DEPARTMENT
Case Study—Acute and Specialty Care
An Unusual Cause of Neonatal Meningitis Sharda Udassi, MD, Jai P. Udassi, MD, Beverly P. Giordano, MS, RN, CPNP, PMHS, & Judy F. Lew, MD
KEY WORDS Intranasal meningocele, meningitis, developmental skull defects
CASE PRESENTATION A 10-day-old White male infant was brought to a local emergency department (ED) with a 1-day history of fever (38.0 C), fussiness, rhinorrhea, coughing, and difficulty breathing (i.e., subcostal retractions but no grunting). The parents brought the infant to the ED because they had received standard infant care instructions (i.e., infants younger than 2 months must be evaluated for any rectal temperature above 38 C) and were concerned that he was not feeding well. The infant had been born at term via a repeat cesarean section. Results of the mother’s serologic studies and group B streptococcal culture were negative. She
Section Editors Karin Reuter-Rice, PhD, CPNP-AC, FCCM, FAAN Corresponding Editor Duke University Durham, North Carolina Terea Giannetta, DNP, RN, CPNP California State University Children’s Hospital Central California Fresno, California
had no history of perinatal or postnatal complications. The infant had received his first hepatitis B vaccine in the newborn nursery. The only abnormal finding of the newborn examination was glandular hypospadias. He had been discharged from the hospital with his mother at 2 days of age. The infant had been feeding well until the day he presented to the ED at 10 days of age. Family/Social History The infant lived at home with his parents and one older sibling. No one at home had been ill with fever, respiratory illness, or skin lesions. The infant was not in day care. Review of Systems On day 10 of life, the infant presented to the ED with a rectal temperature of 38 C, rhinorrhea, breathing difficulties, cough, and a 1-day history of poor feeding. Family members stated that he had been ‘‘congested’’
Jai P. Udassi, Medical Director of Clinical Operations, Pediatric Inpatient Services, and PCICU, Sidra Research and Medical Center, Doha, Qatar. Beverly P. Giordano, Pediatric Nurse Practitioner, Division of General Pediatrics, University of Florida, Gainesville, FL. Judy F. Lew, Professor of Pediatrics, Division of Immunology, Rheumatology, and Infectious Diseases, University of Florida, Gainesville, FL. Conflicts of interest: None to report. Correspondence: Beverly P. Giordano, MS, RN, CPNP, PMHS, 1701 SW 16th Ave, Gainesville, FL 32608; e-mail: bgiordano@ peds.ufl.edu.
Maureen A. Madden, MSN, RN, CPNP-AC, CCRN, FCCM Rutgers Robert Wood Johnson Medical School New Brunswick, New Jersey Bristol Myers Squibb Children’s Hospital New Brunswick, New Jersey
0891-5245/$36.00
Sharda Udassi, Senior Attending Physician, Division of General Pediatrics, Sidra Research and Medical Center, Doha, Qatar.
http://dx.doi.org/10.1016/j.pedhc.2015.03.002
www.jpedhc.org
J Pediatr Health Care. (2015) -, ---. Copyright Q 2015 by the National Association of Pediatric Nurse Practitioners. Published by Elsevier Inc. All rights reserved.
-/- 2015
1
since birth, but they had not observed anything unusual about the shape of his nose or the appearance of his lips. ED staff members noted the presence of rhinorrhea on the initial examination and attributed it to infant’s upper respiratory illness. Physical Examination On the initial physical examination, the infant was noted to have three white blisters on his lower lip. A mass was present in the left nostril, and it enlarged when the infant cried. Some erythema and fullness of the nose was noted, along with clear fluid discharge coming from the left nostril. An oval-shaped mass approximately 2 cm in diameter was visible along the left exterior side of the nose. The infant also had discharge from his left eye. His respiratory rate was 36 breaths per minute; no retractions were present. Oxygen saturation on room air was 97%. The infant’s anterior and posterior fontanelles were not bulging or depressed. The infant had no skin lesions other than those on the lower lip. Diagnostic Testing In the ED, the infant’s blood, urine, and cerebrospinal fluid (CSF) were cultured. A complete blood cell count was significant for leukocytosis (white blood cell [WBC] count, 28,200/mm3; normal, 5,000-20,000/mm3) and bandemia (20%). His C-reactive protein level was elevated at 12.5 mg/L (normal, 0-0.5 mg/dl). His erythrocyte sedimentation rate also was elevated at 44 mm/ hr (normal, 0-4 mm/hr). The platelet count was elevated at 7333/mL (normal, 2523/mL). The CSF obtained from a lumbar puncture was bloody and contained 12,750 red blood cells/mm3; 32 WBCs/mm3; protein, 63 mg/dl; glucose, 60 mg/dl; neutrophils, 70%; and lymphocytes, 30%, but no organisms on gram stain. Complete CSF studies were performed, and results of a herpes simplex virus (HSV) serology study were negative. The initial bacterial culture was negative. Nasal fluid was tested for glucose, but the results were inconclusive. Magnetic resonance imaging (MRI) of the head was obtained to evaluate the nasal mass. The MRI demonstrated a soft tissue (fluid) signal intensity mass in the left nasal cavity extending to the nasal vestibule. The lesion was multiloculated with enhancement of the dura anteriorly and peripherally. There was no brain tissue within the mass. Hospital Admission The infant was admitted to the pediatric unit for continued evaluation and management. Intravenous (IV) administration of prophylactic ampicillin, gentamicin, and acyclovir was initiated to treat possible sepsis and neonatal bacterial and HSV meningitis. By day 2 of admission, the infant’s C-reactive protein had decreased to 0.2 mg/L, the erythrocyte sedimentation 2
Volume - Number -
rate had decreased to 18 mm/hr, the WBC count had decreased to 18,200/mm3, and the platelet count had decreased to 684,000/uL. On day 3 of admission, increased erythema and edema developed over the nasal area, and the infant had persistent fever. A follow-up MRI scan with and without contrast demonstrated enhancement of the meninges. The working diagnosis at this time was meningitis that developed after the initial CSF studies were performed. The patient was transferred to the pediatric intensive care unit (PICU) because of progressive respiratory distress resulting from upper airway obstruction. He was electively intubated. The infant continued to have fever. Culture results from the initial nasal swab were reported as 3+ Staphylococcus aureus that was resistant to oxacillin. The pediatric infectious disease service was consulted. The infant’s parents elected not to repeat the lumbar puncture, because repeat negative CSF cultures would not have ruled out bacterial meningitis in the presence of ongoing antibiotic therapy. The antibiotic was changed from ampicillin to IV vancomycin to cover for methicillin-resistant Staphylococcus aureus (MRSA). Clindamycin was not used initially because it does not adequately diffuse into the CSF (Drugs.com, 2014). Gentamicin was discontinued, and IV cefotaxime was initiated for better central nervous system penetration. The CSF HSV polymerase chain reaction was negative, and the acyclovir was discontinued. The infant received antibiotics for 3 weeks to treat presumed bacterial meningitis caused by an unknown pathogen. On day 4, the infant underwent a left fronto-orbital craniotomy with repair and reconstruction of the anterior fossa floor and meningocele reduction. The neurosurgeon elected to use Dandy’s traditional craniotomy and intracranial surgical approach (Dandy, 1926) because endoscopic sinonasal procedures are difficult when the involved anatomy is complicated and difficult to access. Two days later, the infant underwent a flexible laryngoscopy procedure to assess the patency of the left nasal passage. Mucosal edema was present, but the scope could be passed to the nasopharynx without difficulty. A third head MRI scan demonstrated encephalomalacia of the left frontal lobe as a result of recent resection of the meningocele. Computed tomography of the head noted a dehiscent area in the cribriform plate. One week after surgery, the infant was extubated. When nasopharyngeal cultures confirmed the presence of MRSA that was sensitive to clindamycin, vancomycin was discontinued and treatment with clindamycin was initiated, because the infant was now stable. Treatment with cefotaxime was continued to treat any gramnegative bacteria that may have been present. The infant was discharged 1 month after admission. He had no postoperative complications. He was meeting age-appropriate developmental milestones at Journal of Pediatric Health Care
his recent 6-month well-child checkup. Nurse practitioners were involved in this infant’s care throughout the admission and at his follow-up appointment in the primary care clinic. DISCUSSION Meningoceles are a heterogeneous group of cystic lesions that contain leptomeninges and CSF (Malik, Pandya, & Parteki, 2004). Meningoceles often are grouped with myelomeningoceles, which makes it difficult to know the incidence, genetic factors, and causes (Albright, Pollack, & Adelson, 1999). Congenital meningoceles are relatively rare developmental anomalies (Oner, Uzun, Tokgoz, & Tali, 2004). Intranasal meningoceles occur as a result of meningeal herniation through defects in the floor of the anterior cranial fossa. A CSF pressure gradient that is greater than the tensile strength of the disrupted tissue is a contributing factor in meningeal Intranasal herniation. When meningoceles intracranial pressure is occur as a result of elevated, the weakest anatomic points in the meningeal central nervous system herniation through periphery (i.e., optic defects in the floor nerve sheath, cribriform plate, sellar diaof the anterior phragm, and other cranial fossa. bony dehiscences in the anterior or middle cranial fossae) can act as potential release valves for the high intracranial pressure (Bhat, 2006; Roehm & Brown, 2011). Disruption in the arachnoid and dura mater causes CSF leak, manifested as rhinorrhea (Bhat, 2006). Most cases of CSF rhinorrhea from intranasal meningoceles are of traumatic origin, with only 4% of CSF leaks being spontaneous or due to nontraumatic causes (e.g., developmental skull-based defects with meningocele, skull-based tumor, empty sella, and osteomyelitis; Robertson, Palacios, & D’Antonio, 2013). It was not clear in this infant’s history when the CSF rhinorrhea developed (i.e., after nasal suctioning in the delivery room, when his airway patency was evaluated in the newborn nursery, or if it was spontaneous in origin). Routine intrapartum oropharyngeal and nasopharyngeal suctioning for infants born with clear or meconium-stained amniotic fluid is no longer recommended (Perlman et al., 2010). Although parents are taught to instill saline nose drops and to suction infants’ nares, ‘‘little data exist on their efficacy in improving nasal air movement’’ (Bergeson & Shaw, 2001). An intranasal meningocele can be complicated by meningitis, because intracranial contents are exposed to intranasal organisms when the meningocele ruptures. The risk for meningitis is higher with a spontawww.jpedhc.org
neous CSF fistula than with a traumatic CSF fistula (Robertson et al., 2013). The most common causative organism is Streptococcus pneumoniae, with Haemophilus influenzae the second most common causative organism. In patients younger than 4 months, the most common organisms are gram-negative bacilli (Sirisanthana & Sirisanthana, 1991). In one series of patients with occult anterior cranial fossa defects, there was an average of 4.8 episodes of meningitis per patient (Schwartz & Shaw, 2002). Meningitis occurs in 25% to 50% of persons with untreated traumatic CSF fistulas and in 10% of patients in the first week after head trauma. Spontaneous fistula CSF leaks are often intermittent and persistent in 60% of untreated patients (Robertson et al., 2013). Patients who present with CSF rhinorrhea create a diagnostic challenge. Key historical facts to elicit from any patient with unexplained rhinorrhea include craniofacial trauma or surgery, chronic positional or frontal headache, chronic nasal obstruction symptoms, and previous episodes of meningitis (Schwartz & Shaw, 2002). Infants, such as the one in this case MRI imaging is the study, may often have modality of choice a benign, noncontribufor evaluating tory history before they present with CSF rhilesions with norrhea. potential MRI imaging is the intracranial modality of choice for evaluating lesions extension (e.g., with potential intracraintranasal nial extension (e.g., meningoceles). intranasal meningoceles). Both computed tomography and MRI are often needed to adequately evaluate the bone, brain, and soft tissue components of midface anomalies, especially in congenital masses (Lowe, Booth, Jogler, & Rollins, 2000). Surgical management of intranasal meningoceles has evolved in the past century. Dandy introduced the frontal craniotomy approach to surgical repair of CSF leaks in 1926 (Roehm & Brown, 2011). In the 1950s, extracranial and transnasal approaches replaced the frontal craniotomy approach. Endoscopic techniques were first attempted for CSF leak repairs in 1981 (Bhat, 2006). A traditional craniotomy approach was used for the infant in this case study. SUMMARY Neonates who present with fever, coughing, poor feeding, and rhinorrhea typically undergo evaluations for sepsis, respiratory syncytial virus, and possibly influenza infections. This infant was unusual in that the cause of his poor feeding and rhinorrhea was a ruptured intranasal meningocele. Also unusual was the organism (S. aureus) that caused the meningitis. -/- 2015
3
Intranasal meningoceles, although rare, do occur. Intranasal suctioning is no longer recommended as routine delivery room care, which decreases the risk for rupturing meningoceles that may be present in the newborn’s nose. However, parents are still being taught to use bulb aspirators to clear their infants’ nasal passages. This case study illustrates the dangers that may be associated with this common practice. REFERENCES Albright, A. L., Pollack, I. F., & Adelson, P. D. (1999). Principles and practice of pediatric neurosurgery. New York, NY: Thieme. Bergeson, P. S., & Shaw, J. C. (2001). Are infants really obligatory nasal breathers? Clinical Pediatrics, 40(10), 567-569. Bhat, M. (2006). A case of intranasal meningocele. McGill Journal of Medicine, 9(1), 31-33. Dandy, W. E. (1926). Pneumocephalus (intracranial pneumatocele or aerocele). Archives of Surgery, 12(5), 949-982. Drugs.com. (2014). Clindamycin injection. Retrieved from http:// www.drugs.com/pro/clindamycin-injection.html Lowe, L. H., Booth, T. N., Jogler, J. M., & Rollins, N. K. (2000). Midface anomalies in children. Radiological Society of North America, 20(4), 907-922.
4
Volume - Number -
Malik, R., Pandya, V. K., & Parteki, S. (2004). Frontoethmoidal meningocele. Neuroradiology, 14(4), 379-381. Oner, A. Y., Uzun, M., Tokgoz, N., & Tali, E. T. (2004). Isolated true anterior thoracic meningocele. American Journal of Neuroradiology, 25(10), 1828-1830. Perlman, J. M., Wyllie, J., Kattwinkel, J., Atkins, D. L., Chameides, L., Goldsmith, J. P., . Velaphi, S. on behalf of the Neonatal Resuscitation Chapter Collaborators. (2010). Part 11: Neonatal resuscitation: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Circulation, 122(Suppl. 2), S516-S538. Robertson, H. J. F., Palacios, E., & D’Antonio, M. G. (2013). Cerebrospinal fluid leak imaging. Retrieved from http://emedicine. medscape.com/article/338989-overview Roehm, C. E., & Brown, S. M. (2011). Unilateral endoscopic approach for repair of frontal sinus cerebrospinal fluid leak. Skull Base, 21(3), 139-146. Sirisanthana, V., & Sirisanthana, T. (1991). Etiologic bacterial agents of community-acquired meningitis in pediatric patients at Chiang Mai University Hospital. Journal of Infectious Disease and Antimicrobial Agents, 4, 215-220. Schwartz, M. D., & Shaw, G. J. (2002). Bacterial meningitis secondary to a transethmoidal encephalocele presenting to the emergency department. The Journal of Emergency Medicine, 23(2), 171-174.
Journal of Pediatric Health Care
Case Study—Acute and Specialty Care
An Unusual Cause of Neonatal Meningitis Sharda Udassi, MD, Jai P. Udassi, MD, Beverly P. Giordano, MS, RN, CPNP, PMHS, & Judy F. Lew, MD
KEY WORDS Intranasal meningocele, meningitis, developmental skull defects
CASE PRESENTATION A 10-day-old White male infant was brought to a local emergency department (ED) with a 1-day history of fever (38.0 C), fussiness, rhinorrhea, coughing, and difficulty breathing (i.e., subcostal retractions but no grunting). The parents brought the infant to the ED because they had received standard infant care instructions (i.e., infants younger than 2 months must be evaluated for any rectal temperature above 38 C) and were concerned that he was not feeding well. The infant had been born at term via a repeat cesarean section. Results of the mother’s serologic studies and group B streptococcal culture were negative. She
Section Editors Karin Reuter-Rice, PhD, CPNP-AC, FCCM, FAAN Corresponding Editor Duke University Durham, North Carolina Terea Giannetta, DNP, RN, CPNP California State University Children’s Hospital Central California Fresno, California
had no history of perinatal or postnatal complications. The infant had received his first hepatitis B vaccine in the newborn nursery. The only abnormal finding of the newborn examination was glandular hypospadias. He had been discharged from the hospital with his mother at 2 days of age. The infant had been feeding well until the day he presented to the ED at 10 days of age. Family/Social History The infant lived at home with his parents and one older sibling. No one at home had been ill with fever, respiratory illness, or skin lesions. The infant was not in day care. Review of Systems On day 10 of life, the infant presented to the ED with a rectal temperature of 38 C, rhinorrhea, breathing difficulties, cough, and a 1-day history of poor feeding. Family members stated that he had been ‘‘congested’’
Jai P. Udassi, Medical Director of Clinical Operations, Pediatric Inpatient Services, and PCICU, Sidra Research and Medical Center, Doha, Qatar. Beverly P. Giordano, Pediatric Nurse Practitioner, Division of General Pediatrics, University of Florida, Gainesville, FL. Judy F. Lew, Professor of Pediatrics, Division of Immunology, Rheumatology, and Infectious Diseases, University of Florida, Gainesville, FL. Conflicts of interest: None to report. Correspondence: Beverly P. Giordano, MS, RN, CPNP, PMHS, 1701 SW 16th Ave, Gainesville, FL 32608; e-mail: bgiordano@ peds.ufl.edu.
Maureen A. Madden, MSN, RN, CPNP-AC, CCRN, FCCM Rutgers Robert Wood Johnson Medical School New Brunswick, New Jersey Bristol Myers Squibb Children’s Hospital New Brunswick, New Jersey
0891-5245/$36.00
Sharda Udassi, Senior Attending Physician, Division of General Pediatrics, Sidra Research and Medical Center, Doha, Qatar.
http://dx.doi.org/10.1016/j.pedhc.2015.03.002
www.jpedhc.org
J Pediatr Health Care. (2015) -, ---. Copyright Q 2015 by the National Association of Pediatric Nurse Practitioners. Published by Elsevier Inc. All rights reserved.
-/- 2015
1
since birth, but they had not observed anything unusual about the shape of his nose or the appearance of his lips. ED staff members noted the presence of rhinorrhea on the initial examination and attributed it to infant’s upper respiratory illness. Physical Examination On the initial physical examination, the infant was noted to have three white blisters on his lower lip. A mass was present in the left nostril, and it enlarged when the infant cried. Some erythema and fullness of the nose was noted, along with clear fluid discharge coming from the left nostril. An oval-shaped mass approximately 2 cm in diameter was visible along the left exterior side of the nose. The infant also had discharge from his left eye. His respiratory rate was 36 breaths per minute; no retractions were present. Oxygen saturation on room air was 97%. The infant’s anterior and posterior fontanelles were not bulging or depressed. The infant had no skin lesions other than those on the lower lip. Diagnostic Testing In the ED, the infant’s blood, urine, and cerebrospinal fluid (CSF) were cultured. A complete blood cell count was significant for leukocytosis (white blood cell [WBC] count, 28,200/mm3; normal, 5,000-20,000/mm3) and bandemia (20%). His C-reactive protein level was elevated at 12.5 mg/L (normal, 0-0.5 mg/dl). His erythrocyte sedimentation rate also was elevated at 44 mm/ hr (normal, 0-4 mm/hr). The platelet count was elevated at 7333/mL (normal, 2523/mL). The CSF obtained from a lumbar puncture was bloody and contained 12,750 red blood cells/mm3; 32 WBCs/mm3; protein, 63 mg/dl; glucose, 60 mg/dl; neutrophils, 70%; and lymphocytes, 30%, but no organisms on gram stain. Complete CSF studies were performed, and results of a herpes simplex virus (HSV) serology study were negative. The initial bacterial culture was negative. Nasal fluid was tested for glucose, but the results were inconclusive. Magnetic resonance imaging (MRI) of the head was obtained to evaluate the nasal mass. The MRI demonstrated a soft tissue (fluid) signal intensity mass in the left nasal cavity extending to the nasal vestibule. The lesion was multiloculated with enhancement of the dura anteriorly and peripherally. There was no brain tissue within the mass. Hospital Admission The infant was admitted to the pediatric unit for continued evaluation and management. Intravenous (IV) administration of prophylactic ampicillin, gentamicin, and acyclovir was initiated to treat possible sepsis and neonatal bacterial and HSV meningitis. By day 2 of admission, the infant’s C-reactive protein had decreased to 0.2 mg/L, the erythrocyte sedimentation 2
Volume - Number -
rate had decreased to 18 mm/hr, the WBC count had decreased to 18,200/mm3, and the platelet count had decreased to 684,000/uL. On day 3 of admission, increased erythema and edema developed over the nasal area, and the infant had persistent fever. A follow-up MRI scan with and without contrast demonstrated enhancement of the meninges. The working diagnosis at this time was meningitis that developed after the initial CSF studies were performed. The patient was transferred to the pediatric intensive care unit (PICU) because of progressive respiratory distress resulting from upper airway obstruction. He was electively intubated. The infant continued to have fever. Culture results from the initial nasal swab were reported as 3+ Staphylococcus aureus that was resistant to oxacillin. The pediatric infectious disease service was consulted. The infant’s parents elected not to repeat the lumbar puncture, because repeat negative CSF cultures would not have ruled out bacterial meningitis in the presence of ongoing antibiotic therapy. The antibiotic was changed from ampicillin to IV vancomycin to cover for methicillin-resistant Staphylococcus aureus (MRSA). Clindamycin was not used initially because it does not adequately diffuse into the CSF (Drugs.com, 2014). Gentamicin was discontinued, and IV cefotaxime was initiated for better central nervous system penetration. The CSF HSV polymerase chain reaction was negative, and the acyclovir was discontinued. The infant received antibiotics for 3 weeks to treat presumed bacterial meningitis caused by an unknown pathogen. On day 4, the infant underwent a left fronto-orbital craniotomy with repair and reconstruction of the anterior fossa floor and meningocele reduction. The neurosurgeon elected to use Dandy’s traditional craniotomy and intracranial surgical approach (Dandy, 1926) because endoscopic sinonasal procedures are difficult when the involved anatomy is complicated and difficult to access. Two days later, the infant underwent a flexible laryngoscopy procedure to assess the patency of the left nasal passage. Mucosal edema was present, but the scope could be passed to the nasopharynx without difficulty. A third head MRI scan demonstrated encephalomalacia of the left frontal lobe as a result of recent resection of the meningocele. Computed tomography of the head noted a dehiscent area in the cribriform plate. One week after surgery, the infant was extubated. When nasopharyngeal cultures confirmed the presence of MRSA that was sensitive to clindamycin, vancomycin was discontinued and treatment with clindamycin was initiated, because the infant was now stable. Treatment with cefotaxime was continued to treat any gramnegative bacteria that may have been present. The infant was discharged 1 month after admission. He had no postoperative complications. He was meeting age-appropriate developmental milestones at Journal of Pediatric Health Care
his recent 6-month well-child checkup. Nurse practitioners were involved in this infant’s care throughout the admission and at his follow-up appointment in the primary care clinic. DISCUSSION Meningoceles are a heterogeneous group of cystic lesions that contain leptomeninges and CSF (Malik, Pandya, & Parteki, 2004). Meningoceles often are grouped with myelomeningoceles, which makes it difficult to know the incidence, genetic factors, and causes (Albright, Pollack, & Adelson, 1999). Congenital meningoceles are relatively rare developmental anomalies (Oner, Uzun, Tokgoz, & Tali, 2004). Intranasal meningoceles occur as a result of meningeal herniation through defects in the floor of the anterior cranial fossa. A CSF pressure gradient that is greater than the tensile strength of the disrupted tissue is a contributing factor in meningeal Intranasal herniation. When meningoceles intracranial pressure is occur as a result of elevated, the weakest anatomic points in the meningeal central nervous system herniation through periphery (i.e., optic defects in the floor nerve sheath, cribriform plate, sellar diaof the anterior phragm, and other cranial fossa. bony dehiscences in the anterior or middle cranial fossae) can act as potential release valves for the high intracranial pressure (Bhat, 2006; Roehm & Brown, 2011). Disruption in the arachnoid and dura mater causes CSF leak, manifested as rhinorrhea (Bhat, 2006). Most cases of CSF rhinorrhea from intranasal meningoceles are of traumatic origin, with only 4% of CSF leaks being spontaneous or due to nontraumatic causes (e.g., developmental skull-based defects with meningocele, skull-based tumor, empty sella, and osteomyelitis; Robertson, Palacios, & D’Antonio, 2013). It was not clear in this infant’s history when the CSF rhinorrhea developed (i.e., after nasal suctioning in the delivery room, when his airway patency was evaluated in the newborn nursery, or if it was spontaneous in origin). Routine intrapartum oropharyngeal and nasopharyngeal suctioning for infants born with clear or meconium-stained amniotic fluid is no longer recommended (Perlman et al., 2010). Although parents are taught to instill saline nose drops and to suction infants’ nares, ‘‘little data exist on their efficacy in improving nasal air movement’’ (Bergeson & Shaw, 2001). An intranasal meningocele can be complicated by meningitis, because intracranial contents are exposed to intranasal organisms when the meningocele ruptures. The risk for meningitis is higher with a spontawww.jpedhc.org
neous CSF fistula than with a traumatic CSF fistula (Robertson et al., 2013). The most common causative organism is Streptococcus pneumoniae, with Haemophilus influenzae the second most common causative organism. In patients younger than 4 months, the most common organisms are gram-negative bacilli (Sirisanthana & Sirisanthana, 1991). In one series of patients with occult anterior cranial fossa defects, there was an average of 4.8 episodes of meningitis per patient (Schwartz & Shaw, 2002). Meningitis occurs in 25% to 50% of persons with untreated traumatic CSF fistulas and in 10% of patients in the first week after head trauma. Spontaneous fistula CSF leaks are often intermittent and persistent in 60% of untreated patients (Robertson et al., 2013). Patients who present with CSF rhinorrhea create a diagnostic challenge. Key historical facts to elicit from any patient with unexplained rhinorrhea include craniofacial trauma or surgery, chronic positional or frontal headache, chronic nasal obstruction symptoms, and previous episodes of meningitis (Schwartz & Shaw, 2002). Infants, such as the one in this case MRI imaging is the study, may often have modality of choice a benign, noncontribufor evaluating tory history before they present with CSF rhilesions with norrhea. potential MRI imaging is the intracranial modality of choice for evaluating lesions extension (e.g., with potential intracraintranasal nial extension (e.g., meningoceles). intranasal meningoceles). Both computed tomography and MRI are often needed to adequately evaluate the bone, brain, and soft tissue components of midface anomalies, especially in congenital masses (Lowe, Booth, Jogler, & Rollins, 2000). Surgical management of intranasal meningoceles has evolved in the past century. Dandy introduced the frontal craniotomy approach to surgical repair of CSF leaks in 1926 (Roehm & Brown, 2011). In the 1950s, extracranial and transnasal approaches replaced the frontal craniotomy approach. Endoscopic techniques were first attempted for CSF leak repairs in 1981 (Bhat, 2006). A traditional craniotomy approach was used for the infant in this case study. SUMMARY Neonates who present with fever, coughing, poor feeding, and rhinorrhea typically undergo evaluations for sepsis, respiratory syncytial virus, and possibly influenza infections. This infant was unusual in that the cause of his poor feeding and rhinorrhea was a ruptured intranasal meningocele. Also unusual was the organism (S. aureus) that caused the meningitis. -/- 2015
3
Intranasal meningoceles, although rare, do occur. Intranasal suctioning is no longer recommended as routine delivery room care, which decreases the risk for rupturing meningoceles that may be present in the newborn’s nose. However, parents are still being taught to use bulb aspirators to clear their infants’ nasal passages. This case study illustrates the dangers that may be associated with this common practice. REFERENCES Albright, A. L., Pollack, I. F., & Adelson, P. D. (1999). Principles and practice of pediatric neurosurgery. New York, NY: Thieme. Bergeson, P. S., & Shaw, J. C. (2001). Are infants really obligatory nasal breathers? Clinical Pediatrics, 40(10), 567-569. Bhat, M. (2006). A case of intranasal meningocele. McGill Journal of Medicine, 9(1), 31-33. Dandy, W. E. (1926). Pneumocephalus (intracranial pneumatocele or aerocele). Archives of Surgery, 12(5), 949-982. Drugs.com. (2014). Clindamycin injection. Retrieved from http:// www.drugs.com/pro/clindamycin-injection.html Lowe, L. H., Booth, T. N., Jogler, J. M., & Rollins, N. K. (2000). Midface anomalies in children. Radiological Society of North America, 20(4), 907-922.
4
Volume - Number -
Malik, R., Pandya, V. K., & Parteki, S. (2004). Frontoethmoidal meningocele. Neuroradiology, 14(4), 379-381. Oner, A. Y., Uzun, M., Tokgoz, N., & Tali, E. T. (2004). Isolated true anterior thoracic meningocele. American Journal of Neuroradiology, 25(10), 1828-1830. Perlman, J. M., Wyllie, J., Kattwinkel, J., Atkins, D. L., Chameides, L., Goldsmith, J. P., . Velaphi, S. on behalf of the Neonatal Resuscitation Chapter Collaborators. (2010). Part 11: Neonatal resuscitation: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Circulation, 122(Suppl. 2), S516-S538. Robertson, H. J. F., Palacios, E., & D’Antonio, M. G. (2013). Cerebrospinal fluid leak imaging. Retrieved from http://emedicine. medscape.com/article/338989-overview Roehm, C. E., & Brown, S. M. (2011). Unilateral endoscopic approach for repair of frontal sinus cerebrospinal fluid leak. Skull Base, 21(3), 139-146. Sirisanthana, V., & Sirisanthana, T. (1991). Etiologic bacterial agents of community-acquired meningitis in pediatric patients at Chiang Mai University Hospital. Journal of Infectious Disease and Antimicrobial Agents, 4, 215-220. Schwartz, M. D., & Shaw, G. J. (2002). Bacterial meningitis secondary to a transethmoidal encephalocele presenting to the emergency department. The Journal of Emergency Medicine, 23(2), 171-174.
Journal of Pediatric Health Care
