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Similar to Managing hypercalcaemia presented on CMC, Kol, 1.10.2013
Managing hypercalcaemia presented on CMC, Kol, 1.10.2013
- 1. Speaker: Dr. DibbendhuKhanra Chairperson: Dr. A.K. Banerjee
- 2. Calcium an unparallel hero most abundant mineral of body maintenance of strong bones neuro-mascular action blood clotting, blood pressure hormone regulation -most over-the-counter sold drug - 43% Indian women on supplement - prescribed by doctors commonly
- 3. Calciuma sinister indisguise HypercalcaemiaToday’s concern! ..Some cases.. 3
- 4. Mr. K isa 41 year old patient – Mild depression – Behavioral abnormality – Headache – Fatigue – Difficulty concentrating – TSH - 2.06 (0.5 – 4.00) – calcium 12.4 mg/dl (8.4 – 10.4 mg/dl)
- 5. Mrs. C isa 57 year old patient, well t-score – 1.3 (spine), 2. 8 (femur) Calcium – 12. 5 (8.4 – 10.4 mg/dl) weight loss and generalised weakness Cough and hemoptysis
- 6. • • • • • • • • A 58-year-woman presentedto ER progressive Multiple sclerosis Osteoporosis calcium, 600 mg, 3 times daily 5000-IU cholecalciferol supplement OD tremors Altered sensorium serum calcium 15.2 mg/dL
- 7. • • • • • • 30-year-old female Fever, cough Polyuria,polydypsia, GI upset constipation, confusion, headache CECT chest – hilar lympahedenopathy serum calcium, 13.8 mg/d
- 8. • • • • • 50-year-old male Diabetic for10 years Poorly controlled with OHA HTN, anasarca, anaemia serum calcium 14.8 mg/d
- 9. Calcium metabolism Defining hypercalcaemia Causesof hypercalcaemia Cl/f of hypercalceimia Diagnosis to hypercalcaemia Management
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- 17. A = highcalcium levels means primary hyperparathyroidism unless the PTH is near zero B = normocalcemic" hyperparathyroidism. this is the only group that we believe should have a urinary calcium level performed
- 18. It is IMPOSSIBLEto tell the difference between FHH and primary hyperparathyroidism based upon the results of a 24-hour urine test 1. Urinary calcium can be anything (very low to very high) in Pr HyperPTHism. 2. The arbitrary cut off of urinary ca excretion/ 24 hr 100 lacks any rationality. 3. Nor elevated serum ca neither elevated urinary ca has any association with renal stones. 4. Low urinary ca does not always mean FHH. FHH is so rare, that few doctors will ever see it. FHH is diagnosed incorrectly about 95-99% of the time
- 19. Corrected serum calcium= Ionizedcalcium + 0.8(4-serum albumin) calcium is high and PTH is high, d/g is primary hyperparathyroidism. IF calcium Familial is mildly Hypocalciuric raised in background of Hypercalcemia Sestamibi highly elevated N-scan PTH, then urinary ca can be ordered to rule out FHH 19
- 20. Neuropsychiatric complaints Calcium 12.4mg/dl iPTH – 509 (12-72 pg/ml) Thallium subtraction study: Left lower lobe parathyroid adenoma
- 21. Weight loss andgeneralised weakness Calcium – 12. 5 (8.4 – 10.4 mg/dl) iPTH 21 (10 – 65.0 pg/ml) PTHrp - elevated Lung biopsy with IHC: Well differentiated, low grade squamous cell lung carcinoma
- 22. • • • • calcium, cholecalciferol supplement serumcalcium14.6 mg/dL (15.2 mg/dL) iPTH - 4 pg/mL (N12-65 pg/mL 25-OH D level 103 ng/mL (N>30 ng/ml) Vit D overdose 22
- 23. • • • • • CECT chest –hilar lympahedenopathy serum calcium, 13.8 mg/d iPTH - 4 pg/mL (N12-65 pg/mL 1, 25-OH D level elevated Serum ACEase – highly raised Hilar LN Bx – non caseating granulomas Sarcoidosis 23
- 24. • • • • T2DM CKD serum calcium 14.8mg/d iPTH – 209 (12-72 pg/ml) Hypercalcemia Associated with Renal Failure
- 25. Hypercalcemia Associated withRenal Failure Secondary Hyperparathyroidism Hypocalcaemia is the common denominator Reversible (adaptive) growth of parathyroid gland • Resistance to the normal level of PTH • Increased level of FGF23 • Reduction in 1,25(OH)2 vitamin D Tertiary Hyperparathyroidism • Long-standing, inadequately treated chronic renal failure • True clonal outgrowth (irreversible) 25
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- 27. Critical - >14 mg % 1 Moderate - 12 to 14 mg % 2 Mild – 10.4 to 11.9 mg % 3 • Aggressive therapy • Start therapy • When symptomatic • When PrHyperPTHism • No therapy • Except PrHyperPTHism Normal – 8.5 to 10.3 mg % Hypercalcaemia should always be treated 27
- 28. - thiazide andlithium - volume depletion - prolonged bed rest or inactivity - high calcium diet (>1000 mg/day) 28
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- 30. Dr. Harold Coppisolated calcitonin from salmon sperm
- 31. Bisphos phonate: MOA Osteonecrosis of Jaw (ONJ) mandible> maxilla Matrix metalloproteinase 2
- 32. Treating hypercalcaemia ismultidrug approach In HF, CKD; lowers ca by 1-3 mg/dl Routine use not recommended Do not give bisphosphonates until patient is fully rehydrated contraindicated in patients with cr cl <10 mL/min Caution with NSAIDS, ACE inhibitors, aminoglycosides Calcitonin and hydration provide a rapid reduction, while a bisphosphonate provides a sustained effect
- 33. Monitoring Surgery • Serum calciumlevel Mildly elevated calcium > 1 mg % above normal No previous episodes of • Creatinine clearance life threatening hypercalcemia < 60 ml/minute Normal renal function • Bone density: T score <–2.5 Normal bone status at Any of 3 sites • Age younger than 50 years Serum ca serum creatinine Bone density Significant symptoms – Rx surgery 33
- 34. Minimally Invasive Parathyroidectomy(MIP) an outpatient procedure Pre-op localization with Sestamibi Tc scan cervical block anesthesia minimal surgical incision Intra-op PTH level obtained before and 5 mins after removal If PTH levels fall by greater than 50% operation terminated IF PTH Levels fall by less than 50%, full neck exploration clear-cut cost benefit Accepted in asymptomatic patients not proper for multiple tumour or large tumours
- 35. • If anenlarged gland is found, a • all four glands be normal gland should be sought. sought • if an intra-operative frozen section biopsy of a normal-sized • most of the total parathyroid tissue second gland confirms its mass be removed. histologic normality, no further exploration, biopsy, or excision is • unnecessary surgery & un-acceptable rate needed. of hypoparathyroidism • recurrence rate of hyperand hypocalcamia. parathyroidism may be high if a second abnormal gland is missed. 35
- 36. • totally removethree glands with partial excision of the fourth gland • care is taken to leave a good blood supply for the remaining gland • total parathyroidectomy with immediate transplantation of a portion of a removed, minced parathyroid gland into the muscles of the forearm • surgical excision is easier from the ectopic site in the arm if there is recurrent hyperfunction 36
- 37. calcium 12.4mg/dl (8.4 – 10.4 mg/dl) parathyroid adenoma M/N= Surgery (MIP)
- 38. Malignancy related hypercalcaemia (Breast,Lung, Lymphoma, Thyroid, Kidney, Prostate, Multiple Myeloma) N Saline calcitonin Zoledronic acid
- 39. • Vit Doverdose • Half life of Vit D is very short no further treatment required • Withhold Vit D • Steroid can be used 39
- 40. • • • • Acute symptomatic hypercalcaemia Sarcoidosis(granulomatous disease; DHCC related) NS Steroid 40
- 41. • Hypercalcemia Associatedwith Renal Failure • Secondary hyperparathyroidism • calcitriol
- 42. • Dialysis iflife threatening Secondary hyperparatyroidism • restriction of dietary phosphate, • the use of non-absorbable antacids • careful, selective addition of calcitriol Tertiary Hyperparatyroidism • Partial removal of parathyroid gland 42
- 43. S U M M A R Y Dialysis Controversial Malignancy or VitD associated cases Avoid factors that can aggravate hypercalcemia In CKD 43
- 44. • Most commoncause of hypercalcaemia is primary hyperparathyroidism • Any hypercalcaemia should be worked up and treated. • First investigation to seek for is an intact PTH • Surgery is often provided to apparently aysmptomtic patients of primary hyperparathyroidism • FHH, practically does NOT occur • Hydration is the mainstay of therapy • Managing hypercalcaemia is a multidrug approach • Calcitriol can be given in CKD associated hypercalaemia
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