Hypermagnesaemia

Hypermagnesaemia is an elevated serum magnesium, and is comparatively uncommon because normal kidneys excrete magnesium efficiently. It therefore occurs almost exclusively in the setting of renal impairment combined with a magnesium load, or from iatrogenic administration.

The classic contexts are: magnesium-containing antacids or laxatives in a patient with chronic kidney disease; therapeutic magnesium infusion in pre-eclampsia and eclampsia, where it is the intended treatment and toxicity is a recognised complication requiring active monitoring; treatment of severe asthma or arrhythmia; and, rarely, massive magnesium ingestion.

Because iatrogenic causes dominate, hypermagnesaemia is largely a preventable and anticipatable problem rather than a diagnostic puzzle.

Features progress fairly predictably with rising levels, which is what makes clinical monitoring during magnesium infusion so effective.

Loss of deep tendon reflexes is the earliest and most useful clinical sign, and is the reason reflexes are checked hourly during magnesium infusion in obstetric practice. Their loss precedes respiratory and cardiac toxicity
Nausea, vomiting, flushing and a sensation of warmth
Lethargy, drowsiness and weakness
Hypotension and bradycardia
Respiratory depression progressing to respiratory arrest as levels rise further
Cardiac conduction abnormalities: prolonged PR interval, widened QRS, prolonged QT, and ultimately complete heart block and cardiac arrest

In obstetric practice the monitoring triad is therefore reflexes, respiratory rate and urine output — the last because magnesium is renally cleared and oliguria causes accumulation.

Stop all magnesium administration and all magnesium-containing medications immediately, including antacids and laxatives, which are easily overlooked
Intravenous calcium gluconate (10 mL of 10% solution over 10 minutes, repeated as needed) is the immediate antidote for significant cardiovascular or respiratory toxicity. It directly antagonises magnesium at the neuromuscular junction and myocardium and acts within minutes
Intravenous fluids with a loop diuretic promote renal magnesium excretion in patients with adequate renal function and volume status
Haemodialysis is definitive and is indicated for severe hypermagnesaemia, particularly in renal failure where renal clearance cannot be relied upon
Supportive care: airway protection and ventilatory support for respiratory depression, cardiac monitoring, and treatment of bradyarrhythmia
Monitor magnesium, calcium, potassium and renal function

In the obstetric setting: hourly assessment of deep tendon reflexes, respiratory rate and urine output during magnesium infusion, with calcium gluconate immediately available at the bedside. Reduce the dose or stop the infusion for oliguria or lost reflexes rather than waiting for respiratory compromise.

Prevention: avoid magnesium-containing preparations in chronic kidney disease, and review medication lists specifically for them in any patient with renal impairment.

Referral: nephrology for dialysis; obstetrics and critical care for magnesium toxicity in pre-eclampsia.

Hyperchloraemic Metabolic Acidosis

Also known as: Normal anion gap metabolic acidosis, NAGMA

Hyperchloraemic metabolic acidosis is a normal anion gap metabolic acidosis in which bicarbonate is lost or acid is retained without the accumulation of unmeasured anions. Electroneutrality is maintained by a compensatory rise in chloride, which is what gives the disorder its name.

The distinction from raised anion gap acidosis is the first and most useful step in any metabolic acidosis, because the two have entirely different differential diagnoses. A normal anion gap points toward bicarbonate loss or a renal acidification defect; a raised gap points toward added acid such as lactate, ketones or toxins.

Causes divide into gastrointestinal bicarbonate loss (diarrhoea, which is by far the commonest, alongside high-output stomas, ileostomies, pancreatic and biliary fistulae, and ureteric diversion), renal causes (renal tubular acidosis types 1, 2 and 4, early chronic kidney disease, carbonic anhydrase inhibitors, hypoaldosteronism), and iatrogenic causes, principally large-volume 0.9% saline resuscitation, which is a common and under-recognised contributor in hospital practice.

Calculate the anion gap: Na − (Cl + HCO₃), normal range approximately 8–12 mmol/L. Correct for albumin, adding roughly 2.5 mmol/L for every 10 g/L that albumin falls below 40 g/L, since hypoalbuminaemia masks a raised gap and can make a mixed picture look like a pure normal-gap acidosis
Urinary anion gap (Na + K − Cl) is the key discriminating test once a normal anion gap acidosis is confirmed:

A negative urinary anion gap indicates appropriate renal ammonium excretion, pointing to a gastrointestinal cause such as diarrhoea
A positive urinary anion gap indicates impaired renal ammonium excretion, pointing to renal tubular acidosis

Urine pH: a pH above 5.5 in the presence of systemic acidosis suggests a distal (type 1) renal tubular acidosis, since the distal tubule should be able to acidify maximally
Potassium helps subclassify: low in types 1 and 2 renal tubular acidosis, and high in type 4, which is the commonest form in adults and is typically associated with diabetes, chronic kidney disease, and drugs including ACE inhibitors, ARBs, spironolactone and trimethoprim
Review the fluid chart specifically for saline volume, and the drug chart for acetazolamide and topiramate
Venous blood gas with electrolytes, renal function and albumin

Treat the underlying cause, which is the definitive step in almost every case: manage diarrhoea, address the stoma or fistula output, review and stop contributing drugs, and switch from 0.9% saline to a balanced crystalloid where ongoing resuscitation is required
Bicarbonate replacement is considered for severe acidosis (pH below approximately 7.1–7.2, or bicarbonate below 10–12 mmol/L), for symptomatic patients, and in chronic renal causes where sustained acidosis contributes to bone disease, muscle wasting and progression of chronic kidney disease
Oral sodium bicarbonate is used for chronic replacement, particularly in renal tubular acidosis and chronic kidney disease
Intravenous bicarbonate is reserved for severe acute acidosis, with the recognised caveats that it can worsen intracellular acidosis, cause hypokalaemia as potassium shifts into cells, cause hypocalcaemia, and produce sodium and volume loading
Correct potassium alongside, and anticipate the direction: in types 1 and 2 renal tubular acidosis potassium falls further as bicarbonate is given, whereas type 4 requires management of hyperkalaemia
In type 4 renal tubular acidosis, fludrocortisone is used where hypoaldosteronism is the mechanism, alongside dietary potassium restriction and review of contributing drugs
Monitor gas, electrolytes and renal function during correction

Referral: nephrology for renal tubular acidosis, and for acidosis complicating chronic kidney disease; gastroenterology for high-output stoma or fistula management.

Hypermagnesaemia

Overview

Clinical Features

Management

Overview

Diagnosis

Management