Orbital Defect and Emphysema After Nose Blowing: A Case Report and Literature Review

A 59-year-old man with a history of obstructive sleep apnea presented to the emergency department for acute swelling of the left upper and lower eyelids after nose blowing. The patient denied prior orbital trauma or surgery and examinations were unremarkable for bony step-offs, lacerations, enophthalmos, proptosis, hypoglobus, or extraocular muscle restriction. Imaging confirmed the diagnosis of left anteromedial orbital floor defect with periorbital emphysema. The orbital floor fracture repair was successfully performed with a MEDPOR implant (Stryker, Kalamazoo, Michigan) to seal the persistent orbital floor defect. A review of the literature revealed common predisposing factors, including forceful nose blowing, remote history of trauma, mucosal inflammation, and smoking.


Introduction
Orbital fractures are becoming more frequent in the United States and are most commonly precipitated by physical trauma [1]. Although rare, orbital wall fractures have been associated with increased intranasal pressure seen in nose blowing and sneezing; however, the predisposing factors leading to this type of morbidity are less clear in the existing literature. Herein, we highlight a novel case of acute orbital defect and emphysema after nose blowing and present a succinct literature review of 17 other cases to better define this rare presentation.

Case Presentation
A 59-year-old white male presented to the emergency department (ED) with acute eyelid swelling of the left eye immediately after sneezing. Pertinent medical history included hypertension, hypercholesterolemia, type 2 diabetes mellitus, obstructive sleep apnea (OSA) with eight years of continuous positive airway pressure (CPAP) use, prior cerebrovascular accident, and gastroesophageal reflux disease. The patient also reported being involved in a mild motor vehicle accident (MVA) approximately 10 years prior without relevant sequelae. The surgical history was unremarkable. Home medications included amlodipine, aspirin, citalopram, pantoprazole, metformin, metoprolol, magnesium oxide, and potassium chloride. Social history was significant for daily alcohol and tobacco pipe use.
The patient reported feeling at his baseline prior to the incident. In the ED, he described having an uneventful morning until he blew his nose. The patient denied ocular trauma, eye pain, pain with extraocular movements, changes in vision, headache, sore throat, numbness, tingling, lightheadedness, or loss of consciousness.
Physical exam was notable for non-erythematous left upper and lower eyelid swelling with crepitus and mild swelling of the left upper maxillary region without pain. The patient's visual acuity was not tested by the emergency medicine physician because the patient denied any vision changes. Pupils were equal, round, and reactive to light. Intraocular pressure of the affected eye was 17 mmHg. Extraocular movements were full without restriction, proptosis, or enophthalmos. Anterior segment exam and the remainder of the head, eyes, ears, nose, and throat (HEENT) examination was unremarkable, including the absence of scalp or facial lesions or tenderness, patent ear and nasal canals without erythema or edema, no lesions or erythema of the mouth or pharynx, or palpable lymph nodes.
Labs revealed only a mild anion gap metabolic acidosis. A maxillofacial computed tomography (CT) without contrast revealed extensive orbital emphysema on the left and a bony defect involving the anterior medial margin of the left orbital floor without boney fragments ( Figure 1). There was no evidence of an orbital floor depression fracture or compromise of the medial, lateral, or superior orbital walls. The paranasal sinuses revealed mild mucosal thickening change involving the left maxillary sinus. The ostiomeatal complexes were patent. The patient was ultimately discharged from the ED on oral amoxicillin-clavulanate and instructed to follow up with an oral and maxillofacial surgeon. Repeat imaging one month later with CT of the orbits and sella without contrast showed resolution of the left-sided orbital emphysema, but persistence of the orbital floor defect along the anterior medial margin ( Figure 2). Of note, the paranasal sinuses were clear without mucosal thickening on repeat imaging.

FIGURE 2: Coronal view CT of the orbits and sella without contrast one month after presentation
There is persistence of the anteromedial orbital floor defect (white arrow), with the resolution of orbital emphysema.
Approximately four months after the initial presentation to the ED, the patient was referred to oculoplastic surgery for repair of the orbital floor defect. Visual acuity at the initial presentation to our office was 20/25 in both eyes and intraocular pressures were normal. The examination mirrored the prior exams. Orbital floor fracture repair of the left eye was successfully achieved using a MEDPOR implant (Stryker, Kalamazoo, Michigan) to seal the defect; however, the clinical course was complicated by retrobulbar hemorrhage secondary to premature blood thinner use on the third postoperative day that required lateral canthotomy and inferior cantholysis. At the six-month follow-up, the implant remained in a good position with a resolution of symptoms and return to baseline visual acuity of 20/25 in both eyes.

Discussion
Orbital fractures from all causes most commonly occur in the medial wall, followed by the floor and inferomedial wall [2]. Orbital floor fractures, as in our case, have been well-documented related to physical trauma [1,2]. In a study by Iftikhar et al. (2021) spanning from 2006 to 2017, the two most common causes of orbital floor fractures presenting to the ED were assault (43%) and falls (26%), followed by objects and MVAs [1]. Non-physical causes of orbital floor defects, such as nose blowing and barotrauma, account for a minority of cases.
Mechanisms for orbital wall fracture after nose blowing were postulated in four reports, which primarily implicate prior facial surgery, boney changes of advanced age, and intensity of nose blowing. Kim et al. (2021) proposed that the patient's medial wall fracture after nose blowing was secondary to postoperative changes in the aerodynamics or shock-absorbing capacity of the paranasal sinuses after having an orbital floor fracture repair six years prior [3]. Two cases were in agreement that high intranasal force from vigorous nose blowing could cause an orbital wall fracture consistent with the hydraulic theory [4,5]. Finally, Oluwole and White (1996) in the first case report describing an orbital fracture after nose blowing suggested that the fracture seen in the 70-year-old patient was precipitated by a combination of vigorous nose blowing and natural thinning of the bony wall with age [6].
Based on the known literature, potential predisposing factors in our patient's case include forceful nose blowing, sinusitis, smoking, and a remote history of an MVA; however, it may be possible that CPAP contributed to this presentation. CPAP is known to create dryness and inflammation of the nasal mucosa through continuous airflow. Air travels into the maxillary sinus via the nasal cavity, under the middle concha, and into the middle meatus where the maxillary sinus ostium is located in the hiatus semilunaris. Of note, the primary maxillary ostium is typically located at the junction of the medial maxillary wall and orbital floor, halfway between the anterior and posterior maxillary walls [20]. It is obvious how chronic airflow from CPAP through this pathway can create inflammation and gradual thinning of the maxillary sinus roof and orbital floor. Furthermore, based on the anatomy described above, the defect would most likely occur along the medial orbital floor, because it is the initial contact site when air enters the maxillary sinus through the maxillary ostium. The patient presented in this case report had an anteromedial orbital floor defect, which aligns with this potential mechanism. There is likely slight anatomic variation in the anteroposterior location of the maxillary sinus ostium, explaining why the patient's defect was located more anteriorly.

Conclusions
Nose blowing is an established cause of orbital fracture and emphysema. Predisposing factors have not been fully elucidated, but after a review of the literature, common predisposing factors include forceful nose blowing, remote history of trauma, mucosal inflammation, and smoking. It is thought that CPAP contributed to mucosal irritation and orbital floor thinning in our patient's case. No meaningful associations were observed relating to the age or sex of patients. All orbital fractures affected either the nasal wall or the orbital floor, and nearly all cases presented with periorbital emphysema. Our case with a persistent orbital floor defect was successfully repaired using an orbital implant.

Additional Information Disclosures
Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.