Epidural abscess of the spine

　　Most epidural abscesses are secondary. The primary infection focus can be boils, carbuncles, or cellulitis at nearby or distant sites, or infections of various organs such as lung abscess, ovarian abscess, peritonitis, etc., or complications of systemic sepsis. The site of onset is closely related to anatomical characteristics. The dura mater is formed by the bony periosteum of the vertebral bones and the two layers of the dura mater. The epidural space is filled with richly fatty loose connective tissue and venous plexuses. The two layers are closely connected in front of the dura mater and come into contact with the posterior longitudinal ligament of the spine, actually without any space. The epidural tissue is mainly located on the dorsal and lateral sides, and the space gradually increases from the neck downward. The space between T4 and T8 is 0.5 to 0.7 cm, and the space between T9 and L2 and below gradually becomes narrower, so the most common site of lesions is the dorsal side of the spinal cord and the thoracolumbar segment, rarely occurring in the upper thoracic and cervical segments. The main pathways of infection for this disease are:

　　1. Hematogenous infection, where the pathogenic bacteria reach the epidural space through the blood from nearby or distant infection foci.

　　2. Direct spread of infection from the surrounding purulent infection foci of the spine, such as purulent spondylitic osteomyelitis, infection of the sacrococcygeal fistula, etc.

　　3. Direct entry, such as open wounds connected with the spine, infection caused by lumbar puncture or epidural blockage.

　　Common pathogenic bacteria include Staphylococcus aureus, Staphylococcus albus, Streptococcus, Pseudomonas, Salmonella typhi, and occasionally fungi such as actinomycetes and blastomycetes. After the pathogenic bacteria invade the epidural space, they form蜂窝织炎 within the spaces rich in fat and venous plexuses, with tissue congestion, exudation, and a large number of leukocytes infiltrating. This further develops into necrosis of the fatty tissue, congestion and edema of the dura mater, and the pus gradually increases and spreads, forming an abscess. The abscess is mainly located on the dorsal and lateral sides of the dura mater sac, rarely involving the ventral side. The range of spread from top to bottom can reach several segments, and in some cases, it can involve the entire vertebral canal, even spreading to the intracranial cavity. Most abscesses are solitary, and in a few cases, there are multiple scattered small abscess cavities communicating with a main abscess cavity. The form and dynamic changes of the abscess are related to factors such as the pathogenic bacteria, the immune response of the body and local tissues, the anatomical characteristics of the epidural space, and the structure of the vascular and lymphatic systems. Respiratory movements and vascular pulsations can increase the negative pressure difference within the vertebral canal, which has an

　　After the formation of epidural abscess of the hard spinal meninges, it can also cause inflammatory thrombosis of blood vessels, leading to impaired blood supply to the spinal cord and possibly causing paralysis. Paralysis refers to the reduction or loss of voluntary movement. Clinically, paralysis is divided into functional paralysis and organic paralysis.

　　Most cases of epidural abscess of the hard spinal meninges present with an acute course. In a few cases, the main pathological feature is inflammatory granulation tissue, which may present as a subacute or chronic course. The clinical manifestations of epidural abscess of the hard spinal meninges include the following specific aspects:

　　1. Acute epidural abscess of the hard spinal meninges

　　Acute epidural abscess of the hard spinal meninges is characterized by high fever, chills, malaise, lack of energy, headache, elevated white blood cell count and neutrophil count, systemic signs of infection, and in some cases, meningeal irritation. In the early stage, patients may experience marked pain in the back over the site of infection, with tenderness and percussion pain over the spinous processes at the site or nearby. Local skin may have mild edema, and there may be tenderness and percussion pain in the paraspinal tissues due to inflammation of the nerve roots. The pain may radiate to the chest or abdomen depending on the site of the lesion. A lumbar-sacral abscess may cause leg pain and early urinary retention. As the condition progresses, there may be gradual weakness and numbness of the lower limbs, and signs of pyramidal tract dysfunction. After the appearance of spinal cord symptoms, transverse myelitis often develops rapidly within one to several days, manifested as flaccid paralysis of the limbs, sensory disturbances, and marked urinary sphincter dysfunction.

　　2. Subacute epidural abscess of the hard spinal meninges

　　The clinical course of subacute epidural abscess is similar to that of acute, but with more pronounced and longer-lasting back pain. Nerve root pain appears 1-2 weeks after onset, which worsens with activity or increased abdominal pressure, such as defecation, coughing, or sneezing, and further develops into symptoms of spinal cord dysfunction.

　　3. Chronic epidural abscess of the hard spinal meninges

　　The course of chronic epidural abscess of the hard spinal meninges is long, ranging from 1.5 to 18 months, with a slow onset. Sometimes, there are symptoms of low fever, and the symptoms fluctuate, leading to symptoms of spinal cord compression, manifested as spastic paraplegia, sensory and urinary sphincter dysfunction, which is often difficult to differentiate from intraspinal tumors.

　　The prevention of epidural abscess mainly involves controlling the primary infection foci at various sites to prevent their development into epidural abscess. During the treatment process, patients should follow the doctor's guidance and exercise regularly. They should maintain a regular lifestyle, keep a pleasant mood, correctly face the disease, and build confidence in overcoming the disease. Otherwise, it is easy to worsen the condition. At the same time, the diet should be light, and spicy and heat-promoting foods should be avoided.

　　Lumbar puncture in patients with epidural abscess carries the risk of bringing infection into the subarachnoid space, so this examination should not be performed at will. If it is necessary to perform it, the needle should be inserted carefully, and the needle should be aspirated while inserted to see if there is pus. When pus is aspirated, the needle should not be inserted further to avoid the needle entering the subarachnoid space. The clinical examination methods for epidural abscess mainly include the following aspects:

　　1, X-ray film

　　33% to 65% of patients show abnormal changes in the vertebra and its appendages on X-ray films, of which 70% are seen in chronic epidural abscess, and 10% in acute epidural abscess cases. This is because infection of the vertebra and its appendages leads to bone destruction and hyperplasia, while vertebral collapse and paravertebral infection require time.

　　2, Radionuclide scanning

　　The positive rate of radionuclide scanning is 67% to 100%.

　　3, Myelogram with spinal iodine oil

　　Myelogram with spinal iodine oil was once the main method for diagnosing epidural abscess, which could clearly show the segment and range of the lesion, which was beneficial for surgery.

　　4, CT and CT myelogram

　　Enhanced CT examination has a positive rate of up to 100%, and CT myelogram can also reach 90%, but it is still difficult to clearly show the range of the lesion.

　　5, MRI

　　Magnetic resonance imaging (MRI) is currently the most reliable and accurate method for diagnosing epidural abscess, which can show the range of spondylodiscitis (T1 low signal, T2 high signal), vertebral interspace and soft tissue infection (T2 signal increase), spinal cord compression and displacement, and abscess (T1 low or isosignal), and if MRI and CT still cannot make a clear diagnosis, myelogram with spinal iodine oil should be used.

　　Patients with epidural abscess should pay attention to eating more light and nutritious food, and to dietary balance. They should eat more fresh vegetables and fruits and foods that can enhance immunity to improve the body's ability to resist diseases, and at the same time, they should avoid spicy and stimulating foods.

　　Parietal epidural abscess should be treated as an emergency neurosurgical condition, with urgent surgical decompression and drainage before irreversible spinal cord injury occurs. Clinical practice shows that surgery within 2 hours of paralysis results in satisfactory outcomes, while after >36 hours the outcomes are poor, and surgery after complete paralysis for 48 hours may only save the patient's life. Therefore, shortening the time from paralysis to surgery is the key to improving the efficacy of this disease. The excision of the vertebral lamina should be sufficient and thorough, clearing the pus and granulation tissue, especially the inflammatory granulation tissue which often surrounds and compresses the spinal cord in the epidural space, and should be cleared as cleanly as possible to restore the normal pulsation of the dura mater, achieving complete decompression and preventing the spread of infection. The pus should be subjected to bacterial smears and anaerobic, aerobic, tuberculosis, and fungal cultures. There are three methods for the management of surgical incisions:

　　1. Do not suture the incision and fill it with gauze.

　　2. Partially suture the incision and leave a drain.

　　3. All incisions should be sutured to achieve primary healing. In addition to the skin sutures using silk thread, subcutaneous sutures should be made with catgut. For clean surgical incisions that have not been severely contaminated, the incision can be sutured in one stage after being repeatedly flushed with gentamicin saline to shorten the course of the disease; if there is pus in the muscle layer of the incision or if the wound is contaminated with pus during surgery, the incision should not be sutured or only partially sutured. Some people advocate placing an epidural catheter, performing flushing and injecting antibiotics after surgery, and retaining the catheter for 5 to 7 days. In all these situations, powerful broad-spectrum antibiotics should be administered before and after surgery. The antibiotics should be changed according to the results of bacterial culture and drug sensitivity after the results are out. If the culture results are negative, antibiotics should be selected based on the Gram stain results of the bacterial smear. If there is no accompanying vertebral bone marrow infection, intravenous antibiotics should be given for 3 to 4 weeks after surgery; otherwise, for 6 to 8 weeks. After stopping intravenous administration, oral antibiotics should be continued for several weeks. It is appropriate to use neurotrophic drugs to promote the recovery of nerve function. At the same time, attention should be paid to correcting water and electrolyte imbalances, strengthening nutrition, preventing bedsores and complications.

　　Recently, some people have proposed the use of hyperbaric oxygen therapy, which has achieved satisfactory results. The theoretical basis is that it creates an unfavorable environment for anaerobic bacterial proliferation, which is beneficial to the improvement of poisoning symptoms. The therapeutic effect of this disease is directly related to the severity of the course, the overall condition of the patient, the virulence of the bacteria, the degree of spinal cord compression, especially the timing of surgery. Generally, those who undergo surgery before complete paralysis can recover completely. If complete paralysis occurs for 3 to 5 days or more, it is difficult to recover the function of the spinal cord after surgery. The main causes of death are uncontrollable infection, sepsis, or death from complications, especially urinary tract infection and bedsores.