[Mike MacKinnon]

Acetaminophen Level is > 300

[Mike MacKinnon]

Now that the shock of that level is over.


What phase is this?

What does that mean?

Whats the prognosis?

What should we start and how much and.. will it matter?

Does this explain ALL the symptoms?

[Speed]

I'd guess the phase before death? I'd go with the Muco-myst, I'd have to look it up. Best I can remember: like a gram/kg over 72 hours. 1/10 as a loading dose PO or NG. I can swear that I got an order once to give it by updraft (aerosoled rotten eggs). I think there is an IV solution now. With his symptoms I would think that the ingestion (if all at once) was maybe a day or so ago? I don't know if Muco-myst would do much in the way of prevention of damage. I'm pretty sure it needs to be started within four or six hours to get the biggest bang for the buck. Looks like it's a done deal for him though?

[Sbastian]

Wow! Was I going down the primrose path before? In answer to the questions, and in light of recent developments, I will take another stab at it.

What phase is this?
We are now in phase three of an APAP OD
Phase 2 (18-72 h) Right upper quadrant abdominal pain, anorexia, nausea, vomiting continued rise in serum transaminases levels Tachycardia Hypotension
Phase 3 (72-96 h) Phase 3 Tender hepatic edge, Jaundice Coagulopathy Hepatic encephalopathy Nausea and vomiting, Renal failure, Fatality

What’s the prognosis? Poor

What does that mean? The patient requires transfer to a facility capable of intensive care monitoring and evaluation for potential liver transplantation.

What should we start and how much and. will it matter?
Call poison control at 1-800-222-2221, and they will most likely recommend N-Acetylcysteine (NAC).
Load NAC 140 mg/kg orally. NAC comes as a 20% solution. Dilute to a 5% solution by adding 4:1 apple juice, to prevent further vomiting. To limit odor, place NAC in cup, cover top with plastic cover or plastic wrap, and drink using a straw. If vomiting within 1 hour of NAC dose, then give Ondansetron 8 mg IV and re-dose NAC.
The vast majority of patients requiring NAC therapy can be treated with oral NAC.
NAC Intravenous (NAC-IV) is reserved for patients who cannot take oral NAC due to persistent vomiting, high NG residuals, NPO status, or absolute refusal to drink in a high-risk patient.
The total dose of NAC-IV (Acetadote) is 300 mg/kg administered over 21 hours.
Loading Dose: Dilute 150 mg/kg in 200 mL of 5% dextrose and administer over 60 minutes.
Second Dose: Dilute 50 mg/kg in 500 mL of 5% dextrose and administer over 4 hours.
Third Dose: Dilute 100 mg/kg in 1000 mL of 5% dextrose and administer over 16 hours.
In late presentation of APAP toxicity, >8-24 hours post-ingestion, NAC administration has been associated with decreased incidence of cerebral edema and improved survival.

Does this explain ALL the symptoms? NO

Awaiting further developments.

[LZone]

I have a question... How could he be exhibiting signs of later stage toxicity and his level still be >300? That level is indicative of someone with a recent ingestion, yet his presentation is someone nearing fulminant hepatic failure, maybe even multisystem organ failure. Anyone?

[Sbastian]

LZone, on Jun 17 2008, 08:31 AM, said:

I have a question... How could he be exhibiting signs of later stage toxicity and his level still be >300? That level is indicative of someone with a recent ingestion, yet his presentation is someone nearing fulminant hepatic failure, maybe even multisystem organ failure. Anyone?

He was toxic and they kept giving him APAP, and his liver is shot and can't process the APAP, so the level can't "go down".

[LZone]

The answer to my question about drug level vs. time elapsed leaves me with more questions, such as how did he get toxic to begin with...But for now that is irrelevant, I don't believe at this point there is much that would save him short of an immediate liver transplant. I don't believe NAC will be very effective at this point either, I think that dialysis may buy him some time, although not much to get a liver, provided his other organs have not been damaged to the point of no return. But with a persistent level at >300mg/kg, I think it is game over. I don't know he would even be eligible for such a precious commodity as a liver given his prognosis, especially because his coags must be ridiculous. What are his coags anyway? Unless I missed it, I don't see that they have been posted nor did anyone call for them. Our differential diagnoses may have been narrowed down a little earlier with that info.

[EDMEDIC]

I've got to admit Mike, the zebra got me this time. This man is in the final stages of a serious situation, an APAP OD that I frankly don't think he'll survive. I don't undertsand the abrupt onset of symptoms though. I also have serious doubt that mucomyst is going to do much to change the outcome. We do IV mucomyst here and forego the horrible rotten egg drama that any other form gets you. I guess my big question is , why the sudden onset.Anyone care to give an answer to that?..Brian

[medicerik]

did the crew who transported the patient ever get a reason as to how the bedridden "low-functioning and non verbal" guy got such a massive dose of tylenol?

Erik

[MSDeltaFlt]

medicerik, on Jun 19 2008, 11:48 AM, said:

did the crew who transported the patient ever get a reason as to how the bedridden "low-functioning and non verbal" guy got such a massive dose of tylenol?

Erik

I bet we have 3 guesses, and the first 2 don't count.

[Speed]

medicerik, on Jun 19 2008, 11:48 AM, said:

did the crew who transported the patient ever get a reason as to how the bedridden "low-functioning and non verbal" guy got such a massive dose of tylenol?

Erik

How would that change our treatment plan? I would simply remind the originating and destination staff of the "possible" need for human services to rule out foul play and leave it at that. It could have been an unintentional cumulative toxic does, a lack of knowledge on the care giver's part, or intentional. I enjoy being an interim caregiver and leaving that soap opera to someone else. Going to court sucks, I know nothing.

[medicerik]

It doesn't. It just brings back some bad memories from a 911 call I ran a while back involving a nursing home, a massive Percocet OD, and a patient with basically the same level of function as the guy in this case.

[EDMEDIC]

I agree /c SPEED, how it happened is really immaterial to us right now. Document what you know, and move on /c it. This pt is in phase 3 ( which include "fatality"). I frankly think that is the prognosis. BUT, now the question arises, what do we do now? What measures hould be taken before transport? Is it even appropriate to tranport him? Who will make that decision? Does the receiving Physician know the APAP level found ? From my viewpoint, if we are in fact transporting him, lets get his airway secured and package him up to go. We should hear the aircraft spindling up now....my .02, Brian

[Mike MacKinnon]

So

How could he have such a high APAP level ? Generally, it takes a day orso post ingestion to get to this stage.

[shock360j]

I dont think the APAP OD is necissarily the primary cause for the hepatic problem here. He probably has been recieving Tylenol prn, and the high level is secondary to an already existing hepatic problem (hepatitis, ect). Reviewing his ABG listed previously, if he was indeed this far along in a Tylenol OD, I would expect his pH to be lower than 7.34. That being said, I would suspect this is an unintentional OD caused by the hospital staff not knowing the patient already had a primary hepatic problem, and mucomyst is definately indicated. Since he obviously can't swallow, IV administration would be best. Hopefully, he hasnt already developed an encephalopathy on top of his previous head injury.

[medicerik]

Mike MacKinnon, on Jun 20 2008, 09:49 AM, said:

So

How could he have such a high APAP level ? Generally, it takes a day orso post ingestion to get to this stage.

Could either a chronic ingestion of a APAP containing product with a larger recent ingestion, or an increase in dosage of one of his other medications that is metabolized through the same system in the liver that APAP is do it?


Erik

[MSDeltaFlt]

If I were a LEO, guess where I'd be lookin'?

[medicerik]

So, what's the final result from this case?

Erik

[Mike MacKinnon]

Turns out the guy had been trying to kill himself for 2 days. The only thing he could get his hands on was tylenol (which was in the purse of this caregiver. Unbeknown to her he had take a whole LARGE bottle over this road trip.

The reason his tylenol levels were so high is because he was still taking them the day of arrival in the ER.

Scary huh?

anywho, the caregiver was of little use since apparently she was a "temp" agency person and knew little.

End result this pt died 2 days later in an ICU with nothing to be done.

The moral of the case: many pts come with co-morbidities that confound the diagnosis but that should not preclude following common differentials. If this guy walked into any ER (or was rolled) he would have gotten a UDS and APAP.

Keep everything in perspective at all times and be careful of the 'zebra'

[fire_911medic]

Nice zebra there Mike. My first time playdng and I felt slapped ! Got hooked into thinking the guy had sepsis going on initially. Poor guy had to be in misery with that level. How dd they evntually discoer he had ried to kill himself as he was so confused I'm assuming he didn't relay this? Anyway, i was looking for the zebra and got ran ove by it !

Fire-911medic