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Preventing and treating Meningococcal meningitis.

Meningococcal meningitis (MM) is a severe, often fatal illness that commands astute and rapid intervention. Distinguished by rash, fever, headache, and nuchal rigidity or stiff neck, the disease was first reported in 1805. According to Mehta and Levin (2000), there are 3,000 reported cases of meningitis each year. Prior to the use of antibiotics, the mortality rate for bacterial meningitis was nearly 100% (Mehta & Levin, 2000). Today, even when antibiotics are instituted early in the disease course, morbidity and mortality are high. Of affected adults, 5% to 40% will succumb to the illness (Leib & Tauber, 1999), and more than 25% will suffer neurologic complications (Thomas et al., 1999). The American Academy of Pediatricians recommended HIB (Haemophilus influenzae type b) vaccination for all infants, and consequently, the median age for patients with a reported diagnosis has increased from 15 months in 1986 to 25 years in 1995 (Gold, 1999). Further, neisseria meningitides has replaced H. influenza as the leading cause of meningitis in the United States (Dawson, Emerson, & Burns, 1999).

Numerous variables contribute greatly to increasing the incidence of bacterial meningitis. Socioeconomic factors, including low income, overcrowding, limited access to health care, and lower education level of parents raise relative risk. A compromised immune system and passive or active exposure to cigarette smoke also increase the risk for contracting meningitis (Gold, 1999). The speed in which a diagnosis is made and treatment is begun is the critical factor in caring for patients with meningitis. Adult-health nurses must recognize the pathogenesis of the disease and diagnose and treat the patients quickly.

Pathogenesis

The meninges are the membranes surrounding the brain and spinal cord. When inflammation in this tissue occurs, meningitis results. Bacterial meningitis is the most serious form of meningitis, and is caused by the bacterium Neisseria meningitidis (NM). These bacteria are transmitted by a droplet or discharge from the nose and throat of carriers or infected people. Close contact with a carrier or with a person in the early stages of disease is required for infection to occur. Adolescents and adults are the most frequent carriers of Neisseria meningitides (Stephens, 1999).

Meningococci are commonly found in their nasopharyngeal or tonsillar mucosa. It is not known why only a few individuals develop this potentially fatal disease despite the fact that the colonization of NM in the nasopharynx is very common (Mehta & Levin, 2000). Researchers believe that co-infections or dry air may damage the mucus membrane and allow invasion by the pathogen (Stephens, 1999). This may explain why the incidence of MM is greater in the late winter and early spring months (Stephens, 1999). The occurrence of bacterial meningitis has declined in the Western world as a result of improved social and sanitary conditions (Smeltzer & Bare, 1999).

Bacterial meningitis starts as an infection of the nasopharynx. The venous network of the posterior nasopharynx, middle ear, and mastoid drain toward the brain and are located near the venous system, which drains the meninges. The infection spreads via the blood stream to the subarachnoid layers of the meninges. It then enters the subarachnoid space, which includes the cerebral spinal fluid (CSF) (Smeltzer & Bare, 1999). When the bacteria reach the subarachnoid space, an inflammatory response occurs (Thomas et al., 1999). Consequently, the subarachnoid space becomes lined with purulent exudate. This in turn may obstruct CSF circulation, and can result in increased intracranial pressure (Emergency Nurses Association, 1994).

Signs and Symptoms

Once infected with the bacterium, patients with MM demonstrate a typical progression of symptoms. The most common symptoms associated with infection of the subarachnoid space are headache and fever. The headache is usually severe and is the result of meningeal irritation (Smeltzer & Bare, 1999). Fever is 85% more common in adults than children with MM (Kaplan, 1999). It is generally present throughout the course of the disease (Smeltzer & Bare, 1999). Other signs of meningeal irritation are nuchal rigidity or neck stiffness. This early sign is a result of neck spasms and is considered present if pain occurs during neck flexion and extension. A positive Kernig's sign is present if pain is experienced as the leg is extended at the knee when flexed at the hip (Elliot & Goldberg, 1997). This pain is a result of spasm of the hamstring and is caused by stretching of irritated nerve roots and meninges (Zator Estes, 2002). A positive Brudzinki's sign is present if leg hip flexion occurs when the neck is flexed (Elliot & Goldberg, 1997). This reaction occurs as a result of meningeal irritation (Zator Estes, 2002).

The signs and symptoms seen are variable and can vary notably with respect to the patient's age. However, anorexia and vomiting are common in all ages. Photophobia or an extreme sensitivity to light may be present but the cause remains unclear. Changes in level of consciousness are associated with bacterial meningitis (Smeltzer & Bare, 1999). Lethargy, unresponsiveness, and coma may develop and are the result of the severity of the infection and the patient's response to the disease process (Smeltzer & Bare, 1999).

According to Kaplan (1999), up to 12% of adults with bacterial meningitis experience seizures which occur as a result of cortical irritability (Smeltzer & Bare, 1999). As the disease progresses, classic signs of increased intracranial pressure caused by purulent exudate or cerebral edema may occur. They include widening pulse pressure and bradycardia, respiratory irregularity, headache, vomiting, and depressed levels of consciousness (Smeltzer & Bare, 1999). Focal neurologic abnormalities may be present and are related to increased intracranial pressure or impaired cerebral blood flow. Papilledema, if visualized on fundoscopic exam, is indicative of increased intracranial pressure. Sixth cranial nerve palsies, nystagmus, aphasia, hemiparesis, ataxia, hearing loss, and visual field disturbances may also be present and require additional evaluation by neurologic and infectious disease specialists (Kaplan, 1999).

Testing

When a diagnosis of MM is suspected, a lumbar puncture should be performed on the patient immediately. The cranial vault contains brain tissue, blood, and cerebral spinal fluid. An increase in any one of these components can result in increased intracranial pressure (ICP). The normal ICP is 10 to 20 mmHg (Mellor, 1992). There are several signs associated with this bacterial infection (Dawson et al., 1999). The cerebral spinal fluid is cloudy, and its pressure is elevated. The white blood cell count (WBC) usually ranges from 2,000 to 20,000, and the number of polymorphonu-clear cells is increased. Gram stains are positive in 57% of the patients with neisseria meningitides. Lumbar puncture may cause herniation in patients with intracranial pressure, because a sudden release of pressure can result in brain herniation. As the intracranial pressure increases, the patient becomes stuporous, reacting only to loud auditory or painful stimuli. Precautions should be taken if there is suspicion of an intracranial mass, severely decreased sensorium, or the presence of papilledema. A radiographic evaluation should be conducted prior to performing the lumbar puncture (Kaplan, 1999).

Several other diagnostic tests are performed. These include blood glucose, electrolytes, BUN and creatinine, serum osmolality, blood cultures, clotting studies, urinalysis, and latex agglutination (Emergency Nurses Association, 1994).

Treatment

Before the introduction of antimicrobial agents, bacterial meningitis was considered to be a fatal disease (Saez-Llorens & McCracken, 1999). Because antibiotics have selective toxicity, they are able to kill an invading organism without damaging the cell of the host (Mycek, Harvey, & Champe, 1997). Identifying the infection-carrying organism and determining its sensitivity to antibiotics is necessary in order to choose the most effective agents. In bacterial meningitis, a delay in treatment could result in death for some seriously ill patients. Therefore, some patients require immediate or empiric treatment. Empiric treatment provides for the immediate administration of drugs covering gram-negative and gram-positive microorganisms (Saez-Llorens & McCracken, 1999). In patients with suspected bacterial meningitis, therapy is initiated after cultures have been obtained but before results are available. A gram stain allows the rapid assessment of the nature of the organism. The culture provides a definitive diagnosis and determines what antibiotics the organism is susceptible to (Kaplan, 1999).

Adequate levels of antibiotics must reach the site of infection in order for the antibiotic to be effective. The structure of the brain capillary prohibits many antibiotics from crossing the blood-brain barrier. Effective treatment of meningitis depends on the ability of the antibiotic to cross the blood-brain barrier and enter the cerebrospinal fluid (Saez-Llorens & McCracken, 1999).

Antibiotics will decrease the number of infecting organisms or inhibit further growth of the organism, but the patient's immune system is ultimately responsible for eliminating the infecting organism. Higher doses of antibiotics and longer treatment may be necessary to eradicate the infecting organism in patients with altered immune systems, alcoholism, diabetes mellitus, HIV, malnutrition, or advanced age (Mycek et al., 1997).

Penicillin has been the drug of choice for treating bacterial meningitis for many years. Penicillin G is active against gram-positive and gram-negative cocci. Over the past 15 years the increased prevalence of resistant organisms has forced the change in treatment for meningitis since the susceptibility of the organism is not known at the onset of treatment (Brody, Larner, & Minneman, 1998). Pending results of cultures, ceftriaxone and cefotaxime (third-generation cephlosporines) are currently used to treat NM (Brody et al., 1998). Vancomycin, with or without rifampin, may be added to the regimen in order to cover resistant pneumococci. Both vancomycin and rifampin should be stopped if the identified organism is found to be susceptible to cephlosporins (Saez-Llorens & McCracken, 1999). When the use of cephlosporines is contraindicated, chloramphenicol may be used. Chloramphenicol is bacteriostatic and effective against NM. Chloramphenicol has serious side effects and should only be used when no other drug is suitable (Brody et al., 1998). Once the bacteria is identified and its antimicrobial susceptibility is determined, the patient's drug regimen should be modified. The routine course for antimicrobial treatment is 5 to 7 days. Management should be based on clinical labs and ongoing patient assessment.

The key to effective control of meningitis is immunophrophylaxis. The available vaccine's ability to produce immunity differs in various age groups (Smeltzer & Bare, 1999), and as the patient ages, the presence of antibodies declines (Peltola, 1999). In one study, the use of this vaccine in military recruits reduced the incidence of meningococcal meningitis by 90% (Smeltzer & Bare, 1999). In 1999, the Centers for Disease Control (CDC) recommended that freshman who reside in or plan to reside in a dorm be immunized with one dose of quadrivirulent meningococcal polysaccharide vaccine in order to reduce their risk for disease (Miller, 1999). The CDC also recommended vaccination for tourists traveling to areas where epidemics are occurring (Peltola, 1999; U.S. Department of Health and Human Services, 2000).

In many cases, supportive nursing care can improve patient prognosis. Cerebral edema and increased intracranial pressure can result in seizures, placing the patient at risk for airway obstruction, respiratory arrest, or cardiac dysrhythmia. The nursing team is responsible for continuous assessment of the patient's clinical status and monitoring of the patient's vital signs and intake and output. Nurses intervene to reduce fever and monitor the patient for generalized vasoconstriction, circumoral cyanosis, and cold extremities. Antibiotics are initiated immediately, and patients are placed on respiratory isolation until 24 hours after initiating antibiotic therapy. Family education and patient comfort are ongoing needs.

Predictors of Survival

Patients suffering from MM experience a range of outcomes. Patients, over 60 years of age have a mortality rate of 37%, while those less than 60 years old have a mortality rate of 17% (Kaplan, 1999). Studies demonstrate that the level of consciousness at the time of admission may be a predictor of survival. According to Kaplan (1999), there is a 49% mortality rate among patients who were unresponsive or only responsive to pain at the time of admission. This is in contrast to a 16% mortality rate in patients assessed as alert or lethargic at the time of admission. In one study, patients experiencing seizures within 24 hours of hospitalization had increased mortality or neurologic deficiencies (Kaplan, 1999).

Numerous sequelae associated with meningitis are seen. Hearing impairment can occur as a direct result of inflammation of the inner ear. Obstructive hydrocephalus and damage to the parenchyma of the brain can lead to neurologic sequelae. These include focal sensory motor deficits, mental retardation, and seizure disorder (Kaplan, 1999).

Understandably, the fear of meningitis produces hysteria even though bacterial meningitis is not especially contagious, and recent outbreaks usually involve a limited number of cases (Peltola, 1999). Carriers of the organism are often close contacts of the person infected with meningitis. Prophylaxis is recommended for household members and individuals who have kissed or been otherwise intimate with the patient. Peltola (1999) defines close contacts as individuals who frequently sleep and eat in the same dwelling. Schoolmates are not close contacts even if they are in the same room, unless they sit close to each other. Any health care worker who has direct contact with the patient's secretions should be considered a close contact (Peltola, 1999).

A 2-day course of rifampin, which is bactericidal and is effective against gram-positive and gram-negative organisms, should be provided for all close contacts (Mycek et al., 1997). An intramuscular injection of ceftriaxone is appropriate if the contact is unable to take rifampin (Peltola, 1999).

Prophylaxis will probably not prevent disease if the organism has already invaded and is incubating in the host. Contacts should be cautioned to seek immediate assistance if any signs and symptoms of the disease occur within 1 to 2 weeks following the onset of illness of their contact (Peltola, 1999).

Conclusion

Knowing the epidemiology, pathogenesis, diagnosis, and treatment for MM enables nurses to reduce the mortality and improve clinical outcomes for patients suffering from MM. Because this highly lethal bacterium is so preventable, it is vitally important that nurses promote primary prevention strategies. Identifying populations at risk and encouraging vaccination will lower the incidence of the disease. Once patients are infected, vigilant supportive nursing care can reduce sequelae on survivors.

Additional Readings

Charlton, R. (1998). Concerns about meningitis. Postgraduate Medicine, 104(1), 31-32.

Diaz, P.S. (1999). The epidemiology and control of invasive meningococcal disease. Pediatric Infectious Disease Journal, 18(7), 633-634.

References

Brody, T.M., Larner, J., & Minneman, K.P. (1998). Human pharmacology molecular to clinical. St Louis, MO: Mosby.

Dawson, K.J.G., Emerson, J.C., & Burns, J.L. (1999). Fifteen years of experience with bacterial meningitis. Pediatric Infectious Disease Journal, 18(9), 816-822.

Elliot, D.L., & Goldberg, L. (1997). The history and physical examination case book. Philadelphia: Lippincott- Raven.

Gold, R. (1999). Epidemiology of bacterial meningitis. Infectious Disease Clinics of North America, 13(3), 515-521.

Kaplan, S.L. (1999). Clinical presentation, diagnosis and prognostic factors of bacterial meningitis. Infectious Disease Clinic of North America, 13(3), 579-593.

Leib, S.L., & Tauber, M.G. (1999). Pathogenesis of bacterial meningitis. Infectious Disease Clinic of North America, 13(3), 527-545.

Mehta, N., & Levin, M. (2000). Management and prevention of meningococcal disease. Hospital Practice, 35(8), 75-86.

Mellor, D.H. (1992). The place of computed tomography and lumbar puncture in suspected bacterial meningitis. Archives of Disease in Children, 67(12), 1417-1419.

Miller, J.L. (1999). Use of meningococcal vaccine in college freshman reconsidered. American Journal System Pharmacy, 56(23), 2372.

Mycek, M.J., Harvey, R.A., Champe, P.C. (1997). Lippincott's illustrated reviews: Pharmacology. Philadelphia: Lippincott, Williams & Wilkins.

Peltola, H. (1999). Prophylaxis of bacterial meningitis. Infectious Disease Clinic of North America, 13(3), 685-705.

Saez-Llorens, X., & McCracken, G.H. (1999). Antimicrobial and anti-inflammatory treatment of bacterial meningitis. Infectious Disease Clinic of North America, 13(3), 619-633.

Smeltzer, S.C., & Bare, B.G. (1999). Brunner and Suddarth's textbook of medical surgical nursing. Philadelphia: Lippincott.

Stephens, D.S. (1999). Uncloaking the meningococcus: Dynamics of carriage and disease. Lancet, 353(9157), 941-942.

Thomas, R., Le Tulzo, Y. Bouget, J., Camus, C., Michelet, C., LeCorre, P., & Bellissant, E. (1999). Trail of dexamethasone treatment for severe bacterial meningitis in adults. Intensive Care Medicine, 25(5), 475-480.

U.S. Department of Health and Human Services. (2000). Health information for international travel 1999-2000. Washington, DC: U.S. Government Printing Office.

Zator Estes, M. (2002). Health assessment and physical examination. New York: Delmar.

Patricia A. Michael, MSN, RN, is Director, Capital Health System, Trenton, NJ.
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Date:Feb 1, 2002
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