Hyponatraemia
Red Flags — act before continuing history
| Red flag | Why dangerous | Action |
|---|---|---|
| Seizure or active convulsion | Cerebral oedema from acute severe hyponatraemia (<125 acute) causes life-threatening brain herniation; seizure is a pre-herniation sign | 999 now |
| GCS <13 or acute confusion | Encephalopathy from cerebral oedema; sodium <120 acutely can be fatal within hours without 3% saline | 999 now |
| Na⁺ <120 mmol/L on blood result | Even if chronic, Na⁺ below 120 carries seizure risk and mandates same-day specialist assessment to guide correction rate | Same-day hospital |
| Respiratory depression or SpO₂ fall | Brainstem compression from cerebral oedema; impaired respiratory drive; this is a neurological emergency | 999 now |
| Postural syncope with very low Na⁺ | Severe volume depletion (adrenal crisis, gastrointestinal loss) causing both hypotension and hyponatraemia — haemodynamic emergency | 999 now |
| Suspected Addisonian crisis (hyperpigmentation, hypotension, hyperkalaemia) | Cortisol deficiency causes profound hyponatraemia; hypertensive crisis and cardiovascular collapse can be precipitated by failure to give hydrocortisone before treating Na⁺ | 999 now |
| Rate of fall >5 mmol/L in known chronic hyponatraemia | Previously adapted brain suddenly at risk again; acute-on-chronic can be as dangerous as de novo acute hyponatraemia | Same-day review |
Safeguarding Considerations — Consider in Every Consultation
🏠 Domestic Abuse / Carer Neglect
- Elderly patient with unexplained chronic hyponatraemia and poor nutrition — consider inadequate care
- Carer over-medicating patient with diuretics or restricting food intake
- Conflicting accounts between patient and carer about medication administration
- Patient appears fearful, avoids eye contact, or gives rehearsed answers when carer present
👴 Older Adults / Care Home Residents
- Recurrent hyponatraemia without clear cause in care home — suspect institutional neglect or missed medication review
- Failure of care home to act on flagged blood results — duty to refer to local authority
- Cognitive impairment may mask symptoms; hyponatraemia accelerates dementia progression
- Falls resulting in fractures — check for hyponatraemia as contributing cause even if not the referral reason
🧒 Children / Dependants in the Household
- Infant hyponatraemia from over-diluted formula — consider parental understanding or non-accidental poisoning
- Young child with hyponatraemia and unexplained neurological symptoms — consider Munchausen's by proxy
- Parental mental illness (e.g. causing psychogenic polydipsia) — assess parenting capacity
- Parental alcohol misuse (beer potomania) — assess home environment for children
💊 Self-Harm / Substance Misuse
- MDMA (ecstasy) causes acute SIADH — ask sensitively about recreational drug use
- Intentional water intoxication as self-harm method — rare but documented, particularly in patients with psychosis
- Medication misuse (e.g. doubling diuretics) — screen for mood disorder and deliberate self-harm intent
- Severe hyponatraemia in a young person with eating disorder — assess nutritional intake and purging behaviour
🏠 Social isolation and nutrition
Elderly patients living alone often eat inadequate protein and salt — reducing the solute available to drive urine concentration, impairing free water excretion even in the absence of excess ADH.
"What does a typical day's eating look like for you? Are you managing to eat regular meals?"If nutrition is poor: involve dietitian, social prescribing, and Meals on Wheels; nutritional optimisation directly raises sodium.
🧠 Psychiatric illness and polydipsia
Schizophrenia and affective disorders are strongly associated with primary polydipsia (compulsive water drinking), both as a symptom of the illness and as a side effect of antipsychotics stimulating thirst centres.
"Do you find yourself drinking a lot of water throughout the day? More than you feel you need to?"If positive: quantify fluid intake, involve psychiatry team for behavioural programme, consider antipsychotic review.
😔 Depression and SSRI initiation
The clinical risk is circular: depression is treated with SSRIs, which cause SIADH, worsening cognitive symptoms and potentially worsening mood — leading clinicians to increase the SSRI dose and exacerbate hyponatraemia.
"I know we recently started the antidepressant — how has your mood been? I want to make sure we find a safe option that helps you."If SSRI is causative: switch to mirtazapine or agomelatine (lower SIADH risk); do not simply stop — discuss with prescriber.
🍺 Alcohol and dietary pattern
Beer potomania is a social phenomenon — high alcohol intake with meals replaced by beer, leading to inadequate protein and salt. Repeated episodes are driven by the social context of drinking rather than a biochemical disorder requiring medication.
"Tell me a bit about how alcohol fits into your daily life — when and how much are you typically drinking?"If beer potomania: dietary counselling is more effective than medications; alcohol reduction referral; review social circumstances driving drinking.
😰 Stress and physiological ADH stimulation
Acute psychological stress (bereavement, assault, severe anxiety) triggers ADH release via central pathways. Nausea — a common stress response — is also a potent ADH stimulus. Acutely stressful hospital admissions themselves can precipitate hospital-acquired hyponatraemia.
"Have there been any major stresses or upheavals in your life recently — anything that's been particularly hard?"If significant psychosocial stressor identified: document, offer counselling referral, monitor sodium closely as stressor resolves.
💸 Poverty, heat exposure, and excess sweating
Manual workers, athletes, and patients in poorly ventilated environments may lose substantial sodium through sweat, particularly in summer. If replaced with water alone (not isotonic fluids), dilutional hyponatraemia develops. "Tea and toast" diets in lower-income elderly patients deplete solute.
"What's your home like in warm weather — do you get very hot? And what do you tend to drink when you're thirsty?"If sweat-related: advise isotonic fluids during physical activity; salt supplementation if renal function allows; review home conditions.
- Opening with "Your sodium is low" before asking the patient's story
- Failing to identify the offending drug (SSRI, thiazide) from the medication list
- Not asking about neurological symptoms (seizure, confusion, falls)
- Asking about information already in the notes (e.g. "Do you have heart failure?" when listed)
- Treating hyponatraemia without asking about fluid intake
- Failing to explore ICE — particularly the patient's hidden worry about dementia or cancer
999 or Same-Day Hospital
Call 999 / A&E now- Seizure or status epilepticusAcute cerebral oedema — 2 mL/kg 3% saline IV immediately in hospital
- GCS <13 or acute encephalopathyImminent herniation risk; 999 without delay
- Respiratory arrest or severe hypoventilationBrainstem compression; airway at immediate risk
- Suspected Addisonian crisis (collapse + low Na⁺ + high K⁺)Give IM/IV hydrocortisone 100mg before transport
- Acute Na⁺ <120 mmol/L with any symptomsEven nausea alone — risk of rapid clinical deterioration
- Na⁺ <115 mmol/L any chronicityExtreme caution — specialist guidance essential for safe correction
Same-Day GP / Urgent Referral
Hours to days- Na⁺ 120–129 with mild symptoms (nausea, fatigue, gait instability)Same-day senior GP review; consider same-day medical referral
- Newly identified Na⁺ <130 without clear reversible causeUrgent investigation to exclude malignancy, Addison's, SIADH
- Rapid fall (>10 mmol/L/24h documented)Potentially acute even if number appears "mild"
- Hyponatraemia with suspected new malignancy2-week wait suspected cancer pathway alongside electrolyte correction
- First presentation of SIADH unresponsive to fluid restrictionUrgent endocrinology referral for investigation and tolvaptan consideration
Manage in Primary Care
Weeks with monitoring- Na⁺ 130–135 (mild), clearly drug-induced (e.g. SSRI)Withdraw offending drug; recheck Na⁺ in 5–7 days
- Asymptomatic chronic mild-moderate hyponatraemia (Na⁺ >125)GP investigation and management with monitoring plan
- Beer potomania or psychogenic polydipsia with Na⁺ >130Dietary advice; behavioural plan; repeat bloods 1–2 weeks
- Known cause with stable sodium and asymptomaticOptimise underlying condition; repeat monitoring per cause
- Post-discharge follow-up after inpatient correctionCheck Na⁺ at 1 week, 4 weeks, and 3 months; review cause
- Managing a symptomatic patient with Na⁺ <125 at home without specialist input
- Admitting a truly asymptomatic chronic Na⁺ 132 unnecessarily
- Failing to give safety-netting advice about when to call 999
- Not mentioning the admission route or what will happen next
- Examining only one system without connecting it to the diagnostic question
- Missing postural hypotension in a patient on diuretics
- Performing a full cardiovascular exam without interpreting for volume status
- Not doing a neurological assessment in any confused patient
- Ordering serum sodium without urine sodium and osmolality
- Treating SIADH without ruling out Addison's (cortisol first)
- Not considering malignancy workup in unexplained SIADH over age 40
- Ordering a full battery of investigations without logical sequencing
"Sodium is like the salt in the water your body cells live in. Your blood test shows there's too much water relative to the salt — imagine a salty sea that's been diluted by heavy rain. When the balance tips too far, the cells, especially the brain cells, can swell slightly. That swelling is what causes the tiredness, nausea, and unsteadiness you've been feeling. The good news is that in most cases, once we find the cause — which might be a medication, a hormone imbalance, or too much fluid — we can correct it safely and your symptoms should improve."
"Should I just eat more salt?"
"It's a very reasonable thought, and in a few cases extra salt does help. But the problem here isn't that you're not eating enough salt — it's that your body is holding onto too much water, diluting what salt you do have. Simply eating more salt could make things worse if the underlying cause is still active. Let's find out why first."
"It's probably just my age" or "I always feel tired"
"It might feel like tiredness is normal at your age, and many people do feel worn out sometimes. But the sodium level we found is genuinely below normal and is very likely contributing to how you feel. The encouraging thing is this is treatable — we're not just accepting it as inevitable."
SIADH (drug-induced): SSRIs, thiazides, carbamazepine, NSAIDs — euvolaemic; urine Na⁺ >20; resolves with drug withdrawal
Beer potomania: Dilute urine (<100 mOsm/kg); history of high beer intake; dietary advice curative
Diuretic-induced (thiazide): Hypovolaemic; urine Na⁺ high; stop thiazide; replace K⁺
Hypothyroidism: High TSH; slow reflexes; bradycardia; thyroxine replacement corrects sodium
Psychogenic polydipsia: Very dilute urine; psychiatric history; behavioural fluid restriction
Adrenal insufficiency (Addison's disease)
Hyponatraemia + hyperkalaemia + postural hypotension + fatigue + pigmentation; short synacthen test; emergency if crisis features
SIADH from pulmonary/CNS malignancy
Unexplained SIADH in patient over 40 with weight loss or smoking history; CXR + urgent 2WW referral
Cirrhosis / hepatic hyponatraemia
Ascites, spider naevi, hepatomegaly; MELD-Na score; hepatology referral; tolvaptan consideration
Nephrotic syndrome
Massive proteinuria, low albumin, oedema; nephrology referral; treat underlying glomerulonephritis
Acute severe hyponatraemia (<125, onset <48h) with neurological symptoms
Cerebral oedema; seizure; GCS fall; 3% hypertonic saline 2 mL/kg IV bolus in hospital — not in community
Addisonian crisis
Collapse, hypotension, vomiting; hyponatraemia + hyperkalaemia; give IM hydrocortisone 100mg immediately; 999
Osmotic demyelination syndrome (ODS) risk
If Na⁺ corrected >10 mmol/L/24h; dysarthria, dysphagia, quadriplegia; cannot be reversed; prevention is the only treatment
- Diagnosing SIADH without excluding Addison's first
- Using jargon: "You have SIADH" without explanation
- Failing to name the likely causative drug if identified
- Not acknowledging patient's concern about what low sodium means for their health
- Referring without documenting the current and baseline sodium
- Starting fluid restriction without informing the receiving team
- Failing to stop the causative drug before referral
- Not giving emergency safety-netting at point of referral
Validate — name their expectation
Many patients expect an IV drip of salt water and rapid resolution. Others expect tablets. Naming their expectation prevents antagonism and signals you have understood what they came for.
"I understand you were hoping we might be able to give you something to get this sorted quickly — it's completely reasonable to want that."Explain — share your clinical reasoning
The counterintuitive nature of hyponatraemia management — that giving salty fluid to some patients is dangerous, and restricting fluid in others — needs careful, non-paternalistic explanation.
"The tricky thing with your type of low sodium is that if we correct it too quickly, it can cause problems with the nerves in the brain. So we have to do this gradually and carefully — it's actually safer to go slow."Negotiate — offer something today
Even if the primary treatment is "stop the medication and wait", the patient needs to leave feeling something active has been done. Name what you are doing today.
"What I can do today is stop the medication that's most likely causing this, arrange for blood tests to track your sodium, and get you seen by a specialist — so we're absolutely taking action right now."Reducing water intake decreases the dilutional effect on sodium. Effective only when ADH is driving water retention (SIADH, HF, cirrhosis) — not in volume depletion where it worsens the picture.
Measure all fluids including soups, ice cream, jelly, and fruit high in water. Use a marked jug. Include tea and coffee. Spread fluids throughout the day. Avoid drinking to quench thirst if thirst is pathological (polydipsia).
Free water excretion depends on solute (urea, Na⁺, K⁺) delivery to the kidney. Low-protein diets (beer potomania, tea-and-toast elderly) impair free water excretion even without excess ADH.
Increase protein intake: meat, fish, eggs, lentils, nuts. Urea supplements (15g/day) are available on prescription and used in specialist SIADH management. Do NOT add extra table salt without medical supervision in euvolaemic/hypervolaemic states.
Beer potomania: high volume of beer provides water but inadequate solute (protein, urea, salt). Alcohol also impairs hypothalamic ADH regulation. Both mechanisms contribute in heavy drinkers.
Refer to alcohol liaison if dependent. Advise switching from beer to spirits (lower water volume per unit). Recommend eating food with every drink. Signpost to Drinkline (0300 123 1110).
Exercise-associated hyponatraemia occurs when athletes replace sweat losses with plain water, diluting sodium. High-volume endurance events (marathons, triathlons) carry highest risk, particularly in women.
Drink to thirst rather than prescribed volumes. Use electrolyte drinks (SIS, Lucozade Sport) during events over 60 minutes. Avoid drinking more than sweat losses during exercise — overdrinking is as dangerous as dehydration.
Primary polydipsia in schizophrenia/bipolar is a compulsive behaviour partly driven by antipsychotic-induced thirst. Psychosocial triggers (boredom, anxiety, oral stimulation-seeking) also drive excessive drinking.
Involve community mental health team. Use fluid intake charts. Educate on target volume. Consider antipsychotic review (clozapine and olanzapine most implicated). Structured activity programmes reduce polydipsia behaviour.
Drug-induced SIADH is the commonest reversible cause of hyponatraemia. SSRIs, thiazides, carbamazepine, NSAIDs, PPIs, and desmopressin all contribute. Polypharmacy greatly increases risk — two causative drugs together are synergistic.
Use SMR (structured medication review) framework. Check BNF for SIADH risk of each drug. For SSRIs: switch to mirtazapine. For carbamazepine: discuss AED switch with neurology. For thiazides: switch to loop diuretic if diuresis needed.
0.9% sodium chloride IV (hospital) or oral rehydration (mild, primary care)
- Stop causative drug (thiazide — stop immediately)
- Replace potassium if concurrent hypokalaemia
- Oral rehydration salts (Dioralyte) for mild dehydration without symptoms
- Correct rate no faster than 10 mmol/L in 24h
Fluid restriction 1.0–1.5 L/day + remove causative drug
- Stop SSRI, carbamazepine, NSAID, thiazide as appropriate
- Oral urea 15g/day (Ure-Na) if fluid restriction fails — requires specialist initiation in UK
- Demeclocycline 300–600mg BD: inhibits ADH action — specialist only
- Tolvaptan (vasopressin V2 receptor antagonist): specialist prescribing only; not for heart failure
Fluid restriction + optimise heart failure / cirrhosis / nephrotic syndrome
- HF: optimise ACEi + beta-blocker + spironolactone; loop diuretic for oedema management
- Cirrhosis: spironolactone 100–400mg/day; avoid saline; tolvaptan licensed but specialist only
- Nephrotic: treat glomerulonephritis; albumin infusion occasionally used in hospital
- Hypertonic saline is absolutely contraindicated in hypervolaemic hyponatraemia
3% hypertonic saline (hospital emergency only)
- 2 mL/kg (up to 150 mL) IV over 20 minutes — repeat twice if still seizing
- Target: raise Na⁺ by 5 mmol/L rapidly to abort seizure; then slow rate
- ICU monitoring required; check sodium every 4–6 hours
Treat the endocrine cause first — sodium self-corrects
- Adrenal insufficiency: hydrocortisone 20mg mane + 10mg midday (maintenance); 100mg IM in crisis
- Hypothyroidism: levothyroxine titrated to normal TSH — Na⁺ corrects as thyroid function normalises
- Never restrict fluids in Addison's — will precipitate haemodynamic collapse
Select patient characteristics — management approach appears below
"I'd like you to limit all fluids to a total of 1.5 litres a day — that includes everything: water, tea, coffee, soup, even ice cream. A standard coffee mug is about 250ml, so roughly six mugs total."
Fluid restriction is the single most commonly failed intervention in SIADH — patients return with same sodium because they didn't count all fluid sources. Explain soup, jelly, and fruit count.
"The drip we're giving you contains a salt solution similar to what's naturally in your blood — it will help restore the fluid balance your body has lost. We'll be checking your blood results regularly to make sure we're correcting this at a safe speed."
SCA pearl: in volume-depleted hyponatraemia, giving 0.9% NaCl raises sodium by restoring volume — NOT by adding sodium directly. The kidney then excretes free water, raising Na⁺. Understanding the mechanism is examined.
"This powder works by giving your kidneys more 'cargo' to carry out in the urine — this allows them to remove excess water more effectively. Mix it in fruit juice and take it with food to reduce any nausea."
Oral urea is endorsed in the European 2014 hyponatraemia guidelines as second-line for chronic SIADH. It is underused in UK primary care but increasingly mentioned in MRCGP curricula. Initiate under specialist guidance.
"This medication works differently — it blocks the hormone that makes your kidneys hold onto water, so you'll pass more urine than usual, which helps dilute less of the salt in your blood. It's important you only drink when you're thirsty and don't force fluids."
Tolvaptan is a high-yield SCA topic: candidates frequently asked whether they would prescribe it for heart failure hyponatraemia — the answer is no (EVEREST trial showed harm). Licensed only for cirrhosis and SIADH in UK.
"This replaces a hormone your body isn't making enough of — it's not a steroid in the gym sense. You'll need to increase the dose if you're unwell, having surgery, or under significant physical stress. Always carry your steroid emergency card and wear a medical bracelet."
Sick day rules are essential counselling in Addison's: double the dose for 48h when febrile, vomiting, or having significant physical stress. Give IM hydrocortisone emergency kit to all Addison's patients and train them and a family member to use it.
"This tablet replaces the thyroid hormone your body isn't making enough of. Take it first thing in the morning on an empty stomach, at least 30 minutes before food. Don't take it within 4 hours of iron tablets or calcium supplements as they can block absorption."
Always check cortisol before starting levothyroxine in a patient who might have panhypopituitarism. Thyroxine in an untreated adrenal-insufficient patient can precipitate life-threatening Addisonian crisis by increasing cortisol metabolism. This is a classic SCA exam scenario.
Driving & Road Safety
Hyponatraemia causes cognitive impairment and slowed reaction times equivalent to a blood alcohol level of 50mg/100mL. Patients with Na⁺ <130 may be unsafe to drive.
DVLA guidance: patients should not drive while cognitively impaired. If confusion is present, advise to stop driving and notify DVLA. Hyponatraemia from Addison's or hypothyroidism requires DVLA notification.
Document advice clearly in notes. Advise in writing. DVLA medical enquiries: 0300 790 6806.
"While your sodium is this low, I'd recommend not driving until we've corrected it and rechecked — the confusion and reaction time changes make it genuinely unsafe."Work & Cognitive Function
Even Na⁺ 130–135 causes impaired concentration, working memory deficits, and slower processing — significant for roles requiring precision, numeracy, or complex decision-making.
Patients may need temporary reduced duties or sick leave while sodium is being corrected. Document fitness to work assessment. Fluid restriction can cause embarrassment in social work settings.
Long-term: if cause is ongoing (e.g. chronic SIADH from malignancy), occupational health referral may be needed.
"It's worth knowing that the low sodium can make it harder to concentrate at work — it's nothing to do with your intelligence, it's a physical effect. Things should improve as we correct it."Falls, Balance & Fracture Risk
Hyponatraemia is an independent, dose-dependent risk factor for falls and osteoporosis. Na⁺ <135 chronically reduces bone mineral density and impairs neuromuscular coordination.
Refer to falls prevention service. Ensure vitamin D and calcium assessed. Consider DEXA scan if chronic hyponatraemia has been present for more than 1 year. Mobility aids if unsteady.
Document fall risk assessment at every review. Consider referral to physiotherapy for balance rehabilitation.
"The unsteadiness you've been having is linked to the low sodium — it genuinely doubles the risk of a fall. Once we get your levels up, your balance should improve, but let's also arrange some physio to be safe."Medication Changes & Mental Health
Stopping an SSRI for hyponatraemia at a psychologically vulnerable time creates a complex dilemma. Abrupt SSRI withdrawal causes discontinuation syndrome and may worsen depression.
Never abruptly stop SSRIs — taper over 4–8 weeks. Offer mirtazapine as the lowest SIADH-risk alternative. Coordinate with mental health team if the patient has a serious mental illness.
Monitor mental state during the switch period. Safety-net specifically around mood as well as sodium.
"I know stopping the antidepressant feels worrying at a time when things aren't easy — we won't just take it away; we'll switch you to a safer option and make sure your mental health is supported through this."Fluid Restriction & Social Life
A 1.5-litre fluid restriction is socially restrictive — it affects coffee meetings, restaurant meals, exercise sessions, and the social ritual of sharing drinks. Patients often feel socially isolated by the restriction.
Advise patients to save fluid allocation for social occasions. Acknowledge the restriction is genuinely limiting. Review restriction regularly — aim to relax it as sodium normalises.
Provide written information about the restriction with a practical guide to measuring 1.5 L — most patients underestimate what this looks like.
"I know 1.5 litres a day sounds very restrictive — it's about six mugs of tea total. It won't be forever, and I'll review it as soon as your sodium starts coming up."Cognitive Symptoms & Dementia Fear
Confusion and memory impairment from hyponatraemia closely mimic early dementia — and patients (and families) are often terrified by this. Normalising this as a reversible electrolyte effect rather than early Alzheimer's is deeply reassuring.
Explain explicitly that the cognitive symptoms should reverse as sodium corrects. Arrange formal cognitive reassessment (MMSE/MoCA) at follow-up once sodium is normal to document recovery.
If cognitive symptoms persist after sodium normalises, then dementia workup is appropriate.
"The confusion you're experiencing is very likely coming from the low sodium, not from your memory failing — it is reversible. We'll do a proper memory assessment once your sodium is corrected to confirm this."24–48 hours (same week if managed in primary care)
Repeat Na⁺ to confirm no further fall and document rate of change. Assess whether outpatient management remains safe or whether inpatient escalation is needed. Review whether causative drug has been stopped and whether symptoms have improved or worsened.
5–7 days (1 week review)
Repeat Na⁺ and U&E. Confirm causative drug has been withheld. Check fluid restriction adherence. Review investigation results (cortisol, TFTs, urine studies). Reassess symptom burden, falls, and cognitive function. Escalate if sodium has not risen by at least 3–5 mmol/L.
2–4 weeks
Confirm sodium has normalised or reached safe stable level (>130). Review investigation results and cause. If SIADH unexplained: urgent specialist referral. If drug-induced and stopped: confirm Na⁺ has corrected. Begin relaxing fluid restriction if indicated. Reassess cognition, driving, and functional capacity.
3 months
Post-resolution review: confirm Na⁺ stable. Review specialist letters if referred. Confirm drug substitution established (e.g. mirtazapine in place of SSRI). Reassess ongoing risk factors — is the patient on any new thiazide or NSAID? Document cognitive recovery. Arrange DEXA scan if chronic hyponatraemia confirmed.
Annually (if underlying cause ongoing)
Annual medication reconciliation for all patients with previous hyponatraemia — specifically check for new thiazides, SSRIs, or NSAIDs. Annual Na⁺ check in patients with chronic SIADH, HF, or cirrhosis. Annual bone density review if chronic hyponatraemia has been present. Renal function and cortisol in Addison's patients.
Memory rule — the 10/18 correction rule
Correct sodium by no more than 10 mmol/L in the first 24 hours and no more than 18 mmol/L in the first 48 hours. In patients with high ODS risk (alcoholism, malnutrition, hypokalaemia, liver disease, Na⁺ <120 for >48h), target an even slower rate of 6–8 mmol/L/24h. Check sodium every 2–4 hours in hospital during active correction. Check sodium at 24h and 48h if managing in primary care. If sodium rises too fast, give desmopressin 2mcg IV + 5% glucose to slow correction (hospital only).
⚠ Three scenario-specific phrases — use these verbatim
Why safety-netting matters beyond clinical care
- Closing without summarising the agreed plan
- Not asking a closing question ("Is there anything else?")
- Leaving without naming the 999 symptoms explicitly
- Stopping SSRI without transition plan or mental health safety-net
- Not mentioning the ODS risk to a patient who may attend other services
- Prescribing fluid restriction without written guidance or follow-up plan
- Correct cause identified (drug, volume, hormone, dilutional)
- Causative drug stopped and alternative offered
- Fluid restriction or appropriate treatment initiated
- Monitoring plan (Na⁺ in 5 days) established
- Referral made where appropriate (unexplained SIADH, Addison's, Na⁺ <125)
- All three ICE domains explored (Ideas, Concerns, Expectations)
- Diagnosis explained in plain language with analogy
- Patient's specific fear (dementia, cancer) addressed directly
- Shared decision-making demonstrated (negotiated plan, not imposed)
- Closing question asked and patient given opportunity to ask questions
- Safety-netting delivered specifically, not generically
Who you are
You are Margaret, a 74-year-old retired school librarian who lives alone since her husband died two years ago. You were started on sertraline 50mg six weeks ago for bereavement-related depression by your GP. You also take bendroflumethiazide 2.5mg for blood pressure and amlodipine 5mg. Your daughter brought you in today because she noticed you seemed "not quite yourself" this week.
Hidden agenda
Your primary fear, which you won't volunteer unless sensitively asked, is that the confusion and forgetfulness you've noticed are the early signs of dementia — the same illness your mother had. You haven't told your daughter this fear. You also feel embarrassed about the confusion because you were a librarian and "used to be very sharp." If the doctor addresses dementia specifically and explains the sodium is reversibly affecting your thinking, you feel enormously relieved.
Symptoms if asked directly
- Fatigue: yes, very tired for two weeks, needing afternoon naps
- Nausea: mild, especially in the mornings
- Confusion/memory: you've been leaving the kettle on and forgetting words mid-sentence (very distressing)
- Falls: nearly fell getting up from a chair two days ago; no actual fall
- Seizure: no
- Urine: normal colour; possibly passing more than usual
- Appetite: reduced, eating mainly tea and toast; not much protein
- Alcohol: one small glass of wine with supper occasionally
Lifestyle + bonus details
- Fluid intake: probably 3–4 cups of tea, a couple of glasses of water, and some juice — likely 2+ litres daily
- Diet: mainly toast, biscuits, tea; very little meat or protein since her husband died and she's been eating alone
- Social: goes to a local coffee group Tuesdays but has missed it for two weeks because she felt too tired
- BONUS — only reveal if asked about medications: "I also sometimes take ibuprofen for my knee — is that relevant?"
- Drives herself to the GP — don't volunteer this, but confirm it if asked directly
Resolution: The actor is satisfied if the candidate (1) specifically addresses the dementia fear and explains cognitively symptoms are reversible, (2) explains the sertraline and ibuprofen and thiazide connection in plain English without being alarmist, (3) stops the sertraline with a safe alternative offered and explains the medication change rationale, (4) advises on fluid restriction with practical 1.5-litre guidance, (5) addresses driving safety, and (6) gives a specific safety-net including the 999 trigger symptoms. A candidate who completes all five earns the challenge resolution without resistance.
- Seizure or active convulsion
- GCS <13 / acute confusion
- Suspected Addisonian crisis
- Na⁺ <115 any chronicity
- Acute Na⁺ <120 with any symptoms
- Na⁺ 120–129 with mild symptoms
- Rapid fall >10 mmol/L/24h
- New SIADH — cause unknown
- Malignancy suspected
- Post-surgical / hospital-acquired
- Na⁺ 130–135, asymptomatic
- Drug-induced, cause clear
- Chronic, stable, no neuro signs
- Beer potomania or polydipsia
| Drug / Intervention | Test | Timing | Action threshold |
|---|---|---|---|
| Fluid restriction | Na⁺ + weight | Days 2, 5, 7 then weekly | No rise at 5 days → reassess adherence; escalate to specialist |
| 0.9% NaCl (IV hospital) | Na⁺ | Every 2–4h during infusion | Rise >10 mmol/L/24h → slow/stop infusion; desmopressin if needed |
| Hydrocortisone (Addison's) | Na⁺, K⁺, cortisol | Daily × 48h; weekly × 4 weeks; annually | K⁺ >5.5 or ongoing hyponatraemia → dose review; endocrine input |
| Levothyroxine | TSH, Na⁺ | 6 weeks post-initiation; then annually | TSH still high → increase dose 25mcg; Na⁺ should normalise with euthyroid state |
| Tolvaptan (specialist) | Na⁺, LFTs | Every 4h × 24h then daily × 1 week | Na⁺ rise >12/24h → withhold; LFTs ↑ × 3 ULN → stop permanently |
| SSRI switch to mirtazapine | Na⁺, mental state | 1 week post-switch; then 4 weeks | Na⁺ not rising at 1 week → check adherence; if deteriorating mood → urgent review |