SEPTAL EMPYEMA - keywords
septal empyema
references to bacterial infection, including septal empyema
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septal empyema
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example
An exceptional abnormal behaviour of a midline caivty is due to bacterial infection within the cavum septi pellucidi. Septal “empyema” is a surprise finding during suspicion of ongoing bacterial infection (Li et al. 2002). This also a rare event in children and adults, where it usually leads to neurosrugical drainage.
ventriculitis without septal empyema
After delivery at 31 w GA with premature rupture of the membranes, an uneventful neonatal course was followed by discharge after 5 weeks. Twelve days later, the infant developed fever and irritable crying, later on with seizures. A lumbar puncture yielded turbid cerebrospinal fluid with more than 10,000 leukocytes, an extremely low glucose (0 mg/dL) and increased protein (1038 mg/dL). Urinalysis was normal. Brain echo revealed wall enhancement of the cavum septum pellucidum and debris, MR confirmed. Proteus mirabilis was isolated from CSF. Fourteen days after admission and treatment with antibiotics, the debris in the cavum septum pellucidum disappeared on ultrasound. A lumbar puncture 2 weeks after the initial one revealed leukocytes 44/mm3, a persistently low glucose (28 mg/dL), and increased protein level(426 mg/dL). No bacteria were isolated this time. Progressive hydrocephalus finally led to placement of a ventriculoperitoneal shunt. The ventricular size returned tonormal and the cavum septi pellucidi gradually disappeared. The infant was clinically well on follow-up.
(Li et al. 2002)
septal empyema
example of septal empyema
recent haemorrhage into CSP
Extracerebral effusion (subarachnoid) with debris in the acute stage and meningeal empyema later on can (rarely in ~1 %)) appear as either hypoechoic collections or areas of heterogeneous echogenicity (Yikilmaz et al. 2008, Gupta 2017). A round or biconvex hyperechoic collection is found between bone and cortex. Compression and not dilatation of the underlying sulci allows differentiation from a subarachnoid collection due to CSF retention. The echoreflections in the subdural collection are fine and may show strand formation. Interhemispheric location may occur. Based on CUS alone it can be difficult to differentiate between sterile and purulent effusions although a heterogeneous echogenicity and debris are suggestive of the latter (Raghav et al. 1990, Bockova et al. 2000, Nickerson et al. 2012). While effusion resolves spontaneously, empyema needs aspiration or drainage. Analysis of the fluid confirms the diagnosis.
Foci of hyperechogenicity in white matter may occur in the acute stage around the ventricle and close to the cortex. Such parenchymal abnormalities are caused by vasculitis, haemorrhagic-ischaemic infarction, and abscess formation (Volpe et al. 2018). The lesions are focal or diffuse, often changing in appearance over time. Ischaemic stroke, common in GBS meningitis, is initially difficult to detect but becomes apparent when a scan is repeated beyond 48-72 hours of admission (Hernandez 2011). Typical are infarcts in deep grey matter (perforator stroke) and focal cortical infarctions.
In contrast, liquefaction necrosis is often detected early as a very irregular area of increased echogenicity.
Brain abscesses are uncommon in neonates but when they do occur, they are mostly located in the frontal lobes (Enzmann et al. 1982, Gallagher and Ball 1991, Ries et al. 1993, de Vries et al. 2006, Masand et al. 2015). Usually they start with infarction, then parenchymal necrosis becomes infected and forms an abscess (Volpe et al. 2018). Haematogenous seeding is the alternative. Abscesses can become large, and often multiple. Larger lesions cause mass effect. Their appearance changes as they become demarcated over time, with a hyperechoic rim and central echolucency due to liquefaction and cavitation. The combination of infection and venous infarction (thrombophlebitis) eventually gives rise to periventricular cysts, sometimes of a porencephalic nature.
bacterial encephalitis: ultrasound findings, including septal empyema
A baseline CUS on admission is recommended in neonates with clinical suspicion of CNS infection. If meningitis is confirmed or the condition deteriorates, serial studies rule out complications that need additional monitoring or treatment.
The initial finding during meningitis is brain swelling with slitlike ventricular cavities and limited extracerebral spaces. The sulci may widen and become hyperechoic due to exudation, but also due to increased reflections from the inflamed surrounding (sub)cortex. The latter may indicate the onset of gyral venous infarction (Berman and Banker 1966). During the first few days fine intraluminal linear and nodular reflections may appear, commonly called ‘debris’, usually in the occipital or frontal horns. After some hours the ventricles widen due to exudation and, later, due to obstruction of CSF flow by inflammatory tissue (Hill et al. 1981, Reeder and Sanders 1983, Schellinger et al. 1986, Yikilmaz 2008, Gupta 2017). This may occur at the level of the aqueduct, near the exit foramina of the fourth ventricle or during pericerebellar or pericerebral ascent of CSF. Thick exudate has been reported with many organisms including mycoplasma meningitis (Wolthers et al. 2003).
Common findings are ventriculitis and choroid plexitis, represented by an echoic and thickened lining of the ventricular ependyma, intraventricular strands and debris, and an irregular choroid plexus (Hill et al. 1981). Septation may lead to compartmentalization with multiloculated cavities (Hill et al. 1981, Reeder and Sanders 1983, Schellinger et al. 1986).
In this phase empyema with bulging of the cavum septi pellucidi has been rarely reported (Li et al. 2002). This has to be differentiated from haemorrhage in the cavum, with irregular content in it, and cystic dilatation of the cavity, both without signs of infection. Ventriculitis does not automatically lead to infection within the midline cavities.
septal empyema: summary
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