Al-Azhar University GAZA Palestine Faculty of Medicine

Pain Management
Prepared by :
Ghady Shatat Fatma Shnewra Haneen Abu Aqlain Salwa Al-Khozendar

3nd year students

May , 2013
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Pain Management
What is pain?
Pain has been defined as: an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage American Pain Society (APS) has coined the phrase, Pain: the 5th vital sign.To underscore the importance of pain monitoring and management in patients.

Pain is completely subjective and cannot be proved or disproved. Pain is whatever the experiencing person says it is, existing whenever the experiencing person says it does . Pain is very complex. It is both a sensory and emotional experience.

Substances used in pain:

Neuroscientists know quite a bit about the mechanisms of pain. There are a number of things that promote pain : Substance P, Excitatory aminoacids, Prostaglandins, Kinins, Nerve growth factor, Cytokine, corticotrophin-releasing hormone. We know about elements that attenuate pain : Descending antinociceptive pathways, opioids and opioid receptors, gamma-aminobutyric acid (GABA), cytokines, and CRH.

Factors that Influence Pain perception

What is Pain perception defined as? The process by which pain is recognized and interpreted by the brain. Subjective and dependent on the conditioning of the individual. What are factors that influence perception of pain? Biological factors that can vary pain perception include the persons sex, genetics and number of nociceptors, or pain receptors in the body. Social and cultural factors influencing pain intensity might include an expectation that pain is something you just deal with (less likely to communicate pain) and an overly solicitous family caregiver (more likely to communicate pain). Some psychological issues that can worsen pain follow: Fear of pain, which can lead to a patient not moving, especially when a certain movement caused pain in the past Pain catastrophizing an inability to stop thinking about ones pain and to characterize pain as unbearable, which increases activity in areas of the brain related to anticipation of pain, according to several studies Negative affect (neuroticism) a more irritable or anxious personality, which may be a precursor to pain-related fear or catastrophizing Depression Emotional stress Gender and Genetics Types of pain: According to pain duration, There are 2 types of pain: Acute pain: It is relatively brief in duration(less than 30 day), and is usually due to trauma, surgical procedure, or a specific disease process.usually self limiting as the initial injury heal Increase ANS activity usually accompany acute pain (tachycardia ,tachypnea , HTN, mydriasis and diaphoresis)
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 Chronic pain: may last for years. It usually accompanies a chronic, persisting clinical entity -- rheumatoid arthritis, osteoarthritis, or back pain.. Chronic pain can be quite disabling, often preventing people from working and enjoying life. It can lead to people feeling isolated, angry, frustrated, and guilty

chronic cancer pain: Pain in cancer survivors iccurs in (60-90)% of cancer patients . it is caused by residual tissue damage from the cancer and/or the cancer therapy. Breakthrough pain: Breakthrough pain is pain that comes on suddenly for short periods of time[ and is not alleviated by the patients' normal pain management. It is common in cance rpatients . Forexample , If you take gabapentin for nerve pain, but suddenly experience additional shooting pains, you could be having breakthrough pain.

According to Pain Intensity: Can be broadly categorized as: mild, moderate and severe. It is common to use a numeric scale to rate pain intensity where 0 = no pain and 10 is the worst pain imaginable: Mild: <4/10 Moderate: 5/10 to 6/10 Severe: >7/10 Accodding to pathogenesis: Nociceptive: represents the normal response to noxious insult or injury of tissues such as skin, muscles, visceral organs, joints, tendons, or bones. Examples include: Visceral: hollow organs and smooth muscle; usually referred

 Neuropathic: pain initiated or caused by a primary lesion or disease in the somatosensory nervous system. o Sensory abnormalities range from deficits perceived as numbness to hypersensitivity (hyperalgesia or allodynia), and to paresthesias such as tingling. o Examples include, but are not limited to, diabetic neuropathy, postherpetic neuralgia, spinal cord injury pain, phantom limb (postamputation) pain, and post-stroke central pain Somatic: musculoskeletal (joint pain, myofascial pain), cutaneous; often well localize

Principles of management.
Regularly screen all patients for pain and perform a comprehensive pain assessment when pain is present. Appropriate pain management target. Individualised pain management regimens. Monitoring of pain management regimens and reassessment of patients pain.

Limitations to pain management:

Despite the increased focus on pain management and the implementation of formal guidelines and standards for the management of pain, a significant number of patients continues to experience unacceptable levels of pain. Different factors interfere with proper management of pain; some of them related to the patient, others related to the health care providers, and some to the organizational system. Patient : Some patients don't tell the doctor about their real pain because they are afraid from the injections and drugs or they think that increasing the pain sensation means the disease is getting worse. Socioeconomic factors. Cultural and religious issues. Care provider :
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 Inadequate knowledge and formal training in acute pain management. Opiophobia. System: Lack of standard pain control system. Hospital policies regarding drug administration and resources available.

So for effective pain management , barriers should be recognized, addressed and overcome.

Useful Questions in Assessing Pain:

Onset: When did it begin? How often does it occur? How long does it last? Exacerbating or relieving factors: What brings it on? What makes it better? What makes it worse? Is the pain better lying down or standing up? Is it worse on movement? Localization, Region and Radiation: Where is the pain? Does it move anywhere? Is there more than one site? Quality: What does it feel like? Can you compare it to any pain youve had before? Severity: How intense is your pain? At best? At worst? On average? How bothered are you by the pain? Are there any other symptoms that accompany the pain? Understanding and Impact: What does the pain stop you doing? How are you sleeping? What do you think is causing the pain? What is your goal for the pain? Are there any other views or feelings about the pain that are important to you and your family?

Management of pain :
1- Non pharmacological
2- Pharmacological 1) Non pharmacological : Non-pharmacological therapies are ways to decrease pain in addition to medicine. Each person may respond to these therapies differently. Heat Therapy: Works through vasodilation, which is when blood flow increases in the injured area due to the heat. The blood increases nutrients and oxygen in the area. It also increases the range of motion in muscles and joints, while reducing the likelihood of muscle spasms. Apply heat to the area for 20 to 30 minutes every 2 hours for as many days as directed. Heat can be used to relieve pain caused by chronic conditions of the muscles and joints, such as: Arthritis Old sprains or strains Muscle spasms Muscle stiffness Heat is best for injuries or conditions that are not in the acute phase. In other words, it not used on a fresh injury: this could increase swelling, which in some cases could increase patient's discomfort. In these cases, ice is a better choice. Also, don't apply heat over irritated skin or open wounds (including incisions that are still healing). Finally, people with cancer should not use heat to treat pain, as there is a chance of increased tumor growth. Ice Therapy: When ice is applied to the skin, it has a few different effects on the surrounding tissues. First, it partially numbs the area, which can help temporarily reduce pain. Second, it causes blood vessels to tighten, which decreases the blood flowing into the area. In this way, ice can help decrease swelling and even slow or stop bleeding. In some cases, applying ice to the skin may even prevent some bruising.
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Ice can be beneficial for anyone who has a chronic pain condition that causes (or is caused by) inflammation. Some of the conditions we recommend ice for in our therapy clinic include: Carpal tunnel syndrome Migraine headaches Trigeminal neuralgia Tendinitis Arthritis Massage Therapy: Researchers at McMaster University in Canada found that massage affects the activity of certain genes, directly reducing inflammation in muscles - the same result youd get by taking aspirin or ibuprofen - and boosting their ability to recover from exercise. Researchers found that massage set off a series of molecular events in muscles that helped reverse discomfort related to exercise. Massage dampened the activity of proteins known as inflammatory cytokines, which cause inflammation and pain. It also increased levels of proteins that signal the muscles to produce more mitochondria, the cell structures that produce energy and help muscles recover from activity.

Aromatherapy: This is a way of using scents to relax, relieve stress, and decrease pain. Aromatherapy uses oils, extracts, or fragrances from flowers, herbs, and trees. They may be inhaled or used during massages, facials, body wraps, and baths. . Aromatherapy is effective because it works directly on the amygdala, the brains emotional center, says Mehmet Oz, MD, professor of surgery at Columbia University Medical Center in New York City. Guided imagery: This teaches you ways to put pictures in your mind that will make pain less intense. It may help you learn how to change the way your body senses and responds to pain. Laughter: Laughter may help you let go of stress, anger, fear, depression, and hopelessness. Music: This may help increase energy levels and improve your mood. It may help reduce pain by triggering your body to release endorphins. These are natural body chemicals that decrease pain.

Biofeedback: This teaches your body to respond differently to the stress of being in pain. Caregivers may use a biofeedback machine to help you know when your body is relaxed. Self-hypnosis: This is a way to direct your attention to something other than your pain. For example, you might repeat a positive statement about ignoring the pain or seeing the pain in a positive way. Acupuncture: This therapy uses very thin needles to balance energy channels in the body. This is thought to help reduce pain and other symptoms. Each patient experiences pain differently. It is important to discover the best method for pain control for your patient prior to the onset of pain.

2)Pharmacological : In 1988, the World Health Organization (WHO) declared Cancer Pain management a worldwide emergency and adopted the Canadian 3-step ladder of analgesic agents for control of nociceptive pain. It is NOT a rigid clinical path that must be traversed in the care of every patient. For mild pain start at step one, for moderate pain step two, for severe pain step three. As the severity of pain increases, maximize the dosing at the current step and then, if this is insufficient, move up the ladder. Step 1: Acetaminophen & ASA & NSAIDs They obey first order kinetics and may be dosed up to recommended maximums . Many are available without prescription. Sustained release preparations or drugs with longer half-lives may encourage adherence. Step 2: Several opioid analgesics are conventionally available in combination with either acetaminophen or ASA and are commonly used to manage moderate pain.

 With the exceptions of propoxyphene (that truly has weak analgesic activity), tramadol (that has a unique combination of very weak opioid activity with other analgesic properties) and codeine (that has 1/10 to 1/12 the potency of morphine), the opioids in this class are close in potency to morphine (mg for mg). However, they have been termed "weak" opioids because, in combination, they have a ceiling to their analgesic potency(i.e. 4 gm acetaminophen per 24 hours)

If pain persists, or increases, despite a maximum dose of a step two drug, a step three drug should be prescribed instead Step 3: The pure agonist opioid analgesics comprise step three of the WHO analgesic ladder. Morphine is the prototypical drug because of its ease of administration and wide availability. Many patients with chronic pain are best managed with an appropriately titrated strong opioid that is combined with one or more coanalgesics. In contrast with the step-one and step-2 analgesics, there is no ceiling effect or upper limit to the dose of opioids when titrating to relieve pain. Step 4: In general, "step four" involves invasive approaches for pain relief that can be summarized as follows. Subcutaneous (SC) or intravenous (IV) administration of opioid analgesics and coanalgesics may be required for patients where oral (PO), buccal mucosal, rectal (PR), or transcutaneous approaches are not possible or practical, or where doses of oral opioids lead to undesirable side effects. Side effects may be minimized as a result of the uniform delivery of the drug parenterally, the change in route of administration or the reduction in first pass metabolite production. Subcutaneous administration may be preferable to intravenous approaches as it results in equivalent serum levels and analgesia without the risks of thrombosis or infection, and is much easier to deliver, for much less cost.
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 Administration of opioid analgesics either epidurally or intrathecally may be required in selected patients. Intraventricular application of opioid analgesics and other drugs has been investigated for selected central pain syndromes. Neuroablative techniques such as peripheral neurolytic blockade, ganglionic blockade, cordotomy and cingulotomy may be appropriate in highly selected patients.

Acetaminophen (APAP): Mechanism of action unclear No anti-inflammatory effects Causes liver toxicity at high doses Max dose: 4 gm/day, if no liver disease Newest recommendation 2.6 gm/day Decreases opioid requirements

NSAID& ASA: NSAIDs are anti-inflammatory through their ability to inhibit the enzyme cyclooxygenase that catalyzes the conversion of arachidonic acid to prostaglandins and leukotrienes.

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 Their effect is to decrease the levels of these inflammatory mediators that sensitize nerve endings to painful stimuli. Because analgesia from NSAIDs is achieved through a different mechanism from the opioids and other adjuvant analgesics, they may be combined with these drugs to achieve better pain relief than with a single drug alone. Primary analgesia may be achieved at lower doses than those required for anti-inflammatory action. Therefore, when used as an adjuvant for their anti-inflammatory effects, maximum doses should be used. The side effects of the NSAIDs are related to their mechanism of action. Inhibition of cyclooxygenase leads to inhibition of platelet aggregation, decreased cytoprotection in the gastric mucosa, and decreased renal perfusion. Consequently, bleeding and renal failure are important side effects. The dyspepsia and abdominal pain that limit use of the NSAIDs in some patients do not correlate with significant gastric erosions and gastrointestinal bleeding. Similarly, the use of an H2 blocking antacid (e.g. cimetidine or ranitidine) to treat NSAID dyspepsia and abdominal pain does not prevent gastric erosions and gastrointestinal bleeding. Only misoprostol, which reverses the effect of NSAIDs on the microarteriolar circulation of the stomach, has been shown to heal gastric erosions and reduce the risk of significant gastric bleeding In contrast with the opioids, the NSAIDs and acetaminophen have a ceiling effect to their analgesic potential, do not produce pharmacological tolerance, and are not associated with physical or psychological dependence.

Opioids: Originally derived from poppies Body possesses endogenous opioids enkephalins endorphins
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Opiate Receptors mu delta kappa sigma The opioid analgesics in common usage may be divided into those which are full mu agonists, partial agonists and mixed agonistantagonists. The pure agonist drugs are the most useful in chronic intractable pain.

Side effect of opioids: Common side effects of the opioid analgesics are easily managed. In the majority of patients, pharmacological tolerance develops to all of the common side effects except constipation, within one to two weeks. Consequently, nausea and vomiting may be treated expectantly with antiemetics for the short period that these symptoms are problematic. If nausea and/or vomiting persist, simply changing the opioid or the route of administration may resolve the problem. Similarly, patients should be counseled that the drowsiness they experience when initiating an opioid will usually dissipate after the first week or so. Patients can often tolerate a little drowsiness if they are assured that it wont persist for the entire time they are taking opioid analgesics. In fact, once a stable dose of an opioid has been reached, drowsiness will likely settle completely, function will normalize and most patients on a stable dose of opioid may safely drive a car. Persistent somnolence may be managed by ensuring adequate hydration and renal clearance, changing to a sustained release product to minimize peak effects, changing the opioid, changing the route of administration or by adding a psychostimulant (such as methylphenidate or pemoline). As patients given opioid analgesics will not develop tolerance to constipation, they should be treated with cathartic laxatives (e.g. Senna or Bisacodyl), osmotic laxatives (e.g. magnesium salts or lactulose) or prokinetic agents (e.g. metoclopramide or cisapride) on a routine basis. Simple stool softeners (e.g. sodium docusate) are usually ineffective Persistent side effects of the opioids seem to be somewhat idiosyncratic to the drug and individual. Simply changing to an alternate opioid at an equal analgesic dose will often clear the problem.
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 The uncommon side effects of the opioids are also manageable. The dysphoria and confusion that occasionally occur may be managed by ensuring adequate hydration and renal clearance (thereby minimizing metabolite buildup), lowering the opioid dose, changing the opioid analgesic or by adding low doses of a neuroleptic drug such as haloperidol, chlorpromazine or risperidone. The pruritus and urticaria that occurs with opioids is not immune mediated, but a non-specific release of histamine from mast cells in the skin. This may be managed with long-acting antihistamines or by changing to an alternative opioid analgesic. True allergy presenting as bronchospasm leading to anaphylaxis is extremely rare. Most patients who report allergy have had poorly managed side effects (usually nausea/vomiting and/or constipation) or too much medication too fast (leading to drowsiness and/or confusion). The risk of respiratory depression from opioid analgesics in patients with pain is frequently misunderstood. Pain is a potent stimulus to breathe and a significant stressor. While we cannot be certain of the effects of the first dose in an opioid nave patient, patients develop pharmacological tolerance to the respiratory depressant effects of opioids over the same time course as other side effects. Consequently, in the patient taking opioid analgesics for any significant length of time, it is difficult to demonstrate significant respiratory depression even with large doses of opioids. Too frequently opioids have been withheld or under-dosed because of unsubstantiated fear of respiratory depression or the mismanagement of side effects. In the patient with uncontrolled pain, narcotic analgesics can be judiciously but expeditiously and safely titrated until adequate relief is obtained or intolerable side effects encountered. Opioid overdose: In the setting of pain management, increasing opioid excess presents first as mild drowsiness, proceeds to persistent somnolence, then to a poorly arousable state and finally to respiratory depression. These changes may be associated with increasing restless, agitation, confusion, dreams, hallucinations, myoclonic jerks or even sudden onset of seizures.

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 When assessing a patient for respiratory depression, it is important to remember that a respiratory rate of 8-12 is frequently normal, particularly at nighttime. If early, or even moderate excess is present without major compromise, the opioid can be held and normal metabolism will clear the excess opioid, particularly if the poorly hydrated patient is adequately rehydrated. Naloxone reversal is not normally necessary. If the patient is not arousable, has a respiratory rate less than 6-8 per minute or there is significant hypoxemia or hypotension present, opioid reversal with naloxone may be warranted. Dilute a 0.4 or 1.0 mg ampule of naloxone with 10 cc of saline and administer 0.1-0.2 mg IV boluses every 1-2 minutes. Sc or po administration is not appropriate. As naloxone has a high affinity for opioid receptors, titration any faster, or with larger boluses, may precipitate acute opioid withdrawal that presents as an acute pain crisis, psychosis or severe abdominal pain and precipitates pulmonary edema or even myocardial infarction. Only if several 0.1-0.2 mg boluses are ineffective should the bolus size be increased. Naloxone has a high affinity for lipids and will redistribute itself into adipose tissue within 10-15 minutes of administration. Any improvement frequently appears to disappear within this time frame and signs of toxicity return. Repeated naloxone dosing may be necessary to sustain the reversal until the patient has cleared sufficient of the opioid to be out of danger. If the overdose is severe and considerable naloxone is required, a continuous infusion of naloxone may be required until the crisis is over. If a patient, who has been well managed on a stable dose of opioid for some time suddenly develops signs of overdose, the opioid should be stopped and sepsis or other causes should be ruled out. It is unlikely that the opioid alone will be the cause of the "effective overdose". Addiction and Tolerance: Addiction, the psychological dependence on the drug, is also a vastly overrated and misunderstood consequence of using opioid analgesics. In patients with chronic pain, the incidence of addiction is less than 1:1000 and is usually related to preexisting dependency. Because of its rarity, it is not listed in Table 1 with the other side effects of the opioids.
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 Physical dependence, meaning the development of a withdrawal syndrome upon abrupt discontinuation of the drug, is not evidence of addiction. Physical dependence occurs over the same time course as tolerance develops to the side effects of the opioid analgesics and is the result of changes in the numbers and function of opioid neuro-receptors in the presence of exogenous opioid. If opioid analgesics are tapered instead of abruptly withdrawn, withdrawal symptoms do not occur. Usually the opioid dose can be reduced by 50-75% q2-3days without ill effect. Occasionally a small dose of a benzodiazepine (e.g. 0.5-1.0 mg of lorazepam) or of methadone (with its longer half-life) may be necessary to settle the feeling of slight uneasiness or restlessness that accompanies the tapering process. If restlessness or agitation is anything more than very mild, the rate of tapering should be slowed. Adjuvant analgesics: Adjuvant analgesics are drugs used to enhance the analgesic efficacy of opioids, treat concurrent symptoms that exacerbate pain, and/or provide independent analgesia for specific types of pain. They may be used in all stages of the analgesic ladder. Some of the adjuvants, such as acetaminophen, the NSAIDs, the tricyclic antidepressants and perhaps the antiepileptics have primary analgesic activity themselves and may be used alone or as coanalgesics. Two cancer pain syndromes bear particular mention in this regard. Bone pain from bone metastases is thought to be, in part, prostaglandin mediated. Consequently, the NSAIDs and/or steroids may be particularly helpful in combination with opioids. Cord compression should always be considered if the pain is severe, increasing quickly or associated with motor, bowel or bladder dysfunction. Neuropathic pain is rarely controlled with opioids alone. The tricyclic antidepressants, antiepileptics and steroids are often required in combination with the opioids to achieve adequate relief. Commonly used agents are listed below with a few comments about their use NSAIDs and/or acetaminophen may be added to the opioids for adjuvant analgesia, particularly when inflammatory or peripheral mechanisms are thought to be responsible for the painful stimulus.
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 Corticosteroids provide a range of effects including anti-inflammatory activity, mood elevation, antiemetic activity and appetite stimulation. They reduce pain both by their anti-inflammatory effect of reducing arachidonic acid release to form prostaglandins as well as decreasing swelling and pressure on nerve endings. Undesirable effects such as hyperglycemia, weight gain, myopathy, and dysphoria or psychosis may complicate prolonged therapy. Anticonvulsants (such as carbamazepine, valproate, clonazepam, phenytoin, and gabapentin) are used either alone, or in addition to opioids or other coanalgesics to manage neuropathic pain. They have been particularly advocated for neuropathic pain with a shooting or lancinating quality (such as trigeminal neuralgia or nerve root compression). Tricyclic antidepressants (such as amitriptyline, desipramine, imipramine, nortriptyline) are useful in pain management in general, and neuropathic pain in particular. They have innate analgesic properties and are effective through mechanisms that include enhanced inhibitory modulation of nociceptive impulses at the level of the dorsal horn. If the anticholinergic side effects of tertiary amine tricyclics (amitriptyline, imipramine) are undesirable or troublesome, the secondary amine tricyclics (nortriptyline, desipramine) may be effective analgesics and produce fewer side effects. The selective serotonin reuptake inhibitor class of antidepressants has not been shown to be useful in similar ways to the tricyclic antidepressants. Bisphosphonates (such as pamidronate) and calcitonin have been used as adjuvant analgesics in the management of bone pain from bone metastases. In cancer, bone pain is caused in large part by osteoclastinduced bone resorption rather than the direct effects of the tumor on periosteal or medullary nerve endings. Both the bisphosphonates and calcitonin inhibit osteoclast activity on bone and have been reported to reduce pain significantly in at least some patients. Neuroleptic medications (such as haloperidol, chlorpromazine or risperidone) and anxiolytics (such as lorazepam) are used for the management of specific psychiatric disorders that complicate pain management such as delirium, psychosis, or anxiety disorders. With the exception of methotrimeprazine and clonazepam, none have been shown to have intrinsic analgesic activity.
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Symptoms of Pain in Babies:

Unlike with older children, crying isn't always a reliable pain indicator in babies. That's because crying is a baby's way of expressing a whole host of needs. Here are signs that a baby may be in pain. Changes in crying patterns. A baby's distressed cry sometimes, but not always, sounds different from ordinary crying. Changes in your baby's behavior can also be a tip-off. For example, crying that can't be soothed with a bottle, diaper change, or cuddling could signal pain. Also, a calm baby who becomes unusually fussy could be in pain. Crying while nursing. Sucking can create pressure in the ears. The baby who cries while nursing could very well have a painful ear infection. Prolonged, intense crying, often at the same time each day. This behavior is common with colic, which occurs in infants due to abdominal pain. It often starts at the age of 2 weeks, peaks at 6 weeks, and then gradually declines. Crying and drawing the legs up to the abdomen. Your baby could have colic or a serious medical condition. Withdrawing. Chronic pain can sap a baby's energy, causing him or her to become still, quiet, and to avoid eye contact.

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