Non-hematogenous osteomyelitis: bone involvement
One of the frequent complications of purulent inflammation is non-hematogenous osteomyelitis. It often develops by contact (per continuitatem), when pus directly spreads to the bone tissue from the affected soft tissue area.
Features and clinical forms:
- The risk of contact involvement is highest for bones that closely adjoin the skin and are not covered by muscles.
- Tibial osteomyelitis frequently becomes a complication of the phlegmonous form of erysipelas.
- Bone felon develops as a direct complication of advanced subcutaneous felon.
- Osteomyelitis of the cranial vault develops in infected head wounds when progressive purulent lysis of the epicranial aponeurosis occurs.
- Odontogenic and otogenic osteomyelitis of the jaw or temporal bone occurs when infection spreads from periodontal or ear tissues.
In addition, bone tissue can become infected via a traumatic route in open fractures and gunshot wounds.
Descending mediastinitis: threat to the mediastinum
Phlegmons of the upper half of the torso can be complicated by secondary mediastinitis — purulent inflammation of the mediastinal tissue.
The most frequent scenario is a descending infection from the neck (contact pathway). Infection easily descends downwards in retropharyngeal abscesses, neck phlegmons, and Ludwig's angina (severe putrid-necrotic phlegmon of the floor of the mouth).
In addition to the descending pathway, mediastinitis is provoked by:
- Esophageal injuries: trauma from foreign bodies, burns, ulcerations, or dehiscence of the gastroesophageal anastomosis.
- Extension from bone structures: in osteomyelitis of the sternum, spine, perichondritis, and inflammation of the sternoclavicular joint.
- Lymphogenous and hematogenous pathways: development of metastatic foci in septicopyemia (from the pelvis, limbs).
- Breakthrough from the lungs: spread of pus to the lung root in gangrene or abscess of the lung.
- Trauma: suppuration of mediastinal hematomas after blunt chest impacts.
Phlegmons of the pararectal tissue (Paraproctitis)
Phlegmonous involvement of the perienteric (pararectal) tissue is characterized by marked edema and massive purulent infiltration of loose tissue. It can develop as an independent process or act as a complication of disintegrating pelvic tumors and gunshot wounds.
The causative agents are predominantly mixed microflora: E. coli, staphylococci, and anaerobes. Infection penetrates tissues through:
- Anal fissures and skin scratches.
- Inflamed hemorrhoids and crypts.
- Damage to the rectal mucosa.
- Suppurated perineal hematomas.
Putrid-necrotic paraproctitis represents a special clinical danger. In this condition, tissues disintegrate rapidly while failing to form clearly demarcated abscesses. The process spreads rapidly directly through the pararectal space, as well as via the lymphogenous route to other compartments of the pelvic tissue.
Local purulent complications and neurological symptoms
If the phlegmonous process is localized in the head and neck region (particularly involving major glands), specific complications arise. Inflammation is accompanied by marked edema of the lateral pharyngeal wall and soft palate.
Key manifestations:
- Trismus: sharp restriction of mouth opening due to edema and inflammation of the masticatory musculature.
- Neurological deficit: facial nerve paresis may develop.
- Blood changes: increasing leukocytosis with a left shift in the formula (increase in the number of neutrophils).
In the absence of treatment, purulent melting of the gland capsule occurs. Purulent masses escape into the subcutaneous tissue (forming a secondary phlegmon) and then rupture outward through the skin. This forms fistulas from which pus abundantly discharges along with sequestra — necrotic pieces of parenchyma and capsule.
M-O-P-S: phlegmon complications — Mediastinitis (from neck tissue), Osteomyelitis (contact extension), Paraproctitis (pelvic purulent necrosis), Fistulas (upon tissue melting and skin rupture).
Class and exam questions
Why does contact osteomyelitis occur in phlegmon?
Pus spreads to the bone (per continuitatem) from surrounding affected tissues. This particularly often occurs if the bone closely adjoins the skin and is not protected by muscle mass (for example, the tibia in erysipelas).
Which phlegmon most often leads to secondary mediastinitis?
Descending infection into the mediastinal tissue most commonly becomes a complication of neck phlegmons and Ludwig's angina (severe putrid-necrotic phlegmon of the floor of the mouth).
What is the specificity of putrid-necrotic paraproctitis?
Unlike classic abscesses, this form of inflammation of the perirectal tissue causes extensive tissue disintegration without the formation of a clearly demarcated capsule, which extremely complicates the localization of the process.
How does the blood picture change during progressive purulent tissue melting?
Laboratory blood tests register increasing leukocytosis with a left shift in the leukocyte formula (young neutrophilic forms predominate), indicating a severe systemic inflammatory response.
What else to study on this topic
- Topographic anatomy and fascia of the neck in the context of pus spread pathways
- Classification of localized pararectal abscesses (paraproctitis)
- Pathogenesis and diagnosis of Ludwig's angina
- Differences between hematogenous and non-hematogenous osteomyelitis
- Surgical tactics for the treatment of fistulas and purulent pockets
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Other topics from the section "CHAPTER 11. SURGICAL INFECTION (PURULENT-INFLAMMATORY DISEASES)"
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