Acute hematogenous osteomyelitis, also known as acute osteomyelitis, is an inflammatory disease caused by hematogenous invasion of connective tissue within the bone marrow by septic bacteria in most cases. Rarely, the infection spreads from adjacent soft tissues or is secondary to an open fracture. If left untreated, the bone structure can be destroyed and disability can occur, and the infection can even spread and become life-threatening. In some cases, the disease may become chronic and have a long course. Since it is most often seen in children, it may affect their nutrition and growth.
Causes
(A) Causes
The causative organism is often Staphylococcus aureus hemolyticus, but in recent years there are also more virulent white staphylococcus hemolyticus, occasionally salmonella, pneumococcus or other septic bacteria, most of which are resistant to penicillin and streptomycin. Common primary lesions include pustules, gingival abscesses, and upper respiratory tract infections.
(B) Pathogenesis
For the development of osteomyelitis, the magnitude of bacterial virulence is an extrinsic factor and the systemic condition or local skeletal resistance is an intrinsic factor. The long bone epiphysis has many small terminal arteries with rich circulation and slow blood flow, making it easy for bacteria to multiply. Some bacteria, such as staphylococci, often accumulate in clusters and form emboli in the small arteries, blocking the end of the vessels and leading to local tissue necrosis, which facilitates bacterial growth and the development of infection. Clinically, local tissue injury due to sprains and contusions is often an indirect cause of osteomyelitis.
Bacterial toxins can impair the capillary circulation in the epiphysis 48 h after the onset of infection, generating pus in the epiphysis, which enters the subperiosteum via the Harvard system and Volkmann’s canal, causing periosteal stripping and resulting in the coexistence of bone destruction, necrosis, and the resulting induced repair response (osteomalacia). In the early stage, destruction and necrosis are predominant, with the inner layer of cortical bone receiving blood supply from the epiphysis; after the blood supply is impaired, the bone becomes necrotic and granulation tissue separates it from the surviving bone, forming dead bone fragments. The later stage is dominated by bone proliferation.
After the formation of intraosseous foci of infection, there are mostly severe signs of toxemia because of the surrounding bone and poor drainage. Later, as the abscess expands, the infection spreads in the direction of less local resistance to the surrounding area (Figure 1).
1. Pathways of abscess spread
(1) Abscess spreads to the long bone end. Because the epiphyseal plate has a strong ability to resist infection, the pus does not easily penetrate the epiphyseal plate into the joint cavity, and mostly spreads to the bone marrow cavity, resulting in the involvement of the bone marrow cavity. When the pressure of pus in the marrow cavity increases, it may spread to the subperiosteal layer along the central canal and form a subperiosteal abscess.
(2) Pus breaks through the metaphysis and penetrates into the subperiosteum to form a subperiosteal abscess; when the pressure is further increased, it breaks through the periosteum and flows into the soft tissue. It may also invade the bone marrow cavity along the Harvard canal.
(3) Penetrating into the joint and causing septic arthritis. In children, the epiphyseal plate is a natural barrier against infection and abscesses do not easily enter the joint cavity, but in adults, the epiphyseal plate has no resistance and is more likely to be complicated by arthritis. If the epiphysis is located in the joint capsule (e.g., the femoral neck is located in the hip capsule), the abscess may also penetrate the epiphyseal cortex and enter the joint, resulting in septic arthritis (Figure 2).
Bone nutrition is supplied by the trophoblastic vessels near the bone marrow cavity and by the subperiosteal network of small vessels in the cortical part of the bone close to the periosteum. When the periosteum is lifted by the abscess, the bone cortex in that part loses blood supply from the periosteum, which seriously affects the circulation of bone and causes osteonecrosis. After the pus enters the bone marrow and the central canal, the trophoblastic vessels passing in the canal lumen form thrombi and pus emboli due to inflammation, and the blood supply in the bone is blocked, resulting in osteonecrosis. The distribution and size of the necrotic area depend on the extent of ischemia, and in severe cases, necrosis of the entire bone stem can occur. As the periosteum is peeled off, the osteoblasts in the deeper layer of the periosteum are inflammation stimulated to produce a large amount of new bone, which is wrapped outside the dead bone and forms a shell, which can play a supporting role instead of the diseased bone, from which the pus flows out. Small pieces of dead bone can be absorbed or discharged through the sinus tract, while large pieces of dead bone cannot be discharged or absorbed, the dead cavity cannot be closed, the wound does not heal for a long time and becomes chronic osteomyelitis.
Symptoms
The most common sites of osteomyelitis are the lower femur and upper tibia, followed by the upper femur, humerus and distal radius. However, it can occur in all other bones. Signs and symptoms vary with the severity of the infection, the location, the extent of inflammation, the duration of the disease, the age of the child, and the size of the resistance, and can be broadly classified into three types.
1. septicemia type This type accounts for about 80%. Systemic symptoms are the manifestation of acute sepsis, there may be high fever, coma, delirium and other symptoms. Even toxic shock may occur. Because of blood dissemination, it is often accompanied by serious infections in other sites, such as purulent pericarditis, pneumothorax, brain abscess, etc. Severe cases may be complicated by migratory lesions in the heart, lungs, liver, kidneys and other organs, leading to functional impairment of multiple organs. Local symptoms include persistent severe pain, fear of movement, pressure pain, axial percussion pain, and circumferential swelling of the affected limb. In a few cases, systemic symptoms are the main manifestation, while local signs of the affected bone are late, so early detection of bone lesions is required.
2. Complicated arthritis type This type is mostly in newborns and small infants. The systemic symptoms are often mild and the body temperature is not high, but there is irritability, refusal to eat and weight gain. The lesions are mostly found on the upper femur, upper tibia or upper humerus. Because the epiphysis is included in the joint capsule or the destruction of the epiphysis affects the basis of epiphyseal plate attachment, inflammation spreads easily into the joint and some epiphyseal slippage or destruction occurs, which affects future development.
3. Limited destruction or bone abscess type This type is mostly seen in school-age children, with mild clinical symptoms, localized swelling and pain, and limited movement of nearby joints. Individual children may develop sympathetic joint effusion.
Primary infectious lesions may be seen, and common primary lesions include pustules and gingival abscesses.
Two issues should be addressed in the diagnosis, namely disease diagnosis and etiology diagnosis. The diagnosis should be made early. Because of the late appearance of X-ray manifestations, X-ray findings cannot be used as a basis for diagnosis, and MRI examination can be pursued for those who are in a position to do so. The diagnosis of acute osteomyelitis is a comprehensive diagnosis, and the possibility of acute osteomyelitis should be considered in all cases with the following manifestations: 1.
1. Acute hyperthermia and toxemia.
2. Severe pain in the long epiphysis and reluctance to move the limb.
3. There is a distinct area of pressure pain at the site.
4. The white blood cell count and neutrophil ratio are elevated. Local fractionated puncture has diagnostic value.
Etiological diagnosis lies in obtaining the causative organism. Blood culture with stratified puncture fluid culture is of great value. Repeated blood cultures are required to increase the positive rate.
A definitive diagnosis and appropriate treatment should be made early after the onset of the disease to avoid the development of chronic osteomyelitis. It has been reported in the literature that diagnosis and treatment within 5 days of onset can reduce the chance of acute hematogenous osteomyelitis progressing to the chronic stage.
Diet and Health
Care
Mostly caused by blood-borne infection, sepsis should be actively prevented and treated; actively prevent and treat various infectious diseases of the skin and mucous membranes; actively prevent and treat upper respiratory tract infections, etc.
Treatment
(I) Treatment
Early treatment is necessary. After taking the specimen and sending it for bacterial culture, give antibiotics immediately and do not wait for the culture result. In recent years, high-dose antibiotics are used intravenously. At present, benzocillin (neopenicillin II, benzocillin sodium), ampicillin (ampicillin) or erythromycin are preferred, and chloramphenicol, cephalosporin or gentamicin are also used. When the causative organism and the sensitive antibiotic are clearly identified, the effective drug is changed immediately. Intravenous administration is given for 2 to 3 weeks and can be changed to oral antibiotics for 2 to 3 weeks after the infection is controlled. The affected limb is immobilized in a functional position with a cast or skin traction to ensure rest, reduce pain and prevent the spread of infection and pathological fracture. Systemic supportive therapy should not be neglected, such as antipyretics, fluid replacement, fresh blood transfusion, high protein diet and multivitamins. In severe cases of systemic toxicity, adrenocorticosteroids may be used as appropriate.
Acute osteomyelitis often requires surgical drainage. Early cases within 24 h of onset may be cured by conservative therapy after adequate and effective treatment with decreased body temperature and pain relief. Delayed or delayed diagnosis, such as severe systemic and local symptoms, requires surgical drainage if there is pus on the puncture. Surgical treatment includes incision and drainage with bone drilling or window decompression. Two silicone tubes may be placed in the incision or medullary cavity, one for irrigation with a drip of antibiotic solution and the other for drainage. Wounds with low pus accumulation can be sutured after flushing with antibiotic solution, and half of them can be healed in one stage.
(B) Prognosis
Acute hematogenous osteomyelitis has a high mortality rate in the absence of antibiotics. In the presence of antibiotics the mortality rate decreases to 2%-3%, but the treatment is still not ideal and the course of treatment is long, often calculated on a monthly basis, which seriously affects health. In adult patients the symptoms are heavy and painful. In infants under 1 year of age, osteomyelitis is not diagnosed early because the systemic symptoms are not obvious, and once detected, the epiphysis has been severely damaged, causing impaired limb development and lifelong disability, which can be cured if diagnosed early and treated with timely and effective antibiotics locally and systemically. cunha points out that timely and effective treatment can result in a 92% cure rate for acute hematogenous osteomyelitis.
Examination
Patients with acute septic osteomyelitis have a significant increase in leukocytes and neutrophils in the early stages of the disease, which may be accompanied by anemia and increased sedimentation. The positive rate of early blood bacterial culture is 50% to 75%, and positive blood culture results are usually obtained 24 h after infection. The diagnosis is confirmed by local bone puncture to extract pus and smear to find bacteria. The bacterial sensitivity test should be done along with the bacterial culture of blood and pus in order to select effective antibiotic treatment.
X-ray examination is often unremarkable within 14 days after the onset of the disease, and the onset of X-ray manifestation can be delayed to about 1 month in cases with antibiotics. it is difficult to show bone abscesses less than 1 cm in diameter on X-ray, so the early X-ray manifestation is laminar periosteal reaction with sparse epiphysis. Scattered worm-like bone destruction in the epiphyseal region with extension to the medullary cavity appears on X-ray only when a small bone abscess merges into a larger abscess, when the dense bone becomes thin and irregular changes in the inner and outer layers appear in sequence. The bone destruction results in the formation of dead bone, which may be large or small. Small dead bone may appear as a shadow of increased density, located in the pus cavity, and completely free from the surrounding bone tissue. Large dead bones may be whole segments of osteonecrosis with increased density and no trabecular structures visible. In a few cases, there is pathological fracture.
CT examination can detect subperiosteal abscesses in advance, but it is still difficult to show small bone abscesses.
3. MRI examination can detect inflammatory abnormal signals in the long bone epiphysis and diaphysis at a much earlier stage, and can also show subperiosteal abscesses. Therefore, MRI examination is significantly better than X-ray and CT examination.
4. Radionuclide bone imaging The vasodilatation and increase of blood vessels at the site of the lesion make the 99mTc concentrated in the epiphysis at an early stage, and the positive result is usually available 48h after the onset of the disease. Radionuclide bone imaging can only show the location of the lesion, but cannot make a qualitative diagnosis, so this test is only of indirect diagnostic value.
Differentiation
Diseases that need to be differentiated are as follows.
1. soft tissue cellulitis or deep abscess Swelling is mostly limited to one side of the limb, without axial percussion pain.
2. Scurvy-induced limb pain, pseudo-paralysis and subperiosteal hematoma History of vitamin C deficiency and specific lesions of scurvy in the x-ray epiphysis, with rapid relief of symptoms after vitamin C administration.
3. infantile osteocortical hyperplasia mainly seen in infants under 6 months of age, with mild systemic symptoms, may have low fever, irritability, local swelling, limbs may be pseudo-paralyzed. x-ray is characterized by a large amount of new bone under the periosteum, such as the onset of long bones, the lesion is limited to the bone cadre, never spread to the epiphysis and epiphysis.
4. Acute leukemia with limited bone destruction is often misdiagnosed as osteomyelitis when accompanied by fever and accelerated blood sedimentation with normal white blood cell counts, with localized swelling and tenderness. However, attention to the medical history, diffuse decalcification and the appearance of new affected lesions on X-ray suggest a systemic disorder, which can be diagnosed by bone marrow aspiration.
Complications
The disease is often associated with serious infections in other areas, such as septic pericarditis, pneumothorax, brain abscess, and migrating foci in the heart, lungs, liver, kidneys, etc., leading to toxic shock and functional impairment of multiple organs.