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400 oracic ultrasound
7. Vieillard-Baron A, Prin S, Chergui K et al. Echo-Doppler demonstration of acute cor pulmonale at the bedside in the medical intensive care unit. Am J Respir Crit Care Med 2002; 166: 1310-1319.
8. Vieillard-Baron A, Prin S, Chergui K, Dubourg O, Jardin F. Hemodynamic instability in sepsis bedside assessment by doppler echocardiography. Am J Respir Crit Care Med 2003; 168: 1270-1276.
9. Leung JM, Levine EH. Left ventricular end systolic cavity obliteration as an estimate of intraoperative hypovolaemia. Anaesth 1994; 81: 1102-1109.
10. Cheriex EC, Leunissen KM, Janssen JH et al. Echography of the inferior vena cava is a simple and reliable tool for estimation of ‘dry weight’ in haemodialysis patients. Nephrol Dial Transplant 1989; 4: 563-568.
11. Katzarski KS, Nisell J, Randmaa I et al. A critical evaluation of ultrasound measurement of inferior vena cava diameter in assessing dry weight in normotensive and hypertensive hemodialysis patients. Am J Kidney Dis 1997; 30: 459-465.
12. Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspira-Noninvasive estimation of right atrial pressure from the inspira­tory collapse of the inferior vena cava. Am J Cardiol 1990; 66: 493-496.
13. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest 2008; 134: 172-178.
14. Copetti R, Soldati G, Copetti P. Chest sonography: a usefull tool to differentiate acute cardiogenic pul­monary edema from acute respiratory distress syndrome. Cardiovascular Ultrasound 2008; 6: 16.
15. Lichtenstein D, Meziere G, Biderman P et al. e comet-tail artifact. An ultrasound sign of alveolar­interstitial syndrome. Am J Respir Crit Care Med 1997, 156(5): 1640-1646.
16. Soldati G, Copetti R, Sher S. Sonographic interstitial syndrome. e sound of lung water. J Ultrasound Med 2009; 28: 163-174.
17. Reissig A, Copetti R, Kroegel C. Current role of emergency ultrasound of the chest. Crit Care Med 2011; 39: 839-845.
18. Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest 2008; 134: 117-125.
19. Mathis G, Dirschmid K. Pulmonary infarction: sonographic appearance with pathologic correlation. Eur J Radiol 1993; 17(3): 170-174.
20. Niemann T, Egelhof T, Bongartz G. Transthoracic sonography for the detection of pulmonary embolism-
-a meta-analysis. Ultraschall Med 2009; 30(2): 150-156.
21. Reissig A, Heyne JP, Kroegel C. Sonography of lung and pleura in pulmonary embolism: Sonomorphologic characterization and comparison with spiral CT scanning. Chest 2001; 120: 1977-1983.
22. Mathis G, Blank W, Reissig A et al. oracic ultrasound for diagnosing pulmonary embolism: A pro­spective multicenter study of 352 patients. Chest 2005; 128: 1531-1538.
23. Lichtenstein DA, Meziere G, Lascols N et al. Ultrasound diagnosis of occult pneumothorax. Crit Care Med 2005; 33: 1231-1238.
24. Lichtenstein D, Meziere G, Biderman P, Gepner A. e “lung point”: an ultrasound sign specific to pneumothorax. Intensive Care Med 2000; 26: 1434-1440.
25. Alsalim W, Lewis D. Towards evidence based emergency medicine: Best BETs from the Manchester Royal Infirmary. BET 1: is ultrasound or chest X-ray best for the diagnosis of pneumothorax in the emergency department? Emerg Med J 2009; 26(6): 434-435.
26. Mathis G. oraxsonography – Part I: Chest wall and pleura. Ultrasound Med Biol 1997; 23: 1131-1139.
27. Sajadieh H, Afzali F, Sajadieh V, Sajadieh A. Ultrasound as an alternative to aspiration for determining the nature of pleural effusion, especially in older people. Ann NY Acad Sci 2004; 1019: 585-592.
28. Gehmacher O, Mathis G, Kopf A, Scheier M. Ultrasound imaging of pneumonia. Ultrasound Med Biol 1995; 21(9): 1119-1122.
29. Reissig A, Kroegel C. Sonographic Diagnosis and Follow-Up of Pneumonia: a Prospective Study. Respiration 2007; 74: 537-547.
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30. Parlamento S, Copetti R, Di Bartolomeo S. Evaluation of lung ultrasound for the diagnosis of pneumonia in the ED. Am J Emerg Med 2009; 27(4): 379-384.
31. Lensing AW, Prandoni P, Brandjes D et al. Detection of deep-vein thrombosis by real-time B-mode ultrasonography. N Engl J Med 1989; 320(6): 342-345.
32. Bernardi E, Camporese G, Büller Hr et al.; Erasmus Study Group. Serial 2-point ultrasonography plus D-dimer vs whole-leg color-coded Doppler ultrasonography for diagnosing suspected symptomatic deep vein thrombosis: a randomized controlled trial. JAMA 2008; 300(14): 1653-1659.
33. Agnelli G, Becattini C. Acute pulmonary embolism. N Engl J Med 2010; 363(3): 266-274.
34. Nolan JP, Soar J, Zideman DA et al.; ERC Guidelines Writing Group. European Resuscitation Council Guidelines for Resuscitation 2010 Section 1. Executive summary. Resuscitation 2010; 81(10): 1219-1276.
35. Hernandez C, Shuler K, Hannan H et al. C.A.U.S.E.: Cardiac arrest ultra-sound exam – a better approach to managing patients in primary non-arrhythmogenic cardiac arrest. Resuscitation 2008; 76(2): 198-206.
36. Breitkreutz R, Walcher F, Seeger FH. Focused echocardiographic evaluation in resuscitation management: concept of an advanced life support-conformed algorithm. Crit Care Med 2007; 35(5 Suppl): S150-S161.
37. Blaivas M, Fox JC. Outcome in cardiac arrest patients found to have cardiac standstill on the bedside emergency department echocardiogram. Acad Emerg Med 2001; 8: 616-621.
38. Salen P, Melniker L, Chooljian C et al. Does the presence or absence of sonographically identified car­diac activity predict resuscitation outcomes of cardiac arrest patients? Am J Emerg Med 2005; 23: 459-462.
39. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med 1997; 337(5): 301-306.
40. Salen P, O’Connor R, Sierzenski P. Can cardiac sonography and capnography be used independently and in combination to predict resuscitation outcomes? Acad Emerg Med 2001; 8(6): 610-615.
41. Dellinger RP, Levy MM, Carlet JM et al.; International Surviving Sepsis Campaign Guidelines Com­mittee; American Association of Critical-Care Nurses; American College of Chest Physicians; American College of Emergency Physicians; Canadian Critical Care Society; European Society of Clinical Microbiol­ogy and Infectious Diseases; European Society of Intensive Care Medicine; European Respiratory Society; International Sepsis Forum; Japanese Association for Acute Medicine; Japanese Society of Intensive Care Medicine; Society of Critical Care Medicine; Society of Hospital Medicine; Surgical Infection Society; World Federation of Societies of Intensive and Critical Care Medicine. Surviving Sepsis Campaign: inter­national guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36(1): 296-327.
Updated Bibliography
Kanji HD, McCallum J, Sirounis D, MacRedmond R, Mosas R, Boyd JH. Limited echocardiography-guided therapy In subacute shock is associated with change in management and improved outcomes. J Crit Care 2014; [epub ahead of print].
Ferrada P, Vanguri P, Anand RJ, Whelan J, Duane T, About anos M, Malhotra A, Ivatury R. ABCD echo: limited transthoracic echocardiogram is a useful tool to guide therapy for hypothension in the trauma bay. A pilot study. J Trauma Acute Care Surgery 2013;74:220-223.
Volpicelli G, Lamorte A, Tullio M, Cardinale L, Giraudo M, Stefanone V, Boero E, Nazerian P, Pozzi R, Francisco ME. Point of care multiorgan ultrasonography for the evaluation of undifferentiated hypotension in the emergency department. Intensive Care Med 2013;39.1290-1298.
Studies analyzing the role of ultrasound for the assessment of hypothensive and shock patients.
Anderson KL, Jeng KY, Fields JM, Panebianco NL, Dean AJ. Diagnosing heart failure among acutely dyspneic patients with cardiac, inferior vena cava, and lung ultrasonography. Am J Emerg Med 2013;31:1208-1214.
402 oracic ultrasound
Klein Y, Ramani GV. Assessment and management of cardiogenic shock in the emergency department. Cardiol Clin 2012;30:651-664.
Recent studies addressing the role of ultrasound for the diagnosis and management of critical patients with heart failure and cardiogenic shock.
Hestenes SM, Halvorsen PS, Skulstad H, Remmew EW, Espinoza A, Hyler S, Bugge JF, Fosse E, Nielsen EW, Edvardsen T. Advantages of strain echocardiography In assessment of myocardial function In severe sepsis: an experimental study. Crit Care Med 2014;42:432-440.
Arbo JE, Maslove DM, Beraud AS. Bedsde assessment of right atrial pressure in critically ill septic patients using tissue Doppler ultrasonography. J Crit Care 2013;28.
Harmankaya A, Akilli H, Gul M, Akilli NB, Ergin M, Aribas A, Cander B. Assessment of right ven­tricular functions in patients with sepsis, severe sepsis, and septic shock and its prognostic importance: a tissue Doppler study. J Crit Care 2013;28.
Sepsis and integrated ultrasound.
13
Pleural and lung ultrasound in the
neonatal period and in childhood
e writing of this chapter was carried out with the cooperation and contribution of Dr. Luigi Cattarossi (Director SOC Neonatal Pathology, Azienda Ospedaliera Universitaria, Ospedale Santa Maria della Misericordia, Udine)
Chest radiography is currently the imaging technique commonly used in the study of respiratory failure in the newborn and child. Nuclear magnetic resonance and computed tomography should be considered second-level surveys, and therefore not for routine use. Until now, only few studies have evaluated the usefulness of lung ultrasound in the diag­nosis of respiratory diseases that most commonly affect the newborn and the children. In any case, before our publications on the sonographic di­agnosis of transient tachypnea of the newborn and the hyaline membrane
1-2
disease through an abdominal transhepatic or transplenic approach (Fig . 1) is approach greatly limits the potentiality of lung ultrasound, because no information on changes in the pleural line is obtainable with these projections. In the setting of neonatal respiratory diseases, more than in adult chest ultrasound, a lung full of air has been a taboo for long time.
, the few published papers had only examined the lung bases
3-6
.
Chest radiography has many limitations in neonatal and pediatric age. First of all, it involves the exposure to ionizing radiations. is problem is not negligible, because the risk of developing neoplasms secondary to radiation exposure is greater the younger the patient7. Echography is definitely able to reduce the number of radiographs needed8. Chest radiography has also poor sensitivity in distinguishing carefully the content of an opacity (pleura or parenchyma? alveolo-interstitial edema or consolidation?). Lung ultrasound is definitely more accurate and the possibility of obtaining dynamic images gives it an extraordinary potentiality.
e possibility of performing serial and frequent surveys is another important aspect that is extremely useful in situations of clinical instability.
e execution technique is simple in view of the limited size of the area that needs to be examined and the reduced thickness of the chest wall. High-resolution linear probes are obviously necessary (7.5-13 MHz).
e sonographic findings reported here are the results of over ten years of observations on the most common respiratory diseases in newborns and children. e absolute and constant reproducibility of the sonographic findings is surprising, so that it can be assumed that certain findings are often pathognomonic for a particular disease.
403
404 oracic ultrasound
Figure 1 – Transhepatic and transplenic assessement of the lung bases. From: Bober K et al. Diagnostic utility of ultrasonography for respiratory distress syndrome in neonates. CR440-446.
Med Sci Monit
2006; 12(10):
Execution technique and echographic anatomy
e examination is performed with the infant in a supine position, through longitudinal and transverse scans along the anatomical lines of the chest (parasternal and midclavicular lines, anterior, middle, and posterior axillary lines, and paravertebral lines). e posterior areas may be better viewed in the lateral decubitus position.
e position with the erect trunk is almost never necessary. In ultrasound, the normal lung of the newborn does not differ substantially from that of the
adult. e pleural line is easily viewable beneath the ribs and the pleural gliding motion is easily recognizable (pleural sliding)9 (Clip 1).
Clip 1 – Transverse scan. Pleural sliding in a normal lung (absence of B Lines, evidence of A Lines).
e presence of horizontal artifacts repeated at constant intervals below the pleural line (A Lines10) identifies a normal condition (Figs. 2-3).
At birth it is possible to highlight vertical artifacts (B Lines10). ese artifacts, that indicate disease in the adult (interstitial syndrome) resent residual liquid of the fetal lung. is finding is evident both in infants born by vaginal delivery and Caesarean section. In newborns by the Caesarean section, B Lines are more frequent because of the greater quantity of lung fluid in the lungs. e lower pressure over
11-15
, appear in absolutely healthy infants and rep-
Pleural and lung ultrasound in the neonatal period and in childhood 405
A Lines
Ribs and acoustic shadow cone
Pleural line
A Lines
Figure 2 – Normal lung: transverse scan. Hyperechoic pleural line and horizontal artifacts (A Lines).
Figure 3 – Normal lung: longitudinal scan. Acoustic shadow cones produced by the ribs and hyperechoic pleural line immediately below the ribs. Horizontal artifacts (A Lines).
the rib cage during the transit through the birth canal is probably a causal factor. Newborn B-Lines, though numerous, are not coalescing and are more detectable at the lung bases. Wathever the delivery takes place, there is generally a complete disappearance of the interstitial syndrome within the following 36 hours (Figs. 4-6).
2 hours
2 hours
B Lines
B Lines
Figure 4 – Transverse scan in healthy newborn by Caesarean section 2 hours earlier. Evidence of numerous non-coalescing B Lines.
Transient tachypnea of the newborn
e transient tachypnea of the newborn (TTN) is a common pathological situation, well known to pediatricians and neonatologists. Infants with TTN, within the first hour of life,
406 oracic ultrasound
18 hours
Fig. 5 – Transverse scan in the same healthy newborn after 18 hours from birth. Marked reduction in B Lines.
Fig. 6 – Transverse scan in healthy newborn born by vaginal delivery 2 hours earlier. Presence of some B Lines.
B Lines
show tachypnea and hypoxemia in the absence of carbon dioxide retention. A clinical deterio­ration such as to require mechanical ventilation is very rare. In serious cases the real problem lies in the clinical differential diagnosis with other pathologies.
TTN is due to a delayed clearance of the liquid in the fetal lung, which involves the retention of fluids in the alveoli and interstitium. In vivo studies have shown that the lung epithelium secretes Cl-and fluids throughout pregnancy, but that the capacity to reabsorb Na+ and consequently fluids, occurs only in the late stages of gestation16. At birth the mature lungs reabsorb Na+ and fluids instead of secreting them with Cl. e circulating catecholamines are important in governing this reversal of activity. e increase in oxygen tension that occurs at birth determines an increased capacity of the epithelium to actively absorb sodium and fluids. e concept of pulmonary immaturity at birth expresses the inability to activate these mechanisms. ose born by Caesarean section are more at risk of developing this disease, also for the reduced levels of catecholamines produced during labor, compared with those born by vaginal delivery.
e frequency of TTN is identical throughout the world. About 1% of newborns is suffering from some form of respiratory distress not attributable to infectious diseases. Of this 1%, 33-50% is attributable to TTN. It is more frequent in infants at or near term and tends to resolve spontaneously within 24-72 hours. is disease has low morbidity.
As already said, it is observed more frequently in infants born by Cesarean section for the reduced levels of circulating catecholamines, but also for the non-compression of the rib cage, while during vaginal delivery there is a real “squeezing” of the lung. Milner and colleagues
17
reported that the average volume of gas contained in the chest was 32.7 ml/kg in infants born by vaginal delivery compared to 19.7 ml/kg of births by Caesarean section (same chest circumference). In contrast, the quantity of fluid in the interstitium and alveoli was markedly higher in infants born by Caesarean section.
A higher incidence of TTN has finally been described in infants of asthmatic mothers18. Chest radiograph is still considered the diagnostic standard.
Pleural and lung ultrasound in the neonatal period and in childhood 407
e characteristic findings of Chest X-ray are the presence of prominent perihilar striae at­tributed to lymphatic congestion and the presence of fluid in the fissures. More rarely there are areas of pulmonary infiltrates and small pleural effusions. ese alterations are resolved within 72 hours.
Lung ultrasound in TTN
Ultrasound images of TTN are so specific as to be sufficient for its diagnosis1. Despite the low morbidity of the disease, sometimes the baby shows an early severe respiratory distress requiring differential diagnosis with more high-risk situations (pneumothorax, pneumonia, sepsis, HMD, congenital heart defects, etc.).
Lung ultrasound allows the correct diagnosis resolving the problems related to differential diagnosis. It typically detects the presence of compact B Lines at the bases compared to higher fields, where they are less numerous or even absent (Figs. 7-8). is aspect involves both lungs, although not symmetrically. Frequently, this picture appears more striking for the right lung.
Compact B Lines
Apex
B Lines
Figure 7 – TTN: transverse scan at the upper third of the lung. Numerous but not compact B Lines.
Figure 8 – TTN: transverse scan at the lower third of the lung. Numerous and compact B Lines.
e transition between the lower lung areas with compact vertical artifacts, and the higher areas, is most of the time sudden and it gives the lung a peculiar look. We have defined this sign “double lung point”. is sign is pathognomonic of TTN (Clips 2-6) (Fig. 9).
Clip 2 – TTN: longitudinal scan at the medial third of the right lung. Evident difference between the base, with compact B Lines, and the apex where they are less numerous.
Clips 3, 4 TTN: longitudinal scan at the medial third of the lung showing double lung point.
408 oracic ultrasound
Clip 5 – TTN: longitudinal scan at the apex of the right lung. Evident paucity of B Lines.
Clip 6 – TTN: transverse scan at the base of the right lung. Compact B Lines.
e pleural line is regular, hyperechoic, well-defined and not thickened. e occurrence of pleural effusion is rare.
e artifacts tend to disappear completely within 36-72 hours (Fig. 10).
A
B
C
Figure 9 – TTN: scans at the medial third of the chest, showing the double lung point. (A, B, C)
Pleural and lung ultrasound in the neonatal period and in childhood 409
2 hours
Figure 10 – TTN: scans at the base of the chest 2 and 36 hours after birth. Note the disappearance of the compact B Lines.
36 hours
Pulmonary hyaline membrane disease
e pulmonary hyaline membrane disease (HMD) (respiratory distress syndrome, RDS, accord­ing to Anglo-Saxon authors) occurs almost exclusively in premature infants. e incidence and severity are inversely related to the gestational age of the newborn (45-80% in babies below the 28th week). e outcome of the HMD has improved thanks to the antenatal administration of steroids that accelerate the maturation process of the fetal lung, the early administration of surfactant at birth and ventilatory techniques that reduce the damage to immature lungs19.
Despite all this, the morbidity is still very high (bronchopulmonary dysplasia, pulmonary hemorrhage, persistence of patency of the ductus arteriosus, sepsis, intracranial hemorrhage and/or periventricular leukomalacia, leading to neurological deficits).
HMD is determined by a relative deficiency of surfactant leading to reduced lung compliance and functional residual capacity, with increased dead space. is causes a severe alteration of the ventilation-perfusion, with a right to left shunt that can reach 80% of cardiac output. At microscopic level, the lung shows reduced aeration with distal airway collapse, and large atelectasis areas alternating with tissue showing hyper-insufflated alveoli.
e progression of atelectasis, associated with barotrauma and oxygen toxicity, cause a damage to endothelial and epithelial cells of the distal airways with production of fibrinous material. Hyaline membranes occupying the alveoli are formed within 30 minutes of birth. After 36-72 hours from birth, the epithelium begins the synthesis of surfactant. e healing process is complex. In extremely immature or critical infants a chronic process often occurs, leading to the development of bronchopulmonary dysplasia.
Immaturity is a major risk factor of HMD, but also maternal diabetes and asphyxia have a role. In HDM infants, respiratory distress occur early after birth and consist of dyspnea, expiratory
groan, subcostal and intercostal retractions, nasal flaring and cyanosis. Over the past ten years, the surfactant therapy has reduced mortality of approximately 50%20. Chest X-ray shows a diffuse and bilateral ground glass-like image, consolidations with air
bronchograms and reduced expansion of the lungs. Chest radiologic appearance is useful in