Doug Condit, RPA-C, DFAAPA, USN (ret.)
Editor Emeritus, JAPACVS
Journal of the Association of PAs in Cardiothoracic and Vascular Surgery
Editor-in-Chief
Aaron R. Morton, DMSc, MMSc, PA-C, ATC, FAPACVS Emory University, Atlanta, GA
Associate Editor—International Vicky Vink PA Switzerland
Associate Editor Writer Development
Edward A. Ranzenbach, PA-C, MPAS, CAQ-CVTS, FAPACVS, DFAAPA Forest Ranch, CA
Editorial Board
Matthew Vercauteren MPAS, PA-C, FAPACVS Thoracic Section Editor
Daniel Geersen MPAP, PA-C Vascular Section Editor
Hantz B. Fontaine PA-C
Editorial Member at Large
EDITORIAL MISSION:
The JAPACVS is the official clinical journal of the Association of PAs in Cardiothoracic and Vascular Surgery. The mission of the JAPACVS is to improve Cardiac, Vascular and Thoracic Surgical and CVT Critical Care patient care by publishing the most innovative, timely, practice-proven educational information available for the physician assistant profession.
PUBLISHED CONTENT IN THE JAPACVS: Statements and opinions expressed in the articles and communications herein are those of the authors and not necessarily those of the Publisher or the Association of PAS in Cardiothoracic and Vascular Surgery (APACVS). The Publisher and the APACVS disclaim any responsibility or liability for such material, including but not limited to any losses or other damage incurred by readers in reliance on such content. Neither Publisher nor APACVS verify any claims or other information appearing in any of the advertisements contained in the publication and cannot take responsibility for any losses or other damage incurred by readers in reliance on thereon. Neither Publisher nor APACVS guarantees, warrants, or endorses any product or service advertised in this publication, nor do they guaranty any claim made by the manufacturer of such product or service.
SALES OFFICE
APACVS 1208 Victoria Crossing Festus, MO 63028 Phone (502) 321-6155 admin@apacvs.org
Publisher
David E. Lizotte, Jr. MPAS, PA-C, FAPACVS Executive Director APACVS Fenton, MO
JAPACVS/Journal of the Association of PAs in Cardiothoracic and Vascular Surgery is published quarterly (4 issues per volume, one volume per year) by APACVS 1208 Victoria Crossing, Festus, MO 63028. Volume 5, Number 1, Winter 2023. One year subscription rates: $40 in the United States and Possessions. Single copies (prepaid only): $10 in the United States
© 2023 APACVS, INC. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including by photocopy, recording, or information storage and retrieval system, without permission in writing from the publisher.
Editorial
4 From the Editor’s Desk
Aaron R. Morton, DMSc, MMSc, PA-C, ATC, FAPACVS Editor -In-Chief
5 In Memoriam: Doug Condit, RPA-C, DFAAPA, USN (ret.)
David J. Bunnell, MSHS, PA-C, DFAAPA
6 Tribute to Douglas Condit, RPA-C
John Lee, PA-C, Robert Sammartano, PA-C, Dana Gray, PA-C
Peer Reviewed Content
10 The Application of Transcarotid Artery Revascularization for Treatment of Carotid Artery Stenosis
Matthew Scherschel, DMSc, MPAS, MHA, RRT, PA-C
Peer Reviewed Content
20 Assessment of Malperfusion Syndrome in Aortic Dissection: Defining an Aortic Dissection Lab Panel
Edward Ranzenbach, DMSc, PA-C, CAQ-CVTS, FAPACVS, DFAAPA
APACVS is the only association representing Cardiac, Thoracic and Vascular Surgery and CTV Critical Care PAs. By PAs, For PAs!
We recently lost a champion and a pioneer for Physician Assistants in Cardiothoracic Surgery, in PA Publishing and for our journal. Our own Editor-Emeritus and charter member Mr. Douglas Condit. I will devote my usual space for tributes to Doug with invited content in memorial to a giant in our community.
In honor of Doug, -AM
“I have fought the good fight, I have finished the race, I have kept the faith.”
2 Timothy 7
Doug Condit was the rare individual who was relevant to our profession from the moment he stepped on stage to the moment he died. APACVS Executive Director David Lizotte, MS, PA-C, FAPACVS described him as the prototype for our profession. Former APACVS President Michael Doll, MS, PA-C, FAPACVS, DFAAPA and past Board Member Genie Ball, MS, PA-C, FAPACVS agreed on the precise description in response to my online remembrance“iconic.”
PA Condit was iconic because you can learn the history of our profession by knowing his story. He volunteered to serve in the Vietnam war and became a Navy Corpsman deployed with the Marine Corps where he earned three bronze stars. He had the opportunity to leave Vietnam early, he chose to remain on the battlefield. He declined a seat offered to him at Duke University PA Program to finish his Navy service. He was invited to interview for the University of Alabama Birmingham surgical PA program where he was accepted and introduced to our specialty. During the HIV/AIDs crisis he engaged in scholarship through writing and being the first PA to speak at the Society of Thoracic Surgeons meeting about surgeon’s attitudes about providing care to HIV patients. He educated generations of PA surgical residents at Montefiore Medical Center in Bronx, New York. He was the editor of Surgical PA, CardioVISION, and Editor Emeritus for JAPACVS. He was working in New York during the 2001 terrorist attacks. He was still working when New York City was at the center of the Covid-19 Pandemic in 2020. However, while I admired Doug for his meaningful career, I loved him because he was my friend. We shared a heart for scholarship, a sense of history, and love for patient care. We became close when I started writing with him for CardioVISION which was the predecessor of JAPACVS. We shared emails, phone calls, and frequent social media contact. When I became the Editor of JAPACVS he gave me advice on editorial vision and the challenge of creating and maintaining a scholarly journal. About ten years ago he started sending me emails on anything that made him laugh and it continued until late in 2022. There were so many of these messages
that I could not read them all in real time. It gives me comfort to go back and make sure I read every one.
Doug was full of contradictions. He could be mistaken for someone who was a relic of the past, but he was always engaged with what was happening now. As the song says “he was quick with a joke or a light if you smoke” but he was also a private person. While his direct involvement with American and PA history is significant and he loved to tell the stories, the stories were told without ego or self-aggrandizement. While many of us knew him to be hilarious and down to earth, he was a deeply spiritual man who often spoke with me about our shared Christian faith.
partment of PA Medicine and Director at Large for the American Academy of Physician Associates. He is a former JAPACVS Editor in Chief.
John Lee, PA-C, Robert Sammartano, PA-C, Dana Gray, PA-C
The Physician Assistant/ Associate (PA) profession, particularly the surgical PA community, has sadly lost a pioneer, leader, and surgical PA advocate. He will remain an everlasting surgical PA icon. Doug ‘s national impact on the PA profession was substantial and the honors he had earned do not measure his zeal and determination in effecting recognition for surgical PAs and all PA disciplines through the years.
After graduating from Colorado State University in 1966 and toying around with the idea of law school, he joined the US Navy instead, served in Viet Nam and was honorably discharged as a Hospitalman, receiving several citations for his outstanding military service. Doug’s military career set the tone for his PA life. Doug graduated from University of Alabama’s PA Program in 1970 and subsequently graduated from Montefiore’s Surgical PA Residency Program in 1972 in Montefiore’s first graduating class. Further details of his extensive biography can be accessed at the weblink, https://pahx.org/assistants/condit-doug/.
As a pioneer, he was fearless in overcoming challenges, undeterred by negativity, achieving multiple firsts in his illustrious career. He became the first PA to work in cardiothoracic surgery at Montefiore and was the first PA to present at the Society of Thoracic Surgeon’s national conference. Following a ski trip to the USSR (now Russia), Doug was the first PA to publish the similar roles of Soviet/ Russian “feldshers” to primary care PA’ s.
As a visionary leader, he was a charter member of the Association of PA’s in Cardiothoracic and Vascular Surgery (APACVS) and the American Association of Surgeon’s Assistance (AASA), precursor to the current American Associations of Surgical PA’s (AASPA). He was a prolific writer with over 200 publications. As Editor-in-Chief of Surgical Physician Assistant, along with Susan Lusty (publisher), they were instrumental in uniting the distinctive surgical PA subspecialty organizations. Doug’s spearheading of surgical PA advocacy within the American Academy of Physician Assistants/ Associates (AAPA), AAPA’s Surgical Congress (as Chair), AAPA’s House of Delegates, New York State Society of PA’s (NYSSPA), APACVS, AASA/ AASPA, markedly progressed the influence of surgical PA’s. Never forgetting his military roots, he was a charter member of the AAPA Veteran’s Caucus.
As a mentor, he instilled a passion to learn, teach and proliferate. He personalized Montefiore’s adopted military motto of “be all that you can be” to “you can do it”.
He approached life with humor and out-of-the-box thinking. His quirkiness made him unique and memorable. He remained open-minded exemplified by challenging to the status quo and non-traditional forms of meditation and medical treatments.
We are honored to have known Doug and am grateful for all he’s done for the profession and for each of us professionally. As a steadfast friend, he exuded compassion, support, and sagely advice. In Doug’s words, his hello was typically “ yo’ dude” and he typically ended our joint Christmas cards to hospital staff with “Peace, Love”. Doug, we wish you eternal peace and love.
Carotid artery stenosis can present a risk for transient ischemic attack and stroke. Treatment of carotid artery stenosis with carotid endarterectomy is considered the gold standard but may not be the best treatment option in patients at high-risk for surgical intervention. Transfemoral carotid artery stenting was introduced as a minimally invasive treatment option but has demonstrated poor outcomes compared to carotid endarterectomy. The introduction of transcarotid artery revascularization fills this role by providing outcomes superior to transfemoral carotid artery stenting and consistent with carotid endarterectomy supporting its application for treatment of carotid artery stenosis in patients at high-risk for surgical intervention.
Keywords: carotid artery stenosis, carotid endarterectomy, transcarotid artery revascularization, transfemoral carotid artery stenting, vascular surgery
Learning objectives
• Define symptomatic and asymptomatic carotid artery stenosis.
• Distinguish Centers for Medicare and Medicaid Services guidelines for patients at high-risk for carotid endarterectomy.
• Describe the procedure of transcarotid artery revascularization.
• Recognize patients needing intervention for carotid artery stenosis and recommend treatment based on their clinical picture.
Stroke was the fifth leading cause of death in the United States in 2020 and the leading cause of long-term disability.1,2 It is estimated that strokes cost nearly $53 billion for the provision of healthcare, medication, and missed workdays in the United States.2 Ischemia is the cause of 87% of strokes with carotid artery stenosis (CAS) contributing to approximately 10% of ischemic strokes.2,3 The identification and treatment of CAS is essential for primary and secondary prevention of stroke. Carotid endarterectomy (CEA) is the gold standard treatment for CAS but may not be feasible in individuals at high-risk for surgical intervention.4 Transfemoral carotid artery stenting (TF-CAS) is a minimally invasive treatment option but has been found to have higher rates of stroke and death in the high-risk population.5 The introduction of transcarotid artery revascularization (TCAR) presents a minimally invasive treatment option for individuals at high-risk for surgical intervention if it provides outcomes consistent with CEA.
Atherosclerotic plaque formation in the internal carotid artery results in CAS when it becomes hemodynamically significant. As the degree of stenosis increases, the lumen of the internal carotid artery narrows decreasing blood flow to the brain while also presenting the risk of plaque rupture with embolization distally or thrombus formation within the vessel lumen. These complications of CAS present the risk of ischemic stroke. The estimated global prevalence of CAS in individuals aged 30-79 years is 1.5% with an increase of 59.13% from 2000 to 2020.6
A patient with CAS and no neurologic symptoms or with a history of symptoms greater than six months prior is considered asymptomatic.3 Asymptomatic disease is typically identified during physical examination through auscultation of a carotid bruit or incidentally on imaging studies. The presence of acute neurologic symptoms consistent with amaurosis fugax, transient ischemic attack, or stroke that can be linked to CAS is considered symptomatic.3 Amaurosis fugax will occur on the ipsilateral side and motor or sensory deficits on the contralateral side. Presenting symptoms will depend on the area of the brain affected by limited arterial flow.
Evaluation by neurology will be necessary to rule out other causes for the patient’s symptoms.
Neurologic symptoms including dizziness, lightheadedness, syncope, and vertigo are not typically attributed to CAS as they are symptoms associated with the posterior circulation, while the internal carotid artery blood flow favors the anterior and middle cerebral arteries.3
Carotid duplex ultrasound is considered the first-line evaluation for CAS. Utilized as a screening examination, ultrasound can provide quantification of the degree of stenosis through blood flow velocities in the arterial lumen.3 A velocity of 230 cm/sec or higher is consistent with arterial luminal stenosis of 70% or greater.3 Computed tomography angiography (CTA) provides a more defined evaluation by quantifying the degree of stenosis and characterizing the morphology of the carotid plaque to support medical decision making and surgical planning.3
The Society of Vascular Surgery (SVS) recommends screening for asymptomatic CAS in patients at increased risk due to comorbid conditions shown in Table 1.7 In asymptomatic patients, CEA is recommended for stenosis of greater than 70% with less than 3% risk of perioperative stroke and death and a life expectancy of at least 3 years.7 Symptomatic patients are recommended to undergo CEA with stenosis of 50% or greater.7 Carotid artery stenting should be considered in patients at high-risk for surgical intervention with CEA.7
7
Table
Presence of lower extremity peripheral arterial disease
Those undergoing coronary artery bypass surgery
Age 55 or greater with two atherosclerotic risk factors
Age 55 or greater and current cigarette smoker
Presence of diabetes, hypertension, or coronary artery disease
Presence of silent cerebral infarction on imaging studies
Surgical management of CAS cannot reverse the effects of a neurologic event but is a preventative measure for long-term stroke prophylaxis. Determination of those appropriate for surgical intervention includes consideration of the degree of stenosis, symptom status, preoperative stroke risk,
life expectancy, anatomic risk including contralateral carotid occlusion or prior neck irradiation, and cardiovascular comorbidities that present a physiologic risk.4 CEA remains a wellestablished treatment option for CAS but presents a risk for post operative mortality in those with increased age, contralateral carotid artery stenosis, congestive heart failure, chronic kidney disease, diabetes, and chronic obstructive pulmonary disease.3,8 The Centers for Medicare and Medicaid Services (CMS) has outlined specific physiologic and anatomic high-risk criteria for patients under consideration for CEA shown in Table 2.
Congestive heart failure class III/IV
Left ventricular ejection fraction <30%
Unstable angina
Contralateral carotid occlusion
Recent myocardial infarction
Prior CEA with recurrent stenosis
Prior neck radiation
Evaluation of CEA outcomes from the American College of Surgeons National Surgical Quality Improvement Program database compared patients meeting CMS high-risk criteria guidelines against those determined to be normal risk.4 The exact physiologic or anatomic highrisk factor was unknown to reviewers. Patients with physiologic risk factors were older with higher rates of hypertension, congestive heart failure, diabetes, and chronic kidney disease.4 Those with anatomic risk factors were more likely to have comorbidities including congestive heart failure, chronic obstructive pulmonary disease, and end stage renal disease on hemodialysis.4
High-risk patients were found to have higher rates of adverse events in the first 30 days following CEA than those at normal risk. In 25,788 patients who had undergone CEA, those meeting high-risk physiologic criteria had twice the rate of stroke/death (4.6 vs 2.3%, p<.001) and nearly twice the rate of perioperative cardiac events (3.1 vs 1.6%, p<.001).4 High-risk anatomic patients had elevated rates of stroke/death (3.6 vs 2.3%, p<.001), perioperative cardiac events (2.3 vs 1.6%, p<.01), and cranial nerve injury (4.3 vs 2.5%, p<.001).4 When separated into symptomatic or asymptomatic presentation, those meeting high-risk physiology criteria who
presented asymptomatically had a stroke/death rate significantly higher than normal risk patients (4.7 vs 1.5%, p<.001), well above the 3% recommended in the SVS clinical practice guidelines.4 Individuals meeting high-risk CMS criteria demonstrated worse outcomes than those deemed normal risk with differences in stroke/death rate significantly affected by individuals presenting asymptomatically and with high-risk physiology.
Identifying a minimally invasive treatment option to effectively treat individuals meeting high-risk CMS criteria with comparable outcomes to CEA has been challenging. The introduction of TF-CAS was intended to meet this aim but has not found widespread acceptance due to a higher risk of poor outcomes. The differences in major adverse event outcomes compared to CEA are well documented in the literature with historical studies noting higher rates of stroke following TF-CAS and dramatic increases in those treated for symptomatic CAS.10 One study of 9,753 patients identified a statistically significant higher rate of stroke and death in the perioperative period for symptomatic patients treated with TF-CAS (OR 1.70, 95% CI 1.31 to 2.19; p<0.0001). In asymptomatic patients the rate was found to be higher but not statistically significant.11
The increased rate of stroke and death in TF-CAS patients is likely associated with the point of access that requires an extensive path to be traversed to enter the treatment site. Through a transfemoral artery approach, the guidewire must pass through the aorta and its arch, into the common carotid artery, and up to the internal carotid artery. In high-risk patients, the aorta may be diseased and tortuous creating significant risk during the procedure due to the lack of a protective device during access. Prior to carotid stent placement, an embolic protection device is passed through the stenotic area resulting in the risk of plaque fracturing and thrombus embolization leading to potential ischemic stroke.12 This risk was proven through the utilization of transcranial doppler ultrasound in the operative suite documenting microembolic events during carotid stent placement.13
A new procedure has been developed to overcome the complications associated with TF-CAS. TCAR is a minimally invasive procedure utilizing direct access at the common carotid
artery proximal to the stenosis and employs an embolic protection device to reverse flow in the carotid artery.10 Embolic risk is minimized as the protection device is placed and flow reversal initiated prior to crossing the stenotic area and is utilized throughout the procedure.10 The embolic protection device functions as an arteriovenous circuit between the carotid artery and femoral vein and contains a filter to capture microemboli.10
TCAR avoids the high risk maneuvers completed during TF-CAS, including traversing the aortic arch, cannulation of the common carotid artery at the arch, and crossing the stenotic area without embolic protection.10 Advantages of TCAR include a smaller incision and operative times around 30 minutes less than CEA, contrast volume around 50% of that needed for TFCAS, and in some institutions the procedure is completed under local or regional anesthesia.10 If TCAR can provide improved outcomes compared to TF-CAS and similar outcomes to CEA, this would provide potential protection to patients who meet CMS high-risk criteria for surgical intervention by CEA.
In 2015, TCAR received approval from the United States Food and Drug Administration and CMS with plans for a transcarotid artery revascularization surveillance project. The surveillance project is ongoing with an estimated completion date of December 2024.14 No randomized control trials have been conducted at this time to assess TCAR effectiveness or outcomes.
carotid artery stenting. Utilization of the SVS Transcarotid Artery
Revascularization Surveillance Project database and the Transfemoral Carotid Artery Stent Registry in one study, including 3,286 patients in each cohort, compared outcomes for the procedures.8 Those undergoing TCAR demonstrated a significantly lower in-hospital risk of stroke (1.3% vs 2.4%; absolute difference, -1.10% [95% CI, -1.79% to -0.41%]; RR, 0.54 [95% CI, 0.38 to 0.79]; p=.001) and death (0.4% vs 1.0%; absolute difference, -0.55% [95% CI, -0.98% to –0.11%]; RR, 0.44 [95% CI, 0.23 to 0.82]; p=.008).8 There was no statistically significant difference in myocardial infarction or transient ischemic attack.8 Follow up after one year revealed a statistically significant difference in ipsilateral stroke and death rates in TCAR patients
compared to their transfemoral counterparts (5.1% vs 9.6%; hazard ratio, 0.52 [95% CI, 0.41 to 0.66]; p<.001).8 Similar results have been found in other studies documenting better outcomes for TCAR compared to TF-CAS both perioperatively and long-term.15,16 SVS guidelines now state that TCAR is superior or preferable to TF-CAS in individuals meeting CMS high-risk criteria.7
Carotid endarterectomy. A systematic review and meta-analysis of six studies evaluated outcomes for TCAR compared to CEA.17 No statistical significance was found in stroke or death rates (n = 14,026, OR 1.03, 95% CI 0.77-1.37, p=0.84) and (n = 14,200, OR 1.14, 95% CI 0.67-1.94, p=0.63) respectively.17 The incidence of postoperative myocardial infarction was lower in the TCAR cohort (n = 14,174, OR 0.55, 95% CI 0.36-0.83, p=0.004).17 These results did not change when patients were separated into symptomatic and asymptomatic cohorts.17
Comparable results were achieved in two other studies supporting these findings.10,15 TCAR patients were found to experience a lower rate of cranial nerve injury compared to individuals undergoing CEA (n = 4,012, 0.54% and 1.84%, OR: 0.52, 95% CI: 0.36, 0.74).15
Review
noted patients undergoing TCAR compared to those receiving CEA were older and had more comorbidities including coronary artery disease, congestive heart failure, chronic obstructive pulmonary disease, and on hemodialysis.10 The TCAR patients had operative times of 78 minutes compared to 111 minutes for CEA (p<.001).10 The SVS now recommends TCAR as superior or preferable to CEA in patients meeting CMS high-risk criteria.7
Carotid endarterectomy is the gold standard treatment for CAS. While well validated in the literature, this treatment approach is associated with higher rates of stroke and death in patients meeting CMS high-risk criteria. Utilization of TF-CAS has demonstrated poor outcomes compared to CEA limiting its acceptance. TCAR has shown effectiveness and outcomes comparable to CEA in stroke and death as well as lower myocardial infarction rates post operatively. While still early in its application, TCAR presents a minimally invasive treatment option for CAS that is beneficial to patients meeting CMS high-risk criteria. Continued research and completion
of a randomized controlled trial would be beneficial for the continued evaluation of postoperative outcomes and long-term patency rates.
1. Mortality in the United States, 2020. National Center for Health Statistics. Accessed August 31, 2022. https://www.cdc.gov/nchs/data/databriefs/db427.pdf
2. Tsao CW, Aday AW, Almarzooq ZI, et al. Heart disease and stroke statistics-2022 update: A report from the American Heart Association. Circulation. 2022;145(8):e153-e639. doi:10.1161/CIR.0000000000001052
3. Chaturvedi S, Lalla R, Raghavan P. Trends and controversies in carotid artery stenosis treatment. F1000Res. 2020;9. doi:10.12688/F1000RESEARCH.25922.1/DOI
4. Rao V, Liang P, Swerdlow N, et al. Contemporary outcomes after carotid endarterectomy in high-risk anatomic and physiologic patients. J Vasc Surg. 2020;71(1):104-110. doi:10.1016/J.JVS.2019.05.041
5. Hicks CW, Nejim B, Locham S, Aridi HD, Schermerhorn ML, Malas MB. Association between Medicare high-risk criteria and outcomes after carotid revascularization procedures. J Vasc Surg. 2018;67(6):1752-1761.e2. doi:10.1016/J.JVS.2017.10.066
6. Song P, Fang Z, Wang H, et al. Global and regional prevalence, burden, and risk factors for carotid atherosclerosis: a systematic review, meta-analysis, and modelling study. Lancet Glob Health. 2020;8(5):e721-e729. doi:10.1016/S2214-109X(20)30117-0
7. AbuRahma AF, Avgerinos ED, Chang RW, et al. Society for Vascular Surgery clinical practice guidelines for management of extracranial cerebrovascular disease. J Vasc Surg. 2022;75(1):4S-22S. doi:10.1016/J.JVS.2021.04.073
8. Schermerhorn ML, Liang P, Eldrup-Jorgensen J, et al. Association of transcarotid artery revascularization vs transfemoral carotid artery stenting with stroke or death among pa tients with carotid artery stenosis. JAMA. 2019;322(23):2313-2322. doi:10.1001/
JAMA.2019.18441
9. Medicare National Coverage Determinations Manual Chapter 1, Part 1 (Sections 10-80.12). Centers for Medicare and Medicaid Services. Published September 8, 2021. Accessed August 7, 2022. https://www.cms.gov/Regulations-and-Guidance/Guidance/Manuals/Downloads/ ncd103c1_Part1.pdf
10. Schermerhorn ML, Liang P, Dakour-Aridi H, et al. In-hospital outcomes of transcarotid artery revascularization and carotid endarterectomy in the Society for Vascular Surgery Vascular Quality Initiative. J Vasc Surg. 2020;71(1):87-95. doi:10.1016/J.JVS.2018.11.029
11. Müller MD, Lyrer P, Brown MM, Bonati LH. Carotid artery stenting versus endarterectomy for treatment of carotid artery stenosis. Cochrane Database Syst Rev. 2020;2(2):CD000515. doi:10.1002/14651858.CD000515.PUB5
12. Paraskevas KI, Mikhailidis DP, Veith FJ. Mechanisms to explain the poor results of carotid artery stenting (CAS) in symptomatic patients to date and options to improve CAS outcomes. J Vasc Surg. 2010;52(5):1367-1375. doi:10.1016/J.JVS.2010.04.019
13. Morr S, Vakharia K, Fanous AA, Waqas M, Siddiqui AH. Utility of intravascular ultrasound during carotid angioplasty and stenting with proximal protection. Cureus. 2019;11(6):e4935.
doi:10.7759/CUREUS.4935
14. SVS VQI TransCarotid Revascularization Surveillance Project. ClinicalTrials.gov. Published March 4, 2021. Accessed August 15, 2022. https://clinicaltrials.gov/ct2/show/NCT02850588
15. Naazie IN, Cui CL, Osaghae I, Murad MH, Schermerhorn M, Malas MB. A systematic review and meta-analysis of transcarotid artery revascularization with dynamic flow reversal versus transfemoral carotid artery stenting and carotid endarterectomy. Ann Vasc Surg. 2020;69:426 -436. doi:10.1016/J.AVSG.2020.05.070
16. Galyfos GC, Tsoutsas I, Konstantopoulos T, et al. Early and late outcomes after transcarotid revascularisation for internal carotid artery stenosis: A systematic review and meta-analysis. Eur J Vasc Endovasc Surg. 2021;61(5):725-738. doi:10.1016/J.EJVS.2021.01.039
17. Gao J, Chen Z, Kou L, Zhang H, Yang Y. The efficacy of transcarotid artery revascularization with flow reversal system compared to carotid endarterectomy: A systematic review and metaanalysis. Front Cardiovasc Med. 2021;8:695295. doi:10.3389/FCVM.2021.695295
ASSESSMENT OF MALPERFUSION SYNDROME IN AORTIC DISSECTION: DEFINING AN AORTIC DISSECTION LAB PANEL
Author: Edward Ranzenbach, DMSc, PA-C, CAQ-CVTS, FAPACVS, DFAAPA Assistant Professor - Director of Clinical EducationalPfeiffer
University PA ProgramAlbemarle, NC
Aortic dissection (AD) is a devastating disease process in which the intimal wall of the aorta tears, resulting in a false channel to which blood can enter. As blood enters this false channel, the dissection of the tunica intima away from the tunica media continues to grow, compressing and limiting the flow of blood through smaller arterial branches and possibly even shearing some of them off.
The rate of mortality from AD has been found to be as high as 45% and one of the biggest factors in predicting that mortality is the presence of malperfusion syndrome. In this article we examine the effects of malperfusion syndrome on survivability and the utilization of various laboratory investigations in determining the severity of malperfusion syndrome. The goal of this article is to establish a standard aortic dissection lab panel that should be drawn on every patient suspected of having an AD as soon as they present for diagnosis and treatment in an attempt to provide the cardiothoracic and vascular surgeon with the information necessary to plan the required type and timing of repair.
The aorta arises from the heart and is the conduit for circulation throughout the body. The gateway to the aorta is the aortic valve. The aortic valve is located within the ventricular outflow tract, at the root of the base of the left ventricle. From proximal to distal, the aorta gives
rise to major branches which provide circulation to the left and right main coronary artery, the innominate artery, at the beginning of the proximal arch, which then bifurcates into the right common carotid and the right axillary artery, the left common carotid artery, and the left subclavian artery. From there, the descending trunk of the artery provides branches supplying the vertebral column, the mesentery and abdominal organs, liver, and the renal arteries supplying both kidneys, before branching into the right and left iliac arteries to supply the lower limbs.
The aorta is composed of three layers, the outer layer being the tunica externa. The middle layer is a muscular layer, the tunica media, and provides the artery with the ability to expand and contract to assist in regulation of perfusion throughout the body. The innermost layer of the artery is the tunica intima (see Figure 1).
Aortic dissection occurs when the tunica intima is damaged. This tear in the thin intimal wall of the aorta allows blood to forcefully separate the tunica intima from the tunica media, creating a false lumen or channel. As the false lumen continues to grow, it can compress the true lumen and obstruct flow to branches supplying blood to the organs downstream. Aortic dissection can even shear off smaller arterial takeoffs as well. The end result is decreased perfusion to the tissues supplied by the involved arterial branches.
The incidence of aortic dissection has been estimated to be 4.4 per 100 000 person-years for those age 18 and older. The incidence is almost twice as common for men than women (10.2 versus 5.7 per 100 000 person-years) and increases with age.2 Stanford Type A dissection, involving the ascending aorta as it leaves the heart, is 1.4 times as common as Type B dissection which is defined as dissection originating distal to the takeoff of the left subclavian artery.2 This means that there are approximately 11,000 aortic dissections annually in the United States, approximately 6,400 of those being Stanford Type A.
Seventy-five percent of aortic dissections occur in patients 40 to 70 years of age with the majority occurring between the ages of 50 to 65. Risk factors that predispose one to aortic dissection include hypertension, genetic conditions including Marfan’s syndrome, Ehlers–Danlos syndrome, Turner syndrome, family history, aortic instrumentation during surgery or other invasive procedures, trauma, and inflammatory or infectious diseases that cause vasculitis. Aortic dissection is also a common complication of those congenitally born with a bicuspid aortic valve. This represents about 5% of the population. The bicuspid valve interferes with the laminal flow of blood through the aortic valve and the wall of the ascending aorta can become aneurysmal over time, eventually leading to disruption of the intima and aortic dissection. Use of certain sympathomimetic drugs, such as cocaine or methamphetamines can also lead to aortic dissection and smoking is risk factor as well., One study has demonstrated the incidence of aortic dissection to be between 5.2 and 12.4 cases per hundred thousand people per year, depending on the type of hospital where the patient presents. In another study, 16.7% of aortic dissections were missed in the emergency room, 25% were missed in the first 24 hours after presentation. Khan, and Nair noted that, clinically, pulse deficit was seen in 38% of those presenting with AD. Lower extremity ischemia was 15 – 20%, and neurological deficits in patients with AD have been found to be as high as 18 to 30%.10
Aortic dissections are classified based on the origin of the tear and the extent of the false lumen. In Stanford Type A aortic dissection, the tear originates proximal to the takeoff of the left subclavian artery. The dissection and false lumen may extend retrograde toward the base of the heart, and involve the left and/or right main coronary arteries or the aortic valve, or antegrade downstream. In Stanford type B aortic dissection, the tear, originates distal to the subclavian artery takeoff. The dissection, and false lumen, are constrained and remain distal to the subclavian artery takeoff (see Figure 2).
While surgical intervention for Stanford type B (TBAD) dissections is often delayed, and there are good endovascular treatment options available, Stanford Type A dissections (TAAD) represent an immediate life-threatening surgical emergency. The mortality for TAAD can be as high as 50% in the first 48 hours.2
Aortic dissection can have profound implications for perfusion of multiple organ systems
in the body. As the dissection proceeds antegrade or retrograde from the tear, perforating vessels that supply perfusion to the myocardium, the brain, the spinal cord, the abdominal organs, the liver and kidneys specifically, and the extremities, can all be obstructed or even sheared off leading to ischemic conditions within these organs.
For TAAD, conventional wisdom requires immediate surgical intervention to repair or replace the ascending aorta and redirect blood flow back to critical organ systems downstream. More recent evidence suggests however that those with malperfusion syndrome (MPS), caused by TAAD, suffer significantly higher rates of mortality than those without. Kawahito, and colleagues showed as much as a 5-fold mortality for any malperfusion and the more systems involved, the higher the mortality.
In a landmark and foundational paper from 1997, Deeb, et al. noted that those with MPS suffered a 22% intraoperative mortality, and an 89% in-hospital mortality. They proposed a controversial new approach to TAAD in which they delayed emergency central aortic surgical repair, opting to first attempt percutaneous reperfusion of the malperfused organs, in hopes of better overall survivability. In 2008, Patel and colleagues presented a follow-up long-term analysis of their colleagues Deeb, et al’s results showing that if you survive MPS in the initial phase, your long-term survival rivals that of patients with TAAD sans MPS. Crawford, et al. has shown that MPS occurs in 25 to 30% of TAAD.
Since the initial proposal by Deep and colleagues, other institutions and surgical groups have investigated this approach and found it to be valid., That said, the criteria for determining malperfusion is not well established. Various institutions have defined their own classification.
As an example, in 2015 the “Penn Classification” defined four major classifications:
Classification
Aa Absence of branch vessel malperfusion or circulatory collapse
Ab Branch vessel malperfusion with ischemia
Ac Circulatory collapse with or without cardiac involvement
Abc Both branch vessel malperfusion and circulatory collapse
The Penn classification also noted that any ischemia raises the mortality to 24%. The definitions used in the Penn Classification has led to some confusion about what criteria is used to determine malperfusion in TAAD.
In 2018, Ghoreishi, et al. created a novel risk score to attempt to predict operative mortality based upon values of the patient’s creatinine, lactic acid, and whether or not they had elevated liver enzymes, but even this falls somewhat short, as it fails to address perfusion of the brain, myocardium, and extremities. Indeed, depending upon the surgeon, malperfusion is assessed by clinical exam, by imaging, by laboratory work, or by a combination of any and all of these methods. There is no one codified approach to completely assessing the body systems and their malperfusion.
Life is supported and maintained by several key, critical organ systems within the body. While as an isolated event, some of these systems can be surgically repaired and the loss others can be extrinsically compensated for (i.e. hemodialysis for renal failure), acute ischemic failure of one or more of these systems in a patient with an aortic dissection requiring immediate surgical repair can lead to almost certain mortality. We will examine each of these critical systems, their preoperative assessment using clinical exam, laboratory investigations, and imaging. We will also explore their perioperative risk with respect to mortality.
There is no other organ system in the body that is more susceptible to hypoxia than the brain. Preoperative acute cerebrovascular accident (CVA), or stroke, is typically embolic or ischemic (secondary to compromised blood flow) in the setting of AD. Patients have presented with neurological symptoms, however, and have been found, incidentally, to have AD.
Conversion to Hemorrhagic Stroke. Okada, et al, notes that 41% of embolic cerebral strokes will convert to hemorrhagic strokes at a median of 20 days post original event (range 3 –47). The conversion rate was found to be higher in those 70 years-old and above (51%), and with the size of the infarct (moderate to large ~51%) similarly influencing the conversion rate as well.21 Although the incidence of conversion was not affected by thrombolytic or anticoagulant therapy, in cases where hemorrhagic conversion (HC) occurred, and those modalities were applied, the resulting hematoma was massive.
In a more recent study, Hong and colleagues note that HC is rare within the first six hours and usually occurs within the first four days. If treated with thrombolysis or thrombectomy however, it occurs usually within the first 24 hours after the initial CVA.22 They also note that patients with an acute embolic CVA are at risk for additional ischemia, especially in situations where they are hypotensive. The use of anti-hypertensive agents to keep the patient normal to hypotensive is a frequent initial treatment strategy to prevent further aortic dissection or rupture while the patient is awaiting availability of surgical intervention.
Repair of a TAAD utilizing extracorporeal bypass and deep hypothermic arrest requires the patient to be systemically heparinized with tens of thousands of units of heparin given. Because of these issues, surgeons have classically considered stroke to be an independent mortality predictor in TAAD and in many cases surgeons have demurred or consigned patients to medical treatment and the eventual mortality that that confers.
Cerebral Malperfusion and Immediate Surgical Repair. Jensen and Chen, in their recent work, note that patients undergoing surgical repair of their TAAD with pre-operative cerebral malperfusion (CMP) have double the in-house mortality (25.7% versus 12%, p < 0.001)
than those who present as neurologically intact. At one year post-operatively, their survival is 62.6% versus 81.3% (p >0.001), respectively.23 That said, they propose that the vast majority of patients who present with TAAD and neurological symptoms, and even coma, are appropriate for immediate surgical intervention. They review studies from a number of authors who have taken patients with significant neurological impairment to surgery with remarkable rates of survival and resolution of their neuro- deficits. In one such study, Tsukube, et al, took 24 patients with a Glascow Coma Score (GCS) of 6.5 ± 2.4, indicating coma, for immediate surgical repair. Of those patients, the mean age was 71 ± 11 years. Of this group, 79% of patients had recovery of consciousness and 50% went on to achieve a modified Rankin Score of 3, indicating the patient has moderate disability; requiring some external help but able to walk without the assistance of another individual. The cumulative survival rate of these patients was 48.2% after 10 years.25
Jensen and Chen propose an assessment and treatment strategy for patients with cerebral malperfusion (CMP).23 In general, only those patients who have been in a coma for greater than six hours, or who have intracranial hemorrhage demonstrated on their head CT, should undergo delayed or deferred surgical repair.23 They do acknowledge a study by Fukuhara, et al that demonstrated that the presence of internal carotid artery (ICA) occlusion was an absolute harbinger of mortality secondary to cerebral edema and herniation syndrome. By contrast, 79% of those patients with unilateral or even bilateral common carotid artery occlusion, but no ICA occlusion, survived to hospital discharge (p < .001).27 In such cases where CMP is suggested, Jensen and Chen recommend the surgeon consider dedicated angiography of the head and neck vessels but warn that the time necessary to obtain such studies must be weighed against the possible delay of immediate surgical intervention.
As the focus of this paper is to establish a standard set of laboratory studies for all patients presenting with possible aortic dissection, we look to the brain for such markers of injury. In 1985, Nordby and Urdal noted the presence of fractionated creatinine kinase, type BB (CK-BB) in the blood of patients that had recent contusion of the brain. More recently, Carr, and colleagues examined CK-BB as a marker for soldiers who had experienced mild traumatic brain injury. While their study failed to show results significant enough to support the use of
this marker in making the diagnosis, the low number of subjects in the study indicates the need for more research in this area. Elevated levels of CK-BB have been found in patients with certain breast tumors and other malignancies,, so the presence of CK-BB in the blood is not necessarily pathognomonic for cerebral malperfusion syndrome.
While physical assessment and imaging will remain the primary modalities for assessment of neurological status in patients with TAAD, this author suggests that including creatinine kinase BB in a standard lab panel for this patient population adds no risk and presents an area of possible research that could benefit these patients in the future.
Aortic dissection can extend retrograde into the left and/or right main coronary arteries, causing an insufficient blood flow to the myocardium resulting in ischemia and infarction. Acute myocardial infarction in AD has been reported to be from 5.7 to 11.3%.
When considering the role of the heart in AD, primary evaluation is concerned with two specific goals:
(1) determining if the patient has a myocardial infarction, which could impact the surgical approach necessary to correct the aortic dissection by re-establishing normal coronary artery blood flow, and
(2) determining if the heart itself is viable and will allow the patient to be weaned from extracorporeal bypass and survive the surgery.
Typically, patients undergoing emergent repair for TAAD undergo trans-esophageal echocardiography (TEE). The TEE probe is inserted, and the patient is imaged, prior to the incision, and the ascending aorta is evaluated for the presence of a flap and false lumen. This allows the surgeon to determine what portions of the aorta are involved, what cannulation strategy will be possible, and the need for deep hypothermic cardiac arrest. Additionally, the function of the heart is assessed including aortic insufficiency, which is associated with retrograde dissection into the root. Also assessed, are wall motion abnormalities in the ejection fraction of the left ventricle can be calculated as well. This imaging is key to understanding the viability of the myocardium and how it will impact the patient’s ability to survive surgery.
By now, it is well-established that cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are the gold standard tests for determining myocardial damage. At least one of these tests is readily available at all hospitals and cTnT levels > 0.1 μg/L and cTnI levels of > 0.1 to 2 μg/L (accounting for local laboratory variants in the assay) are indicators of myocardial damage.
Boden, et al, examined the size of infarct and outcomes based on cTnT levels. They reported a 6.4% mortality at 1 year with levels averaging just 3.15 μg/L (1.21 to 7.22 ).34 Small positive values indicate minor myocardial damage. That said, there are numerous conditions that can elicit a troponin leak including end-stage renal disease, acute heart failure exacerbation, pulmonary embolism, stroke, and sepsis, among others, and in TAAD itself. Vrsalovic demonstrated that 26.8% of TAAD patients were significantly associated with increased risk of short-term mortality (OR 2.57; 95% CI 1.66–3.96). Larger values (40 – 50 μg/liter) can indicate substantial myocardial infarction and very-large values (>140 μg/liter) would indicate a severely damaged organ in which the viability is questionable. Either of these labs should be included in the AD lab panel.
Visceral ischemia occurring in TBAD is as high as 25%, with in-hospital mortality as high as 11%.16 The operative mortality for patients with TAAD and visceral ischemia is reported as high as 43%.16 Moreover, a dissection that extends into the celiac trunk or the superior or inferior mesenteric arteries may not be totally relieved with reestablishment of flow through the true lumen of the dissected aorta. Thus, dissection involving these arteries may need to be addressed independently, and possibly preceding surgical correction of aortic dissection.
Abdominal Pain. Ohle, et al, note that abdominal pain had a 28.4% sensitivity and 88.4% specificity for AD.9 Thus, the presence of abdominal pain, in and of itself, is not a reliable indicator for AD. Moreover, abdominal pain in and of itself does not denote visceral ischemia. Diagnosis of visceral ischemia would be aided by the presence of elevated liver function tests (LFTs) and lactic acidosis.
Acidosis as an Indicator of Mortality. Overall acidosis and calculation of a base
deficit is available through arterial blood gasses (ABGs), and one study has shown that 92% of patients with a base deficit of ≥ 10 in the presence of abdominal malperfusion perished. The value of lactate levels in visceral malperfusion is somewhat less definitive. In their work on ischemic colitis after cardiac surgery, Arif and colleagues note that although high blood lactate is a frequent finding, it cannot be used to effect early detection of ischemic colitis. This would seem to be supported by Studer, and colleagues, who found that elevated lactate values measured within 24 hours before surgery for ischemic bowel demonstrated a moderate correlation, but no statistical significance with the length of bowel necrosis (r2=0.257, p=0.058). That said, the study by Studer, and colleagues, had an in-hospital mortality rate of 42.9% with the nonsurvivors having a statistically significant higher lactate level than those who survived (5.6±4.8 vs. 3.0±2.2 mmol/L, p=0.024).40 We would postulate that lactate levels are an important part of a comprehensive laboratory investigation and should be viewed in the context of other complimentary lab values and the patient’s overall clinical picture.
Although it is an abdominal organ, liver failure in cardiac surgery has been shown to have its own impact on mortality, and we consider it individually.
The rate of liver failure post cardiac surgery is relatively low but, when present, the mortality exceeds 60%. Pre-existing liver failure would obviously not bode well for the patient’ s survival in AD. Even with novel extracorporeal blood purification treatments, the death rate remains 23% at 30 days.41 Although elevated LFTs in and of themselves have only been shown to be 15% sensitive, they have been shown to be 90.6% specific for a diagnosis of AD.9 Liver failure is easily detected as part of a comprehensive metabolic panel, that can be drawn at any hospital and the results should be available to the surgeon prior to incision.
Patients with acute kidney injury (AKI) have a five-fold risk of death following cardiac surgery, and AKI requiring the use of continuous renal replacement therapy (CRRT) has been associated with a 50% post-operative mortality. Bhavsar, et al, have shown that a creatinine
kinase level of 1,250 U/L or more was 93.3% predictive of subsequent acute renal failure secondary to rhabdomyolysis. Thus, knowing the patient’s renal history and testing their renal function pre-aortic dissection repair for acute changes is key to understanding their postoperative course. A renal panel is part of a comprehensive metabolic panel is required as part of a comprehensive workup for any patient suspected of having AD. Unfortunately, serum creatinine elevations can lag behind acute kidney injury (AKI) by as much as 24 to 48 hours. Moreover, a dissection leaving one kidney malperfused and the other healthy and functioning, may not evoke a significant creatine rise. There are newer technologies (i.e nephro-check) on the horizon that will be able to detect AKI much sooner and as these become available their incorporation into this evaluation should be considered. Finally, an elevated creatinine kinase level would indicate possible renal failure secondary to rhabdomyolysis and should be tested as well. These results should be available to the surgeon prior to incision.
One of the key diagnostic indicators of AD is pulse deficit. Acute differences in blood pressure readings in the upper extremities or lower extremities, or complete lack of pulses in an extremity was found by Ohle, et al to have 20.6% sensitivity and 99.3 specificity for the diagnosis of AD.9 In a systematic review, Gargiulo, et al showed that lower extremity malperfusion occurs in up to 40% of TBAD and is seen in up to 71% of TBAD with associated malperfusion syndrome. The 30-day mortality in these cases was high and 97% of these patients developed lower limb complications.46 Lower limb malperfusion was the only clinically detected malperfusion in 52% of patients presenting with TBAD, and it was associated with renal malperfusion 40% of the time and visceral malperfusion 25% of the time. 46 An elevated plasma creatinine kinase has been associated with a 56% need for limb amputation and is a good indicator of significant lower limb ischemia. This would be a devastating complication to a patient that already has a high risk of mortality from aortic dissection. Moreover, elevated creatinine kinase is an indicator of rhabdomyolysis, and is a precursor to renal failure.
In addition to the laboratory investigations mentioned so far, we would be remiss not to discuss others that, while not indicative of malperfusion syndrome, can be diagnostic of AD, or will aid in its surgical treatment.
Profound anemia in AD is a morbid sign and can indicate rupture, either contained or uncontained.
A prothrombin time (PT) and partial thromboplastin time (PTT) are part of the standard workup for any patient going to cardiac surgery. A fibrinogen level could also be of use if there is suspicion of massive or slow, long-term hemorrhage. Other indicators of platelet function should also be considered if patient’s home regimen includes platelet inhibitors.
While any patient going to cardiac surgery needs to be typed, screened, and crossmatched for blood, this need is especially true for AD. Guan, and colleages, in their paper exploring hemostatic disturbances in patients undergoing AD surgery demonstrate the need not only for red cells, but fresh frozen plasma and platelets as well, with inter-operative blood losses averaging 1.4 L, and 2.2 L postoperatively.
d-dimer and C-Reactive Protein
The presence of thrombus, which forms in the false lumen in an aortic dissection, will lead to the activation of the intrinsic and extrinsic clotting cascade. Part of this reaction produces fibrinolysis resulting in the production of d-dimer, a degradation product of cross-linked fibrin. Ohle, et al, showed that a d-dimer of > 500 ng/dL was 96.7% sensitive and 71.7% specific for diagnosis of AD.9
C-reactive protein (CRP) is a nonspecific indicator of inflammation produced by the liver, and is frequently elevated in AD.
Wen, et al, examined the levels of d-dimer and CRP in patients with AD, specifically with respect to measured levels and their survival. There were 114 patients included in their study of
which 83 survived (27% mortality).50 All the subjects in their study had normal preoperative hepatic and renal function. Those patients that survived had a d-dimer of 4.28 µg/ml ± 1.99 while the d-dimer in those who died was 9.84 µg/ml ± 3.53 (P < 0.001).50 The surviving patients had a CRP of 11.18 mg/L ± 1.85 while those who succumbed to their AD had a CRP of 14.08 mg/ L ± 2.8 (P < 0.001). 50 While this is a single center experience, the preoperative predictive value of d-dimer and CRP should not be underestimated.
Based upon the above discussion, the author suggests that the following lab panel be drawn on any patient presenting with acute onset pain described as tearing sensation, chest or back pain with neuro- symptoms, acute abdomen, or signs of malperfusion in an extremity (i.e. swelling, mottling, cold to the touch, lack of distal pulses, deconjugate blood pressures), undergo the following labs, in addition to CT angiography of the chest abdomen and pelvis:
• Complete Blood Count (CBC)
• Comprehensive Metabolic Panel (CMP)
• Arterial Blood Gas (ABG)
• Lactic Acid (lactate)
• Creatinine Kinase (CK) with MB, BB, and MM fractions
• Troponin
• d-dimer
• C-Reactive Protein (CRP)
• Prothrombin Time (PT) with International Normalized Ratio (PT/INR)
• Partial Thromboplastin Time (PTT)
• Fibrinogen
• Type and Screen
• Crossmatch for six units of packed red cells
The values in the table above represent an aggregate of critical MPS values, and the associated mortalities that have been documented.
The proposed laboratory investigations should be organized into a standard panel designated the “aortic dissection panel,” and should be ordered STAT. Additionally, three units of fresh frozen plasma, two units of platelets, and two cryoprecipitate should also be reserved for this patient until a decision to proceed with surgery has been made.
As previously mentioned, Ghoreishi, et al, have proposed a novel mortality risk score for TAAD.20 This score, as presented in Table 3, is based on the lactic acid level, the creatinine, and whether or not there is liver failure:
Our analysis is that this score presents an incomplete picture and, although it is predictive of mortality risk, there are additional factors that should be considered. We would suggest that a multicenter study, utilizing the data points from the proposed standardized lab panel could be used to further refine this equation. This is an area that we would recommend for additional study.
Acute aortic dissection is a devastating disease with extremely high potential for mortality and morbidity. The presence of malperfusion syndrome can significantly increase the patient’ s risk and in some cases can predict the inability to prevent mortality even with surgical repair.
The hallmark of assessing malperfusion syndrome is, and always will remain, a combination of examination, imaging, and laboratory assessment. Laboratory assessment, however, has been shown to have predictive value when determining the patient survivability. The establishment of a standard panel of laboratory investigations that can be ordered and resulted prior to the patient undergoing surgery can provide the surgeon with the necessary tools to plan or modify their approach, or even to forgo a predictively futile attempt to save the patient’s life by surgical intervention.
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