Ketorolac IG
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Transcript of Ketorolac IG
By : IG
Derifat asam asetic heterocyiclic Analgesic potent tapi anti inflamasi
moderatgol. NSAID menghasilkan efek
analgesi melalui penghambatan sintesis prostaglandin
Struktur kimia :
Sebagian besar NSAIDs bekerja sbg non-selective inhibitors dari enzyme cyclooxygenase,
Menghambat : cyclooxygenase-1 (COX-1) cyclooxygenase-2 (COX-2) isoenzymes.
Cyclooxygenase mengkatalisa formasi prostaglandins & thromboxane dari arachidonic
acid (itself derived from the cellular phospholipid bilayer by phospholipase A2).
Prostaglandins act (among other things) as messenger molecules in the process of inflammation. This mechanism of action was elucidated by John Vane (1927-2004), who later received a Nobel Prize for his work
Diindikasikan untuk manajemen nyeri jangka pendek (<5 hari)
Sangat berguna untuk manajemen nyeri post operatif yg segera
Efek analgesinya pada dosis terapi setara 6-12 mg morfin dgn onset yang sama (20-30menit) tapi durasi lebih panjang (6-8jam)
Bekerja di perifir dan tidak menembus sawar darah otak sehingga efek ke SSP minimal
Spesifik : tidak mendepresi pernapasan, mual, muntah,mengantuk.
Sering digunakan untuk manajemen nyeri operasi ortopedi dan obgyn tapi lebih jarang digunakan pada operasi intra abdominal
Menghambat agregasi platelet, memperpanjang bleeding time
Penggunaan jangka panjang bisa berakibat toksis ke ginjal (nekrosis papiler)
GIT bisa berakibat perdarahan dan ulserasi bahkan perforasi
Karena eliminasinya di ginjal tidak disarankan diberikan pd pasien dgn ggn fungsi ginjal
Kontra indikasi pada pasien yang alergi aspirin atau NSAID lainya
Pasien dg rwyt asma insiden hipersensitif terhadap aspirin meningkat (10%)polip nasal(20%)
NSAID
↑ Leukocyte-EndothelialInteractions
Capillary Obstruction
IschemicCell Injury
Proteases +Oxygen Radicals
Endo/EpithelialCell Injury
Mucosal Ulceration
Loss of
PGE 2 an
d PGI 2 m
ediat
ed in
hibition
of ac
id secre
tion an
d cytop
rotec
tive e
ffect Loss of PGI2 induced inhibition of LTB4 mediated
endothelial adhesion and activation of neutrophils
Dosis awal 60mg IM atau 30mg IV loading dose
Maintenance 15-30mg /6jamPasien usia tua perlu dosis
penyesuaian / pengurangan dosis karena fx ginjal menurun
Aspirin menurunkan protein binding ketorolac sehingga perlu dosis yang lebih besar.
Ketorolac tidak mempengaruhi MAC agen anestesi inhalasi serta tidak mempengaruhi hemodinamic pasien yang dibius
Ketorolac bisa menurunkan kebutuhan analgetik opiat post operatif
Non spesifik COX inhibitor (ketorolac, diclofenac dosis : 1mg/kgbb IV)
Selectif COX-2 inhibitor (parecoxib) punya toxicitas lebih rendah dan efek ke GIT yang lebih rendah,serta efek ke agregasi platelet yang lebih rendah pula dosis (20-40mg IV)
1. NSAIDs are effective analgesics for the acute pain of surgery, low back pain and renal colic (Level I*).
2. NSAIDs are effective adjunct to opioids (Level I).
3. NSAIDs given in addition to paracetamol improve analgesia (Level I).
I Evidence obtained from a systematic review of all relevant randomised controlled trials.
II Evidence obtained from at least one properly designed randomised controlled trial
III-1 Evidence obtained from well-designed pseudo-randomised controlled trials (alternate allocation or some other method)
NHMRC 1999
NNT (95%CI)Codeine 60 mg 16.7 (11-48)Paracetamol 1000 mg 3.8 (3.4-4.4)Morphine 10 mg (IM) 2.9 (2.6-3.6) Ketorolac 10 mg 2.6 (2.3-3.1)Ibuprofen 400 mg 2.4 (2.3-2.6)Diclofenac 50 mg 2.3 (2.0-2.7)Paracetamol 1G/ Codeine 60 mg 2.2 (1.7-2.9)Parecoxib 40 mg (iv) 2.2 (1.8-2.7)Lumiracoxib 400mg 2.1 (1.7-2.5)Diclofenac 100mg 1.9 (1.6-2.2)
Oxford acute pain league table www.jr2.ox.ac.uk/bandolier/booth/painpag/Ac
utrev/Analgesics/Leagtab.html
Small increased risk of thrombotic attacks.
Diclofenac (150 mg ) = etoricoxib. Ibuprofen 1200mg or below - no
increase of myocardial infarction.Naproxen - lower incidence of
thrombotic risk than coxibs.All NSAIDs - risk greater with high
doses, long term Rx.
Clinical anestesiology,G Edward MORGANJr, Fourt edition.2006 chapter 15 page 282-283
Pharmakology & physiology in Anesthetic practice,fourt edition, Robert K STOELTING, lipincot & walkins chapter 11 page 287-288