2017-5-30 Hypocalcaemia - Wikipedia

Hypocalcaemia
From Wikipedia, the free encyclopedia

Hypocalcaemia, also spelled hypocalcemia, is low calcium

levels in the blood serum.[1] The normal range is 2.1–
Hypocalcemia
2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L) with levels
less than 2.1 mmol/L defined as hypocalcemia.[2][3][4]
Mildly low levels that develop slowly often have no
symptoms.[5][6] Otherwise symptoms may include
numbness, muscle spasms, seizures, confusion, or cardiac Calcium within the periodic table
arrest.[2][5] Classification and external resources

Common causes include hypoparathyroidism and vitamin D Specialty Endocrinology

deficiency.[5] Others causes include kidney failure, ICD-10 E83.5 (http://apps.who.int/classification
pancreatitis, calcium channel blocker overdose, s/icd10/browse/2016/en#/E83.5)
rhabdomyolysis, tumor lysis syndrome, and medications eMedicine article/241893 (http://emedicine.medsca
such as bisphosphonates.[2] Diagnosis should generally be pe.com/article/241893-overview)
confirmed with a corrected calcium or ionized calcium
Patient Hypocalcemia (http://patient.info/doctor/
level.[5] Specific changes may be seen on an UK Hypocalcaemia)
electrocardiogram (ECG).[2]

Initial treatment for severe disease is with intravenous calcium chloride and possibly magnesium sulfate.[2]
Other treatments may include vitamin D, magnesium, and calcium supplements. If due to hypoparathyroidism,
hydrochlorothiazide, phosphate binders, and a low salt diet may also be recommended.[5] About 18% of people
who are in hospital have hypocalcemia.[6]

Contents
1 Signs and symptoms
2 Causes
3 Mechanism
4 Diagnosis
5 Management
6 See also
7 References Video explanation
8 External links

Signs and symptoms

The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect due to the
decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits
depolarization of nerve and muscle fibers, reduced calcium lowers the threshold for depolarization.[7] The
symptoms can be recalled by the mnemonic "CATs go numb" - Convulsions, Arrhythmias, Tetany, and
numbness/parasthesias in the hands and feet and around the mouth.

Petechiae which appear as on-off spots, then later become confluent, and appear as purpura (larger
bruised areas, usually in dependent regions of the body).
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Oral, perioral and acral paresthesias, tingling or 'pins and needles' sensation in and around the mouth and
lips, and in the extremities of the hands and feet. This is often the earliest symptom of hypocalcaemia.
Carpopedal and generalized tetany (unrelieved and strong contractions of the hands, and in the large
muscles of the rest of the body) are seen.
Latent tetany
Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and
maintaining the cuff pressure above systolic)
Chvostek's sign (tapping of the inferior portion of the cheekbone will produce facial spasms)[8]
Tendon reflexes are hyperactive
Life-threatening complications
Laryngospasm
Cardiac arrhythmias
Effects on cardiac output
Negative chronotropic effect, or a decrease in heart rate.
Negative inotropic effect, or a decrease in contractility

ECG changes include the following:

Intermittent QT prolongation, or intermittent prolongation of the QTc (corrected QT interval) on
the EKG (electrocardiogram) is noted. The implications of intermittent QTc prolongation
predisposes to life-threatening cardiac electrical instability (and this is therefore a more critical
condition than constant QTc prolongation). This type of electrical instability puts the patient at high
risk of torsades de pointes, a specific type of ventricular tachycardia which appears on an EKG (or
ECG) as something which looks a bit like a sine wave with a regularly increasing and decreasing
amplitude. (Torsades de pointes can cause death, unless the patient can be medically or electrically
cardioverted and returned to a normal cardiac rhythm.)

Causes
Hypoparathyroidism is a common cause of hypocalcemia. Calcium is tightly regulated by the parathyroid
hormone (PTH). In response to low calcium levels, PTH induces the kidneys to reabsorb calcium, the kidneys
to increase production of calcitriol (the active form of vitamin D) thereby increasing intestinal absorption of
calcium, and the bones to release calcium. These actions lead to a re-balance in the blood calcium levels.
However, in the setting of absent, decreased, or ineffective PTH hormone, the body loses this regulatory
function, and hypocalcemia ensues. Hypoparathyroidism is commonly due to surgical destruction of the
parathyroid glands via parathyroidectomy or neck dissection for head and neck cancers. Hypoparathyroidism
may also be due to autoimmune destruction of the glands.

Eating disorders
Prolonged vomiting (e.g. with a viral illness)
Exposure to mercury, including infantile acrodynia
Excessive dietary magnesium, as with supplementation.
Excessive dietary zinc, as with supplementation (causes rapid hypocalcemia).
Prolonged use of medications/laxatives containing magnesium
Chelation therapy for metal exposure, particularly EDTA
Osteoporosis treatment or preventive agents, such as bisphosphonates and denosumab.
Agents for the treatment of hypercalcemia, such as Calcitonin.
Chronic kidney failure
Absent active vitamin D
Decreased dietary intake
Decreased sun exposure
Defective Vitamin D metabolism
Anticonvulsant therapy
Vitamin-D dependent rickets, type I
Ineffective active vitamin D
Intestinal malabsorption
Vitamin-D dependent rickets, type II
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Pseudohypoparathyroidism
Severe acute hyperphosphataemia
Tumour lysis syndrome
Acute kidney failure
Rhabdomyolysis (initial stage)
Exposure to hydrofluoric acid
As a complication of pancreatitis
Alkalosis, often caused by hyperventilation
As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic
alkalosis, the concentration of freely ionized calcium, the biologically active component of blood
calcium, decreases. Because a portion of both hydrogen ions and calcium are bound to serum
albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing
up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total
serum calcium. For every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L.
This hypocalcaemia related to alkalosis is partially responsible for the cerebral vasoconstriction
that causes the lightheadedness, fainting, and paraesthesia often seen with hyperventilation.
Tetany may also be seen with this condition.
Neonatal hypocalcemia
Very low birth weight (less than 1500 grams)
Gestational age less than 32 weeks

Mechanism
Physiologically, blood calcium is tightly regulated within a narrow range for proper cellular processes. Calcium
in the blood exists in three primary states: bound to proteins (mainly albumin), bound to anions such as
phosphate and citrate, and as free (unbound) ionized calcium. Only the ionized calcium is physiologically
active. Normal blood calcium level is between 8.5 to 10.5 mg/dL (2.12 to 2.62 mmol/L) and that of ionized
calcium is 4.65 to 5.25 mg/dL (1.16 to 1.31 mmol/L).

Diagnosis
Because a significant portion of calcium is bound to albumin, any alteration in the level of albumin will affect
the measured level of calcium. A corrected calcium level based on the albumin level is: Corrected calcium
(mg/dL) = measured total Ca (mg/dL) + 0.8 * (4.0 - serum albumin [g/dL]).[9] Another way to determine the
calcium level is to measure directly the ionized calcium level.

Management
Intravenous calcium gluconate 10% can be administered, or if the hypocalcaemia is severe, calcium
chloride is given instead. This is only appropriate if the hypocalcemia is acute and has occurred over a
relatively short time frame. But if the hypocalcemia has been severe and chronic, then this regimen can
be fatal, because there is a degree of acclimatization that occurs. The neuromuscular excitability, cardiac
electrical instability, and associated symptoms are then not cured or relieved by prompt administration of
corrective doses of calcium, but rather exacerbated. Such rapid administration of calcium would result in
effective over correction – symptoms of hypercalcemia would follow.
However, in either circumstance, maintenance doses of both calcium and vitamin-D (often as 1,25-
(OH)2-D3, i.e. calcitriol) are often necessary to prevent further decline.

See also
Calcium metabolism
Hypercalcaemia
Milk fever (hypocalcemia in animals)
Calcium deficiency (plant disorder)
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Hypomagnesemia with secondary hypocalcemia

References
1. LeMone, Priscilla; Burke, Karen; Dwyer, Trudy; Levett-Jones, Tracy; Moxham, Lorna; Reid-Searl, Kerry (2015).
Medical-Surgical Nursing (https://books.google.ca/books?id=MDXiBAAAQBAJ&pg=PA237). Pearson Higher
Education AU. p. 237. ISBN 9781486014408.
2. Soar, J; Perkins, GD; Abbas, G; Alfonzo, A; Barelli, A; Bierens, JJ; Brugger, H; Deakin, CD; Dunning, J; Georgiou,
M; Handley, AJ; Lockey, DJ; Paal, P; Sandroni, C; Thies, KC; Zideman, DA; Nolan, JP (October 2010). "European
Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances:
Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac
surgery, trauma, pregnancy, electrocution.". Resuscitation. 81 (10): 1400–33. doi:10.1016/j.resuscitation.2010.08.015
(https://doi.org/10.1016%2Fj.resuscitation.2010.08.015). PMID 20956045 (https://www.ncbi.nlm.nih.gov/pubmed/20
956045).
3. Pathy, M.S. John (2006). Principles and practice of geriatric medicine (http://onlinelibrary.wiley.com/doi/10.1002/04
7009057X.app01/pdf) (4. ed.). Chichester [u.a.]: Wiley. p. Appendix. ISBN 9780470090558.
4. Minisola, S; Pepe, J; Piemonte, S; Cipriani, C (2 June 2015). "The diagnosis and management of hypercalcaemia.".
BMJ (Clinical research ed.). 350: h2723. doi:10.1136/bmj.h2723 (https://doi.org/10.1136%2Fbmj.h2723).
PMID 26037642 (https://www.ncbi.nlm.nih.gov/pubmed/26037642).
5. Fong, J; Khan, A (February 2012). "Hypocalcemia: updates in diagnosis and management for primary care." (https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267). Canadian family physician Medecin de famille canadien. 58 (2):
158–62. PMC 3279267 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279267)  . PMID 22439169 (https://www.
ncbi.nlm.nih.gov/pubmed/22439169).
6. Cooper, MS; Gittoes, NJ (7 June 2008). "Diagnosis and management of hypocalcaemia." (https://www.ncbi.nlm.nih.g
ov/pmc/articles/PMC2413335). BMJ (Clinical research ed.). 336 (7656): 1298–302.
doi:10.1136/bmj.39582.589433.be (https://doi.org/10.1136%2Fbmj.39582.589433.be). PMC 2413335 (https://www.n
cbi.nlm.nih.gov/pmc/articles/PMC2413335)  . PMID 18535072 (https://www.ncbi.nlm.nih.gov/pubmed/18535072).
7. Armstrong, C.M., Cota, Gabriel. (1999). "Calcium block of Na+ channels and its effect on closing rate" (https://ww
w.ncbi.nlm.nih.gov/pmc/articles/PMC22436). Proceedings of the National Academy of Sciences of the United States
of America. 96 (7): 4154–4157. Bibcode:1999PNAS...96.4154A (http://adsabs.harvard.edu/abs/1999PNAS...96.4154
A). doi:10.1073/pnas.96.7.4154 (https://doi.org/10.1073%2Fpnas.96.7.4154). PMC 22436 (https://www.ncbi.nlm.nih.
gov/pmc/articles/PMC22436)  . PMID 10097179 (https://www.ncbi.nlm.nih.gov/pubmed/10097179).
8. Durlach, J; Bac, P; Durlach, V; Bara, M; Guiet-Bara, A (June 1997). "Neurotic, neuromuscular and autonomic
nervous form of magnesium imbalance". Magnesium research. International Society for the Development of
Research on Magnesium. 10 (2): 169–95. PMID 9368238 (https://www.ncbi.nlm.nih.gov/pubmed/9368238).
9. Fluids & Electrolytes: A 2-in-1 Reference for Nurses (https://books.google.ca/books?id=Ap2Gc5U0TPwC&pg=PA12
2). Lippincott Williams & Wilkins. 2006. p. 122. ISBN 9781582554259.

External links

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Categories: Electrolyte disturbances Calcium

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