohol, strong acids/all 1 hour unless slow emptying (opiates)
Entero-hepatic recirculating - carbamazepine, theophylline (4 hours)
Whole bowl irrigation - polyethylene glycol NG, rapid expulsions
Elimination Forced alkaline diuresis —> iv Sodium bicarb with loop, urine pH>6.5 Acidic drugs are ionic and can’t be reabsorption Aspirin, methotrexate
RRT if small, water soluble, low protein binding
Haemoperfusion - charcoal cartridge in HD
Types of toxidrome
There are six commonly described toxidromes
Anticholinergic
- Antihistamines, Antidepressants, especially TCAs, Antipsychotics, Antispasmodics, Anti-Parkinsonian, drugs
-CVS Tachycardia, arrhythmias
- CNS Myoclonus, seizures, mydriasis
- Neuropsychiatric Delirium
- GU Retention
- GI Reduced bowel sounds
- Metabolic Hyperthermia, flushed/dry skin
Cholinergic
-Organophosphates Nerve agentsm, Cholinesterase inhibitors, e.g. in patients with MG
- RS Bronchorrhoea, bronchospasm, progressive paralysis leading to respiratory failure/arrest, asphyxiation
- CVS Tachy-/bradycardia
- CNS Lacrimation, miosis weakness, paralysis seizures
- GU Urinary incontinence
- GI Salivation, cramping nausea and vomiting, diarrhoea
- Metabolic Diaphoresis
Narcotic
- opiods
- RS Respiratory depression
- CVS Bradycardia, hypotension
- CNS ↓GCS, hyporeflexia, miosis
- Metabolic Hypothermia, rhabdomyolysis
Sedative
- Benzodiazepines, Alcohol, Barbiturates
- RS Respiratory depression
- CVS Bradycardia, hypotension
- CNS ↓GCS, hyporeflexia
- Metabolic Hypothermia
Serotoninergic
- TCAs, SSRIs, MAOIs, Cocaine, Amphetamines, Tramadol, pethidine
- CVS Tachycardia, hypo-/hypertension
- CNS Tremor, fasciculations, extrapyramidal side effects, hyperreflexia, seizures
- Neuropsychiatric Confusion, agitation
- Metabolic Hyperthermia, rhabdomyolysis
Sympathomimetic
- Cocaine, Amphetamines, Decongestants, Caffeine, Theophyllines
- CVS Tachycardia, hypo-/hypertension, arrhythmias
- CNS Hyperreflexia, myoclonus, seizures, mydriasis
- Neuropsychiatric Agitation, delusions, paranoia
- Metabolic Hyperthermia, diaphoresis, rhabdomyolysis
Pathophys of paracetamol OD
Metabolised by sulphation and glucuronidation
Small part by cp450 to NAPQINAPQI detoxed by glutathione
OD - sulphate/gluc stopped
Switching to cp450 —> more NAPQI, glutathione depletes
Degree of toxicity is directly proportional to magnitude of overdose
Factors aggregating a paracetamol OD
Pre-existing glutathione depletion —> eating disorder, chronic alcohol, CF, HIV
Induction of the cP450 system - phenytoin, rifampicin, carbamazepine
Why does lactate rise in paracetamol OD
Impaired mitochondrial dysfunction —> anaerobic respiration
Due to hepatic failure
How does NAC work
Provides reservoir of sulphydryl groups
Stimulates glutathione
Side effects of NAC
Rash
Angiooedema
Bronchospasm
THESE ARE NOT A CI ….slow the rate, give an antihistamine
Features of salicylate poisoning
Toxic level - CTZ activated, N&V.
Resp centre activated—> resp alkalosis
High levels, uncouple cellular resp —> lactic acidosis
Fever
Tinnitus
Hypoglyc
Vertigo
Visual loss
Coag
Pulmonary oedema
Management of aspirin oD
AC in one hour
Forced alkaline diuresis —> pH 7.40-7.50
urine to >6.5HD
Mechanism of TCA overdose
Cholinergic antagonisms
Na blockade
Features of TCA OD
CVS - tachy, arrhymia, hypotension
Neuro - Dilated pupils, blurred vision, seizures
Resp - depression
GI - dry mouth, prolonged transit
Warm dry skin urine retention
Key Ix of TCA OD
ECG, 12 lead and continuous monitor (wide QRS)
ABG
Management of TCA od
ABCDE
Activated charcoal, and can be repeated
Intubation if low GCS
observe QRS and BP, (>100ms)
increase pH
hyperventilate
iv sodium bicarbonate (also high sodium load to prevent blockade)
Arrhythmia - bicarb, magnesium, lidocaine
Care reports of lipid emulsions
Seizure - benzos
