Growing skull fracture

Growing skull fracture, cause, type and management

1. Growing skull fracture Dr Abhishek Rai Resident neurosurgery

2. Introduction A skull fracture is a break in one or more of the eight bones that form the cranial portion of the skull, usually occurring as a result of blunt force trauma. Any significant blow to the head results in a concussion, with or without loss of consciousness.

3. Compound fracture A fracture in conjunction with an overlying laceration that tears the epidermis and the meninges, or runs through the paranasal sinuses and the middle ear structures, bringing the outside environment into contact with the cranial cavity is called a compound fracture. Compound fractures can either be clean or contaminated . Compound elevated fracture : Its rare type of skull fracture where the fractured bone is elevated above the intact outer table of the skull.

4. Types Cranial vault Linear/ Fissure fracture Depressed Elevated Comminuted Pond fracture Gutter fracture Diastatic Basilar Growing skull fracture Cranial burst fracture Fracture of skull base Ring fracture Hinge fracture ACF fracture MCF fracture PCF fracture

5. Linear/Fissure fracture Linear skull fractures are breaks in the bone that transverse the full thickness of the skull from the outer to inner table. They are usually with no bone displacement . The common cause of injury is blunt force trauma where the impact energy transferred over a wide area of the skull. Not easily detectable in radiology. Mc type(70%) Line of fracture runs parallel to axis of compression

6. Linear fracture Linear skull fractures are usually of little clinical significance unless they parallel in close proximity or transverse a suture, or they involve a venous sinus groove or vascular channel. The resulting complications may include suture diastasis , venous sinus thrombosis , and epidural hematoma . In young children, although rare, the possibility exists of developing a growing skull fracture especially if the fracture occurs in the parietal bone

7. Depressed fracture A depressed skull fracture aka Fracture a la signature , since it reflects the type of weapon used. It occurs if the fractured bone is driven inwards to distance equivalent to thickness of skull table . Sometime only involve outer table. Risk of post traumatic epilepsy is 15% .

8. Depressed fracture Depressed skull fractures present a high risk of increased pressure on the brain, or a hemorrhage to the brain that crushes the delicate tissue. In complex depressed fractures, the dura mater is torn. Depressed skull fractures may require surgery to lift the bones off the brain if they are pressing on it by making burr holes on the adjacent normal skull .

9. Comminuted fracture Spider web/Mosaic fracture 2 or more intersecting lines of fracture dividing the bone into 3 or more fragments. Cause : Significant force striking over broad surface area. Complications of linear and depressed fracture

10. Pond fracture Smooth concave dent resulting from in-buckling of skull. Occurs in pliable skull (<4 years) Inner table not fractured. Brain and meninges are not damaged. Cause : Obstetric fracture Forcible delivery

11. Gutter fracture Part of thickness of skull is removed to form gutter. Cause: Oblique bullet wound Associated with irregular depressed fracture of outer table of skull. Dura and brain may be torn.

12. Diastatic fracture Separation of sutures due to blow on the head with blunt weapon. Young children Mc Sagittal suture Widening of the sutures may be appreciated on plain radiograph and is better still appreciated on CT The following widths are considered to be diagnostic of sutural diastasis >10 mm at birth >3 mm at two years >2 mm at three years

13. Growing skull fracture Linear or non-linear skull fractures in children that enlarge with time are termed growing skull fractures . Growing skull fractures are rare and occur, almost exclusively, during the first years of life. Also described as traumatic ventricular cysts , craniocerebral erosions , cranial malacia , and leptomeningeal cysts , among others. They appear most frequently as soft, subgaleal collections overlying an enlarging bony defect at the site of a previous diastatic fracture .

14. History Howship was the first to report a patient with a growing skull fracture. In 1816, he described a 9-month-old child in whom an enlarging defect in his parietal bone developed after an injury. The defect was apparent within 2 weeks after the injury and never resolved. The first account of the pathology of this condition was by Rokitansky in 1856. He reported 5 month old who struck his head during a seizure and subsequently an enlarging scalp mass developed. Therapeutic puncture of the mass was performed, after which meningitis developed and the child died. At autopsy a large bone defect was found along with an associated dural tear and injury to the underlying brain.

15. History Dyke introduced the term leptomeningeal cyst in 1937. Other observations have failed to confirm the central role of leptomeningeal cysts in the pathogenesis of growing fractures. Penfield and Erickson described a patient with an enlarging defect at the site of a childhood fracture. At surgery, brain, but no cyst was found in the defect. Tenner and Stein also described herniated brain within the ossification defects in children with growing fractures and highlighted the importance of local brain injury and swelling in their development. Rosenthal and associates found that both the dura and arachnoid had to be opened to produce an enlarging fracture and that concomitant injury to the brain did not increase the likelihood that a growing fracture.

16. History Many of the children described have had significant neurological deficits from the time of their injury, there are several reports of progressive dysfunction that develops months or years after the event. This has been attributed to brain injury caused by (1) local brain herniation and consequent ischemia (2) repetitive trauma to the exposed brain on the bone edge or by direct concussion, (3) physical distortion of the brain related to its displacement Growing fractures occur only in settings in which there is rapid brain growth or, much less commonly , increased intracranial pressure .

17. Epidemiology They account for less than 1% of skull fractures in large pediatric series and, for practical purposes, are never seen in adults. Almost all enlarging fractures are found in children younger than 3 years ; two thirds of them occur in children younger than 1 year. Neurological deficit more than 50% in most case series, and for the incidence of posttraumatic seizures, which is also around 50%

18. Natural history 3 stages of development of GSF : Stage I : Aka Prephase : Skull fracture (linear or comminuted) with dural laceration and herniation of brain tissue or arachnoid membrane through torn dura. Stage II : Early phase . It last approx. 2 months, Bone defect is small, deformity relatively limited, mild neurologic deficit, Entrapped tissue prevents fracture healing. Stage III : Late stage , after 2 months, bone defect significantly enlarges, brain tissue and CSF extend between bony edge of fracture through torn dura and arachnoid

19. Pathophysiology Although the development of growing skull fractures is multifactorial, the predominant factor in their causation is the presence of lacerated dura mater. The pulsatile force of the brain during its growth causes the fracture in the thin skull to enlarge. This interposition of tissue prevents osteoblasts from migrating to the fracture site and inhibiting healing. 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.

20. Pathophysiology The brain extrusion may be present shortly after diastatic linear fracture in neonates and young infants resulting in focal dilation of the lateral ventricle near the growing fracture.

21. Evaluation The typical patient with a growing fracture is Being younger than 3 years Has a subgaleal fluid collection overlying the fracture, (although the collection may resolve soon after injury) Has a neurological deficit caused by the injury Has skull radiographs that demonstrate a diastatic fracture with at least 3.5-mm separation of the bone edges Some authors have advised obtaining skull radiographs 6 weeks and again several months after the injury while others asked to see these patients in the clinic after 8 weeks.

22. Evaluation Common initial complaints are pain at the fracture site Epilepsy progressive neurological deficit. On examination : Palpable ossification defect , larger than the one initially present, that is usually but not always overlain by a soft, often pulsatile subgaleal collection. - Operative The ossification defect is small or only minimally different than it was at initial evaluation, and no overlying collection is present. - re-examine these children several weeks later.

23. Radiology On plain radiographs, they appear as smooth edged ossification defects, often scalloped and occasionally, with sclerotic margins. CT demonstrates the same bony abnormalities and almost uniformly injury and cystic degeneration of the underlying brain. Frequently, brain tissue is seen to protrude into the fracture; ventricular asymmetry, with the ventricles drawn to the fracture site, is also common.

24. Radiology MRI adds little but a clear delineation of the parenchymal injury. Angiography is of minimal value in this setting, but reported cases show vessels outside the skull in the bone defect.

25. Classification Classification of the growing skull fractures into three types suggested here was found to be helpful in explaining these diversities and planning the treatment

26. Classification Classification of the growing skull fractures into three types suggested here was found to be helpful in explaining these diversities and planning the treatment

27. Classification Duro -cranioplasty was the correct treatment in type 1. A shunting procedure required as an initial or definitive management for type II and III fractures with raised intracranial pressure.

28. Treatment Successful repair requires identification of the dural margin, repair of the dural defect, and coverage of the missing bone. A large incision is needed; it must extend well beyond the margins of the skull defect. The skin flap is reflected in the subgaleal plane and the bony defect is defined. The dural edge has a tendency to recede and is often located well back from the edge of the bone. It can be found by progressively removing bone from the margins of the defect until the dura is circumferentially exposed. A burr hole can be placed a few centimeters from the bone edge.

29. Treatment Circumferential craniotomy Once the dural defect is exposed, the underlying brain is carefully dissected. If a large area of cortex is herniating through the dural defect, an attempt to reduce it should be made. Resection of herniated gliotic tissue Closure of the dural defect is necessary to prevent recurrence f the growing fracture. Primary closure rarely possible, so some graft material must be used.

30. Treatment Several options are available for bone coverage, the most frequently used of which are split-thickness calvarial grafts, full thickness calvarial autografts, synthetic materials, and split rib grafts. VP Shunt

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