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  1.  Introduction  Pathophysiology  Epidemiology  Clinical Features  Differential Diagnosis  Complications  Management  Prognosis  Prevention
  2.  Meningitis is a potentially life-threatening infection of the meninges-the tough layer of tissue that surrounds the brain and the spinal cord.  If not treated, meningitis can lead to brain swelling and cause permanent disability, coma, and even death.  Meningitis can be life-threatening because of the inflammation's proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency.
  3.  Meningitis can be caused by a variety of things, including bacteria (the most serious), viruses, fungi, reactions to medications, and environmental toxins such as heavy metals.  Although bacterial and fungal meningitis require extended hospitalization, meningitis caused by viruses can often be treated at home and has a much better outcome.
  4.  Although meningitis is a notifiable disease in many countries, the exact incidence rate is unknown.  In sub-SaharanAfrica, large epidemics of meningococcal meningitis occur in the dry season, leading to it being labeled the "meningitis belt"; annual rates of 500 cases per 100,000 are encountered in this area, which is poorly served by medical care.
  5. A. Bacterial  Bacterial meningitis is usually part of a bacteraemic illness, although direct spread from an adjacent focus of infection in the ear, skull fracture or sinus can be causative.  The types of bacteria that cause bacterial meningitis vary by age group;
  6. In premature babies and newborns up to three months old, common causes are group B streptococci ,Escherichia coli & Listeria monocytogenes. Older children are more commonly affected by Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) .
  7. Under five by Haemophilus influenzae type B  In adults, N. meningitidis and S. pneumoniae together cause 80% of all cases of meningitis, with increased risk of L. monocytogenes in those over 50 years old. Recent trauma to the skull gives bacteria in the nasal cavity the potential to enter the meningeal space i.e staphylococcus,
  8.  Immune deficiencies such as complement deficiency, which predisposes especially to recurrent meningococcal meningitis  Tuberculous meningitis, meningitis due to infection with Mycobacterium tuberculosis
  9.  Viruses are the most common cause of meningitis, usually resulting in a benign and self-limiting illness requiring no specific therapy.  Occurs mainly in children or young adults, with acute onset of headache, irritability and the rapid development of meningism.  Headache is usually the most severe feature.
  10.  There may be a high pyrexia but focal neurological signs are rare  Viruses that can cause meningitis include; Enteroviruses- most common  Herpes simplex virus type 2- mollarets meningitis (and less commonly type 1)
  11.  Varicella zoster virus (known for causing chickenpox and shingles)  Mumps virus- where there is no immunization program  HIV CMV
  12.  The term aseptic meningitis refers to all cases of meningitis in which infection can be demonstrated.
  13.  Meningitis may occur as the result of several non- infectious causes: Spread of cancer to the meninges (malignant meningitis)  Certain drugs (mainly non-steroidal anti- inflammatory drugs, antibiotics and intravenous immunoglobulins).  Inflammatory conditions such as sarcoidosis  Connective tissue disorders such as systemic lupus erythematosus and certain forms of vasculitis (inflammatory conditions of the blood vessel wall)
  14.  Chronic meningococcaemia is a rare condition in which the patient can be unwell for weeks or even months with recurrent fever, sweating, joint pains and transient rash.  Usually occurs in the middle-aged and elderly, and in those who have previously had a splenectomy
  15.  A number of factors influence the development of bacterial meningitis, including virulence of the strain, host defenses, and bacteria-host interactions.  Bacterial seeding usually occurs by hematogenous spread. In those without an identifiable source of infection, local tissue and bloodstream invasion by bacteria colonized in the nasopharynx may be a common source.  Meningeal seeding also may occur with a direct bacterial inoculate during trauma, neurosurgery, or instrumentation
  16.  Once in the CSF, the paucity of antibodies, complement components, and white blood cells (WBCs) allows the bacterial infection to flourish.  Bacterial cell wall components initiate a cascade of complement- and cytokine-mediated events that result in at least 3 critical events: increased permeability of the blood-brain barrier, cerebral edema, and presence of toxic mediators in the CSF.  Replicating bacteria, increasing numbers of inflammatory cells, cytokine-induced disruptions in membrane transport, and increased vascular and membrane permeability perpetuate the infectious process and account for the characteristic changes in CSF cell count, pH, lactate, protein, and glucose.
  17.  Exudates extend throughout the CSF, particularly to the basal cisterns, damaging cranial nerves (eg, cranial nerve VIII, with resultant hearing loss), obliterating CSF pathways (causing obstructive hydrocephalus), and inducing vasculitis and thrombophlebitis (causing local brain ischemia.  As intracranial pressure (ICP) continues to rise and brain edema progresses, CNS autoregulatory processes begin to fail.This pivotal event may occur when the transient increase in cerebral blood flow (CBF) reverses and begins to decrease.  CBF reduction correlates with the patient's decreasing alertness and changes in mental status.
  18.  Without medical intervention, the cycle of decreasing CBF, worsening cerebral edema, and increasing ICP proceeds unchecked.  Ongoing endothelial injury may result in vasospasm and thrombosis, further compromising CBF, and may lead to stenosis of large and small vessels.  Systemic hypotension (septic shock) also may impair CBF, and the patient soon dies from systemic complications or from diffuse CNS ischemic injury.
  19.  Approximately 25% of patients with bacterial meningitis present acutely within 24 hours of onset of symptoms.  Other patients with bacterial meningitis and most patients with viral meningitis present with subacute neurologic symptoms developing over 1-7 days.  Chronic symptoms lasting longer than 1 week suggest meningitis caused by some viruses as well as tuberculosis, syphilis, fungi (especially cryptococci), and carcinomatous meningitis
  20.  Classic symptoms include :  Headache  Nuchal rigidity (generally not present in children <1 y or in patients with altered mental status)  Fever and chills, Photophobia  Phonophobia,Vomiting  Prodromal upper respiratory infection (URI) symptoms (viral and bacterial)  Seizures (30-40% in children, 20-30% in adults)  Focal neurologic symptoms (including focal seizures)  Altered sensorium (confusion may be sole presenting complaint, especially in elderly)
  21.  Signs of meningeal irritation Nuchal rigidity or discomfort on neck flexion Kernig sign: Positive Brudzinski sign: Positive  Papilledema is present in only one third of meningitis patients with increased ICP.  Focal neurologic signs: Isolated cranial nerve abnormalities (principally III, IV,VI,VII) in 10- 20% of patients
  22.  Systemic findings:  Extracranial infection (eg, sinusitis, otitis media, mastoiditis, pneumonia, urinary tract infection) may be noted.  Arthritis is seen with N meningitidis, less commonly with other bacteria.  Nonblanching petechiae and cutaneous hemorrhages are seen classically with N meningitidis; however, these also can occur with other bacterial and viral infections.  Endotoxic shock with vascular collapse is characteristic of severe N meningitidis infection.
  23.  Risk factors: Aged 60 years or older Aged 5 years or younger Immunosuppressed patients Splenectomy and sickle cell disease Alcoholism and cirrhosis Dural defect (eg, traumatic, surgical, congenital) Ventriculoperitoneal shunt
  24.  Brain Abscess  Neoplasms, Brain  DeliriumTremens  Pediatrics, Febrile Seizures  Encephalitis  Herpes Simplex  Subarachnoid Hemorrhage
  25.  Sepsis  Disseminated intravascular coagulation  Gangrene  Focal seizures  Abnormalities of the cranial nerves:Visual symptoms and hearing loss  Encephalitis or cerebral vasculitis  Severe meningococcal and pneumococcal infections may result in hemorrhaging of the adrenal glands, leading to Waterhouse- Friderichsen syndrome, which is often lethal.
  26. A. Investigations  Complete blood count  Serum glucose  BUN and/or creatinine and liver profile to assess organ functioning and adjust antibiotic dosing  Coagulation profile and platelets  Cultures : blood, nasopharynx, respiratory secretions, urine, and skin lesions
  27.  Head CT scan with contrast or MRI with gadolinium Imaging is indicated in patients with evidence of head trauma, altered mental status, or focal findings. Rule out brain abscess, sinus or mastoid infection, skull fracture, and congenital anomalies. Presence of papilledema in raised ICP
  28.  Chest x-ray As many as 50% of patients with pneumococcal meningitis also have evidence of pneumonia on initial chest x-ray  Lumbar puncture General patterns in CSF pressure measurement and analysis in bacterial, viral, and fungal (cryptococcal) meningitis may support a diagnosis.
  29. Types of meningitis Glucose Protein Cells Acute bacterial low high PMNs, often >300/mm³ Acute viral normal Normal/high Mononuclear, <300/mm³ TB low high Mononuclear & PMNs, <300/mm³ Fungal low high <300/mm³ Malignant low high Usually mononuclear
  30.  PCR- uses enzymes to enhance the presence of bacterial or viral DNA in CSF.  Serology -may be useful in viral meningitis  Diagnosis of cryptococcal meningitis can be made using an India ink stain of the CSF.
  31.  There is an untreated mortality rate of around 80%, so action must be swift.  In meningococcal disease, mortality is doubled if the patient presents with features of septicaemia rather than meningitis.
  32.  Initial treatment Intravenous fluids should be administered if hypotension or shock are present Mechanical ventilation may be needed if the level of consciousness is very low, or if there is evidence of respiratory failure
  33. Treatments to decrease the intracranial pressure with medication (e.g. Dexamethasone). Seizures are treated with anticonvulsants.
  34.  Empiric antibiotics must be started immediately, even before the results of the lumbar puncture and CSF analysis are known.  Third-generation cefalosporin such as cefotaxime or ceftriaxone  In young children and those > 50 years of age, immunocompromised, addition of ampicillin is recommended to cover Listeria monocytogenes
  35.  Adjuvant treatment with corticosteroids (usually dexamethasone) reduces rates of severe hearing loss and neurological damage in adults but have no effect on overall mortality.  Alternatively;  Vancomycin  Chloramphenicol  Clindamycin
  36.  Viral meningitis typically requires supportive therapy only, such as fluid, bedrest, and analgesics.  Fungal meningitis, such as cryptococcal meningitis, is treated with long courses of highly dosed antifungals, such as amphotericin B and fluconazole.
  37.  Untreated, bacterial meningitis is almost always fatal.  Viral meningitis, in contrast, tends to resolve spontaneously and is rarely fatal.  With treatment, mortality -newborn patients (20–30%), older children (about 2%) but rises again to about 19–37% in adults.
  38.  Meningitis caused by H. influenza and meningococci has a better prognosis compared to cases caused by group B streptococci, coliforms and S. pneumoniae.  In adults, 66% of all cases emerge without disability.The main problems are deafness (in 14%) and cognitive impairment (in 10%).
  39.  For some causes of meningitis, prophylaxis can be provided in the long term with vaccine, or in the short term with antibiotics  Meningococcus vaccines exist against groups A, C, W135 andY but not group B serogroup  Routine vaccination against Streptococcus pneumoniae with the pneumococcal conjugate vaccine (PCV).  Childhood vaccination with BCG significantly reduce the rate of tuberculous meningitis.
  40. Adults who can benefit from Haemophilus influenza type B (Hib) vaccine-  Sickle cell anaemia,  Leukemia,  HIV/AIDS,  post splenectomy,  bone marrow transplantation  those receiving chemotherapy for cancer.
  41.  Antibiotic prophylaxis, particularly for meningococcal meningitis- (2Days oral rifampicin or single dose of ciprofloxacin/ ceftriaxone)