Pathophysiology of Postoperative Pain• 6 problems: 1. Peripheral sensitization 2. Constant bombardment of the CNS with noxious input 3. Noxious input processed by the CNS 4. Pathophysiological consequences of acute pain 5. Sensitization of the CNS response, called wind- up 6. Induced sensitivity in the nervous system outlasts the stimulus
2. Constant bombardment of the CNS with noxious input
3. Noxious input processed by the CNS• Adverse spinal reflexes, such as muscle spasm and sympathetic stimulation, are provoked.• Supraspinal reflexes incite the mediators of the stress response.
A M u lt im o d a l A p p r o a c h t o C o n t r o l P o s t o p e r a t iv e P a t h o p h y s io lo g y a n d R e h a b ilit a t io n in P a t ie n t sU n d e r g o in g A b d o m in o t h o r a c ic E s o p ha g e c to myB r o d n e r G, P o g a t z k i E , V a n A k e n H, e t a l . A n e s t hMultimodal regimen:g 1 9 9 8 ;8 6 :2 2 8 – 3 4 An a l2. Effective thoracic epidural analgesia • Establishing epidural blockade intraoperatively • Patient-controlled postoperative epidural analgesia (PCEA) • Continuous evaluation and treatment of postoperative pain by an acute pain service3. Early tracheal extubation4. Forced mobilization
Physiologic Impact of Epidural Analgesia• Lower rates of deep venous thromboses• Lessening myocardial ischemia• Decreasing pulmonary morbidity• Positive consequences on recovery of gastrointestinal function
5. Sensitization of the CNS response• Central sensitization refers to enhanced excitability of dorsal horn neurons and is characterized by: 1. increased spontaneous activity 2. Enlarged receptive field area 3. An increase in responses evoked by large and small caliber primary afferent fibers• Windup refers to the progressive increase in the magnitude of C-fiber evoked responses of dorsal horn neurons produced by repetitive activation of C-fibers.• Triggered by neurotransmitter glutamate and neurokinin peptides (substance P)
R e v e r s in g T is s u e In ju r y - In d u c e d P la s t icChanges i n t h e S p i n a l C o r d :T h e S e a r c h f o r t h e M a g ic B u lle t R a j a S N, Do u g h e r ty P M. R e g An e s th Pa i n Me d 2 0 0 0 ;2 5 :4 4 1 – 41. 4 glutamate & 3 substance P receptor subtypes2. Different neurochemical mechanism mediated by differing pain states3. There may be no single “magic bullet” that blocks central sensitization and the result secondary hyperalgesia.
6. Induced sensitivity in the nervous system outlasts the stimulus sClinical pain hPhysiologic pain – Low-threshold – High-threshold – Sensitization – Serve to warm the following injury organism of harm • Allodynia • Hyperethesia • hyperpathia? Ca n we a v o i d to ta l a n a l g e s i a a n d b l o c k o n l y th ec l i n i c a l pa i n? Th e s o ph i s ti c a te d g o a l o f pr e e m pti v e a n a l g e s i a toa c h i e v e a d i f f e r e n ti a l e f f e c t o n ph ys i o l o g i c a n dc l i n i c a l pa i n
P r e e m p t iv e E p id u r a l A n a lg e s ia a n d R e c o v e r y F r o m R a d ic a l P ro s ta te c to myGo t t s c h a l k A , S mit h DS , J o b e s DR , e t a l . J AMA 1 9 9 8 ; 2 7 9 :1 0 7 6 – 8 2 .
Applying What We Know toPostoperative Pain Management1. Prevent sensitization or stimulation of peripheral receptors – Antihistamines – NSAIDs – Local anesthetics
Applying What We Know toPostoperative Pain Management2. Diminish or eliminate the bombardment of the CNS with nociceptive input – Peripheral nerve blocks – Intrathecal or epidural analgesia – Systemic opioids – Small-dose IV ketamine
S m a ll-D o s e K e t a m in e E n h a n c e s M o r p h in e -In d u c e d A n a lg e s ia A f t e r O u t p a t ie n t S urg e ryM a n z o S u z u k i, K e n t a r o T s u e d a , e t a l . A n e s t h A n a l g 1 9 9 9 ;8 9 :9 8 - 1 0 3 IV coadministration of ketamine 50-100 μg/kg with morphine 50 μg/kg 15 min before the end of the operation 1. Although opiates produce antinociception through μ receptor agonist activity, they activate NMDA receptors, resulting in hyperalgesia and the development of tolerance to opiates. • The marked reduction in both pain score and morphine requirement may be explained by the interaction of ketamine with NMDA receptors that had been activated by perioperative nociceptive inputs, as well as by the administration of morphine.
Applying What We Know toPostoperative Pain Management3. Continue treatment until the inflammatory reaction that fuels the nociceptive input is minimized – Sustained release opioids – Consultation with a pain psychologist
• For humanitarian reasons…• Why postoperative pain must be treated effectively…• The value of “multimodal” or “balanced analgesia” in postoperative pain management…
(A) LOC AL A N E S T H E S IA :• Injection site: Pain, haematoma, Nerve trauma, infection• Vasoconstrictors: Ischemic necrosis• Systemic effects of LA agent: Allergic reactions, toxicity
( B ) S P IN A L , E P ID U R A L & C AUDAL A N E S T E S IA :• Technical failure• Headache due to loss of CSF• Intrathecal bleeding• Permanent N. or spinal cord damage• Paraspinal infection• Systemic complications (Severe hypotension)
(C ) G ENERAL A N E S T E S IA :• Direct trauma to mouth or pharynx.• Slow recovery from anesthesia due to drug interactions OR in- appropriate choice of drugs or dosage.• Hypothermia due to long operations with extensive fluid replacement OR cold blood transfusion.
• Allergic reactions to the anesthetic agent: Minor effects eg: Postoperative nausea & vomiting Major effects eg: Cardiovascular collapse, respiratory depression)• Haemodynamic Problems: Vasodilation & shock