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Dr. Minnu Panditrao's Dexmedetomidine for intraoperative sedation & analgesia
 

Dr. Minnu Panditrao's Dexmedetomidine for intraoperative sedation & analgesia

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Prof. Minnu Panditrao shares her own ideas about the use dexmedetomidine for various indications i.e. for sedation, intra and post operative analgesia.

Prof. Minnu Panditrao shares her own ideas about the use dexmedetomidine for various indications i.e. for sedation, intra and post operative analgesia.

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    Dr. Minnu Panditrao's Dexmedetomidine for intraoperative sedation & analgesia Dr. Minnu Panditrao's Dexmedetomidine for intraoperative sedation & analgesia Presentation Transcript

    • DexmedetomidineFor IntraoperativeSedation&Analgesia
    • Dr. Mrs. Minnu M. PanditraoCONSULTANTDEPARTMENT OF ANESTHESIOLOGY &INTENSIVE CAREPublic Hospital Authority’sRAND MEMORIAL HOSPITALFREEPORT, GRAND BAHAMACOMMONWEALTH OF THE BAHAMAS
    • FORMERLY:ProfessorDepartment of Anaesthesiology and CriticalCareDr. D Y Patil Medical CollegePimpri, Pune, India
    • alpha 2 Adrenergic Receptor Agonists• Imidazole class of drugs• Older drugs : xylazinedetomidinemedetomidinein veterinary medicine!• Clonidine : first agent ( in humans)•Clarke KW, Hall LW. “Xylazine” a new sedative for horse and cattle. Vet rec1969; 85: 512-517•Tamsent A, Gordh T. Epidural clonidine produces analgesia, Lancet1984; 2:231-232
    • alpha 2 Adrenergic Receptor AgonistsDexmedetomidineWhat is so special about it?
    • Dexmedetomidine• a D – enantiomer of medetomidine• New Entrant in this class• approved in 1999 by FDA for clinicalapplication in humans• Structure:
    • Actions• CentralSedation, anxiolysis and analgesiaBradycardia and hypotension• PeripheralDecreased GI secretions, inclusive of salivaDecreased GI motilityInhibition of rennin-Angiotensin (RA) system anddecreased release of renninIncreased Glomerular Filtration Rate (GFR),Increased excretion of Na, water and thus diuresisDecreased intra-ocular pressureDecreased insulin release
    • MECHANISMCLINICAL (CNS) EFFECTS• neither the nerve/ terminal is allowed to getstimulated, nor it can transmit/ propagate thesignal forwards.• at supra-spinal level as well as at spinal levelSupra-spinal: Locus coeruleus:– Brainstem center - modulates wakefulness– Major site for hypnotic actions (sedation,anxiolysis)– Mediated via various efferent pathways:• Thalamus and subthalamus cortex• Nociceptive transmission via descending spinal tracts• Vasomotor center and reticular formation
    • MECHANISMCLINICAL (CNS) EFFECTS• Spinal: Spinal cord Binding to 2 receptors analgesiaAt Substantia gelatinosa (Lamina II), closing the gate at the dorsal horn tostimuli coming from Aδ and C fibers Inhibit release of nociceptive humoraltransmitters like Substance Prelease of substance P•Kuraishi Y, Hirota N, Sato Y, et al Noradrenergic inhibition of the release of Substance P from the primary afferents in the rabbit spinalcord dorsal horn. Brain res.1985; 309: 177- 182
    • CNS ACTIONSDexmedetomidine• Sedation – central, G-proteins (inhibition)• Analgesia – spinal cord, Substance P
    • CELLULAR MECHANISMCa++Ca++Ca++–– +Decrease ininflux of Ca++Decrease in actionpotential due tohyperpolarization2A2ARGo Gk K+K+K+
    • CNS ACTIONS• Sedation, resembles the physiologic sleepwith less prominent respiratory depression• Action is supposed to be mediated throughα2A subset of receptors and is very specificfor dexmedetomidine as compared toclonidine• Are easily arousable and additional sedative/adjuvant is not needed to maintain thesedation•Hunter JC, Fontana DJ, Hedley LR et al. Assessment of the role of alpha 2 adrenoceptor subtypes in anti nociceptive , sedative andhypothermic action of dexmedetomidine in transgenic mice Br J Pharmacol1997; 122: 1339-1344•Venn RM, Bradshaw CJ, Spencer R et al. Preliminary UK experience of dexmedetomidine, a novel agent for post operative sedationin intensive care unit. Anaesthesia 199; 54: 1136-1142
    • Actions on Cardio-Vascular system• Totally devoid of any direct effects onmyocardium• Transient increase in BP : attributable toperipheral vasoconstriction due tostimulation of α2B adrenoreceptors inperipheral vascular smooth muscles.• Significant bradycardia & Hypotensionsecondary to central inhibitory α2A agonisteffect• All these effects can be offset or overcomewith use of atropine, ephedrine or volumeloading
    • Clinical Uses of Dexmedetomidine• Craniotomy:aneurysm, AVM• Cervical spinesurgery• Conventional CABG• Off-pump CABG• Vascular surgery• Thoracic surgery• Bariatric surgery• Back surgery, evokedpotentials• Head injury• Burn• Trauma• Awake intubation
    • Clinical Uses of DexmedetomidineSedation in CT and MRI imaging studiesMason K, Ped Anesth 2008Koroglu A, Anesth Analg 2006Outpatient third molar surgeryUstin Y, J Oral Maxilfac Surg 2006Cheung C, Anaesthesia 2007Cataract surgeryAlhashemi J, Br J Anaest 2006Cardiac catheterizationTosun Z, J Card Vasc Anesth 2006Mester R, Am J Therap 2008GI ProceduresDemiraran Y, Can J Gastroenter 2007Dex may be a good alternative to midazolam for upperendoscopy
    • Dex: Use in Coronary Artery SurgeryCoronary Artery Surgery PatientsDexmedetomidine : Herr study, n=300: Dex vs. controls [propofol]• Faster time to extub in dex gp - by 1 hr• 70% did not require morphine vs. 34% controls• Dex pts had less Afib (7 vs 12 pts)Herr DL: Crit Care Med 2000;28:M248. Washington HospitalCABG and Lung Disease• RCT, n= 20. Dex started at end of surgery, 0.2 to 0.7 ug/kg/hr, + continued 6hr after extubation vs. controls (propofol)Dexmedetomidine• Faster time to extub: 7.8 + 4.6 h v. 16.5 + 11.8 h• No difference in PaCO2 between gps 30 min after extub: 37.9 v. 34.9 mmHgSumping ST: CCM 2000;28:M249. Duke
    • Dex: Use in Thoracotomy + ThoracoscopyThoracotomy + thoracoscopy patients• COPD, pleural effusion, marginal pulmonary function, pCO2 + pO2 with opioids• Thoracic epidural: mainly for thoracotomy, Dex: mainly for thoracoscopyDexmedetomidine• Patients are arousable, but sedated• Does not ventilatory drive• Greatly need for opioids• Alternative to thoracic epidural• Continue after extubationVascular surgery• Usually at risk for CAD, ischemia, HTN, tachycardia• Dex attenuates periop stress response• Dex attenuates BP w AXC, especially thoracic aortaDexmedetomidine: RCT, n=41. Dex continued 48 hr postop• HR in dex gp at emergence- 73 + 11 v. 83 + 20 bpm• Better control of HR, Plasma NE levels in dex groupTalke et al: Anesth Analg 2000;90:834. Multicenter
    • Dex: Use in Other Surgical ProceduresAbdominal surgery• Dexmedetomidine provides analgesia without respiratory depression• Especially useful in elderly undergoing colon resections, TAH, + other stressfulproceduresBariatric surgery• Dexmedetomidine Improves Postop Pain Mgt after Bariatric Surgery• Morphine use in dex gp• Pain score better in dex gp: 1.8 vs 3.4 , % time pain free in PACU in dex gp: 44% vs 0• Better control of HR in dex gpNeck + back surgery• Dex causes minimal effect on SSEP monitoring• Smooth emergence, especially cervical spine• Easy to evaluate neuro function prior to + after extubationRamsay MA, et al: Anesthesiology, 2002: A-910 and A-165. Baylor
    • Dex: Use in Other Surgical ProceduresBurns patients• 2 agonist effect assists in the management of burn patients; bluntscatecholamine surge•Use in intubated and non-intubated burn patients•Outpatient dressing changes instead of ketamineTrauma and Alcohol withdrawal patients•Benzodiazepines typically used- Intubation and ventilation oftenrequired if extreme agitation•Dexmedetomidine is an alternative to BZD- Spontaneous breathing,Hemodynamic stability, Adequate sedation, Prevention of autonomiceffects of withdrawal, Pain control
    • Dex: Use in Neuro anesthesiaEffect of Dexmedetomidine on Cerebral Blood Flow• Animal models– Dex causes a reduction in CBF up to 45%– Dex has no effect on the CMRO2– Dex produces the concentration-dependent constriction of pial arteries and veins– Dex limits hypercapnea- and hypoxia-induced cerebral vasodilationZornow MH et al, Anesth Analg; 1990Fale A et al, Anesth Analg; 1994Karlsson et al, Anesth Analg; 1991• Human study (TCD)– Mean CBF velocity decreased with an increase in plasma concentration of Dex– Pulsatility index increased at higher level of Dex (indicates an increase in CVR)Zornow MH et al, J Cereb Blood Flow Metab; 1993Cognitive Function• There is strong evidence that a2 – agonists improve prefrontal cortical function (PFC)Arnstein et el. Arch Gen Psychiatry 1996
    • Dex: Use in Neuro anesthesiaEffect on ICP• Animal model– ICP was unchanged despite an increase in systemic blood pressurein rabbits– ICP was decreased in the presence of intracranial hypertensionZornow MH et al, Anesth Analg 1992• Human study– Dex has no effect on lumbar CSF pressure in patients undergoingtransphenoidal pituitary tumor resectionTalke P et al. Anesth Analg 1997Effect on SSEPs and AEP• There is a lack of effect on cortical AEP• Dex does not affect cortical (P25-N35) response• Dex depresses median nerve P15-N20 amplitudesThornton C et al. Br J Anaesth 1999
    • Dex: Use in Neuro anesthesiaAntinociception· a2 – Agonists attenuate hemodynamic responses to laryngoscopy and intubationLawrence CJ et al Anaesthesia 1997· a2 – Agonists decrease peri operative oxygen consumption Taittonen MT Br J Anaesth1997• Dex reduces NE level during emergence from anesthesia (2 to 3 times lower than placebo)Talke P et al. Anesth Analg 2000Effect on BIS• BIS values after Dex infusion for 1 hour were: 65 at 0.2 mg/kg/hr, 60 at 0.6 mg/kg/hr• Volunteers readily awakened from hypnosis by talking ; BIS returned to awake levelBIS before and after subjects were asked to perform various tasksHall JE et al. Anesth Analg 2000
    • Dex: Use in Neuro anesthesia- Neuro protective effects• Inhibition of ischemia induced NE release may be associated withneuroprotection• Dex prevents delayed neuronal death after focal ischemia• Dex decreased total ischemic volume by 40% compared to placeboJolkkonen J et al. Euro J Pharm 1999Hoffman WE et al Anesthesiology 1991• Dex enhances glutamine disposal by oxidative metabolism inastrocytesHuang R et al. J Cereb Blood Metab 2000
    • Dexmedetomidine: Use in CraniotomyCraniotomy for Aneurysm / AVMAnesthesia considerations• Smooth induction + emergence, Prevent rupture• Avoid cerebral ischemia, Hypothermia (33 oC) CMRO2, CBF, CBV, CSF, ICPDexmedetomodine• sympathetic stimulation• or no change in ICP• shivering w/o respiratory depression• Preserved cognitive function- reliable serial neuro examsDoufas AG et al: Stroke 2003;34. Louisville, KYCraniotomy• Postoperative infusion of Dex in patients recovering from transphenoidalhypophysectomy reduced plasma catecholamines by 70%Talke P et al Anesth Analg 1997
    • Dex Use in Neuro: Clinical ExperienceSpinal Fusion• Intraoperative switching from a propofol infusion to Dex in patients undergoingcervical fusion resulted in:– A neurological examination that was successfully performed in the OR on anintubated patient– Clinically insignificant hemodynamic changes during and after the switchoverBloom M et al J Neurosurg Anesth 2001
    • Dex Use in Neuro: Clinical ExperienceCarotid Endartrectomy• A combination of superficial and deep cervical plexus blocks is the mostcommon regional anesthetic technique in the NYU medical center• Sedation with dexmedetomidine (0.2-0.4 mcg/kg/hr) offers a comfortableand cooperative patient during the operation• Less agitation and respiratory depression than with a continuous infusionof propofol or repeated doses of fentanyl and/or midazolamFunctional Neurosurgery• Dex infusion at 0.1 – 0.2 mcg/kg/hr allowed us to achieve a tranquil statesufficient to complete neuropsychiatric testing required for mapping of thecortical speech area, as well as to perform an awake tumor resection• A lack of respiratory depression offers an advantage over other techniqueBekker A et al. Anesth Analg 2001
    • Dex Use in Ophthalmology:Effect of dexmedetomidine premedication on the intraocular pressurechanges after succinylcholine and intubation: BJABritish Journal of Anaesthesia 100 (4): 485–9 (2008) February 19, 2008Details - 40 patients with no pre-existing eye disease undergoing GA, Randompremedication with Dex 0.6 mcg/kg or saline, HR, MAP, and IOP measured• IOP- Succinylcholine and intubation increased IOP in both groups.However, in the Dex group, the IOP rise was not different from the baselinevalue and was significantly lower than in the saline group .• MAP- After intubation, the MAP in the control group was higher than thatin the dex group and exceeded the baseline value• HR- HR also showed less fluctuation in the dex group than in the salinegroupResult:• Premedication with a dose dex 0.6 mg/kg over 10 min blunted the ↑IOPcaused by succinylcholine & intubation• Attenuated the hemodynamic response to laryngoscopy & intubation.
    • Dex Use in Ophthalmology: Conclusion  of IOP with succinylcholine & endotracheal intubation can beblunted with i.v. dexmedetomidine premedication. Hemodynamic stability is an additional advantage Dex could be a beneficial premedication in open globe injuries Single i.v. dose of dexmedetomidine 0.6 mcg/kg  IOP by 34% The present study (0.6 mcg/kg) was based on a previous clinical study,where the selected dose resulted in a significant  IOP and preventedIOP response to intubationDexmedetomidine attenuates sympathoadrenal responses to tracheal intubation. Br J Anaesth 1992; 68: 126–31
    • PROCEDURAL SEDATION• Koroglu A, Br J Anaesth 2005;94:821– Dex vs midazolam for MRI sedation– 80 patients, 1-7 yrs– Dex: 1ug/kg bolus, then 0.5 ug/kg/hr– Midazolam: 0.2 mg/kg, then 0.36 mg/kg/hr– Efficacy: 32/40 (dex) vs 8/40 (midazolam)– Onset: 19 min (dex) vs 35 min (midazolam)– Similar CV effects - nothing significant• Concl: dex > efficacy vs midazolam• Problem – midaz rarely sole agent for MRI
    • PROCEDURAL SEDATION• Koroglu A, Anesth Analg 2006;103:63– Dex vs propofol for MRI sedation– 60 patients aged 1-7 yrs– Dex: 1ug/kg bolus, then 0.5 ug/kg/hr– Propofol: 3 mg/kg bolus, then 6 mg/kg/min– Efficacy similar: 83% (dex) vs 90% (propofol)– Onset – 11 min (dex) vs 4 min (propofol)– rec time with dex (27 vs 18 min)– hypoxia with dex (0% vs 13%)• Concl: Consider as alternative to propofol
    • Dex Use in MRI• 80 children aged 1-7 years• Randomly assigned to eitherdexmedetomidine or midazolam– 10-minute loading doses:1 mcg/kg dexmedetomidine,0.2 mg/kg midazolam– Infusions: 0.5 mcg/kg/hdexmedetomidine,6 mcg/kg/h midazolam1• The quality of MRI wassignificantly better (P<.001) andthe rate of adequate sedation wassignificantly higher (P<.001) withdexmedetomidineQuality of MRI0102030401 2 3NumberofPatientsMidazolamDexmedetomidine
    • Clinical Administration• Onset of 30 minutes as compared to that ofmidazolam 3-5 minutes and that of propofol30-50 secondscan be decreased by infusion of standardloading dose of 1µg/kg, over 10 minutes• Offset of sedative action in 5 minutes, whilemidazolam has about 2 to 6 hours andpropofol has 3-8 minutes.• Duration of analgesic action of about 4 hoursas compared to that of Fentanyl up to 60-80minutes
    • Indications & Dosage• A pre-anaesthetic medication and as apsychosedation in short outpatient surgicalprocedures• initial loading dose of intra venous infusionof dexmedetomidine 1- 6 µg / kg for 10minutes till 3 on Mackenzie’s Sedationassessment score (till the patient showedawakening responses to calling in spite ofclosed eyes) and maintained on0.4 µg/kg/hr•Taniyama K, Oda H, Okawa K et al. Psychosedation with dexmedetomidine hydrochloride duringminor oral surgery. Anesth Prog 2009; 56:n75-80
    • Indications & Dosage• In the dose of 0.2 to 0.7 µg/kg/hr, found toattenuate the stress induced sympathoadrenal responses to laryngoscopy,endotracheal intubation, surgical stimulationand provide overall increased hemodynamicstability & as an adjuvant to otheranaesthetic agents, including inhalationalagents like isofluraneBhatia P. Dexmedetomidine: a New agent in Anaesthesia & Critical care Practice. http://dexmedtomidine.comAanta R, Jaakola ML, Kallio A, Kanto J. Reduction of minimum alveolar concentration of isoflurane by dexmedetomidine.Anesthesiology 1997;80 : 1055-1060
    • Indications & Dosage• Can be used to obtund the autonomicpressor response due to laryngoscopy andendotracheal intubation• In the dose of 1 µg / kg diluted in 100ml ofsaline solution, infused over 15 minutes• After a stabilization period of 5 minutes• Suitably induced, relaxed & tracheaintubated
    • Indications & Dosage• an intra-operative analgesic in GA as analternative to opioids• Infusion of standard loading dose of 1µg/kg,over 10 minutes followed by maintenance of 0.2-0.7 µg/kg/hr. diluted in 0.9 % normal salineScheinin B, Lindgren L, Bandel T, Scheinin H, Scheinin M. Dexmedomidine attenuates sympatho adrenal responses totracheal intubation and reduces need for thiopentone and peri-operative fentanyl Br J Anaesth 1992; 68: 126-131Menda F, Koner O, Sayin M, Ture H et al. Dexmedetomidine as an adjunct to anaesthetic induction to attenuatehemodynamic response to endotracheal intubation in patients undergoing fast track CABG. Ann Can J Anaesth 2010’13: 16-21
    • Indications & Dosage• It has been found to provide neuro-protective effect by decreasing cerebralblood flow without increasing either withcerebral metabolic rate (CMRO2) or intracranial pressure (ICP)• sole sedating agent with local anestheticagents in a high risk patient• used as anti-shivering and forthermoregulation•Zornov MH, Maze M, Dyek JB. Shafer SL. Dexmedetomidine decreases cerebral blood flow velocity in humans JCereb Blood Flow Metab 1993; 13: 350-352•Rich JM. Dexmedetomidine as a sole sedating agent with local anesthesia in a high risk patient for axillo-femoralbypass graft: a case report. AANA Journal2005; 73:357-360
    • alpha 2 Adrenergic ReceptorAntagonistAtipamezole• Effectively reverses Psychomotor side-effects• Reverses Sedation & Sympatholysis• Reverses Analgesia• t ½ is 1 ½ - 2 hours.
    • To compare the efficacy ofDexmedetomidine vs Fentanylas sedative & analgesic in short generalanaesthesia in day care obstetric &gynaecological surgeries
    • AIMS AND OBJECTIVES• To compare the time required for onset and offsetof sedation, quality of intra-operative & post-operative analgesia and the time required for post-operative recovery using Inj. Dexmedetomidineand Inj. Fentanyl• To evaluate cardio-respiratory and any othersystemic side effects at equal doses
    • METHODOLOGY• Age group 18 - 65 years of ASA-I & II•Randomized into two equal groups of 20 each by computergenerated model•Pre-medicated with Inj. Glycopyrrolate 0.2mg i.v.• Group A: patients received Inj. Dexmedetomidine1μg/kg i.v. 10 min. prior to induction by infusion• Group B: patients received Inj. Fentanyl 1μg/kg i.v.10 min. prior to induction by infusion
    • • Induction done with Inj. Propofol i.v in titrated doses• Maintained with 66% N2O, 33% Oxygen & Isoflurane ( titratedconcentration) with the patient breathing spontaneously onMagill circuit• Time to eye opening at the conclusion of surgery was recorded• In post anaesthesia care unit patients were evaluatedperiodically for- vitals- sedation using Ramsay sedation scale- visual analog scale- time of rescue analgesia (when VAS >5)- Standard Aldrete score for post anaesthesia recoveryMETHODOLOGY
    • RESULTS• Demographic profile for Age, Sex and ASA grade had nostatistical significance & hence were comparable• The requirement of Propofol was significantly reduced in DexGroup• Comparison of pulse rate in Dexmedetomidine Groupshowed significant fall immediately after pre medication ,without any intervention it returned to baseline, & remainedequivalent to that in Fentanyl Group throughout surgery•Line diagram showing comparision of pulse rate in study groups0102030405060708090On table AFT PMD AFT IND At 5 min At 10 min At 15 min At end Post - opPRAverageGroup AGroup BP < 0.05 after premedication.
    • RESULTS• No significant change in blood pressureseen in Dex. group whereas continuousfluctuation of systolic BP seen infent.group• No significant change in diastolic BP &Respiratory rate seen in any of the groups• significant fall in saturation was observedwith Fentanyl group• The time of eye opening is highlysignificantly early in Dex. group (p<0.001)and delayed eye opening seen withfentanyl groupLine diagram showing comparision of systolic blood pressure in studygroups9095100105110115120125On table AFT PMD AFT IND At 5 min At 10 min At 15 min At end Post - opSBP (mm Hg)AverageGroup AGroup BLine diagram showing comparision of SPO2 in study groups0102030405060708090100110On table AFT PMD AFT IND At 5 min At 10 min At 15 min At end Post - opSPO2AverageGroup AGroup B01234567AverageEye opening after surgery (min)Bar chart showing comparison of eye opening after surgery in studygroupGroup AGroup B
    • RESULTS• The post operative analgesia duration wasmore in Dex. group (approx. 4-6 hrs.),whereas in Fentanyl group patients requiredrescue analgesia within 1 – 1.5 hrs of surgery• The sedation was highly significantlyprofound in fentanyl group according toRamsay sedation score (p < 0.001) after 15min of surgery• The quality of recovery was highlysignificantly better (Aldrete score = 9+)wasobserved in most of the patients after 30 minin Dex.group & Similar results were seenonly after 1.5 – 2 hrs. in Fentanyl GroupLine diagram showing comparision of VAS score in study groups02468At End of surgery At 30 min At 1 hr At 1.5 hr At 2 hrVAS ScoreAverageGroup AGroup BLine diagram showing comparision of Ramsay sedation in post operative in studygroups01234End of surgery At 15 min At 30 min At 1 hr At 2 hrRamsay sedationAverageGroup AGroup BP < 0.001 at 1.5 hrs.P < 0.001 at 15 min.Line diagram showing comparision of standard aldrete score in post operative in studygroups024681012End of surgery At 15 min At 30 min At 1 hr At 1.5 hr At 2 hrStandard aldrete scoreAverageGroup AGroup BP < 0.001 at 15,30, 60 min.
    • TO EVALUATE THE EFFECTOF ADDITION OFDEXMEDETOMIDINE TO 0.5%HYPERBARIC BUPIVACAINEINTRATHECALLY
    • AIMS & OBJECTIVES• To study the onset and duration of analgesia with theaddition of 10 µg Dexmedetomidine to 0.5% heavyBupivacaine in sub-arachnoid block• To evaluate the quality of block and post operativeanalgesia as compared to control i.e. 0.5% heavyBupivacaine• To observe any side effects of intrathecal administrationof Dexmedetomidine with 0.5% Bupivacaine intraoperatively and post operatively
    • METHODOLOGY• Patients of ASA I,II and age group 18-65 years wererandomized into two equal groups of 20 each by acomputer generated model• Group A (Dexmedetomidine Group) were given 3ml of0.5% heavy Bupivacaine + 0.5ml (10 µg) ofDexmedetomidine• Group B (Control Group) were given 3ml of 0.5% heavyBupivacaine + 0.5ml of Water for injection• Patients will be preloaded with Ringer Lactate solution10 ml/kg body• Spinal anaesthesia was given using a 26G Quincke’sneedle in sitting position through a midline approach
    • METHODOLOGY• Sensory block was tested by pinprick method till T6sensory level• Degree of motor blockade was assessed by modifiedBromage scale• Intraoperative vitals were monitored• Hypotension: SBP < 90 mm Hg or a decrease of >20%from baseline. Hypotension was treated with a bolusadministration of 250 ml Ringer lactate and 6 mg of i.v.Mephentermine if required• Bradycardia was defined as HR < 50 bpm and wastreated with 0.6 mg of i.v. Atropine• Postoperatively, 2 segment sensory regression, motorregression and time to rescue analgesia were monitored
    • • No statisticallysignificant differencefor age, height ,weight, Sex wise andASA distribution inboth groupsRESULTS
    • • Difference in sensory onsetnot statistically significant• Motor onset significantlyshorter in DexmedetomidineGroup (t value-2.54,p value < 0.05)• Difference in peak sensoryinsignificant• Peak motor significantlylonger in Dex Group(t value-4.59, p value<0.0001)RESULTS012345678AverageTime of Peak sensory (T3) Time of Peak motor(T4)After spinal anesthesiaMultiple bar diagram showing comparison of time of sensory and motorPeak after spinal anesthesia in study groupsGroup AGroup B
    • • 2 segment sensoryregression• motor regressionand• time of rescueanalgesiasignificantly longerin Dex. GroupRESULTSParameters Group A Group B tValueP ValueMean SD(n=20)Mean SD(n=20)2 segment sensoryregression (T5)190.3 34.80 98.65 14.95 10.81 <0.0001Motor regression(T6)265.05 57.50 138.7 14.76 9.51 <0.0001Time of rescueanalgesia (T7)342.75 76.94 189 20.71 8.62 <0.0001050100150200250300350Average2 segment sensoryregression (T5)Motor regression(T6)Time of rescueanalgesia (vas > 7)(T7)Level of sensory blockadeMultiple bar diagram showing comparison of level of sensory blockadein study groupsGroup AGroup B
    • • Both groups withmanageableBradycardia &Hypotension01234No.ofcasesBradycardia HypotensionSide effectMultiple bar diagram showing side effect wise distribution of cases instudy groupsGroup AGroup BLine diagram showing comparision of heart rate in study groups0102030405060708090100Pre–opAt3minAt10minAt15minAt30minAt45minAt60minEndofSurgeryPost-opHR (min)AverageGroup AGroup BLine diagram showing comparision of systolic blood pressure in studygroups020406080100120140Pre–opAt3minAt10minAt15minAt30minAt45minAt60minEndofSurgeryPost-opSBP (mm Hg)AverageGroup AGroup BLine diagram showing comparision of diastolic blood pressure in studygroups0102030405060708090Pre – op At 3 min At 10minAt 15minAt 30minAt 45minAt 60minEnd ofSurgeryPost -opDBP (mm Hg)AverageGroup AGroup B
    • Indications: Future plans• Use of dexmedetomidine as anadjuvant to Local Anaesthetic Mixture,in peri- bulbar block
    • Summarizing• Quest for an ‘Ideal’ peri-operative sedative-analgesic goes on… &… on…&….on!!• α2 agonists are unique class of drugs, withmany desirable properties!!• Clonidine and now dexmedetomidine, areversatile, multi-faceted and potent drugs!!!• It has been successfully employed in Cardiac,Neuro-surgical, abdominal, Head & NeckSurgeries and Procedural sedation !!!!
    • Conclusion!• Dexmedetomidine can be considered a suitableagent for providing pre-operative sedation &pre-anaesthetic anxiolysis• Useful in the day care procedures likeconscious sedation and procedural sedation• changing our viewpoint of providing intra &post operative analgesia, without any potentialand significant side-effects of existing agentsemployed for this purpose.