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Neonatal Meningitis Medication

  • Author: David C Dredge, MD; Chief Editor: Amy Kao, MD  more...
 
Updated: Dec 14, 2015
 

Medication Summary

Aggressive antimicrobial intervention is lifesaving in neonates with suspected meningitis. Because distinguishing viral from bacterial meningitis is difficult early in the clinical course, a combination of agents is often necessary, providing coverage for both types of infection.

In most institutions, acyclovir is the preferred antiviral therapy, but the best antibacterial therapy remains subject to debate. The combination of ampicillin and gentamicin is a common regimen. Many centers use cefotaxime in addition to or instead of gentamicin, particularly when gram-negative infections are suspected. Selection of antibiotics should be based on likely pathogens, local patterns of antibacterial drug sensitivities, and hospital policies.

In addition to the medications listed below, pleconaril is an experimental agent that interferes with attachment, entry, and uncoating of enteroviruses. It was shown to be well tolerated by neonates in a single, small, double-blinded study. Data supporting the efficacy of pleconaril are limited, although a larger clinical trial is currently under way. At present, this drug is available only for compassionate use or in clinical trials.

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Antivirals, Other

Class Summary

Antiviral agents inhibit viral replication and activity.

Acyclovir (Zovirax)

 

Acyclovir is the preferred treatment for herpes simplex virus (HSV) meningitis. Intravenous (IV) therapy is treatment of choice for neonatal HSV infection, regardless of clinical presentation. Acyclovir is activated by herpes-specific thymidine kinase; it prevents viral replication by inhibiting viral DNA polymerase. Because it is excreted primarily by the kidneys, dosing must be modified in patients with renal impairment.

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Antibiotics, Other

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Either gram-positive or gram-negative organisms may cause bacterial sepsis and meningitis. Combination therapy is necessary.

Ampicillin

 

Ampicillin has bactericidal activity against susceptible organisms. The combination of ampicillin with an aminoglycoside is the initial treatment of choice for neonates with presumptive group B streptococcal (GBS) meningitis and for most other suspected bacterial infections of the central nervous system (CNS).

Penicillin G (Pfizerpen)

 

Penicillin G interferes with synthesis of cell-wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms. It can be given alone to treat GBS meningitis when susceptibility of CSF isolates to the drug has been demonstrated.

Cefotaxime (Claforan)

 

Cefotaxime is a third-generation cephalosporin with a gram-negative spectrum of activity; it has lower efficacy against gram-positive organisms. It arrests bacterial cell-wall synthesis, which, in turn, inhibits bacterial growth.

Whereas ampicillin plus an aminoglycoside remains the initial treatment of choice for bacterial meningitis, some investigators recommend ampicillin plus a cephalosporin (eg, cefotaxime) as initial treatment. The rapid emergence of cephalosporin-resistant strains limits the use of the latter combination, unless gram-negative bacterial meningitis strongly suspected. Treatment typically lasts 21 days, with most authorities recommending 14-21 days from the first negative CSF culture.

Gentamicin

 

Gentamicin is the prototypical aminoglycoside for combining with ampicillin to treat neonatal meningitis, but organism sensitivities and hospital protocols vary widely. Evolving bacterial resistance may necessitate the use of higher doses.

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Anticonvulsants, Other

Class Summary

Anticonvulsants prevent seizure recurrence and terminate clinical and electrical seizure activity.

Phenobarbital

 

Phenobarbital increases the activity of gamma-aminobutyric acid, an inhibitory neurotransmitter in the central nervous system. This medication is typically used as the first-line agent in the treatment of neonatal seizures. An IV dose may require approximately 15 minutes to attain peak levels in the brain. Typically, a loading dose of 20 mg/kg IV is given initially, with additional bolus doses of 5-10 mg/kg if seizure activity persists, to a maximum total dose of 40 mg/kg.

Fosphenytoin (Cerebyx)

 

Fosphenytoin is the diphosphate ester salt of phenytoin and acts as a water-soluble prodrug of that agent. After administration, plasma esterases convert fosphenytoin to phosphate, formaldehyde, and phenytoin. Phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.

To eliminate the need to perform molecular weight-based adjustments when converting between fosphenytoin and phenytoin sodium doses, express the dose in terms of phenytoin sodium equivalents (PE). Although fosphenytoin can be administered either IV or IM, IV administration is preferable and should be used in emergency situations.

Fosphenytoin is typically considered the second choice of anticonvulsants in neonates if phenobarbital does not control seizures.

Lorazepam (Ativan)

 

Lorazepam is a benzodiazepine anticonvulsant that is used in cases that are refractory to phenobarbital and phenytoin. By increasing the action of gamma-aminobutyric acid (GABA) the major inhibitory neurotransmitter in the brain, lorazepam may depress all levels of the CNS, including the limbic system and the reticular formation.

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Contributor Information and Disclosures
Author

David C Dredge, MD Attending Physician, Pediatric Neurology, Baystate Children's Hospital; Assistant Professor of Pediatrics, Tufts University Medical School

David C Dredge, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, Child Neurology Society, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Kalpathy S Krishnamoorthy, MD Associate Professor of Pediatrics and Neurology, Harvard Medical School; Consulting Staff, Division of Pediatric Neurology, Massachusetts General Hospital

Disclosure: Nothing to disclose.

Chief Editor

Amy Kao, MD Attending Neurologist, Children's National Medical Center

Amy Kao, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Have stock from Cellectar Biosciences; have stock from Varian medical systems; have stock from Express Scripts.

Acknowledgements

Sarah M Barnett, MD, MPH Fellow in Neonatal Neurology, Division of Pediatric Neurology, Massachusetts General Hospital

Sarah M Barnett, MD, MPH is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Public Health Association, Child Neurology Society , and Massachusetts Medical Society

Disclosure: Nothing to disclose.

David A Griesemer, MD Professor, Departments of Neuroscience and Pediatrics, Medical University of South Carolina

David A Griesemer, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine, American Academy of Neurology , American Epilepsy Society, Child Neurology Society, and Society for Neuroscience

Disclosure: Nothing to disclose.

J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Volpe JJ. Bacterial and fungal intracranial infections. Neurology of the Newborn. 5th. Philadelphia, Pa: Saunders Elsevier; 2008. 916-56.

  2. Volpe JJ. Viral, protozoal, and related intracranial infections. Neurology of the Newborn. 5th. Philadelphia, Pa: Saunders Elsevier; 2008. 851-915.

  3. Krebs VLJ, Costa GAM. Clinical outcome of neonatal bacterial meningitis according to birth weight. Arq. December 2007. 65:1149-1153. [Medline].

  4. Davies PA, Rudd PT. Incidence; The Developing Brain. Neonatal Meningitis. Cambridge, England: Cambridge University Press; 1994. Ch 1.

  5. Klinger G, Chin CN, Beyene J, et al. Predicting the outcome of neonatal bacterial meningitis. Pediatrics. 2000 Sep. 106(3):477-82. [Medline].

  6. Heath PT, Nik Yusoff NK, Baker CJ. Neonatal meningitis. Arch Dis Child Fetal Neonatal Ed. 2003 May. 88(3):F173-8. [Medline].

  7. Tiskumara R, Fakharee SH, Liu C-Q, Nuntnarumit P, Lui K-M, Hammoud M, et al. Neonatal infections in Asia. Arch Dis Child Fetal Neonatal Ed. March 2009. 94:F144-8. [Medline].

  8. Zaidi AK, Thaver D, Ali SA, Khan TA. Pathogens associated with sepsis in newborns and young infants in developing countries. Pediatr Infect Dis J. 2009 Jan. 28(1 Suppl):S10-8. [Medline].

  9. Puopolo KM, Madoff LC, Eichenwald EC. Early-onset group B streptococcal disease in the era of maternal screening. Pediatrics. 2005 May. 115(5):1240-6. [Medline].

  10. CDC. Trends in perinatal group B streptococcal disease - United States 2000-2006. Morb Mortal Wkly Rep. February 2009. 58:109-112. [Medline].

  11. CDC. Enterovirus surveillance--United States, 2002-2004. MMWR Morb Mortal Wkly Rep. 2006 Feb 17. 55(6):153-6. [Medline].

  12. Tebruegge M, Curtis N. Enterovirus infections in neonates. Semin Fetal Neonatal Med. March 2009. 1-6. [Medline].

  13. Levorson RE, Jantausch BA, Wiedermann BL, Spiegel HM, Campos JM. Human parechovirus-3 infection: emerging pathogen in neonatal sepsis. Pediatr Infect Dis J. 2009 Jun. 28(6):545-7. [Medline].

  14. Selvarangan R, Nzabi M, Selvaraju SB, Ketter P, Carpenter C, Harrison CJ. Human parechovirus 3 causing sepsis-like illness in children from midwestern United States. Pediatr Infect Dis J. 2011 Mar. 30(3):238-42. [Medline].

  15. Hunter JH, Petrosyan M, Ford HR, Prasadarao NV. Enterobacter sakazakii: An emerging pathogen in infants and neonates. Surg Infect (Larchmt). October 2008. 9:533-539.

  16. Kimberlin D. Herpes simplex virus, meningitis, and encephalitis in neonates. Herpes. 2004. 11 Supp 2:65A-76A. [Medline].

  17. Thaver D, Zaidi AK. Burden of neonatal infections in developing countries: a review of evidence from community-based studies. Pediatr Infect Dis J. 2009 Jan. 28(1 Suppl):S3-9. [Medline].

  18. de Louvois J, Halket S, Harvey D. Effect of meningitis in infancy on school-leaving examination results. Arch Dis Child. 2007 Nov. 92(11):959-62. [Medline].

  19. Chang CJ, Chang HW, Chang WN, Huang LT, Huang SC, CHang YC. Seizures complicating infantile and childhood bacterial meningitis. Pediatr Neurol. September 2004. 32:165-171. [Medline].

  20. Stevens JP, Eames M, Kent A, et al. Long term outcome of neonatal meningitis. Arch Dis Child Fetal Neonatal Ed. 2003. 88:F179-184. [Medline].

  21. Bedford H, de Louvois J, Halket S, et al. Meningitis in infancy in England and Wales: follow up at age 5 years. BMJ. 2001 Sep 8. 323(7312):533-6. [Medline].

  22. Pong A, Bradley JS. Bacterial meningitis and the newborn infant. Infect Dis Clin North Am. 1999 Sep. 13(3):711-33, viii. [Medline].

  23. Unhanand M, Mustafa MM, McCracken Gh, Nelson JD. Gram-negative enteric bacillary meningitis: a twenty-one year experience. J Pediatr. January 1993. 122:15-21. [Medline].

  24. Miyairi I, Causey KT, DeVincenzo JP, Buckingham SC. Group B streptococcal ventriculitis: a report of three cases and literature review. Pediatr Neurol. May 2006. 34:395-399. [Medline].

  25. Ment LR, Ehrenkranz RA, Duncan CC. Bacterial meningitis as an etiology of perinatal cerebral infarction. Pediatr Neurol. September/October 1986. 2:276-279. [Medline].

  26. Fitzgerald KC, Golomb MR. Neonatal arterial ischemic stroke and sinovenous thrombosis associated with meningitis. J Child Neurol. July 2007. 22:818-822. [Medline].

  27. Bao X, Wong V. Brainstem auditory-evoked potential evaluation in children with meningitis. Pediatr Neurol. 1998 Aug. 19(2):109-12. [Medline].

  28. Committee on Medical Liability, American Academy of Pediatrics. Berger JE ed, Deitschel CH Jr ed. Medical Liability for Pediatricians. 6th ed. 2004. 163, 169.

  29. Malbon K, Mohan R, Nicholl R. Should a neonate with possible late onset infection always have a lumbar puncture?. Arch Dis Child. 2006 Jan. 91(1):75-6. [Medline].

  30. Garges HP, Moody MA, Cotten CM, et al. Neonatal meningitis: what is the correlation among cerebrospinal fluid cultures, blood cultures, and cerebrospinal fluid parameters?. Pediatrics. 2006 Apr. 117(4):1094-100. [Medline].

  31. Shah DK, Daley AJ, Hunt RW, Volpe JJ, Inder TE. Cerebral white matter injury in the newborn following Escherichia coli meningitis. Eur J Paediatr Neurol. 2005. 9:13-17. [Medline].

  32. Malik GK, Trivedi R, Gupta A, Singh R, Prasad KN, Gupta RK. Quantitative DTI assessment of periventricular white matter changes in neonatal meningitis. Brain Dev. May 2008. 30:334-341. [Medline].

  33. Klinger G, Chin CN, Otsubo H, et al. Prognostic value of EEG in neonatal bacterial meningitis. Pediatr Neurol. 2001 Jan. 24(1):28-31. [Medline].

  34. Poblano A, Gutierrez R. Correlation between the neonatal EEG and the neurological examination in the first year of life in infants with bacterial meningitis. Arq Neuropsiquiatr. September 2007. 65:576-580. [Medline].

  35. Stoll BJ, Hansen N, Fanaroff AA, et al. To tap or not to tap: high likelihood of meningitis without infection in very low birthweight infants. Pediatrics. 2004. 113:1181-6. [Medline].

  36. Alarcon A, Pena P, Salas S, Sancha M, Omenaca F. Neonatal early onset Escherichia coli sepsis: trends in incidence and antimicrobial resistence in the era of intrapartum antimicrobial prophylaxis. Pediatr Infect Dis J. April 2004. 23:295-299. [Medline].

  37. Pickering LD, ed. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2006.

  38. Thaver D, Ali SA, Zaidi AK. Antimicrobial resistance among neonatal pathogens in developing countries. Pediatr Infect Dis J. 2009 Jan. 28(1 Suppl):S19-21. [Medline].

  39. Chaudhuri A. Adjunctive dexamethasone treatment in acute bacterial meningitis. Lancet Neurol. 2004 Jan. 3(1):54-62. [Medline].

  40. Wellman MB, Sommer DD, McKenna J. Sensorineural hearing loss in postmeningitic children. Otol Neurotol. 2003 Nov. 24(6):907-12. [Medline].

 
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Acute bacterial meningitis (same patient as in the other two images). This axial nonenhanced CT scan shows mild ventriculomegaly and sulcal effacement.
Acute bacterial meningitis (same patient as in the other two images). This axial T2-weighted MRI shows only mild ventriculomegaly
Acute bacterial meningitis (same patient as in the other two images). This contrast-enhanced, axial T1-weighted MRI shows leptomeningeal enhancement (arrows).
Meninges of the central nervous parts
Neisseria meningitidis
Neonate with a lumbar myelomeningocele with an L5 neurologic level. Note the diaphanous sac filled with cerebrospinal fluid and containing fragile vessels in its membrane. Also, note the neural placode plastered to the dorsal surface of the sac. This patient underwent closure of his back and an untethering of his neural placode. The neural placode was circumnavigated and placed in the neural canal. A dural sleeve was fashioned in such a way to reconstruct the neural tube geometry.
This anteroposterior skull radiograph demonstrates the craniolacunia or Luckenschadel seen in patients with myelomeningocele and hydrocephalus. Mesodermal dysplastic changes cause defects in the bone. The thin ovoid areas of calvaria are often surrounded by dense bone deposits. They are most likely the result of defective membranous bone formation typical of neural tube defects and not increased intracranial pressure as once thought. These characteristic honeycomb changes are seen in about 80% of the skulls in children with myelomeningocele and hydrocephalus
Sagittal T1-weighted MRI image of a child after closure of his myelomeningocele. Child is aged 7 years. Note the spinal cord ends in the sacral region far below the normal level of T12-L1. It is tethered at the point in which the neural placode was attached to the skin defect during gestation. The MRI showed dorsal tethering, and the child complained of back pain and had a new foot deformity on examination. By definition, all children with a myelomeningocele have a tethered cord on MRI, but only about 20% of children require an operation to untether the spinal cord during their first decade of life, during their rapid growth spurts. Thus, the MRI must be placed in context of a history and examination consistent with mechanical tethering and a resultant neurologic deterioration.
Sagittal T1 MRI image of a child with a myelomeningocele and associated Chiari II malformation. Note the cerebellar vermis and part of the brainstem has herniated below the foramen magnum and into the cervical canal (arrow). This patient had multiple brainstem symptoms and findings to include stridor and cranial nerve paresis (cranial nerves III, VI, IX, X) despite having a well-functioning ventricular-peritoneal shunt. He required a posterior fossa decompression of his hindbrain in order to relieve the symptoms of hindbrain herniation and brainstem compression. A minority of myelomeningocele patients require a Chiari II decompression. Those that do usually present in their first year of life with similar symptoms, stridor and cranial nerve paresis. A functioning shunt is imperative prior to exploring the posterior fossa in these children. Often times, especially in older children, a shunt revision may alleviate some of the symptoms of hindbrain compression. Tube Defects in the Neonatal Period
Neonate with a large occipital encephalocele lying in the prone position prior to surgical intervention. Note the large skin-covered sac that represents a closed neural tube defect. Often called cranium bifidum, it is a more serious condition that represents a failure of the anterior neuropore to close. In this patient, a defect in the skull base (basicranium) was associated with this large sac filled with cerebrospinal fluid and a small, disorganized remnant of brain. The patient fared satisfactorily after the surgery in which the encephalocele was excised. However, the patient needed placement of a ventricular-peritoneal shunt to treat the resultant hydrocephalus, which is not uncommon. At age 5 years, the child was doing well and had only moderate developmental delay.
Autopsy specimen on a child with anencephaly. This is one of the most common CNS malformations in the West. The neonate, like almost all with such a severe forms of neural tube defects, did not survive more than a few hours or days. This malformation represents a failure of the anterior neuropore to close. This photograph also reveals an absence of the calvaria and posterior bone elements of the cervical canal, as well as the deficiency in the prosencephalon. Photo courtesy of Professor Ron Lemire.
Ventral view of a child with anencephaly that, like the previous picture, shows the loss of cranium and enclosed nervous tissue. In addition to the primary defect in development, a secondary destruction of nervous tissue occurs. Direct exposure to the caustic amniotic fluid causes progressive destruction of the remaining neural structures and secondary proliferation of a thin covering of vascular and glial tissue. Photo courtesy of Professor Ron Lemire.
These 2 photographs depict the lumbar regions on 2 different children with closed neural tube defects. Both children have lipomyelomeningocele. The child in the left has a dorsal lipoma that is pedunculated. The child on the right has a more common-appearing lipomatous mass that is heaped up beneath the skin. Both lipomas lead from the subcutaneous tissue, through the dura and into the intradural space, where they are attached to the spinal cord. Photos courtesy of Professor J.D. Loeser.
Photograph of a child undergoing a neurosurgical procedure in which the spinal cord is being detached (untethered) from the intradural and extradural lipomatous mass that fixes it to the subcutaneous tissue. The white arrow shows the laser char on the lipoma that has been shaved off the spinal cord and was connected to the extradural mass. The black arrow shows the extradural lipoma, which crept through the dura and attached to the spinal cord, thereby firmly fixing the spinal cord at too low and too dorsal a location in the sagittal plane.
The lumbar region of a newborn baby with myelomeningocele. The skin is intact, and the placode-containing remnants of nervous tissue can be observed in the center of the lesion, which is filled with cerebrospinal fluid (CSF).
Axial T1-weighted MRI scan of an 8-week-old girl who presented with enlarging head circumference. Considerable ventricular dilatation is shown on the lateral and third ventricles. Periventricular lucency is observed around the frontal horns, indicating raised intraventricular pressure.
Sagittal T1-weighted MRI scan of an 8-week-old girl who presented with enlarging head circumference. The third and lateral ventricles are dilated, whereas the fourth ventricle is of normal size. Aqueductal stenosis is shown. The appearance is typical of this condition.
Phase-contrast MRI scan of an 8-week-old girl who presented with enlarging head circumference, obtained 3 months after endoscopic third ventriculostomy. A large signal void is shown in the prepontine region, corresponding to the flow through the stoma in the floor of the third ventricle, indicating that the ventriculostomy is functioning well.
Axial T1-weighted MRI scan of a 15-year-old girl who was born with thoracic myelomeningocele, hydrocephalus, and Arnold-Chiari II syndrome. She was treated with a ventriculoperitoneal shunt. The ventricular system has a characteristic shape, with small frontal and large occipital horns, which are typical in patients with spina bifida. The shunt tube is shown in the right parietal region.
Sagittal T1-weighted MRI scan of a 15-year-old girl who was born with thoracic myelomeningocele, hydrocephalus, and Arnold-Chiari II syndrome. Significant hindbrain hernia and low-lying fourth ventricle are shown in the context of the Arnold-Chiari II syndrome. Damaged shunt valve removed during shunt revision from a 22-year-old woman with hydrocephalus and spina bifida. The material of the valve has dramatically disintegrated.
Damaged shunt valve removed during shunt revision from a 22-year-old woman with hydrocephalus and spina bifida. The material of the valve has dramatically disintegrated.
 
 
 
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