TOXICOLOGY

Case of Acetaminophen
 1
ACETAMINOPHEN
POISONING CASE
CASE
A thirty-six-year-old male patient comes to the ED and reports
taking an “overdose” earlier that day in an attempt to commit
suicide. Apparently he was discharged from his job one day prior
and had “given up.” He reports some abdominal pain
approximately and two episodes of emesis 3–4 hours prior to
arrival in the ED. Initially he refused to identify what substance he
ingested during the suicide attempt. He denied regular or recent use
of prescription or over the-counter medications or dietary
supplements as well as regular consumption of alcoholic beverages.
No other medical history is available
Physical Examination The Vital Signs

blood pressure 138/88

pulse 92/min and regular
respiratory rate 20/min temperature 37.2 Celsius
temperature 37.2 Celsius
awake
alert and oriented
responded to questions appropriately
mild epigastric tenderness
the rectal examination was normal
The neurologic examination was within normal limits
Acetaminophen
Paracetamol (acetaminophen) is an
analgesic and antipyretic drug that
is widely used in the world as a
first-line drug since 1950.
Acetaminophen is a free drug and
is very easy to obtain so that the
risk of acetaminophen abuse is
greater.
 Paracetamol tends to be safe when used in accordance with
the dose and can cause hepatotoxic in the use of more than 4 grams.
The Food and Drug Supervisory Agency BPOM said that
Indonesia had a number of cases from 2002-2005 as many as 201
cases with 175 cases including suicide attempts. In the United States
the FDA recorded 307 cases of hepatotoxics related to the use of
paracetamol from January to 2001.
 Percentage Of
Hepatotoxic Sufferers
60% p a t i e n t wi t h s e ve r e l i ve r f a i l u r e

sufferer dies
40%

Q1 Q2
 Paracetamol is generally converted by the cytochrome P-450

enzyme in the liver into its reactive metabolite called N-Acetil

P-Benzoqinoneimin (NAPQI). This process is called

metabolite activation, and NAPQI acts as a free radical.

 Under normal circumstances, NAPQI will be detoxified

quickly by the glutathione enzyme from the liver. Glutathione

contains sulfhydryl groups which will covalently bind to the

free radical NAPQI, producing cysteine ​conjugates.

 Some will be acetylated to be the conjugate of mercapturic

acid, which can then be excreted in urine. At therapeutic

doses, NAPQI is hepatotoxic, where in excess doses the

production of hepatotoxic metabolites increases beyond the

ability of glutathione to detoxify, so that these metabolites

react with liver cells and the emergence of centro-lobular

necrosis. Therefore in the treatment of paracetamol poisoning

therapy is intended to stimulate the synthesis of glutathione

Causes of Poisoning
• Overdose
• There are contraindications to liver
function
• Taking the next dose too quickly without
giving enough time lag
• Take several drugs that contain
paracetamol at the same time
• Consuming peracetamol with too high a
dose (same as if it's not like number 1
time)
• The interaction of drugs with drinks, for
example paracetamol with milk.
 Symptomps
Phase III
Phase I recurring events
Phase I
Jaundice (symptoms of liver failure)
Nausea and Vomiting
Hypoglycemia
No appetite

Phase II Phase IV
If extensive and progressive liver
Enlarged liver (hepatomegaly) damage can occur, sepsis
Disseminated Intravascular
Increased bilirubin
Coagulation (DIC) and death
Blood clots become slow

Decreased urine volume

Handling and Medication

Activated carbon 100 gr in

200 ml

N-acetylcysteine ​140 mg / kg
body weight
Thanks!
Any questions?