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_3781_Библиотеки_им_академика_М_И_Перельмана
.pdf
32 Lung Transplantation
https://t.me/medicina_free
Fig. 32.3 Lung hilum
dissection. The donor lungs,
transported in cold
preservation solution and
triple-bagged, are dissected
on the back table prior to
implantation. The hilar
structures— left atrial cuff/
pulmonary veins (a),
bronchus (b), and pulmonary
artery (c)—are identied and
dissected out
– During all aspects of dissection and explanation of the lungs, it is crucial to
protect the phrenic, vagus, and recurrent laryngeal nerves.
• Implant technique.
361
– The donor lungs are split on the back table if harvested en bloc and prepared
for implantation (Fig.32.3). The lungs are sequentially transplanted. The lung
with worse function is removed rst, with single lung ventilation via the contralateral lung. If there is a discrepancy in lung function, the right lung is
implanted rst because the anatomy is more favorable.
– There are three anastomoses in a lung transplant—the bronchial, pulmonary
artery, and left atrial cuff/pulmonary vein anastomoses. The order of anastomoses
and surgical technique varies across institutions. Generally, the bronchial anastomosis (most posterior) is done rst, followed by the pulmonary artery anastomosis and, lastly, the pulmonary vein anastomosis.
The bronchial anastomosis is an “end-to-end” anastomosis, sewn with running absorbable suture (PDS) around the entire circumference of the airway.
To prevent ischemia, the donor airway is cut back to within one ring of the
upper lobe take off as it is devascularized during explant. The bronchial anastomosis is often reinforced with an intercostal muscle or pericardial ap to
separate it from the vascular anastomoses and prevent the formation of a stula between the airway and the vasculature.
The pulmonary artery anastomosis is similarly sewn with a running prolene
suture, and the pulmonary vein anastomosis with a running prolene suture.
After the anastomoses are complete, the lung is carefully deaired and gradually reperfused over the course of 10–15 min as rapid exposure of the
362
https://t.me/medicina_free
implanted lung to signicant cardiac output can lead to ischemia reperfusion
injury. The surgical eld is carefully inspected for hemostasis.
– Two or more chest tubes are placed in each pleural cavity at the conclusion of the
case. Sternal wires are used to reapproximate the sternum and the incision closed
in layers. A postoperative bronchoscopy is performed to inspect the patency and
caliber of the bronchial anastomoses and perform pulmonary toilet to eliminate
accumulated blot and mucus.
E. D. Hompe and A. A. Osho
Immunosuppression [12, 13]
• Patients who undergo lung transplantation are started on immunosuppression to
prevent rejection. At the time of transplant, high-dose immunosuppressive agents
are administered to dampen the T-cell immune response and, over time, the
immunosuppression is gradually down titrated to maintenance dosing.
• High-dose glucocorticoids (IV methylprednisolone) are administered prior to
lung perfusion, usually during completion of the rst vascular anastomosis, to
decrease reperfusion injury.
• An induction immunosuppression agent may be given at the time of transplant to
reduce the risk of acute organ rejection. Most patients who undergo lung transplantation in the United States receive induction therapy (80.9%).
• The most common induction agents used are basiliximab (monoclonal antibody
(mAb) against the interleukin-2 receptor), rabbit anti-thymocyte globulin (T-cell
depleting agent), and alemtuzumab (mAb against CD52 and T-cell depleting agent).
– One important contraindication to giving induction therapy is if the patient is
at high risk for certain postoperative infections, such as in cases of CMV
mismatch (CMV+ organ is transplanted into a CMV− recipient).
• For maintenance immunosuppression, most patients are on tacrolimus (a calcineurin inhibitor), mycophenolate mofetil (a nucleotide blocking agent), and a
glucocorticoid such as prednisone.
– Patients are monitored closely for side effects of these medications and take
prophylaxis against potential opportunistic infections.
Outcomes [13–15]
• In the most recent report on outcomes of lung transplantation in the United
States, post-transplant survival was 89.4% at 1year, 74.8% at 3years, and 61.2%
at 5years. The incidence of acute rejection was reported to be 14.6%, but multiple other studies describe higher rates of acute rejection, approaching 30–40%.
32 Lung Transplantation
https://t.me/medicina_free
363
Chronic lung allograft dysfunction (bronchiolitis obliterans) was reported in
5.7% of recipients at 1year and 40.2% at 5years.
• The average time to transplant for candidates on the waitlist was 1.4months. In
recent years, there has been a notable increase in transplant rates for adults
65years and older and patients with restrictive lung disease.
• Other contributors to post-transplant morbidity and mortality include infections,
particularly in the rst year after transplant, the development of renal insufciency (often secondary to calcineurin inhibitors) and malignancies (posttransplant lymphoproliferative disorder, skin cancer, and solid organ tumors) in
the long term.
• With the increase in the number of DCD donors, it is important to compare outcomes and survival rates in patients who receive DBD versus DCD lungs. Recent
data showed no difference in 5-year survival in DCD recipients compared to
DBD recipients. In addition, while primary graft dysfunction was shown to be
worse for DCD lungs in the immediate postoperative setting, it was noted to
improve rapidly and there was ultimately no difference in graft function at 72h.
• Innovations to address the donor shortage, such as increased use of DCD donors,
organ engineering and xenotransplantation, as well as strategies to prevent and
treat chronic lung allograft dysfunction, will ultimately be needed to make meaningful progress in the eld.
References
1. Weill D. Lung transplantation: indications and contraindications. J Thorac Dis.
2018;10(7):4574–87.
2. Weill D, Benden C, Corris PA, Dark JH, Davis RD, Keshavjee S, etal. A consensus document for the selection of lung transplant candidates: 2014—an update from the Pulmonary
Transplantation Council of the International Society for Heart and Lung Transplantation. J
Heart Lung Transplant. 2015;34(1):1–15.
3. Lyu DM, Goff RR, Chan KM.The lung allocation score and its relevance. Semin Respir Crit
Care Med. 2021;42(3):346–56.
4. Puri V, Patterson GA, Meyers BF.Single versus bilateral lung transplantation: do guidelines
exist? Thorac Surg Clin. 2015;25(1):47–54.
5. Thabut G, Christie JD, Ravaud P, Castier Y, Brugière O, Fournier M, etal. Survival after bilateral versus single lung transplantation for patients with chronic obstructive pulmonary disease:
a retrospective analysis of registry data. Lancet. 2008;371(9614):744–51.
6. Weiss ES, Allen JG, Merlo CA, Conte JV, Shah AS. Survival after single versus bilateral lung transplantation for high-risk patients with pulmonary brosis. Ann Thorac Surg.
2009;88(5):1616–25.
7. Chaney J, Suzuki Y, Cantu E III, van Berkel V. Lung donor selection criteria. J Thorac Dis.
2014;6(8):1032–8.
8. Lardinois D, Banysch M, Korom S, Hillinger S, Rousson V, Boehler A, et al. Extended
donor lungs: 11 years experience in a consecutive series. Eur J Cardiothorac Surg.
2005;27(5):762–7.
9. Puri V, Patterson GA. Adult lung transplantation: technical considerations. Semin Thorac
Cardiovasc Surg. 2008;20(2):152–64.
364
https://t.me/medicina_free
10. Sundaresan S, Trachiotis GD, Aoe M, Patterson GA, Cooper JD.Donor lung procurement:
assessment and operative technique. Ann Thorac Surg. 1993;56(6):1409–13.
11. Gust L, D'Journo XB, Brioude G, Trousse D, Dizier S, Doddoli C, etal. Single-lung and
double-lung transplantation: technique and tips. J Thorac Dis. 2018;10(4):2508–18.
12. Chung PA, Dilling DF.Immunosuppressive strategies in lung transplantation. Ann Transl Med.
2020;8(6):409.
13. Valapour M, Lehr CJ, Skeans MA, Smith JM, Miller E, Goff R, etal. OPTN/SRTR 2020
annual data report: lung. Am J Transplant. 2022;22(Suppl 2):438–518.
14. Van Raemdonck D, Keshavjee S, Levvey B, Cherikh WS, Snell G, Erasmus M, etal. Donation
after circulatory death in lung transplantation-5-year follow-up from ISHLT Registry. J Heart
Lung Transplant. 2019;38(12):1235–45.
15. Villavicencio MA, Axtell AL, Spencer PJ, Heng EE, Kilmarx S, Dalpozzal N, etal. Lung
transplantation from donation after circulatory death: United States and single-center experience. Ann Thorac Surg. 2018;106(6):1619–27.
E. D. Hompe and A. A. Osho
Chapter 33
https://t.me/medicina_free
Adult Congenital Heart Disease
SelenaS.Li andJordanP.Bloom
Adult Presentation ofCommon Congenital Heart Defects
In the modern era, over 90% of children with congenital heart defects survive into
adulthood, and the prevalence of CHD has shifted from infancy/childhood to adulthood [1]. The presentation of adults with congenital heart defects encompasses both
those who diagnosed and treated in childhood, as well as new diagnoses. Over 75%
of ACHD patients have had prior palliative surgeries and interventions and have
established care with cardiology and cardiac surgery. However, the remaining 25%
can present with either new symptoms of a known defect or a previously undetected
diagnosis [2]. The symptoms of CHD that manifest later in life differ from those
that present in childhood and can often be misdiagnosed.
S. S. Li · J. P. Bloom (*)
Division of Cardiac Surgery, Massachusetts General Hospital, Boston, MA, USA
e-mail: ssli@mgb.org; jpbloom@mgh.harvard.edu
Switzerland AG 2024
J. P. Bloom, T. M. Sundt (eds.), Cardiac Surgery Clerkship, Contemporary
Surgical Clerkships, https://doi.org/10.1007/978-3-031-41301-8_33
365© The Author(s), under exclusive license to Springer Nature
366
https://t.me/medicina_free
Atrial septal
defect (ASD)
and patent
foramen ovale
(PFO)
Partial
anomalous
pulmonary
venous return
(PAPVR) [3]
Ventricular
septal defect
(VSD)
Coronary
anomalies [4]
S. S. Li and J. P. Bloom
Denition Presenting symptoms in the adult
ASD=membranous defect
in interatrial septum,
resulting in connection
between the right and left
atria
PFO=failure of closure of
foramen ovale, with
persistent connection
between the right and left
atria
Pulmonary veins drain
erroneously to right heart
(SVC, IVC, RA) instead of
to LA
Defect in membranous or
muscular interventricular
septum, resulting in
connection between RV
and LV
May include anomalies of
coronary vessel:
– Origin
– Course
– Termination
– Collateral vessels
Isolated ASD/PFO
• Exam
– Fixed, split S2
From delayed closure of the
pulmonary valve (PV)
– Systolic murmur at upper left sternal
border
Increased blood ow across
pulmonary valve (PV)
– Mid-diastolic murmur at lower left sternal
border
Increased ow across tricuspid valve
• Paradoxical embolism
– Stroke
– Peripheral embolism
– Mesenteric ischemia
• Right heart failure
– Elevated jugular venous pressure (JVP)
– Peripheral edema
– Hepatic congestion
• Eisenmenger syndrome (right-to-left shunt)
– Cyanosis
– Shortness of breath
– Clubbing
– Hemoptysis
*May also present associated with other
congenital syndromes
*Depends on degree of left-to-right shunting
• Shortness of breath
• Peripheral edema
• Chest pain/discomfort
• Palpitations
*Most common congenital heart defect
• Exam
– Loud S1 with wide, xed split S2
– Holosystolic murmur at left sternal
border
Left-to-right shunt
• Right heart failure
• Elevated JVP
• Peripheral edema
• Orthopnea
Eisenmenger syndrome (right-to-left shunt)
• See above
• Incidental nding on CT/CTA
• Chest pain/angina
• Dyspnea on exertion
• Syncope
• Sudden cardiac death
– Higher risk in anomalous LEFT coronary
artery
Pulmonary
septal defect
hypertrophy
33 Adult Congenital Heart Disease
https://t.me/medicina_free
367
Tetralogy ofFallot
Tetralogy of Fallot (ToF) is the most common cyanotic congenital heart disease, and
historically, the rst to be palliated surgically.
Anatomy/Pathophysiology
• Infundibular portion of ventricular septum is displaced anteriorly into the right
ventricular outow tract (RVOT)—remember the mnemonic “PROVe”
(Fig.33.1).
– Pulmonary stenosis.
– Right ventricular (RV) hypertrophy (resulting from pulmonary stenosis).
– Overriding aorta.
– VSD.
Initial Operation
• Neonatal repair (Fig.33.2).
– Principles:
1. VSD closure.
2. Relief of RVOT obstruction.
Fig. 33.1 Tetralogy of
Fallot anatomy
stenosis
Infundibular
stenosis
Overriding aorta
Ventricular
Right ventricular
368
https://t.me/medicina_free
Patch repairing
septal defect
Fig. 33.2 Surgical repair of tetralogy of Fallot with transannular patch
S. S. Li and J. P. Bloom
Transannular patch
to right ventricular
outflow tract
• Pulmonary valvotomy and augmentation of the infundibulum.
• Transannular patch.
• RV to PA conduit.
Common Complications
• Severe pulmonary regurgitation.
– RV dilation or dysfunction (usually much later in life).
• Risk for arrhythmia and sudden cardiac death.
• Heart failure.
• Aortic root dilation and aortic regurgitation.
Reoperative Surgery
• Principles:
– Prior surgical repair techniques (transannular patch) result in PR which leads
to risk of RV dilation and arrhythmia in adulthood.
33 Adult Congenital Heart Disease
https://t.me/medicina_free
– Reoperative surgery involves pulmonary valve replacement (PVR).
• Indications for PVR.
– Severe PR and symptoms or decreased exercise tolerance.
– Asymptomatic severe PR and any of the following:
Moderate to severe RV dysfunction.
Moderate to severe RV enlargement.
Symptomatic or sustained arrhythmia.
Moderate to severe TR.
• Surgery versus catheter-based intervention.
– Percutaneous PVR.
Current studies have focused on use in patients with previous surgical
RVOT conduits [5].
Short-term results comparable to surgical cohorts in terms of reductions in
pulmonary regurgitation and RV volume.
No randomized trials that directly compare the two.
Coronary Artery Anomalies
369
Coronary artery anomalies can broadly be categorized as anomalies of origin,
course, or termination of the artery, or abnormal collateral vessels. Discussed here
are anomalous coronary arteries originating from the wrong sinus as it is the anomaly most frequently associated with sudden cardiac death.
Anomalies ofOrigin
Anomalous right coronary (RCA) Anomalous left coronary (LCA)
Epidemiology
[6]
Workup – Imaging (CT, MRI, intravascular
Treatment Asymptomatic, negative stress test:
– 0.28% originating from left sinus of
Valsalva
– 0.003% from pulmonary artery [4]
– Increased risk with ToF or double
outlet RV
US, left heart catheterization)
– Nuclear stress test
– Regular follow-up
Symptomatic or positive stress:
– PCI w/stent
– Surgery
– 0.03% from right sinus of
Valsalva
– 0.008% from pulmonary
artery [4]
– Imaging (CT, MRI,
intravascular US, left heart
catheterization)
– Nuclear stress test
Age <35
– Surgery (regardless of
symptoms)
Age ≥35
– Surgery if symptomatic or
positive stress
370
https://t.me/medicina_free
Fig. 33.3 Courses of anomalous coronary arteries
S. S. Li and J. P. Bloom
Imaging
• CT superior to MRI for denition of course of anomalous coronary artery
(Fig.33.3).
Prepulmonary (anterior) – Courses anterior to pulmonary artery
Retroaortic – Courses posterior to aorta
Transseptal – Courses through interventricular septum
Interarterial – Courses between aorta and pulmonary artery
– Higher risk of compression—>ischemia
• Increasing role of intravascular US to dene anomalous origins.
Risk ofSudden Cardiac Death [4]
• Higher risk in:
– Anomalous LCA from right sinus.
– Interarterial course. (There is debate about whether this leads to higher risk)
– Intramural course (in which the coronary artery courses through the media of
the aorta) [7]
– Slit-like orice opening.
– Anomalous LCA from pulmonary artery
– Atresia of LCA.
Surgical Repair
• Coronary artery unroong (excising common wall between aorta and anomalous
coronary, Fig.33.4).
Соседние файлы в папке Библиотека им академика М.И. Перельмана