Hypochlorite alkalosis

Introduction Low-chlorine alkalosis is a type of metabolic alkalosis, which is more common in the pediatric intensive care unit. Metabolic alkalosis is harmful to the body. In addition to causing acid-base balance and electrolyte imbalance, severe cases can be life-threatening. Because it occurs in critically ill children and is based on other diseases (such as respiratory system, digestive system, nervous system, etc.), it is often covered by the primary disease, and the clinical manifestations are diversified and lack specificity. It is easily overlooked, and often the condition is delayed or aggravated by the inability to diagnose and treat it in time.

Cause

Chloride deficiency: Since Cl- is the only anion in the renal tubule that is easily reabsorbed with Na+, when the [Cl-] in the original urine is reduced, the renal tubules strengthen the discharge of H+ and K+ in exchange for the weight of Na+, HCO3- The absorption increases to produce NaHCO3. Therefore, due to the loss of H+, K+ and the increase in NaHCO3 reabsorption due to loss of hypochloremia, it can lead to metabolic alkalosis. At this time, the patient's urine Cl- is reduced. In addition, the aforementioned furosemide and diuretic acid can inhibit the active reabsorption of Cl- in the thick segment of the medullary ascending branch, thereby causing the lack of Cl-.

At this time, the distal curved tube strengthens the rows H+ and K+ to exchange for too much Na+ reaching the distal curved tube. Therefore, it can also cause metabolic alkalosis. At this time, the patient's urine Cl- is elevated. Loss of HCl by vomiting means loss of Cl-, decrease of Cl- in plasma and urine, and metabolic alkalosis occurs through the above-mentioned Cl-reduction mechanism in the original urine. In the case of alkalosis, the body will be compensated by 1. extracellular fluid buffer 2. ion exchange 3. respiratory compensation 4. kidney compensation, etc. By compensating regulation, the ratio of HCO3-/H2CO3 can be kept within the normal range. Within, it is a compensatory metabolic alkalosis; otherwise, it is called a decompensated metabolic alkalosis Breakline.

an examination

Clinical manifestations include dehydration, thirst and oliguria (following the diuretic period), numbness of the hands and feet during alkalosis, and sometimes quadriplegia with hypokalemia. Lighter patients have no obvious symptoms, and severe ones have shallow and slow breathing, or mental and neurological abnormalities such as lethargy, confusion or paralysis. May be associated with clinical manifestations of hypokalemia and water shortage. In severe cases, there may also be low blood medicine teaching | Yu network to collect and organize calcium performance. A preliminary diagnosis can be made based on the medical history. Blood gas analysis can confirm the diagnosis and understand its severity. Decompensation. Blood pH and HC03- were significantly increased, and PaC02 was normal. The blood pH of the compensated period can be basically normal, but HC03- and BE (base residual) have a certain degree of increase.

Differential diagnosis

1. Too much hydrogen ion loss

(1) Loss of gastric juice: Frequent vomiting in pyloric obstruction or high intestinal obstruction, direct loss of gastric acid (HCl). Gastric gland wall cells produce HCl, H+ is the reaction of gastric gland wall cells from CO2+H2OH2CO3H++HCO3-, and Cl- is derived from plasma. The presence of carbonic anhydrase in the parietal cells facilitates the rapid progress of this reaction. H+ and Cl- form HCl secreted into the stomach in the gastric gland lumen. After entering the small intestine, HCl is neutralized with NaHCO3 in an alkaline digestive juice such as intestinal juice, pancreatic juice, and bile. The secretion of alkaline fluid is caused by the stimulation of H+ into the intestine. Therefore, if HCl is lost due to vomiting, NaHCO3 secretion in intestinal fluid is reduced, and there will be retention in the body; in addition, NaHCO3 which has been secreted into the intestine is not neutralized by HCl, which is bound to cause an increase in [HCO3-] in the intestinal fluid. Increased absorption. This causes the blood [HCO3-] to rise and cause metabolic alkalosis.

The loss of gastric juice can be accompanied by the loss of Cl+, K+ and the decrease of extracellular fluid volume. These factors are also related to the occurrence of hypokaline alkalosis at this time. In the case of low blood Cl-, the same symbol negative ion HCO3- is increased to compensate, H+ is transferred into the cell due to ion transfer when K+ is low, and Na+ reabsorption is promoted due to increased aldosterone secretion when the extracellular fluid volume is decreased, and H+ and K+ are discharged. These can cause metabolic alkalosis.

(2) Excessive H+ in the kidney: Excessive H+ excretion in the kidney is mainly caused by increased aldosterone secretion. Aldosterone promotes the release of H+ and K+ from the distal convoluted tubules and collecting ducts, while enhancing the reabsorption of Na+. The increase in H+ emission is due to the reaction of H2COH3H++HCO3-, and the formation of HCO3- is increased, and the reabsorption is accompanied by Na+, which causes metabolic alkalosis and hypokalemia.

Increased aldosterone secretion is seen in the following cases:

1 primary aldosteronism.

2 Cushint's Syndrome - often caused by pituitary secretion of ACTH tumors, primary adrenal hyperplasia or tumors. The production and release of cortisol and other hormones increase, and cortisol also has mineralocorticoid activity, which can also lead to metabolic alkalosis.

3 congenital adrenal hyperplasia - can be divided into two types, 17-hydroxylase-deficient (non-masculine) and 11-hydroxylase-deficient (masculine). Because of the lack of these enzymes, cortisol synthesis is reduced, and the decrease in blood cortisol levels feedbackly causes the pituitary to secrete excess ACTH, promote adrenal synthesis and secrete more deoxycorticorticosterone (DOC) and corticosterone. DOC has significant mineralocorticoid activity.

4Bartter Syndrome - This is a syndrome characterized by hyperplasia of the near ball device and increased renin secretion. Alginosterone secretion is increased by the reninangiotensinaldosterone system, and the patient has no hypertension because of the reduced reactivity of his blood vessels to angiotensin II. Due to the increased secretion of prostaglandins in patients, it has been proposed in recent years that sympathetic nerves are excited and the prostaglandins are increased to cause an increase in renin secretion. For example, the use of indomethacin to inhibit prostaglandin synthesis can reduce the levels of renin and aldosterone in patients, and restore metabolic alkalosis and Na+ and K+ to normal.

5 near ball device tumor, its cells can secrete a large amount of renin, causing hypertension and metabolic alkalosis.

6 When licorice and its preparations are used in a large amount for a long time, since glycyrrhizic acid has mineralocorticoid activity, it can cause metabolic alkalosis similar to aldosteronism.

7 When the extracellular fluid volume is reduced, it causes an increase in aldosterone secretion to enhance Na+ reabsorption and maintain capacity, which can cause metabolic alkalosis. Common in urine, diuretic and other medullary diuretic urine or when a large amount of gastric juice is lost. In this case, for every 1 liter of extracellular fluid, plasma [HCO3-] increased by about 1.4 mmol/L. In addition to the reduction of extracellular fluid, furosemide and uric acid can inhibit the reabsorption of Cl- and Na+ by the ascending branch of the renal tubules, which leads to the increase of Na+ reaching the distal curved tube and the replacement of the distal curved tube H+ for Na+. The process is strengthened, which is also related to the occurrence of metabolic alkalosis.

8 In the stress response during trauma and surgery, there is an increase in the secretion of adrenocortical hormone, often accompanied by metabolic alkalosis.

2. Excessive intake of alkaline substances

(1) Excessive intake of bicarbonate: for example, patients with ulcers take excessive amounts of sodium bicarbonate, and when neutralizing gastric acid leads to a significant increase in NaHCO3 in the intestine, especially in patients with impaired renal function, the ability of the kidney to regulate HCO3- decreases. Can cause alkalosis. In addition, when correcting acidosis, an excessive amount of sodium bicarbonate is also added to cause alkalosis.

(2) Excessive intake of sodium lactate: HCO3- is produced by metabolism in the liver. Seen in the excessive correction of sodium lactate solution when correcting acidosis.

(3) excessive intake of sodium citrate: the fluid used in blood transfusion is anticoagulated with sodium citrate. There is 16.8mEq of sodium citrate per 500 ml of blood, and HCO3- can be produced by liver metabolism. Therefore, metabolic alkalosis can occur when a large number of blood transfusions (for example, rapid input of 3000 to 4000 ml).

3. Potassium deficiency

A decrease in serum potassium caused by various causes can cause an increase in plasma NaHCO3 and metabolic alkalosis. The mechanism is that when the serum K+ decreases, the K+ of the renal tubular epithelial cells decreases correspondingly, and the H+ increases, and the Na+ and HCO3- increase. Metabolic alkalosis at this time, unlike alkaline alkalosis when it is alkaline, it is acidic, called abnormal aciduria. 2 When serum potassium is lowered, K+ is moved outside the cell to supplement K+ of the extracellular fluid due to ion exchange, and H+ enters the cell to maintain electrical neutrality, resulting in metabolic alkalosis (in this case, intracellular acidosis) Of course, the intracellular substance can buffer H+ into the cell.

Clinical manifestations include dehydration, thirst and oliguria (following the diuretic period), numbness of the hands and feet during alkalosis, and sometimes quadriplegia with hypokalemia. Lighter patients have no obvious symptoms, and severe ones have shallow and slow breathing, or mental and neurological abnormalities such as lethargy, confusion or paralysis. May be associated with clinical manifestations of hypokalemia and water shortage. In severe cases, there may also be low blood medicine teaching | Yu network to collect and organize calcium performance. A preliminary diagnosis can be made based on the medical history. Blood gas analysis can confirm the diagnosis and understand its severity. Decompensation. Blood pH and HC03- were significantly increased, and PaC02 was normal. The blood pH of the compensated period can be basically normal, but HC03- and BE (base residual) have a certain degree of increase.

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