169
CLINEU 00174
Case report
Brain abscess after esophageal dilatation fur stenosis L, Algoed”, I? Boonb, M. De Vosc, K. Van Den Abeele”, P. Santensb, J. De Reuckb and L. Calliauw”’ Depurtments
of “Neurosurgery, hNeurology, and ‘Gostro-~nterok)~~~
Univcwity Hospitul, Glwnt, Belgiurrr
(Received 24 June, 1991) (Revised, received I4 October, I99 L) (Accepted 14 October, 1991) Kq
wortds:
Brain abscess; Esophageal dilatation
Summary
The case is presented of a 2%year-old female with a brain abscess after esophageal dilatation for stricture, secondary to an acute necrotizing esophagitis. Other causes of brain abscess were excluded. To our knowledge this is the first documented case of brain abscess after dilatation for esophageal stricture in adult life. Some reports in the pediatric literature have been published previously.
Introduction
A brain abscess arises either as a direct result from infections within the cranial cavity, from infections secondary to skull fracture or neurosurgical procedures, or as metastasis from infections elsewhere in the body. Metastatic abscesses in the brain are commonly seen secondary to a suppurative process in the lungs or heart [I]. A very rare cause of brain abscess is esophageal dilatation. This condition has been described in children after accidental ingestion of chemical agents [2-S]. We report here a Z&year- old woman who presented with a brain abscess after repeated esophageal dilatations for peptic stenosis secondary to an acute necrotizing esophagitis.
Case report
A 2%year-old
woman
was hospitalized
with com-
c’orr-erpot,di~~?~~~ 10: L. Algoed, Department of Neurosurgery, University Hospital. De Pintelaan 185. 9000 Ghent, Belgium.
plaints of abdominal pain and hematemesis. At that time the patient was 38 weeks pregnant. She underwent a laparatomy because of an acute abdomillai syndrome with signs of peritonitis. Appendectomy and right ovariectomy were performed but no signs of inflammation were found. The delivery 4 days later was uneventful. The next day a gastroscopy was done because of persistent vomiting and retrosternal pain upon eating. The distal half of the esophagus appeared ulcerative with black necrotic plaques. Superficial erosions were noted in the stomach. No cultures or biopsies were taken. The patient was treated with omneprazole and cisapride. Her condition improved temporarily. However, after 1 month she conlpl~l~ned ofdysphagia. On endoscopy tubular narrowing of the distal esophagus was seen. The pink, friable and granular mucosa was covered by a thick white exsudate. Dilations with Savary bougies were started on day 1. This procedure was repeated 10. 22, 29 and 38 days later. No antibiotic prophylaxis was given. On day 45, the patient started to experience a progressive weakness of the right arm and leg. A few days later. she had the im-
Fig. 1. Stereotaxic CT scan with administration of contrast medium showing a ring-like enhancement with perilesional edema in the left parietal lobe.
pression
that her speech was less fluent and on day 54 she
was admitted to the neurological department. Neurological examination on admission showed operative
patient
side, a deviation
with a central of the tongue
ate right hemiparesis
a co-
facial palsy on the right
with Babinski
sign. There
scan of the brain showed a left parietal a ring-like enhancement after contrast scan visualised
aspiration
of the abscess,
lesion with moderate
showed
contrast
only a small residual
enhancement
(see Fig. 2).
to the right and a moderwas no
fever, meningeal irritation or fundoscopic abnormalities. Routine laboratory examination revealed a microcytic anemia and a slightly elevated sedimentation rate. CT
1). A Tc brain
Fig. 2. CT scan with administration of contrast medium 6 weeks after aspiration showing only a small residual lesion in the left parietal lobe.
hypodensity with infusion (see Fig.
an increased
focal activity
at the same site. Other paraclinical investigations total body scan. transesophageal echo Doppler,
such as abdomi-
nal echography, sinus and lung x-rays were normal. Gynecological, ophthalmological and otorhinological examinations revealed no abnormalities. On day 65, the patient underwent a stereotactically guided aspiration of the brain lesion (see Fig. 1). Pus was evacuated and the following organisms were cultured: Streproeoccus milleri (preponderant). Ekonellu mrrodens, Veillonellu sp. and Bucttwides nwluninogenicus. On further treatment with intravenous antibiotics for 6 weeks (cefotaxim, metronidazole and penicilline), the patient improved and the hemiparesis resolved almost completely. A control CT scan, performed 6 weeks after
Discussion In this patient with a metastatic brain abscess no other source than the esophagus has been found; 6 weeks before the onset of neurological derwent
a first esophageal
symptoms
Bacteremia, secondary to esophageal been demonstrated in different studies [15] suggested
in 1940 that
moms could metastasize
the patient
un-
dilatation.
abdominal
dilatation, has [lo-141. Batson and
pelvic
to the brain via retrograde
tuflow
in lumbar and perivertebral veins. A similar mode of spread might explain the occurrence of brain abscesses following esophageal dilatations. Peri-esophageal venules interconnect with vertebral veins so that blood may be forced into the brain in a retrograde fashion [2]. The other proposed mechanism is transient bacteremia induced by disruption of the esophageal mucosa with arterial seeding into the brain [3]. This appears more likely due to the supratentorial location of the abscess in the presented case.
171 TABLE I CASES OF BRAIN ABSCESS AFTER DILATATION
REPORTED
IN THE LITERATURE
Author (patient’s age and sex)
No. of dilatations
Antibiotics peri-dilatation
Steroids
Organism
Schlitt [4] 1.17 mo, M
2
yes
no.
B. meluninogenicus,
Neisseriu sp.,
no.
Peptococcus sp. B. melaninogenicus,
microaerophilic
Streptococcus H. paraprophilus
2.4 yrs, F
9
yes
3
yes
yes (2 d)
Golladay et al. [6] 6.5 yrs, M
8
NA (given perioperatively)
NA (given perioperatively)
Kotler et al. [8] 1.17 mo, F 2.2 yrs. F 3.15 yrs. F
multiple NA multiple
yes ( 1 course) yes ( 1 course) yes ( 1 course)
yes (1 course)
S. aureus
yes ( 1 course)
NA NA
Leahy et al. [7] I .4 mo. NA 2.6 yrs. M
4 multiple
NA NA
NA NA
NA Microaerophilic
3
NA
NA
Streptococcus, Staphylococcus epidermidis, Group B Streptococcus S. aureus
Neuman et al. [2] 16 mo, M
NA
NA
NA
Streptococcus
Harp et al. [3] 16 mo, M
4
NA
NA
Microaerophilic group F, betahemolytic Streptococcus
Lui [5] I .5 yrs. M 2.16 mo, M
4 7
NA NA
NA NA
Sterile
Rontal et al. [9] 17 yrs. M
multiple
yes (initially and perioperatively)
yes (initially and perioperatively)
Sterile
Present study 28 yrs. F
5
no
no
Streptococcus milleri, Ekonella corrodens, Bacteroides
3,4.5 yrs, M
3.4 yrs. F
S. aureus
viridans
Pepto-, Streptococcus
meluninogenicus,
anaerobic
Veillonelka
NA = not available.
Various authors (Table 1) have reported cases of brain abscess after esophageal dilatation [2Z 91. All these previously reported patients were in the pediatric age group
and all had supratentorial abscesses. The isolated organisms belong, like in this patient, to the normal oropharyngeal bacterial flora. The origin of brain abscess of
172 these children
can be explained
since steroid tients,
has been the routine
immunosuppression
thogenesis.
by two mechanisms
On
the other
fluid intake
might
play a role in the pachildren
are perhaps
dehydration
because
due to the esophageal
This causes physiological crease
polycythemia,
the flow of the microcirculation
formation
and subsequent
is then more prone the bacteremic developed
leading
to cloth
in the brain.
an abscess
phase after dilatation.
a brain
of
stricture.
which might de-
microinfarcts
to develop
It
focus during
Why our patient
abscess is not clear. There was no evi-
dence
of immunosuppression.
acute
necrotizing
The initial
esophagitis
event
[16], of which
was an
the patho-
genesis remains unclear. The CT scan findings on admission (day 54) corresponded with a stage of capsule formation of the abscess of more than 14 days [17,18]. Keeping also in mind that the neurological signs started on day 45, we can pressume that the dilatation performed on day 29 or 38 caused the spread of the bacteria leading
to the brain abscess.
The use of prophylactic antibiotics by esophageal dilatation is controversial; however, it is only generally accepted for cardiac
patients
4 Schlitt,
A. ( 1977) Bacteremia following esophageal dilation and esophago-gastroscopy. Aust. N.Z. J. Med., 7: 32-35. W.J., McKee. J., Wilkinson, D., 12 Welsh, J.D., Griftiths.
particularly during adult life. Anyhow, the clinician should be alert to this condition in the presence of persistent fever and neurological signs in patients with a his-
I4
Berg, L. and De Marchena, 0. (1989) Focal infections. In: Rowland, L. (Ed.), Merritt’s Textbook of Neurology, Lea & Febiger, Philadelphia-London, pp. 8896. Neuman, A., Lernau, O.Z., Goldberg, M., Hod, G. and Nissan. S. (I 986) Brain abscess. A complication of esophageal dilatations. Z. Kinderchir., 41: 4344. Harp, D., Schlitt, M.D., Williams, P. and Shamoun, J. (I 989) Brain abscess following dilatation of esophageal stricture. Clin. Imag., 13: 140&141.
report
Metastatic abscess as a complication of retrograde esophageal dilatation. Ann. Otol., 82: 643-648. IO Botoman. A. and Surawicz, C. (1986) Bacteremia with gastrointestinal endoscopic procedures. Gastrointest. Endosc. 32 (5): 342-346. II Stephenson, P.M., Dorrington. L., Harris, O.D. and Rao,
13
References
G. et al. (1985) Brain ab-
Cerebral abscess in children secondary to esophageal dilatation. Pediatrics, 59: 300-30 1. 8 Kotler, R.. Schild, J.A. and Holinger, P.H. (1975) Delayed CNS complications. Laryngoscope, 85: 137991386. 9 Rental. E.. Meyerhoff, W. and Duval, A.J., III. (1973)
with a high risk of endocardi-
dilatation.
L., Zorn,
5 Lui, T.N., Lee, S.T., Chang, C.N. and Wang, H.S. (1988) Brain abscess after dilatation of esophageal Stricture. Pediat. Neurosci.. 14: 250-253. 6 Golloday, ES., Tepas, J.J., 111, Pickard, L.R.. Siebert, J.J.. Brown, R.W. and Haller. J.A. (1980) Bacteremia after esophageal dilation: a clinical and experimental study. Ann. Thorac. Surg. 30: 19-23. 7 Leahy. W.R., Toyka, K.V. and Fischbeck, K.H.. Jr. (1977)
tis [17]. The occurrence of brain abscesses after esophageal dilatation for stricture remains a very rare complication,
tory of esophageal
M., Mitchem,
scess after esophageal dilatation for caustic stricture: of three cases. Neurosurgery. 17(6): 947-95 1.
in these pa-
hand,
more easily in a state of chronic decreased
treatment
[5]:
15
I6
Flournoy, D.J. and Mohr, J. (1983) Bacteremia associated with esophageal dilation. J. Clin. Gastroenterol. 5: 109--I 12. Raines. D.R.. Brache, W.C., Anderson. D.L. and Boyce, W.H. The occurrence of bacteremia after esophageal dilation. Gastrointest. Endosc., 22: 86-87. Yin. T.P.. Ellis. R. and Dellipiani, A.W. (1983) The incidence of bacteremia after outpatient Hurst bougienage in the management of benign esophageal strictures. Endoscopy, 15: ‘89-790. Batson. O.V. ( 1940) The function of the vertebral veins and their role in the spread of metastases. Ann. Surg.. 112: 138149. Goldenberg, S., Wain. S. and Marignani, P. (1990) Acute
necrotizing esophagitis. Gastrbenterology, 98: 493496. I7 Britt, R., Enzmann. D. and Yeager. A. ( 198 1) Neuropathological and computerized tomographic findings in experimental brain abscess. J. Neurosurg.. 55: 590-603. 18 Britt. R. and Enzmann, D. (1983) Clinical stages of human brain abscesses on serial CT scans after contrast infusion. J. Neurosurg.. 59: 972-989. 19 Neu. H. and Fleischer. D. (1989) Recommendations for antibiotic prophylaxis before endoscopy. Am. J. Gastroenterol., 84: 148881491.
CLINEU 00174
Case report
Brain abscess after esophageal dilatation fur stenosis L, Algoed”, I? Boonb, M. De Vosc, K. Van Den Abeele”, P. Santensb, J. De Reuckb and L. Calliauw”’ Depurtments
of “Neurosurgery, hNeurology, and ‘Gostro-~nterok)~~~
Univcwity Hospitul, Glwnt, Belgiurrr
(Received 24 June, 1991) (Revised, received I4 October, I99 L) (Accepted 14 October, 1991) Kq
wortds:
Brain abscess; Esophageal dilatation
Summary
The case is presented of a 2%year-old female with a brain abscess after esophageal dilatation for stricture, secondary to an acute necrotizing esophagitis. Other causes of brain abscess were excluded. To our knowledge this is the first documented case of brain abscess after dilatation for esophageal stricture in adult life. Some reports in the pediatric literature have been published previously.
Introduction
A brain abscess arises either as a direct result from infections within the cranial cavity, from infections secondary to skull fracture or neurosurgical procedures, or as metastasis from infections elsewhere in the body. Metastatic abscesses in the brain are commonly seen secondary to a suppurative process in the lungs or heart [I]. A very rare cause of brain abscess is esophageal dilatation. This condition has been described in children after accidental ingestion of chemical agents [2-S]. We report here a Z&year- old woman who presented with a brain abscess after repeated esophageal dilatations for peptic stenosis secondary to an acute necrotizing esophagitis.
Case report
A 2%year-old
woman
was hospitalized
with com-
c’orr-erpot,di~~?~~~ 10: L. Algoed, Department of Neurosurgery, University Hospital. De Pintelaan 185. 9000 Ghent, Belgium.
plaints of abdominal pain and hematemesis. At that time the patient was 38 weeks pregnant. She underwent a laparatomy because of an acute abdomillai syndrome with signs of peritonitis. Appendectomy and right ovariectomy were performed but no signs of inflammation were found. The delivery 4 days later was uneventful. The next day a gastroscopy was done because of persistent vomiting and retrosternal pain upon eating. The distal half of the esophagus appeared ulcerative with black necrotic plaques. Superficial erosions were noted in the stomach. No cultures or biopsies were taken. The patient was treated with omneprazole and cisapride. Her condition improved temporarily. However, after 1 month she conlpl~l~ned ofdysphagia. On endoscopy tubular narrowing of the distal esophagus was seen. The pink, friable and granular mucosa was covered by a thick white exsudate. Dilations with Savary bougies were started on day 1. This procedure was repeated 10. 22, 29 and 38 days later. No antibiotic prophylaxis was given. On day 45, the patient started to experience a progressive weakness of the right arm and leg. A few days later. she had the im-
Fig. 1. Stereotaxic CT scan with administration of contrast medium showing a ring-like enhancement with perilesional edema in the left parietal lobe.
pression
that her speech was less fluent and on day 54 she
was admitted to the neurological department. Neurological examination on admission showed operative
patient
side, a deviation
with a central of the tongue
ate right hemiparesis
a co-
facial palsy on the right
with Babinski
sign. There
scan of the brain showed a left parietal a ring-like enhancement after contrast scan visualised
aspiration
of the abscess,
lesion with moderate
showed
contrast
only a small residual
enhancement
(see Fig. 2).
to the right and a moderwas no
fever, meningeal irritation or fundoscopic abnormalities. Routine laboratory examination revealed a microcytic anemia and a slightly elevated sedimentation rate. CT
1). A Tc brain
Fig. 2. CT scan with administration of contrast medium 6 weeks after aspiration showing only a small residual lesion in the left parietal lobe.
hypodensity with infusion (see Fig.
an increased
focal activity
at the same site. Other paraclinical investigations total body scan. transesophageal echo Doppler,
such as abdomi-
nal echography, sinus and lung x-rays were normal. Gynecological, ophthalmological and otorhinological examinations revealed no abnormalities. On day 65, the patient underwent a stereotactically guided aspiration of the brain lesion (see Fig. 1). Pus was evacuated and the following organisms were cultured: Streproeoccus milleri (preponderant). Ekonellu mrrodens, Veillonellu sp. and Bucttwides nwluninogenicus. On further treatment with intravenous antibiotics for 6 weeks (cefotaxim, metronidazole and penicilline), the patient improved and the hemiparesis resolved almost completely. A control CT scan, performed 6 weeks after
Discussion In this patient with a metastatic brain abscess no other source than the esophagus has been found; 6 weeks before the onset of neurological derwent
a first esophageal
symptoms
Bacteremia, secondary to esophageal been demonstrated in different studies [15] suggested
in 1940 that
moms could metastasize
the patient
un-
dilatation.
abdominal
dilatation, has [lo-141. Batson and
pelvic
to the brain via retrograde
tuflow
in lumbar and perivertebral veins. A similar mode of spread might explain the occurrence of brain abscesses following esophageal dilatations. Peri-esophageal venules interconnect with vertebral veins so that blood may be forced into the brain in a retrograde fashion [2]. The other proposed mechanism is transient bacteremia induced by disruption of the esophageal mucosa with arterial seeding into the brain [3]. This appears more likely due to the supratentorial location of the abscess in the presented case.
171 TABLE I CASES OF BRAIN ABSCESS AFTER DILATATION
REPORTED
IN THE LITERATURE
Author (patient’s age and sex)
No. of dilatations
Antibiotics peri-dilatation
Steroids
Organism
Schlitt [4] 1.17 mo, M
2
yes
no.
B. meluninogenicus,
Neisseriu sp.,
no.
Peptococcus sp. B. melaninogenicus,
microaerophilic
Streptococcus H. paraprophilus
2.4 yrs, F
9
yes
3
yes
yes (2 d)
Golladay et al. [6] 6.5 yrs, M
8
NA (given perioperatively)
NA (given perioperatively)
Kotler et al. [8] 1.17 mo, F 2.2 yrs. F 3.15 yrs. F
multiple NA multiple
yes ( 1 course) yes ( 1 course) yes ( 1 course)
yes (1 course)
S. aureus
yes ( 1 course)
NA NA
Leahy et al. [7] I .4 mo. NA 2.6 yrs. M
4 multiple
NA NA
NA NA
NA Microaerophilic
3
NA
NA
Streptococcus, Staphylococcus epidermidis, Group B Streptococcus S. aureus
Neuman et al. [2] 16 mo, M
NA
NA
NA
Streptococcus
Harp et al. [3] 16 mo, M
4
NA
NA
Microaerophilic group F, betahemolytic Streptococcus
Lui [5] I .5 yrs. M 2.16 mo, M
4 7
NA NA
NA NA
Sterile
Rontal et al. [9] 17 yrs. M
multiple
yes (initially and perioperatively)
yes (initially and perioperatively)
Sterile
Present study 28 yrs. F
5
no
no
Streptococcus milleri, Ekonella corrodens, Bacteroides
3,4.5 yrs, M
3.4 yrs. F
S. aureus
viridans
Pepto-, Streptococcus
meluninogenicus,
anaerobic
Veillonelka
NA = not available.
Various authors (Table 1) have reported cases of brain abscess after esophageal dilatation [2Z 91. All these previously reported patients were in the pediatric age group
and all had supratentorial abscesses. The isolated organisms belong, like in this patient, to the normal oropharyngeal bacterial flora. The origin of brain abscess of
172 these children
can be explained
since steroid tients,
has been the routine
immunosuppression
thogenesis.
by two mechanisms
On
the other
fluid intake
might
play a role in the pachildren
are perhaps
dehydration
because
due to the esophageal
This causes physiological crease
polycythemia,
the flow of the microcirculation
formation
and subsequent
is then more prone the bacteremic developed
leading
to cloth
in the brain.
an abscess
phase after dilatation.
a brain
of
stricture.
which might de-
microinfarcts
to develop
It
focus during
Why our patient
abscess is not clear. There was no evi-
dence
of immunosuppression.
acute
necrotizing
The initial
esophagitis
event
[16], of which
was an
the patho-
genesis remains unclear. The CT scan findings on admission (day 54) corresponded with a stage of capsule formation of the abscess of more than 14 days [17,18]. Keeping also in mind that the neurological signs started on day 45, we can pressume that the dilatation performed on day 29 or 38 caused the spread of the bacteria leading
to the brain abscess.
The use of prophylactic antibiotics by esophageal dilatation is controversial; however, it is only generally accepted for cardiac
patients
4 Schlitt,
A. ( 1977) Bacteremia following esophageal dilation and esophago-gastroscopy. Aust. N.Z. J. Med., 7: 32-35. W.J., McKee. J., Wilkinson, D., 12 Welsh, J.D., Griftiths.
particularly during adult life. Anyhow, the clinician should be alert to this condition in the presence of persistent fever and neurological signs in patients with a his-
I4
Berg, L. and De Marchena, 0. (1989) Focal infections. In: Rowland, L. (Ed.), Merritt’s Textbook of Neurology, Lea & Febiger, Philadelphia-London, pp. 8896. Neuman, A., Lernau, O.Z., Goldberg, M., Hod, G. and Nissan. S. (I 986) Brain abscess. A complication of esophageal dilatations. Z. Kinderchir., 41: 4344. Harp, D., Schlitt, M.D., Williams, P. and Shamoun, J. (I 989) Brain abscess following dilatation of esophageal stricture. Clin. Imag., 13: 140&141.
report
Metastatic abscess as a complication of retrograde esophageal dilatation. Ann. Otol., 82: 643-648. IO Botoman. A. and Surawicz, C. (1986) Bacteremia with gastrointestinal endoscopic procedures. Gastrointest. Endosc. 32 (5): 342-346. II Stephenson, P.M., Dorrington. L., Harris, O.D. and Rao,
13
References
G. et al. (1985) Brain ab-
Cerebral abscess in children secondary to esophageal dilatation. Pediatrics, 59: 300-30 1. 8 Kotler, R.. Schild, J.A. and Holinger, P.H. (1975) Delayed CNS complications. Laryngoscope, 85: 137991386. 9 Rental. E.. Meyerhoff, W. and Duval, A.J., III. (1973)
with a high risk of endocardi-
dilatation.
L., Zorn,
5 Lui, T.N., Lee, S.T., Chang, C.N. and Wang, H.S. (1988) Brain abscess after dilatation of esophageal Stricture. Pediat. Neurosci.. 14: 250-253. 6 Golloday, ES., Tepas, J.J., 111, Pickard, L.R.. Siebert, J.J.. Brown, R.W. and Haller. J.A. (1980) Bacteremia after esophageal dilation: a clinical and experimental study. Ann. Thorac. Surg. 30: 19-23. 7 Leahy. W.R., Toyka, K.V. and Fischbeck, K.H.. Jr. (1977)
tis [17]. The occurrence of brain abscesses after esophageal dilatation for stricture remains a very rare complication,
tory of esophageal
M., Mitchem,
scess after esophageal dilatation for caustic stricture: of three cases. Neurosurgery. 17(6): 947-95 1.
in these pa-
hand,
more easily in a state of chronic decreased
treatment
[5]:
15
I6
Flournoy, D.J. and Mohr, J. (1983) Bacteremia associated with esophageal dilation. J. Clin. Gastroenterol. 5: 109--I 12. Raines. D.R.. Brache, W.C., Anderson. D.L. and Boyce, W.H. The occurrence of bacteremia after esophageal dilation. Gastrointest. Endosc., 22: 86-87. Yin. T.P.. Ellis. R. and Dellipiani, A.W. (1983) The incidence of bacteremia after outpatient Hurst bougienage in the management of benign esophageal strictures. Endoscopy, 15: ‘89-790. Batson. O.V. ( 1940) The function of the vertebral veins and their role in the spread of metastases. Ann. Surg.. 112: 138149. Goldenberg, S., Wain. S. and Marignani, P. (1990) Acute
necrotizing esophagitis. Gastrbenterology, 98: 493496. I7 Britt, R., Enzmann. D. and Yeager. A. ( 198 1) Neuropathological and computerized tomographic findings in experimental brain abscess. J. Neurosurg.. 55: 590-603. 18 Britt. R. and Enzmann, D. (1983) Clinical stages of human brain abscesses on serial CT scans after contrast infusion. J. Neurosurg.. 59: 972-989. 19 Neu. H. and Fleischer. D. (1989) Recommendations for antibiotic prophylaxis before endoscopy. Am. J. Gastroenterol., 84: 148881491.
