1 / 24

ACETAMENOPHEN TOXICITY

ACETAMENOPHEN TOXICITY. BY: Dina Saad Alagamy Dina Mostafa Shata.

antonios
Download Presentation

ACETAMENOPHEN TOXICITY

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. ACETAMENOPHEN TOXICITY BY: Dina Saad Alagamy Dina Mostafa Shata

  2. A 18 year old female was admitted to the Emergency after trying to commit a suicide by taking a large number of analgesic & antipyretic tablets, she was suffering from sever vomiting, nausea, pallor, anorexia and malaise. She stayed in the emergency for further investigation, after 24 hours lab investigation revealed elevated liver enzymes & serum bilirubin.

  3. What is the possible diagnosis? ACETAMINOPHEN TOXICITY

  4. What is the lab investigation can you do?A) ToxicologicalB)Routine

  5. A)Toxicological Investigation1- plasma acetaminophen level “it's the basic diagnosis even no symptoms” determine 4h post ingestion more than 150mg/ml indicated liver toxicity

  6. 2-Rumack Mathew nomogram correlate serum acetaminophen level with time after ingestion it's use only to acute toxicity not for chronic

  7. B) Routine investigation1-liver function test ALT& AST ,bilirubin ,prothrombin should monitored daily ,there's sharp rise of ALT by 3rd day then decline after that2-electrolytes ,glucose ,BUN .3-Renal function test, urine analysis.

  8. What is the toxic action of acetaminophen ?

  9. Normally: >90% is directly converted to non toxic glucuronide & sulfate conjugates 5% is oxidized by Cytochrome P450 to (N-acetyl-p-benzoquinoneimine) <5% excreted unchanged in urine

  10. In toxicity:Sulphate & glucuronide pathway become saturated Acetaminophen shunt to cytochrome p450 increase NAPQI Glutathione depletion NAPQI remains in its toxic form Hepatic & renal damage

  11. What's the expected clinical presentation?

  12. Stage 1: “GIT Irritation” 0.5 – 24 hours post-ingestion

  13. Stage 2: “Apparent recovery”24 – 48 hours post-ingestionsymptoms less sever, patient looks normalincrease SGOT & SGPTIncrease BilirubinProlonged PT

  14. Stage 3: “Hepatic necrosis”3–5dayspost-ingestion

  15. Stage 4: “Actual recovery”5 days – 2 weeksStarting from the 5th dayLiver function test returns to normalHepatic architecture returns to normal with fibrosiswithin 3 months

  16. How to management this case?

  17. A)Emergency & Supportive measures1-2-

  18. B)GIT Decontamination1-gastric lavage2-Activated charcoal3-Soduim sulphate cathartics

  19. C)Antidotes :1-NAC or Mucomyst 20%2-Methionine tab 250 mg

  20. NAC or Mucomyst 20% Time: 8-10 hours Mechanism :

  21. NAC or Mucomyst 20% Dose : 1) Oral :- Loading dose = 140 mg/kg Maintenance dose = 70 mg/kg every 4h for 17 doses 2)IV infusion :- Loading dose = 150 mg/kg in 200 ml dextrose 5% over 30 min Maintenance dose = 50 mg/kg in 250 ml dextrose 5% over 4h THEN 100 mg/kg in 500 ml dextrose 5 % over 16h

  22. NAC or Mucomyst 20% Indications: Level above the possible risk line Level more20mg/ml &unknown time of ingestion Evidence of hepatic toxicity &history of excessive dose Precautions: Do not stop NAC early if monogram indicated toxic possibility Any dose vomited within 1hour of administration should be repeated If emesis persists anti emetics may be used If evidence of liver injury develops NAC is continued until LFT are improve

  23. D) Enhance Elimination:1-massive ingestion with very high levels & complicated with coma or acidosis2-Acute renal failure

More Related