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Q1: What further investigations would you perform and how would they help you?
Apart from the routine investigations, serum and urinary osmolality, urinary excretion of sodium, short Synacthen test (for adrenal reserve), and thyroid function would help in distinguishing the various causes of hyponatraemia. Hypovolaemic hyponatraemia (common causes being fluid loss from skin, gastrointestinal tract, respiratory system, third space collections, renal loss, and HIV infection) is characterised by serum osmolality of <280 mosmol/kg and clinical dehydration. Isovolaemic hyponatraemia (common causes being the polydipsias, hypokalaemia, renal failure, hypothyroidism, and adrenal insufficiency) is associated with a serum osmolality of >280 mosmol/kg. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterised by urine osmolality greater than 200 mosmol/kg with a spot urinary sodium >20 mmol/l in the presence of normal adrenal, renal, and thyroid function. A spot urine sodium of <30 mmol/l is suggestive of an extrarenal cause of hypovolaemia.
Q2: What is “short bowel” syndrome and how does it cause hyponatraemia?
“Short bowel” syndrome refers to the clinical sequel as a result of excision of a substantial length of bowel. Sodium homoeostasis in health depends largely on renal regulation of its urinary excretion, thirst, and antidiuretic hormone secretion. Losses of sodium from bowel are small in health. The usual common sources of massive sodium losses are from the intestinal tract and kidneys.1 The pathophysiological consequences depend on extent and site of resection, adaptation and integrity of the remaining bowel, and whether the colon has been preserved or not.2 Patients with jejunostomy have a higher faecal output of water, sodium, and divalent cations and they often need a permanent parenteral supply of saline if their small bowel length is less than 200 cm and “parenteral” nutrition support if they retain <100 cm small bowel. In contrast, 50 cm of the jejunum often suffices for adequate oral nutrition if most of the colon is preserved2 as the colon is believed to take on some small bowel features (especially absorption of salt and water) and result in more efficient fermentation. Ileum and colon avidly absorb sodium against a concentration gradient. In the model of short gut syndrome, the major adaptive change is said to be decreased intestinal flow rate related to delayed gastroduodenal emptying.3
Although hyponatraemia has been classically associated with hypothyroidism, thyrotoxicosis can also precipitate hyponatraemia in patients with short bowel syndrome.
A variety of restorative adaptive mechanisms occur in patients with short bowel syndrome to maintain physiological equilibrium.
Hyponatraemia is a common in-hospital electrolyte abnormality and there should be a reasonable investigation protocol set-up for the work-up of such patients.
Q3: What is the diagnosis here and how did this possibly cause hyponatraemia?
The patient described was clinically dehydrated with a reduced serum osmolality of 248 mosmol/kg and urinary excretion of sodium less than 10 mmol/l. This would be consistent with hypovolaemic hyponatraemia and extrarenal sodium loss. Synacthen test was normal but thyroid function revealed a free thyroxine of 35 pmol/l (normal 9.8–23 pmol/l), a free triiodothyronine of 9.0 pmol/l (normal 3.5–6.5 pmol/l), and a suppressed thyroid stimulating hormone of 0.01 IU/l (normal 0.35–5.5 IU/l) in keeping with thyrotoxicosis. Thyroid antibodies were undetectable.
Hyponatraemia is well recognised in patients with primary hypothyroidism, especially in severe forms4,5 and can also develop in patients with secondary hypothyroidism.5 However, hyponatraemia associated with thyrotoxicosois is rare and very few cases have been described in literature. Thyrotoxicosis is characterised by changes in the cellular content of sodium and potassium while fluctuations in the intracellular fluid composition are less important and less stable. Diurnal urinary excretion, glomerular filtration rate, and excretion of sodium and creatinine has been shown to be increased in mild to moderately severe thyrotoxicosis.6 Thyrotoxicosis is also classically known to be associated with increased intestinal motility and gastric emptying.7 This together with the fact that the patient had ileostomy (short bowel syndrome) probably led to an increase in sodium and water loss through the ileostomy resulting in hyponatraemia. Low urinary sodium excretion further supports the hypothesis that sodium loss was extrarenal, presumably gastrointestinal, and reflects increased bowel activity secondary to thyrotoxicosis (unfortunately, we were not able to quantify sodium loss through the ileostomy).
Thus, we describe a patient with long standing uncomplicated ileostomy and associated new onset thyrotoxicosis which was probably coincidental, but nevertheless instrumental in precipitating the acute onset of hyponatraemia. Hyponatraemia is a common in-hospital electrolyte abnormality. Since its pathophysiology is quite varied, accurate diagnosis of the cause of hyponatraemia is essential for the implementation of correct management. Thus, thyrotoxicosis should be considered in the differential diagnosis when hyponatraemia occurs in patients with short bowel syndromes.
Thyrotoxicosis precipitating hyponatraemia in short bowel syndrome.
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