Prof RJ Harvey

Nose Picking, Crusting and Septal Perforations: The Missing Part of the Story

Nose picking is one of the most common human behaviours that almost nobody wants to discuss honestly. In most people, it is harmless. It is not a disease, and it is not automatically a psychiatric problem. It is usually just a way of clearing dried mucus from the nose. In rhinology, however, the subject matters. For years, many surgeons were taught that chronic septal crusting, septal ulceration and septal perforation were mainly explained by drying from nasal airflow. That explanation is partly true. The nose conditions a large volume of air every day. Depending on activity, climate and physiology, roughly 15,000–20,000 litres of air may pass through the nasal cavity in a day. Airflow can dry secretions, thicken mucus, and contribute to crusting. But airflow is not the whole story. In many patients, the missing mechanical factor is the finger. A crust forms, the patient feels blocked, they clear it, the surface bleeds or becomes raw, a new crust forms, and the cycle repeats. The patient is not being “bad”. They are often trying to breathe. The problem is that the wound surface is being reset every day.

Nose picking: normal behaviour versus a medical problem

The medical term often used for compulsive nose picking is rhinotillexomania. That term is useful, but it can also confuse the discussion. Most people who pick their nose do not have rhinotillexomania. The available survey data make this clear. Jefferson and Thompson’s adult survey reported that nose picking was an almost universal adult behaviour and concluded that, in most people, it should be regarded as a habit rather than a psychiatric disorder. A later adolescent survey found that almost the entire adolescent sample admitted to nose picking, with a median frequency of four times per day. In that study, 7.6% reported picking more than 20 times per day, and nearly 17% considered that they had a serious nose-picking problem. The practical distinction is therefore important: - Common nose picking is occasional clearing of dried mucus or crust. - Clinically relevant nose picking is repeated mechanical trauma to vulnerable nasal mucosa. - Rhinotillexomania is compulsive, repetitive picking that may be difficult to control and may require behavioural or psychological support. This distinction is now specifically recognised in the rhinology literature. Alobid and colleagues have described self-induced nasal septal perforation from rhinotillexomania as a different entity from ordinary nose picking, with management that may require behavioural therapy, multidisciplinary care, silicone sheets, and septal repair where appropriate. For clinicians, the key question is not whether the behaviour is embarrassing. The key question is whether it is affecting healing.

Why the old “dry airflow” explanation is incomplete

Drying from nasal airflow is real. It is particularly relevant in patients with: - a dry anterior septum - exposed cartilage or bone - postoperative crusting - a septal perforation - inflammatory nasal disease - prior intranasal drug exposure - mucosal injury from sprays, trauma, infection or surgery But if airflow were the only driver, the clinical patterns would often be more predictable. What we commonly see is more focal and more mechanical. The anterior septum is exactly where the finger reaches most easily. It is also where small areas of trauma can become chronic. A patient feels a dry crust or sharp edge, removes it, and creates a raw area. The raw area bleeds or weeps, then dries into another crust. The patient again feels blocked and clears it. This is the crust–pick–crust cycle.

and excerpt from: Alobid I, Garaycochea O, Rojas-Lechuga MJ, Harvey RJ, Hopkins C, et al. International Consensus Statement on Nasal Septal Perforation. Rhinology. In press. The recent International Consensus Statement on Nasal Septal Perforation supports this model. It describes a pathophysiological sequence from mucosal excoriation to ischaemia, ulceration and perforation. During that process, crust and eschar formation occur, and repeated removal of those crusts can further disrupt mucosal healing. In the associated Delphi process, consensus was reached that nose picking driven by nasal crusting can be a factor in the pathogenesis of nasal septal perforation, and that nose picking can contribute to enlargement of an existing perforation. That is a major shift in thinking. Dryness may start the crust. The finger may stop it healing.

Scenario 1: chronic septal crusting without a perforation

The first clinical situation is the patient with chronic anterior septal crusting, but no established septal perforation. These patients often say something like: “I know I shouldn’t touch it, but I can feel something there. It blocks the airway. I just need to clear it.” That statement is clinically important. The patient is not describing an irrational act. They are describing a sensory trigger. The crust feels obstructive, rough, dry, bloody or irritating. Removing it gives short-term relief. The long-term effect is the opposite: the area fails to heal. On endoscopy, the surgeon may see: - focal anterior septal crusting - a raw mucosal patch beneath the crust - bleeding after crust removal - squamous metaplasia or thickened unhealthy mucosa - early ulceration over septal cartilage - repeated crusting at the same reachable location

Persisent finger trauma results in the focal area of septal crusting   In selected patients, this becomes more than a moisturising problem. If the surface has become chronically unstable, it may need a reconstructive solution. A small mucosal graft can help restore a healthier epithelial surface and allow the area to re-mucosalise.

a simple free graft to the seputm can be used at any stage of the crusting to perforation stage to help with healing The rationale is consistent with broader endoscopic rhinology experience. Free mucosal grafting has been used to accelerate re-epithelialisation, reduce crusting and stabilise healing surfaces in skull base surgery, frontal sinus surgery and septal reconstruction. The aim is not simply to “cover a sore spot”. The aim is to interrupt the cycle of crusting, finger trauma and delayed healing.

Scenario 2: the already perforated septum

Septal perforations are often explained as airflow problems. That is partly correct. A hole in the septum changes airflow. Air moves abnormally through the perforation, secretions dry, and crusts form. Patients may develop obstruction, whistling, bleeding, crusting and impaired quality of life. But the perforation itself also creates a target. One of the most revealing clinical observations is crusting at the posterior edge of a septal perforation. Traditionally, that crusting might be explained by abnormal airflow across the back edge of the defect. In some cases, that is true. But it is not always the dominant factor. Endoscopic video can show the finger entering the nose and picking directly at the posterior edge of the perforation. That image changes the explanation. The crust is not simply forming because air has passed over it. It is also being mechanically disturbed because the patient is trying to clear the obstruction. This matters because ongoing picking can: - enlarge the perforation - maintain crusting at the perforation margin - trigger recurrent bleeding - prevent epithelial stability - compromise the success of repair

The areas of finger trauma are obvious in these patients with septal perforations. Our own septal perforation repair cohort reflects how common this issue is in clinical practice. In a 90-patient series, picking was documented as present in 34.4% of patients, and picking was recorded as an aetiological factor in 22.2%. Most perforations were anterior, with 88.6% located anteriorly. Those numbers are not trivial. They suggest that nose picking is not an occasional incidental detail. It is a recurring clinical factor. The same cohort also shows why restoring a stable mucosal surface matters. Before repair, crusting was present in 74.1% of patients. After repair, crusting fell to 12.9%. Ulceration fell from 14.0% to 2.3%, and anatomical closure was achieved in 90.0% of patients. Free mucosal graft integration was complete in 85.6% overall, and complete in 92.6% of patients who achieved successful anatomical closure. These data support a practical point: if the mucosa is restored and protected, crusting and ulceration often improve substantially. But if the crust–pick–crust cycle continues, even technically sound repair may be placed at risk. This is especially relevant when discussing perforations related to cocaine or other intranasal injury. The initiating factor may be chemical, vascular, traumatic or inflammatory. But the later non-healing phase often includes crusting, awareness, manipulation and repeated mucosal trauma.

Scenario 3: early septal trauma after septoplasty

The third situation is early septal trauma after an otherwise well-performed septoplasty. Historically, when surgeons saw an early anterior septal ulcer or developing perforation after septoplasty, the explanation was often “poor blood supply”. Sometimes vascular compromise can occur. But that explanation does not always make anatomical sense. The anterior septum has a rich blood supply. For matching injuries to occur on both sides of the septum, at the same anterior reachable location, purely from isolated vascular failure would be unusual. A more plausible explanation in many patients is early mechanical trauma. After septoplasty, patients may feel: - dried blood - crusts - sutures - splints - thick mucus - obstruction - sharp or rough edges - anxiety that something is “stuck” in the nose The natural reaction is to clear it. Unfortunately, the early postoperative septum is vulnerable. Fingertip trauma can remove healing mucosa, expose cartilage, and create bilateral opposing raw areas. If this is not recognised, a small area of trauma may progress to ulceration and then perforation. The practical observation is that these areas often heal very well when protected. Silastic sheets can shield the mucosa, reduce shear, maintain a moist environment and prevent direct finger trauma. In selected cases, mucosal grafting can also help restore the epithelial surface and get the healing process back on track.

Simple silastic or silicone sheets are very helpful to ensure good healing and always best considered before crusting occurs That response undermines the simplistic idea that the problem is always poor blood supply. If the tissue heals when protected from trauma and desiccation, then the issue was not simply irreversible vascular failure.

How to talk about this with patients

The conversation has to be direct, but not judgemental. Shame makes patients deny the behaviour. Denial prevents treatment. A useful phrase is: “I can see why you are clearing it. It feels blocked and uncomfortable. The problem is that every time the crust is removed with a finger, the healing surface is pulled off again. Our goal is not just to moisturise the nose. It is to stop the wound being reset every day.” That explanation works because it validates the patient’s experience. The patient is not being accused of causing everything. They are being shown how one understandable behaviour can prevent healing. Treatment usually involves several layers: - saline irrigation or spray to soften crusts - ointment or moisturising gel to reduce dryness - avoidance of direct finger trauma - careful debridement only when appropriate - treatment of infection or inflammation if present - protection with silastic sheets in selected cases - mucosal grafting for focal non-healing areas - septal perforation repair when the underlying drivers are controlled - behavioural or psychological support when picking is compulsive For true rhinotillexomania, the issue is not solved by telling the patient to “just stop”. Compulsive picking may sit within the broader group of body-focused repetitive behaviours and may require structured behavioural therapy, habit-reversal strategies and sometimes mental health support.

A message for surgeons

Surgeons need to ask about nose picking. Not aggressively. Not sarcastically. Just plainly. In septal crusting, septal ulceration, septal perforation and early postoperative septal trauma, the question is clinically relevant. If the behaviour is not recognised, the surgeon may keep treating the crust while missing the mechanism that recreates it. This is now part of the modern septal perforation conversation. At Prof Isam Alobid’s International Septal Perforation Repair Course in Barcelona, where many of the major contemporary flap techniques are discussed, the role of crusting, mucosal injury and patient behaviour has become an important part of the discussion. I have jokingly been called the “nose picking expert” in this setting. It is not the most glamorous title in rhinology, but it is clinically useful.

Happy to known as the "Nose picking" expert, its a big part of clinical presentations. The point is simple: good surgery still needs good healing conditions. If finger trauma continues, even technically excellent surgery may fail. If the behaviour is recognised and managed, many areas of septal crusting, ulceration and early trauma can recover.

Conclusion

Nose picking is common. Most of the time, it is harmless. But in the wrong clinical setting, it becomes important. Chronic septal crusting, posterior-edge crusting in septal perforations, and early septal trauma after septoplasty are not always explained by airflow and dryness alone. The finger may be the missing mechanical factor. The best approach is not blame. It is recognition. Patients pick because something feels blocked, dry, sharp or irritating. The surgeon’s job is to explain the crust–pick–crust cycle, reduce the crusting, protect the healing surface, and use reconstructive techniques such as silastic sheeting or mucosal grafting when needed. Dry air may start the crust. The finger may stop it healing.

References

- Jefferson JW, Thompson TD. Rhinotillexomania: psychiatric disorder or habit? J Clin Psychiatry. 1995;56(2):56–59. - Andrade C, Srihari BS. A preliminary survey of rhinotillexomania in an adolescent sample. J Clin Psychiatry. 2001;62(6):426–431. - Alobid I, Arango Cabezas N, Yuen-Ato KC, Hopkins C, et al. Self-induced nasal septal perforation: rhinotillexomania — a different entity from nose picking. Laryngoscope. 2025;135(5):1590–1597. doi:10.1002/lary.31913. - Alobid I, Garaycochea O, Rojas-Lechuga MJ, Harvey RJ, Hopkins C, et al. International Consensus Statement on Nasal Septal Perforation. Rhinology. In press. - Campion NJ, Couto AM, Hua R, Qiao J, Gendeh H, Rosenbaum A, Darbari Kaul R, Alvarado R, Choy C, Sacks PL, Campbell RG, Kalish L, Harvey RJ. Free mucosal grafting as a simple adjunct to achieve rapid re-epithelialization in septal perforation repair. Laryngoscope. In press. - Downs BW, Sauder HM. Septal Perforation. In: StatPearls. Treasure Island, FL: StatPearls Publishing; updated 2023.

FAQ

Is nose picking normal?

Yes. Nose picking is common and usually harmless. It becomes medically important when repeated picking damages vulnerable nasal lining, causes bleeding, worsens crusting, or prevents a septal wound from healing.

Can nose picking cause a septal perforation?

Nose picking can contribute to septal ulceration and perforation, especially when it repeatedly injures the same area of the anterior septum. It is rarely the only factor. Surgery, intranasal drugs, inflammation, infection, trauma and sprays may also contribute.

Why does septal crusting keep coming back?

Septal crusting can recur because of dryness, abnormal airflow, inflammation, exposed cartilage, infection or repeated mechanical trauma. In some patients, removing the crust with a finger repeatedly resets the wound surface and prevents stable healing.

Why does the back edge of a septal perforation crust?

The back edge of a septal perforation may crust because airflow through the perforation dries mucus. In some patients, however, the posterior edge is also repeatedly reached and traumatised by a finger when the patient tries to clear the crust.

Can picking after septoplasty cause problems?

Yes. Early after septoplasty, the nasal lining is healing and may be vulnerable. Picking at crusts, dried blood or sutures can injure the mucosa and, in some cases, contribute to septal ulceration or perforation.

How can septal crusting be treated?

Treatment usually includes saline sprays or irrigations, moisturising ointment or gel, treatment of infection or inflammation, and avoidance of direct trauma. In selected cases, silastic sheets or mucosal grafting may help protect and restore the healing surface.

Achieving a bloodless surgical field in endoscopic sinus surgery

Why the surgical field matters in sinus surgery

Endoscopic sinus surgery is performed through narrow corridors, close to the orbit, skull base, optic nerve, carotid artery and anterior ethmoidal artery. In this environment, bleeding is not just an inconvenience. It degrades orientation.

A poor field makes it harder to recognise anatomical landmarks, identify sinus outflow pathways, complete the operation efficiently and avoid complications. It may also increase postoperative scarring and the risk of incomplete surgery. These principles have been central to rhinology teaching for decades: haemostasis affects visibility, operative time, completeness of surgery and the surgeon’s ability to stay oriented during dissection.

The aim is not simply to reduce the number of millilitres of blood loss. A case can have modest total blood loss but still have a poor endoscopic field if there is persistent mucosal ooze across the lens and operative target. The real goal is a quiet field where anatomy remains visible and decisions remain precise.

This is why many rhinologists use the Boezaart scale, also known as the Fromme-Boezaart scale, to describe intraoperative bleeding. It is a 0-to-5 surgical field scale in which 0 represents no bleeding and 5 represents severe bleeding that prevents surgery. It was popularised in endoscopic sinus surgery by Boezaart and colleagues in their comparison of sodium nitroprusside- and esmolol-induced controlled hypotension for functional endoscopic sinus surgery.¹

A movement from a Boezaart 3 or 4 field to a Boezaart 1 or 2 field is not a small change. It is often the difference between repeatedly suctioning blood and being able to operate deliberately.

A bloodless field is built in layers

No single manoeuvre reliably creates the ideal field. The best results come from stacking several modest but evidence-supported interventions:

early topical vasoconstriction and local mucosal injection reverse Trendelenburg positioning perioperative tranexamic acid bradycardic, carefully controlled anaesthesia mucosal-preserving surgical technique

Each component may improve the surgical field by a modest amount. Across the operation, the cumulative difference can be large. It is reasonable to think of many of these interventions as moving the field by roughly half a Boezaart grade or more, depending on the patient and disease process.

That is not a formal mathematical equation. The trials do not prove simple additivity across all interventions. But clinically, the cumulative effect is obvious. A case performed flat, with inhalational anaesthesia, no tranexamic acid, late or weak vasoconstriction and mucosal stripping is a different operation from one performed with a complete haemostatic strategy.

1. Start early: topical vasoconstriction and local mucosal injection

The nose is highly vascular. The sinonasal mucosa contains resistance vessels, capacitance vessels, venous sinusoids and mucosal microvasculature. Effective vasoconstriction needs to start before the first incision or instrument trauma.

Our principle is early application of high-concentration, non-selective alpha agonist vasoconstriction, most commonly topical adrenaline / epinephrine where appropriate. The rationale is that alpha-1 activity constricts resistance vessels, while alpha-2 activity contributes to venous capacitance vessel constriction. By contrast, partial alpha agonists such as oxymetazoline and phenylephrine are useful decongestants but may produce less complete mucosal vasoconstriction than adrenaline-based preparation.²

In our practice, topical preparation commonly uses 1:2000 adrenaline with 1% ropivacaine. This is applied early and allowed time to work. Topical preparation remains the most important local step because it treats a broad mucosal surface before bleeding has started.

For clarity, 1:2000 adrenaline is equivalent to 0.5 mg/mL adrenaline. 1% ropivacaine is equivalent to 10 mg/mL ropivacaine. These concentrations require local institutional approval, anaesthetic awareness and disciplined use. The purpose of providing the details is to describe a reproducible rhinology workflow, not to replace local medication governance.

Local mucosal injection is then used as a second step, not as a substitute for topical preparation. A typical 10 mL syringe mixture is:

8 mL of 1% ropivacaine 1 mL of 1:10,000 adrenaline 1 mL of tranexamic acid, using 1 mL from a 1000 mg / 10 mL ampoule, equivalent to 100 mg TXA

This gives a final 10 mL solution containing:

ropivacaine: 80 mg total, or 8 mg/mL, equivalent to 0.8% adrenaline: 0.1 mg total, or 10 micrograms/mL, equivalent to 1:100,000 tranexamic acid: 100 mg total, or 10 mg/mL, equivalent to 1%

The raw ingredients are often more useful to surgeons than the final concentrations because they allow the mixture to be replicated consistently within local pharmacy and anaesthetic governance. The dose still needs to be checked against patient weight, cardiovascular risk, renal function, maximum local anaesthetic dosing, anticoagulant status and institutional protocols.

Topical adrenaline in nasal surgery has been studied for systemic catecholamine effects. Van Hasselt and colleagues compared plasma catecholamine levels after topical application versus infiltration of adrenaline for nasal surgery.³ The practical point is not that topical adrenaline is risk-free; it must be used with appropriate anaesthetic communication, dosing discipline and cardiovascular awareness. But when used correctly, it remains one of the most effective tools for mucosal preparation.

The sequence also matters. If a weaker partial agonist is applied first, there is a theoretical risk of occupying receptors before a stronger non-selective vasoconstrictor is used. This is one reason many high-volume rhinology units standardise preparation rather than relying on ad hoc topical sprays immediately before surgery.

2. Position: reverse Trendelenburg is not cosmetic

Positioning is one of the simplest and most underused interventions for surgical field quality.

A 15- to 20-degree reverse Trendelenburg position reduces venous congestion and improves the endoscopic field. Hathorn and colleagues randomised patients undergoing FESS to 15-degree reverse Trendelenburg or horizontal positioning and concluded that the 15-degree reverse Trendelenburg position improved the field of view and reduced blood loss.⁴ Gan and colleagues later studied 5-, 10- and 20-degree reverse Trendelenburg positioning in a double-blind randomised controlled trial.⁵

The mechanism is straightforward. Head-up positioning lowers venous pressure in the operative field. In prior surgical teaching material, reverse Trendelenburg positioning is highlighted as reducing central venous pressure and nasal mucosal blood flow. The practical clinical effect is that less venous congestion is delivered into the operative field.

Ideal positioning for hemostatic control is 15-20deg and appears more than expected. simple iphone utilities help with inital judgement

The important clarification is that reverse Trendelenburg is not the same as dangerous cerebral hypoperfusion. A 15- to 20-degree head-up position is generally well tolerated under modern anaesthesia, with the anaesthetist maintaining appropriate cerebral perfusion and systemic parameters. The aim is controlled venous unloading, not extreme hypotension.

In practical terms, this is often the single easiest improvement to implement. If the patient is flat, the surgeon is already accepting avoidable venous congestion.

3. Tranexamic acid: antifibrinolysis for a better field

Tranexamic acid is a synthetic lysine analogue that inhibits fibrinolysis by blocking plasminogen binding to fibrin. It stabilises clot rather than causing vasoconstriction.⁶

For endoscopic sinus surgery, the strongest current evidence is the 2023 Cochrane review by Lourijsen and colleagues. It included 14 randomised controlled trials with 942 participants. Tranexamic acid, administered topically or intravenously, probably reduced surgical field bleeding score, with a standardised mean difference of -0.87 using Boezaart or Wormald grading systems. It also reduced intraoperative blood loss by a mean of 70.32 mL and reduced operative time by about 13 minutes. No seizures or thromboembolic events were reported within 24 hours in the included studies, although longer-term adverse-event data were limited.⁷

The usual perioperative dose used in many sinus surgery studies is approximately 10–15 mg/kg intravenously at induction, commonly translating to about 1000 mg in an adult. This should still be individualised for renal function, thrombotic history and local anaesthetic protocols.

The pooled result demonstrated that tranexamic acid probably reduces the surgical field bleeding score, with a standardised mean diHerence (SMD) of -0.87 (95% confidence interval (CI) -1.23 to -0.51; 13 studies, 772 participants; moderate-certainty evidence). A SMD below -0.70 represents a large eHect (in either direction).

The safety profile of intravenous tranexamic acid has also been examined beyond rhinology. Taeuber and colleagues analysed 216 randomised trials involving 125,550 patients and found no association between intravenous tranexamic acid and increased overall thromboembolic events; events occurred in 2.1% of TXA patients versus 2.0% of controls.⁸ That does not remove the need for case selection, but it counters the common reflex that TXA is inherently unsafe.

The practical message is simple: tranexamic acid is cheap, pharmacologically rational and supported by sinus surgery-specific Cochrane evidence.

4. Anaesthesia: hypotension is not the whole goal

The old phrase “hypotensive anaesthesia” can be misleading. In sinus surgery, the goal is not simply to push the blood pressure as low as possible. The field is influenced by cardiac output, heart rate, venous pressure, mucosal vasodilation, anaesthetic technique and local surgical trauma.

A more accurate target is often bradycardic, mildly hypotensive, low-flow physiology under carefully monitored anaesthesia.

Total intravenous anaesthesia, particularly propofol-remifentanil-based techniques, has repeatedly shown advantages in surgical field visibility compared with inhalational anaesthesia. Kolia and Man’s 2019 meta-analysis of randomised trials found TIVA superior to inhalational anaesthesia for visual field, estimated blood loss and operative time.⁹ Moffatt and colleagues’ 2021 meta-analysis similarly found that TIVA had superior intraoperative visibility scores and blood loss compared with inhalational anaesthesia.¹⁰

There is also Cochrane-level evidence that deliberate hypotension with propofol can improve the surgical field in FESS.¹¹ But the nuance matters: hypotension without control of heart rate and venous congestion is not the same as a good endoscopic field. Esmolol-based approaches in the original Boezaart work are relevant because they emphasise the importance of heart rate and flow, not merely arterial pressure.¹

The anaesthetic plan should therefore be discussed before the case begins. The surgeon and anaesthetist should agree on the field objective, expected complexity, acceptable haemodynamic range and whether TIVA, remifentanil, beta-blockade or other approaches are appropriate for the patient.

5. Technique: do not create bleeding that drugs cannot fix

The final step is surgical discipline.

Vasoconstrictors work on smooth-muscle-containing vessels. They do not solve bleeding from stripped mucosa, exposed cancellous bone or bony Haversian channels. Once mucosa is avulsed and raw bone is exposed, the surgeon has created a bleeding surface that is less responsive to topical vasoconstriction.

The principle is simple: preserve mucosa wherever possible.

This means biting rather than pulling, using through-cutting forceps correctly, avoiding mucosal stripping, using the microdebrider in a controlled fashion, maintaining a clean suction tip, and respecting tissue planes. In prior teaching material, the surgical message was deliberately blunt: “No stripping of mucosa” and “mucosa-bone-mucosa.”

This is not just aesthetic surgical technique. It is haemostatic technique. A surgeon who strips mucosa creates their own bleeding problem and then blames the anaesthetist.

What the Boezaart scale teaches us

The Boezaart scale is useful because it converts a subjective frustration into a shared operative language. A one-point difference is clinically meaningful. A two-point difference is major.

The evidence for any individual intervention is often modest: a better field with reverse Trendelenburg, a better field with TIVA, a better field with tranexamic acid, a better field with proper vasoconstriction and careful technique. But in real surgery these do not occur in isolation. They stack.

The goal is not to perform surgery in a dry-looking field for cosmetic satisfaction. The goal is orientation. The cleaner the field, the easier it is to identify the skull base, lamina papyracea, frontal recess, sphenoid face, posterior ethmoid partitions and vascular landmarks.

That is the difference between operating on anatomy and operating through blood.

Patient factors still matter

Not every case can be made bloodless. Severe eosinophilic polyposis, active infection, fungal disease, revision surgery, anticoagulation, hypertension, vascular tumours and distorted anatomy all increase bleeding risk.

Preoperative medical optimisation may help in selected patients, particularly those with nasal polyposis. Earlier evidence syntheses have suggested that preoperative steroids may improve blood loss, operative time and surgical field grade in polyp surgery, although this needs to be balanced against the goal of preserving tissue for biopsy, histology and endotyping in modern CRS care.¹²

A bloodless field is therefore not simply an anaesthetic trick or a drug protocol. It starts with correct patient selection, control of inflammation where appropriate and knowing what disease process is being operated on.

Why patients should care

Patients do not usually ask about Boezaart scores. They ask whether surgery will be safe and effective.

A clear surgical field contributes directly to that. It allows the surgeon to see the skull base, orbit, lamina papyracea, frontal recess, sphenoid face, posterior ethmoid partitions and vascular landmarks. It helps the surgeon complete the planned dissection rather than stopping early because the field is unsafe. It reduces unnecessary trauma and may reduce operative time.

For surgeons, the surgical field is a technical outcome. For patients, it is a safety outcome.

What about PPF injections?

Pterygopalatine fossa injection can be a useful adjunct in selected sinus surgery cases, but it is not required in every operation and should not be presented as one of the core five steps.

The injection is performed by infiltration through the greater palatine canal, targeting the pterygopalatine fossa region. It is sometimes loosely referred to as a “PPF injection,” but the practical route is the greater palatine canal.

We use this selectively when initial topical vasoconstriction or local mucosal injection is difficult, such as in patients with a very large polyp load, obstructing inflammatory disease or selected vascular tumour cases. In these situations, the early field can be poor before the surgeon has adequate access to place topical patties or perform precise local infiltration.

There is evidence supporting both haemostatic and analgesic benefit. Hwang and colleagues’ systematic review and meta-analysis found that greater palatine canal injections with local anaesthetic and vasoconstrictor reduced operative bleeding during endoscopic sinus surgery.¹³ A separate meta-analysis of sphenopalatine block in endoscopic sinus surgery found reductions in intraoperative bleeding, postoperative pain, nausea and vomiting, and recovery from sedation, without significant adverse effects in the included studies.¹⁴

The technique is demonstrated in this prior teaching video:

This video uses the phrase “PPF canal,” but anatomically the injection is performed through the greater palatine canal to access the pterygopalatine fossa region. The technique should be framed as an adjunct, not a replacement for the core haemostatic strategy. The main pillars remain topical vasoconstriction, reverse Trendelenburg positioning, tranexamic acid, appropriate anaesthesia and mucosal-preserving surgical technique.

The practical recipe

A reproducible approach to endoscopic sinus surgery haemostasis is:

prepare the mucosa early with effective topical vasoconstriction use local mucosal injection when appropriate place the patient in 15–20 degrees reverse Trendelenburg consider perioperative tranexamic acid, commonly 10–15 mg/kg or about 1 g IV, where not contraindicated use TIVA and aim for controlled bradycardic, mildly hypotensive physiology rather than crude hypotension alone preserve mucosa and avoid exposing raw bone unnecessarily consider greater palatine canal / pterygopalatine fossa injection as an adjunct in selected cases where early topical or local access is difficult

The best field is not achieved by one heroic manoeuvre. It is achieved by making several sensible decisions before and during every case.

A bloodless field is not about making surgery look elegant. It is about making endoscopic sinus surgery safer, more efficient, more complete and more anatomically controlled..

Related articles

Chronic rhinosinusitis https://richardharvey.sydneyentclinic.com/2022/02/12/do-i-really-have-sinusitis-chronic-sinus-symptoms/

References

When the nose feels blocked but the airway is open: functional nasal obstruction and low-value nasal surgery

A common referral in tertiary rhinology is the patient who says: “I am a mouth breather,” “I never get enough oxygen,” or “my nose is ruining my sleep and energy.” Sometimes that patient has obvious nasal obstruction: a severe septal deviation, enlarged inferior turbinates, nasal polyps, allergic rhinitis or nasal valve collapse. In that setting, treatment can be high value.

But sometimes the nasal airway is already open.

The examination is unremarkable. The nose looks patent on endoscopy. Objective airflow testing is normal or near normal. The patient’s main concern is not really a blocked nostril, but fatigue, poor sleep, low energy, breathlessness, anxiety about breathing, or a general sense of not getting enough air.

That is a different clinical problem.

The nose filters, warms, humidifies and senses airflow. It is important for comfort, smell, airway protection and perceived sleep quality. But the nose does not oxygenate the blood. Gas exchange occurs in the lungs. Widening an already adequate nasal airway is unlikely to fix tiredness, poor energy, unexplained breathlessness or the feeling of “not getting enough oxygen.”

This is where Ray’s Rules become useful.

The turbinates are dynamic, not fixed

The inferior turbinates are vascular organs. They are not simply “large” or “small.” Their size changes through the day depending on posture, autonomic tone, allergy, rhinitis, irritants, infection, medication use and the normal nasal cycle.

Two normal physiological processes are especially important.

The first is the nasal cycle. This is the spontaneous alternating congestion and decongestion of the nasal mucosa. One side of the nose becomes more congested while the other side opens. This is driven by dilation and constriction of venous cavernous tissue in the turbinates and septum. Approximately 70–80% of healthy adults demonstrate a nasal cycle, although the pattern is not always perfectly regular or symmetrical. The cycle length may vary from 30 minutes to several hours.¹

The second is postural congestion. When a person moves from sitting upright to lying flat, central venous pressure may increase by up to approximately 8 mmHg because of hydrostatic pressure. This increases congestion of the nasal mucosa and nasal airway resistance. The effect is often greater when lying on one side, where the lower, dependent nasal cavity becomes more congested.¹,²

These normal physiological changes are amplified when the nasal lining is already inflamed or vascularly reactive, as occurs in allergic rhinitis, non-allergic rhinitis and inferior turbinate hypertrophy.

This explains why patients with true turbinate-driven obstruction often say:

“It swaps sides.” “It is worse when I lie down.” “It blocks on the side I sleep on.” “A decongestant spray opens it clearly.”

That history is not incidental. It is diagnostic information.

Ray’s Rules: a practical test of turbinate physiology

Ray’s Rules are a simple clinical heuristic for deciding whether a patient’s symptoms behave like vascular turbinate obstruction.

They ask whether the patient has:

Cycling nasal congestion — the blocked side changes from side to side. Postural congestion — the nose blocks when lying flat or on the dependent side. A clear response to topical decongestant — the airway improves when the vascular turbinate component is temporarily reduced.

These features suggest that the patient has an intact sensory perception of nasal airflow and a dynamic turbinate component to their obstruction. In other words, the symptoms behave like turbinate disease.³,⁴

This does not mean that every patient with positive Ray’s Rules needs surgery. Many still need medical management first: saline irrigation, intranasal corticosteroids, antihistamines, allergen avoidance, immunotherapy where appropriate, and treatment of rhinitis. But if symptoms persist despite well-conducted medical therapy, and the examination confirms inferior turbinate hypertrophy, turbinate reduction may be a rational intervention.

The important point is the reverse: patients who do not demonstrate these features may be poor candidates for turbinate surgery, particularly when objective findings are mild.

Ray's rules provide a simple pathophysioology linked screen for patients likely to benefit from turbinate reduction

When nasal surgery is more likely to be high value

Nasal surgery is more likely to be high value when there is a match between the patient’s symptoms, examination and objective findings.

For example, a patient with visible inferior turbinate hypertrophy, alternating nasal obstruction, night-time postural blockage and a strong response to decongestant has a plausible vascular turbinate problem. If medical treatment fails, turbinate reduction may address the mechanism of obstruction.

Similarly, a patient with a clear anterior septal deviation, nasal valve compromise, or fixed unilateral obstruction has a structural problem that may be improved by septoplasty, septorhinoplasty or valve surgery.

In both settings, the treatment target is clear: improve nasal airflow through a mechanically or physiologically obstructed nasal airway.

When nasal surgery may be low value

Surgery becomes low value when the patient’s main symptoms are not actually explained by the nose.

A common example is the patient who presents with “nasal congestion” but, on closer questioning, is primarily concerned about:

poor sleep waking unrefreshed fatigue low daytime energy reduced exercise tolerance breathlessness feeling they are “not getting enough oxygen” anxiety around breathing a general belief that mouth breathing is damaging their health

Many of these patients have become more aware of nasal breathing through popular health culture. Books such as James Nestor’s Breath: The New Science of a Lost Art have brought attention to nasal breathing, slow breathing, mouth breathing, breathwork and the relationship between breathing habits and health.⁵ This public discussion has been useful in many respects. Nasal breathing is physiologically preferable to chronic mouth breathing. It filters and humidifies air, supports nasal airflow sensation, and contributes to airway comfort.

But the popular message can become distorted. Some patients begin to attribute almost every symptom — fatigue, poor sleep, reduced concentration, exercise limitation, anxiety or “low oxygen” — to minor nasal findings. That is not good medicine.

If the nasal airway is open, airflow testing is normal, and the patient does not describe cycling congestion, postural congestion or decongestant response, then turbinate surgery is unlikely to solve the true problem. In that situation, it is more useful to look for other contributors: sleep apnoea, insomnia, stress, anxiety, poor sleep routine, medication effects, cardiopulmonary disease, anaemia, endocrine issues, deconditioning or broader health factors.

Telling the patient that nasal surgery is not indicated is not dismissive. It may be the most honest and protective answer.

Nasal breathing and sleep: important, but not magic

There is good evidence that treating nasal disease can improve subjective sleep quality. A systematic review and meta-analysis of allergic rhinitis and nasal septal deviation found that treatment improved patient-reported sleep measures, including Epworth Sleepiness Scale and Pittsburgh Sleep Quality Index scores.⁶

However, the same review found insufficient evidence that objective sleep metrics improve in the same way.⁶ This distinction matters.

A patient may feel that sleep is better after nasal treatment. That is a valid outcome. Better nasal airflow can reduce discomfort, reduce mouth breathing, improve CPAP tolerance in selected patients, and improve sleep-related quality of life. But improvement in nasal airflow sensation is not the same as better sleep function.

But nasal surgery should not be presented as a reliable treatment for objective sleep architecture, oxygenation, sleep apnoea or global fatigue unless the broader sleep disorder has been properly assessed. The nose contributes to sleep comfort. It is not the whole sleep system.

Functional nasal obstruction and unrealistic expectations

The most difficult group is the patient with severe symptoms, minimal objective obstruction and high expectations of benefit from surgery.

Some patients describe nasal obstruction in a way that resembles breathlessness, air hunger or anxiety about breathing. In the empty nose syndrome and functional nasal obstruction literature, this mismatch between symptoms and objective findings has become increasingly important. Patients may present before surgery with nasal airflow symptoms that are not explained by anatomy, then remain symptomatic or worsen after a technically adequate septal or turbinate procedure.³,⁴

This does not mean the symptoms are fake. It means the mechanism may not be surgically correctable.

In this setting, further surgery can be harmful. It may reinforce the belief that the problem is purely structural, create disappointment when the expected gains in sleep or energy do not occur, and expose the patient to the risks of an operation without a realistic chance of solving the primary complaint.

Ray’s Rules help identify the patient whose symptoms behave like turbinate physiology. They also help identify the patient in whom turbinate surgery may be the wrong tool. A terrific summary article by Professor Sacks is availiable here.

Why the profession needs to own this problem

Functional nasal surgery is under increasing scrutiny. In 2025, ENT UK expressed concern about South-East England ICB decisions to suspend funding for septoplasty, turbinate surgery and functional septorhinoplasty.⁷ Media coverage reported that some patients would receive NHS septoplasty funding only in exceptional circumstances.⁸

Blunt funding restrictions are not the right way to manage nasal obstruction. Some patients have severe, genuine, surgically correctable nasal airway disease. They need access to high-value nasal surgery.

But the profession also needs to be clear about where surgery is less likely to help. If surgeons do not define high-value nasal surgery carefully, funders may define it crudely.

A simple heuristic of “failed nasal steroid spray, therefore septoplasty and turbinate reduction” is not enough. Good decision-making should include the patient’s symptom pattern, endoscopy, objective airflow assessment where appropriate, response to decongestant, allergy/rhinitis evaluation and the patient’s expectations of benefit.

The practical message

Ray’s Rules are not a formal score. They are a practical clinical safeguard.

If the nose blocks from side to side, worsens with posture, and opens with decongestant, the symptoms are behaving like turbinate physiology. If examination confirms turbinate hypertrophy and medical therapy has failed, turbinate surgery may be a reasonable high-value intervention.

If the patient’s main concern is sleep, fatigue, tiredness, breathlessness or not getting enough oxygen, and the nasal airway is objectively adequate, nasal surgery is unlikely to solve the real problem.

A good rhinologist does not just widen noses. A good rhinologist decides when widening the nose is likely to help — and when it is not.

References

Pendolino AL, Lund VJ, Nardello E, Ottaviano G. The nasal cycle: a comprehensive review. Rhinology Online. 2018;1:67–76. doi:10.4193/RHINOL/18.021. Harvey RJ, Roland LT, Schlosser RJ, Pfaar O. Chief Complaint: Nasal Congestion. J Allergy Clin Immunol Pract. 2024;12(6):1462–1471. doi:10.1016/j.jaip.2024.04.028. Kanjanawasee D, Campbell RG, Rimmer J, Alvarado R, Kanjanaumporn J, Snidvongs K, Kalish L, Harvey RJ, Sacks R. Empty nose syndrome pathophysiology: a systematic review. Otolaryngol Head Neck Surg. 2022;167(3):434–451. doi:10.1177/01945998211052919. Png LH, Kalish L, Sacks R. Empty nose syndrome: the case for “functional nasal obstruction” as a predisposing risk prior to nasal surgery. Curr Otorhinolaryngol Rep. 2023;11:422–429. doi:10.1007/s40136-023-00487-w. Nestor J. Breath: The New Science of a Lost Art. New York: Riverhead Books; 2020. Fried J, Yuen E, Zhang K, Li A, Rowan NR, Schlosser RJ, Nguyen SA, Gudis DA. Impact of treatment for nasal cavity disorders on sleep quality: systematic review and meta-analysis. Otolaryngol Head Neck Surg. 2022;166(4):633–642. doi:10.1177/01945998211029527. ENT UK. Statement concerning the suspension of funding for functional nasal surgery. Published 10 October 2025. Tapper J. NHS cuts will “severely impact” those who struggle to breathe. The Observer. Published 6 October 2025

FAQ

What is functional nasal obstruction?

Functional nasal obstruction describes a situation where a patient feels significantly blocked, but the nasal airway is open or near normal on examination and objective testing. The symptom is real, but the mechanism may not be a surgically correctable narrowing of the nose.

What are Ray’s Rules?

Ray’s Rules are a practical rhinology heuristic used to identify whether symptoms behave like turbinate-driven obstruction. The three features are cycling nasal congestion, postural congestion and a clear response to topical nasal decongestant.

What is cycling nasal congestion?

Cycling nasal congestion means the blocked side changes from one side of the nose to the other. This often reflects the normal nasal cycle, where one side of the nose becomes more congested while the other side opens.

What is postural nasal congestion?

Postural nasal congestion is nasal blockage that worsens when lying flat or lying on one side. It occurs because venous pressure and vascular congestion increase in the nasal lining, especially around the inferior turbinates.

Does a blocked nose cause low oxygen levels?

Usually no. The nose filters, warms, humidifies and senses airflow, but gas exchange occurs in the lungs. A blocked nose can affect comfort, perceived sleep quality and mouth breathing, but persistent breathlessness or concern about oxygen levels should be assessed beyond the nose.

Can nasal surgery improve sleep?

Nasal surgery and rhinitis treatment can improve patient-reported sleep quality in selected patients. However, evidence that nasal surgery reliably improves objective sleep measurements, sleep architecture or oxygenation is limited.

When is turbinate surgery more likely to help?

Turbinate surgery is more likely to help when symptoms behave like turbinate physiology: the blockage cycles from side to side, worsens with posture, improves with decongestant, and examination confirms inferior turbinate hypertrophy.

When is nasal surgery less likely to help?

“Septal deviation and big turbinates” is not a diagnosis: why nasal obstruction often returns after surgery

One of the commonest referral patterns I see as a tertiary rhinologist is the patient who has had nasal surgery, initially felt better, and then slowly developed the same sense of nasal blockage again. These patients often arrive disappointed, sometimes angry, and usually confused. They have been told they had a “septal deviation and big turbinates”, underwent septoplasty, turbinate reduction or both, and expected a durable solution.

The problem is that “septal deviation and enlarged turbinates” is not a diagnosis. It is a description of anatomy.

That distinction matters. A diagnosis should explain why the nose feels blocked, why the problem developed, why it behaves the way it does, and why a particular treatment should work. A deviated septum may explain unilateral nasal obstruction, particularly if it follows trauma or has been present since adolescence. But it is a weaker explanation for progressive, bilateral nasal congestion that has developed over time without injury.

When the obstruction is generalised, alternates from side to side, worsens when lying flat, or is clearly affected by irritants, seasons or indoor environments, the cause is usually more than fixed anatomy. It is often rhinitis. The next question should be: what type of rhinitis, and what is driving it?

Congestion and obstruction are not always the same thing

Patients and clinicians often use the same words differently. Patients may use “congestion” to mean blocked airflow, pressure in the face, mucus in the throat, heaviness in the head or even headache. In contrast, rhinologists usually reserve “obstruction” for impaired nasal airflow and “congestion” for mucosal swelling or vascular engorgement.

This mismatch has been formally described. In a study of how patients and clinicians define “nasal congestion”, patients were much more likely than clinicians to include pressure-related symptoms, mucus-related symptoms and other non-obstructive symptoms in their definition of congestion. This is why a patient can have a scan report mentioning a deviated septum or turbinate hypertrophy and still not have a useful diagnosis. The finding may be real, but it may not be the dominant cause of the symptom.

This issue is also central to our forthcoming Medicine Today feature article, How we breathe: Nasal congestion and treatment strategies, selected as the May feature article. The article emphasises that nasal congestion is more than a blocked nose: patient perceptions of pressure, mucus and airflow often diverge from clinical definitions, complicating diagnosis and management.

A practical distinction is this: a fixed anatomical obstruction tends to be consistent, often affecting one side more than the other, and may relate to trauma, nasal development, prior rhinoplasty or valve collapse. A physiological or inflammatory obstruction tends to vary. It may cycle from side to side, worsen when lying down, respond temporarily to decongestant spray, fluctuate with allergen exposure, or worsen in certain environments.

The second pattern is commonly turbinate-based and vascular, but the driver is often inflammatory, allergic, neurogenic or irritant-related rather than simply “large turbinates”.

The nose is not just a pipe

A simple but misleading model is that nasal breathing improves if the surgeon makes a larger tunnel. That is only partly true.

Humans do not directly “measure” airflow through mechanical airflow receptors in the nose. The sensation of clear nasal breathing is strongly influenced by cooling of the nasal lining as air passes across the mucosa. Trigeminal cold receptors, including TRPM8 receptors, help generate the perception of nasal patency. This explains why menthol, eucalyptus or similar products can make the nose feel clearer without objectively increasing airflow.

The nose on the left is not affected by allergy and has normal mucosa. The patient on the right has normal airflow but feels congested due the rhinitis reaction.

It also explains why surgery that creates space but does not restore healthy airflow over responsive mucosa may not solve the patient’s perceived congestion. Inflamed mucosa, thick mucus, vascular engorgement and tissue remodelling can all reduce the cooling signal. The patient may feel blocked even when the airway is not severely narrowed.

Conversely, after turbinate surgery, the early mechanical improvement may be obvious. But if the allergic or inflammatory drive persists, mucosal swelling and tissue remodelling can return.

The common mistake: treating the consequence, not the disease

Inferior turbinate hypertrophy is often the visible consequence of a long-standing mucosal disease. In allergic rhinitis, repeated allergen exposure can produce chronic inflammation, venous engorgement, glandular change and tissue remodelling. The turbinate becomes the visible structure that attracts surgical attention, but the allergy is the engine that keeps driving the process.

This is especially relevant in patients who do not present with classic “hay fever”. Many allergic patients do not volunteer itch, sneeze, watery rhinorrhoea or conjunctivitis. Their dominant symptom is obstruction. They may not intuitively think of allergy, and if the clinician does not test or examine for it, the disease is missed.

A more accurate formulation for many of these patients is not “septal deviation and big turbinates”. It is closer to:

Persistent rhinitis, often allergic or locally allergic, with turbinate and septal swell body tissue remodelling producing dynamic bilateral nasal obstruction.

That diagnosis leads to a different treatment plan.......not just surgery.

A negative allergy test does not always exclude allergy in the nose

Skin-prick testing and serum-specific IgE testing are important, but they are not perfect reflections of what is happening in the nasal mucosa. Some patients have negative skin and blood allergy tests but still react to allergen challenge directly in the nose. This is known as local allergic rhinitis.

Although epicutaneous tests for allergy are the gold standard, many patients with clear allergic rhinitis will have negative skin and serum tests. This doesnt mean that they dont have allergy, its just not present in surrogate markers for allergy in the nose. It can be as high 30%.

The concept is often referred to as “entopy” — allergy localised to the target organ rather than detectable systemically. A useful Australian shout-out belongs to Professor Simon Carney, whose work helped establish the idea that patients could show evidence of allergy in the absence of conventional systemic atopy. The term “entopy” was later used in the local allergy paradigm literature to describe this nose-localised allergic response.

This matters clinically. If a patient has a strongly allergic history — for example, seasonal symptoms, indoor dust mite pattern, morning congestion, turbinate oedema or mucus changes on endoscopy — a negative skin or serum test should not automatically close the door on allergy.

Hamizan and colleagues systematically reviewed nasal allergen provocation testing in allergic and non-allergic rhinitis. Across 46 studies, nasal allergen reactivity was present in 86.3% of patients classified as allergic rhinitis by systemic testing, but also in 24.7% of patients classified as non-allergic rhinitis. The authors concluded that local allergen reactivity is demonstrated in about one quarter of patients previously considered non-allergic.

That finding is not academic hair-splitting. It changes how patients should be treated. A patient labelled “non-allergic” may still have an allergic reaction in the nose and may still be suitable for allergy-directed therapies.

Why turbinate surgery can feel good — then fade

Turbinate reduction can be very effective. It creates space, reduces vascular tissue volume, and can improve nasal airflow. The issue is not that turbinate surgery is poor surgery. The issue is that it is often being asked to do the wrong job.

Surgery can reduce the tissue burden. It does not, by itself, switch off the allergic or inflammatory process that enlarged the tissue in the first place.

The long-term data are important here. De Corso and colleagues prospectively followed 305 patients with rhinitis who underwent radiofrequency volumetric inferior turbinate reduction. Early results were favourable, with significant improvement in nasal stuffiness, nasal obstruction and mouth breathing. But symptoms worsened after 36 months, with progressive recurrence, especially in allergic patients.

The relapse-free probability is the key figure. In the whole cohort, the cumulative probability of remaining relapse-free was 0.848 at 36 months but fell to 0.531 at 60 months. In allergic patients, it fell from 0.807 at 36 months to 0.357 at 60 months. In plain terms, the benefit was real, but it diminished over time, and allergic rhinitis was associated with worse durability.

This does not mean turbinate surgery “failed”. It means the underlying biology kept operating.

The diminshing effects of a simple turbinate procedure over time (De Corso E, Bastanza G, Di Donfrancesco V, Guidi ML, Morelli Sbarra G, Passali GC, et al. Radiofrequency volumetric inferior turbinate reduction: long-term clinical results. Acta Otorhinolaryngol Ital. 2016;36(3):199-205.)

A later systematic review of surgical interventions for inferior turbinate hypertrophy also supports the general effectiveness of turbinate surgery, showing meaningful improvements in subjective nasal obstruction and objective airflow measures across multiple techniques. But this should not be interpreted as a licence to label every bilateral blocked nose as a turbinate problem. The better conclusion is that turbinate surgery works best when the turbinate is genuinely the limiting structure and the disease process driving turbinate swelling has been identified.

This is the clinical pattern patients often describe: “It worked at first, then slowly stopped working.”

That slow loss of benefit should not automatically be interpreted as poor surgical technique. In many cases, the real problem is that the underlying rhinitis was never properly diagnosed, treated or modified.

Why intranasal steroid failure does not prove the problem is surgical

Another common heuristic is: try a nasal steroid spray; if it does not work, diagnose septal deviation and enlarged turbinates; then operate.

That is too simplistic.

A failed nasal spray trial does not prove that anatomy is the primary cause. It may mean the spray was poorly delivered, poorly adhered to, not strong enough, not the right treatment for the mechanism, or introduced too late to reverse established tissue remodelling. Or simply the initial benefit is not in align with patient expectations.

But patients with normal airflow on testing are the greatest risk from low benefit from septal and turbinate surgery in particular.

In persistent allergic rhinitis, especially house dust mite–driven disease, the relevant question is often not “did a spray help?” but “is this a chronic allergic airway disease requiring disease modification?”

Allergen immunotherapy is fundamentally different from symptom suppression. Antihistamines and intranasal corticosteroids may reduce symptoms while being used. Immunotherapy aims to reduce the immune response to the allergen itself. That is why, in selected patients, it should be considered earlier rather than after years of progressive tissue change.

This does not mean every patient needs immunotherapy. It means the diagnosis should be made properly before surgery is offered as the next step.

The pattern that should make clinicians pause

A simple septal deviation can explain unilateral obstruction. A single-sided blocked nose after trauma is a different problem from a patient who says:

“My nose blocks on both sides.”

“It changes sides.”

“It is worse lying flat.”

“It is worse overnight or in the morning.”

“It improves briefly with decongestant spray.”

“It has slowly developed over years.”

“I never had trauma.”

“I had turbinate surgery and it helped for a while, then wore off.”

That pattern should trigger a rhinitis workup, not just an anatomical label.

Assessment may include nasal endoscopy, allergy testing, objective airflow testing where available, decongestant response, and careful separation of airflow symptoms from pressure, mucus, sleep, fatigue and anxiety-related breathing concerns.

Rhinomanometry and nasal peak inspiratory flow can be useful because they test whether obstruction is truly airflow-related and whether it is reversible. This matters before offering more surgery to a patient whose main symptom may not be mechanical obstruction.

Surgery still has a role — but it must be integrated

The correct conclusion is not “avoid turbinate surgery”. That would be just another simplistic rule.

Turbinate surgery can be valuable when tissue remodelling has become a major contributor to obstruction. In some patients, immunotherapy or pharmacotherapy improves the inflammatory component, but the remodeled turbinate or septal swell body remains too bulky. In those patients, surgery can restore airflow while disease-modifying therapy reduces the risk of the same process recurring.

This is also why the sequence of care matters. A patient who has substantial allergic inflammation and turbinate remodelling may need both disease modification and anatomical optimisation. Surgery may improve the airway, but immunotherapy or other medical strategies may be needed to prevent the same mucosal process from continuing.

The better model is integrated treatment:

First, define the symptom: airflow obstruction, congestion, pressure, mucus or mixed symptoms.

Second, identify the mechanism: fixed anatomy, allergic rhinitis, local allergic rhinitis, nasal hyperreactivity, irritant exposure, medication effect, rhinitis medicamentosa, chronic rhinosinusitis or a functional overlay (anxiety/hyperventilation/panic disorder/SSD).

Third, match treatment to mechanism: immunotherapy for relevant allergic drivers, pharmacotherapy for symptom control, irritant cessation where relevant, and surgery where anatomy or tissue remodelling is genuinely limiting airflow.

This is particularly important for patients who have already had “low-value” nasal surgery. Many are not wrong about their symptoms. They are wrong about the explanation they were given — or the explanation was incomplete.

The key message

“Septal deviation and enlarged turbinates” is a finding. “Congested nose” is a symptom. Neither is a proper diagnosis.

When patients have progressive bilateral nasal obstruction, alternating congestion, postural blockage or loss of surgical benefit over time, the clinician should look beyond anatomy. The question is not simply whether the septum is bent or the turbinates are large. The question is why the nasal airway is behaving that way.

In many patients, the answer is rhinitis — often allergic rhinitis or local allergic rhinitis — with turbinate-based vascular congestion and tissue remodelling. Surgery may still help, but only if it is used as part of a broader plan that addresses the disease process driving the obstruction.

Patients do better when treatment is directed at the cause, not the label.

References

McCoul ED, Mohammed AE, Debbaneh PM, Carratola M, Patel AS. Differences in the intended meaning of congestion between patients and clinicians. JAMA Otolaryngol Head Neck Surg. 2019;145(7):634-640. doi:10.1001/jamaoto.2019.1073 Harvey RJ, Roland LT, Schlosser RJ, Pfaar O. Chief complaint: nasal congestion. J Allergy Clin Immunol Pract. 2024;12(6):1462-1471. doi:10.1016/j.jaip.2024.04.028 Sozansky J, Houser SM. The physiological mechanism for sensing nasal airflow: a literature review. Int Forum Allergy Rhinol. 2014;4(10):834-838. doi:10.1002/alr.21368 Carney AS, Powe DG, Huskisson RS, Jones NS. Atypical nasal challenges in patients with idiopathic rhinitis: more evidence for the existence of allergy in the absence of atopy? Clin Exp Allergy. 2002;32(10):1436-1440. doi:10.1046/j.1365-2745.2002.01494.x Powe DG, Bonnin AJ, Jones NS. ‘Entopy’: local allergy paradigm. Clin Exp Allergy. 2010;40(7):987-997. doi:10.1111/j.1365-2222.2010.03536.x Hamizan AW, Rimmer J, Alvarado R, Sewell WA, Kalish L, Sacks R, Harvey RJ. Positive allergen reaction in allergic and nonallergic rhinitis: a systematic review. Int Forum Allergy Rhinol. 2017;7(9):868-877. doi:10.1002/alr.21988 De Corso E, Bastanza G, Di Donfrancesco V, Guidi ML, Morelli Sbarra G, Passali GC, Poscia A, de Waure C, Paludetti G, Galli J. Radiofrequency volumetric inferior turbinate reduction: long-term clinical results. Acta Otorhinolaryngol Ital. 2016;36(3):199-205. doi:10.14639/0392-100X-964 Zhang K, Pipaliya RM, Miglani A, Nguyen SA, Schlosser RJ. Systematic review of surgical interventions for inferior turbinate hypertrophy. Am J Rhinol Allergy. 2023;37(1):110-122. doi:10.1177/19458924221134555 Chin D, Marcells G, Malek J, Pratt E, Sacks R, Harvey RJ. Nasal peak inspiratory flow as a diagnostic tool for differentiating decongestable from structural nasal obstruction. Rhinology. 2014;52(2):116-121. doi:10.4193/Rhino13.123

FAQ

Is a deviated septum always the cause of nasal obstruction?

No. A deviated septum can cause nasal obstruction, especially when symptoms are one-sided or followed nasal trauma. Progressive bilateral nasal congestion is often driven by rhinitis, allergy, turbinate swelling, nasal hyperreactivity or mucosal inflammation rather than septal anatomy alone.

Why did my turbinate surgery work at first and then stop working?

Australia has one of the most accessible and high-quality radiology ecosystems in the world. In NSW in particular, a competitive private imaging market has delivered rapid access, excellent technology, and broad geographic coverage. For patients, this is a clear strength.

For clinicians, however, it has introduced a growing problem:

fragmentation of imaging care and over-reliance on radiology reports

These two issues intersect in a way that directly affects how we diagnose and manage sinus disease.

The Core Principle: Look at the Scan

In rhinology, one principle remains fundamental:

Always review the images—not just the report

Radiology reports almost never conclude that the sinuses are “normal.” Instead, they frequently describe:

mucosal thickening partial opacification retention cysts “features of sinusitis”

For non-specialists—and for patients reading their own reports—this language implies disease. But in many cases, it does not reflect clinically meaningful pathology.

What Does “Normal” Actually Look Like?

We addressed this directly in our systematic review of sinus imaging in asymptomatic populations.

Across 16,966 individuals with no sinus symptoms, the findings were clear (1):

Mean Lund-Mackay score: 2.24 ~15% had a score ≥4 13% had mucous retention cysts 17.7% had mucosal thickening ≥2 mm

The implication is straightforward:

Incidental sinus findings are common—and often normal

This is a critical point for both clinicians and patients. CT imaging is highly sensitive, but it does not distinguish between physiological variation and disease.

Simple mucosal cysts are present in 13% of all patients and thickening of mucosa of 2-4mm is common in normal asymptomatic patients.

The Clinical Disconnect

Radiologists are doing exactly what they should—describing structural findings.

But sinus disease is not defined by imaging alone.

It requires:

symptoms (nasal obstruction, discharge, smell loss, etc.) objective findings (endoscopy ± imaging) clinical context

Without this, imaging findings risk being over-interpreted.

This leads to a familiar pattern:

patients labelled with “sinusitis” based on imaging antibiotics prescribed unnecessarily referrals driven by reports rather than symptoms persistent confusion when treatment fails

Why Reviewing the Images Matters

A written report cannot fully capture:

distribution of disease (localised vs diffuse) anatomical variation surgical relevance correlation with symptoms

When you review the scan yourself, you can distinguish between:

incidental change → common, non-contributory clinically relevant disease → requiring treatment

For example:

mild maxillary mucosal thickening in an asymptomatic patient → likely normal diffuse ethmoid disease with anosmia → clinically significant

This level of interpretation cannot be outsourced.

A New Problem: Fragmentation of Imaging Access

At the same time, accessing imaging has become more difficult.

Despite improved availability, we now face:

multiple radiology providers separate portals for each group different usernames, passwords, and 2FA systems locked accounts from failed logins difficulty accessing prior imaging across providers

The result is paradoxical:

More imaging—but less usable continuity

For surgeons, this affects:

comparison over time surgical planning confidence in decision-making

A Practical Solution: A Central Access Resource

To address this, I have created this page as a practical tool for ENT surgeons and referrers.

Instead of searching for individual radiology portals each time, you can:

select your state choose the radiology provider access the image portal directly

👉 Bookmark this page and use it as a central access point.

Radiology Image Access Finder

Select your state, then choose a radiology provider. The button will open the doctor / referrer image access portal.

Loading radiology access data...

State Select state NSW ACT QLD VIC SA NT TAS WA Radiology Group Select radiology group Open Doctor / Referrer Image Access Portal

This is a simple step—but one that can significantly reduce friction in daily clinical practice. Message me if there is update or correction required.

For Patients: Bring the Images

Patients should be encouraged to:

bring their imaging (USB or digital access) use consistent providers where possible understand that reports may not reflect disease

A report is helpful—but it is not definitive.

Listen to the Evidence

For a deeper discussion of incidental sinus findings and their clinical implications, you can listen to our podcast

OTO: Sinus Radiological Findings in General Asymptomatic Populations: A Systematic Review of Incidental Mucosal Changes

:

Conclusion

Modern rhinology requires more than access to imaging—it requires interpretation, context, and clinical judgement.

CT scans are sensitive—but not specific Reports describe findings—but do not define disease Access to imaging is improving—but continuity is worsening

The responsibility remains with the clinician.

If you don’t review the scan yourself, you risk treating the report—not the patient.

Reference 

Razi B, Perkovic A, Alvarado R, Stroud A, Ho J, Kalish LH, Campbell RG, Sacks R, Harvey RJ. Sinus radiological findings in general asymptomatic populations: a systematic review of incidental mucosal changes. Otolaryngol Head Neck Surg. 2022;167(1):16–24.

FAQ section

Why should ENT surgeons review sinus CT images themselves?

Because radiology reports describe findings, but ENT surgeons must decide whether those findings are clinically relevant.

Are minor sinus CT abnormalities common?

Yes. Studies show that mucosal thickening, retention cysts, and low Lund-Mackay scores are common even in people without sinus symptoms.

Does mucosal thickening mean sinusitis?

Not always. Mild mucosal thickening may be incidental and must be interpreted alongside symptoms and endoscopy.

Why are prior scans important?

Prior scans allow clinicians to compare changes over time, which is often essential for diagnosis and surgical planning.

Why is radiology access difficult in Australia?

The Septal Swell Body: The Missing Target in Nasal Obstruction Surgery

Despite decades of refinement in nasal airway surgery, one structure continues to be consistently overlooked: the septal swell body (SSB). While inferior turbinate reduction and septoplasty dominate surgical thinking, the SSB remains poorly understood, inconsistently addressed, and often misinterpreted as a simple septal deviation.

This is increasingly difficult to justify.

A growing body of anatomical, radiological, and clinical evidence now demonstrates that the SSB is not merely a structural bystander, but a dynamic, glandular, and clinically relevant contributor to nasal obstruction. Yet, many surgeons still lack a systematic approach to managing it—even in patients with persistent symptoms after otherwise adequate surgery.

More Than a Septal Thickening: A Distinct Anatomical Structure

The SSB—also referred to as the nasal septal turbinate or septal body—is located anteriorly, superior to the inferior turbinate and just anterior to the middle turbinate. Importantly, it is not simply the bony-cartilaginous junction of the septum, but a fusiform, soft tissue structure with substantial mucosal volume .

Histologically, it is markedly different from the surrounding septum. Studies consistently show that the SSB contains:

abundant seromucinous glands (~50%) venous sinusoids and erectile tissue thickened mucosa with vascular capacity

This composition closely resembles inferior turbinate tissue rather than septal mucosa .

This distinction is critical. It reframes the SSB as a functional structure, capable of active physiological change, rather than a passive anatomical variant.

A Dynamic Contributor to Nasal Airflow

The SSB behaves like a turbinate.

Radiological evidence demonstrates that it is dynamic in size, with measurable changes over time that correlate directly with inferior turbinate variation. In a longitudinal CT-based study, changes in SSB width significantly correlated with turbinate size changes (r = 0.35, p = 0.04), supporting a shared role in nasal cycling and airflow regulation .

This has practical implications:

Enlargement of the SSB contributes to internal nasal valve narrowing It increases nasal airway resistance It participates in the nasal cycle alongside turbinates

Despite this, most surgical paradigms still focus almost exclusively on the lateral wall.

Hypertrophy in Disease: Allergy and Inflammation

The SSB is not static—it responds to disease.

Multiple radiographic studies demonstrate that the SSB is significantly enlarged in patients with sinonasal disease, particularly those with allergic rhinitis and turbinate hypertrophy.

In a large CT-based study of 405 patients:

SSB dimensions were significantly greater in diseased vs control groups For example, middle segment thickness: 12.74 mm vs 10.47 mm (p=0.001)

Similarly, Hizli et al. demonstrated that:

SSB size is significantly larger in patients with inferior turbinate hypertrophy Allergy has an additive effect, further increasing SSB area and width (p < 0.001)

This reinforces a key concept:

The septal swell body undergoes the same inflammatory hypertrophy as the inferior turbinate

Yet, while turbinate hypertrophy is routinely treated, SSB hypertrophy is often ignored.

The septal swell body or septal turbinate undergoes the same tissue remodelling as the IT.

The Evidence for Treatment: Not Just Theory

The most compelling argument for addressing the SSB is clinical outcomes.

A recent systematic review and meta-analysis (2025) evaluated septal swell body volume reduction (SSBVR) across seven studies (n=232 patients). The findings were clear:

Significant improvement in nasal obstruction scores (SMD 2.54) Reduction in nasal airway resistance (SMD –0.67) Increased cross-sectional area (SMD –1.05) Benefits sustained up to 12 months

Perhaps more importantly:

Adding SSB reduction to turbinate surgery improved outcomes compared to turbinate surgery alone (SMD 0.47)

This directly challenges current surgical practice.

If turbinate surgery alone is inferior, then failing to address the SSB may represent incomplete surgery.

Why Is the SSB Still Ignored?

Despite this growing evidence, many surgeons do not routinely treat the SSB.

There are several reasons:

Misidentification as septal deviation Lack of emphasis during surgical training Perception that intervention is unnecessary or risky Absence of consensus guidelines

A systematic review of the nasal septal turbinate concluded that it remains an “overlooked surgical target”, despite consistent anatomical and early clinical evidence supporting its relevance .

This aligns with real-world experience. Many international observers—across Europe, Asia, and South America—report no exposure to SSB surgery during training, highlighting a global gap in rhinologic education.

Safety: Addressing a Common Concern

One concern often raised is the risk of septal perforation.

However, this appears overstated.

Across intervention studies:

Treating a Watery Nose (Rhinorrhea): Why Targeted Nerve Surgery Is Changing Practice

A persistently watery nose—rhinorrhea—is one of the most common yet poorly understood symptoms we see in rhinology. Patients often arrive having been treated repeatedly for “allergies” or “sinus problems,” yet their dominant complaint remains unchanged: a constant need for tissues, social embarrassment, and a sense that their nose is never dry. Although, we all might suffer a watery nose when skiing, going for a jog on an early morning or from eating spicy foods, this can be a daily occurence for those patients with a neurogenic rhinitis.

For clinicians, the challenge is that rhinorrhea is not a diagnosis—it is a physiological output. The underlying driver, in many patients, is not inflammation alone but neurogenic dysregulation of nasal secretion, particularly in non-allergic, neurogenic or mixed rhinitis. Nasal hyper-reactivity is the contemporary term. This distinction explains why conventional therapies frequently fail—and why surgery, when appropriately selected, can be transformative.

From Vidian Neurectomy to Targeted Nasal Denervation

Historically, vidian neurectomy was the definitive surgical solution for refractory rhinorrhea. By interrupting parasympathetic input at the level of the vidian nerve, the procedure reduces glandular secretion across the nasal mucosa. A systematic review demonstrated consistent improvement in rhinorrhea across studies (1). Gustatory rhinitis was the classic condition cured by vidain neurectomy. We use to see it commonly after bariatric surgery.

While dry eye is commonly reported, it is usually temporary, resolving over time. However, the small risk of persistent symptoms must be balanced against the fact that rhinorrhea is a benign, non-progressive condition, which has driven a shift toward more targeted interventions (1).

The Rationale for Posterior Nasal Nerve (PNN) Surgery

Modern surgical management focuses on the posterior nasal nerve (PNN), a distal parasympathetic pathway supplying the nasal mucosa. Rather than interrupting the system proximally, PNN surgery targets secretion at its effector site.

Anatomical work shows that autonomic fibres are distributed across multiple nasal nerve branches, supporting the need for targeted but adequate denervation (2).

Clinically, PNN offers:

effective reduction in rhinorrhea preservation of lacrimal function lower morbidity than vidian neurectomy

Identifying the Right Patient

Successful outcomes depend on selecting the right patient.

Typical features include:

persistent clear, watery rhinorrhea poor response to intranasal steroids and antihistamines non-allergic or mixed rhinitis phenotype

These patients often describe triggers such as cold air, eating, or environmental irritants, and frequently report postnasal drip and cough.When it co-exists with allergy, immunotherapy is almost alwasy done first as most nasal hyperactivity disappears when the allergic component is treated.

Prognostication: The Role of Ipratropium

A trial of intranasal ipratropium bromide is one of the most useful tools in clinic.

Nasal iaptropium is no longer sold as "Nasal" atrovent but can be compounded or found in other forms locally and in NZ

A positive response indicates parasympathetic-driven secretion, helping predict response to intervention. Studies show that ipratropium responsiveness predicts outcomes in PNN ablation procedures, although surgical PNN remains effective even in non-responders (3).

The Rise—and Limits—of In-Office Ablation

Cryotherapy and radiofrequency ablation of the PNN have gained popularity as office-based procedures.

Short-term results are encouraging, with 70–80% of patients improving (4). However, durability remains the key limitation.

A multicentre study showed:

84% initial improvement ~95% recurrence over time mean recurrence at ~5 months (4)

This reflects partial nerve injury rather than definitive transection.

Patients should therefore understand:

benefit is often temporary repeat procedures may be required

Morbidity and Patient Experience

Although marketed as minimally invasive, these procedures are not trivial.

Patients frequently report:

significant discomfort under local anaesthesia post-procedural pain and crusting occasional epistaxis requiring intervention (5)

In the Australian context, this raises practical considerations. Many patients prefer a single definitive day surgery procedure, rather than repeated uncomfortable outpatient treatments.

Why Surgical PNN Remains My Preferred Approach

In my practice, I favour endoscopic posterior nasal nerve neurectomy.

The advantages are clear:

Durability: true nerve division reduces recurrence Low morbidity: avoids lacrimal complications Efficiency: single day procedure Reliability: less dependent on pre-selection

The Septal Swell Body: The Missing Piece in Rhinorrhea Surgery

John Craig and i discusssed one of the most overlooked contributors to persistent rhinorrhea is the septal swell body (SSB).

Often dismissed as a minor septal thickening, it is in fact a distinct functional structure.

Histologically, the SSB contains dense seromucinous glands—up to 50% glandular tissue, significantly greater than surrounding septum (6). It also demonstrates specialised architecture and vascularity, distinguishing it from typical septal mucosa (7).

Functionally, the SSB behaves dynamically. Imaging studies show that its size varies with turbinate changes, suggesting a role in nasal cycling (8). Physiological studies further demonstrate that targeted decongestion improves airflow, comparable to turbinate decongestion (9).

This has direct relevance to rhinorrhea.

The SSB is:

a glandular structure contributing to secretion a vasoactive region influencing airflow likely involved in neurogenic reflex pathways

Importantly, parasympathetic fibres are not confined to the PNN. John's own research show that autonomic input also arises from other pathways, including the anterior ethmoid nerve (2).

This raises an important point:

PNN surgery alone may not fully address all sources of nasal secretion

The SSB may represent a residual driver of rhinorrhea, particularly in patients with incomplete response.

A Practical Surgical Strategy

As no practical way to selectively perform an Anterior Ethmoid Neurectomy has been described, there has been growing interest in treating the SSB using radiofrequency techniques, with studies demonstrating significant symptom improvement (10). However, these approaches add cost and risk thermal injury.

In my practice, I favour a simple mechanical reduction:

endoscopic shaving of the SSB no thermal injury low cost and reproducible

This integrates naturally with:

PNN neurectomy turbinate surgery

A critical technical point is that the area heals by secondary intention. To prevent desiccation and optimise healing, I routinely use a:

👉 0.5 mm silicone (silastic) sheet

to protect the mucosa during recovery.

Moving Toward Precision Rhinology

Rhinorrhea is not a single-site disease. It is a distributed physiological process involving:

neural pathways glandular tissue vascular structures

Treatment should reflect this.

We now have a spectrum:

medical therapy ipratropium (diagnostic + therapeutic) ablation (selected patients) PNN surgery (durable neural control) SSB reduction (glandular + anterior contribution)

Conclusion

The management of a watery nose has evolved from broad autonomic interruption to precision, physiology-driven surgery.

While newer technologies offer convenience, their limitations—particularly durability—must be acknowledged.

For many patients, the goal is not temporary relief but long-term control with minimal morbidity.

Combining posterior nasal nerve surgery with targeted treatment of the septal swell body represents a more complete and modern approach to rhinorrhea.

References (Vancouver)

Marshak T, Yun WK, Hazout C, Sacks R, Harvey RJ. A systematic review of the evidence base for vidian neurectomy in managing rhinitis. J Laryngol Otol. 2016;130(S4):S7–S28. Craig JR, Dunn RT, Ray A, Keller CE, Peterson EL, Eide JG. Cadaveric analysis of autonomic nerve fiber density in posterior nasal, posterolateral nasal, and anterior ethmoid nerves. Int Forum Allergy Rhinol. 2023;13(11):2109–2112. Maddineni S, Hwang PH, Ayoub NF, Patel ZM, Nayak JV, Chang MT. Predictive value of ipratropium responsiveness on posterior nasal nerve neurectomy outcomes in chronic rhinitis. Otolaryngol Head Neck Surg. 2026;174(2):359–365. Craig JR, Mack C, Vidovich A, Wilson C, Nguyen TV, Kuan EC. Rhinorrhea recurrence after posterior nasal nerve cryoablation: a multicenter cohort study. Laryngoscope. 2025;135:1928–1934. Lin CC, Hwang YL, Liao JY, Teng HL, Shih TY, Huang CY. Radiofrequency ablation versus laser neurolysis of the posterior nasal nerve in patients with chronic rhinitis. Otolaryngol Head Neck Surg. 2026;174(4):954–962. Wexler D, Braverman I, Amar M. Histology of the nasal septal swell body. Otolaryngol Head Neck Surg. 2006;134:596–600. Şişman AS, Acıoğlu E, Yiğit Ö, et al. Nasal septal turbinate: cadaveric study. Am J Rhinol Allergy. 2014;28:e173–e177. Wong EH, Noussair M, Hasan Z, et al. Physiological changes in septal swell body size correlate with inferior turbinate changes. J Laryngol Otol. 2020;134:323–327. Wong EH, Deboever N, Chong J, et al. Isolated topical decongestion of the septal swell body improves nasal airflow. Am J Rhinol Allergy. 2020;34:417–421. Pritikin J, Silvers S, Rosenbloom J, et al. Temperature-controlled radiofrequency treatment of the septal swell body: 12-month outcomes. Int Forum Allergy Rhinol. 2024;14:1549–1557. What causes a constantly runny nose?

A persistent watery nose is often caused by overactive nerve signals (non-allergic rhinitis), not just allergies or infection.

What is posterior nasal nerve (PNN) surgery?

PNN surgery is a procedure that reduces nasal secretion by interrupting parasympathetic nerve signals to the nasal lining.

Why might PNN surgery not fully stop rhinorrhea?

Other areas, such as the septal swell body, may continue to produce mucus due to additional nerve pathways.

What is the septal swell body?

It is a gland-rich area of the nasal septum that contributes to nasal airflow and mucus production.

Is surgery better than in-office treatments?

Repairing a spontaneous nasal CSF leak in the lateral sphenoid is one of the more misunderstood operations in endoscopic skull base surgery.

At a recent national meeting, I was struck by how often panelists used the term “transpterygoid approach” while clearly describing different operations. That confusion is not trivial. It affects teaching, operative planning, and ultimately outcomes.

The issue is visible even in recent classification work. The new international sphenoid classification lists type 2C transpterygoid sphenoidotomy as “partial or complete removal of the anterior sphenoid sinus wall with partial resection of the pterygoid process”. Yet the same paper defines type 2B complete sphenoidotomy as removal of the anterior sphenoid wall extending from skull base to sphenoid floor and from septum to orbit. In practice, that means some surgeons are calling an extended sphenoid opening “transpterygoid,” (maybe vworking throguh an antrostomy) while others mean a true direct lateral transmaxillary route to the lateral recess and working lateral to the neural structures.

Those are not the same operation.

The core question should not be, “Is this transpterygoid?” The real question is:

Are we reaching a lateral defect through a direct corridor, or are we still working around corners?

Endoscopic transmaxillary / transpterygoid approach to the lateral sphenoid recess, previously via a medical maxillectomy and now done via prelacrimal. A) removal of the inferior turbinate with preservation of the inferior turbinate head, B) modified medial maxillectomy with excision of medial maxillary wall, C) removal of posterior maxillary wall, D) identification and ligation of the internal maxillary artery, E) blunt dissection through pterygopalatine and infratemporal fossa contents, F) identification of lateral pterygoid plate (arrowhead) and descending palatine nerve (arrow) which is reflected medially and preserved if possible, G) partial removal of lateral pterygoid plate and bone over lateral sphenoid recess, H) identification of meningocele defect within the lateral sphenoid recess, I) excision of meningocele and repair of defect using duragen and bone graft.

That distinction matters because most lateral sphenoid meningoceles and encephaloceles are exactly what the name suggests: lateral. In our recent prelacrimal-transmaxillary series, the defects were shown to be lateral to V2 and the foramen rotundum, and often facing laterally, which makes angled medial-to-lateral work much harder to visualize and reconstruct.

Left lateral sphenoid recess encephaloceles. Lateral to CNV2 and directed laterally. Very hard to visualize via a tranethmoid/antral approach

That is why I believe the direct route—either through a medial maxillectomy or, preferably, a prelacrimal / peri-lacrimal transmaxillary corridor—is often the most rational approach. The prelacrimal-transmaxillary technique creates a straight-line trajectory through the maxillary sinus to the posterior wall, then through the pterygoid process to the lateral sphenoid recess, allowing direct 0-degree endoscopic access and straight instruments. By contrast, the classic modified transpterygoid routes described through large antrostomies often still require surgeons to work with angled endoscopes and curved instruments “around corners”.

In our Laryngoscope technical paper, that difference is made explicit. The prelacrimal-transmaxillary approach is favored when the lateral recess is truly lateral. If the defect sits directly behind the descending root of CNV2, a wide sphenoidectomy with angled instruments may suffice. But once the defect is lateral to CNV2 and the foramen rotundum, the direct transmaxillary window is the better corridor. It also preserves the vidian bundle, the descending root of V2, and the pterygopalatine ganglion. The lateral trans-orbital root also offers access wihtout affecting these structures, but an endoscopic surgeon simply "extending" a transethmoid sphenoidectomy via an antrostomy is not.

The other concept that deserves retiring is “Sternberg’s canal”. Too often, lateral sphenoid CSF leaks are still explained as though they arise from a congenital canal in the lateral recess. That is not how I think about these patients. The defect usually behaves like an acquired weak point in a pneumatized lateral sphenoid, not a magic embryologic tunnel in the recess itself. My understanding, consistent with the position advanced by Bradford Woodworth and colleagues, is that if Sternberg’s canal exists, it is an embryologic cleft in the lateral wall of the sphenoid, not the typical lateral recess defect surgeons are closing in modern endoscopic practice.

But even that debate is secondary to the most important truth:

The hole is not the disease.

For most spontaneous lateral sphenoid CSF leaks, the underlying problem is idiopathic intracranial hypertension (IIH). The international consensus statement emphasizes that spontaneous CSF rhinorrhea is closely linked to IIH and that elevated ICP must be assessed and definitively managed after closure to avoid recurrence and long-term sequelae.

That is why we use a lumbar drain differently from many surgeons. I do not see it as a routine drain-first device. In our postoperative IIH management chapter, the preferred strategy is to clamp the lumbar drain at the end of surgery and use it to monitor ICP in the first 24 hours. If pressure is elevated, then it becomes a tool for diversion and medical decision-making. In other words, it is not there primarily to “rest” the repair. It is there to tell you whether the patient has a pressure problem that still needs treatment.

For readers who want practical numbers, the commonly used ranges are:

Normal ICP: about 10–20 cm H₂O Borderline / mildly elevated: 20–25 cm H₂O Abnormal / consistent with raised ICP: greater than 25 cm H₂O

The consensus statement specifically supports definitive management when ICP is >25 cm H₂O. In our chapter, we also note that lumbar drains are particularly useful in higher-risk patients, including those with opening pressures >30 cm H₂O, and that persistent pressures >35 cm H₂O or poor acetazolamide response may push management toward permanent CSF diversion.

This matters because untreated IIH is not just a recurrence problem. It is also a vision problem. The consensus document recommends fundoscopy and visual assessment in these patients and stresses that long-term ICP control is needed to avoid the sequelae of untreated IIH. That is also why weight loss is critical. In our postoperative management chapter, a 6–10% reduction in weight is cited as enough to resolve IIH in some patients.In an era of GLP-1 durgs such as Ozempic, Wegovy and Monjaro, this is very achievable.

So when I look at a lateral sphenoid CSF leak, I do not think in reductionist terms.

I think: Is the defect truly lateral? Is my corridor direct? Am I sparing vidian, greater palatine and Int Forum Allergy Rhinol - 2014 - Illing - Spontaneous sphenoid lateral recess cerebrospinal fluid leaks arise from V2 when I can? And once the defect is closed, have I actually treated the disease?

Because the best repair of a lateral sphenoid leak is not just a patch. It is the right corridor plus long-term pressure control.

FAQ

What causes a nasal CSF leak in the lateral sphenoid?

Most spontaneous lateral sphenoid CSF leaks are linked to elevated intracranial pressure rather than trauma or a simple congenital hole. The defect is often part of a broader IIH problem.

What is the best surgical approach to a lateral sphenoid CSF leak?

For truly lateral defects, a direct transmaxillary route such as a prelacrimal or medial maxillectomy corridor usually provides better access than an indirect medial route.

Is Sternberg’s canal the usual cause of lateral sphenoid CSF leak?

Probably not. The modern view is that most lateral sphenoid leaks are acquired defects related to pressure and skull base thinning rather than a classic congenital canal in the lateral recess.

Why use a lumbar drain after CSF leak repair?

In selected patients, a lumbar drain is useful as an ICP monitoring tool after closure, rather than for routine drainage. It helps determine whether additional pressure management is needed.

What ICP is considered abnormal after CSF leak repair?

Normal ICP is usually around 10–20 cm H2O. Pressures above 25 cm H2O are generally considered abnormal and may require definitive treatment.

Why is weight loss important in IIH-associated CSF leak?

Weight loss helps reduce intracranial pressure and lowers the risk of recurrence and long-term complications, including visual loss

The management of chronic rhinosinusitis (CRS)—particularly diffuse type-2 disease such as CRSwNP or eosinophilic CRS—has entered a new era.

Biologic therapies have transformed outcomes. But an important question remains:

Can biologics replace surgery—or is the combination the optimal approach?

In a recent presentation at the ASOHNS ASM in Hobart, I explored the evolving role of surgery in the biologic era and why combining surgery and biologics in CRS is often essential to achieving remission.

The Traditional Pathway—and Its Limitations

Patients with diffuse CRS typically follow a familiar pathway:

topical corticosteroids short courses of oral steroids endoscopic sinus surgery revision surgery in refractory cases

Biologics such as dupilumab, mepolizumab, and tezepilumab now offer a powerful new option.

This has led to a natural question:

Why not just use biologics and avoid surgery altogether?

The answer is more nuanced.

Surgery Still Matters in the Biologic Era

Randomised trials of biologics show clear efficacy, but they also reveal an important signal:

👉 Patients with prior surgery behave differently

Post-hoc analyses from both mepolizumab and dupilumab trials suggest that:

prior surgery is often a marker of more severe disease but also of greater responsiveness to biologics

This may reflect:

reduced tissue remodelling improved drug access altered inflammatory burden

But beyond this, we must consider what surgery actually achieves.

Surgery Is Not Just About Access

It is often said that surgery improves topical drug delivery.

That is true—but incomplete.

Surgery also:

removes inflammatory tissue reduces polyp burden improves mucociliary clearance addresses mechanical obstruction removes co-pathologies such as REAH or mucus plugging

These are not trivial effects.

They fundamentally alter the disease environment.

The Importance of Surgical Completeness

One of the most important concepts emerging from recent work is extent of surgery.

Studies using the ACCESS score and similar metrics show that:

👉 More complete surgery is associated with better outcomes in biologic-treated patients

Lower ACCESS scores (i.e. more complete surgery) → better symptom outcomes Greater surgical completeness predicts response to dupilumab In multivariate analysis, extent of surgery may be the dominant predictor of outcome

This aligns with our own work:

Extent of sinus surgery is associated with disease control in biologic-treated CRS

In this cohort:

~49% achieved remission/control overall Remission rates were dramatically higher with extended surgery: Draf III: ~61% Draf IIc: ~68% Draf IIa: ~9% Draf I: 0%

👉 Extent of surgery, not comorbdiites like AERD/Asthma, once on biologics, was the key determinant of outcome

Complete sinus surgery is asscoiated with better outcomes in diffuse CRS

Timing Matters: Surgery vs Biologics—or Both?

Another key question is sequencing:

biologic first? surgery first? or combination?

Emerging evidence suggests:

👉 Combination therapy outperforms biologics alone

Randomised and real-world studies show:

improved outcomes when biologics are combined with surgery greater symptom control reduced steroid dependence

Importantly, patients with incomplete prior surgery appear to benefit significantly from revision procedures—even when already on biologics. This work from Prof Palmer and UPenn on COSI supports this statement.

This reinforces a critical point:

Biologics do not correct structural disease. Surgery does.

The Goal Has Changed: Remission

Historically, we aimed to “improve symptoms.”

That is no longer enough.

The goal in 2026 is:

no systemic steroids stable endoscopic findings low symptom burden durable disease control

👉 Remission

Achieving this requires addressing both:

the inflammatory pathway (biologics) the structural and mechanical disease (surgery)

Avoiding Reductionist Thinking

One of the risks in the biologic era is reductionism:

viewing CRS as purely an inflammatory disease treatable with drugs alone

But diffuse CRS is more complex.

It includes:

tissue remodelling polyp formation mucus stasis structural dysfunction coexisting pathologies

No single therapy addresses all of these.

The Future: Combination Therapy

The message from current evidence is clear:

Surgeons need biologics Patients need surgery Outcomes are best when both are used appropriately

👉 Combination therapy offers the highest likelihood of remission

As we move forward, the question is no longer:

Surgery or biologics?

But rather:

How do we combine them optimally for each patient?

📺 Watch the full presentation here: https://youtu.be/4dW-ZwKegW4

FAQ Section

Can biologics replace sinus surgery in CRS?

No. Biologics treat inflammation but do not address structural disease, tissue remodelling, or mucus obstruction.

Does surgery improve biologic response?

Yes. More complete surgery is associated with better outcomes and higher remission rates in biologic-treated CRS.

What is the goal of treatment in CRS today?

The goal is remission—no steroids, stable disease, and long-term control.

When should surgery be combined with biologics?

Why “Chronic Sinusitis” and “Nasal Polyps” Are Misleading Terms

Understanding why modern rhinology is moving beyond these outdated disease labels

For decades, patients and doctors alike have used the term chronic sinusitis to describe persistent inflammation of the sinuses. It is one of the most commonly used diagnoses in ear, nose and throat (ENT) practice.

But there is a problem.

The term chronic sinusitis — or chronic rhinosinusitis (CRS) — is not actually a disease.

It is a description of inflammation, not an explanation of why that inflammation occurs.

In many ways, using the term “chronic sinusitis” today is like respiratory physicians describing asthma, COPD, bronchiectasis, and interstitial lung disease collectively as “chronic lungitis.”

No respiratory specialist would accept such a vague diagnosis. Yet in rhinology, we still routinely use a similarly imprecise term.

As our understanding of sinus disease improves, it is becoming increasingly clear that CRS is not one disease, but a group of very different conditions that share a common symptom — chronic inflammation of the sinus lining.

The Problem With the Term “Chronic Sinusitis”

The word sinusitis simply means inflammation of the sinuses.

But inflammation is a final pathway, not a diagnosis.

Inflammation can be caused by many different mechanisms:

allergy

immune dysregulation from the epithelial barrier

infection

genetic disease

mucociliary dysfunction

Grouping all of these under the same label risks oversimplifying the disease and potentially misdirecting treatment.

Nasal polyps are msimply the endpoint of chronic inflmmation and dont describe a specidfic disease condition

Historically, CRS was classified using a simple system:

CRS with nasal polyps

CRS without nasal polyps

While simple, this system ignores the biological diversity of sinus disease.

As research has advanced, it has become clear that these categories fail to reflect the underlying causes or mechanisms of inflammation.

Why “Nasal Polyps” Is Also a Misleading Diagnosis

The term nasal polyps is equally problematic.

A polyp is not a disease — it is a tissue response to chronic inflammation.

In other words, polyps are an endpoint of tissue remodeling, not the cause of the disease itself.

Many different conditions can produce tissue changes that look like nasal polyps.

Examples include:

Primary diffuse type-2 inflammatory CRS

Allergic fungal sinusitis (AFS)

Cystic fibrosis

Central compartment atopic disease (CCAD)

Respiratory epithelial adenomatoid hamartoma (REAH)

Antrochoanal polyps

These conditions have very different causes and treatments, yet they may all be described using the same label: “nasal polyps.”

Video:Polypoid degeneration of the sinus mucosa in cystic fibrosis. We understand that this condition wont respond to modern day biologics but then we dont discuss the ambiguity when treating non-CF CRS patients

This is why saying a patient “has nasal polyps” is often clinically incomplete.

It is similar to diagnosing someone with “a lung nodule” without explaining whether it is infection, inflammation, or cancer.

A Shift Toward Precision Medicine in Sinus Disease

Modern medicine is moving toward precision medicine — tailoring treatment based on the underlying mechanism of disease.

This approach has transformed the treatment of many inflammatory diseases, particularly asthma.

Asthma is no longer considered a single disease. Instead, it is divided into different endotypes, each driven by distinct inflammatory pathways.

The same shift is now occurring in rhinology.

Researchers and clinicians increasingly recognize that different forms of CRS require different treatments.

This is particularly important in the era of biologic therapies, including:

dupilumab

mepolizumab

tezepelumab

These medications target specific immune pathways and can cost tens of thousands of dollars per year.

Using them effectively requires accurate identification of the underlying disease mechanism.

The EPOS 2020 Classification of CRS

Recognising these challenges, the European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS2020) proposed a more biologically meaningful classification of sinus disease.

Instead of focusing on the presence or absence of polyps, the new framework classifies primary CRS based on:

Anatomic distribution

Inflammatory endotype

This approach helps identify different clinical phenotypes that require different treatments.

Figure: Contemporary classification of primary chronic rhinosinusitis based on anatomical distribution and inflammatory endotype, adapted from EPOS2020 and Grayson et al. Step 1: Anatomical Distribution

Primary CRS may be divided into:

Localized disease

Examples include:

isolated frontal sinusitis

isolated sphenoid sinusitis

ostiomeatal complex disease

These conditions often behave more like mechanical or obstructive diseases.

Diffuse disease

Diffuse disease involves broader inflammation across the sinus system and is typically associated with systemic inflammatory pathways.

This category includes conditions such as:

eosinophilic CRS

central compartment atopic disease

allergic fungal sinusitis

Step 2: Inflammatory Endotype

The next layer of classification focuses on the dominant immune pathway.

Two major patterns are recognised:

Type-2 (Th2) inflammation

This pathway involves cytokines such as IL-4, IL-5, and IL-13 and is associated with:

eosinophilic inflammation

asthma

nasal polyps

corticosteroid responsiveness

Many modern biologic drugs target this pathway.

Non–Type-2 inflammation

These conditions involve different immune pathways and often behave differently clinically.

Examples include:

older onset disease

smokers

corticosteroid-resistant CRS

From Classification to Real Clinical Phenotypes

When anatomical distribution and inflammatory endotype are combined, a range of distinct CRS phenotypes emerges.

Examples include:

Central compartment atopic disease (CCAD)

Eosinophilic CRS (eCRS)

Allergic fungal sinusitis (AFS)

Non-eosinophilic CRS

Each has characteristic patterns of symptoms, imaging findings, and treatment responses.

CRS is not all the same and it dictates treatment

Understanding these phenotypes allows clinicians to move beyond a simple “one size fits all” approach to sinus disease.

Why This Matters for Patients

For patients, the terminology used to describe disease can directly influence treatment decisions.

Two people diagnosed with “chronic sinusitis” may actually have completely different diseases requiring different therapies.

For example:

A patient with localized sinus obstruction may benefit primarily from surgery.

A patient with type-2 inflammatory disease may benefit from:

corticosteroids

biologic therapy

long-term inflammatory control.

Without recognising these differences, treatment can become trial-and-error.

Rethinking the Language of Sinus Disease

Medicine evolves as knowledge grows.

Just as asthma has evolved from a single diagnosis into multiple inflammatory subtypes, sinus disease is undergoing a similar transformation.

The terms “chronic sinusitis” and “nasal polyps” remain useful as broad descriptions, but they should not be considered final diagnoses.

Instead, they are starting points.

Behind those labels lies a complex group of conditions with distinct causes, biology, and treatments.

Recognising these differences is essential if we are to move toward precision medicine in rhinology.

And perhaps one day, the term chronic sinusitis will seem just as outdated as calling every lung disease “chronic lungitis.”

References

Fokkens WJ, Lund VJ, Hopkins C, et al. European Position Paper on Rhinosinusitis and Nasal Polyps 2020. Rhinology. 2020.

Grayson JW, Hopkins C, Mori E, Senior B, Harvey RJ. Contemporary classification of chronic rhinosinusitis beyond polyps vs no polyps. JAMA Otolaryngol Head Neck Surg. 2020.

Grayson JW, Cavada M, Harvey RJ. Clinically relevant phenotypes in chronic rhinosinusitis. J Otolaryngol Head Neck Surg. 2019.

Frequently Asked Questions About Chronic Sinusitis

What is chronic sinusitis (CRS)?

Chronic sinusitis, also called chronic rhinosinusitis, describes persistent inflammation of the sinus lining lasting more than 12 weeks. It is not a single disease but a group of conditions with different underlying causes.

Are nasal polyps a disease?

No. Nasal polyps are not a disease themselves. They are a tissue response to chronic inflammation and can occur in many different sinus conditions.

What causes chronic sinusitis?

Many different processes can cause chronic sinus inflammation including allergy, immune dysfunction, infection, microbial imbalance, genetic diseases such as cystic fibrosis, and type-2 inflammatory conditions.

Why is CRS classification important?

Different types of CRS respond to different treatments. Understanding the underlying inflammatory pathway helps doctors choose the most effective therapy, including surgery, steroids, or biologic medications.

What is type-2 inflammation in sinus disease?

Type-2 inflammation is an immune pathway involving cytokines such as IL-4, IL-5 and IL-13. It is commonly associated with eosinophilic CRS, asthma, and nasal polyps and is the target of modern biologic therapies.

What is the EPOS classification of CRS?

Why “Blocked Nose” Doesn’t Always Mean Blocked Airflow

The importance of objective testing in nasal breathing

Many patients come to clinic saying they have a “blocked nose” or “nasal congestion.” It is one of the most common symptoms in ENT practice. Yet what patients describe as congestion can mean very different things medically.

Some patients truly have restricted airflow through the nose, while others have a sensation of stuffiness caused by inflammation, mucus, or nerve signalling in the nasal lining. These two problems feel similar, but they are not the same — and they require very different treatments.

At the Sydney ENT Clinic NoseLab, we use specialised testing to determine whether a patient’s symptoms are caused by real airflow obstruction or by other nasal conditions. This distinction is critical before recommending treatments such as medication, allergy therapy, or surgery.

You can learn more about the facility here: https://richardharvey.sydneyentclinic.com/services/nose-lab/

Nasal congestion vs nasal obstruction: not the same thing

Patients often use the word “congestion” to describe several different sensations:

difficulty breathing through the nose

pressure in the face or sinuses

a “stuffy” or heavy feeling

mucus in the nose or throat

However, these symptoms do not always reflect a physical blockage of airflow.

Research comparing patient and doctor interpretations of “nasal congestion” shows that patients often associate it with pressure, mucus, or headaches, whereas clinicians define congestion primarily as reduced airflow through the nose.

Understanding this difference is essential because treatments aimed at improving airflow (such as septoplasty or nasal valve surgery) may not help symptoms caused by inflammation or nerve signalling.

How the nose senses airflow

The sensation of nasal breathing is not produced by airflow sensors. Instead, it is generated by cooling of the nasal lining as air passes through it.

Cold-sensitive receptors in the trigeminal nerve (TRPM8 receptors) detect this cooling effect and signal to the brain that airflow is present.

Medicine today outline_RJH_edit…

This explains several common experiences:

Menthol or eucalyptus inhalers can make the nose feel clearer without actually improving airflow.

Allergic inflammation or thick mucus can make the nose feel blocked even when airflow is normal.

Patients sometimes feel severe obstruction despite adequate nasal airway space.

In other words, perception and physiology do not always match.

Why objective testing matters

Because symptoms alone can be misleading, objective testing is increasingly important in nasal medicine.

At the NoseLab we combine:

detailed nasal endoscopy

functional airflow testing

physiological assessment of nasal resistance

These tools allow us to determine whether symptoms are caused by:

Structural obstruction Examples include septal deviation, nasal valve narrowing, or turbinate enlargement.

Inflammatory congestion Often related to allergy, rhinitis, infection, or environmental irritants.

Functional or sensory disorders Where the perception of airflow does not correspond with measurable airflow.

Objective testing helps prevent unnecessary surgery and ensures the correct treatment is chosen.

Rhinomanometry: measuring nasal airflow

One of the most useful tools for evaluating nasal breathing is rhinomanometry.

This test measures:

airflow through each side of the nose

pressure changes during breathing

nasal airway resistance

By quantifying nasal resistance during normal breathing, rhinomanometry helps distinguish:

fixed anatomical obstruction

reversible congestion caused by inflammation

It is considered one of the most reliable objective tests for evaluating nasal airflow and monitoring treatment response.

A respiratory scientist undertakes testing to determine true airflow

For example:

If airflow improves significantly after a nasal decongestant, the problem is likely inflammatory (such as allergy).

If airflow remains restricted, a structural issue such as nasal valve narrowing may be present.

This information helps guide decisions about medical therapy, allergy treatment, or surgery.

What research tells us about nasal symptoms

Interestingly, research shows that symptoms do not always correlate strongly with objective airflow measurements.

Studies from our group and others have demonstrated that patients’ perception of nasal obstruction can be influenced by multiple factors, including mucosal inflammation and even emotional health.

This highlights an important point: treating the structure of the nose alone does not always solve the problem.

Instead, effective management requires understanding the full physiological picture.

Using nasal endoscopy to identify inflammation

Nasal endoscopy provides a detailed view of the inside of the nose and sinuses.

Certain endoscopic findings can suggest allergy-driven inflammation, including:

middle turbinate oedema

watery secretions

inferior turbinate hypertrophy

These features have been shown to correlate with allergic airway disease in systematic reviews of nasal endoscopy findings.

Our research group has contributed extensively to understanding these patterns of disease.

You can see an example of nasal examination techniques here: Endoscopic features of inhalant allergy

And examples explaining nasal obstruction and congestion: 2024-Harvey et al Cheif complaint nasal congestion

The role of the NoseLab

The NoseLab at Sydney ENT Clinic is designed to provide comprehensive evaluation of nasal breathing using advanced diagnostic tools.

Testing may include:

rhinomanometry

nasal endoscopy

airflow resistance testing

assessment before and after decongestants

evaluation of nasal valve function

This approach allows us to move beyond simple visual examination and measure how the nose actually functions during breathing.

Rhinomanometry is the most reliable testing and measures true airflow (a & b). Nasal peak inspiratory flow (c) measures collapsibility and the shape or cross-sectiona is measured by acoustic rhinomanometry (d)

The goal is to provide patients with:

accurate diagnosis

personalised treatment plans

avoidance of unnecessary procedures

When should you consider objective testing?

Objective nasal airflow testing can be helpful if you experience:

persistent nasal blockage despite treatment

poor sleep related to nasal breathing

ongoing symptoms after nasal surgery

uncertainty about whether surgery may help

complex symptoms where scans appear normal

Understanding whether symptoms reflect true airflow obstruction or inflammatory congestion is the first step toward effective treatment.

Many patients are unsure whether their nasal congestion is caused by true airflow obstruction or by inflammation within the nose. The following questions address common concerns about nasal breathing and objective airflow testing.

Frequently Asked Questions About Nasal Congestion and Nasal Airflow Testing

What is the difference between nasal congestion and nasal obstruction?

Nasal congestion and nasal obstruction are often used interchangeably, but they are not the same. Nasal obstruction refers to a physical restriction of airflow through the nose, usually caused by structural problems such as a deviated septum or nasal valve narrowing. Nasal congestion, however, often refers to the sensation of a blocked or stuffy nose caused by inflammation, mucus, or swelling of the nasal lining. Many patients feel congested even when airflow through the nose is normal.

How can doctors measure whether my nose is actually blocked?

Doctors can objectively measure nasal airflow using specialised tests such as rhinomanometry. This test measures the pressure and airflow through each side of the nose during normal breathing. By calculating nasal airway resistance, rhinomanometry helps determine whether symptoms are caused by a true airflow obstruction or by inflammatory congestion from conditions such as allergy or rhinitis.

What is rhinomanometry?

Rhinomanometry is a diagnostic test used to measure nasal airflow and nasal resistance during breathing. It works by measuring the pressure difference between the front and back of the nose while airflow is recorded. The results show whether the nasal airway is physically restricted and whether the obstruction improves after using a nasal decongestant.

Why do some people feel blocked even when their nose is open?

The sensation of nasal breathing depends largely on cooling of the nasal lining as air flows through it. Nerve receptors in the nose detect this cooling effect and signal the brain that airflow is present. When inflammation, mucus, or swelling interfere with this cooling sensation, patients may feel congested even if airflow is normal.

Can allergy cause nasal congestion without blocking airflow?

Yes. Allergic rhinitis and other inflammatory conditions can cause swelling of the nasal lining, increased mucus production, and nerve irritation. These changes can create a strong sensation of congestion even when the airway remains relatively open.

When should someone consider objective nasal airflow testing?

Objective testing may be helpful if you experience:

persistent nasal blockage despite treatment

difficulty breathing through the nose during sleep

ongoing symptoms after previous nasal surgery

uncertainty about whether surgery may improve breathing

symptoms of nasal congestion despite normal scans or examinations

Testing helps determine whether symptoms are due to structural obstruction or inflammatory congestion.

Can nasal airflow testing help decide if surgery is necessary?

Yes. Objective airflow testing can help determine whether surgery is likely to improve breathing. If testing shows that airflow obstruction is caused by structural narrowing, procedures such as septoplasty or nasal valve surgery may help. If airflow is normal, treatment may instead focus on allergy control or medical therapy.

What tests are performed in a specialised nasal airflow laboratory?

In a specialised nasal function clinic such as the NoseLab, testing may include:

rhinomanometry to measure airflow resistance

nasal endoscopy to visualise internal structures

nasal airflow measurements before and after decongestants

evaluation of nasal valve function

assessment of inflammatory conditions such as allergy or rhinitis

These tests help provide a comprehensive evaluation of nasal breathing.

Why is my nose always blocked at night?

Many people notice that their nose feels more blocked when lying down at night. This occurs because body position changes blood flow to the nasal lining. When you lie down, increased venous pressure causes the turbinates (structures inside the nose) to swell slightly. This is part of the normal nasal cycle, where one side of the nose becomes more congested while the other opens. In people with allergy, inflammation, or structural narrowing, this normal cycle can become exaggerated and produce significant nighttime congestion.

Can a deviated septum cause nasal congestion?

Yes. A deviated septum, where the cartilage or bone dividing the nasal passages is off-centre, can narrow one or both sides of the nasal airway and reduce airflow. However, many people with septal deviation breathe normally and do not experience symptoms. Nasal congestion is often caused by inflammation from allergy or rhinitis rather than septal anatomy alone. Objective airflow testing can help determine whether a septal deviation is actually responsible for breathing problems.

Why does menthol make my nose feel clearer?

Menthol and similar substances stimulate cold-sensitive nerve receptors in the nasal lining. These receptors signal to the brain that air is moving through the nose, creating a sensation of improved airflow. However, menthol usually does not change the physical size of the nasal airway or improve airflow resistance. It simply alters the perception of breathing, which is why products containing menthol, eucalyptus, or similar compounds can make the nose feel clearer without treating the underlying cause of congestion.

Learn more

If you would like to learn more about advanced nasal testing and evaluation, visit:

NoseLab: https://richardharvey.sydneyentclinic.com/services/nose-lab/

Remission in Chronic Rhinosinusitis with Nasal Polyps (CRSwNP): Why “Feeling Better” Is No Longer Enough

For years, success in chronic rhinosinusitis with nasal polyps (CRSwNP) meant one thing: the patient feels better.

But in 2025, that is no longer our goal.

With the arrival of biologic therapies for nasal polyps—including dupilumab, mepolizumab, and benralizumab—the target has shifted. In other airway diseases, especially asthma, the conversation has moved beyond symptom improvement toward a more ambitious endpoint: remission. Severe asthma remission has been defined as a composite state (no exacerbations, no systemic corticosteroids, sustained symptom control, stable objective measures, over time).(1) Real-world studies show that remission is achievable in a meaningful subset of biologic-treated asthma patients.(2,3)

CRSwNP shares overlapping type 2 inflammatory biology with asthma and responds to targeted biologics.(4–7) So the obvious question is:

Should we aim for remission in nasal polyps too?

The answer is yes—but CRS is structurally different.

Why Sinus Surgery Changes the Remission Conversation

Unlike asthma, we can surgically modify the anatomy in CRSwNP.

Procedures such as complete sphenoethmoidectomy and extended surgery (e.g., Draf IIc/III) reshape the inflammatory environment, improve topical access, and reduce persistent diseased compartments.(8–10) Distribution studies demonstrate that extended frontal procedures can improve irrigation penetration compared with more limited frontal approaches.(9)

Recent evidence also shows that surgical completeness predicts disease trajectory and may influence response to subsequent biologic therapy. CT-based measures of completeness such as ACCESS (Amsterdam Classification of Completeness of Endoscopic Sinus Surgery) quantify how complete surgery is and have been linked to outcomes.(11) Similarly, the Completion of Surgery Index (CoSI) provides another structured approach to capturing adequacy of surgical extent.(12)

Our recent study—Extent of sinus surgery is associated with disease control in biologic treated type-2 dominant CRS—found that extended neo-sinuis surgery  was strongly associated with achieving disease control in biologic-treated patients.(13) Clincial remisison achieved in 60%+ of patients.

In other words: surgical completeness matters.

So remission in CRSwNP cannot be defined by symptoms alone.

CRSwNP Remission vs. Symptom Improvement

Traditionally, studies report:

Change in SNOT-22

Change in polyp score

Corticosteroid use

Avoidance of revision surgery

These are essential metrics and remain central in consensus guidance.(14,15) But they measure improvement, not a stable disease state.

A patient can be polyp-free yet still require repeated systemic corticosteroids. That is not remission.

That is partial control.

Partial control in nasal polyps

What Should Remission in Nasal Polyps Look Like?

A practical remission framework for CRSwNP should include multiple domains, similar to other inflammatory diseases:

Complete Clinical Remission (≥12 months)

HHT Nosebleeds Treatment in Australia: A Specialist ENT Algorithm for Refractory Epistaxis

Hereditary hemorrhagic telangiectasia (HHT) is a genetic vascular disorder characterised by fragile, abnormal blood vessels. The most common and often most disabling manifestation is recurrent epistaxis. For many patients in Australia, HHT-related nosebleeds progress from occasional inconvenience to chronic haemorrhagic disease requiring iron infusions, transfusions, repeated procedures and multidisciplinary care. This article outlines an evidence-based treatment framework for HHT nosebleeds and presents a practical, phenotype-driven escalation strategy for patients who fail lubricants, tranexamic acid and ablation therapy. Its my professional modification of the Consensus statement  with the evidence basis for what surgical procedures and when.

Why Are Nosebleeds So Common in HHT?

HHT is caused by mutations affecting angiogenesis pathways, most commonly involving ENG or ACVRL1 genes. The result is abnormal vascular development. Within the nasal cavity this leads to superficial telangiectasias with thin walls and reduced structural support, predisposing to recurrent bleeding with airflow, dryness and minor trauma.

Stepwise Management of HHT Epistaxis

The Second International HHT Guidelines provide a structured management framework . However, once initial therapy fails, escalation should reflect bleeding phenotype rather than follow a purely linear pathway. Step 1: Moisturising Therapy Daily saline sprays, gels and humidification form the foundation of management. Reducing crusting and mucosal trauma decreases bleeding frequency but does not alter angiogenic drive.

nasal bleeding blood nose epistaxis septal perforation Step 2: Tranexamic Acid Oral tranexamic acid stabilises clot formation and can reduce bleeding severity in patients with persistent epistaxis . It does not modify telangiectasia formation but is useful adjunctive therapy.

Tranexamic acid for nasal bleeding Step 3: Ablative Therapies KTP laser, radiofrequency ablation, coblation and sclerotherapy reduce bleeding by coagulating visible telangiectasias. While effective, benefits are often temporary, and repeated ablation may result in septal damage .

When Ablative therapy and TXA Fail: A Phenotype-Driven Strategy

Phenotype 1: Multi-System Bleeding Patients with severe anaemia, transfusion dependence or concurrent gastrointestinal bleeding represent a systemic angiogenic phenotype. In this group, intravenous bevacizumab targets VEGF-mediated angiogenesis and has demonstrated reductions in Epistaxis Severity Score and improvements in haemoglobin levels .

Bevacizumab as an intravenous agent. Evidence does not suggest benefit from local use. Phenotype 2: Nasal-Dominant Refractory Disease In patients with predominantly nasal bleeding and limited systemic involvement, septodermoplasty may provide durable benefit. This surgical technique replaces fragile septal mucosa with a split-thickness skin graft, reducing telangiectasia density and mechanical trauma . Phenotype 3: Temporary Stabilisation Silicone (Silastic) septal splints reduce airflow trauma and may provide temporary control or serve as bridging therapy in selected patients .

Silastics sheeting for stabilizing nose bleeds Salvage Therapy: Nasal Closure Nasal closure (Young’s procedure) eliminates airflow through the nose and remains the definitive salvage option for life-threatening or transfusion-dependent epistaxis after failure of other interventions .

Practical Specialist Algorithm

Step 1: Moisturisation and iron optimisation Step 2: Tranexamic acid Step 3: Coblation, Laser or ablative therapy Step 4: Stratify phenotype • Multi-system bleeding → Intravenous bevacizumab • Nasal-dominant disease → Septodermoplasty • Temporary control required → Silicone splints • Catastrophic refractory disease → Nasal closure Escalation should reflect disease biology rather than simply symptom severity.

Frequently Asked Questions About HHT Nosebleeds

Can HHT nosebleeds be cured?

Hereditary hemorrhagic telangiectasia (HHT) is a genetic condition and cannot be cured. However, the frequency and severity of nosebleeds can often be substantially reduced. Management includes regular nasal moisturising therapy, tranexamic acid, targeted ablative procedures such as laser treatment, and escalation to systemic or surgical options in refractory cases.

When should tranexamic acid be used for HHT epistaxis?

Tranexamic acid is typically considered when regular moisturising therapy alone does not provide adequate control. It works by stabilising clot formation and may reduce bleeding severity. It is usually used in conjunction with local ENT measures rather than as a standalone treatment.

What is the role of laser/Coblation therapy in HHT nosebleeds?

Laser and other ablative therapies treat visible telangiectasias within the nasal cavity. These procedures can reduce bleeding frequency and improve quality of life. However, because HHT is driven by ongoing angiogenesis, new telangiectasias may form over time, and repeat treatments or escalation may be necessary.

When is bevacizumab considered for HHT-related nosebleeds in Australia?

Intravenous bevacizumab may be considered in severe or refractory cases, particularly in patients with multi-system bleeding, recurrent iron infusions, or transfusion dependence. Bevacizumab targets vascular endothelial growth factor (VEGF) and addresses the underlying angiogenic drive of the disease. Suitability and access require specialist assessment.

What is septodermoplasty and who is it for?

Septodermoplasty is a surgical procedure in which fragile septal mucosa is replaced with a split-thickness skin graft. It is generally considered in patients with nasal-dominant, refractory HHT epistaxis who have not achieved adequate control with medical therapy and laser treatment.

When is nasal closure (Young’s procedure) used?

Nasal closure is a salvage procedure reserved for severe, refractory epistaxis, particularly when bleeding is life-threatening or transfusion-dependent and other treatments have failed. The procedure permanently stops nasal airflow and requires careful counselling before proceeding.

References

Have you noticed a hard lump on your forehead that feels like bone and doesn’t move when you press it?

Many patients in Sydney present after searching:

“Why do I have a lump on my forehead?”

“Is a bony growth on my forehead dangerous?”

“Do I need surgery for a forehead osteoma?”

In most cases, a firm, painless, slow-growing bump on the forehead is a forehead osteoma — a benign bony tumour arising from the outer layer of the frontal bone .

Although medically harmless, these lesions often cause cosmetic concern. Advances in minimally invasive endoscopic surgery now allow removal as a day surgery procedure in Sydney, with hidden incisions, rapid recovery and excellent cosmetic outcomes .

What Is a Forehead Osteoma?

A forehead osteoma is a benign tumour composed of mature compact bone. It most commonly arises from the outer table of the frontal bone .

Endoscopic removal of a forehead osteoma through a single-port hairline incision.

Key features:

Benign (non-cancerous)

Extremely slow growing

Well circumscribed

Homogeneously dense on CT imaging

No malignant transformation reported

Osteomas are among the most common benign bone-forming lesions of the skull .

Having a Hard Lump on My Forehead

A typical forehead osteoma presents as:

A firm, rock-hard lump

Fixed to underlying bone

Painless

Slowly enlarging over years

Normal overlying skin

Patients frequently describe it as:

“It feels like part of my skull.”

Most outer-table osteomas are discovered incidentally or due to cosmetic asymmetry rather than symptoms .

What Causes a Bony Growth of the Forehead?

The exact cause of a bony growth of the forehead remains unclear.

Proposed mechanisms include:

Developmental overgrowth

Reactive bone formation

Genetic predisposition (rare)

Association with Gardner syndrome (rare and usually multiple lesions)

In most adult patients, osteomas arise spontaneously and grow slowly over time.

Can a Forehead Osteoma Turn Into Cancer?

No. There are no reports of malignant transformation of a true osteoma .

Natural History: Will a Forehead Osteoma Go Away?

Forehead osteomas:

Odontogenic Sinusitis: The Overlooked Source of Sinus Disease

Understanding Odontogenic Sinusitis Odontogenic sinusitis (ODS) represents a distinct and often under-recognised subset of chronic rhinosinusitis (CRS). It is defined as sinus inflammation secondary to a dental or odontogenic process—hence sometimes referred to as secondary CRS. While CRS is classically associated with mucosal disease of nasal origin, a surprising proportion arises from dental pathology extending into the maxillary sinus. In the modern rhinology clinic, understanding, recognising, and optimally managing ODS is critical for effective patient outcomes. According to the European Position Paper on Rhinosinusitis and Nasal Polyps 2020 (Fokkens et al.), odontogenic processes should always be considered in unilateral sinus disease, particularly when maxillary involvement predominates. Epidemiology and Clinical Suspicion Unilateral disease is the first red flag. Studies show that nearly half of all unilateral maxillary opacifications have an odontogenic origin. Turfe et al. (2019) analysed 45 % of unilateral cases and found: - 44 % reported a foul smell, - 87 % had middle-meatal purulence, - 66 % had no mention of ODS on radiology, and - 88 % involved extra-maxillary extension—most commonly into the frontal sinus (60 %). Even more strikingly, in dental literature summarised by Vitali et al. (2023), the pooled global prevalence of ODS among affected sinuses reached 51 % (range 40–61 %). Risk factors included: - Apical lesions (odds ratio 4.03), - Periodontitis (OR 5.49), and - Bone loss—moderate (OR 2.57) to severe (OR 13.8). This data illustrates that half of what we call “maxillary sinusitis” is actually dental in origin.

Mechanisms: How Dental Pathology Breaches the Sinus The proximity of upper posterior teeth roots to the maxillary sinus floor creates a delicate anatomical relationship. Periapical infection, periodontitis, tooth extraction, or implant manipulation can disrupt the sinus membrane, providing a conduit for bacteria, foreign material, and inflammatory mediators to invade the sinus cavity. This invasion triggers mucosal inflammation, impaired mucociliary clearance, and eventual pan-sinus spread if untreated. As the disease evolves, secondary sinus involvement—especially of the ethmoid and frontal sinuses—is common, explaining why patients often present with broad sinonasal symptoms despite an odontogenic origin. Predictive Clinical Features Clinically, ODS can mimic routine sinusitis but carries several predictive hallmarks: Predictive Factor ODS Non-ODS p-Value Posterior discharge 63 % 45 % 0.004 Frontal involvement 58 % 38 % 0.019 (Goyal et al., 2021). A patient with posterior nasal discharge, unilateral frontal sinus opacification, or a foul odour should immediately prompt the clinician to review dental history, imaging, and examine the upper molars.

The Curious Experience of Nasal Breathing: A Deep Dive into Human Perception

When we think about breathing, it often feels like a straightforward, mechanical process: air flows in through our nose or mouth, fills our lungs, and sustains life. Yet the subjective experience of nasal breathing is anything but simple. For millions around the world, the sensation—or disruption—of nasal airflow can heavily impact comfort, sleep, and even emotional well-being. Surprisingly, this perception is not merely about how much air passes through the nostrils, but also how the nasal mucosa "feels" that airflow. Recent research sheds light on the complex sensory and psychological mechanisms underlying nasal breathing. Understanding this can not only reshape how we view common complaints like nasal congestion but also revolutionize treatments for conditions like chronic rhinitis/ rhinosinusitis and empty nose syndrome.: Interpreting Nasal Congestion: Bridging the Blockage vs Pressure/Mucus Divide The symptom of nasal congestion often reflects a striking disconnect between patient and clinician interpretations. McCoul et al. (2019) revealed that while clinicians narrowly define congestion as nasal blockage due to mucosal swelling, patients frequently describe congestion using a much broader palette of sensations—including facial pressure, mucus accumulation, and even headache. Critically, the study found that patients were 39% more likely to associate congestion with pressure-related symptoms and 51% more likely to relate it to mucus symptoms compared to clinicians. For example, 50% of patients identified "pressure in the face" as part of congestion, compared to only 16% of doctors. Similarly, "postnasal drip" was tied to congestion by 38% of patients but merely 3.5% of clinicians. This discrepancy highlights a clinical pitfall: if physicians focus only on airway patency and physical obstruction, they may miss the true sources of patient distress. As Harvey et al. (2024) further emphasized, "nasal congestion" is often an umbrella term encompassing blockage, pressure, mucus, and even pain. Anatomical evaluations and airflow measures like rhinomanometry may therefore fail to capture the complex, multifaceted experience patients report.

the difference between what clinicans and patients mean when they refer to 'nasal congestion' Effective communication is crucial. Physicians should actively inquire whether a patient's "congestion" refers to airflow restriction, facial pressure, or mucus-related symptoms. Tailoring treatment accordingly—whether decongestants, anti-inflammatory therapies, or mucus modulators—can dramatically improve satisfaction and outcomes. In summary, nasal congestion is not synonymous with obstruction. Addressing pressure and mucus symptoms alongside physical airway management is essential for truly meeting patient needs.

The Anatomy of Perception: Airflow vs. Sensation

At first glance, one might think that the brain senses airflow in the nose directly. However, human nasal perception is primarily thermosensory, not purely mechanosensory. In other words, what we feel as "easy breathing" largely depends on how cool our nasal lining becomes, not necessarily how much air moves through the nose. When air passes through the nasal passages, it causes evaporative and radiant cooling of the mucosal surfaces. This subtle temperature change is detected by specific nerve endings, particularly those belonging to the trigeminal nerve. Interestingly, despite measurable increases in airflow after procedures like septoplasty or turbinate reduction, many patients still report persistent nasal obstruction if the mucosal cooling effect is not restored. Simple objective airflow measurements often correlate poorly with subjective improvements in breathing sensation.

A high septal deflection on the left is relatively minor but prevent airflow to the upper part of the left nasal cavity and brings about a disproportionate sense of nasal obstruction compared to the anatomical cross-sectional area comprimsed by that anatomical abnormality Thus, enhancing mucosal cooling—not merely enlarging airway diameter—is critical to optimizing the subjective nasal breathing experience.

TRP Channels: The Molecular Guardians of Nasal Sensation

The key players in detecting nasal mucosal cooling are transient receptor potential (TRP) channels, a family of ion channels involved in sensory transduction. TRPM8, a specific subtype of TRP channels, is particularly crucial. It responds to: - Temperatures between 8°C and 22°C - Chemical agents like menthol and eucalyptol When activated, TRPM8 channels stimulate sensory neurons that transmit signals to the brainstem and cortex. This leads to the subjective experience of "clear" and "easy" nasal breathing.

it is evaporative cooling of the nose that triggers the sense of nasal breathing It's why mentholated lozenges, nasal sprays, or even cool air can create a powerful illusion of improved nasal airflow, even when objective measurements remain unchanged. TRPM8 receptors are located predominantly on trigeminal nerve endings within the nasal epithelium, mucous glands, and vessels, making them essential sensors of the nasal environment.

How Cooling Becomes Consciousness: The Neural Pathway

Once the TRPM8 receptors are activated by cooling, they: - Depolarize sensory neurons - Send signals to the spinal trigeminal nucleus - Cross over to ascend the trigeminospinothalamic tract - Activate higher brain regions such as: - The insula cortex (emotional processing) - The anterior cingulate cortex (attention and decision making) - The somatosensory cortex (sensory mapping) - The precentral gyrus (motor control) This complex neurocircuitry illustrates why nasal obstruction isn't merely a physical complaint. It deeply ties into emotion, cognition, and even motor readiness, explaining why nasal blockage can feel so distressing and distracting.

Beyond the Nose: Anxiety and the Sensation of Air Hunger

An often overlooked factor in nasal perception is the role of psychological states, particularly anxiety. Feelings of "not being able to breathe" strongly overlap with symptoms seen in anxiety disorders: - Air hunger - Dyspnea - A sensation of suffocation In conditions like empty nose syndrome (ENS), patients paradoxically feel congested despite having wide, open nasal passages post-surgery. This mismatch between objective nasal patency and subjective breathing difficulty is thought to involve maladaptive cortical processing, especially in the emotional centers of the brain. Thus, treating nasal obstruction might, in some cases, require a dual approach: - Physical: Correcting anatomical issues and restoring mucosal cooling - Psychological: Managing underlying anxiety or sensory integration disorders

Clinical Implications: Reframing Treatment Goals

Traditional interventions for nasal congestion have heavily focused on restoring airflow. However, newer insights emphasize that restoring mucosal cooling sensation is just as, if not more, important. Strategies include: - Create mucosal separation throughout the nasal cavity during surgery to enable evaporative cooling - Treat underling inflammatory mucosal disease - Avoiding offering surgery to patients that have enormous expectations of benefit to fatique, sleep and energy levels - Screening patients for anxiety or emotional dysregulation pre- and post-surgery Furthermore, in chronic rhinosinusitis with nasal polyps (CRSwNP), effective treatments like biologics (e.g., anti-IL-5, anti-IL-4/13 agents) not only reduce polyp burden but may also improve mucosal health, enhancing cooling sensation and breathing perception.

Emerging Therapies: Biologics and Beyond

In chronic inflammatory conditions like type 2 CRSwNP, biologics targeting eosinophils (anti-IL-5) or broader type 2 pathways (anti-IL-4/IL-13) are changing the landscape. By reducing mucosal inflammation, they indirectly restore: - Mucosal smoothness - Normal vascular function - Effective TRPM8 signaling Clinical trials like SYNAPSE (mepolizumab) and dupilumab real-world studies have shown significant improvements in nasal symptom burden, often including improvements in breathing perception. Yet not all patients respond equally. In non-responders, other factors like local allergen-driven IgE pathways, anatomic variations, or even psychological overlays may still drive symptoms.

Conclusion: Breathing is More Than Air