Bacterial Meningitis

Pathophysiology
NURS 256
Jessica Bray

1
Meningitis is an inflammation of the pia mater and arachnoid membranes that surround the brain and

spinal cord. The sub arachnoid space between the two layers contains CSF which may reflect the signs

and sx. of meningitis. In bacterial meningitis a bacterial pathogen is responsible for the infection. The

organisms responsible vary with the age and immune status of the patient. The mortality rate is 5% (

). Bacterial meningitis is usually more serious than viral meningitis. It is not self limiting as viral

meningitis is and permanent CNS damage may be caused by the inflammation associated with the

bacterial infection instead of the pathogen itself. Purulent exudates may result in vasculitis and

cerebral vasospasm that may lead to cerebral edema. Bacterial meningitis is usually spread by droplet

precautions. This disease first presents itself through Pathophysiology when “the host becomes

infected with a pathogen that commonly causes meningitis such as, S. pneumoniae and N.

meningitides. The bacteria colonize the nasopharynx by attaching to NP epithelial cells. Bacteria are

transported across epithelial cells to the intravascular space or invade the intravascular space by

creating separations in the junctions of epithelial cells. Once in the bloodstream, bacteria are able to

avoid phagocytosis by neutrophils and classic complement–mediated bactericidal activity due to the

presence of a polysaccharide capsule. Bloodborne bacteria can reach the intraventricular choroid

plexus of the brain and directly infect its epithelial cells, and subsequently gain access to the CSF.

Some bacteria, such as S. pneumoniae, can adhere to cerebral capillary endothelial cells and

subsequently migrate through or between these cells to reach the CSF. Bacteria are able to multiply

rapidly within CSF because of the absence of effective host immune defenses. Normal CSF contains

few white blood cells (WBCs) and relatively small amounts of complement proteins. The small number

of the latter two prevents effective phagocytosis of bacteria by neutrophils. CSF is less conducive to

phagocytosis than a solid tissue substrate” (. These factors contribute to the rapid onset on

meningococcal infection. Classic symptoms are fever, headache, and nuchal rigidity. Older patients

may display altered mental status whereas children display behavioral changes, arching of the neck

and back, a blank stare, feeding intolerance, and seizure activity. Petechial rashes may be present.

Patients often complain of photophobia. Neck tenderness, altered breathing pattern, listlessness and

bulging anterior fontanel bulging is usually present in infants. There are two signs that indicate

positive meningeal irritation (Brudzinski’s and Kernig’s signs).

2
The pathogenesis of bacterial meningitis is critically influenced by the inflammatory reaction induced

by the invading bacteria. Many of the neurologic manifestations and complications of bacterial

meningitis result from the immune response to the invading pathogen rather than from direct

bacteria-induced tissue injury. As a result, neurologic injury can progress even after the CSF has been

sterilized by antibiotic therapy.

Bacterial lysis with the release of cell-wall components (toxins) into the subarachnoid space is the

initial step of the inflammatory response and the formation of purulent exudates in the subarachnoid

space. “Bacterial cell-wall components, such as the lipopolysaccharide (LPS) molecules of gram-

negative bacteria and teichoic acid and peptidoglycans of S. pneumoniae, induce meningeal

inflammation by stimulating the production of inflammatory cytokines and chemokines by nerve cells,

astrocytes, monocytes, microvascular endothelial cells, and CSF leukocytes . This cytokine response

leads to an increase in CSF protein concentration and leukocytosis. Cytokines that induce chemotactic

migration in leukocytes and a variety of other proinflammatory cytokines are also produced and

secreted by leukocytes and tissue cells that are stimulated by IL-1 and TNF”.

(www.merckmanuals.com/professional). In addition, bacteremia and the inflammatory responses

induce the production of excitatory amino acids, reactive oxygen, nitrogen, and other mediators that

can induce death of brain cells.

Diagnostic evaluation is usually made by performing a lumbar puncture for collection and

examination of CSF. CSF that is positive for meningitis will have a turbid or cloudy appearance. The

patient will have elevated CSF pressure. The CSF will contain an elevated amount of

polymorphonuclear cells. The glucose level of the fluid will be reduced while proteins are elevated.

The gram stain will be positive as will the culture identifying the causative organism. Additional

laboratory studies include. A CBC (this will usually show increased total WBC count, with a large

number being young neutrophils in the diff.) Blood, urine, and nasopharyngeal swabs may be done in

an attempt to find the source of infection. In severely ill patients platelet count, serum electrolytes,

glucose, BUN, and Creatinine may be monitored as these values may be critical in patients with

severe meningitis. MRI and or CT scans may be performed to rule out other disorders or to detect

abscesses. www.accessmedicine.com

3
 The management of meningitis is a team approach through nursing, infectious disease

specialists, neurology, internal medicine, and otolaryngologist, and laboratory staff. IV antibiotics are

started immediately and are modified if necessary after C&S has been done. IV corticosteroids are

given to manage the inflammation; this may lead to GI bleeding and mask clinical responses to

infection. Steroids are confined to patients greater than 6 weeks of age. Experimental treatment with

plasmaphoresis has been used to remove cytokines from the blood. If the source of infection is

neurosurgical procedures therapy is indicated for MRSA and other gram negative bacteria.

Complications of bacterial meningitis (especially in children) may result in deafness, learning

difficulties, spasticity, paresis, or cranial nerve disorders. Seizures occur in 20-30% of patients

(Lippincott, pp.503). Increased ICP may result in cerebral edema, decreased perfusion, and tissue

damage. Severe edema may result in herniation or compression of the brainstem. In some instances

pupura have been associated with DIC.

Nursing assessment includes a detailed history of recent exposure to infections, assessment of

neurological status and vital signs. Performance of tests that indicate meningeal irritation, and

assessment of sensorineaural function (sight, hearing, facial nerve palsy), and diminished cognitive

function. Nursing interventions to reduce fever include administration of antimicrobial agents on

schedule, monitoring temperature and administering antipyretics as ordered, and institution of other

cooling methods such as hypothermia blankets. Nursing interventions directed towards maintaining

fluid balance include prevention of IV fluid overload (to prevent increase cerebral edema), close

monitoring of I&O. Measures used to enhance cerebral perfusion include assessment of LOC, vitals,

and neurological status frequently. The nurse will maintain a calm and dimly lit environment to

prevent agitation which can increase ICP and relieve photophobia. Preparing the patient for lumbar

puncture is often a nursing intervention. The nurse must notify the healthcare provider of signs of

deterioration: increasing temp, decreasing LOC, seizure activity, or altered respirations. Nursing

interventions aimed at reducing pain include administration of analgesics and monitoring response.

Opiods are avoided as they may mask true LOC. Assistance with positioning to comfort for neck or

back stiffness is done. Elevating the bed will decrease ICP and therefore reduce pain.

4
REFERENCES

1. Roos Karen L, Tyler Kenneth L, "Chapter 376. Meningitis, Encephalitis, Brain Abscess, and

Empyema" (Chapter Harrison's Principles of Internal Medicine), 17e: retrieved 11/25/2010 from:

http://www.accessmedicine.com/content.aspx?aID=2906668.

2. Jacewicz, David MD, (full review/revision December 2009 ), Acute bacterial meningitis. Retrieved

11/23/2010 from http://www.merckmanuals.com/professional/sec16/ch218/ch218b.html

3. Lippincott Williams & Wilkins, 2006 Lippincott manual of nursing practice8th Edition, Neurologic

disorders, pp. 503-505, Ambler , PA: Lippincott Raven Publishers.