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Hypercalcemia. Carol S. Viele RN MS Clinical Nurse Specialist Hematology-Onc-BMT UCSF. Objectives. At the completion of this presentation the participant will be able to: Describe 2 side effects of hypercalcemia Define 2 agents utilized to treat hypercalcemia - PowerPoint PPT Presentation
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HypercalcemiaHypercalcemia
Carol S. Viele RN MSCarol S. Viele RN MSClinical Nurse SpecialistClinical Nurse Specialist
Hematology-Onc-BMTHematology-Onc-BMTUCSFUCSF
ObjectivesObjectives
At the completion of this presentation the At the completion of this presentation the participant will be able to:participant will be able to:– Describe 2 side effects of hypercalcemiaDescribe 2 side effects of hypercalcemia– Define 2 agents utilized to treat Define 2 agents utilized to treat
hypercalcemiahypercalcemia– Describe at least 2 nursing interventions for Describe at least 2 nursing interventions for
hypercalcemiahypercalcemia
PrevalencePrevalenceMost common metabolic complication of Most common metabolic complication of cancercancer
10-20% of all cancer patients per year will 10-20% of all cancer patients per year will be diagnosed with hypercalcemiabe diagnosed with hypercalcemia
Associated MalignanciesAssociated Malignancies
Lung-35% ( NSCL)- 15% occurrenceLung-35% ( NSCL)- 15% occurrence
Breast- 40-50%Breast- 40-50%
Multiple Myeloma-20-40%Multiple Myeloma-20-40%
Head and Neck-6%Head and Neck-6%
Genitourinary-6%Genitourinary-6%
Other/Unknown primary-15%Other/Unknown primary-15%
Mechanism of Calcium RegulationMechanism of Calcium Regulation
Bone formation and resorption (99%) in Bone formation and resorption (99%) in bonebone
GI absorptionGI absorption
Urinary excretionUrinary excretion
Hypercalcemia in CancerHypercalcemia in Cancer
Due to increased bone resorption and Due to increased bone resorption and release of calcium from bonerelease of calcium from bone
Three mechanismsThree mechanisms– Osteolytic metastases with local release of Osteolytic metastases with local release of
cytokinescytokines– Tumor secretion of parathyroid hormone-Tumor secretion of parathyroid hormone-
related proteinrelated protein– Tumor production of calcitriolTumor production of calcitriol
Hormonal ControlHormonal ControlParathyroid hormone- released from the Parathyroid hormone- released from the parathyroid in response to a drop in calcium, parathyroid in response to a drop in calcium, acts directly on bone by stimulating osteoclast acts directly on bone by stimulating osteoclast formation and inhibiting osteoblastsformation and inhibiting osteoblasts
Vitamin D (1,25-dihydroxycholecalciferol)-Vitamin D (1,25-dihydroxycholecalciferol)-increase calcium and phosphorous absorption increase calcium and phosphorous absorption from the intestinal mucosafrom the intestinal mucosa
Calcitonin-reduces calcium release into Calcitonin-reduces calcium release into circulation as a result of bone resorptioncirculation as a result of bone resorption
Pathogenesis of Skeletal Pathogenesis of Skeletal MetastasesMetastases
tumour cell
osteoblast
mineralized bone
Imunecell
IL-1, TNFGM-CSF
activatd TGFß IL-6
IL-1 IL-6 TNF TGF EGF
PGs PTHrPcathepsins
OIF / OAF
osteoclast
Osteolytic MetastasesOsteolytic Metastases
Osteolytic mets are the result of direct induction Osteolytic mets are the result of direct induction of local osteolysis by the tumor cellsof local osteolysis by the tumor cells
Breast and Non–small cell lungBreast and Non–small cell lung
In Breast cancer adminstration of estrogen and In Breast cancer adminstration of estrogen and antiestrogen Tamoxifen) can lead to antiestrogen Tamoxifen) can lead to hypercalcemiahypercalcemia
Cytokines play a major role Cytokines play a major role – Tumor necrosis factorTumor necrosis factor– Interleukin-1Interleukin-1
Osteoclast Activating FactorsOsteoclast Activating Factors
Multiple Myeloma can release these factors by Multiple Myeloma can release these factors by tumor cellstumor cellsCytokines active in osteoclastic activityCytokines active in osteoclastic activity– Interleukin-1-betaInterleukin-1-beta– LymphotoxinLymphotoxin– Tumor necrosis factorTumor necrosis factor– IL-6IL-6– Macrophage colony stimulating factorMacrophage colony stimulating factor– Macrophage inflammatory proteinMacrophage inflammatory protein– Vascular cell adhesion molecule-1Vascular cell adhesion molecule-1– Hepatocyte growth factor ( This is produced by Hepatocyte growth factor ( This is produced by
myeloma cells in culture)myeloma cells in culture)
Pathogenesis of Skeletal Pathogenesis of Skeletal MetastasesMetastases
tumour cell
osteoblast
mineralized bone
Imunecell
IL-1, TNFGM-CSF
activatd TGFß IL-6
IL-1 IL-6 TNF TGF EGF
PGs PTHrPcathepsins
OIF / OAF
osteoclast
Clinical ManifestationsClinical ManifestationsDehydrationDehydration
PolydipsiaPolydipsia
PolyuriaPolyuria
GastointestinalGastointestinal– AnorexiaAnorexia– Nausea/VomitingNausea/Vomiting– ConstipationConstipation– Abdominal painAbdominal pain
Clinical ManifestationsClinical Manifestations
Bone painBone pain
Pathologic fracturePathologic fracture
Weakness Weakness
LethargyLethargy
HyporeflexiaHyporeflexia
DepressionDepression
Clinical ManifestationsClinical Manifestations
StuporStupor
ComaComaConfusionConfusionVisual disturbancesVisual disturbancesApathyApathyRestlessnessRestlessness
Clinical ManifestationsClinical Manifestations
GenitourinaryGenitourinary–PolyuriaPolyuria–PolydipsiaPolydipsia–NocturiaNocturia–Calcium nephropathyCalcium nephropathy–HypercalciuriaHypercalciuria–NephrolithiasisNephrolithiasis
Clinical ManifestationsClinical Manifestations
CardiovascularCardiovascular– HypertensionHypertension
– BradycardiaBradycardia
– Cardiac arrhythmiasCardiac arrhythmias
– Cardiac arrestCardiac arrest
– Heart blockHeart block
– Digitalis sensitivityDigitalis sensitivity
DiagnosisDiagnosis
Laboratory testsLaboratory tests–Ionized calcium or free calcium is Ionized calcium or free calcium is
the physiologically active form of the physiologically active form of calcium circulating in the bloodcalcium circulating in the blood
–50% of serum calcium is ionized50% of serum calcium is ionized
–Results < 1.30Results < 1.30
DiagnosisDiagnosisNormal serum calcium 9-11mg/dl Normal serum calcium 9-11mg/dl
Hypercalcemia can be estimated via a Hypercalcemia can be estimated via a formula:formula:– Corrected Ca (mg/dl) = Ca divided by 4 minus Corrected Ca (mg/dl) = Ca divided by 4 minus
albumin(gm/dl) times ) 0.8albumin(gm/dl) times ) 0.8
Medical ManagementMedical Management
Mild hypercalcemiaMild hypercalcemia–Calcium < 12Calcium < 12
–AsymptomaticAsymptomatic
–TherapyTherapyActivityActivity
Avoid salt restrictionAvoid salt restriction
Discontinue thiazide diureticsDiscontinue thiazide diuretics
Medical ManagementMedical ManagementModerate to severe hypercalcemiaModerate to severe hypercalcemia– Moderate 12-13 mg/dlModerate 12-13 mg/dl– Severe >13.5 mg/dlSevere >13.5 mg/dl
TherapyTherapy– RehydrationRehydration– Diuretics- FurosemideDiuretics- Furosemide– Discontinue thiazide diureticsDiscontinue thiazide diuretics
Medical ManagementMedical Management
Antiresorptive therapyAntiresorptive therapy–CalcitoninCalcitonin
–BisphosphonatesBisphosphonatesEtidronate-DidronelEtidronate-Didronel
Pamidronate- ArediaPamidronate- Aredia
Zoledronic acid- ZometaZoledronic acid- Zometa
Ibandronate- BonivaIbandronate- Boniva
Risedronate- ActonelRisedronate- Actonel
Mechanism of action of Mechanism of action of BisphosphonatesBisphosphonates
inhibit osteoclast formation, migration and osteolytic activity, promote apoptosis
local release during bone resorption
concentrated in newly mineralizing bone and under osteoclasts
modulate signalling from osteoblasts to osteoclasts
Current Therapeutic Approaches for Current Therapeutic Approaches for
Skeletal Complications ofSkeletal Complications of MalignanciesMalignanciesRadiotherapyRadiotherapy
Endocrine therapy Endocrine therapy
ChemotherapyChemotherapy
Orthopedic interventions Orthopedic interventions
AnalgesiaAnalgesia
BisphosphonatesBisphosphonates11
– Treatment of choice in hypercalcaemia of malignancy Treatment of choice in hypercalcaemia of malignancy (HCM)(HCM)
– Potent inhibitors of pathologic bone resorptionPotent inhibitors of pathologic bone resorption– Effective therapy for skeletal complications of bone Effective therapy for skeletal complications of bone
metastasesmetastases1. Body JJ, et al. J Clin Oncol. 1998.
1. Green J, et al. J Bone Miner Res. 1994.2. Evans CE, Braidman IP. J Bone Miner Res. 1994.3. Derenne S, et al. J Bone Miner Res. 1999.4. Boissier S, et al. Cancer Res. 2000.5. Marion G, et al. Bone. 1998.
Zoledronic Acid—Mechanisms of Zoledronic Acid—Mechanisms of ActionAction
Zoledronic acid reduces bone resorption by Zoledronic acid reduces bone resorption by potently inhibiting osteoclast hyperactivitypotently inhibiting osteoclast hyperactivity
Proposed mechanisms of action include:Proposed mechanisms of action include:– Functional suppression of mature osteoclastFunctional suppression of mature osteoclast11
– Inhibition of osteoclast maturationInhibition of osteoclast maturation22
– Inhibition of osteoclast recruitment to the siteInhibition of osteoclast recruitment to the site22
– Reduction in the production of cytokines, eg, IL-Reduction in the production of cytokines, eg, IL-1, IL-61, IL-633
– Inhibition of tumour-cell invasion and adhesion Inhibition of tumour-cell invasion and adhesion to bone matrixto bone matrix4,54,5
Overall Safety ConclusionsOverall Safety Conclusions
ZOMETA ZOMETA (4 mg) via 15-minute infusion (4 mg) via 15-minute infusion is safe and is safe and well tolerated, with a safety profile comparable to well tolerated, with a safety profile comparable to that of pamidronate (90 mg) via 2-hour infusion, that of pamidronate (90 mg) via 2-hour infusion, including renal tolerability including renal tolerability
Similar overall safety profile to that of other Similar overall safety profile to that of other intravenous bisphosphonates intravenous bisphosphonates
Laboratory abnormalities (grade 3 and 4) were Laboratory abnormalities (grade 3 and 4) were similar for ZOMETA and placebosimilar for ZOMETA and placebo
EfficacyEfficacy
Zoledronic acid is the only Zoledronic acid is the only bisphosphonate to be proven effective bisphosphonate to be proven effective across tumor types in patients with both across tumor types in patients with both lytic and blastic bone lesionslytic and blastic bone lesions
Nursing ManagementNursing ManagementEducationEducation– PatientPatient– Significant othersSignificant othersRehydrationRehydration– I&OI&O– WeightsWeightsActivityActivity– Encourage ambulationEncourage ambulation
Nursing ManagementNursing ManagementSafetySafety– Falls preventionFalls prevention– Do not allow patient to overstress bonesDo not allow patient to overstress bones– Do not pull on arms or legsDo not pull on arms or legs– Have patient report all bone painHave patient report all bone pain– Be very gentle when assisting patientBe very gentle when assisting patient– Use assistive devicesUse assistive devices– Safety assessment for home via Safety assessment for home via
PT/Home HealthPT/Home Health
Nursing ManagementNursing Management
Decrease anxietyDecrease anxietyEducationEducation
ReferencesReferencesJensen, G., “Hypercalcema of Malignancy” in Jensen, G., “Hypercalcema of Malignancy” in Oncology Nursing SecretsOncology Nursing Secrets, R Gates and R Fink , R Gates and R Fink (eds), Philadelphia: Hanley and Belfus, (eds), Philadelphia: Hanley and Belfus, 2008,523-5262008,523-526
Paines, H., “How to manage metabolic Paines, H., “How to manage metabolic emergencies”, emergencies”, Contemp OncolContemp Oncol, 3 (9), 54-57, , 3 (9), 54-57, 1993 1993
2009 UpToDate, ‘Treatment of Hypercalcemia’ 2009 UpToDate, ‘Treatment of Hypercalcemia’ www.http://UPTODATE accessed 7/9/09 accessed 7/9/09
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