Pathophysiology of Meningitis

Pathophysiology of Meningitis

Predisposing factors include upper airway infection, otitis media, mastoiditis, sickle cell anemia and other hemoglobinopatis, a new neurosurgical procedure, head trauma and immunological effects. Venous channels through the posterior nasopharynx, middle ear and mastoid tract to the brain and the veins near the channel meningen; all of these links that support the growth of bacteria.

Organisms enter the bloodstream and cause an inflammatory reaction in the meningen and under the cortex, which can cause thrombus and decreased cerebral blood flow. Cerebral tissue due to impaired metabolism meningen exudate, vasculitis and hypoperfusion. Purulent exudate may spread to the base of the brain and spinal cord. Inflammation also spread to the wall membrane of the cerebral ventricles. Bacterial meningitis associated with intracranial physiological changes, which consisted of increased permeability of the blood, the defense area of the brain, cerebral edema and increased intra-cranial pressure.

In acute infection patients died due to bacterial toxins, before the meningitis. The infection most of these patients with adrenal damage, circulatory collapse and associated with widespread hemorrhage (at sindromWaterhouse-Friderichssen) as a result of endothelial damage and necrosis of blood vessels caused by the meningococcus.

Pathophysiology of Meningitis

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