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PLEURAL EFFUSION - Complete Clinical Guide

History Taking

• Dyspnea - onset (acute vs gradual), severity, positional (orthopnea suggests heart failure, platypnea suggests hepatopulmonary syndrome)
• Pleuritic chest pain - sharp, worse on inspiration (suggests exudate - infection, PE, malignancy, RA, lupus)
• Cough - dry or productive, hemoptysis
• Fever/rigors - suggests parapneumonic effusion or empyema
• Weight loss/night sweats - TB or malignancy
• Ankle swelling/orthopnea/PND - heart failure (bilateral transudates)

• Heart failure, liver cirrhosis, nephrotic syndrome (transudates)
• TB exposure, HIV status
• Malignancy (especially lung, breast, lymphoma - commonest causes of massive effusion)
• Autoimmune: RA, SLE
• Recent MI or cardiac surgery (Dressler's/post-cardiac injury syndrome)
• Pulmonary embolism risk factors (DVT, immobility, malignancy, OCP use)
• Pancreatitis (left-sided effusion, high amylase in fluid)

• Methotrexate, bleomycin, mitomycin, busulfan, procarbazine
• Nitrofurantoin (chronic use)
• Amiodarone
• Ergotamine, methysergide (antimigraine)
• Bromocriptine

• Smoking (lung cancer)
• Alcohol (cirrhosis - hepatic hydrothorax; 85% right-sided)
• Occupational exposure: asbestos (mesothelioma - massive effusion, no mediastinal shift)
• Travel history (TB endemic areas)

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Key Examination Findings to Know

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Investigations - Viva Favourites

Chest X-Ray Signs

• Small effusion (<200-500 mL): Blunting of costophrenic angles (posterior then lateral)
• Moderate: Homogeneous opacity, concave meniscus (higher laterally - meniscus sign)
• Large (~1000 mL): Reaches 4th anterior rib
• Massive: Dense hemithorax opacification + contralateral mediastinal shift
• No mediastinal shift despite massive effusion = consider mesothelioma, or collapsed lung on same side

Lateral Decubitus CXR

• Detects small effusions (fluid layers out)
• Now largely replaced by ultrasound

Ultrasound

• Best initial tool for detection and guided thoracentesis
• Empyema: echogenic, septate fluid
• Simple transudate: anechoic

CT Chest

• Best for identifying underlying cause (pleural nodules, lung mass, mediastinal nodes)
• MRI: superior contrast resolution for malignant vs benign; T1 bright = blood (subacute) or chyle

FDG PET/CT

• Can help differentiate exudate (FDG uptake) from transudate
• Not routine - used for malignant vs benign pleural disease

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Light's Criteria - MUST KNOW VIVA POINT

Viva trap: ~25% of transudates (especially in heart failure patients on diuretics) are misclassified as exudates by Light's criteria. In that setting, use serum albumin - pleural fluid albumin gradient: if >1.2 g/dL it is a true transudate.

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Causes Summary Table

• Right-sided: heart failure, ascites/cirrhosis, liver abscess
• Left-sided: pancreatitis, pericarditis, oesophageal rupture, aortic dissection
• Bilateral exudate: metastatic disease, lymphoma, SLE, RA, pulmonary embolism, myxoedema, post-cardiac injury

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Pleural Fluid Analysis - Viva Points

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Management - Viva Points

• Asymptomatic transudate: Treat underlying cause (diuretics for HF, etc.)
• Therapeutic thoracentesis: Symptom relief; don't drain >1.5 L at once (re-expansion pulmonary oedema risk)
• Chest drain (intercostal tube): Empyema, hemothorax, large symptomatic effusion
• Pleurodesis: Recurrent malignant effusion (talc is most effective agent)
• Indwelling pleural catheter (IPC): Recurrent malignant or hepatic hydrothorax - bridge/palliation
• TIPS: Hepatic hydrothorax refractory to diuretics (70-80% initial response)
• VATS/medical thoracoscopy: Undiagnosed exudative effusion; pleural biopsy if needle biopsy non-diagnostic; no difference in diagnostic yield between the two
• Conventional chest tube NOT recommended for hepatic hydrothorax (protein/electrolyte loss, infection, renal failure risk)

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HEART HOLES (CONGENITAL SEPTAL DEFECTS) - Complete Clinical Guide

Classification of Congenital Heart Disease (CHD)

CHD
├── Acyanotic (left-to-right shunt initially)
│   ├── With increased pulmonary flow: VSD, ASD, PDA, AVSD (endocardial cushion defect)
│   └── Obstructive: Pulmonary stenosis, Aortic stenosis, Coarctation of aorta
└── Cyanotic (right-to-left shunt)
    ├── Decreased pulmonary flow: Tetralogy of Fallot, Tricuspid atresia, Pulmonary atresia
    └── Increased pulmonary flow: TGA, Truncus arteriosus, TAPVR

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Ventricular Septal Defect (VSD)

History Taking

• Most common congenital cardiac defect - 20-25% of all CHD
• Spontaneous closure in 30-40% overall, 50-70% of small VSDs
• Ask about: feeding difficulty/poor feeding (infant equivalent of exertional dyspnoea), failure to thrive, frequent chest infections, sweating during feeds
• Symptoms appear from 4-8 weeks of age when pulmonary vascular resistance naturally falls

• Small VSD: Asymptomatic (maladie de Roger)
• Large VSD: CHF signs from ~2-3 months - tachypnoea, poor feeding, recurrent respiratory infections, failure to thrive

• Eisenmenger's syndrome (pulmonary HTN leading to reversal to R-to-L shunt, cyanosis)
• Infective endocarditis
• Aortic regurgitation (high VSDs)
• Pulmonary hypertension

Examination/Signs

• Harsh pansystolic murmur at left lower sternal border (smaller VSD = louder murmur - maladie de Roger)
• Thrill if loud murmur
• Loud P2 if pulmonary hypertension develops
• Signs of CHF: hepatomegaly, tachycardia, tachypnoea, failure to thrive

Viva Points - VSD

• Most common CHD
• Pressure in RV = pressure in LV if large VSD (pulmonary HTN)
• Eisenmenger's: when shunt reverses R-to-L, patient becomes cyanotic and is no longer operable
• ECG: biventricular hypertrophy (large VSD)
• CXR: cardiomegaly, increased pulmonary vascular markings
• Echo: confirmatory - shows size, location, flow direction
• Location types: perimembranous (most common), muscular, inlet (AVSD), supracristal (outlet - risk of AR)

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Atrial Septal Defect (ASD)

History Taking

• Can remain asymptomatic until adulthood (unlike VSD)
• Adults: exertional dyspnoea, palpitations (AF), recurrent chest infections
• Children: often picked up incidentally on examination
• Paradoxical embolism - stroke in young patient (ask about DVT, PE, migraine with aura)
• Ask about family history (ASD has genetic associations - Holt-Oram syndrome, Down syndrome)

Examination/Signs

• Ejection systolic murmur at pulmonary area (2nd left intercostal space) - due to increased flow across pulmonary valve
• FIXED WIDE SPLITTING of S2 - the most important sign (splitting does not vary with respiration)
• Loud P2 if pulmonary hypertension
• Right ventricular heave (parasternal)
• AF in older patients

Viva Points - ASD

• Fixed splitting of S2: RA already volume-loaded so RV fills equally in inspiration and expiration
• Types: Ostium secundum (most common, ~70%), Ostium primum (near AV valves, associated with Down syndrome and AV canal defect), Sinus venosus (near SVC/IVC), Coronary sinus
• ECG: right axis deviation + incomplete RBBB (secundum); left axis deviation + prolonged PR (primum)
• CXR: right heart enlargement, prominent pulmonary vasculature
• Paradoxical embolism explains cryptogenic stroke in young adults
• Treatment: closure (catheter-based device for secundum; surgical for others) when Qp:Qs >1.5:1

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Presentation Timing by Defect (Key Viva Table)

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Eisenmenger's Syndrome - Viva Must-Know

• Prolonged large left-to-right shunt causes pulmonary vascular disease and irreversible pulmonary hypertension
• Shunt reverses to right-to-left → cyanosis (late-onset)
• Patient becomes inoperable at this stage (closing the defect would kill the patient - the shunt is now the safety valve)
• Presents in: large unrepaired VSD, ASD, PDA
• Managed: heart-lung transplant, pulmonary vasodilators (bosentan, sildenafil)

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Tetralogy of Fallot - Viva Summary (Most Common Cyanotic CHD)

1. VSD (large, non-restrictive)
2. Overriding aorta
3. Pulmonary stenosis (right ventricular outflow tract obstruction)
4. Right ventricular hypertrophy

• Triggered by: crying, defecation, feeding, fever - anything that drops SVR
• SVR drops → more R-to-L shunt through VSD → severe hypoxia + metabolic acidosis → hyperpnoea → worsens shunt (vicious cycle)
• Management of tet spell:
  1. Knee-chest position (increases SVR, decreases shunt)
  2. Supplemental oxygen
  3. Morphine 0.1-0.2 mg/kg IV/IM (reduces hyperpnoea, decreases infundibular spasm)
  4. Sodium bicarbonate 1 mEq/kg IV if acidotic
  5. Fentanyl/Midazolam as alternatives
  6. Propranolol (reduces infundibular spasm)

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Ductal-Dependent Lesions - Must-Know Viva List

• Tetralogy of Fallot, Tricuspid atresia, Pulmonary atresia, Hypoplastic right heart, TGA

• Severe coarctation of aorta, Severe aortic stenosis, Hypoplastic left heart syndrome

Key point: In neonates with ductal-dependent lesions, DO NOT give indomethacin (closes ductus). Give prostaglandin E1 (alprostadil) to keep the ductus open while arranging surgery.

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Quick Viva Differentiator Table

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