Necrotizing fasciitis of the abdominal wall

　　First, the cause of onset

　　This disease often occurs in patients with low body immunity and small vascular lesions, and can occur from neonates to elderly over 60 years old, especially in elderly patients with diabetes, atherosclerosis, or malignant tumors receiving chemotherapy or immunosuppressants, who are more prone to occur. The vast majority are secondary necrotizing fasciitis, and there are reasons or risk factors that can be found; 15% to 18.2% of acute necrotizing fasciitis have unknown causes, belonging to idiopathic infections.

　　1, Risk factors:According to the literature reports, the risk factors related to the onset of this disease include:

　　(1) Surgery and trauma: It often occurs after abdominal surgery and trauma, especially after appendectomy, colorectal surgery, abdominal trauma with colorectal injury, or abdominal wall trauma after combined colorectal injury, it is easier to occur abdominal wall necrotizing fasciitis. Casall et al. reported that 12 cases of necrotizing fasciitis had a history of abdominal injury or abdominal surgery. Other surgical treatments (such as percutaneous transhepatic intrahepatic portosystemic shunt, surgical puncture, drainage of abscess under the guidance of CT or ultrasound, urogenital instrument operation, external application of herbal medicine or moxibustion, local block treatment, etc.) and abscesses after scratching are prone to cause this disease.

　　(2) Chronic diseases: Diabetes, chronic renal insufficiency, congenital leukopenia, etc., among which diabetes is the most common disease factor and risk factor.

　　(3) Vascular diseases: Atherosclerosis, hypertension, peripheral vascular diseases, etc.

　　(4) Infection diseases: Umbilical erysipelas, abdominal infection (such as acute appendicitis, cholecystitis, peritonitis, etc.), syphilis, typhoid fever, etc.

　　(5) Malignant diseases: Malignant tumors, leukemia, AIDS, etc.

　　(6) Old age and physical weakness, malnutrition, etc.

　　(7) Abuse or long-term use of glucocorticoids and immunosuppressants.

　　(8) Chemotherapy, radiotherapy.

　　(9) Other: Alcoholism, drug abuse, obesity, urinary extravasation, penile priapism, excessive sexual intercourse, etc.

　　2, Pathogenic bacteria:There are many pathogenic bacteria that cause necrotizing fasciitis, and most of them are normal flora of the skin, intestines, and urinary tract, especially related to the distribution of normal flora in the adjacent areas of trauma and incisions. Common aerobic bacteria include staphylococcus aureus, group A streptococcus, escherichia coli, enterococcus, proteus, pseudomonas, klebsiella, etc.; common anaerobic bacteria include anaerobic streptococcus, bacillus fragilis, clostridium perfringens, etc.; and they often cause pathogenicity through the synergistic action of aerobic and anaerobic bacteria.

　　3, Susceptible factors and pathogenic bacteria:Recent studies have found that different susceptible factors are closely related to different pathogenic bacteria. For example, after trauma, clostridium perfringens is often found in the pathogenic bacteria; in patients with diabetes, the pathogenic bacteria are often bacillus fragilis, escherichia coli, and staphylococcus aureus; in patients with malignant tumors and immunosuppression, pseudomonas and escherichia coli are most common.

　　The pathogenic bacteria of secondary necrotizing fasciitis of the abdominal wall mainly侵入 through wounds, and most of them are mixed infections of bacteria. Ruose et al. reported 16 cases of necrotizing fasciitis, with a total of 75 species of aerobic and anaerobic bacteria cultured, and some scholars reported that bacteria from 81 patients were cultured to 375 species, with some patients having up to 5-6 species of bacteria. Some research results show that necrotizing fasciitis in all parts, including the abdominal wall, is most commonly seen in mixed infections of anaerobic and aerobic bacteria, accounting for about 68% of the total; those with pure anaerobic bacteria are the next most common, accounting for about 22%; and those with aerobic bacteria are the least, accounting for only 10%. It is not difficult to see that anaerobic bacteria are the most common pathogenic bacteria. The incidence rate of anaerobic bacteria in the inguinal region and lower abdominal wall necrotizing fasciitis is the highest. Many patients have negative anaerobic bacteria cultures, which may be related to problems in specimen collection, storage, transportation, or culture inoculation conditions, and/or not meeting the experimental requirements.

　　The cause of idiopathic necrotizing fasciitis of the abdominal wall is unclear. Studies have shown that immune dysfunction, especially factors such as the presence of malignant tumors, diabetes, arteriosclerosis, the use of glucocorticoids, and immunosuppressants, are closely related to it. The pathogenic bacteria may spread from other parts of the body to the affected area hematogenously, such as from the teeth, throat, and tonsils, among other places.

　　Two, Pathogenesis

　　Necrotizing fasciitis begins in the fascia and subcutaneous tissue, initially the skin is not involved. As the infection rapidly spreads along the fascial surface and the condition progresses, the large-scale reproduction of aerobic bacteria also leads to the massive consumption of oxygen in the infected tissue, as well as the formation of fibrinoid thrombi in the subcutaneous small arteries and veins of the affected area and the adjacent healthy tissue with inflammatory reaction, resulting in poor tissue perfusion and a significant decrease in oxygen supply, which can lead to a decrease in PaO2 of 2.66-3.99 kPa. In addition, when neutrophils aggregate at the lesion site to perform the function of phagocytizing invasive bacteria, the oxygen consumption can increase by more than 20 times, further reducing the already low PO2 in the local tissue, even to zero. This not only seriously affects the ability of neutrophils to phagocytize bacteria but also favors the proliferation of anaerobic bacteria, leading to more severe pathological damage to the locally invaded tissue, thereby causing a large-scale hypoxia and necrosis of the skin, subcutaneous tissue, and fascia. Due to the large-scale reproduction and growth of anaerobic bacteria and the production of tumor necrosis factor, streptokinase, hyaluronidase, and other substances, the tissue structure is further decomposed and destroyed; in addition, the tissue between the abdominal fascia and muscle is relatively loose, and infections by some gas-producing bacteria such as anaerobic streptococci and Escherichia coli can produce gas, causing air to accumulate in the tissue spaces and pressure to rise, making it difficult to confine the infection. The infection rapidly spreads along the subcutaneous fascia to surrounding areas, such as the chest wall and buttocks. The affected subcutaneous tissue and fascia show inflammatory edema and necrosis, with inflammatory cells, bacterial infiltration, malodorous purulent, and bloody secretions covering the necrotic fascia and muscle.

　　Large abdominal surgeries, severe abdominal trauma, and abdominal infections can suppress or damage the immune system of the body, such as bacteria and (or) toxins that can keep the immune function of immune organs like the spleen in an inhibitory state, lowering the production levels of P factor (properdin), opsonic protein, and complement, resulting in weakened phagocytic activity of polymorphonuclear leukocytes and phagocytes in the blood circulation, further aggravating and accelerating the progression of infection. With the absorption of a large amount of toxins, and the entry of bacteria or pus clots into the blood, patients quickly develop systemic toxic symptoms, including chills, high fever, or unregulated body temperature, toxic shock, DIC. Severe cases may quickly develop multiple organ dysfunction or failure.

　　Necrotizing fasciitis of the abdominal wall often complicates with the invasion and rupture of large blood vessels, leading to hemorrhagic shock in cases where bleeding is not promptly treated, and the formation of venous and arterial thrombosis, septic emboli. It may also cause mediastinitis, pericarditis, pleurisy; muscle paralysis, polyneuritis; cholecystitis, peritonitis, intestinal paralysis, or acute pancreatitis, etc. Severe cases may also develop sepsis, which is an acute organ dysfunction secondary to infection. Clinical manifestations include fever, chills, tachycardia, changes in consciousness, and increased white blood cells. Essentially, it is a systemic effect caused by the invasion of pathogenic microorganisms, leading to the massive release of inflammatory mediators.

　　Most cases occur 1 to 3 days after abdominal surgery or trauma, with shorter onset times that can be as brief as a few hours. Sometimes, the disease may occur even 10 to 14 days after trauma. The disease has an abrupt onset and rapid progression. If not treated promptly, the mortality rate can reach 20% to 73%. For neonates with umbilical erysipelas complicated with necrotizing fasciitis of the anterior abdominal wall, the mortality rate can be as high as 93.8%, and those occurring on the posterior abdominal wall (retroperitoneum) often prove fatal.

　　1. Local manifestations

　　Secondary to surgery and trauma, the wound and its surrounding area may appear painful, congested, and swollen, followed by skin discoloration, necrosis, accompanied by malodorous pus or coffee-colored exudate from the incision or wound; for those without a history of surgery or trauma, the early lesions may only manifest as sudden pain, local redness, tenderness, and palpable hard masses (nodules) in the soft tissue, often misdiagnosed as cellulitis. With the occlusion of nutritional vessels and exhaustion of oxygen within the tissue, the skin quickly becomes pale, followed by purple-black necrosis. The skin surface often appears with scattered blood blisters of varying sizes, which may gradually merge and ulcerate, leading to the shedding of the epidermis and exposing the black dermis after ulceration. The subcutaneous tissue and superficial and deep fascia undergo progressive widespread necrosis and liquefaction, with the skin floating on top. Local puncture may yield malodorous purulent fluid mixed with gas, and this process usually occurs within 36h to 4 days after the onset of infection symptoms.

　　Before tissue gangrene, the affected area has abnormal pain, and the pain decreases and sensory loss or painless sensation appear with the occlusion of the perforating blood vessels between the skin and fascia and the necrosis of the nerves.

　　The local clinical manifestations of necrotizing fasciitis are related to the type of pathogen, such as enterobacter, anaerobic bacterial infection is characterized by gas production, so palpation can have crepitus, and it is often necessary to differentiate from gas gangrene; Staphylococcus aureus infection spreads relatively slowly, pus is thick, and has a 'localized trend'; Streptococcus group A pus is thin,呈血性, spreads relatively rapidly, with marked edema; Bacteroides pus has a foul smell, etc.

　　Two, General manifestations

　　Due to the entry of a large amount of toxins, bacteria, or pus clots into the blood, patients often have severe sepsis, septicemia, and other infections, with severe systemic toxic manifestations.

　　1, Chills, high fever, body temperature up to 39℃～41℃.

　　2, Restlessness, delirium, apathy.

　　3, Blood pressure drop, weak pulse, oliguria, and other toxic shock symptoms.

　　Severe cases may have multiple organ dysfunction or failure.

　　The key to preventing this disease is to avoid over-exertion,外伤 and cold, actively treat the primary disease, and prohibit the abuse or long-term use of corticosteroids and immunosuppressants. Early appropriate treatment of abdominal diseases that may cause necrotizing fasciitis of the abdominal wall is the fundamental measure to prevent necrotizing fasciitis of the abdominal wall. Any abdominal surgery, even including abdominal puncture, should be strictly performed under sterile conditions. Antimicrobial drugs should be administered orally before intestinal surgery to reduce the occurrence of necrotizing fasciitis of the abdominal wall.

　　One, Blood routine examination:The red blood cells and hemoglobin of most patients are lower than normal; the white blood cell count is elevated, even >30×109/L, neutrophils >0.80, and toxic granules appear.

　　Two, Bacteriological examination:Secretion from the wound or puncture aspiration of pus for smearing or culture can find hemolytic streptococcus, Staphylococcus aureus, anaerobic bacteria, and other pathogenic bacteria.

　　Three, Pathological examination:In recent years, some scholars have proposed to make small incisions locally, take tissue biopsy and rapid frozen section, and observe inflammatory reaction and formation of arteriovenous thrombosis, and can also perform pus swab bacterial culture.

　　Four, Ultrasound examination:It is used for early diagnosis and guiding puncture aspiration of pus for culture, and can show: skin edema and thickening, irregular fascial deformation, diffuse thickening, abnormal effusion along the fascial surface, abscess cavity, subcutaneous gas.

　　Five, X-ray examination:

　　1. X-ray film:X-ray films show that soft tissue gas is more sensitive than physical examination, showing soft tissue swelling, thickening, and mediastinum, retroperitoneal and other soft tissue gas shadows, pleural effusion, and so on.

　　2, CT scan:CT is superior to X-ray film in detecting deep infections, soft tissue necrosis, and the extent of effusion, but it is less sensitive than MRI in showing deep fascial fluid, mainly used for infection localization and determination of lesion depth, CT signs:

　　(1) Skin and subcutaneous tissue diffuse edema and thickening, subcutaneous fat in a strip-like, reticular enhancement;

　　(2) Fascia thickening, in general, the superficial fascia is involved, while the superficial, middle, and deep layers of the deep fascia may be involved to different degrees;

　　(3) Soft tissue air shadow, usually distributed along the fascial surface, continuous, there is generally no isolated gas accumulation in the soft tissues such as muscles;

　　(4) Local effusion, pus shadow, can involve multiple different anatomical spaces at the same time, or located between subcutaneous fat and muscle or along the muscle distribution;

　　(5) Early muscle is often not involved or shows mild inhomogeneity, with the progression of the disease and the involvement of adjacent muscles, it shows varying degrees of thickening, enhancement, and destruction;

　　(6) Contrast agent extravasation, manifested as the appearance of high-density shadows in the interstitial effusion soon after the injection of contrast agent, which is due to the necrosis and rupture of the arterial or venous wall;

　　(7) Internal jugular vein or other deep vein thrombosis or septic embolism;

　　(8) Lymph node reactive enlargement, etc.

　　3, MRI:MRI can display minor signal changes in soft tissues including skin, subcutaneous fat, superficial and deep fascia, muscles, etc., and can clearly show the anatomical distribution of the disease, which is helpful to determine the best biopsy site and implement treatment plans, and monitor treatment response. In predicting necrosis or myositis, it is more accurate than the increase of plasma creatine kinase, lactate dehydrogenase, or myoglobinuria. The sensitivity of MRI diagnosis of necrotizing fasciitis is 100%, specificity 86%, accuracy 94%, but its scanning time is long, not suitable for critically ill patients.

　　MRI signs:

　　(1) Subcutaneous tissue thickening, T1-weighted imaging shows low signal, T2-weighted imaging shows high signal, may have enhancement;

　　(2) Superficial and deep fascia thickening, effusion, T2-weighted imaging shows high signal, most呈 homogeneous, clear, dome-shaped high signal area, if there is a large mass signal increase in the deep fascia T2-weighted imaging, necrotizing fasciitis can be diagnosed;

　　(3) Gadolinium enhancement scan shows necrosis or abscess as low signal on T1-weighted imaging, high signal on T2-weighted imaging, without enhancement or central part without enhancement, with a peripheral enhancement ring. Inflammatory tissue shows low signal on T1-weighted imaging, high signal on T2-weighted imaging, and uniform enhancement on T1-weighted imaging enhancement scan;

　　(4) Gadolinium contrast agent quickly enhances in the adjacent T2-weighted high signal area, indicating damage to the perivascular network, leading to increased early contrast agent extravasation. This is a sign of invasive infection, while the typical ring enhancement showing abscess formation suggests a small degree of invasive infection;

　　(5) T2-weighted imaging shows mild diffuse increase in muscle signal, T1-weighted imaging enhancement scan shows diffuse enhancement of muscle discontinuity, but the degree of muscle signal enhancement is lighter than that of fascia changes, which is due to edema, muscle abscess (ring-shaped muscle effusion), and the wall may be enhanced.

　　1. Dietetic recipes for abdominal wall necrotizing fasciitis

　　1. Yam and date porridge:Yam 150 grams, 9 dates, 100 grams of rice. Wash the yam, peel it, and cut into small pieces; clean and prepare the dates and rice. Add an appropriate amount of water to the pot, add the dates and rice to cook the porridge. When it is five-thirds done, add the yam pieces and continue to cook until the porridge is done. Eat 1-2 times a day, and it can be eaten long-term. Yam has the effects of invigorating the spleen and lung, nourishing the kidney and consolidating essence. Dates have the effects of reinforcing the middle energizer, nourishing the stomach and spleen, and nourishing the blood and calming the mind. It is used to treat dyspepsia caused by weakness of the spleen and stomach, postoperative abdominal distension, and abdominal pain.

　　2. Taro and pork shreds porridge:Fresh taro 100 grams, lean pork 60 grams, corn flour 100 grams. Peel and wash the taro, cut into small pieces; slice the lean pork for later use. Add an appropriate amount of water to the pot, bring to a boil, sprinkle in the corn flour (stirring continuously to prevent sticking), then add the pork slices to cook the porridge. When it is five-thirds done, add the taro pieces and continue to cook until the porridge is done. Eat twice a day, and it can be eaten long-term. Taro has the effects of regulating the middle energizer, harmonizing the stomach, softening hard lumps, and dispersing nodules. Pork has the effects of nourishing the kidney yin, nourishing the liver blood, and moistening the skin. Corn is nutritious and has the effects of regulating the middle energizer and benefiting the brain. It is used to treat postoperative abdominal distension and various symptoms of dyspepsia.

　　2. Mung bean and pork shreds porridge:

　　1. Eat more foods rich in vitamin A, B-complex, and vitamin C, such as oranges, apples, tomatoes, and other fruits and vegetables.

　　2. Strengthen nutrition by eating diets rich in protein and vitamins, such as chicken, lean meat, shrimp, milk, tofu, and beans.

　　3. To prevent infection, foods such as needlefish, loach, crucian carp, chrysanthemum flowers, rapeseed, taro, mung beans, adzuki beans, malan tou, etc. can be eaten.

　　3. Foods to avoid for abdominal wall necrotizing fasciitis

　　1. Eat less cold foods in daily life, as this is not conducive to blood circulation. Common cold foods include duck eggs, duck blood, pork intestines, pork brain, seafood, persimmons, pomegranates, bananas, longans, kiwis, sugarcane, watermelons, bitter melons, melons, tomatoes, bamboo shoots, and raw lotus roots, etc.

　　2. Avoid smoking, drinking, greasy, fried, moldy, or salted foods.

　　3. Avoid spicy foods such as garlic and mustard greens.

　　4. Avoid eating overly sour, spicy, or salty foods.

　　1. Treatment

　　1. Large-dose combined use of antibiotics:The pathogenic bacteria of necrotizing fasciitis are often mixed. Before the results of bacterial culture and drug sensitivity test are available, large doses of combined antibiotics or broad-spectrum antibiotics should be used; thereafter, adjustments should be made in a timely manner based on the results of bacterial culture and drug sensitivity test. Common broad-spectrum antibiotics include cephalosporins, metronidazole, or tinidazole, etc.

　　2. Surgical treatment:Once the disease is diagnosed, immediate incision and drainage should be performed. The operation should pay attention to:

　　(1) Extensive incision: Multiple incisions reaching the deep fascia to completely open or enlarge the incision, so as to achieve the purpose of sufficient drainage.

　　(2) Complete debridement: Thoroughly remove necrotic tissue until healthy bleeding tissue is reached. This is the key to ensuring the effectiveness of surgery. Necrotic fascial tissue between the muscles should be removed as much as possible while retaining normal nerves and blood vessels.

　　(3) Destroy the anaerobic environment: Apply hydrogen peroxide (peroxide) or 1:5000 potassium permanganate solution for repeated flushing of the surgical area after debridement.

　　These measures can increase the redox potential difference inside the incision, creating an environment unfavorable for the growth of anaerobic bacteria, which is conducive to controlling the further spread and diffusion of infection.

　　(4) Adequate drainage: Place Optuss solution gauze strips or iodophor gauze strips for drainage. The gauze should be loosely placed and reach the deep part, do not stuff it too tightly or leave any ineffective cavity.

　　3. Dressing change after surgery:Change the dressing frequently after surgery to accelerate the shedding of necrotic tissue. Generally, the wound should be flushed with chlorhexidine (hexidine), hydrogen peroxide (peroxide), or 1:5000 potassium permanganate solution at least three times a day. Then, use gauze strips soaked in hydrogen peroxide (peroxide) to dress the wound, drain and cover the wound, until granulation tissue begins to grow inside the wound and there is no necrotic tissue. At this point, change to gauze strips soaked in saline for dressing, drain and cover the wound. Bacterial culture should be repeated during dressing changes to detect secondary infection early. When the wound infection is controlled and the granulation tissue is fresh, skin grafting can be performed to cover the wound.

　　4. Strengthen the application of inflammatory mediator antagonists:In recent years, it has been found that inflammatory mediators such as endotoxins, TNFα, IL-1, etc., play an extremely important role in the occurrence, development, and changes of this disease. Blocking the excessive release of inflammatory mediators at different levels and actively supplementing severely insufficient endogenous inhibitors has a positive significance. At present, indomethacin (inflammatory pain), ibuprofen, anti-endotoxin monoclonal antibodies, IL-1 receptor antagonists, anti-TNFα, and other non-steroidal anti-inflammatory drugs and cytokine regulators are commonly used.

　　5. General supportive therapy:Supportive treatment is an important guarantee for treatment success. For patients with good general condition and the ability to eat, high-calorie, high-protein, and vitamin-rich diets should be provided; for patients with significant systemic symptoms and severe illness, it is necessary to correct hypoproteinemia and electrolyte imbalance in a timely manner, strengthen enteral and parenteral nutritional support, and the nutritional calories should be at least twice the basal metabolic calories. According to the condition, fresh whole blood or plasma can be infused.

　　6. Hyperbaric oxygen adjuvant therapy:Under hyperbaric oxygen conditions, the oxygen partial pressure of the body tissues is higher, which has the following therapeutic effects on necrotizing fasciitis: inhibiting the growth and reproduction of anaerobic bacteria; improving the ability of neutrophils to phagocytize bacteria; oxidizing the sulfhydryl groups of aerobic bacteria to disulfide, causing metabolic disorders and inhibiting growth and reproduction; hyperbaric oxygen can cause significant vasoconstriction, thereby reducing permeability, decreasing inflammatory exudation, and rapidly alleviating tissue edema; under hyperbaric oxygen, the oxygen concentration in the blood increases, and the blood PaO2 rises, which can quickly correct local tissue ischemia, hypoxia, and metabolic disorders, promote granulation tissue regeneration, accelerate the formation and establishment of collateral circulation, and is conducive to the elimination of inflammation and necrotic tissue, and accelerate the improvement of local diseases.

　　Therefore, once the disease is confirmed or suspected clinically, hyperbaric oxygen therapy should be performed immediately in addition to debridement and the use of effective antibiotics.

　　7. Treatment of complications:In the case of severe infection, attention should be paid to strengthen heart function, protect renal function, and other comprehensive treatments, be vigilant and treat severe complications such as sepsis and toxic shock, and actively provide respiratory and circulatory support for patients with concurrent respiratory and circulatory failure.

　　8. Immunotherapy:Injectable interferon-gamma 1 million U, once a day, for a total of 10 times.

　　9. Control existing systemic diseases, such as diabetes.

　　Second, prognosis

　　Although significant progress has been made in the early diagnosis and treatment of the disease in recent years, its mortality rate is still 0% to 50%. A comprehensive review of the literature reports that factors affecting prognosis include:

　　1. The patient's own resistance, such as the presence of chronic diseases such as diabetes, chronic renal insufficiency, congenital leukopenia, malignant tumors, AIDS, etc., or the use of chemotherapy, radiotherapy, immunosuppressive therapy, as well as aging, malnutrition, and infection, etc., have a poor prognosis. Some scholars reported that the survival rate is 79% and the mortality rate is 17% for those with fewer than 3 risk factors, and the predicted mortality rate is 50% for those with 3 or more risk factors.

　　2. Early diagnosis and surgical drainage Freischlag believes that the timing of surgery is directly related to mortality. When the skin appears extensive blackening and necrosis, shock, and DIC, the progression of the disease is often difficult to reverse, and treatment opportunities are often lost. He found that patients who underwent surgical drainage within 24 hours of onset had a mortality rate of 36%; beyond 24 hours or later, it reached 70%; Ivan et al. reported that patients who underwent early diagnosis (within 0-4 days after onset, with an average of 21 hours) by frozen section diagnosis of the wound tissue and early surgical treatment had good effects, with only 1 death in 8 patients; while those diagnosed later based on clinical manifestations had a higher mortality rate due to delayed early treatment opportunities. Some Chinese scholars have also found that the main factor for treatment failure is insufficient understanding of the pathological changes of the disease, which delays the timing of surgical treatment, leading to severe complications such as infection, absorption of toxins causing sepsis, multiple organ failure, and ultimately leading to patient death. Therefore, early diagnosis and early surgical drainage are one of the key factors to improve survival rates and improve prognosis.