A 23 year old man presented to the accident and emergency department of a university hospital after an alleged assault. He had sustained a blow to the left side of his head with the stiletto heel of a shoe. On arrival he was fully conscious and the only apparent injury was a two cm wound in the scalp superior to the left ear. There was no history of loss of consciousness. The wound was cleaned and sutured and the patient discharged home with head injury instructions.

On returning home he became increasingly unwell with intermittent speech difficulties. He was taken to an A&E department of his local hospital 48 hours after the injury.

After initial assessment, a plain skull x ray revealed a minor depressed skull fracture of the left parietal bone. Computed tomography (CT) confirmed the presence of the fracture, together with underlying contusion of the parietal lobe. He was transferred to the regional neurosurgical unit for further assessment.

On arrival at the neurosurgical unit he had a mild expressive dysphasia and a temperature of 37.8°C. He was initially managed conservatively with intravenous antibiotics (certriaxone and metronidazole) which had been started in the A&E department. However, after three days his expressive dysphasia worsened. CT was repeated and now showed cerebral swelling and oedema extending down to the left temporal lobe, with areas of patchy contrast enhancement. The radiological appearances were consistent with cerebritis. At this stage, there was no obvious cerebral abscess and conservative treatment was continued, with the addition of flucloxacillin. Despite these measures, the patient deteriorated clinically and developed a left third cranial nerve palsy and a decreased level of consciousness. Further CT showed a large cerebral abscess beneath the fracture site (fig 1).

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Figure 1

 Cranial computed tomography showing a large cerebral abscess.

A craniectomy and debridement was performed and 20 ml of pus was aspirated. Staphylococcus aureus was isolated following culture of the pus. The patient improved clinically, and postoperative CT showed resolution of the abscess. He was discharged after completion of a 21 day course of intravenous antibiotics. The patient was well at follow up three months later, with a mild expressive dysphasia which had resolved at a 12 month follow up.

DISCUSSION

Open depressed skull fractures can occur in a variety of settings.¹ To our knowledge there has not been any previous report of a stiletto heel causing such an injury. This could in part reflect the relative strength of the particular heel involved in this case. We are informed that such heels are may be customised and reinforced when worn by members of the transsexual/transvestite community, of which the alleged assailant was a member.

Fractures of the skull vault are influenced by various factors, which include the thickness of the vault and the force of the impact. Rapid dynamic loading occurred in this case, with the force probably acting for a very short time (<200 ms). The size of impacting device (that is, the heel) and the force of impact are directly related to the magnitude of the dynamic load.² In this case, a large amount of kinetic energy made contact with the skull over a small area (∼1 cm²). The degree of local deformation in this case was enough to cause penetration and fracture of the skull.

The complications and sequelae of compound depressed fractures of the skull are minimised by early diagnosis and appropriate treatment.³ Frequently, as in our case, there is no associated neurological injury, so depressed fractures may be missed because radiographic investigations are not done.

The Society of British Neurological Surgeons issued guidelines in 1998 for the indications for skull x ray following recent head trauma.⁴ These include a history of loss of consciousness or amnesia, suspected penetrating injury, a scalp laceration >5 cm long, bruising or swelling, CSF leak from the nose or ear, and a violent mechanism of injury.

Even when a skull x ray is obtained, the depression is often not appreciated.³ This case illustrates the need for careful examination. The scalp is relatively mobile and any area of depression may not lie directly beneath the laceration. Visual exploration of the skull through the scalp laceration may fail to reveal a fracture. Careful digital exploration of the scalp wound with a gloved finger can reveal a bone edge, a depression, or a mobile bone fragment.⁵ Exploration under local anaesthesia and aseptic conditions using a finger sweep technique should be mandatory in such cases.

The management of choice in preventing infection from open depressed skull fractures is operative debridement and thorough irrigation,⁶ though there is evidence that select cases can be safely managed without operation.^6,7

The distinction between antibiotic treatment and prophylaxis is blurred, as contamination of the wound has already occurred at the time of injury.⁸ The prevalence of infective complications (abscess, empyema, meningitis) after compound depressed skull fractures ranges from 4% to 10%.^9,10

This case highlights the need for clearly determining the mechanism of injury and undertaking appropriate investigations. A high index of suspicion should be maintained if a pointed object is implicated in assaults involving the skull.