Myopathy nephrotic metabolic syndrome

Introduction to myopathy nephrotic metabolic syndrome With the development of vascular surgery, the treatment of acute arterial embolization has made gratifying progress, but the mortality rate and amputation rate of the affected limb are still quite high. The main cause of this result is ischemic rhabdomyolysis and the resulting muscle red. Protein, ion disorder, oxygen free radicals and other metabolic syndrome (myonephropathic-metabolic syndrome, MMS), which is a metabolic syndrome of myopathy and nephropathy, has not paid enough attention to this metabolic change in the past, so the patient's prognosis is poor. According to recent literature statistics, the incidence of MMS after acute arterial occlusion is 7% to 37.5%, and its true incidence is still unknown. basic knowledge The proportion of illness: 0.0035% Susceptible people: no specific population Mode of infection: non-infectious Complications: hyperkalemia

Cause of myopathy, nephrotic metabolic syndrome

As the disease progresses, it can be divided into two stages: acute ischemic phase (vascular occlusion phase) and blood supply reconstruction and reperfusion phase.

Acute ischemic period

It is characterized by severe pain in the affected limb, low skin temperature, pale skin, cyanosis, abnormal feeling or disappearance. Exercise or examination of the limbs will aggravate the pain. The most typical clinical manifestation in this period is stiffness or necrosis after the limb, especially the distal end. Joints such as knees, sputum, "freezing" phenomenon, limb stiffness indicates the occurrence of metabolic syndrome, 12 to 24 hours after the limbs are severely swollen, throughout the affected limb, sometimes the thigh is more prominent than the calf, edema mainly occurs in the muscle In the tissue, the swollen limbs can be soft, tight, and woody, non-depressed. Because of the low skin temperature and cyanosis, they are often misdiagnosed as "femoral bruises". The main difference between them is that the edema occurs in the muscles. Internal rather than subcutaneous tissue, patients often have agitation, delirium and disorientation. These neurological symptoms may be caused by azotemia and other metabolic substances acting together on brain tissue. This period is often accompanied by varying degrees of metabolic disorders such as : Acidosis, azotemia and hyperkalemia, if not corrected in time, can cause serious complications and even death.

2. Blood supply is re-established

(1) Causes of the disease

Acute arterial occlusion

(1) Acute arterial embolism.

(2) Non-embolic arterial occlusion, including:

1 acute thrombosis of abdominal aorta or abdominal aortic aneurysm;

2 femoral artery cannulation during cardiopulmonary bypass;

3 arterial trauma;

4 clamps block the blood flow when the large artery is reconstructed.

2. Ischemic muscle necrosis.

3. Non-traumatic myopathy muscle damage, long-term coma, drug toxicity, infection, burns, metal poisoning.

(two) pathogenesis

1. Ischemic changes Within a few hours after acute arterial occlusion, the limbs may appear pale and swollen. This change is more pronounced at 24 hours. At this time, the muscles can be cut to give a fish-like appearance. After 24 hours, the muscles are affected. When it is congested and purple, it becomes hard. When the fascia is cut, the viable muscle turns pink, and it is cut from the fascia. If it can not be relieved, the edema will be further aggravated after the blood supply is restored. Muscles may present varying degrees of necrosis.

Microscopically, some muscle fibers can maintain a complete appearance at the beginning of the lesion. Some muscle fibers have nuclear loss and slight cytoplasmic coagulation, which is a granular change. This is a characteristic change in early hypoxia. After 24 hours, some muscle fibers are swollen and glassy. In the late stage (48-72h), the transverse lines and nucleus of the muscle fibers disappeared. The amputation specimens showed mild to moderate degeneration and even necrosis of the regenerated muscle fibers.

Skeletal muscle accounts for about 42% of the body's body weight, and contains a large amount of biochemical substances in its complex structure, making this muscle tissue extremely sensitive to hypoxia. In the state of hypoxia, these biochemical substances are released into the blood, some of which are The damage of the human body is even fatal, and it is also the main factor causing MMS. The muscle fiber cell membrane plays an important role in the pathophysiology of skeletal muscle. At the time of ischemia, the adenosine triphosphate (ATP) in the myocytes is significantly reduced. Abnormal changes in membrane permeability, causing severe damage to the internal and external spatial configuration of the sarcoplasmic reticulum, resulting in abnormal transmembrane exchange of various biochemical substances, resulting in a series of metabolic syndrome, in revascularization and reperfusion Period, the affected limb produces a large number of oxygen free radicals, mainly including superoxide anion, hydrogen peroxide and hydroxyl groups. The oxygen radicals are unstable in nature, have strong reactivity, and are cytotoxic. Oxygen free radicals are easily associated with thiol enzymes and proteins. Lipids and DNA react to destroy the chemical structure of tissue cells. Polyunsaturated fatty acids in cell membranes are the most susceptible to oxygen free radicals. , causing changes in the integrity of the biofilm, further causing biochemical substances in the muscle cells to enter the blood, leading to necrosis of MMS and muscle cells.

2. Metabolic syndrome

Metabolic syndrome can be temporary or delayed, and this is especially true after blood supply is reconstituted.

(1) Metabolic acidosis: almost all patients, but to varying degrees, metabolic acidosis stems from the accumulation of acidic metabolites: tissue ischemia and hypoxia lead to a decrease in aerobic metabolism and anaerobic glycolysis, resulting in A large amount of lactic acid and pyruvic acid, in the initial stage, the two kinds of acid increased in degree. After that, the lactic acid level increased faster than pyruvic acid, the blood pH and CO 2 content decreased, and the number of anions and cations increased significantly.

Before blood supply reconstruction, the pH value of the reflux venous blood of the affected limb decreased, lower than or equal to 7.2, indicating a poor prognosis. If the pH value continues to decrease after reconstruction, the prognosis is worse.

(2) Changes in electrolytes: Most of the serum sodium ions are in the normal range, and the potassium ions are also in the normal range at the initial stage. After revascularization, the muscle cells dissolve and release a large amount of potassium into the blood, and the blood potassium is obviously increased, and the blood vessels are suddenly removed. Clips may lead to cardiac arrest, hyperkalemia can cause arrhythmia and cardiac arrest, more than half of patients with low calcium, hyperphosphatemia and oliguria, oliguria calcium and phosphorus ratio changes due to myocyte membrane pass Due to the permeability change, under normal circumstances, the extracellular calcium ion concentration is 3 to 4 times higher than the intracellular calcium ion concentration. If the myocyte membrane is destroyed, the intracellular calcium ion concentration is increased until the intracellular and extracellular calcium ions are equal. Increased contractility of myocytes, resulting in ischemic limb stiffness and partial MMS patients with muscle spasm in renal failure.

(3) Enzymatic changes: Before the blood supply for reconstruction, the plasma content of Creatine Phosphokinase (CPK) increased slightly, and the content of venous blood in the affected limb was very high. After the blood supply was reconstructed, CPK increased again. High, CPK, especially its isoenzyme CPK-MM elevation is a direct evidence of muscle damage. High levels of CPK usually reflect progressive muscle necrosis. At this time, if the skin color is normal, it often leads to wrong judgment, and the skin is intact. Reflecting the deep muscle tissue is normal, in the mild, CPK decreased within a few hours or 1-2 days after the recovery of blood supply, in more serious cases, CPK rose to 1000 ~ 2000U in a few days, 10 to 12 days after recovery Normally, in severe cases and deaths, CPK is progressively elevated to more than 20,000 U. All patients have elevated levels of Lactate Dehydrogenase (LDH) and Serum Glutamic-Oxaloacetic Transaminase (SGOT). The elevated level of SGOT is directly proportional to the degree of ischemia, and the continuous elevation of SGOT indicates that the muscle has irreversible pathological damage.

Both LDH and CPK are elevated in both MMS and myocardial infarction, but their changes are different and should be identified.

(4) Myoglobinuria: Within a few hours after vascular occlusion, the amount of urine is often reduced, because the urine contains myoglobin released by skeletal muscle dissolution and presents cherry red, and myoglobinuria peaks at 48h for several days. The increase is related to the extent and extent of muscle solubilization. The myoglobin that appears in the urine is a guaiac resin-positive, or benzidine-positive, or positive-base-positive granule, while the urine has no red blood cells, while the plasma is Clarified, myoglobinuria is often misdiagnosed as hemoglobinuria, Berman proposed the following identification methods: red plasma + red urine hemoglobinuria; clarified plasma + red urine myoglobinuria, myoglobin specific qualitative test method Including: chemical methods, spectrophotometry and immunological methods, Markowiz reported a quantitative assay for urinary myoglobin, which makes early detection of blood and urinary myoglobin possible.

(5) Myoglobinemia: Renal exclusion of myoglobin is sometimes delayed, and only a small amount is excreted in the early stage. It is difficult to confirm the presence of myoglobinuria and thus misdiagnosis. Therefore, when no myoglobin hematuria is detected, the height is In patients suspected of having rhabdomyolysis, we should test myoglobin in the blood.

(6) Acute renal failure: The degree of renal function damage varies with the degree of muscle ischemia, acidosis and myoglobinuria. In mild to moderate cases, renal function is only temporary and reversible damage, and the amount of urine output is reduced. Most patients There is oliguria or no urine, followed by rapid increase of blood urea nitrogen and creatinine in patients, severe cases of severe acidosis with prolonged myoglobinuria, if not immediately dialysis, there will be irreversible kidney damage, and even death Histological examination showed the presence of myoglobin tube type in the renal tubules, containing a small amount of epithelial cells. The degree of acute tubular necrosis depends on the extent to which myoglobin blocks the renal tubules. This pathological change is often called myoglobin nephropathy, sometimes This kidney disease synergizes with the glomerular sclerosis damage of the patient, which seriously affects the prognosis. According to the data obtained from animal experiments and human autopsy, the myocardial mechanical blockage caused by myoglobin has a causal relationship with acute renal failure, but Whether or not myoglobin is directly toxic to the renal tubules is controversial because experiments have shown that injection of myoglobin does not cause acute renal failure.

And the reperfusion period of this period, the clinical symptoms vary with the degree of ischemia. In severe cases, although the blood supply is restored, but the distal tissue perfusion is incomplete, the pain is not alleviated but worsened. The perfusion is not completely because the intermuscular artery branches are more trunk. The obstruction is severe, the blood supply is not easy to recover, but the muscle and joint stiffness are relieved. The affected calf or forearm gap syndrome still exists. After the blood supply is restored, the microthrombus of platelet and fibrin tissue can enter the pulmonary circulation, causing serious complications. .

All patients with MMS should consider the possibility of MMS. The early prominent manifestations are muscle contraction, joint stiffness and non-concave edema of the affected limb. Patients may have psychiatric symptoms due to pain, metabolic disorders and azotemia. The prominent manifestations of the reconstruction and reperfusion period are non-concave edema, cherry red urine, oliguria or anuria and impaired cardiac function.

Myopathy, nephrotic metabolic syndrome prevention Strengthen exercise, enhance physical fitness, and improve immunity. Regular participation in physical exercise, such as health gymnastics, practicing Qigong, Tai Chi, doing radio gymnastics, walking, etc., is of great benefit. Anyone who insists on physical exercise will have a strong body and strong disease resistance, and rarely suffer from illness.

Myopathy, nephrotic metabolic syndrome, complications Complications hyperkalemia

Patients often have agitation, delirium and disorientation.

Myopathy, nephrotic metabolic syndrome symptoms, common symptoms, severe pain, pale skin, cyanosis, edema, urinary azotemia, no urine, dynamism, directional stress, metabolic acidosis

As the disease progresses, it can be divided into two stages: acute ischemic phase (vascular occlusion phase) and blood supply reconstruction and reperfusion phase.

Acute ischemic period

It is characterized by severe pain in the affected limb, low skin temperature, pale skin, cyanosis, abnormal feeling or disappearance. Exercise or examination of the limbs will aggravate the pain. The most typical clinical manifestation in this period is stiffness or necrosis after the limb, especially the distal end. Joints such as knees, sputum, "freezing" phenomenon, limb stiffness indicates the occurrence of metabolic syndrome, 12 to 24 hours after the limbs are severely swollen, throughout the affected limb, sometimes the thigh is more prominent than the calf, edema mainly occurs in the muscle In the tissue, the swollen limbs can be soft, tight, and woody, non-depressed. Because of the low skin temperature and cyanosis, they are often misdiagnosed as "femoral bruises". The main difference between them is that the edema occurs in the muscles. Internal rather than subcutaneous tissue, patients often have agitation, delirium and disorientation. These neurological symptoms may be caused by azotemia and other metabolic substances acting together on brain tissue. This period is often accompanied by varying degrees of metabolic disorders such as : Acidosis, azotemia and hyperkalemia, if not corrected in time, can cause serious complications and even death.

2. Blood supply re-establishment and reperfusion period

The clinical symptoms of this period vary with the degree of ischemia. In severe cases, although the blood supply is restored, but the perfusion of the distal tissue is incomplete, the pain is not alleviated but the exacerbation is incomplete. The perfusion is not completely due to the severe obstruction of the intermuscular artery branch. It is not easy to recover, but the muscle and joint stiffness are relieved. The affected calf or forearm gap syndrome still exists. After the blood supply is restored, the microthrombus of platelet and fibrin tissue can enter the pulmonary circulation, causing serious complications.

Examination of myopathy nephrotic metabolic syndrome

Blood test

The degree of elevation of serum potassium, CPK, SGOT and LDH reflects the extent and extent of skeletal muscle necrosis; elevated blood myoglobin may be noted for renal failure; blood pH decreases, especially after revascularization, pH decreases further to prognosis Not good.

2. Urine check

When there is myoglobin in the urine, you should be alert to the occurrence of renal failure.

3. Oxygen free radical detection

Because of its unstable chemical properties and short half-life, it is difficult to detect the indirect determination of the presence of oxygen free by measuring the malondialdehyde acid proportional to the increase in lipid hydrogen peroxide.

Diagnosis and diagnosis of myopathy nephrotic metabolic syndrome

All patients with MMS should consider the possibility of MMS. The early prominent manifestations are muscle contraction, joint stiffness and non-concave edema of the affected limb. Patients may have psychiatric symptoms due to pain, metabolic disorders and azotemia. The prominent manifestations of reconstruction and reperfusion are non-concave edema, cherry red urine, oliguria or anuria and impaired heart function.

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