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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

ECG, electrolyte and bone-health complications

Psychiatry · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Electrical instability or severe electrolyte disturbance

Syncope, seizure, chest pain, arrhythmia, awake pulse below 40 beats/minute, prolonged QTc, potassium below 2.5 mmol/L, severe sodium disturbance, hypoglycaemia or falling phosphate need urgent monitored medical management.

Action: Assess ABCDE and glucose, obtain a 12-lead ECG and repeat electrolytes including magnesium and phosphate, stop or review contributors and seek senior medical or paediatric advice. Correct severe abnormalities in an appropriate monitored setting and continue necessary nutrition under a refeeding plan rather than treating the laboratory value in isolation.

Overview

Interpret cardiac, biochemical and skeletal complications of eating disorders, recognise when monitoring or acute correction is needed, and use NICE bone-health recommendations accurately.

Cardiac risk in eating disorders arises from several interacting mechanisms: low energy availability and reduced cardiac mass, reduced circulating volume, autonomic adaptation, electrolyte loss, refeeding shifts and medication. Sinus bradycardia is common in restrictive illness and usually improves with nutrition, but it is not automatically benign. MEED treats an awake heart rate below 40 beats/minute as red. Syncope, postural collapse, arrhythmia, conduction change or prolonged QTc requires urgent correlation rather than an ECG label alone.

QTc interpretation needs context. Measure the underlying rhythm and review the correction formula, because extreme heart rates can distort automated values. Compare with age- and sex-relevant reference ranges and look for T-wave change, ectopy, pauses and heart block. Review potassium, magnesium and calcium plus every prescribed, over-the-counter and non-prescribed substance. NICE recommends ECG monitoring when cardiac-compromising medication is used in the presence of hazards such as bradycardia below 40, hypokalaemia or prolonged QT.

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PsychiatryOriginal SBA

Bone-density timing

An adult with anorexia nervosa has remained underweight for just over two years without previous scanning. Which statement best reflects NICE bone-health guidance?

Choose one answer, then submit
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Sources and review status3 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • NICE NG69 eating disorders recommendationsECG indications, electrolyte management and bone-health recommendations.
  • RCPsych CR233 Medical Emergencies in Eating DisordersCardiac thresholds and biochemical emergency management.
  • NHS anorexia nervosa overviewCurrent patient-facing cardiovascular, neurological and skeletal complications.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
Biochemistry reflects behaviour but is not a lie detector. Vomiting or diuretics often produce hypokalaemic, hypochloraemic alkalosis; laxative diarrhoea may produce acidosis; water loading can cause dilutional hyponatraemia. Renal conservation can transiently mask total-body depletion, and electrolytes can change rapidly after the test. Phosphate and magnesium require specific measurement, especially during refeeding. Severe correction is specialist work because renal impairment, rapid sodium correction and concentrated intravenous potassium can themselves cause harm.

Low bone mineral density results from prolonged low energy availability, hypogonadism, altered bone turnover and impaired attainment of peak bone mass. The central treatment is nutritional recovery and restoration of a healthy weight for age. NICE advises discussing the purpose of scanning before ordering it, considering DXA after 1 year of underweight in children and young people or 2 years in adults, and scanning earlier for bone pain or recurrent fractures. Children need bone-size-adjusted interpretation such as bone mineral apparent density.

Hormonal and bone medicines are not simple substitutes for recovery. NICE says not to routinely offer oral or transdermal oestrogen to children or young people solely for low bone density and advises specialist paediatric or endocrine input before hormonal treatment. It gives tightly defined circumstances for physiological oestrogen in young women aged 13–17 and says bisphosphonates may be considered for women aged 18 and over with long-term low weight and low bone density after discussion of benefits and teratogenic risk. Apply these sex-linked recommendations through relevant physiology, bone age, hormone exposure and reproductive potential rather than gender label alone, with specialist input. Osteoporosis also requires avoiding high-impact or high-fall-risk activity.

Key points

  • Order ECG according to rapid loss, excessive exercise, purging, bradycardia, hypotension, weakness, electrolyte imbalance, rhythm history, caffeine and prescribed or non-prescribed medication.
  • Sinus bradycardia commonly reflects starvation adaptation, but an awake heart rate below 40, symptoms, conduction disease, arrhythmia or prolonged QTc requires urgent assessment.
  • Vomiting commonly causes chloride and potassium depletion with metabolic alkalosis; laxative diarrhoea may cause potassium and bicarbonate loss with metabolic acidosis.
  • Hyponatraemia may result from water loading, medication or volume disturbance; correction must be cautious and guided by cause, chronicity, symptoms and urine studies.
  • NICE recommends oral electrolyte replacement unless absorption is impaired or the disturbance is severe; route and dose depend on level, ECG, renal function and ongoing losses.
  • The main way to prevent and treat low bone density in anorexia is reaching and maintaining a healthy weight or BMI for age, not prescribing hormones without nutritional restoration.
  • Consider bone-density scanning after 1 year of underweight in children and young people and after 2 years in adults, or earlier for bone pain or recurrent fractures.
  • Do not repeat bone-density scans more often than annually unless bone pain or recurrent fractures develop; paediatric results need adjustment for bone size.

Aetiology

01

Chronic energy deficit

Sustained undernutrition reduces cardiac and endocrine function and prevents normal bone formation, especially during peak bone-mass acquisition.

02

Compensatory losses

Vomiting, laxatives, diuretics, water loading and excessive exercise disturb fluids, electrolytes and acid-base balance through different mechanisms.

03

Treatment interaction

Refeeding and prescribed or non-prescribed medicines can expose depleted stores, alter QT risk and change replacement requirements quickly.

Pathophysiology

  1. 1
    Electrical vulnerability

    Potassium, magnesium and calcium abnormalities alter cardiac repolarisation, while bradycardia and QT-active drugs can increase arrhythmic risk.

  2. 2
    Volume and autonomic change

    Low circulating volume and starvation adaptation produce hypotension, postural tachycardia or bradycardia and reduced exercise tolerance.

  3. 3
    Bone remodelling imbalance

    Low energy availability, hypogonadism and altered endocrine signals reduce bone formation and may increase resorption, weakening skeletal structure.

  4. 4
    Intracellular electrolyte shift

    Insulin release during refeeding moves phosphate, potassium and magnesium into cells, potentially causing rapid serum falls and organ dysfunction.

Clinical features and red flags

Starvation bradycardia

Slow sinus rate may be an energy-conserving adaptation, but extreme rate, symptoms, postural compromise or another ECG feature shifts concern.

Purging chemistry

Potassium, chloride, bicarbonate and renal patterns can suggest vomiting, diuretic or laxative effects while never proving or excluding the behaviour.

Refeeding phosphate fall

A declining phosphate after nutrition begins signals intracellular shift and can precede weakness, oedema, respiratory failure and cardiac dysfunction.

Low bone density

Fractures, bone pain, delayed puberty and prolonged underweight identify skeletal risk, but absence of symptoms does not ensure normal bone mass.

Medication interaction

QT-prolonging, electrolyte-altering or bradycardic drugs become more hazardous when malnutrition, purging and dehydration reduce physiological reserve.

Red flags requiring action

  • Preserved consciousness and a sinus rhythm do not make an awake pulse below 40 safe; MEED recommends physician or paediatric assessment with postural observations, bloods and ECG.
  • Prolonged QTc, heart block, ventricular ectopy, new T-wave change or syncope requires review of rate correction, electrolytes and prescribed or non-prescribed drugs.
  • Potassium below 2.5 mmol/L is a MEED red finding and may need initial intravenous correction with ECG monitoring when oral treatment is unsafe or ineffective.
  • Falling phosphate after nutrition begins may be the earliest refeeding warning and can progress to respiratory, cardiac and neuromuscular failure.
  • Bone pain, recurrent fracture, loss of height or high-impact exercise in established osteoporosis requires prompt skeletal and activity review.

Investigations

  1. 01
    Twelve-lead ECGFirst step
    Why
    Assess rate, rhythm, conduction, repolarisation and QTc under standard resting conditions.
    Interpretation and limitations
    Manually review suspicious automated values and interpret with heart rate, age, sex, electrolytes, symptoms and medication; significant abnormality needs senior advice.
  2. 02
    Electrolyte and renal panel
    Why
    Measure sodium, potassium, chloride, bicarbonate, urea, creatinine, magnesium, phosphate and calcium when risk indicates.
    Interpretation and limitations
    Use trends and the clinical behaviour; severe values, symptoms, ECG change or impaired renal function determine correction route and monitoring intensity.
  3. 03
    Fluid and urine assessment
    Why
    Differentiate dehydration, water loading and other causes of sodium or weight fluctuation.
    Interpretation and limitations
    Fluid balance, paired serum and urine osmolality and urinary electrolytes may clarify cause; rapid unstructured fluid administration can be dangerous.
  4. 04
    Bone-density scan
    Why
    Quantify bone mineral density when duration of underweight, pain or fractures makes the result clinically useful.
    Interpretation and limitations
    Use paediatric bone-size correction and specialist explanation; repeat no more than yearly unless new pain or recurrent fracture justifies earlier assessment.
  5. 05
    Endocrine and fracture review
    Why
    Assess puberty, gonadal suppression, thyroid adaptation, vitamin D, calcium intake and fracture risk.
    Interpretation and limitations
    Amenorrhoea or low testosterone supports low energy availability but is not required; treatment priorities remain nutrition, safe activity and specialist advice.

Differential diagnosis

01

Athletic bradycardia

Training can slow pulse, but undernutrition, symptoms, postural findings, ECG features and energy availability must be assessed before reassurance.

02

Primary rhythm disorder

Congenital long-QT, heart block, myocarditis and cardiomyopathy require consideration when ECG findings exceed expected nutritional adaptation.

03

Renal or endocrine electrolyte disease

Renal tubular disorders, adrenal disease and other endocrine conditions can mimic purging-related chemistry or coexist with it.

04

Primary osteoporosis

Glucocorticoids, coeliac disease, endocrine disease and genetic bone disorders may add risk beyond low weight and need targeted assessment.

Management

01Cardiac symptomsLink ECG to physiologyFirst stepSyncope, palpitations, chest pain, bradycardia, purging or QT-active medication raises concern.+
  1. 1Obtain ECG, glucose and urgent potassium, magnesium, calcium and renal testing while assessing postural and hydration status.
  2. 2Place severe electrolyte disturbance, significant ECG abnormality or symptomatic extreme bradycardia in a monitored setting with senior input.
  3. 3Correct the cause, review medication and provide nutrition; do not use pacing or antiarrhythmics reflexively for starvation sinus bradycardia.
02Electrolyte changeCorrect cause and deficitBloods show potassium, sodium, phosphate, magnesium or acid-base abnormality.+
  1. 1Identify ongoing vomiting, diarrhoea, diuretics, water loading, renal impairment, medication and timing relative to refeeding.
  2. 2EscalationUse oral replacement when appropriate and escalate severe, symptomatic or poorly absorbed deficits to a monitored specialist protocol.
  3. 3Repeat testing at a clinically justified interval and confirm a sustainable plan to stop ongoing loss or dilution.
03Skeletal riskRestore energy and protect boneProlonged underweight, pubertal disruption, bone pain, fracture or osteoporosis raises concern.+
  1. 1Prioritise weight restoration, adequate calcium and vitamin D intake and reduction of unsafe exercise with eating-disorder and dietetic support.
  2. 2Order DXA at NICE intervals or earlier for pain or recurrent fractures and obtain age-appropriate specialist interpretation.
  3. 3Seek endocrine expertise before hormonal or bone-active treatment and discuss reproductive implications and high-impact activity restrictions.

Complications

01

Malignant arrhythmia

Severe electrolyte disturbance, QT prolongation and conduction disease can produce syncope, seizure-like collapse and sudden cardiac death.

02

Neuromuscular failure

Low potassium, phosphate or magnesium can cause profound weakness, rhabdomyolysis, respiratory impairment and acute neurological symptoms.

03

Fragility fracture

Low bone density increases stress and fragility fractures, pain and loss of activity, with potentially incomplete recovery of peak bone mass.

04

Iatrogenic harm

Rapid sodium correction, unsafe concentrated potassium, unmonitored QT medication and inappropriate exercise advice can add preventable injury.

Monitoring and follow-up

  • Repeat ECG after clinically important electrolyte correction, medication change or recurrent symptoms and document the rate and QT-correction method used.
  • Trend potassium, magnesium, phosphate, sodium, bicarbonate and renal function according to purging, refeeding and replacement rather than at arbitrary intervals.
  • Monitor oral or intravenous replacement for overcorrection, renal accumulation, diarrhoea, tissue injury and recurrence from ongoing behaviour.
  • Follow growth, puberty, weight restoration, fracture symptoms and activity; revisit whether DXA results will alter management before repeating a scan.
  • Review every QT-active or electrolyte-altering medicine and non-prescribed product at transitions between medical and psychiatric care.

Special situations

QTc is calculated

Automated QTc can mislead at extreme rates, so the trace, formula and clinical context matter more than copying one machine number.

Serum can mask depletion

Homeostasis may preserve a serum electrolyte despite low total-body stores until purging, fluids or insulin-driven refeeding exposes the deficit.

Weight restoration treats bone

Hormone replacement without adequate nutrition does not address the central low-energy mechanism and may create false reassurance about recovery.

Children need size correction

Short stature and smaller bones can artifactually lower areal DXA values, making bone-size-adjusted analysis and paediatric expertise important.

Exercise can be treatment-limiting

High-impact loading is not therapeutic when osteoporosis, fracture risk or medical instability makes continued sport unsafe.

Common pitfalls

  1. 01

    Calling all bradycardia benign athletic conditioning without examining malnutrition and postural compromise.

  2. 02

    Trusting automated QTc without checking rhythm, heart rate, formula, electrolytes and medication.

  3. 03

    Replacing potassium repeatedly while ignoring vomiting, laxatives, water loading or renal impairment.

  4. 04

    Using oral contraceptive withdrawal bleeding as proof that bone physiology has recovered.

  5. 05

    Ordering frequent DXA scans that do not change care and expose the patient to repeated weight-focused discussion.

  6. 06

    Prescribing oestrogen or bisphosphonate without the age-specific NICE conditions and specialist counselling.