Clinical
The management of hypercalcaemia in advanced cancer Annie Pettifer, Sarah Grant
H
ypercalcaemia is a clinical condition that occurs when the serum calcium level rises above 2.6 mmol/l (Samphao et al, 2010). For patients with a diagnosis of advanced cancer, hypercalcaemia is the most common life-threatening metabolic condition and is associated with a low survival rate, with a median survival of 3–4 months (Bower and Cox, 2010). Hypercalcaemia affects between 10% and 30% of patients with cancer, depending on the characteristics of the sample studied (Watson et al, 2005). It is most frequently found in multiple myelomas and breast cancers, but is also common in squamous cell carcinomas of the head and neck, lung, kidney, and cervix uteri. It is much less common in cancer of the prostate, small cell lung cancer, and gastric and large bowel tumours (Twycross et al, 2009). Hypercalcaemia can be distressing for both patients and families. In the main, once diagnosed it can be treated effectively, but without treatment it is potentially fatal. This article reviews the physiology of normal calcium regulation and the mechanisms by which this may alter in patients with malignancy. It also describes the clinical manifestation of hyper calcaemia, diagnostic testing, and therapeutic management. The implications of this distressing complication for patients and carers are discussed together with the care that should be given to reduce the effects of this potentially life-threatening condition. The care of patients with hyper calcaemia in advanced cancer is illustrated by a case example that demonstrates the importance of advance care planning.
© 2013 MA Healthcare Ltd
Physiology of normal calcium regulation Calcium is the most common mineral in the human body and is crucial to normal human functioning, particularly in muscle and nerve action and blood clotting (Clancy and McVicar, 2009). Serum calcium is normally maintained between 2.12 and 2.65 mmol/l (Tadman and
International Journal of Palliative Nursing 2013, Vol 19, No 7
Abstract
Hypercalcaemia is common in patients with advanced cancer. If detected, it usually responds to palliative treatment and patients’ distressing symptoms will improve markedly. However, if left untreated hypercalcaemia is potentially fatal. It can be difficult to detect as its symptoms can also be attributed to other common aspects of advanced malignancy. It is therefore essential that nurses are aware of the underlying physiology and can identify which patients are at risk of becoming hypercalcaemic. Hypercalcaemia often recurs and can become increasingly difficult to treat. Such refractory hypercalcaemia requires sensitive and considered management with advance care planning, particularly as difficult treatment dilemmas may arise if and when malignancy advances. Key words: Hypercalcaemia l Malignancy l Cancer l Advance care planning l Nursing
Roberts, 2007) by homeostatic mechanisms operating within the bone, gastrointestinal (GI) tract, and kidneys. Bone and teeth act as a calcium reservoir, storing around 90% of total calcium levels (Montague et al, 2005). Calcium in bone is found crystallised into hydroxyapatite, which makes up the bone matrix. Bone matrix is not static, but is constantly regenerating as calcium and phosphate are released from bone by the action of osteoclasts. The converse action of osteoblasts re-forms calcium and phosphate into bone to maintain serum calcium levels. The GI tract and the kidneys also have a role in calcium homeostasis although, unlike the bone, they have no calcium storage function. Calcium is ingested into the GI tract from foods such as dairy products and green leafy vegetables (Clancy and McVicar, 2009). Once within the GI tract, depending on the demand for it, calcium may be absorbed into the serum or excreted within the faeces. Similarly, extracellular calcium can be reabsorbed into the serum as it passes through the kidney or can be excreted within the urine as required to maintain constant optimal serum levels.
Annie Pettifer is Senior Lecturer in Adult Nursing, Coventry University, Priory Street, Coventry, CV1 5FU, England; Sarah Grant is Macmillan Palliative Care Clinical Nurse Specialist, St Michael’s Hospice, The Cottage, 50 Lancaster Park Road, Harrogate, HG2 7SX, England Email: A.Pettifer@ coventry.ac.uk Or: sarah.grant2@ saintmichaelshospice.org
327
onal Journal of Palliative Nursing. Downloaded from magonlinelibrary.com by 193.061.135.112 on November 24, 2015. For personal use only. No other uses without permission. . All rights r
Clinical
Table 1. Mechanisms and frequency of hypercalcaemia in different tumour types* Mechanism
Frequency
Common tumour type(s)
Parathyroid hormone-related protein production
80%
Squamous: cell, renal, ovarian, endometrial, and breast cancers
Action of cytokines
20%
Breast cancer, myeloma, lymphoma
Increased 1,25-dihydroxycholecalciferol (vitamin D) production
The management of hypercalcaemia in advanced cancer Annie Pettifer, Sarah Grant
H
ypercalcaemia is a clinical condition that occurs when the serum calcium level rises above 2.6 mmol/l (Samphao et al, 2010). For patients with a diagnosis of advanced cancer, hypercalcaemia is the most common life-threatening metabolic condition and is associated with a low survival rate, with a median survival of 3–4 months (Bower and Cox, 2010). Hypercalcaemia affects between 10% and 30% of patients with cancer, depending on the characteristics of the sample studied (Watson et al, 2005). It is most frequently found in multiple myelomas and breast cancers, but is also common in squamous cell carcinomas of the head and neck, lung, kidney, and cervix uteri. It is much less common in cancer of the prostate, small cell lung cancer, and gastric and large bowel tumours (Twycross et al, 2009). Hypercalcaemia can be distressing for both patients and families. In the main, once diagnosed it can be treated effectively, but without treatment it is potentially fatal. This article reviews the physiology of normal calcium regulation and the mechanisms by which this may alter in patients with malignancy. It also describes the clinical manifestation of hyper calcaemia, diagnostic testing, and therapeutic management. The implications of this distressing complication for patients and carers are discussed together with the care that should be given to reduce the effects of this potentially life-threatening condition. The care of patients with hyper calcaemia in advanced cancer is illustrated by a case example that demonstrates the importance of advance care planning.
© 2013 MA Healthcare Ltd
Physiology of normal calcium regulation Calcium is the most common mineral in the human body and is crucial to normal human functioning, particularly in muscle and nerve action and blood clotting (Clancy and McVicar, 2009). Serum calcium is normally maintained between 2.12 and 2.65 mmol/l (Tadman and
International Journal of Palliative Nursing 2013, Vol 19, No 7
Abstract
Hypercalcaemia is common in patients with advanced cancer. If detected, it usually responds to palliative treatment and patients’ distressing symptoms will improve markedly. However, if left untreated hypercalcaemia is potentially fatal. It can be difficult to detect as its symptoms can also be attributed to other common aspects of advanced malignancy. It is therefore essential that nurses are aware of the underlying physiology and can identify which patients are at risk of becoming hypercalcaemic. Hypercalcaemia often recurs and can become increasingly difficult to treat. Such refractory hypercalcaemia requires sensitive and considered management with advance care planning, particularly as difficult treatment dilemmas may arise if and when malignancy advances. Key words: Hypercalcaemia l Malignancy l Cancer l Advance care planning l Nursing
Roberts, 2007) by homeostatic mechanisms operating within the bone, gastrointestinal (GI) tract, and kidneys. Bone and teeth act as a calcium reservoir, storing around 90% of total calcium levels (Montague et al, 2005). Calcium in bone is found crystallised into hydroxyapatite, which makes up the bone matrix. Bone matrix is not static, but is constantly regenerating as calcium and phosphate are released from bone by the action of osteoclasts. The converse action of osteoblasts re-forms calcium and phosphate into bone to maintain serum calcium levels. The GI tract and the kidneys also have a role in calcium homeostasis although, unlike the bone, they have no calcium storage function. Calcium is ingested into the GI tract from foods such as dairy products and green leafy vegetables (Clancy and McVicar, 2009). Once within the GI tract, depending on the demand for it, calcium may be absorbed into the serum or excreted within the faeces. Similarly, extracellular calcium can be reabsorbed into the serum as it passes through the kidney or can be excreted within the urine as required to maintain constant optimal serum levels.
Annie Pettifer is Senior Lecturer in Adult Nursing, Coventry University, Priory Street, Coventry, CV1 5FU, England; Sarah Grant is Macmillan Palliative Care Clinical Nurse Specialist, St Michael’s Hospice, The Cottage, 50 Lancaster Park Road, Harrogate, HG2 7SX, England Email: A.Pettifer@ coventry.ac.uk Or: sarah.grant2@ saintmichaelshospice.org
327
onal Journal of Palliative Nursing. Downloaded from magonlinelibrary.com by 193.061.135.112 on November 24, 2015. For personal use only. No other uses without permission. . All rights r
Clinical
Table 1. Mechanisms and frequency of hypercalcaemia in different tumour types* Mechanism
Frequency
Common tumour type(s)
Parathyroid hormone-related protein production
80%
Squamous: cell, renal, ovarian, endometrial, and breast cancers
Action of cytokines
20%
Breast cancer, myeloma, lymphoma
Increased 1,25-dihydroxycholecalciferol (vitamin D) production
