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Nausea and vomiting in a patient with increasing thirst

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Q1: Describe the finding on computed tomography and MRI and give a differential diagnosis

Enhanced axial computed tomography of the brain with iodine based contrast (iodine 300 mg I/ml) demonstrates a 1.5 cm diameter enhancing lesion in the suprasellar cistern involving the pituitary stalk.

The supplementary T1 weighted MRI scan with gadolinium DPTA enhancement shows this lesion to be based in the pituitary stalk with involvement of the floor of the hypothalmamus. There was preservation of the normal high signal in the posterior pituitary gland.

In a patient with known breast carcinoma this would represent a pituitary stalk metastasis. For radiological differential diagnoses see table 1.1

Table 1

Radiological differential of a suprasellar mass

Q2: What three simple biochemical tests would you perform, and what result would you expect and why?

The simple biochemical tests would be a serum urea and electrolytes, a corrected serum calcium, and osmolality of the serum and urine. The anticipated finding on the serum urea and electrolytes would be a raised sodium, because of the dehydration of the polyuria. You may have expected the serum calcium to be raised from the history of breast cancer due to either skeletal metastases or secondary to chemotherapy. The raised calcium could contribute to a potential nephrogenic diabetes insipidus.

On the osmolality testing you would have suspected a normal to high serum osmolality and a low urine osmolality.2

A serum fasting blood glucose would be another reasonable biochemical investigation. For biochemical results in our patient see table 2.

Table 2

Biochemical results in patient studied

Q3: What special biochemical test would you perform, and what result would you expect and why?

To confirm the clinical diagnosis of cranial diabetes insipidus you should perform a water deprivation test, demonstrating that the urine does not become more concentrated as serum becomes more concentrated. When desmopressin 20 μg is given intranasally you would expect the urine osmolality to increase at least approximately 1.5 times, confirming a cranial cause for the diabetes insipidus. If it does not increase after desmopresssin one’s suspicion of a nephrogenic cause is strengthened considerably. For causes of diabetes inspidius see table 3.1,3,4

Table 3

Causes of cranial diabetes insipidus

This was not performed in our patient as the imaging demonstrated a lesion in an appropriate site for a cause of cranial diabetes insipidus.

Q4: How does the anatomical location succinctly explain the symptoms?

The pituitary stalk lesion extends from the hypothalamus and floor of the third ventricle. The stalk lesion will cause pressure effects on axons coursing from the supraoptic nucleus and paraventricular nucleus of the hypothalamus to the posterior pituitary. This will interfere in the axonal flow of antidiuretic hormone and its carrier protein to the posterior pituitary, hence explaining in part the diabetes insipidus despite a normal appearing posterior pituitary gland on MRI. As the lesion extends up into the hypothalamus, it will involve the suproptic nucleus directly.

Adjacent in the hypothalamic region are the satiety centre in the ventromedial nucleus and regulation of hunger from the dorsomedial nucleus. The blood supply to the pituitary stalk and pituitary is different from the rest of the brain, it has a portal circulation from the hypothalamus (particularly the arcuate nucleus) that is essential for the neuroendocrine regulation of the anterior pituitary, with a systemic arterial supply the inferior, middle, and superior hypophyseal arteries from the cavernous and supraclinoid portions of the internal carotid artery. Thus metastases are more common here, particularly the pituitary stalk and posterior pituitary.5 Because of the neuroendocrine function of the pituitary and its stalk, there is an absence of the blood-brain barrier, hence explaining why metastases can present here earlier than the remainder of the brain.3,5

Final diagnosis

Cranial diabetes insipidus.

Acknowledgments

The author thanks Mr J Summerlin, superintendent radiographer, CT scanner, Nottingham City Hospital.

References

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