Posterior Reversible Encephalopathy Syndrome: Pattern on ¹⁸F-Fluorodeoxyglucose Positron Emission Tomography-Computed Tomography Correlated with Magnetic Resonance Imaging in Pediatric Hypertensive Encephalopathy

An 11-year-old female child presented to the pediatric emergency department with acute altered sensorium and multiple episodes of seizures for 1month. On evaluation, she was found to be hypertensive. Further investigations were done for workup of hypertension and associated seizure episodes. Ultrasound abdomen and renal Doppler study revealed normal left kidney and small right kidney with no definite evidence of renal artery stenosis. Computed tomography(CT) angiography revealed evidence of wall thickening and enhancement involving arch and descending aorta. For the evaluation of vasculitis and to look for any seizure foci, whole-body and brain ¹⁸F-fluorodeoxyglucose positron emission tomography-computed tomography (¹⁸F-FDG PET-CT) was planned. Scan revealed hypometabolism in bilateral parieto-occipital region in the axial and sagittal sections [Figure 1a-f, white arrows]. Also noted was diffuse increased FDG uptake in the wall of ascending and arch of aorta and patchy mild FDG uptake in descending aorta. Coronal section showing increased FDG uptake in the ascending aorta is shown in Figure 1g (black arrow), correlating with wall thickening and enhancement in CT angiography (image not shown here), suggesting metabolically active inflammatory involvement in large vessels. To correlate these incidental brain hypometabolism changes, magnetic resonance imaging (MRI) brain was done which revealed edematous cortical gyri in bilateral parieto-occipital lobes in T1 [Figure 2a, red arrow] showing hyperintensity on T2-weighted [Figure 2b, yellow arrow] and fluid-attenuated inversion recovery sequences [Figure 2c and d, white arrows]. No significant restriction of diffusion was seen on diffusion-weighted images [Figure 2e and f]. The overall findings suggested posterior reversible encephalopathy syndrome(PRES) secondary to acute hypertensive encephalopathy in the current clinical scenario.

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Figure 1 Axial and sagittal sections of positron emission tomography and fused ¹⁸F-fluorodeoxyglucose positron emission tomography-computed tomography images (a-f) of brain showing decreased fluorodeoxyglucose uptake in bilateral parietal and occipital lobes (white arrows). Coronal sections of whole-body ¹⁸F-fluorodeoxyglucose positron emission tomography images (g) showing increased fluorodeoxyglucose uptake in relation to ascending and arch of aorta (black arrow), suggestive of metabolically active inflammatory involvement

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Figure 2 Axial T1-weighted image (a) showing edematous cortical gyri in bilateral parieto-occipital lobes (a, red arrow) showing hyperintensity on T2 (b, yellow arrow), and fluid-attenuated inversion recovery sequences (c and d, white arrow). There is no restriction of diffusion seen on diffusion-weighted image (e) and apparent diffusion coefficient map (f). These features are suggestive of posterior reversible encephalopathy syndrome

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PRES is a clinicoradiological entity presenting clinically with headache, visual disturbances, seizures, and altered mental status.[12] Underlying causes include hypertension, cytotoxic medications, preeclampsia or eclampsia, autoimmune and systemic conditions, including thrombotic thrombocytopenic purpura, systemic lupus erythematosus, and sepsis.[3] It typically affects parieto-occipital region, but other regions can be involved.[4] Pathogenesis involves dysregulation of normal autoregulatory vasoconstriction, whenever there is sudden increase in systemic blood pressure causing endothelial damage, thrombotic microangiopathy, resulting in fluid leakage from the intravascular space to the interstitial compartment causing vasogenic edema.[567] It is usually a reversible phenomenon and resolves if underlying cause is corrected. Sometimes, it is a diagnostic challenge when it presents with overlapping and atypical symptoms. In the acute setting, CT helps for rapid assessment and also exclude other causes presenting with overlapping symptoms including, cerebral hemorrhage and space-occupying lesions, but CT can also be normal with no significant changes.[8] MRI typically shows bilateral white-matter abnormalities in vascular watershed areas in the posterior regions of cerebral hemispheres, most commonly involving parieto-occipital lobes. Atypical findings including hemorrhage and isolated involvement of the frontal lobes can be seen.[9] Based on these clinical and imaging features, diagnosis of PRES secondary to hypertensive encephalopathy was made. The patient was started on oral steroids and antihypertensive drugs and patient responded well to treatment. She is currently discharged from the hospital in stable condition.