Atlas of pathophysiology, 2 Edition
Part II - Disorders
In meningitis, the brain and the spinal cord meninges become inflamed, usually because of bacterial infection. Such inflammation may involve all three meningeal membranes—the dura mater, arachnoid, and pia mater.
Meningitis is usually a complication of bacteremia, especially due to:
Other infections associated with the development of meningitis include:
· otitis media
· brain abscess, usually caused by Neisseria meningitidis, Haemophilus influenzae, Streptococcus pneumoniae, and Escherichia coli.
Meningitis may follow trauma or invasive procedures, including:
· skull fracture
· penetrating head wound
· lumbar puncture
· ventricular shunting.
Aseptic meningitis may result from a virus or other organism. Sometimes no causative organism can be found.
Meningitis commonly begins as an inflammation of the pia-arachnoid, which may progress to congestion of adjacent tissues and destroy some nerve cells. The microorganism typically enters the central nervous system by way of blood; direct communication between cerebrospinal fluid (CSF) and the environment (trauma); along cranial or peripheral nerves; or through the mouth or nose. Microorganisms can reach a fetus through the intrauterine environment.
The invading organism triggers an inflammatory response in the meninges. In an attempt to ward off the invasion, neutrophils gather in the area and produce an exudate in the subarachnoid space, causing the CSF to thicken. The thickened CSF flows less readily around the brain and spinal cord, and it can block the arachnoid villi, causing hydrocephalus.
The exudate also:
· exacerbates the inflammatory response, increasing the pressure in the brain
· can extend to the cranial and peripheral nerves, triggering additional inflammation
· irritates the meninges, disrupting their cell membranes and causing edema.
The consequences are elevated intracranial pressure (ICP), engorged blood vessels, disrupted cerebral blood supply, possible thrombosis or rupture and, if ICP isn't reduced, cerebral infarction. Encephalitis may also ensue as a secondary infection of the brain tissue.
In aseptic meningitis, lymphocytes infiltrate the pia-arachnoid layers, but usually not as severely as in bacterial meningitis, and no exudate is formed. Thus, aseptic meningitis is self-limiting.
Signs and symptoms
· Fever, chills, and malaise
· Headache, vomiting and, rarely, papilledema
· Signs of meningeal irritation:
§ Nuchal rigidity
§ Positive Brudzinski's and Kernig's signs
§ Exaggerated and symmetrical deep tendon reflexes
· Irritability, delirium, deep stupor, coma, and photophobia, diplopia, or other vision problems
An infant may show signs of infection, but most are simply fretful and refuse to eat. In an infant, vomiting can lead to dehydration, which prevents formation of a bulging fontanel, an important sign of increased ICP.
Diagnostic test results
· Lumbar puncture shows elevated CSF pressure (from obstructed CSF outflow at the arachnoid villi), cloudy or milky-white CSF, high protein level, positive Gram stain and culture (unless a virus is responsible), and decreased glucose concentration.
· Cultures of blood, urine, and nose and throat secretions reveal the offending organism.
· Chest X-ray reveals pneumonitis or lung abscess, tubercular lesions, or granulomas secondary to a fungal infection.
· Sinus and skull X-rays identify cranial osteomyelitis or paranasal sinusitis as the underlying infectious process, or skull fracture as the mechanism for entrance of the microorganism.
· White blood cell count reveals leukocytosis.
· Computed tomography scan reveals hydrocephalus, cerebral hematoma, hemorrhage, or tumor.
· Electrocardiogram reveals sinus arrhythmia.
· I.V. antibiotics for at least 2 weeks, followed by oral antibiotics selected by culture and sensitivity testing
· I.V. fluids
· Agents to control arrhythmias
· Anticonvulsant (usually given I.V.) or a sedative
· Aspirin or acetaminophen
Health care workers should take droplet precautions (in addition to standard precautions) for meningitis caused by H. influenzae or N. meningitidis, until 24 hours after the start of effective therapy.
MENINGES AND CEREBROSPINAL FLUID FLOW
INFLAMMATION IN MENINGITIS