Abstract
We report an 80 year old man in the terminal stage of cancer receiving home care. On the 18th day after starting home care, he experienced a sudden onset of impaired consciousness, unsteadiness of gait, and ophthalmoplegia. Based on the clinical symptoms and a prolonged loss of appetite, Wernicke encephalopathy (WE) was suspected. Thiamine 100 mg was administered intravenously, and 20 minutes later, the patient responded to verbal stimuli. After 1 h, he was able to engage in conversation. When impaired consciousness occurs in cancer patients receiving home care, it is important to consider WE as a differential diagnosis.
Keywords: cancer, home care, terminal care, thiamine deficiency, Wernicke encephalopathy
1. INTRODUCTION
Terminal‐stage cancer patients exhibit various physical and psychological symptoms. 1 Loss of appetite is a common symptom, and one of the conditions associated with this is thiamine deficiency (TD). Tissue storage of thiamine is very limited; thus, depletion of the body stores can occur rapidly after about 18 days of unbalanced nutrition in healthy individuals, and after 3–5 days in patients with chronic diseases.2, 3, 4 The clinical manifestations include mental status changes, ocular abnormalities, and incoordination of gait. Treatment involves the administration of a large dose of thiamine. 5 With early detection and appropriate treatment, the condition can be cured without sequelae. However, the diagnosis of this disease is not easy, and it is often overlooked. 2
As terminal‐stage cancer patients receiving home care often experience a decrease in appetite, it is expected that some will develop TD or WE. However, there has been only one reported case of WE. 6
Herein, we report a terminal‐stage cancer patient receiving home care who developed sudden onset of impaired consciousness. The patient was diagnosed with WE; however, with appropriate treatment, his symptoms improved dramatically in a short time, leading to an enhancement in his QOL in the terminal stage.
2. CASE REPORT
The patient was an 80 year old man who was diagnosed with gastric cancer 4 years previously. He underwent gastrectomy and chemotherapy; however, his physical condition worsened. One month prior, he was hospitalized because of difficulty in moving. However, as he wished to spend the final stage of his life at home, the decision was made to proceed with home care.
On the day of discharge, the home care physician made the initial visit. No impairment of consciousness was observed. Physical findings included a height of 158 cm, a weight of 55 kg (BMI = 22), body temperature of 36.5°C, blood pressure of 122/73 mmHg, pulse rate of 69 bpm, respiratory rate of 20 bpm, and his SaO2 was 97%. In addition, he complained of persistent abdominal pain, dizziness, and fatigue. His appetite was reduced, but he was eating small amounts of his favorite foods. He had no past medical history of psychiatric illness or alcohol or drug abuse. Subsequent home visits were conducted on days 7 and 14, during which no impairment of consciousness was observed, and he was able to walk independently.
On day 18 of home care, he experienced a sudden onset of impaired consciousness, prompting an emergency house call by the home care doctor. The patient's body temperature was 36.2°C, blood pressure 153/53 mmHg, pulse rate 95 bpm, respiratory rate 12 bpm, and SaO2 97%. Neurological findings included an inability to focus the eyes and a lack of response to the physician's questions. The patient had urinary incontinence and was unable to walk. His score on the Glasgow Coma Scale was E3 V2 M1 for a total of six points.
Blood tests were conducted to investigate the cause of the patient's delirium (Table 1). The blood biochemical findings revealed anemia, hypoalbuminemia, liver dysfunction, and elevated ammonia levels, but no abnormalities that could explain the condition were identified. Based on the patient's reduced appetite 3 and the presence of mental status changes, ocular abnormalities, and incoordination of gait, WE was suspected, and blood tests, including the examination of vitamin B1 levels, were performed. Intravenous administration of a combination drug containing 100 mg of vitamin B1, 100 mg of B6, and 1 mg of B12 (Vitamedin®) 7 was provided over 1 h. Further, because of the slightly elevated ammonia level, the patient received the intravenous administration of branched‐chain amino acids (Aminoleban®) 500 mL. 8
TABLE 1.
Patient blood biochemical findings.
| Item | Results | Reference range | Unit |
|---|---|---|---|
| White blood cell count | 7.80 | 3.30–8.60 | ×1000/μ |
| Red blood cell count | 3.23 | 4.35–5.55 | ×million/μ |
| Hemoglobin level | 8.4 | 13.7–16.8 | g/dL |
| Hematocrit | 27.4 | 40.7–50.1 | % |
| Mean corpuscular volume | 84.8 | 83.6–98.2 | fL |
| Mean corpuscular hemoglobin | 26 | 27.5–33.2 | pg |
| Mean corpuscular hemoglobin concentration | 30.7 | 31.7–35.3 | g/dL |
| Platelet count | 159 | 158–348 | ×1000/μ |
| Total protein | 7.0 | 6.6–8.1 | g/dL |
| Albumin | 2.9 | 4.10–5.10 | g/dL |
| AST (GOT) | 29 | 13.00–30.00 | U/L |
| ALT (GPT) | 20 | 10.00–42.00 | U/L |
| Lactate dehydrogenase (LD_IFCC) | 244 | 124.00–222.00 | U/L |
| Alkaline phosphatase (ALP_IFCC) | 203 | 38.00–113.00 | U/L |
| γGTP | 242 | 13.00–64.00 | U/L |
| Creatinine | 0.76 | 0.65–1.07 | mg/dL |
| eGFR(Female) | 74.5 | 60≦ | mL/min/1 |
| Uric acid | 4.0 | 3.7–7.8 | mg/dL |
| Ammonia | 104.0 | 12–66 | μg/dL |
| Blood glucose | 104 | 70.00–109.00 | mg/dL |
| Hemoglobin A1c | 5.3 | 4.90–6.00 | % |
| Sodium | 142 | 138–145 | mEq/L |
| Chloride | 109 | 101–108 | mEq/L |
| Potassium | 4.0 | 3.6–4.8 | mEq/L |
| Calcium | 8.7 | 8.8–10.1 | mg/dL |
| Total bilirubin | 0.7 | 0.4–1.5 | mg/dL |
| CRP | 1.56 | 0–0.14 | mg/dL |
| Activated partial thromboplastin time (APTT) | 34.3 | 24–39 | s |
| Prothrombin time (PT) | 12.8 | 11.0–13.0 | s |
| PT% | 101 | 80–1200 | % |
| PT‐INR | 1.00 | 0.90–1.10 | |
| Fibrinogen | 290 | 200–400 | mg/dL |
| Fibrin and fibrinogen degradation products | 13.8 | 0–4.9 | μg/mL |
| D‐dimer | 5.15 | 0–0.99 | μg/mL |
| Free T3 | 1.94 | 2.15–4.24 | pg/mL |
| Free T4 | 1.35 | 0.90–1.70 | ng/dL |
| TSH | 0.90 | 0.50–5.00 | μIU/mL |
| Vitamin B1 | 19 | 24.0–66.0 | ng/mL |
At ~ 20 min after the start of the intravenous infusion, the patient began to respond to the healthcare provider's voice and was able to shake hands when asked, indicating an improvement in consciousness. One hour later, the patient was able to engage in simple conversation and recognize the attending physician, showing a clear improvement in consciousness. Further, the oral administration of a combination drug containing vitamin B1, B6, B12 (Vitamedin®) was started from that day forward at a dose of 2 two tablets per day.
The following day, the patient was able to walk to the toilet with the help of a family member. Oral intake was also possible, and the patient was able to consume some food, although in small amounts. Three days after the emergency home visit, the patient was found sitting on the edge of his bed during a follow‐up visit. His level of consciousness had returned to previous levels, and the patient was able to take food and medication orally.
Subsequently, it was found that his vitamin B1 level had significantly decreased to 19 ng/mL (normal range 24–66 ng/mL) (Table 1).
The patient showed no further impairment of consciousness disturbances for ~ 3 weeks, but weakness subsequently progressed and the patient passed away on Day 51 of home care.
3. DISCUSSION
We observed WE in a patient receiving terminal‐stage home care.
The trigger for the diagnosis was the acute onset of impaired consciousness, in this case delirium. As delirium is an acute brain dysfunction caused by some underlying factor, it is essential to conduct a thorough investigation to identify the cause. 9 There has only been one reported case of WE in a terminally ill cancer patient receiving home care. 6 However, among cancer patients admitted to palliative care units, 28% have significantly lowered thiamine levels, 10 and in consideration of the fact that patients receiving end‐of‐life care at home often experience a reduced appetite, it is possible that WE has not been diagnosed in home‐care settings to date.
In the case presented herein, decreased appetite was the key to diagnosis; however, in patients in a critically ill condition, the thiamine requirement increases, 4 and this may have contributed to disease onset.
In conclusion, when delirium is diagnosed in patients receiving home care, it is necessary to include WE in the differential diagnosis with the aim of improving the patient's QOL. Further, it is important to consider the possibility of WE because of vitamin B1 deficiency being misdiagnosed as terminal delirium.
AUTHOR CONTRIBUTIONS
Minoru Saiki: Writing – original draft; writing – review and editing; conceptualization; investigation; resources. Mayumi Ishida: Conceptualization; writing – original draft; writing – review and editing; investigation; methodology. Yoshitaka Ooya: Conceptualization; writing – review and editing; investigation. Nozomu Uchida: Conceptualization; investigation; writing – review and editing; project administration. Hideki Onishi: Conceptualization; writing – original draft; writing – review and editing; project administration.
CONFLICT OF INTEREST STATEMENT
Authors declare no conflict of interests for this article.
CONSENT FOR PUBLICATION
Written informed consent was obtained from the patient for publication of this case report.
ETHICS STATEMENT
We got written informed consent from the patient. Our institution do not require Ethics Approval for case report.
ACKNOWLEDGMENTS
This work was supported by JSPS KAKENHI Grant Number 19K11722.
Saiki M, Ishida M, Ooya Y, Uchida N, Onishi H. Wernicke encephalopathy observed in a cancer patient receiving terminal‐stage home care. J Gen Fam Med. 2025;26:626–629. 10.1002/jgf2.70050
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