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752 SECTION 12: Pediatrics The condition of children with hypoxemia, respiratory distress, hypo tension, and tachycardia may deteriorate when they are positioned for lumbar puncture, so resuscitation and empiric administration of IV antibiotics is needed prior to lumbar puncture. In children with thrombocytopenia or factor deficiencies, replace platelets or factor before attempting lumbar puncture.  PATIENT PREPARATION Anticipate the procedure and its difficulties. Assemble a needle of the correct size, the appropriate specimen containers, and preprinted labels, and ensure a quiet environment without interruptions. Explain the procedure to the caregivers. In some institutions, written informed consent for lumbar puncture is required. Describe the process of procedural sedation if it is needed and obtain consent. Apply a topical anesthetic cream or spray prior to needle insertion to reduce pain and improve the success rate of the lumbar puncture. 54,55 For infants, sucking on a pacifier dipped in sucrose solution is analgesic and calming and decreases crying. Prepare the skin using sterile technique.  POSITION Have an experienced healthcare provider, the “holder, ” restrain the infant or child. Wrapping the child in sheets may help limit leg move ment. Flexing the hips is more important than flexing the neck. In addition, flexing the neck may lead to respiratory difficulty. Continuous pulse oximetry may be helpful in monitoring for airway obstruction. Whether to choose the lateral recumbent position or the sitting position depends upon the preference of the physician. In some studies, using US to measure the width between the spinous processes in the sitting position was found to be better than the lateral decubitus position. 56,57 Although the sitting position may improve flexion of the hips, this position may be more difficult for the holder to maintain.  LUMBAR PUNCTURE TECHNIQUE Most lumbar punctures are performed with a 22-gauge lumbar puncture needle, usually 1 1/2 in. in length for infants, 21/2 in. for children 2 years to 8 years, and 31/2 in. for older children. In obese patients, choosing a lumbar puncture needle may be more difficult. One study calculated that a lumbar puncture needle length (in centimeters) of 1 + [17 × (weight in kilograms/height in centimeters)] was most accurate. 58 Lumbar punc ture depth was measured on abdominal CT scans to derive this formula. Lumbar needles with a clear hub show cerebrospinal fluid flow sooner than those with metal or opaque hubs. Insert the LP needle between the L4 and L5 spinous processes in the intervertebral space in the midline of the back and direct the needle toward the umbilicus. This interspace is easily located because it lies in line between the iliac crests. Introduce the needle with the bevel of the needle up. Insert the needle until the characteristic “pop” identifies introduction into the subarachnoid space. An alternative method is to remove the stylet from the needle after the needle pierces the skin. Advance the needle, without the stylet, incrementally until cerebrospi nal fluid flows. Occasionally rotating the lumbar needle clockwise or counterclockwise up to 360 degrees may help improve flow if the bevel of the needle is sideways. When removing the lumbar needle, replace the stylet. Bonadio originally reported early stylet removal as the “Cincinnati method” in 1992.

ntil cerebrospi nal fluid flows. Occasionally rotating the lumbar needle clockwise or counterclockwise up to 360 degrees may help improve flow if the bevel of the needle is sideways. When removing the lumbar needle, replace the stylet. Bonadio originally reported early stylet removal as the “Cincinnati method” in 1992. 59 Early experience with hollow-bore needles without a stylet associated this technique with the development of epidermoid tumors after the procedure. However, by puncturing the epidermis with the stylet in place and removing the stylet after introduction through the epidermis, this complication should be eliminated. Two separate reports found that the use of this Cincinnati method and the administration of topical anesthetics were associated with improved success rates. 54,55 After successful entry into the subarachnoid space, collect three tubes of cerebrospinal fluid, each with at least 0.5 mL of fluid. Send the first tube for cell count, which includes WBC and red blood cell counts; send the second tube for protein and glucose measurement; and send the third tube for routine bacterial culture and Gram staining (Table 119-3). Additional tubes may be collected for polymerase chain reaction testing for bacteria and viruses as needed (e.g., enterovirus, herpes simplex virus). If the child has been pretreated with antibiotics, latex agglutina tion testing may be performed for H. influenzae type b, S. pneumoniae , group B streptococci, E. coli, and N. meningitidis serogroups A, B, C, Y , and W135. However, latex agglutination testing has poor sensitivity for bacterial infection. Polymerase chain reaction assays for pathogenic organisms, including panels for multiple viral and bacterial pathogens, are also available. After a failed attempt, obtain a new needle and restart the procedure. Insertion into the L3 to L4 intervertebral space or the L5 to S1 inter vertebral space may be successful. US- or fluoroscopy-guided lumbar needle insertion may be necessary when all else fails. REFERENCES The complete reference list is available online at www.TintinalliEM.com. TABLE 119-3 Normal Cerebrospinal Fluid (CSF) Values by Age CSF Parameter 0–4 wk 4–8 wk >8 wk WBCs/mm3 0–19 cells/mm 3 0–9 cells/mm 3 0–9 cells/mm 3 Glucose (milligrams/dL) 30–60 40–70 50–80 CSF/blood glucose ratio 60% 60% 60% Protein (milligrams/dL) 60–100 50–80 15–45 Source: Adapted with permission from Tenenbein M, Macias CG, Sharieff GQ, Yamamoto LG, Schafermeyer RW (eds): Strange and Schafermeyer’s Pediatric Emergency Medicine, 5th ed. New York: McGraw-Hill Education, Inc. © 2019. Table 59-1, p. 389. Meningitis in Infants and Children Amy Levine INTRODUCTION AND EPIDEMIOLOGY Meningitis is an inflammation of the leptomeninges, tissues that cover the brain and spinal cord. Untreated bacterial meningitis has a mortality of nearly 100%, so treat suspected bacterial meningitis promptly. Unfortunately, even with rapid antibiotic treatment, long-term neuro logic sequelae occur. Viral meningitis has a range of severity: mild cases resolve without sequelae; however, some viruses, such as herpes virus, can cause severe infections. Meningoencephalitis is an inflammation of the brain as well as the meninges. It is less common than meningitis but can be devastating. The most common causes of bacterial meningitis vary with the child’s age (Table 120-1). Vaccination programs have had a huge impact on the epidemiology of bacterial meningitis in developed countries. For instance, Haemophilus influenzae vaccine has almost eliminated H. influenzae meningitis in countries where the vaccine is utilized and has decreased overall bacterial meningitis rates by 55%.

able 120-1). Vaccination programs have had a huge impact on the epidemiology of bacterial meningitis in developed countries. For instance, Haemophilus influenzae vaccine has almost eliminated H. influenzae meningitis in countries where the vaccine is utilized and has decreased overall bacterial meningitis rates by 55%. 1 The introduction of the polyvalent vaccinations for Streptococcus pneumoniae (PCV7 in 2000 and PCV13 in 2010) has markedly decreased meningitis caused by that organism, although it remains the most frequent cause of pediatric meningitis. 2 Neisseria meningitidis remains an important cause of meningitis in children, and vaccines against serotype B have recently been introduced. Other important causes of bacterial meningitis in children include Mycobacterium tuberculosis and Borrelia burgdorferi, the caus ative agent of Lyme disease. N. meningitidis commonly colonizes the upper respiratory tract, but does not commonly cause invasive disease in the Western hemisphere, although worldwide, there are endemic regions, such as the African meningitis belt. In childhood, there are two peaks of infection, one in CHAPTER Tintinalli_Sec12_p0669-0996.indd 752 8/2/19 7:50 PM

s commonly colonizes the upper respiratory tract, but does not commonly cause invasive disease in the Western hemisphere, although worldwide, there are endemic regions, such as the African meningitis belt. In childhood, there are two peaks of infection, one in CHAPTER Tintinalli_Sec12_p0669-0996.indd 752 8/2/19 7:50 PM CHAPTER 120: Meningitis in Infants and Children 753 TABLE 120-1 Causes and Treatment of Bacterial Meningitis by Age Group Age Group Most Common Organisms Treatment Comments Neonates (0–28 d) Group B Streptococcus, Escherichia coli Ampicillin 100 milligrams/kg every 8 h (age <7 d) or 75 milligrams every 6 h (age 7–28 d) AND Gentamicin 4 milligrams/kg every 24 h Less common organisms: Streptococcus pneumoniae, other gram-negative organisms, Listeria monocytogenes, Haemophilus influenzae type b, Neisseria meningitidis Herpes simplex virus type 2 in infected mothers If herpes suspected, add acyclovir 20 milligrams/kg every 8 h Young infants (28–90 d) Group B Streptococcus, gram-negative bacilli Ampicillin 100 milligrams/kg every 6 h AND Gentamicin 2.5 milligrams/kg every 8 h Cefotaxime 100 milligrams/kg every 8 h Less common organisms: S. pneumoniae, N. meningitidis Herpes simplex virus type 2 If herpes suspected, add acyclovir 20 milligrams/kg every 8 h Older infants (>3 months) and children S. pneumoniae, N. meningitidis, H. influenzae type b Vancomycin 15 milligrams/kg every 6 h AND Ceftriaxone* 50 milligrams/kg every 12 h Cefotaxime † 100 milligrams/kg every 8 h Approximately half of meningitis in the United States is viral Immunization makes infection with H. influenzae unlikely in the older infant and child Herpes simplex virus type 2 If herpes suspected, add acyclovir 20 milligrams/kg every 8 h *For penicillin/β-lactam allergy, substitute chloramphenicol 50 milligrams/kg every 12 hours.11 †For penicillin/β-lactam allergy, substitute chloramphenicol 25 milligrams/kg every 6 hours.11 children less than 2 years of age and another in adolescents. The dis ease can be rapidly progressive and fulminant or present with more nonspecific symptoms. For this reason, it is important to maintain a high index of suspicion. Viral meningitis is much more common than bacterial meningitis. Enteroviruses are the leading cause worldwide. 4 Meningoencephalitis can be caused by enteroviruses, arboviruses (including West Nile virus), and herpes viruses. Herpes simplex virus type 1 infection occurs sporadically and causes a severe meningoencephalitis in children and adults. Herpes simplex virus type 2 develops in neonates born to infected mothers. Varicella-zoster virus can cause CNS infections including acute cerebellar ataxia. Many other viruses can cause CNS infections, including cytomegalovirus, Ebstein-Barr virus, mumps virus, adenovirus, influenza virus, parainfluenza virus, rubeola virus, rubella virus, and rabies virus. More recently, chikungunya and Zika viruses have emerged as important pathogens to consider in patients with his tory of travel in South and Central America, although cases have been diagnosed elsewhere. Fungal meningitis can occur in both normal and immunocompromised hosts. Important causes include Cryptococcus neoformans, Coccidioides immitis, and Candida albicans . Parasite infections can cause eosinophilic meningitis, defined as meningitis with at least 10 eosino phils/mm3 of cerebrospinal fluid (CSF). The main causes are Angiostrongylus cantonensis, Gnathostoma spinigerum , and Taenia solium . These are endemic in the tropics but are spreading due to travel.6 PATHOPHYSIOLOGY Bacterial meningitis in children usually results from bacteremia arising from organisms colonizing the nasopharynx.

cerebrospinal fluid (CSF). The main causes are Angiostrongylus cantonensis, Gnathostoma spinigerum , and Taenia solium . These are endemic in the tropics but are spreading due to travel.6 PATHOPHYSIOLOGY Bacterial meningitis in children usually results from bacteremia arising from organisms colonizing the nasopharynx. Less commonly, meningitis is caused by direct spread of bacteria from a contiguous site of infection, such as sinusitis, or from penetration of the CSF space from trauma, dermal sinus tracts, or open neural tube defects. Viral respira tory infections can increase the likelihood of meningitis when the nasopharynx is colonized. Meningitis starts with breakdown of the blood–brain barrier. Then organisms enter the subarachnoid space. Once there, they can multiply quickly because the CSF has low levels of complement, antibodies, and other host defenses. Bacterial cell wall components and toxins produce an inflammatory response that increases vascular permeability and attracts leukocytes. The inflammatory response is responsible for much of the damage that ensues. Viral pathogens also produce damage by direct tissue destruction as well as inflammation. CLINICAL FEATURES  HISTORY Infants ≤30 days old are at risk for meningitis due to an immature immune response. Symptoms in this age group are variable and non specific and include both fever and hypothermia. Neonates can present with a history of lethargy, poor feeding, fussiness, bulging fontanelle, vomiting, diarrhea, seizures, grunting, or respiratory distress. Elements in the birth history that increase the likelihood of bacterial meningitis include prematurity, low birth weight, delivery complications, mater nal infection, and maternal colonization with group B streptococci or herpes simplex. Some neonates present with few symptoms early in the course of their illness, so maintain a high degree of suspicion for early meningitis when confronted with a potentially sick newborn.  SIGNS AND SYMPTOMS OF BACTERIAL VERSUS VIRAL MENINGITIS Bacterial Meningitis Certain signs and symptoms are especially helpful for diagnosing bacterial meningitis in infants and children. Caregiver reports of bulging fontanelle (likelihood ratio [LR] 8, 95% confidence interval [CI] 2.4–26), or neck stiffness (LR 7.7, 95% CI 3.2–19), or seizures (outside of the febrile seizure range of 6 months to 6 years; LR 4.4, 95% CI 3.0–6.4), or reduced feeds (LR 2, 95% CI 1.2–3.4) are concern ing for meningitis. 7 Children with meningitis can present with the rapid onset of shock and altered mental status or with more gradual symptoms including fever, headaches, photophobia, upper respiratory symptoms, GI symptoms, irritability, and rash. The World Health Organization’s Pocket Book of Hospital Care for Children reported the performance of signs and symptoms for bacterial meningitis in infants and children and did not find any single clinical feature distinctive enough to make a “robust diagnosis of bacterial meningitis. ” However, the combination of fever, seizures, meningeal signs, and altered consciousness was consistently associated with bacterial meningitis. Tintinalli_Sec12_p0669-0996.indd 753 8/2/19 7:50 PM

ildren and did not find any single clinical feature distinctive enough to make a “robust diagnosis of bacterial meningitis. ” However, the combination of fever, seizures, meningeal signs, and altered consciousness was consistently associated with bacterial meningitis. Tintinalli_Sec12_p0669-0996.indd 753 8/2/19 7:50 PM 754 SECTION 12: Pediatrics Viral Meningitis Infants with viral meningitis typically present with irritability and decreased activity. Headache and fever are the usual complaints in children. Other symptoms include photophobia, rashes, nausea, vomiting, and pain in the neck, back, and legs. Most children with West Nile virus will be asymptomatic or have mild illness. Severe neurologic illness from West Nile virus is more common in adults than in children. 9 Arboviruses can cause viral meningitis, encephalitis, or acute flaccid paralysis. A recent outbreak of enterovirus D68 was also associated with acute flaccid paralysis. Herpes simplex virus can cause devastating infection in neonates. Both type 1 and type 2 herpes simplex virus can cause neonatal disease. Infection can present in three ways: (1) as disseminated disease with involvement of the CNS in 60% to 75% of cases; (2) as primary CNS disease; or (3) as disease localized to the skin, eyes, and/or mouth. About two thirds of infants with disseminated or CNS disease will have skin lesions, but these may not be present at the time of diagnosis. Herpes infection can be transmitted through an infected maternal genital tract but may also be transmitted from a nongenital infection as well. Herpes simplex encephalitis (herpes simplex virus type 1) beyond the neonatal period presents with fever, altered mental status, seizures, and focal neurologic findings. It occurs sporadically. PHYSICAL EXAMINATION Neonates and infants (<90 days old) may have fever, normal temperature, or hypothermia. A normal temperature does exclude meningitis. Toxic appearance, lethargy, mottling, bulging fontanelle, abnormal cry, grunting, respiratory distress, and increased or decreased tone are all supportive of the diagnosis, but these signs can be absent. Jaundice or rash may occasionally be seen. Infants in the first months of life are unlikely to have a stiff neck. Fever in neonates (rectal temperature of 100.5°F [38.0°C] or higher) should always prompt suspicion for meningitis. In the absence of fever, a clinician should be concerned about infants who are ill appearing, have the signs or symptoms listed earlier, or are just not “acting right” according to their caregivers. Older infants (>90 days old) with meningitis may also have fever, hypothermia, toxic appearance, lethargy, mottling, bulging fontanelle, abnormal cry, grunting, and respiratory distress at presentation. Chil dren (>36 months of age) may have fever and nuchal rigidity. The Kernig sign (with the patient lying supine and the hip flexed at 90 degrees, the patient cannot extend the knee fully without pain) and Brudzinski sign (with the patient lying supine, there is involuntary flexion of the legs with passive neck flexion) may be present. Patients may have altered mental status, shock, focal neurologic signs, or signs of increased intracranial pressure. Rash or another focal sign of infection may be present. Patients may have symptoms of an upper respiratory infection, myalgias, or arthralgias. Look for evidence of methicillinresistant Staphylococcus aureus when examining the skin, although S. aureus meningitis is most commonly associated with a history of a neurosurgical procedure. 12 Consider bacterial meningitis in the child with fever and seizures, outside the range of 6 months to 6 years. DIAGNOSIS  DIFFERENTIAL DIAGNOSIS In neonates, the most common causes of meningitis in the United States are group B Streptococcus and Escherichia coli.

sociated with a history of a neurosurgical procedure. 12 Consider bacterial meningitis in the child with fever and seizures, outside the range of 6 months to 6 years. DIAGNOSIS  DIFFERENTIAL DIAGNOSIS In neonates, the most common causes of meningitis in the United States are group B Streptococcus and Escherichia coli. Other organisms that cause meningitis include S. pneumoniae, Listeria monocytogenes, other streptococci, nontypeable H. influenzae, Staphylococcus species, Klebsiella, Enterobacter, Pseudomonas, Treponema pallidum, and M. tuberculosis. Neonates can develop meningitis from primary viral infection with herpes simplex virus or enteroviruses. The differential diagnosis of neonatal sepsis and meningitis includes infection from fungi ( Candida) and protozoa (malaria crosses the placenta, and maternal malaria can infect the neonate). Noninfectious illnesses that can appear similar to sepsis and meningitis include cardiac disease, necrotizing enterocolitis, congenital adrenal hyperplasia, inborn errors of metabolism, and intra cranial hemorrhage. In older infants and children , the usual dilemma is differentiating acute viral and bacterial meningitis. The typical bacterial causes are S. pneumoniae, N. meningitidis, and H. influenzae type b. Less common organisms include M. tuberculosis, Nocardia species, T. pallidum, and B. burgdorferi. 14 Fungal infections and parasitic infections can produce infection of the CNS. Infections around the brain and spinal cord may appear similar to meningitis. Collagen vascular disease, malignancy, and certain drugs and toxins should also be included in the differential diagnosis.  LABORATORY TESTING Check a bedside glucose in all acutely ill infants and children with altered mental status. All children suspected of having meningitis should undergo a lumbar puncture when they are clinically stable. Although establishing a diagnosis is important, patients who are unstable but suspected of having bacterial meningitis should receive antibiotics as quickly as possible (Table 120-1). Defer lumbar puncture until the child is stabilized and can tolerate the procedure. Positioning an infant or child for lumbar puncture before stabilization can result in hypoxia and hypotension. There are a few contraindications to lumbar puncture in children besides hypoxia and clinical instability. These include focal neurologic findings, thrombocytopenia, local infection at the lumbar site, and vertebral abnormalities. See Chapter 119, “Fever and Serious Bacterial Illness in Infants and Children, ” for details of pediatric lumbar puncture. Children with focal neurologic signs should receive antibiotics promptly, without waiting for a CT scan or lumbar puncture; the next step is a head CT scan prior to lumbar puncture. CSF abnormalities of meningitis, such as neutrophilic pleocytosis, low glucose, and high protein, will persist for days despite antibiotic treatment. Bacteria are generally not evident on Gram stain after antibiotics have penetrated the CSF (time intervals for clearance of bacteria in the CSF range from 15 minutes to several hours; see later section, “The Child Pretreated with Antibiotics”). Spinal fluid should be sent for cell count, protein, glucose, Gram stain, and culture. In the event of a traumatic tap, send fluid for culture and use clinical judgment in the interpretation of other results. Decision rules correcting the WBC count based on the number of red cells may not be reliable. The CSF of patients with bacterial meningitis tends to have lower glucose, higher protein, higher WBC counts, and a more frequent predominance of neutrophils relative to the CSF of patients with viral meningitis, but there is considerable overlap between the two groups.

d on the number of red cells may not be reliable. The CSF of patients with bacterial meningitis tends to have lower glucose, higher protein, higher WBC counts, and a more frequent predominance of neutrophils relative to the CSF of patients with viral meningitis, but there is considerable overlap between the two groups. The Bacterial Meningitis Score14 (Table 120-2) identifies any one risk factor associated with bacterial meningitis and has been independently validated in multiple settings. 16-18 A recent meta-analysis showed that procalcitonin had good differentiation between bacterial and viral meningitis. In the same analysis, C-reactive protein did not perform as well.19 In another systematic review, procalcitonin levels of ≥2 ng/mL had a TABLE 120-2 Pediatric Bacterial Meningitis Score14* Pediatric Bacterial Meningitis Score •  Positive  cerebrospinal fluid (CSF) Gram stain (2 points) •  CSF  protein >80 mg/dL (1 point) •  Blood  absolute neutrophil count ≥10,000 cells/mm3 (1 point) •  Seizure  at or before presentation (1 point) •  CSF  neutrophil count ≥1000 cells/mm3 (1 point) Interpretation •  0  points: Aseptic meningitis very likely •  1  point: Aseptic meningitis less likely •  2  points: Bacterial meningitis more likely Source: Adapted with permission from Nigrovic LE, Malley R, Kuppermann N. Cerebrospinal fluid pleocytosis in children in the era of bacterial conjugate vaccines. Distinguishing the child with bacterial and aseptic meningitis. Pediatr Emerg Care 25: 112–120, 2009. [PMID: 19225382]. Copyright Lippincott Williams & Wilkins. Tintinalli_Sec12_p0669-0996.indd 754 8/2/19 7:50 PM

ey R, Kuppermann N. Cerebrospinal fluid pleocytosis in children in the era of bacterial conjugate vaccines. Distinguishing the child with bacterial and aseptic meningitis. Pediatr Emerg Care 25: 112–120, 2009. [PMID: 19225382]. Copyright Lippincott Williams & Wilkins. Tintinalli_Sec12_p0669-0996.indd 754 8/2/19 7:50 PM CHAPTER 120: Meningitis in Infants and Children 755 sensitivity of 40% to 50% and a specificity of 90% for predicting the presence of a bacterial infection. Using the cutoff of <0.5 ng/mL to predict low risk of bacterial infection had a sensitivity of 80% and a specificity of 70%. 20 Polymerase chain reaction has been used in the past mainly for diagnosing viral meningitis. More recently, multiplex polymerase chain reaction diagnostics capable of detecting all of the major bacterial and viral causes of meningitis have been licensed. 21,22 Line probe assays based on hybridization of multiplex polymerase chain reaction have also been developed. 23 As such diagnostics become more widely available, they can decrease the time to diagnosis and allow for the detection of causative organisms in patients pretreated with antibiotics. ED TREATMENT  ANTIBIOTICS Antibiotics may have difficulty penetrating the blood–brain barrier. Therefore, doses used to treat meningitis are frequently higher than the doses used for other pediatric infections ( Table 120-1). For neonates, presumptive therapy for meningitis is generally ampicillin and cefotaxime or gentamicin. For older infants and children, Table 120-1 lists empiric treatment that will cover the three major bacterial causes of meningitis in the United States ( N. meningitidis , S. pneumoniae, and H. influenzae type b). Patients with viral meningitis and meningoencephalitis generally receive supportive treatment, although acyclovir should be used when HSV infection is suspected. Lyme disease, tuberculous meningitis, fun gal meningitis, and parasitic infections of the CNS all require specific therapy. STEROIDS Much of the damage caused by bacterial meningitis results from the inflammatory response in the CNS. In particular, labyrinthitis can result from bacterial meningitis, producing sensorineural hearing loss. For that reason, dexamethasone therapy to reduce CNS inflammation has been proposed as an adjunct to antibiotic therapy. Data supporting the benefits of dexamethasone treatment have been mixed in children. Dexamethasone was shown to reduce the likelihood of hearing loss in children with meningitis due to H. influenzae type b in the 1980s, when that was the predominant organism. 25,26 With the emergence of S. pneumoniae as the dominant strain, the data are less robust. A recent Cochrane review showed that patients with meningitis due to S. pneumoniae who were treated with dexamethasone had a lower death rate, whereas no effect on mortality was seen with meningitis due to H. influenzae or N. meningitidis. Steroids decreased the rate of hearing loss in patients with meningitis due to H. influenzae but not due to other bacteria. In the Cochrane analysis, patients in high-income countries treated with steroids were more likely to have reduced hearing loss or neurologic sequelae than patients in low-income countries. 27 The American Academy of Pediatrics stated in 1990 that dexamethasone may be considered for treatment of infants and children with meningitis due to H. influenzae type b, but does not recommend steroid use in other bacterial forms of meningitis. 28 If used for bacterial meningitis, dexa methasone needs to be given before or with the first dose of antibiotics to be most effective. The dose of dexamethasone is 0.15 milligram/kg IV every 6 hours.

ith meningitis due to H. influenzae type b, but does not recommend steroid use in other bacterial forms of meningitis. 28 If used for bacterial meningitis, dexa methasone needs to be given before or with the first dose of antibiotics to be most effective. The dose of dexamethasone is 0.15 milligram/kg IV every 6 hours. DISEASE COMPLICATIONS Mortality from bacterial meningitis has been reduced to <10% with antibiotics and supportive care.29 However, survivors can experience sensorineural hearing loss, visual impairment, seizures, hydrocephalus, cognitive impairment, learning disabilities, and emotional problems.30 Factors predicting hearing loss include S. pneumoniae as the etiologic agent and low glucose levels in CSF . Factors predicting mortality include coma, seizures, shock, respiratory distress, neutropenia, and a high protein level in CSF . Factors predicting adverse neurologic consequences in general include coma, seizures, fever for at least 7 days, and a low WBC count in CSF . Additional, although less robust, predictors include symptoms for more than 48 hours, male gender, fever, and absence of petechiae. In the ED, physicians may see respiratory compromise, shock, seizures, hypoglycemia, and hyponatremia in children with meningitis. Hypo glycemia results from sepsis and physiologic stress and is treated with administration of dextrose. Hyponatremia most commonly results from the syndrome of inappropriate antidiuretic hormone secretion due to brain inflammation. If syndrome of inappropriate antidiuretic hormone secretion is suspected, initiate fluid restriction to 75% of maintenance requirements after treating shock and dehydration. Low sodium can also be due to home oral rehydration with hypotonic liquids. Seizures can be due to brain inflammation, hypoglycemia, or hyponatremia, so correct glucose and sodium before administering antiepileptic medications. Children with meningitis can also develop subdural effusions, empy emas, and strokes during treatment for bacterial meningitis, but these are not usually present at the time of ED presentation. Viral meningitis and meningoencephalitis can range from mild to fulminant illness leading to death or permanent neurologic disability. Some lasting effects, such as learning disorders, can be subtle. Fungal meningitis can cause death or severe disability, particularly in immunocompromised hosts. Eosinophilic meningitis from helminth infection is generally self-limited and does not require antifungal therapy. DISPOSITION AND FOLLOW-UP In almost all circumstances, admit children with suspected bacterial or viral meningitis for definitive diagnosis, treatment, and supportive care. After discharge, children need long-term monitoring for neurodevelopmental problems and hearing loss. SPECIAL CONSIDERATIONS AND SPECIAL PATIENTS  THE CHILD WITH A VENTRICULOPERITONEAL SHUNT One of the most common causes of shunt failure in patients with shunted hydrocephalus is shunt infection. Most infections occur soon after shunt placement. The predominant organism is Staphylococcus epidermidis, suggesting that the infecting organism is likely introduced at the time of surgery. Other infecting agents include S. aureus, gramnegative rods, Enterococcus faecalis , and Propionibacterium species. Predictors of shunt infection include premature birth, use of a neuro endoscope during shunt placement, and replacement of an infected shunt. 32 Only about 10% of shunt infections occur more than 1 year after shunt surgery. Patients with late infections frequently develop peritonitis, often from appendicitis. 33 Shunt infections can present with symptoms of increased intracranial pressure, fever, redness or swelling along the shunt, or abdominal pain. Treatment should include vancomycin and a third-generation cephalosporin.

shunt surgery. Patients with late infections frequently develop peritonitis, often from appendicitis. 33 Shunt infections can present with symptoms of increased intracranial pressure, fever, redness or swelling along the shunt, or abdominal pain. Treatment should include vancomycin and a third-generation cephalosporin. Add an aminoglycoside if the Gram stain shows gram-negative rods. Transfer to a tertiary care center for CSF shunt tap is the best option (See Video: VP Shunt Aspiration). Imaging to assess whether the shunt is intact and is functioning should be pursued if there is any question about shunt integrity.  THE UNVACCINATED CHILD Widespread immunization against H. influenzae type b and S. pneumoniae has drastically reduced the rate of serious bacterial illness or meningitis from these two organisms. Children who are not immunized benefit from herd immunity. Nevertheless, when unvaccinated neo nates or children develop fever, consider meningitis. Prior to the age of 18 months, children are less likely to develop meningismus, and it is difficult to exclude meningitis on clinical grounds alone. The septicappearing infant or child with no immunizations should be managed conservatively with a lumbar puncture to exclude meningitis. The real question is what to do with the unimmunized child with a fever who is not toxic appearing and has no obvious source for fever on physical examination. In children who have not been immunized, obtain Tintinalli_Sec12_p0669-0996.indd 755 8/2/19 7:50 PM