Traumatic subdural effusion (TSDE), also known as subdural hygroma (SDG), is a common complication following traumatic brain injury (TBI) and refers to a pathological state of excessive collection of cerebrospinal fluid (CSF) in the subdural space caused by traumatic arachnoid laceration [1]. In early stages, TSDE can be easily ignored or masked by the symptoms of primary TBI. Even if TSDE is identified by a computed tomography (CT) scan early, it may increase progressively or evolve into chronic subdural hematoma (CSDH) later. Both types tend to require surgical treatment and are often only detected when symptoms of neurological dysfunction are present [2]. The definition of TSDE versus CSDH depends on the nature of the subdural space contents. A subdural collection is classified as hematoma when it contains more than 105/mm3 of red blood cells or more than 0.5 g/dl of hemoglobin or when the CT value is greater than 20Hu [3], [4]. Presently, the mechanism of TSDE remains unclear, and it is challenging to predict subsequent changes in effusion in actual clinical practice. It would be of great significance to clinical medicine if the risk of TSDE deterioration could be predicted early.

There are some reports on the risk factors for the occurrence of TSDE, but they focus mainly on patients with subdural effusion after craniectomy [5], [6]. A recent study by Wei et al [7]. found that the application of a nomogram could effectively predict the risk of TSDE for those suffering from mild TBI. However, there are few reports on the tendency of effusion deterioration or improvement after the appearance of TSDE. Similarly, the factors contributing to effusion changes have not been extensively studied. This study is the first to report a nomogram model for predicting the possibility of effusion deterioration within six months of the onset of TSDE. The model is valuable for early identification in high-risk groups, as well as for the management and prevention of effusion deterioration.