Craniofacial Fracture Symptoms

6.1  Combined Skull Base and Midface

Fractures

Apart from the classical midface fracture signs, there are certain (direct) and uncertain (indirect) clinical symptoms indicating additional skull base fractures. Liquorrhea, clinically visible bony prolaps, dislocated bony fragments and intracranial air (CCT) or dislocated skull base fragments (CCT) indicate skull base fractureswithdurallaceration(HausamenandSchmelzeisen 1996; Messerklinger and Naumann 1995; Joss et al. 2001).

Signs of open skull base fractures

•Clinical evidence of a liquorrhea

•Brain prolapse

•Visible bone defects due to dislocated bony fragments

•Intracranial air in CCT

•Dislocation of skull base fragments, basal fissures and bone diastasis in CCT

6.1.1  Certain Signs of Skull Base

and Dural Injuries

6.1.1.1  Liquorrhea

Nasal liquorrhea is an obvious sign of an open skull base fracture (Probst 1971, 1986; Entzian 1981; Loew et al. 1984; Weerda 1995). Nasal liquorrhea indicates a liquor fistula, an open communication between the intracranial intradural space and the pneumatized sinuses of the viscerocranium.

Liquor loss from the left or the right nostril might indicate the location of the osseous skull base defect, although this cannot be relied on. The sinus septum can also be damaged in fractures of the posterior wall of the frontal sinus, thus causing diagnostic confusion as liquor might drain on the opposite side. On the other hand, liquorrhea from both nostrils does not necessarily indicate a bilateral cranio-nasal fistula (Kessel et al. 1971; Kastenbauer and Tardy 1995).

Fistulas

There are varying excretory pathways for liquor (Loew et al. 1984; Rosahl et al. 1996). The liquor can flow directly through an osseous defect in the cribriform region. Indirect pathways run through fractures in the paranasal sinus system using natural drainage outlets: e.g., the nasofrontal duct, via the ethmoid bone or over the drainage system of the sphenoid sinus.

According to Waller (1977), direct cranio-nasal fistulas (cribriform plate fistulas) are the cause of liquorrhea in 51% of the cases, whereas indirect cranio-sino-nasal fistulas (frontonasal/fronto-ethmoidal-nasal/sphenoidal- nasal) represent 48% of the cases. Sphenoid fistulas occur in about 5% of the cases (Fig. 6.1).

Multiplicity

According to Probst and Tomaschett (1990), 59% of the frontal skull base injuries are associated with dural injuries. Thirty-five percent of the dural tears are unilateral, 24% bilateral and in 44% of these patients multiple dural lacerations are found.

In unilateral fractures with dural lacerations, 79% of the dural tears are ipsilateral and 21 % bilateral, in

Fig. 6.1  CSF leaks: the most frequent locations of dural defects after frontal skull base injuries (mod. a. Ewers et al. 1995). 1 Fronto-nasal CSF leak (direct cranio-nasal), 2 fronto-ethmoido- nasal CSF leak (indirect cranio-sino-nasal), 3 spheno-nasal CSF leak (indirect cranio-sino-nasal)

bilateral fractures 65% of the dural lacerations are bilateral and 33% unilateral located (Schroth et al. 2004).

According to Lewin (1974), bilateral dural tears occur mostly in central midface injuries (80% bilateral dural fistulae). According to Godbersen and Kügelgen (1998), one can expect several dural tears, especially in frontocranial injuries of type III (posterior sinus wall fractures).

In lateral skull base fractures, however, only 20% of the patients have dural injuries, but in 52% multiple dural lacerations are found (Lewin 1974).

In our own patients, approximately 56% of the craniofacial fractures had concomitant dural injuries, of which 12% were bilateral and 44% unilateral.

Time of Manifestation

There is a distinction between early and late onset of liquorrhea (Lewin 1974; Spetzler and Zambramski 1986; Kaestner et al. 1998).

Statistically, a liquorrhea starts in 63% of the cases within the first 24 h following trauma. In 51–80% of the cases the onset of a liquorrhea can be observed within 48 h (Lewin 1974; Founier 2007). A late onset between 2 and 12 weeks following the craniofacial

injury occurs in 30% of the cases, in 14% after 2–6 months and in 7% after 7–12 months (Lecuire and Mounier-Kuhn 1961).

Average manifestation of liquorrhea following frontal skull base injury, in relation to posttraumatic time (Lewin 1974)

The eventuality of a late onset of liquorrhea does not exclude a dural injury in skull base injuries (Paillas et al. 1967). However, one has to keep in mind that a clinically apparent liquorrhea may stop spontaneously within a week in about 85% of the patients (Georgiade et al. 1987; Schmidek and Sweet 1988) (see also Sect. 7.2)

A clinically apparent loss of liquor weeks or even months following trauma may be caused by necrosis of brain tissue squeezed between fractured bones. The necrosis destroys the dural barrier. As the arachnoidal space is only separated from the paranasal sinuses by incomplete and unstable scarred connective tissue (Russell and Cummings 1984; Kaestner et al. 1998), a sudden intracranial pressure increase may cause the scar tissue to break and a liquor fistula will appear (Probst 1986).

Clinical Evidence of Liquorrhea

Every suspicion of liquorrhea must either be confirmed or excluded by further examination. Standard clinical methods are:

•Rhinoscopy: obvious liquor loss from the paranasal sinuses, visualization of defects

•The “handkerchief” test: nose secretion does stiffen on a hankerchief, liquor does not

•The swab/sponge test: liquorrhea gives a liquor border around the bloodstain, whereas regular nose secretion does not

•The Queckenstedt test: pressing the jugular vein will raise the intracranial pressure resulting in increased liquor leakage

•Nasal endoscopy: with the aid of fluorescence identification