Complications Of Paranasal Sinusitis Research Articles

Odontogenic orbital cellulitis in a young man with complete vision loss – a case report

Abstract Odontogenic inflammation in humans can spread to adjacent anatomical structures, causing pathological changes that are dangerous to health and, in some cases, life. In this paper, we present an unusual case of odontogenic orbital cellulitis caused by both Lactobacillus rhamnosus and Enterococcus avium, which resulted in blindness of the eye in a 25-year-old man. Orbital cellulitis is more common in children due to the relative immaturity of their immune systems whereas it is rare in adults – in most cases, it occurs as a complication of paranasal sinusitis. An accurate diagnosis requires not only a thorough clinical examination but also appropriate imaging tests (such as a computed tomography or nuclear magnetic resonance test). Successful treatment largely depends on the earliest possible implementation of pharmacological therapy. In cases where it is justified, surgical procedures to decompress and drain the abscess should also be considered. However, in the case described in this publication, the patient did not regain vision in the affected eye despite the implementation of both intensive pharmacological treatment and surgical treatment, probably due to ischemic optic neuropathy and central retinal artery occlusion caused by severe infraorbital oedema.

A Severe Case of Septic Cavernous Sinus Thrombosis Caused by a Rare Pathogen

SESSION TITLE: Student/Resident Case Report Poster - Critical Care IV SESSION TYPE: Student/Resident Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM INTRODUCTION: Cavernous Sinus Thrombosis (CST) is thrombophlebitis in the cavernous sinuses. Before the availability of antibiotics, this dramatic and lethal illness carried a 100% mortality, therefore, the onus is on the clinician to have early recognition of this disease and treatment options, which include antibiotics, anticoagulation, and surgery. Although there have been case reports of CST as a complication of paranasal sinusitis, otitis media, and pharyngitis in pediatric population, literature review reveals few cases of CST in adults causing multi-organ impairment similar to our patient. We report a case of CST causing cranial nerve palsy and internal carotid artery narrowing from ethmoid and sphenoid sinusitis secondary to Group C, Beta Hemolytic Streptococcus. This is a common flora of upper airways and skin and bacteremia is almost always seen in immunocompromised individuals and rarely seen in an immunocompetent patient like ours. CASE PRESENTATION: 36 year old female with no significant past medical history presented to the ED with a three day history of left sided headaches, subjective fevers, diplopia and left periorbital swelling. On exam, she was febrile with left eye proptosis and left lateral gaze palsy. Labs revealed significant leukocytosis with left shift and elevated inflammatory markers. CTA head and neck showed left cavernous sinus thrombosis/thrombophlebitis as well as narrowing of left internal carotid artery with MRI/MRV confirming these findings. Imaging also revealed bilateral complete opacification of sphenoid and ethmoid cells suggestive of severe sphenoiditis and ethmoiditis. She was admitted to ICU and her course was complicated by septic shock and acute hypoxemic respiratory failure requiring pressors and mechanical ventilation as per ARDS protocol. Further septic workup revealed the patient to have beta hemolytic, group C strep bacteremia with nasal culture showing the same speciation. She was started on IV antibiotics and heparin drip in ICU and was later discharged home on oral warfarin and IV ceftriaxone. DISCUSSION: The likely mechanism in our patient is that she initially had ethmoiditis causing orbital inflammation and thrombophlebitis of the ophthalmic vein, which extended posteriorly to cause septic CST. Literature review shows that S. aureus encompasses two-thirds of the cases followed by streptococci, especially pneumococci, but there have been no cases, to our knowledge, of group C beta hemolytic strep causing CST. CONCLUSIONS: Aggressive multidisciplinary approach to management remains key in these patients due to high mortality if there is a delay in early and proper diagnosis. Sinusitis and ethmoiditis are relatively common and a physician should be aware of the potential adverse consequences, especially in the setting of ptosis, proptosis, and external opthalmoplegia. Reference #1: Hiroshi Sakaida, Masayoshi Kabayashi, Ai Ito. Cavernous Sinus Thrombosis: linking a swollen red eye and headache. Lancet 2014: 384: 928 DISCLOSURE: The following authors have nothing to disclose: Hemal Mehta, Anthony Saleh, Ravish Singhal No Product/Research Disclosure Information

Parafalcine Subdural Empyema in a Woman with Recurrent Acute Otitis Media

Subdural empyema (SDE) most frequently arises as a complication of paranasal sinusitis and is a serious intracranial infection. Parafalcine SDE, resulting from acute otitis media, is a rare phenomenon. Here, we report the case of 57 year old woman, with a history of nasopharyngeal carcinoma (NPC) with radiotherapy, 28 years ago and recent diagnosis of recurrent acute otitis media, who was admitted to the emergency department with a 2 days history of progressive right-sided limb weakness. Neurological examination revealed right-sided hemiparesis without meningeal signs. Non-enhanced computed tomography (CT) scans of the brain revealed a hypodense lesion in the left parafalcine region. Gadolinium-enhanced magnetic resonance imaging demonstrated layers of rim-enhancing subdural fluid collection and swelling of the surrounding brain, suggestive of empyema. The patient underwent surgical evacuation of empyema and was treated with intravenous antibiotics for 6 weeks. The patient recovered well without neurological deficits. Follow-up brain CT 6 weeks later showed complete resolution of previous lesions. Acute otitis media complicated by SDE is a rare clinical phenomenon that carries a high mortality rate. The complication risk may be higher in NPC patients following radiotherapy. Early diagnosis of SDE and prompt surgical evacuation of purulent material can result in a full recovery.

Skull Base Osteomyelitis

Skull base osteomyelitis may develop as a complication of paranasal sinusitis or other regional infectious process or as an unfortunate sequelae of iatrogenic injury or trauma. Afflicted patients generally have some form of systemic immunocompromise, most often diabetes, or a history of external beam radiotherapy for a head and neck malignancy with the radiation portal encompassing the area of the skull base. Before the era of systemic antimicrobial therapy, skull base osteomyelitis was almost universally fatal. Acute osteomyelitis often results in rapid lytic destruction of the skull base bone commonly associated with cranial nerve palsy/paralysis, and rarely, with craniovertebral instability and intracranial abscess formation. It may or may not be associated with a deep fascial, orbital or intracranial soft tissue component. Chronic osteomyelitis, as seen in granulomatous conditions, is often much more indolent and slowly progressive. Patients may still exhibit cranial nerve palsies, albeit usually more slowly. As such, they are often able to compensate for these losses over time and hence often delay their clinical presentation. In contradistinction to malignant otitis externa (otologic skull base osteomyelitis), nonotologic skull base osteomyelitis may pose a significant diagnostic clinical challenge. There are no pathognomic findings on clinical or radiographic examination which confirm skull base osteomyelitis. Tissue diagnosis is the key to both diagnosis and management of this rare entity. Preoperative CT or MRI-guided fine needle aspiration of accessible lesions is warranted for all skull base lesions. Unfortunately, this is not feasible in many cases due to inaccessibility. Thus, advanced open and/or endoscopic craniofacial approaches are required to allow for safe exposure of the affected areas. Preoperatively, it may not be possible to differentiate infectious from neoplastic entities that can present in a similar fashion. Once access has been achieved, confirmatory biopsy should be sent for pathologic analysis. If osteomyelitis is confirmed, then aggressive surgical debridement of grossly affected bone, preserving neurovascular anatomy whenever possible, followed by culturedriven systemic antibiotic therapy (generally for 6 weeks) is the mainstay of treatment. Initial or suspected nonotologic osteomyelitis should be treated empirically to provide coverage for Staphylococcus aureus. This is in contradistinction again to otologic osteomyelitis where empiric coverage for Pseudomonas aeruginosa should be provided. Cultures should always be sent to evaluate for possible fungal and tuberculosis pathologies as well. Serial gallium scans may be useful to follow these patients postoperatively as a marker of response to treatment. Serial CT and MRI scanning seems to be less useful in this regard. With aggressive surgical debridement facilitated by the broad exposure provided by modern craniofacial approaches, followed by tissue-guided systemic antimicrobial therapy, one can anticipate resolution of the progressive radiographic findings, and often times, note reversal or improvement of neural deficits (especially those of recent onset). Refractory cases and those arising in a radiated field may benefit from the adjunctive use of hyperbaric oxygen therapy (minimum of 30 dives). The major difficulty encountered by the clinician treating this patient population remains that of establishing a sound diagnosis and differentiating this lesion from a neoplastic process.