Skip to content
Eye Trauma

Orbital Roof Fracture

An orbital roof fracture is a fracture of the upper wall (roof) of the orbit, resulting from trauma to the forehead or frontal bone. It often occurs as an extension of a fracture of the superior orbital rim.

It occurs in 1–9% of patients with craniofacial trauma 1, 4) and accounts for 12–19% of all orbital wall fractures. In adults, isolated fractures are rare; a strong force is required to fracture this area, often resulting from severe head injury. According to a review of 526 cases by Lucas et al., the most common mechanisms are traffic accidents (39.5%), falls (30.3%), and assaults (11.8%).

In children, isolated fractures are more common and can occur from relatively minor trauma. This is because children have a larger cranium relative to the face and incomplete pneumatization of the frontal sinus 3, 4).

Blow-in fractures are a type where the orbital roof is displaced downward, thought to be caused by a sudden increase in intracranial pressure (ICP) at the time of injury 1). In cases with severe traumatic brain injury (TBI), there is a unique condition where bone fragments move in conjunction with ICP fluctuations.

Q Can orbital roof fractures occur in children?
A

In children, it can occur even with minor trauma. Unlike adults, isolated fractures are common and many cases are managed conservatively. On the other hand, growing skull fracture, in which proptosis appears after a latent period of several months to years after injury, is a condition unique to children 3).

  • Diplopia: Caused by ocular movement disorders due to entrapment of extraocular muscles or cranial nerve palsy.
  • Decreased visual acuity: Occurs when traumatic optic neuropathy is complicated.
  • Pain on eye movement: Due to entrapment or inflammation of extraocular muscles.
  • Pain when blowing the nose: Caused by communication between the paranasal sinuses and the orbit in cases involving the frontal sinus.
  • Delayed onset of eyelid swelling and proptosis: Growing skull fracture in children. Latent period is 4 months to 12 years 3).
  • Difficulty reporting symptoms due to impaired consciousness: In cases complicated by severe traumatic brain injury, patients often cannot provide a subjective history.

Closed fractures may be accompanied by vasovagal reflex, which is common in young people. Systemic symptoms such as severe eye pain, nausea/vomiting, syncope, and bradycardia occur, and misdiagnosis as increased intracranial pressure can delay diagnosis.

Orbital and Ocular Findings

Periorbital hematoma/edema: Subconjunctival hemorrhage and chemosis are also common.

Proptosis: Occurs in blow-in fractures, intraorbital hematoma, or brain herniation.

Enophthalmos: Occurs when the orbital cavity is enlarged due to a large fracture.

Hypoglobus: Due to the position of bone fragments or pseudomeningocele.

Pulsatile exophthalmos: A delayed finding suggesting brain tissue herniation (encephalocele/meningocele) through a superior wall defect.

Neurological and Functional Findings

Ocular misalignment and restricted eye movement: Due to extraocular muscle entrapment or cranial nerve palsy.

Cranial nerve palsy (CN III, IV, VI): Diplopia and restricted eye movement; CN IV palsy presents with head tilt4, 5).

rAPD (relative afferent pupillary defect): Positive when traumatic optic neuropathy is present.

Globe rupture: Occurs in 4–9.5% of superior orbital wall fractures.

Orbital emphysema: Caused by air inflow from the frontal sinus when the frontal sinus is involved.

Q Can a superior orbital wall fracture cause blindness?
A

Globe rupture occurs in 4–9.5% of cases, and traumatic optic neuropathy can cause vision loss, while cranial nerve palsy can cause eye movement disorders. The incidence of corneal abrasion and eyelid laceration is also reported to be higher than in other orbital wall fractures.

Mechanism of injury: High-energy trauma such as traffic accidents, falls, and assaults accounts for the majority. In adults, isolated fractures require significant force, while in children, relatively minor trauma can cause them.

Anatomical features: The superior orbital wall is paper-thin at the frontal sinus. The floor of the frontal sinus forms the superior orbital wall, which is composed of the frontal bone and the lesser wing of the sphenoid bone. Trauma to the frontal eminence causes buckling of this bone.

Pediatric risk: Because the skull is relatively large compared to the face and the frontal sinus is not fully pneumatized, impact is more directly transmitted to the superior orbital wall3, 4).

Elevated ICP: In patients with severe traumatic brain injury, elevated intracranial pressure may promote downward displacement of bone fragments in blow-in fractures1).

The main imaging tests are shown below.

TestFeaturesIndications
CT (thin-slice coronal)Gold standard. Depicts fracture size and location.First choice
MRIUseful for differentiating brain herniation, CSF, and hematoma.Cases suspected of encephalocele or pseudomeningocele2, 3)
3D CTUseful for depicting fractures of the orbital rim and frontal bone.Preoperative planning for complex fractures

CT does not require contrast, and it is important to scan both soft tissue and bone windows. Bone windows are used to detect subtle fractures, while soft tissue windows are used to observe soft tissue entrapment or strangulation. In cases with severe traumatic brain injury, serial CT scans are needed to monitor bone fragment displacement 1).

  • Visual acuity and optic nerve function: Record early at the initial visit.
  • Pupillary examination (rAPD): Essential for evaluating the presence of traumatic optic neuropathy.
  • Red saturation test and color vision test: Useful as an adjunct for assessing optic nerve function.
  • Exophthalmometry: Quantitative assessment of proptosis or enophthalmos.
  • Hess chart and binocular single visual field test: Objective evaluation of diplopia.
  • Forced duction test: Used to determine the indication for surgical reduction, but often imaging and clinical findings are sufficient. It is not actively performed under awake conditions due to pain.

Exclude other orbital wall fractures, optic canal fractures, skull base fractures, and ocular injuries. In pseudomeningocele, differentiation from orbital cellulitis and periorbital contusion is necessary 2).

Isolated, non-displaced orbital roof fractures often do not require surgery. In a review by Lucas et al., 40% of 526 cases were managed conservatively.

Basic patient instructions for conservative treatment are as follows:

  • Do not blow the nose: Strictly prohibited within 2 weeks after injury because blowing the nose can worsen emphysema.
  • Contact sports prohibited: 6–8 weeks.
  • Oral antibiotics: Prescription varies by physician.
  • Oral steroids: May be used to reduce edema.

Strabismus after orbital trauma may improve spontaneously over 4–6 months of observation. Conservative management of diplopia includes occlusion, Fresnel prisms, prism glasses, and botulinum toxin injection.

Surgery is considered in the following cases:

  • Extraocular muscle entrapment in closed fracture: Risk of muscle necrosis; requires emergency reduction within 24 hours of injury.
  • Soft tissue entrapment: Surgery should be performed as early as possible (usually within 2 weeks).
  • Proptosis, enophthalmos, or globe displacement: When cosmetic or functional problems are significant.
  • Bone fragment compressing the optic nerve: Cases with vision loss or positive rAPD.
  • Elevated ICP or vision changes: Blow-in fracture with severe traumatic brain injury1).

Early surgery (within 2 weeks) has been reported to achieve good functional and cosmetic results in 80% of cases4). If significant ocular trauma (globe rupture, retinal detachment) is present, orbital surgery should be postponed.

Transpalpebral Approach

Indications: Isolated orbital roof fracture (no need for intracranial access).

Features: Minimally invasive. Approach to the superior orbital wall via an upper eyelid crease incision.

Risks: Scarring, infection, temporary sensory disturbance of the superior orbit.

Coronal incision + frontal craniotomy

Indications: Comminuted displaced fractures requiring anterior skull base injury or intracranial access. Used in 94.8% of surgical cases in the Lucas review.

Features: Performed with multidisciplinary collaboration involving neurosurgery and otolaryngology.

Risks: Meningitis, brain injury, stroke.

The most common implant material is titanium miniplates (46.2%), with autologous skull bone graft being the gold standard. PPE and nylon foil can also be used. For growing skull fractures in children, PMMA, titanium mesh, and bioabsorbable materials are selected 3). If CSF leak is present, primary closure plus collagen graft on-lay repair is performed 1).

After surgery, avoid blowing the nose and strenuous exercise. Follow-up examination after 1 week, then according to progress. Explain to the patient that final healing takes several months, including resolution of edema, hematoma, and bone fusion.

Q Can it heal without surgery?
A

Isolated, non-displaced fractures often do not require surgery; in the Lucas review, 40% were managed conservatively. If eye movement disorder or diplopia is mild and imaging changes are reversible, observation is appropriate.

Q How long does recovery take after surgery?
A

Due to postoperative edema, hematoma, and bone healing, final recovery takes several months. In early surgery for extraocular muscle entrapment, recovery may occur early postoperatively; Irfan Syahputra et al. reported complete recovery of CN III and VI palsy on POD6 4).

6. Pathophysiology and Detailed Mechanisms

Section titled “6. Pathophysiology and Detailed Mechanisms”

Similar to orbital floor and medial wall fractures, both the hydraulic theory and buckling theory are involved. Blunt trauma causes increased intraorbital pressure and direct force to the orbital wall, resulting in fracture and herniation of orbital contents into the fracture site.

The mechanism of blow-in fractures is characterized by a sudden spike in ICP that pushes the orbital roof downward 1).

Rao et al. (2024) demonstrated in two cases that the position of the bone fragment correlated with ICP changes on serial CT. When ICP was <5 mmHg, the bone fragment moved upward (8.3→3.0 mm), and when ICP was 14–22 mmHg, it moved downward again (7.9 mm) 1). This finding supports the importance of ICP monitoring in determining surgical timing.

Mechanism of growing skull fracture (children): dural tear → arachnoid protrudes into fracture line → CSF pulsation erodes and enlarges bone edges → brain herniation → proptosis 3). Most common in children under 3 years, with an incidence of 0.05–0.1%. Latency ranges from 4 months to 12 years.

Formation of pseudomeningocele: dural tear → CSF leaks into the orbit through the orbital roof defect → formation of a fibrous capsule 2). Presents with pulsatile or non-pulsatile proptosis, globe ptosis, diplopia, restricted eye movement, and vision loss.

Q How are intracranial pressure and fracture related?
A

In blow-in fractures with severe traumatic brain injury, increased ICP can cause the bone fragment to move downward, worsening compression of orbital contents. When ICP decreases, the bone fragment moves upward; thus, ICP management directly affects the severity of orbital roof fractures 1).


7. Latest Research and Future Perspectives (Investigational Reports)

Section titled “7. Latest Research and Future Perspectives (Investigational Reports)”

Major recent reports are shown below.

Author/YearContentSignificance
Rao et al. 20241)Confirmation of ICP-driven bone fragment movement by serial CTUse of ICP for surgical timing
Mirkin et al. 20252)Extraorbital extension of pseudomeningocele (first report in literature)Recognition of a new complication
Gupta et al. 20253)CAD/CAM custom PMMA implantNew technique for pediatric bone defect repair

CAD/CAM and 3D printing technology enables precise assessment of bone defects and preoperative fabrication of custom implants.

Gupta et al. (2025) fabricated a PMMA implant (5 mm thick) using a 3D-printed skull model for a 4-year-old girl with a growing skull fracture, and performed coronal incision, dural repair, and PMMA placement. The procedure was screwless and accounted for pediatric growth, with improvement in proptosis and pain at 2 weeks postoperatively3).

Extraorbital extension of pseudomeningocele was first reported by Mirkin et al. (2025). A case of extension to the extraorbital (periorbital subcutaneous) region after lumbar drain dislodgement was confirmed, highlighting the importance of including pseudomeningocele after orbital roof fracture in the differential diagnosis2).


  1. Rao V, Gerndt CH, Ong V, Strong EB, Shahlaie K. Worsening orbital roof “blow-in” fractures following traumatic brain injury: A report of two cases. Surg Neurol Int. 2024;15:316.
  2. Mirkin S, Patel J, Wang W, Engel C. A rare case of traumatic orbital pseudomeningocele. Cureus. 2025;17(1):e77881.
  3. Gupta AK, Gupta R, Saini A, Narula V, Singh RK. Innovative solutions in orbital fracture management: The role of computer-aided design and computer-aided manufacturing technology. Contemp Clin Dent. 2025;16:49-52.
  4. Irfan Syahputra B, Yudoyono F, Ompusunggu SE, et al. Recovery of ocular motility after surgical intervention in orbital roof fracture-induced cranial nerve injuries. Surg Neurol Int. 2025;16:296.
  5. Dubey S, Bansal O, Kekunnaya R, Sachdeva V. Canine tooth syndrome due to orbital roof fracture. BMJ Case Rep. 2022;15:e248733.

Copy the article text and paste it into your preferred AI assistant.