Diabetic Ketoacidosis – Harvard Health

What is it?

Diabetic ketoacidosis is a potentially fatal complication of diabetes that occurs when you have much less insulin than your body needs. This problem causes the blood to become acidic and the body to become dangerously dehydrated. Diabetic ketoacidosis can occur when diabetes is not treated adequately, or it can occur during times of serious sickness.

To understand this illness, you need to understand the way your body powers itself with sugar and other fuels. Foods we eat are broken down by the body, and much of what we eat becomes glucose (a type of sugar), which enters the bloodstream. Insulin helps glucose to pass from the bloodstream into body cells, where it is used for energy. Insulin normally is made by the pancreas, but people with type 1 diabetes (insulin-dependent diabetes) don’t produce enough insulin and must inject it daily.

Your body needs a constant source of energy. When you have plenty of insulin, your body cells can get all the energy they need from glucose. If you don’t have enough insulin in your blood, your liver is programmed to manufacture emergency fuels. These fuels, made from fat, are called ketones (or keto acids). In a pinch, ketones can give you energy. However, if your body stays dependent on ketones for energy for too long, you soon will become ill. Ketones are acidic chemicals that are toxic at high concentrations.

In diabetic ketoacidosis, ketones build up in the blood, seriously altering the normal chemistry of the blood and interfering with the function of multiple organs. They make the blood acidic, which causes vomiting and abdominal pain. If the acid level of the blood becomes extreme, ketoacidosis can cause falling blood pressure, coma and death.

Ketoacidosis is always accompanied by dehydration, which is caused by high levels of glucose in the blood. Glucose builds up in the blood if there is not enough insulin to move glucose into your cells. During an episode of ketoacidosis, it is common for blood sugar to rise to a level over 400 milligrams per deciliter. When blood sugar levels are so high, some sugar “overflows” into the urine. As sugar is carried away in the urine, water, salt and potassium are drawn into the urine with each sugar molecule, and your body loses large quantities of your fluid and electrolytes, which are minerals that play a crucial role in cell function. As this happens, you produce much more urine than normal. Eventually it may become impossible for you to drink enough fluids to keep up with amounts that you urinate. Vomiting caused by the blood’s acidity also contributes to fluid losses and dehydration.

People with type 1 diabetes are at risk of diabetic ketoacidosis. If you have type 1 diabetes, ketoacidosis can occur because you have stopped taking your insulin injections or because your insulin dose is too low. It can be triggered by an infection or severe physical stress, such as an injury or surgery, because your body can need more insulin than usual during these stresses.

Ketoacidosis is less likely to occur in people with type 2 diabetes. In most people who have type 2 diabetes, blood insulin levels usually do not get low enough to signal the liver to make ketones.

In about 25% of children with diabetes, symptoms from ketoacidosis are the first sign that they have diabetes.

Symptoms

Symptoms of diabetic ketoacidosis include:

• Frequent urination
• Extreme thirst
• Dry mouth
• Cool skin
• Nausea and vomiting with or without abdominal pain

As blood ketone levels increase, the person’s breathing pattern may become slow and deep, and his or her breath can have a fruity odor. A person with ketoacidosis may seem to be tired or confused or may have trouble paying attention. Without prompt treatment in the first day of symptoms, the illness may cause low blood pressure, a loss of consciousness, coma or death.

If you have type 1 diabetes, it is important to frequently measure your blood glucose levels. If your levels are running high or you are prone to ketoacidosis, you will want to test your urine for ketones. If the urine test strip reads “moderate” or “large,” it’s possible you have ketoacidosis.

Diagnosis

People with diabetic ketoacidosis are always treated in a hospital. Your doctor will test your blood for levels of glucose, ketones, and electrolytes such as sodium and potassium. If you have been taking your insulin without missed doses, your doctor will want to determine if you have an infection.

Expected duration

Symptoms of diabetic ketoacidosis can develop over a period of a few hours, and treatment results in rapid recovery. Commonly, people who develop ketoacidosis will remain in the hospital for one to three days.

Prevention

If you have type 1 diabetes, you usually can prevent diabetic ketoacidosis by following the insulin regimen and diet prescribed by your doctor and by testing your blood glucose regularly. If your body is stressed by an infection, ketoacidosis can develop within hours, and you may not be able to prevent it. It is important for you to check your blood sugar more frequently during an infection, so you can adjust your treatment. It is also important for you to recognize that vomiting and abdominal pain may be signs of ketoacidosis, so that you can get medical help quickly.

To help make sure that you receive proper emergency treatment for diabetic ketoacidosis if you are away from home, wear a medical identification necklace or bracelet that identifies you as a diabetic. This will help emergency personnel to recognize your problem quickly if you are among strangers and you are too sick to speak for yourself.

Treatment

Diabetic ketoacidosis requires treatment in a hospital, often in the intensive care unit. You will receive a large volume of fluids intravenously (through a vein) and insulin to lower your blood sugar and to correct the acidosis. Your blood sugar and acid levels will be monitored frequently, and you will be given potassium supplements to restore your body’s supply of this essential mineral. Until your blood chemistry returns to normal, your vital signs (temperature, pulse, respirations, blood pressure) and urine output will be monitored closely. If an infection has triggered your episode of ketoacidosis, antibiotics or other medications will be used to treat the infection.

When to call a professional

If you have type 1 diabetes and feel unwell, check your blood sugar levels often. Also test your urine for ketones. Call your doctor if you have:

• Unexplained nausea and vomiting with or without abdominal pain,
• Moderate or high levels of urine ketones, or
• Your blood sugar is high and you can’t lower it by adjusting your insulin dose.

Prognosis

With prompt treatment, more than 95 percent of patients recover from diabetic ketoacidosis.

Additional info

National Institute of Diabetes and Digestive and Kidney Diseases

https://www.diabetes.niddk.nih.gov/

Diabetic Ketoacidosis (DKA): Practice Essentials, Background, Pathophysiology

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KETOACIDOSIS AND KETOACIDOTIC COMA | Demidova I.Yu.

Diagnosis of diabetic ketoacidosis in established diabetes mellitus is not difficult. Cases when diabetes mellitus manifests in a state of ketoacidosis require special attention. Recommendations for the treatment of this condition and its complications are presented.

To diagnose diabetic ketoacidosis in documented diabetes mellitus presents no difficulties. Emphasis should be laid on the cases in which diabetes mellitus is manifestative in the presence of ketoacidosis. Recommendations for treatment of this condition and its complications are given.

I.Yu. Demidov – Department of Endocrinology, MMA named after. THEM. Sechenov (head – Academician of the Russian Academy of Medical Sciences Prof. I.I. Dedov)

I.Yu. Demidova — Department of Endocrinology (Head Prof. I.I. Dedov, Academician of the Russian Academy of Medical Sciences, I.M. Sechenov Moscow Medical Academy

By , etoacidosis and ketoacidotic coma are one of the main causes of death in patients with diabetes mellitus (DM) at the age up to 20 years.More than 16% of patients suffering from insulin-dependent DM (IDDM) die precisely from ketoacidosis or ketoacidotic coma. The risk of a fatal outcome of ketoacidosis increases especially in cases where the factor provoking the occurrence of this acute complication of diabetes is a severe intercurrent disease.
Identification of IDDM in the early stages reduced the incidence of manifestations of this disease in a state of ketoacidosis to 20%. Education of patients suffering from diabetes, the principles of self-control and tactics of behavior in emergency conditions has significantly reduced the risk of ketoacidosis – up to 0.5-2% of cases per year.
The study of the nuances of the pathogenesis of ketoacidosis and the creation of optimal treatment regimens for this condition have led to a decrease in the frequency of deaths, but the mortality rate from ketoacidotic coma is 7-19%, and in non-specialized medical institutions this figure is higher.

Pathogenesis

The most common provoking factors for decompensation of DM and the development of ketoacidosis are any intercurrent diseases (acute inflammatory processes, exacerbations of chronic diseases, infectious diseases), surgical interventions, injuries, violations of the treatment regimen (administration of expired or incorrectly stored insulin, errors in prescribing or administering a dose of a drug, malfunctioning insulin delivery systems, emotional stress, pregnancy, and stopping insulin for suicidal intent.
The leading role in the pathogenesis of ketoacidosis is played by absolute insulin deficiency, which leads to a decrease in glucose utilization by insulin-dependent tissues and, accordingly, hyperglycemia, and severe energy starvation in them. The latter circumstance is the cause of a sharp increase in the blood level of all counter-insulin hormones (glucagon, cortisol, catecholamines, ACTH, growth hormone), stimulation of glycogenolysis, proteolysis and lipolysis, supplying substrates for gluconeogenesis in the liver and, to a lesser extent, in the kidneys. Gluconeogenesis in combination with a direct impairment of glucose utilization by tissues due to absolute insulin deficiency is the most important cause of rapidly increasing hyperglycemia, increased plasma osmolarity, intracellular dehydration and osmotic diuresis.
These factors lead to severe extracellular dehydration, hypovolemic shock, and significant electrolyte disturbances. Dehydration and hypovolemia cause a decrease in cerebral, renal and peripheral blood flow, which, in turn, enhances the existing hypoxia of the central nervous system and peripheral tissues and leads to the development of oliguria and anuria. Hypoxia of peripheral tissues contributes to the activation of anaerobic glycolysis processes in them and a gradual increase in the level of lactate. The relative deficiency of lactate dehydrogenase in insulin deficiency and the impossibility of complete utilization of lactate in the Cori cycle are the cause of lactic acidosis in decompensated IDDM. Insulin deficiency and a sharp increase in the concentration of all counter-insulin hormones are the cause of the activation of lipolysis and the mobilization of free fatty acids (FFA), which contributes to the active production of ketone bodies. Enhanced formation of acetyl-CoA, a precursor of acetoacetate (and acetone during its decarboxylation), and B-hydroxybutyrate is provided under these conditions by the active intake of FFAs into the liver due to their mobilization from peripheral tissues and the predominance of lipolysis processes over lipogenesis in the liver cell itself.
The rapid increase in the concentration of ketone bodies during decompensation of DM is due not only to their increased production, but also to a decrease in their peripheral utilization and excretion in the urine due to dehydration and oliguria, which replaced polyuria. The dissociation of ketone bodies is accompanied by an equimolar production of hydrogen ions. Under conditions of DM decompensation, the production of ketone bodies and, consequently, the formation of hydrogen ions exceed the buffer capacity of tissues and body fluids, which leads to the development of severe metabolic acidosis [1].
The severity of the condition in ketoacidosis is due to a sharp dehydration of the body, decompensated metabolic acidosis, a pronounced deficiency of electrolytes (potassium, sodium, phosphorus, magnesium, etc.), hypoxia, hyperosmolarity (in most cases) and often concomitant intercurrent disease.

Clinical picture

Ketoacidosis develops gradually over several days. In the presence of severe concomitant infection, the clinical picture of ketoacidosis unfolds in a shorter time.
Early clinical symptoms of ketoacidosis are typical signs of DM decompensation, such as increasing dryness of the mucous membranes and skin, thirst, polyuria, subsequently replaced by oliguria and anuria, weakness, headache, drowsiness, loss of appetite, weight loss, the appearance of a slight smell of acetone in the exhaled air. In case of failure to provide timely assistance, metabolic disorders are aggravated, and the clinical signs described above are supplemented by nonspecific symptoms of intoxication and acidosis, such as headache, dizziness, nausea and vomiting, which soon becomes more frequent and becomes indomitable. The vomit in ketoacidosis often has a bloody brownish tint and doctors mistake this for “coffee grounds” vomit. As ketoacidosis increases, the smell of acetone in the exhaled air increases, and breathing becomes frequent, noisy and deep (respiratory compensation, Kussmaul breathing).
A symptom that is observed in more than half of the patients deserves special attention – the so-called “abdominal syndrome” of ketoacidosis, manifested by the “acute abdomen” clinic. Often, the combination of abdominal pain, vomiting, and leukocytosis observed in ketoacidosis leads to diagnostic errors and surgical interventions that are unacceptable in this state, often ending in death. The risk of such errors is especially high in the case of manifestation of diabetes in a state of ketoacidosis.
An objective examination shows pronounced signs of dehydration (in severe cases, patients lose up to 10-12% of body weight). Tissue turgor is sharply reduced. The eyeballs become soft, and the skin and visible mucous membranes become dry. Tongue coated with thick brown coating. Muscle tone, tendon reflexes, body temperature and blood pressure are reduced. A frequent pulse of weak filling and tension is determined. The liver, as a rule, protrudes significantly from under the edge of the costal arch and is painful on palpation. Kussmaul’s breath is accompanied by a pungent odor of acetone in the exhaled air.
When examining patients in a state of ketoacidosis, it is necessary to clarify the cause that provoked decompensation of diabetes as soon as possible. If there is a concomitant intercurrent disease, treatment should be started immediately.
From the first signs of DM decompensation, patients show signs of first mild, and then more and more pronounced CNS depression. So, at first, patients complain of a headache, become irritable, and then lethargic, apathetic, drowsy. The developing state of stunnedness is characterized by a decrease in the level of wakefulness, a slowdown in conscious reactions to stimuli, and an increase in periods of sleep. As metabolic disorders worsen, a state of stupor, often called a precomatous state, is clinically manifested by deep sleep or unresponsiveness similar to it in behavioral reactions. The final stage of the growing depression of the central nervous system is a coma, characterized by a complete lack of consciousness.
In a blood test, hyperglycemia, hyperketonemia, an increase in the level of urea nitrogen, creatinine and, in some cases, lactate are determined. Plasma sodium levels are usually low. Despite a significant loss of potassium with osmotic diuresis, vomit and stool, leading to a pronounced deficiency of this electrolyte in the body, its plasma concentration may be normal or even slightly elevated in anuria. In the study of urine, glucosuria, ketonuria and proteinuria are determined. The acid-base state (ACS) reflects decompensated metabolic acidosis, with blood pH dropping below 7.0 in severe cases. The ECG may show signs of myocardial hypoxia and conduction disturbances.
In the event that it is known that the patient has diabetes, the diagnosis of ketoacidosis and ketoacidotic coma is not difficult. The diagnosis is confirmed by the clinical picture described above, laboratory parameters (primarily hyperglycemia, the presence of glucose and ketone bodies in the urine) and CBS, indicating the presence of decompensated metabolic acidosis. In the case of manifestation of diabetes immediately in a state of ketoacidosis or coma, one should first of all focus on the presence of severe dehydration, signs of acidosis (Kussmaul respiration) and significant weight loss in a short period of time. At the same time, the CBS study excludes respiratory alkalosis as the cause of hyperventilation and confirms the presence of metabolic acidosis in the patient. In addition, the smell of acetone in the exhaled air should lead the doctor to the idea that the patient has ketoacidosis. Lactate acidosis, uremia, alcoholic ketoacidosis, poisoning with acids, methanol, ethylene glycol, paraldehyde, salicylates (other causes of metabolic acidosis) are not accompanied by such pronounced dehydration and significant weight loss, and also manifest a typical clinical picture for them. The presence of hyperglycemia and ketonuria confirms the diagnosis of DM and ketoacidosis.

Treatment

Treatment of patients in a state of decompensated diabetes, and even more so in a state of ketoacidosis or ketoacidotic coma, should begin immediately. Patients are hospitalized in a specialized department, and in a state of coma – in the intensive care unit.
The main goals of ketoacidosis therapy are to combat dehydration and hypovolemic shock, restore physiological acid-base balance, normalize electrolyte balance, eliminate intoxication and treat concomitant diseases.
Immediately before the start of therapy, the patient’s stomach is washed with a solution of sodium bicarbonate. A urinary catheter is inserted to monitor kidney function and account for diuresis. In order to improve tissue oxygenation, oxygen inhalation is established. Considering hypothermia, the patient must be warmly covered, and the solutions should be administered warm.
To monitor the effectiveness of the therapy, glycemia, blood pH, pCO ₂ , the level of K, Na, lactate and ketone bodies in the blood, glucosuria and ketonuria, blood pressure, ECG, hemoglobin level, hematocrit, respiratory rate (RR) are monitored before the start of treatment , pulse. Subsequently, it is necessary to hourly monitor glycemia, blood pH, pCO ₂ , BP, ECG, RR, pulse. You can evaluate other indicators every 2 – 3 hours.
An important prognostic value (especially in a state of coma) is the assessment of the reaction of pupils to light. A weak reaction or its complete absence indicates the development of structural changes in the brain stem and a low probability of a favorable outcome of the disease.
Rehydration is very important in the treatment of diabetic ketoacidosis due to the large role of dehydration in the chain of metabolic disorders in this condition. The volume of lost fluid is replenished with physiological (or hypotonic with hyperosmolarity) and 5-10% glucose solutions. Termination of infusion therapy is possible only with a full recovery of consciousness, the absence of nausea, vomiting and the possibility of fluid intake by the patient per os. During the first hour, 1 l 0.9 is injected intravenously% NaCl solution. In the presence of hyperosmolarity, saline may be replaced with a hypotonic 0.45% NaCl solution.
The effective osmolarity is calculated using the following formula:
Osmolarity = 2 [Na + K (mmol/l)] + blood glucose (mOsm) (mmol/l), normal = 297 ± 2 mOsm/l
Over the next two hours from the start of therapy, 500 ml of a 0.9% NaCl solution are injected hourly. In the following hours, the rate of fluid administration should usually not exceed 300 ml/h. After reducing the level of glycemia below 14 mmol / l, the physiological solution is replaced with a 5 – 10% glucose solution and injected at the rate indicated above. The appointment of glucose at this stage is dictated by a number of reasons, among which the main one is maintaining the necessary blood osmolarity. A rapid decrease in the level of glycemia and the concentration of other high-osmolar blood components during infusion therapy often causes an undesirable rapid decrease in plasma osmolarity.
Insulin therapy is started immediately after the diagnosis of ketoacidosis. In the treatment of ketoacidosis, as well as any other urgent condition in diabetes, only short-acting insulin is used (Actrapid MS, Actrapid NM, Humulin R, Insuman Rapid, etc.). Before the normalization of CBS and the decrease in the level of glycemia below 14.0 mmol / l, insulin is administered only intravenously by drip or intramuscularly into the rectus abdominis muscle. Upon reaching the indicated level of glycemia and normalization of the CBS, the patient is transferred to the subcutaneous injection of short-acting insulin.
The dose of insulin in the first hour of treatment is 10 units intravenously by bolus or 20 units intramuscularly. In the case of concomitant severe purulent infection, the first dose of insulin can be doubled.
Subsequently, an average of 6 IU of short-acting insulin is administered hourly intramuscularly or together with physiological NaCl solution intravenously. To do this, 10 IU of insulin for every 100 ml of physiological saline is added to a separate container with a 0.9% NaCl solution. The resulting mixture is thoroughly shaken. In order to adsorb insulin on the walls of the system, 50 ml of the mixture is passed through it in a jet. The use of previously used albumin solutions for the same purpose is now considered optional. 60 ml of this mixture is injected intravenously every hour. In the event that during the first 2-3 hours from the start of therapy the level of glycemia does not decrease, it is recommended to double the dose of insulin in the next hour.
Upon reaching the level of glycemia 12 – 14 mmol / l, the dose of injected insulin is reduced by 2 times – up to 3 units hourly (30 ml of a mixture of insulin and saline). At this stage of therapy, it is possible to transfer the patient to intramuscular injections of insulin, however, it should be borne in mind that the insulin syringes used and the various individual systems for administering the hormone are equipped with needles only for subcutaneous insulin injection.
One should not strive to reduce the level of glycemia below 10 mmol / l, since this increases the risk of not only hypoglycemia, but, above all, hypomolarity. However, if glycemia falls below 10 mmol/l with persistent acidosis, it is recommended to continue to inject insulin hourly and reduce the dose to 2 to 3 U/h. With the normalization of CBS (mild ketonuria may persist), the patient should be transferred to subcutaneous insulin, 6 IU every 2 hours, and then every 4 hours at the same dose.
In the absence of ketoacidosis on the 2-3rd day of treatment, the patient can be transferred to 5-6 single injections of short-acting insulin, and later on to conventional combined insulin therapy.
Restoration of electrolyte balance , especially potassium deficiency, is an important component of complex treatment of ketoacidosis. Usually, the introduction of KCl is started 2 hours after the start of infusion therapy. However, if before the start of treatment there are already ECG or laboratory signs confirming hypokalemia in the absence of anuria, potassium administration can be started immediately, since the administration of liquid and insulin contributes to a rapid decrease in the level of potassium in the blood by diluting its concentration and normalizing the transport of potassium into the cell .
The dose of KCL solution administered by intravenous drip depends on the concentration of potassium in the plasma. So, at a potassium level below 3 mmol / l, it is necessary to inject 3 g / h (dry matter), at 3 – 4 mmol / l – 2 g / h, at 4 – 5 mmol / l – 1.5 g / h, at 5 – 6 mmol / l – 0.5 g / hour. Upon reaching a plasma potassium level of 6 mmol / l, the administration of the KCl solution should be discontinued.
As a rule, patients do not need additional correction of hypophosphatemia. The question of the need for the introduction of potassium phosphate arises only if the level of phosphorus in plasma decreases below 1 mg%.
Recovery of KOS begins literally from the first minutes of the treatment of ketoacidosis, thanks to the appointment of liquid and the introduction of insulin. The restoration of fluid volume triggers physiological buffer systems, in particular, the ability of the kidneys to reabsorb bicarbonates is restored. The administration of insulin suppresses ketogenesis and thereby reduces the concentration of hydrogen ions in the blood. However, in some cases, the question arises of the need to prescribe sodium bicarbonate in order to correct the CBS. It was noted above that even a significant peripheral metabolic acidosis is not always accompanied by an equally pronounced CNS acidosis, due to the presence of a number of protective and adaptive mechanisms. According to J. Ohman et al. J. Posner and F. Plum [2], in patients with diabetic ketoacidosis before therapy, the pH of the cerebrospinal fluid is usually within the normal range. Attempts to correct plasma acidosis using intravenous sodium bicarbonate can lead to the rapid development of CNS acidosis and a sharp deterioration in the patient’s state of consciousness. Taking into account the described side effects with the introduction of soda, very strict criteria for the appointment of sodium bicarbonate in diabetic ketoacidosis have been developed. The question of the advisability of introducing soda should be considered only at a blood pH level below 7.0. It should be emphasized that in this case it is very important to constantly monitor changes in acid-base balance, and when a pH value of 7.0 is reached, the introduction of bicarbonate should be stopped. Use a 4% solution of sodium bicarbonate at the rate of 2.5 ml per 1 kg of actual body weight intravenously drip very slowly. With the introduction of sodium bicarbonate, a solution of KCl is additionally injected intravenously at the rate of 1. 5–2 g of KCl of dry matter [2].
In order to treat or prevent inflammatory diseases broad-spectrum antibiotics are prescribed.
To improve the blood rheological properties and prevent disseminated intravascular coagulation, twice on the first day of treatment, 5000 units of heparin are administered intravenously under the control of a coagulogram.
In order to normalize oxidative processes, 150 – 200 ml of cocarboxylase and 5 ml of a 5% solution of ascorbic acid are added.
With low blood pressure and other symptoms of shock, therapy is carried out aimed at increasing and maintaining blood pressure and cardiac activity.
After removing the patient from the state of ketoacidosis, a sparing diet rich in carbohydrates, proteins, and potassium is prescribed. Fats are excluded from the diet for at least a week.

Complications of ketoacidosis

Among the complications that occur during the treatment of ketoacidosis, the greatest danger is cerebral edema, which ends in death in 70% of cases (R. Couch et al., 1991; A. Glasgow, 1991). The most common cause of cerebral edema is a rapid decrease in plasma osmolarity and glycemia levels during infusion therapy and insulin administration. In the case of the use of sodium bicarbonate in order to correct acidosis, additional prerequisites are created for the occurrence of this formidable complication. An imbalance between the pH of peripheral blood and cerebrospinal fluid contributes to an increase in the pressure of the latter and facilitates the transport of water from the intercellular space to brain cells, the osmolarity of which is increased. Typically, cerebral edema develops 4 to 6 hours after the start of therapy for diabetic ketoacidosis. In the case when the patient’s consciousness is preserved, the signs of the onset of cerebral edema are deterioration of health, severe headache and dizziness, nausea, vomiting, visual disturbances, as well as eye strain, hemodynamic instability, and increasing fever. As a rule, the listed clinical symptoms appear after a “bright” period of improvement in well-being against the background of an obvious positive dynamics of laboratory parameters.
It is much more difficult to suspect the onset of cerebral edema in patients in a state of ketoacidotic coma. A sure sign of this complication at the initial stage is the absence of positive dynamics in the state of consciousness of the patient against the background of an objective improvement in carbohydrate metabolism. The clinical signs of cerebral edema described above are accompanied by a decrease or absence of pupillary response to light, ophthalmoplegia, and edema of the optic nerve. Ultrasound encephalography and computed tomography confirm the diagnosis.
Treatment of cerebral edema is much more difficult than the diagnosis of this condition. When confirming the presence of cerebral edema in a patient, osmotic diuretics are prescribed – intravenous drip of a mannitol solution at the rate of 1 – 2 g / kg. Following this, 80-120 mg of lasix and 10 ml of hypertonic sodium chloride solution are injected intravenously by jet [4]. The question of the advisability of prescribing glucocorticoids (preference is given exclusively to dexamethasone due to its minimal mineralocorticoid properties) has not been fully resolved. It is believed that the greatest effect from the appointment of these hormones is observed with cerebral edema on the background of an injury or tumor. However, given the ability of glucocorticoids to reduce pathologically increased vascular permeability and the blood-brain barrier, normalize ion transport through the cell membrane and inhibit the activity of lysosomal enzymes of brain cells, the question of the advisability of their appointment for cerebral edema in ketoacidosis should be decided individually. To ongoing therapeutic measures are added brain hypothermia and active hyperventilation of the lungs in order to reduce intracranial pressure due to the resulting vasoconstriction. In some cases, a craniotomy should be considered.
Other complications of ketoacidosis and its therapy include disseminated intravascular coagulation, pulmonary edema, acute cardiovascular failure, hypokalemia, metabolic alkalosis, asphyxia due to aspiration of gastric contents.
Strict monitoring of hemodynamic parameters, hemostasis, electrolytes, changes in osmolarity and neurological symptoms makes it possible to suspect the above complications in the early stages and immediately take effective measures aimed at their elimination.

Literature:

1. Krane E. Diabetic Ketoacidosis. Ped Clinics N Amer 1987;34:935–60.
2. Plum F., Posner J.B. Diagnosis of stupor and coma. Translated from English: Medicine, 1986. – 544 p. ill.
3. Beaser R. Diabetic emergencies. Joslin Diabetes Center. lecture notes. October, 1992:12.
4. Diabetic ketoacidosis – A Scheme for management. In: Diabetes in the Young. ISGD. Official Bulletin 1990;23:13–5.

WARNING – ARMED Diabetic ketoacidosis

Korolenko GG,
Head of Endocrinology Department
,
Candidate of Medical Sciences

Diabetic ketoacidosis is one of the most common complications of diabetes mellitus. All patients with this disease experience it to one degree or another. However, with type 1 diabetes, people are more susceptible to diabetic ketoacidosis, and in them this formidable complication proceeds in a more severe form.

Without timely medical attention, ketoacidosis can lead to severe consequences, including coma. Therefore, it is so important to be able to detect an increase in the level of ketones in time and prevent pathological changes in the body.

Causes

The main cause of diabetic ketoacidosis in diabetes mellitus is an increase in the body’s need for insulin. The level of glucose in the blood in this case can be from 10 mmol / l to 30 mmol / l or even higher.

The most common causes of spikes in blood sugar due to an acute lack of insulin are the following: wrong dose of insulin or skipping an injection, dietary problems, severe stress, viral diseases or exacerbation of other diseases that also require a lot of insulin to ensure metabolic processes . If the need for insulin is not restored in time and the attack of hyperglycemia is not stopped, the concentration of ketone bodies in the patient’s blood begins to rise, which are toxins and can cause severe poisoning.

The fact is that with a lack of insulin, the patient’s body experiences an acute shortage of glucose, which is the main source of energy for cells. In order to somehow compensate for energy hunger, the body begins to process fats to obtain the necessary energy. The end product of fat processing is ketone bodies. In conditions of insulin deficiency, their number increases like an avalanche.

Ketone bodies are extremely hazardous to human health and can cause severe intoxication.

Symptoms

The first symptoms of intoxication in diabetes are in many ways similar to food poisoning, which often misleads patients. Trying to get rid of unpleasant symptoms, patients take drugs for indigestion, which do not bring them relief.

At this time, the level of ketone bodies in the blood continues to rise, thereby increasing the toxic effect of toxins on the body. Often such self-treatment ends with an emergency hospitalization of the patient, and in the most severe cases, a coma.

For this reason, it is important for people with diabetes to be able to distinguish between ordinary food poisoning and diabetic ketoacidosis. This will allow you to make the correct diagnosis in time and start adequate treatment without wasting time.

Symptoms diabetic ketoacidosis diabetic:

1. Extreme thirst
2. Severe nausea and vomiting;
3. Diarrhea up to 10 times a day;
4. Weakness, malaise;
5. Headache, dizziness;
6. Frequent and profuse urination;
7. Abdominal pain;
8. Dry skin;
9. Heavy rapid and noisy breathing;
10. Smell of acetone from the mouth;
11. Double vision;
12. Pain in the region of the heart.
13. Inhibited reactions, indicating damage to the central nervous system.

Severe vomiting, diarrhea and copious urination lead to a large loss of fluid, which can cause severe dehydration. Signs indicating the development of such a condition are dryness and flaking of the skin, cracks in the lips, pain in the eyes, and a complete absence of saliva.

When dehydrated, the patient’s blood becomes thick and viscous, which further increases the concentration of glucose and puts a tremendous strain on the heart and blood vessels. Such consequences of intoxication are especially dangerous for people suffering from diseases of the cardiovascular system, as they can lead to a heart attack or stroke. In addition, a high level of acetone has a negative effect on the tissues of the entire urinary system.

In an attempt to get rid of acetone, the body excretes it in the urine, which poisons the kidney cells and can lead to severe kidney failure.

Treatment

Since the vast majority of cases of diabetic ketoacidosis in diabetes mellitus are caused by elevated blood sugar levels, the main method of its treatment is the introduction of short-acting insulin. Self-monitoring should be carried out every 4 hours and injections of short-acting or ultra-short-acting insulin should be done, depending on the obtained glycemic values ​​(4-10 units of insulin) until blood glucose normalizes.

In particularly severe cases, to accelerate the action of the insulin preparation, it is introduced into the body using a dropper or intravenous injection.

But it is important to emphasize that injections of insulin into a vein should only be performed in the presence of a doctor, as they require special skill and accurate dosage calculation. Otherwise, they can cause a severe attack of hypoglycemia and further increase the intoxication of the body.

With severe vomiting, diarrhea and profuse urination, the patient should drink as much liquid as possible, which will compensate for the loss of moisture and protect the body from dehydration. It is important to emphasize that in this condition, the patient should drink only mineral water without gas, and not coffee, tea or other drinks.

The following drugs are not recommended for dehydration:

1. Diuretics;
2. ACE inhibitors;
3. Angiotensin receptor blockers;
4. Anti-inflammatory drugs, including ibuprofen.