Meningitis Nursing Care Management and Study Guide

Meningitis is inflammation of the meninges, and it can kill fast. Viruses, bacteria, and fungi all cause it, and the bacterial form is the emergency. Recognize fever, headache, neck stiffness, and altered mental status, get the lumbar puncture and antibiotics moving, and protect the brain while the infection is brought under control.

What is Meningitis?

CNS infections split into those involving the meninges (meningitis) and those confined to the parenchyma (encephalitis). Meningitis is inflammation of the meninges, the three layers of membranes enclosing the brain and spinal cord: the dura (tough outer membrane), the arachnoid (lacy, weblike middle membrane), and the subarachnoid space (delicate fibrous inner layer carrying many of the vessels that feed the brain and cord). Anatomically it divides into inflammation of the dura (pachymeningitis, less common) and leptomeningitis (inflammation of the arachnoid and subarachnoid space, more common).

Pathophysiology

Most cases start from an infectious agent that has colonized or set up a localized infection elsewhere. The organism invades the submucosa by getting past host defenses (physical barriers, local immunity, phagocytes or macrophages). Bloodstream invasion and seeding is the most common spread, but meningeal seeding can also follow direct inoculation during trauma, neurosurgery, or instrumentation. Once organisms cross the disrupted blood-brain barrier, they are partly shielded from the immune system and spread. The immune response makes it worse: vessels leak, letting fluid, WBCs, and infection-fighting particles into the meninges and brain, which swells the brain and cuts blood flow to regions, worsening the picture. In bacterial meningitis, replicating bacteria, rising inflammatory cells, cytokine-driven disruption of membrane transport, and increased vascular and membrane permeability keep the process going.

Statistics and Incidences

Incidence varies by agent and by a nation's medical resources. With almost 4100 cases and 500 deaths annually in the United States, bacterial meningitis remains a major source of morbidity and mortality; the annual US incidence is 1.33 cases per 100,000 population. Neonatal bacterial meningitis runs 0.25-1 case per 1000 live births, with 0.15 cases per 1000 full-term births and 2.5 cases per 1000 premature births. N meningitidis causes about 4 cases per 100,000 children aged 1-23 months, and the risk of secondary meningitis is 1% for family contacts and 0.1% for daycare contacts. S pneumoniae meningitis runs 6.5 cases per 100,000 children aged 1-23 months. Newborns carry the highest risk for acute bacterial meningitis, and after the first month of life the peak incidence is in infants aged 3-8 months.

Causes

Causes include bacteria, viruses, fungi, parasites, and drugs (NSAIDs, metronidazole, IV immunoglobulin [IVIg]). The most common bacterial cause is S pneumoniae, a gram-positive coccus. Enteroviruses cause most aseptic meningitis in children, with nonpolio enteroviruses (NPEVs) responsible for about 90% of viral meningitis cases where a pathogen is identified; mumps virus is the most common cause of aseptic meningitis in unimmunized populations, occurring in 30% of all mumps patients. Fungal causes include Cryptococcus neoformans (a ubiquitous encapsulated yeastlike fungus), Coccidioides immitis (a soil-based dimorphic fungus in mycelial and yeast/spherule forms), and Blastomyces dermatitidis (a dimorphic fungus endemic in North America, in the Mississippi and Ohio River basins). Parasites include Angiostrongylus cantonensis, the rat lungworm, which causes eosinophilic meningitis (pleocytosis with more than 10% eosinophils), and Gnathostoma spinigerum, a GI parasite of wild and domestic dogs and cats, which may cause eosinophilic meningoencephalitis.

Clinical Manifestations

Only about 44% of adults with bacterial meningitis show the classic triad of fever, headache, and neck stiffness. Fever appears first and worsens. As bacterial meningitis progresses, seizures can occur at any age (30% of adults and children, 40% of newborns and infants). Neck stiffness is part of the triad. Kernig's sign is positive when the leg cannot fully extend with the thigh flexed on the abdomen. Brudzinski's sign is positive when neck flexion produces flexion of the knees and hips, and passive flexion of one lower extremity produces the same in the opposite leg. Subacute bacterial meningitis and most viral meningitis present with neurologic symptoms developing over 1-7 days. Infants may show high-pitched crying, lethargy or irritability (an infant may simply appear slow or inactive), and photalgia (photophobia, discomfort in bright light).

Assessment and Diagnostic Findings

Whenever meningitis is strongly considered, perform a prompt lumbar puncture; CSF examination is the cornerstone of diagnosis. A screening head CT may precede LP to assess herniation risk. In bacterial meningitis, CBC with differential shows polymorphonuclear leukocytosis with a left shift. As many as 50% of patients with pneumococcal meningitis also show pneumonia on initial chest radiography. Cultures matter most when LP is delayed for imaging to rule out herniation, in which case antimicrobials are started before CSF is obtained. Serum procalcitonin (PCT) is increasingly used to help distinguish bacterial from aseptic meningitis in children.

Medical Management

If the patient is in shock or hypotensive, infuse crystalloid until euvolemia. If mental status is altered, use seizure precautions, treat seizures per protocol, and consider airway protection. If the patient is alert and stable with normal vital signs, give oxygen, establish IV access, and arrange rapid transport to the ED.

Pharmacologic Management

Start empiric antibiotics by age and overriding conditions. Sulfonamides (trimethoprim and sulfamethoxazole) inhibit bacterial synthesis of tetrahydrofolic acid. Tetracyclines inhibit protein synthesis by binding the 30S and possibly 50S ribosomal subunits. Carbapenems, including meropenem, inhibit cell wall synthesis by binding penicillin-binding proteins. Fluoroquinolones inhibit DNA gyrase and topoisomerases, blocking DNA synthesis. Vancomycin (a glycopeptide) blocks glycopeptide polymerization in the cell wall and covers many gram-positive infections. Aminoglycosides bind 16S ribosomal RNA within the 30S subunit and are mainly bactericidal against aerobic gram-negative bacilli. Third-generation cephalosporins are less active against gram-positive organisms than first-generation agents but highly active against Enterobacteriaceae, Neisseria, and H influenzae. Antivirals interfere with viral replication for viral meningitis, and systemic antifungals treat fungal disease. Inactivated bacterial vaccines induce active immunity against meningitis pathogens. Corticosteroids improve outcomes in certain bacterial meningitis (H influenzae, tuberculous, pneumococcal). Mannitol, an osmotic diuretic, lowers subarachnoid pressure by creating an osmotic gradient between CSF and plasma. Furosemide, a loop diuretic, blocks chloride cotransport and inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal tubule. Anticonvulsants aggressively control seizures, since seizure activity raises ICP.

Nursing Management

Nursing Assessment

Continually assess neurologic status and vital signs. Use pulse oximetry and arterial blood gas values to quickly identify the need for respiratory support.

Nursing Diagnosis

Major diagnoses include risk for infection related to the contagious organism; acute pain related to headache, fever, and neck pain from meningeal irritation; impaired physical mobility related to IV infusion, nuchal rigidity, and restraining devices; activity intolerance related to fatigue and malaise; risk for impaired skin integrity related to immobility, dehydration, and diaphoresis; risk for injury related to restlessness and disorientation; interrupted family process related to the critical situation and uncertain prognosis; anxiety related to treatment and risk of death; and risk for ineffective therapeutic regimen management.

Nursing Care Planning & Goals

Goals are protection against injury, prevention of infection, restoring normal cognitive function, and preventing complications.

Nursing Interventions

Assess neurologic status and vital signs constantly, and determine oxygenation from ABGs and pulse oximetry. Insert a cuffed endotracheal tube (or tracheostomy) and place the patient on mechanical ventilation as prescribed. Monitor blood pressure (usually via arterial line) for incipient shock, which precedes cardiac or respiratory failure. Give rapid IV fluid replacement if prescribed, but avoid overhydration because of cerebral edema risk. Reduce high fever to cut the oxygen demand on heart and brain. Protect the patient from injury from seizures or altered LOC. Monitor daily body weight, serum electrolytes, and urine volume, specific gravity, and osmolality, especially if SIADH is suspected. Prevent immobility complications such as pressure injury and pneumonia. Maintain infection control precautions until 24 hours after antibiotics begin (oral and nasal discharge is infectious). Keep the family informed and allow visits at appropriate intervals.

Evaluation

Expected outcomes are avoidance of injury, avoidance of infection, restoration of normal cognitive function, and prevention of complications.

Discharge and Home Care Guidelines

At home, the patient should alternate rest and activity to conserve energy, eat safe and clean foods, use simple infection control at home, and recognize and promptly report signs of an infectious process.

Documentation Guidelines

Document the client's description of and acceptable level of pain, prior medication use, current physical findings, the client's understanding of individual risks and safety concerns, availability and use of resources, current and previous level of function and its effect on independence and lifestyle, lab and diagnostic results, mental status or cognitive evaluation, the plan of care and teaching plan, responses to interventions, attainment or progress toward outcomes, and modifications to the plan.