Eduardo Miñambres MD, PhDa, , Javier Burón MDa, Borja Suberviola MDa, Miguel Angel Hernández MDa, Alejandro González-Castro MDa and Andrés González-Mandly MDa
Department of Intensive Care, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain Department of Radiology, Hospital Universitario Marqués de Valdecilla, 39008 Santander, Spain
Posttraumatic spinal epidural hematomas (SEHs) occur infrequently in neurosurgical practice. They present as an acute spinal cord compression, and usually, emergent surgical treatment is recommended for most patients to decompress the spinal canal. We report the case of a healthy 22-year-old man who developed a symptomatic thoracic epidural hematoma after a severe thoracic trauma. He was treated with nonsurgical management, and the hematoma resolved spontaneously. The patient remained asymptomatic over a year of follow-up.
A healthy, previously asymptomatic 22-year-old man was admitted to the Emergency Department after a traffic accident. There was no loss of consciousness at the scene, and on arrival, the patient had a Glasgow coma score of 15. Initial physical examination revealed a severe chest trauma with multiple rib fractures and dorsal back pain. Neurologic examination did not identify any focal signs. He was admitted to our Trauma Intensive Care Unit (ICU). On arrival at the ICU, he was taken for helicoidal computed tomography of the neck (normal) and thorax that confirmed the presence of the rib fractures and showed a bilateral lung contusion and T8 vertebral compression fracture with minimal invasion of the spinal canal (less than 10%). Eight hours after the trauma, he developed neurologic symptoms of posterior cord compression which consisted in paraesthesiae in the lower limbs, with 5 strength (of a possible 5) in both lower extremities and symmetrical, normal reflexes. Neurosurgery was immediately consulted and emergent magnetic resonance imaging (MRI) of the spine was scheduled. The MRI revealed a posterior SEH. Methylprednisolone 30 mg/kg was administered intravenously and a drip of 5.4 mg/kg per hour initiated. Because of his additional lesions and the mild neurologic deficit, the patient was treated with a plan for nonsurgical management with strict bed rest and serial neurologic examination. After 24 hours, symptoms were totally resolved with normal sensitivity. He remained in Trauma ICU for 7 days (because of the chest trauma). Ten days after admission, the patient was scheduled for spinal stabilization, with no complications, and was discharged from the hospital by the ninth postoperative day. At the 1-year follow-up, the patient remained asymptomatic and returned to normal activities. The exact incidence of posttraumatic SEH has not been determined, although some authors estimate it as less than 1% of all spinal injuries [2]. The real incidence has increased since the advent of imaging techniques, namely, computed tomography and MRI, so epidural hematomas may be much more common than what was previously thought [3]. However, a posttraumatic SEH is believed to be a very rare finding. It occurs more commonly associated with ankylosing spondylitis or rheumatoid arthritis in elderly patients but is very uncommonly associated to trauma injuries in previously healthy patients [4]. However, the exact mechanisms of the bleeding remain controversial. An epidural hematoma can arise from either an arterial or a venous source. Because our patient had resolution without operative treatment, we can only assume that he had a hematoma of venous origin. Composed of thin valveless vessels, the intrarachidial venous plexus may be vulnerable to rupture with abrupt changes in venous pressure, possibly resulting from blunt trauma. Hemorrhage from the epidural arteries could also be the source of SEH from sheer stress or direct impact, causing stretching and rupture of the arterial system [5]. Posttraumatic SEH generally presents with symptoms immediately after the traumatic event, although they have also been described presenting with a delayed onset [6]. They classically present as acutely painful episodes and progressive neurologic compromise and then often evolve to complete neurologic dysfunction at the level of the cord compression. A majority of patients have sensory and motor deficits that develop within minutes to hours from the injury, as in our case. One third of posttraumatic SEHs occur in T spine and are thought to become symptomatic with smaller hematomas due to anatomically narrower canal of the thoracic spine when compared with the cervical or lumbar spine [7] and [8]. Early surgical evacuation of the hematoma remains the treatment of choice for most patients with symptomatic SEH [1] and [9]. Recently, nonsurgical treatment has been proposed in selected cases of SEH with good neurologic recovery [6], [10], [11], [12] and [13]. This population includes patients with mild neurologic deficits and those who demonstrate early, rapid, and progressive improvement in neurologic function within the first 24 hours, as in our patient. Torres et al [14], in a series of 22 patients with spontaneous or traumatic SEH, recommended early surgical evacuation when the patients presented severe neurologic deficits (Frankel A-B) and conservative treatment in patients with minimal neurologic involvement. Thoracic SEH is an uncommon condition that may present after trauma with significant neurologic compromise. Although there are only a few reports of successful conservative treatment, we believe that, if the neurologic deficit is not severe and if there is clinical improvement with initial steroid therapy, nonsurgical treatment remains an option, especially in traumatic patients as ours in whom emergency surgery could be problematic because of the presence of additional lesions. Further studies are necessary to understand the real role of nonsurgical treatment of these lesions.
The American Journal of Emergency Medicine. Volume 24, Issue 1 , January 2006, Pages 134-136.
