3. 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
6. 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.
7. 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 s
U 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 my
B 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 h
Multimodal regimen:g 1 9 9 8 ;8 6 :2 2 8 – 3 4
An a l
2. 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 service
3. Early tracheal extubation
4. Forced mobilization
10. Physiologic Impact of Epidural
Analgesia
• Lower rates of deep venous
thromboses
• Lessening myocardial ischemia
• Decreasing pulmonary morbidity
• Positive consequences on recovery
of gastrointestinal function
11. 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)
12. 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 ic
Changes 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 – 4
1. 4 glutamate & 3 substance P receptor subtypes
2. Different neurochemical mechanism mediated
by differing pain states
3. There may be no single “magic bullet” that
blocks central sensitization and the result
secondary hyperalgesia.
13. 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 e
c 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 to
a 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 d
c l i n i c a l pa i n
14. 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 my
Go 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 .
15. Applying What We Know to
Postoperative Pain Management
1. Prevent sensitization or
stimulation of peripheral
receptors
– Antihistamines
– NSAIDs
– Local anesthetics
16. Applying What We Know to
Postoperative Pain Management
2. Diminish or eliminate the
bombardment of the CNS with
nociceptive input
– Peripheral nerve blocks
– Intrathecal or epidural analgesia
– Systemic opioids
– Small-dose IV ketamine
17. 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 ry
M 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.
18. Applying What We Know to
Postoperative Pain Management
3. Continue treatment until the
inflammatory reaction that fuels
the nociceptive input is
minimized
– Sustained release opioids
– Consultation with a pain psychologist
19. • For humanitarian reasons…
• Why postoperative pain must be
treated effectively…
• The value of “multimodal” or
“balanced analgesia” in
postoperative pain
management…
20. (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
21. ( 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)
22. (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.
23. • Allergic reactions to the anesthetic
agent:
Minor effects
eg: Postoperative nausea & vomiting
Major effects
eg: Cardiovascular collapse,
respiratory depression)
• Haemodynamic Problems:
Vasodilation & shock
