The inferior rectus muscle is one of the six extraocular muscles responsible for controlling eye movement, primarily functioning to depress the eye (looking downward). Inferior rectus entrapment is a serious, acute medical condition where this muscle becomes physically trapped within the bony structure of the eye socket. This mechanical restriction usually occurs as a direct consequence of blunt force trauma to the orbital region. Prompt recognition and intervention are necessary because the muscle’s restricted movement and potential lack of blood flow can lead to permanent vision problems.
How Orbital Floor Fractures Cause Entrapment
The bony eye socket, or orbit, is comprised of several thin walls, with the floor being one of the weakest areas. A sudden, forceful impact increases intraorbital pressure, causing the orbital floor to fracture in a blowout fracture. This pressure forces the soft contents of the orbit, including the inferior rectus muscle and surrounding fatty tissue, to herniate into the fracture site.
The fracture often involves the roof of the maxillary sinus, the bony plate directly beneath the eyeball. When the muscle and soft tissues are pushed through this defect, they become mechanically incarcerated, severely limiting eye movement. In children, this is often a “trapdoor fracture,” where elastic bone snaps back into place, tightly capturing the tissue. This tight entrapment puts the inferior rectus muscle at immediate risk of ischemia (lack of sufficient blood supply).
Recognizing the Distinctive Clinical Signs
Patients with inferior rectus entrapment typically present with specific symptoms. The most common finding is a marked restriction of vertical eye movement, particularly an inability to look upward, because the trapped inferior rectus muscle acts as a tether. This mechanical restriction results in diplopia (double vision), which is often most pronounced when the patient attempts to look up or when looking straight ahead.
Another important clinical sign is pain, which often intensifies when the patient attempts to move the affected eye. This pain, combined with the muscle traction, can trigger the oculocardiac reflex, a vagal response that is especially relevant in pediatric patients. Activation of this reflex can cause a sudden and significant drop in heart rate (bradycardia), nausea, and vomiting. Some patients may also exhibit a sunken appearance of the eyeball, known as enophthalmos, if a large volume of orbital tissue has herniated into the sinus.
Confirming the Diagnosis Through Imaging
Objective confirmation of inferior rectus entrapment relies on medical imaging, with computed tomography (CT) being the preferred method. The CT scan provides detailed cross-sectional views of the bony orbit and soft tissues, allowing clinicians to precisely visualize the injury. Coronal and sagittal views are particularly useful, clearly showing the orbital floor and the muscle’s position relative to the fracture. Characteristic findings include the entrapment of the inferior rectus muscle mass within the bone defect and the “rounding” of the muscle, which indicates swelling and edema. Given the risk of muscle ischemia, especially in trapdoor fractures common in children, the CT findings dictate the urgency of surgical intervention.
Surgical Intervention and Recovery
Surgical intervention is the standard treatment for inferior rectus entrapment and is often performed urgently, sometimes within 48 hours, to prevent irreversible damage. The procedure’s primary goal is the decompression and release of the entrapped muscle and surrounding tissue from the fracture site. Surgeons gain access to the orbital floor, often through a small incision, to carefully lift and free the incarcerated tissue. Once the muscle is safely released, the second goal is to repair the orbital floor defect.
This is typically accomplished by placing an implant, such as a thin plate or synthetic material, over the fractured area to restore the floor’s integrity and prevent future tissue herniation. Following the operation, patients typically experience immediate or rapid improvement in their eye movement and a reduction in pain. The post-operative recovery involves monitoring for residual double vision, which may persist temporarily due to muscle swelling or nerve bruising. While many patients achieve a full range of ocular motility, some may require additional observation or secondary corrective procedures if diplopia remains.