Do you give benzo's to a hypoglycemic seizure?

[Asysin2leads]

Anyone notice how quicky 1EMT-P shut the hell up when I pointed out he was full of crap about the NYC protocols? The higher on their horse they are, the longer the trip on the way down is. Man I love making arrogant condescending jerks look foolish.

[THE_DITCH_DOCTOR]

Man I love making arrogant condescending jerks look foolish.

Me too. Nice work.

[sharon.simmons]

I've been diabetic since `82. My first seizure was in `84. I've had several through the years all due to hypoglycemia. I can see why this would be an issue for EM T's everywhere. If I may, let me put it in perspective:

You can not process the drugs without glucose, in your bloodstream, and brain to do so.

Without glucose, the plug has been pulled, and there is nothing else to discuss.

Glucogon has been saving my life from seizures for decades.

I prefer D50 because it doesn't give me the nasty headaches.

My doctor still prescribes glucogon.

Once you give a diabetic sugar...well, I for one don't mind you being extra cautious if no one is there to tell you I don't have a seizure disorder.

But, my brain can't process.

What it can't process.

And, without glucose on board, no matter how you do it, it can't process anything!

I'm just saying--

[Ace844]

I've been diabetic since `82. My first seizure was in `84. I've had several through the years all due to hypoglycemia. I can see why this would be an issue for EM T's everywhere. If I may, let me put it in perspective:

You can not process the drugs without glucose, in your bloodstream, and brain to do so.

Without glucose, the plug has been pulled, and there is nothing else to discuss.

Glucogon has been saving my life from seizures for decades.

I prefer D50 because it doesn't give me the nasty headaches.

My doctor still prescribes glucogon.

Once you give a diabetic sugar...well, I for one don't mind you being extra cautious if no one is there to tell you I don't have a seizure disorder.

But, my brain can't process.

What it can't process.

And, without glucose on board, no matter how you do it, it can't process anything!

I'm just saying--

"sharon.simmons",

Just FYI, the benzo's which you are most likely to be given for your "Seizures" when they occur, DO NOT Rely on glucose to wither reah an effective PK, or be metabolized. Here's the ifo for those drugs...

1.) Valium::"Pharmacokinetic information of diazepam following rectal administration was obtained from studies conducted in healthy adult subjects. No pharmacokinetic studies were conducted in pediatric patients. Therefore, information from the literature is used to define pharmacokinetic labeling in the pediatric population.Diazepam rectal gel is well absorbed following rectal administration, reaching peak plasma concentrations in 1.5 hours. The absolute bioavailability of diazepam rectal gel relative to diazepam injectable solution is 90%. The volume of distribution of diazepam rectal gel is calculated to be approximately 1 L/kg. The mean elimination half-life of diazepam and desmethyldiazepam following administration of a 15 mg dose of diazepam rectal gel was found to be about 46 hours (CV=43%) and 71 hours (CV=37%), respectively. Both diazepam and its major active metabolite desmethyldiazepam bind extensively to plasma proteins (95-98%).

Metabolism and Elimination: It has been reported in the literature that diazepam is extensively metabolized to one major active metabolite (desmethyldiazepam) and two minor active metabolites, 3-hydroxydiazepam (temazepam) and 3-hydroxy-N-diazepam (oxazepam) in plasma. At therapeutic doses, desmethyldiazepam is found in plasma at concentrations equivalent to those of diazepam while oxazepam and temazepam are not usually detectable. The metabolism of diazepam is primarily hepatic and involves demethylation (involving primarily CYP2C19 and CYP3A4) and 3-hydroxylation (involving primarily CYP3A4), followed by glucuronidation. The marked inter-individual variability in the clearance of diazepam reported in the literature is probably attributable to variability of CYP2CI9 (which is known to exhibit genetic polymorphism; about 3-5% of Caucasians have little or no activity and are “poor metabolizersâ€) and CYP3A4. No inhibition was demonstrated in the presence of inhibitors selective for CYP2A6, CYP2C9, CYP2D6, CYP2EI, or CYP1A2, indicating that these enzymes are not significantly involved in metabolism of diazepam."

2.) Versed::"Midazolam's activity is primarily due to the parent drug. Elimination of the parent drug takes place via hepatic metabolism of midazolam to hydroxylated metabolites that are conjugated and excreted in the urine. Six single-dose pharmacokinetic studies involving healthy adults yield pharmacokinetic parameters for midazolam in the following ranges: volume of distribution (Vd), 1.0 to 3.1 L/kg; elimination half-life, 1.8 to 6.4 hours (mean approximately 3 hours); total clearance (Cl), 0.25 to 0.54 L/hr/kg. In a parallel group study, there was no difference in the clearance, in subjects administered 0.15 mg/kg (n=4) and 0.30 mg/kg (n=4) IV doses indicating linear kinetics. The clearance was successively reduced by approximately 30% at doses of 0.45 mg/kg (n=4) and 0.6 mg/kg (n=5) indicating non-linear kinetics in this dose range.

Absorption: The absolute bioavailability of the intramuscular route was greater than 90% in a crossover study in which healthy subjects (n=17) were administered a 7.5 mg IV or IM dose. The mean peak concentration (C max ) and time to peak (T max ) following the IM dose was 90 ng/mL (20% CV) and 0.5 hour (50% CV). C max for the 1-hydroxy metabolite following the IM dose was 8 ng/mL (T max =1.0 hour).

Following IM administration, C max for midazolam and its 1-hydroxy metabolite were approximately one-half of those achieved after intravenous injection.

Distribution: The volume of distribution (Vd) determined from six single-dose pharmacokinetic studies involving healthy adults ranged from 1.0 to 3.1 L/kg. Female gender, old age, and obesity are associated with increased values of midazolam Vd. In humans, midazolam has been shown to cross the placenta and enter into fetal circulation and has been detected in human milk and CSF (see Special Populations ).

In adults and pediatric patients older than 1 year, midazolam is approximately 97% bound to plasma protein, principally albumin.

Metabolism: In vitro studies with human liver microsomes indicate that the biotransformation of midazolam is mediated by cytochrome P450 3A4. This cytochrome also appears to be present in gastrointestinal tract mucosa as well as liver. Sixty to seventy percent of the biotransformation products is 1-hydroxy-midazolam (also termed alpha-hydroxy-midazolam) while 4-hydroxy-midazolam constitutes 5% or less. Small amounts of a dihydroxy derivative have also been detected but not quantified. The principal urinary excretion products are glucuronide conjugates of the hydroxylated derivatives.

Drugs that inhibit the activity of cytochrome P450 3A4 may inhibit midazolam clearance and elevate steady-state midazolam concentrations.

Studies of the intravenous administration of 1-hydroxy-midazolam in humans suggest that 1-hydroxy-midazolam is at least as potent as the parent compound and may contribute to the net pharmacologic activity of midazolam. In vitro studies have demonstrated that the affinities of 1- and 4-hydroxy-midazolam for the benzodiazepine receptor are approximately 20% and 7%, respectively, relative to midazolam.

Excretion: Clearance of midazolam is reduced in association with old age, congestive heart failure, liver disease (cirrhosis) or conditions which diminish cardiac output and hepatic blood flow.

The principal urinary excretion product is 1-hydroxy-midazolam in the form of a glucuronide conjugate; smaller amounts of the glucuronide conjugates of 4-hydroxy- and dihydroxy-midazolam are detected as well. The amount of midazolam excreted unchanged in the urine after a single IV dose is less than 0.5% (n=5). Following a single IV infusion in 5 healthy volunteers, 45% to 57% of the dose was excreted in the urine as 1-hydroxymethyl midazolam conjugate. "

3.)Ativan::"Injectable lorazepam is readily absorbed when given intramuscularly. Peak plasma concentrations occur approximately 60 to 90 minutes following administration and appear to be dose-related (e.g., a 2.0 mg dose provides a level of approximately 20 ng/ml and a 4.0 mg dose approximately 40 ng/ml in plasma). The mean half-life or lorazepam is about 16 hours when given intravenously or intramuscularly. Lorazepam is rapidly conjugated at the 3-hydroxyl group into its major metabolite, lorazepam glucuronide, which is then excreted in the urine. Lorazepam glucuronide has no demonstrable CNS activity in animals. When 5 mg of intravenous lorazepam was administered to volunteers once a day for four consecutive days, a steady state of free lorazepam was achieved by the second day (approximately 52 ng/ml of plasma three hours after the first dose and approximately 62 ng/ml three hours after each subsequent dose, one day apart). At clinically relevant concentrations, lorazepam is bound 85% to plasma proteins."

My short answer to this long response is thus. It is dangerous/Fatal for the provider/practioner to assume ANYTHING.. The other part of this is if we miss another cause or assume just one it could kill and or seriously/permenantly cause harm to a patient. Are you willing to accept this happening to you or a soemone you care for...I'm willijng to bet not!!!!

Hope this helps,

Ace844

[NCFD18]

I see it like this Hypoglycemia can cause seizures! That being said D50 should treat the underlying problem while at the same time making an unconcious patient concious, which is your main concern.

[NCFD18]

Status epilepticus is as potentially fatal as hypoglycemia. Normally I would advise treatment of the underlying cause (low blood sugar) to correct the situation (seizures). But in this case I agree that without IV access your choices are limited. Glucagon takes a long time to kick in, relative to D50. What is your definition of status?? Some texts refer to status as seizures with greater than 30 minute duration, and others consider 2 or more seizures in succession without consciousness to be status. With hypoglycemia, the next step beyond seizure is probably arrest.

With this presentation, I would run with Diazepam 5 mg PR to break the seizure. Follow with glucometer to confirm hypoglycemia and then go with 100 mg thiamine and D50. Our region also allows ativan, but I personally do not like the drug at all.

Break the seizure as quickly as possible and then treat the underlying cause.

You can stop the seizures and the unconciousness all at once. It would be dangerous waisting time w/ diazapam esspessially if you live here where you have to call in orders for diazapam.

BTW i've never started an IV on a seizing pt but ive seen it done, not only seizing a diabetic low sugar fighting with the first responders lol. Its not impossible.

[iditacom]

Give the glucose (no matter what form) first before going with other treatment. Use the KISS method always in EMS, go for other methods after u rule out the basics.

[flightmedic608]

Hello, I think we should back up and start from the beginning...are you securing the patients airway? If so, how? In the case of someone seizing from being hypoglycemic...hmm which came first...has the person been seizing so long that they are using their metabolic stores? Is there a different pathophyisology of the seizure...known disease, head bleed etc? There are a lot of factors that you need to discuss before you can just state to give this medication or that. This is a good post...it shows that people are out there trying to learn and find the right way to treat a patient. You should get used to looking at the patient as a whole picture and trying to assess in that standard.

Fly safe.

[NCFD18]

Hello, I think we should back up and start from the beginning...are you securing the patients airway? If so, how? In the case of someone seizing from being hypoglycemic...hmm which came first...has the person been seizing so long that they are using their metabolic stores? Is there a different pathophyisology of the seizure...known disease, head bleed etc? There are a lot of factors that you need to discuss before you can just state to give this medication or that. This is a good post...it shows that people are out there trying to learn and find the right way to treat a patient. You should get used to looking at the patient as a whole picture and trying to assess in that standard.

Fly safe.

Yeah the pt is having hypoglycemic seizures we have esatblished this.

[Asysin2leads]

You know, I'd love to see these guys sitting around scratching their chins, reading their medical textbooks, and playing Colombo M.D. searching for the exact cause while they have an actively seizing patient spitting up a mixture of saliva, blood, and vomit all over a hysterical families living room.