Traumatic CSF leakage is very rare in children because the skull is flexible and the sinuses are underdeveloped. Traumatic CSF leakage occurs in 2% of all pediatric TBIs and in 12–30% of cases with skull base fractures and is most common in calcaneal fractures of the frontal sinus, ethmoid sinus, and temporal bone. In particular, even if only a simple skull fracture is seen in an infant, it is recommended to fully explain the possibility of progression to GSF to the parent, and to conduct a physical examination and imaging study follow-up for 3 months after the initial head trauma. In conclusion, early diagnosis and treatment of GSF are important in preventing the progression of neurological deficits and cranial deformities. Some authors have reported that a ventriculoperitoneal shunt operation is often required after surgery to prevent hydrocephalus or CSF leakage. If surgery is performed with epileptic seizures, electrophysiological monitoring should be performed during the removal of lesions that cause epileptic seizures. The operator should be careful not to remove functional brain tissue while removing the exposed brain through the skull defect during surgery. For cranioplasty, autologous bone is mainly used, and an alloplastic material (polymethyl methacrylate, titanium) can be used when the skull defect is wide. If the dural defect is wide, fascia lata, cadaveric dural grafts, and artificial dura are often used. In the treatment of GSF, surgery should be performed to prevent further brain damage, and the most important technique is watertight closure of the dura mater, which includes removal of the leptomeningeal cyst and encephalomalacia. The treatment of GSF involves surgical repair of the dura mater tear and cranioplasty. In such cases, MRI shows herniated brain tissue through the skull defect, as well as a leptomeningeal cyst or encephalomalacia. However, these diagnostic methods are not useful for diagnosing early-stage GSF. CT demonstrates the same bony abnormalities and evidence of injury in the underlying brain during the early period, as well as leptomeningeal cyst, ventricular asymmetry, focal dilatation of the lateral ventricle, and herniation of the brain tissue into the bony defect. Simple radiographs of GSF usually show an enlarged diastatic fracture and linear lytic lesions in the skull with scalloped margins. Simple skull lateral (A) and three-dimensional computed tomography (CT) (B) showing a widened fracture line in the left parietal bone in a patient with growing skull fracture, and axial CT showing a bulging leptomeningocele that occurred through the bone segments (C). 1) however, if necessary, magnetic resonance imaging (MRI) may be needed. Radiological diagnosis of GSF is mostly possible with simple radiography and computed tomography (CT) ( Fig. Common clinical presentations of GSF are pulsatile scalp swelling that grows when a child cries, headache, epileptic seizures, and neurological deficits. In the early stage of GSF, clinical presentations and radiological examinations are the most useful diagnostic clues. Several studies have reported a diagnosis of GSF, and early diagnosis is the most important. The parietal bone is the most common site of GSF, followed by the occipital and frontal bones. The resorption of the adjacent bone by the continuous pressure from tissue herniation through the bone gap adds to the progression of the fracture line. This interposition of herniated elements prevents osteoblasts from migrating to the fracture site, inhibiting healing. The pulsatile force of the brain during growth causes the fracture in the thin skull to enlarge. The pathogenesis of GSF is skull fracture with dura mater tearing accompanied by arachnoid adhesions. In addition, more than 90% of these GSFs occur under 3 years of age, and most occur chronically. It has an incidence of approximately 0.05% to 1.6%. GSF is a rare complication that occurs in infants and children, first described clinically by Howship in 1816.
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