This retrospective study examined the incidence of RBH in a large dataset of facial trauma patients, focusing on variations across fracture types and patient demographics. Results revealed a markedly higher rate of acute RBH in orbital fracture patients (1.3%) than previously reported (0.45–0.6%) [1, 2]. Changes in pupillary reflex and tenting on CT imaging were identified as potential indicators for vision loss.

Fracture type, mechanism of injury, and patient age have been linked to a higher incidence of RBH. Especially fractures involving the orbital roof have shown a strong association [1, 3], possibly due to their fissural nature, which obstructs blood drainage and raises IOP. In this study, RBH was most frequent in bilateral orbital fractures —likely because of the higher prevalence of high-energy trauma— and unilateral orbital roof fractures, although cases were observed across all fracture types. Importantly, RBHs can occur across all age groups. In this study, the youngest patient to undergo immediate haematoma evacuation was 9 years old.

Only a small number of RBH progress to vision-threatening OCS. The exact mechanism behind vision loss remains unclear. Recovery after prompt orbital decompression suggests that both IOP and timely intervention play critical roles. Animal studies have shown that once a critical pressure threshold is exceeded, the duration of pressure may be more detrimental to neuronal survival than its intensity [17]. Intervention within 60 to 120 min of RBH onset is considered crucial [2, 10, 11]. In our study, patients who experienced vision impairment received slightly delayed treatment (median 8.4 h vs. 6.5 h). However, RBH may not develop immediately after injury [7,8,9], complicating the determination of the treatment window. In addition, vision loss has been documented in RBH patients even without elevated pressure [6]. Some studies also report poor vision recovery despite timely intervention within the recommended two-hour window [18]; conversely, others document recovery even with prolonged delays [19,20,21]. It is, therefore, difficult to establish general threshold values for treatment timing.

Identifying clinical and radiological markers of vision impairment is crucial for early recognition of at-risk patients. Christie et al. [4] reported that among OCS patients, 44% experienced vision changes, 40% had proptosis, 35% had pupillary abnormalities, 30% showed restricted eye movement, 16% had elevated IOP, and 15% reported pain. Popat et al. [22] suggested that RBH might be predicted by three or more of the following signs: pain, proptosis, chemosis, diplopia, subconjunctival haemorrhage, elevated IOP, tense globe, reduced vision, restricted movement, or loss of pupillary reflex. However, the clinical relevance of many of these indicators is debated. Signs like chemosis, subconjunctival haemorrhage, diplopia, vision changes, and restricted movement lack specificity, as they are common in orbital fractures but often unrelated to RBH. Pain is also unreliable, as many patients present with severe trauma or are unconscious on admission.

Similarly, IOP assessment has its limitations. Retrobulbar pressure does not always correlate with IOP [23], and many emergency departments lack the necessary equipment for accurate measurement. Readings obtained with improper techniques have been reported to vary even by 50–100% [24]. When IOP measurement is infeasible, globe palpation is sometimes used, although it remains highly subjective and imprecise.

In unconscious patients, the absence of a pupillary response is considered a strong indicator [1] and our results support this, as all patients with vision loss exhibited non-reactive, light-stiff pupils. However, systemic conditions, intracranial injuries, or the effects of substances and medications may complicate diagnosis. Proptosis is another indicator commonly used for unconscious patients, but it does not directly correlate with IOP. Other causes —such as bony displacement into the orbit (blow-in fracture) [25], orbital bleeding [26], or retrobulbar swelling [1, 27] — must also be considered.

The role of CT imaging in diagnostics remains debated. Some studies advocate for clinical evaluation alone [3, 28], while others highlight the value of CT in identifying haematoma characteristics [29] and associated findings such as orbital fractures and intracranial injuries. In our study, tenting—a tulip-like appearance on CT—emerged as another significant indicator of permanent visual impairment, observed in five of the seven patients with vision loss. Previous studies have similarly recognized the tulip-like bulb [15, 30, 31] as a key radiological finding in acute RBH.

Haematoma location is also thought to be a significant factor in determining vision loss; however, the rarity of RBHs presents challenges for studying RBH confined to specific areas. Reddy et al. [32] reported that intraconal haematomas and those adjacent to the optic nerve were associated with poor visual outcome. In this study, vision loss was most prevalent among patients with haematomas located in the superior orbit or at multiple sites.

The primary limitation of this study is the small number of RBH patients, which restricted the statistical analysis. Additionally, certain variables, such as pain, could not be assessed retrospectively. Despite these limitations, this study is one of the most comprehensive investigations of RBH in orbital fracture patients, with an extensive nine-year study period and a large dataset encompassing all facial fracture patients treated at a tertiary trauma centre during this time. To prevent future RBH-related visual impairments, it is crucial to enhance awareness of acute RBH and the critical predictors—particularly tenting on CT scans and changes in pupillary reflex—among clinicians. Further multicentre studies are needed to better understand the underlying causes of RBH-related vision loss, improve the identification of at-risk patients, and establish standardized treatment protocols for those requiring urgent intervention.