Our 12th episode focuses on a topic common in otolaryngology and primary - chronic rhinosinusitis. Join us to discuss the evaluation of a patient with chronic rhinosinusitis and some pearls for the OR!

Show Notes

Intro:

Hey everyone and welcome to The Oto Approach, a podcast created by medical students for medical students, to teach you about all things otolaryngology. I'm your host Aileen, and today we're going to talk about Chronic Rhinosinusitis. Tag along for a discussion about this common presentation in otolaryngology and family medicine. 

Rhinosinusitis broadly refers to inflammation of the mucosa in the paranasal sinuses and the nose. Hence its name, rhino- refers to nose, sinus- refers to the sinuses, and itis- refers to inflammation. Rhinosinusitis can be subclassified into acute, sub-acute, and chronic. Acute refers to rhinosinusitis which lasts < 4 weeks; subacute is 4 to <12 weeks, and chronic is >/= 12 weeks [1]. Chronic rhinosinusitis is the focus of this episode.

Chronic rhinosinusitis, also known as CRS, is a common condition, with an estimated prevalence of ~10% in the population [2,3]. CRS is also found to have a detrimental impact on the physical and mental health of patients and results in increased healthcare resource utilization [3]. In fact, a study by Metson has shown that patients with CRS report worse social functioning and pain control than patients with back pain, chronic obstructive pulmonary disease, angina, and congestive heart failure [4]. 

Anatomy:

Before diving deeper into CRS, let’s review some anatomy. The nose is structured superiorly by the nasal bones and inferiorly by the upper and lower cartilages. Inside the nose, the nasal cavity is divided by the nasal septum. The nasal septum is made up of cartilaginous and bony septum with overlying mucosa. The bony aspects of the septum are vomer, palatine crest, perpendicular plate of the ethmoid bone and maxillary crest [5]. The quadrangular cartilage makes up the cartilaginous septum anteriorly [5]. The roof of the nasal cavity is the skull base, specifically the cribriform plate of the ethmoid bone [5].

The paranasal sinuses are found in the bones of the face and skull, and they surround and drain into the nasal cavities [6]. The paranasal sinuses function to decrease the weight of the skull, increase the resonance of the voice, and provide immunological defense [6]. There are four pairs of paranasal sinuses named after the bones that house them - the frontal, sphenoid, maxillary, and ethmoid sinuses. They each have openings within the meatuses of the nose (otherwise known as ostium) to allow drainage of fluid into the nose [6]. Meatuses of the nose are drainage passageways from the sinuses and are housed by the turbinates. In both nasal cavities, there are usually three nasal turbinates that look a bit like shelves - the superior, middle, and inferior turbinates [7]. Some patients may have an incidental finding of a supreme nasal turbinate [8].  The nasal turbinates project from the lateral nasal cavity walls, and their primary function is to warm and humidify the air entering the nose [7]. The sphenoid and posterior ethmoid sinuses drain into the sphenoethmoidal recess near the back of the nasal cavity [6]. The ethmoid infundibulum is a three dimensional pyramidal space that facilitates drainage of the maxillary, anterior ethmoid, and frontal sinuses in the middle meatus [6]. The hiatus semilunaris is a two-dimensional gap that empties the ethmoid infundibulum [6]. The uncinate process is a projection of the ethmoid bone and protects the opening of these sinuses in the middle meatus [9]. Overall, the region of the ostia (or openings) of the anterior ethmoid, maxillary, frontal sinuses is termed the osteomeatal complex [6]. Finally, the nasolacrimal duct drains into the inferior meatus [6]. Hasner’s valve protects the opening of the nasolacrimal duct into the inferior meatus [5]. 

The nose and paranasal sinuses are lined by pseudostratified, keratinized columnar epithelium - otherwise known as respiratory epithelium [5].

Patho-physiology:

CRS is inflammation of the nose and the paranasal sinuses. The pathogenesis of this inflammation is still being studied, but contributing factors appear to be multifactorial. It is hypothesized that impaired mucociliary clearance, sinonasal epithelial barrier abnormalities, tissue remodeling, and host immune responses all play a role [10]. It is important to note that CRS is typically not an acute infection that was unsuccessfully treated.

CRS can broadly be separated into two categories - CRS with and without polyposis. Many more phenotypes of CRS exist, but are out of the scope of this podcast, for the medical student level the broad separation of CRS with and without polyposis is sufficient. Nasal polyps are benign outgrowths of nasal and paranasal mucosa that can significantly impact patients’ function and quality of life. The treatment options differ depending on the presence and absence of polyps [11]. However, polyps are beginning to be further sub classified based on the clinical picture and pathological findings of the polyps. These are described as the phenotype and endotype, respectively [12-14].

The presence of nasal polyps can change the treatment pathway for patients with CRS - but, we’ll get into that a bit later though! 

Diagnosis/investigations:

How do we diagnose CRS? There are a variety of criteria, but many Canadian Otolaryngologists will use the 2011 Canadian guidelines which provided the mnemonic CPODS. CPODS stands for congestion; facial pressure or pain; nasal obstruction or blockage; purulent anterior or posterior nasal drainage; and change in the sense of smell [15]. To diagnose CRS the patient must have at least 2 CPODS symptoms for at least 8 weeks, and at least one of these must be either the O or the D - obstruction or discharge [15]. In addition, the objective finding of sinus/nose inflammation upon nasal endoscopy or computed tomography (CT) is required [15]. 

Endoscopy is typically completed in the otolaryngology clinic using flexible nasopharyngoscopy. It is important to consider patient comfort while ensuring proper visualization. Clinicians will have different tactics to achieve this - varying from lubrication of the scope, nasal decongestion prior to endoscopy often with Otrivin (xylometazoline), (meh taz o leen)  and/or topical lidocaine analgesia sprays. The attending physician will typically perform nasopharyngoscopy, this allows opportunities for medical students to view various anatomy. As medical students become more comfortable, the physician may allow them to perform endoscopy under direct supervision. In the nasal cavity look for septal deviations, bony spurs, and turbinate hypertrophy, inferior turbinate hypertrophy is a common finding in patients with CRS [16]. Assess the external and internal nasal valve areas [16]. These are the opening of the nostrils and the opening into the nasal cavity just past the nasal hairs. Inside the nasal cavity, look for nasal obstruction, mucopurulent debris, and erythematous and edematous (otherwise inflamed) nasal mucosa [16]. Also look at the sinus drainage, looking for obvious signs of inflammation or obstruction [16]. Look for signs of bleeding or septal perforations [16]. Finally, look for polyps. Polyps look like pale, fleshy pouches of tissue that are often described as looking like peeled grapes. They are most commonly seen in the middle meatus and can be found in the nasal cavity in more severe cases. The finding of polyps can change the management of CRS and is therefore important to identify.

The Lund-Mackay scoring system can be used to assess CT scans of the paranasal sinuses and osteomeatal complex [17]. Each sinus (frontal, anterior ethmoid, posterior ethmoid, maxillary, sphenoid) and the osteomeatal complex are assigned a score from 0 to 2 [16]. 0 = no abnormality/opacification; 1 = partial opacification; and 2 = complete opacification [17]. Each side is scored separately and a combined score of 24 is possible [17].  

Presentation/history:

Patients presenting with CRS will commonly present with a long-standing history of breathing concerns. It is important to take a detailed head and neck history - start with the OPQRST questions in your HPI - Onset? Precipitating factors? Relieving factors? Quality? Radiation? Severity? Time frame? Of course, don’t forget to ask the diagnostic “CPODS” questions mentioned earlier. Precipitating and relieving factors can be especially important as they can identify potential triggers that bring on or worsen symptoms. Ask if it is intermittent or constant, uni or bilateral, ask if they snore or have consistent tearing [5]. Ask what patients have tried so far to help their symptoms and what effect it has had. How did they tolerate previous treatments? Along these lines - it is important to take a good medical history asking about allergies, current medications, previous and current medical conditions, and previous surgery or trauma (specifically in the head and neck area). Seasonal allergies can worsen CRS symptoms. 

There are also medical conditions that can predispose patients to CRS such as asthma and cystic fibrosis [5]. In fact, asthma and CRS are highly correlated. A study has reported that 88% of patients with mild-moderate asthma have sinus CT abnormalities consistent with CRS, and 70% have symptoms consistent with CRS [18,19]. In patients with severe asthma, these numbers increased to 100% with CT findings, and 74% with CRS symptoms [18,19]. It is thought that asthma and CRS are associated because both are inflammatory conditions of the respiratory tract. The unified airway theory or “one airway, one disease”, suggests that the respiratory tract is not separated into partitions, but is rather one functional unit. [20,21]. As such, it is thought that the pathophysiology behind inflammatory diseases of the respiratory tract, such as asthma and CRS are not individual and separate, but rather are linked through the unified airway [20,21]. 

When asking about medications, inquire about over-the-counter nasal decongestant use. Patients often assume anything over the counter is safe to use as much as needed; when in reality, these medications can actually make symptoms worse, with rebound vasodilatation and patients can become dependent on these medications. This condition is called rhinitis medicamentosa [22]. To prevent  rhinitis medicamentosa, duration of topical decongestant use is recommended to be less than 3-5 days. 

Social history is vital in the assessment of a patient with CRS. Asking about their environment both at home and at work is important. Asking about dust exposure, the heating system, do they have carpets or flooring, what kind of pillows do they use, do they have any pets? Further, ask about smoking or vaping habits, or exposure to secondhand smoke. The use of recreational drugs and alcohol is important as well, especially recreational drugs which are ingested intranasally, such as cocaine. 

It is also important to ask about family history and their past experiences with CRS.  A family history of allergies or other medical conditions can provide helpful information to guide treatment and identify contributing allergens. For patients with CRS, it is extremely important to assess how the condition is affecting the patient’s quality of life through FIFE questions (feelings, ideas, function, and expectations) because the management approach is partially driven by how limiting the condition is to individual patients. 

On physical examination look for external signs of head and neck trauma. Check the bridge of the nose for deviation, step deformity or signs of a previous fracture, perform anterior rhinoscopy to look for mucosal inflammation, inferior turbinate hypertrophy, nasal polyps, or septal deviation/perforation. Watch the patient breathe, occlude each nostril individually and watch them breathe again. Observe for internal or external nasal valve collapse/obstruction. It is important to complete a full head and neck exam, by examining the ear, ear canal, and tympanic membrane; palpating the head and neck for masses; and examining the subsites of the oral cavity and oropharynx. Finally, nasopharyngoscopy should be performed as described earlier in the diagnostic criteria.

Treatment:

Treatment of CRS typically follows a ladder approach, going from least to most invasive. 

Conservative

First-line treatment is typically avoidance of irritants such as smoke, dust, and allergens along with nasal saline lavage. One step above this on the ladder is the addition of intranasal corticosteroid sprays such as mometasone (Nasonex). Topical or oral antihistamines can also be prescribed, if there is a suspected allergic component to the patient’s presentation. Pediatric patients with CRS symptoms may also be referred for allergy testing. Moving up the ladder again is the use of budesonide (Pulmicort) nebuamps, these can be mixed into nasal saline lavage for regular use, most commonly once or twice daily for ongoing maintenance therapy. Nasal steroid irrigations provide greater distribution of the corticosteroid throughout the nasal cavity and sinuses than steroid sprays, resulting in better relief of CRS [23]. The final medical option varies depending on if the patient has CRS with or without polyposis, a short course of systemic antibiotics can be prescribed for patients suffering from CRS without polyposis, or a short course of oral steroids can be prescribed for patients suffering from CRS with polyposis. 

FESS

If medical intervention does not provide symptomatic relief, surgical intervention may be appropriate. Functional endoscopic sinus surgery (otherwise known as FESS) is typically used to treat chronic rhinosinusitis [24]. FESS is a minimally invasive technique that has revolutionized the field of sinus and nasal cavity surgeries [24]. FESS is typically performed by an otolaryngologist under general anesthesia using a rigid endoscope [24]. However, there is a growing field of doing endoscopic sinus surgery under local anesthesia, which may be especially beneficial for patients with contraindications to general anesthesia or comorbidities that predispose them to greater risks related to general anesthesia [25]. During sinus surgery, the sinus ostia are widened to improve drainage from the sinuses. The main goals are to open up the nasal cavity and sinuses to maximize the exposure of nasal mucosa to steroid irrigations, to re-establish ventilation and improve mucociliary clearance to the paranasal sinuses [23,24].  The degree of surgery and the sinuses which are addressed, is determined on a case by case basis.

Operation on the frontal sinuses is more challenging and has a greater risk of complications [5]. Operation on the frontal sinuses is classified by the DRAF criteria [5]. DRAF I is an anterior ethmoidectomy with exposure of frontal sinus outflow tract [5]. DRAF IIa is frontal sinusotomy with the removal of agger nasi and frontal recess cells, exposing frontal sinus ostium between lamina papyracea and middle turbinate [5]. DRAF IIb is the removal of the head of the middle turbinate and widening frontal sinus ostium from lamina papyracea to septum [5]. DRAF III is the removal of the entire floor of the frontal sinus, inter-sinus septum, and anterosuperior nasal septum [5].

Pre-operatively, it is important to inform the patient of the risks and benefits of FESS, especially to facilitate informed consent. As with any surgery, FESS has risks of general anesthesia, bleeding, and infection. With FESS, instruments are often used near the skull base and orbital cavities. As such, there is a risk of cerebrospinal fluid (CSF) leak through damage to the cribriform plate, along with this there is a risk of infection spreading to the brain resulting in meningitis [5]. Clear fluid seen draining during surgery should make you suspicious of a CSF leak, this can be repaired with grafts intra-operatively. There is also risk of damage to the structures within the orbital cavity, damage to the optic nerve can cause blindness, penetration of the orbital fat can cause a retrobulbar hematoma, retrobulbar or pre-septal emphysema may occur from micro-fracturing the lamina papyracea, diplopia (double vision) can occur due to extraocular eye muscle injury, and epiphora (excessive tear formation) can result from injury to the nasolacrimal duct system [5]. Finally, important arteries live around the nose and paranasal sinuses and damage to these can cause major hemorrhage - specifically at risk is the anterior ethmoid, posterior ethmoid, sphenopalatine and carotid arteries [5]. Damage to the carotid artery is a very rare, but very severe potential complication and it requires urgent management [5]. 

To reduce the risk of these serious complications, intraoperative image guidance systems have been used for sinus surgeons [5]. These systems work as a GPS navigation system to guide sinus surgery, giving surgeons the ability to track their instruments in the nasal cavity with real-time correlation with the patient’s preoperative CT scan. 

The CLOSE checklist is a systematic approach to CT evaluation pre-FESS/endoscopic skull base surgery. C stands for cribriform plate - which is typically assessed using the Keros classification [26]. The Keros classification, classifies the depth of the olfactory fossa based on the height of the lateral lamella of the cribriform plate [27]. The deeper the olfactory fossa, the higher the Keros classification, which means more of the thinner parts of the cribriform plate are exposed, resulting in a higher risk of trauma to the skull base [27]. Keros Type 1 has a depth of 1-3 mm, type 2 has a depth of 4-7 mm, and type 3 has a depth of 8-16 mm [27]. L stands for lamina papyracea (the thin bone separating the orbit from the nasal sinuses) - you are assessing for remote orbital fractures, orbital prolapse into the ethmoid sinus, the uncinate process and its attachment site and the presence of Haller cells [28]. Haller cells are ethmoid air cells lateral to the maxillo-ethmoidal suture line along the inferomedial orbital floor; their presence can result in inadvertent entry into the orbit, if not properly recognized pre-operatively [28]. O stands for Onodi cell [29]. An Onodi air cell is a sphenoethmoidal air cell, an anatomical variant. These air cells, if present, lie in close proximity to the optic nerve and internal carotid artery [29]. S stands for sphenoid sinus pneumatization [26]. It is important to identify the pneumatization pattern of the sphenoid sinus (conchal, presellar or sellar) and identify carotid canal or optic nerve dehiscence [26]. Finally, E stands for (anterior) ethmoidal artery - look to identify the ethmoidal notch and presence of supraorbital pneumatization [26].

FESS has reported outcomes ranging from ~80-90% in the literature [24]. However, patient education is crucial to success in FESS. Re-establishment of mucociliary clearance and sinus drainage allows pathways for increased penetrance/access of intranasal saline lavage and corticosteroids. Patient adherence with medical management can significantly impact perceived outcomes of FESS.

Clinical Pearls 

Biologic therapy and research for use in CRS patients have been a developing field in recent years. It is being increasingly recognized that type 2 immune responses may contribute to the pathophysiology of CRS [30,31]. These immune responses have shown the ability to respond to biologics in other disease states [30,31]. These biologic therapies may play a significant role in the treatment of CRS patients, specifically in those with polyposis, in the near future. In fact, the Rhinology Working Group of the Canadian Society of Otolaryngology-Head and Neck Surgery, recently released consensus statement guidelines for the use of biologics in patients with CRS [30]. 

It is important to be aware of variations in patient presentation. For example, aspirin-exacerbated respiratory disease (AERD) is defined by Samter’s triad as asthma, nasal polyps, and an allergy to aspirin [32]. This is a more severe form of CRS which is more challenging to treat. Different treatment modalities along with those mentioned earlier can be employed for these patients. Aspirin desensitization therapy where patients are exposed to increasingly higher doses of aspirin in a controlled setting is a unique treatment for AERD which can be beneficial for these patients [32]. 

Unilateral rhinosinusitis symptoms should prompt you to consider other causes including but not limited to paranasal tumors, odontogenic etiology - often due to periapical abscess of the maxillary molars, and fungal involvement potentially a fungal ball (mycetoma) [5]. Rhinosinusitis is common in untreated HIV patients, who are at increased risk of invasive fungal sinusitis [5].

Further, acute sinusitis is commonly caused by viral pathogens and can be self-limiting [5]. However, acute-bacterial sinusitis and acute frontal sinusitis can have severe complications resulting from intracranial and intraorbital spread of infection [5]. These topics regarding acute sinusitis and associated complications will be covered in a future episode.

Thank you to Kalpesh Hathi for developing this script. 

We would like to extend our sincerest thanks to the Saint John Regional Hospital Department of Surgery within the Horizon Health Network for their generous support. 

Thank you so much for listening to our podcast! We hope you’ll tune in to our next episode! Please head to our website at www.theotoapproach.com for our show notes, and to sign up for our newsletter to stay up to date with our latest episodes. 

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