Giperkaltsiyemichesky encephalopathy
Contents:
- Description
- Symptoms of Giperkaltsiyemichesky encephalopathy
- Reasons of Giperkaltsiyemichesky encephalopathy
- Treatment of Giperkaltsiyemichesky encephalopathy
- a href="javascript:if(confirm(%27medicalmeds.eu/consult_new.php?src_razd=bolezn&src_id=3154&vc_spec=14 \n\nThis file was not retrieved by Teleport Pro, because it is addressed on a path excluded by the site\%27s Robot Exclusion parameters. (Teleport Pro\%27s compliance with this system is optional; see the Project Properties, Netiquette page.) \n\nDo you want to open it from the server?%27))window.location=%27medicalmeds.eu/consult_new.php?src_razd=bolezn&src_id=3154&vc_spec=14%27" tppabs="medicalmeds.eu/consult_new.php?src_razd=bolezn&src_id=3154&vc_spec=14">
see also:
- Atherosclerotic encephalopathy of Binswanger
- Encephalopathy
- Hepatic encephalopathy
- Distsirkulyatorny encephalopathy
- a href="" class="spoiler_links">To show all list
Description:
It is one of the most frequent disturbances of metabolism at patients of a hospital of the general profile. As well as at other metabolic encephalopathies, extent of dysfunction of TsNS depends on the speed of change of concentration of sodium in blood serum.
Symptoms of Giperkaltsiyemichesky encephalopathy:
Extremely high concentration of calcium leads to consciousness disturbance, development of a myoclonus, asteriksis, epileptic seizures and, sometimes, choreiform movements.
Reasons of Giperkaltsiyemichesky encephalopathy:
Heavy degree of gipernatriyemichesky dehydration (Na> 155 ¼Ý¬ó/l) is observed at not diabetes mellitus, the neketotichesky diabetic coma expressed to diarrhea and at patients in a condition of a sopor if they do not receive liquid.
Treatment of Giperkaltsiyemichesky encephalopathy:
Treatment of a hypercalcemia: elimination of the reason of a hypercalcemia (an oncotomy, the termination of reception of vitamin D and t of), reduction of intake of calcium in an organism, increase in its removal, purpose of the means interfering a calcium exit from bones, and the drugs strengthening intake of calcium in a bone. The most important components of treatment - recovery of volume of extracellular liquid. - 3 l of isotonic solution of sodium of chloride a day under control of the central venous pressure) and correction of electrolytic composition of plasma. Furosemide (100 - 200 mg intravenously each 2 h) strengthens calcium excretion while tiazida have opposite effect. At intravenous administration of phosphates (Na2 HPO4 or NaH2PO4) calcium level in plasma also decreases, however phosphates are contraindicated at a renal failure. A resorption of a bone tissue the calcitonin, glucocorticosteroids oppress. Decrease in level of calcium in plasma begins in several hours after introduction and reaches a maximum for the 5th day of treatment. Mitramitsin causes thrombocytopenia, damage of a liver and has to be used in the absence of effect of other treatment. For the emergency decrease in content of calcium in blood use of a hemodialysis or peritoneal dialysis with a beskaltsiyevy dialysis fluid is possible (it is put generally at patients with the accompanying heart and renal failure into practice). At the tumoral hypercalcemia connected with excess products of PGE 2 (metabolites are found in urine), indometacin and other inhibitors of synthesis of prostaglandins give gipokaltsiyemichesky effect. The hypercalcemia accompanying a thyrotoxicosis is quickly stopped by purpose of propranolol intravenously in a dose of 10 mg/h. Glucocorticosteroids do not exert impact on a hypercalcemia at primary hyperparathyreosis therefore the test with a hydrocortisone is used for the differential diagnosis of a hypercalcemia.