Sinus pericranii (SP) is predominantly a congenital condition, but it can also develop secondary to head trauma. Trauma-induced SP is exceptionally rare, with only several documented cases in the literature (1, 2). While the diagnosis of SP is generally straightforward, it is crucial not to overlook potential underlying conditions such as craniosynostosis, cephalocele, arteriovenous malformation (AVM), venous angioma, cavernous angioma, hydrocephalus and other congenital anomalies, which can lead to SP (3–11). This venous anomaly may initially be mistaken for a simple scalp swelling and improperly treated, necessitating increased vigilance. Moreover, rapid enlargement of SP within a short period demands even greater vigilance (4). Although the prognosis for SP patients is relatively favorable, achieving aesthetically pleasing and precise management, especially for frontal SP, remains challenging. This case report aims to present our experience in managing trauma-induced frontal SP and to review the existing literature, providing valuable insights for the diagnosis and treatment of this rare condition.

G. Stromeyer (12) first introduced the term “Sinus pericranii” in 1,850 to describe a blood-filled reservoir on the skull bones that communicates with the dura mater sinuses via the diploic veins. Although the exact incidence of SP is not clearly documented, it is known to be a rare vascular malformation, typically presenting as a sporadic scalp mass, with most cases being congenital (9, 13–16). Traumatic frontal SP is an even rarer, with only a few dozen cases reported (1, 2, 17). The limited data hinders a comprehensive understanding of SP, and no established treatment protocol exists. A significant proportion of cases are misdiagnosed as simple scalp masses and excised, which poses substantial risks (18, 19).

The hidden risks are primarily due to two main factors: First, SP is often classified into two types: (a) Secondary: often caused by trauma, hydrocephalus, intracranial hypertension; (b) Congenital: most common in craniosynostosis and frequently accompanied by various venous malformations and developmental anomalies (6–9). Treating SP as a simple scalp mass, regardless of its type, obscures the underlying condition and overlooks the true problem. Second, SP can be categorized as dominant (if the majority of venous flow communicates through the SP) or accessory (if only a portion of the intracranial venous flow communicates through the SP): For accessory SP, treatments such as surgical excision or vascular intervention are feasible; However, for dominant SP, excision as a simple scalp mass can lead to severe complications such as cerebral edema (20). Therefore, early and precise diagnosis of SP is crucial for determining the appropriate treatment, reducing complications, and optimizing therapeutic outcomes.

When diagnosing SP, imaging studies are more critical than physical examinations and medical history. Three-dimensional CT scans can clearly reveal any thinning, defects, or holes in the skull beneath the mass and assess for craniosynostosis (7, 11, 21, 22). CT with contrast or Magnetic Resonance Venography (MRV) can demonstrate the presence of extracranial blood vessels within the mass. If necessary, Digital Subtraction Angiography (DSA) can be used to confirm the communication between extracranial veins and intracranial venous sinuses or dural venous lakes (10, 23, 24). By integrating these imaging findings with the patient's medical history and symptoms, a diagnosis of SP can be established (3, 4, 25–27). However, not all imaging studies are necessary in every case.

In our case, the patient, a 31-year-old man, presented with an asymptomatic mass. A three-dimensional CT scan was performed to identify skull abnormalities and exclude hydrocephalus, intracranial lesions and hypertension. The patient had a clear history of frontal trauma at the site of the mass during childhood. Angiography also ruled out intracranial vascular malformations and the type of dominant SP. Based on these findings, a diagnosis of SP was confirmed, and surgical excision was deemed appropriate.

The treatment of SP is challenging due to its low incidence, which results in limited reports and a lack of established diagnostic or treatment guidelines. Currently, endovascular embolization and surgical resection are the two main treatment methods (4, 10, 14, 20, 23, 28). After excluding secondary factors such as malformations and hydrocephalus, surgical resection can be performed. Given the reports of recurrence following resection, we reviewed the relevant literature and combined it with our experiences to propose the following measures for preventing postoperative recurrence: For the initial treatment of typical SP, it is essential to coagulate and remove all abnormal vessels and seal all holes with bone wax; For patients with high-risk factors for recurrence, such as an unusually large number of emissary veins or rich circulation between intra- and extracranial venous systems, we recommend coagulating and severing all veins at their point of departure from the sinus; In case of large bone defects, it is advisable to use autologous bone grafts or artificial bone graft materials, such as acrylic resin, to seal the defects and the surrounding thinned skull, followed by covering the lesion with periosteum; For patients with concurrent conditions like raised intracranial pressure, hydrocephalus, cerebral vascular malformations, or increased intracranial venous pressure, it is crucial to first address these primary conditions before proceeding with the resection of SP (1, 3–9, 14, 15, 21, 22, 25–34).

In this case, we describe a patient with traumatic frontal SP. The choice of incision site, complete resection, and prevention of recurrence are crucial for both cosmetic outcomes and effective treatment of frontal SP. Pathological examination is essential for confirming diagnosis. Through this rare case and a review of the existing literature, we aim to provide valuable insights for the diagnosis and management of SP.