Delirium due to Trousseau syndrome in a patient with cancer and a history of recurrent infection-induced delirium: a case report and mini literature review
Case Report | Psychiatric, Psychological, Social, and Spiritual Issues in Palliative Medicine and Palliative Care

Delirium due to Trousseau syndrome in a patient with cancer and a history of recurrent infection-induced delirium: a case report and mini literature review

Junji Yamaguchi ORCID logo, Ryoichi Sadahiro ORCID logo, Saho Wada, Eri Nishikawa, Kentaro Horiuchi, Tatsuto Terada, Rika Nakahara, Hiromichi Matsuoka ORCID logo

Department of Psycho-Oncology, National Cancer Center Hospital, Tokyo, Japan

Contributions: (I) Conception and design: J Yamaguchi; (II) Administrative support: J Yamaguchi, R Sadahiro, H Matsuoka; (III) Provision of study materials or patients: J Yamaguchi, R Sadahiro, T Terada; (IV) Collection and assembly of data: J Yamaguchi; (V) Data analysis and interpretation: J Yamaguchi; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Junji Yamaguchi, MD, CP. Department of Psycho-Oncology, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. Email: j.yamaguchi.1981@gmail.com.

Background: It is common for patients with cancer to present with delirium during cancer treatment due to various causes, such as infection, electrolyte abnormalities, medications, and brain metastasis. Furthermore, delirium may also occur when a patient with cancer develops Trousseau syndrome. Delirium due to Trousseau syndrome in a cancer patient with a history of repeated delirium might be mistaken for previous episodes, which could lead to overlooking a stroke.

Case Description: A male aged 90 years with gallbladder cancer was admitted to the hospital. During hospitalization, he experienced recurrent episodes of cholangitis and fever, accompanied by delirium. His inflammatory response decreased, and his fever resolved following antibiotic treatment. After recovery, he experienced a loss of appetite, and olanzapine (2.5 mg/day) was started on Day 17 of hospitalization. However, early on Day 21, he suddenly became restless, moaned loudly, and exhibited signs of delirium. Initially, delirium due to olanzapine or reinfection was suspected. However, a new stroke was suspected because of speech impairment as well as the sudden onset of delirium. Head magnetic resonance imaging revealed a fresh stroke in the right basal ganglia, which was identified as the cause of the delirium.

Conclusions: Patients with cancer are more prone to developing stroke due to the hypercoagulable state associated with malignancy. Even in the absence of obvious neurological signs, such as hemiplegia, the possibility of Trousseau syndrome needs to be considered when a patient presents with atypical or sudden-onset delirium.

Keywords: Cancer; delirium; stroke; Trousseau syndrome; case report

Submitted Jul 10, 2025. Accepted for publication Oct 17, 2025. Published online Nov 19, 2025.

doi: 10.21037/apm-25-65

Highlight box

Key findings

• Some cases of Trousseau syndrome develop with delirium.

• Delirium due to Trousseau syndrome in a cancer patient with a history of repeated delirium might be confused with the same delirium as in the past, leading to the risk of overlooking a stroke.

What is known and what is new?

• Trousseau syndrome is generally regarded as unexplained thrombotic events that precede the diagnosis of an occult visceral malignancy or occur concomitantly with the tumor.

• We have experienced a case of Trousseau’s syndrome in which delirium was the initial onset without obvious neurological findings such as paralysis. The possibility of stroke was considered because of the speech impairment and the sudden onset of delirium that was not consistent with the patient’s general condition.

What is the implication, and what should change now?

• Patients with cancer are more prone to developing stroke due to the hypercoagulable state associated with malignancy.

• Even in the absence of obvious neurological signs, such as hemiplegia, the possibility of Trousseau syndrome needs to be considered when a patient presents with atypical or sudden-onset delirium.

Introduction

Patients with cancer sometimes experience delirium due to various factors during treatment. Early detection of prodromal symptoms of delirium has been demonstrated to reduce symptom severity (1,2), and the importance of early intervention for delirium in patients with cancer has been emphasized (3). The diverse causes of delirium in patients with cancer include electrolyte abnormalities, medications, infections, or brain metastases, each requiring different treatment approaches. Therefore, accurate identification and classification of the underlying cause of delirium are essential for the safe continuation of cancer therapy. Repeated episodes of delirium are occasionally observed in some patients with cancer. Specifically, delirium often recurs and is prolonged by recurrent infections and associated fever. In such cases, when delirium occurs from a different cause, availability bias might lead medical professionals to attribute the delirium to the same cause as before, potentially resulting in poor prognosis and even fatal outcomes.

Patients with cancer are known to be prone to stroke due to an elevated hypercoagulable state caused by malignancy (4), commonly referred to as Trousseau syndrome. Trousseau syndrome is generally defined as unexplained thrombotic events that precede the diagnosis of an occult visceral malignancy or occur concomitantly with the tumor (5-8). The main clinical manifestations of Trousseau syndrome include various fatal conditions, including pulmonary embolism, deep vein thrombosis, and ischemic stroke (9,10). Suppose delirium due to Trousseau syndrome newly develops in a cancer patient with a history of recurrent delirium. In such cases, stroke might be overlooked or misdiagnosed, leading to a poor prognosis. Here, we report a case of delirium due to Trousseau syndrome in a patient with gallbladder cancer who had a history of repeated delirium caused by infection and fever. When delirium presents atypically or abruptly, a new stroke needs to be considered as a potential underlying cause. We present this case in accordance with the CARE reporting checklist (available at https://apm.amegroups.com/article/view/10.21037/apm-25-65/rc).

Case presentation

A 90-year-old male with gallbladder cancer (adenocarcinoma, stage IIIA). The patient married in his 20s and has lived with his wife until now, running a rice shop. He had no history of mental illness. At X–3 years, he suffered an epidural hematoma due to a fall, but recovered without any sequelae. However, his cognitive function declined with age, and mild memory loss and inattentiveness were observed.

At Y–3 months (X years), the patient was diagnosed with unresectable gallbladder cancer with liver invasion. At Y months, he was admitted to National Cancer Center Hospital to initiate gemcitabine plus cisplatin plus pembrolizumab therapy. On Day 3 of admission, he developed cholangitis accompanied by fever and became delirious. The delirium, primarily characterized by insomnia and disorientation, persisted with fluctuations but was not severe enough to require psychotropic medications. Blood cultures were positive for Acinetobacter species. Treatment with tazobactam plus piperacillin (13.5 g/day, intravenous, Days 3–5) was initiated, followed by ampicillin plus sulbactam (12.0 g/day, intravenous, Days 6–29). The first percutaneous transhepatic cholangio drainage (PTCD) was performed on Day 5, followed by a stent exchange on Day 11, and a second PTCD on Day 14. Although he gradually recovered and delirium resolved, anorexia and mild nausea persisted. On Day 17, olanzapine (2.5 mg/day, oral) was initiated to treat anorexia and nausea. No apparent mental or physical changes were observed between Days 17 and 20. However, on the night of Day 21, he suddenly became confused and delirious, grunting loudly and having difficulty communicating with others. The patient was considered to be agitated due to delirium, and we, as the liaison team, were asked to manage his psychiatric symptoms. The attending physician requested management for delirium, assuming it was a recurrence of delirium associated with the infection. Initially, we suspected delirium due to infection. However, the patient presented neither fever nor laboratory abnormalities, such as elevated inflammatory markers (Table 1). Although olanzapine-induced delirium was also considered, the delirium did not occur on the day of or the day following olanzapine initiation, making this cause unlikely.

Table 1

Laboratory findings of the patient

Blood test items Days after admission
1 5 12 15 20 21 24 27
WBC (103/μL) 7.3 5.7 8.4 5.0 4.3 3.8 6.0 5.7
RBC (104/μL) 353 332 383 371 343 340 358 352
PLAT (104/μL) 28.0 10.9 15.7 26.5 1.6 4.6 4.7 8.0
BUN (mg/dL) 11 32 20 24 56 55 29 26
eGFR (mL/min/1.73 m2) 61 53 60 65 26 29 60 63
Cre (mg/dL) 0.88 1.00 0.89 0.83 1.91 1.73 0.90 0.85
AST (U/L) 38 97 32 26 41 35 77 50
ALT (U/L) 34 70 39 30 45 39 94 86
Na (nmol/L) 137 134 136 137 137 140 142 142
K (nmol/L) 4.2 4.3 5.0 4.3 3.8 3.8 3.6 3.8
Ca (mg/dL) 8.5 7.6 7.4 7.2 7.0 7.3 7.4 7.2
Alb (g/dL) 3.3 2.4 2.3 1.9 1.4 1.9 2.2 2.0
CRP (mg/dL) 0.25 22.86 10.33 11.94 6.31 4.37 0.81 0.50
D-dimer (μg/mL) – – – – – 3.5 5.4 –
PT-INR 1.11 1.2 – – – 1.36 1.27 –
APTT (s) 29.7 33.4 – – – 51.6 37.9 –

On Day 21, delirium developed despite a decreasing trend in the inflammatory response, while blood coagulation abnormalities also developed. These findings are consistent with the clinical course of a new stroke. Alb, albumin; ALT, alanine aminotransferase; APTT, activated partial thromboplastin time; AST, aspartate aminotransferase; BUN, blood urea nitrogen; Ca, calcium; Cre, creatinine; CRP, C-reactive protein; eGFR, estimated glomerular filtration rate; K, potassium; Na, sodium; PLAT, platelet; PT-INR, prothrombin time-international normalized ratio; RBC, red blood cell; WBC, white blood cell.

Upon examination, although no obvious neurological signs such as paralysis were observed, the patient suddenly became unable to communicate and only grunted loudly with restlessness, leading us to suspect a disturbance of consciousness and speech impairment due to a possible stroke. Additional laboratory findings on Day 21 showed abnormalities in the blood coagulation system, including D-dimer (Table 1), after the onset of delirium and speech impairment. These results and the very sudden onset of clinical symptoms led us to suspect the possible brain stroke related to cancer. Head magnetic resonance imaging (MRI) revealed a fresh cerebral infarction in the right basal ganglia, consistent with Trousseau syndrome (Figure 1). In this case, we did not attempt echocardiography or carotid ultrasound. This is partly because the patient’s psychiatric symptoms were relatively unstable, which made it hard for him to stay still during the examination. Given the patient’s very advanced age, we determined that the benefits of administering sedation with psychotropics for the examination were minimal. Fortunately, his level of consciousness spontaneously improved within approximately half a day. Due to his advanced age and the small size of the infarct, anticoagulation therapy and surgery were not performed, and the patient was carefully monitored. He recovered without sequelae and underwent physical rehabilitation, which further gradually improved his general condition. The patient affirmed that he had no mental problems, and no specific psychiatric changes were noted. On Day 38 of hospitalization, he was discharged, and home visit treatment was initiated (Figure 2).

Figure 1 A head MRI of the patient was taken on Day 21 of hospitalization. A new stroke (indicated by the arrow) is recognized in the right basal ganglia with the development of delirium and aphasia, which is regarded as a Trousseau syndrome. MRI, magnetic resonance imaging.
Figure 2 Clinical course of the patient. PTCD, percutaneous transhepatic cholangio drainage.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

According to the latest review by the American Heart Association/American Stroke Association, stroke includes both ischemic and thrombotic conditions (11). Ischemic stroke is defined as “An episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction.” (11). On the other hand, a stroke caused by cerebral venous thrombosis is defined as “Infarction or hemorrhage in the brain, spinal cord, or retina due to thrombosis of a cerebral venous structure. Symptoms or signs caused by reversible edema without infarction or hemorrhage do not qualify as stroke.” (11). While the definitions share many similarities, as shown in Table 1, we observed an increase in D-dimer levels along with the onset of impaired consciousness and speech difficulties. Additionally, given the mechanism by which Trousseau syndrome arises from tumor-induced thrombosis, we estimate that this case is more likely to be derived from a stroke due to cerebral venous thrombosis.

In this case, the stroke was fortunately small, and although the patient initially presented with delirium, his level of consciousness spontaneously recovered over time. However, delirium caused by Trousseau syndrome may be easily mistaken for delirium due to other causes. If a new stroke is overlooked, patients may be at increased risk of a poor prognosis. In addition, both drug-induced and stroke-related delirium often have a relatively rapid onset. In this case, the absence of apparent neurological signs such as paralysis, combined with the use of olanzapine, complicated the diagnosis process. Although this was not a case of olanzapine-induced delirium, several such cases have been reported (12-14). The anticholinergic effects of olanzapine have been suggested as a possible mechanism (15), and the disturbance of the limbic system neurotransmitters is speculated to be involved (16).

Cancer often causes hypercoagulable states and is a risk factor for venous and arterial thromboembolism (4,6-8). Cerebral infarction has been noted to be the most common consequence of embolism and is primarily associated with hypercoagulability and nonbacterial thromboendocarditis (4). Furthermore, patients with cancer have been noted to develop an increased rate of short-term recurrence of stroke and sudden death (4). The accumulation of intratumoral regulatory T cells via neuropilin-1 signaling has been suggested as an important molecular mechanism contributing to the exacerbation of ischemic brain damage in cancer-bearing mice (17).

A study involving 956 lung cancer patients showed that the median age for Trousseau syndrome was 65 years (18). The most common histological type was adenocarcinoma (78.9%), and the brain was the most frequent site of thromboembolism (84.2%) (18). Additionally, high survival rates after the onset of Trousseau syndrome were linked to non-adenocarcinoma histology, epidermal growth factor receptor gene mutations, and treatment with immune checkpoint inhibitors (18). Another study involving 20 pancreatic cancer patients found that common clinical manifestations of Trousseau syndrome included paralysis (31%), language disorder (31%), and difficulty walking (11%) (19). The median survival time from the onset of Trousseau syndrome was 2.0 months (19).

Venous thromboembolism is one of the most serious clinical outcomes associated with Trousseau syndrome, and its frequency has been noted to vary depending on the cancer type. Specifically, the cancers with the highest incidence rates were reported as follows: pancreatic (8.1%), renal (5.6%), ovarian (5.6%), lung (5.1%), and gastric (4.9%) cancers (8). This suggests that the frequency of Trousseau syndrome also varies depending on the type of cancer, and the possibility of Trousseau syndrome should be especially suspected when atypical delirium occurs in these cancers. Typical clinical manifestations of stroke in patients with cancer are altered mental status and unilateral hemiplegia (20). Additionally, multiple arterial infarcts are more common than single arterial infarcts (20), and elevated D-dimer levels are associated with cerebral infarction (4,20,21). Furthermore, some cases of Trousseau syndrome-induced delirium are accompanied by psychiatric symptoms, and the combination of perospirone and memantine was effective (22).

However, in this case, no hemiplegia was noted, and the only obvious neurological symptoms were delirium and speech defects, with no apparent psychiatric symptoms, all of which made the detection of a new stroke difficult. Additionally, the decline in cognitive function in the patient made neurological assessment more difficult.

Generally, delirium following acute stroke is common, occurring in 13–48% of patients (23). Delirium after stroke is more frequent in older patients (24,25), hemorrhagic stroke (24,25), and thalamic stroke (23). Strokes presenting with delirium alone, without obvious neurological signs or symptoms, are rare (26,27), although a notable feature of clinical findings in cancer patients is the high frequency of asymptomatic stroke (21).

In this case, we suspected a new stroke due to the unusual and sudden onset of delirium. The atypical course of the patient, characterized by language impairment and worsening delirium despite decreasing inflammatory markers, along with the absence of other identifiable causes, prompted consideration of delirium secondary to a new stroke. Typically, prodromal symptoms of delirium include sleep disturbance, hallucinations, and irritability (28). However, in this case, these symptoms were absent, and consciousness suddenly deteriorated. Furthermore, despite the onset of delirium, the patient’s most recent laboratory tests were unremarkable, vital signs were stable, and no fever was reported. In contrast, previous episodes of delirium coincided with elevated inflammatory markers and fever associated with exacerbation of cholangitis. However, the abrupt onset of delirium in the context of a stable physical condition deviated from the patient’s prior clinical course, with speech impairment, leading us to suspect delirium related to a new stroke.

There is concern that when delirium develops due to Trousseau syndrome in a patient with a history of recurrent delirium, it might be misattributed to the same previous cause, increasing the risk that a new stroke will be overlooked. This suggests that failure to properly assess the cause of delirium in patients with cancer may have potentially fatal consequences. Furthermore, stroke in patients with cancer has been associated with a notable incidence of recurrent stroke, transient ischemic attacks, and increased mortality (29). Therefore, prompt investigation for a new stroke is warranted when a patient with cancer presents with sudden delirium that deviates from their typical clinical course.

Conclusions

We believe it is important to exclude Trousseau syndrome as a differential diagnosis for delirium in patients with cancer, since they are at a high risk of stroke due to increased blood coagulation. Since overlooking this risk can be fatal, the accumulation of more case reports of stroke-induced delirium in patients with cancer is necessary.

Acknowledgments

The authors thank the patient and his family for their participation in this study.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://apm.amegroups.com/article/view/10.21037/apm-25-65/rc

Peer Review File: Available at https://apm.amegroups.com/article/view/10.21037/apm-25-65/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://apm.amegroups.com/article/view/10.21037/apm-25-65/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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Cite this article as: Yamaguchi J, Sadahiro R, Wada S, Nishikawa E, Horiuchi K, Terada T, Nakahara R, Matsuoka H. Delirium due to Trousseau syndrome in a patient with cancer and a history of recurrent infection-induced delirium: a case report and mini literature review. Ann Palliat Med 2025;14(6):617-623. doi: 10.21037/apm-25-65

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