Hypoglycemia - what is it? Hypoglycemia: symptoms, causes, signs, treatment, diet. Hypoglycemic state and hypoglycemic coma (clinical picture)
In most cases, hypoglycemic conditions develop in patients with diabetes mellitus during insulin therapy or therapy with second-generation sulfonylurea drugs (glibenclamide - maninil - daonil; gliquidone - glu-renorm; gliclazide - diabeton - predian; glipizide), as well as during treatment with the first generation drug, chlorpropamide, the half-life of which is 36 hours. Hypoglycemic conditions are usually associated with disturbances in the rhythm of food intake or drug overdose.
The occurrence of severe hypoglycemic conditions is observed when using hypoglycemic drugs in patients with chronic renal failure, Addison's disease, and in patients with acetylation defects (“slow acetylators”).
Much less frequently, spontaneous hypoglycemic states are caused by insulinomas and other extrapancreatic tumors, early stage diabetes mellitus, glycogen storage diseases, and functional hyperinsulinism. Finally, severe hypoglycemic conditions occur due to poisoning with hypoglycemic drugs.
The development of hypoglycemic conditions when using sugar-lowering drugs is potentiated by alcohol intake, physical overload, P-blockers, salicylates, amphetamine, haloperidol, phenothiazines, quinine, ethionamide.
It should be noted that p-blockers not only potentiate hypoglycemic states, but also mask their clinical manifestations by eliminating adrenergic components.
Alcohol intake can provoke the development of a hypoglycemic state even without the participation of sugar-lowering drugs, both with a single dose and in chronic alcoholics with eating disorders. Data have been published on the occurrence of hypoglycemic conditions in febrile children when they are repeatedly wiped with alcohol.
Prehospital physicians often come into contact with patients who are in a state of hypoglycemia. The glycemic level must be examined in every comatose patient, in patients with convulsive syndrome, with strange behavior in drivers during transport accidents.
Clinical picture. Glucose is the main source of energy for brain tissue. Therefore, the clinical manifestations of hypoglycemic conditions are based on central nervous system dysfunction.
With the rapid development of hypoglycemic conditions, mental disorders (disorientation, inappropriate behavior) predominate; with a slow development, neurological disorders predominate. At the stage of precursors of hypoglycemic conditions (this stage is absent in patients with depletion of glycogen reserves of the liver - in chronic alcoholics, with liver pathology, with prolonged decompensation of diabetes mellitus), the patient experiences suddenly developing sensations of weakness, hunger, anxiety, headache, and less often - a sensation of numbness of the tip tongue and lips (the latter is a specific symptom). If at this stage the hypoglycemic state is not relieved by the intake of carbohydrates, agitation, disorientation, then stupor, convulsions, and stupor develop.
At the stage of advanced hypoglycemia, the patient has impaired consciousness or loss of consciousness, sweating, tachycardia, and sometimes increased blood pressure, clonic and tonic convulsions; tissue turgor is normal.
Symptoms of glycemic conditions tend to appear at glycemic levels< 2,78-3,33 ммоль/л. Редко гликемические состояния могут сочетаться с ке-тоацидозом.
Differential diagnosis. Hypoglycemic conditions can simulate cerebrovascular pathology, brain tumors, psychoses, i.e. neurological, psychiatric and even cardiovascular pathology. Differential diagnosis is based on a quick positive effect intravenous administration glucose in hypoglycemic conditions.
Differentiation of hypoglycemic states, diabetic ketonemic coma and diabetic non-ketonemic hyperosmolar coma is based on the absence of dehydration, ketonuria, and hyperglycemia in hypoglycemic states.
Alcohol-induced hypoglycemia develops 2-10 hours after drinking alcohol. The patient is usually in a coma and responds only to painful stimulation. A blood test reveals hypoglycemia and alcohol. In the urine there is ketonuria without glucosuria.
Emergency treatment. The basis of therapy for hypoglycemic conditions is intravenous or oral administration of glucose. There is evidence that, on average, 20 g of glucose is sufficient to relieve a hypoglycemic state. If there is no possibility of oral administration of glucose, the latter is administered internally.
approximately in the amount of 50 ml of 40% solution. If there is no effect, the administration should be repeated.
After restoration of consciousness in uncomplicated hypoglycemic conditions, the patient should be fed foods high in carbohydrates (bread, porridge, potatoes).
For refractory hypoglycemic conditions, second-line drugs are glucagon (1 mg intravenously or intramuscularly, can be administered twice) or adrenaline (1 mg subcutaneously). Patients with refractory hypoglycemic conditions and hypoglycemic conditions caused by taking sulfonylureas (especially chlorpropamide), patients with poisoning with antihyperglycemic drugs, patients with hypoglycemia complicated by acute cerebral or coronary circulatory disorders are hospitalized.
Main dangers and complications. Severe, long-term, uncontrollable hypoglycemia progresses to cerebral coma; cramps and sweating stop; areflexia, often hyperthermia, progressive arterial hypotension, and cerebral edema develop. Achieving and stabilizing normoglycemia or hyperglycemia at this stage of hypoglycemic conditions does not lead to success.
In patients with coronary disease heart or brain hypoglycemic conditions can provoke acute disorder coronary or cerebral circulation. Patients are advised to undergo ECG monitoring and urgent hospitalization.
Severe hypoglycemic conditions are the cause of death in 3-7% of patients with type I diabetes mellitus.
Basic diagnostic and therapeutic measures at the hospital stage. Therapy for refractory hypoglycemic conditions should be long-term and intensive. At the hospital stage, intravenous administration of a 10-20% glucose solution is continued to achieve normoglycemia or moderate hyperglycemia (8.3-11.1 mmol/l). If combination therapy(glucose + adrenaline) is ineffective; against the background of continued intravenous administration of glucose, slow (over 30 minutes) intravenous administration of 300 mg of diazoxide every 4 hours is recommended. Significant arterial hypotension does not occur.
To prevent relapse of hypoglycemic conditions, the patient is prescribed intravenous administration of 100-200 mg of hydrocortisone hemisuccinate.
When the patient's condition is stabilized and moderate hyperglycemia persists against the background of intravenous administration of a 5% glucose solution, the administration of the latter can be stopped.
Treatments are carried out while monitoring ECG, pH and blood gases. Acute adrenal insufficiency
Acute adrenal insufficiency develops as a result of sharp decline or cessation of secretion of gluco- and mineralocorticoids by the adrenal cortex during its primary or secondary lesions. Lesions of the medulla
adrenal glands producing catecholamines is compensated by their extra-adrenal production and is not clinically manifested.
Most cases acute failure adrenal glands is associated with an unrecognized or inadequately treated primary chronic failure adrenal cortex with its autoimmune, tuberculous lesions (Addison's disease), amyloidosis, hemochromatosis, sarcoidosis, AIDS.
The development of acute adrenal insufficiency in patients in this group is provoked by acute infections, surgical interventions and other stressful situations.
Acute damage to the adrenal cortex can be caused by vascular thrombosis without previous damage due to meningococcemia and sepsis of another etiology - Waterhouse-Friderichsen syndrome. In adults, this syndrome is caused by hemorrhages in the adrenal glands during acute infections, injuries, burns, and during treatment with fibrinolytics and anticoagulants.
The likelihood of acute adrenal insufficiency threatens patients who have been receiving glucocorticoids for a long time after their withdrawal, patients after bilateral adrenalectomy for Itsenko-Cushing syndrome, and congenital virilizing hyperplasia of the adrenal cortex.
All of the above causes of acute adrenal insufficiency are associated with primary damage to the adrenal glands.
Secondary adrenal insufficiency and the possibility of developing acute adrenal insufficiency are caused by insufficient production of ACTH or ACTH-releasing hormone. These relatively rare variants of acute adrenal insufficiency are the result of organic lesions hypothalamic-pituitary structures (tumors, granulomas), postpartum hypopituitarism (Sheehan syndrome).
An acute decrease in the concentration of gluco- and mineralocorticoids (cortisol, aldosterone) circulating in the blood triggers a cascade of pathological phenomena: water and electrolyte disorders with loss of fluid, sodium, chlorides, accumulation of potassium to toxic concentrations, hypoglycemia, damage to vascular tone. Electrolyte and fluid losses are aggravated by vomiting and diarrhea.
Delayed diagnosis and onset intensive care end in severe collapse, coma and death of the patient.
Clinical picture and diagnosis. Clinically, acute adrenal insufficiency is manifested by acutely developing dehydration, vascular collapse, neuropsychiatric and gastrointestinal manifestations. The severity of each component may vary in individual patients.
In patients with chronic adrenal insufficiency, acute adrenal insufficiency syndrome is preceded by a prodromal period, the duration of which is from several hours to several days. During this time, the symptoms of asthenia, muscle weakness progress, loss of appetite, nausea, vomiting are observed, loose stool, abdominal pain, weight loss, arterial hypotension.
In patients with primary damage to the adrenal glands, skin pigmentation develops, especially noticeable in places where clothing rubs, on the palmar folds, in the area
postoperative scars. Pigmentation may be combined with areas of leukoderma (vitiligo).
With secondary lesions of the adrenal glands, pigmentation is absent.
Body temperature in acute adrenal insufficiency may be normal or decreased. With hemorrhages and infarctions of the adrenal glands, severe hyperthermia occurs within several hours.
Waterhouse-Friderichsen syndrome often has a petechial rash.
Psychoneurological disorders are manifested by meningeal symptoms, paresthesia, disorders of superficial and deep sensitivity, convulsions, disturbances of consciousness, and delirium. Patients are diagnosed with severe arterial hypotension (systolic blood pressure within 70 mm Hg and below), frequent small pulse, muffled heart sounds, shortness of breath, cyanosis.
Patients with preserved consciousness complain of abdominal pain, which, subjectively and with objective detection of pain, is difficult to distinguish from pain in acute inflammatory processes abdominal cavity. Vomit may be coffee-colored. Diagnostic errors and unjustified surgical interventions become fatal for patients.
For the diagnosis of acute adrenal insufficiency, anamnestic data and the presence of medical documents indications of pathology of the adrenal glands, autoimmune diseases, tuberculosis, long-term use glucocorticoids, adrenalectomy or nephrectomy (for kidney tuberculosis).
On prehospital stage blood sugar testing helps recognize acute adrenal insufficiency, since hypoglycemia is a significant component of acute adrenal insufficiency.
The ECG can detect changes characteristic of hyperkalemia: flattening of the P wave, blockade of conduction at various levels, the appearance of replacement rhythms, shortening of the ST segment, high-amplitude T waves.
Differentiation of acute adrenal insufficiency from vascular collapse and shock of other origin is based on therapeutic effect intravenous administration of hydrocortisone, sodium chloride solutions, if these measures are carried out in a timely manner.
Emergency therapy at the prehospital stage of an acute adrenal insufficiency crisis is carried out by administering water-soluble hydrocortisone preparations (hydrocortisone hemisuccinate): 150 mg of the drug is administered intravenously, the same amount is administered intramuscularly. In the absence of this drug, 60 mg of prednisolone is injected intravenously and the same amount is administered intramuscularly. In the absence of water-soluble preparations of hydrocortisone or prednisolone, 250 mg of hydrocortisone acetate is administered intramuscularly, using several injection sites (50 mg each) to accelerate the absorption of the drug.
The patient is rehydrated by intravenous drip administration of 0.9% sodium chloride solution and 5% glucose solution at a rate of 0.5 l/h. The first 200-300 ml of solution is administered as a stream, after which, switching to drip administration, 10 ml of 10% sodium chloride solution is injected intravenously.
If consciousness is preserved and there is no vomiting, treatment can begin with the appointment of 150 mg of tableted cortisone acetate and 50 mg of fludrocortisone (Cortinef) orally.
In case of severe arterial hypotension, 1 ml of 0.2% norepinephrine solution (per 1 liter of solution) or 1-2 ml of 1% mesatone solution should be added to the intravenously administered isotonic sodium chloride solution.
The patient is transported to the intensive care unit of the hospital by a resuscitation ambulance team.
At the hospital stage, intramuscular administration of hydrocortisone gemisuccinate (or succinate, Solu-Cortef) 50-100 mg every 3 hours, intravenous drip administration of 0.9% sodium chloride solution and 5% glucose solution (with or without norepinephrine) are continued under condition control patient, when monitoring blood pressure, central venous pressure, ECG, electrolyte concentrations, glycemia, creatinine content, hourly diuresis.
Blood, urine, and X-ray examination chest, area of the adrenal glands for tuberculosis.
In the absence of water-soluble preparations of hydrocortisone or prednisolone, intramuscular administration of a suspension of hydrocortisone acetate 50-100 mg every 3-4 hours is continued, followed by a dose reduction.
The mineralocorticoid drug Cortineff is prescribed 50-100 mg per day orally until the crisis is relieved.
After the patient’s condition improves and the crisis is stopped, the dose of administered glucocorticoids is reduced by half, and then their maintenance dose is selected. Patients are shown parenteral administration ascorbic acid.
Antibiotics and anti-tuberculosis drugs are prescribed if necessary after consultation with a phthisiatrician.
Special studies (cortisol levels, 17-OX in blood and urine) are of secondary importance. Waiting for the results of these studies should not delay intensive care.
The clinical picture of a hypoglycemic state consists of two groups of symptoms caused by neuroglycopenia and energy starvation nerve cells and sympathetic-adrenal response to hypoglycemia.
A hypoglycemic state usually develops when blood sugar levels drop to less than 2.75 mmol/L (50 mg%). However, in its occurrence it is important not only absolute value glycemia, but also the rate of its decrease. Often, with a slow decrease in sugar concentration, the patient feels well with a glycemia of 2.75-2.25 mmol/l (50-50 mg%) and even 1.7 mmol/l (30 mg%), and with prolonged adaptation of the brain to high content blood sugar, its sharp decrease even to a normal level is accompanied by a clinical picture of hypoglycemia. Cases of a hypoglycemic state have been described with a rapid decrease in glycemia from 22.2 mmol/l (400 mg%) to 11.1 mmol/l (200 mg%).
The hypoglycemic state usually occurs acutely, with the patient feeling general weakness, hunger, sweating, hand trembling, sometimes headache or dizziness, palpitations. Facial paresthesia (numbness of the lips, tongue, chin) and diplopia are considered very characteristic of a hypoglycemic attack.
In most cases, this period lasts long enough for an experienced patient who has already experienced similar episodes to take the necessary measures (quickly eat a piece of sugar, bread, candy, drink sweet tea). If this is not done, then excitement increases, sweating becomes profuse, and signs of disorientation appear.
The patient becomes angry, aggressive, sometimes hallicinates, often commits senseless acts, screams, tries to fight with others, categorically refuses the offer to eat, give an injection of glucose. During this period, the patient gives the impression of being drunk, and if an attack occurs in the absence of people who know about it illness, he often ends up in the police or a sobering-up center. Subsequently, clonic or tonic convulsions occur, sometimes a real epileptic seizure.
Psychomotor agitation gives way to general apathy, stupor, drowsiness, and then coma develops. With a short coma, the skin is usually pale, moist, its turgor and the tone of the eyeballs are normal. The tongue is wet, tachycardia, blood pressure is normal or slightly elevated. Breathing is normal. There is no smell of acetone from the mouth. The temperature is normal. Muscle tone, tendon and periosteal reflexes are increased. May be positive symptom Babinsky. As the coma deepens and increases in duration, sweating stops, breathing becomes more frequent and shallow, blood pressure decreases, and sometimes bradycardia appears.
Changes in the neurological status are clearly increasing: appear pathological symptoms(nystagmus, anisocoria, phenomena of meningism, pyramidal signs), muscle tone decreases, tendon and abdominal reflexes are inhibited.
Hypoglycemic attacks are especially dangerous in elderly people suffering from coronary heart and brain disease. Hypoglycemia can be complicated by myocardial infarction or stroke, so ECG monitoring is mandatory after relief of the hypoglycemic state. Mild hypoglycemic episodes usually pass without a trace, but severe, prolonged or frequent ones gradually lead to encephalopathy, and then to personality degradation. In addition, hypoglycemia contributes to the progression of microangiopathy, as confirmed by dynamic monitoring of diabetic retinopathy.
In each case of hypoglycemia, it is necessary to thoroughly and immediately determine its causes. Patients with a hypoglycemic state that developed without warning, essentially with sudden loss consciousness.
No less dramatic are hypoglycemic attacks in patients who, understanding what is happening to them, are unable to perform the simplest actions- take a piece of sugar out of your pocket, drink a glass of tea, etc. The insulin therapy regimen for such persons should be such as to prevent the recurrence of hypoglycemia.
“Diabetes mellitus”, A.G. Mazowiecki
When examining a patient in a state of ketoacidemic coma, signs of dehydration attract attention. The skin is dry, cold, sometimes flaky, with traces of scratching. Lips are dry, covered with caked crusts. Facial features are pointed, eyes are deeply sunken, eyeballs soft when pressed due to dehydration. Skin turgor and skeletal muscle tone are reduced. The face is usually pale, and sometimes there is diabetic rubeosis. Body temperature…
To stimulate oxidative processes in a dropper with isotonic solution sodium chloride add a complex of vitamins: 1 ml of a 5% solution of vitamin B12, 200 mcg of vitamin HCG, 5 ml of a 5% solution of ascorbic acid, as well as 100 mg of cocarboxylase. If signs of atony and fullness of the stomach appear (bloating of the upper abdomen, splashing noise), it is necessary to empty it and rinse it with a solution of bicarbonate...
Without gastric dyspepsia Almost no case of diabetic ketoacidosis is avoided. Repeated vomiting plays an important role in aggravating water and electrolyte imbalance. However, in some patients, even in the precoma stage, intense pain in the abdomen appears, usually without clear localization, increasing, with tension in the muscles of the anterior abdominal wall and symptoms of peritoneal irritation. At the same time, it is observed dyspeptic syndrome…
The patient begins to feed after the return of consciousness. On the first day they give alkaline mineral water, potassium-rich fruits and vegetable juices, compotes, jelly. From the second day, pureed vegetables and fruits (potatoes, carrots, applesauce), crackers, kefir, pureed soups, semolina and oatmeal are allowed. From the 4th-5th day cottage cheese is included in the diet, boiled fish, pureed or chopped...
If the abdominal (pseudoperitonic) variant of ketoacidotic coma is usually observed in individuals young, then in older patients its cardiovascular (cardiovascular) form is more common. Presenter clinical manifestation- severe collapse with a significant decrease in arterial and venous pressure, tachycardia, threadlike pulse, various disorders heart rate, cyanosis and coldness of the extremities. Hypovolemia plays a leading role in the pathogenesis of this form...
Hypoglycemia is a condition of the body that is characterized by a drop in glucose levels in the blood to such levels that, first of all, brain cells and the entire body experience energy starvation due to an insufficient amount of glucose. This disrupts their functions, which are manifested by various clinical symptoms.
Hypoglycemia can be true or false (no less dangerous). With false hypoglycemia, blood sugar levels can be either normal or elevated. This is usually associated with a rapid decrease in blood sugar levels from fairly high values to low indicators, for example, from 20–25 to 10–15 mmol/l.
True hypoglycemia is characterized by blood sugar levels below 3.3 mmol/l, so it can be argued that hypoglycemia is a peculiar reaction of the body to a rapid drop in blood sugar levels below usual values. When blood sugar decreases, the formation of glucose from glycogen, as well as the action of insulin, is suppressed. Then some mechanisms are activated that help the body additionally form carbohydrates, so consciousness is gradually restored even without appropriate treatment. However, this does not mean that hypoglycemia should not be treated, because for all tissues and organs, especially for the brain, starvation occurs, which is characterized by a peculiar symptomatic picture.
Hypoglycemia causes
Hypoglycemia develops for a number of reasons, which include: increased production insulin in the pancreas; enough high rate insulin, as well as others medications in patients with diabetes mellitus; changes in the functioning of the pituitary gland and adrenal glands; disturbance of carbohydrate metabolism in the liver.
Also, hypoglycemia can be conditionally divided into a drug-dependent disease and not. As a rule, hypoglycemia, which is dependent on medications, occurs among patients diagnosed with. The second variant of the pathological condition is observed as fasting hypoglycemia, which occurs after fasting, and in the form of a reactive form of hypoglycemia, which occurs after ingesting carbohydrate foods.
Very often, hypoglycemia can be caused by insulin or sulfonylurea drugs, which are prescribed to patients with diabetes to lower blood sugar levels. If the dose of the drug is too high in relation to the food eaten, the drug can reduce sugar to too much low values. Patients getting sick severe form diabetes, are generally at risk of hypoglycemia. As a rule, this is due to insufficient production islet cells the pancreas produces glucagon, and the adrenal glands produce adrenaline. But it is these hormones that play a direct role in the mechanisms of first defense against this hypoglycemia. This disease can also be caused by other drugs.
Very often hypoglycemia is diagnosed in psychiatric unbalanced people who secretly take sugar-lowering medications or self-administer insulin. This is due to free access to medicines.
Quite severe hypoglycemia, and sometimes stupor, can be observed in persons in drunkenness, as well as those who abuse alcohol and neglect proper nutrition. As a result, the liver runs out of carbohydrates.
Stupor during hypoglycemia can occur even with a small amount of alcohol in the blood, but below the level that is allowed for driving. Therefore, it is not always the traffic police inspector or medical worker will be able to determine that a person has a stupor as a result of a disease, and not a symptom of a drunken state.
Sometimes hypoglycemia can occur in a healthy person who has had strenuous physical activity. With prolonged fasting, symptoms of hypoglycemia can occur simultaneously with pathology of the adrenal glands or pituitary gland, as well as after alcohol abuse. IN in this case is happening severe exhaustion carbohydrates, which cannot maintain normal blood glucose levels. But in some cases, hypoglycemia appears immediately after fasting. In children with a disorder of any liver enzyme system, signs of hypoglycemia occur between breakfast, lunch and dinner.
The nutritional form of hypoglycemia occurs in people who have undergone gastrectomy. In this case, sugar is absorbed too quickly, which stimulates the production of insulin, which in large quantities causes a decrease in blood sugar. If hypoglycemia of the nutritional type develops without visible reasons, then this is idiopathic nutritional hypoglycemia.
The reasons that cause the disease include some foods containing fructose or galactose, which prevent the release of glucose from the liver. And leucine is involved in stimulating excess insulin in the pancreas. Thus, these products reduce blood sugar after a certain amount of time after eating.
In addition, insulinomas can provoke hypoglycemia as a result of excessive insulin production. Very rarely, tumors that are not localized in the pancreas can cause the development of the disease.
A rare cause of a hypoglycemic state is a disease associated with an autoimmune abnormality. In this case, the body tries to produce insulin antibodies, which leads to sharp fluctuations, since the pancreas produces an excess amount of insulin to neutralize the antibodies. This condition can be found both in patients with diabetes and in those who do not have this disease.
The development of hypoglycemia may be influenced by cardiac or renal failure, severe infections, malignant pathologies in the form of tumors, irrational and poor nutrition, shock, viral and cirrhosis. All of these diseases can cause a hypoglycemic state.
Hypoglycemia symptoms
The clinical picture of hypoglycemia consists of symptoms that can be divided into certain categories. They are characterized general violations, vegetative, neurological and metabolic. It is not always possible to differentiate them and correlate blood sugar levels. But there is a certain pattern: with hypoglycemia, the glucose concentration decreases to almost 3 mmol/l. That's when they appear general symptoms and vegetative, with a small number of neurological manifestations. But when the sugar concentration is from 2.3 to 2.7 mmol/l, hypoglycemic coma develops.
The general symptoms of hypoglycemia are characterized by anxiety, headaches, irritability, nervousness, constant hunger and a burning sensation in the epigastric region. However, all these symptoms cannot indicate hypoglycemia, but with their complex combination, a hypoglycemic state can be diagnosed.
Autonomic disorders are caused by tachycardia and the appearance of muscle tremors. Then a pulsation is felt in the head and on the periphery of the body, which is associated with the rapid movement of blood.
Among autonomic disorders, adrenergic and parasympathetic symptoms are distinguished. In the first case, the clinical picture of hypoglycemia consists of the appearance of tachycardia, with a predisposition to it, pallor of the skin, hand tremors (tremor), arterial hypertension and increased respiratory rate. But the symptoms of the parasympathetic clinic consist of a feeling of hunger, rumbling in the stomach, as a result of increased peristalsis in the stomach and intestines, as well as the appearance of a burning sensation in the epigastric region. All this clinical picture characteristic of the very onset of hypoglycemia, so it is very important to always differentiate these symptoms from various pathologies metabolism.
With the neurological symptoms of hypoglycemia, there is a feeling of relative energy deficiency in the brain, which is characterized by dizziness, pain in the head and pulsation in the blood vessels. The disease then progresses to severe form, so parts of the cerebral cortex are partially turned off. Marked focal symptoms in the form of sensory disturbances in some parts of the body, and sometimes motor activity is partially lost.
One of the most severe violations Hypoglycemia is hypoglycemic coma, which develops as a result of a sharp decrease in glucose. This causes loss of consciousness with lack of sensation in the various shapes irritation, even pain. After emerging from a coma, patients experience weakness throughout the body, a feeling of fear and disorientation, tremors in the muscles, inappropriate behavior, appear pathological reflexes. Sometimes, with deep damage to the cerebral cortex, patients do not remember everything that happened before the onset of hypoglycemic coma.
All these symptoms are observed until loss of consciousness. But the patient does not have time to notice this, since consciousness switches off quite quickly. It is this clinical picture that makes it possible to differentiate hypoglycemic coma from hyperglycemic, ketoacidotic and hyperosmolar coma. They are characterized by a gradual loss of consciousness with a number of neurological, general and metabolic signs.
Signs of hypoglycemia
In hypoglycemia, a distinction is made between a hypoglycemic state and a hypoglycemic coma. Signs of the disease do not always appear gradually. Sometimes, even suddenly, a soporous manifestation of hypoglycemia, convulsions or acute form psychotic syndrome.
Signs initial stage hypoglycemia are severe hunger, hand tremors and autonomic disorders in the form of sweating, headaches, general condition weakness, increased heart rate, causeless irritability, aggressiveness and fear. If these signs are not eliminated in a timely manner with the help of foods that contain easily absorbed carbohydrates, some others, characteristic of this state signs. Among them are tremors in the body, profuse sweating, double vision, fixed gaze and hemiplegia.
Hypoglycemia is characterized by signs of mental reactions, namely: aggression, agitation, inability to navigate around, and sometimes hallucinations. Very often these signs are mistaken for intoxication, as a result of alcohol, or hysteria. If the hypoglycemic state is not eliminated at this stage, then convulsive contractions of some muscle groups, in particular, in the facial area, and the excited state also intensifies, vomiting appears with one or two-sided Babinski's symptoms, clonic and tonic convulsions that provoke epilepsy, blackouts also occur and then coma occurs.
A characteristic sign of hypoglycemia is a change in the cardiovascular system, which is expressed in a decrease in blood pressure, the appearance of an increased heart rate, arrhythmia in the form of extraordinary contractions of the heart, less often a low heart rate, sinus arrhythmia. And the ECG shows suppression of the S-T segment, and the amplitude of the T wave decreases. Patients with a sharp decrease in blood sugar levels experience angina attacks. The blood shows slight leukocytosis and lymphocytosis, and sometimes leukopenia.
In the compensated form of diabetes mellitus, hypoglycemia has negative values of sugar in the urine and a reaction to acetone. But hypoglycemia of decompensated diabetes is characterized by an increase in hormones such as glucocorticoids, growth hormone, catecholamines and ACTH, which help develop ketoacidosis and form acetone in the urine.
Another sign of hypoglycemia is hypoglycemic coma, which is characterized by sweating, wet skin, pale face, increased muscle tone, trembling, increased tendon reflexes and convulsions. Also, in particular, diastolic blood pressure decreases, the pupils dilate, the eyeballs are in normal tone or slightly decreased, mental signs with delusional hallucinations are noted. Blood sugar levels are quite low and there is no acetone in the urine. Sometimes, during studies at the beginning of the disease, a slight sugar content in the urine of about 1% may be detected. And repeated laboratory research after 30 minutes they give a negative answer with urinary sediment without changes.
Hypoglycemia in children
This condition in children does not apply to rare pathology. Very often, the causes of childhood hypoglycemia can be various diseases of the nervous and endocrine systems, as well as stress, physical activity and other balanced diet.
Symptoms of a hypoglycemic state in children manifest themselves in the form of lethargy, drowsiness, irritability, pallor, sweating, hunger and heart rhythm disturbances. Blood sugar levels are less than 2.2 mmol/l.
Hypoglycemia is very dangerous for a child’s life, as it disrupts the body’s metabolism and coordination of movement, provokes pain in the head, and contributes to the appearance of seizures and fainting. Frequent hypoglycemic attacks negatively affect mental and physical development children.
As a rule, hypoglycemia in children can occur like other diseases. Thus, it is necessary to thoroughly examine the child, since the younger his age, the more often he may experience dangerous defeats nervous system, mental retardation or epileptic seizures as a result of the sensitivity of its nerve cells to blood sugar variability.
Older children experience the same symptoms of hypoglycemia as adults. For them this manifests itself in the form anxiety state, pallor of the face, chills throughout the body, blurred vision and loss of coordination. In addition, convulsions appear, tachycardia becomes more frequent, they experience strong feeling hunger and lose consciousness.
There are two underlying reasons development of childhood hypoglycemia, such as increased levels of ketone bodies in the blood and leucine intolerance.
During hypoglycemia in children, acetone appears in the blood in the form of ketone bodies, which is characterized by a peculiar acetone smell from mouth. Since acetone is a toxic substance, the corresponding signs of its effect on the nervous system are poisoning with nausea, vomiting, dizziness and fainting. In this situation, the child’s stomach is washed soda solution or mineral water, causing vomiting. And to replenish glucose, give a little honey or sugar, or maybe tableted glutamic acid. After suffering an attack, the child must be monitored by a specialist; he must constantly measure blood sugar, as well as have a urine test done for the presence of ketone bodies.
Used for the treatment of children with hypoglycemia balanced diet with the exception of animal fats and simple carbohydrates. Preference is given to dairy products and seafood, juices, fruits and vegetables. It is important to take food seven times a day and in small quantities.
IN in rare cases As a result of congenital metabolic disorders, children experience incompatibility of the body with the leucine amino acid, which is part of proteins. This phenomenon is called leucine hypoglycemia, which occurs mainly in young children. Not a large number of Something sweet may improve the patient's situation a little. But a balanced diet with this form of hypoglycemia is very difficult to maintain, since the growing body constantly needs protein. As a general rule, you should exclude eggs and milk, as well as pasta, nuts and fish. Therefore, to create a diet for sick children with leucine hypoglycemia, the help of a nutritionist is necessary.
It is important to remember that early identification of symptoms of hypoglycemia in a child will allow its causes to be detected as early as possible, and this will lead to a successful treatment outcome. Also, to avoid complications with childhood hypoglycemia, it is necessary to monitor the amount of blood sugar and its stable content.
Hypoglycemia treatment
The period of treatment of hypoglycemia in the first stage, before hospitalization of the patient, consists of sufficient intake of food that contains carbohydrates and is included in the patient’s usual diet with the presence of sweet tea and fruit juices.
In the second stage of hypoglycemia, it is necessary to immediately consume foods with easily digestible carbohydrates, such as jam, compote with sugar, sweet tea, candies, fruit syrup. As a rule, such foods containing fructose and sucrose prevent the progression of the hypoglycemic state and normalize the glycemic level and the patient’s condition. Without certain indications, patients are not hospitalized.
In the third stage of hypoglycemia, in order to provide effective emergency assistance, it is necessary to immediately administer intravenously a 40% Glucose solution up to 100 ml to avoid the occurrence of brain swelling. The patient is usually hospitalized in this condition in order to prevent the early consequences of hypoglycemia and adjust sugar-lowering therapy.
Hypoglycemic coma or the fourth and fifth stages of hypoglycemia are treated either in the intensive care unit or in the intensive care unit. For this form of hypoglycemia, an intravenous jet of 80–100 ml of a 40% Glucose solution and an intramuscular injection of 1 ml of Glucagon are first prescribed, followed by an intravenous drip of 200 to 400 ml of a 5% Glucose solution. Be sure to maintain blood sugar levels between 6 and 9 mmol/l. If it is not possible to achieve effectiveness in treatment, Adrenaline is administered subcutaneously. Basically, all these manipulations restore the patient’s consciousness. It is only important to remember that the administered hormones are closely related to the action of endogenous glucose, as well as glycogen from the liver. Thus, frequent use of these drugs is not recommended, as this may worsen the patient's condition.
If the measures taken do not restore the patient’s consciousness, then hydrocortisone is administered intramuscularly or intravenously. As a rule, after this the patient’s condition stabilizes, but consciousness does not return immediately. In this case, the administration of Glucose and Insulin continues, and Potassium preparations are taken. To improve the processes of glucose utilization, Ascorbic acid is introduced.
WITH for preventive purposes For cerebral edema, slow intravenous administration of magnesium sulfate or intravenous drip administration of Mannitol from 200 to 250 ml is used. Patients are also given oxygen therapy. Sometimes fresh donor blood is transfused.
As soon as the patient is brought out of the coma, he is prescribed drugs that improve the processes of microcirculation and stimulation of proteins and carbohydrates in the cells of the central nervous system. These include Glutamic acid, Cerebrolysin, Aminalon, Cavinton for three to six weeks, according to indications.
To prevent hypoglycemia, it is necessary to prescribe adequate hypoglycemic therapy using Insulin, thus, overdose of the drug must be avoided. And the second component of prevention is the correct distribution of carbohydrates in the diet, as well as moderate regulation of physical activity throughout the day and additional consumption of carbohydrates.
Diet for hypoglycemia
It is believed that postprandial hypoglycemia is favorably influenced by limited carbohydrate intake in the diet. Although the methods of such control in dietary treatment have never been carried out. However, if you look from a physiological point of view, this approach can have positive results, because attacks of hypoglycemia usually develop after eating glucose-containing foods.
Dietary measures can help most patients, especially in the first stages of the disease, in which medications in rare cases.
There is some controversy regarding the degree of carbohydrate restriction. One category of authors adheres to a diet with a fairly small amount of carbohydrates, about one hundred grams. But they cause ketosis, impair glucose tolerance and reduce amino acid storage after eating protein. Incredibly, even healthy people who adhere to such a diet heavy load glucose can become hostage to hypoglycemia. It is for this reason that the intake of carbohydrates cannot be completely excluded, as this can provoke the appearance of characteristic clinical symptoms if you don't follow a diet. Therefore, treatment begins with a slight restriction of carbohydrates from 120 to 150 g.
It is very important to limit not only the amount of carbohydrates, but also the type of foods that contain them. It is absolutely necessary to exclude simple sugars. Carbohydrates should be consumed as starch in foods such as pasta, bread, potatoes, rice, which should be consumed before three times per day in small portions with the same number of snacks in the form of light snacks. If you are unable to achieve success using this dietary nutrition, then resort to greater carbohydrate restriction.
In some cases, diet has no effect at all positive results, and sometimes even worsens the symptoms of hypoglycemia, which should make the doctor wary about fasting hypoglycemia or, in general, talk about the absence of this disease with corresponding patient complaints. If dietary nutrition is ineffective in limiting carbohydrates and in the absence of hypoglycemic genesis, drug therapy is prescribed.
As a rule, for hypoglycemia it is prescribed. In this case, conditions are created that normalize the metabolism of carbohydrates in the body. Dishes are prepared from certain foods that contain small amounts of both carbohydrates and fats. It is strictly forbidden to consume sugar, honey and jam, as well as various sweets and confectionery. These products are used to relieve attacks of hypoglycemia, or as a snack before significant physical activity.
The peculiarity of the diet for hypoglycemia is that it is necessary to keep a daily diary calculating the amount of fats, carbohydrates and proteins in food. It is also important to control chemical composition dishes.
Patients diagnosed with diabetes mellitus generally have a significantly increased appetite and are in a state of constant feeling hunger. Thus, patients with this diagnosis need to eat dishes that satiate the stomach, contain a large amount of fiber, but with low calorie content, that is, vegetables.
On the menu daily ration for the treatment of hypoglycemia in diabetes mellitus should include products such as black (240g) or White bread(180g), butter(15g), vegetable oil(10g), carrots (200g) or apples, potatoes (200g), pasta (20g), cereal (60g), cheese (20g), egg (1 pc.), fish, boiled or baked meat. Sugar is replaced with sweeteners.
The products are subject to normal culinary processing, but it is advisable to limit the consumption of fried foods and not to over-salt the food. In addition, the body must receive sufficient amounts of vitamins, especially from group B and ascorbic acid. Meals should be small and frequent. Almost half of the diet should include carbohydrates, and these are legumes, cereals, fruits, grains, and pasta. Of course, it is better to give preference to foods that are rich in fiber, as they gradually increase the amount of glucose in the blood.
The hypoglycemic state is associated with a decrease in blood glucose levels - hypoglycemia. This acute pathological condition develops mainly during competitions in long and ultra-long distance running, during long-hour road races in cycling, when cross-country skiers cross long distances, during marathon swims, etc.
As is known (see the biochemistry textbook), carbohydrates are the main sources of energy that provide intense muscle activity. Their oxidation requires significantly less oxygen than, for example, the oxidation of fats. Carbohydrates in the form of glycogen are found in the liver and skeletal muscles. Total such reserves are usually about 400 g, of which in the liver - up to 100 g.
During physical activity, due to the release of adrenaline, glycogen is converted into glucose, which is delivered by blood from the liver to the nervous system and working muscles.
IN normal conditions Blood glucose levels range from 80 to 120 mg%. Prolonged and intense physical activity leads to a decrease in blood sugar. If it's just a little smaller lower limit norms, no pathological reactions are observed in athletes. If the blood sugar level decreases significantly, to 40 mg% and below (V.S. Farfel), a dangerous hypoglycemic state may develop. The reason for this is a decrease in the delivery of glucose to the central nervous system, which does not have reserves of this carbohydrate. As a result, its work is disrupted and a complex of nonspecific and specific symptoms for the activity of the nervous system is revealed.
One of the early signs of a hypoglycemic state is an acute feeling of hunger. Then weakness and dizziness develop, and the athlete breaks out in a cold sweat. Following this, there appear specific symptoms, indicating serious violation functioning of the central nervous system: confusion, speech impairment, an athlete at a distance can perform ridiculous actions (for example, suddenly change the direction of movement and continue running from finish to start).
When observing an athlete with a developing hypoglycemic state, attention is drawn to the pallor of the skin (sometimes they acquire a greenish color), the pupils dilate, practically do not react to light, the pulse is difficult to palpate, and blood pressure drops sharply.
A hypoglycemic state develops more often in insufficiently trained athletes. Pathological signs may appear in them when the blood sugar level drops to 65-60 mg%.
Insufficient acclimatization to unusual competition conditions plays a certain role in the development of a hypoglycemic state. Poor readiness to participate in competitions in high altitudes, in unusually warm or cold conditions, and disruption of biorhythms due to long-distance travel may play a role here. The nutritional regime preceding the competition is also important.
In highly qualified athletes, a hypoglycemic state can develop during participation in competitions in a state of fatigue or when admission to them is untimely after illness.
All of the above refers to predisposing factors. Along with them, it is important good nutrition before the start of the competition and during the distance. Performing long hours of work without specialized nutrition is unacceptable. Eating carbohydrates before the start of competition is necessary in order to increase the body's carbohydrate reserves. Thus, before long and ultra-long distance competitions, it is recommended to take sugar, but its amount should not exceed 100-120 g. The fact is that when there is an excess amount of sugar in the blood, it begins to be excreted by the kidneys. In addition, a large amount of glycogen increases the athlete’s own weight, since 1 g of this substance binds 2.7 g of water. Therefore, increasing the glycogen reserve, for example to 700 g, increases the athlete’s weight by 2 kg (Astrand). Thus, taking excess sugar is ineffective.
Nutrition at a distance is provided in the form of liquid mixtures containing required amount easily digestible carbohydrates (at a distance of 50 km, a skier can take up to 1 liter of a mixture containing 350 g of sugar). IN as a last resort the liquid mixture can be replaced with lump sugar or chocolate. The number of nutrition points depends on the length of the distance. The first such point can be organized already at the 10-15th kilometer of the distance, depending on the type of sport (but no further than at the 25th kilometer). During marathon races, feeding stations can be located every 5 km, and during cross-country skiing at 50 km - somewhat less often.
A moderate hypoglycemic state can also be observed immediately after competitions and training. To prevent its development, it is advisable to take carbohydrates after the finish.
If a hypoglycemic state develops, it is necessary to provide assistance to the victim. First of all, you should invite him to drink a glass of warm sugar syrup with bread or eat a few lumps of sugar or granulated sugar washed down with water. If a more severe hypoglycemic state develops, accompanied by confusion, immediate medical attention is required.
Hypoglycemia is a condition of the body caused by a sharp decrease in blood sugar levels and insufficient supply of glucose to the cells of the central nervous system. The most severe manifestation of a hypoglycemic state is hypoglycemic coma.
Hypoglycemic conditions in diabetes mellitus can occur due to:
a) overdose of administered insulin or sulfonamide antihyperglycemic drugs.
b) eating disorders due to untimely eating after an insulin injection or eating food with an insufficient amount of carbohydrates,
c) increased sensitivity to insulin (especially in childhood and adolescence),
d) decreased insulin-activating ability of the liver and kidneys (insufficient production of insulinase or activation of its inhibitors);
e) alcohol intoxication (slowing down the breakdown of glycogen);
f) chronic renal failure (increased circulation time of glucose-lowering drugs as a result of slower excretion in the urine);
g) compensatory insulinism on early stages diabetes mellitus;
h) taking salicylates, sulfa drugs, adrenergic blockers when prescribed in combination with insulin or tableted hypoglycemic drugs.
Pathogenesis
The basis of the pathogenesis of hypoglycemia is a decrease in glucose utilization by CNS cells. It is known that free glucose is the main energy substrate for brain cells. Insufficient supply of glucose to the brain leads to the development of hypoxia with subsequent progression of metabolic disorders of carbohydrates and proteins in the cells of the central nervous system. Different parts of the brain are affected in a certain sequence, which determines the characteristic change in symptoms as the hypoglycemic state progresses. First of all, the cerebral cortex suffers from hypoglycemia, then the subcortical structures, the cerebellum, and ultimately the functions of the medulla oblongata are impaired.
The brain receives its nutrition from carbohydrates, but little glucose is deposited in it. The energy needs of CNS cells are high. Brain tissue consumes 30 times more oxygen than muscle tissue. Glucose deficiency is accompanied by a decrease in oxygen consumption by the cells of the central nervous system, even with sufficient oxygen saturation in the blood, and therefore the symptoms of hypoglycemia are similar to the signs of oxygen deficiency.
In the pathogenesis of hypoglycemia, the decisive factor is the ability to utilize glucose, therefore hypoglycemic states can be observed even with normal blood glucose levels, but when the processes of glucose entering the cell are suppressed. Due to a lack of glucose in the cells of the most differentiated parts of the brain (cortex and diencephalic structures), irritability and anxiety occur. Dizziness, drowsiness, apathy, inappropriate speech or behavior. In case of damage to phylogenetically more ancient parts of the brain (medulla oblongata, upper parts of the spinal cord), tonic and clonic convulsions, hyperkinesis, inhibition of tendon and abdominal reflexes, anisocoria, and nystagmus develop.
Hypoglycemia is an adequate stimulator of the sympathoadrenal system, which leads to an increase in the content of catecholamines in the blood. This is manifested by characteristic autonomic symptoms: weakness, sweating, tremor, tachycardia. At the same time, hypoglycemia causes irritation of the hypothalamus with subsequent activation of contrainsular neurohormonal systems (corticotropin - glucocorticoids - somatotropin). An increase in the activity of the contrainsular systems is a compensatory reaction of the body aimed at eliminating hypoglycemia. A significant place in the elimination of hypoglycemia through self-regulation belongs to glucagon, which activates the breakdown of glycogen, primarily in the liver.
Prolonged carbohydrate starvation and brain hypoxia are accompanied not only by functional, but also by morphological changes, including necrosis or edema of certain areas of the brain. Excess catecholamines during hypoglycemia leads to disruption of cerebral vascular tone and blood stasis in them. Slowing blood flow leads to increased thrombus formation with subsequent complications. It has been suggested that one of the causes of neurological disorders during hypoglycemia may be a decrease in the formation of amino acids and peptides necessary for normal neuronal activity. It should be remembered that a hypoglycemic state promotes ketogenesis. The mechanism here is as follows: with a decrease in blood glucose and the development of energy deficiency, the secretion of catecholamines and somatotropin increases, increasing lipolysis, which creates conditions for the accumulation of β-hydroxybutyric and acetoacetic acids in the blood - the main substrates of ketosis.
Depending on the individual sensitivity of the central nervous system to glucose deficiency, a hypoglycemic state occurs when different levels glycemia – from 4.0 to 2.0 mmol/l and below. In some cases, hypoglycemic conditions can develop with a rapid decrease from very high level(for example, from 20 or more mmol/l) to normal and even slightly increased blood glucose levels (5.0-7.0 mmol/l).
Clinical picture
The development of hypoglycemic coma is preceded by the following: clinical stages hypoglycemia:
1st stage
Pathogenetically caused by hypoxia of cells of the higher parts of the central nervous system, mainly the cerebral cortex.
Clinical signs are very varied. They are characterized by agitation or depression, anxiety, mood changes, and headaches. During an objective examination, moisture in the skin and tachycardia can be noted. Unfortunately, not all patients experience a feeling of hunger, and therefore do not regard their condition as a manifestation of a hypoglycemic reaction.
2nd stage
Its pathogenetic basis is damage to the subcortical-diencephalic region.
Clinical symptoms are characterized by inappropriate behavior, mannerisms, motor agitation, tremor, profuse sweating, severe tachycardia and arterial hypertension; headache, uncontrollable hunger, but consciousness at this stage is not impaired.
3rd stage
Hypoglycemia is caused by a violation of the functional activity of the midbrain and is characterized by a sharp increase in muscle tone, the development of tonic-clonic convulsions reminiscent of an epileptic seizure, the appearance of Babinski's symptom, and dilated pupils. Pronounced moisture of the skin, tachycardia and high blood pressure remain. Sometimes delusions and hallucinations are added.
The course of this stage may be accompanied by the development of either depression or aggressiveness in the patient’s behavior.
4th stage
Associated with damage to the upper parts of the medulla oblongata (coma itself) - characterized by muscle hypertonicity with the development of convulsive syndrome and loss of consciousness.
Tendon and periosteal reflexes are increased. The tone of the eyeballs is also increased, the pupils are dilated. Skin wet. Body temperature is normal or slightly elevated. Breathing is normal, the smell of acetone is usually absent. Heart sounds may be increased, the pulse may be rapid, and blood pressure may be elevated or normal.
5th stage
Damage to the lower parts of the medulla oblongata is characterized by deep coma, hypotension, tachycardia; the respiratory and vasomotor centers can be involved in the process, and then death occurs.
The clinical picture of this stage reflects the progression of the comatose state. In this case, areflexia is observed. Muscle tone decreases, profuse sweating stops, breathing problems, a drop in blood pressure, and heart rhythm disturbances may occur.
It should be emphasized that in some cases atypical hypoglycemic reactions are observed, the pathogenetic basis of which is damage to the limbic-reticular region. In such cases, clinical signs of hypoglycemia are characterized by nausea, vomiting, bradycardia, and euphoria.
A life-threatening condition that accompanies hypoglycemia is cerebral edema. The development of cerebral edema is caused by several factors: late diagnosis coma, erroneous administration of insulin or overdose of hypertonic (40%) glucose solution.
The clinical picture of cerebral edema is characterized by meningeal symptoms, vomiting, fever, respiratory and heart rhythm disturbances.
The consequences of hypoglycemic conditions can be divided into early and late. The first develop several hours after a hypoglycemic state. These include hemiparesis, hemiplegia, aphasia, myocardial infarction and cerebrovascular accident.
Long-term effects are observed several days, weeks or months after the development of a hypoglycemic state. They are manifested by encephalopathy, progressing with repeated hypoglycemia, epilepsy, and parkinsonism.
A hypoglycemic state due to alcohol intoxication is particularly dangerous in terms of adverse consequences.
An essential diagnostic criterion for a hypoglycemic state is a positive reaction to intravenous glucose.
Treatment (pre-hospital)
To relieve the first stage of a hypoglycemic state, a meal containing carbohydrates is sufficient. Included in the patient’s usual diet (bread, porridge, potatoes, jelly).
At the second stage of hypoglycemia, additional easily digestible carbohydrates (sugar, jam) are needed. Typically, a quick meal containing sucrose and fructose. Allows you to prevent the progression of a hypoglycemic state and normalize the level of glycemia and the patient’s condition. If there are no special indications, patients do not require hospitalization.
To provide effective emergency care at stage 3 of a hypoglycemic state, immediate administration of a 40% glucose solution is required in the amount necessary to completely eliminate the clinical symptoms of a hypoglycemic state, but not exceeding 80 ml (to avoid cerebral edema). The patient must be hospitalized to prevent the early consequences of hypoglycemia and adjust the dose of glucose-lowering therapy.
Treatment of stages 4 and 5 (hypoglycemic coma) is carried out in the intensive care unit.
Loading...
