A loculated pus accumulation in the subdural space between the dura mater and arachnoid is characterized as an intracranial subdural empyema. Subdural empyema is also classified as Focal intracranial infection.
The subdural space is uninterrupted and possesses no anatomical barrier hence empyema spread in the vast contours of the brain between both hemispheres.
Epidemiology
Children and young adults are most affected by intracranial subdural empyema. Males are affected more frequently than females, with a male to female ratio of 3:1. Its prevalence has been estimated to be 11 cases per 100,000 people. Subdural empyema, which develops in the spinal canal, is infrequent.
Anatomy
Pathophysiology
The most common causative factor is a localized infection. This infection further spreads to the intra-cranial compartments due to the lack of valves in diploic veins. Since the veins are valveless, the bacterial infection spreads intracranially due to blood flow in either direction.
It can also occur after cranial operative procedures, and subdural empyema develops due to the inoculated microorganisms in the subdural space.
Etiology
Polymicrobial infections are common in this condition. Streptococcus pneumoniae, Haemophilus influenzae, Streptococci, Staphylococci, and other gram-negative bacilli are among the most prevalent microbes. Staphylococcus aureus is associated with cases of cranial trauma and surgical intervention.
Moreover, in cases of paranasal sinusitis, anaerobic and aerobic streptococci are frequently documented microorganisms. Purulent meningitis is considered a complication in infants, and exposure to bacterial foci in children of older age gives rise to subdural empyema. Subdural empyema caused by bacterial meningitis is rare in adults.
The risk factors include infected hematoma, subdural effusion, prior cranial surgery, penetrating head injury, and trauma with open skull fractures. Prior failed treatment of ear and sinus infections (most associated with otitis media).
Genetics
Prognostic Factors
This condition is often associated with severe neurological complications such as cerebral edema, cerebral abscess, seizures, hydrocephalus, sepsis, septic shock, electrolyte imbalances, infection in adjacent cranial bones, and residual neurological deficits. Comatose, supine patients with severe disease progression have a higher mortality risk.
Patients with co-morbidities, secondary infection, and cranial surgery are at higher risk of neurological deficit. The prognosis of the disease depends upon the level of consciousness, the intervention’s time frame, and the treatment’s aggressiveness.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
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References
https://www.ncbi.nlm.nih.gov/books/NBK557829/
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A loculated pus accumulation in the subdural space between the dura mater and arachnoid is characterized as an intracranial subdural empyema. Subdural empyema is also classified as Focal intracranial infection.
The subdural space is uninterrupted and possesses no anatomical barrier hence empyema spread in the vast contours of the brain between both hemispheres.
Children and young adults are most affected by intracranial subdural empyema. Males are affected more frequently than females, with a male to female ratio of 3:1. Its prevalence has been estimated to be 11 cases per 100,000 people. Subdural empyema, which develops in the spinal canal, is infrequent.
The most common causative factor is a localized infection. This infection further spreads to the intra-cranial compartments due to the lack of valves in diploic veins. Since the veins are valveless, the bacterial infection spreads intracranially due to blood flow in either direction.
It can also occur after cranial operative procedures, and subdural empyema develops due to the inoculated microorganisms in the subdural space.
Polymicrobial infections are common in this condition. Streptococcus pneumoniae, Haemophilus influenzae, Streptococci, Staphylococci, and other gram-negative bacilli are among the most prevalent microbes. Staphylococcus aureus is associated with cases of cranial trauma and surgical intervention.
Moreover, in cases of paranasal sinusitis, anaerobic and aerobic streptococci are frequently documented microorganisms. Purulent meningitis is considered a complication in infants, and exposure to bacterial foci in children of older age gives rise to subdural empyema. Subdural empyema caused by bacterial meningitis is rare in adults.
The risk factors include infected hematoma, subdural effusion, prior cranial surgery, penetrating head injury, and trauma with open skull fractures. Prior failed treatment of ear and sinus infections (most associated with otitis media).
This condition is often associated with severe neurological complications such as cerebral edema, cerebral abscess, seizures, hydrocephalus, sepsis, septic shock, electrolyte imbalances, infection in adjacent cranial bones, and residual neurological deficits. Comatose, supine patients with severe disease progression have a higher mortality risk.
Patients with co-morbidities, secondary infection, and cranial surgery are at higher risk of neurological deficit. The prognosis of the disease depends upon the level of consciousness, the intervention’s time frame, and the treatment’s aggressiveness.
https://www.ncbi.nlm.nih.gov/books/NBK557829/
medtigo
Subdural Empyema
Updated :
September 17, 2022
A loculated pus accumulation in the subdural space between the dura mater and arachnoid is characterized as an intracranial subdural empyema. Subdural empyema is also classified as Focal intracranial infection.
The subdural space is uninterrupted and possesses no anatomical barrier hence empyema spread in the vast contours of the brain between both hemispheres.
Children and young adults are most affected by intracranial subdural empyema. Males are affected more frequently than females, with a male to female ratio of 3:1. Its prevalence has been estimated to be 11 cases per 100,000 people. Subdural empyema, which develops in the spinal canal, is infrequent.
The most common causative factor is a localized infection. This infection further spreads to the intra-cranial compartments due to the lack of valves in diploic veins. Since the veins are valveless, the bacterial infection spreads intracranially due to blood flow in either direction.
It can also occur after cranial operative procedures, and subdural empyema develops due to the inoculated microorganisms in the subdural space.
Polymicrobial infections are common in this condition. Streptococcus pneumoniae, Haemophilus influenzae, Streptococci, Staphylococci, and other gram-negative bacilli are among the most prevalent microbes. Staphylococcus aureus is associated with cases of cranial trauma and surgical intervention.
Moreover, in cases of paranasal sinusitis, anaerobic and aerobic streptococci are frequently documented microorganisms. Purulent meningitis is considered a complication in infants, and exposure to bacterial foci in children of older age gives rise to subdural empyema. Subdural empyema caused by bacterial meningitis is rare in adults.
The risk factors include infected hematoma, subdural effusion, prior cranial surgery, penetrating head injury, and trauma with open skull fractures. Prior failed treatment of ear and sinus infections (most associated with otitis media).
This condition is often associated with severe neurological complications such as cerebral edema, cerebral abscess, seizures, hydrocephalus, sepsis, septic shock, electrolyte imbalances, infection in adjacent cranial bones, and residual neurological deficits. Comatose, supine patients with severe disease progression have a higher mortality risk.
Patients with co-morbidities, secondary infection, and cranial surgery are at higher risk of neurological deficit. The prognosis of the disease depends upon the level of consciousness, the intervention’s time frame, and the treatment’s aggressiveness.
https://www.ncbi.nlm.nih.gov/books/NBK557829/
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