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260 oracic ultrasound
expiratory diaphragmatic excursion in the first second may be considered analogues of vital capacity and forced expiratory volume in the first second (FEV1). According to this, the ratio between forced expiratory diaphragmatic excursion in the first second and maximum expiratory diaphragmatic excursion, represents an M-Mode index of obstruction (MIO). In a recent study, a MIO < 77 was identified as a possible cutoff for suspecting an obstructive spirometric pattern, with a 95.5% positive predictive value59 (Fig. 17).
Figure 17 – First second diaphragm motion in forced expiration analyzed using M Mode ultrasound in an anterior subcostal approach. The ratio between forced expiratory diaphragmatic excursion in the first second and maximum expiratory diaphragmatic excursion, represents an M Mode index of obstruction (MIO).
Finally, diaphragm thickening between total lung capacity and residual volume is inversely related to air trapping indices60.
Sniff test
e sniff test is a fluoroscopic procedure used for years for the functional evaluation of the diaphragm. is examination is simple to perform and the results are easy to interpret. In our opinion ultrasound allows to perform a sonographic sniff test much more easily and without radiant exposure61.
On quiet and deep inspiration, both hemidiaphragms move downward as the anterior chest wall moves upward. is movement is evaluated by a convex transducer placed under the costal arch and directed superiorly, taking advantage of the acoustic windows of the liver and spleen. is maneuver may not be possible to the left for the interposition of the colon. In this case the location of the probe in the intercostal and semicoronal position can permit an evalua­tion. e M-mode function allows to obtain a trace of the movement depending on time
1,62
For sniffing, the patient can be explored upright (if possible) and in supine position. He or she first takes in a deep breath, then breathes all the way out, and finally, with the mouth closed, breathes in as fast and deeply as possible. On sniffing, both hemidiaphragms move rapidly downward and M-Mode trace registers a quick positive deflection.
Normally, during a voluntary sniff test the diaphragm shows an excursion of 2.5-3 cm (2.9 ± 0.6 cm in men and 2.6 ± 0.5 cm in women for the right hemidiaphragm, 3.1 ± 0.6 cm in men and 2.7 ± 0.5 in women for the left hemidiaphragm) (Fig. 18).
In diaphragmatic paralysis orthograde excursion is absent and there may be paradoxical mo­tion even on quiet and deep inspiration, but on sniffing there is usually paradoxical motion.
.
Pathology of the diaphragm 261
Figure 18 – Sniff test. M-Mode.
In diaphragmatic weakness excursion is reduced and/or delayed on quiet and deep inspiration, while on sniffing motion it is usually paradoxical. erefore a pathological sniff test show­ing paradoxical diaphragmatic movement indicates diaphragmatic dysfunction, but when a hemidiaphragm is paralyzed, there is no orthograde motion on quiet or deep inspiration.
In eventration, excursion of the affected segment is reduced on quiet and deep inspiration and the sniff test may be abnormal. However, the posterior aspect of the hemidiaphragm shows normal motion.
If the patient becomes dyspneic or hypoxemic in the supine position, an ultrasound evalua­tion of the diaphragmatic dynamics with the patient lying down is useful. Normally, in the supine position, the diaphragm is higher and its excursion is reduced because the muscle works against abdominal pressure. A large decrement in diaphragm excursion and lung volume with the patient supine may be therefore diagnostic.
Bibliography
1. Nason LK, Walker CM, McNeeley MF, Burivong W, Rigner CL, Godwin JD. Imaging the diaphragm: Anatomy and function. Radiographics 2012; 32.
2. Maish MS. e Diaphragm. Surg Clinics North Am. 2010;90:955-68.
3. Fell SC. e Respiratory Muscles. Chest Surg Clinics North Am. 1998;8: 281-94.
4. Kantarci F, Mihmanli I, Demirel MK et al. Normal diaphragmatic motion and the effects of body com­position. Determination with M-Mode sonography. J Ultrasound Med 2004; 23: 255-260.
5. Testa A, Soldati G, Giannuzzi R et al. Ultrasound M-Mode assessment of diaphragmatic kinetics by anterior transverse scanning in healty subjects. Ultrasound Med Biol 2011; 37: 44-52.
6. McKenzie DKS, Gandevia C, Gorman RB, Southon CG. Dynamic changes of the zone of apposition and diaphragm lenght during maximal respiratory efforts. orax 1994; 49: 634-638.
262 oracic ultrasound
7. Wait JL, Johnson RL. Patterns of shortening and thickening of the human diaphragm. J Appl Physiol 1997; 83: 1123-1132.
8. Laghi F, Tobin MJ. Disorders of the respiratory muscles. Am J Resp Crit Care Med. 2003;168.10-48.
9. Brink JA, Heiken JP, Semenkovich J. Abnormalities of the diaphragm and adjacent structures: findings on multiplanar spiral CT scan. Am J Roentgenol 1994;163:307-310.
10. De Troyer A. Effect of hyperinflation on the diaphragm. Eur Respir J. 1997;10:708-713.
11. Gibson GJ. Diaphragmatic paresis: pathophysiology, clinical features and investigation. orax 1989;44:960-970.
12. Gottesman E, McCool FD. Ultrasound evaluation of the paralyzed diaphragm. Am J Resp Crit Care Med 1997;155:1570-1574.
13. Kumar N, Folger WN, Bolton CF. Dyspnea as the predominant manifestation of bilateral phrenic neuropaty. Mayo Clin Proc 2004;79:1563-1565.
14. McCool FD, Tzelepis GE. Dysfunction of the diaphragm. N Engl J Med 2012;366:932-942.
15. Aboussouan LS. Respiratory disorders in neurologic diseases. Cleveland Clin J Med 2005;72:511-520.
16. De Palo VA, McCool FD. Respiratory muscle evaluation of the patient with neuromuscular disease. Semin Resp Crit Care Med 2002;23:201-209.
17. Aliotta A, Rapaccini GL, Pompili M, Grattagliano A, Cedrone A, Trombino C, De Luca F, De Vitis I. Ultrasonographic signs of sliding gastric and hiatal hernia: their prospective evaluation. J Ultrasound Med 1994;13:665-669.
18. Tovar JA. Congenital diaphragmatic hernia. Orphanet J Rare Dis 2012;7:1.
19. Garne E, Haeusler M, Barisic I et al. Congenital diaphragmatic hernia: evaluation of prenatal diagnosis in 20 european regions. Ultrasound Obstet Gynecol 2002;19:329-333.
20. Taylor GA, Atalabi OM, Estroff JA. Imaging of congenital diaphragmatic hernias. Pediatr Radiol 2009;39:1-16.
21. Kotecha S, Barbato A, Bush A et al. Congenital diaphragmatic hernia. Eur Respir J 2012;39:820-829.
22. Yeh HC, Halton KP, Gray CE. Anatomic variations and abnormalities in the diaphragm seen with US. Radiographics 1990;10:1019-1030.
23. Wilcox PG, Pardy RL. Diaphragmatic weakness and paralysis, Lung 1989;167:323-341.
24. Mier-Jedrzejowicz A, Brophy C, Moxham J, Green M. Assessment of diaphragm weakness. Am Rev Respir Dis 1988;137:877-883.
25. Matamis D, Soilemezi E, Tsagourias M, Akoumianaki E, Dimassi S, Boroli F, Richard JCM, Brochard L. Sonographic evaluation of the diaphragm in critically ill patient. Technique and clinical applications. Intensive Care Med 2013;39.801-810.
26. Chawla J, Gruener G. Management of critical illness polyneuropathy and myopathy. Neurol Clin 2010;28:961-977.
27. Grosu HB, Lee IY, Lee J, Eden E, Eikermann M, Rose KM. Diaphragm muscle thinning in patients who are mechanically ventilated. Chest 2012;142:1455-1460.
28. Lloyd T, Tang YM, Benson MD, King S. Diaphragmatic paralysis: the use of M-Mode ultrasound for diagnosis in adults. Spinal Cord 2006;44:505-508.
29. Cohn D, Benditt JO, Eveloff S, McCool D. Diaphragm thickening during inspiration. J Appl Physiol 1997;83:291-296.
30. Vivier E, Mekontso Dessap A, Dimassi S, Vargas F, Lyazidi A, ille AW, Brochard L. Diaphragm ultrasonography to esptimatthe work of breathing during non invasive ventilation . Intensive Care Med 2012;38:796-803.
31. Summerhill EM, El Sameed YA, Glidden TJ, McCool FD. Monitoring recovery from diaphragm paralysis with ultrasound. Chest 2008,133.737-743.
Pathology of the diaphragm 263
32. Boles JM, Bion J, Connors A, Herridge M, Marsh B, Melot C, Pearl R, Silverman H, Stanchina M, Vieillard-Baron A, Welte T. Weaning from mechanical ventilation. Eur Respir J 20017;29:1033-1056.
33. Eskandar N, Apostolakos MJ. Weaning from mechanical ventilation. Crit Care Clin 2007;23:263-274.
34. Heunks L, Van der Hoeven JG. Clinical review: e ABC of weaning failure -a structured approach. Crit Care 2010,14:245.
35. Ferrari G, De Filippi G, Elia F, Panero F, Volpicelli G, Aprà F. Diaphragm ultrasound as a new index of discontinuation from mechanical ventilation. Critical Ultrasound Journal 2014;6:8.
36. Soldati G, Inchingolo R, Smargiassi A, Sher S, Nenna R, Inchingolo CD, Valente S. Ex vivo lung so­nography: morphologic-ultrasound relationship. Ultrasound Med Biol. 2012;38:1169-79.
37. Soldati G, Smargiassi A, Inchingolo R, Sher S, Nenna R, Valente S, Inchingolo CD, Corbo GM. Lung ultrasonography may provide an indirect estimation of lung porosity and airspace geometry. Respiration 2014 DOI 10.1159/000368086 in press.
38. Soummer A, Perbet S, Brisson H, Arbelot C, Constantin JM, MD, Lu Q, Rouby JJ, and the Lung Ultrasound Study Group. Ultrasound assessment of lung aeration loss during a successful weaning trial predicts postextubation distress. Crit Care Med 2012;40:2064-2012.
39. Criner GJ. Measuring diaphragm shortening using ultrasonography to predict extubation success. orax 2014;69:402-404.
40. Kim WY, Suh HJ, Hong SB, et al. Diaphragm dysfunction assessed by ultrasonography: influence on weaning from mechanical ventilation. Critical Care Med 2011;39:2627-2630.
41. DiNino E, Gartman EJ, Sethi JM, McCool FD. Diaphragm ultrasound as a predictor of successful extubation from mechanical ventilation. orax 2014;69:423-427.
42. Lerolle N, Guerot E, Dimassi S, Zegdi R, Faisy C, Fagon JY, Diehl JL. Ultrasonographic diagnostic criterion for severe diaphragmatic dysfunction after cardiac surgery. Chest 2009;135:401-407.
43. Kim SH, Na S, Choi JS, NaH, Shin S, Koh SO. An evaluation of diaphragmatic movement by M-Mode sonography as a predictor of pulmonar dysfunction after upper abdominal surgery. Anesth Analg 2010;110:1349-54.
44. Subotic D, Stevic R, Gajic M, Vesovic R. Diaphragm motion and lung function prediction in patients operated for lung cancer – a pilot study on 27 patients. Journal of Cardiothoracic Surgery 2013;8:213.
45. McKenzie DK, Butler JE, Gandevia SC. Respiratory muscle function and activation in chronic obstruc­tive pulmonary disease. J Appl Physiol 2009;107:621-629.
46. Ottenheijm CAC, Heunks LMA, Sieck GC, Zhan WZ, Jensen SM, Degens H, DeBoo T, Dekhuijzen R. Diaphragm dysfunction in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2005;172:200-205.
47. Dos Santos Yamaguti WP, Paulin E, Shibao S, Chammas MC, Salge JM, Ribeiro M, Cukier A, Carvalho CRF. Air trapping: the major factor limiting diaphragm mobility in chronic obstructive pulmonary disease patients. Respirology 2008;13:138-144.
48. Ottenheijm CAC, Heunks LMA, Dekhuijzen RPN. Diaphragm adaptations in patients with COPD. Respiratory Research 2008;9:12.
49. Ottenheijm CAC, Heunks LM, Dekhuijzen PNR. Diaphragm muscle fiber dysfunction in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2007;175:1233-1240.
50. O’Donnell DE. Hyperinflation, dyspnea, and exercise intolerance in chronic obstructive pulmonary disease. Proc Am orac Soc 2006;3:180-184.
51. Braun NMT, Arora NS, Rochester DF. Force-length relationships of the normal human diaphragm. J Appl Physiol Environ Exercise Physiol 1982;53:405-412.
52. Sharp JT, Danon J, Druz WS, Goldberg NB, Fishman H, Machnach W. Respiratory muscle function in patients with chronic obstructive pulmonary disease: its relationship to disability and to respiratory therapy. Am Rev Respir Dis 1974;110:154-167.
264 oracic ultrasound
53. Rochester DF, Braun NMT. Determinants of maximal inspiratory pressure in chronic obstructive pul­monary disease. Am Rev Respir Dis 1985;132:42-47.
54. Gerscovich EO, Cronan M, McGahan JP, Jain K, Jones CD, McDonald C. Ultrasonographic evaluation of diaphragmatic motion. J Ultrasound Med 2001;20:597-604.
55. McKenzie DK, Gorman RB, Tolman J, Pride NB, Gandavia SC. Estimation of diaphragm lenght in patients with severe chronic obstructive pulmonary disease. Respir Physiol 200;123:225-234.
56. Kang HW, Kim TO, Lee BR, Yu JY, Chi SY, Ban HJ, Oh IJ, Kim KS, Kwon YS, Kim YI, Kim YC, Lim CS. Influence of diaphragmatic mobility on hypercapnia in patients with chronic obstructive pulmonary disease. J Korean Med Sci 2011; 26: 1209-1213.
57. MacIntyre NR. Muscle dysfunction associated with chronic obstructive pulmonary disease. Respiratory Care 2006;51:840-848.
58. Gorman RB, McKenzie DK, Pride NB, Tolman JF, Gandevia SC. Diaphragm length during tidal breath­ing in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2002;166:1461-1469.
59. Zanforlin A, Smargiassi A, Inchingolo R, di Marco Berardino A, Valente S, Ramazzina E. Ultrasound analysis of diaphragm kinetics and the diagnosis of air way obstruction: the role of M-Mode index of ob­struction. Ultrasound Med Biol 2014;40:1065-1071.
60. Smargiassi A, Inchingolo R, Tagliaboschi L, Di Marco Berardino A, Valente S, Corbo GM. Ultrasonographic assessment of the diaphragm in chronic obstructive pulmonary disease patients: relationships with pulmonary function and the influence of body composition – a pilot study. Respiration 2014;87:364-371.
61. Kharma N. Dysfunction of the diaphragm: imaging as a diagnostic tool. Curr Opin Pulm Med 2013;19:394-398.
62. Alexander C. Diaphragm movements and the diagnosis of diaphragmatic paralysis. Clin Radiol 1966;17:79-83.
9
oracic trauma
oracic trauma occurs in 60% of poly-injured patients and represents an important cause of mortality and morbidity. Both closed and penetrating traumas commonly produce intrathoracic injuries, which contribute to 20-25% of the overall mortality of the injuried patient.
Table 1 reports the different organs and pathologies involved in thoracic
1
trauma Road accidents are the leading cause of closed thoracic injuries (70-80%)
e overall mortality directly tied to these events is around 8/100,000.
Open thoracic traumas are mainly linked to the use of weapons and are more characteristic of particular urban realities or war contexts3. Most of these traumas concern the chest wall and the pleural cavity. A fair amount of pulmonary contusions (26%) is often underestimated or unrecognized.
e general diagnostic and therapeutic approach to the thoracic injuries begins with the ABCD (Airways, Breath, Circulation, Disability) of the resuscitation, according to the criteria proposed in the Advanced Trauma Life Support Course (ATLS)4. Instrumental investigations must observe an appropriate timing considering needs, priorities and integration of methods5. ATLS criteria point out an approach that is both diagnostic and therapeutic to life-threatening conditions such as asphyxia and circulatory arrest.
e clinician who evaluates an injured patient first considers the nature of the event, its dynamics (as a function of involved mechanical energy) and the clinical objectivity. In the
Table 1 – Injuries associated with thoracic trauma
Chest wall 45%
Lung 26%
Hemothorax 25%
Pneumothorax 20%
Heart 09%
Diaphragm 07%
Aorta and great vessels 04%
Esophagus 0.5%
Miscellany 21%
. e vast majority of trauma associates different injuries.
chest, much more than in other location, priority is given to the patency of airways and to ventilation (A and B).
e first diagnosis should aim to remove critical situations for vital functions. Any diagnostic act must be immediate and directed to a therapeutic act, which is the resolution or at least the control of a com­promised vital function.
e operating algorithm must therefore be simple and functional. To each “yes” from the diagnostic input (ABCD related), a damage control action must match
2
.
265
266 oracic ultrasound
(example: B, massive pneumothorax = immediate drainage). e negation of a diagnostic hypothesis induces a fast operative shift (example from Breath to Circulation). However, periodic revaluations of the previous steps are essential in this approach.
It is obvious that this kind of logic can hardly lean on complex instrumental investigations requiring time and interrupting the contact with patients. In the Emergency Room, during ABCD, the functional impairment is tested on a clinical basis, using traditional physical examination or little more.
erefore, inspection, auscultation and palpation have a primary role in the assessment of an injured subject during the primary survey. e diagnostic accuracy of these actions is high with regard to A and B, but not for minor damage. However, it is low with regard to incipient hemodynamic instability or impeding shock. is latter aspect is true for the chest and for the abdomen.
e clinical accuracy of non-massive hemoperitoneum does not exceed 40%. A low sensitivity of the clinical examination for hemothorax is characteristic6.
With a closed chest trauma, hemodynamic instability indicates hypovolemia (hemothorax, intrathoracic vessels injuries, external bleeding) or a mechanical reason (massive pneumotho­rax, haemopericardium or blunt cardiac trauma). Of course, in the injured patient an agonal hemodynamic instability preceding cardiac arrest is seen in all the situations that cause acute respiratory failure and severe hypoxia (airway obstruction rupture, bilateral pneumothorax, massive hemothoraces etc.). e delayed recognition of these situations considerably worsens the patient’s prognosis.
In the chest, airway damage is associated with hemodynamic impairment and, conversely, bleeding in the chest may alter the dynamics of breath. ese pathophysiological bidirec­tional links must be borne in mind for many practical reasons, but also because they hugely complicate the clinical objectivity.
In chest trauma, an altered respiratory mechanics is an inspective finding. More specifically, the problem may be a parietal modification (flail chest), the occupation of the pleural cavity and/or the pulmonary structural integrity and compliance, as in contusions and in ARDS.
After controlling airways and breathing, the recognition of bleeding is a priority (Circulation). Inside the chest cage, hemorrhage cannot only induce shocks, as in other body areas as well, but it is a cofactor of respiratory and cardiac failure.
Finally, chest trauma can affect myocardial function through a direct damage of the heart muscle, valves and great vessels.
About 85% of patients with closed chest trauma can be treated conservatively: for these sub­jects clinical observation, thoracostomy, pain control, respiratory support and physiotherapy are sufficient. e majority of invasive interventions in chest trauma includes the treatment of pneumothorax or hemothorax7 and represents a complex problem. e identification and early treatment of pleural injuries avoids important complications as the retained hemothorax and empyema, while the control of lung contusions is a precautionary tool for ARDS and respiratory failure. Only 10-15% of all patients with closed chest trauma requires thoracotomy to treat uncontrollable parenchymal airway and vascular lesions.
e approach to open chest trauma is more stringent. Patients with hemodynamic instability usually require immediate surgery, and echocardiography is probably the only necessary diag­nostic test. In these cases, the most important question is what type of thoracotomy incision
oracic trauma 267
should be used. Patients with hemodynamic stability benefit of the use of CT, which is very accurate in defining existing lesions8.
X-ray diagnostics in chest trauma
Radiographic tests9, conventional radiography and computed tomography (CT), have an eminently functional and practical purpose for the evaluation of chest trauma. Each di­agnostic test, however performed, is aimed at the type of trauma to which it is addressed. In this perspective, clinically obvious and serious lesions (e.g. pneumothorax with tracheal deviation, hemodynamic instability and respiratory effort) do not have to wait for radio­graphic scans, but should be treated. For example, CT may be appropriate for diagnosing a hemopericardium, but, in front of a hypotensive patient with jugular turgor, there is no time for a complex diagnostics. e first option is immediate treatment, possibly preceded by a quick bedside investigation.
ATLS rules give indication to perform a chest X-ray early in the secondary survey10. It is ac­cepted that the radiography is performed in suboptimal technical conditions, resulting less sensitive and specific than a standard two-view-X-ray with the patient in the upright position.
erefore, chest X-ray is widely used in the emergency room for assessing parietal or bone damages and pleural or pulmonary lesions (hemothorax and pneumothorax). A “screening” examination is used for the vast majority of traumatized patients and it remains an excel­lent tool for early detection of life threatening thoracic injuries. In the emergency room, a radiologic “quick read” helps out in patient triage. Moreover, chest X-ray is used to detect the correct positioning of the devices (endotracheal tube, central venous access), and to identify subtle signs of mediastinal or vascular injuries.
However, many thoracic injuries are difficult to recognize in chest radiography and the use of CT has been steadily increasing in recent years.
Not technically perfect chest X-ray can miss 50% or more of hemothoraces and 50% of pneumothorax and it has very low sensitivity for lung and mediastinal lesions. Anyway, the appreciation for chest-X-ray lies in its historical weight, in its overview ability and, last but not least, in the absence of more sensitive but equally practical alternative methods. Currently CT with intravenous contrast is the diagnostic gold standard for thoracic injuries.
ere is no doubt that if every subject with chest injury underwent CT, false negativities would be drastically reduced, at the cost of overdiagnosis in a number of cases and with an economic and biologic burden.
CT is hugely sensitive for pneumothorax, pleural effusions and parenchymal lung damage, and it is sufficiently accurate for vascular lesions. In patients with chest trauma and normal chest X-ray, CT scan showed lesions in 39% of cases, but influenced treatment decisions only in 5% of cases. However, literature reports a more important role of this exam in influencing clinical decisions (30%). is suggests that CT has a maybe too high sensitivity11 for situations with low clinical relevance and that it would be reserved for patients with high probability of injury (elders, with associated injuries of the abdomen and pelvis)12. Finally, accurate diagnosis of aortic and mediastinal lesions can be made only with the use of angiographic methods (angio-CT)13. Unfortunately, CT is not commonly performed at the bedside in the Emergency Room. In addition, every reasonable protocol currently requires that any subject undergoing CT is in hemodynamically stable conditions.
268 oracic ultrasound
e current trend is to refer to CT any patient with significant chest trauma. According to this strategy, hemodynamically stable subjects with minor trauma are studied. However, difficulties would arise on more severe, hemodynamically unstable patients for the temporal gap due to stabilization before performing CT scans.
In many institutions hemodynamically stable blunt trauma patients routinely receive a su­pine chest X-ray in the trauma room and many of these patients also receive CT imaging of the chest, cervical spine, abdomen and pelvis. According to the previous considerations, a practical approach based both on chest X-ray and chest CT is redundant, time consuming and expensive. eoretically, omitting routine chest X-ray would eliminate an unnecessary test that, in this population, does not add useful information, and incurs significant costs as well as unnecessary radiation exposure.
Chest X-ray, with its documented low diagnostic accuracy is located between clinical ex­amination and CT. is diagnostic gap might be filled by an instrumental survey capable of improving the diagnostic power of chest X-ray. We think that ultrasound is a good candidate.
Recently, a decision instrument (NEXUS chest) for selective chest imaging in blunt trauma has been proposed. Its role is the identification of blunt trauma patients with very low risk of thoracic injuries on chest imaging. Seven clinical criteria (age >60 years, rapid deceleration mechanism (fall >20 ft, MVC >40 mph), chest pain, intoxication, abnormal mental status, distracting painful injury, tenderness to chest wall palpation) are risk factors. Chest imaging is unnecessary in patients without risk criteria (sensitivity 98.8%, negative predictive value
98.5%). In our opinion, chest ultrasound may be the elective investigation in low-risk subjects that did not undergo traditional chest imaging.
Applications of ultrasound in thoracic traumatology
Until recently, the indications for chest ultrasonography in trauma patients were inusual and only the FAST (Focused Assessment with Sonography for Trauma)14 used the left ascend­ing subcostal and coronal projections of pleural sacs for the evaluation of pleuropericardial effusions.
A more anatomic use of chest ultrasound for lung injury appeared as an excess, because it was believed that the lung was not an optimal target for ultrasound and that it could be studied with a simple X-ray (Fig. 1).
However, the growing practice of placing the ultrasound probe in the intercostal spaces and experiences of pleural ultrasound have shown that some diagnosis (pneumo- and hemothorax, hemopericardium) could be possible with echography, obviating the need to carry radiology equipment and staff in emergency areas. On the other hand, the increased use of CT created a diagnostic gold standard in this setting, showing the limitations of chest radiography.
is new vision has progressively increased with the increasing skills that emergency and ICU physicians acquired in this field.
e consequence was the birth of “focused” and “point of care” ultrasound, no longer as a radiological tool, but relevant to various professionals who needed to make diagnosis15. In few years, from 2005 to 2010, a cultural growth got ultrasound off the ground, in emergency and intensive care. Ultrasound was just a particular examination helping eyes, hands and ears of physicians.
According to this perspective, ultrasound must be applied to each chest trauma, even if it had, for the critical condition of the injured patient, the same diagnostic accuracy of chest X-ray.
oracic trauma 269
Figure 1 – Chest X-ray performed in the emergency department in a polyinjured supine patient. The quality is not good. It allows to effectively monitor the positioning of the devices (note the thoracostomic bilateral tubes and the endotracheal tube into the right bronchus), but it does not effectively allow the determination of the effects of trauma on rib cage, pleura, lung and mediastinum.
e preceding pages on non-traumatic pathology showed the diagnostic potential of ultra­sound to assess many chest pathologies, indicating stereotyped but typical expressions of echographic imaging.
e implementation of ultrasound in chest trauma patients is relatively easy by virtue of the common general principles that govern the production of pleuropulmonary images in ultrasound.
For these reasons, we believe that in injured subjects echography, according to the concept of focused examination (such as FAST) can and should extend far above the diaphragm with synthetic directions: study of pleural dynamics and content, evaluation of the acoustic lung properties and assessment of the heart and pericardium16.
A coordinated approach to the injured patient, generally referred as extended FAST or E-FAST, has already had its initial and convincing validation in the literature, at least regarding its use in the Emergency Room.
In the following pages, the use of chest ultrasound in trauma patients will be described, con­sidering its benefits and limitations, the possibility to select secondary surveys, its applications for studying lung parenchyma and the patient monitoring.
Methodology
To perform ultrasound in thoracic trauma, 3.5-5 MHz convex and sector probes are used, depending on the explored organs (pleural fields, lung, heart), and the resolution or the depth required. According to the principles of chest ultrasound, the linear probe (7-10 MHz) is used when the pleural details have to be exalted, as it can occur in the difficult diagnosis of pneumothorax.
e thorax is studied performing anterior, lateral and, if possible, posterior scans, placing the probe in the intercostal spaces or longitudinally on the skin. e cardiac area is explored through subdiaphragmatic, parasternal, apical and suprasternal scans.