Lactic acidosis is a pathological condition that develops with a persistent increase in the level of lactic acid in the blood to 5 mmol / l or more. It is manifested by symptoms of intoxication – nausea, vomiting, dizziness, anxiety. In the later stages, breathing disorders with pronounced hyperventilation of the lungs, confusion in the form of stupor and coma are characteristic. The main diagnostic methods are laboratory blood and urine tests. Treatment includes hemodialysis, artificial ventilation of the lungs, infusion of glucose solution, drug correction of concomitant diseases.
ICD 10
E87.2 Acidosis
Meaning
Lactic acidosis in Latin means “lactic acid”. The condition is also called lactic acidemia, lactic acid coma, hyperlactatacidemia, lactic acidosis. In ICD-10 pathology is attributed to the group of violations of water-salt and acid-base balance (class – Diseases of the Endocrine system). This is an extremely rare complication. Exact epidemiological data have not been determined, but it has been established that about half of the cases are diagnosed in patients diagnosed with diabetes mellitus. Among this group of patients, according to American studies, the frequency of lactic acidosis is 0.006-0.008%. The development of the complication does not depend on gender, it is significantly more often registered in people aged 35 to 84 years.
Causes
Lactic acidosis can be caused by increased lactate production, its insufficient excretion through the renal tubules and / or metabolic disorders in the liver, in which the processes of pyruvate breakdown, glucose formation from non-carbohydrate compounds suffer. The causes of these metabolic shifts are:
- Hereditary pathology of metabolism. There is a genetically determined form of acidosis. With it, there are violations at the level of key enzymes of carbohydrate metabolism, symptoms are observed immediately after birth.
- Diabetes mellitus. Often the accumulation of lactate is caused by the use of biguanides – hypoglycemic drugs. The risk of a violation increases with insufficient liver and kidney functions, oxygen starvation of muscle tissues after physical exertion, respiratory syndromes, vitamin deficiency, alcohol consumption, pregnancy.
- Cardiovascular diseases. Lactic acidemia is formed in heart pathologies burdened with circulatory problems, after cardiological operations using AIC, with sepsis, hypovolemic and cardiogenic shock with DIC syndrome. The symptoms of acidosis are rapidly increasing.
- Resuscitation conditions. Lactic acidosis can develop in oncological diseases (especially with pheochromocytoma), in patients in a comatose or shock state. Also, the complication is provoked by deep, extensive lesions of the kidneys and liver.
- Intoxication. The risk of lactic acidosis increases with alcoholism. Who is potentiated by the intake of carbon monoxide, ethylene glycol, methanol, salts of salicylic and prussic acid, chlorides into the body.
Pathogenesis
Lactic acidosis is characterized by a persistent increase in lactic acid indicators, acidification of arterial blood. Lactic acid is a source of energy, but, unlike glucose, its metabolism occurs anaerobically (without the inclusion of oxygen in the reaction). It is produced by erythrocytes, skeletal muscles, skin and central nervous system tissues, kidneys, gastrointestinal mucosa, retina, and tumor neoplasms. Increased lactate formation is often caused by hypoxia, against which it becomes impossible to convert glucose into adenosine triphosphate.
In addition, lactic acidosis is caused by insufficient utilization of acid by the kidneys and liver. The key pathological mechanism is a violation of gluconeogenesis, in which lactate normally turns into glucose or is completely oxidized in the chain of reactions of citric acid synthesis. An additional way of disposal – excretion through the kidneys – is activated when the threshold value of lactic acid is exceeded equal to 7 mmol / l. With hereditary lactic acidosis, there are congenital defects in the synthesis of enzymes necessary for the reactions of the breakdown of pyruvic acid or the conversion of non-carbohydrate compounds into glucose.
Classification
According to the severity of the clinical picture, the severity of the course, there are three stages of lactic acidosis: early, medium and late. Their development occurs extremely quickly, within a few hours the symptoms increase from general weakness to coma. Another classification is based on the etiopathogenetic mechanisms underlying the complication. According to it , there are two types of hyperlactatacidemia:
- Acquired (type A). Usually debuts after 35 years. It is caused by a violation of the supply of oxygen and blood to the tissues. There are clinical signs characteristic of metabolic acidosis – the functions of the central nervous system are suppressed, the respiratory rate and heart rate change. There is a direct link between the level of lactic acidemia and neurological symptoms. With diabetes, there is a high probability of shock, a sharp decrease in blood pressure.
- Congenital (type B). It manifests itself from birth, less often from early childhood, refers to hereditary forms of metabolic disorders. From the first days of life, neurological and respiratory disorders are determined: myotic hypotension, areflexia, confusion, dyspnea, polypnea, symptoms characteristic of asthma.
Symptoms
For acquired lactic acidemia, acute development is typical, the full clinical picture unfolds in 6-18 hours. Symptoms-harbingers are usually absent. At the first stage, acidosis manifests itself nonspecifically: patients note general weakness, apathy, muscle and chest pains, digestive disorders in the form of vomiting, loose stools, abdominal pain. The middle stage is accompanied by an increase in the amount of lactate, against which the phenomena of hyperventilation of the lungs occur. The gas exchange function of the lungs is disrupted, carbon dioxide accumulates in the circulatory system. Changes in respiratory function are called Kussmaul’s breathing. There is an alternation of rare rhythmic cycles with deep breaths and heavy noisy exhalations.
Signs of severe cardiac and vascular insufficiency are detected. Patients have sharply reduced blood pressure, hypotension is constantly increasing, can lead to collapse. The formation of urine slows down, oliguria develops, then anuria. Various neurological symptoms are revealed – areflexia, spastic paresis, hyperkinesis. Motor anxiety and delirium are increasing. By the end of the middle stage, the DIC syndrome unfolds. Thrombosis with hemorrhagic necrotic lesions is often diagnosed. At the last stage, psychomotor agitation is replaced by sopor and coma. The work of the nervous, cardiovascular, respiratory and urinary systems is suppressed.
With lactic acidosis type B, symptoms most often appear in the first days of a child’s life. Respiratory disorders come to the fore: dyspnea – shortness of breath, a feeling of lack of air; polypnea – rapid shallow breathing; asthma–like conditions – choking cough, whistling, difficulty inhaling and exhaling. Among the neurological symptoms, muscle hypotension, areflexia, isolated convulsions, episodes of clouded consciousness are determined. There is a refusal of breast and artificial mixture, frequent vomiting, abdominal pain, skin rash, jaundice of the integument. In the future, a delay in mental and physiological development is often revealed.
Complications
Lactic acidosis is a serious threat due to the high risk of brain edema and death. The probability of death increases in the absence of medical care in the coming hours after the onset of the first symptoms. Vascular hypotension and hypoxia of the brain lead to the development of various brain disorders, neurological deficits. After an acute period, patients complain of dizziness and chronic headache for a long time. Speech and memory disorders are possible, requiring rehabilitation measures.
Diagnostics
Examination of patients is carried out on an emergency basis. The diagnosis is handled by an endocrinologist, and a neurologist’s consultation is additionally prescribed. Lactic acidosis is very difficult to detect clinically – symptoms vary, only muscle pain is specific throughout all stages. Otherwise, the picture is similar to some types of encephalopathy, with hypoglycemia, with the development of which the amount of lactate remains normal. The diagnosis is confirmed based on the data of a comprehensive laboratory study. It includes:
- Blood test. It is carried out in order to detect metabolic changes in the concentration of lactic acid and glucose. The lactate level is more than 3 mmol/ l, an increased amount of glucose and nitrogen–containing compounds of peptide metabolism, an abnormal increase in the concentration of lipids, the ratio of lactic and pyruvic acid is 1:10.
- Urinalysis. According to the final data, the preservation of kidney function, the degree of lactate excretion is diagnosed. The results of the urine test indicate a high level of acetone, glucose.
- Assessment of blood pH. Tests can reveal the status of oxygenation and pH balance of the body. With lactatacidemia, the bicarbonate concentration level is less than 10 mmol / l, the pH value is from 7.3 to 6.5.
Treatment
Therapy of the congenital form of lactatacidemia is carried out in stages. First, acidotic shifts in the pH balance are eliminated, after that a special diet is prescribed: violations of gluconeogenesis are corrected by frequent feeding of the child with food rich in carbohydrates; failures in the pyruvate oxidation cycle require an increase in the amount of fats in the diet, their content should reach 70% of the daily caloric content. Treatment of acquired forms of lactic acidosis is aimed at restoring electrolyte balance, combating acidosis, hyperglycemia, shock and oxygen starvation. The following procedures are performed:
- Hemodialysis, infusions. Purifying the blood outside the body is the most effective way to deactivate excess lactate in the peripheral circulatory system. Glucose solution is also injected intravenously. Insulin injections are performed in parallel. Such a complex stimulates the activity of pyruvate dehydrogenase and glycogen synthetase enzymes.
- Artificial ventilation of the lungs. The removal of carbon monoxide formed as a result of a violation of the pH balance is performed by the ventilator method. The resumption of alkaline equilibrium occurs when the concentration of carbon dioxide in the plasma decreases to 25-30 mmHg. This mechanism lowers the concentration of lactate.
- Taking cardiotonic medications. Medications of this group stimulate the contractile activity of the heart muscle, restore the rhythm. Cardiac glycosides, adrenergic agents, non-glycoside cardiotonics are used.
Prognosis and prevention
The outcome of lactic acidosis is relatively favorable with successful therapy of the underlying disease, timeliness and adequacy of infusion therapy. The prognosis also depends on the form of lactic acidemia – survival is higher among people with type A pathology (acquired). Prevention is reduced to the prevention of hypoxia, intoxication, proper treatment of diabetes mellitus with strict adherence to the individual dosage of biguanides and their immediate cancellation in case of intercurrent infections (pneumonia, influenza). Patients from high–risk groups – those diagnosed with diabetes in combination with pregnancy, old age – need to carefully monitor their own condition, at the first signs of muscle pain and weakness, seek medical advice.
Literature
- Lactic acidosis in diabetes mellitus / Limanskaya G.F., Cheban A.K.// Problems of endocrinology. – Vol. 19, No. 4.
- Internal diseases. Part 2/ Harrison T.R. – 1992.
- A course of lectures on resuscitation and intensive care/ Spas V.V. – 2009.