Xiebeilu studio WeChat add369456 Henoch-Schonlein purpura is a kind of vascular responsive disease in children, due to antigen-antibody compound. The deposits deposit on the walls of blood vessels, causing widespread capillary vasculitis and even necrotizing systemic small vessel vasculitis, which eventually leads to bleeding and edema of multiple tissues throughout the body. Digestive system involvement now appears to be common, and 2/3 of children with allergic purpura have gastrointestinal symptoms. The cause of intra-abdominal symptoms is bleeding and edema under the mucous membranes and serosa. Spontaneous intestinal perforation is considered to be one of the most serious intra-abdominal complications of Henoch-Schonlein purpura. It is an important cause of death in Henoch-Schonlein purpura. The incidence rate is less than 0.1%. Its pathogenesis is vasculitis leading to thrombosis and continuous serious The ischemia leads to thickening and necrosis of the entire intestinal wall and eventually perforation. The age of onset is often lower than the average age of purpura. The specific reason is not completely clear, and it may be related to the poor constitution of young children and the development of children’s immune system with age. The small intestine is the most common perforation location, with statistics accounting for 64.7%, and reports of perforation in the stomach, duodenum, and large intestine. Perforation is usually single, but there are many reports of perforation. Until the 1970s, the mortality of allergic purpura with spontaneous intestinal perforation was almost 100%. Since then, correct understanding and surgical treatment have improved survival rates. Spontaneous intestinal perforation has typical manifestations of chemical peritonitis, but because children often have obvious abdominal distension before perforation, it is difficult to diagnose by clinical signs alone, and auxiliary examination is very important. Ultrasound and CT can be used to confirm the involvement of the intestinal tract, show the thickening of the intestinal wall and hematoma, and the progress of the intestinal involvement. A series of ultrasound can prove whether the thickening of the intestinal wall has subsided or worsened to show the progress of gastrointestinal involvement, and has become a good clinical aid. Regarding the progress of intra-abdominal involvement of purpura, B-ultrasound has been found to have 100% sensitivity and specificity. In two independent large-scale studies, it can detect early intestinal edema and gas intestinal wall, which are mostly bead-like Single gas is rare for gas accumulation. Abdominal upright film is a classic examination to diagnose digestive tract perforation. In our case, the diagnosis was confirmed by CT, B-ultrasound and abdominal radiograph. Since the risk of spontaneous intestinal perforation is extremely high, once a case of suspected spontaneous intestinal perforation is found, surgical exploration is required as soon as possible. The application of glucocorticoids is also one of the possible causes of intestinal perforation. At present, this possibility has only been discussed in relevant literature reports. There is no definitive conclusion and further research is needed. In conclusion, spontaneous intestinal perforation is a serious complication of allergic purpura, and delayed diagnosis and treatment often result in death. Early diagnosis and surgery are necessary.
Xiebeilu studio WeChat add369456 Allergic purpura is a kind of capillary allergic disease, often manifested as skin purpura, abdominal pain, blood in the stool, joint swelling and pain, nephritis, etc., but the pathological basis of this disease is the inflammation of small arteries throughout the body, often It involves multiple organ damage, causing some rare complications. Familiar with these complications is undoubtedly of great significance for improving the diagnosis and treatment of allergic purpura. 1. The clinical manifestation of purpuric heart damage is 1. How mild the heart symptoms are, and may have palpitations. Chest tightness, discomfort in the precordial area, etc. In some cases, heart enlargement, galloping rhythm, wet lung rales are present. , Hepatomegaly, lower extremity edema and other cardiac insufficiency performance; 2. There may be low blunt heart sounds, premature beats, transient apical systolic murmurs or pericardial friction sounds. It has been reported that 6.2% of patients with purple scars have hypertension and increased myocardial enzymes in some patients; 3. ECG can be found ST changes, low voltage, atrioventricular hypertrophy, Q-T prolongation, and sinus tachycardia or bradycardia, Bundle branch block, atrioventricular block. Premature beats and other arrhythmias; 4. Heart damage often occurs 2 to 15 days after the onset of purple paralysis, which is the peak of allergy. Often heart damage also improves with purple epilepsy. Recovery; 5. Allergic purpura with heart damage is mostly mixed, followed by kidney type, indicating that abnormal allergies affect a wide range of people, the chance of heart involvement is correspondingly increased. Because of the mildness of purpuric heart damage. Clinical missed diagnosis. Therefore, patients with allergic purpura should observe the heart dynamically. Once evidence of heart involvement is found, it can also exclude diseases such as rheumatic or viral myocarditis and lupus erythematosus. That is, purpuric heart damage should be considered and treated early to avoid serious consequences such as cardiac insufficiency. 2. The clinical manifestations of purpura nervous system damage are 1. Light headache only. Dizziness, severe cases can be subarachnoid hemorrhage, cerebral hemorrhage and multiple neuritis; 2. Sometimes headache can occur before purpura appears, May be accompanied by nausea, vomiting, convulsions, convulsions, seizures, and even coma; 3. Emotional instability, irritability, apathy, and other mental abnormalities; 4. Aphasia, hemiplegia, chorea, cortical hemianopia, ataxia, etc. Damage; 5. Can also be involved in facial nerve, ulnar nerve, femoral nerve, sciatic nerve and other peripheral nerve involvement performance; 6. Prognosis is generally good. Most of them can be cured by active treatment. A few serious cases may leave sequelae or cause death. 3. The clinical manifestations of purpura skin necrosis are swelling, pain, coldness, and cyanosis in the hands and feet, and then it becomes black and shows dry necrosis. The skin of the two toes began to darken and dry out. Two weeks later, the toes gradually showed carbon black, shriveled, and hard hair. The diagnosis of fulminant purpura caused dry necrosis of the two toes. 4. Clinical features of purpura intestinal necrosis 1. All have typical skin purple scars and obvious abdominal pain, vomiting, blood in the stool; 2. Abdominal carbuncle is unbearable, sweating drought. It is persistent abdominal pain. Abdominal diffuse tenderness, but abdominal muscle Tension and rebound pain may not be obvious. Bowel sounds decrease; 3. Intestinal perforation cases often have a sudden increase in body temperature before perforation, liver dullness disappears after perforation, free gas can be seen below, the total number of white blood cells and neutrophils increase; 4. Perforation often occurs 4 to 15 days after skin purpura. Some people say that perforation easily occurs when the abdominal pain of fresh purpura intensifies again after remission of purpura. Because most of the disease is treated with corticosteroids, it often masks the typical signs of intestinal necrosis and is likely to cause missed diagnosis. Therefore, those with abdominal purpura with persistent diffuse abdominal pain and obvious tenderness should be alert to the possibility of purple scar intestinal necrosis or intestinal perforation.