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Symptoms: Head Wound, Headache, Nausea

Wiler, Jennifer L. MD, MBA

doi: 10.1097/01.EEM.0000340950.69012.8d
Quick Consult

A 39-year-old man is transferred from an outside ED after he was assaulted with a crowbar. He claims he lost consciousness for an unknown period of time. He complains of a headache and nausea, but denies vomiting, paresthesias, focal weakness, neck pain, or vision changes. His only past medical history is an eye enucleation secondary to trauma. The patient is confused but able to follow commands.



The photograph shows what you see on evaluation. Sutures were placed to grossly approximate the gaping wound prior to transfer to your facility. What is the likely diagnosis, and how would you manage this condition in the ED?

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Diagnosis: Depressed Skull Fracture

The skull is made up of eight cranial bones protected by hair, skin, connective tissue, adipose, fascia, and muscle. Blunt force can cause these bones to fracture, but depressed skull fractures typically require significant blunt force, and are commonly associated with underlying brain injury and subsequent neurologic deficits. The more pronounced the bony fragment depression, the more likely dural tears, cortical lacerations, and worse outcomes. (Childs Nerv Syst 1996;12[6]:323.) Depressed skull fractures most commonly occur in the frontoparietal area (75%) where the bone is relatively thinner.

It is estimated that skull fractures are diagnosed in two percent to 20 percent of children who present to the ED for evaluation of head injury. (Ann Emerg Med 2001;37[1]:65.) Of those, approximately 30 percent have subsequent intracranial injury. Skull fractures in infants tend to be secondary to falls or abuse, but in older children are usually the result of bicycle accidents. In adults, skull fractures are typically the result of motor vehicle collisions or violence. One case series reported that six percent of head injuries were complicated by depressed skull fractures, of which 90 percent were open (compound) fractures. (J Trauma 1993;35[3]:441.) Patients with compound depressed skull fractures are at risk of serious complications including infection (10%), neurological impairment (11%), development of late epilepsy (15%), and death (as high as 19%). (Neurosurgery 2006; 58[3 Suppl]:S56.)



Patients with depressed skull fractures typically present with localized head trauma. A palpable bony deformity “step off” may be appreciated. Depending on the bone disrupted and extent of underlying intracranial injury, patients may have evidence of hemotympanum, cranial nerve deficits and palsies, facial ecchymosis (raccoon eyes), CSF rhinorrhea or otorrhea, hemiplegia, or paralysis. Mentation at presentation also can range from normal (GCS 15) to obtunded/coma, and some may present with a report of seizure activity. Despite these potential high-acuity presentations, 25 percent of patients with depressed skull fracture interestingly do not report a history of loss of consciousness.

Clinical and diagnostic evaluation of infants with potential head injury and skull fractures can be challenging. Depressed skull fractures may be palpable on examination, but isolated clinical evaluation is insufficient to rule out underlying skull injury especially in children. (Ann Emerg Med 1997;30[3]:253.) One study reported that 71 percent of children with isolated skull fractures had at least one of the following indicators of serious head injury: initial loss of consciousness, seizures, vomiting, lethargy, irritability, depressed mental status, and focal neurologic findings. As James Roberts, MD, notes in his articles about evaluating head injury in children (EMN 2006;28[11]:17 and 2006;28[12]:21), seizure, loss of consciousness, and vomiting tend to correlate poorly with underlying intracranial injury (Pediatrics 1999;104[4 Pt 1]:861) while a change in mental status is a common indicator of intracranial injury. A complete neurological evaluation should be performed, and baseline laboratory studies are typically warranted, especially if the patient is considered an operative candidate.

Delayed diagnosis and surgical evacuation of intracranial hematomas is known to increase morbidity and mortality so expeditious evaluation and management of suspected depressed skull fracture is recommended. (N Engl J Med 1981;304[25]:1511.) If the index of suspicion of a skull fracture is high enough to warrant imaging, then evaluation of the intracranial anatomy is warranted and skull radiographs are unnecessary. Computerized tomography, therefore, is the modality of choice for evaluating suspected skull fractures and underlying intracranial injury. (Pediatrics 1999;104[6]:1407 and Ann Fr Anesth Reanim 2000;19[4]: 296.) Poor prognostic indicators include deep displacement of bony fragments, and decreased mental status (GCS 8 or less). (Childs Nerv Syst 1996; 12[6]:323.)

All patients with a depressed skull fracture require neurosurgical evaluation. In the past, surgical elevation of the depressed fragment was considered standard treatment with the intent of decreasing infection rates. Today, more conservative management is recommended because elevation may not prevent seizure, infection, or neurological deficits. In adults with open (compound) skull fractures, conservative (nonoperative) management is acceptable if there is no evidence of dural disruption, significant intracranial hematoma, frontal sinus involvement, wound infection, gross wound contamination, unacceptable cosmetic deformity, pneumocephalus, or depression greater than 1 cm. Early surgical intervention is recommended for those with closed (simple) depressed fracture fragments greater than the cranium thickness. (Neurosurgery 2006; 58[3 Suppl]:S56.) Recommendations are similar for children. (J Neurosurg 1987;66[4]:506 and Childs Nerv Syst 1996;12[6]:323.) More well-designed randomized trials, however, need to be performed to validate the current practice recommendations.

At this time, there is no consensus on using prophylactic antibiotics for patients with depressed skull fractures (Emerg Med J 2002;19[6]:552,) but their use for open depressed skull fracture is recommended by some. (Neurosurgery 2006;58[3 Suppl]:S56 and Ann R Coll Surg Engl 1994;76[3]:147.)

Seizures are a known complication of traumatic brain injury. They can occur early (within one week) after the inciting event and are less likely to recur while late onset seizures are more likely to develop into epilepsy. The risk of early seizures in patients with depressed skull fractures and intracerebral contusions is estimated to be as high as 30 percent. (Epilepsia 2003;44[Suppl 10]:18.) Patients with early post-traumatic brain injury are typically started on anti-epileptic therapies because of the concern for status epilepticus and the theoretical risk of decreased brain perfusion and subsequent intracranial pressure elevation. The ideal duration of treatment is unclear. The use of prophylactic anti-epileptic medications for traumatic brain injury is controversial. Advocates note the significant potential disability of epilepsy, but studies have yet to demonstrate that prophylactic anti-epileptic medications significantly prevent the development of post-traumatic brain injury epilepsy.

Traumatic brain injury post-concussive syndrome (including chronic headaches, dizziness, cognitive and psychological or mood impairment) is a well known consequence of brain injury. Severity of symptoms and morbidity correlate with extent of brain injury, including those with depressed skull fracture. Other complications include intracerebral vascular injury, delayed hematoma formation, cranial nerve injury, direct brain injury, and hydrocephalus so serial imaging is typically performed. Other complications including pneumonia, gastric “stress” ulcers, and deep vein thrombosis are well known to affect the critical care patient and must also be addressed. (Neurosurg Clin N Am 1991;2[2]:411.)

This patient was found to have a open depressed skull fracture in the left occipital region immediately adjacent to the sagittal sinus, a linear skull fracture in the right temporal region, a small right temporal and left occipital lobe contusion, and subarachnoid hemorrhage. The decision was made by neurosurgery not to elevate the depressed bone fragments because of their close proximity to the sagittal sinus.

© 2009 Lippincott Williams & Wilkins, Inc.