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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.

Dr. Irene Petrides received her doctorate in pharmacy from Duquesne University in 2008 with a concentration in geriatric pharmacotherapy. Upon graduation, Dr. Petrides practiced in a community pharmacy as the Pharmacist Manager at CVS Pharmacy in Concord, North Carolina. She joined Delta Care in 2013 as a hospice clinical pharmacist.

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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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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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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Irene Petrides, PharmD

Oral Hygiene in End of Life Care

Oral mouth discomfort is often seen in advanced illness and this can strongly affect quality of life. It is therefore important to keep a close watch on a patient’s oral hygiene and make it a priority in the plan of care. Oral health issues can include but are not limited to dysphagia, nutrition and taste problems, thick mucus, difficulty speaking, denture related issues, nausea and vomiting, stomatitis, hypersalivation, mucositis, thrush, and xerostoma.1

Assessment of the patient’s self-care ability is the first step. This will help determine the level of support a patient a will require. Not all patients need full care, a simple reminder or assistance by a caretaker may provide a basic approach in order to stay on the right path of the daily oral regimen. Once a care plan is established, there are measures that can be taken in order to avoid complications which include using a soft toothbrush, avoid mouthwashes that contain alcohol, rinse with saline or soda water, or use moist gauze to wipe cheeks after each meal.2,7 In addition, it is imperative to review medications in order to rule out any undesired oral mucosa effects associated with medication therapy.1 The goal is to maintain optimal oral hygiene with minimal discomfort. Most of the time a proactive approach is desired however in hospice we are often using a palliative oral care approach in symptoms that already exist. Once preventative and standard oral hygiene procedures have been properly assessed and addressed, it may become necessary to treat common complications.

Mucositis is a painful condition that often presents as red or white lesions in the mucosal lining of mouth, pharynx and digestive tract. In the late stages it is associated with fibrosis of connective tissue and hypovascularity. It is most often seen in patients who have received toxic chemotherapy and radiotherapy in head and neck cancer.1,6 Palliative treatment includes viscous lidocaine 2%, combination oral rinse (lidocaine, diphenhydramine, sorbitol and Mylanta), and chlorhexidine gluconate.1

Oropharyngeal Candidiasis (oral thrush) is a condition where white patches can be located in the mouth, inner cheeks, throat, palate and tongue and also is associated with pain. The tissue under the white patches is often raw and sore. The patient may have bad breath, unpleasant taste in the mouth, or dry mouth. Medications that can cause thrush include corticosteroids, antibiotics, and chemotherapy. Patients who have a higher prevalence of candidiasis are those who have cancer, HIV, uncontrolled diabetes, and smokers.3,7 Treatment includes antifungal mouthwash (nsystatin) or lozenges (clotrimazole). Administration of systemic fluconazole or itraconazole may be necessary in the management of more severe cases.1 It is important to remember that if a patient wears dentures they must also be treated separately with antifungal mouth rinse.5

Xerostoma is a symptom referring to dry mouth. Nearly 75% of hospice patients are affected by xerostoma, which is the most common cause of malnutrition in palliative patients. It is often associated with difficulty chewing, altered taste burning sensation, and thick saliva.1,3 Causes of xerostoma may include dehydration, vomiting or diarrhea, medications with anticholinergic activity, benzodiazepines and opioids, radiation, HIV/ AIDS, diabetes, renal failure, and Sjogrens syndrome.1,3 Treatment includes oral hydration such as humidifiers, stimulating salivary reflexes with medications like xylitol, administration of the cholinergic agonist pilocarpine, or using saliva substitutes such Biotene®.

Hypersalivation also known as sialorrhea is an increase in salivary flow. Patients who have neurological conditions such as Parkinson’s disease or amyotrophic lateral sclerosis may find it difficult to manage hypersalivation. Often medications are contraindicated in the treatment due to the side effects associated with anticholinergic drugs. If the patient’s quality of life is affected, anticholinergic medications such as atropine, glycopyrrolate, or scopolamine can be used.1

Dysphagia, or difficulty swallowing effectively, is a common symptom seen in hospice care. Food debris and saliva accumulate in the oral cavity which can increase bacterial growth. Inadequate oral hygiene at this point in care may increase the patient’s risk of developing aspiration.4 Therefore dysphagia may not only have a negative impact on oral health but also on the systemic health of a hospice patient. Despite minimizing debris in the oral cavity with adequate oral hygiene other preventative measures are necessary in order to avoid undesired complications. The most common non-invasive approaches include pleasure feeding, pureed diet, and crushing medications.1,4

Awareness of oral hygiene in the hospice patient should be an extension of the palliative care plan. Identifying oral health barriers, preventing major complications and treating oral conditions is the mainstay of managing oral hygiene. In conclusion comfort care and palliative treatment are established in oral care if a patient can eat and drink adequately with minimal pain or discomfort.


References:

1. Mulk BS, Chintamaneni RL, Mpv P, Gummadapu S, Salvadhi SS. Palliative Dental Care- A Boon for Debilitating. Journal of Clinical and Diagnostic Research : JCDR. 2014;8(6):ZE01-ZE06. doi:10.7860/JCDR/2014/8898.4427.

2. Chen X, Chen H, Douglas C, Preisser JS, Shuman SK. Dental treatment intensity in frail older adults in the last year of life. Journal of the American Dental Association (1939). 2013;144(11):1234-1242.

3. Alt-Epping B, Nejad RK, Jung K, Groß U, Nauck F. Symptoms of the oral cavity and their association with local microbiological and clinical findings—a prospective survey in palliative care. Supportive Care in Cancer. 2012;20(3):531-537. doi:10.1007/s00520-011-1114-z.

4. Gallagher R. Swallowing difficulties: A prognostic signpost. Canadian Family Physician. 2011;57(12):1407-1409.

5. Saini R, Marawar P, Shete S, Saini S, Mani A. Dental Expression and Role in Palliative Treatment. Indian Journal of Palliative Care. 2009;15(1):26-29. doi:10.4103/0973-1075.53508.

6. Davies, Andrew, and Ilora G. Finlay, eds. Oral care in advanced disease. Oxford University Press, 2005.

7. O’Reilly M. Oral care of the critically ill: a review of the literature and guidelines for practice. Australian Critical Care. 2003;16(3):101-110. doi:10.1016/s1036-7314(03)80007-3.

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