Pulmonary Embolism

Also known as: PE, Venous thromboembolism

Obstruction of pulmonary arterial circulation, most commonly by thrombus embolized from deep vein thrombosis of the lower limbs/pelvis (>90% of cases), causing ventilation-perfusion mismatch, increased pulmonary vascular resistance, and potential right ventricular strain/failure.

Classified by severity:

Low-risk (non-massive): hemodynamically stable, no RV dysfunction
Intermediate-risk (submassive): hemodynamically stable but with RV dysfunction (echo/CT) and/or elevated carintermediate; further subdivided intermediate-low/intermediate-high
High-risk (massive): hemodynamic instability (sustained hypotension SBP<90, requiring vasopressors, or pulseless); highest mortality, requires aggressive reperfusion

Sudden onset dyspnea (most common symptom), pleuritic chest pain, cough, hemoptysis (suggests pulmonary infarction)
Tachycardia, tachypnea, hypoxia; syncope/pre-syncope (suggests significant hemodynamic compromise; high-risk feature)
Examination: often unremarkable beyond tachycardia/tachypnea; signs of DVT present in a minority; signs of RV strain in massive PE ; raised JVP, loud P2, right-sided S3, hypotension
Risk factors (Virchow's triad): recent surgery/immobilization, malignancy, pregnancy/postpartum, estrogen therapy, prior VTE, inherited thrombophilia, long-haul travel, obesity, trauma, central venous catheter
Massive PE: shock, syncope, cardiac arrest ; PEA arrest should always prompt consideration of PE as a reversible cause

Clinical probability assessment first (Wells or Geneva score):
- Low/intermediate probability: D-dimer : if negative, PE effectively excluded; if positive, proceed to imaging
- High probability: proceed directly to imaging (D-dimer not useful for exclusion at high pre-test probability)
D-dimer: sensitive but non-specific (elevated in pregnancy, malignancy, infection, recent surgery, elderly) ; age-adjusted cutoffs improve specificity in older patients
CT pulmonary angiography (CTPA): investigation of choice; direct visualization of filling defect, also assesses RV size/strain (RV:LV ratio >1 suggests significant strain)
V/Q scan: alternative if CTPA contraindicated (renal impairment, contrast allergy) or in pregnancy
ECG: sinus tachycardia most common; S1Q3T3, right heart strain (T-wave inversion V1-4), RBBB ; classic but insensitive
Echocardiography: bedside assessment of RV strain in unstable patients when CTPA not immediately feasible
Troponin/BNP: elevated in RV strain, prognostic marker for risk stratification
Lower limb Doppler: confirms DVT source if positive, though normal doesn't exclude PE

Differentials: ACS, pneumonia, pneumothorax, pericarditis, musculoskeletal chest pain, anxiety, aortic dissection, COPD/asthma exacerbation.

Hemodynamically stable (low/intermediate-risk):

Anticoagulation : start promptly once diagnosis confirmed (or strongly suspected while awaiting imaging in high pre-test probability):
- DOAC (apixaban, rivaroxaban) : first-line for most; apixaban 10mg bd x7 days then 5mg bd; rivaroxaban 15mg bd x21 days then 20mg od
- LMWH (enoxaparin 1mg/kg bd) : preferred in pregnancy, severe renal impairment, active malignancy, or if intervention anticipated
- Warfarin: requires LMWH bridging until INR therapeutic (2-3), largely superseded except specific indications (mechanical valve, severe renal impairment, antiphospholipid syndrome)
Duration: minimum 3 months for provoked PE with reversible risk factor; longer/indefinite for unprovoked PE or ongoing risk factors ; individualized bleeding vs. recurrence assessment
Intermediate-high risk: closer monitoring, low threshold for escalation

Hemodynamically unstable (high-risk/massive PE) ; reperfusion indicated:

Systemic thrombolysis: alteplase 100mg IV over 2 hours (or accelerated regimens) : first-line for confirmed massive PE with shock
Catheter-directed thrombolysis/thrombectomy: alternative where contraindications to systemic thrombolysis exist or expertise available
Surgical embolectomy: for absolute contraindication to thrombolysis with appropriate surgical support
Supportive: cautious IV fluid (small boluses only : aggressive fluid worsens RV strain), vasopressor (noradrenaline) for hypotension, avoid excessive positive pressure ventilation if intubated
ECMO: bridge to definitive therapy in refractory cardiogenic shock/cardiac arrest

IVC filter: for absolute contraindication to anticoagulation with ongoing high VTE risk, or recurrent PE despite adequate anticoagulation.

Pregnancy-specific: LMWH is anticoagulant of choice (DOACs and warfarin contraindicated), continue through pregnancy and minimum 6 weeks postpartum, total duration ≥3 months.

Referral: respiratory/cardiology for risk stratification, hematology for thrombophilia workup if unprovoked/recurrent, ICU for massive PE.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Asthma

Chronic inflammatory airway disease characterized by variable, reversible airflow obstruction, airway hyperresponsiveness, and chronic inflammation involving eosinophils, mast cells, T-helper 2 (Th2) lymphocytes, and in some phenotypes neutrophils.

Bronchial smooth muscle hyperreactivity leads to episodic wheeze, breathlessness, chest tightness, and cough, typically worse at night/early morning and triggered by identifiable stimuli.

Classified by:

Phenotype: allergic/atopic (childhood-onset, IgE-mediated, eosinophilic), non-allergic (adult-onset, often neutrophilic), exercise-induced, occupational, aspirin exacerbated respiratory disease (AERD; asthma + nasal polyps + NSAID sensitivity), obesity-associated
Severity (based on treatment step needed for control, per GINA): mild, moderate, severe
Control status: well-controlled, partly controlled, uncontrolled (based on symptom frequency, reliever use, exacerbations, lung function)

Episodic symptoms: wheeze (expiratory, polyphonic), dyspnea, chest tightness, dry cough (may be sole symptom: cough-variant asthma)
Diurnal variability: worse at night/early morning
Triggers: allergens (dust mites, pollen, pet dander), viral URTIs, exercise, cold air, irritants (smoke, strong odors), NSAIDs/aspirin, beta-blockers, emotional stress, occupational exposures
Examination: expiratory wheeze on auscultation (may be absent between exacerbations — "silent chest" in severe attack is an ominous sign of minimal air movement), prolonged expiratory phase, hyperinflated chest in poorly controlled disease
Personal/family history of atopy: eczema, allergic rhinitis, food allergy

Acute exacerbation severity grading (critical for triage):

Mild–moderate: PEFR ≥50% predicted/best, talks in sentences, RR normal-increased, no accessory muscle use
Severe: PEFR 33–50%, unable to complete sentences in one breath, RR ≥25/min, HR ≥110/min, accessory muscle use
Life-threatening: PEFR <33%, silent chest, cyanosis, feeble respiratory effort, exhaustion, bradycardia/hypotension, arrhythmia, confusion/reduced consciousness, SpO2 <92%
Near-fatal: raised PaCO2 (normal or rising CO2 in an asthmatic tachypneic patient is a red flag;suggests fatigue and impending respiratory failure) and/or requiring mechanical ventilation.

Clinical suspicion + objective demonstration of variable airflow obstruction.

Spirometry: obstructive pattern; FEV1/FVC <0.7 (or below lower limit of normal); bronchodilator reversibility test: FEV1 improvement ≥12% AND ≥200mL post-salbutamol confirms diagnosis
Peak expiratory flow rate (PEFR): diurnal variability >10% (amplitude % mean) over 2 weeks supports diagnosis; useful for home monitoring and exacerbation severity
FeNO (fractional exhaled nitric oxide): >40ppb supports eosinophilic airway inflammation (adults); helpful when spirometry equivocal
Bronchial challenge testing (methacholine/histamine): used when diagnosis uncertain and spirometry normal; positive if PC20 <8mg/mL (specialist setting)
Allergy testing (skin prick or specific IgE) to identify triggers in atopic phenotype
CXR: usually normal; used to exclude alternative diagnoses or complications (pneumothorax, consolidation) during severe exacerbation

Differentials: COPD (fixed obstruction, smoking history, older age ;overlap syndrome ACO possible), vocal cord dysfunction/paradoxical vocal fold motion, heart failure ("cardiac asthma"), bronchiectasis, foreign body aspiration (esp. children), pulmonary embolism, GERD-related cough, ABPA (allergic bronchopulmonary aspergillosis ;consider if poorly controlled with high IgE, eosinophilia, central bronchiectasis).

Chronic/maintenance therapy : GINA stepwise approach (current guidelines favor ICS-containing reliever over SABA-only, given SABA-monotherapy mortality risk):

Step 1 (mild, infrequent symptoms): as needed low dose ICS - formoterol (e.g., budesonide-formoterol) preferred over SABA alone
Step 2: low dose maintenance ICS (e.g., budesonide 200–400mcg/day or equivalent) + as needed ICS-formoterol or SABA
Step 3: low-dose ICS-LABA maintenance (e.g., budesonide-formoterol 200/6mcg one puff bd) + as-needed reliever
Step 4: medium-dose ICS-LABA
Step 5: high-dose ICS-LABA + add-on: LAMA (tiotropium), or biologic therapy if severe eosinophilic/allergic phenotype : omalizumab (anti-IgE), mepolizumab/benralizumab (anti-IL5/5R, eosinophilic), dupilumab (anti-IL4/13); oral corticosteroids as last resort, lowest effective dose, given long-term toxicity

Leukotriene receptor antagonists (montelukast 10mg od adults): add-on option, especially in aspirin-sensitive or exercise-induced asthma; counsel on neuropsychiatric side effects (mood changes, nightmares)
Inhaler technique and adherence review at every visit: major cause of "poor control" is technique failure, not undertreatment
Trigger avoidance, smoking cessation, weight management if obese, treat comorbid allergic rhinitis/GERD

Acute exacerbation management:

Oxygen: titrate to SpO2 94–98%
Salbutamol (SABA): nebulized 5mg (or 2.5mg in children) repeated/continuous in severe cases, or via spacer 4–10 puffs every 20 min for 1 hour in mild-moderate
Ipratropium bromide: nebulized 500mcg 4-6 hourly, added in moderate-severe/life-threatening exacerbations
Systemic corticosteroids: prednisolone 40–50mg PO od for 5–7 days (adults), or IV hydrocortisone 100mg 6-hourly if unable to tolerate oral/severe: start early, within 1 hour of presentation
Magnesium sulfate: IV 1.2–2g over 20 minutes for severe/life-threatening exacerbations not responding to initial bronchodilators
IV salbutamol or aminophylline: considered in life-threatening cases unresponsive to above (specialist/ICU setting, aminophylline loading 5mg/kg over 20 min if not on theophylline, then infusion, with levels monitored)
Escalate to ICU/anesthetics for intubation if: exhaustion, rising PaCO2, deteriorating consciousness, or failure to improve despite maximal therapy

Discharge criteria: PEFR >75% predicted/best, stable on reliever ≥4 hourly, inhaler technique checked, written asthma action plan provided, steroid course completed/prescribed, follow-up arranged within 2–7 days.

Monitoring: step down treatment after 3 months of good control; step up if uncontrolled (assess adherence/technique/triggers before escalating). Annual review including spirometry, exacerbation history, and comorbidity screening.

References

Global Initiative for Asthma (GINA)

Pulmonary Embolism

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management