PULMONOLOGY — CASE-BASED CLINICAL SCENARIOS

CASE 1 — WHAT WENT WRONG?

1. What is the diagnosis?
2. What went wrong in the management?
3. What is the correct approach to oxygen therapy in this condition?

1. Acute exacerbation of COPD with hypercapnic (Type II) respiratory failure.
2. High-flow O₂ was given inappropriately — in chronic hypercapnic COPD patients, high FiO₂ blunts the hypoxic drive and worsens CO₂ retention (hypercapnic coma). Controlled oxygen supplementation was not used.
3. Controlled oxygen at 24–28% via Venturi mask targeting SpO₂ 88–92%; add non-invasive ventilation (NIV/BiPAP) if acidosis persists; continue short-acting bronchodilators, systemic corticosteroids, and antibiotics. (Fishman's Pulmonary Diseases)

CASE 2 — WHAT WENT WRONG?

1. What is the diagnosis?
2. What went wrong in the management?
3. What is the correct treatment?

1. Acute severe / near-fatal asthma (PEFR <50%, SpO₂ <92%, unable to complete sentences = severe; silent chest/altered consciousness = life-threatening).
2. Only one nebulization was given; patient was discharged without reassessment or hospitalization. Near-fatal asthma requires ICU admission, not discharge.
3. Admit to HDU/ICU; continuous back-to-back salbutamol nebulization + ipratropium, IV magnesium sulfate (2g over 20 min), IV hydrocortisone, controlled O₂, and consider mechanical ventilation if deteriorating. (ROSEN's Emergency Medicine; Fishman's Pulmonary Diseases)

CASE 3 — WHAT WENT WRONG?

1. What is the correct diagnosis?
2. What went wrong in the management?
3. What is the immediate treatment?

1. Tension pneumothorax (primary spontaneous pneumothorax progressing to tension).
2. Diagnosis was missed — the classic triad (absent breath sounds, hyperresonance, tracheal deviation) and hypotension were ignored; no chest imaging was done; analgesics were given instead of emergency decompression.
3. Immediate needle thoracostomy (2nd intercostal space, mid-clavicular line) as a temporizing measure, followed by chest tube insertion (tube thoracostomy). Do NOT wait for imaging if hemodynamically unstable. (ROSEN's Emergency Medicine)

CASE 4 — WHAT WENT WRONG?

1. What type of effusion was this actually, and what does it indicate?
2. What went wrong in the management?
3. What is the correct next step?

1. Exudative effusion by Light's criteria (pleural protein/serum protein >0.5; pleural LDH/serum LDH >0.6). This indicates a cause other than pure heart failure — likely parapneumonic effusion or malignancy.
2. The effusion was misclassified as transudative; the exudative biochemistry was ignored. No further workup (cytology, cultures, pH) was done to identify the cause.
3. Repeat thoracentesis with pleural fluid culture, cytology, and pH. A pH <7.2 suggests complicated parapneumonic effusion requiring chest tube drainage. Treat underlying infection with antibiotics. (Murray & Nadel's Textbook of Respiratory Medicine; Harrison's Principles)

CASE 5 — WHAT WENT WRONG?

1. What is the diagnosis now?
2. What went wrong in the initial management?
3. What is the correct management?

1. Severe CAP complicated by septic shock / respiratory failure.
2. A CURB-65 score ≥3 indicates high severity and mandates hospital admission ± ICU — outpatient oral monotherapy was inappropriate for this risk category. Inadequate coverage (amoxicillin alone misses atypical pathogens).
3. ICU admission; IV broad-spectrum antibiotics (β-lactam + macrolide, or respiratory fluoroquinolone); aggressive fluid resuscitation; supplemental oxygen with preparation for mechanical ventilation; blood and sputum cultures before antibiotics. (Harrison's Principles; Murray & Nadel's Textbook)

• Case 1: COPD exacerbation + oxygen toxicity
• Case 2: Acute severe asthma
• Case 3: Tension pneumothorax
• Case 4: Pleural effusion misclassification (Light's criteria)
• Case 5: Pneumonia severity scoring (CURB-65)

PULMONOLOGY — PG-LEVEL CASE-BASED SCENARIOS

CASE 6 — WHAT WENT WRONG?

1. What is the diagnosis and risk stratification?
2. What went wrong in the management?
3. What is the correct treatment strategy?

1. Massive (high-risk) pulmonary embolism — defined by haemodynamic instability (systolic BP <90 mmHg), extensive bilateral thrombus, and RV dysfunction (RV:LV ratio >1 on CT). Accounts for 5–10% of PE cases with highest mortality risk.
2. LMWH anticoagulation alone is insufficient for massive PE — systemic thrombolysis (or surgical embolectomy if thrombolysis is contraindicated) is the treatment of choice. The haemodynamic compromise and RV failure required urgent reperfusion, not just anticoagulation.
3. Systemic thrombolysis with alteplase (tPA) 100 mg IV over 2 hours is indicated for haemodynamically unstable massive PE. If thrombolysis fails or is contraindicated, consider catheter-directed thrombolysis or surgical pulmonary embolectomy. Unfractionated heparin (UFH) should accompany or follow thrombolysis (not LMWH, due to need for hour-to-hour control). Resuscitation with vasopressors, cautious fluids (avoid RV overload), and ICU monitoring are mandatory.

Reference: Harrison's Principles of Internal Medicine, 22E — Chapter 290, "Pulmonary Embolism"; classification of massive PE and anticoagulation strategies, pp. 2202–2206. Sabiston Textbook of Surgery, "Acute Pulmonary Embolism", Chapter 27.

CASE 7 — WHAT WENT WRONG?

1. What is the diagnosis?
2. What went wrong in the ventilation strategy?
3. What is the correct approach?

1. Severe ARDS (PaO₂/FiO₂ ≤100 mmHg; bilateral infiltrates; non-cardiogenic; onset within 7 days of insult — Berlin definition 2012). Pancreatitis is a known indirect cause of ARDS.
2. TV of 10 mL/kg actual body weight is volutrauma — in ARDS, ventilation must use 6 mL/kg of predicted body weight (PBW) with plateau pressure <30 cmH₂O. High TV causes barotrauma/volutrauma to the small remaining aerated ("baby lung") regions. PEEP of 5 cmH₂O was also suboptimal for severe ARDS.
3. Lung-protective ventilation: TV 6 mL/kg PBW, plateau pressure ≤30 cmH₂O, titrate PEEP (higher PEEP tables for severe ARDS). Target pH >7.25 with permissive hypercapnia if needed. Prone positioning (>16 hours/day) for PaO₂/FiO₂ <150. Consider ECMO if refractory. Manage bilateral pneumothoraces with chest drains. This strategy (ARMA trial, ARDS Network) reduced mortality from 40% to 30%.

Reference: Miller's Anesthesia, 10E — "Acute Respiratory Distress Syndrome and Lung-Protective Ventilation", Chapter 79, pp. 11884–11886. Harrison's Principles, 22E — Berlin definition of ARDS.

CASE 8 — WHAT WENT WRONG?

1. What is the most likely diagnosis?
2. What went wrong in management?
3. What is the correct treatment?

1. Idiopathic Pulmonary Fibrosis (IPF) — the HRCT pattern of subpleural basal honeycombing with traction bronchiectasis is a UIP (Usual Interstitial Pneumonia) pattern, which is diagnostic of IPF when consistent clinical context is present (age >60, non-smoker, progressive restriction, bilateral Velcro crackles, clubbing).
2. IPF does not respond to corticosteroids — this is a critical and common error. High-dose steroids are not only ineffective in IPF but cause significant systemic harm. IPF is characterized by progressive irreversible fibrosis, not reversible inflammation. Steroids are reserved for other ILDs like NSIP or hypersensitivity pneumonitis.
3. Antifibrotic therapy: Nintedanib (a tyrosine kinase inhibitor) or Pirfenidone (inhibits TGF-β-mediated fibrosis) — both slow the rate of FVC decline. Refer for lung transplant evaluation in eligible patients. Pulmonary rehabilitation, supplemental O₂, and management of comorbidities (pulmonary hypertension, GERD) are important adjuncts. Avoid steroids unless co-existing inflammatory component is confirmed.

Reference: Fishman's Pulmonary Diseases and Disorders, 2E — "Idiopathic Pulmonary Fibrosis"; nintedanib and pirfenidone evidence. Murray & Nadel's Textbook of Respiratory Medicine — "Usual Interstitial Pneumonia", UIP pattern HRCT criteria. Goldman-Cecil Medicine — "Histopathologic Features of UIP", nintedanib/pirfenidone RCTs.

CASE 9 — WHAT WENT WRONG?

1. What is the diagnosis?
2. What went wrong in the management?
3. What is the correct treatment?

1. Ventilator-Associated Pneumonia (VAP) caused by MRSA — defined as pneumonia developing ≥48 hours after endotracheal intubation, with a new or progressive infiltrate plus clinical features (fever, purulent secretions, leukocytosis).
2. Two errors: (a) Initial empirical antibiotic choice — ceftriaxone has no MRSA coverage and is inappropriate for late-onset VAP (>4 days) where multi-drug-resistant organisms (MRSA, Pseudomonas, Acinetobacter) are expected. (b) Failure to de-escalate or escalate antibiotics based on culture results despite MRSA identification — this constitutes inadequate targeted therapy and risks clinical failure, resistance, and mortality.
3. Switch to vancomycin (IV, targeting trough 15–20 mg/L or AUC 400–600) or linezolid (may have superior lung penetration for MRSA VAP). De-escalate after clinical improvement and culture sensitivity. Duration: 7–8 days is sufficient for uncomplicated VAP. Non-pharmacological VAP prevention: elevate head of bed 30–45°, oral chlorhexidine, minimize sedation, ventilator weaning protocol.

Reference: Harrison's Principles of Internal Medicine, 22E — Hospital-acquired and Ventilator-Associated Pneumonia chapter. Murray & Nadel's Textbook of Respiratory Medicine — "Diagnostic Approach", nosocomial pneumonia management.

CASE 10 — WHAT WENT WRONG?

1. What was the diagnostic error?
2. What went wrong in the management?
3. What is the correct diagnostic algorithm?

1. V/Q scan is not the first-line imaging in PE — it is a second-line test (used when the patient cannot tolerate IV contrast). In COPD patients, V/Q scans are frequently non-diagnostic/indeterminate due to underlying ventilation abnormalities, making them particularly unreliable.
2. Two major errors: (a) CT pulmonary angiography (CTPA) should have been the primary imaging modality — it provides direct visualization of thrombus, assesses RV size, and identifies alternative diagnoses. (b) A patient with high clinical probability (Wells ≥5) and hemodynamic instability should receive immediate anticoagulation (UFH) while awaiting imaging — withholding anticoagulation for 12 hours was dangerous. Anticoagulation is indicated if PE probability is high and bleeding risk is acceptable, even before imaging confirmation.
3. Correct algorithm (per Harrison's 22E): For high clinical likelihood (Wells >4) → skip D-dimer → go directly to CTPA. If CTPA confirms PE → risk stratify → if haemodynamically unstable (massive PE) → systemic thrombolysis or embolectomy. McConnell's sign on echo (RV free wall hypokinesis + hyperkinetic apex) is highly specific for acute PE and should prompt emergency action while CTPA is being arranged.

Reference: Harrison's Principles of Internal Medicine, 22E — "Pulmonary Embolism", Wells score algorithm, CTPA as first-line imaging, McConnell's sign, pp. 2202–2209 (Chapter 290). Harrison's 22E also describes V/Q scanning as second-line: "used mostly for patients who cannot tolerate intravenous contrast."

Quick Reference Summary

PULMONOLOGY — MISDIAGNOSIS CASES (PG Level)

CASE 11 — THE GREAT MASQUERADER

1. What was the misdiagnosis?
2. What is the correct diagnosis, and what clue was missed?
3. How should the diagnostic workup be revised?

1. Misdiagnosis: Acute decompensated heart failure. The bilateral infiltrates, elevated BNP, and leg oedema led the team to anchor on CHF without considering an alternative.
2. Correct diagnosis: Pulmonary embolism (PE) superimposed on CHF. The critical clue: "when occult PE occurs concomitantly with overt CHF or pneumonia, clinical improvement often fails to ensue despite standard medical treatment of the concomitant illness" — this is the hallmark PE warning in Harrison's. Additional clues: recent immobility post-orthopedic surgery (major VTE risk factor), persistent tachycardia despite diuresis, and SpO₂ not improving despite fluid offload. BNP elevation in PE is due to RV strain, not LV failure — it does not reliably distinguish the two.
3. Calculate Wells score (recent surgery + immobility = 1.5; tachycardia = 1.5; alternative diagnosis less likely = 3 → score >4, high probability). Skip D-dimer in high probability; proceed directly to CT pulmonary angiography (CTPA). Check lower limb doppler for DVT. If confirmed PE → anticoagulation ± risk-stratified escalation.

Reference: Harrison's Principles of Internal Medicine 22E — "PE is known as 'the great masquerader.' Diagnosis is difficult because symptoms and signs are nonspecific... When occult PE occurs concomitantly with overt CHF or pneumonia, clinical improvement often fails to ensue." Chapter 290, p. 2202. Wells PE Clinical Decision Rule, Table 290-2.

CASE 12 — THE RECURRING CONSOLIDATION

1. What is the misdiagnosis?
2. What is the correct diagnosis?
3. What are the key diagnostic clues, and what should have been done?

1. Misdiagnosis: Recurrent community-acquired pneumonia. Antibiotics were started empirically each time without questioning why the same lobe was repeatedly affected.
2. Correct diagnosis: Obstructive pneumonia secondary to endobronchial lung carcinoma. A centrally obstructing tumour prevents drainage of a lung segment, leading to recurrent post-obstructive pneumonia in the same anatomical location. This is a classic presentation of central (endobronchial) lung cancer.
3. Key clues: (a) Same lobe each time — recurrent consolidation in the same segment is a red flag; true recurrent CAP almost never recurs in an identical location. (b) Weight loss — a B-symptom strongly suggesting malignancy. (c) Heavy smoking history — high prior probability of lung cancer. The correct step after the first non-resolving or recurrent same-lobe pneumonia is a post-treatment CXR at 6 weeks to confirm clearance. Persistent or recurrent opacity demands CT thorax, followed by bronchoscopy and biopsy to exclude malignancy. PET-CT for staging if malignancy confirmed.

Reference: Murray & Nadel's Textbook of Respiratory Medicine — Obstructive pneumonia as a presentation of central endobronchial tumours; post-treatment radiographic follow-up in pneumonia. Goldman-Cecil Medicine — Lung cancer presentations.

CASE 13 — THE FARMER'S "ASTHMA"

1. What was the misdiagnosis?
2. What is the correct diagnosis?
3. What are the distinguishing features, and what is the management?

1. Misdiagnosis: Bronchial asthma. The episodic breathlessness was labelled as asthma without considering the occupational exposure history, spirometry pattern, or systemic features (fever, bilateral nodular infiltrates).
2. Correct diagnosis: Acute/subacute Hypersensitivity Pneumonitis (HP) — also called extrinsic allergic alveolitis. Exposure to thermophilic actinomycetes in stored hay (Farmer's Lung) or avian proteins (Bird Fancier's Lung) causes immune-mediated alveolar inflammation 4–8 hours post-exposure.
3. Key distinguishing features:
   • Asthma: obstructive spirometry, improves with bronchodilators, no fever, no infiltrates.
   • HP: restrictive spirometry + reduced DLCO, fever, bilateral infiltrates, work-relatedness (worse at work, better on days off).
   • Per Goldman-Cecil's occupational misdiagnosis table: "Symptoms typically resolve within days and recur on re-exposure to the same trigger — acute HP can be misdiagnosed as acute viral respiratory illness or pneumonia."
   • Management: Remove antigen exposure (primary treatment). Acute/severe: systemic corticosteroids (prednisolone 40–60 mg/day, tapered over 4–6 weeks). Chronic HP with fibrosis: antifibrotics may be considered. Occupational history is mandatory in all respiratory patients.

Reference: Goldman-Cecil Medicine — Table 10: "Examples of Occupational Respiratory Diseases That Could Be Misdiagnosed as Common Non-occupational Respiratory Disease" — Acute HP listed as misdiagnosed as asthma/viral pneumonia. Goldman-Cecil Medicine International Edition, Chapter on Occupational Lung Disease.

CASE 14 — THE "ASTHMATIC" WITH THE FIXED WHEEZE

1. What was the misdiagnosis?
2. What is the correct diagnosis?
3. What specific findings confirm the correct diagnosis, and what is the management?

1. Misdiagnosis: Late-onset bronchial asthma. The key errors: failing to recognize that asthma produces a polyphonic, expiratory wheeze that varies; not investigating a fixed unilateral wheeze; and dismissing an abnormal flow-volume loop.
2. Correct diagnosis: Upper airway/central airway obstruction — e.g., tracheal stenosis, subglottic tumour, or extrinsic tracheal compression (goitre, mediastinal mass). A fixed extrathoracic obstruction produces characteristic features that are entirely unlike asthma.
3. Confirming features:
   • Fixed monophonic wheeze — same pitch and location, unlike variable polyphonic asthma wheeze.
   • Louder over the trachea than the chest — indicates central, not peripheral airway obstruction.
   • Flow-volume loop: plateau (truncation) of BOTH inspiratory AND expiratory curves — the hallmark of a fixed large airway obstruction. In asthma, only the expiratory curve is affected (variable intrathoracic obstruction).
   • Spirometry non-responsive to bronchodilators.
   • Next step: CT neck and thorax to identify structural cause; flexible bronchoscopy for direct visualisation and biopsy if needed.
   • Management depends on cause: tracheal dilation, endobronchial stenting, surgical resection, or treatment of goitre/mediastinal mass.

Reference: Murray & Nadel's Textbook of Respiratory Medicine — Upper airway obstruction and flow-volume loop interpretation. Fishman's Pulmonary Diseases and Disorders — Differential diagnosis of wheeze; fixed vs. variable airway obstruction patterns.

CASE 15 — THE "PNEUMONIA" WITH BILATERAL HILAR SHADOWS

1. What was the misdiagnosis?
2. What is the correct diagnosis?
3. What investigations confirm it, and why was the initial diagnosis wrong?

1. Misdiagnosis: Pulmonary Tuberculosis. TB was assumed based on constitutional symptoms and hilar shadows, without confirming microbiological evidence or considering alternative diagnoses.
2. Correct diagnosis: Sarcoidosis — a multisystem granulomatous disease of unknown aetiology characterised by non-caseating granulomas. Classic presentation: young adult (often Black African or Northern European), bilateral symmetric hilar lymphadenopathy, erythema nodosum, dry cough, negative TB workup.
3. Why TB was wrong:
   • TB hilar adenopathy is typically unilateral or asymmetric; bilateral symmetric BHL strongly favours sarcoidosis.
   • Negative Mantoux and negative AFB smears ×3 argue against TB.
   • Erythema nodosum + BHL = Löfgren's syndrome — a specific clinical diagnosis of sarcoidosis (benign, self-limiting form).
   • Anti-TB drugs are unnecessary and potentially harmful in sarcoidosis.
   Confirming investigations:
   • Serum ACE (elevated in ~60% of sarcoidosis).
   • Serum calcium (hypercalcaemia due to extrarenal 1,25-OH vitamin D production by granulomas).
   • HRCT thorax (BHL ± perilymphatic nodules).
   • Tissue biopsy (bronchoscopy with BAL + transbronchial biopsy, or EBUS-TBNA): non-caseating epithelioid granulomas without AFB = confirms sarcoidosis.
   • Management: Löfgren's syndrome often resolves spontaneously — NSAIDs for erythema nodosum, systemic corticosteroids only if symptomatic or organ-threatening disease.

Reference: Goldman-Cecil Medicine — Table 10: "Sarcoidosis" listed as a disease that can be misdiagnosed as silicosis or beryllium disease (and vice versa) based on occupational and exposure history; bilateral hilar lymphadenopathy differential. Harrison's Principles of Internal Medicine 22E — Sarcoidosis: Chapter on Granulomatous Pulmonary Disease; Löfgren's syndrome.

Summary Table

PULMONOLOGY MISDIAGNOSIS QUIZ

UG Senior / Intern Level

CASE A — THE FEVER THAT WOULDN'T BREAK

1. What was the misdiagnosis, and why was it wrong?
2. What is the correct diagnosis?
3. What is the pathognomonic sign and how is it formed?
4. What is the treatment?

1. Misdiagnosis: Typhoid fever. Typhoid does not cause bilateral pulmonary infiltrates, thrombocytopenia, or the characteristic skin lesion. Failure to fully undress and examine the patient is a critical error — the eschar was missed.
2. Correct diagnosis: Scrub typhus — caused by Orientia tsutsugamushi, transmitted by the larval stage (chigger) of the trombiculid mite. Found predominantly in the "scrub typhus triangle": South Asia, China, Southeast Asia, Indonesia.
3. Eschar — the pathognomonic sign. It forms at the site of the chigger bite: the organism causes local tissue necrosis → a painless black crusted ulcer with a red halo. Common hidden sites: axilla, groin, behind ears, scalp, skin folds. Not always present (reported in ~50–80% of cases), but when found, it clinches the diagnosis.
4. Doxycycline 100 mg twice daily for minimum 7 days (until ≥3 days afebrile). Alternative in pregnancy/children: Azithromycin 500 mg daily for 3 days. Doxycycline is the first choice for virtually all rickettsial infections. Prompt treatment causes rapid defervescence — diagnostic in itself.

Reference: Brenner & Rector's The Kidney — "Scrub typhus: high fever, skin rash, headache, myalgia, lymphadenopathy... a typical eschar occurs at the site of the bite." Sherris Medical Microbiology — Orientia tsutsugamushi. Dermatology 5E — Treatment of rickettsial diseases, Table 76.3.

CASE B — THE ESCHAR THAT CRIED WOLF

1. What is the complete diagnosis?
2. Why is the P/F ratio important here, and what does it indicate?
3. What went wrong in the management?
4. What is the correct treatment?

1. Scrub typhus complicated by ARDS (Scrub ARDS) — Orientia tsutsugamushi infection causing severe systemic vasculitis, increased alveolar-capillary permeability, and non-cardiogenic pulmonary oedema meeting ARDS criteria. This is a life-threatening complication and a major cause of death in scrub typhus. The groin eschar was the diagnostic clue.
2. P/F ratio (PaO₂/FiO₂) = 86 → Severe ARDS by Berlin definition (2012):
   • Mild ARDS: P/F 201–300
   • Moderate ARDS: P/F 101–200
   • Severe ARDS: P/F ≤100 All measured with PEEP ≥5 cmH₂O. Bilateral infiltrates not explained by cardiac failure = fulfils ARDS criteria.
3. The underlying cause — scrub typhus — was not identified or treated. Starting antibiotics without doxycycline is ineffective. Standard antibiotics do not cover intracellular organisms like O. tsutsugamushi.
4. Two-track treatment:
   • Treat scrub typhus: Doxycycline 100 mg IV/BD urgently — this is the single most important step. Rapid defervescence expected within 24–48 hours.
   • Manage ARDS: Lung-protective mechanical ventilation — tidal volume 6 mL/kg predicted body weight, plateau pressure <30 cmH₂O, titrated PEEP, permissive hypercapnia (pH >7.25 acceptable). Prone positioning if P/F <150. Vasopressors for shock.

Reference: Brenner & Rector's Kidney — "Severe disease is characterized by ARDS, AKI, bleeding, coagulation disorders, meningoencephalitis, and shock. Respiratory distress and encephalitis are the major causes of death." Current Surgical Therapy 14E — Berlin Definition ARDS, Box 1 (P/F ratios and PEEP criteria). Dermatology 5E — Doxycycline treatment, Table 76.3.

CASE C — BREATHLESS ON THE WARD

1. What was misdiagnosed as post-op pain?
2. Name three specific risk factors for this diagnosis present in this patient.
3. What simple bedside score would have flagged this immediately?
4. What is the emergency treatment?

1. Pulmonary embolism (PE). Pleuritic chest pain + sudden onset dyspnoea post-orthopaedic surgery = PE until proven otherwise. This is haemodynamically unstable → Massive PE.
2. Three risk factors (Virchow's triad):
   • Venous stasis: prolonged immobility post-surgery
   • Endothelial injury: surgical trauma to vessels
   • Hypercoagulability: post-surgical prothrombotic state Additional: orthopaedic lower limb surgery is one of the highest VTE risk surgical procedures.
3. Wells PE Score — tachycardia (1.5) + immobility/surgery (1.5) + alternative diagnosis less likely than PE (3.0) = score >6 = high probability. No D-dimer needed at high probability — go directly to CTPA (or echo/treat empirically if haemodynamically unstable).
4. Massive PE emergency treatment:
   • Immediate IV unfractionated heparin (UFH) bolus
   • Systemic thrombolysis: Alteplase (tPA) 100 mg IV over 2 hours — drug of choice for haemodynamically unstable PE
   • If thrombolysis fails/contraindicated: surgical pulmonary embolectomy or catheter-directed therapy
   • Vasopressors (noradrenaline) for shock; cautious IV fluids (avoid RV overload)

Reference: Harrison's Principles of Internal Medicine 22E — Wells PE score (Table 290-2), PE masquerader, haemodynamic classification; anticoagulation and thrombolysis strategies, Chapter 290.

CASE D — THE WHEEZE THAT DIDN'T RESPOND

1. What was misdiagnosed as asthma?
2. What does the flow-volume loop finding tell you?
3. What occupational disease must be considered given his work history?
4. What is the next investigation?

1. Fixed large airway (central airway) obstruction — likely from extrinsic tracheal compression or endobronchial lesion. This was misdiagnosed as asthma because of wheeze, but asthma produces: polyphonic expiratory wheeze, obstructive spirometry, bronchodilator response — none of which were present here.
2. Truncation (plateau) of BOTH inspiratory AND expiratory limbs of the flow-volume loop = Fixed upper/central airway obstruction. In asthma: only the expiratory curve is affected (variable intrathoracic obstruction). A fixed obstruction behaves the same in both breathing phases — a classic differentiating sign.
3. Silicosis — 15-year exposure to granite (crystalline silica) dust in a quarry. Silicosis causes progressive massive fibrosis, upper lobe nodular opacities, and predisposes to TB. It could also mimic IPF and would appear on Goldman-Cecil's list of occupational diseases misdiagnosed as non-occupational ILD.
4. CT thorax (to assess tracheal/bronchial pathology and parenchymal lung) + flexible bronchoscopy for direct visualisation and biopsy. Also: CXR for silicotic nodules (upper lobe, "eggshell" hilar calcification). HRCT for lung parenchyma if silicosis suspected.

Reference: Murray & Nadel's Respiratory Medicine — Fixed large airway obstruction and flow-volume loop interpretation. Goldman-Cecil Medicine — Occupational misdiagnosis table: silicosis misdiagnosed as IPF or sarcoidosis.

CASE E — KEPT GOING BACK FOR THE SAME COUGH

1. What is the misdiagnosis, and what is the correct diagnosis?
2. What does the supraclavicular swelling and hoarseness suggest?
3. Why does the same lobe keep getting infected?
4. List the investigations in order.

1. Misdiagnosis: Recurrent CAP. Correct diagnosis: Central (endobronchial) lung carcinoma causing post-obstructive pneumonia. In true recurrent CAP, consolidation rarely recurs in the exact same anatomical segment. Recurrence in the same lobe = red flag for an obstructing lesion.
2. • Right supraclavicular lymphadenopathy = likely N3 nodal metastasis (Virchow's-equivalent in lung cancer staging) → advanced/metastatic disease
   • Hoarseness = involvement of the left recurrent laryngeal nerve (loops around aortic arch) by mediastinal spread → suggests mediastinal invasion, often from a right-sided tumour with lymph node compression
3. A central tumour obstructs a bronchus → mucus and secretions accumulate distally → bacteria colonise the stagnant pool → post-obstructive pneumonia recurs in the same segment every time antibiotics clear the infection, but the obstruction remains.
4. Investigations in order:
   • CXR (compare all three — same lobe!)
   • CT thorax + abdomen + pelvis with contrast (assess tumour, nodes, distant metastases)
   • Flexible bronchoscopy + biopsy (for tissue diagnosis and histological type)
   • PET-CT for staging
   • Pulmonary function tests (pre-treatment assessment)
   • Biopsy of supraclavicular node if accessible (easiest tissue for diagnosis)

Reference: Murray & Nadel's Textbook of Respiratory Medicine — Obstructive pneumonia as a presentation of endobronchial malignancy; post-treatment radiological follow-up. Harrison's Principles 22E — Lung cancer presentations, recurrent pneumonia, mediastinal lymphadenopathy.

Quick Reference for the Quiz