7. High risk people:
-1.Conditions of CYP induction (e.g. heavy
alcohol consumption, those on anticonvulsant
drugs)
-2.Condition of GSH depletion (e.g. fasting or
malnutrition)
-3.With pre-existing liver disease.
8. TOXIC DOSE
• SINGLE DOSE - > 7 TO 10G
• FATAL DOSE > 15 TO 25G
• HEAVY DRINKERS > 2TO 6 G
• USUAL TOXIC DOSE - >150MG/KG
• THERAPEUTIC DOSE – 15MG/KG
9. STAGES
Stage 1 Stage 2 Stage 3 Stage 4
LESS THAN 24HOUR
- Non specific
symptom
- Asymtomatic
- Lab studies-
normal
24 TO 72 HOUR :
-Enzymes start
raising
-AKI ,pancreatitis
72 TO 96 HOURS
- Severe
hepatoxicity
- Death most
common
- HEPATIC STAGE
4 DAYS TO 2 WEEKS
- RECOVERY
PHASE
- Gradually
improves
10. AKI
Renal impairment - less than 2 percent.
AKI is due primarily - ATN.
Usually spontaneously improves.
NAC wont affect – kidney prognosis
11. INDICATORS OF POOR PROGNOSIS
• HEPATIC COMA
• ACIDOSIS PH<7.3
• PT PROLONGATION
• CREATNINE RAISE >3.3
• FALLING ALT WITH WORSENING PT
13. • N-acetylcysteine - all patients who r at
significant risk for hepatotoxicity.
• Start therapy before the onset of (ALT)
elevation.
• This is accomplished by initiating treatment
within 8 hours of an acute ingestion.
20. SUMMARY
• NAPQI – MAIN TOXIC PRODUCT RESPONSIBLE
• C.F IN FOUR STAGES
• TOXIC DOSE- >150MG/KG
• MODIFIED RUMACK MATHEW NOMOGRAM
• N-ACETYLCYSTINE – 20 HR IV PROTOCOL AND 70
HOUR ORAL PROTOCOL.
THANK YOU …. .bmpinternalmedicine@gmail.com
Editor's Notes
SIRS has been something that has been beat into our heads as medical students. The derivation occurred in the year 1991 when the focus was on the hosts inflammatory response.
Another task force constituted in the year 2001 recognized the limitations but really did not offer any alternatives.
So what we have been left with is the sepsis definition largly unchanged for more than 2 decades.