Barbiturate Overdose
Barbiturates cause severe CNS and respiratory depression and may mimic brain death
Barbiturates cause severe CNS and respiratory depression and may mimic brain death
Digoxin toxicity is characterised by gastrointestinal distress, hyperkalemia and life-threatening dysryhthmias, including increased automaticity and AV nodal blockade
Activated Charcoal: decontamination agent; absorbing molecules of drug on its surface -> inhibiting their absorption by as much as 50% -> excretion in faeces
Opioid Withdrawal
Opioid Overdose: miosis; CNS depression; respiratory depression; complications of hypoxia: seizures, dysrrhythmia, brain injury
Paraquat Poisoning; highly toxic herbicide; common agent in suicide in 3rd world; leading single agent causing death from pesticide poisoning in many countries including Sri Lanka
The patient's form a heterogeneous group that requires a systematic approach based on early resuscitation where needed, risk assessment to guide further management and early consideration of the underlying psychosocial issues.
Reviewed and revised 24 May 2014 OVERVIEW MECHANISM OF ACTION TOXICOKINETICS RISK ASSESSMENT CLINICAL FEATURES Effects include: Complications INVESTIGATIONS (Guided by clinical assessment) Laboratory tests MANAGEMENT Resuscitation Supportive care and monitoring Decontamination Disposition References and Links Journal articles
Ethanol (ethyl alcohol) is an aliphatic alcohol, C2H5OH. The primary effect of ethanol is CNS depression, which is additive with other CNS depressants
High-dose Insulin Euglycaemic Therapy (HIET) is primarily used in the therapy of severe calcium channel blocker toxicity. HIET can also be used for severe beta blocker toxicity and potentially other toxicities/ presentations requiring inotropic support
Sympathomimetic syndrome with potential for life-threatening vascular complications (ischemia, dissection and haemorrhage). Note: ecstasy is also associated with hyponatraemia
Drug withdrawal in ICU is more common than generally appreciated.