Chvostek's
Shafiepour ,m MD.
Kerman university of medical sciences
38-year-old man presented to the emergency
Department with facial paresthesias and upperextremity muscle cramping.
His symptoms were progressive, beginning as mild
paresthesias on postoperative day 1; by the time he
presented, they had been getting worse for about
24 hours.
His medical history
was noteworthy only for papillary thyroid
carcinoma, for which he had undergone
a total thyroidectomy 2 days earlier.
Physical examination revealed apparent
Chvostek’s sign and Trousseau’s sign and
a result of postsurgical acquired
hypoparathyroidism.
On physical examination, a Chvostek's sign
(twitching of the circumoral muscles in response
to gentle tapping of the facial nerve just anterior
to the ear) may be elicited, although it is also
present in10% of normal individuals.
Carpal spasm may be induced by inflation of a
blood pressure cuff to 20 mmHg above the
patient's systolic blood pressure for 3 min
(Trousseau's sign). Severe hypocalcemia can
induce seizures, carpopedal spasm,
bronchospasm, laryngospasm, and prolongation
of the QT interval.
His total calcium level was 5.8 mg per deciliter
(normal range, 8.4 to 10.3) (1.45 mmol per liter
[2.1 to 2.6]), his free calcium level was 1.68 mEq
per liter (normal range, 2.24 to 2.64) (0.84 mmol
per liter [1.12 to 1.32]), and his serum phosphate
level was 6.6 mg per deciliter (normal range, 2.7 to
4.5) (2.13 mmol per liter [0.87 to 1.45]). The
parathyroid hormone level was 7 pg per milliliter
(normal range, 15 to 65).
Chvostek’s sign is described as the twitching of
facial muscles in response to tapping over the area
of the facial nerve. Trousseau’s sign is carpopedal
spasm that results from
ischemia, such as that induced by pressure applied
to the upper arm from an inflated
sphygmomanometer cuff
Chvostek’s sign is neither sensitive nor specific for
hypocalcemia, since it is absent in about one third of
patients with hypocalcemia and is present in
approximately 10% of persons with normal calcium
levels. Trousseau’s sign, however, is more sensitive
and specific; it is present in 94% of patients with
hypocalcemia and in only 1% of persons with normal
calcium levels.
Our patient’s symptoms resolved with
intravenous administration of calcium
gluconate, and he was discharged with
instructions to begin oral calcium supplementation
and to maintain close follow-up with his
endocrinologist.
Acute, symptomatic hypocalcemia is initially managed
with calcium gluconate, 10 mL 10% wt/vol (90 mg or
2.2 mmol) intravenously, diluted in 50 mL of 5% dextrose
or 0.9% sodium chloride, given intravenously over 5 min.
Continuing hypocalcemia often requires a constant
intravenous infusion (typically 10 ampuls of calcium
gluconate or 900 mg of calcium in 1 L of 5% dextrose or
0.9% sodium chloride administered over 24 h).
Accompanying hypomagnesemia, if present, should be
treated with appropriate magnesium supplementation.
Chronic hypocalcemia due to Hypoparathyroidism
is treated with calcium supplements (1000–1500
mg/d elemental calcium in divided doses) and
either vitamin D2 or D3 (25,000–100,000 U daily)
or calcitriol [1,25(OH)2D, 0.25–2 g/d].
Other vitamin D metabolites (dihydrotachysterol,
alfacalcidiol) are now used less frequently.