Subdural empyema (S.E) is a rare intracranial infection that .usually arises as a complication of meningitis in infants and as a complication of paranasal sinusitis, otitis or trauma in older children or adults (FEUERMAN et all). Subdural empyema by analogy with pleural empyema - is an appropriate generally accepted term for the diseases, since it is a collection of pus in preformed space. The first thorough clinico - pathological description of the disease were by KUBIK and ADAMS (1943) and COURVILLE (1944). The (S.E) is one of the most serious intracranial infections, so much that the preantibiotic era subdural empyema was almost universally fatal, and that despite surgical and antibiotic treatment, there is still a mortality of 15-40 per cent and a high morbidity rate in the reported scries.
MATERIALS AND METHODS
The author has operated only 9 cases of subdural empyema: this is 8.3 per cent of all intracranial infections of surgical interest operated in the same period of time (10% for BEDUSCHI and MAROSSERO 1960). The age breakdown in this series is in Table 1.
Table 1: Age of patients with subdural empyema
Out of 9 patients, seven were below forty and of these 3 were babies 10-11 months old. Six of the patients were males and 3 females. The subdural empyema was located in all cases at the convexity.
The presenting symptoms in this series were similar to those previously reported - fever, headache, nausea and vomiting, meningitism in the early stages, altered mental status focal neurological deficits, focal or generalised seizures in the late referral. Table 2. Shows the clinical breakdown.
Table 2: Clinical presentation of patients with subdural empyema.
|Fever + Meningitis||9|
|Raised Intracra. pressure||6|
The duration from the onset of symptoms until the time of surgery ranged from few days to sixty days. The infectious source of the subdural empyema was related to the age of the patient. In all three babies 10-11 months age the S.E. was secondary to meningitis. one following measles, one other concomitant with otitis media. In the 6 eases over the age of 10 years, 3 were secondary to head injuries, 2 to frontal sinusitis and one to chronic oto mastoiditis. All the cases of this series were in the pre C.T. Scanning era: 6 cases had carotid angiography with typical findings of subdural collection and in three babies two subdural taps and one ventriculography confirmed the diagnosis.
The pathogenesis of subdural empyema secondary to paranasal sinusitis, was first delineated in the classic paper by COURVILLE. The direct mechanism of infection of the subdural space is by erosion through the posterior wall ofthe frontal sinus and dura; as in two cases of frontal purulent sinusitis, and one case of chronic oto mastoiditis. The indirect mechanism of infection of the subdural space involves the interconnecting venous system of the extracranial and intracranial spaces. Retrograde spread of septic trombophlebitis occurs from the superficial mucosal veins into the dural venous sinuses, cortical bridging veins and cortical veins because these veins are valveless, and eventually the invasion of the subdural space.
Table 3: Presumed source of infection in cases with subdural empyema.
In infants, and young there is a diflerent pathogenetic mechanism. These patients nearly always has meningitis associated with the S.E. as opposed to adults. It has been hypothesized that in this young children a subdural effusion forms secondary to meningitis ( 12 per cent of cases); this effusion subsequently becomes infected forming a subdural empyema. Trauma has an important role in the S.E.; not only the penetrating wounds may be the cause, hut also post operative empyemas. Trauma may infect the subdural space even in closed head injuries when a linear fracture involves the posterior wall of the frontal sinus or the ethmoidal sinuses, where the dura is thin and strictly adherent to the bone, may lacerate the dura putting the subdural space in communication with the sinuses: this happened to one of our cases. In cases following a head injury with the information of a subdural haematoma characterised by progressive headache after a free interval of time a sudden onset of high fever, rapid deterioration of the menial status, epilepsy and severe neurological deficits with signs of meningism indicate that the subdural hematoma has become infected and transformed in a subdural empyema: this happened in two of our cases in which one the infection of the subdural hematoma was probably due to associated chest infection and where a streptococcus was isolated and the second, where the infection of the subdural hematoma was probably due to a gastrointestinal infection and where an Escherichia coli was isolated. Most probably the infections of these subdural hematomas is due to a "locus minoris resistentiae" in patients carrying a concomitant infective disease. Facial infections and rupture of an intracerebral abscess may also be considered in the pathogenesis of the subdural empyema. Hematogenous seeding of the subdural space must be exceptional because only DE GROOD (1951) has reported two cases, one following a parotitis and the other consequent to a lung abscess due to actinomicosis. Following DE GROOD, the infection follows the hematic stream, forms a small cortical abscess that opens in the subdural space.
Table 4: Organism in subdural Empyema
|Staphylococcus aureus hemoliticus||Trauma||1|
In infants the most common organisms found in S.E. is the Hemophilus Influenza and Aerobic Streptococcus as in two of our babies. In 5 other cases the bacteriology showed: Staphylococcus aureus hemolyticus, staphylococcus aureus, anaerobic streptococcus in two cases, bacterium coli in one case. In two cases the pus was sterile.
Rapid diagnosis, surgical removal of the irritating pus and appropriate antibiotic therapy are the principles that form the cornerstone for management of subdural empyema. (FEUERMAN et all 1989). The rapid diagnosis of S.E. is not always easy, but when the classic syndrome of headache, nausea, vomiting, fever and meningism followed-by neurological deficits and seizures is present in conjunction with parasanal sinusitis, otitis or mastoiditis, the diagnosis of intracranial suppuration (either sudural empyema or brain abscess) is clear. When no history ofotorhinologic disease is present, the diagnosis is difficult between that from brain abscess, meningitis, cerebritis or viral encephalitis. But in the suspicion of S.E. or brain abscess, mainly in the presence of focal neurological deficit or focal seizures, neuro-radiological investigations (angiography where scanning is not available), C.T. scan with contrast and even better M.R.I, are mandatory. The M.R.I, will help also to identify, in case ofS.E., the possible extension of empyema in the interhemisperic fissure, the opposite side and in the posterior fossa.
It has been reported by various authors (BANNISTER et al) that the CT Scan may be normal or not indicative of a subdural empyema. In this cases it is suggested tisal if the clinical evidence is in favour of subdural empyema and considering the gravity of the infection, a surgical exploration is indicated, or else, the use of angiography or better M.R.I.
Once the diagnosis is radiologically confirmed immediate surgical drainage should be undertaken. Since the advent of C.T. scan with usually accurate localization of the empyema, selective burr holes with irrigation of the cavity through the burrholes has been advocated (RENAUDIN et al-1980). BANNISTER et al (1981) take exception to this approach in their publication. They reviewed their experience with 66 cases and a further 309 cases that has been reported in the literature by 1980 and reach the conclusion that a better outcome was achieved by draining the pus via craniotomy rather than burrholes.
They attributed this improvement to more complete removal of pus, which can be loculated, thick and tenacious. Thus, burr hole drainage, even with catheter irrigation, may not adequately drain an empyema. This recommendation is substantiated by the experience of FEUERMAN et al (1989) and by our modest experience of 3 cases published in 1961 and other nine cases treated in Kenya.
Table 5: Type of surgery and outcome in cases of subdural empyema
|Type of operation||Number||Mortality||Percentage|
|Burrhole followed by craniot.||2||1||50|
In our series two cases had burr holes as a first treatment: the first case a subdural empyema was evacuated elsewhere through burr hole: he was later referred to us in coma and a craniotomy was performed but the patient died. The second case a baby had a ventriculography and drainage of a subdural empyema during the procedure, required craniotomy 4 days after with complete recovery. The other 7 cases had all primary craniotomies with one death and one patient recovered (a baby) with severe hemiparesis. In our series of 9 cases there is a mortality of 50% in cases in which the burrhole was the first treatment followed by craniotomy, and a mortality of 14.2% in the case: treated with primary craniotomy. The total mortality rate was of 2 cases over 9 (22.2 percent).
The drug of choice before the culture results are hand, and usually afterwards, is chloramphenicol that has been used in all our cases. It penetrates the blood-brain barrier and the brain tissues well (BANNISTER et all -1981). Topical chloramplienicole was used in the first 4 cases: in the last 5 cases topical Rifampicine was used. The dura was closed in 8 cases and left open in one case. A subdural drain was left in all cases but have not been used for irrigation post-operatively. In all cases the bone flap was removed to avoid possible risks of post operative osteitis and also as decompressive measure.
In conclusion, an early diagnosis followed by radical removal of pus at the earliest possible stage by a large craniotomy and antibiotic treatment seems to be today the treatment of choice.