Post on 29-Dec-2015
Hypercalcemia
Chief Complaint: review lab results (June 30)
History of Illness: seen by GP in April c/o bilateral shoulder pain. Recently started exercise program O/E full ROM but weakness rotator cuff muscles & tender supraspinatus.
Xrays -> bilateral calcification in rotator cuff Ca+ 2.88 May 5th PTH normal. Repeat calcium normal. Dx rotator cuff tendonitis. Plan: repeat calcium. Exercise. NSAIDS.
May 20th calcium 3.01 PTH normal
Hypercalcemia
June 30th Presented at clinic for lab results. c/o “normal aches and pains”, itchy eyes, drippy nose
Sent for TSH, PTHrp, ionized calcium, Vit D 1,25 & Vit D 25
July 8th : c/o hx crampy abdominal pain, constipation, nausea, fatigue, skin “feels dry”, headache, irritability, leg weakness & trouble concentrating; sx for 2-3 weeks, thought was dehydrated so took Pedialyte...sx improved.
similar episode 4 months ago, lasted only 2 days.
Hypercalcemia
Past Medical History: lichen sclerosis. Mild depression
Allergies: palm oil -> wheezingMeds: Trazadone 50 mg po HS. No antacids. Calcium 1 gm/day. Vit D 800 IU/day Family History: older sister with lupus. Younger sister with arthritis. 4 sisters & niece
with thyroid problems. Father, 2 sisters, daughter with depression. Mother deceased breast cancer age 62. younger sister with early CRC
Social History: quit smoking 25 yrs ago. Drinks 1-5 beer &/or wine a day; can take it or leave it. CAGE neg
Hypercalcemia
Physical Exam
General Appearance: alert, slim 57 yr old female; appears her stated age. No acute distress.
BP 112/65 HR 68, regular RR 16
EENT: normal. No enlarged nodes. Thyroid not enlarged.
Chest clear
CVS: S1S2 normal. No murmurs
Abd: soft, nontender. No masses.
Neuro: CN II-XII normal. 5+ strength bilateral UE, LE. DTR 2+
Labs: Calcium 3.25 ionized calcium 1.89
TSH, CBC, PTH, CK, lytes, Bun, creatinine Vit D normal
Hypercalcemia
Differential Dx: ?
Plan: ?
Refer to Internal Medicine
Pt went to Prince George for 3 wks.
Hypercalcemia
• Results when calcium entering circulation exceeds calcium excreted in urine or deposited in bone
• Due to: increased bone resorption, increased GI absorption, decreased renal excretion.
• Hyperparathyroidism & malignancy make up 90% of cases
Hypercalcemia
Causes of increased bone resorption
1. Primary hyperparathyroidism: (usually not > 3.25) increased PTH -> increased bone resorption & increased
serum calcium increased calcium absorption in GI tract
2. 2nd ary hyperparathyroidism: often assoc with CKD; low or normal calcium; can increase with prolonged disease
3. Malignancy: hypercalcemia associated with many tumors eg. Bone mets, multiple myeloma PTHrp assoc with nonmetastatic solid tumors
4. Thyrotoxicosis: mild hypercalcemia in 15-20% of pts
Hypercalcemia
Causes of increased calcium absorption
• High calcium intake alone rarely causes hypercalcemia (elevated serum calcium -> PTH )
• High calcium intake plus reduced urinary excretion ->
1. CKD: decreased calcium excretion/elevated serum phosphate/decreased calcitriol synthesis
2. Milk-Alkali syndrome: excess milk or calcium carbonate -> hypercalcemia, metabolic alkalosis & renal insufficiency
Hypercalcemia
3. Excessive Vit D: increases calcium absorption & bone resorption
1,25 -> results from:
a) excess intake calcitriol
eg. tx for hypoparathyroidism, or hypocalcemia/2nd’ary hyperparathyroidism of renal failure.
Lasts 1-2 days; tx with salt & fluids, stopping calcitriol.
b) Increased endogenous production
eg pts with lymphoma, chronic granulomatous disorders (sarcoidosis, Wegeners)
high 25OHD from excess Vit D or calcidiol intake
lasts longer; more aggressive tx needed
Hypercalcemia
Other less common causes of hypercalcemia Lithium -> increased PTH secretion Thiazide diuretics -> decreases urinary calcium excretion Pheochromocytoma -> rare; ?due to concurrent hyperparathyroidism
Adrenal insufficiency Rhabdomyolysis & diuretic phase of ARF Theophylline toxicity Familial hypocalciuric hypercalcemia Metaphyseal chondrodysplasia: rare form of dwarfism
Hypercalcemia
Diagnostic Approach Clinical & lab evaluation to distinguish between hyperparathyroidism
& malignancy
PTH-mediated: 1’ary hyperparathyroidism, familial hyperparathyroid syndromes
Non PTH-mediated: malignancy, Vit D excess, granulomatous dx
1. Repeat sample to confirm hypercalcemia2. Clinical evaluation, duration of high calcium, presence of sx, FH, &
meds may give clues.3. PTH: frankly elevated or in upper half of normal -> primary
hyperparathyroidism4. PTH < 20 pg/ml: look for other causes. 5. PTHrp & Vit D metabolites
Hypercalcemia
Symptoms of hypercalcemia Polyuria, altered mentation, nausea, vomitting, constipation Life-threatening -> arrythmia, ++volume depletion due to polyuria
Chronic mild hyperparathyroidism Usually no symptoms Increased risk osteopenia, renal calculi, nephrocalcinosis
Hypercalcemia
Interpretation of serum calcium
Hypercalciumemia due to ionized (free) calcium
40-45% calcium bound to albumin
Increased protein-binding can cause elevation in serum total calcium but not ionized calcium. Occurs in pts with hyperalbuminemia due to severe dehydration & rarely MM.
Hypoalbuminemia -> normal total calcium, but elevated ionized calcium.
Hypercalcemia
Degree of hypercalcemia useful
< 2.75 mmol/L more likely primary hyperparathyroidism
> 3.25 mmol/L more common with malignancy
10-20% of pts with 1’ary hyperparathyroidism have PTH in upper end of normal
Hypercalcemia
Key PointsKnow when to check calciumKnow what to look for if elevatedComprehensive hx can give clues