Puke and the Pill Bottles

[Richard B the EMT]

RCMP= Royal Canadian Mounted Police

Ipecac is not in my protocols any more, but I have (sometimes) a long memory.

[jonas salk]

damn, had a nice reply, lost after accidentally clicking on an ad.

Okay, here we go. Given the the amount of ASA he took, along with his tachypnea i'm thinking he's put himself into a nice acidotic state. I'd want to have etCO2 hooked up and do my best to help blow off the excess CO2. Initiate transport, and if he starts giving us trouble in back by being the jackass that he probably is, some midazolam IV/IN. And if you got it maybe some NaHCO₃?

Edited June 17, 2010 by jonas salk

[DartmouthDave]

damn, had a nice reply, lost after accidentally clicking on an ad.

Okay, here we go. Given the the amount of ASA he took, along with his tachypnea i'm thinking he's put himself into a nice acidotic state. I'd want to have etCO2 hooked up and do my best to help blow off the excess CO2. Initiate transport, and if he starts giving us trouble in back by being the jackass that he probably is, some midazolam IV/IN. And if you got it maybe some NaHCO₃?

Hello,

His ETCO2 is 19mmHg.

Also, I think that an amp of NaHCO3 is a reasonable plan.

He is loaded up in the ambulance and you are getting geared up to go to the hospital.

[jonas salk]

Hello,

His ETCO2 is 19mmHg.

Also, I think that an amp of NaHCO3 is a reasonable plan.

He is loaded up in the ambulance and you are getting geared up to go to the hospital.

any change in condition after the bicarb is in?

I'm quickly running out of ideas of what I could do during transport, other than assist ventilations, and monitor.

I also expected the ETCO2 to be much higher...

Also what does the waveform look like? Any change in etco2 with bagging and the bicarb?

[DartmouthDave]

Hello,

Here is a decent link about ASA OD:

ASA OD

There were two goals I had with this case study.

1. ASA and glucose

2. Airway Management

First, there is an interesting tidbit glucose utilization. ASA in toxic levels can inhibit utilization of glucose within the CNS despite a normal serum glucose level. So, an altered LOC with a suspected should get some glucose in most cases.

"Increased cellular metabolic activity due to uncoupling of oxidative phosphorylation may produce clinical hypoglycemia, although the serum glucose levels may sometimes be within the normal range. As intracellular glucose is depleted, the salicylate may produce discordance between levels of plasma and cerebrospinal fluid (CSF) glucose and symptoms of CNS hypoglycemia (eg, altered mental status) may occur even when blood glucose levels are within the reference range."

I based this case study on a fellow that came into the ED and then the ICU. He was given an amp of D50W and D5W with NaHCO3 was started.

Second, airway management. Most sources (Up to Date, ect...) stated that intubation of an ASA OD should be avoided. ASA OD causes central nervous system hyperventilation. Which cause a profound resp. alkalosis. This helps prevent binging of H+ to the Sal- to for HS (acid). Anything that disrupts this can cause a rise in HS (acid) in the blood.

They only time intubation is warranted if if their is depressants on board. Which is the case in the scenario. Really, a good argument can be made for intubation as well as avoiding it.

Cheers

any change in condition after the bicarb is in?

I'm quickly running out of ideas of what I could do during transport, other than assist ventilations, and monitor.

I also expected the ETCO2 to be much higher...

Also what does the waveform look like? Any change in etco2 with bagging and the bicarb?

Hello,

I am sorry to say I am very weak on ETCO2 waveforms. What I can say is the ETCO2 is correct.

Here is the thing with the CO2. An ASA OD causes central nervous system hyperventilation. Thereby causing a resp alkalosis. At the same time an ASA OD will cause a medabolic acidosis (low HCO-). An ABG would show a mixed resp alkalosis and a medabolic acidosis. Without the hyperventilation the acidosis would be much worse!

The ETOH and MSIR is bad news here. It lowers the resp rate and volume. Thereby, taking away the compensation caused by the hyperventilation. This is why the Narcan was a good idea. Plus, the NaHCO3- for the acidosis (worsen by the hyopventilation).

A low CO2 is a good thing here.

Cheers

[jonas salk]

Hello,

Here is a decent link about ASA OD:

ASA OD

There were two goals I had with this case study.

1. ASA and glucose

2. Airway Management

First, there is an interesting tidbit glucose utilization. ASA in toxic levels can inhibit utilization of glucose within the CNS despite a normal serum glucose level. So, an altered LOC with a suspected should get some glucose in most cases.

"Increased cellular metabolic activity due to uncoupling of oxidative phosphorylation may produce clinical hypoglycemia, although the serum glucose levels may sometimes be within the normal range. As intracellular glucose is depleted, the salicylate may produce discordance between levels of plasma and cerebrospinal fluid (CSF) glucose and symptoms of CNS hypoglycemia (eg, altered mental status) may occur even when blood glucose levels are within the reference range."

I based this case study on a fellow that came into the ED and then the ICU. He was given an amp of D50W and D5W with NaHCO3 was started.

Second, airway management. Most sources (Up to Date, ect...) stated that intubation of an ASA OD should be avoided. ASA OD causes central nervous system hyperventilation. Which cause a profound resp. alkalosis. This helps prevent binging of H+ to the Sal- to for HS (acid). Anything that disrupts this can cause a rise in HS (acid) in the blood.

They only time intubation is warranted if if their is depressants on board. Which is the case in the scenario. Really, a good argument can be made for intubation as well as avoiding it.

Cheers

Hello,

I am sorry to say I am very weak on ETCO2 waveforms. What I can say is the ETCO2 is correct.

Here is the thing with the CO2. An ASA OD causes central nervous system hyperventilation. Thereby causing a resp alkalosis. At the same time an ASA OD will cause a medabolic acidosis (low HCO-). An ABG would show a mixed resp alkalosis and a medabolic acidosis. Without the hyperventilation the acidosis would be much worse!

The ETOH and MSIR is bad news here. It lowers the resp rate and volume. Thereby, taking away the compensation caused by the hyperventilation. This is why the Narcan was a good idea. Plus, the NaHCO3- for the acidosis (worsen by the hyopventilation).

A low CO2 is a good thing here.

Cheers

Yeah, after I posted the question about the ETCO2 I took some time to think about it and realised that I was mistaken for the very reasons you just posted. Would have gone back to modify my comments but the iPhone version of this form doesn't have the edit button.

This is was an excellent scenario. ASA can be a very dangerous drug, not quite as dangerous as Tylenol, but it's up there.

[HBEMT]

I'm thinking dt's from morphine, given the drenched clothes and empty pill bottles...he was probably thinking there wasn't enough aspirin or alcohol in the world to solve that problem... Wonder what his glucose levels are? and is it possible he seized or did he just pass out?

[zippyRN]

I'm with Kiwi and Dartmouth Dave on this ... in that we've got someone with 2 lots of depressants on board ( the Booze and Morphine) and a I doubt the Gabapentin is helping either, who is likely to be acidotic because of what's happened and what he's got on board ( the Aspirin) . the Glucose stuff definitely bears consideration as well.

HBEMT - DTs ? from an opiate - especially in acute overdose I'm not sure where you are coming from if you mean DT as in delirum tremens or other withdrawl symptoms ... or do you mean DTs as in something else

[DartmouthDave]

I'm thinking dt's from morphine, given the drenched clothes and empty pill bottles...he was probably thinking there wasn't enough aspirin or alcohol in the world to solve that problem... Wonder what his glucose levels are? and is it possible he seized or did he just pass out?

Hello,

Typically, a patient suffering from withdrawal (etoh, benzo, opiates, ect...) will demonstrate psychmotor agitation, fever, tachycardiac, hypertension, N+V and diarrhea.

In fact, I got burned once by a Nun. I thought it was an acute abdomen because of diffuse abd pain, N+V, diarrhea, temp (38 degrees). She looked like hell (nice pun).

This fellow has a mixed OD of MSIR and ASA.

His glucose is normal. But, an ASA OD can block the uptake of glucose in the brain.

Time for pre-night shift nap.

Cheers

[promedEMT]

Hello,

The RCMP request assistance at a downtown residence. They responded to a domestic dispute to find a 45 year-old male confused and agitated. They were concerned and requested medical assistance.

On arrival you are greeted by an RCMP member. She tells that they have been here many times for domestic disputes. Recently, the wife moved out. She returned to get her stuff and found her husband to be 'scary' and 'nuts'. The wife is in the back of a police car. She was intoxicated and became disruptive and violent as well.

The scene is safe. The RCMP escort you and your partner into the living room. The patient is slumped over on the coach with his eyes closed. His hands are cuffed behind his back. One of the RCMP says that he just passed out. But, just before he passed out he was breathing very fast.

Around the room you see numerous empty alcohol bottles, pill bottles and pools of emesis. The room smells of stale urine, sweat, and emesis. The patient appears very flushed and his clothing is soaked in sweat.

You are an ALS unit. You can call ALS or BLS backup if you wish.

Cheers....

ABC's

check vitals

assist ventilations as necessary or place on high flow high con O2

narcan probably wouldnt be a bad idea

Four lead EKG and run a strip to check for cardiac issues.

Have a line ready to go in case he codes

LOAD and GO

have LE accompany you in the back enroute in case the patient becomes violent

Edited March 9, 2011 by promedEMT