What Are Lactic Acidosis Symptoms?

Lactic acid is reduced by pyruvate, which is a sugar intermediate metabolite. When hypoxia or pyruvate is not oxidized, it is reduced to lactic acid. Acidosis caused by elevated blood lactic acid levels for various reasons is called lactic acidosis.

Basic Information

English name

lactic acidosis

Visiting department

Endocrinology

Common causes

Hypoxia, drug use, systemic diseases, congenital metabolic abnormalities

Common symptoms

Nausea, abdominal pain, decreased appetite, dizziness, drowsiness, slightly deeper breathing, severe coma or shock in severe cases

Causes of lactic acidosis

Hypoxia

The human body can significantly increase the production of lactic acid under hypoxia. Heart and lung dysfunction or vascular obstruction can cause insufficient oxygen supply.In addition, various shocks (cardiogenic, endotoxin, hypovolemic), anemia, heart failure, asphyxia, CO poisoning, etc. also cause the body to be hypoxic. the reason.

2. Drug application

Biguanide, sorbitol, xylitol, methanol, ethanol and other alcohol drugs, paracetamol and salicylate can all cause lactic acid accumulation in the body. Among them, biguanide drugs, especially Jiangtangling, can enhance anaerobic fermentation, inhibit the liver and muscles from taking up lactic acid, and inhibit gluconeogenesis, so it has the effect of causing lactic acidosis.

3. Systemic disease

Found in diabetes, malignant tumors (leukemia, etc.), liver disease (acute viral or drug-toxic hepatitis with failure), severe infections (septicemia, etc.), uremia, convulsions, pancreatitis, and gastrointestinal diseases. Systemic diseases often cause liver and kidney dysfunction in the body, causing excess lactic acid in the body not to be metabolized and excreted, causing lactic acid accumulation.

4. Congenital metabolic abnormalities

People with congenital glucose 6-phosphatase deficiency (type 1 glycogen accumulation disease), pyruvate dehydrogenase and carboxylase deficiency, fructose 1, 6 diphosphatase deficiency, and oxidative phosphorylation deficiency can cause lactate metabolism abnormalities in the body , Leading to acidosis.

Clinical manifestations of lactic acidosis

The clinical manifestation of lactic acidosis is not very specific, and it varies depending on the cause.

It is worth noting that lactic acidosis is an acute complication of diabetic patients, which is common in diabetic patients who take large amounts of biguanide drugs. Those with mild symptoms can only have nausea, abdominal pain, decreased appetite, dizziness, drowsiness, and deeper breathing. Severe or severe patients may have nausea, vomiting, headache, dizziness, tenderness, lip cyanosis, hypotension, hypothermia, weak pulses, fast heart rate, dehydration, deep breathing, disturbance of consciousness, reduced limb reflexes, pupil dilation , Deep coma or shock.

Lactic acidosis test

Urine and blood acidity increased significantly, blood pH <7.0; CO ₂ binding power dropped below 20%; blood lactic acid> 5mmol / L, sometimes up to 35mmol / L (most of those who died> 25mmol / L were cured); pyruvate also increased High as 0.2 1.5mmol / L; Lactic acid / pyruvate 30 / 1; HCO ₃ ^- decreased; blood glucose often increased; Na ⁺ , Cl ^- changed little, Na ⁺ sometimes high; K ⁺ often increased or normal; white blood cells Most of the counts increased, sometimes up to 60,000 / mm ³ ; the anion gap [Na ⁺ + K ⁺ -(HCO ₃ ^- ten Cl-)] is often> 18mmol / L, but the ketone body is not much higher, which can be diagnosed as Lactic acidosis.

Diagnosis of lactic acidosis

The lactic acid concentration in normal fasting venous blood (at rest) is 0.4 1.4mmol / L, and the pyruvate concentration is 0.07 0.14mmol / L. The ratio of the two is 10: 1, generally L (some consider it> 5mmol / L) , HCO ₃ ^- 10mmol / L, lactic acid / pyruvate> 10 and other causes of acidosis can be ruled out.

Differential diagnosis of lactic acidosis

1. Hyperosmotic non-ketogenic diabetic coma

The elderly are multiple people, and may also have dehydration, shock, and coma, but blood glucose often exceeds 33.3mmol / L, blood sodium exceeds 155mmol / L, plasma osmotic pressure exceeds 330mmol / L, and blood ketone bodies are negative or weakly positive. However, lactic acidosis had a significant increase in blood lactic acid (over 5 mmol / L), little change in Na ⁺ and an anion gap of more than 18 mmol / L.

2. ethanolic acidosis

He has a habit of drinking alcohol, and usually develops after drinking a lot of alcohol. The patient's blood beta-hydroxybutyric acid is increased due to severe vomiting, and blood ketones can be positive.

3. Hypoglycemic coma

The patient had a history of inadequate food intake, acute onset, drowsiness, and coma, but had negative urine glucose and ketone, low blood sugar, and had a history of excessive insulin injection or excessive hypoglycemic medication.

4. Starvation ketosis

As a result of inadequate eating, the patient's fat was decomposed, blood ketones were positive, but urine glucose was negative, and blood sugar was not high.

5. Acute pancreatitis

More than half of the patients with diabetic ketoacidosis will have non-specific elevations in blood and urine amylase, and sometimes the increase is greater.

Lactic acidosis treatment

1. Actively treat primary disease

Such as heart, lung dysfunction, vascular obstruction, shock, anemia, asphyxia, CO poisoning and so on. For those with diabetic lactic acidosis, glucose and insulin can be dripped intravenously to reduce the anaerobic fermentation of sugars and help to eliminate blood lactic acid.

2. Correct acidosis and disorders of water and electrolyte metabolism

(1) Replenish alkali with 5% sodium bicarbonate. When pH> 7.25, stop alkali infusion to avoid alkali poisoning. Alkali supplementation should not be too much or too fast, otherwise CO _{2 will} not be easily eliminated and lead to aggravated hypoxia and intracranial acidosis.

(2) Rehydration quickly corrects dehydration. Rehydration and volume expansion in treatment of shock can improve tissue perfusion, correct shock, diuretic and acid discharge, and supplement with normal saline to maintain sufficient cardiac output and tissue perfusion. The amount of fluid replacement depends on the patient's dehydration and cardiopulmonary function.

3. Oxygen, potassium, hemodialysis

If necessary, make a tracheotomy or supply oxygen with a respirator. According to the situation of acidosis, blood glucose, serum potassium, supplement potassium as appropriate. If the patient cannot tolerate the retention of sodium and water, especially lactic acidosis caused by hypoglycemic, lactate-free dialysate can be used for blood or peritoneal dialysis.