Pain & Management PDF

Pain & Management Pain can be deﬁned as: An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. Acute pain may be thought of as a physiological process having a biological function, allowing the patient to avoid or minimize injury. Persistent pain, on the other hand, may be described more as a disease than a symptom. Aetiology and Neurophysiology Neuroanatomy of pain transmission The majority of tissues and organs are innervated by special sensory receptors (nociceptors) connected to primary afferent nerve ﬁbers of differing diameters. Small myelinated Aδ ﬁbers and unmyelinated C ﬁbers are responsible for the transmission of painful stimuli to the spinal cord where these afferent primary ﬁbers terminate in the dorsal horn. Neurotransmitters and pain Various neurotransmitters in the dorsal horn of the spinal cord are involved in pain modulation. These include amino acids such as glutamate and γ-aminobutyric acid (GABA), monoamines such as noradrenaline and 5-hydroxytryptamine (5-HT, serotonin) and peptide molecules, of which the opioid peptides are the most important. Opioid receptors are found in both the CNS and the periphery; in the CNS they are found in high concentrations in the limbic system, the brainstem and the spinal cord. The natural ligands (molecules that bind to the receptor) at opioid receptors are a group of neuropeptides including the endorphins. Opioid analgesics mimic the actions of these natural ligands and exert their effect through the μ, δ and, to a lesser extent, the κ receptors. These receptors mediate the analgesic effect of morphine-like drugs. Assessment of pain Evaluation of pain should include a detailed description of the pain and an assessment of its consequences. There should be a full history, psychosocial assessment, medication history and assessment of previous pain problems, & factors that inﬂuence the pain. Diagnostic laboratory tests, imaging, including plain radiography, computer tomography (CT) and magnetic resonance imaging (MRI), and Visual analogue and verbal rating scales are also used: Different questionnaires scales designed to evaluate the severity of pain (scores). Questionnaire help to describe other aspects of the pain, and pain diaries record the inﬂuence of activity and medication on pain. Types of pain Acute pain can be important for the body to tell the brain that there is something wrong and help to avoid harm. Chronic pain is pain that goes on for a long time. It needs regular assessment and a different approach to treatment Management Acute pain usually results from noxious stimulation as a result of tissue damage or injury. It can be managed effectively using analgesic drugs and is often self-limiting. Persistent pain may be considered as pain which continues beyond the usual time required for tissue healing. Treatment may involve specialist pain management services, and a multidisciplinary approach that assesses and Non-medical treatments Physical therapy and various psychological techniques including cognitive behavioural therapy may also form part of a multimodal treatment program. Pain can be modulated using non-pharmacological techniques: for example, stimulation produced analgesia such as transcutaneous electrical nerve stimulation (TENS), acupuncture and massage, or invasive procedures such as neurosurgery or neurolytic nerve blocks. Analgesic ladder The World Health Organization (WHO) analgesic ladder forms the basis of many approaches to the use of analgesic drugs. There are essentially three steps: non-opioid analgesics, weak opioids and strong opioids. The analgesic eﬃcacy of non-opioids, such as paracetamol and non-steroidal anti-inﬂammatory drugs (NSAIDs) (e.g. aspirin, ibuprofen and diclofenac), is limited by side effects and ceiling effects, that is, beyond a certain dose, no further pharmacological effect is seen. If pain remains uncontrolled, then a weak opioid, such as codeine or dihydrocodeine, may be helpful. There may be additional beneﬁt in combining a weak opioid with a non-opioid drug. Strong opioids, of which morphine is considered the gold standard, have no ceiling effect and therefore increased dosage continues to give increased analgesia but side effects often limit effectiveness. Adjuvant drugs, such as corticosteroids, WHO analgesic ladder Analgesic drugs Paracetamol The mechanism by which paracetamol exerts its analgesic effect remains uncertain. Inhibition of prostaglandin synthesis within the CNS has been proposed. although this is probably not the only mechanism. Interaction with the serotonin and endocannabinoid neurotransmitter systems have been demonstrated in animal models. With normal doses, the majority of paracetamol are metabolized and inactivated in the liver, undergoing a phase II conjugation reaction with glucuronic acid. A small proportion of a dose is metabolised using a cytochrome P450 mediated reaction that forms a reactive intermediate, N-acteylp- benzoquinimine (NAPQI). Usually, NAPQI can be deactivated by conjugation with glutathione in the liver. However, following ingestion of a large amount of paracetamol the hepatic stores of both glucuronic acid and glutathione become depleted leaving free NAPQI, which causes liver damage. The usual therapeutic dose for adults is paracetamol 1 g taken four times daily. It is very important that this dose is not exceeded, otherwise hepatotoxicity is more common. Compared with other analgesics, paracetamol is not as potent; however, when taken in combination with a NSAID or opioid, there is an additive analgesic effect. Non-steroidal anti-inﬂammatory drugs NSAIDs exert their analgesic and anti- inﬂammatory effects through inhibition of the enzyme cyclooxygenase. NSAIDs are used widely to relieve pain, with or without inﬂammation, in people with acute and persistent musculoskeletal disorders. In single doses, NSAIDs have superior analgesic activity compared to paracetamol. In regular higher dosages, they have both analgesic and anti-inﬂammatory effects, which makes them particularly useful for the treatment of continuous or regular pain associated with inﬂammation. NSAIDs have been shown to be suitable for the relief of pain in dysmenorrhoea, toothache and some headaches and to treat pain caused by secondary bone tumours, which result from lysis of bone and release of prostaglandins. Differences in anti-inﬂammatory activity between NSAIDs are small, but there is considerable variation in individual patient response as well as the incidence and type of side effects. The potential treatment beneﬁts of an NSAID must be weighed against the risks. NSAIDs are contraindicated in patients with known active peptic ulceration and should be used with caution in the elderly and in those with renal impairment or asthma. COX-2 selective drugs COX- Cyclooxygenase exists in two forms: cyclo- oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2). COX-1 is a constitutive enzyme that is expressed under normal conditions in a variety of tissues, including the gastro-intestinal tract and kidney, where it catalyze the formation of prostaglandins required for homeostatic functions. It does not have a role in nociception or inﬂammation. COX-2 is an inducible enzyme that appears in damaged tissues shortly after injury and leads to the formation of inﬂammatory prostaglandins within these tissues. COX-2 selective NSAIDs should, theoretically, inhibit the formation of inﬂammatory prostaglandins without affecting the activity of COX-1 in areas such as the gut. In practice, use of COX-2 speciﬁc drugs is associated with reduced risks of gastro- intestinal side effects when compared with non-selective drugs. However, their use has also been linked with adverse effects including ischemic cardiac events and this may limits their use. Guidance on NSAID use Prescribing should be based on the safety proﬁles of individual, NSAIDs or COX-2 selective inhibitors, on individual patient risk proﬁles, for example, gastro- intestinal and cardiovascular. The lowest effective dose of NSAID or COX-2 selective inhibitor should be prescribed for the shortest time necessary. The need for long-term treatment should be Concomitant aspirin, and possibly other antiplatelet drugs, greatly increases the gastro-intestinal risks of NSAIDs and severely reduces any gastro-intestinal safety advantages of COX-2 selective inhibitors. Aspirin should only be co-prescribed if absolutely necessary. Opioids Potency (morphine = 1) Drug 0.1 Codeine 0.1 Dihydrocodeine 0.2 Tramadol 0.1 Pethidine 1 Morphine 2.5 Diamorphine 7 Hydromorphone )with repeat dosing (10–2 Methadone 150 Fentanyl (transdermal) Weak opioids Weak opioids are prescribed frequently, either alone or in combination with other analgesics, for a wide variety of painful disorders. There are three major drugs in this group, codeine, dihydrocodeine and dextropropoxyphene, which are recommended as step 2 of the WHO analgesic ladder for pain that has not responded to non- opioid analgesics. Codeine Codeine is the prototypical drug in this group. It is structurally similar to morphine and about 10% of the codeine is demethylated to form morphine. It is a powerful cough suppressant as well as being very constipating. In combination with NSAIDs, the analgesic effects are usually additive but the variability in response is considerable. Dihydrocodeine Dihydrocodeine is chemically similar to codeine. It has similar properties to codeine when used at the same dosage and may be slightly more potent. Dextropropoxyphene Dextropropoxyphene was prescribed in combination with other analgesics such as paracetamol (co-proxamol). It is associated with problems in overdose. Patients with hepatic dysfunction and poor renal function are particularly at risk. Strong opioids Morphine Morphine is the ‘gold standard’ strong opioid analgesic. It is available for administration by a range of administration routes, including oral, rectal and injectable formulations and has a duration of action of about 4 h after oral administration. There is no ceiling effect when the dose is increased, daily doses of up to 1 or 2 g of morphine may be required for some cancer Other strong opioids Pethidine and dextromoramide offer little advantage over morphine in that they are generally weaker in action with a relatively short duration of action (2 h). Dipipanone is only available in a preparation which contains an antiemetic (cyclizine), and increasing doses lead to sedation and the risk of developing a tardive dyskinesia with long-term use. Methadone has a long elimination half-life of 15–25 h,. It has minimal side effects with long-term use and some patients who experience serious adverse effects with morphine may tolerate methadone. Hydromorphone and oxycodone are synthetic opioids. Some patients appear to tolerate hydromorphone or oxycodone better than Fentanyl is available as a transdermal formulation for long-term use. The patch is designed to release the drug continuously over 3 days. Alternative analgesic therapy should be continued for at least the ﬁrst 12 h until therapeutic levels are achieved. Patches are replaced every 72 h. Agonist-antagonist and partial agonists Most of the drugs in this category are either competitive antagonists at the μ opioid receptor, where they can bind to the site but exert no action, or they exert only limited actions; that is, they are partial agonists. Those that are antagonists at the μ opioid receptor can play a role in withdrawal syndrome in patients receiving concomitant opioid agonists such as morphine. Buprenorphine is a semi-synthetic, highly lipophilic opioid that is a partial agonist at the μ opioid receptor and an antagonist at both the δ and κ receptors. It has high receptor aﬃnity and, through this property, a duration of action of 6 h. The long duration of action and high bioavailability would suggest a role for buprenorphine in the management of persistent pain. Pentazocine, a benzomorphan derivative, is an agonist and at the same time a very weak antagonist at the μ opioid receptor. It produces analgesia that is clearly different from morphine and is probably due to agonist actions at the κ-receptor. Tramadol is a centrally acting analgesic that has opioid agonist activity and also has potent monoamine reuptake properties similar to many antidepressants. It is not as potent as morphine and eﬃcacy is limited by side effects, including high risk of drowsiness and nausea and vomiting. Its monoaminergic activity appears to be valuable in the management of neuropathic pain and hence may be an acceptable alternative to a weak opioid. Adverse effects of opioids The adverse effects of opioids are nearly all dose related, and tolerance develops to the majority with long-term use. Respiratory depression is potentially dangerous in patients with impaired respiratory function, but tolerance develops rapidly with regular dosing. It can be reversed by naloxone (non-selective and competitive opioid receptor antagonist), and its binding aﬃnity is highest for the μ-opioid receptor, then the δ-opioid receptor, and lowest for the κ-opioid receptor. Nausea and vomiting Antiemetics should be co-prescribed routinely with opioids for the ﬁrst 10 days. Choice of antiemetic will depend upon the cause, and a single drug will be suﬃcient in two-thirds of patients. Where nausea is persistent, another antiemetic is used, it should have a different mode of action. Constipation Opioids reduce intestinal secretions and peristalsis, causing a dry stool and constipation. Unlike other adverse effects constipation tends not to improve with long-term use, and when opioids are used on a long-term basis most patients need a stool softener (e.g. docusate sodium) and a stimulant laxative (e.g. senna) regularly. Tolerance, dependence and addiction Persistent treatment with opioids often causes tolerance to the analgesic effect, When this occurs the dosage should be increased or, alternatively, another opioid can be substituted. Addiction is very rare when opioids are prescribed for pain relief. Smooth muscle spasm Opioids cause spasm of the sphincter of Oddi in the biliary tract and may cause biliary colic, as well as urinary sphincter spasm and urinary retention. Thus, in biliary or renal colic, it may be preferable to use another drug without these effects. Pethidine was believed to be the most effective in these circumstances but still with variable effect. Local anaesthetics Local anesthetic drugs, such as lidocaine and bupivacaine, produce reversible blockade of neural transmission in autonomic, sensory and motor nerve ﬁbers by binding to sodium Channels, preventing sodium ion entry during depolarization. The concentration of local anesthetic and dose used determine the onset, density and duration of the block. If the maximum dose is exceeded, serious cardiovascular and CNS effects (convulsions) may be Non-opioid analgesics Nefopam is a drug which is chemically related to orphenadrine and diphenhydramine. However, it is neither an opioid, anti-inﬂammatory drug nor an antihistamine. The mechanism of analgesic action remains unclear. As a non-opioid, it is not associated with the problems of dependence and respiratory depression. Nefopam may be useful in asthmatic patients and in those who are intolerant of NSAIDs Adjuvant medication In some types of pain, such as cancer pain or neuropathic pain, the addition of non-analgesic drugs to analgesic therapy can enhance pain relief. Antidepressants, anti-epileptics, intravenous anaesthetic agents, skeletal muscle relaxants, steroids, antibiotics, antispasmodics, hormones, bisphosphonates & others. Adjuvant drugs used in the treatment of pain Example Type of pain Drug class Carbamazepine Neuropathic pain Anti-epileptics Sodium valproate Migraine Gabapentin Cluster headache Pregabalin Lamotrigine Amitriptyline Neuropathic pain Antidepressants Imipramine Musculoskeletal Venlafaxine Duloxetine Ketamine Neuropathic pain Intravenous Burn pain anaesthetic Cancer pain agents Baclofen Muscle spasm Skeletal muscle Dantrolene Spasticity relaxants Botulinum toxin (type A) Example Type of pain Drug class Dexamethasone Raised intracranial Steroids Prednisolone pressure Nerve compression As indicated by culture and Infection Antibiotics sensitivity Hyoscine butylbromide Colic Antispasmodics Loperamide Smooth muscle spasm Calcitonin Malignant bone pain Hormones/ Octreotide Spinal stenosis hormonal Intestinal obstruction analogues Pamidronate Bone pain (caused Bisphosphonates (for cancer pain) by cancer or Alendronate osteoporosis) Headac he Headache is a symptom of which there are many causes. It is the most common pain compliant. The international headache society (HIS) classiﬁed headache into primary headache and secondary headache : 1-Primary headache disorders: which include migraine headache, tension headache and cluster headache Migraine headache and tension headache: Migraine headache: A dull ache that intensiﬁes over a period of minutes or hours to throbbing headache which worsen with each pulse. Pain usually suﬃcient to interfere with daily Headache is either unilateral (in about 70% but can change from side to side from attack to attack usually over the forehead) or bilateral Typically migraine attack last between a few hours and 3 days. Migraine may precipitated by stress, (e.g. pressure at work), or after a period of stress (in holiday or weekends), and it is about three times more common in women than in men and may be associated with menstrual cycle. Aura may present in about 25% of migraine: Visual disturbances (blind spots, photophobia, zigzag lines, ﬂashing lights) or neurological disturbances (paresthesia start in hand---go to arm------go to face and lips). Tension headache: A dull ,diffuse pain rather than throbbing. pain usually not suﬃcient to interfere with daily activities. bilateral headache which occur in a hatband distribution around the head (may be described as a band around the head). may last between a few hours and several days e.g. a week or more. not associated with nausea and vomiting. may occur during or after stress, fatigue, anxiety. Aura is not present Cluster headache: cluster headache involve (as its name indicate) a number of headaches one after one. It is a rare (around 0.24 % of the general population). It is more prevalent in men than women. Cluster headache is characterized by intermittent attacks of severe unilateral headache, accompanied by symptoms such as conjunctival congestion (red eye), lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis (small pupil), ptosis (droopy eye lid) and eyelid oedema. The headache is sudden in onset, frequently occurs around the eyes and is often described as a boring sensation. There are two forms of cluster headache: episodic and chronic. Episodic cluster headache is more common (80-90 per cent of patients) and is characterized by periods of headache lasting from weeks to months, interspersed by months to years of remission. In contrast, the 10-20 per cent of patients who experience chronic cluster headache has symptoms for more than one year with pain free periods of less than 14 days. 2-Secondary headache disorders: A-Sinusitis: Sinusitis may complicate respiratory viral infection (e.g. cold) the pain is felt behind and around the eye (orbital) and usually only one side is affected (unilateral), pain typically worsen by bending forward or lying down. And may be associated with rhinorrhoea or nasal congestion. B-Subarrachnoid hemorrhage: Which causes sever intense pain located in the occipital region. Nausea, vomiting and decreased consciousness is often present. C- Conditions causing raised intracranial pressure (e.g. brain tumor, haematoma, abscess) The pain is localized or diffuse but it is usually worse in the morning and improve during the day, worsen by coughing, sneezing, bending or lying down. After a period, neurological symptoms (nausea, vomiting, confusion decreased consciousness, diﬃculty with speech…) start to become evident. D- Temporal arteritis (usually occur in elderly): The temporal arteries -----can inﬂamed---may become red and painful to touch-----urgent referral (may lead to blindness). Note: these signs are not always present but unilateral pain is experienced and person generally feels unwell with fever, myalgia, and general malaise. E- Eye problems: Eye strain: headache associated with a period of reading, writing or other close work ----may be due to deteriorating eyesight -----in 1 st instance, patient should referred to optician for routine eye checking. Glaucoma: in which there is a frontal headache, with pain around the eye, blurred vision, cornea lock cloudy, and sometimes the eye appear red. F- Hypertension: Occasionally, headache is caused by hypertension, but contrary to the popular opinion----such headaches are not common and only occur when the BP is extremely high. G- Depression: Depression often present with tension –like headache---- -check for other symptoms of depression (loss of appetite, weight loss, sleep disturbances, and constipation). Patient assessment with Headache: The most common type of headache are tension headache, migraine and sinusitis. Careful questioning can distinguish causes that are potentially serious. Headache associated with menstrual cycle or certain* Frequency.times, e.g. weekend or holidays, suggest migraine :and timing Headache that occurs in clusters at same time / night *.suggests cluster headache Headache that occur on most days with same pattern*.suggest tension headache *lying down make cluster headache worse Trigger Food (in about 10% sufferers), menstruation, and*.relaxation after stress are indicative of migraine Pain that worsen on exertion, coughing or bending may *.suggests a tumor Typically migraine attack last between a few hours and 3 * Attack days duration Tension headache may last between a few hours and * several days e.g. a week or more.Cluster headaches last between 15 and 180 minutes (3 hours) * In early childhood or as young adult, primary headache* Onset of is most likely. After 50 years of age the likelihood of a headache.secondary cause is much greater Headache and fever at the same time imply an*.infectious cause Headache that follows a head trauma might indicate post- *.concussive headache or intracranial pathology Mild to moderate dull and band-like pain suggest tension * Severity of.headache pain Severe or intense ache or throbbing suggests haemorrhage *.or aneurysm Moderate to severe throbbing pain that often start as a dull *.ache suggests migraine.Piercing, boring, searing eye pain suggests cluster headache * Cluster headache is nearly always unilateral in frontal, * Location of.orbital or temporal pain Migraine headache is either unilateral(in about 70% but * can change from side to side from attack to attack Tension is often bilateral headache which occur in a hatband * distributionn around the head (may be described as a band.around the head)

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