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African Journal of Neurological Sciences
Pan African Association of Neurological Sciences
ISSN: 1015-8618
Vol. 16, Num. 1, 1997
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SUBDURAL EMPYEMA IN THE KENYAN AFRICAN'
SUBDURAL EMPYEMA IN THE KENYAN AFRICAN'
R.F. RUBERTl
African Neurological Diseases Research Foundation Nairobi,
Kenya.
Code Number:NS97003
SUMMARY
Nine cases of subdural empyema in the Kenyan
African are reported. This rare but very serious intracranial
infection arises as a complication of meningitis in infants and as
a complication of paranasal sinusitis, otitis or trauma in older
children and adults. In two cases with chronic posttraumatic
subdural haematoma, the hematoma became infected by haematogenous
seeding. It is the Author's opinion that the treatment has a better
outcome by draining the pus via craniotomy rather than burr holes.
The operative mortality was of two cases (22.2 per cent).
RESUME
Neuf cas d'empyeme subdural observes au
Kenya sont rapportes. Ces rares mais graves infections
intracraniennes sont une complication des meningites chez le jeune
enfant, et des sinusites, des otites et des traumatismes craniens
chez les enfants plus ages ou les adultes. Dans deux cas avec un
hematome subdural chronique posttraumatique, l'infection etait
d'origine sanguine. D'apres les auteurs, le traitement par drainage
du pus est preferable apres une craniotomie plutet que par des
trous de trepan. La mortalite operatoire a ete de 2 cas
(22,2%).
Key words: Subdural Empyema - Kenya
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 in the preantibiotic era
subdural empyema was almost tmiversally 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
series.
Materials and methods
The Author has operated only 9 cases of
subdural empyema: this is 8.3 per cent of all intr-acranial
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.
Age |
Number |
0-10 |
3 |
11-20 |
2 |
21-40 |
2 |
40+ |
2 |
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 eases
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.
Symptoms/signs |
Number |
Fever + meningitis |
9 |
Raised intracra. Pressure |
6 |
Neurological deficits |
4 |
Epileptic seizures |
3 |
Coma |
4 |
The duration from the onset of symptoms until
the time of surgery ranged ffom few days to sixty days. The
intectious 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 tbllowing measles, one other
concomitam with otitis media. In the 6 cases over the age of 10
years, 3 were secondary to head injuries, 2 to frontal sinusiris
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.
Pathogenesis
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 of the
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.
Origin |
Number |
Percentage |
Trauma |
3 |
33 |
Paranasal |
2 |
22 |
Otitic |
2 |
22 |
Meningitic |
2 |
22 |
In infants and young there is a different
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, but 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 alter a free
interval of time a sudden onset of high fever, rapid deterioration
of the mental 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.
Organism |
Origin |
Number |
Streptococci |
- |
|
Aerobic Streptococcus |
Meningitic |
1 |
Anaerobic Streptococcus |
Paranasal |
2 |
Staphylococci |
- |
|
Staphylococcus aureus hemoliticus |
Trauma |
1 |
Staphylococcus aureus |
Trauma |
1 |
Hemophilus Influenza |
Meningitis |
1 |
Escherichia coli |
Trauma |
1 |
Sterile |
Otitic-Meningitis |
2 |
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.
Treatment
Rapid diagnosis, surgical removal of the
irritating pus and appropriate antibiotic therapy are the
principles that form the cornerstone for management of subdural
empyema (FEURERMAN 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
of otorhinologic 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. TheM.R.I. will help also to identify, in case of S.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 that 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 burr
holes 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 burr holes.
They attributed this improvement to more
complete removal of pus, which can be 1oculated, 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 FEURERMAN 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 |
Burr hole followed by craniot. |
2 |
1 |
50 |
Primarycraniotomy |
7 |
1 |
14 |
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 burr hole was the first treatment followed by
craniotomy, and a mortality of 14.2% in the cases 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 chloramphenicole that has been
used in all our cases. It penetrates the blood-brain barrier and
the brain tissues well (BANNISTER et all -1981). Topical
chloramphenicole 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 a decompressive measure.
In conclusion, an early diagnosis followed by a
radical removal of pus at the earliest possible stage by a large
craniotomy and antibiotic treatment seems to be today the treatment
of choice.
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