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Three-Dimensional Reconstruction of Orbital Fractures
Published on: May 16, 2025
Orbital wall infarction in child with sickle cell disease
1Department of Paediatrics, University of Antwerp, Antwerp University Hospital , Belgium.
Insights
Sickle cell disease can cause orbital wall infarction in young patients, presenting as periorbital edema. Early diagnosis and conservative treatment are key for vision preservation.
Area of Science:
- Hematology
- Ophthalmology
- Pediatrics
Background:
- Sickle cell disease (SCD) is a genetic blood disorder characterized by abnormal hemoglobin.
- Vaso-occlusive crises are common in SCD, leading to blocked capillaries and tissue damage.
Observation:
- A 17-year-old male with homozygous sickle cell disease presented with generalized pain and bilateral periorbital edema and proptosis.
- Initial treatment included hydration, oxygen, analgesia, and IV antibiotics for suspected osteomyelitis.
Findings:
- Magnetic resonance imaging (MRI) confirmed orbital wall infarction with bone anomalies in the orbital and frontal bones.
- Ophthalmological examination showed no optic nerve compression, and the patient improved with conservative management.
Implications:
- Orbital wall infarction should be considered in the differential diagnosis of young SCD patients with periorbital symptoms.
- Prompt recognition and appropriate management, potentially including corticosteroids or surgery for orbital compression, are crucial for preserving vision in these patients.
Abstract:
We present the case of a 17-year-old boy, known with homozygous sickle cell disease, who was admitted because of generalised pain. He developed bilateral periorbital oedema and proptosis, without pain or visual disturbances. In addition to hyperhydration, oxygen and analgesia IV antibiotics were started, to cover a possible osteomyelitis. Patients with sickle cell disease are at risk for vaso-occlusive crises, when the abnormally shaped red blood cells aggregate and block the capillaries. Such a crisis typically presents at a location with high bone marrow activity, as the vertebrae and long bones. At an early age, the bone marrow is still active at other sites, for example the orbital wall, and thus infarction can also occur there. Thus, in young persons with sickle cell disease, it is important to consider orbital wall infarction in the differential diagnosis, since the approach is different from osteomyelitis. If the disease is complicated by an orbital compression syndrome, corticosteroids or surgical intervention may be necessary to preserve the vision. In our patient, an MRI of the orbitae demonstrated periorbital oedema with bone anomalies in the orbital and frontal bones, confirming orbital wall infarction. Ophthalmological examination revealed no signs of pressure on the nervus opticus. The patient recovered gradually with conservative treatment.

