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Sunday, April 25, 2021

Nonsteroidal anti-inflammatory drug

From Wikipedia, the free encyclopedia
 
Nonsteroidal anti-inflammatory drug

200mg ibuprofen tablets.jpg
Coated 200 mg tablets of generic ibuprofen, a common NSAID
Class identifiers
Pronunciation/ˈɛnsɛd/ EN-sed
SynonymsCyclooxygenase inhibitor, Cyclooxygenase enzyme inhibitor, Nonsteroidal anti-inflammatory agents/analgesics (NSAIAs), Nonsteroidal anti-inflammatory medicines (NSAIMs)
UsePain, fever, Inflammation, Antithrombosis
ATC codeM01A
Mechanism of actionEnzyme inhibitor
Biological targetCOX-1 and COX-2

Nonsteroidal anti-inflammatory drugs (NSAIDs) are members of a drug class that reduces pain, decreases fever, prevents blood clots, and in higher doses, decreases inflammation. Side effects depend on the specific drug but largely include an increased risk of gastrointestinal ulcers and bleeds, heart attack, and kidney disease.

The term nonsteroidal distinguishes these drugs from steroids, which while having a similar eicosanoid-depressing, anti-inflammatory action, have a broad range of other effects. First used in 1960, the term served to distance these medications from steroids, which were particularly stigmatised at the time due to the connotations with anabolic steroid abuse.

NSAIDs work by inhibiting the activity of cyclooxygenase enzymes (COX-1 or COX-2). In cells, these enzymes are involved in the synthesis of key biological mediators, namely prostaglandins, which are involved in inflammation, and thromboxanes, which are involved in blood clotting.

There are two types of NSAIDs available: non-selective and COX-2 selective. Most NSAIDs are non-selective and inhibit the activity of both COX-1 and COX-2. These NSAIDs, while reducing inflammation, also inhibit platelet aggregation (especially aspirin) and increase the risk of gastrointestinal ulcers/bleeds. COX-2 selective inhibitors have less gastrointestinal side effects but promote thrombosis and some of these agents substantially increase the risk of heart attack. As a result, certain older COX-2 selective inhibitors are no longer used due to the high risk of undiagnosed vascular disease. These differential effects are due to the different roles and tissue localisations of each COX isoenzyme. By inhibiting physiological COX activity, all NSAIDs increase the risk of kidney disease and through a related mechanism, heart attack. In addition, NSAIDs can blunt the production of erythropoietin resulting in anaemia, since haemoglobin needs this hormone to be produced. Prolonged use is dangerous and case studies have shown the health risk with celecoxib.

The most prominent NSAIDs are aspirin, ibuprofen, and naproxen, all available over the counter (OTC) in most countries. Paracetamol (acetaminophen) is generally not considered an NSAID because it has only minor anti-inflammatory activity. Acetaminophen treats pain mainly by blocking COX-2 and inhibiting endocannabinoid reuptake almost exclusively within the brain, but not much in the rest of the body.

Medical uses

NSAID identification on label of generic ibuprofen, an OTC NSAID

NSAIDs are usually used for the treatment of acute or chronic conditions where pain and inflammation are present.

NSAIDs are generally used for the symptomatic relief of the following conditions:

Aspirin, the only NSAID able to irreversibly inhibit COX-1, is also indicated for antithrombosis through inhibition of platelet aggregation. This is useful for the management of arterial thrombosis and prevention of adverse cardiovascular events like heart attacks. Aspirin inhibits platelet aggregation by inhibiting the action of thromboxane A2.

In a more specific application, the reduction in prostaglandins is used to close a patent ductus arteriosus in neonates if it has not done so physiologically after 24 hours.

NSAIDs are useful in the management of post-operative dental pain following invasive dental procedures such as dental extraction. When not contra-indicated they are favoured over the use of paracetamol alone due to the anti-inflammatory effect they provide. When used in combination with paracetamol the analgesic effect has been proven to be improved. There is weak evidence suggesting that taking pre-operative analgesia can reduce the length of post operative pain associated with placing orthodontic spacers under local anaesthetic. Combination of NSAIDs with pregabalin as preemptive analgesia has shown promising results for decreasing post operative pain intensity.

The effectiveness of NSAIDs for treating non-cancer chronic pain and cancer-related pain in children and adolescents is not clear. There have not been sufficient numbers of high-quality randomized controlled trials conducted.

Inflammation

Differences in anti-inflammatory activity between NSAIDs are small, but there is considerable variation in individual response and tolerance to these drugs. About 60% of patients will respond to any NSAID; of the others, those who do not respond to one may well respond to another. Pain relief starts soon after taking the first dose and a full analgesic effect should normally be obtained within a week, whereas an anti-inflammatory effect may not be achieved (or may not be clinically assessable) for up to 3 weeks. If appropriate responses are not obtained within these times, another NSAID should be tried.

Contraindications

NSAIDs may be used with caution by people with the following conditions:

  • Irritable bowel syndrome
  • Persons who are over age 50, and who have a family history of GI (gastrointestinal) problems
  • Persons who have had past GI problems from NSAID use

NSAIDs should usually be avoided by people with the following conditions:

Adverse effects

The widespread use of NSAIDs has meant that the adverse effects of these drugs have become increasingly common. Use of NSAIDs increases risk of a range of gastrointestinal (GI) problems, kidney disease and adverse cardiovascular events. As commonly used for post-operative pain, there is evidence of increased risk of kidney complications. Their use following gastrointestinal surgery remains controversial, given mixed evidence of increased risk of leakage from any bowel anastomosis created.

An estimated 10–20% of people taking NSAIDs experience indigestion. In the 1990s high doses of prescription NSAIDs were associated with serious upper gastrointestinal adverse events, including bleeding. Over the past decade, deaths associated with gastric bleeding have declined.

NSAIDs, like all medications, may interact with other medications. For example, concurrent use of NSAIDs and quinolone antibiotics may increase the risk of quinolones' adverse central nervous system effects, including seizure.

There is an argument over the benefits and risks of NSAIDs for treating chronic musculoskeletal pain. Each drug has a benefit-risk profile and balancing the risk of no treatment with the competing potential risks of various therapies should be considered. For people over the age of 65 years old, the balance between the benefits of pain-relief medications such as NSAIDS and the potential for adverse effects has not been well determined.

In October 2020, the U.S. Food and Drug Administration (FDA) required the drug label to be updated for all nonsteroidal anti-inflammatory medications to describe the risk of kidney problems in unborn babies that result in low amniotic fluid. They are recommending avoiding NSAIDs in pregnant women at 20 weeks or later in pregnancy.

Combinational risk

If a COX-2 inhibitor is taken, a traditional NSAID (prescription or over-the-counter) should not be taken at the same time. In addition, people on daily aspirin therapy (e.g., for reducing cardiovascular risk) must be careful if they also use other NSAIDs, as these may inhibit the cardioprotective effects of aspirin.

Rofecoxib (Vioxx) was shown to produce significantly fewer gastrointestinal adverse drug reactions (ADRs) compared with naproxen. The study, the VIGOR trial, raised the issue of the cardiovascular safety of the coxibs. A statistically significant increase in the incidence of myocardial infarctions was observed in patients on rofecoxib. Further data, from the APPROVe trial, showed a statistically significant relative risk of cardiovascular events of 1.97 versus placebo—which caused a worldwide withdrawal of rofecoxib in October 2004.

Use of methotrexate together with NSAIDs in rheumatoid arthritis is safe, if adequate monitoring is done.

Cardiovascular

NSAIDs, aside from aspirin, increase the risk of myocardial infarction and stroke. This occurs at least within a week of use. They are not recommended in those who have had a previous heart attack as they increase the risk of death or recurrent MI. Evidence indicates that naproxen may be the least harmful out of these.

NSAIDs aside from (low-dose) aspirin are associated with a doubled risk of heart failure in people without a history of cardiac disease. In people with such a history, use of NSAIDs (aside from low-dose aspirin) was associated with a more than 10-fold increase in heart failure. If this link is proven causal, researchers estimate that NSAIDs would be responsible for up to 20 percent of hospital admissions for congestive heart failure. In people with heart failure, NSAIDs increase mortality risk (hazard ratio) by approximately 1.2–1.3 for naproxen and ibuprofen, 1.7 for rofecoxib and celecoxib, and 2.1 for diclofenac.

On 9 July 2015, the Food and Drug Administration (FDA) toughened warnings of increased heart attack and stroke risk associated with nonsteroidal anti-inflammatory drugs (NSAIDs) other than aspirin.

Possible erectile dysfunction risk

A 2005 Finnish survey study found an association between long term (over 3 months) use of NSAIDs and erectile dysfunction.

A 2011 publication in The Journal of Urology received widespread publicity. According to the study, men who used NSAIDs regularly were at significantly increased risk of erectile dysfunction. A link between NSAID use and erectile dysfunction still existed after controlling for several conditions. However, the study was observational and not controlled, with low original participation rate, potential participation bias, and other uncontrolled factors. The authors warned against drawing any conclusion regarding cause.

Gastrointestinal

The main adverse drug reactions (ADRs) associated with NSAID use relate to direct and indirect irritation of the gastrointestinal (GI) tract. NSAIDs cause a dual assault on the GI tract: the acidic molecules directly irritate the gastric mucosa, and inhibition of COX-1 and COX-2 reduces the levels of protective prostaglandins. Inhibition of prostaglandin synthesis in the GI tract causes increased gastric acid secretion, diminished bicarbonate secretion, diminished mucus secretion and diminished trophic effects on the epithelial mucosa.

Common gastrointestinal side effects include:

Clinical NSAID ulcers are related to the systemic effects of NSAID administration. Such damage occurs irrespective of the route of administration of the NSAID (e.g., oral, rectal, or parenteral) and can occur even in people who have achlorhydria.

Ulceration risk increases with therapy duration, and with higher doses. To minimize GI side effects, it is prudent to use the lowest effective dose for the shortest period of time—a practice that studies show is often not followed. Over 50% of patients who take NSAIDs have sustained some mucosal damage to their small intestine.

The risk and rate of gastric adverse effects is different depending on the type of NSAID medication a person is taking. Indomethacin, ketoprofen, and piroxicam use appear to lead to the highest rate of gastric adverse effects, while ibuprofen (lower doses) and diclofenac appear to have lower rates.

Certain NSAIDs, such as aspirin, have been marketed in enteric-coated formulations that manufacturers claim reduce the incidence of gastrointestinal ADRs. Similarly, some believe that rectal formulations may reduce gastrointestinal ADRs. However, consistent with the systemic mechanism of such ADRs, and in clinical practice, these formulations have not demonstrated a reduced risk of GI ulceration.

Numerous "gastro-protective" drugs have been developed with the goal of preventing gastrointestinal toxicity in people who need to take NSAIDs on a regular basis. Gastric adverse effects may be reduced by taking medications that suppress acid production such as proton pump inhibitors (e.g.: omeprazole and esomeprazole), or by treatment with a drug that mimics prostaglandin in order to restore the lining of the GI tract (e.g.: a prostaglandin analog misoprostol). Diarrhea is a common side effect of misoprostol, however, higher doses of misoprostol have been shown to reduce the risk of a person having a complication related to a gastric ulcer while taking NSAIDs. While these techniques may be effective, they are expensive for maintenance therapy.

Hydrogen sulfide NSAID hybrids prevent the gastric ulceration/bleeding associated with taking the NSAIDs alone. Hydrogen sulfide is known to have a protective effect on the cardiovascular and gastrointestinal system.

Inflammatory bowel disease

NSAIDs should be used with caution in individuals with inflammatory bowel disease (e.g., Crohn's disease or ulcerative colitis) due to their tendency to cause gastric bleeding and form ulceration in the gastric lining.

Renal

NSAIDs are also associated with a fairly high incidence of adverse drug reactions (ADRs) on the kidney and over time can lead to chronic kidney disease. The mechanism of these kidney ADRs is due to changes in kidney blood flow. Prostaglandins normally dilate the afferent arterioles of the glomeruli. This helps maintain normal glomerular perfusion and glomerular filtration rate (GFR), an indicator of kidney function. This is particularly important in kidney failure where the kidney is trying to maintain renal perfusion pressure by elevated angiotensin II levels. At these elevated levels, angiotensin II also constricts the afferent arteriole into the glomerulus in addition to the efferent arteriole it normally constricts. Since NSAIDs block this prostaglandin-mediated effect of afferent arteriole dilation, particularly in kidney failure, NSAIDs cause unopposed constriction of the afferent arteriole and decreased RPF (renal perfusion flow) and GFR.

Common ADRs associated with altered kidney function include:

These agents may also cause kidney impairment, especially in combination with other nephrotoxic agents. Kidney failure is especially a risk if the patient is also concomitantly taking an ACE inhibitor (which removes angiotensin II's vasoconstriction of the efferent arteriole) and a diuretic (which drops plasma volume, and thereby RPF)—the so-called "triple whammy" effect.

In rarer instances NSAIDs may also cause more severe kidney conditions:

NSAIDs in combination with excessive use of phenacetin or paracetamol (acetaminophen) may lead to analgesic nephropathy.

Photosensitivity

Photosensitivity is a commonly overlooked adverse effect of many of the NSAIDs. The 2-arylpropionic acids are the most likely to produce photosensitivity reactions, but other NSAIDs have also been implicated including piroxicam, diclofenac, and benzydamine.

Benoxaprofen, since withdrawn due to its liver toxicity, was the most photoactive NSAID observed. The mechanism of photosensitivity, responsible for the high photoactivity of the 2-arylpropionic acids, is the ready decarboxylation of the carboxylic acid moiety. The specific absorbance characteristics of the different chromophoric 2-aryl substituents, affects the decarboxylation mechanism.

During pregnancy

NSAIDs are not recommended during pregnancy, particularly during the third trimester. While NSAIDs as a class are not direct teratogens, they may cause premature closure of the fetal ductus arteriosus and kidney ADRs in the fetus. Additionally, they are linked with premature birth and miscarriage. Aspirin, however, is used together with heparin in pregnant women with antiphospholipid syndrome. Additionally, indomethacin is used in pregnancy to treat polyhydramnios by reducing fetal urine production via inhibiting fetal kidney blood flow.

In contrast, paracetamol (acetaminophen) is regarded as being safe and well tolerated during pregnancy, but Leffers et al. released a study in 2010, indicating that there may be associated male infertility in the unborn. Doses should be taken as prescribed, due to risk of liver toxicity with overdoses.

In France, the country's health agency contraindicates the use of NSAIDs, including aspirin, after the sixth month of pregnancy.

In October 2020, the U.S. Food and Drug Administration (FDA) required the drug label to be updated for all nonsteroidal anti-inflammatory medications to describe the risk of kidney problems in unborn babies that result in low amniotic fluid. They are recommending avoiding NSAIDs in pregnant women at 20 weeks or later in pregnancy.

Allergy and allergy-like hypersensitivity reactions

A variety of allergic or allergic-like NSAID hypersensitivity reactions follow the ingestion of NSAIDs. These hypersensitivity reactions differ from the other adverse reactions listed here which are toxicity reactions, i.e. unwanted reactions that result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug. Some NSAID hypersensitivity reactions are truly allergic in origin: 1) repetitive IgE-mediated urticarial skin eruptions, angioedema, and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and 2) Comparatively mild to moderately severe T cell-mediated delayed onset (usually more than 24 hour), skin reactions such as maculopapular rash, fixed drug eruptions, photosensitivity reactions, delayed urticaria, and contact dermatitis; or 3) far more severe and potentially life-threatening t-cell-mediated delayed systemic reactions such as the DRESS syndrome, acute generalized exanthematous pustulosis, the Stevens–Johnson syndrome, and toxic epidermal necrolysis. Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favor of forming metabolites that promote allergic symptoms. Afflicted individuals may be abnormally sensitive to these provocative metabolites or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1. Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are: 1) exacerbations of asthmatic and rhinitis (see aspirin-induced asthma) symptoms in individuals with a history of asthma or rhinitis and 2) exacerbation or first-time development of wheals or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema.

Possible effects on bone and soft tissue healing

It has been hypothesized that NSAIDs may delay healing from bone and soft-tissue injuries by inhibiting inflammation. On the other hand, it has also been hypothesized that NSAIDs might speed recovery from soft tissue injuries by preventing inflammatory processes from damaging adjacent, non-injured muscles.

There is moderate evidence that they delay bone healing. Their overall effect on soft-tissue healing is unclear.

Other

The use of NSAIDs for analgesia following gastrointestinal surgery remains controversial, given mixed evidence of an increased risk of leakage from any bowel anastomosis created. This risk may vary according to the class of NSAID prescribed.

Common adverse drug reactions (ADR), other than listed above, include: raised liver enzymes, headache, dizziness. Uncommon ADRs include an abnormally high level of potassium in the blood, confusion, spasm of the airways, and rash. Ibuprofen may also rarely cause irritable bowel syndrome symptoms. NSAIDs are also implicated in some cases of Stevens–Johnson syndrome.

Most NSAIDs penetrate poorly into the central nervous system (CNS). However, the COX enzymes are expressed constitutively in some areas of the CNS, meaning that even limited penetration may cause adverse effects such as somnolence and dizziness.

NSAIDs may increase the risk of bleeding in patients with Dengue fever For this reason, NSAIDs are only available with a prescription in India.

In very rare cases, ibuprofen can cause aseptic meningitis.

As with other drugs, allergies to NSAIDs might exist. While many allergies are specific to one NSAID, up to 1 in 5 people may have unpredictable cross-reactive allergic responses to other NSAIDs as well.

Drug interactions

NSAIDs reduce kidney blood flow and thereby decrease the efficacy of diuretics, and inhibit the elimination of lithium and methotrexate.

NSAIDs cause decreased ability to form blood clots, which can increase the risk of bleeding when combined with other drugs that also decrease blood clotting, such as warfarin.

NSAIDs may aggravate hypertension (high blood pressure) and thereby antagonize the effect of antihypertensives, such as ACE inhibitors.

NSAIDs may interfere and reduce efficiency of SSRI antidepressants. NSAIDs, when used in combination with SSRIs, increases the risk of adverse gastrointestinal effects.  NSAIDs, when used in combination with SSRIs, increases the risk of internal bleeding and brain hemorrhages.

Various widely used nonsteroidal anti-inflammatory drugs (NSAIDs) enhance endocannabinoid signaling by blocking the anandamide-degrading membrane enzyme fatty acid amide hydrolase (FAAH).

NSAIDs may reduce the effectiveness of antibiotics. Tests on cultured bacteria found that antibiotic effectiveness was reduced by 18-30% on average compared to tests which did not include NSAIDs.

Immune response

Although small doses generally have little to no effect on the immune system, large doses of NSAIDs significantly suppress the production of immune cells. As NSAIDs affect prostaglandins, they affect the production of most fast growing cells. This includes immune cells. Unlike corticosteroids, they do not directly suppress the immune system and so their effect on the immune system is not immediately obvious. They suppress the production of new immune cells, but leave existing immune cells functional. Large doses slowly reduce the immune response as the immune cells are renewed at a much lower rate. Causing a gradual reduction of the immune system, much slower and less noticeable than the immediate effect of Corticosteroids. The effect significantly increases with dosage, in a nearly exponential rate. Doubling of dose reduced cells by nearly four times. Increasing dose by five times reduced cell counts to only a few percent of normal levels. This is likely why the effect was not immediately obvious in low dose trials, as the effect is not apparent until much higher dosages are tested.

Mechanism of action

Most NSAIDs act as nonselective inhibitors of the cyclooxygenase (COX) enzymes, inhibiting both the cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) isoenzymes. This inhibition is competitively reversible (albeit at varying degrees of reversibility), as opposed to the mechanism of aspirin, which is irreversible inhibition. COX catalyzes the formation of prostaglandins and thromboxane from arachidonic acid (itself derived from the cellular phospholipid bilayer by phospholipase A2). Prostaglandins act (among other things) as messenger molecules in the process of inflammation. This mechanism of action was elucidated in 1970 by John Vane (1927–2004), who received a Nobel Prize for his work.

COX-1 is a constitutively expressed enzyme with a "house-keeping" role in regulating many normal physiological processes. One of these is in the stomach lining, where prostaglandins serve a protective role, preventing the stomach mucosa from being eroded by its own acid. COX-2 is an enzyme facultatively expressed in inflammation, and it is inhibition of COX-2 that produces the desirable effects of NSAIDs.

When nonselective COX-1/COX-2 inhibitors (such as aspirin, ibuprofen, and naproxen) lower stomach prostaglandin levels, ulcers of the stomach or duodenum and internal bleeding can result.

NSAIDs have been studied in various assays to understand how they affect each of these enzymes. While the assays reveal differences, unfortunately, different assays provide differing ratios.

The discovery of COX-2 led to research to the development of selective COX-2 inhibiting drugs that do not cause gastric problems characteristic of older NSAIDs.

Paracetamol (acetaminophen) is not considered an NSAID because it has little anti-inflammatory activity. It treats pain mainly by blocking COX-2 mostly in the central nervous system, but not much in the rest of the body.

However, many aspects of the mechanism of action of NSAIDs remain unexplained, and for this reason, further COX pathways are hypothesized. The COX-3 pathway was believed to fill some of this gap but recent findings make it appear unlikely that it plays any significant role in humans and alternative explanation models are proposed.

NSAIDs interact with the endocannabinoid system and its endocannabinoids, as COX2 have been shown to utilize endocannabinoids as substrates, and may have a key role in both the therapeutic effects and adverse effects of NSAIDs, as well as in NSAID-induced placebo responses.

NSAIDs are also used in the acute pain caused by gout because they inhibit urate crystal phagocytosis besides inhibition of prostaglandin synthase.

Antipyretic activity

NSAIDs have antipyretic activity and can be used to treat fever. Fever is caused by elevated levels of prostaglandin E2, which alters the firing rate of neurons within the hypothalamus that control thermoregulation. Antipyretics work by inhibiting the enzyme COX, which causes the general inhibition of prostanoid biosynthesis (PGE2) within the hypothalamus. PGE2 signals to the hypothalamus to increase the body's thermal setpoint. Ibuprofen has been shown more effective as an antipyretic than paracetamol (acetaminophen). Arachidonic acid is the precursor substrate for cyclooxygenase leading to the production of prostaglandins F, D, and E.

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Pain management

From Wikipedia, the free encyclopedia

Opium poppies such as this one provide ingredients for the class of analgesics called opiates
Pain Medicine Physician
Occupation
Names
  • Physician
Occupation type
Specialty
Activity sectors
Medicine
Description
Education required
Fields of
employment
Hospitals, Clinics

Pain management, pain killer, pain medicine, pain control or algiatry, is a branch of medicine that uses an interdisciplinary approach for easing the suffering and improving the quality of life of those living with chronic pain. The typical pain management team includes medical practitioners, pharmacists, clinical psychologists, physiotherapists, occupational therapists, physician assistants, nurses, and dentists. The team may also include other mental health specialists and massage therapists. Pain sometimes resolves quickly once the underlying trauma or pathology has healed, and is treated by one practitioner, with drugs such as analgesics and (occasionally) anxiolytics. Effective management of chronic (long-term) pain, however, frequently requires the coordinated efforts of the pain management team. Effective pain management does not mean total eradication of all pain.

Medicine treats injuries and diseases to support and speed healing. It treats distressing symptoms such as pain to relieve suffering during treatment, healing, and dying. The task of medicine is to relieve suffering under three circumstances. The first being when a painful injury or pathology is resistant to treatment and persists. The second is when pain persists after the injury or pathology has healed. Finally the third circumstance is when medical science cannot identify the cause of pain. Treatment approaches to chronic pain include pharmacological measures, such as analgesics, antidepressants and anticonvulsants, interventional procedures, physical therapy, physical exercise, application of ice or heat, and psychological measures, such as biofeedback and cognitive behavioral therapy.

In the nursing profession, one common definition of pain is any problem that is "whatever the experiencing person says it is, existing whenever the experiencing person says it does".

Pain management includes patient communication about the pain problem. To define the pain problem, a health care provider will likely ask questions such as:

  • How intense is the pain?
  • How does the pain feel?
  • Where is the pain?
  • What, if anything, makes the pain lessen?
  • What, if anything, makes the pain increase?
  • When did the pain start?

After asking such questions, the health care provider will have a description of the pain. Pain management will then be used to address that pain.

Adverse effects

There are many types of pain management. Each have their own benefits, drawbacks, and limits.

A common challenge in pain management is communication between the health care provider and the person experiencing pain. People experiencing pain may have difficulty recognizing or describing what they feel and how intense it is. Health care providers and patients may have difficulty communicating with each other about how pain responds to treatments. There is a risk in many types of pain management for the patient to take treatment that is less effective than needed or which causes other difficulties and side effects. Some treatments for pain can be harmful if overused. A goal of pain management for the patient and their health care provider is to identify the amount of treatment needed to address the pain without going beyond that limit.

Another problem with pain management is that pain is the body's natural way of communicating a problem. Pain is supposed to resolve as the body heals itself with time and pain management.[5] Sometimes pain management covers a problem, and the patient might be less aware that they need treatment for a deeper problem.

Physical approach

Physical medicine and rehabilitation

Physical medicine and rehabilitation uses a range of physical techniques such as heat and electrotherapy, as well as therapeutic exercises and behavioral therapy. These techniques are usually part of an interdisciplinary or multidisciplinary program that might also include pharmaceutical medicines. Spa therapy has showed positive effects in reducing pain among patients with chronic low back pain. However there are limited studies looking at this approach. Studies have shown that kinesiotape could be used on individuals with chronic low back pain to reduce pain. The Center for Disease Control recommends that physical therapy and exercise can be prescribed as a positive alternative to opioids for decreasing one's pain in multiple injuries, illnesses, or diseases. This can include chronic low back pain, osteoarthritis of the hip and knee, or fibromyalgia. Exercise alone or with other rehabilitation disciplines (such as psychologically based approaches) can have a positive effect on reducing pain. In addition to improving pain, exercise also can improve one's well-being and general health.

Manipulative and mobilization therapy are safe interventions that likely reduce pain for patients with chronic low back pain. However, manipulation produces a larger effect than mobilization.

Specifically in chronic low back pain, education about the way the brain processes pain in conjunction with routine physiotherapy interventions may provide short term relief of disability and pain.

Exercise interventions

Physical activity interventions, such as tai chi, yoga and Pilates, promote harmony of the mind and body through total body awareness. These practices incorporate breathing techniques, meditation and a wide variety of movements, while training the body to perform functionally by increasing strength, flexibility, and range of motion. Physical activity and exercise may improve chronic pain (pain lasting more than 12 weeks), and overall quality of life, while minimizing the need for pain medications. More specifically, walking has been effective in improving pain management in chronic low back pain.

TENS

Transcutaneous electrical nerve stimulation (TENS) is a self-operated portable device intended to help regulate and create chronic pain via electrical impulses. Limited research has explored the effectiveness of TENS in relation to pain management of Multiple Sclerosis (MS). MS is a chronic autoimmune neurological disorder, which consists of the demyelination of the nerve axons and disruption of nerve conduction velocity and efficiency. In one study, electrodes were placed over the lumbar spins and participants received treatment twice a day and at any time when they experienced a painful episode. This study found that TENS would be beneficial to MS patients who reported localized or limited symptoms to one limp. The research is mixed with whether or not TENS helps manage pain in MS patients.

Transcutaneous electrical nerve stimulation has been found to be ineffective for lower back pain. However, it might help with diabetic neuropathy as well as other illnesses.

tDCS

Transcranial direct current stimulation (tDCS) is a non-invasive technique of brain stimulation that can modulate activity in specific brain cortex regions, and it involves the application of low-intensity (up to 2 mA) constant direct current to the scalp through electrodes in order to modulate excitability of large cortical areas. tDCS may have a role in pain assessment by contributing to efforts in distinguishing between somatic and affective aspects of pain experience. Zaghi and colleagues (2011) found that the motor cortex, when stimulated with tDCS, increases the threshold for both the perception of non-painful and painful stimuli. Although there is a greater need for research examining the mechanism of electrical stimulation in relation to pain treatment, one theory suggests that the changes in thalamic activity may be due the influence of motor cortex stimulation on the decrease in pain sensations.

In relation to MS, a study found that after daily tDCS sessions resulted in an individual's subjective report of pain to decrease when compared to a sham condition. In addition, the study found a similar improvement at 1 to 3 days before and after each tDCS session.

Fibromyalgia is a disorder in which an individual experiences dysfunctional brain activity, musculoskeletal pain, fatigue, and tenderness in localized areas. Research examining tDCS for pain treatment in Fibromyalgia has found initial evidence for pain decreases. Specifically, the stimulation of the primary motor cortex resulted in significantly greater pain improvement in comparison to the control group (e.g., sham stimulation, stimulation of the DLPFC). However, this effect decreased after treatment ended, but remained significant for three weeks following the extinction of treatment.

Acupuncture

Acupuncture involves the insertion and manipulation of needles into specific points on the body to relieve pain or for therapeutic purposes. An analysis of the 13 highest quality studies of pain treatment with acupuncture, published in January 2009 in the British Medical Journal, was unable to quantify the difference in the effect on pain of real, sham and no acupuncture. A systematic review in 2019 reported that acupuncture injection therapy was an effective treatment for patients with nonspecific chronic low back pain, and is widely used in Southeast Asian countries.

Light therapy

Research has not found evidence that light therapy such as low level laser therapy is an effective therapy for relieving low back pain.

Interventional procedures

Interventional procedures - typically used for chronic back pain - include epidural steroid injections, facet joint injections, neurolytic blocks, spinal cord stimulators and intrathecal drug delivery system implants.

Pulsed radiofrequency, neuromodulation, direct introduction of medication and nerve ablation may be used to target either the tissue structures and organ/systems responsible for persistent nociception or the nociceptors from the structures implicated as the source of chronic pain. Radiofrequency treatment has been seen to improve pain in patients for facet joint low back pain. However, continuous radiofrequency is more effective in managing pain than pulsed radiofrequency.

An intrathecal pump used to deliver very small quantities of medications directly to the spinal fluid. This is similar to epidural infusions used in labour and postoperatively. The major differences are that it is much more common for the drug to be delivered into the spinal fluid (intrathecal) rather than epidurally, and the pump can be fully implanted under the skin.

A spinal cord stimulator is an implantable medical device that creates electric impulses and applies them near the dorsal surface of the spinal cord provides a paresthesia ("tingling") sensation that alters the perception of pain by the patient.

Intra-articular ozone therapy

Intra-articular ozone therapy has been seen to efficiently alleviate chronic pain in patients with knee osteoarthritis.

Psychological approach

Acceptance and Commitment Therapy

Acceptance and Commitment Therapy (ACT) is a form of cognitive behavioral therapy that focuses on behavior change rather than symptom change, includes methods designed to alter the context around psychological experiences rather than to alter the makeup of the experiences, and emphasizes the use of experiential behavior change methods. The central process in ACT revolves around psychological flexibility, which in turn includes processes of acceptance, awareness, a present-oriented quality in interacting with experiences, an ability to persist or change behavior, and an ability to be guided by one's values. ACT has an increased evidence base for range of health and behavior problems, including chronic pain. ACT influences patients to adopt a tandem process to acceptance and change, which allows for a greater flexibility in the focus of treatment.

Recent research has applied ACT successfully to chronic pain in older adults due to in part of its direction from individual values and being highly customizable to any stage of life. In line with the therapeutic model of ACT, significant increases in process variables, pain acceptance, and mindfulness were also observed in a study applying ACT to chronic pain in older adults. In addition, these primary results suggested that an ACT based treatment may significantly improve levels of physical disability, psychosocial disability, and depression post-treatment and at a three month follow-up for older adults with chronic pain.

Cognitive behavioral therapy

Cognitive behavioral therapy (CBT) helps patients with pain to understand the relationship between their pain, thoughts, emotions, and behaviors. A main goal in treatment is cognitive (thinking, reasoning or remembering) restructuring to encourage helpful thought patterns. This will target healthy activities such as regular exercise and pacing. Lifestyle changes are also trained to improve sleep patterns and to develop better coping skills for pain and other stressors using various techniques (e.g., relaxation, diaphragmatic breathing, and even biofeedback).

Studies have demonstrated the usefulness of cognitive behavioral therapy in the management of chronic low back pain, producing significant decreases in physical and psychosocial disability. CBT is significantly more effective than standard care in treatment of people with body-wide pain, like fibromyalgia. Evidence for the usefulness of CBT in the management of adult chronic pain is generally poorly understood, due partly to the proliferation of techniques of doubtful quality, and the poor quality of reporting in clinical trials. The crucial content of individual interventions has not been isolated and the important contextual elements, such as therapist training and development of treatment manuals, have not been determined. The widely varying nature of the resulting data makes useful systematic review and meta-analysis within the field very difficult.

In 2020, a systematic review of randomized controlled trials (RCTs) evaluated the clinical effectiveness of psychological therapies for the management of adult chronic pain (excluding headaches). There is no evidence that behaviour therapy (BT) is effective for reducing this type of pain, however BT may be useful for improving a persons mood immediately after treatment. This improvement appears to be small, and is short term in duration. CBT may have a small positive short-term effect on pain immediately following treatment. CBT may also have a small effect on reducing disability and potential catastrophizing that may be associated with adult chronic pain. These benefits do not appear to last very long following the therapy. CBT may contribute towards improving the mood of an adult who experiences chronic pain, which could possibility be maintained for longer periods of time.

For children and adolescents, a review of RCTs evaluating the effectiveness of psychological therapy for the management of chronic and recurrent pain found that psychological treatments are effective in reducing pain when people under 18 years old have headaches. This beneficial effect may be maintained for at least three months following the therapy. Psychological treatments may also improve pain control for children or adolescents who experience pain not related to headaches. It is not known if psychological therapy improves a child or adolescents mood and the potential for disability related to their chronic pain.

Hypnosis

A 2007 review of 13 studies found evidence for the efficacy of hypnosis in the reduction of pain in some conditions. However the studies had some limitations like small study sizes, bringing up issues of power to detect group differences, and lacking credible controls for placebo or expectation. The authors concluded that "although the findings provide support for the general applicability of hypnosis in the treatment of chronic pain, considerably more research will be needed to fully determine the effects of hypnosis for different chronic-pain conditions."

Hypnosis has reduced the pain of some harmful medical procedures in children and adolescents. In clinical trials addressing other patient groups, it has significantly reduced pain compared to no treatment or some other non-hypnotic interventions. The effects of self hypnosis on chronic pain are roughly comparable to those of progressive muscle relaxation.

Hypnosis with analgesic (painkiller) has been seen to relieve chronic pain for most people and may be a safe and effective alternative to medications. However, high quality clinical data is needed to generalize to the whole chronic pain population.

Mindfulness meditation

A 2013 meta-analysis of studies that used techniques centered around the concept of mindfulness, concluded, "that MBIs [mindfulness-based interventions] decrease the intensity of pain for chronic pain patients." A 2019 review of studies of brief mindfulness-based interventions (BMBI) concluded that BMBI are not recommended as a first-line treatment and could not confirm their efficacy in managing chronic or acute pain.

Mindfulness-based pain management

Mindfulness-based pain management (MBPM) is a mindfulness-based intervention (MBI) providing specific applications for people living with chronic pain and illness. Adapting the core concepts and practices of mindfulness-based stress reduction (MBSR) and mindfulness-based cognitive therapy (MBCT), MBPM includes a distinctive emphasis on the practice of 'loving-kindness', and has been seen as sensitive to concerns about removing mindfulness teaching from its original ethical framework within Buddhism. It was developed by Vidyamala Burch and is delivered through the programs of Breathworks. It has been subject to a range of clinical studies demonstrating its effectiveness.

Medications

The World Health Organization (WHO) recommends a pain ladder for managing pain relief with pharmaceutical medicine. It was first described for use in cancer pain. However it can be used by medical professionals as a general principle when managing any type of pain. In the treatment of chronic pain, the three-step WHO Analgesic Ladder provides guidelines for selecting the appropriate medicine. The exact medications recommended will vary by country and the individual treatment center, but the following gives an example of the WHO approach to treating chronic pain with medications. If, at any point, treatment fails to provide adequate pain relief, then the doctor and patient move onto the next step.

Common types of pain and typical drug management
Pain type typical initial drug treatment comments
headache paracetamol /acetaminophen, NSAIDs doctor consultation is appropriate if headaches are severe, persistent, accompanied by fever, vomiting, or speech or balance problems; self-medication should be limited to two weeks
migraine paracetamol, NSAIDs triptans are used when the others do not work, or when migraines are frequent or severe
menstrual cramps NSAIDs some NSAIDs are marketed for cramps, but any NSAID would work
minor trauma, such as a bruise, abrasions, sprain paracetamol, NSAIDs opioids not recommended
severe trauma, such as a wound, burn, bone fracture, or severe sprain opioids more than two weeks of pain requiring opioid treatment is unusual
strain or pulled muscle NSAIDs, muscle relaxants if inflammation is involved, NSAIDs may work better; short-term use only
minor pain after surgery paracetamol, NSAIDs opioids rarely needed
severe pain after surgery opioids combinations of opioids may be prescribed if pain is severe
muscle ache paracetamol, NSAIDs if inflammation involved, NSAIDs may work better.
toothache or pain from dental procedures paracetamol, NSAIDs this should be short term use; opioids may be necessary for severe pain
kidney stone pain paracetamol, NSAIDs, opioids opioids usually needed if pain is severe.
pain due to heartburn or gastroesophageal reflux disease antacid, H2 antagonist, proton-pump inhibitor heartburn lasting more than a week requires medical attention; aspirin and NSAIDs should be avoided
chronic back pain paracetamol, NSAIDs opioids may be necessary if other drugs do not control pain and pain is persistent
osteoarthritis pain paracetamol, NSAIDs medical attention is recommended if pain persists.
fibromyalgia antidepressant, anticonvulsant evidence suggests that opioids are not effective in treating fibromyalgia

Mild pain

Paracetamol (acetaminophen), or a nonsteroidal anti-inflammatory drug (NSAID) such as ibuprofen will relieve mild pain.

Mild to moderate pain

Paracetamol, an NSAID or paracetamol in a combination product with a weak opioid such as tramadol, may provide greater relief than their separate use. A combination of opioid with acetaminophen can be frequently used such as Percocet, Vicodin, or Norco.

Moderate to severe pain

When treating moderate to severe pain, the type of the pain, acute or chronic, needs to be considered. The type of pain can result in different medications being prescribed. Certain medications may work better for acute pain, others for chronic pain, and some may work equally well on both. Acute pain medication is for rapid onset of pain such as from an inflicted trauma or to treat post-operative pain. Chronic pain medication is for alleviating long-lasting, ongoing pain.

Morphine is the gold standard to which all narcotics are compared. Semi-synthetic derivatives of morphine such as hydromorphone (Dilaudid), oxymorphone (Numorphan, Opana), nicomorphine (Vilan), hydromorphinol and others vary in such ways as duration of action, side effect profile and milligramme potency. Fentanyl has the benefit of less histamine release and thus fewer side effects. It can also be administered via transdermal patch which is convenient for chronic pain management. In addition to the intrathecal patch and injectable fentanyl formulations, the FDA (Food and Drug Administration) has approved various immediate release fentanyl products for breakthrough cancer pain (Actiq/OTFC/Fentora/Onsolis/Subsys/Lazanda/Abstral). Oxycodone is used across the Americas and Europe for relief of serious chronic pain. Its main slow-release formula is known as OxyContin. Short-acting tablets, capsules, syrups and ampules which contain OxyContin are available making it suitable for acute intractable pain or breakthrough pain. Diamorphine, and methadone are used less frequently. Clinical studies have shown that transdermal Buprenorphine is effective at reducing chronic pain. Pethidine, known in North America as meperidine, is not recommended for pain management due to its low potency, short duration of action, and toxicity associated with repeated use. Pentazocine, dextromoramide and dipipanone are also not recommended in new patients except for acute pain where other analgesics are not tolerated or are inappropriate, for pharmacological and misuse-related reasons. In some countries potent synthetics such as piritramide and ketobemidone are used for severe pain. Tapentadol is a newer agent introduced in the last decade.

For moderate pain, tramadol, codeine, dihydrocodeine, and hydrocodone are used, with nicocodeine, ethylmorphine and propoxyphene or dextropropoxyphene (less commonly).

Drugs of other types can be used to help opioids combat certain types of pain. Amitriptyline is prescribed for chronic muscular pain in the arms, legs, neck and lower back with an opiate, or sometimes without it or with an NSAID.

While opiates are often used in the management of chronic pain, high doses are associated with an increased risk of opioid overdose.

Opioids

In 2009, the Food and Drug Administration stated: "According to the National Institutes of Health, studies have shown that properly managed medical use of opioid analgesic compounds (taken exactly as prescribed) is safe, can manage pain effectively, and rarely causes addiction." In 2013, the FDA stated that "abuse and misuse of these products have created a serious and growing public health problem".

Opioid medications can provide short, intermediate or long acting analgesia depending upon the specific properties of the medication and whether it is formulated as an extended release drug. Opioid medications may be administered orally, by injection, via nasal mucosa or oral mucosa, rectally, transdermally, intravenously, epidurally and intrathecally. In chronic pain conditions that are opioid responsive, a combination of a long-acting (OxyContin, MS Contin, Opana ER, Exalgo and Methadone) or extended release medication is often prescribed along with a shorter-acting medication (oxycodone, morphine or hydromorphone) for breakthrough pain, or exacerbations.

Most opioid treatment used by patients outside of healthcare settings is oral (tablet, capsule or liquid), but suppositories and skin patches can be prescribed. An opioid injection is rarely needed for patients with chronic pain.

Although opioids are strong analgesics, they do not provide complete analgesia regardless of whether the pain is acute or chronic in origin. Opioids are effective analgesics in chronic malignant pain and modestly effective in nonmalignant pain management. However, there are associated adverse effects, especially during the commencement or change in dose. When opioids are used for prolonged periods drug tolerance, chemical dependency, diversion and addiction may occur.

Clinical guidelines for prescribing opioids for chronic pain have been issued by the American Pain Society and the American Academy of Pain Medicine. Included in these guidelines is the importance of assessing the patient for the risk of substance abuse, misuse, or addiction. Factors correlated with an elevated risk of opioid misuse include a history of substance use disorder, younger age, major depression, and the use of psychotropic medications. Physicians who prescribe opioids should integrate this treatment with any psychotherapeutic intervention the patient may be receiving. The guidelines also recommend monitoring not only the pain but also the level of functioning and the achievement of therapeutic goals. The prescribing physician should be suspicious of abuse when a patient reports a reduction in pain but has no accompanying improvement in function or progress in achieving identified goals.

The list below consists of commonly used opioid analgesics which have long-acting formulations. Common brand names for the extended release formulation are in parentheses.

*Methadone and buprenorphine are each used both for the treatment of opioid addiction and as analgesics

Nonsteroidal anti-inflammatory drugs

The other major group of analgesics are nonsteroidal anti-inflammatory drugs (NSAID). They work by inhibiting the release of prostaglandins, which cause inflammatory pain. Acetaminophen/paracetamol is not always included in this class of medications. However, acetaminophen may be administered as a single medication or in combination with other analgesics (both NSAIDs and opioids). The alternatively prescribed NSAIDs such as ketoprofen and piroxicam have limited benefit in chronic pain disorders and with long-term use are associated with significant adverse effects. The use of selective NSAIDs designated as selective COX-2 inhibitors have significant cardiovascular and cerebrovascular risks which have limited their utilization. Common NSAIDs include aspirin, ibuprofen, and naproxen. There are many NSAIDs such as parecoxib (selective COX-2 inhibitor) with proven effectiveness after different surgical procedures. Wide use of non-opioid analgesics can reduce opioid-induced side-effects.

Antidepressants and antiepileptic drugs

Some antidepressant and antiepileptic drugs are used in chronic pain management and act primarily within the pain pathways of the central nervous system, though peripheral mechanisms have been attributed as well. They are generally used to treat nerve brain [DJS -- "nerve pain" ?] that results from injury to the nervous system. Neuropathy can be due to chronic high blood sugar levels (diabetic neuropathy). These drugs also reduce pain from viruses such as shingles, phantom limb pain and post-stroke pain. These mechanisms vary and in general are more effective in neuropathic pain disorders as well as complex regional pain syndrome. A common anti-epileptic drug is gabapentin, and an example of an antidepressant would be amitriptyline.

Cannabinoids

Evidence of medical marijuana's effect on reducing pain is generally conclusive. Detailed in a 1999 report by the Institute of Medicine, "the available evidence from animal and human studies indicates that cannabinoids can have a substantial analgesic effect". In a 2013 review study published in Fundamental & Clinical Pharmacology, various studies were cited in demonstrating that cannabinoids exhibit comparable effectiveness to opioids in models of acute pain and even greater effectiveness in models of chronic pain.

Other analgesics

Other drugs which can potentiate conventional analgesics or have analgesic properties in certain circumstances are called analgesic adjuvant medications. Gabapentin, an anticonvulsant, can reduce neuropathic pain itself and can also potentiate opiates. Drugs with anticholinergic activity, such as orphenadrine, cyclobenzaprine, and trazodone, are given in conjunction with opioids for neuropathic pain. Orphenadrine and cyclobenzaprine are also muscle relaxants, and are useful in painful musculoskeletal conditions. Clonidine, an alpha-2 receptor agonist, is another drug that has found use as an analgesic adjuvant.

Self-management

Self-management of chronic pain has been described as the individual's ability to manage various aspects of their chronic pain. Self-management can include building self-efficacy, monitoring one's own symptoms, goal setting and action planning. It also includes patient-physician shared decision-making, among others. The benefits of self-management vary depending on self-management techniques used. They only have marginal benefits in management of chronic musculoskeletal pain.

Society and culture

The medical treatment of pain as practiced in Greece and Turkey is called algology (from the Greek άλγος, algos, "pain"). The Hellenic Society of Algology and the Turkish Algology-Pain Society are the relevant local bodies affiliated to the International Association for the Study of Pain (IASP).

Undertreatment

Undertreatment of pain is the absence of pain management therapy for a person in pain when treatment is indicated.

Consensus in evidence-based medicine and the recommendations of medical specialty organizations establish guidelines to determine the treatment for pain which health care providers ought to offer. For various social reasons, persons in pain may not seek or may not be able to access treatment for their pain. The Joint Commission, which has long recognized nonpharmacological approaches to pain, emphasizes the importance of strategies needed to facilitate both access and coverage to nonpharmacological therapies. Users of nonpharmacological therapy for pain management generally have lower insurance expenditures than those who did not use them. At the same time, health care providers may not provide the treatment which authorities recommend. The need for an informed strategy including all evidence-based comprehensive pain care is demonstrated to be in the patients' best interest. Healthcare providers' failure to educate patients and recommend nonpharmacologic care should be considered unethical.

In children

Acute pain is common in children and adolescents as a result of injury, illness, or necessary medical procedures. Chronic pain is present in approximately 15–25% of children and adolescents. It may be caused by an underlying disease, such as sickle cell anemia, cystic fibrosis, rheumatoid arthritis. Cancer or functional disorders such as migraines, fibromyalgia, and complex regional pain could also cause chronic pain in children.

Assessment
Young children can indicate their level of pain by pointing to the appropriate face on a children's pain scale.

Pain assessment in children is often challenging due to limitations in developmental level, cognitive ability, or their previous pain experiences. Clinicians must observe physiological and behavioral cues exhibited by the child to make an assessment. Self-report, if possible, is the most accurate measure of pain. Self-report pain scales involve younger kids matching their pain intensity to photographs of other children's faces, such as the Oucher Scale, pointing to schematics of faces showing different pain levels, or pointing out the location of pain on a body outline. Questionnaires for older children and adolescents include the Varni-Thompson Pediatric Pain Questionnaire (PPQ) and the Children’s Comprehensive Pain Questionnaire. They are often utilized for individuals with chronic or persistent pain.

Nonpharmacologic

Caregivers may provide nonpharmacological treatment for children and adolescents because it carries minimal risk and is cost effective compared to pharmacological treatment. Nonpharmacologic interventions vary by age and developmental factors. Physical interventions to ease pain in infants include swaddling, rocking, or sucrose via a pacifier. For children and adolescents physical interventions include hot or cold application, massage, or acupuncture. Cognitive behavioral therapy (CBT) aims to reduce the emotional distress and improve the daily functioning of school-aged children and adolescents with pain by changing the relationship between their thoughts and emotions. In addition this therapy teaches them adaptive coping strategies. Integrated interventions in CBT include relaxation technique, mindfulness, biofeedback, and acceptance (in the case of chronic pain). Many therapists will hold sessions for caregivers to provide them with effective management strategies.

Pharmacologic

Acetaminophen, nonsteroidal anti-inflammatory agents, and opioid analgesics are commonly used to treat acute or chronic pain symptoms in children and adolescents. However a pediatrician should be consulted before administering any medication.

Professional certification

Pain management practitioners come from all fields of medicine. In addition to medical practitioners, a pain management team may often benefit from the input of pharmacists, physiotherapists, clinical psychologists and occupational therapists, among others. Together the multidisciplinary team can help create a package of care suitable to the patient.

Pain physicians are often fellowship-trained board-certified anesthesiologists, neurologists, physiatrists or psychiatrists. Palliative care doctors are also specialists in pain management. The American Board of Anesthesiology, the American Osteopathic Board of Anesthesiology (recognized by the AOABOS), the American Board of Physical Medicine and Rehabilitation, and the American Board of Psychiatry and Neurology each provide certification for a subspecialty in pain management following fellowship training. The fellowship training is recognized by the American Board of Medical Specialties (ABMS) or the American Osteopathic Association Bureau of Osteopathic Specialists (AOABOS). As the field of pain medicine has grown rapidly, many practitioners have entered the field, some non-ACGME board-certified.

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