Secondary Logo

Journal Logo

Fire up to beat the threat of bacterial meningitis

Miller, April MSN, RN, CCRN, CNS

doi: 10.1097/01.NURSE.0000437473.22627.01
Feature
Free

When bacterial meningitis strikes, rapid assessment, diagnosis, and treatment can save the patient's life. Be prepared to act fast to prevent death or serious complications such as brain damage.

April Miller is an RN at Memorial Hospital of Carbondale in Carbondale, Ill.

The author has disclosed that she has no financial relationships related to this article.

Figure

Figure

WITHOUT A DOUBT, bacterial meningitis in adults is a frightening diagnosis with an alarming mortality. The good news is that this devastating disease is on the decline in the United States. Based on surveillance data from 1998 to 2007, the incidence of bacterial meningitis has declined from 2 cases per 100,000 to 1.38 per 100,000.1

The bad news? While the incidence is dropping, the mortality of about 15% has changed little.1 In developing countries without access to good healthcare and vaccines, the mortality is much higher.2,3 About 20% of meningitis survivors suffer long-term consequences, including brain damage, renal failure, hearing loss, and amputations.4

In many clinical situations, healthcare providers prefer a slow and methodical diagnostic workup favoring noninvasive, cost-effective methods. In the case of bacterial meningitis, however, a rapid assessment, workup, and diagnosis can be life saving. Because this disease can turn deadly very quickly, establishing the diagnosis and starting appropriate treatment as early as possible is critical. This article explains how these steps can be achieved.

Back to Top | Article Outline

Looking into the neurologic system

Meningitis occurs when the leptomeninges, the thin tissues surrounding the brain and spinal cord, are inflamed, and the cerebrospinal fluid (CSF) contains an abnormally large number of white blood cells (WBCs). The meninges are made up of the pia, arachnoid, and dura maters. In bacterial meningitis, the arachnoid mater and the CSF are infected in both the subarachnoid space and the cerebral ventricles.5 (See Getting inside the meninges.)

Bacterial rarely penetrate the blood-CSF barrier. But when penetration does occur, bacteria can enter the subarachnoid space and cause meningitis.2

Back to Top | Article Outline

Understanding the epidemiology

Meningitis can be caused by several types of microorganisms, which can be classified as bacterial or nonbacterial, including viruses.6

When diagnosing bacterial meningitis, healthcare providers consider certain patient characteristics. Factors related to age, immunosuppression, geographic region, and recent infections and surgeries can predispose a patient to bacterial meningitis.2,3 Otitis, sinusitis, and pneumonia are some common conditions linked to bacterial meningitis.3

The three leading causes of bacterial meningitis in the United States are Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae.7 Bacterial meningitis can also be caused by group B streptococcus and Listeria monocytogenes.1,7–9

S. pneumoniae, which causes pneumococcal meningitis, is the most common cause of meningitis in the United States, and has a mortality around 15%.1 Older adults and immunocompromised patients are at greatest risk for pneumococcal meningitis.

Meningococcal meningitis, caused by N. meningitidis, is most common in adolescents and young adults. Nearly 15% of meningococcal disease occurs in this age-group.10 Meningococcal disease is associated with crowded living conditions, such as college dormitories.2,10 The mortality of meningococcal meningitis is about 10%.1

The incidence of H. influenzae infection has declined dramatically in recent years because of vaccination against H. influenzae. However, H. influenzae remains a common cause of bacterial meningitis in adults and unvaccinated infants and children, especially in those with diminished humoral immunity.5

Back to Top | Article Outline

Pathophysiology

Bacterial meningitis develops when bacteria in the CSF replicate and undergo lysis. This process releases endotoxins or fragments of cell walls, which in turn initiate the release of inflammatory mediators. These substances start a complex sequence of events that allows pathogens, neutrophils, and albumin to move into the CSF by crossing capillary walls.11

When the pathogens move into the subarachnoid space, they cause inflammation and a purulent exudate. Vascular congestion and infarction may develop in the surrounding tissues due to thrombophlebitis of the bridging veins and dural sinuses or obliteration of arterioles by inflammation. Finally, the meninges thicken and adhesions form. These adhesions may impinge on the cranial nerves, causing cranial nerve palsies, or may prevent CSF outflow, causing hydrocephalus.11

Back to Top | Article Outline

Clinical presentation

The classic triad of acute bacterial meningitis consists of fever, nuchal rigidity (stiff neck), and altered mental status. At least one of these findings is almost always present in patients with this disease.3 A severe, generalized headache is also a common symptom.5 Other possible symptoms include photophobia, nausea, and vomiting.

Patients age 65 and older are more likely to have seizures and hemiparesis and less likely to have a headache and nuchal rigidity than younger patients.3

Two well-known physical assessment findings often associated with meningeal irritation and inflammation are a positive Kernig sign and a positive Brudzinski sign.12 (See Sizing up the signs.)

Some patients may present with a petechial rash. Although most commonly seen with meningococcal disease caused by N. meningitidis, it's also seen with H. influenzae or S. pneumoniae infections.3,13

Back to Top | Article Outline

Diagnostic studies

Lab studies include a complete blood cell count, blood cultures, serum chemistry tests, coagulation studies, and C-reactive protein tests.9

Anytime bacterial meningitis is suspected, a lumbar puncture should be performed as soon as possible (unless contraindicated) to obtain cerebral spinal fluid specimens for analysis, including culture and sensitivity. In general, a low CSF glucose level, an elevated CSF protein concentration, and a high CSF leukocyte count indicate bacterial meningitis. (See Classic CSF findings in acute bacterial meningitis.)

A lumbar puncture performed on a patient with increased intracranial pressure (ICP) can result in cerebral herniation, so under certain circumstances, such as the presence of a focal neurologic deficit, a computed tomography (CT) scan of the brain may be performed prior to lumbar puncture.2

In these patients, specimens for blood cultures should be obtained and empiric antibiotic therapy initiated before the CT scan is performed.2,8 If the CT scan is normal, the lumbar puncture should be performed.

As long as the patient hasn't received antibiotics before the CSF specimen was obtained, the culture will be positive 70% to 85% of the time.8 Unfortunately, it can take 48 hours to obtain these results. In the meantime, a Gram stain can help to correctly identify the organism 60% to 90% of the time.8

Back to Top | Article Outline

Antibiotic therapy

Promptly administering antibiotics is a priority immediately after the lumbar puncture is performed or, if a CT of the head is needed before lumbar puncture, immediately after blood cultures are obtained.2,3 Antibiotic therapy should target the presumptive organism identified on the Gram stain. If the lumbar puncture can't be obtained immediately, then empirical antibiotic therapy should be initiated.8

Table C

Table C

The Infectious Diseases Society of America has published clinical guidelines for the treatment of bacterial meningitis. If the causative organism is S. pneumoniae, vancomycin plus a third-generation cephalosporin is recommended. Recommended antimicrobial therapy for N. meningitidis is a third-generation cephalosporin. Duration of antibiotic therapy is related to the causative organism and the patient's clinical response to treatment.8 Dexamethasone should be considered in patients with suspected pneumococcal meningitis. This drug may diminish some of the negative consequences of inflammation in the central nervous system (CNS).8,14

Back to Top | Article Outline

Nursing considerations

  • The conjugate vaccines for H. influenzae type b and S. pneumoniae have been very successful in preventing meningitis.2,6 The meningococcal vaccine is routinely given to adolescents and should be given to people with certain risk factors. (See Who should receive the meningococcal vaccine, and which one?)
  • If at all possible, patients with bacterial meningitis should be admitted to a neurologic ICU. This setting allows for close monitoring of neurologic status and for complications.
  • The CDC recommends that patients with suspected or proven meningitis caused by either N. meningitidis or H. influenzae type b be placed on droplet precautions for the first 24 hours of antibiotic therapy.13,15
  • Deterioration in clinical status can occur rapidly, so frequently assess the patient's neurologic status, especially level of consciousness and vital signs. Report new focal signs immediately.13
  • Try to minimize increases in the patient's ICP. Appropriate measures may include keeping the patient's head of bed elevated to 30 degrees, keeping the head midline, minimizing suctioning, using sedation, keeping the room quiet and dark, and avoiding hypercapnia.13,14
  • Patients with bacterial meningitis may develop dehydration, shock, syndrome of inappropriate secretion of antidiuretic hormone, and/or intracranial hypertension. Closely monitor for fluid and electrolyte imbalances.3,9
  • Analgesics may be required to treat headache. Darkening the room may help if the patient complains of photophobia.13
  • The patient's hearing should be assessed before discharge because hearing loss is a common late complication of bacterial meningitis.5,14,16
  • Keep in mind that because N. meningitidis is easily spread from person to person, secondary cases need to be prevented. Suspected meningococcal disease should be reported to the local public health department. People in close contact with an infected person should receive chemoprophylaxis.14,16
Back to Top | Article Outline

Outcome measurement

Survivors of bacterial meningitis may experience long-lasting problems that aren't apparent during the acute period. Besides hearing loss, patients may experience renal dysfunction and neurologic complications.

Those who develop seizures during the course of the illness may require long-term antiepileptic drugs.14 Even patients who make a full recovery may require psychological support after surviving this devastating illness.17

Back to Top | Article Outline

Need for speed

By being alert to signs and symptoms of bacterial meningitis and realizing the need for speed for patients suspected of having this potentially deadly disease, nurses can help their patients survive and minimize complications. And simply reminding appropriate patients of the benefits of vaccination is another way nurses can fight back against bacterial meningitis.

Back to Top | Article Outline

Getting inside the meninges

Inside the skull and vertebral column, the brain and spinal cord are loosely suspended and protected by several connective tissue sheaths called the meninges, as shown in this figure. The surfaces of the spinal cord, brain, and segmental nerves are covered with a delicate connective tissue layer called the pia mater (Latin for “delicate mother”). The surface blood vessels and those that penetrate the brain and spinal cord are encased in this protective tissue layer. A second very delicate, nonvascular, and waterproof layer, called the arachnoid, encloses the entire CNS. The arachnoid layer is named for its spider-web appearance. The CSF is contained in the subarachnoid space. Arachnoid villi, shown within the superior sagittal sinus, are one site of CSF absorption into the blood. Immediately outside the arachnoid is a continuous sheath of strong connective tissue, the dura mater (Latin for “tough mother”), which provides the major protection for the brain and spinal cord. The cranial dura often splits into two layers, with the outer layer serving as the periosteum of the inner surface of the skull.

Figure

Figure

Source: Porth CM. Essentials of Pathophysiology. 3rd ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams and Wilkins; 2011.

Back to Top | Article Outline

Sizing up the signs

Neck mobility. First, ensure that the patient has been properly evaluated by a healthcare provider to rule out the potential for spinal column or spinal cord injury. Patients with no history of trauma who are supine should be able to flex the neck forward until the chin touches the chest, if possible. Normally, the neck is supple, and the patient can easily bend the head and neck forward.

Brudzinski sign. As the patient flexes his or her neck, observe the hips and knees in reaction to this maneuver. Normally they should remain relaxed and motionless. Flexion of the hips and knees is a positive Brudzinski sign suggesting meningeal inflammation.

Kernig sign. Flex the patient's leg at both the hip and knee, and then straighten the knee. Although some discomfort behind the knee during full extension is common, this maneuver shouldn't produce pain. Pain and increased resistance to extending the knee are a positive Kernig sign. When bilateral, it suggests meningeal irritation.

Figure

Figure

Source: Bickley LS, Szilagyi PG. Guide to Physical Examination and History Taking. 10th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams and Wilkins; 2009.

Back to Top | Article Outline

Who should receive the meningococcal vaccine, and which one?18,19

People at risk for bacterial meningitis who should be vaccinated include the following:

  • adolescents
  • students living in dormitories
  • military recruits
  • anyone exposed to meningococcal bacteria in labs
  • anyone traveling to or living in parts of the world where meningococcal disease is common
  • people who are immunocompromised
  • anyone who may have been exposed to someone with bacterial meningitis.

Meningococcal conjugate vaccine (MCV4) is the preferred vaccine for people age 55 or younger. Meningococcal polysaccharide vaccine (MPSV4) is the only meningococcal vaccine licensed for people older than 55. People with certain medical conditions and most adolescents need two doses for adequate protection. For more information about vaccination schedules in adults and children, see http://www.cdc.gov/vaccines/vpd-vac/mening/.

Back to Top | Article Outline

REFERENCES

1. Thigpen MC, Whitney CG, Messonnier NE, et al. Bacterial meningitis in the United States, 1998–2007. N Engl J Med. 2011;364(21):2016–2025.
2. Bhimraj A. Acute community-acquired bacterial meningitis in adults: an evidence-based review. Cleve Clin J Med. 2012;79(6):393–400.
3. Bamberger DM. Diagnosis, initial management, and prevention of meningitis. Am Fam Physician. 2010;82(12):1491–1498.
4. National Meningitis Association. Overview. About meningococcal disease. 2013. http://www.nmaus.org/meningitis/.
5. Tunkel AR.Clinical features and diagnosis of acute bacterial meningitis in adults. UpToDate. 2012. http://www.uptodate.com.
6. Abd Nasir AI, Omar FM, Lau TF, et al. The overview of meningitis and its treatment. Category: infectious diseases. 2011;2(12):WMC002767. http://www.webmedcentral.com/article_view/2767.
7. Brouwer MC, Tunkel AR, van de Beek D. Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis. Clin Microbiol Rev. 2010;23(3):467–492.
8. Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis. 2004;39(9):1267–1284.
9. Blewitt J. Meningitis part 1: causes, diagnosis and treatment. Br J Sch Nurs. 2010;5(6):278–282.
10. National Meningitis Association. Who is at risk? 2013. http://www.nmaus.org/meningitis/who-is-at-risk.htm.
11. Porth CM. Essentials of Pathophysiology. 3rd ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams and Wilkins; 2011.
12. Ward MA, Greenwood TM, Kumar DR, Mazza JJ, Yale SH. Josef Brudzinski and Vladimir Mikhailovich Kernig: signs for diagnosing meningitis. Clin Med Res. 2010;8(1):13–17.
13. Hoffman O, Weber JR. Pathophysiology and treatment of bacterial meningitis. Ther Adv Neurol Disord. 2009;2(6):1–7.
14. Chaudhuri A, Martinez-Martin P, Kennedy PG, et al. EFNS guideline on the management of community-acquired bacterial meningitis: report of an EFNS Task Force on acute bacterial meningitis in older children and adults. Eur J Neurol. 2008;15(7):649–659.
15. Fahey BJ.Meningitis: bacterial vs. viral. Advance Healthcare Network for Nurses. http://nursing.advanceweb.com/article/meningitis-bacterial-vs-viral.aspx.
16. Watkins J. Recognising the signs and symptoms of meningitis. Br J Sch Nurs. 2013;7(10):481–483.
17. Beckett G. Meningitis and septicaemia: diagnosis and prevention—immunization and vaccination. Practice Nurs. 2010;21(8):398–402.
18. Centers for Disease Control and Prevention. Vaccines and preventable diseases: meningococcal: who needs to be vaccinated? 2011. http://www.cdc.gov/vaccines/vpd-vac/mening/who-vaccinate.htm.
19. Centers for Disease Control and Prevention. Vaccine information statements (VIS). Meningococcal VIS. 2011. http://www.cdc.gov/vaccines/hcp/vis/vis-statements/mening.html.
© 2013 by Wolters Kluwer Health | Lippincott Williams & Wilkins.