Hypokalemia

Introduction to hypokalemia The serum potassium concentration is lower than 3.5 mmol/L (3.5 mEq/L, and the normal human serum potassium concentration ranges from 3.5 to 5.5 mmol/L) is called hypokalemia. In hypokalemia, the total potassium content of the body does not necessarily decrease, as is the case when extracellular potassium is transferred to the cells. However, in most cases, patients with hypokalemia are also associated with a reduction in total potassium (potassiumdeficit). The severity of clinical manifestations depends on the degree of potassium deficiency inside and outside the cell and the rate of potassium deficiency. The symptoms of acute hypokalemia are more severe than those of chronic hypokalemia with the same level of potassium deficiency. Acute hypokalemia should be treated with urgent measures. For chronic hypokalemia, as long as the blood potassium is not less than 3mmol/L, the cause can be checked first, and then the cause can be treated. Potassium supplementation should be determined according to the level of blood potassium. If the potassium level is 3.5~4mmol/L, you don't need extra potassium. You only need to encourage patients to eat more potassium-containing foods, such as fresh vegetables, juices and meat. When the potassium level is between 3.0 and 3.5 mmol/L, it is necessary to determine whether or not to supplement potassium according to the specific conditions of the patient. basic knowledge The proportion of sickness: 0.01% Susceptible population: patients who cannot eat normally, have severe diarrhea and vomiting Mode of infection: non-infectious Complications: arrhythmia hyperkalemia

Cause of hypokalemia

Causes

Reduced potassium intake (30%):

Generally, the diet contains more potassium, so as long as it can eat normally, the body will not be deficient in potassium, digestive tract obstruction, coma, and patients who have fasted for a long time after surgery cannot eat. If these patients are given intravenous nutrition, there is no simultaneous Potassium supplementation or potassium supplementation can lead to potassium deficiency and hypokalemia. However, if the lack of intake is the only cause, the degree of potassium deficiency in a certain period of time can be caused by the potassium retention function of the kidney. When the intake is insufficient, the urinary potassium excretion can be reduced to less than 20mmol/L within 4 to 7 days, and can be reduced to 5-10mmol/L within 7 to 10 days. The normal urinary potassium excretion is 38-150mmol/L. .

Excessive potassium excretion (20%):

1. Loss of potassium through the gastrointestinal tract: This is the most important cause of potassium loss in children. It is common in patients with severe diarrhea and vomiting, such as loss of digestive juice. The concentration of K+ in feces during diarrhea can reach 30-50 mmol/L. Potassium lost with feces can be 10 to 20 times more than normal, and the increase in fecal potassium content is due to the reduction of potassium absorption in the small intestine due to diarrhea and the reduction in blood volume due to diarrhea. Aldosterone secretion increases, and aldosterone can not only increase the excretion of urinary potassium, but also strengthen the role of potassium secretion in the colon. Since the potassium content in gastric juice is only 5-10 mmol/L, the loss of gastric juice is not the main cause of potassium loss during severe vomiting. And a large amount of potassium is lost through the kidney with urine, because metabolic alkalosis caused by vomiting can increase the potassium excretion of the kidney, and the reduction of blood volume caused by vomiting can also promote renal potassium excretion through the increase of secondary aldosterone.

2, potassium loss by the kidney: This is the most important cause of potassium loss in adults, the common factors that cause increased potassium excretion in the kidney are:

1 long-term continuous use or excessive use of diuretics: for example, inhibition of proximal convoluted tubule sodium, water reabsorption of diuretic carbonic anhydrase inhibitor acetazolamide, inhibition of medullary ascending branch thick segment Cl- and Na + reabsorption Diuretic furosemide, diuretic acid, thiazide, etc., can increase the flow of raw urine reaching the distal renal tubule, and the increase of the flow here is an important reason for promoting the increase of renal tubular potassium secretion. The above diuretic can also make The amount of Na+ reaching the distal convoluted tubule is increased, which leads to the loss of potassium through the Na+-K+ exchange. Many diuretics also have a common mechanism for causing an increase in renal potassium excretion: an increase in aldosterone secretion due to a decrease in blood volume, furosemide, The role of diuretic acid and thiazide is to inhibit the reabsorption of Cl- by the thick segment of the medullary ascending branch and also inhibit the reabsorption of Na+. Therefore, the long-term use of these drugs can lead to both hyponatremia and low Chloremia, it has been shown that hypochloremia caused by any cause can increase the potassium excretion of the kidney. One of the possible mechanisms is that hypochloremia may directly stimulate the potassium secretion of the distal renal tubule.

2 Certain kidney diseases: In the case of distal renal tubular acidosis, due to the hydrogen dysfunction of the distal convoluted tubules, H+-Na+ exchange is reduced and K+-Na+ exchange is increased, resulting in potassium loss, proximal renal tubular acidosis The reabsorption of HCO3- in the proximal convoluted tubule is reduced, and the increase in HCO3- reaching the distal convoluted tubule is an important reason for promoting the increase of potassium excretion in the distal convoluted tubule. Details, post-urinary phase of acute tubular necrosis, due to urea in renal tubule fluid Increased osmotic diuresis, as well as the function of re-absorption of water and electrolyte by the neonatal tubular epithelium, can cause an increase in potassium excretion.

3 Excessive adrenal cortex hormone: When the original and secondary aldosterone increase, the exchange of Na+-K+ in the distal convoluted tubules and collecting ducts increases, thus acting as a potassium-sparing sodium. In Cushing syndrome, the corticosteroid cortisol Increased secretion, cortisol also has a certain mineralocorticoid-like effect, a large number, long-term increase in cortisol can also promote the exchange of Na+-K+ in the distal convoluted tubule and collecting duct, resulting in increased potassium excretion in the kidney.

4 The number of anions that are not easily reabsorbed in the far-curved tubules is increased: HCO3-, SO42-, HPO42-, NO3-, -hydroxybutyric acid, acetoacetic acid, penicillin, etc. belong to this, and they increase in the distal convoluted tubule Can not be reabsorbed to increase the negative charge of the original urine, so K + easy to enter the luminal fluid from the renal tubular epithelial cells and with the loss of urine.

5 magnesium deficiency: magnesium deficiency often causes hypokalemia. The potassium reabsorption of the medullary ascending branch depends on the Na+-K+-ATR enzyme in the renal tubular epithelial cells, which in turn requires the activation of Mg2+. The enzyme may be inactivated due to the loss of intracellular Mg2+, and thus potassium reabsorption occurs and potassium is lost. Animal experiments have also shown that magnesium deficiency can also cause an increase in aldosterone, which may also be the cause of potassium loss.

6 alkalosis: In the case of alkalosis, the renal tubular epithelial cells have a decrease in H+, so the H+-Na+ exchange is strengthened, so the potassium is increased with the urine.

3, potassium loss through the skin: sweat contains only 9mmol / L of potassium, under normal circumstances, sweating does not cause hypokalemia, but in heavy-earth labor in high-temperature environment, a lot of sweat can also lead to the loss of potassium.

Extracellular potassium transfer to the cells (20%):

When extracellular potassium is transferred to the cells, hypokalemia can occur, but the total potassium content in the body is not reduced.

1. Low-potassium periodic paralysis: extracellular potassium is transferred to the cells during seizures, which is a familial disease.

2, alkalosis: intracellular H + moved to the outside of the cell to compensate, while extracellular K + into the cell.

3. Excess insulin: When using high-dose insulin to treat diabetic ketoacidosis, there are two mechanisms for hypokalemia:

1 Insulin promotes cell glycogen synthesis, potassium is required for glycogen synthesis, and plasma potassium enters cells with glucose to synthesize glycogen.

2 Insulin may directly stimulate Na+-K+-ATPase on the skeletal muscle cell membrane, so that Na+ excretion in myocytes increases and extracellular K+ enters myocytes.

4. Scorpion poisoning: A large number of cases of rickets occurred in a certain place in Sichuan during the Anti-Japanese War. The clinical manifestations were mainly muscle weakness and paralysis. In severe cases, death was caused by respiratory muscle paralysis. The study by Chinese scholar Du Gongzhen confirmed the disease. The reason is cockroach poisoning, but the mechanism of sputum poisoning caused by sputum poisoning has not yet been elucidated. It has been confirmed that the mechanism of sputum poisoning caused by sputum poisoning is that sputum poisoning causes hypokalemia. When sputum poisoning, Na+-K+-ATPase on the cell membrane continues. Activity, so potassium in the extracellular fluid continuously enters the cell, but the pores of potassium outflow from the cell are specifically blocked, resulting in hypokalemia, which is caused by some acid-soluble barium salts such as barium acetate. , barium carbonate, barium chloride, barium hydroxide, barium nitrate and barium sulfide.

Crude cotton oil poisoning (20%):

In the past two or three decades, a hypokalemia has occurred in some cotton producing areas in China, and in some provinces it has been called soft disease. Its main clinical features are extremely weak muscles or flaccid paralysis. Severe cases often die due to respiratory muscle paralysis, serum potassium concentration is significantly reduced, often in the same area, there are many people with the disease, the cause is closely related to the consumption of crude cottonseed oil, crude cotton oil is some small oil plants in rural areas and squeeze The production process of these factories is not in conformity with the specifications. The cottonseed is not fully steamed or even used for oil extraction. The extracted oil is not refined according to the regulations. Therefore, many toxic substances in cottonseed are stored. In oil, the occurrence of "soft disease" and the subsequent series of studies are all gossypol gossypol, the mechanism of hypokalemia in "soft disease" has not yet been elucidated, the discovery of "soft disease" and the subsequent series The research is carried out by Chinese scholars. So far, there are no records of the disease in foreign books and periodicals.

Pathogenesis

The physiological function of K has been as described above. When intracellular potassium is deficient in extracellular potassium and acidosis, if the intracellular K decreases, the K exchanged with extracellular H decreases, so potassium deficiency is often accompanied by metabolic acidosis, chronic Potassium deficiency can be seen in potassium-deficient nephropathy, which mainly manifests renal tubular insufficiency. The decrease of serum potassium can also increase the resting potential of myocardial cells, prolong the action potential, and reflect the ST segment reduction on the electrocardiogram, and the T wave amplitude is reduced and flat. Or inversion, u wave appears and can be fused with T wave. Due to the decrease of K in cardiomyocytes, the self-discipline of myocardial pacemaker cells increases, and the myocardial conduction is inhibited, it is easy to produce new ectopic excitatory lesions and cause various heart rhythms. Qi, severe cases of ventricular fibrillation leading to death, can also occur atrioventricular block.

Hypokalemia prevention

Prevention of this disease is the focus, the cause of this disease is many, especially in the process of clinical treatment, it should pay attention to the prevention of the occurrence of this disease, one is to remove the cause in time, and the second is the possibility of potassium deficiency, such as long-term fasting, body fluids If you lose more people, you should add potassium in time.

Hypokalemia complications Complications arrhythmia hyperkalemia

The disease can mainly cause the following complications:

1, hypokalemia with low calcium, low magnesium, low calcium often manifested as hand and foot spasm, their symptoms can also be confused with each other, should pay attention to the addition of appropriate calcium and magnesium while supplementing potassium.

2, hypokalemia can cause various types of arrhythmia.

3, hyperkalemia: for patients with hypokalemia, due to excessive potassium supplementation during treatment, may cause hyperkalemia because of improper treatment, so in order to prevent hyperkalemia, potassium chloride can be used Add 5% to 10% glucose solution.

4, hypokalemia can also cause renal function of the disease, so the urine volume should be strictly observed during treatment.

Symptoms of hypokalemia Common symptoms Excessive potassium excretion Metabolic low potassium expression indifferent nausea Lower limbs or soft sputum peristalsis slows down convulsions constipation atrioventricular block

The severity of clinical manifestations depends on the degree of potassium deficiency inside and outside the cell and the rate of potassium deficiency. The symptoms of acute hypokalemia are more severe than those of chronic hypokalemia with the same level of potassium deficiency.

1. Neuromuscular system: common symptoms are muscle weakness and paroxysmal soft palate. The latter may have muscle weakness before the attack. Although the seizure is related to the absolute level of plasma [K], it is more related to the [K] gradient inside and outside the cell. Close, the larger the gradient, the greater the difference between the resting potential and the threshold potential, so that the muscle excitability is reduced, and the sputum can also occur when the plasma [K] rises. The seizures are more late and tired, and the affected muscles are the most limbs. Commonly, the head and neck muscles are generally not tired, but may involve breathing muscles and have difficulty breathing. There may be numbness of the limbs before the attack, and then fatigue, and finally the autonomic activity completely disappears. Generally, the proximal muscles are slightly milder than the distal muscles. Can not stand, walk, sit or squat can not stand up, the lighter reliable supportive support stand up, sleep in bed can not turn over themselves, can also occur painful sputum or hand and foot convulsions, the central nervous system is mostly normal, mind Awake, there may be mental symptoms such as apathy, depression, sleepiness, memory and loss of orientation or loss, cranial nerves are rarely affected, and shallow nerve reflexes are weakened or completely disappeared. However, deep reflections and abdominal wall reflections are less affected.

2, the cardiovascular system: low potassium can reduce myocardial stress and a variety of arrhythmias and conduction block, mild sinus tachycardia, atrial or ventricular premature contraction, atrioventricular block Severe cases of paroxysmal atrial or ventricular tachycardia, and even ventricular fibrillation, potassium deficiency can aggravate digitalis and expectorant poisoning, can lead to death, peripheral peripheral blood vessels dilate, blood pressure can be reduced, myocardial tension can be reduced Heart enlargement, heart failure occurs in severe cases, electrocardiogram changes have been described in pathophysiology, EKG appears u wave, often suggesting that the body loses potassium at least 500mmol / L.

3, urinary system: long-term low potassium can damage the renal tubules and cause potassium-deficient nephropathy, renal tubular concentration, ammonia synthesis, hydrogen secretion and Cl- reabsorption function can be reduced or enhanced, sodium excretion function or reabsorption of sodium The function can also be reduced, and the net result can lead to metabolic low potassium and low chloride alkalosis.

4, endocrine metabolic system: hypokalemia may have impaired glucose tolerance, long-term potassium deficiency in children with delayed growth, hypokalemia patients, urinary potassium excretion is reduced (<30mmol / 24h), but by renal tubular acid Inflammation and acute renal failure caused by increased urinary potassium excretion (>40mmol/24h), urinary potassium excretion still increased in the case of hypokalemia, often suggesting increased aldosterone secretion, is a clue to the diagnosis of aldosteronism.

5, the digestive system: potassium deficiency can slow bowel movements, mild potassium deficiency only appetite deficiency, abdominal distension, nausea and constipation, severe potassium deficiency can cause paralytic intestinal obstruction.

Hypokalemia check

1. Blood test indicators: serum potassium concentration decreased, <3.5mmol/L, blood pH was at normal high limit or >7.45, sodium ion concentration was at normal low limit or <135mmol/L.

2, urine test indicators: urinary potassium concentration decreased, urine pH value is acid, urine sodium discharge is more.

3, ECG examination: the earliest performance is ST segment depression, T wave pressure is low, widened, inverted, wave appears, QT time is prolonged, the above changes can be improved after potassium supplementation.

Diagnosis and identification of hypokalemia

diagnosis

Blood K is called mild hypokalemia at 3.0 to 3.5 mmol/L, and the symptoms are few. Blood K is moderately hypokalemia between 2.5 and 3.0 mmol/L, and may have symptoms. Blood K <2.5mmol / L for severe hypokalemia, severe symptoms.

The diagnosis of hypokalemia includes: determining hypokalemia and determining the cause of hypokalemia.

1, determine hypokalemia: according to: 1 serum potassium is lower than 135mmol / L. 2 ECG examination has a low potassium image. 3 clinical manifestations in line with hypokalemia.

2, determine the cause of hypokalemia: including: 1 detailed medical history, such as feeding, gastrointestinal symptoms, urination and nocturia and diuretics, smoking and drinking history. 2 laboratory tests: in addition to potassium, sodium, chlorine, should also check blood calcium, magnesium, low calcium, low magnesium and acidosis can aggravate hypokalemia, determine urinary potassium concentration, if urinary potassium concentration <20mmol / L, Most of them are potassium in the gastrointestinal tract. >20mmol/L, mostly for extra-renal potassium, but <20mmol/L does not rule out potassium loss in the kidney, especially in patients with low sodium intake and freshly used potassium diuretics, blood and urine pH values, both Alkaline, suggesting an increase in aldosterone. Blood is acidic, urine is alkaline, suggesting renal tubular acidosis.

The incidence of hypokalemia is high, and its symptoms are often concealed by the primary disease, which is easy to be misdiagnosed. Therefore, for long-term food intake, fasting, diuresis or massive vomiting, patients with diarrhea should be promptly supplemented with potassium salt, in addition, in metabolic acid In case of poisoning, serum potassium may not be low, and hypokalemia may occur when acidosis is corrected.

Differential diagnosis

For further identification, blood volume status and blood pressure should be observed. If blood pressure is increased, consider aldosteronism, hypercortisolism, liddle syndrome and other diseases. If the blood pressure is normal, consider Batter syndrome, Getelman syndrome and other diseases.

In addition, when hypokalemia complicated with arrhythmia, it needs to be differentiated from other types of arrhythmia, such as supraventricular tachycardia, because some patients may have no other clinical symptoms, only arrhythmia, so for some Patients with a history of heart disease, if there is arrhythmia, should be suspected of the disease, if the cause of the disease exists, laboratory tests should be performed, generally can be diagnosed.

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