RESUMO
Background: Cerebral microdialysis (CMD) is an FDA-approved multimodal invasive monitoring technique that provides local brain metabolism measurements through continuous interstitial brain fluid sampling at the bedside. The past applications in traumatic brain injury and subarachnoid hemorrhage show that acute brain injury (ABI) can lead to a metabolic crisis reflected by changes in cerebral glucose, pyruvate, and lactate. However, limited literature exists on CMD in spontaneous intracerebral hemorrhage (ICH). Case Description: A 45-year-old woman presented with a Glasgow Coma Scale of 8T and left frontal ICH with a 6 mm midline shift. She underwent craniotomy and ICH evacuation. Intraoperatively, CMD, brain tissue oxygenation (PbtO2), intracranial pressure (ICP), and cerebral blood flow (CBF) catheters were placed, targeted toward the peri-hematoma region. Postoperatively, ICP was normal; however, PbtO2, CBF, glucose, and lactate/ pyruvate ratio were abnormal. Due to concern for the metabolic crisis, poor examination, and hydrocephalus on computed tomography of the head (CTH), she underwent external ventricular drainage (EVD). Post-EVD, all parameters normalized (P < 0.05 on Student's t-test). Monitors were removed, and she was discharged to a nursing facility with a modified Rankin scale of 4. Conclusion: Here, we demonstrate the safe implementation of CMD in ICH and the use of CMD in tandem with PbtO2/ICP/CBF to guide treatment in ICH. Despite a normal ICP, numerous cerebral metabolic derangements existed and improved after cerebrospinal fluid diversion. A normal ICP may not reflect underlying metabolic-substrate demands of the brain during ABI. CMD and PbtO2/CBF monitoring augment traditional ICP monitoring in brain injury. Further prospective studies will be needed to understand further the interplay between ICP, PbtO2, CBF, and CMD values in ABI.
RESUMO
BACKGROUND: Glioblastoma multiforme (GBM) has a dismal prognosis despite aggressive therapy. Initial diagnosis and measurement of response to treatment is usually determined by measurement of gadolinium-enhanced tumor volume with magnetic resonance imaging (MRI). Unfortunately, many GBM treatment modalities can cause changes in tumor gadolinium enhancement patterns that mimic tumor progression. The lack of a definitive imaging modality to distinguish posttreatment radiographic imaging changes (PTRIC), including pseudoprogression and radiation necrosis, from true tumor progression presents a major unmet clinical need in the management of GBM patients. METHODS: The authors discuss current modalities available for differentiating PTRIC and tumor progression, describe development of an animal model of PTRIC, and consider potential molecular and cellular pathways involved in the development of PTRIC. RESULTS: An animal model using glioma cells transfected with a luciferase reporter has been developed, and after conventional GBM therapy, this animal model can be evaluated with posttreatment bioluminescence imaging and various MR tumor imaging modalities. CONCLUSIONS: Posttreatment radiographic changes that mimic tumor progression can influence clinicians to make treatment decisions that are inappropriate for the patient's actual clinical condition. Several imaging modalities have been used to try to distinguish PTRIC and true progression, including conventional MRI, perfusion MRI, MR spectroscopy, and positron emission tomography (PET); however, none of these modalities has consistently and reliably distinguished PTRIC from tumor growth. An animal model using glioma cells transfected with a luciferase reporter may enable mechanistic studies to determine causes and potential treatments for PTRIC.
