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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2935_Библиотеки_им_академика_М_И_Перельмана
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Pleural Disease116
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Figure 6.5 Investigation and management of unilateral pleural effusion.
Respiratory Medicine
6.2 Pleural Effusion
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Figure 6.6
ne icidMeyrotarpiseR
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Pleural Disease118
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MICRO-references
Flowcharts adapted from the British Thoracic Society Pleural Disease
Guidelines 2023, available at:
https://www.brit-thoracic.org.uk/quality-improvement/guidelines/
pleural-disease/
8. COMPLICATIONS
Complications may be a consequence of the primary pathology e.g. malig-
•
nancy or heart failure.
Complications of effusion:
•
• Atelectasis.
• Passive lobar collapse due to volume of fluid.
• Pleural thickening and fibrosis.
• Pseudochylothorax: cholesterol-rich effusion due to chronic pleural
inflammation, usually >5 years.
• Trapped lung secondary to visceral pleural thickening.
Complications of treatment:
•
• Pneumothorax secondary to thoracocentesis.
• Re-expansion pulmonary oedema.
9. PROGNOSIS
Prognosis is related to underlying cause.
•
• Malignancy of the pleural cavity reflects incurable disease.
MICRO-case
You are a respiratory physician clerking a 70-year-old gentleman, Mr.
Tyler, who has been referred by his GP with shortness of breath and
pleuritic chest pain. On clinical examination he has a dull percussion
note and reduced breath sounds on the left side. Apleural effusion is
confirmed on CXR; however the aetiology is not clear based on the clinical history.
You arrange for pleural aspiration to be performed under ultrasound
guidance and send the sample for analysis, requesting protein and LDH
levels; microbiology; cytology and pH. In addition you send blood for
serum protein and LDH levels.
The results show a protein level of 35 g/L. As this is close to the
threshold of 30 g/L, you use Light’s criteria to confirm that the fluid is
exudative as the pleural protein: serum protein ratio is 0.6
Respiratory Medicine
and the pleural LDH: serum LDH ratio is 0.68. Cytology
continued…
6.2 Pleural Effusion
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continued…
You suspect lung cancer on the basis of Mr. Tyler’s smoking history of 50
pack-years which is confirmed on CT thorax.
As MrTyler is likely to benefit from intervention and the lung is considered re-expandable, you decide to drain the effusion and perform
talc pleurodesis. This procedure is successful.
Key Points
Light’s criteria are used in borderline cases to determine whether an
•
effusion is transudative or exudative.
Malignancies are the main cause of exudative pleural effusions.
•
The primary malignancies most commonly associated with pleural
•
effusions include lung cancer, breast cancer and lymphoma.
Management of malignant effusions is guided by prognosis and
•
symptomatic improvement.
of the aspirate reveals the presence of malignant cells.
Respiratory Medicine
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Pulmonary
Embolism
1. DEFINITION
Occlusion of the pulmonary vasculature, usually caused by a thrombus
•
which arises from the deep veins of the pelvis or lower limb.
Amniotic fluid, air embolism and fat embolism can also occur.
•
2. EPIDEMIOLOGY
e risk of venous thromboembolism is 11- .5 per 1000 person-years, but
•
varies widely depending on risk factors (see below)
Other causes of pulmonary embolism are less common.
•
3. AETIOLOGY AND RISK FACTORS
e risk factors for venous thromboembolism are:
•
• Surgery: particularly major abdominal/pelvic or lower limb surgery or
intensive care treatment post-operatively.
• Pregnancy and puerperium.
• Caesarean section.
• Lower limb fracture.
• Immobility.
• Malignancy: particularly advanced disease or abdominal/pelvic cancer.
• Trauma.
• Hormone replacement therapy/oral contraceptive pill.
• rombotic disorders.
– Factor V Leiden, protein C and S deficiency, antithrombin
deficiency.
• Myeloproliferative disorders.
• Nephrotic syndrome.
• Long-distance sedentary travel.
4. PATHOPHYSIOLOGY
Effects of the pulmonary embolism are determined by the amount of pulmo-
•
nary circulation that is affected.
• Massive pulmonary embolism:
DOI: 10.1201/9781315113937-8
Pulmonary Embolism
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– PE with haemodynamic instability:
◯
Hypotension: SBP < 90 mmHg.
◯
Postural BP drop.
◯
Syncope.
– Associated significant thrombus load on CTPA causing right ventricu-
lar outflow obstruction, with radiological features of right heart strain
– Hypoxaemia in massive PE occurs due to ventilation-perfusion
mismatch:
◯
Affected areas of the lung are ventilated but not perfused due to
obstruction of pulmonary blood flow.
◯
Increased blood flow to unaffected areas of the lung can also occur.
◯
ese alveoli are unable to sufficiently oxygenate the additional
blood volume, resulting in low PaO2.
Figure 7.1 Pathophysiology of haemodynamic instability in massive PE.
• Submassive pulmonary embolism:
– Significant thrombus load causing signs of right heart strain on
imaging tests but with absence of cardiovascular compromise.
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5. CLINICAL FEATURES
Clinical features of PE and DVT are summarised in Table 7.1.
•
Table 7.1 Clinical features of PE and DVT.
SYMPTOMS OF PE SIGNS OF PE SIGNS OF DVT
Dyspnoea Cyanosis Leg swelling
Pleuritic chest pain Tachycardia Tenderness
Haemoptysis Tachypnoea Erythema
Dizziness Hypotension/Postural Warmth
Syncope Raised JVP Engorged superficial veins
Respiratory Medicine
BP drop
Pleural rub
Pleural effusion
Gallop rhythm
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7.1 CLINICAL MANAGEMENT OF PE
1. INVESTIGATIONS
Basic investigations
•
• A number of generic tests will be required if PE is suspected.
• CXR: often normal and more helpful in excluding other diagnoses.
Findings can only be suggestive, not diagnostic, of PE.
– Atelectasis.
– Fleischner’s sign: prominent central pulmonary artery.
– Westermark’s sign: oligaemia in PE area of distribution (see Figure 7.1)
– Small pleural effusion.
• ECG: not diagnostic as an isolated test.
– Sinus tachycardia.
– New right axis deviation.
– New right bundle branch block (See Figure 7.2).
– Atrial fibrillation
– SQ
• ABG: hypoxia and hypocapnia are suggestive of PE.
TS
- wave in lead I, with Q wave and inverted T wave in lead III.
13
3
Figure 7.2 An ECG showing right bundle branch block.
Respiratory Medicine
Clinical risk scoring
•
• Any further investigations will be determined by the clinical judgement
and clinical risk scoring.
7.1 Clinical Management of PE
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• e most commonly used clinical risk scores are the Wells score (see
Table 7.2) or the Geneva score (see Table 7.3).
• e Wells score is simpler and used more commonly in the UK.
– Wells score:
◯
>4 – high risk
◯
≤4 – a low risk (although 8% of low risk patients will have a PE).
– Geneva Score:
◯
≤4 – low probability ( 10% )
◯
5–8 – intermediate probability ( 38%)
◯
>8 – high probability (81% )
• e pre-test score determines choice of investigation (See Figure 7.4).
Table 7.2 Wells Score for PE.
CLINICAL FEATURE SCORE
Clinical signs and symptoms of DVT. Yes: +3
PE most, or equally most, likely possibility. Yes: +3
Heart rate >100. Yes: +1.5
Immobilisation for at least 3 days, or surgery in previous 4 weeks. Yes: +1.5
Previous history of PE/DVT Yes: +1.5
Haemoptysis Yes: +1
Malignancy: palliative or with treatment in last 6 months. Yes: +1
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Table 7.3 Geneva Score for PE.
VARIABLE CRITERIA SCORE
Age 60–79 years 1
Past history PE/DVT 2
Surgery within last 4 weeks 3
Heart rate >100 bpm 1
PaCO
2
PaO
2
Chest X-ray findings Band atelectasis 1
>80 years 2
Respiratory Medicine
<35 mmHg 2
35–39 mmHg 1
<49 mmHg 4
49–59 mmHg 3
60–71 mmHg 2
72–82 mmHg 1
Elevated hemidiaphragm 1
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•
Respiratory Medicine
Further Tests:
• If there is sufficient clinical suspicion or the clinical risk scoring indi-
cates, further tests are required:
• D-dimer has a 96% sensitivity, but low specificity.
– Should not be used as a routine test but can be useful to exclude PE
if there is a low-risk Wells score.
◯
A low-risk Wells score and negative D-dimer indicates a very low
likelihood PE and usually is interpreted as excluding the diagnosis of PE.
◯
In other situations a negative D-dimer lacks negative predictive
value and further tests are required to confirm or exclude.
• Ventilation-perfusion nuclear medicine (VQ) scan
– A gamma camera is used to record the distribution of inhaled and
peripherally infused radio-labelled technetium. e images from
the two phases are compared to look for unmatched defects in
perfusion.
– May be offered as an alternative to CTPA in certain patients:
◯
Allergy to contrast media
◯
Severe renal impairment
◯
High risk from irradiation
– Does not provide additional diagnostic or prognostic information
although can provide an estimation of clot burden.
• CT pulmonary angiogram (CTPA) is a highly specific test for the diag-
nosis of a PE (See Figure 7.3):
– is is the most commonly used diagnostic test.
– e contrast agent may cause nephrotoxicity in patients with signifi-
cant renal impairment.
– Provides clear visual assessment of the clot burden, can show signs of
right heart strain (for prognostication) and may provide an alternative diagnosis if PE is not seen.
– More limited in ability to detect small subsegmental clots especially
if breathing artefact or incorrect timing of contrast injection.
• Pulmonary angiography: the gold standard for the diagnosis/exclu-
sion of a PE.
– It is invasive (right heart catheterisation) and has associated morbid-
ity and mortality.
– Rarely performed unless mechanical disruption or thrombectomy is
anticipated.
• Transthoracic echo (TTE): may be done in patients to identify right
ventricular (RV) strain, but not often used acutely as RV strain can be
recognised on CTPA.
7.1 Clinical Management of PE
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Figure 7.3 ACTPA scan in a patient with a central PE.
– May occasionally identify a thrombus in the right heart.
• Cardiac biomarkers: used to predict prognostic course.
– BNP/NT-proBNP: increased levels reflect the severity of haemody-
namic compromise.
– Troponin T: a marker of myocardial damage, associated with a
poorer prognosis.
• Investigations for malignancy should be considered in all patients
with unprovoked DVT/PE:
– Assessment should include:
◯
Review of medical history
◯
Baseline blood tests including FBC, U&E, liver function tests,
and physical examination
Respiratory Medicine
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