Chronic tophaceous gout in a 72-year-old male presenting with fatal hypertensive hemorrhagic stroke: a case report

Abstract

Background

Chronic tophaceous gout is a well-recognized consequence of long-standing hyperuricemia. Although epidemiological evidence increasingly links hyperuricemia with elevated cerebrovascular risk, the co-occurrence of advanced tophaceous gout and fatal hemorrhagic stroke is infrequently reported, particularly from South Asian populations.

Case presentation

A 72-year-old Nepali male with a 15-year history of hypertension and a 12-year history of poorly controlled gouty arthritis presented following a fall with decreased consciousness. He was in hypertensive crisis (200/100 mmHg) with a Glasgow Coma Scale of 11/15 and left-sided hemiparesis. Physical examination incidentally revealed extensive subcutaneous tophi at bilateral elbows, left second metacarpophalangeal joint, bilateral first metatarsophalangeal joints, right Achilles tendon, and bilateral knees. Investigations showed hyperuricemia (serum uric acid 10.2 mg/dL), mildly elevated creatinine (peak 1.8 mg/dL), a normal coagulation profile, and absence of thrombocytopenia (platelets 172,000/μL). HbA1c was 5.1%, excluding diabetes. Neuroimaging confirmed a right thalamic hemorrhage with intraventricular extension. Despite ICU management, he deteriorated neurologically and was discharged against medical advice. He died five days after discharge.

Conclusions

This fatal hemorrhagic stroke occurred in a patient with coexisting advanced tophaceous gout and long-standing hypertension. While the stroke was attributable to hypertensive crisis, the incidental finding of extensive tophi highlights the systemic burden of uncontrolled hyperuricemia. The case underscores the importance of sustained urate-lowering therapy and cardiovascular risk management in patients with gout, and the serious consequences of medication non-adherence.

Background

Hyperuricemia has been increasingly recognized as an independent risk factor for cardiovascular and cerebrovascular disease [1, 2]. A 2025 meta-analysis of 22 prospective studies involving over 770,532 adults found hyperuricemia to be significantly associated with both stroke incidence (pooled RR 1.42; 95% CI 1.31–1.53) and stroke mortality (pooled RR 1.53; 95% CI 1.18–1.99), with a modest but significant association for hemorrhagic stroke mortality (pooled RR 1.13; 95% CI 1.02–1.26) [3]. The proposed mechanisms include nitric oxide depletion, endothelial dysfunction, NLRP3 inflammasome activation, and promotion of oxidative stress [4, 5].

Chronic tophaceous gout, the most advanced stage of gout, represents a visible marker of sustained, inadequately treated hyperuricemia [6]. While the epidemiological link between hyperuricemia and stroke is established, clinical reports documenting the co-occurrence of extensive tophaceous disease and hemorrhagic stroke are sparse. Herein, we describe a case of fatal hypertensive hemorrhagic stroke in a 72-year-old Nepali male in whom advanced tophaceous gout was incidentally detected on physical examination.

Case presentation

A 72-year-old male was brought to the emergency department of Hospital in Chitwan, Nepal, following a witnessed fall at home with subsequent decrease in consciousness. His medical history included systemic hypertension diagnosed 15 years prior and progressive gouty arthritis for 12 years. He had been prescribed febuxostat 40 mg daily, colchicine 0.5 mg daily, and indomethacin, but reported inconsistent adherence throughout his illness. He consumed alcohol occasionally and followed a predominantly non-vegetarian, high-carbohydrate diet.

On arrival, blood pressure was 200/100 mmHg; other vital signs were within normal limits. Neurological assessment revealed a Glasgow Coma Scale (GCS) score of 11/15 (E3V3M5), left-sided hemiparesis, and right-sided facial deviation. Initial laboratory investigations revealed marked hyperuricemia with serum uric acid of 10.2 mg/dL(normal range 3.5–7.2 mg/dL). Additional investigations revealed a serum creatinine of 1.2 mg/dL (rising to 1.8 mg/dL by day 3, consistent with acute-on-chronic renal impairment), blood urea nitrogen of 24.3 mg/dL, and serum sodium of 138 mEq/L. Coagulation profile showed a prothrombin time of 14.7 s and INR of 1.13, excluding a coagulopathic contribution to the hemorrhage. Complete blood count revealed a total platelet count of 172,000/μL and hemoglobin of 12.8 g/dL. Lipid profile showed total cholesterol 170 mg/dL, LDL cholesterol 103.2 mg/dL, HDL cholesterol 35 mg/dL, and triglycerides 159 mg/dL. HbA1c was 5.1% (32.6 mmol/mol), excluding concurrent diabetes mellitus. Thyroid function tests were within normal limits. C-reactive protein was mildly elevated at 6.5 mg/L. The patient had a history of systemic hypertension with documented inconsistent medication adherence; he had no prior stroke or transient ischemic attack. Cardiovascular and respiratory examinations were unremarkable. Echocardiography demonstrated moderate concentric left ventricular hypertrophy, grade I diastolic dysfunction, normal LV systolic function (LVEF 65%), mild tricuspid regurgitation, and mild pulmonary artery hypertension, consistent with long-standing hypertensive heart disease. Physical examination incidentally revealed extensive chronic tophaceous gout with multiple firm, non-tender subcutaneous tophi at olecranon regions, left second metacarpophalangeal joint, bilateral first metatarsophalangeal joints, right Achilles tendon, and bilateral knees (Figs. 1, 2and3). The tophi had been progressively enlarging over several years.

Fig. 1.

Arrow showing Subcutaneous tophi over the bilateral olecranon process and left second metacarpophalangeal joint

Fig. 2.

Arrow showing Tophi at bilateral first metatarsophalangeal joints and right Achilles tendon

Fig. 3.

Arrow showing Tophi at the right knee

Non-contrast CT of the brain confirmed a right thalamic hemorrhage with intraventricular extension (IVH), consistent with a hypertensive bleed at this location. No midline shift or hydrocephalus was documented on initial imaging. MRI was not performed during the admission. The patient was admitted to the intensive care unit under neurosurgery and managed with intravenous mannitol and 3% hypertonic saline for cerebral edema, and aggressive blood pressure control with intravenous labetalol transitioning to oral amlodipine–losartan. Neurosurgical intervention was not pursued given the deep thalamic location and poor neurological baseline.

Over four days, neurological status deteriorated to GCS 8/15. Neurosurgical consultation recommended conservative management given the thalamic location. Despite counseling regarding the guarded prognosis, the family elected to discharge the patient against medical advice (AMA) on nasogastric tube feeding. The patient died five days after discharge (day 9 from presentation) (Table 1).

Table 1.

Clinical timeline of the patient

Time point	Event
15 years prior	Diagnosis of systemic hypertension
12 years prior	Onset of gouty arthritis; prescribed ULT; inconsistent adherence
Day 0	Fall with decreased consciousness; ED: BP 200/100, GCS 11/15, left hemiparesis; extensive tophi incidentally noted; CT: right thalamic hemorrhage with IVH
Days 1–4 (ICU)	IV mannitol, 3% NaCl, labetalol, amlodipine; GCS declines to 8/15
Day 4	Discharged AMA on NG feeding
Day 9	Death confirmed on follow-up

ULT Urate-lowering therapy; ED Emergency department; BP Blood pressure; GCS Glasgow Coma Scale; CT Computed Tomography; IVH Intraventricular hemorrhage; IV Intravenous; AMA Against medical advice; NG Nasogastric

Discussion

The primary cause of stroke in this patient was almost certainly his hypertensive crisis in the context of long-standing, poorly controlled hypertension. Tophaceous gout was an incidental finding on physical examination, not the proximate cause of the hemorrhagic event. We report this case not to claim a causal relationship between tophaceous gout and hemorrhagic stroke, but to highlight two clinically important observations.

First, the presence of extensive tophi across seven anatomical sites served as a visible indicator of years of sustained hyperuricemia and medication non-adherence. While this patient’s stroke was driven by hypertension, epidemiological evidence increasingly supports hyperuricemia as an independent contributor to cerebrovascular risk. Jiang et al. (2025) demonstrated significantly increased stroke incidence and mortality in hyperuricemic individuals [3], and Mendelian randomization studies suggest this association may be partly causal, mediated through nitric oxide depletion and NLRP3 inflammasome activation [4, 5]. In patients with both hypertension and chronic hyperuricemia, these vascular insults may act additively, though establishing individual-level causality from a single case is not possible.

Second, this case illustrates the challenges of chronic disease management in resource-limited settings. Our patient’s inconsistent adherence to prescribed febuxostat and colchicine, a well-documented problem in gout, with non-adherence rates exceeding 50% within the first year of therapy [7] contributed directly to the progression of tophaceous disease over several years [6, 8]. In Nepal, where healthcare infrastructure presents challenges for chronic disease follow-up, advanced tophaceous disease persists at rates rarely seen in high-income countries.

A comparable case was reported by Cardoza and Hoque (2025), describing a 62-year-old male with advanced tophaceous gout discovered incidentally during admission for acute ischemic stroke [9]. Silva Veiga et al. (2024) described an 85-year-old with giant tophaceous gout and a history of prior hemorrhagic stroke [10]. Our case adds to this limited literature a fatal outcome and a South Asian context.

Limitations

This case has several limitations. First, the diagnosis of tophaceous gout was clinical and was not confirmed by polarized light microscopy or synovial fluid crystal analysis; while the clinical picture is highly consistent with tophaceous gout, histological confirmation was not performed. Second, as a single case report, no causal inference can be drawn regarding the relationship between hyperuricemia or tophaceous gout and hemorrhagic stroke; the association between these conditions is epidemiological, not mechanistically established at the individual level. Third, longitudinal cardiovascular and metabolic data were unavailable, including prior serum uric acid trends, duration of hyperuricemia, prior echocardiographic data, and adherence history beyond patient self-report. These gaps limit the completeness of the clinical picture and restrict broader generalizability of the findings.

Conclusion

This case documents a fatal hypertensive hemorrhagic stroke in a 72-year-old male with coexisting advanced chronic tophaceous gout detected incidentally on examination. While the stroke was attributable to hypertensive crisis rather than gout per se, the extensive tophaceous burden reflects the systemic consequences of sustained hyperuricemia and medication non-adherence. Clinicians encountering advanced tophaceous gout should recognize it as a marker of metabolic derangement warranting comprehensive cardiovascular risk assessment, strict blood pressure control, and sustained urate-lowering therapy targeting serum uric acid below 6.0 mg/dL.

Learning points

• Extensive tophaceous gout is a visible marker of chronic hyperuricemia and medication non-adherence, not merely a musculoskeletal problem.

• Hyperuricemia is epidemiologically associated with increased stroke incidence and mortality, though individual-level causality cannot be inferred from case reports.

• Patients with tophaceous gout warrant comprehensive cardiovascular risk assessment, including strict blood pressure control.

• Discharge against medical advice in the setting of cerebral edema carries a high risk of fatal outcome and confounds assessment of disease prognosis.

• Medication non-adherence remains the most important modifiable risk factor for progression to advanced tophaceous gout.

Abbreviations

AKI

Acute kidney injury

AMA

Against medical advice

BP

Blood pressure

BUN

Blood urea nitrogen

CI

Confidence interval

CT

Computed tomography

ED

Emergency department

GCS

Glasgow coma scale

ICU

Intensive care unit

IV

Intravenous

IVH

Intraventricular hemorrhage

NG

Nasogastric

NLRP3

NLR family pyrin domain containing 3

RR

Relative risk

ULT

Urate-lowering therapy

Author contributions

ASK and UKS were involved in the conceptualization and design of the case report. ASK, RD, and AL performed the literature search and drafted the initial manuscript. UKS and NP provided clinical management of the patient and supervised the data collection. NP and ASK performed critical revisions of the manuscript for important intellectual content. All authors read and approved the final manuscript.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Data availability

No datasets were generated or analyzed during the current study.

Declarations

Ethics approval and consent to participate

Our institution does not require ethical approval for reporting individual cases or case series.

Consent for publication

Written informed consent was obtained from the patient's next of kin for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare no competing interests.