Rare brain computed tomography image findings of hyperosmolar hyperglycemic state due to acute ischemic stroke-induced stressed hyperglycemia: A case report

INTRODUCTION

Hyperosmolar hyperglycemic state (HHS) is a severe and potentially fatal complication, most often seen in patients with poorly controlled diabetes mellitus (DM).^[1] It is typically triggered by acute illnesses such as stroke, infection, or surgery.^[2] This case report describes the progression of stroke-induced stress hyperglycemia into HHS in an elderly patient with pre-existing DM and hypertension.

CASE REPORT

A 68-year-old woman presented to the emergency department with recurrent seizures beginning that morning. The episodes started as focal jerking of the right limbs, progressing to generalized tonic–clonic convulsions, occurring up to 5 times that day.

On admission, she was alert but had right-sided weakness predating the seizures. There were no sensory deficits or cranial nerve signs. Her history included hypertension and type 2 DM, without prior stroke.

Vital signs were stable, with blood pressure 170/50 mmHg, heart rate 73 bpm, respiratory rate 20, and temperature 36.3°C. Laboratory tests revealed marked hyperglycemia (glucose 839 mg/dL), elevated creatinine (2.5 mg/dL), hyponatremia (sodium 124 mmol/L), potassium imbalance, and mildly raised fibrinogen.

A non-contrast head computed tomography (CT) scan [Figure 1] revealed hyperdense lesions (51 HU) in the right lentiform nucleus, right corona radiata, right caudate nucleus, and left caudate nucleus. To identify the seizure, electroencephalography (EEG) revealed mild diffuse encephalopathy, suggesting global cerebral insult, possibly due to metabolic derangements or acute ischemia.

Close

Figure 1:

Axial non-contrast head computed tomography shows hyperdense lesion in the (a, b, c) right nucleus lentiformis and nucleus caudatus (red arrow) ; (d) right and left nucleus caudatus (red arrows).

Export to PPT

Due to the complexity of the case, a multidisciplinary team of neurologists and endocrinologists provided coordinated care, addressing both the stroke and HHS. This approach supported the patient’s stabilization and clinical improvement.

After 48 h of intensive treatment, including intravenous fluids, electrolyte correction, and insulin therapy, blood glucose levels normalized. Renal function improved, seizures ceased, and right-sided weakness partially resolved.

The stroke was managed conservatively, as thrombolysis or thrombectomy was not indicated. Secondary prevention included antiplatelet therapy, blood pressure control, and statin administration. Early neurorehabilitation was initiated to support motor recovery.

DISCUSSION

Hyperglycemia in acute illness, especially in the context of stroke, can result from stress-induced hormonal changes, such as increased cortisol, catecholamines, and glucagon.^[3] These counter-regulatory hormones promote gluconeogenesis and glycogenolysis, leading to elevated blood glucose levels.^[4] Acute ischemic stroke can also trigger significant inflammation and oxidative stress, further impairing glucose metabolism.^[5] Given the initial CT scan findings and the patient’s severe hyperglycemia, it is likely that metabolic factors played a predominant role in her neurological deterioration.

HHS is defined by severe hyperglycemia (usually >600 mg/dL), marked dehydration, and absent significant ketosis. The patient had negative serum ketones, confirming the absence of significant ketosis. Elevated serum osmolarity and fluctuating potassium levels further aligned with classic HHS presentation. Her hemoglobin A1c (HbA1c) was 17.2%, reflecting chronic poor glycemic control.^[1] Given her renal impairment (peak creatinine 2.5 mg/dL), careful monitoring was crucial to prevent acute kidney injury. Hyponatremia can also occur in HHS due to the effects of hyperglycemia on fluid and electrolyte balance.

These findings aligned with HHS, which is characterized by extreme hyperglycemia, hyperosmolarity, and dehydration without ketoacidosis. Neurological manifestations, including seizures and encephalopathy, can occur during acute hyperglycemic episodes.^[6] The bilateral involvement of the caudate nuclei and right-sided lesions suggested widespread neurological dysfunction, even in the absence of hyperkinetic movements.

The pathophysiology underlying these imaging findings remains debated. The most widely supported hypothesis attributes hyperdensity to reactive astrocyte hydration layers, though others suggest chronic ischemic injury. Stroke-induced hyperglycemia may exacerbate cerebral injury, further contributing to radiological abnormalities.^[7] Although radiological abnormalities may persist longer than clinical symptoms, outcomes generally improve with prompt insulin therapy and glucose normalization.^[8]

In addition, the CT scan demonstrated brain atrophy, a common finding in elderly patients with long-standing diabetes and hypertension. Chronic hyperglycemia is associated with accelerated neurodegeneration, microvascular dysfunction, and cortical atrophy, all of which may increase the risk of seizures and cognitive decline.^[9,10] These imaging findings underscored the role of metabolic and structural brain changes in the patient’s clinical presentation.

This case highlights the progression of stroke-induced stress hyperglycemia to HHS, a potentially fatal complication in elderly patients with underlying diabetes. Acute illnesses, particularly strokes, precipitate stress-induced hyperglycemia, a phenomenon exacerbated by insulin resistance and counter-regulatory hormone secretion.^[3] The stroke likely induced a metabolic cascade, impairing glucose utilization and promoting increased glucose production, culminating in HHS.

Several factors contributed to the patient’s progression to HHS: (1) long-standing poorly controlled diabetes, as evidenced by her elevated HbA1c, increasing her vulnerability to severe hyperglycemia during stress; (2) the severe physiological stress response to stroke, triggering hormonal changes that elevated blood glucose levels and reduced insulin sensitivity;^[3] and (3) global cerebral dysfunction, as indicated by EEG findings, possibly exacerbated by severe hyperosmolarity and dehydration.^[5] The absence of metabolic acidosis or significant ketonuria confirmed HHS rather than diabetic ketoacidosis.

Although the patient recovered from the acute crisis, HHS may worsen neurodegeneration and contribute to vascular cognitive decline in elderly stroke survivors with poorly controlled diabetes. This highlights the need for long-term monitoring of cognitive and neurological function. Future studies should examine how acute hyperglycemia affects stroke outcomes and whether early glucose control improves prognosis.

CONCLUSION

This case illustrates the complex interplay between stroke, stress-induced hyperglycemia, and HHS. Early recognition of this triad, along with timely, aggressive management, is crucial to improving outcomes. Understanding the underlying mechanisms linking acute cerebrovascular events and metabolic disturbances can guide clinicians in anticipating and mitigating life-threatening complications in vulnerable patient populations.