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\begin{document}

\title{Acute type A Intramural Hematoma with cerebral ischemia treated with
tPA.}



\author[1]{Megan Wang}%
\author[2]{Shinichiro Ikeda}%
\author[2]{Benjamin Youdelman}%
\author[3]{Elias Wan}%
\affil[1]{SUNY Downstate Medical Center}%
\affil[2]{Maimonides Medical Center}%
\affil[3]{Affiliation not available}%


\vspace{-1em}



  
  \date{May 22, 2024}


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\selectlanguage{english}
\begin{abstract}
A 68-year-old female patient presented to the emergency department with
left-sided weakness. Tissue plasminogen activator (tPA) was started for
stroke, however, the patient was later found to have a type A intramural
hematoma (IMH). TPA was subsequently discontinued. She was
hemodynamically stable and was treated medically due to the risk of
bleeding from tPA. Fortunately, the patient had a complete neurological
recovery. She underwent an aortic repair 6 weeks after initial
presentation and was discharged home without any complications. Aortic
dissection and IMH should always be in the differential diagnosis when
treating patients with signs of cerebral ischemia. This is the first
documented case of accidental administration of tPA in a patient with
intramural hematoma (IMH), and illustrates a successful case of delayed
surgical repair for high risk IMH in patients recovering from cerebral
ischemia.%
\end{abstract}%



\sloppy


\textbf{Introduction}

Patients with acute aortic dissection (AD) and intramural hematoma (IMH)
can present with a variety of symptoms including cerebral ischemic in
addition to classical chest pain. Catastrophic outcomes in AD cases
mistakenly treated with tissue plasminogen activator (tPA) have been
reported {[}1-2{]}. It is crucial to rule out AD/IMH in stroke patients.
Moreover, treatment of type A IMH with stroke is controversial and our
case illustrates success with a delayed surgical repair.

\textbf{Case presentation}

A 68-year-old Chinese female patient presented to the Emergency
Department (ED) 45 minutes after sudden onset of left-sided weakness.
The patient was exercising in the park, then collapsed and was found to
have left-sided weakness and slurred speech. She had a mild headache and
denied all other complaints including chest pain.

Upon arrival to the emergency department, she was afebrile, blood
pressure was 86/62 mmHg, heart rate 61 bpm, respiratory rate 15 bpm and
oxygen saturation 98\% on room air. Electrocardiography showed sinus
rhythm, 62 bpm, with no ST changes or T-wave inversions. Her physical
exam showed left hemiparesis, slurred speech, gaze palsy, homonymous
hemianopsia, and hemisensory loss, with a National Institutes of Health
Stroke Scale of 14. Complete blood count and basic metabolic panel were
within normal limits.

Her past medical history was significant for an abdominal aortic
aneurysm repaired with endovascular aneurysmal repair and thoracic
aortic aneurysm. The ascending aorta was 4.5 cm and proximal descending
aorta was 5.4 cm, confirmed by computed tomography angiogram (CTA) one
week prior to this event. No significant trauma, family, or social
history was reported.

Non-contrast computed tomography (CT) of the head and CTA of the head
and neck were obtained (Fig. 1), which showed possible early ischemic
changes in the right insula and a large vessel occlusion in the right
middle cerebral artery. ASPECT score was 9. Furthermore, a thrombus in
the right internal carotid artery and a possible IMH or atherosclerotic
plaque in the aortic arch was found (Fig.1-A).

Initially, the defect in the aortic arch of the head and neck CT was not
recognized. Neurology deemed her a candidate for intravenous tissue
plasminogen activator (tPA) which was started within one hour of symptom
onset. After starting tPA, the radiologist informed the ED team of a
possible IMH in the aortic arch. Close examination of the head and neck
CTA suggested a possible thrombus in the right internal carotid, common
carotid, and aortic arch (Fig.1-A). Our aortic center team was
consulted. tPA was stopped within 20 minutes (25mg, half of the planned
dose, was given). A chest CTA demonstrated a type A IMH involving the
aortic root, ascending aorta, and aortic arch with a significantly
enlarged ascending aorta (5.1cm), aortic arch (4.7 cm) and proximal
descending aorta (5.4 cm). The patient was hemodynamically stable and
would pose a high risk of bleeding or hemorrhagic conversion from tPA,
so surgery was not performed. She was monitored in the intensive care
unit and her neurological condition improved. A follow-up CT scan showed
a decrease in IMH size from 10 mm to 5 mm (Fig. 2-A, B), and
demonstrated no new aortic dissection or expansion. She was discharged 5
days after the onset of stroke. During a follow-up visit in our
outpatient office, she demonstrated complete neurological recovery. The
ascending aorta, aortic arch and proximal descending aorta were dilated
(5.1 cm, 4.7 cm, and 5.4 cm, respectively). Therefore, a decision was
made to proceed with the planned repair of the aorta 6 weeks after the
initial presentation. We performed total arch replacement with a frozen
elephant trunk under deep hypocirculatory arrest at
18\textsuperscript{o}C using retrograde cerebral perfusion. She suffered
no neurologic injuries postoperatively and was discharged on
post-operative day 6 (Fig. 2-C).

\textbf{Discussion:}

AD and IMH are serious cardiovascular emergencies that classically
present with sudden chest and back pain. However, 15\% of patients
report no significant pain {[}1{]}. Painless AD/IMH can remain
undetected and the diagnosis can be missed upon initial evaluation.
Furthermore, ischemic stroke is prevalent in 6 \% of patients with AD
{[}2{]}.

In order to prevent misdiagnosis of AD/IMH, a patient's medical history
and family history should be screened for aortic pathology and a
thorough physical exam including signs of malperfusion on all
extremities should be performed. D-dimer has a high sensitivity and
specificity (100\% and 94.8\%, respectively) for AD/IMH and can be
measured {[}5{]}. Upper mediastinal widening on chest X ray can be a
sign of AD/IMH. Bedside carotid duplex ultrasound to evaluate for
thrombus or carotid artery dissections should also be considered. CTA
should be performed if there is any suspicion of AD/IMH. Our patient's
head and neck CTA findings, as well as her history of abdominal and
thoracic aortic aneurysm, should have raised the suspicion of aortic
pathology as the cause of her cerebral malperfusion.

Immediate surgical intervention is the gold standard for type A AD and
acceptable outcomes of immediate surgery for type A AD in the setting of
ischemic stroke are reported, but the treatment of type A IMH remains
controversial especially when it is complicated with stroke {[}6{]}.
Surgery for a Type A IMH is recommended for patients with high risk
features defined as total aortic diameter more than 50 mm, hematoma
thickness more than 11 mm, and ulcer-like projections {[}7{]}.~Our
patient's ascending aorta and aortic arch had these risks and if it had
not been for stroke and the administration of tPA, she would have met
criteria for emergent open aortic surgery. TPA significantly increases
the risk of surgical bleeding and operating patients suffering ischemic
stroke have a potential risk of hemorrhagic conversion. Therefore, we
delayed surgery until the patient completely recovered from stroke.

\textbf{Conclusion:}

Given that patients with AD/IMH could present with symptoms of cerebral
ischemia, AD/IMH should always be ruled out before initiating tPA.
Delayed surgery for acute type A IMH recovering from stroke could be an
appropriate treatment strategy.

\textbf{Ethical Approval:}

We did not obtain IRB approval as this is a case report.

\textbf{References:}

1. Hong KS, Park SY, Whang SI, et al. Intravenous recombinant tissue
plasminogen activator thrombolysis in a patient with acute ischemic
stroke secondary to aortic dissection. J Clin Neurol. 2009
Mar;5(1):49-52.

2. Morihara R, Yamashita T, Deguchi K, et al. Successful Delayed Aortic
Surgery for a Patient with Ischemic Stroke Secondary to Aortic
Dissection. Intern Med. 2017 Sep 1;56(17):2343-2346.

3. Mussa FF, Horton JD, Moridzadeh R, et al. Acute Aortic Dissection and
Intramural Hematoma:~A Systematic Review.~\emph{JAMA.}
~2016;316(7):754--763.

4. Gorla R, Erbel R, Kahlert P, et al. Diagnostic role and prognostic
implications of D-dimer in different classes of acute aortic syndromes.
Eur Heart J Acute Cardiovasc Care. 2017 Aug;6(5):379-388.

5. Di Eusanio M, Patel HJ, Nienaber CA, Montgomery DM, et al. Patients
with type A acute aortic dissection presenting with major brain injury:
should we operate on them? J Thorac Cardiovasc Surg. 2013 Mar;145(3
Suppl): S213-21.

6. Estrera AL, Garami Z, Miller CC, et.al. Acute type A aortic
dissection complicated by stroke: can immediate repair be performed
safely? J Thorac Cardiovasc Surg. 2006 Dec;132(6):1404-8.

7. S. Christopher M, Wilson YS., Monika H, et al. 2021 The American
Association for Thoracic Surgery Expert Consensus Document: Surgical
Treatment of Acute Type A Aortic Dissection, J J Thorac Cardiovasc Surg,
2021.

Figure legends:

Figure 1. CT angiography of head and neck with contrast (A) and CT of
the head without contrast (B).

A. Thrombosis in the right internal carotid artery (Red arrow) and
intramural hematoma in the aortic arch (Yellow arrow). B. Initial
concern of large vessel occlusion in the right middle cerebral artery
(Red arrow).

Fig.2. CTA on day 0, day 5, and postoperative image.

A. An initial CTA demonstrated type A intramural hematoma (IMH) in the
ascending aorta just above the aortic root and extending as far as the
transverse arch proximal to the left subclavian artery. The size of the
ascending aorta was 5.1 cm. The distal arch and proximal descending
aorta were dilated to 5.4 cm.

B. A follow-up CTA on day 5 showed the ascending aorta was stable in
size. The size of IMH decreased from 10mm to 5mm.

C. Total arch replacement with frozen elephant trunk and previous
endovascular stent graft for abdominal aortic aneurysm.\selectlanguage{english}
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