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![Corrected total calcium (mg%) =
[(Measured total calcium mg%) +
{(4.4 - measured albumin g%) x 0.8}]
Example:
[12.0 + {(4.4 – 2.4) x 0.8}] =
[ 12.0 + (2 x 0.8)] = 12.0 + 1.6 = 13.6
mg%
9](https://image.slidesharecdn.com/hypercalcemia-230329060818-c8b1a8f8/75/Hypercalcemia-ppt-9-2048.jpg)
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Hypercalcemia.ppt
- The document discusses evaluation and management of hypercalcemia. The most common causes are primary hyperparathyroidism and malignancy. Diagnostic workup includes serum calcium, PTH, and history of medications. Hypercalcemic crisis is a medical emergency requiring aggressive intravenous hydration and diuretics, calcitonin, bisphosphonates, or dialysis. Optimal treatment involves identifying and addressing the underlying cause of hypercalcemia.
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Hypercalcemia.ppt
- 1.
- 2. • Commonly encounteredin Practice • Diagnosis often is made incidentally • The most common causes are primary hyperparathyroidism and malignancy • Diagnostic work-up includes measurement of serum calcium, intact parathyroid hormone (I-PTH), h/o any medications • Hypercalcemic crisis is a life-threatening emergency 2
- 3. • Most oftenasymptomatic – Incidental Dx • Mild Hypercalcemia is asymptomatic • Most important cause is hyper parathyroid • DD is needed to decide the treatment • Optimal step by step evaluation is a must. 3
- 4. • 98% ofthe body calcium is in the skeleton • Only 2% is circulation and only half of this is free calcium (ionized Ca++) • This only is physiologically active • The reminder 1% is bound to proteins • Direct measurement of free Calcium ?? 4
- 5. 5 Parathyroid Hormone 1,25 DHCor Vitamin D3 Calcitonin
- 6. 6 Bone Resorption Intestinal Absorption Renal Excretion
- 7.
- 8. Hormone Effect BoneGut Kidney PTH Ca Po4 Increases Osteoclasts Indirect via Vit. D Ca reab Po4 exr. Vitamin D3 Ca Po4 No direct action Ca Po4 absorption No direct effect Calcitonin Ca Po4 Inhibits Osteoclasts No direct effect Ca & Po4 excretion 8
- 9. Corrected total calcium(mg%) = [(Measured total calcium mg%) + {(4.4 - measured albumin g%) x 0.8}] Example: [12.0 + {(4.4 – 2.4) x 0.8}] = [ 12.0 + (2 x 0.8)] = 12.0 + 1.6 = 13.6 mg% 9
- 10.
- 11. Second hydroxylation inthe Kidney at first position 1,25 dihydroxy Cholecalciferol Active Vitamin D (Calcitriol) Successive hydroxylations of Cholecalciferol 25 hydroxylation in the Liver 25 hydroxy Cholecalciferol Vitamin D is a steroid hormone From dietary sources Action of Sunlight on skin 11
- 12. PTH • 4 PTglands • 84 AA hormone • Low Ca stimulates it Calcitriol (D) • Active bone formation • Main effect is on the Gut • PTH Vit. D Calcitonin • Para follicular C of Thyroid • 34 AA hormone • On Kidney 12
- 13. 13 Critical - >14 mg % Moderate - 12 to 14 mg % Mild – 10.4 to 11.9 mg % Normal – 8.5 to 10.3 mg %
- 14.
- 15.
- 16. • More than90 percent of hypercalcemia cases are Primary hyperparathyroidism and malignancy • These conditions must be differentiated early to provide optimal treatment & accurate prognosis • Humoral hypercalcemia of malignancy implies a very limited life expectancy — only a matter of weeks • Primary hyperparathyroidism has a benign course. 16
- 17. • Primary hyperparathyroidism •Sporadic, familial, associated with Multiple Endocrine Neoplasia (MEN I or II) • Tertiary hyperparathyroidism • Associated with chronic renal failure • PTH due to Vitamin D deficiency 17
- 18. • Vitamin Dintoxication • Iatrogenic Vitamin D injections • Usually 25-hydroxyvitamin D2 in over-the-counter supplements • Granulomatous disease – Sarcoidosis, Berylliosis, Tuberculosis • Hodgkin’s lymphoma 18
- 19. • Humoral hypercalcemiaof malignancy (mediated by PTHrP) – common cause • Solid tumors, especially lung, head and neck squamous cancers • Renal Cell Carcinoma (RCC) • Local osteolysis (mediated by cytokines) • Multiple Myeloma • Breast cancer 19
- 20. • Thiazide diuretics(usually mild) - common • Lithium for depressive illnesses • Milk-alkali syndrome (calcium + antacids) • Vitamin A intoxication (including analogs used to treat acne) 20
- 21. • Hyperthyroidism • Adrenalinsufficiency • Acromegaly • Pheochromocytoma 21
- 22. • Familial hypocalciurichypercalcemia (FHH) mutated calcium-sensing receptor gene • Immobilization, with high bone turnover (e.g., Paget’s disease, bedridden child) • Recovery phase of Rhabdomyolysis 22
- 23. • CNS • GIT •SKELETON • KIDNEY STONES BONES GROANS MOANS 23
- 24. Renal “stones” • Nephrolithiasis •Nephrogenic Diabetes Insipidus • Dehydration • Nephrocalcinosis 24
- 25. Skeleton “bones” • Bonepains • Arthritis • Osteoporosis • Osteitis fibrosa cystica in HPTH 25
- 26. Abdominal “Moans” • Nausea,vomiting • Severe anorexia, weight loss • Constipation (not relieved by Rx.) • Abdominal pain (vague and diffuse) • Pancreatitis • Peptic ulcer disease 26
- 27. Psychological “Groans” • Impairedconcentration • Impaired memory, Depression • Confusion, stupor, coma • Lethargy and severe fatigue • Extreme muscle weakness • Corneal calcification (band keratopathy) 27
- 28. Cardiovascular • Hypertension, Increasedrisk of CHD • ECG changes of shortened QT interval, PR prolonged, QRS widened, ST , Bradycardia • Cardiac arrhythmias; Vascular calcification Others • Itching (Generalized Pruritus) • Keratitis, conjunctivitis 28
- 29. 29 ? Suspect Calcium Serum Calcium 8.5to 10.3 > 10.3 mg % < 8.0 mg % Hypocalcemia Normal calcium
- 30. Medications > 10.3 mg%I-PTH High/Normal Pri PTH Suppressed Vit D Toxicity Milk Alkali Cancers/ Lymphoma Suppressed PTHrP 30
- 31. PTHrP Low or Normal Low or Normal 1,25 Vit. D If Low Cancer If High Lymphoma High 24 hr. urine calcium Low – FHH N or Sestamibi 31 Endocrine
- 32.
- 33. 33 • Increased screeningfor serum Ca++ and • Wider availability of I-PTH assay • 80% of cases single parathyroid adenoma • Usually benign adenoma or hyperplasia • Rarely parathyroid cancer • High PTH in the setting of hypercalcemia • Slowly progressive – Sestamibi N-scan • 25% require surgery – RLN paralysis
- 34. 34 64 yrs male- “hyper parathyroid storm” with a serum calcium level of 16.4 mg%
- 35. • Serum calciumlevel > 12 mg % at any time • Episodes of hyper parathyroid crisis • Marked hypercalciuria (urinary Ca++ > 400 mg /day) • Nephrolithiasis; Impaired renal function • Osteitis fibrosa cystica – Thinning of cortical bone • Reduced bone density by DEXA scan (Z score < 2) • Classic neuromuscular symptoms, Proximal muscle weakness and atrophy, Hyper reflexia and ataxia • Age younger than 50 years 35
- 36. 36 • 25 OH- Vitamin D2 is the supplemental Vit D • Level of 25 OH – Vitamin D3 is to be measured • Macrophages in the granulomas, lymphomas cause extra renal conversion of 25 OH form to the1,25 hydroxy derivative –the active Calcitriol • PTH levels are suppressed; Calcitriol levels • Stop the offending use of Vitamin D • Glucocorticoids – for over one month or more • Manage hypercalcemia vigorously
- 37. 37 • Most commonlymediated by systemic PTHrP • Humoral Hypercalcemia of malignancy • PTHrP mimics the bone & renal effects of PTH • Normal Calcitriol and suppressed PTH levels • Excessive bone lysis due to primary or bone secondaries can cause hypercalcemia • MM and metastatic Br Ca present in this way. • In Osteolytic hypercalcemia, SAP is markedly • Hodgkin’s lymphoma – production of Calcitriol
- 38. • Thiazide diureticsincrease renal calcium resorption and cause mild hypercalcemia • Resolves after discontinuing the drug • Thiazide unmasks hyperparathyroidism • Milk–alkali syndrome – Ca + Antacids • Lithium – the set point for PTH • Excess Vitamin A - bone resorption and causes hypercalcemia. 38
- 39. • FHH –Familial Hypocalciuric Hypercalcemia • AD – 100% penetrance – Ca-R gene mutation • Moderate hypercalcemia with normal/ PTH • 24 hour urinary calcium is very low • No benefit from parathyroidectomy • High bone turnover in Paget’s disease or prolonged immobilization • Recovery phase of Rhabdomyolysis 39
- 40. • Ca <12but > 10.3 mg% – no appreciable clinical benefit – they need evaluation • Any patient with Serum Ca > 12 mg% should be aggressively treated • Ca > 14 mg% is Hypercalcemic crisis • Always correct the Ca value for Sr Albumin 40
- 41.
- 42. • Vigorous I.V.Nacl Diuresis – N Saline • Adequate hydration – urine out put must be maintained 200 ml/hour = 5 L /day • The safest and most effective treatment of Hypercalcemic crisis is saline rehydration • Once the urine out put is maintained – give I.V. Furosemide – a loop diuretic in low doses of 10 to 20 mg • ERT - might be beneficial in PMW – new RCT 42
- 43. • In severehypercalcemia refractory to saline diuresis • Calcitonin (Zycalcit, Miacalcin) 6 -8 U/kg IM/SC (400 i.u) given every six hours. • This treatment has a rapid onset but short duration of effect • Patients develop tolerance to the calcium- lowering effect of Calcitonin. 43
- 44. • Zoledronic acid(Zometa) - 4 mg IV diluted in 100 ml of N Saline - over at least 15’ once a M • Pamindronate (Pamidria) - 60 mg IV infusion over 4 h initial – repeated after a month • Etidronate (Didronel) - 7.5 mg/kg IV over 4 h daily for 3-7 d; dilute in at least 250 ml of sterile N Saline • They inhibit bone resorption, inhibit the Osteoclastic activity. 44
- 45. • Dialysis forrefractory Hypercalcemic crisis • Parathyroidectomy for adenomas • Rx. of the underlying cause – Eliminate drugs • Plicamycin (Mithracin) 25 mcg/kg/d IV for 4 d • Gallium nitrate (Ganite) 100 mg/m2/d IV for 5 days in 1 L of NS or 5% Dextrose • Cinacalcet (Sensipar) - 30 mg PO od – (increases sensitivity of calcium sensing receptor) 45
- 46. • Hypercalcemia isoften asymptomatic • Screen all suspected by doing Sr Calcium • If elevated, do I-PTH and follow algorithm • 90% Hyperparathyroidism and malignancy • Vitamin D toxicity is an important cause • Thiazide diuretics common cause, Vitamin A • Adequate hydration - N Saline + Furosemide • Calcitonin + Zoledronic acid main stay of Rx. 46