Initial Management of Hyponatraemia

Initial management will always start with DRS ABCD. 

• Assess patients fluid status and attempt to assign them as either hypovolaemic, euvolaemic or hypervolaemic  
  1. Includes assessing weight change, postural BPs and urine output 
• Check for chronicity by looking up previous sodium levels 
  1. If hyponatraemia is not acute, then we need to be slow and calculated in raising sodium to prevent cerebral pontine demyelination 
• Check other UEC/CMP and manage other electrolyte disturbances accordingly

If patient is hypervolaemic or euvolaemic, fluid restriction is a good initial management strategy

• Fluid restriction is usually to around 1 litre
• More strict restrictions can be used, especially if the hyponatraemia is severe
• It is always easier to relax fluid restrictions than to tighten them

If patient is hypovolaemic, consider IV therapy

As an intern, initiating initial management with either restriction or replenishment of fluids is not unreasonable (if you are confident in your assessment of fluid status) while you await further instructions from your registrar or endocrinology. 

Drug Chart Review for Hyponatraemia

Acute hyponatraemia which is thought to be drug related will most likely be caused by drugs that are newly introduced or have had their doses altered, therefore it is important to obtain a comprehensive drug history. 

Drugs which commonly cause hyponatraemia include:

• Diuretics
• Antidepressants - SSRIs, MAO inhibitors, SNRIs, mirtazepine 
• ACE inhibitors and ARBs
• NSAIDs
• PPIs
• Opiates 
• Sulfonlylureas 
• Anticonvulsants - carbamazepine, gabapentin

If you can identify a drug which is newly introduced or has had a dose change, undoing the modification should return the sodium to normal levels (assuming all other variables have stayed the same).

When identifying drugs on a chart which may be contributing to hyponatraemia, it is not unreasonable to withhold the next dose of the medication to buy you time to discuss with your team about ongoing management and drug changes. 

More comprehensive lists of drugs causing hyponatraemia can be found here, as well as their potential mechanisms of action. 

Investigations for Hyponatraemia

Our initial tests help us to ascertain whether we have a reduction in total body sodium, an excess of total body water and tells us how sodium is being managed as it runs through the kidneys.

Initial tests to run include:

• UEC 
  • Assess plasma sodium levels and renal function 
• Serum osmolality 
  • Helps to differentiate between true hyponatraemia and pseudohyponatraemia 
• Urine osmolality
  • Tells us about the kidneys ability to concentrate urine 
  • A low osmolality indicates dilute urine, as would be expected in polydipsia with functioning kidneys
  • A high osmolality indicates concentrated urine, as may be expected in SIADH 
• Urinary sodium
  • Helps to differentiate between hypovolaemia and SIADH
  • Low urinary sodium indicates hypovolaemia 
  • High urinary sodium is associated with SIADH - especially when coupled with high osmolality 
• BSL 
  • Hyperglycaemia can cause hyponatraemia due to shifts of water out of cells to dilute the glucose
• Cholesterol/triglycerides 
  • Hypertriglyceridaemia can cause a pseudohyponatraemia due to the way sodium levels are run in labs - it is not a true hyponatraemia and should be ruled out 

A referral to endocrinology can help interpretation of the results and guidance on other required tests.

Ongoing Management of Hyponatraemia

Return to normal sodium levels should be done in a slow and controlled fashion, to help prevent cerebral pontine demyelination. 

• Frequent measurement of UECs to assess trajectory of sodium levels
  • Guidance on frequency will be given by endocrinology
  • Initially this may be required BD (or perhaps more frequent), with the frequency dropping as levels stabilise 
  • Consider organising a PICC line for your patient, particularly if they are difficult to venepuncture, if they are going to require frequent testing 
• Gradual reintroduction of withheld drugs 
  • Drugs which can cause hyponatraemia should be slowly reintroduced (if still indicated) with careful monitoring of sodium levels 
  • Start with drugs the patient had been on long term 
  • Consider switching drugs/therapeutic class if possible to reduce the number of drugs which can cause hyponatraemia
• Gradual easing of fluid restriction 
  • On advice of endocrinology, as the sodium levels stabilise we can usually start to relax the fluid restriction (assuming we have treated the underlying cause of hyponatraemia)
• Monitor for signs and symptoms of hyponatraemia
• Control BSLs and cholesterol/triglycerides 

Acute Management of Hypernatraemia

Initial management always starts with DRS ABCD.

Hypernatraemia is most often chronic (i.e. lasting 48 hours) and thus treatment is aimed at a slower return to normal levels. 

• Assess fluid status
  • Patients are usually hypovolaemic 
  • Includes weight changes, postural BPs and urine output
  • Includes assessing ongoing losses as these will need to be replaced 
• Check for chronicity by looking up previous sodium levels
• If hypovolaemic, start fluid replacement - including accounting for ongoing losses 
  • PO fluid replacement is ideal, especially if hypernatraemia is not severe
  • If IVT is required, use dextrose 5% as this will not increase the sodium load 
  • The eTG has a table on how to calculate the rate of 5% dextrose to prescribe 
• Remeasure UEC/VBG levels to assess rate of rise of Na 
  • Aim less than 10mmol/L in 24 hours
    
    
• If hypervolaemic and hypernatraemic, treatment will require diuresis to rid the body of total body sodium while replenishing with dextrose 5% to maintain a euvolaemic status. Seek senior assistance.

References: eTG , UpToDate

Drug Chart Changes for Hypernatraemia

Few commonly used drugs are implicated in hypernatraemia. 

• Diuretics 
  • Causing loss of total body water in excess to loss of total body sodium
  • Cease/withhold, especially if the patient is hypovolaemic 
• Sodium chloride  
  • Excess sodium load via IVT resulting in hypernatraemia is less common but should be considered

Investigating the Cause of Hypernatraemia

The most common cause of hypernatraemia is dehydration/loss of total body water. 

This may be as a result of:

• Inadequate water intake 
• GI losses
• Severe burns
• Diuretics
• Diabetes insipidus (central or nephrogenic) 
  • Check urine outputs (usually >3L in 24 hours)
  • Check urine osmolality (usually dilute and <300 mOsm/kg)
  • Plasma ADH levels 
  • Urine dipstick - will show low specific gravity 

Less commonly, hypernatraemia may be due to sodium overload such as from excess hypertonic NaCl solution. 

Source: eTG, Medscape

Ongoing Management of Hypernatraemia

Ongoing management will largely revolve around maintaining euvolaemic status for the majority of patients 

• Assess ongoing losses and ensure they are factored into ongoing daily IVT rates
  • Transition to PO intake as sodium levels start to stabilise and the underlying cause is treated 
• Monitor UEC and CMP especially if losses are secondary to increased GI losses as other electrolytes may be affected
• Reinstate diuretics if still clinically indicated once patient becomes euvolaemic and sodium levels stabilise with initially more frequent checking of electrolyte levels 
• Use of desmopressin if related to central diabetes insipidus - will require endocrinology input

Initial Management of Hypokalaemia

Initial management always starts with DRS ABCD. 

• Classify K level as mild (3.1 - 3.5mmol/L), moderate (3 - 2.5mmol/L) or severe (<2.5mmol/L) hypokalaemia
  • If mild - is replacement required or may monitoring be sufficient?
  • If moderate or severe - consider confirming potassium level with repeat testing
• Are there any contraindications for immediate initiation of potassium replacement? 
  • Consider escalation especially if medically complex patient such as renal transplant or dialysis patients
• PO vs IV vs both
  • Generally speaking, IV is reserved for severe hypokalaemia, if there are ECG changes or if PO intake is not possible
  • PO options:
    • Potassium Chloride SR 600mg tabs (Slow-K): 8mmol of K per tab
    • Potassium Chloride effervescent tabs (Chlorvesent): 14mmol of K per tab
  • IV options:
    • 10mmol KCl in 100mL NaCl 0.29% - infused over 1 hour minimum
    • 40mmol KCl in 1000mL NaCl 0.9% - infused over 4 hours minimum 
    • As a rough guide, expect a rise of  0.1mmol/L for each 10mmol infused
• Repeat potassium levels
  • 1 hour after IV replacement
  • 4 hours after PO replacement

QLD Health guidelines on electrolyte replacement

Drug Chart Review for Hypokalaemia

One of the most common drug classes implicated in hypokalaemia are diuretics. 

Your decision on how to manage the diuretics will depend on the clinical situation. You should consider whether there is an ongoing need for diuresis:

• If yes - can we switch to or supplement with potassium sparing diuretics?
  • This may involve reducing the dose of the non-potassium sparing diuretic (e.g. hydrochlorothiazide) and adding in a potassium sparing diuretic (e.g. spironolactone)
  • If ongoing diuresis with non-potassium sparing diuretics is indicated, consider supplementation with potassium chloride
• If no - can we withhold or cease diuresis?

Many other drugs/drug classes may be implicated in hypokalaemia, especially in high doses or in overdose: 

• Insulin
• Beta-agonists
• Verapamil 
• Quetiapine
• Penicillins

Your decision to alter the existing medications on the drug chart will depend on the severity of the hypokalaemia and the clinical situation.

Here is a list of medications which can be implicated in hypokalaemia. 

Investigations for Hypokalaemia

The two broad categories for reduced electrolyte levels are reduced intake or increased excretion.
There can also be shifts of electrolytes intracellularly from the ECF - such as from use of insulin or beta-agonists. 

Reduced oral intake of potassium is seldom the single cause for hypokalaemia requiring treatment; it is more likely to be a contributing factor. 

Excess excretion is more likely to be causative of total body potassium depletion.  

Look for common signs of excessive secretion

•  Polyuria 
  • May be diuretic related - including endogenous diuretic states such as the normal increase in aldosterone which occurs as part of the endocrinological stress response to surgery
• Vomiting
  • Complex mechanism: hypokalaemia occurs due to hypovolemia resulting in increased aldosterone activity  
• Diarrhoea 
  • Due to direct potassium excretion due to the high potassium content in the lower GI system
  • Includes patients undergoing bowel prep for endoscopy

Initial investigations will include: UEC, CMP, VBG and ECG.

• VBG is useful for rapid test results, but also gives you important information such as acid base status and lactate levels
• Hypomagnesia is often seen in patients with hypokalaemia, but it itself can be a cause for potassium losses  
• There are a variety of ECG changes that can occur. Look for premature atrial complexes, AF or AV block

These are the more common causes of hypokalaemia, especially in patients who have previously been known to have normal K levels. It is especially prudent to look for other underlying causes of hypokalaemia in patients who have persistent hypokalaemia. 

Ongoing Management of Hypokalaemia

Ongoing management will consist of:

• Monitoring hypokalaemia 
  • Inpatient
    • Frequency of repeating UECs will depend on severity of hypokalaemia and replacement strategy 
    • May need increased checking if severe or ongoing losses expected (even up to BD), reducing over time to daily, alt daily, three times/week, weekly etc. depending on how long the patient is an inpatient for
  • Outpatient
    • GP follow up with repeat UEC +/- ECG especially if potassium stability has not yet been obtained on discharge, if there is ongoing increased losses or if patient is on potassium supplementation on discharge 
• Prescription of maintenance oral potassium supplementation 
  • Slow-K (potassium chloride MR 600mg) is the most common formulation prescribed on discharge
  • If it is a new medication for the patient, consider prescribing a reduced quantity to prompt patient to follow up with GP for ongoing review of its indication
• Investigation and treatment of underlying cause 

Initial Management of Hyperkalaemia

Initial management always starts with DRS ABCD. 

Upon receipt of a hyperkalaemia result:

• Classify hyperkalaemia as mild (5.5-5.9mmol/L), moderate (6.0-6.4mmol/L) or severe (>6.5mmol/L) to help frame the management pathway you will likely take
  • Mild hyperkalaemia without ECG changes may be amenable to conservative therapy and monitoring
• Call the bedside nurse/NIC/a colleague for assistance in organising:
  • Repeat VBG +/- UEC
  • IV access (ideally at least 1 large bore in a reasonable sized vein)
  • ECG - the presence of ECG changes automatically classifies the hyperkalaemia as severe 
  • BSL to exclude diabetic ketoacidosis in T1DM 
  • A clinical assistant to run help run the bloods down to pathology urgently 

The principles of hyperkalaemia management involve:

Drug Chart Review for Hypokalaemia

Many drugs are implicated in electrolyte disturbances, including hyperkalaemia. 

The decision to withhold or cease certain medications will depend on the level of hyperkalaemia and the indication of the drug. 

Some common medication classes known to cause hyperkalaemia include:

• ACE Inhibitors 
• AT II receptor antagonists 
• Potassium sparing diuretics
• NSAIDs
• Beta-blockers
• Digoxin 

A more complete list can be found here. 

In general, it is not unreasonable to withhold a dose of a medication which either a) can worsen hyperkalaemia or b) has increased toxicity in hyperkalaemia while you seek advice from seniors to decide whether it is appropriate to continue the medication.

If you're unsure whether to withhold a drug or not, you can put the rest of the days doses up for review (and communicate this to the nurses). 

Investigations for Hyperkalaemia

Look for causes of increased intake, reduced clearance or intracellular shift of potassium. The aforementioned drugs would be implicated in either reduced clearance or intracellular shifts of potassium. 

Increased intake of potassium is unlikely to be a major contributor to hyperkalaemia. 

The number of investigations undertaken will depend on what the clinical suspicion for the cause is. 

Reduced urinary clearance of potassium is found in:

• Acute and/or chronic kidney impairment
• Reduced aldosterone secretion or response to aldosterone

The altered aldosterone activity is most likely due to drugs, but investigations into underlying aldosterone disorders could be undertaken. 

Increased potassium shift out of cells is found in:

• Hyperglycaemia (such as in diabetes)
• Metabolic acidosis  
• Beta-blockade 
• Exercise
• Pseudohyperkalaemia 

Therefore, it would be prudent to monitor renal function (UEC) and blood glucose levels and pH (VBG) as part of ongoing monitoring. 

Causes of hyperkalaemia can be found here.

Ongoing Management of Hyperkalaemia

Ongoing management of hyperkalaemia will include: 

• Monitoring of UEC
  • Frequency of testing will depend on the stability of the patients and how stable the potassium levels have been  
• Monitoring of ECG
• Ongoing medications to aid excretion of total body potassium 
  • Potassium sacrificing diuretics (e.g. Furosemide)
  • Sodium polystyrene resins (e.g. Resonium-A)
  • Once potassium levels have stabilised in the normal range, these medications should be weaned and ceased if no other indication exists for them 

Acute Management of Hypomagnesia

Initial management always starts with DRS ABCD

• Perform an ECG and look for rhythm abnormalities (and compare with previous)
  • if abnormalities present, then discuss with senior 
• If nil rhythm abnormalities and patient can take oral medications then consider replacement, especially if ongoing losses are expected 
  • Magnesium aspartate 500mg tablets are the standard tablets given - usually 2-4 tablets/day in divided doses 
  • BioMag contains a higher amount of elemental magnesium and as an alternative to standard magnesium aspartate 
• if oral replacement is not possible (e.g. pt NBM or vomiting), consider IV replacement
  • use magnesium sulfate 10mmol in 100mL 0.9% NaCl 

Drug Chart Changes for Hypomagnesia

Diuretics are the most common cause of drug related hypomagnesia, specifically loop and thiazide diuretics.  

Consider withholding or ceasing diuretics if appropriate (considering indication of diuretics and whether therapeutic goals have been achieved), alternatively the hypomagnesia may need to be corrected using supplementation. 

Other drugs implicated in hypomangesia are typically due to nephrotoxicity resulting in increased urinary excretion of magnesium. These drugs include:

• Digoxin
• Aminoglycoside antibiotics
• Calcineurin inhibitors
• Amphotericin B

A more complete list can be found here. 

Investigation of Hypomagnesia

Hypomagnesia can be caused by GI losses, renal losses or inadequate intake.

GI losses are predominated by diarrhoea compared to vomiting, and GI losses can be exacerbated by lack of oral intake.  

A physical examination to assess hydration status may help to determine the aetiology of hypomagnesia.

• if hypovolaemic - may indicate increased GI losses resulting in hypomagnesia
• if hypervolaemic - may indicate fluid overload resulting in dilution of magnesium and resultant hypomagnesia

Patients with a history of alcoholism may also present with hypomagnesia as a result of renal tubular dysfunction. 

Investigations include

• CMP
  • For evaluation of magnesium levels 
  • Associated hypocalcaemia can be seen in some genetic conditions
• UEC
  • Hypomagnesia can be associated with refractory hypokalaemia 
  • eGFR to assess renal function 
• ECG
  • Look for rhythm abnormalities
• Lipase
  • Not a routine investigation however pancreatitis can be a cause of hypomagnesia 

See this UpToDate article for causes of hypomagnesia.

Ongoing Management of Hypomagnesia

Ongoing management of hypomagnesia will include:

• Monitoring of UEC and CMP 
  • Assessment of renal function if renal losses are the primary cause 
  • Assessment of electrolyte stabilisation
• Oral replacement
  • While the underlying cause for hypomagnesia is going 
  • Magnesium aspartate or BioMag
  • Request outpatient follow up with GP so they can cease the oral replacement when appropriate once Mg levels have stabilised and underlying cause for hypomagnesia

Acute Management of Hypermagnesia

Initial management always starts with DRS ABCD

Hypermagnesia is uncommon in the absence of magnesium supplementation or renal impairment. 

The effects of hypermagnesia as generally concentration related. A list of symptoms corresponding to magnesium levels can be found here. 

Initial management involves:

• Look for symptoms of hypermagnesia - such as altered conscious state, diminished deep tendon reflexes, hypotension
• Perform an ECG 
• Measure UEC and CMP if not already done
• Withholding magnesium supplementation is typically enough to return levels to normal. 
  • Can consider giving a loop or thiazide diuretic if hypermagnesia is severe
  • Few patients will require dialysis for their hypermagnesia  

Drug Chart Changes for Hypermagnesia

Excessive intake of magnesium or renal impairment are the common causes of hypermagnesia. 

Therefore:

• Cease magnesium supplementation (oral and IV)
• Consider withholding nephrotoxic drugs if AKI present

Investigating Cause of Hypermagnesia

Given the most common causes of hypermagnesia as excessive intake and renal impairment, a UEC to measure Creatinine/eGFR would be the most useful test. 

If an AKI is found, investigating the root cause would be the next step. 

There are other less significant causes for mild hypermagnesia which can be found here.  

Ongoing Management of Hypermagnesia

Ongoing management would involve:

• Ensuring resolution of AKI, if present
• Measuring magnesium levels to ensure stabilisation

Acute Management of Hypophosphataemia

Initial management always starts with DRS ABCD

In acute hypophosphataemia, replacement can be via the oral or IV route. 

• Soluble Phosphate 500mg tabs (Phosphate Sandoz) provides 16.1mmol phosphorous per tablet 
• IV replacement is typically via sodium dihydrogen phosphate 10mmol in 100mL sodium chloride 0.9%

Oral replacement is preferred in patients who are stable and can tolerate PO intake.

Drug Chart Changes for Hypophosphataemia

Hypophosphataemia may occur as a result of the following drug treatments:

• Excessive use of antacids 
• Insulin therapy 
• Diuretics (esp. loop)
• Phosphate binders

Assess the indication for any medications implicated in hypophosphataemia, as well as the severity and clinical significance of the hypophosphataemia, before withholding or ceasing medications. 

A full list of medications implicated in hypophosphataemia can be found here. 

Investigating Cause of Hypophosphataemia

Investigations into the underlying cause for hypophosphataemia include:

• CMP
  • Hypercalcaemia coupled with hypophosphataemia points towards primary hyperparathyroidism 
  • Hypocalcaemia coupled with hypophosphataemia suggests vitamin D deficiency
  • Hypomagnesia coupled with hypophosphataemia may suggest refeeding 
• UEC
  • Hypokalaemia coupled with hypophosphataemia may suggest refeeding
• PTH
  • If CMP is suggestive of a parathyroid pathology
• ABG
  • If respiratory alkalosis is thought to be the cause of hypophosphataemia 
• CK
  • If there is concerns for rhabdomyolysis
• Vitamin D levels
  • Low Vitamin D can result in poor absorption of phosphate

Ongoing Management of Hypophosphataemia

Ongoing management will depend on the underlying pathology causing hypophosphataemia

• Measurement of electrolytes to ensure return to normal (UEC and CMP) 
• Replacement of vitamin D (including loading if necessary) if vitamin D is low 
• Predicting and preventing refeeding syndrome in the first instance, or treating it with electrolyte replacement and gradual reintroduction of caloric intake
• Oral phosphate replacement can be used to supplement low phosphate but it's ongoing need should be reviewed regularly

Acute Management of Hyperphosphataemia

Initial management always starts with DRS ABCD.

Hyperphosphataemia is often asymptomatic, and incidental hyperphosphataemia may be amenable to conservative treatment.  

• Limit phosphate intake
• Measure UEC to assess renal function
• If correction is deemed necessary, can consider diuresis with loop diuretics (with fluid repletion as necessary)
• If severe renal impairment is present, can utilise phosphate binders - however their effects will not be as rapid as diuresis

Drug Chart Changes for Hyperphosphataemia

There are not many drugs which are implicated directly in hyperphosphataemia, besides phosphate supplements which should be ceased.

If an AKI (or AOCKD) is noted, nephrotoxics should be withheld.  

>Investigating Cause of Hyperphosphataemia  

• UEC 
  • Severe AKI will result in lack of phosphate excretion and thus elevated serum phosphate 
  • Hyperkalaemia may point towards Tumour Lysis Syndrome if the patient has a large tumour load present 
• CMP
  • Low calcium with hyperphosphataemia can be indicative of renal failure or hypoparathyroidism 
• Urate
  • Hyperuricaemia will point towards Tumour Lysis Syndrome if the patient has a large tumour load present 
• PTH
  • Hypoparathyroidism can be a cause of hyperphosphataemia 

Ongoing Management of Hyperphosphataemia  

• If there is an AKI, the underlying cause will need to be treated to return phosphate levels to normal
• If there is CKD, then ongoing management will likely be via phosphate binders
• The frequency of monitoring of UEC and CMP will depend on the chronicity and stability of the hyperphosphataemia
  • If the patient is being sent home not at their baseline eGFR or Phosphate levels then follow up blood tests with the GP would be useful to guide ongoing treatment

Initial Management of Hypocalcaemia

Initial management will always start with DRS ABCD

• Make an assessment of the severity of hypocalcaemia
  • if found incidentally and pt is asymptomatic it will likely be mild
  • if experiencing symptoms such as muscle cramps, spasms, or paraesthesia then likely moderate
  • if experiencing tetany, laryngospasm or seizures then likely severe 
• Order an ECG to look for hyper-excitability and rhythm abnormalities
• Order UEC and CMP to assess renal function, magnesium and phosphate levels 
  • Hypomagnesia will need to be corrected concurrently as calcium repletion is inefficient in the setting of hypomagnesia
  • Phosphate levels can help determine the underlying cause
• If hypocalcaemia is severe:
  • Prescribe IV calcium gluconate 10% 20mL in NaCl 0.9% 100mL as a slow push (20 mins) followed by IV calcium gluconate 10% 100mL in NaCl 0.9% 900mL starting at 50mL/hr and titrated to calcium levels/response 
  • Measure CMPs every 3 hours and monitor ECG while infusion running
• If hypocalcaemia is moderate, or initial severe hypocalcaemia has been treated:
  • Calcium carbonate 1.5g BD 

References: eTG, BMJ

Drug Chart Changes for Hypocalcaemia

Hypocalcaemia is less commonly secondary to drugs. 

Implicated drugs which may be withheld if clinically indicated, such as in severe hypocalcaemia with symptoms, include:

• Loop diuretics
• PPIs (mostly long term use)
• Bisphosphonates 
• Phenytoin
• SSRIs
• Gentamicin 

Investigating the Cause of Hypocalcaemia

Common causes of hypocalcaemia include post-surgical (parathyroid damage), vitamin D deficiency, hypomagnesia and hyperventilation. 

Investigations should include: 

• LFTs
  • Hypoalbuminaemia will mean there is less bound, and thus total, calcium in the body. 
  • However it is ionised calcium which is the active form, therefore if there is hypoalbuminaemia then the ionised calcium level should be calculated (use this calculator) to determine if there is a clinical hypocalcaemia 
• PTH levels
  • Useful to determine if the hypocalcaemia is as a result of parathyroid damage or reduced parathyroid function
• Vitamin D
  • Low vitamin D will reduce calcium absorption 
• Magnesium
  • Hypomagnesia will be indicative of parathyroid dysfunction 
• UEC
  • Check renal function to ensure AKI is not the cause of electrolyte imbalance
• ECG
  • Hypocalcaemia may show prolongation of ST segment and QT interval. If present, will have increased risk of VT. 

References: eTG, LITFL, Medscape

Ongoing Management of Hypocalcaemia

Ongoing management will primarily involve ensuring resolution of any underlying cause. 

Ongoing management will primarily involve ensuring resolution of any underlying cause. 

• Lab tests
  • UEC and CMP
    • Monitor renal function and electrolyte status to help guide ongoing pharmacological treatment
  • Disease specific testing
    • For example, measuring PTH or vitamin D levels if they showed to be low on initial testing 
• Pharmacological treatment
  • Oral calcium supplementation can be used to treat hypocalcaemia
    • Often come combined with other drugs such as vitamin D which can help treat disease specific states
  • Replacement of other electrolytes, such as magnesium, if necessary
• Management of underlying condition to help prevent hypocalcaemia recurrence  

Acute Management of Hypercalcaemia

Initial management will always start with DRS ABCD.

• Confirm hypercalcaemia and measure PTH levels concurrently 
  1. Including trying to ascertain a timeline of how rapidly the hypercalcaemia has occurred 
• Correct for albumin abnormalities
  1. Using this calculator 
  2. Ionized calcium is the active form and therefore if calcium alterations are suspected an ionized calcium level could be obtained 
• Check for symptoms 
  1. Assess fluid status of patient as hypercalcaemic patients may be dehydrated
  2. Assess GCS as severe hypercalcaemia may cause the patient to be obtunded 
  3. "Stones, bones, groans and psychiatric moans"
• Classify as mild, moderate or severe based on serum levels and symptoms
  1. Mild can generally be monitored with encouragement of increased PO fluid intake
  2. Moderate hypercalcaemia may require hydration with IVT to help dilute and excrete calcium
  3. Severe hypercalcaemia (>3.0mmol/L) will require urgent management, typically with IV hydration and bisphosphonates 
     • 4-6 litres of NaCl 0.9% over 24 hours 
     • Bisphosphonate initiation should only be performed after discussion with your registrar and/or endocrinology 

Drug Chart Changes for Hypercalcaemia

Look for drugs which will make hypercalcaemia worse and withhold or consider ceasing:

• Thiazide diuretics
• Vitamin D
• Calcium supplementation 

Chart the appropriate quantity of IVT 

• NaCl 0.9% is the preferred solution
• Ensure you chart enough without causing the patient to become fluid overloaded – this may be an issue if they have an AKI or have poor urine output 
• Link the orders together so the nursing staff are aware that we want multiple bags to be given over a period of time

Reference: UpToDate

Investigating the cause of Hypercalcaemia

90% of non-transient hypercalcaemia is caused by malignancy or hyperparathyroidism. 

Hypercalcaemia of malignancy often causes higher calcium levels with more rapid rises in calcium levels and will likely be associated with other symptoms of malignancy. 

Hyperparathyroidism on the other hand will cause less elevated calcium levels with a longer chronicity and the patients may often be asymptomatic and otherwise stable. 

Labs to order

• PTH
  1. Elevated PTH will point towards a primary hyperparathyroidism as the cause
  2. Low PTH will point towards a non-PTH mediated hypercalcaemia and increases suspicion for hypercalcaemia of malignancy 
• Vitamin D 
  1. Elevated vitamin D points towards vitamin D intoxication as the cause 
• UEC and CMP 
  1. Especially if diuretic related, we want to see alterations in other electrolytes as well as renal function 

UpToDate has a table with all causes of hypercalcaemia, including those which are less common. 

You can also find a diagnostic approach flowchart to aid in clinical diagnosis of the underlying cause for hypercalcaemia. 

Ongoing Management of Hypercalcaemia

Ongoing management will consist of dietary advice, medication changes and treatment of underlying condition

• Avoid excessive dietary calcium 
• Increase oral hydration, aiming 8 glasses of water per day (as long as no fluid restrictions are in place)
• Cease calcium and vitamin D supplementation
• If the cause is malignancy, then treatment of the underlying condition should result in resolution