Ketoacidotic coma ICD 10. Diabetic ketoacidosis and diabetic ketoacidotic coma

Diabetic ketoacidosis(DKA) is an emergency condition that develops as a result of absolute (usually) or relative (rarely) insulin deficiency, characterized by hyperglycemia, metabolic acidosis and electrolyte disturbances. The extreme manifestation of diabetic ketoacidosis is ketoacidotic coma. Statistical data. 46 cases per 10,000 patients suffering from diabetes. The predominant age is up to 30 years.

Code according to the international classification of diseases ICD-10:

Causes

Risk factors. Late diagnosis of diabetes. Inadequate insulin therapy. Associated acute diseases and injuries. Previous dehydration. Pregnancy complicated by early toxicosis.

Etiopathogenesis

Hyperglycemia. Lack of insulin reduces glucose utilization in the periphery and, along with excess glucagon, causes increased glucose formation in the liver due to stimulation of gluconeogenesis, glycogenolysis and inhibition of glycolysis. Protein breakdown in peripheral tissues provides a supply of amino acids to the liver (the substrate for gluconeogenesis).

As a result, osmotic diuresis, hypovolemia, dehydration and excessive excretion of sodium, potassium, phosphate and other substances in the urine develop. A decrease in blood volume leads to the release of catecholamines, which interfere with the action of insulin and stimulate lipolysis.

Ketogenesis. Lipolysis, resulting from a lack of insulin and an excess of catecholamines, mobilizes free fatty acids from storage in adipose tissue. Instead of re-esterifying incoming free fatty acids into triglycerides, the liver switches their metabolism to the formation of ketone bodies. Glucagon increases the level of carnitine in the liver, which ensures that fatty acids enter the mitochondria, where they undergo b - oxidation to form ketone bodies. Glucagon reduces the content of malonyl in the liver - CoA, fatty acid oxidation inhibitor.

Acidosis. Increased production of ketone bodies (acetoacetate and b-hydroxybutyrate) in the liver exceeds the body's ability to metabolize or excrete them. The hydrogen ions of the ketone bodies combine with bicarbonate (buffer), which leads to a drop in serum bicarbonate and a decrease in pH. Compensatory hyperventilation leads to a decrease in p a CO 2 .. Due to increased levels of plasma acetoacetate and b - hydroxybutyrate, the anion gap increases.. The result is metabolic acidosis with an increased anion gap.

Symptoms (signs)

Clinical picture ketoacidotic coma is determined by its stage.

Stage I (ketoacidotic precoma).. Consciousness is not impaired.. Polydipsia and polyuria.. Moderate dehydration (dry skin and mucous membranes) without hemodynamic disturbances.. General weakness and weight loss.. Deterioration of appetite, drowsiness.

Stage II (beginning ketoacidotic coma).. Stupor.. Kussmaul-type breathing with the smell of acetone in the exhaled air.. Severe dehydration with hemodynamic disturbances (arterial hypotension and tachycardia).. Abdominal syndrome (pseudoperitonitis)... Tension of the muscles of the anterior abdominal wall. .. Symptoms of peritoneal irritation... Repeated vomiting in the form of “coffee grounds” is caused by diapedetic hemorrhages and the paretic state of the vessels of the gastric mucosa.

Stage III (complete ketoacidotic coma).. No consciousness.. Hypo- or areflexia.. Severe dehydration with collapse.

Diagnostics

Laboratory research. Increasing the concentration of glucose in the blood to 17-40 mmol/l. An increase in the content of ketone bodies in the blood and urine (nitroprusside, which reacts with acetoacetate, is usually used to determine the content of ketone bodies). Glucosuria. Hyponatremia. Hyperamylasemia. Hypercholesterolemia. Increased urea content in the blood. Serum bicarbonate<10 мЭкв/л, рH крови снижен. Гипокалиемия (на начальном этапе возможна гиперкалиемия) . Уменьшение р a СО 2 . Повышение осмолярности плазмы (>300 mOsm/kg) . Increase in anion gap.

Diseases affecting results. With concomitant lactic acidosis, a lot of b-hydroxybutyrate is formed, so the acetoacetate content is not so high. In this case, the reaction with nitroprusside, which determines only the concentration of acetoacetate, may be weakly positive even with severe acidosis.

Special studies. ECG (especially if MI is suspected). As a rule, sinus tachycardia is detected. Chest X-ray to rule out respiratory tract infection.

Differential diagnosis. Hyperosmolar non-ketoacidotic coma. Lactic acid diabetic coma. Hypoglycemic coma. Uremia.

Treatment

TREATMENT

Mode. Admission to the intensive care unit. Bed rest. The goals of intensive therapy are to accelerate the utilization of glucose by insulin-dependent tissues, relieve ketonemia and acidosis, and correct water and electrolyte imbalances.

Diet. Parenteral nutrition.

Drug therapy. Soluble insulin (human genetically engineered) intravenously at an initial dose of 0.1 U/kg, followed by infusion of 0.1 U/kg/h (approximately 5-10 U/h). Correction of dehydration.. 1000 ml of 0.9% sodium chloride solution for 30 minutes IV, then.. 1000 ml of 0.9% sodium chloride solution for 1 hour, then.. 0.9% solution. - sodium chloride at a rate of 500 ml/h (approximately 7 ml/kg/h) for 4 hours (or until dehydration stops), then continue infusion at a rate of 250 ml/h (3.5 ml/kg/h) , controlling the glucose level in the blood.. When the glucose concentration decreases to 14.65 mmol/l - 400-800 ml of 5% glucose solution with 0.45% sodium chloride solution during the day. Reimbursement of losses of minerals and electrolytes.. With the concentration of potassium in the blood serum<5,5 ммоль/л — препараты калия (например, калия хлорид со скоростью 20 ммоль/ч) .. При рН артериальной крови ниже 7,1 — натрия гидрокарбонат 3-4 мл/кг массы тела.. Фосфаты — 40-60 ммоль со скоростью 10-20 ммоль/ч.

Observation. Monitoring the mental state, vital functions, diuresis every 30-60 minutes until the condition improves, then every 2-4 hours during the day. The blood glucose level is determined every hour until the concentration reaches 14.65 mmol/l, then every 2-6 hours. K+ level, HCO 3 -, Na+, base deficiency - every 2 hours. Phosphate content, Ca 2 +, Mg 2 + - every 4-6 hours.

Complications. Brain swelling. Pulmonary edema. Venous thrombosis. Hypokalemia. THEM. Late hypoglycemia. Erosive gastritis. Infections. Respiratory distress syndrome. Hypophosphatemia.

Course and prognosis. Ketoacidotic coma is the cause of 14% of hospitalizations in patients with diabetes and 16% of deaths in diabetes. Mortality is 5-15%.

Age characteristics. Children. Serious mental disorders often occur. Treatment is intravenous bolus administration of mannitol 1 g/kg in the form of 20% solution. If there is no effect, hyperventilation to p a CO 2 2-28 mm Hg. Elderly. Particular attention should be paid to the condition of the kidneys; chronic heart failure is possible.

Pregnancy. The risk of fetal death in ketoacidotic coma during pregnancy is about 50%.

Prevention. Determination of blood glucose concentration under any stress. Regular administration of insulin.
Abbreviations. DKA - diabetic ketoacidosis.

ICD-10. E10.1 Insulin-dependent diabetes mellitus with ketoacidosis. E11.1 Non-insulin-dependent diabetes mellitus with ketoacidosis. E12.1 Diabetes mellitus associated with malnutrition with ketoacidosis. E13.1 Other specified forms of diabetes mellitus with ketoacidosis. E14.1 Diabetes mellitus, unspecified, with ketoacidosis.

Note. The difference is anionic- the difference between the sum of measured cations and anions in plasma or serum, calculated by the formula: (Na+ + K+) - (Cl- + HCO 3 -) = 20 mmol/l. May be increased in diabetic acidosis or lactic acidosis; not changed or reduced in metabolic acidosis with loss of bicarbonate “cation-anion difference.

Pediatric ketoacidosis- a heterogeneous group of conditions accompanied by the appearance of ketone bodies in the blood and urine. Ketone bodies are the main carriers of energy from the liver to other tissues and the main source of energy obtained from lipids by brain tissue. Main reasons ketoacidosis in newborns - diabetes, glycogenosis type I (232200), glycinemia (232000, 232050), methylmalonic aciduria (251000), lactic acidosis, succinyl-CoA-acetoacetate transferase deficiency.

Code according to the international classification of diseases ICD-10:

• E88. 8 - Other specified metabolic disorders

Insufficiency of succinyl-CoA-acetoacetate transferase (#245050, EC 2. 8. 3. 5, 5p13, defect of the SCOT, r gene) - an enzyme of the mitochondrial matrix that catalyzes the first step of the breakdown of ketone bodies.

Clinically

severe recurrent ketoacidosis, vomiting, shortness of breath.

Laboratory

deficiency of succinyl-CoA-3-acetoacetate transferase, ketonuria.

Richards-Randle syndrome (*245100, r) is ketoaciduria with mental impairment and other symptoms.

Clinically

mental retardation, ataxia, poor development of secondary sexual characteristics, deafness, peripheral muscle atrophy.

Laboratory

ketoaciduria. Synonym: syndrome of ataxia - deafness - developmental delay with ketoaciduria.

Lactic acidosis - several types caused by mutations in various enzymes of lactic acid metabolism: . deficiency of lipoyl transacetylase E2 (245348, r, À); . deficiency of the component of the pyruvate dehydrogenase complex containing X - lipoyl (*245349, 11p13, PDX1, r gene); . congenital infantile form of lactic acidosis (*245400, r); . lactic acidosis with the release of D - lactic acid (245450, r). General symptoms are lactic acidosis, delayed psychomotor development, muscle hypotonia. Some forms have specific manifestations, such as microcephaly, muscle twitching, baldness, necrotizing encephalopathy, etc.

Ketoadipic aciduria (245130, r).

Clinically

congenital skin pathology (collodion skin), swelling of the back of the hands and feet, developmental delay, muscle hypotonia.

Laboratory

hyperexcretion of a-ketoadipic acid in urine.

ICD-10. E88. 8 Other specified metabolic disorders.

Tags:

Did this article help you? Yes - 0 No - 0 If the article contains an error Click here 310 Rating:

Click here to add a comment to: Ketoacidosis in children(Diseases, description, symptoms, traditional recipes and treatment)

E10.1 Insulin-dependent diabetes mellitus with ketoacidosis

E11.1 Non-insulin-dependent diabetes mellitus with ketoacidosis

E13.1 Other specified forms of diabetes mellitus with ketoacidosis

E12.1 Diabetes mellitus associated with malnutrition, with ketoacidosis

E14.1 Diabetes mellitus, unspecified with ketoacidosis

R40.2 Coma, unspecified

Causes of diabetic ketoacidosis and diabetic ketoacidotic coma

The development of diabetic ketoacidosis is based on a severe insulin deficiency.

Causes of insulin deficiency

• late diagnosis of diabetes mellitus;
• withdrawal or insufficient dose of insulin;
• gross violation of diet;
• intercurrent diseases and interventions (infections, injuries, operations, myocardial infarction);
• pregnancy;
• the use of medications that have insulin antagonist properties (glucocorticosteroids, oral contraceptives, saluretics, etc.);
• pancreatectomy in persons who have not previously suffered from diabetes.

Pathogenesis

Insulin deficiency leads to a decrease in glucose utilization by peripheral tissues, liver, muscles and adipose tissue. The glucose content in cells decreases, resulting in activation of the processes of glycogenolysis, gluconeogenesis and lipolysis. Their consequence is uncontrolled hyperglycaemia. Amino acids formed as a result of protein catabolism are also included in gluconeogenesis in the liver and aggravate hyperglycemia.

Along with insulin deficiency, excessive secretion of contrainsular hormones, primarily glucagon (stimulates glycogenolysis and gluconeogenesis), as well as cortisol, adrenaline and growth hormone, which have a fat-mobilizing effect, i.e. stimulating lipolysis and increasing the concentration of free fatty acids, is of great importance in the pathogenesis of diabetic ketoacidosis. acids in the blood. An increase in the formation and accumulation of FFA breakdown products - ketone bodies (acetone, acetoacetic acid, b-hydroxybutyric acid) leads to ketonemia, the accumulation of free hydrogen ions. The concentration of bicarbonate in the plasma decreases, which is used to compensate for the acid reaction. After the buffer reserve is depleted, the acid-base balance is disturbed, and metabolic acidosis develops. The accumulation of excess CO2 in the blood leads to irritation of the respiratory center and hyperventilation.

Hyperventilation causes glucosuria, osmotic diuresis with the development of dehydration. In diabetic ketoacidosis, body losses can be up to 12 liters, i.e. 10-12% of body weight. Hyperventilation increases dehydration due to water loss through the lungs (up to 3 liters per day).

Diabetic ketoacidosis is characterized by hypokalemia due to osmotic diuresis, protein catabolism, as well as a decrease in the activity of K + -Na + -dependent ATPase, which leads to a change in membrane potential and the release of K + ions from the cell according to a concentration gradient. In persons with renal failure, in whom the excretion of K + ions in the urine is impaired, normo- or hyperkalemia is possible.

The pathogenesis of the disorder of consciousness is not completely clear. Impaired consciousness is associated with:

• hypoxic effect on the head of ketone bodies;
• cerebrospinal fluid acidosis;
• dehydration of brain cells; due to hyperosmolarity;
• hypoxia of the central nervous system due to an increase in the level of HbA1c in the blood, a decrease in the content of 2,3-diphosphoglycerate in erythrocytes.

Brain cells have no energy reserves. The cells of the cerebral cortex and cerebellum are most sensitive to the lack of oxygen and glucose; their survival time in the absence of O2 and glucose is 3-5 minutes. Cerebral blood flow decreases compensatoryly and the level of metabolic processes decreases. Compensatory mechanisms also include the buffering properties of cerebrospinal fluid.

Symptoms of diabetic ketoacidosis and diabetic ketoacidotic coma

Diabetic ketoacidosis usually develops gradually over several days. Frequent symptoms of diabetic ketoacidosis are symptoms of decompensated diabetes mellitus, including:

• thirst;
• dry skin and mucous membranes;
• polyuria;
• weight loss;
• weakness, adynamia.

Then they are joined by symptoms of ketoacidosis and dehydration. Symptoms of ketoacidosis include:

• smell of acetone from the mouth;
• Kussmaul breathing;
• nausea, vomiting.

Symptoms of dehydration include:

• decreased skin turgor,
• decreased tone of the eyeballs,
• decrease in blood pressure and body temperature.

In addition, signs of an acute abdomen are often observed due to the irritating effect of ketone bodies on the gastrointestinal mucosa, pinpoint hemorrhages in the peritoneum, peritoneal dehydration and electrolyte disturbances.

In severe, uncorrected diabetic ketoacidosis, disturbances of consciousness develop, including stupor and coma.

The most common complications of diabetic ketoacidosis include:

• cerebral edema (rarely develops, more often in children, usually leads to the death of patients);
• pulmonary edema (most often caused by improper infusion therapy, i.e. administration of excess fluid);
• arterial thrombosis (usually caused by an increase in blood viscosity due to dehydration, decreased cardiac output; myocardial infarction or stroke may develop in the first hours or days after the start of treatment);
• shock (it is based on a decrease in circulating blood volume and acidosis, possible causes are myocardial infarction or infection with gram-negative microorganisms);
• addition of a secondary infection.

Diagnosis of diabetic ketoacidosis and diabetic ketoacidotic coma

The diagnosis of diabetic ketoacidosis is made on the basis of a history of diabetes mellitus, usually type 1 (however, it should be remembered that diabetic ketoacidosis can also develop in people with previously undiagnosed diabetes mellitus; in 25% of cases, ketoacidotic coma is the first manifestation of diabetes mellitus with which the patient goes to the doctor), characteristic clinical manifestations and laboratory diagnostic data (primarily an increase in the level of sugar and beta-hydroxybutyrate in the blood; if it is impossible to test for ketone bodies in the blood, ketone bodies in the urine are determined).

Laboratory manifestations of diabetic ketoacidosis include:

• hyperglycemia and glycosuria (in persons with diabetic ketoacidosis, glycemia is usually > 16.7 mmol/l);
• the presence of ketone bodies in the blood (the total concentration of acetone, beta-hydroxybutyric and acetoacetic acids in the blood serum during diabetic ketoacidosis usually exceeds 3 mmol/l, but can reach 30 mmol/l with a norm of up to 0.15 mmol/l. The beta- hydroxybutyric and acetoacetic acids in mild diabetic ketoacidosis is 3:1, and in severe diabetic ketoacidosis - 15:1);
• metabolic acidosis (diabetic ketoacidosis is characterized by the concentration of bicarbonate and serum
• electrolyte imbalance (often moderate hyponatremia due to the transition of intracellular fluid into the extracellular space and hypokalemia due to osmotic diuresis. The level of potassium in the blood may be normal or elevated as a result of the release of potassium from the cells during acidosis);
• other changes (possible leukocytosis up to 15,000-20,000/μl, not necessarily associated with infection, increased hemoglobin and hematocrit levels).

Also of great importance for assessing the severity of the condition and determining treatment tactics is the study of the acid-base state and electrolytes in the blood. An ECG can reveal signs of hypokalemia and heart rhythm disturbances.

Differential diagnosis

In diabetic ketoacidosis and especially in diabetic ketoacidotic coma, it is necessary to exclude other causes of impaired consciousness, including:

• exogenous intoxications (alcohol, heroin, sedatives and psychotropic drugs);
• endogenous intoxication (uremic and hepatic coma);
• cardiovascular:
  • collapse;
  • Adams-Stokes attacks;
• other endocrine disorders:
  • hyperosmolar coma;
  • hypoglycemic coma;
  • lactic acid coma
  • severe hypokalemia;
  • adrenal insufficiency;
  • thyrotoxic crisis or hypothyroid coma;
  • diabetes insipidus;
  • hypercalcemic crisis;
• cerebral pathology (reactive hyperglycemia is often possible) and mental disorders:
  • hemorrhagic or ischemic stroke;
  • subarachnoid hemorrhage;
  • episyndrome;
  • meningitis,
  • traumatic brain injury;
  • encephalitis;
  • cerebral sinus thrombosis;
• hysteria;
• cerebral hypoxia (due to carbon monoxide poisoning or hypercapnia in patients with severe respiratory failure).

Most often it is necessary to differentiate between diabetic ketoacidotic and hyperosmolar precoma and coma with hypoglycemic precoma and coma.

The most important task is to distinguish these conditions from severe hypoglycemia, especially in the prehospital stage, when blood sugar levels cannot be determined. If there is the slightest doubt about the cause of the coma, trial insulin therapy is strictly contraindicated, since in case of hypoglycemia, the administration of insulin can lead to the death of the patient.

Treatment of diabetic ketoacidosis and diabetic ketoacidotic coma

Patients with diabetic ketoacidosis and diabetic ketoacidotic coma must be urgently hospitalized in the intensive care unit.

After diagnosis and initiation of therapy, patients need constant monitoring of their condition, including monitoring of basic hemodynamic parameters, body temperature and laboratory parameters.

If necessary, patients undergo artificial ventilation (ALV), catheterization of the bladder, installation of a central venous catheter, nasogastric tube, and parenteral nutrition.

Carry out in the intensive care unit.

• express blood glucose analysis once an hour with intravenous glucose administration or once every 3 hours when switching to subcutaneous administration;
• determination of ketone bodies in blood serum 2 times a day (if impossible, determination of ketone bodies in urine 2 times a day);
• determination of K and Na levels in the blood 3-4 times/day;
• study of the acid-base state 2-3 times a day until stable normalization of pH;
• hourly monitoring of diuresis until dehydration is eliminated;
• ECG monitoring;
• monitoring blood pressure, heart rate (HR), body temperature every 2 hours;
• chest x-ray;
• general blood and urine analysis once every 2-3 days.

The main directions of treatment for patients are: insulin therapy (to suppress lipolysis and ketogenesis, inhibit liver glucose production, stimulate glycogen synthesis), rehydration, correction of electrolyte disturbances and acid-base disorders, eliminating the cause of diabetic ketoacidosis.

Pre-hospital rehydration

To eliminate dehydration, administer:

Sodium chloride, 0.9% solution, intravenous drip at a rate of 1-2 l/h in the 1st hour, then 1 l/h (in the presence of heart or renal failure, the infusion rate is reduced). The duration and volume of the injected solution are determined individually.

Further measures are carried out in intensive care units.

Insulin therapy

An ICD is inserted in the NICU.

• Soluble insulin (human genetically engineered or semi-synthetic) IV slowly 10-14 units, then IV drip (in 09% sodium chloride solution) at a rate of 4-8 units/hour (to prevent insulin adsorption on plastic for every 50 units of insulin add 2 ml of 20% albumin and bring the total volume to 50 ml with 0.9% sodium chloride solution.When glycemia decreases to 13-14 mmol/l, the insulin infusion rate is reduced by 2 times.
• Insulin (human genetically engineered or semi-synthetic) IV drip at a rate of 0.1 U/kg/hour until diabetic ketoacidosis is eliminated (125 U diluted in 250 ml of sodium chloride 0.9%, i.e. 2 ml of solution contains 1 unit of insulin), when glycemia decreases to 13-14 mmol/l, the rate of insulin infusion is reduced by 2 times.
• Insulin (human genetically engineered or semi-synthetic) IM 10-20 units, zitem 5-10 units every hour (only if it is impossible to quickly install an infusion system). Since comatose and precomatous states are accompanied by impaired microcirculation, the absorption of insulin administered intramuscularly is also impaired. This method should only be considered as a temporary alternative to IV administration.

When glycemia decreases to 11-12 mmol/l and pH > 7.3, they switch to subcutaneous insulin administration.

• Insulin (human genetically engineered or semi-synthetic) - subcutaneously 4-6 units every 2-4 hours; The first subcutaneous injection of insulin is made 30-40 minutes before stopping the IV infusion of drugs.

Rehydration

For rehydration use:

• Sodium chloride, 0.9% solution, intravenous drip at a rate of 1 liter during the 1st hour, 500 ml during the 2nd and 3rd hours of infusion, 250-500 ml in the following hours.

When blood glucose levels

• Dextrose, 5% solution, intravenous drip at a rate of 0.5-1 l/h (depending on the volume of circulating blood, blood pressure and diuresis)
• Insulin (human genetically engineered or semi-synthetic) intravenously 3-4 units for every 20 g of dextrose.

Correction of electrolyte disturbances

Patients with hypokalemia are administered a solution of potassium chloride. Its rate of administration in diabetic ketoacidosis depends on the concentration of potassium in the blood:

Potassium chloride IV drip 1-3 g/hour, the duration of therapy is determined individually.

For hypomagnesemia, administer:

• Magnesium sulfate - 50% p-p, IM 2 times a day, until hypomagnesemia is corrected.

Only in individuals with hypophosphatemia (blood phosphate levels

• Potassium phosphate monobasic IV drip 50 mmol phosphorus/day (for children 1 mmol/kg/day) until correction of hypophosphatemia or
• Potassium phosphate dibasic IV drip of 50 mmol phosphorus/day (for children 1 mmol/kg/day) until hypophosphatemia is corrected.

In this case, it is necessary to take into account the amount of potassium introduced into the phosphate

Errors and unreasonable assignments

The introduction of a hypotonic solution at the initial stages of treatment for diabetic ketoacidosis can lead to a rapid decrease in plasma osmolarity and the development of cerebral edema (especially in children).

The use of potassium even during moderate hypokalemia in individuals with oligo- or anuria can lead to life-threatening hyperkalemia.

The administration of phosphate in renal failure is contraindicated.

Unjustified administration of bicarbonates (in the absence of life-threatening hyperkalemia, severe lactic acidosis, or at a pH > 6.9) can lead to side effects (alkalosis, hypokalemia, neurological disorders, tissue hypoxia, including the brain).

14.1