History: 2-month premature infant developed jerking of extremities at age two weeks. (Section would be a bit larger to include more history in a real case submission)
Physical exam: Afebrile, (rest of vital signs). Lethargic infant who demonstrates tonic-clonic seizures with increased tone of the extremities between jerks. (this section would be larger in a real case submission to include a more comprehensive exam).
Differential diagnosis: Hypoxic-ischemic encephalopathy, hemorrhage, meningitis/cerebritis, mass, seizure disorder, mass, toxic/metabolic encephalopathy, accidental trauma, non-accidental trauma.
Laboratory results: WBC of 17.5K and anemia. Lumbar puncture yielded bloody fluid that grew no organisms.
Imaging findings: Head ultrasound shows markedly dilated lateral, third and fourth ventricles that are filled with heterogeneous moderately echogenic material. Parenchyma is compressed. Decreased sulci due to prematurity.
Differential diagnosis based on imaging: Intraventricular hemorrhage vs pus.
Clinical course: The patient was started on phenobarbital, with resolution of tonic-clonic seizure activity. Right ventricular tap was performed to relieve intracranial pressure, with drainage of purulent material, which eventually grew Escherichia coli. The patient expired four days later.
Diagnosis:Escherichia coli meningitis
Discussion: Meningitis is a common cause of hydrocephalus and neurological problems worldwide. It usually results from seeding of the choroid plexus in the setting of sepsis. Meningeal inflammation leads to vasculitis, cortical infarcts, and diffuse cerebral edema. In infants, Group B streptococcus, Escherichia coli, and Listeria monocytogenes are responsible for most cases of meningitis and cerebritis.
If US is performed in the acute phase, it may demonstrate thick, echogenic meninges, prominent cortical vessels, and unusually wide sulci. Increased subarachnoid fluid may be seen. As the disease progresses, the ventricles fill with exudate that is less echogenic than acute hemorrhage. It evolves to appear more uniformly complex and lacy than chronic hemorrhage, allowing differentiation. Intraventricular cysts and isolated entrapped ventricles may form secondary to adhesions.
In the acute phase, ventriculitis and adhesions at the cerebral aqueduct or the fourth ventricular foramina may cause obstructive hydrocephalus. Hydrocephalus may alternatively arise from extra axial impaired resorption of fluid. In the chronic phase, hydrocephalus may be either obstructive or secondary to global parenchymal loss.
Parenchymal foci of increased echogenicity represent infection, hemorrhage, or ischemia. The entire brain may appear edematous due to extensive cerebritis. Especially in the setting of Citrobacter koseri, vasculitis may lead to infarction, necrosis, liquefaction, and abscess formation. Brain abscess initially demonstrates increased echogenicity and hypervascularity, evolving to a complex mass and eventual cavitation with marginal hyperemia.