Basilar By Jerry
Skull Fractures in Childhood Cranial Nerve Involvement
L. Kitchens,
Diller B. Groff,
Louisville, l Cranial nerve palsies developed in 23% of 73 children with basilar skull fractures. The majority occurred in patients 10 years of age or older. Our overall incidence was higher than that in a review indiscriminately ence with
in which basilar skull fractures
were
included with all head injuries.’ Our experi-
meningitis
was
similar
to that
present
in the
literature and would seem to support avoidance of prophylactic antibiotics.
Because there was no improvement
in neuro-
logical deficits in patients treated with steroids (the only case of meningitis
in our series was associated with steroids), we
believe
their
that
use is unwarranted.
discuss the prognosis
with
although the majority
(53.3%)
It is important
the patient’s
family,
to
because,
of cases resolve completely,
those with residual deficits can have significant morbidity. Copyright
o 1991 by W.B. Saunders Company
INDEX WORDS:
Basilar skull fractures;
cranial nerve injury.
B
ASILAR SKULL FRACTURES are uncommon in the pediatric population with a reported incidence of 6% to 14% of children with head injuries.‘12 There are few reports on cranial nerve deficits associated with pediatric head trauma or, more specifically, basilar skull fractures. It is thought that these deficits are caused by either direct trauma to the nerve or some degree of vascular compromise.3 Steroids have been used empirically to minimize edema, but there are no reports to support this practice. More importantly, a significant percentage of patients will have resolution of their cranial nerve deficit without intervention. We reviewed the experience of Kosair Children’s Hospital, Louisville, Kentucky, with basilar skull fractures and associated cranial nerve deficits over a 5-year period (May 1984 to June 1989) with a primary goal of documenting the incidence and clinical course of these deficits. We also wanted to determine the incidence of meningitis and seizure disorders as complications of basilar skull fractures.
From the Department of Surgery, Division of Pediattic Surgery, University of Louisville School of Medicine, Louisville, KY. Presented at the Jens G. Rosenkrantz Resident Competition at the 42nd Annual Meeting of the Surgical Section of the American Academy of Pediatrics, Boston, Massachusetts, October 67,199O. Address reprint requests to Diller B. Groj$ MD, Pediatric Surgery, Kosair Children’s Hospital, PO Box 35070, Louisville, KY 402325070. Copyright o 1991 by W. B. Saunders Company 0022-3468/91/2608-0020$03.OOlO
992
Hirikati
S. Nagaraj,
With
and Mary
E. Fallat
Kentucky MATERIALS
AND
METHODS
Between 1984 and 1989, 73 patients with basilar skull fractures were admitted to Kosair Children’s Hospital, Louisville, KY. The criteria for diagnosis included the presence of hemotympanum, tympanic membrane perforation with blood in the external auditory canal, otorrhea, rhinorrhea, or roentgenographic confirmation of a fracture. Seventeen (23%) of 73 patients had cranial nerve deficits diagnosed during their hospitalization. These were grouped according to the cranial nerve involved and the duration of the deficit. All deficits present at 6 months were considered permanent.3A subset of patients was identified with persistent cerebrospinal fluid (CSF) drainage for more than 24 hours. The patient population comprised 45 boys and 28 girls between the ages of 17 months and 17 years. Of the 17 patients with cranial nerve deficits, 12 (70.1%) were 10 years of age or older whereas 28 (50%) of the patients without neurological sequelae were age 10 years or older. The mechanism of injury varied. Passengers in motor vehicle accidents accounted for 37% of the injuries, falls accounted for 26%, bicycle accidents for 15.1%, and 11% were pedestrians struck by automobiles. The remaining 11% involved a variety of activities. Orthopedic injuries were present in 16 patients, thoracic injuries in 3 patients, and facial fractures in 10 patients. There were no abdominal injuries in this series and there were no fatalities. All patients were evaluated by the Pediatric Surgical and Neurosurgical Services at the time of admission. In addition, patients with deficits of cranial nerves (CN) II, III, IV, VI were evaluated by the Ophthamology Service. Otolaryngology was consulted for those patients with deficits of CN VII and VIII. RESULTS
Of 73 patients with basilar skull fractures, 17 (23%) had CN deficits. A total of 30 CN palsies were identified; 14 (46.7%) were permanent and 16 (53.3%) were temporary. Eight of these patients had multiple deficits whereas the remaining deficits were solitary. CN deficits were present in 29% of patients with associated injuries (Table 1). One patient (1.1% of the total patient population) complained of anosmia (CN I). There was no improvement in this deficit. Unilateral blindness (CN II) was experienced by five patients (6.8%); four of whom progressed to optic atrophy (80%) while one patient (20%) had significant improvement with only a mild field defect. Three patients (4.1%) were noted to have an oculomotor nerve (CN III) deficit, and two patients (66.7%) recovered complete function. A trochlear nerve (CN IV) deficit was identified in two patients (2.7%) and both had complete resolution of their deficit. There were seven cases (9.6%) of abducens nerve (CN VI) involvement. Six (85.7%) resolved completely. Facial nerve (CN VII) deficits Journalof Pediatric Surgery, Vol 26, No 8 (August), 1991: pp 992-994
993
BASILAR SKULL FRACTURES WITH CN INVOLVEMENT
Table 1. Cranial Nerve Deficits in 17 Patients NO.
Permanent
Temporary 0
CNI
1
1
CN II
5
4
1
CN III
3
1
2
CN IV
2
0 -
CNV
2 -
CN VI
7
1
6
CN VII
7
4
3
CN VIII
5
3 -
CN IX-XII Total
30
14 (47%)
2 16 (53%)
were identified in seven patients (9.6%); four (57.1%) were permanent. Although all patients with hemotympanum or perforated tympanic membrane had conductive hearing deficits by audiogram, five patients (6.8%) had proven deficits of the auditory nerve (CN VIII). Of these patients, three (60%) had residual deficits. There were no reported deficits involving either the trigeminal nerve (CN V) or the basal cranial nerves (CN IX to XII). Eleven patients experienced persistent CSF leak for more than 24 hours. All cases were treated with head elevation and all sealed spontaneously by 11 days. Three of these patients received prophylactic antibiotics. There were no cases of meningitis reported in this subgroup with CSF leakage. In our entire series, 10 patients (13.7%) received prophylactic antibiotics either for their basilar skull fracture or for other associated injuries. None of the patients receiving antibiotics developed meningitis. Of the four patients (5.4%) treated with steroids, three had CN deficits, none of whom had resolution of the deficit. None of the four patients received prophylactic antibiotics; one developed meningitis. This was the only case of meningitis in the whole group, representing 1.4% of patients with basilar skull fracture. There was only one patient (1.4%) with a documented seizure in the immediate postinjury period with no long-term sequelae. DISCUSSION
These data indicate that even though basilar skull fractures occur less commonly in the pediatric population than in the adult population, a large number of children will have either single or multiple CN palsies. Not only is the prognosis variable depending on the CN involved, the morbidity associated with these deficits varies significantly. Therefore, it would seem prudent to discuss each cranial nerve separately. The incidence of CN I impairment varies from 3% to 10%. It is age dependent, and is more common in older patients.’ While partial lesions usually resolve, anosmia present 2 months after injury rarely im-
proves.3 We encountered only one case (1.4%) of olfactory nerve palsy that presented as anosmia. There was no improvement in this deficit. CN II palsies carry a significant morbidity. There is a reported incidence of 4.8% in pediatric head injuries.4 In this series, the incidence was 6.8%, and 80% of these patients had total blindness without improvement. One patient had improvement (20%) of his deficit, but with a residual lower field defect. Rarely is the optic canal involved in these cases, and operative intervention is not indicated unless there is early, progressive deterioration. The incidence of CN III palsies among pediatric head injuries varies greatly in the literature, from 1% to 15.9%.1,4 According to one source, over 75% of these patients recover.3 The chief complaint is of diplopia caused by external strabismus. Three patients had with oculomotor nerve involvement (4.1%); two (66.7%) recovered completely. One patient (33.3%) had no improvement in his diplopia. Patients with isolated CN IV deficits experience diplopia on downward gaze. Two patients (2.7%) had CN IV palsies, and both were associated with total ophthalmoplegia. These lesions were temporary. Much more common is the CN IV palsy which has a reported incidence of 11.6% to 13% of head injuries.4,’ These patients present with internal strabismus. Because of the nerve’s long course along the floor of the cranium, it is very sensitive to increased intracranial pressure (ICP) and may explain why many patients improve in a few days as ICP normalizes.3 There were 7 patients with abducens palsy (9.6%) 6 of whom (85.7%) recovered completely. Two of these cases were associated with total ophthalmoplegia. Facial nerve deficits are associated with petrous bone fractures. In fact, 50% of the longitudinal fractures and 25% of the transverse fractures of the petrous bone result in facial nerve involvement.6 The reported incidence of CN VII palsies is 3% to 4%.3 Rates of complete recovery vary between 60% and 75% within 3 months’ whereas patients with deficits beyond this time are considered permanent.’ We had seven patients (9.6%) with CN VII palsies, five (71.4%) of whom had petrous ridge fractures on radiological examination. Although four of the patients (57%) had permanent deficits, which is a higher percentage than in literature,’ three of the four patients had only slight residual weakness of a branch of CN VII. Loss of hearing is a frequent complaint among patients with basilar skull fractures, most commonly caused by conductive defects associated with hemotympanum. Deafness due to neurological sequelae is
994
KITCHENS ET AL
reported to occur in 0.8% of head injuries. This is typically a mild high-frequency loss with minimal morbidity.3 We had five patients (6.8%) with CN VII deficits documented by audiogram; three (60%) were permanent. Trigeminal nerve palsies are very rare and are usually associated with crush injuries to the lateral skull. There were no CN V deficits in our series. Deficits of the basilar cranial nerves (IX to XII) are exceedingly rare and none were noted in our series. Steroids were used in four patients (5.4%) for
either increased ICP or CN palsies. None of the three patients receiving steroids for CN involvement improved significantly. The one case of meningitis in this series occurred in a patient who had received steroids. Although one cannot prove a causal relationship, we feel that it would be prudent to avoid steroid usage in these patients. Of the 11 patients with CSF leaks, three received antibiotics. Because none of these patients developed meningitis, and because the overall incidence of this complication is so low, we feel antibiotics are not warranted.
REFERENCES 1. Meaty .I: Pediatric Head Injuries. Springfield, IL, Thomas, 1968, pp 88-136 2. Hendrick EB, Harwood-Hash MR, Hundson AR: Head injuries in children. Clin Neurosurg 11:46-64,1964 3. Bakay L, Glasauer FE: Head Injury, Cranial Nerve Injuries. Boston, MA, Little, Brown, 1980, pp 263-276 4. Jacobi G, Ritz A, Eurich R: Cranial nerve damage after pediatric head trauma: A long-term follow-up study of 741 cases. Acta Paediatr Hung 27:173-187,1986
5. Engels EP: Basilar skull fractures involving the sella turcica. Clin Radio1 12:177, 1961 6. Karnik PP, Kirtane MV, Wagh SP, et al: Otoneurological problems in head injuries and their management. Int Surg 60:466469,1975 7. McHugh HE: Facial paralysis in birth injury and skull fractures. Arch Otol Rhino1 Laryngol78:443-455,1963 8. Harris P: Head injuries in childhood. Arch Dis Child 32:448491,1957
Discussion A. Cooper (New York, NY): This article adds an important piece to our knowledge of serious head trauma in children, because there has been, to my knowledge, only one other reported study of this problem. I was surprised to learn that all of the patients in this series survived, because many of the basilar skull fractures we have observed were associated with fatal head trauma. The nearly 25% incidence rate of cranial nerve damage found in this series, half of which was permanent, suggests that we should pay more attention to this problem, particularly because there is now data to support preservation of nerve function associated with the administration of corticosteroids. Although this study found no benefit associated with the use of corticosteroids in
this population, it is possible that the drugs were not given early enough to make a difference. The study also confirms the experience most of us have had with meningitis following CSF leaks and the need for prophylactic antibiotics: they do not appear to be necessary. However, the main value of this study is that it calls our attention to a problem that in the initial resuscitation evaluation, is sometimes overlooked. D. Groff (response): When there are four neurosurgeons in consultation, it’s difficult to devise specific protocols. We don’t have a figure for exactly when steroid use was started, but it’s something that would be very important.
Skull Fractures in Childhood Cranial Nerve Involvement
L. Kitchens,
Diller B. Groff,
Louisville, l Cranial nerve palsies developed in 23% of 73 children with basilar skull fractures. The majority occurred in patients 10 years of age or older. Our overall incidence was higher than that in a review indiscriminately ence with
in which basilar skull fractures
were
included with all head injuries.’ Our experi-
meningitis
was
similar
to that
present
in the
literature and would seem to support avoidance of prophylactic antibiotics.
Because there was no improvement
in neuro-
logical deficits in patients treated with steroids (the only case of meningitis
in our series was associated with steroids), we
believe
their
that
use is unwarranted.
discuss the prognosis
with
although the majority
(53.3%)
It is important
the patient’s
family,
to
because,
of cases resolve completely,
those with residual deficits can have significant morbidity. Copyright
o 1991 by W.B. Saunders Company
INDEX WORDS:
Basilar skull fractures;
cranial nerve injury.
B
ASILAR SKULL FRACTURES are uncommon in the pediatric population with a reported incidence of 6% to 14% of children with head injuries.‘12 There are few reports on cranial nerve deficits associated with pediatric head trauma or, more specifically, basilar skull fractures. It is thought that these deficits are caused by either direct trauma to the nerve or some degree of vascular compromise.3 Steroids have been used empirically to minimize edema, but there are no reports to support this practice. More importantly, a significant percentage of patients will have resolution of their cranial nerve deficit without intervention. We reviewed the experience of Kosair Children’s Hospital, Louisville, Kentucky, with basilar skull fractures and associated cranial nerve deficits over a 5-year period (May 1984 to June 1989) with a primary goal of documenting the incidence and clinical course of these deficits. We also wanted to determine the incidence of meningitis and seizure disorders as complications of basilar skull fractures.
From the Department of Surgery, Division of Pediattic Surgery, University of Louisville School of Medicine, Louisville, KY. Presented at the Jens G. Rosenkrantz Resident Competition at the 42nd Annual Meeting of the Surgical Section of the American Academy of Pediatrics, Boston, Massachusetts, October 67,199O. Address reprint requests to Diller B. Groj$ MD, Pediatric Surgery, Kosair Children’s Hospital, PO Box 35070, Louisville, KY 402325070. Copyright o 1991 by W. B. Saunders Company 0022-3468/91/2608-0020$03.OOlO
992
Hirikati
S. Nagaraj,
With
and Mary
E. Fallat
Kentucky MATERIALS
AND
METHODS
Between 1984 and 1989, 73 patients with basilar skull fractures were admitted to Kosair Children’s Hospital, Louisville, KY. The criteria for diagnosis included the presence of hemotympanum, tympanic membrane perforation with blood in the external auditory canal, otorrhea, rhinorrhea, or roentgenographic confirmation of a fracture. Seventeen (23%) of 73 patients had cranial nerve deficits diagnosed during their hospitalization. These were grouped according to the cranial nerve involved and the duration of the deficit. All deficits present at 6 months were considered permanent.3A subset of patients was identified with persistent cerebrospinal fluid (CSF) drainage for more than 24 hours. The patient population comprised 45 boys and 28 girls between the ages of 17 months and 17 years. Of the 17 patients with cranial nerve deficits, 12 (70.1%) were 10 years of age or older whereas 28 (50%) of the patients without neurological sequelae were age 10 years or older. The mechanism of injury varied. Passengers in motor vehicle accidents accounted for 37% of the injuries, falls accounted for 26%, bicycle accidents for 15.1%, and 11% were pedestrians struck by automobiles. The remaining 11% involved a variety of activities. Orthopedic injuries were present in 16 patients, thoracic injuries in 3 patients, and facial fractures in 10 patients. There were no abdominal injuries in this series and there were no fatalities. All patients were evaluated by the Pediatric Surgical and Neurosurgical Services at the time of admission. In addition, patients with deficits of cranial nerves (CN) II, III, IV, VI were evaluated by the Ophthamology Service. Otolaryngology was consulted for those patients with deficits of CN VII and VIII. RESULTS
Of 73 patients with basilar skull fractures, 17 (23%) had CN deficits. A total of 30 CN palsies were identified; 14 (46.7%) were permanent and 16 (53.3%) were temporary. Eight of these patients had multiple deficits whereas the remaining deficits were solitary. CN deficits were present in 29% of patients with associated injuries (Table 1). One patient (1.1% of the total patient population) complained of anosmia (CN I). There was no improvement in this deficit. Unilateral blindness (CN II) was experienced by five patients (6.8%); four of whom progressed to optic atrophy (80%) while one patient (20%) had significant improvement with only a mild field defect. Three patients (4.1%) were noted to have an oculomotor nerve (CN III) deficit, and two patients (66.7%) recovered complete function. A trochlear nerve (CN IV) deficit was identified in two patients (2.7%) and both had complete resolution of their deficit. There were seven cases (9.6%) of abducens nerve (CN VI) involvement. Six (85.7%) resolved completely. Facial nerve (CN VII) deficits Journalof Pediatric Surgery, Vol 26, No 8 (August), 1991: pp 992-994
993
BASILAR SKULL FRACTURES WITH CN INVOLVEMENT
Table 1. Cranial Nerve Deficits in 17 Patients NO.
Permanent
Temporary 0
CNI
1
1
CN II
5
4
1
CN III
3
1
2
CN IV
2
0 -
CNV
2 -
CN VI
7
1
6
CN VII
7
4
3
CN VIII
5
3 -
CN IX-XII Total
30
14 (47%)
2 16 (53%)
were identified in seven patients (9.6%); four (57.1%) were permanent. Although all patients with hemotympanum or perforated tympanic membrane had conductive hearing deficits by audiogram, five patients (6.8%) had proven deficits of the auditory nerve (CN VIII). Of these patients, three (60%) had residual deficits. There were no reported deficits involving either the trigeminal nerve (CN V) or the basal cranial nerves (CN IX to XII). Eleven patients experienced persistent CSF leak for more than 24 hours. All cases were treated with head elevation and all sealed spontaneously by 11 days. Three of these patients received prophylactic antibiotics. There were no cases of meningitis reported in this subgroup with CSF leakage. In our entire series, 10 patients (13.7%) received prophylactic antibiotics either for their basilar skull fracture or for other associated injuries. None of the patients receiving antibiotics developed meningitis. Of the four patients (5.4%) treated with steroids, three had CN deficits, none of whom had resolution of the deficit. None of the four patients received prophylactic antibiotics; one developed meningitis. This was the only case of meningitis in the whole group, representing 1.4% of patients with basilar skull fracture. There was only one patient (1.4%) with a documented seizure in the immediate postinjury period with no long-term sequelae. DISCUSSION
These data indicate that even though basilar skull fractures occur less commonly in the pediatric population than in the adult population, a large number of children will have either single or multiple CN palsies. Not only is the prognosis variable depending on the CN involved, the morbidity associated with these deficits varies significantly. Therefore, it would seem prudent to discuss each cranial nerve separately. The incidence of CN I impairment varies from 3% to 10%. It is age dependent, and is more common in older patients.’ While partial lesions usually resolve, anosmia present 2 months after injury rarely im-
proves.3 We encountered only one case (1.4%) of olfactory nerve palsy that presented as anosmia. There was no improvement in this deficit. CN II palsies carry a significant morbidity. There is a reported incidence of 4.8% in pediatric head injuries.4 In this series, the incidence was 6.8%, and 80% of these patients had total blindness without improvement. One patient had improvement (20%) of his deficit, but with a residual lower field defect. Rarely is the optic canal involved in these cases, and operative intervention is not indicated unless there is early, progressive deterioration. The incidence of CN III palsies among pediatric head injuries varies greatly in the literature, from 1% to 15.9%.1,4 According to one source, over 75% of these patients recover.3 The chief complaint is of diplopia caused by external strabismus. Three patients had with oculomotor nerve involvement (4.1%); two (66.7%) recovered completely. One patient (33.3%) had no improvement in his diplopia. Patients with isolated CN IV deficits experience diplopia on downward gaze. Two patients (2.7%) had CN IV palsies, and both were associated with total ophthalmoplegia. These lesions were temporary. Much more common is the CN IV palsy which has a reported incidence of 11.6% to 13% of head injuries.4,’ These patients present with internal strabismus. Because of the nerve’s long course along the floor of the cranium, it is very sensitive to increased intracranial pressure (ICP) and may explain why many patients improve in a few days as ICP normalizes.3 There were 7 patients with abducens palsy (9.6%) 6 of whom (85.7%) recovered completely. Two of these cases were associated with total ophthalmoplegia. Facial nerve deficits are associated with petrous bone fractures. In fact, 50% of the longitudinal fractures and 25% of the transverse fractures of the petrous bone result in facial nerve involvement.6 The reported incidence of CN VII palsies is 3% to 4%.3 Rates of complete recovery vary between 60% and 75% within 3 months’ whereas patients with deficits beyond this time are considered permanent.’ We had seven patients (9.6%) with CN VII palsies, five (71.4%) of whom had petrous ridge fractures on radiological examination. Although four of the patients (57%) had permanent deficits, which is a higher percentage than in literature,’ three of the four patients had only slight residual weakness of a branch of CN VII. Loss of hearing is a frequent complaint among patients with basilar skull fractures, most commonly caused by conductive defects associated with hemotympanum. Deafness due to neurological sequelae is
994
KITCHENS ET AL
reported to occur in 0.8% of head injuries. This is typically a mild high-frequency loss with minimal morbidity.3 We had five patients (6.8%) with CN VII deficits documented by audiogram; three (60%) were permanent. Trigeminal nerve palsies are very rare and are usually associated with crush injuries to the lateral skull. There were no CN V deficits in our series. Deficits of the basilar cranial nerves (IX to XII) are exceedingly rare and none were noted in our series. Steroids were used in four patients (5.4%) for
either increased ICP or CN palsies. None of the three patients receiving steroids for CN involvement improved significantly. The one case of meningitis in this series occurred in a patient who had received steroids. Although one cannot prove a causal relationship, we feel that it would be prudent to avoid steroid usage in these patients. Of the 11 patients with CSF leaks, three received antibiotics. Because none of these patients developed meningitis, and because the overall incidence of this complication is so low, we feel antibiotics are not warranted.
REFERENCES 1. Meaty .I: Pediatric Head Injuries. Springfield, IL, Thomas, 1968, pp 88-136 2. Hendrick EB, Harwood-Hash MR, Hundson AR: Head injuries in children. Clin Neurosurg 11:46-64,1964 3. Bakay L, Glasauer FE: Head Injury, Cranial Nerve Injuries. Boston, MA, Little, Brown, 1980, pp 263-276 4. Jacobi G, Ritz A, Eurich R: Cranial nerve damage after pediatric head trauma: A long-term follow-up study of 741 cases. Acta Paediatr Hung 27:173-187,1986
5. Engels EP: Basilar skull fractures involving the sella turcica. Clin Radio1 12:177, 1961 6. Karnik PP, Kirtane MV, Wagh SP, et al: Otoneurological problems in head injuries and their management. Int Surg 60:466469,1975 7. McHugh HE: Facial paralysis in birth injury and skull fractures. Arch Otol Rhino1 Laryngol78:443-455,1963 8. Harris P: Head injuries in childhood. Arch Dis Child 32:448491,1957
Discussion A. Cooper (New York, NY): This article adds an important piece to our knowledge of serious head trauma in children, because there has been, to my knowledge, only one other reported study of this problem. I was surprised to learn that all of the patients in this series survived, because many of the basilar skull fractures we have observed were associated with fatal head trauma. The nearly 25% incidence rate of cranial nerve damage found in this series, half of which was permanent, suggests that we should pay more attention to this problem, particularly because there is now data to support preservation of nerve function associated with the administration of corticosteroids. Although this study found no benefit associated with the use of corticosteroids in
this population, it is possible that the drugs were not given early enough to make a difference. The study also confirms the experience most of us have had with meningitis following CSF leaks and the need for prophylactic antibiotics: they do not appear to be necessary. However, the main value of this study is that it calls our attention to a problem that in the initial resuscitation evaluation, is sometimes overlooked. D. Groff (response): When there are four neurosurgeons in consultation, it’s difficult to devise specific protocols. We don’t have a figure for exactly when steroid use was started, but it’s something that would be very important.
