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Chapter: Medical Surgical Nursing: Management of Patients With Neurologic Infections, Autoimmune Disorders, and Neuropathies

Meningitis - Infectious Neurologic Disorders

Meningitis - Infectious Neurologic Disorders
The infectious disorders of the nervous system include meningitis, brain abscesses, various types of encephalitis, and CreutzfeldtJakob and new-variant Creutzfeldt-Jakob disease.

Infectious Neurologic Disorders

The infectious disorders of the nervous system include meningitis, brain abscesses, various types of encephalitis, and CreutzfeldtJakob and new-variant Creutzfeldt-Jakob disease. The clinical manifestations, assessment, and diagnostic findings as well as the medical and nursing management are related to the specific infectious process.


Meningitis is an inflammation of the meninges, the protective membranes that surround the brain and spinal cord. Meningitis is classified as aseptic or septic. In aseptic meningitis, bacteria are not the cause of the inflammation; the cause is viral or secondary to lymphoma, leukemia, or brain abscess. Septic meningitis refers to meningitis caused by bacteria, most commonly Neisseria meningitidis, although Haemophilus influenzae and Streptococcus pneumoniae are also causative agents.

Outbreaks of N. meningitidis infection are most likely to occur in dense community groups, such as college campuses and military installations. Though infections occur year round, the peak incidence is in the winter and early spring. Factors that increase the risk for developing bacterial meningitis include tobacco use and viral upper respiratory infection because they increase the amount of droplet production. Otitis media and mastoiditis increase the risk of bacterial meningitis because the bacteria can cross the epithelium membrane and enter the subarachnoid space. Persons with immune system deficiencies are also at greater risk for developing bacterial meningitis. Between 1992 and 1996 there was a 28% increase in the number of new cases reported in the 12-to-29-year-old age group (Rosenstein, Perkins, Stephens et al.,2001). This increase focused attention on the need to develop a vaccine for high-risk populations.


Meningeal infections generally originate in one of two ways:through the bloodstream as a consequence of other infections, or by direct extension, such as might occur after a traumatic injury to the facial bones, or secondary to invasive procedures.

N. meningitidis concentrates in the nasopharynx and is transmitted by secretion or aerosol contamination. Bacterial or meningococcal meningitis also occurs as an opportunistic infection in patients with acquired immunodeficiency syndrome (AIDS) and as a complication of Lyme disease (Chart 64-1). S. pneumoniae is the most frequent causative agent of bacterial meningitis associated with AIDS (Rosenstein, Perkins, Stephens et al., 2001).

Once the causative organism enters the bloodstream, it crosses the blood–brain barrier and causes an inflammatory reaction in the meninges. Independent of the causative agent, inflammation of the subarachnoid space and pia mater occurs. Since there is little room for expansion within the cranial vault, the inflammation may cause increased intracranial pressure. Cerebrospinal fluid (CSF) flows in the subarachnoid space, where inflammatory cellular material from the affected meningeal tissue enters and accumulates in the subarachnoid space, thereby increasing the CSF cell count (Coyle, 1999).

The prognosis for bacterial meningitis depends on the causative organism, the severity of the infection and illness, and the timeliness of treatment. In acute fulminant presentations there may be adrenal damage, circulatory collapse, and widespread hemorrhages (Waterhouse-Friderichsen syndrome). This syndrome is the result of endothelial damage and vascular necrosis caused by the bacteria. Complications include visual impairment, deafness, seizures, paralysis, hydrocephalus, and septic shock.



Clinical Manifestations

Headache and fever are frequently the initial symptoms. Fever tends to remain high throughout the course of the illness. The headache is usually severe as a result of meningeal irritation. Meningeal irritation results in a number of other well-recognized signs common to all types of meningitis:

·        Nuchal rigidity (stiff neck) is an early sign. Any attempts at flexion of the head are difficult because of spasms in the muscles of the neck. Forceful flexion causes severe pain.

·        Positive Kernig’s sign: When the patient is lying with the thigh flexed on the abdomen, the leg cannot be completely extended (Fig. 64-1).

·       Positive Brudzinski’s sign: When the patient’s neck is flexed, flexion of the knees and hips is produced; when passive flex-ion of the lower extremity of one side is made, a similar movement is seen in the opposite extremity (see Fig. 64-1).

·      Photophobia: extreme sensitivity to light; this finding is common, although the cause is unclear.


A rash can be a striking feature of N. meningitidis infection, occurring in about half of patients with this type of meningitis. Skin lesions develop, ranging from a petechial rash with purpuric lesions to large areas of ecchymosis.


Disorientation and memory impairment are common early in the course of the illness. The changes depend on the severity of the infection as well as the individual response to the physiologic processes. Behavioral manifestations are also common. As the illness progresses, lethargy, unresponsiveness, and coma may develop.


Seizures and increased intracranial pressure (ICP) are also as-sociated with meningitis. Seizures occur secondary to focal areas of cortical irritability. Intracranial pressure increases secondary to accumulation of purulent exudate. The initial signs of in-creased ICP include decreased level of consciousness and focal motor deficits. If ICP is not controlled, the uncus of the temporal lobe may herniate through the tentorium into the brain stem. Brain stem herniation is a life-threatening event causing cranial nerve dysfunction and depressing the centers of vital functions, such as the medulla (Rowland, 2000).


A fulminating infection occurs in about 10% of patients with meningococcal meningitis, with signs of overwhelming sep-ticemia: an abrupt onset of high fever, extensive purpuric lesions (over the face and extremities), shock, and signs of disseminated intravascular coagulopathy (DIC). Death may occur within a few hours of onset of the infection.

Assessment and Diagnostic Findings

When the clinical presentation points to meningitis, diagnostic testing to identify the causative organism is conducted. Bacterial culture and Gram staining of CSF and blood are key diagnostic tests (Fischbach, 2002). The presence of polysaccharide antigen in CSF further supports the diagnosis of bacterial meningitis (Rosenstein et al., 2001).



In 1971, the military began vaccinating all new recruits against meningococcal meningitis, resulting in a dramatic decrease in the incidence. Researchers suggested vaccination of college freshman as surveillance studies indicated that freshmen living in dormito-ries were at highest risk for developing meningococcal meningitis. At this time vaccination is not required for college freshmen; however, the American Academy of Pediatrics provides informa-tion to college freshmen and their parents about the risk of dis-ease and the availability of vaccination (Bruce et al., 2001; Centers for Disease Control and Prevention [CDC], 2000).


People in close contact with patients with meningococcal meningitis should be treated with antimicrobial chemopro-phylaxis using rifampin (Rifadin), ciprofloxacin hydrochloride (Cipro), or ceftriaxone sodium (Rocephin) (CDC, 2000). Ther-apy should be started as soon as possible after contact; a delay in the initiation of therapy will limit the effectiveness of the pro-phylaxis (Rosenstein et al., 2001). Vaccination should also be considered as an adjunct to antibiotic chemoprophylaxis for any-one living with a person who develops meningococcal infection. Vaccination for children and at-risk adults should be encouraged to avoid meningitis caused by H. influenzae and S. pneumoniae.


Medical Management


Successful outcomes depend on the early administration of an anti-biotic that crosses the blood–brain barrier into the subarachnoid space in sufficient concentration to halt the multiplication of bac-teria. Penicillin antibiotics (eg, ampicillin, piperacillin) or one of the cephalosporins (eg, ceftriaxone sodium, cefotaxime sodium) may be used. Vancomycin hydrochloride alone or in combina-tion with rifampin may be used if resistant strains of bacteria are identified. High doses of the appropriate antibiotic are adminis-tered intravenously.


Dexamethasone has been shown to be beneficial as adjunct therapy in the treatment of acute bacterial meningitis and in pneumococcal meningitis if given 15 to 20 minutes before the first dose of antibiotic and every 6 hours for the next 4 days. Studies indicate that dexamethasone improves the outcome in adults and does not increase the risk of gastrointestinal bleeding (de Gans & van de Beek, 2002).


Dehydration and shock are treated with fluid volume ex-panders. Seizures, which may occur in the early course of the dis-ease, are controlled with phenytoin (Dilantin). Increased ICP is treated as necessary.


Nursing Management


The patient may be critically ill; therefore, so many of the nurs-ing interventions are collaborative with those of the physician, respiratory therapist, and other members of the health care team. The patient’s prognosis may depend on the supportive care provided.


Neurologic status and vital signs are continually assessed. Pulse oximetry and arterial blood gas values are used to quickly identify the need for respiratory support as the increasing ICP compromises the brain stem. Insertion of a cuffed endotracheal tube (or tracheotomy) and mechanical ventilation may be neces-sary to maintain adequate tissue oxygenation.


Arterial blood pressures are monitored to assess for incipient shock, which precedes cardiac or respiratory failure. Rapid intra-venous (IV) fluid replacement may be prescribed, but care is takento prevent fluid overload. Fever also will increase the workload of the heart and cerebral metabolism. ICP will increase in response to increased cerebral metabolic demands. Therefore, measures are taken to reduce body temperature as quickly as possible.

Other important components of nursing care include:


·      Monitoring body weight, serum electrolytes, and urine vol-ume, specific gravity, and osmolality, especially if the syn-drome of inappropriate antidiuretic hormone (SIADH) secretion is suspected

·      Protecting the patient from injury secondary to seizure ac-tivity or altered level of consciousness

·      Preventing complications associated with immobility, such as pressure ulcers and pneumonia

·      Instituting droplet precautions until 24 hours after the ini-tiation of antibiotic therapy (oral and nasal discharge is con-sidered infectious)


Any sudden, critical illness can be devastating to the family. Because the patient’s condition is often critical and the progno-sis guarded, the family needs to be informed about the patient’s condition and permitted to see the patient at intervals, even though the priority is to address the patient’s need for immediate and intensive treatment. An important aspect of the nurse’s role is to support the patient and to assist the family in identifying others who can be supportive to them during the crisis.

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