Complications of abscess

Complications of odontogenic abscesses

Abscesses of the maxillofacial region often occur as an outcome of exacerbated chronic apical periodontitis, suppurated radicular cysts, or inflammation of the tooth socket. The infection spreads primarily by contact and is capable of causing a number of critical conditions:

• Soft tissue lesions: formation of secondary abscesses and phlegmon in the fascial spaces of the neck and face. Of particular note is Ludwig's angina—a putrid-necrotic phlegmon affecting the loose connective tissue of the parapharyngeal and pterygomandibular spaces and the floor of the mouth (pathogen: group A streptococci).
• Intracranial complications: the infection penetrates the cranial cavity, causing septic thrombosis of the cavernous sinus, purulent meningitis, and brain abscesses.
• Pathologies of the neck and thoracic cavity: development of purulent mediastinitis and laryngeal edema.
• Bone tissue involvement: severe osteomyelitis of the jaw bones and systemic odontogenic sepsis.

Complications and outcomes of liver abscesses

Purulent lesions of the liver frequently develop as a result of ascending cholangitis (due to biliary tract obstruction) or microbial embolism via the portal vein (e.g., in abscess-forming appendicitis).

If purulent inflammation progresses, significant periportal necrosis occurs. The pathogenesis of the complications is as follows:

1. Fibrosis: connective tissue septa form, linking portal areas with the centers of hepatic lobules.
2. Abnormal regeneration: focal proliferation of hepatocytes grossly disrupts the normal lobular structure of the organ.
3. Outcome: biliary micronodular monolobular cirrhosis is formed.

The main causes of death in such patients are hepatic failure and secondary infectious processes (abscess formation, sepsis, bilateral bronchopneumonia).

Septicopyemia and purulent metastases

Generalisation of infection from a primary abscess or other purulent focus (port of entry) leads to the development of septicopyemia. In this case, the infection spreads via metastasis of pus, accompanied by purulent lymphangitis and thrombophlebitis. Most often, the process is caused by gram-positive flora (staphylococci, streptococci), as well as Pseudomonas aeruginosa or fungi of the genus Candida.

Bacteria settle in organs, forming embolic abscesses (purulent metastases):

• Embolic purulent nephritis occurs in the kidneys.
• Multiple secondary abscesses form in the liver.
• Purulent osteomyelitis develops in the bone marrow.
• Suppuration of infarctions is observed in the lungs.

Key pathomorphological feature: unlike foci of other etiologies, a capsule does not form for a long time around septic abscesses.

In addition, the heart is affected with the development of acute septic polypous-ulcerative endocarditis (with purulent deposits on the valves). The immune response manifests as splenomegaly ("septic spleen" weighing up to 1500 g with a tense capsule) and myeloid metaplasia of lymph nodes. Fatty degeneration increases in parenchymatous organs due to hypoxia and intoxication.

Class and exam questions

What else to study on this topic

• Pathogenesis of intrahepatic cholestasis
• Microscopic picture of a cystogranuloma
• Morphological changes of the spleen in sepsis
• Differences between septicopyemia and septicemia

Other topics in the "Additional Topics" section

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