Pain Management

Dr Shahzad Mengal
PGR II Surgical Unit III
Objectives
• Definition
• Causes
• Pain classification
• Physiology of pain
• Response to pain
• Clinical assessment of pain
• Evaluation of pain
• Management of pain
Definition
• Pain is a protective mechanism
• It is an unpleasant sensory and emotional experience associated with
actual or potential tissue damage or described in terms of such
damage
Causes of pain
• Inflammatory causes due to any infection or infestations.
• Hypoxia due to poor blood supply like in myocardial infarction, peripheral
vascular disease.
• Trauma.
• Obstruction like intestinal obstruction.
• Colicky pain like ureteric, biliary, intestinal.
• Compression over nerve roots like in inter vertebral disc prolapse.
• Advanced malignancies cause severe distressing pain, which requires
proper pain control.
• Ulcers, perforation, peritonitis, abscess formation are all other causes.
Types of pain
• Acute pain ; lasts only through the expected recovery period whether it has a sudden or
slow onset and regardless of intensity.
• Chronic pain ; is prolonged, usually recurring or persisting over 6 months or more and
interferes with functioning.
• Superficial pain: It is sharp usually localised pain, due to irritation of peripheral nerve
endings in superficial tissue by chemical/mechanical/thermal/electrical injury.
• Segmental pain: It occurs due to irritation of particular nerve trunk/ root; located in
particular dermatome of the body supplied by the sensory nerve trunk or root.
• Deep pain: It is due to irritation of deeper structures like
muscles/tendons/bones/joints/viscera.
• It is vague and diffuse when compared to superficial pain. It is often referred to common
segmental areas of representation. Often spasm of skeletal muscle of same spinal cord
segment can occur.
• Psychogenic pain: It may be functional/emotional/hysterical.
Pain physiology
• Fibers that carry pain are C fibers very slow, unmylenated, asso; with dull aching,
throbbing and diffuse pain. A delta fibers slow, myelinated asso: sharp, pricking
and well localized pain. A Beta fibers fast, large diameter, myelinated carries AP
from mechanoreceptors.
• Nociceptive pain occurs in 5 phases: 1) Transduction, 2) Conduction, 3)
Transmission, 4) Modulation, 5) Perception.

• 1.Transduction: begins when peripheral terminals of nociceptive C fibers and A-

delta (Aδ) fibers are depolarized by noxious mechanical, thermal, or chemical
energy. The membranes of these terminals contain proteins and voltage-gated
ion channels that convert thermal, mechanical, or chemical energy into an action
potential (AP). Nociceptor terminals are spread densely throughout the skin. They
are found less on periosteum, joints, tendons, muscles, and least on the surface
of organs.
• Conduction: An AP generated in nociceptor terminals is conducted across the peripheral
process to the central process were it depolarizes the presynaptic terminal. The
presynaptic terminal interfaces with a network of interneurons and second order
neurons in the dorsal horn. Interneurons can facilitate or inhibit transmission to second
order neurons.
• Transmission: begins when a nociceptive AP reaches the presynaptic terminal in the
dorsal horn. The AP causes the presynaptic terminals of Að and C fibres to release a
variety of pro-nociceptive substances into the synaptic cleft. C-fiber presynaptic
terminals are known to release glutamate which activates postsynaptic α-amino-3-
hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors; substance P which
activates postsynaptic NK1 receptors; and calcitonin gene–related peptide, which
activates postsynaptic CGRP receptors. Activation of postsynaptic receptors results in an
influx of ions that depolarize second order neurons and interneurons. When a secondary
neuron is depolarized it generates an action potential that is relayed through the
contralateral spinothalamic tract (STT) or to the medulla and brain stem via the
spinoreticular & spinomesencephalic tracts or to the hypothalamus via the
spinohypothalamic tract.
• Modulation: is an adaptive process involving both excitory and inhibitory mechanisms.
• Divided into peripheral and central modulation of Nociception
Peripheral modulation can be accomplished
by:
a) inhibiting the sensitization of nociceptor terminals with medications such as cyclooxygenase
inhibitors, e.g. aspirin, ibuprofen.
b) inhibiting depolarization and repolarization of the axonal membrane. Local anesthetics like
lidocaine prevent the generation or conduction of an action potential by blocking the influx of
sodium through voltage-gated sodium channels located along first and second order afferents.
c) inhibiting the inflammatory response to trauma with hydrocortisone. Hydrocortisone is
believed to stimulate the production of lipocortin-1, which inhibits the biosynthesis of
prostaglandins and leukotrienes from arachidonic acid by inhibiting the cytosolic enzyme
phospholipase A2. Lipocortin-1 is also believed to inhibit leukocytic inflammatory events including:
epithelial adhesion, emigration, chemotaxis, phagocytosis.
d) stimulating the large fast Aβ fibers in the area of injury can induce interneurons in the dorsal
horn to release GABA and glycine which inhibit the release of glutamate from the primary afferent
terminal, thereby preventing depolarization of the second order neuron. Mechanical stimulation
and transcutaneous electrical nerve stimulation (TENS) are believed to reduce the perception of
pain by activating fast Aβ fibers (Gate control theory).
Central Modulation of Nociception
• a) Exogenous opioids like hydromorphone, morphine and oxycodone produce analgesia by mimicking endogenous endorphins.
Opioids are able to activate the endorphin receptors: Mu, Kappa and Delta. Mu receptors are responsible for most of the analgesic
effect of opioids and are present on neurons in the spinal cord, brainstem and midbrain.
• In the dorsal horn, Mu receptor act by closing voltage sensitive calcium channels on the primary afferent presynaptic terminal.
Blocking the influx of Ca++ inhibits depolarization and the subsequent release of the neurotransmitters glutamate and substance P.
Mu receptors also increase the efflux of K+ from the second order postsynaptic terminal, which increases the internal (-) charge,
creating a hyperpolarized state.
• In the brainstem and midbrain, activated Mu receptors turn off GABAergic interneurons responsible for suppressing the
antinociceptive decending pathway. In other words, opioids enhance the activity of the descending pathway which results in
increased release of antinociceptive serotonin and norepinephrine from the descending neuron terminals into the dorsal horn.
b) Endogenous opioids (endorphins) work in a manner similar to exogenous opioids. The existence of endorphins has been
demonstrated by the application of stimulation produces analgesia (SPA). Electrical stimulation of the periaqueductal gray (PAG)
elicits the release of endorphins which produce an analgesia that can be blocked by the opioid antagonist naloxone.
c) Antidepressants are believed to enhance the analgesic activity of the descending pathway by increasing the availablity of
synaptic monoamines. The monoamines serotonin and norepinephrine are the primary neurotransmitters released by descending
pathway neuron terminals. Descending pathway neurons arise in the brainstem and terminate in close proximity to primary
afferent terminals, interneurons and synaptic membrane of second order neurons located in the dorsal horn.
 • • Stimulation of the nucleus raphe magnus in the brainstem results in antinociception
attributed to the release of serotonin (5-HT) within the dorsal horn. "Agents that block 5-HT
synthesis attenuate stimulation-produced analgesia, and the application of some 5-HT
agonists in the spinal cord results in inhibition of cells responsive to nociceptive stimuli."
Selective serotonin-reuptake inhibitors can contribute to the modulation of nociception.
• Stimulation of the locus coeruleus in the medulla results in antinociception attributed to
the release of norepinephrine within the dorsal horn. Presynaptically noradrenaline increases
inhibitory transmitters from interneurons and depresses glutamate release from both Aδ and
C afferent terminals.•

• Perception of nociceptive pain is dependant upon neural processing in the

spinal cord and several brain regions. Pain becomes more than a pattern of
nociceptive action potentials when they reach the brain. Action potentials
ascending the spinothalamic tract are decoded by the thalamus, sensorimotor
cortex, insular cortex and the anterior cingulate to be perceived as an unpleasant
sensation that can be localized to a specific region of the body. Action potentials
ascending the spinobulbar tract are decoded by the amygdala and hypothalamus
to generate a sense of urgency and intensity. It is the intergration of sensations,
emotions and cognition that result in our perception of pain.
Gate Control Theory
• The gate control theory of pain asserts that non-painful input closes the
nerve "gates" to painful input, which prevents pain sensation from
traveling to the central nervous system.
• Gate control system is located at the junction of first and second
• neuron. Large diameter ‘A’ fibre is stimulated by temperature
• and touch. Fine ‘C ‘ fibre is stimulated by pain. If ‘A’ fibre
• once gets stimulated, blocks the gate mechanism, then pain
• from ‘C’ fibre cannot pass through the gate to reach the brain
• for perception.
• Pain modulators like endorphins and opioid peptides in brain
• and spinal cord inhibit the release of substance ‘P’.
Response to pain
• The body’s response to pain has both physiologic and psychologic aspect. The sympathetic nervous system responds
resulting in fight and flight response with notable increase in blood pressure and pulse.
• The person may hold his breath or may have short and shallow breath produces atelectasis, lowers circulating oxygen
increases cardiac load.
• Pain interefere with sleep, appetite, lower quality of life for both patient and his family members.
• Natural response is to stop the activity, tense muscles and withdraw from pain provoking activities may produce muscle
atrophy and painful spasm.
• Uncontrolled pain impairs immune f.unction which slows healing and increase susceptibility to infection and dermal ulcers.
Clinical Assessment of pain
• Original site of pain is very important. In acute appendicitis original site of pain is in umbilicus; but later it is
referred to RIF.
• Time and mode of onset of pain—it is sudden onset and rapidly progressive in acute appendicitis; it is of
insidious onset and of long duration with episodic nature in chronic peptic ulcer.
• Type/nature of pain—superficial/deep; dull ache or sharp severe/pricking/bursting/vague aching
(continuous mild pain), throbbing, scalding (burning sensation particularly felt during urination in cystitis,
pyelonephritis, urethritis), pins and needles pricking sensation in peripheral nerve injury or irritation,
shooting pain (seen in intervertebral disc prolapse and sciatica—pain shoots along the course of nerve),
stabbing (sudden, severe, sharp, episodic—seen in perforated duodenal ulcer), colicky pain is due to
muscular contraction in a hollow tube in an attempt to obviate the obstruction by forcing the content out—
gripping, episodic pain with vomiting and sweating (seen in intestinal colic, ureteric colic of stone, biliary
colic of stone), twisting pain of bowel volvulus/twisted ovarian cyst/torsion testis, constricting pain around
the chest by angina, etc.
• Severity of the pain: In acute conditions like peritonitis and abscess pain will be severe compared to chronic
one.
• Periodicity of pain: Pain appears, persists for few weeks and then disappears for few weeks; again reappear. Such periodicity is often
observed in chronic peptic ulcer; trigeminal neuralgia.
• Precipitating/aggravating factors: Abdominal pain may get worsened by taking food like in gastric ulcer. Pain due to appendicitis, ureteric
stone aggravates by change of position, walking, jolting. Pain of urinary bladder stone aggravates in standing position. In reflux oesophagitis
pain increases while scooping. Pain in pancreatitis increases while lying down. Pain in intervertebral disc prolapse aggravates by lifting the
weight.
• Relieving factors of pain: Pain reduce by certain methods and patient uses that method to relieve the pain. Hunger pain of early morning in
duodenal ulcer is relieved by taking food. Pain of pancreatitis is relieved in sitting and bending forward. Propped up position relieves pain of
reflux oesophagitis. In acute peritonitis, pain reduces temporarily by lying still.
• Associated symptoms: Acute pain may be associated with pallor, sweating and vomiting. Migraine pain with vomiting and visual
disturbances; intestinal/ureteric colic with sweating, vomiting and cold periphery; acute pyelonephritis and urinary infections with
chills/rigors and fever; ureteric colic with haematuria; biliary colic with jaundice and pale stool are other examples of such association.
• Time of occurrence of pain In duodenal ulcer, hunger pain occurring in early morning or later evening is typical. Migraine occurs in early
morning; frontal sinusitis induced headache occurs a few hours after getting up.
• Pain may move from one place to other:
• Radiation of pain
• It is extension of pain from original site to another site withpersisting of
pain at original site. This radiating pain is of same character of original site.
Penetration of duodenal ulcer posteriorly causes pain both in epigastrium
and back—is an example. Pain of pancreatitis radiates to back.
• Referred pain:
• Pain is not felt at the site of the disease but felt at distant site.
Diaphragmatic irritation causes referred pain at the tip of shoulder through
same segmental supply of diaphragm (phrenic nerve C4, C5) and shoulder
(cutaneous supply C4, C5). Hip joint pathology may cause referred pain in
knee joint—through articular branches of femoral, obturator and sciatic
nerves. Other examples—referred ear pain from carcinoma tongue through
lingual and auriculotemporal nerve; referred pain in the epigastrium from
the heart; referred pain in the abdomen from pleura; referred pain over
the testis from the ureter
• Shifting/migration of pain: Originof pain is one site; later pain shifts
to another site and pain at original site disappears. Pain when begins
in viscera, it is felt at the same somatic segmental area in the body;
but once parietal layer is involved by inflammation/pathology pain is
felt at the anatomical site. Example is pain of acute appendicitis
where original visceral pain is at the umbilicus (T9 and T10 segments
supply both umbilicus and appendix) shifts later to right iliac fossa
when once the parietal peritoneum of that area is inflamed.
Pain Evaluation scale
Pain Management
• Acute Pain Management;
• If pain occurs, there should be prompt oral administration of drugs in the
following order: nonopioids (aspirin and paracetamol); then, as necessary,
mild opioids (codeine); then strong opioids such as morphine, until the
patient is free of pain. To calm fears and anxiety, additional drugs –
“adjuvants” – should be used.
• To maintain freedom from pain, drugs should be given “by the clock”, that
is every 3-6 hours, rather than “on demand” This three-step approach of
administering the right drug in the right dose at the right time is
inexpensive and 80-90% effective. Surgical intervention on appropriate
nerves may provide further pain relief if drugs are not wholly effective.
Chronic Pain Management
• When pain persists for 3 to 6 months is called chronic pain.
• Chronic pain may present for treatment of the cause (e.g. pancreatitis,
malignancy) or concomitant benign pathology. Acute pain after surgery
may progress to chronic pain and is believed to be due to inadequate
treatment of acute pain itself.

• persistent pain from a variety of disorders including chronic inflammatory

disease, recurrent infection,degenerative bone or joint disease, nerve
injury and sympathetic dystrophy. This may result from persistent
excitation of the nociceptive pathways causing spontaneous firing of pain
signals at N-methyl-d-aspartate receptors in the ascending pathways. This
pain does not respond to opiates or neuroablative surgery.
 Chronic Non malignant pain

• Who ladder for pain relief should be applied in case of chronic pain.
• Drugs in chronic non-malignant pain
• Paracetamol and the non-steroidal anti-inflammatory drugs (NSAID) are
the mainstay of musculoskeletal pain treatment.
• The tricyclic antidepressant drugs and anticonvulsant agents are often
useful for the pain of nerve injury, although side effects can prove
troublesome and reduce compliance. Both pregabalin and gabapentin
reduce spontaneous neuronal activity and are now used for managing the
neuropathic chronic pain. In more severe and debilitating non-malignant
chronic pain, opioid analgesic drugs are used in slow release oral
preparations of morphine and oxycodone, and transcutaneous patches
delivering fentanyl and buprenorphine. Combinations of drugs often prove
useful to achieve the optimum of efficacy with minimal side effects.
• Local anaesthetic and steroid injections can be effective around an
inflamed nerve and they reduce the cycle of constant pain
transmission with consequent muscle spasm. Epidural injections are
used for the pain of nerve root irritation associated with minor disc
prolapse along with active physiotherapy to promote mobility.
• • Nerve stimulation procedures such as acupuncture, transcutaneous
nerve stimulation, and spinal cord stimulators increase endorphin
production in the central nervous system. Nerve decompression
craniotomy rather than percutaneous coagulation of the ganglion is
now performed for trigeminal neuralgia.
 Chronic Malignant pain control
• WHO pain ladder is applied initially.
• Oral opiate analgesia is necessary when the less powerful analgesic agents no longer control pain
on movement, or enable the patient to sleep. Fear that the patient may develop an addiction to
opiates is usually not justified in malignant disease. It is also important to distinguish between the
addiction and dependence; the former being a psychosocial phenomenon while the latter is a
pure physiological response to a given drug. Some patients experience ‘breakthrough pain’
(acute, excruciating and incapacitating), which occurs either spontaneously or in relation to a
specific predictable or unpredictable trigger, experienced by patients who have relatively stable
and adequately controlled background pain. Oral morphine, often used for chronic pain, can be
prescribed in short-acting liquid or tablet form and should be administered regularly every 4
hours until an adequate dose of drug has been titrated to control the pain over 24 hours. Once
this is established, the daily dose can be divided into two separate administrations of enteric-
coated, slow-release morphine tablets (MST morphine) every 12 hours. Additional short-acting
opioids (morphine/fentanyl) can then be used to cover episodes of breakthrough pain. Nausea
treated using anti-emetic agents does not usually persist, but constipation is a frequent and
persistent complication requiring regular prevention with laxatives.
• Infusion of subcutaneous, intravenous, intrathecal or epidural opiate drugs
• The infusion of opiates is necessary if a patient is unable to take oral drugs.
Subcutaneous infusion of diamorphine is simple and effective to administer.
Epidural infusions of diamorphine with an external pump can be used on mobile
patients. Intrathecal infusions with pumps programmed by external computer are
used, however, there is a possibility of developing infection with catastrophic
effects. Intravenous narcotic agents may be reserved for acute crises, such as
pathological fractures.
• Neurolytic techniques in cancer pain
• These should only be used if the life expectancy is limited and the diagnosis is
certain. The useful procedures are:
• • Subcostal phenol injection for a rib metastasis.
• • Coeliac plexus neurolytic block with alcohol for pain of pancreatic, gastric or
hepatic cancer.
• Intrathecal neurolytic injection of hyperbaric phenol.
• Percutaneous anterolateral cordotomy divides the spinothalamic ascending pain
pathway. It is a highly effective technique in experienced hands, selectively
eliminating pain and temperature sensation in a specific limited area.
• Alternative strategies include:
• • The development of anti-pituitary hormone drugs, such as
tamoxifen and cyproterone, enables effective pharmacological
therapy for the pain of widespread metastases instead of pituitary
ablation surgery.
• • Palliative radiotherapy can be most beneficial for the relief of pain
in metastatic disease.
• Adjuvant drugs, such as corticosteroids to reduce cerebral oedema or
inflammation around a tumour, may be useful in symptom control.
Tricyclic antidepressants, anticonvulsants and flecainide are also used
to reduce the pain of nerve injury
• In the management of chronic pain, a multidisciplinary approach by a
team of medical and nursing staff working with psychologists,
physiotherapists and occupational therapists can often achieve much
more benefit than the use of powerful drugs.