Neurol Sci
https://doi.org/10.1007/s10072-017-3158-4

BRIEF COMMUNICATION

Intravenous thrombolysis in SLE-related stroke: a case report
and literature review
Xiaodong Chen 1,2

& Gelin Xu

1

Received: 11 May 2017 / Accepted: 12 October 2017
# Springer-Verlag Italia S.r.l. 2017

Abstract Patients with systemic lupus erythematosus (SLE)
bear an increased risk of ischemic stroke. However, evidences
for treating acute stroke due to artery thrombosis in SLE patients are extremely limited. A 45-year-old woman experienced sudden left hemiplegia. She was transported to the
emergency department of our hospital 2 hours after the initial
symptom. According to the medical records, the patient was
diagnosed with SLE at the age of 28. CT scanned 150 min
after the initial symptom showed no evidence of acute changes
or hemorrhage. Magnetic resonance angiography (MRA) revealed occlusion of the right proximal middle cerebral artery
(MCA). Ischemic stroke was diagnosed and NIHSS scored
11. The occluded MCA was successfully recanalized with
intravenous rtPA. Sequent vascular imaging and serological
results indicated that the etiology of the occlusion in right
MCA was SLE vasculitis. The patient attained a mRS of 3 at
the 3-month follow-up. The case is the first one in the literature that acute ischemic stroke related to SLE vasculitis was
treated successfully with intravenous rtPA thrombolysis. The
feasibility of intravenous thrombolysis for stroke related to
SLE warrant further study.
Keywords Thrombolysis . Stroke . Systemic lupus
erythematosus . Vasculitis
Xiaodong Chen and Gelin Xu contributed equally to this work and should
be considered co-first authors.
* Xiaodong Chen
163chenxd@163.com

1

Department of Neurology, Jinling Hospital, Southern Medical
University, Nanjing, Jiangsu Province 210002, China

2

Department of Neurology, Shuyang People’s Hospital,
Shuyang, Jiangsu Province 223600, China

Systemic lupus erythematosus (SLE) is an important etiology
of ischemic stroke, especially in young patients [1].
Inflammation-induced endothelial injury and subsequent
thrombosis have been regarded as the remaining pathogenesis
for SLE-related stroke [2]. However, experiences for treating
acute stroke due to artery thrombosis in SLE patients are very
limited. To our knowledge, only three cases of SLE-related
stroke being treated with intravenous rtPA have been reported
[3–5]. Here, we present a case of acute ischemic stroke due to
right middle cerebral artery (MCA) occlusion in a 45-year-old
woman with previous history of SLE. The occluded right
MCA was successfully recanalized after intravenous administration of rtPA. We then reviewed the literatures concerning
the intravenous thrombolysis and endovascular treatment of
ischemic stroke related to SLE.

Case report
A 45-year-old female experienced sudden left hemiplegia. She
was transported to the emergency department of our hospital
2 hours after the initial symptom. According to the medical
records, the patient was diagnosed with SLE at the age of 28.
She had experienced mild to moderate fever for 12 days. She
was currently on prednisone 10 mg/day and azathioprine
50 mg/day. She had no history of seizure, illicit drug use, or
oral contraceptive use. On admission, the patient was alert and
oriented. The axillary temperature was 37.4 °C. The blood
pressure was 154/94 mmHg, and pulse 111 beats per minute.
Overt left central facial palsy and left hemiplegia were observed during physical examination. National Institute of
Health Stroke Scale (NIHSS) scored 11. Routine blood test
revealed that the white blood cell count was 15.3 × 109/L, with
76% as neutrophils. There was mild hypoferric anemia (hemoglobin as 95.2 g/L). Serum CRP level (> 120.0 mg/L)

Neurol Sci

increased remarkably. Serum fibrinogen (4.16 g/L) and Ddimer levels (2.0 mg/L) also increased. Both platelet count
and routine coagulation parameters were normal. The capillary blood glucose level was 6.83 mmol/L. The renal function
was normal, as were blood levels of other electrolytes, calcium, magnesium, and cholesterol, and results of hepatic function tests.
Non-contrast computed tomography (CT) scanned
150 min after the initial symptom showed no evidence of
acute changes or hemorrhage (Fig. 1a). Acute ischemic
stroke was then diagnosed. Intravenous rtPA (0.9 mg/kg,
5.5 mg as bolus followed by 49.5 mg as infusion) was
initiated 195 min after the stroke onset. Magnetic resonance imaging (MRI), scanned 200 min after the stroke

onset, revealed abnormal signals in right basal ganglia
and temporal lobe. Magnetic resonance angiography
(MRA) revealed occlusion of the right proximal MCA,
(Fig. 1b, c). The volume of the diffusion abnormality was
less than 25 mL, and therefore the patient was likely to
benefit from endovascular thrombectomy, but the patient
refused it after receiving adequate information.
Sixty minutes after the bolus of rtPA, the strength of left
extremities improved gradually. Twenty-four hours later, her
NIHSS score was 7. She did not have any complications post
thrombolysis. A repeated CT, scanned 24 h after rtPA thrombolysis, showed acute infarction in right basal ganglia (Fig.
1d). Contrast-enhanced MR (CE-MR) showed partial enhancement in the infarction core (Fig. 1e). CE-MRA revealed

a

b

c

d

Fig. 1 a Axial CT image before thrombolysis showed no evidence of
early changes or hemorrhage; b and c MRI after the bolus of rtPA, DWI
showed acute infarction in the territory of right MCA; MRA revealed
occlusion of proximal right MCA; d Axial CT scanned 24 h after
thrombolysis shows acute infarction; e and f Contrast-enhanced MR
24 h after thrombolysis revealed partial reinforcement in the infarction
area (white arrow); MRA shows an abrupt drop off of signal in the right

MCA (red arrow) with an inhomogenous distribution of blood distally
(yellow arrowheads), which indicated vasculitis as the etiology of the
stroke; g, h, and i High-resolution, black-blood MRI after gadolinium
injection scanned at 3-month follow-up demonstrating a strong, smooth,
and concentric vessel wall enhancement in right MCA (yellow arrow and
yellow circle)

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e

f

g

h

i

Fig. 1 continued.

recanalization of right MCA and partially recovered distal
blood flow (Fig. 1f). The stenosis in right MCA as shown in
MRA suggested that the etiology of the occlusion was
vasculitis.
After intravenous rtPA treatment, the patient underwent further examinations to determine the etiology of the stroke. The
results of carotid and vertebral ultrasound scan, transesophageal
ECHO, ECG Holter were unremarkable. Blood test showed
normal levels of serum protein C, protein S, factor V Leiden,
antithrombin III, homocysteine, and antiphospholipid antibodies. Of noted, ANA, anti-SSA levels increased in both serum
and cerebrospinal fluid (CSF), but serum C1q (102 mg/L), C3
(0.83 g/L), C4 (0.06 g/L), and immunoglobulin M (0.31 g/L)
levels decreased. Erythrocyte sedimentation rate (ESR)

increased remarkably (83 mm/h). CSF was colorless, with a
total protein level of 670 mg/L, and elevated immunoglobulin
G (0.1 g/L). According to criteria by the American College of
Rheumatology [6], stroke related to SLE was diagnosed. We
consulted the immunologist. Thereafter, the patient started a
treatment with intravenous 1 g methylprednisolone daily for
3 days followed by 60 mg prednisone daily, cyclophosphamide
(1 g/day), and lifelong oral warfarin anticoagulation with regular INR monitoring (target 2–3).
At the 3-month follow-up, strength in left extremities further improved. She could walk independently and move her
left arm freely, but she could not take articles with her left
hand. mRS scored 3, and there were no further stroke during
90 days after the index stroke.

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Discussion and review of literature
Stroke and transient ischemic attacks (TIA) occurred in
0.5 to 15% of patients with SLE [7]. The related stroke
can be attributed to several factors, such as Libman Sacks
endocarditis, inflammatory-mediated atherosclerosis,
hypercoagulation secondary to anticardiolipin antibodies,
and vasculitis [8, 9].
In the present case, ischemic stroke due to right MCA occlusion was evidenced by CT, MRI, and MRA results. A diagnosis of SLE was indicated by elevated serum inflammatory
markers, positive lupus serologic results, CSF changes, and
abnormal signal of right MCA in CE-MRA images. This diagnosis was further supported by the gradual improvement of
the patient after being treated with high-dose glucocorticoid.
The first case of stroke related to SLE-treated with intravenous thrombolysis was reported in 2015 by Loharia and colleagues [3]. A 37-year-old female with acute MCA stroke
attained excellent outcome after rtPA thrombolysis (10 mg
as IV bolus followed by 80 mg as IV infusion, treatment
initiated at 4 h after stroke onset). The patient was subsequently diagnosed with antiphospholipid syndrome (APS) [3].
Recently, Lemarroy et al. [4] reported a case of acute ischemic
stroke involving a large territory of the right MCA. This 22year-old woman also attained good clinical outcome after intravenous rtPA treatment (0.6 mg/kg, treatment started at
150 min after stroke onset), despite concomitant thrombocytopenia and prolonged prothrombin times due to SLE and
APS. Success treatments of these two cases emphasized the
need for further evaluating the feasibility of intravenous
thrombolysis in stroke patients with SLE, especially in those
with secondary APS and/or thrombocytopenia.
Recently, Stadler et al. [10] reported a case of acute ischemic stroke with concomitant APS and thrombocytopenia.
This 48-year-old woman was treated successfully with mechanical thrombectomy. The occluded MCA was recanalized
using stent-like clot retriever 150 min after symptom onset.
She attained favorable outcome after the endovascular
procedure.
There is only one case reported in literature concerning the
use of rtPA for treating stroke related to SLE vasculitis [5].
A 40-year-old woman with acute ischemic stroke was
treated with rtPA (0.9 mg/kg, treatment imitated at
90 min after symptom onset). She had a previous history
of SLE with secondary APS. Although there was no hemorrhagic transformation, the patient attained no significant
improvement after thrombolysis. Subsequent MRI scan revealed a large infarction in right hemisphere, and the MRA
revealed signs of vasculitis [5].
In non-SLE patients, both definite and possible vasculitis can increase the risk of intracranial hemorrhage after
intravenous rtPA thrombolysis [11, 12]. CNS vasculitis
can result in intracranial hemorrhage by damaging vessel

wall and promoting aneurysm formation. In rare cases,
SLE has been associated with changed blood coagulation
factors and necrotized vasculitis in cerebral vessels, both of
which might be devastating in the presence of rtPA [13].
Given the potential risk of intracranial hemorrhage,
the use of thrombolysis in stroke patients with history
of CNS vasculitis should be considered with extra caution. In the management of acute ischemic stroke, the
benefit of intravenous thrombolysis is crucially time-dependent. On the other hand, early hemorrhagic transformation, either due to reperfusion injury or damage of
the blood-brain barrier, is also time-dependent. Time,
therefore, should be considered preferentially when
making the treatment decisions for these patients.
Considering the successful experiences from this case
and others reported previously, the feasibility of intravenous thrombolysis for stroke related to SLE warrant
further study.
Compliance with ethical standards
Conflict of interest The authors declare that there are no conflicts of
interests.

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