michaeltt said:
hey man my bad, i really didnt know what the drug was he was talking about, but i thought it would likely be an opiate. thats pretty crazy about what happens during severe liver failure.. are you a doctor bro?
nope, not a doctor, no one is a doctor on the internet, never believe that.
I studied acetaminophen overdose about a dozen years ago. I have met and seen personally those who have tried to commit suicide by acute ingestion of tylenol etc...
It rarely works. I have however seen many people die of liver failure secondary to alcohol abuse and its the worst death possible.
I met a kid that took literally 50grams at least of acetaminophen and now his liver after a year and a half is near normal.
There are so many variables that one cannot say 26 tabs is going to do anything however, the death will take days if it leads to that, but it just may. I actually refreshed my memory a bit on this. Not that it makes a whit of difference if he doesnt act.
But, these are numbers are very conservative as far as lethal dose. When I studied it, I can remember that it is very rare in the US but seems to occur more frequently in the UK. TT is in Scotland so infrastructure of 911 is different and such.
The chances of the kid dying is directly correlated with how soon he gets treatment. I deal strictly with the heart but see patients that have liver failure on occasion needing transplant.
He can be alright if this is isolated and the dose is taken fine by the body, he may have destroyed a large section of his liver which regenerates over time given that other caustic substances are no longer ingested allowing it to regenerate, ie, no more cider for a long time.
Or could pass the point of no return, either liver transplant or a very slow, very, very, very agonizing death.
Liver filters toxins and also produces clotting factors and other necessary agents.
Im not an internal medicine guy per se being strictly cardiac as a primary focus but seen all kinds of messed up livers, last one was full of mets from breast cancer.
here, I googled something for the tylenol overdose
Background: Acetaminophen is the most widely used analgesic and the most commonly used drug in pediatrics. It is available in various formulations, including liquid, tablet, capsule, and suppository. The chemical structure of acetaminophen is N-acetyl-p-aminophenol (APAP). It has an excellent safety profile in therapeutic doses, but hepatotoxicity can develop with overdoses. N-acetylcysteine (NAC) is an effective antidote for APAP toxicity resulting from an acute single overdose.
Pathophysiology: Acetaminophen is rapidly absorbed in therapeutic doses, with peak levels in 1-2 hours and 2-4 hours in the overdose setting. Therapeutic levels range from 10-20 mcg/mL. Small protein binding of 10% occurs, with a volume of distribution of 0.9 L/kg. Metabolism is primarily hepatic; the half-life is 2-4 hours. Acetaminophen, the parent compound, is nontoxic, but hepatic metabolism leads to formation of a toxic metabolite, N-acetyl-benzoquinoneimine (NAPQI). The liver metabolizes more than 90% of acetaminophen to glucuronide and sulfate conjugates, which are eliminated in the urine. In children, sulfation is the primary pathway until age 10-12 years; glucuronidation predominates in adolescents and adults. Only a small amount of acetaminophen (2%) is excreted unchanged by the kidney. Hepatotoxicity is the result of formation of the reactive and toxic metabolite NAPQI by the cytochrome P-450 system.
Glutathione can bind NAPQI and lead to excretion of nontoxic mercapturate conjugates. As glutathione stores are diminished, NAPQI is not detoxified and covalently binds to the lipid bilayer of hepatocytes causing centrilobular necrosis. Glutathione must be replaced by sulfhydryl compounds from the diet or medication such as NAC. Glutathione stores are affected by age, diet, liver disease, and medical conditions such as fasting, gastroenteritis, chronic alcoholism, or HIV disease. Inducers of cytochrome P-450 2E1 such as ethanol, isoniazid (INH), rifampin, phenytoin, barbiturates, and carbamazepine can lead to increased production of NAPQI.
Frequency:
In the US: Acetaminophen is the drug most commonly ingested in overdoses and is a common co-ingestant. Acetaminophen-induced hepatic failure is the second leading cause of liver transplantation.
Mortality/Morbidity:
Since the introduction of NAC, the mortality rate from APAP toxicity is low.
Age:
In acute exposures, mortality and morbidity are decreased in pediatric patients compared to mortality and morbidity in adults. Whether this difference in mortality is due to age-related differences in metabolism, increased glutathione stores, or low ingested doses is unclear. Recently, concern has arisen about chronic toxicity in young febrile children.
CLINICAL Section 3 of 10
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography
History:
Phase 1
The first phase lasts up to 24 hours.
Patients typically experience anorexia, nausea, and vomiting.
Some patients may have no initial symptoms, but they have the potential to develop significant clinical toxicity.
The presence of neurologic, respiratory, and cardiac symptoms is rare in this phase.
Phase 2
The second phase typically occurs 24-48 hours postingestion.
Patients present with right upper quadrant pain and tenderness that coincides with transaminase elevation.
Phase 3
Phase 3 develops 3-4 days postingestion.
Patients have symptoms of hepatic failure with jaundice, bleeding, or encephalopathy.
Only about 3.5% of patients who develop hepatotoxicity eventually develop fulminant hepatic failure.
Death may occur due to cerebral edema or sepsis.
Phase 4
Phase 4 occurs 4-14 days postingestion.
Depending on the extent of damage, patients may have complete recovery of liver function or death.
Physical:
Phase 1: Physical findings are nonspecific and include pallor, malaise, vomiting, and diaphoresis.
Phase 2
The patient may develop right upper quadrant tenderness.
Tachycardia and hypotension may occur with volume loss.
Phase 3: Physical findings include jaundice, gastrointestinal bleeding, abdominal pain, and encephalopathy.
Phase 4: The final phase involves resolution of physical findings or death.
Causes:
The maximum daily dose of acetaminophen is 4 g in adults and 90 mg/kg in children. A single ingestion of 7.5 g in an adult or more than 150 mg/kg in a child is a potentially toxic dose of APAP.
Production of NAPQI by the cytochrome P-450 system is the cause of liver toxicity.
as I said, off the top of my head, I believe that 25grams ,was the median dose for fatality, but that was a loonnng time ago when I studied it, basically, he may or may not be ok.
Only going to the hospital with bloodwork can confirm that.
The thing is, if TT doesnt act is my point. He may be responsible for a friend going through a truly nightmarish death. No joke, bleeding from every orifice type of hemorrhagic fever type of death
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