Sonographic findings in bacterial meningitis in neonates and young infants
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Cranial sonography plays an important role in the initial evaluation of infants with suspected bacterial meningitis and in monitoring for complications of the disease. Echogenic widening of the brain sulci, meningeal thickening and hyperemia suggest the diagnosis in an at-risk population. Sonography can identify the presence of extra-axial fluid collections, and color Doppler sonography can be very helpful in differentiating benign enlargement of subarachnoid spaces from subdural effusions. Intraventricular debris and stranding, and an irregular and echogenic ependyma are highly suggestive findings associated with ventriculitis. Sonography can play an important role in the detection of postinfectious hydrocephalus, in the determination of the level of obstruction, and in the evaluation of intracranial compliance. Focal or diffuse parenchymal involvement can represent parenchymal involvement by cerebritis, infarction, secondary hemorrhage or early abscess.
KeywordsMeningitis Ultrasonography Doppler Bacterial infections Central nervous system infections Children
Bacterial meningitis is an uncommon but serious condition in the newborn and infant child. The incidence of bacterial meningitis has shown a dramatic decline in the last 25 years in the United States . But despite a number of recent advances in neonatal intensive care, rapid bacteriological assays, and potent antibiotics, neonatal bacterial meningitis remains an important cause of neurological disability worldwide [2, 3, 4]. Early diagnosis of the primary disease and its complications is essential for the prevention of neurodevelopmental sequelae. Cranial sonography is often the first imaging modality used in the evaluation of critically ill infants with suspected meningitis. Thus, familiarity with the pathophysiology and sonographic appearance of bacterial meningitis is important for the radiologist and neonatologist taking care of these patients. In this article we review and update the US features of bacterial meningitis and its complications with emphasis on the relationship between imaging findings and underlying pathological changes.
Pathophysiology of meningitis
Bacterial meningitis usually occurs as a result of bacteremia and sepsis, with initial seeding of the central nervous system via the choroid plexus. The infection then spreads into the cerebrospinal fluid (CSF) and can cause inflammation of the ventricular system (ventriculitis). Inflammation of the meninges typically follows [2, 5]. A key feature of arachnoiditis is the presence of vasculitis, predominantly in small and medium-size veins that traverse the subarachnoid space . Meningeal inflammation extends to the walls of the bridging and cortical veins to cause thrombophlebitis and vascular occlusion, which is associated with cortical infarcts [5, 6]. A number of bacterial virulence factors and inflammatory cytokines contribute to the inflammatory process, resulting in diffuse cerebral edema, increased intracranial pressure, and alterations of cerebral blood flow [7, 8, 9]. Lipopolysaccharides found in the bacterial cell wall can lead to a disruption in the blood–brain barrier and invasion of microorganisms into deeper cerebral structures [10, 11]. Arachnoiditis and ventriculitis might also contribute to a more generalized encephalopathy characterized by neuronal loss, gliosis and periventricular leukomalacia . Later pathological findings include diffuse cerebral cortical and white matter atrophy, hydrocephalus, which can also be seen in the early phase, multicystic encephalomalacia, porencephaly and ventricular septations [2, 3, 5, 12, 13].
In the acute phase of meningitis, marked vasodilatation of cortical vessels is often present as the result of potent vasogenic effects of bacterial toxins. In later stages of the disease, there is a global reduction in cerebral blood flow attributed to impairment of cerebral autoregulation and brain edema .
In the newborn infant, streptococcus group B, Escherichia coli, and Listeria monocytogenes are the most commonly isolated organisms in CSF. Although other gram-negative enteric organisms such as Klebsiella species and Citrobacter species are less common, they can have far more devastating consequences .
Sonographic features of meningitis
Sonographic abnormalities are present in approximately 65% of infants with acute bacterial meningitis [3, 16, 17, 18, 19, 20, 21, 22]. However, the frequency of imaging abnormalities in patients with a clinical presentation complicated by persistent seizures, abnormal neurological findings and a deterioration of CSF examination within the first 48 h can be as high as 100% . The high incidence of positive sonograms in infants with suspected complications resulted in the recommendation by some authors to use sonography only when there is a clinical suspicion of a complication . Han et al.  found that no infant without a clinical indication of complications of meningitis had clinically significant findings on sonography. However, other authors suggest a sonographic examination should be used on every infant with or without evidence of complications on the basis of reports of a high incidence of positive findings in infants without any clinical indication of complications [17, 23, 24]. Rosenberg et al.  suggest an initial examination at the time of diagnosis of bacterial meningitis and a follow-up study within 1 week if the initial study demonstrates any parenchymal or ventricular abnormality.
We recommend cranial sonography as a baseline study in every infant who has an adequate size fontanel if the diagnosis of bacterial meningitis is suspected clinically. Because the major advantage of sonography is its ability to be safely repeated, a second study should be performed if any clinical deterioration occurs, such as increasing head circumference, occurrence of new neurological findings, and lack of response to therapy. However, in patients with complicated bacterial meningitis whose clinical situation is sufficiently stable to leave the nursery, MRI should be the next study of choice. In children, MRI is widely accepted for its safety and high soft-tissue resolution. It is superior to sonography in showing the existence and extension of the complications, especially in the posterior fossa. It has the further advantage of not using ionizing radiation.
It is essential to use state-of-the-art equipment with optimized settings including linear, curved and vector probes with variable megahertz in order to perform a complete evaluation of the meninges because of the often subtle sonographic changes of bacterial meningitis [25, 26].
Meningeal and extra-axial findings
Although histopathological studies have shown exudative inflammation of the choroid plexus (plexitis) and of the ependymal lining (ventriculitis) in up to 93% of those autopsied [5, 13], only those with more severe involvement exhibit abnormal findings on cranial sonography [3, 16, 20, 28]. By US examination, the choroid plexus can appear more echogenic and its contours irregular and poorly defined [16, 28, 38, 39]. The ependyma can have a thick, irregular and echogenic appearance, as well [20, 28, 37, 38, 39].
Abnormal parenchymal echogenicity
Areas of abnormal brain echogenicity have been reported in 12% to 65% of infants with bacterial meningitis [3, 20, 28]. Lesions can be focal or diffuse and can represent parenchymal involvement by cerebritis, infarction, secondary hemorrhage or early abscess [3, 17, 40]. The presence and size of parenchymal lesions are associated with significant neurological sequelae and are indicators of a poor prognosis .
One of the most devastating complications of bacterial meningitis is abscess formation. It has been reported with a frequency of between 1% and 18% in newborns with meningitis [2, 3, 16, 21, 28]. Mortality rates are significant (15–75%), and up to 66% of survivors develop neurological sequelae [41, 42].
Most cerebral abscesses are caused by a member of the Enterobacteriaceae family (Citrobacter and Enterobacter species) [43, 44]. Citrobacter koseri (formerly C. diversus) is the main causative agent leading to abscess formation in the brain [43, 45]. Up to 77% of infected patients develop an intracerebral abscess. The major pathological feature of Citrobacter meningitis is vasculitis followed by infarction, with necrosis and liquefaction of large portions of the white matter of the hemispheres [45, 46]. Hemorrhagic necrosis and liquefaction can also occur [43, 46]. Surgical drainage of these lesions is not recommended to avoid further damage to surrounding brain parenchyma .
Diffuse cerebral atrophy, multicystic encephalopathy, and porencephaly might be seen as the end-stage of complications of bacterial meningitis.
Ventricular dilatation is present in 14–65% of infants with bacterial meningitis and can occur in either the acute or the chronic phase of the disease [16, 17, 18, 19, 20, 21, 28]. The level of obstruction to CSF flow is usually outside the ventricular system but can occur within the narrowest portions of the ventricles as a result of ependymitis and secondary adhesion. Common locations for intraventricular obstruction include the aqueduct of Sylvius and the exit foramina of the fourth ventricle .
Pulsed Doppler interrogation of the anterior cerebral artery before and after compression of the anterior fontanel can be a useful adjunct in the serial monitoring of infants with postinfectious hydrocephalus [53, 54, 57]. Increasing response to fontanel compression as manifested by increasing changes in arterial RI can be an indication for shunt placement in infants with rapidly progressive hydrocephalus.
Sonographic evaluation of the thoracolumbar spine in infants with meningitis might reveal the presence of echogenic debris within the spinal subarachnoid space. This finding has been associated with a higher risk of progressive hydrocephalus .
Cranial sonography continues to be an excellent front-line imaging modality in the initial diagnosis and monitoring of infants with acute bacterial meningitis and its potential complications. Its utility is enhanced by the use of alternative scanning approaches and Doppler techniques for identification of ventriculitis, extra-axial fluid collections, and hemodynamic alterations. Spinal sonography might also play a role in assessing the risk of progressive hydrocephalus.
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