Abdominal wall necrotizing fasciitis
Introduction
Brief introduction of abdominal wall necrotizing fasciitis The necrotizing of abdominal wall is a necrotic soft tissue infection that occurs in the abdominal wall. There are many pathogenic bacteria. The infection mainly involves the deep abdominal wall and superficial fascia, and it can also invade the skin, but it does not involve the muscle in the early stage. The disease can occur in any part of the abdominal wall (such as the anterior abdominal wall, lateral abdominal wall, groin area and posterior ventral wall), especially in abdominal trauma or surgical cutting (invasive) mouth and adjacent areas, but also for the buttocks, The infection of the perineum spread, sometimes after a small stab wound or insect bite, the incidence of necrotizing fasciitis is sharp, rapid progress, and the condition is dangerous. Delayed diagnosis and treatment often lead to death of the patient. basic knowledge The proportion of illness: 0.003%-0.004% Susceptible people: no special people Mode of infection: non-infectious Complications: peritonitis, acute pancreatitis
Cause
Causes of abdominal wall necrotizing fasciitis
Risk factors (30%):
Comprehensive literature reports that the risk factors associated with the disease are:
(1) Surgery and trauma: more often after abdominal surgery and trauma, especially after appendectomy, after colorectal surgery, abdominal injury or abdominal wall injury combined with abdominal wall injury is more likely to occur abdominal wall necrotizing fasciitis, Casall I have reported that 12 cases of necrotizing fasciitis have a history of abdominal injury or abdominal surgery, and other surgical treatments (interventional procedures such as transjugular intrahepatic portosystemic shunt, surgical puncture, CT or ultrasound guided transabdominal abscess drainage, Urinary genital device operation, external application of herbs or AI fire burning, partial closure treatment, etc.) and carbuncle can easily induce the disease after scratching.
(2) Chronic diseases: diabetes, chronic renal failure, congenital leukopenia, etc., among which diabetes is the most common predisposing factor and risk factor.
(3) vascular disease: arteriosclerosis, hypertension, peripheral vascular disease, etc.
(4) Infectious diseases: umbilical inflammation, abdominal infection (acute appendicitis, cholecystitis, peritonitis, etc.), syphilis, typhoid and other infections.
(5) Malignant diseases: malignant tumors, leukemia, AIDS, etc.
(6) Old age, malnutrition, etc.
(7) Abuse or long-term use of glucocorticoids and immunosuppressive agents.
(8) chemotherapy, radiotherapy.
(9) Others: alcoholism, drug abuse, obesity, extravasation of urine, abnormal erection of the penis, excessive sexual intercourse, etc.
Pathogens (30%):
There are many pathogens causing necrotizing fasciitis, and most of them are the normal flora of skin, intestines and urethra, especially related to the distribution of normal flora in the vicinity of wounds and incisions. The common aerobic bacteria are Staphylococcus aureus. Group A Streptococcus, Escherichia coli, Enterococcus, Proteus, Pseudomonas, Klebsiella, etc.; common anaerobic bacteria are anaerobic streptococci, Bacteroides fragilis, Clostridium, etc.; Aerobic bacteria and anaerobic bacteria synergistically cause disease.
Susceptibility factors (20%):
In recent years, studies have found that different susceptibility factors are closely related to different pathogens. For example, post-traumatic infection, Clostridium is more common in pathogenic bacteria; infection occurs in diabetic patients, pathogenic bacteria are Bacteroides fragilis, Escherichia coli, Staphylococcus aureus See; infections in malignant tumors and immunosuppressed patients, most commonly with Pseudomonas, Escherichia coli, etc.
The main wounds of secondary abdominal necrotic fasciitis are invasive, and most of them are mixed infections of bacteria. Ruose et al reported 16 cases of necrotizing fasciitis, and a total of 75 aerobic and anaerobic bacteria were cultured. 81 cases of bacteria were reported to be cultured in 375 species, and some patients may have up to 5 to 6 species of bacteria. Some studies have shown that anaerobic fasciitis and anaesthesia in all parts including the abdominal wall Oxygen bacteria mixed infection is the most common, accounting for 68% of the total; anaerobic bacteria culture is the second, accounting for 22%; aerobic bacteria culture is the least, only 10%, it is not difficult to see Anaerobic bacteria are the most common pathogens. In the clinical inguinal region, the anaerobic rate of anaerobic fasciitis in the lower abdominal wall is the highest. Many patients are negative for anaerobic culture and may be collected, stored, transferred or collected with specimens. There are problems in the cultivation of inoculation conditions and/or non-compliance with the experimental requirements.
The cause of idiopathic abdominal wall necrotizing fasciitis is unclear. Studies have shown that immune dysfunction, especially with malignant tumors, diabetes, arteriosclerosis, glucocorticoids and immunosuppressive agents, is closely related to its pathogens. Blood in other parts of the body spreads to the affected area, such as from the teeth and throat and tonsils.
The disease occurs in patients with low systemic immune function and small vascular disease, from neonates to the elderly over 60 years old, especially in elderly patients with diabetes, arteriosclerosis or malignant tumors are more susceptible to chemotherapy or immunosuppressive agents. Occurred, the majority of secondary necrotizing fasciitis, have causes or risk factors can be investigated; 15% to 18.2% of acute necrotizing fasciitis for unknown reasons, is an idiopathic infection.
Pathogenesis
Necrotizing fasciitis begins in the fascia and subcutaneous tissue. The initial skin is not affected. As the infection spreads rapidly along the fascia and the disease progresses, the aerobic bacteria multiply and the oxygen in the infected tissue is consumed. And the affected area and the adjacent subcutaneous arterioles of healthy tissue with inflammatory reaction, small vein fibrin-like thrombosis, resulting in poor tissue perfusion, a large drop in oxygen supply, can reduce the PaO2 drop by 2.66 ~ 3.99kPa, in addition, When neutrophils accumulate in the lesions and play the role of phagocytic invading bacteria, they can increase the oxygen consumption by more than 20 times, so that the PO2 of the local tissue has been reduced further, even to zero, which not only seriously affects the neutral particles. The ability of cells to phagocytose bacteria is more conducive to the proliferation of anaerobic bacteria, resulting in more pathological damage to the invaded local tissues, resulting in a wide range of skin, subcutaneous tissue and fascia hypoxia, necrosis, due to the proliferation of anaerobic bacteria And the production of tumor necrosis factor, streptokinase, hyaluronidase, etc., the tissue structure is further broken down; plus abdominal fascia and muscle More woven, and anaerobic streptococci, Escherichia coli and other gas-producing bacteria infection can produce gas, so that the interstitial gas accumulation, increased pressure, so that the infection is not easy to limit, along the subcutaneous fascia rapidly spread to the surrounding, to The chest wall, buttocks and other adjacent areas, affected subcutaneous tissue, inflammatory edema, necrosis, inflammatory cells, bacterial infiltration, odorous purulent, bloody secretions covering the necrotic fascia and muscle.
Some large abdominal surgery, severe abdominal trauma and abdominal infection can inhibit or damage the body's immune system. For example, bacteria and/or toxins can inhibit the immune function of immune organs such as the spleen, P factor (properdin), conditioning The production levels of opsonic proteins and complements are reduced, resulting in impaired phagocytosis of polymorphonuclear leukocytes and phagocytic cells in the blood circulation, further aggravating the progression of infection, with the absorption of large amounts of toxins, bacteria or pus When the plug enters the blood, the patient quickly develops symptoms of systemic poisoning, chills, high fever or body temperature, toxic shock, DIC, and severe multiple organ dysfunction or failure.
Prevention
Abdominal wall necrotizing fasciitis prevention
Necrotizing fasciitis is often accompanied by immune damage to the whole body and local tissues, such as secondary skin damage caused by bruises, contusions, insect bites, etc. After the operation of the hollow organ, perianal abscess drainage, extraction, and abdominal cavity After the operation of the mirror, it is very traditional to find and treat it in time. In addition, the body's immunity should be improved, and the primary systemic disease and local skin damage should be actively treated.
Complication
Complications of abdominal wall necrotizing fasciitis Complications, peritonitis, acute pancreatitis
The disease often complicated by large blood vessel invasion and rupture, arteriovenous thrombosis, sepsis embolism formation; mediastinal inflammation, pericarditis, pleurisy; muscle paralysis, multiple nerve paralysis; cholecystitis, peritonitis, intestinal paralysis or acute pancreatitis.
Symptom
Abdominal wall necrotizing fasciitis symptoms Common symptoms Necrotizing fasciitis High fever venous thrombosis irritability Shallow fasciitis Swollen chills gangrene
More in abdominal surgery, 1 to 3 days after trauma, the onset time is only a few hours, sometimes even 10 to 14 days after trauma, the disease begins rapidly, the disease develops rapidly, such as diagnosis and treatment is not timely, mortality Up to 20% to 73%, and neonatal umbilical inflammation associated with anterior abdominal necrotizing fasciitis, the mortality rate can be as high as 93.8%, occurring in the posterior abdomen (peritoneal) are often fatal.
Partial performance
Secondary to surgery and trauma, there is pain, congestion, edema in the wound and its surroundings, followed by cyanosis, necrosis, malodorous pus outflow or brown exudate in the incision or wound; no history of surgery, traumatic history, early lesions Can only be manifested as sudden pain, local redness, tenderness and soft tissue lumps (knot), often misdiagnosed as cellulitis, with nutrient vascular embolization and oxygen depletion in the tissue, the skin quickly pale, followed by Purple-black necrosis, the surface of the skin often appears to be scattered in the blood bubble, can gradually fuse and rupture, the epidermis sheds, reveals the black dermis after rupture; subcutaneous tissue and shallow deep fascia progressive extensive necrosis, skin Floating on it, local puncture can extract the odorous purulent liquid and mix with gas, which usually occurs 36h to 4 days after the infection symptoms appear.
Before the tissue gangrene, the lesion is abnormally painful. With the embolization of the perforating vessel between the skin and the fascia and nerve necrosis, the skin pain of the affected area is alleviated and there is a feeling of loss or no pain.
The local clinical manifestations of necrotizing fasciitis are related to the species of pathogenic bacteria. For example, Enterobacter, the characteristic of anaerobic infection is gas production, so palpation can have sputum pronunciation, which is often associated with gas gangrene identification; Staphylococcus aureus infection The expansion is relatively slow, the pus is thick, and there is a "limited trend"; the group A streptococcus pus is thin, bloody, relatively rapid expansion, and obvious edema; the bacillus pus has a foul odor.
2. Whole body performance
Due to a large number of toxins, bacteria or pustules entering the blood, patients are often accompanied by severe toxemia, sepsis and other infections, systemic poisoning is serious.
(1) chills, high fever, body temperature up to 39 ° C ~ 41 ° C.
(2) irritability, embarrassment, indifference.
(3) toxic shock, such as decreased blood pressure, weak pulse, and low urine.
(4) Severe cases may have multiple organ dysfunction or failure manifestations.
Examine
Examination of abdominal wall necrotizing fasciitis
1. Blood routine examination: Most patients have red blood cells, hemoglobin is lower than normal; white blood cell count is increased, even >30×109/L, neutrophils>0.80, and poisoning particles appear.
2. Bacterological examination: Take the wound secretion or puncture and pus to smear or culture, and find pathogens such as hemolytic streptococcus, staphylococcus aureus and anaerobic bacteria.
3. Pathological examination: In recent years, some scholars have proposed local small incision, taking tissue biopsy and rapid frozen section, showing inflammatory reaction and arteriovenous thrombosis, and can also be used for bacterial culture of pus swab.
4.B-ultrasound: for early diagnosis and guided puncture and pus culture, it can show: skin edema thickening, irregular fascia deformation, diffuse thickening, abnormal effusion along the fascial surface, abscess, subcutaneous gas .
5. X-ray inspection
(1) X-ray plain film: X-ray plain film shows that soft tissue gas is sensitive to physical examination, visible soft tissue swelling, thickening and mediastinum, retroperitoneal and other soft tissue gas, pleural effusion.
(2) CT scan: CT is superior to X-ray film in the detection of deep infection, soft tissue necrosis and gas accumulation, but it is less sensitive than MRI in displaying deep fascial fluid, mainly used for infection localization and determination of lesion depth. , CT signs:
1 skin, subcutaneous tissue diffuse edema thickening, subcutaneous fat strips, reticular reinforcement;
2 fascia thickening, under normal circumstances, superficial fascia is involved, and the degree of shallow, medium and deep involvement of deep fascia can be different;
3 soft tissue gas shadow, more along the fascial surface distribution, continuous, muscles and other soft tissues generally do not have isolated gas accumulation;
4 local effusion, empyema, can involve multiple different anatomical gaps at the same time, can also be located in subcutaneous fat, between muscles or along muscles;
5 Early muscles are often unaffected or manifested as mild inhomogeneity. As the disease progresses and the adjacent muscles are involved, it shows varying degrees of thickening, strengthening, and destruction;
6 contrast agent extravasation, which appears as a high-density shadow in the interstitial effusion soon after the injection of the contrast agent, which is caused by necrosis of the artery or vein wall;
7 internal jugular vein or other deep vein thrombosis or sepsis embolus;
8 lymph node reactive swelling and so on.
(3) MRI: MRI can show soft tissue including skin, subcutaneous fat, deep fascia, muscle and other small signal changes, can clearly show the anatomical distribution of the disease, help determine the best biopsy site and implementation of treatment options, and monitor treatment response In terms of predicting necrosis or muscle abscess, it is more accurate than plasma creatine kinase, lactate dehydrogenase or myosinuria. MRI is sensitive to necrotizing fasciitis with 100% sensitivity and specificity of 86%. 94%, but its scan time is long, not suitable for critically ill patients.
MRI signs:
1 The subcutaneous tissue is thickened, the T1 weighted image is low signal, and the T2 weighted image is high signal, which can be strengthened;
2 shallow, deep fascia thickening, effusion, T2 weighted image showing high signal, most of them are homogenous boundary clear dome-shaped high signal area, such as deep fascia T2 weighted image with massive signal increase, you can diagnose Necrotizing fasciitis; 3 sputum enhanced scan, necrosis or abscess showed T1 weighted image with low signal, T2 weighted image with high signal, no enhancement or central part without enhancement, surrounded by intensive ring, inflammation tissue showed T1, The weighted image is low signal, the T2 weighted image is high signal, the T1 weighted image is enhanced scanning, and the uniformity is strengthened. The 4 injection contrast agent is quickly strengthened in the adjacent T2 weighted image high signal region, and the system is close to the capillary network damage, resulting in contrast. The early extravasation of the agent is caused by the invasiveness of the infection, while the typical annular enhancement shows the abscess formation, suggesting that the infection is less invasive; the 5T2-weighted image shows a slight diffuse increase in the muscle signal, and the T1-weighted image is enhanced. Scanning showed discontinuous intensification of muscles, but the degree of muscle signal enhancement was lighter than that of fascia, caused by edema, muscle abscess (in the form of annular muscle effusion), and the wall could be strengthened.
Diagnosis
Diagnosis and differentiation of abdominal wall necrotizing fasciitis
Diagnostic criteria
Early necrotizing fasciitis lacks specific clinical manifestations, so the diagnosis is difficult, the clinical should be vigilant, strengthen observation, comprehensive analysis.
1. History:
According to the predisposing factors of this disease, focus on the recent history of trauma and history.
(1) History of trauma: It is mainly to know whether there is a history of abdominal surgery in the near future, whether there are any trauma, stab wounds or insect bites in the abdominal wall, groin area or adjacent areas.
(2) History of illness: pay attention to whether you have diabetes (recessive), atherosclerosis, obesity or bloating, etc.; whether you have recently received radiotherapy, chemotherapy, glucocorticoids or immunosuppressive drugs.
2. Clinical features
(1) Partial: Incision (incision) pain is intensified, and the adjacent area is red, swollen and hot, and progresses rapidly. There is brown exudate or malodorous pus out; the surrounding skin appears purple or necrotic, and the affected area can touch the hair.
(2) Whole body: accompanied by chills, high fever, irritability, ambiguity or apathy, blood pressure drop, pulse weakness and other poisoning performance.
(3) drug effect: combined with the application of a sufficient amount of antibiotics, the symptoms are not improved, should be highly suspected of the disease may be.
3. Blood: The white blood cell count is significantly increased, the neutrophils are elevated and poisoning particles appear.
4. Bacterial culture: For cases suspected of necrotizing fasciitis of the abdominal wall, take the blister exudate or the smear of the skin lesion area for gram staining and bacterial culture, if there is aerobic and anaerobic culture. The diagnosis is clear. If the anaerobic culture is negative, factors such as systemic antibiotics or specimens should be excluded.
5. Imaging examination: showing skin, subcutaneous tissue, fascial edema thickening; soft tissue accumulation, local effusion and empyema, and distributed along the fascia surface, or located under the skin fat, between muscles or along the muscle; contrast agent Characteristics of osmolarity and muscle involvement.
6. Tissue biopsy: Rapid frozen sections showed inflammatory response and arteriovenous thrombosis.
Differential diagnosis
1. Acute cellulitis: acute, diffuse, suppurative infection of subcutaneous, subfascial, intermuscular or deep loose connective tissue. Its clinical features are:
(1) The pathogenic bacteria are mainly hemolytic streptococcus, followed by Staphylococcus aureus and anaerobic bacteria.
(2) The image shows thickening of the subcutaneous tissue, increased density of adipose tissue, irregular reinforcement with cord-like, with or without subcutaneous and superficial fascial effusion, and the deep structure is normal.
(3) necrotizing fasciitis MRIT2: weighted images show that the deep fascia is mostly homogeneous and clear dome-shaped high signal area, while uncomplicated infectious cellulitis is more T2-weighted than necrotizing fasciitis The dome-shaped area of the signal is smaller and thinner, and the boundary is unclear.
(4) Most cases of acute cellulitis can be cured by using antibiotics alone. Antibiotics for necrotizing fasciitis are not effective, but require more surgical treatment. When the operation is seen, the pale fascia of the fascia is old cotton-like, and the toughness is poor. However, the muscles are not necrotic or affected, and the subcutaneous tissue is extensively damaged or pitted-like necrosis occurs, and the skin edge is sneaked.
Due to the pathogenic bacteria of acute cellulitis, the pathological and clinical features are similar, especially the acute cellulitis caused by anaerobic bacteria (anaerobic streptococcus, enterococci, Bacteroides, non-C. difficile, etc.) At the cellulite, fascia and skin can also be necrotic, and it has the characteristics of rapid spread, not easy to be limited, systemic symptoms are severe, pus is stinky, and the body is also pronounced, which is very similar to the clinical manifestations of necrotizing fasciitis. In most cases, clinically relying on physical examination, imaging examination is difficult to identify, the purpose of diagnosis is to determine the treatment plan, although by observing the effect of antibiotic treatment may be able to get a part of the identification basis, but the significance of its identification and For the determination of the value of the treatment plan will be greatly reduced, because necrotizing fasciitis must be treated with early surgery, therefore, for suspected necrotizing fasciitis is difficult to rule out the diagnosis of acute cellulitis, early surgical treatment, and through surgery Tissue biopsy is performed by rapid frozen section inspection to avoid delays in surgery and adverse consequences.
2. Gas gangrene: an acute infection caused by Clostridium, mainly in patients with extensive muscle damage, less incision in the abdominal wall, manifested as skin edema around the wound, nervous, pale, rapidly changing It is purple-black and has blister of different sizes, with extensive muscle necrosis; local and systemic symptoms are more serious than necrotizing fasciitis, and the disease progresses more rapidly; the smears of wound secretions are examined by Gram staining and found a large number of leathers. Blue staining positive for crude bacilli, white blood cell count decreased, and X-ray examination showed gas between wound muscle groups.
3. Myositis and non-gangrene muscle necrosis: caused by soft tissue infections between muscles, characterized by: significant muscle involvement, pain, hyperesthesia, signs of systemic poisoning; presence of creatinine phosphokinase in the blood, presence of muscle cells in hematuria Protein, CT showed that muscles involved in myositis were thickened with or without heterogeneous enhancement. Muscle necrosis showed low-density areas or muscle rupture in the muscle strengthening part. MRI T2-weighted images showed suppurative myositis lesions. In the high-signal area of the spindle-shaped or rounded border, the musculoskeletal involvement of the necrotizing fasciitis is secondary, caused by the spread of the primary fascia infection to adjacent muscles, and the imaging changes after the fascia and soft tissue changes.
4. Other diseases: such as peritonitis.
