PE, Pneumothorax and Pleural Effusion Flashcards
PE - Causes
Usually arise from a venous thrombosis in the pelvis or legs – clots travel to the right side of the heart before lodging in the pulmonary circulation.
Rare causes include right ventricular thrombus (post MI), septic emboli (endocarditis), fat, air or amniotic fluid embolism, neoplastic cells or parasites.
PE - Risk Factors
Recent surgery (especially abdominal, pelvic or hip/knee replacement), thrombophilia (e.g. antiphospholipid syndrome), leg fracture, prolonged bed rest or reduced mobility, malignancy, pregnancy or in the postpartum period, taking the contraceptive pill or HRT and previous PE.
PE - Clinical Features
Depend on the number, size and distribution of the emboli:
- Symptoms – acute breathlessness, pleuritic chest pain, haemoptysis, dizziness and syncope.
- Signs – pyrexia, cyanosis, tachypnoea, tachycardia, hypotension, JVP, pleural rub or effusion.
PE - Wells Criteria
0 – low probability, 1-2 moderate probability and >3 high probability of DVT:
- Active cancer or treatment within 6 months.
- Paralysis, paresis or recent plaster immobilisation of the lower limbs.
- Recently bed ridden for >3 days or major surgery within 4 weeks.
- Localised tenderness along venous system.
- Entire leg swollen.
- Calf circumference >3cm more than other side 10cm below tibial tuberosity.
- Pitting oedema > than in asymptomatic leg.
- Collateral superficial veins
- Alternative diagnosis as likely or more likely than DVT.
PE - Investigations
- Bloods - FBC, Us and Es, baseline clotting and ABG (may show low PaO2 and PaCO2).
- Imaging – chest x-ray – may be normal or show a dilated pulmonary artery, linear atelectasis, small pleural effusion, wedge shaped opacities or cavitation. CT pulmonary angiography – this has replaced VQ scanning as first line and can show emboli down to the 5th order pulmonary arteries. Bilateral leg ultrasound – may also be sufficient to confirm but not exclude PE.
- ECG – may be normal or show tachycardia, right bundle branch block, right ventricular strain (inverted T waves V1 to V4) or SI QIII TIII – deep S waves in I, Q waves and inverted T waves in III.
- D-dimer – a negative result excludes PE in those with low or moderate clinical probability and imaging is not required. However a positive test does not confirm PE so imaging must be done.
PE - Management
Anti-coagulate with low molecular weight heparin (LMWH).
Start warfarin and when the INR is >2 stop heparin and continue with warfarin for at least 3 months aiming for an INR of 2-3.
PE - Prevention
Give heparin e.g. 2500U dalteparin SC OD to all immobile patients, prescribe compression stockings and encourage early immobilisation, stop the OCP pre-op (if reliable with another form of contraception) and if family history of thromboembolism consider investigation for thrombophilia.
Pneumothorax - Causes
Often spontaneous (particularly in young, thin men) due to rupture of a sub-pleural bulla.
Other causes include asthma, COPD, TB, pneumonia, lung abscess, carcinoma, cystic fibrosis, lung fibrosis, sarcoidosis, connective tissue disorders (e.g. Marfan’s or Ehlers-Danlos syndrome), trauma, iatrogenic (subclavian CVP line insertion, pleural aspiration, biopsy or positive pressure ventilation).
Pneumothorax - Clinical Features
- Symptoms – may be asymptomatic or present with sudden onset dyspnoea and/or pleuritic chest pain. Patients with asthma or COPD may present with a sudden deterioration.
- Signs – reduced expansion, hyper-resonance to percussion and diminished breath signs. With a tension pneumothorax the trachea will also be deviated away from the affected side.
Pneumothorax - Management
- Tension – do not perform a chest x-ray as it will delay immediate necessary treatment. Insert a large bore (14-16G) needle with a syringe (partially filled with 0.9% saline) into the 2nd intercostal space in the mid-clavicular line. Remove the plunger to allow the trapped air to bubble through the syringe (with the saline acting as a water seal) until a chest drain is placed.
- Non-tension – if dyspnoea or a rim of air >2cm on chest x-ray attempt aspiration of the air. If unsuccessful you can repeat or consider a chest drain and if successful patient is discharged.
Pleural Effusion - Definition
* Fluid in the pleural space* – effusions can be divided by their protein content – transudates contain <25g/L and exudates contain >35g/L.
Other fluid in pleural space - blood is a haemothorax, pus is an empyema, chyle (lymph and fat) is a chylothorax and blood and air is a haemopneumothorax.
Pleural Effusion - Transudates
Can be due to increased venous pressure (cardiac failure, constrictive pericarditis or fluid overload), hypoproteinaemia (cirrhosis, nephrotic syndrome or malabsorption), hypothyroidism or Meig’s syndrome (right pleural effusion and ovarian fibroma).
Pleural Effusion - Exudates
Due to increased permeability of pleural capillaries secondary to infection, inflammation or malignancy – e.g. in pneumonia, TB, pulmonary infarction, rheumatoid arthritis, SLE, bronchial carcinoma, malignant metasteses, lymphoma or mesothelioma.
Pleural Effusion - Symptoms and Signs
- Symptoms – may be asymptomatic or present with dyspnoea and pleuritic chest pain.
- Signs – there will be decreased expansion, stony dull percussion and diminished breath sounds on the affected side. Tactile vocal fremitus and vocal resonance will also be decreased. With larger effusions there may be tracheal deviation away from the side of the effusion.
Pleural Effusion - Associated Diseases
Malignancy (clubbing, lymphadenopathy, radiation marks or mastectomy scar), chronic liver disease, cardiac failure, hypothyroidism, rheumatoid arthritis or SLE.
Pleural Effusion - Investigations
- CXR – small effusions may only blunt the costophrenic angle but larger ones can be seen as a water dense shadow with a concave upper border.
- Ultrasound – useful in identifying presence of pleural fluid and in guiding aspiration or biopsy.
- Diagnostic aspiration - percuss the upper border of the pleural effusion and choose site 1 or 2 intercostal spaces below it. Infiltrate down to the pleural with 5-10mL of 1% lidocaine. Attach a 21G needle to a syringe and insert it just above the upper border of an appropriate rib (to avoid neurovascular bundle) and draw off 10-30mL of pleural fluid.
- Pleural biopsy – performed with a Abram’s needle if fluid analysis is inconclusive.
Pleural Effusion - Fluid Analysis
- Gross appearance – clear or straw coloured in transudate or exudate, turbid and yellow in empyema or haemorrhagic in trauma, malignancy or infarction.
- Cytology – neutrophils in para-pneumonic effusion or PE, lymphocytes in TB, malignancy, RA, SLE or sarcoidosis or mesothelial cells in pulmonary infarction.
- Clinical chemistry – protein is <25g/L in transudates and >35g/L in exudates or glucose and pH are low and LDH high in empyema, malignancy, TB, RA or SLE.
- Immunology – rheumatoid factor in rheumatoid arthritis, antinuclear antibodies in SLE or low complement levels in infection, malignancy, RA or SLE.
Pleural Effusion - Management
Treat the underlying cause where possible.
- Drainage – if effusion is symptomatic drain it (repeatedly if necessary) – best removed slowly at <2L/24 hours. Can be aspirated in same way as a diagnostic tap or using an intercostal drain.
- Pleurodesis – adhesion of pleura with tetracycline, bleomycin or talc if recurrent effusions.
- Surgery – persistent collections or thickening of the pleura on ultrasound requires surgery.
Sarcoidosis - Definition
A multisystem granulomatous disorder of unknown cause. It usually affects adults aged between 20-40 years. It is more common in women and more common and severe in Afro-Caribbean’s.
Sarcoidosis - Pulmonary Features
90% have an abnormal chest x-ray with bilateral hilar lymphadenopathy ± infiltrates or fibrosis.
Symptoms – dry cough, progressive dyspnoea, decreased exercise tolerance and chest pain. In 10-20% symptoms progress with deterioration of lung function.
Sarcoidosis - Non-pulmonary Features
Lymphadenopathy, hepatomegaly, splenomegaly, conjunctivitis, enlargement of lacrimal and parotid glands, terminal phalangeal bone cysts, subcutaneous nodules, erythema nodosum, Bell’s palsy, neuropathy, meningitis, space occupying lesions, cardiomyopathy, arrhythmia’s, hypercalcaemia and uria, renal stones or pituitary dysfunction.
Sarcoidosis - Staging
CXR – abnormal in 90% and used to stage the disease – stage 1 is BHL, stage 2 is BHL and pulmonary infiltrates, stage 3 is infiltrates only and stage 4 is progressive fibrosis and bulla.
Sarcoidosis - Investigations
- Bloods – lymphopenia, ESR is raised, LFTs deranged, calcium and immunoglobulin’s will be raised. 24 hour urine will show high calcium and tuberculin skin test is negative in 66%.
- CXR – abnormal in 90% and used to stage the disease.
- ECG – may show arrhythmia’s or bundle branch block due to cardiomyopathy.
- Lung function tests – can be normal or show impaired gaseous exchange and restrictive defect.
- Tissue biopsy – of the lung, liver, lymph nodes, skin nodules or lacrimal gland is diagnostic.
- Bronchoalveolar lavage – shows lymphophilia in active disease and neutrophilia with fibrosis.
- Ultrasound – of the abdomen may show renal calcification or hepatosplenomegaly.
- Bone x-rays – may show ‘punched out’ lesions in the terminal phalanges.
Sarcoidosis - Management
Patients with BHL alone do not need treatment as most recover spontaneously.
- Steroids – indicated with parenchymal lung disease, uveitis, hypercalcaemia or neurological or cardiac involvement – 40mg Prednisolone PO OD for 4-6 weeks then decrease over 1 year.
- Severe disease – give IV Methylprednisalone or immunosuppressants e.g. Methotrexate.
Sarcoidosis - Prognosis
In 60% the disease resolves over 2 years and a further 20% respond to steroid therapy.
Interstitial Lung Disease
A generic term used to describe a number of conditions that primarily affect the lung parenchyma in a diffuse manner.
They are characterised by chronic inflammation and/or progressive fibrosis and share a number of clinical and pathological features.
Interstitial Lung Disease - Features
Dyspnoea on exertion, non-productive paroxysmal cough, abnormal breath sounds, abnormal chest x-ray and high resolution CT and a restrictive picture on spirometry.
ILD - Classification
- With a known cause – occupational (e.g. asbestosis, berylliosis, silicosis or cotton workers lung), drugs (e.g. nitrofurantoin, bleomycin, amiodarone, sulfasalazine or busulfan), infections (e.g. TB, fungi or viral) or hypersensitivity reaction (e.g. extrinsic allergic alveolitis).
- Associated with systemic disease – sarcoidosis, rheumatoid arthritis, SLE, systemic sclerosis, Sjogren’s syndrome, ulcerative colitis, renal tubular acidosis or autoimmune thyroid disease.
- Idiopathic – idiopathic pulmonary fibrosis, cryptogenic or lymphocytic interstitial pneumonia.
Extrinsic Allergic Alveolitis - Definition and Causes
In sensitised individuals inhalation of allergens (e.g. fungal spores or avian proteins) provokes a hypersensitivity reaction. In the acute phase the alveoli are infiltrated with acute inflammatory cells. With chronic exposure granuloma formation and obliterative bronchiolitis occur.
Causes – bird fanciers or pigeon fanciers lung (proteins in bird droppings), farmer’s and mushroom worker’s lung, malt workers lung (aspergillus clavatus).
EAA - Features and Management
- Clinical features - Acute - 4-6 hours post-exposure – fever, rigors, myalgia, dry cough, dyspnoea and crackles. Chronic – dyspnoea, weight loss, exertional dyspnoea, type 1 failure or cor pulmonale.
- Management - **Acute**– remove allergen, give 35-60% O2 and give oral prednisolone (reducing dose). Chronic – avoid exposure to allergens or wear a face mask and long term steroids.
Idiopathic Pulmonary Fibrosis
There is inflammatory cell infiltration and pulmonary fibrosis of unknown cause – this is otherwise known as cryptogenic fibrosing alveolitis. It is the most common cause of interstitial lung disease.
IPF - Clinical Features
- Symptoms – dry cough, exertional dyspnoea, malaise, weight loss and arthralgia.
- Signs – cyanosis, finger clubbing and fine end inspiratory crackles.
- Complications – it can lead to respiratory failure and there is an increased risk of malignancy.
IPF - Investigations
Bloods – raised CRP and immunoglobulins and ABG – hypoxia and hypercapnia. CXR –shows decreased lung volume, bilateral lower zone reticulo-nodular shadowing and in advanced stages honeycomb appearance. Spirometry – restrictive picture and lung biopsy for definitive diagnosis.
IPF - Management
Supportive – oxygen, pulmonary rehabilitation, opiates, palliative care input. Steroids should not be used unless the diagnosis is doubt. Patients can be considered for a lung transplantation.
Prognosis – 5 year survival is 50%.
