DYSHYDRIAS
1). Dehydration
A. Cellular — true, primary or aqueous: arises as a result of the initial loss of water or the excess of salt, decrease of water entry. In the process, water is "evaporated" from the extracellular space and Na-concentration remains high, therefore, cell water goes to the extracellular space.
Clinical picture: excruciating thirst, dryness of the tongue and mucous membranes, oliguria with high concentration of urine, symptoms of pachyemia, periods of anxiety, psychoses, hallucinations and coma.
Losses of 2% of the total water in the organism cause thirst, 5% — dryness of the tongue, 10% — coma. Nausea and vomiting are absent.
Laboratory data: Na+ and K+ contents are increased in the urine, VICF is decreased or not changed.
Treatment: 5% glucose i/v, per os. Electrolytic solutions are contraindicated, since they increase extracellular hypertension and cause edema. About effective treatment we may judge by disappearance of thirst, increase of diuresis and decrease of specific gravity of the urine (late symptom).
B. Extracellular (salt deficient) — arises in connection with losses of salt, therefore, it is secondary or hypotonic.
Etiopathogenesis: losses of salt as a result of vomiting, diarrhea, fistulas of GIT, insufficient supply of salt, adrenal insufficiency, when, owing to a decrease of aldosterone level, Na+ resorption in the kidneys lowers, as well as in osmotic diuresis, polyuria, hyperkalemia, excessive application of diuretics, increased excretion of exudate through skin in burns, etc.
Clinical picture: it is due to hypovolemia (AP decrease, thready pulse, veins are empty, collapsed, tendency to collapse), cellular hyperhydration (absence of thirst, headache, vomiting, a little loss of weight).
Laboratory data: hemoconcentration, high Ht, increase of nitrogen are noted, as well as oliguria with hyposthenuria since kidneys retain salt. If the patient is allowed an enteral intake of water — polyuria arises because without salt water cannot be retained.
Treatment: to restore a level of salt by administration of hypertonic solu tions.
A combination o f hypertonic N aCl solutions with glucose is contraindicated, since glucose is metabolized with formation of endogenic water that may lead to the edema of the brain. ^S»W* t*\o} \<~&\ Ut^ f^-t
A tendency to an increase of CI-level in the urine means the onset of compensation. Glucocorticoids may be used since they retain Na+.
4 C. General dehydration is characterized by negative water balance in both sectors as a result of extreme water losses or stopping a liquid intake.
Water losses are accompanied by salt losses (GIT stricture, cholera).
Clinical picture: pale sallow colour of skin, sunken eyes, cyanosis of lips, loss of skin elasticity, decrease of body weight, severe thirst, but not unquenchable.
Laboratory data: VICF is decreased, hemoconcentration, elevated level of protein, Na+, H+, urea and uric acid, oliguria are marked.
Treatment: should be started with isotonic glucose solutions, then gradually NaCl and ADH are added.
Hypertonic solutions are categorically forbidden!
Mineralocorticoids and conserved blood should be avoided.
2). Hyperhydration
A. Cellular is the result of the excess of pure water or excessive isotonic
infusions in normal or decreased osmotic level. In shortage of electrolytes water goes from the interstitial space into the cell and swelling of tissues develops.
Clinical picture: headaches, depression, convulsions, syncopes; cerebral edema— the main cause of death. There is no thirst, mucous membranes and tongue are moist, osmotic pressure is decreased, increase of the volume of total (cellular and extracellular) water, a lowering of Na1" and elevation of K.+ levels in plasma.
Treatment: in acidosis, CO poisoning — to restore metabolism, anabolics, 30% glucose with insulin are used. To limit administration of liquid and to prescribe vitamins C, P, B, 10% NaCl hypertonic solutions — 40-80 ml slowly! In acidosis — soda, lactate, trisamine.
B. Extracellular hyperhydration as a result of water retention or edema.
C Mechanisms of edemas:
1. Capillary edema is a consequence of variations of hydrostatic and oncotic pressure at the level of capillary and an increase of endothelial permeability.
The increase of HSP in the capillary leads to water migration into the interstitial space, protein concentration and oncotic pressure in the vascular bed decrease.
As a result of anoxia, acidosis, inflammation and hyperhistaminemia, an increase of capillary permeability takes place that leads to coming out of proteins from capillaries into interstitial space and contributes to the elevation of oncotic pressure in the interstitial space in decreased OP in the capillary.
2. Renal edema. In its basis lie glomerulo-tubular disorders with Na+ retention and normal filtration. Aldosterone clearance is increased in cardiac edemas. The cause is the elevation of VP and aldosterone activity.
Clinical picture: anuria, decrease of protein content, ascitis, etc.
Laboratory data: increase of ECF in renal edema and increase of ICF in capillary edema. Extracellular osmotic pressure is normal or decreased, in capillary edema a level of blood proteins is low, and in the interstitial fluid their number is increased.
Treatment: limitation of salts, administration of large quantities of liquids in order to decrease the concentration of Na"1" ions, vitamins C, P, antihistamine agents. In case of normal Na" content one must limit the intake of liquid and prescribe diuretics.
C. General hyperhydration. It is a true poisoning of the organism with water as a result of its overloading with water and its insufficient excretion. All three sectors are overloaded. A concentration of salts is proportionally decreased.
Etiopathogenesis: renal failure, excessive hyperhydration with endogenic water.
Clinical picture: edemas, elevated AP, cerebral hemorrhage, left ventricular failure, pulmonary edema, hemodilution, dilution of electrolytes.
Treatment: water restriction, prohibition of salt, diuretics, laxatives, glucose 300 g/day with insulin, vitamins C, B, hormones, testosterone 50-100 mg, retabolil.
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