A comprehensive view on the consensus statement Multimodality Monitoring in Neurocritical Care


Few days ago a joint commission published a consensus on neuromonitoring in Neurocritical Care. There was no such explicit guideline before. This lead to a wide variety of approaches and opinions how to perform that crucial task. Some of these recommendations were rather surprising for me. An example is the recommendation against the use of serum NSE for prognostication in hypoxic-ischemic encephalopathy in patients treated with therapeutic hypothermia. In the following days I try to comment every subchapter of the consensus agenda. Today I start reviewing the subchapter “Clinical Evaluation”

1. We recommend that assessments with either the GCS (combined with assessment of pupils) or the FOUR score be routinely performed in comatose adult patients with acute brain injury.

The FOUR Score is not widely used in Germany and even among neurologist not wide known. The score is quiet more powerful assessing the comatose patient taking in account the pattern of breathing und pupillar reaction.

2. We recommend using the NRS 0–10 to elicit patient’s self-report of pain in all neurocritical care patients wakeful enough to attempt this. This is the gateway to a concept of analgosedation with a clear emphasis on analgesia.

If you do not asses pain, you don´t treat it proper. Be sure to asses this in a somnolent or even comatose patient. These are the next two points.

3. We recommend in the absence of a reliable NRS patient self-report, clinicians use a behavior-based scale to estimate patient pain such as the BPS or CCPOT.

4. We recommend use of the revised NCS-R to estimate pain for patients with severely impaired consciousness such as VS or MCS, using a threshold score of 4.

I will link all scales used in the show notes.

5. We recommend monitoring sedation with a validated and reliable scale such as the SAS or RASS.

RASS should be the next tool to do a reasonable sedation especially in ventilated patients. In a protocol controlled analgesia and sedation these two parameters should be assessed every shift by the nurse. We should turn our back to a one size fits all analgesia.

6. We recommend against performing sedation interruption or wake-up tests among brain-injured patients with intracranial hypertension, unless benefit out-weighs the risk.

This goes along with my personal experience. Brain injured go freaking if you wham-bam turn off analgesia and sedation. ICP is sure to sky rocket. So this should be a gradual process. I prefer to quarter analgesia and sedation every quarter of an hour and hold this maneuver in case of severe ICP reaction and vegetative instability.

7. We suggest assessment of delirium among neurocritical care patients include a search for new neurologic insults as well as using standard delirium assessment tools.

8. We recommend attention to level of wakefulness, as used in the ICDSC, during delirium screening to avoid confounding due to residual sedative effect. Delirium in NICU is associated with increased mortality and long-term cognitive impairment.

Scores like the CAM-ICU test have been validated for a general ICU population. In one trial the CAM-ICU was feasible only in some patients on a stroke unit. 55% of patients where excluded due to higher NIH stroke scales and lower GCS. Of the remaining patient there was a delirium incidence of 43%. I guess delirium screening should only be performed in awake patients. In particular testing takes time.

Le Roux, Peter, et al., “Consensus summary statement of the International Multidisciplinary Consensus Conference on Multimodality Monitoring in Neurocritical Care.” Intensive care medicine 40.9 (2014): 1189-1209.

Mitasova, Adela, et al., “Poststroke delirium incidence and outcomes: Validation of the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU)*.” Critical care medicine 40.2 (2012): 484-490.


http://www.icudelirium.org/docs/CAM_ICU_training_German.pdf http://geriatriceducation.duke.edu/resources/resource/cam-icu-assessment-demonstration-videos



FOUR Score:








Do it Right – Vancomycin Dosing


  After a discussion at work I’ve been looking to current recommendations for proper vancomycin dosing in the ICU and ER.

Drug monitoring should be performed. Through serum concentrations just before the next dose at steady state are recommended. Steady state is achieved normally just before the fourth dose. The minimum through serum concentration should be above 10mg/L to avoid the resistance and at least moderate concentration at the infection theatre. If you have a MRSA with a Minimal Inhibition Concentration (MIC) of 1mg/L or above minimum through concentrations of 15-20mg/L should be targeted. To achieve optimal through concentrations doses of 15-20mg/kg actual body weight (ABW) should be given every 8-12 hours with normal renal function. In case of a MIC of 2 or above conventional dosing regimes fail. If you have a serious ill patient the authors recommend a loading dose of 25-30mg/kg ABW.  Vancomycin Induced Nephrotoxicity is defined as two or three increases in serum creatinine concentrations (0,5mg/dL or 50% above baseline) after several days of therapy. Frequent monitoring is not recommended if there is no risk for renal failure. The authors suggest a weekly monitoring for stable patients. Every patient should receive at least one through serum level and repeated as deemed clinically appropriate.

So dose right, know your MIC.

Rybak, Michael, et al. “Therapeutic monitoring of vancomycin in adult patients: a consensus review of the American Society of Health-System Pharmacists, the Infectious Diseases Society of America, and the Society of Infectious Diseases Pharmacists.” American Journal of Health-System Pharmacy 66.1 (2009): 82-98.

MarylandCC Project - Vanc & Zosyn is NOT the Answer to Everything

EMCrit – Proper Vancomycin Dosing

PRINCIPLE – First details published

As a part of the poster presentation first details were published.
PRINCIPLE – Predictors of Re-Intubation in Neurological Criticall Ill Planned for Extubation found these predictors and could calculate a significant score to use in daily business. Strengest predictor for itself was tracheal secretion.


We are hoping on an interview with Dr. Steidl.

There is already an article about PRINCIPLE on the site of the Department of Neurology, here is the link.

Awake Hypothermia


Cooling and temperature management are key features of any ICU. NICU tend to cool longer than their counterparts in cardiology1. Also neurologists like their patients awake so that they can perform a neurological examination.
A way to reach that goal is to keep your patient awake in the process of cooling. Kama Guluma2 published in 2006 an article in which he described the feasibility of awake cooling in a small patient collective. He used an endovascular cooling device in 10 ischemic stroke patients. Cooling started as soon as possible. In case of systemic thrombolysis the placement of the femoral iv catheter was performed 30 minutes after completion of the t-PA infusion.
On initiation a meperidine drip was started at 30mg/h. A convective surface warming blanket was applied. 24h of cooling.
Shivering was countered by boluses of merepidine. There was no feeding. There was no significant shivering in the study period.

After all this could be a possible way to cool patients in the near future who received definitive treatment of a large vessel occlusion to prevent cerebral edema and hemorrhagic transformation3.


1.         Kollmar R, Schwab S. Hypothermia and Ischemic Stroke. Current treatment options in neurology 2012.

2.         Guluma KZ, Hemmen TM, Olsen SE, Rapp KS, Lyden PD. A trial of therapeutic hypothermia via endovascular approach in awake patients with acute ischemic stroke: methodology. Acad Emerg Med 2006;13:820-7.

3.         Hong JM, Lee JS, Song HJ, Jeong HS, Choi HA, Lee K. Therapeutic hypothermia after recanalization in patients with acute ischemic stroke. Stroke; a journal of cerebral circulation 2014;45:134-40.



Rebleeding after aSAH – TXA a way to go

Rebleeding after aSAH is a serious problem. Mortality increases in such a case up to 80% (1). Especially ultra-early rebleeding is underestimated (2). So it is reasonable to treat the bleeding. There are basically two methods to perform a definitive bleeding protection. One way to go is the endovascular approach by coiling the aneurysm. The open way done by neurosurgery is clipping the aneurysm.
The decision what way to go should by made in a dialogue between the treating specialities.
In an ideal scenario there would be no delay between diagnosing and treating the aneurysm. But that is not the path we are taking most of the time in a world of limited resources.
An answer is the very detailed guideline of the AHA/ASA for the management of aneursymal subarachnoid haemorrhage (3). They give three conservative recommendations to prevent rebleeding.

1. Between the time of aSAH symptom onset and aneurysm obliteration, blood pressure should be controlled with a titratable agent to balance the risk of stroke, hypertension-related rebleeding, and maintenance of cerebral perfusion pressure (Class I; Level of Evidence B). (New recommendation)

2. The magnitude of blood pressure control to reduce the risk of rebleeding has not been established, but a decrease in systolic blood pressure to <160 mm Hg is reasonable (Class IIa; Level of Evidence C). (New recommendation) 

3. For patients with an unavoidable delay in obliteration of aneurysm, a significant risk of rebleeding, and no compelling medical contraindications, short-term (<72 hours) therapy with tranexamic acid or aminocaproic acid is reasonable to reduce the risk of early aneurysm rebleeding (Class IIa; Level of Evidence B). (Revised recommendation from previous guidelines)

Let us have a look at recommendation three. Antifibrinolytic therapies were tested during the last decades. After all they showed no benefit with the main complication of thromboembolic events. These studies had a maximum of 14d to include a patient to the first dose of TXA (tranexamic acid 4-9g/d) or EACA (epsilon aminocaproic acid 24g/d) and treated the patients up to 6 weeks. For a reduction of rebleeding events of about 50% they suffered for an increase of ischemic events by about 50%. So with no benefit at hand that kind of therapy was dimissed (9).
In 2002 Hillmann et. all. published a prospective randomised trial in which they administered TXA directly after diagnosing an aSAH. They gave 1g immediately and 1g each 6h until aneurysma occlusion or 72h. Tranexamic acid, a synthetic derivative of the amino acid lysine, is an antifibrinolytic agent that acts by binding to plasminogen and blocking the interaction of plasmin(ogen) with fibrin, thereby preventing dissolution of the fibrin clot (4). 254 patients received TXA and 251 placebo. The incidence of rebleeding was reduced from 10,8% to 2,4%. This result were repeated by Harrigan (5) and Starke (6). In the retrospective study ogf Harrigan is of note, three of the five rebleeds never received the drug before they bled.

For the future there is a randomized controlled trial (ULTRA) (7) in the Netherlands. They are looking for potential benefit in preventing rebleeding as well as preventing DINDs. The aim of this study is to investigate whether ultra-early and short-term administration of the antifibrinolytic agent tranexamic acid (TXA), as add-on to standard SAH management, leads to better functional outcome. I await a positive result. Take a look at existing data and you know, it is just a problem of underpowered trials.

Baharoglu et. all. (8) published in September 2013 a chochrane report on TXA in which they not recommended the use in case of SAH. In the end they stated in contrast to the older cochrane report (9) that the ultra early giving of antifibrinolytics shows promise. In their point of view the current level of evidence is not sufficient to use it outside of clinical trials. this is what they actually do (7).

My personal opinion  goes alongside with the AHA/ASA guideline. Especially if you bled under PAH therapy TXA should be administered.

1. Ameen A, Illingworth R. Anti-fibrinolytic treatment in the pre-operative management of subarachnoid haemorrhage caused by ruptured intracranial aneurysm. Journal of Neurology, Neurosurgery & Psychiatry 1981;44:220-6.
2. Fujii Y, Takeuchi S, Sasaki O, Minakawa T, Koike T, Tanaka R. Ultra-early rebleeding in spontaneous subarachnoid hemorrhage. J Neurosurg 1996;84:35-42.
3. Connolly ES, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke; a journal of cerebral circulation 2012;43:1711-37.
4. McCormack PL. Tranexamic Acid. Drugs 2012;72:585-617.
5. Harrigan MR, Rajneesh KF, Ardelt AA, Fisher III WS. Short-term antifibrinolytic therapy before early aneurysm treatment in subarachnoid hemorrhage: effects on rehemorrhage, cerebral ischemia, and hydrocephalus. Neurosurgery 2010;67:935-40.
6. Starke RM, Kim GH, Fernandez A, et al. Impact of a protocol for acute antifibrinolytic therapy on aneurysm rebleeding after subarachnoid hemorrhage. Stroke; a journal of cerebral circulation 2008;39:2617-21.
7. Germans MR, Post R, Coert BA, Rinkel GJ, Vandertop WP, Verbaan D. Ultra-early tranexamic acid after subarachnoid hemorrhage (ULTRA): study protocol for a randomized controlled trial. Trials 2013;14:143.
8. Baharoglu, M. I., Germans, M. R., Rinkel, G. J. E., Algra, A., Vermeulen, M., van Gijn, J., & YBWEM, R. (2013). Drugs for preventing blood clot dissolution (antifibrinolytic therapy) to reduce the occurrence of rebleeding in aneurysmal subarachnoid haemorrhage. Health.
9. Roos, Y. B., Rinkel, G. J., Vermeulen, M., Algra, A., & Van Gijn, J. (2003). Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev, 2.