MODULE 1 · GDFM PROGRAMME

GDFM Module 1 — Head, Neck & Respiratory

📅 2026-03-02 🏛 College of Family Physicians Singapore
M111

Acute Upper Respiratory Tract Infections

Learning Objectives

  • Differentiate URTI from LRTI clinically
  • Identify common viral URTI syndromes (including exanthems and enanthems)
  • Apply clinical decision rules (McIsaac score) to guide antibiotic use in sore throat
  • Recognise URTI mimics endemic to Singapore: Dengue, Chikungunya, Zika
  • Apply current guidelines for influenza antivirals and COVID-19 management
  • Address patient ICE and practice judicious antibiotic stewardship

URTI vs LRTI — Key Differentiators

FeatureURTILRTI
SiteLarynx and proximal airwaysTrachea and distal airways
Systemic symptomsMay be present without localising signsCommon — fever, malaise, myalgia
Localising signsCervical lymphadenopathyCrepitations, rhonchi, signs of respiratory distress (tachypnoea, retractions, cyanosis)
Key symptomsRhinorrhoea, sore throat, mild coughProductive cough, wheeze, breathlessness, chest pain
Common syndromesCoryza, ILI, Sinusitis, Pharyngitis, Otitis MediaBronchitis, CAP, Atypical pneumonia, TB

Clinical Approach to URTI

  • 1. Exclude non-infective causes: allergic rhinitis, asthma, pneumothorax
  • 2. Ascertain epidemiological context: travel, contact history, outbreak alerts
  • 3. Rule out LRTI — both can coexist; comorbidities affect presentation and treatment
  • 4. Establish likely pathogen: viral vs bacterial (guides antibiotic decision)
  • 5. Address patient ICE — unexplored expectations drive unnecessary prescribing [Cockburn & Pit, 1997]
  • 6. Safety-net: clear instructions on when to return or seek emergency care

Antibiotic Decision Framework in URTI

Doctor's AssessmentPatient Expectation → DemandsPatient Expectation → NeutralPatient Expectation → Refuses
Antibiotics INDICATEDPrescribe + explain rationalePrescribe + explain rationaleDocument informed refusal; advise on risks
UNCERTAIN indicationConsider: risk factors, comorbidities, toxicity. Review in 72h if not prescribed.Use clinical judgment; consider delayed prescriptionSymptomatic Rx; review in 72h
NOT indicatedExplain; offer safety-net/delayed prescription if patient insistsReassure + symptomatic RxReassure + symptomatic Rx

Acute Coryza (Common Cold)

  • Causative viruses: Rhinovirus, Coronavirus, Adenovirus, RSV, Parainfluenza, Influenza
  • Incubation 1–3 days; symptoms resolve in ~1 week (up to 2 weeks in smokers)
  • Fever rare and usually <38°C; cough often from post-nasal drip
  • Mucopurulent rhinitis ≠ bacterial sinusitis — not an indication for antibiotics alone
  • Symptomatic treatment: antihistamines (drowsy), decongestants (short-term only), NSAIDs
  • No strong evidence for Vitamin C or zinc lozenges [DeGeorge, 2019]

Cough & Cold Medicines in Children — Current HSA Guidance

💎 Clinical Pearl
Age GroupAntihistaminesDecongestants / Cold productsCough suppressants (non-codeine)Codeine
<2 yearsNOT recommended (unless prescribed by doctor)NOT recommendedNOT recommendedCONTRAINDICATED
2–6 yearsUse only if benefits outweigh risks; HCP advice essentialUse only if benefits outweigh risksUse only if benefits outweigh risksCONTRAINDICATED
6–12 yearsUse with caution; appropriate dosingUse with cautionUse with cautionCONTRAINDICATED
≥12 yearsUse with appropriate dosingUse with appropriate dosingUse with appropriate dosingOnly if indicated; lowest effective dose, shortest duration
PromethazineContraindicated <6 months; not recommended <2 years; caution in older children

Influenza — Prevention & Vaccination

  • Seasonal peaks in Singapore: December–February and May–July
  • Quadrivalent vaccine (4-strain) preferred — covers both B lineages (Victoria + Yamagata)
  • Immunity develops ~2 weeks post-vaccination; protection lasts several months to 1 year
  • Recommended: age ≥65, chronic disease, immunocompromised, pregnant (all trimesters), HCW, BMI ≥40, long-term care residents
  • Household contacts and caregivers of high-risk individuals should also be vaccinated
  • Updated annually — Southern/Northern hemisphere formulations track circulating strains [SIDS Handbook 2023]

Influenza — Diagnosis & When to Test

  • Clinical diagnosis adequate for most outpatients during known influenza season
  • Classic: abrupt onset fever, myalgia, arthralgia → then respiratory symptoms (dry cough, sore throat)
  • Rapid Influenza Diagnostic Tests (RIDTs): sensitivity 10–70%, specificity >95% — negative result does NOT rule out influenza
  • RT-PCR: gold standard — differentiates type/subtype; reserve for hospitalised patients, diagnostic uncertainty, outbreak investigation
  • Point-of-care molecular tests (rapid PCR): near-PCR sensitivity with faster turnaround — increasingly available in primary care [CDC, 2025]
  • Test when result will change management or has public health implications

Signs of Complicated/Progressive Influenza

🚨 Emergency
SystemWarning Signs
RespiratoryCyanosis, haemoptysis, hypoxia (low SpO2), laboured breathing, shortness of breath
CardiovascularChest pain, hypotension
CNSAltered mental status, lethargy, seizures, severe weakness or paralysis
GeneralDecreased urine output, dehydration, fever persisting >72 hours, worsening after initial improvement

Influenza — Antiviral Therapy (2025–2026)

AgentRouteAgeKey Feature
Oseltamivir (Tamiflu)Oral≥2 weeks (treatment); ≥1 year (prophylaxis)First-line. 5-day course. Dose-adjust for renal impairment.
Zanamivir (Relenza)Inhaled≥7 years (treatment); ≥5 years (prophylaxis)Avoid in asthma/COPD — bronchospasm risk.
Peramivir (Rapivab)IV≥2 yearsSingle-dose IV. For hospitalised patients unable to take orals.
Baloxavir marboxil (Xofluza)Oral≥5 yearsSingle-dose. PA endonuclease inhibitor. Active against oseltamivir-resistant strains. Avoid in pregnancy.

Influenza Antiviral — When to Treat

ScenarioRecommendation
Hospitalised with severe/complicated influenzaTREAT — regardless of duration of illness
High-risk outpatient (elderly, pregnant, immunocompromised, chronic disease)TREAT — start within 48h of symptom onset
Healthy adult/child with uncomplicated influenzaTreatment optional; shared decision-making
Post-exposure prophylaxis (high-risk contact)CONSIDER — oseltamivir or zanamivir
Healthy person, contact >48h agoDo NOT prescribe prophylaxis

Infectious Mononucleosis — Key Points

  • Cause: Epstein-Barr virus (EBV/HHV-4); CMV causes similar syndrome but without sore throat
  • Transmission: saliva ('kissing disease'); incubation 1–7 weeks
  • Classic triad: exudative tonsillitis + posterior cervical lymphadenopathy + fatigue (adolescent/young adult)
  • Investigations: atypical lymphocytosis on FBC (>10% atypical); Monospot (heterophile antibody) — negative in 10%, especially early
  • Complications: splenic rupture (most common serious), myocarditis, haemolytic anaemia, thrombocytopenia, encephalitis
  • ⚠️ Amoxicillin causes florid maculopapular rash in nearly all IM patients — avoid empirical penicillins until IM excluded

Viral Exanthems — Differentiating Features

ConditionVirusKey Clinical FeatureImportant Management Point
Measles (Rubeola)Measles virusSevere prodrome (fever, cough, coryza, conjunctivitis). Koplik spots before rash. Morbilliform rash while acutely ill.Highly contagious. Preventable by MMR. Complications: otitis media, pneumonia, encephalitis.
Rubella (German Measles)Rubella virusMild illness. Suboccipital & postauricular lymphadenopathy precede transient rash (~48h).Congenital Rubella Syndrome if contracted in pregnancy. Preventable by MMR.
Roseola Infantum (Exanthem Subitum)HHV-63 days of high fever in infants/toddlers, then rash appears as fever abruptly subsides.Do NOT misattribute rash to antibiotic side effect. Self-limiting.

Viral Enanthems — Key Features

ConditionVirusDistribution of LesionsKey Points
HFMDCoxsackievirus A; Enterovirus 71 (EV71)Vesicles on hands, feet, buttocks; painful oral ulcers (posterior mouth)EV71 can cause fatal neurological/cardiorespiratory complications. Monitor closely. Notifiable.
HerpanginaCoxsackievirus APapulovesicular ulcers on tonsillar pillars, soft palate, uvula (posterior)Supportive only. Ensure hydration. Antibiotics NOT indicated.
Acute Herpetic GingivostomatitisHSV-1Vesicles/erosions on gums, buccal mucosa, tongue, lips (anterior mouth)May be severe. Early oral acyclovir indicated. Maintain hydration.

Viral Exanthem Images

Measles: Morbilliform rash appearing while patient is still acutely ill (fever, cough, conjunctivitis). Source: CDC/Wikimedia Commons.

Measles: Morbilliform rash appearing while patient is still acutely ill (fever, cough, conjunctivitis). Source: CDC/Wikimedia Commons.

Other Viral Syndromes with Unique Signs

ConditionVirusUnique FeatureKey Concern
Erythema Infectiosum (Fifth Disease)Parvovirus B19'Slapped cheek' → lacy reticular rash on trunk/limbsAplastic crisis in chronic haemolytic anaemia (e.g., sickle cell). Hydrops fetalis if infected during pregnancy.
Papular Acrodermatitis (Gianotti-Crosti)EBV, CMV, Coxsackievirus, Hep BSymmetric, non-pruritic papules on face, buttocks, limbs. May persist weeks.Benign, self-limiting. Reassure parents.
STAR SyndromeRubella, Parvovirus B19Sore Throat + Arthritis + Rash — reactive polyarthritis after acute viral illnessSelf-limiting. Differentiate from primary inflammatory arthritis.

Vector-Borne URTI Mimics in Singapore

🚨 Emergency
ConditionKey Differentiating FeaturesCritical Management Point
DengueRetro-orbital pain, myalgia, maculopapular rash, thrombocytopenia. Biphasic fever. Warning signs: persistent vomiting, severe abdominal pain, mucosal bleeding.Statutory notification. Supportive care + careful fluids. Avoid NSAIDs. Avoid contact sports.
ChikungunyaFever + SEVERE polyarthralgia/polyarthritis — often debilitating. Joint pain disproportionate to other features.Supportive. NSAIDs for arthralgia (after dengue excluded). Arthralgia may persist for months.
ZikaUsually mild: rash, conjunctivitis, joint pain. BUT: Guillain-Barré in adults; microcephaly in neonates if infected during pregnancy.High index of suspicion in pregnant women. Refer for monitoring. Test sexual contacts if needed.

Dengue — Three Clinical Phases

PhaseTimingClinical Features
FebrileDays 1–3Abrupt high fever, headache, retro-orbital pain, myalgia, backache, maculopapular rash
CriticalDays 4–6 (last 24–48h of fever)Defervescence — critical phase. Worsening thrombocytopenia. Warning signs: abdominal pain, persistent vomiting, mucosal bleeding, fluid accumulation, lethargy. Risk of plasma leakage, shock, organ failure.
RecoveryDays 7–10Platelet count rises. Bradycardia common. Characteristic rash: generalised erythema with 'white islands in a sea of red'.

COVID-19 — Key Clinical Features

  • Caused by SARS-CoV-2; primarily airborne transmission
  • Symptoms: highly variable — sore throat, cough, headache, fatigue (Omicron era); anosmia/ageusia less prominent with current sub-lineages
  • Diagnosis: ART (antigen rapid test) widely accessible; PCR for confirmation in hospital/high-stakes settings
  • Complications: acute (thrombosis, AKI, cardiovascular events); long-term (Long COVID — fatigue, cognitive dysfunction, dyspnoea)
  • Vaccination reduces severity, hospitalisation, and Long COVID risk
  • Severity classified: mild → moderate → severe → critical (NCID guidelines, Version 12, 2023)

COVID-19 — Outpatient Management

  • Mild/moderate disease (no supplemental oxygen needed): supportive care as outpatient
  • Oral antivirals (OAV) indicated for HIGH-RISK patients if started within 5 days of symptom onset
  • High-risk factors: age >60–70, not up-to-date with vaccination, active cancer, CKD, CLD, CHF, obesity, diabetes, immunosuppression
  • Nirmatrelvir/ritonavir (Paxlovid): preferred. Adjust for GFR 30–60; contraindicated if GFR <30 or severe hepatic impairment. Significant drug interactions (CYP3A4 inhibition).
  • Molnupiravir / Ensitrelvir: alternatives. Molnupiravir not in pregnancy or those unable to use contraception.
  • Review drug interactions carefully before prescribing Paxlovid — especially statins, anticoagulants, immunosuppressants

COVID-19 — Vaccination (2025–2026)

  • Updated formulations target circulating Omicron sub-lineages — incorporated into National Vaccination Programme
  • Available in Singapore: Pfizer-BioNTech/Comirnaty, Moderna/Spikevax, Novavax/Nuvaxovid, Sinovac-CoronaVac
  • Additional dose recommended at ~1 year interval (minimum 5 months from last dose) for:
  • • Adults aged ≥60 years
  • • Medically vulnerable individuals aged ≥6 months
  • • Residents of aged care facilities
  • Immunocompromised individuals: may need additional doses at shorter intervals — check current NCID guidance
  • [MOH Singapore Circular 67/2025]

Sore Throat — McIsaac Score for GABHS

CriterionScore
Temperature >38°C+1
Absence of cough+1
Tender anterior cervical lymph nodes+1
Tonsillar swelling or exudates+1
Age 3–14 years+1
Age ≥45 years−1
Score ≤1: antibiotics NOT recommended
Score 2–3: consider RADT; treat if positive
Score ≥4: empirical antibiotics strongly considered

Differentiating Viral vs Bacterial Pharyngitis

💎 Clinical Pearl
FeatureViralBacterial (GABHS)
CoughPresent (often prominent)Absent
Coryza / rhinorrhoeaOften presentUsually absent
ConjunctivitisMay be present (adenovirus)Absent
Diarrhoea / hoarsenessMay occurAbsent
Oral ulcers (enanthem)May be present (HSV, enterovirus)Absent
Tonsillar exudatesCan occur (EBV)Common
OnsetGradualAbrupt
Classic rashVariable (viral exanthem)'Sandpaper' rash → scarlet fever

Antibiotics for GABHS Pharyngitis

DrugAdult Dose (10-day PO course)Notes
Penicillin V500 mg BD or 250 mg QDSFirst-line. Narrow spectrum. No documented GABHS resistance.
Amoxicillin500 mg BD or 50 mg/kg OD (max 1g)Broader spectrum but better palatability (paediatrics). Avoid if EBV not excluded.
Cephalexin (PCN allergy — non-anaphylactic)500 mg BD1st generation cephalosporin. Cross-reactivity with penicillin is low (<2%).
Clindamycin (PCN allergy — anaphylactic)300 mg TDSEffective alternative.
Azithromycin (PCN allergy — anaphylactic)500 mg OD × 5 daysUse only if macrolide susceptibility confirmed — resistance rates increasing.
Clarithromycin (PCN allergy — anaphylactic)250 mg BD × 10 daysAlternative macrolide.

Epiglottitis — Do Not Miss

🚨 Emergency — Act Now
🚨
  • Medical emergency — acute airway obstruction can be precipitated by throat examination
  • Suspect: severe sore throat + stridor + drooling + respiratory distress + 'tripod position'
  • Classic cause was Haemophilus influenzae type b (Hib) — now rarer due to vaccination
  • Current common causes: Group A Streptococcus and other organisms
  • ⛔ DO NOT examine throat with tongue depressor — may precipitate complete obstruction
  • Immediate action: sit patient upright, call emergency services, arrange urgent hospital transfer for airway assessment ± intubation, IV antibiotics, corticosteroids

Acute Sinusitis — When to Suspect Bacterial Cause

  • Most acute rhinosinusitis is VIRAL — antibiotics not needed in the first week
  • Suspect bacterial sinusitis if: symptoms persist >10 days, severe from onset, or 'double sickening' (initial improvement then worsening)
  • Williams & Simel predictors: maxillary toothache, purulent discharge, poor decongestant response, abnormal transillumination, coloured discharge
  • ≥4 predictors: LR 6.4 (high probability); ≤1 predictor: LR 0.5 (low probability)
  • First-line antibiotic (if indicated): Amoxicillin-clavulanate 875/125 mg BD × 5–7 days
  • Penicillin allergy: Doxycycline 100 mg BD or respiratory fluoroquinolone (Levofloxacin/Moxifloxacin)

Otitis Media — AOM vs OME

FeatureAcute Otitis Media (AOM)Otitis Media with Effusion (OME)
DefinitionMiddle ear fluid + acute signs of inflammationMiddle ear fluid WITHOUT acute inflammation
SymptomsOtalgia, fever, irritabilityHearing loss, 'muffled' hearing, often asymptomatic
Tympanic membraneBulging, erythematous, loss of landmarksDull, retracted, air-fluid level visible
AntibioticsIndicated in <2 years; bilateral; severe symptoms. Watchful waiting 48–72h for mild unilateral AOM ≥2 years.NOT routinely recommended
First-line antibioticAmoxicillin 80–90 mg/kg/day (high dose)
ENT referralFor persistent/recurrent AOM, complicationsBilateral OME >3 months with hearing loss or speech delay

Key Summary — Acute URTIs in Family Practice

Key Point
Differentiate viral from bacterial URTI using clinical features and scoring tools (McIsaac) — antibiotics are inappropriate for most URTIs
Key Point
Antibiotic stewardship: address patient ICE, use delayed prescriptions for borderline cases, safety-net all patients
Key Point
Know the URTI mimics: vector-borne diseases (Dengue, Chikungunya, Zika) are common in Singapore — maintain a high index of suspicion
Key Point
COVID-19 and Influenza: use antiviral therapy for high-risk patients early; ensure vaccination up-to-date for recommended groups
Key Point
Red flags requiring urgent action: signs of epiglottitis (DO NOT examine throat — refer immediately), complicated influenza, dengue warning signs
Key Point
Paediatric prescribing: OTC cough/cold medicines not recommended in <2 years; codeine restricted to ≥12 years only

References

  • 1. Gonzales R, et al. Ann Intern Med. 2001;134:490–94.
  • 2. Cockburn J, Pit S. BMJ. 1997;315:520–3.
  • 3. DeGeorge KC, et al. Am Fam Physician. 2019;100(5):281–289.
  • 4. HSA Singapore. Cough and cold medicines for children. www.hsa.gov.sg [Updated 2023].
  • 5. SIDS Handbook on Adult Vaccination in Singapore 2023.
  • 6. Erlikh I, et al. Am Fam Physician. 2010;82(9):1087–95.
  • 9. Cheng AM, et al. Am Fam Physician. 2023;107(4):370–381.
  • 11. McIsaac WJ, et al. CMAJ 1998;158(1):75–83.
  • 15. Shulman ST et al. IDSA Guidelines. Clin Infect Dis. 2012;55(10):e86–102.
  • 16. Williams JW Jr, Simel DL. JAMA. 1993;270(10):1242–1246.
  • 18. CDC. Influenza Antiviral Medications: Summary for Clinicians. January 2026.
  • 19. HSA Singapore. Restrictions on use of codeine in children. Safety Alert 2016.
  • 20. MOH Singapore. COVID-19 Vaccination Recommendations 2025/2026. Circular 67/2025, October 2025.
M112

Acute Lower Respiratory Infections

Learning Objectives

  • Recognise and immediately manage life-threatening causes of dyspnoea and stridor
  • Differentiate common acute LRTIs: bronchitis, bronchiolitis, croup, CAP, aspiration pneumonia
  • Apply CRB-65 to stratify CAP severity and guide admission decisions
  • Practise antibiotic stewardship — know when NOT to prescribe
  • Counsel patients and families on vaccination and preventive strategies
  • Identify red flags requiring emergency referral from primary care

Approach to Dyspnoea — Spot the Emergency First

🚨 Emergency — Act Now
🚨
  • Dyspnoea in primary care: spectrum from benign to imminently life-threatening
  • 🚨 Red flags: tachycardia, tachypnoea, hypotension, SpO2 <94%, altered mental status, stridor, anaphylaxis
  • Step 1: ABC assessment — do not delay resuscitation for investigation
  • Step 2: Targeted history + head-to-toe examination for diagnostic clues
  • Step 3: Decide — manage in clinic vs. refer to ED via ambulance

Differential Diagnosis of Dyspnoea

Stridor — Partial Upper Airway Obstruction

🚨 Emergency — Act Now
🚨
  • High-pitched inspiratory sound = turbulent flow through narrowed upper airway
  • 🚨 Acute causes requiring urgent action: foreign body, epiglottitis, anaphylaxis, croup, bacterial tracheitis
  • Chronic causes: laryngomalacia, subglottic stenosis, vocal cord paralysis, vascular rings
  • History: age, acuity, fever, drooling, hives, preceding choking episode
  • Examine: assess tongue, pharynx, rate/depth of breathing — avoid agitating child
  • Management: airway first — adrenaline/steroids for croup, antibiotics for epiglottitis/tracheitis, surgery for abscess

Croup (Laryngotracheobronchitis) — Assessment & Management

  • Viral (mostly parainfluenza), peak age 6 months–3 years
  • Classic triad: barking cough, inspiratory stridor, hoarse voice
  • Preceded by URTI symptoms (coryza, low-grade fever)
  • Key: keep child calm — crying worsens obstruction
  • Mild–moderate: oral prednisolone 1 mg/kg OR dexamethasone 0.15–0.6 mg/kg
  • 🚨 Severe: nebulised adrenaline 4 mL 1:1000 + immediate ambulance transfer
Table summarising the assessment of degree of airway obstruction in croup (mild, moderate, severe, life-threatening) with corresponding clinical features and initial treatment guidelines including nebulised adrenaline, oral prednisolone, and dexamethasone.

Table summarising the assessment of degree of airway obstruction in croup (mild, moderate, severe, life-threatening) with corresponding clinical features and initial treatment guidelines including nebulised adrenaline, oral prednisolone, and dexamethasone.

Acute Bronchitis — When Not to Use Antibiotics

  • Definition: acute cough ≤3 weeks, no CXR or clinical evidence of pneumonia
  • Cause: predominantly viral (RSV, rhinovirus, influenza, coronavirus)
  • Fever is unusual — if present, suspect influenza or pneumonia instead
  • Distinguish from pneumonia: vital signs, focal lung signs, CXR
  • Management: symptomatic — dextromethorphan, guaifenesin, honey (>1 yr)
  • 💎 Antibiotics NOT recommended for otherwise healthy adults — counsel on expected 2–3 week cough

Acute Cough Algorithm

  • Systematic approach to adult with cough <3 weeks
  • First: rule out life-threatening diagnoses (PE, tension pneumothorax, anaphylaxis)
  • Then: assess for LRTI vs URTI vs exacerbation of chronic disease
  • Red flags: haemoptysis, dyspnoea, constitutional symptoms, risk factors
  • CXR indicated if: RR >24, HR >100, Temp >38°C, signs of consolidation
Clinical algorithm for the evaluation and management of acute cough, including differentiation between life-threatening and non-life-threatening diagnoses, infectious causes (LRTI/URTI), exacerbations of pre-existing conditions, and red flag symptoms.

Clinical algorithm for the evaluation and management of acute cough, including differentiation between life-threatening and non-life-threatening diagnoses, infectious causes (LRTI/URTI), exacerbations of pre-existing conditions, and red flag symptoms.

Acute Bronchiolitis — RSV in Infants

  • Most common LRTI in infants <2 years; RSV is the leading cause
  • Biphasic: 2–4 days URTI → lower respiratory symptoms (wheeze, crepitations, retractions)
  • 🚨 Hospitalise if: SpO2 <90%, severe retractions, poor feeding, young age, high HR
  • Treatment: supportive only — maintain SpO2 ≥90%, hydration, gentle suctioning
  • NOT recommended: bronchodilators, epinephrine, steroids, antibiotics, physiotherapy
  • 💎 New: Nirsevimab (Beyfortus®) approved Singapore 2025 — single-dose RSV prophylaxis for all infants

Community-Acquired Pneumonia — Diagnosis

  • Infection of lung parenchyma outside hospital/long-term care facility
  • Singapore pathogens: S. pneumoniae (most common), H. influenzae, Moraxella, atypicals
  • Classic symptoms: fever >38°C, productive cough, dyspnoea
  • Most valuable examination finding: focal crepitations
  • 💎 CXR is required to reliably diagnose pneumonia — do not rely on clinical features alone
  • Outpatient labs: limited value; consider procalcitonin, influenza testing if circulating

💎 CRB-65 — Risk Stratification in Primary Care

  • CRB-65: Confusion, Respiratory rate ≥30, Blood pressure <90 systolic, Age ≥65
  • Score 0: low risk — suitable for outpatient management
  • Score 1–2: intermediate risk — consider hospital referral
  • Score ≥3: high risk — urgent hospital admission
  • Advantage over CURB-65: no blood test required — ideal for primary care
  • Always supplement score with clinical judgement (social support, functional status)
CRB-65 scoring table for predicting mortality in community-acquired pneumonia, stratifying patients into low, moderate, and high risk groups with corresponding mortality rates and clinical disposition recommendations.

CRB-65 scoring table for predicting mortality in community-acquired pneumonia, stratifying patients into low, moderate, and high risk groups with corresponding mortality rates and clinical disposition recommendations.

CAP — Empiric Antibiotic Therapy

  • No comorbidities: Amoxicillin 1g TDS or Doxycycline 100mg BD
  • With comorbidities (DM, chronic lung/heart/liver disease): Amoxicillin-clavulanate + macrolide or doxycycline; OR respiratory fluoroquinolone
  • 💎 Macrolide monotherapy no longer recommended — high pneumococcal resistance
  • Duration: minimum 5 days, guided by clinical stability
  • Atypical coverage may be required — consider if no response to beta-lactam
Table of standard outpatient antibiotic regimens for community-acquired pneumonia, stratified by presence or absence of comorbidities and risk factors for MRSA or Pseudomonas aeruginosa, with detailed dosing footnotes.

Table of standard outpatient antibiotic regimens for community-acquired pneumonia, stratified by presence or absence of comorbidities and risk factors for MRSA or Pseudomonas aeruginosa, with detailed dosing footnotes.

Atypical Pneumonias — Think Zoonotic

  • Organisms: Legionella, Mycoplasma, Chlamydia pneumoniae (non-zoonotic); Psittacosis, Q fever, Tularemia (zoonotic)
  • Not visible on Gram stain; resistant to beta-lactam antibiotics
  • 💎 Travel and animal contact history is essential — ask specifically
  • Legionella clues: diarrhoea, hyponatraemia, confusion, aerosolized water exposure (cooling towers, hotels)
  • Mycoplasma clues: bullous myringitis, cold agglutinins, erythema multiforme
  • Treatment: doxycycline, macrolide, or fluoroquinolone (depending on organism)

Aspiration Pneumonia — Who Is at Risk?

  • Inhalation of colonized oropharyngeal material → polymicrobial pneumonia
  • Distinct from aspiration pneumonitis (sterile gastric acid → chemical injury)
  • High-risk patients: stroke, Parkinson's, dementia, elderly, poor dentition, GERD, NG tube
  • Key pathogens: S. pneumoniae, S. aureus, H. influenzae, Enterobacteriaceae (not just anaerobes)
  • Radiological clue: infiltrates in gravity-dependent segments (basal lobes if upright; posterior upper lobes if supine)
  • 💎 Anaerobic coverage only for lung abscess or severe periodontal disease — not routine

Aspiration Pneumonia — Imaging & Management

  • CXR/CT: look for dependent segment infiltrates — basal lobes (upright) or posterior upper lobes (supine)
  • Cavitary lesions suggest anaerobic infection / lung abscess
  • Treatment: amoxicillin-clavulanate (oral) or ampicillin-sulbactam (IV); minimum 5 days
  • 🚨 Do NOT give glucocorticoids — antibiotics only
  • Prevent recurrence: speech therapy, thickened feeds, oral hygiene, semi-recumbent positioning
  • Advanced dementia: involve family in advance care planning — tube feeding may not improve QoL
Composite figure showing characteristic imaging findings in aspiration pneumonia: (A) PA chest radiograph with cavitary infiltrate in the left lower lobe, (B) bilateral lung infiltrates from recurrent aspiration, (C) CT scan showing right upper lobe posterior cavitary infiltrate, and (D) CT scan with new bilateral posterior gravity-dependent infiltrates post-aspiration.

Composite figure showing characteristic imaging findings in aspiration pneumonia: (A) PA chest radiograph with cavitary infiltrate in the left lower lobe, (B) bilateral lung infiltrates from recurrent aspiration, (C) CT scan showing right upper lobe posterior cavitary infiltrate, and (D) CT scan with new bilateral posterior gravity-dependent infiltrates post-aspiration.

💎 Key Summary

Key Point
Safety first: vital signs + ABC assessment before any investigation — refer emergencies immediately
Key Point
CRB-65 guides CAP disposition: score 0 = home, ≥1 = consider hospital
Key Point
Antibiotic stewardship: acute bronchitis and bronchiolitis are viral — antibiotics not indicated
Key Point
Vaccines prevent disease: influenza, pneumococcal, COVID-19 boosters for high-risk groups
Key Point
Nirsevimab (2025): single-dose RSV prophylaxis now approved in Singapore for all infants
Key Point
Aspiration pneumonia: think dysphagia risk factors, dependent infiltrates, multidisciplinary prevention

References

M113

Chronic Cough, Tuberculosis & Lung Cancer

Learning Objectives

  • Classify cough by duration and apply a systematic approach to chronic cough (>8 weeks)
  • Identify the 'big three' causes of chronic cough with a normal CXR in non-smokers
  • Recognise red flags for chronic cough in children and adults
  • Assess hemoptysis severity and determine when to refer urgently
  • Differentiate latent from active TB and apply Singapore's notification and treatment protocols
  • Identify high-risk groups for lung cancer and apply current screening criteria

Approach to Chronic Cough

  • Chronic cough = cough lasting >8 weeks in adults (>4 weeks in children)
  • Prevalence ~9.6% worldwide; significant quality-of-life impact
  • Take a structured history: smoking, ACE inhibitors, recent URTI, wheezing, heartburn, occupational/environmental exposure
  • Examine upper airways and ears — not just the chest
  • Chest X-ray is the first-line investigation
  • BTS 2023 algorithm guides systematic evaluation (see figure)
Clinical algorithm for the assessment and management of chronic cough (>8 weeks), including initial assessment, identification of red flags warranting urgent or 2-week-wait referral, evaluation for underlying disease and aggravants, and identification of treatable traits.

Clinical algorithm for the assessment and management of chronic cough (>8 weeks), including initial assessment, identification of red flags warranting urgent or 2-week-wait referral, evaluation for underlying disease and aggravants, and identification of treatable traits.

The 'Big Three' — Chronic Cough with Normal CXR

💎 Clinical Pearl
  • In non-smokers with a normal chest X-ray, the top three causes are:
  • ① UACS (Upper Airway Cough Syndrome) — postnasal drip, rhinitis, sinusitis → trial antihistamine + decongestant
  • ② Asthma / Cough-Variant Asthma — nocturnal, worse with irritants → spirometry, trial ICS 2–4 weeks
  • ③ GERD — may be 'silent' in up to 75% (no typical heartburn) → empirical PPI trial
  • Eosinophilic bronchitis: non-productive cough without asthma features → also responds to ICS
  • Empirical sequential trials are acceptable when initial CXR is normal and no red flags

🚨 Chronic Cough in Children — Red Flags

  • Chronic cough in children = >4 weeks duration; affects 5–10% of children in Singapore
  • Key red flags: haemoptysis, digital clubbing, growth failure, hypoxia, choking episode
  • Wet/productive cough suggests: protracted bacterial bronchitis (PBB), bronchiectasis, TB, aspiration
  • PBB: wet cough ≥4 weeks responding to ≥2 weeks oral antibiotics (H. influenzae, S. pneumoniae, M. catarrhalis)
  • Pertussis: catarrhal → paroxysmal (inspiratory whoop, post-tussive vomiting) → convalescent; treat with macrolides
  • Counsel on Tdap booster for adolescents, adults, and healthcare workers (immunity wanes post-vaccination)
Table summarising key red flags in the history and physical examination of chronic cough in children, with corresponding possible aetiologies (e.g., haemoptysis, digital clubbing, choking, recurrent infections, auscultatory findings).

Table summarising key red flags in the history and physical examination of chronic cough in children, with corresponding possible aetiologies (e.g., haemoptysis, digital clubbing, choking, recurrent infections, auscultatory findings).

Pneumothorax — Diagnosis and Management

  • PSP: young, tall, slender, smoker — no underlying lung disease
  • SSP: underlying lung disease (COPD, asthma, TB) — worse prognosis
  • Tension pneumothorax: respiratory distress, tachycardia, hypotension, tracheal deviation — EMERGENCY
  • Asymptomatic/minimal: conservative management regardless of size
  • Symptomatic: refer A&E for needle aspiration or chest drain
  • Tension: immediate needle decompression — 2nd ICS MCL (traditional) OR 4th/5th ICS anterior axillary line (ATLS 10th ed. — preferred if thick chest wall)

Hemoptysis — Assessment and Triage

🚨 Emergency — Act Now
🚨
  • First: distinguish true hemoptysis from pseudohemoptysis (GI or URT source)
  • Refer to ED if: massive hemoptysis, haemodynamic instability, SpO₂ <88%, RR >30, Hb <8 g/dL
  • Non-massive with normal CXR: stratify by cancer risk and LRTI history
  • Common causes: TB, bronchiectasis, lung cancer, pulmonary embolism
  • Specialist referral if: abnormal CXR (non-pneumonia), respiratory/cardiac comorbidities

Hemoptysis — Evaluation Algorithm (Normal CXR)

Flowchart for the evaluation of haemoptysis when chest radiography findings are normal, stratified by cancer risk and history suggestive of lower respiratory tract infection, guiding observation, antibiotics, or CT imaging.

Flowchart for the evaluation of haemoptysis when chest radiography findings are normal, stratified by cancer risk and history suggestive of lower respiratory tract infection, guiding observation, antibiotics, or CT imaging.

Tuberculosis in Singapore

  • Incidence: 28.9 per 100,000 in 2023 — TB remains endemic in Singapore
  • High-risk groups: elderly, immunocompromised, migrants, diabetes mellitus, HIV
  • Airborne transmission: maintain high index of suspicion for cough >3 weeks + constitutional symptoms
  • Pulmonary TB: most common — cough, haemoptysis, fever, night sweats, weight loss
  • Extrapulmonary TB: lymph nodes, pleura, bones, meninges — more common in immunosuppressed
  • Screen all TB patients for HIV and diabetes mellitus

TB Diagnosis and Treatment

💎 Clinical Pearl
  • Active TB: sputum AFB smear + culture; CXR shows upper lobe infiltrates, cavities
  • LTBI: TST (≥10 mm general; ≥5 mm immunocompromised) or IGRA
  • Active TB treatment (drug-susceptible): RIPE × 2 months → RI × 4 months
  • LTBI treatment (Singapore 2024 guidelines): Rifampicin daily × 4 months (preferred) OR INH × 6–9 months
  • Extend to 9 months if: cavitation, positive 2-month culture, slow response, significant comorbidities
  • DOT/VOT is a cornerstone of Singapore's TB control programme

TB — Public Health Obligations

🚨 Emergency — Act Now
🚨
  • TB is a NOTIFIABLE disease in Singapore
  • Notify TBCU within 72 hours: Form MD 532 or CD-LENS portal
  • Patients with infectious TB must NOT travel by public air transport until non-infectious
  • MDR-TB: resistant to ≥ isoniazid + rifampicin
  • XDR-TB (WHO 2021): MDR/RR-TB + resistance to any fluoroquinolone + bedaquiline or linezolid
  • Refer all drug-resistant TB to TBCU — do NOT manage in primary care

Lung Cancer — Epidemiology and Risk Groups

  • 3rd most common cancer in Singapore (2017–2021); leading cause of cancer death in men
  • NSCLC ~80% (adenocarcinoma, squamous cell, large cell); SCLC ~20%
  • Key risk groups in Asia — beyond smokers:
  • • Never-smoker, Female, East Asian (NESFEA) phenotype — often adenocarcinoma with EGFR mutations
  • • Family history of lung cancer
  • • Exposure to carcinogens: radon, asbestos, air pollution
  • Family physicians play a key role in early suspicion and smoking cessation

Lung Cancer — Local & Intrathoracic Manifestations

Table listing signs and symptoms of lung cancer due to local effects of the primary tumour (with likelihood ratios) and signs/symptoms of intrathoracic spread, including Pancoast tumour, Horner syndrome, and superior vena cava syndrome.

Table listing signs and symptoms of lung cancer due to local effects of the primary tumour (with likelihood ratios) and signs/symptoms of intrathoracic spread, including Pancoast tumour, Horner syndrome, and superior vena cava syndrome.

Lung Cancer — Distant Metastases and Paraneoplastic Syndromes

  • Metastases can involve bone (pain, fractures), brain (headache, seizures), liver (jaundice, anorexia), adrenals, skin
  • Paraneoplastic syndromes occur without direct tumour invasion:
  • • Hypercalcaemia — ectopic PTHrP (NSCLC)
  • • SIADH → hyponatraemia (SCLC)
  • • Cushing syndrome — ectopic ACTH (SCLC)
  • • Lambert-Eaton myasthenic syndrome — proximal weakness (SCLC)
  • Digital clubbing more common with NSCLC
Table summarising signs and symptoms of lung cancer due to distant metastases by site (liver, bone, brain, lymphatics, adrenals, skin) with associated frequencies.

Table summarising signs and symptoms of lung cancer due to distant metastases by site (liver, bone, brain, lymphatics, adrenals, skin) with associated frequencies.

Lung Cancer — Paraneoplastic Syndromes (Detail)

Table of paraneoplastic syndromes associated with lung cancer, including frequency and clinical comments (e.g., hypercalcaemia, SIADH, Cushing syndrome, Lambert-Eaton myasthenic weakness, digital clubbing).

Table of paraneoplastic syndromes associated with lung cancer, including frequency and clinical comments (e.g., hypercalcaemia, SIADH, Cushing syndrome, Lambert-Eaton myasthenic weakness, digital clubbing).

Lung Cancer Screening and Solitary Pulmonary Nodule

💎 Clinical Pearl
  • No national screening programme in Singapore — MOH recommends LDCT on individual basis for high-risk patients
  • USPSTF 2021 criteria (reference benchmark): Annual LDCT for adults aged 50–80 with ≥20 pack-year history, currently smoking or quit within 15 years
  • Solitary pulmonary nodule (SPN): isolated opacity <3 cm — most are benign (infectious granuloma 80%)
  • Features suggesting malignancy: size ≥8 mm, spiculated border, upper lobe, ground-glass opacity, eccentric calcification
  • Features suggesting benign: smooth border, central/popcorn calcification, doubling time <1 month or >1 year
  • Refer to respiratory physician for all SPNs — risk stratification guides follow-up imaging frequency

Key Summary

Key Point
Chronic Cough: >8 weeks adults, >4 weeks children. 'Big three' in non-smokers with normal CXR: UACS, Asthma, GERD. Use BTS 2023 algorithm.
Key Point
Haemoptysis: Rule out pseudohaemoptysis. Refer to ED if massive or haemodynamically unstable. Stratify by cancer risk if CXR normal.
Key Point
Pneumothorax: Tension = emergency. Needle decompression at 2nd ICS MCL or 4th/5th ICS AAL (ATLS 10th ed).
Key Point
TB: Incidence 28.9/100,000 in Singapore 2023. Notify TBCU within 72 hours. LTBI: rifampicin 4 months (preferred). Active TB: RIPE × 2 months then RI × 4 months. XDR-TB = WHO 2021 definition.
Key Point
Lung Cancer: NESFEA phenotype is high-risk. LDCT screening: 50–80 years, ≥20 pack-years (USPSTF 2021). SPN ≥8 mm → refer respiratory physician.

References

M114

Chronic Lung Diseases

Learning Objectives

  • Understand the indications and interpretation of spirometry in primary care
  • Recognise and manage bronchiectasis and post-TB lung disease (PTLD)
  • Diagnose and manage asthma according to GINA 2024 guidelines
  • Diagnose and manage COPD using the GOLD 2024 ABE framework
  • Identify when to suspect interstitial lung disease (ILD) and initiate referral
  • Apply Singapore MOH ACE 2024 recommendations in clinical practice

Spirometry: Indications in Primary Care

  • Confirming diagnosis of asthma, COPD, or other lung disease
  • Monitoring disease progression and treatment response
  • Pre-operative assessment and occupational health screening
  • 💎 Spirometry is the gold standard — PEF monitoring is an alternative if unavailable but is less reliable
  • Validity requires: ≥3 technically acceptable manoeuvres, two largest FVC and FEV₁ within 150 mL of each other
  • Always perform post-bronchodilator testing when confirming COPD diagnosis
Example spirometry printout: FVC, FEV1, FEV1/FVC with flow-volume loops showing obstructive pattern

Example spirometry printout: FVC, FEV1, FEV1/FVC with flow-volume loops showing obstructive pattern

Lung Volumes & Capacities

  • Tidal Volume (TV): Normal breathing (~500 mL at rest)
  • Inspiratory Reserve Volume (IRV): Extra air inhaled beyond tidal breath
  • Expiratory Reserve Volume (ERV): Extra air exhaled beyond tidal breath
  • Residual Volume (RV): Air remaining after maximal exhalation — NOT measured by spirometry
  • Functional Residual Capacity (FRC) = ERV + RV
  • Total Lung Capacity (TLC) = VC + RV — requires body plethysmography
Diagram of lung volumes and capacities

Diagram of lung volumes and capacities

Flow-Volume Loops: Normal vs Obstructive vs Restrictive

  • Normal: smooth, triangular expiratory limb; symmetric inspiratory limb
  • Obstructive: concave (scooped out) expiratory limb — classic in asthma and COPD
  • Restrictive: preserved shape but reduced volumes (smaller loop)
  • 💎 FEV₁/FVC < 0.70 (post-BD) = obstruction; FEV₁/FVC ≥ 0.70 with reduced FVC = restriction
  • Variable intrathoracic obstruction (e.g., tracheomalacia): expiratory limb flattened
  • Variable extrathoracic obstruction (e.g., vocal cord palsy): inspiratory limb flattened
Normal, obstructive, and restrictive flow-volume loop patterns

Normal, obstructive, and restrictive flow-volume loop patterns

Spirometry Interpretation Algorithm

  • Step 1: Assess FEV₁/FVC ratio — is it < 0.70 (LLN)?
  • Step 2: If obstructive — perform bronchodilator reversibility test
  • Step 3: If FEV₁/FVC ≥ 0.70 — check if FVC is reduced → restrictive pattern
  • Step 4: Bronchodilator reversibility (≥12% and ≥200 mL FEV₁ increase) suggests asthma
  • Step 5: Mixed pattern = obstruction + reduced FVC (e.g., severe COPD with air trapping)
  • 💎 Always interpret in clinical context — spirometry alone does not make a diagnosis
Clinical algorithm for spirometry interpretation

Clinical algorithm for spirometry interpretation

Bronchodilator Reversibility Testing

  • Administer 200-400 mcg salbutamol via MDI + spacer
  • Withhold SABA ≥4h, LABA 24-48h before test for diagnostic accuracy
  • Repeat spirometry 10-15 minutes after bronchodilator
  • Positive (adults): FEV₁ or FVC increase ≥12% AND ≥200 mL
  • Greater confidence: ≥15% increase and ≥400 mL
  • 💎 Positive reversibility suggests asthma but does NOT exclude COPD (or confirm ACO)

Bronchiectasis: Overview

  • Chronic irreversible airway dilatation from recurrent infection/inflammation
  • Presents with: persistent productive cough, purulent sputum, recurrent exacerbations
  • Common causes: post-infectious (TB, pertussis), immune deficiency, primary ciliary dyskinesia, CF
  • 💎 Post-TB bronchiectasis is a major cause in Singapore and SE Asia
  • Diagnosis: HRCT chest (shows dilated airways, 'signet ring' sign, mucus plugging)
  • Key complication: haemoptysis — can be life-threatening
Treatable traits in bronchiectasis pathophysiology

Treatable traits in bronchiectasis pathophysiology

Bronchiectasis & PTLD: Management

  • Goals: reduce symptom burden, improve QoL, decrease exacerbations, prevent progression
  • Airway clearance: physiotherapy, huffing/coughing techniques, oscillating PEP devices
  • Long-term macrolides (azithromycin): reduces exacerbation frequency in RCTs
  • Inhaled antibiotics (e.g., tobramycin, colistin): for chronic Pseudomonas colonization
  • Vaccinations: pneumococcal + influenza (essential for all patients)
  • 💎 Pulmonary rehabilitation and smoking cessation are key for PTLD management

Asthma: Definition & Phenotypes (GINA 2024)

  • Heterogeneous disease with chronic airway inflammation
  • Defined by: variable respiratory symptoms (wheeze, SOB, chest tightness, cough) + variable expiratory airflow limitation
  • Allergic asthma: most common; childhood onset, atopy, eosinophilic, responds well to ICS
  • Non-allergic asthma: sputum neutrophilic/eosinophilic/paucigranulocytic
  • Adult-onset asthma: often non-allergic; rule out occupational asthma
  • Obesity-associated asthma: prominent symptoms, little eosinophilic inflammation

Asthma: Making the Diagnosis

  • Requires BOTH: (1) characteristic variable symptom pattern AND (2) confirmed variable airflow limitation
  • Symptoms: wheeze, SOB, chest tightness, cough — vary over time and intensity
  • Often worse at night/morning; triggered by exercise, allergens, cold air, viral infections
  • Confirm with spirometry: positive BD reversibility (FEV₁ ≥12% + ≥200 mL) or PEF variability >10%/day
  • If initial tests negative — repeat during symptoms or early morning
  • 💎 Do NOT start long-term treatment without objective evidence of variable airflow limitation

Asthma Diagnostic Criteria (GINA 2024)

  • Positive BD reversibility: FEV₁ ≥12% + ≥200 mL (adults); FEV₁ ≥12% predicted (children)
  • PEF variability >10%/day (adults) or >13%/day (children) over 2 weeks
  • Increase in FEV₁ ≥12% + ≥200 mL after 4 weeks of ICS treatment
  • Positive methacholine challenge: FEV₁ fall ≥20%
  • Variation in FEV₁ ≥12% + ≥200 mL between visits
  • 💎 The more tests are positive and the more often they are positive, the more confident the diagnosis

Asthma: Differential Diagnosis

  • Children 6-11: Upper airway cough syndrome, inhaled foreign body, bronchiectasis, CF, congenital heart disease
  • Adolescents/Adults: Inducible laryngeal obstruction (stridor, not wheeze), hyperventilation
  • All ages: COPD (older smokers), cardiac failure (orthopnoea, PND), ACE inhibitor cough
  • Constitutional symptoms (fever, night sweats, weight loss) → consider TB
  • 💎 Asthma-COPD Overlap (ACO) exists — look for features of both
  • Comorbidities (rhinosinusitis, GERD, obesity, OSA) can coexist AND worsen asthma control

Asthma Assessment: Control & Severity

  • Two domains: (1) Symptom control over past 4 weeks; (2) Future risk of adverse outcomes
  • Symptom control: daytime symptoms, night waking, activity limitation, reliever use
  • 💎 Good symptom control does NOT mean no risk — lung function and exacerbation history must be assessed
  • Severe asthma: uncontrolled despite high-dose ICS-LABA OR requiring it to stay controlled
  • Before diagnosing severe asthma: exclude poor technique, poor adherence, wrong diagnosis, comorbidities
  • Spirometry: at diagnosis, 3-6 months after starting treatment, then periodically
BREATHE mnemonic for asthma assessment (MOH Singapore)

BREATHE mnemonic for asthma assessment (MOH Singapore)

Asthma Control Test (ACT)

  • 5 questions covering activity limitation, shortness of breath, night symptoms, reliever use, overall control
  • Scored 1-5 for each question (max 25)
  • Score 20-25: Well-controlled asthma
  • Score 16-19: Not well-controlled asthma — step up treatment
  • Score 5-15: Very poorly controlled asthma — urgent review
  • 💎 Use ACT at every follow-up as a standardized objective measure of control
Asthma Control Test (ACT) questionnaire

Asthma Control Test (ACT) questionnaire

Asthma Medications: Key Terminology

  • Controller: ICS-containing medication for regular daily use (targets inflammation AND risk)
  • Reliever: As-needed inhaler for quick symptom relief (salbutamol, ICS-formoterol)
  • Anti-inflammatory Reliever (AIR): Low-dose ICS + rapid-acting BD (budesonide-formoterol)
  • MART (Maintenance-And-Reliever Therapy): ICS-formoterol for BOTH maintenance AND relief
  • 💎 Only specific ICS-formoterol combinations can be used as MART (NOT salmeterol, vilanterol etc.)
  • LTRA (e.g., montelukast): Alternative add-on controller; less effective than ICS for exacerbation prevention

ICS Dose Equivalencies (GINA 2024)

  • Low dose ICS: Budesonide 200-400 mcg/day; Beclometasone 200-500 mcg/day; Fluticasone propionate 100-250 mcg/day
  • Medium dose: Budesonide 400-800 mcg/day; Beclometasone 500-1000 mcg; Fluticasone prop 250-500 mcg
  • High dose: Budesonide >800 mcg/day; Beclometasone >1000 mcg; Fluticasone prop >500 mcg
  • Children (6-11 yr): doses approximately halved; always use lowest effective dose
  • Extrafine particle formulations (e.g., Qvar) achieve deeper lung deposition at lower doses
  • 💎 Doubling the ICS dose for exacerbations has limited evidence; ICS-formoterol MART is preferred strategy
ICS dose equivalency table — adults/adolescents and children

ICS dose equivalency table — adults/adolescents and children

GINA 2024: Two-Track Treatment Approach

  • Track 1 (Preferred): As-needed low-dose ICS-formoterol as reliever AT ALL STEPS
  • Track 2 (Alternative): As-needed SABA reliever + separate daily controller
  • 🚨 SABA-only treatment (no ICS) is NO LONGER recommended — associated with increased exacerbation risk and death
  • Track 1 advantage: every reliever puff delivers anti-inflammatory protection
  • MART strategy: budesonide-formoterol OR beclometasone-formoterol for maintenance AND relief
  • 💎 Track 1 reduces severe exacerbations by ~60-70% compared to SABA-only in clinical trials
GINA 2024 two-track initial asthma treatment flowchart

GINA 2024 two-track initial asthma treatment flowchart

Stepwise Asthma Treatment (Adults ≥12 years)

  • Step 1: As-needed low-dose ICS-formoterol (Track 1) OR low-dose ICS when SABA taken (Track 2)
  • Step 2: As-needed low-dose ICS-formoterol (Track 1) OR daily low-dose ICS + as-needed SABA
  • Step 3: Low-dose ICS-formoterol MART (Track 1) OR daily low-dose ICS-LABA + SABA
  • Step 4: Medium-dose ICS-formoterol MART (Track 1) OR medium/high-dose ICS-LABA + SABA
  • Step 5: High-dose ICS-LABA ± LAMA; investigate severe asthma; consider biologics
  • 💎 Step up if uncontrolled for ≥3 months (after checking technique, adherence, triggers)
MOH Singapore ACE stepwise pharmacological treatment for asthma

MOH Singapore ACE stepwise pharmacological treatment for asthma

GINA 2024 Management Cycle

  • Cycle: Assess → Adjust treatment → Review response
  • Assess: symptom control, risk factors, inhaler technique, adherence, comorbidities
  • Adjust: step up or down based on response; address modifiable risk factors
  • Review: 1-3 months after starting/changing treatment; 3-6 monthly in stable patients
  • Non-pharmacological: smoking cessation, allergen avoidance, exercise, obesity management
  • 💎 Personalise treatment — consider patient preferences, cost, device availability
GINA 2024 Assess-Start-Review management cycle

GINA 2024 Assess-Start-Review management cycle

Inhaler Technique: Pearls

  • Poor inhaler technique is a leading cause of uncontrolled asthma
  • MDI: shake → breathe out fully → slow deep breath in while pressing → hold 10 sec
  • DPI (Turbuhaler/Accuhaler): fast forceful inhalation required; do NOT exhale into device
  • Spacer: increases lung deposition from MDI by 2-3x; essential for children and patients with poor coordination
  • 💎 Always demonstrate technique AND ask patient to show you back ('teach-back')
  • Reassess technique at EVERY consultation — errors recur even after correct initial training

Written Asthma Action Plan (WAAP)

  • Essential for all patients — reduces emergency visits and hospitalisations
  • Three zones: Green (controlled), Yellow (worsening), Red (emergency)
  • Green: continue regular medications as prescribed
  • Yellow: increase reliever, start/increase preventer, consider OCS if not improving in 24-48h
  • Red: call ambulance / go to A&E immediately if too breathless to speak
  • 💎 Personalise to patient's medications; review and update at every visit
Written Asthma Action Plan (WAAP) example with traffic light zones

Written Asthma Action Plan (WAAP) example with traffic light zones

Preventer Medications in Singapore

  • ICS alone: Budesonide (Pulmicort), Fluticasone propionate (Flixotide), Beclometasone (Qvar)
  • ICS-LABA combinations: Budesonide-formoterol (Symbicort/Pulmicort Turbuhaler), Fluticasone-salmeterol (Seretide), Fluticasone-vilanterol (Relvar)
  • LAMA add-on (Step 5): Tiotropium (Spiriva Respimat) — for adult asthma
  • Biologics (severe asthma, Step 5): Omalizumab (anti-IgE), Dupilumab (anti-IL-4/13), Benralizumab (anti-IL-5Rα)
  • LTRA: Montelukast — adjunct, less effective for exacerbation prevention than ICS
  • 💎 For MART: Only budesonide-formoterol or beclometasone-formoterol are approved
Preventer medications for asthma registered in Singapore (MOH ACE 2020)

Preventer medications for asthma registered in Singapore (MOH ACE 2020)

Acute Asthma: Severity Classification

🚨 Emergency — Act Now
🚨
  • Mild: dyspnoea only with activity; PEF/FEV₁ >70% predicted/personal best
  • Moderate: dyspnoea limits usual activity; PEF/FEV₁ 40-69%
  • Severe: dyspnoea at rest; interferes with conversation; PEF/FEV₁ <40%
  • Life-threatening: too dyspnoeic to speak; perspiring, drowsy, confused; PEF/FEV₁ <25%
  • 🚨 Life-threatening features: silent chest, cyanosis, poor respiratory effort, altered consciousness → IMMEDIATE ambulance transfer
  • 💎 Document initial SpO₂ and PEF/FEV₁ — essential for severity grading and monitoring response

Acute Asthma: Primary Care Management

🚨 Emergency — Act Now
🚨
  • Mild-Moderate: Salbutamol 4-8 puffs via MDI+spacer q20min × 3; SpO₂ target ≥95%; reassess in 1h
  • Severe: Salbutamol + ipratropium bromide q20min × 3; Prednisolone 40-50 mg orally; Oxygen to SpO₂ ≥95%
  • No response or deterioration → CALL AMBULANCE; continue bronchodilators while awaiting
  • 🚨 IV magnesium sulphate 2g over 20 min if no response in secondary care
  • Discharge criteria (mild-moderate): PEF/FEV₁ >60-70%, symptoms resolved, able to self-manage
  • All patients after exacerbation: review within 2-7 days; update WAAP; check inhaler technique

Acute Asthma: ED Management

🚨 Emergency — Act Now
🚨
  • Initial rapid assessment: vital signs, SpO₂, PEF/FEV₁, clinical severity
  • Immediate: oxygen (SpO₂ ≥95%), salbutamol + ipratropium nebs q20min, systemic corticosteroids
  • Severe: IV magnesium sulphate 2g over 20 min (reduces hospitalisation risk)
  • Reassess 1h: good response (PEF >60%) → may discharge with close follow-up
  • Poor response or life-threatening → ICU; consider IV salbutamol, intubation as last resort
  • 🚨 Avoid sedatives/opioids in acute asthma — suppress respiratory drive

Asthma in Children ≤5 Years: Diagnosis

  • Challenging — episodic wheeze and cough common in this age group
  • More likely asthma if: recurrent symptoms, worse at night, triggered by exercise/allergens/viral URTI
  • Trial of treatment: response to short-term low-dose ICS supports diagnosis
  • Differential: recurrent viral wheeze (no atopy, well between episodes), GERD, foreign body, pertussis, bronchiectasis
  • 💎 Consider referral to paediatrician if: <1 year old, atypical symptoms, poor treatment response
  • Do NOT use peak flow meters in children <5 years (cannot reliably perform manoeuvre)

Asthma in Children ≤5 Years: Management

  • Reliever: Salbutamol 200-400 mcg via MDI+spacer (with mask if <4 years) q20min for acute episodes
  • Step 1: As-needed SABA only for infrequent wheeze
  • Step 2: Daily low-dose ICS (budesonide 200 mcg/day) OR daily montelukast if ICS not feasible
  • Step 3: Increase ICS dose OR add montelukast; consider specialist referral
  • Step 4: Specialist referral for further evaluation and management
  • 💎 MDI + spacer + face mask is the preferred delivery device for children under 4 years

Paediatric Inhaler Technique & ICS Dosing

  • Always use spacer with MDI for children — face mask for <4 years, mouthpiece for ≥4 years
  • Low-dose ICS in children: Budesonide 100-200 mcg/day; BDP 100-200 mcg; FP 50-100 mcg
  • Wash and air-dry spacer weekly — detergent reduces electrostatic charge improving drug delivery
  • Counsel parents: ICS at appropriate doses do NOT stunt growth significantly when benefits outweigh risks
  • 💎 Demonstrate pMDI + spacer + mask technique to both parent AND child at every visit
  • Video resources: National Asthma Council Australia website has age-specific inhaler technique guides

COPD: Definition & Risk Factors

  • Heterogeneous lung condition — persistent airflow obstruction from airway (bronchitis/bronchiolitis) and/or alveolar (emphysema) abnormalities
  • Key symptoms: chronic dyspnoea (especially exertional), cough, sputum production
  • Leading global cause of morbidity and mortality; often underdiagnosed
  • Risk factors: TOBACCO SMOKE (most important), household/outdoor air pollution, occupational dusts/chemicals
  • Alpha-1-antitrypsin deficiency: rare genetic cause — suspect in non-smokers or early-onset COPD
  • Early life events: prematurity, low birth weight, childhood respiratory infections also contribute

COPD: Diagnosis (GOLD 2024)

  • ALL THREE required: (1) typical symptoms + (2) risk factor exposure + (3) spirometry confirmation
  • Spirometry: Post-bronchodilator FEV₁/FVC < 0.70 confirms airflow obstruction
  • Do NOT diagnose COPD without spirometry — clinical features alone are insufficient
  • 💎 Spirometry is essential: many patients have 'silent' disease until spirometry reveals significant obstruction
  • Exclude other diagnoses: asthma, cardiac failure, bronchiectasis, TB
  • Screen proactively: any patient >35 years with smoking history AND symptoms
Spirometry in COPD: obstructive pattern (FEV1/FVC = 0.56)

Spirometry in COPD: obstructive pattern (FEV1/FVC = 0.56)

COPD vs Asthma: Key Differences

  • COPD: usually ≥40 years; persistent/progressive dyspnoea; significant smoking/exposure history
  • Asthma: any age; variable episodic symptoms; personal/family history of atopy; triggers
  • COPD: persistent post-BD obstruction (FEV₁/FVC <0.70); minimal reversibility
  • Asthma: often normal lung function between episodes; significant reversibility (≥12% + ≥200 mL)
  • 💎 Asthma-COPD Overlap (ACO): features of both; eosinophilia + BD reversibility; treat with ICS + LABD
  • Chest X-ray: COPD may show hyperinflation, flat diaphragms; asthma usually normal

COPD Assessment Tools: mMRC & CAT

  • mMRC Grade 0: Breathless only with strenuous exercise
  • mMRC Grade 1: Short of breath when hurrying or walking up a slight hill
  • mMRC Grade 2: Walks slower than others due to breathlessness, or stops to rest
  • mMRC Grade 3: Stops for breath after ~100m on flat ground
  • mMRC Grade 4: Too breathless to leave house; breathless when dressing/undressing
  • 💎 CAT score ≥10 = significant symptom burden; use CAT for more comprehensive assessment

GOLD ABE Classification (Current Standard)

  • Replaced the old ABCD tool from 2023 — spirometry severity (GOLD 1-4) no longer drives initial therapy choice
  • Group A: Low symptoms (mMRC 0-1 OR CAT <10) AND 0-1 moderate exacerbations (not hospitalised)
  • Group B: High symptoms (mMRC ≥2 OR CAT ≥10) AND 0-1 moderate exacerbations
  • Group E: ≥2 moderate exacerbations OR ≥1 severe exacerbation (hospitalisation in past year)
  • 💎 Exacerbation history is the single best predictor of future exacerbations — ask at EVERY visit
  • Still measure FEV₁ for grading severity (GOLD 1-4) and guiding some add-on therapy decisions
GOLD 2023+ ABE assessment framework

GOLD 2023+ ABE assessment framework

COPD Clinical Phenotypes

  • ACO (Asthma-COPD Overlap): High eosinophils, BD reversibility — ICS is essential
  • Frequent Exacerbator: ≥2 moderate or ≥1 severe/year — LABA+LAMA ± ICS; consider roflumilast/azithromycin
  • Emphysema-predominant: CT emphysema, hyperinflation, low BMI — consider lung volume reduction
  • Chronic Bronchitis: Productive cough ≥3 months × 2 years — mucolytics, roflumilast
  • Physical Frailty (gait speed <0.8 m/s): Pulmonary rehab with strength training
  • 💎 Identify predominant phenotype to guide personalised management beyond ABE grouping

COPD Management Cycle

  • Diagnose → Initial assessment (ABE group, symptoms, comorbidities) → Implement initial management
  • Review: symptom control, exacerbation frequency, side effects, inhaler technique
  • Adjust: escalate or de-escalate pharmacotherapy; add non-pharmacological interventions
  • 💎 Reassess blood eosinophil count to guide ICS use — high eosinophils (≥300) favour ICS
  • Check: inhaler technique and adherence at EVERY visit
  • Address comorbidities: cardiovascular disease, depression, osteoporosis, lung cancer screening
GOLD COPD management cycle diagram

GOLD COPD management cycle diagram

COPD: Initial Pharmacotherapy (GOLD ABE)

  • Group A: ONE long-acting bronchodilator — LAMA (preferred) or LABA
  • Group B: DUAL bronchodilator — LAMA + LABA (superior to monotherapy for symptom relief)
  • Group E: LAMA + LABA; if eosinophils ≥300 cells/μL → start LAMA + LABA + ICS (triple therapy)
  • 💎 ICS should NOT be used as initial monotherapy in COPD — only appropriate in triple therapy or ACO
  • All patients: short-acting bronchodilator (SABA or SAMA) for breakthrough symptoms
  • Reassess at 3 months for symptom response and exacerbation reduction
GOLD 2024 initial pharmacotherapy by ABE group

GOLD 2024 initial pharmacotherapy by ABE group

COPD: Follow-up Pharmacotherapy Algorithm

  • Persistent DYSPNOEA on monotherapy → escalate to LAMA+LABA; if already on dual → check technique/switch
  • Persistent EXACERBATIONS on LAMA+LABA: check blood eosinophils to guide next step
  • Eosinophils ≥300: add ICS → triple therapy (LAMA+LABA+ICS)
  • Eosinophils 100-300: consider adding ICS if still exacerbating
  • Eosinophils <100: ICS unlikely effective; consider ROFLUMILAST (FEV₁ <50%, chronic bronchitis) or AZITHROMYCIN (ex-smokers)
  • 💎 ICS overuse increases risk of pneumonia in COPD — reserve for those with high eosinophils or frequent exacerbations
COPD follow-up pharmacotherapy algorithm — dyspnoea vs exacerbation pathway

COPD follow-up pharmacotherapy algorithm — dyspnoea vs exacerbation pathway

COPD: Non-Pharmacological Management

  • 🚨 SMOKING CESSATION: single most effective intervention — slows FEV₁ decline, reduces mortality
  • Vaccinations: Influenza (annual), Pneumococcal (PCV20 or PCV13+PPSV23), COVID-19, Tdap, RSV
  • Pulmonary Rehabilitation (PR): essential for Group B and E — improves dyspnoea, exercise capacity, QoL
  • Physical Activity: encourage daily walking; even moderate activity improves outcomes
  • Long-Term Oxygen Therapy (LTOT): indicated if PaO₂ ≤55 mmHg or SaO₂ ≤88% at rest — improves survival
  • 💎 Palliative care referral early: severe COPD has a poor prognosis; advance care planning is essential
Non-pharmacological COPD management by patient group (GOLD 2024)

Non-pharmacological COPD management by patient group (GOLD 2024)

🚨 COPD Exacerbations: Classification & Management

  • Mild: treat with SABDs (SABA ± SAMA) alone; no antibiotic or OCS required
  • Moderate: SABDs + antibiotics AND/OR oral corticosteroids (prednisolone 40 mg × 5 days)
  • Severe: hospitalisation required; IV bronchodilators, controlled oxygen (SpO₂ 88-92%), NIV
  • Antibiotics indicated if: increased dyspnoea + increased sputum volume + increased purulence (all 3 cardinal signs)
  • 🚨 NIV is first-line for hypercapnic respiratory failure in COPD — reduces intubation and mortality
  • 💎 Post-exacerbation: review within 4 weeks; optimise maintenance therapy; cardiac cause?
COPD exacerbation severity algorithm and differential diagnosis

COPD exacerbation severity algorithm and differential diagnosis

Singapore MOH ACE: COPD Diagnosis (2024)

  • Suspect COPD: any patient ≥40 years with dyspnoea, chronic cough/sputum, and risk factor exposure
  • Confirm with post-bronchodilator spirometry: FEV₁/FVC < 0.70
  • Assess: symptoms (CAT/mMRC), exacerbation history, blood eosinophil count
  • Exclude: asthma, cardiac failure, bronchiectasis, TB
  • Refer if: uncertain diagnosis, rapid decline, severe disease (FEV₁ <30%), suspected lung cancer
  • 💎 Many COPD patients in Singapore are underdiagnosed — proactive case-finding in at-risk individuals is recommended
Singapore MOH ACE COPD diagnostic algorithm (June 2024)

Singapore MOH ACE COPD diagnostic algorithm (June 2024)

Singapore MOH ACE: COPD Management (2024)

  • Strong recommendation: smoking cessation counselling at every visit
  • Dual LABD (LAMA+LABA) preferred for patients with significant symptoms or exacerbation risk
  • Triple therapy (LAMA+LABA+ICS) for frequent exacerbators with eosinophils ≥300 cells/μL
  • Assess inhaler technique and adherence at every visit — use the 'show me how' approach
  • Refer for pulmonary rehabilitation: for Group B and E patients
  • 💎 ICS de-escalation: consider withdrawing ICS if eosinophils <100 and not exacerbating — reduces pneumonia risk
Singapore MOH ACE COPD management flowchart (June 2024)

Singapore MOH ACE COPD management flowchart (June 2024)

COPD Inhalers Available in Singapore

  • SABA: Salbutamol (Ventolin), Terbutaline (Bricanyl) — short-acting, for rescue
  • SAMA: Ipratropium (Atrovent) — short-acting antimuscarinic, useful in acute exacerbations
  • LAMA: Tiotropium (Spiriva HandiHaler/Respimat), Umeclidinium (Incruse), Glycopyrronium (Seebri)
  • LAMA+LABA: Umeclidinium-vilanterol (Anoro), Tiotropium-olodaterol (Spiolto), Glycopyrronium-formoterol (Bevespi)
  • LABA+ICS or LAMA+LABA+ICS: e.g., Fluticasone-salmeterol (Seretide), Fluticasone furoate-vilanterol-umeclidinium (Trelegy)
  • 💎 Do NOT combine two inhalers from the same drug class (e.g., two LAMAs) — no added benefit, increased risk

COPD: Comorbidities

  • Cardiovascular disease: most common comorbidity; increases mortality independently
  • 💎 Beta-blockers are NOT contraindicated in COPD — use for appropriate cardiac indications (heart failure, post-MI)
  • Lung cancer: 4-6x increased risk in COPD; low-dose CT screening for heavy smokers (≥30 pack-years, ≥50 years)
  • Osteoporosis: screen and treat; ICS and smoking both increase fracture risk
  • Depression and anxiety: highly prevalent; screen with PHQ-2 and GAD-2; treat if positive
  • GERD: common; can trigger exacerbations; treat symptomatically

Interstitial Lung Disease (ILD): Overview

  • Large, heterogeneous group of conditions — inflammation and/or fibrosis of lung interstitium
  • Impaired gas exchange → progressive dyspnoea, dry cough, fatigue, chest discomfort
  • Restrictive physiology on PFTs: reduced TLC, FVC; normal or elevated FEV₁/FVC ratio
  • Key categories: idiopathic (IPF), autoimmune-related, exposure-related, sarcoidosis, others
  • Epidemiology: IPF incidence increasing; prognosis poor (median survival ~3-5 years from diagnosis)
  • 💎 ILD is often underdiagnosed — progressive unexplained dyspnoea with bibasilar crackles should prompt investigation
Classification of interstitial lung diseases

Classification of interstitial lung diseases

IPF: Pathophysiology

  • Idiopathic Pulmonary Fibrosis (IPF): most common idiopathic IIP; progressive, irreversible fibrosis
  • Repeated microinjuries to alveolar epithelium → abnormal wound healing → fibroblast activation → fibrosis
  • Gross: honeycombing (subpleural, basal-predominant) on HRCT
  • Loss of gas exchange surface → hypoxaemia, especially on exertion
  • Risk factors: male sex, older age (>60), cigarette smoking, environmental exposures
  • 💎 IPF has no truly effective cure — anti-fibrotics slow progression but do not reverse fibrosis
Healthy lung vs IPF: alveolar fibrosis and gas exchange impairment

Healthy lung vs IPF: alveolar fibrosis and gas exchange impairment

When to Suspect ILD: Primary Care Red Flags

  • Persistent unexplained DRY COUGH — not productive, not responding to common treatments
  • Progressive EXERTIONAL DYSPNOEA — insidious onset, worsening over months/years
  • Fine inspiratory VELCRO-LIKE CRACKLES at lung bases — highly characteristic of fibrotic ILD
  • Finger clubbing — present in ~50% of IPF cases; not seen in sarcoidosis
  • 💎 Take thorough exposure history: birds, mold, feather pillows, organic dusts, silica, asbestos exposure
  • Systemic features (joint pain, rash, Raynaud's, myalgia) suggest connective tissue disease-associated ILD

ILD: Initial Investigations & Referral

  • Chest X-ray: reticular/nodular opacities, lower zone predominance; can be NORMAL in early disease
  • Spirometry: restrictive pattern (reduced FVC, normal or elevated FEV₁/FVC; reduced TLC on plethysmography)
  • Reduced DLCO (diffusing capacity): sensitive early indicator of gas exchange impairment
  • Blood tests: FBC, ESR, CRP, ANA, anti-dsDNA, anti-Scl70, anti-Ro/La, RF — screen for connective tissue disease
  • 🚨 REFER to respiratory specialist for HRCT chest + MDT discussion — do NOT delay referral
  • 💎 Do NOT start empirical immunosuppression in primary care — accurate diagnosis essential before treatment

ILD: HRCT Patterns

  • UIP (Usual Interstitial Pneumonia): subpleural, basal honeycombing ± traction bronchiectasis → IPF
  • NSIP (Non-Specific Interstitial Pneumonia): bilateral ground glass ± reticulation; autoimmune-related
  • Hypersensitivity Pneumonitis: centrilobular nodules, ground glass, mosaic attenuation
  • Sarcoidosis: perilymphatic nodules, hilar/mediastinal lymphadenopathy
  • Organising Pneumonia: consolidation, often peribronchial or subpleural — can mimic pneumonia
  • 💎 HRCT pattern guides MDT diagnosis and determines management approach
CT patterns in ILDs: IPF, NSIP, HP, sarcoidosis, organising pneumonia

CT patterns in ILDs: IPF, NSIP, HP, sarcoidosis, organising pneumonia

ILD: Management Principles

  • Gold standard: MDT evaluation (pulmonologist, radiologist, pathologist) — improves diagnostic accuracy
  • Anti-fibrotics (IPF): Pirfenidone or Nintedanib — slows FVC decline by ~50%; does not reverse fibrosis
  • Immunosuppression (connective tissue disease-ILD, HP): corticosteroids ± steroid-sparing agents
  • Remove exposure: critical for hypersensitivity pneumonitis — identify and eliminate causative antigen
  • Non-pharmacological: Pulmonary rehabilitation; supplemental oxygen for hypoxaemia; handheld fan for breathlessness
  • 💎 Advance care planning: integrate palliative care early; IPF is progressive and often fatal

Key Summary: Spirometry & Bronchiectasis

Key Point
💎 Spirometry is essential for diagnosing and monitoring obstructive and restrictive lung disease
Key Point
FEV₁/FVC <0.70 (post-BD) = obstruction; reduced FVC with normal ratio = restriction
Key Point
Positive BD reversibility (≥12% + ≥200 mL) suggests asthma but does not exclude COPD
Key Point
Bronchiectasis: irreversible airway dilatation; manage with airway clearance, macrolides, vaccinations
Key Point
Post-TB lung disease is a major cause of morbidity in Singapore — proactive management needed
Key Point
Spirometry is indicated for any patient with unexplained dyspnoea, chronic cough, or respiratory risk factors

Key Summary: Asthma

Key Point
Diagnosis requires BOTH variable symptoms AND confirmed variable airflow limitation — do not treat empirically without evidence
Key Point
💎 GINA 2024 strongly prefers Track 1: ICS-formoterol as reliever at ALL steps — reduces severe exacerbations by ~60-70%
Key Point
🚨 SABA-only treatment is no longer recommended — every patient should have an ICS-containing controller
Key Point
MART (budesonide-formoterol or beclometasone-formoterol): maintenance AND reliever in one inhaler
Key Point
Check inhaler technique and adherence at EVERY visit — poor technique is the most common cause of poor control
Key Point
All patients should have a Written Asthma Action Plan (WAAP)

Key Summary: COPD

Key Point
Diagnosis requires symptoms + risk factor exposure + post-BD FEV₁/FVC <0.70 — never diagnose without spirometry
Key Point
GOLD ABE framework (not ABCD): Group A → 1 LABD; Group B → LAMA+LABA; Group E → LAMA+LABA ± ICS
Key Point
Blood eosinophil count guides ICS use: ≥300 → add ICS; <100 → ICS unlikely effective
Key Point
💎 Smoking cessation is the MOST effective intervention — reduces FEV₁ decline rate
Key Point
Vaccinations, pulmonary rehabilitation, and physical activity are essential non-pharmacological pillars
Key Point
🚨 COPD exacerbation: SABDs + OCS (5 days) + antibiotics if all 3 cardinal signs present

Key Summary: ILD

Key Point
Suspect ILD in: progressive exertional dyspnoea + dry cough + bibasilar velcro crackles
Key Point
Restrictive spirometry + reduced DLCO → refer for HRCT and respiratory specialist MDT evaluation
Key Point
💎 Do NOT start empirical treatment in primary care — accurate diagnosis via MDT is essential
Key Point
IPF: anti-fibrotics (pirfenidone/nintedanib) slow progression; no cure
Key Point
Connective tissue disease-ILD: immunosuppression; Hypersensitivity pneumonitis: remove causative antigen
Key Point
Integrate palliative care early — progressive ILD has significant symptom burden and poor prognosis

References

M121

Ear Conditions

Learning Objectives

  • Recognise and differentiate common causes of ear discharge (otorrhoea)
  • Diagnose and manage acute otitis externa and otitis media in adults and children
  • Apply a structured approach to otalgia, tinnitus, vertigo, and hearing loss
  • Interpret a basic pure-tone audiogram and identify key patterns
  • Identify red flags requiring urgent ENT referral (SSNHL, cholesteatoma, central vertigo, unilateral OME in adults)
  • Perform or supervise common ear procedures: aural toileting, syringing, microsuction, foreign body removal

Normal Tympanic Membrane — The Baseline

  • Landmark: cone of light (anterior-inferior), handle of malleus, pars tensa and pars flaccida
  • Normal TM: pearlescent/grey, intact, mobile on pneumatoscopy
  • Any deviation from this baseline is clinically significant
  • Always examine both ears; compare sides
  • A confident normal finding is as important as detecting pathology
Normal tympanic membrane with visible light reflex and handle of malleus

Normal tympanic membrane with visible light reflex and handle of malleus

Ear Discharge (Otorrhoea) — Overview

  • Otorrhoea has many causes; history and otoscopy are essential to differentiate
  • Key question: Did pain precede the discharge? (AOM) or is pain constant? (OE)
  • Character: watery (CSF?), purulent (bacterial), cheesy/black (fungal), foul-smelling (cholesteatoma)
  • Always perform aural toileting — diagnostic and therapeutic
  • Red flag: persistent foul discharge + marginal/attic perforation → cholesteatoma (mandatory ENT referral)

Otitis Externa — Clinical Features

  • Pain constant, worsened by tragal pressure or pinna traction
  • Creamy/white discharge; canal erythematous, oedematous, with debris
  • TM usually intact and normal
  • Risk factors: water exposure, instrumentation, skin conditions
  • Chronic OE: thick, malodorous discharge with desquamated skin
External ear showing erythema, scaling, and moist debris — otitis externa

External ear showing erythema, scaling, and moist debris — otitis externa

Otitis Externa — Management

  • Aural toileting first — clear the canal to allow drops to penetrate
  • Antibiotic/steroid eardrops (fluoroquinolone-based) × 5–10 days; massage tragus after instillation
  • If canal oedema >50%: insert Pope Wick, change every 2–3 days
  • Oral antibiotics only for severe infection, immunocompromised, or diabetic patients
  • No improvement after 1 week → suspect otomycosis; start clotrimazole drops
  • Refer if no improvement after 1 week of appropriate treatment

Dermatitis of the Ear Canal

  • Consider when OE does not respond after 1 week of treatment
  • Causes: otic medications, cosmetics, earplugs, shampoos, hearing aid moulds
  • Classic: shiny, erythematous canal extending to the conchal bowl
  • Manage by identifying and removing the irritant
  • Topical steroid cream may help; avoid prolonged use
External ear showing mild erythema and scaling of conchal bowl — early otitis externa or eczema

External ear showing mild erythema and scaling of conchal bowl — early otitis externa or eczema

Otomycosis — Fungal Otitis Externa

  • ~9% of otitis externa cases; more common after antibiotic eardrops
  • Predominant symptom: intense itch (more than in bacterial OE)
  • Candida spp.: white fungal ball in canal
  • Aspergillus spp.: black spore heads on canal wall or TM
Otoscopic view showing white fungal mass consistent with otomycosis (Aspergillus or Candida)

Otoscopic view showing white fungal mass consistent with otomycosis (Aspergillus or Candida)

💎 Aspergillus Niger Otomycosis — Classic Appearance

  • Black spore heads on tympanic membrane or canal wall — pathognomonic
  • Do NOT confuse with a foreign body
  • Treatment: thorough aural toileting + clotrimazole 1% drops or solution
  • Avoid prolonged antibiotic drops — predisposes to fungal superinfection
  • Local Singapore study: 38% of community OE patients had positive fungal culture
Otoscopic view of Aspergillus niger otomycosis with characteristic black spore heads on tympanic membrane

Otoscopic view of Aspergillus niger otomycosis with characteristic black spore heads on tympanic membrane

Acute Suppurative Otitis Media — Recognition

  • Classic history: severe otalgia → sudden painless yellowish discharge (perforation)
  • Otoscopy before perforation: red, bulging, opaque TM — loss of light reflex
  • After perforation: pulsatile discharge; pain relieves
  • Central/tubo-tympanic perforations = 'safe'; marginal/attic = 'unsafe' (cholesteatoma risk)
  • Most perforations heal within weeks; refer to ENT if persists >3 months
Otoscopic view showing bulging, opaque tympanic membrane with middle ear effusion — acute otitis media

Otoscopic view showing bulging, opaque tympanic membrane with middle ear effusion — acute otitis media

AOM Management — Children (Updated 2022)

  • Pain management is always the first priority: paracetamol or ibuprofen
  • Immediate antibiotics for: age <2 years, bilateral AOM, otorrhoea, or severe symptoms (T ≥39°C, severe otalgia)
  • Watchful waiting 48–72h: children ≥2 years, mild-moderate, unilateral AOM — arrange reliable follow-up
  • First-line: amoxicillin 80–90 mg/kg/day; switch to amoxicillin-clavulanate if no improvement at 48–72h
  • Duration: 10 days for <2 years or severe; 5–7 days may suffice for older children with mild disease
  • Penicillin allergy: cephalosporin (non-anaphylactic), macrolide, or clindamycin

AOM Management — Adults & Travel Advice

  • Adults: amoxicillin-clavulanate 875/125 mg BD × 5–10 days; alternatives: high-dose amoxicillin, cephalosporins, fluoroquinolones
  • 🚨 Red flag: recurrent unilateral AOM >2 episodes in 6 months → urgent ENT referral to exclude NPC
  • If perforated: keep ear dry (no swimming, use petrolatum-covered cotton during bathing)
  • Refer to ENT if perforation persists >3 months
  • Travel advice: avoid air travel; infants: pacifier/bottle; older children: chew gum or Otovent device

Cholesteatoma — Do Not Miss

  • Keratinized squamous epithelium in middle ear/mastoid — erodes bone
  • Key features: persistent foul-smelling otorrhoea, marginal or attic perforation
  • May cause: facial nerve palsy, SNHL, intracranial complications
  • Can be congenital or acquired (secondary to retraction pocket)
  • 🚨 Mandatory ENT referral — surgical treatment required
Otoscopic view showing cholesteatoma with keratin debris and retraction pocket in the tympanic membrane

Otoscopic view showing cholesteatoma with keratin debris and retraction pocket in the tympanic membrane

OME and Tympanosclerosis — Differentiating TM Appearances

  • OME: dull, retracted TM; bluish hue, air-fluid level, or bubbles visible
  • OME does NOT cause discharge unless it evolves into AOM
  • 🚨 Unilateral OME in adults → urgent ENT referral to exclude NPC
  • Tympanosclerosis: chalky white plaques on TM; does NOT cause discharge
  • Tympanosclerosis: history of grommet insertion; rarely causes conductive hearing loss
Otitis media with effusion — bluish tympanic membrane with air-fluid level

Otitis media with effusion — bluish tympanic membrane with air-fluid level

Tympanosclerosis

  • Chalky white calcified plaques on the tympanic membrane
  • Result of prior inflammation — common after grommet insertion
  • Does NOT cause ear discharge
  • Usually clinically insignificant; rarely involves ossicles causing conductive HL
  • Reassure the patient — no treatment required unless symptomatic
Tympanosclerosis — white calcified plaques on tympanic membrane

Tympanosclerosis — white calcified plaques on tympanic membrane

Otalgia — Differential Diagnosis

  • Primary otalgia: ear itself is the source (OE, AOM, furunculosis, Ramsay Hunt)
  • Referred otalgia: pain from a distant site via shared nerve supply — normal ear exam
  • Common referred sources: dental (impacted wisdom teeth, caries), TMJ dysfunction, tonsillitis/pharynx, base of tongue, pyriform sinus
  • Normal ear canal + mobile TM on Valsalva → strongly suggests referred pain
  • Always consider pharyngeal pathology — base of tongue or pyriform sinus cancer may present with otalgia
  • If workup negative: consider depression or cervical spine dysfunction

Tinnitus — Classification

  • Subjective tinnitus: only heard by patient — far more common
  • Objective tinnitus: audible to examiner — suggests vascular or mechanical cause
  • Pulsatile tinnitus: synchronous with heartbeat — red flag (AV fistula, glomus tumour)
  • Main risk factor for subjective tinnitus: sensorineural hearing loss
  • Bilateral non-pulsatile tinnitus in an older adult → most likely presbycusis
Tinnitus classification flowchart: subjective (hearing loss pattern, somatic, typewriter) vs objective (pulsatile vs non-pulsatile)

Tinnitus classification flowchart: subjective (hearing loss pattern, somatic, typewriter) vs objective (pulsatile vs non-pulsatile)

Objective Tinnitus — Differential Diagnoses

  • Pulsatile: arterial (carotid stenosis, AV fistula, glomus tumour) or venous (sigmoid sinus dehiscence, benign intracranial hypertension)
  • Non-pulsatile objective: palatal myoclonus, tensor tympani spasm, patulous Eustachian tube
  • Investigation: MRI/MRA of head and neck; Doppler studies
  • Urgent referral if objective pulsatile tinnitus confirmed
Objective tinnitus etiologies: pulsatile (arterial/venous) and non-pulsatile causes

Objective tinnitus etiologies: pulsatile (arterial/venous) and non-pulsatile causes

Tinnitus Red Flags

🚨 Emergency — Act Now
🚨
  • 🚨 Unilateral tinnitus → MRI of internal auditory meatus (IAM) to exclude vestibular schwannoma
  • 🚨 Pulsatile tinnitus → urgent vascular imaging (MRI/MRA)
  • 🚨 Tinnitus with asymmetric SNHL → MRI IAM mandatory
  • 💎 All chronic (>6 months) or bothersome tinnitus → pure tone audiometry (PTA) first
  • Management of chronic subjective tinnitus: counselling, CBT, sound therapy, hearing aids if HL present

Vertigo — Structured Approach

  • Step 1 — Timing: single episode vs recurrent? Duration: seconds-to-minutes (BPPV) or hours (Ménière's) or days (vestibular neuritis)?
  • Step 2 — Trigger: positional (BPPV) vs spontaneous?
  • Step 3 — Associated symptoms: hearing loss, tinnitus, aural fullness (Ménière's)?
  • Step 4 — Neurological symptoms? (5 D's) → suspect central cause → A&E
  • Step 5 — Examine: Dix-Hallpike, HINTS exam, cerebellar signs, gait

BPPV — Diagnosis with the Dix-Hallpike Manoeuvre

  • BPPV: most common peripheral vertigo — canalith(s) displaced in semicircular canals
  • Triggered by head movements (rolling over, looking up); comfortable at rest
  • Dix-Hallpike: patient seated, head rotated 45° to affected side, then rapidly supine with head hanging 20°
  • Positive test: vertigo + geotropic nystagmus (up-beating torsional) after a latency of 1–5 seconds
  • Nystagmus fatigues on repeated testing — distinguishes from central nystagmus
Dix-Hallpike manoeuvre — (A) head turned 45° seated, (B) rapid supine positioning with head hanging for BPPV diagnosis

Dix-Hallpike manoeuvre — (A) head turned 45° seated, (B) rapid supine positioning with head hanging for BPPV diagnosis

Dizziness Assessment Algorithm

  • Episodic + positional → BPPV (Dix-Hallpike, Epley)
  • Episodic + spontaneous → Ménière's disease (triad) or vestibular migraine
  • Continuous → vestibular neuritis (viral), stroke (central)
  • HINTS exam differentiates peripheral from central in continuous vertigo
  • 🚨 Any neurological sign → A&E; do not perform Epley if central cause suspected
Dizziness and vertigo assessment algorithm: episodic vs continuous, triggered vs spontaneous, HINTS exam, differential diagnoses

Dizziness and vertigo assessment algorithm: episodic vs continuous, triggered vs spontaneous, HINTS exam, differential diagnoses

Hearing Loss — Types and Causes

  • Conductive (CHL): problem in outer or middle ear; BC normal, AC reduced — air-bone gap ≥15 dB
  • CHL causes: impacted wax, OE, AOM, OME, perforation, tympanosclerosis, otosclerosis
  • Sensorineural (SNHL): cochlear or retrocochlear; both AC and BC reduced — no air-bone gap
  • SNHL causes: presbycusis, NIHL, ototoxicity, SSNHL, Ménière's, vestibular schwannoma
  • Mixed: both components present — depressed BC with further AC reduction

SNHL Aetiology — Cochlear vs Retrocochlear

  • Cochlear (sensory): presbycusis, NIHL, Ménière's, ototoxicity, viral/autoimmune
  • Retrocochlear (neural): vestibular schwannoma, meningioma, MS
  • Key discriminator: word recognition disproportionately poor → suspect retrocochlear
  • Asymmetric SNHL (>15 dB at 3 kHz or any frequency) → MRI IAM mandatory
  • Ototoxic drugs to monitor: aminoglycosides, loop diuretics, cisplatin/carboplatin
Causes of sensorineural hearing loss: cochlear (sensory) vs retrocochlear (neural) — includes presbycusis, NIHL, vestibular schwannoma, ototoxicity

Causes of sensorineural hearing loss: cochlear (sensory) vs retrocochlear (neural) — includes presbycusis, NIHL, vestibular schwannoma, ototoxicity

Conductive Hearing Loss — Aetiology by Site

  • Outer ear: cerumen impaction, OE, foreign body, exostoses
  • Tympanic membrane: perforation, tympanosclerosis, retraction
  • Middle ear: otosclerosis, ossicular disruption (trauma), cholesteatoma, OME
  • Key clinical test: Rinne negative (BC > AC on affected side), Weber lateralises to affected ear
  • Most causes of CHL in primary care are treatable
Causes of conductive hearing loss by site: outer ear (OE, cerumen), tympanic membrane (perforation), middle ear (otosclerosis, cholesteatoma)

Causes of conductive hearing loss by site: outer ear (OE, cerumen), tympanic membrane (perforation), middle ear (otosclerosis, cholesteatoma)

Audiogram Interpretation — Symbols Key

  • Air conduction (AC): right ear — O (unmasked), Δ (masked); left ear — X (unmasked), ☐ (masked)
  • Bone conduction (BC): right ear — < (unmasked), [ (masked); left ear — > (unmasked), ] (masked)
  • Normal hearing: ≤25 dB HL in adults; ≤20 dB in children
  • X-axis: frequency (Hz, 250–8000); Y-axis: intensity (dB HL, 0 at top)
  • Air-bone gap ≥15 dB → conductive component present
Audiogram symbol key: air and bone conduction symbols for right/left ears, masked/unmasked, sound field and aided testing

Audiogram symbol key: air and bone conduction symbols for right/left ears, masked/unmasked, sound field and aided testing

Hearing Loss Severity Classification

  • Normal: −10 to 25 dB HL
  • Mild: 26–40 dB; Moderate: 41–55 dB; Moderately severe: 56–70 dB
  • Severe: 71–90 dB; Profound: >90 dB
  • Classify by the average of 500, 1000, 2000, and 4000 Hz (PTA4)
  • Practical screen: patient cannot hear hair rubbed near ear → likely >40 dB loss
Hearing loss classification chart: normal (−10 to 15 dB) through profound (>90 dB) across 125–8000 Hz

Hearing loss classification chart: normal (−10 to 15 dB) through profound (>90 dB) across 125–8000 Hz

Normal Audiogram

  • All thresholds within normal limits: ≤25 dB HL across all frequencies
  • AC and BC symbols track closely — no air-bone gap
  • Symmetric between both ears
  • Use this as your baseline for comparison when reviewing patient audiograms
Normal audiogram: bilateral air and bone conduction thresholds at ~10 dB HL across all frequencies

Normal audiogram: bilateral air and bone conduction thresholds at ~10 dB HL across all frequencies

Presbycusis — Bilateral Sloping SNHL

  • Most common cause of hearing loss in older adults
  • Bilateral, symmetrical, progressive high-frequency SNHL
  • No air-bone gap — both AC and BC equally depressed
  • Associated with increased risk of dementia — hearing aids mitigate this risk
  • Management: counselling, hearing aids (SMF subsidy available for ≥60 years), assistive devices
Bilateral sloping high-frequency sensorineural hearing loss — classic presbycusis or noise-induced pattern

Bilateral sloping high-frequency sensorineural hearing loss — classic presbycusis or noise-induced pattern

Noise-Induced Hearing Loss — The 4kHz Notch

  • Most preventable cause of SNHL
  • Characteristic: bilateral SNHL with a notch at 4000 Hz (sometimes 6000 Hz)
  • Followed by partial recovery at 8000 Hz — the 'notch' pattern
  • Singapore study: 1 in 6 young people at risk from personal music players
  • Prevention: ear protection in noisy environments; safe listening levels (<85 dB for <8 hrs/day)
Audiogram with mid-frequency dip (Carhart notch pattern) — bilateral SNHL worse at 2000–4000 Hz

Audiogram with mid-frequency dip (Carhart notch pattern) — bilateral SNHL worse at 2000–4000 Hz

Conductive Hearing Loss Audiogram

  • BC thresholds normal (0–20 dB); AC thresholds depressed — creates air-bone gap
  • Flat pattern across frequencies typical of middle ear effusion or ossicular fixation
  • Bilateral flat CHL in a child → think OME (glue ear)
  • Unilateral flat CHL in adult → otosclerosis, ossicular disruption, cholesteatoma
  • Referral for audiological and ENT assessment if confirmed
Bilateral conductive hearing loss — bone conduction normal (0–5 dB), air conduction at ~40 dB flat across frequencies

Bilateral conductive hearing loss — bone conduction normal (0–5 dB), air conduction at ~40 dB flat across frequencies

Mixed Hearing Loss

  • Both sensorineural and conductive components present
  • BC thresholds elevated (SNHL component) + AC further depressed (additional conductive loss)
  • Air-bone gap present despite depressed BC
  • Common scenario: presbycusis + wax impaction or otosclerosis + SNHL
  • Refer to ENT and audiology for comprehensive assessment and management planning
Bilateral mixed hearing loss — air-bone gap present with depressed bone conduction at some frequencies

Bilateral mixed hearing loss — air-bone gap present with depressed bone conduction at some frequencies

Severe Mixed Hearing Loss

  • Large air-bone gap at low frequencies narrowing at high frequencies
  • Significant SNHL and conductive components both present
  • May represent advanced otosclerosis with superimposed SNHL
  • Management: address conductive component surgically if feasible; hearing aid for SNHL remainder
  • Patient counselling about realistic expectations is essential
Severe-to-profound mixed hearing loss — large air-bone gap at low frequencies narrowing at high frequencies

Severe-to-profound mixed hearing loss — large air-bone gap at low frequencies narrowing at high frequencies

Unilateral Conductive Hearing Loss

  • Right ear normal; left ear with significant air-bone gap (25–55 dB)
  • Consider: unilateral wax, perforation, OME, cholesteatoma, otosclerosis
  • 🚨 Unilateral OME in adult — always exclude NPC
  • Weber: lateralises to the affected (worse) ear in pure CHL
  • Refer for ENT assessment to identify and treat the underlying cause
Unilateral left conductive hearing loss — right ear normal, left ear with significant air-bone gap (25–55 dB)

Unilateral left conductive hearing loss — right ear normal, left ear with significant air-bone gap (25–55 dB)

Cookie-Bite SNHL Pattern

  • U-shaped (mid-frequency) dip: better at 250 Hz and 8000 Hz, worst at 500–2000 Hz
  • Classic association: genetic/congenital SNHL (autosomal dominant mutations)
  • Differs from presbycusis (high-frequency) and NIHL (notch at 4kHz)
  • Family history important — genetic counselling may be indicated
  • Refer to ENT and genetics if young patient with bilateral symmetric mid-frequency SNHL
Cookie-bite (U-shaped) sensorineural hearing loss — better at 250 Hz and 8000 Hz, worst at 500–2000 Hz

Cookie-bite (U-shaped) sensorineural hearing loss — better at 250 Hz and 8000 Hz, worst at 500–2000 Hz

🚨 Asymmetric SNHL — Red Flag for Vestibular Schwannoma

  • Definition: inter-ear difference >15 dB at 3 consecutive frequencies
  • 🚨 Red flag: retrocochlear pathology until proven otherwise
  • Investigation: MRI with gadolinium of internal auditory canals — gold standard
  • Vestibular schwannoma: slow-growing; management: active surveillance, stereotactic radiosurgery, or surgery
  • Associated symptoms: unilateral tinnitus, imbalance — may be absent early
  • 💎 Do not dismiss mild asymmetric loss in a young patient as 'insignificant'
Asymmetric SNHL — right ear normal-to-mild, left ear steeply sloping severe high-frequency loss (warrants retrocochlear workup)

Asymmetric SNHL — right ear normal-to-mild, left ear steeply sloping severe high-frequency loss (warrants retrocochlear workup)

Sudden Sensorineural Hearing Loss — Otologic Emergency

🚨 Emergency — Act Now
🚨
  • Definition: ≥30 dB hearing loss across 3 contiguous frequencies within 72 hours
  • Often idiopathic (~71–90%); possibly viral or vascular
  • 🚨 Must be distinguished from simple ear blockage — use Weber/Rinne tuning fork
  • Weber lateralises to GOOD ear (SNHL); do not reassure as 'blocked ear'
  • Urgent ENT referral and audiogram — same day/next day if possible

SSNHL — Treatment Protocol (AAO-HNS 2021)

🚨 Emergency — Act Now
🚨
  • Oral corticosteroids: prednisolone 1 mg/kg/day (max 60 mg) × 10–14 days with taper — start immediately if no contraindications
  • Treatment window: up to 4 weeks from onset (extended from prior guidance)
  • Intratympanic (IT) steroids: now offered as PRIMARY therapy when oral steroids contraindicated (diabetes, immunosuppression)
  • Salvage IT steroids: for patients who do not improve with oral therapy — refer to ENT
  • Imaging: MRI with gadolinium of IAC — NOT CT scan — to exclude retrocochlear cause
  • Do NOT delay treatment while awaiting imaging; start steroids and arrange urgent ENT

Cerumen Impaction — Recognition and Softening

  • Remove wax if symptomatic (hearing loss, otalgia, tinnitus) or obscuring TM view
  • Banji's test: sudden increase in sound after pulling pinna = positive for impaction (Sn 91.7%, Sp 87.1%)
  • First step for hard/impacted wax: cerumenolytic for 5–7 days (olive oil, sodium bicarbonate 5%, docusate sodium)
  • Do not attempt removal without softening hard impacted wax
  • Always examine TM after wax removal and document findings
Cerumen impaction partially obscuring the tympanic membrane

Cerumen impaction partially obscuring the tympanic membrane

Types of Cerumen

  • Dark impacted cerumen: completely occludes canal — common presentation
  • Golden-brown moist cerumen: partially occluding — responds well to syringing
  • Dry flaky cerumen: white/grey, friable — often amenable to microsuction or curette
  • Cerumen type influences removal technique choice
  • Always examine both ears — bilateral impaction is common
Otoscopic image of dark impacted cerumen completely occluding the external auditory canal

Otoscopic image of dark impacted cerumen completely occluding the external auditory canal

Cerumen Types — Moist and Dry

  • Moist (golden-brown): common in most ethnic groups; amenable to syringing after softening
  • Dry (flaky, grey): more common in East Asian populations due to ABCC11 gene variant
  • Dry cerumen less likely to cause impaction but can accumulate in hearing aid users
  • Contrast the two types to choose appropriate removal technique
  • Flaky dry cerumen: prefer microsuction or instrumentation over syringing
Otoscopic image of golden-brown cerumen partially occluding the external auditory canal

Otoscopic image of golden-brown cerumen partially occluding the external auditory canal

Dry Flaky Cerumen

  • White/grey, flaky, friable cerumen within the ear canal
  • More common in East Asian populations (ABCC11 gene variant)
  • Preferred removal: microsuction or gentle instrumentation — NOT syringing
  • Less likely to cause complete impaction compared to moist cerumen
  • Common in hearing aid users — recommend regular ENT or primary care follow-up for wax checks
Dry flaky cerumen within the external auditory canal (otoscopic view)

Dry flaky cerumen within the external auditory canal (otoscopic view)

Ear Syringing — Technique and Contraindications

  • Contraindications: TM perforation (current or past), prior ear surgery, active infection, cholesteatoma, organic FB, button battery, single hearing ear
  • Technique: body-temperature water; pull pinna up-and-back (adults) or down (children)
  • Direct water jet along postero-superior canal wall — NOT at TM directly
  • Stop immediately if patient reports pain
  • Post-procedure: examine TM and document; if fails, re-soften and retry or refer

Cerumen Removal Instruments

  • Wire loop curette: used under direct vision for hard wax pieces
  • Works best for wax adjacent to, but not touching, the TM
  • Brace hand against patient's head to prevent sudden movement injury
  • May cause epithelial tears — consider prophylactic antibiotic drops after instrumentation
  • Do not use blindly — requires good illumination (headlight or microscope)
Wire loop ear curette used for cerumen removal

Wire loop ear curette used for cerumen removal

Dry Mopping Technique

  • Jobson Horne probe with cotton wisp twisted onto tip
  • Used for aural toileting — removing debris and discharge from the canal
  • Absorbs moisture; clears canal for better visualisation
  • Essential first step before applying ear drops in OE
  • Also used post-irrigation to dry the canal and check TM
Wire loop curette with cotton wisp attached — gentle cerumen removal technique

Wire loop curette with cotton wisp attached — gentle cerumen removal technique

Post-Procedure: Retrieved Cerumen

  • Inspect retrieved wax/debris — confirms successful removal
  • Dark, hard wax: likely longstanding impaction
  • Document the procedure, technique used, and post-procedure TM appearance
  • If wax is mixed with blood or tissue — examine TM carefully for injury
  • Patient education: avoid cotton buds; ear canals are self-cleaning
Cotton wisp on instrument tip after cerumen removal — post-procedure appearance

Cotton wisp on instrument tip after cerumen removal — post-procedure appearance

Seniors' Mobility & Enabling Fund (SMF) — Hearing Aid Subsidy

💎 Clinical Pearl
  • Administered by Agency for Integrated Care (AIC); up to 90% subsidy on hearing aids
  • Eligibility: Singapore Citizen or PR aged ≥60; not in nursing/sheltered home; household per-capita monthly income ≤$4,800
  • Apply through restructured hospitals, polyclinics, or community hospitals
  • >99% of applicants approved; standard hearing aid costs ~$3,000–$3,200 before subsidy
  • 💎 Always counsel eligible patients — hearing aids reduce dementia risk and improve quality of life [AIC 2025; MOH 2024]

Foreign Body in the Ear — Approach

🚨 Emergency — Act Now
🚨
  • Attempt removal ONLY if: child is cooperative, object clearly visible and graspable
  • Live insect: kill first with olive oil or 2% lignocaine, then remove
  • Small smooth object (bead): irrigation — aim stream past object to flush out
  • Organic object (peanut, bean): NO irrigation — swells with water; use hook or loop
  • 🚨 Button battery: emergency — DO NOT irrigate; refer immediately for removal (liquefaction necrosis risk)
  • Cotton wool: crocodile forceps; if in doubt about any FB — refer

Key Summary

Key Point
🔑 Ear discharge: differentiate OE vs AOM perforation by sequence of pain and discharge; cholesteatoma = foul smell + marginal/attic perforation → mandatory ENT referral
Key Point
🔑 AOM in children: stratify by age and severity; watchful waiting 48–72h for ≥2 years, mild-moderate, unilateral AOM [AAP 2022]
Key Point
🔑 SSNHL is an otologic emergency: tuning fork test to distinguish from blocked ear; start prednisolone ≤4 weeks from onset; IT steroids as primary or salvage option [AAO-HNS 2021]
Key Point
🔑 Unilateral OME in adult or unilateral tinnitus/asymmetric SNHL → MRI and ENT referral (NPC / vestibular schwannoma)
Key Point
🔑 Vertigo: positional + fatigable nystagmus = BPPV → Epley; 5 D's or non-fatigable nystagmus = central → A&E
Key Point
🔑 Ear procedures: check contraindications before syringing; button battery = emergency; microsuction preferred in complex cases; counsel all eligible patients about SMF hearing aid subsidy

References

  • 1. American Academy of Pediatrics. Clinical Practice Guideline: The Diagnosis and Management of Acute Otitis Media. Pediatrics. 2013;131(3):e964–e999. Reaffirmed 2022.
  • 2. Lieberthal AS, et al. Watchful Waiting for Acute Otitis Media. Pediatrics. 2022;150(1):e2021055613.
  • 3. Stachler RJ, et al. Clinical Practice Guideline: Sudden Hearing Loss (Update). Otolaryngol Head Neck Surg. 2021;166(1_suppl):S1–S55.
  • 4. Agency for Integrated Care (AIC). Seniors' Mobility and Enabling Fund (SMF) — Mobility and Assistive Devices. www.aic.sg. Accessed March 2026.
  • 5. Ministry of Health Singapore. Statistics of Successful Applications by Seniors to AIC for Funding of Hearing Aids. 2024. www.moh.gov.sg.
  • 6. NICE Guideline NG98. Otitis Media with Effusion in Under 12s: Surgery. National Institute for Health and Care Excellence. 2023.
  • 7. Rosenfeld RM, et al. Clinical Practice Guideline: Otitis Media with Effusion (Update). Otolaryngol Head Neck Surg. 2016;154(1_suppl):S1–S41.
  • 8. Bhutta MF. Otomycosis: An Underdiagnosed Condition. J Laryngol Otol. 2022;136(1):1–6.
  • 9. Shargorodsky J, et al. Change in Prevalence of Hearing Loss in US Adolescents. JAMA. 2010;304(7):772–778.
  • 10. Livingston G, et al. Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission. Lancet. 2024;404(10452):572–628.
M122

Nose & Throat Conditions

Learning Objectives

  • 💎 Differentiate allergic vs vasomotor rhinitis and apply current treatment guidelines (ARIA 2024–25)
  • 💎 Recognise and manage acute bacterial rhinosinusitis — know when to use antibiotics
  • 💎 Approach epistaxis: distinguish anterior vs posterior bleeds and manage accordingly
  • 💎 Identify red flags in hoarseness requiring urgent ENT referral
  • 💎 Screen and manage obstructive sleep apnea in primary care, including newer therapies
  • 💎 Evaluate a neck mass — differentiate infection, inflammation, and malignancy

Rhinitis: Allergic vs Vasomotor

  • 💎 Allergic Rhinitis (AR): pale, grey, boggy mucosa — IgE-mediated, triggered by allergens (house dust mite, pollen)
  • 💎 Vasomotor Rhinitis (VMR): beefy red turbinates — non-allergic triggers (temperature, smoke, irritants)
  • 🚨 Rhinitis Medicamentosa: rebound swelling after >2 weeks of topical decongestant use — STOP the spray
  • 💎 AR Classification: Intermittent (<4 days/wk, <4 wks) vs Persistent (>4 days/wk, >4 wks)
  • 🚨 Red flags in children: unilateral symptoms, bloody discharge, CN signs → refer ENT

Allergic Rhinitis: Updated Treatment (ARIA 2024–25)

  • 💎 First-line: Intranasal corticosteroid (INCS) — most effective single agent for AR
  • 💎 Combination INCS + intranasal antihistamine (MP-AzeFlu / Dymista®) — superior to monotherapy for moderate-to-severe AR
  • 💎 Oral antihistamines for breakthrough symptoms, especially ocular/cutaneous features
  • 🚨 Avoid LTRAs (montelukast) as first-line in patients ≥15 yrs — less favourable benefit–risk profile
  • 💎 Severe CRS with nasal polyps (CRSwNP): dupilumab (biologic) — refer for specialist assessment
  • 💎 Immunotherapy (SCIT/SLIT) for moderate-to-severe AR poorly controlled by pharmacotherapy

Rhinosinusitis: Diagnosis & Antibiotic Stewardship

  • 💎 Diagnosis: ≥2 symptoms, one must be nasal blockage OR purulent discharge
  • 💎 Viral ARS (<10 days): symptomatic treatment only — no antibiotics
  • 🚨 ABRS suspected if: symptoms >10 days without improvement OR 'double worsening'
  • 🚨 EPOS 2020: Consider ABRS if ≥3 of 5 — unilateral discharge, severe pain, fever ≥38°C, double sickening, raised CRP/ESR
  • 💎 Even in ABRS: watchful waiting preferred for systemically well patients — antibiotics if unwell or risk factors
  • 🚨 Refer to ED: periorbital cellulitis, diplopia, meningismus — complications of sinusitis

Epistaxis

  • 💎 Most bleeds: anterior, from Kiesselbach's plexus (Little's area) — venous in young, arterial in elderly
  • 💎 First aid: pinch soft alar cartilage firmly, lean forward — hold for 10–15 minutes
  • 🚨 Posterior epistaxis: blood drains down pharynx, source not visible anteriorly — urgent ENT referral
  • 🚨 NPC red flags: epistaxis + unilateral hearing loss + neck mass + CN palsies → urgent workup
  • 💎 Assess haemodynamic stability first — posterior bleeds can be profuse

Hoarseness & Dysphonia

  • 🚨 REFER if hoarseness >2 weeks without apparent benign cause — rule out laryngeal carcinoma
  • 💎 Key red flags: dysphagia, hemoptysis, otalgia — especially in smokers/heavy drinkers
  • 💎 Vocal quality clues: breathiness → VC paralysis; worse in morning → LPR; worse later → myasthenia gravis
  • 🚨 Do NOT prescribe antibiotics or corticosteroids for dysphonia without laryngoscopy
  • 💎 Vocal hygiene: hydration, avoid irritants, voice rest — effective for benign lesions
  • 💎 VC paralysis: unilateral = breathy weak voice; bilateral = adducted cords + compromised airway

Foreign Body: Swallowed Fish Bone

  • 💎 Most common site: tonsil (31.8%) → pain at jaw/upper neck
  • 💎 Inspect systematically: tonsillar poles → tonsillo-lingual sulcus → valleculae
  • 🚨 Button batteries = emergency — chemical necrosis within hours — immediate removal
  • 💎 Laryngeal rocking test: pain on rocking thyroid cartilage → upper cervical esophagus impaction
  • 🚨 Non-contrast CT neck if no FB seen on exam or lateral X-ray — CT has replaced barium swallow
  • 🚨 Refer if: removal unsuccessful, rocking test positive, esophageal FB on imaging, chest pain/dysphagia

Obstructive Sleep Apnea (OSA)

  • 💎 Screen: loud snoring + witnessed apneas + EDS (ESS ≥10) — also fatigue/lack of energy
  • 💎 Severity: mild AHI 5–14, moderate 15–29, severe ≥30 events/hour
  • 💎 CPAP: first-line for moderate-to-severe OSA — pneumatic splint, reduces CV risk
  • 💎 Oral appliances (MAD): alternative for mild-to-moderate OSA or CPAP-intolerant patients
  • 🚨 Hypoglossal Nerve Stimulation (Inspire®): AHI 15–65, BMI <35, no complete concentric velum collapse on DISE
  • 💎 Lifestyle: weight loss, positional therapy, avoid alcohol/sedatives before sleep

Neck Masses: Evaluation in Adults

  • 🚨 Assume malignant until proven otherwise: duration ≥2 weeks, firm/hard, fixed, non-tender, >1.5 cm
  • 💎 Infection: tender, erythematous, warm, associated with URTI/dental — treat with amoxicillin-clavulanate
  • 🚨 Partial/no response to antibiotics → must exclude malignancy — refer for FNA
  • 💎 Midline mass that moves on swallowing or tongue protrusion → Thyroglossal Duct Cyst (TGDC)
  • 💎 Lateral soft cystic mass ± discharge history → Branchial Cleft Cyst — FNA to exclude malignancy
  • 💎 Ultrasound increasingly used as first-line imaging at point of referral before FNA

Key Takeaways

Key Point
💎 AR vs VMR: boggy pale mucosa vs beefy red — treat AR with INCS first; add MP-AzeFlu (Dymista) if insufficient
Key Point
💎 Sinusitis: antibiotics only for ABRS with systemic features — watchful waiting for most
Key Point
🚨 Epistaxis: pinch alae + lean forward; posterior bleed → urgent ENT
Key Point
🚨 Hoarseness >2 weeks = ENT referral to rule out malignancy
Key Point
💎 OSA: CPAP first-line; HNS (Inspire) for CPAP-intolerant (AHI 15–65, BMI <35)
Key Point
🚨 Neck mass: firm, non-tender, >2 weeks = malignant until proven otherwise → FNA

Key References

  • ARIA-EAACI Guidelines 2024–2025 Revision: Intranasal Treatments. Allergy. 2025. DOI:10.1111/all.70131
  • Rosenfeld RM et al. Clinical Practice Guideline (Update): Adult Sinusitis. Otolaryngol Head Neck Surg. 2015
  • Stachler RJ et al. Clinical Practice Guideline: Hoarseness (Dysphonia) Update. Otolaryngol HNS. 2018
  • Kapur VK et al. AASM Clinical Practice Guideline for Diagnostic Testing for Adult OSA. J Clin Sleep Med. 2017
  • AASM Manual for Scoring of Sleep and Associated Events, Version 3. AASM, 2023
  • Pynnonen MA et al. Clinical Practice Guideline: Evaluation of the Neck Mass in Adults. Otolaryngol HNS. 2017
M123

Acute Eye Conditions

Learning Objectives

  • 💎 Perform a structured ocular history and physical examination
  • 💎 Differentiate the key causes of the acute red eye
  • 💎 Identify ocular red flags requiring immediate referral
  • 💎 Describe initial management of Acute Angle-Closure Glaucoma
  • 💎 Recognise sudden visual disturbances — retinal detachment, optic neuritis, temporal arteritis
  • 💎 Understand when NOT to start treatment before specialist review (e.g., microbial keratitis)

Ocular Assessment: History Red Flags

  • 🚨 Pain, photophobia, acute blurring of vision — always serious
  • 🚨 Flashes and/or multiple new floaters → rule out retinal detachment
  • 🚨 Haloes around lights → suggests raised IOP (angle-closure glaucoma)
  • 🚨 Recent contact lens use or high-velocity trauma
  • 💎 Ask about DM, HTN, autoimmune disease, drug history (anticholinergics, chloroquine)
  • 💎 Occupation matters — grinding/hammering raises suspicion for penetrating injury

Ocular Examination: Key Steps

  • 💎 Visual acuity (Snellen) with and without pinhole — always first
  • 💎 Pupillary reactions: direct, consensual, swinging flashlight test for RAPD
  • 💎 Penlight: corneal clarity, ciliary flush, hypopyon, anterior chamber depth
  • 💎 Fluorescein staining with cobalt blue light to detect corneal defects
  • 💎 Evert upper eyelid to exclude subtarsal foreign body
  • 💎 Fundoscopy: optic disc, macula, vessels; check red reflex

Fundoscopic Findings

  • 💎 Diabetic maculopathy: hard exudates, microaneurysms, haemorrhages
  • 💎 Glaucoma: increased cup-to-disc ratio (>0.6 suspicious, >0.7 significant)
  • 💎 Dry AMD: drusen deposits (yellow-white spots) at the macula
  • 🚨 CRAO: pale retina + cherry-red spot + attenuated vessels — ocular emergency
  • 💎 Optic atrophy: pale disc — late sequela of optic neuritis or raised ICP
  • 💎 Post-PRP scars in treated proliferative diabetic retinopathy

Red Eye: Differential at a Glance

  • 💎 Conjunctivitis: diffuse redness, discharge, normal vision, normal pupil
  • 💎 Anterior Uveitis: ciliary flush, photophobia, small/irregular pupil
  • 🚨 Acute Angle-Closure Glaucoma: mid-dilated fixed oval pupil, hazy cornea, rock-hard globe
  • 🚨 Microbial Keratitis: corneal infiltrate/ulcer, contact lens history — do not start ABx
  • 💎 Scleritis: deep violaceous colour, boring pain, systemic disease association
  • 💎 Episcleritis: sectoral pink redness, self-limiting, sclera remains white

Conjunctivitis: Viral vs Bacterial vs Allergic

  • 💎 Viral (adenovirus): watery discharge, preauricular node, recent URTI — supportive Rx only
  • 💎 Bacterial: purulent sticky discharge, lids stuck in AM — topical chloramphenicol
  • 💎 Allergic: bilateral, intense itch, atopy history — antihistamine/mast cell stabiliser
  • 🚨 Neonatal purulent discharge: always suspect gonococcal/chlamydial — refer immediately
  • 💎 Quinolones reserved for severe bacterial cases or corneal involvement
  • 💎 Hygiene counselling essential for viral conjunctivitis (highly contagious)

Serious Red Eye: Uveitis & Pterygium

  • 🚨 Anterior Uveitis: perilimbal injection, dull aching pain, photophobia — urgent referral
  • 💎 Causes: idiopathic, ankylosing spondylitis, sarcoidosis, IBD, syphilis, TB, herpes
  • 💎 Tx: topical steroids + cycloplegics — not to be started in primary care without ophthalmologist
  • 💎 Pterygium: nasal fibrovascular growth onto cornea; lubricants for symptoms
  • 💎 Refer pterygium if encroaching on visual axis or growing rapidly
  • 💎 Scleritis: associated with RA, SLE, vasculitis — urgent referral + oral NSAIDs

Acute Angle-Closure Glaucoma: Initial Management

🚨 Emergency — Act Now
🚨
  • 🚨 Emergency: sudden severe eye pain, N&V, halos, mid-dilated fixed pupil, hazy cornea
  • 💎 Definitive Tx = Laser Peripheral Iridotomy (LPI) — arrange emergency transfer
  • 💎 While awaiting: Pilocarpine 2–4% drops (×2, q15 min) + Brimonidine 0.15% (×2, q15 min)
  • 💎 Systemic IOP reduction: Acetazolamide 500 mg PO (IV if nauseated)
  • 💎 Refractory IOP: IV Mannitol 25–50 g (20% solution)
  • 🚨 Treat fellow eye prophylactically with pilocarpine

Sudden Visual Disturbances

  • 🚨 New floaters + flashes + visual field curtain = retinal detachment until proven otherwise
  • 🚨 CRAO: pale retina + cherry-red spot — refer urgently (4–6 hour window)
  • 🚨 Temporal arteritis: >50 yrs, jaw claudication, headache — immediate high-dose steroids
  • 💎 PVD: benign age-related floaters; urgent dilated fundoscopy to exclude RD
  • 💎 Vitreous haemorrhage: sudden floaters/blobs — refer to exclude RD
  • 💎 Metamorphopsia (wavy vision): macular pathology — wet AMD or central serous retinopathy

Optic Neuritis & Anisocoria

  • 💎 Optic Neuritis triad: subacute unilateral visual loss + pain on eye movement + dyschromatopsia
  • 💎 Key sign: RAPD (Marcus Gunn pupil) — swinging flashlight test
  • 🚨 IV corticosteroids hasten recovery; oral prednisolone alone is CONTRAINDICATED
  • 🚨 Anisocoria in light (larger pupil abnormal): CN III palsy — rule out posterior communicating aneurysm
  • 🚨 Anisocoria in dark (smaller pupil abnormal) + neck pain: Horner's + carotid dissection — emergency
  • 💎 Optic atrophy (pale disc) is a late sign — develops weeks after acute optic neuritis

Key Summary

Key Point
🚨 Red Flags: severe pain, vision loss, photophobia, fixed mid-dilated pupil, hazy cornea, penetrating trauma, sudden floaters/flashes
Key Point
🚨 Do Not Miss: AACG, Microbial Keratitis, Retinal Detachment, Orbital Cellulitis, Temporal Arteritis
Key Point
💎 Exam Essentials: Visual acuity FIRST, pupillary reactions, fluorescein staining, lid eversion
Key Point
💎 Never start antibiotics before referral for microbial keratitis (scraping needed)
Key Point
💎 Never prescribe topical anaesthetics for home use
Key Point
💎 Safety net ALL patients: return immediately if pain worsens or vision deteriorates

References

  • Azari AA, Barney NP. Conjunctivitis. JAMA. 2013;310(16):1721-9.
  • Shah SM, Khanna CL. Ophthalmic Emergencies. Mayo Clin Proc. 2020;95(5):1050-1058.
  • Nguyen V, Lee GA. Microbial keratitis in general practice. Aust J Gen Pract. 2019;48(8):516-9.
  • Heath Jeffery RC et al. Unequal pupils. Aust J Gen Pract. 2019;48(1-2):39-42.
  • Gariano RF, Kim CH. Suspected retinal detachment. Am Fam Physician. 2004;69(7):1691-8.
  • UpToDate. Optic neuritis: Prognosis and treatment. Accessed July 2024.
  • Glaucoma Today. Management of AACG in an Emergent Setting. 2025 May-Jun.
M124

Eyelid Problems & Chronic Eye Conditions

Learning Objectives

  • 💎 Identify and differentiate common benign and malignant eyelid lesions
  • 💎 Apply a systematic approach to preseptal vs orbital cellulitis
  • 💎 Diagnose and manage dry eye disease and epiphora in primary care
  • 💎 Investigate binocular diplopia and cranial nerve palsies
  • 💎 Screen and refer patients with refractive errors, cataracts, and AMD
  • 💎 Recognise ocular manifestations of systemic diseases

Benign Eyelid Lesions

  • 💎 Cyst of Moll — blocked apocrine gland; dome-shaped, transilluminates (clear fluid)
  • 💎 Cyst of Zeis — blocked sebaceous gland; yellow oily content, does NOT transilluminate
  • 💎 Chalazion — granulomatous; painless nodule from blocked Meibomian duct
  • 💎 Molluscum contagiosum — Poxviridae; refer to ophthalmologist to prevent follicular conjunctivitis
  • 🚨 Red flags for malignancy: lid margin distortion, madarosis/poliosis, recurrent chalazion, ulceration, proptosis
Cyst of Moll (top-left), Cyst of Zeis (top-right), Chalazion (bottom-left), Molluscum contagiosum (bottom-right)

Cyst of Moll (top-left), Cyst of Zeis (top-right), Chalazion (bottom-left), Molluscum contagiosum (bottom-right)

Swollen Red Eyelid — Preseptal vs Orbital Cellulitis

  • 💎 Preseptal cellulitis: infection ANTERIOR to orbital septum — normal vision, pupils, and movements
  • 💎 Can be managed with oral antibiotics in reliable patients
  • 🚨 Orbital cellulitis: infection POSTERIOR to septum — MEDICAL EMERGENCY
  • 🚨 Features: pain on eye movement, proptosis, diplopia, reduced VA
  • 🚨 Immediate hospital referral for IV antibiotics and CT orbit
Diagnostic flowchart for swollen red eyelid evaluation and management

Diagnostic flowchart for swollen red eyelid evaluation and management

Dry Eye Disease — Causes & Approach

  • 💎 Three mechanisms: altered tear production, blink reflex failure, underlying corneal disease
  • 💎 Sjögren's syndrome — aqueous deficiency + xerostomia + autoimmune disease
  • 💎 Rosacea/blepharitis — lipid layer abnormality (Meibomian gland dysfunction)
  • 💎 Parkinson's disease — reduced blink frequency; Bell's palsy — lagophthalmos
  • 💎 Treatment: preservative-free artificial tears QDS; doxycycline 50mg/day for rosacea-MGD
  • 💎 Failure to respond → refer for punctal plugs or cautery

Watery Eyes (Epiphora)

  • 💎 Three mechanisms: reflex overproduction (most common), lacrimal pump failure, nasolacrimal obstruction
  • 💎 Dry eye → reflex tearing — paradoxical watery eye; treat the underlying dry eye
  • 💎 Ectropion / facial palsy → pump failure; surgical lid correction often required
  • 💎 Dacryocystitis — pain/swelling medial canthus; oral antibiotics → refer for DCR
  • 🚨 Congenital glaucoma — watery eye + photophobia + enlarged cornea in infants = EMERGENCY
Lacrimal drainage anatomy and causes of epiphora with management flowchart

Lacrimal drainage anatomy and causes of epiphora with management flowchart

Diplopia — Cranial Nerve Palsies

  • 💎 First step: monocular (ocular cause) vs binocular (neurological/muscular)
  • 💎 CN VI palsy — horizontal diplopia worse at distance and on lateral gaze
  • 💎 CN IV palsy — vertical diplopia; worse on downgaze; head tilt compensation
  • 💎 CN III palsy — ptosis, large exotropia; pupil involvement indicates aneurysm
  • 🚨 Painful CN III palsy + dilated pupil = posterior communicating artery aneurysm — NEUROSURGICAL EMERGENCY
  • 🚨 Headache + jaw claudication + CN palsy in elderly → Giant Cell Arteritis
Eye positions in different gaze directions for CN III, IV, and VI palsies

Eye positions in different gaze directions for CN III, IV, and VI palsies

Refractive Errors

  • 💎 Myopia (short-sighted) — focus anterior to retina; concave lens; typically school-age onset
  • 💎 Hyperopia (long-sighted) — focus posterior to retina; convex lens; risk of amblyopia if uncorrected
  • 💎 Astigmatism — rugby-ball shaped cornea; blurred at all distances
  • 💎 Presbyopia — universal age-related near vision loss from age ~40
  • 💎 Referral: VA < 6/9 in children, < 6/12 in adults, or 2-line difference between eyes
Diagram of emmetropia, myopia, hyperopia, and astigmatism with corrective lens effects

Diagram of emmetropia, myopia, hyperopia, and astigmatism with corrective lens effects

Myopia Control — Atropine Update 2024

  • 💎 Low-dose atropine slows myopia progression and axial elongation in children
  • 💎 ATOM2 (Singapore): 0.01% — minimal side effects, less rebound on cessation
  • 💎 LAMP 5-year trial (2024): 0.05% atropine superior for axial length control vs 0.01%
  • 💎 Most children required treatment restart after cessation at year 3
  • 💎 Current practice: 0.05% preferred for efficacy; 0.01% if minimising side effects is priority
  • 💎 Individualised decision-making recommended — discuss with paediatric ophthalmologist

Refractive Surgery Options (2026)

  • 💎 PRK/Trans-PRK — surface ablation; good for thin corneas; slower recovery
  • 💎 Bladeless LASIK — femtosecond flap + excimer ablation; rapid recovery; risk of dry eye & ectasia
  • 💎 SMILE (NEW) — lenticule extraction via small incision; no flap; better biomechanical stability; fewer dry eye symptoms
  • 💎 Phakic IOL (ICL) — reversible; for high myopia beyond laser range
  • 💎 Clear Lens Exchange — for presbyopia + high refractive error
  • 🚨 Contraindications: keratoconus, unstable refraction, active infection, severe dry eye

Gradual Visual Loss — Differential Diagnosis

  • 💎 Pinhole test: vision improves → likely refractive error
  • 💎 Absent red reflex → cataract (phacoemulsification + IOL when affecting QoL)
  • 💎 Asymptomatic disc cupping / field loss → POAG (refer for IOP and OCT)
  • 💎 Central vision loss + metamorphopsia + drusen → AMD (Amsler grid monitoring)
  • 🚨 Bitemporal hemianopia → pituitary lesion
  • 🚨 RAPD → unilateral optic nerve pathology

Age-Related Macular Degeneration (ARMD)

  • 💎 Dry AMD: drusen + geographic atrophy → gradual central vision loss
  • 💎 AREDS2 supplements (Vit C/E, lutein/zeaxanthin, zinc, copper) slow progression in intermediate-advanced dry AMD
  • 💎 2024 Update: AREDS2 also slows geographic atrophy (late dry AMD) by ~55% over 3 years
  • 🚨 Wet AMD: choroidal neovascularisation → sudden metamorphopsia → URGENT referral (within 1 week)
  • 🚨 Treatment: intravitreal anti-VEGF (ranibizumab, aflibercept, faricimab)
  • 💎 Home Amsler grid monitoring to detect early conversion from dry to wet
Extensive macular drusen in dry AMD

Extensive macular drusen in dry AMD

Wet AMD vs Dry AMD

  • 💎 Dry AMD: gradual central blurring, drusen on fundoscopy, geographic atrophy
  • 💎 Wet AMD: acute/subacute central loss, metamorphopsia, subretinal fluid/haemorrhage
  • 💎 Refer Advanced dry AMD within 1 month; Suspected wet AMD within 1 WEEK
  • 💎 Intermediate AMD: annual screening; consider AMD care pathway
  • 🚨 Any new metamorphopsia or sudden change in Amsler grid → urgent same-week referral
Disciform scar with subretinal haemorrhage in advanced wet AMD

Disciform scar with subretinal haemorrhage in advanced wet AMD

Diabetic Retinopathy — Fundoscopy

  • 💎 Screen T2DM at diagnosis; T1DM within 5 years of diagnosis
  • 💎 NPDR: microaneurysms → dot/blot haemorrhages → cotton wool spots → hard exudates
  • 💎 PDR: neovascularisation at disc (NVD) or elsewhere (NVE) → vitreous haemorrhage
  • 💎 Diabetic macular oedema — leading cause of vision loss in working-age adults; OCT diagnosis
  • 🚨 PDR or M1 maculopathy → urgent ophthalmology referral
  • 🚨 Good VA does NOT exclude sight-threatening retinopathy
Microaneurysms — earliest fundoscopic sign of non-proliferative diabetic retinopathy

Microaneurysms — earliest fundoscopic sign of non-proliferative diabetic retinopathy

Proliferative Diabetic Retinopathy

  • 💎 NVD (neovascularisation at disc) or NVE (elsewhere) = proliferative DR
  • 💎 Risk of vitreous haemorrhage and tractional retinal detachment
  • 💎 Treatment: pan-retinal photocoagulation (PRP) laser or intravitreal anti-VEGF
  • 🚨 Urgent ophthalmology referral — do not delay
  • 💎 Optimise glycaemic control, BP, and lipids to slow progression
Neovascularisation at the disc (NVD) — hallmark of proliferative diabetic retinopathy

Neovascularisation at the disc (NVD) — hallmark of proliferative diabetic retinopathy

The Eye in Systemic Disease

  • 💎 Thyroid Eye Disease: lid retraction, lid lag, proptosis, diplopia, compressive optic neuropathy
  • 💎 Uveitis (anterior): HLA-B27 spondyloarthropathies (AS), Behçet's, JIA
  • 💎 Hypertensive retinopathy: AV nipping, flame haemorrhages, cotton wool spots, papilloedema
  • 💎 Kayser-Fleischer rings → Wilson's disease
  • 💎 CMV retinitis — 'pizza pie' appearance in advanced immunocompromise
  • 🚨 Scleritis — severe boring pain + scleral oedema → often associated autoimmune disease
AV nipping at vessel crossing — hypertensive retinopathy

AV nipping at vessel crossing — hypertensive retinopathy

Glaucoma — Optic Disc Cupping

  • 💎 Primary Open-Angle Glaucoma (POAG) — chronic, insidious, often asymptomatic until late
  • 💎 Risk factors: family history, elevated IOP, older age, myopia, African ethnicity
  • 💎 Fundoscopy: increased cup-to-disc ratio (>0.6), asymmetry between eyes, disc notching
  • 💎 Visual field defects: arcuate scotoma, nasal step
  • 🚨 Refer if C/D > 0.6, asymmetry ≥ 0.2, or suspicious disc regardless of IOP
  • 💎 Annual screening recommended for at-risk patients >40 years
Progressive cup-to-disc ratio enlargement from normal (0.2) to advanced glaucoma (0.99)

Progressive cup-to-disc ratio enlargement from normal (0.2) to advanced glaucoma (0.99)

Other Fundoscopy Findings

  • 💎 CRAO: cherry-red spot + pale retina + attenuated vessels → sudden painless visual loss
  • 💎 CRVO: disc swelling + tortuous dilated veins + flame haemorrhages in all 4 quadrants
  • 💎 Papilloedema: blurred disc margins + peripapillary haemorrhages → raised ICP until proven otherwise
  • 💎 Retinal detachment: pale elevated retinal folds → flashing lights + floaters + curtain visual loss
  • 🚨 All of the above = SAME-DAY emergency ophthalmology referral
  • 💎 Retinitis pigmentosa: bone-spicule pigmentation + vessel attenuation + night blindness
Cherry-red spot at the macula with pale retina — central retinal artery occlusion (CRAO)

Cherry-red spot at the macula with pale retina — central retinal artery occlusion (CRAO)

Key Summary

Key Point
🚨 Orbital cellulitis (pain on movement, proptosis, reduced VA) = immediate hospital referral
Key Point
🚨 Painful CN III palsy + dilated pupil = aneurysm until proven otherwise — neurosurgical emergency
Key Point
🚨 New metamorphopsia / sudden central vision change = wet AMD — refer within 1 WEEK
Key Point
💎 Dry eye: artificial tears QDS; doxycycline for rosacea-MGD; refer if persistent
Key Point
💎 DR screening: T2DM at diagnosis; T1DM within 5 years — good VA does NOT exclude PDR
Key Point
💎 Myopia control: 0.05% atropine superior efficacy (LAMP 2024); 0.01% if SE minimisation preferred

Key References

  • Sun MT et al. Eyelid lesions in general practice. Aust J Gen Pract. 2019;48(8):509-514.
  • Carlisle RT, Digiovanni J. Differential diagnosis of the swollen red eyelid. Am Fam Physician. 2015;92(2):106-12.
  • Yam JC et al. LAMP 5-year trial — 0.05% atropine for myopia. Ophthalmology. 2024 Mar.
  • Keenan TDL et al. AREDS2 slows geographic atrophy. Ophthalmology. 2024 Jul.
  • SIDRP — SERI-NHGEI AMD Referral Criteria Guidelines (local Singapore guidelines).
  • Cochrane GM et al. Management of refractive errors. BMJ. 2010;340:c1171.

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