Ketoacidosis in diabetes mellitus - what is it and what is it eaten with?

One of the most common diseases of the endocrine system is diabetes mellitus, the decompensation of which can manifest itself in four types of comatose states:

• Ketoacidosis, and ketoacidotic coma, which is its extreme manifestation. Symptoms of ketoacidotic coma
• Insulin therapy
• Infusion therapy

Ketoacidotic coma is the most common coma in diabetes mellitus; the mortality rate in ketoacidotic coma is 2-4%.

Possible causes leading to decompensation of diabetes mellitus:

• belated referral (diagnosis) of the patient to a doctor, with the development of insulin-dependent diabetes mellitus;
• insulin therapy errors;
• incorrect behavior of the patient: errors in diet, alcohol abuse, incorrect dosage of insulin);
• acute diseases, especially purulent infections;
• physical or mental injuries;
• pregnancy;
• surgical interventions.

As a result of insulin deficiency, when there is a discrepancy between the production of endogenous insulin or the delivery of exogenous insulin and the body's needs for it, energy starvation of the body develops with excessive concentrations of glucose in the blood and extracellular fluid, which is a source of energy.

Unutilized glucose, gradually accumulating, leads to an increase in plasma osmolarity, as a result of which part of the interstitial and later intracellular fluid, together with the trace elements contained in it, passes into the vascular bed, causing serious cellular dehydration and a decrease in the intracellular content of electrolytes, and, above all, , potassium. When the glucose concentration increases so much that it exceeds the renal permeability threshold, glycosuria develops with the formation of generalized severe dehydration. The blood thickens, its rheological properties are impaired, thrombus formation increases, and the volume of renal perfusion decreases.

The described pathological cascade, caused by a high concentration of sugar in the blood, can be conditionally considered the first link in the pathogenesis of decompensated diabetes mellitus.

The second conditional link in the decompensation of diabetes mellitus is ketosis (excessive accumulation of ketone bodies in the blood), which turns into ketoacidosis. Ketone bodies, which have the properties of weak acids, cause the accumulation of hydrogen ions in the body, and a decrease in the number of sodium bicarbonate ions - metabolic acidosis develops.

Diabetic ketoacidosis, accompanied by insulin deficiency and excessive secretion of contrainsular hormones, causes severe metabolic disorders that cause the development of a coma. It is currently believed that the cause of death in ketoacidotic coma is dehydration of brain neurons, which occurs against the background of plasma hyperosmolarity.

What is diabetic ketoacidosis

• Diabetic ketoacidosis (DKA) is the result of dehydration associated with insulin deficiency, high blood sugar and organic acids called ketones.
• Diabetic ketoacidosis is associated with significant disturbances in body chemistry that can be corrected with proper therapy.
• Diabetic ketoacidosis usually occurs in people with type 1 diabetes, but can also develop in anyone with diabetes.
• Because type 1 diabetes usually affects people under the age of 25, diabetic ketoacidosis is most common in this age group, but the condition can develop at any age. Men and women are affected equally.

“Acidosis” is translated from Latin as “sour” and means a shift in the body’s acid-base balance towards increased acidity. Since the cause of this process is an increase in the concentration of ketone bodies, the prefix “keto” is added to the word “acidosis”.

What is the connection between metabolic dysregulation and diabetes mellitus? Let's try to explain. Normally, the main source of energy is glucose, which enters the body with food. The missing amount is compensated by glycogen, which accumulates in the muscles and liver.

Since glycogen reserves are limited, and its volume is calculated for about a day, it is the turn of fat deposits. Fat is broken down into glucose, and thus compensates for its deficiency. The breakdown products of fats are ketones, or ketone bodies - acetone, acetoacetic and beta-hydroxybutyric acid.

An increase in the concentration of acetone can occur during physical activity, diets, and an unbalanced diet with a predominance of fatty foods and a minimum amount of carbohydrates. In a healthy body, this process does not cause damage due to the kidneys, which promptly remove ketone bodies, and the PH balance is not disturbed.

Diabetic ketoacidosis develops very quickly even with a normal diet and lack of physical activity. The reason lies in the deficiency or complete absence of insulin, because without it glucose cannot penetrate into the cells. A situation of “hunger amid plenty” arises, when there is enough glucose, but there are no conditions for its use.

Fat and glycogen cannot affect the process, and glucose levels continue to rise. Hyperglycemia increases, the rate of fat breakdown increases, and as a result, the concentration of ketone bodies becomes alarming. When the renal threshold increases, glucose enters the urinary system and is actively excreted by the kidneys.

The kidneys work to the limit of their capabilities, and sometimes they fail, and a significant amount of fluid and electrolytes is lost. Due to significant loss of fluid, the blood thickens, and oxygen starvation occurs in the tissues. Tissue hypoxia promotes the formation of lactic acid (lactate) in the blood, which is fraught with the development of lactic acid coma - lactic acidosis.

Normally, the pH value of the blood is on average 7.4; if it is below 7, there is a direct threat to human life. Diabetic ketoacidosis can lead to this decline in just a few hours, and within a day or a little more, a ketoacidotic coma sets in.

The term “acidosis” comes from the Latin “sour” and means a decrease in the body’s pH. The prefix “keto” indicates that the increase in acidity occurred due to an increase in the concentration of ketone bodies in the blood. Let's take a closer look at why this happens and how diabetes mellitus affects the acid-base balance.

In normal metabolism, the leading source of energy is glucose, which is supplied daily with food in the form of carbohydrates. If it is not enough, glycogen reserves are used, which are stored in the muscles and liver and serve as a kind of depot. This storage facility can quickly open and replenish a temporary lack of glucose; it lasts for a maximum of a day.

We encounter the formation of acetone in the body quite often: during weight loss, significant physical activity, and when eating fatty, low-carbohydrate foods. In a healthy person, this process goes unnoticed, the kidneys promptly remove ketones from the body, intoxication and pH shifts are not observed.

In diabetes mellitus, ketoacidosis occurs much faster and develops more rapidly. Even with sufficient nutrition, cells do not have enough glucose. This is explained by the absolute absence of insulin or its severe deficiency, because it is insulin that opens the door for glucose into the cell. The broken down glycogen and fat reserves are not able to improve the situation; the resulting glucose only increases hyperglycemia in the blood.

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Ketones during pregnancy

During pregnancy, it is also important to test urine for ketoacidosis as often as possible. With daily analysis, it will be possible to notice deterioration as early as possible, prescribe treatment and prevent the development of diabetic ketoacidosis, which is extremely dangerous for both the woman herself and her child.

The doctor may advise the expectant mother to carry out diagnostics not with urine, but directly with blood. To do this, as mentioned above, you can use a glucometer and test strips for it.

Ketoacidosis during pregnancy develops due to a lack of insulin; the danger is that it only takes a day from the moment of the first symptoms to coma. Also, treatment can have a detrimental effect on the condition of the mother and fetus, and its absence will lead to death. Reasons for development:

• Diagnosis of type 1 diabetes mellitus during pregnancy.
• Insufficient amount of insulin. In pregnant women, insulin needs increase; the doctor must take into account and change the dosage of the drug.
• Eating excessive amounts of flour, sudden weight gain.
• Diabetes mellitus accompanied by infectious diseases.
• Lack of glucose control.

Classification and symptoms

Ketoacidosis develops in three stages:

• ketoacidotic precoma, stage 1;
• onset of ketoacidotic coma, stage 2;
• complete ketoacidotic coma, stage 3.

In most cases, about 2.5-3 days pass from the first to the last stage. There are exceptions when a coma occurs in no more than a day. Together with increased blood glucose levels and other metabolic disorders, the clinical picture becomes more pronounced.

Symptoms of diabetic ketoacidosis are divided into early and late. The first signs of hyperglycemia appear:

• dry mouth, feeling of constant thirst;
• frequent urination;
• weight loss and weakness.

Next, characteristic symptoms of increased ketone production occur - a change in respiratory rhythm called Kussmaul breathing. The person begins to breathe deeply and noisily, while inhaling air less frequently than usual. In addition, there is a smell of acetone from the mouth, nausea and vomiting.

The nervous system reacts to the development of ketoacidosis with headache, drowsiness, lethargy and nervousness - ketoacidotic precoma occurs. With an excess of ketones, the gastrointestinal tract also suffers, which is caused by dehydration and is manifested by abdominal pain, decreased intestinal motility and tension in the anterior abdominal wall.

All of the above symptoms are indications for emergency hospitalization. Since the manifestations of ketoacidosis are similar to other diseases, the patient is often brought to a surgical or infectious diseases hospital. Therefore, it is very important to first measure the patient’s blood sugar and check for the presence of ketone bodies in the urine.

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Patients with ketoacidosis may experience complications - pulmonary edema, thrombosis of various locations, pneumonia and cerebral edema.

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Treatment

At the stage of ketosis, therapy is aimed at eliminating the causes of the pathology - the amount of fat in the patient’s diet is reduced, the person needs to drink a lot of alkaline mineral water. Regidron helps eliminate dehydration and restore water-salt balance. To eliminate intoxication and improve liver function, it is necessary to take enterosorbents, hepatoprotectors - Essentiale, Enterosgel, Polyphepan.

If there is no therapeutic effect, an injection of rapid insulin is given, and the drugs Splenin and Cocarboxylase are administered intramuscularly. If ketosis does not progress, the level of sugar and ketone bodies is within the acceptable range, the patient is discharged, data on the therapy performed is entered into the medical history, and further treatment takes place at home. In case of severe ketosis, which is accompanied by manifestations of decompensated diabetes, the patient is hospitalized in a hospital.

Treatment methods:

• administration of injections of simple insulin, while blood sugar values ​​​​cannot be reduced quickly, the optimal speed is no more than 5.5 mmol/l per hour;
• infusion therapy - saline solution is administered using droppers, the dose is calculated taking into account the severity of the pathology and the person’s age;
• administration of potassium if necessary daily;
• if the pH in the blood is less than 7 units, sodium bicarbonate is administered;
• Heparin is administered to elderly patients to prevent the development of thrombosis;
• when infectious complications occur, penicillin and cephalosporin antibiotics are administered intramuscularly;
• if signs of cerebral edema are observed, treat with corticosteroids and diuretics;
• in case of vomiting, gastric lavage is performed; if spontaneous breathing is impaired, the person is connected to a ventilator.

In the first 12 hours, the total amount of fluid administered to the patient should not exceed 10% of the patient’s weight, otherwise pulmonary edema may occur. Patients diagnosed with ketoacidosis are under round-the-clock supervision by medical personnel; they regularly take blood and urine tests to determine the levels of sugar, acetone, sodium, potassium, and pH. An ECG is also performed, blood pressure and temperature are measured.

Important! Doctors recommend checking urine for ketone levels if sugar levels exceed 13.4 mmol/l; for colds and flu, self-diagnosis should be performed every 5-6 hours.

Nutrition rules

Diet is one of the important components of therapy for ketoacidosis. However, in diabetes mellitus, adequate insulin therapy plays a major role. The condition can be corrected solely by diet only with “hungry” acidosis, which develops in people without diabetes, more often in children.

Sample menu for 3 days:

1. 1 day – cereal porridge, natural jam with xylitol or sorbitol, honey, 1.5–3 liters of Borjomi or other alkaline mineral water.
2. Day 2 – oatmeal, mashed potatoes, low-fat fermented milk products, dried bread.
3. Day 3 – light broths, pureed lean meat.

If the patient cannot feed on his own, he is given parenteral fluids, a 5% glucose solution.

Degrees

Based on the severity of the condition, ketoacidosis is divided into 3 degrees, each of which differs in its manifestations.

The mild degree is characterized by:

• a person suffers from a frequent urge to urinate. Excessive fluid loss is accompanied by constant thirst;
• “dizzy” and headache, constant drowsiness is felt;
• against the background of nausea, appetite decreases;
• pain in the epigastric region;
• The exhaled air smells like acetone.

The average degree is expressed by a deterioration of the condition and is manifested by the fact that:

• consciousness becomes confused, reactions slow down;
• tendon reflexes are reduced, and the size of the pupils almost does not change from exposure to light;
• tachycardia is observed against the background of low blood pressure;
• from the gastrointestinal tract, vomiting and loose stools are added;
• the frequency of urination is reduced.

Severe degree is characterized by:

• falling into unconsciousness;
• inhibition of the body's reflex responses;
• constriction of the pupils with a complete lack of reaction to light;
• noticeable presence of acetone in exhaled air, even at some distance from a person;
• signs of dehydration (dry skin and mucous membranes);
• deep, rare and noisy breathing;
• enlarged liver, which is noticeable upon palpation;
• an increase in blood sugar levels to 20-30 mmol/l;
• high concentration of ketone bodies in urine and blood.

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Features in children

Most often, signs of complications appear suddenly and in an acute form.

This is associated with early undetected type 1 diabetes mellitus. Symptoms of the disease in children are identical to those in adults, only in not fully formed organisms the course of ketoacidosis accelerates several times.

The reasons may be incorrect dosage of insulin-containing drugs or their irregular administration; stressful situations can also harm the child. If you suspect this disease, it is necessary to test for acetone in the urine and show the child to a specialist as soon as possible.

Signs indicating the development of ketoacidosis in children are completely no different from the symptoms that appear in adults. Therefore, if you notice one or more signs in a child that confirm a dangerous condition, be sure to take appropriate measures.

The ketoacidotic state is dangerous for children of any age, as the disease develops very quickly. At first, it all begins with a deterioration in the child’s general condition; lethargy and lack of appetite are observed.

Parents should be concerned about suspicious symptoms and conduct a rapid blood sugar test and a urine test to detect the presence of a toxic component. Causes of the disease:

• lack of parental control over the systematic administration of insulin;
• carbohydrate metabolism disorders, non-compliance with diet;
• living in families with a low standard of living, where children are exposed to stress.

Signs

A person with diabetic ketoacidosis may experience one or more of the following symptoms:

• excessive thirst
• frequent urination
• general weakness
• vomit
• loss of appetite
• confusion
• abdominal pain
• dyspnea
• Kussmaul's breath
• sick look
• dry skin
• dry mouth
• increased heart rate
• low blood pressure
• increase in breathing rate
• characteristic fruity odor on breath
• loss of consciousness (diabetic ketoacidotic coma)

• The first sign of this is an increase in blood sugar levels, resulting in insulin deficiency. If the patient begins to experience thirst, which is not quenched even by drinking water, his mucous membranes and skin become dry. In this case, urination becomes more frequent, the patient may suddenly lose weight, and there is general weakness and malaise.
• Next, a state of ketoacidosis develops due to the accumulation of ketone bodies - the patient’s body becomes intoxicated. This manifests itself in the form of nausea, frequent vomiting, bad breath, rapid or deep breathing.
• Against the background of disruption of processes, a disturbance of the nervous system occurs - a patient with diabetic ketoacidosis experiences severe headaches, a kind of lethargy appears, increased drowsiness, the patient is too irritated. The condition rapidly worsens, leading the patient to loss of consciousness and coma.
• In parallel to the main symptoms, gastrointestinal disorders develop - its cells suffer from a catastrophic deficiency in fluid. As a result, dehydration occurs, and the remains are removed from the body along with vital potassium. The patient experiences spasmodic pain in the abdomen, a tense state of the stomach walls, and weak intestinal motility.

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Diet

A low carbohydrate diet includes:

• Limit carbohydrate intake to 10–12 XE (bread units) per day. 1 XE corresponds to 10–12 g of carbohydrates.
• Exclusion of quickly digestible carbohydrates (sugar, juices, chocolate, fruits).
• When receiving insulin as a result of treating ketoacidosis, count and adjust the amount of carbohydrates consumed so that the opposite condition does not develop when glucose levels become as low as possible (hypoglycemia).
• In addition to low-carbohydrate nutrition, it is important to reduce fat intake. It is necessary to drink plenty of fluids.

Type 2 diabetes mellitus is a chronic metabolic disease characterized by impaired carbohydrate metabolism and the development of hyperglycemia (high blood glucose levels) due to insulin resistance (cell insensitivity to the hormone insulin). The most serious complication of diabetes mellitus is ketoacidosis and, as a consequence, ketoacidotic coma.

Ketoacidosis is an acute complication that manifests itself as hyperglycemia, ketonemia (the presence of ketone substances in the blood) and metabolic acidosis (the formation of acidic reaction products during metabolism). It is rare in type 2 diabetes.

The main clinical manifestations of diabetic ketoacidosis include:

Causes of diabetes in dogs

The processes that cause endocrine disruption are primarily associated with poor nutrition and hormonal dysfunction. Diabetes may have secondary symptoms, such as a pathology that occurs against the background of hormonal disorders. The main driving factors influencing the development of diabetes in dogs are:

• Genetically determined heredity.
• Poor nutrition and the development of obesity.
• Hormonal disorders, including those caused by hormone therapy.
• Age over 6-7 years.
• Digestive disorders (chronic pancreatitis).
• Destruction of the pancreas due to severe stress, viral damage, and the appearance of autoimmune pathologies.
• Specific pregnancy or estrus.

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Tests and diagnostics

To make a diagnosis, studying the clinical picture may be sufficient. In addition, ketoacidosis as persistent decompensated diabetes manifests itself in the form of:

• elevated glycemic over 15-16 millimol/l;
• achieving glycosuria 40-50 g/l or more;
• leukocytosis;
• exceeding the ketonemia above 5 millimol/l and detecting ketonuria (more than ++);
• reducing blood pH below 7.35, as well as the amount of standard serum bicarbonate to 21 millimol/l or less.

In 25% of cases, ketoacidosis is idiopathic - occurring for no apparent reason.

Types of diabetes

Diabetic pathology in dogs differs into types, which differ in different mechanisms of occurrence of carbohydrate metabolism disorders and beta cell dysfunction. Most often, diabetes in a pet is not completely cured.

The animal requires constant monitoring of nutrition and medication (insulin therapy). If the disease is caused by hormonal imbalances, which can be eliminated over time, then diabetes goes away completely.

Types of diabetes in dogs:

1. Insulin dependent. This type of pathology is characterized by complete insulin deficiency due to pancreatic dysfunction. Symptoms of insulin-dependent disease include high levels of glucose in the blood, extreme thirst and frequent urination. Genetic predisposition plays a special role in the development of this type of pathology.
2. Insulin-independent. This type of disease is caused by excess production of insulin due to improper, excessive nutrition of the animal. Metabolic metabolism is disrupted and glucose is not absorbed properly by the dog’s body. Due to decreased sensitivity to insulin, sugar is not absorbed by the animal’s tissues and is contained in the blood in excess of the norm. Typically, this type of pathology is accompanied by increased weight in the dog. If you follow proper nutrition and lose weight, your pet's condition can be stabilized. If over time the animal's pancreas becomes depleted and is unable to produce insulin, insulin therapy is required.
3. Secondary pathology. Develops against the background of a primary disease as a consequence of the development of endocrine disorders. It may occur during hormone therapy or as a result of pathologies associated with digestive pathologies (pancreatitis). When the symptoms of the primary disease are eliminated, the dog’s blood sugar in most cases stabilizes.
4. Pregnancy diabetes. Develops in bitches immediately after estrus or in the last stages of pregnancy. It appears due to the animal’s body’s tolerance to glucose due to a sharp increase in certain hormones, including progesterone and growth hormone. Most often, the disease resolves spontaneously immediately after childbirth.

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The main reasons for the development of pathology

Ketone bodies begin to be produced due to a disruption in the interaction of cells with insulin, as well as during severe dehydration.

This can happen in type 2 diabetes, when cells lose sensitivity to the hormone, or in type 1 diabetes, when the damaged pancreas stops producing enough insulin. Since diabetes causes intense urine output, this combination of factors causes ketoacidosis.

The following reasons can provoke ketoacidosis:

• taking hormonal, steroid drugs, neuroleptics and diuretics;
• diabetes during pregnancy;
• prolonged fever, vomiting or diarrhea;
• surgical intervention, pancreatectomy is especially dangerous;
• injuries;
• duration of type 2 diabetes mellitus.

Another reason can be considered a violation of the schedule and technique of insulin injections:

• using a hormone that has expired;
• rare measurement of blood sugar concentration;
• violation of dietary nutrition without insulin compensation;
• damage to the syringe or pump;
• self-medication using traditional methods with skipping injections.

Ketoacidosis occurs as a result of an error in the diagnosis of diabetes mellitus and, accordingly, a delayed start of insulin treatment.

Symptoms and signs

The disease develops over a long period of time, so the owner of a diabetic dog cannot always determine its onset. However, the typical symptoms of diabetes in dogs are:

• Increased thirst.
• Frequent urination.
• Significant weight loss.
• Excessive appetite.

Veterinary medicine has identified additional signs of diabetes in dogs:

• Lethargic appearance of the animal, general fatigue.
• Hair loss.
• Urine and saliva may emit a sour-fruity odor.
• Frequent heartbeat.
• Enlarged liver.
• The appearance of various types of dermatitis.
• Dry mouth and viscous saliva.
• Non-healing wounds.

Often, when the disease is advanced, cataracts begin to form, causing the lens of the eye to become cloudy. The dog can be so exhausted that with increased nutrition, the ribs appear under the fur.

The most difficult thing for a diabetic dog is the development of ketoacidosis. This is a condition in which the body is poisoned by toxic ketones. Vomiting and weakness appear; if the dog does not receive medical assistance, it falls into a coma.

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Diagnosis of pathology

So, having looked at diabetic ketoacidosis in children and adults, and knowing what it is, we need to consider how to diagnose this condition in a diabetic.

Diagnostic measures are carried out before hospitalization of the patient through blood and urine tests. In a situation where it is not possible to obtain a urine test, since it cannot be collected, a biological fluid (blood) is examined, a small amount of which is applied to a test strip to determine the presence of ketone bodies in the urine.

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Then the stage of development of the complication is determined. It is very important to distinguish diabetic ketoacidosis in children and adults from hyperosmolar syndrome and other diseases.

Diagnosis of the disease is differential, so it is necessary to distinguish the disease from other acute conditions:

• Alcoholic ketoacidosis.
• Acidosis due to hunger.
• Overdose of medications.
• Overdose of medications containing methyl alcohol.
• Poisoning the body with ethyl alcohol.

It should be said that the patient may have normal or decreased body temperature, but this does not mean that there are no infectious and inflammatory processes.

The renal form of coma is characterized by frequent urination, which is replaced by anuria.

Ketoacidotic coma

Ketoacidotic coma is an acute complication of diabetes mellitus resulting from insulin deficiency due to inadequately selected insulin therapy. This condition is life-threatening and can be fatal. According to statistics, this complication occurs in 40 patients out of 1000 patients.

In 85-95% of cases, coma ends favorably, and in 5-15% of cases it ends in death for the patient. People over 60 years of age are most vulnerable. For older people, it is especially important to explain the correctness of insulin therapy and compliance with the dosage of the drug.

Etiology of occurrence

There are several reasons why such a serious complication occurs. All of them are due to non-compliance with the therapy regimen, violation of recommendations prescribed by the doctor, as well as the addition of a secondary infection. If we analyze the reasons in more detail, we can identify the following factors that provoke the development of such an illness as ketoacidotic coma:

• drinking alcohol in large quantities;
• discontinuation of antihyperglycemic drugs without a doctor’s permission;
• unauthorized transition to the tablet form of treatment for insulin-dependent diabetes mellitus;
• missed insulin injection;
• violation of technical rules for administering insulin;
• creating unfavorable conditions for metabolic disorders;
• the addition of infectious and inflammatory diseases;
• injuries, surgical interventions, pregnancy;
• stress;
• stroke, myocardial infarction;
• taking medications that are not combined with insulin therapy.

The occurrence of complications in all of the above cases is due to a decrease in the sensitivity of tissue cells to insulin or an increase in the secretory function of counter-insular hormones (cortisol, adrenaline, norepinephrine, growth hormone, glucagon). In approximately 25% of cases of ketoacidotic coma, the cause of its occurrence cannot be identified.

Pathogenesis of ketoacidotic coma

After the onset of the action of some provoking factors for the development of complications of diabetes mellitus, a chain of pathological processes begins in the body, which lead to the development of symptoms of the complication, as well as to possible consequences. How does ketoacidotic coma and its symptoms develop?

Firstly, insulin deficiency appears in the body, as well as the production of excess amounts of counter-insular hormones. This disorder leads to insufficient provision of tissues and cells with glucose and a decrease in its utilization. In this case, glycolysis is suppressed in the liver and a hyperglycemic state develops.

Secondly, under the influence of hyperglycemia, hypovolemia occurs (decrease in blood volume), loss of electrolytes in the form of potassium, sodium, phosphates and other substances, as well as dehydration (dehydration).

Thirdly, due to a decrease in circulating blood volume (CBV), increased production of catecholamines begins, which cause an even greater deterioration in the functional effect of insulin in the liver. And in this condition, when there is an excess of catecholamines and a lack of insulin in this organ, the mobilization of fatty acids from adipose tissue begins.

The final stage of the complication mechanism is the increased production of ketone bodies (acetone, acetoacetate, beta-hydroxybutyric acid).

Due to this pathological condition, the body is unable to metabolize and eliminate ketone bodies, which bind to the accumulated hydrogen ions, resulting in a decrease in blood pH and bicarbonate levels and the formation of metabolic acidosis.

The body's compensatory response occurs in the form of hyperventilation and a decrease in the partial pressure of carbon dioxide. Ketoacidotic coma under the influence of such pathogenesis begins to show symptoms.

Symptoms of complications

Symptoms of complications develop gradually and take from several hours to several days. At the very beginning of ketoacidotic coma, the patient notes dry mouth, thirst and polyuria.

All these symptoms indicate decompensation of diabetes mellitus.

Further, the clinical picture is supplemented by itching due to dry skin, loss of appetite, weakness, adynamia, pain in the limbs and headaches.

Due to loss of appetite and loss of electrolytes, abdominal pain, nausea and vomiting of “coffee grounds” begin. Abdominal pain can sometimes be so acute that pancreatitis, ulcer or peritonitis is initially suspected.

Increasing dehydration increases intoxication of the body, which can lead to irreversible consequences.

Scientists have not fully studied the toxic effect on the central nervous system, but the main assumptions of death are dehydration of brain neurons, which occurs as a result of plasma hyperosmolarity.

The main clinical picture of ketoacidotic coma is the typical symptoms for this complication, expressed in rapid but deep breathing (Kussmaul breathing) with the smell of acetone on exhalation.

Patients have reduced skin turgor (elasticity), and the skin and mucous membranes are dry. Due to a decrease in blood volume, the patient may experience orthostatic hypotension, accompanied by confusion, gradually turning into a coma.

It is very important to notice the presence of these symptoms in time in order to provide timely assistance.

Treatment

Inpatient treatment of a patient involves combating hypovolemic shock and dehydration, normalizing electrolyte balance, eliminating intoxication, restoring the physiological functions of the body and treating concomitant diseases.

Principles of care and treatment for ketoacedotic coma:

1. Rehydration. An important link in the chain of eliminating complications. With ketoacidosis, dehydration of the body occurs and physiological fluids in the form of 5-10% glucose and 0.9% sodium chloride solution are administered to replenish lost fluid. Glucose is prescribed to restore and maintain blood osmolarity.
2. Insulin therapy. This treatment method begins immediately after the diagnosis of ketoacidonic coma. In this case, as well as in other urgent conditions of diabetes mellitus, short-acting insulin is used (Insuman Rapid, Actrapid NM, Actrapid MS, Humulin R). Initially, it is administered intramuscularly into the rectus abdominis muscle or intravenously. After the glucose level reaches 14 mmol/l, the patient begins to administer short-acting insulin subcutaneously. As soon as the glycemic level is fixed at 12-13 mmol/l, the dose of administered insulin is halved. Glycemia should not be reduced below 10 mmol/l. Such actions can provoke the onset of the development of a hypoglycemic state and blood hyposmolarity. As soon as all the symptoms of ketoacedomic coma are eliminated, the patient is transferred to 5-6 single injections of short-acting insulin, and with stabilizing dynamics, combination insulin therapy is then carried out.
3. Restoration of electrolyte balance and hemostasis. Such events are an important part of the therapy. By introducing the necessary drugs, calcium deficiency and the acid-base state of the blood are restored, thereby ensuring the normalization of kidney function to reabsorb bicarbonates.
4. Improving the rheological properties of blood. And also to prevent intravascular coagulation, intravenous heparin can be prescribed, always under the control of a coagulogram.
5. Treatment of secondary infections. If the patient experiences a secondary infection, broad-spectrum antibiotics can be prescribed to prevent their occurrence.
6. Symptomatic therapy. To restore blood pressure and eliminate the consequences of shock, therapeutic measures are carried out aimed at improving cardiac activity. In addition, after a coma, the patient is prescribed a gentle diet rich in potassium, carbohydrates and proteins. Fats are excluded from the diet for at least 7 days.

Prevention of ketoacedotic coma

Nothing is better than just not getting sick. If a moment occurs in life when a chronic disease requires increased attention, you should treat this circumstance with special responsibility.

Firstly, you need to pay special attention to all recommendations prescribed by your doctor. Secondly, you need to monitor the expiration date of insulin, follow the administration technique, dosage and injection time.

The drug must be stored according to all rules.

If the patient feels unwell and worsening of his condition, which he cannot cope with on his own, he should immediately consult a doctor, where he will be provided with emergency care.

Complications of coma

Ketoacedotic coma, with a correct diagnosis and timely correction of biochemical disorders, has a favorable outcome and does not cause serious consequences. The most dangerous complication of this condition can be cerebral edema, which is fatal in 70% of cases.

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Prevention of CC

Only the diabetic himself can prevent the onset of coma. The main condition is normal compensation of the disease. The closer the sugar level is to the target, the less likely there are acute complications. If glucose often exceeds 10 or even 15 mmol/l, any deviation from the normal course of life can lead to coma: illness, poor diet, severe anxiety.

Do not try to cope with an incipient coma alone if you feel drowsy or very tired. Consciousness in this state can fade away in a matter of minutes. If you have high sugar and feel unwell, call an ambulance, call your neighbors, open the front door so that doctors can quickly get into your apartment if you cannot get out of bed.

Check them out for yourself and let your loved ones read about them. Print out the first aid rules and place them in a visible place. In your passport, wallet, or phone screen, place information about your type of diabetes, prescribed treatment, and other diseases. Notify your colleagues and friends that you have diabetes, tell them what symptoms you should call an ambulance for. The prognosis of a coma largely depends on the correct actions of others and emergency doctors.

What will happen if left untreated?

Experts say that invasive methods of treating diabetic ketoacidosis help the patient fully recover from a serious illness. Death is extremely rare (approximately 2% of all cases).

But, if a person ignores the disease, then unforeseen complications may arise.

If a diabetic does not treat ketoacidosis, he can expect:

• severe cramps of the limbs;
• cerebral edema;
• reduction in glucose levels to a critical level;
• heart failure;
• accumulation of fluid in the lungs.

Etiology

The most common cause of severe ketoacidosis is type 1 diabetes mellitus.
Diabetic ketoacidosis occurs due to an absolute or relative deficiency of insulin that develops over several hours or days. I.
In patients with newly diagnosed insulin-dependent diabetes mellitus, partial or complete deficiency of endogenous insulin is caused by the death of beta cells of the pancreatic islets.
II.
In patients receiving insulin injections, the causes of ketoacidosis may be: 1. inadequate therapy (prescription of too small doses of insulin);
2. violation of the insulin therapy regimen (skipped injections, expired insulin); 3. a sharp increase in the need for insulin in patients with insulin-dependent diabetes mellitus: a) infectious diseases: sepsis (or urosepsis); pneumonia ; other upper respiratory and urinary tract infections; meningitis; sinusitis; periodontitis; cholecystitis, pancreatitis; paraproctitis. b) concomitant endocrine disorders: thyrotoxicosis, Cushing's syndrome, acromegaly, pheochromocytoma; c) myocardial infarction, stroke; d) injuries and/or surgical interventions; e) drug therapy: glucocorticoids, estrogens (including hormonal contraceptives); f) pregnancy; g) stress, especially in adolescence. In all of the above cases, the increase in the need for insulin is due to increased secretion of counter-insular hormones - adrenaline (norepinephrine), cortisol, glucagon, growth hormone, as well as insulin resistance - increased tissue resistance to the action of insulin. III.
In a quarter of patients, the cause of diabetic ketoacidosis cannot be determined.