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Diagnosis and Work Up

Diagnosis of peritonsillar abscess is usually made clinically by any of the following features:

  • Unilateral swelling of the peritonsillar area
  • Non-resolving acute tonsillitis with persistent unilateral tonsillar enlargement
  • A bulge on the unilateral soft palate with anterior displacement of the ipsilateral tonsil

Laboratory Investigations

  • Complete blood count (CBC) and electrolytes
  • Heterophile antibody test (to rule out suspicion of infectious mononucleosis)
  • Pus culture sensitivity from needle aspirate of the abscess
  • C-reactive protein blood culture might be required in patients presenting with features of sepsis

Headache abscess

The frequency of common symptoms and signs is as follows:

  • A headache (69% to 70%) the most common medical symptom.
  • Mental status changes (65%) lethargy progressing to coma is indicative of severe cerebral edema and a poor prognostic sign.
  • Focal neurologic deficits (50% to 65%) occur days to weeks after the onset of a headache.
  • Pain is usually localized to the side of the abscess, and its onset can be gradual or sudden in nature. The pain is most severe in intensity and not relieved by over-the-counter pain medications.
  • Fever (45% to 53%)
  • Seizures (25% to 35%) can be the first manifestation of brain abscess. Grand mal seizures are particularly common in frontal abscesses.
  • Nausea and vomiting (40%) are mostly seen with raised intracranial pressure
  • Nuchal rigidity (15%) are most commonly associated with occipital lobe abscess or an abscess that has leaked into a lateral ventricle.
  • Third and sixth cranial nerve deficits.
  • Rupture of abscess usually presented with suddenly worsening headache and followed by emerging signs of meningismus.

Evaluation

Routine tests: CBC count with differential and platelet count, ESR, serum C-reactive protein, serologic test, blood cultures (at least 2; preferably before antibiotic therapy).

Lumbar puncture: Rarely required and only should be performed with a prior CT and MRI scan after ruling out increased intracranial pressure because of the potential for cerebrospinal fluid (CSF) herniation and death. In circumstances of acute presentation of patients or suspicion of meningitis, blood cultures can be used for initiation of antibiotic therapy. The results are mostly nonspecific consisting of an elevated protein level, pleocytosis with the variable neutrophil count, typically a normal glucose level, and sterile cultures. A lumbar puncture in the case of rupture when WBC count becomes high in addition to elevated CSF lactic acid and abundant RBCs in the CSF.

Stereotactic CT or Surgical Aspiration: Samples obtained can be employed for culture, Gram stain, serology, histopathology, and polymerase chain reaction.

Computed Tomography

Imaging findings depend on the stage of the lesion. Early cerebritis often appears as an irregular low-density area that does not enhance or may show infrequent patchy enhancement. As cerebritis evolves, a more conspicuous rim-enhancing lesion becomes visible.  Enzmann et al. reported that CT findings of patchy enhancement in early cerebritis evolve to a rim of enhancement in late cerebritis which later on forms the brain abscess. A key histopathologic difference is that rim enhancement of late cerebritis is not associated with collagen deposition as seen in abscess where it surrounds a purulent cavity.  Serial CT examinations in patients with late abscess show progressively decreasing edema and mass effect. Brain abscess wall is usually smooth and regular with 1 mm to 3 mm thickness with surrounding parenchymal edema. The ring of enhancement may not be uniform in thickness and can be relatively thin on the medial or ventricular surface in the deep white matter, where vascularity is less abundant. Edema and contrast enhancement is suppressed by administration of steroids. Multi-location with subjacent daughter abscesses or satellite lesions is frequently seen. Gas if presently is suggestive of gas-forming organisms.

Magnetic Resonance Imaging

MRI is the imaging modality of choice for diagnosis as well as follow-up of lesions. It is more sensitive for early cerebritis and satellite lesions particularly those present in the brain stem as well as estimating the necrosis and extent of the lesion.  It allows for a greater contrast between cerebral edema and the brain and is also more sensitive for detecting the spread of inflammation into the ventricles and subarachnoid space.

Conventional spin echo imaging with contrast: Classic MR imaging findings of an abscess include a contrast-enhanced rim surrounding a necrotic core. Rim is T1 isointense to hyperintense relative to white matter and T2 hypointense. On  MRI  characteristic smooth tri-laminar structure of the rim on T2W imaging proves helpful in differentiating from other ring-enhancing lesions. Central necrosis shows variable hyperintensity on T2 depending upon the degree of protein content and hypointense on T1.

Diffusion-weighted magnetic resonance imaging: (DWI) is capable of distinguishing brain abscess from other ring-enhancing brain lesions. Abscesses are typically hyperintense on DWI (indicating restricted diffusion, characteristic of viscous materials, such as pus), while neoplasms like glioma as lack restricted diffusion appearing hypointense or variable hyperintense much lower than an abscess.

Diffusion-Tensor Imaging is based on three-dimensional diffusivity and commonly employed for evaluation of white matter tracts.Fractional anisotropy, a quantitative variable is calculated by diffusion-tensor imaging. This variable reflects the degree of tissue organization and quite higher in abscess supposedly due to organized leukocytes in the abscess cavity.

Proton MR Spectroscopy probe tissue metabolism. Spectral analysis reveals elevated succinate, although not commonly seen is quite specific for an abscess. Other significant metabolites include elevated acetate, alanine, and lactate signals. Amino acids from neutrophil-driven protein breakdown suggest a pyogenic abscess. MR spectroscopy may be used to further differentiate anaerobic from aerobic metabolism by elevated succinate and acetate peaks which are only observed in anaerobic infections due to glycolysis and subsequent fermentation. Also, lactate peaks are lowest in strict anaerobes owing to metabolic lactate consumption.

Radiological Investigations

  • X-ray of the soft tissue of the neck
  • Contrast-enhanced CT is required in a very young patient where clinical diagnosis or in cases with other complications like the development of parapharyngeal or retropharyngeal abscess is not feasible.
  • Intraoral ultrasonography is a simple, non-invasive imaging modality proposed to differentiate peritonsillitis from a peritonsillar abscess. Another important use is in the exact localization of site for abscess drainage.

Treatment / Management

Treatment involves draining the abscess, providing antibiotic support, pain control and removal of infectious tooth source. Often oral antibiotics with timely dentist appointment for dental carries intervention is sufficient. Dental abscesses may not require an admission to the hospital and administration of intravenous (IV) antibiotics unless the patient presents with worrisome features that include fever, dyspnea or airway compromise secondary to swelling. Most dental abscesses can be treated with antibiotics to cover gram negatives, facultative anaerobes, and strict anaerobes.

Penicillins and cephalosporins can be used in odontogenic infections, but there is increasing antimicrobial resistance due to B-lactamase production. This increase in resistance would make using penicillins in conjunction with other antimicrobials such as metronidazole or an antibiotic with an extended spectrum like ampicillin-sulbactam and ampicillin-clavulanate more appropriate.

  • Dosing: Ampicillin-sulbactam 3 g intravenously (IV) every 6 hours
  • Dosing: Amoxicillin-clavulanate: 875 mg orally every 12 hours
  • Dosing: Penicillin G 2 to 4  IV every four to 6 hours PLUS Metronidazole 500 mg IV or orally every 8 hours
  • Dosing: Cefoxitin: 1 to 2 g IV every 4 hours
  • Dosing: Cefotetan: 2 g IV every 12 hours

Macrolides should not be used the first line unless the patient has penicillin or cephalosporin allergy. There is increased resistance to macrolides and the bacterial species that exhibit resistance are anaerobic Streptococci and Prevotella species that are major colonizers of the oropharynx and often culprits in a dental abscess.

Metronidazole has excellent coverage against anaerobic organisms but lacks sufficient coverage against aerobic gram-positive organisms. It is recommended to use metronidazole in conjunction with penicillin to extend antimicrobial coverage to include aerobic gram-positive organisms.

  • Dosing: Penicillin G 2 to 4 IV every 4 to 6 hours PLUS Metronidazole 500 mg IV or orally every 8 hours

Clindamycin is a good option for patients with allergies to penicillins and cephalosporins. Clindamycin overs coverage against gram-positive organisms, anaerobes, B-lactam resistant organisms and has good bone penetration. It was demonstrated that Clindamycin was equally as effective in treating severe odontogenic infections as Penicillin V (Gilmore et al.).

  • Dosing: Clindamycin 600 mg IV every 6 to 8 hours

For severe infections or in immunocompromised patients. Anti-pseudomonal antibiotics like fourth-generation or higher cephalosporins or extended spectrum penicillins like piperacillin-tazobactam should be considered. Carbapenems like meropenem should also be reserved for severe infections. Meropenem has activity against gram-positive and gram-negative organisms as well as resistant organisms.

  • Dosing: Piperacillin-tazobactam 4.5 g IV every 6 hours
  • Dosing: Meropenem 1 g IV every 8 hours
  • Dosing: Cefepime 1 to 2 g IV every 12 hours

References

  • https://www.ncbi.nlm.nih.gov/books/NBK493149/
  • https://www.ncbi.nlm.nih.gov/books/NBK519546/
  • https://www.ncbi.nlm.nih.gov/books/NBK6937/
  • https://www.ncbi.nlm.nih.gov/books/NBK459170/
  • https://www.ncbi.nlm.nih.gov/books/NBK538230/
  • https://www.ncbi.nlm.nih.gov/books/NBK519520/
  • https://www.ncbi.nlm.nih.gov/books/NBK441841/
  • https://www.ncbi.nlm.nih.gov/books/NBK519573/
  • https://www.ncbi.nlm.nih.gov/books/NBK513141/
  • https://www.ncbi.nlm.nih.gov/books/NBK441873/
  • https://www.ncbi.nlm.nih.gov/books/NBK6955/
  • https://www.ncbi.nlm.nih.gov/books/NBK459132/
  • https://www.ncbi.nlm.nih.gov/books/NBK430832/
  • https://www.ncbi.nlm.nih.gov/books/NBK545292/
  • https://www.ncbi.nlm.nih.gov/books/NBK535450/
  • https://www.ncbi.nlm.nih.gov/books/NBK436004/
  • https://www.ncbi.nlm.nih.gov/books/NBK459167/

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