Hypomagnesaemia: diagnosis and management in the emergency department
Intended for healthcare professionals
Evidence and practice    

Hypomagnesaemia: diagnosis and management in the emergency department

Alexander Cushny Staff nurse, Accident and Emergency, Withybush General Hospital, Pembrokeshire, Wales
Rachel Rees Advanced nurse practitioner, Accident and Emergency, Withybush General Hospital, Pembrokeshire, Wales

Why you should read this article:
  • To understand the role of magnesium in human physiological functioning

  • To learn how hypomagnesaemia, a deficiency of magnesium, can affect the neuromuscular, cardiovascular and renal systems

  • To enhance your knowledge of the clinical management of patients with hypomagnesaemia

Magnesium is an intracellular electrolyte and is a vital element in human physiological functioning. A deficiency in magnesium, termed hypomagnesaemia, can affect the neuromuscular, cardiovascular and renal systems. Hypomagnesaemia may be more prevalent in patients with cancer than in the general population. The increasing numbers of cancer diagnoses in the UK means that emergency department (ED) nurses are likely to be involved in care of this population, including those with suspected hypomagnesaemia. This article describes some of the causes and signs and symptoms of hypomagnesaemia and outlines the diagnosis and clinical management of patients with the condition. The article includes a case study of a patient with cancer who was admitted to an ED with hypomagnesaemia.

Emergency Nurse. doi: 10.7748/en.2022.e2141

Peer review

This article has been subject to external double-blind peer review and checked for plagiarism using automated software

@kushnikov

Correspondence

cushlex@gmail.com

Conflict of interest

None declared

Cushny A, Rees R (2022) Hypomagnesaemia: diagnosis and management in the emergency department. Emergency Nurse. doi: 10.7748/en.2022.e2141

Published online: 26 July 2022

Introduction

Magnesium is the second most abundant intracellular electrolyte in the human body after potassium and the fourth most abundant extracellular cation (a positively charged ion) in the human body (Jahnen-Dechent and Ketteler 2012). It is also an abundant mineral in nature and is readily available through ingestion of plant and animal foods, for example green leafy vegetables, legumes, nuts, seeds and whole grains and red meat, although processed foods have a lower magnesium content (Ahmed and Mohammed 2019, Katopodis et al 2020).

Magnesium is a vital element in human physiological functioning and is involved in many enzyme systems that regulate various biochemical reactions in the body, including protein synthesis, muscle and nerve function, blood glucose control and blood pressure regulation (Katopodis et al 2020). Magnesium is required for energy production and glycolysis and synthesis of deoxyribonucleic acid (DNA) and ribonucleic acid (RNA). It also contributes to the structural development of bone and is involved in active transport of calcium and potassium ions across cell membranes, which affects nerve impulse conduction, muscle contraction and heart rhythms (Abraham and Schellack 2016). A deficiency in magnesium, termed hypomagnesaemia, can affect the neuromuscular, cardiovascular and renal systems (Schwalfenberg and Genuis 2017).

In the UK there are around 375,000 new cancer diagnoses every year, which equates to over 1,000 per day. Around 45% of patients diagnosed with cancer have surgery as part of their primary cancer treatment, 27% have radiotherapy and 28% have chemotherapy (Cancer Research UK 2022). Magnesium can be depleted through reduced food intake, intestinal malabsorption and increased renal excretion; the latter two factors can be influenced by pharmacokinetics (Jahnen-Dechent and Ketteler 2012). Patients with cancer, therefore, may be susceptible to these risk factors due to reduced appetite and/or gastrointestinal (GI) disturbances and/or increased urinary production caused by side effects of surgery, chemotherapy or other medicines. Hypomagnesaemia may be more prevalent in patients with cancer than in the general population for these reasons (Saif 2008).

This article outlines the causes of hypomagnesaemia and the diagnostic process and describes the clinical management of patients with the condition in the emergency department (ED). The article includes a case study of a patient with cancer who was admitted to the ED with suspected hypomagnesaemia (Case study 1).

Case study 1. Dorothy

Dorothy (a pseudonym) was a 58-year-old woman with grade III local advanced invasive ductal carcinoma. Dorothy had completed four courses of chemotherapy, consisting of neoadjuvant docetaxel, carboplatin, trastuzumab and pertuzumab, and had been discharged home after her fourth course.

Dorothy experienced diarrhoea and developed tremors and a tingling sensation in her lips and tongue, which prompted her to attend her GP surgery. She was referred by the GP to the medical team at the local hospital with suspected hypomagnesaemia.

On arrival at the ED, Dorothy’s baseline observations and an initial summary of presenting signs and symptoms were taken.

At this stage no tremors were observed. Blood tests, including serum magnesium levels, and an ECG were undertaken as part of the assessment. The ECG showed normal sinus rhythm, however the serum magnesium level was 0.23mmol and was therefore classified as ‘grade 4, life threatening’ (Table 2).

The team decided it was likely that hypomagnesaemia had been caused by the diarrhoea, which was a side effect of the chemotherapy.

Dorothy was prescribed 20mmol magnesium sulfate via intravenous infusion over three hours in line with local trust guidelines. Cardiac monitoring was continued during this period.

Dorothy was also prescribed and administered oral loperamide to manage the diarrhoea. Dorothy was admitted to the medical unit from the ED for further magnesium infusions.

Following discharge, Dorothy attended the ambulatory care unit to receive intermittent magnesium infusions over the next few months until her magnesium levels returned to normal.

Key points

  • Magnesium is a vital element in human physiological functioning and is involved in many enzyme systems that regulate biochemical reactions in the body

  • Early signs of magnesium deficiency may include loss of appetite, nausea, vomiting, fatigue and weakness

  • The most common test for evaluating a patient’s magnesium levels is serum magnesium concentration, particularly where there is a need for rapid assessment

  • Clinical management of patients with hypomagnesaemia involves replacement with magnesium sulfate, administered either intravenously or orally

Hypomagnesaemia

Signs and symptoms

Ahmed and Mohammed (2019) have suggested that magnesium is a ‘forgotten’ electrolyte due to a lack of understanding of its physiology among professionals, lack of attention in the literature compared with electrolytes such as sodium, potassium and calcium, and because patients are often asymptomatic until plasma serum levels of magnesium are very low. Symptoms associated with hypomagnesaemia are rare unless plasma serum levels are depleted to values <0.4mmol/L; severe effects at magnesium concentrations of <0.4mmol/L can include seizures, drowsiness, confusion and coma (Ayuk and Gittoes 2011, National Institute for Health and Care Excellence (NICE) 2013). Hypomagnesaemia has also been associated with atrial and ventricular arrhythmias, although the underlying mechanism is unknown (Ayuk and Gittoes 2011).

Early signs of magnesium deficiency may include loss of appetite, nausea, vomiting, fatigue and weakness and may progress to numbness, tingling, muscle contractions, cramps, seizures, sudden changes in behaviour caused by excessive electrical activity in the brain, personality changes, abnormal heartbeat and coronary spasms as the deficiency deteriorates (Jahnen-Dechent and Ketteler 2012). There may be no clinical symptoms even in patients with severe hypomagnesaemia, however there may be a greater likelihood of symptoms in patients who experience a rapid decrease in serum magnesium concentration compared with a more gradual change (Jahnen-Dechent and Ketteler 2012).

The long-term effects of hypomagnesaemia include coronary artery disease due to endothelial cell dysfunction (Ahmed and Mohammed 2019.)

Causes of hypomagnesaemia

Table 1 summarises the causes of hypomagnesaemia. Patients with cancer may be at risk of hypomagnesaemia due to decreased nutritional intake, for example through loss of appetite, nausea or vomiting associated with cancer treatments, and transcellular shift or GI and/or kidney losses through increased excretion caused by the side effects of surgery or chemotherapy (Bruera and Sweeney 2000, Schuchardt and Hahn 2017).

Table 1.

Causes of hypomagnesaemia

GastrointestinalRenalTranscellular shift (from extracellular to intracellular fluid)Transdermal
  • Diarrhoea

  • Vomiting

  • Dietary deficiency (including protein-calorie malnutrition, parenteral and enteral feeding with inadequate magnesium, alcoholism and pregnancy)

  • Familial magnesium malabsorption

  • Gastrointestinal fistula

  • Inflammatory bowel disease

  • Laxative abuse

  • Surgical resection

  • Malabsorption – sprue (impaired absorption of nutrients by the small intestine), steatorrhea (oily stool), chronic pancreatitis and nasogastric suction

  • Alcoholism

  • Diabetes

  • Diuretics (thiazides, loop diuretics and osmotic diuretics)

  • Hypoparathyroidism

  • Hyperthyroidism

  • Hyperaldosteronism

  • Syndrome of inappropriate antidiuretic hormone secretion

  • Excessive vitamin D

  • Ketoacidosis

  • Hypercalcaemia and/or hypophosphataemia

  • Tubular defects (primary magnesium wasting, Gitelman syndrome, renal tubular acidosis)

  • Acidosis (correction of)

  • Blood transfusion (massive)

  • Epinephrine

  • Hungry bone syndrome

  • Insulin/glucose/ refeeding syndrome

  • Pancreatitis (acute)

  • Excessive sweating

  • Massive burns

Diagnosis

The most common test for evaluating a patient’s magnesium levels is serum magnesium concentration, particularly where there is a need for rapid assessment (Jahnen-Dechent and Ketteler 2012). According to the Association for Clinical Biochemistry and Laboratory Medicine (2012), reference intervals for serum magnesium levels in adults are as follows:

  • Age <60 years: 0.66-1.07mmol/L.

  • Age 60 to 90 years: 0.66-0.99mmol/L.

  • Age >90 years 0.70-0.95mmol/L.

Approximately 60% of total body magnesium is located in bone, 38% in soft tissues and less than 2% in the extracellular fluid compartment (Saif 2008). However, serum magnesium levels do not necessarily reflect the status of total body stores due to the complex process of magnesium absorption and homeostasis (Saif 2008). Magnesium is mainly absorbed in the small intestine, homeostasis is maintained by the intestine, bone and kidneys, and excess magnesium is excreted by the kidneys and faeces (Jahnen-Dechent and Ketteler 2012). This might suggest that a urine sample would be a more reliable and valid test. Indeed, the Association for Clinical Biochemistry and Laboratory Medicine (2012) recommends measurement of 24-hour urine magnesium if GI or renal losses cannot be distinguished. However, the active reabsorption of magnesium from the urine within the kidneys, to maintain homeostasis, prevents evaluation of the precise concentration – in simple terms, urine collected over 24 hours would not show accurate levels as homeostasis would have altered the levels (Schuchardt and Hahn 2017).

The accuracy of blood analysis is also questionable due to the process of homeostasis (Razzaque 2018). The amount of magnesium that the body requires at any given time, and therefore the amount that is absorbed, fluctuates. No matter how much magnesium is ingested through food or supplements the amount that is absorbed will be regulated by the magnesium transporters and/or bioavailability (exogenous factors) and by endogenous factors such as age and health status (Walker et al 2003, Coudray et al 2005, Kappeler et al 2017). Some cancer treatments will disrupt this process of absorption and homeostasis due, for example, to side effects such as diarrhoea which will reduce the overall amount of magnesium available in the body (Schuchardt and Hahn 2017).

It is important that prescribing clinicians understand the absorption and homeostasis process and that the type of magnesium supplementation and route of administration will depend on the aetiology, symptoms and grading severity of serum magnesium levels and other associated electrolytes (Ahmed and Mohammed 2019).

There are no UK national, standardised guidelines for the diagnosis and treatment of patients with acute hypomagnesaemia, however the National Cancer Institute (2017) Common Terminology Criteria for Adverse Events Version 5.0 provides a grading severity scale for hypomagnesaemia (Table 2).

Table 2.

Grading severity scale for hypomagnesaemia

GradeSerum magnesium levels
Grade 1 (mild)<0.5mmol/L
Grade 2 (moderate)<0.5-0.4mmol/L +
Grade 3 (severe)<0.4-0.3mmol/L
Grade 4 (life threatening)<0.3mmol/L

Although diagnosis is based on serum magnesium levels, the results do not indicate the cause of the hypomagnesaemia (Association for Clinical Biochemistry and Laboratory Medicine 2012). Therefore, nurses and other healthcare professionals must conduct a comprehensive assessment of the patient’s presenting signs and symptoms, past and current medical history and previous and current medicines, as well as their family and social history. This can inform diagnosis and assist in identification of the underlying cause, which will require treatment (Ahmed and Mohammed 2019).

Clinical management

Clinical management of patients with hypomagnesaemia involves replacement with magnesium sulfate administered either intravenously (IV) or orally. The type and amount of magnesium sulfate replacement is based on serum magnesium levels and grading severity. As mentioned above, there are no standardised national UK guidelines on magnesium replacement therapy, however the Intensive Care Society (2020) has published recommendations on standard concentrations for continuous infusion of magnesium sulfate with the aim of improving patient safety. Nurses and other healthcare professionals should adhere to their local trust guidelines and policies on management of patients with hypomagnesaemia.

Administration of IV magnesium sulfate

The strength of magnesium prescribed and the method of administration will depend on the patient’s serum magnesium levels and grading, and prescribers should adhere to local trust guidelines which should be accessible on the intranet (Kraft et al 2005). Nurse prescribers and other clinicians can also consult the British National Formulary information on magnesium sulfate (Joint Formulary Committee 2022).

Table 3 shows an example of serum magnesium level and replacement options for adult clinical haematology patients (Oxford University Hospitals NHS Foundation Trust 2015). The serum magnesium levels and grading in Table 3 are based on the National Cancer Institute (2009) Common Terminology Criteria for Adverse Events Version 4.0.

Table 3.

Example of serum magnesium level and replacement options for adult clinical haematology patients

Grade 1 (mild) 0.5-0.7mmol/LGrade 2 (moderate) 0.4-0.5mmol/LGrades 3 and 4 (severe/life threatening) ≤0.4mmol/LNotes
Only replace if the patient is symptomatic
First line oral:
  • First option: magnesium aspartate 10mmol sachets – 1 sachet twice daily

  • Second option: magnesium glycerophosphate 8mmol (2x4mmol tablets) three times a day



Second-line intravenous (IV):
  • 10mmol magnesium sulfate in 100mL-1L sodium chloride 0.9% or glucose 5% over 90 minutes

  • (10mmol magnesium sulfate = 5mL magnesium sulfate 50% injection)

Either
Oral:
  • First option: magnesium aspartate 10mmol sachets – 1 sachet twice daily

  • Second option: magnesium glycerophosphate 8mmol (2 × 4mmol tablets) three times a day


OR
IV:
  • 20mmol magnesium sulfate in 100mL-1L sodium chloride 0.9% or glucose 5% over 3-12 hours

  • (20mmol magnesium sulfate = 10mL magnesium sulfate 50% injection)

IV:
  • 20mmol magnesium sulfate in 100mL-1L sodium chloride 0.9% or glucose 5% over 3-12 hours

  • (20mmol magnesium sulfate = 10mL magnesium sulfate 50% injection)

Oral replacement:
  • Oral magnesium salts commonly cause and may worsen diarrhoea


IV replacement:
  • 10mmol over 90 minutes or 20mmol over 3 hours are acceptable infusion rates (on the Oxford University Hospitals NHS Foundation Trust haematology day treatment unit)

  • A slower rate (6-12 hours) should be used on the ward

  • Solution must be diluted before IV administration and mixed thoroughly

  • Maximum concentration for peripheral IV infusion is 20% (for example 0.8mmol/mL) using a large peripheral vein

  • Maximum infusion rate is 36mmol/hour

Patients should have an electrocardiograph (ECG) before and after administration of IV magnesium replacement therapy and cardiac monitoring during the infusion, particularly those with underlying cardiac issues such as arrythmias. The patient’s vital signs should be monitored and recorded using the National Early Warning Score (NEWS) 2 (Royal College of Physicians 2017) and urinary output should be measured and recorded on the fluid balance chart. Adverse reactions, such as loss of patellar reflexes, weakness, nausea, sensation of warmth, flushing, drowsiness, double vision and slurred speech (Joint Formulary Committee 2022), should be documented.

The magnesium sulfate infusion should be documented on the patient’s fluid chart to monitor fluid balance. In patients with diarrhoea, a stool chart should be used to record the amount of loss and consistency of stool and a stool sample may be sent for analysis to identify the cause.

Conclusion

Patients with cancer may be at risk of developing hypomagnesaemia due to inadequate nutritional intake and/or diarrhoea or increased renal excretion as a side effect of treatments and interventions. Patients referred to the ED with suspected hypomagnesemia will require analysis of blood serum magnesium levels and clinical management will depend on the results and grading of severity. Although diagnosis is confirmed by blood analysis this does not identify the cause. Therefore, nurses must take a comprehensive patient history to determine possible causes of magnesium depletion.

There are no UK national, standardised guidelines on the treatment and management of patients with hypomagnesaemia. Nurses and other healthcare professionals should, therefore, consult and adhere to local trust policies on magnesium level and replacement options for patients with hypomagnesaemia.

References

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