Neurocritical Care Society Presidents

NCS Presidents

  Name Years served
1 Thomas P. Bleck, MD 2002-2004
2 Michael N. Diringer, MD 2004-2007
3 Cherylee W. J. Chang, MD 2007-2009
4 Stephan A. Mayer, MD 2009-2011
5 Gene Sung, MD 2011-2013
6 J. Claude Hemphill III, MD 2013-2014
7 Romergryko G. Geocadin, MD 2014-2015
8 Edward Manno, MD 2015-2016
9 Michel T. Torbey, MD, MPH, FAHA. FCCM, FNCS 2016-2017
10 Gretchen M. Brophy, PharmD, BCPS, FCCP, FCCM, FNCS 2017 to current

NCS Presidents (MS Word format)


Reference: (2019). Past Presidents – Neurocritical Care Society. [online] Available at: [Accessed 17 May 2019].


Neurocritical Care Society Annual Meetings

Neurocritical Care Society was formed in 2002 with Dr. Thomas P. Bleck as the founding president.  Here is a listing of the dates of the NCS Annual Meetings from 2003 onwards.  I’m missing 2004 – so anyone who knows when and where the second annual conference (2004) was held, message me.

 Dr. Thomas Bleck


1st – 2003 – First annual conference, Phoenix, Arizona

2nd – 2004 – ????

3rd – 02/25-27/2005 Hilton Scottsdale Resort and Villas, Scottsdale, Arizona

4th – 11/4-5/2006, Baltimore, MD

5th – 11/2-3/2007 – Rio Suite Hotel & Casino, Las Vegas, Nevada

6th – 10/23-25/2008 Doral Resort, Miami, Florida

7th – 11/11-14/2009 – Hilton New Orleans Riverside, New Orleans, Louisiana

8th 09/15-18/2010 San Francisco Marriott Marquis, San Francisco, California

9th – 09/21-24/2011 Hilton Montreal Bonaventure Montreal, Canada

10th – 10/4-7/2012 Realizing the Vision Sheraton Denver Downtown Hotel Denver, Colorado

11th – 10/1-4/2013 Enhancing Best Practices Worldwide, Philadelphia Marriott Downtown, Philadelphia PA

12th – 09/11-14/2014 Improving Outcomes Through Interdisciplinary Collaborations The Westin Seattle, Seattle Washington

13th – 10/7-10/2015 Scottsdale, Arizona

14th – 09/15-18/2016, Together We Move Forward, Gaylord National Resort and Convention Center, National Harbor, MD, Gaylord National Harbor

15th – Oct, 2017 Hilton Waikoloa Village, Hawaii, the Big Island Wakoloa Hawaii

16th – Without Borders – Boca Raton, Florida

17th – 10/15-18/2019 Vancouver Convention Center, Vancouver, British Columbia, Canada

18th 09/22-25/2020 Phoenix Convention Center, Phoenix, Arizona

Guidelines for DVT Prophylaxis in Neurocritical Care (from NCS)

DVT Chemoprophylaxis Guideline Recommendations (summary) from the Neurocritical Care Society (published in 2016).



  1. We recommend initiating VTE pharmacoprophylaxis as soon as is feasible in all patients with acute ischemic stroke. (Strong recommendation and high-quality evidence)
  2. In patients with acute ischemic stroke and restricted mobility, we recommend prophylactic-dose LMWH over prophylactic-dose UFH in combination with IPC. (Strong recommendation and high-quality evidence)
  3. Due to insufficient evidence, the panel could not issue a recommendation regarding the use of CS for VTE prophylaxis although their use does not appear to be harmful.
  4. In stroke patients undergoing hemicraniotomy or endovascular procedures, we suggest the use of UFH, LMWH, and/or IPC for VTE prophylaxis in the immediate postsurgical or endovascular epoch except when patients have received rTPA, in which case prophylaxis should be delayed 24 h. (Weak recommendation and low-quality evidence)


  1. We recommend the use of IPC and/or GCS for VTE prophylaxis over no prophylaxis beginning at the time of hospital admission. (Strong recommendation and high-quality evidence)

  2. We suggest using prophylactic doses of subcutaneous UFH or LMWH to prevent VTE in patients with stable hematomas and no ongoing coagulopathy beginning within 48 h of hospital admission. (Weak recommendation and low-quality evidence)

  3. We suggest continuing mechanical VTE prophylaxis with IPCs in patients started on pharmacologic prophylaxis. (Weak recommendation low-quality evidence)



  1. We recommend VTE prophylaxis with UFH in all patients with aSAH (Strong recommendation and high-quality evidence) except in those with unsecured ruptured aneurysms expected to undergo surgery. (Strong recommendation and low-quality evidence)

  2. We recommend initiating IPCs as VTE prophylaxis as soon as patients with aSAH are admitted to the hospital. (Strong recommendation and moderate-quality evidence)

  3. We recommend VTE prophylaxis with UFH at least 24 h after an aneurysm has been secured by surgical approach or by coiling. (Strong recommendation and moderate-quality evidence)


  1. We recommend initiating IPC for VTE prophylaxis within 24 h of presentation of TBI or within 24 h after completion of craniotomy as supported by evidence in ischemic stroke and postoperative craniotomy. (Weak recommendation and low-quality evidence)
  2. We recommend initiating LMWH or UFH for VTE prophylaxis within 24–48 h of presentation in patients with TBI and ICH, or 24 h after craniotomy. (Weak recommendation and low-quality evidence).
  3. We recommend using mechanical devices such as IPC for VTE prophylaxis in patients with TBI, based on data from other Neurological injuries such as ischemic stroke. (Weak recommendation and low-quality evidence).


We recommend VTE prophylaxis with either LMWH or UFH upon hospitalization for patients with brain tumors who are at low risk for major bleeding and who lack signs of hemorrhagic conversion. (Strong recommendation and moderate-quality evidence).


  1. We recommend initiating VTE prophylaxis as early as possible, within 72 h of injury. (Strong recommendation and high-quality evidence)
  2. We recommend against using mechanical measures alone for VTE prophylaxis. (Weak recommendation and low-quality evidence)
  3. We recommend LMWH or adjusted dose UFH for VTE prophylaxis as soon as bleeding is controlled. (Strong recommendation and moderate-quality evidence)
  4. If VTE prophylaxis with LMWH or UFH is not possible, we suggest mechanical prophylaxis with IPC. (Weak recommendation and low-quality evidence)


  1. We recommend using prophylactic doses of UFH (bid or tid) LMWH, or fondaparinux as the preferred method of VTE prophylaxis. (Strong recommendation and moderate-quality evidence)
  2. We recommend using IPC for VTE prophylaxis for patients in whom the bleeding risk is deemed too high for pharmacologic prophylaxis. (Strong recommendation and moderate-quality evidence)
  3. We suggest combining pharmacologic and mechanical VTE prophylaxis (with IPC) in patients with neuromuscular disease. (Weak recommendation and low-quality evidence)
  4. We suggest using GCS only for VTE prophylaxis in patients in whom neither pharmacologic prophylaxis nor IPC use is possible. (Weak recommendation and low-quality evidence)
  5. We suggest continuing VTE prophylaxis for an extended period of time, at a minimum for the duration of the acute hospitalization, or until the ability to ambulate returns. (Weak recommendation and very low-quality evidence)


  1. Ambulatory back surgery with unique positioning strategies such as prone or kneeling has been associated with zero rates of VTE, and we suggest considering the use of IPC only for VTE prophylaxis in this surgical population. (Weak recommendation and low-quality evidence)
  2. In standard elective spine surgery, we recommend using ambulation with mechanical VTE prophylaxis (GCS or IPC) alone, or combined with LMWH. In patients with increased risk for VTE, we recommend combined therapy with ambulation, GCS or IPC, and LMWH. (Strong recommendation and moderate-quality evidence).
  3. Because of the increased risk of bleeding, we recommend using UFH only as an alternative to other methods of VTE prophylaxis. (Strong recommendation and moderate-quality evidence)


  1. We recommend using IPC with LMWH or UFH. (Strong recommendation and moderate-quality evidence)
  2. We recommend against the routine use of IVC filters in the setting of severe spinal cord injury or complicated spine surgery. (Weak recommendation and low-quality evidence)
  3. We suggest considering a removable prophylactic IVC filter as a temporary measure only in patients with PE and DVT or those with DVT at risk for PE who cannot be anticoagulated. (Weak recommendation and low-quality evidence)


  1. We recommend using IPC with either LMWH or UFH within 24 h after craniotomy. (Strong recommendation and moderate-quality evidence)
  2. We recommend the use of IPC with LMWH or UFH within 24 h after standard craniotomy in the setting of glioma resection. (Strong recommendation and moderate-quality evidence)


  1. We suggest the use of CS and IPC until the patient is ambulatory. (Weak recommendation and low-quality evidence)
  2. We suggest immediate prophylactic anticoagulation with LWMH or UFH. (Weak recommendation and low-quality evidence)


  1. We recommend initiating pharmacoprophylaxis with UFH and/or mechanical VTE prophylaxis with IPC or CS in patients with hemiparesis from stroke or other neurological injury within 24 h if activated prothrombin time is measured. (Weak recommendation and low-quality evidence) If during the procedure rTPA or other thrombolytics are used, then extra caution is advised, and delay of initiation of chemoprophylaxis only for at least 24 h after the procedure should be considered. (Weak recommendation and low-quality evidence)
  2. Patients undergoing elective procedures may not require LMWH or UFH, but may benefit from early ambulation, and/or mechanical prophylaxis with IPC or CS. (Weak recommendation- very low-quality evidence)



Nyquist, P., Bautista, C., Jichici, D., Burns, J., Chhangani, S., DeFilippis, M., Goldenberg, F., Kim, K., Liu-DeRyke, X., Mack, W. and Meyer, K. (2015). Prophylaxis of Venous Thrombosis in Neurocritical Care Patients: An Evidence-Based Guideline: A Statement for Healthcare Professionals from the Neurocritical Care Society. Neurocritical Care, 24(1), pp.47-60.


Isopropanol Ingestion

Interesting case reported in NEJM (Case 13-2019) which reminded me of a similar case I encountered during residency (unexplainable rise in serum creatinine with AGMA in a patient who had a psychiatric disorder).

Case summary, middle-aged male patient admitted for alcoholic intoxication, improving but suddenly presented on day 5 with acute delirium, lethargy, tachycardia, tachypnea and abdominal distensión. Work-up unrevealing. Next morning more awake, then had coffee-ground emesis in the afternoon.

Initial work-up for AMS included (note – nice checklist for AMS)

  1. BMP, fingerstick, UA (no hypo/hyper glycemia, natremia, no hypercalcemia), ammonia
  2. EKG, CXR
  3. CT head – rule out a new anatomical event in CNS (stoke, ICH)
  4. EEG (showed generalized theta slowing, no epileptiform abnormalities) – no obvious seizures or post-ictal state
  5. ABG (AGMA of uncertain cause, metabolic alkalosis from vomiting with respiratory compensation) – no hypoxemia or hypercarbia

Other considerations

  1. empiric treatment with naloxone – no effect
  2. Rule out cardiogenic or septic shock
  3. Large PE (if chest pain, hypoxic, hemodynamic compromise)
  4. Drug or toxin ingestion

The clue to the diagnosis was seen in the ABG (which showed anion gap metabolic acidosis).

Consider 5 categories for AGMA (instead of MUDPILES)

  1. Inborn errors of metabolism (proprionic acidemia, FA oxidation defects, etc.) – present at birth or diagnosed in infancy
  1. Lactic acidosis – labs only measure L-lactate (form produced by humans); D-lactic acidosis can be caused by IM injections with propylene glycol which is metabolized into both D and L-lactate stereoisomers (s.a. Phenobarbital)
  1. Ketoacidosis – alcohol, diabetic, starvation ketoacidosis
  1. Renal failure – retention of H+ ions and anions (sulfate, phosphate, irate)
  1. Drug or toxin ingestion -long list of substances; methanol, ethylene glycol, chronic acetaminophen ingestion (5-oxoproline acidosis), isopropyl alcohol

What happened? Patient ingested hand sanitizer which contains isopropanol. This leads to urine ketones (alcohol is metabolized into acetone) and causes severely altered mental status.

How to test? Blood volatile substances screening – which is a gas chromatography-based test which detects presence of toxic alcohols (s.a. Acetone, methanol, ethanol, isoproanol).

Tests came back negative for isopropanol but positive for acetone. Why? Isopropanol is metabolized to acetone by alcohol dehydrogenase, a ketone that does not undergo further oxidation by aldehyde dehydrogenase. Isopropanol has short half-life of 3-7 hours. Acetone has longer half-life (>20 hours)

Diagnosis? Isopropanol intoxication (rapid onset inebriation followed by hemorrhagic gastritis, hallmark feature is ketones in urine and serum without metabolic acidosis)


Fenves, A., Mojtahed, A., Nisavic, M. and Massoth, L. (2019). Case 13-2019: A 54-Year-Old Man with Alcohol Withdrawal and Altered Mental Status. New England Journal of Medicine, 380(17), pp.1657-1665.

Serum Alcohol Level

Our labs report ETOH level as mg/dL (i.e. x1000 of g/dL). See two tables below – which may be helpful to determine if ETOH is cause of altered mental status.

Also, ETOH metabolic rate is about 20 mg/dL/hour. This formula can be useful to calculate the peak ETOH levels. For example, a patient who comes in with ETOH level of 136 mg/dL who stopped drinking 10 hours ago probably had a peak ETOH level of 336 mg/dL (10 hours x 20mg/dL/hr = 200mg/dL).


Fenves, A., Mojtahed, A., Nisavic, M. and Massoth, L. (2019). Case 13-2019: A 54-Year-Old Man with Alcohol Withdrawal and Altered Mental Status. New England Journal of Medicine, 380(17), pp.1657-1665.

Elshiere, et al. Serum alcohol levels correlate with injury severity and resource utilization. South African Journal of Surgery.

Noninvasive ICP Monitoring with Transcranial Doppler Ultrasonography

Interesting case report published in Neurocritical Care Journal describes the use of TCDs in a patient where invasive ICP monitoring was contraindicated.

TCD can measure cerebrovascular hemodynamic parameters that can serve as indirect marker for trends in ICP and cerebral perfusion.

Some common TCD variables include blood flow velocities s.a. peak systolic veolocity (PSV), end-diastolic velocity (EDV), mean flow velocity (MFV) and pulsatility index (PI).

PI is the difference between systolic and diastolic flow velocities divided by the mean velocity. It measures variability of blood velocity and describes distal cerebrovascular resistance.

Normal TCD waveform shows low resistance pattern with sharp systolic upstroke and slow diastolic decay.

With increasing ICP:

  1. Cerebral vessel compliance decreases
  2. Increased resistance to flow – high PI
  3. Waveform shows sharper systolic decay, low EDV, decreased amplitude

TCD waveform analysis + trends in MFV and PI can estimate ICP.

In the case report, the TCD changes with increasing ICP are as follows:

  • normal MFV, high PIs, waveform with rapid systolic decay (concerning for increased ICP, no hemodynamic compromise)
  • Higher PI, sharper waveform, lower MFV (suggests increasing R to flow, evolving hemodynamic compromise)
  • ICP-lowering therapies able to show improvement in waveforms
  • Eventually, waveform shows improved compliance, MFV, PIs – sedation weaned

Continuous TCD measurements may help measure trends in cerebral hemodynamics and compromise of flow.


Ghoshal, S., Gomez, J. and Sarwal, A. (2019). Noninvasive ICP Monitoring by Serial Transcranial Doppler in Coagulopathic Patient. Neurocritical Care.