Non-pitting edema of the extremities

Introduction Non-concave edema: refers to the use of a finger to press the edema of the limb, non-concave edema is not immediately present, mainly seen in mucinous edema caused by hypothyroidism. 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, etc. cause myelphropathic-metabolic syndrome (MMS), which is myopathy and nephrotic metabolic syndrome. In the past, this metabolic change has not been given enough attention, 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. All patients with MMS should consider the possibility of MMS. Early prominent manifestations were muscle contraction, joint stiffness, and non-concave edema of the affected limb. Patients may develop psychiatric symptoms due to pain, metabolic disorders, and azotemia. The prominent manifestations of revascularization and reperfusion are non-concave edema, cherry red urine, oliguria or anuria and impaired cardiac function.

Cause

(1) Causes of the disease

Acute arterial occlusion

(1) Acute arterial embolism.

(2) Non-embolic arterial occlusion.

include:

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: pale and swelling of the affected limb can occur within a few hours after acute arterial occlusion, and this change is more pronounced at 24 hours. At this time, the muscle is cut and can be fish-like. After 24 hours, the muscles become purple and hard due to congestion. When the fascia is cut, the viable muscles turn pink and cut from the fascia. If it can not be relieved, after the blood supply is restored, the edema will be further aggravated, and the muscle may show different 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, which is a characteristic change in early hypoxia. After 24 hours, some muscle fibers were swollen and glassy. In the late stage (48-72h), the transverse lines and nucleus of the muscle fibers disappeared. Specimens after amputation showed mild to moderate degeneration and even necrosis of 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, and some of them are even fatal to the human body, and are also the main factors causing MMS. The muscle fiber cell membrane plays an important role in the pathophysiology of skeletal muscle.

During ischemia, intracellular adenosine triphosphate (ATP) is significantly reduced, resulting in abnormal membrane permeability changes, causing severe disruption of the internal and external spatial configuration of the sarcoplasmic reticulum, resulting in transmembrane exchange of various biochemical substances. An abnormality has occurred, resulting in a series of metabolic syndromes. During revascularization and reperfusion, the affected limb produces a large number of oxygen free radicals, including superoxide anion, hydrogen peroxide and hydroxyl. Oxygen free radicals are unstable in nature, highly reactive, and cytotoxic. Oxygen free radicals react easily with sulfhydryl enzymes, proteins, lipids and DNA to destroy the chemical structure of tissue cells. Polyunsaturated fatty acids in cell membranes are the most susceptible to oxygen free radicals, resulting in biofilm integrity. The change further causes the 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, especially after blood supply is rebuilt.

(1) Metabolic acidosis: occurs in almost all patients, but to varying degrees. Metabolic acidosis results from the accumulation of acidic metabolites: tissue ischemia and hypoxia lead to a decrease in aerobic metabolism and enhanced anaerobic glycolysis, producing large amounts of lactic acid and pyruvate. In the early stage, the two kinds of acid increased in the same degree. After that, the lactic acid level increased faster than pyruvic acid, the blood pH and CO2 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: serum sodium ions are mostly in the normal range. Potassium ions are also in the normal range at the initial stage. After revascularization, myocyte lysis releases a large amount of potassium into the blood, and the blood potassium is obviously increased. Sudden removal of the blood vessel clip may lead to cardiac arrest. Hyperkalemia can cause arrhythmia and sudden cardiac arrest. About half of the patients have low calcium, hyperphosphatemia and oliguria. The change in calcium-phosphorus ratio during oliguria is due to changes in muscle cell membrane permeability.

Under normal circumstances, the extracellular calcium ion concentration is 3 to 4 times higher than the intracellular calcium ion concentration. If the muscle cell membrane is destroyed, the intracellular calcium ion concentration is increased until the intracellular and extracellular calcium ion concentrations are equal, the muscle cell contractility is enhanced, and the ischemic limb stiffness occurs and some MMS patients develop muscle spasm during renal failure.

(3) Enzymatic changes: Before the blood supply was reconstituted, the plasma content of Creatine Phosphokinase (CPK) was slightly increased, and the content of venous blood in the affected limb was high. After the blood supply was rebuilt, CPK increased again. CPK, especially its isoenzyme CPK-MM elevation, is a direct evidence of muscle damage, and high levels of CPK usually reflect progressive muscle necrosis. At this time, if the skin color is normal, it often leads to a wrong judgment. The intact skin does not reflect the normal muscle tissue in the deep surface. In mild cases, CPK decreased within a few hours or 1-2 days after recovery of blood supply. In more severe cases, CPK rose to 1000-2000 U in a few days, and returned to normal after 10-12 days.

In severe cases and deaths, CPK progressively increased to more than 20,000 U. All patients had 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 continued increase in SGOT indicates an irreversible pathological damage to the muscle.

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, and the urine is reddish by the myoglobin released by skeletal muscle dissolution. Myoglobinuria peaked at 48h for several days, and its elevation was 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 there is no red blood cells in the urine, and the plasma is clear. 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 examination methods include: chemical methods, spectrophotometry, and immunological methods. Markowiz reported a quantitative assay for urinary myoglobin, making early detection of blood and urine myoglobin possible.

(5) Myoglobinemia: Renal exclusion of myoglobin is sometimes delayed, and only a small amount is excreted in the early stage, and it is difficult to confirm the presence of myoglobinuria, thereby misdiagnosing. Therefore, in patients with highly suspected rhabdomyolysis, we should test myoglobin in the blood when myoglobin hematuria is not detected.

(6) Acute renal failure: The degree of renal impairment varies with the degree of muscle ischemia, acidosis, and myoglobinuria. In mild to moderate cases, renal function is only temporary and reversible damage, urine output is reduced, and most patients have oliguria or no urine. Following the patient's blood urea nitrogen and creatinine increased rapidly. In severe cases, severe acidosis with persistent myoglobinuria, if not immediately dialysis, will cause irreversible kidney damage, or even death. Histological examination revealed the presence of myoglobin casts in the renal tubules, with a small number 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 glomerular sclerosis damage in patients, which seriously affects prognosis. According to the data obtained from animal experiments and human autopsy, there is a causal relationship between renal tubular mechanical obstruction caused by myoglobin and acute renal failure, but whether myoglobin has direct toxicity to renal tubules is controversial because the experiment shows that the muscle is injected. Red albumin does not cause acute renal failure.

The clinical symptoms of this period and reperfusion period 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 increased. Infusion is not completely because the branch of the intermuscular artery is severely blocked compared with the trunk, and the blood supply is not easy to recover. However, muscle and joint stiffness have been alleviated. The affected calf or forearm gap syndrome still exists. After blood supply is restored, microthrombus in platelets and fibrin tissue can enter the pulmonary circulation, causing serious complications.

an examination

Related inspection

Blood routine urine routine serum potassium blood electrolyte examination serum potassium (K+, K)

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

1. Acute ischemic period: manifested as severe pain in the affected limb, low skin temperature, pale skin, cyanosis, paresthesia or disappearance. Exercise or examination of the limbs may aggravate the pain. The most typical clinical manifestation of this period is stiffness of the affected limb or rigidity after necrosis. Especially in the distal joints such as knees and ankles, "freezing" occurs. The stiffness of the limbs indicates the occurrence of metabolic syndrome. After 12 to 24 hours, the limbs were severely swollen and spread throughout the affected limb, sometimes the thigh was more pronounced than the calf.

Edema mainly occurs in muscle tissue, and the swollen limb can be soft, tight, and woody, non-depressed. Because of the low skin temperature and cyanosis, it is often misdiagnosed as "femoral bruising". The main difference between the two is that the edema occurs in the muscle rather than the subcutaneous tissue. Patients often have agitation, delirium, and disorientation. These neurological symptoms may be the result of a combination of azotemia and other metabolic substances on brain tissue. This period is often accompanied by varying degrees of metabolic disorders such as acidosis, azotemia and hyperkalemia, which can cause serious complications or even death if not corrected in time.

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 distal tissue perfusion is incomplete, the pain is not alleviated but increased. Infusion is not completely because the branch of the intermuscular artery is severely blocked compared with the trunk, and the blood supply is not easy to recover. However, muscle and joint stiffness have been alleviated. The affected calf or forearm gap syndrome still exists. After blood supply is restored, microthrombus in platelets and fibrin tissue can enter the pulmonary circulation, causing serious complications.

Related checks:

1. 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 A further decline in value suggests a poor prognosis.

2. Urine examination: 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 proportionally increased with the action of lipid hydrogen peroxide.

Patients often have agitation, delirium, and disorientation.

Differential diagnosis

Edema, also known as edema, refers to the retention of water in the subcutaneous tissue, which can be divided into concave edema and non-concave edema.

1 can be concave edema: press the edema with your fingers, and immediately appear concave can be concave edema.

2 non-concave edema: use the finger to press the edema site, not immediately appear concave is non-concave edema, mainly seen in hypothyroidism caused by mucinous edema.

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

1. Acute ischemic period is characterized by severe pain in the affected limb, low skin temperature, pale skin, cyanosis, paresthesia or disappearance. Exercise or examination of the limbs may aggravate the pain. The most typical clinical manifestation of this period is stiffness of the affected limb or rigidity after necrosis. Especially in the distal joints such as knees and ankles, "freezing" occurs. The stiffness of the limbs indicates the occurrence of metabolic syndrome. After 12 to 24 hours, the limbs were severely swollen and spread throughout the affected limb, sometimes the thigh was more pronounced than the calf. Edema mainly occurs in muscle tissue, and the swollen limb can be soft, tight, and woody, non-depressed. Because of the low skin temperature and cyanosis, it is often misdiagnosed as "femoral bruising". The main difference between the two is that the edema occurs in the muscle rather than the subcutaneous tissue.

Patients often have agitation, delirium, and disorientation. These neurological symptoms may be the result of a combination of azotemia and other metabolic substances on brain tissue. This period is often accompanied by varying degrees of metabolic disorders such as acidosis, azotemia and hyperkalemia, which can cause serious complications or even death if not corrected in time.

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 distal tissue perfusion is incomplete, the pain is not alleviated but increased. Infusion is not completely because the branch of the intermuscular artery is severely blocked compared with the trunk, and the blood supply is not easy to recover. However, muscle and joint stiffness have been alleviated. The affected calf or forearm gap syndrome still exists. After blood supply is restored, microthrombus in platelets and fibrin tissue can enter the pulmonary circulation, causing serious complications.

Related checks:

1. 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 A further decline in value suggests a poor prognosis.

2. Urine examination: 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 proportionally increased with the action of lipid hydrogen peroxide.

Patients often have agitation, delirium, and disorientation.

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