Lung ultrasound in the critically ill - The BLUE protocol: Part 2

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Part II The BLUE-Protocol in Clinical Use The Ultrasound Approach of an Acute Respiratory Failure: The BLUE-Protocol Severe dyspnea is one of the most distressing situations for a patient. Aiming at a therapy based on immediate diagnosis is a legitimate target. The acute incapacity to breathe is one of the most distressing situations one can live [1]. The BLUE-protocol concentrates 18 years of efforts (mainly repeated submissions) aiming at promptly relieving these patients. The idea of performing an ultrasound examination in time-dependent patients was not far from a blaspheme in 1985, definitely not envisageable according to the rules. Our approach possibly intrigued some doctors and nurses in the ERs of our institutions. During the management of these critical situations, time was not for quiet explanations. What the emergency doctors (who had to rush to the next patient in the overcrowded ER and eventually rushed after duty for a deserved nap, end of the story) did not fully see was that, after a few minutes, we were able to give to the nurse therapeutic options, while organizing the transfer to the ICU. And what they did not see at all (occupied by 1,000 other tasks, medical, administrative, familial, etc.: this was not time for international guidelines on lung ultrasound) was that these options were in accordance with the final diagnosis. In the emergency setting, we use familiar tools since decades and centuries, mainly physical 20 examination [2] and radiography [3], two basic tools, yet increasingly known for having limited precision. The crowded emergency room is not the ideal place for serene work, an acknowledged issue [4–8]. One-quarter of the patients of the BLUE-protocol in the first hour of management received erroneous or uncertain initial diagnoses, and many more received inappropriate therapy. The online document of Chest 134:117–125 details these 26 % of wrong diagnoses. CT seems a solution, but Chap. 29 will demonstrate its heavy drawbacks. One day, the community will maybe find this tool definitely too much irradiating [9]. We initiated this long work using an ADR4000 (from 1982) then shifted for our Hitachi-405 (from 1992, last update 2008). Their 3 MHz sectorial probe and 5 MHz microconvex probe were perfectly suitable. The Spirit of the BLUE-Protocol Basically, the BLUE-protocol is a protocol. Yet it was designed for being a flexible one. Some protocols are possibly built for exempting doctors to think, but this one requires to keep on being a doctor. It is permanently “piloted.” In some situations, it will just confirm an obvious diagnosis. In others, it will confidently invalidate a diagnosis which looked the likely one. For being perfectly understood (and anticipating remarks), the BLUE-protocol should be D.A. Lichtenstein, Lung Ultrasound in the Critically Ill: The BLUE Protocol, DOI 10.1007/978-3-319-15371-1_20, © Springer International Publishing Switzerland 2016 157 158 20 The Ultrasound Approach of an Acute Respiratory Failure: The BLUE-Protocol considered as an “intellectual exercise,” a tool just designed for using the minimal bunch of data for the maximal accuracy, when used alone. Countless articles are now using lung ultrasound, and many propose various algorithms including echocardiography and other items, advocating a “multiorgan approach.” This is not the spirit of our protocol: it associates these various items but does not include them (the difference is substantial). Comparing these studies with our approach would therefore make little sense. Regarding, for instance, the heart, see at the end of this chapter and at the end of Chap. 24 that we did not “forget” it (it is known that searchers may sometimes be absent minded, but up to forgetting the heart, there is a substantial step!); we just deleted it from our data. The accuracy of “BLUE-protocol plus echocardiography” is anyway featuring at end of this chapter, and we invite the readers to make an opinion. Same remark for all clinical signs. Some academicians reproached to the BLUE-protocol to forget these precious signs [10] (don’t miss the discussion at the end of Ref. [10]). The clinical signs are, ironically, in the center of the Extended BLUE-protocol, for an improved accuracy (Chap. 35). The BLUE-profiles are here, available, up to this respected physician to integrate his favorite clinical data at will in his clinical approach. The Design of the BLUE-Protocol The BLUE-protocol was conceived in an observational study in a Parisian universityaffiliated teaching hospital. We performed ultrasonography on admission, in the climax of dyspnea, on serial patients with acute respiratory failure. Acute respiratory failure was defined based on clinical criteria requiring admission to the ICU. The gold standard was the final diagnosis considered in the hospitalization report, made by a medical ICU team (expert panel) who did not take into account the lung ultrasound data and used traditional approaches. Uncertain diagnoses, multiple diagnoses, and rare causes (frequency <3 %) were excluded (see Chap. 21). After years necessary for the publication of the preliminary background (mostly lung terminology), we were able to propose the analysis of three items at the lung area – with dichotomous answer, collected at standardized points (upper and lower BLUE-points, PLAPS-point). 1. Abolished anterior lung sliding (yes or no) 2. Lung rockets at the anterior wall (present or absent) 3. Alveolar and/or pleural syndrome (called PLAPS if posterior or/and lateral) (yes or no) We added an adapted venous analysis (indicated in 54 % of cases). Note that the venous analysis takes the major time (2 min of a 3 min examination), which is nonetheless short, since we use a simple machine with fast start-up, the same microconvex probe, time-saving maneuvers, only one setting, and a contact product which allows major time savings. This will be repeated again, intentionally. The BLUE-Profiles: How Many in the BLUE-Protocol? A work of a “profiler,” based on analysis of hundreds of pre-data, was done during 7 years. From this observational work, the profiles of the BLUE-protocol were defined (Fig. 20.1). There are eight profiles. The anterior analysis, which initiates the BLUE-protocol, can describe six situations. Five of them conclude the protocol: the B-, B′-, A/B-, C-, and A′-profile. One of them is the A-profile (Video 10.1). The A-profile designates an anterior chest wall with predominant A-lines and lung sliding. The A-profile opens to three more profiles (A-DVT, A-no-VPLAPS, and nude profile). Here are the profiles, which were assimilated to specific diseases. The term “profile” assumes an association of signs (two), plus a location (Fig. 20.2). 1. The A-profile plus DVT was assimilated to pulmonary embolism. The term “DVT” or “no DVT” was fully detailed in Chap. 18, because it is integrated in a specific, adapted protocol. 2. The A-no-V-PLAPS profile is a temporary label which designates an A-profile with no The BLUE-Profiles: How Many in the BLUE-Protocol? 159 (anterior BLUE-points) Lung sliding B-profile Pulmonary edema Present Any A-profile A/B-profile C-profile Sequential venous analysis Thrombosed vein The BLUE protocol Abolished A'-profile B'-profile PNEUMONIA PNEUMONIA Plus lung point Without lung point Free veins Pneumothorax Pulmonary embolism Stage 3 Need for other diagnostic modalites (PLAPS-point) (A-DVT-profile) PLAPS Pneumonia (A-noV-PLAPS-profile) no PLAPS COPD or Asthma (nude profile) This decision tree is not designed for providing 100 % of diagnoses of acute dyspnea. It has been simplified with the target of overall accuracy just > 90 % (90.5 %) Fig. 20.1 The decision tree of the BLUE-protocol. A decision tree using lung and venous ultrasound to guide the diagnosis of acute respiratory failure: the BLUE- protocol (Adapted from Lichtenstein and Mezière [11], with the authorization of Chest) Fig. 20.2 Regular distributions. The main regular profiles of the BLUE-protocol. Note that this figure uses a particular representation of the B-profile and the B′-profile in static images: on M-mode, lung sliding is materialized by this succession of vertical white and black stripes (it reminds real-time images done with vascular probes), since the B-lines come and go through the shooting line of the M-mode. Abolished lung sliding generates a homogeneous MM-space in M-mode: hyperechoic if the shooting line strings a B-line (like here) and hypoechoic if done between two B-lines. Note for the C-profile than only one point is required. The A′-profile does not feature for space management (already dealt with) DVT and with a PLAPS (uni- or bilateral). Called in some of our articles the A-VPLAPS-profile, it is now slightly longer but more logical, thus hopingly easier to remember. When “A-no-V-PLAPS” is spelled slowly, we can understand “A,” i.e., no pneumothorax and no pulmonary edema; then “no V,” i.e., schematically, pulmonary embolism unlikely; and then “PLAPS,” making at this step COPD/ asthma unlikely. The A-no-V-PLAPS profile was assimilated to pneumonia. 3. The nude profile is a normal profile, i.e., A-profile with no DVT and no PLAPS. It was assimilated to asthma or COPD, two bronchial 160 20 The Ultrasound Approach of an Acute Respiratory Failure: The BLUE-Protocol diseases put together because of a same origin (bronchial obstruction), a roughly same therapy, and a same pathophysiological absence of interstitial, alveolar, pleural, or venous signs. 4. The B-profile designates anterior predominant bilateral lung rockets associated with lung sliding (Video 13.1). It was assimilated to hemodynamic pulmonary edema. 5. The B′-profile is a B-profile with abolished lung sliding (Video 13.2). It was assimilated to pneumonia. 6. The A-/B-profile designates anterior predominant lung rockets at one side and predominant A-lines at the other. It was assimilated to pneumonia. 7. The C-profile designates anterior lung consolidation, regardless of size and number. The C-profile was assimilated to pneumonia. 8. The A′-profile is an A-profile with abolished lung sliding (Video 14.2). When a lung point was associated, it was assimilated to pneumothorax. Once these profiles were predefined as written, the study could begin. We then assessed the concordance between profiles and diseases. Some Terminology Rules We specify the precise language used in the BLUE-protocol for enabling other teams to reproduce our results. When the first of the four anterior BLUEpoints shows lung sliding with A-lines, labeling it a “quarter of A-profile” indicates that the user has understood that the “A-profile” is defined on the four anterior points. We prefer to read that a given patient had “four quarters of B-profile” (i.e., a B-profile, clearly expressed). One of the four anterior points with a lung consolidation, even minute (C-line), makes a C-profile. One isolated B-line visible at all four anterior BLUE-points: this is such a rare pattern that we do not know its clinical relevance. We should temporarily consider this profile as an A-profile. Some profiles should not generate too much troubles (Fig. 20.3). A quarter of B-profile visible on three of the four anterior BLUE-points makes sensu stricto “three-quarters of a B-profile.” It should probably be linked to a B-profile. A quarter of B-profile at the right upper BLUE-point with a quarter of B-profile at the left lower BLUE-point and a quarter of B-profile at the right upper BLUE-point with a quarter of B-profile at the left upper BLUE-point are rare profiles, rare enough for not having been seen in the BLUE-protocol. We think wise and logical to link such profiles to an irregular A/B-profile (much more than a B-profile) – suggesting pneumonia/ARDS. Two-quarters of B-profile at the two lower BLUE-points: this profile, seen in 5 % of cases of hemodynamic pulmonary edema, should probably be considered as an irregular B-profile Fig. 20.3 Atypical distributions. Some atypical distributions of anterior lung rockets The Results 161 (patient under beginning of depletive therapy?). Three-quarters of A-profile with one-quarter of B-profile must be assimilated to an A-profile. This is usually a pneumonia, which will be recognized using the long sequence of the BLUEprotocol: no venous thrombosis and a PLAPS usually present: “A”-no-V-PLAPS-profile. The Results At the submission of the manuscript, 302 patients were analyzed. After exclusion of 16 patients for unknown diagnosis, 16 for double diagnosis, and 9 for rare diagnosis, 260 dyspneic patients with one definite diagnosis were considered. The main causes of acute respiratory failure seen in our walls were pneumonia (31 %), pulmonary edema (24 %), decompensated COPD without cause (18 %), severe asthma (12 %), pulmonary embolism (8 %), and pneumothorax (3 %). Table 20.1 details our results. In this population, the BLUE-protocol alone provided the correct diagnosis in 90.5 % of cases [11]. Each of the BLUE-profiles warranted a specificity for the considered disease greater than 90 %. Table 20.1 details the accuracy of ultrasound for each diagnosis. All these major causes of acute respiratory failure in the adult have characteristic patterns. Acute hemodynamic pulmonary edema: nearly all cases, i.e., 62 of 64, yielded bilateral disseminated anterior lung rockets, a pattern always associated to lung sliding: the B-profile. PLAPS were present in 56 of 62 cases. Pneumonia: of 83 cases, 74 had one of four characteristic profiles. The A-no-V-PLAPSprofile was seen in 35 cases, the C-profile in 18, the A/B profile in 12, and the B′-profile in 9. Each of these four profiles was infrequent, but the sum made an 89 % sensitivity, and these patterns were 94 % specific to pneumonia. Exacerbated COPD, severe asthma: patients had usually a normal pattern (nude profile). Of 49 cases of COPD, 7 had pathologic patterns. These results will be commented below (“missed” cases of the BLUE-protocol). Pulmonary embolism: patients had nearly always (20 of 21) an anterior normal surface (A-profile). None had anterior lung rockets (in the B, A/B, or B′ variant). Eighty-one percent had visible deep venous thrombosis. Half of the cases had PLAPS. Table 20.1 Accuracy of the BLUE-protocol Mechanism of dyspnea Acute hemodynamic pulmonary edema Exacerbated COPD or severe asthma Pulmonary embolism Pneumothorax Pneumonia Profiles of BLUE-protocol B-profile Nude profile (A-profile with no DVT and no PLAPS) A-profile with deep venous thrombosis A′-profile (with lung point) 1. B′-profile 2. A/B-profile 3. C-profile 4. A-no-V-PLAPS profile The four profiles Adapted from Lichtenstein and Mezière [11] Brackets: No. of patients Sensitivity 97 % (62/64) Specificity 95 % (187/196) Positive Negative predictive value predictive value 87 % (62/71) 99 % (187/189) 89 % (74/83) 97 % (172/177) 93 % (74/79) 95 % (172/181) 81 % (17/21) 99 % (238/239) 94 % (17/18) 98 % (238/242) 88 % (8/9) 100 % (251/251) 100 % (8/8) 99 % (251/252) 11 % (9/83) 14.5 % (12/83) 21.5 % (18/83) 42 % (35/83) 100 % (177/177) 100 % (177/177) 99 % (175/177) 96 % (170/177) 100 % (9/9) 100 % (12/12) 90 % (18/20) 83 % (35/42) 70 % (177/251) 71.5 % (177/248) 73 % (175/240) 78 % (170/218) 89 % (74/83) 94 % (167/177) 88 % (74/84) 95 % (167/176) 162 20 The Ultrasound Approach of an Acute Respiratory Failure: The BLUE-Protocol Pneumothorax: all had abolition of anterior lung sliding with the A-line sign (A′-profile). Eight of nine had a lung point. These profiles and results will be sharply explained, detailed, and commented in the following chapters. Pathophysiological Basis of the BLUE-Protocol The pathophysiology fully explains the scientific basis of the BLUE-protocol and the results. It is detailed in devoted chapters, one per disease (see Chaps. 23, 24, 25, 26, and 27). A-lines indicate air, which can be physiological (normal lung surface seen in COPD, asthma, pulmonary embolism, and anterior wall of posterior pneumonia) or pathological (pneumothorax). Lung rockets indicate interstitial syndrome. Hemodynamic pulmonary edema and some cases of pneumonia display anterior and symmetric lung rockets. Alveolar and pleural changes are usually posterior (defining PLAPS) and are common to pulmonary edema, pneumonia, and pulmonary embolism (even pneumothorax), therefore not of major discriminating potential if used alone. Anterior consolidations are typical of pneumonia. PLAPS not associated with anterior interstitial changes are seen in pneumonia and pulmonary embolism. PLAPS have a discriminative value only in patients with A-profile and without venous thrombosis: this provides a BLUE diagnosis of pneumonia, likely. Lung sliding is seen in hemodynamic pulmonary edema, a disease which creates a transudate. Transudate is a kind of oil, allowing us to breathe from birth to death without burning. Lung sliding is also seen in pulmonary embolism, COPD, and some pneumonia. It is present in asthma, although of limited amplitude in very severe cases. Abolished lung sliding is seen in many cases of pneumonia, a group of diseases which create exudate. Exudate acts like glue, sticking the lung to the wall. Pneumothorax always abolishes lung sliding. The Decision Tree of the BLUEProtocol (Fig. 20.1) To get a 90.5 % accuracy in a few minutes, we first check for anterior lung sliding. Its presence discounts pneumothorax. Anterior B-lines are then sought. The B-profile calls for pulmonary edema. B-′, A/B-, and C-profile call for pneumonia. The A-profile prompts a search for venous thrombosis. If present, the BLUE-diagnosis is pulmonary embolism. If absent, PLAPS are sought. Their presence (A-no-V-PLAPS-profile) calls for pneumonia and their absence (nude profile) for COPD or asthma. To get a far higher accuracy, read Chap. 35. The Missed Patients of the BLUEProtocol. What Should One Think? An Introduction to the Extended BLUE-Protocol These critical points are developed through the textbook. The BLUE-protocol was designed for using the simplest decision tree for reaching the highest accuracy. The target to reach was the value of “90 %” (it was, actually, 90.5 %). Wanting to reach 91, 92 %, etc., would have complicated this decision tree, and so on, up to the theoretical value of 100 %. Reminder, the BLUEprotocol is only a protocol. It should be considered as a tool, permanently piloted by the physician. Using basic clinical data, some simple tests (ECG, D-dimers, etc.), the common sense (a precious tool), and some more developed ultrasound tools (in one sentence, performing an Extended BLUE-protocol), the accuracy climbs substantially. Please consider the BLUE-protocol as an initial approach (with already an overall 90.5 % accuracy, just used alone). In 9.5 % of included patients, the BLUEprotocol yielded a profile which was not in agreement with the official diagnosis. We must consider two groups. 1. Some are real limitations (4 %). Pulmonary embolism without visible venous thrombosis (19 %) is a typical limitation of the BLUE-protocol. Pneumonia with the When Is the BLUE-Protocol Performed B-profile (7 %) looks like hemodynamic pulmonary edema. Piloting the BLUE-protocol would correct this kind of limitation. Just a short example, in a pneumonia with a B-profile, considering simple signs (history, fever, white cells, etc.) and simple emergency cardiac sonography, the physician enters into the Extended BLUE-protocol and usually corrects the error. See Chap. 22, and don’t forget to read, once basic data are integrated, Chap. 35. 2. Other cases (5.5 %) possibly indicate a failure of the gold standard. When a patient has standardized ultrasound signs of lung consolidation and receives the official diagnosis of exacerbated COPD, there is likely a failure in the traditional tools. This patient has likely a superadded diagnosis (radio-occult pneumonia, pulmonary embolism). Patients with the B-profile but officially considered COPD are other possible mistakes. Patients without the B-profile but considered pulmonary edema are again possible mistakes. These cases are detailed in Chaps. 24 and 25. All in all, while accepting the final diagnosis as a gold standard, we consider that the Fig. 20.4 Integration of the BLUE-protocol in the traditional management. This figure illustrates the usual steps of management of an acute respiratory failure, and the place that the BLUE-protocol and the simple emergency cardiac sonography can take, between the clinical examination and the first paraclinical tests. One main aim of the BLUE-protocol is to relief the patient before – or in 163 90.5 % rate of correct diagnoses is below the reality. We may calculate an officious rate of 90.5 + 5.5 %, i.e., 96 % (−1 % for the science, say 95 %), yet this kind of calculation would violate the rules of scientific publications. In any honest study, the gold standard cannot be always perfect, but how to prove it, when it is the gold standard? Just common sense can alert. Commercial pilots make mistakes; we assume doctors are not exempt from some mistakes too. When Is the BLUE-Protocol Performed The raison d’être of the BLUE-protocol, which uses ultrasound alone, is to be inserted in the first stages of the usual management of an acute dyspnea. In this traditional management, one can describe three steps (Fig. 20.4): 1. Step 1: The physician receives the patient and, time permitting, learns the history and makes the physical examination. This step is decisive. A young dyspneic patient with fever has not the same disease with an apyretic old cardiopathic one, e.g. substitution to – the usual late tests (Step 3). We aim at making the simple clinical examination, the BLUEprotocol, the simple cardiac sonography, and the initial current basic tests the fab four in acute respiratory failure management. The integration of the BLUE-protocol within these three other major tools is part of the definition of the Extended BLUE-protocol 164 20 The Ultrasound Approach of an Acute Respiratory Failure: The BLUE-Protocol 2. Step 2: Simple tests are done, like ECG, D-dimers, and basic venous blood tests (see below). 3. Step 3: With all these elements in hand, the doctor decides whether sophisticated examinations will be ordered. This is usually time for asking a CT scan or a sophisticated echocardiography. The BLUE-protocol aims at being inserted between Step 1 and Step 2. Its 90.5 % official rate of accuracy will be dramatically enhanced using basic data, making the need for the traditional Step 3 less mandatory (see below), for reaching the LUCIFLR spirit (Chap. 29). The Timing: How Is the BLUEProtocol Practically Used The BLUE-protocol is usually done in Stage 1′ (semirecumbent patient). We apply the probe on the right upper BLUE-point (1″). We identify the bat sign (2″). Then we search for lung sliding. With experience, two seconds are enough to recognize lung sliding (2″). Pneumothorax is instantaneously ruled out. Then we analyze the Merlin’s space. A-lines should be rapidly identified (2″). A pulmonary edema is ruled out. A routine Carmen’s maneuver indicates that no B-line is visible. This takes 3″. The lower BLUE-point is then analyzed (10 more seconds). The left lung analysis adds 20″. Facing a B-profile, an A/Bprofile, a C-profile (one point is enough, in terms of specificity), or a B′-profile, the protocol is over. The rest of the lung will of course be analyzed but outside the protocol (searching for PLAPS after detecting a B′-, C-, or A/B-profile is redundant), same remark for the venous network. The A-profile calls, using the same probe, for a venous analysis. If no venous thrombosis is detected (2 min), the diagnosis of pulmonary embolism is not ruled out of course, but the user comes back to the lung posteriorly. Stage 3 is performed (6″ for setting the patient) and the PLAPS-point is analyzed, searching either air artifacts or PLAPS (7″). This step prioritizes the diagnosis of pneumonia if PLAPS are present or COPD/asthma if PLAPS are absent. Facing an A′-profile, a lung point is sought for, laterally, posteriorly, etc. (a matter of half a minute). Once the BLUE-protocol is over, the physician decides if this information is in agreement with the Steps 1 (history, etc.) and 2 (basic tests, ECG, etc.), making a part of Extended BLUE-protocol, and initiates active therapy or goes up to Step 3 (CT, etc.) if necessary. All in all, scanning the patient in the longest sequence takes 3 min and 6 s. This is done in the case of asthma/COPD (the longest sequence). In the case of the A′-, B′-, C-, and A/B-profiles, the test takes a few seconds. As one example of how to pilot the BLUEprotocol, a patient with the B-profile will have a priority diagnosis of hemodynamic pulmonary edema. If meanwhile, the simple history learns that this patient is followed for a chronic interstitial disease, the diagnosis will of course be shifted to the profit of exacerbated chronic interstitial disease, statistically 16 times less frequent [11]. The Extended BLUE-protocol uses this history, some echocardiographic data (showing here rather right heart anomalies), and studies the PLAPS-point, which is not required in the native BLUE-protocol but will here provide basic data: PLAPS favors the diagnosis of a chronic interstitial disease complicated by something (edema, embolism, pneumonia, etc.); absence of PLAPS will suggest a simple exacerbation with no visible factor of complication (read Chap. 35). We routinely make a comprehensive venous analysis in patients without A-profile, but this is done outside the protocol, again. The BLUE-Protocol and Rare Causes of Acute Respiratory Failure They are dealt with mainly in Chaps. 21 and 35. Frequently Asked Questions Regarding the BLUE-Protocol All these questions are answered in the specific sections through the book. Here are some: Why isn’t the heart featuring in the BLUE-protocol? Why just three points and no lateral analysis? A Small Story of the BLUE-Protocol What should one think of the “missed” patients of the BLUE-protocol? Didn’t the exclusion of patients create a bias limiting the value of the BLUE-protocol? Challenging patients? What about the mildly dyspneic patients (simply managed in the emergency room)? What happens when the BLUE-protocol is performed on non-blue patients? What is the interest of the PLAPS concept? Can the BLUE-protocol allow a distinction between hemodynamic and permeabilityinduced (ARDS) pulmonary edema? How about patients with severe pulmonary embolism and no visible venous thrombosis? What about pulmonary edema complicating a chronic interstitial disease? Will the BLUE-protocol work everywhere? Will multicentric studies be launched for validating the BLUE-protocol on huge numbers? Are 3 min really possible? Is the BLUE-protocol only accessible to an elite? By the way, why “BLUE” protocol? A Whole 300-Page Textbook Based on 300 Patients It may be one more FAQ. Any honest physician knows that huge numbers do not change a reality. Using 3,000 or 30,000 patients would have made only slight changes. The countless patients we managed once the study was submitted (years and years from the printing of this textbook) and the countless patients we could “pilot” from our world laboratory, i.e., all the information we received from hundreds of physicians through the planet, just confirmed the value of this series, based on logic. Our aim is to see this method aging well and see it used by increasing critical care physicians – and all other fields concerned. 165 Combining our lung and (adapted) venous approaches should result in considering the simple emergency cardiac sonography as a new, valuable entity. 2. Less irradiation will be provided. Physical examination, BLUE-protocol, simple cardiac sonography, and basic tests (without arterial puncture) should summarize the investigation of most patients (Fig. 20.4). The decrease of requirement for Step 3 examinations (mainly CT) is one of our major satisfactions. Chapter 29 will show the drawbacks of CT. The traditional arterial puncture was placed among these targets. The simple perspective of decreasing this test would have fully awarded our 18-year research. This test is painful: patients remember it. We guess that these blue patients are hypoxic. So the question becomes: “Why do we need blood gases?” Searching to know the CO2 level for making a diagnosis indicates how blind we are (without ultrasound) facing acute dyspnea. We keep this test in the ICU, on an arterial line, for monitoring circulatory status in sedated patients. As to expert echocardiography Doppler, we see no drawback to see this test performed, provided the team is already equipped and trained, in a patient who already received the initial therapy and in the countries where this option is envisageable. 3. We appreciate this possibility to immediately relieve the acutely dyspneic patient by providing appropriate therapy (full O2, e.g.). The rate of deaths which are the immediate or remote consequence of initial errors should decrease – not to speak of the comfort of the patients and the satisfaction to see simplicity winning in this demanding field of medicine. A Small Story of the BLUE-Protocol How Will the BLUE-Protocol Impact Traditional Managements? Three main fields should be affected: 1. If the lung is admitted in the court of ultrasound, the heart will be the definite winner. Read if there’s time the introduction of this textbook, describing when, where, and how the real work began. Having had the privilege of working in a pioneering ICU developing echocardiography in the critically ill since 1989, we had easy access to
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