Multimodal monitoring
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I will be giving high-impact, rapid-fire talks on assessing stroke symptoms, using EEG after acute brain injury, and advanced multimodality monitoring
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Multimodal monitoring
- 1. Multimodality Monitoring By Brandon foreman md @neurollama
- 2. a) Why MMM is better than a single measurement for inferring brain injury patterns? b) What are multimodality measurements that can be used clinically? c) What is the literature on safety and utility? >Objectives
- 6. Fly by sight Fly by gauges
- 9. Parenchyma, 1200 cc CSF, 150 cc Blood, 150 cc >Pressure Ko 2013
- 10. Ko 2013,Aries 2012 ICPICP r = PRx >Pressure 0 5 10 15 20 25 30 35 40 45 50 0 20 40 60 80 100 Mean Arterial Pressure ICP(mmHg) 0 5 10 15 20 25 30 35 40 45 50 0 20 40 60 80 100 Mean Arterial Pressure ICP(mmHg)
- 11. PbtO2 >Metabolism Rosenthal 2008, De Georgia 2014
- 15. >MMM ICP + PbtO2 + Temp rCBF dEEG
- 16. >MMM
- 19. 193 MONTHS LATER
- 20. >end
Editor's Notes
- 39 y/o s/p MVC, initial GCS 10->8T; now HD9 c/b ARDS and ICP
- “The ICP came down to 13”
- This is YOU about to take care of a patient
- In patients who are awake, you use your clinical acumen to detect clinical changes and treat your patient. But in a comatose patient, you don’t have those cues and you have use the tools you DO have.
- But no single measurement gives you the entire picture about whats happening with the 1984 300zx. Multimodal monitoring then is simply a way of putting together multiple measurements in order to infer where our care is going and what’s happening to the brain tissue. The key is to do this in a rational way.
- Definition of Multimodality Monitoring Multiple sources of information integrated and interpreted to provide more complete information regarding about an organ system. Central Use of Multimodality Neuromonitoring The prevention or detection and management of secondary brain injury. Not every hospital can perform MMM on individual patients but insights from MMM may be generalizable to your resus goals for patients with similar injuries.
- Pressure refers really to PERFUSION PRESSURE. This is the amount of forward pressure necessary to maintain blood flow against resistance. That resistance is what is inferred by the “intracranial pressure” concept that most of us are familiar with. If the resistance is high, the perfusion is low. When the pressure is high for longer periods of time, it might be analogous to a low-flow state, such as hypoperfusion in sepsis. This relationship was made clear by Guiza et al when they found that in N=261 adults, the amount of pressure/time stratified the odds for poor outcome. Shorter time and higher pressure and longer time at even acceptable pressure could increase the odds for poor outcome by a factor of nearly 4. Everyones familiar with BEST:TRIP, the study of N=324 sTBI age >12 in South America. This study randomized to goal-directed protocol based on clinical exam and imaging vs. goal-directed protocol based on an ICP value (goal<20 mmHg). Results suggested more days of brain-specific tx in the non-ICP group (4.8 vs. 3.4; p=0.002), but no difference in 6-mo mortality (44% vs. 39%; p=0.40) after controlling for age and injury severity. But there were problems: 44% one or both pupils unreactive; no rehab after discharge; 1-2% EVD rate. Caution with interpreting the results of this study. Currently the BTF Guidelines suggest with Class IIa evidence the use of ICP monitoring in select patients with sTBI.
- So what’s the input pressure? It’s the mean arterial pressure. The brain normal has a stably low resistance pressure but we’re all familiar with the wide range of MAPs that patients exhibit – how does the brain maintain regular flow? Through autoregulation – that is, pressure-flow regulation. CBF = CPP*pi*r^4 / 8*viscosity*length Because CBF is related to CBV and therefore intracranial volume and pressure, you can use it to map the response of the ICP to the MAP, a correlation coefficient knows as the PRx. In a study by Aries, et al in N=327 patients with TBI, 70% had an optimal CPP wherein this PRx value was minimized. 50% of non-survivors were treated <CPPopt (p<0.01, univariate) and there was a significant association with mortality and with morbidity > +/- 10mmHg outside of the optimum. Go below this and you risk losing blood flow -> ischemia.
- Ultimately, CMRO2 = CBF *AVDO2, which suggests that the measurement of tissue oxygenation is really related to flow and oxygenation, however changes in the oxygen extraction fraction of the brain tissue itself can change the brain tissue oxygen. Either way, this measurement has been well-studied and is entering Phase III clinical trials. In a systematic review of 3 studies in TBI; n=150, OR 4.0 for non-survival with PbtO2<10 (Maloney-Wilensky 2009). In prospective studies to target PbtO2 after TBI, the first included N=145; trend at 3 months with 79% good outcome vs. 61% control (p=0.09; McCarthy 2009). Most recently, the BOOST II study showed in N=119; reduction in hypoxia from 44% to 15% with trend toward better outcome at 6-months (Okonwko 2017). To increase PbtO2 – Increase CPP (with or without rCBF depending on pressure reactivity), increase vessel radius, or decrease fluid viscosity; alternatively, can try to drive increase dissolved oxygen via supporting oxygen delivery from increasing hgb. Increased PaO2 alone is poorly usable, results in vasoconstriction (Nakjima 1983) or increased lactate and pyruvate (Magnoni 2003) with no increase in CMRO2 (Diringer 2007)
- Markers: Pyruvate, Lactate, Glucose, Glycerol, Glutamate Brain is 2% body weight yet makes up 20% of total O2 consumption. In a retrospective observational cohort of n=223 patients, LPR was found to best correlate with mortality and unfavorable outcome with an optimal cutpoint of 25 mg/dL (Timofeev 2011). Others have found similar results (Zeiler 2017 meta-analysis). Persistent lactate elevations predict frontal atrophy (Vespa 2008). Bottom line: avoid hypoglycemia and maintain both brain tissue oxygenation and perfusion pressure Glucose <80 mg/dL leads to cerebral hypoglycemia Maintain 120-180 mg/dL (intermediate range)
- Definition of Multimodality Monitoring Multiple sources of information integrated and interpreted to provide more complete information regarding about an organ system. Central Use of Multimodality Neuromonitoring The prevention or detection and management of secondary brain injury.
- When we looked at our first N=43 (mean age 41.6+/-17.5 years) we were able to use MMM starting a median 12.5 (9.0-21.4) hours from injury for mean of 94.3+/-50.5 hours. 72% in right frontal lobe (31/43) All modalities monitored in 90.7% (39/43) Only n=1 (2.4%) had significant tract hemorrhage (non-operative) Median lag from placement to reliable PbtO2 8.3 (4.0-19.8) hours
- 21 y/o s/p high-speed MCC Initial post-resus GCS 6T Initial CT with likely DAI Initially admitted to SICU An MRI was performed confirming diffuse axonal injuries. He was still in the SICU; someone began talking with the parents about potentially withdrawing care.
- MMM Placed 51 hours from injury, PTD2.
- MMM Placed 51 hours from injury, PTD2.
- MegaMan2