PITUITARY ADENOCARCINOMA AND CSF RHINORRHOEA

PITUITARY ADENOCARCINOMA AND CSF RHINORRHOEA

Kishore B Sandu*, S B Ogale**, Gautham K***, Vikas Kumar****
*Lecturer; **Head of the Dept.; ***Registrar; ****Resident, Department of ENT, KEM Hospital, Parel, Mumbai 400 012.

Leaking of the CSF from nose is symptom of failed containment of the CSF to its subarachnoid compartment. It indicates a communication with the subarachnoid space and therefore an opening in the arachnoid, dura and bone to permit exit of CSF through the nose. A CSF fistula presenting as rhinorrhoea poses a diagnostic and therapeutic challenge to even the most experienced surgeon.

Here we present an interesting case of CSF rhinorrhoea (CSFR) which was through an extensive break in the sphenoid sinus in a patient who was operated for a pituitary tumour followed by radiotherapy.

55 year old Mr. DS presented in September 1994 to the Department of Neurosurgery in our institution with generalised headache since 10 years. He had poor vision in the left eye and was diagnosed to be having primary optic atrophy. Immediately after admission he became blind in the left eye. Vision in the right eye was 6/24. He was also noticed to have partial third nerve weakness. An urgent CT scan showed a large enhancing mass in the sellar and parasellar region, causing severe destruction of bone and extending superiorly up to the third ventricle. The patient was taken for an urgent exploration and left frontal craniotomy was performed. Intraoperatively the tumour was seen underneath the second and third nerves and the temporal lobe. Third nerve was severely compressed between the tumour displaced to the opposite side and the cavernous was ballooned due to tumour infiltration. Due to these findings only a partial excision of the tumour was done and the specimen sent for histopathological examination, which turned out to be an adenocarcinoma of the pituitary gland. The patient then completed radiotherapy in November 1994. He then presented with CSFR with no other neurological deficits about 4 months after completing the radiotherapy.

The neurosurgeons attempted a sublabial, trans-septal closure of CSFR, but the patient continued to have the leakage till he presented to us in March 1999. Clinical and biochemical examination of nasal fluid confirmed CSFR. A dedicated metrizimide CT cisternography revealed a large defect in the superior and lateral wall of the sphenoid sinus with a free flow of the CSF through its ostium.

We planned an endoscopic trans nasal closure of the CSFR. The patient was taken under hypotensive GA. Posterior and inferior portions of the middle turbinate and the posterior bony septum was excised for a wider exposure of the anterior wall of the sphenoid sinus. The mucous membrane of the sphenoid sinus was stripped to bare the bone of the sinus. Fascia lata graft and fat from the thigh was harvested. A large piece of fat and nasal septal cartilage was plugged into the dural defect. The fascia lata graft was enveloped round a piece of Gel foam which facilitated better placement and spreading of the graft. The sinus was packed with the fat and nasal tamponade was given with Merocel.

Postoperatively the patient was given broadspectrum antibiotics, stool softeners, antitussives, acetazolamide. Lumbar puncture or sub-arachnoid catheter was not advocated. The Merocel pack was removed after 10 days and the patient was advised light work for three months. Patient has been asymptomatic for 6 months and in view of his extensive lesion a repeat cisternography was done which did not show any evidence of CSFR.

The aetiology of CSFR can be divided into traumatic and spontaneous causes. In order to enter the nose the CSF must successfully cross the arachnoid, the duramater, the bone plate and then the soft tissues of the nose and the paranasal sinuses. CSF may enter the nose through the cribriform plate, the ethmoidal roof, sphenoid sinus, posterior wall of the frontal sinus and the petrous ridge into the middle ear and into the nose through the eustachian tube. The dura is tightly adhered at the thin cribriform plate and the anterior ethmoid roof, which is the commonest site for the CSF leak.

In non traumatic cases the leakage is more obscure and may be associated with pituitary tumours, meningiomas, AV malformations or any inflammatory diseases. We have observed that there is always a vague history of trauma many years prior to a spontaneous leak or the patient may be having a history of recurrent attacks of meningitis. Raised intracranial pressure and the pulsating brain matter contribute to the breaking of an incomplete fracture line followed by a CSF leakage. Johnston believed that a persistent remnant of a craniopharyngeal canal provided a channel for spontaneous leaks. In this case report we present an interesting case of a patient who had CSFR due to the primary cause of pituitary adenocarcinoma. The diagnosis of this was made by a detailed clinical examination, biochemical analysis of nasal fluid and more importantly documenting by a metrizimide CT cisternography. The sinus endoscope has been put to its maximum utility in closure of this CSFR which otherwise would have required an extensive neurosurgical intervention which had failed on a previous occasion.

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