AssessmentsRetropharyngeal and peritonsillar abscesses
Retropharyngeal and peritonsillar abscesses
Peritonsillar infections are generally preceded by tonsillitis or pharyngitis, and progresses from cellulitis to .
Content Reviewers:Rishi Desai, MD, MPH
A retropharyngeal abscess develops behind the pharynx - in the tissue that lies just behind the back of the throat.
A peritonsillar abscess develops around the tonsils, particularly the palatine tonsils which are at the back of the throat.
Let’s start by better defining the locations of these spaces.
The retropharyngeal space is the region between the pharynx and vertebrae and is bound posteriorly, closer to the vertebrae, by the alar fascia and anteriorly, closer to the pharynx, by the buccopharyngeal fascia.
These fascial layers are thin fibrous layers that coat muscles, tendons, and bones muscle, and between them in the retropharyngeal space are lymph nodes.
These lymph nodes are like surveillance stations that bring in lymphatic fluid from the throat and other nearby tissue.
If there are pathogens in that lymphatic tissue, immune cells in the lymph node can respond and try to destroy the invading pathogens.
Next, is the peritonsillar region which refers to the palatine tonsils.
The palatine tonsils are on either side of the oropharynx and are attached to the soft palate at the back of the oral cavity. They’re basically dense collections of lymphatic tissue wrapped within a fibrous capsule - like tiny lymph burritos, that help defend against pathogens in the food and air.
When pathogens like bacteria invade tissues in the mouth they’re brought to nearby lymph nodes.
Often times, the first immune cells at the scene are neutrophils, which release chemicals and enzymes that kill bacteria and dissolve pieces of of dead cells, creating a pool of dead material.
This is a specific type of acute inflammatory response called suppurative inflammation, which simply means that pus is created in the process.
From a macroscopic view, this is sometimes referred to a liquefactive necrosis, because the area of dead tissue turns to liquid.
As those immune cells get to a point where they can’t withstand the environment, they die too, and become part of that pool.
Initially the debris might be intermixed with healthy tissue, but over time it can coalesce into a single area - a process that is often sped up when more immune cells get involved.
Around this pool of pus, a wall of fibrinogen - which is the same protein that holds together blood clots - starts to harden into a barrier.