Isolated traumatic retroclival hematoma: case report and review of literature

Retroclival subdural hematoma (rcSDH) has been reported less often than epidural hematoma (rcEDH). However, both can co-present, particularly in violent injuries [10]. Tables 1, 2, 3, and 4 summarize the available English literature. In the pediatric population, there have been 30 cases of rcEDH and 16 cases of rcSDH; in the adult population, there have been 8 cases of rcEDH and 21 cases of rcSDH. The tectorial membrane helps define the distinction between the epidural space and the subdural space, where the former is ventral to the membrane and the latter is dorsal to the membrane [11]. The tectorial membrane is the rostral continuation of the posterior longitudinal ligament, attached inferiorly to the posterior body of the axis and superiorly to the occipital bone along the clivus [11]. RcEDH are restricted by the boundaries of the membrane (that is, from the mid-portion of the clivus to the middle of the body of the axis); rcSDH are not restricted and can disseminate from the intracranial to the spinal subdural space [11]. The MRI (Fig. 2a, 2b) from our patient demonstrated stripping of the tectorial membrane, with focal areas of disruption; the ventral fluid collection tracking down to the mid body of the odontoid is consistent with an epidural hematoma; however, there is also a collection that exists posterior to the tectorial membrane and tracks more inferiorly to the posterior of the C3 body; this collection is consistent with a subdural collection.

The most common etiology is a traumatic event that induces hypermobility of the neck. Either hyperflexion or hyperextension can lead to soft tissue injury or fractures, causing a retroclival hematoma. The preponderance of reported pediatric cases relative to adult cases may be attributed to the anatomical differences at the craniocervical junction. Compared to adults, children possess certain features (large head-to-body proportion, small occipital condyles, shallow facet joints, and weak cervical muscles) that increase the mobility of the spine and augment the risk for injury [12, 13]. Disruption of the tectorial membrane (i.e., from its insertion into the clivus) can cause venous bleeding from the surrounding basilar venous plexus and dorsal meningeal branch of the meningohypophyseal trunk, leading to an epidural collection [11]. In children, the dura can be more easily detached from the bone, which makes them more vulnerable to forceful traction [14]. Clival fractures have been associated with rcEDH, likely due to bone bleeding as well as injury to the tectorial membrane [15, 16]. Similarly, odontoid fractures have been reported; dislocation of the dens can cause damage to the transverse ligament and traction to the tectorial membrane, prompting hemorrhage [17, 18]. Shearing forces may lead to rcSDH via rupture of the bridging petrosal and small veins near the foramen magnum; the tectorial membrane is usually unharmed, remaining attached to the clivus; this feature is an important characteristic which differs from rcEDH [11]. Other traumatic injuries associated with retroclival hematoma include atlanto-occipital dislocation [19, 20], atlanto-axial dislocation, rupture of the transverse ligament [17], fractures of the occipital condyles [21], spheno-occipital synchondrosis diastasis [22], brain stem contusion [17], and intraventricular hemorrhage [17].

There are a variety of non-traumatic causes of retroclival hematoma. A common etiology is pituitary apoplexy. Hemorrhage can spread through the diaphragm sella into the subdural space, constrained by the posterior arachnoid membrane of the prepontine cistern [1, 23]; on the other hand, a defect in the dorsum can permit blood flow into the epidural space [24]. Rare cases of rcSDH have been associated with aneurysmal rupture [25, 26]. Moreover, pressure changes (spontaneous intracranial hypotension [7] and posterior fossa decompressive craniectomy [27]), thrombocytopenia [28], and hemophilia [29] have been linked with rcSDH. Several cases have occurred spontaneously with negative work-up and no history of trauma [3‐8].

Clinical presentation can be variable. Neurological impairment may be related to stretching, direct compression, or contusion of surrounding nerves and brain parenchyma. The most frequently injured cranial nerve is the sixth cranial nerve (unilateral [16, 30] or bilateral [6, 14, 15, 19, 31‐35]). Other affected nerves include the optic, oculomotor, trigeminal, facial, glossopharyngeal, and hypoglossal nerves. Patients may also exhibit hemiparesis or quadriparesis. The rare extreme cases include brain stem contusion with cardiorespiratory compromise [17‐20, 36] and progressive hydrocephalus [19].

These hematomas may be overlooked on axial CT due to beam hardening artifacts in the posterior fossa [16], requiring reformatted CT images or MRI to elucidate the diagnosis and assess for ligamentous damage. Common etiologies can typically be inferred based on clinical presentation (history of trauma or presence of pituitary adenoma). Work-up for concurrent blunt traumatic vascular injury may be warranted. With no obvious mechanism, work-up for vascular pathology or coagulopathy should ensue [28]. The presence of ligamentous instability and brain injury or spinal cord injury will determine the appropriate management [11]. The possibility of brainstem compression or instability mandates initial close observation, reasonably within an ICU setting [30]. Although rare, the extra-axial hematoma can cause mass effect on the brainstem and cranial nerves, necessitating surgical evacuation [19, 35, 37, 38]. Of the 33 traumatic cases of rcEDH, twelve patients exhibited a cranial nerve palsy, five patients required surgical stabilization of the craniocervical junction [19, 38, 39], one patient required an external ventricular drain for progressive hydrocephalus [20], and six patients died. Of the 17 traumatic cases of rcSDH, no patient required surgical stabilization; one patient died. Of the 12 cases of pituitary apoplexy, all but 1 patient exhibited cranial nerve palsies; overall, surgical resection of the hemorrhagic pituitary adenoma has led to good outcomes [1, 24].

Except for the rare cases that lead to death [17, 18, 20, 28, 29, 37, 39], the majority of patients exhibit good outcomes with minimal long-term neurological deficits with conservative management. Tubbs et al. [39] noted no relationship between hematoma size and presenting symptoms; moreover, initial GCS did not correlate with outcomes. Hematoma appears to resolve within 2–11 weeks [14, 36, 39]. On admission, our patient exhibited bilateral 6th nerve palsies, consistent with prior reports. At discharge, 19 days after the accident, he exhibited intact eye movements. Flexion and extension films demonstrated no cervical instability, and his cervical spine was cleared.