Otological complications following basal skull fractures
J.L. LANCASTER*, D.J. ALDERSON#, J.W.A. CURLEY*
*Royal Preston Hospital, Preston, and # Arrowe Park Hospital, Wirral, Merseyside, U.K.
A retrospective review is presented of 50 patients, with a basal skull fracture, who had radiological or clinical evidence of temporal bone involvement. The study looks at the incidence of significant otological symptoms reported during the admission and we review the subsequent patient management. We propose that all patients presenting with a head injury, and one or more of a number of symptoms characteristic of a temporal bone fracture, should automatically have an otological assessment. This will facilitate the early detection and subsequent follow up of potentially correctable middle ear disorders. We review the literature to highlight the high incidence of complications associated with these fractures.
Keywords: head injury, otological assessment, basal skull fracture, temporal bone
J.R.Coll.Surg.Edinb., 44, April 1999, 87-90
UK hospitals receive in the region of 1 000 000 new attendees each year secondary to head injury alone.1 Many of these patients will have sustained other, life threatening, injuries which usually take priority in the initial treatment. In the seriously head injured patient, it is important not to overlook the management of non life threatening injuries in an attempt to try and improve their subsequent quality of life. Unrecognised otological complications are one such group of injuries which, if left uncorrected, may add to the difficulties in rehabilitation, and adversely affect the overall quality of life. The purpose of this study was to look at the incidence of temporal bone involvement in patients with a basal skull fracture, and to review the otological complications and sub-sequent patient management.
The case notes of 250 consecutive admissions to a busy district general hospital, (which was also the regional tertiary referral centre for neurosurgery), from 1990 to 1995 were obtained. All these patients had been diagnosed as having a basal skull fracture on either clinical or radiological grounds. Information was gathered by careful retrospective review of the histories. From these cases, only fifty patients fulfilled our selection criteria of a clear history or evidence of a head injury, with one or more of the following findings: computerised tomography (CT) evidence of a temporal bone fracture, cerebrospinal fluid (CSF) otorrhoea, otohaemator-rhea, and/or clinical evidence of a haemotympanum.
The patients selected were between the ages of 2 and 87 years of age, with a male to female ratio of 2:3. The site of impact of the head injury was occipital in 42%, parietal in 22%, temporal in 20%, frontal in 12% and multiple in 6% of cases. On admission, 80% of patients were noted to be bleeding from the external auditory meatus, and 18% were noted to have CSF otorrhoea. Documented examination of 28% of patients revealed a haemotympanum. However, there was no record of an otoscopic examination in 38% of patients. In total, 54% required respiratory support in the form of mechanical ventilation, and they were subsequently admitted to an intensive care unit.
On hospital admission, 43 patients (86%) had a cranial CT scan; 20 ( 40% ) patients were reported as having a temporal bone fracture, and a further 9 (18%) more specifically as having a petrous temporal bone fracture. Figure 1 illustrates the typical course of longitudinal and transverse fracture lines in the petrous temporal bone.
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| Figure 1: Typical course of a longitudinal fracture line (A) and transverse fracture line (B) within a petrous temporal bone, shown with the following landmarks; posterior clinoid process (C), foramen ovale (D), foramen lacerum (E), internal acoustic meatus transmitting vestibulocochlear and facial nerves (F), jugular foramen (G ), auditory ossicles (H), tympanic membrane (I), outline of the pathway of the external auditory canal within the temporal bone (J), and the sigmoid sinus (K) | |
An otological opinion was sought from the Department of Otolaryngology on 18 (36%) patients. The range and frequency of otological symptoms and signs reported are shown in Table 1. Pure tone audiometry was performed on 16 patients ( 32% ), the remaining two patients being too unwell for such an investigation. A second audiogram, at either 3 or 6 monthly review, was available for comparison in 12 out of 16 of these patients. Five patients were lost to review, either from failure to attend, or because of transfer back to the original referral source for convalescence. Only two patients had a documented lower motor neurone lesion of the facial nerve; one was not graded whilst the other was assessed as being grade six on the House-Brackman classification. The latter patient underwent facial nerve decompression and the palsy subsequently improved to a grade two.
Table 1: Documented otological symptoms and signs during admission (n=50)
| Otological features | Percentage of patients (n) |
|---|---|
| Deafness | 42 ( 21) |
| Tinnitis | 2 ( 1 ) |
| Vertigo | 20 ( 10) |
| Facial nerve palsy | 4 ( 2 ) |
| Chorda tympani dysfunction | 2 ( 1 ) |
| CSF rhinorrhoea | 18 ( 9 ) |
| Otohaematorrhoea | 80 ( 40) |
| Haemotympanum | 28 ( 14) |
Complications secondary to temporal bone fractures are relatively common. However, the majority of the complications are not life threatening.2 Hearing loss is the commonest complication and is classified as being either sensori-neural,
conductive or mixed. Trauma to the cochlea, auditory nerve or intracranial auditory pathways can result in a sensori-neural hearing loss. This may be transient or permanent. Sensori-neural hearing loss may occur following even minor head injuries in which no skull fracture is sustained. In Griffith's study of 84 patients admitted with concussion but no skull fracture following head injury, a total of 66 ears exhibited a sensori-neural pattern of hearing loss.3 After six months, 86% (36/42) of these patients presenting with a low frequency type loss had recovered, whilst only 12.5 % (3/24) of those with a high frequency type hearing loss had recovered.
The second type of hearing loss is conductive, in which the patient has an air-bone gap in their pure tone audiogram. This implies that the cochlea and intracranial pathways for hearing are intact. The conducting pathways for sound, which include the external auditory canal, tympanic membrane, and middle ear ossicles, however, are in some way dysfunctional. Hence, pure tone audiometry demonstrates a difference between the inner ear hearing potential, measured by the bone conduction, and the actual hearing level to air conducted sound, resulting in an 'air-bone gap'. This is frequently due to the existence of a tympanic membrane perforation or haemotympanum, both of which usually resolve spontaneously over 2 to 3 months. In our study there was a mean improvement in the air bone gap of 7.5dB over a 3 to 6 month period of follow-up (see Table 2).
Table 2: This table shows the mean improvement of the air-bone gap, as a function of improvement in conductive hearing, and mean improvement in bone conduction thresholds, as a function of improvement in sensori-neural hearing (n = 12 over 3-6 months )
| Improvement in the air-bone gap over a 3-6 month period (dB) | Improvement in the mean bone conduction thresholds over 3-6 months ( dB ) |
|---|---|
| 30 | 11 |
| 26 | 1 |
| 19 | 2 |
| 14 | -8 |
| 12 | -4 |
| 5 | 0 |
| 2 | 2 |
| 2 | 22 |
| 1 | 13 |
| 0 | 4 |
| -7 | 2 |
| -14 | 0 |
| Mean=7.5 | Mean=3.8 |
Should the air bone gap fail to close after a period of three months then one should consider an ossicular discontinuity or fixation as a cause for the persisting deafness. This occurred in 3 out of 12 patients within our series. Most would agree that corrective tympanoplasty for suspected ossicular discontinuity should be delayed for at least this interval to allow a period for transient defects to correct themselves spontaneously.4
Ossicular discontinuity is considered to be the commonest surgically correctable complication of temporal bone fractures; Schubiger (1986) found its incidence to be 25.8% in a series of 89 temporal bone fractures.5 The commonest ossicular chain injury seen involves disruption of the incudostapedial joint. Other frequently seen injuries include gross displacement of the incus, (in which articulation is lost with the malleus, fossa incudis and stapedial head ), and fractures of the stapedial arch.6
An alternative to surgery in a conductive hearing loss may involve the simple provision of a hearing aid, and in many cases this is appropriate. Previous studies have looked at the incidence of hearing loss after head injury, but few have looked at this in relation to the specific type of fracture.7,8
Often, the diagnosis of a temporal bone fracture is difficult to make both clinically and radiologically. What is clear is that otoscopic findings lend important clinical weight to the diagnosis and in some cases may be the only demonstrable sign of the injury. Previous studies have shown that routine otoscopy is as important as radiology in the diagnosis of basal skull fractures.9 We found that in 38% of the 50 patients in our series, there was no recorded otoscopic examination.
We found cerebrospinal fluid rhinorrhoea was documented in 18% of patients, all of whom were initially managed conservatively and without the use of prophylactic antibiotics. Most patients will settle spontaneously following a period of bed rest, with or without the insertion of a lumbar drain. Those cases which persist are at risk of developing intracranial sepsis and, therefore, require exploration and repair. In our series, only one case failed to settle spontaneously and required surgical closure of the leak following the development of meningitis.
Our series revealed the incidence of facial palsy to be 4%. It is not within the remit of this paper to discuss the complex neuro-otological management of post-traumatic facial palsies, and it still remains a topic of debate amongst otolaryngologists. We stress the importance of the involvement of an otolaryngologist in all post traumatic facial palsies at the earliest opportunity.10 We also recommend referral to an otolaryngologist in all cases where there is clinical or radiological suspicion of auditory damage.
In Schubinger's study of 89 temporal bone fractures, he found a 48% incidence of otological complications potentially correctable by surgery.5 The non-surgical management of patients with post-traumatic sensori-neural hearing loss, tinnitus and vertigo may be equally important for these patients. Appropriate rehabilitation can be co-ordinated following assessment by an otolaryngologist. A high index of suspicion is needed for referral to an otolaryngologist after head injury.
The diagnosis of a basal skull fracture can be difficult to make, and is greatly aided by otoscopy findings. We stress that this examination forms an important part of the initial patient assessment. A large number of patients admitted with a basal skull fracture will have clinical or radiological evidence of temporal bone involvement. Of those with temporal bone involvement, many will have otological complications, which may warrant surgical intervention. In some cases this should be performed as soon as the patient is fit enough for the procedure, however in most, a period of observation is necessary for evaluation. Both post-traumatic facial palsy and CSF otorrhoea require the involvement of the otolaryngology team as soon as the patient's other life threatening conditions have been treated.
We recommend an automatic otological referral of all patients with clinical or radiological evidence of a temporal bone fracture. Screening would initially involve a thorough history, examination, and audiometry, with evoked response audiometry and high resolution computerised tomography scans of the temporal petrous bones being requested if indicated.
Copyright date: 18th August 1998
Correspondence: Mr JL Lancaster, Department of Otolaryngology, Royal Preston Hospital, Sharoe Green Lane North, Fulwood, Preston, PR2 9HT, UK
©1999 The Royal College of Surgeons of Edinburgh, J.R.Coll.Surg.Edinb., 44; 2:87-90