symptoms of PE
Acute breathlessness, pleuritic chest pain, haemoptysis; dizziness; syncope. Ask about risk factors (above), past history or family history of thromboembolism.
• Classically presents with sudden onset, pleuritic chest pain, associated with breathlessness and haemoptysis. Additional symptoms include postural dizziness or syncope.
• Massive PE may present as cardiac arrest (particularly with electromechanical dissociation) or shock.
• Presentation may be atypical, i.e. unexplained breathlessness or unexplained hypotension or syncope only.
• Pulmonary emboli should be suspected in all breathless patients with risk factors for DVT or with clinically proven DVT (see Cardiac emergencies p.[link]).
• Recurrent PEs may present with chronic pulmonary hypertension and progressive right heart failure.
signs of PE
Pyrexia; cyanosis; tachypnoea; tachycardia; hypotension; raised jvp, pleural rub; pleural effusion. Look for signs of a cause, eg deep vein thrombosis.
• Examination may reveal tachycardia and tachypnoea only. Look for postural hypotension (in the presence of raised JVP).
• Look for signs of raised right heart pressures and cor pulmonale (raised JVP with prominent ‘a’ wave, tricuspid regurgitation, parasternal heave, right ventricular S3, loud pulmonary closure sound with wide splitting of S2, pulmonary regurgitation).
• Cyanosis suggests a large PE.
• Examine for a pleural rub (may be transient) or effusion.
• Examine lower limbs for obvious thrombophlebitis.
• Mild fever (>37.5°C) may be present. There may be signs of coexisting COPD.
risk factors for PE
• Recent surgery, especially abdominal/pelvic or hip/knee replacement
• Thrombophilia, eg antiphospholipid syn. ([link])
• Leg fracture
• Prolonged bed rest/reduced mobility
• Pregnancy/postpartum; Pill/HRT
• Previous PE
diagnostics of PE
• ABG: normal ABG does not exclude a PE. ↓PaO2 is invariable with larger PEs. Other changes include mild respiratory alkalosis and ↓PaCO2 (due to tachypnoea) and metabolic acidosis (2° to shock).
• ECG: commonly shows sinus tachycardia ± non-specific ST- and T-wave changes in the anterior chest leads. The classical changes of acute cor pulmonale such as S1Q3T3, right axis deviation, or RBBB are only seen with massive PE. Less common findings include AF.
• CXR: may be normal and a near-normal chest film in the context of severe respiratory compromise is highly suggestive of a PE. Less commonly may show focal pulmonary oligaemia (Westermark’s sign), a raised hemidiaphragm, small pleural effusion, wedge-shaped shadows based on the pleura, sub-segmental atelectasis, or dilated proximal pulmonary arteries.
• Blood tests: there is no specific test. FBC may show neutrophil leukocytosis; mildly elevated CK, troponin, and bilirubin may be seen.
• Echo/TOE: insensitive for diagnosis but can exclude other causes of hypotension and raised right-sided pressures (e.g. tamponade, RV infarction, see Cardiac emergencies p.[link]). In PE it will show RV dilatation and global hypokinesia, with sparing of apex (McConnell’s sign), and pulmonary artery dilation.
• A highly sensitive, but non-specific test.
• Useful in ruling out PE in patients with low or intermediate probability.
• Results can be affected by advancing age, pregnancy, trauma, surgery, malignancy, and inflammatory states.
Ventilation/perfusion (V/Q) lung scanning
A perfusion lung scan (with IV technetium-99 labelled albumin) should be performed in all suspected cases of PE.
• This is the recommended initial lung imaging modality in patients with non-massive PE.
• Allows direct visualization of emboli as well as other potential parenchymal disease, which may explain alternative explanation for symptoms.
• Sensitivity and specificity are high (>90%) for lobar pulmonary arteries but not so high for segmental and sub-segmental pulmonary arteries.
• A patient with a positive CTPA does not require further investigation for PE.
• A patient with a negative CTPA in the context of a high/intermediate probability of a PE should undergo further investigation.
Evaluation of leg veins with US
• Not very reliable. Almost half of patients with PE do not have evidence of a DVT and therefore a negative result cannot rule out a PE.
• Useful second-line investigation as an adjunct to CTPA/V/Q scan.
• Outcome studies have demonstrated that it would be safe not to anticoagulate patients with a negative CTPA and lower limb US who have an intermediate/low probability of a PE.
• Is the ‘gold standard’ investigation.
• It is indicated in patients in whom diagnosis of embolism cannot be established by non-invasive means. Look for sharp cut-off of vessels or obvious filling defects.
• Invasive investigation and can be associated with 0.5% mortality.
• If there is an obvious filling defect, the catheter or a guide wire passed through the catheter may be used to disobliterate the thrombus.
• After angiography, the catheter may be used to give thrombolysis directly into the affected pulmonary artery (see Cardiac emergencies).
• The contrast can cause systemic vasodilatation and haemodynamic collapse in hypotensive patients.
Management of PE
1. Stabilise patient:
• Obtain venous access and start IV fluids (crystalloid or colloid).• Give LMWH or UFH to all patients with high or intermediate risk of PE until diagnosis is confirmed. Meta-analysis of multiple trials has shown LMWH to be superior to UFH with a reduction in mortality and bleeding complications. For doses consult local formulary.• If there is evidence of haemodynamic instability (systemic hypotension, features of right heart failure) or cardiac arrest, patients may benefit from thrombolysis with rtPA or streptokinase—same doses used for treatment of STEMI
• Patients may respond to oral NSAIDs.
• Opiate analgesia to be used with caution. The vasodilatation caused by these drugs may precipitate or worsen hypotension. Give small doses (1–2mg diamorphine IV) slowly. Hypotension should respond to IV colloid.
• Avoid IM injections (anticoagulation and possible thrombolysis).
• Start LMWH when PE is suspected
• Start warfarin when PE is confirmed, continue LMWH until INR is therapeutic (2–3)
• IV fluids if hypotensive
• If there is evidence of haemodynamic instability: consider thrombolysis.
management of PE after stabilising
• In patients who have contraindications to thrombolysis and are in shock requiring inotropic support, there may be a role for embolectomy if appropriate skills are on site.
• This can be performed percutaneously in the catheterization laboratory using a number of devices or surgically on cardiopulmonary bypass.
• Percutaneous procedures may be combined with peripheral or central thrombolysis.
• Seek specialist advice early. Best results are obtained before onset of cardiogenic shock.
• Radiological confirmation of extent and site of embolism is preferable before thoracotomy.
• Mortality is ~25–30%.
• Infrequently used as little to suggest improved short- or long-term mortality.
• Filters are positioned percutaneously and if possible patients must remain anticoagulated to prevent further thrombus formation.
• Most are positioned infrarenally (bird’s nest filter), but can also be suprarenal (Greenfield filter).
• Indications for IVC filter use include:
• Anticoagulation contraindicated: e.g. active bleeding, heparin-induced thrombocytopenia, planned intensive chemotherapy
• Anticoagulation failure despite adequate therapy
• Prophylaxis in high-risk patients: e.g. progressive venous thrombosis, severe pulmonary hypertension.
• LMWHs have now superseded UFH for management of both DVT and PE. They require no monitoring on a daily basis and also allow outpatient treatment.
• There must be period of overlap between LMWH/UFH therapies and anticoagulation with warfarin until INR is within therapeutic range and stable.
• LMWH are administered primarily as a once-daily SC injection and dosage is determined by patient weight.
• Always anticoagulate with LMWH/UFH before starting warfarin. Protein C (a vitamin K-dependent anticoagulant) has a shorter half-life than the other coagulation factors and levels fall sooner resulting in a transient pro-coagulant tendency.
• If DVT is confirmed commence warfarin and maintain on LMWH/UFH until INR >2.
• Anticoagulate (INR 2–2.5) for 3 months.
• If recurrent DVT, or patient at high-risk of recurrence, consider lifelong anticoagulation.
pulmonary embolism AETIOLOGY
Virchow's triad is still the preferred aetiological model for DVT and PE. 
Vessel wall damage: endothelial cell damage promotes thrombus formation, usually at the venous valves. Damage to the vessel wall can occur after a number of insults including trauma, previous DVT, surgery, venous harvest, and central venous catheterisation. 
Venous stasis: poor blood flow and stasis promote the formation of thrombi. Venous stasis and congestion result in valvular damage, further promoting thrombus formation. Increased venous stasis is associated with age >40 years, immobility, general anaesthesia, paralysis, spinal cord injury, myocardial infarction, prior CVA, varicose veins, advanced CHF, and advanced COPD.
Hypercoagulability: a number of other conditions (both inherited and acquired) increase the risk of PE. These include cancer, high-oestrogen states (obesity, pregnancy, and hormone replacement), inflammatory bowel disease, nephrotic syndrome, sepsis, blood transfusion, and inherited thrombophilia (factor V Leiden mutation, prothrombin gene mutation, protein C and S deficiency, antithrombin III deficiency, and antiphospholipid antibody syndrome).
ARDS/ pulmonary oedema
Acute respiratory distress syndrome (ARDS) is a non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates critical illness.
The diagnosis of ARDS is based on fulfilling 3 criteria: acute onset (within 1 week), bilateral opacities on CXR, and a PaO2/FiO2 (inspired oxygen) ratio of ≤300 on PEEP or CPAP ≥5 cm H2O.  If no risk factor for ARDS is present, then heart failure as a cause of acute pulmonary oedema should be ruled out.
• Acute breathlessness, cough, frothy blood-stained (pink) sputum
• Collapse, cardiac arrest, or shock
• Associated features may reflect underlying cause:
• Chest pain or palpitations: ?IHD/MI, arrhythmia
• Preceding history of dyspnoea on exertion: ?IHD, poor LV
• Oliguria, haematuria: ?acute renal failure
• Seizures, signs of intracranial bleed
causes of pulmonary oedema
Increased pulmonary capillary pressure (hydrostatic)
• ↑Left atrial pressure
• Mitral valve disease
• Arrhythmia (e.g. AF) with pre-existing mitral valve disease
• Left atrial myxoma
• Aortic valve disease
• Uncontrolled hypertension
• Pericardial constriction
• Fluid overload
• High output states (anaemia, thyrotoxicosis, Paget’s, AV fistula, beri-beri)
• Reno-vascular disease
↑Pulmonary venous pressure
• L → R shunt (e.g. VSD)
• Veno-occlusive disease
• Intracranial haemorrhage
• Cerebral oedema
• Post ictal
↑ pulmonary capillary permeability
- Acute lung injury
• ↓intravascular oncotic pressure
↓ intravascular oncotic pressure
• ↑losses (e.g. nephrotic syndrome, liver failure)
• ↓production (e.g. sepsis)
• Dilution (e.g. crystalloid transfusion)
management of Pulmonary oedema
Stabilize the patient
• Patients with acute pulmonary oedema should initially be continuously monitored and managed where full resuscitation facilities are available.
• Sit the patient up in bed.
• Give 60–100% O2 by facemask (unless contraindicated, COPD).
• If the patient is severely distressed, summon the ‘on-call’ anaesthetist and inform ITU. If dyspnoea cannot be significantly improved by acute measures (see following text) the patient may require CPAP or mechanical ventilation.
• Treat any haemodynamically unstable arrhythmia—urgent synchronized DC shock may be required.
• Diamorphine 2.5–5mg IV (caution abnormal ABGs)
• Metoclopramide 10mg IV
• Furosemide 40–120mg slow IV injection.
• Secure venous access and send blood for urgent U&Es, FBC, and cardiac enzymes (including troponin).
• Unless thrombolysis is indicated take ABG.
• If the SBP is ≥90mmHg and the patient does not have aortic stenosis:
• Give sublingual GTN spray (2 puffs)
• Start IV GTN infusion 1–10mg/hour, increase the infusion rate every 15–20min, titrating against BP (aiming to keep SBP ~100mmHg).
• If the SBP is <90mmHg treat patient as cardiogenic shock (see Cardiac emergencies p.[link]).
• Insert a urinary catheter to monitor urine output.
• Repeat ABG and K+ if the clinical condition deteriorates/fails to improve, or after 2h if there is improvement and the original sample was abnormal.
• Monitor pulse, BP, respiratory rate, O2 saturation with a pulse oximeter (if an accurate reading can be obtained) and urine output.
key points in pulmonary oedema management
• Sit the patient up in bed.
• IV diamorphine (+metoclopramide).
• IV furosemide.
• IV GTN infusion (titrate according to BP).
• Look for and treat underlying cause (e.g. ischaemia, arrhythmia).
• Consider CPAP or mechanical ventilation if dyspnoea is not improved by acute measures.
- Urinary catheter
- Pulmonary artery catheter
special considerations for cause and management in pulmonary oedema
• Conditions that require specific treatment:
• Acute aortic and mitral regurgitation p.[link]
• Diastolic left ventricular dysfunction p.[link]
• Fluid overload p.[link]
• Renal failure p.[link]
• Severe anaemia
• Hypoproteinaemia p.[link].
pulmonary oedema management 2
Assess the patient’s respiratory function
• Wheeze may be caused by interstitial pulmonary oedema. If there is a history of asthma, give nebulized salbutamol (2.5–5mg), nebulized ipratropium bromide (500mcg), and hydrocortisone (200mg) IV. Consider commencing aminophylline infusion. This will relieve bronchospasm, as well as ‘off-load’ by systemic vasodilatation (see Cardiac emergencies p.[link]). However, it may worsen tachycardia and it can be arrhythmogenic and lower K+ (supplement to ensure K+ 4–5mmol/L).
• Indications for further respiratory support include:
• Patient exhaustion or continuing severe breathlessness
• Persistent PaO2 <8kPa
• Rising PaCO2
• Persistent or worsening acidosis (pH <7.2).
• CPAP: this may be tried for cooperative patients, who can protect their airway, have adequate respiratory muscle strength, and are not hypotensive. The positive pressure reduces venous return to the heart and may compromise BP.
• Endotracheal intubation and mechanical ventilation may be required and some positive end expiratory pressure (PEEP) should be used (see Cardiac emergencies p.[link]).
• Discuss the patient with the on-call anaesthetist or ITU team early.
haemodynamic assessment of a patient with Pulmonary Oedema
It is important to distinguish between cardiogenic and non-cardiogenic pulmonary oedema, as further treatment is different between the two groups. This may be difficult clinically. A PA (Swan–Ganz) catheter must be inserted if the patient’s condition will allow.
• Non-cardiogenic pulmonary oedema occurs when the hydrostatic pressure within the capillary system overcomes the plasma oncotic pressure. In patients with hypoalbuminaemia this will occur at PCWP <15mmHg. The critical PCWP may be estimated by serum albumin (g/L) × 0.57. Thus a patient with a serum albumin of 15g/L will develop hydrostatic pulmonary oedema at a LA pressure of 8mmHg; a serum albumin of 30g/L will require an LA pressure of >17mmHg, etc.
• Cardiogenic pulmonary oedema is often associated with significant systemic hypotension or low output states. Contributing factors include conditions where there is ‘mechanical’ impairment to forward flow (e.g. valvular heart disease (especially if acute) VSD) or severe myocardial disease (large MI, myocarditis, cardiomyopathy).
• The gradient between PA diastolic pressure and PCWP (PAD–PCWP) is generally <5mmHg in cardiogenic and >5mmHg in non-cardiogenic pulmonary oedema (e.g. ARDS).
• The pulse and BP are most commonly elevated due to circulating catecholamines and over activity of the renin–angiotensin system. Examination reveals sweating, cool ‘shut-down’ peripheries, high pulse volume (assess carotid or femoral pulses).
The lungs are covered by a thin serous layer (the visceral pleura). The pleura is then reflected on to the chest wall and pericardium (the parietal pleura). The lung hila 'connect' the visceral and parietal pleura. There is normally a small amount of fluid in the 'pleural space' between the parietal and visceral pleura, which lubricates movement between them. A pleural effusion is when the volume of this fluid is substantially greater than normal.
aetiology of pleural effusion
When a pleural effusion is present, it is caused by disease which can be pulmonary, pleural or extrapulmonary.
Benign pleural effusions are twice as common as malignant effusions.
Effusions are usually classified as either transudates or exudates. However, blood (haemothorax), pus (empyema) or chyle (chylothorax) can also accumulate in the pleural space:
- A transudative pleural effusion occurs when there is disruption of the hydrostatic and oncotic forces operating across the pleural membranes.
- An exudative pleural effusion occurs when there is increased permeability of the pleural surface and/or capillaries, usually as a result of inflammation.
Impaired lymphatic drainage and abnormal sites of entry (for example, passage of fluid across the diaphragm in people with ascites) can also be underlying causes of pleural effusions.
Causes of transudates:
Most common causes:
Less common causes:
Pulmonary embolism (tends to produce a comparatively small effusion but disproportionate dyspnoea and pleuritic pain; 80% are exudates, 20% are transudates)
Superior vena cava obstruction (usually due to lung cancer)
Meigs' syndrome (benign ovarian tumour, ascites and pleural effusion)
Causes of exudates:
Malignancy (most commonly, lung cancer in men and breast cancer in women; large unilateral pleural effusions are most commonly due to malignancy)
Less common causes:
Pulmonary infarction (usually resulting from pulmonary embolism)
Autoimmune disease, especially rheumatoid arthritis
Complication of acute myocardial infarction (Dressler's syndrome)
Yellow nail syndrome (yellow nails, lymphoedema, pleural effusion and bronchiectasis)
Adverse drug reactions (the most common are methotrexate, amiodarone, nitrofurantoin and phenytoin)
causes of chylothorax
usually occurs because of disruption of the thoracic duct
Neoplasm: lymphoma, metastatic carcinoma
Trauma: operative and penetrating injuries
TB, sarcoidosis, cirrhosis, amyloidosis
Transudate or exudate?
Exudates have a protein level of >30 g/L; transudates have a protein level of <30 g/L.
How is unilateral pleural effusion investigated?
Does the clinical picture suggest a transudate (eg, left ventricular failure (LVF), hypoalbuminaemia, dialysis)? It is often possible to identify transudative effusions by clinical assessment alone.
- If YES, treat the cause. This may result in resolution. If it doesn't, continue with pleural aspiration, as below.
- If NO, perform pleural aspiration
Pleural aspiration (thoracentesis) >> what tests with the aspirates?
send aspirated fluid for cytology; protein; lactate dehydrogenase (LDH); pH; Gram stain, culture and sensitivity; acid-alcohol fast bacilli (AAFB) stains and culture.
If the pleural fluid protein is between 25 and 35 g/L, Light's criteria should be applied to differentiate transudates and exudates accurately.
Light's criteria state that the pleural fluid is an exudate if one or more of the following criteria are met:
Pleural fluid protein divided by serum protein >0.5
Pleural fluid LDH divided by serum LDH >0.6
Pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
typical presentation with pleural effusion
• Chest discomfort or sensation of heaviness
• Symptoms of malignancy: loss of appetite, weight, energy
• Symptoms of infection: fever, cough, sputum, night swe