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Monday, August 18, 2025

Snoring


Introduction

Snoring is defined as a harsh or hoarse sound produced during sleep due to turbulent airflow causing vibration of the soft tissues in the upper airway, particularly the soft palate, uvula, tonsillar pillars, and base of the tongue. It is one of the most common sleep-related breathing disorders, affecting an estimated 40–60% of men and 20–40% of women over the age of 40. In children, prevalence ranges from 10–15%.

While occasional snoring may be harmless, chronic and loud snoring can indicate underlying obstructive sleep apnea (OSA) or other airway pathologies, with implications for cardiovascular, metabolic, and neurocognitive health.

Anatomy and Physiology of Snoring

The upper airway includes the nose, pharynx, and larynx. Normally, airflow during sleep remains laminar. However, when the muscles of the pharynx relax excessively, narrowing occurs, causing turbulent airflow. This turbulence vibrates surrounding tissues, producing the characteristic snoring sound.

Key anatomical contributors:

  • Nasal cavity: Deviated septum, turbinate hypertrophy, congestion.

  • Oropharynx: Enlarged tonsils, long uvula, soft palate collapse.

  • Tongue base: Macroglossia, obesity-related fat deposition.

  • Neck soft tissue: Adipose tissue narrowing airway.

Etiology and Risk Factors

1. Structural Abnormalities

  • Deviated nasal septum.

  • Nasal polyps.

  • Enlarged adenoids or tonsils (common in children).

  • Retrognathia or micrognathia.

  • Long uvula or soft palate.

2. Obesity and Fat Distribution

  • Central obesity increases fat deposition around pharyngeal walls, reducing lumen size.

  • Neck circumference >40 cm is a predictor of snoring and OSA.

3. Lifestyle and Environmental Factors

  • Alcohol consumption: relaxes pharyngeal muscles.

  • Sedative medications: benzodiazepines, antihistamines, hypnotics.

  • Smoking: causes mucosal inflammation and edema.

  • Sleep position: supine sleeping worsens airway collapse.

4. Medical Conditions

  • Allergic rhinitis or chronic sinusitis.

  • Hypothyroidism (mucopolysaccharide deposition).

  • Acromegaly (macroglossia).

  • Pregnancy: weight gain and mucosal edema.

5. Age and Gender

  • Snoring increases with age due to reduced muscle tone.

  • Men are more commonly affected due to airway anatomy differences.

Pathophysiology

  1. Airway narrowing due to anatomical obstruction or functional relaxation.

  2. Turbulent airflow generates tissue vibration.

  3. Partial obstruction results in snoring, while complete obstruction leads to apnea (cessation of breathing).

  4. Repeated obstructions cause intermittent hypoxia, sympathetic activation, and sleep fragmentation, progressing to OSA.

Clinical Presentation

  • Primary symptom: audible snoring during sleep, often reported by bed partners.

  • Associated symptoms:

    • Daytime sleepiness and fatigue.

    • Morning headaches.

    • Dry mouth and sore throat upon waking.

    • Restless sleep, frequent awakenings.

    • Nocturia (frequent urination at night).

  • In children: hyperactivity, learning difficulties, poor school performance.

Red flags suggesting sleep apnea:

  • Witnessed apneas.

  • Choking or gasping during sleep.

  • Severe daytime somnolence.

  • Resistant hypertension.

Diagnostic Evaluation

1. Clinical History

  • Snoring frequency, intensity, positional relation.

  • Daytime symptoms (fatigue, sleepiness).

  • Medical history: obesity, nasal congestion, cardiovascular disease.

  • Medication and alcohol use.

2. Physical Examination

  • BMI and neck circumference.

  • Nasal inspection (septal deviation, polyps).

  • Oral exam (tonsils, uvula, palate).

  • Mallampati classification (visualization of oropharynx).

3. Investigations

  • Polysomnography (gold standard): Records sleep stages, respiratory effort, airflow, oxygen saturation, and apnea-hypopnea index (AHI).

  • Home sleep apnea testing (simplified polysomnography).

  • Nasopharyngoscopy: Endoscopic evaluation for structural obstructions.

  • Imaging: CT or MRI for craniofacial abnormalities.

Classification

  • Primary Snoring (Simple Snoring): No apnea or oxygen desaturation.

  • Obstructive Sleep Apnea (OSA): Snoring with apneas/hypopneas and desaturations.

  • Upper Airway Resistance Syndrome (UARS): Snoring with increased respiratory effort and arousals without apneas.

Management

1. Lifestyle and Behavioral Measures

  • Weight loss: Reduces pharyngeal fat; even 10% reduction improves snoring.

  • Sleep position therapy: Avoiding supine sleep (tennis ball technique, positional devices).

  • Alcohol and sedative avoidance: Particularly 4–6 hours before bedtime.

  • Smoking cessation: Reduces airway inflammation.

  • Regular sleep hygiene.

2. Medical Management

A. Nasal Decongestion

  • Topical nasal corticosteroids for allergic rhinitis:

    • Fluticasone propionate nasal spray 50 mcg per spray, 1–2 sprays in each nostril once daily.

    • Mometasone furoate nasal spray 50 mcg, 2 sprays each nostril once daily.

  • Oral antihistamines for allergic component:

    • Cetirizine 10 mg orally once daily.

    • Loratadine 10 mg orally once daily.

B. Pharmacological Muscle Tone Enhancement (Investigational)

Some trials explore agents like atomoxetine (40 mg orally nightly) combined with oxybutynin (5 mg orally nightly) to improve upper airway muscle tone in OSA. Still experimental and not first-line.

C. Treatment of GERD (when reflux worsens snoring)

  • Proton pump inhibitors:

    • Omeprazole 20–40 mg orally once daily.

3. Non-Pharmacological Interventions

A. Continuous Positive Airway Pressure (CPAP)

  • Mainstay for OSA-related snoring.

  • Provides pneumatic splint to keep airway open.

  • Effective in eliminating snoring and improving cardiovascular outcomes.

B. Mandibular Advancement Devices (Oral Appliances)

  • Custom-made dental devices that advance mandible forward, enlarging airway.

  • Useful in mild to moderate OSA and primary snoring.

C. Nasal Dilators

  • External nasal strips or internal nasal stents to improve airflow.

4. Surgical Management

Indicated for structural abnormalities or refractory cases:

  • Uvulopalatopharyngoplasty (UPPP): Resection of uvula, soft palate tissue.

  • Radiofrequency tissue ablation: Reduces soft palate volume.

  • Septoplasty/turbinate reduction: For nasal obstruction.

  • Tonsillectomy and adenoidectomy: Especially effective in children with enlarged tonsils/adenoids.

  • Maxillomandibular advancement surgery: For craniofacial abnormalities.

  • Hypoglossal nerve stimulation devices: Newer therapy for OSA-related snoring.

5. Pediatric Snoring Management

  • Adenotonsillectomy is the first-line treatment for most children with snoring and OSA due to enlarged tonsils/adenoids.

  • Intranasal corticosteroids and leukotriene receptor antagonists (e.g., Montelukast 4–5 mg chewable tablet once daily) may be used in mild pediatric cases.

Complications

  • Daytime consequences: Fatigue, cognitive impairment, reduced quality of life.

  • Cardiovascular risks: Hypertension, arrhythmias, myocardial infarction, stroke (especially with OSA).

  • Metabolic risks: Insulin resistance, type 2 diabetes.

  • Behavioral and emotional issues: Particularly in children (hyperactivity, poor school performance).

  • Marital/relationship strain: Due to sleep disturbance of bed partners.

Precautions and Patient Counseling

  • Encourage weight loss and exercise.

  • Advise avoidance of alcohol, sedatives, and late heavy meals.

  • Stress adherence to CPAP therapy when prescribed.

  • Explain importance of long-term follow-up for cardiovascular risk monitoring.

  • In children, emphasize ENT evaluation for adenoid/tonsil hypertrophy.

Drug Interactions

  • Intranasal corticosteroids (fluticasone, mometasone): Risk of systemic corticosteroid interactions is minimal but possible with CYP3A4 inhibitors (ketoconazole, ritonavir).

  • Antihistamines (cetirizine, loratadine): May have additive sedation when combined with alcohol or sedatives.

  • Proton pump inhibitors (omeprazole): Interacts with clopidogrel (reduces antiplatelet effect).

  • Atomoxetine (investigational use): Interacts with MAO inhibitors, SSRIs (risk of serotonin syndrome).

  • Montelukast (pediatrics): May interact with CYP2C9 inducers such as rifampin.

Prognosis

  • Primary snoring without OSA is generally benign, but may progress if risk factors persist.

  • Snoring with OSA requires long-term management due to associated morbidity and mortality.

  • Children generally have excellent outcomes with adenotonsillectomy.

  • Weight reduction and lifestyle interventions can significantly reduce or eliminate snoring in many cases.




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