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The contents of this blog contain topics relevant to end of life care written by our own hospice clinical pharmacists. Continue to check this site regularly for the newest post or subscribe to the RSS feed below.
Lori Osso-Connor, PharmD, CGP

Review of Addison’s Diease

Addison’s disease or adrenal insufficiency is a very rare hormonal disorder. It is so rare that this condition is often not discussed in end of life care. It can be useful to understand Addison’s disease and the management of this condition as many of these patients are on steroid therapy that may overlap with the hospice plan of care. This highlights importance of obtaining a complete and accurate medical history on admission to ensure that we have a full understanding of why the patient is on a current medication therapy.

Addison’s disease is a result of a hormanal change in the adrenal glands. The adrenal glands are walnut sized organs that sit on top of the kidneys. Their function is to produce cortisol, aldosterone, and DHEA (dehydroepiandrosterone) which are necessary for many functions in the body. There are two types of adrenal insufficiency: primary adrenal insufficiency and secondary adrenal insufficiency. Primary adrenal insufficiency occurs when the adrenals cannot produce enough cortisol and/or aldosterone due to some type of damage to the adrenals caused by an infection, virus, or autoimmunity. Approximately 80% of Addison’s disease is caused by an autoimmune disorder. This is when the body’s immune system attacks its own organs. Secondary adrenal insufficiency occurs when the pituitary in the brain fails to produce ACTH (adrenocortisotropin). Secondary adrenal insufficiency may be caused by the abrupt discontinuation of high doses of steroids, surgical removal of pituitary tumor, or a change in the pituitary gland function. ACTH is needed to stimulate the production of cortisol. If the ACTH is low, the cortisol will also be low.

The HPA axis (hypothalamic-pituitary-adrenal axis) is a negative feedback mechanism which functions to control cortisol levels. In the brain, the hypothalamus releases corticotrophin releasing hormone(CRH) which then signals the pituitary to release ACTH. ACTH signals the adrenals to make cortisol. When cortisol levels peak, there is a negative feedback that tells the hypothalamus to stop releasing CRH and thus the pituitary to stop making ACTH.

Cortisol, a glucocorticoid, aldosterone, a mineralcorticoid, and DHEA, sex hormones, have many functions in the human body. Cortisol helps to maintain blood pressure, regulate metabolism, and slows the inflammatory response. Aldosterone works to maintain blood pressure and balance sodium and potassium. If aldosterone is low, sodium is decreased and potassium is increased. DHEA makes the sex hormones androgen and estrogen.

The symptoms of adrenal insufficiency include: weight loss, fatigue, abdominal pain, muscle weakness, nausea and vomiting, hypotension, dizziness, hypoglycemia, and salt craving. Additionally, hyperpigmentation can occur in primary adrenal insufficiency. This is due to the high ACTH stimulation the melanocytes in the skin especially in the skin folds, elbows, knees, and palms of the hands.

The primary treatment for adrenal insufficiency is the replacement of oral hydrocortisone (a glucocorticoid) plus or minus fludrocortisone (a mineralcorticoid). If the patient becomes ill or has an accident and is unable to swallow, the injectable form of hydrocortisone must be administered. Events such as surgery or pregnancy would also cause those with adrenal insufficiency to be managed with the injectable formulation instead of oral. When a patient becomes ill, they must follow a stress dosing plan by doubling or tripling the steroid doses dependent on the numerical value of the fever as the body requires more cortisol to deal with the acute illness.

Patients must be very compliant or they could end up in an Addisonian crisis which could lead to shock and death. Symptoms of an adrenal crisis include: low blood pressure, low blood sodium, low blood glucose, and high blood potassium.

Adrenal insufficiency is diagnosed through blood and urine tests. This will help to determine the cortisol level. If the cortisol level is low, an ACTH stimulation test will be done. The patient will be given an IV injection of synthetic ACTH and samples of blood, urine or both are taken before and after the injection. If the cortisol rises in response to the ACTH, Addison’s can be ruled out. A little or no increase indicates adrenal insufficiency. If the ACTH test is abnormal, a CRH stimulation test can be done to determine the cause of the adrenal insufficiency. A patient is injected with synthetic CRH and blood is taken before, 30, 60, 90, 120 minutes after the injection. Addison’s patients will produce a high ACTH with no cortisol response. Those with secondary adrenal insufficiency will fail to produce ACTH or it is delayed. If it is delayed, the hypothalamus is the cause. If no ACTH is produced, the pituitary is the cause. Other tests may include an ultrasound of the abdomen to see if there are structural abnormalities in the adrenals, a tuberculin test, and antibody blood tests.

Those with adrenal insufficiency should always wear a medic alert bracelet to indicate that they are cortisol dependant. They also need to always carry the injectable form of the corticosteroid in the event of an emergency.

There is still a lot to learn with adrenal insufficiency. The recent article, The Diagnosis and Treatment of Primary Adrenal Insufficiency in the Journal of Clinical Endocrinology acknowledges that diagnostic procedures and treatment strategies are far from optimal. They also state that the validity of the adrenal function tests are questionable. Salivary cortisol testing which has been done by functional medicine for many years is only recently being acknowledged in the medical world as a biomarker. Liquid chromatography testing is also being studied as a diagnostic test. Additionally, replacing cortisol has no effect on the HPA axis and ACTH levels remain high. Drugs such as rituximab and tetracosactide has resulted in regeneration of cortisol production. Immunomodulatory treatment to stop the autoimmune response may eventually be the treatment for those with autoimmune adrenal insufficiency. They have also documented a successful adrenal transplantation. As you can see, much work needs done so that adrenal insufficiency can have a cure and not just a treatment.


References:
1. Bornstein, SR, Bruno A, Wiebke A, Andreas B, Don-Wauchope A, Hammer GD, et al. "Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline." The Journal of Clinical Endocrinology & Metabolism 101.2 (2016): 364-89. Web.
2. Loechner, K. "Adrenal Insufficiency and Addison's Disease." N.p., May 2014. Web. 12 Feb. 2016.

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Irene Petrides, PharmD

Management and Treatment of Gout

2016 07 15 8 42 15Gout is a syndrome of acute or chronic recurrent arthritis and pain. The incidence of this condition continues to rise with increasing age. Therefore, this condition is a common comorbidity for many hospice patients. Reviewing the characteristics of gout and how to most appropriately manage this condition can help us to also best manage our hospice patients.  

Gout is characterized by having chronic hyperuricemia. Hyperuricemia is defined as having urate levels greater than 6.8 mg/dl which is considered the level at which the physiological saturation threshold is exceeded.5 Hyperuricemia is the result of overproduction or underexcretion of uric acid. Increased production of uric acid is less common but is seen in myeloproliferative disorders or lymphoproliferative disorders.1 The risk of developing gout can be associated with medications, renal disease, obesity, and hypothyroidism.2 Medication that are most frequently associated with gout are thiazide and loop diuretics. Stress, trauma or alcohol ingestion may also result in an acute gout attack. Due to multiple comorbid conditions with combination of medication use, the elderly have an increased occurrence of developing gout.5

The clinical presentation of an acute gouty attack includes the abrupt onset of joint inflammation causing pain and swelling. This can occur at any time of the day be seems to present most often during the night. Gout commonly affects the first metatarsophalangeal joint and can also affect the feet, ankles, heels, knees wrist, fingers, and elbows. Symptoms include fever, chills, warmth, swelling, erythema, and intense pain of the involved joint.2 An untreated, mild gout attack will usually subside within 3 to 10 days. However, nephrolithiasis, nephropathy, or urate deposits in affected joints can occur in severe cases.1 Treatment of an acute gout attack should start immediately following symptoms and include the use of nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and/or corticosteroids.2

Due to excellent efficacy NSAIDs are considered first line therapy for gout management. Indomethacin, naproxen, and sulindac are approved for labeling by the Food and Drug administration for the treatment of gout. Note other NSAIDs can be used in the treatment of gout but they do not all have the labeled indication for treating gout. Therapeutic success is based on how quickly the drug is initiated. High dose therapy should be initiated and continued for 24 hours after complete resolution of gout and then taper down over 2 to 3 days. After initiating therapy, resolution of gout should occur within 5 to 8 days.2 NSAIDs should be monitored closely or avoided in patients with cardiovascular disease, severe chronic kidney disease, and peptic ulcer disease. Common adverse effects include gastrointestinal intolerance and worsening of renal function.

Colchicine is a medication which is highly effective at treating an acute gout attack and produces a response within hours of administration. Colchicine should be reserved for patients who are unable to take NSAID therapy. However, if colchicine is not administered within the first 48 hours of onset of an acute attack, then efficacy is substantially diminished.  Abdominal cramping and diarrhea may be reported with colchicine therapy. Recommendation include to start colchicine therapy at initial dose of 1.2mg followed 1 hour later by another 0.6mg and not to exceed 1.8mg on the first day of therapy. Therapy with continue at a dose of 0.6mg daily or twice daily until gout attack resolves.2 Due to multiple drug interactions including lipid lower agents, colchicine should be used with extreme caution due to risk of toxicity. Therefore, colchicine should be avoided in patients with renal or hepatic disease and would not be the drug of choice.

Corticosteroids are reserved for patients where NSAID therapy and colchicine therapy are contraindicated or in patients who do not have clinical response to NSAIDs or colchicine.1,4 Patients with gout in multiple joints may benefit from the use of an oral corticosteroid.2 High dose therapy is initiated at onset of gout for 3 to 5 days and then should be tapered gradually over 10 to 14 days in order to avoid a rebound attack. Although most patients tolerate oral corticosteroids, common adverse effects may include mood changes, flood retention, hyperglycemia and increased blood pressure.5

Allopurinol is indicated for prophylactic therapy. Allopurinol is usually initiated after the first gout attack or after the passage of the first renal stone. If the first gout attack was mild and quickly responded to therapy, allopurinol does not need to be initiated.2 Initial dose of allopurinol is 100mg per day and titrated up 100mg per week to achieve a uric acid level of 6 mg/dL or less with a maximum dose of 800mg per day. Adverse effects include skin rash, leukopenia, gastrointestinal problems, headache and urticarial.4

When treating gout, a comprehensive treatment strategy is required. This includes lifestyle changes including a restricted diet. Comorbidity and medication use need to be taken into account. Initiate immediate treatment of acute gout flares with NSAIDS, colchicine or corticosteroids. When indicated, initiate uric acid lowering therapy (allopurinol) at the proper time usually weeks after an acute flare is subsided. Recognizing the signs and symptoms of gout in a timely manner is the primary contributing factor to a desired therapeutic outcome. The goal of therapy is to reduce pain and disability with minimal adverse effects.


References

  1. Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi, T. Terkeltaub, R. (2012). 2012 American College of Rheumatology guidelines for management of gout. Part 1: Systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res Arthritis Care & Research, 64(10), 1431-1446.

  2. Khanna D, Khanna PP, Fitzgerald JD, Singh MK, Bae S, Neogi T, Terkeltaub, R. (2012). 2012 American College of Rheumatology guidelines for management of gout. Part 2: Therapy and antiinflammatory prophylaxis of acute gouty arthritis. Arthritis Care Res Arthritis Care & Research, 64(10), 1447-1461.

  3. Edwards N, Sundy J, Forsythe A, Blume S, Pan F, Becker M. (2010). Work productivity loss due to flares in patients with chronic gout refractory to conventional therapy. Journal of Medical Economics, 14(1), 10-15.

  4. Edwards N, Sundy J, Forsythe A, Blume S, Pan F, Becker M. (2010). Work productivity loss due to flares in patients with chronic gout refractory to conventional therapy. Journal of Medical Economics, 14(1), 10-15.

  5. Mandell, BF. (2008). Clinical manifestations of hyperuricemia and gout. Cleveland Clinic Journal of Medicine, 75(Suppl_5).

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Shane Donnelly, PharmD

Estimating Risk for Thromboembolism in Atrial Fibrillation: The ATRIA Risk Score

2016 06 28 9 45 57Atrial fibrillation, or Afib, is essentially a temporary, semi-permanent, or permanent change in the electrophysiology of the atria of the heart. Afib is the abnormal rapid contraction of the atria, resulting in an irregular atrioventricular contraction rhythm. This decreases the heart’s ability to eject blood through the body efficiently (decreased cardiac output), thus increasing stasis of pooled blood within the chambers of the heart. Patients with atrial fibrillation are at an increased risk for arterial thromboembolic events because of the procoagulant effect of hemostasis.

The most common arterial thromboembolic event correlated with atrial fibrillation is ischemic stroke. Determining the risk for thromboembolism in these patients is multifactorial and risk factors such as concurrent valvular heart disease (i.e. mitral valve stenosis, prosthetic valves etc.), significantly increase the risk for thromboembolism.1 In patients with valvular heart disease, the risk for thromboembolism high and anticoagulation or antiplatelet therapy should be utilized, barring significant contraindications to either warfarin (Coumadin) or aspirin. Hospice patients with prosthetic valves, mechanical valves, or significant valvular stenosis should maintain anticoagulation or antiplatelet therapy until the patient loses the ability to swallow, or a bleeding diathesis poses a greater risk to the patient and family than the benefit of preventing an ischemic stroke.

In patients with non-valvular atrial fibrillation, the risk of stroke is less significant and warrants an investigation into the patient’s risk of having an ischemic event. There are several modalities by which to estimate risk for thromboembolism in patients with non-valvular atrial fibrillation. The CHADS2 and CHA2DS2-VASc scores are the most common scoring tools utilized by clinicians. Each scoring system is briefly described below.2

CHADS2 - Assigns points to patients based upon risk factors proven in various trials to increase the risk for ischemic stroke in patients with atrial fibrillation. Does not take into account previous history of arterial vascular disease (aortic plaque, myocardial infarction, peripheral arterial disease, etc.) or sex. Assigns 1 point for: congestive heart failure, hypertension, age greater than 74, or the presence of diabetes mellitus. Assigns 2 points to patients with a history of stroke/TIA. In this scoring system, patients with a score of 0 are considered low risk, a score of 1 equates to a moderate risk, and 2 or greater indicates a high risk patient.

CHA2DS2-VASc - Broadens stroke risk assessment for patients between the ages of 65-74, adds increased risk points for age greater than 74, and includes history of arterial vascular disease and female sex as additional risk factors. Assigns 1 point for: congestive heart failure, hypertension, presence of diabetes mellitus, arterial vascular disease, age between 65-74, or female sex. Assigns 2 points for an age greater than 74 years and history of stroke/TIA. This risk estimation system utilizes the same risk score-based anticoagulation parameters as CHADS2.

The 2014 AHA/ACC/HRS guidelines recommends utilizing vitamin K antagonists (i.e. warfarin) or novel oral anticoagulants (rivaroxaban [Xarelto ®] or apixaban [Eliquis ®]) with a CHADS2 or CHA2DS2-VASc score of 2 or greater (moderate-high risk).3 The downfall to utilizing these risk assessments is the underestimation of low risk in patients who fit parameters for high risk of stroke.

The ATRIA (Anticoagulation and Risk Factors in Atrial Fibrillation) risk score is a novel tool designed to more accurately define high risk versus low risk patients.4 The ATRIA score includes risk factors addressed with CHADS2/CHA2DS2-VASc and adds the presence of renal dysfunction as an additional risk factor (eGFR < 45 mL/min or ESRD and proteinuria). The ATRIA risk score, however, stratifies patients into two categories based on the presence/absence of stroke/TIA in the past medical history. This unique feature of ATRIA may provide additional clinical significance in avoiding anticoagulation when it may actually not be clinically necessary.

In hospice patients, the need for anticoagulation is a clinical conundrum that frequently leaves clinicians wondering if anticoagulation is necessary. Patients may or may not be able to swallow, which complicates matters further. The ATRIA risk score may provide hospice clinicians a better picture as to whether anticoagulation is necessary. The scoring system is more time-intensive in comparison to the CHADS2/CHA2DS2-VASc stroke risk scores, but in the end may be able to help prevent adverse bleeding events and can become a cost-effective approach to anticoagulation in hospice patients. The scoring system is as follows:4

Risk Factor Points without prior stroke Points with prior stroke
Age (years)
            85 or greater 6 9
               75-84 5 7
               65-74 3 7  
               Less than 65 0 8
Female 1 1
Diabetes 1 1
CHF 1 1
Hypertension 1 1
Proteinuria 1 1
eGFR less than 45 mL/min 1 1

In patients with an ATRIA risk score of 6 or below, the risk of stroke per 100 patient years is approximately that of a CHADS2/CHA2DS2-VASc stroke risk score or 0-1.2 In patients scoring above a 6, the benefits of stroke prevention most likely outweigh the risk of major bleeding with anticoagulation. In patients with a score less than 6, it may be feasible to discontinue anticoagulation or downgrade the intensity of anticoagulation. Downgrading anticoagulation could include discontinuing warfarin or the novel oral anticoagulants, discontinuing clopidogrel, and switching the patient to low-dose aspirin (81 mg orally once daily). If the patient’s ATRIA scores are as low as 2, anticoagulation is most likely unnecessary.

Most clinicians are familiar with the CHADS2/CHA2DS2-VASc stroke risk scores. Some hospice patients may require a more rigorous assessment of stroke risk, and the benefits of anticoagulation should be weighed versus the risks of adverse bleeding events, drug interactions, and the evolving issue of polypharmacy. It may be advantageous to consider utilizing the ATRIA risk score to assist with anticoagulation decision making at the end-of-life in patients with non-valvular atrial fibrillation. Populations that may particularly benefit from an ATRIA risk assessment include patients with no history of stroke/TIA and those at an older age without renal dysfunction or other significant comorbidities.


References:
1. Nishimura R, Otto C, Bonow R et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(23):2440-2492. Accessed December 14th 2015.
2. Friberg L, Rosenqvist M, Lip G. Evaluation of risk stratification schemes for ischaemic stroke and bleeding in 182 678 patients with atrial fibrillation: the Swedish Atrial Fibrillation cohort study. European Heart Journal. 2012;33(12):1500-1510. Accessed December 14th 2015.
3. January C, Wann L, Alpert J et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary.Journal of the American College of Cardiology. 2014;64(21):2246-2280. Accessed December 15th 2015.
4. Singer D, Chang Y, Borowsky L et al. A New Risk Scheme to Predict Ischemic Stroke and Other Thromboembolism in Atrial Fibrillation: The ATRIA Study Stroke Risk Score. Journal of the American Heart Association. 2013;2(3):e000250-e000250. Accessed December 17th 2015.

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Irene Petrides, PharmD

Management of Orthostatic Hypotension

2016 06 01 14 58 09

Orthostatic hypotension affects 20-30% of the population over 65.1 Orthostatic hypotension or postural hypotension is a form of low blood pressure that occurs when you stand up from a sitting or lying down position. It is defined as a drop in systolic blood pressure by ≥20 mmHg and ≥10 mmHg for diastolic blood pressure. Normal individuals only have a 5-10 mmHg drop in their systolic blood pressure when standing. There are many pharmacologic and nonpharmacologic therapies used to treat orthostatic hypotension. Examples of pharmacologic therapy include midodrine and fludrocortisone, whereas nonpharmacologic therapies involve body manipulation, postural changes and diet. Note that the use of fludrocortisone in the management of orthostatic hypotension is considered an off-label use of this medication.

Midodrine targets the alpha adrenergic receptors on the vasculature, but does not target the central nervous system therefore this medication is not associated with central nervous side effects because it does not cross the blood brain barrier. Midodrine is often dosed 2-3 times daily at a starting dose of 2.5mg with peak effect at 25-30 minutes. Doses are often increased rapidly until response is achieved with a maximum of 30mg per day.2 Potential adverse effects include uterine contractions, tachycardia, headaches, palpitations and arterial hypertension, especially in supine position.2 Final doses of midodrine should be taken 4 hours prior to bedtime in order to reduce supine hypertension.

Fludrocortisone is a mineralocorticoid. This medication stimulates the release of salt into the bloodstream. By increasing blood volume there is a rise blood pressure. Therapy is initiated at 0.1mg per day. Peak effect occurs in 1-2 weeks therefore dosing should be increased at weekly or biweekly intervals. Most patients obtain optimal blood pressure control at 0.3-0.4mg per day. Potential adverse effects include hypokalemia and hypomagnesemia, supine hypertension, and headache.3 In addition, the patient may gain up to 8 pounds in weight when maximal effect of therapy is achieved.3

Nonpharmacologic therapy in orthostatic hypotension can provide an integral role in reducing a blood pressure drop upon standing. Therapies include an addition of salt to the diet or salt tablets in order to correct salt depletion due to polyuria and poor oral intake. Moderate physical exercise has been shown to improve orthostatic tolerance. Compression stockings and abdominal binders have been shown to be effective, although if patient can tolerate, abdominal binders have been shown to be more effective. Physical maneuvers such as crossing the legs or bending forward can help raise blood pressure. Another approach to a nonpharmacologic treatment for orthostatic hypotension is sleeping in the head up position. Although, the efficacy of head tilt has not been determined. It is important to have the patient stand up slowly from the supine position. Also, prolonged exposure to heat can exacerbate orthostatic hypotension. Therefore, reducing exposure can limit complications.4

In concluding, a combination of pharmacological and nonpharmacological therapies should be considered in treating orthostatic hypotension. The methods summarized in this article can provide beneficial outcomes. Using these methods, it is possible to reduce undesired issues with orthostatic hypotension such as falls, loss of consciousness and even broken bones.


References:
1. Rutan G, Hermanson B, Bild D, Kittner S, LaBaw F, Tell G. Orthostatic hypotension in older adults. The Cardiovascular Health Study. CHS Collaborative Research Group. Hypertension. 1992;19(6_Pt_1):508-519. doi:10.1161/01.hyp.19.6.508..

2. Doyle. Midodrine: use and current status in the treatment of hypotension. Br J Cardiol. 2012;19(1). doi:10.5837/bjc.2012.007.

3. Medow M, Stewart J, Sanyal S, Mumtaz A, Sica D, Frishman W. Pathophysiology, Diagnosis, and Treatment of Orthostatic Hypotension and Vasovagal Syncope. Cardiology in Review. 2008;16(1):4-20. doi:10.1097/crd.0b013e31815c8032.

4. Thompson, P., Wright, J., & Rajkumar, C. (2011). Non-pharmacological treatments for orthostatic hypotension. Age and ageing, 40(3), 292-293.

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Michelle Mikus, PharmD

The Opioid-Induced Hyperalgesia Phenomenon

2016 06 02 10 28 25

Morphine is the gold standard of pain relief in hospice, so anytime it is administered there is at least some degree of pain relief, right? Not always! In 1943 an interesting paradoxical reaction to morphine was being reported in peer-reviewed literature and became known as Opioid Induced Hyperalgesia (OIH). While still not fully understood, it is important to recognize that this phenomenon can occur when caring for patients that have long-term opioid use.

Clinically, OIH can present one of two ways. The first is simply hyperalgesia, which is increase response to painful stimuli. The second is allodynia, which is a painful response to typically non-painful stimuli (a feather, for example). The pain that presents is often a different quality of pain and at times is in a different location.

Most research regarding OIH has been conducted in laboratory animals and has yielded results that are linear: increased opioid use = increased OIH. Unfortunately, there is not enough human data to support this correlation, but fortunately, it does not seem to be so linear. At the center of the current discussion is whether OIH results from an increasing tolerance to opioid pain medications or from taking the medications themselves (with the medication causing the perceived pain). At this point, the only thing that is certain is that OIH is quite complex and differs among patients.

One interesting observation showed that as chronic pain patients were tapered appropriately off of opioids, a portion of the patients rated their pain the same or even better. One very preliminary study that was done to look at the cause of OIH pointed to a natural progression of chronic pain. If that proves to be true, OIH would be better stated as a natural state of hyperalgesia from chronic pain.

Managing patients with OIH is largely dependent on alternative methods of pain relief. The dose of opioid should be reduced and that alone may help reduce the experienced pain. Doses can be reduced up to 50% and if appropriate, low dose methadone can be added. Withdrawal should be avoided as this can worsen pain. Rotation from a morphine derivative to fentanyl, methadone or buprenorphine may also be effective. Ketamine has been used also. Alternative pharmacologic agents can be used in combination with a lower dose of the same opioid or a different opioid. Other pharmacologic options include antidepressants (duloxetine, tri-cyclic compounds such as nortriptyline), anticonvulsants (carbamazepine, gabapentin, pregabalin), and NSAIDs (ibuprofen, naproxen, meloxicam, diclofenac). Note that the use of carbamazepine in the management of pain is considered an off-label use of this medication. Nerve blocks and spinal cord stimulation have also been used along with cognitive behavioral therapy as non-pharmacological interventions.

Caring for patients with OIH can be a significant clinical challenge as it is not well understood yet. It is important to recognize that if a patient is in pain and a larger dose of an opioid is given that effectively manages the pain, the patient likely does not have OIH. For patients that experience an increase in pain or a different quality of pain as a result of an increased opioid dose, look to alternative pharmacologic therapies to help increase quality of life.


References: 
1. Lee M, Silverman SM, et al. A comprehensive review of opioid-induced hyperalgesia. Pain Physician. 2011 Mar-Apr;14(2):145-61. 
2. Melville N. Complexities of Opioid-Induced Hyperalgesia Poorly Understood. Medscape Multispecialty. March 31, 2015. http://www.medscape.com/viewarticle/842359#vp_1. Accessed Dec 30, 2015. 
3. Schug S. Opioid-induced hyperalgesia: What to do when it occurs? Ann Palliat Med 2012;1(1):6-7. 
4. Tompkins DA, Campbell CM. Opioid-Induced Hyperalgesia: Clinically Relevant or Extraneous Research Phenomenon? Curr Pain Headache Rep. 2011 Apr; 15(2): 129–136.

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