In protracted and severe vomiting, as occurs with pyloric obstruction or stenosis, gastric fluid is lost in large amounts and a hypochloremic (acid-losing) alkalosis develops. Gastric contents have a relatively low sodium content and water loss relatively exceeds electrolyte loss. Despite relatively low electrolyte content, significant quantities of electrolytes are lost with the fluid, leading to some depletion of total body sodium. The dehydration from fluid loss is partially counteracted by increased secretion of arginine vasopressin (AVP, or vasopressin; antidiuretic hormone, ADH) in response to decreased fluid volume. AVP promotes fluid retention. Whether hyponatremia, normal-range serum sodium values, or hypernatremia will develop depends on how much fluid and sodium are lost and the relative composition and quantity of replacement water and sodium, if any. Oral or parenteral therapy with sodium-free fluid tends to encourage hyponatremia. On the other hand, failure to supply fluid replacement may produce severe dehydration and even hypernatremia. Serum potassium values are most often low due to direct loss and to alkalosis that develops when so much hydrochloric acid is lost. Similar findings are produced by continuous gastric tube suction if continued over 24 hours.

In severe or long-standing diarrhea, the most common acid-base abnormality is a base-losing acidosis. Fluid loss predominates quantitatively over loss of sodium, chloride, and potassium despite considerable depletion of total body stores of these electrolytes, especially of potassium. Similar to what occurs with vomiting, decrease in fluid volume by fluid loss is partially counteracted by increased secretion of AVP (ADH). Again, whether serum sodium becomes decreased, normal, or increased depends on degree of fluid and electrolyte loss and the amount and composition of replacement fluid (if any). Sufficient electrolyte-free fluids may cause hyponatremia. Little or no fluid replacement would tend toward dehydration, which, if severe, could even produce hypernatremia. The diarrhea seen in sprue differs somewhat from the electrolyte pattern of diarrhea from other causes in that hypokalemia is a somewhat more frequent finding.

In extensive sweating, especially in a patient with fever, large amounts of water are lost. Although sweat consists mostly of water, there is a small but significant sodium chloride content. Enough sodium and chloride loss occurs to produce total body deficits, sometimes of surprising degree. The same comments previously made regarding gastrointestinal (GI) content loss apply here also.

In extensive burns, plasma and extracellular fluid (ECF) leak into the damaged area in large quantities. If the affected area is extensive, hemoconcentration becomes noticeable and enough plasma may be withdrawn from the circulating blood volume to bring the patient close to or into shock. Plasma electrolytes accompany this fluid loss from the circulation. The fluid loss stimulates AVP (ADH) secretion. The serum sodium level may be normal or decreased, as discussed earlier. If the patient is supported over the initial reaction period, fluid will begin to return to the circulation after about 48 hours. Therefore, after this time, fluid and electrolyte replacement should be decreased, so as not to overload the circulation. Silver nitrate treatment for extensive burns may itself cause clinically significant hyponatremia (due to electrolyte diffusion into the hypotonic silver nitrate solution).

Diabetic acidosis and its treatment provide very interesting electrolyte problems. Lack of insulin causes metabolism of protein and fat to provide energy that normally is available from carbohydrates. Ketone bodies and other metabolic acids accumulate; the blood glucose level is also elevated, and both glucose and ketones are excreted in the urine. Glucosuria produces an osmotic diuresis; a certain amount of serum sodium is lost with the glucose and water, and other sodium ions accompany the strongly acid ketone anions. The effects of osmotic diuresis, as well as of the accompanying electrolyte loss, are manifested by severe dehydration. Nevertheless, the serum sodium and chloride levels are often low in untreated diabetic acidosis, although (because of water loss) less often they may be within normal range. In contrast, the serum potassium level is usually normal. Even with normal serum levels, considerable total body deficits exist for all of these electrolytes. The treatment for severe diabetic acidosis is insulin and large amounts of IV fluids. Hyponatremia may develop if sufficient sodium and chloride are not given with the fluid to replace the electrolyte deficits. After insulin administration, potassium ions tend to move into body cells as they are no longer needed to combine with ketone acid anions. Also, potassium is apparently taken into liver cells when glycogen is formed from plasma glucose under the influence of insulin. In most patients, the serum potassium level falls to nearly one half the admission value after 3-4 hours of fluid and insulin therapy (if urine output is adequate) due to continued urinary potassium loss, shifts into body cells, and rehydration. After this time, potassium supplements should be added to the other treatment.

Role of the kidney in electrolyte physiology

In many common or well-recognized syndromes involving electrolytes, abnormality is closely tied to the role of the kidney in water and electrolyte physiology. A brief discussion of this subject may be helpful in understanding the clinical conditions discussed later.

Urine formation begins with the glomerular filtrate, which is similar to plasma except that plasma proteins are too large to pass the glomerular capillary membrane. In the proximal convoluted tubules, about 85% of filtered sodium is actively reabsorbed by the tubule cells. The exchange mechanism is thought to be located at the tubule cell border along the side opposite the tubule lumen; thus, sodium is actively pumped out of the tubule cell into the renal interstitial fluid. Sodium from the urine passively diffuses into the tubule cell to replace that which is pumped out. Chloride and water passively accompany sodium from the urine into the cell and thence into the interstitial fluid. Most of the filtered potassium is also reabsorbed, probably by passive diffusion. At this time, some hydrogen ions are actively secreted by tubule cells into the urine but not to the extent that occurs farther down the nephron (electrolyte pathways and mechanisms are substantially less well known for the proximal tubules than for the distal tubules).

In the ascending (thick) loop of Henle, sodium is still actively reabsorbed, except that the tubule cells are now impermeable to water. Therefore, since water cannot accompany reabsorbed sodium and remains behind in the urine, the urine at this point becomes relatively hypotonic (the excess of water over what would have been present had water reabsorption continued is sometimes called “free water” and from a purely theoretical point of view is sometimes spoken of as though it were a separate entity, almost free from sodium and other ions).

In the distal convoluted tubules, three processes go on. First, sodium ions continue to be actively reabsorbed. (In addition to the sodium pump located at the interstitial side of the cell, which is pushing sodium out into the interstitial fluid, another transport mechanism on the tubule lumen border now begins actively to extract sodium from the urine into the tubule cells.) Intracellular hydrogen and potassium ions are actively excreted by the tubule cells into the urine in exchange for urinary sodium. There is competition between hydrogen and potassium for the same exchange pathway. However, since hydrogen ions are normally present in much greater quantities than potassium, most of the ions excreted into the urine are hydrogen. Second, the urinary acidification mechanisms other than bicarbonate reabsorption (NaHPO4 and NH4) operate here. Third, distal tubule cells are able to reabsorb water in a selective fashion. Permeability of the distal tubule cell to water is altered by a mechanism under the influence of AVP (ADH). There is a limit to the possible quantity of water reabsorbed, because reabsorption is passive; AVP (ADH) simply acts on cell membrane permeability, controlling the ease of diffusion. Therefore, only free water is actually reabsorbed.

In the collecting tubules, the tubular membrane is likewise under the control of AVP (ADH). Therefore, any free water not reabsorbed in the distal convoluted tubules plus water that constitutes actual urine theoretically could be passively reabsorbed here. However, three factors control the actual quantity reabsorbed: (1) the state of hydration of the tubule cells and renal medulla in general, which determines the osmotic gradient toward which any reabsorbed water must travel; (2) the total water reabsorption capacity of the collecting tubules, which is limited to about 5% of the normal glomerular filtrate; and (3) the amount of free water reabsorbed in the distal convoluted tubules, which helps determine the total amount of water reaching the collecting tubules.

Whether collecting tubule reabsorption capacity will be exceeded, and if so, to what degree, is naturally dependent on the total amount of water available. The amount of water reabsorbed compared to the degree of dilution (hypotonicity) of urine reaching the collecting tubules determines the degree of final urine concentration.