(2022) 22:303
Ling et al. BMC Surgery
https://doi.org/10.1186/s12893-022-01753-2

Open Access

CASE REPORT

Hemophilia A developing cerebral infarction
after surgical treatment of giant hemophilic
pseudotumor: a case report
Yiqing Ling1†, Zhenyu Shi1†, Chenying Su2, Xiaochen Liu3, Lingxin Zheng4, Xiaohao Pan4, Yan Sun4,
Xuan Zhang4, Jinling Wei5, Ju Li1, Peijian Tong1 and Taotao Xu1*   

Abstract
Background: Cerebral infarction (CI) is an unusual complication in patients with bleeding disorders. To our knowledge, this is the first case of postoperative internal border-zone infarction (I-BZI) from Hemophilia A.
Case presentation: We present a case of Hemophilia A developing I-BZI, after surgical treatment of giant hemophilic pseudotumor. A 36-year-old man was introduced from other hospital by Hemophilia with giant hemophilic
pseudotumor in his left thigh. Patient and his relatives did not have a history of thrombophilia. After excluding the
relevant surgical contraindications, we performed the operation of pseudotumor resection. Prior to surgery, blood
tests revealed hemoglobin of 137 g/L. FVIII activity was 1.5%. Activated partial thromboplastin time (APTT) was 71.50 s
and D-dimer was 3.33 mg/L FEU. Immediately before surgery, the patient received an intravenous infusion of FVIII
products ­(Xyntha®) at a dose of 3500 IU for his body weight of 80 kg. Post-operative day two (POD2), patient developed vomiting, decreased response, and dysarthria. Hemoglobin was 54 g/L with blood pressure of 110/70 mmHg.
Magnetic resonance imaging of the brain showed there were multiple acute cerebral infarctions in bilateral lateral
ventricles (internal border zone) and multiple ischemic foci in the white matter areas and basal ganglia of the bilateral
cerebral hemispheres. This case suggested that acute severe anemia can be one of the causes of I-BZI.
Conclusions: For the treatment of I-BZI caused by acute anemia from Hemophilia A, volume expansion, red blood
cell supplement and continuous improvement of coagulation with suitable dose of factor VIII (FVIII) should be considered to improve prognosis.
Keywords: Hemophilia A, Factor VIII deficiency, Cerebral infarction, Hemophilic pseudotumor, Case report
Background
Hemophilia is an X-linked recessive congenital bleeding disorder characterized by the absence or deficiency
in factor VIII/IX pro-coagulant function [1]. The majority of bleeding episodes in hemophilic patients occur
†

Yiqing Ling and Zhenyu Shi contributed equally to this work.

*Correspondence: xut@zcmu.edu.cn
1
The First Affiliated Hospital of Zhejiang, Chinese Medical University, You Dian
Road No.54, Hangzhou 310006, Zhejiang Province, People’s Republic of China
Full list of author information is available at the end of the article

within the musculoskeletal system, mainly in the joints
[2]. However, approximately 30% of cases involve the
muscles, especially muscles with a rich blood supply [3,
4]. Recurrent bleeding in the muscles may lead to the
complication of pseudotumor, which has a reported incidence of 1%-2% in patients with severe coagulation factor deficiency [5]. A hemophilic pseudotumor, also called
a hemophilic cyst, is characterized by an encapsulated
and slowly expanding hematoma, which may enlarge
progressively and become life-threatening [6]. Surgical
resection, embolisation or bone graft to the emptied area

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Ling et al. BMC Surgery

(2022) 22:303

followed by rational factor replacement therapy is effective in treating hemophilic pseudotumor. Presently, there
are few reports of ischemic cerebral infarction (CI), especially internal border-zone infarction (I-BZI) in patients
with Hemophilia [7]. More importantly, the etiology of
the ischemia needed to be identified as it will govern the
appropriate treatment. In this case report, we present a
case of Hemophilia A developing cerebral infarction after
surgical treatment of giant hemophilic pseudotumor.

Case report
A 36-year-old male with severe Hemophilia A presented
with a mass in his left thigh. The mass was noticed
10 years ago at which time patient declined intervention. Patient had inconsistent factor VIII (FVIII) treatment since patient was 12 years old. Patient and his
relatives did not have a history of thrombophilia. In Jan
2021, the patient was admitted for swelling in the left
thigh. Physical examination on admission showed flexion contracture of the left knee due to severe pain and a

Page 2 of 6

hard mass over the anterolateral left thigh with pressure
pain (Fig. 1A). Neurologic exam of the lower extremity
was normal. There were symmetrical and strong pulses
in bilateral dorsalis pedis artery on palpation. Radiographs, CT, and MRI showed a 45 cm × 13 cm × 12 cm
pseudotumor in the anterolateral left thigh with multiple large irregular cystic lesions. There was no cortical
destruction of the left femur (Fig. 1B–H). A focal ultrasound revealed a giant intramuscular pseudotumor with
irregular borders and mass effect on adjacent structures.
No definite feeding artery was identified. The neighboring blood vessel around the mass was difficult to detect
via the vascular ultrasound due to the shadowing from
the giant mass. However, an undisturbed blood flow was
seen in the distal portion of the pseudotumor. Blood tests
on 01/26/2021 revealed hemoglobin of 137 g/L. FVIII
activity was 1.5%. Activated partial thromboplastin time
(APTT) was 71.50 s and D-dimer was 3.33 mg/L FEU
(Table 1). The FVIII inhibitor test and human immunodeficiency virus (HIV) screening was negative.

Fig. 1 Preoperative photograph of left thigh showing a giant mass on the anterolateral region of left thigh (A). Anteroposterior radiograph of
the left thigh showing a giant soft-tissue mass located at the left thigh without periosteal reaction of femur shaft (B). Coronal and axial Magnetic
resonance imaging (MRI) of the left thigh showing the large pseudotumor masses on the anterolateral region of left thigh (C, D). Axial computerized
tomography of leg showed intramuscular hematoma in left thigh (E–H). Diffusion weighted MRI and T2 weighted MRI of the brain showed there
were multiple acute cerebral infarctions in bilateral lateral ventricles (internal border zone) and multiple ischemic foci in the white matter areas and
basal ganglia of the bilateral cerebral hemispheres (I–L)

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Table 1 Summary of laboratory analysis and coagulation factor administration at different time point in this study
Date

Hemoglobin Platelet ­(109/L) FVIII
(g/L)
activity
(%)

APTT (s) D-dimer
FIB (g/L) Blood
(mg/L FEU)
pressure
(mmHg)

Volume of coagulation
factor administration

01/26/2021 (on admission)

137

204

1.5

71.50

3.33

3.11

145/96

–

01/28/2021 (prior to
surgery)

–

223

50.4

43.90

4.48

2.94

112/63

01/29/2021 (POD1)

83

180

29.8

47.10

1.06

2.74

134/75

Bolus dose of
3500 IU + 1000 IU

Maintenance dose of
2000 IU q8h

01/30/2021 (POD2:
patient with slurred
speech and decreased
responsiveness)

54

173

17.7

52.70

0.71

4.77

110/70

Bolus dose of 4000 IU
and maintenance dose of
4000 IU q8h

01/30/2021 (after intravenous injection with RBC
2U and plasma 390 ml)

62

176

43.5

40.60

0.66

4.53

115/72

Maintenance dose of
4000 IU q8h

01/31/2021 (POD4:
patient with worsening
alteration of consciousness)

47

157

76.0

46.40

0.66

3.83

120/70

Maintenance dose of
4000 IU q8h

01/31/2021 (after intravenous injection with RBC
3U and plasma 350 ml)

73

213

96.2

38.90

0.46

6.65

140/80

Maintenance dose of
4000 IU q8h

The patient underwent pseudotumor resection under
general anesthesia on 01/28/2021. Immediately prior
to surgery, the patient received an intravenous infusion
of FVIII products ­(Xyntha®) at a dose of 3500 IU for
his body weight of 80 kg. According to his FVIII activity (Table 1), we appropriately adjusted the volume of
coagulation factor administration. Intracapsular resection of the pseudotumor was performed because of the
ill-defined borders and unknown malignant potential
of the mass. Intra-operative dissection of the pseudotumor revealed several liters of brown-greyish fluid. Ossified hematoma and old blood clots were found within
the pseudotumor capsule. The resected mass weighed
2000 g. The resection cavity was subsequently irrigated
with dilute hydrogen peroxide solution and betadine.
After which the cavity was packed with gelatin sponge
and the dead space was closed using overlapping sutures.
Total blood loss during surgery was 900 ml, and 2 U of
red blood cell were transfused.
On 01/29/2021, the patient’s vital signs were stable. The
left thigh was slightly swollen. Bloody liquid of 110 ml was
drawn from the drainage tube, and the incision was dry
and clean. Coagulation factor VIII was changed to maintain at a dose of 2000 IU q8h. The result of hemoglobin,
FVIII activity, APTT and D-dimer are summarized on
Table 1. Until the night of 01/30/2021, patient had two
episodes of vomiting and developed slurred speech
with decreased responsiveness. Heart rate on ECG was
110 bpm with blood pressure about 110/70 mmHg, and

oxygen saturation was 98–100% under oxygen inhalation
(3 L/min). Physical exam revealed that patient was aphasic but was able to follow commands. Upper extremities
were within normal limits. The abdomen was soft and
nontender. The right lower extremity was normal. The
left thigh was swollen, and the left leg had pitting edema.
Patient was not able to move it upon command. Bilateral Babinski’s signs were positive. Blood work showed
hemoglobin was 54 g/L, FVIII activity was 17.7%, APTT
was 52.70 s, and D-dimer was 0.71 mg/L FEU (Table 1).
Craniocerebral CT scan showed no obvious abnormal
changes in brain parenchyma. After intravenous injection of 4000 IU coagulation factor, 4000 IU q8h maintained, and RBC 2 U and plasma 390 ml were infused.
Blood work showed hemoglobin was 62 g/L, FVIII activity was 43.5%, APTT was 40.60 s, and D-dimer was
0.66 mg/L FEU (Table 1). In the morning of 01/31/2021,
the patient’s continued to have worsening alteration of
consciousness. Blood work showed hemoglobin was
47 g/L, FVIII activity was 76.0%, APTT was 46.40 s, and
D-dimer was 0.66 mg/L FEU (Table 1). Blood gas analysis showed that pH was 7.460, partial pressure of oxygen
was 152.0 mmHg, partial pressure of carbon dioxide was
36.8 mmHg, and lactic acid was 0.90 mmol/L. The inhibitor test revealed FVIII inhibitor < 0.60BU. After intravenous injection of RBC 3U, plasma 350 ml were infused.
Blood work showed the hemoglobin was to 73 g/L, FVIII
activity was 96.2%, APTT was 38.90 s, and D-dimer was
0.46 mg/L FEU (Table 1). Magnetic resonance imaging

Ling et al. BMC Surgery

(2022) 22:303

of the brain showed there were multiple acute cerebral
infarctions in bilateral lateral ventricles (internal border zone) and multiple ischemic foci in the white matter
areas and basal ganglia of the bilateral cerebral hemispheres (Fig. 1I–L).
After multidisciplinary consultation, supportive treatment with RBC and plasma infusion and coagulation
factor administration continued. On 02/02/2021, patient
started to gradually recover starting with single syllable
and continued with double syllables the next day. One
week after the initially neurologic deficit, the patient was
at near baseline consciousness and normal speech.

Discussion
Border zone infarction (BZI) occur at the anastomotic
watershed areas of two main arteries [8]. This type of
infarction accounts for about 10% of all CI [9]. The
pathophysiology is thought to be ischemic damage due
to hypoperfusion of the distal vascular territory. BZI was
divided into cortical border-zone infarction (C-BZI) or
internal border-zone infarction (I-BZI). C-BZI is associated with embolic pathogenesis and less frequently due to
hemodynamic compromise. I-BZI is from hypoperfusion
caused mainly by arterial stenosis, occlusion, or hemodynamic compromise [10, 11]. The internal border-zone is
supplied by the superficial and deep perforating arteries
of the middle cerebral artery (MCA) and the anterior cerebral artery (ACA) [10]. In general, hemodynamic compromise is considered as hypotension in patients with
severe arterial stenosis or acute hypotension [12]. However, Amin-Hanjani et al. found that the hypoperfusion
symptoms alone correlated poorly with actual hemodynamic compromise as assessed by quantitative magnetic
resonance angiography [13].
Recently, researchers have noticed and revealed the
potential correlations among bleeding, anemia, and CI
[14, 15]. Previous research has considered that bleeding and subsequent anemia to be a precipitant for CI
and proposed that the hemodynamic compromise and
enhanced thrombosis were the mainly pathogenic mechanisms. In addition, Tsai et al. reported 12 patients with
acute anemia in the case of acute blood loss, without systemic hypotension [16]. The study found that all bilateral
BZI had I-BZI thought to be because acute anemia led
to cerebral blood flow insufficiency and oxygen carrying capacity reduction resulting in CI when hemoglobin
levels drop below the critical level, especially in patients
with intracranial stenosis. In our case, no clear embolic
source was found. When the patient was considered
to have bilateral I-BZI, that is, at the beginning of neurological deficit (110/70mmhg), there was no systemic
hypotension. Patient refused to undergo cerebral magnetic resonance angiography due to rapid recovery and

Page 4 of 6

financial reasons. Ambulatory electrocardiogram showed
no atrial fibrillation, and echocardiography showed no
atrial fibrillation and mural thrombus. No obvious plaque
is found in carotid artery by B-ultrasound, so thrombembolia is not considered as the cause of I-BZI. Taking
into account of the watershed location, patient’s young
age, and his rapid recovery, the root cause was thought
to be due to postoperative acute blood loss secondary
to Hemophilia A. And while the blood pressure did not
decrease significantly, there were signs of acute anemia
(hemoglobin 54 g/L). This resulted in ineffective perfusion and decreased oxygen carrying capacity leading
to tissue hypoxia and hemodynamic damage. Miyazaki
et al. presented the first case of acquired Hemophilia A
patient with pseudotumor and I-BZI [7]. The patient
was not treated surgically, and laboratory tests showed
severe anemia (hemoglobin of 5.5 g/dL), APTT of 99.4 s.
In our case, preoperative hemoglobin of the patient was
137 g/L, whereas the postoperative hemoglobin dropped
to 54 g/L. Postoperative day one, hemoglobin continued
to drop 47 g/L. In addition, while hemophilic pseudotumor is a slow process, I-BZI occurs in acute or chronic
anemia as shown by both Masayuki and our report. On
the other hand, several studies have documented that
severe or chronic iron-deficiency anemia patients were
accompanied by reactive thrombocytosis, which was
considered as a risk factor for carotid artery thrombus
formation and might lead to CI [14, 17]. However, Tsai
et al. considered that reactive thrombocytosis was not a
possible contributing factor to CI in patients with acute
anemia because thrombocytosis was not present at all
in any of patients with acute anemia and CI [16]. In our
case, on POD2 and POD4, the levels of APTT, D-dimer
and FIB were mildly elevated, while the hemoglobin was
54 g/L and 47 g/L, respectively, and platelets were within
normal range (Table 1), indicating acute anemia contributes to CI via the decrease of oxygen carrying capacity
rather than the change of coagulation and fibrinolysis.
Nevertheless, the definite mechanisms of their associations between CI and acute anemia require investigation
in future studies.
In the treatment of cerebral ischemia, the etiology
of the ischemia is vital to determining the treatment
options. Our patient with Hemophilia A was high risk
of massive bleeding from the surgical intervention. The
combination of repetitive hemorrhage and acute blood
loss postoperatively resulted in the watershed infarction
of bilateral lateral ventricles and multiple ischemic foci
in the white matter areas and basal ganglia of the bilateral cerebral hemispheres. Although the treatment for
thrombotic and stenotic ischemia is thrombectomy or
thrombolysis, it is essential to urgent blood transfusion
and rapid correction of the underlying cause of acute

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bleeding. Volume repletion and expansion is needed to
address the hypoperfusion. Especially for patients with
acute anemia, only expansion is not enough, but also the
supplement of red blood cells is needed to increase oxygen carrying capacity and improve ineffective perfusion.
On the other hand, improvement of the patient’s coagulation function was essential for the underlying Hemophilia
A, while this strategy seems to be paradoxical to CI. It is
worth mentioning that prothrombin complex is one of
the commonly used coagulation drugs in Hemophilia
patients, but some studies have shown that prothrombin
complex has been reported to increase the probability of
cerebral infarction [18]. Accordingly, as to I-BZI caused
by acute anemia in hemophilic patients, the maintenance
infusion with FVIII seems to be recommended. Admittedly, the present study has a limited number of patients
with I-BZI caused acute anemia, and the preliminary
results should be interpreted cautiously. More case collection and awareness are required to clarify how to rapid
correction of the underlying cause of acute bleeding in
hemophilic patients.

Conclusions
I-BZI can occur in acute or chronic anemia if hemoglobin is below a certain level. Further studies will have
to be done to determine the threshold. For the treatment
of I-BZI caused by acute anemia from Hemophilia A, volume expansion, red blood cell supplement and continuous improvement of coagulation with suitable dose of
FVIII should be considered to improve prognosis.
Abbreviations
FIB: Fibrinofen; MCA: Middle cerebral artery; ACA​: Anterior cerebral artery; BZI:
Border-zone infarction; C-BZI: Cortical border-zone infarction; APTT: Activated
partial thromboplastin time; HIV: Human immunodeficiency virus; CI: Cerebral
infarction; POD2: Post-operative day two; POD4: Post-operative day four; FVIII:
Factor VIII; I-BZI: Internal border-zone infarction; RBC: Red blood cell; ECG:
Electrocardiogram.
Acknowledgements
The authors thank the participants for their involvement in this case report.
Author contributions
All authors have made substantial contributions to all of the following: YL,
ZS, CS and TX: obtained patient consent, collected initial data, and critically
revised the manuscript. XL and LZ: interpreted data and wrote the first and
final draft of the manuscript. XP, YS and XZ: involved in the acquisition of data,
analysis, and interpretation of data. PT, JL and TX: critically revised the article
for important intellectual content and approved the final version for submission. All authors read and approved the final manuscript.
Funding
This work was supported by grants from the National Natural Science Foundation of China (No. 81904223); Medical Health Science and Technology Program
of Zhejiang Province (No. 2020KY659); Bethune Charitable Foundation (No.GX-2020-1107-17); Talent Cultivation Project of Zhejiang Association for Science
and Technology (No. CTZB-2020080127); Youth Research and Innovation Fund
of Zhejiang Chinese Medical University (No. KC201933).

Page 5 of 6

Availability of data and materials
The original contributions presented in the study are included in the article/
supplementary material, further inquiries can be directed to the corresponding author/s.

Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent was obtained from the patient for publication of
this case report and accompanying images.
Competing interests
The authors declare that they have no competing interests.
Author details
1
The First Affiliated Hospital of Zhejiang, Chinese Medical University, You
Dian Road No.54, Hangzhou 310006, Zhejiang Province, People’s Republic of China. 2 The First Affiliated Hospital of Wenzhou Medical University,
Wenzhou 325000, Zhejiang, People’s Republic of China. 3 University of Toledo
Medical Center, Toledo, OH 43614, USA. 4 Zhejiang Chinese Medical University,
Hangzhou 310053, Zhejiang, People’s Republic of China. 5 Tongde Hospital
of Zhejiang Province, Hangzhou 310007, Zhejiang, People’s Republic of China.
Received: 17 November 2021 Accepted: 2 August 2022

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