JRSM >
Volume 94, Number 6 >
Pp. 293-294
Department of Neurosurgery, Hurtswood Park Neurological Centre, Haywards Heath, West Sussex RH16 4EX, UK
Correspondence to: Mr K Ashkan, Department of Neurosurgery, Atkinson Morley's Hospital, Copse Hill, Wimbledon, London SW20 ONE, UK
In a patient with an old head injury, violent nose-blowing can have dangerous consequences.
CASE HISTORY
A man aged 54 had a three-week history of nasal discharge and reduced hearing with pain in the left ear. The earache, accompanied by a sensation of fluid in the ear but no discharge, had begun after an episode of violent nose-blowing. He also had a persistent watery nasal discharge, which he had been trying to relieve by further blowing of the nose. His general practitioner treated him unsuccessfully for otitis, with antibiotics and syringing. A few hours before admission to hospital the patient had become confused and disoriented. In his medical history the only noteworthy incident was a childhood left occipital depressed skull fracture without any intracranial injuries.
One admission to our department the Glasgow Coma Score was 11 (eyes 4, verbal 1, motor 6). He had fluid behind the left tympanic membrane and temperature was 37.3°C; there were no focal neurological deficits. Leaning him forward produced large amounts of watery fluid leakage from his nose.
A computed tomographic scan revealed extensive intraventricular air in the lateral and third ventricles. There was also evidence of previous skull trauma with underlying encephalomalacia in the left occipital region but no base-of-skull fractures (Figure 1). A magnetic resonance scan ruled out a cerebral abscess. There was no evidence of infection in cerebrospinal fluid (CSF) obtained by lumbar puncture. Subsequently, a left mastoidectomy was performed; a CSF fistula was found and repaired and a lumbar drain was left in situ for 5 days. Postoperatively the Glasgow Coma Score improved to 15. There was no further CSF leak, and he was discharged home with strict instructions not to blow his nose.
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COMMENT
The term pneumocephalus—a collection of air within the skull—was coined by Wolff in 19141, but Chiari in 1884 was the first to report a case of intracranial pneumocephalus, in a patient with severe ethmoiditis2. Most cases of pneumocephalus today are due to head trauma3,4, followed in order of frequency by neoplasia, infections (such as otitis3,5, sinusitis3,6 and intracranial infection3,7) and medical interventions3.
Two main theories have been suggested for the pathophysiological basis of pneumocephalus. The first is the ‘ball-valve’ mechanism, whereby air enters the intracranial space (by coughing, sneezing or nose-blowing) through a cranial defect and becomes trapped by the meninges or brain, increasing the intracranial pressure. Usually there is no associated CSF leak8. The second is the ‘inverted-bottle’ mechanism: as CSF leaks from the intracranial space, negative pressure within the cranium causes air to be sucked in3.
In our case pneumocephalus developed unusually late after trauma. Following the childhood head injury, the breeched dura and mastoid air cells were separated only by a thin plate of bone. This was eventually fractured by violent blowing of the nose, causing CSF to leak first into the mastoid air cells and then into the middle ear, down the eustachian tube and out through the nose. The CSF leak in turn caused intracranial hypotension, permitting air entry into the cranial cavity. The initial pneumocephalus therefore seems in this case to have developed through the inverted-bottle mechanism. The pneumocephalus, however, was made worse by the patient's continuous nose-blowing to clear the troublesome rhinorrhoea. A ball-valve mechanism therefore may also be implicated here whereby air entered the cranial cavity via the middle ear and the eustachian tube as a result of a rise in the nasopharyngeal pressure during nose blowing8. Air reached the intraventricular space either by direct migration or through the foramina of Luschka and Magendie. Initially, the patient's ventricular system was buffering against changes in intracranial pressure until it was sufficiently drained of CSF such that it could no longer compensate, leading to symptomatic intracranial hypotension.
This case illustrates how post-traumatic pneumocephalus can develop many years after a head injury. In a patient with transient watery nasal discharge and a history of cranial trauma, the possibility of CSF rhinorrhoea should be borne in mind.
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