HYPOCALCEMIA

R. RodríguezMay 21, 2013

Calcium Metabolism

Bones = insoluble salts• Protect, weight, levers

ECF = soluble ions (1%)• Ionized• Protein bound

PTH secretion – regulated by free Ca2+

PTH Kidney

Bone

A 17 year-old female with a history of total thyroidectomy was sent to the emergency department (ED) for an abnormal lab study.

The patient reported a previous history of electrolyte problems with which she felt "twitchy," yet reported no symptoms during this ED evaluation.

A blood pressure cuff was placed on the patient's right arm and inflated to a pressure above the patient's systolic blood pressure.

After approximately 2 minutes, the patient's right hand developed a contracted position. Within seconds of release of the cuff, the patient's hand returned to a normal position.

Hypocalcemia

Abnormally low serum concentration of:

Ionized calcium < 4.7

Or total serum Ca < 8.5

Etiology:• Renal failure: 1,25-hydroxy Vit D deficiency Vit D

deficiency (nutritional)

• Hypomagnesemia: failure of release of PTH

• Hypoparathyroidism: from surgery and stunned hypoparathyroidism, neck radiation, autoimmune destruction or Ca-sensing receptor auto-Ab

• Drug induced: Phenytoin – damages vitamin DFoscarnet, Cinacalet – inhibits PTH release

Pseudohypoparathyroidism• Peripheral tissue resistance to PTH

Primery site = renal tubules Bone osteitis fibrisa cystica

• Ia and Ib: end organ resistance• Ia:• serum PTH • skeletal abnormalities• Mental retardation• Short stature

Hypoproteinemia:• nephrotic syndrome, • chronic illness, • malnutrition, • cirrhosis• volume overexpansion.

• Corrected Calcium:[N(Alb) – P(Alb)] x 0.8 + (Ca)

Each 1.0 Alb = 0.8 Ca

Vit D deficiency:1. Crohn’s disease2. Celiac sprue3. Pancreatic insufficiency4. Nutritional/Sunlight

• PTH levels are high • Alk phos can be elevated

Hyperphosphatemia:• Excessive enteral or parenteral

phosphate administration

• The tumor lysis syndrome

• Rhabdomyolysis- induced acute renal failure

Pancreatitis• Libereted FA chelate Ca2+

Sepsis:• Hypocalcemia is associated with a

worse prognosis.

• Most often reported with gram-negative sepsis

• Has occurred in toxic shock syndrome caused by staph

• The pathophysiology of hypocalcemia in this setting is unknown.

Clinical manifestations• Neuromuscular irritability: • perioral paresthesias, • cramps, • + Chvostek’s,• + Trousseau’s, • laryngospasm• irritability, depression,• psychosis, • ICP, seizures, • QT interval

Clinical manifestations:• Rickets and/or osteomalacia: • Chronic vit D low Ca2+,

low PO43- low

bone/cartilage mineralization

• growth failure, • bone pain, • muscle weakness

Clinical manifestations:• Renal osteodystrophy • ( vit D & PTH in renal failure)

• osteomalacia • ( mineralization of bone due to

Ca and 1,25-(OH)2D)

• osteitis fibrosa cystica • (due to PTH)

Diagnostic studies• Ca• alb• PTH• 25-(OH)D• 1,25(OH)2D (if renal failure or rickets)• Mg• PO4

• Alk phos• UCa

Treatment

• Symptomatic: intravenous Ca gluconate (1–2 g IV over 20 mins) + calcitriol* (most effective in acute hypocalcemia, but takes hrs to work)

• Asymptomatic and/or chronic: oral Ca (1–3g/d) & vitamin D (ergocalciferol* 50,000 IU PO q wk x 8-10wks)

• Chronic renal failure: phosphate binder(s), oral Ca, calcitriol or analog

Resources

• Fischer, Conrad; Internal medicine clerkship: Survive clerkship & ace the shelf. 1st Edition. Kaplan Publishing. Hypocalcemia, pages: 86-87.

• Sabastine, Mark; Pocket medicine: The massachsetts General Hospital Handbook of Internal Medicine. Fourth Edition. Lippincott Williams & Wilkins. Calcium disorders, page: (7-12)

• Goldman's Cecil Medicine: Expert Consult Premium 24th Edition. Saunders. Hypocalcemia, pages 1113 - 1119

QUESTIONS?