Here's a report published in the British Medical Journal about my case - seems I was quite a find! There's a lot
of medical terminology in there, so feel free to highlight the easier to understand bits by clicking the button below.
An 11 year old, tall boy presented with symptoms typical of pituitary apoplexy. A large necrotic and
haemorrhagic tumour was removed, which was shown to be an adenoma secreting growth hormone and prolactin.
Subsequent treatment comprised cranial irradiation and hormone replacement. Eighteen months after operation
growth was static and plasma growth hormone and prolactin concentrations were undetectable.
Pituitary apoplexy is caused by infarction or haemorrhage, or both, into a pituitary tumour. The symptoms
and signs are usually typical, with the sudden onset or worsening of headache, vomiting, visual
deterioration, fever, drowsiness, and coma. There may be evidence of previous pituitary dysfunction such
as acromegaly, Cushing's syndrome, or hyperprolactinaemia. The condition commonly presents as a
neurosurgical emergency requiring prompt decrompression of the pituitary mass to restore vision. This
decrompression not only relieves pressure on vital intercranial structures but also confirms the presence
of a haemorrhagic necrotic tumour characteristic of the condition. Pituitary apoplexy has been reported
as occurring in 5-10% of patients with pituitary tumour.
We report results of clinical and endocrine studies in a tall boy who developed symptoms of acute raised
intracranial pressure after pituitary apoplexy associated with a pituitary adenoma secreting growth hormone
An 11 year old boy presented with severe frontal headache, vomiting, fever, and blurred vision of 12 days'
duration. Intermittent headaches over several months had been treated as migraine. Rapid growth had started
at age 8, but the rate had slowed during the previous year. On examination he was tall (169cm; +3SD over
the normal mean), but there no obvious signs of acromegaly. He was pale, febrile, yet fully conscious.
He had decreased visual acuity, bilateral optic atrophy, and a bitemporal hemianopia. Blood pressure
was normal. There was no gynaecomastia, but he had galactorrhoea on expression; he was in early puberty. The
cerebro-spinal fluid was normal.
Radiography of the skull showed an enlarged pituitary fossa; computed tomography showed a mass that
enhanced homogeneously, filling much of the pituitary fossa, with some suprasella extension.
Preoperative serum thyroxine concentration was 57 nmol/l (4.4ug/100ml) (normal 60-150 nmol/l (4.7-11.7 ug/100ml));
triidothyronine 1.2 nmol/l (0.8ng/ml) (normal 1.2-3.1 nmol/l (0.8-2.0 ng/ml)); thyroid stimulating hormone
< 2.5mU/l (normal <5mU/l) diurnal plasma cortisol < 28 nmol/l (<1.0ug/100ml); random serum growth hormone
during sleep 1.8mU/1; and plasma testesterone 1.4 nmol/l (0.4 ng/ml) (prepubertal). There was no response to
thyroid stimulating hormone, gonadotrophin, or prolactin to combined stimulation with thyroid releasing hormone
and leteinising hormone releasing hormone. The table shows the plasma glucose, insulin, and growth hormone
concentrations in response to an oral glucose load (1.75g/kg). Glucose tolerance was normal with an early,
exaggerated insulin response at 30 minutes; growth hormone concentration were consistently low.
A large necrotic and haemorrhagic pituitary tumour that compressed the optic nerves on both sides was removed via
a right frontotemporal craniotomy. Histological examination showed an acidophillic adenoma with numerous foci of
calcification. Immunoperoxidase staining was positive for growth hormone and prolactin antibodies. His
vision recovered postoperatively. He was given cranial irradiation and hormone replacement treatment with
desmopressin, thyroxine and cortisone acetate. Growth was static 18 months after surgery, and plasma growth hormone
and prolactin concentrations were undetectable.
Plasma concentrations of glucose, insulin, and growth
hormone in response to oral glucose load of 1.75 g/kg (75g)
Pituitary apoplexy associated with gigantism in childhood is rare.
Our patient is the youngest patient with pituitary apoplexy to have been
reported on. Impairment of the infundibular circulation by impaction of the
of the enlarging tumour at the diaphragmatic notch may cause infarction or
haemorrhage, or both, into the pituitary gland.