Severe Exertional Heat Stroke with Intestinal Edema and Concurrent Hippocampal Abnormal Signals and Lacunar Infarction: A Case Report

Abstract

Introduction

Heat stroke is a life-threatening condition characterized by hyperthermia and central nervous system (CNS) dysfunction, and often leads to multiorgan damage. Both intestinal and neurological complications have been individually reported in severe cases of exertional heat stroke (EHS); however, their concurrent presentation is rare.

Case Presentation

We hereby report the case of a 48-year-old man with a history of untreated hypertension, who collapsed when working outdoors in hot and humid weather. He was brought in a comatose condition with hypotension and a core body temperature of 40.6°C. Initial whole-body computed tomography (CT) revealed intestinal edema. Brain CT indicated no abnormalities; however, magnetic resonance imaging (MRI) on Day 3 revealed diffusion-weighted imaging hyperintensities in the bilateral hippocampi and right putamen, consistent with hippocampal ischemia and lacunar infarction. Cognitive assessments using the Mini-Mental State Examination (MMSE), Frontal Assessment Battery (FAB), and Trail Making Test (TMT) identified persistent memory impairment and executive dysfunction. These findings correlated with the MRI report and corroborated the hippocampal and frontal-subcortical involvement. The putaminal infarct was attributed to microvascular vulnerability intensified by dehydration and hypercoagulability.

Conclusion

This is the first reported case of EHS presenting with concurrent intestinal edema, hippocampal abnormalities, and lacunar infarction. Early systemic and neurological imaging, along with detailed neuropsychological assessment, are crucial for identifying the extent of CNS injury. Intestinal edema on early CT imaging may serve as a radiological marker of systemic endothelial injury and potential CNS involvement in severe EHS, thereby alerting clinicians to the possibility of intracranial complications.

Introduction

Heat stroke is a life-threatening condition characterized by a core body temperature that exceeds 40°C and is accompanied by central nervous system (CNS) dysfunction [1–3]. While neurological injuries, including ischemic damage in the basal ganglia and hippocampus are commonly observed to accompany a heat stroke, gastrointestinal manifestations such as intestinal edema are also common occurrences in severe cases [4–6]. However, their direct association and potential interplay with CNS damage have not been sufficiently reported. The current case highlights the importance of identifying the symptoms of intestinal and neurological involvement in cases of severe exertional heat strokes (EHSs) and underscores the role of neuroimaging and systemic assessments in guiding treatment options. To the best of our knowledge, this is the first case study documenting the simultaneous presentation of intestinal edema and abnormal hippocampal signals and acute lacunar infarction in the context of heat stroke.

Case Presentation

A 48-year-old male construction worker with a medical history of untreated hypertension was working outdoors in the month of June, a period of high-temperature and high-humidity season in Japan. On that day, the weather conditions reported were a maximum temperature of 30.0°C, 40% humidity, and a recorded wet bulb globe temperature of 25.1°C. The patient commenced work at 7:00 a.m. and continued working until 1:00 p.m., with very brief rest periods. He started exhibiting signs of disorientation in the afternoon and was emergently transferred to our hospital. At admission, he was diagnosed with a Glasgow Coma Scale (GCS) of 1-1-1 and his pupils were 3.0 mm bilaterally with positive light reflexes. Further examination revealed a blood pressure of 78/46 mm Hg, heart rate of 127 bpm, and bladder temperature of 40.6°C. He did not complain of headache, vomiting, or vertigo throughout his clinical course. There was no evidence of diarrhea, bloody stools, or other gastrointestinal symptoms. Head computed tomography (CT) revealed no abnormal findings; however, a whole-body CT scan revealed fluid retention and edema in the small intestine and colon, which was suggestive of intestinal edema (Fig. 1). Blood tests revealed elevated liver transaminases, increased creatine kinase, and acute kidney injury. White blood cell counts and C-reactive protein levels were within the normal range and coagulation abnormalities were limited to mild thrombocytopenia. Other systemic markers of endothelial dysfunction and intestinal permeability, such as cytokine levels (e.g., interleukin [IL]-6, IL-10, tumor necrosis factor-alpha [TNF-α]) or I-FABP, were not assessed. The D-dimer level was elevated at 0.9 μg/mL, suggesting potential activation of the coagulation cascade. There was no diagnosis of disseminated intravascular coagulation. Blood cultures did not reveal any evidence of a bacterial infection.

Fig. 1.

Initial head and abdominal computed tomography (CT) scan revealing intestinal edema without CNS abnormalities. a Head CT performed on admission revealed no evidence of intracranial hemorrhage or infarction. b Axial and coronal views of abdominal CT scans revealed intestinal wall thickening and fluid retention (white arrows), consistent with intestinal edema. These findings were present despite the absence of gastrointestinal symptoms such as diarrhea or bloody stools, indicating that the systemic vascular permeability changes were related to the heat stroke.

The patient was diagnosed with severe EHS. Immediate treatment included tracheal intubation and cooling measures that included intravenous fluid replacement, cold air therapy, and intravascular cooling catheter placement via the right femoral vein. His body temperature was reduced to below 37.0°C within 1 h.

On Day 2, after an improvement in his consciousness level to GCS 4-4-6, he was extubated; however, he exhibited cognitive dysfunction, primarily characterized by memory impairment, along with symptoms associated with the frontal lobe (Mini-Mental State Examination [MMSE] 19, Frontal Assessment Battery [FAB] 13, Trail Making Test part A [TMT-A]: 42 s, TMT part B [TMT-B]: 127 s). On Day 3, magnetic resonance imaging with diffusion-weighted imaging revealed hyperintensities in the bilateral hippocampi and basal ganglia, particularly the putamen and globus pallidus, together with a subtle lesion in the right internal capsule (Fig. 2). By Day 18, the hippocampal and basal ganglia abnormalities had resolved, leaving only a persistent right internal capsule lesion on FLAIR imaging, which indicated a true lacunar infarction. This concise description clarifies the temporal distinction between transient heat-induced changes and permanent ischemic injury. While his cognitive function improved partially, his memory impairment persisted (MMSE 19, FAB 17, TMT-A: 34 s, TMT-B: 77 s). On Day 22, he was transferred to a rehabilitation hospital with a modified Rankin Scale (mRS) score of 3. He returned to work on Day 52, although mild memory impairment persisted with an mRS score of 1. At a 6-month and 1-year follow-up, the patient remained employed and functionally independent with an mRS score of 1. Although mild memory impairment persisted, there was no deterioration in his cognitive or physical function, suggesting favorable long-term outcomes following EHS with hippocampal injury.

Fig. 2.

Serial brain MRI and cognitive assessments demonstrating reversible hippocampal injury and persistent lacunar infarction Day 3 diffusion-weighted imaging (DWI) and fluid-attenuated inversion recovery (FLAIR) revealed hyperintensities in the bilateral hippocampi and right internal capsule (white arrows). By Day 18, these lesions had resolved except for residual FLAIR hyperintensity in the right internal capsule (white arrowhead), consistent with lacunar infarction. Neuropsychological test scores (MMSE, FAB, TMT-A/B) are shown below. MRA, magnetic resonance angiography.

Discussion

EHS can cause profound neurological and systemic complications resulting from hyperthermia-induced ischemic injury and inflammatory responses [1, 2, 4, 5]. During hyperthermia, blood flow redistribution prioritizes peripheral circulation, which results in reduced cerebral perfusion and causes ischemia in metabolically demanding areas like the hippocampus and basal ganglia [4, 5]. The vulnerability of the hippocampus often results in memory dysfunction. Putamen, which is supplied by small perforating arteries, is at risk of microvascular occlusion in dehydration-induced hypercoagulability [7]. Thus, CNS damage can be concurrently caused by multiple ischemic pathways. Although the patient did not meet the criteria for overt disseminated intravascular coagulation, the D-dimer level was mildly elevated (0.9 μg/mL), suggesting subclinical activation of coagulation and possible endothelial dysfunction. This supports the hypothesis that microthrombosis may have contributed to the observed lacunar infarction.

It is crucial to differentiate true infarcts from reversible ischemic lesions, particularly in deep gray matter regions such as the basal ganglia, where both types of lesions might coexist on diffusion-weighted imaging. In the current case, a true lacunar infarction was supported by the persistent FLAIR hyperintensity in the right internal capsule at follow-up, while the resolution of other lesions underscored the need for serial imaging to avoid overdiagnosis of stroke in heat-related CNS injury.

The patient also exhibited intestinal edema, highlighting systemic endothelial dysfunction. In heat stroke, a widespread injury is caused to vascular endothelium due to hyperthermia. Systemic inflammatory responses triggered by hyperthermia may compromise gut permeability, potentially contributing to intestinal wall edema, facilitating endotoxin entry into the circulation [6]. This process exacerbates systemic inflammation and CNS damage via cytokine-mediated blood-brain barrier disruption. Interestingly, there are reports of similar mechanisms of intestinal dysfunction being observed in patients with severe traumatic brain injury (TBI). The disruption of autonomic regulation, catecholamine surge, and systemic inflammatory responses following TBI can result in impaired gastrointestinal perfusion and enhanced intestinal permeability. The concept of a vulnerable brain-gut axis in neurologically injured patients has further been supported by some animal models, that have demonstrated histological mucosal injury, increased gut permeability, and bacterial translocation following TBI [8, 9]. These parallels indicate that the intestinal edema observed in our patient could not necessarily only reflect systemic hyperthermia-related injury but might also share common pathophysiological pathways with other acute CNS injuries, including TBI. Notably, in heat stroke, intestinal edema was observed before CNS findings on early imaging, raising the clinical implication that gastrointestinal findings may precede intracranial complications. Although inflammatory cytokines were not measured in this case, prior studies have implicated IL-6 and TNF-α in the pathogenesis of endothelial dysfunction and blood-brain barrier disruption during EHS. These cytokines promote increased vascular permeability and leukocyte infiltration, potentially contributing to both intestinal edema and cerebral ischemia observed in severe EHS cases [5].

In the current patient, cognitive dysfunction following EHS was not limited to memory impairment but was systematically evaluated using MMSE, FAB, and TMT. Several studies have demonstrated the correlation of performance on these neuropsychological assessments with hippocampal structure and function. MMSE scores have been associated with hippocampal volume, particularly in cases of cognitive decline [10]. Similarly, in patients with early dementia, subtests of the FAB have demonstrated relationships with hippocampal atrophy [11]. TMT-B performance requires cognitive flexibility and working memory and has been linked to hippocampal activity [12]. These correlations support the interpretation that the patient’s cognitive deficits were an indication of the underlying hippocampal involvement caused by heat stroke-related ischemia.

The importance of early cognitive rehabilitation in EHS survivors was highlighted by the partial cognitive recovery despite structural normalization. This case demonstrates that the window of plasticity may remain open even after reversible ischemic injury, and standardized cognitive screening tools such as MMSE, FAB, and TMT could guide the timing and intensity of the neurorehabilitation interventions.

Additionally, certain patient factors, including preexisting conditions such as untreated hypertension, obesity, dehydration, and advanced age, can predispose individuals to heat stroke-related complications [13]. Hypertension, particularly if untreated, can impair cerebral autoregulation and exacerbate vascular dysfunction under hyperthermic conditions. Hypertension is well established as the most common risk factor and etiology of lacunar infarctions. However, in a small subset of cases (less than 5%), lacunar infarcts may arise from alternative causes such as hematologic disorders or infectious/inflammatory arteritis. Given that the underlying etiology can influence therapeutic decisions, an accurate diagnosis is important when evaluating lacunar infarctions [14]. Furthermore, environmental factors such as high ambient temperature and humidity that are commonly experienced in Japan during the month of June, can also contribute to increased susceptibility to heat strokes.

In this case, intestinal edema was identified on initial imaging prior to the emergence of CNS abnormalities. This suggests that intestinal edema may serve as an early radiological marker of systemic endothelial dysfunction and impending neurological injury. Recognizing intestinal edema at presentation could prompt clinicians to implement earlier and more intensive neurological monitoring, consider early brain imaging even in the absence of overt CNS signs, and prepare for timely cognitive rehabilitation strategies. Therefore, gastrointestinal imaging findings in severe EHS cases may have broader implications for anticipating CNS complications and guiding multidisciplinary care.

Limitations

This report describes a single case, which limits the generalizability of the findings. Detailed inflammatory and permeability-related biomarkers were not assessed, and while the patient remained functionally independent up to 1 year, formal neuropsychological testing was not performed after discharge. These factors limit the ability to draw definitive conclusions regarding the mechanisms and long-term neurocognitive outcomes of EHS with intestinal and CNS involvement.

Future studies are warranted to determine whether intestinal edema consistently precedes CNS injury in EHS and whether it can be used as a predictive marker for neurological complications. Larger case series and prospective studies incorporating biomarkers of endothelial dysfunction, gut permeability, and neuroimaging may help establish the clinical utility of abdominal findings in predicting CNS outcomes. Additionally, research into the brain-gut axis in heat-related illness may provide new insights into systemic and neurological interplay.

Conclusion

We have reported a rare case of a patient suffering from severe EHS with intestinal edema, hippocampal injury, and lacunar infarction. The combination of these findings has rarely been reported. An early CT scan indicating intestinal edema might serve as a warning sign for CNS complications. Timely systemic and neurological assessments are critical in treating heat strokes. Further studies are warranted for understanding this multiorgan impact and guiding neurocritical care strategies.

Acknowledgment

The authors would like to thank Enago (www.enago.jp) for the English language review.

Statement of Ethics

Ethical review and approval were not required for this case report in accordance with the institutional and national guidelines. Written informed consent was obtained from the patient for the publication of this case report and accompanying images, in accordance with the CARE guidelines. The CARE Checklist for this case report is provided as an online supplementary file (for all online suppl. material, see https://doi.org/10.1159/000549492).

Conflict of Interest Statement

The authors declare that the report was conducted without any commercial or financial relationships that could be construed as a potential conflict of interest.

Funding Sources

This study was not supported by any sponsor or funder.

Author Contributions

Junzo Nakao: conceptualization, data curation, formal analysis, investigation, visualization, and writing – original draft. Suguru Tanaka, Yu Amemiya, Junji Hatakeyama, Kazuma Yamakawa, and Ryo Hiramatsu: writing – review and editing. Masahiko Wanibuchi and Akira Takasu: supervision and writing – review and editing.

Funding Statement

This study was not supported by any sponsor or funder.

Data Availability Statement

The data supporting the findings of this case report are not publicly available due to patient privacy and ethical restrictions. Any de-identified data relevant to the conclusions of this report may be made available upon reasonable request to the corresponding author, subject to institutional approval.