Etiology and pathogenesis
The development of inflammation in the middle ear is a combination of anatomical predispositions and infection. In children under 2 years of age, the auditory (Eustachian) tube is positioned low, and is short, wide, and straight. This creates ideal conditions for bacteria to enter from the nasopharynx.
The primary bacterial agents are Streptococcus pneumoniae and Haemophilus influenzae (the latter often causes a recurrent course). In infants during the first months of life, Escherichia coli may be the cause, and in approximately 10% of cases, viruses are the sole causative agents.
Cascade of pathological changes:
- Against the background of a runny nose (rhinitis) during an acute respiratory viral infection (ARVI), nasopharyngeal edema or adenoid hypertrophy occurs.
- Dysfunction (obstruction) of the auditory tube develops.
- Negative pressure forms within the isolated tympanic cavity, causing transudation of fluid from the vessels.
- Bacteria actively multiply in the fluid, forming a purulent exudate.
- Under the mechanical pressure of pus and the enzymatic action of bacteria, the tympanic membrane perforates, and pus discharges outward.
Clinical presentation and forms
The disease typically starts as a complication of ARVI accompanied by marked rhinitis. The child becomes extremely restless (especially due to nasal congestion), and body temperature rises.
The key symptom is otalgia (earache). Pain typically worsens upon swallowing, which frequently causes children to refuse food.
Clinically and morphologically, two forms of the disease are distinguished, which can transition into one another:
- Catarrhal form: the initial stage of inflammation without pus.
- Purulent form: characterized by the accumulation of purulent exudate and ending in rupture of the tympanic membrane followed by otorrhea.
Otoscopic and laboratory diagnostics
The diagnosis is established based on patient complaints and visual assessment of the tympanic membrane.
In catarrhal inflammation, the membrane becomes dull, and its landmarks are smoothed out. Vascular injection is visible initially, which rapidly progresses to total hyperemia. The light reflex disappears (note: in newborns, it normally appears only by the 1st month of life).
For the purulent stage, the pathognomonic and most prominent sign is bulging of the tympanic membrane. A complete blood count (CBC) reveals classic markers of acute bacterial inflammation: elevated ESR and neutrophilic leukocytosis.
Complications and consequences
Despite its apparent commonality, middle ear inflammation can lead to severe consequences. Complications are divided into three groups:
- Local: transition to a chronic form, involvement of the mastoid process (mastoiditis) or mastoid antrum (antritis), labyrinthitis, and peripheral facial nerve palsy.
- Intracranial (less than 1%): bacterial meningitis, brain or epidural abscess, sigmoid sinus thrombosis.
- Long-term: frequent recurrences cause adhesion formation in the tympanic cavity. This leads to progressive hearing loss, which critically impairs speech development in a child. Otitis media suffered in childhood accounts for up to 25% of all adult sensorineural hearing loss cases.
Principles of treatment
Therapy is aimed at sanitizing the nasopharynx, eliminating the pathogen, and relieving pain.
- Restoration of auditory tube function: thorough toilet of the nasal cavity, irrigation therapy, vasoconstrictor drops (decongestants). Antihistamines are added in cases of concomitant atopy.
- Antibacterial therapy:
- Local therapy: ear drops (ciprofloxacin), nasal sprays, inhaled forms of antibiotics.
- Systemic therapy: aminopenicillins, macrolides, or cephalosporins are prescribed only for purulent processes, the threat of complications, or if local remedies fail.
- Symptomatic treatment: ibuprofen or paracetamol to relieve fever and pain. Drops containing anesthetics (lidocaine) are used locally.
- Surgical treatment: under strict indications, an ENT specialist performs incision of the tympanic membrane (paracentesis, tympanocentesis) to ensure the outflow of pus.
Pathogenesis cascade «OTIS»: Organ/nasopharyngeal edema (Edema) → Tube closed (negative pressure) → Infection in transudate → Suppuration and perforation.
Class and exam questions
Why does ear pain worsen when swallowing?
Swallowing movements contract the muscles that open the pharyngeal opening of the auditory tube. This causes movement of the inflamed tissues and a sharp change in pressure within the tympanic cavity, which triggers the pain syndrome.
Is it mandatory to prescribe systemic antibiotics for any earache?
No, systemic drugs are prescribed strictly according to indications. These include ineffectiveness of local therapy, progression from the catarrhal to the purulent stage, or a high risk of developing complications.
What does the prevention of the disease entail?
It includes the prevention of ARVI (vaccination, hardening, breastfeeding) and the prevention of tubal infection through timely and adequate treatment of rhinitis.
What else to study on this topic
- Methodology and indications for paracentesis (tympanocentesis)
- Specific features of otitis media caused by atypical intracellular pathogens
- The role of adenoid hypertrophy in the recurrent course of the disease
- Differential diagnostics of catarrhal and purulent forms via otoscopy
- Pathogenesis of sensorineural hearing loss as a long-term consequence
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