Late complications of diabetes mellitus: prevention and treatment. Diabetic hand and foot syndrome
LATE COMPLICATIONS OF DM
The social significance of diabetes mellitus (DM) is that it leads to early disability and mortality, which is caused by the presence of late vascular complications diabetes Patients with diabetes are at greatest risk of developing cardiovascular diseases. More than 40% of all amputations lower limbs(not caused by trauma) is carried out in connection with diabetic foot syndrome And gangrene of the lower extremities. Distal polyneuropathy and autonomic neuropathy are the cause of low quality of life, disability and disability in large quantity patients with diabetes.
Late complications of diabetes include:
1. microangiopathies - damage to capillaries, arterioles and venules, the clinical manifestation of which is retinopathy, nephropathy, as well as neuropathy, where a significant place is given to primary damage to the vessels involved in the blood supply to the peripheral parts of the nervous system.
2. macroangiopathies - damage to large and medium-sized vessels, leading to heart attack myocardium, stroke, diabetic foot syndrome and gangrene of the lower extremities.
3. neuropathy.
4. osteoarthropathy. Pathogenesis.
The pathogenesis of angiopathy is multifactorial. It is believed that in the pathogenesis angio- two main factors are involved:
- internal factor - genetic predisposition, i.e. inheritance of angiopathy (most likely, there is a polygenic type of transmission).
- external factors- for the implementation of a genetic predisposition to the development of angiopathy, the participation of external factors is necessary, the role of which is primarily hyperglycemia and the associated cascade of metabolic, hormonal, rheological and other disorders. Without the participation of the latter factors, the realization of a genetic predisposition to angiopathy is impossible.
Despite significant general mechanisms pathogenesis of macro- and microangiopathy in diabetes mellitus, the clinical and pathomorphological characteristics of these lesions are different.
Diabetic microangiopathies(DM) is a complex of pathological changes in microcirculation vessels and peri-microvascular zones that develop in diabetes mellitus and other disorders of glucose tolerance.
With DM, all links of the microcirculation chain are affected: arterioles, capillaries, venules, intermicrovascular anastomoses. Pathological changes develop in all elements of the vascular wall: endothelium, basal and elastic membranes, smooth muscle cells, fibrous structures, pericytes and adventitia. Damage to the endothelium and basement membrane of microvessels.
An important factor in damage to endothelial cells in diabetes mellitus under conditions of hyperglycemia is increased sorbitol pathway of glucose metabolism. Activation of aldose reductase with subsequent accumulation of sorbitol in endothelial cells leads to osmotic edema and destruction of the latter, up to the development of hyperosmolar “explosions” of cells.
Normally, in response to damage to endothelial cells, their regeneration occurs since endothelial cells, as well as pericytes and smooth muscle cells, produce a large amount of substances that stimulate reparative processes in blood vessels (fibroblast and platelet growth factors, endothelial growth factor, angiopoietins and etc.). In diabetes mellitus, the restoration of damaged microvascular endothelium is sharply impaired. It is known that endothelial cells produce a wide range of factors that regulate the homeostasis system. Under conditions of chronic hyperglycemia, the glycosylation process captures protein elements predominantly of the anticoagulant system, which is additional factor local thrombosis. Free radical processes and glycosylation of endothelial cell components lead to a decrease in the production of vasodilators, such as NO and prostacyclin. The resulting spasm of arterioles aggravates hypoxia and; hence, free radical damage to endothelial cells.
Red blood cells containing glycosylated hemoglobin have an altered surface s-potential, which leads to stasis, agglutination and sludge of red blood cells. The finale of these processes is microthrombosis, which creates local circulatory and hemic hypoxia, activation of lipid peroxidation with damage to the cytoplasmic membranes of endothelial cells.
BM lesions have a complex genesis, consisting of three main mechanisms: metabolic, hypoxic, and immune complex. Metabolic damage to the BM is based on the processes of enzymatic and non-enzymatic glycosylation of its proteins. In this case, the network-like structure of type IV collagen is disrupted. With hyperglycemia, the synthesis of fibrous structures and the architectonics of the BM are sharply disrupted. Such a change in the structure of the latter not only disrupts, but also suppresses growth and regeneration nerve fibers,
which includes the neuropathic component of MD. Hypoxia, characteristic of BM (discussed above), activates lipid peroxidation of BM, which also leads to an increase in its permeability to plasma proteins. The significance of immune complex damage to the BM is obvious in autoimmune diabetes mellitus. They are deposited on the BM of microvessels subendothelially or on the “bare” BM. immune complexes(IR) different composition. These ICs contain insulin, its precursors and metabolites as antigens (autoantigens); proteins of smooth muscle fibers and fibroblasts; surface and cytoplasmic antigens of islet (especially P) cells of the pancreas; antigens of other organs and tissues (adrenal cortex, stomach, etc.); immunoglobulins G, as well as many other substances that perform the function of antigens. The role of autoantibodies in IC is usually performed by immunoglobulins A, M, G. It should be noted that immune damage to the BM is probably carried out not only by IC, but also by autoantibodies. Regeneration of the BM damaged in diabetes mellitus is sharply reduced and distorted due to damage to the cells that carry it out (EC, SMC, pericytes) and disruption of membrane-cellular and intercellular interactions in microvessels.
DIABETIC RETINOPATHY Epidemiology.
In patients with type 1 diabetes, after 5-7 years, clinically detectable symptoms of DR are found in 15-20% of cases, after 10 years - in 50-60%, and after 30 years in almost all patients. In type 2 diabetes, due to late diagnosis, signs of DR are detected already at diagnosis of diabetes in 15-30% of cases, after 10 years - in 50-70%, and after 30 years - in more than 90% of patients. The most severe stage of retinal damage - proliferative retinopathy - is observed in 10-30% of all cases of diabetes. Pathogenesis.
The pathogenetic mechanisms of DR are diverse and are far from fully studied. Undoubtedly, all of them are directly or indirectly related to hyperglycemia. Hyperglycemia is especially dangerous for insulin-independent tissues (in particular for the vascular endothelium and pericytes), the transport of glucose into which does not require the presence of insulin.
An increased concentration of glucose in cells in the presence of the enzyme aldose reductase causes the development of its metabolism along the polyol pathway with the formation of fructose and sorbitol. The accumulation of sorbitol leads to disruption of osmotic and electrolyte balance, swelling, disruption of cell structure and function.
The endothelium of the retinal vessels is the main structure in the blood-ophthalmic barrier system; at the local level it supports blood circulation
in accordance with the needs of the neural retina, regulates platelet activity, prevents parietal fibrin deposition and the formation of intravascular platelet and coagulation thrombi. Violation of the integrity and function of the endothelium is an important link in the pathogenesis of DR.
It is believed that this mechanism plays a significant role in the death of pericytes, dysfunction of the capillary endothelium and its partial loss. The vascular wall becomes “porous”, like a sieve. Through such a changed wall, the liquid part of the blood with proteins, fats, etc. dissolved in it begins to leak out of the vessel. At the stage of non-proliferative diabetic retinopathy, changes in the arterial and venous vessels, multiple small intraretinal hemorrhages, areas of impaired blood supply, areas of edema, where the retina is thickened due to accumulated fluid and intraretinal deposits of protein-fat complexes - "solid exudates". This is how retinal swelling occurs, it becomes thickened, connections between nerve cells are disrupted, and some retinal cells die.
Pericytes strengthen the mechanical structure of the capillary and participate in autoregulation capillary blood flow. Loss of pericytes contributes to capillary atony and microaneurysm formation. The death of some endothelial cells is combined with the active proliferation of others, thickening of the basement membrane and the formation of microthrombi. The vascular bed of the retina becomes uneven. It combines areas not perfused with blood with areas of dilated capillaries and venous vessels. In places of impaired blood circulation and nutrition of the retina, "infarction" zones arise, in which part of the retina dies. nerve cells. In these areas, the retina is no longer capable of perceiving light information. When examining the fundus, they appear as whitish foci, "cotton wool" lesions, or "soft exudates."
Hypoxic zones serve as sources of proliferative factors, especially vascular endothelial growth factor (VEGF), which are produced by endothelium, Müller cells and astroglia. The accumulation of growth factors causes the development of proliferative processes with the appearance of not only newly formed vessels, but also fibroglial cords and membranes, complicated by hemorrhages and tractional retinal detachment. The spread of growth factors through the vitreous humor (VT) into the anterior chamber of the eye leads to the development of iris rubeosis and neovascular glaucoma.
The development of DR is significantly influenced by the anatomy of the retinal vascular system, including the dichotomous division of each arteriole, the terminal nature of the blood supply to the retinal zones (absence of anastomoses), and the tight junction of endothelial cells. Clinical
the significance of the dichotomous division of the arteriole is that with an increase in the resistance to blood movement along one of its branches, the blood flow is redistributed in favor of the other branch (the phenomenon of stealing). This contributes to the emergence of focal ischemic foci characteristic of DR in combination with areas of increased perfusion. Classification (E. Kohner and M. Porta). There are three stages of development of DR:
1. non-proliferative
2. preproliferative,
3. proliferative.
In the first stage varicose veins, a limited number of microaneurysms, single intraretinal lipid foci (“hard exudates”) and microhemorrhages (“soft exudates”) are observed.
In the preproliferative stage all the above symptoms increase quantitatively. Changes in the veins are characterized not only by their expansion, but also by uneven caliber, sometimes constrictions, a distinct appearance, tortuosity, and the formation of loops. Very sharp changes in venous
vessels indicate the appearance of glial constrictions along their course. In addition to hard exudative foci, soft foci appear, caused by acute focal ischemia in the retinal nerve fiber layer. The amount of hemorrhage increases; which can be not only intraretinal, but also superficial, streaky and even preretinal. Fluorescein angiography of the fundus reveals areas of the retina that are not perfused with blood and arteriovenular shunts, leakage of fluorescein from retinal vessels and microaneurysms, and reduction of paramacular capillaries.
Proliferative DR is characterized by the appearance of newly formed vessels on disk optic nerve, near it or along the way large branches retinal vessels, the formation of fibroglial films, cords. In cases where there is no posterior vitreal detachment, the neovascular process and gliosis can spread along the Aaloid membrane of the CT.
The consequences of proliferative DR include preretinal hemorrhages, hemophthalmos, retinoschisis, traction retinal detachment and neovascular glaucoma.
A serious complication of DR, which can occur at any stage, is maculopathy, leading to a decrease in central vision. Maculopathy can be caused by edema, deposits of lipid exudate from the parafoveolar capillaries, the traction effect on the retina of the hyaloid membrane of the CT, epiretinal membrane, or a pronounced reduction of the capillary network (ischemic maculopathy)! Non-proliferative diabetic retinopathy.
Dilatation of veins and capillaries ■ Microaneurysms
Hemorrhages (mainly in the paramacular zone)
Retinal edema (in the macular area or along large vessels)
Single exudative foci (mainly in the central part of the fundus)
Vision is not impaired.
Preproliferative diabetic retinopathy.
Venous abnormalities (clearness, tortuosity, duplication, loops, pronounced fluctuations in vessel caliber) Multiple retinal hemorrhages
■ Multiple exudative lesions (hard and soft)
■ Decreased visual acuity (changes in the fundus also affect the macular area)
Proliferative diabetic retinopathy.
Neovascularization of the optic nerve head and other parts of the retina, with penetration into the vitreous body
■ Rubeosis (newly formed vessels of the iris)
Repeated hemorrhages into the vitreous body, preretinal hemorrhages with formation fibrous tissue(vitreoretinal cords)
■ Possible tractional retinal detachment
Reduced severity vision up to blindness.
Ophthalmological examination.
Ophthalmological examination of patients with diabetes and DR performs the following tasks:
Making a diagnosis of DR, including determining the stage of the disease; - control over the dynamics of the process; assessment of the effectiveness of the therapy;
Revealing side effects and making adjustments to the course of treatment. The examination, in addition to the usual methods of examining an eye patient, includes:
Biomicroscopy of the fundus,
Retinography,
Fluorescein angiography of the retina (if indicated).
The condition of the vessels of the anterior segment of the eye can be judged using biomicroscopy and fluorescein angiography.
Ultrasound and electrophysiological research methods are especially useful when a detailed visual examination of the fundus of the eye is impossible (cataracts, hemorrhages or opacities of the eye fundus). Primary and secondary prevention.
Patients with diagnosed diabetes without clinical signs of DR should be examined by an ophthalmologist every 1-3 years. After the appearance of symptoms of DR, the timing of visiting an ophthalmologist is set individually, but not less than 1-2
times during the year. Deterioration of vision requires an immediate visit to the ophthalmologist. Great importance is given to teaching a patient with diabetes meth- ods of self-control, proper diet, physical exercise, quitting smoking and alcoholic beverages, and reducing stress.
The basis for the prevention and treatment of DR is optimal compensation of carbohydrate metabolism. In case of severe hyperglycemia, the decrease in blood glucose levels should be carried out slowly, over several weeks, in order to avoid deterioration not only of the patient’s well-being, but also the condition of the retina and even possible loss of vision. Surgery.
The purpose of surgical interventions for DR is the prevention and treatment of those complications that are the main causes of decreased vision or blindness. Surgical methods include
Photo - or * cryocoagulation of the retina,
Vitrectomy,
■ operations for retinal detachment and neovascular glaucoma.
Photocoagulation of the retina is carried out with lasers operating in green, yellow, or red. infrared zones of the light spectrum. Argon or krypton lasers are especially often used.
Three main methods of laser photocoagulation are used: /. Focal laser photocoagulation, which consists of applying coagulates in places where fluorescein is translucent during angiography, in areas where microaneurysms are localized, minor hemorrhages, exudates. 2. Barrier laser photocoagulation, which consists of applying small coagulates paramacularly in several rows. This method is used for non-proliferative diabetic retinopathy in combination with macular edema.
In successful cases, PRFC leads not only to the suspension of the processes of neovascularization and gliosis, but also to the partial or complete disappearance of previously formed newly formed vessels. The frequency of positive outcomes of timely PRFC reaches 80-90%. However, in some cases additional laser interventions or vitrectomy are necessary.
When the transparent media of the eye are clouded, especially with hemophthalmia, PRFC cannot be performed. In such cases, transconjunctival or transscleral cryocoagulation of the septum is used. This procedure accelerates the resorption of hemorrhage and stops or slows down the progression of proliferative DR.
In the most severe cases of proliferative DR, complicated by persistent hemophthalmos, formation of glial and fibrovascular membranes, traction maculopathy or retinal detachment, vitrectomy is used with removal or segmentation of the epiretinal and posterior hyaloid membrane, focal or panretinal endolaser photocoagulation and, if necessary, gas or silicone tamponade.
DIABETIC NEPHROPATHY.
The leading cause of death in patients with type 1 diabetes worldwide is chronic renal failure (CRF) due to progression diabetic nephropathy(DN).
Kidney damage in diabetes.
/. Specific kidney damage(actually diabetic nephropathy-
tia): diffuse glomerulosclerosis, nodular glomerulosclerosis (Kim-
Melstila-Wilson).
2. Nonspecific kidney damage
Infectious: bacteriuria, pyelonephritis, kidney carbuncle, kidney abscess, papillary necrosis.
Vascular: atherosclerotic nephrosclerosis, hypertensive nephrosclerosis.
Toxic: with the introduction of contrast agents, abuse of non-narcotic analgesics.
Neurogenic: atony Bladder.
Immunoinflammatory: glomerulonephritis, interstitial nephritis.
Tumor: paraneoplastic nephropathies.
Urolithiasis disease.
Kidney damage in diabetes is represented by a wide spectrum, in which diabetic glomerulosclerosis, pyogenic
lonsfritis and infection urinary tract, atherosclerotic nephrosclerosis, hypertensive nephrosclerosis. These changes are primarily related to the characteristics metabolic disorders with diabetes with characteristic micro-macroangiopathies, a tendency to infectious complications and an increased risk cardiovascular pathology.
Features of kidney damage in type 2 diabetes may be due to morphological changes of an age-related nature, such as sclerosis of small renal arteries and arterioles (especially efferent ones) with hyperperfusion of the medulla and a decrease in the cortical fraction, interstitial fibrosis of the medulla, focal glomerulosclerosis. A decrease in filtration function (slower than concentration ability) is associated with a decrease in cortical blood flow (by 10% every decade) and the progression of glomerulosclerosis so that by the age of 80 the total number of glomeruli is almost halved. A favorable background in addition to age-related disorders renal hemodynamics are reduced immune reactivity, impaired urodynamics (hypokinesia of the ureters, bladder, prostate adenoma), hypertonic disease, hyperlipidemia with an established “nephrotoxic” effect of lipids. Even moderate effects of dysmetabolism created by diabetes can decompensate the kidney in elderly people.
In diabetes, there is a dependence of the frequency of development of DN on the duration of the disease; however, the course and clinical manifestations of DN in type 2 diabetes are somewhat different from kidney damage in type 1 diabetes.
Hyperfiltration, i.e., high flow rate, is characteristic of the early stages of DN in patients with type 1 diabetes. glomerular filtration(more than 140 ml/min), is not detected in patients with type 2 diabetes, which is probably due to the severity of sclerotic changes in the renal tissue already at the onset of the disease in the latter. Microalbuminuria in patients with type 1 diabetes is the most important precursor clinical stage DN, in patients with type 2 diabetes, this indicator is more associated with the development of cardiovascular pathology (55-60% of patients with type 2 diabetes with microalbuminuria die from myocardial infarction or stroke and only 3-5% from uremia. Etiopathogenesis.
The basis of pathomorphological changes in diabetic nephropathy is cell proliferation of the endothelium and thickening of the basement membrane.
From a morphological point of view, there are two main types of lesions of the renal glomeruli in diabetes - nodular and diffuse. Diffuse glomerulosclerosis (intracapillary) is more often observed, which progresses to
quite slowly and rarely leads to chronic renal failure. Morphological changes with this form, they are present throughout the kidney.
The second form, nodular, is observed, as a rule, from the very beginning of diabetes (usually type 2 diabetes) and rapidly progresses with the development of diabetic glomerulocapillary microaneurysms located on the periphery or in the center of the glomerulus, narrowing or completely clogging the lumen of the capillaries.
Along with changes in the glomerular capillaries, lesions of the arterioles are observed with thickening of the intima, with deposition in the intercapillary space (glomerular mesangium) of lipids and proteins that contribute to the development of sclerotic changes leading to occlusion of the glomeruli (the increased volume of mesangium begins to compress the vascular network of the glomeruli), atrophy of the renal tubules and impaired filtration function of the kidneys. Lesions affect both the afferent and efferent vessels, which is especially typical for diabetes.
Currently, the role of the following 2 groups of factors involved in the development of DN, which are closely intertwined and interrelated with each other, has been proven:
■ metabolic: hyperglycemia, hyperlipidemia;
■ hemodynamic: intraglomerular hypertension, arterial hypertension.
Hyperglycemia is a triggering metabolic factor in the development of diabetic kidney damage. In the absence of hyperglycemia, changes in renal tissue characteristic of diabetes are not detected. The mechanisms of the nephrotoxic effect of hyperglycemia were clarified only at the very end of the 90s:
Non-enzymatic glycosylation of kidney membrane proteins, changing their structure and function;
polyol pathway of glucose metabolism, leading to the accumulation of osmotically active sorbitol in tissues;
direct toxic effect of glucose on kidney tissue, leading to activation of the enzyme protein kinase C, which increases the permeability of renal vessels;
■ activation of oxidative reactions contributing to the formation of large amounts free radicals having a cytotoxic effect. Hyperlipidemia is another metabolic factor in the progression of DN,
also leading to changes in the structure of the renal membranes and the progression of glomerulosclerosis. Intraglomerular hypertension (high hydraulic pressure in the capillaries of the renal glomeruli) is a leading hemo-
dynamic factor in the progression of DN. It has been established that the cause of the development of intraglomerular hypertension is the high activity of the renal renin-angiotensin system, namely the hyperactivity of angiotensin II. It is this vasoactive hormone that plays a key role in the disruption of intrarenal hemodynamics and the development of structural changes in kidney tissue in diabetes.
Arterial hypertension, arising secondary to diabetic kidney damage, becomes the most powerful factor in the progression of renal pathology, the strength of its damaging effects being many times greater than the influence of the metabolic factor (hyperglycemia and hyperlipidemia).
Classification of diabetic nephropathy
(CE. Mogensen et al. (1983), based on laboratory and clinical
/. Hyperfunctional hypertrophy(1st stage) Without clinical manifestations
It is characterized by hyperperfusion, hyperfiltration and normoalbuminuria (less than 30 mg/day). Detectable V In some cases, microalbuminuria is reversible with insulin therapy.
■ Glomerular filtration rate is high but also reversible. 2. Stage of initial structural changes(2nd stage)
No clinical manifestations
■ Appears 2-5 years from the onset of diabetes
■ Characterized by thickening of the glomerular basement membrane and an increase in the volume of the mesangium;
■ Manifested by hyperfiltration and normoalbuminuria (less than 30 mg/day). Microalbuminuria is not constant - it is detected with decompensation of diabetes and with physical activity.
Glomerular filtration rate was significantly increased. 2. Beginning nephropathy(3rd stage).
■ Without clinical manifestations
■ Develops more than 5 years from the onset of the disease, more often after 10-15 years.
■ Microalbuminuria is constant.
Glomerular filtration rate is moderately increased or normal. Blood pressure tends to increase, especially during physical activity.
Blood pressure increases
Clinical nephropathy(4th stage)
Develops 15-20 years from the onset of the disease.
Microalbuminuria develops into clinical proteinuria (contents
protein more than 0.5 g per day). ■ Glomerular filtration rate decreases.
Is almost constant arterial hypertension.
End stage renal failure, or uremia stage(5th stage), characterized by a very low glomerular filtration rate (less than 10 ml/min); total diffuse or nodular glomerulosclerosis.
First three stages of diabetic nephropathy are preclinical and occur without clinical symptoms. An objective sign of the presence of nephropathy during this period is microalbuminuria. Normally, no more than 30 are excreted mg albumin per day, which is equivalent to an albumin concentration of less than 20 mg/l V one-time urine test. When proteinuria occurs, albumin excretion from urine exceeds 300 mg/day. Therefore, the range of microalbuminuria is 30 to 300 mg/day or 20 to 200 mcg/min.
In Russia in 2000, the Ministry of Health of the Russian Federation approved a new classification of DN, including three stages of development this complication.
stage of microalbuminuria
the stage of proteinuria with preserved nitrogen excretory function of the kidneys the stage of chronic renal failure (CRF)
With careful control of glycemia and normalization of intrarenal hemodynamics and kidney volume, which can be achieved with long-term use of angiotensin-converting enzyme inhibitors, stabilization and slowdown of the progression of nephropathy are possible. The appearance of proteinuria indicates a significant destructive process in the kidneys, in which about 50-75% of the glomeruli are already sclerotic, and the morphological and functional changes have become irreversible. It has been shown that from this time (the appearance of proteinuria) the glomerular filtration rate progressively decreases at a rate of 1 ml/min per month or about 10 ml/min per year, which leads to end-stage renal failure 7-10 years after the onset of proteinuria.
Clinical manifestations of diabetic nephropathy.
The clinical manifestations of diabetic nephropathy are highly dependent on the type of diabetes. In type 1 diabetes, the first symptom is proteinuria, which at first rarely exceeds 1 g/l and is not accompanied by changes in urinary sediment, edema and arterial hypertension. Almost always, already at this stage, changes in the fundus in the form of diabetic retinopathy are observed. Subsequently, other symptoms appear and constantly increase: proteinuria reaches 10 g/l, hypoalbuminuria, edema and arterial hypertension develop. Often, signs of neuropathy are observed (impaired sensitivity, pain, decreased tendon reflexes). All these clinical phenomena are accompanied by an increase in the total amount of lipids, especially cholesterol, while the level total protein reduced (nephrotic syndrome). Disturbances in concentration and excretory functions kidney
At the stage of chronic renal failure, glycemia, glucosuria and the need for insulin can be significantly reduced due to a decrease in the rate of insulin degradation and its excretion in the urine. .
In addition to specific changes in the kidneys, inflammatory diseases of the kidneys are often observed in diabetes mellitus. In the urine of such patients, bacteriuria is detected, which is asymptomatic or with a clinical picture of pyelonephritis. Purulent pyelonephritis in patients diabetes mellitus occurs in the form of apostematous nephritis, abscess or carbuncle of the kidneys. Cystitis is often associated. This is facilitated not only by the presence of glucosuria (an environment for the proliferation of microbes), but also by autonomic neuropathy, leading to the syndrome of incomplete bladder emptying.
Kidney infection can lead to the formation of an abscess or carbuncle of the kidney, which can occur with the clinical picture of cholecystitis, appendicitis, pancreatitis, etc. The septic nature of the temperature curve and relative resistance to antibiotic therapy, despite the absence of a typical pain syndrome (autonomic neuropathy), are indicators possible abscess or carbuncle of the kidney. Ultrasonography in some cases it helps to establish correct diagnosis, and surgical treatment saves the lives of patients. In addition, in diabetes mellitus hydronephrosis occurs, caused by “atonic” (neurogenic) bladder. Diagnosis of diabetic nephropathy.
The earliest and most reliable method for diagnosing DN is the microalbuminuria test. The term "microalbuminuria" refers to the excretion of albumin in urine in low quantities (from 30 to 300 mg/day). This amount of protein is not determined by traditional routine blood test.
chi, and therefore the earliest stage of DN may not be diagnosed. But this stage is the only one reversible with timely administration of pathogenetic therapy. Screening for microalbuminuria should be performed
in patients with type 1 diabetes:
Once a year after 5 years from the onset of DM (at the onset of DM after
puberty);
Once a year from the moment of diagnosis of DM (at the onset of DM in
period of puberty);
in patients with type 2 diabetes:
Once a year from the moment of diagnosis of diabetes.
Prevention and treatment of diabetic nephropathy depending on its stage.
With normal urinary albumin excretion In the presence of microalbuminuria.
1. Careful correction carbohydrate metabolism:
A regimen of intensified insulin therapy for type 1 diabetes and transfer to insulin therapy for patients with type 2 diabetes in case of poor compensation when taking oral hypoglycemic agents;
2. Correction blood pressure:
Start antihypertensive therapy if blood pressure rises above 140/90 mmHg. Art., among antihypertensive drugs, it is preferable to prescribe therapy with angiotensin-converting enzyme (ACE) inhibitors.
Avoid prescribing medications that worsen carbohydrate and lipid metabolism ( non-selective P-blockers- obsidan, anaprilin, thiazide diuretics such as hypothiazide).
3. Correction of intrarenal hemodynamics:
ACE inhibitors (even with normal blood pressure levels). In the presence of proteinurgsh.
1. Correction of carbohydrate metabolism.
2. Correction of blood pressure with the preferred prescription of ACE inhibitors.
At the stage of microalbuminuria, protein intake is limited to 1 g/kg body weight.
At the stage of proteinuria up to 0.7 - 0.8 g per 1 kg of body weight.
At the stage of chronic renal failure - up to 0.5 - 0.6 g per 1 kg of body weight,
It is advisable to replace animal protein with vegetable protein. Extension allowed carbohydrate diet to cover energy costs. The patient's diet should be prepared with the participation of a nutritionist. 4. Correction of lipid metabolism:
An increase in proteinuria, as a rule, is accompanied by the development of hyperlipidemia with a predominance of atherogenic lipid fractions, and therefore it is recommended to follow a lipid-lowering diet. When increasing total cholesterol more than 6.5 mmol/l (norm up to 5.2) and serum triglycerides more than 2.2 mmol/l (norm up to 1.7), it is recommended to add medications that normalize the lipid spectrum of the blood.
At the stage of chronic renal failure (CRF):
In patients with type 1 diabetes with progression of chronic renal failure daily requirement in insulin decreases sharply (due to inhibition of the activity of renal insulinase, which metabolizes insulin). In this regard, the frequency of hypoglycemic conditions increases, which requires a reduction in the dose of insulin;
In patients with type 2 diabetes receiving therapy with oral hypoglycemic agents, with the development of chronic renal failure, transfer to insulin therapy is recommended, since most of these drugs are metabolized and excreted in batches. An exception is the drug glyurenorm (gliquidone), excreted through the biliary tract, which allows its use in patients with early stage chronic renal failure (serum creatinine not more than 200 µmol/l);
When serum creatinine increases to more than 200 µmol/l (or 2.2 mg%), it becomes necessary to manage patients together with a nephrologist to decide on the tactics of conservative treatment of such patients;
When serum creatinine increases to more than 500 µmol/l (or 5.5 mg%), the issue of preparing patients for extracorporeal (hemodialysis, peritoneal dialysis) or surgical (kidney transplantation) treatment methods is decided.
Indications for extracorporeal and surgical methods treatment of diabetic nephropathy Kidney transplant
When serum creatinine increases to 8-9 mg% (600-700 µmol/l) and glomerular filtration rate decreases< 25 мл/мин
Hemodialysis or peritoneal dialysis
when serum creatinine increases to mg% (µmol/l) and filtration rate decreases< 10 мл/мин
Detection of microalbuminuria or proteinuria is a mandatory indication for initiating active drug treatment for DN. At the moment, the issue of choosing the most effective drug that can slow down the progression of the pathological process in the kidneys in diabetes has been clearly resolved in favor of ACE inhibitors (captopril, enalapril, perindopril, ramipril, fosinopril, trandolanpril, etc.). This is due to the fact that ACE inhibitors, by blocking the formation of a powerful vasoconstrictor - angiotensin II, not only have a pronounced effect hypotensive effect, but also a specific protective effect on kidney tissue, regardless of their effect on blood pressure levels. It has been established that the local renal concentration of angiotensin II is thousands of times higher than its content in the blood plasma. Mechanisms pathogenic action angiotensin II on kidney tissue is due not only to its vasoactive effect, but also to proliferative, prooxidant and prothrombogenic activity.
According to the latest WHO recommendations (1999) ACE inhibitors are recognized as first-line drugs of choice for the treatment of DN. ACE inhibitors are capable of normalizing not only systemic, but also intraglomerular hypertension, which plays a role in vital role in the progression of diabetic kidney damage. These drugs, by blocking the formation of angiotensin II, provide expansion of the efferent (efferent) glomerular arteriole, thereby significantly reducing intraglomerular hydrostatic pressure. The unique nephroprotective properties of ACE inhibitors allow them to be used to treat the earliest stage of DN (microalbuminuria stage) even with normal levels of systemic blood pressure. In patients with diabetes and arterial hypertension, the antiproteinuric effect of ACE inhibitors is enhanced significant decrease systemic blood pressure.
Relatively recently, it appeared on the pharmaceutical market a new group drugs that can block the action of angiotensin II at the level of receptors on which this peptide acts. These drugs are called angiotensin receptor antagonists. These include losartan, irbesartan, valsartan, etc. Perhaps a combination of an ACE inhibitor and an angiotensin receptor antagonist, which allows blocking the activity of the renin-angiotensin system, will be most effective in preventing the progression of diabetic kidney damage, but this question still remains open.
Economic aspects of diabetic nsphropathy.
Treatment of patients with diabetes with end-stage renal failure requires enormous costs. In the USA, the cost of treating 1 patient on hemodialysis is thousands. $ per year. Using the same amount of money, it is possible to conduct:
Screening for microalbuminuria (MAU) in 4000 patients with diabetes or
Provide therapy with ACE inhibitors for a year to 400 patients with diabetes at the MAU stage, which in 50% of cases will completely stop the progression of nephropathy
Provide therapy with ACE inhibitors for a year to 200 patients with diabetes at the stage of proteinuria, which will stop the progression
DN and its transition to the stage of chronic renal failure in 50% of patients. t
DIABETIC NEUROPATHY
Neuropathy occupies a special place among the late complications of diabetes mellitus. The first clinical signs of neuropathy can occur already in the early stages of development of the disease and, as a rule, are accompanied by subjective symptoms that significantly affect the quality of life of patients (for example, pain). In addition, neuropathy can cause the formation of a neuropathic foot ulcer, influence the course of diabetes mellitus itself. For example, the consequence of neuropathic gastroenteropathy may be significant variability in the absorption of food in the intestine (in particular carbohydrates) and, as a result, unpredictable fluctuations in postprandial glycemia. The consequence of autonomic neuropathy is the loss of the ability of patients to recognize hypoglycemia.
Today, the pathogenetic pathways of damage to the nervous system are reduced to two main complementary theories: metabolic and vascular. Moreover, if previously more attention and, accordingly, a greater share in the development of neuropathy was attributed to vascular changes, united under the concept of diabetic microangiopathy, today the results of a number of studies indicate a close relationship between metabolic changes and the state of endoneural blood flow.
As a cause of diabetic foot syndrome, including gangrene, peripheral sensory and autonomic polyneuropathy plays a significant role.
Tia. Patients with neuropathically infected feet make up 60-70% of all patients with diabetic foot syndrome.
Hyperglycemia, competitively inhibiting the transport of myoinositol into the cell, leads to a decrease in its intracellular concentration, which, along with disruption of myelin synthesis, leads to a decrease in Na-K-ATPase activity and, as a consequence, demyelination of nerve fibers, loss of the ability to transmit nerve impulses along the fiber and slowing down the speed of nerve stimulation.
With diabetic neuropathy, microcirculatory disorders develop in the system of intraneural vessels. The key role here is played by an increase in the formation of advanced glycation end products, which is a consequence of long-term hyperglycemia with disruption of the structure of the vascular wall and, in particular, the basement membrane of the capillaries. At the same time, the formation of low-density lipoproteins is induced and their accumulation in vascular wall, proliferation of smooth muscle cells. A certain role is also played by the influence exerted by lipid peroxidation, which significantly increases the formation of free radicals that have a destructive effect on the endothelium, as well as suppression of the synthesis of prostacyclin, which has vasodilating properties and is a physiological inhibitor of platelet aggregation. Classification and clinical manifestations of diabetic neuropathy A variant classification was proposed by Thomas and Ward: ■ Peripheral polyneuropathy Autonomic neuropathy
In its turn peripheral neuropathy divided into: Symmetrical polyneuropathies Sensory or sensorimotor Acute or subacute motor Focal or polyfocal neuropathies Cranial form Proximal motor neuropathy Mononeuropathy of the limb and trunk Clinical forms of autonomic neuropathy ■ Cardiovascular Sinus tachycardia at rest Silent myocardial infarction Orthostatic hypotension Sudden death
Gastrointestinal
Esophageal dysfunction, gastropathy, slow gastric evacuation function, diabetic diarrhea, constipation, fecal incontinence.
Urogenital
Erectile dysfunction. Retrograde ejaculation (infertility). Bladder dysfunction.
Impaired ability to recognize hypoglycemia
Sweating dysfunction sweating of the face, upper half torso when eating.
Distal anhidrosis.
Diabetic osteoarthropathy (PDA, Charcot foot) is non-infectious bone and joint destruction caused by diabetic neuropathy. Unlike typical forms of osteoporosis, osteoarthropathy is a lesion bone tissue exclusively local in nature. It is believed that PDA is caused by a special form of diabetic neuropathy with predominant damage to myelinated nerve fibers and relative preservation of non-myelinated nerve fibers, which leads to impaired microvascular tone, which entails increased blood flow in bone tissue. These pathological processes serve as a prerequisite for the manifestation of PDA - osteoporosis of the distal parts of the lower extremities, which reduces the resistance of the bone to damaging influences.In this case, a damaging factor (minimal trauma while walking, surgery on the foot, etc.) leads to increased blood flow in the bone or its damage, and as a result, activation of osteoclasts with subsequent “launch” of the process of osteolysis.The course of PDA has 4 stages.
1. Acute stage. It is characterized by swelling of the foot, moderate hyperemia and local hyperthermia. Pain and fever are not typical. X-ray images reveal osteoporosis of the bones of the feet, possibly the presence of microfractures.
2. Subacute stage. Fragmentation and onset of foot deformation (typically flattening of the arch of the foot). Swelling and inflammation are reduced. X-ray - fragmentation of bone structures.
3. Chronic. Severe deformation of the foot, the presence of spontaneous fractures and dislocations. The function of the foot is completely disrupted; in typical cases, loads on the foot when walking lead to deformation of the foot like a “rocking foot”; in more severe cases, the foot can be figuratively compared to a “bag of bones”. X-ray - fragmentation of bone structures, periosteal and paraosseous calcification.
4. Stage of complications. Overload individual areas foot leads to the formation of ulcerative defects; when they become infected, phlegmon of the foot, osteomyelitis, and gangrene develop.
Diagnosis is based on medical history (long-term diabetic sensorimotor neuropathy), clinical picture(if a patient with diabetes mellitus has unilateral swelling of the foot, especially if the skin is intact, it is necessary to exclude a PDA), radiological and biochemical (bone isoenzyme of alkaline phosphatase, hydroxyproline, collagen fragments, etc.) markers. It is known that PDA does not develop in patients with circulatory disorders of the lower extremities. Disturbance of the main blood flow and diabetic PDA- mutually exclusive diseases, and the use of vasoactive drugs worsens the prognosis for PDA. Treatment.
1. Complete unloading of the foot until signs of inflammation disappear, wearing an orthosis, and then orthopedic shoes (required).
2. In the acute phase, it is possible to use drugs that inhibit the process of bone tissue resorption (xidifon, phosphamax, clodronate, calcitonin).
3. Drugs that stimulate bone tissue development (active metabolites of vitamin D3), anabolic steroids, calcium supplements.
4. Auxiliary products (NPVN, elastic bandaging limbs, diuretics) are used to reduce swelling.
5. In case of ulcers, antibacterial therapy.
DIABETIC FOOT SYNDROME
Diabetic foot syndrome combines pathological changes in the peripheral nervous system, arterial and microcirculatory beds, and osteoarticular apparatus, which pose an immediate threat to the development of ulcerative necrotic processes and gangrene of the foot.
Despite a sufficient amount of information on the pathogenesis, diagnosis, methods of treatment and prevention of complications of diabetes, data on the frequency and outcome of lesions of the lower extremities still remain disappointing. The results of epidemiological studies conducted in various countries indicate that in the structure of all non-traumatic lower limb amputations, patients with diabetes account for 50-75%.
In the pathogenesis of the development of diabetic foot syndrome, the leading place is occupied by three main factors: neuropathy;
■ damage to the arteries of the lower extremities;
■ infection.
The last factor, as a rule, is concomitant with respect to the first two. Based on the predominance of neuropathic changes or peripheral blood flow disorders, two main clinical forms of diabetic foot syndrome are distinguished:
neuropathic; ■ ischemic.
Along with the two main forms of damage to the lower extremities in diabetes mellitus, a third is also distinguished:
mixed (neuro-ischemic).
In neuropathic form There is damage to the somatic and autonomic nervous system when the arterial segments of the lower extremities are intact. Neuropathy can lead to the following three types of foot lesions:
■ neuropathic ulcer;
osteoarthropathy (with subsequent development of Charcot's joint); neuropathic edema.
Long-term sensorimotor neuropathy leads to a characteristic deformation of the foot, which prevents its normal position when walking and standing. This deformation is caused by an imbalance between the flexors And extensors, leads to bulging of the heads of the metatarsal bones, the formation of separate areas on the plantar surface of the foot that experience excess load pressure. Constant pressure on these areas leads to To inflammatory autolysis of soft tissues and ulcer formation. This is the reason for the most common location of ulcers in the area projections heads metatarsal bones on the sole. Decline pain sensitivity And joint feeling leads to the fact that the formation of an ulcer goes unnoticed by the patient. Often, due to reduced sensitivity, patients are deprived of protection from various damaging influences external environment, for example, exposure to high temperatures or ultraviolet rays.
Autonomic dysfunction often accompanies somatic neuropathy and is characterized by a decrease or complete absence of sweating function (dry, thin skin). The consequence of autonomic neuropathy, which can be characterized as autosympathectomy, is calcification of the arterial media, which is often called Mönckeberg sclerosis. Autonomic neuropathy leads to increased blood flow in the superficial vessels of the skin, which causes elevated temperature skin of the feet, increased blood flow and contouring of skin veins, even in a horizontal position of the patient. These changes are a consequence of the formation of arteriovenous shunts, through which arterial blood, bypassing the capillary network, is discharged into the venous bed, leading to an actual decrease in capillary blood flow. Elevated skin temperature of the foot is more likely to indicate the presence of an active process of osteoarthropathy than the state of peripheral blood flow.
Very often, the formation of ulcerative lesions occurs due to improper selection of shoes. As mentioned above, sensorimotor neuropathy leads to a characteristic foot deformity. On the other hand, there is the presence of neuropathic edema (fluid accumulation in the tissues of the lower extremities associated with neuropathy). The causes of neuropathic edema have not been fully elucidated, but it can be assumed that they are a consequence of disorders in the autonomic nervous system, the formation of multiple arteriovenous shunts and disruption of hydrodynamic pressure in the microvasculature. Thus, the patient’s foot changes not only its shape, but also its size. At the same time, shoes are selected by patients based on knowledge of their previous sizes, and one or two measurements are taken into account. Reduced sensitivity does not allow the patient to detect discomfort in a timely manner new shoes and, as a consequence of this, leads to the formation of abrasions and ulcers.
Patients' feet may be exposed to various damaging factors. Due to the increased sensitivity threshold, patients may not feel the effects of high temperature, for example, a burn on the dorsum of the foot when sunbathing, or on the plantar surface of the foot when walking barefoot on hot sand. From chemical factors It should be noted the damaging effect of keratolytic ointments containing salicylic acid, which can lead to the formation of ulcers.
Ulcerative defects are often infected with staphylococci, streptococci, and colibacteria. Often there is an addition of anaerobic microflora. An infected foot lesion may be accompanied by the formation of gas in the soft tissues, which is detected both by palpation and x-ray. This condition is usually accompanied by hyperthermia and leukocytosis. In such cases, urgent surgical intervention with necrectomy, administration of adequate antibiotic therapy, and careful monitoring of glycemia are necessary.
The ischemic form develops as a consequence of atherosclerotic damage to the arteries of the lower extremities, which leads to disruption main blood flow. In this case, neuropathic changes may also occur. The ischemic form is characterized by pain symptoms, usually pain at rest. In this case, some relief occurs when the patient changes his body position, for example, by giving an elevated position to the head end of the bed or hanging his legs from the bed. In order to relieve pain symptoms, lumbar sympathectomy is sometimes performed, but no improvement in the hemodynamics of the lower extremities is observed.
Externally skin the feet may be pale or cyanotic, or have a pinkish-red hue due to dilation of the superficial
pillars in response to ischemia. In contrast to the neuronatic form, the ischemic form of the lesion has cold feet. Ulcerative defects occur as acral necrosis (fingertips, marginal surface of the heels). Provoking factors in terms of the occurrence of ulcerative defects are: wearing tight shoes, the presence of deformation, swelling of the foot. A secondary infection, both aerobic and anaerobic, is often associated. The cause of impaired blood flow is the development of obliterating atherosclerosis of the arteries of the lower extremities. At the same time, there is a clear tendency towards generalized damage to arteries of medium and small caliber. In patients with diabetes mellitus, atherosclerotic changes develop much more often than in the general population.
CHARACTERISTIC SIGNS AND SYMPTOMS ARISING FOR MACROANGIOPATHY LOWER LIMB
1. Intermittent claudication
2. Cold to the touch foot
3. Night pain
4. Pain at rest
5. No pulse
6. Pallor of the limb in an elevated position
7. Slow filling of veins with preliminary elevated position of the limb
8. Skin rubeosis in combination with pinpoint petechiae
9. Atrophy of subcutaneous adipose tissue 10. Presence of acral necrosis
11. Gangrene Diagnosis.
The main objectives of diagnostic measures are to determine the clinical form of diabetic foot syndrome, the severity of neuropathy and/or ischemia, the depth of ulcerative lesions, assess the condition of bone structures, identify pathogenic flora in an ulcerative defect.
Diagnosis of foot lesions in patients with diabetes is based on the following principles:
■ careful history taking,
■ examination of the legs,
Assessment of the state of arterial blood flow,
X-ray of feet and ankle joints, bacteriological examination of wound discharge.
What matters is the duration of the disease, the type of diabetes, the treatment given, whether the patient at the time of examination or previously had symptoms of neuropathy (stabbing or burning pain in the legs, cramps in the calf muscles, feeling of numbness, paresthesia).
A history of ulcers or amputations is an important predictor of the development of new foot lesions. With other late complications of diabetes (retinopathy and nephropathy, especially the terminal stage), there is a high probability of developing a peptic ulcer. It is necessary to determine the patient's awareness of the possibility of foot damage in diabetes, its causes and preventive measures. Based on anamnestic data, the first step can be taken in the differential diagnosis of neuropathic and ischemic forms of diabetic foot syndrome.
The complaint of intermittent claudication is characteristic feature macroangiopathies. In this case, the time of onset of pain, the distance that the patient walks before the first pain appears, and the presence of pain at rest are taken into account. Unlike ischemic pain, which can also occur at night, neuropathically caused pain syndrome is relieved by walking. Ischemic pain is somewhat relieved by hanging the legs over the edge of the bed.
Foot examination is the simplest and effective method identifying foot lesions. It is important to pay attention to the following signs:
1. color of the limbs: red (with neuropathic edema or Charcot arthropathy), pale, acidic (with ischemia), pink in combination with pain symptoms and absence of pulsations (severe ischemia);
2. deformities: hammertoes, hooked toes, hallux valgus, hallux varus, protruding metatarsal bones of the foot, Charcot arthropathy;
3. edema: bilateral - neuropathic, as a result of cardiac or renal failure; unilateral - with an infected lesion or Charcot arthropathy;
4. condition of nails: atrophic with neuropathy and ischemia, discoloration in the presence of fungal infection;
5. hyperkeratoses: especially pronounced in areas of the foot that experience excessive pressure during neuropathy, for example, in the area of the projection of the heads of the metatarsal bones;
6. ulcerative lesions: in neuropathic forms - on the sole, in ischemic forms - they form in the form of acral necrosis;
7. pulsation: pulsation on the dorsal and posterior tibial arteries of the foot is reduced or absent on both limbs in the ischemic form and normal in the neuropathic form;
8. skin condition: dry, thin skin with neuropathy.
Assessment of neurological status. Neurological examination includes testing of vibration sensitivity using a graduated
tuning fork. The vibration sensitivity threshold increases with age, so adjustment for age or comparison of the results obtained with the normogram is necessary. Neuropathic lesions are characterized by an increase in the threshold of vibration sensitivity, which corresponds to a decrease in indicators on the tuning fork scale below 3.0 conventional units; For ischemic lesion indicators correspond to the age norm. Determination of pain, tactile and temperature sensitivity using standard methods.
Assessment of the state of arterial blood flow. The most commonly used non-invasive methods for assessing the state of peripheral blood flow are Dopplerometry, Dopplerography (they allow one to assess the level of stenosis or thrombosis, as well as its extent); measurement is being carried out systolic pressure in the arteries of the thigh, leg and foot, the level of occlusion is determined by the pressure gradient. Indicators of the ankle-brachial index (the ratio of the systolic pressure in the artery of the leg and the systolic pressure in the brachial artery) reflect the degree of reduction in arterial blood flow.
X-ray of feet and ankle joints. This method allows you to identify signs of diabetic osteoarthropathy, diagnose spontaneous fractures of small bones of the foot, suspect the presence of osteomyelitis, exclude or confirm the development of gas gangrene.
Bacteriological research detachable wound defect is of paramount importance for the selection of adequate antibiotic therapy.
Differential diagnosis.
There is often a need to differentiate between neuropathic and ischemic pain that occurs at night or at rest. Neuropathic pain, even with slight physical exertion on the legs, weakens, while with ischemia it worsens. Patients with macroangiopathy note some relief of pain in certain positions of their legs, when lowering them from the bed, so they are often forced to sleep while sitting. The reduction in pain is explained by a relative improvement in blood supply associated with increased blood flow due to the formation of arteriovenous shunts, due to a decrease or complete loss of sympathetic vascular tone. This also explains the temporary relief of pain symptoms in patients with obliterating disease.
rosclerosis during sympathectomy. It should be emphasized that sympathectomy does not lead to a significant restoration of reduced blood flow and a decrease in the degree of ischemia, but aggravates the manifestations of autonomic neuropathy, resulting in the development of Charcot foot.
Differential diagnosis of diabetic foot forms
Neuropathic | Ischemic |
■ A history of ulcers, toe amputations, deformities of the feet, fingers, and nail plates. Long course diseases Alcohol abuse Dry skin, areas of hyperkeratosis in areas of excess load pressure ■ Deformation of the feet, fingers, ankle joints - specific, bilateral swelling Pulsation in the arteries of the feet is preserved on both sides ■ Ulcerative defects in points of excess load pressure, painless Characteristic absence subjective symptoms | ■ A history of cardiovascular diseases, atherosclerotic lesions of cerebral vessels. Hypertension and/or dyslipidemia. Smoking abuse ■ Skin color - pale or cyanotic, atrophic, often cracked ■ Deformation of fingers and feet is not specific Pulsation in the arteries of the feet is reduced or absent ■ Acral necrosis, sharply painful Intermittent claudication |
Conditions that should be differentially diagnosed in the presence of pain when walking: arthritis, muscle pain, neuropathic pain, radicular pain, compression of the spinal roots, anemia, myxedema, thrombophlebitis.
Timely and adequate conservative therapy for neuropathic infected forms of foot lesions allows one to avoid surgical intervention in 95% of cases. Treatment for neuropathic foot infection includes the following main components: 1.Optimization metabolic control.
To ensure conditions conducive to healing, it is important to achieve a state of compensation of carbohydrate metabolism. Intensive insulin therapy is carried out. The body's need for insulin may increase significantly due to
the presence of an infectious-inflammatory process and high temperature, therefore this requires a corresponding increase in the dose of administered insulin. Patients with type 2 diabetes who are treated with oral hypoglycemic drugs, in the presence of non-healing non-iropathic ulcers or severe pain, are recommended to be transferred to insulin therapy.
2. Unload the affected area.
Complete rest And offloading the foot can cause even years-old ulcers to heal within weeks. In this case, both a wheelchair, crutches, and special unloading shoes can be used.
3. Local wound treatment.
Local treatment of the wound includes removal of necrotic tissue, treatment of the edges of the ulcer and ensuring asepticity wound surface and nearby areas of the foot. Solutions should not have coloring properties (iodine), since it is difficult to judge the dynamics of the inflammatory process from the colored skin around the wound. Dressing materials must provide sufficient moisture inside the wound; hydrogel dressings are used for this purpose; have sufficient hydrophilicity; ensure unhindered gas exchange, be atraumatic for the wound defect, especially when removing the bandage; be impermeable to bacteria. The choice of dressings is made V depending on the stage of the wound process /. Removal of areas of hyperkeratosis.
If there are areas of hyperkeratosis, it is necessary to remove them in a timely manner using a scalpel with a shortened blade. This procedure is performed by specially trained medical personnel. In some cases, after removal of the callus, an ulcerative defect is discovered.
6. Correct selection And wearing special shoes.
7. Antibiotic therapy.
If there is an infection of the soft tissues of the foot, antibiotic therapy is necessary. The type, dose of the drug and duration of treatment are determined based on the data of a bacteriological study of the microflora of the wound discharge, the severity of the process and the rate of healing of the ulcer.
When it is not possible to quickly obtain test results, antibiotic therapy is prescribed immediately. wide range actions. The main groups of antibacterial drugs and possible combinations used in the treatment of patients with infected forms of foot lesions: penicillin group, ampicillin group, group of penicillinase-resistant penicillins; a group of broad-spectrum penicillins; cephalosporins, aminoglycosides gentamicin, kanamycin; macrolides, erythromycin, clarithromycin, azithromycin, roxithromycin, lincomycin, clindamycin; quinolones, ciprofloxacin, ofloxacin, pefloxacin.
Treatment of the non-schemic form of diabetic foot syndrome
1. Use of conservative methods of therapy (see above).
2. Relief of the phenomena of critical ischemia of the foot;
Drug therapy aimed at improving macro- and microhemodynamics of the affected limb is a combination of rheological solutions (reopolyglucin, rheomacrodex) with disaggregants (curantil, trental) and antispasmodics (papaverine, no-shpa). The course of treatment is for 7-10 days. If there is clinical improvement, manifested in the relief of pain and improvement of the local status of the ulcer (the appearance of active granulations and marginal epithelization), standard conservative therapy can be continued for another 7-10 days, followed by a transition to tablet preparations.
The most effective treatment for patients with ischemic DS is intravenous administration of prostaglandin E1 (vasaprostan). The drug is administered at a dose of 60 mg/day for? 250 ml of saline solution for 10-14 days. If necessary, the course of therapy with vazaprostan can be continued for up to 28 days until the phenomena of critical ischemia are completely relieved. If the phenomena of critical ischemia are stopped by the primary course, then the patient is transferred to standard disaggregant therapy.
If the implementation is ineffective conservative therapy the question is raised about the possibility of reconstructive surgery. The choice of reconstruction method depends on the level and type of lesion:
a) percutaneous transluminal angioplasty;-
b) thrombarterectomy;
c) distal bypass with vein in situ.
Diabetic gangrene. In case of extensive purulent-necrotic lesions, amputation is performed, while the most favorable in terms of post-amputation rehabilitation are amputations at the level lower third shins. Issues of post-amputation rehabilitation are resolved by orthopedic surgeons. Important in the future has prosthetics and selection orthopedic shoes.
Economic aspects.
Direct costs for one limb amputation in a patient with diabetes (according to the group for the study of the economics of diabetes, 1999) amount to 60 thousand rubles. For comparison: the level of expenses for training 1 patient is 2000 rubles, opening a diabetic foot office is 15-20 thousand rubles. The operation of one “diabetic foot” office for 1 year, with the ability to provide therapeutic and diagnostic assistance to 1,500 patients, costs 40 thousand rubles.
MINISTRY OF HEALTH OF THE RUSSIAN FEDERATION
Irkutsk State Medical University
KHAMNUEVA L. Y., ANDREEVA L. S., SHAGUN O. V.
COMPLICATIONS OF DIABETES MELLITUS:
PATHOGENESIS, CLASSIFICATION, CLINIC, DIAGNOSIS, TREATMENT, PREVENTION
Tutorial
There are two groups of complications in diabetes: acute and chronic. Acute complications of diabetes develop within hours or days; chronic complications develop over several months, but more often over years or even decades. That's why chronic complications DM is also called “late”.
Acute complications of diabetes mellitus.
Acute complications of diabetes include ketoacidotic, hyperosmolar (hyperglycemic) and lactic acidotic coma. Hypoglycemic coma, which can complicate glucose-lowering therapy for diabetes, is considered separately. Laboratory signs of diabetic comas are given in table. 6.
Ketoacidotic coma ranks first in prevalence among acute complications of endocrine diseases and is typical for T1DM. The mortality rate for this coma reaches 6-10%, and in children with T1DM this is the highest common reason of death. A rapidly progressing insulin deficiency leads to the development of coma.
Predisposing factors are:
prescribing too small doses of insulin during treatment;
violation of the insulin therapy regimen (skipped injections, expired insulin);
a sharp increase in the need for insulin, which occurs during infectious diseases, injuries and operations, stress, concomitant endocrine disorders with overproduction of counter-insular hormones (thyrotoxicosis, acromegaly, pheochromocytoma, Cushing's disease), pregnancy;
Mechanisms of damage in ketoacidotic coma associated with intoxication with ketone bodies, metabolic acidosis, hypovolemia, hypoxia and cell dehydration.
Ketone bodies, especially acetone, actively interact with lipid components cell membranes, and also suppress the normal functioning of many intracellular enzymes. The phospholipid-rich structures of the central nervous system are particularly affected.
In severe cases, hypovolemia leads to a decrease in renal blood flow, which is accompanied by a weakening of glomerular filtration and a decrease in diuresis (oliguria). This entails an increase in azotemia and worsening acidosis due to a weakening of the kidneys' excretion of nitrogenous wastes and secreted H + ions. Azotemia and acidosis cause disturbances in all organ systems, with the greatest threat to life associated with suppression of the functions of the central nervous system that regulate blood circulation and respiration.
Symptoms of ketoacidosis are loss of appetite, nausea, vomiting, abdominal pain, then blurred vision, darkness and loss of consciousness, depressed reflexes, drop in blood pressure, the appearance of Kussmaul breathing (rare, deep, noisy), symptoms of dehydration (decreased tissue turgor, soft eyeballs), fruity (with a noticeable admixture of acetone) odor of exhaled air.
Laboratory signs of ketoacidotic coma are given in Table. 6. Noteworthy hyperglycemia, but not maximum, increase ketone bodies and acidosis. Hyperlipidemia and hypercholesterolemia are also characteristic, which indicates active lipolysis.
Hyperosmolar (hyperglycemic) coma more common in older people with mild to moderate T2DM. In 30% of patients it turns out to be the first manifestation of T2DM, i.e. In almost 1/3 of patients with hyperosmolar coma, the diagnosis of diabetes is first made only at the time of coma development. This leads to the fact that the mortality rate in hyperosmolar coma reaches 30%, while in the “more expected” ketoacidotic coma in persons observed for T1DM, the mortality rate is no more than 10%, i.e. 3 times less.
Cause of hyperosmolar coma– a relative deficiency of insulin caused by insulin resistance, the amount of which in the body is sufficient to prevent the processes of enhanced lipolysis and ketogenesis, but not enough to counteract increasing hyperglycemia. Most often, coma occurs as a result of an increase in the need for insulin due to increased action of endogenous contrainsular hormones in conditions of a developing “acute phase response” (infectious diseases, mechanical injuries and operations, burns and frostbite, acute pancreatitis, myocardial infarction, etc.) or when concomitant endocrine disorders (thyrotoxicosis, acromegaly, pheochromocytoma, Cushing's disease).
Cases have been described of the development of hyperosmolar coma when it is impossible to quench thirst in lonely bedridden elderly patients, as well as when using concentrated glucose solutions (prescribed for parenteral nutrition) in people with initially unrecognized diabetes.
Mechanisms of damage in hyperosmolar coma associated with dehydration of all tissues caused by hyperosmolality of blood plasma (>350 mOsmol/kg) against the background of pronounced hyperglycemia (> 40 mmol/l) and a decrease in blood volume.
Dehydration of brain structures with sharp drop intracranial pressure leads to general depression of the central nervous system, manifested in the form of neurological disorders, an increasing disorder of consciousness, turning into its loss, i.e. in a coma. Hemocoagulation disorders associated with hypovolemia can provoke the development of disseminated intravascular coagulation syndrome, arterial (myocardial infarction, stroke) and venous (especially often in the inferior vena cava basin) thrombosis.
Symptoms of hyperosmolar coma. Over the course of several days or weeks, symptoms such as thirst, polyuria, polydipsia, weight loss and weakness increase. The mechanism of these symptoms is the same as in ketoacidotic coma and is associated with hyperglycemia, osmotic diuresis, increasing dehydration and loss of electrolytes. However, dehydration in hyperosmolar coma reaches a much greater degree, and therefore cardiovascular disorders caused by hypovolemia in these patients are more pronounced. Characteristic laboratory signs: very high plasma glucose concentration and osmolality, no ketoacidosis, normal pH.
Lactic acidemic coma.
IN pure form Lactic acidemic coma in diabetes is much less common than ketoacidosis and hyperosmolar coma. The accumulation of lactate in an amount exceeding the body’s ability to utilize it in the liver and kidneys (more than 3400 mmol/day) leads to lactic acidosis, in which the lactic acid content increases to 2 mmol/l or more.
Predisposing factors for lactic acidemic coma:
any conditions accompanied by severe tissue hypoxia - shock, blood loss, severe heart and pulmonary failure. In this case, glycolysis is compensatory activated, leading to the accumulation of lactic acid;
severe damage to the liver and kidneys, i.e. organs in which lactic acid is metabolized;
any conditions causing acidosis with pH values<7,2 (при рН<7,2 подавляется распад лактата в печени и почках).
Many diseases progress without treatment and cause changes in the functioning of the entire body. Complications are especially dangerous for people with diabetes. Metabolic disorders lead to kidney failure and the development of other dangerous diseases.
Why complications develop in diabetes mellitus
The causes of concomitant ailments depend on the type of disease. In type I diabetes, complications develop when the patient does not administer insulin in a timely manner.
The patient may simply systematically deviate from the injection schedule, which will lead to the appearance of concomitant diseases.
Mechanism of development of complications:
- The amount of insulin in the blood decreases, and glucose increases.
- There is a strong feeling of thirst, polyuria (increased volume of urine).
- The concentration of fatty acids in the blood increases due to massive lipolysis (breakdown of fats).
- All anabolic processes slow down, tissues are no longer able to ensure the breakdown of ketone bodies (acetone formed in the liver).
- Intoxication of the body occurs.
In type II diabetes mellitus (non-insulin-dependent), problems arise due to the fact that patients do not want to follow a diet and do not take glucose-lowering medications. Nutritional correction is mandatory in the treatment of chronic hyperglycemia (excess blood sugar) and insulin resistance (reduced sensitivity of insulin-dependent cells to the action of insulin).
Complications of type 2 diabetes occur as follows:
- The level of glucose in the blood gradually increases.
- Due to an excess of sugar, the functioning of internal organs begins to deteriorate.
- Intracellular hyperglycemia develops, leading to glucose neurotoxicity (impaired nervous system functions) and other diseases.
Factors that increase the risk of complications
The patient's condition rarely worsens without reason. Factors that increase the risk of diabetes complications:
- Genetic predisposition. The patient’s risk of developing complications increases 5-6 times if one of his parents suffered from severe diabetes.
- Excess weight. This is especially dangerous for type 2 disease. Regular diet violations lead to an increase in body fat. Specific cellular receptors can no longer actively interact with insulin, and over time their number in tissues decreases.
- Alcohol consumption. People with all forms of diabetes will have to give up alcohol, because it causes hypoglycemia and reduces vascular tone.
- Non-compliance with diet. For type 2 diabetes, it is prohibited to consume sweet fruits and foods containing fast carbohydrates and trans fats (ice cream, chocolate, margarine, etc.). If you have any type of illness, you should not eat fast food. “Insulin” diabetics should completely exclude sweets from their diet. If you don't follow the diet, your sugar levels will rise and fall sharply.
- Lack of physical activity. Neglecting exercise and physical therapy leads to a slowdown in metabolism. Decay products stay in the body for too long and poison it.
- Chronic cardiovascular diseases. With hypertension, coronary heart disease, and atherosclerosis, tissue sensitivity to insulin decreases.
- Stress, strong psycho-emotional stress. Adrenaline, noadrenaline, and glucocorticoids have a bad effect on the functioning of the pancreas and the production of insulin.
- Pregnancy. The tissues of the female body absorb their own insulin less due to the active production of hormones.
Acute complications of diabetes mellitus
These conditions are dangerous because they develop quickly and suddenly, can lead to the death of the patient, and are accompanied by serious metabolic disorders. Acute complications include:
- various forms of hyperglycemia;
- hypoglycemia.
Hyperglycemic conditions
Large amounts of glucose in the blood can kill a person with diabetes. Hyperglycemic conditions require hospitalization for further treatment. They come in 3 types:
| State | Reasons for development | Symptoms | Main methods of treatment |
| Ketoacidosis |
|
|
|
| Hyperosmolar state |
|
|
|
| Lactic acidotic coma (lactic acidosis) |
|
|
|
Hypoglycemia
The development of the disease is provoked by low blood sugar. To normalize the patient’s condition, doctors administer glucose drips. Hypoglycemia can be caused by an overdose of insulin, alcohol, too strict a diet, or excessive exercise. Symptoms of the disease:
- aggression, a state of unreasonable fear or anxiety;
- increased sweating, pale skin;
- rapid pulse - from 100 to 400 beats per minute;
- muscle tremors or cramps;
- nausea, vomiting;
- double vision;
- headache, severe dizziness.
Chronic complications of diabetes
Not all problems with metabolic disorders appear immediately. A number of diseases occur due to prolonged disruption of metabolic processes and concomitant intoxication. Organs and cells stop doing their job. Late complications of type I diabetes:
- Loss of vision. When the disease is initially diagnosed, 32% of patients are diagnosed with retinopathy (retinal damage). If left untreated, a diabetic rapidly develops cataracts and then blindness.
- Diabetic nephropathy. The circulatory system of the kidneys is affected. They cannot filter the plasma properly, and protein appears in the urine. The disease develops almost asymptomatically until the terminal stage.
- Damage to the circulatory system of the lower extremities. Type 2 diabetes is one of the leading causes of leg amputation that is not associated with physical trauma or accidents. Gangrene with this disease progresses slowly. The patient may not pay attention to foci of necrosis for a long time until amputation of the foot or the entire limb is required.
- Damage to the central nervous system (CNS).
- Angiopathy.
With non-insulin-dependent diabetes, the patient may develop the following late complications:
- Kidney failure. At the terminal stage, the patient requires a kidney transplant.
- Damage to the cardiovascular system. The main cause of death in patients with type 2 diabetes is stroke or heart attack. The vessels of the heart and brain, under the influence of excess glucose, begin to lose their elasticity, and atherosclerotic plaques appear on their surface.
- Problems with the central nervous system and peripheral nervous system.
- Poor blood supply to the lower extremities.
- Vision problems.
Angiopathy
The diseases are accompanied by damage to large and small vessels. With angiopathy, the blood circulation of the lower extremities, the functioning of the kidneys, eyes, heart, and brain are disrupted.
Diseases are treated with drugs to lower cholesterol, prevent blood clots, and improve tissue metabolism.
Symptoms of angiopathy:
- frequent urination;
- pale skin;
- arrhythmia;
- localized swelling;
- decreased visual acuity;
- impaired coordination and memory;
- high blood pressure.
Damage to the central nervous system
In diabetes mellitus, the blood supply to all organs is disrupted. Damage to the central nervous system is expressed in the development of encephalopathy. Patients experience asthenia, vegetative-vascular dysfunction, neuroses, and convulsions. The disease can be diagnosed using MRI and electroencephalography.
For the treatment of encephalopathy in diabetes mellitus the following is prescribed:
- Drugs to maintain normal blood glucose concentrations.
- Medicines to improve blood microcirculation, nootropics.
- Medicines that lower blood pressure.
- B vitamins, alpha lipoic acid, vitamin E for normal functioning of the central nervous system.
- Sedatives, tranquilizers.
Diabetic foot syndrome
Anatomical and functional changes occur against the background of osteoarthropathy, neuropathy, and angiopathy. Disorders in diabetic foot develop in the distal parts of the lower extremities, i.e. on fingers and pads. Ulcerative-necrotic processes affect soft and bone tissues. Approximately 90% of cases of the syndrome occur in patients with type 2 diabetes mellitus. Diabetic foot comes in three forms:
- Neuropathic. Develops against the background of diabetic multiple lesions of peripheral nerves (polyneuropathy).
- Neuroischemic. The cause of the development of this form of the disease is angiopathy.
- Osteoarthropathic. The form has 3 stages: acute, subacute, chronic. The cause of the disease is osteoporosis.
Consequences of diabetes in children
The main reason for the onset of the disease at a young age is genetic predisposition. If a child often suffers from viral diseases or has a weak immune system, then he is also at risk of developing diabetes. Children have the following complications:
- Problems with kidney function. The disease develops due to the fact that increased glucose damages the filtering elements of the kidneys. Proteinuria (the appearance of protein in the urine) is the main symptom of nephropathy. Patients with diseased kidneys are advised to diet and take medications that normalize blood pressure and lipid metabolism. For infections of the genitourinary system, antibiotics are prescribed.
- Decreased visual acuity. When glucose levels are high, the blood vessels and nerve fibers of the eye are damaged. Against the background of these processes, vision deteriorates. The patient complains of blurriness and “floaters” before the eyes. Treatment consists of normalizing the blood supply to the fundus of the eye with the help of medications and reducing glucose levels.
Treatment of complications of diabetes mellitus
When drawing up a treatment plan, the patient's condition plays an important role. There are three main areas of treatment:
- Decreased glucose levels. All patients should follow a low-carbohydrate diet. For type 1 of the disease, insulin therapy is indicated, and for type 2, the use of glucose-lowering drugs.
- Compensation of metabolic processes. An individual nutrition plan is developed for the patient, and injections of vitamins and beneficial acids are prescribed. Physical therapy is required.
- Treatment. The treatment plan is developed in accordance with the type and severity of the concomitant disease. For example, infectious lesions of the limbs or genitourinary system are treated with antibiotics.
