Nakamura et al.

BMC Neurology (2018) 18:190

https://doi.org/10.1186/s12883-018-1194-1

CASE REPORT Open Access

Posterior reversible encephalopathy

syndrome with extensive cytotoxic edema
after blood transfusion: a case report and
literature review
Yoshitsugu Nakamura1,3*, Masakazu Sugino1,3, Akihiro Tsukahara1,3, Hiroko Nakazawa2, Naomune Yamamoto2 and
Shigeki Arawaka3

Abstract
Background: Posterior reversible encephalopathy syndrome (PRES) is described as a clinical-radiological disease
entity with good prognosis. In brain MRI, PRES generally presents with vasogenic edema. Although PRES is induced
by various causes, a small number of PRES cases have occurred after red cell blood transfusion. It is unclear whether
there are characteristic features in PRES after blood transfusion.
Case presentation: Here, we report a case of 75-year-old Japanese woman who had acute exacerbation of
subacute anemia by bleeding from gastric ulcer. After receiving a red cell blood transfusion, she showed
disturbance of consciousness with extensive cytotoxic and small vasogenic edema in the occipitoparietal area
on brain MRI. She was diagnosed as PRES and suffered irreversible impairments of visual acuity and fields in
both eyes. We summarized and discussed clinical features of cases with PRES after blood transfusion.
Conclusions: A total of 21 cases including the present one have been reported as PRES after blood transfusion. Of the
cases, 20 of 21 were female, and 15 of 17 developed PRES in the course of chronic anemia lasting over 1 month. Anemia
was severe in 15 of 20 cases, with hemoglobin levels < 3.5 g/dl. In 14 of 17 cases, hemoglobin levels increased to 5 g/dl
by red cell blood transfusion until the onset of PRES. On brain MRI, 2 of 21 cases showed cytotoxic edema and 3 of 21
cases showed irreversible neurological disturbance. In this patient, the occurrence of PRES in subacute anemia and the
presence of extensive cytotoxic brain edema with irreversible neurological deficits were characteristic points. When
treating severe anemia, even with a subacute progression, we should consider a possibility that PRES occurs after blood
transfusion with extensive cytotoxic brain edema and irreversible neurological changes.
Keywords: Posterior reversible encephalopathy syndrome, Blood transfusion, MRI, Cytotoxic edema, Neurological
sequelae, Case report

Background disturbance, headache, seizure, and various visual distur-

Posterior reversible encephalopathy syndrome (PRES) was bances. Vasogenic edema was observed in the bilateral
first described as a clinical and radiological disease entity parieto-occipital regions as elevation of apparent diffusion
by Hinchey and colleagues in 1996 [1]. Usually, PRES pre- coefficient (ADC) values in brain magnetic resonance im-
sents subcortical vasogenic brain edema in patients with aging (MRI) [1, 2]. The prognosis of PRES is generally
acute neurological symptoms, such as conscious good in terms of improvement and reversal of radiological
and clinical findings. However, a previous paper reported
* Correspondence: [email protected] atypical cases. These showed cytotoxic edema, neuro-
1
Division of Neurology, Aino Hospital, 11-18 Takadacho, Osaka, Ibaraki logical sequelae, and lack of hypertension [2]. Cytotoxic
567-0011, Japan
3
Division of Neurology, Department of Internal Medicine IV, Osaka Medical edema was observed as hyperintensity on diffusion
College, 2-7 Daigakumachi, Takatsuki, Osaka 569-8686, Japan
Full list of author information is available at the end of the article

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Nakamura et al. BMC Neurology (2018) 18:190 Page 2 of 7

weighted images (DWI) and decrease of ADC values in matter of the bilateral occipital and occipitoparietal
brain MRI. lobes. DWI also showed high signal intensities in these
PRES occurs in association with severe hypertension, lesions, while ADC maps show low signal intensities in
renal failure, eclampsia, autoimmune disorders, and ex- the cortical and subcortical regions with small high sig-
posure to immunosuppressive agents. The clinical features nal intensities in the surrounding area. These image pat-
of PRES caused by preeclampsia-eclampsia or calcineurin terns indicated that the lesions were damaged by
inhibitors are shown to be different from those caused by extensive cytotoxic edema with restricted vasogenic
other triggers [3–5]. PRES is seen after red cell blood edema (Fig. 1). Magnetic resonance angiography (MRA)
transfusion in a small number of patients [6–21]. How- showed no stenosis or occlusion of brain arteries. MR
ever, there was no study analyzing these cases of PRES venography and 3-dimensional CT angiography was
after blood transfusion. The clinical features of PRES after negative for sinus thrombosis, although the left trans-
blood transfusion remains unclear. Here, we report a verse sinus was hypoplastic.
patient who had PRES after being treated for severe During this process, the maximum systolic blood pres-
anemia with red cell blood transfusion. This case showed sure was 130 mmHg. Laboratory examinations showed
cytotoxic edema in the occipitoparietal regions on brain no abnormality in liver and coagulatory functions. The
MRI, and developed irreversible visual disturbance. These level of serum creatinine was stable. Autoantibodies,
features were different from typical PRES. We review pre- such as anti-nuclear antibody, anti-thyroid antibody, and
vious cases of PRES after red cell blood transfusion and anti-neutrophil cytoplasmic antibody, were negative.
discuss the features of these cases with the supposed There was no mutation at position 3243 of the mito-
mechanism of brain damages caused by an increase in the chondrial DNA. The cerebrospinal fluid was clear, color-
hemoglobin (Hb) concentration. less and acellular with a total protein level of 41 mg/dl
and a glucose level of 79 mg/dl. Transthoracic echocar-
Case presentation diography showed that myocardial wall motion was nor-
A 75-year-old woman (height 132 cm, weight 34 kg) mal without foramen ovale or left ventricular thrombus.
consulted a medical doctor with loss of appetite lasting Holter electrocardiogram showed no atrial fibrillation.
for 1 week. She had taken aspirin, celecoxib, and amlodi- From these examination results, the clinical course, and
pine because of angina and hypertension. Laboratory characteristic MRI findings, we considered the possibility
examinations showed that her Hb decreased modestly to of PRES and performed conservative treatment by moni-
10.7 g/dl. Two weeks later, she was admitted to our hos- toring the fluctuations of blood pressure and vital signs.
pital because her anorexia had worsened day by day. On On admission day 7, her responsiveness to external
admission day 1, she was alert and fully oriented. Her stimulation improved. However, her visual acuity had
blood pressure and pulse rate were stable. Laboratory declined to 20/100 in the right eye and 20/200 in the left
examinations showed that the levels of Hb and eye, and visual field test showed defects of the left lower
hematocrit decreased remarkably to 4.8 g/dl and 15%, quadrants in both eyes. Her optic disc and retina were
respectively. The values for white blood count and normal. Two months later, her Mini-Mental State Exam-
C-reactive protein (CRP) increased slightly to 9900 ination score improved to 16 from 8 on admission day
/mm3 and 4.64 mg/dl, respectively. Additionally, her al- 14. However, the disturbances of visual acuity and fields
bumin level decreased to 2.5 g/dl and the creatine level remained unrecovered. When compared with MRI find-
increased slightly to 1.14 mg/dl (estimated glomerular ings, high signal intensities on DWI images were dimin-
filtration rate was 41.7 ml/min). Chest and abdominal ished on admission day 7 (Fig. 1). In addition, high
computed tomography (CT) failed to detect abnormal signal intensities on FLAIR images were diminished until
lesions. On admission day 2, she vomited large amounts 4 months after onset, and these lesions alternatively
of bright red blood. Her Hb level further decreased to involved low signal intensities, indicating cystic change
2.9 g/dl. She underwent an urgent transfusion of 560 ml (Fig. 2). There were no findings showing cardiogenic
of red blood cells. Endoscopic examination detected embolism and cerebral venous thrombus. The cystic
active bleeding from a gastric ulcer, and endoscopic clip- lesion in posterior lobe seemed to represent ischemic
ping was performed against the bleeding lesion. change, because PRES is reported to cause ischemic
The next day, her Hb improved to 8.9 g/dl. However, change as a complication [22].
she did not respond to verbal or pain stimuli despite her
eyes having opened. She showed normal light reflexes Discussion and conclusions
without anisocoria. On brain MRI (fluid-attenuated in- Methods
version recovery, FLAIR), high signal intensities were This review was based on a literature search for articles
seen in the bilateral cerebellar hemispheres, bilateral concerning PRES after blood transfusion that were pub-
watershed regions, right thalamus, and white and gray lished from 1997 through August 2017. By using the
Nakamura et al. BMC Neurology (2018) 18:190 Page 3 of 7

Fig. 1 On admission day 2, axial fluid-attenuated inversion recovery (FLAIR) images show abnormal hyperintense areas bilaterally in the cerebellar
hemispheres, watershed regions, and white and grey matter of the occipital and occipitoparietal lobes. Axial FLAIR images show hyperintense
areas in white matter predominating in the periventricular region indicating leukoaraiosis (a, b, c, d, e). Axial diffusion weighted image (DWI)
images show hyperintense areas in these lesions and the right thalamus (f, g, h, i, j). Apparent diffusion coefficient (ADC) map shows low signal
intensities in the bilateral cerebellar hemispheres and watershed regions (k, o). ADC map shows low signal intensities in the cortical and subcortical
regions with small areas of high signal intensity in the surrounding area (l, m, n). These image patterns indicate that the lesions were damaged by
extensive cytotoxic edema with restricted vasogenic edema. Most hyperintense areas on DWI on 2 days after admission disappeared by 7 days after
admission (p, q, r, s, t)

Fig. 2 Hyperintense areas on axial fluid-attenuated inversion recovery (FLAIR) image at 2 days after admission (a, b, c) gradually disappear at
2 months after admission (d, e, f) and 4 months after admission (g, h, i). However, at 4 months after admission several cystic changes remained
in the cerebellar hemisphere, occipital region, and right thalamus (g, h, i)
Nakamura et al. BMC Neurology (2018) 18:190 Page 4 of 7

Medline database (PubMed, National Library of Medi- Discussion

cine, Bethesda, MD; keywords: posterior reversible en- Although the exact mechanism of PRES after blood
cephalopathy syndrome and blood transfusion) and transfusion is unclear, a rapid increase in the Hb level
further checking the reference lists of articles, 20 cases and viscosity by the blood transfusion is thought to trig-
of PRES after red cell blood transfusion were identified. ger the occurrence of PRES. This increase could induce
In this report, a total of 21 cases including the present acute vascular endothelium dysfunction and an elevation
one, were reviewed. of vascular resistance, leading to endothelial damage and
The distribution of brain lesions was divided into three extravascular leakage of fluid and macromolecule in the
areas: anterior circulation (AC), posterior circulation brain. Also, the velocity of brain blood flow is shown to
(PC), and deep structure (DS) territories. AC includes increase in patients with severe anemia [25]. It raises an
the frontal, temporal and parietal lobes. PC includes the idea that rapid elevation of vascular resistance or vascu-
occipital lobe, cerebellum and brainstem. DS includes lar constriction factors in blood products damages vas-
the basal ganglia, deep white matter and corpus callo- cular endothelial cells [26]. Consequently, these changes
sum [23]. Patients with sickle cell anemia who developed are thought to cause PRES [6]. However, a previous
PRES after blood transfusion were excluded because paper showed that anemia itself caused PRES under a
sickle cell anemia itself was reported to cause PRES [24]. hemorrhagic shock state with sepsis or multiple organ
failure [27]. The present patient was not consistent with
Results of literature review that prior case because our patient had no signs or
Table 1 shows the characteristics of 21 cases of PRES after symptoms of sepsis or multiple organ failure. There was
blood transfusion. The mean age of onset was 43.6 years a possibility that rapid elevation of Hb levels affected the
(range 6–77 years). Twenty cases (95%) were in females, occurrence of PRES. The elevation of Hb levels by blood
and all adult cases were in females. The primary causes of transfusion is dependent on the volume of circulating
anemia varied, such as gynecological disease (10 cases), blood, which is associated with the body weight [28]. It
renal failure (3 cases), iron deficiency anemia (2 cases), is possible that Hb levels rapidly elevated from 2.9 g/dl
aplastic anemia (2 cases), cancer surgery (2 cases), thalas- to 8.9 g/dl by transfusing 560 ml of blood, because the
semia (1 case), and gastrointestinal bleeding (1 case). In the body weight of this patient was low. This rapid elevation
majority of PRES cases after blood transfusion (15 (88%) of of Hb levels may affect the occurrence of PRES.
17 assessable cases) had been affected by chronic anemia There are two characteristic points distinguishing the
lasting over 1 month. The mean Hb value before blood present patient. First, the patient presented with exten-
transfusion was 3.4 g/dl (range 1.4–9.2). Severe anemia sive cytotoxic edema on brain MRI. In cases with PRES
(Hb < 3.5 g/dl) was observed in 15 (75%) of 20 assessable after blood transfusion, the frequency of cytotoxic edema
cases. The mean Hb value after blood transfusion was was less than that of vasogenic edema. Cytotoxic edema
6.7 g/dl (range 3.2–10.4). Hb increased to ≥5 g/dl in 14 was found in only 11–30% of previous cases with PRES
(82%) of 17 assessable cases just before the onset of PRES. [2, 29]. However, it is unclear how cytotoxic edema oc-
The mean onset of neurological symptoms after blood curs in PRES after blood transfusion, and whether the
transfusion was 7.1 days (range 1–18 days). The period cytotoxic edema in PRES causes irreversible damages is
from blood transfusion to the occurrence of PRES is known under debate [2, 4, 22, 29–33]. In addition, the present
to depend on some factors, including the patient’s condi- patient showed cytotoxic edema over an extensive area
tion, disease complication, and total amount and speed of as compared with other cases with cytotoxic edema. In
blood transfusion [19]. Neurological symptoms were en- the present patient, this extensive cytotoxic edema may
cephalopathy (9 cases, 43%), seizure (15 cases, 71%), head- have helped to cause the irreversible visual disturbance.
ache (13 cases, 62%), visual disturbance (11 cases, 52%), Indeed, while the number of cases with extensive cyto-
and focal deficit (2 cases, 10%). The number of cases with toxic edema is very small, those cases are generally asso-
hypertension was small (8 cases, 38%), in contrast to the ciated with irreversible changes and incomplete clinical
data showing that 80–85% cases of PRES exhibit hyperten- recovery [2, 22, 29–32]. Therefore, the clinical course of
sion [2]. Neurological sequelae, such as consciousness dis- the present patient may suggest that rapidly correcting
turbance, visual disturbance and hemiplegia, were found in anemia with red cell blood transfusion should be
3 cases (14%). PRES brain lesions after blood transfusion avoided to prevent PRES. It supports an idea that cyto-
were seen in the PC territory (20 cases, 95%), the AC terri- toxic edema causes irreversible damages in PRES. To
tory (13 cases, 62%), and the DS territory (3 cases, 14%). address this issue, it is necessary to collect similar cases
On brain MRI, 2 cases (9%) presented with cytotoxic with neurological sequelae.
edema, and vasoconstriction was identified in 9 cases Second, the period of anemia in the present patient
(43%). Vasoconstriction was caused by cerebral angiography was shorter those that reported in previous cases. Most
in 3 cases and MR angiography in 6 cases. cases (88% of all reported cases of PRES after blood
Table 1 Previous reports PRES after blood transfusion and our case
Patient No. Age/ Cause of Course of Hb(g/dl) pre/ Volume of Symptom onset Clinical Lesion Cytotoxic Vasoconstriction Hypertension Sequelae Reference
Sex anemia anemia post BT BT (ml) after BT (days) finding distribution edema
Nakamura et al. BMC Neurology

1 45/F Myoma uteri Chronic 2.0/10.0 800 2 S, H AC, PC No Yes Yes None 6
2 48/F Myoma uteri Chronic 3.0/8.0 1000 6 E, S, F AC, DS No Yes No None 7
3 47/F Aplastic anemia Chronic 1.5/10.9 NR 7 E, S, H, V PC No Yes No None 8
4 58/F Cancer surgery NR 7.7/10.9 1400 9 E, S PC No No Yes E 9
(2018) 18:190

5 77/F Cancer surgery Acute 9.2/13.3 2800 18 E, S PC No No Yes None 9

6 32/F Myoma uteri Chronic 5.7/12.5 1600 5 H PC No Yes No None 10
7 11/M Iron deficiency anemia NR NR/NR NR NR S, V AC, PC No No No None 11
8 42/F Renal failure Chronic 5.7/11.7 400 6 S, H, V PC No Yes No None 12
9 56/F Corpus uteri cancer Chronic 2.0/9.2 2000 6 E, S, V PC No No Yes None 13
10 28/F Aplastic anemia Chronic 3.2/9.6 1640 8 H, V AC, PC No No No None 14
11 57/F Iron deficiency anemia Chronic 2.0/10.0 1120 10 S, H AC, PC No No Yes None 14
12 50/F Hypermenorrhea Chronic 1.5/NR 3000 NR S, H AC, PC No Yes Yes None 15
13 46/F Myoma uteri Chronic 1.4/NR 2500 15 H, V AC, PC Yes Yes Yes None 15
14 36/F Hypermenorrhea Chronic 1.4/11.3 1120 12 E, S AC, PC, DS No No No V, F 16
15 6/F Thalassemia NR 4.8/NR 280 2 E, H PC No No No None 17
16 36/F Myoma uteri Chronic 1.7/8.8 560 2 E, S, H, V AC, PC No No Yes None 18
17 45/F Renal failure Chronic 3.4/7.9 800 4 H, V AC, PC No Yes No None 19
18 47/F Renal failure Chronic 3.0/10.4 750 NR S, H, V PC No Yes No None 19
19 40/F Hypermenorrhea Chronic 3.1/8.6 840 4 S, H, V, F AC, PC No No No None 20
20 35/F Abortion NR 3.4/13.8 700 10 S AC, PC No No No None 21
21 75/F Gastrointesional bleeding Subacute 2.9/8.9 560 1 E, V AC, PC, DS Yes No No V Our case
Abbreviations: PRES posterior reversible encephalopathy syndrome, NR not reported, Hb hemoglobin, BT blood transfusion, E encephalopathy, S seizure, H headache, V visual disturbance, F focal deficit, AC anterior
circulation, PC posterior circulation, DS deep structure
Page 5 of 7
Nakamura et al. BMC Neurology (2018) 18:190 Page 6 of 7

transfusion) had had chronic anemia lasting over and it caused irreversible damages. Clinical findings of
1 month [6–8, 10, 12–16, 18–20]. In these typical cases, this patient suggest that irreversible damages may be
it assumed that a rapid improvement of oxygenation by caused by extensive development of cytotoxic edema in
blood transfusion induces PRES by disturbing the bal- the brain. Additionally, if the anemia is urgently cor-
ance of vessels, which is maintained by chronic hypoxic rected by blood transfusion, clinicians should check for
vasodilation [6]. In the present patient, the period of the presence of risk factors, including elevation of CRP
anemia during which Hb decreased from 10.7 to 2.9 was levels, hypoalbuminemia, renal injury, and female sex,
14 days. The presence of other factors may exacerbate and perform the blood transfusion slowly with carefully
the occurrence of PRES. Severe anemia itself (Hb 2.9 g/ monitoring the increase of Hb levels.
dl) may affect the occurrence of PRES. Also, previous re-
Abbreviations
ports have demonstrated that elevation of CRP levels AC: Anterior circulation; ADC: Apparent diffusion coefficient; CRP: C-reactive
[34], hypoalbuminemia [35, 36], and renal injury [37] are protein; CT: Computed tomography; DNA: Deoxyribonucleic acid; DS: Deep
candidate factors affecting the occurrence of PRES. Ele- structure; DWI: Diffusion weighted image; FLAIR: Fluid attenuated inversion
recovery; Hb: Hemoglobin; MRA: Magnetic resonance angiography; MRI: Magnetic
vation of CRP levels has been shown to exacerbate PRES resonance imaging; PC: Posterior circulation; PRES: Posterior reversible
by increasing the vulnerability of the blood–brain barrier encephalopathy syndrome
by inflammation-associated endothelial damage [34]. Hy-
Acknowledgments
poalbuminemia affects the development of edema in Not applicable.
PRES by reducing colloid osmotic pressure [35, 36].
Renal injury is reported to mediate endothelial cell dam- Funding
No funding was received for this study.
age, which is a poor prognosis factor [37]. The present
patient presented with elevated CRP levels, hypoalbu- Availability of data and materials
minemia, and renal injury. These factors may affect the The dataset supporting the conclusion of this article is included within the
article.
occurrence of PRES after blood transfusion in patients
with subacute severe anemia. Authors’ contributions
Finally, most cases of PRES after blood transfusion YN and MS examined and scripted the manuscript. AT, HN, and NY helped
to draft the manuscript and performed analyses. SA supported for the critical
are female. The proportion of female PRES patients revision of the manuscript for intellectual content. All authors approved the
after blood transfusion is much greater than the pro- contents of this case report.
portion of female patients among all PRES patients,
Ethics approval and consent to participate
including eclampsia, because previous reports show The authors declare that ethics approval was not required for this case
that female patients account for 56–68% of all PRES report.
patients [22, 29, 33, 34, 36–40]. The reason why
Consent for publication
many cases with PRES after blood transfusion were
Written informed consent was obtained directly from both the patient and
female remained unclear. About half of PRES after the patient’s husband for publication of this case report and any accompanying
blood transfusion accompanied vasoconstriction. In images at the same time.
general, the frequency of vasoconstriction is reported
Competing interests
to be 18% in PRES [22, 37]. This suggests that the The authors declare that they have no competing interests.
frequency of vasoconstriction in PRES after blood
transfusion is higher than that in PRES induced by Publisher’s Note
other causes. Decrease in estrogen levels may affect Springer Nature remains neutral with regard to jurisdictional claims in
to cause vasoconstriction [41, 42], because estrogen published maps and institutional affiliations.

suppresses vascular constriction [43]. Also, there is a Author details

1
tendency that almost papers concerning PRES after Division of Neurology, Aino Hospital, 11-18 Takadacho, Osaka, Ibaraki
blood transfusion were published from Asia [6, 8–17, 567-0011, Japan. 2Division of Internal Medicine, Aino Hospital, 11-18
Takadacho, Osaka, Ibaraki 567-0011, Japan. 3Division of Neurology,
19, 21]. To clarify whether genetic factors associate Department of Internal Medicine IV, Osaka Medical College, 2-7
with the occurrence of PRES after blood transfusion, Daigakumachi, Takatsuki, Osaka 569-8686, Japan.
it is necessary to further analyze clinical features by
Received: 4 November 2017 Accepted: 31 October 2018
accumulating cases with PRES after blood transfusion.

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