PAIN MANAGEMENT Show Final Objective: On completion of this module you will be able to evaluate and manage acute and chronic pain. Enabling Objective: To achieve this goal, you should be able to:
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Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage. (IASP) Pain is subjective and multi-dimensional. It can be divided into four categories: nociception, pain, suffering and pain behaviour. Nociception is the detection of tissue damage by receptors and the transmission of this information to the central nervous system. Pain is the perception and interpretation of this information within the brain. Suffering is the negative response to pain and other emotional events such as fear, anxiety, isolation or depression. Pain behaviour is the person’s response to pain that can inform others that the person is suffering from noxious stimuli. DEFINITIONS Allodynia Pain due to a stimulus that does not normally provoke pain. The stimulus may be mechanical or thermal. Analgesia Absence of pain in response to a stimulus that would normally be painful. Causalgia (Complex Regional Pain Syndrome type 2) A syndrome of constant burning pain and allodynia and hyperpathia (greatly exaggerated pain sensation) following nerve injury. It is often combined with vasomotor and sudomotor dysfunction followed by trophic changes. Central Pain Pain caused by a lesion or dysfunction of the central nervous system. Dysesthesia An unpleasant abnormal sensation. It can occur in response to a stimulus or without a stimulus. Hyperalgesia An increased response to a stimulus that is not normally painful. Hyperesthesia An increased sensitivity to stimulation, excluding the special senses. It includes allodynia and hyperalgesia Hyperpathia Abnormally painful and exaggerated reaction to a stimulus, especially repetitive, where the stimulus is perceived initially less intense. Neuralgia and neuropathic pain Pain initiated or caused by a primary lesion or dysfunction of the peripheral or central nervous system. Nociceptor A receptor preferentially sensitive to a noxious stimulus. Pain Threshold The least experience of pain that a person can recognize. Paresthesia An abnormal sensation, spontaneous or evoked. It is not unpleasant. Peripheral sensitisation A reduction in the threshold and increase in the responsiveness of the peripheral terminals of nociceptors such that the terminals are activated by non-noxious stimuli, and noxious stimuli evoke a greater response. Inflammatory mediators drive this and all forms of tissue injury and inflammation generate peripheral sensitisation. Central sensitisation Nociceptive neurons in the dorsal horn of the spinal cord become sensitised by peripheral tissue damage or inflammation and are hyper excitable so that normal inputs produce abnormal responses. The increased excitability is triggered by a burst of activity in the nociceptors which then alter the strength of the synaptic connections between the nociceptor and the neurons of the spinal cord. PHYSIOLOGY AND ANATOMY OF PAIN Nociceptive Pain Nociceptive pain is caused by mechanical, inflammatory, chemical or thermal stimuli at the somatic or visceral tissue nociceptors. Injury leads to the release of pain producing chemicals that cause vasodilation, inflammation and oedema. Chemical and mechanical stimuli activate peripheral sensory organs, which are free nerve endings, also called the nociceptors. The nociceptors are widely distributed throughout the body. An electrical signal is generated that is conducted by primary afferent nerve fibres (A-delta and C fibres) to the cell bodies of these nerves in the dorsal root ganglia and then into the spinal cord. The central terminals of the C and A delta fibres project to the dorsal horn of the spinal cord where the signal is modulated before ascending in the spinothalamic tract to the brain stem and brain. Potassium ions, prostaglandins and bradykinins are released from damaged tissue and substance P is released from nerve endings. Vasodilatation and oedema leads to the release of more bradykinins, leukotrienes, histamine, serotonin and noradrenaline from vessels in the area of injury. These chemicals can modify the sensitivity of nociceptors and cause primary hyperalgesia, which is an increased response to a painful stimulus, leading to allodynia. Once the nociceptors have been activated, the sensory impulses travel to the central nervous system via myelinated A-delta fibres and unmyelinated C fibres (primary afferent fibres). The small myelinated A-delta fibres carry the initial response to pain, and the slower, unmyelinated C fibres carry the prolonged nociceptive impulses that continue after the injury occurs. These primary afferent terminals contain excitatory neurotransmitters such as glutamate, aspartate and substance P. After tissue damage occurs, if there is constant uncontrolled pain transmission to the CNS, there can be sufficient changes in nerve function that results in the touch and pressure impulses transmitted via the A-beta fibres being interpreted as painful. When the nociceptive neurons (primary afferents) enter via the dorsal horn of the spinal cord, they synapse with interneurons, where they are subjected to modulating influences coming from higher centres. This supraspinal modulation involves the GABA (gamma-amino butyric acid), opioid, NMDA (N-methyl D-aspartate), noradrenergic and serotonergic receptors. Some nociceptive impulses pass directly to the anterior horn of the spinal cord, where they stimulate sympathetic neurons and release noradrenaline. Other impulses pass to the brain stem and brain to provoke pain behaviour. Neuropathic pain Neuropathic pain is due to a lesion or damage in peripheral nerves, nerve roots or within the central nervous system. It serves no adaptive function and is pathologic. Some examples of peripheral neuropathic pain include, diabetic neuropathy and carpal tunnel syndrome. Examples of central neuropathic pain include the syndromes associated with thalamic strokes and spinal cord trauma. The diagnosis of neuropathic pain is made when there are both positive and negative symptoms and signs. Positive symptoms include the presence of allodynia, hyperalgesia and dysesthesia. Negative symptoms and signs are loss of function such as sensory loss in a region of pain hypersensitivity, muscle weakness and absent reflexes. Unlike inflammatory pain, neuropathic pain causes alterations in nociceptive processing that persist long after the resolution of the initial insult to the nervous system. Dysfunctional pain Dysfunctional pain is defined as pain in the absence of an identifiable noxious stimulus, tissue damage, inflammation or lesion in the nervous system. The mechanisms involve abnormal function of the nervous system. Tension-type headache, fibromyalgia and irritable bowel syndrome are examples of dysfunctional pain. ASSESSMENT OF PAIN Assessment A proper assessment and measurement of pain is essential for diagnosis of the cause of pain, selecting the appropriate analgesic regime and for evaluation/modification of the therapy according to patient’s response. Methods of assessment must take into account the physiological, psychological and environmental factors that influence the pain experience. The assessment of pain must include a general medical history and physical examination, a specific “pain history” and an evaluation of associated disability. A complete pain history provides diagnostic clues that may distinguish different underlying pain states such as nociceptive or neuropathic pain. Measurement Pain is an individual, multi-factorial experience influenced by culture, previous pain events, mood, fear, anxiety, prognosis and the ability to cope. Hence, most measures of pain in clinical use are based on self-report. These measures have been shown to produce sensitive and consistent results if done properly. In certain situations self-reporting measures may not be suitable (for example, patients with cognitive impairment, reduced conscious states, children, language differences, inability to cooperate or severe anxiety). In these patients, other measures of pain assessment will be needed. Recording of pain aims to increase awareness and utilization of pain assessment. Regular and repeated measurements of pain as determined by duration and severity of pain, patient needs, type of intervention(s) and response to that intervention(s) may lead to improved pain management. Such measures should ideally include assessments of static (rest) and dynamic (on sitting, coughing or moving the affected part) pain. There are several methods used to measure the severity of pain. None are able to measure pain perfectly, as many patients are unable to assign a “number” to their pain. The scales are grouped into the uni-dimensional and multi-dimensional scales. The uni-dimensional scales include the Visual Analog Scale (VAS), Verbal Numeric Rating Scale (VNRS) and categorical scales (the Verbal Rating Scale or VRS and the Wong-Baker faces pain rating scale). These are able to measure the severity of pain, but cannot provide an accurate assessment of function. The VAS is a linear analog scale of 10 cm in length with one end marked “no pain” and the other end marked “worst possible pain”. The patient is asked to mark a point on the scale to indicate the severity of pain. The VAS is used in research, but less often in clinical practice. The VNRS is commonly used in clinical settings. The patient is asked to rate the pain out of a maximum score of 10. The faces pain rating scale is used for children aged over 5 or 6 years of age and those patients who cannot communicate well. Multi-dimensional scales include the McGill Pain Questionnaire and the Brief Pain Inventory. They are used to measure the subjective impact of pain on activity and functional capability. They are used for the assessment of complex pain problems and chronic pain. Children present a challenge due to the observer’s inability to distinguish pain and distress due to other causes such as hunger, separation and fear. Pain has the same negative effects in children as it does in adults. In the very young pre-verbal child, the signs of pain are increased blood pressure, increased heart rate, sweating, reduced oxygen saturation, crying and restlessness. The CHIPPS (Children and Infants Postoperative Pain Scale) uses some of these signs to score pain in the very young child. A score between zero and 2 is assigned to each of the following: crying, facial expression, posture of the trunk, posture of the legs and motor restlessness. This is an example of observational assessment as it involves the interpretation of pain behavior by a trained observer. Importantly, the inability to communicate does not mean that pain is absent. Any measurement of pain should be performed repeatedly in the acute setting. This improves pain management and allows one to assess the adequacy of analgesic therapy. ACUTE POSTOPERATIVE PAIN Effective pain management in the surgical patient helps to improve the quality of life for the patient, facilitate rapid recovery and return to full function and reduce morbidity. Acute pain is experienced immediately after surgery and typically, lasts up to seven days. Pain that lasts more than 3 months after the injury is classified as chronic pain. Acute pain is protective as it induces immobilization and allows healing. However, there are adverse effects of severe untreated acute pain including, cardiovascular side effects such as tachycardia and hypertension, increased oxygen consumption, sleep disturbance, emotional and physical suffering including cognitive dysfunction, impaired bowel movement, inability to cough and deep breathe (leading to atelectasis, retention of secretions and pneumonia) and deep venous thrombosis secondary to immobilization. The humoral stress response to pain can lead to hyponatremia secondary to excessive antidiuretic hormone secretion and to metabolic effects such as protein wasting. Untreated acute postoperative pain predisposes to the development of chronic pain and there is a risk of behavioural changes in children. Acute pain management for surgery begins intraoperatively. The anaesthetist should be aware that intravenous induction or inhalational anaesthetic agents do not produce analgesia. (With the notable exceptions of ketamine, which also has analgesic effects, and nitrous oxide, which contributes to intraoperative analgesia.) Adequate intraoperative analgesia will allow the patient to emerge from anaesthesia with less pain and make it easier to manage pain in the recovery room. The options for intraoperative analgesia include the administration of paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs) preoperatively, intraoperative opioids (including fentanyl for short low pain intensity procedures only and morphine for operations expected to produce pain well into the postoperative period), local anaesthetic infiltration and regional blockade. Different types of surgery produce different levels of pain and the pain experience is very individual. The anaesthetist should be aware that the same surgery might produce different degrees of pain and suffering in different patients. A multi-modal approach to the management of acute pain is desirable. Two or more analgesic agents that act by different mechanisms are used to achieve a greater analgesic effect without increasing adverse events that are associated with increased doses of single agents. For example, intravenous opioids can be administered in combination with non-steroidal anti-inflammatory agents (NSAIDs) and paracetamol to reduce the amount of opioid required. Balanced, or multi-modal analgesia is the method of choice for the management of pain wherever possible. Paracetamol and NSAIDs are used for low intensity pain, with opioids and/or local analgesia techniques being added for moderate and high intensity pain. Treatment options will vary according to the magnitude of postoperative pain expected following surgery. Mild intensity pain produced by operations such as inguinal hernia repair and diagnostic laparoscopy can be managed with paracetamol, wound infiltration with local anaesthetic, non-steroidal anti-inflammatory drugs (NSAIDs) (unless contraindicated), regional block analgesia and with a weak opioid. Small intravenous increments of a strong opioid in the recovery room may be required. Moderate intensity pain is produced by operations such as hip replacement, hysterectomy or jaw surgery and can be managed with paracetamol, wound infiltration with local anaesthetic, NSAIDs, and peripheral nerve block or opioid injection such as intravenous patient controlled analgesia with morphine (IV PCA). Severe intensity pain can be expected after operations such as thoracotomy, upper abdominal surgery, aortic surgery and knee replacement. It can be managed with regular paracetamol, wound infiltration with local anaesthetic, NSAIDs and epidural local anaesthesia or major peripheral nerve or plexus block or opioid injection (IV PCA). Acute pain can progress to chronic pain. Chronic post surgical pain is common (up to 30% for some procedures). The chronic pain can be severe and lead to significant disability. The risk factors for the progression of acute to chronic pain include the severity of pre and postoperative pain, intraoperative nerve injury and psychological vulnerability. Specific early interventions may reduce the incidence of chronic pain after surgery. PAIN RELIEVING MEDICATIONS The four main groups of analgesic drugs used to manage postoperative pain are: 1. Non-opioid analgesics 2. Weak opioids 3. Strong opioids 4. Adjuvant medications Opioids are the mainstay of acute pain treatment. They are used systemically alone or in combination with other analgesics. Higher doses are usually required in the first 24 - 48 hours after surgery when pain tends to be severe and patients are unable to tolerate oral medications. Opioids act on endogenous opioid receptors located in the spinal cord, brain and peripheral tissues. The three important receptor types are the mu, delta and kappa receptors. Potent opioid analgesics are mu-1 receptor agonists. The activation of mu receptors causes analgesia, euphoria, respiratory depression, nausea and vomiting, bradycardia, miosis, decreased gastrointestinal motility and dependence. The kappa and delta receptors also mediate analgesia. All opioids given in equianalgesic doses produce the same analgesic effect. They can be administered via different routes. The oral route is preferred when the patient is able to take oral medications. Morphine is a naturally occurring opioid. It is the most widely used opioid in the management of acute pain. The dose requirements of morphine vary with age, with the elderly requiring less morphine that the young adult. The average dose requirements of morphine for the first 24 hours postoperatively can be estimated using the formula 100-Age (in years). It is important to note that the dose requirements vary greatly between patients and the patient’s response to morphine should be monitored frequently. When establishing analgesia for acute severe pain, it is best given in small increments intravenously. The patient is reassessed every 3-5 minutes for degree of pain and sedation before further doses are given. For the patient less than 70 years of age, doses of 1 mg to 4 mg may be given intravenously until the patient is comfortable. The 4 mg dose is usually administered as the first dose, with 1-2 mg doses every 3-5 minutes thereafter until the pain has reached a tolerable level. It may take up to 15 minutes for morphine to reach its maximum effect, so the patient is observed closely during this time. The most worrisome effects of morphine are excessive sedation and respiratory depression, so it is important for a patient who is receiving intravenous boluses for acute pain control to be closely monitored. Where PCA morphine is unavailable, morphine can be very effectively administered as a subcutaneous bolus every 2 to 3 hours for acute pain once pain control is achieved in the recovery room following surgery. The dose requirements vary with age. The typical doses required are: Age (years) 20-39 40-59 60-69 70-85 >85 Morphine dose (mg) Morphine is metabolised to morphine-3-glucuronide and morphine-6-glucuronide in the liver. These are excreted by the kidneys and can accumulate in renal failure. M6G is analgesic and M3G may cause hyperalgesia, myoclonus and seizures with long-term morphine use. Morphine induces histamine release and rapid bolus injection may produce local erythema, hypotension and rarely, bronchospasm. It has a poor oral bioavailability, so the oral dose is 3 times the parenteral dose. Fentanyl is a synthetic opioid that is 50-80 times as potent as morphine. It is very lipid soluble and does not cause histamine release. It is used in doses of 2 mcg per kg intraoperatively for analgesia. The time to peak effect is 5 minutes after intravenous administration. Its short duration of action (30-60 minutes) makes it unsuitable for ongoing analgesia except when given via an IV PCA device or in combination with local anaesthetic agents in an epidural. Tramadol is a centrally acting analgesic with some mu receptor activity. Its analgesic effect is also due to its ability to inhibit noradrenaline and serotonin reuptake. It causes less sedation, respiratory depression and constipation than other opioids, but it can cause nausea and vomiting. It has significant drug interactions, and may induce the serotonin syndrome when given with selective serotonin reuptake inhibitors or tricyclic antidepressants. Tramadol can be given orally or as an injection. The doses are similar for both routes. The doses are 2-3 mg per kilogram as a loading dose, then 1-2 mg per kg (50-100 mg for adults) every 4-6 hours, up to 600 mg per day. The non-steroidal anti-inflammatory drugs inhibit cyclooxygenase, which is an enzyme in the arachidonic acid pathway that is involved in prostaglandin production. They act as analgesics and antiinflammatory agents. They are useful adjuncts in multimodal analgesic regimes. The NSAIDs have a ceiling effect for analgesia and are not sufficient to produce effective pain relief on their own after major surgery. (The ceiling effect refers to the property of increasing doses of a given medication to have progressively smaller incremental effect). There is no sedation or respiratory depression associated with the use of NSAIDs and they are very useful when combined with morphine, as they can reduce the requirement for morphine by 30-50%. The adverse effects of NSAIDs are due to the inhibition of the cyclooxygenase type 1 enzyme. This can result in gastrointestinal upset and peptic ulceration, decreased platelet aggregation and changes in glomerular filtration. Other side effects include a rise in blood pressure, fluid retention and precipitation of bronchospasm in asthmatics who are sensitive to aspirin. Diclofenac, ibuprofen and metamizole are examples of non-steroidal medications. Metamizole is no longer used in many countries due to its propensity to cause agranulocytosis. Diclofenac is given in doses of 25-50 mg 2 or 3 times daily. It reaches its peak effect in 2 hours. Ibuprofen takes 30 to 90 minutes to reach its peak effect and is given in doses of 200-400 mg every 6-8 hours. Paracetamol is an analgesic and antipyretic agent that has central and some peripheral action. It has few side effects and may be administered via the oral, rectal or intravenous routes. The time to peak analgesic effect is one to two hours. It is a weak analgesic and can be used on its own to treat mild to moderate pain. It is useful for treating moderate pain when combined with opioids. The dose of paracetamol in adults is one gram four times per day. The maximum dose in adults is 4 grams per day. In children over 3 months of age, the dose is 15-20 mg/kg every 6 hours with a maximum daily dose of 90 mg/kg per day. Toxicity related to paracetamol overdose can cause liver failure. It is more likely if there is a chronic illness or malnutrition. If overdose occurs, N-acetylcysteine is administered to prevent liver damage. Ketamine is a useful adjunctive medication in the management of acute pain, especially in the situation of acute opioid tolerance. Persistent pain may activate NMDA receptors in the spinal dorsal horn, producing central sensitisation (spinal cord neuron hyperexcitability, which leads to hyperalgesia and allodynia) and inadequate response to opioids. NMDA receptor antagonists such as ketamine may attenuate central sensitisation. By reducing central sensitisation, it can theoretically reduce the likelihood of developing chronic pain. Severe postoperative pain in an adult may be reliably treated with a loading dose of 0.5 – 1 mg/kg intramuscularly or 0.1 – 0.2 mg/kg intravenously plus an infusion at 0.1- 0.2 mg/kg/hr. PATIENT CONTROLLED ANALGESIA Patient Controlled Analgesia (PCA) involves the use of a pump with a microprocessor that can be programmed to allow the patient to self-administer a bolus dose of opioid medication upon pressing a button. The clinician programs the dose of medication and a lockout period is programmed so that it is not possible to administer another dose of opioid even after the button is depressed during the lockout period. The typical prescription for morphine is a one mg bolus with a five-minute lockout period. It is believed that a PCA device is safer than a morphine infusion, as there is no need to guess a patient’s opioid requirements. The patient themselves will deliver their own dose by activation of the button. If the patient is too sedated, they will not press the button for another dose of opioid. Use of a PCA allows for the safer administration of intravenous opioid and allows the patient to be “in control” of their own pain management. There are some limitations to the use of a PCA. The patient’s pain must be controlled well before a PCA device is used, as it will not be possible for the patient to administer a loading dose of medication to achieve rapid pain control using the typical prescription as described above. It is only a means of maintaining analgesia, not establishing analgesia. The patient is the only person allowed to activate the PCA; otherwise it is possible to overdose the patient on opioid medication. The intravenous line for the administration of PCA opioid should not be used for anything else. The patient’s pain score and sedation score needs to be carefully monitored. Other disadvantages of PCA is the expense of the equipment and syringes, the fact that the patient needs to be able to understand how to trigger the device, and the potential for overdose if there is incorrect programming or use of the device. INTRAVENOUS INFUSIONS OF MORPHINE After achieving control of acute pain with boluses of morphine, a steady plasma level of morphine can be maintained with the use of an infusion of morphine. This avoids the problem of high peak plasma concentrations and of the need to wait for the return of pain at the end of an intermittent dosing interval. A typical prescription for a young adult is 3-5 mg of morphine per hour via the infusion pump and much lower doses are required for the elderly (1 mg per hour). Importantly, it is important to closely monitor a patient on a morphine infusion and close observation for sedation and respiratory depression is required. This usually means that the patient needs to be nursed in a high dependency unit. If there is an inadequate rate of infusion, it is possible to administer an intravenous bolus to re-establish adequate analgesia and increase the infusion rate. If too high an infusion rate is used, respiratory depression and excessive sedation will occur. REGIONAL AND LOCAL ANAESTHETIC TECHNIQUES Regional techniques can stop pain transmission and are therefore an excellent way of providing acute pain relief, particularly in the postoperative setting. Local anaesthetics can be applied topically or injected subcutaneously to numb a small area, or they can be infiltrated into the surgical site or administered as a regional nerve block or major neuraxial block such as spinal or epidural analgesia. Regional techniques can reduce the prevalence of chronic postoperative pain. This is particularly true for epidural analgesia and thoracotomy pain. Epidural analgesia Epidural analgesia is a very useful technique for the management of severe postoperative pain. It provides superior analgesia for knee replacement, major abdominal and thoracic procedures. Patients who are having major vascular reconstructions obtain a benefit from the sympathetic block and vascular graft patency is improved. Epidural analgesia can reduce the stress response to surgery, decrease the amount of blood loss and help to prevent some postoperative pulmonary complications. The contraindications to epidural analgesia include: the patient’s refusal of the technique, coagulation disorders, systemic bacteraemia or infection at the potential insertion site and uncorrected hypovolemia. Relative contraindications include spine pathology and neurologic disorders. The epidural is inserted at the middle dermatomal level of the incision site. A loss of resistance technique is used to identify the epidural space and a catheter is threaded to allow for the ongoing administration of local anaesthetics and opioid medications. Local anaesthetics act by inhibition of nerve conduction via sodium channel blockade. In high enough concentrations, they will block autonomic, sensory and motor nerve fibres. The smaller fibres are most sensitive and therefore it is relatively easy to block autonomic (C fibres) and pain sensory fibres (A-delta and C fibres). By using low concentrations of local anaesthetics, a differential block may be produced. This means that the larger motor and touch fibres can be partially spared. The extent of the epidural block is measured by assessment of temperature sensation and monitoring the degree of motor block. The same nerve fibres carry temperature sensation as pain sensation. The dermatomes with decreased temperature sensation will also have decreased pain sensation. It is desirable to have minimal motor block. Checking for foot movement, movement at the knee and hip flexion assesses the degree of motor block. An increase in the extent of the epidural block without change to the infusion solution or bolus administration should prompt the clinician to suspect spinal cord compression from either an epidural or spinal abscess or haematoma. If this occurs, decompression surgery should be performed within six hours to avoid permanent paralysis. A bolus dose local anaesthetic will increase the degree of sympathetic block and cause vasodilatation in the anaesthetised areas. This may cause hypotension due to decreased venous return to the heart. After a bolus dose, the patient is observed for 20-30 minutes with regular (5 minutely) blood pressure and heart rate monitoring to detect hypotension. Hypotension may be corrected with an intravenous fluid bolus or vasoconstrictors. Opioid medications can be infused into the epidural space to act on the opioid receptors in the dorsal horn of the spinal cord. Opioids administered via the epidural space will also be taken up into the systemic vasculature and produce central effects, thus creating the potential for sedation and respiratory depression, particularly if they are used with other systemic opioids and sedative agents. The more lipid soluble opioids (such as fentanyl) will undergo more systemic absorption but the more water-soluble agents (such as morphine) will tend to diffuse into the cerebro-spinal fluid. They can both produce respiratory depression albeit via different mechanisms. The morphine may produce delayed respiratory depression via diffusion into the CSF to the ventricular system. Opioids can be used safely in epidurals so long as the patient is monitored for sedation and respiratory depression. The most significant complications of epidural block include: failed block, post-dural puncture headache, epidural haematoma (rare) and epidural abscess (rare). The benefits of epidurals include superior analgesia, reduced pulmonary complications, increased vascular graft patency, reduced incidence of myocardial infarction, less perioperative blood loss and earlier return of bowel function following bowel surgery. CHRONIC PAIN Chronic pain is defined as pain that persists beyond normal tissue healing time. It may result from persistent tissue damage and inflammation, leading to ongoing activation of the nociceptive pain pathways. Chronic pain may also result from neurologic injury (leading to neuropathic pain) or it may be a manifestation of abnormal function of the nervous system independent of peripheral pathology or lesions to the nervous system (dysfunctional pain). Nociceptive pain has a protective function but neuropathic and dysfunctional pain do not and in this case, the pain can be considered a disease. Pain hypersensitivity results from changes in the function, chemistry and structure of both the peripheral and central nervous system. As the initial injury heals or the inflammation resolves, the sensitisation normally resolves, but it can persist. Central sensitisation is a principal element of chronic pain syndromes. The assessment of chronic pain is based on a full pain history, clinical examination and investigations. An assessment of mood is important and may reveal depression that is related to the pain itself, the failure of diagnosis and treatment and the functional impact of the pain. An important question to ask is what the patient considers to be the cause of the pain. The pain history should include an assessment of the site, character, duration, exacerbating and relieving factors, pattern of physical activity and the impact of the pain, the effect on sleep, treatment, the effect on employment and relationships, past medical history and family history. Examination of the patient will involve a complete physical assessment. The area in question is examined for bony deformity and tenderness, joint swelling and limitation of movement, neurological function, muscle power, tone and tenderness, and the skin is examined for signs of sympathetic dysfunction such as temperature change, loss of hair growth, vascular changes and discolouration and disorders of sensation. The measurement of pain will not only measure severity, but the loss of function, and the effect on the patient’s life (including psychological effects). Many patients will have had multiple investigations that have not been able to find the cause of the pain. That does not mean that the pain is not real. The management of chronic pain usually requires multimodal therapies that are chosen on the basis of the underlying mechanisms. These therapies will include pharmacologic, behavioural, physical and procedural modalities. It is important to note that pain states will not necessarily be “cured” and that the aim of therapy is to control the pain and improve function. There are two categories of pharmacologic agents used for pain: the analgesics and the anti-neuropathic agents. The analgesics include the opioids, such as morphine and simple analgesics such as the NSAIDs and paracetamol. They are used according to the World Health Organisation analgesic ladder in a stepwise manner, starting with paracetamol and NSAIDs, then adding weak opioids and finally adding stronger opioids. It is desirable to use the oral route of administration. The anti-neuropathic agentsinclude the tricyclic antidepressants (which are first line agents for neuropathic pain), anti-epileptic agents and tramadol. Ketamine acts in nociceptive as well as neuropathic pain states. Combination therapy with more than one agent is usually required for the treatment of chronic pain states. Neuropathic pain does not respond to simple analgesics. In these patients, a tricyclic antidepressant it started, then an anti-epileptic followed by an opioid. Unfortunately opioids can induce hyperalgesia, pharmacologic tolerance, and other side effects. It is important to balance their side effects with their benefits. Initiation of therapy is usually with small doses (such as 10 mg of morphine orally every 4 hours) and increased according to effect (the dose is usually increased by 50% increments every 3 days). The aim is to maintain the dose at the lowest effective dose to minimise side effects. Once the required daily dose is established, the daily dose may be given as a long acting sustained release preparation two times per day. The sedative and respiratory depression produced by morphine may predispose to pneumonia. Non-pharmacological therapies are very important in the management of chronic pain. Modern pain rehabilitation aims to modify maladaptive behaviours, overcome psychosocial influences, allow restoration of function and improve coping skills. This usually involves physical therapy (exercise), cognitive behavioural therapy, relaxation and stress management and rehabilitation for the return to work. Chronic Pain Conditions Prolonged postoperative pain Chronic post surgical pain is common. It may be severe and may lead to significant disability. The risk factors that predispose patients to the development of chronic post surgical pain include the severity of pre and postoperative pain, intra-operative nerve injury and psychological vulnerability. Early analgesic interventions may reduce the incidence of chronic pain after surgery. Cancer Pain Cancer pain may be acute or chronic. It may have multiple mechanisms, particularly as disease progresses. It may have somatic, visceral or neuropathic components. Progressive tissue destruction will cause pain. There will be a significant psychological contribution to cancer pain that will be influenced by social, cultural and spiritual issues. Some treatments will include analgesia medications as already outlined, but chemotherapy, radiotherapy, surgery and invasive analgesic technique can be useful. The risks of escalating the doses of analgesics, particularly opioids, need to be balanced with the need for comfort and quality of life. Neuropathic Pain Neuropathic pain can be acute or chronic. It is pathological pain resulting from sustained transmission of pain signals in the absence of ongoing tissue injury or activation of pain sensitive afferent peripheral nerves. The clinical features of neuropathic pain include, decreased sensation or increased threshold for sensation, increased sensitivity to a stimulus, paraesthesia, dysesthesia, hyperalgesia, allodynia, hyperpathia and causalgia. Some peripheral neuropathies can cause pain and they include: diabetic peripheral neuropathic pain, HIV/AIDS related neuropathy, carpal tunnel syndrome, post-herpetic neuralgia, meralgia paresthetica, trigeminal neuralgia, and occipital neuralgia. Central pain is a deafferentation pain that can result from any lesion in the central nervous system. The onset of pain may be delayed by several months after the initial insult. The pain usually correlates to the anatomic sits of the causative lesion. The most common cause is stroke, but multiple sclerosis, brain abscess, encephalitis and tumours can cause central pain. Spinal cord central pain can result from spinal cord injury or other spinal lesions. Most commonly, cauda equina and central cord injuries cause pain. Some post surgical pain syndromes, complex regional pain syndrome types 1 and 2 and phantom limb pain (after amputation) are examples of neuropathic pain. Sympathetically maintained pain (Complex Regional Pain Syndrome CRPS) Nerves in damaged tissues appear to be very sensitive to sympathetic stimulation from noradrenaline released from the nerve endings and from circulating catecholamines. This pathophysiologic mechanism is marked by an improvement of pain when sympathetic blockade is performed. Complex regional pain syndrome is considered to be a neuropathic pain syndrome that is sympathetically maintained. There are two types of CRPS. It involves a limb in most cases with a history of noxious traumatic injury with or without nerve involvement. Direct injuries to the central nervous system may cause CRPS. The exact mechanism is not known. The diagnostic criteria are: 1. The presence of an initiating noxious event or cause of immobilisation. 2. Continuing pain, allodynia or hyperalgesia, with pain disproportionate to the inciting event. 3. Evidence of oedema, changes in skin blood flow or abnormal sudomotor (sweating) activity in the region of pain. 4. Diagnosis is excluded by the existence of conditions that would otherwise account for the degree of dysfunction. Type 1: Without evidence of major nerve damage Type 2: With evidence of major nerve damage SELF-ASSESSMENT QUESTIONS 1. Compare the different methods of evaluating acute pain. Which methods are appropriate for assess pain in children under the age of 3 years? 2. How do opioids work? 3. What are the consequences of severe acute postoperative pain after an upper abdominal procedure? 4. What are the advantages and disadvantages of epidural analgesia for major abdominal surgery? ASSIGNMENT Describe the pharmacology of morphine in detail. Discuss the place of morphine in the management of acute severe postoperative pain. Outline its advantages and side effects when used for severe acute pain. Briefly compare the pharmacology of morphine and fentanyl. PAIN MANAGEMENT CASE STUDIES Case 9.1 Tungaa is a 37-year-old mother of three who has come in for a mastectomy and axillary clearance. She is concerned about pain after her surgery. What are the options for pain management after a mastectomy? What is multi-modal analgesia? She receives a general anaesthetic and has been given fentanyl for intraoperative analgesia. After a two-hour procedure she wakes in the recovery room complaining of severe pain. How will you assess the severity of her pain? What other medications could you offer for management of her acute pain? The recovery room nurse is concerned about the fact that she has given Tungaa over 20 mg of morphine but that she is still complaining of pain. She appears drowsy but is still easily rousable. What is her sedation score? Is it reasonable to offer further doses of morphine for analgesia? Tungaa begins to vomit and states that she is very nauseated. How will you manage her nausea and vomiting? Case 9.2 A fifteen-year-old boy is brought to you hospital with a femoral fracture after falling off his horse. It has taken over two hours for the family to bring him to the hospital and he appears very distressed. Outline your initial management of his pain in detail. He will require surgery this afternoon. What anaesthetic will you offer him and why? After the anaesthetic he is suffering severe pain in the recovery room. You have already administered morphine, a non-steroidal analgesia agent and paracetamol. What other measures could you use to treat his pain?
A Fifty five year old smoker presents with chronic pain following his thoracotomy and pneumonectomy five years age. He describes severe chest wall pain that has a typical intercostal nerve distribution. What is neuropathic pain? Discuss the pathophysiology of neuropathic pain. What factors will increase the probability of developing neuropathic pain? Which medications may be useful in the management of neuropathic pain? Discuss their mechanisms of action. Which condition is heightened response that occurs after exposure to a noxious stimulus?Hyperalgesia. Hyperalgesia is an increased painful sensation in response to additional noxious stimuli.
What are the 3 types of pain?When describing pain, the types will fall into three categories: Nociceptive Pain, Neuropathic Pain and Mixed Pain.
What is chronic pain syndrome?Chronic or persistent pain is pain that carries on for longer than 12 weeks despite medication or treatment. Most people get back to normal after pain following an injury or operation. But sometimes the pain carries on for longer or comes on without any history of an injury or operation.
Which of the following is a physiologic response to pain?Physiological signs of pain may include: dilatation of the pupils and/or wide opening of the eyelids. changes in blood pressure and heart rate. increased respiration rate and/or depth.
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Which condition is a heightened response that occurs after exposure to a noxious stimulus?
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