Summary table of reported cases of HHS mimicking stroke
| Case report | Presentation | Imaging | Clinical course | Discussion |
|---|---|---|---|---|
| Bala et al 20207 | A 55-year-old man with a background of T2DM. 72 hours' right homonymous hemianopia BGL 27.6 mmol/L and hyperosmolality. | MRI: subcortical lesion of left occipital lobe. EEG: no abnormality. | Both symptoms and MRI changes (repeat scan at 3 months) resolved following normalisation of glucose. | Theorised that hyperglycaemia and hyperosmolality can result in hypoxic-ischaemic injury to the brain and consequent release of free radicals. |
| Shah et al 20148 | A 67-year-old woman with a background of T2DM, hypertension, hyperlipidaemia and previous ischaemic lacunar stroke. Sudden onset left MCA syndrome: global aphasia, left gaze deviation and right hemiplegia (NIHSS 32). BGL 45.8 mmol/L. | CT of the brain: intracerebral haemorrhage excluded. MRI / MRA / MR perfusion at 6 hours: no diffusion restriction or large vessel occlusion. Small area of increased time to peak and mean transit time with normal cerebral blood volume in left posterior temporal lobe. Non-specific EEG findings (slowing) likely representing hyperglycaemia. MRI with DWI (day 5): no evidence of stroke or pathology consistent with left MCA syndrome. | Thrombolysis given within 3 hours. Treated with IV fluids, nicardipine (for blood pressure control) and insulin. Symptoms improved with reduction of blood glucose: NIHSS of 17 at glucose 23.3 mmol/L. Within 24 hours of admission, full resolution of symptoms. | Resolution of symptoms correlated with normalisation of blood glucose. MR and clinical findings not in keeping with seizure or post-ictal Todd's paresis. MR perfusion findings in conjunction with EEG findings suggest an area of lower perfusion due to lower energy demand, not hypoperfusion. However, the mechanism by which hyperglycaemia causes this is unknown. |
| Our case | A 74-year-old man with a background of T2DM, hypertension, obstructive sleep apnoea, asthma and previous bladder cancer. Collapse, left-sided weakness and slurred speech. BGL 51.0 mmol/L. | CT of the brain at admission: normal. CT of the brain at deterioration: normal (haemorrhage excluded). MRI with DWI (day 4): tiny right parieto-occipital region infarct. | Deterioration early in admission with NIHSS worsening from 3 to 20. Treated for HHS with IV fluids and insulin. Treated for hypertension with GTN infusion. Treated for stroke with aspirin. IV antibiotics (for pneumonia). NIHSS 0 at day 2 of admission. | HHS can accentuate stroke symptoms. HHS can also mimic stroke but important to exclude concurrent ischaemic stroke given prothrombotic state. If possible, urgent CT angiography / MRI could aid thrombolysis decision. |
BGL = blood glucose level; CT = computed tomography; DWI = diffusion-weighted imaging; EEG = electroencephalography; GTN = glyceryl trinitrate; HHS = hyperosmolar hyperglycaemic state; IV = intravenous; MCA = middle cerebral artery; MR = magnetic resonance; MRA = magnetic resonance angiography; MRI = magnetic resonance imaging; NIHSS = National Institutes of Health Stroke Scale; T2DM = type 2 diabetes mellitus.