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Decreased morbidity from acute bacterial spinal epidural abscesses using computed tomography and nonsurgical treatment in selected patients.

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Decreased Morbidity from Acute Bacterd
Spinal Epidural Abscesses Using Computed
Tomography and Nonsurgical Treatment in
Selected Patients
D. Leys, MD," F. Lesoin, MD,? C. Viaud, MD,S F. Pasquier, MD," M. Rousseaux, MD," M. Jomin, MD,f
and H. Petit, MD*
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We describe 5 patients with spinal epidural abscesses in whom computed tomographic scanning confirmed diagnosis
without the use of myelography. One patient required urgent surgery because of rapidly deteriorating neurological
status, but the other 4 were treated nonsurgically. The medical treatment of these patients and 9 others described in
the literature consisted of antibiotics administered parenterally for a minimum of 8 weeks, followed by oral antibiotic
therapy. Early diagnosis with computed tomographic scanning and a benign neurological state at the onset of treatment were associated with good results.
Leys D, Lesoin F, Viaud C, Pasquier F, Rousseaux M, Jomin M, Petit H: Decreased morbidity from acute
bacterial spinal epidural abscesses using computed tomography and nonsurgical treatment in selected
patients. Ann Neurol 17~350-355, 1985
Recently, medical treatment has been employed increasingly to treat brain abscesses [12, 141 as well as
intracranial subdural [S} and extradural[9} empyemas.
This new approach depends heavily on the use of computed tomographic (CT) scanning [12, 151 for early
diagnosis and follow-up. Extending this principle, we
have used CT scanning for diagnosis and follow-up in
5 patients with spinal epidural abscesses, 4 of whom
were treated nonsurgically.
Case Reports
Patient 1
A 62-year-old man with cirrhosis of the liver had intermittent back pain for 2 weeks. The pain increased, and fever and
urinary incontinence developed. On admission 30 days later,
his body temperature was 40°C. There was cervical, thoracic,
and lumbar paraspinal spasm, and severe tenderness over
T9-Tl0. He was incontinent for urine and feces. Neurological examination indicated sensory loss from S 1 to
S3 on the left and from S3 to S5 bilaterally; reflexes were
absent in the legs. White blood cell count (WBC) was
14,200 per cubic millimeter (80% polymorphonuclear cells
[PMNs]) and erythrocyte sedimentation rate (SR) was 80
mm per hour. Standard thoracic and lumbar spinal roentgenograms were normal. A spinal CT scan (Fig l), performed without myelography but after intravenous administration of contrast agent, showed from T10 to S2 there was a
From the Departments of *Neurology, tNeurosurgery, and
SNeuroradiology, University of Lille, France.
Received Dec 27, 1983, and in revised form Feb 9, July 19, and Sept
5, 1984. Accepted for publication Sept 15, 1984.
350
loss of the physiological low density associated with epidural
fat tissue normally found around the spinal cord, and a discrete area of higher density, where the contrast material had
fixed at the level of the dural sheath. There was no sign of
spondylodiscitis, and perispinal soft tissue was normal. A
guided puncture at the level of L1 yielded thick pus, from
which Staphylococcus aweus was isolated, and framycetine, 10
mg, was administered locally. The patient received cefotaxh e (8 gm intravenously [IV]), fosfomycine (12 gm IV), and
tobramycin (225 rng intramuscularly [IM]) daily for 6 weeks.
The cause of the epidural abscess was not found. Because of
the cirrhosis, as well as abnormalities of coagulation, surgery
was withheld.
Ten days later the patient was afebrile and had less lumbar
pain. Reflexes became normal in the legs, and continence
returned. Six weeks after the onset of treatment, all symptoms had disappeared, but sensory loss remained from S3 to
S5 on the left. At that time parenteral therapy was stopped,
and a two-month course of rifampicine (600 mg daily orally)
followed. Standard thoracic and lumbar spinal roentgenograms and a CT scan obtained after this treatment were normal. One year later a small sensory loss persisted from S3 to
S5 on the left side, without functional discomfort.
Patient 2
A 57-year-old woman was first examined because of progressive lumbar pain without radicular irradiation in May
1983. In July the pain became worse, confining her to bed.
Address reprint requests to Prof Petit, Service de Neurologie,
HBpital B, 59037 Lille Ckdex, France.
A
B
Fig I . (Patient I .) (A) Before treatment, computed tomographic
scan shwed the loss of the physiological low density associated
with epiduralfat tissue (arrow). (B) After antibiotic treatment,
the low density reappeared (double arrows).
She became constipated and developed urinary retention.
Neurological examination revealed no other abnormalities.
Spinal percussion of T12 and L2 was painful, and intense
paravertebral spasm extended to the thoracic region. Her
body temperature fluctuated between 37.5 and 38°C. SR was
119 and 130 mm per hour. WBC was 9,700, with 79%
Fig 2. (Patient 2.) (A) Before treatment, computed tomographic
scan showed an epiduralfixation of contrast (arrow) posteriorly
and laterally t o the right, and abnormalfixation of intravenous
contrast at the level of the dural sheath (double arrows). (3)
After antibiotic treatment, these abnormalities have disappeared.
A
neutrophils. Standard lumbar spinal roentgenograms and
tomograms were normal. A spinal CT scan (Fig 2) from T10
to L2 showed epidural fixation of contrast material posteriorly and laterally to the right. Abnormal projections
arose from the anterior portion of the upper surface of the
L3 vertebra, mainly on the right. The physiologically normal
fat tissue was not visualized in the epidural space. A hypodense-appearing lesion was found on the right side on the
vertebral surface, corresponding to a “punched-out” area.
The perispinal tissue was normal. The signs indicated a posterolateral epidural abscess extending from T11 to L2. A
guided puncture yielded thick pus from which Streptococcus
sanguis was isolated. No point of entry or septicemia was
found. During the puncture 10 mg of framycetine was administered locally. Treatment consisted of cefotaxime (8 gm
IV), fosfomycine (12 gm IV), and tobramycin (225 mg IM)
daily for 5 weeks. Within one month the patient recovered
clinically, and the abscess was no longer visible on CT scan.
B
Leys et al: Spinal Epidural Abscess 351
A
B
A second set of vertebral tomograms demonstrated spondylodiscitis. A two-month course of amoxicillin (6 gm daily
orally) followed. Total recovery had occurred by November
1983.
F ig 3. (Patient 3.) (A)Befre treatment, computed tomogruphic
scan showed an abnormalfixation of contrast in the dural
sheath (arrow) and a loss offat tissue (double arrows). ( B )A$
ter antibiotic treatment, the lw density appearance typical of fat
tissue reappeared (arrow).
Patient 3
A 63-year-old man was first seen in August 1983 with inoperable carcinoma of the sigmoid colon treated by colostomy
because of pelvic extension. Five days later he became febrile
(39°C) but had no other pathological signs. Blood culture
isolated Proteus mirabilis. Twenty-four hours later severe
lumbar pain occurred, with irradiation to the L5 root on the
right. The patient's temperature was 39.2"C, his neck was
supple, and Kernig's sign was absent. There was percussion
tenderness from T5 to L5, with weakness and sensory loss in
the L5 territory on the right. Reflexes were absent in the
legs, and urinary and fecal retention were present. WBC was
18,000 (80% PMNs), and SR was 104 mm per hour. Standard spinal roentgenograms were normal. Spinal C T scan
(Fig 3 ) from T4 to S1 showed little fixation of the contrast
material at the level of the wall of the dural sheath and an
extended area of high density adjacent to it, from T5 to L5,
without sign of spondylodiscitis or perispinal soft tissue infection. Epidural fat tissue was not seen. Guided puncture
discharged thick pus from which no organism was isolated,
and 10 mg of framycetine was administered locally. Treatment consisted of cefotaxime (6 gm IV) and trimethoprimsulfamethoxazole (320 to 1,600 mg IV) daily for 8 weeks,
the sulfamethoxazole having already been initiated. Fever
and back pain decreased in about 2 weeks. Weakness of the
right leg disappeared and reflexes returned to normal after a
month. Sensory loss and urinary retention resolved during
the third month; at this time standard roentgenograms and
CT scans were normal. Parenteral therapy was stopped in
October 1783 and followed by a two-month course of amoxicillin (6 gm daily orally). Treatment was stopped and there
had been no relapse as of six months later.
Patient 4
A 30-year-old man was treated on November 28, 1783, by
chemonucleolysis for a herniated left S1 lumbar disc. Twenty
352
Annals of Neurology
Vol 17 No 4
April 1785
hours later he became febrile (40°C),lumbar pain developed,
and the radicular pain increased. Clinical examination revealed weakness and sensory loss in the S1 territory on the
left, leg areflexia, constipation, urinary retention, and perianal anesthesia. WBC was 25,600 (80% PMNs), and SR
was 76 mm per hour. Standard roentgenograms were
normal, but a C T scan (Fig 4) showed an area of anterior
and posterior high density at the S1 level. Because of rapid
neurological deterioration, laminectomy was performed a
few hours after admission to evacuate an epidural abscess at
L5-S1. No organism was isolated (antibiotic therapy was
started before admission). A course of cefotaxime (6 gm IV
daily), fosfomycine (12 gm IV daily), and tobramycin (225
mg IM daily) was maintained for two months. Fever disappeared, but signs of cauda equina compression persisted,
with urinary retention, perianal sensory loss, and areflexia. A
C T scan showed signs of spondylodiscitis. Parenteral therapy
was stopped, and a 6-week course of pristinamycin (3 gm
orally daily) followed; five months after onset urinary retention persisted.
Patient 5
A 52-year-old man became febrile following surgery in August 1983 for an L4-L5 herniated disc. The patient received
6 gm of ampicillin intravenously daily for 2 weeks. O n day
20 fever had disappeared but lumbar pain appeared and increased slowly.
By December 1983 lumbar radicular (L4) pain was severe
and sphincter involvement had developed. Body temperature was 37.5%. Physical examination showed no motor or
sensory loss, but knee jerk reflexes were absent. WBC was
normal, but SR was 64 and 112 mm per hour. Standard
roentgenograms and tomograms revealed signs of spondylodiscitis at L4-L5, including loss of disc thickness, conden-
A
B
F i g 4. (Patient 4.1 (A)Before treatment, computed tomographic
scan showed an area of higher density (arrow) surrounding an
area of lwer density (double arrows). (B) After laminectomy
and antibiotic treatment, the abnormalities disappeared.
Fig 5 . (Patient 5 .I Computed tomographic scan obtained before
antibiotic treatment revealed mainly signs of spondylodiscitis (arrow) but also a small area of epidural infection near the bone
(double arrows).
up, tomograms showed only residual healed spondylodiscitis
without signs of epiduritis.
Discussion
Use o f CT Scan for Diagnosis
To localize an acute bacterial spinal epidural abscess,
myelography with water-soluble contrast material has
been recommended { 131, but this procedure may be
dangerous 141. In our 5 cases CT scanning of the spine
without myelography but after intravenous administration of meglumine iothalamate (1.5 mglkg) revealed
the abscess. The most common sign, present in all 5
patients, was the loss of the physiological epidural fat,
which reappeared a few weeks later (see description
of Patient 3). Another sign consisted of an unusual
fixation of the contrast material at the level of the dural
sheath, which was surrounded by an area of higher
density situated between bone and the dural sheath
(see description of Patient 2). CT scanning revealed
the epidural abscess, specified its height, localization,
and volume, and guided the subsequent epidural puncture, which isolated the causative organism in 3 of 4
medically treated patients. In 3 cases CT scanning revealed infection of the bone.
Nonsurgical Treatment of Spinal Epidural Abscesses
sation of the upper surface of the body of LS and the lower
surface of L4, and the presence of a “punched-out” area. CT
scan (Fig 5 ) confirmed the signs of spondylodiscitis and revealed a small area of epidural inflammation near the bone
infection; epidural fat tissue was not found, and a small area
of higher density replaced it. Gallium 67 uptake was increased at L4-L5. No organism was isolated. The patient
received cefotaxime (8 gm IV), fosfomycin (12 gm IV), and
tobramycin (225 mg IM) daily for 8 weeks, after which back
pain decreased, fever disappeared, and sphincter function
became normal. Parenteral therapy was stopped, and a twomonth course of pristinamycin, 3 gm orally daily, followed.
By the completion of this course of treatment, symptoms
had disappeared and WBC and SR were normal. On follow-
Antibiotics alone are effective therapy for spinal epidural abscesses. Among our 4 patients, 3 have recovered completely and the fourth has minor sequelae.
Some authors have already treated spinal epidural abscesses with antibiotic therapy alone; these cases, including 6 of ours {lo}, are summarized in Table 1. In
these 13 patients treated without surgery, neurological
signs of compression of the spinal cord o r cauda equina
were often limited ( { l l } ;our Patients 1-3, 5 ) and
paraplegia was often incomplete 14, 7, 10, 17). Nevertheless, in 3 cases of complete paraplegia C4, lo}, partial or complete recovery was also obtained. Of these
13 patients, 10 recovered completely, 1 has minor sequelae, and 2 have severe sequelae. These results are
Leys et al: Spinal Epidural Abscess
353
TaHe 1. Patients Treated Without Surgwy
Author
Reason for
Nonsurgical Treatment
Janbon et al 1947 C71
?
Gautier and Luthier
?
1974 t41
Messer et a1 1977 [ l l ] Poor state of health
Neurological State
Basis of Diagnosis
Clinical Outcome
Signs of cauda equina
compression
Total paraplegia
EP
TR
EP
TR
No sign of com-
Myelography and EP
TR
IP
Myelography and EP
TR
IP
IP
Myelography and EP
Myelography and EP
TR
TR
IP
Total paraplegia
Myelography and EP
Myelography and EP
TR
Major sequelae
Total paraplegia
Myelography and EP
Major sequelae
IP
IP
C T scan and EP
C T scan and EP
Minor sequelae
TR
IP
1P
C T scan and EP
C T scan
TR
TR
pression
Leys et a1 1984 [lo]
1
2
3
4
5
6
Present cases
1
2
3
5
Minor neurological
signs
Poor state of health
Minor neurological
signs
Length of infection
Complete and old
paraplegia
Complete and old
paraplegia
Poor state of health
Minor neurological
signs
Poor state of health
Minor neurological
signs
IP = incomplete paraplegia; EP = epidural puncture; TR = total recovery; CT = computed tomographic.
Table 2. Clinical Outcome with Use of Surgey in Six Series
No. of Patients
~~~~~~
Author
Hancock 1973 [6]
Baker et a1 1975 El]
Russel et al 1979 El61
Hakin et al 1979 [ 5 ]
Phillips and Jefferson
1979 ri31
Leys et al 1984 [lo]
Total
Total
Total Recovery
Minor Sequelae
Major Sequelae
0
2
6
5
4
14
6
13
5
8
3
4
25
4
12
11
23
11
3
2
2
1
34 (22%)
1
43 (28%)
49
34
29
17
155
10
64 (41%)
better than those obtained with emergency surgical
treatment with associated antibiotic therapy. Table 2
summarizes 155 sugically treated cases in six reported
series. A total of 14 deaths (9%), 43 cases with major
sequelae (28(%), 34 cases with minor sequelae (22%),
and 64 patients with total recovery (41%) were observed. The better results with nonsurgical treatment
can be explained at least partly by the fact that 10 of
the 13 patients had less severe neurological involvement at the onset of treatment. A second factor is that
354 Annals of Neurology Vol 17 No 4 April 1985
Deaths
1
5
14 (9%)
the infectious process is not enclosed 141, and the antibiotics easily diffuse into it.
Even if surgical treatment becomes necessary, certain principles govern the use of antibiotic therapy: (1)
The agents must be active against Staphylococcus alcreiw,
the causative organism in most cases 14, 6, lo]. ( 2 )
They must be able to diffuse into bone so as to treat
spondylodiscitis 16, lo]. ( 3 )They must have low toxicity so as to permit prolonged treatment (13 to 16
weeks in our cases; a little less elsewhere in the litera-
ture). We prefer the combined use of cefotaxime, fosfomycine, and tobramycin. In one case trimethoprimsulfamethoxazole replaced fosfomycine and tobramycin;
this modification was necessitated by antibiotic therapy
prescribed before admission. Parented therapy must
be prolonged, in our experience a minimum of 8
weeks, and oral therapy must follow. Antibiotic therapy is, of course, adjusted to the causative organism. In
3 cases we started treatment by administering framycetine (10 mg) at the time of epidural puncture.
Based on the 13 cases summarized here, we recommend that the following patients with spinal epidural
abscess receive exclusively medical treatment:
Patients who represent poor surgical candidates because of severe concomitant medical problems.
Those whose abscess involves a considerable length
of the vertebral canal and who have an epiduritis
from the cervical to the lumbar level.
Patients not suffering severe loss of spinal cord or
cauda equina function.
Patients who have complete paralysis for more than
3 days.
Patients with a localized spinal epidural abscess who
neurologically probably
should be operated on as soon as possible ({lo, 111;
our Patient 4). In such cases an extensive laminectomy
must be performed 113, 141, with evacuation of pus
and local administration of antibiotics 121. We have no
experience with the suction irrigation technique, proposed in 1983 by Garrido and Rosenwasser {3],which
requires prior laminectomy.
are rapidly deteriorating
The authors thank Elias H. Sarkis, MD, and Joanna L. Schmidt, MA,
for revision of the English manuscript.
References
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epidural abscess. N Engl J Med 293:463-468, 1975
2. Ferguson JF, l r s c h WM: Extradural empyema following thoracic extradural block; case report. J Neurosurg 41:762-764,
1974
3. Garrido E, Rosenwasser RH: Experience with the suctionirrigation technique in the management of spinal epidural infection. Neurosurgery 12:678-679, 1983
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9:509-515, 1974
5. Hakin RN, Burt AA, Cook JB: Acute spinal epidural abscess.
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6. Hancock DO: A study of 49 patients with acute spinal extrad u a l abscess. Paraplegia 10:285-288, 1973
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13. Phillips GE, Jefferson A: Acute spinal epidural abscess: observations from fourteen cases. Postgrad Med J 55:712-715, 1979
14. Rosenblum ML, Hoff JT, Norman D, et al: Nonoperative treatment of brain abscesses in selected high risk patients. J
Neurosurg 52:217-225, 1980
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Leys
et al: Spinal Epidural
Abscess
355
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