OVERVIEW
Liver is the metabolic regulator of human body, playing an important role in regulating water, electrolyte and acid-base balance. Cirrhosis can cause water, electrolyte and acid-base balance imbalance, resulting in internal environmental disorders, including hyponatremia, hypokalemia, hypochloremia, hypocalcemia, etc., which is one of the more common complications of cirrhosis, especially in the period of hepatic dysfunction, and the degree of electrolyte disorders has a close relationship with the severity of cirrhosis, the therapeutic effect and the prognosis.
Causes
1.Hyponatremia
(1) Insufficient intake: patients with liver cirrhosis and ascites, often adopt low-salt diet and restrict sodium intake to avoid ascites growth. (2) increased excretion: in cirrhosis, due to metabolic dysfunction, nausea, vomiting, anorexia, diarrhea and other symptoms often occur, so that a large number of sodium-containing gastrointestinal fluid is lost, thus producing electrolyte disorders such as low sodium. At the same time, repeated diuresis, release of ascites, and make a large loss of sodium.
(3) Dilutional low sodium: due to water metabolism disorder in cirrhosis, resulting in water and sodium retention, and as a result, the total body fluid volume increases. The relative decrease of sodium content in body fluids causes hyponatremia.
(4) Metabolic alkalosis: due to the patient’s vomiting and diarrhea causing low potassium and low chloride alkalosis, the blood potassium decreases, causing intracellular potassium to move to the outside of the cell and extracellular sodium to move to the inside of the cell, resulting in the decrease of extracellular sodium.
2. Hypokalemia
(1) Insufficient intake: due to lack of appetite or fasting, patients with cirrhosis have insufficient potassium intake, while the renal potassium excretion function is normal, resulting in potassium deficiency.
(2) Increased excretion: patients with cirrhosis ascites vomit, diarrhea, upper gastrointestinal bleeding, a large amount of potassium is lost from digestive fluid, while the application of large amounts of potassium-excreting diuretics, as well as the release of ascites also cause a large amount of potassium to be discharged.
(3) Abnormal distribution in the body: when alkalosis, excessive insulin application, potassium enters into the cell from the outside of the cell, resulting in lower blood potassium.
3. Hypochloremia
(1) Reduced source: In order to prevent and treat rupture bleeding of esophageal- fundic varices in patients with liver cirrhosis, proton pump inhibitors are taken to reduce gastric acid secretion, which is one of the causes of hypochloremia.
(2) Increased loss: secondary to increased aldosterone, long-term application of diuretics to increase urine output, resulting in increased urinary chlorine excretion and decreased serum chlorine concentration. Loss of gastric fluid during vomiting further reduces serum chloride concentration.
4. Hypocalcemia
(1) Vitamin D metabolism disorder: Since vitamin D3 must be hydroxylated to 25-(OH)2D3 by the liver, and then further hydroxylated to active 1,25-(OH)2D3 in the kidneys, 1,25-(OH)2D3 production decreases in hepatic disorders, which affects calcium absorption.
(2) Vitamin D malabsorption: intestinal absorption is impaired in cirrhosis, leading to vitamin D malabsorption.
(3) Magnesium ion deficiency: Cirrhosis is often accompanied by hypomagnesemia, magnesium deficiency makes calcium inappropriate for release from the bones, and can lead to decreased secretion of parathyroid hormone, which leads to low calcium.
(4) When accompanied by renal insufficiency, 1,25-(OH)2D3 synthesis is impaired and blood phosphorus is elevated.
(5) Decreased parathyroid function leads to decreased parathyroid hormone secretion.
Symptoms
1. Hyponatremia
There are clinical manifestations of increased intracranial pressure such as headache, vomiting, optic disc edema and impaired consciousness. Patients with decompensated cirrhosis may have hypotonic encephalopathy and hepatic encephalopathy at the same time. When hepatorenal syndrome occurs, it manifests as spontaneous oliguria or anuria, azotemia, dilutional hyponatremia and hyponatremia, but there is no important pathological changes in the kidney.
2. Hypokalemia
(1) Neuromuscular symptoms: muscle weakness is the earliest manifestation, usually the limbs muscle weakness first, followed by flaccid paralysis, and in severe cases, respiratory muscle paralysis may occur, and there may be dysphagia, choking on drinking water, flaccid paralysis, and tendon reflexes may be weakened or disappeared.
(2) Symptoms of cardiovascular system: palpitation, muffled heart sound, decreased blood pressure, arrhythmia. Electrocardiogram changes appear in the early stage of T-wave lowering, widening, biphasic or inverted, followed by ST-segment lowering, prolonged QT interval and u-wave.
(3) Gastrointestinal symptoms: bitter mouth, nausea, vomiting, abdominal distension, intestinal obstruction and intestinal paralysis.
(4) Abnormal renal function: polyuria and hypospecific gravity urine are sometimes seen in patients with severe hypokalemia.
(5) Neurological symptoms: lethargy, irritability, drowsiness, poor orientation, and hepatic coma may be induced.
3. Hypochloremia
It is often accompanied by hyponatremia and hypokalemia, causing hyponatremia, hypokalemia and hypochloremic alkalosis and inducing hepatic encephalopathy. Hypochloremia can also aggravate alkalosis in erythrocytes, aggravate tissue hypoxia, induce hepatic encephalopathy, and is not conducive to the recovery of liver function.
4. Hypocalcemia
Patients have generalized bone pain or lumbar and leg pain, numbness of hands and feet, slow movement, etc., which are often covered by the symptoms of liver cirrhosis. Some patients may have tachycardia.
Examination
Laboratory blood electrolyte examination.
Diagnosis
1. Hyponatremia
Serum sodium concentration below 135 mmol/L.
2. Hypokalemia
Serum potassium concentration less than 3.5 mmol/L.
3. Hypochlorhydria
Serum chloride concentration less than 100 mmol/L.
4. Hypocalcemia
When the serum protein concentration is normal, the serum calcium concentration is lower than 2.2mmol/L. The normal reference value of calcium concentration may vary slightly in different hospitals.
Treatment
1. Hyponatremia
For patients with decompensated cirrhosis, first of all, we should actively treat the primary disease and monitor the blood sodium concentration. Avoid blind or excessive salt-restricted diet, use of diuretics, and release of ascites. Sodium and diuretics should be selected according to the condition in order to maintain the blood sodium level above 130 mmol/L. If blood sodium is less than 120 mmol/L, water intake should be restricted, intravenous sodium supplementation should be considered, and diuretics should be suspended. When treating dilutional hyponatremia, conventional diuretics may exacerbate electrolyte loss from the body, which in turn may worsen hyponatremia or cause other electrolyte imbalances.
2. Hypokalemia
(1) Correct the cause of hypokalemia.
(2) Dietary potassium supplementation: give foods rich in potassium, such as fish, meat, beans.
(3) Oral potassium supplementation: 10% potassium chloride solution or tablets, 10% potassium citrate and potassium magnesium mentholatum can be given.
(4) Intravenous potassium supplementation: in principle, see urine potassium supplementation, should not be too much too fast, the amount of potassium supplementation can be initially determined with reference to the results of blood potassium measurement.
3. Hypochloremia
Possible causes of hypochloremia should be actively removed, and hypokalemia and hyponatremia should be corrected in time, and arginine hydrochloride can be given intravenously if necessary.
4. Hypocalcemia
(1) Firstly, treat the primary disease and correct alkalosis.
(2) Mild or moderate calcium deficiency can be treated with oral calcium gluconate, calcium chloride and calcium lactate.
(3) Intravenous calcium supplementation, 10% calcium gluconate or calcium chloride can be injected intravenously.
(4) Supplement 1,25-(OH)2D3.