The Hidden Risks of Nasal Surgery: ENS, Breathing Difficulties, and Systemic Health Impacts

Quick Overview of the Consequences of Nasal Surgery

Surgical Procedures in the Nose and Their Consequences:

Turbinate reduction (turbinoplasty), septoplasty, spreader graft surgery, and medial maxillectomy (a sinus surgery where the wall between the nose and maxillary sinus is removed) lead to excessive nasal opening, resulting in a loss of normal airflow resistance. Additionally, these procedures impair the filtration, warming, and humidification of inhaled air and cause damage to the nerves and receptors responsible for airflow perception.

Impaired Nitric Oxide Production:

• Epithelial cells in the nasal mucosa produce nitric oxide (NO), which mixes with inhaled air and contributes to bronchodilation, improved oxygenation, and protection against infections.
• Turbinoplasty amputates or damages epithelial cells, reducing NO production.
• ENS can lead to secondary atrophic rhinitis and further loss of NO-producing epithelial cells.
• Consequences: Impaired oxygenation, increased risk of infections, and worsening respiratory problems.

Sensory and Nerve-Related Effects:

• Nerve damage and loss of mucosa containing TRPM8 receptors (thermoreceptors) lead to:
  • Impaired sensory feedback to the brain.
  • Reduced natural pause between exhalation and inhalation.
  • Decreased airflow sensation, which can cause:
    • Air hunger → Feeling of suffocation → Feeling of drowning → Tension → Stress response → Severe sleep disturbance.
• Amputation or destruction of nasal structures and mucosa leads to:
  • Loss of part of the respiratory system.
  • Disrupted autonomic regulation of sympathetic and parasympathetic balance.
  • Reduced nasal resistance, affecting breathing depth and heart rate regulation.

Dysfunction in Breathing Regulation:

• Altered breathing rhythm and hyperventilation:
  • Without normal airflow resistance, air flows too quickly in and out of the nose → Overventilation → Abnormally high minute ventilation → Excessive loss of carbon dioxide from the blood → Hypocapnia → Alkalosis → Systemic effects.
  • Nerve damage eliminates the natural breathing pause between exhalation and inhalation. This leads to more breaths per minute and excessive minute ventilation → Hypocapnia → Alkalosis → Systemic effects.
• Loss of TRPM8 receptors can lead to:
  • Increased tidal volume (airflow per normal breath) – If airflow is not felt, breathing depth may increase → Overventilation of the lungs.
  • Inability to sense airflow also leads to air hunger and reduced pause between exhalation and inhalation → More breaths per minute → Increased minute ventilation → Excessive loss of carbon dioxide from the blood.
• Low carbon dioxide levels (hypocapnia) cause:
  • Alkalosis → Systemic effects.
  • Vasoconstriction → Impaired oxygenation.
  • Reduced oxygen uptake at the cellular level (Bohr effect).

Autonomic and Metabolic Stress Response:

• Chronic sympathetic dominance ("fight or flight").
• Increased lactate production and metabolic dysfunction.
• Compensatory increase in hematocrit (B-ERV) and MCHC to improve oxygenation.
• Alkalosis causes a compensatory decrease in blood bicarbonate concentration.
• Electrolyte disturbances, including low ionized potassium and calcium.
• Impact on the renin-angiotensin-aldosterone system (RAAS) → Blood pressure dysregulation and sodium/potassium imbalances.

Heart and Circulation:

• Oxygen deficiency (Bohr effect) leads to:
  • Compensatory increased blood pressure.
  • Stress and low carbon dioxide levels cause vasoconstriction.
  • Increased heart strain, impaired oxygen supply to the heart muscle, and sleep deprivation.
  • Risk of left ventricular hypertrophy.
  • Further reinforced sympathetic overactivity.

Neurological and Cognitive Impact:

• Reduced cerebral perfusion → Impaired oxygen delivery to the brain.
• Sleep problems, reduced deep sleep, and increased beta-amyloid accumulation.
• Increased risk of neurodegeneration and cognitive impairment.
• Mitochondrial dysfunction → Fatigue and brain fog.
• Impact on dopamine and serotonin balance → Increased risk of depression and anxiety.

Long-Term Systemic Complications:

• Chronic inflammation and oxidative stress.
• Weakened immune system → Increased susceptibility to infections (e.g., pneumonia).
• Higher risk of heart attack, stroke, and other circulatory diseases.
• Impaired gastrointestinal function → Reduced motility and nutrient absorption.

Quality of Life and Social Consequences:

• Severe impairment of functional ability.
• Social isolation and loss of relationships.
• Increased risk of suicide, statistically highest in years 1–2 after ENS onset and years 4–8.
• Inability to work and premature aging.
• Loss of career and colleagues.
• Financial ruin – Poverty.

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Potential Nocturnal Hypoventilation in ENS

In ENS, breathing regulation is disrupted, typically leading to hyperventilation. However, in some cases, nocturnal hypoventilation can occur, meaning inadequate ventilation of the lungs, resulting in excessive carbon dioxide buildup in the blood.

During sleep, breathing depth naturally decreases due to lower metabolic activity, reduced diaphragm movement, and altered central breathing regulation. In individuals with ENS, these normal changes may be exacerbated by the lack of nasal airway resistance and other physiological factors, further disrupting the breathing pattern at night.

Possible Causes of Nocturnal Hypoventilation:

• Reduced intrathoracic pressure → Decreased airway resistance can affect pressure conditions in the chest, impairing lung expansion.
• Reduced intra-abdominal pressure → Impact on diaphragm movement can lead to reduced stability and inefficient breathing.
• Impaired lung expansion → Reduced diaphragm resistance (air resistance) during inhalation can result in shallower breaths, especially during sleep.
• Premature lung collapse during exhalation due to lack of nasal resistance → Normally, nasal resistance creates a certain backpressure during exhalation, helping keep airways open longer and maintaining optimal gas exchange. In ENS, the absence of this resistance can lead to faster lung emptying and potentially premature collapse of smaller airways (atelectasis), reducing the time required for effective carbon dioxide clearance and alveolar gas exchange.