Diabetic ketoacidosis (DKA) induced cerebral edema complicating small chronic subdural hematoma/hygroma/ at Zewuditu memorial hospital: a case report

Background While both DKA & CSDH/subdural hygroma/ are known to cause significant morbidity and mortality, there is no a study that shows the role & effect of DKA on CSDH/subdural hygroma/ & vice versa to authors’ best knowledge; hence this work will show how important relation does exist between DKA & CSDH/ hygroma. Case summary This study highlights the diagnostic & management challenges seen for a case of a 44 years old female black Ethiopian woman admitted with a diagnosis of newly diagnosed type 1 DM with DKA + small CSDH/subdural hygroma/ after she presented with sever global headache and a 3 month history of lost to her work. She needed burrhole & evacuation for complete clinical improvement besides DKA’s medical treatment. Conclusion DKA induced cerebral edema on the CSDH/subdural hematoma/ can have a role in altering any of the parameters (except the thickness of CSDH) for surgical indication of patients with a diagnosis of both CSDH +DM with DKA. Hence, the treating physicians should be vigilant of different parameters that suggests tight brain &/ cerebral edema (including midline shift, the status of cisterns, fissures & sulci) and should not be deceived of the thickness of the CSDH/subdural hygroma/alone; especially when there is a disproportionately tight brain for the degree of collection. Whether DKA induced cerebral edema causes a subdural hygroma is unknown and needs further study.

Evaluation and Prediction of Post-stroke Cerebral Edema Based on Neuroimaging

Cerebral edema is a common complication of acute ischemic stroke that leads to poorer functional outcomes and substantially increases the mortality rate. Given that its negative effects can be reduced by more intensive monitoring and evidence-based interventions, the early identification of patients with a high risk of severe edema is crucial. Neuroimaging is essential for the assessment and prediction of edema. Simple markers, such as midline shift and hypodensity volume on computed tomography, have been used to evaluate edema in clinical trials; however, advanced techniques can be applied to examine the underlying mechanisms. In this study, we aimed to review current imaging tools in the assessment and prediction of cerebral edema to provide guidance for using these methods in clinical practice.

Microvascular Dysfunction in Blood-Brain Barrier Disruption and Hypoperfusion Within the Infarct Posttreatment Are Associated With Cerebral Edema

Background and Purpose: Factors contributing to cerebral edema in the post-hyperacute period of ischemic stroke (first 24–72 hours) are poorly understood. Blood-brain barrier (BBB) disruption and postischemic hyperperfusion reflect microvascular dysfunction and are associated with hemorrhagic transformation. We investigated the relationships between BBB integrity, cerebral blood flow, and space-occupying cerebral edema in patients who received acute reperfusion therapy. Methods: We performed a pooled analysis of patients treated for anterior circulation large vessel occlusion in the EXTEND-IA TNK and EXTEND-IA TNK part 2 trials who had MRI with dynamic susceptibility contrast-enhanced perfusion-weighted imaging 24 hours after treatment. We investigated the associations between BBB disruption and cerebral blood flow within the infarct with cerebral edema assessed using 2 metrics: first midline shift (MLS) trichotomized as an ordinal scale of negligible (<1 mm), mild (≥1 to <5 mm), or severe (≥5 mm), and second relative hemispheric volume (rHV), defined as the ratio of the 3-dimensional volume of the ischemic hemisphere relative to the contralateral hemisphere. Results: Of 238 patients analyzed, 133 (55.9%) had negligible, 93 (39.1%) mild, and 12 (5.0%) severe MLS at 24 hours. The associated median rHV was 1.01 (IQR, 1.00–1.028), 1.03 (IQR, 1.01–1.077), and 1.15 (IQR, 1.08–1.22), respectively. MLS and rHV were associated with poor functional outcome at 90 days ( P<0 .002). Increased BBB permeability was independently associated with more edema after adjusting for age, occlusion location, reperfusion, parenchymal hematoma, and thrombolytic agent used (MLS cOR, 1.12 [95% CI, 1.03–1.20], P =0.005; rHV β, 0.39 [95% CI, 0.24–0.55], P <0.0001), as was reduced cerebral blood flow (MLS cOR, 0.25 [95% CI, 0.10–0.58], P =0.001; rHV β, −2.95 [95% CI, −4.61 to −11.29], P =0.0006). In subgroup analysis of patients with successful reperfusion (extended Treatment in Cerebral Ischemia 2b-3, n=200), reduced cerebral blood flow remained significantly associated with edema (MLS cOR, 0.37 [95% CI, 0.14–0.98], P =0.045; rHV β, −2.59 [95% CI, −4.32 to −0.86], P =0.004). Conclusions: BBB disruption and persistent hypoperfusion in the infarct after reperfusion treatment is associated with space-occupying cerebral edema. Further studies evaluating microvascular dysfunction during the post-hyperacute period as biomarkers of poststroke edema and potential therapeutic targets are warranted.

Spontaneous intracranial hypotension complicated by diffuse cerebral edema and episodes of severely elevated intracranial pressure: illustrative case

BACKGROUND Spontaneous intracranial hypotension (SIH) is a well-documented condition that typically follows a defined clinical course. Previously published studies describing the pathophysiology of SIH have demonstrated extensive evidence of low intracranial pressure (ICP) driving the clinical features of the condition. Through lumbar puncture and use of intracranial monitoring devices, however, both low and normal cerebrospinal fluid (CSF) pressures have been documented. This report outlined and discussed the unique finding of elevated ICP associated with clinical features of SIH. OBSERVATIONS Here, the authors presented a case of a patient with spontaneous spinal CSF leak who developed tonsillar herniation, cerebral edema, and subsequent episodes of elevated ICP. Although more diverse presentations of SIH are being reported, the authors believed the case to be unique because SIH was accompanied by elevated ICP. LESSONS This case adds to the growing body of literature surrounding SIH by demonstrating that patients can develop elevated CSF pressures associated with acute encephalopathy.