Sedatives OD
Benzos
Barbs
Chloral
hydrate
Incr GABA activity via incr f of opening of channels
High lipid soluble; large VOD; cross placenta and breast milk; involved in 1/3 DSH’s; alprazolam OD can
have more coma
Interactions: diazepam incr metabolism of ETOH and phenytoin; coingestants incr risk
In paeds: 1-2 tabs causes mild sedation and ataxia within 2hrs
Sx: hypotonia, nystagmus, forced downward asymmetric movement with caloric testing; aspiration
pneumonia, hypothermia, DVT, rhabdo
Charcoal: if significant toxicity (not usually required)
Flumazenil: pure competitive benzo antagonist; max effect 5mins; DOA 45mins; useful as diagnostic
agent / post op (may also be used in isolated paed OD; but otherwise isolated benzo OD rarely causes
resp dep severe enough to require flumazenil); may not reverse airway reflexes despite improved LOC;
CI if benzo dependence, unknown OD, TCA / other seizure causing drug, seizure disorder, incr ICP, QRS
prolongation (as suggests TCA OD); risk of patient absconding; may cause withdrawal; may get
seizures; 0.1-0.2mg/min to max 2mg (if doesn’t work, benzo not cause of LOC)  if works, 0.10.2mg/hr
Incr GABA activity via incr duration of opening of channels; also antagonise glutamate
Long acting = phenobarb (HL 35-140hrs), primidone; short acting = pentobarb, ultra-short acting =
thiopental
Sx: onset in secs-mins if IV, 1-2hrs if PO
NS: Miosis, vertigo, nystagmus, decr tone, can mimic brain death (unreactive pupils, loss of dolls eye
reflex, arreflexia)
Other: Decr RR/ BP/T/BSL, ARDS, decr bowel sounds; 5% barb burns (bullous lesions due to direct
epidermal toxicity)
Ix: levels correlate well with CNS depression; serial levels if comatose and may guide enhanced
elimination trt’s
Mng: charcoal
MDAC if significant (interrupts enterohepatic and enteroenteric circulation; do if intubated)
Haemodialysis/perfusion/filtration if severe (>100mg/L or levels rising despite MDAC or ileus
so cannot use MDAC); ETT early if decreasing LOC
Disposition: observe 6hrs
>2g toxicity (>8mg/kg), >4g death; can cause severe GI irritation  haemetemsis, ulceration,
strictures; HL 4-14hrs (up to 35hrs in OD)
pear scent
Sx: rapid onset (<30mins) decr LOC, ataxia,
, myocardial depression, incr sens to
catecholamines and shortened refractory period (arrhthmyias with instrumentation, VF, VT, TdP,
asystole, multifocal V ectopics, AF, SVT); decr BP; hypothermia
Ix: serial ECG’s; gastroscopy if large ingestion
Mng: ETT if CNS / CV Sx; beta-blockers for arrhythmias (other anti-arrhythmics not helpful inc MgSO4;
may be worsened by inotropes; metoprolol 5mg (0.1mg/kg in children) slow IV and repeat at 5mins 
esmolol infusion); IVF for hypotension; charcoal OK; haemoperfusion/dialysis if severe (refractory
arrhythmia / CV instability)
GHB
Acts on GHB and GABA receptors at pons, hippocampus, cortex, caudate nucleus; also incr dopamine in
striatum and cortex; incr Ach and 5-HT; peak effect 30-60mins; 25mg/kg  sleep, 50mg/kg  coma
In paeds: any ingestion can cause coma and be potentially lethal
Sx: cycling agitation and coma; vomiting; agitation 15%; seizures 5%; hypotonia and decr reflexes;
nonreactive pupils / miosis; myoclonic movements; bradycardia; U waves on ECG; resp depression;
hypothermia; loss of airway reflexes; Sx last 4-6hrs with sudden recovery characterised by delirium
and vomiting
Mng: ventilation may be needed for 3-6hrs; prognosis good; atropine / inotropes / pacing only needed
if hypotension or end organ hypoperfusion noted; consider alternative diagnosis of coma lasts >6hrs
Withdrawal Withdrawal  GABA XS; onset Sx within 2-10/7; can cause syndrome similar to DT’s; Sx similar to
alcohol withdrawal (agitation, incr HR, seizures); give longer acting benzo and wean over wks; manage
as per ETOH withdrawal