Meningitis refers to an infection of the cerebrospinal fluid (CSF) that bathes the brain, whereas encephalitis is an infection of the brain itself. Most meningitis pathogens enter the CSF space by hematogenous spread. More unusually, pathogens may enter through a mechanical disruption (e.g., a fracture of the base of the skull) or by direct extension from a local infection (e.g., ear, mastoid air cells, sinuses, or orbit). Once the blood–brain barrier has been breached, natural defense mechanisms are less able to stop the multiplication of organisms. Since 1990, the incidence of bacterial meningitis in children under 18 years of age has declined by approximately one-third due to the widespread uptake of the highly effective vaccines against Haemophilus influenzae type B (1990), Streptococcus pneumoniae (7-valent 2000; 12-valent 2010), and Neisseria meningitidis (2005). The predominant bacterial pathogens for children older than 2 months of age remain S. pneumoniae and N. meningitidis, and for the youngest infants Group B streptococcus and Escherichia coli.¹

The younger a child with meningitis, the less specific the presenting signs and symptoms will be. Neonates and young infants are likely to present with fever, poor feeding, irritability, inconsolability, or listlessness. Older children with meningitis may present with “classic” signs and symptoms of meningitis which include headache, photophobia, stiff neck, change in mental status, bulging fontanel, nausea, and vomiting. The Brudzinski sign (neck flexion causes the hips and knees to flex involuntarily) and the Kernig sign (hip flexed prevents full extension of the leg) are both late signs of meningeal irritation. However, these clinical signs have poor diagnostic accuracy in identifying cases of bacterial meningitis.²

In the early phases, meningitis may be confused with gastroenteritis or intussusception, respiratory infections (e.g., pneumonia), or deep neck space infections (e.g., retropharyngeal abscess or cervical adenitis). For children with altered mental status, encephalitis, cerebral hemorrhage or abscess, or toxic ingestions must also be considered.

The initial management of an unstable patient with suspected meningitis must focus on assuring airway, breathing, and cardiovascular stability. Supplemental oxygen is always administered. (See Chapter 20 for management of shock.) If signs of increased intracranial pressure develop, clinicians should elevate the head slightly and initiate controlled hyperventilation (target PaCO₂ between 30 and 35 mmHg). Children unresponsive to initial therapy may benefit from the use of mannitol (0.25–1 g/kg). Associated seizures are controlled with rapid-acting benzodiazepines followed by an appropriate second-line agent (see Chapter 53). If hypoglycemic (defined as a blood glucose of <40 mg/dL), children require an intravenous glucose infusion and monitoring.

If the child with suspected meningitis is unstable or has evidence of potential elevated intracranial pressure, lumbar puncture should be delayed.³ Although the early administration of antibiotics may prevent recovery of the organism from CSF culture⁴ and impact CSF profiles,³ appropriate antibiotics should be administered early. Of note, bacterial pathogens are isolated from blood culture in approximately half of children with bacterial meningitis and may help guide decisions about duration and type of parenteral antibiotics.

Stable patients with suspected meningitis should have prompt blood testing and diagnostic lumbar puncture, especially in children at higher risk of bacterial infections (e.g., neonates, immunocompromised children, and close contacts of a confirmed bacterial meningitis case). The initial laboratory evaluation should include a complete blood count (CBC) with differential,⁵ peripheral glucose, as well as CSF white blood cell (WBC) with differential, red blood cell (RBC) count, glucose, protein, and Gram stain. In children without bacterial meningitis, CSF glucose should be approximately 60% of peripheral glucose.⁶ Cultures of blood and CSF should also be obtained.

Normal CSF parameters are age related (Table 59-1).^6–9 Traumatic lumbar punctures occur commonly, especially in the youngest children, which may complicate the interpretation of CSF cell counts. Correction formulas are designed to correct CSF WBC for the presence of CSF RBCs for the interpretation of traumatic CSF. Application of a 1000:1 CSF RBC to CSF WBC correction formula has been shown to reduce the number of infants with CSF pleocytosis without misclassifying many additional infants with bacterial meningitis.¹⁰ The introduction of peripheral blood also elevates the CSF protein by approximately 1.1 mg/dL per 1000 RBCs per mm.¹¹