Edema of the brain and convulsions

Edema of the brain is characterized by a violation of consciousness andconvulsive attacks. Etiology and pathogenesis The cerebral edema differs in etiological non-specificity. | Infectious diseases. | Toxic and hypoxic conditions. Acute neuroinfections. | TBI. Epileptic status. | Violation of cerebral circulation. | Tumors of the brain. | Somatic diseases. Pathogenesis distinguishes between vasogenic, cytotoxic, osmotic and hydrostatic edema of the brain. CLINICAL PICTURE | General anxiety, "brain cry," vomiting, muscle twitching, convulsions. | Disturbances of consciousness (up to sopor and coma), delirium, hallucinations. | Meningeal symptoms, the presence of pathological reflexes, hyperesthesia. | Malignant hyperthermia. Hemodynamic disorders (increasing, and then lowering blood pressure, collapse, bradycardia), breathing disorders. | Identify "stagnant discs of the optic nerves" when examining the fundus. ACTION ON THE CHALLENGE Treatment The method of administration and dosage of medicines used in the treatment of cerebral edema are listed in Table. 17-13. Table 17-13. Drugs used for edema of the brain

Drug, dose, method of administration

Decongestant and dehydration therapy

Dexamethasone 0.5-2 mg / kg body weight every 4 hoursin / m or iv or hydrocortisone at 20 mg / kg body weight, or prednisolone 5 mg / kg body weight Mannitol in a dose of 0.5-1 g / kg body weight IV drip Glycerol oral by 0.5-1 , 5 g / kg body weight through the probe 3 times a day Albumin iv drip Furosemid at a dose of 2 mg / kg body weight IV in struyno in 2-4 admission

Correction of electrolyte homeostasis under controlblood ionograms CLINICAL PHARMACOLOGY OF MEDICINAL PRODUCTS | Provide the patient with an elevated position in bed, carry out sanation of the upper respiratory tract, oxygen therapy, in severe cases, intubation of the airways and ventilation. | Mannitol: the initial dose is 50% daily; the first 33% is injected slowly or iv droplet at a rate of 100 drops / min, then 30-40 drops / min. | Anticonvulsant therapy: if diazepam is ineffective, inhalation or barbiturate anesthesia is indicated. | Hospitalization in the intensive care unit is necessary.

  1. Abstract. Internal Diseases, 2007
    Emergency care in a polyclinicAspiration pneumonia in children Colon's disease Crohn's disease Glomerulonephritis Bronchial asthma IHD. Angina pectoris Infectious myocarditis Edema Quincke Pulmonary edema Pneumoconiosis Pneumonia Gout Renal failure Cirrhosis Stomach ulcer Ulcerative
  2. Edema of the brain
    Increase the water content in the brain can beis due to several mechanisms. Most often there is vasogenic edema caused by an increase in the permeability of the blood-brain barrier, which is accompanied by the release of plasma into the brain tissue. Elevated blood pressure promotes vaso-genic edema. The causes of vasogenic edema: mechanical trauma, inflammatory diseases of the brain, brain tumors, arterial
  3. Prevention
    A prerequisite for normal developmentpregnancy are providing the animals with sufficient exercise and feeding according to the norms compiled on the basis of the timing of pregnancy. The content and feeding of pregnant animals. Diagnosis of pregnancy in dogs and cats is performed by examination and palpation. Upon examination, a change in the contour of the abdomen is detected (saggy
  4. Scleroderma
    Observed at any age, women are sicksomewhat more often than men. The disease develops slowly, gradually. There are three stages of the disease - edema, induration and atrophy. There is swelling of the skin and subcutaneous tissue in the face, trunk and extremities. The skin above the affected areas is shiny, elastic, with pressure the finger does not leave depressions. In the stage of induction, the skin and subcutaneous
  5. OTEK QUEEN
    Clinic. Quincke's edema is characterized by the rapid development of limited edema of the skin, which is most often observed in the area of ​​the lips, eyelids and the rear of the hand. Less common is swelling of the oral mucosa, nasopharynx and respiratory tract. Usually, edema occurs without pests and grows for several weeks, after which it begins to decrease and disappears without leaving a trace. Swelling can seize large areas
  6. Anthrax.
    Infection of man S. I. possibly by contact, aerogenic, alimentary and transmissible routes. Pathogenesis. Entrance gate - damaged skin, mucous membranes of the respiratory tract and gastrointestinal tract. Exotoxin causes coagulation of proteins, tissue swelling, anthrax carbuncle develops - an inflammation of the nose, a necrosis of the skin in the center of the focus with the formation of a brownish-black crust. Macrophages are recorded in the reg / nodes.
  7. Edema of pregnant women
    Swelling of the pregnant (hydrops gravidarum)is characterized by accumulation in the subcutaneous tissue and skin of the extremities and the lower abdominal wall of the transudate. The disease is observed mainly in cows and mares. The causes of this disease may be insufficient movement and blood circulation disorder in pregnant animals. The predisposing factor for the appearance of edema is feeding
  8. PULMONARY EDEMA
    With swelling of the lungs, due to overfilling with bloodpulmonary veins and capillaries, swelling of the blood plasma and, as a consequence, blood stasis, which starts in the lower parts of the lungs, enter the lumen of the bronchi and bronchioles. The mucous membranes of the bronchi also swell. Pulmonary edema can develop as a result of physical overload, with heat and sunstroke, with the plague of carnivores and some others
  9. anthrax
    Pathogen - anthrax bacillusEpidemiology. The source of infection are sick animals. Infection of man S. I. possibly by contact, aerogenic, alimentary and transmissible routes. Pathogenesis. Entrance gate - damaged skin, mucous membranes of the respiratory tract and gastrointestinal tract. Exotoxin causes protein coagulation, tissue swelling, anthrax carbuncle develops - asp-nekr
  10. Meningococcal infection.
    The causative agent is Neisseria meningitidis. The source of infection is the patient and the carrier, the air way. Pathogenesis - introduction into the mucosa of the nasopharynx, bronchus - local inflammation - lymphogenically in the blood - meningococcemia - destruction by antibodies - endotoxin - vascular reaction - through the BBB - serous, then purulent meningitis - sometimes encephalitis. The incubation period is 2-10 days. Clinical picture.
  11. Phlegmonous (infiltrative-purulent) laryngitis
    Phlegmonous laryngitis - infiltrative purulentinflammation of the submucosal layer, muscular and ligamentous apparatus and adnexa of the cartilages of the larynx. More often the process occurs in men, localized in the epiglottis or an arytenoid cartilage. Etiologicheskim faktorom is an infection (streptococcus, staphylococcus, etc.), penetrating into the larynx tissue or from the surface in trauma
  12. PULMONARY EDEMA
    Lung edema - a pathological increase in volumeextravascular fluid in the lungs. The main role in this is the increase in hydrostatic pressure in the pulmonary vessels, a decrease in the plasma CODE, an increase in the permeability of the vascular wall. In 1896 E.G. Starling substantiated the theory of vascular resorption of fluid from connective tissue spaces into small vessels, according to which Qr = K (deltaP -