Haemophilus Meningitis Workup

Updated: Mar 02, 2016
  • Author: Pranatharthi Haran Chandrasekar, MBBS, MD; Chief Editor: Niranjan N Singh, MD, DM  more...
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Approach Considerations

Laboratory tests should be performed as appropriate. Lumbar puncture should be strongly considered in all infants aged 2-12 months with a history suggestive of Haemophilusinfluenzae meningitis and the finding of meningismus on physical examination. Brain imaging studies may be of importance. Electroencephalography (EEG) is indicated in some situations. All patients should undergo brainstem auditory evoked response (BAER) testing either during hospitalization or soon thereafter.

Go to Meningitis for more complete information on this topic.


Complete Blood Count

At presentation, the majority of patients with H influenzae type b (Hib) meningitis have an elevated white blood cell (WBC) count, with a left shift. As with Hib epiglottitis, counts in excess of 20,000/µL may be found.


Measurement of Serum Glucose Concentration

Serum glucose values should be measured, for the sake of comparison with cerebrospinal fluid (CSF) glucose levels (see below). Serum glucose values are often abnormal (low or high) in cases of acute bacterial meningitis.


Serum and Urine Chemistry Studies

Serum and urine chemistry, in particular sodium values, should be ascertained immediately and monitored at intervals throughout treatment. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) develops in approximately half of all cases of Hib meningitis. It may cause stupor or seizure and may contribute to the elevation of intracranial pressure.

Diagnostic criteria for SIADH are as follows:

  • Serum sodium less than 135 mEq/L
  • Serum osmolality less than 270 mOsm/L
  • Urine osmolality greater than twice serum osmolality
  • Urine sodium greater than 30 mEq/L
  • No evidence of confounding hypovolemia or dehydration

In some instances, low serum sodium is due to cerebral salt wasting rather than SIADH. Unlike SIADH, cerebral salt wasting is associated with a decline rather than an increase in patient mass. In other instances, hyponatremia is produced by the excessive intravenous administration of hyposmolar fluids.


Blood Cultures

Hib may be grown from blood cultures in at least 50-80% of cases if the patient has received no prior treatment with antibiotics. Accurate etiologic diagnosis of meningitis may be more complicated in developing countries, where often there is widespread use of antibiotics before blood or CSF cultures can be obtained. This approach is understandable if one considers the delay that may be encountered in some nations in rapidly obtaining access to healthcare facilities capable of performing such studies.


Other Tests

Lumbar puncture is critical in the evaluation of patients with suspected meningitis. Lumbar puncture results may confirm the diagnosis of meningitis or suggest an alternative diagnosis. In cases of bacterial meningitis, CSF Gram stain and culture may identify the organism causing meningitis, which is advantageous in that treatment and prognostication can be adjusted to the specific organism. Identification of increased pressure by lumbar puncture may also modify the therapy provided.

CSF abnormalities are found in approximately 16-20% of children who are evaluated by lumbar puncture for possible meningitis. Of the children with abnormalities, 60-68% have viral infection, 20-26% have bacterial infection, and the cause remains unclear or unknown in 5-10%.

Indications and contraindications

Lumbar puncture should be performed unless some specific contraindication exists. In young febrile children, lumbar puncture should be performed if meningitis cannot be otherwise excluded (after appropriate consideration of such contraindications as asymmetrical space-occupying lesion).

Lumbar puncture should also be strongly considered if another definite source of infection and fever cannot be found and outpatient antibiotic therapy is to be provided. In such cases, performing puncture avoids the diagnostic difficulties associated with partially treated meningitis in the event that the infant returns within the next few days with clinical worsening.

Care must be taken not to perform lumbar punctures in patients who are at risk for brain herniation or are manifesting signs of impending herniation. Although the scientific underpinnings of allegations that there is a relationship between lumbar puncture and herniation are in many cases weak, they may not appear to be so in the minds of nonmedical personnel called upon to review such an alleged relationship in retrospect in a courtroom.

Findings that may indicate the onset of herniation or impending herniation include focal brainstem signs, especially if present unilaterally (eg, dilation of a pupil, diminution or loss of pupillary reactivity, diminution or loss of abducens function); head tilt; meningismus; deterioration in mental status; visual field defect; focal seizures; vomiting; increased tone in the lower extremities; Cushing reflex (ie, elevated blood pressure with slow heart rate); and hyperventilation or other disturbances of breathing rhythm consistent with brainstem regulatory failure.

Papilledema is a very important sign, but it may not develop until after several hours of increased intracranial pressure (ICP), and a large segment of the medical community cannot reliably determine the pertinent early funduscopic changes. Venous pulsation presence may be reassuring, but the absence of pulsations is of greatest value only in cases where they were known to be present prior to the current urgent presentation.

In cases where concern is raised by any of these signs, deferring lumbar puncture until after brain imaging can be obtained is appropriate. However, in all such cases wherein the diagnosis of meningitis is entertained, obtaining a blood culture and initiating appropriate broad-spectrum antibiotic therapy immediately afterward is crucial, so that performance of the brain scan does not delay initiation of treatment.

The authors re-emphasize the point that the performance of brain imaging studies should never delay the initiation of treatment for increased intracranial pressure or seizures. Note that even in cases where intravenous (IV) antibiotics have been administered immediately before a computed tomography (CT) scan, CSF from a lumbar puncture performed after the completion of the scan seldom has been sterilized by the antibiotics.

In the absence of focal neurologic findings (such as those noted above), the risk of herniation in cases of Hib meningitis is low, and one can safely proceed to lumbar puncture without imaging. In general, evidence of raised ICP is not considered a categorical contraindication to lumbar puncture, as long as no signs suggesting focal space-occupying lesions are found. If evidence exists for increased ICP, a small needle (#22 gauge) should be employed by the most skilled available person, and only as much CSF as is needed for essential tests should be collected.

General considerations

Opening pressure should be recorded. This should be done only when patients are in the lateral recumbent position and are as relaxed and calm as possible.

In bacterial meningitis, opening pressure is frequently elevated, which may have an impact on treatment. In small calm infants, pressures should be less than 160 mm water. Older infants and children should have pressures less than 180 mm water. In some obese individuals, normal pressures are as high as 250 mm water. In fulminant cases of Hib meningitis, pressures as high as 300 mm water to more than 500 mm water may be recorded.

CSF should be collected in a sterile manner in sufficient quantity and immediately submitted to the laboratory. If extra CSF is available, freeze it and store it for possible future evaluation.

Assessment of CSF appearance

The appearance of the CSF should be noted. Normal CSF is clear. In bacterial meningitis, however, the presence of greater than 200 WBCs/µL, greater than 400 red blood cells (RBCs)/µL, greater than 100 mg/dL protein, or greater than 105 colony-forming units (CFU) of bacteria may cause the CSF to appear cloudy. This change may be subtle and is best appreciated by flicking the bottom of the firmly held tube and observing for a shimmer of iridescence. In severe cases, the CSF may appear purulent. Protein values of greater than 150 mg/dL cause the fluid to appear xanthochromic.

Gram staining of CSF

Gram staining of the CSF may reveal the Hib pleomorphic gram-negative coccobacilli. If the CSF is cloudy, the stain should be performed on fresh uncentrifuged CSF. If the CSF is clear, it should be performed on the pellet of centrifuged CSF.

The probability of visualizing bacteria depends on the concentration of bacteria in CSF. Bacteria are identifiable in 60-90% of all cases of acute bacterial meningitis, particularly in cases where more than 105 CFU/mL are present. The specificity of a positive Gram stain for bacterial meningitis is approximately 95%. Gram staining does not provide a definitive identification of the bacteria and does not, of course, provide information concerning antibiotic sensitivities.

Oral or IV pretreatment with antibiotics may disable the identification of organisms by Gram stain. Indeed, the presence of organisms on Gram stain 24 hours after IV treatment has been initiated may be an important indicator of treatment failure.

CSF white blood cell count

CSF should be examined promptly for WBCs because these cells generally begin to disintegrate within about 90 minutes of the lumbar puncture. WBC levels greater than 10/µL are usually considered abnormal, as is the presence of even 1 polymorphonuclear (PMN) leukocyte.

WBC differential counts from cytocentrifuged CSF may falsely elevate the PMN leukocyte count. The occurrence of a preceding convulsive seizure may elevate the WBC count, particularly the PMN leukocyte count. When modest CSF pleocytosis is due to seizure and not meningitis, opening pressure is usually normal, CSF is clear, fewer than 80 WBC/µL are found, and CSF glucose is normal.

The typical finding in Hib meningitis is PMN leukocyte–predominant pleocytosis, as is the case in most other forms of bacterial meningitis. CSF WBC counts in Hib meningitis are greater than 100/µL in more than 90% of cases and greater than 1000 in 65-70% of cases. The mean CSF WBC counts for Hib meningitis approach 1100/µL.

Note, however, that although lymphocytes typically predominate in the fully developed CSF pleocytosis of viral meningitis, PMN leukocytes may predominate in as many as 20-75% of lumbar puncture samples obtained in the early phases of viral encephalitis, and they may be found in 5-8% of viral encephalitides even after fully developed pleocytosis has been achieved. On the other hand, approximately 10-30% of bacterial meningitis cases have early lymphocytic predominance, especially in cases where the CSF WBC count is fewer than 1000/µL.

In at least half of all patients who receive appropriate antibiotic therapy for bacterial meningitis, the CSF WBC count remains elevated for at least 1 week after initiation of therapy. In some cases, the elevation persists for several weeks. However, falling CSF WBC counts on repeat lumbar punctures should be considered a reassuring indication of response to appropriate treatment.

Relatively low CSF WBC counts in a very ill child with Hib meningitis may indicate a poor prognosis, especially if large numbers of nonengulfed Hib organisms are observed on the CSF Gram stain.

Measurement of CSF glucose concentration

CSF glucose concentrations lower than 40 mg/dL are found in approximately two thirds of all cases of acute bacterial meningitis. Comparison must always be made to serum glucose concentrations measured at the time of the lumbar puncture. The CSF-to-serum-glucose ratios should be approximately 2:3 (ie, 0.6).

In the presence of an elevated serum glucose concentration, a CSF glucose concentration within the reference range may not actually be normal, because the CSF value must be interpreted with respect to the serum value. A CSF-to-serum-glucose ratio of less than 0.31 is observed in 70% of patients with bacterial meningitis. Low CSF-to-serum glucose ratios are also found in fungal and carcinomatous meningitides.

In as many as 80% of patients who receive appropriate IV antibiotic treatment for bacterial meningitis, CSF glucose concentration returns to the reference range by day 3 of that treatment. Even with appropriate treatment, however, some patients continue to exhibit low CSF glucose concentrations for 7-10 days.

Measurement of CSF protein concentration

As happens with any process that disturbs the function of the blood-brain barrier, CSF protein concentrations increase in bacterial meningitis. In Hib meningitis, this value for lumbar CSF is typically greater than 50 mg/dL, with a typical range of 100-500 mg/dL. If ventricular CSF is available for analysis, note that protein values greater than 15 mg/dL are abnormal. In the event of a traumatic tap, protein values may be grossly estimated by subtracting 1 mg/dL of protein for every 1000 RBCs/µL.

Measurement of CSF lactate concentration

In the setting of bacterial meningitis, CSF lactate is frequently elevated. Values in excess of 3.5-3.8 mmol/L are sensitive indicators of acute bacterial meningitis, found in as many as 92% of cases. The specificity of this finding is comparatively low, although elevation of lactate to the concentrations noted above is more strongly indicative of bacterial than viral meningitis. However, elevation of lactate does not exclude the diagnosis of viral meningitis.

Whether CSF lactate as a diagnostic test adds information that cannot be obtained from CSF cell counts, glucose, and protein is not clear. Moreover, elevated CSF lactate may be due to other potential alternative diagnoses (eg, closed head injury, smothering and other causes of hypoxic-ischemic brain injury, neoplasia, or prolonged seizures from any of a wide variety of causes).

Elevation of CSF lactate in Hib meningitis may be due to cerebral edema or changes in cell membranes or cellular energy metabolism leading to anaerobic glycolysis. CSF lactate may remain elevated for a fairly long time after effective antimicrobial therapy has resulted in amelioration of brain edema and restoration of ICP to the reference range.

Repeated lactate estimation (by lumbar CSF analysis or magnetic resonance imaging [MRI] spectroscopically) may provide a method for estimating possible deleterious effects of fluid restriction in cases of Hib meningitis–induced brain swelling. Inadequate systemic volume may be deleterious in such cases because of the high ICP and pressure-passive nature of dysregulation of cerebral circulation in meningitis.

CSF culture

Culture of the CSF yields the most specific information; unfortunately, that information is not immediately available. CSF cultures are positive within 48 hours in approximately 75-80% of cases, with a sensitivity of 95% and a specificity of 99%. Hib in culture can be considered the cause of meningitis most confidently when the organism was found on Gram stain of the initial CSF.

A positive culture is the most valuable single test in confirming the diagnosis of bacterial meningitis. Although in some instances a false-positive CSF culture is obtained, these cultures tend to contain skin commensals such as Staphylococcus alba, and a false-positive CSF culture containing Hib is likely very rare. Moreover, ascribing such a positive culture to contamination is so risky that the physician rarely has any choice other than to complete the usual course of therapy for meningitis.

A positive CSF culture provides the additional benefit of permitting the determination of antimicrobial sensitivity in subcultures of recovered organisms and thus allowing the adjustment of antibiotic selection. However, several additional days after recovery of the organism may be necessary to obtain such results.

Implications of CSF evaluation for management

Although CSF assays may be less sensitive or specific than positive cultures and Gram stains (unless the CSF findings are very abnormal), the results of CSF analysis are critical for the initial management of Hib meningitis. Evidence suggests that in cases where the clinical picture is consistent, any of the following CSF results predict bacterial meningitis with 99% certainty:

  • CSF glucose less than 34 mg/dL
  • CSF-to-serum-glucose ratio less than 0.23
  • CSF leukocyte count greater than 2000/µL
  • CSF neutrophil counts greater than 1180/µL

Moreover, in cases where individuals have been treated with antibiotics within the week before the lumbar puncture, the less-irrefutable approach of diagnosing meningitis by CSF cell counts and chemistries must nonetheless be relied upon for decisions concerning initiation and continuation of therapy. Two careful prospective studies indicate that as many as one third of children with Hib meningitis have received recent antibiotic treatment, usually for suspected otitis media.

Previous treatment with oral antibiotics may significantly reduce the yield of CSF culture and Gram stain; indeed, these may be rendered negative within 24 hours of such treatment. CSF protein concentration and neutrophil percentage are also decreased. On the other hand, previous treatment has not been shown to significantly decrease the yield of blood culture, total CSF WBC count, CSF glucose concentration, or CSF-to-serum-glucose ratio.

The reduced significance of some of these indicators of bacterial meningitis was thought to be due to the fact that oral antibiotics, while not preventing the development of meningitis, had attenuated the severity of illness. This concept is supported by the finding that among children whose Hib meningitis was preceded by otitis media or upper respiratory illness, the interval between the preceding illness and the development of meningitis was several days longer in children who received antibiotic treatment than in untreated children.

Studies of the effects of IV antibiotic administration on CSF characteristics of children with meningitis have shown that as many as several days of IV treatment with appropriate antibiotics does not significantly alter CSF protein, glucose, or WBC concentrations, although the yield of Gram stain and culture is lost.

No results of CSF cell counts or chemistries can be used to irrefutably rule out a meningitis diagnosis in a patient who has clinical indications of possible meningitis. This is particularly true because of the possibility of viral meningitis in such cases.

Other CSF tests

Bacterial antigen tests such as counterimmunoelectrophoresis or latex agglutination immunologically detect the soluble antigens on many bacteria, including those of Hib. The tests are very rapid but detect only the most common meningitis pathogens. The latex particle agglutination antigen tests for Hib have a sensitivity of 97% and a specificity of 95%.

Polymerase chain reaction (PCR) is an emerging technique that may ultimately be useful in identifying the organism when the Gram stain and culture results are negative. However, its application to bacterial meningitis has been limited by a significant number of false-positive results caused by amplification of contaminating DNA and mispriming.

An advantage of both bacterial antigen tests and PCR is that the results are not affected by treatment with oral antibiotics before presentation.

Various studies have been published concerning the utility of testing for fibrin degradation products, lactate dehydrogenase, creatine kinase, or other potential CSF constituents in evaluation of children who may have meningitis. As yet, no compelling evidence indicates that such testing is valuable.


Brain Imaging

Brain imaging studies may be of importance in patients with Hib meningitis. These studies are appropriately obtained in the acute setting to identify mass lesions that are in the differential diagnosis (eg, focal encephalitis, brain abscess, empyema, parasitism, subdural hemorrhages) not only for diagnostic purposes, but also to evaluate possible risks of lumbar puncture. Hence, evidence of focal neurologic dysfunction (ie, seizures, focal neurologic deficits) or of papilledema should prompt consideration of scanning.

Other indications for scanning during the initial or subsequent phases of hospitalization include persistently depressed or unexplained deterioration in neurologic status and prolonged fever despite treatment.

Scanning should never be performed before other critical management decisions have been made and acted instituted. If lumbar puncture is deferred until after scanning, adequate IV access must be established, blood cultures must be drawn, and broad-spectrum antibiotic coverage pertinent to any suspected meningitic agent should be administered.

If a scan is ordered because of seizures, full IV loading with an anticonvulsant should be considered. The authors regard phenobarbital as the drug of choice for this in young children because its sedative properties may make other forms of sedation unnecessary.

The wide therapeutic window of phenobarbital permits multiple additional doses to be administered if seizures are resistant to treatment, and this agent is easier to manage than phenytoin because of the nonlinear kinetics of phenytoin, if an anticonvulsant is judged necessary at discharge. Phenobarbital may also have beneficial effects in cases of increased ICP by reducing irritability and cerebral metabolic demand.

Brain imaging studies obtained at presentation are usually justified to identify an alternative diagnosis to meningitis (eg, brain abscess, subdural empyema) that may contraindicate a lumbar puncture. Results of imaging studies do not confirm the diagnosis of meningitis, which can only truly be confirmed by the performance of lumbar puncture. In instances where lumbar puncture is contraindicated, the presumption of meningitis may be made when the imaging results or clinical circumstances and other testing do not disclose an alternative diagnosis.

Go to Imaging in Bacterial Meningitis for more complete information on this topic.

Choice of imaging modality

Either CT or MRI may provide information concerning the usual space-occupying lesions or other complications that may result from Hib meningitis and either modality provides information concerning some alternative diagnoses. Generally, CT is obtained because it is usually more readily available and requires less time. Patients must be monitored by qualified personnel during imaging because seizures or critical elevation in ICP may develop while the study is being performed.

The most common imaging findings in cases of Hib meningitis at or shortly after presentation are meningeal, ependymal, or choroidal enhancement due to meningitic inflammation. Inflammatory exudate may be demonstrable in the basilar cisterns, especially the foramen magnum. The accumulation of inflammatory exudate tends to widen the basilar cisterns and the cortical sulci (particularly over the convexities of the forebrain hemispheres).

Findings on CT scanning may be fully normal in the acute stage of Hib meningitis. MRI scanning, if performed, may reveal the abnormalities noted above with even greater sensitivity and definition than CT scanning.

Abnormalities indicative of meningitic inflammation and exudate support the diagnosis of meningitis but are not very specific with regard to organism and usually do not modify therapy or prognosis. Thus, for example, the extent of meningeal enhancement is not indicative of prognosis. Rarely, adults may present with Hib meningoventriculitis, evident as ventricular debris, periventricular hyperintense signal, and periventricular ependymal enhancement. [18]

Other important abnormalities that scans may detect tend to develop later in the course of Hib meningitis and constitute complications of the disease. In many cases, these abnormalities are better defined by MRI than by CT scanning. Indications for obtaining such scans, whether CT or MRI, include the following:

  • Persistence of fever after several days of appropriate IV antibiotic therapy (occurs in approximately 10% of all cases of Hib meningitis)
  • Return of fever after achievement of an afebrile state with appropriate IV antibiotic therapy
  • Evidence suggesting increased ICP (eg, bulging fontanelle, Cushing reflex, obtundation, meningismus, cranial nerve signs suggestive of herniation), hydrocephalus, large subdural effusion, or empyema
  • Focal neurologic deficits
  • Prolonged obtundation or coma

On CT scanning performed because of these various indications, abnormalities are found in slightly more than 50% of all such scans. However, in most instances, these abnormalities do not require specific interventions, and their detection may not prove helpful in estimating prognosis.

Transependymal movement of CSF may be detected, especially in instances where noncommunicating hydrocephalus develops. Brain swelling may be found, and on MRI, diffuse increased T2-weighted signal may be found, representing interstitial cerebral edema. These various changes may indicate the need for management of increased ICP.

On CT scanning, brain edema causes loss of differentiation of gray and white matter. Care must be taken not to overinterpret the watery appearance of white matter in the brains of very young infants; this appearance may be normal because of the larger water content of unmyelinated tissue. Loss of sulcal markings and of the usually distinct suprasellar, perimesencephalic, and quadrigeminal cisterns may occur. Ventricular compression imparting a slitlike contour to the frontal horns may occur.

Subdural effusions

Subdural effusions are common in Hib meningitis and are usually the result of an inflammation-induced increase in the permeability of capillaries and veins of the inner dural surface, permitting leakage of sterile fluid into the subdural space.

On CT imaging, subdural effusions are crescentic extra-axial collections between the outer surface of the brain and the inner surface of the skull, and their density is quite low, appearing similar to CSF. They are often bilateral and, if large, may flatten the anterior portions of the brain and may displace the frontal horns posteriorly. To some extent, the displacement posteriorly may be the artificial result of the recumbent positioning of the patient in the scanner. They do not usually enhance after contrast administration.

Subdural effusions are generally benign and do not cause symptoms and should in general be left alone. Eventually they resorb spontaneously, as the meningitis resolves. On occasion, however, subdural effusions can create local mass effect with involvement of local tissue. They may even result in elevated ICP, herniation, or focal signs. The development of new or progressive deficits, such as hemiparesis, during the course of illness may indicate that a subdural effusion has begun to exert mass effects.

Subdural effusions may become infected. On brain imaging, infection is suggested by the fact that the purulent material within the effusion produces an imaging appearance that is of higher density than CSF. IV contrast administration results in enhancement, especially at the border between cortex and subdural surface.


Hydrocephalus, either communicating or obstructive, may occur in Hib meningitis. Such a process should be suspected if the patient has progressive or prolonged altered consciousness despite appropriate antibiotic treatment. Communicating hydrocephalus probably develops because the inflammatory exudate across the vertices impairs the resorptive function of arachnoid granulations. Noncommunicating hydrocephalus usually develops because of exudative blockage of the foramina of Magendie and Luschka.

In distinction to the changes of edema, communicating hydrocephalus enlarges the entire ventricular system, including the fourth ventricle and, in some instances, the extra-axial spaces. Transependymal movement of CSF may result in periventricular lucency of the frontal ventricular horns.

In obstructive hydrocephalus, these periventricular lucencies are even more pronounced and the ventricular enlargement is limited to the lateral and third ventricles without enlargement of the fourth ventricle or extra-axial spaces. Obviously, the periventricular changes are even more evident on MRI than on CT scanning and consist of bright signal on T2 weighting.

Cerebral infarction

Cerebral infarction as a consequence of meningitic vasculitis may be found. CT scanning may show low-density lesions corresponding to a particular vascular territory. Hib meningitis–associated infarction tends to be found in the subcortical white matter, cerebellum, and brainstem. Administration of contrast results in gyriform, nodular, or ring enhancement of the infracted area. Infarctions may be hemorrhagic, a feature that CT scanning is particularly likely to reveal.

MRI is more likely to demonstrate bland infarction, particularly when sequences designed to demonstrate restricted diffusion are employed. These abnormalities tend to be found in subcortical white matter, cerebellum, and brainstem and resemble the changes that may be found in hypoxic-ischemic encephalopathy. Lesions such as these should be suspected when patients with Hib meningitis manifest focal deficits or seizures.


The low-density changes of cerebritis may be quite difficult to identify by CT scanning, although after contrast administration, the margins of areas of cerebritis are sometimes surrounded by a rather indistinct and nonhomogeneous halo. Occasionally, contrast is also found in the center of such regions. Evolution of brain abscess in such regions results in a ring of low density surrounded by contrast enhancement that is itself contained within a larger low-density area of brain edema. These changes are much more distinct on MRI.

Unlike some other types of meningitis, abscess formation is uncommon in Hib meningitis. Abscess formation may be detected in scans obtained because the patient has developed focal deficits or seizure.



EEG is sometimes indicated to evaluate for seizure activity. Indications include persistent depressed mental status without obvious evidence of seizure activity. Nonconvulsive status epilepticus is common in this population, although altered mental status is more often caused by metabolic disarray.


Brainstem Auditory Evoked Response Testing

Hearing impairment is a common complication in Hib meningitis. It is usually permanent. Hearing may be difficult to assess clinically; therefore, all children should have BAER testing at some point during hospitalization or in the early period of posthospitalization recovery.

The results of BAER testing do not influence acute management, and to that extent, the timing of BAER testing is not important. However, the value of BAER testing in predicting permanent sensorineural hearing loss from bacterial meningitis is limited if test results are abnormal before resolution of conductive loss (due to the presence of otitis media, which frequently precedes Hib meningitis) or other possible forms of acute inflammation of neural tissue. Thus, the test should be repeated some weeks or months later if results are initially abnormal.

On the other hand, if the test results are normal during the acute phase of the disease, their predictive value for normal hearing is excellent. Unlike other focal complications of meningitis, sensorineural hearing loss is not a risk factor for epilepsy. However, sensorineural hearing loss is associated with language and learning delays. Thus, if present, children should be referred for further hearing and speech evaluations and therapies.