scribd01.pptx Acute bacterial meningitis

Acute bacterial meningitis

1. Acute Bacterial meningitis Bacterial meningitis is an acute purulent infection within the Subarachnoid space ↓ Consciousness,seizures , ↑ICP, and stroke Common form of suppurative CNS infection Community acquired Bacterial meningitis: • Streptococcus pneumoniae ~50% • Neisseria meningitidis ~25% • Group B streptococci ~15% • Listeria monocytogenes ~10% • Hemophilus influenzae type B <10%

2. ETIOLOGY • S. pneumoniae • N. meningitidis • Gram negative bacilli • Group B sreptococcus • L. monocytogenes • H. influenzae type b • S. aureus & coagulase negative staphylococci

3. PATHOPHYSIOLOGY • Colonize the Nasopharynx • Transported across the epithelial cells

4. CLINICAL PRESENTATION • Fever, Headache, Neck Rigidity • Decreased level of Consciousness • Nausea, Vomiting, Photophobia • Nuchal Rigidity • Kernig’s Sign • Brudzinski’s Sign • Seizures Focal- Generalized •Raised ICP-Cushing’s Reflex

5. DIAGNOSIS Blood Cultures should be obtained immediately • CSF Examination • Neuroimaging • Petechial Lesion biopsy for meningococci

6. TREATMENT

7. Dexamethasone The use of adjunctive corticosteroids is controversial. Based on the existing current evidence they are not recommended in low- and middle-income countries as they do not demonstrated benefit If used; Dexamethasone 10 mg IV QID for 04 days

8. Encephalitis Encephalitis is defined as an inflammation of the brain caused either by infection, usually with a virus, or from a primary autoimmune process

9. CLINICAL PRESENTATION Commonly has an altered level of consciousness Hallucinations, agitation, personality change, behavioral disorders Focal or generalized seizures Focal neurologic disturbance

10. Involuntary movements Involvement of the hypothalamic-pituitary axis may result in Temperature dysregulation , Diabetes insipidus SIADH

11. CSF Examination The characteristic CSF profile Lymphocytic pleocytosis Mildly elevated protein concentration, Normal glucose concentration. A CSF pleocytosis occurs in >95% of immunocompetent patients CSF cell counts exceed 500/ μL in only about 10% of patients with encephalitis.

12. CSF PCR Primary diagnostic test for CMV, EBV, HHV-6, and enteroviruses The sensitivity (~96%) and specificity (~99%) of HSV CSF PCR Enteroviral (EV) CSF PCR appears to have a sensitivity and specificity of >95%.

13. TREATMENT Basic management and supportive therapy Acyclovir HSV Severe encephalitis due to VZV or EBV. Ganciclovir and foscarnet CMV-related CNS infections

14. Normal intracranial pressure (ICP) is defined as < 15 mm Hg, whereas pathologically increased ICP is any pressure ≥ 20 mm Hg.

15. Clinical Presentation Management of increased ICP headaches and papilledema . History Intense headache Visual symptoms: Blurry vision Photophobia Drowsiness Projectile vomiting Recent medical history: Trauma Stroke Cancer Metabolic diseases

16. Eye exam: Papilledema on ophthalmoscopy Cranial nerve (CN) VI ( abducens nerve) palsy Spontaneous periorbital bruising Cushing triad (possibly due to brainstem compression): Widened pulse pressure (↑ difference between systolic and diastolic blood pressure) Bradycardia Irregular respiration

17. Altered mental status (coma in some individuals) Seizures Focal and progressive neurologic changes can be seen due to Local effects of mass lesions Herniation

18. Urgent neuroimaging : brain CT or MRI- Signs of brain edema: Loss of gray/white matter differentiation Compression of the ventricles Obliteration of sulci Localized edema = midline shift Herniation Lumbar puncture (LP): Indicated if there are no structural abnormalities on neuroimaging Done after brain imaging to avoid herniation from a rapid decrease in ICP Elevated opening pressure (> 250 mm H2O) confirms the diagnosis CSF studies for infection, blood, other testing

19. Initial management: Immediate support of oxygenation and blood pressure Paralytic agents and adequate sedation to minimize further increases in ICP (if intubation is needed) Close monitoring of vitals and ECG Avoid hypotonic fluids to prevent worsening of brain edema.

20. Measures to decrease ICP: Elevate the head of the bed > 30º → promotes venous return Hyperventilation (decrease pCO2 to 25–30 mm Hg) → decreases cerebral blood flow (CBF) Mannitol : reduces intravascular volume → results in osmotic gradient → fluid moves from the extracellular to the intravascular space → brain edema is reduced Hypertonic saline (bolus or continuous infusion): Tonicity of the blood increases → concentration gradient is created → fluid moves from the extracellular to the intravascular space → brain edema is reduced Monitor serum Na Maintain euvolemia Acetazolamide = a diuretic to decrease the production of CSF Induced coma ( propofol ): reduces sympathetic activity and metabolic demand Anticonvulsants if seizures Antipyretics if febrile (e.g., with encephalitis)

21. ICP monitoring: Intraventricular = gold standard Intraparenchymal Subarachnoid Epidural Removal of CSF: if hydrocephalus is identified → ventriculostomy drainage Surgery: decompressive craniectomy Normalizes ICP by opening the skull Definitive treatment for masses (e.g., blood clots, tumors)

22. REFERNCES Harrison principle of Internal Medicine 21st ed. page 4118-4180 STG for General Hospitals 4th ed.(2021) Up todate