The daily intake of water and electrolytes can vary greatly, but the daily excretion also varies, so that water and electrolytes are often kept in dynamic balance in the body. This constant change and maintenance of the balance of water and electrolytes in the human body is mainly accomplished by the body’s internal regulatory ability. If this regulatory function is disrupted by various factors such as disease and trauma, disorders of water and electrolytes will develop, and the imbalance of body fluid balance can be expressed as volume imbalance, concentration imbalance or composition imbalance. Volume imbalance refers to the isotonic decrease or increase of body fluid volume, which only causes the change of extracellular fluid volume, and the occurrence of water deficiency or water excess. Concentration dysregulation is an increase or decrease in the amount of water in the extracellular fluid such that there is a change in the concentration of osmotic particles, i.e., a change in osmolarity, such as hyponatremia or hypernatremia. Although changes in the concentration of other ions in the extracellular fluid can have their own pathophysiological effects, they do not significantly change the osmolarity of the extracellular fluid due to the small amount, so they only cause component disorders, such as acidosis or alkalosis, hypokalemia or hyperkalemia, and hypocalcemia or hypercalcemia. Wu Chunfu, Department of Surgery, Wuxi Hospital of Traditional Chinese Medicine
I. Disorders of water and sodium metabolism
The relationship between water and sodium is very close, so water deficiency and sodium loss often exist at the same time. The causes of water and sodium metabolism disorders are different, and the degree of water deficiency and sodium loss can also be different. Water and sodium can be lost in proportion to each other, or water deficiency can be more than sodium deficiency, or water deficiency can be less than sodium deficiency. Thus, the pathophysiological changes and some clinical manifestations caused are also different.
(a) Isotonic dehydration, also known as acute dehydration or mixed dehydration. Surgical patients are most prone to this type of dehydration. Water and sodium are lost in proportion to each other, while serum sodium remains in the normal range and the osmolarity of extracellular fluid remains normal. It causes a rapid decrease in the amount of extracellular fluid (including circulating blood volume). The pressure receptors in the walls of the small renal inflow arteries are stimulated by the decrease in intratubular pressure and the decrease in Na+ in the distal tubular fluid due to the decrease in glomerular filtration rate, causing excitation of the renin-aldosterone system and an increase in aldosterone secretion. Aldosterone promotes sodium reabsorption in the distal tubule, and there is an increase in the amount of water that is reabsorbed along with sodium, causing the amount of extracellular fluid to rebound. Since the lost fluid is isotonic and basically does not change the osmotic pressure of the extracellular fluid, initially intracellular fluid is not transferred to the extracellular space to compensate for the lack of extracellular fluid. Therefore, the amount of intracellular fluid does not change. However, after this fluid loss lasts for a long time, the intracellular fluid will gradually move out and be lost along with the extracellular fluid, causing cellular dehydration.
The common causes are: (1) acute loss of digestive fluid, such as massive vomiting, intestinal fistula, etc.; (2) loss of body fluid in infected areas or soft tissues, such as intraperitoneal or retroperitoneal infections, intestinal obstruction, burns, etc. These lost fluids have basically the same composition as extracellular fluid.
Clinical manifestations The patient has scanty urination, anorexia, nausea, and weakness, but is not thirsty. The tongue is dry, the eyes are not sunken, and the skin is dry and flaccid. When the loss of body fluid reaches 5% of body weight in a short period of time, i.e., 25% of extracellular fluid, the patient shows symptoms of hypovolemia such as rapid pulse rate, cold extremities, and unstable or falling blood pressure. When the loss of body fluid continues to reach 6% to 7% of body weight (equivalent to 30% to 35% loss of extracellular fluid), the manifestations of shock are more severe. This is often accompanied by metabolic acidosis. If the loss of body fluid is mainly gastric fluid, the patient may develop metabolic alkalosis and some clinical manifestations of alkalosis because of the large loss of CI-.
Diagnosis Mainly depends on medical history and clinical manifestations. Detailed questions should be asked about the presence of large loss of digestive or other body fluids; how long the fluid loss or inability to eat has lasted; how much the estimated daily fluid loss is, and the nature of the fluid loss. Laboratory tests may reveal a significant increase in red blood cell count, hemoglobin mass and red blood cell pressure product, indicating hemoconcentration. Serum Na+ and CI- are generally not significantly decreased. Urine specific gravity is increased. If necessary, blood gas analysis or carbon dioxide binding capacity measurement is performed to determine whether there is acid (or alkaline) toxicity.
Treatment Treat the cause of isotonic dehydration simultaneously to reduce the loss of water and sodium, if possible. In response to the decrease in extracellular fluid volume, replenish blood volume as soon as possible with balanced salt solution or isotonic saline. Symptoms such as fine pulse rate and decreased blood pressure often indicate loss of extracellular fluid up to 5% of body weight, and the patient may be given a rapid drip of approximately 300 ml (based on 60 kg body weight) of the above solution intravenously to restore blood volume. If there is no blood volume deficiency, the patient can be given 1/2 to 2/3 of the above amount, i.e., 1500 to 2000 ml, to replenish the water deficiency, or the amount of rehydration can be calculated according to the red blood cell pressure volume. In addition, the daily requirement of water should be supplemented with 2000ml and sodium 4.5g.
Isotonic saline contains 154mmol/L each of Na+ and CI-, while the serum Na+ and CI- content are 142mmol/L and 103mmol/L respectively. The normal kidney has the function of retaining HCO-3 and excreting CI-, so the large amount of CI- entering the body does not cause hyperchloremic acidosis. However, in a state of severe dehydration or shock, renal blood flow is reduced and the chloride excretion function is affected. Infusion of large amount of isotonic saline from intravenous has the risk of causing high blood CI- and causing hyperchloremic acidosis. Balanced saline solutions with similar electrolyte content and intraplasma content are ideal for treating dehydration, avoiding excessive CI- input and helping to correct acidosis. At present, the commonly used balanced salt solutions are sodium lactate and compound sodium chloride solution (1.86% sodium lactate solution and compound sodium chloride solution ratio of 1:2) and sodium bicarbonate and isotonic water solution (1.25% sodium bicarbonate solution and isotonic saline ratio of 1:2). After the correction of dehydration, the excretion of bets increases and the K+ concentration is diluted by the increase of extracellular fluid, so attention should be paid to the occurrence of hypokalemia. Generally, potassium oxide should be supplemented after the urine volume reaches 40 ml/h.
(ii) Hypotonic dehydration Also called chronic dehydration or secondary dehydration. Water and sodium are lost at the same time, but water deficiency is less than sodium deficiency, so serum sodium is lower than the normal range and extracellular fluid is hypotonic. The body reduces the secretion of antidiuretic hormone, so that the reabsorption of water in the renal tubules is reduced and the urinary output is increased to raise the osmolarity of the extracellular fluid. However, the amount of extracellular fluid in turn decreases even more, and intertissue fluid enters the circulation, which partially compensates for the blood volume, but makes the decrease in intertissue fluid more than the decrease in plasma. Faced with a significant reduction in circulating blood volume, the body will no longer take into account the osmotic pressure and try to maintain blood volume. Excitation of the renin-aldosterone system leads to a decrease in renal sodium excretion and an increase in CI- and water reabsorption. Therefore, the sodium chloride content in the urine is significantly reduced. The decrease in blood volume in turn stimulates the posterior pituitary gland, resulting in increased secretion of antidiuretic hormone and increased water reabsorption, leading to oliguria. If the blood volume continues to decrease, shock will occur when the above compensatory function is no longer able to maintain blood volume. This kind of shock caused by massive sodium loss is also called hyponatremic shock.
The main causes are: (1) continuous loss of gastrointestinal digestive juices, such as repeated vomiting, long-term gastrointestinal tract suction or chronic intestinal obstruction, resulting in the loss of sodium with a large amount of digestive juices; (2) chronic leakage from large trauma; (3) excessive renal excretion of water and sodium, such as the application of sodium-removing diuretics (chlorothiazide, diuretic acid, etc.), without paying attention to the amount of sodium supplementation, resulting in the body sodium deficiency relatively more than water deficiency.
Clinical manifestations vary with the degree of sodium deficiency. Common symptoms include dizziness, blurred vision, weakness, fine and rapid pulse rate, and easy fainting when rising. When the circulating blood volume decreases significantly, the filtration volume of kidney decreases accordingly, resulting in retention of metabolites in the body, which may lead to confusion, myoclonic pain, weakened tendon reflex and coma.
According to the degree of sodium deficiency, hypotonic dehydration can be divided into three degrees.
1. mild sodium deficiency The patient feels tired, dizzy, numbness of hands and feet, and thirst is not obvious. Na+ in urine is reduced. Serum sodium is below 135 mmol/L, and sodium chloride deficiency is 0.5g per kg body weight.
2. Moderate sodium deficiency In addition to the above symptoms, there are also nausea, vomiting, fine and rapid pulse, unstable or decreased blood pressure, small pulse pressure, superficial venous atrophy, blurred vision, standing fainting. Urine output is low, and sodium and chloride are almost absent in the urine. Serum Na+ is below 130 mmol/L, and sodium chloride deficiency is 0.5-0.75g per kg body weight.
3. Severe sodium deficiency The patient is confused, with muscle spasmodic twitching and weakened or absent tendon reflexes; there is xerosis and even coma. Shock often occurs. Serum Na+ is below 120 mmol/L, and sodium chloride deficiency is 0.75-1.25 g per kg body weight.
Diagnosis Based on the patient’s history of fluid loss with the above characteristics and clinical manifestations, the diagnosis of hypotonic dehydration can be made initially. Further, urine Na+ and CI- can be measured, and there is often a significant decrease. In mild sodium deficiency, although serum sodium may not yet have significant changes, the content of sodium chloride in urine is often reduced. ②Serum sodium measurement, according to the measurement results, the degree of sodium deficiency can be determined; serum sodium below 135 mmol/L indicates hyponatremia. ③Red blood cell count, hemoglobin amount, red blood cell pressure volume, blood non-protein nitrogenated sodium and urea are increased, while urine specific gravity is often below 1.010.
Treatment Actively address the causative agent. For extracellular fluid sodium deficiency more than water deficiency and blood volume deficiency, intravenous infusion of salt-containing solution or hypertonic saline is used to correct the hypotonicity of body fluids and replenish blood volume.
1. Mild and moderate sodium deficiency The amount of fluid to be resupplied is estimated according to the degree of clinical sodium deficiency. For example, if a patient weighs 60kg and the serum sodium is 135mmol/L, it is estimated that 0.5g of sodium chloride is lost per kg of body weight, and the total sodium deficiency is 30g. Generally, half of it can be given first, i.e. 15g, plus the daily sodium requirement of 4.5g, totaling 19.5g, which can be done by intravenous infusion of 5% glucose saline about 2000ml. In addition, the daily fluid requirement of 2000ml should be given, and according to the degree of dehydration, some more rehydration should be added. The remaining half of the sodium can be recharged on the second day.
2. Severe sodium deficiency For those who appear to be in shock, the blood volume should be replenished first to improve microcirculation and perfusion of tissues and organs. Crystal solutions such as lactic acid compound sodium chloride solution, isotonic saline and colloidal solutions such as hydroxyethyl starch, dextrose and plasma protein solution can be applied. However, the dosage of crystalloid solution is generally 2 to 3 times larger than that of colloid solution. Next, intravenous hypertonic saline (generally 5% sodium chloride solution) 200-300ml is administered to correct low blood sodium as soon as possible to further restore the amount of extracellular fluid and osmotic pressure, so that water can be moved from the edematous cells. Later, depending on the condition, it will be decided whether hypertonic saline needs to be continued or changed to isotonic saline.
The amount of sodium salt to be replenished can generally be calculated according to the following formula.
Amount of sodium salt to be replenished (mmol) = [normal value of blood sodium (mmol/L) – measured value of blood sodium (mmol/L)] * body weight (kg) * 0.60 (0.50 for women).
The amount of sodium chloride supplementation was calculated based on 17 mmol Na+ = 1 g of sodium salt. Half of the daily requirement of 4.5g was given on the same day, of which 2/3 was given in 5% NaCl solution, and the rest was given in isotonic saline. Later, serum Na+, K+, CI- and blood gas analysis can be measured as reference for further treatment.
3. Sodium deficiency with acidosis After replenishment of blood volume and sodium, acidosis can often be corrected at the same time due to the compensatory regulation function of the body, so it is generally not necessary to treat with alkaline drugs at the beginning. If the acidosis is still not completely corrected by blood gas analysis, 100-200ml of 1.25% sodium bicarbonate solution or 200ml of balanced salt solution can be injected intravenously, and the decision to continue the supplementation will be made later depending on the situation. After the urine volume reaches 40ml/h, potassium salt should be replenished.
(iii) Hypertonic dehydration, also known as primary dehydration. Although water and sodium are missing at the same time, but the water deficiency is more than sodium deficiency, so the serum sodium is higher than the normal range and the extracellular fluid is hypertonic. The thirst center located in the lower part of the optic thalamus is stimulated by hyperosmolarity, and the patient feels thirsty and drinks water to increase water in the body in order to lower the osmotic pressure. On the other hand, hypertonicity of extracellular fluid can cause increased secretion of antidiuretic hormone, resulting in increased reabsorption of water by the renal tubules and decreased urine output, which reduces the osmolarity of extracellular fluid and restores its volume. If dehydration continues, a significant decrease in circulating blood volume causes increased secretion of aldosterone, which enhances the reabsorption of sodium and water to maintain blood volume. In severe cases of water deficiency, the osmolarity of extracellular fluid increases, causing intracellular fluid to move to the extracellular space, with the result that there is a decrease in both intracellular and extracellular fluid volumes. Finally, the degree of intracellular fluid dehydration exceeds the degree of extracellular fluid dehydration. Water deficiency in brain cells will cause brain dysfunction.
Etiology The main causes are: ① Insufficient intake of water, such as dysphagia in esophageal cancer, insufficient water administration in critically ill patients, nasal feeding of highly concentrated elemental diet or intravenous injection of large amount of hypertonic saline solution. ② Excessive loss of water, such as high fever with massive sweating (sweat containing 0.25% sodium chloride), burn exposure therapy, diabetic coma, etc.
Clinical manifestations vary with the degree of dehydration. According to the severity of symptoms, hypertonic dehydration is generally divided into three degrees.
1. Mild dehydration No other symptoms except thirst. The amount of water deficiency is 2% to 4% of body weight.
2. moderate dehydration Extreme thirst. Weakness, low urine and increased specific gravity of urine. Dry lips and tongue, poor skin elasticity, sunken eye sockets. Irritability often occurs. Water deficiency is 4% to 6% of body weight.
3. Severe water deficiency In addition to the above symptoms, symptoms of brain dysfunction such as mania, hallucinations, delirium, and even coma appear. The water deficiency is more than 6% of body weight.
Diagnosis The diagnosis of hypertonic dehydration can generally be made based on the medical history and clinical manifestations. Laboratory tests often reveal: ① high specific gravity of urine. (ii) Mildly increased red blood cell count, hemoglobin volume, and red blood cell pressure product. ③Serum sodium is elevated, above 150 mmol/L.
Treatment The cause should be removed as early as possible so that the patient no longer loses fluid to facilitate the body’s own regulatory function. For patients who cannot be given orally, a 5% glucose solution or 0.45% sodium chloride solution should be given intravenously to replenish the lost fluid. There are two ways to estimate the amount of fluid lost: ① Estimated by the percentage of body weight lost according to the severity of clinical manifestations. For every 1% of body weight lost, 400-500 ml of fluid should be replenished. ② Calculation based on blood Na+ concentration. The amount of rehydration (ml) = [blood sodium measurement (mmol/L) – normal blood sodium value (mmol/L)] * body weight (kg) * 4. The calculated amount of rehydration should not be rehydrated on the same day, to avoid water intoxication. Generally, it can be divided into two days. Half of the amount of water should be given on the same day, and the remaining half should be given on the next day. In addition, the daily requirement of 200ml should be replenished.
It must be noted that although the serum Na + measurement has increased, but because of the same time there is a lack of water, blood concentration, the total amount of sodium in the body is actually still reduced. Therefore, appropriate sodium supplementation should be given along with water supplementation to correct sodium deficiency. If there is a potassium deficiency to be corrected at the same time, the potassium should be supplemented after the urine volume exceeds 40 ml/h to avoid causing excessive blood potassium. If the acidosis is not corrected after rehydration treatment, sodium bicarbonate solution can be given.
(iv) Excessive water, also known as water intoxication or dilute hyponatremia. It means that the total amount of water into the body exceeds the amount of drainage, resulting in water retention in the body, causing a decrease in blood osmotic pressure and an increase in circulating blood volume. Water overload occurs less frequently. Only in the case of excessive secretion of antidiuretic hormone or renal insufficiency, the body takes in too much water or receives too much intravenous fluids, causing water to accumulate in the body, resulting in water intoxication. At this time, the amount of extracellular fluid increases, serum sodium concentration decreases, and osmotic pressure decreases. Because the osmotic pressure of intracellular fluid is relatively high, water moves into the cells, with the result that the osmotic pressure of both intracellular and extracellular fluid decreases and the amount increases. In addition, the increased amount of extracellular fluid inhibits the secretion of aldosterone, which reduces the reabsorption of Na+ by the distal tubule and increases the excretion of Na+ from the urine, thus reducing the serum sodium concentration even more.
Clinical manifestations can be divided into two categories.
1. acute water intoxication The onset is acute. Brain cell swelling and brain tissue edema cause increased intracranial pressure, resulting in various neurological and psychiatric symptoms, such as headache, aphasia, confusion, disorientation, drowsiness, agitation, convulsions, delirium, and even coma. Sometimes brain herniation can occur.
2. Chronic water intoxication There may be weakness, nausea, vomiting, drowsiness, etc., but they are often masked by the symptoms of the primary disease. The patient’s weight is significantly increased, and the skin is pale and moist. Sometimes saliva and tears are increased. There is usually no sunken edema.
Laboratory tests may reveal decreased red blood cell count, hemoglobin volume, red blood cell pressure volume and plasma protein volume; decreased plasma osmolality, as well as increased mean red blood cell volume and decreased mean red blood cell hemoglobin concentration. This indicates an increase in both intracellular and extracellular fluid.
Treatment Prevention is more important than treatment. Water intake should be strictly limited in those prone to excessive secretion of antidiuretic hormone, such as pain, blood loss, shock, trauma and major surgery; in patients with acute renal insufficiency and in patients with chronic cardiac insufficiency. For patients with water intoxication, water intake should be stopped immediately, after the body excretes excess water, the less severe, water intoxication can be lifted. In addition to water prohibition, diuretics should be used to promote water excretion in more severe cases. Generally, osmotic diuretics, such as 20% mannitol or 25% sorbitol 200ml intravenous rapid drip, are used to reduce brain cell edema and increase water discharge. Also can be intravenous tab diuretics, such as tachyphylaxis and diuretic acid. Intravenous 5% sodium chloride solution can also be given to rapidly improve the hypotonicity of body fluids and reduce brain cell swelling.
Potassium abnormalities
There are hypokalemia and hyperkalemia, with the former being the most common.
(A) Hypokalemia The normal value of serum potassium is 3.5-5.5 mmol/L. Lower than 3.5 mmol/L indicates hypokalemia. The common causes of potassium deficiency or hypokalemia are: ①Long-term inadequate food intake. (2) Application of diuretics such as tachykinuria and diuretic acid, renal tubular acidosis, and excessive salt corticosteroids, which cause excessive potassium excretion from the kidneys. ③The rehydration patient receives fluids without potassium salts for a long time. ④Inadequate potassium salt supplementation in intravenous nutrition fluids. ⑤ Loss of potassium from extrarenal route by vomiting, continuous gastrointestinal decompression, fasting, intestinal fistula, colonic villous adenoma and ureterosigmoid anastomosis. In general, persistent low serum potassium often indicates severe potassium deficiency in the body.
Clinical manifestations Myasthenia gravis is the earliest manifestation, usually starting with weakness of the extremity muscles and later extending to the trunk and respiratory muscles. Sometimes there may be difficulty in swallowing, so that food or water may choke into the respiratory tract. Later on, there may be flaccid paralysis and diminished or absent tendon reflexes. Patients have symptoms of altered gastrointestinal function such as bitterness in the mouth, nausea, vomiting and intestinal paralysis. Cardiac involvement is mainly manifested by conduction and rhythm abnormalities. Typical ECG changes are early onset of lowered, widened, biphasic or inverted T waves, followed by lowered ST segments, prolonged QT intervals and U waves (Figure 3-1). However, patients with hypokalemia do not always present with ECG changes, so the presence of hypokalemia cannot be determined solely on the basis of ECG changes. It should be noted that some of the clinical manifestations of hypokalemia may be less pronounced in patients with severe extracellular fluid depletion; instead, symptoms of hypokalemia may appear only as a result of water and sodium deficiency, but after correction of the water deficiency, some symptoms of hypokalemia may appear due to further dilution of potassium. In patients with severe potassium deficiency, polyuria sometimes occurs because potassium deficiency prevents the action of antidiuretic hormone, so that the kidneys lose the function of concentrating urine. In addition, when the serum potassium is too low, K+ is removed from the cells and the exchange with Na+ and H+ increases (for every 3 K+ removed, 2 Na+ and 1 H+ are transferred into the cells), and the H+ concentration in the extracellular fluid decreases; while the distal tubular excretion of K+ decreases and the excretion of H+ increases. As a result, alkalosis occurs and the patient shows some of the symptoms of alkalosis, but the urine is acidic (paradoxical aciduria).
Figure 3-1 Electrocardiographic changes in hypokalemia
The diagnosis of hypokalemia can usually be made based on the history and clinical presentation. Although electrocardiography can be helpful, it is generally not advisable to wait for the electrocardiogram to show typical changes before making a firm diagnosis. Serum potassium measurements are often decreased.
Treatment The cause of hypokalemia should be treated as early as possible to reduce or stop the continued loss of potassium.
The degree of potassium deficiency is difficult to determine clinically. A preliminary determination of potassium supplementation can be made by referring to the results of serum potassium measurements. If the serum potassium is less than 3 mmol/L, K+ 200-400 mmol can increase the serum potassium by 1 mmol/L. If the serum potassium is 3.0-4.5 mmol/L, K+ 100-200 mmol can increase the serum potassium by 1 mmol/L. The total amount of potassium in the extracellular fluid is only 60 mmol, so if the potassium-containing solution is fed into the vein too quickly, the blood potassium can increase a lot in a short time. If intravenous potassium solution is given too quickly, the blood potassium can increase a lot in a short period of time, causing fatal consequences. The rate of potassium supplementation should not exceed 20mmol/h, and the daily amount of potassium supplementation should not exceed 100-200mmol. If the patient is in shock, crystal or colloidal solution should be given first to restore blood volume as soon as possible. After the urine volume exceeds 40 ml per hour, potassium chloride solution should be given intravenously. There are other uses for potassium chloride infusion. Since hypokalemia is often accompanied by extracellular alkalosis, CI-, which is given together with potassium, may help to reduce the alkalosis. In addition, chlorine deficiency can affect the kidney’s ability to conserve potassium, so KC1 infusion can be beneficial in the treatment of hypokalemia by enhancing the kidney’s ability to conserve potassium in addition to replenishing K+. It takes a long time to completely correct potassium deficiency in the body, and the patient can take potassium salts after being able to take them orally.
(B) Hyperkalemia is called hyperkalemia when the serum potassium exceeds 5.5 mmol/L. The cause of hyperkalemia is mostly related to hyperalgesia. Most of the reasons for this are related to the inability of the kidneys to excrete potassium effectively from the urine due to reduced kidney function. Common causes include: (1) an increase in the amount of potassium entering the body (or blood), such as oral or intravenous potassium chloride, drugs, tissue damage, and large amounts of stored blood. (ii) Decreased renal excretion, such as acute renal failure, application of potassium-preserving diuretics (e.g., aminoglutethimide, ampicillin), and salt corticosteroid deficiency. (iii) Abnormal distribution of transcellular cells, such as acidosis, application of succinylcholine, and infusion of arginine.
Clinical manifestations There are usually no specific symptoms, sometimes there is mild confusion or indifference, abnormal sensation and limb weakness. Severe hyperkalemia has manifestations of microcirculatory disorders, such as pale skin, chills, bruising, and hypotension. A slow heartbeat or arrhythmia, or even cardiac arrest, is often present. Hyperkalemia, especially when the blood potassium exceeds 7 mmol/L, almost always has electrocardiographic changes. Typical ECG changes are early high T waves with prolonged sharp QT intervals, followed by widening of the QRS and prolonged PR intervals (Figure 3-2).
Figure 3-2 Electrocardiographic changes in hyperkalemia
When a patient with a cause of hyperkalemia presents with clinical manifestations that cannot be explained by the original cause, the possibility of hyperkalemia should be considered and an electrocardiogram should be performed. Serum potassium is often elevated.
Treatment In addition to treating the primary disease and improving renal function, the following should be considered when hyperkalemia is detected.
1. stop giving all drugs or solutions with potassium, and try not to eat foods with high potassium content to avoid an increase in blood potassium.
2. Reduce the serum potassium concentration
(1) Temporary transfer of K+ into the cells: ①After intravenous injection of 60-100ml of 5% sodium bicarbonate solution, continue intravenous injection of 100-200ml of sodium bicarbonate. hypertonic alkaline solution can increase the blood volume, K+ will be diluted, and K+ will be transferred into the cells or excreted by urine, which will help the treatment of acidosis. The injected Ka+, also counteracts the effect of K+. ② Use 100-200ml of 25% glucose solution and 1u of insulin for every 3-4g of sugar for intravenous infusion, which can transfer K+ into the cells and temporarily reduce the serum potassium concentration. If necessary, repeat the dose every 3~4 hours. (3) For those who have renal insufficiency and cannot infuse too much fluid, 100ml of 10% calcium gluconate solution, 50ml of 11.2% sodium lactate solution, 400ml of 25% glucose solution, add 30u of insulin, and continue intravenous infusion for 24 hours at 6 drops per minute.
(2) Application of cation exchange resin: 15g orally four times a day, which can carry away more potassium ions from the digestive tract. At the same time, take sorbitol or mannitol orally to induce diarrhea to prevent the occurrence of fecal mass intestinal obstruction. Can also add 10% glucose solution 200ml for retention enema.
(3) Dialysis therapy: there are peritoneal dialysis and hemodialysis, which are generally used when the above mentioned therapies still cannot reduce the serum potassium concentration.
(3) Anti-arrhythmia: Intravenous injection of 20ml of 10% calcium gluconate solution. calcium has an antagonistic effect with potassium and can relieve the toxic effect of K+ on the myocardium. Calcium gluconate can be used repeatedly. Also available 30 ~ 40ml of calcium gluconate added to intravenous rehydration solution within the drip.
Third, the magnesium abnormal
Normal adult body magnesium total is about 1000mmol, about magnesium 23.5g. About half of the magnesium exists in the bone, the rest almost all exist in the cell, only 1% exist in the extracellular fluid. The normal value of serum magnesium concentration is 0.70~1.20mmol/L. Although there is a decrease in serum magnesium concentration, renal magnesium excretion does not stop. In many diseases, often can appear abnormal magnesium metabolism.
(A) magnesium deficiency long period of gastrointestinal digestive fluid loss, such as intestinal fistula or large part of the small intestine after resection, coupled with eating less, is the main reason for magnesium deficiency. Other reasons are long-term application of magnesium-free solution treatment, intravenous high nutrition without adding the right amount of magnesium as a supplement and acute pancreatitis.
The common symptoms of hypomagnesemia are memory loss, nervousness, easily agitated, confusion, irritability, tachycardia-like movement, etc. The patient’s face is pale and atrophied. Severe magnesium deficiency may have seizures.
For patients who have triggering factors and some symptoms of hypomagnesemia, magnesium deficiency should be suspected. Because magnesium deficiency often and potassium deficiency and calcium deficiency at the same time, in some hypokalemia patients, after potassium supplementation still does not improve the situation, should be considered to have magnesium deficiency. Measurement of serum magnesium concentration is generally of little value to confirm the diagnosis. Because magnesium deficiency does not necessarily appear low serum magnesium, and low serum magnesium does not necessarily indicate a magnesium deficiency. If necessary, can be magnesium load test, help the diagnosis of magnesium deficiency. Normal people in the intravenous infusion of magnesium chloride or magnesium sulfate 0.2 5mmol/kg, 90% of the injected amount is quickly excreted from the urine, while in magnesium deficiency patients, after injecting the same amount of solution, 40% to 80% of the input magnesium can be retained in the body or even daily excretion of magnesium from the urine only 1mmol.
Generally can be supplemented by 0.25mmol/(kg.d) dose of magnesium salt. If the patient’s renal function is normal, and magnesium deficiency is serious, can be supplemented by 1mmol/(kg. d) magnesium salt. Commonly used magnesium chloride solution or magnesium sulfate solution intravenous drip. When the patient has convulsion, generally use magnesium sulfate solution intravenous drip, can be faster to control the convulsion. Dosage to give 10% magnesium sulfate 0.5ml per kilogram of body weight. Intravenous magnesium should be given to avoid giving too much magnesium, too fast, so as not to cause acute magnesium poisoning and cardiac arrest. If magnesium poisoning, should be intravenous injection of calcium gluconate or calcium chloride solution to act as an anti-agent. Complete correction of magnesium deficiency takes a long time, so after lifting the symptoms, still should continue to supplement magnesium daily for 1 to 3 weeks. The general dosage is 50% magnesium sulfate 5 ~ 10mmol (equivalent to 50% magnesium sulfate 2.5 ~ 5ml), intramuscular injection or dilution after intravenous injection.
(B) magnesium excess mainly occurs in the renal insufficiency, met in the process of applying magnesium sulfate for eclampsia. Early burns, extensive injuries or surgical stress, severe extracellular fluid deficiency and severe acidosis can also cause an increase in serum magnesium.
Clinical manifestations include fatigue, weakness, loss of tendon reflexes and decreased blood pressure. When there is a large increase in serum magnesium concentration, cardiac conduction dysfunction occurs and ECG shows prolonged PR interval, widened QRS and elevated T wave, similar to the ECG changes in hyperkalemia. Respiratory depression, drowsiness and coma, and even cardiac arrest may occur in the late stages.
Treatment should start with slow intravenous administration of 2.5-5 mmol calcium gluconate or calcium chloride solution to counteract the inhibition of magnesium on the heart and muscles. At the same time to actively correct acidosis and dehydration, stop giving magnesium . If the serum magnesium concentration still does not fall or symptoms still do not reduce, should be used early dialysis therapy.
Fourth, the calcium abnormalities
Most of the calcium in the body is stored in the bone in the form of calcium phosphate and calcium carbonate. The normal value of serum calcium concentration is 2.5 mmol/L. 45% of them are ionized calcium, which plays the role of maintaining the stability of neuromuscular, about half of them are non-ionized calcium with the same combination of serum protein, 5% are non-ionized calcium combined with other substances in the fluid between plasma and tissue. The ratio of ionized to nonionized calcium is influenced by the fact that a decrease in pH can increase ionized calcium and an increase in pH can decrease ionized calcium. Disorders of calcium metabolism generally rarely occur in surgical patients.
(i) Hypocalcemia can occur in patients with acute pancreatitis, necrotizing fasciitis, renal failure, pancreatic and small bowel fistulas, and parathyroid gland damage. Clinical manifestations are mainly caused by increased neuromuscular excitability, such as easy agitation, perioral and finger (toe) numbness and pins and needles, hand and foot twitching, muscle and abdominal cramps, hyperactive tendon reflexes, and positive Chvostek’s and Trousseau’s signs. The diagnosis is basically confirmed when serum calcium is measured below 2 mmol/L. For treatment, the primary disease should be treated, and 10% calcium gluconate 20 ml or 5% calcium chloride 10 ml should be given intravenously to relieve the symptoms. If there is alkalosis, it should be corrected at the same time to increase the concentration of ionized calcium in the blood. If necessary, multiple doses can be given (1g of calcium gluconate contains Ca2+2.5mmol; 1g of calcium chloride contains Ca2+10mmol). For patients who need long-term treatment, calcium lactate can be taken or supplemented with vitamin D at the same time.
(ii) Hypercalcemia occurs mainly in hyperparathyroidism, followed by bone metastatic carcinoma, especially in bone metastatic breast cancer treated with estrogen. Early symptoms include fatigue, weakness, malaise, loss of appetite, nausea, vomiting and weight loss. Further increase in serum calcium concentration may result in severe headache, back and limb pain, thirst, and polyuria. An increase in serum calcium up to 45 mmol/L is life threatening. Surgical treatment should be performed for hyperparathyroidism to fundamentally resolve hypercalcemia. For patients with bone metastatic cancer, low-calcium diet and sufficient water can be given to prevent dehydration to reduce symptoms and pain. Symptomatic treatment may include rehydration, ethylenediaminetetraacetic acid (EDTA), steroids and sodium sulfate to temporarily reduce serum calcium concentration.