(1)
Hôpital Ambroise Paré Service de Réanimation Médicale, Boulogne (Paris-West University), France
Pulmonary embolism has a special place in most minds, probably because of the risk of sudden death if the diagnosis is not immediate. Atypical cases, generating delays in the therapy, are the most dangerous. Any help should be studied with interest, especially if noninvasive.
This disease was the guest star of our previous edition, featuring in six chapters (DVT, pleural effusion, alveolar syndrome, interstitial syndrome, echocardiography, all acute situations). It benefits here from a synthesis.
The BLUE-protocol aims at expediting the diagnosis. We no longer ask whether ultrasound examination should be ordered or not. We just do it routine. It allows most of the time to avoid transportation of unstable patients to the CT room. Or worse, to initiate blind heparin therapy or blind thrombolysis in this shocked patient without major proof. Finding here evidence of embolism, or there differential diagnoses (pneumonia, pulmonary edema, abdominal disorders with thoracic pain, etc.), our simple approach should find interest to the intensivist.
Pathophysiological Reminder of the Disease
For various reasons, a thrombosis is formed in the venous network. This thrombosis extends, is dislodged, and creates an embolism when the cross section of the vessel prevents further migration. Very large clots are stopped at main branches of the pulmonary arteries, creating massive circulatory disorders. Transversal roads avoid distal ischemia. If very small clots migrate up to the deep areas of the lung, hemodynamic disorders are minimal (unless the clots are very small but numerous), but the distal circulation is altered, resulting in local areas of infarction, hemorrhage, etc. Lung vessel occlusion is not supposed to be accessible using transthoracic ultrasound. Pulmonary embolism does not yield interstitial change.
The Usual Ways of Diagnosis
Obvious cases raise minor issues, when, e.g., a patient with risk factors (contraceptive pill, e.g.) has chest pain, dyspnea, painful leg, etc. In other instances, the diagnosis is more subtle. Sometimes, pulmonary embolism generates an acute circulatory failure, sometimes mimicking septic shock. Cardiac arrest is another familiar presentation.
We don’t know any direct and specific clinical sign of embolism. The radiograph is traditionally and schematically normal, of importance for the logic of the BLUE-protocol. Subtle signs are in actual fact often present (plane atelectasis, elevated cupola, among others). The ECG can show the signs of the series of Stein [1]. Blood gases show hypoxia and hypocapnia. D-dimers are positive. The pulmonary artery angiography has long been replaced by the angio-CT, which shows the clots within the branches of the pulmonary arteries. Traditional echocardiography shows signs of acute right failure. Transesophageal echocardiography can rarely show the embolus within a branch of the pulmonary artery [2]. This is a direct sign. In exceptional, privileged cases, simple ultrasound with the microconvex probe can expose the main pulmonary arteries and demonstrate the clot (Fig. 26.1). The most direct way should probably be endovascular ultrasound [3] that could possibly be done at the bedside (read Anecdotal Note 1).
Fig. 26.1
The right pulmonary artery. This artery (PA) is seen through its short axis, surrounded by the aortic arch (A). Suprasternal scan (only short footprints, and inconstantly, can achieve this route). Floating tissular patterns can here directly demonstrate acute pulmonary embolism in an extreme emergency. The conjunction of a chancy window and a rare pattern using external route makes a rather rare sign – which should deserve however to be routinely sought for
For this daily concern, many issues are raised. The clinical data have notorious insufficiencies [4, 5], an issue when the risk of death from undiagnosed cases is 40% [1, 6]. The usual diagnostic tools were, and still are, risky [6]. Their accuracy can be debated [7]. D-dimers raise increasing reluctance. Helical CT, the gold standard, is not perfect [8]. It misses very distal clots, a real issue if they are numerous (and generate circulatory troubles). Giving inappropriate therapy has an 11% risk of major bleeding and a lethal risk between 0.7% and 1.8% [9–11]. The abundance of current protocols indicates the importance of the issues generated by this disease in the physicians’ minds.
When to Proceed to the BLUE-Protocol? Which Signs? Which Accuracy?
In the BLUE-protocol, the diagnosis of pulmonary embolism is prioritized (compared to COPD, asthma, posterior pneumonia), because these critically ill patients are at high risk of suddenly worsening.
The A-Profile
Massive pulmonary embolism typically generates an A-profile, found in 95% of cases with acute respiratory failure. Sensitivity is 95 % [12].
Venous Thrombosis
It was found in 81 % of cases in the BLUE-protocol (i.e., an 81 % sensitivity [12]). This number stabilizes around 78 % with large number of cases (under submission). These data were acquired using a specific tool and a specific method.
The location of the DVT is usually correlated with the severity of embolism. We never saw caval thrombosis at the time of diagnosis. In data under submission, common femoral location is present in 1/4 of cases, low femoral location in 1/2 of cases, and calf location in 2/3 of cases. The more severe the embolism, the more distal the remaining thrombosis.
The A-Profile and Deep Venous Thrombosis
The association of A-profile plus DVT has a 99 % specificity [12].
Lung Consolidations
Posterolateral locations are found in half of the cases (52 % precisely), often located against the diaphragm, usually of small volume, often associated with small pleural effusions [12]. Note that a posterolateral analysis is not required in the BLUE-protocol once an A-profile and a DVT have been found, since the diagnosis is done, with or without PLAPS. Anterior locations of lung consolidation were 5 % [12].
Echocardiographic Signs
We remind that they are not included in the BLUE-protocol. They were long standardized [2]. The dilatation of the right ventricle is of major relevance in acute circulatory failure (the relevance is more moderate in acute respiratory distress, where several causes can create it). The BLUE-protocol has demonstrated that a patient with acute respiratory failure and an A-profile (the usual presentation of pulmonary embolism) has no left heart failure – since there is no sign of pulmonary edema. This patient has usually the right heart failure common to embolism, pneumonia, COPD, etc. The place of echocardiography can therefore be simplified.
Value of the BLUE-Protocol for Ruling Out Other Diseases
The DVT, when found, is more than a strong argument for pulmonary embolism. However, in the BLUE-protocol, it is advised to begin by the lung (showing an A-profile); this association provides a 99% specificity. If no attention is paid to the lung, the specificity losses five points: the positive predictive value of deep venous thrombosis alone was 89 %, but 94 % if associated with the A-profile [12].
The A-profile has a low specificity (50 %): it is seen in quite all cases of COPD, asthma, and posterior pneumonia with no anterior interstitial extension. In all these diseases, there is no reason for finding a DVT. If a DVT has been found in patients with known COPD or asthma, this DVT is likely the cause of the acute exacerbation. The A-profile is seen in all healthy subjects.
Ultrasound Pathophysiology of Pulmonary Embolism
The physiopathology of pulmonary embolism explains the A-profile. There is no factor able to abolish lung sliding. Interstitial signs are not expected. Anterolateral lung rockets are uncommon. The normality of the ultrasound lung examination is the equivalent of the normal chest X-Ray. The PLAPS may be explained by the hemorrhages, infarctions, and atelectatic areas.
Why Not 100 % Accuracy? The Limitations of the BLUE-Protocol
How About Patients With Severe Pulmonary Embolism and No Visible Venous Thrombosis?
The main limitation comes from these 19 % of patients who had no, or no longer, visible DVT. How to manage such cases?
The clue is simple: common sense (a synonym of “Extended BLUE-protocol”). We remind that the BLUE-protocol is only a protocol, and the physician, who has already a diagnosis in mind, must permanently “pilot” this BLUE-protocol. When the clinical setting points on a possible embolism, explorations should go further. A young lady who has no history of asthma, has a recent orthopedic surgery, complains from sudden chest pain and acute respiratory failure, and displays an A-profile, with positive D-dimers and pathologic ECG is a perfect suspect. As a rule, a patient with the nude profile (A-profile, no DVT, no PLAPS, in other words, normal lungs, normal veins) is diagnosed “COPD or asthma” by the BLUE–protocol. If the history does not point out such diseases, although we can face a first crisis, pulmonary embolism must be envisaged by the physician.
How About Patients with Lung Rockets Instead of the A-Profile?
The B-profile was not seen in the patients of the BLUE-protocol. Its frequency in larger groups stabilizes around 2 % (and the A/B profile in 2 %, study on submission). In these rare cases of lung rockets, they were septal rockets. We still wait our first case of massive pulmonary embolism (not complicating a chronic interstitial syndrome, not complicating an ARDS) with a bilateral ground-glass rocket pattern. In other words, the ground-glass-profile (i.e., bilateral ground-glass rockets) has up to now a 100 % negative predictive value for pulmonary embolism. There is no reason to see a B′-profile. An A′-profile will be seen in all patients with chronic abolition of lung sliding (history of pleural diseases), and there cannot be any lung point there.
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