hypomagnesemia
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Etiology
- endocrine disorders
- hypoparathyroidism
- hyperaldosteronism
- diabetes mellitus via glucose-induced osmotic diuresis
- disorders of calcium metabolism
- resistance to effects of PTH (pseudohypoparathyroidism)
- hungry bone syndrome
- gastrointestinal disorders
- malabsorption of Mg+2 in the ileum
- celiac sprue, steatorrhea
- pancreatitis[1]
- radiation injury to the bowel
- bowel resection
- small bowel bypass
- excessive GI secretions
- malabsorption of Mg+2 in the ileum
- redistribution from extracellular to intracellular space
- 'hungry bone' syndrome after parathyroidectomy
- osteoblastic metastases
- acute respiratory alkalosis
- insulin therapy
- inappropriate renal excretion (decreased tubular reabsorption)
- Bartter's syndrome
- idiopathic magnesium wasting
- obstructive uropathy
- renal transplantation
- chronic interstitial renal disease
- chronic poor nutritional status
- alcoholism
- recovery from acute renal failure
- pharmaceutical agents
- extracellular volume expansion
- cirrhosis
- intravenous (IV) fluid administration
- genetic disorders (see OMIM correlations)
* proton pump inhibitors cannot be stopped in patients with Barrett esophagitis[5]
Epidemiology
- up to 65% of patients in intensive care units
Pathology
- hypomagnesemia causes functional hypoparathyroidism & hypocalcemia
- lower PTH secretion & end-organ resistance to PTH
- hypomagnesemia associated iwth hypokalemia due to urine K+ wasting
Genetics
Physiology
- unbound magnesium is freely filtered at the glomerulus
- > 95% of filtered magnesium is reabsorbed by the kidney
- magnesium is reabsorbed primarily at the ascending loop of Henle
- the last site of regulation is the distal convoluted tubule[4]
Clinical manifestations
- complaints related to hypomagnesemia are nonspecific
- most patients asymptomatic
- patients may become symptomatic with serum magnesion < 1.2 mg/dL[1]
- cardiac arrhythmias: tachycardia
- CNS manifestations
- altered mental status in severe cases
- vertigo, ataxia, depression
- lethargy, anorexia nausea
- seizure activity
- neuromuscular irritability[1]
- positive Chvostek's sign
- positive Trousseau's sign
- carpopedal spasms
- neuromuscular hyperexcitability convulsions
- muscle weakness is not common
- muscle cramping
- tremors, fasciculations[1]
- dysarthria & dysphagia from esophageal dysmotility
* also see Laboratory: & Diagnostic Procedures/Special laboratory (below)
Laboratory
- serum Mg+2, serum Ca+2, serum K+, serum phosphorus
- hypokalemia is common
- hypocalcemia is common
- hypophosphatemia may occur
- BUN & serum creatinine
- blood glucose
- inappropriately normal or low PTH
- 24 hour urine Mg+2
- > 20-50% retention of IV magnesium sulfate 2.4 mg/kg suggests Mg+2 depletion
- urine Mg+ secretion of > 24 mg/day suggest renal Mg+2 wasting
- renal Mg+2 wasting defined as fractional excretion of Mg+2 = serum creatinine x urine Mg+2/ 0.7 x serum Mg+2 x urine creatinine
- if > 4% or daily urinary Mg+2 excretion of >1 mmol/day (24 mg/day)[4]
Diagnostic procedures
electrocardiogram (ECG) & cardiac monitor
- findings are non-specific
- ST segment depression
- tall, peaked T waves
- flat T waves or depression in the precordium
- U waves; loss of voltage
- PR prolongation
- widened QRS
- cardiac arrhythmias
- due to hypomagnesemia alone or concomitant hypokalemia
- paroxysmal atrial & ventricular dysrhythmias
- repolarization alternans
Complications
- magnesium deficiency can cause hypocalcemia with impaired PTH secretion[1][3]
Management
- stop offending medications (diuretics, proton pump inhibitors) if feasible*
- intravenous magnesium sulfate 1-2 g IV every 6 hours to a total dose of 8-12 g for serum Mg+2 > 1 mg/dL[1]
- oral replacement with slow-release magnesium citrate, magnesium oxide, magnesium gluconate in divided doses (NEJM)[5]
- hypokalemia & hypocalcemia may correct with Mg+2 replacement
- treat seizures with benzodiazepines
* proton pump inhibitors cannot be stopped in patients with Barrett esophagitis[5]
More general terms
More specific terms
Additional terms
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Medical Knowledge Self Assessment Program (MKSAP) 11, 14, 16, 18, 19. American College of Physicians, Philadelphia 1998, 2006, 2012, 2018, 2021
Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022 - ↑ eMedicine: hypomagnesemia http://www.emedicine.com/emerg/TOPIC274.HTM
- ↑ 3.0 3.1 Iwasaki Y, Asai M, Yoshida M, Oiso Y, Hashimoto K. Impaired parathyroid hormone response to hypocalcemic stimuli in a patient with hypomagnesemic hypocalcemia. J Endocrinol Invest. 2007 Jun;30(6):513-6 PMID: https://www.ncbi.nlm.nih.gov/pubmed/17646727
- ↑ 4.0 4.1 4.2 Tucker BM et al Urinary Magnesium in the Evaluation of Hypomagnesemia. JAMA. Published online October 30, 2020 PMID: https://www.ncbi.nlm.nih.gov/pubmed/33125046 https://jamanetwork.com/journals/jama/fullarticle/2772654
- ↑ 5.0 5.1 5.2 5.3 5.4 5.5 NEJM Knowledge+ Endocrinology
- ↑ Ahmed F, Mohammed A. Magnesium: The Forgotten Electrolyte-A Review on Hypomagnesemia. Med Sci (Basel). 2019 Apr 4;7(4):56. PMID: https://www.ncbi.nlm.nih.gov/pubmed/30987399 PMCID: PMC6524065 Free PMC article. Review.