Dry necrosis of the ear shell

Introduction Dry necrosis of the ear shell is one of the clinical manifestations of diffuse intravascular coagulation. Diffuse intravascular coagulation (DIC) is not a single disease, but a complex pathological process and clinical syndrome caused by multiple causes. Embolization in clinical manifestations, the general symptoms of embolism are local congestion, hemorrhage or extremity cyanosis, long-term embolization of the distal part can lead to rhinitis, dry necrosis of the ear shell. It is characterized by extensive platelet aggregation and fibrin deposition in the microcirculation, resulting in diffuse microthrombus formation, secondary coagulation factors and massive consumption of platelets, and fibrinolysis, resulting in microcirculatory disorders, hemorrhage, hemolysis A series of serious clinical manifestations. The condition of acute disseminated intravascular coagulation is progressing rapidly, and if it is not treated in time, it is often life-threatening.

Cause

There are many causes of DIC. According to the analysis of a group of domestic materials, infection is common, accounting for more than 1/3 of the total number of cases, followed by malignant tumors (including acute promyelocytic leukemia), which together account for about 2/3 of the cause. . Extensive surgery, tissue damage, obstetric accidents, and extracorporeal circulation are also common causes of DIC.

The pathogenesis of DIC in various causes is not exactly the same. The main mechanisms for causing DIC are as follows:

(a) infection

Both Gram-negative and positive bacterial sepsis can be caused, but Gram-negative bacteria are more common, such as Escherichia coli, Proteus, Pseudomonas aeruginosa, and bacillus, Gram-positive bacteria such as Staphylococcus aureus, typhoid fever Bacillus, etc., Gram-positive bacteria such as Staphylococcus aureus, hemolytic streptococcus, Clostridium, and the like. Non-bacterial infections are less common, such as viruses, ricketts, protozoa, spirochetes, and fungal infections. The incidence of bacterial infection mainly includes the factors of bacterial infection itself and the endotoxin produced. After bacterial infection, vascular endothelial cells are damaged, which can release a large amount of tissue factor into the blood, promote coagulation, complement is also related to coagulation, fibrinolysis and activation of kinin system. Regarding endotoxin, it has been demonstrated in experiments that the addition of endotoxin of Gram-negative bacteria to blood in a test tube can cause tissue factor activity on the primary membrane of monocytes. If the rabbits are injected with endotoxin after consumption of mononuclear cells with a large amount of alkylating agent, DIC will not occur, and endotoxin exposure to vascular endothelial cells will also produce tissue factor activity. However, it has also been found that the ratio of Peptidogyciw (a peptide sugar induced by DIC) to the content of techoic acid in the cell wall of the bacteria-positive bacteria is also related to the occurrence of DIC. It is obvious that the pathology of DIC caused by infection is complicated and also In contrast, bradykinin has a strong relaxing effect on blood vessels, which is one of the causes of blood pressure drop and shock in infection.

(two) malignant tumor

In cancer, pancreas, kidney, prostate, bronchial and other cancers, DIC is more common, acute promyelocytic leukemia is also easy to develop DIC. In cancer DIC, it is particularly prone to cases with extensive metastasis or massive tissue necrosis, because in these cases, tumor cells secrete a large amount of mucin, tissue factor, procoagulant, proteolytic enzyme, which promotes coagulation. And promote the pathological role of DIC. Trousseau syndrome is a case of chronic DIC in malignant tumors, which is characterized by recurrent migratory arteriovenous thrombosis and may even be the first manifestation.

(3) Obstetric accident

Including amniotic fluid embolism, early placental ablation, hypertonic saline abortion, pregnancy toxemia, stillbirth retention, uterine rupture, caesarean section, etc., DIC can be seen, the mechanism of the disease is mainly due to a large number of tissue factors in tissues such as amniotic fluid and placenta Into the blood circulation, promote blood coagulation, in addition, hypercoagulable state and abnormal changes in blood vessels and blood flow may also be the cause of the disease.

(4) Others

1 Severe head injury complicated by DIC may enter the blood circulation and promote blood coagulation due to the destruction of the blood-brain barrier by factors with potential coagulation activity.

2 venomous snake bites cause DIC, in addition to tissue damage released a large number of tissue factors, into the blood to promote coagulation, venom itself secretion substances also have the role of fibrinogen to fibrin.

3 immune diseases such as systemic lupus erythematosus, rejection of grafts, etc. cause DIC, mainly due to abnormal immune mechanisms in the disease causing extensive vascular endothelial cell damage, and complement activation is related to the promotion of coagulation mechanism.

4 liver diseases such as acute liver necrosis, cirrhosis and other cases of severe liver damage, are also prone to DIC, the reasons for which are due to the similar vascular endothelial damage and procoagulant substances, on the other hand It is due to the weakening of the function of phagocytosis and clearance of procoagulant substances in liver diseases.

5 elevated body temperature, acidosis, shock, hypoxia caused by vascular endothelial cell damage, can induce or aggravate DIC, hemolytic disease or hemolytic reaction, red blood cells can also promote procoagulant substances induced or aggravated DIC.

The most important change in the pathogenesis of DIC is due to the consequences of both thrombin and plasmin. The effects of both have produced many coagulation and fibrinolytic activities in the body. The role of the two can be different for different causes, the severity of the disease varies, and can also produce different changes in different phases of the disease, after a series of laboratory tests to find out, in the role of thrombin, first Is to break down fibrinogen to protein peptide A, form a fibrin monomer, monomers polymerize into fibrin, and form a thrombus under the cross-linking of factor VIII, but fibrin (original) can also be associated with fibrin cleavage products (FDP) forms a soluble complex. Thrombin can also activate factors V, VIII, XIII, protein C system and platelets, and stimulate the production of various active mediators such as platelet activating factor (PAF), prostacyclin, VW factor, etc. Thrombin can also affect the fibrinolytic system through vascular endothelial cells, so changes in the activity of thrombin in the body cause various changes in the body related to biochemical coagulation active substances. The combined results are that fibrinogen, factor II, V, VIII, XIII, protein C, and platelets are reduced due to large consumption, and platelet function is abnormal. Plasminogen is in various activators and also in tissue fibrinolysis. The zymogen activator is activated to convert to lysozyme. The action of fibrinolytic enzyme on fibrin (former) to form FDP/fdp and FDP can inhibit the formation and polymerization of fibrin, inhibit platelet activation, decompose and inactivate coagulation factors, and make fibrin, factors V, VIII and IX. cut back. From the results of the above two effects, the changes in coagulation and fibrinolysis in the body are extremely complicated in the occurrence of DIC.

In addition, anticoagulant substances in DIC include antithrombin III, protein C system components, tissue pathway inhibitors and the like.

an examination

Related inspection

Combined calcium cross test (CRT, PRT) Otolaryngology CT examination

(1) There are primary diseases that can induce diffuse intravascular coagulation and factors that contribute to the onset of disseminated intravascular coagulation.

(2) Have more than two of the following clinical manifestations:

1 repeated, severe or multiple site bleeding tendency, difficult to explain with the primary disease.

2 Unexplained refractory hypotension or shock.

3 The lungs, brain, liver, skin, subcutaneous and limb embolism appear, causing symptoms and signs of microcirculatory disorders, especially the acute renal function or pulmonary insufficiency that is not consistent with the primary disease.

4 rapid development of progressive anemia that is difficult to explain in the primary disease.

5 Heparin or other anticoagulant therapy is effective.

(3) Laboratory tests meet the following criteria:

1 The following three abnormalities occur simultaneously: one is that the platelet count is lower than 100×109/L or progressively decreased. Second, plasma fibrinogen is less than 150 mg / dl or progressive decline. Third, prothrombin time is prolonged by more than 3s.

2 If only 2 of the above 3 experimental tests are abnormal, there must be 1 or 2 of the following 4 abnormalities. The clotting time is prolonged for more than 5s, the 3P test is positive, or one of the ethanol gel test, the staphylococcal aggregation test, and the FDP quantification is abnormal. The euglobulin lysis time is less than 70 min or the plasma plasminogen content is decreased, and the blood film is more than 2%. Fragment of red blood cells and various shaped red blood cells.

Differential diagnosis

1. Primary fibrinolysis: This disease is clinically rare. It is due to certain factors that enhance the activity of plasminogen activin, resulting in the conversion of a large amount of plasminogen to plasmin, causing fibrinogen and Decomposition of factor V, VIII and other coagulation factors. Clinical manifestations of bleeding at various sites. Primary fibrinolysis is common in severe liver disease and liverless liver transplantation, and the production of anti-plasminogen activin and antiplasmin is reduced due to liver disease. In addition, the disease can also be seen in the lungs, prostate, uterus and other serious lesions, or certain drug poisoning, can occur fibrinolysis, there are unexplained fibrinolysis, but organ dysfunction is not obvious, generally not Leading to acute renal failure and shock, the main clinical manifestations of fibrinolysis are extensive and severe bleeding. The platelet count in the laboratory was normal or slightly decreased, the 3P test was negative, the euglobulin lysis time was significantly shortened, FVIII: C was normal, and platelet -TG was normal. Treatment with anti-fibrin solvent has a good effect and heparin treatment is ineffective.

2. Insufficient fibrinogen production: If the normal plasma fibrinogen content is less than 60% to 80%, there will be clinical bleeding. Insufficient hereditary fibrinogenesis is rare. Patients will have varying degrees of bleeding symptoms for life. Half of the patients have umbilical cord bleeding after birth as the first symptom, in addition to nasal discharge, blood in the stool, vomiting blood or hematuria. About 21% of patients have joint bleeding, and menorrhagia is rare. Laboratory examination: reduced platelet count and hyperfibrinolysis, prolonged clotting time, complete lack of fibrin determination, blood non-coagulation, prolonged prothrombin time.

3. Severe liver disease bleeding

Clinical Classification

(1) acute type: acute onset, often in a few hours or 1 ~ 2d onset, the condition is dangerous, rapid progress, bleeding, shock and other symptoms are obvious and serious. It is common in acute intravascular coagulation induced by acute infection, acute trauma and major surgery, acute hemolysis caused by blood transfusion, amniotic fluid embolism and other reasons.

(2) Subacute type: Onset within a few days to several weeks, the condition is more moderate than the acute type. Common in a variety of cancer and acute leukemia, stillbirth retention.

(3) Chronic type: The onset is slow, and the course of the disease can sometimes be several months to several years. Found in chronic liver disease, pregnancy poisoning, connective tissue disease, giant hemangioma. Clinical bleeding is mild, shock and thrombosis are rare, often found after laboratory tests.

The above clinical types are often related to the amount and speed of the procoagulant into the bloodstream. If the procoagulant substance enters the bloodstream rapidly, it often appears as an acute type. When a small amount of procoagulant substance is added and slowly enters the bloodstream, it is often expressed as Subacute or chronic.

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