International Journal of Pediatric Otorhinolaryngology, 24 (1992) 217-226 0 1992 Elsevier Science Publishers B.V. All rights reserved 0165-5876/92/$05.00
217
PEDOT 008 13
Central nervous system complications secondary to oto-rhinologic infections. An analysis of 39 pediatric cases Mordechai
Kraus and Ferit Tovi
Department of Otolaryngology, Soroka University Hospital and Center for Health Sciences and Sercices, Ben-Gurion University of the Negeq Beer-Sheva (Israel)
(Received 18 July 1991) (Revised version received 16 December 1991) (Accepted 26 December 1991)
Key words: Brain abscess; Meningitis; Subdural empyema; Lateral sinus thrombosis; Extradural abscess
Abstract Fifty-eight central nervous system complications were noted in 39 pediatric patients with a primary oto-rhinological infection. The ages ranged from 1 to 15 years. Eleven patients (25%) had more than one complication. 12.8% of the cases died. Leptomeningitis was the most common intracranial complication (54%) Lateral sinus thrombosis (LST) occurring in 10 patients (26%) was accompanied with other intracranial abnormalities in 80% of cases. Brain abscess as an initial or concomitant complication was associated with the highest mortality rates (40%). In two of’ these fatal cases multiple brain abscesses were detected. The low incidence of intracranial infections secondary to oto-rhinologic infections and the masking effect of antibiotics present difficulties in the early recognition of the CNS complication. Despite the value of the modern imaging techniques in the investigation of the CNS complication, the clinical oto-rhinologic examination is of paramount importance in detecting the original infection in the pneumatic spaces of the upper respiratory tract. Additionally, bone scans were found of value in demonstrating the osteitic process of these cases.
Correspondence to: Dr. F. Tovi, Department Beer-Sheva 84101. Israel.
of Otolaryngology, Soroka Medical Center, P.O. Box 151,
218
Introduction With the advent of antimicrobial drugs, the incidence of central nervous system secondary to otorhinologic infections has decreased (CNS) complications, [4,8,17,23,25]. But still, due to the masking effect of antibiotics and/or the lack of familiarity of the new generation of primary care clinicians with these complications, the early diagnosis of intracranial sepsis may be delayed [8,17,23]. Moreover, diverse intracranial purulencies in childhood exhibit similar clinical manifestations [24]. Hence, recognition of the nature of the CNS sepsis may be difficult. Our data are presented to alert the clinician to the ever-present possibility of CNS complications related to upper respiratory tract infections.
Patients and clinical data Over a period of 18 years (1972-19901, 60 patients with CNS complications secondary to otorhinological infections were treated in the Otolaryngology Department of of Soroka Medical Center. The 39 patients (67%) in our series ranged from 1 month to 15 years and the median age was 8 years. The male/female ratio was 28 : 11. The results of clinical examination, the imaging investigations and other pertinent data were analyzed.
Results The middle ear in 28 patients (71%) and the paranasal sinuses in 8 patients (20%) were the site of the initial infection. In the other 3 patients (9%‘0),fracture of the midface, mucormycosis of the palate and infratemporal fossa infection precipitated the intracranial sepsis. The patients’ data of the CNS complications are summarized in Table 1. The mortality rate was 12.8% (5 out of 39 patients).
Discussion The close anatomic relationship of the pneumatic spaces, related via the upper respiratory tract to the CNS, make’s the latter vulnerable during the course of middle ear cleft and paranasal sinus infections [17,23]. Performed pathways, venous connections, congenital dehiscences in the base of the skull and acquired bone defects play an important role in the intracranial spread of the ear and sinus infections [6,14,18]. The majority of CNS complications of the upper respiratory tract infections occur in the pediatric population, and are distributed at the same frequency as in the pre-antibiotic era [4]. The mortality rate in CNS complications of ear and rhinological diseases is still alarming [23]. In our series, death occurred in 5 patients, accounting for 12.8% of the cases. In two of these cases, the primary infection remained undiagnosed until
26%
20%
4
10
8
4 5
Pachimeningitis
Lateral sinus thrombosis
Brain abscess
Subdural empyema Extradural abscess 2% 2% 2% 2% 2% 2%
10% 13%
* AOM-15 ** COM-5 Sinusitis-l COM-1 Sinusitis-3 COM-5 AOM-2 Silent-OM-3 COM-5 Sinusitis-l AOM-1 *** ITF-1 Sinusitis-4 AOM-1 COM-4 Sinusitis-l COM-1 COM-1 AOM-1 AOM-1 Palatal infection-l
Site of primary infection
* AOM = Acute otitis media. Some of the cases (11) had multiple complications: n = 39 * * COM = Chronic otitis media. No. of complications = 58 * * * ITF = Infratemporal fossa.
Sagittal sinus thrombosis Straight sinus thrombosis Otitic hydrocephalus CSF liquorrhea Osteomyelitis of base of skull Mucormycosis
54%
21
Leptomeningitis
10%
Incidence of complications
No. of cases with specific complications
CNS complications
Types of intracranial complication in 39 patients
TABLE I
1
1
_
1 1 1 1
1 4
5
1
2
Concomitant CNS purulencies
3 1
3
9
4
19
Primary CNS complication
1
_
1
1
1
1
Mortality rates according to CNS primary complications
220
the occurrence of intracranial sepsis. Silent infection (masked mastoiditis) of the middle ear cleft was the initial cause of the CNS complication in 3 (7.6%) of the patients. This entity has been recognized after the advent of antimicrobial drugs. Inadequate or inappropriate use of antibiotics may partially treat the disease and provide relief of the symptomatology [13]. Yet, due to occlusion of the tympanic isthmus or aditus ad antrum by the inflamed mucosa or polypoid changes, the mastoid air cell system becomes partially or totally separated from the middle ear cavity [15]. Due to the nature of the colonizing flora in non-aerated mastoid cells, the mastoid inflammation progresses into a low-grade bone disease. The signs and symptomatology of this entity are not as overt as those occurring in the acute mastoiditis, and the ear drum may appear normal or with minimal inflammatory changes [8]. In our experience, a bone scan appeared to be of value in the detection of the osteitic process in otherwise normal looking ears. CNS involvement in otorhinologic infections occurs by direct spread of the primary lesion or by thrombo-embolic process. While in chronic ear and paranasal sinus infections percontiguous spread is the main mechanism in the CNS involvement, acute diseases have a tendency to spread by the hematogenous. route. The latter is less frequently seen nowadays [183. Meningitis
Meningitis is the most frequent CNS complication of the middle ear cleft and paranasal sinus infections [16-181. In 21 patients this complication occurred in the form of leptomeningitis and in the other 4 patients as pachimengingitis. The latter is a localized reaction of the dura to the adjacent focus of inflammation in the base of the skull 1201.The usual development of this complication is by percontiguous propagation of the primary infection. In one case chronic otitis media and in three cases ethmoiditis precipitated this complication. Apart from one patient with sinusitis, leptomeningitis was always secondary to middle ear cleft infections. Fifteen patients initially suffered from acute and 5 from chronic otitis media. In another patient with paranasal sinus infection, leptomeningitis progressed to subdural empyema. Only one patient in this series died from the complication. He had initially been treated without the attention of an otolaryngologist. Hence, the chronic middle ear disease remained initially undiagnosed. Upon the apparent resolution of the meningeal infection, he was discharged and but later became unconscious. The patient was readmitted and this time chronic middle ear disease was detected. CT examination showed an ipsilateral temporal lobe abscess and lateral sinus thrombosis. Despite decompression of the abscess and thrombectomy the patient remained in a coma of fatal outcome. This case serves as an example for the risk of undiagnosed primary disease. Of the young generation of physicians some may not be aware of the fact that otorhinologic infection may precipitate an intracranial sepsis [4]. The treatment regimen of meningeal infections, in our series, consisted of elimination of the primary focus of infection (paracentesis and appropriate antibiotics) in acute middle ear infections. In chronic disease alongside the antibiotics, surgical eradication of the middle ear cleft infection was performed.
221
Lateral sinus thrombosis
Lateral sinus thrombosis &ST) was considered as the second most frequent complication of otogenic disease in the preantibiotic era [21]. Although antibiotics have drastically reduced the frequency of LST, they have done little in decreasing mortality rates which remain as high as 15-36% [21]. The anatomic proximity of this dural sinus with the mastoid air cells makes it vulnerable at the course of middle ear infections. Before the advent of antibiotics LST occurred most frequently in acute ear infections [18]. Today, it is most frequently seen in neglected chronic ears as well as in low-grade middle ear cleft infections [12,21]. In our study two patients developed LST secondary to acute middle ear infection and three others developed LST as a consequence of masked mastoiditis. In the rest of the patients this complication was due to chronic otitis media. Although septic fever is a frequent sign of the disease, it is not pathognomonic and at times may be absent [18,21]. Headache and meningeal signs occur frequently [21]. Four of our patients had meningeal signs and were initially diagnosed and treated as meningitis. Unresponsiveness to antibiotics raised a high index of suspicion of LST. Contrast-enhanced CT showed perisinus dural enhancement compatible with the circumscribed perisinus inflammation, and considered as an early CT finding of LST [21] (Fig. 1). The circumscribed perisinus meningitis occurs by perisinus abscess in the sinus plate area with subsequent sinus thrombosis [18]. In one of our cases LST was precipitated by acute otitis media. In such cases, thrombophlebitis originating from the middle ear mucosa transmits the infection to the sinus [18]. High doses of antibiotics covering a mixed and anaerobic flora, surgical eradication of the mastoid infection associated with thrombectomy constitute the management of this condition in chronic middle ear disease [18,21]. Bone scan may prove the presence of middle ear cleft disease in masked infections. When this complication develops secondary to acute otitis media, decompression of the middle ear, together with the initiation of appropriate antibiotics usually solve the problem
WY. In our series meningitis, brain abscess, extradural abscess and cerebellitis were concomitant complications accompanying LST. One of our patients succumbed to the disease. This patient had concomitant multiple brain abscesses. Brain abscess
Brain abscess due to middle ear infections occurs in the temporal lobe more often than in the cerebellum [19]. Those secondary to frontal sinusitis develop usually in the frontal or fronto-parietal lobes [16]. In 6 of our patients with middle ear disease the abscess developed in the temporal lobe and in another patient, with paranasal sinus infection, it developed in the frontoparietal lobe. In 5 out of 8 patients with brain abscess, other intracranial processes (meningitis, LST, subdural empyema) preceded this complication, The pathogenesis of brain abscess secondary to otorhinologic infections may be by direct extension of the primary infection or by by retrograde thrombophlebitis. Infection of the brain initially produces an episode of encephalitis characterized by
222
Fig. 1. Post-contrast axial CT shows right perisinus meningeal enhancement, surrounding a filling defect in the area of the lateral sinus. All these, compatible with thrombosis of the right lateral sinus.
and headaches [19]. By the latent stage, localization of the initial encephalitis occurs and the symptoms usually subside. Upon the encapsulation of the site of encephalitis, signs of CNS pressure may occur such as projectile vomiting, focal seizures, cranial nerve dysfunction, slowing of the pulse and coma. It is worthwhile to note that in two of our patients who were already hospitalized because in the stage of the initial disease (frontal sinusitis and midface fracture) behavioral changes led us to perform a CT of the brain, which detected the abscess at an early stage. CT provides also an accurate diagnosis of the brain abscess. It also differentiates between the stages of encephalitis and abscess formation [31. Antibiotics may be of primary efficacy in the early stages [ll]. Serial scans are also of value in monitoring the development and/or the resolution of brain abscess (Figs. 2a, b and c). CT also appears of importance for indicating the right time for surgery [31. The therapy regimen for brain abscess in our patients consisted of appropriate antibiotics and removal of the abscess as well as surgical eradication of the primary site of infection. In two cases the abscess developing in the proximity of the fever
223
Fig. 2. (a, b and c) Sequential
axial CT scans of the brain show resolution by transmastoid drainage and antibiotics.
of the brain
abscess
treated
tegmen tympani was drained through mastoidectomy. In six other patients the drainage was done by a neurosurgical approach. Death occurred in one out of three patients in whom a brain abscess was the sole CNS complication. In cases where the brain abscess was accompanied by other intracranial purulencies, the mortality rates were higher (60%).
224
Subdural empyema
Subdural empyema occurs when purulent material collects in the subdural space. Most frequently it develops secondary to childhood meningitis but it may also present as a complication of middle ear or paranasal sinus infections in older children [16]. In our series, this complication occurred always secondary to paranasal sinus infection. The overall mortality rate from this complication was lower in comparison with the preantibiotic era [16]. If not recognized early, subdural empyema can be a rapidly fatal disease. Since there are no anatomic barriers in the subdural space, the empyema may spread rapidly on the central cortex and in the interhemispheric area. The early stages of this entity may be similar to meningitis. Cortical vein thrombophlebitis is a common concomitant complication that may give rise to abscess formation [1,2,9], as was seen in one of our patients. Nowadays the disease is recognized by modern imaging techniques. Sometimes it may not be detected by CT and angiography may be helpful in demonstrating the cortical comparison covered by the empyema [5,7]. Proper management of subdural empyema consists of prompt evacuation of the collection as well as appropriate antimicrobial therapy [5,7]. In our patients surgical drainage was done by burrhole aspiration followed by fronto-ethmoidectomy. Although the introduction of antibiotics has significantly improved the outlook of this disease, the mortality rates are still in the range of 20-40% [5,7]. In our series the death rate was 25%. Extradural abscess
Extradural abscess is considered as the most common complication of chronic middle ear cleft infection [18]. It develops upon bone erosion of the tegmen tympani or the sinus plate. A localized osteitis of the posterior frontal sinus wall may also cause an extradural abscess in the anterior fossa [161. This complication, when occurring at the lateral sinus area, is also called a perisinus abscess [lo]. Clinical features of this condition present with headaches. In neglected cases, the extradural collections may rupture and progress to subdural empyema, LST or brain abscess. In our series, extradural abscess occurred in five cases of otitis media. In four of these patients it was accompanied by other intracranial lesions such as LST, meningitis, cerebellitis, brain, abscess and CSF liquorrhea. No death occurred in this group of patients.
Conclusions (1) Despite the liberal use of antibiotics. and the advantages provided by the primary care medicine in cur area, CNS complications of otorhinologic infections are still encountered and even accompanied by an alarming mortality rate. (2) Modem imaging techniques are of value in localizing and demonstrating the nature of the intracranial disease. A complete otorhinologic examination is the
225
initial part of the investigation in order to diagnose the initial extracranial focus of infection. The undetected primary ear or rhinologic infection may precipitate further metastatic complications. In the present series masked middle ear cleft infection was the cause of the intracranial sepsis in 7.6% of patients. In these cases a bone scan was of value in depicting the osteitic process. (3) Brain abscess either as initial or concomitant complications resulted in the highest mortality rates in our series. (4) LST, due to its presentation in different clinical settings, and mostly in the form of meningitis, poses diagnostic difficulties. The CT sign of the perisinus meningeal reaction is of paramount importance in the early recognition of this condition.
References 1 Courvilee, C.B. and Rosenwald, L.K. Intracranial complications of infection of nasal cavities and accessory sinuses. Arch. Otolaryngol., 27 (1938) 692-731. 2 Farmer, T.W. and Wise, G.R. Subdural empyema in infants, children and adults. Neurology, 23 (1973) 254-261. 3 Freeman, J., Changing concepts in the management of otitic intracranial infection. Use of computerized axial tomography in early detection and monitoring of cerebritis. Laryngoscope, 94 (1984) 907-911. 4 Gower, D. and McGuirt, W.F. Intracranial complications of acute and chronic infectious ear disease: a problem still with us. Laryngoscope, 93 (19831 1028-1033. 5 Heilbron, Y.D., Tovi, F., Hirsch, M. and Ronen, J. Subdural empyema of sinus origin in children. Inter. J. Pediatr. Otolaryngol., 6 (1983) 205-211. 6 Hilsinger, R.L. and Caparora, R.J. Otogenic brain abscess. Laryngoscope, 80 (1970) 697-711. 7 Hitchcock, E. and Andreas, H. Subdural empyema: a review of 29 cases. J. Neurol. Neurosurg. Psychiatry, 27 (1964) 422-434. 8 Holt, G.R. and Gates, G.A., Masked mastoiditis. Laryngoscope, 93 (1983) 1034-1037. 9 List, C.F. Interhemispheric subdural suppuration. J. Neurosurg., 7 (1950) 313-324. 10 Mafee, M.F., Goldino, E., VaIVassor, I., Kumar,. A. et al. Otogenic intracranial inflammation. Role of CT. Otolaryngol. Clinic of North America, 21(2) (1988) 245-263. 11 Mariglia, A.J., Van Buren, J.M., Bruce, W.B. et al. Intracranial abscesses secondary to ear and paranasal sinuses infections. Otolaxyngol. Head and Neck Surg., 88 (1980) 670-680. 12 Meyerhoff, W.L., Kim, C.S. and Paparella, M.M., Pathology of chronic otitis media. Ann. Otol. Rhinol. Laryngol., 87 (1978) 749-760. 14 Myers, E.N. and Ballantine, M.T., The management of otogenic brain abscess. Laryngoscope, 75 (1965) 273-288. 13 Mawson, S. In: M. Ballantyne and J. Grove, Eds. Scott-Brown’s Disease of the Ear, Nose and Throat. Butterworth Co. Ltd., London, 1979, pp. 190. 15 Proctor, B. Attic otitis block and tympanic diaphragm. Ann. Otol. Rhinol. Laryngol., 80 (19711 810-814. 16 Remmler, D. and Bales, R., Intracranial complications of frontal sinusitis. Laryngoscope, 90 (1980) 1814-1824. 17 Samuel, J., Fernandes, C.M.C. and Steinberg, J.L., Intracranial otogenic complications: a persisting problem. Laryngoscope, 96 (1986) 272-277. 18 Shambaugh, G.E. Jr. and Glasscock, M.E. III. Surgery of the Ear. W.B. Saunders, Co. Philadelphia, 1980, pp. 289-318. 19 Shambaugh, G.E. Jr. and Glasscock, M.E. III. Surgery of the ear, W.B. Saunders Co, Philadelphia, 1980, pp, 317-326.
20 Smith, B.H., Infections of the cranial dura and the dura sinuses. In P.J. Vinken and G.N. Bruyn (Eds) Handbook of Clinical Neurology, Vol. 33, Ch. 10, North Holland Publication Co., Amsterdam, 1983, pp. 149-162. 21 Teichgraber, J.F., Per-Lee, J.H. and Turner, J.S. Jr., Lateral sinus thrombosis: a modern perspective. Laryngoscope, 92 (1982) 744-750. 22 Tovi, F. and Hirsch, M. CT diagnosis of lateral sinus thrombosis. Ann. Oto. Rhinol-Laryngol. 100 (1991) 79-82. 23 Wolfowitz, B.L. Otogenic intracranial complications. Arch. Otolaryngol., 96 (1972) 220-222. 24 Vaughan, V.C., McKay, R.J. Jr. and Behrman, R.E. In: Nelson Textbook of Pediatrics. W.B. Saunders, Philadelphia, 1970, pp. 717-720. 25 Whitaker, C.W. Intracranial complications of ear, nose and throat infections. Laryngoscope, 81 (9) (1980) 1375-1380.
217
PEDOT 008 13
Central nervous system complications secondary to oto-rhinologic infections. An analysis of 39 pediatric cases Mordechai
Kraus and Ferit Tovi
Department of Otolaryngology, Soroka University Hospital and Center for Health Sciences and Sercices, Ben-Gurion University of the Negeq Beer-Sheva (Israel)
(Received 18 July 1991) (Revised version received 16 December 1991) (Accepted 26 December 1991)
Key words: Brain abscess; Meningitis; Subdural empyema; Lateral sinus thrombosis; Extradural abscess
Abstract Fifty-eight central nervous system complications were noted in 39 pediatric patients with a primary oto-rhinological infection. The ages ranged from 1 to 15 years. Eleven patients (25%) had more than one complication. 12.8% of the cases died. Leptomeningitis was the most common intracranial complication (54%) Lateral sinus thrombosis (LST) occurring in 10 patients (26%) was accompanied with other intracranial abnormalities in 80% of cases. Brain abscess as an initial or concomitant complication was associated with the highest mortality rates (40%). In two of’ these fatal cases multiple brain abscesses were detected. The low incidence of intracranial infections secondary to oto-rhinologic infections and the masking effect of antibiotics present difficulties in the early recognition of the CNS complication. Despite the value of the modern imaging techniques in the investigation of the CNS complication, the clinical oto-rhinologic examination is of paramount importance in detecting the original infection in the pneumatic spaces of the upper respiratory tract. Additionally, bone scans were found of value in demonstrating the osteitic process of these cases.
Correspondence to: Dr. F. Tovi, Department Beer-Sheva 84101. Israel.
of Otolaryngology, Soroka Medical Center, P.O. Box 151,
218
Introduction With the advent of antimicrobial drugs, the incidence of central nervous system secondary to otorhinologic infections has decreased (CNS) complications, [4,8,17,23,25]. But still, due to the masking effect of antibiotics and/or the lack of familiarity of the new generation of primary care clinicians with these complications, the early diagnosis of intracranial sepsis may be delayed [8,17,23]. Moreover, diverse intracranial purulencies in childhood exhibit similar clinical manifestations [24]. Hence, recognition of the nature of the CNS sepsis may be difficult. Our data are presented to alert the clinician to the ever-present possibility of CNS complications related to upper respiratory tract infections.
Patients and clinical data Over a period of 18 years (1972-19901, 60 patients with CNS complications secondary to otorhinological infections were treated in the Otolaryngology Department of of Soroka Medical Center. The 39 patients (67%) in our series ranged from 1 month to 15 years and the median age was 8 years. The male/female ratio was 28 : 11. The results of clinical examination, the imaging investigations and other pertinent data were analyzed.
Results The middle ear in 28 patients (71%) and the paranasal sinuses in 8 patients (20%) were the site of the initial infection. In the other 3 patients (9%‘0),fracture of the midface, mucormycosis of the palate and infratemporal fossa infection precipitated the intracranial sepsis. The patients’ data of the CNS complications are summarized in Table 1. The mortality rate was 12.8% (5 out of 39 patients).
Discussion The close anatomic relationship of the pneumatic spaces, related via the upper respiratory tract to the CNS, make’s the latter vulnerable during the course of middle ear cleft and paranasal sinus infections [17,23]. Performed pathways, venous connections, congenital dehiscences in the base of the skull and acquired bone defects play an important role in the intracranial spread of the ear and sinus infections [6,14,18]. The majority of CNS complications of the upper respiratory tract infections occur in the pediatric population, and are distributed at the same frequency as in the pre-antibiotic era [4]. The mortality rate in CNS complications of ear and rhinological diseases is still alarming [23]. In our series, death occurred in 5 patients, accounting for 12.8% of the cases. In two of these cases, the primary infection remained undiagnosed until
26%
20%
4
10
8
4 5
Pachimeningitis
Lateral sinus thrombosis
Brain abscess
Subdural empyema Extradural abscess 2% 2% 2% 2% 2% 2%
10% 13%
* AOM-15 ** COM-5 Sinusitis-l COM-1 Sinusitis-3 COM-5 AOM-2 Silent-OM-3 COM-5 Sinusitis-l AOM-1 *** ITF-1 Sinusitis-4 AOM-1 COM-4 Sinusitis-l COM-1 COM-1 AOM-1 AOM-1 Palatal infection-l
Site of primary infection
* AOM = Acute otitis media. Some of the cases (11) had multiple complications: n = 39 * * COM = Chronic otitis media. No. of complications = 58 * * * ITF = Infratemporal fossa.
Sagittal sinus thrombosis Straight sinus thrombosis Otitic hydrocephalus CSF liquorrhea Osteomyelitis of base of skull Mucormycosis
54%
21
Leptomeningitis
10%
Incidence of complications
No. of cases with specific complications
CNS complications
Types of intracranial complication in 39 patients
TABLE I
1
1
_
1 1 1 1
1 4
5
1
2
Concomitant CNS purulencies
3 1
3
9
4
19
Primary CNS complication
1
_
1
1
1
1
Mortality rates according to CNS primary complications
220
the occurrence of intracranial sepsis. Silent infection (masked mastoiditis) of the middle ear cleft was the initial cause of the CNS complication in 3 (7.6%) of the patients. This entity has been recognized after the advent of antimicrobial drugs. Inadequate or inappropriate use of antibiotics may partially treat the disease and provide relief of the symptomatology [13]. Yet, due to occlusion of the tympanic isthmus or aditus ad antrum by the inflamed mucosa or polypoid changes, the mastoid air cell system becomes partially or totally separated from the middle ear cavity [15]. Due to the nature of the colonizing flora in non-aerated mastoid cells, the mastoid inflammation progresses into a low-grade bone disease. The signs and symptomatology of this entity are not as overt as those occurring in the acute mastoiditis, and the ear drum may appear normal or with minimal inflammatory changes [8]. In our experience, a bone scan appeared to be of value in the detection of the osteitic process in otherwise normal looking ears. CNS involvement in otorhinologic infections occurs by direct spread of the primary lesion or by thrombo-embolic process. While in chronic ear and paranasal sinus infections percontiguous spread is the main mechanism in the CNS involvement, acute diseases have a tendency to spread by the hematogenous. route. The latter is less frequently seen nowadays [183. Meningitis
Meningitis is the most frequent CNS complication of the middle ear cleft and paranasal sinus infections [16-181. In 21 patients this complication occurred in the form of leptomeningitis and in the other 4 patients as pachimengingitis. The latter is a localized reaction of the dura to the adjacent focus of inflammation in the base of the skull 1201.The usual development of this complication is by percontiguous propagation of the primary infection. In one case chronic otitis media and in three cases ethmoiditis precipitated this complication. Apart from one patient with sinusitis, leptomeningitis was always secondary to middle ear cleft infections. Fifteen patients initially suffered from acute and 5 from chronic otitis media. In another patient with paranasal sinus infection, leptomeningitis progressed to subdural empyema. Only one patient in this series died from the complication. He had initially been treated without the attention of an otolaryngologist. Hence, the chronic middle ear disease remained initially undiagnosed. Upon the apparent resolution of the meningeal infection, he was discharged and but later became unconscious. The patient was readmitted and this time chronic middle ear disease was detected. CT examination showed an ipsilateral temporal lobe abscess and lateral sinus thrombosis. Despite decompression of the abscess and thrombectomy the patient remained in a coma of fatal outcome. This case serves as an example for the risk of undiagnosed primary disease. Of the young generation of physicians some may not be aware of the fact that otorhinologic infection may precipitate an intracranial sepsis [4]. The treatment regimen of meningeal infections, in our series, consisted of elimination of the primary focus of infection (paracentesis and appropriate antibiotics) in acute middle ear infections. In chronic disease alongside the antibiotics, surgical eradication of the middle ear cleft infection was performed.
221
Lateral sinus thrombosis
Lateral sinus thrombosis &ST) was considered as the second most frequent complication of otogenic disease in the preantibiotic era [21]. Although antibiotics have drastically reduced the frequency of LST, they have done little in decreasing mortality rates which remain as high as 15-36% [21]. The anatomic proximity of this dural sinus with the mastoid air cells makes it vulnerable at the course of middle ear infections. Before the advent of antibiotics LST occurred most frequently in acute ear infections [18]. Today, it is most frequently seen in neglected chronic ears as well as in low-grade middle ear cleft infections [12,21]. In our study two patients developed LST secondary to acute middle ear infection and three others developed LST as a consequence of masked mastoiditis. In the rest of the patients this complication was due to chronic otitis media. Although septic fever is a frequent sign of the disease, it is not pathognomonic and at times may be absent [18,21]. Headache and meningeal signs occur frequently [21]. Four of our patients had meningeal signs and were initially diagnosed and treated as meningitis. Unresponsiveness to antibiotics raised a high index of suspicion of LST. Contrast-enhanced CT showed perisinus dural enhancement compatible with the circumscribed perisinus inflammation, and considered as an early CT finding of LST [21] (Fig. 1). The circumscribed perisinus meningitis occurs by perisinus abscess in the sinus plate area with subsequent sinus thrombosis [18]. In one of our cases LST was precipitated by acute otitis media. In such cases, thrombophlebitis originating from the middle ear mucosa transmits the infection to the sinus [18]. High doses of antibiotics covering a mixed and anaerobic flora, surgical eradication of the mastoid infection associated with thrombectomy constitute the management of this condition in chronic middle ear disease [18,21]. Bone scan may prove the presence of middle ear cleft disease in masked infections. When this complication develops secondary to acute otitis media, decompression of the middle ear, together with the initiation of appropriate antibiotics usually solve the problem
WY. In our series meningitis, brain abscess, extradural abscess and cerebellitis were concomitant complications accompanying LST. One of our patients succumbed to the disease. This patient had concomitant multiple brain abscesses. Brain abscess
Brain abscess due to middle ear infections occurs in the temporal lobe more often than in the cerebellum [19]. Those secondary to frontal sinusitis develop usually in the frontal or fronto-parietal lobes [16]. In 6 of our patients with middle ear disease the abscess developed in the temporal lobe and in another patient, with paranasal sinus infection, it developed in the frontoparietal lobe. In 5 out of 8 patients with brain abscess, other intracranial processes (meningitis, LST, subdural empyema) preceded this complication, The pathogenesis of brain abscess secondary to otorhinologic infections may be by direct extension of the primary infection or by by retrograde thrombophlebitis. Infection of the brain initially produces an episode of encephalitis characterized by
222
Fig. 1. Post-contrast axial CT shows right perisinus meningeal enhancement, surrounding a filling defect in the area of the lateral sinus. All these, compatible with thrombosis of the right lateral sinus.
and headaches [19]. By the latent stage, localization of the initial encephalitis occurs and the symptoms usually subside. Upon the encapsulation of the site of encephalitis, signs of CNS pressure may occur such as projectile vomiting, focal seizures, cranial nerve dysfunction, slowing of the pulse and coma. It is worthwhile to note that in two of our patients who were already hospitalized because in the stage of the initial disease (frontal sinusitis and midface fracture) behavioral changes led us to perform a CT of the brain, which detected the abscess at an early stage. CT provides also an accurate diagnosis of the brain abscess. It also differentiates between the stages of encephalitis and abscess formation [31. Antibiotics may be of primary efficacy in the early stages [ll]. Serial scans are also of value in monitoring the development and/or the resolution of brain abscess (Figs. 2a, b and c). CT also appears of importance for indicating the right time for surgery [31. The therapy regimen for brain abscess in our patients consisted of appropriate antibiotics and removal of the abscess as well as surgical eradication of the primary site of infection. In two cases the abscess developing in the proximity of the fever
223
Fig. 2. (a, b and c) Sequential
axial CT scans of the brain show resolution by transmastoid drainage and antibiotics.
of the brain
abscess
treated
tegmen tympani was drained through mastoidectomy. In six other patients the drainage was done by a neurosurgical approach. Death occurred in one out of three patients in whom a brain abscess was the sole CNS complication. In cases where the brain abscess was accompanied by other intracranial purulencies, the mortality rates were higher (60%).
224
Subdural empyema
Subdural empyema occurs when purulent material collects in the subdural space. Most frequently it develops secondary to childhood meningitis but it may also present as a complication of middle ear or paranasal sinus infections in older children [16]. In our series, this complication occurred always secondary to paranasal sinus infection. The overall mortality rate from this complication was lower in comparison with the preantibiotic era [16]. If not recognized early, subdural empyema can be a rapidly fatal disease. Since there are no anatomic barriers in the subdural space, the empyema may spread rapidly on the central cortex and in the interhemispheric area. The early stages of this entity may be similar to meningitis. Cortical vein thrombophlebitis is a common concomitant complication that may give rise to abscess formation [1,2,9], as was seen in one of our patients. Nowadays the disease is recognized by modern imaging techniques. Sometimes it may not be detected by CT and angiography may be helpful in demonstrating the cortical comparison covered by the empyema [5,7]. Proper management of subdural empyema consists of prompt evacuation of the collection as well as appropriate antimicrobial therapy [5,7]. In our patients surgical drainage was done by burrhole aspiration followed by fronto-ethmoidectomy. Although the introduction of antibiotics has significantly improved the outlook of this disease, the mortality rates are still in the range of 20-40% [5,7]. In our series the death rate was 25%. Extradural abscess
Extradural abscess is considered as the most common complication of chronic middle ear cleft infection [18]. It develops upon bone erosion of the tegmen tympani or the sinus plate. A localized osteitis of the posterior frontal sinus wall may also cause an extradural abscess in the anterior fossa [161. This complication, when occurring at the lateral sinus area, is also called a perisinus abscess [lo]. Clinical features of this condition present with headaches. In neglected cases, the extradural collections may rupture and progress to subdural empyema, LST or brain abscess. In our series, extradural abscess occurred in five cases of otitis media. In four of these patients it was accompanied by other intracranial lesions such as LST, meningitis, cerebellitis, brain, abscess and CSF liquorrhea. No death occurred in this group of patients.
Conclusions (1) Despite the liberal use of antibiotics. and the advantages provided by the primary care medicine in cur area, CNS complications of otorhinologic infections are still encountered and even accompanied by an alarming mortality rate. (2) Modem imaging techniques are of value in localizing and demonstrating the nature of the intracranial disease. A complete otorhinologic examination is the
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initial part of the investigation in order to diagnose the initial extracranial focus of infection. The undetected primary ear or rhinologic infection may precipitate further metastatic complications. In the present series masked middle ear cleft infection was the cause of the intracranial sepsis in 7.6% of patients. In these cases a bone scan was of value in depicting the osteitic process. (3) Brain abscess either as initial or concomitant complications resulted in the highest mortality rates in our series. (4) LST, due to its presentation in different clinical settings, and mostly in the form of meningitis, poses diagnostic difficulties. The CT sign of the perisinus meningeal reaction is of paramount importance in the early recognition of this condition.
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