Eng / Meningeal syndrome

Differential diagnosis of meningitis

based on analysis:

epidemiological data (seasonality, source of infection, route of infection, age)

clinical data (time of onset of meningeal syndrome and its severity, the presence of other clinical signs of the disease: the presence of exanthema, lymphadenopathy, hepatosplenomegaly, kidney damage)

Laboratory (OAK, OAM, CSF study, biochemical studies) instrumental methods of research (ultrasound, radiography, CT, MRI, REG, EchoEG)

Bacteriological and serological examination of blood and cerebrospinal fluid, ELISA, PCR of cerebrospinal fluid for fungi, bacteria, viruses, Mycobacterium tuberculosis

CLINIC of serous meningitis

Prodromal condition (headache, drowsiness, malaise) with measles, chicken pox, mumps, influenza develops within 14 days after the onset of infection. Body temperature 38-40 degrees.

Meningeal syndrome: headache, aggravated by head movements, changes in the level of consciousness, inappropriate behavior, back pain, photophobia, neck stiffness, symptoms of Kernig, Brudzinsky.

Syndrome of intracranial hypertension: bursting headache, vomiting without previous nausea, depression of consciousness, convulsions, respiratory failure, congestive optic discs.

serous meningitis

Neurological symptoms: aphasia, hemiparesis, cranial nerve damage, cerebellar ataxia, subcortical automatism, convulsions, mental disorders.

Diagnosis: after CT and MRI, a lumbar puncture is performed.

CT may show cerebral edema in the temporal and frontal lobes.

The cerebrospinal fluid has an increased protein content, the number of lymphocytes is 50-1500 per 1 mm 3 .

complications of purulent meningitis

septic shock,

DIC,

multiple organ failure syndrome

Intracranial complications of purulent meningitis

cerebral edema,

syndrome of inappropriate secretion of antidiuretic hormone,

subdural effusion,

hypothalamic dysfunction,

ventriculitis,

ependymatitis,

heart attack,

hydrocephalus,

dislocation syndrome,

herniation syndromes;

Edema - swelling of the brain

Has no etiological specificity

Symptoms are determined by the localization and severity of the process

In the early stages of development before the onset of dislocation, the symptoms of CNS damage are determined by lesions of the meninges with the development of an inflammatory process in them and cerebral hypertension due to CSF hyperproduction, which are manifested by meningeal syndrome

Pathogenesis Edema - swelling of the brain

Toxic damage to cerebral vessels

Microcirculatory disorders

Brain hypoxia

Increased BBB permeability

Entry into cells of sodium and water

An increase in the volume of the brain in a confined space leads to the dislocation of the medulla oblongata with the descent of the cerebellar tonsils into the foramen magnum (death from respiratory paralysis).

The following factors play a role in pathogenesis:

Vascular factor - violation of vascular permeability, damage to cell membranes (penetration of protein and other plasma components into the brain tissue. As a result, there is an increase in the osmolarity of the intercellular fluid (and water tends to go from the vessels into the tissue)

Circulatory factor:

Inflammatory factors cause the expansion of the arteries of the brain, causing a significant increase in pressure in its capillaries.

Water is filtered from them into the intercellular space, as a result, tissues are damaged.

Tissue factor

The brain increases in volume (swelling) with limited intracranial space - compression of the brain;

HMO increases ICP - decreased cerebral perfusion pressure

(difference between blood pressure and ICP);

A violation of cerebral circulation (cerebral ischemia) develops;

As a result, the brain tissue metabolism switches to an anaerobic type.