Introduction
MIVS gained popularity due to its rapid progress and nowadays preferred over full thoracotomy because of its more favorable outcomes in terms of post-surgery complications in native
and redo cases [1]. However, MIVS might come with an increased risk for phrenic nerve palsy, stroke, or IAD. IAD is a very
rare and severe complication, with an incidence of` only 0.15%
during or after non-aortic surgery and high mortality between
30-50% [2]. So far, only cases of IAD after Minimally Invasive
Aortic Valve Surgery and Right Atrial Cryoablation during port
access have been discussed [3]. And presenting our experience
of an IAD during MIMVS, will bring more light to surgeons to
better manage these cases as this procedure is innovative and
little is known about how to manage IAD.
Patient’s information
A 61-year-old woman, with no pre-existing medical conditions, was admitted to our hospital with effort intolerance;
shortness of breath during physical activity for about 2 weeks.
Examination
Auscultation showed normal vesicular breath sounds and a
pan-systolic murmur (3/6) at the apex, radiating to the left axilla, left lung base, with a mid-systolic click. Normal jugular vein
pressure and no pedal edema were noted.
Table 1: Examination findings on admission.
Blood pressure |
117/64 mmHg |
Arterial pO2 |
76mmHg |
ECG |
Mild left ventricular
hypertrophy
(Sokolow-Lyon-Index 4,6mV)
Sinus rhythm (82 bpm)
|
TTE |
Mild displacement of the
mitral leaflets (P1) into
the left atrium during
systole, slight leaflet
thickness and stiffness. EF=72%
LA=30mm, LV =42mm, IVS =
10mm
|
Doppler color flow imaging
|
Mitral valve orifice area =
7.9 cm Tricuspid valve
pressure gradient = 21 mmHg
mild pulmonary regurgitation
|
Sonography of vessels |
Carotid artery (7mm),
jugular vein (8 mm) and
femoral artery (7.2 mm) and
vein (7.9 mm) were without
pathological findings.
|
Thoracic Contrast Tomography
(CT) scan
|
Mild calcification of aortic
wall Pleura slightly
thickened
|
Coronary CT scan |
Mild stenosis (about 10%) of
the proximal RCA
|
Brain CT scan |
Small focal infarction in
the basal ganglia region
Mild cerebral atrophy
|
Lung function |
FEVI = 2.1L MVV= 81 L/min
|
Diagnosis
Investigations were done, (as shown in Table 1). It was determined to be primary MR due to a posterior mitral valve prolapse. Mitral valve repair is mostly selected over mitral valve
replacement in primary MR. As symptomatic patients have
poor long-term prognosis, early surgical intervention in highthroughput centers with good expectable outcomes should be
targeted.
Surgical management
Post general anesthesia, a Central Venous Catheter (CVC, Arrow International Inc. Pennsylvania, 19605, USA) and a guidewire for later Superior Vena Cava (SVC) cannulation into the
inner jugular vein were placed. Afterwards, we made a 2-cm
incision at the right groin to prepare the femoral vessels. After heparinisation and sufficient Activated Clotting Time (ACT),
Cardiopulmonary Bypass (CPB) was installed by cannulating the
femoral vessels and SVC via jugular vein and connected them to
the heart-lung machine. The operation was carried out under
constant TEE control. Invasive blood pressure monitoring was
installed in the right radial artery and rectal temperature was
followed.
Whilst still creating the endoscopic access, we asked the Perfusionist to run simultaneously the CPB and decrease the body
temperature in order to continue the surgery without disturbance.
The surgical field was exposed using the anterolateral port
access approach in the proximal axillary line of the 4th right intercostal space [4]. Subsequently, the thoracic endoscope was
inserted; a slight adhesion of the pleural leaflets was detached,
exposing the surgical field. A hematoma was observed in ascending aorta (Figure 2A). The Anaesthesiologist noted a drop
in BP, pulse, a spike in CVP. TEE confirmed the hematoma in ascending aorta and diagnosis of a type a acute Aortic Dissection
was made (Figure 2B).
Immediately, a shift to full median sternotomy was performed. Suspecting the dissection might originate from falselumen cannulation of the femoral artery, we immediately
stopped the CPB. The heart rate decreased considerably but
not fully stopped.
Post-thoracotomy, a thinned aortic wall with intermural hematoma was conspicuously seen, confirming IAD. Ventricular
fibrillation was noted.
Worsening of the situation; an impending asystole, hypothermia and lack of time, we urgently needed an alternative circulation. As a retrograde dissection caused by the tip of the cannula
was suspected, peripheral femoral cannulation was aborted in
favor of direct ascending aortic cannulation for a new CPB (Figure 2C). Axillary cannulation was not also preferred due to the
emergency. RCA involvement was ruled out.
Histidine-Tryptophan-Ketoglutarate (HTK) solution (Custodiol; Dr. Franz Kohler, Chemie GmbH, Bensheim, Germany) was
administered into both coronary sinuses for myocardial protection. Once reconstitution of body perfusion attained, Deep Hypothermic Circulatory Arrest (DHCA) was induced. No intimal
damage or entry site was visible in the ascending aorta and
aortic arch. We implanted an elephant stent-graft (MicroPort
Medical Co, Ltd, Shanghai, China) into the true lumen of the
aortic arch and the proximal part of the descending aorta. After inflation of the stent-graft, we fenestrated the part covering
the three arch branches by an island anastomosis with interrupted 2-0 prolene suture, fixing the branches to the window
of the stent. To elongate the proximal end of the stent-graft, we
sewed an artificial vessel to the attached vascular graft, gaining
space for the cannula insertion. In the next step, we clamped
the artificial vessel and cannulated the descending aorta via the
artificial vessel. We reinforced the proximal end through vascular patches and wrapped the artificial vessel with a slice of the
autologous pericardium. After 19 minutes of DHCA, we reconstituted the body perfusion and started to increase the temperature slowly; this gave us time to reinforce the aortic root using
a modified sandwich technique, as described by Tang et al [5].
Lastly, we connected the aortic root to the artificial vessel to
complete the aortic repair. (Figure 2D). A shunt was established
between the artificial chamber and the right atrium via an endto-side anastomosis with an artificial blood vessel. After stabilizing the vitals, we opened the left atrium, exposing the mitral
valve apparatus. The mitral valve was slightly thickened, with
ruptured P1, P2 papillary muscles and mitral prolapse. Standard
mitral valve repair employing the “Loop in Loop” technique was
performed (Figure 2E). When the water probe indicated a satisfying closure and no significant regurgitation, we implanted
a #28 mitral annulus (Medtronic® semi-rigid band) (Figure 2F).
After the air exclusion with the head-down position, the atrial
septum incision was closed. The heart started to beat again after an external 200 Joules defibrillation. Blood was returned to
the patient and she was finally weaned off the CPB. Total CPB
time was 280 minutes, aortic cross-clamp time was 115 minutes. Three drainage tubes were inserted followed by chest closure. The patient was transferred to the ICU.
Post-surgical management
The same night; a re-thoracotomy was performed for hemostasis, requiring massive blood transfusion.
Patient’s ICU stay was 17 days. Total intubation time was 3
days, with Bi-Level Positive Airway Pressure (BIPAP) assistance
for another 6 days and double channel oxygen for 8 days. Furthermore, CT scan, X-ray, transthoracic echocardiography and
blood gas analysis were routinely performed.
Follow-up and Outcomes
The patient’s recovery was good. TEE showed normal EF of
LV (55%). Day 32 post-operative, the patient was discharged in
stable condition. One, three, six months of postoperative examinations were normal.
Discussion
Preoperatively, the typical risk factors for AD were not found.
Sonographic evaluation of femoral and jugular vessels did not
show pathological findings. However, pre-operative assessment
of aortic wall by angiography was not done, as no history of
peripheral vascular disease was reported and examination results were normal. We assumed a retrograde dissection from
femoral cannulation. The cannula tip might have hurt the intima
layer of the fragile aortic arch, inducing a Stanford type A aortic
dissection. The most common entry site for IAD in non-aortic
cardiac surgery is the abdominal aorta [6,7].
Dissection can be identified as follows: Blue discoloration
and expansion of the ascending aorta, intractable bleeding
from aortic sites, and high perfusion line pressures with associated systemic hypotension. In our case, we started the CPB at a
point under TEE surveillance; however, we had not yet obtained
visual control of the surgical field. IAD was confirmed at the moment both by TEE and the naked eye. Although coming with an
increased risk for unobserved AD allows the induction of hypothermia while still establishing the surgical field, this practice is
timesaving. A delayed induction of hypothermia after complete
set up would require the entire team to wait for an additional
10-15 minutes. By starting CPB before pericardiotomy and soon
after thoracotomy, minimally invasive cardiac surgery becomes
feasible in patients unable to bear unilateral lung ventilation
[8]. We suggested that CPB is started only when the surgical
field and TEE monitoring are already seen at the same time to
minimize the risk of IAD.
Once IAD is confirmed, the surgeon discontinued the CPB immediately and secure an alternative peripheral site of cannulation. This ensures that the blood flow is through the true aortic
lumen. We described direct aortic cannulation as an emergency
method to reconstitute bridging perfusion under a very urgent
situation of low blood pressure.
To maintain an adequate perfusion pressure, we directly
cannulated the ascending aorta after probing for the true lumen and assessing the intimal condition, similar to the “Samurai” cannulation method proposed by Kitamura et al. However
under different circumstances [9].
Conclusion
To summarize; close attention, discovery on time, effective
treatment is required in a modern minimally invasive surgery
team. Regarding the effective management of IAD, the surgeon’s experience, degree of specialization, and ability are decisive.
Abbreviations: MIVS: Minimally Invasive Valve Surgery; IAD:
Iatrogenic Aortic Dissection; MIMVS: Minimally Invasive Mitral
Valve Surgery; TEE: Trans-Esophageal Echocardiography; MR:
Mitral Regurgitation; ACT: Activated clotting time; CPB: Cardiopulmonary bypass; RCA: Right Coronary Artery.
Declarations
Ethics Statement and Informed Consent: The written consent of the patient was taken for the publication of any potential images or data published in this article.
Authors Contribution: All the authors have contributed
equally in writing this article.
Conflict of interest: No conflicts of interest relevant.
Supplementary Material: The Supplementary Material for
this article can be found online.
Acknowledgements: We are grateful to Dr Wajeehullahi Akilu from Tongji Medical College for language editing and revising
this manuscript.
Disclosures: There are no relationships with industry.
References
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