HYPOCALCEMIA

R. Rodrguez
May 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 Casensing receptor auto-Ab
Drug induced:
Phenytoin damages vitamin D
Foscarnet, 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.
2.
3.
4.

Crohns disease
Celiac sprue
Pancreatic insufficiency
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,
+ Chvosteks,
+ Trousseaus,
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
(12 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 24 th
Edition. Saunders. Hypocalcemia, pages 1113 - 1119

QUESTIONS?