Lecture 5 Opioids, NSAIDS, Antiarthritics, PCA PDF

OPIOID M A R I LYN T HOM P SON ODOM , ANALGESICS P H. D.  Endogenous Opioids Our bodies also have endogenous opioids: endorphins, enkephalins Regulate functions such as pain relief, euphoria induction, stress resilience, CV protection, food intake contro...

OPIOID M A R I LYN T HOM P SON ODOM , ANALGESICS P H. D.  Endogenous Opioids Our bodies also have endogenous opioids: endorphins, enkephalins Regulate functions such as pain relief, euphoria induction, stress resilience, CV protection, food intake control.  Opioid Analgesics Patients often take these after surgery and trauma, pain with advanced cancer, end-of-life-care Group of drugs that can relieve moderate to severe pain Produce substance use disorder and tolerance can occur Classified as a controlled substance in the US Morphine is the original prototype  Three major categories of opioid receptors: Mu-opioid receptor Kappa-opioid receptor Delta-opioid receptor Each receptor class has several subclasses Stimulation of any of these 3 causes Opioid analgesia Receptors Receptors exist throughout the body; distribution varies based on organs Mu receptors are located in the brain and spinal cord and are the most important for mediating the analgesic effects of many opioids especially morphine The more significant side effects result from Mu receptor stimulation Respiratory depression and constipation Opioid abuse and addiction  Opioids are classified as: Strong agonists Mild-to-moderate Classification agonists Mixed agonist- antagonists Antagonists  Used to treat severe pain Interact primarily with mu opioid receptors in the CNS Strong Agonists Best known: morphine (MS Contin) Other examples: Fentanyl Meperidine (Demerol) Methadone (Methadose)  Mild-to-Moderate Agonists Efficacy and affinity are reduced relative to strong agonists More effective at treating moderate pain Examples: Codeine Hydrocodone Oxycodone  Exhibit some agonist and some antagonist (or partial agonist) activity because they act different at different classes of opioid receptors Cause analgesia - bind to and activate kappa receptors (kappa agonists) while they are blocking mu receptors (mu receptor antagonists) Mixed-Agonist- Produce adequate analgesia with less side effects (respiratory Antagonists depression) Reduced risk of fatal overdose Fewer addictive qualities Example: Buprenorphine-partially activates mu receptors, but an May produce psychotropic effects: hallucinations, vivid dreams antagonist at kappa receptor; used for opioid treatment disorders Maximal analgesic effect is not as great as that of a strong agonist Antagonists Block all opioid receptors with an increased affinity for the mu receptors Will not produce analgesia Will displace opioid agonists from the receptors are can be used to treat opioid overdoses and addiction Example: naloxone (Narcan) Can be given in emergency situations when a patient is in respiratory distress from opioid overdose Will reverse the respiratory depression within 1-2 minutes  Pharmacokinetics Administration: oral, suppository form Long-acting formulas (extended release) Subcutaneous and intramuscular injection are necessary for some opioids due to poor intestinal absorption or the effects of first pass Some are administered via IV Transdermal patches can be used: fentanyl Steady, prolonged administration into the systemic circulation Iontophoresis can be used to enhance the effects of these Some opioids can be administered systemically through lozenges or lollipops (dissolve in mouth)  Distributed equally in all body tissues Main effect occurs after they reach the CNS Pharmacokinetics Metabolic inactivation takes place in the liver with a small amount occurring in the lungs, kidneys, and CNS Excreted in the urine  Opioids act on neuronal receptors in the brain, spinal cord and peripheral tissues. Mechanism of Action Analgesic effect is due to modifying synaptic activity at these  Spinal Effects Act at the spinal cord to inhibit painful impulses from being sent from the periphery to the brain (afferent) Supraspinal (Brain) Effects Sites of Opioid receptors are found at several locations in the brain Opioid Opioids bind to these and remove inhibition in descending pathways that decrease pain (efferent) Effects Peripheral Effects of Opioids Opioid receptors are found in the periphery Opioids bind to these and provide analgesic effects by decreasing the excitability of these sensory neurons Inhibit the neuron from initiating transmission of painful stimuli toward the spinal cord  Opioid analgesics work best on moderate to severe pain that is constant in duration Not as effective on sharp, intermittent pain Used clinically for: surgery, trauma, MI, and chronic pain with cancer Oral administration of a mild-to-moderate Treatment of Pain opioid agonist should be used first Then stronger agonists are used orally and then parenterally Opioids often alter the pain perception more than eliminating the pain Patient no longer perceives that they are in pain and experience a euphoria and a sense that they are floating  Parenteral routes may be more effective in chronic, severe pain Using an epidural or intrathecal space may be optimal Catheters are often surgically implanted so that the tip is in the epidural or intrathecal space Programmable drug delivery systems can then be used Continuous infusion can cause Treatment of Pain nausea and constipation Patient controlled anesthesia (PCA) is an example of this – patient controls how much medicine they receive Oral opioids are most effective when given at regular intervals – patient should not wait until they feel pain Need to keep plasma levels at a therapeutic range Other Uses Opioids are also used as premedication or an adjunct to general anesthesia Cough suppressors Codeine Decrease GI motility so can be used to control severe diarrhea  Adverse Effects Sedative properties, mental slowing and drowsiness Euphoria Respiratory depression is the most serious side effect Within a few minutes of administration can see slowing of the breathing rate which can last for several hours GI distress: N & V, constipation  Addiction When an individual repeatedly ingests the drug for mood-altering and pleasure or to get a “high” Tolerance The need to progressively Addiction, increase the dosage of the Tolerance and drug to achieve a therapeutic effect when the Dependence drug is used for prolonged periods The number and sensitivity of the receptors for opioids can decrease over time causing tolerance and the need to increase dosage  Physical Dependence Onset of withdrawal symptoms when the drug is abruptly removed Opioid withdrawal is evident 6-10 hours after the last dose of the drug and will continue for 5 days Symptoms of opioid withdrawal: Body aches Addiction, Diarrhea Tolerance and Fever Dependence Goosebumps Irritability Shivering Sweating Tachycardia N&V Weakness/fatigue The risk of tolerance and dependence is low with opioid drugs are used appropriately  Opioid Induced Hyperalgesia Some patients may fail to respond to opioids or may report increased pain (hyperalgesia) when given the drugs Maybe be due to genetic factors If the patient’s pain does not improve or it increases after beginning an opioid the physician needs to be notified  Methadone is the drug used to treat opioid addiction This is an opioid agonist like morphine It has milder withdrawal symptoms than other opioids Methadone is substituted for the opioid that the patient is Treating Addiction of addicted to (example: heroin) Opioids and then it is slowly withdrawn as the patient goes through counseling and is monitored Buprenorphine and naltrexone are also used for opioid dependence Buprenorphine—mixed agonist antagonist Naloxone—opioid antagonist  Side effects like sedation and GI discomfort can be bothersome during therapy Pain relief from opioids will allow much better tolerance to therapy sessions PT should be scheduled during Rehab their peak effect Considerations Remember that these drugs can cause respiratory depression Regarding Use of Hypoxia and hypercapnia can be Opioids seen Respiratory response to rehab exercises can be blunted Opioid addicts may c/o diffuse mm aches Modalities may help with the discomforts of opioid withdrawal Nonsteroidal Anti- Inflammatory Drugs (NSAIDs) NSAIDs Decrease Relieve mild to inflammation moderate pain Decrease risk of Reduce fever blood clotting (inhibit platelet aggregation) NSAIDs Aspirin is the original NSAID Acetaminophen is similar to aspirin in pain and fever relief, but it is NOT an NSAID because it does not have anti-inflammatory properties or anticoagulant properties NSAIDs NSAIDs work by interfering with the synthesis of an endogenous compound called prostaglandins All cells in the body (except RBC) can produce prostaglandins They are hormones that help regulate cell function under normal conditions as well as pathological conditions Production of prostaglandins increases when a cell has undergone trauma Prostaglandins During injury our body naturally increases prostaglandin production Inflammation: prostaglandins play an important role in inflammation; inhibition of this will help manage acute and chronic inflammation Pain: increase prostaglandins increase the sensitivity of pain receptors Fever: increased prostaglandins promotes fever How NSAIDs Work Aspirin and other NSAIDs are This enzyme is the first step in the synthesis of prostaglandins all inhibitors of the Inhibiting this enzyme will inhibit cyclooxygenase enzyme (COX) prostaglandin production COX-1 COX enzyme has 2 subtypes: COX-2 COX-1 and COX-2 COX-1 enzyme produces prostaglandins that help regulate normal cell activity and maintain cell homeostasis Prostaglandins produced by this enzyme are generally beneficial COX-2 enzyme is produced primarily in injured cells It then produces prostaglandins that mediate pain and other aspects of the inflammatory response Prostaglandins produced by this enzyme are more harmful COX-1 and COX-2 Best clinical results will be achieved by inhibiting the prostaglandins produced by COX-2 and sparing those produced by COX-1 Aspirin and traditional NSAIDs are non-selective and do not act in this manner Decrease pain and inflammation by blocking COX-2 Decreases platelet aggregation by irreversibly inhibiting formation of prostaglandin derivative, thromboxane A2 Decrease the production of beneficial and protective prostaglandins which is why gastric damage and kidney damage can occur Aspirin Acetylsalicylic acid Oldest NSAID Used to manage pain in musculoskeletal and joint disorders, after surgery (decreased need for as much opioids) Used to prevent clots; conditions such as heart attack, CVA Can be used to treat fever in adults Ibuprofen is also frequently used for fever in adults and children Aspirin Cancer prevention Regular aspirin use decreases chances of colorectal cancer May also help prevent GI cancers (stomach, esophagus) and non-GI cancers (bladder, breast, prostate) Aspirin helps prevent tumor growth by inhibiting the COX-2 enzyme which inhibits prostaglandins which could cause abnormal cell division in these tissues Side Effects of NSAIDs Primary side effect is GI damage GI hemorrhage, ulceration due to loss of protective prostaglandins Take aspirin with meals to reduce the risk Use of other drugs with aspirin can help prevent or treat GI side effects Proton pump inhibitors: inhibit the secretion of gastric acid from mucosal cells which can decrease the risk of ulcers Side Effects of NSAIDs Cardiovascular Decreased platelet activity and reduce the risk of clots Can increase blood pressure which ultimately increases the risk of thrombotic events This risk is greatest in those who have HTN at baseline or other cardiac risk factors These risks are greatest in the COX-2 selective drugs COX-2 enzyme causes vasodilation so the selective drugs cause vasoconstriction which increases BP Side Effects of NSAIDs Aspirin drugs can cause adverse changes in hepatic function in patients with liver disease or when taken in excessive doses Aspirin drugs can also cause problems with the kidneys when given to patients who have impaired renal function, DM, heart failure, or those with decreased body water Aspirin overdose is known as aspirin intoxication or poisoning Symptoms: HA, tinnitus, difficulty hearing, confusion, GI distress, metabolic acidosis Side Effects of NSAIDs Aspirin is also associated with Reye’s syndrome High fever, vomiting, liver dysfunction, and increasing unresponsiveness, delirium, coma and even death Only occurs in children and teenagers so it is recommended that they not take aspirin Aspirin can also inhibit bone healing so it should not be taken in anyone who has a healing fracture or s/p spinal fusion Aspirin vs. NSAIDs No evidence that Nonaspirin NSAIDs Certain NSAIDs are less NSAIDs are better than have less GI discomfort toxic to other organs aspirin as an anti- but overall can have (liver and kidneys) than inflammatory drug or some stomach aspirin pain medication irritation Patients should be Non-prescription Cost of prescription prescribed the NSAID NSAIDs (Ibuprofen) can NSAIDs is 10-20x more that provides them cost up to 5x more than aspirin with the best response than aspirin at the least cost COX-2 Selective Drugs Aspirin and most NSAIDs are nonselective (inhibit both COX-1 and COX-2) Selective COX-2 inhibitors (example: Celebrex) have less gastric irritation They do cause an increase in upper respiratory tract infections Cause an increased risk in heart attack and stroke in patients with cardiac risk factors – HTN, heart disease Many of the COX-2 selective drugs have been taken off of the market because of this risk (example: Vioxx) Only COX-2 selective drug still on the market is celecoxib (Celebrex) Acetaminophen Tylenol Often equal to NSAIDs and aspirin for pain relief and fever reduction Not associated with upper GI irritation Used widely in treating non-inflammatory conditions that have mild to moderate pain, especially if there is a history of gastric damage (ulcers) First drug used in early stages of OA and other non- inflammatory musculoskeletal conditions Used for children and teenagers with fever Acetaminophen May also activate descending MOA not fully serotonergic inhibitory pathways in CNS elucidated Antipyresis is due to inhibition of the hypothalamic heat-regulating center High doses of acetaminophen People with preexisting liver disease or individuals who are alcoholics may be can be toxic to susceptible to liver damage if they take the liver and can acetaminophen be fatal (15 g) Thoughts for Physical Therapists The drugs discussed can create analgesia without sedation Stomach discomfort is a concern Patients may inquire about the differences of over- the-counter medications such as aspirin, acetaminophen and ibuprofen Management of RA & OA Rheumatoid Arthritis (RA) Chronic, systemic disorder that causes synovitis and destruction of the articular cartilage Pain, stiffness and inflammation of the small synovial joints in the hands, feet and in larger joints (knee) Progressive disease that can lead to severe joint destruction and bone erosion Juvenile rheumatoid arthritis is RA that is diagnosed in children younger than 16 drug treatment is like adult RA Rheumatoid Arthritis (RA) The joint damage causes pain and suffering, disability, and decreased quality of life Increased incidence of cardiovascular disease and other comorbidities RA is caused by an autoimmune response in genetically susceptible individuals Drug Treatment of RA Two goals: Decrease joint inflammation Decrease or stop the progression of the disease Three categories of drugs: NSAIDs Glucocorticoids Disease-modifying antirheumatic drugs (DMARDs) NSAIDs Aspirin and NSAIDs used to be the first medications used for RA This changed with the development of DMARDs which slow the progression of RA NSAIDs are still used for reducing inflammation and pain Glucocorticoids reduce inflammation to a greater extent but NSAIDs have fewer side effects Choosing the right NSAID for RA treatment is based on trial and error NSAIDs COX-2 inhibitors and traditional NSAIDs are associated with heart attack and increased CVA risk so there is concerns about using these long term COX-2 inhibitors are less toxic on the stomach and other tissues than other NSAIDs Acetaminophen is not recommended for use with RA. Why? NSAIDs Most common side effect: stomach irritation Gastric ulceration, hemorrhage The use of NSAIDs, even COX-2 inhibitors, have decreased with the development of DMARDs but they do still have an important role in the management of RA Glucocorticoids (corticosteroids) Effective anti- Example: Prednisone inflammatory agents Early use of these in RA progression can decrease Provide symptomatic joint erosion and damage relief by decreasing joint (which slows disease inflammation and the progression) pain associated with RA High doses are required to actually have this effect which can have serious side effects Glucocorticoids Effective as a supplement to DMARDs throughout all phases of RA DMARDs take several weeks to become effective so using a glucocorticoid initially with a DMARD can help control pain and inflammation until the DMARD takes effect Many patients take low doses of glucocorticoids in combination with DMARDs throughout their entire disease process Glucocorticoids Can be used during acute Can be injected directly flare-ups or exacerbations into the joint in order to of RA manage exacerbations Can even be given in high doses Only 2-3 injections per joint per for a week or two if needed year during a flare up Glucocorticoids Mechanism of Action Bind to a receptor in the cytoplasm of certain cells and form a glucocorticoid-receptor complex The complex moves to the cell’s nucleus where it binds to genes that regulate the inflammatory process By binding to these genes, the production of pro- inflammatory substances are inhibited, and production of anti-inflammatory proteins occurs Glucocorticoids Adverse Effects Osteoporosis – especially when used at higher doses for prolonged periods of time Muscle wasting and weakness HTN Aggravation of DM Glaucoma Cataracts Increased risk of infection **These side effects all need to be considered and glucocorticoid use should be limited in those with RA Disease-Modifying Antirheumatic Drugs (DMARDs) Medications that halt or slow the progression of RA Early and aggressive use of these can slow the disease progression and promote remission before the joints become too damaged When used with NSAIDs and glucocorticoids the long term outcomes are improved and improvements in quality of life are noted They inhibit certain aspects of the immune response that is the cause of RA Disease-Modifying Antirheumatic Drugs (DMARDs) Antimalarials Nonbiological DMARDs Biological DMARDs Tumor Necrosis Factor Inhibitors Other DMARDs Antimalarials These are a group of nonbiological traditional DMARDs Only hydroxychloroquine is FDA approved for RA Chloroquine may be prescribed off label These drugs work by affecting immune cell responses Antimalarials Side effects: High doses can cause irreversible retinal damage Doses for RA are usually below what would cause this Recommend regular eye exams for patients Considered very safe compared to other DMARDs Small risk of headache and GI distress Methotrexate Used in the treatment of cancer Used to treat RA in children and adults Shows the effects of RA: decreases synovitis, decreases bone erosion and decreases the narrowing of the joint space Has greater therapeutic effects than other DMARDs Rapid onset - only 2-3 weeks Much lower dose than that used for chemotherapy Methotrexate Side Effects Very toxic drug GI tract: loss of appetite, nausea, intragastrointestinal hemorrhage Pulmonary problems Hematological disorders Liver dysfunction Hair loss Side effects are noted primarily with long term use Tumor Necrosis Factor Inhibitors Tumor necrosis factor-α is a protein that is released from cells involved in inflammatory responses TNF- α promotes joint erosion and inflammation with RA By inhibiting TNF- α the progression of the destructive effects of RA are slowed TNF- α is a biological DMARD because it affects a biological response to a specific protein Tumor Necrosis Factor Inhibitors They can also be used Must be given TNF- α can be used as as a substitute for other parenterally: an initial treatment for DMARDs when patients subcutaneous injection RA have not responded or by slow IV fusion well to them Tumor Necrosis Factor Inhibitors Side Effects: Prone to upper respiratory infections and other infections such as sepsis Contraindicated in people who have infections Should be discontinued if an infection develops Malignancy (lymphoma) Liver disease Heart failure Lupuslike disease Demyelinating disorders that mimic MS JAK inhibitors Used when TNFα-inhibitors fail Not a “biologic”; still considered a DMARD Orally administered Risk of serious cardiovascular problems (MI, stroke, pulmonary embolus); gastrointestinal perforation risk Other DMARDs Physicians may also prescribe other immunosuppressants for RA management These drugs are more toxic and are reserved for patients who have not responded to traditional DMARDs like methotrexate Examples: immunosuppressants that are used to prevent rejection s/p transplant, to treat cancer, or to treat IBS Combining DMARDs DMARDs can be used simultaneously when treating RA A combination of 2 or more drugs can have optimal benefits and a low dose can be used of each Methotrexate is typically the cornerstone drug with other DMARDs added to it Often TNF-α is combined with it Increased potential for toxicity and drug interactions when combining DMARDs Combining DMARDs may provide the best success though for RA remission Diet and RA Some RA symptoms can be reduced through diet Diets high in fish oil and omega-3 fatty acids are beneficial because they help control inflammation Foods with antioxidant properties are beneficial (fruits, vegetables) Diets high in meat and protein can exacerbate symptoms Cigarette smoking can increase the risk of RA in susceptible populations Osteoarthritis (OA) 50% of those 65 and older have OA Not caused by an immune system response Due to an intrinsic defect in the remodeling of the joint cartilage and underlying subchondral bone Progressive deterioration of articular cartilage that is accompanied by degenerative bone changes Osteoarthritis (OA) Treatment of joint inflammation is not a major focus in OA Inflammatory synovitis does occur in OA, but this is secondary to the articular damage Focus should be on nonpharmacological interventions: PT, weight loss, joint replacements in advanced stages Osteoarthritis (OA) New drugs have emerged Drug therapy is used to Focus has been that slow or reverse the manage pain and acetaminophen and pathological changes: maintain active lifestyle NSAIDs to relieve pain disease-modifying OA drugs (DMOADs) OA: Acetaminophen and NSAIDs Acetaminophen is often the first drug used to treat OA NSAIDs are used to treat pain with OA also Used for analgesic properties but the anti-inflammatory properties can help the mild synovitis that occurs due to joint destruction Some NSAIDs can be applied topically over the joint: will give pain relief without side effects such as GI discomfort These drugs do not change the course of OA Viscosupplementation One type of disease-modifying OA drugs (DMOADs) Uses a substance known as hyaluronan (hyaluronic acid) to restore the lubricating properties of synovial fluid in arthritic joints Injected into the arthritic joint to maintain or restore viscosity which limits joint destruction progression Also improves pain and function  Viscosupplementation 3-5 weekly injections can be Pain usually decreases Beneficial for 6 months – 1 Can delay the need for given within days year after a series of more aggressive treatment injections such as joint replacements Glucosamine & Chondroitin Sulfate Dietary supplements may help protect articular cartilage or reverse the joint deterioration found in OA These are 2 key ingredients needed to produce synovial fluid and articular cartilage Available as a nonprescription dietary supplement Another form of disease-modifying OA drugs (DMOADs) More Facts About Pain Meds Acetaminophen dosages Geriatric patient: 2500 mg is the max per day (or 2.5 g); for healthy normal adult 4.0 g/day is the limit Regular Tylenol has 325mg acetaminophen Extra Strength Tylenol has 500 mg Norco has 325mg acetaminophen and it also has hydrocodone in it NORCO® 7.5/325 and NORCO® 10/325 Pain medication commonly used in geriatrics opioid Percocet has 325 mg acetaminophen Acetaminophen and oxycodone Opioid 2.5mg/325mg; 5mg/325mg; 7.5mg/325mg; 10mg/325mg What Kind of Pain Medication is it? Opioid NSAID Acetaminophen Tramadol (Ultram) (Rx) Aspirin (OTC) Tylenol (OTC) Hydrocodone (Rx) Celecoxib (Celebrex) (Rx) Oxycodone (Rx) Diclofenac (Voltaren) (OTC) NORCO (Rx) Ibuprofen (Motrin, Advil) (OTC) Percocet (Rx) Meloxicam (Mobic) (Rx) Meperidine (Demerol) Naproxen (Naprosyn) (OTC) Morphine (MS Contin) Codeine OTC = over the counter; Rx = prescription required Comparison of Side Effects Opioids NSAIDs Aspirin Acetaminophen Sedative properties: Gastric damage Hepatotoxicity or Can be toxic to the liver mental slowing, (hemorrhage, ulcers) impaired liver function in high doses drowsiness (those with liver disease) Respiratory depression Kidney damage in those Kidney damage in those (slowed breathing rate) with kidney disease with kidney disease GI distress: nausea, Increase BP (COX-2 Aspirin poisoning: HA, constipation, vomiting selective drugs) tinnitus, difficulty hearing, confusion, GI distress, metabolic acidosis Addiction, tolerance, Inhibit bone healing Reye syndrome physical dependence Experience euphoria Inhibit bone healing Patient- Controlled Analgesia (PCA) Patient-Controlled Analgesia Patient can self administer small doses of a pain medication (often opioid) at frequent intervals Typically delivered through an IV or into the spinal canal by a type of pump Allows the patient to have some control over pain – as pain increases the patient can administer more medication Used s/p surgery, in patients with cancer and other chronic pain conditions Patient-Controlled Analgesia In order to control pain drugs should be delivered into the bloodstream or target tissues in a constant and predictable manner With traditional pain medication there are periods of time when the concentration of the drugs falls below the therapeutic window, and this causes the pain to increase Patient-Controlled Analgesia Side effects are nearly non- With PCA the drug levels existent with PCA because are kept more constant and the concentration does not remain in the therapeutic rise above the therapeutic window window PCA Terminology Loading Initial large dose given to bring the level of analgesia to the therapeutic window dose Demand Amount of drug that can be self administered by the patient each time dose they activate the PCA Lockout Minimum amount of time allowed between each demand dose interval PCA Terminology Background infusion rate Small amount of analgesic that can be continuously administered Provides low background level of analgesia Can lead to increased risk of side effects Not routinely used Successful versus total demands PCA systems record the total times the patient demanded the medication vs. how many times they were allowed to have it Types of Analgesia used for PCAs Non-opioid analgesics can Opioids are the primary PCA be combined with opioid PCAs can also deliver local medication analgesics to reduce the anesthetics quantity of opioids needed PCAs are a safer way to Example: epidural used administer opioids during childbirth because they keep plasma levels stable without large fluctuations PCA Pumps Pumps can be: External Implantable PCA Routes IV Epidural Regional IV PCA Most common way to use PCA is through intravenous administration Small intermittent doses of the drug are administered through a catheter and directly into systemic circulation Effective for a short period of time – first few days after surgery If it is needed for a longer period of time, then a central venous access point is recommended Port is located directly under the skin Epidural PCA Drugs are administered directly into the area outside of the meninges surrounding the spinal cord Can also be administered directly into the subarachnoid space: spinal or intrathecal administration Epidural is the preferred method – its safer and there is less risk of damaging the meninges Epidural PCA gives more effective analgesia with less drug as compared to IV PCA Drug is closer to the spinal cord and gets into systemic circulation quicker Regional PCA & Oral Route Patient self-administers the drug directly into Provides localized pain an anatomical site: peripheral joint, relief without side effects peripheral nerve, or into a wound on other tissues or organs Bedside device provides a Oral route pill when activated by the patient Comparison of PCA to other analgesics Patients report increased satisfaction with PCA as compared to other methods of analgesic administration Continuous infusions are another method that are rated very highly by patients They tend to supply more quantity of the drug though which places the patient at risk for increased side effects PCA Adverse Effects When opioids are used in PCAs the side effects are the same as with other opioid administration Sedation, GI problems, respiratory depression Decreased or equal risk to these side effects as with other methods of administration Rehab Implications Patients who are using PCA for pain management typically have less sedation and are more alert PCA decreases the need to schedule therapy around medication administration since plasma concentrations are constant Patients may be more mobile with PCA than with traditional pain methods: increased pain relief means the patient is out of bed sooner Rehab Implications PTs should monitor for signs of problems or malfunction with PCA If patient shows signs of respiratory depression or excessive sedation it could indicate that the patient has been overdosed by the PCA system