Spinal  anaesthesia  is  the  most  commonly  used  technique  for lower abdominal surgeries as it is  very economical and easy to  administer.    However,  postoperative  pain  control  is  a major  problem  because  spinal  anaesthesia  using  only local anaesthetics  is  associated  with  relatively  short  duration  of action, and thus early analgesic intervention is needed in the postoperative   period.   A   common   problem   during   lower abdominal  surgeries under spinal anaesthesia is visceral pain, nausea, and vomiting.[1]

Local  anaesthetic  lignocaine  was  used  for  shorter  procedures that  can  be  lasted  for  1.5  hours  or  less.  It is  associated  with shorter  duration  of  action  and  it  was  later  replaced  by Bupivacaine.  Bupivacaine  is  the  most  commonly  employed local    anaesthetic    for    sub    arachnoid    block.    Though bupivacaine  is  longer  acting  than  lignocaine  it  has  its  own demerits  like  cardio  toxicity  and  its  duration  of  action  lasts only  for  3  hours,  so  early  need  for  rescue  analgesic  in  post operative period.[2]

Many  adjuvants  are  commonly  used  to  prolong  the  duration of  analgesia.  The addition of  opioids  to  local  anaesthetic solution have disadvantages, such as pruritus and respiratory depression.  So  our  concern  is  to  choose  an  adjuvant  with bupivacaine which provides early onset of sensory and motor blockade, stable intra operative condition and prolonging the post operative analgesia with minimal side effects.[3,4]

Neostigmine  is  an  anticholinesterase  agent,  which  inhibits the    hydrolysis    of    acetyl    choline.    Spinal    neostigmine apparently  activates  descending  pain  inhibitory  systems  that rely    on    a    spinal    cholinergic    interneuron,    probably exacerbating  a  cholinergic  tonus  that  is  already  activated during  the  post  operative  period  and  seems  to  be  extremely efficient for alleviating somatic pain.[5]

Dexmedetomidine, a new highly selective α2-agonist, acts by binding to presynaptic C fibers and postsynaptic dorsal horn neurons.  Their  analgesic  action  is  a  result  of  depression  of the  release  of  C-fiber  transmitters  and  hyper  polarisation  of postsynaptic dorsal horn neurons. The prolongation of effect may result from synergism between local anaesthetic and α2 -adrenoceptor  agonist,  while  the  prolongation  of  the  motor block of spinal anaesthetics may result from the binding of α2 -adrenoceptor agonists to motor neurons in the dorsal horn.[6]

This prospective, randomized, double-blinded, clinical study   aims   to   determine   the   effect   of   intrathecal administration   of   Neostigmine   and   Dexmedetomidine   as adjuvants  on  the  onset  and  duration  of  sensory  and motor block   and   postoperative   analgesia   produced   by spinal Bupivacaine.

This study will be carried out under the Department of Anaesthesiology and Critical Care Medicine, Gauhati Medical College.

REFERENCES:

1.Rajni     Gupta     et     al:     A     Comparative     study     of     intrathecal dexmedetomidine and fentanyl as adjuvants to Bupivacaine: Journal of Anaesthesiology  Clinical  Pharmacology.2011;  Volume:  27,  Issue:  3, Page: 339-343

 2.David  L.  Brown:  spinal,Epidural,  and  Caudal  Anesthesia:  Miller’s anesthesia: 7thedition: chapter 51: 1611 -1638

 3.Dr.Yoga   Narasimha   N   et   al:   A   clinical   study   of   perioperative effectiveness of adjuvant Neostigmine with intrathecal Bupivacaine for lower  abdominal  surgeries:  IOSR  Journal  of  Dental  and  Medical Sciences: Volume 2, Issue 3 (Nov- Dec2012), PP 35-39

 4.Robert W. Hurley : Acute Postoperative Pain: Miller’s anesthesia : 7th edition : chapter 87 : page : 2757-2780

 5.Calvey  TN  et  al  :  Pharmacokinetics  and  pharmacological  effects  of neostigmine in man : Br J Clin Pharmacology : 1979 Feb;7(2):149-55

6.Panzer   O   et   al   :   Pharmacology   of   sedative-analgesic   agents   – Dexmedetomidine,  remifentanil,  ketamine,  volatile  anaesthetics  and The role of Mu antagonists: Critical Clin : 2009;25:451-69