Which ONE of the following is a cause for pseudohyponatraemia?
Answer: C Pseudohyponatraemia is hyponatraemia in the setting of normal plasma osmolality (POsm 275–295). High levels of plasma proteins and lipids increase the non-aqueous and non-Na+ containing fraction of plasma which analysers misread as a factitious lower value of [Na+ ] than the serum truly contains. Hence, a pseudohyponatraemia. It is also known as factitious hyponatraemia. Causes of pseudo or factitious hyponatraemia include hyperlipidaemia and hyperproteinaemic states such as multiple myeloma and Waldenstrom macroglobulinaemia.
Hyperglycaemia causes a hypertonic hyponatraemia (POsm > 295) by causing water to move from the ICF to the ECF. This causes a subsequent decrease in [Na+ ]. The corrected Na+ can be calculated by the formula:
Sodiumcorrected = glucose (mmol/L)/3.5 + measured [Na+ ]
SIADH and liver cirrhosis are both causes of hypotonic hyponatraemia (POsm < 275).
Reference:
Which ONE of the following is NOT one of the criteria required in making a diagnosis of SIADH?
Answer: D: SIADH is generally a diagnosis of exclusion. It is a cause of euvolaemic hypotonic hyponatraemia, though some patients may have slightly increased ECF volume, however, are generally not clinically fluid overloaded. Total body sodium is nearly normal despite the presence of hyponatraemia. SIADH is characterised by six criteria:
The most common causes of SIADH can be categorised into three groups:
Malignant causes:
Pulmonary causes:
Neurological causes:
References:
A 68-year-old man is brought in seizing from a nursing home. His initial [Na+ ] on a venous blood gas is found to be 176 mmol/L.
Which ONE of the following drugs may be responsible for this finding?
Answer: B: This man is likely to be seizing due to his elevated sodium concentration. Hypernatraemia is defined as a serum sodium of >150 mmol/L and can be caused by either a decrease in total body water or, less likely, from an increase in sodium load (decreased excretion or increased intake). It has a high mortality rate of around 50% due to the combination of both the effects on the body of hypernatraemia, and due to the severity of the underlying disease itself. Nearly all hypernatraemia seen in the ED is due to volume depletion. However, overly rapid correction (unless acute hypernatraemia) can be almost as harmful, leading to cerebral oedema, further seizures and permanent neurological sequelae.
Diabetes insipidus is one of the causes of hypernatraemia seen in the ED. This disease can cause marked hypotonic urine excretion and consequently significant total body water loss, leading to severe dehydration particularly in the elderly. Causes of diabetes insipidus may be central or nephrogenic. Central causes include tumours, trauma or idiopathic, and nephrogenic causes include drugs, renal disorders, haematological and familial disorders.
Lithium is a drug well known for causing nephrogenic diabetes insipidus.1 Consequently, morphine, NSAIDs and carbamazepine are all drugs that have the potential to cause a euvolaemic hyponatraemia.
Which ONE of the following treatments is NOT recommended in the treatment of hypercalcaemia?
Answer: A: The normal total serum calcium concentration is 2.15–2.55 mmol/L, and hypercalcaemia can be defined as a level higher than this. It is a relatively common condition with more than 90% of causes being attributed to hyperparathyroidism or malignancy. Treatment should be initiated in any symptomatic patient or if the [Ca2+ ] is >3.5 mmol/L. There are four primary treatment goals:
Hydration replaces the ECF volume thereby diluting the calcium concentration and increasing calcium clearance. Normal saline is the fluid of choice, and Hartmann’s solution or colloids are best avoided as they contain calcium.
Enhanced renal excretion, though a modest effect, is achieved by the use of loop diuretics such as frusemide once the patient is adequately hydrated. Thiazide diuretics should be avoided as they actually enhance calcium reabsorption in the distal convoluted tubule. While they rarely cause hypercalcaemia in isolation as the result of this enhanced reabsorption, thiazide diuretics can unmask hypercalcaemia due to other causes.
In the treatment of hypercalcaemia, corticosteroids assist only in a selected population of patients such as haematological malignancies, vitamin D toxicity and sarcoidosis. Generally, it is an ineffective treatment for hypercalcaemia due to solid tumour cancers (though breast cancer may be an exception).
Bisphosphonates inhibit osteoclast activity and therefore reduce mobilisation of calcium from bone.
A 53-year-old woman is brought to the emergency department (ED) with confusion. Her only past medical history is that of breast cancer. Her serum calcium level has returned as 3.63 mmol/L.
Which ONE of the following would you NOT expect to see during her ED work-up?
Answer: D: Hypercalcaemia should be immediately considered as one of the potential causes of this patient’s confusion. It can cause a wide range of disturbances of the neurological, gastrointestinal, cardiovascular, renal and musculoskeletal systems. Signs and symptoms expected to be seen include all of confusion, polyuria, hyporeflexia and constipation. The rhyme: stones (urinary calculi, polyuria, polydipsia), bones (bony pain), groans (abdominal pain from constipation, peptic ulcer disease, pancreatitis) and psychic moans (confusion, irritability, hallucinations) can be used to easily remember the key clinical features of hypercalcaemia.
The ECG abnormalities of hypercalcaemia include depressed ST segments, widened T waves, and shortened ST segments and QTc segments. It can progress to bradyarrhythmias, bundle branch blocks and eventually complete heart block. It is hypocalcaemia that causes a prolonged QTc.
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