Diagnosis
It is mainly based on history and clinical manifestations. Serum potassium measurement blood K + <3.5 mmol / L, the symptoms can be diagnosed. However, serum K+ may not show a decrease in dehydration or acidosis. In addition, according to the electrocardiogram, it can reflect the low potassium situation more sensitively, and the main manifestations of the electrocardiogram are prolongation of the Q-T interval, decrease of the S-T segment, T-wave hypoplasia, widening, biphasia, inversion, or the appearance of U-wave.
Therapeutic measures
(1), generally use oral potassium, adult prophylactic dose of 10% potassium chloride 30~40ml/d (each g of potassium chloride contains 13.4mmol of potassium). Oral potassium chloride is easy to have gastrointestinal reaction, available potassium citrate is better (1g of potassium citrate contains 4.5mmol of potassium).
(2) Intravenous infusion of potassium chloride is used in patients who cannot take it orally or who have severe potassium deficiency. Commonly used concentration of 5% dextrose solution 1.0L added 10% potassium chloride 10 ~ 20ml, each g of potassium chloride must be evenly titrated for more than 30 ~ 40min, can not be pushed intravenously. The amount of potassium supplementation depends on the condition, as prevention, usually adults supplement potassium chloride 3～4g/d, as treatment, it is 4～6g or more.
(3) Points for attention of potassium supplementation: a. The urine output must be above 30ml/h before considering potassium supplementation, otherwise it may cause high blood potassium. b. For those with acidosis, high blood chloride or liver function impairment, the application of potassium glutamate can be considered, each 6.3g contains 34mmol of potassium, which can be added to 0.5L of glucose solution for IV drip. c. Too high a concentration of intravenous potassium chloride may stimulate the veins and cause pain, even venous spasm and hemorrhagic spasm. d. The concentration of intravenous potassium chloride is too high, causing pain and even venous cramps. e. The concentration of potassium chloride is too high, causing pain, even venous spasm and venous spasm. f. The amount of potassium chloride should be determined according to the condition. It can cause pain, even venous spasm and thrombosis. d. Do not drip too fast, the sudden increase of serum potassium concentration can lead to cardiac arrest. e. K+ enters into the cell very slowly, about 15h to reach the balance of intracellular and extracellular, and in the case of cellular insufficiency such as hypoxia, acidosis, etc., the equilibrium time of potassium is even longer, about 1 week or longer, so correcting the lack of potassium needs to be a few days, don't be too hasty or stop replenishment. f. The potassium deficiency should be corrected over several days. g. The potassium deficiency should be treated with a special treatment. h. The potassium deficiency should be treated with a special treatment. i. The potassium deficiency should be treated with a special treatment. Do not be too hasty or stop the supplementation in the middle. f. When potassium deficiency is accompanied by hypokalemia, attention should be paid to calcium supplementation, because the symptoms of hypokalemia are often concealed by hypokalemia, and after the correction of hypokalemia, hypokalemic convulsions may occur. g. When large amounts of potassium are supplemented in a short period of time or for a long period of time, regular observation is required, and the measurement of serum potassium and electrocardiogram is required to avoid hyperkalemia. h. When a large amount of potassium is supplemented for a long period of time, regular observation is required.
Etiology and pathogenesis
1. Decreased potassium intake General diet is rich in potassium. Therefore, as long as you can eat normally, your body will not be deficient in potassium. Patients with gastrointestinal obstruction, coma, and long time fasting after surgery cannot eat. If nutrition is given intravenously to these patients without concomitant or insufficient potassium supplementation, potassium deficiency and hypokalemia can result. However, if inadequate intake is the sole cause, the degree of potassium deficiency can be less severe over a period of time because of the potassium-conserving function of the kidneys. When potassium intake is inadequate, urinary potassium excretion can be reduced to less than 20 mmol/L in 4 to 7 days and to 5 to 10 mmol/L in 7 to 10 days (normal urinary potassium excretion is 38 to 150 mmol/L).
2. Excessive potassium excretion
(1) Loss of potassium via gastrointestinal tract: This is the most important cause of potassium loss in children, and it is common in patients with severe diarrhea and vomiting accompanied by loss of large amounts of digestive fluids. In diarrhea, the concentration of K+ in feces can reach 30-50mmol/L. At this time, the loss of potassium with feces can be 10-20 times more than normal. The reason why the fecal potassium content increases, on the one hand, because of diarrhea and make potassium absorption in the small intestine is reduced, on the other hand is due to diarrhea caused by the reduction of blood volume can make aldosterone secretion increase, and aldosterone not only can make the urinary potassium discharge increase, but also can make the colon secretion of potassium to strengthen the role. Since gastric juice contains only 5-10 mmol/L of potassium, the loss of gastric juice is not the main cause of potassium loss during severe vomiting, and a large amount of potassium is lost via the kidneys in the urine, because the metabolic alkalosis caused by vomiting can increase renal excretion of potassium (more details later), and the reduction of blood volume caused by vomiting can also promote renal excretion of potassium through the increase of aldosterone secondary to vomiting.
(2) Transrenal potassium loss: this is the most important cause of potassium loss in adults. The common factors that cause the increase of renal potassium excretion are:
①The long-term continuous use of diuretics or excessive dosage: for example, inhibit the proximal tubular sodium, water reabsorption of diuretics (carbonic anhydrase inhibitor acetazolamide), inhibit the medullary collaterals of the ascending branch of the thick section of Cl- and Na + reabsorption of diuretics (tachycardia, diuretic acid, thiazides, etc.) can make the distal tubular flow of primary urine increased, and the increase of flow is the promotion of the renal tubular potassium. This increase is important in promoting increased tubular potassium secretion. The above diuretics also increase the amount of Na+ reaching the distal tubule, which leads to potassium loss through enhanced Na+-K+ exchange. Many diuretics also have a ****same mechanism for causing increased renal potassium excretion: increased aldosterone secretion through a decrease in blood volume. Tachycardia, diuretics, and thiazides act by inhibiting the reabsorption of Cl- and thus Na+ in the thick segment of the ascending branch of the medullary collaterals. Therefore, prolonged use of these drugs can lead to both hyponatremia and hypochloremia. Hypochloremia of any cause has been shown to increase renal potassium excretion. One possible mechanism for this is that hypochloremia appears to directly stimulate potassium secretion in the distal renal tubule.
②Some renal diseases: such as distal renal tubular acidosis, due to the distal tubular hydrogen secretion dysfunction, thus reducing the H+-Na+ exchange and increasing the K+-Na+ exchange, resulting in potassium loss. In proximal tubular acidosis, the decrease in proximal tubular HCO3- reabsorption and the increase in HCO3- reaching the distal tubule is an important reason for the increase in potassium excretion from the distal tubule (see later). In the polyuric phase of acute tubular necrosis, increased potassium excretion can occur because of osmotic diuresis due to increased urea in the tubular fluid and inadequate reabsorption of water and electrolytes by the neoplastic tubular epithelium.
3 adrenocorticotropic hormone excess: primary and secondary wai aldosterone increase, the renal distal tubule and collecting duct Na + - K + exchange increased, thus playing a role in the discharge of potassium and sodium protection. cushing syndrome, the secretion of the glucocorticoid hormone cortisol increased greatly. Cortisol also has some salocorticoid-like effects. A large, prolonged increase in cortisol also promotes Na+-K+ exchange in the distal tubules and collecting ducts leading to increased renal potassium excretion.
④Increase of anions that are not easily reabsorbed in the distal tubule: HCO3-, SO42-, HPO42-, NO3-, β-hydroxybutyric acid, acetoacetate, penicillin, and so on belong to this. They increase in the distal tubular fluid, due to the inability to be reabsorbed and increase the negative charge of the original urine, and thus K + easily from the renal tubular epithelial cells into the tubular lumen fluid and lost with the urine.
⑤Magnesium deficiency: magnesium deficiency often causes hypokalemia. Potassium reabsorption in the ascending branch of the medullary collaterals depends on the Na+-K+-ATR enzyme in the epithelial cells of the renal tubules, and this enzyme needs to be activated by Mg2+. In magnesium deficiency, this enzyme may be inactivated by the absence of intracellular Mg2+, and potassium reabsorption at this site is impaired, resulting in potassium loss. Animal experiments have also demonstrated that magnesium deficiency can also cause an increase in aldosterone, which may also be the cause of potassium loss.
6 Alkalosis: In alkalosis, the H+ excretion by renal tubular epithelial cells decreases, so the H+-Na+ exchange is strengthened, so the potassium excretion in urine increases.
(3) Loss of potassium through skin: sweat contains only 9mmol/L. Under normal circumstances, sweating does not cause hypokalemia. In general, sweating does not cause hypokalemia, but when heavy physical labor is performed in a hot environment, a large amount of sweating can also lead to the loss of potassium.
3. Extracellular potassium transfer to intracellular Hypokalemia can occur when extracellular potassium is transferred to intracellular, but the total amount of potassium in the body does not decrease.
1) Hypokalemic periodic paralysis: episodes of extracellular to intracellular potassium transfer, a familial disease.
(2) Alkalosis: intracellular H+ moves to the extracellular to compensate, while extracellular K+ enters the cell.
(3) Excess insulin: When high dose insulin is used to treat diabetic ketoacidosis, hypokalemia occurs by two mechanisms:
(1) Insulin promotes cellular glycogen synthesis, which requires potassium, and plasma potassium enters the cell with glucose to synthesize glycogen.
②Insulin may directly stimulate the Na+-K+-ATPase on the membrane of skeletal muscle cells, thus increasing the discharge of Na+ from myocytes and increasing the entry of extracellular K+ into myocytes.
(4) barium poisoning: anti-Japanese war period in Sichuan, a large number of cases of "party disease", the clinical manifestations of the main muscle weakness and paralysis, the serious often due to respiratory muscle paralysis and death. After China's scholars Du Gongzhen and other research, to determine the cause of the disease is barium poisoning. However, the mechanism of paralysis caused by barium poisoning has not been clarified. Now it is confirmed that the mechanism of paralysis caused by barium poisoning is hypokalemia caused by barium poisoning. In barium poisoning, the Na+-K+-ATPase on the cell membrane continues to be active. Therefore, potassium in the extracellular fluid keeps entering the cell. However, the pore through which potassium flows out of the cell is specifically blocked, and thus hypokalemia occurs. Barium poisoning is caused by some barium salts dissolved in acid such as barium acetate, barium carbonate, barium chloride, barium hydroxide, barium nitrate and barium sulfide.
4. Crude raw cotton oil poisoning In the past two or three decades, in some cotton production areas in China, a kind of hypokalemic paralysis, in some provinces is also known as "soft disease". Its main clinical feature is the limb muscles are extremely weak or flaccid paralysis, often due to severe respiratory muscle paralysis and death, serum potassium concentration is significantly reduced. Often there are many cases in the same area. The etiology is closely related to the consumption of crude raw cottonseed oil. Crude raw cottonseed oil is produced by some small oil factories and presses in rural areas. The production process of these factories is substandard. Cotton seeds are not fully steamed or even without shelling is used to extract oil, and the extracted oil is not in accordance with the provisions of the alkali refining. As a result, many toxic substances in the cotton seeds are stored in the oil. With the occurrence of "soft disease" and a series of subsequent studies, are cotton phenol (gossypol). The mechanism of hypokalemia in "soft disease" has not been elucidated. The discovery of "soft disease" and a series of subsequent studies were conducted by our scholars. So far, there is no record of this disease in foreign books and journals
.