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Metabolism decompensation (ketoacidosis, diabetic coma hyperosmolar acidotic or non-acidotic, lactic acidosis)

Correction of acidosis compared with treatment with high doses of insulin is somewhat later (Soler et al.). Depending on the amount and method of administration of insulin, the speed of correction of hyperglycemia and acidosis, according to Soler et al., Is different:
Insulin
Dose
Introduction
Small
intramuscularly
Mostly intravenous under pressure Large
(intravenously
(injection)
Blood sugar ↓ (9.0 ± 4,5) ↓↓ (5.9 ± 2.5) ↓↓ (5.7 ± 2.3)
Acidosis ↓ (12.8 ± 7.0) ↓ (13.6 ± 7.6) ↓↓ (10.7 ± 7.4)
The time interval between the correction of hyperglycemia and acidosis About 5 h About 9 h About 6 h
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With the introduction of large doses of insulin, there is a tendency to hypoglycemia and hypokalemia, a greater increase in growth hormone and more. slowing down lactate levels (Alberti et al.). Artificial B cells are only available for a small number of institutions, so their use has no practical significance.
Preference is given to small doses of insulin. The question of whether to inject them intramuscularly or intravenously is still under discussion (Alberti et al., Hayton et al., Soler et al.).
Depending on the technical equipment, the following method is practically recommended:
- without the introduction of infusion solutions: first 12–16–20 U of simple insulin intravenously and / or intramuscularly, then 8 IU of simple insulin every 30 minutes or hourly intramuscularly, or especially with resistant at the beginning or increasing hyperglycemia, as well as poor blood circulation intravenously (Clumeck et al.). If the level of sugar reaches 300 mg / dl, then an infusion solution of glucose 50 and a small amount of insulin are administered [4–8–12 IU with 2–4-hour intervals subcutaneously depending on the level of sugar in the blood (Alberti ,. Menzel, Bigergeil, Mohnike et al.)].
It is necessary to remember about the half-cycle of the assimilation of simple insulin: when administered intravenously, about 4-5 minutes (Turner et al.), And the duration of action is about 60 minutes (Clumeck et al.); with intramuscular injection - about 2 hours (Winder), with subcutaneous administration - about 4 hours (Binder). It is more correct to inject insulin at first intramuscularly, but not subcutaneously!
- when administered with infusion solutions: 6–8–12 U of simple insulin per hour in an electrolyte infusion solution 153 with human albumin 0.1–0.2 g added to prevent insulin from adsorbing on the infusion system, see 3.10.2.2) as long infu-sia (Genuth, Page et al., Kidson et al., Sempe et al.). If blood sugar drops to 300 ml / dl, then infusion of glucose 50 and insulin are administered, as mentioned above.
To use fructose, sorbitol, xylitol as carriers of calories is not necessary, since there is a sufficient amount of glucose.
A decrease in blood sugar does not depend on the severity of ketosis or the treatment of insulin that has already been administered, but on concomitant infectious processes (Alberti).
Fluid injection
In order to replace water and electrolytes, it is necessary to begin the introduction of fluid before obtaining data on the sugar content in the blood!
Hyperosmolar acidotic coma: only with extremely pronounced hyperosmolarity (plasma sodium level above 150 meq / l) can hypotonic solutions be used (electrolyte infusion solution 70, electrolyte infusion solution 105) .105 meq Na +, 51 meq C1 - and 54 meq HCO 3 - on 1 d
Introduction of potassium
Potassium loss reaches 200-700 mEq (Alberti). With the beginning of the introduction of fluid and insulin, the flow of fluid into the intracellular space begins, with the flow of potassium into the cells ahead of the flow of glucose. Even in the early stage of coma treatment, more than 50% of the injected potassium is excreted through the kidneys. Despite the fact that with the increase in the oxidation of ketonic acids, potassium can again enter into exchange, simultaneously with the reverse development of acidosis, hypokalemia increases.
The introduction of potassium, if there are no contraindications for this - hyperkalemia (ECG, potassium content in plasma), anuria or oliguria, should be started under the control of the monitor. The dosage is adjusted individually (20–40 mEq / h, sometimes up to 80–100 mEq / h - Alberti, Ritz et al.). The optimal dose is 250-350 mEq / 24 h.
Acid-base state
Acidosis is a consequence of insulin deficiency. Insulin therapy, along with reimbursement of volume, is given the most importance in the fight against acidosis. An hour after the start of treatment, the first positive changes in the acid-base state are detected, even without bicarbonate therapy. After 24 hours, there are still minor deviations (King et al.). Therapy with bicarbonate is currently carried out only when cardiovascular diseases require urgent elimination of acidosis (Assal et al., Alberti, Kind et al.).
Hasty compensation of acidosis is fraught with consequences (Alberti, Freirich): a sharp drop in the pH of the cerebrospinal fluid due to the increased influx of CO2 into the cells (Alberti, Assal et al.); a slow fall in the osmolality of the cerebrospinal fluid; hypokalemia; reduced CO2 dissociation due to the shift of the O2 dissociation curve with alkalosis appearing later and difficult to correct.
Excessive buffer therapy should be avoided (Richter, Heine!)
If alkalization therapy is carried out, then you should not strive for pH values ​​below 7.1 (Alberti, French)!
Treatment of disorders of the cardiovascular system
As a rule, 1/4 mg of strophanthin is prescribed per day. In case of heart failure, the dose should be greater. If renal function is impaired, then digoxin is used instead of strophanthin. If during the treatment of coma the blood pressure suddenly drops (the systolic pressure becomes lower than 110 mm Hg. St.), Then levarterenol (norepinephrine hydrochloride) 5 mg / 100 ml is administered. However, it is necessary to exclude hypovolemia!
Other events
Antibiotics; with vomiting, nausea or atony of the stomach, prolonged aspiration of gastric contents; warming the patient.
Phosphate injections: As the coma is treated with insulin and liquids for 24 hours, the plasma phosphate concentration drops below 1 mg / dl and only on the following days does their level return to normal. To improve the dissociation of O2 and at the same time improve the supply of oxygen to the tissues during coma therapy, the early introduction of phosphate is recommended (Ditzel, Ditzel, Standl). When phosphate deficiency decreases 2,3-diphospho-glycerate (2,3-DFG), which facilitates the transfer of oxygen to the tissue (Ditzel, Ditzel, Standl).
If extrarenal renal failure is excluded (hypovolemia!), Then comatose patients with anuria, high creatinine and a poor prognostic index can perform hemodialysis (Schneider, Ziegelasch). It is necessary to remember about errors when determining creatinine associated with the presence of ketone bodies in the plasma (1 meq of acetoacetate gives a false increase in creatinine up to 2 mg / dl, according to Kattermann).
Dangerous complications of coma therapy
- Belated start of treatment. Immediate administration of insulin is necessary even before blood sugar levels are obtained.
- Hypoglycemia. With the introduction of small doses of insulin with artificial b-cells or infusion solutions, it can be avoided.
- Hypokalemia. Potassium is administered from the very beginning, if there are no contraindications: oliguria, hyperkalemia (plasma potassium control, monitoring observation).
- Edema of the brain - the so-called secondary shock - disquilibrium syndrome. It develops with a rapid drop in plasma osmolality (hyponatremia below 125 meq! - Duck et al.) Due to the preservation of hyperosmolarity in the cerebrospinal fluid and brain cells. Edema of the brain can be avoided with a gradual decrease in osmolality, the use of isotonic solutions, careful use of hypotonic solutions.
- Forced alkalization therapy.
- A sharp decrease in the concentration of sugar in the blood: you should only gradually eliminate metabolic disorders.
In a diabetic coma, the patient cannot be operated on, since surgery and anesthesia exacerbate the hopelessness of the situation (disturbances associated with surgery are added to metabolic disorders due to insulin deficiency!). The exception is the opening of abscesses in the unconscious state of the patient without anesthesia. If, in a bad state of metabolism, there are vital indications for surgery, before the operation it is necessary to bring the metabolism to a satisfactory condition as soon as possible with the means of treating diabetic coma.
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Metabolism decompensation (ketoacidosis, diabetic coma hyperosmolar acidotic or non-acidotic, lactic acidosis)

  1. Coma with ketoacidosis (ketoacidotic). Ketoacidosis
    ICD-10 code number Coma with ketoacidosis (ketoacidotic). E10.0 E11.0 E12.0 E13.0 Ketoacidosis E14.0 E10.1 E11.1 E12.1 E13.1 E14.1 When making a diagnosis Mandatory Level of Consciousness, blood pressure, heart rate, respiratory rate, body temperature, ECG Laboratory studies : blood glucose, CBS indices, blood gases, hemoglobin, electrolytes (K, Na, Cl, Mg, Ca), leukocytes, blood formula, urea, creatinine,
  2. DIABETIC KETOACIDOSIS
    Definition Diabetic ketoacidosis (DKA) is called metabolic acidosis associated with high levels of ketoacids (acetoacetate and betahydroxybutyrate) in the blood and urine of a diabetic patient. Etiology Absolute or relative insufficiency of insulin, causing mobilization and oxidation of fatty acids, which leads to the formation of keto acids. Typical cases in patients with diabetes
  3. Diabetic ketoacidosis
    Diabetic ketoacidosis (DKA) is an acute complication of diabetes mellitus (DM), which is characterized by elevated blood glucose levels> 14 mmol / l, severe ketonemia and the development of metabolic acidosis. This is a life-threatening condition that usually develops in patients with type I diabetes and is sometimes the debut of the disease. In rare cases, diabetic ketoacidosis can
  4. Diabetic ketoacidosis
    Predisposing factors Diabetic ketoacidosis (DKA) is a common and serious condition, with mortality ranging from 5 to 15%, despite intensive treatment. DKA is a result of insulin deficiency, usually with a relative excess of contrainsular hormones. Most often, DKA is caused by a failure to follow a diet or drug treatment regimen, although it often contributes
  5. Hyperosmolar nonacidotic coma
    Hyperosmolar coma is a variant of diabetic coma, the features of which are high hyperglycemia, a significant increase in blood osmolarity, the absence of ketoacidosis. As a rule, it occurs in people older than 50 years. Observed in children, more often in young children. Among all children with diabetic coma, the hyperosmolar coma is 8.2% (M.I. Martynova, 1976). Etiology. Typical
  6. Hyperosmolar nonacidotic coma
    Examination volume 1. More often develops in children under 2 years of age, against the background of Down's disease or a delayed psychomotor development of another genesis; in non-severe diabetes mellitus without a tendency to ketoacidosis, as a complication of treatment with diuretics, gaukocorticoids, etc. 2. It manifests itself with symptoms of dehydration: the skin is dry, the touch is hot, the tone of the eyeballs and tissues is reduced, hyperthermia;
  7. Diabetic non-conservative hyperosmolar coma
    DIAGNOSIS Diabetic non-congenital hyperosmolar coma, as a rule, complicates the course of unrecognized type 2 diabetes in patients over 40 years of age. It is observed much less frequently than a diabetic ketonemic coma. They provoke the development of diabetic non-conservative hyperosmolar coma, decompensation of diabetes, febrile diseases, surgical interventions,
  8. Diabetic ketonemic coma
    D - ka: In most cases, diabetic ketonemic coma complicates the course of type I diabetes. In the period of precursors (precoma) for several days there are signs of diabetes decompensation, which are joined by increasing weakness, lethargy, nausea, vomiting. Acute inflammatory diseases accelerate the development of severe ketoacidosis, diabetic
  9. Diabetic non-conical hypersmolar coma
    D - ka: Diabetic non-ketonemic hypersmolar coma, as a rule, complicates the course of unrecognized diabetes mellitus type II in patients older than 40 years. It is much less common than diabetic ketonemic coma. They provoke the development of diabetic non-conservative hyperosmolar coma, decompensation of diabetes, febrile diseases, surgical interventions,
  10. Diabetic ketonemic coma
    DIAGNOSIS In most cases, diabetic ketonemic coma complicates the course of type 1 diabetes mellitus. During precursors (precoma) for several days, there are signs of decompensation of diabetes mellitus, which are accompanied by increasing weakness, lethargy, nausea, vomiting, polyuria. Acute inflammatory diseases accelerate the development of severe ketoacidosis,
  11. Diabetic (ketoacidotic) coma
    Ketoacidosis and ketoacidotic coma are one of the main causes of death for patients with diabetes. Pathogenesis. In diabetes mellitus (diabetes mellitus), insulin deficiency, an islet hormone of the pancreatic islet apparatus, contributes to impaired glucose uptake, turning it into glycogen, there is a gross disruption of carbohydrate metabolism. The blood sugar content rises -
  12. Diabetic hyperketonemic coma
    The development of diabetic hyperketonemic (ketoacidotic) coma in children is promoted by factors: untreated and undiagnosed diabetes; discontinuation of insulin or a significant reduction in its dose; acute infectious and other intercurrent diseases, especially purulent; gross violations of the diet and regime; surgical interventions, injuries (physical and mental) and other stressful
  13. Ketoacidotic diabetic coma
    - This is a terrible complication of diabetes mellitus (DM), which is a consequence of pronounced insulin deficiency and reduced glucose utilization by the tissues, which leads to severe ketoacidosis, disruption of all types of metabolism, disorder of the function of all organs and systems, primarily the nervous system and loss of consciousness. Causes: 1) infection (urinary tract, pneumonia, osteomyelitis,
  14. Hereditary metabolic diseases
    Hereditary metabolic diseases - monogenic pathology, in which gene mutation entails certain pathochemical disorders. The classification is as follows. 1. Hereditary diseases of amino acid metabolism: Alcaptonuria, albinism, hypervalinemia, histidinemia, homocystinuria, leucinosis, tyrosinosis, phenylketonuria. 2. Hereditary diseases of carbohydrate metabolism: galactosemia, glycogenosis, disaccharidase
  15. Phytotherapy of metabolic diseases
    Metabolism (metabolism) is the basis of life and is the most important specific sign of living matter, distinguishing living from nonliving. Its essence is the process of continuous entry into the body from the outside of various organic and inorganic compounds, their assimilation, alteration and release into the environment of the formed decomposition products. Metabolism
  16. Special treatment of metabolic disorders
    Metabolic disorders in diabetes, regardless of the various pathogenetic aspects, are based on insulin deficiency. Diet, muscular work and the use of insulin and perorad antidiabetic drugs for over 20 years have been the basis of treatment in each case. Treatment methods Oral diabetes therapy, medications, see table. 25. Insulin: Drugs Used
  17. Heart damage in metabolic disorders
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