A 23 yo male with history of admission for head injury ~ 6 month back, frontal lobe contusions and fractures of floor of anterior cranial fossa.
Now readmission for recent onset severe headache and neck stiffness, clinically signs of meningitis.
Immediate Post admission MRI Axial FLAIR image of Brain shows:
1. Focal cortical Gliosis involving frontal lobes near orbital surface more obvious on right side, possible secondary to previous head injury.
2. A focal dural thickening in left frontal region near floor of anterior cranial fossa.
3. Mild diffuse cerebral odema, T2 hyperintensity in the region of cortical sulci particularly in the dependent portions of brain suggestive of meningitis.
4. Marked mucosal thickening and collection ethmoid air cells.
A focal dural thickening in left frontal region near floor of anterior cranial fossa, mild diffuse cerebral odema, T2 hyperintensity in the region of cortical sulci in the dependent portions of brain suggestive of meningitis. An associated mucosal thickening and collection ethmoid air cells appears to be related to each other secondary to a possible fracture involving floor of anterior cranial fossa which may not be seen on MRI.
Conclusion: Meningitis as a delayed complication of head injury.
Post-traumatic meningitis in head injured patients is uncommon, reported in 0.38-2.03%.
A skull fracture with accompanying dural tear results in a CSF fistula is typical, allows the subsequent passage of microorganisms into the cranial compartment. While CSF leak may resolve spontaneously, patients remain at risk for PTM as dural healing may be absent. Pneumocephalus which is seen in 86% of those with skull base fractures, is indicative of a dural tear with passage of air into the cranial cavity from an adjacent paranasal sinuses or mastoid. PTM has also been reported with fractures across infected paranasal sinuses, middle ear structures, and mastoid air cells without a dural tear.
Clinical presentation
The time between injury and diagnosis of PTM ranges from less than 24 hours to many years.
Signs and symptoms in PTM are variable. Fever (in 86-100%), deterioration in consciousness (in 97-100%) may be extremely rapid and progressive.
Triad of fever, stiff neck, and change in mental status.
Headache is also common (in 57-86%)
Causative agents for PTM include a wide range of both gram-positive and gram-negative organisms. Streptococcus pneumoniae is the most common agent and is isolated in 52-100% of cases. Other often reported gram-positive organisms include Staphylococcus aureus and streptococcal species. Gram-negative organism encountered in 17-100% and is most often noted with open cranial wounds or lengthy hospitalizations. Commonly isolated gram-negative bacteria include Escherichia coli, Klebsiella pneumoniae, Neisseria meningitidis, Haemophilus influenzae and Pseudomonas aeruginosa.
The diagnosis of PTM is usually made by CSF cultures. Cultures may fail to yield an isolate; negative cultures have been reported in up to 27% of cases. The reason may be patient is already receiving prophylactic antibiotics.
Antibiotics should be chosen in accordance with the clinical situation and ability to penetrate the blood-brain barrier. Broad spectrum antibiotics are the choice.
Pneumonia, deafness, anosmia, mental retardation, or other major neurologic deficits are the common complications of PTM.
Now readmission for recent onset severe headache and neck stiffness, clinically signs of meningitis.
Immediate Post admission MRI Axial FLAIR image of Brain shows:
2. A focal dural thickening in left frontal region near floor of anterior cranial fossa.
3. Mild diffuse cerebral odema, T2 hyperintensity in the region of cortical sulci particularly in the dependent portions of brain suggestive of meningitis.
4. Marked mucosal thickening and collection ethmoid air cells.
A focal dural thickening in left frontal region near floor of anterior cranial fossa, mild diffuse cerebral odema, T2 hyperintensity in the region of cortical sulci in the dependent portions of brain suggestive of meningitis. An associated mucosal thickening and collection ethmoid air cells appears to be related to each other secondary to a possible fracture involving floor of anterior cranial fossa which may not be seen on MRI.
Conclusion: Meningitis as a delayed complication of head injury.
POST TRAUMATIC MENINGITIS
A skull fracture with accompanying dural tear results in a CSF fistula is typical, allows the subsequent passage of microorganisms into the cranial compartment. While CSF leak may resolve spontaneously, patients remain at risk for PTM as dural healing may be absent. Pneumocephalus which is seen in 86% of those with skull base fractures, is indicative of a dural tear with passage of air into the cranial cavity from an adjacent paranasal sinuses or mastoid. PTM has also been reported with fractures across infected paranasal sinuses, middle ear structures, and mastoid air cells without a dural tear.
Clinical presentation
The time between injury and diagnosis of PTM ranges from less than 24 hours to many years.
Signs and symptoms in PTM are variable. Fever (in 86-100%), deterioration in consciousness (in 97-100%) may be extremely rapid and progressive.
Triad of fever, stiff neck, and change in mental status.
Headache is also common (in 57-86%)
Causative agents for PTM include a wide range of both gram-positive and gram-negative organisms. Streptococcus pneumoniae is the most common agent and is isolated in 52-100% of cases. Other often reported gram-positive organisms include Staphylococcus aureus and streptococcal species. Gram-negative organism encountered in 17-100% and is most often noted with open cranial wounds or lengthy hospitalizations. Commonly isolated gram-negative bacteria include Escherichia coli, Klebsiella pneumoniae, Neisseria meningitidis, Haemophilus influenzae and Pseudomonas aeruginosa.
The diagnosis of PTM is usually made by CSF cultures. Cultures may fail to yield an isolate; negative cultures have been reported in up to 27% of cases. The reason may be patient is already receiving prophylactic antibiotics.
Antibiotics should be chosen in accordance with the clinical situation and ability to penetrate the blood-brain barrier. Broad spectrum antibiotics are the choice.
Pneumonia, deafness, anosmia, mental retardation, or other major neurologic deficits are the common complications of PTM.
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