skymedic
02-01-2000, 04:27 PM
A south African colleague of mine, recently conveyed her concern regarging the safety of Tramal (Tramadol hydrochloride, a synthetic narcotic). This follows several incedents experienced by her colleagus, plus two of which she bore the brunt.
In all cases, the patients concerned were either initially hypovolemic, hypotensive, or both. Following the administration of Tamadol at the recommednded dosages of 2mg/kg slow IVI, these patients (most of whom were GCS 15/15 initially) experienced grand mal seizures within ten minutes of receiving Tramal. Most of these had to be intubated and ventilated after Diazepam administration, and some required further sedation for adequate management.
I suspect that the above is caused by one or more of the following:
1. Low hematocrit
2. Altered diffusion gradients and pressure gradients on the brain due to hypotension.
2. Cerebral hypoxia (though most patients were 15/15 at time of administration)
3. Electrolyte imbalances
4. Altered neurotransmitter enhanced/impaired
5. Pharmacokinetics of the drug are altered and/or affected by one of the above scenarios.
If anyone has experienced a similar case or can provide any insight to into the matter, please advise.
Thanks
Michael Dollenberg
N.Dip AET, ACLS PALS
PS. I've since found out that in clinical trials of Tramadol on lab rats (apparently their neuro structure and response is similar to ours), convulsions were induced after dosages of 25mg/kg.
Here's a theory:
If the patient is compensating by means of vasoconstriction (fit, young and healthy), then he would effectively have an increased concentration of tramadol in cerebral circulation (due to decreased peripheral circ.). thus increased risk of high cerbral doses???
Any thoughts??
[This message has been edited by skymedic (edited February 02, 2000).]
[This message has been edited by skymedic (edited February 03, 2000).]
In all cases, the patients concerned were either initially hypovolemic, hypotensive, or both. Following the administration of Tamadol at the recommednded dosages of 2mg/kg slow IVI, these patients (most of whom were GCS 15/15 initially) experienced grand mal seizures within ten minutes of receiving Tramal. Most of these had to be intubated and ventilated after Diazepam administration, and some required further sedation for adequate management.
I suspect that the above is caused by one or more of the following:
1. Low hematocrit
2. Altered diffusion gradients and pressure gradients on the brain due to hypotension.
2. Cerebral hypoxia (though most patients were 15/15 at time of administration)
3. Electrolyte imbalances
4. Altered neurotransmitter enhanced/impaired
5. Pharmacokinetics of the drug are altered and/or affected by one of the above scenarios.
If anyone has experienced a similar case or can provide any insight to into the matter, please advise.
Thanks
Michael Dollenberg
N.Dip AET, ACLS PALS
PS. I've since found out that in clinical trials of Tramadol on lab rats (apparently their neuro structure and response is similar to ours), convulsions were induced after dosages of 25mg/kg.
Here's a theory:
If the patient is compensating by means of vasoconstriction (fit, young and healthy), then he would effectively have an increased concentration of tramadol in cerebral circulation (due to decreased peripheral circ.). thus increased risk of high cerbral doses???
Any thoughts??
[This message has been edited by skymedic (edited February 02, 2000).]
[This message has been edited by skymedic (edited February 03, 2000).]