Unsteadiness, nausea and a sodium of 122

For three weeks he has been nauseated, mildly headachy and increasingly unsteady. His daughter noticed slowed thinking and two unusual lapses. He has had two near-falls but no seizure, vomiting, collapse or reduced consciousness. These symptoms may be attributable to hyponatraemia and must not be dismissed as mild merely because he is awake.

Sertraline 50 mg daily began six weeks ago. Other medicines are amlodipine, tamsulosin and intermittent paracetamol. He has never taken a diuretic and uses no supplements or recreational drugs. The chronology makes drug-associated SIAD a strong explanation, but not a diagnosis by chronology alone.

He drinks eight or nine mugs of tea plus water daily, unchanged for years. There is no vomiting, diarrhoea, heavy beer intake, oedema, orthopnoea, weight loss, night sweats, new cough, haemoptysis, thyroid history or glucocorticoid exposure. He has a 41 pack-year smoking history.

His wife died ten months ago. He fears that the word ‘confused’ will lead his daughter to place him in a care home. Sertraline has helped him cope, and abrupt withdrawal feels like abandonment. Ask directly about current depression, hopelessness, self-harm or suicidal thoughts, support and who will own follow-up if the drug is stopped.

Pulse 78, BP 138/76 lying and 134/74 standing, respiratory rate 16, oxygen saturation 96% on air, temperature 36.7°C, glucose 5.2 mmol/L. He is alert and orientated but scores 8/10 on an abbreviated cognitive screen. Gait is broad-based and hesitant; there is no focal deficit, cerebellar syndrome, papilloedema or seizure activity.

The absence of coma or seizure does not make persistent nausea, headache and cognitive change benign. They fit the Society for Endocrinology category of moderately severe symptoms if attributable to hyponatraemia.

JVP is visible and not raised, mucous membranes are moist, capillary refill is normal, there is no postural drop, oedema, ascites or clinical heart failure. He appears euvolaemic, while acknowledging that bedside volume assessment is imperfect.

No goitre, hyperpigmentation, lymphadenopathy, clubbing, focal chest finding, organomegaly or signs of cirrhosis. These negatives refine probability but do not independently establish SIAD or exclude malignancy.

Serum sodium 122 mmol/L, potassium 4.1, serum osmolality 254 mOsm/kg, urine osmolality 486 mOsm/kg and urine sodium 58 mmol/L. Creatinine, glucose, lipids, protein, liver profile and calcium do not suggest pseudohyponatraemia or a major renal, hepatic or hyperglycaemic explanation.

This is hypotonic hyponatraemia with inappropriately concentrated urine in an apparently euvolaemic patient. Interpret urine results with medicines, recent fluids and clinical context.

TSH and free T4 are normal. A 09:00 cortisol of 465 nmol/L is reassuring only in its assay and clinical context; seek endocrine advice or dynamic testing if adrenal insufficiency remains plausible. Chest radiograph is clear. Do not convert a normal radiograph into an automatic cancer exclusion, nor order CT solely because sodium remains low without reassessing the whole case.

This is symptomatic hypotonic hyponatraemia with persistent nausea, headache, cognitive change and gait instability, probably chronic over weeks. Sertraline-associated SIAD is the leading cause after initial assessment, but symptom severity and safe correction take priority over proving the cause.

Recommend admission to a monitored setting, urgent senior/endocrine input and treatment under the current local hypertonic-saline protocol. The Society for Endocrinology pathway uses controlled 3% sodium chloride boluses for severe or moderately severe symptoms, with an early small rise rather than normalisation as the goal. Use the local protocol for preparation, delivery and sampling rather than improvising a regimen.

Record neurological status and sodium before treatment, recheck frequently and set explicit correction ceilings. Be ready to stop or reverse excessive correction under specialist direction. Chronicity, malnutrition, alcohol excess, hypokalaemia and liver disease alter osmotic demyelination risk. Treat the patient and the trajectory, not a target of ‘138’.

At the same time confirm medicines, repeat paired samples when appropriate, assess thyroid and adrenal function, and investigate pulmonary, neurological or malignant causes only when history, examination or persistence after drug withdrawal justifies them.

Withhold sertraline as a likely contributor and discuss alternative depression care with the GP or liaison team. Check for withdrawal and self-harm risk. Later fluid management must be individualised to cause and response; do not give reflex isotonic saline to an apparently euvolaemic SIAD pattern, and do not present a fixed one-litre restriction as universal.

Explain that the low sodium is a treatable reason for his unsteadiness and slowed thinking. Admission is intended to protect independence, not remove it. Agree who will update his daughter and who will review mood treatment.

Escalate immediately for seizure, reduced consciousness, vomiting, worsening headache, new focal neurology, cardiorespiratory instability or an unexpectedly rapid sodium rise. Handover symptom severity, likely duration, volume assessment, paired osmolalities, medicines, treatment already given, sodium trajectory, next sample and correction ceiling.

This is severe symptomatic hyponatraemia: immediate ABC care, monitored hypertonic-saline protocol, senior/endocrine/critical-care help and frequent sodium checks. Do not delay therapy for final cause classification.

The cause and fluid strategy change. Restore circulating volume under monitored guidance and anticipate rapid water diuresis and overcorrection once antidiuretic drive switches off.

The kidney is appropriately suppressing antidiuretic hormone. Reassess primary polydipsia and low-solute intake, quantify intake and anticipate rapid autocorrection when the driver changes; do not call this SIAD.

Stop active correction, seek immediate expert help and use the local overcorrection-rescue pathway. Document timing, fluids, urine output and every sodium result.

Strong: Recognises moderately severe symptoms and treats promptly under a monitored protocol.

Incomplete: Identifies SIAD but starts only cause-directed therapy.

Unsafe: Waits for seizure before considering hypertonic saline.

Strong: Combines volume state, paired osmolalities, urine sodium and exclusions.

Incomplete: Calls the pattern SIAD from sertraline timing alone.

Unsafe: Gives generic fluid advice without classifying the patient.

Strong: States monitoring, correction ceilings and an overcorrection plan.

Incomplete: Says ‘correct slowly’ without numbers being protocol-led or tracked.

Unsafe: Targets rapid normalisation.

Strong: Connects treatment to preserving independence and provides mental-health continuity.

Incomplete: Stops sertraline without exploring what it means to him.

Unsafe: Dismisses grief, capacity or self-harm risk.