Stridor: Pathophysiology, Causes, and Tracheostomy Tubes

What is Stridor?

Stridor is a high-pitched sound caused by the turbulent flow of air through a partially obstructed airway. It must be distinguished from stertor and wheeze:

• Stertor is an inspiratory sound resembling snoring, caused by partial obstruction of the airway at the nasopharynx or oropharynx — above the level of the larynx.
• Wheeze originates in the smaller airways (bronchi) and is predominantly expiratory, as seen in asthma and COPD.
• Stridor arises from obstruction at or below the larynx.

Phase of Stridor and Level of Obstruction

The phase during which stridor is heard gives important diagnostic information about the anatomical level of obstruction:

• Inspiratory stridor is characteristic of supraglottic and glottic obstructions (above or at the level of the vocal cords). During inspiration, negative intrathoracic pressure sucks air inward through the narrowed segment, generating turbulence that is loudest on the inspiratory phase. Common causes include epiglottitis, supraglottitis, and laryngomalacia.
• Expiratory stridor occurs when the obstruction is in the smaller airways, such as the bronchi. During expiration, positive intrathoracic pressure compresses already narrowed airways further. More commonly called wheeze — seen in bronchiolitis and asthma.
• Biphasic stridor (both inspiratory and expiratory) occurs with lesions of the subglottis and trachea, where the airway is critically narrowed in both phases. The classic example is croup (laryngotracheobronchitis).

Common Causes of Stridor on Call

In Adults

• Trauma to the airway: Blunt neck trauma can cause laryngeal fracture or haematoma. Suspect this in any patient with a hoarse voice, neck tenderness, and stridor after direct neck injury.
• Anaphylaxis: A life-threatening hypersensitivity reaction causing rapid supraglottic and glottic oedema. Treat immediately with IM adrenaline 0.5 mg (1:1000), chlorphenamine, and hydrocortisone. Call the resuscitation team.
• Laryngeal oedema due to epiglottitis, supraglottitis, or laryngitis: Bacterial infection causes rapidly progressive inflammatory oedema. Epiglottitis in adults is often caused by Streptococcus or Staphylococcus species (Haemophilus influenzae type B is more typical in unvaccinated children). Do not examine the throat without anaesthetic support.
• Neoplastic lesions of the larynx: Progressive hoarseness followed by stridor is the classic presentation of laryngeal SCC. The stridor is typically gradual in onset. These patients need urgent ENT and oncology review.
• Bilateral vocal cord paralysis: Causes biphasic stridor and may follow thyroid surgery (bilateral recurrent laryngeal nerve injury), or be due to malignant infiltration. Flexible nasendoscopy confirms the diagnosis.

In Children

• Laryngomalacia: The most common cause of chronic stridor in infants. The supraglottic structures are immature and collapse inward during inspiration. Characteristic intermittent inspiratory stridor typically beginning in the first few weeks of life, worsening when supine or crying, and improving in the prone position. Usually self-resolves by 18 months. Rarely requires surgical intervention (supraglottoplasty).
• Croup (laryngotracheobronchitis): Usually affects children aged 6 months to 3 years. Caused predominantly by parainfluenza virus. Presents with a barking "seal-like" cough, biphasic stridor, and low-grade fever. Managed with dexamethasone and nebulised adrenaline for moderate to severe cases.
• Epiglottitis: Now rare in vaccinated populations due to the Hib vaccine but still encountered — particularly in unvaccinated children and adults. Classic tripod positioning, drooling, high fever, and a toxic appearance. A medical and surgical emergency — do NOT examine the throat or cause distress.
• Inhaled foreign bodies: Children who suddenly develop choking, stridor, or unilateral wheeze should be suspected of foreign body inhalation. Peanuts, coins, and small toy components are common culprits. Chest X-ray (inspiratory and expiratory views) may show air-trapping or mediastinal shift. Removal is performed under general anaesthesia using a rigid bronchoscope.
• Angioneurotic oedema (hereditary angioedema or allergic angioedema): Episodic non-pitting oedema of the face, lips, tongue, and larynx caused by bradykinin or histamine-mediated mechanisms. Hereditary angioedema (HAE — C1-esterase inhibitor deficiency) does not respond to adrenaline or antihistamines — treat with C1-inhibitor concentrate, icatibant, or fresh frozen plasma. Allergic angioedema responds to adrenaline and antihistamines.

Management in Adults

1. Position: Allow the patient to sit or lie in the position they find most comfortable. Do not force them to lie down — many patients with upper airway obstruction maintain their airway better when upright.
2. Oxygen or Heliox: Administer high-flow oxygen. If available and the patient does not require high FiO2, consider Heliox (a mixture of 79% helium and 21% oxygen). The lower density of helium reduces turbulence through the narrowed airway and reduces the work of breathing, buying time for other treatments to take effect.
3. Nebulised racemic adrenaline: 5 ml of 1:1000 adrenaline (5 mg) nebulised. Causes mucosal vasoconstriction and rapidly reduces airway oedema. Onset within minutes; duration 30 to 60 minutes. Monitor for rebound oedema after the effect wears off.
4. Intravenous cannula, dexamethasone or hydrocortisone: Insert IV access and administer systemic corticosteroids. Dexamethasone 8 mg IV or IM is the preferred agent for acute airway oedema. Hydrocortisone 200 mg IV is an alternative if dexamethasone is unavailable.
5. Monitor vital signs: Record oxygen saturations, respiratory rate, pulse, and blood pressure continuously. A falling oxygen saturation is a pre-terminal sign — act before this point is reached.
6. Call the anaesthetist: Do this early. The anaesthetist will need time to prepare for a potentially difficult intubation. In epiglottitis or suspected total airway obstruction, the call should be made immediately on first assessment.
7. Keep the crash tracheostomy kit ready: Ensure the tracheostomy trolley (or at minimum a surgical airway kit — scalpel, dilator, cuffed tracheostomy tube) is immediately available at the bedside.
8. Call the ENT registrar: The ENT team provides surgical airway backup. Do not delay this call.
9. Brief targeted history: Once the acute phase is controlled, take a concise relevant history from the patient or relatives, focusing on the likely diagnosis: onset, preceding illness, foreign body ingestion, drug exposure (including ACE inhibitors — which can cause angioedema), recent surgery, vaccination history.
10. Arterial blood gases (ABG): If clinically feasible, an ABG provides information on oxygenation (PaO2), ventilation (PaCO2 — rising CO2 is a pre-arrest finding), and acid-base status. Do not delay treatment to obtain an ABG.
11. Flexible nasendoscopy: Once the patient is stabilised and the stridor has improved, a flexible nasendoscope can be passed (via the nose, through the nasopharynx, and down to the level of the vocal cords) to directly visualise the larynx. This identifies the cause and level of obstruction. If you are not trained in flexible nasendoscopy, the ENT registrar will perform this.
12. Neck and chest X-rays: Anteroposterior and lateral neck X-rays may show subglottic narrowing (the "steeple sign" in croup), a swollen epiglottis (the "thumb sign" in epiglottitis), or soft tissue emphysema. A chest X-ray assesses for foreign body and pulmonary pathology. These investigations should not delay treatment in an acutely deteriorating patient.

Management in Children

1. Minimise distress: Sit the child on a parent's lap in a quiet room. Do not attempt to examine the throat, insert a cannula, or perform any procedure that may agitate the child — distress worsens airway obstruction by increasing oxygen demand and respiratory effort, and in epiglottitis can precipitate complete obstruction.
2. Call a senior paediatric consultant: A paediatric consultant and paediatric anaesthetist should be called immediately for any child with significant stridor.
3. Inform the ENT registrar: The ENT team should be available for emergency surgical airway if needed.
4. Monitor non-invasively: Monitor the respiratory rate. Accept that other monitoring (oxygen saturation probe, ECG) may not be tolerated by a distressed child — do not fight to apply it. Observe carefully for signs of deterioration: increasing respiratory rate, increasing work of breathing (tracheal tug, intercostal recession, subcostal recession, use of accessory muscles), cyanosis, reduced level of consciousness, and drooling.
5. Communicate the severity: When calling for help, be specific about the severity of stridor. Describe the presence or absence of tachypnoea, drooling, tracheal tug, intercostal indrawing on inspiration, respiratory effort, ability to speak or cry, cyanosis, and level of consciousness and responsiveness. This allows the arriving team to prepare appropriately.

Tracheostomy Tubes — Identification and Components

Any doctor working in a hospital where tracheostomy patients are managed must be able to identify and handle the most common tracheostomy tubes. The two most commonly encountered tubes in UK practice are the Shiley and the Fuller's (Portex) tracheostomy tubes. The key components of any tracheostomy tube are:

• Outer cannula: The main tube, which sits within the tracheal stoma. It has a fixed 15 mm connector (universal ventilator attachment) and neck flanges for securing the tube with tapes.
• Inner cannula: A removable lining tube that sits inside the outer cannula. Crucially, the inner cannula can be removed for cleaning without disturbing the outer tube, which maintains the airway. Blocked inner cannulae are the most common cause of tracheostomy obstruction on the ward — always remove and clean the inner cannula first.
• Obturator (introducer): A blunt-tipped solid rod that fits inside the outer cannula during initial insertion to prevent the tube tip from traumatising the tracheal wall. It is removed immediately after the tube is inserted. It should never be left in the tube during use.
• Cuff: An inflatable balloon around the lower portion of the outer cannula that seals the trachea below the tube, preventing aspiration and directing all ventilation through the tube. Cuff pressure should be monitored regularly (target 20 to 25 cmH2O) — overinflation causes tracheal mucosal ischaemia and stenosis.
• Pilot balloon: A small external balloon connected to the cuff, used to assess cuff inflation status. If the pilot balloon is flat, the cuff may be deflated or ruptured.

Emergency Management of a Blocked or Displaced Tracheostomy

Follow this systematic approach:

1. Suction the tracheostomy tube with a soft suction catheter.
2. Remove the inner cannula, clean it under running water, and reinsert — this resolves the majority of ward tracheostomy emergencies.
3. If the tube is still blocked, attempt to pass a suction catheter through the outer cannula to assess and restore patency.
4. If completely obstructed, remove the outer tube entirely. If the stoma is mature (more than 7 to 10 days old), re-intubate via the stoma using a new tube or a flexible airway. If the stoma is immature, secure the airway orally or nasally while calling ENT urgently.
5. Call ENT and anaesthetics immediately if airway cannot be maintained.