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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.
Holly Lassila, DrPH, MSEd, MPH, RPh

Acute Myocardial Infarction in Women

2016 12 28 10 12 46The American Heart Association recently released a scientific statement concerning Acute Myocardial Infarction in Women.1 Cardiovascular disease is still the leading cause of death in women in the United States and globally and of the 2.7 million women with a history of an (myocardial infarction) MI, more than 53,000 have died of an MI, and an estimated 262,000 were hospitalized for AMI and unstable angina. The differences in the clinical presentation between men and women have consequences for timely identification of symptoms, appropriate triage, diagnostic testing and treatment. Compared with men women are more likely to have pain in the upper back, arm, neck, and jaw as well as unusual fatigue, flu-like symptoms, dyspnea, indigestion, nausea/vomiting, palpitations, weakness, and a sense of dread and anxiety feeling.

Mehta LS, et al reported the top ten things to know about acute myocardial infarction in women:

1. Although there has been a reduction in cardiovascular mortality death in women in the US, there has not been a substantial decline in acute MI event rates or MI deaths in young women. 

2. Compared with older women, younger women are trending with worse risk factor profiles and higher mortality.

3. Plaque characteristics differ for women, and recent data have suggested a greater role of microvascular disease in the pathophysiology of coronary events among women even though epicardial coronary artery atherosclerotic disease remains the basic cause of acute MI in both men and women.

4. Date from autopsy studies have shown that women have an increased prevalence of plaque erosion compared to men, and that MI without obstruction coronary artery disease (CAD) is more common at younger ages and among women.

5. Any young woman who presents with an acute coronary syndrome without typical atherosclerotic risk factors should be suspected of having spontaneous coronary artery dissection (SCAD). This is a very rare condition and occurs more frequently in women. The clinical presentation of SCAD can be unstable angina, MI, ventricular arrhythmias, and sudden cardiac death.

6. Recent evidence suggests that depression in women is a powerful predictor of early-onset MI, showing a strong association with MI and cardiac death in young and middle-aged women than in men of similar ages. In the general population, depression is 2 times more prevalent in women than in men.

7. Women with risk factors such as high blood pressure and diabetes have an increased risk of heart attack compared to men.

8. As mentioned above, women are more likely to present with pain in the upper back, arm, neck, and jaw, as well as unusual fatigue, dyspnea, indigestion, nausea/ vomiting, palpitations, weakness, and a sense of dread, compared with men who present with central chest pain.

9. Research suggests that women are delayed in seeking treatment for acute MI compared to men. Reasons for the delay include living alone, interpreting symptoms as non urgent and temporary, consulting with a physician or family member and fear and embarrassment.

10. Women, compared to men, tend to be undertreated and are less likely to participate in cardiac rehabilitation after a heart attack.


 Submitted by: Holly Lassila, DrPH, MSEd, MPH, RPh; Hospice Clinical Pharmacist at Delta Care Rx


 References:
1. Mehta LS, et al; on behalf of the American Heart Association Cardiovascular Disease in Women and Special Populations Committee of the Council on Clinical Cardiology, Council on Epidemiology and Prevention, Council on Cardiovascular and Stroke Nursing, and Council on Quality of Care and Outcomes Research. Acute myocardial infarction in women: a scientific statement from the American Heart Association [published online ahead of print January 25, 2016]. Circulation. doi: 10.1161/CIR.0000000000000351.

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Sydney Janusey, PharmD

HAART and Palliative Care: A Combined Approach

2016 12 28 9 53 55

Drug therapies continue to evolve so often that the goals of their intended care for certain disease states also change. A classic example of this shift would be the medications used to treat HIV and AIDS. Less than a few decades ago the medications for HIV/AIDS were purely thought as palliative and were used to keep patients from suffering near the end of life. Now with highly active antiretroviral therapy (HAART) as a first line treatment option, patients are living without an imminent threat to their health status. However, there are a few points to consider when looking at HAART and patients at the end of their life in need of symptom management and palliation. The drugs used to treat HIV/AIDS come with a lot of side-effects and drug interactions, particularly interactions with medications used in palliative care. Palliative care in HIV/AIDS does not always have to be an alternative treatment, but one that can be combined with disease-state focused therapy1.

Important goals of palliative care include treating pain, fatigue, weight loss, nausea, vomiting, and depression. Here are some examples of medications appropriate for treating these signs.
1. For the symptom of fatigue, consider managing with prednisone, dexamethasone, or methylphenidate.2

2. For the symptom of weight loss, consider managing with prednisone, dexamethasone, or megestrol acetate (non-preferred).2
3. For the symptom of nausea and vomiting, consider managing with metoclopramide, haloperidol, prochlorperazine, promethazine, lorazepam, or corticosteroids.2
4. For the symptom of depression, consider managing with methylphenidate, prednisone, or dexamethasone.2

As medications are added to a patient’s care plan it is very important to consider a few crucial interactions between HAART and commonly used palliative care medications.2 The protease inhibitors ritonavir, indinavir, nelfinavir, saquinavir and amprenavir as well as non-nucleoside reverse transcriptase inhibitor (NNRTI) delavirdine interact with commonly used antidepressants including fluoxetine, paroxetine and sertraline. The NNRTIs efavirenz and nevirapine interact with anticonvulsants carbamazepine, phenytoin, and phenobarbital. In addition to these interactions on the basis of the cytochrome P450 enzyme the following medications should also be used with caution: meperidine, methadone, codeine, morphine, fentanyl, dronabinol, benzodiazepines and zolpidem.2

Inevitably there will come a time when discontinuation of HAART is warranted.2 With this discussion comes the question of benefit versus. risk of therapy.2 The benefit is based on the patient’s prognosis and treatment goals for their end of life care. The benefits of continuing therapy include protection against encephalopathy or dementia, relief of constitutional symptoms and a psychological benefit from comfort that treatment is being maintained.2 The risk includes the continued build up of adverse effects from medications no longer truly working, patient comfort, and complication of end of life care and advance planning.2

As palliative care services continue to grow and play a greater role the trend is shifting towards palliation of symptoms.2 These medications should be given much earlier in care allowing patients to be comfortable for a longer period of time than just at the end of life.2 Eventually, however, removing HAART with a heavy side-effect profile and focusing on symptom palliation will lead to the most comfort for the patient and ideal treatment for their last days.1


 Submitted by: Sydney Janusey, PharmD; Hospice Clinical Pharmacist at Delta Care Rx


References:
1. O’Neill, Joseph F et al. A Clinical Guide to Supportive and Palliative Care for HIV/AIDS. US Department of Health and Human Services. Health Resources and Services Administration. HIV/AIDS Bureau. 2003. Accessed February 28, 2016.

2. Selwyn, Peter A; Forstein, Marshall. Overcoming the False Dichotomy of Curative vs Palliative Care for Late-Stage HIV/AIDS. JAMA, Vol 290, No 6. August 13, 2003.Accessed February 16, 2016.

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Michelle Mikus, PharmD

Purple is NOT the New Yellow: A Clinical Look at Purple Urine Bags

From orange to red and all shades of yellow, most clinicians can list reasons for discolored urine. When urine appears purple, however, both patients and clinicians are taken off guard. Interestingly enough, Purple Urine Bag Syndrome (PUBS) is a very real however rare clinical phenomenon that cannot go unnoticed.

Purple urine bags are just that -the bags themselves appear to have a purple tint. The urine itself is not discolored. This happens when gram-negative bacteria that produce two specific enzymes (phosphatase and sulfatase) are present in the urine and react with PVC urinary catheters and bags. While urinary tract infections are common, especially among patients in long term care facilities, PUBS is not common since it is dependent on bacteria producing those specific enzymes.

Patients that present with PUBS are often geriatric females with a history of constipation and are catheterized. Patients most often have multiple comorbid conditions, however this could be coincidental due to the age and environment of care of the patient population from many case studies. Alkaline urine plays an important role as does dehydration. Constipation allows for an overgrowth of bacteria which introduces more potential pathogens to the body (including E. Coli). The final component of the purple color is the presence of tryptophan in the body, which when in the presence of sulfatase and phosphatase in an alkaline environment is converted to indigo (blue) and indirubin (red). When indigo and indirubin combine, they appear purple to the eye.

A purple urine bag is very apparent indication of a urinary tract infection that needs treated. If not treated quickly, septicemia can occur and outcomes can be fatal, especially considering the population this most often occurs in. By treating the underlying infection and therefore eliminating the presence of phosphatase and sulfatase in the urine, the urine bag for a catheterized patient will no longer turn purple in color when replaced.


 Submitted by: Michelle Mikus, PharmD; Hospice Clinical Pharmacist at Delta Care Rx; Pharmacy Manager at ProCure Pharmaceutical Services


 References:

  1. Lin CH. Huang HT. Chien CC, et al. Purple urine bag syndrome in nursing homes: ten elderly case reports and a literature review. Clin Interv Aging. 3:729-34. 2008

  2. Harun NS, Nainar SK, Chong VH. Purple urine bag syndrome: a rare and interesting phenomenon. South Med J. 100:1048-50. 2007

 

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Delta Campus Pharmacy Student

Lack of E-Prescribing Controlled Substances by Doctors

2016 08 22 14 07 33A recent article in USA Today discussed the fact that although electronic prescribing of prescriptions, specifically controlled substances, would be a great way to cut down on abuse and fraud the majority of the United States is not utilizing this system. Only 7% of doctors are electronically prescribing controlled substances today. Currently only three states actually require that controlled substances be e-prescribed, however, only two of these three actually enforce this law. The three states that require controlled substances to be e-prescribed include Minnesota, New York and Maine.

Minnesota was the first state to require e-prescribing of controlled substances, although they do not allow physicians to be penalized for not doing so. New York requires physicians to check the online database to see if patients are getting controlled substances elsewhere before prescribing. They are then required to e-prescribe these prescriptions or they could face legal action. Maine became the third state to require e-prescribing of controlled substances in April 2016 and starting January 2017 physicians could face fines and/or jail time for not doing so.

Opioid abuse is one of the leading causes of death in the country currently, much of the abuse stemming from prescription painkillers. Physicians e-prescribe non-controlled medications on a regular basis and now that they have the ability to electronically send prescriptions to pharmacies for controlled substances they should be utilizing this software. Eliminating paper prescriptions can ensure that the patient is not altering the prescription in anyway, it would lessen the chance of patients ‘doctor-shopping’ to get multiple prescriptions, and it could prevent the chance of physician prescription pads being stolen which we see in the news all too often. Some people are afraid that although e-prescribing may make it harder for drug users to get their hands on controlled substances it could lead to these individuals turning to heroin to get their fix instead. Either way you look at the issue it is amazing that so few physicians are taking advantage of this new technology simply as an easier way to keep records if nothing else.

Hospices utilizing e-prescribe technology automatically meet federal and state regulations regarding how prescriptions are issued for controlled substances. Delta Care Rx is the only hospice pharmacy benefit manager in the United States that has developed their own proprietary e-prescribing platform for hospice clients. Currently, more than 250 clinicians use the Delta Care Rx e-prescribing tool. The number of hospice clinicians utilizing the Delta Care Rx e-prescribing technology is expected to quadruple by 2017 says Drew Mihalyo, PharmD who is the President and COO of Delta Care Rx.


Submitted by: Stephanie Stuparitz, PharmD Candidate 2017, Duquesne University


Reference:
O’Donnell J. Most doctors don’t use e-prescribing for opioids. USA Today. May 19, 2016: 3A.

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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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Delta Campus Pharmacy Student

Anticoagulation Bridging Chart

There are several patient specific factors that need to be taken into account when selecting an oral anticoagulant. At times, a patient may no longer be appropriate for their current anticoagulant and need to be converted to another agent. The below chart is to serve as a guide when making clinical decisions on how to convert a patient from one anticoagulant to another agent and/or safe practices for discontinuing an anticoagulant.

Drug

Bridging Required

Indication/Dosing D/C Plan for Standard Bleeding Risk Procedure D/C Plan for High Bleeding Risk Procedure
Dabigitran (Pradaxa®)

DVT and pulmonary embolism: YES

Administer 150 mg twice daily after 5 to 10 days of parenteral anticoagulation

Dabigitran to warfarin: YES

Dabigitran contributes to INR elevation; warfarin’s effect on the INR will be better reflected only after dabigitran has been stopped for ≥2 days.

Start time must be adjusted based on CrCl:

CrCl >50 mL/minute: Initiate warfarin 3 days before discontinuation of dabigitran

CrCl 31 to 50 mL/minute: Initiate warfarin 2 days before discontinuation of dabigitran

CrCl 15 to 30 mL/minute: Initiate warfarin 1 day before discontinuation of dabigitran

CrCl  There are no recommendations provided in the U.S. manufacturer’s labeling.

Warfarin to dabigitranNO

Discontinue warfarin and start dabigitran when INR is less than 2

Atrial Fibrillation: CrCl >30, 150mg BIDif CrCl 15-30 then 75mg BID, CrCl

DVT/PE: CrCl >30 150mg BID, if CrCl

CrCl ≥ 50 Stop dabigitran 2 days before procedure

CrCl 30-50 stop dabigitran 3 days before procedure

CrCl ≥ 50 Stop dabigitran 3 days before procedure

CrCl 30-50 stop dabigitran 4-5 days before procedure

Rivaroxaban

(Xarelto®)

Rivaroxaban to warfarin: YES

Typically in general practice, clinicians stop rivaroxaban and start both a parenteral anticoagulant and warfarin at the time the next rivaroxaban dose should have been taken

Warfarin to rivaroxabanNO

Discontinue warfarin and start rivaroxaban as soon as the INR is below 3 to avoid insufficient anticoagulation

Non-valvular Atrial Fibrillation: CrCl >50, 20mg QD w/ evening mealif CrCl 15-50 then 15mg QD

DVT/PE

Treatment: 15mg BID w/ food for first 21 days then 20mg QD w/ food for remaining treatment

Risk Reduction: 20mg QD w/ food

Prophylaxis after surgery:

-Hip replacement: 10mg QD for 35 days

-Knee replacement: 10mg QD for 12 days

CrCl ≥ 50 Stop rivaroxaban 2 days before procedure

CrCl 30-50 stop  rivaroxaban 2 days before procedure

CrCl 15-30 stop  rivaroxaban 3 days before procedure

CrCl ≥ 50 Stop rivaroxaban 3 days before procedure

CrCl 30-50 stop  rivaroxaban 3 days before procedure

CrCl 15-30 stop  rivaroxaban 4 days before procedure

Apixaban (Eliquis®) 

Apixaban to warfarinYES

Discontinue apixaban, and begin both a parenteral anticoagulant and warfarin at the time when the next dose of apixaban should have been taken. Then stop parenteral anticoagulant once INR reaches goal range

Warfarin to apixabanNO

Apixaban should be started when INR is < 2

Atrial Fibrillation: 5mg BID

Any two of the following:  ≥ 80 y/o,  Scr ≥ 1.5 mg/dl or ≤ 60 kg: 2.5 mg BID

ESRD on hemodialysis: 5mg BID

On hemodialysis + ≥ 80 y/o or ≤ 60 kg: 2.5mg BID

CrCl <25: Not recommended

Hip replacement: 2.5mg BID 12-24 hrs after surgery for 35 days

Knee replacement: 2.5mg BID 12-24 hrs after surgery for 12 days

DVT/PE

Treatment: 10mg BID for 7 days then 5mg BID for 6 months

Risk reduction: 2.5mg BID for at least 6 months after DVT/PE

CrCl ≥ 50 Stop apixaban 2 days before procedure

CrCl 30-50 stop apixaban 3 days before procedure

CrCl ≥ 50 Stop apixaban 3 days before procedure

CrCl 30-50 stop apixaban 4 days before procedure

Edoxaban (Savaysa™)

DVT and pulmonary embolism: YES

Oral: 60 mg once daily after 5 to 10 days of initial therapy with a parenteral anticoagulant

Edoxaban to warfarin: YES

Oral: For patients taking edoxaban 60mg once daily, reduce dose to 30mg once daily and begin warfarin concomitantly. For patients taking edoxaban 30mg once daily reduce the dose to 15mg once daily and begin warfarin concomitantly. Measure INR at least weekly and discontinue edoxaban once INR ≥2 and continue warfarin therapy

LMWH and other oral anticoagulants other than warfarin to edoxaban: YES

Start edoxaban at the time of the next scheduled dose, when transitioning from unfractionated heparin, discontinue the infusion and start edoxaban four hours later

Warfarin to edoxaban: NO

Discontinue warfarin and start edoxaban when the INR is ≤ 2.5

Atrial fibrillation: CrCl >50 and CrCl  >95 AVOID USE

DVT/PE

Treatment: CrCl>50 60mg QD after 5 to 10 days of initial therapy with a parenteral anticoagulant, CrCl 15-50  30mg QD,  CrCl

Discontinue at least 24 hours before surgery or invasive procedure Discontinue at least 24 hours before surgery or invasive procedure

Submitted by: Alisha Ensell, PharmD Candidate 2016 and Shelby Scott, PharmD Candidate 2016


References:
1. Metzger A, Nagaraj T. New Oral Anticoagulants: Clinical Parameters and Uses in Practice. Consult Pharm. 2015;30(6):329-45.
2. Lexicomp Online. Lexicomp Web site. http://www.crlonline.com.authenticate.library.duq.edu/lco/action/home

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Delta Campus Pharmacy Student

Tube Feeding Considerations in End of Life Care

Enteral feeding tubes may be helpful for nutrition support in patients that cannot eat but have a working gastrointestinal tract. Administering medication in these tubes is useful for patients that cannot take it another route, but issues can arise. This article discusses some factors that can affect medications given this route and ways to avoid common issues related to administration down a feeding tube.

The placement site of the tube can alter the medication efficacy. Most oral medications are absorbed in the small intestine. Some medications, for example antacids, sucralfate, and bismuth, act locally in the stomach and would provide minimal benefit if administered in a tube that bypasses the stomach. In addition, if medications that rely on extensive first-pass metabolism, such as opioids, beta-blockers, or tricyclic antidepressants, are administered in a tube that ends in the jejunum, they will have increased absorption and greater efficacy possibly leading to more adverse effects. First-pass metabolism is a result of the drug entering the liver after absorption in the gut resulting in much of the drug being metabolized before reaching the systemic circulation. This is taken into consideration when dosing this type of medication and if it is bypassed, by administering into the jejunum, it leads to a higher concentration of drug than intended

The tube size also plays an important part in deciding medication administration. Small bore tubes are more comfortable for the patient but are more likely to clog, especially with medication administration. Only liquid medications should be used in a Dobhoff tube to prevent clogging. Large bore tubes are less likely to clog, but it is important to know that if the tube is being used for suctioning, medications should not be given down that tube because they might be removed before absorption.

Medications should not be administered or mixed with tube feedings because they can interact and lead to negative effects. Phenytoin is the most well-known medication in this situation, decreasing blood levels of the drug up to 75% when administered with tube feeds. It is recommended to hold feedings 2 hours before and after each dose if possible. Warfarin efficacy is reduced when administered through a feeding tube and INR should be monitored more closely. Other medications can form precipitates with tube feedings, such as iron supplements and sucralfate. Liquid medications prepared as syrups can be acidic and denature proteins in the feeding, causing clumps and leading to clogs.

Liquid dosage forms are the preferred form for enteral administration of medications. Suspensions and elixirs are preferred over syrups because they are less likely to clog. Many liquid preparations contain large amounts of sorbitol which can cause GI upset or diarrhea. There are also liquid medications with high osmolality, above 1000 mOsm/kg, which will draw water into the GI tract and lead to cramping, diarrhea, or vomiting. A few examples of medications with high osmolality include acetaminophen elixir, cimetidine solution, metoclopramide hydrochloride syrup, and lithium citrate syrup.

Medications that should not be crushed include tablets that are controlled-release, enteric-coated, teratogenic, or irritants. Disrupting the controlled-release mechanism can cause toxic blood levels of the drug and enteric-coated drugs do not crush well and when mixed with water will bond together creating a clog. If the medication is teratogenic it should not be crushed for the safety of the staff. Capsules with microencapsulated pellets, such as Depakote Sprinkle and Effexor XR, can be opened and the pellets can be administered in large bore feeding tubes.

The tube should be flushed with a small amount of water both before and after medication administration. Flushing helps prevent clogs and interactions between different medications or tube feeds. Also, if medications are scheduled to be administered at the same time, they should not be given down the tube at the same time but rather administered separately while flushing the tube in between each medication. This is important because medications can precipitate or interact if given together increasing the risk of clogs or decreasing efficacy. Also, it is recommended to hold feeding for 30 minutes before and after the medication is administered if it requires administering on an empty stomach and the tube ends in the stomach. No holding is required if the tube ends in the intestine rather than the stomach.

If clogging does occur it is recommended to intervene as soon as possible by flushing with warm water. It is not recommended to try flushing with acidic liquids, such as soda or cranberry juice, because it has not shown to be more effective than water and might compound the issue by precipitating proteins from the feedings. Instead, an alkalized enzyme solution should be used. It is prepared by crushing one sodium bicarbonate 324mg tablet and one pancrelipase tablet mixed together with 5mL of water.

Overall, medication use in feeding tubes can be complicated with many different factors involved. Problems such as clogged feeding tubes and disruption of medication efficacy negatively affect both the patient and the staff. It is important to recognize why these problems can occur and to follow proper administration guidelines to prevent them in the future.


Submitted by: Alexander Fringes, PharmD Candidate 2016


References:
1. PL Detail-Document. A Stepwise Approach: Selecting Meds for Feeding Tube Administration. Pharmacist’s Letter/Prescriber’s Letter. June 2014. 
2. Williams NT. Medication administration through enteral feeding tubes. Am J Health-Syst Pharm. 2008; 65(24): 2347-57. doi: 10.2146/ajhp080155.
3. Beckwith CM, Feddema SS, Barton RG, Graves C. A Guide to Drug Therapy in Patients with Enteral Feeding Tubes: Dosage Form Selection and Administration Methods. Hosp Pharm. 2004; 39(3): 225-37.
4. Emami S, Hamishehkar H, Mahmoodpoor A, Mashayekhi S, Asgharian P. Errors of oral medication administration in a patient with enteral feeding tube. J Res Pharm Pract. 2012; 1(1):37-40. doi:10.4103/2279-042X.99677.

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Joseph Thomas, PharmD

Cognitive Screening Assessments for Dementia Patients

When it comes to assessing a dementia patient’s cognitive status, there are many different tests that can help determine the patient’s level of impairment. The purpose of these assessments and scales is to help reduce subjectivity in clinical situations. An ideal assessment should have face validity, construct validity, concurrent validity, and inter-rater reliability. Face validity means that clinicians, family members, and patients can agree that the questions are relevant and meaningful. Construct validity means that the assessment accurately tests what it was designed to measure. Concurrent validity means that the assessment can be validated by another gold standard assessment. Inter-rater reliability is when two or more raters can use the same assessment scale and get the same answers.

When it comes to dementia patients, assessments are available to test specifically for function, behavior, and quality of life, but cognition is the coveted characteristic that is attempted to be measured. The most popular cognitive screening test administered is the Mini-Mental State Examination (MMSE). This test is designed to test cognition in areas such as memory, attention, and orientation. It is limited to a low sensitivity to change and it has floor and ceiling effects. Due to copyright enforcement issues surrounding the MMSE, it has started to fall out of favor due to fear of litigation and the Montreal Cognitive Assessment (MOCA) is gaining in popularity due to their promotion of open permission to clinicians to use their assessment without paying for licensing fees or worrying about copyright litigation. The MOCA is a 30 point based assessment and it is more sensitive than the MMSE. It is also useful to assess patients with vascular dementia. It assesses executive function, memory, language, abstraction, orientation, and delayed recall.

The National Hospice and Palliative Care Organization (NHPCO) recommends the Functional Assessment Staging Test (FAST). The FAST scale is designed to evaluate patients when the MMSE cannot reflect changes in a clinically meaningful way and it identifies progressive steps of functional decline. FAST stage 7a is the minimum staging level for hospice enrollment. An assessment used to determine overall dementia severity is the Clinical Dementia Rating (CDR). It is a comprehensive interview based test that assesses memory, orientation, judgement, function, and caregiver burden. Despite being a very useful assessment, one major downside of this assessment is the amount of time it takes to administer.

With many different types of assessments available to clinicians, it is important to select and use a test properly. Many standardized assessments with demonstrated reliability for screening of dementia are available. Clinicians should understand the specifics of an assessment before administering a test. Most tests have training guides to help ensure the correct usage of the assessment. Clinicians should implement the training guides and familiarize themselves with proper administration technique to ensure the validity and reliability of the assessment.


References: 
1. Fast Fact #150. (n.d.). 
2. MoCA Montreal - Cognitive Assessment. (n.d.).
3. Sheehan, B. (2012). Assessment scales in dementia. Therapeutic Advances in Neurological Disorders, 5(6), 349–358.http://doi.org/10.1177/1756285612455733
4. Tsoi KF, Chan JC, Hirai HW, Wong SS, Kwok TY. Cognitive Tests to Detect Dementia: A Systematic Review and Meta-analysis. JAMA Intern Med. 2015;175(9):1450-1458. doi:10.1001/jamainternmed.2015.2152.

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Jessica Horsley, PharmD

Medication Reconciliation and Transitions of Care at End of Life

According to The Joint Commission, medication reconciliation is the process of comparing a patient's medication orders to all of the medications that the patient has been taking. This reconciliation is done to avoid medication errors such as omissions, duplications, dosing errors, or drug interactions. It should be done at every transition of care in which new medications are ordered or existing orders are rewritten. Transitions in care include changes in setting, service, practitioner or level of care. Accurate and complete medication reconciliation can prevent numerous prescribing and administration errors. Medication errors related to medication reconciliation typically occur at the "interfaces of care"—when a patient is admitted to, transferred within, or discharged from a health care facility. Common causes of medication reconciliation errors include inaccuracies or omission during transcription, poor documentation, communication breakdown, and workflow disruption.

Additionally, in hospice and palliative care, some patients may be too ill, injured, young, or disabled to actively participation the medication reconciliation process. Patients may need the assistance of another person (e.g., family member, significant other, surrogate decision maker) if they are overwhelmed in managing their condition, are not proficient in speaking or reading English, or face health literacy challenges that might prevent them from understanding medication use directions. When the patient is unable to actively or fully participate in the medication reconciliation process and has requested assistance from another person, involve the authorized person(s) in the medication reconciliation process. This involvement should occur at all interfaces of care . 

Medication Reconciliation Best Practices:

1. The hospice has a standardized medication reconciliation process in place that is completed and reviewed by the IDT within 5 days of the initiation of care.

a.Medication reconciliation needs to be performed at every nursing visit comparing most current medication sheet from EMR to med sheet that is in patient's home.
b.Medication reconciliation occurs at every IDT meeting where patient cases are reviewed.

2. Any discrepancies that are identified are clarified with the physician and/or pharmacy consultant within 24 hours.

3. There is a process in place to review current medications to determine which ones are related to the primary and secondary diagnosis and therefore the financial responsibility of the hospice.

a. First Verify – collect an accurate list of ALL medications the patient is taking. This becomes the “ONE TRUE SOURCE”
b. Second, Clarify – any questions about which drugs, which dose and which frequency.
c. Third, Reconcile by reviewing this list with the hospice physician and/or pharmacy consultant along with any questions or concerns in order to obtain clarification or revised orders.


4. Provide medication and medication reconciliation education to staff and consider as yearly competency.

a. Assure Staff Training includes at least the following:
        i. Ask the patient/caregiver before the first visit to collect all of the patient’s medications. 
        ii. Note any discrepancy between the prescription on the bottle and what the patient states he/she is taking. 
        iii. Ask about the use of non-prescription medications. 
      iv. Identify any combination of medications that may be contraindicated or medications that seem to be inappropriate such as those on the Beers Criteria.

5. Assure staff has access to AND a process in place to use up to date medication information and software programs to analyze medication interactions, duplication, adverse effects etc.

6. Assessment of the patient and caregiver's ability to administer medication should be done at every nursing visit so that teaching can be customized to their needs and to enhance the safety of medication administration.  Hospice staff can consult with the Delta Care pharmacist during the visit to ensure that questions are answered.

Many of these “best practices” are already in place for your hospice by using Delta Care Rx on-demand pharmacist services. Utilizing a staff properly trained for appropriate medication reconciliation with the patient or caregiver paired with the consultation and information provided by Delta Care pharmacists is an important partnership to prevent dangerous medications errors and curb symptom management issues that may be due to inappropriate medication use and interactions. Although data specifically related to medication errors in hospice and palliative care are sparse, one study found that all hospice patients had at least one medication discrepancy, with an average of eight per patient. Most commonly these discrepancies were omission of medications. Most drug interactions identified were moderately severe. Owing to the fact that polypharmacy often increases as a patient ages and/or becomes more ill, it is prudent to always perform accurate medication reconciliation at each transition of care and provide timely updates to medication profile to ensure that an accurate medication list is always at the ready.


References:
1. The Joint Commission. Using medication reconciliation to prevent errors. Sentinel Event Alert. January 2006; 35. Available from:http://www.jointcommission.org/assets/1/18/SEA_35.PDF
2. Visiting Nurses Association of America. Patient Safety: Medication reconciliation and management. VNAA Blueprint for excellence. Available from: http://0101.nccdn.net/1_5/3d0/168/33c/A-Guide-to-Medication-Reconciliation-and-Management.pdf
3. Kemp L, Narula P, McPherson M, Zuckerman I. Medication reconciliation in hospice: a pilot study. Am J Hosp Palliat Care [serial online]. June 2009;26(3):193-199. Available from: MEDLINE Complete, Ipswich, MA. 

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Shane Donnelly, PharmD

Renal Dosing for Commonly Used Oral Antibiotics

The kidneys are one of the most important organs responsible for eliminating substances from the body. Structural damage to the excretion mechanisms of the kidneys slows the filtration and elimination process down, allowing drug metabolites to stay in the body for longer periods of time. For some medications with inactive and harmless metabolites, this is not a relevant issue. However, for medications with active metabolites or medications that are not completely metabolized by the liver, this poses a potentially significant problem. The inability to efficiently eliminate active drug molecules puts patients at risk for harmful adverse effects. Antibiotics are particularly interesting in this regard. When dosed appropriately and efficiently eliminated by the body, side effect profiles are often mild and harmless. However, when dosed inappropriately in a patient with renal impairment, active drug molecules or metabolites can build up and may induce or exacerbate neurological, cardiac, or pulmonary comorbid conditions.

The table below provides a foundation for dosing common antibiotics in patients with renal impairment. It is important to utilize this table in the manner in which it was intended; purely as a reference point. Individualize treatment based on the patient and the indication that is being treated.

Renal Dosing Guide for Commonly Used Oral Antibiotics  
 
Antibiotic Renal-Dosing Special Considerations  
Amoxicillin (Amoxil) Amoxicillin + Clavulanate Potassium (Augmentin)

Severe Impairment (CKD Stage 4) give 250-500 mg amoxicillin q12h

End-Stage Disease (CKD Stage 5) give  250-500 mg amoxicillin q24h

All products containing

875 mg of Amoxicillin or extended-release formulations should be avoided in patients with severe impairment.

 
Azithromycin (Z-Pack, Zithromax) None. Use with caution. No specific renal dosing required in manufacturer's labeling.  
Cefaclor (Ceclor) None. Use with caution. No specific renal dosing required in manufacturer’s labeling.  
Cefuroxime (Ceftin)

Severe Impairment (CKD Stage 4) give the indicated dose q24h

End-Stage Disease (CKD Stage 5) give the indicated dose q48h

Alternatively, may dose at 15 mg/kg/dose q24h in patients with End-Stage Disease.  
Cephalexin (Keflex)

Moderate-Severe Impairment (CKD Stage 3-4) give 500 mg q8-12h

End-Stage Disease (CKD Stage 5) give 500 mg q12-24h

Cost-effective option for treating skin and soft tissue infections and may be used as an alternative agent for uncomplicated UTIs.  
Ciprofloxacin (Cipro)

Moderate Impairment (CKD Stage 3) give 250-500 mg q12h

Severe Impairment (CKD Stage 4) give 250-500 mg q18h

End-Stage Disease (CKD Stage 5) give 250-500 mg q24h

If using extended-release formulation, dose at 500 mg q24h with Severe Impairment.  
Clarithromycin (Biaxin) Severe Impairment (CKD Stage 4) decrease the dose by 50% Many drug interactions. May need to decrease dose with certain HIV medication.  
Clindamycin (Cleocin) None Potential alternative to penicillin due to allergy.  
Doxycycline Monohydrate (Vibramycin) None Potential safe alternative for community-acquired pneumonia or MRSA in patients with renal dysfunction.  
Erythromycin (Ery-Tab) None Medication can be used to induce gastric motility.  
Levofloxacin (Levaquin)

Moderate Impairment (CKD Stage 3) give 250 mg q24h +/- 500 mg loading dose (or) 750 mg q48h

Severe Impairment (CKD Stage 4) give 250-500 mg q48h +/- 500-750 mg loading dose

Dosing largely depends on indication. Utilize dose of that fits the suspected organism/infection.  
Metronidazole (Flagyl) None. Use with caution. Metabolites may accumulate in patients with End-Stage Renal Disease.  
Nitrofurantoin (Macrobid, Macrodantin) Moderate Impairment (CKD Stage 3) note that use is contraindicated Some literature1 suggests nitrofurantoin can be used safely in patients with a CrCl >40 mL/min for short-term treatment of uncomplicated UTI's (<1 week).  
Penicillin V Potassium (Pen VK) Use with caution. Excretion of penicillin is prolonged in patients with renal impairment.  
Sulfamethoxazole/ Trimethoprim (Bactrim, Septra)

Severe Impairment (CKD Stage 4) decrease the dose by 50%

End-Stage Disease (CKD Stage 5) note that use is not recommended

Dosing is highly dependent on indication.

*Per LexiComp, Wolters Kluwer Health 2
**Degree of Impairment and estimated Glomerular Filtration Rate: Moderate Impairment (CKD Stage 3): CrCl < 60 mL/min; Severe Impairment (CKD Stage 4): CrCl < 30 mL/min; End-Stage Disease (CKD Stage 5): CrCl < 15 mL/min

Age over 65 years old, hypertension, cardiovascular disease, diabetes, tobacco use, and obesity are all risk factors for developing chronic kidney disease 4. Many patients admitted to hospice have at least one of these risk factors. Awareness of the common signs of chronic kidney disease (known risk factors, consistent itching, changes in urine output, etc.4 can help the team to safely utilize medication.

Ultimately, the decision to treat and effectively dose antibiotics relies on the constant vigilance of the palliative care/hospice team. Awareness of the common dosing of antibiotics, the indications, and dosing for renal impairment can lead to better outcomes for patients who experience the uncomfortable reality of their diseases.


References:
1. Oplinger M and Andrews CO. “Drug Information Rounds: Nitrofurantoin Contraindication in Patients With a Creatinine Clearance Below 60 mL/min: Looking for the Evidence,” Ann Pharmacother, 2013, 47(1):106-11. 
2. LexiComp. Hudson, Ohio: Wolters Kluwer Health; c1978-2015. https://online.lexi.com/lco/action/home. 
3. The National Kidney Foundation. GFR. 2014. Available at: https://www.kidney.org/kidneydisease/siemens_hcp_gfr. 
4. Mayoclinic.org. Chronic kidney disease Risk factors - Mayo Clinic. 2015. Available at: http://www.mayoclinic.org/diseases-conditions/kidney-disease/basics/risk-factors/con-20026778.

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Michelle Mikus, PharmD

Rectal Medication Seizure Management Options

In end of life care, often times the oral route of medication administration is not an option. However, it is important that seizure prophylaxis be maintained beyond the patient's ability to swallow and that treatment options are known. The good news about rectal administration of seizure medications is that many antiepileptics that patients take orally can be given rectally. In addition, the dosages of these medications do not need adjusted from oral to rectal.

Phenobarbital is one of the oldest medications used for seizure prophylaxis. This medication is weight based and also takes 4-5 hours to reach peak concentration. For that reason, phenobarbital should not be used for acute seizure episodes. Dosages are most often 1-3mg/kg orally or rectally in divided doses (1-2 times daily). Note phenobarbital is sedating.

Carbamazepine immediate release tablets can be used rectally. Ideally, the same daily oral dosage is given rectally in 6-8 small, divided doses and the crushed tablets are put in a gelatin capsule when possible. Most patients require daily doses between 800-1200mg. Note carbamazepine serum concentrations should be monitored. Carbamazepine suspensions can also be used and would need to be diluted with an equal volume of water.

Valproic acid and divalproex sodium are of the most commonly used medications for seizure prophylaxis. Fortunately, they too can be used rectally when oral administration is not possible. If using the liquid formulations, dilute with an equal volume of water. Optimal response is seen at doses below 60mg/kg/day, in divided doses.

Lastly, a lamotrigine rectal suspension can be prepared out of the immediate release or chewable tablets. This is done by crushing the tablets and mixing into 6-10mL of room temperature water. Most patients find success at a dose of 250mg twice daily.

Benzodiazepines such as diazepam and lorazepam are commonly used rectally for acute seizures and should not be excluded from this overview.

There are many reasons that a patient may need to be on an antiepileptic drug: epilepsy, brain metastases, and even disease progression, to name a few. Using the above information, management of these medications beyond the oral route is possible and dose conversions are not necessary.


References:
1. Connelly, J., & Weissman, D. Fast Fact #229: Seizure Management in the Dying Patient. Retrieved September 4, 2015, fromhttps://www.capc.org/fast-facts/229-seizure-management-dying-patient/
2. Krouwer H, Pallagi J, Graves N. Management of seizures in brain tumor patients at the end of life. J Palliat Med. 2000;3:465-475

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Lori Osso-Connor, PharmD, CGP

Serotonin Syndrome in the Elderly

Serotonin Syndrome or serotonin toxicity occurs when there is overstimulation of the peripheral and central serotonin receptors which causes serotonin to accumulate in the body. Increased serotonin levels can occur through the following mechanisms: increased serotonin production, inhibition of serotonin reuptake, inhibition of serotonin metabolism, increased serotonin release, and/or stimulation of the serotonin receptor. Any medication or combination of medications that can increase the concentration of serotonin can cause serotonin syndrome. The medications most likely to be involved in contributing to serotonin syndrome include selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitor (SNRIs), tricyclic antidepressants (TCAs) or serotonin modulator antidepressants (trazodone).

SSRIs are often used in the treatment of depression. The elderly population is at increased risk of experiencing depression due to disability, co-morbid conditions, and/or the death of loved ones. Therefore, the use of antidepressants in the elderly is common. SSRIs exert their effect by blocking the reuptake of CNS neuron serotonin in the brain. Some examples of SSRIs include: Prozac (fluoxetine), Paxil (paroxetine), Celexa (citalopram), Lexapro (escitalopram), and Zoloft (sertraline).

Serotonin syndrome is often underdiagnosed and clinicians must be aware and identify early symptoms. Serotonin syndrome is diagnosed through clinical symptoms. The hallmark feature of serotonin syndrome is agitation. The common signs are usually a triad of features including: neuromuscular excitation (clonus, rigidity, hyperreflexia), autonomic stimulation (tachycardia, fever, sweating, diarrhea, hypertension), and changes in mental status (confusion, agitation, coma). The Hunter Serotonin Toxicity Criteria is recommended for diagnosing serotonin syndrome.

Serotonin syndrome may occur within minutes to hours of use of the offending medication(s). The severity could range from mild to severe, even resulting in death. Treatment consists of discontinuing the causative medication. Diazepam has been used to decrease hypertonicity. Serotonin antagonists such as cyproheptadine and chlorpromazine also have been used.
It is important for the pharmacist to be aware of medications that have the potential to cause serotonin syndrome and recognize to the signs and symptoms associated with it.

Medication Class Examples
Selective Serotonin Reuptake Inhibitors (SSRIs) citalopram (Celexa), fluoxetine (Prozac), fluvoxamine (Luvox), olanzapine/fluoxetine (Symbyax), paroxetine (Paxil)
Selective Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) duloxetine (Cymbalta), sibutramine (Meridia), venlafaxine (Effexor)
Triptans

almotriptan (Axert), eletriptan (Relpax), frovatriptan (Frova), naratriptan (Amerge), rizatriptan (Maxalt), sumatriptan (Imitrex),

zolmitriptan (Zomig)

Miscellaneous

Medications- buspirone (Buspar), carbamazepine (Tegretol), cocaine, cyclobenzaprine (Flexeril), Fentanyl, 5-hydroxytryptophan, linezolid (Zyvox), lithium, L-tryptophan, meperidine (Demerol), methadone (Dolophine), methamphetamine (Desoxyn), methylene blue, metoclopramide (Reglan), mirtazapine (Remeron), ondansetron (Zofran), phenelzine (Nardil), selegiline (Eldepryl), St. John’s wart, tramadol (Ultram), tranylcypromine (Parnate), trazodone (Oleptro), valproic acid

Medication Classes- Ergot alkaloids, Tricyclic antidepressants

 


References:
1. Brown, Charles. "Drug-Induced Serotonin Syndrome." U.S. Pharmacist 17 Nov. 2010: Web. 27 Aug. 2015. 
2. Nguyen, Timothy, and Billy Sin. "A Case of an Older Adult Patients and Drugs Associated with Serotonin Syndrome." The Consultant Pharmacist 30.8 (2015): 455-57. 

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Irene Petrides, PharmD

Hyperkalemia in the Elderly

Hyperkalemia or a rise in serum potassium concentration is an electrolyte disorder that has the potential to be a life threating condition. With increased aged there is increased risk for hyperkalemia. In the elderly, the loss of renal mass and comorbid conductions results in decreased renal function.1,2 Therefore the common regulatory mechanism of managing potassium is disrupted.3 Many medications can be associated with contributing to hyperkalemia including potassium supplements, potassium sparing diuretics, nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors, beta adrenergic blocking agents, heparin, digoxin, and trimethoprim-sulfamethoxazole.4 In order to avoid hyperkalemia certain precautions should be taken. This includes renal dosing and avoiding concomitant use of potassium altering medications. Signs and symptoms of hyperkalemia often are associated muscle paralysis, dyspnea, palpitations, nausea or vomiting and paresthesia. It is imperative to recognize these signs and symptoms as for hyperkalemia can be quickly fatal, resulting in respiratory paralysis or cardiac arrest.3

Management of hyperkalemia depends on severity and renal function. In patients with moderate potassium elevation and normal renal function, treatment simply results in identifying and removing the source of increased potassium levels and/or increasing the excretion of potassium.3 This includes a loop diuretic, aldosterone analogue, or initiating the controversial cation exchange resin (Kayexalate®).2 In patients with severe hyperkalemia and impaired renal function, aggressive treatment may comprise of intravenous insulin along with glucose, inhaled nebulized intravenous beta-2 agonist, intravenous calcium for cardiac toxicity, sodium bicarbonate to correct severe metabolic acidosis, and ultimately emergency dialysis.3

Kayexalate® (sodium polystyrene sulfonate) is a medication used in treatment of hyperkalemia. However it is important to keep in mind the safety label posted by the US Food and Drug administration in 2009.1 Kayexalate® is reported to cause colonic necrosis and other serious gastrointestinal adverse events including bleeding, ischemic colitis, and perforation.1,2 Therefore it is not recommended to use Kayexalate® with Sorbitol®.1,2,3 Due to this labeling, a more appropriate strategy in the treatment of mild to moderation hyperkalemia may be decreasing potassium intake increasing potassium depletion with the use of loop diuretics.1,2

In conclusion it is important to keep in mind prevention is key. A drug medication review is always necessary. All medications need to be evaluated especially over the counter medications. Many patients are on potassium supplements, non-steroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors. Decreased renal function in addition to medications associated with drug induced hyperkalemia is a recipe for disaster in the aging population Ultimately, appropriate prevention is desired in addition to close monitoring as well as treatment when necessary.3,4


REFERENCES:

1 Kamel, K. S., and M. Schreiber. 'Asking The Question Again: Are Cation Exchange Resins Effective For The Treatment Of Hyperkalemia?'. Nephrology Dialysis Transplantation 27.12 (2012): 4294-4297. Web.

2 Sterns, R. H. et al. 'Ion-Exchange Resins For The Treatment Of Hyperkalemia: Are They Safe And Effective?'. Journal of the American Society of Nephrology 21.5 (2010): 733-735. Web.

3 Elliott, M. J. et al. 'Management Of Patients With Acute Hyperkalemia'. Canadian Medical Association Journal 182.15 (2010): 1631-1635.

4 Perazella, Mark A., and Rex L. Mahnensmith. 'Hyperkalemia In The Elderly'. J Gen Intern Med 12.10 (1997): 646-656. Web.

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Jessica Horsley, PharmD

Intranasal Medication Administration: Suitable Drugs and Devices

Compared to intravenous (IV) and other invasive routes of administration, intranasal (IN) administration of medications provides several benefits with regard to safety and efficacy. This route of administration is needleless, requires no sterile technique and is pain-free and well tolerated by patients. The transmucosal drug absorption offered by this route offers a rapid onset of action, with dosing and bioavailability similar to IV dosing.

Variability in intranasal drug absorption can be attributed to both drug and patient-related factors. Drug formulations should be concentrated and potent and of a volume of less than 1mL (preferably less than 0.2mL if possible). Physicochemical drug properties are of importance, as optimal absorption is dependent on the molecular weight and hydro- or lipophilicity of the drug. Lipophilic medications with a molecular weight of less than 300 Da are most suitable for IN administration. The patient’s transepithelial passage proves to be another variable affecting drug absorption. Abnormal nasal blood flow, rhinosinusitis, radiation to the head/neck, diseases affecting mucociliary clearance like cystic fibrosis, and cigarette smoking may all affect mucosal health, and therefore IN drug absorption. Drug interactions for IN administration are considered relative and include phenylephrine and oxymetazoline.

With regard to IN administration, most nursing professionals and even patients are familiar with nose drops or aerosol sprays like sodium chloride nasal spray or fluticasone. For those medications without a commercial nasal dosage form available, options for administration in the past have included compounding into drops/spray, or using a syringe and cotton ball. These methods may prove problematic due to immediate swallowing, rapid clearance, and posterior delivery of medication. A new option, drug atomization, now exists to address these failures in IN drug delivery. An atomized spray delivers small particles to the nasal mucosa rapidly and without regard to patient positioning. Three commercial devices exist for IN drug atomization: Mucosal Atomization Device, Accuspray Nasal Spray and Kurve Controlled Particle Dispersion. Although considered off-label use, the therapeutic uses of IN-administered drugs include seizures, hypoglycemia, opioid overdose, epistaxis and anesthesia. Suitable medications for IN administration applicable to the hospice population include fentanyl, benzodiazepines, ketamine, naloxone and lidocaine.1

2016 06 29 12 57 45

For information regarding nasal atomization products:

LMA MAD Nasal
http://www.lmana.com/pwpcontrol.php?pwpID=6359

BD Accuspray SCF
http://www.bd.com/pharmaceuticals/products/nasal-spray.asp

Kurve CPD
http://www.kurvetech.com/nasaltechnology.asp 

 


References:

1 Jen, C. No IV access, get MAD! Powerpoint presentation at: the American Society for Health-System Pharmacists Midyear Clinical Meeting; Dec 7-11 2014; Anaheim, CA.

2 Wolfe TR, Braude DA. Intranasal medication delivery for children: a brief review and update. Pediatrics. 2010;126(3):532-7.

3 Gallagher EJ. Nasogastric tubes: hard to swallow. Ann Emerg Med. 2004;44:138-41.

4 Pandey RK, Bahetwar SK, Saksena AK, Chandra G. A comparative evaluation of drops versus atomized administration of intranasal ketamine for the procedural sedation of young uncooperative pediatric dental patients: A prospective crossover trial. J Clin Pediatr Dent. 2011;36:79–84.

5 Tsze DS, Steele DW, Machan JT, Akhlaghi F, and Linakis JG. Intranasal ketamine for procedural sedation in pediatric laceration repair: a preliminary report. Pediatr Emerg Care. 2012 Aug;28(8):767-770.

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Delta Campus Pharmacy Student

Use of Nebulized Morphine for the Management of Dyspnea

Dyspnea, or shortness of breath, is a very common complaint in hospice and palliative care. Up to 70% of end stage cancer or COPD patients experience dyspnea.1 Opioids, such as morphine, have been used to relieve the uncomfortable sensation associated with dyspnea. Oral and parenteral morphine are the most well studied routes of administration for this indication. Unfortunately, systemic absorption of opioids can cause adverse events that may be considered unbearable in the hospice population such as nausea, vomiting, drowsiness, constipation, and respiratory depression. Oral administration of morphine takes 15-30 minutes to take effect and lasts about four hours.2,3 While parenteral administration of morphine takes 6-10 minutes to take effect and also last about four hours. Inhaled opioids have a faster onset of action than the oral route and considered less invasive than the parenteral route.2

The use of nebulized opioids can be considered an appealing option compared to the oral and parenteral routes of administration. However, nebulized opioids are not routinely recommended. This is because there is conflicting data as to their benefit. There are no large-scale studies testing the efficacy of nebulized opioids, and smaller studies show conflicting evidence. Some studies show that nebulized opioids are less effective compared to oral or parenteral administration while others show that nebulized morphine is equally efficacious to subcutaneous morphine.1,4 Some patients are noted to prefer nebulized morphine over other routes of administration.4

A systematic review of 18 clinical trials that evaluated all routes of opioids in the management of dyspnea found a statistically significant benefit with the oral and parenteral routes of administration but found the nebulized route of administration to be no more effective than nebulized saline. However, the authors of this review did note that there might have been insufficient data with the nebulized route of administration to make this claim.8 Another review of 9 clinical trials looking at efficacy of nebulized morphine in the management of dyspnea found that 3 of the trials had positive results, but the rest failed to show improvement after treatment. The authors note that the small number of subjects, variety of disease states, and different outcome measures limited the interpretation of the results.9 Based upon these varying results, the use of nebulized opioids for the management of dyspnea are not routinely recommended. If you are going to consider a trial of a nebulized opioid, then it is recommended to use an injectable vial and not the oral morphine concentrate. A review of the literature will find no place where the oral concentrate has been evaluated and one article that directly states that the oral elixir should not be used.10 There is some belief that the sugar-free formulation of the oral morphine solution can be used via nebulizer, however, there is not literature to support this. It is of note that all current oral morphine solutions are sugar free and that the sugar containing oral morphine solutions are no longer on the market.7 There is some concern if the injectable vial needs to be preservative free for use via nebulizer. This concern comes from the fact the preservatives can induce bronchospasm in some patients. This is a rare but sometimes serious side effect. The preservatives of most concern are sulfites and edetate disodium (EDTA), found in both oral and parenteral preparations of morphine.5,6 It is not necessary to use preservative-free morphine, but caution should be used in patients susceptible to bronchospasms. If you are not using a preservative free product, then it is recommended to monitor your patient during the first administration of the nebulized opioid for this side effect. Typical starting dose for nebulized morphine is 2.5-10 mg; this can be titrated up to 30 mg per dose. Alternatives to morphine include hydromorphone 0.25- mg or fentanyl 25 mcg.1 Doses can be repeated every 4 hours as needed.3 Morphine for injection should be diluted to 2 mL volume with normal saline solution, if needed.1


Submitted by: Shawn Millsop, PharmD Candidate 2016 at Duquesne University School of Pharmacy and Lorin Yolch, PharmD, CGP, FASCP, Director of Professional Education at Delta Care Rx


References

1 Ferraresi V. Inhaled opioids for the treatment of dyspnea. Am J Health-Syst Pharm. 2005; 62: 319-320.

2 Bausewein C, Simon ST. Inhaled nebulized and intranasal opioids for the relief of breathlessness. Curr Opin Support Palliat Care. 2014; 8: 208-212.

3 Sarhill N, Walsh D, Khawarm E, Tropiano P, Stahley MK. Nebulized hydromorphone for dyspnea in hospice care of advanced cancer. Am J Hosp Palliat Care. December 2000; 17(6): 389-391.

4 Bruera E, Sala R, Spruyt, et al. Nebulized Versus Subcutaneous Morphine for Patients with Cancer Dyspnea: A Preliminary Study. J Pain Symptom Manage. June 2005: 29(6): 613-618.

5 Excipients in the label and package leaflet of medicinal products for human use. European Commission. http://www.ema.europa.eu/docs/en_GB/document_library/Scientific_guideline/2009/09/WC500003412.pdf Published July 2003. Accessed June 2, 2015.

6 Beasley R, Fishwick D, Miles JF, Hendeles L. Preservatives in nebulizer solutions: risk without benefit. Pharmacotherapy. January-February 1998; 18(1): 130-139.

7 Gold Standard, Inc. Morphine. Clinical Pharmacology [database online]. Available at: http://www.clinicalpharmacology.com. Accessed June 25, 2015.

8 Jennings AL, Davies AN, Higgins JP, Gibbs JSR, Boardley KE. A Sytematic Review of the use of Opioids in the management of dyspnoea. Thorax. 2002;57:939-44.

 9 Brown SJ, Eichner SF, Jones JR. Nebulized Morphine for Relief of Dyspnea Due to Chronic Lung Disease. The Annals of Pharmacotherapy. June 2005;29:1088-92.

10 Ahmedzai S, Davis C. Nebulised drugs in palliative care. Thorax. 1997;52(Suppl 2):S75-77.

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Shane Donnelly, PharmD

Prescription Drug Misuse, Dependence, and Abuse in the Elderly

Older adults are often left out of the discussion when it comes to prescription drug misuse, dependence, and abuse. Prescription drug abuse is an epidemic in this country, and it’s not just confined to the younger patient population. It is estimated that 11% of elderly patients abuse prescription medication.1

The elderly consume roughly one quarter of the prescriptions sold in the United States.1 Elderly patients often have chronic pain, anxiety, or insomnia that requires the use of potentially addictive medication. Additionally, elderly patients may not be adequately treated with their current therapies. These risk factors, along with social isolation, depression, and limited functionality, make the geriatric population particularly at risk for substance misuse and abuse.

Providing safe and effective care for elderly patients requires that signs of prescription misuse, dependence, and abuse are recognized quickly. The medications that are often abused can lead to events such as falls and accidents that require these patients to be admitted to inpatient units or nursing homes. To effectively manage prescription medication misuse and abuse in this population, the definition of substance misuse, dependence, tolerance, and abuse should be addressed.

Misuse- Prescription medication misuse is the improper taking of medication by the patient. It is most commonly by accident, but can also be intentional. Assess your patient’s ability to take medication correctly. It may be necessary to provide pharmaceutical education to your patient.  Examples include.2

• Taking medication differently than directed on the label due to poor eyesight or reading ability

• Doubling up on doses

• Borrowing medication from friends or family members

• Acquiring medication online to treat self-diagnosed conditions

Physical dependence and Tolerance- Physical dependence evolves from the continued regular use of a substance that results in withdrawal symptoms upon discontinuation. Tolerance to medication occurs when patients need higher doses of medication to achieve adequate symptomatic relief. Patients with physical dependence and tolerance may display drug-seeking behavior that can be misconstrued as psychological dependence (addiction).2 Assess the patient’s current condition and medication profile. The patient’s therapy may be inadequate due to tolerance or lack of efficacy. Communicate concerns with the patient’s physician. The patient may then cease to engage in drug-seeking behavior.

Psychological dependence (addiction)- Psychological dependence is a state that demonstrates loss of control and/or compulsive drug-seeking behavior.3 These patients engage in medication use despite the potential for adverse consequences. These patients need professional help to overcome both physical and psychological dependence. At this point, it is important to understand that these patients are potentially putting themselves and others in immediate danger.

In hospice, it is rare for a patient to become psychologically dependent on medication. It is important to be aware of any signs of substance abuse among family members or caregivers. Recognizing signs of caregiver abuse is important to protect patients and provide the best possible care for the end-of-life stage. It’s important to listen your patient’s concerns regarding their medication and to assess the root cause of medication discrepancies.


References:

1 Culbertson JW, Ziska, M. Prescription drug misuse/abuse in the elderly. Geriatrics. 2008; 63(9): 22-31.

2 Agins, A. Prescription drug abuse: from bad to worse. CEdrugstorenews.com March/April 2012. Retrieved July 5, 2012 at: http://www.cedrugstorenews.com/userapp//lessons/lesson_view_ui.cfm?lessonuid=401-000-12-201-H01.

3 American Psychiatric Association. Diagnostic and Statistical Methods of Mental Disorders (Fourth Edition, Text Revision). Washington, DC: American Psychiatric Association. 2000;199-273

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