- Metabolized to cysteine → Regeneration of sulphydril groups and glutathione
- acting as an alternate substrate for conjugation
- reduces disulfide bonds in mucoproteins

Reversal of MoP receptor effects such as sedation, hypotension, respiratory depression, and the dysphoric effects of partial agonists
Will precipitate acute withdrawal symptoms in opiate addicts

- unclear
- may involve establishment of concentration gradient away from primary site of action of LA

- Reduces hepatotoxicity
- mucolytic

- CVS: > 0.3 mg/kg → ↑MAP
- RESP: nil
- CNS: Drowsiness at high dose, Decreased pain tolerance
- OTHER: Sphincter of oddi spasm

- energy substrate (essential fatty acids)
- managing lipophilic drug overdose by binding and facilitating clearance

PO: BA low

91% absorption but Oral BA 2% due to extensive first-pass metabolism

IV only

66-97%
Albumin

46%

None

0.5 L/kg

2 L/kg
Highly lipid soluble

Wide - distributed to fat and tissues

Liver
Deacetylated to cysteine -> normal metabolism (Rapid)

Liver
via glucuronidation to naloxone-3-glucouronide

Liver
Broken down to Fatty acids and glycerol

Unchanged: 40% urine, 3% feces

Liver and kidneys

25 ml/min/kg

5.5 hrs

0.5-1.5 hrs

not well defined

usually in 1st hr:
- rash around infusion site
- angiooedema
- bronchospasm
- hypo/hyper tension

Mx: stop, give antihistamine, then restart at slowest infusion rate

Rapid onset of withdrawal symptoms in opioid drug addiction
At High Doses:
- Hypertension
- Tachycardia
- Arrhythmias

- Fat embolism
- Hyperlipidemia, pancreatitis
- Hepatic dysfunction
- Allergic reactions

Synthetic derivative of cysteine

substituted oxymorphone derivative.
pKa = 8.0

fat emulsion

Antidote

Antidote

Antidote

Antidotes

- paracetamol overdose
- non-paracetamol induced fulminant hepatic failure
- prevention of contrast nephropathy
- mucolytic therapy

- the reversal of respiratory depression due to opioids
- the diagnosis of suspected opioid overdose and has been used in the
treatment of.
- clonidine overdose

- TPN mixtures
- Local anaesthetic toxicity with or without circulatory arrest
- Prevention of essential fatty acid deficiency syndrome

Level 3

Level 3

Level 3

antioxidant and glutathione inducer

competitive antagonist at mu-, delta-,
kappa-, and sigma-opioid receptors

- Energy substrate
- Reverse local anaesthetic cardiotoxicity

Duration: short

Onset: 1-3 mins
Peak effect: 15 mins
Duration: 30 mins
> Less than the effect site time of most opioids → requirement for repeat dosing or infusion.

(For LA tox)
onset: minutes
peak: 15-30mins

IV or oral formulation
200mg/mL
compatible with 5% dextrose

clear solution for injection containing 0.02/0.4 mg/ml of naloxone hydrochloride

white, oil-water emulsion with 20% soybean oil, egg yolk phospholipids, glycerin, sodium hydroxide and water

IV, PO, Neb (inhaled)

IV:
1st : 150mg/kg in 200ml dextrose over 15mins
2nd : 50mg/kg in 500ml over 4hrs
3rd : 100mg/kg in 1l over 16hrs

IV/IM

- Reversal of post-operative respiratory depression and coma: 20-40mcg IV PRN
- For opioid overdose reversal 0.4-2 mg IM/IV → Via infusion a 5mcg/kg/hr
- Reversal of S/Es of opioids: 1-4 mcg/kg
- Increased cardiac contractility in septic shock at doses 1mg/kg IV

IV

For LA tox: 1.5ml/kg bolus over 1 minute →
Infusion 15 ml/kg/hr

If not stabilized, two subsequent boluses may be given 5 mins apark.
Then rate doubled to 30ml/kg/hr

Max cumulative dose 12ml/kg

effective in alleviating the pruritus, nausea,
and respiratory depression associated with the epidural or spinal administration of opioids.

serum amylase or lipase should be monitored for
2 days