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Richard Choi, DO

Follow @rkchoi

Sep 25 • 20 tweets • 13 min read

Get ready for a wild ride! We will be going down a 🐰🕳 and 🔎 multiple issues along the way. Buckle up! As always, all cases deidentified and never published while admitted. #tweetorial #neurotwitter #medtwitter #FOAMed #MedEd #Neurology
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Middle aged person with opioid abuse, bipolar, hip abscess, who p/w dysarthria, 🤢🤮. Patient is admitted and has sudden change in MS, undergoes stroke alert. CT with mild ventriculomegaly but no other acute process
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Blood🩸 cultures return with GPC in pairs and clusters 🦠 and vancomycin is started. They remain altered and repeat CT head 2 days later now shows worsening hydrocephalus (🧠💧) with transependymal flow. Cultures finalize to MRSA.
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Remember that transependymal edema occurs when the intraventricular pressure is higher than surrounding tissue and CSF starts to push through the ependymal lining of the ventricles.

https://twitter.com/vmargar/status/1160804049312190466?s=20&t=-L89QUfLwlgWpg2_zP-dFw

They undergo MRI L spine, T1 post gad representative images shown. Patient has diffuse enhancement of cauda 🐴 and subdural empyemas
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They undergo MRI brain, T1 post gad representative images shown. Patient with meningitis, ependymitis and ventriculitis & known communicating 🧠💧 (for the difference between communicating and non-communicating (aka obstructive) hydro, see:

https://twitter.com/StefanTigges/status/1516046390916308993?s=20&t=-L89QUfLwlgWpg2_zP-dFw

)
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So it seems they have a florid MRSA infection of the 🧠 leading to the 🧠💧. But MRI of the 🧠 also shows small ischemic strokes in multiple territories (DWI shown)
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They undergo ventriculostomy placement. CSF analysis supports this with 64 WBC, 46 RBC, protein 58, Glucose 42, 51% neutrophilic. What is going on???
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Patient undergoes CT/A/V given these strokes are of unclear etiology and this shows severe vasospasm in all arteries, and no venous sinus thrombosis and a developing right parietal area of suspected ischemia! 😵‍💫😵🥴
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Patient undergoes angiogram which confirms severe diffuse vasospasm. They receive intraarterial verapamil and balloon angioplasty to MCA/ACA/BA. Daily TransCranial Dopplers (TCDs) and nimodipine are started.
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The vasospasm pathophysiology in meningitis is even less well understood than in SAH, but is related to NO, endothelin-1, IL1, IFN g and TNF (see pubmed.ncbi.nlm.nih.gov/25610703/).
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Management is largely driven by SAH protocols, with BP augmentation and CCB form the core of this management (see oatext.com/treatment-of-v…) as well as endovascular management, though in some cases, revascularization has been used (see: ncbi.nlm.nih.gov/pmc/articles/P… )
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What do you do now?
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We throw the kitchen sink. She receives IT vancomycin and nicardipine. We start vasopressors to augment her BP. Her TCDs trend up over the next several days. She is requiring multiple pressers, and her BP drops every time she receives nimodipine. What do you do?
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Remember from Physics that flow is proportional to radius to the 4th power, so any changes in radius will have significant implications in velocity to maintain flow, and this is the principle applied when we monitor velocities with TCDs.
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There is a retrospective review demonstrating that when patients get > of their nimodipine as scheduled, their outcomes are better, but this is retrospective: pubmed.ncbi.nlm.nih.gov/26690937/. Meanwhile 2D echo and TEE negative for vegetations.
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They self d/c’d the ventric after about 15 days but fortunately did not develop further 🧠💧. They gradually improved but had a challenging dispo due to the IVDA history. They went to rehab after 2 months with residual aphasia (receptive>expressive) and generalized weakness.
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