Introduction
Pulmonary embolism
Natural history of PE
Epidemiology
Pathophysiology
Clinical presentation
Assessment of pretest clinical probability
d-dimer testing
Imaging tests
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V/P imaging with SPECT (V/PSPECT) or in rare situations planar scintigraphy (V/Pplanar). Occasionally, perfusion-only lung scanning is performed. V/PSPECT may also be combined with low-dose computed tomography (CT), V/PSPECT/CT
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Computed tomography of the pulmonary arteries (CTPA)
Basic principles of PE diagnosis
Radiopharmaceuticals for V/PSPECT
Ventilation
Radiopharmaceutical | Administered activity (MBq) | Critical organ (mGy/MBq) | Effective dose (mSv/MBq) |
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99mTc-MAA [52] | 40–120 | 0.067 lungs | 0.017 |
99mTc-DTPA [53] | 20–30 | 0.047 bladder | 0.007 |
99mTc-Technegas [54] | 20–30 | 0.11 lungs | 0.015 |
81mKr [55] | 40–400 | 0.0068 lungs | 0.0007 |
Perfusion
Quality control and injection practice
Imaging protocols
Ventilation | Perfusion | |
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Administration | Inhalation | Intravenous injection |
Radiopharmaceutical administered activity | Technegas® or DTPA 25–30 MBq to reach the lung | 99mTc-MAA 120–160 MBq |
Particle size | 0.005–0.2 μm or 1.2–2 μm | 15–100 μm |
Time of imaging | ≈ 11 min | ≈ 5 min |
Acquisition protocol | ||
Reconstruction | Iterative reconstruction, e.g. OSEM with 8 subsets and 4 iterations |
Image presentation
Interpretation and reporting of findings
Ventilation/perfusion patterns
Semiology | Diagnosis | Probability that the semiologic pattern is diagnostic | Level of evidence | ||
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Pattern | Distribution | Area | |||
Mismatch | Segmental | 1 segment | PE* | Very high | |
≥ 2 subsegments | PE* | Very high | |||
≤ 1 subsegment | Non-PE | High | |||
Total lung unperfused | Total lung | Tumour# | High | ||
Abscess# | High | ||||
Massive PE | Very low (rare) | Very rare condition | |||
Nonsegmental | Systematically antigravitational redistribution | Heart failure | High | ||
Irregular | Vasculitis | Very low (rare) | Very rare condition, expert opinion | ||
Match | Segments or lobules | No stripe sign | Tumour | Depends on clinical context | |
Atelectasia | |||||
Empyema | |||||
Stripe sign | Pneumonia evolutioned stage | High | |||
Reverse mismatch§ | Segments or lobules | Stripe sign | Pneumonia initial stage | High | |
No stripe sign | COPD | High |
Criteria for acute pulmonary embolism
PE: • V/P mismatch of at least one segment or two subsegments in keeping with the pulmonary vascular anatomy (wedge-shaped defects with the base projecting to the lung periphery). | |
No PE: • Normal perfusion pattern in keeping with the anatomic boundaries of the lungs. • Matched or reversed-mismatched V/P defects of any size, shape or number in the absence of mismatch. • Mismatch that does not follow a lobar, segmental or subsegmental pattern. | |
Nondiagnostic for PE: • Widespread V/P abnormalities not typical of specific diseases. |
Pitfalls in the interpretation of V/PSPECT
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Technical artefacts may arise from preinjection handling of the 99mTc-MAA. The withdrawal of blood into the syringe that contains the solution of 99mTc-MAA can cause the aggregation of particles that can produce hotspots in the images. A similar consequence can appear from failure to resuspend 99mTc-MAA particles before the administration.
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Planar imaging may underestimate the presence or extent of perfusion abnormalities because of normal perfusion masking embolised regions, also known as the shine through of normal areas. This problem is eliminated by V/PSPECT.
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In rare cases, vasculitis and congenital vascular anomalies may lead to segmental/lobar mismatches.
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Mismatched perfusion defects without a clear segmental character may be seen in older, partly resolved PE, but not related to acute PE. These nonsegmental mismatched defects are observed in several lung disorders including lung cancer, mediastinal lymphadenopathy, postradiation pneumonitis/fibrosis and heart failure. V/PSPECT facilitates the identification of segmental perfusion defects, which are particularly well visualised when using rotating 3D volumetric images.
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Unilateral absence of perfusion in a whole lung with preserved ventilation and without any V/P mismatch in the other lung is generally not due to PE [80, 81]. In such cases, chest CT may reveal the presence of other pathologies such as tumour, aortic dissection, other mediastinal processes or congenital pulmonary vascular abnormalities.
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Fissure artefacts are a common finding along the line of the oblique fissure, especially in perfusion SPECT. It may produce a nonsegmental mismatch [57].
Additional considerations
Quantification of PE extent
Follow-up
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Assess therapy effect
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Differentiate between new and old PE when there is a suspicion of PE recurrence
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Explain physical incapacity after PE
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Applicability to all patients
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Low radiation dose
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High sensitivity to allow estimation of resolution of even small emboli and occurrence of new ones
V/PSPECT/CT
CTPA
Risks of CTPA
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Iodine hypersensitivity. Severe pseudoallergic reactions are generally very rare (approx. 0.04%, rarely fatal [102]). In an emergency scenario when CT cannot be withheld, intravenous premedication may be suitable.
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Thyroid dysfunction. Induction of hyperthyroidism and in rare cases also hypothyroidism is another complication associated with iodinated contrast media [103]. In an iodine-deficient geographical region, 2% of patients developed subclinical hyperthyroidism [104]. In unselected patients, overt hyperthyroidism occurred in 0.25% within 12 weeks [105]. Iodine-induced thyrotoxicosis is often overlooked in the elderly [106], and in the worst case, it may even cause a thyroid storm with cardiac arrest [107]. Risk factors are (potentially undiagnosed) Graves’ disease and/or thyroid autonomy [108]. Patients with thyroid storm should not receive iodinated contrast media at all; in other cases, premedication with oral sodium perchlorate (and thiamazole) may be helpful. Under emergency conditions, this treatment may be initiated directly after contrast exposure. Thyroid function is routinely monitored prior to contrast application in the vast majority of radiological institutions through serum baseline TSH.
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Renal dysfunction. The most severe complication of CTPA is contrast media-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI). CI-AKI is defined as an increase in serum creatinine within 48–72 h after intravenous administration of low- or isoosmolarity iodinated contrast media. It carries a risk of chronic renal insufficiency, dialysis and death [100, 109]. The assumption of causality between intravenous contrast media administration and AKI has been challenged in recent publications, but data are controversial. The baseline glomerular filtration rate (eGFR) was found to be an independent predictor of AKI [110]. In two multivariate analyses, patients with an eGFR ≤ 43.6 mL/min [111] or eGFR < 60 mL/min [112], respectively, had the potential to develop CI-AKI. The odds ratios in the incidence of CI-AKI between contrast-enhanced CT and noncontrast CT increased below an eGFR < 30 mL/min [113]. In two meta-analyses, contrast-enhanced CT, compared with non-contrast-enhanced CT, was not significantly associated with AKI [114, 115]. In a large single-centre retrospective cohort study, the probability of developing AKI was 10.6%, 10.2% and 10.9% in the contrast-enhanced, unenhanced and non-CT group [116]. However, a selection bias must be considered as only a minority of patients with a baseline serum creatinine > 1.5 mg/dL received contrast media and factors that may have influenced the clinical decision to administer contrast media could not be perceived. Randomisation of patients to receive intravenous contrast media, once not considered ethically feasible, will be necessary to fully understand the role of contrast media in precipitation of renal dysfunction [116]. Current guidelines consider intravenous contrast administration to be safe to a creatinine clearance of 30 mL/min/1.73 m2 [117]. In almost every radiological institution, a baseline serum creatinine level and/or eGFR is determined prior to intravenous contrast administration to identify patients at risk. CI-AKI was considered to be the third most common cause in hospital acquired AKI [118]; now strong evidence is provided that the incidence of CI-AKI is substantially lower [109]. AKI is a multifactorial entity, and usually more than one risk factor (contrast media, nephrotoxic drugs, hypertension, age > 70 years, reduced cardiac output, diabetes mellitus and others) is involved [102].
Comparison of V/PSPECT and CTPA (see also Table 4)
V/PSPECT | CTPA | Comment | |
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Availability | Limited | Wide | Makes CTPA indispensable |
Feasibility | Near 100% | Up to 50% | Makes V/PSPECT indispensable |
Rate of nondiagnostic studies | |||
Sensitivity | ≥ 96% | ≥ 78% | In high clinical probability, 40% needs further exam |
Specificity | ≥ 97% | ≥ 98% | V/PSPECT and CTPA equivalent |
Effective radiation dose | 1.2–2 mSv | ||
Absorbed breast radiation dose | ≈ 0.8 mGy | V/PSPECT crucial for young women | |
Additional diagnoses | Common, important | Common, important | Highest documented rate—V/PSPECT |
Diagnostics of chronic pulmonary embolism | Reference method? | Not useful but needed prior to surgery? | V/PSPECT is gold standard |
Follow-up and research | Optimal | V/PSPECT offers quantitative data |
Accuracy of PE diagnosis
Radiation exposure
Additional diagnostic contributions of V/PSPECT
Chronic obstructive pulmonary disease
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Grade 1: uneven aerosol distribution through the lung seen in mild COPD.
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Grade 2: uneven aerosol distribution and reduced Technegas® penetration to the periphery, with deposition of aerosols in small airways, seen as hotspots. This indicates moderate COPD.
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Grade 3: a severely impaired Technegas® penetration to the periphery and a central deposition of Technegas® in large airways, usually with large areas of reduced/absent ventilation. This indicates severe COPD. Figure 8 presents a case with severe COPD, emphysema and PE.
Left heart failure
Pneumonia
Chronic pulmonary embolism and chronic thromboembolic pulmonary hypertension
Lung cancer radiotherapy planning
Pregnancy
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The incidence of PE in pregnancy is about fivefold higher than in nonpregnant females of a similar age and is the leading nonobstetric cause of death during pregnancy in developed countries. The incidence of PE and DVT is about 1 and 3‰, respectively [171]. The incidence is similar in all 3 trimesters [172]. The diagnostic accuracy of any test is compromised by a low prevalence of PE in this collective [147, 173].
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CTPA leads to unique radiation hazards to the maternal breast [180].