How to interpret electrolyte blood results to identify abnormalities (2025)

Accurate interpretation of electrolyte blood results is key to patient diagnosis and management. Read our guide.

Abstract

Interpreting electrolyte blood results is fundamental to clinical practice because abnormal electrolyte levels can signify underlying diseases and conditions. Accurate interpretation of electrolyte levels underpins diagnostic reasoning in practice, empowering advanced practitioners to deliver informed and holistic patient care. This article, the last in an assessment and interpretation series for advanced clinical practitioners, reviews the basic physiology of four significant electrolytes, their abnormalities and the consequences of electrolyte imbalance.

Citation: Slade D (2025) How to interpret electrolyte blood results to identify abnormalities. Nursing Times [online]; 121: 1.

Author: Deborah Slade is senior lecturer in advanced practice, Oxford Brookes University.

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Introduction

Electrolytes are minerals that have an electrical charge when dissolved in water/body fluids (for example, blood, urine and cells) (Murphy et al, 2019). These negatively charged (anions) and positively charged (cations) electrons are vital for cellular reactions/functions (Ernstmeyer and Christman, 2021). Electrolytes maintain acid-base balance, electrical neutrality in cells, generation/conduction of action potentials in nerves and muscles, fluid regulation and blood clotting (Shrimanker and Bhattarai, 2024).

The body obtains electrolytes from food and fluids. Normal target ranges for electrolytes are narrow, and slight abnormalities can devastate bodily functions (Ernstmeyer and Christman, 2021). Electrolyte blood results in biochemistry testing convey molecular-level changes in the body’s cellular processes, giving understanding of conditions and diseases, such as dehydration, diabetes mellitus (DM), kidney dysfunction and acid-base imbalances (Murphy et al, 2019).

This article reviews the electrolytes sodium (Na), potassium (K), calcium (Ca) and magnesium (Mg) as measured in a blood serum test, their basic physiology, abnormalities and the consequences of electrolyte imbalance. Advanced practitioners must analyse electrolyte results alongside patient history, clinical presentation and examination findings to understand the patient’s condition, guide further diagnostic investigations and develop management strategies.

Table 1 shows normal ranges and imbalances of Na, K, Ca and Mg. All electrolytes must be considered together, as they affect each other.

How to interpret electrolyte blood results to identify abnormalities (1)

Sodium (Na)

Na maintains blood plasma volume (extracellular fluid (ECF)), acid-base balance, transmission of nerve impulses and normal cell function (Lee and Mather, 2022; Lieberman and Peet, 2022). Na is the principal extracellular (EC) positively charged cation (Na+) (Fig 1) and a major contributor to the osmolality (particle concentration dissolved in a fluid) of the blood (Najem et al, 2024).

How to interpret electrolyte blood results to identify abnormalities (2)

Around 60% of body weight is water (~40litres (L) in an adult weighing 70kg) (Overgaard-Steensen and Ring, 2018). In health, total body Na is constant because essentially Na excretion matches food and fluid intake. However, the gastrointestinal (GI) tract is often a major route of Na loss (Lee and Mather, 2022; Lieberman and Peet, 2022).

Hypernatraemia

Hypernatraemia is when Na in the blood is too high due to reduced fluid intake or excess fluid loss (Overgaard-Steensen and Ring, 2018). Hypernatraemia is less common than hyponatraemia (low blood Na), but more clinically significant if it develops rapidly (mortality >50%) (Overgaard-Steensen and Ring, 2018). The clinical presentation is dehydration (Table 2). Causes are outlined below:

  • Water depletion – although total body Na is constant, decreased water intake and continued insensible water losses (through the skin and lungs) lead to decreased ECF volume; examples include reduced oral fluid intake (especially in infants or older people) and diaphoresis (excessive sweating) with fever or heat stroke (Murphy et al, 2019). Patients with diabetes insipidus lose too much water in the urine due to the impaired release of anti-diuretic hormone (ADH) from the pituitary gland (Waugh and Grant, 2018). This prevents the renal tubules from conserving water, causing hypernatraemia, seen in individuals with traumatic brain injury or pituitary tumours (Murphy et al, 2019; Waugh and Grant, 2018). Nephrogenic diabetes insipidus occurs when renal tubule cells fail to respond to ADH due to lithium use (medication for mood disorders) or hypokalaemia (low K levels) (Murphy et al, 2019). Treating the underlying cause of hypernatraemia is paramount alongside replacement fluids;
  • Water and Na depletion – deficits of water over Na (water > Na) – when the body loses more water than sodium – may occur with increased urine production/osmotic diuresis due to glucosuria (excess glucose in the urine) in patients with DM (Murphy et al, 2019). Similarly, urea diuresis occurs with high-protein feeds/diets without adequate water supplementation. Deficits of water > Na also occurs with burn injuries, excessive sweating and excess watery diarrhoea (Overgaard-Steensen and Ring, 2018);
  • Increased Na content of ECF – this can occur with intravenous (IV) administration of sodium bicarbonate (NaHCO3); a concentration of 8.4% of 1,000mmol/L Na, used to treat acidosis, may be mitigated by considering a less concentrated solution of NaHCO3 (1.26% Na 150mmol/L) (Overgaard-Steensen and Ring, 2018). Excess secretion of aldosterone (a steroid hormone controlling serum Na and K) causes Na retention in renal tubules; hypernatraemia occurs in patients with benign tumours on the adrenal glands, Conn’s syndrome (adrenal glands make too much aldosterone) and renal disease (Murphy et al, 2019; Overgaard-Steensen and Ring, 2018).

How to interpret electrolyte blood results to identify abnormalities (3)

Hyponatraemia

A decrease in serum Na levels relative to water is called hyponatraemia and causes dilution of body fluids (low osmolality) (Banu and Flanagan, 2019); up to 40% of inpatients can have serum Na <138mmol/L (Al Mawed et al, 2018). To excrete excess water, the osmoregulatory hypothalamus in the brain stimulates the pituitary gland to secrete less ADH, to regulate healthy nephrons to excrete water and reabsorb Na (Overgaard-Steensen and Ring, 2018).

Table 2 highlights presenting symptoms of hyponatraemia. Causes include:

  • Non-oedematous hyponatraemia – an increase in body fluid with the total body Na remaining constant. One example is syndrome of inappropriate antidiuretic hormone (SIADH), in which not enough water is excreted, causing very concentrated urine (Yasir and Mechanic, 2023); however, this condition shows no signs of fluid volume excess, blood pressure is normal (normotensive), and glomerular filtration rate (GFR), serum urea and creatinine (measures of kidney function) remain in range. SIADH may occur in patients with pneumonia, subphrenic abscess (fluid accumulation between the diaphragm, liver, and spleen), malignancy and abdominal surgery; it can also be induced by drugs, such as thiazide diuretics and chlorpropamide (Murphy et al, 2019). Non-oedematous hyponatraemia can also be caused by drinking too much water (intoxication) to try to rehydrate after a long period of not drinking; it can also occur after IV 5% glucose infusions (glucose is metabolised leaving free water) (Banu and Flanagan, 2019);
  • Na loss – hypotension and Na loss can occur due to chronic or acute GI losses, such as vomiting or watery diarrhoea (Murphy et al, 2019). Increased Na excretion and ECF depletion leads to thirst, dyspnoea, vomiting, abdominal cramps, confusion and lethargy (Murphy et al, 2019). Individuals show signs of dehydration, such as sunken eyes, dry tongue and buccal mucosa (soft, moist lining of the mouth), postural hypotension and tachycardia; life-threatening sodium depletion may present with serum Na in the normal range, so the patient’s history and clinical signs must be prioritised (Murphy et al, 2019).

Potassium (K)

K is the principal positively charged ion cation (K+) in the intracellular fluid (ICF) (98% of total body K in the intracellular (IC) space and 2% in the EC space). As the body cannot conserve K, it must be ingested daily in the diet; cellular uptake of K is stimulated by insulin (Li and Vijayan, 2014).

Na and K have a reciprocal relationship. The kidneys reabsorb Na and excrete K in response to aldosterone secretion (Murphy et al, 2019). Small changes in K concentration can affect the excitability of nerve and muscle tissue; for example, the heart’s vulnerability to K fluctuations can cause life-threatening arrhythmias (Li and Vijayan, 2014).

ECF gains K when cells are destroyed and IC K is released, and also when K shifts from ICF to ECF – for example, in acidosis, which redistributes K from the IC to EC space in exchange for hydrogen ions (H+). Once the cause of acidosis is corrected, K is transported back to the IC space reducing K in the blood; caution is, therefore, needed with K replacement/ management during acidosis (Morton and Thurman, 2023). The kidneys have no mechanism to combat K loss as it is excreted, even when plasma levels are low (Laurin and Leblanc, 2018; Chernecky et al, 2005).

Hyperkalaemia

Hyperkalaemia is when the serum or plasma K+ level is above the upper limits of normal. In patients at risk of hyperkalaemia, it is important to be aware of presenting signs (Table 2). Causes include:

  • Renal failure – hyperkalaemia can occur in a variety of patient conditions, for example, poor excretion of K because of low GFR, kidney damage due to DM, systemic lupus erythematosus and sickle cell disease (Laurin and Leblanc, 2018). Premature babies are at high risk of hyperkalaemia within 48 hours of birth because of their immature renal function (Bonilla-Félix, 2017). Older adults are at risk due to: deteriorating renal function; reduced renal blood flow (reduced GFR); reduced oral intake of K; and decreasing plasma renin and aldosterone, which reduce excretion of K (Morton and Thurman, 2023). Older adults with polypharmacy (regular simultaneous use of five or more medications) are more likely to take medications that may interfere with K excretion, such as non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors and K-sparing diuretics (Varghese et al, 2024);
  • Subcutaneous heparin therapy – this can interfere with aldosterone production, thereby decreasing K excretion (Amdetsion et al, 2023);
  • Addison’s disease – both Addison’s disease (reduced aldosterone excretion/ hypoaldosteronism) and aldosterone antagonist drugs (for example, spironolactone) decrease K excretion (Scott et al, 2023);
  • Cell damage – K release from ICF in patients with burns, rhabdomyolysis (muscle tissue breakdown resulting in the release of toxic components into the bloodstream and kidneys), trauma, malignancy, haemolysis and chemotherapy (Murphy et al, 2019).
  • Blood transfusions with stored blood – these may cause hyperkalaemia when K leaks from cells due to failure of the Na+/K+ ATPase pump (which transports Na+ and K+ ions across cell membranes against their concentration gradients). The K plasma level may increase by 0.5 -1.0mmol/L per day of refrigerated blood storage (Opoku-Okrah et al, 2015);
  • Insulin deficiency – low cellular uptake of K results in hyperkalaemia (Murphy et al, 2019).

Hypokalaemia

Hypokalaemia is when K in the blood becomes too low due to inadequate intake or excess loss (Murphy et al, 2019). Clinical features include muscle and heart symptoms (Table 2). Causes include:

  • GI losses – for example, due to prolonged vomiting (loss of gastric acid leads to alkalaemia), diarrhoea (quick transit through the colon prevents absorption), surgical fistula and laxative misuse (Castro and Sharma, 2024; Chernecky et al, 2005);
  • Renal losses – for example, due to renal disease, administration of diuretics (thiazides and frusemide), hyperaldosteronism (excess K is excreted), alcoholism, a newly transplanted kidney, glycosuria (high glucose in the urine)/osmotic diuresis, Mg depletion and high stress (Castro and Sharma, 2024);
  • Drug-induced hypokalaemia – this may occur with thiazide diuretics, corticosteroids and adrenaline (Murphy et al, 2019);
  • Alkalosis – this stimulates a shift of K+ from the EC to IC space in exchange for H+; therefore, correcting the cause of alkalosis is essential when considering K+ replacement therapy (Chernecky et al, 2005);
  • IV dextrose administration – large amounts may cause increased endogenous insulin release and, hence, hypokalaemia (insulin stimulates cellular K uptake) (Morton and Thurman, 2023);
  • Reduced dietary intake – reduced intake of K-rich food, such as chocolate, dried fruit, nuts, seeds, fruit (oranges, bananas, apricots), meat and vegetables (beans, potatoes, mushrooms, tomatoes and celery);
  • Insufficient oral intake – administration of K-deficient IV fluid and lack of K supplement in total parenteral nutrition will predispose a patient to hypokalaemia (Morton and Thurman, 2023).

Calcium (Ca)

Approximately 99% of Ca is stored in bones and teeth, and 1% in the ECF and soft tissue (Waugh and Grant, 2018). Some bone is reabsorbed daily and Ca is returned to the ECF; to maintain Ca balance an equal amount of bone formation must occur (Morton and Thurman, 2023). Ca: maintains cell structure and function; helps maintain cell membrane stability and long-term permeability control; facilitates nerve-impulse transmission for contraction of cardiac, smooth and skeletal muscle; and is integral to the clotting cascade and release of certain hormones (Morton and Thurman, 2023).

Ca binding

Serum Ca concentration is kept within a very narrow range. Approximately 45% is bound to plasma proteins (primarily albumin), 15% to small anions such as PO4³- and citrate, and 40% is in free or ionised state (Ca++), which is the active form (Goyal et al, 2023); as such, reduced serum albumin (hypoalbuminemia) leads to reduced bound/serum Ca, but the level of free/ionised Ca++ is unaffected (Gozzolino et al, 2018).

Acid-base disturbances affect the binding capacity of Ca to albumin and exchange of Ca++ and H+ ions between the IC and EC space (Goyal et al, 2023). If blood pH rises (alkalosis), more Ca binds with proteins so the level of free/ionised Ca++ drops and the patient with alkalosis develops hypocalcaemia (Murphy et al, 2019). However, when blood pH drops (acidosis), less Ca binds with proteins and free/ionised Ca++ rises, causing hypercalcaemia (Murphy et al, 2019).

As special equipment is required to measure free/ionised Ca++, biochemistry tests usually measure total serum Ca concentration, corrected for the blood albumin level (Goyal et al, 2023).

Homeostasis

Ca is absorbed across the intestinal mucosa; net absorption must equal daily urinary loss to maintain homeostasis (Yu and Sharma, 2024). Hormones regulate Ca transport in the gut, kidneys and bone; these are primarily parathyroid hormone (PTH), 1,25-dihydroxyvitamin D-3 (Vitamin D3) and calcitonin (Yu and Sharma, 2024).

PTH maintains Ca within tight limits for nerve function, cell membrane permeability, muscle contraction and glandular secretion (Goyal et al, 2023). As PTH is dependent on free/ionised Ca++, patients with low albumin are not hypocalcaemic (low blood Ca) and the laboratory adjusts the Ca level to reflect normal albumin (Murphy et al, 2019). PTH is secreted in response to low free/ionised Ca++ and causes bone resorption, liberating Ca from bone and promoting reabsorption in kidney tubules. Consequently, increased PTH secretion in response to low free/ionised Ca++ can lead to bone disease if left untreated (Murphy et al, 2019).

Calcitonin (released by the thyroid gland) acts transiently as an antagonist to PTH; it inhibits bone resorption, decreasing gut absorption and promoting excretion of Ca (Chernecky et al, 2005).

Gut absorption of Ca by sterol hormones depends on Vitamin D and PTH (Chernecky et al, 2005). Vitamin D also promotes Ca resorption from bone, as well as Ca kidney reabsorption, to raise serum/total Ca levels (Goyal et al, 2023).

Hypercalcaemia

Raised levels of serum/total Ca (hypercalcaemia) are more common than hypocalcaemia. Patients may be asymptomatic in the early stages, but clinical presentation in severe cases can include: neurological and psychological signs; muscle weakness, leading to cardiac and gut problems; kidney failure; and bone pain (Table 2). Causes include:

  • Increased Ca resorption from bone – this is a primary cause due to hyperparathyroidism (increased serum PTH levels) (Turner, 2017). Hyperparathyroidism can be due to familial predisposition (abnormalities in several potential genes) or a parathyroid adenoma tumour that secretes PTH, independent of feedback control of free/ionised Ca++ (Morton and Thurman, 2023; Turner, 2017);
  • Hypercalcaemia of malignancy – this occurs when tumours invade and destroy bone, releasing a PTH-related protein that raises serum/total Ca levels (for example, squamous cell carcinoma of lung; myeloma, a cancer of the bone marrow; Hodgkin’s lymphoma; renal cell carcinoma; or breast cancer) (Murphy et al, 2019);
  • Increased Ca absorption/reduced excretion – increased absorption in the GI tract and reduced excretion from the kidneys (Morton and Thurman, 2023);
  • Inappropriate Vitamin D or metabolites – when treating renal disease or hypoparathyroidism (Murphy et al, 2019);
  • Hyperthyroidism raising levels of thyroid hormones – this can accelerate bone turnover, especially osteoclastic activity (the breaking down of bone, which is essential for bone modelling and growth). This leads to raised serum/total Ca levels from increased bone resorption (Morton and Thurman, 2023);
  • Immobilisation or multiple fractures – these can increase Ca release from bone, especially in people with Paget’s disease in whom thickened, disorganised bone structure is prone to fracture (Murphy et al, 2019);
  • Hypophosphataemia (low phosphate (PO4)) – this increases free/ionised Ca++ because Ca has an inverse relationship with PO4, with PTH regulating levels of Ca and PO4 in the blood (Morton and Thurman, 2023);
  • Ca therapy – routine Ca containing solutions given during cardiac surgery, abuse of certain antacids (calcium carbonate), side-effects of lithium or thiazide diuretics that reduce renal excretion of free/ionised Ca++, and increased Vitamin A (increases bone resorption) can all predispose a patient to hypercalcaemia; these should be checked when biochemistry results show a raised serum/total Ca level (Murphy et al, 2019).

Hypocalcaemia

Characterised by low levels of serum/total Ca, mild cases can be asymptomatic; however, if hypocalcaemia is severe, presenting symptoms can include neuromuscular and cardiac symptoms (Table 2). Causes include:

  • Low serum albumin – this occurs with low blood albumin levels because most of the body’s Ca is bound to albumin; therefore, serum/total Ca should always be corrected for the albumin level before hypocalcaemia is diagnosed (Goyal et al, 2023). There is a ~0.25mmol/L drop in serum/total Ca concentration for every 10g/L reduction in the serum albumin concentration; this can be caused by cirrhosis, nephrosis, malnutrition, burns, chronic illness and sepsis (Murphy et al, 2019);
  • Poor dietary intake – for example, a lack of green leafy vegetables, dairy, whole grains, nuts and legumes. Most at-risk individuals are older adults and post-menopausal women lacking oestrogen (reduces Ca absorption); alcoholics are especially prone due to poor diet, poor Ca absorption and low Mg levels that induce PTH resistance (Goyal et al, 2023; Morton and Thurman, 2023);
  • Vitamin D deficiency – due to malabsorption, inadequate diet and little exposure to sunlight. Certain anticonvulsant drugs (for example, phenytoin, sodium valproate) interfere with vitamin D metabolism (Lee and Mather, 2022), leading to osteomalacia (softening of the bones) in adults and rickets in children;
  • Increased intestinal activity – when this leads to malabsorption or loss of Ca salts in faeces, hypocalcaemia occurs. Examples include patients with persistent diarrhoea, laxative misuse, chronic malabsorption or pancreatic insufficiency (Morton and Thurman, 2023);
  • Reduced activity/inactivity – this can lead to a loss of Ca from bones (serum/total Ca levels may be normal). In the long term, this may accelerate the development of osteoporosis (Lombardi et al, 2020);
  • Hypoparathyroidism (decreased serum PTH levels) – this can be due to damaged parathyroid glands (post surgery or due to autoimmune effects), abnormal regulation of PTH production and secretion, or abnormal parathyroid gland development (Goyal et al, 2023). Post-surgery damage is the most common reason for hypoparathyroidism (Goyal et al, 2o23). Low PTH as a cause of hypocalcaemia is determined by repeated serum/total Ca levels (measured at least two weeks apart), combined with inappropriately low PTH levels (Goyal et al, 2023);
  • Mg deficiency – as normal Mg levels are needed to produce parathyroid hormone, Mg deficiency can decrease Ca absorption in the gut and kidneys; the aminoglycoside antibiotic, gentamicin, lowers serum Mg and may decrease Ca resorption from bone (Morton and Thurman, 2023);
  • Substantial blood transfusion – this can cause an acute decline in free/ionised Ca++ due to Ca binding with citrate (used as an anticoagulant in stored blood), which renders it unavailable for use; at risk are children and patients receiving a massive transfusion (Goyal et al, 2023; Li and Xu, 2015).

Magnesium (Mg)

Mg++ (the active form of Mg) is the fourth most abundant cation in the human body and the second most abundant IC cation after PO4³- (Hansen and Bruserud, 2018). Mg tends to be bound to albumin or other substances; Mg++ cannot be measured so biochemistry laboratory results will reflect the total circulating amount of Mg, making it important to also measure serum albumin levels (Murphy et al, 2019).

Mg is a co-factor in ~300 enzyme systems that control diverse biochemical reactions in the body, including:

  • Protein synthesis;
  • Muscle and nerve function through cell membrane transport of K and Ca;
  • Blood–glucose control and glycolysis (splitting of glucose into two pyruvate molecules);
  • Aerobic/oxidative metabolism (chemical process using oxygen to produce energy from carbohydrates) (Murphy et al, 2019).

Mg also facilitates normal function of the cardiac and vascular systems, affecting blood pressure control (vasodilation) and contractility of cardiac muscle. It is an integral part of chlorophyll, so green leafy vegetables are a dietary source (30% is absorbed from the small intestine and distributed to metabolically active tissue) (Murphy et al, 2019).

Hypermagnesaemia

A high level of serum Mg (hypermagnesaemia) is uncommon but may be seen in: renal failure/dysfunction; untreated DKA; or in patients receiving Mg-containing antacids, laxatives, supplements and rectal enemas (Morton and Thurman, 2023). Clinical features include cardiovascular, cardiac, respiratory and neurological manifestations (Table2).

Hypomagnesaemia

Low Mg (hypomagnesaemia), when severe, may cause hypoparathyroidism and hypo-calcaemia (Morton and Thurman, 2023). Patients with vascular disease and hypo-magnesaemia are at higher risk of strokes (Morton and Thurman, 2023). The condition affects ~10% of critically ill hospitalised patients (mainly due to GI and/or renal disorders), and may lead to secondary hypokalaemia and hypocalcaemia, causing severe neuromuscular and cardiovascular manifestations (Hansen and Bruserud, 2018).

Symptoms of hypomagnesaemia are similar to those of hypocalcaemia and hypokalaemia, and include impaired neuromuscular and cardiac function and CVS symptoms (Table 2). Causes include:

  • Dietary insufficiency and intestinal malabsorption – for example, due to severe vomiting, diarrhoea or fistula losses, and following prolonged nasogastric aspiration/suction (Morton and Thurman, 2023). Alcohol overuse triggers the kidneys to excrete more Mg, exacerbated by poor diet and vomiting (Morton and Thurman, 2023).
  • Insufficient oral intake – for example, in IV fluid therapy, total parenteral nutrition (delivered intravenously) or enteral feeding;
  • Compromised gut absorption – excess Ca and PO4 in the GI tract impair Mg absorption, and may be seen in patients with infection, inflammation, surgery, and cancer (Morton and Thurman, 2023);
  • Pancreatitis – Mg forms soaps, with fatty acids taking Mg out of the circulation, leading to low serum levels (Morton and Thurman, 2023);
  • Loss from the kidneys – for example, in patients with osmotic diuresis, due to: hyperglycaemia/DKA; prolonged
    use of loop or thiazide diuretics; glomerulonephritis (inflammation/damage to the glomeruli or filtering part of the kidneys); pyelonephritis (kidney infection); renal tubular acidosis; or impaired renal reabsorption, caused by anticancer cytotoxic drug therapy (Morton and Thurman, 2023);
  • Excessive loss of body fluids – for example, due to burns, chronic diarrhoea or breast feeding (Morton and Thurman, 2023).

Conclusion

Accurate interpretation of electrolyte results is crucial as imbalances can have significant, sometimes life-threatening, implications, particularly in acute/critically ill patients or those who have complex medical conditions. It is used to monitor organ function, guide fluid management, diagnose underlying conditions, prevent complications and monitor responses to therapies, and recognise and manage critical situations.

Also in this series

  • How to conduct a clinical consultation in advanced practice
  • History taking for advanced clinical practitioners: what should you ask?
  • Assessing frailty in older people as part of holistic care
  • How to carry out a respiratory assessment in advanced practice
  • How to interpret chest radiographs (X-rays): a systematic approach
  • How to conduct a cardiovascular assessment in advanced practice
  • How to assess and examine a patient with abdominal symptoms
  • Performing a cranial nerve examination and interpreting the findings
  • Understanding microbiology tests and interpreting the results
  • How to assess patients presenting with musculoskeletal conditions
  • How to interpret haematology results to inform diagnosis and management

Advanced practitioners

This series is aimed at nurses and midwives working at or towards advanced practice. Advanced practitioners are educated at masters level and are assessed as competent to make autonomous decisions in assessing, diagnosing and treating patients. Advanced assessment and interpretation is based on a medical model and the role of advanced practitioners is to integrate this into a holistic package of care.

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