Efek Parasetamol Intravena terhadap Regresi Sensorik Anestesi Spinal dengan Bupivakain Hiperbarik 0,5%

Hadi Sumitro Jioe, Maribelle A. Reyes

Abstract


Penggunaan anestesi spinal untuk operasi besar saat ini umum dilakukan dan telah dipraktikkan dalam jangka waktu cukup lama. Parasetamol merupakan obat analgetik yang telah dikenal cukup lama dan saat ini digunakan untuk mengontrol nyeri baik selama operasi maupun pascaoperasi. Parasetamol memiliki efek analgetik pada susunan saraf pusat (SSP) melalui penghambatan jalur siklo-oksigenase dan berpengaruh secara tidak langsung terhadap sistem serotoninergik serta ditemukan dalam konsentrasi yang signifikan dalam cairan serebrospinal setelah pemberian melalui infus. Penelitian ini bertujuan mengevaluasi pengaruh pemberian parasetamol intravena dosis tunggal sebelum operasi terhadap regresi blok anestesi spinal pada pasien yang akan dilakukan operasi besar. Sebanyak 30 pasien dengan klasifikasi American Society of Anesthesiologist (ASA) I dan II dengan rentang usia 18–55 tahun yang dilakukan operasi besar dengan anestesi spinal diikutsertakan ke dalam uji acak terkontrol buta ganda yang dilakukan periode Februari–Juni 2015 di Operating Theatre-East Avenue Medical Center, Quezon City, Philippines. Pasien dialokasikan menjadi 2 grup secara acak dan diberikan infus 100 mL parasetamol 1 gram (Grup A; n=15) atau 100 mL NaCl 0,9% (Grup P; n=15) selama 20 menit sebelum pemberian obat pada anestesi spinal. Penilaian nyeri dinilai menggunakan visual analog scale (VAS), serta dicatat pada saat diberikan bantuan obat analgetik. Data dianalisis dengan uji chi-kuadrat dengan nilai p<0,05 dianggap bermakna. Regresi blok sensorik tertunda secara signifikan pada Grup A pada jam ke-2 (T5–T7; n=11) dibanding dengan grup P pada jam ke-2 (T5–T7; n=2) dengan nilai p<0,05. Simpulan, pemberian infus parasetamol intravena 20 menit sebelum dilakukan anestesi spinal dengan bupivakain hiperbarik 0,5% dapat menunda regresi blok sensorik.

Kata kunci: Anestesi spinal, bupivakain hiperbarik, parasetamol intravena, regresi sensorik


Effect of Intravenous Paracetamol on Sensory Regression of Spinal Anesthesia with Bupivacaine Heavy 0.5%

Spinal anesthesia is a long-accepted anesthesia that is commonly used for major surgery. Paracetamol intravenous infusion is a known analgesics that is recently used for intra-operative as well as post-operative pain control. Paracetamol has an analgesic effect, primarily to the central nervous system (CNS), through the cyclooxygenase pathway, and probably has an indirect influence on the serotoninergic system which is supported by the fact that paracetamol is found in significant concentration in the cerebrospinal fluid (CSF) after infusion. This study was designed to evaluate the effect of single pre-operative intravenous infusion of paracetamol on sensory regression of spinal blockade in patients undergoing major surgery. Thirty ASA I and II patients aged 18–55 years undergoing major surgery under spinal anesthesia were included in this randomized controlled trial double blind study during the period of February–June 2015 at the Operating Theatre – East Avenue Medical Center, Philippines. Patients were randomly allocated to receive either 1 gr/100 mL Paracetamol (Group A; n=15) or 100 mL Normal Saline (Group P; n=15) drip for 20 minutes before administration of spinal anesthesia. The intensity of pain was assessed by Visual Analog Scale (VAS) Score. Time of rescue analgesic administration was also recorded. Data were analyzed by Chi-Square Test with p value of <0.05 considered significant. Sensory regression was delayed in Group A (T5-T7; n=11) when compared to Group P (T5 – T7; n=2), which was statistically significant (p<0.05). Therefore, the administration intravenous Paracetamol 20 minutes prior to spinal anesthesia administration with Bupivacaine Heavy 0.5% can delay regression of sensory blockade.

Keywords: Bupivacaine heavy, intravenous paracetamol, sensory regression, spinal anesthesia



Keywords


Anestesi spinal; Bupivakain hiperbarik; Parasetamol intravena; Regresi sensorik

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References


Bhattacharya D, Roy S, Sribastav S, Chanda R, Paul S, Chowdhury G. Intravenous paracetamol infusion can prolong duration of spinal anesthesia in patients undergoing major gynecological surgeries. Int J Sci Nat. 2013;4(1):23–8.

Hindle A. Intrathecal opioids in the management of acute postoperative pain. Br J Anaesth. 2008;8(3):81–5.

Ayoub SS, Colville-Nash PR, Willoughby DA, Botting RM. The involvement of a cyclooxygenase 1 gene – derived protein in the antinociceptive action of paracetamol in mice. Eur J Pharmacol. 2006;538:57–65.

Mitchell JA, Akarasereenont P, Thiemermann C, Flower RJ, Vane JR. Selectivity of nonsteroidal anti-inflammatory drugs as inhibitors of constitutive and inducible cyclooxygenase. Proc Natl Acad Sci. 1993;90:11693–7.

Pickering G, Loriot MA, Libert F, Eschalier A, Beaune P, Dubray C. Analgesic effect of acetaminophen in humans: first evidence of a central serotonergic mechanism. Clin Pharmacol Ther. 2006;79:371–78.

Kumpulainen E, Kokki H, Halonen T, Heikkinen M, Savolainen J, Laisalmi M. Paracetamol penetrates readily into the cerebrospinal fluid of children after intravenous administration. Pediatrics. 2007;119:766–71.

Huseyin Sen, Yalcin Kulahci, Enis Bicerer, Sezai Ozkan, Guner Dagh, Alparslan Turan. The analgesic effect of paracetamol when added to lidocaine for intravenous regional anesthesia. Anesth Analg. 2009;109:1327–30.

Saricaoglu CM, Canbay F, Dal O, Uzumcigil D, Leblebicioglu A, Aypar G. The analgesic effect of paracetamol when added to lidocaine for intravenous regional anesthesia. Minerva Anestesiol. 2011.

Alessandra O, Sheila L, Maurizio S, Anna F, Alfio B, The analgesic activity of paracetamol is prevented by the blockade of cannabinoid CB1 receptors. Eur J Pharmacol. 2006;531(1–3):280–1.

Sandrini M, Pini LA, Vitale G. Differential involvement of central 5-HT1B and 5-HT3 receptor subtypes in the antinociceptive effect of paracetamol. Inflamm Res. 2003;52:347–52.

Hogesstat ED, Jonsson BA, Ermund A, Andersson DA, Björk H, Alexander JP. Conversion of acetaminophen to the bioactive N – acylphenolamine AM404 via fatty acid amide hydrolase – dependent arachidonic acid conjugation in the nervous system. J Biol Chem. 2005;280:31405–12.

Borazan, Hale, Erde, Tuba B, Kececioglu M, Otelcioglu Seref. Prevention of pain on injection of propofol: a comparison of lidocaine with different doses of paracetamol. Eur J. Anesth. 2010;27:253–7.

Colletti AE, Vogl HW, Rahe T, Zambraski EJ. Effect of acetaminophen and ibuprofen on renal function in anesthetized normal and sodium depleted dogs. J Appl Physiol. 1999;86:592–7.

Muth-Selbach US, Tegeder I, Brune K, Geisslinger G. Acetaminophen inhibits spinal prostaglandin E2 release after peripheral noxious stimulation. Anesthesiology. 1999;91:231–9.

Bjorkman R. Central antinociceptive effects of non-steroidal anti-inflammatory drugs and paracetamol: experimental studies in the rat. Acta Anaesthesiol Scand. 1995;103(suppl):1–44.

Nakayama Y, Omote K, Kawamata T, Namiki A. Role of prostaglandin receptor subtype EP1 in prostaglandin E2-induced nociceptive transmission in the rat spinal dorsal horn. Brain Res. 2004;1010:62–8.

Alonso JD, Aguado T, Wu CS, Palazuelos J, Hofmann C, Patricia G. The CB1 cannabinoid receptor drives corticospinal motor neuron differentiation through the Ctip2/Satb2 transcriptional regulation axis. J Neurosci. 2012;32(47):16651–5.




DOI: https://doi.org/10.15851/jap.v6n3.1367

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