**CCrISP Pain Notes**
An unpleasant emotional and sensory experience, associated with actual
or potential tissue damage, or described in terms of such damage.'
- ie the pt may suffer pain without tissue injury.
Somatic or visceral damage --> psychic experience of pain.
Arises from abnormal nerve activity.
Influenced by pts mind - memory, stress, malingering.
Transmission of information about noxious stimuli.
Involves four processes.
Free nerve endings are well distributed through body.
- absent from solid viscera but present in their capsules
- absent from serosa of hollw viscera, but present under epithelium and
A potential is generated proportional to intensity of stimulation
--> evokes an action potential if large enough.
Stimulation can be chemically
- H+, K+, bradykinins, serotonin.
- usually released from damagedcells
- or produced by inflammatory response
- H+ produced by ischaemia
PGs don't evoke pain, but facilitate response
- eg substance P, released in periphery when nociceptive nerves stimuli
- ther promotes vasodilation and enhances inflammation
Mechanical nociception is poorly understood
- occurs on stretching of collagen.
- involves deformation of a lattice of nerves when under tension.
2. Peripheral Transmission
Nociception is mediated by multi-function nerve
- carried by Ad or C neurones
Ad fibres normally carry mechanical stimuli
- low intensity felt as pressure
- higher as pain.
- increased frequency of discharge tells brain of pain
- Ad can also carry temperature sensation
- pain evoked with >45oC.
C fibres carry mechanical, thermal, chemical
- some responsive only in noxious range
- others activated by chemicals released by damage / inflammation
Nociceptive afferents enter cord by dorsal roots
- some do come in via ventral roots also.
- first distributed 1-3 levels rostrally and caudally in dorsolateral
- multiple collaterals then enter grey matter.
- ramify in lamellae I,II,III of dorsal horns
- undertake many simple or complex connections with interneurones and
second-order neurones in grey-matter.
- this is the first site of pain 'control'.
3. Central Transmission
Marginal neurones (large neurones in lamina I) are specialist
Wide-dynamic-range neurones (lamina V) transmit touch and pressure as
well as nociception.
- they synapse with interneurones in II and III from nociceptive
- they receive collaterals from posterior columns (non-noxious)
- hence they allow control.
Principle transmitters are glutamate and substance P
Receptors are AMPA, NMDA, NK-1
Glutamate acts on AMPA to produce brief depolarisation
- glutamates chief target however is NMDA but its Ca channel is blocked
- the previous AMPA stimulation removes the Mg
- this causes a strong depolarisation with Ca influx.
Substance P is very slow
- acts on NK-1 for a long strong depolarisation
- initiates intracellular events also (G-protein & phospholipase C
in cell membranes)
--> phosphatidyl inositol transformed to inositol triphosphate and
diaglycerol + Ca
- Ca translocates in cell membrane, facilitating NMDA receptor function.
- hence enhances effect of glutamate.
- diaglycerol, protein kinase and Ca also promote c- fos (a
- intracellular Ca & calmodulin & NADPH activates NO
All of these allows control:
- a small glutamate release will only activate AMPA
- NMDA is only activated after a sustained glutamate release
- only with prolonged glutamate release will substance P be active
--> strong and sustained response far outlasting the initial stimulus
--> CNS responds
The role of C-fos is poorly understood
- perhaps in chrnoic pain, c-fos activity causes hyperexcitability
NO causes hyperalgesia, spread beyond initial pain site.
Axons of marginal and wide-dynamic-range neurones leave the grey matter
- cross midline to anterior white commissure
--> anterolateral funiculus
- a minority also ascend ipsilaterally.
The anterior funiculus was previously known as the anterior &
lateral spinothalamic tracts
- now understood this segregation is nonsense
- touch and nociception is carried in both.
Ascending axons have two destination
- the neospinothalamic system relays to the ventral posterior
lateral (VPL) and central lateral (CL) nuclei of the thalamus.
- from the VPL nucleus info is carried to the parietal lobe
--> this conveys the locus of the stimulus.
- the CL nuclei projects to the reticular formation of the thalamus to
the limbic system
--> this evokes the aversive and emotional experience.
- the paleospinothalamic system relays to the reticular formation of
- principally the nucleus reticularis gigantocellularis
- collaterals from neospinothalamic system also meet here.
--> local projections effect modulation.
- ascending projections reinforce aversion to pain from CL nucleus.
Brainstem neurones exert a tonic inhibitory effect on the spinal cord
- prevents the spinal cord and CNS from becoming overloaded.
- allows transmission of important information only.
- noxious stimuli are important
- upon receiving nocicpetiv info, the nervous system dampens other
spinal info (through descending inhibition) to enhance the clarity of
the nociceptive info.
Ascending nociceptive axons activate the NRGC
--> activates the nucleus raphe magnus
--> and the periaqueductal grey matter
--> and other sites eg locus coeruleus and lateral medullary
reticular formation (LMRF)
- neurones desced to spinal cord from here
--> effect an inhibitory action on afferent traffic.
- negative feedback called 'centre-surround inhibition'.
- directed at segments adjacent to active segment
- hence enhancing the perception of the incoming signal.
- and thus the signal-to-noise ratio.
Neurones descending from the NRM use serotonin
- noradrenalin is used by locus coeruleus and LMRF.
- interneurones use enkaphalin and GABA
--> most analgesic tenchniques mimic these transmitters.
Pain transmitted by nerves not related to the actual source of pain.
The nociceptive system is poorly organised somatotopically.
- poor correlation between stimulation site and neurone transmitting
info about it in the CNS
Particularly true for deep tissue pain
- innervated in a convergent manner, so various sites converge on
synapse with same second-order neurone.
- many second-order neurones converge on the same third-order thalamic
--> hence parietal lobe can't specify site exactly.
- at best +/- 1 level of spinal cord accurate
--> parietal lobe instead registers pain as arising from among
tissues innervated by those segments of the spinal cord
Hence deep pain is perceived over a wide area with indistinct boundaries
- but centred over a particular region of the body.
Evolutionarily this makes sense
- an organism could not escape pain from pancreatitis or PUD
- but can from eg the skin
- hence redundant to wire nervous system to exact deep sources
Skin also has touch receptors so is generally very well localised.
- hence palpation allows the location of pain to be inferred from
relationship to skin
- but also blurs things a little by enhancing deep pain and modulation.
A pt reports a deep pain by indicating a certain body region.
The surgeon recognises the segments pertaining to that region.
Hence can form a differential diagnosis.
Hence a comprehensive knowledge of segmental innervation is required.
Segmental innervation is spread through intercostal spaces indicated by
Similar but without the help of ribs.
The lower six (bony) ribs point into abdominal region and respective
pass into ambomen also.
- hence umbilicus belongs to 10th rib as that is where it points.
- T7-T9 evenly dispersed between sternum to umbilicus
- T11-L1 are dispersed from umbilicus to pubis.
Report of pain
Pain felt in these regions relates to bones, joints, ligaments,
or viscera innervated by the spinal cord of same number.
Stomach: T5-6 (top)
Stomach: T6-10 (bottom)
Small bowel: T9-10
Bladder T11-L2? S2-4?
Ascending C.: T10
Transverse C.: T11
Descending C.: T12
Sigmoid C.: L1-2
Pain is not referred to dermatomes
- referred deeply to segments of the body wall or limbs
- in the thorax, the dermatome happens to correspond to the body wall
of same number.
- this is not true for the head or limbs.
Pain in any region does not imply relationship to underlying viscera.
- eg while pain of PUD is felt in epigastrium
- pain of t. colon is felt suprapubically
Segmental pattern is twisted and blended
Reasonable approximation can be made based on innervation of muscles
Pain caused by damage to the nerves of the noceceptive system.
Arises from axons of peripheral nerves.
Eg peripheral neuropathy, post-hepetic neuralgia or neuroma.
- incompletely understood.
- perhaps ectopic discharge in diseased axons or their cell bodies.
- or loss of inhibition in spinal cord.
- in neuromas, sprouts form from the nerve end and seek a target, if
don't they form a spontaneously active and sensitive tangle.
Second or third order neurones are oversensitive.
'Deafferentation' pain when they lose their accustomed afferent inputs
- eg brachial plexus avulsion.
- the nerve becomes unstable, discharging spontaneously
- pt reports pain from the segmental distribution.
Or thalamic pain due to infarction of cells inhibiting nociceptive
A concept, not an actual entity.
Assumes some pts experience pain due to mental influences, not
The biological basis for this cannot be tested.
A default diagnosis fraught with problems
- may reflect a lack of proper diagnosis
- or inability to determine true neurogenic or nociceptive pain.
- remember RA, UC, spinal cord injury pain and PUD have all been blamed
psychogenic states in the recent past.
Disease or injury
- treat cause
- NSAIDs (inhibit PGs from tissue damage)
- LA, neurotomy
- TENS works when electrodes interposed between source of pain and CNS,
distal upper limb lesions (otherwise ineffective)
- mode of TENS action thought to be stimulation of larger afferents
smaller nocicpetive afferents.
- spinal cord stimulation
- spinal opioids (interrupt transmission by mimicking enkephalin)
- opioids (reduce tonic descending inhibition, decreasing signal/noise
- tricyclics (?enhance inhibitory action of serotonin in the dorsal
- acupuncture (?diffuse noxious inhibitory control - the noxious needle
evokes widespread activation of descending inhibition, inhibiting
- cord/brain stimulation (signal corruption)
- ?NSAIDS (exert their major effect here)
- paracetamol (unknown but thought CNS)
- these two have similar efficacy for musculoskeletal disorders
CCrISP Pain Notes
Pain control is not only humanitarian
- pain--> sympathetic drive, vasoconstriction, increased O2 demand,
--> may promote MI, inhibits lung fx, promoting pneumonia
But pain is not all bad; an important stimulus for daily behaviour
Not to abolish pain, but to make people comfortable, and allow rapid
return to function.
1. Prevent it:
-avoid tension in surgical closure, prevent drains from pulling on
sutures, relieve urinary retention
- drugs are more effective at preventing pain than treating established
2. Recgnise new problems:
- escalating analgesia requirements are suspicious
- ischaemia, anastomotic leak, compartment syndrome and bleeding are
--> 'breakthrough' pain in a previously controlled pt is a surgical
complication until proved otherwise.
3. Manage expectations
- expectations of pts and staff are essential factors
- tell pts to expect pain, but it should be controlled.
4. Surgical considerations
- upper abdo incisions hurt more and cause more pulmonary disturbance.
- infiltrate long-acting local intra-operatively
- employ epidurals, caudal blocks, intercostal blocks, ilioinguinal
Role in the Pain Team
hospital should have an MDT pain team
- liase with them and be aware of protocols.
--> is pain relief contributing to poor progress?
--> is the method of analgesia inhibiting this pt?
Remember pain is often sedative
- these effects may last 3 nights post op.
- continue O2 for 72 hrs in high-risk pts after major surgery receiving
- it is more common that a pt slips into resp failure due to insufficient analgesia than oversufficient opioids.
- sedation is a much better indicator of impending opioid overdosage
- hypoxaemia may occur in the presence of normal RR
- assess the depth of respiration, rate, and check ability to cough.
- abg and sats are useful adjuncts.
- persistant tachycardia/hypertension may potentiate MI
- remember pts with
sympathetic blockade (epidural) are very sensitive to inadequate volume
replacement and should have losses quickly corrected.
--> accurate fluid balance charts are essential.
--> but have a high index of suspicion for concealed bleeding.
Declining GCS is an early marker of opioid toxicity.
Full Pt Assessment
- is adequate analgesia prescribed?
- is is being given?
- is the treatment appropriate?
- verbal, facial or physiology cues are good predictors of pain
- but remember in some people they can be way out.
Severity Scoring system
Record when pt taking deep breaths, coughing and moving
Verbal 0=absent; 1=mild;
2=discomfort; 3=distressing; 4=excruciating
Visual analogue scales
- can you move? cough?
Investigate and Plan
- resp fx is important: evaluate with ABG, CXRs, sputum culture
If pain relief is adequate, continue and review
- is it due to analgesia failure
- incorrect implementation of method chosen?
- surgical complications?
Managing Acute Pain
The Analgesic Ladder
- as pain escalates, so does support
- supplement, don't replace the lower agents
- use opioids by just one route at a time
- usually a regular balanced multimodal therapy is more effective than
a single agent.
Safe, effective if regular
- the basis of most regimens
Increasingly used to reduce opioid consumption
- often contraindicated in the critically ill due to gastric and renal
Gold standard in severe pain,
- codeine: weak analgesic;
same efficacy as paracetamol in clinical trials; profoundly
constipating, nauseating; but often useful in combination therapy
- tramadol: many opioid
effects but without resp/dependence effects; but markedly emetic in
- oral morphine:
bioavailability low, titrate to requirement; side effects same; start
with elixer, move to slow release tabs
- iv morphine: useful in
boluses to desired effect; 5mg initially, then 1-2mgs until controlled;
often 20-30mg may be needed in an average-sized pt; best to move to a
pca if ongoing requirement.
- im opioids: superceeded and
no longer used.
Occurs even at therapeutic doses, showing pCO2>40.
--> resp rate is easy to measure and it is extremely unlikely respiratory
depression will occur if rate says above 12/min
Nausea / vomiting
Distressing, common, dose-related
- there is little evidence that prophylactic antiemetics (maxalon,
cyclizine etc) have any
Treat with nalaxone increments of 100ug if hypoxic/over-sedated
- remember side effects, avoid rapid return of pain and remember short
"Patient Controlled Analgesia"
- reduces the fear of uncontrolled pain
- pts administer bolus doses (usually 1mg) until pain controlled
- a 'lock-out' time prevents over-administration
- well accepted, easy, effective, pt-centred, safe & may reduce
--> but at night they may wake with pain that takes a few pushes to
Blocks afferent pain pathways with local anaesthetic
- beware that many anaesthetists will not want to insert an epidural if
even one dose of clexane is given.
One dose is given in theatre
- then an infusion is established (bupivacaine 0.1-0.125% & an
opioid, eg fentanyl 2-4ug/ml
--> pain relief is desired, but with minimal sympathetic effects and
no motor block
1. Breakthrough pain
- a new surgical problem until proved otherwise.
- alternatively the pain team may have to review dose, placement etc.
- relatively common with epidurals, particularly in younger pts and
- due to sympathetic block and vasodilation
- exclude other causes before blaming the epidural
- correct and hypovolaemia
--> then correct with vasoconstrictors (anaesthetist domain)
Remember that this is more often produced by inadequate post-op analgesia than overuse.