In Empty Nose Syndrome, these and other nerve endings have been destroyed, primarily due to surgery or amputation of the turbinates, and secondarily due to the subsequent dryness that occurs when the nose remains wide open 24/7. Over time, this dryness leads to a degenerative process where metaplasia occurs. This is an adaptive cellular change where the mucosal cells transform to resemble ordinary skin cells. As this process progresses, more and more of the mucosal function and sensation are lost. Consequently, complete Empty Nose Syndrome often develops months to years after the initial surgery, leaving surgeons without accountability.
According to Dr. Eugene Kern, the residual functional nasal mucosa typically fails within an average of 6.1 years following a turbinectomy. This information is discussed in Dr. Eugene Kern's lecture, specifically around the 20-minute mark.
Empty Nose Syndrome: A degenerative condition with a delayed onset
Below is an excerpt from a summary of a research report in which Kern participated
Note: Turbinectomy refers to the amputation of the nasal turbinates
Martinez conducted a follow-up study on 29 of the 40 patients who had undergone a turbinectomy two years earlier and found that only 3 patients (7.5%) had developed excessive dryness and crusting in the nasal mucosa. Later, 3 to 5 years after the turbinectomy, Moore conducted a follow-up on 18 of these 40 patients and found that 89% had now developed bilateral crusting in the nasal mucosa. Additionally, 39% of these patients had thick, foul-smelling discharge. He thus concluded that total amputation of the nasal turbinates should not be performed due to the poor long-term outcomes.
Here we find the reason why the medical community believes that only a few individuals will develop atrophic rhinitis after amputation of the nasal turbinates. The follow-up is conducted too soon. If one waits 5 to 10 years after the surgery, the majority of the operated individuals will have suddenly developed a degenerative condition in the nasal mucosa. A condition that is a combination of secondary Atrophic rhinitis and empty nose syndrome (ENS).
HYPER-ventilation and Empty Nose Syndrome
In Empty Nose Syndrome, hyperventilation is observed in approximately 75-80% of cases, which is often neurologically related but also due to insufficient nasal resistance. Without optimal resistance, the lungs cannot fully expand during inhalation, and the airflow moves too quickly in and out of the lungs for optimal gas exchange. This combination leads to a constant fight-or-flight reaction, which in turn impairs the ability to sleep, concentrate, and relax.
As mentioned in the scientific study bellow, Stress activation in the limbic system is observed in Empty Nose Syndrome because the brain loses its ability to sense airflow through the nose. However, when study participants with ENS were exposed to menthol, which activates the remaining TRPM8 receptors in the nasal lining, they regained a slight sensation of airflow. This resulted in a reduction of the stress response in the limbic system.
Source: Empty Nose Syndrome: Limbic System Activation Observed by Functional Magnetic Resonance Imaging DOI: 10.1002/lary.21903
Adequate levels of spO2 in the blood, yet simultaneous oxygen deprivation in the body's tissues
From the text above we know that hyperventilation is very common in ENS. During hyperventilation, the amount of carbon dioxide in the blood decreases, leading to an increase in blood pH (making it more alkaline). As the blood becomes more alkaline, the ability of hemoglobin to release oxygen to the tissues is altered. This phenomenon is known as the Bohr effect.
Under normal circumstances, carbon dioxide contributes to lowering blood pH, which in turn reduces hemoglobin's affinity for oxygen, allowing oxygen to be more readily released to the tissues. However, during hyperventilation, the following occurs:1. As carbon dioxide levels in the blood drop, pH increases, making the blood more alkaline.
2. This causes hemoglobin to maintain a tighter grip on oxygen molecules.
3. Consequently, oxygen molecules find it more difficult to dissociate from hemoglobin. As a result, less oxygen is released to the body’s tissues, potentially leading to oxygen deprivation in muscles and other tissues, even though blood oxygen levels may appear adequate.
This can result in symptoms such as dizziness, tingling, and a sensation of breathlessness.
In ENS-Hyperventilation, Test Lactate Instead of SpO2 to Assess Oxygen Delivery Capacity
When assessing oxygenation in ENS-related hyperventilation, it is crucial to recognize that measurements based on blood spO2 alone are not reliable. This is because we cannot determine how much oxygen is released from hemoglobin (As previously explained). Another method to evaluate how well the body is oxygenated is to measure lactate levels. Lactate is produced when cells do not receive enough oxygen, and the normal range during inactivity should be between 0.5 and 2.2 mmol/L. Levels exceeding this range suggest that hyperventilation related to ENS may have caused hypoxia in the body, even if spO2 blood levels appear normal.
It is worth noting that a member of our ENS group recently consulted Dr. Weiss in Mannheim for several respiratory tests. One of these tests measured lactate levels before and after physical exertion. The results indicated a lactate level of 4.2 mmol/L at rest and 14.7 mmol/L post-exercise. This increase can likely be attributed to a combination of ENS related hyperventilation, a deficiency in nasal nitric oxide, which normally enhances lung ventilation. And insufficient nasal resistance, resulting in an inability to fully utilize lung capacity during inhalation (explanation further below).
Let us now review the study:
"How Breath-Control Can Change Your Life: A Systematic Review on Psycho-Physiological Correlates of Slow Breathing: doi: 10.3389/fnhum.2018.00353"
The study shows that nasal breathing in healthy, non-nasally operated individuals affects brain activity, particularly in areas such as the piriform cortex, amygdala, and hippocampus, which are associated with emotions and memory. This suggests that nasal breathing can enhance cognitive functions and concentration.
Electroencephalography (EEG) during slow breathing shows increased activity of delta and theta waves, which are associated with relaxation and awareness, similar to deep meditation.
Slow breathing also affects the autonomic nervous system, with measurable changes in heart rate variability (HRV) and respiratory sinus arrhythmia (RSA), indicating a balanced function between the sympathetic and parasympathetic nervous systems.
The conclusion of the study was that slow breathing and nasal breathing can improve both psychological and physiological well-being, with benefits including improved concentration, reduced anxiety, and increased calmness.
The effects described in the above study are due to nasal breathing stimulating various types of receptors (nerve endings) in the nose, which in turn stimulate the brain and vagus nerve, leading to psychological well-being, harmony, and balance between sympathetic and parasympathetic activation in the autonomic nervous system. When the nasal mucosa is amputated or damaged, the calming effect on the nervous system ceases, leaving individuals with ENS trapped in sympathetic activation. This stress activation is further exacerbated by hyperventilation observed in 75-80% of ENS cases, which is not mentally induced but has physiological causes resulting from the surgery. These causes are a combination of receptor damage/loss and the nose being physiologically too open for calm and deep breathing that fully expands the lungs.
Nasal Nitric Oxide, effects on vasodialation of lung vessels Additionally, it should be noted that individuals with ENS have had a large portion of their nasal mucosa removed and destroyed. This mucosa normally produces the majority of the nitric oxide (NO) combined in the nose and sinuses. Studies have shown that individuals with ENS have significantly lower levels of exhaled NO. Since NO is a gas that dilates blood vessels, this affects the entire body, including the brain, which now receives less blood, resulting in reduced cognitive function.In the following study: Nasal Nitric Oxide in Relation to Psychiatric Status of Patients with Empty Nose Syndrome https://doi.org/10.1016/j.niox.2019.07.005, it was found that:
"Nitric oxide (NO) affects important neurotransmitters involved in neuropsychiatric disorders, and NO is proposed to play a 'dual role' in these conditions. Levels of L-arginine and NO metabolites decrease in patients with severe depression. A national survey showed that depression is linked to lower fractional levels of exhaled nitric oxide."
To note: Depression is extremely common among Turbinate reduction victims who have ENS.
Results from the scientific study: "We included 19 patients with Empty Nose Syndrome (ENS) and 12 patients with chronic rhinitis (CHR). Nasal nitric oxide (nNO) levels were significantly lower in ENS patients compared to CHR patients." (CHR patients = Nasal congestion patients)
"Our results indicated that NO levels in the sinonasal area may be related to changes in depression and anxiety status in patients with Empty Nose Syndrome."
Impact of Reduced Nasal Resistance on Respiratory and Cardiovascular Function
Turbinates and Airflow Regulation: The turbinates play a role in regulating nasal airflow resistance by swelling (due to increased blood flow) and contracting (due to reduced blood flow). This is part of the normal nasal cycle. This function optimizes gas exchange in the lungs by ensuring that the volume of inhaled air matches the blood flow to the lungs, facilitating efficient perfusion of respiratory gases. For example: During physical exercise, the turbinates shrink to reduce airflow resistance, allowing for increased ventilation to meet the body’s higher oxygen demand. Conversely, during rest or low activity, the turbinates slightly enlarge, increasing airflow resistance, which lowers respiratory rate. This supports the dominance of the parasympathetic nervous system, promoting relaxation and digestion
Lungexpansion in Relation to Nasal Resistance:
When the turbinates are significantly reduced or removed during surgery, the nasal airflow resistance diminishes. As a result, the body no longer needs to generate as much negative pressure to draw air into the lungs. This reduction in resistance decreases the workload on the diaphragm and intercostal muscles, which are responsible for expanding the thoracic cavity during inhalation. With less demand for negative pressure to inhale, breathing becomes shallower, and the lungs fail to fully expand, utilizing only 50-60% of their capacity. This incomplete lung expansion leaves a significant portion of the alveoli, the tiny air sacs responsible for gas exchange, underutilized. As a result, the efficiency of gas exchange is compromised, limiting the amount of oxygen entering the bloodstream.
Empty Nose Syndrome: Under and over ventilation at the same time?
When the lungs do not fully expand, there is a risk of re-inhalation of CO2. In one reported case of ENS, nightly HYPO-ventilation and CO2 accumulation were detected using the FDA-approved Sentec device. (This was observed without any signs of sleep apnea)
Note: HYPER-ventilation is a common issue associated with Empty Nose Syndrome, as documented in scientific literature, and leads to abnormally low levels of CO2 in the blood. This results in increased blood alkalinity (respiratory alkalosis) and vasoconstriction, which impairs oxygen delivery to tissues by affecting hemoglobin’s ability to release oxygen. Symptoms may include dizziness, tingling or numbness in the hands, feet, or face, as well as fatigue, tiredness, difficulty concentrating, or confusion.
However, HYPER-ventilation in ENS differs from that caused by emotional factors. Emotional HYPER-ventilation typically involves very rapid, deep breaths through the mouth. Whereas ENS-related HYPER-ventilation is characterized by shallow nasal breathing that does not fully utilize lung capacity due to a lack of normal nasal airflow resistance and nasal nerve injury. Additionally, it is not as rapid as emotional HYPER-ventilation. As a consequence of the loss of full lung expansion in ENS, UNDER ventilation can occur even with a high respiratory rate. Medically, this under ventilation is referred to as HYPO-ventilation and leads to hypercapnia and a build up of harmful levels of CO2 in the blood.
To accurately measure ENS-related HYPO-ventilation (PCO2), it is crucial to conduct the measurement at night, as the body has greater difficulty expelling CO2 during sleep and periods of inactivity. Consequently, some individuals with Empty Nose Syndrome may experience HYPER-ventilation during the day and HYPO-ventilation at night.
Regardless of whether HYPER- or HYPO-ventilation occurs in cases of Empty Nose Syndrome, the underlying causes of the respiratory disturbances are usually similar. Both conditions arise from disruptions due to a lack of normal nasal airflow resistance, reduced levels of nasal nitric oxide, and the loss of receptors that enable the brain and lungs to receive neurological signals indicating that breathing is occurring through the nose. Without this neurological feedback system from the nose to the brain, there will be a chronic feeling of air hunger and dyspnea, triggering a fight-or-flight response.
Modified "Control Pause-Test" to understand the neurological part of ENS
What is known is that breathing rate is regulated by the levels of carbon dioxide in the blood. However, what is less commonly known by the public is that both breathing rate and depth are also regulated by neurofeedback from the nose to the brain. In ENS, that nose-brain connection has been destroyed or at least heavily compromised by the surgery and the subsequent mucosal degeneration.
The neurological part of ENS-related air hunger can be tested by performing a so-called Control Pause Test. In this case, however, we will modify the second part of the test. The test involves starting by breathing normally through the mouth and then holding your breath until you feel the urge to take another breath. You will measure the time from the moment you exhaled your last breath until you feel the first impulse to take a new breath. After completing this first part, you should have recorded a certain number of seconds during which it felt comfortable for you to hold your breath without feeling strained.
Now we move on to part two of the test, which is modified to show the effect of mucosal nerve stimulation on breath holding time. This modified CP test begins with you breathing normally through your mouth for 60 seconds while simultaneously blocking your nose completely with your fingers. Once 60 seconds have passed, exhale normally and then start timing until you feel the first urge to take another breath. Stop the timer here and record the result. (Note that you should continue to block your nose throughout this second part of the test.)
What you will likely notice is that you were able to hold your breath comfortably significantly longer during the first part of the test when you breathed through your mouth while keeping your nose open. What does this indicate? It suggests that it is not only the level of carbon dioxide in the blood that determines when you initially feel the need for a new breath, but also that there are additional factors.
To understand what these factors are, we first need to explain that during part 1 of the test, even though you were breathing through your mouth, there was still about 10-20% airflow through your nose. This is how we are designed, and this airflow is more than sufficient to activate the thousands of receptors that are normally present in a healthy, non-operated nose. This neurological feedback from the nasal mucosa to the lungs and brain has a calming effect. Allowing the autonomic nervous system to remain in a state of parasympathetic dominance for longer during your breath holding time. This nerve and receptor stimulation is what allows you to feel relaxed without experiencing shortness of breath for a longer duration during the first part of the test.
This modified CP test thus demonstrates that the feeling of air hunger is not solely controlled by the level of carbon dioxide in the blood, but also by neurological feedback from the nose to the brain and from the nose to the lungs. Now imagine what happens in Empty Nose Syndrome when the nasal nerves and receptors are amputated and destroyed. The brain lacks signals from the nose, leaving you in a constant state of air hunger even though the nose is physiologically open.
For your information regarding spirometry and lung expansion in ENS:
The reduced lung expansion we discussed earlier in can be assessed using nasal spirometry. To test how lung expansion is affected by nasal resistance, you need to start the test by breathing normally through the nose using spirometry equipment modified for nasal breathing. After completing part 1 of the test, you move on to part 2, where cotton implants are placed in the fully open ENS nostril to restore normal nasal airflow resistance. Once this is done, the test is repeated in the same manner. Afterward, you compare the utilized lung volume between test 1 and test 2.
Note: Keep in mind that despite ENS, you may still have some nasal cycle left that can affect the test results. Recently, a spirometry test of an individual affected by ENS showed that lung expansion increased by 80% after the cotton implants. For your information, such a test can be performed in Germany at: Dr. Thomas Weiss Praxis in Mannheim
Tips for measuring end-tidal carbon dioxide and partial pressure of carbon dioxide in the blood:
To measure end-tidal carbon dioxide (etCO2), a capnometer can be used. This device measures the exhaled level of carbon dioxide (CO2) per breath. For more robust evidence, it's advisable to measure blood carbon dioxide (pCO2), which is the partial pressure of carbon dioxide. The normal range for etCO2 and pCO2 is 35-45 mmHg.
Of interest regarding HYPO-ventilation and ENS: Not all individuals with Empty Nose Syndrome are likely to experience HYPO-ventilation, which refers to insufficient ventilation of carbon dioxide (CO2) from the blood. For this to occur, the nasal passages would likely need to be extremely opened due to surgery. However, HYPER-ventilation is a well-known condition in research related to ENS, believed to occur in about 75-80% of cases.
Nasal resistance: Impact on Intrathoracic and Intra-Abdominal Pressure
The expansion of the thoracic (lung) cavity typically creates a downward force on the abdominal cavity, aiding in venous return from the abdomen to the thoracic cavity. However, with reduced nasal resistance, lung expansion decreases and the negative intrathoracic pressure diminishes. This reduction in thoracic pressure leads to a corresponding decrease in intra-abdominal pressure (stomach pressure), which impairs the effectiveness of venous return to both the heart and the lungs.
Compromised Venous Return and Cardiac Output:
The decreased negative pressure in both the thoracic and abdominal cavities results in diminished venous return to the heart. With less blood returning to the heart and lungs, cardiac output decreases. This reduction in cardiac output impairs overall circulation and limits the volume of blood available to deliver oxygen and nutrients to various tissues.
Impaired Gas Exchange Efficiency:
The reduced blood flow through the pulmonary vessels due to decreased venous return negatively impacts gas exchange. Less blood flow means that oxygen uptake and carbon dioxide elimination are compromised, leading to inefficient gas exchange. This reduction in gas exchange efficiency significantly affects respiratory health and overall oxygenation of the blood.
Conclusion:
In summary, ENS leads to reduced nasal resistance, which in turn decreases the need for negative pressure during inhalation. This results in less lung expansion, lower negative intrathoracic and intra-abdominal pressures, compromised venous return, and decreased cardiac output. The overall impact is impaired gas exchange and reduced efficiency in delivering oxygen to tissues, including the brain.
Individuals with surgically reduced nasal resistance may experience symptoms such as impaired cognition, fatigue, dizziness, and decreased exercise tolerance, all due to compromised circulation and impaired gas exchange.
Further more, since the turbinates and the nasal mucosa is an extremely important part of the autonomic nervous system that controls sympathetic and parasympathetic dominance ENS also affects mental aspects. When the turbinates are heavily destroyed or removed most individuals will struggle severely to sleep and relax and will found themselves in constant fight and flight mode. Severe insomnia is one of the most common aspects of nasal turbinate reduction / destruction.
So, removing or destroying a person’s turbinates and nasal structures while claiming that it has no adverse effects is a grave injustice that inflicts severe suffering on the individual. This suffering has, tragically, led to numerous cases of self-destruction. Surgeons who undertake such procedures without adequately informing patients of the potential consequences must be held accountable for their actions.
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