Meningitis is an inflammation of the pia mater and arachnoid membranes that surround the brain and the spinal cord. The subarachnoid space between these two meninges contains CSF that may reflect the signs and symptoms of meningitis.
Pathophysiology and Causes of Meningitis
Viral meningitis is the most common form. More than 10,000 cases are reported annually, but the actual incidence may be as high as 75,000. It is usually self-limiting; management is supportive. It is usually caused by a nonpolio enterovirus (90%). The incidence of viral meningitis drops with age. As a general rule, the younger the patient, the greater the risk of viral meningitis. This organism is spread by the faecal-oral route and through sewage.
In the United States, the incidence of acute, bacterial meningitis is approximately three cases per 100,000 per year. The mortality is 10% to 30%, and many who recover are left with long-term problems (eg, hearing deficit).
Bacterial meningitis may cause damage to the CNS from the inflammatory process rather than the pathogen. The organisms causing these infections seem to vary depending on the age and immune status of the patient. Bacterial meningitis is usually more serious than viral meningitis. It is typically caused by Streptococcus pneumoniae (pneumococcal meningitis), a gram-positive diplococci, and Neisseria meningitidis (meningococcal meningitis), a gram-negative diplococci.
- Most bacteria that cause meningitis begin by colonizing the nasopharynx, then invade the circulation and CSF, causing an inflammatory response mediated by cytokines.
- Bacterial meningitis can result in brain damage due to chemicals released by bacteria that kill or damage neurons, purulent exudates that may result in vasculitis and vasospasm, and increased ICP that causes cerebral edema.
Fungal meningitis, particularly Cryptococcus neoformans, affects immunosuppressed patients (eg, human immunodeficiency virus [HIV]–positive) through soil contaminated with excrement from pigeons and chickens. Cryptococcal antigen, or culture, is found in the CSF, but meningeal signs may be minimal. In HIV-positive patients, tuberculous meningitis, tuberculomas, and atypical mycobacterial infections of the brain may be noted.
Parasitic meningitis is usually cause by flukes, worms, or amoeba Hospital-acquired post craniotomy meningitis, caused predominantly by gram-negative bacilli, can result in mortalities of 30%; multiple craniotomy operations place the patient at even higher risk. It develops approximately 7 to 8 days postoperatively.
Neoplastic meningitis affects approximately 3% to 8% of patients who have systemic cancers. The mean survival time is approximately 5 to 8 months. In neoplastic meningitis, malignant cells infiltrate the leptomeninges as a complication of breast cancer, lung cancer, malignant melanoma, non-Hodgkin’s lymphoma, and acute leukemia.
Meningitis is the primary intracranial complication of acute and chronic sinusitis (sphenoid sinusitis most common). S. pneumonia and Staphylococcus aureus are the most common organisms.
Listeria monocytogenes, gram-positive bacilli, may cause meningitis through contaminated hot dogs, cold meats, and unpasteurized dairy products.
The incidence of Haemophilus influenzae meningitis has decreased due to the haemophilus b conjugate vaccine.
Signs and Symptoms of Meningitis
- Classic symptoms are fever, headache, and nuchal rigidity. Constitutional symptoms of vomiting, diarrhea, cough, and myalgias appear in more than 50% of patients. History of temperature elevation occurs in 76% to 100% of patients who seek medical attention. A common patternm is low-grade fever in the prodromal stage and higher temperature elevations at the onset of neurologic signs.
- Altered mental status; confusion in older patients.
- Petechial (appears like “rug” burn) or purpuric rash from coagulopathy, especially with N. meningitidis.
- Photophobia.
- Neck tenderness or a bulging anterior fontanel in infants.
- Children may exhibit behavioral changes, arching of the back and neck, a blank stare, refusal to feed, and seizures. Viral meningitis can cause a red, maculopapular rash in children.
- Positive Brudzinski’s and Kernig’s signs
- Neonates may exhibit poor feeding, altered breathing patterns, or listlessness.
- Onset may be over several hours or several days depending on the infectious agent, the patient’s age, immune status, comorbidities, and other variables. Some viruses cause rapid onset of symptoms, while others may involve prodromal nonspecific flu-like symptoms, such as malaise, myalgia, and upper respiratory symptoms. In many cases, symptoms have a biphasic pattern; the nonspecific flu-like symptoms and lowgrade fever preceding neurologic symptoms by approximately 48 hours. With the onset of neck stiffness and headache, the fever usually returns.
Diagnostic Evaluation for Meningitis
- Complete blood count (CBC) with differential is indicated to detect an elevated leukocyte count in bacterial and viral meningitis, with a greater percentage of polymorphonuclear leukocytes (90%) in bacterial and (less than 50%) in viral meningitis (normal 0% to 15%).
- Blood cultures are obtained to indicate the organism.
- CSF evaluation for pressure, leukocytes, protein, glucose— CSF normally has five or fewer lymphocytes or mononuclear cells/mm3.
- In acute bacterial meningitis, the CSF may indicate elevated pressure, elevated leukocytes (several thousand), elevated protein, low glucose. A culture and smear will identify the organism. WBC differential should be done by a stained smear of sediment.
- In viral encephalitis, the CSF may indicate normal/ moderately elevated pressure, few/elevated leukocytes (fewer than 1,000), normal or slightly elevated protein, normal glucose.
- MRI/CT scan with and without contrast rules out other disorders. A CT scan with contrast must be done to detect abscesses.
- Latex agglutination may be positive for antigens in meningitis.
- Low CD4 counts indicate immunosuppression in HIVpositive patients and other patients with immunosuppressive disorders.
- In patients with acquired immunodeficiency syndrome (AIDS), MRI is used to detect meningeal irritation, evidence of a sinus infection, or brain abscess.
Treatment of Meningitis
- The assessment and management of meningitis should be approached through a team effort with nursing, infectious disease and otolaryngology specialists, neurology, internal medicine, and laboratory and diagnostic staff.
- Most patients are given I.V. antibiotics as soon as possible until the laboratory findings determine the type of meningitis (eg, viral, bacterial). However, cultures should be taken before initiating antibiotics.
- To manage inflammation, dexamethasone (Decadron) or another corticosteroid is given I.V.
- This may result in GI bleeding and mask clinical responses to treatments (eg, resolved fever).
- This steroid should be used before or with the first dose of antibiotics (I.V. 0.6 mg/kg/day in four divided doses for the first 4 days of antibiotics) and should be confined to patients older than age 6 weeks.
- Plasmapheresis may be used experimentally to remove cytokines in some cases.
- Temozolomide (Temodar), a second-generation alkylating agent, is effective against many cancers that result in neoplastic meningitis. External beam radiation may be used in conjunction with chemotherapy (eg, intrathecal thiotepa or methotrexate).
- Cochlear implantation rehabilitation due to deafness caused by meningitis should be considered. Realistic goals must be set, because the patient may develop only environmental sound awareness and still have to deal with learning disabilities.
- If meningitis is suspected after neurosurgical procedures, consider potential I.V. line bacteremia, CSF leak, or immunosuppression.
- Antifungal agents, such as amphotericin B (Fungizone) and the triazoles, fluconazole (Diflucan) and itraconazole (Sporanox), are indicated for cryptococcal meningitis. Relapse is common if the patient does not have chronic suppressive therapy with fluconazole or another antifungal agent.
- Empiric antituberculosis drugs must be initiated if infection by Mycobacterium tuberculosis is suspected.
Complications of Meningitis
- Bacterial meningitis, particularly in children, may result in deafness, learning difficulties, spasticity, paresis, or cranial nerve disorders.
- Increased ICP in AIDS patients with cryptococcal meningitis can result in severe visual losses.
- Seizures occur in 20% to 30% of patients.
- Increased ICP may result in cerebral edema, decreased perfusion, and tissue damage.
- Severe brain edema may result in herniation or compression of the brain stem.
- Purpura may be associated with disseminated intravascular coagulation.
Nursing Assessment of Meningitis
- Obtain a history of recent infections such as upper respiratory infection and exposure to causative agents. Meticulous history taking is essential and must include evaluation of exposure to ill contacts, mosquitoes, ticks, and outdoor activities in areas of endemic Lyme disease, travel history with possible exposure to tuberculosis, as well as history of medication use, intravenous drug use, and sexually transmitted disease risk. Another important part of history is prior antibiotic use, which may alter the clinical picture of bacterial meningitis.
- Assess neurologic status and vital signs.
- Evaluate for signs of meningeal irritation.
- Assess sensorineural hearing loss (vision and hearing), cranial nerve damage (eg, facial nerve palsy), and diminished cognitive function.
Nursing Diagnoses of Meningitis
- Hyperthermia related to the infectious process and cerebral edema.
- Risk for Imbalanced Fluid Volume related to fever and decreased intake.
- Ineffective Tissue Perfusion (cerebral) related to infectious processes and cerebral oedema.
- Acute Pain related to meningeal irritation.
- Impaired Physical Mobility related to prolonged bed rest.
Nursing Interventions of Meningitis
Reducing Fever
- Administer antimicrobial agents on time to maintain optimal blood levels.
- Institute other cooling measures, such as a hypothermia blanket, as indicated.
- Monitor temperature frequently or continuously, and administer antipyretics as ordered.
Maintaining Fluid Balance
- Prevent I.V. fluid overload, which may worsen cerebral edema.
- Monitor intake and output closely.
- Monitor CVP frequently.
Enhancing Cerebral Perfusion
- Assess LOC, vital signs, and neurologic parameters frequently. Observe for signs and symptoms of increased ICP (eg, decreased LOC, dilated pupils, widening pulse pressure).
- Maintain a quiet, calm environment to prevent agitation, which may cause an increased ICP.
- Prepare patient for a lumbar puncture for CSF evaluation, and repeat spinal tap, if indicated. Evaluate patient for ICP prior to lumbar puncture.
- Notify the health care provider of signs of deterioration: increasing temperature, decreasing LOC, seizure activity, or altered respirations.
Reducing Pain
- Administer analgesics as ordered; monitor for response and adverse reactions. Avoid opioids, which may mask a decrease in LOC.
- Darken the room if photophobia is present.
- Assist with position of comfort for neck stiffness, and turn patient slowly and carefully with head and neck in alignment.
- Elevate the head of the bed to decrease ICP and reduce pain.