Keywords
aorta - dissection - acute - bleeding
Introduction
In spite of improvement of surgical treatment, Type-A acute aortic dissection (AAAD)
is so far associated with relatively high mortality. Low incidence and diversity of
clinical manifestations of AAAD sometimes lead to wrong diagnosis. Coagulopathy developing
in the settings of the main disease[1] is significantly compromised by unreasonably administered antiaggregants and anticoagulants
that leads inevitably to the increase of risk of perioperative bleeding as one of
the most dangerous life-threatening complications.[2]
[3] Surgical aggression, malperfusion syndrome, duration of procedure, blood loss, and
many other factors inevitably decrease the patients' survival chances. In this article,
we would like to share our experience of successful treatment of a patient with 18-L
perioperative blood loss in DeBakey Type-I acute aortic dissection with drug-induced
hypocoagulation and malperfusion of a lower extremity.
Case Presentation
A 59-year-old man was urgently hospitalized in September 2017 with complaints of chest
pain, a pain in the left lower extremity and numbness in the left foot. According
to the patient, he had been injected with nonsteroidal anti-inflammatory drugs in
unknown doses by an emergency response physician (it was not documented in referral
medical documents). Computed tomography angiogram of the chest was performed and demonstrated
dilatation of the ascending aorta with DeBakey Type-I dissection and radiological
signs of asymptomatic dissection of the brachiocephalic trunk, left common carotid,
right coronary and left renal arteries, and common iliac and common femoral arteries
on the left side. Echocardiography showed a DeBakey Type-I aortic dissection and dilatation
of ascending aorta to 49-mm, tricuspid aortic valve (AV) with regurgitation ++ + .
Left side of the heart was enlarged with preserved ejection fraction (EF). Triplex
sonography (TS) of the lower extremities' arteries showed absence of blood flow in
the major arteries distal to the left common femoral artery. The electrocardiogram
(ECG) was without any ischemic sings and coronary angiography demonstrated intact
coronary arteries. Laboratory results showed decreased platelet aggregation with adenosine
5′-diphosphate to 31%; creatine kinase was increased to 314 U/L. The patient underwent
a two-stage surgical procedure.
As a first stage, a cross right-to-left femoral-femoral bypass with an Intergard heparin-knitted
10 mm graft, was performed. After the blood flow restarted, pulsation in the major
arteries of the left lower extremity was detected on palpation along the entire length.
The TS of the lower extremity arteries was performed intraoperatively; the blood flow
in the arteries of the right and left lower extremities was satisfactory. By the end
of the first stage, acid-base imbalance in the blood was revealed. The diagnostics
of ischemia-reperfusion injury markers was performed, the creatine phosphokinase level
reached 1,544.70 U/L; the MB fraction was normal. Taking into account the admissible
values of laboratory results and the absence of growth of biochemical markers of tissue
injury, repair of the ascending aorta and aortic arch using the INTERGARD vascular
graft was performed as the second stage. Distal “hemiarch” anastomosis and reimplantation
of the AV into the neoaorta proximally ([Fig. 1]) were performed.[4] The bypass time was 320 minutes, cross-clamp time was 167 minutes, and duration
of circulatory arrest was 29 minutes. After administration of protamine sulfate, persistent
oozing and bleeding was observed at the sites of the vascular implant punctures and
along the suture lines. After prolonged and unsuccessful hemostasis, the modified
Cabrol shunt was performed between the perigraft space to right atrial appendage using
a bovine pericardial patch ([Fig. 2]). The transverse sinus was blocked with local hemostatic materials.
Fig. 1 The reimplanted aortic valve.
Fig. 2 The modified Cabrol shunt between the perigraft space to right atrial appendage using
a bovine pericardial patch.
The total operative time was 8 hours and intraoperative blood loss was 9 L. In the
end of procedure, pericardium, anterior mediastinum, and both pleural cavities were
drained. In the early postoperative period the bleeding was continuing, its correction
required massive transfusion therapy with 6,700 mL of packed red blood cells, 6,600 mL
of fresh frozen plasma, and 600 mL of platelets. Using a cell saver, 5,200 mL of autologous
blood was returned. The total volume of blood loss in first 6 hours after surgery
was 9 L. After intensive conservative therapy, the rate of bleeding decreased from
1,000 to 200 mL per hour. The drainage tubes were removed on day 6. The late postoperative
period was complicated by prolonged (20 days) intubation and renal failure. On day
44 after surgery, the patient was discharged in satisfactory condition. The patient
was followed-up 1 year after surgery: he was active and did not have any complaints,
but he was limping on the left leg. Good AV function and preserved EF of left ventricle
were observed.
Discussion
Early initiation of antiplatelet therapy is definitely recommended to reduce mortality
in patients with acute coronary syndrome (ACS). Unfortunately for aortic surgeons,
ACS cannot always be confirmed by specific ECG changes, which increases the level
of cardiac biomarkers, so one-third of AAAD cases get dual antiplatelet therapy[5]
[6] and a surgeon faces a situation of impossibility of complete hemostasis.
The current guidelines do not contain sufficient information regarding management
of the patients with AAAD in the settings of antiplatelet agent exposure. The drug-induced
platelet dysfunction together with hemodilution, total heparinization, hypothermia,
metabolic acidosis, allogeneic blood product transfusion, malperfusion syndrome, etc.,
significantly compromises consumption coagulopathy.[1]
[2]
[3]
[6]
[7]
Such difficult cases, including those presented here, require high concentration of
medical team to develop an individual multicomponent treatment approach, especially
in blood loss control. Taking into account the fact the manifestation of consumption
coagulopathy occurs in the first hours of acute dissection, it requires an increased
volume of blood components in the perioperative period. So, according to data of Danish
authors,[5] in drug-induced hypocoagulation among patients with acute aortic syndrome, the requirement
of blood components markedly increases. We compared our conventional data on transfusion
supply of patients who underwent surgery for AAAD with data presented by Chemtob et
al.[5] The volume of blood components that we used was several times less. Even though
such surgical techniques as various modification of Cabrol's shunt[8] have significantly improved the control of bleeding they, in our opinion, do not
always guarantee sufficient hemostasis, especially in patients with coagulopathy.
In spite of apparentness of this unsolved problem, centers, and clinics performing
urgent surgeries of aorta will still have to work in complicated conditions of inadequate
supply of materials for coagulopathy control. Although coagulopathy and high rate
of intraoperative mortality are inevitably associated with acute aortic dissection,
the surgery is the only survival chance for a patient.
