The Eyes Have It

History and Physical

A 10-year-old, previously healthy girl suffered a direct left frontal impact into a wall while driving a motorcycle without a helmet. Bystanders estimated a collision speed of approximately 40 km/h with immediate loss of consciousness that lasted seconds, two episodes of emesis, agitation, and disorientation. When she arrived three hours later at the emergency department, she was confused and combative. Her GCS was 12 (O=3; V=3; M=6), and the Full Outline of Unresponsiveness (FOUR) scale was 14 (O=4; M=3; TC=3; R=4). Her left pupil was dilated with a diameter of 5 mm and showed poor response to light. The right pupil was normal. Palpebral and ocular movements were normal in both eyes. Visual acuity was not evaluable at that time, but light stimulus showed response only in the right eye. Fundoscopy was normal in both eyes. Motion, sensation, and reflexes were normal in all four extremities, with negative Babinski signs. Airway was clear and respiration was normal with a respiratory rate 22/min and oxygen saturation 92% on room air. Heart rate was 64/min, blood pressure 106/58, and ECG showed normal sinus rhythm. There were multiple bruises, lacerations, and swelling over the left face and eyelid, nose, and left leg. Medications (per discussion with family) were propranolol 2 mg/kg/day for rectal hemangioma. Her consciousness improved before being transported to radiology, with the patient answering questions and making eye contact. GCS scale was up to 14 (O=4; V=4; M=6).

Diagnostic Workup

Head CT showed left temporoparietal epidural/subdural hematomas with midline shift <5 mm ( Fig. 61.1 ), left orbital floor fracture, and intrasinus hemorrhage ( Fig. 61.2 ). This corresponded to a Rotterdam CT score of 1 and Marshall classification of grade II traumatic brain injury (TBI). CT cervical spine, chest radiograph, and Focused Assessment with Sonography in Trauma (FAST) exam were normal. The patient was admitted to the PICU with GCS of 15, normal neurologic examination, and normal vital signs. Ophthalmological evaluation identified a dilated left pupil with no response to light and blindness of the left eye. Consensual left pupillary reflex was noted when stimulating the right eye. The next day, orbital CT showed a fracture of the left lamina papyracea with hemorrhage surrounding the proximal intraorbital optic nerve ( Fig. 61.3 ). A traumatic injury of the left optic nerve was diagnosed.

A panel of two head C T scans labeled A and B shows a left parietal subdural hematoma marked by an arrow and a temporal subdural hematoma marked by an arrowhead. The panel presents axial head C T views. Scan A shows a crescent shaped hyperdensity along the left parietal convexity marked by an arrow. Scan B reveals a similar hyperdense area in the left temporal region marked by an arrowhead. — Fig. 61.1

A coronal C T scan shows a left orbital floor fracture marked by an arrow and a maxillary sinus hemorrhage marked by an asterisk. The coronal C T section shows disruption of the continuity in the left orbital floor marked by an arrow. Below the fracture site, the maxillary sinus on the same side appears filled with soft tissue density marked by an asterisk, consistent with hemorrhage. The nasal turbinates and septum remain midline and intact. — Fig. 61.2

A panel of two orbital C T scans labeled A and B shows a left lamina papyracea fracture and perineural hemorrhage around the proximal intraorbital optic nerve marked by an arrow respectively. The panel contains two axial C T scans. Panel A shows a bony window where an arrow indicates a disruption in the continuity of the left lamina papyracea. Panel B presents a soft tissue window where an arrowhead marks a region of increased density surrounding the proximal portion of the left intraorbital optic nerve, consistent with hemorrhage. — Fig. 61.3

Clinical Differential Diagnoses

Anisocoria and mydriasis are clinical red flags following acute head trauma because of their association with increased ICP and brain herniation. Pupillary asymmetry or anisocoria greater than 1 mm (physiologic limits) should raise concern for intracranial mass effect until proven otherwise. Other clinical signs are often present, including unconsciousness, contralateral motor deficit, posturing, or Cushing reflex.

Optic nerve injury is signified by a relative afferent pupillary defect with less pupillary constriction in the affected eye (Marcus-Gunn pupil). Posttraumatic ischemia of the occipital lobe could also explain visual field defects or blindness.

Additional causes of anisocoria can include use of dilating eye drops or nebulized ipratropium bromide. Prone positioning has also been associated with unilateral mydriasis.

Imaging Differential Diagnoses

In a patient who develops anisocoria after brain trauma, imaging should be performed to evaluate for intracranial hypertension and herniation caused by cerebral edema or hemorrhage. In the absence of intracranial pathology, especially if severe facial lesions are present, optic nerve injury should also be suspected as the cause of anisocoria. Risk factors on facial CT include intraconal hematoma or emphysema, optic canal fracture, and hematoma along the posterior globe. Sphenoid bone fractures are also associated with optic nerve injury in 50% of cases ( Fig. 61.4 ).