Hypocalcaemia

OVERVIEW

  • calcium is a highly regulated cation
  • involved in: cell death, duration and strength of cardiac muscle contraction, muscle contraction in blood vessels, airways and uterus, coagulation, bone metabolism, neurotransmitter and hormone release…
  • Ca2+ exists in the extracellular plasma two states:
    1. free ionized state and
    2. bound to other molecules (mostly albumin, rest – beta-globulins, phosphate, citrate)
  • ionized Ca2+ concentration is inversely related to pH -> an increase in pH results in a decrease in ionized Ca2+

Calcium levels

  • total Ca2+ range = 2.2-2.5mmol/L (55% bound, 45% ionized)
  • ionized Ca2+ range (50%) = 1.1-1.3mmol/L
  • protein bound Ca2+ range (40%) = 0.95-1.2mmol/L
  • complex Ca2+ (10% – calcium phosphate, salts) = 0.05mmol/L

CALCIUM METABOLISM

Vitamin D

  • group of related sterols
    cholecalciferol is formed in the skin
    -> in liver to 25-hyrdroxcholecalciferol
    -> in kidney proximal tubules to 1,25-dihydroxycholecalciferol
    -> this then helps calcium absorption in the intestine
  • controlled by parathyroid hormone

-> increases intestinal absorption of Ca2+
-> increases renal Ca2+ reabsorption
-> mobilises bone Ca2+ & PO43-

Parathyroid hormone

  • secretion increased by hypocalaemia and hypomagnesaemia
  • secretion decreased by hypercalcaemia and hypermagnesaemia

-> mobilses Ca2+ from bone
-> increases renal Ca2+ reabsorption
-> increases renal PO43- excretion
-> increases formation of 1, 25-dihyroxycholecalciferol

Calcitonin

  • antagonist of parathyroid hormone
  • secreted by the parafollicular cells of the thyroid gland in response to:
    – hypercalcaemia
    – catecholamines
    – gastrin

-> inhibits the mobilisation of bone Ca2+
-> increases renal Ca2+ & PO43- excretion

SUMMARY OF CAUSES

Intake reduced:

  • Ca2+
  • vitamin D
  • phenytoin (increased metabolism of vitamin D)

Redistribution:

  • alkalosis
  • citrate toxicity
  • hyperphosphataemia
  • pancreatitis
  • tumour lysis syndrome
  • rhabdomyolysis
  • decreased bone turnover
  • hypoparathyroidism
  • drugs (bisphosphonates, PPI’s, SSRI’s, gentamicin)

Output increased:

  • urinary – ethylene glycol, cis-platin, protamine, loop diuretics
  • non-urinary – bleeding, plasmapheresis, citrate RRT

CAUSES OF HYPOCALCAEMIA AND ACID-BASE DISTURBANCE

  • Metabolic alkalosis – citrate toxicity
  • Metabolic acidosis – acute renal failure, tumour lysis, rhabdomyolysis, pancreatitis, ethylene glycol poisoning, hydrofluoric acid, sepsis, burns

HISTORY

  • perioral numbness
  • paresthesias
  • muscle cramps
  • mild mental status changes (irritability)
  • seizures
  • tetany
  • collapse
  • to find cause: diet, drugs, symptoms specific to cause
  • laryngospasm

EXAMINATION

  • Chvostek sign (tapping facial nerve anterior to ear -> spasm of facial muscles)
  • Trousseau sign (inflate BP cuff -> trap median nerve -> carpal spasm)
  • hypotension
  • arrhythmias (long QT)
  • heart failure
  • signs specific to cause

INVESTIGATIONS

  • Ca2+ (total and ionized)
  • PO43-
  • Mg2+
  • PTH
  • ECG: prolongation of ST segment and QT interval -> VT
  • albumin
  • lipase (rule out pancreatitis)
  • U+E – renal failure, hyperkalaemia
  • CK and urate – rhabdomyolysis

MANAGEMENT

  • treat cause
  • proportional to severity
  • oral Ca2+
  • replace Mg2+
  • vitamin D
  • IV calcium (10mL gluconate = 2.3mmol = 93mg, 10mL chloride = 6.8mmol = 272mg)
  • indications for IV calcium therapy:

-> symptomatic hypocalcaemia
-> ionized Ca2+ <0.8mmol/L
-> hyperkalaemia
-> Ca2+ channel blocker OD
-> hypermagnesaemia
-> hypocalcaemia with high inotrope requirement
-> massive transfusion
-> post cardiopulmonary bypass


References and Links


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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