Overdose Flashcards
MOA of benzodiazepines toxicity
Potentiates and increases affinity of activity of GABA
Clin features of Benzo overdose
CNS
- CNS Effects:
• depressed LOC
Drowsiness
• Slurred speech
• Ataxia (uncoordinated movements)
• Confusion
• Dizziness
• Amnesia
• Coma (in severe cases) - Respiratory Effects:
• Usually mild or absent respiratory depression in isolated overdose
• Marked respiratory depression if combined with other CNS depressants (e.g., opioids, alcohol) - Cardiovascular Effects:
• Generally stable
• May have mild hypotension or bradycardia in large overdoses
Other
Hypotonia
Serotonin syndrome
Hypothermia
Specific diagnostic test for Benzo overdose
Urine tox screen
(Detects oxazepam which is a metabolite of diazepam and chlordiazepam)
A negative screen doesn’t rule it out
Management of benzodiazepine
Mostly supportive care and monitoring
Abcs
Intubate if unable to ventilate
IV line, take your bloods and and start fluids if needed.
Bloods: VBG, hGT, serum glucose
Correct , FBC, UEC, paracetamol level
Correct electrolytes
Activated charcoal if 1-2hpost ingestion
Dialysis is ineffective
Flumazenil 0.2mg IV over 15s (max dose 3mg) but controversial, certain indications and contraindications
Flumazenil can be considered once significant sedation is observed and you’ve confirmed it’s:
• An acute, isolated benzodiazepine overdose
• No contraindications
Indications of Flumazepine
Conscious sedation (Benzo overdose)
Accidental paediatric sedation
Diagnostic tool to avoid further investigations
Contraindications to Flumazenil
Suspected it known dependence to benzos
Coingestion with other toxins (TCAs, aminophylline, Cocain , lithium, INH, MOAs)
Known epileptic
Long term care plan in Benzo overdose?
Psychiatric review
Social worker
Rehab referral
How to manage benzo overdose as inpatient
Mild sedation can be managed supportively and observed for at least 4 hours after
ingestion with particular attention to blood pressure, pulse and respiratory rate.
Patients who have significant CNS depression and require intubation or should be
admitted to intensive care unit.
What are the iron formulations
Ferrous sulphate 60mg
Ferrous sulphate (dried)65mg
Iron furamate 65mg
Iron gluconate 35mg
Risk assessment in iron overdose
<20mg/kg Asymptomatic
• 20-60mg/kg GI symptoms
• 60-120g/kg Systemic symptoms
• >120mg/kg Potentially letha
How to calculate iron toxicity
(Elementary iron*no. Of pills) / weight in kg
Phases of iron toxicity
Phases 1: GI phase
0-6hours
N&V, diarrhea, GI bleeding
Phase 2: latent phases
6-24hours
Clinical improvement after rescuscitation Or ongoing cellular toxicity (lactic acidosis production)
Phase 3: Shock phase
12-72hours
Recurrent GI sx, metabolic acidosis with anion gap, shock, multi organ involvement (cardiac, renal, coagulopathy, CNS)
Phase 4: Fulminant hepatic failure
2-3 days post ingestion
High fatality
Phase 5: Sequale
3-6 weeks post ingestion
GI scaring, strictures, gastric outlet obstruction
Investigation for Iron toxicity
4.Investigations
Bedside:
• VBG-Lactate, HAGMA
• Glucose level
• Urine pregnancy test
• ECG
Labs:
• Fe level at 4 hours post ingestion (levels peak 4-6hrs post ingestion then begin to fall). Level
>90Umol/L or 500mcg/dl are thought to be predictive of systemic toxicity
• FBC
• Coagulation studies
• Liver function test
• Paracetamol level-R/o co-ingestion
• CEU
Abdo X-rays to visualise fragments
Indications for deferoxamine
Fe level >500mcg/dl or 90umol/L
Systemic illness (shock, acidosis, altered mental state)
SE of deferoxamine
Side effects of DFO:
• Early: Urticaria and hypotension-infusion rate related.
• Late: ARDS related to a duration >24hrs; Yersinia sepsis (DFO promotes its growth
When can you dc a patient post Iron overdose
- If asymptomatic at 6 hours can discharge
• A child who has ingested <40mg/kg and is asymptomatic or an adult who has ingested
<60mg/kg and is asymptomatic at 6 hours can be discharged.
• Admit patients with systemic toxicity depending on severity to ward, high care or ICU.
• In children presenting with toxicity consider child neglect and consult social workers
• Psychiatric assessment in patients with an intentional overdo
Managemt of Iron toxicity
6.Treatment
(i) ABC and ongoing cardiac monitoring
(ii) Supportive and symptomatic care-Volume resuscitation with crystalloid 10-20mls/kg ;
antiemetics; treat haemorrhagic gastritis ,give blood if needed; correct electrolyte abnormalities
(iii) Decontamination
- Activated charcoal does not bind Fe
- Whole bowel irrigation can be considered if large pill burden visualized on Abdominal Xray
(iv) Antidote= Deferoxamine (Chelating agent)
Indications: Systemic illness (shock, acidosis, altered mental state); Fe level> 90umol/L (>500mcg/dl)
- Binds only to Free Fe and forms ferrioxamine which is excreted in the urine, giving it a “Vin-rose”
colour. Dose 15mg/kg/hr I.V can be titrated upwards, must not exceed 80mg/kg in first 24h
Dose of deferoxamine in iron overdose
15mg/kg/hour IV (can be tut rated upwards, don’t exceed 80mg/kg in first 24hours)
Opiod overdose toxidrome
Coma
Pinpoint pupils
Resp depression
Hypotension
Hyporeflexia
Hypothermia
Antidote for opiod overdose and dosage
0.04mg and titrate up q2-3min as need for ventilation to 0.5mg, 2mg, 5mg up to max 10-15mg
Specific test for opioid overdose
Qualitative: morphine and heroin metabolites can be
detected on a standard urine drug screen for up three
Acute opioid toxicity is a clinical diagnosis; the
management of a patient with an opioid toxidrome is
unchanged by the result of a urine opioid scre
Management of opiod overdose on presentation
Supportive care
Airway and breathing: intubate if unable to ventilate, oxygenate or low GCS
Circulation: fluids and/ or inotropes if needed
Correct electrolytes derangements
Activated charcoal if 1-2 hours post ingestion
There is no routine role for gastric lavage, or dialysis
Antidote:
Naloxone
Dose: Starting dose 0.04mg, incremental increases every 2-3min, followed by an
infusion.
Excessive amounts of naloxone can precipitate opioid withdrawal.
Intravenous (IV) route is preferred, however it may be given nasally, subcutaneously
or intramuscularly if IV access is unattainable.
Naloxone lasts 20 mins to 2 hours, shorter than most opiates.
The goal of therapy should be adequate ventilation and not normal level of
consciousness
What is the toxicity dose for paracetamol
> 10g in 24hours
200mg/kg in 24hours
Stages of acetaminophen toxicity
- 0-24hours : preclinical
- 24-72hours : Hepatotoxicity
- 72-96hours Hepatic failure with encephalopathy
- > 96hours Survival or death
What do you use to plot paracetamol level
Rumack Matthew nomogram
Management of paracetamol overdose
Supportive is mainstay
ABSc
A – intubation if there is intractable vomiting with risk of aspiration or a low GCS
B – Ventilator support or O2 if there is hypoventilation/aspiration
C – Inotropy/vasopressors as needed
IV access and check glucose
Paracetamol specific
If within 2hours of presentation give 50mg activated charcoal (if no contraindications)
Treat with antiemetics if vomiting
Paracetamol level at 4hours
If suspicious that a toxic dose was ingested (>10g) give antidote even before level is available
Antidote:
N acetylcholine cysteine
Should be administered within 8hours of overdose
It can be given orally, but ideally via IV route
150mg/kg over 1 hour in 5% dextrose
Then 50mg/kg over 4 hours in 5% dextrose
Then 100mg/kg over 16 hours in 5% dextrose
It may cause anaphylactoid reactions – slow the infusion of NAC and administer anti-histamines, do not stop NAC
Patients who ingest very high doses of Paracetamol may benefit from haemodialysis, but this topic is controversial
Once liver failure has set in, the only viable form of treatment is supportive care until liver transplant can be performed
Pathophysiology of TCA overdose
Inhibition of norepinephrine and serotonin reuptake at nerve terminals: This accumulation of excitatory neurotransmitters is thought to be the mechanism by which seizures occur in TCA overdose.
Anticholinergic action: The build-up of the neurotransmitter Acetylcholine in the CNS can cause disorientation, agitation, euphoria or dysphoria and sensory hallucinations.
Direct alpha-adrenergic blockade: This can cause profound hypotension.
Membrane-stabilizing effect on the myocardium by blocking the cardiac myocyte fast sodium channels: TCAs decrease the sodium influx through the fast sodium channels and consequently decrease the slope of phase 0, leading to the widened QRS complex that is typically seen on ECGs of individuals with CA poisoning.
Clinical features of TCA overdose
CVS: palpitations , chest pain, hypotension
CNS: decreased level of consciousness, drowsiness, coma, seizures, Resp depression,
Peripheral autonomic system: dry mouth, dry skin, urinary retention, blurred vision, blurred vision
Management of TCA overdose
INVESTIGATIONS:
ECG
Arterial Blood Gas
TCA concentration
Paracetamol levels
MANAGEMENT:
Symptomatic:
Sodium Bicarbonate 0.5 – 2 mEq/kg IV bolus followed by infusion
Aim for pH 7.45-7.55
Monitor Sodium and Potassium levels
Seizures: Diazepam
Ongoing Seizures: Phenobarbital (Not Phenytoin, which is also a Sodium Channel blocker)
REFERRAL / ADMISSION CRITERIA:
Admit Symptomatic patients – depending on clinical condition. Symptomatic patients requiring Ventilatory support may require ICU.
