HYPOCALCEMIA

Normal serum calcium is 2.15 to 2.65 mmol/litre. Hypocalcemia may present as asymptomatic case, acute life threatening condition or may be chronic in nature.

Etiology:

ClinicalPresentations:

  1. Latent tetany: it can be elicited by one of the following signs:
  • Chvostek’s sign: When the facial nerve in front of ear lobe is tapped it leads to contraction of facial muscles.
  • Trousseau’s sign: A sphygmomano meter cuff is applied to upper arm and pressure is maintained above systolic pressure for 1to 5 minutes. Presence of carpal spasm is considered positive sign.
  • Increased muscle excitability to galvanic stimulation also known as Erb’s sign.
  1. Symptomatic:
  • Acute severe presentation: Laryngospasm,broncho spasm or seizures of all types.
  • Tetany, Carpopedal spasms.
  • Tingling/ numbness in circum oral region and periphery of limbs.
  • Muscle Cramps.
  • Prolonged QT interval on ECG.

Differentialdiagnosis:

Treatment:

Acute hypocalcemia: calcium gluconate 10ml 10% IV, diluted in 50ml 5% dextrose by slow infusion(>5 minutes). 10 ampoules of 10 % calciumgluconate 10 ml in 1 litre 5 % dextrose may be given in infusion at 50ml/hour.Associated hypomagnesia must be corrected first. Vitamin D orally may be given.

Persistent hypocalcemia:

  • Oral calcium supplementation.
  • Vitamin D preparation e. g. vitamin D3 (Cholecalciferol), vitamin D2 (ergocalciferol), Alfacalcidol (1,25 – dihydroxycholecalciferol).

Hypoparathyroidism:

It is a disease characterized by insufficiency of or resistance to the action of parathyroid hormone.

Etiology:

  1. Acquired:Surgery (most common cause)
  • Radiation
  • Iron overload (thalassaemia)
  • Hypomagnesaemia
  • Infiltration by metastasis
  • Infiltration by systemic disease (sarcoidosis,amyloidosis, Wilson’s disease)
  • Neonatal hypocalcemia.
  1. Idiopathic
  2. Genetic syndromes:
    • Pseudohypoparathyroidism and hypomagnesaemicsyndroms
  • Parathyroid agenesis.
  1. Autoimmune:
    • Polyglandular (Type I)
  • Isolated

Causes of hypomagnesaemia:

  1. Inadequate intake:
    • Prolonged intake of low magnesium diet.
  • Prolonged infusion of low magnesium solution.
  • Protein energy malnutrition
  • Chronic alcoholism
  1. Malabsorption:
    • Inflammatory bowel disease
  • Bypass surgery
  • Post radiation
  • Familial hypomagnesaemia
  1. Drug induced:
    • Diuretics (non potassium sparing)
  • Nephrotoxic drugs
  1. Latrogenic:
    • Post parathyroidectomy
  • Post renal transplant
  1. Renal tubular dysfunction:
    • Hyperaldosteronism
  • Post renal obstruction
  • Batter’s syndrome
  • Defective renal tubular transplant
  1. Miscellaneous:
    • Post myocardial infarction
  • Post starvation
  • Acute pancreatitis
  • Post diabetic ketoacidosis

Clinical features:

  1. Severe:
    • Laryngospasm
  • Bronchospasm
  • Seizures of all types
  • Carpopedal spasm
  • Heart failure
  1. Mild:
    1. Mental symptoms:
      • Fatigue
  • Hyper – irritability
  • Anxiety
  • Major psychosis
  1. Parathesthesia
  2. Muscle cramps
  3. Perioral numbness
  4. Ectodermal changes:
    1. Nails: These become brittle, develop ridges and may fall off.
    2. Delayed detention, enamel hypoplasia.
    3. Dry and sparse hands.
    4. Cataract
    5. Vesicular or eczematous eruptions in skin
    6. Fissures at angles of mouth
  5. Raised inracarnial tension and papilloedema
  6. Intracranial calcification may be seen in basalganglia region as symmetrical punctuate opacities.
  7. Organic brain syndromes:
    • Dementia
  • Psychosis
  1. Extrapyramidal disorders:
    • Chorea
  • Athetosis
  • Tremor
  • Hemiballismus

Pseudohypoparathyroidism: This condition is characterized by end-organ resistance to PTH with result anthypocalcemia. It has been found associated with Albright’s hereditaryosteodystrophy (AHO) characterized by short stature, obesity subcutaneouscalcification, mental retardation, round facies and brachydactyly.

There are three major variants of pseudohypoparathyroidismdescribed:

Variant                                                                 PTHresistant     Sometic features of AHO

PHPla                                                                             +                                   +

PHPIb                                                                             +                                    -

PPHP (pseudohypoparathyroidism)                 -                                     +

Features of PTHresistant: hypocalcemia, hyperphosphataemia, elevated serum PTH, absence of increase in serum and urinary cyclic AMP and urinary phosphate after PTH IVinfusion.

Treatment:

It is essentially aimed at to raise the plasma calcium to alevel that will alleviate the symptoms. Treatment methods include:

  1. IV calcium gluconate slow injections every 5 -10minutes.
  2. Continuous IV calcium gluconate infusion.
  3. Oral calcium supplement
  4. Vitamin D supplementation (Calcitriol,alfacalcidol, dihydrotachysterol or ergocalciferol).
  5. Avoidance of drugs that may cause hypocalcemia such as loop diuretics, sex steroids, glucorticoids and anti-convulsants.

Alternative experimental therapies:

  1. Parathyroid hormone replacement
  2. Parathyroid gland all transplantation.