PAIN
1. Explain the Gate-Control theory of pain.
Pain is an unpleasant sensory and emotional experience that is associated with
actual or potential tissue damage, or described in terms thereof. Tissue injury
is detected peripherally by nociceptors and transmitted via small C fibres
(slow pain i.e. pressure) and small Aδ fibres (fast pain, i.e. sudden heat) to the
CNS where it is interpreted and perceived by the brain. It is suggested that
within the CNS are circuits that modulate incoming pain information; the gate
control theory is one such example.
In the mid-1960s, Melzack and Wall proposed a theory that the transmission
of a peripheral painful stimulus to the CNS occurs via a ‘gate’ at the spinal
cord level. The concept is that a non-painful input closes the ‘gate’ to the
painful input, thereby preventing further transmission of the painful stimulus
and suppressing the perception of pain. The gate is thought to be an inhibitory
interneuron in the substantia gelatinosa of the dorsal horn of the spinal cord.
It can be stimulated or inhibited pre-synaptically by different non-noxious
afferent inputs, e.g. touch or vibration sensation via Aβ fibres.
Clinical applications of this theory include the use of neuro-modulatory
techniques for chronic pain, such as transcutaneous electrical nerve
stimulation (TENS) and spinal cord stimulators. TENS units produce two
different current frequencies below the painful threshold in order to produce
analgesia via the gate control theory mechanism. Following on from the
TENS system, Shealy and colleagues proposed the use of spinal cord
stimulators to produce a similar effect and they have been used in neuropathic
pain, complex regional pain syndrome, angina pectoris and peripheral
vascular disease.
2. Describe the anatomy of the Coeliac plexus.
The coeliac plexus, also known as the Solar plexus, is the largest sympathetic
plexus. It supplies the upper abdominal organs. The coeliac plexus is
retroperitoneal and anterior to the abdominal aorta at the root of the coeliac
artery - 𝐿1 (𝑇12 − 𝐿1 ).
It originates from the coeliac ganglia, the left and right closely related to the
crura of the diaphragm. These ganglia are formed bilaterally from the greater
splanchnic nerve (𝑇5 -𝑇9/10 ), the lesser splanchnic nerve (𝑇10/11 ) and least
splanchnic nerve (𝑇11/12 ).
The relations of the coeliac plexus are;
- Posteriorly – abdominal aorta
- Anteriorly – pancreas, stomach and omental bursa
- Laterally – adrenal glands, inferior vena cava
- Superiorly – crura of the diaphragm
3. Describe the technique of the Coeliac plexus block. What are its
indications?
 Take informed consent and, as with all major nerve blocks, secure
intravenous access and the help of a skilled assistant.
 Intra-venous fluids are required pre-block to reduce the risk of hypotension
after the procedure.
 There are three popular approaches:
o The retro-crural (classic) approach
o The antero-crural approach
o Neurolysis of the splanchnic nerves
 The block is performed using a C-arm with contrast, intravenous sedation,
local anaesthetic infiltration of the superficial layers, with the patient in the
prone position.
 It normally takes two needle insertions, one on each side to block both of the
coeliac ganglia, but on some occasions good spread to both sides is achieved
just using a single injection.
 The needle entry point is just below the tip of the 12th rib 5-7cm from the
midline.
 Using X-ray screening in two planes, the tip of the needle is then directed
toward the body of L1 for the retro-crural and antero-crural approaches and to
the body of T12 for neurolysis of the splanchnic nerves.
 The needle is withdrawn slightly and then redirected forwards until it is in the
area of the coeliac plexus, avoiding the aorta and inferior vena cava. Radioopaque dye is injected to confirm the correct placement of the needle, and then
the appropriate mixture is injected:
- For non-malignant pain: 10 ml 0.5% chirocaine on each side
- For malignant pain: 5 ml 6% aqueous phenol + 5 ml 0.5% chirocaine
on each side
 CT and ultrasound facilitate a transabdominal approach in patients who are
unable to tolerate either the prone or lateral decubitus position or if the liver
is so enlarged that a posterior approach is not feasible.
As the block causes dilatation of the upper abdominal vessels, venous pooling can
occur, leading to hypotension. This can be exacerbated by pre-existing dehydration,
hence the need for IV hydration before performing the block.
Indications
- For relief of pain from non-pelvic intra-abdominal organs.
o Acute pain - may be performed during surgery for postoperative pain
relief.
o Chronic pain - useful for any condition that causes chronic severe upper
abdominal visceral pain - e.g. chronic pancreatitis (local anaesthetic blocks
only).
o Cancer pain - useful for upper abdominal organ cancer pain, and is
frequently used for carcinoma of the pancreas - initial diagnostic local
anaesthetic block, followed by neurolytic block.
4. Outline the options for postoperative analgesia in a 71/M who is S/P
pneumonectomy for adenocarcinoma of the lung.
Thoracotomy is among the most painful of all operative procedures. Good
analgesia is essential not only for obvious compassionate reasons, but also
because hypoventilation due to pain may increase the risk of postoperative
pulmonary complications.
- Systemic opioids: Systemic opioids remain the mainstay of post-thoracotomy
analgesic techniques. Their major clinical limitation is a narrow therapeutic
window. It is important to appreciate that the inter-individual variability in opioid
requirement following thoracotomy varies by a factor of up to ten. Hence Patient
Controlled Analgesia (PCA) is the preferred technique, after adequate loading
has occurred. However, a well-controlled opiate infusion may provide
comparable analgesia.
- NSAIDS:
NSAIDs
have
opioid-sparing
benefits
when
commenced
postoperatively. They do not produce respiratory depression and with short-term
use, complications such as gastrointestinal bleeding and renal dysfunction are
rarely a problem.
- Epidural analgesia: A wide variety of epidural techniques have been trialled,
including lumbar versus thoracic, local anaesthetic alone versus opiates alone and
in various combinations. Thoracic epidural infusions of opiates appear to be more
effective than lumbar, especially for relatively non-lipophilic opiates such as
pethidine. Highly lipophilic opiates may cause acute respiratory depression due
to systemic absorption; several studies have demonstrated that epidural
administration of fentanyl may be equivalent to the intravenous route.
Hydrophilic opiates such as morphine have the potential to produce delayed
respiratory depression due to rostral spread to the brainstem. Thoracic local
anaesthetic infusions are ineffective as sole agents and are associated with an
unacceptably high incidence of hypotension and excessive motor block. Thoracic
epidural combinations of dilute local anaesthetic and opiates have recently
become popular, although some studies show no benefit from the addition of
local anaesthetic compared with opiates alone.
- Intercostal nerve blocks: Intercostal nerve blocks performed intraoperatively are
of benefit for a short period immediately postoperatively. Sustained benefit can
be obtained by the use of local anaesthetic infusion into intercostal catheters
placed under direct vision above and below the incision prior to wound closure.
- Interpleural analgesia: Interpleural analgesia is performed by directly infusing
local anaesthetic into the pleural cavity. It is of limited value following
thoracotomy in adults. Analgesia is unreliable and loss of local anaesthetic occurs
through the chest drain.
- Cryo-analgesia: Cryo-analgesia of intercostal nerves performed prior to wound
closure produces intercostal blockade lasting several months. Despite the
theoretical attractions, in one of the few controlled trials of the technique it did
not produce improved pain scores or respiratory function. In addition, cryoanalgesia may lead to the development of intercostal neuralgia.
5. What is the mechanism of action of gabapentin and when may it be useful
in the management of chronic pain?
Gabapentin is a gabapentinoid, or a ligand of the auxiliary α2δ subunit site of certain
voltage-dependent calcium channels (VDCCs), and thereby acts as an inhibitor of
α2δ subunit-containing VDCCs. There are two drug-binding α2δ subunits, α2δ-1
and α2δ-2, and gabapentin shows similar affinity for (and hence lack of selectivity
between) these two sites. Gabapentin is selective in its binding to the α2δ VDCC
subunit. Despite the fact that gabapentin is a GABA analogue, and in spite of its
name, it does not bind to the GABA receptors, does not convert into GABA or
another GABA receptor agonist in vivo, and does not modulate GABA transport or
metabolism. There is currently no evidence that the effects of gabapentin are
mediated by any mechanism other than inhibition of α2δ-containing VDCCs. In
accordance, inhibition of α2δ-1-containing VDCCs by gabapentin appears to be
responsible for its anticonvulsant, analgesic, and anxiolytic effects.
Neuropathic pain comes from damaged nerves. It is different from pain messages
that are carried along healthy nerves from damaged tissues. Neuropathic pain is often
treated by different drugs to those used for pain from damaged tissue, which we
often think of as painkillers. Medicines that are sometimes used to treat depression
or epilepsy can be effective in some people with neuropathic pain. One of these is
gabapentin. Gabapentin at doses of 1800 mg to 3600 mg daily can provide good
levels of pain relief to some people with postherpetic neuralgia and peripheral
diabetic neuropathy. Evidence for other types of neuropathic pain is very limited.
The outcome of at least 50% pain intensity reduction is regarded as a useful outcome
of treatment by patients, and the achievement of this degree of pain relief is
associated with important beneficial effects on sleep interference, fatigue, and
depression, as well as quality of life, function, and work.
6. Define the following terms
a. Nociception - Refers to the processing of a noxious stimulus resulting in the
perception of pain by the brain.
b. Allodynia - refers to central pain sensitization (increased response of neurons)
following normally non-painful, often repetitive, stimulation.
c. Hyperalgesia - is an abnormally increased sensitivity to pain, which may be
caused by damage to nociceptors or peripheral nerves and can cause
hypersensitivity to stimulus.
d. Neuropathic pain - is pain caused by damage or disease affecting the
somatosensory nervous system.