Case history
Case history #1
A 62-year-old man presents to the accident and emergency department with worsening dyspnoea and peripheral oedema. Past history is relevant for prior myocardial infarction followed by cardiomyopathy with an ejection fraction of 20%. He has been taking an ACE inhibitor, beta-blocker, and furosemide, but he ran out of these medications several days ago. His blood pressure is 100/60 mmHg. Jugular vein distention is present. Chest examination reveals rales to halfway up his lungs, a third heart sound, and a soft systolic murmur. He has minimal ascites and marked peripheral oedema to the knee. Routine electrolyte panel shows a serum sodium level of 125 mmol/L and serum potassium level of 3.6 mmol/L. Serum glucose levels and liver function tests are normal.
Case history #2
A 73-year-old woman presents to the A&E department after a fall in which she sustained a right hip fracture. She has a previous history of hypertension and depression. She is currently taking an ACE inhibitor, chlortalidone, and sertraline. She has been experiencing loss of balance over the past several weeks. Her blood pressure is 130/75 mmHg and her pulse is 82 beats per minute and regular. Other than the fracture to her right hip, physical examination appears normal. Her oral mucosa is moist and skin turgor is normal. She has no oedema. Routine electrolyte panel shows a serum sodium level of 125 mmol/L and serum potassium level of 3.5 mmol/L. Serum glucose levels and liver function tests are normal.
Other presentations
Hyponatraemia can present as a complication of many conditions. Hyponatraemia that occurs in patients with cirrhosis, nephrotic syndrome, or congestive heart failure may present similarly, although this depends on the underlying aetiology.[3] Patients with syndrome of inappropriate antidiuretic hormone (SIADH) may be asymptomatic but have hyponatraemia upon laboratory testing. SIADH can be due to a known or occult malignancy (e.g., small cell lung cancer, gastrointestinal tract cancers), central nervous system disorders (e.g., subarachnoid haemorrhage, meningitis, encephalitis), pulmonary disease (e.g., pneumonia), or other non-specific causes (e.g., medications, pain, nausea, stress, general anaesthesia).[3][4]
Other less common causes of hyponatraemia include primary polydipsia and potomania. Primary polydipsia manifests as acute mental status changes and/or seizures associated with markedly increased water intake over a short period of time. Distinct from other causes of hyponatraemia, a very low urine osmolality is typically present in these patients.[5] Patients may also present with chronic, paucisymptomatic hyponatraemia caused by high fluid intake in the setting of very low solute and electrolyte intake. This can occur in association with heavy beer drinking (beer potomania), inadequate diets (i.e., very low-calorie diets with high fluid intake, including the ‘tea and toast’ diet) or crash diets. In these patients, urine osmolality is intermediate (i.e., not as low as in polydipsia, but not markedly elevated as in SIADH).
Acute, symptomatic hyponatraemia may occur with any of the conditions described above, particularly if, for example, hyponatraemia develops rapidly in patients with euvolemic hyponatraemia caused by a medication or a high fluid intake. This leads to symptoms of cerebral oedema including nausea, vomiting, headache, altered mental status, and ultimately, seizures or coma. This is a medical emergency requiring prompt management.
Use of this content is subject to our disclaimer