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Subdural empyema
- 1. SUBDURAL EMPYEMA DR ADARSH I NATH SENIOR RESIDENT DEPT OF NEUROSURGERY
- 3. INTRODUCTION • Suppuration in the “preexisting space” between the dura and arachnoid. • Also known as – Pachymeningitis Interna/ Purulent Pachymeningitis. • Serious illness associated with frequent neurologic sequalae , resulting in mortality rates up to 10-20%. • It constitutes to about 13-23% of all the intracranial bacterial infections & presents as a fulminant picture • Surgical Emergency
- 4. • ETIOLOGY • CLINICAL FEATURES • INVESTIGATIONS • MICROBIOLOGY • MANAGEMENT • DIFFERENTIAL DIAGNOSIS
- 7. • ETIOLOGY • CLINICAL FEATURES • INVESTIGATIONS • MICROBIOLOGY • MANAGEMENT • DIFFERENTIAL DIAGNOSIS
- 8. ETIOLOGY • Most commonly supratentorial • Generally as secondary spread • Paranasal sinus infection – (40-80%)- Retrograde thrombosis/ Direct Spread • Otitis Media/ Mastoiditis – (10-20%)- Direct Spread- Temporal & Occipital • Trauma/ Iatrogenic – 20%- Less fulminant, • Subdural Effusion • Meningitis- Neonates (2-10%) The mechanism of the development in infants is through infection of sterile, reactive subdural effusions secondary to meningitis. • Hematogenous (distant) – 5% of the cases.
- 9. • ETIOLOGY • CLINICAL FEATURES & PATHOPHYSIOLOGY • INVESTIGATIONS • MICROBIOLOGY • MANAGEMENT • DIFFERENTIAL DIAGNOSIS
- 10. CLINICAL FEATURES • Usually Dramatic/ Fulminant • Mainly due to the Bacterial Toxins & Cortical Venous Thrombosis – Infarction. • Altered Sensorium • Features of Raised ICP – (Cerebral Oedema & Hydrocephalus) • Speech disturbances/ Hemiparesis/ Seizures may also been seen • Generally symptoms to diagnosis is usually 4 days • Diagnosed Clinically – High Index of suspicion. • Post OP- Sepsis + Seizures ( 25%), Generally by 1 month
- 12. • Therefore the clinical features of the Subdural Empyema is due to • 1) Features of Raised ICP • 2) Meningeal Irritation ( 80%) • 3) Focal Cortical Inflammation • * In cases secondary to Post OP, Previous Antibiotic, Infected Subdural Hematoma & Hematogenous – Patients are generally less symptomatic & presents with seizures.
- 13. PATHOPHYSIOLOGY • Subdural empyema most often occurs due to the direct extension of local infection. • The infection can spread to the intracranial compartment due to the valveless diploic veins of Breschet. • As a result, blood may flow in either direction, causing the spread of bacterial infection intracranially • They can also occur after cranial surgical procedures secondary to the inoculation of microorganisms into the subdural space, further developing into a subdural empyema.
- 14. • Fulminant Nature of the Subdural Empyema • 1) Lack of Fibrin Capsule within the subdural space • 2) Lack of Anatomical Barriers.
- 16. • ETIOLOGY • CLINICAL FEATURES • INVESTIGATIONS • MICROBIOLOGY • MANAGEMENT • DIFFERENTIAL DIAGNOSIS
- 17. INVESTIGATIONS • Blood Routine –Leukocytosis with Left sided shift - Neutrophils • CRP/ ESR – Inflammatory Markers. • Blood Culture • LP – Not Indicated. • Imaging
- 19. IMAGING • CT Head- When using CT as an imaging modality, SDE will appear crescentic in shape over the cerebral convexity with a surrounding rim that is enhanced with the use of contrast. • MRI Brain – The diagnostic imaging study of choice for intracranial subdural empyema is a magnetic resonance imaging (MRI) with intravenous gadolinium enhancement • High signal Intensity on DWI, Low signal on ADC, ADC Value less than normal cortical Grey Matter • Diffusion MRI – Can differentiate between Subdural Empyema and Subdural Effusion.
- 25. • ETIOLOGY • CLINICAL FEATURES • INVESTIGATIONS • MICROBIOLOGY • MANAGEMENT • DIFFERENTIAL DIAGNOSIS
- 26. MICROBIOLOGY • Culture & Sensitivity is generally negative in ( 7-53%) • Paranasal Sinusitis- Aerobic/ Microaerophilic Streptococci, Anaerobes • Post Traumatic / Iatrogenic – Staph Aureus • Meningitis – H. Influenzae / Streptococcus Pneumoniae. • Rarer Organisms- Salmonella/ E.Coli / Other Organisms • Dural Allografts – Propionibacterium Acnes.
- 28. • ETIOLOGY • CLINICAL FEATURES • INVESTIGATIONS • MICROBIOLOGY • MANAGEMENT • DIFFERENTIAL DIAGNOSIS
- 29. MANAGEMENT • Neurosurgical emergency • Early Surgery – Craniotomy/ Craniectomy/ Evacuation of Empyema • Followed by Antibiotics • Vancomycin + 3rd Generation Cephalosporins • Continued for 4 to 6 weeks & A follow up scan to be planned during this period
- 30. SURGICAL MANAGEMENT • Craniotomy – (11-8 %) • CT Guided Burr Holes – ( 23.3%)
- 31. SEQUALE
- 32. • ETIOLOGY • CLINICAL FEATURES • INVESTIGATIONS • MICROBIOLOGY • MANAGEMENT • DIFFERENTIAL DIAGNOSIS
- 33. DIFFERENTIAL DIAGNOSIS • Subdural Hygroma • Subdural Effusion • Epidural Abscess • Cerebral Abscess
- 34. EPIDURAL ABSCESS • Between the skull & Dura • Generally in frontal region – as a result of contiguous spread from PNS • Indolent Lesion ( Dura Mater protects the brain ) • Fever/ Headache/ Neurologic Signs – Due to the mass effect rather than infiltration. • Treatment is mainly conservative with antibiotics • If Untreated- It can spread intracranially – Septic Thrombophlebitis • MRI Shows – Thickened Dural Surface.
- 35. SUBDURAL HYGROMA • Excess fluid in the subdural space (may be clear, blood tinged, or xanthochromic and under variable pressure). • Mechanism of formation of hygroma is probably a tear in the arachnoid membrane with resultant CSF leakage into the subdural compartment. Hygroma fluid contains pre-albumin, which is also found in CSF but not in subdural hematomas. • Another possible mechanism is post-meningitis effusion. • May increase in size (possibly due to a flap-valve mechanism) • On CT, the density of the fluid is similar to that of CSF. • Signal characteristics on MRI follow those of CSF
- 36. SUBDURAL EFFUSION/ CHRONIC SDH • Classically CSDHs contain dark “motor oil” fluid which does not clot. • Blood within the subdural space evokes an inflammatory response. Within days, fibroblasts invade the clot and form neomembranes on the inner (cortical) and outer (dural) surface. • This is followed by ingrowth of neocapillaries, enzymatic fibrinolysis, and liquefaction of blood clot. • Patients may present with minor symptoms of headache, confusion, language difficulties (e.g. word Finding difficulties or speech arrest, usually with dominant hemisphere lesions), or TIA-like symptoms
- 37. CEREBRAL ABSCESS • Adults: no findings are specific for abscess, and many are due to edema surrounding the lesion. • Most symptoms are due to increased ICP (H/A, N/V, lethargy). Hemiparesis and seizures develop in 30–50% of cases. Symptoms tend to progress less rapidly than with empyema • It takes at least 2 weeks to progress through this maturation process, • Diffusion MRI: DWI → bright, ADC → dark (restricted diffusion suggesting viscous fluid)
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