Necrotizing vasculitis

Introduction to necrotizing vasculitis Nodular vasculitis is actually nodular polyarteritis, also known as nodular periarteritis and necrotizing arteritis, polyarteritis, etc. It is characterized by significant inflammation of the whole layer of small arteries and middle arteries. Lesions occur in the branches of the arteries, causing multiple aneurysms, thrombosis and infarction, and fibrin-like necrosis. The specific cause is still unclear, and may be the same as the etiology and pathogenesis of other systemic necrotizing vasculitis. It is an immune complex vasculitis caused by exogenous substance allergies, extensive lesions, multiple system damage, representing several clinical Syndrome. Factors such as serum, drugs, bacteria, and viral infections can cause vascular inflammatory lesions. The specific pathogenesis is not very clear, and may be related to the immune dysfunction and allergy of the body. Various factors activate the body's allergic reaction, forming a soluble circulating immune complex that settles on the vessel wall, resulting in enhanced permeability of the vessel wall, activation of complement, infiltration of immune-active cells, and vascular inflammatory lesions or necrosis. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: non-infectious Complications: gas gangrene, hemolytic streptococcal gangrene

Causes of necrotizing vasculitis

Cause:

The specific cause is still unclear, and may be the same as the etiology and pathogenesis of other systemic necrotizing vasculitis. It is an immune complex vasculitis caused by exogenous substance allergies, extensive lesions, multiple system damage, representing several clinical Syndrome. Factors such as serum, drugs, bacteria, and viral infections can cause vascular inflammatory lesions. The specific pathogenesis is not very clear, and may be related to the immune dysfunction and allergy of the body. Various factors activate the body's allergic reaction, forming a soluble circulating immune complex that settles on the vessel wall, resulting in enhanced permeability of the vessel wall, activation of complement, infiltration of immune-active cells, and vascular inflammatory lesions or necrosis.

Pathogenesis:

The pathogenesis is generally thought to be related to allergic reactions, and the toxic scale in the blood causes its own immune inflammation and invades the damaged blood vessels. Patients may have increased erythrocyte sedimentation rate, bilateral lower extremity skin lesions, and pigmentation.

Necrotizing vasculitis prevention

Necrotic vasculitis is a primary vasculitic lesion with no relevant preventive measures.

Necrotic vasculitis complications Complications, gas gangrene, hemolytic streptococcal gangrene

If you have necrotizing vasculitis, you should treat it early. If you don't treat it in time, it will cause ulceration and gangrene in the affected area, and even the risk of amputation or death.

Necrotic inflammatory symptoms Common symptoms Joint pain, weakness, joint migration pain, swelling, kidney damage, reticular subcutaneous nodules, nausea and vomiting, arrhythmia

Clinical manifestations of nodular vasculitis

Mainly due to the onset of illness, often have fever, joint muscle pain, fatigue and other performance.

Skin damage:

1 The rash is seen in 50% of patients with pleomorphism such as dermatitis, bleeding, erythema, claw-shaped erythema, purpura and reticular bluish.

2 subcutaneous nodules, 0.5 to 1 cm in size, distributed along the superficial superficial artery, or gathered near the blood vessels, pain and tenderness. The center of the nodule often forms ulcers due to necrosis.

Kidney damage:

Found in 70% to 80% of patients, manifested as proteinuria and hematuria, often with rapid hypertension with edema, increased blood urea nitrogen, and ultimately renal failure.

Heart damage:

Common coronary artery involvement, may have myocardial ischemia, arrhythmia, severe myocardial infarction, heart failure can occur in the late stage.

Digestive system damage:

30% to 50% have gastrointestinal symptoms, manifested as severe abdominal pain, nausea, vomiting, ulcers, bleeding or perforation in the intestinal tract when severe. When the pancreas, gallbladder, or hepatic and bile ducts are involved, symptoms of acute hemorrhagic pancreatitis, acute necrotizing cholecystitis, or acute hepatic necrosis may occur.

Damage to the nervous system:

It is more common in peripheral neuritis, distributed along the nerve, and has pain or painfulness. Central nervous system involvement can cause dyskinesia and stroke.

Examination of necrotizing vasculitis

Laboratory inspection

The most common changes were elevated white blood cells to 20,000 to 40,000/l (80% of patients), proteinuria (60%), and microscopic hematuria (40%). Temporary or persistent eosinophilia is uncommon, but can be seen in patients with a long course of disease, or with Churg-Strauss syndrome, pulmonary involvement, or asthma attacks. In addition, there are often thrombocytosis, accelerated erythrocyte sedimentation rate, anemia (caused by blood loss or renal failure), hypoproteinemia and elevated serum immunoglobulin. Although autoimmune antibodies are common in other collagen vascular diseases, the disease is rarely positive.

Diagnosis and differentiation of necrotizing vasculitis

Diagnostic criteria

In patients with unexplained fever, abdominal pain, kidney failure or high blood pressure, or when suspected nephritis or heart disease is accompanied by eosinophilia or unexplained symptoms and joint pain, muscle tenderness and muscle weakness, subcutaneous nodules, Nodular polyarteritis can be diagnosed when skin purpura, pain in the abdomen or limbs, or rapidly developing hypertension. Especially when other fevers and multiple organ damage have been ruled out, clinical and laboratory results usually indicate a diagnosis. Systemic disease with peripheral neuritis (usually multiple, ie multiple mononeuritis) with bilateral or symmetrical or asymmetrical involvement of the main nerve trunk (eg, phrenic nerve, phrenic nerve, sciatic nerve) suggesting nodular polyarteritis The previous clinical manifestations of healthy middle-aged men also suggested nodular polyarteritis.

Because nodular polyarteritis has no specific serum response, it can only be diagnosed based on the pathological changes of necrotic arteritis seen in typical lesion biopsy, or the typical aneurysm shown in angiography of medium blood vessels. A blind biopsy of an unaffected tissue is useless. Due to the focal nature of the lesion, biopsy may sometimes not yield a positive result. Therefore, biopsy should be performed on skin, subcutaneous tissue, calf nerves or muscles with clinical manifestations. In the absence of clinical symptoms, EMG and nerve conduction measurements can help to select muscle or nerve biopsy sites. Because the gastrocnemius muscle has the risk of developing venous thrombosis after surgery, it is not suitable for biopsy unless it is the only muscle with symptoms. Testicular biopsy should be advocated (microscopic lesions are more common here), but testicular biopsy should be avoided if there are other suspicious sites. If other sites do not provide the materials needed for diagnosis, a renal biopsy is performed for those with nephritis, and a liver biopsy for patients with severe liver dysfunction is desirable. In the absence of a positive histological diagnosis, selective angiography can also be diagnosed by the presence of small aneurysms in the kidney, liver, and celiac vessels.

Differential diagnosis

Different from multiple vasculitis and nodular vasculitis.

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