12.4 Asthma, COPD and Respiratory Emergencies

4. Respiratory Disease: Asthma and Chronic Obstructive Pulmonary Disease (COPD)

Respiratory disease impairs alveolar gas exchange and airway mechanics, presenting acute hazards during dental operative procedures.

Asthma: Pathophysiology and Clinical Triggers

Asthma is a chronic inflammatory disorder of the conducting airways characterized by bronchial hyperresponsiveness, reversible airflow limitation, mucosal oedema, and excessive mucous secretion.

• Dental Triggers: In the dental environment, acute bronchospasm can be provoked by: acute psychological stress and fear, inhalation of cold dry air, dental stone/plaster dust, airborne powder from latex gloves, methyl methacrylate monomer vapour from acrylics, impression material colophony, and sulfite preservatives.
• The Local Anaesthetic Preservative Trap: Local anaesthetic cartridges that contain a vasoconstrictor (such as adrenaline) also contain sodium metabisulfite or potassium metabisulfite as an antioxidant to prevent catecholamine oxidation. In approximately 5% to 10% of asthmatic patients (particularly steroid-dependent asthmatics), sulfites can trigger severe, acute IgE-mediated or non-IgE-mediated hypersensitivity reactions and life-threatening bronchospasm. If a patient gives a confirmed history of sulfite allergy, plain local anaesthetics (e.g., 3% mepivacaine plain or 4% prilocaine plain) must be used.

Aspirin-Exacerbated Respiratory Disease (AERD / Samter's Triad)

Aspirin-sensitive asthma affects up to 10% to 20% of adult asthmatic patients. It is characterized by the classic Samter's triad (or Widal's syndrome):

1. Severe bronchial asthma.
2. Chronic rhinosinusitis with recurrent nasal polyposis.
3. Severe hypersensitivity to aspirin and non-steroidal anti-inflammatory drugs (NSAIDs).

                    Arachidonic Acid
                           │
        ┌──────────────────┴──────────────────┐
        ▼                                     ▼
  Cyclooxygenase-1 (COX-1)              5-Lipoxygenase (5-LOX)
  [BLOCKED by Aspirin & NSAIDs]               │
        │                                     ▼
  Loss of Prostaglandin E2 (PGE2)       Massive Surge of Cysteinyl Leukotrienes
  (Loss of Bronchoprotective Tone)              (LTC4, LTD4, LTE4)
                                              │
                                              ▼
                                        Profound Bronchoconstriction,
                                        Mucosal Oedema & Fatal Bronchospasm

• Molecular Mechanism: Aspirin and traditional non-selective NSAIDs (ibuprofen, naproxen, diclofenac, ketoprofen) irreversibly or reversibly block the cyclooxygenase-1 (COX-1) enzyme. This shunts all uninhibited arachidonic acid metabolism into the 5-lipoxygenase pathway, generating an uncontrolled surge of cysteinyl leukotrienes ($LTC_4$, $LTD_4$, $LTE_4$). Concurrently, the synthesis of prostaglandin $E_2$ ($PGE_2$), which exerts baseline bronchodilator and mast-cell stabilising effects, is abolished. The resulting leukotriene surge causes massive bronchoconstriction, mucosal hyperaemia, and rapid, potentially fatal asphyxiation.
• Clinical Mandate: Aspirin and all NSAIDs are strictly contraindicated in patients with asthma who have a history of aspirin sensitivity or nasal polyposis. In clinical practice, paracetamol (or paracetamol with codeine) is the analgesic of choice. If paracetamol is insufficient, weak opioids (dihydrocodeine) may be considered, while monitoring for respiratory depression.

Chairside Asthma Management and Emergency Protocol

• Pre-treatment Check: The patient must place their short-acting selective beta-2 adrenergic agonist inhaler (Salbutamol 100 mcg/actuation, blue inhaler) directly on the bracket table. Verify that the canister is not empty.
• Ultrasonic Scalers and Aerosols: Avoid ultrasonic scaling, air-polishers, and excessive water spray during periods of unstable asthma or in patients with active wheezing. Aerosol clouds and aspirating cool water mist trigger hyper-reactive bronchial smooth muscle contraction.
• Acute Asthma Attack Protocol in the Dental Chair:
  1. Stop dental treatment; remove all oral instruments and rubber dam.
  2. Sit the patient upright and lean them slightly forward; do NOT lay the patient down (supine positioning increases work of breathing and orthopnoea).
  3. Administer Salbutamol (100 mcg/puff): deliver 2 to 4 puffs immediately, preferably via a large-volume spacer device (Volumatic / AeroChamber). Instruct the patient to take 4 to 5 tidal breaths per puff.
  4. Reassure the patient and administer high-flow oxygen (10–15 L/min via non-rebreather reservoir mask).
  5. If symptoms fail to resolve, administer 1 puff of Salbutamol every 30 to 60 seconds, up to a total of 10 puffs.
  6. Call 999 immediately if the patient is unable to complete sentences in one breath, displays silent chest (absence of wheezing due to severe airflow cessation), develops cyanosis, has an oxygen saturation $< 92%$, or fails to improve following 10 puffs of salbutamol.
  7. If the patient becomes exhausted, drowsy, or loses consciousness, prepare for intramuscular adrenaline (0.5 mg IM [0.5 mL of 1:1,000] in anterolateral thigh) as emergency bronchodilator therapy, assist ventilation with bag-valve-mask, and initiate basic life support.

Chronic Obstructive Pulmonary Disease (COPD)

COPD is a progressive, irreversible pulmonary disorder encompassing chronic bronchitis (chronic productive cough for $\ge 3$ consecutive months in $\ge 2$ successive years) and emphysema (abnormal permanent enlargement of airspaces distal to terminal bronchioles with destruction of alveolar walls and loss of elastic recoil).

Dental Considerations for COPD

1. Chair Positioning (Avoid Fully Supine): Patients with moderate-to-severe COPD suffer from significant diaphragmatic flattening and reduced chest wall compliance. Placing the dental chair in a flat or supine position forces the abdominal viscera superiorly against the diaphragm, causing acute mechanical orthopnoea, respiratory exhaustion, and severe dyspnoea. Always treat COPD patients in a semi-erect or fully upright position (at an angle of $\ge 45\text{ degrees}$).
2. The Loss of Hypoxic Drive and Oxygen Hazard:
   • Pathophysiology: In healthy individuals, central chemoreceptors in the medulla oblongata are exquisitely sensitive to changes in arterial carbon dioxide ($PaCO_2$), which acts as the primary respiratory drive. In patients with end-stage chronic bronchitis and severe hypercapnia, the central chemoreceptors become chronically desensitized to elevated $PaCO_2$. Consequently, respiratory drive is maintained entirely by peripheral chemoreceptors (located in the carotid and aortic bodies) that fire in response to low arterial oxygen tension ($PaO_2$)—the so-called hypoxic drive.
   • The Danger of High-Flow Oxygen: If uncontrolled high-flow oxygen (e.g., 10–15 L/min via non-rebreather mask, delivering $>60-80%\text{ }O_2$) is administered to a severe COPD patient with chronic CO2 retention, the acute elevation of $PaO_2$ abolishes the peripheral chemoreceptor firing. The sole remaining drive to breathe is abruptly extinguished, precipitating acute hypoventilation, hypercapnic respiratory acidosis, carbon dioxide narcosis, coma, and respiratory arrest.
   • Emergency Oxygen Guidance: If emergency oxygen is required in a COPD patient with respiratory distress, deliver controlled low-concentration oxygen via a 24% or 28% Venturi mask (at 2–4 L/min), targeting oxygen saturations strictly between 88% and 92%, pending emergency medical arrival.
3. Sedation, Narcotics, and Rubber Dam Hazards:
   • Conscious Sedation: Intravenous midazolam is contraindicated in severe COPD due to its potent central respiratory depressant effects. Inhalation sedation with nitrous oxide/oxygen must be used with extreme caution or avoided in bullous emphysema, as nitrous oxide diffuses into closed air spaces 34 times faster than nitrogen leaves, expanding pulmonary bullae and precipitating a life-threatening spontaneous tension pneumothorax.
   • Opioid Analgesics: Opioids (codeine, dihydrocodeine, morphine) depress the medullary respiratory centre and suppress the cough reflex, promoting mucus plugging and hypoventilation. Avoid opioids; rely on paracetamol and non-opioid regimens.
   • Rubber Dam: In severe COPD patients who are obligatory mouth-breathers, placing a rubber dam can induce acute sensations of suffocation and severe respiratory distress. If rubber dam isolation is indispensable, use a nasal cannula for supplemental low-flow air/oxygen and ensure the nares remain completely unobstructed.

5. Clinical Traps, Pitfalls, and Worked Scenarios

[!CAUTION] Clinical Trap: Demands for Antibiotic Prophylaxis in High-Risk Patients: A 65-year-old male with a mechanical aortic valve replacement presents for surgical extraction of a fractured lower molar. The patient insists that his previous dentist always gave him 3 g of oral amoxicillin before treatment and demands a prescription, stating he will hold you legally responsible if he contracts endocarditis. Under UK GDC standards and NICE CG64, routine antibiotic prophylaxis is not indicated. Acceding to patient pressure without clinical justification violates UK antimicrobial stewardship. The correct management is to provide empathetic, structured explanation: explain that current UK evidence demonstrates antibiotics do not prevent endocarditis, that daily toothbrushing poses a greater cumulative risk, and that amoxicillin carries significant risks of fatal allergic reactions and antibiotic resistance. Document the detailed discussion in the clinical notes. If the patient refuses treatment without prophylaxis, offer to liaise with their cardiologist.

[!WARNING] Clinical Trap: Misdiagnosing Jaw Pain as Odontogenic in Ischaemic Heart Disease: Myocardial ischaemia does not always present with classic retrosternal chest tightness. In up to 10% to 15% of patients—especially women, diabetics, and the elderly—cardiac ischaemia presents atypically as referred craniofacial pain. Ischaemic visceral afferent fibres travelling via cardiac sympathetic nerves (T1–T4) enter the spinal cord and converge with somatic pathways, projecting via interneurons to the spinal trigeminal nucleus. Consequently, angina or an acute MI may manifest solely as cramping, burning, or aching pain radiating to the left angle of the mandible, lower jaw, or teeth, provoked by walking or climbing stairs and relieved by rest. Extracting a sound mandibular molar because of "unexplained lower jaw pain" in a patient with cardiovascular risk factors is a catastrophic diagnostic blunder. Always take a complete cardiovascular history and inquire whether jaw pain is provoked by physical exertion.

Worked Clinical SBA Scenario

Scenario: A 71-year-old male presents to your dental surgery complaining of severe, constant throbbing pain from tooth 47. Medical history reveals a 15-year history of severe Chronic Obstructive Pulmonary Disease (COPD) with long-term home oxygen therapy, alongside Stage 2 hypertension treated with amlodipine. Clinical examination reveals acute periapical periodontitis associated with a non-restorable retained root of 47. Pre-operative blood pressure is recorded at $158/94\text{ mmHg}$, and his baseline oxygen saturation on room air is $89%$. While in the dental chair, the patient develops severe wheezing, breathlessness, and acute agitation.

Question: What is the immediate, correct sequence of clinical management for this patient regarding chair positioning, oxygen administration, and pharmacological intervention?

Analysis and Clinical Governance: The patient is experiencing an acute bronchospastic exacerbation of his severe COPD. Placing him flat in the dental chair would induce diaphragmatic splinting and worsen respiratory failure; he must be maintained upright or semi-reclined at $\ge 45\text{ degrees}$. Crucially, administering high-flow oxygen via a non-rebreather mask ($10-15\text{ L/min}$) is contraindicated because his baseline $SpO_2$ of $89%$ reflects chronic CO2 retention dependent on peripheral hypoxic drive; high-flow oxygen will suppress breathing and trigger carbon dioxide narcosis. The correct management is to administer Salbutamol (2–4 puffs via spacer), sit the patient upright, and if supplemental oxygen is required, titrate via a 24% or 28% Venturi mask targeting an $SpO_2$ strictly within 88% to 92%. If acute respiratory distress fails to resolve, summon an emergency ambulance (999). Tooth extraction is deferred until the acute respiratory exacerbation has resolved.