Binds excess digoxin or digitoxin molecules circulating in the blood
- Fab fragment-digoxin complex excreted by kidney - Net shifts the equilibrium away from binding of digoxin to receptors

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

- 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

-

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

IV only

-

46%

None

0.3 L/kg [DigiFab]
0.4 L/kg [Digibind]

2 L/kg
Highly lipid soluble

Wide - distributed to fat and tissues

Nil

Liver
via glucuronidation to naloxone-3-glucouronide

Liver
Broken down to Fatty acids and glycerol

Urine

Liver and kidneys

25 ml/min/kg

Unbound: 11 hrs
Bound: 15-20 hrs

0.5-1.5 hrs

not well defined

Anaphylaxis – rare
Digoxin Withdrawal: AF, heart failure, hypokalemia

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

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

Monoclonal antibody (mAB) FAB (Fragment antigen-binding) fragment from sheep immunized with digoxin derivative

substituted oxymorphone derivative.
pKa = 8.0

fat emulsion

Antidote

Antidote

Antidote

Antidotes

- For treatment of acute and chronic digoxin overdose
- Treatment of toxicities of other cardiac glycosides: oleander, bufotoxin (cane toad), Chinese medicines

- 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

Binds Digoxin Molecules

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

- Energy substrate
- Reverse local anaesthetic cardiotoxicity

Onset: 0-60min
Peak: 30-360min

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

powder
contains 38-40mg of digoxin-specific Fab fragments (which binds approx. 0.5mg Digoxin)
reconstitute with sterile water

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

Empiric: 10vials of Fab fragments

Known dose, no level:
Total body load = Dose (in mg) x 0.8 (BA of digoxin)
Number of vials = TBL x 2

Known concentration:
No of vials = [(serum digoxin concentration in ng/mL) x (patient's weight in kg)]/ 100

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