Sodium Disorders — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Margaret Chen, 78 years old. [1]

Presenting complaint: Brought to the emergency department by ambulance after a fall at home. Her daughter reports five days of progressive drowsiness and confusion, with decreased oral intake. She did not lose consciousness with the fall and has no head injury, but she has been unable to walk safely. [1]

Past history:

• Hypertension for 20 years
• Osteoporosis (wrist fracture 3 years ago)
• Mild cognitive impairment (MoCA 22 last year)
• Cholecystectomy 10 years ago
• No known allergies [1]

Current medications:

• Hydrochlorothiazide 25 mg daily — commenced 3 weeks ago by her GP for a blood pressure of 158/92
• Amlodipine 5 mg daily
• Alendronate 70 mg weekly
• Calcium and vitamin D
• Paracetamol as needed [1]

Social history: Widowed, lives alone, normally independent in activities of daily living. Her daughter visits daily. Does not smoke, drinks alcohol rarely. [1]

Examination findings (trainee elicits):

• Alert but drowsy, GCS 13 (E4 V4 M5). Oriented to name only.
• Dry mucous membranes, reduced skin turgor.
• HR 92, BP 142/78 lying, 118/66 standing. JVP low.
• Cardiovascular: no apex displacement, no added sounds.
• Respiratory: clear.
• Abdomen: soft, non-tender, no organomegaly, no ascites.
• No peripheral or sacral oedema.
• Neurological: no focal deficits, no asterixis, GCS 13. No signs of head injury.
• No buccal or palmar crease pigmentation. [1]

Investigations:

• Na 116 mmol/L, K 2.9 mmol/L, Cl 82, HCO3 26, urea 11 mmol/L, creatinine 95, glucose 6.2
• Serum osmolality 248 mOsm/kg
• Urine osmolality 380 mOsm/kg, urine sodium 48 mmol/L, urine potassium 26
• TSH 3.1 mU/L, free T4 14 pmol/L
• Morning cortisol 480 nmol/L
• FBC normal, LFTs normal
• ECG: sinus rhythm, minor ST changes, QTc 470 ms
• CT brain (done for the fall and confusion): no acute haemorrhage, mild chronic small vessel disease, no fracture [1]

Candidate's structured presentation (model)

Opening statement (SASPOP format): [1]

"Mrs Chen is a 78-year-old widowed woman with a background of hypertension, osteoporosis, and mild cognitive impairment, who presents with five days of progressive confusion and drowsiness culminating in a fall, on a background of severe hyponatraemia from a thiazide diuretic commenced by her general practitioner three weeks ago. [1]

Her main problems are:

1. Severe hypotonic hyponatraemia — sodium 116 — with cerebral symptoms, and competing risks of cerebral oedema versus osmotic demyelination
2. Thiazide-induced hyponatraemia — the drug is the cause, confirmed by the renal salt-wasting pattern in a volume-depleted patient with a normal cortisol
3. Hypovolaemia with a postural drop and prerenal urea
4. Hypokalaemia — 2.9 — which contributes to the hyponatraemia and raises the osmotic demyelination risk
5. A fall on a background of cognitive impairment — assess for injury, distinguish delirium from dementia, and address the postural hypotension
6. Polypharmacy and the need for an alternative antihypertensive
7. Osteoporosis with an ongoing falls risk [1]

Her dominant clinical threats are, in order: cerebral oedema if her conscious state deteriorates, osmotic demyelination if I correct too fast given her hypokalaemia and age, and the consequences of the fall. I will manage her with the recognition that sodium disorders are water disorders, that symptom severity not the absolute number drives urgency, and that the correction ceiling is eight to ten millimoles per litre in twenty-four hours." [1]

Investigation summary: [1]

"Her serum osmolality of 248 confirms true hypotonic hyponatraemia — there is no pseudo- or hypertonic component. Her urine osmolality of 380 confirms that vasopressin is inappropriately active, ruling out primary polydipsia and low-solute intake. Her urine sodium of 48 in a clinically volume-depleted patient indicates a renal salt-wasting mechanism — the thiazide — rather than extra-renal loss. Her TSH and morning cortisol are normal, formally excluding hypothyroidism and adrenal insufficiency, the two treatable mimics of SIADH. Her urea of 11 with a normal creatinine reflects prerenal physiology from her hypovolaemia. Her prolonged QTc is consistent with hypokalaemia and warrants ECG monitoring during correction. Her CT brain shows no acute intracranial cause for her confusion, supporting the hyponatraemia as the driver of her encephalopathy. The picture is a textbook thiazide-induced hyponatraemia with hypokalaemia in a vulnerable elderly woman." [1]

Management plan: [1]

1. Immediate — the emergency assessment and the competing-risk framework:

   • Admit to high dependency. Cardiac and neuro-obs.
   • Stop the hydrochlorothiazide immediately and permanently.
   • Secure IV access; set up sodium checks every 2 to 4 hours for 24 hours.
   • Have desmopressin (DDAVP) 1 to 2 micrograms drawn up and available. [1]

2. Correction strategy — symptom-driven, ceiling-bound:

   • If her GCS falls or she seizes: 3% hypertonic saline 100 mL over 10 minutes, repeat up to a maximum of three boluses, target 4 to 5 mmol/L rise in 4 hours.
   • Otherwise: cautious volume repletion with 0.9% saline (she is hypovolaemic), with the expectation that stopping the thiazide and repleting volume will suppress vasopressin and allow a controlled sodium rise.
   • 24-hour ceiling: 8 mmol/L (the lower end — her hypokalaemia and age raise the ODS risk). Target sodium no higher than 124 in 24 hours.
   • 48-hour ceiling: 18 mmol/L.
   • If she overcorrects (sodium rises above ceiling): relower with DDAVP plus 5% dextrose; recreate a controlled hyponatraemia. [1]

3. Correct the potassium:

   • IV potassium chloride, targeting K above 4.0. This both corrects the deficit and itself raises the sodium as potassium moves back into cells and sodium moves out. Continuous ECG monitoring given her prolonged QTc. [1]

4. Confirm the diagnosis formally:

   • Document the response to thiazide cessation and volume repletion.
   • Repeat urine osmolality and sodium during correction.
   • A short Synacthen test only if the morning cortisol had been borderline (480 is reassuringly normal in the acute setting). [1]

5. Address the fall and cognitive state:

   • Once the sodium has stabilised and delirium has resolved, reassess cognition — distinguish the reversible delirium of hyponatraemia from her underlying mild cognitive impairment.
   • Formal falls assessment: orthostatic blood pressures (she has a postural drop), medication review (amlodipine contributes), vision, gait, home safety.
   • Occupational therapy and physiotherapy input.
   • Reassess her blood pressure targets — she may have been over-treated. [1]

6. Long-term hypertension management:

   • Switch from the thiazide to an ACE inhibitor (perindopril) or a calcium channel blocker, recognising her postural hypotension and fall risk.
   • Document the thiazide adverse reaction clearly and communicate it to the GP, the patient, and her daughter.
   • Consider a 24-hour ambulatory blood pressure once she is stable to guide targets. [1]

7. Osteoporosis and falls prevention:

   • Continue alendronate, calcium, and vitamin D.
   • Check for an occult fracture from the fall (already done — CT brain negative; consider plain films if any focal pain).
   • Home safety assessment; consider a personal alarm. [1]

8. Communication:

   • Explain to Mrs Chen and her daughter that the new water pill caused the problem, that she must never take a thiazide again, and that the sodium will be corrected slowly to protect her brain.
   • Provide written medication guidance and a thiazide-alert card.
   • Comprehensive discharge summary to the GP with the integrated plan. [1]

Examiner discussion questions

Q1: "Her sodium rose from 116 to 131 in the first 24 hours. What happened, and what do you do?" [1]

"She overcorrected — a rise of 15 millimoles per litre exceeds my eight-millimole ceiling. The mechanism is an autonomous water diuresis after I stopped the thiazide and repleted her volume: once the non-osmotic vasopressin drive was switched off, her kidney excreted the retained free water briskly and the sodium overshot. This is the classic overcorrection pattern in thiazide-induced hyponatraemia, and it is exactly why I was checking her sodium every two to four hours and why I had desmopressin ready. The immediate management is to relower her sodium into a safe range. I give desmopressin 1 to 2 micrograms subcutaneously or intravenously every 8 hours, combined with free water — oral if she can drink, or 5 percent dextrose intravenously. This recreates a controlled hyponatraemic state. I target a sodium in the low 120s. The evidence suggests that prompt relowering reduces the risk of osmotic demyelination. Once she is stable in the target range, I taper the desmopressin and allow a slow, controlled rise within the ceiling going forward. I would also reassess her neurologically and consider an MRI brain if she develops any new focal signs, to look for early osmotic demyelination." [1]

Q2: "Why is hypokalaemia a risk factor for osmotic demyelination, and what is the mechanism?" [1]

"Hypokalaemia raises the risk of osmotic demyelination through two mechanisms. First, potassium depletion impairs the brain's ability to reaccumulate the organic osmoles it shed during chronic hyponatraemia — the astrocytes need normal intracellular potassium to mount the osmolyte reaccumulation that protects them during correction. Second, hypokalaemia itself causes a form of osmotic stress on astrocytes that compounds the stress of rising extracellular tonicity. The clinical implication is that hypokalaemic patients should be corrected more slowly — at the lower end of the 8 to 10 millimole per 24-hour range — and the potassium should be corrected first and concurrently. In Mrs Chen's case, I replaced her potassium aggressively from the outset, both to protect her from ODS and because correcting the potassium itself raises the serum sodium as potassium moves back into cells and sodium moves out." [1]

Q3: "How would your management differ if her morning cortisol had been 180 nmol/L?" [1]

"A morning cortisol of 180 in a sick patient is in the indeterminate range and would not exclude adrenal insufficiency. Cortisol normally exerts tonic inhibition of vasopressin release, so glucocorticoid deficiency produces a syndrome biochemically indistinguishable from SIADH — euvolaemic hyponatraemia with inappropriately concentrated urine and a high urine sodium. I would not wait for confirmation to treat: I would give a dose of intravenous hydrocortisone — 100 milligrams stat — as empirical cover while I performed a short Synacthen test the next morning. If the Synacthen test confirms adrenal insufficiency, she would need lifelong glucocorticoid and, if it is primary adrenal insufficiency with aldosterone deficiency, mineralocorticoid replacement as well. The key point is that missing adrenal insufficiency is fatal, and it is one of the two mimics of SIADH — the other being hypothyroidism — that must be excluded before any patient is labelled with SIADH." [1]

Q4: "Six months later she is well, on perindopril and amlodipine, and her sodium is 138. Her GP asks if she can restart a low-dose thiazide for her blood pressure. What do you say?" [1]

"I would say no, absolutely and permanently. A documented episode of thiazide-induced hyponatraemia is a contraindication to future thiazide use — rechallenge carries a high risk of recurrence, often more severe. The mechanism is an individual susceptibility to the diluting defect and potassium-wasting of thiazides, which persists. I would advise her GP to manage her blood pressure with an ACE inhibitor, a calcium channel blocker, or, given her age and cardiovascular risk, an SGLT2 inhibitor — none of which cause hyponatraemia by this mechanism. If her blood pressure is not controlled on perindopril and amlodipine, I would add a low-dose loop diuretic only if strictly necessary, with electrolyte monitoring, and avoid all thiazides and thiazide-like diuretics including indapamide and chlorthalidone. I would document this clearly and issue her a thiazide-alert card." [1]

DCE Short Case — Volume Status Assessment

Instruction

"Examine this hyponatraemic patient. Assess the volume status and look for signs suggesting the underlying cause. You have 7 minutes for examination and 8 minutes for discussion." [1]

Key signs the patient demonstrates (hypovolaemic model)

• Hands and general: dry mucous membranes, reduced skin turgor over the sternum, no pigmentation, no clubbing, pulse 92 regular.
• Neck: low jugular venous pressure (2 cm), no elevation.
• Cardiovascular: postural blood pressure drop (lying 142/78 to standing 118/66), no apex displacement, no added sounds, no third heart sound.
• Respiratory: clear — no consolidation to suggest a pneumonia-driven SIADH, no crackles to suggest heart failure.
• Abdomen: soft, no ascites, no hepatomegaly, no spider naevi, no caput medusae, no ballotable masses.
• Legs: no peripheral or sacral oedema.
• Neurological: drowsy, GCS 13, no focal deficits, no asterixis. [1]

Presentation template

"I examined this hyponatraemic patient's volume status and looked for signs of the underlying cause. Beginning at the hands, there is no palmar or buccal pigmentation to suggest Addison's disease, the pulse is 92 and regular, the skin turgor is reduced and the mucous membranes are dry. In the neck the jugular venous pressure is low at 2 centimetres. Cardiovascular examination reveals a postural blood pressure drop from 142 over 78 lying to 118 over 66 standing, with no apex displacement and no third heart sound. The respiratory examination is clear, with no consolidation and no crackles. The abdomen is soft with no ascites, no hepatomegaly, and no stigmata of chronic liver disease. There is no peripheral or sacral oedema. Neurologically the patient is drowsy with a Glasgow Coma Scale of 13 but no focal deficits. [1]

In summary, this patient is hypovolaemic, with a postural drop, a low jugular venous pressure, dry mucous membranes, and reduced skin turgor. There are no signs of an oedema-forming state. The absence of hyperpigmentation, hyperkalaemia, and hypotension argues against primary adrenal insufficiency. Given the hypovolaemic picture with a renal salt-wasting pattern on the urine biochemistry, the most likely cause is a thiazide diuretic. I would review the medication chart and check a morning cortisol and TSH to formally exclude the mimics." [1]

Discussion

1. Summarise findings and conclusion: "The patient is hypovolaemic with a renal salt-wasting pattern. The differential for hypovolaemic hyponatraemia divides into extra-renal losses — vomiting, diarrhoea, burns, third spacing — where the urine sodium is under 20; and renal losses — thiazide, loop diuretic, adrenal insufficiency, cerebral salt wasting, bicarbonaturia — where the urine sodium is over 20. Her urine sodium of 48 points to a renal cause, and the medication chart will reveal the thiazide." [1]

2. What signs would have indicated a hypervolaemic cause? "A raised jugular venous pressure, peripheral or sacral oedema, a third heart sound, crackles, and ascites. The hypervolaemic causes are heart failure, cirrhosis, and advanced chronic kidney disease — all oedema-forming states where effective arterial volume is low despite total volume overload, driving non-osmotic vasopressin release and free water retention." [1]

3. What signs would have indicated adrenal insufficiency? "Hyperpigmentation of the palmar creases, buccal mucosa, gums, and recent scars — from elevated pro-opiomelanocortin driving melanocyte-stimulating hormone. Hyperkalaemia and hypotension from mineralocorticoid deficiency in primary adrenal insufficiency. Hypoglycaemia, weight loss, abdominal pain, and salt craving. Secondary adrenal insufficiency from pituitary disease spares aldosterone (the renin-angiotensin axis is intact), so it presents without hyperkalaemia and is easily mislabelled as SIADH — which is why a morning cortisol is mandatory in every euvolaemic hyponatraemic patient." [1]

4. When would you give 3% hypertonic saline? "Only for severe symptomatic hyponatraemia — a seizure, coma, or signs of cerebral herniation — regardless of the absolute sodium value. The regimen is 100 millilitres over 10 minutes, repeated up to a maximum of three boluses, aiming for a 4 to 5 millimole per litre rise in the first four hours. I would not give it for asymptomatic or mildly symptomatic hyponatraemia, where the correction ceiling and the risk of osmotic demyelination dominate. And I would always have desmopressin available to relower if the correction overshoots." [1]

5. How does this patient's cognitive impairment interact with her hyponatraemia? "Hyponatraemia causes or worsens confusion, falls, and cognitive impairment, particularly in the elderly. Her mild cognitive impairment likely lowered her baseline reserve, making her more vulnerable to the encephalopathic effects of the hyponatraemia. The fall may have been both a cause (she became hypovolaemic and postural from reduced intake) and a consequence (the confusion caused the fall). Once the sodium is corrected I must reassess her cognition to distinguish the reversible delirium from her underlying impairment, and address her falls risk before discharge — she is at high risk of further falls and fractures, and her osteoporosis makes the consequences severe." [1]