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Cns infection 2018
- 1. CNS INFECTION EXTERN. SARISASOOTTIWONG 6TH YEARS MEDICAL STUDENT,THAILAND 2018 Tel. +66846299844
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- 3. SKULL OSTEOMYELITIS Skull ishighly vascular and resistant to infections Pathogen S. aureus S. epidermidis Pathogenesis Direct inoculation(More common) ex. pyogenic sinus disease, infected penetrating trauma Hematogenous spreading
- 4. SKULL OSTEOMYELITIS Clinical feature Fever Signsof inflammation Fluid collection/Discharge Pott’s puffy tumor
- 5. SKULL OSTEOMYELITIS Diagnosis Hx,PE Elevate ESR, CRP (Non specific) Fluid collection for G/S, C/S Treatment Combination Surgical debridement Antibiotic i.v. first 2 wks then high dose oral form after surgery 6- 12 wks
- 6. ATB FOR CSFPENETRATING
- 7. EPIDURAL ABSCESS OFBRAIN
- 8. EPIDURAL ABSCESS OFBRAIN Pathogen S. aureus S. epidermidis Pathogenesis เเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเเ เเเเเเเเเ เเเเ Air sinus infection, Skull osteomyelitis
- 9. EPIDURAL ABSCESS OFBRAIN Clinical feature Fever, headache Focal neurologic deficit Signs of increased intracranial pressure Meningeal irritation signs Stiff neck Seizure
- 10. EPIDURAL ABSCESS OFBRAIN Diagnosis CT/MRI c contrast Finding -> Extradural enhancing collection (LP frequently fails to yield the offending organism and risks herniation due to mass effect) Treatment Emergency condition Craniectomy + Drainage ATB 6-12 wks
- 11. EPIDURAL ABSCESS OFBRAIN Brain magnetic resonance images without and with contrast Metastatic Epidural Bacterial Abscess
- 12.
- 13. SUBDURAL EMPYEMA Collection ofpus in the subdural space Widely spreading more than Epidural and Brain abscess Pathogenesis contiguous spread ex Air sinus infection, ear infection, Mastoiditis, Epidural abscess After surgery/ device insertion beneath Dura Infection of pre-existing subdural blood: septicemia
- 14. SUBDURAL EMPYEMA Pathogens: Aerobicstreptococcus 30-50% Staphylococcus 15-20% Microanaerobic and anaerobic 15-25% Streptococci Aerobic gram negative rods 5-10% Other anaerobe 5-10%
- 15. SUBDURAL EMPYEMA Clinicalfeature More severe than Epidural abscess Rapidly progressive Lacks significant barriers ex compartmentalization, septation Status epilepticus may occur Diagnosis CT/MRI c contrast Enhancing collection in subdural space Severe brain edema
- 16. SUBDURAL EMPYEMA Magnetic resonanceimaging revealing a right subdural empyema with meningeal enhancement
- 17.
- 18. SUBDURAL EMPYEMA Treatment Emergency -> Drainage + lavage to decrease inflammatory material causing CorticalVein thrombosis Burr hole drainage or small craniotomy 1 to 2 months of antibiotics 10% to 20% mortality risk chronic sequelae : seizure disorder, residual hemiparesis.
- 19.
- 20. BRAIN ABSCESS • Afocal intracranial infection that is initiated as an area of cerebritis and evolves into a collection of pus surrounded by a vascularized capsule
- 21. EPIDEMIOLOGY Higher incidencein developing countries Men more common than women Differences in age are based on the primary site of infection Otitic focus : < 20 years or > 40 years Paranasal sinuses : 30 - 40 years.
- 22. RISK FACTORS pulmonaryabnormalities congenital cyanotic heart disease bacterial endocarditis penetrating head trauma AIDS
- 23.
- 24. PATHOGENESIS o Contiguous sourceof infection o Usually single brain abscess o Infections in the middle ear , mastoid cells , or paranasal sinuses • Otitis media : temporal lobe or cerebellum • Paranasal sinusitis : frontal lobe • Sphenoid sinusitis : temporal lobe or sella turcica • Dental infections (molar teeth) : frontal lobe
- 25. PATHOGENESIS Hematogenous (10-15%) •Multiple , multiloculated abscesses , grey-white matter junction(site of greatest blood flow) • The most common sources : lung • Chronic pyogenic lung diseases : lung abscess • Bronchiectasis • Empyema • Cystic fibrosis
- 26. PATHOGENESIS • Hematogenous dissemination •Other : wound & skin infections , osteomyelitis , pelvic infections , and intra-abdominal infections • Cyanotic heart disease (TOF ,TGA) : common cause in pediatrics • Bacterial endocarditis
- 27. PATHOGENESIS Direct penetratingtrauma Open head injury Neurosurgical procedure Foreign body No obvious source 25%
- 28. MICROBIOLOGY • Bacteria isthe most common • Streptococcus spp. • Enteric gram-negative bacilli • Proteus spp. , Escherichia coli, Klebsiella spp. , Pseudomonas aeruginosa and Enterobacter spp. • Staphylococcus aureus • Anaerobes • Bacteroides spp. and Prevotella spp
- 30. MICROBIOLOGY • Fungus • mostcommon : Candida spp. • Risk factor • The use of broad-spectrum antimicrobial agents • Corticosteroids • Diabetes mellitus
- 32. PATHOPHYSIOLOGY Early cerebritis Late cerebritis Earlycapsule formation Late capsule formation
- 33. PATHOPHYSIOLOGY 1.Early cerebritis (Day0-3) Histopathology - Central zone of necrosis - local inflammatory response - Marked peri-lesion edema - Poor demarcation from adjacent brain CT - Poor marginated area of hypodensity - Minimal if any enhancement with IV contrast
- 34. PATHOPHYSIOLOGY 2. Late cerebritis Day 4-9 Histopathology - Pus - Enlargement of necrotic center - Maximal cerebral edema - Reticulin network as precu rsor to capsule
- 35. 2. LATE CEREBRITIS(CON’T) CT - Hypodensity area still may show poor margination - Patchy enhancement duri ng early part of phase - Rim-enhancement begins late r in phase - Central hypodense areas fil ls in with contrast on delayed scans
- 36. 3. Early capsuleformation Day 10-14 Histopathology - Continue formation of pus - Development of collagen capsule - Cerebral edema surrounding capsule CT - Well-defined rim enhancing - mass; an outer hypodens rim (double rim sign)
- 37. 4. Late capsuleformation Day >14 Histopathology 5 distinct zone (a) Necrotic center filled with pus (b) Peripheral zone of inflammatory cell and fibroblasts (c) Dense collagen capsule (d) Layer of neovascularity with residual cerebritis (e) Zone of edema and reactive gliosis
- 38. 4. Late capsule formation(con’t) CT - Rim enhancing lesion - Thickned capsule - Diminisned hypodense central cavity
- 39. HISTOLOGIC STAGING OFCEREBRAL ABSCESS
- 40. CLINICAL FEATURES • Signs& symptom : related to size, location ,virulence of the organism • Classical triad <50% : • headache • fever • focal neurological deficit • Sudden worsening of the headache & new onset of meningismus, may signify rupture of the abscess into the ventricular space
- 42. INVESTIGATION BLOODWORK - PeripheralWBC: may be normal or only mildly elevated in 60-70% of cases (usually > 10,000) - Blood cultures: usually negative - ESR: may be normal - C-reactive protein (CRP): infection anywhere in body can raise the level. Patients with brain tumor and other inflammatory condition (e.g. dental abscess) may have and elevated CRP level. Sensitivity is 90%, specificity is 77%
- 43. INVESTIGATION Lumbar puncture No characteristic finding diagnostic of abscess Open pressure is usually increase,WBC count and protein may be elevated Organism can rarely identified from CSF by LP Risk of transtentorial herniation,especially with large lesions Due to the risk and the low yield of useful information,avoid LP if not already done
- 44. INVESTIGATION • Imaging • MRI: gold standard • CT with contrast : Rim enhancing lesion, smooth & thin wall with surrounding edema
- 46. TREATMENT Medical Abscess <3 cm Multiple small abscesses Difficult area Early cerebritis phase High surgical risk ATB 6-8 wk Empirical tx : Vancomycin Cloxacillin+ Ceftriazone+ Metronidazole Supportive treatment Dexamethasone Anticonvulsant
- 48. SURGICAL MANAGEMENT • Needleaspiration after burr-hole • Indication Well encapsulated > 3 cm Nearly to ventricle • No response to antibiotics • Preferable
- 49. SURGICAL MANAGEMENT • Completeexcision after craniotomy • Indication • Multiloculated abscess • Traumatic brain abscess (to remove bone fragment or foreign body) • Encapsulated fungal brain abscess • Gas-forming lesion
- 51. CLINICAL COMPLICATIONS Abscessrupture transforms localized infection -Meningitis -Ventriculitis Elevated ICP may cause uncal hernia and subsequently death Seizure
- 52. OUTCOME Mortality ranged form40-60% With improvement in antibiotics, surgery, and the improved ability to diagnose and follow response with CT and/or MRI, mortality rate has been reduced to 10% But morbidity remains high with permanent neurologic deficit or seizures in up to 50% of cases A worse prognosis is associated with poor neurologic function, intraventricular rupture of abscess
- 54.
- 55. SPINAL ABSCESS Intraspinalabscess เเเเเเเเเเเเเเเเเเเเเเ เเเเเ Morbidity เเเ Mortalityเเเ เเเเเเเเ Spinal epidural abscess (most common) Spinal subdural abscess Intramedullary abscess
- 56. SPINAL EPIDURAL ABSCESS Posteriorly, the epidural space contains fat, small arteries, and the venous plexus Anteriorly, the epidural space is a potential space with the dura tightly adherent to the vertebral bodies and ligaments Most spinal epidural abscesses occur in the thoracic area, which is anatomically the longest of the spinal regions
- 57. PATHOGENESIS Hematogenous :bacterial endocarditis, infected indwelling catheters, urinary tract infection, peritoneal and retroperitoneal infections, and others. Symptoms progress rapidly Direct extension : from vertebral osteomyelitis, Psoas abscess , Epidural injections or catheters. Slow progression of symptoms
- 59. PATHOGENSIS Staphylococcus aureus Staphylococcus and Pseudomonas species, Escherichia coli, Brucella, and Mycobacterium tuberculosis. MRSA : history of MRSA abscesses, spinal surgery, or implanted devices Fungal infections : Immunosuppressed patients
- 60. RISK FACTOR DM IVDU Alcoholism chronic immunosuppression, older adult hemodialysis patients
- 61. CLINICAL FEATURES Fourphases I. localized spinal pain II. radicular pain and paresthesias III. muscular weakness, sensory loss, and sphincter dysfunction IV. paralysis Fever 30% Headache & neck pain
- 62. INVESTIGATION Imaging MRIis the procedure of choice CT myelography : intraspinal extramedullary mass LP is relatively contraindicated : risk of introducing purulent material into the subarachnoid space
- 63. TREATMENT Laminectomy +Drainage ATB 6-8 wk
- 64.
- 65. TUBERCULOMA Tuberculoma เเเเเเเเเเเเเเเเเเเเเเเเ เเเเเเเเเเเเเเเเเเเเเเเเเเเเ เเเเเเเเเเเเเเเ เเเเเเเเเเเเเเเเเ เเเเเเ เเเเเเเเเเเเเเเเ เเเเเเเเเ caseous necrosis
- 66. TUBERCULOMA Clinical feature เเเเเเเเเเเเเเเเเเเเเเเเเเเเ เเเเเเเเเเเเเเเเเเเเเเเเเเ เเเเเเ Investigation CT brain c contrast Mass Hydrocephalus CXR -> Pulmonary TB Film skull -> Calcified tuberculoma
- 67.
- 68. TUBERCULOMA Treatment Anti TBdrug Surgical removal เเเเเเเเเเเเเเเเเเเเเเเเเเเเเ
- 69.
- 70. CEREBRAL CYSTICERCOSIS Ingestionof eggs of Taenia solium Most common parasitic disease of the nervous system Pathogenesis เเเเเเเเเเเเเเเเเเเเเเเเเเเ เเเเเเเเเเเเเเเเเเเเเเเเเเ Scolex เเเเเเ เเเเเเเเเเเเเเเเเเเเเ เเเ เเ infarct เเเเเเเเเเ เเเเเเเเเเเเเเเเเเเเเเเเเเเเเเ เเเเเเเเเเ Hydrocephalus เเเเเเ 1.5-2 เเ เเเเเ เเเ Scolexเเเเเ เเเเเเเ เเเเเเเเ เเ Calcified
- 72. CEREBRAL CYSTICERCOSIS Pathology4 ชชชชชชชชชชชชชชช Meningeal form Parenchymatous form Ventricalar form Mixed form
- 73. CEREBRAL CYSTICERCOSIS Clinicalfeature Epilepsy: Most common presentation (70%) Headache, dizziness Neuropsychiatric dysfunction Cognitive decline Dysarthria severe dementia
- 74. CEREBRAL CYSTICERCOSIS Clinicalfeature Stool exam 10-15% taeniasis CSF Mononuclear pleocytosis Eosinophilia Normal or low glucose levels Elevated protein levels Immunology ELISA for neurocysticercosis CT brain
- 77. CEREBRAL CYSTICERCOSIS Medicaltreatment Anticonvulsant Steroid Anti helminthic therapy : Praziquantel Surgical treatment Indication Hydrocephalus V-P shunt,V-A shunt Mass effect -> Obstructive hydrocephalus Surgical removal
Editor's Notes
- #4 The decline of fulminant osteomyelitis of the skull from a routine event to a rare occurrence has largely paralleled the emergence of potent antibiotics. Today, osteomyelitis of the skull usually presents as a chronic process that occasionally complicates craniotomies and scalp injuries
- #5 non-neoplastic complication of acute sinusitis characterised by subperiosteal abscess and osteomyelitis opacified frontal sinus with stranding and swelling of the overlying scalp. Bone algorithm will often demonstrate a defect in the anterior wall of the sinus.
- #6 ESR provides a useful marker to monitor the efficacy of therapy using serial determinations CRP levels rise and fall rapidly after surgery, thus making it a good indicator of acute infections, recovery, and relapse osteopenia, subtle erosion of inner and outer tables, and gross lytic destruction
- #10 Inflammation of cortical blood vessels, leading to thrombosis and stroke Cerebritis
- #11 LP frequently fails to yield the offending organism and risks herniation due to mass effect ไม่ว่าจะขนาดเล็กแค่ไหนก็ตาม เพราะอาจเกิด Subdural empyema หรือ Cortical vein thrombosis ตามมาได้
- #27 Brain abscess เพิ่มมากขึ้นหากมี Cerebral infarction
- #41 shows signs of meningitis but examination revealsno pathological changes in the meninges. headache,neck stiffness
- #56 Posteriorly, the epidural space contains fat, small arteries, and the venous plexus Anteriorly, the epidural space is a potential space dura adherent to vertebral bodies and ligaments
- #78 due to inflammation and fibrosis of the arachnoid villi or inflammatory reaction to the meninges and subsequent occlusion of the foramina of Luschka and Magendie Noncommunicating hydrocephalus may be a consequence of intraventricular cysts.