Chapter 50 Meningitis
PATHOPHYSIOLOGY
Meningitis is an acute inflammation of the meninges. The organisms responsible for bacterial meningitis invade the area either directly as a result of a traumatic injury or indirectly when they are transported from other sites in the body to the cerebrospinal fluid (CSF). A variety of agents can produce an inflammation of the meninges including bacteria, viruses, fungi, and chemical substances.
Since the introduction and widespread use of the Haemophilus influenzae type B (HIB) vaccine, this organism has been largely controlled in the developed world. The principal bacterial pathogen in children and adults is Streptococcus pneumoniae, followed by Neisseria meningitidis. In infants 0 to 3 months of age, the most common causes are group B Streptococcus, Escherichia coli, and Listeria monocytogenes.
Aseptic meningitis is usually caused by enteroviruses and affects young adults more often than children. Older children usually manifest a variety of nonspecific prodromal signs and flulike symptoms that last for 1 to 2 weeks. Although fatigue and weakness may persist for a number of weeks, sequelae are uncommon. The child is evaluated and treated until bacterial meningitis is ruled out. Viral meningitis usually requires only a brief hospitalization; supportive care at home is the primary intervention.
Otitis media, sinusitis, or respiratory tract infections may constitute the initial stage of infection. Newer technology, such as cochlear implants, may also lead to meningitis. Head injuries, penetrating wounds, and neurosurgery may also provide an opening into the meninges, leading to meningitis. In addition, a predisposition resulting from an immune deficiency increases the likelihood of occurrence of this disorder. Once the meninges are infected, the organisms are spread through the CSF to the brain and adjacent tissues.
Prognosis varies depending on the individual’s age, the infecting organism, the speed with which antibiotic therapy is initiated, and the presence of complicating factors. Neonatal meningitis is associated with a high mortality rate and an increased incidence of neurologic sequelae. Meningococcal meningitis can also be rapidly fatal. In many affected individuals, bacterial meningitis can result in long-term behavioral changes, motor dysfunction, hearing loss, and cognitive changes such as perceptual deficits and learning disorders.
Ensuring vaccination with HIB vaccine during the infant and toddler years, and meningococcal vaccine during preteen years or before college entry can go a long way in prevention of meningitis. All children with cochlear implants should also receive pneumococcal vaccine to prevent meningitis caused by S. pneumoniae. Children with immune deficiencies are also recommended to have these vaccines.
INCIDENCE
1. Of all bacterial meningitis cases, 90% are in children younger than 5 years of age.
2. More males than females contract meningitis.
3. Age range of peak incidence is 6 to 12 months.
4. Age range with the highest rate of morbidity is birth to 4 years.
5. Meningitis occurs mostly during winter and early spring.
6. About 171,000 people worldwide die from bacterial meningitis yearly.
CLINICAL MANIFESTATIONS
LABORATORY AND DIAGNOSTIC TESTS
1. Lumbar puncture and culture of cerebrospinal fluid (CSF) with the following results:
2. Serum glucose level—elevated
3. Complete blood count with differential, platelet count
4. Blood culture—to identify causative organism
5. Urine culture and urinalysis—to identify causative organism
6. Nasopharyngeal culture—to identify causative organism
7. Serum electrolyte levels—elevated if child is dehydrated; increased serum sodium (Na); decreased serum potassium (K)
8. Urine osmolarity—increased with increased secretion of antidiuretic hormone
MEDICAL MANAGEMENT
Meningitis is considered a medical emergency requiring early recognition and treatment to prevent neurologic damage. The child is placed in respiratory isolation for at least 24 hours after the initiation of therapy with intravenous (IV) antibiotics to which the causative organism is sensitive. Steroids may be administered as an adjunct to decrease the inflammatory process. Intravenous hydration therapy is instituted to correct electrolyte imbalances, in addition to providing hydration. With this fluid administration, the infused volume must be assessed frequently to prevent fluid overload complications such as cerebral edema. Frequent assessment of neurologic status is crucial. Treatment is then directed toward the identification and management of complications of the disease process. The most common complications are subdural effusion, DIC, and shock.
NURSING INTERVENTIONS
1. Monitor infant’s or child’s vital signs and neurologic status as often as every hour.
2. Monitor child’s hydration status.
3. Monitor child for seizure activity (see Chapter 69).
4. Institute isolation procedures with respiratory precautions to protect others from infectious contact; keep child in isolation for 24 hours after antibiotic therapy is started.
5. Monitor IV infusion and side effects of medications.
6. Provide comfort measures in environment that is quiet and has minimal stressful stimuli.
7. Position child with head of bed slightly elevated to decrease cerebral edema; monitor administration of fluids.
8. Reduce temperature through use of tepid sponge baths or antipyretics agents (acetaminophen, ibuprofen).
9. Provide emotional support when child undergoes lumbar puncture and other tests.
10. Provide emotional and other support to family.
11. Provide age-appropriate diversional activities (see relevant section in Appendix F).
Discharge Planning and Home Care
1. Instruct parents about administration of medications and monitoring for side effects.
2. Instruct parents in monitoring for long-term complications and their signs and symptoms (learning disabilities and other educational difficulties).
3. Assess immunization status and recommend that parents consult child’s primary care provider regarding needed immunizations.
Centers for Disease Control [2006 Childhood Immunization Schedule (website)] www.cdc.gov/mmwr/preview/mmwrhtml/mm5451-Immunizationa1.htm. Accessed January 13, 2006
Halket S, et al. Long term follow up after meningitis in infancy: Behaviour of teenagers. Arch Dis Child. 2003;88(5):395.
Mandelco BL, Potts NL. Neurological alterations. In: Potts NL, Mandleco BL. Pediatric nursing: Caring for children and their families. Clifton Park, NY: Delmar, 2002.
Medscape News Feature. Possible link between cochlear implants and bacterial meningitis. [Medscape (serial online)] www.medscape.com/viewarticle/439607. Accessed January 1, 2006
Nigrovic LE, Kupperman N, Malley R. Development and validation of a multivariable predictive model to distinguish bacterial from aseptic meningitis in children in the post-Haemophilus influenza era. Pediatrics. 2002;110(4):712.
Porter V. Bacterial meningitis: A deadly but preventable disease. [Medscape (serial online)] www.medscape.com/viewarticle/481019. Accessed January 1, 2006
Rusk J. Shift seen in burden of bacterial meningitis since 1998. Infect Dis Child. 2006;19(1):26.
Waknine Y:. FDA warns of continuing meningitis risk in cochlear implant recipients. [Medscape (serial online)] www.medscape.com/viewarticle/523106. Accessed February 15, 2006
