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Clinical Case Report

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Wernicke’s encephalopathy due to malnutrition
and parenteral nutrition in a patient with cerebral
infarction
A case report
Xiaojiao Lian, MSa,b, Meng Wu, MSa,b, Haixia Fan, MScc, Yi Zhang, MScc, Ping Sun, MSa,

∗

Abstract
Introduction: Wernicke’s encephalopathy (WE) is a severe neuropsychiatric disorder, which results from a nutritional deficiency of

thiamine. The occurrence of WE is rarely reported in patients with cerebral infarction, who often have complications of malnutrition.
Cerebral infarction is a neurological disease, patients with cerebral infarction may show symptoms such as disturbance of
consciousness and gait instability, which is difficult to differentiate from WE. Thus, early recognition and differential diagnosis of WE
are important. We report a rare case of cerebral infarction patient who developed WE due to malnutrition and parenteral nutrition.

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Patient concerns: A 65-year-old woman was admitted to our hospital with cerebral infarction. She had lost 15 kg of weight in the
past month or so and was diagnosed with malnutrition. In order to correct malnutrition, parenteral nutrition and intravenous glucose
without thiamine were administered. Cognitive dysfunction, laloplegia, sleep rhythm inversion, somnolence and bilateral lower limbs
weakness were presented 20 days after admission.
Diagnosis: Brain magnetic resonance imaging confirmed the diagnosis of WE.
Interventions: The patient was given thiamine and nutrition support therapy.
Outcomes: The patient’s cognitive impairment, laloplegia and sleep condition improved within 4 days. Neurological status

continued to improve and physical activity recovered gradually within 2 weeks. She received rehabilitation training when her condition
was relatively stable, and her muscle strength of limbs and physical function gradually improved.
Conclusion: Infarction-related malnutrition may result in nutrient deficiency-related neurological complications, such as WE. Thus,
it is important to pay close attention to the nutritional status of patients with cerebral infarction. In addition, early recognition and
differential diagnosis of WE in patients with infarction-related malnutrition are necessary, early treatment of replete thiamine
supplementation and nutrition support therapy can reduce the risk of WE and improve the prognosis.
Abbreviations: MRI = magnetic resonance imaging, WE = Wernicke’s encephalopathy.
Keywords: cerebral infarction, malnutrition, parenteral nutrition, thiamine, wernicke’s encephalopathy

characterized by a typical triad of altered mental status, ataxia of
gait and ocular sign.[2] Only 16% of WE patients showed the
typical triad syndrome and 19% had no documented clinical
signs.[3] Although the current level of diagnosis and treatment has
improved, there is still a potential underdiagnosis of WE.
WE is commonly caused by chronic alcoholism. Besides, WE
also frequently occurs in people with fasting, starvation,
malnutrition, malignant disease, gastrointestinal disease, and
surgery,[4] bariatric surgery,[5] and hyperemesis gravidarum.[6]
Because stroke can affect the nutritional status of patients,
malnutrition is often observed in such patients,[7] which is a risk
factor for WE. Cerebral infarction, a neurological disease
accompanied with symptoms of disturbance of consciousness
and gait instability, is difficult to differentiate from WE.
However, WE is rarely reported in patients with cerebral
infarction.
Here, we report a case of WE due to malnutrition and
parenteral nutrition in a patient with cerebral infarction.

1. Introduction
Wernicke’s encephalopathy (WE), first described by Carl
Wernicke in 1881, is a severe neuropsychiatric disorder due to
a nutritional deficiency of thiamine (vitamin B1).[1] WE is
Editor: N/A.
The authors have no conflicts of interest to disclose.
a

Department of Nutrition, the First Hospital of Shanxi Medical University,
Department of Nutrition and Food Hygiene, School of Public Health, Shanxi
Medical University, c Department of Geriatrics, the First Hospital of Shanxi
Medical University, Taiyuan, Shanxi, China.
b

∗

Correspondence: Ping Sun, Department of Nutrition, the First Hospital of Shanxi
Medical University, Jiefangnanlu Street No.85, Taiyuan 030001, Shanxi, China
(e-mail: sunping888@126.com).

Copyright © 2020 the Author(s). Published by Wolters Kluwer Health, Inc.
This is an open access article distributed under the Creative Commons
Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
How to cite this article: Lian X, Wu M, Fan H, Zhang Y, Sun P. Wernicke’s
encephalopathy due to malnutrition and parenteral nutrition in a patient with
cerebral infarction: a case report. Medicine 2020;99:16(e19799).

2. Case report

Received: 23 May 2019 / Received in final form: 18 January 2020 / Accepted: 4
March 2020

A 65-year-old woman showed weakness of the left limbs,
lethargy and confusion with no obvious incentive on November

http://dx.doi.org/10.1097/MD.0000000000019799

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13th, 2017, so she visited a primary hospital and was diagnosed
with cerebral infarction by brain magnetic resonance imaging
(MRI). She experienced nausea and vomiting intermittently, even
developed into poor appetite. Then intravenous hydration was
administered and the specific condition was not clear, but the
treatment produced little effect. Finally, the patient hospitalized
in the Department of Geriatrics of our hospital on December
20th, 2017. At the time of admission, the height of the patient was
158 cm, the weight was 50.0 kg and the BMI was 20.0 kg/m2. Her
weight had fallen by 15 kg for about a month. The NRS2002
nutritional risk screening tool scored 5 points.[8] She was
diagnosed with malnutrition. She suffered from hypertension for
years and took levamlodipine besylate tablets orally. She also had
a history of type 2 diabetes for more than one year and took
metformin hydrochloride tablets orally. In addition, the patient
had no history of smoking or alcoholism.
The patient cooperated well with the physical examination on
admission. She manifested as the decline in numeracy and
comprehension, right-left disorientation, tiny right horizontal
nystagmus. The left finger-to-nose test was positive, and the heelknee-tibia test could not be completed. Abdominal ultrasonography revealed gallbladder enlargement and the possibility of
cholecystitis with cholestasis. Computerized tomography of the
upper abdomen also showed gallbladder enlargement and
cholestasis. Cardiac ultrasound revealed mild left atrial enlargement, mild mitral incompetence, and aortic sclerosis. Carotid
artery ultrasound indicated bilateral carotid atherosclerosis with
plaque formation. Initial laboratory findings were as follows:
white blood cell count 6.4∗109/L, elevated erythrocyte
(5.66∗1012/L), hemoglobin level 145.0 g/L, platelet count
172∗109/L, alanine aminotransferase level 21U/L, aspartate
aminotransferase level 22U/L, elevated total bilirubin (36.4 m
mol/L), elevated urea nitrogen (9.49mmol/L), creatinine level
61.3 mmol/L, hypokalemia (3.23mmol/L), serum sodium level
(137mmol/L), hypochloremia (96.0mmol/L). The patient received intravenous hydration and symptomatic treatment. She
received ondansetron to improve nausea and vomiting, with no
significant improvement of symptoms. Considering the patient’s
disease status and nutritional status, the patient was finally given
central venous nutrition. Because clinicians lacked systematic
cognition of nutrition therapy, the central venous nutrition given
to the patient only contained 50% glucose injection, compound
amino acid injection (18AA-II), and 20% long chain fat emulsion
injection, which made the nutrition imbalanced and vitamin
deficient.
On January 9th, 2018, the patient was critically ill and
suddenly showed cognitive dysfunction, laloplegia, sleep rhythm
inversion and then developed into somnolence. Bilateral lower
limbs weakness and reduced activity were presented. The muscle
strength of the right limbs was at the 1 level, the muscle tone was
reduced. The heel-knee-tibia test could not be completed and
bilateral babinski signs were positive. Therefore, the suspicion of
a recurrence of cerebral infarction or the occurrence of a new
lesion could not be ruled out. Acute laboratory results revealed
low serum sodium (127mmol/L, normal range: 137–147mmol/L)
and low serum chlorine (96mmol/L, normal range: 99–110mmol/
L) levels, so hyponatremia and hypochloraemia should also be
considered to be involved in altered mental status. Finally, MRI
of the brain revealed abnormal signal in the dorsal thalamus,
mamillary bodies, periaqueductal gray matter, left central
anterioposterior cortex (Fig. 1), which was consistent with the
diagnosis of WE.[4]

After confirmed the diagnosis, the patient received 100 mg of
thiamine intramuscularly 3 times daily for 9 days and then 100
mg of thiamine intramuscularly two times daily for 4 days. At the
same time, the patient asked for consultation of Department of
Nutrition. We firstly recommended a gradual transition from
parenteral nutrition to enteral nutrition to restore her intestinal
function gradually. Considering that she had dysphagia and poor
food intake due to cerebral infarction, we suggested to use an
indwelling nasogastric tube. Initially, she was given partial
parenteral nutrition and partial enteral nutrition for 6 days. That
is 250 mL of compound amino acids (18AA-II) was administered
once daily in partial parenteral nutrition. As for partial enteral
nutrition, the intacted protein-based enteral nutrition powder
was prepared into a nutrition solution with a concentration of
20% to 25%, and pumped into the nasogastric tube at a constant
speed. Then, according to the patient’s gastrointestinal tolerance,
she gradually transitioned to total enteral nutrition, that is, the
compound amino acid injection (18AA-II) was replaced by whey
protein powder. In the first 3 days of the start of nutrition
therapy, she was given 900 kcal of energy and 50 g of protein.
Then, the energy and protein supplements were increased to 1300
kcal and 70 g, respectively. In addition, considering her long-term
poor diet, she was given water-soluble vitamins, fat-soluble
vitamins and trace elements supplements in enteral nutrition.
Interestingly, after regular thiamine and nutritional treatment,
her cognitive impairment, laloplegia and sleep condition
significantly improved within 4 days. Her neurological status
continued to improve and physical activity gradually recovered
within 2 weeks. Subsequently, the patient, whose condition was
relatively stable, was given 10 mg of thiamine orally three times
daily and transitioned from enteral nutrition to food homogenate
(low-salt and low-fat diabetes homogenate). As expected, her
nutrition-related laboratory indicators and electrolytes gradually
returned to normal level. Laboratory data are shown in Table 1.
On January 17th, 2018, the patient was transferred to
Department of Rehabilitation Medicine for further rehabilitation
training, and her muscle strength of limbs increased gradually. As
her swallowing function gradually recovered, the nasogastric
tube was removed and the oral diet was started. The patient
finally achieved the goal of rehabilitation and was discharged on
February 9th, 2018.
The patient provided informed consent for publication of the
case report.

3. Discussion
We report a case of WE in a patient with cerebral infarction,
which is uncommon. In this case, the patient was diagnosed with
anxiety and depression, which resulted in nausea, vomiting and
poor appetite, it was defined as psychogenic nausea and vomiting
and psychogenic poor appetite. Previous studies have shown that
lesions in the right temporal lobe of stroke patients can cause
emotional changes and are related to anxiety and depression.[9]
Thus, in this case, the patient’s temporal lobe infarction caused
anxiety and depression, which further led to nausea, vomiting
and poor appetite. These factors ultimately resulted in malnutrition and thiamine deficiency. The early stages of thiamine
deficiency can inversely cause gastrointestinal symptoms such as
slow gastric emptying, nausea and vomiting.[10] Thus a vicious
circle was formed. Her weight spiraled down. Attributing to
sharp fall in her weight, the patient was diagnosed with
malnutrition. Previous studies have shown that rapid weight
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Figure 1. A. Fluid-attenuated inversion-recovery coronal images showing hyperintense signal alteration at the level of the periaqueductal gray matter and at the
level of the mamillary bodies. B. Diffusion-weighted imaging images showing hyperintense signal alteration at the level of the mamillary bodies and at the level of the
dorsal thalamus. C. Fluid-attenuated inversion-recovery coronal images showing hyperintense signal alteration at the level of the dorsal thalamus. D. Fluidattenuated inversion-recovery coronal images showing hyperintense signal alteration at the level of the left central anteroposterior cortex.

full attention. When patients are diagnosed with malnutrition, a
reasonable and personalized nutrition therapy should be
administered by a professional clinical nutritionist to correct
malnutrition in a timely manner. In this way, somatic
complications caused by malnutrition, such as WE, can be
avoided.
WE is diagnosed primarily by the typical triad syndrome,[15]
but only 16% of WE patients had the typical triad syndrome and

loss and malnutrition can result in WE, and the occurrence of WE
is directly linked to rapid weight loss.[11,12]
Dysphagia is a commonly complaint after strokes. A systematic
review found that the reported incidence of dysphagia was 64%
to 78% with instrumental testing in stroke patients.[13]
Dysphagia can cause severe complications of malnutrition and/
or dehydration in up to 25% of stroke patients.[14] Therefore,
malnutrition in patients with cerebral infarction should be given

Table 1
Change in laboratory data from nutritional intervention to discharge.
Intervention day
Total protein (g/L)
Albumin (g/L)
Urea nitrogen (mmol/L)
Creatinine (umol/L)
Hemoglobin (g/L)
Serum potassium(mmol/L)
Serum sodium(mmol/L)
Serum chlorine(mmol/L)

Pre-intervention

2

3

4

5

7

15

29

Reference range

70.0
44.0
10.08
65.1
144
4.27
127
96.0

61.2
37.7
13.12
72.4
122
4.07
127
93.8

58.0
36.7
9.57
44.3
103
3.50
136
104.0

57.1
34.6
5.17
30.7
97
3.43
142
105.3

–
–
–
–
102
3.04
138
101.0

68.1
34.0
4.42
39.7
104
4.60
141
101.5

72.5
39.2
4.29
42.4
114
3.74
139
100.8

71.4
41.8
6.45
61.3
120
3.88
141
102.1

65–85
40–55
2.8–7.6
49–90
115–150
3.5–5.5
137–147
99–110

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19% had no documented clinical signs.[3] MRI typically show an
high T2 signal in the paraventricular regions of the thalamus, the
hypothalamus, mamillary bodies, the periaqueductal region, the
floor of the fourth ventricle and midline cerebellum, which was
consistent with our report.[16] The sensitivity and specificity of
MRI for diagnosing WE are 53% and 93% respectively, the
positive predictive value of MRI is 89%.[17] The high specificity
can be used to rule out other intracranial pathologies, but the
sensitivity is low. In patients with WE, positive MRI results are
associated with altered mental status, but are not related to the
other two of the typical triads.[11] computerized tomography is
not useful for diagnosing WE.[17] There are the operational
criteria proposed by Caine for the diagnosis of WE, which require
2 of the following 4 signs:

and 1.2 mg/d for women, and increase in children, pregnancy,
lactation, malignant diseases, and the high caloric or high
carbohydrate diet.[16] The body is capable of storing 30 to 50 mg
of thiamine.[21] Because the body’s storage of thiamine are
adequate for up to 18 days.[22] When a healthy individual takes
imbalanced nutrition lasting 2 to 3 weeks, it may result in
thiamine depletion and WE.[16] Vomiting, intravenous glucose
without thiamine and parenteral nutrition are predisposing
factors of WE.[23] Due to prolonged emesis and poor appetite, the
body of the patient was depleted of thiamine. The clinician gave
her intravenous glucose without thiamine and parenteral
nutrition, which aggravated her thiamine deficiency.
WE is a rare neuropsychiatric disorder with specific symptomatic treatment, and thiamine repletion is the only treatment for
WE. Intravenous treatment with either 100 or 200 mg thiamine
has cured WE in non-alcoholics based on many case reports.[4]
According to the European Federation of Neurological Societies
and the Royal College of Physicians, it is recommended to
administer 500 mg of thiamine intravenously three times daily in
alcoholic patients until symptoms of acute WE resolve.[4,24] The
EFNS also recommends that suspected or manifest WE should be
given 200 mg of thiamine 3 times daily and preferably by
intravenous rather than intramuscular route until symptoms and
signs are not further develop.[4] Thiamine should be administered
before any carbohydrate, and a balanced diet should be
established immediately after thiamine.[4] In this case, thiamine
supplementation and balanced nutritional therapy were given
immediately after the diagnosis of WE.
If the diagnosis and treatment are delayed, WE will progress to
chronic Korsakoff syndrome, which is characterized by amnestic
disorder and confabulation.[19] In order to avoid unnecessary
delay, clinicians should administer thiamine at the earliest
awareness of risk factors for thiamine deficiency or suspicion of
WE.[2]
In summary, patients with cerebral infarction often have the
complications of malnutrition, which may result in nutrient
deficiency-related neurological complications, such as WE.
Therefore, it is important to pay close attention to the nutritional
status of patients with cerebral infarction, and correct the
malnutrition reasonably. There were delays in diagnosis and
treatment of WE in this case, suggesting that we could use Caine’s
criteria for early diagnosis. Besides, early recognition and
differential diagnosis of WE in patients with infarction-related
malnutrition are necessary, and early treatment of replete
thiamine supplementation and nutrition support therapy can
reduce the risk of WE and improve the prognosis.

(1) dietary deficiencies,
(2) oculomotor abnormalities,
(3) cerebellar dysfunction, and
(4) either an altered mental state or mild memory impairment.[18]
In a previous systematic review, the use of the criteria in the
diagnosis of WE was found that Caine’s criteria had a higher
sensitivity than the typical triad.[2] In this case report, the patient
had poor appetite because of the onset of cerebral infarction
approximately 1 month before admission. At the time of
admission, she had lost 15 kg of body weight (weight loss rate
was 23.1%), and was diagnosed with malnutrition after a
nutritional assessment, which proved that the condition of
dietary deficiency was existed. In addition, the patient manifested
as tiny right horizontal nystagmus on admission. Therefore,
according to Caine’s criteria, she should be diagnosed with WE at
this point. Her delayed diagnosis might result from the clinicians’
low awareness of these criteria. Achieving the early diagnosis of
WE remains a challenge for clinicians, and the use of Caine’s
criteria could increase the early diagnosis of WE. Besides, the
diagnosis of WE may be masked by other diseases because its
symptoms are common to many illness.[19] Cerebral infarction
can cause the instability of gait, nystagmus (ie, basilar artery
occlusion), disturbance of consciousness, which can also occur in
patients with WE. These symptoms cause cerebral infarction to
be difficult to distinguish from Wernicke’s encephalopathy. WE is
a brain disorder with a clear response to thiamine treatment, but
cerebral infarction does not recover in the short term based on
nutrient supplementation. Thiamine therapy can rapidly improve
ataxia, ophthalmoplegia and nystagmus, as well as confusional
state in patients with WE.[20] It has been reported that eye
movement disorders can be improved after a few hours of
treatment. The recovery of ataxia occurs after a few days. The
changes in mental state tend to improve after 2 to 3 weeks of
treatment.[16] This aspect can be used as a good identification
point between WE and cerebral infarction. Caine’s criteria use the
broadest definition of clinical symptoms rather than the narrower
classic triad, and emphasize the importance of malnutrition.[19]
For patients with cerebral infarction, if there are dietary
deficiencies or malnutrition, preventive thiamine supplementation should be administered to prevent further progression of the
disease. And the level of suspicion for WE should be high in
cerebral infarction patients whose clinical condition may lead to
thiamine deficiency.
Thiamine is an essential water-soluble vitamin. In addition,
thiamine is an essential coenzyme for numerous biochemical
pathways of the nervous system. The Chinese recommended
nutrient intake of dietary thiamine in adults is 1.4 mg/d for men

Acknowledgments
We would like to thank the patient for his informed consent and
contribution to the publication of this case report. We also thank
the doctors of Department of Geriatrics and Department of
Nutrition for their advice and help.

Author contributions
Conceptualization: Ping Sun, Xiaojiao Lian.
Supervision: Xiaojiao Lian, Meng Wu, Haixia Fan, Yi Zhang,
Ping Sun.
Writing – original draft: Xiaojiao Lian.
Writing – review & editing: Xiaojiao Lian, Meng Wu, Ping Sun.
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[14] Rofes L, Vilardell N, Clavé P. Post-stroke dysphagia: progress at last.
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[15] Hutcheon D. Malnutrition-induced Wernicke’s encephalopathy following a water-only fasting diet. Nutr Clin Pract 2015;30:92–9.
[16] Sechi G, Serra A. Wernicke’s encephalopathy: new clinical settings and
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[19] E , I-G , HEK , et al. Wernicke-Korsakoff-syndrome: under-recognized
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[20] Sarayu Vasan AK. Wernicke Encephalopathy. Treasure Island (FL):
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[21] Thomson AGME. Wernicke’s encephalopathy: role of thiamine. Pract
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[22] Tanphaichitr V. Shils MEOJ, Shike M, Ross AC. Thiamin. Modern
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