Ige O.A.

Consultant Anaesthetist
 The IASP defines pain as “an unpleasant
sensory and emotional experience
associated with actual or potential tissue
damage, or described in terms of such
damage”.
 Acute pain – Is that which is caused by noxious
stimulation due to injury, a disease process, or
abnormal function of muscle or viscera.
 It is pain of recent onset and of short duration,
lasting no more than days or weeks.
 Examples are post traumatic, post operative,
obstetric pain and acute illnesses –MI,
pancreatitis, renal calculi.
 It can be somatic or visceral.
 Somatic pain is divided into superficial
(skin, mucous memb, subcut tissues) and
deep (muscles, tendons, joints and bones).
 Superficial pain is well localized, sharp pain
while deep somatic pain is dull, aching, not
well localized.
 Visceral pain may be due to a disease
process or abnormal function of internal
organ or its covering.
 Chronic pain is defined as that which persists
beyond the usual course of an acute disease or
after a reasonable time for healing to occur.
This time varies from 3-6 months.
 It is not just a physical sensation. It usually has
underlying cultural and psychological
background on which the painful condition is
superimposed. It has emotional and financial
consequence that the painful condition has
caused.
 It can occur in spite of negative physical
findings and investigations.
 Pain is conducted along three neural pathways:
 First order neurons. Neural body located in the dorsal root ganglia
at the vertebral foramina. Single axon that bifurcates sending one
end to the peripheral tissues it innervates and the other to the
dorsal horn of the spinal cord.
 Second order neurons. After synapsing with the first order neuron
in the dorsal horn, they cross the mid-line and ascend in the
spinothalamic tract to the thalamus, the reticular formation, the
nucleus raphe magnus and the periaqueductal gray area. Second
order neurons are either nociceptive specific or wide dynamic
range neurons which also receive other stimuli apart from pain.
 Third order neurons. Synapse with second order neurons in the
thalamus then send projections to the post-central gyrus of the
cerebral cortex through the internal capsule and corona radiata.
 Most nociceptors are free nerve endings that sense
tissue damage. They sense alogens like bradykinin,
histamine, serotonin (5HT), H+, K+ and some
prostaglandins.
 Noxious sensation is divided into a fast, sharp and well
localized pain conducted by Aδ fibers and a dull, slow
onset, poorly localized pain conducted by C fibers.
 The neurotransmitters are excitatory (substance P,
calcitonin gene-related peptide, glutamate, aspartate,
ATP) or inhibitory (somatostatin, acetylcholine,
encephalins, adenosine, GABA and glycine).
 Transduction: The process by which a noxious stimulus is
converted to an electrical stimulus in appropriate sensory nerve
endings. Noxious stimulus can be from direct nerve injury or
from factors released from damaged cells – Potassium ion,
Hydrogen ion, Histamine, Serotonin, ATP, Bradykinin,
Arachidonic acid and prostaglandins.
 Transmission: Transmission occurs along myelinated A-delta
and unmyelinated C fibers to the dorsal horn of the spinal cord.
 Modulation: It alters pain transmission. There are both
inhibitory and excitatory mechanisms modulating impulse
transmission both in the central and peripheral nervous
systems.
 Perception: Pain perception lies at the level of the thalamus.
The cortex is responsible for discrimination of specific sensory
experiences.
 Successful management of patients begins with a
thorough and accurate assessment of their complaints
 Self report: trust the patients self report
 Evaluate psychological and functional impact of pain on
patient and family: depression, anxiety, coping style of
patient and family and substance abuse
 Determine the cause of pain
 Careful physical and neurological examination
 Relevant laboratory and radiological evaluation e.g. x-
ray, CT scan, NMRI
 Evaluate disease activity that might be associated with
progressive tissue damage and increasing pain e.g.
tumour markers or CD4 counts
 Rule out other causes of pain
 Visual analog scale
 Verbal rating scale
 Numerical pain rating scale.
 Pharmacological and non-pharmacological
 Pharmacological method constitutes the
mainstay of treatment of most pain.
 The Gold standard for pharmacologic
treatment is
 By mouth
 By the clock
 By the ladder
 For the individual
 With attention to detail
 According to the WHO analgesic ladder, begin
pharmacologic therapy with
 Non-opioid analgesic: They do not produce
physical dependence or tolerance but they
have an intrinsic ceiling on their analgesic
efficacy e.g. NSAIDs and acetaminophen.
 Weak opioids: Used in moderate pain not
responsive to non-opioids e.g. codeine,
hydrocodone, oxycodone,butophanol,
nalbuphin, pentazocine, DF118 and tramadol.
 Strong opioids: Used for severe pain that is not
relieved by weak opioids e.g. morphine,
hydromorphone, methadone and fentanyl.
 Adjuvants can be added at all levels to improve pain
relief: TCA (analgesic, mood elevation, potentiates
opioids) e.g. Amitriptyline, Nortriptyline.
Corticosteroids (anti-inflammatory, reduce
perineural oedema, useful in brain and spinal cord
lesions, antiemetic, appetite stimulant, mood
elevating) e.g. dexamethazone, prednisolone.
Phenothiazines e.g. methotrimeprazine (has
analgesic property)
 Non-pharmacological therapy
 Surgical treatment: used for pain refractory to analgesic or
anaesthetic interventions. Cordotomy and myelotomy may be
performed.
 Neuroblative procedures: they provide pain relief by modifying pain
pathways. Agents used include local anaesthetics, cryotherapy,
radiofrequency lesions and neurolytic agents like phenol and ethyl
alcohol
 Stimulation induced analgesia: TENS, Acupuncture.
 Physiotherapy
 Psychological therapy. Introduce early - Useful in almost all pain
syndromes to treat coexisting anxiety and to improve patient and
family coping strategies. Based on patient education. They are
thought to identify negative thoughts and to control them using
imagery, distraction and relaxation therapy.
 Support groups
 Other therapeutic modalities e.g. Chemotherapy, Radiation therapy
 POSTOPERATIVE PAIN
 Preemptive Treatment of Postoperative Pain: Recent
evidence points to advantages of administering
potent analgesics or nerve block techniques prior to
surgical stimulation (preemptive treatment). Intense
noxious stimulation can sensitize portions of the
central nervous system to subsequent input. Such
stimulation, in the form of a surgical incision, may
lead to functional changes in the central nervous
system (CNS) (sometimes called "windup") that later
cause postoperative pain to be perceived as more
"painful" than it would otherwise have been.
 Systemic Opioids: Effective doses of
appropriate drugs can be administered by the
oral, rectal, transdermal, or sublingual route,
or by subcutaneous, intramuscular, or
intravenous injection or infusion. Of these
options, intramuscular opioids have been the
most common treatment choice for patients
after surgery.
 Patient-Controlled Analgesia: the self-administration of small
doses of opioids by patients when they experience pain. Most
intravenous PCA devices consist of a microprocessor-controlled
pump triggered by depressing a button. When triggered, a preset
amount (incremental dose) of opioid is delivered into the patient's
intravenous line. A timer in the pump prevents administration of
an additional bolus until a specified period (lockout interval) has
elapsed.
 Regional Anesthetic Techniques: these include wound infiltration,
nerve blocks and epidural analgesia.
 Nonsteroidal Anti-Inflammatory Drugs e.g. ketorolac.
 Ketamine: Although systemically administered ketamine may
have a place as a short-term analgesic, sedation, unpleasant
emergence delirium, and hallucinations have limited its use.