Concept Of Pain In Ayurveda

Pain is the commonest of all symptoms. Pain is the biggest problem since the beginning of
mankind. All the systems of philosophy have taken origin in search of the method to relieve pain. The
word “disease” itself denotes painful situation.

The main object of medicine and surgery is to ameliorate the sufferings of living beings.
Ayurveda came into existence to eliminate the pain and suffering of living being.

Charaka clearly says that “Health is Happiness and Disease is Pain” and the same basis it has
been classified in “Sukh” and “Dukh” (happiness and pain). There are many terms for pain in Ayurveda
such as Shool, Vedna, Ruja , Dukh, Pidha etc. Shool or Vedna has been described as symptom and
complication in many diseases.

It has been mentioned in Sushruta Samhita that once lord Shiva became angry with Kamdev
who disturbed him during meditation and Lord Shiva threw his trishool towards Kamdev. He became
afraid and escaped into the body of Lord Vishnu. Lord Vishnu diverted the trishool towards earth and
that trishool on earth arouse shool in human beings. As it was originated from a trishool it was called
shool.

In Shalya tantra this problem has been more predominant because of the traumatic nature of
ailments which afflicted the body and mind with severe pain. This requires urgent management of the
problems by the surgeons who applied the necessary methodology to manage the situation effectively.

In Shalya tantra there were many treatises prevalent during those days. Some of which like
Bhoj, Pushklwat, Vishwamitra, Karvirya, etc. are found only as quotations in latter commentaries. But
unfortunately no other texts except Sushruta Samhita is available and that is why it has been regarded
as the representative of the surgical school of the Ayurveda.

One can find the important information from these texts and also valuable clues for further
research in this direction. The theory of Tridosha is the basis of Ayurveda, one will have to consider this
also while studying the present problem. Tridosha is concerned with life and is the primary factor for
maintaining and controlling the biological phenomena of the living beings.

As soon as life emerges the three doshas take up their respective functions and start working
constantly till death. Even a single cell has all the three doshas which regulate the different functions of
the living cells.

The equilibrium of the three doshas has to be maintained at every cost because if it is disturbed
the disorder would appear. While applying a drug the mode of action has to be kept in mind in relation
to the three doshas because of the final criteria of the remedy would be the equilibrium of doshas.

Even in case of the management of pain or anesthesia one has to find effective drug and study
them on the basis of tridosha on one side and Rasa, Guna, Virya, Vipaka, and Prabhva on the other side.
 Pain is pathological symptom predominantly caused by Vata. Hence while screening the drug for
this problem we shall have to keep these in mind and select some outstanding drugs which may prove
useful in this regard. But there may be some other drugs which might be effective due to the Prabhava,
i.e. specific action which cannot be explained on the lines of Rasa, Guna, Virya, Vipaka. Acharya Charaka
has classified drugs and made group Vednasthapniya.

The word Vedna may be interpreted in two ways. It may denote pain and also sensation in
general, therefore, it indicates that the problem of pain was hurting in the mind of ancient ages equally
as we are anxious today to find out some effective drug.

Definition -
Hindi

Description of exact nature of pain and various methods to relieve it have been described widely
in Ayurvedic literature. Acharya Charaka depicts pain as “VEDNA” which is both physical and mental.
Manas is responsible for both happiness and miseries and mind plays a major role in manifestation of
pain.

Acharya Charaka has clearly mentioned that shoola in any part of the body or in any disease is
always caused by ‘provoked and vitiated vata’. The derivation of the word ‘Shoola’ dealt within
‘Vaiyakaran sidhanta kaumidi’ by ‘Bhattoji Dixit’ in 16th century AD, based on description of Panini’s
Asthadhaya. The word Shoola has been derived from the root ‘shool’ (shooldhatu No. 526, Vyadhipraran
43, vayikaran sidhanta kaumidi).

The word ‘Shoola’ is completed by root ‘Shoola’ +’k’ suffix. The suffix is employed where
‘Shoola’ has meaning as ‘Pain’. Due to the sensation of pain (ruja) the diseases are called as ‘roga’.

Sites of Vedna/ Pain

The sense organs are the most important sites for the manifestation of happiness and miseries.
In ayurvedic literature attention has been directed towards origin, nature of pain as well as classification
of pain.

The word “Shoola” is also used for painful sensation. Indeed Ayurveda has not only considered
shoola as a symptom or as an independent disease entity but they have taken more comprehensive
view regarding the etiology, pathology and management of pain. Shoola has been described as outcome
of Vatavyadhi. There cannot be pain (Shoola) without involvement of vata (Su. Sutra. 17/12) but pitta
and kapha influences the nature and intensity of pain. Thus all three doshas (vata, pitta, kapha) as a
whole are responsible for the origin, development and perception of pain. Su.Su17/12.
Types of Vedna/Pain
In Sushruta Samhita, there is description of different types of Shoola (pain) in Uttar tantra
“Gulampratishedhaadhyaya”

i. Vataj Shoola
ii. Pittaja Shoola
iii. Kaphaja Shoola
iv. Sannipataja Shoola
v. Mutra Shoola
vi. Hrit Shool
vii. Parsva Shoola
viii. Vasti Shoola
ix. Vit Shoola
x. Avipakaj Shoola

Vataja Shoola –

This is perceived by patient, as a violent colic pain when he is empty stomach and also complains
of difficulty in respiration. Numbness is seen in limbs or seems stuffed and there is great difficulty in
evacuating flatus, stool and urine. These symptoms mark the Vataja type of the disease.

Pittaja Shoola –

Thirst and burning sensation in the body attended with an excruciating pain, giddiness, loss of
consciousness, desire for cold things and amelioration on application of cooling measures are the
specific features of Pittaja Shoola.

Kaphaja Shoola –

An agonizing pain with nausea, excessive heaviness of stomach and sense of numbness in limbs
are features which distinguish Kaphaja Shoola. Kapahaja Shoola is not as severe and colic in nature as
Vataja Shoola.

Sannipataja Shoola –

When there is vitiation of all the three doshas of body due to above mentioned various
etiological factors, body experiences all series of symptoms which are said to be incurable.

Hritshoola –

The vitiation of Vata aggravates vitiated Rasa and incarcerates in the region of heart through
the action of deranged Pitta and Kapha produces Shool in the cardiac region and give rise to difficulty in
respiration. The cardiac origin of pain (Hritshoola )is aggravated through the action of the deranged
Vayu and Rasa of the body.
Parsva Shoola-

The vitiation of Kapha in the region of Parsva (sides) arrests the course of local Vayu, which thus
is irritated and causes an immediate distention of abdomen with rumbling sounds in intestines. A
pricking pain is felt in the affected part, which seems as being pierced with needles. The patient
complains of insomnia and has no relish of food. His respiration becomes painful and difficult. Parsva
Shoola is brought by the action of vitiated Vata and Kapha.

Kukshi Shoola –

The deranged and aggravated bodily Vayu, affecting the Agni of digestion and incarcerated in
the region of Kukshi interferes with digestion of previously taken food which in these consequences
remains stiff and undigested. The patient breaths heavily owing to the accumulation of undigested
matter and tosses due to the agony of pain, finding no relief in any posture whether sitting or lying. Due
to indigestion of food there is vitiation of bodily Vayu and Kukshi Shoola is produced.

Vasti Shoola-

In this type of Shoola there is pain in bladder, groin, and umblical region. Vata is vitiated by
suppression of stool, urine and flatus in the region of Vasti. This vitiated Vata further hampers the
excretion of these waste products and thus vicious cycle gets activated.

Mutra Shoola –

Due to the action of deranged bodily Vayu the patient feels a cutting pain in the genital region
as well as on the sides of inguinal region causing suppression of urine.

The pain is intensified during the process of micturition.

Vitshoola –

Due to the impairment of digestive Agni and improper digestion, vata vitiates which obstructs
the excretion of faecal matter accumulated in large intestine and give rise to excruciating pain. The pain
is first experienced in right and left groin region but soon spreads over whole abdomen. Thirst becomes
unquenchable and the patient feels no relief even after evacuation of bladder and bowel.

Avipakaj Shoola

Excessive eating in an impaired state of digestive Agni aggravates the local vayu due to which
food taken remains undigested in the Kukshi . The undigested food causes intolerable colic which brings
about distension of abdomen, epileptic fits, nausea and vomiting with an attack of vilambika. The
patient complains of vomiting, shivering, diarrhea and even loses consciousness.

Pain described in Dukha

In Sushruta Samhita there is description of Dukha which is mainly of 3 types-

i. Adhyatmik Dukha (psychosomatic pain)

ii. Adhibhautik Dukha (pain due to animate and inanimate objects)
iii. Adhidaivik Dukha (pain due to divine and evil sources)

Further Adhyatmik Dukha is divided into 2 types

i. Sharirika dukha (physical sufferings)

ii. Mansika Dukha (psychological suffering)

Maharishi patanjili, has described “Pratikula Vedna” as Dukha.

The Dukha is the diseased condition of both mind and body. Acharya Charaka has described that a
clinician always treat the pain of past, present, and future of an individual or patients.

On the basis of intensity pain maybe of three types –

i. Tivra (Severe)
ii. Madhyam (Moderate)
iii. Mridu (Mild)

The presentation of pain depends on the cause and type of Vrana

i. Vataja - Severe pain

ii. Pittaja - Burning pain
iii. Kaphaja - Mild and diffuse pain

Shalyaj Pain- These are acute pains.

Pain as symptom

In Vranasravidhyaniya Adhyaya, Acharya Sushruta mentioned about different kinds of

presentation of pain in vrana according to dosha involvement.

Vataja Vranavedna -

 Todan - Pricking pain

 Bhedan - Stabbing pain
 Chedna - Cutting pain
 Ayam - Stretching pain
 Manthana - Gripping pain
 Vikshepana - Throwing pain
 Chimchimayana - Irritating pain
 Nirdahana - Burning pain
 Avabhanjana - Breaking pain
  Sphotan - Bursting pain
 Vidaarna - Tearing pain
 Utpaatna - Driving pain
 Kampana - Cramping pain
 Vishleshana - Dividing pain
 Vikirana - Radiating pain
 Stambhana - Stable pain
 Purana - Filling pain
 Swapana - Numbness
 Akunchana - Cramping pain
 Ankushika - Penetrating pain
 Muhurmuhuraagachhytati - Spasmodic pain
 Vividha - Vague pain

Pittaja Vrana Vedna -

 Osha - Burning
 Chosha - Sucking
 Paridaha - Generalized burning
 Dhumayan - Like smoke from wound
 Gatramangaravikaranameva- Like whole body kept in fire
 Ksharavasiktra Vedna - Like kshara applied over the wound
 Ushma abivrutti - Increased heat in the body.

Kaphaja Vrana Vedna –

 Kandu - Itching
 Alpavedan - Mild pain
 Guruta - Heaviness
 Suptata - Numbness
 Updeha - Like covered with paste
 Stabda - Stable
 Shaitya - Coldness

MARMA AND PAIN

If there is vyadhana of Rujakara marma it will produce severe pain. Pain is mentioned as the
symptom of Mamsa, Sira, Snayu, Asthi and Sandhimarma vedna.

Dosha responsible for pain –

 In Ayurvedic literature many references showed that pain is produced due to Vata Dosha.

Acharya Sushruta clearly described that ..hindi..meaning. There will not be any pain without
vata. Pain is mentioned as one of Aatmarupa and karma of vata.

Acharya Madhavkar also said that pain is produced mainly by vata dosha. Vata is the main
dosha involved in pain. It is the main factor for generating and spreading pain but for specific type of
pain in specific region a specific fraction of vayu is responsible. For example

For generalized pain - Vayan Vayu

Headache - Prana and Vyan Vayu

Abdominal pain - Samaan Vayu

Chest pain - Vyan and Prana Vayu

Although vitiated Vayu is the main factor pain, but pitta and kapha also alter the nature of pain.
As Acharya Charaka has mentioned, though there is predominance of one dosha in disease, other dosha
may also get vitiated. Due to avaran of marga/srotas and dhatushaya there is vataprakopa. This avaran
may be due to Kapha dosha.

Samprapti Abhigat

Vata Prakopa

Shool/ Vedna

Samprapti Ghatak

Dosha - Vata

Dushya - Rakta, Mamsa, Meda

Updhatu - Sira, Snayu

Srotas - Raktvaha, Mamsavaha, Medavaha

Srotodushti Prakara - Attipravriti

Sthana - Abhighataja Sthana

Upshaya - Vishranti

Sadhya-asadhyata - Sadhya

Pain describes as a complication in different procedures

Additional application of lepa or stale lepa application over the affected part would result in
pain, burning sensation and increased amount of heat at the site. If the excision is wide it will produce
pain.

Psycological aspect of pain in Ayurveda

This is universal truth that perception of same degree will be different for different individuals
and severity of pain will also differ for same individual at the different times (Kaal) and place (Desha).
This can be explained by description of psychosomatic behavior. The pain endurance is mainly related to
state of individual Satva that is state of mind. Acharya Charaka has said that this pain has got inverse
relationship with endurance (satva) of the patient. The satva (mind) in conjunction with soul controls
the body.

According to Charaka, Satva of an individual is of 3 types-

i. Pravara (high)
ii. Madya (medium)
iii. Avara (low)

Sushruta has described it under three headings of Satvika, Rajasa, Tamasa. Persons of Pravara Satva
are full of ‘Sara’ and inspite of small body due to abundance of Satva guna, are capable of high degree
of pain endurance. A person of Madhya Satva is mainly of Madhya Sara and has less pain bearing
capacity than Pravara Satva. A person of Avara or Hina Satva inspite of having larger body, have least
capacity of pain endurance.

Some other references are also available:-

 Friends who talk Anukula and Priya by giving assurance to patient and by talking
 Different stories reduce pain of the wound.
 Sheetal sparsha and Sukha Sparsha in Vata Kantaka to reduce pain
 Chanting of mantras to reduce pain of women in labor is mentioned by Acharya Charaka.

Thus, it is quite clear that the ancient Acharyas knew about both physical and mental aspects of pain
as well as their management very minutely.

It is clearly mentioned in Ayurvedic literature that all the three body Doshas i.e Vata, Pitta, Kapha
should remain in balance state for health. Vata in its vitiated form is main factor of producing pain.
Modern view
Concept of pain
French Philospher Simone Weil noted that

“Pain is the root of Knowledge”

In 1982, singer John Mellencamp proudly sang that it

“Hurt so good”

This International Association for the Study of Pain (IASP) defines pain as “an unpleasant
sensory and emotional experience associated with actual or potential tissue damage, or described in
terms of such damage.” This classification further states that pain is always subjective and that it is a
sensation in part of the body .At the same time it is unpleasant and therefore also has an emotional
component. It is to be noted that pain is not just a physical sensation. It is also an emotional experience.
It varies from person to person and in the same person time to time.

A simple no-nonsense definition of pain is

“Pain is what patient says, hurts.”

The emphasis is on the patient’s experience. Pain is unpleasant sensation no doubt, but on the
whole it is usually beneficial to the man or animal. Pain makes us conscious for the removal of cause and
precipitating factors of the injurious agent by appropriate measures.

The peripheral nerve ending (nociceptor) transmits the pain impulse to the dorsal horn of the
spinal cord, where it gets modified before onward transmission to the brain.

Any pain caused by primarily by stimulation (heat, cold, vibrations, stretch, and chemical stimuli
released from damaged cells) of the nociceptor can be said to be nociceptive pain. If pain is not caused
by a stimulus applied to the nociceptor, but is caused by impulse generation within the pathway
proximal to the nociceptor, but is caused by impulse generation within the pathway proximal to the
nociceptor (this could be in the nerve, the spinal cord or the brain), it is called neuropathic pain .Pain
being generated by nerve cell dysfunction.
Physiology of Nociception

The term ‘nociception’, which is derived from noci (Latin word for harm or injury), is used to
describe the neural response only to traumatic or noxious stimuli. All nociception produces pain, but not
all pain results from nociception.

Nociceptors are characterizes by a high threshold for activation and encode the intensity of
stimulation by increasing their discharge rates in a graded fashion.

Most nociceptors are free nerve endings that sense heat, mechanical and chemical tissue
damage . There are mechano-nociceptors which respond to pinch and pinprick, silent nociceptors, which
respond only in the presence of inflammation and the Polymodalmechanoheatnociceptors . The last are
more prevalent and respond to excessive pressure, extremes of temperatures and algogens (bradykinin,
histamine, serotonin, H+,, K+, some prostaglandins, ATP etc.).

Sensation (pain) is often described as either protopathic (noxious) or epicritic (non-anxious).

Epicritic sensation (light, touch, pressure, proprioception and temperature discrimination) is
characterized by low threshold receptors and is generally conducted by large myelinated nerve fibers.
While protopathic sensation (pain) is subserved by high threshold receptors and conducted by smaller,
less myelinated (Aδ) and unmyelinated (C) nerve fibers.

Pain Pathways

Pain is conducted along three neuron pathways that transmit noxious stimuli from the periphery
to the cerebral cortex. Primary afferent neurons are located in the dorsal root ganglion, which lie in the
vertebral foramina at each spinal cord level. Each neuron has a single axon that bifurcates, sending one
end to the peripheral tissues it innervates and the other into the dorsal horn the primary afferent
neuron synapses with a second order neuron whose axon cross the midline and ascend in the
contralateral Spinothalamic tract (STT) to reach the thalamus. Second order neuron synapses in thalamic
nuclei with third order neurons, which in turn sends projection through the internal capsule and corona
radiate to the Post Central Gyrus (PCG) of the cerebral cortex.

First order neurons

The majority of the first order neuron sends the proximal end of their axons into the spinal cord
via dorsal (spinal) sensory root at each cervical, thoracic, lumbar and sacral level. Some unmyelinated
afferent (C) fibers have been shown to enter spinal cord via the ventral nerve root, accounting for
observation that some patients continue to feel pain even after transaction of the dorsal nerve root and
report pain following ventral root stimulation. The axons of first-order neuron may also synapse with
the interneurons, sympathetic neurons and ventral horn motor neurons.

Second order neurons

Pain fibers may ascend or descend one to three spinal segments in Lissauer’s tract before synapsing
with second order neuron in the grey matter of the ipsilateral dorsal horn. In many instances they
communicate with them through inter neurons. Spinal cord grey matter was divided by Rexed into 10
laminas. Second order neuron may be either nociceptive specific or WDR (wide dynamic range) neurons,
also receive non-noxious afferent input from Aδ, C fibers. WDR which is more abundant in lamina I, IV, V
while Aδ fibers synapse mainly in laminas I, V, X. Lamina I responds primarily to noxious stimuli from
Cutaneous and deep somatic tissues. Lamina II, is also called the Substantia Gelatinosa contains many
interneurons and is believed to play a major role in processing and modulating nociceptive input from
cutaneous nociceptors. It is a major site of action of opioids. Visceral afferents terminate primarily in
lamina V, and to a lesser extent lamina I. These two laminas represent points of central convergence
between somatic and visceral inputs. Traditionally C fibers represent a large number of fibers in
peripheral nerves which are unmyelinated and transmit dull aching, burning and poorly localized pain,
have large receptive fields and have input that does not fatigue or extinguish with repeated stimulation.
Aδ fibers are also called mechanoreceptors because they increase their firing rate with increased
stimulus and are myelinated. Hence associated with fast pain perception, have specificity, and well
localized but are lesser in number than C fibers.

The spinothalamic tract –

The axons of most second order neurons cross the midline close to their level of origin to the
collateral side of spinal cord before they form the spinothalamic tract and send their fibers to the
thalamus, the reticular formation, the Nucleus Raphe Magnus, and the periaqueductal gray. The
spinothalamic tract, which is classically considered the major pain pathways, lays anterolaterally in the
white matter of spinal cord. This ascending tract can be divided as lateral and medial. The lateral
spinothlamic tract (neospinothalamic) projects mainly to the ventral posterolateral nucleus of the
thalamus and carries discriminative aspects of pain, such as location, intensity and duration.

The autonomic and unpleasant emotional perceptions of pain .Some spinothalamic fibers also
projects to the periaqueductal gray and thus may be an important link between ascending and
descending pathways.

Alternate pain pathways diffusely, ipsilaterally, and contralaterally .Hence some patients continue to
perceive pain following ablation of the contralateral STT. The spino-reticular tract is thought to mediate
arousal and autonomic responses to pain. Spino-mesencephalic tract may be important in activating
antinociceptive , descending pathways, because it has some projections to PAG. The spino-
hypothalamic and spino-telencephalic tracts activate the hypothalamus and evoke emotional behavior.
The spino-cervical tract ascends uncrossed to the Lateral cervical nucleus, which relays the fibers to the
contra-lateral thalamus and is a major alternate pain pathway. Some fibers in the dorsal columns are
responsive to pain, they ascend medially and ipsilaterally.

Integration with the sympathetic and motor systems

Somatic and visceral afferents are fully integrated with the skeletal motor and the sympathetic
systems in the spinal cord, brainstems, and higher centers. Afferent dorsal horn neurons synapse both
directly and indirectly with the anterior horn motor neurons. These synapses are responsible for reflex
muscle activity whether normal or abnormal. Similarly synapses between afferent nociceptive neurons
and sympathetic neurons in the intermedial-lateral columns results in reflex sympathetically mediated
vasoconstriction, smooth muscle spasm, and the release of catecholamine ‘s both locally and from the
adrenal medulla.

Third order neurons

Third order neurons are located in the thalamus and fibers to somatosensory areas I and II in the
Post Central Gyrus of the parietal cortex and the superior wall of Sylvian fissure respectively. Perception
and discrete localization of pain take place in these cortical areas.

Chemical mediators of pain

Most important of these are substance P (peptide) and Calcitonin Gene Related Peptide (cGRP).
Glutamate is the most important excitatory amino acid. Substance P (sP) is synthesized and released by
first order neuron both peripherally and in the dorsal horn and facilitates neurotransmission. It
sensitizes nociceptors , degranulates histamines from mast cells and serotonin from platelets and is a
potent vasodilator and chemo-attractant for leucocytes. Since sP releasing neurons also innervate the
viscera and send collateral fibers to Para-vertebral sympathetic ganglion, intense stimulation of viscera
can cause direct post-ganglionic sympathetic discharge. Inhibitory neurotransmitters include opioids like
β endrophins, Enkephalins and GABA, glycins, adenosine, serotonin etc.

Modulation of pain

Modulationof pain occurs peripherally at the nociceptors, in the spinal cord or in the supra
spinal structures. This can either inhibit or facilitate pain.

Peripheral modulation

When repetitive stimulation of dorsal horn neurons involved in the pain response occurs, the
frequency of discharge can be shown with neurophysiological techniques to increase. This phenomenon
is called sensitization or “wind up”. Thus stimuli that is normally not painful such as lightly stroking the
skin cause patient agony because the nervous system response is augmented by maladaptive changes in
the processing of sensory input.

Primary Hyperalgesia

This sensitization leads to decrease in pain threshold, an increase in frequency response to the
same stimulus intensity, a decrease in response latency, and spontaneous firing even after cessation of
the stimulus. Primary hyperalgesia is mediated by the release of algogens from damaged tissues.

Prostglandins are produced following tissue damage by the action of phospholipase A2 on

phospholipids released from cell membranes to form arachidonic acid (AA). The cyclo-oxygenase (COX)
pathway then converts the latter into endoperoxides, which in turn are transformed into prostacyclin
and prostaglandin E2 (PGE2). PGE2 directly activates free nerve endings, while prostacyclin potentiates
edema from bradykinin. The lipoxygense pathway ultimately converts AA to leukotrienes which also
potentiate certain types of pain. Acetaminophen and NSAIDs produce analgesia by inhibition of cyclo-
oxygenase enzymes.

Secondary Hperalgesia

Neurogenic inflammation also called secondary hyperalgesia, play an important role in

peripheral sensitization following injury. It is manifested by the triple response of a red flush around the
site of injury, local tissue edema and sensitization to noxious stimuli which is primarily due to anti-
dromic effect of release of sP (and probably cGRP) from collateral axons of the primary afferent neuron.
Substance P degranulates histamines and 5-HT, results in vasodilation and causes tissue edema, and
induces formation of leukotrienes.

Central Modulation

A. Facilitation

Three mechanisms are mainly responsible for central sensitization in the spinal cord.

i. Wind up and sensitization of second order neurons.

ii. Receptor field expansion
iii. Hyperexcitibility of flexion reflexes

Neurochemical mediators of central sensitization include sP, cGRP, VIP, Cholecystokinin (CCK),
angiotensin, and galanin as well as the excitary amino acids L-Glutamate and L-Aspartate. These
substances trigger changes in membrane receptors on neurons, activating intracellular second
messengers which in turn, phosphorylate substrate proteins. A common pathway is an increase in
intracellular calcium concentration.

Glutamate and Aspartate play an important role in wind-up via activation on NDMA and non-
NDMA receptor mechanism. Activation of NMDA increases intracellular calcium concentration in
spinal neurons and activates phospholipase c (PLc) helps in information of IP3 and DAG (Diacyl
Glycerol) which function as second messenger.

Activation of NMDA receptors also includes nitric oxide formation. Both prostaglandins and
nitric oxide facilitates the release of excitatory amino acids in the spinal cord. Hence COX inhibitors
such as aspirin and NSAIDs also appear to have important analgesic actions in the spinal cord.

B. Inhbition

Inhibition takes place both in the cord itself and descending neural activity from Supraspinal
centers.

Segmental inhibition

Activation of large afferent fibers sub serving epicritic sensation inhibits WDR neurons and STT
activity. Also activation of noxious stimuli in non-contiguous part of the body inhibits WDR neurons
at other levels i.e pain in one part of the body inhibits pain in other part of the body. That such sites
existed was proposed by Gate Control theory by Melzack and Wall in 1965. Glycine and GABA are
amino acids that functions as inhibitory neurotransmitters. They likely play an important role in
segmental inhibition antagonism of glycine and GABA which results in powerful facilitation of WDR
neurons and produces Allodynia and hyperesthesia. There are two subtypes of GABA: GABAa and
GABAb Segmental inhibition is mediated by GABAb receptor activity which increases K+ receptor
conductance across cell membrane. The GABAa receptor functions as Cl- channel which increases Cl-
conductance across the membrane. Benzodiazepines potentiate this action. Activation of glycine
receptors also increases Cl- conductance across neuron cell membranes. Adenosine also modulates
nociceptive activity in the dorsal horn. At least two receptors are known A1 which inhibits
adenylcyclase and A2 which stimulates adenylcyclase. The A1 receptor mediates adenosine’s anti-
nociceptive action. Methylxanthines can reverse this effect through phosphordiestrase inhibition.

Supraspinal inhibition

Several Supraspinal structures send fibers down the spinal cord to inhibit pain in the dorsal horn
which originate mostly in the PAG, reticular formation, and NRM .Axon from PAG act presynaptically
on primary afferent neurons and postsynaptically on second order neurons. These pathway mediate
their anti-noiciceptive action via α2 adrenergic, Serotonergic, opiate (µ, δ, Ƙ) receptor mechanism.
The role of monoamines in pain inhibition explains the analgesic action of anti-depressants that
block reuptake of catecholamine’s and serotonin. Activity at these receptors activates secondary
intracellular calcium concentration.

The endogenous opiate system acts (Primarily the NRM and reticular formation) via methionine
encephalin, leucine enkephalin and β endorphin, which are antagonized by naloxone. PAG have high
concentration of endogenous opioid neurotransmitters. These opiates act presynaptically to
hyperpolarize primary afferent neurons and inhibit the release of sP. They also appear to cause
postsynaptic inhibition. Exogenous opioids may ct principally postsynaptically on the second order
neuron or interneurons in the Substantia Gelatinosa.

Nor-epinephrine and Serotonin are also implicated in these inhibitory/ modulatory circuits. Since
pain transmission neurons can be activated by modulatory neurons, it is theorectically possible to
generate a pain signal with no peripheral noxious stimulus.

Pathophysiology of Acute pain

Tissue damage and inflammation

Noxious stimuli sufficient to cause tissue damage and are associated with release of numerous
inflammatory mediators. Inflammatory mediators may be directly algogenic or enhance the
algogenic effect of other stimuli. Chemical mediators of inflammation exert their effect on
membrane ion channels of nociceptive neurons either by direct coupling to membrane receptors for
specific substance (Hydrogen ion, adenosine triphosphate, serotonin 5-HT3) or more commonly by
an indirect action mediated by intracellular second messengers, (Bradykinin, Cytokines, Prostanoids,
Histamine H1, Serotonin 5-HT3).

Some mediators act on other parts of the neuron to control the release of mediators by the
other cells. Other mediators such as platelet activating factor enhance the process by acting on
blood vessels and inflammatory cells to evoke long lasting arteriolar vasodilation. Important
mediator’s involved in inflammatory hyperalgesia include bradykinin, cytokines and eicosanoids.

Inflammatory medaitors

Bradykinin

The autacoids bradykinin is cleaved form inactive precursor in response to tissue damage.
Bradykinin is potent algogenic agent which also sensitizes nociceptors to the action of other
algogens, increase vascular permeability and enhances leukocyte chemotaxis. Bradykinin receptors
activation releases prostaglandins from sympathetic fibers as well as from other tissues. Binding
sites for bradykinin are found on sensory nerve fibers and in the dorsal horn.

Catecholamine

Catecholamines have been implicated in nociceptive stimulus at the spinal cord level, the effect
being mediated by the α2-adrenoceptors.

Cytokines

Cytokines are regulatory peptides produced in all cells. They have pleiotropic action. Anti-
inflammatory cytokines and growth factors contribute to inflammatory hyperalgesia. Thus, TNF-α
release is stimulated by bradykinin. This stimulates the production of IL-1 and IL-6 which induce
hyperalgesia via the production of cyclo-oxygenase products. The effect of IL-8 is mediated via
sympathetic nerve fibers.

Histamine

Histamine released from damaged cells and mast cells in response to substance and nerve
growth factor causes activation of nociceptors vasodilation and edema.

Protons

Inflammatory exudates tend to be acidic and there is evidence that protons at the site of tissue
damage, enhances the action of algogenic substance as well as exciting neurons directly.

Prostaglandins

Tissue damage releases phospholipids from cell membranes which are broken down by
phospholipase A2 to from arachidonic acid. Cyclo-oxygenase catalyzed oxidation of archidonic acid
 results in the production of cyclic prostaglandins. The cyc;o-oxygenase enzyme is encoded by two
genes and two forms of enzyme (COX1 and COX2) have been characterized.

COX1 is produced in quiescent condition and is a constitutive member of normal cells ,

prostaglandins have protective function such as gastric mucus production and renal blood flow
maintenance. COX2 the inducible form at the enzyme, is the major isozyme associated with
inflammation. COX2 is induced in endothelial cells, macrophages and synovial fibroblasts, mast cells,
chondrocytes and osteoblast after tissue trauma by inflammatory agents. Prostaglandins sensitize
nociceptors to the action of their substance and to mechanical stimuli.

Leucotrienes

The lipoxygenase products of arachidonic acid metabolism may also have algogenic properties.

Classification of Pain

A. According to clinical usefulness

1. Acute Pain 2. Chronic Pain

Acute pain is a signal of ongoing or impending tissue damage that provokes the patient to
escape from injurious event or seek treatment. Acute pain is primarily due to nociception. Chronic pain
is defined as that which persists beyond the usual course of an acute pain or after a reasonable time for
healing to occur, which varies between 1-6 months in most definitions. Chronic pain may be due to
nociception but in this physiological and behavioural factors often play a major role, it may be
nociceptive neuropathic or mixed.

B. According to pathophysiology

1. Nociceptive 2. Non-nociceptive

a. Somatic (i) Superficial (i) Neuropathic

(ii) Deep (ii) Sympathetic

b. Visceral (i) Tue localized visceral pain (iii) Referred visceral pain
(ii) Localized parietal pain (iv) Referred parietal pain

Nociceptive pain arises from the stimulation of specific pain receptors. These receptors can
respond to heat, cold, vibration, stretch and chemical stimuli released from damaged cells.

Non-nociceptive pain arises from within the peripheral and central nervous system. Specific
receptors do not exist here, pain being generated by nerve cell dysfunction.
 Somatic pain

Source-

Tissues such as skin, muscle, joints, bones and ligaments- often known as musculoskeletal pain.

Receptors activated –

Specific receptors (nociceptors) for heat, cold, vibration, stretch (muscles), inflammation (e.g.
cuts and sprains which cause tissue disruption), and oxygen starvation (ischemic muscle cramps).

Characterstics-

Ofte sharp and well localized, and can often be reproduced by touching or moving the area or
tissue involved. Although, deep somatic pain may be dull, aching and less well localized than
superficial somatic pain.

Visceral Pain

Source- Internal organs of the three main body cavities-

a) Thorax (heart and lungs)

b) Abdomen (liver, kidneys, spleen and bowels)
c) Pelvis (bladder, womb and ovaries)

Receptors activated-

Specific receptors (nociceptors) for stretch, inflammation, and oxygen starvation (ischemia).

Characterstics-

True visceral pain is dull, diffuse and usually midline. It is frequently associated with abnormal
sympathetic or parasympathetic activity causing nausea, vomiting, sweating and changes in B.P and
heart rate. Parietal pain is typically sharp and localized or referred to a distant site. The phenomenon of
visceral or parietal pain referred to cutaneous areas, results from patterns of embryonic development,
migration of tissues and the convergence of visceral and somatic afferent input into the CNS.

Nerve Pain

Source-

From within the nervous system itself, pain may originate from the peripheral nervous system
(the nerves between the tissues and the spinal cord), or from the central nervous system (the nerves
between the spinal cord and the brain).

Causes- May be due to any one of the following process-

 Nerve degeneration- Multiple sclerosis, Stroke, Brain hemorrhage and Oxygen starvation
  Nerve pressure- Trapped nerve
 Nerve inflammation- Torn or slipped disc
 Nerve infection- Shigellas and other viral infections.

Characteristics-

These signals are then interpreted by the brain as pain, and can be associated with the signs of
nerve malfunction such as hypersensitivity (touch, vibration, hot ,cold), tingling, numbness and
weakness. There is often referred pain to an area where that nerve would normally supplye.g. in sciatica
from a slip disc irritating the L5 spinal nerve produces pain down the leg to the outside shin and big toe
i.e. the normal territory in the leg supplied by the L5 spinal nerve. Nerve pain is often described as
shooting, burning and hypersensitive.

Sympathetic pain-

Source

Due to possible over activity of sympathetic nervous system, and central/peripheral nervous
system mechanisms controls blood flow to issues such as skin and muscle, sweating by the skin and the
speed and responsiveness of the peripheral nervous system.

Causes-

Occurs more commonly after fractures and soft tissue injuries of the arms and legs, and these
injuries may lead to Complex Regional Pain Syndrome (CRPS). CRPS was previously known as Reflex
Sympathetic Dystrophy.

Receptors activated-

Like nerve pain there are no specific pain receptors (non-nociceptive). The same nerve
processes as mentioned above may be operated in CRPS.

Characterstics-

Presents as extreme hypersensitivity in the skin around the injury and also peripherally in the
limb (Allodynia), and is associated with abnormalities of sweating and temperature control in the area.
The limb is usually so painful, that the sufferer refuses to use it causing secondary problems after a
period of time with muscle wasting, joint contracture, and osteoporosis of the bones. It is possible that
the syndrome is initiated by trauma to small peripheral nerves close to the injury.

Measurement of pain

The measurement of pain is important to provide information about its severity and cause and
to determine and evaluate treatment. This is a challenge, however, because pain is subjective
experience that is influenced by psychological, cultural and other variables.
 1. Visual analogue scale (VAS)-

The visual analogue scale is one of the most widely used measures of pain intensity. It consists of a
10 cm line marked at one end with ‘No pain’ and at other with ‘Worst pain ever.’ The patient marks a
point on this line to represent their current status. It can be used for various parameters such as pain,
mood, pain relief and disability. The value is taken as the distance of the mark along the scale from the
origin. Current opinion in that visual analogue scales are reliable when used with the appropriate group
of patients and under controlled circumstances. These scales are not suitable for very young children or
the visually impaired.

2. Verbal and numerical rating scales-

Verbal pain rating scale such as none, mild, moderate, and severe have been used for many years
and provide as simple tool measure pain intensity. Verbal pain relief scale may br used to measure the
effect of particular treatment and may be more sensitive at detecting an improvement than looking for
a change in pain score. Numerical pain rating scales are similar to the visual analogue scale but replace
the line with the number 0-10. Measurement of pain using verbal and numerical rating scale correlates
with pain measured by the VAS.

3. Book word descriptor ranking-

Here assessment is dependent on a choice of a word descriptor from list. The assessment is
obtained by scoring for each word to give a pain rating index. An alternatively using free choice from
non-scored word lists, the total number of word chosen can be recorded. This method can adapted for
visually impaired patients.

4. Mc Gill pain questionnaire-

It was first described by Melzack 1975. It consists of a body map and word descriptor section for
evaluating the intensity and other characteristics of pain. It is a relatively questionnaire taking around
twenty min or more to complete, depending on patient’s skill. This limits its application since it is not
suitable for children, highly anxious patients or patients in the immediate post- operative period. It is
commonly used in research.

Post-operative Pain

Pain has been defined as the sensory appreciation of afferent nociceptive stimuli which elicits an
affective (or autonomic) component;

Both are subjected to rational interpretation by the patient. Post-operative pain differs from
other types of pain in that it is usually transitory with progressive improvement over a relatively short
time source and there requirement for immediate relief which dictate the development of suitable
management protocols. Typically the affective component tends towards an anxiety state associated
with diagnosis of the condition and fear of delay in provision of analgesic therapy by attendants.
 Postoperative pain can be divided into acute pain and chronic pain: Acute pain is experienced
immediately after surgery (up to 7 days). Pain which lasts more than # months after the injury is
considered to be chronic pain.

Positive role of pain

Acute pain plays a useful “positive” physiological role by:

 Providing warning of tissue damage

 Inducing immobilization to allow appropriate healing.

Negative effects of pain

Short term negative effects of acute pain include:

 Emotional and physical suffering for the patient.

 Sleep disturbance( with negative impact on mood and mobilisation)
 Cardiovascular side effects (such as hypertension and tachycardia)
 Increased oxygen consumption( with negative impact in the case of coronary artery disease)
 Impaired bowel movement (while opioids induce constipation or nausea, untreated pain may
also be an important cause of impaired bowel movement or PONV)
 Negative effects on respiratory function(leading to atelectasis, retention of secretions and
pneumonia
 Delays mobilization is one of the major causes for delayed mobilization).

Need for post-operative analgesia

1. Relieving suffering: First and foremost, pain is suffering and it is our duty to relieve suffering.

2. Muscle spasm: Pain causes reflex muscle spasm. This has two negative implication:

a. It can be cause respiratory embarrassment. Musclespasm can cause regional hypoventilation and
contribute to post-operative respiratory problems.

b. The muscle spasm itself can be a major cause of pain. Even short term muscle spasm can cause
severe pain- for example, backache.

3. Untreated pain will be keep getting worse. There are several neurophysiological reasons for this:

a. Recruitment of nociceptors: Silent or ‘sleepy’ nociceptors are those that do not respond to noxious
stimuli normally; but are activated in the inflamed tissues. Once they are recruited, the same degree of
electrical impulses, thereby resulting in worsening of pain.

b. Central recruitment: With persisting pain, adjacent spinal segments (or adjacent suprapinal areas)
get recruited, so that pain gradually spreads to larger areas .This could be the reason for the occasional
patient with cancer pain or some chronic pain to complain of pain from “head to foot”.
 c. Sensitization of nociceptors : The nociceptors get sensitized with time so that response threshold is
lowered.

d. Central sensitization (wind-up “phenomenon”): The dorsal horn cells get sensitized. It manifests as:

i. An increase in the receptive in the receptive field for sensitized dorsal horn neurons.
ii. An increase in the duration of response.
iii. A reduction in response threshold.
iv. N-Methyl D Aspartate (NMDA) is believed to be the most important neurotransmitter involved
in the “wind-up” mechanism.

4. Anatomical and genetic changes: It has been clearly proved now that persistent unrelieved pain can
cause anatomical changes in the nervous system, as well as genetic changes in the dorsal horn cell.

As have been mentioned in introduction of this work in the beginning, despite recent advances
in post-operative pain management a recent survey showed that most adults still aspect to have
significant post-operative pain after surgery which is their primary concern, and a number of patients
still experience moderate to severe pain post-operative.

Hence effective treatment of post-operative pain should be high the agenda of all staff looking
after post-operative patients. Often, pain control after surgery can be less than optimal. The reasons for
this are multifactor but include staffing and resource issues, over reliance on single analgesic agent
regimens, under estimation of effective dosages, over estimation of analgesic duration of action and
misconceptions about particular side effects and the potential for addiction.

Cause of variation in Analgesic requirements

There is marked inter individual variation in analgesic requirements. Unfortunately there is no way
of predicting in advance the extent of opioid requirements of individual patients .Various factors
responsible for these facts are:-

i. Site of surgery- In general upper abdominal surgery produces greater pain than the lower
abdominal surgery, which in turn is associated with greater pain than peripheral surgery, which
in turn is associated with greater pain than peripheral surgery. Few exceptions are surgery of
richly innervated digits. Operations to joints are associated with sharp pain whereas abdominal
surgery is associated with two types of pain: a continuous dull nauseating pain induced by
coughing and movement.
ii. Aged gender and body weight- Analgesic requirements of females are identical for similar types
of surgery. However there is reduction in analgesic requirements with advancing age. There is
no evidence that variation in body weight in the adult population affects opioid requirements.
iii. Psychological factors- The patient’s personality affects pain perception and response to
analgesic drugs. Further the extent of patient’s anxiety also differ pain perception. Some other
facts have been mentioned previously.
 iv. Wound movement- Movement at a wound site exacerbates pain, thus, the classic response to
injury is to avoid movement at that site. This explains the greater observed pain in abdominal
and thorax, where wounds are necessarily subjected to the movement of respiration
Immobilization such as used when splinting and long bone fracture reduces pain.
v. Pharmcokinetic variability- After i.m. injection of an opioid there is a three to seven fold
difference between patients in the rate at which peak plasma concentrations of the drug occur
and a two to five fold difference in the peak plasma concentrations achieved. This
pharmacokinetic variability helps to explain the relatively poor response to a single i.m injection
given for the post-operative pain.
vi. Pharmacodynamic variability- Major reason for variation in pain sensitivity is Pharmacodynamic
actions i.e. inherent sensitivity of pin receptors. It is possible to define a steady state plasma
concentration of a opioid/NSAID at which analgesia concentration (MEAC). This MEAC level
varies four to five folds between individual patients and is affected by age and differences in
psychological profile.

Clinical factors related to post-operative pain

Pain causes an increase in the sympathetic response of the body with subsequent rise in heart
rate, cardiac work and oxygen consumption. Prolonged pain can reduce physical activity and lead to
venous stasis and an increased risk of deep vein thrombosis and consequent pulmonary embolism. In
addition, there can be widespread effects on gut and urinary tract motility which may in turn lead to
postoperative ileus, nausea, vomiting and retention. These problems are unpleasant for the patient and
may prolong hospital stay.

The choice of pain relieving techniques may be influenced by the site surgery. Equally, it may be
influenced by drug availability and familiarity with different methods of analgesia. For example,
although patient controlled analgesia (PCA) has often shown to be better than the intermittent delivery
of intramuscular opioids it does not produce as much pain relief as epidural opioid analgesia. Equally, a
local anesthetic block can effectively relieve pain, but only for the duration of the particular agent used.
Choice of technique will also be influenced will also be influenced by the degree of training and
expertise to the staff.

Improvement can be achieved by better education for all staff concerned with the delivery of
post -operative pain relief and by making the assessment and recording of pain levels part of the routine
management of each patient. Ideally, a named individual should be responsible in each hospital for the
delivery and teaching of acute pain management.

Adverse effectsof post-operative pain

1. Respiratory effects –
Pain is a disincentive to normal deep respiration and coughing. Most patients will show
an impairment of pulmonary function but this is most marked in patient undergoing upper
abdominal or thoracic surgery. It leads to basal atelectasis, mucous plugging and subsequent
bacterial infection. Painful surgical incision involving the upper abdomen results in a reflex
 mediated increase in tone in the abdominal muscles during expiration and a decrease in
diaphragmatic function. Increased muscle tone is a contributing factor for increased oxygen
consumption and increased lactic acid production. Distended bowel associated with post-
operative ileus or tight dressings may further decrease ventilation and fear of aggravating pain
may further cause patients to avoid breathing deeply of coughing.
2. Cardiovascular effects-
The risk of myocardial ischemia or infarction, deep vein thrombosis may be increased
when fear of aggravating pain results in reduced physical activity, venous stasis and platelet
aggregation. The simplest and most effective prophylaxis against thromboembolic disease in the
post-operative period in the post-operative period is early mobilization. The sympathetic
adrenergic response to pain results in increased cardiovascular stress and increases platelet
adhesion. The latter may explain the relatively high incidence of preoperative myocardial
infarction and thrombo-embolism.
3. Gastrointestinal and urinary complications-
Enhanced sympathetic tone increases sphincter tone and decreases intestinal and
urinary motility, promoting ileus and urinary retention respectively. Nauses, vomiting and
constipation are common. Abdominal distension further aggravates lossof lung volume and
pulmonary dysfunction. Pain can also cause hyper motility of the urethra and bladder and
consequent difficulty with urination. Adequate analgesia has been shown to speed up return of
bowel function.
4. Stress response
a. Neuroendocrine and metabolic effects-
The stress response has been termed ‘The integrated adaptive living web of
neuroendocrine, immunologic and intercellular biochemical signals evoked by tissue injury’.
The neuroendocrine response to pain involves hypothalamic pituitary adrenocortical and
sympathoadrenal interactions. Suprasegmental reflex response to pain result in increased
sympathetic tone, hypothalamic stimulation, increased catecholamine’s and catabolic
hormone secretion and decrease anabolic hormone viz. insulin, testosterone secretion. The
result for this include increased protein catabolism with subsequent inhibition of tissue
healing and depressed immune function with reduced resistance to infection and sodium
and water retention, increased blood glucose , free fatty acids, ketone bodies and lactate.
Pain is thought to be a major trigger in the response and it has been shown in the effective
analgesia, in particular epidural analgesia is associated with a reduced stress response. Also
there is evidence to support an associated reduction in post-operative morbidity and
mortality.
b. Psycological responses-
Perioperative pain can be major source of fear and anxiety. When prolonged, it can lead
to anger, resentment and adversarial relationships with doctor and nurses. Insomnia may
also occur which is detrimental recovery.

Methods of post-operative pain management

 Optimal management of acute post-operative pain requires planning, patient and staff
education and tailoring to the type of surgery and the needs of individual patients; Effective post-
operative pain relief has numerous benefits and should be administered according to protocol of
increasing strength as recommended by W.H.O.

Pharmacological interventions

i. Opioids-

Opioids given by the intravenous (IV) route provide rapid and predictable pain control when
compared with intramuscular (IM) administration. In the post-operative period the systemic absorption
of IM morphine may be variable due to hypothermia, hypervolemia and peripheral vasoconstriction. If
not precluded, opioids can be given effectively by the subcutaneous or oral route.

Opioids are predominantly inactivated in the liver with metabolites excreted in the bile and the
urine. Care must be exercised in patients with renal impairment to avoid the accumulation of active
metabolites such as morphine-6-glucuronide. Opioids act against dull, poorly localized pain resulting
from stimulation of supraspinal and spinal pathways. Not all types of pain are equally sensitive to
opioids and it is important to recognize at the outset that opioids in the management of post-operative
pain. Other desirable effects are sedation and anxiolysis. Adverse effects include bradycardia,
hypotension and vasodilation due to reduced sympathetic drive, histamine release and specific vagal
effects. GI complications include delayed gastric emptying, increased smooth muscle tone and reduced
peristalsis leading to constipation and contraction of the gallbladder and sphincter of Oddi.

Nausea and vomiting caused by dopamine (DA) and serotonin (5-HT3) receptor stimulation in
the chemo receptor trigger zone can be problematic for the patient. Respiratory depression due to
opioids is a dose dependent phenomenon where the depth and rate of breathing are reduced as a result
of decreased sensitivity of the respiratory center to carbon dioxide. These effects can be reversed by
opioid antagonists such as naloxone.

ii. PCA(Patient Controlled Analgesia)-

PCA allows the patient to be self-administer small doses of intravenous opioid at frequent
intervals, providing better post-operative pain relief than intermittent IM injections. PCA allows for
variations in opioid requirement as a result of tolerance variability in pharmacokinetics and changes in
pain intensity. To use PCA effectively, the patient must grasp its concept and retain the instructions into
the post-operative period. In the elderly the patients the failure rate of PCA increases, there should be
careful assessment of the patient’s age, cognitive function, drug history, co-morbidity etc. and the
proposed surgical procedure prior to prescription of the PCA. PCA requires frequent monitoring by
trained nurses. Additional prescription of oxygen, anti-emetics and opioid antagonists should be clear.

iii. Pre-emptive analgesia-

 Trauma or inflammation results in sensitization of pain pathways. Locally, mediators sensitize the Aδ
and C fibers so that slow intensity stimuli create pain sensation. Centrally, sensory bombardment results
in changes such that input by normal low threshold Aβ fibers is sensed as pain. Pre-emptive analgesia is
based on the hypothesis that these changes can be prevented and that this will result in better
analgesia. At present, the benefits of pre-emptive analgesia are not established.

iv. Tramadol-

Tramadol is a synthetic analgesic that is weak opioid receptor agonist. It also exerts analgesia via
inhibition of Noradrenaline and serotonin reuptake and increases the release of 5-HT to modify
nociceptive transmission through the activation of inhibitor descending pathways in the CNS. Though it
can cause nausea, Tramadol is an analgesic that causes minimal sedation, respiratory depression and GI
stasis.

v. Paracetamol-

Paracetamol has an important role in balanced analgesia. In adults the regular prescription of
paracetemol has been shown to have a significant opioid sparing effect in post-operative patients,
typically of the order of 20-30%. Paracetemol for the most part is used as an adjunct in the
management of post-operative pain and evidence suggests that it is a weaker analgesic than NSAIDs.

vi. Non-steroidal anti-inflammatory drugs(NSAIDs)-

NSAIDs are heterogeneous class of drugs that exert their anti-inflammatory effects through the
inhibition of cyclo-oxygenase (COX) and hence reduce the production of inflammatory prostaglandins
(PG) NSAIDs are generally considered to be inadequate as sole agents in the control of immediate post-
operative pain, but in conjunction with opioids work synergistically and have a significant opioid sparing
effect. However the effect of PG inhibition is not restricted to inflamed tissue and this explains why their
use is often limited. There are four principle adverse effects associated with NSAIDs-

a. Loss of PG mediated cytoprotection in gut resulting in gastrointestinal ulceration.

b. Renal PGs are important in the maintenance of renal blood flow and glomerular filtration when
blood flow is borderline and therefore the use of NSAIDs can precipitate renal dysfunction in
susceptible patients and should be used judiciously in the elderly, those on ACE inhibitors and in
the presence of hypervolemia, dehydration and hypotension.
c. NSAIDs increase the prostacyclin, TXA2 inhibitors and ais in the abnormal platelet function that
may impair hemostasis.
d. Aspirin induced asthma: COX inhibition leads to increased levels of arachidonic acid (AA) and
increased metabolism through the alternative lipoxygenase pathway to form an abundance of
leukotrienes which can mediate bronchoconstriction and anaphylaxis.
vii. COX2 inhibitors-

Various clinical trials support the hypothesis that specific COX-2 inhibitors may provide a
significantly improved risk benefit ratio in terms of GIT safety as compared with conventional (acidic)
NSAIDs. Though well controlled studies are needed to define clinical utility of these in patients at risk of
renal disease, hypertension or CHF. Cardiovascular risk of COX-@ inhibitors remains controversial. The
prevailing assumption was COX-2 is not expressed constitutively (i.e in basal condition), but only after
tissue damage and inflammation. But recent evidence has shown that COX-2 is expressed constitutively
in human kidney and CNS. Their use in the post-operative setting is yet to be fully evaluated.

viii. Local anesthetics-

Local anesthetics can be used in a variety of ways to provide analgesia in the post-operative period
from wound infiltration to administration via an epidural catheter. Local Anesthetics act on sodium
channels to inhibit transmission of impulses along peripheral nerves but all excitable tissues can be
affected and if sufficient amounts enter the circulation toxic effects will be seen. Many studies have
shown the benefit of local anesthetic wound infiltration in minor surgical procedures in terms of
improved analgesia, better pain scores and reduced opioid consumption when compared with placebo.
Long acting local anesthetics are preferred e.g. Bupivacaine since they produce longer analgesia. In
contrast, studies involving major abdominal surgery, demonstrate minimal, if any, benefit over placebo.

ix. Epidural

Epidural analgesia is produced by the administration of appropriate drugs into the epidural space
just outside the dural sac usually via an indwelling catheter. Local anesthetic, opioid or a combination of
both can be used to provide epidural analgesia. This allows improved mobilization and activity and
earlier return to normal functioning which should be the aim of post-operative analgesia. Adverse
effects depend on the drug used. Hypotension, motor block and urinary retention are the major adverse
effects associated with this technique.

x. Nerve blocks-

Peripheral nerve blocks such as the ilioinguinal block for hernia repair are relatively easy to perform
and can provide effective post-operative pain relief. Peripheral nerve block can be used alone or more
commonly is conjunction with other analgesics as part of a balanced analgesic technique.

xi. Nitrous oxide-

The old laughing gas is available with 50% oxygen in premixed cylinders. It is a potent analgesic,
probably superior to the opioids in the control of acute somatic pain such as when drain tubes are
removed or dressings changed. Of course, it must be breathed for a sufficient time (at least 5 minutes)
to establish analgesia.

xii. NDMA antagonists-

The activation of amino acids (glutamate) of spinal cord dorsal horn N-Methyl-D-Asparate(NMDA)
receptors antagonist. Low dose subcutaneous or intravenous Ketamine infusion (5-15mg/hr) produces
significant pain relief after surgery. Unfortunately the side effect of ketamine, including hallucination
limits its use.
Non pharmacological interventions-

A careful explanation of what the patient can expect to experience after the operation can
significantly reduce morphine requirements. Other simple measures which reduce pain include ensuring
a comfortable well supported position in bed and splinting the extremities. Relaxation therapy,
acupuncture and transcutaneous electrical nerve stimulation9TENS) also reduced analgesic
requirements, but by themselves are usually inadequate for post-operative pain. Hypnosis is effective in
some, nut is very time consuming. Operative neurolysis (e.g. cryotherapy) can be very effective, but
recovery of nerve function is slow and neuralgias may follow.

Inference

The relationship between good quality analgesia and improved surgical outcome has not yet
been conclusively demonstrated. However, the relief of pain and suffering are fundamental aspects of
patient care and we are to improve post-operative pain management we should treat this subject
seriously and give to it the time and energy it deserves.

Caudal Anesthesia
Caudal epidural anesthesia is one of the most commonly used regional techniques in pediatric
patients. It may also be used in anorectal surgery in adults. The caudal space is the sacral portion of the
epidural space . Caudal anesthesia involves needle and/or catheter penetration of the sacrococcygeal
ligament covering the sacral hiatus that is created by the unfused S4 and S5 laminae.

Adult caudal blockade has fallen from favour in the anesthesia community. The majority of
anesthesia provider use lumbar epidurals and spinals for surgeries that can be done with confidence by
anesthetists who are willing to learn the anatomy, basic skills, and limitations entailed in this lost
technique.

Anatomy

The sacrum is a triangular bone that is composed of five fused sacral vertebrae. It articulates
with lumbar spine superiorly, the iliac bones laterally, and the coccyx inferiorly. The lack of fusion or the
absence of the S4 and S5 laminae gives rise to the sacral hiatus between the sacral cornua. This area is
covered posteriorly by the dense sacrococcygeal ligament that is formed from the supraspinus and
interspinus ligament, “as well as the ligamentum flavum.” Penetration of this inverted V-shaped
ligament by a needle provides direct access to the caudal limit of the epidural space in the sacral canal.
It is in the area where there is considerable variation in the normal anatomy of adult patients.
The contents of te sacral canal

The contents of the sacral canal

The sacral canal contains the terminal portion of the dural sac, which typically ends cephalad to
a line joining the posterior superior iliac spines, or S2, the anterior and posterior divisions, and the
dorsal root gangli of the sacral nerves. The sacral canal contains a venous plexus and some loose fat and
areolar tissue.

Anatomical abnormalities of the sacrum

i. Upward and downward displacement of the hiatus

ii. Pronounced narrowing or partial obliteration of the sacral canal, making needle insertion
difficult.
iii. Ossification of the sacrococcygeal membrane.
iv. Dural extension to the level of the 3rd sacral vertebra.
v. Dural extension to the level of the 3rd sacral vertebra.
vi. The hiatus may be of many different shapes, the extradural space below it may range from
being deep to excessively shallow.

Technique for performing caudal epidural

The technique of caudal anesthesia relies on the same four P’s as spinal anesthesia, with minor
modifications- Preparation, Position, Projection and Puncture.

Preparation-

Before commencing it is important to examine the patient, explain the procedure, and obtain
written consent. Patient should be fasted. All the relevant equipment’s, drugs and monitoring
instruments should be checked and an i/v infusion must always be inserted and a full aseptic technique
with cleansing of skin done before performing caudal block.

Position

Three positions are available for caudal anesthesia, with the prone position most often chosen
in adults, the lateral decubitus position in children, and the knee-chest position infrequently used. The
lateral decubitus position is used in children because it is easier to maintain block a patent airway in this
position than in the prone position, and the landmarks are more easily palpable than in adults.

When placing a patient in the prone position, a pillow should be inserted beneath the iliac crests
to rotate the pelvis and make cannulation of the caudal canal easier. An additional help is to spread the
lower extremities about 20 degrees with the heels rotated laterally, which minimizes gluteal muscle
contraction and eases needle insertion.

Projection and Puncture

Projection and Puncture

Caudal anesthesia requires identification of the sacral hiatus. The sacrococcygeal ligament (i.e.
extension of ligamentum flavum) overlying the sacral hiatus lies between the sacral cornua. To facilitate
locating the cornua, the posterior superior iliac spines should be located and, by using the line between
them as one side of an equilateral triangle, the location of the sacral hiatus should be approximated.

After the sacral hiatus is identified, the index and middle fingers of the palpating hand are
placed on the sacral cornua, and a 21 gauge hypodermic needle or 22 gauge canula is inserted at an
angle of approximately 45 degrees to the scrum. While advancing the needle, a decrease in resistance to
needle insertion should be appreciated as the needle enters the caudal canal. The needle is advanced
until bone (i.e. dorsal aspect of the ventral plate of the sacrum) is contacted and then slightly
withdrawn, and the needle is redirected so that the angle of insertion relative to the skin surface is
decreased.

In male patients, this angle is almost parallel to the coronal plane; in female patients, a slightly
steeper angle (15 degrees) is necessary. During redirection of the needle and after loss of resistance is
again encountered, the needle is advanced is not attempted because dural puncture and unintentional
intravascular cannulation become more likely. The needle should be aspirated looking for CSF or blood,
if negative aspiration proven, injection is performed.

Confirmation of needle placement

The classic “pop”, felt as sacrococcygeal membrane is pierced is usually sought for proper caudal
needle placement. The absence of subcutaneous bulging and the lack of resistance upon injection of
local anesthetic are additional signs of proper needle placement, Aspiration of the needle should be
clear of blood and CSF and a negative response to a test dose of epinephrine should be also used to rule
out intrathecal and intravascular placement, Other tests to confirm proper needle placement include
the “whoosh” test, and the use of nerve stimulation The “whoosh” test requires the injection of 2.5 ml
of air through the caudle needle , with a “whoosh” being heard with a stethoscope placed over the
thoracolumbar spine. However, this can lead to a patchy block. More importantly, it can cause a venous
air embolism if the needle is inserted into epidural vessels especially in small infants. The “whoosh”
technique avoids these problems by injecting local anesthetic or saline in place of air but the benefit of
confirming needle placement prior to local anesthetic injection is lost. Excessive saline injection may
dilute subsequent local anesthetic injections and lead to an adequate block.

Factor affecting the duration of block

 Dose of the drug

 Concentration of the anesthetic drug.
  Types of drug used- Bupivacine has prolonged block than lignocaine.
 Added vasoconstrictors increase the duration by 10-50%

Dose and duration

According to the text book of anesthesia by Aitkenhead-lidocaine2% with oe without adrenaline

and bupivcine 0.5% are suitable agents. In an adult 10 ml of solution block anal sensation consistently
within 15-20 minutes.

Indications

Caudal blockade can be used whenever the surgical area is primarily innervated by the sacral
and lower lumbar nerve roots. The following procedures are appropriate for caudal blockade:

1. Anal surgery, especially hemorrhoidectomy and anal dilation.

2. Surgery on the vulva and vagina.
3. Surgery on the scrotal skin and penis.
4. Surgery on a lower limb.
5. Obstetric analgesia for 2nd stage of instrumental delivery.
6. Frequently used in post-operative analgesia in children (e.g. after circumcision and
orchidopexy).

Contraindications

1. Patient refusal.
2. Infection near the site of injection.
3. Coagulopathy.
4. Pilonidal sinus.
5. Congenital abnormalities of the sacrum cause unclear or impalpable anatomy.

Complications

 Intravascular or intraosseous injection. This may lead to grand mal seizures

and/or cardio-respiratory arrest.
 Dural puncture- Extreme care must be taken to avoid this as a total spinal block
will occur if the dose for ta caudal block is injected into the subarachnoid space.
If this occurs then the patient will become rapidly apneic and profoundly
hypotensive.
 Perforation of the rectum.
 Sepsis- This should be a very rare occurrence if strict aseptic procedures are
followed.
  Urinary retention.
 Hematoma.
 Puncture of fetal head during obstetric analgesia.
 May cause temporary inability to ejaculate in male patient.

The adult caudal block has specific indications and distinct advantages compared to other
regional techniques. It can be performed with great success when there is knowledge of the pertinent
anatomy and the practical experience to go along with it. Once these two factors have been mastered,
the use of a caudal block in adult patients can become a welcome addition to the anesthetist’s
repertoire of anesthesia techniques.