What Is Diabetes Fatigue?

Diabetes is a group of lifelong metabolic diseases characterized by chronic hyperglycemia caused by multiple causes. Long-term increase in blood glucose, damage to large blood vessels and microvessels, and endangers the heart, brain, kidney, peripheral nerves, eyes, feet, etc. According to World Health Organization statistics, there are more than 100 complications of diabetes, which is currently the most known one. disease. More than half of the deaths from diabetes are due to cardiovascular and cerebrovascular diseases, and 10% are due to renal disease. Patients with amputation due to diabetes are 10 to 20 times more than non-diabetics. Clinical data show that about 10 years after the onset of diabetes, 30% to 40% of patients will have at least one complication, and once the complication occurs, it is difficult to reverse drug treatment, so it is emphasized to prevent complications of diabetes as soon as possible.

Basic Information

English name

diabetes complications

Visiting department

Endocrinology

Multiple groups

Diabetics

Common locations

Heart, brain, kidney and eyes

Common causes

High blood sugar, untimely treatment, poor diet control, etc.

Common symptoms

Diabetic nephropathy, cardiovascular disease and diabetic foot, etc.

Causes of complications of diabetes

Diabetes complications can be divided into acute and chronic categories according to the severity of the onset of complications and pathological differences.

1. Causes of acute complications of diabetes

Including diabetic ketoacidosis, hyperglycemia and hypertonic state, lactic acidosis, etc., the main causes are due to severe lack of insulin activity and inappropriate rise of glycemic hormone, which leads to excessive blood sugar, which causes sugar, fat and protein Metabolic disorders that cause the body's water, electrolytes, and acid-base balance to become imbalanced.

2. Causes of chronic complications of diabetes

Chronic complications are the main causes of disability and death of diabetes, mainly including: major vascular complications, such as cerebrovascular, cardiovascular and lower extremity vascular lesions. Microvascular complications, such as kidney disease and fundus disease. Neuropathy, including sensory nerves responsible for the senses, motor nerves that govern physical activity, and autonomic neuropathy that manages internal organs, blood vessels, and endocrine functions.

At present, it is generally believed that the polyol bypass, protein kinase C, hexosamine activation, the amount of advanced glycosylation products (AGEs), and the increase of mitochondrial reactive oxidation products (ROS) induced by hyperglycemia may be chronic complications of diabetes And the common basis of the development of the disease.

Complications of diabetes

Diabetic nephropathy

It is one of the most important comorbidities for patients with diabetes. The incidence rate in China is also on the rise, and it has become the second cause of end-stage renal disease, second only to various glomerulonephritis. Due to its complex metabolic disorders, once it progresses to end-stage renal disease, it is often more difficult to treat than other kidney diseases. However, active and appropriate interventions can significantly reduce and delay the occurrence of diabetic nephropathy, especially in the early course of the disease.

2. Diabetic eye complications

(1) Diabetic retinopathy is the most important manifestation of diabetic microangiopathy, is a fundus lesion with specific changes, and is one of the serious complications of diabetes. Clinically, according to the presence or absence of retinal neovascularization, diabetic retinopathy without retinal neovascularization is referred to as non-proliferative diabetic retinopathy (or simple or background type), and diabetes with retinal neovascularization will be formed. Retinopathy is called proliferative diabetic retinopathy.

(2) There are four cases of uveitis related to diabetes: uveitis related to diabetes itself; infectious uveitis, the chance of endogenous infectious endophthalmitis in patients with diabetes is more normal There is a significant increase in people; accompanied by some specific types of uveitis, but the two are accidental coincidences, or have an internal connection; infective endophthalmitis or sterile endophthalmitis after internal eye surgery. Occurred in middle-aged and elderly patients with diabetes.

(3) Diabetic cataracts occur in young diabetic patients whose blood sugar is not well controlled. Most of them are onset in both eyes and develop rapidly. They can even become completely cloudy within days, weeks, or months.

3. Diabetic Foot

The foot is a complex target organ for diabetes, a multisystem disease. Peripheral neuropathy and peripheral vascular disease combined with excessive mechanical stress in diabetic patients can cause the destruction and deformity of the soft tissue of the foot and the bone and joint system, and then cause a series of foot problems from mild neurological symptoms to severe ulcer , Infection, vascular disease, Charcot joint disease, and neuropathic fractures. In fact, similar pathological changes can also occur in the upper limbs, face and trunk, but the incidence of diabetic foot is significantly higher than other parts.

4. Diabetic cardiovascular complications

Including microvascular disease, myocardial disease, and cardiac autonomic neuropathy on the heart and large blood vessels, the leading cause of death in patients with diabetes. Coronary heart disease is a major macrovascular complication of diabetes. Studies have shown that the risk of death from coronary heart disease in patients with diabetes is three to five times higher than in non-diabetic patients. The pathological mechanism is atherosclerosis, high blood sugar, high systolic blood pressure, high cholesterol, increased low-density lipoprotein, decreased high-density lipoprotein, age, gender, smoking, and family history are all risk factors for its onset.

5. Diabetic cerebrovascular disease

It refers to intracranial macrovascular and microvascular diseases caused by diabetes. According to statistics, 20% to 40% of patients with type 2 diabetes will develop cerebrovascular disease, which is mainly manifested as cerebral arteriosclerosis, ischemic cerebrovascular disease, and cerebral hemorrhage. , Brain atrophy, etc., is one of the main causes of death in patients with diabetes.

6. Diabetic neuropathy

The most common type of diabetic neuropathy is chronic distal symmetrical sensorimotor polyneuropathy, which is a diabetic peripheral neuropathy with a high incidence. Some patients already have peripheral neuropathy when they are newly diagnosed with diabetes. Unfortunately, In terms of treatment, especially in the eradication of diabetic neuropathy, its focus is also on preventing its occurrence and controlling its development.

Clinical manifestations of diabetes complications

Acute complications of diabetes

(1) Diabetic ketoacidosis The onset of this disease is acute, usually less than 24 hours. Most patients have polyuria, thirst, fatigue, and other symptoms of diabetes that worsen or appear for the first time. If left untreated, nausea may occur. , Vomiting, loss of appetite and other symptoms, a small number of patients may have abdominal pain. As the disease progresses, patients may suffer from varying degrees of consciousness and even coma. During the physical examination, the patient was found to have dehydration, and some patients had a rotten apple smell in their breath. Laboratory tests showed that urine glucose and ketone bodies were strongly positive; blood glucose increased, usually between 16.7 and 33.3 mmol / L; blood ketone bodies increased, mostly at 4.8 mmol / L; blood pH and carbon dioxide binding power and HCO ₃ decreased, and anions The gap is significantly increased.

(2) Hypertonic hyperglycemia. The onset is hidden, and the typical clinical manifestations from the onset to the appearance are generally 1 to 2 weeks. It is more common in elderly patients with type 2 diabetes over 60 years of age. In the early stage, the symptoms of diabetes such as polydipsia and polyuria are only worsened. As the disease progresses, severe dehydration and central nervous system damage may occur. Laboratory tests showed strong positive urine glucose, negative or weak positive urinary ketone bodies; blood glucose increased significantly, generally above 33.3 mmol / L; blood ketone bodies were normal or slightly higher; effective plasma osmotic pressure increased, generally above 350 mmol / L .

(3) Lactic acidosis often occurs in patients taking a large amount of biguanide drugs or with systemic diseases. The onset is relatively rapid. Patients have deep breathing, blurred mind, stiffness, and coma. Blood lactic acid concentration is a specific indicator for the diagnosis of lactic acidosis. The concentration of lactic acid is more than 5mmol / L, sometimes up to 35mmol / L.

2. Chronic complications of diabetes

(1) Diabetic nephropathy According to the course and pathophysiological evolution of diabetic nephropathy, Mogensen proposed to divide diabetic nephropathy into the following five stages: The initial changes in glomerular hyperfiltration and renal hypertrophy are consistent with high blood glucose levels Partial relief can be obtained after control. There were no histopathological injuries in this period. Normal albuminuria The glomerular filtration rate (GFR) is higher than normal. The renal pathological manifestations were thickened glomerular basement membrane, increased mesangial matrix, increased urinary albumin excretion rate (UAE) (> 20 g / min) after exercise, and returned to normal after rest. If the blood glucose is well controlled during this period, the patient can stay in this period for a long time. GFR begins to decrease to normal in the early stage of diabetic nephropathy . Renal pathology showed glomerular nodular lesions and arteriolar vitreous changes. UAE continued to increase to 20-200 g / min, resulting in microalbuminuria. The patient's blood pressure increased during this period. Clinical diabetic nephropathy. Typical KW nodules appear pathologically. Persistent massive albuminuria (UAE> 200g / min) or proteinuria is greater than 500mg / d, about 30% of patients may develop nephrotic syndrome, and GFR continues to decline. This period is characterized by no decrease in urinary protein as GFR decreases. Once a patient enters stage IV, the condition often progresses sexually. If not actively controlled, GFR will drop by an average of 1 ml / min per month. GFR of end-stage renal failure <10ml / min. Urinary protein decreases due to glomerulosclerosis. Uremic symptoms are obvious and dialysis is needed. The above stages are mainly based on type 1 diabetic nephropathy, while type 2 diabetic nephropathy is not obvious.

The nephrotic syndrome of diabetic nephropathy is often more markedly edema than general glomerular disease, and often accompanied by severe hypertension. Due to the high transmembrane pressure of glomerular capillaries and severe damage to the glomerular filtration membrane protein barrier, some patients with end-stage renal failure may also have a large amount of proteinuria.

(2) Diabetic eye complications Diabetic retinopathy The pathological changes of retinal capillaries are aneurysms, bleeding spots, hard exudation, cotton wool spots, vein beading, microvascular abnormalities in the retina, and macular edema. Extensive ischemia can cause retinal or optic disc neovascularization, preretinal hemorrhage, and traction retinal detachment. The patient has severe visual impairment. Diabetes can cause two types of retinopathy, proliferative and non-proliferative retinopathy. Diabetic retinopathy is one of the major causes of blindness. In proliferative retinopathy, retinal damage stimulates the growth of new blood vessels. The growth of new blood vessels is not good for the retina, it can cause fibrous hyperplasia, and sometimes retinal detachment. New blood vessels can also grow into the vitreous, causing vitreous hemorrhage. Compared with non-proliferative retinopathy, proliferative retinopathy is more harmful to vision, which can cause severe vision loss or even complete blindness. Uveitis associated with diabetes The first onset is usually acute anterior uveitis, with sudden onset, eye pain, photophobia and tears. Examination revealed ciliary congestion, a large number of fine dusty corneal deposits, anterior chamber flashes (+ ++), anterior chamber inflammatory cells (++ ++++), and a small number of patients with a large amount of fibrosis in the anterior chamber. Exudation, even pus in the anterior chamber, will eventually lead to complications such as post-iris adhesions, iris neovascularization, concurrent cataracts, and secondary glaucoma. Diabetic cataracts Diabetic cataracts occur in young diabetic patients whose blood sugar is not well controlled. It is usually onset in both eyes and develops rapidly. It can even become cloudy and completely cloudy within a few days, weeks, or months. At the beginning, typical white spots or snow flakes appear under the anterior and posterior capsules, which rapidly expands to completeness Cataract, more common in the lower part of the posterior capsule; often accompanied by refractive changes, when blood glucose is elevated, myopia; when blood glucose is reduced, hyperopia.

(3) Diabetic foot Early sensation changes usually show a sock-like appearance, involving the distal end of the limb first, and then developing toward the proximal end. Light touch, proprioception, temperature, and pain are all weakened; motor neuropathy is manifested by atrophy of the intrinsic muscles of the foot and claw-shaped toe deformities; autonomic nerve involvement is manifested by normal perspiration of the skin, loss of temperature and blood flow regulation, resulting Local tissues are less flexible, forming thick ridges and are more susceptible to breaking and cracking. Late stage In addition to the above-mentioned symptoms caused by early neuropathy, ulcers, infections, osteomyelitis, and Charcot arthropathy can also occur.

(4) Diabetic heart disease Coronary artery disease in diabetic patients is often of severe stenosis, which can be manifested as angina pectoris, acute coronary syndrome, myocardial infarction, cardiogenic shock, sudden death, etc. It is worth noting that as diabetic patients often have autonomic neuropathy, asymptomatic coronary heart disease is more common, or manifested as fatigue, atypical dyspnea, gastrointestinal symptoms and other atypical symptoms.

(5) Diabetic cerebrovascular disease Cerebral arteriosclerosis The incidence of cerebral arteriosclerosis in diabetic patients with a disease course of more than 5 years can reach 70%, which is mainly manifested as headache, dizziness, insomnia, forgetfulness, inattention, moodiness Stability and other neurasthenia symptoms. Physical examination of the nervous system usually showed no positive signs. Asymptomatic stroke refers to a stroke that is asymptomatic or mild and has not been noticed and has not been revealed or identified. Among them, asymptomatic cerebral infarction (including lacunar cerebral infarction and non-lacunar cerebral infarction) accounted for 74%, and asymptomatic cerebral hemorrhage accounted for about 26%. Acute cerebrovascular disease is mainly manifested by cerebral thrombosis, with small and medium arterial infarction and multiple lesions more common. Clinical symptoms are often mild, but often recurrent, progressively worsened, and difficult to recover.

(6) Diabetic peripheral neuropathy is the most common type of diabetic neuropathy . More than 50% of patients may have symptoms, which are manifested as burning pain, electric shock or acupuncture-like sensations, hypersensitivity and numbness, and often worsen at night. Sock and glove-like distribution when feet and hands are involved. Some patients are asymptomatic, and abnormalities can be found only during neurological examination. Diabetic peripheral neuropathy can be diagnosed if there are 2 or more abnormalities in the following 5 tests: abnormal temperature sensation; abnormal vibration sensation; knee reflex disappears; nylon wire examination, foot sensation or Disappeared; Nerve conduction velocity (NCV) slowed down by 2 or more.

Treatment of diabetes complications

Acute complications

The treatment principles of ketoacidosis and hypertonic hyperglycemia are the same, including rehydration as soon as possible to restore blood volume and correct dehydration; lower blood sugar; correct electrolyte disorders and acid-base disorders; actively seek and eliminate incentives; closely observe changes in the condition To prevent complications and reduce mortality.

Patients with lactic acidosis have a high mortality rate. Therefore, patients with hyperlactic acidemia (ie, no acidemia, but lactic acid> 2.5mmol / L) need to treat various potential causes in time and actively prevent them. The most fundamental treatment of lactic acidosis is the treatment of the cause, such as correcting shock and improving circulation; timely correcting acidosis; supplementing insulin and glucose; when the condition is critical, dialysis treatment should be timely.

2. Diabetic nephropathy

Treatment of diabetic nephropathy should be comprehensive, including controlling blood sugar, controlling blood pressure, diet treatment, and correcting lipid metabolism disorders, etc .:

(1) Control of blood sugar Glycosylated hemoglobin should be controlled as low as 6.5% as much as possible.

(2) Blood pressure control Angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor antagonist is the first choice for antihypertensive drugs. Urine protein d, blood pressure should be controlled at 130 / 80mmHg; Urine protein> 1g / d, blood pressure should be controlled at 125 / 75mmHg,

(3) Diet The protein intake should be limited to 0.8g / (kg · d) in the early stage, and it can be reduced to 0.6g / (kg · d) in patients who have a lot of proteinuria and renal failure. Patients with intermediate and advanced renal impairment should be supplemented with a-keto acid.

(4) Lipid-lowering statins should be used to strictly correct lipid disorders.

3. Diabetic eye complications

(1) Basic treatment of diabetic retinopathy Early and strictly control blood sugar, reduce blood sugar fluctuations, pay attention to blood pressure reduction, lipid regulation, and improve microcirculation treatment. Avoid smoking harmful factors such as drinking and drinking. Photocoagulation laser treatment is considered to be an effective method for the treatment of diabetic retinopathy. Clinical experiments have shown that photocoagulation has a beneficial effect on the pathogenesis of the disease in two aspects: one is to cause the degradation of new blood vessels and prevent them from regenerating; the other is to reduce macular edema. Condensation therapy Condensation is mainly used for patients who are not suitable for photocoagulation therapy or supplementary therapy for photocoagulation therapy, such as patients with refractive interstitial opacity or photocoagulation of peripheral retina lesions that cannot be treated. Vitreotomy For diabetic retinopathy, the basic indication for vitrectomy is vitreous hemorrhage and severe proliferative lesions. It is generally believed that vitrectomy should be performed for those who cannot absorb spontaneously for more than 3 months.

(2) Diabetes-related uveitis Diabetes should be treated with standard medications, and uveitis should be determined according to the type, severity, and degree of blood glucose elevation. Anterior uveitis is mainly treated with glucocorticoids, ciliary muscle paralysis agents, and non-steroidal anti-inflammatory drugs. Later, middle, and whole uveitis, oral glucocorticoids can be given in the case of good blood glucose control; for those with markedly elevated blood sugar and accompanied by refractory uveitis, nitrogen mustard and cyclophosphate Amide, etc.

(3) Actively treat diabetes at the early stage of onset of diabetic cataract . The opacity of the lens may partially subside, and vision can be improved to different degrees. Drops are used to treat cataract eye drops. When cataract significantly affects vision, cataract extraction can be performed under blood glucose control. If there is no proliferative diabetic retinopathy, it can be implanted into the posterior chamber intraocular lens; postoperatively prevent infection and bleeding.

4. Diabetic Foot

(1) Treatment of ulcers The treatment of diabetic foot ulcers requires the cooperation of multiple departments. Based on the control of blood glucose, improvement of microcirculation, and nutritional support, decompression, debridement, wound dressing, infection control, Vascular reconstruction, amputation and other measures were used for treatment.

(2) Treatment of Charcot arthropathy. Most Charcot neuroarthropathy can be treated conservatively. Surgical fixation does not accelerate healing. On the contrary, surgery may cause new instability and may have fractures around the internal fixation, resulting in delayed healing of the diseased area. Non-surgical treatment has been successful in more than 70% of cases. However, the success rate was lower in patients with Charcot arthropathy in the back of the foot and ankle. End-stage neuroarthropathy can leave serious deformities, requiring patients to continue wearing foot braces, such as rear shell-like ankle and foot braces, hind foot rests or special shoes to reduce the incidence of subsequent ulcers.

5. Diabetic heart disease

First, we should actively treat the primary disease of diabetes, strictly control blood sugar, and correct disorders of glucose metabolism; second, lifestyle interventions, including smoking cessation, alcohol control, sodium restriction, and appropriate exercise; Oxidants, vasoactive drugs, antithrombotic drugs. Fourth, control risk factors and prevent and manage hypertension, obesity, and hyperlipidemia. Some patients with diabetic heart disease cause recurrent angina pectoris, and those who fail medical treatment can be treated with percutaneous angioplasty, vascular stent or coronary artery bypass graft. In order to detect diabetic heart disease early, regular ECG examination is necessary.

6. Diabetic cerebrovascular disease

The treatment principle is the same as that of non-diabetic cerebrovascular disease. The following points should be noted in the treatment:

(1) Control and monitoring of blood glucose In patients with diabetic stroke, too high or too low blood glucose will affect the prognosis, so controlling blood glucose in a suitable range is the basis for the treatment of diabetic cerebrovascular disease.

(2) Antiplatelet drugs Platelet antagonists can reduce stroke mortality. Due to abnormal platelet function in most patients with diabetes, patients with diabetes and atherosclerosis need long-term antiplatelet therapy.

(3) Antihypertensive treatment In diabetic stroke, especially in the acute phase of bleeding, the indications and degree of antihypertensive treatment should be carefully grasped. Antihypertensive treatment cannot pursue rapid antihypertensive effect.

(4) Lipid-lowering statins Lipid-lowering drugs can reduce the incidence of cerebrovascular accidents in diabetic patients by lowering blood cholesterol.

7. Diabetic peripheral neuropathy

(1) Etiological treatment Actively and strictly control hyperglycemia and keep blood sugar stable; improve microcirculation, commonly used drugs such as prostaglandin E ₂ , pentoxifylline, anisodamine, cilostazol, blood circulation and blood stasis, etc. For repair, methyl vitamin B ₁₂ (methylcobalamin), neurotrophic factor, C peptide, etc. are commonly used; for antioxidative stress, commonly used drugs such as a-lipoic acid.

(2) Symptomatic treatment is mainly to control pain in order to minimize the pain caused by diabetic neuropathy. Patients are usually relieved in the following order: mecobalamin and a-lipoic acid, traditional and new generation anticonvulsants, duloxetine, tricyclic antidepressants, opioid analgesics, etc.