Medical Conditions Affecting the Nervous System

Subtopic:

Meningitis

The term “meningitis” originates from the Greek word meninx meaning “membrane,” combined with the medical suffix -itis, indicating “inflammation.”

Meningitis is characterized by a sudden inflammation of the protective membranes surrounding the brain and spinal cord. These membranes are collectively called the meninges.

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

WHAT ARE MENINGES?

Meninges are a set of three membranes that, along with cerebrospinal fluid, function to encapsulate and safeguard the brain and spinal cord, forming the central nervous system. These three layers, listed from the innermost to outermost, are:

  • Pia Mater: This is the innermost layer, a very thin and delicate membrane. It is impermeable and tightly adheres to the surface of the brain, closely following all of its intricate folds and contours.

  • Arachnoid Mater: Positioned above the pia mater, the arachnoid mater is named for its spiderweb-like appearance. It is structured as a loose sac, not tightly bound to the pia mater below. The space between the arachnoid mater and the pia mater is termed the subarachnoid space, and this area is filled with cerebrospinal fluid.

  • Dura Mater: As the outermost layer, the dura mater is a tough, thick, and durable membrane. It is attached to both the arachnoid membrane underneath it and to the inner surface of the skull itself.

The meninges play a crucial role in forming a blood-brain barrier. This barrier acts to impede pathogens present in the bloodstream from directly entering the brain tissue. However, some infectious agents can still breach this barrier and cause diseases within the central nervous system. Beyond this barrier function, the meninges also provide a physical cushion, protecting the delicate brain tissue from direct physical trauma and injury.

Causes of Meningitis and their Mode of Transmission

Meningitis can be triggered by a range of infectious and non-infectious agents.

  1. Bacterial Causes:

    • Streptococcus pneumoniae: A frequent bacterial culprit, spread occurs through the inhalation of respiratory droplets expelled by infected individuals when coughing or sneezing.

    • Group B Streptococci (especially subtype III): These bacteria commonly reside in the vaginal tract of women and are a primary cause of meningitis in newborns during their first week of life, often contracted during birth.

    • Escherichia coli (with K1 antigen): Typically found in the human digestive system, E. coli can pose a risk to newborns, particularly during delivery as they pass through the birth canal.

    • Listeria monocytogenes (serotype IVb): This bacterium can be transmitted from mother to child before birth, posing a threat primarily to newborns.

    • Neisseria meningitidis (meningococcus): More prevalent in older infants and young children, particularly around 6 years of age. Transmission happens through respiratory droplets.

    • Haemophilus influenzae type B: A significant cause of meningitis in children under 5 years old, particularly in countries where Hib vaccination is not widespread. It is also spread via respiratory droplets.

    • Mycobacterium tuberculosis: More commonly seen in individuals from regions where tuberculosis is widespread. Transmission occurs via respiratory droplets.

    • Treponema pallidum (syphilis) and Borrelia burgdorferi (Lyme disease): These bacteria have different transmission routes. Treponema pallidum (syphilis) is sexually transmitted. Borrelia burgdorferi (Lyme disease) is transmitted through the bite of infected ticks.

    Note: Aseptic meningitis, where no bacteria are identified as the cause, is most often due to viral infections.

  2. Viral Causes:

    • Enteroviruses: These viruses are typically spread via the fecal-oral route, meaning through contact with fecal matter and subsequent ingestion.

    • Herpes simplex virus (especially type 2): Usually transmitted through direct physical contact with active lesions, most commonly genital sores.

    • Varicella-zoster virus: The virus that causes chickenpox (primary infection) and shingles (reactivation). It is transmitted through airborne respiratory droplets.

    • Mumps virus: Spread through respiratory droplets and direct contact with saliva of infected individuals.

    • HIV (Human Immunodeficiency Virus): Transmitted through direct contact with infected bodily fluids, including blood, sexual contact, and from mother to child during pregnancy, childbirth, or breastfeeding.

    • LCMV (Lymphocytic choriomeningitis virus): Transmission occurs through contact with bodily fluids – urine, droppings, saliva – or nesting materials of infected rodents.

  3. Fungal Causes:

    • Cryptococcus neoformans: Infection usually occurs through the inhalation of fungal spores present in the environment, often associated with bird droppings or decaying vegetation.

    • Coccidioides immitis, Histoplasma capsulatum, Blastomyces spp.: These fungal infections also initiate through the inhalation of fungal spores that are found in soil and the environment in specific geographic areas.

  4. Parasitic Causes:

    • The presence of a high proportion of eosinophils in cerebrospinal fluid (CSF) can suggest a parasitic etiology.

    • Cerebral malaria: Transmitted by the bite of infected Anopheles mosquitoes carrying the Plasmodium falciparum parasite.

    • Amoebic meningitis (e.g., Naegleria fowleri): Contracted when contaminated freshwater enters the nose, allowing the amoeba to travel to the brain.

    • Angiostrongylus cantonensis, Gnathostoma spinigerum, Schistosoma: These parasites have diverse transmission pathways, including ingestion of contaminated food or water and, in the case of Schistosoma, through contact with contaminated freshwater containing snail intermediate hosts.

    • Cysticercosis, Toxocariasis, Baylisascariasis, Paragonimiasis: These parasitic infections are acquired through different routes, often involving ingestion of contaminated food or water containing parasite eggs or larvae.

  5. Non-infectious Conditions:

    • Neoplastic: Meningitis can arise as a result of cancer that has spread (metastasized) to the meninges from other parts of the body.

    • Sarcoidosis: This inflammatory condition of unknown origin can sometimes affect the meninges.

    • Systemic lupus erythematosus (SLE): This autoimmune disease can involve inflammation of the meninges.

    • Granulomatosis with polyangiitis (GPA, formerly Wegener’s granulomatosis): An autoimmune disorder that can cause inflammation of blood vessels and may affect the meninges.

    • Behçet’s disease: An autoimmune disorder characterized by blood vessel inflammation that can, in some cases, involve the meninges.

    • Drug-Induced Meningitis: Certain medications can induce meningeal irritation that mimics meningitis. These include:

      • Nonsteroidal anti-inflammatory drugs (NSAIDs)

      • Intravenous immunoglobulin (IVIG)

      • Intrathecal agents administered directly into the spinal fluid

      • Specific antibiotics, for example, trimethoprim-sulfamethoxazole

Risk Factors for Meningitis:

Several factors can increase an individual’s susceptibility to developing meningitis.

  1. Immunocompromised State (Immunosuppression): A weakened immune system makes individuals more vulnerable to infections, including meningitis. This can be due to:

    • Use of immunosuppressant medications, often post-organ transplant.

    • HIV/AIDS infection, which significantly compromises immune function.

    • Age-related immune decline, particularly in the elderly.

    • Associated Pathogens: In immunocompromised individuals, meningitis may more commonly be caused by opportunistic pathogens like Staphylococci, Pseudomonas, and various Gram-negative bacteria.

  2. Recent Skull Trauma: Head injuries, especially those that fracture the skull, can create a direct pathway for bacteria from the nasal passages to enter the meningeal space, bypassing normal protective barriers.

  3. Presence of Brain or Meningeal Devices: Medical devices implanted in the brain or meninges, such as:

    • Cerebral shunts used to drain excess cerebrospinal fluid.

    • Extraventricular drains (EVDs) used for monitoring and drainage of CSF.

    • Ommaya reservoirs used for chemotherapy administration.
      These devices can serve as conduits for infection.

  4. Head and Neck Infections: Infections in the head and neck region can sometimes spread to the meninges, including:

    • Otitis media (middle ear infection).

    • Mastoiditis (infection of the mastoid bone behind the ear).

  5. Cochlear Implants: These devices, surgically implanted to improve hearing, can, in rare instances, increase the risk of meningitis.

  6. Persistent Anatomical Defects: Congenital or acquired anatomical abnormalities that create an abnormal connection between the external environment and the central nervous system can increase vulnerability to meningitis.

  7. Age Extremes: Individuals at the extremes of age are at higher risk:

    • Children, especially those under 5 years old, have immature immune systems.

    • Adults over 50 years old may have age-related immune system decline and other comorbidities.

  8. Systemic Infections: Certain systemic infections can increase the risk of meningitis as bacteria can spread through the bloodstream:

    • Endocarditis (infection of the heart’s inner lining).

    • Pneumonia (lung infection).
      These conditions can lead to bacterial seeding of the meninges.

  9. Asplenia (Absence or Dysfunction of the Spleen): The spleen plays a vital role in filtering bacteria from the bloodstream. Individuals lacking a functioning spleen are more susceptible to bloodstream infections and subsequently, meningitis.

Pathophysiology of Meningitis:
  1. Entry of Infectious Agents:

    • (a) Routes of Entry:

      • Direct Penetration: Organisms can enter directly, for example, through open skull fractures.

      • Hematogenous Spread: Invasion may occur via the bloodstream, allowing pathogens to reach the brain from distant sites of infection.

      • Extension from Adjacent Infection: Infection can spread from nearby infected areas, such as sinus or ear infections.

  2. Bloodstream Invasion and Meningeal Access: Pathogenic organisms, having entered the body, gain access to the bloodstream and subsequently reach the meningeal membranes surrounding the brain and spinal cord. Upon their arrival at the meninges, these organisms are recognized by the body’s immune system as foreign invaders.

  3. Initiation of Immune Response: The identification of pathogens triggers the body’s immune defenses. A complex interaction ensues between immune cells and the invading organisms.

    • Cytokine Release: Astrocytes and microglia, resident immune cells in the brain, respond by releasing cytokines. These signaling molecules act to recruit more immune cells to the site of infection and stimulate local tissues to mount an inflammatory response.

  4. Increased Blood-Brain Barrier Permeability: The inflammatory process leads to alterations in the blood-brain barrier, making it more permeable than normal.

    • Vasogenic Edema: This increased permeability results in vasogenic cerebral edema. Fluid leaks out of blood vessels into the brain tissue, causing brain swelling.

    • White Blood Cell Infiltration: A significant influx of white blood cells into the cerebrospinal fluid (CSF) and meninges occurs. This massive cellular infiltration contributes to intense meningeal inflammation and also causes interstitial edema, further swelling the brain tissue.

  5. Cerebral Vasculitis:

    • Inflammation of Cerebral Vessels: The walls of cerebral blood vessels become inflamed, a condition known as vasculitis. This inflammation compromises blood flow within the brain.

    • Cytotoxic Edema: As blood flow is reduced and cellular damage occurs, cytotoxic edema develops. This type of edema involves swelling directly within brain cells.

  6. Elevation of Intracranial Pressure (ICP):

    • Combined Edema Effects: The cumulative effect of vasogenic, interstitial, and cytotoxic edema leads to a marked increase in intracranial pressure (ICP) within the confined space of the skull.

    • Impaired Cerebral Blood Flow: The elevated ICP impedes blood flow into the brain, making it progressively harder for oxygenated blood to reach brain tissue.

    • Oxygen Deprivation and Cell Death: Brain cells are deprived of sufficient oxygen due to compromised blood flow. This oxygen starvation triggers apoptosis, or programmed cell death, in brain neurons and other brain cells, leading to neuronal injury and loss.

  7. Brain Swelling and Clinical Manifestations:

    • CSF Circulation Blockage: Significant brain swelling disrupts and may block the normal flow of cerebrospinal fluid (CSF) within the brain and around the spinal cord.

    • Clinical Signs Emerge: The combination of inflammation, edema, and elevated ICP leads to the development of characteristic clinical signs and symptoms of meningitis, including severe headache, seizures, and other neurological deficits.

  8. Progression of Untreated Meningitis:

    • Widespread Brain Involvement: If left untreated, the inflammatory process continues to spread and affect more extensive areas of the brain.

    • Development of Complications: Serious complications can arise, such as:

      • Encephalitis (inflammation of the brain tissue itself).

      • Further increase in intracranial pressure (ICP).

      • Brainstem dysfunction, impacting vital functions.

      • Multi-organ dysfunction syndrome, affecting systems throughout the body.

    • Fatal Outcome: Without timely and effective medical intervention, the progressive damage from meningitis can ultimately lead to death.

CLINICAL FEATURES

Meningitis presents with a range of signs and symptoms. Key clinical features include:

  1. Fever: An elevated body temperature is a common and important indicator, often signaling a systemic infection such as meningitis.

  2. Headache: Characterized by severe pain in the head. This is a very frequent symptom, occurring in nearly 90% of cases of bacterial meningitis.

  3. Neck Stiffness (Nuchal Rigidity): Marked by increased tension and stiffness in the neck muscles. This classic sign strongly suggests meningeal irritation and is commonly observed in both adults and children with meningitis.

  4. Photophobia: Intolerance and abnormal sensitivity to bright light. This symptom reflects an increased sensitivity of the eyes likely due to meningeal inflammation.

  5. Phonophobia: Intolerance to loud or sudden noises. Similar to photophobia, phonophobia indicates a heightened sensory sensitivity, suggesting meningeal involvement.

  6. Irritability (in Small Children): Manifests as changes in behavior, often seen as increased fussiness, restlessness, and inconsolability in young children.

  7. Unwell Appearance (in Small Children): A general impression that the child is sick and uncomfortable, indicating overall illness. While non-specific, this observation supports other, more distinct meningitis symptoms.

  8. Fontanelle Bulging (in Infants): A noticeable bulging of the fontanelle, the soft spot on an infant’s head. This is specific to infants, particularly those up to 6 months old, and is a critical sign indicating increased intracranial pressure.

  9. Leg Pain: Discomfort or pain experienced in the legs. This may arise from the systemic inflammatory response associated with meningitis.

  10. Cold Extremities: Hands and feet that are cool to the touch. This is a peripheral manifestation of systemic inflammation, resulting in altered circulation. Physical examination will reveal extremities that are palpably cooler than normal.

  11. Abnormal Skin Color: Changes in the normal skin tone. This is another sign of peripheral circulatory disturbances resulting from systemic inflammation. Altered skin coloration is typically noted during a physical examination.

  12. Positive Kernig’s Sign: Pain that limits the ability to passively extend the knee when the hip is flexed at 90 degrees. This is a specific test for meningitis and suggests meningeal irritation. The test is performed with the patient lying on their back (supine); pain and resistance to knee extension indicates a positive sign.

  13. Positive Brudzinski’s Sign: Neck flexion causes involuntary knee and hip flexion. Specific for meningitis; reflects meningeal irritation. Neck flexion
    triggers involuntary leg movements.
  14. Jolt Accentuation Maneuver: Determines likelihood of meningitis in those with fever and headache. A procedure is done where Rapid horizontal
    head rotation; worsening headache indicates possible meningitis. Simple bedside test aiding diagnostic decision-making.
  15.  Rapidly Spreading Petechial Rash (Meningococcal Meningitis): Small, reddish-purple spots on the skin. Specific to meningococcal meningitis;
    requires urgent medical attention. May precede other symptoms, aiding early identification.
  16. . Confusion or Altered Consciousness: Mental state changes, disorientation. Indicates severe cases with potential neurological involvement.
    Altered mental status evident during examination.
  17. . Vomiting: Forceful expulsion of stomach contents.
  18. Nonspecific Symptoms in Young Children: Irritability, Drowsiness, Poor Feeding:
    Irritability: Behavioral changes.
    Drowsiness: Increased sleepiness.
    Poor Feeding: Reduced appetite or feeding reluctance
Diagnosis and Investigations

1. History Taking and Physical Examination:

  • Classic Triad of Diagnostic Signs: Historically, diagnosis considered three core signs:

    1. Nuchal Rigidity: Examine for stiffness and resistance in neck movement.

    2. Sudden High Fever: Measure body temperature to detect significant elevation.

    3. Altered Mental Status: Assess for any changes in alertness, confusion, or disorientation.

    • Diagnostic Accuracy: Be aware that this classic triad is observed in less than half of bacterial meningitis cases (approximately 44–46%).

    • Additional Physical Signs: Look for other indicators such as a positive Kernig’s sign (pain on knee extension with hip flexion) or Brudziński sign (involuntary hip and knee flexion with neck flexion).

  • CSF Findings in Meningitis: Cerebrospinal Fluid (CSF) analysis is crucial.

    • Parameters Assessed: Laboratory examination of CSF focuses on:

      • Glucose Levels: Measuring sugar content.

      • Protein Levels: Quantifying protein concentration.

      • White Blood Cell Count: Determining the number and type (predominantly polymorphonuclear cells in bacterial meningitis) of white blood cells.

    • Diagnostic Differentiation: Variations in these CSF parameters help distinguish between different types of meningitis (bacterial, viral, fungal, etc.).

  • Blood Tests and Imaging:

    • Inflammatory Markers: Blood tests include:

      • C-Reactive Protein (CRP): To assess general inflammation levels.

      • Complete Blood Count (CBC): To evaluate white blood cell count and other blood cell parameters.

    • Blood Cultures: Obtain blood samples for culture to attempt to identify the causative pathogen in the bloodstream.

    • Electrolyte Monitoring: Regularly check electrolyte levels, particularly sodium, to manage potential complications like hyponatremia (low sodium).

    • Imaging (CT or MRI): Neuroimaging is recommended before lumbar puncture in a significant proportion of adult meningitis cases (around 45%).

      • Indications for Imaging: To rule out:

        • Brain masses (tumors or abscesses).

        • Elevated intracranial pressure (ICP) which could make lumbar puncture risky.

  • Lumbar Puncture (Spinal Tap): This is the definitive diagnostic procedure.

    • Procedure: A needle is inserted into the lumbar space within the dural sac to collect CSF for analysis.

    • Contraindications: Lumbar puncture should be avoided if there is suspicion of:

      • Brain mass.

      • Significantly elevated intracranial pressure (ICP).

    • Opening Pressure Measurement: Measure the CSF pressure during the procedure; it is typically elevated in bacterial meningitis.

    • CSF Appearance: Observe the visual characteristics of the CSF sample; cloudy or turbid CSF may suggest increased protein, white blood cells, red blood cells, and/or bacterial presence.

  • Specialized Tests for Meningitis Type Differentiation: Advanced tests aid in identifying the specific cause.

    • Latex Agglutination Test:

      • Positive Results May Indicate: Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Escherichia coli, and group B streptococci.

      • Routine Use: Typically reserved for cases where initial CSF tests are inconclusive.

    • Limulus Lysate Test:

      • Positive Result Suggests: Presence of Gram-negative bacteria.

    • Polymerase Chain Reaction (PCR):

      • Purpose: To amplify and detect bacterial or viral DNA directly in the CSF sample.

      • Diagnostic Value: Highly sensitive and specific, capable of detecting minute quantities of pathogen DNA.

    • Tuberculous Meningitis Diagnostics: Specific methods for diagnosing TB meningitis:

      • Ziehl-Neelsen Stain: Acid-fast staining for mycobacteria, but has low sensitivity.

      • Tuberculosis Culture: Traditional culture of CSF for Mycobacterium tuberculosis, but is time-consuming.

      • PCR for TB: Increasingly used for faster and more sensitive detection of Mycobacterium tuberculosis DNA.

MANAGEMENT OF MENINGITIS

Meningitis demands urgent medical attention as it is a potentially fatal condition if untreated. Rapid initiation of treatment is critical to improve outcomes. Initial management focuses on immediate antibiotic administration and sometimes antiviral agents. Corticosteroids may be added to reduce inflammation-related complications.

Immediate Intervention:

  • Patient Reception and Admission: Upon arrival:

    • Admit the patient to an isolation room within the male medical ward, ensuring dimmed lighting.

    • Provide a comfortable bed and position the patient to maximize comfort.

  • Rapid Patient Assessment: Conduct a quick evaluation of the patient’s condition:

    • Assess level of consciousness using the Glasgow Coma Scale (GCS).

    • Record baseline vital signs: Temperature (T), Pulse (P), Respiration (R), and Blood Pressure (BP).

  • Patient and Family Reassurance: Provide calm reassurance to both the patient and their family to reduce anxiety and fear.

  • Physician Notification: Immediately inform the doctor about the patient’s condition and assessment findings.

  • Emergency Measures (Concurrent Actions):

    • Oxygen Administration: Initiate oxygen therapy, especially if the patient is unconscious or showing signs of respiratory distress.

    • Intravenous Access: Establish an Intravenous (IV) line for fluid resuscitation and medication delivery. Draw blood samples for initial hematological and biochemical tests.

  • Doctor-Ordered Investigations (Anticipate): Prepare for likely requests such as:

    • Cerebrospinal Fluid (CSF) analysis: for volume, appearance, and laboratory analysis.

    • Chest X-ray and Ultrasound: To investigate potential primary infection sites or sources.

Continuous Care:

  • Fluid Balance and Monitoring:

    • Insert a urinary catheter to accurately monitor urine output and maintain a 24-hour fluid balance chart.

    • Insert a nasogastric (NG) tube for enteral nutrition if the patient cannot maintain adequate oral intake.

  • Fever Management: Implement tepid sponging to help lower fever and enhance patient comfort.

  • CSF Monitoring: Continuously monitor CSF drainage (if applicable) for changes in quality, quantity, and appearance, noting any concerning changes.

  • Infection Control: Implement rigorous infection control measures:

    • Collect all patient discharges carefully and ensure proper disinfection.

    • Use safe disposal methods for all contaminated materials to prevent cross-infection.

Following Doctor’s Review and Prescription (Antibiotic Therapy Examples):

  • Streptococcus pneumoniae Meningitis (10-14 day course, up to 21 days in severe cases):

    • Benzylpenicillin: 3-4 Million Units (MU) IV or IM every 4 hours.

    • Alternative: Ceftriaxone 2 grams IV or IM every 12 hours.

  • Haemophilus influenzae Meningitis (10-day course):

    • Ceftriaxone: 2 grams IV or IM every 12 hours.

  • Neisseria meningitidis Meningitis (up to 14-day course):

    • Benzylpenicillin: 5-6 MU IV every 6 hours.

    • Alternatives:

      • Ceftriaxone 2 grams IV or IM every 12 hours.

      • Chloramphenicol 1 gram IV every 6 hours (or IM if IV access is problematic).

  • Meningitis in Adults Over 50 Years: Empiric regimens often cover a broader spectrum of pathogens:

    • Cefotaxime: 2 grams IV every 6 hours.

    • Alternative: Ceftriaxone 2 grams IV every 12 hours.

    • Combination Therapy (consider for Listeria coverage):

      • Co-trimoxazole 50mg/kg IV daily in 2 divided doses plus Ampicillin 2 grams IV every 4 hours.

      • Or, if broader Gram-negative cover is needed: Co-trimoxazole 50mg/kg IV daily in 2 divided doses alone may be considered in specific contexts.

Continuous Nursing Care (Ongoing Supportive Measures):

  • Patient and Relative Reassurance: Continue providing emotional support and reassurance.

  • Pressure Ulcer Prevention: Implement a 2-hourly turning schedule to prevent pressure sores, and repositioning to avoid aspiration, particularly in patients with reduced consciousness.

  • Hygiene and Comfort: Maintain hygiene:

    • Regularly clean IV infusion sites.

    • Provide bed baths for patient hygiene.

    • Ensure regular oral care to maintain oral hygiene and comfort.

    • Change bed linens and soiled linen frequently to maintain a clean and comfortable environment.

  • Nutritional Support: Ensure the patient receives a balanced diet, considering enteral or parenteral routes as needed based on oral intake ability.

  • Promote Mobility: Encourage patient exercises and range of motion activities as tolerated to promote circulation and healing and prevent complications of immobility.

  • Bowel Management: Provide a bedpan or commode readily accessible to manage bowel movements as needed.

  • Health Education: Educate the patient (if conscious and alert) and family about meningitis: its causes, symptoms, treatment, and preventive measures, including vaccination and hygiene practices.

Specific Interventions (Management of Meningitis Complications):

  • Mechanical Ventilation: Initiate mechanical ventilation for patients with significantly reduced level of consciousness or exhibiting respiratory failure to ensure adequate oxygenation and ventilation.

  • Raised Intracranial Pressure (ICP) Management:

    • ICP Monitoring: Implement ICP monitoring if indicated to continuously assess intracranial pressure.

    • Optimize Cerebral Perfusion Pressure (CPP): Manage blood pressure and ICP to maintain adequate cerebral perfusion.

    • ICP-Lowering Treatments: Utilize therapies to reduce ICP, such as:

      • Medications like mannitol (osmotic diuretic).

      • Elevation of the head of the bed.

      • Controlled hyperventilation in specific circumstances.

  • Seizure Management:

    • Administer anticonvulsant medications promptly to control active seizures and prevent seizure recurrence.

  • Hydrocephalus Management:

    • For hydrocephalus (obstruction of CSF flow), interventions may include:

      • Temporary CSF drainage through serial lumbar punctures.

      • Insertion of a lumbar drain for continuous CSF drainage.

      • Long-term CSF diversion via a cerebral shunt placement, if necessary.

Bacterial Meningitis Specifics:

  • Antibiotic Selection: Choice of antibiotics may include:

    • Cefotaxime

    • Vancomycin

    • Chloramphenicol

    • Ampicillin

    • Antibiotics may be used in combination based on suspected pathogen and local resistance patterns.

  • Empirical Therapy Considerations: Initial antibiotic choice is often empirical, guided by:

    • Patient age.

    • History of head trauma.

    • Recent neurosurgical procedures.

    • Presence of cerebral shunt or other implanted devices.

    • Listeria monocytogenes Coverage: Ampicillin is often included in empirical regimens for:

      • Young children.

      • Individuals over 50 years of age.

      • Immunocompromised patients.
        This is to ensure coverage against Listeria monocytogenes.

  • Tuberculous Meningitis Treatment:

    • Requires prolonged antibiotic therapy, typically lasting a year or longer, using a multi-drug regimen tailored to TB.

  • Steroid Use (Adjunctive Therapy):

    • Adjunctive treatment with corticosteroids, particularly dexamethasone, may provide benefits in bacterial meningitis, including:

      • Reduction in the risk of hearing loss.

      • Improved short-term neurological outcomes.

    • The specific role and benefit of steroids can vary between children and adults and depends on the causative organism.

Viral Meningitis Management:

  • Supportive Care: Viral meningitis treatment is mainly supportive, focusing on symptom management and allowing the body’s immune system to clear the infection.

  • Antiviral Medications: Antiviral drugs, such as aciclovir, may be used in specific cases, particularly for meningitis caused by:

    • Herpes simplex virus (HSV).

    • Varicella-zoster virus (VZV).

  • Home Management (Mild Cases): Mild viral meningitis cases can often be managed at home with:

    • Rest.

    • Hydration.

    • Pain relief with over-the-counter analgesics.

Fungal Meningitis Management:

  • Antifungal Therapy: Treatment requires prolonged courses of high-dose antifungal medications:

    • Amphotericin B (often as an initial induction therapy).

    • Flucytosine (often in combination with amphotericin B).

  • Intracranial Pressure Management: Frequent lumbar punctures or placement of a lumbar drain may be necessary to relieve elevated intracranial pressure associated with fungal meningitis.

Note on Prognosis:

  • Untreated Bacterial Meningitis: Almost invariably fatal without medical intervention.

  • Viral Meningitis: Typically resolves spontaneously with supportive care and is rarely fatal.

  • Bacterial Meningitis with Treatment: Mortality rates vary with age and the causative organism. Mortality is highest in:

    • Newborns (20–30%).

    • Adults (19–37%).

Note; in managing meningitis; (general) Key Management Principles

  1. Isolation Precautions: Implement isolation protocols, especially for bacterial meningitis, to prevent transmission. This includes single-room isolation and appropriate personal protective equipment (PPE) for healthcare staff and visitors.

  2. Prompt Antimicrobial Therapy: Initiate broad-spectrum antibiotics immediately upon suspicion of bacterial meningitis, without waiting for definitive diagnostic test results.

  3. Optimal Hydration Maintenance: Administer intravenous fluids to ensure adequate hydration, especially addressing fluid losses from fever, vomiting, and poor oral intake.

  4. Ventilation Support: Monitor respiratory status closely and provide ventilatory support, including mechanical ventilation if needed, to maintain oxygenation and manage respiratory distress.

  5. Intracranial Pressure Reduction: Implement measures to monitor and reduce elevated intracranial pressure (ICP) to prevent brain damage; this may include osmotic therapy (mannitol), head elevation, and potentially surgical decompression in severe cases.

  6. Bacterial Shock Management: Be vigilant for and aggressively manage septic shock if it develops, using vasopressors, fluid resuscitation, and other supportive measures to stabilize hemodynamics.

  7. Seizure Control: Administer anticonvulsants to manage and prevent seizures, thereby protecting the brain from seizure-related injury.

  8. Temperature Regulation: Control fever with antipyretics and physical cooling measures to prevent hyperthermia, which can worsen neurological outcomes.

  9. Anemia Correction: Address anemia if present through appropriate interventions, ensuring adequate oxygen-carrying capacity of the blood.

  10. Complication Management: Proactively identify and treat complications such as hydrocephalus, subdural effusions, cranial nerve palsies, and neurological sequelae, using targeted therapies to improve recovery and minimize long-term disability.

Intravenous fluids are critical for hypotension and shock management, and Intensive Care Unit (ICU) admission should be considered for unstable patients. Mechanical ventilation may be needed for reduced consciousness or respiratory failure. Raised intracranial pressure requires monitoring and interventions like mannitol and potential CSF drainage. Seizures are managed with anticonvulsants. Hydrocephalus may necessitate CSF diversion via temporary or permanent shunts.

Prevention of Meningitis:

Behavioral Measures:

  • Good Personal Hygiene Practices: Regular handwashing, especially after being in public places and before eating, is a key step in minimizing the spread of both bacterial and viral meningitis.

  • Respiratory Hygiene: To reduce transmission via respiratory droplets, it’s important to practice respiratory etiquette. This includes covering your mouth and nose when coughing or sneezing and avoiding close contact, such as kissing, with others, especially when feeling unwell.

  • Awareness of Fecal-Oral Transmission: Certain viruses that cause meningitis, like enteroviruses, can spread through fecal-oral pathways. Maintaining good hygiene practices, particularly around toilet use and food preparation, helps lower the risk of infection from this route.

Vaccination:

  • Haemophilus influenzae Type B (Hib) Vaccine: Routine immunization of infants and young children with the Hib vaccine is a highly effective measure. Since its introduction in the 1980s, Hib vaccination programs have dramatically decreased the occurrence of meningitis caused by Haemophilus influenzae type B in many countries.

  • Pneumococcal Conjugate Vaccine (PCV): Vaccination against Streptococcus pneumoniae using the Pneumococcal Conjugate Vaccine (PCV) is crucial in preventing pneumococcal meningitis, particularly in vulnerable populations like young children and older adults.

  • Bacillus Calmette-Guérin (BCG) Vaccine: Childhood BCG vaccination, primarily known for tuberculosis prevention, has also been linked to a reduced incidence of tuberculous meningitis, a severe form of the disease.

Antibiotics:

  • Short-Term Antibiotic Prophylaxis: In specific situations of high exposure risk to certain types of meningitis, short-term antibiotic administration can be used as a preventive measure. This prophylactic approach is particularly considered for individuals in high-risk categories, such as those who have sustained basilar skull fractures, to prevent bacterial meningitis development.

Complications of Meningitis:
  1. Sepsis: Meningitis can initiate sepsis, a serious condition where the body’s response to infection spirals out of control. This systemic inflammatory reaction can lead to disruptions in blood pressure, heart rate, body temperature, and respiration. Organ dysfunction may follow as a result of insufficient blood supply to vital organs.

  2. Disseminated Intravascular Coagulation (DIC): DIC is a disorder of blood clotting that can be triggered by meningitis. It involves excessive activation of the clotting system throughout the bloodstream. This over-activation can paradoxically lead to both blood clots obstructing small blood vessels and an increased risk of bleeding due to depletion of clotting factors. In severe cases of meningococcal disease, DIC can lead to gangrene in the limbs due to circulatory compromise.

  3. Increased Intracranial Pressure (ICP): Brain tissue swelling from meningitis can elevate pressure within the skull. This increased ICP is a dangerous complication that can lead to brain herniation, a life-threatening condition where brain tissue is squeezed and displaced. Signs of elevated ICP and herniation include decreased level of consciousness, loss of the pupillary light reflex (pupils not reacting to light), and abnormal body posturing. Furthermore, inflammation from meningitis can obstruct the normal pathways for cerebrospinal fluid (CSF) circulation, resulting in hydrocephalus (an accumulation of CSF in the brain).

  4. Seizures: Seizures are a frequent occurrence, particularly in the early stages of meningitis. While often presenting acutely, seizures can become a recurring issue and lead to the development of epilepsy, a chronic seizure disorder. Approximately 30% of children with meningitis experience seizures.

  5. Cranial Nerve Abnormalities: Inflammation caused by meningitis can extend to and affect the cranial nerves. These nerves are responsible for various functions, and their compromise can result in problems such as abnormal eye movements, facial muscle weakness or paralysis, and hearing impairments. Visual disturbances and hearing loss may persist as long-term sequelae even after recovery from the acute infection.

  6. Brain Inflammation and Vascular Issues: Meningitis may progress to involve inflammation of the brain tissue itself (encephalitis) or the cerebral blood vessels (cerebral vasculitis). These complications can manifest as neurological deficits including muscle weakness, sensory loss, or abnormal movements affecting different parts of the body depending on the specific brain areas impacted by the inflammation and vascular compromise.

  7. Long-Term Consequences: Even with treatment, meningitis can leave lasting effects. Long-term complications may include permanent hearing loss (deafness), epilepsy as a result of brain damage, persistent hydrocephalus requiring ongoing management, and cognitive deficits affecting memory, learning, and executive functions. These long-term issues are more likely if treatment is delayed or if the initial infection is particularly severe.