Hypercalcemia effects and treatment for Palliative Care patient

Essay by kathy23University, Bachelor'sB+, December 2008

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Hypercalcemia49-year-old lady with 13-year history of ca breast with known bone and lung metastasis is admitted with increased confusion, constipation and increasing pain.

Mary had been living independently with her adult son.

Her treatment and therapies so far had includedBilateral mastectomies with axillary clearanceRadiotherapyChemotherapyIntraehteal pump for pain reliefMonthly APDHormone therapyHYPERCALCEMIA, a common life-threatening disorder, occurs in approximately 10%-20% of individuals with cancer (Chisholm). Occurrences of hypercalcemia have been reported in most types of malignancies with the most frequently reported tumours including carcinomas of the breast, lung and multiple myeloma. Immediate management of cancer-related acute hypercalcemia to prevent death or provide symptomatic relief may be warranted. With proper use of antihypercalcemic agents, the severe consequences of acute hypercalcemia can be prevented.

Calcium is the most common mineral found in the body. Calcium in the body is found predominantly in bone and teeth 99% while the remainder is found in extra cellular fluid.

There are a number of roles of calcium in the body:StructureCalcium is a major structural element in bones and teeth. The mineral component of bone consists mainly of hydroxyapatite crystals, which contain large amounts of calcium and phosphorus (about 40% calcium and 60% phosphorus) (Heaney).

Bone is a dynamic tissue that is remodelled throughout life. Bone cells called osteoclasts begin the process of remodelling by dissolving or resorbing bone. Bone-forming cells called osteoblasts then synthesize new bone to replace the bone that was resorbed. During normal growth, bone formation exceeds bone resorption.

Intracellular messengerCalcium plays a role in mediating the constriction and relaxation of blood vessels (vasoconstriction and vasodilation), nerve impulse transmission, muscle contraction, and the secretion of hormones.

Excitable cells, such as skeletal muscle and nerve cells, calcium channels in their cell membranes that allow for rapid changes in calcium concentrations. For example, when a muscle fiber receives a nerve impulse that stimulates it to contract, calcium channels in the cell membrane open to allow a few calcium ions into the muscle cell. These calcium ions bind to activator proteins within the cell that release a flood of calcium ions from storage vesicles inside the cell. The binding of calcium to the protein, troponin-c, initiates a series of steps that lead to muscle contraction (Weaver)Regulation of CalciumMaintenance of the body Ca stores and plasma Ca concentration ultimately depends on dietary Ca intake, absorption of Ca from the GI tract, and renal Ca excretion.When blood calcium decreases, calcium-sensing proteins in the parathyroid glands send signals resulting in the secretion of parathyroid hormone (PTH). PTH stimulates the conversion of vitamin D to its active form, calcitriol, in the kidneys. Calcitriol increases the absorption of calcium from the small intestine. Together with PTH, calcitriol stimulates the release of calcium from bone by activating osteoclasts (bone resorbing cells), and decreases the urinary excretion of calcium by increasing its reabsorption in the kidneys. When blood calcium rises to normal levels, the parathyroid glands stop secreting PTH and the kidneys begin to excrete any excess calcium in the urine (http://www.merck.com/pubs/mmanual/section2/chapter12/A002-012-0675). Calcium is released from the bones in several ways. Parathyroid hormone (PTH) and calcitonin are hormones that are important for calcium balance. PTH controls kidney excretion and reabsorption of calcium (Mundy & Guise, 1997).

Hypercalcemia is defined as a serum calcium level greater than 2.56 mmol/L. Because calcium binds to albumin and only the unbound (free) calcium is biologically active, the serum level must be adjusted for abnormal albumin levels. This is significant for palliative care clients as people with terminal illness often have a lower albumin level due to decreased oral intake.

To calculate corrected calcium level there is a formalueCorrected calcium (mmol/L) = measured calcium + 0.022 x (42 – albumin (g/l)).

Hypercalcemia in breast cancer it is caused by increased bone resorption and impairment of the renal function, which reduces the clearing of calcium from the blood. Immobility, dehydration, anorexia, nausea and vomiting may also increase the calcium levels.

Tumour release of PTH-related protein causes the bones to release calcium and the distal renal tubules to reabsorb it as the proximal tubules excrete it (Barnett, 1999). Calcitonin counteracts PTH but plays a minor role in calcium regulation.

Signs and Symptoms of HypercalcemiaSymptom prevalence among patients treated for hypercalcemia of malignancy stratified by corrected serum total calcium concentrations at presentation(http://www.meb.uni-bonn.de/cancernet/304462.html)Table 1Serum Calcium Concentration-------------------------------Symptoms <3.5 mmol/L >/= 3.5 mmol/L------------------------------------------------------------------------------CNS symptoms 41% 80%constipation 21% 25%malaise-fatigue 65% 50%anorexia 47% 59%nausea and/or vomiting 22% 30%polyuria and/or polydipsia 34% 35%pain 51% 35%Signs and symptoms of hypercalcemia are related to the enhanced effect of calcium on specific body systems, including the heart, kidneys, gastrointestinal tract, and neuromuscular function (Siegelski & Tittle, 1996). Calcium plays a major role in cell membrane permeability, particularly that of muscle and nerve cells (Lang-Kummer, 1997). Cardiac effects include arrhythmias and alterations in heart rate and blood pressure (increase or decrease). Renal impairment and polyuria may occur. Gastrointestinal side effects include nausea, vomiting, constipation, and abdominal muscle cramps. Confusion, disorientation, muscle weakness, or bone pain indicates impaired neuromuscular function (Siegelski & Tittle).

Mary has present with a number of symptoms of hypercalcemia these are increased tiredness, constipation, nausea and vomiting and pain. These can be dismissed as simply consistent with a diagnosis of cancer. The assessment process that needs to be undertaken for Mary may confirm the diagnosis.

Patients with high calcium levels should be examined for the following symptoms:•Nerves and muscles (muscle strength, muscle tone, reflexes, tiredness, indifference, depression, confusion, restlessness)•Heart (high blood pressure,changes in heart function, irregular heartbeats, digitalis poisoning)•Kidneys (production of too much urine, noctural urination, glucosuria, excessive thirst)•Gastrointestinal (loss of appetite, nausea, abdominal pain, constipation, abdominal bloating)•Other (muscle and bone pain, itching)Base line blood tests would includeFull blood count this was to assess haemoglobin and white cell count this ruled out anaemia and/or infection as cause of symptoms.

Blood Chemistry - results Calcium 2.99 mmol/lAlbumin 32 g/lTherefore corrected calcium = measured calcium + 0.022 x (42 – albumin (g/l)) = 3.21mmol/LBase line bloods show raised calcium it had been three weeks since her last APD infusion.

There are a number of treatments for hypercalcemia these include –Rehydration – this will increase extracellular fluid increasing urine output and clearance of calcium.

Bisphosphonates – Pamidronate is a potent inhibitor of osteoclastic bone resorption. Calcitonin - Calcitonin is a rapidly acting peptide hormone secreted in response to hypercalcemia by the parafollicular cells (C cells) of the thyroid. A commercial preparation of salmon calcitonin is available. The combination of salmon calcitonin and prednisone may control plasma Ca for up to several months in some patients with malignancy. It’s limited by its short duration of action and the lack of response in up to 25% of patients. (http://www.merck.com/pubs/mmanual/section2/chapter12/A002-012-0675)Mary had been treated monthly with Pamidronate since July 1999. This had not been for hypercalcemia but to reduce the incidence and rate of skeletal events as discussed by Pavlakis and Stockler (2002).

Treatment for Mary:Mary was encouraged to increase her fluid intake and subcutaneous fluids 1500mls over 24hrs to increase extracellular fluid.

Regular anti emetics.

Calcitonin 300IU over 6 hours subcutaneously for three daysCommencement of dexamethasone which can assist to decrease nausea and improve appetite (Pereira). Then Pamidronate two days later.

Mary aperients were increased and bowels started to function on a daily basis.

Mary did not complete Calcitonin because of the side effects; she had serve itching of the palms and a skin rash on both hands and arms. Mary found this side effect unbearable and decided that the burden of treatment was too great.

Mary’s Calcium level did reduce to 2.57mmols and her symptoms reduced to enable her to attend her son’s wedding three weeks into her admission.

Three days after Mary’s sons wedding she got up to the toilet and spontaneously fractured her left femur.

Mary became bed bound and it was discussed with Mary the issue of treatment again if she became hypercalcemic, Mary opted for no treatment just symptom control. Mary died four weeks later.

Barnett, M.L. (1999). Hypercalcemia. Seminars in Oncology Nursing, 15, 190-201.

Chisholm, M.A. & Taylor, A.T. Acute Hypercalceamia http://www.uspharmacist.com/NewLook/DisplayArticle.cfm?item_num=8Heaney, R.P. Calcium, dairy products, and osteoporosis. Journal of the American College of Clinical Nutrition. 2000; volume 19: pages 83S-99S.

Lang-Kummer, J. (1997). Hypercalcemia. In S.L. Groenwald, M.H. Frogge, M. Goodman, & C.H. Yarbro (Eds.), Cancer nursing: Principles and practice (4th ed.) (pp. 684-701). Boston: Jones and Bartlett.

Mundy, G.R., & Guise, T.A. (1997). Hypercalcemia of malignancy. American Journal of Medicine, 103, 134-145.

Pavlakis N, Stockler M. Bisphosphonates in breast cancer (Cochrane Review). In: The Cochrane Library, Issue 1, 2002. Oxford: Update Software.

Pereira J. Management of Bone Pain. In Portenoy RK. Bruera E. eds. Topics in Palliative Care Volume 3. New York Oxford University Press 1998, pp79-116.

Siegelski, S.A., & Tittle, M. (1996). Hypercalcemia in the critically ill cancer patient. American Journal of Nursing, 96(Suppl. 6), 12-15Warrell RP Jr: Metabolic emergencies. In: DeVita VT Jr, Hellman S, Rosenberg SA, eds.: Cancer: Principles and Practice of Oncology. Philadelphia, Pa: Lippincott-Raven Publishers, 5th ed., 1997, pp 2486-2493.

Weaver, C.M. & Heaney, R.P. Calcium. In Shils, M. et al. Eds. Nutrition in Health and Disease, 9th Edition. Baltimore: Williams & Wilkins, 1999: pages 141-155.