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  • Complications of diabetes mellitus

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    Acute complications of diabetes mellitus

    Acute complications of diabetes mellitus pose a serious threat to life. Acute complications include hyperglycaemic and hypoglycemic coma. The most often develops a state of hypoglycemia, which occurs with a rapid decrease in the glucose level in the blood. Hyperglycemic coma( due to excessive increase in blood sugar) is divided into ketoacidotic, hyperosmolar and hyperlactacidemic( lactic acid).

    Ketoacidosis and ketoacidotic coma

    Diabetic ketoacidosis is an acute disturbance of metabolic processes as a result of progressive insulin deficiency, which is manifested by a sharp increase in the level of glucose and ketone bodies in the blood, as well as by the development of metabolic acidosis( shift of blood pH to the acid side as a result of accumulation of toxicproducts of disturbed metabolism).

    The metabolic disorder during the development of ketoacidosis proceeds in several stages. The first stage - the violation of metabolic processes - is manifested by the presence of signs of excessive blood sugar and the appearance of sugar in the urine( in the norm it is not).The second stage is ketoacidosis. There is a progression of the metabolic disorder, symptoms of intoxication are observed, which is expressed by oppression of consciousness in the form of stun or confusion, as well as other characteristic manifestations. At laboratory inspection the raised or increased level of Saccharum of a blood, sharply positive reaction to acetone in urine is marked. The third stage is the precommission. There is a more pronounced depression of consciousness, down to stupor. The fourth stage is a coma. There is a profound violation of all kinds of metabolism, consciousness is completely absent. This state is a threat to life. Quite often, acute metabolic disorders in diabetes mellitus, which are accompanied by high levels of sugar, the appearance of ketones in the urine( see above), acidosis( shift of blood pH to the acid side), and violation of consciousness of any degree are combined with the term "diabetic ketosis".This condition is most typical for type I diabetes mellitus.

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    In most cases, the state of ketoacidosis develops as a result of a change in treatment regimen in the form of a long pass or complete unauthorized withdrawal of medications. For the most part, people with diabetes mellitus do so in the absence of appetite, fever, nausea, vomiting. Quite often a break in taking tablets of sugar-reducing drugs is several months or even years. The second place among the causes of the development of ketoacidosis is occupied by acute inflammatory diseases, exacerbation of chronic and infectious diseases. There can be a combination of both. Also, the development of ketoacidosis can be caused by errors in the treatment of insulin preparations, such as inadequate dosage or the administration of an unfit drug. Both the cause and the effect of ketoacidosis can be myocardial infarction and stroke. The development of ketoacidosis is possible in pregnancy, when there is an increase in the need for insulin and the appearance of relative resistance of tissues to it. Ketoacidosis occurs in a stressful state, such as shock, sepsis, trauma, surgery.

    The main role in the development of ketoacidosis belongs to a sharp deficiency of insulin. As a result, there is a decrease in the intake of glucose into the cells and, as a consequence, its blood level rises. When the utilization of glucose by cells in tissues is impaired, energy hunger develops. This causes an increase in the release of blood hormones such as glucagon, cortisol, adrenaline. These hormones have an effect opposite to insulin, that is, they cause an increase in the processes of glucose formation in the liver. The resulting glucose enters the bloodstream, as a result of which its level rises even more. Hyperglycemia leads to the fact that the fluid from the cells goes into the vascular bed. If a certain threshold is exceeded, glucose enters the urine, that is, glucosuria develops. Together with it, water and electrolytes( sodium, potassium, calcium, fluoride, chlorides) enter the urine. As a result, the dehydration of the body, severe electrolyte disorders develop, there is a thickening of blood, leading to the formation of blood clots. As a result of severe dehydration and a decrease in the volume of circulating blood in the vessels, the intensity of renal and cerebral blood flow decreases, resulting in insufficient intake of oxygen to these organs.

    Reduction of renal blood flow causes a decrease in the amount of urine, which leads to a rapid increase in blood glucose."Oxygen starvation" of tissues causes a metabolic disorder, resulting in the accumulation of excess lactic acid in the body - lactate. The excess of this substance helps to shift the pH of the blood to the acidic side. In addition, the activation of fat splitting in adipose tissue occurs. As a result, the blood increases the content of free fatty acids, which in excess enter the liver. Free fatty acids in this case are the main source of energy. As a result of numerous chemical transformations, ketone bodies( acetic acid, acetone) are formed from them. The number of ketone bodies in the blood is rapidly increasing, which is associated not only with the increase in their formation, but also with the fact that their excretion from the body decreases with urine. Ketone bodies, as well as lactate, contribute to a shift in blood pH to the acid side. This condition manifests itself as a violation of breathing, as well as the appearance of pain in the abdomen. Also, with diabetic ketoacidosis, heart function is disrupted, digestive system disorders occur, and many others leading to cerebral edema. First of all, in the case of metabolic disorders, the central nervous system suffers, which is manifested by a progressive impairment of consciousness.

    The development of ketoacidotic coma is preceded by three stages: ketosis, ketoacidosis, precoma. Each stage as it approaches comatose state is characterized by aggravation of metabolic disorders, which leads to greater inhibition of consciousness. The ketoacidotic coma in most cases develops over several days. The stages of ketosis are characterized by the following symptoms: dryness of the mucous membranes and skin of a progressive nature;thirst appears;the amount of urine released increases, the weakness grows;decreased appetite and body weight;there is a headache and increased drowsiness. The surrounding may note the presence in the exhaled air of a weak odor of acetone. To detect ketosis, urine analysis must be performed, in which ketonic bodies are detected in this disorder. With the progression of metabolic disorders, the stage of ketoacidosis develops. It is manifested by the appearance of signs of excess fluid loss by the body: dryness of the mucous membranes, tongue, skin, muscle tone and skin turgor is reduced, there is a tendency to lower blood pressure, palpitations increase, and urine output decreases. In most cases, as a result of intoxication, nausea and vomiting appear. With the progression of ketoacidosis, vomiting becomes more frequent, exacerbating the dehydration of the body. Usually emetics have a blood-brown hue. The rhythm of breathing is disturbed. The smell of acetone in the exhaled air is more clearly defined. There is an expansion of the blood capillaries, which causes the appearance of a diabetic blush. Quite often there are pains in the abdomen without a clear localization, there is a strain of the muscles of the anterior abdominal wall. These symptoms appear as a result of irritation of the peritoneum and solar plexus by ketone bodies, small hemorrhages in the peritoneum, as well as violations of the motor activity of the intestine. The stage of precoma differs in the progression of the disturbance of consciousness, aggravation of dehydration and intoxication. In the absence of treatment, the lesion of the central nervous system progresses, which ends with the development of coma. Coma is characterized by a complete lack of consciousness. There is a sharp smell of acetone, breathing is disturbed, the face is pale, a blush appears on the cheeks. Characteristic signs of dehydration: dryness of mucous membranes, tongue, and skin. Turgor tissues are reduced, as well as muscle tone and eyeballs. Arterial pressure is reduced, the pulse is frequent, weak. Reflexes and all kinds of sensitivity are reduced or absent, which depends on the depth of the coma.

    Treatment of this condition is carried out exclusively in the intensive care unit.

    Hyperosmolar coma

    A condition in which an elevated blood content of compounds such as sodium and glucose is called hyperosmolarity. As a result of insufficient intake of these substances, a rather distinct pressure difference exists between the outside and intracellular fluid inside the cells. As a result, first the excess fluid loss of cells develops, which further leads to a general dehydration of the body. Dehydration is primarily the cells of the brain. The greatest risk of development of hyperosmolarity occurs in type II diabetes, most often in elderly streets.

    The development of hyperosmolar coma provokes dehydration and insulin deficiency. Dehydration, in turn, provokes such conditions as vomiting, diarrhea, acute pancreatitis or cholecystitis, blood loss, prolonged use of diuretics, impaired renal function, etc. To increase insulin deficiency in diabetes mellitus, various injuries, surgical interventions, long-term use of hormonalpreparations.

    The appearance of signs of hyperosmolar coma occurs slowly - a few days or weeks. Initially, there is an increase in signs of diabetes mellitus, such as thirst, weight loss and an increase in the amount of urine. At the same time, there are muscle twitchings, which are constantly amplified and turn into convulsions of local or generalized nature. Violations of consciousness can be noted already in the first days of the disease. First, these disturbances are manifested by a decrease in orientation in the surrounding space. Constantly progressing, disturbances of consciousness can go to a state of coma, which is preceded by the appearance of hallucinations and delirium. Hyperosmolar coma is characterized by the fact that signs of damage to the nervous system are very diverse and are manifested by convulsions, paresis and paralysis, speech disorders, the appearance of involuntary movements of eyeballs, signs of meningitis. Usually the aggregate of these signs is considered as an acute disorder of cerebral circulation. Externally, you can identify the manifestation of pronounced dehydration of the body: dry skin and visible mucous membranes;turgor of the skin, muscle tone and tone of the eyeballs are reduced;pointed facial features. Breathing becomes superficial, frequent. The smell of acetone in the exhaled air is absent. There is a decrease in blood pressure, a frequent pulse. Quite often the body temperature rises to high figures. Usually the final stage is the development of shock, the cause of which are severe circulatory disorders.

    Treatment of this type of coma is also carried out in conditions of intensive care units.

    Lactacidosis and hyperlactacidemic coma

    Lactacidosis is a state of shifting the pH of the internal environment of the body to the acidic side, which results from an increased content of lactic acid in the blood. The development of lactic acidosis can be triggered by various diseases and conditions, which are accompanied by a decreased intake of oxygen to the tissues of the body, as well as an increase in the intensity of formation and a decrease in the utilization of lactic acid. The more frequent development of lactic acidosis in diabetes mellitus is explained by the fact that it promotes the state of chronic oxygen starvation of tissues. In addition, quite often patients with type II diabetes, especially the elderly, have several concomitant diseases. Most often, such diseases are pathologies from the cardiovascular system, which are characterized by a state of chronic hypoxia.

    Lactacidosis initially manifests increased fatigue, increasing weakness, drowsiness, nausea, vomiting. These signs resemble decompensation of diabetes mellitus. The main symptom that can cause suspicion of lactic acidosis is the appearance of muscle pains, which are caused by the accumulation of lactic acid in them. The expressed disturbance of a condition can develop literally in some hours. Usually its signs are a violation of breathing, the expansion of peripheral vessels, a sharp decrease in blood pressure, heart rhythm disturbances, confusion, stupor or coma. The cause of death in lactacidosis is, as a rule, acute cardiovascular failure or respiratory arrest.

    Treatment is conducted in the intensive care unit.

    Hypoglycemia and hypoglycemic coma

    Hypoglycemia most often complicates the course of diabetes in those people who receive insulin or tableted hypoglycemic agents. Hypoglycemia is a syndrome caused by a pathologically low level of glucose in the blood. Hypoglycemia can be easy when it can be adjusted by taking enough carbohydrates. In the case of severe hypoglycemia, loss of consciousness is noted, which requires intravenous glucose. Especially often, the condition of hypoglycemia develops in elderly people with type II diabetes and who receive glibenclamide group preparations with a hypoglycemic aim. Quite often, hypoglycemia in such people is repeated periodically. The extreme manifestation of the hypoglycemic state is a hypoglycemic coma. It is defined as an acute condition, threatening to life, caused by a rapid and pronounced decrease in the level of glucose in the blood, which in turn causes the development of energy starvation of the cells of the body, edema of the brain substance, and in far-reaching cases - death of the cortex oreven the brain itself. Typically, hypoglycemia in diabetes mellitus occurs with a rapid decrease in glucose levels to the lower limit of normal - 3.3 mmol / l. However, signs of hypoglycemia can develop already at a blood sugar level of 4.6 mmol / l. In such cases, there is a pronounced difference in blood sugar levels over a short period of time.

    The main reason for the development of hypoglycemia is the excess of insulin in the body in relation to the amount of carbohydrates coming from food or from other sources( the production of glucose by the liver), as well as the accelerated utilization of carbohydrates in intensive muscular work. The development of hypoglycemia is triggered by the following factors: excessive physical stress, alcohol consumption, a violation of a diet in the form of an improper diet or insufficient carbohydrate intake, and an overdose of insulin or tableted hypoglycemic drugs. Development of hypoglycemia is facilitated by the first trimester of pregnancy, childbirth, chronic hepatitis and hepatosis in diabetes mellitus, kidney disease with kidney failure, insufficiency of the adrenal cortex and thyroid gland, as well as taking certain medications, for example salicylates.

    Reducing blood glucose primarily affects the state of the central nervous system. With the lowering of blood glucose level below the physiological level, its intake into the brain cells decreases, which leads to their energy starvation. This condition is called neuroglycopenia. It manifests itself at different stages with various neurological disorders, which ultimately lead to loss of consciousness and development of coma. Separate structures of the central nervous system have different sensitivity to energy hunger. Initially, hypoglycemia affects cells of gray matter located in the cerebral cortex, because they have the greatest intensity of metabolic processes. This fact explains the appearance of neuroglycopenia symptoms with any more or less pronounced decrease in blood glucose level. The least sensitive to hypoglycemia are such centers as respiratory and vasomotor. This explains the fact that breathing, vascular tone and cardiac activity persist for a long time even in cases when prolonged hypoglycemia leads to an irreversible loss of the cerebral cortex. All compensatory mechanisms that activate when the state of hypoglycemia develop can maintain the viability of the brain for a relatively short period of time. If the duration of hypoglycemic coma is less than 30 minutes, then, with adequate treatment and rapid recovery of the consciousness of complications and consequences, as a rule, is not observed. Prolonged hypoglycemia represents a danger to life. As a result of prolonged energy starvation, edema of the brain material develops, small-scale hemorrhages develop in the brain tissues. Ultimately, these changes are the cause of violations in the cells of the cortex, and subsequently - their deaths.

    Hypoglycemic coma is characterized by sudden development against a background of satisfactory condition. The development of coma is preceded by a state of mild hypoglycemia, which can be eliminated by the intake of a sufficient amount of carbohydrates. The period of hypoglycemia is accompanied by the appearance of coma harbingers. They are manifested by a number of signs, such as excessive sweating, hunger, anxiety, anxiety, palpitation, dilated pupils and increased blood pressure. If the state of hypoglycemia develops, nightmares begin to disturb during sleep. Quite often, the first signs of neuroglycopenia appear, which include inadequate behavior, disorientation in the space, aggressiveness, mood changes, amnesia, dizziness and headache, as well as visual disorders in the form of double vision, the appearance of "fog" and flashing "flies".In the absence of treatment, neuroglycopenia is aggravated, which is manifested by the development of psychomotor agitation, increased muscle tone, convulsions. This state continues for a short time and is replaced by a coma. Hypoglycemic coma is characterized by the following symptoms: increased sweating, increased muscle tone, the appearance of convulsive syndrome. The precursors of hypoglycemic coma do not appear in all cases. If hypoglycemic coma lasts a long time, then there are signs of cerebral edema. Also, the appearance of superficial breathing, lowering of arterial pressure, reflexes decrease or completely drop out, palpitations decrease. Lethal outcome occurs as a result of death of the cortex or substance of the brain. A sign of the onset of these states is the lack of pupillary response to light.

    Treatment should be immediate and carried out in the intensive care unit. The lack of treatment within 2 hours of the onset of hypoglycemic coma significantly worsens the prognosis for life.

    Prevention of hypoglycemia

    In the case of upcoming physical exertion, it is necessary to increase the amount of carbohydrates by 1-2 grain ED.The intake of this amount of carbohydrate is made before and after exercise. If physical activity is planned for more than 2 hours, the amount of insulin administered on that day should be reduced by 25-50%.The amount of spirits should be limited to 50-75 g. Also, adherence to the dietary regime is important for the prevention of hypoglycemia. In order to prevent hypoglycemia at night, in the evening you must include foods that contain protein. In order to restore the normal blood sugar level with mild hypoglycemia, you can take sugar or a sweet carbonated drink.

    Late complications of diabetes mellitus

    Late complications of diabetes mellitus include lesions of blood vessels( diabetic angiopathies).Diabetic angiopathy is a generalized vascular lesion that extends to both small vessels and medium to large caliber vessels. With the defeat of small vessels, such as arterioles, venules and capillaries, microangiopathy develops. With lesions of medium and large caliber vessels, macroangiopathy develops. Microangiopathies lead to damage to the kidneys and eyes. In macroangiopathies, the vessels of the heart, brain and large vessels of the lower extremities are affected. The main role in the development of diabetic angiopathy belongs to the increase in the level of sugar in the blood.

    Diabetic nephropathy

    Diabetic nephropathy is a specific kidney damage in diabetes, which ultimately leads to the development of chronic renal failure. The initial signs of diabetic nephropathy are revealed after 5-10 years from the onset of diabetes mellitus. This complication is the main cause of death in type 1 diabetes mellitus.

    Diabetic kidney damage is characterized by several stages: microalbuminuria( urinary excretion of a small amount of protein), proteinuria( urinary excretion of large amounts of protein), chronic renal failure. The stages of microalbuminuria and proteinuria during routine examination are not detected. The stage of microalbuminuria is characterized by an increase in the release of protein albumin with urine in an amount of 30 to 300 mg per day. At the general analysis of urine the protein is not revealed. Characteristic manifestations at this stage does not develop. In some cases, there may be a slight increase in blood pressure. The stage of proteinuria is characterized by an increase in the release of protein in the urine of more than 300 mg per day. If proteinuria is more than 3.5 grams per day, this indicates the development of a nephrotic syndrome, which is manifested by swelling on the face. Increased blood pressure develops in 65-80% of individuals, while both systolic and diastolic blood pressure increase. Arterial hypertension with diabetic kidney damage is stable and lack of sensitivity to drugs designed to lower blood pressure. Nephrotic syndrome leads to a decrease in the amount of protein per unit volume of blood. Since the time when persistent proteinuria is established, all the signs characteristic of chronic renal failure are added. This stage has a progressive course, the rate of which can be different. The most powerful factor in the progression of chronic renal failure is arterial hypertension( increased blood pressure).In most cases, at this stage, there are various inflammatory processes of the urinary system, such as pyelonephritis and some others.

    The first two stages of diabetic nephropathy are detected in the case of detection of a protein in the urine with two or more of its studies. The stage of chronic renal failure is characterized by a massive loss of protein in the urine - more than 3.5 grams per day, - a decrease in the amount of protein in the blood, an increase in serum cholesterol.

    To achieve a positive effect, treatment should begin already in the first stage of diabetic kidney damage. The goal of treatment at this stage is to normalize the blood pressure level. The drugs of choice are enalapril, perindopril, lisinopril. Preparations of this group normalize the indices of arterial pressure, and also improve the blood flow in the kidneys. In the case of a normal level of blood pressure, the drugs of this group should also be used, but in a small dose. Treatment at the stage of proteinuria should include the use of insulin preparations( in the case of type II diabetes), compliance with a diet with a reduced amount of salt( in the case of hypertension).Correction of blood pressure is carried out by the same drugs. The level of arterial pressure to be achieved is no more than 130/85 mm Hg. Art. In the case of inefficacy of enalapril and similar drugs, additional use of such drugs as verapamil or diltiazem is necessary. In addition, you can use atenolol, diuretics( such as furosemide) and some others. Treatment for the development of chronic renal failure is determined by its stage. Distinguish the conservative stage and terminal. The main method of treatment in a conservative stage is to follow a diet. In the case of high blood pressure, the amount of table salt is limited to 3 g per day. The amount of carbohydrates should be increased in order to cover energy costs. Of the medicines at this stage, insulin and preparations of the enalapril group are mandatory. In the case of the terminal stage of chronic renal failure, treatment is conducted in specialized nephrological hospitals. Methods of treatment are chronic hemodialysis or peritoneal dialysis. If there is a need and a possibility, kidney transplantation is performed.

    Diabetic retinopathy

    Diabetic retinopathy - affection of the capillaries, arteries and veins of the retina.

    With diabetes mellitus, there is a narrowing of the vessels, which is accompanied by a decrease in their blood filling. There are degenerative changes in blood vessels with the formation of small saccular protrusions of the walls of blood vessels. With a prolonged lack of oxygen, which comes with blood to the retina of the eye, calcium salts and lipids are deposited in it. The deposition of lipids in the retina leads to the formation of dense patches. As a result of all pathological changes in the vessels of the retina, infiltrates and scars form on it. When the process is far gone, retinal detachment and blindness can occur. Discontinuities of pathologically dilated vessels and infarcts lead to hemorrhages in the vitreous of the eye. In addition, glaucoma can develop.

    For the detection of diabetic retinopathy it is necessary to undergo a series of studies, both objective and instrumental. Methods of examination include: external examination of the eyes, determination of visual acuity and visual fields, examination of the cornea, iris and angle of the anterior chamber of the eye using a slit lamp. In the case of opacity of the vitreous and lens, ultrasound of the eye is performed. If there is a need, then the retinal vessels are explored and the ocular fundus is photographed.

    The main principle in the treatment of this complication is to achieve compensation for metabolic processes in diabetes mellitus. To prevent blindness, laser retina photocoagulation is performed. This technique can be used at any stage of diabetic damage to the eye, but the greatest effect is achieved when used in the early stages. The purpose of this technique is to stop the functioning of newly formed retinal vessels. If there is a need, then it is possible to perform vitrectomy - removal of the vitreous body.

    Diabetic neuropathy

    Diabetic neuropathy implies the defeat of the central and peripheral nervous system in diabetes mellitus. The key point in the development of this complication is a chronic increase in blood sugar levels. There are three theories of the development of diabetic neuropathy. According to the first theory, as a result of high blood sugar in the blood inside the nerve, a significant increase in glucose concentration occurs. Since glucose in excess amounts is not subjected to complete metabolism, it contributes to the formation of sorbitol. This substance is osmotically active, that is, it "pulls" water behind it. As a result of increasing the concentration of sorbitol inside the nerve, edema of a progressive nature occurs. The essence of the second theory is that as a result of the defeat of vessels supplying the nerve, there is an insufficient supply of oxygen to them, which in turn leads to metabolic disorders and the occurrence of microcirculation. According to the third theory, the proteins that form the basis of any nerve are damaged.

    The manifestation of diabetic neuropathy depends on its type.

    Sensory neuropathy initially exhibits a disturbance in vibration sensitivity. The detection of this disorder is done using a graduated tuning fork, which is mounted on the head of the first bone of the tarsus. The detection of this violation is based on the human experience of vibrating the tuning fork. The most frequent sign of this complication of diabetes is the appearance of numbness and "crawling" in the lower extremities. The usual manifestation of damage to the nervous system in diabetes mellitus is a feeling of chilliness in the legs, which feel warm to the touch. Sensomotor neuropathy is characterized by the appearance of the syndrome of restless legs. This syndrome consists in a combination of increased sensitivity and the appearance of a sensation of "creeping crawl" at night. As the disease progresses, these sensations appear in the hands, as well as in the chest and abdomen. With prolonged course of diabetes mellitus, small painful nerve fibers die, which is manifested by spontaneous cessation of pain in the extremities. Sensory motor neuropathy can be accompanied by a decrease in sensitivity, the manifestation of which is the loss of sensitivity by the type of "stocking and gloves"( that is, on hands sensitivity is reduced in the area corresponding to that when putting on gloves, and on the legs - stockings).In addition, there may be difficulties in moving, as well as disruption of coordination of movement. Since there is a disturbance of pain sensitivity, people often do not notice small foot injuries, which are then easily infected.

    Cardiovascular( cardiovascular) form of neuropathy is characterized by an increase in heart rate( tachycardia) at rest, that is, without any physical exertion. Progression of the disease leads to the defeat of the sympathetic nervous system, which is manifested by a slight decrease in tachycardia. All these changes in the nervous regulation of the activity of the heart muscle lead to a disruption of its adaptation to physical exertion.

    Gastrointestinal( gastrointestinal) form of diabetic neuropathy develops as a result of the disturbance of the nervous regulation of the activity of the gastrointestinal tract. This form of lesion is manifested by a violation of the passage of food through the esophagus, the development of inflammation of the esophagus wall as a result of throwing acidic gastric contents into it( reflux-esophagitis), there is a paresis( violation of the motor activity) of the stomach, in which both the deceleration and the acceleration of its emptying can occur. As a result of impaired motor function of the intestine, there is an alternation of diarrhea and constipation. In addition, there is a violation of the pancreas formation of digestive juices. Often often salivating, as well as dyskinesia of the biliary tract, which increases the tendency to the formation of stones in the bile ducts.

    The urogenital form is a consequence of the spread of the process to the sacral nerve plexus. In this case, the regulation of the function of the urogenital tract is impaired. This form of diabetic neuropathy is manifested by the lack of tonus of the ureters and bladder, by reverse casting( from the ureters into the bladder or from the bladder to the kidneys) or stagnation of urine, by an increased tendency to infection of the urinary system. In 50% of men, there is a violation of erection and ejaculation, and a violation of the pain sensitivity of the testicles is also noted. In women, a vaginal moisturizing disorder may occur.

    Impaired ability to recognize a decrease in blood sugar levels. Normally, with a decrease in the level of sugar, an emergency release of the glucagon hormone into the bloodstream takes place, which stimulates the formation of glucose in the body from various substances. Its initial release occurs as a result of stimulation of the pancreas through the nervous system. With the development of diabetic neuropathy, as a result of a disturbance in the function of the nervous system, the release of this hormone into the blood does not occur. There is also a loss of symptoms, which are precursors of lowering blood sugar levels. All these disorders lead to the fact that a person loses the ability to recognize the approaching state of hypoglycemia.

    Diabetic neuropathy is accompanied by impaired pupillary function, which is manifested by impairment of vision adaptation in the dark.

    Violation of the function of sweat glands develops as a result of a violation of the innervation of the skin. Since the function of sweat glands falls out, the skin becomes dry - an anhydrosis develops.

    Treatment of for this complication is carried out in three stages. The first stage is to achieve a normal course of metabolic processes in diabetes mellitus. To this end, intensive treatment with insulin preparations is carried out. The second stage of treatment is to stimulate the restoration of damaged nerve fibers. To this end, lipoic acid preparations and B vitamins are used. Under the influence of lipoic acid preparations, the energy balance in the nervous formations is restored, and their further damage is prevented. The duration of such treatment is 3-6 months. The third stage is to carry out treatment aimed at eliminating all adverse manifestations, which depend on the form of diabetic neuropathy.

    Diabetic Foot Syndrome

    Diabetic Foot Syndrome is a pathological condition of the foot in diabetes mellitus, which appears against the background of peripheral nerves, skin and soft tissues, bones and joints and is manifested by acute and chronic ulcers, osteoarticular lesions and purulent necrotic processes.

    There are three forms of the syndrome of the diabetic foot: neuropathic, ischemic and mixed( neuroischemic).60-70% of cases of diabetic foot syndrome development are neuropathic form.

    Neuropathic form. Initially, with the development of diabetic neurological damage, lesions are continued beyond the located nerve sections, with the longest nerves being affected. As a result of the damage to the special fibers that make up these nerves, a deficiency of "nutritional" impulses to muscles, tendons, ligaments, bones and skin develops, which leads to their exhaustion. A consequence of this is the deformation of the affected foot. In this case, there is a redistribution of the load on the foot, which is accompanied by an excessive increase in the load on individual sections. Such areas may be the heads of metatarsal bones, which will be manifested by thickening of the skin in these areas. As a result of the fact that these areas of the foot experience constant pressure, the soft tissues of these areas undergo inflammatory fusion. All these mechanisms eventually lead to the formation of a ulcerative defect. Since there is a violation of the function of the sweat glands, the skin becomes dry and cracks appear easily on it. As a result of a violation of the pain sensation type, a person may not notice this. In the future, infection of lesions occurs, which leads to the appearance of ulcers. Their formation is promoted by an immunodeficiency, arising at an aggravation of a diabetes. The development of the neuropathic form of the diabetic foot is accompanied by a change in the vessels of the limb. As a result of the expansion of the vessels of the foot, its swelling and temperature increase develops. Due to the violation of blood flow in these vessels, oxygen deficiency develops, which enters the tissues of the foot, which also contributes to the aggravation of the process. Under the influence of the edema of the foot, there may be an increase in compression of arterial vessels( a symptom of the "blue finger").

    This type of foot injury in diabetes mellitus is characterized by three types of lesions. These include ulcers, lesions of the bones and joints of the foot, and swelling. Ulcers are most often located in the area of ​​the sole, as well as in the intervals between the toes. With neuropathy, spontaneous bone fractures can occur. In some cases, these fractures are painless. In this case, the foot becomes swollen, its redness is noted. Destructive processes in the bone-ligament apparatus can take quite a long time. This is usually accompanied by the formation of a pronounced bone deformation, which is called the joint of Charcot. Edema develops as a result of a disturbance in the regulation of the tone in the small vessels of the foot and the emergence of them into the tissues of the liquid part of the blood.

    Treatment of includes several activities: achieving the normalization of all metabolic processes in diabetes mellitus, the use of antibiotics, wound treatment, rest and unloading of the foot, removal of the thickening of the skin and wearing specially selected shoes.

    The ischemic form of the of the diabetic foot syndrome develops when the main blood flow in the limb is disturbed, which occurs when the arteries are atherosclerotic.

    Skin covers on the affected foot take a pale or cyanotic tinge. In more rare cases, as a result of the expansion of the surface capillaries, the skin acquires a pinkish-red hue. The expansion of these vessels occurs with oxygen deficiency in the blood. With the ischemic form of the diabetic foot, the skin becomes cold to the touch. Ulcers are formed at the tips of the toes and on the edge surface of the heel. In many cases, this form of complication of diabetes is characterized by the appearance of pain.

    Instrumental research methods are used to determine the state of arterial blood flow in the vessels of the lower limbs. For this, the method of Doplerography, angiography of vessels of lower extremities, computed tomography, magnetic resonance tomography, and ultrasound scanning of these vessels are used.

    As with the neuropathic form, it is necessary to achieve the normalization of metabolic processes. The defeat of the lower limb with a given form of diabetic foot can be of different severity. The usual method of treatment, which is preferred in the ischemic form of the diabetic foot, is an operation to restore normal blood flow to the limb due to the plasticity of the vessels. In the event that necrotic and ulcerative lesions are absent, walking is recommended for 1-2 hours per day, which contributes to the development of blood flow in the limb. To prevent the formation of blood clots in blood vessels is recommended the use of aspirin in 1/4 tablets per day, as well as special drugs that prevent blood clotting in the vessels. If there are already thrombi, drugs used to promote their melting. In the case when the purulent-necrotic process with any variant of the diabetic foot is quite extensive, the issue of amputation of the lower limb is being decided.

    The main method of preventing the development of diabetic foot syndrome is adequate treatment of diabetes mellitus and maintenance of metabolic processes at the optimal level. Each visit to the doctor requires an examination of the lower limbs. Such examinations should be conducted at least once every 6 months. It is also important not to forget about the elementary rules of foot care. It is necessary to maintain the cleanliness and dryness of the legs, hold warm foot baths, apply a cream to prevent the appearance of cracks in the skin.

    Hygiene of a diabetic patient

    Hygiene plays a very important role in the life of people with diabetes. This includes not only the observance of personal hygiene, maintenance of home hygiene, clothing, nutrition, but also the development of dosed physical exercise, complexes of therapeutic physical training, hardening, exclusion of bad habits. Physical exercises and subsequent water procedures( rubbing, dousing, showering or bathing) harden the body well, increasing its resistance to diseases.

    Oral hygiene.

    In diabetes mellitus, care should be given to the oral cavity, because with it, diseases of the teeth and gums develop more often and flow more heavily. A diabetic patient should visit the dentist regularly( every six months), timely dental caries treatment, and remove tartar.

    Foot care.

    Danger of leg injuries in diabetes mellitus is very high. There is even the concept of the syndrome of the "diabetic foot".When peripheral nerve endings and vessels are damaged, the sensitivity and blood supply of various parts of the lower extremities decreases sharply. In these cases, ordinary shoes can cause foot deformation, ulceration, and the development of diabetic gangrene. Deformation of the foot leads to the formation of areas of increased pressure on the plantar surface. As a result, inflammation of the soft tissues of the foot occurs, followed by the formation of ulcers. In addition, any damage to the skin with an increased level of glycemia and poor blood supply leads to the infection of wounds with the spread of infection to the ligamentous and osteoarticular apparatus. Treatment of the diabetic foot is a complex and lengthy process. But diseases and complications can be avoided by performing individual preventive measures for foot care.

    Foot control.

    Every diabetic patient must thoroughly examine his legs every day in good light. Particular attention should be paid to: skin changes in the interdigital spaces. With fungal infections, immediately consult a dermatologist. Horny skin, cracks, calluses on the fingers - all this can cause the development of the infectious process.

    Wash your feet in the morning and in the evening, using warm water with a temperature of 37-38 ° C.

    Use a soft sponge and neutral soap to wash your feet.

    The duration of the foot baths is no more than 5 minutes.

    After washing, thoroughly wipe the feet, especially the interdigital spaces, with a soft towel.

    When handling the feet, never use sharp objects( blades, pointed scissors, razors), corn plasters, ointments. Rinse the skin with a pumice stone.

    For cutting nails, use scissors with rounded ends and cut the nails only straight.

    Selection of shoes.

    If you choose the right shoes and insoles, you can avoid the development of the syndrome of "diabetic foot".

    Normally shoes should give stability( shoes on laces well fix the joints of the foot);A wide, low heel is a reliable support for the feet.

    Shoes should be in size: the width of the shoe should correspond to the width of the foot( at the level of the first joint of the thumb).

    The top of the shoe should be made of natural materials.

    Choose shoes in the afternoon. Legs by this time swell, before putting on shoes, check it with your hand to exclude irregularities( wrinkles, rough seams).

    The deformation or bending of the shoe is a sign of an abnormal gait. In this case it is better to consult a doctor.

    If you have injured your leg, you need to do the following:

    disinfect the wound with antiseptic agents( avoid using dye solutions: iodine, diamond greens, as they hide the inflammation zone);

    should not be used with ointment or bactericidal plaster without a doctor's recommendation;

    , place a dry sterile swab and bandage on the wound.

    In everyday life it is better to use simple socks( stockings), your size or a number larger and with a small inclusion of synthetic fibers. Socks or stockings should be changed daily. Even at home you should not walk barefoot, it is undesirable also to wear shoes with open toes.

    Compliance with rhythm in everyday life is an important factor in maintaining health. First of all, we are talking about the alternation of work and rest, wakefulness and sleep. Among all kinds of rest, the most physiologically important is sleep. Its impairments significantly impair the effectiveness of diabetes care. To ensure fast falling asleep and deep sleep, the following are recommended:

    • last meal at least 2 hours before bedtime( exception is only permissible for patients who use insulin for prolonged action and are prone to hypoglycemic conditions - such patients are desirable for 30-40 minutesbefore a dream to take an easy additional supper - fruit, kefir);

    • half-hour evening walk in the open air;

    • sleep in a well-ventilated place;

    • in bed should take a comfortable, familiar position, relax;

    • to properly relax the muscles, you can resort to self-hypnosis.

    The question of the need for sleeping pills and sedatives is decided by the doctor individually.

    Psychotherapy

    Diabetes mellitus is a disease that accompanies a person for life. This situation in many patients often causes depression, loss of interest in the world around them. The endocrinologist must constantly conduct psychotherapeutic conversations with patients and members of his family, emphasizing at the same time that under the right treatment and treatment the patient can lead a normal life, fulfill his professional duties and not feel his own defectiveness. It is very important to create a favorable psychological situation for the patient at work, in the family, to surround him with understanding, care.

    Day mode.

    Compliance is particularly important for people on insulin. Here it should be mentioned that the time of insulin administration in connection with food intake is different. Insulin can be injected just before meals, 10-15 minutes before meals, etc. The interval between insulin injection and food intake should not exceed one hour. The time of insulin administration in connection with food intake is strictly individual. This is set by the doctor. Not everyone in the home, working environment can establish an approximate daily routine, close to the sanatorium. Despite this, patients with diabetes mellitus are required to observe the daily routine, based on real possibilities. The condition of the patient with diabetes mellitus, well-being, working capacity is very much dependent on compliance with the regime, which does not necessarily have to resemble a spa.

    Going to the spa treatment, some patients with diabetes mellitus, in anticipation of good results for some time before the trip and on the road cease to comply with the prescribed regime, which is harmful to health. To eliminate the consequences, it is necessary to spend extra time in the resort to return the patient to a normal state and start a full-fledged treatment. The same should be emphasized for patients who complete the course of sanatorium treatment when they allow themselves to violate the prescribed regime at the end of their stay and sometimes on their way home.

    The success of sanatorium treatment, like any other treatment, can be persistent for diabetics only if the prescribed regimen is strictly observed. In the assigned mode, all its constituent elements( nutrition, insulin, correct alternation of work with rest, observance of hygienic rules, gymnastics, sports, etc.) are important, only this contributes to the preservation of health.

    Reminder for the patient

    To maintain good health, keep high work activity and prevent complications of a diabetic patient in daily life, a special treatment and prophylactic regimen should be observed. Its main requirements are as follows:

    1. Dietary nutrition is the basis of treatment for all forms of diabetes. From the daily diet should be excluded sugar, confectionery, semolina, fatty sausages, alcohol, beer, grapes, fruit juices on sugar. Limit the consumption of food products containing easily digestible carbohydrates( bakery products, potatoes and cereals, sweet fruit varieties).Diet should include vegetables, fruits, milk, cottage cheese. Especially important is the intake of food at a strictly defined time in accordance with the introduction of insulin.

    2. A clear mode of the day is needed. Morning up, work( study), insulin administration, eating and medication, active rest, going to sleep should be done at a certain time. Do not allow mental and physical overwork. Sundays should be fully used for outdoor activities.

    3. Observe the rules of personal hygiene and hygiene of the home. Physical culture, sports( not power kinds) have a beneficial effect on metabolism, enhance the absorption of glucose, reduce the need for insulin, ease the course of the disease, increase efficiency.

    4. The prescribed medication should be taken at a specific time. Replacement of the drug, changing the dose and even more so that they can not be canceled without the knowledge of the doctor.

    5. Observe the purity and sterility of insulin administration. Places of injections should be changed so that repeated injections into the same site were not more often 1-2 times a month.

    In patients receiving insulin, hypoglycemic conditions may develop. The first signs are weakness, trembling of hands, sweating, numbness of lips, tongue, hunger, confusion of consciousness, down to unconsciousness( hypoglycemic coma).This is facilitated by late or inadequate intake of food, the introduction of an excessive dose of insulin, excessive physical activity, the intake of alcohol( especially strong spirits).To eliminate acute hypoglycemia, you need to eat 20 g of glucose, 200 ml of sugar-containing drinks, 4-5 pieces of sugar, candy, which should always be carried along with a diabetic passport. In addition to daily self-monitoring, if you feel unwell, more often measure blood sugar and urine sugar, examine urine for acetone, continue treatment with insulin or sugar-reducing tablets, seek medical help.

    6. Acute infectious disease, untimely and insufficient insulin administration, mental and physical fatigue, gross violations of the day and nutrition regimen and other causes can lead to decompensation of diabetes and development of coma.

    7. When choosing a profession and working activity, people with diabetes should take into account the limitations caused by the characteristics of the disease, the need to prevent its complications. Relatives and friends should know the rules of care for hypoglycemia.

    8. Compensated diabetes mellitus can not become an obstacle to marriage and normal family life. With the purpose of early detection and prevention of diabetes mellitus it is necessary to periodically( 1 2 times a year) examine their children.

    9. To prevent complications, among which the most frequent lesions of the eyes, kidneys, liver, legs, diseases of the nervous system, gums, a patient with diabetes should be under constant medical supervision, be on dispensary records.

    Indicators of diabetes compensation are: good general well-being, retention of work capacity, lack of thirst, dry mouth, no signs of eye, kidney, liver, nervous system, legs, mouth, 1.5-2 l urine per day and absenceor traces of sugar in it, the sugar content in the blood to 7.8-8 mmol / l without sudden fluctuations in its concentration during the day.

    A diabetic patient should always carry with him and keep the "Diabetes Card" in an accessible place, which is necessary for the timely provision of emergency medical care in case of development of a coma( unconscious) state.

    If you feel that there is a lack of appropriate materials or specific medical care for effective diabetes control, contact your local diabetic association.