Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2693_Библиотеки_им_академика_М_И_Перельмана.pdf
9 Aortic Stenosis
are exertional dyspnea (inability to increase cardiac output and elevated pulmonary
capillary pressure), angina pectoris, and exertional syncope (caused by decreased
arterial pressure associated with vasodilatation in the exercising muscles or arrhythmias). Care must be taken to avoid intravascular volume depletion [Mulligan M,
Cousins M.Chapter 4. In: Lichtor JL, editor. Preoperative preparation and intraoperative monitoring. Philadelphia: Current Medicine; 1997. (Miller RD, editor. Atlas
of anesthesia; vol. 3)] Caption adapted from original
165
Disease Course
• After the onset of symptoms, patients with severe aortic stenosis have a survival rate as low as 50% at two years and 20% at ve years without aortic
valve replacement.
Related Evidence
Papers of particular interest have been highlighted as:
** Of key importance
Practice Guideline
Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd, Guyton RA,
O'Gara PT, Ruiz CE, Skubas NJ, Sorajja P, Sundt TM 3rd, Thomas JD, Anderson
JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Creager MA, Curtis LH,
DeMets D, Guyton RA, Hochman JS, Kovacs RJ, Ohman EM, Pressler SJ, Sellke
FW, Shen WK, Stevenson WG, Yancy CW; American College of Cardiology;
American College of Cardiology/American Heart Association; American Heart
Association. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines. J Thorac Cardiovasc Surg.
2014 Jul;148(1):e1-e132.
24939033. http://www.ncbi.nlm.nih.gov/pubmed/24939033 **
Vahanian A, Aleri O, Andreotti F, Antunes MJ, Barón-Esquivias G, Baumgartner
H, Borger MA, Carrel TP, De Bonis M, Evangelista A, Falk V, Lung B, Lancellotti
P, Pierard L, Price S, Schäfers HJ, Schuler G, Stepinska J, Swedberg K,
Takkenberg J, Von Oppell UO, Windecker S, Zamorano JL, Zembala M; ESC
Committee for Practice Guidelines (CPG); Joint Task Force on the Management
of Valvular Heart Disease of the European Society of Cardiology (ESC);
European Association for Cardio-Thoracic Surgery (EACTS). Guidelines on the
https://doi.org/10.1016/j.jtcvs.2014.05.014. PMID:
166
C. V. Pollack, Jr. et al.
management of valvular heart disease (version 2012): the Joint Task Force on the
Management of Valvular Heart Disease of the European Society of Cardiology
(ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Eur
J Cardiothorac Surg. 2012 Oct;42(4):S1–44.
https://doi.org/10.1093/ejcts/
ezs455. PMID: 22922698. http://www.ncbi.nlm.nih.gov/pubmed/22922698 **
Holmes DR Jr, Mack MJ, Kaul S, Agnihotri A, Alexander KP, Bailey SR, Calhoon
JH, Carabello BA, Desai MY, Edwards FH, Francis GS, Gardner TJ, Kappetein
AP, Linderbaum JA, Mukherjee C, Mukherjee D, Otto CM, Ruiz CE, Sacco RL,
Smith D, Thomas JD; American College of Cardiology Foundation; American
Association for Thoracic Surgery; Society for Cardiovascular Angiography and
Interventions; Society for Thoracic Surgeons; American Heart Association;
American Society of Echocardiography; European Association for CardioThoracic Surgery; Heart Failure Society of America; Mended Hearts; Society of
Cardiovascular Anesthesiologists; Society of Cardiovascular Computed
Tomography; Society for Cardiovascular Magnetic Resonance. 2012 ACCF/
AATS/SCAI/STS expert consensus document on transcatheter aortic valve
replacement: developed in collaboration with the American Heart Association,
American Society of Echocardiography, European Association for CardioThoracic Surgery, Heart Failure Society of America, Mended Hearts, Society of
Cardiovascular Anesthesiologists, Society of Cardiovascular Computed
Tomography, and Society for Cardiovascular Magnetic Resonance. Ann Thorac
Surg. 2012 Apr;93(4):1340–95. https://doi.org/10.1016/j.athoracsur.2012.01.084.
PMID: 22300625. http://www.ncbi.nlm.nih.gov/pubmed/22300625 **
Meta-Analysis
Giordana F, D'Ascenzo F, Nijhoff F, Moretti C, D'Amico M, Biondi Zoccai G,
Sinning JM, Nickenig G, Van Mieghem NM, Chieffo A, Dumonteil N, Tchetche
D, Barbash IM, Waksman R, D'Onofrio A, Lefevre T, Pilgrim T, Amabile N,
Codner P, Kornowski R, Yong ZY, Baan J, Colombo A, Latib A, Salizzoni S,
Omedè P, Conrotto F, La Torre M, Marra S, Rinaldi M, Gaita F.Meta-Analysis
of Predictors of All-Cause Mortality After Transcatheter Aortic Valve
Implantation. Am J Cardiol. 2014 Nov 1;114(9):1447-1455. https://doi.
org/10.1016/j.amjcard.2014.07.081. PMID: 25217456. http://www.ncbi.nlm.
nih.gov/pubmed/25217456
Sannino A, Losi MA, Schiattarella GG, Gargiulo G, Perrino C, Stabile E, Toscano
E, Giugliano G, Brevetti L, Franzone A, Cirillo P, Imbriaco M, Trimarco B,
Esposito G.Meta-analysis of mortality outcomes and mitral regurgitation evolution in 4,839 patients having transcatheter aortic valve implantation for severe
aortic stenosis. Am J Cardiol. 2014 Sep 15;114(6):875–82. https://doi.
org/10.1016/j.amjcard.2014.06.022. PMID: 25092192. http://www.ncbi.nlm.
nih.gov/pubmed/25092192
Coffey S, Cox B, Williams MJ.The prevalence, incidence, progression, and risks of
aortic valve sclerosis: a systematic review and meta-analysis. J Am Coll Cardiol.
9 Aortic Stenosis
167
2014 Jul 1;63(25 Pt A):2852–61. https://doi.org/10.1016/j.jacc.2014.04.018.
PMID: 24814496. http://www.ncbi.nlm.nih.gov/pubmed/24814496 **
Review
Singh A, Steadman CD, McCann GP.Advances in the understanding of the pathophysi-
ology and management of aortic stenosis: role of novel imaging techniques. Can J
Cardiol. 2014 Sep;30(9):994–1003. https://doi.org/10.1016/j.cjca.2014.03.008.
PMID: 2501569. http://www.ncbi.nlm.nih.gov/pubmed/2501569 **
Iung B, Vahanian A.Epidemiology of acquired valvular heart disease. Can J Cardiol.
2014 Sep;30(9):962–70.
24986049. http://www.ncbi.nlm.nih.gov/pubmed/24986049 **
Pandian NG, Ramamurthi A, Applebaum S.Role of echocardiography in aortic
stenosis. Prog Cardiovasc Dis. 2014 Jul-Aug;57(1):47–54.
org/10.1016/j.pcad.2014.05.006. PMID: 25081401. http://www.ncbi.nlm.nih.
gov/pubmed/25081401
Thaden JJ, Nkomo VT, Enriquez-Sarano M.The global burden of aortic stenosis.
Prog Cardiovasc Dis. 2014 May-Jun;56(6):565–71. https://doi.org/10.1016/j.
pcad.2014.02.006. PMID: 24838132. http://www.ncbi.nlm.nih.gov/pubmed
/24838132 **
Saikrishnan N, Kumar G, Sawaya FJ, Lerakis S, Yoganathan AP.Accurate assess-
ment of aortic stenosis: a review of diagnostic modalities and hemodynamics.
Circulation. 2014 Jan 14;129(2):244–53. https://doi.org/10.1161/
CIRCULATIONAHA.113.002310. PMID: 24421359. http://www.ncbi.nlm.nih.
gov/pubmed/24421359 **
Dill KE, George E, Abbara S, Cummings K, Francois CJ, Gerhard-Herman MD,
Gornik HL, Hanley M, Kalva SP, Kirsch J, Kramer CM, Majdalany BS, Moriarty
JM, Oliva IB, Schenker MP, Strax R, Rybicki FJ.ACR appropriateness criteria
imaging for transcatheter aortic valve replacement. J Am Coll Radiol. 2013
Dec;10(12):957–65.
24183748. http://www.ncbi.nlm.nih.gov/pubmed/24183748 **
Akerström F, Barderas MG, Rodríguez-Padial L. Aortic stenosis: a general over-
view of clinical, pathophysiological and therapeutic aspects. Expert Rev
Cardiovasc Ther. 2013 Feb;11(2):239–50. https://doi.org/10.1586/erc.12.171.
PMID: 23405844. http://www.ncbi.nlm.nih.gov/pubmed/23405844 **
McLean KM, Lorts A, Pearl JM.Current treatments for congenital aortic stenosis.
Curr Opin Cardiol. 2006 May;21(3):200–4. PMID: 16601457. http://www.ncbi.
nlm.nih.gov/pubmed/16601457
https://doi.org/10.1016/j.cjca.2014.03.022. PMID:
https://doi.
https://doi.org/10.1016/j.jacr.2013.09.002. PMID:
Use PubMed Clinical Queries to nd the most recent evidence. Use this search
strategy:
“Aortic Valve Stenosis”[Mesh] OR “Aortic Stenosis”
Chapter 10
Aspiration
ChristopherJ.Rees, RichardM.Cantor, CharlesV.Pollack,Jr.,
andVictoriaG.Riese
Name andSynonyms
Aspiration; Aspiration Pneumonia; Aspiration Pneumonitis; Chemical Pneumonitis
Incidence/Epidemiology
• About half of all healthy adults aspirate to some degree during sleep, but this
is usually not clinically signicant. Healthy people have physiologic defenses
(such as cough and glottic closure) against aspiration that helps to limit the
damage that can be caused.
• Aspiration becomes clinically signicant when the patient has some underlying condition that compromises the usual defenses.
• Up to 15 % of cases of typical community-acquired pneumonia (CAP) are
due to aspiration of pathogenic bacteria from the oro-pharyngeal cavity and
the stomach. The incidence increases with age, and up to 20 % of CAP in the
elderly is from aspiration.
C. J. Rees
Emergency Department, Pennsylvania Hospital, Philadelphia, PA, USA
R. M. Cantor
Department of Emergency Medicine and Pediatrics, State University of NewYork Upstate
Medical University, Syracuse, NY, USA
C. V. Pollack,
Department of Emergency Medicine, Thomas Jefferson University,
Philadelphia, PA, USA
V. G. Riese
Librarian Consultant, Eldersburg, MD, USA
C. V. Pollack, Jr. (ed.), Differential Diagnosis of Cardiopulmonary Disease,
https://doi.org/10.1007/978-3-319-63895-9_10
Jr. ()
169© Springer Nature Switzerland AG 2019
170
• It is felt that the majority of hospital- and nursing home-acquired pneumonias
are due to aspiration.
• Factors that can increase the risk of aspiration include: decreased level of
consciousness; neurologic disorders that affect swallowing; mechanical
disruption of the oro-pharynx, epiglottis, trachea, and esophagus, such as
endotracheal intubation; nasogastric feeding tubes; tracheostomy, etc.
C. J. Rees et al.
Differential Diagnosis
• Aspiration, especially aspiration of gastric contents causing aspiration pneumonitis, can present as acute shortness of breath with both tachypnea and
hypoxia. As such, the differential is broad, and contains all the usual causes of
acute dyspnea and respiratory compromise, such as ACS, pulmonary embolism, and pulmonary edema/CHF, among others.
• Aspiration pneumonia may present as typical CAP or HAP, with fever and
cough with purulent sputum, but can also present sub-acutely when caused
predominately by anaerobes.
Pathophysiology andEtiology
• Aspiration results in three broad clinical syndromes, often presenting with
overlapping features:
• Aspiration pneumonitis (chemical pneumonitis)
• Bacterial Infection causing pneumonia, empyema, and/or pulmonary abscess
• Airway obstruction from larger, solid matter
• The pathophysiology starts similarly in all syndromes. They are caused by the
abnormal entry of endogenous secretions, uids, and/or particulate matter
into the lower airway.
• Aspiration/Chemical Pneumonitis. In this syndrome, there is aspiration of
materials that have a direct, toxic effect on the lower airways and lung tissue.
The best-known and studied substance is gastric acid, and serves as the pathophysiologic model for all other substances.
• The airways and lungs are relatively resistant to injury. For clinically sig-
nicant issues to result, there needs to be a large amount of aspirate (generally more than 25ml in an adult), and the pH must be below 2.5.
• When this condition is met, rapid physiologic changes occur (within 3
minutes), including atelectasis, peribronchial hemorrhage, pulmonary
edema, and rapid death of bronchial epithelial cells.
• After 4 hours, the alveolar spaces will become lled with an inammatory
exudate composed of inammatory cells, brin, and desquamated tissue.
10 Aspiration
• Within 2 days there will be hyaline membrane formation, and the lungs will
be edematous and hemorrhagic with consolidation of the alveolar spaces.
• Lungs that have been injured by acid or other directly toxic materials are
more susceptible to subsequent bacterial infection.
• Bacterial Infection/Aspiration Pneumonia. The bacteria that cause aspiration
pneumonia generally originate in the upper airways or stomach.
• Classically, oral anaerobes (Peptostreptococcus, Fusobacterium nuclea-
tum, Prevotells, and Bacteroides spp.) and streptococci caused aspiration
pneumonia.
• More recently, hospital- and healthcare-acquired aspiration pneumonia has
been associated with more virulent organisms, such as Staphylococcus
aureus, Pseudomonas aeruginosa, and gram-negative bacilli.
• Airway obstruction. Airway obstruction may result from either uids or solid
material aspiration.
• The ingestion of uids that are not directly toxic to lung tissue (saline,
barium, etc.) can initiate a reex airway closure, such as in drowning.
• Solid objects cause differing levels of obstruction based upon their size
relative to the airways.
• Most foreign body aspirations occur in children between the ages of one
and three.
• Large objects can obstruct at the larynx, proximal trachea, tracheal bifur-
cation, or main stem bronchus. They cause nearly immediate respiratory
distress, inability to talk, and cyanosis. Unless removed quickly, they can
rapidly lead to death.
• Smaller objects cause local atelectasis, and the patient will have a cough or
focal wheezing.
171
Presentation
Typical/“Classic”
• Aspiration/Chemical Pneumonitis:
• Acute onset of symptoms with profound dyspnea, and associated
hypoxemia.
• Often seen in the setting of known risk-factors for aspiration.
• Bacterial Infection. Presentation is variable, and depends upon the causative
organisms and the overall health status of the affected patient.
• Most patients present somewhat acutely with the typical symptoms of
pneumonia, fever, productive cough, and dyspnea, especially when the
infection is due to organisms other than anaerobes (such as Staph, Strep,
Pseudomonas, etc.).
172
• Infections from anaerobic organisms often present more slowly, over days
and weeks. There is often necrotic-smelling sputum, and a notable lack of
rigors. Most patients with anaerobic aspiration pneumonia will have an
easily recognized risk factor for aspiration, and poor dental health.
• Airway Obstruction.
• Large particle airway obstruction causes acute respiratory compromise and
failure, with severe dyspnea, inability to talk, hypoxia/cyanosis, and rapid
cardiovascular collapse if not removed.
• Small particle airway obstruction can present in a more subtle fashion,
with an indolent, irritative cough, associated with dyspnea that is sometimes present only with exertion.
C. J. Rees et al.
Atypical
• There is a wide-spectrum of clinical presentations and syndromes for aspiration. As above, aspiration syndromes typically present acutely, but depending
upon many factors, may be sub-acute or indolent. Also, as noted above, atypical presentations occur especially with aspiration pneumonia caused by
anaerobic organisms, airway obstruction caused by small particles, or aspiration pneumonitis caused by small volume, higher pH substances.
Primary Differential Considerations
• Differential considerations for aspiration include:
• Respiratory Distress Syndrome
• Other respiratory failure
• Status asthmaticus
• Circulatory shock
• RSV infection in children
History andPhysical Exam
Findings That Conrm Diagnosis
• A witnessed aspiration event, followed by the typical clinical syndrome of
aspiration pneumonitis, conrms the diagnosis.
10 Aspiration
Factors That Suggest Diagnosis
• A patient who presents with community- or hospital-acquired pneumonia, has
risk factors for aspiration, and/or has inltrates in the dependent lung zones
(lower lobes if aspiration occurred in the upright position, or superior segments
of the lower lobes and/or posterior segment of the upper lobes if aspiration
occurred in the supine position) should be further evaluated for aspiration and
swallowing difculties.
Factors That Exclude Diagnosis
• Finding another cause for the dyspnea/respiratory distress makes aspiration
unlikely.
Ancillary Studies
Laboratory
• Laboratory abnormalities in aspiration pneumonitis are usually non-specic.
There may be a moderately elevated white blood cell count. Patients may be
hypoxic with a respiratory acidosis on blood gas analysis, especially in the
acute setting when they are tachypneic.
• Patients with bacterial pneumonia caused by aspiration will usually have laboratory ndings of acute infection with a leukocytosis with bandemia and/or
a leftward shift. These patients may also be hypoxic.
173
• Sputum culture has a limited role in aspiration pneumonia. Most infections
are polymicrobial, and many of the causative organisms are difcult to
culture. Coughed sputum samples are not useful for culture, as the normal
ora of the mouth and upper airway contaminates them.
• Laboratory studies are not helpful in the diagnosis of airway obstruction from
particulate matter.
Imaging
• CXR ndings in aspiration pneumonitis typically appear about 2 hours after
an aspiration event. Typically, there are inltrates in the dependent lung zones.
These are the lower lobes when the patient was in an upright position during
the aspiration event, and the superior segments of the lower lobes and posterior segments of the upper lobes if the patient was in the supine position during the aspiration event. Over time, if the disease progresses, the CXR may
show evidence of ARDS with diffuse, uffy inltrates.
174
C. J. Rees et al.
Aspiration pneumonia with infection: image progression. a Several hours after
aspiration of gastric content, there are patchy inltrates at both lung bases medially.
b Three days after aspiration, the consolidation has increased in density and extent.
At this phase, aspiration pneumonitis should be improving. This suggests secondary
infection. c Four days after aspiration, computed tomography reveals dense consolidation in the posterior and lateral basal segments of both lower lobes. This degree
of consolidation is more than one usually sees with uncomplicated aspiration pneumonitis. [Goodman LR. Imaging the Intensive Care Patient. In: Hodler J, von
Schulthess GK, Zollikofer CL, editors. Diseases of the Heart and Chest, Including
Breast 2011–2014 [Internet]. Milano: Springer Milan; 2011 [cited 2015 May 22].
p.66–9. Available from: http://link.springer.com/10.1007/978-88-470-1938-6_10]
Caption adapted from original
• The CXR in aspiration pneumonia caused by bacteria will also typically
reveal an inltrate in one or more of the dependent lung zones.
• Patients with pneumonia caused by anaerobic bacteria can have more indo-
lent presentation and may develop either lung abscess or empyema that can
be revealed on the CXR.
10 Aspiration
175
The chest radiograph and computed tomography scan showed pleural empyema
without lung abscess. [From article: Lung abscess predicts the surgical outcome in
patients with pleural empyema. Journal of Cardiothoracic Surgery. 2010;5(1):88.
https://doi.org/10.1186/1749-8090-5-88, at http://link.springer.com/article/10.1186
%2F1749-8090-5-88; by Hung-Che Huang, Heng-Chung Chen, Hsin-Yuan Fang,
Yi-Chieh Lin, Chin-Yen Wu, Ching-Yuan Cheng, © Huang etal; licensee BioMed
Central Ltd. 2010; licensed under Creative Commons Attribution License BY 2.0
http://creativecommons.org/licenses/by/2.0] Caption from original