The early and late complications following treatment of severe craniofacial injuries cannot always be differentiated from those of the injury itself. Complications may develop with or without and despite or because of a surgical intervention (Sprick 1988; Schmidek and Sweet 1988).

Complications which develop within a short period of time after the injury (<1 month) are classified as early complications. Late complications develop after an inter­ val of 2-3 months (Hardt and Steinhäuser 1979).

Postoperative complications are dependent on various modalities:

•Severity of the injury

•Time of treatment

•Quality of treatment

•Absence of primary treatment

Postoperative complications

Postoperative complications cause specific problems (Kretschmer 1978; Schmidek and Sweet 1988), such as:

•Subgaleatic, epidural, subdural, intracerebral abscesses

•Epidural-subdural hemorrhage/hematoma

•Osteomyelitis of replanted bone fragments or autogenous bone grafts

•Hygroma

•Sinus complications

•Recurrent liquorrhoea

•Elevated intracranial pressure

Own statistics

Our own postoperative early and late complications following treatment of craniofacial fractures are distributed as follows (Neidhardt 2002):

Postoperativecomplicationsandlatesequelaefollowingcraniofacial reconstruction

13.1  Infections and Abscesses

The postoperative complications in our group of patients proved to be relatively low. The most common complication was infection (15%).These infections can be divided into:

•Localized (early) infections:

subgaleatic, epidural, abscesses/empyemas

•Late infections: osteomyelitis

Localized infections were observed in 11%. Staphylo­ coccus aureus could be detected in most of these of cases:

•3% subgaleatic infections

•4% epidural abscesses

•4% infected seromas

The infected seromas were found in the temporal area away from the actual fracture site and were caused by harvesting large temporal muscles patches. The epidural abscesses resulted from epidural dead space caused by failing expansion of the brain.

Subgaleatic and epidural abscesses require urgent revision of the operation site with facultative removal

Fig. 13.1  Subgaleatic infection. (a) Infection following insufficient transfacial primary treatment. (b) State following craniotomy. Removal of infected fragments and osteosynthesis material, fronto- facial-osteotomy, and skull base revision. (c) Reconstruction of the frontal region. Closure of the remaining defect with bone dust and titanium mesh. (d) Postoperative situation

a1

a2

d1

b

c1

c2

d2

of the osteosynthesis material and obligate removal of the infected bone fragments, a selective antibiotic therapy and drainage (Figs. 13.1 and 13.2).

13.2  Osteomyelitis

Despite adaequate reconstruction and sufficient perioperative antibiotic prophylaxis, infection or necrosis of local bone fragments or grafts may occur. Osteomyelitis can develop with varying latency in areas of insufficiently revitalized bone.

Besides general signs of infection and local inflammatory changes of the galea, there is radiological evidence of a permeative osteolysis of the bone. If recurrent swelling, pain, and fistulae occur, the operation site has to be revised due to the vital danger of osteomyelitis.

In 4% of our own patients, osteomyelitis was the cause for revision of the frontofacial operation site:

•Osteomyelitis of local bone (2%)

•Osteomyelitis of bone grafts (2%)

Therapy consists of removing the osteosynthesis material from the infected and neighboring areas and removing the affected bone (sequestrotomy) until vital bony margins are found. The dural reconstruction has to be examined.

Bony reconstruction can be postponed and a titanium mesh inserted for immediate contour restoration. Imme­ diate reconstruction with cancellous bone and titanium mesh, however, also proved to be successful (Esser and May 1990; Kuttenberger et al. 1996) (Figs. 13.3 and 13.4).

13.3  Recurrent Liquorrhea

The most common complication following skull base treatment in combination with midface fractures is

b

persisting or recurrent liquorrhea. The following causes may be responsible (Boenninghaus 1974; Kretschmer 1978; Myers and Sataloff 1984; Probst 1986; Brachvogel et al. 1991):

•Insufficient repair of dural defects

•Displacement of dural reconstruction (grafts, membranes) through manipulation (e.g., midface reduction following skull base treatment)

•High intracranial pressure

•False diagnosis of skull base fractures with dural injuries

•Iatrogenic dural injuries

To detect the reasons for recurrent liquorrhea, specific radiograph examinations are necessary (CT/JotrolanCT/MRI/liquor scintigraphy).To locate persisting liquor fistulae, intraoperative liquor marking with sodium fluorescein has proved its value (see Chap. 8).

The frequency of recurrent liquorrhea not only depends on the surgical technique but also on the type of injury. According to the modern literature it varies between 2% and 6% (Probst 1986; Lange et al. 1995).

Recurrent liquorrhea following dural and skull base repair (Donald 1998)

*cited by Probst 1971 - see the reference fruther down

**cited by Donald P. J., 1998 - see the reference further down No star – These authors are cited on there own in the reference list

Fig. 13.3  Frontal osteomyelitis. Reconstruction of the craniofrontal region with cancellous bone and titanium mesh. (a) Frontal cutaneous fistula formation following frontofacial reconstruction. (Gun shot injury of the midface and frontal skull

base.) (b) CT: osteolysis of the frontal bone with sequestration. (c) Reconstruction with cancellous bone graft and titanium mesh after sequestrotomy. (d) Postoperative X-ray and CT control