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.
