The Handicapped Nose Breathing

Prof. W. Bachmann The handicapped nose breathing

Basic diagnostics:

Anamnesis, inspection, rhinomanometrics and allergology Prof. Dr. W. Bachmann ATMOS MedizinTechnik GmbH & Co. KG Kaiser-Wilhelm-Straße 5 Ludwig-Kegel-Straße 16 76530 Baden-Baden 79853 Lenzkirch Germany Germany

phone +49 7653 689-0 fax +49 7653 689-190

2 Preface Measurement of nasal resistance, especially, has taught us in recent years to understand better the associations between the form and function of the nose. This is still true today. Without comparing the patient’s history and findings on inspection with the measurements of resistance, a functional assessment of narrow points and anatomical abnormalities cannot be made.

Error-free investigation and treatment of obstructed nasal breathing can often be achieved only by the precise quantification and differentiation of nasal resistance (constant anatomical resistance, variable turbinate resistance, the ratio between the two sides, flow increase etc.) with the aid of rhinomanometry. In recent years, the diagnostic process has become standardised. Unfortunately, however, there has hitherto been no short practical introduction to:

. rhinomanometry and the sources of error

. history, inspection and rhinomanometry as a diagnostic unit

. basic features of the investigation of nasal allergies and hyperreactivity

. basic clinical and functional anatomical information

I hope that this brief introduction, limited to what is important and accepted will prove useful for rhinologists, allergists, pulmonologists, occupational and sports physicians and medical technical staff both as an introduction and as a reference book for routine clinical practice.

August 2000 Prof. W. Bachmann

3 Table of contents 1.0 Introduction: why rhinomanometry? 6

2.0 Nasal resistance 2.1 Nasal resistance graphs: respiratory pliers, spread, quantification 8 2.2 Physiological spread, representative graph 9 2.3 Quantification of nasal resistance, 2 parameters 9 2.3.1 Clinically oriented parameters: V150 and Δ V% 10 2.3.2 Equivalent tube sizes 11

3.0 Performing rhinomanometry 3.1 Structure and mode of function of a rhinomanometer 12 3.2 Guidelines on performing rhinomanometry 13 3.3 Anterior measurement of choanal pressure with adapter 15 3.4 Posterior measurement of choanal pressure with oral probe 16 3.5 Synchronous measurement of pressure difference and flow through half-mask with measuring tube 17

4.0 Investigation of obstructed nasal breathing 4.1 The nose as flow channel: form and function as one unit 18 4.2 Clinically important basic concepts 21 4.3 Three leading symptoms (often in combination), important groups of illnesses 23 4.4 History: basic investigations 24 4.5 Anterior and posterior rhinoscopy (endoscopy). Basic investigations 25 4.6 Rhinomanometry (basic investigations) 26

4 5.0 Nasal hyperreactivity 5.1 Definition, pathomechanisms 29 5.2 Non-allergic hyperreactive rhinitis 30 5.3 The allergic type I reaction (hyperreactivity in 3 phases) 32 5.3.1 Clinically important basic data concerning nasally acting allergens (3 groups) 33 5.3.2 Baseline investigations to find the current allergen 36 5.3.3 Allergy history (family, personal, symptoms, environmental history) 36 5.3.4 Targetted search for the current allergen by classifing the predominant symptoms into 4 main groups 38 5.3.5 Skin testing – RAST 39 5.3.6 Emergency treatment of allergic incidents 42 5.3.7 Nasal provocation 43 5.3.8 Investigation of oral allergens with nasal symptoms (cross allergies, pseudo-allergies) 47

6.0 Appendix 6.1 Brief history of rhinomanometry 49 6.2 Conclusion 49 References 50 6.4 Division of rhinomanometric measuring curves 32 6.5 Flow SUM...... 32 6.6 Flow INC...... 32

5 1.0 Introduction: Why rhinomanometry?

Evaluation of nasal resistance is difficult, as it is a parallel, alternating and partial resistance of the entire airways, and it also possesses a bypass – mouth breathing. Obstructed nasal breathing can be caused by different factors, alone or in combination.

Assessment of nasal resistance by the patient is often incorrect and misleading because of his lack of knowledge of the physiological and pathological relations. Assessment by inspection, endoscopy or acoustic rhinometry is reliable only in extreme cases, since an exact quantitative conclusion about the measurable patency cannot be drawn from the measured cross section because of the complicated flow physics.

Quantification by rhinomanometry is therefore essential! This is the only method that allows:

. distinguishing of anatomical defects of the supporting skeleton, hyperreactivity, non-nasal factors in mouth breathing and erroneous subjective assessment when there are combined causes, . determination of objective operative indications (nonphysiological bottlenecks, anatomical defects increasing turbulence or narrowing the lumen, turbinate factors, side asymmetry), . clarification of operative contraindications (nasal cavity too wide), . confirmation of the current state of nasal allergies by measuring the reduction in flow after nasal provocation, . support for the diagnosis of nasal hyperreactivity by clarifying the turbinate factor and excluding nasal allergens by provocation, . objective identification of non-nasal factors (oral, dental, jaw anomalies, pulmonary, cardiac dyspnoea, psychological factors) in mouth breathing by obtaining normal measurements, . identification of false subjective estimates of patency by comparing with the measurements,

6 . quantification of alterations in patency after: . diagnostic measures (resolving swelling, provocation etc.) . therapeutic measures (operative, medical, physical) . experimental measures (hot and cold stimuli, changes of position).

7 2.0 Nasal resistance 2.1 Nasal resistance graphs: Respiratory pliers, spread, quantification

Nasal resistance is a preset regulatory resistance for the optimum ventilation of the sinuses, ears and lungs. It is greater than lung resistance, hence its clinical importance and the indispensability of measuring it!

. Figure 1. “Respiratory Flow V (cm³/s) pliers” according to Exspiration li. Inspiration re. BACHMANN using anterior measurement = ∆ p (Pascal) right and left side present a mirror image. Ter- minology: international Exspiration re. Inspiration li. standard, see also page 16.

. Typically curved resistance graphs as a result of the resistance changing during a breath. (simple quantification is therefore impossible.) . Principle of measurement: synchronous measurement of 2 parameters: Pressure difference Δ p (Pascal) between nasal opening and choana. Flow V. (cm³/s) = volume of air flowing through each cross section per second or per minute. . Analysis: flow at 75, 150, 300 Pascal. Roughly: . The smaller V. 150, the closer the graph is to the x axis, the greater the unilateral resistance and the lower the nasal patency. . The lower V.150 bilat, the narrower the respiratory pliers and the greater the total resistance. . False graphs see page 13.

8 2.2 Physiological spread, representative graph

Several breaths in one measurement have a scatter of up to 15%. However, a single representative graph is required for quantification. Since outliers often occur, simple averages are insufficient. It should be stated in describing the device what method is used for drawing a representative graph (weighting, re- gression graph, CAR etc). The representative graphs of immediately repeated measurements can have a scatter of up to 15 %.

2.3 Quantification of nasal resistance, 2 parameters

Quantification of the resistance graph is problematic, since it has 3 phases: . A purely laminar initial phase. This is extremely brief (approx. 0 - 30 cm³/s flow) and therefore clinically insignificant. This is also an area of very high measurement precision. . A large laminar-turbulent mixed phase due to increasing turbulence. It is the most important zone physiologically. . An end phase. There is individual variation, and it has either a still obvious laminar component or is predominantly turbulent or completely turbulent or demonstrates inspiratory narrowing of the lumen with an increasingly straight-line graph.

For diagnosis 2 parameters which allow a comparison are sufficient: . with the history to clarify subjective false estimates . with inspection to elucidate: . pathological bottlenecks (i.e. narrower than a normal isthmus, page 18). . anatomical defects (deviations, spines etc.), which disturb the flow as the pressure difference increases due to turbulence, deflection, eddies etc. . anatomical defects which cause inspiratory narrowing of the lumen (valve stenosis).

9 2.3.1 Clinically oriented parameters: V.150 and Δ V% (BACHMANN, BACHERT)

Both are clear and easy to measure as they simply quantify the increase in flow between 0 and 150 and 150 and 300 Pascal and compare it with a purely laminar flow (figure 2). They can be read directly from the graph or printed as a table with graph. They allow a conclusion to be drawn about the type of flow (laminar, turbulent, mixed) and its causes (bottlenecks, anatomical defects) and to identify subjective false estimates.

. . V 150, the increase in flow between 0 and 150 Pascal. It is dominated by the narrowest point and is the inverse of the 4th-5th power of the hydraulic diameter*). Relative to this, turbulence, eddying etc. is still low and not very relevant diagnostically.

. . ∆ V %, the percentage increase in flow between 150 and 300 Pascal. Since it is 100 % with purely laminar flow, lower levels indicate abnormalities of laminarity (turbulence etc.) caused by anatomical defects, and also inspiratory narrowing of the lumen. The lower the Δ V. %, the greater the abnormality and the significance of the anatomical defect (figure 2):

. . ∆ V . between 100 and 80 %: Predominantly laminar flow. Often in the case of a narrow nose, when there is no great difference between the cross section of the isthmus and that of the nasal cavity. . . ∆ V between 80 and 41 %: Laminar-turbulent mixed flow due to anatomical defects such as an excessively wide cavity, deviations, spines etc. . . ∆ V 41 %: Purely turbulent flow. The graph forms a parabola. . . ∆ V between 41 and 25 %: Additional eddies, deflection etc. due to marked anatomical defects or slight inspiratory narrowing of the lumen. . . ∆ V less than 25 %: Definite inspiratory narrowing of the lumen due to extremly tender wings of nose, floating polyps (valve stenosis).

10 Calculation of Δ V.%: V 300 divided by V. 150. The two places after the decimal correspond to the increase in flow in %. If V 300 is not reached, the patient should be asked to breathe harder!

. V cm³/s Laminar flow, since flow is doubled when Δ p is doubled Disturbance of laminarity (turbulence etc.)

Increase in flow Δ V. The lower this figure, the Nasal resistance greater the disturbance of laminarity. graph Δ V. % = percentage V. increases relative to V. 150.

Increase in flow V. 150. The lower this is, the higher the resistance due to dominant narrowest point.

∆ p 150 300

Figure 2. Clinical parameters V. 150, V. 300 and Δ V. %

2.3.2 Equivalent tube sizes (MLYNSKI)

Comparison with the diameter d and coefficient of friction λ of round tubes of the same resistance is not useful clinically, since it only quantifies the purely laminar or purely turbulent zone, but not the physiologically important laminar- turbulent zone. The equivalent quantities d and λ are difficult to calculate and not clearly useful for the physician.

*) In this way, non-round tubes can be compared to round tubes (dh = 4 x area / circumference).

11 3.0 Performing rhinomanometry 3.1 Structure and mode of function of a rhinomanometer







Figure 3. ATMOS® Rhino 31 made by ATMOS MedizinTechnik GmbH & Co. KG

Structure: . Recording measurements . Measuring probe with olives  or Half mask for flow, can be attached to the flow measuring tube . Pressure probe and hose  or Tube with nasal adapter for ∆ p . Handle  . Rhinomanometer with operating buttons, electromechanical pressure transducer, amplifier, analogue-digital transducer, programs for the ENT physician and allergist to calculate clinical parameters. Display for essential monitoring of procedure and test result. . integrated printer

Function: Rhinomanometers are easy to operate nowadays (measurement of both sides takes under 3 minutes). The synchronously measured pressure difference and flow are converted by sensitive pressure sensors into electrical voltage, ampli- fied and digitalised. With these data, the microprocessor calculates the desired clinical parameters while eliminating outliers.The measurement process is mo- nitored online as a graph by appearing on a display. The graphs obtained and the calculated relevant parameters are stored and printed when required.

12 Measurement accuracy: For technical reasons and because of the curve of the graph, there are different errors in measuring the pressure difference and the flow. The pressure difference has a measurement inaccuracy of at least ± 0.5 Pascal. In the case of flow, the percentage inaccuracy is greatest close to zero and falls as the initial levels increase. Thus, with a measurement diaphragm with a diameter of 8 mm an inaccuracy of less than 5 % is only obtained with a flow of approx. 100 cm³/s. Results obtained below this threshold are therefore very inaccurate (e.g. the equivalent tube diameter d according to MLYNSKI, page 11).

3.2 Guidelines on performing rhinomanometry

Requirements, preparation of apparatus Incorrect results are nearly always due to incorrect attachment of the pressure adapter and the mask. It should first be practised on one’s own person. . After acute inflammation or nasal operations, patency stabilises only after about 6 - 8 weeks! . Because of the regulatory function of the nose, the patient has to adapt to the atmosphere of the room for at least 10 minutes during the heating period. It should also not be preceded by major physical exertion (e.g. climbing stairs). . Enquire about last use or application of nasally-acting medication. . Before commencing measurement, the patient must be asked about present patency (very good, good, poor, very poor) and this should be recorded, otherwise subjective false estimates cannot be identified. . Then switch on the rhinomanometer, select the program and set to zero without inserting the nasal adapter and without putting on the mask, otherwise a correct measurement cannot be made.

13 Measurement – 10 rules . Rhinomanometry is usually performed with the patient seated. . The patient should blow his nose if necessary. . After informing the patient briefly about the procedure, the appropriate nasal adapter for the anterior technique (page 15) or the oral probe for the posterior technique (page 17) is placed to measure the pressure difference. . Then press the mask onto the face to measure the flow (Figure 9). Ensure that it fits closely without blocking the nasal entrance by excessive pressure. The most frequent side air is in the eye-nose angle. . The patient now has to breathe in and out with the mouth closed. . Observe the display to see whether the normally S-shaped graph demonstrates:

 . extreme deviations around the V 0-point,   extreme scattering,  or large loops. 

In such cases, eliminate the cause (mouth breathing, side air?) or start ∆ p the measurement again without mask 300 and adapter!!

 the 300 Pascal line is reached   during inspiration. If not, the patient should be asked to breathe a bit harder. Figure 4. Typical false graphs

. The actual measurement program is only started when “test breaths” are normal. After 3-5 “proper” breaths, the table of results (page 28) is retrieved and the mask and adapter are removed. . This procedure is repeated on the other side. . Apart from this general procedure, different operating instructions should be noted with different rhinomanometers.

14 3.3 Anterior recording of choanal pressure with adapter

Anterior technique = method of choice Closed side of the nose acts like an elongated tube as far as the choana. Disadvantages of the anterior method: . The method cannot be used in the presence of perforated or floating septum. . Only one side can be measured at a time! . Bilateral flow must always be calculated with the Measuring hose Nose for choanal adapter same Δ p, normally 150 Pascal. E.g. V. 150 bilat = pressure V. 150 r + V. 150 l Figure 5. . By closing one side, an artificial stenosis occurs with reactive dilation of the free side. As a result, the calculated bilateral result is slightly higher than the bilateral result measured posteriorly.

Right lumen impression from in front . Note oblique vestibular axis. . Isthmus = physiologically narrowest point in the cavity between septum and lateral mucocuta- Cavum neous junction (concave, narrow above, wide Cavity entrance below, flexible lateral margin) for rapid alterations of resistance. Produces 60 % of the resistance of

one side (page 18). Isthmus Vestibulum . Cavity entrance: large, round-oval, bordered by limen nasi = mucocutaneous junction between vestibule and cavity (medial border = upper edge of mobile septum). Figure 6.

15 Correct insertion of the nasal adapter . Because of the oblique vestibular axis, the adapter is placed so that its opening touches the bottom of the septum. It is then advanced ver- tically upwards into the vestibule until the patient feels that the adapter is airtight in place. . It is possible to check that it is airtight: the adapter tube is pressed closed, the free nostril is also held closed and the patient is asked to sniff in and out. If the adapter is firmly in place, the nostrils move inwards and outwards. . Foam with closed pores is usually used as adapter. Figure 7

3.4 Posterior measurement of choanal pressure with oral probe

Recording the choanal pressure by an oral probe is successful in only about 2/3 of cases since the probe often causes a reflex raising of the ton- gue or soft palate. The method is therefore not suitable for daily routine practice. Tube for measuring choanal pressure Figure 8

Advantages: . The bilateral resistance can be obtained with one measurement. . Measurement is also possible in the presence of a perforated septum.

16 3.5 Synchronous recording of the pressure difference and flow through a half-mask with tube

After application of the adapter: . Push the mask with tube up into the chin furrow  . Press it onto the face (dotted line)  . Ensure a close fit, but avoid excessive pressure, otherwise nasal entrance is distorted. . Commonest site of leak: eye-nose angle

Nasal olives are not allowed for recording flow according to the recommen- dations of the European Committee for Standardising Rhinomanometry, as considerable scattering of the results Right! is provoked by uncontrollable exclusion of isthmus resistance. Wrong: mouth not closed Three principal errors in attaching the sensor: . Mask has side air on the face. Resis- tance appears too high! Figure 9. . Mouth not closed (relatively frequent)! Resistance appears too low! . Pressure tube is not securely airtight in the nostril. Patency appears too good!

17 4.0 Investigation of obstructed nasal breathing 4.1 The nose as flow channel: form and function as a unit

Form without function is a corpse. Function without form is a ghost (VOGEL, WAINRIGHT).

. Typical: curve at the start (oblique vestibule, Figure 6) and at the end (choanae). . An anterior jet-like narrow point (isthmus) and a wide cavity. . A mobile lateral wall (lateral soft tissue wall, turbinates capable of swelling). . The slit-like nasal lumen is divided into vestibular, valve and turbinate area, where the vestibule and valve area form an anterior functional unit.

1)  Vestibule Directs air through the cavity entrance obliquely to the most anterior part of the septum (collision surface for large foreign bodies). Anatomical defects, e.g. saddle or snub nose, can alter this.

2)  -  Valve area. . Central physiological and clinical importance! . Scaffolding: septum, lateral cartilage, piriform aperture, floor of the nose. . The valve area corresponds to the anterior cavity, i.e. from the cavity entrance as far as the aperture. . Upper valve gap according to MINK (), between the septum and lateral cartilage. . Cavity entrance area (), arched over by the lateral wall of the vestibule. Typical stenosis septal haematoma. Boundaries of cavity entrance see figure 13. . Isthmus region (), isthmus as far as the head of the inferior turbinate. Site of most stenoses. Isthmus (LEGLER, BACHMANN) boundaries and shape see figures 6, 12, 13.

18 Importance: . High (approx. 60 %), rapidly regulatable (since flexible laterally) series resistance for optimum ventilation of the sinuses, the middle ear and the lungs. . Distribution of the air in the entire cavity but reduced into the narrow upper half of the cavity (region of smell), increased into the wide lower half that is crucial for patency. . Early turbulence (jet) for exchange processes in the turbinate area. Pathological importance: . If isthmus not curved, no optimum distribution of the flow of air into the cavity. . If isthmus too narrow, resistance too high, i.e. V. 150 very low. . If isthmus too wide, poor ventilation of sinuses, middle ear and lungs, since in- and expiratory alternating pressure too low! . If lower lateral margin too rigid (e.g. postoperatively) rapid changes in resistance impossible (incorrectly ascribed to the poorly flexible Mink valve). . Area of head of turbinate(), part of the valve area, since the head of the inferior turbinate exceeds the aperture!

3) Turbinate area. If the space in the cavity is too wide (atrophy, large turbinate reduction) turbulence too high dryness, little capacity for swelling for long-lasting changes in resistance (climate adaptation), small climatic and immunological exchange surface.  The larger the cross section of the cavity relative to the isthmus, the greater the turbulence (jet effect). Example: atrophic rhinitis (V 150 good, but Δ V % < 35% = much turbulence).

Figure 10. Division of the lumen into vestibule, valve and turbinate areas.

\\\\\\: Olfactory region  Bold: Isthmus and aperture Grey: lower half of lumnen Shaded: isthmus region ()

    Body of Choana Valve area turbinate

19 Figure 11. The lower half of the lumen is crucial for nasal patency. This applies also for the valve area. Example: upper valve crevice narrow on right, lower lumen wide = good patency. R L Figure 12. Concave isthmus surface. Narrowest cross section.

Hook in the pocket at the tip of the nose

Lower edge of the lateral cartilage = cranial isthmus and medial boundary of cavity (not or crus slightly flexible).

Mucocutaneous fold in the incisura of the medial aperture = lateral isthmus and border of border of cavity (very flexible). isthmus Fissure in cavity with inferior turbinate septum Vestibule, thin medial wall (mobile septum) and broad mobile septum lateral wall (side of the nose). Resulting oblique entrance to cavity.

Edge of nostril

Hook in the posterior pocket of the vestibule

Figure 13. View into the left nasal lumen. Isthmus, entrance to cavity.

Isthmus ( ) = Physiologically narrowest point (approx. 0.6 – 0.8 cm²) in the anterior cavity, shown by vertical projection of the craniolateral mucocutaneous junction onto the septum (- - - - -). There is no structural boundary! Shape: concave, narrow above, wide below. Flexible lateral margin!

20 Entrance to cavity ( ) = Large round-oval oblique boundary between vesitbule and cavity. Extends from the upper border of the columella to the joint lateral boundary of the isthmus and cavity. Its boundary is identical with the entire mucocutaneous junction (limen nasi).

4.2 Clinically important basic concepts

The diagnostic evaluation of nasal resistance is difficult, as it is a parallel resistance (R+L), an alternating resistance (isthmus, turbinates) and a partial resistance (approx. 50 - 60% of the total airways), and also possesses a bypass – mouth breathing.

. Definition of obstructed nasal breathing: constant or intermittent mouth breathing when sitting or lying or during light exertion (walking quickly, climbing short stairs) after excluding non-nasal causes (page 23).

. The patient’s sensation of nasal resistance can have a nasal or non-nasal origin. Quantitatively often not identical with the objective (measurable) resistance.

. . . Physical: resistance R = ∆ p / V , Patency D = V / ∆ p When flow is not purely laminar, R applies only to each point on the graph.

Because of the changing patency, both uni- and bilateral, depending on the atmosphere, previous exertion, sitting or lying, investigation should distinguish the following:

. Constant anatomical or skeletal resistance due to cartilage and bone structures is the residual resistance after the maximum fall in swelling (2 x in 10 minutes!).

. The variable turbinate resistance for slow but long-lasting changes (e.g. climate change etc.) corresponds to the difference between resting resis- stance and the resistance after maximum subsidence of swelling.

21 . The variable isthmus resistance for rapid changes during physical exertion derives from the tone of the nasal muscles. It is seldom tested in isolation (dilatation test).

. Momentary (current) uni- or bilateral patency (P.) Every diagnosis requires a comparison between the history, inspection and rhinomanometry. A precondition for this is the same measure for patency: very good, good, bad, very bad. Unfortunately, the information obtained from the patient is often unreliable. It is more reliable when he is asked to make comparisons: is your nasal breathing better or worse? Then: good or very good or bad or very bad? An answer of middling is not useful for quantification. Assessment by inspection is also uncertain, except in extreme cases. Measurement of the subjective estimate and assessment from inspection is therefore essential.

. The bilateral mean (average) patency (P) It is found most reliably from the frequency of mouth breathing: never, seldom, often, constantly (equivalent to: very good, good, bad, very bad).

. We speak of permanent or intermittent stenosis in the presence of constantly or temporarily pathologically increased resistance. We speak of pseudostenosis if obstructed breathing without mouth breathing is reported (page 24).

. The physiological shalf-side rhythm . Unilateral control measurements possible only short-term, since one side of the nose swells every 4 - 8 hours, and the other subsides to about the same degree. . In contrast, bilateral patency remains the same under the same external conditions with a scatter of approx. 10 - 15 %. This allows us to speak of an average patency P–bilaterally.

Figure 14.

22 4.3 Three leading symptoms (often in combination), important groups of illnesses

1.Reduced patency (definition see page 21) Uni- or bilateral anatomical defect: permanent stenosis, no secretion (pathological V. 150- and/or other results see page 12). V. bilat. In operative region, coincides with the assessment of “poor”.The type and site of the stenosis are determined by inspection. Space-occupying processes: foreign bodies, benign tumours (nasal polyps: genuine, mucoviscidosis, Kartagener‘s syndrome, Woake’s syndrome etc.), malignant tumours.

2. Abnormal secretion (too little, too much, pathological secretion) Rhinitis sicca: endogenous, postinfectious, medication-related. No secretion, possibly crust formation, sometimes hyposmia, V.150bilat > 700 cm³/s, frequent Δ V. < 35%. Blocked sensation due to abnormal mucosal sensitivity, sometimes with mouth breathing. . Atrophic rhinitis with mouth breathing (V 150 bilat > 700 cm³/s, Δ V. often < 35%): broad nose = no “physiological preset resistance” = shallow breathing = too little distension of alveoli = sensation of obstructed nasal breathing = tran- sition to mouth breathing. (This sensation is less frequent during exertion, as breathing is forced anyway.) Rhinitis, Sinusitis (purulent secretion): Fluctuating permanent stenosis. High reduction of swelling. Cytokines and neuropeptides play a part when changing from viral headcold to a chronic state (duration despite treatment of more than 8 weeks). As co-transmitters, they have a direct effect on blood vessels and glands, especially substance P. Brady- kinin is predominant among the mediators. Cause: bacterial, viral, mycotic. Rare specific infections: TB, lues, leprosy, rhinoscleroma etc. Systemic diseases, e.g. Wegener’s disease, immunglobulin deficiencies. Nasale allergy (ubiquious, non-ubiquitous, oral allergens): Usually a triad of symptoms: intermittent stenosis (frequently also alternate sides), i.e. free or less severe intervals, non-purulent secretion, irritation. Often excessively poor estimate of current patency. Usually swollen livid mucosa. High reduction in swelling (> 120 cm³/s), rhinomanometric provocation tests elucidate current involvement of the allergens. Non-allergic hyperreactivity: similar symptoms as allergic rhinitis. CSF fistula: purely watery secretion. Tumours, ulcers: bloody secretion.

23 3. Subjective false assessment (due to effect ofnon -nasal factors) Excessively poor estimate of current patency. Why? . Mouth not closed, despite closed teeth, since upper lip is too short and front teeth are too long. Often mistaken for “tension nose”. . Oral, dental, jaw anomalies; marked tonsil hypertrophy, adenoids. . Mouth breathing because of dyspnoea of pulmonary, cardiac or other origin. . Mouth breathing because of Rh. sicca / atrophic rhinitis (see above). . In allergic or non-allergic intermittent stenosis, worse periods are often refer- red to the current situation. . Underestimation of improvement of infections of the upper/lower airways. . Stress: “being fed up”. Excessively good estimate of current patency. Why? . Medication improving airway resistance (cortisone, anti-asthmatic drugs). . Insensibility to discomfort, particularly in young persons because accessory respiratory muscles are still strong. Errors in diagnosis and treatment usually result from false estimates of patency (P) by patient and physician (because of complicated flow physics): . Non-indicated septum or turbinate correction. . Failure to perform operation despite medical indication (page 26) or in the case of a combination of hyperreactive rhinitis with anatomical defects. . Hyposensitisation despite unproven involvement of the allergen.

4.4 History: baseline investigations

Duration: recent, moderate or prolonged? Right or left-sided, bilateral? Alter- nating sides? Type of nasal breathing: permanent stenosis (anatomical abnormality)? Inter- mittent stenosis (allergictype)? Pseudostenosis (subjective false estimate, page 13)? 2 forms: . No mouth breathing, but “blocked feeling” (typical of atrophic rhinitis/ rhinitis sicca) . Mouth breathing of non-nasal origin is interpreted as nasal in origin Degree of current nasal breathing: very good, good, poor, very poor? In both cases, the degree of patency can be determined only by rhinomanometry. Degree of average patency: very good, good, poor, very poor? Identical with frequency of mouth breathing at rest, lying down, on mild exertion: never, rarely, often, always?

24 Other symptoms: secretion (serous, mucous, purulent, bloody)?, irritation (sneezing, itching)? Medications acting on the nose? Operations (nose, sinuses)?

4.5 Anterior and posterior rhinoscopy (endoscopy). Baseline investigations

. Clarification of non-nasal causes of mouth breathing: . Oral, dental, jaw anomalies? Dyspnoea of cardiac/pulmonary origin? . Psychological factors (stress, lack of pain perception)?, disorders of central regulation?

. Clarification of nasal causes of mouth breathing: . Narrowing of the lower lumen because of defects of the bony/cartilaginous skeleton? . Narrowing of lumen (secretion, swelling of turbinates, foreign body, neoplasm)? . High turbulence when cavity too wide relative to isthmus? Deviations, spine? . Inspiratory narrowing of lumen due to wide alae nasi, mobile polyps etc.? . Nonphysiological difference between sides?

. Rules of thumb for estimating unilateral patency (= current findings!) . Estimation of obstruction due to bottlenecks/anatomical defects unreliable except in extreme cases. . The narrowest point of the lower half of the lumen (vestibule, cavity below the lateral cartilage and middle turbinate), normally the isthmus, is always definitive. All cross sections narrower than a normal isthmus are pathological. . Of 2 areas of the same size, the more circular has the lower resistance. . Increased turbulence due to an excessively wide cavity or deflection due to deviated septum, spines or ridges, and also inspiratory narrowing of the lumen, have an adverse effect. . Topical classification of stenosis according to relevant cross sections:

25  Nostril: stenosis rare.  Entrance to nasal cavity: typical stenosis.: septal haematoma.  Isthmus region (shaded) between isthmus (bold) and head of turbinate: stenosis very frequent.  Head of turbinate: stenosis Figure 15. frequent.  Body of turbinate: spines leading to deflection of flow are important, longitudinal ridges less so.  Choanae: adenoids, space- occupying processes.      

. The three degrees of septal deviation according to COTTLE are not suitable for estimating patency. The residual lumen is crucial (e.g. good patency despite ridges/spines in contact with turbinates or residual lumen on the floor of the nose in the presence of nasal polyps).

. Rules of thumb for estimating bilateral patency: the wider side is definitive because the two sides are in parallel. Example: good on the right and poor on the left = good both sides. Marked asymmetry has a deleterious effect for physiological reasons. Example: very good on the right and poor on the left = good both sides (instead of very good).

4.6 Rhinomanometry (baseline investigations, see also page 4 and 5)

Before starting the measurement, it is necessary to elucidate, note or program whether nasal breathing now is better or worse or the same, better or worse than usual. Diagnostic comparison between the measured and estimated levels is not possible otherwise.

a) Pathological results: diagnostic significance . Pathological bottleneck: unilateral V. 150 < 250 cm³/s. Operation? . Pathological nasal breathing: V. 150 bds < 700 cm³/s. (Operation? See below)

26 . Form error, turbulence-increasing type: ∆ V. 150 bds < 700 cm³/s. (Operation? See below) . . Form error, lumen-narrowing type: ∆ V < 25 %. Cause: aspiration of too soft alinasals, floating polyps . Asymmetry between sides: L/R < 0.6 (if L < R) or greater than 1.5 (if L > R). . Turbinate factor: Difference in V. 150 before and after maximum subsidence of swelling >120 cm³/s . Subjective fasle estimate: current estimated level and measured level do not coincide V. 150 bilat. Cause: non-nasal factors, Rh. sicca, hyperreactivity etc.

. b) Final comparison: V 150 bilateral  – current estimated level   =  Measured result good (> 700), estimated level good: currently normal nasal breathing

 =  Measured result poor (< 700), estimated level poor: swelling subsidence test obligatory! In context with history and inspection clear operative indication: . Correction of defects of the skeleton if V. 150 bilat < 700 cm³/s or side ratio > 1.5 bzw. < 0.6 after subsidence of swelling. . Single or additional turbinate correction is turbinate factor > 120 cm³/s.

 <  Measured result poor (< 700), but estimated level good. Why? . Since the patient is happy, operation only for medical reasons (recurrent respiratory tract infections, snoring, stenosis headache etc.). . Very good side symmetry (L/R 0.83 - 1.2) or little turbulence (Δ V.> 70 %) can explain the good estimated level. . Otherwise, causes for the subjective false estimate should be sought (e.g. corticosteroids, antiasthma drugs, diminished pain perception etc., see page 13).

 >  Measured result good (> 700), but estimated level poor. Why? . Caution with operations! Patients usually unsatisfied afterwards. Possible exception: very poor side difference or valve stenosis. . Asymmetry (L/R < 0.6 oder > 1.5) or turbulence-increasing/lumen-narrowing anatomical defect Δ V < 35, < 25 %) may explain the subjective false estimate.

27 . Otherwise, causes for the subjective false estimate should be sought (Rh. sicca, non-nasal mouth breathing, intermittent stenosis etc.). Often problem cases. Repeat measurement?

c) Elucidation of average patency (P) . In permanent stenosis P – must logically equal the momentary patency. If a different value is reported for P– a subjective false estimate is suspected. . In intermittent stenosis the test of subsidence of swelling is critical. It distin- guishes constant anatomical resistance from the momentary (variable) turbinate resistance, thus giving an objective assessment of operative indications.

d) Alterations in patency after diagnostic (provocation), therapeutic (conserva- tive or operative) or experimental measures are usually measured only with the comparison level V. 150, when the normal scatter should be noted, along with physiological half-side rhythm in the case of unilateral measurement.

e) For the pulmonologist, comparison with lung resistance is not important, but whether the nasal breathing is pathological from the ENT aspect and for what reason (e.g. bottleneck, excessive difference between sides, lumen too wide, valve stenosis etc.).

Fig. 16. Printout of ATMOS® Rhino 31 made by AT- MOS MedizinTechnik GmbH & Co. KG For technical reasons, the following abbrevia- tions are used in the printout: . V = Fl. . V bds = Fl.R+L . ∆ V % = Fl Inc Ratio between sides SQ = Fl.L/R . Resistance = ∆ p / V = Res

28 5.0 Nasal Hyperreactivity 5.1 Definition, pathomechanisms

. Hyperreactivity is a response to non-allergic and/or allergic stimuli that is increased compared to the normal response.

. A diagnostic distinction must be made between allergic and non-allergic hyperreactivity, often in combination with non-hyperreactive causes, e.g.: . Anatomical abnormalities of the nose. Operation if there is mouth breathing, otherwise increased invasion of an allergen into the lung and change of level. Rhinomanometric investigation is essential. Many failures result from its omission. . Decongestant nasal agents. With prolonged use, sometimes even after 10 - 14 days fatigue of the constrictor mechanism with hyperaemia. Abuse in approx. 1 % of cases in an ENT practice. It is seldom mentioned by the patient. . Antihypertensive agents. There is often swelling of the turbinates with a sensation of dryness (blocked nose) due to inhibition of the precapillary sphincters when lying down. This obstruction must not be mistaken for an allergy to mites or bedding materials. Whether obstruction was present before the start of blood pressure treatment is crucial. Even young patients suffer from high blood pressure! . Bacterial (purulent) rhinitis, sinusitis. Allergic persons have an increased predisposition. Conspicuous: a change in symptoms (headache, purulent (!) secretion).

Pathomechanisms of hyperreactive rhinitis: . Disorders of neurovegetative balance (parasympathetic dominance). . Immunological abnormality of mediators, neurotransmitters, neuropeptides. . Increased response of the receptors on blood vessels, glands, nerves. . Resulting abnormality of vascular and gland control (figure 17)

29 Diagram of vascular and gland control by 2 balanced regulatory cycles: 1) Vasodilating and increasing secretion: . neuropeptide NP I: vasoactive intestinal polypeptide, histidine. . parasympathetic (cholinergic) 2) Vasoconstricting and inhibiting secretion (grey): . NP II: neuropeptide Y, somatostatin, neurotensin . sympathetic (adrenergic): noradrenaline . humoral: adrenaline

1st regulatory cycle Cortex

Klimareize Transmitters Ganglia Hypothalamus gasserian ganglion (SP) sensitive \\\\////\\\ Central facial area (NP I) parasympathisch  N. petrosus major Gg. pterygo-palatinum

Axonreflex (NP II)

medullary N. petrosus profundus bulbar sympathisch klimatisierte centres adrenaline Atemluft vasopressin acts through ACTH T 1-5 the lung Gg. cervicalis on blood O , nd 2 Humoral 2 regulatory CO2, pH system cycle Presso- and chemoreceptors, peripheral nerves Figure 17.

5.2 Non-allergic hyperreactive rhinitis

Since there is no direct evidence, 3 points should be noted: 1) Allergy suspected (if necessary, baseline allergy investigations): . Previously absent bilaterally blocked nasal breathing, with or without non- purulent secretion or irritation, without inflammatory or medication origin . Allergies (pollen-induced rhinitis, asthma, neurodermatitis) or hyperergies (rheumatoid, erythema nodusum etc.) and migraine, personal (PH) or family (FH) history of food or drug intolerance. . Other increased organ manifestations in the FH or PH (e.g. bronchitis).

30 . Commencement of symptoms in youth or middle age. . Commencement on changing usual environment (change of home, occupation, new cosmetic and personal hygiene items, clothing, animal contact, new acquisitions etc.) . Obvious relation of exposure to time, place, activity . (Total IgE and interleukin 4 raised)

2) Eosinophilic forms – Triggering causes: . NARES (non-allergic rhinitis with eosinophilia syndrome). Controversial! . Pseudoallergy. Non-IgE-mediated effector stimulation (possible abnormality of arachidonic acid metabolism). No previous sensitisation. Preedominantly a problem of orally ingested substances: foods and their additives, drugs, particular analgesics (aspirin etc.). Often begins with obstruction and facial erythema. Often the only symptoms without the familiar dramatic asthma attacks. Triggers:

Pharmacological liberators nonspecific effects external source of: e.g. acetylsalicylic acid, e.g. strawberries histamine: sauerkraut, food additives wines serotonin: bananas tyramine: chocolate etc.

Complement system Mast cell Effector cell

3) Non-eosinophilic forms – Trigger factors: . Direct stimuli (irritant and toxic) of the nasal mucosa (solvents, formaldehyde, volatile chlorides, bases, acids etc., decongestant abuse)? . Distant stimuli (reflex) of optical type (dazzling), taste (spices), mechanical, thermal (cold feet, draught)? Mostly sneezing and/or strong watery secretion (sneezer). . Dependence on position (mostly obstruction of the lower side)? . Psychological factor (stress nose)? . Hormonal factor (pregnancy, puberty, thyroid disease)? . Medicines (central α-sympathomimetics, antisympathomimetics, 1-receptor blockers, ergot alkaloids, anticholinergics, antihistamines, antidepressants, ACE inhibitors, hormonal contraceptives?

31 5.3 The allergic type I reaction (hyperreactivity in 3 phases)

. Sensitisation on first contact with the allergen: formation of specific IgE antibodies by the interaction between T- and B-lymphocytes and filling of mast cells and basophils. . Immediate reaction on second contact: through binding of the allergen to the IgE antibody, release of mediators from mast cells and basophils and eosinophils. They produce the typical allergic symptoms via receptors on the blood vessels and glands. . Late reactions: cellular inflammatory sequence of reactions after 4 - 8 hours. Patient with marked late reaction has a tendency to asthma.

pollen mites fungi bacteria

Severity Blocked nasal breathing

much secretion Secretion type little secretion

frequent

Sneezing stimulus slight

frequent

Itchy eyes slight

Severity BNSA BNS BNS BNS

Combination of symptoms

mehrere Symptome 1 oder 2 Symptome gleich stark im Vordergrund

B = blocked nose S = secretion N = sneezing E = itchy eyes

Figure 18. Typical symptoms of ubiquitous allergens

32 5.3.1 Clinically important baseline data concerning nasal acting allergens (3 groups)

1) Ubiquitous allergens (pollen, mites, moulds, bacteria) . Frequent. Possible everywhere that conditions for existence are appropriate. . Typical symptoms (figure 18) . Pollen: for seasonal flowering times and clinical importance see figure 19. Increased symptoms in dry windy weather and often in the morning. Mites: Perennial. Moist bed heat, organic bedding materials (feathers, horsehair etc.), increased in the morning. Hay mites more in rural areas, food mites more in urban areas. The allergens are the faeces. Moulds require: moisture, heat, sheltered habitat with little air movement, organic food substrate. Incidence 10 - 15 %, however very varied regionally. Usually primarily asthma. Often problem cases. 3 groups are distinguished: . Extramural fungi: seasonal pollen-like symptoms, but lasting until late summer. Increased in warm humid weather. Occurs only on living organic material. Important: Alternaria, Cladosporium. . Extra- and intramurally living fungi: seasonal but lasting until November/ December. Perennial. If intramural on dead organic material (e.g. hay, leaves, stored fruit/vegetables). Main symptoms in the afternoon. Important: Asper- gillus. . Mural fungi: perennial. Only on dead organic material (e.g. wallpaper, wooden floorboards, worn clothes or shoes, pot plants, in bathrooms, store rooms, hobby rooms). Room atmosphere often musty. Important: Penicillium. The so-called big four: Alternaria, Cladosporium, Aspergillus, Penicillium.

33 2) Non-ubiquitous (milieu-dependent) allergens (often problem cases) . Definition: inhaled dusts or aerosols of plant origin (wood or flour dust, latex etc), animal origin (contact with animals or animal products: feathers, wool, silk, fur or leather in bed, cushions, home textiles etc.) or chemical origin (hy.- giene, cosmetic, washing, cleaning agents, occupational allergens) with sources especially in the individual surroundings. . No typical symptoms, but often non-ubiquitous, place- or activity-related symptom predominance, detailed environmental history usually needed. . Important: animal epithelium approx. 15 %! . Occupational allergens occupy a special position. . Typical: worsening during working hours. Colleagues with the same symptoms. Contact with certain raw, intermediate, end products, aids and cleaning agents, paints, varnishes, adhesives etc. . Occupational groups at special risk: Farmers: animal epithelium, insects, fertilisers etc. (ubiquitous: pollen, moulds) Industry: wood, textile, chemical and metal sectors Trades: baker, painter, carpenter, hairdresser, laundry Medicine, science: disinfectants, latex, experimental animals etc.

3) Bowel wall produces too much IgE. Relatively rare (between 0.5 – 0.7 %). Usually problem cases, since rarely time-or place-related and reaction times up to 6 hours (since often only metabolites are allergenic). Other organs usually involved also. Principal allergens: milk, egg, fish. Cross allergies have common allergen core (usually plant proteins).

Figure 19. Flowering calendar of seasonal allergens. Sporulation times of extramural fungi. They are classified roughly into before, during and after grass flowering.

34 Feb. Mar. Apr. Ma< Jun. Jul. Aug. Sep. Oct. Pollen types Clinical relevance

Trees

Hazel ***

Alder ***

Poplar **

Elm **

Birch ***

Ash *

Willow *

Beech *

Oak *

Hornbeam *

Grasses

Meadow foxtail ***

Sweet vernal grass ***

Orchard grass ***

Rye grass ***

Smooth-stalked meadow grass ***

Meadow fescue ***

Large-leaved timothy ***

Cereals

Rye ***

Oats **

Barley **

Wheat **

Plants

Dandelion *

Ribwort ***

Pellitory of the wall *

Common nettle *

Goosefoot *

Sorrel ***

Mugwort ***

Fungi

Alternaria alternata ***

Aspergillus species ***

Cladosporium species ***

Clinical importance, ***=high, **= less high, *= low Main flowering Pre-/post-flowering (or sporulation) (or sporulation)

35 5.3.2 Baseline investigations to find the current allergen

History  Seek allergy, confirm if current.

Skin testing,  confirms sensitisation of the patient without proving RAST that it is currently involved in the nose.

Provocation  Direct proof that allergen is currently involved.

5.3.3 Allergy history (family, personal, symptoms, environmental history)

The history leads in about 80 % of cases to the guilty allergen. However, problem cases require “the patience of an ass and the feel of a criminologist ”.

Family history Allergies, asthma, allergic rhinitis, eczema?

Personal history Other allergies? Respiratory diseases? Hyperergies (rheumatoid etc.) migraine? intolerance? Operations on the nose, sinuses? Medications: analgesics, antihy- pertenxives, decongestants, anti-allergic drugs etc.? Allergy tests? Hyposensitisation? Other?

. Start: first time? Now? After changes of environment (home, occupation, cosmetics, clothing, animals, new acquisitions etc.)?

. Course: episodic? Chronic? Increasing, the same?

Symptom history (Symptoms, predominant symptoms) . Symptoms (S) and predominant symptoms (PS) often lead directly to the allergen. If not: environment history.

. The nasal relevance of a suspected allergen is confirmed by reactivation of symptoms on renewed contact and improvement in symptoms when the allergen is absent, e.g. when there is a change of milieu (holiday, change of home, occupation etc.)

36 . It is useful to analyse the last or most severe occurrence of the symptoms (S and PS), since patients remember these better. . Symptoms: non-ubiquitous? Ubiquitous (Figure 18)? Elucidate ecodata (page 33)!!! . Main symptoms: obstruction, secretion (purulent, watery, mucous), irritation? . Accompanying symptoms: eyes, ears, bronchi? . Distant symptoms: stomach, intestine (suggesting foods), skin?

. Predominant symptoms (PS): when, where, how? Allows targetted search for allergen. When (time of year/day)? Where (intra-, extramural)? Doing what (working at home, leisure, at work, subsidiary occupation)? After taking foods, medications? When using personal consumer articles (clothing, cosmetics etc.)?

Environment history This means looking for sources of allergens in the entire private/occupational environment (often perennial allergy), and only in this area in the case of clear PS. Ask about:

. Ubiquitous allergens (typical symptoms and ecodata, page 33)

. Non-ubiquitous allergens (dusts, aerosols, page 20): animal, plant, chemical origin. Criteria: . Local/room atmosphere: wet, dry, sunny, windy, musty, well/badly ventila- ted. . Vegetation: garden, meadow, field, wood etc., what house plants? . Type of building: own home, apartment block, wooden building, old or new building. . Furnishing: wood panelling, home textiles, furs, constituents of bedding, cushions etc. . Use: store for foods, old clothes etc., keeping animals. . Activities: materials employed etc. . Special features: keeping pets, exotic woods etc.

37 5.3.4 Targetted search for the current allergen (•) by classifying the predominant symptoms (PS) into 4 main groups:

1) Seasonal (spring to the start of winter) and ubiquitous (also with change of place and environment) PS Flowering calendar (Figure 19) . Pollen: typical symptoms and ecodata Frequent cross allergies (common allergen core): Birch, hazel, alder: malaceous and stone fruits, nuts, almonds, kiwi, anise and others Mugwort: celery, carrot, paprika, garlic, camomile, curry, nutmeg, ginger, cinnamon, other spices Grasses, rye: soya, cereal flour, muesli, peanuts Bananas: latex allergy!! PS Sporulation times (Figure 19) . Extramural fungi: typical symptoms and ecodata

2) Perennial (at any time of year, irregular intervals) and ubiquitous PS Heating period . Mites (bedclothes): typical symptoms and ecodata (page 33) . Extra- and intramural fungi: typical symptoms and ecodata (page 33) PS Common cold periods . Bacteria (controversial)

3) Perennial and non-ubiquitous (only in certain situations) Non-ubiquitous allergens mimic ubiquitous symptoms if exposure is constant (e.g. cosmetics, clothing). The same work always in the same place make it difficult to distinguish place and activity dependence.

Location points PS Immediate surroundings: local climate? Vegetation? Industry? . Pollen, moulds? PS Inside rooms: bedroom, living room, bathroom, workroom, store room, hobby rooms etc.. . intramural fungi: typical local and room atmosphere, organic food substrate . Dusts: animal, plant, chemical origin (see environment history, page 22)

38 Activities PS Housework . House dust . intramural fungi (typical ecodata in workplace, page 33) PS Main or subsidiary occupation, hobbies: see occupational allergens, page 33)

Other points PS Personal items: nontypical symptoms . Hygiene, cosmetic, washing articles, powder, sprays . Clothing made of natural products (wool, silk, leather, fur, latex etc.) PS Animals: pets, large and small animals (cat, hamster, rabbit, horse etc.) PS Certain plants

Oral points PS Foodstuffs: foods, beverages, other consumables. Note: other additional organ manifestions. Up to 6 hours latent period. PS Medications: analgesics etc.

4) Perennial without clear central points (mainly problem cases) . Repeat allergy history, especially of most recent symptoms, since patients remember these better. . Precise environmental history for ubiquitous and non-ubiquitous allergens in the entire private and occupational area (page 33). . Food allergy . Testing if still unclear (page 39).

5.3.5 Skin testing – RAST

. Both confirm only sensitisation, not current involvement of the nose, so cannot replace provocation. . The RAST demonstrates specific IgE circulating in the blood. Classes II to IV should be regarded as positive.

39 . With regard to skin testing, attention is drawn to the partly modified BACHERT screening plan and figure 20 and 21. (e.g. of further small animals, etc.) . Every skin test should always include a NaCl and histamine control in order to identify false-positive or false-negative reactions. . One should be prepared for incidents (see emergency treatment page 42).

bold = mixed allergen Prick i.c. RAST NP* 1 NaCl 2 Histamine 3 Grasses 4 Rye 5 Trees I 6 Trees II 7 Birch 8 Hazel 9 Alder 10 Weeds 11 Plantain 12 Mugwort 13 Mite I 14 Mite II 15 Lepidoglyphus d. (Hay mite) 16 Acorus siro (flour mite) 17 Tyrophagus p. (food mite) 18 Fungi I 19 Fungi II 20 Alternaria 21 Cladosporium 22 Aspergillus 23 Penicillium 24 Feathers 25 Cat 26 Guineapig 27 Egg 28 Cow’s milk Other: *) Nasal provocation

40 Allergen solution

Prick test

Allergen solution (dusts or foodstuffs brought along) Scratched skin NaClNaCl

Scratch test

Intracutaneous test

Figure 20. The principle of the prick, scratch and intracutaneous test (they confirm only sensitisation, not the current involvement of the allergen in the nose.) Diameter of wheal Erythem + 2 - 3 3 - 5

++ 3 6 - 10

+++ 4 - 6 11 - 20

++++ > 6 > 20 Pseudopodien

Figure 21. The strength of the skin test, assessed by the size of the wheal and erythema.

41 5.3.6 Emergency treatment of allergic incidents Note: itching in the throat, palms of hands and soles of feet

General measures . Positioning of the patients: head down, legs raised, head turned to side to avoid aspiration. . Apply blood pressure cuff. Expose brachial vein, insert i.v. cannula.

Severe schock, major drop in blood pressure Call emergency doctor (Phone: ______) or alternative doctor (Phone: ______). . Apply blood pressure cuff. Obtain and secure intravenous access. . Rapid infusion (500 ml in 5 minutes) Ringer lactate DAB 7 or similar. . 1 ampoule Urbason solubile forte or Volon A solubile 40 mg i.v. . 1 mg adrenaline s.c. distributed over several sites. . If nec. 0.25 – 0.5 ml intravenously of an adrenaline solution (1 ml 1:10 000) or drip. . Oxygen inhalation.

Warning: ventricular fibrillation . Monitor carotid pulse. . Response to adrenaline disappears at the start of acidosis. Give sodium bicarbonate also if necessary!

Cardiac arrest . Cardiac massage

Respiratory arrest . Mouth-to-mouth breathing, artificial ventilation

Uvula and palatal oedema . Touch with adrenaline

Glottal oedema . If possible, drip on 2 - 3 drops of adrenaline. . Corticosteroids intravenously (e.g. 1 g Urbason solubile forte). . 1 ampoule Tavegil (5 ml) i.v. . Adrenaline inhalation (Medihaler).

42 . Corticosteroid inhalation (Pulmicort, Viarox). . Oxygen inhalation. . If necessary, intubation or tracheotomy (coniotomy).

Bronchial obstruction . Euphyllin 1 - 2 ampoules (10 ml) slowly i.v. (over 5 minutes) or i.m. . Corticosteroids i.v. (e.g. 1 g Urbason solubile forte or Volon A solubile 40 mg). . Adrenaline inhalation (Medihaler). . Corticosteroid inhalation (Pulmicort, Sanasthmyl). . B2-adrenergic inhalation (e.g. Sultanol Aerosol). . Oxygen inhalation.

Excessive local skin reaction . Tourniquet proximal to injection site. . Inject around the injection site with 1 ml adrenaline solution 1:1000. . Hydrocortisone ointment.

5.3.7 Nasal provocation

Skin test and RAST do not prove current involvement of an allergen in the nose, but only sensitisation of the patient. Thus, there is a high percentage of false-positive skin tests, particularly with fungi, house dust, mites, tree pollen and weeds.

Indications for nasal provocation . elucidation of current involvement, if skin test/RAST and history do not agree. . Perennial allergens, especially mites, moulds, house dust. . Simultaneous occurrence of different allergens, if it is not possible to separate them in the history, e.g. pollen – extramural fungi. . Exclusion of weaker allergens in the case of multiple allergy in order to produce an effective therapeutic solution. . Control of treatment after hyposensitisation, medications. . Inadequate therapeutic effect in the case of multiple allergy to elucidate which allergen did not react or reacted only slightly. . Avoiding bronchial provocation in the case of simultaneous nasal and bronchial symptoms.

43 Requirements for nasal provocation . Symptom-free or low symptom condition. . No nasal corticosteroid spray, rauwolfia preparations or psychoactive drugs for at least 2 weeks. . No oral corticosteroid or antihistamine preparations for at least 1 week. . Not less than 8 weeks after nasal operations or acute inflammation. With unilateral control measurements of V. 150 under 250 cm³/s clarification of anatomical defects first (ENT physician).

Dosage, special provocation solutions, storage . Single allergens are tested (exception: grass mixtures). . 1 spray of pollen and mites, 2 sprays in the case of fungi and other weakly reacting allergens. 1 push = 0.04 - 0.05 ml of the test solution. . Stabilising agents added to the skin test solutions can have an irritant effect (false-positive results). Only glycerine-free solutions should therefore be used for provocation (approx. 30 % less irritation). . Because of the short shelf-life of these special solutions, ensure correct storage and observe the expiry date.

Emergency treatment (page 42) When the allergen is applied as described below, practically no spread of the allergen into the deep airways can be expected (oedema of the uvula or soft palate, asthma attack). Nevertheless, one should always be prepared for severe incidents.

Application of the allergen Pump dosing sprays are most suitable for routine practice. Ensure only that the spray is held as horizontally as possible, directed towards the inferior turbinate. The method allows it to be directed. It is important to avoid deep inspiration of the allergens!

44 The patient should therefore be asked: . to inspire deeply and then . hold his breath. In this phase, spray the allergen, wait briefly and then . have the patient sniff back and forth while bending the head forward and . then breathe out. Figure 22.

Rhinomanometrically controlled provocation The only internationally standardised and surest method is active anterior rhinomanometry of separate sides.

3 measurement procedures:

Initial measurement bilaterally . Used to determine the momentarily better side of the nose. This is provoked. Unilateral V. 150 levels under 250 cm³/s indicate anatomical defects (ENT specialist!). Levels below 100 cm³/s are unsuitable for provocation.

Control or solvent measurement . Apply the solvent without the allergen to the inferior turbinate on the better side. Measurement after 15 minutes. . Used to indicate further nonspecific hyperreactivity, if markedly worse than 10 - 15 % relative to the initial measurement. . Also used to calculate the reduction in flow after provocation.

First measurement . In the case of pollen 10 - 15 minutes after provocation. Mites, house dust and moulds react more slowly, so measure only after 20 - 40 minutes. . Used to calculate the change in flow relative to the control measurement or initial measurement, if this is worse than the control result. . Second measurement if the reduction in flow is between 20 and 40 %. A further rise in the event of a slow allergen reaction indicates current involvement.

45 Obstruction the most reliable test parameter. 2 exceptions: . Despite obvious secretion/irritation, obstruction cannot be confirmed, as it is also absent as a lead symptom in the medical history. . There is a false histamine reaction. A test using 2 drops of histamine is recommended. If no reaction occurs, the result of provocation should not be analysed. This false reaction is not constant, so the test should be repeated another day.

Elucidation of current involvement by measuring the percentage reduction . in V 150 The only objective method. Calculated and stored by computer nowadays.

. The provocation is positive if – with reference to the control V. 150 level – the reduction in flow is greater than 40 % in the 1st or 2nd measurement. . The provocation requires a second test if the reduction in flow in the 1st test is between 20 and 40 % and the point score is below 3 points (see below). . The provocation is negative if the reduction in flow in the 1st test is ‚ immediately below 15 % or it remains below 40 % in the 2nd test.

A symptom score should also be recorded. It is positive if greater than 3.

Points Secretion Sneezing Distant symptoms 1 none 0 - 2 times none 2 slight 3 - 5 times lacrimation, itchy eyes 3 marked > 5 times conjunctivitis, dyspnoea, urticaria

If the reaction is negative, a second provocation test can be performed the same day with a different allergen.

46   

Figure 23. Positive provocation result

Printout of a provocation of the right side of the nose with mite:  Control measurement on the right at 150 Pa = 428 ccm/s  1st measurement after provocation = 328 ccm/s, i.e. the reduction in flow was 24 %. A second test was necessary.  2nd measurement = 164 ccm/s, i.e. the reduction in flow was 62 %. The provocation was now positive and current involvement of mite allergy was confirmed.

5.3.8 Investigation of oral allergens with nasal symptoms (cross allergies or pseudoallergies)

. History

Nontypical symptoms, no association with location or time, other organ manifestations, up to 6 hours latency time . Skin test With foodstuffs (milk, egg) and contaminating moulds. Skin tests are up to 30 - 40 % false-negative. Often only the metabolites are allergenic. . Nasal provocation (NP) With skin-positive moulds or foods (provided they can be used in the nose, e.g. flour). NP positive = current involvement.

47 . Allergen-free diet Only tea with sugar or potatoes or rice cooked without milk for 10 - 14 days if nasal provocation not possible, questionable or negative. If no improvement in symptoms, food allergy unlikely, no oral provocation. . Oral provocation If improvement in symptoms after allergen-free diet. First oral provocation with moulds clearly or weakly positive on skin test or nasal provocation. Investigation of foodstuffs only after that (exclusion or provocation diet, search or addition diet). For method and interpretation of the complex tests, see special literature.

Nasal provocation in pseudoallergy due to aspirin Acetylsalicylic acid intolerance is the cause of about 10 % of cases of nasal polyps combined with asthma. Oral or inhalational provocation should only be undertaken in hospital because of possible severe side effects. In contrast, nasal provocation is also possible on an ambulant basis (MERTENS). Lysine-ASA is dripped onto the inferior turbinate in increasing dosage (2, 4, 10 mg dissolved in 0.2 ml distilled water) at 30-minute intervals. The nasal resistance is measured 3 times between administrations. The test is positive if flow is reduced by 40%. Because of the high specificity, oral provocation can be omitted if the test is positive, but not if the test is negative. In the presence of polyposis, the test is possible only if nasal patency is still adequate.

48 6.0 Appendix 6.1 Brief history of rhinomanometry

1902 Coutarde publishes the anterior method of measurement. 1925 Zwaardemarker introduces inherent flow measurement. 1958 Semerak founds modern rhinomanometry: first synchronous measurement! In the following period, because of advances in electrical engineering and elec- tronics, introduction of electro-mechanical transducers, amplifiers, 2-channel and X/Y recorders. Then the use of analogue-digital transducers and microprocessors to calculate clinical parameters. Documentation using printers. Development of small portable rhinomanometers.

6.2 Conclusion

Assessment of nasal resistance, like that of lung resistance, is a question of measurement and interpretation. It can only be answered in the context of the history, inspection and rhinomanometry and so is a task for the physician.

49 6.3 References

Bachert, C.: Die chronisch verstopfte Nase - Zur Klassifikation der nasalen Hyperreaktivität. Deutsches Ärzteblatt, 1996, 93(16):1034-1038

Bachmann, W.: Die Funktionsdiagnostik der behinderten Nasenatmung. Ein- führung in die Rhinomanometrie. Springer, Berlin, 1982

Bachmann, W., Bachert C.: Die behinderte Nasenatmung, ein diagnostisches Vademekum. Dustri, München-Deisenhofen, 1987

Bachmann, W.: Eine neue Methode zur diagnostisch-therapeutischen Bewer- tung rhinomanometrischer Ergebnisse. HNO, 1993, 41:19-23

Bachmann, W.: In: Oto-Rhino-Laryngologie in Klinik und Praxis. Band II. Thieme, Stuttgart, 1992

Broms, P.: Rhinomanometrie. Thesis, Malmö, 1980

Clement, P.A.R., Hirsch, C.: Rhinomanometry - A Review. ORL, 1984, 46:173-193

Jessen, M., Malm, L.: Longterm follow up of patients with nasal stuffines and normal NAR. Acto Otolaryng, Stockholm, 1984, 214:95-98

Legler, U.: Zur Morphologie und Nomenklatur des Vestibulum nasi. Z Laryngol Rhinol, 1968, 47:640

Masing, H.: Die klinische Bedeutung der Nasenwiderstandsmessung. Arch Ohren Nasen Kehlkopfheilk, 1965, 185:763-768

Mlynski, G., Löw, J.: Die Rhinoresistometrie - eine Weiterentwicklung der Rhino- manometrie. Laryngo Rhino Otol, 1993, 72

Nolte, H.: Allergie. Dustri, München-Deisenhofen, 1992

Semerák, A.: Objektive Beurteilung der Nasendurchgängigkeit. Z Laryngol Rhi- nol, 1958, 37:248-261

50 6.4 Division of rhinomanometric measuring curves a) b)

6.5 Flow SUM

Sum of flow in left and right-hand side of nose at differential pressure 150 Pa Obstruction 0 to 200 cm³s-1 + 35 cm³s-1 high level 200 to 400 cm³s-1 ± 35 cm³s-1 medium level 400 to 500 cm³s-1 ± 35 cm³s-1 low level over 500 cm³s-1 – 35 cm³s-1 not obstructed

6.6 Flow INC

Flow INC. R or L Clinical Significance above 35% increasing laminar flow. matches a normal curve between 35% and 25% Increasingly poorer aerodynamics due to additional vertices, secondary flows, etc. below 25% Found with valvular stenosis, additional narrowing of the lumen as a result of sides of nose being sucked in or due to floating polyps, etc.

51 ATMOS MedizinTechnik GmbH & Co. KG Ludwig-Kegel-Str. 12, 14–16, 18 79853 Lenzkirch / Germany 2013-08 Index: 02 . Tel: +49 7653 689-0 [email protected] P093.1023.1 www.atmosmed.com