Parotid abscess

A parotid abscess is an infection of the parotid gland, a major salivary gland localized in the retromandibular fossa, which can arise from ascending infection via Stensen’s duct, or from bacteraemia or viremia.

Bacterial and (more rarely) viral infection of the intra-parotideal and periparotideal lymph nodes, or of the glandular parenchyma, can lead to suppurative changes, which can result in abscess formation. If the process continues pus penetrates the capsule and invades the surrounding tissue, and extends downward into the deep facial planes of the neck, backward into the external auditory canal, or outward into the facial skin.^[1]

It is suppuration of the parotid space deep cervical fascia splits into two layers,superficial and deep,to enclose the parotid gland and its associated structures parotid space lies deep to its superficial layer. Contents of parotid space include parotid gland and its associated parotid lymph nodes, facial nerve,external carotid artery, and retromandibular vein. Facial layer is very thick superficially but very thin on the deep side of the parotid gland where the parotid abscess can burst to form parapharyngeal abscess and hence spread to the mediastinum.^[2]

Aetiology

The predisposing conditions and precipitating factors include: dehydration, poor oral hygiene, dental infection,oral trauma, xerostomia, ductal obstruction, certain drugs (anticholinergics and antihistamines), certain chronic diseases (Sjogren’s syndrome and diabetes mellitus), mal- nutrition, pre-existing parotid Warthin’s tumour, immune suppression, and sialolithiasis.^[3] Infection from the oral cavity travels it via the stenson’s duct to invade the parotid gland. Multiple small abscesses may form in the parenchyma. They may then coalesce to form a single abscess so.^[4]

Bacteriology, virology and parasitology

The most common pathogen associated with acute bacterial parotitis and head and neck abscesses is Staphylococcus aureus both in adults, and in paediatrics patients,^[5] while in infant recurrent parotitis, Streptococcus species are the most recurrent isolated organisms.^[6] Other infection-inducing pathogens reported in literature include Streptococcus, Hemophilus, Pseudomonas, Mycobacterium tuberculosis, anaerobic bacteria and others. Other viral agents associated with parotid infection are coxsackie viruses, Epstein Barr virus, influenza A virus, lymphocytic-choriomeningitis virus, para influence viruses, herpes simplex virus, and cytomegalovirus.^[7]

Clinical features

An acute infection of the parotid gland is characterized by variety of symptoms such as the sudden onset of erythematous swelling in parotideal region, pain, fever, facial asymmetry, facial nerve palsy, and less frequently, pus/ blood in the oral cavity and dysphagia. Acute inflammation frequently evolves into abscesses, which are characterized by liquid or semiliquid content and sometimes gives rise to a fistula toward either the surface or the deepest layers of the gland. A parotid abscess, in some cases, can be a life-threatening disease, as the inflammation can spread to the head and neck causing the formation of abscesses in these zones.^[8] Tuberculosis of the parotid gland is a rare clinical entity even in countries where the disease is endemic.^[9][10] Clinically, it generally presents as a localized, unilateral, slow-growing parotid mass with a certain degree of fixation indistinguishable from salivary gland tumors,^[11] in this cases the histopathological examination is characterized by tuberculoid granulomas, with caseous necrosis, Langhans giant cells and epithelioid cells. Fluctuation is difficult to elicit due to thick capsule. Opening of the stenson's duct become congested and may exude pus on pressure over the parotid.^[12]

Diagnosis: USG Appearance

Among the various imaging modalities, sonography is considered first-line imaging for the evaluation of the parotid gland as, thanks to its superficial position, most parts are accessible by high-frequency linear probes (9–18 MHz) and only a little portion of the parotid gland may be hidden by the acoustic shadow of the mandible. Routine US examination is performed with the patient in the supine position, it include transverse and longitudinal scans over the mandibular angle covering the preauricular, infraauricular, retroauricular and cervical regions; it is crucial to examine the gland bilaterally because some diseases may occur bilaterally, or for comparison. The parotid gland, which is localized in the retromandibular fossa, is divided into superficial and deep lobes by a plane at the level of the facial nerve, which is not normally visualized with ultrasound, although its position can be inferred as it lies just lateral to the main intraparotid vessels, which are readily identified. Usually, the normal intraglandular ducts and the main duct (Stenson’s duct) are rarely visualized even with high-frequency transducers in a non-dilated status. The echo structure of the gland is usually homogeneous and the echogenicity is similar to that of the thyroid gland. Very frequently in the parotid parenchyma can be observed normal lymph nodes, which appear elliptical and hypoechoic with a hyperechoic, fatty, central hilum. When a parotid inflammatory process is occurring, the gland sonographically appears increased in volume. The boundaries of the gland are slightly faded and the parenchyma is dishomogeneously hypoechoic due to the edematous state of the parenchyma. The abscessual evolution of the inflammation is characterized by hypo-anechoic lesion, with irregular margins. An important signal of the above-mentioned inflammatory state is the appearance of vessels with a linear and reasonably regular path which subsequently becomes more irregular and characterized by numerous anastomoses, which can be highlighted by the increase in intensity of the Color Doppler signal. In the abscessual forms, the Color Doppler signal have a peripheral typology, as in this case the vessels entwine in the area which is peripheral to the abscess. Another important aspect is the presence of enlarged lymph nodes with characters of reactivity; in advanced stages may appear areas of necrosis. Frequently, the abscessual evolution gives rise to a fistula towards the surface. Sonographic findings, in case of tubercular abscess, are characterized by an enlarged parotid gland that shows a focal lesion, with pseudo-solid, inhomogeneous, appearance, and fairly regular margins (caseous necrosis).

Treatment

Correct the dehydration,improve oral hygiene and promote salivary flow. Intravenous antibiotics are instituted. Surgical drainage under local or general anaesthesia is carried out by a preauricular incision as employed for parotidectomy. Skin flap is raised to expose surface of the gland, and the abscess or abscesses are bluntly opened working parallel to the branches of the 7th nerve. Skin incision is loosely approximated over a drain and allowed to heal by secondary infection.

Depending upon the site of abscess, incisions are made along the line of blood vessels and nerves and not across it. Where possible natural skin crease is selected in a dependent area. Most often the point where it fluctuates the most may be utilized. The length of the incision will depend upon the width and depth of the abscess. Generally, incision is made through most of the width of the abscess.

Once skin incision is made, drainage is done as follows:

An opening is made into the abscess using a sinus forceps or a closed blunt hemostat and when the abscess is entered open the jaws of the sinus forceps or hemostat allowing the purulent material to escape (Hilton's method). For an abscess of larger size, the index finger is inserted through the opening into the abscess cavity and pus is evacuated carefully palpating for deep pockets if any. Make sure that the finger does not open normal tissue space. Once all the purulent material is evacuated the cavity may be irrigated with normal saline using a bulb syringe. At this point the cavity could be packed with saline gauze part of which hangs out of the wound and also a corrugated rubber drain may be utilized for deeper pockets. Initial dressings are best managed by packing with saline gauze, Gamji pads and bandages or adhesive tapes as necessary. Abscesses are preferably dressed at least once a day and as often as necessary when it gets soaked with purulent drainages with eachdressing further saline irrigation may be carried out particularly if the pockets are deep. Local application of antibiotics or use of betadine or chlorhexidine in the cavity does not seem to help particularly where abscesses have been adequately drained and dressed with saline gauze. Dressings can be facilitated particularly in the extremities utilizing warm saline soaks in clean bowls. Elevation of the extremities involved, above the level of the heart adds to the comfort of the patient and helps in early healing. It is always desirable to get a culture and sensitivity of the purulent material drained and while awaiting the final report, antibiotic is started. At times a gram stain may indicate the nature of the organisms and help in the selection of antibiotics.

References