Lakhasly

Meningeal infections generally originate in one of two ways: through the bloodstream as a consequence of other infections or by direct spread, such as might occur after a traumatic injury to the facial bones or secondary to invasive procedures.An acute fulminant infection occurs in about 10% of pa- tients with meningococcal meningitis, producing signs of over- whelming septicemia: an abrupt onset of high fever, extensive purpuric lesions (over the face and extremities), shock, and signs of disseminated intravascular coagulation (DIC).Bacter- ial or meningococcal meningitis also occurs as an oppor- tunistic infection in patients with acquired immunodefi- ciency syndrome (AIDS) and as a complication of Lyme disease (Chart 64-1).Acute fulminant presenta- tion may include adrenal damage, circulatory collapse, and widespread hemorrhages (Waterhouse-Friderichsen syn- drome).Once the causative organism enters the bloodstream, it crosses the blood-brain barrier and proliferates in the cere- brospinal fluid (CSF).The host immune response stimu- lates the release of cell wall fragments and lipopolysaccha- rides, facilitating inflammation of the subarachnoid and pia mater.CSF circulates through the subarach- noid space, where inflammatory cellular materials from the affected meningeal tissue enter and accumulate.

Meningeal infections generally originate in one of two ways: through the bloodstream as a consequence of other infections or by direct spread, 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. Bacter- ial or meningococcal meningitis also occurs as an oppor- tunistic infection in patients with acquired immunodefi- ciency syndrome (AIDS) and as a complication of Lyme disease (Chart 64-1).
Once the causative organism enters the bloodstream, it crosses the blood–brain barrier and proliferates in the cere- brospinal fluid (CSF). The host immune response stimu- lates the release of cell wall fragments and lipopolysaccha- rides, facilitating inflammation of the subarachnoid and pia mater. Because the cranial vault contains little room for

expansion, the inflammation may cause increased intracra- nial pressure (ICP). CSF circulates through the subarach- noid space, where inflammatory cellular materials from the affected meningeal tissue enter and accumulate.
The prognosis for bacterial meningitis depends on the causative organism, the severity of the infection and illness, and the timeliness of treatment. Acute fulminant presenta- tion may include adrenal damage, circulatory collapse, and widespread hemorrhages (Waterhouse-Friderichsen syn- drome). This syndrome is the result of endothelial damage and vascular necrosis caused by the bacteria. Complications include visual impairment, deafness, seizures, paralysis, hy- drocephalus, and septic shock.

Seizures can occur and are the result of areas of irritabil- ity in the brain. ICP increases secondary to diffuse brain swelling or hydrocephalus (van de Beek, et al., 2006). The initial signs of increased ICP include decreased level of con- sciousness and focal motor deficits. If ICP is not controlled, the uncus of the temporal lobe may herniate through the tentorium, causing pressure on the brain stem. Brain stem herniation is a life-threatening event that causes cranial nerve dysfunction and depresses the centers of vital func- tions, such as the medulla. See Chapter 61 for discussion of the patient with a change in level of consciousness (LOC) or increased ICP.
An acute fulminant infection occurs in about 10% of pa- tients with meningococcal meningitis, producing signs of over- whelming septicemia: an abrupt onset of high fever, extensive purpuric lesions (over the face and extremities), shock, and signs of disseminated intravascular coagulation (DIC). Death may occur within a few hours after onset of the infection.