A primer of neurologic emergencies: summary from the American Thoracic Society Meeting 2016

A primer of neurologic emergencies: summary from the American Thoracic Society Meeting 2016

Luis Fiallo1, Atul Malhotra1, Jamie Nicole LaBuzetta2

1Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, 2Division of Neurocritical Care, Department of Neurosciences, University of California San Diego, La Jolla, CA, USA

Correspondence to: Jamie Nicole LaBuzetta, MD. 200 W Arbor Dr, Mail Code 8465, San Diego, CA 92103, USA. Email: jlabuzetta@ucsd.edu.

Submitted Jun 28, 2016. Accepted for publication Jul 01, 2016.

doi: 10.21037/jtd.2016.07.25

At the American Thoracic Society Meeting in 2016, there were a number of interesting sessions focused on neurological critical care. Tom Bleck, MD provided a lecture, some portion of which is summarized here. In addition we have added information from other talks and recent publications in this area.

Ischemic infarct

As compared with placebo, intravenous alteplase [IV tissue plasminogen activator (tPA)] administered between 3 and 4.5 hours after onset of symptoms significantly improved clinical outcomes in patients with acute ischemic stroke; tPA was more frequently complicated by symptomatic intracranial hemorrhage (1). Regardless of whether IV tPA is administered, in patients with anterior circulation proximal arterial occlusion seen on angiography, a small infarct core, and moderate-to-good collateral circulation, intra-arterial therapy is safe and can be considered (2). In patients undergoing endovascular thrombectomy, studies support decreased mortality and improved functional outcomes (3,4). Early IV magnesium sulfate therapy does not improve outcomes in ischemic stroke (5).

In patients with malignant edema, surgical decompression can be considered within 48 hours of stroke onset potentially to decrease mortality and poor outcome. However, this decision should be one that is made with an emphasis on the patient’s previously understood wishes related to survival and dependency (6).

Intracerebral hemorrhage

There is a trend towards improved functional outcomes with SBP <140 mmHg in INTERACT II (7), though no difference in functional outcome or mortality was seen in ATACH-2 with aggressive SBP management <140 mmHg (8). 3-factor or 4-factor PCC should be administered rather than FFP to patients with vitamin-K antagonist-associated intracranial hemorrhage and INR >1.4 (9).

There is no difference in functional outcome with craniotomy for supratentorial hemorrhage, though there may be a small survival benefit in superficial intracerebral hemorrhage without intraventricular blood (10). Minimally invasive surgery with instillation of tPA decreases hematoma volume and perihematomal edema (11); it is yet unknown whether this approach affects outcomes, but there is an active trial underway. In patients with large intraventricular hemorrhage and small intracerebral hemorrhage meeting appropriate criteria, there was a reported mortality benefit following protocolized administration of intraventricular tPA (CLEAR III preliminary results presented at International Stroke Conference, Los Angeles, 2016).

Aneurysmal subarachnoid hemorrhage (SAH)

Nimodipine should be administered to patients with aneurysmal SAH (12). The addition of statins was not associated with reduction in vasospasm or improvement in outcomes (13). Intravenous magnesium sulfate does not improve clinical outcome after SAH, and therefore routine administration cannot be recommended (14).

Aneurysmal SAH is often complicated by seizures; among patients treated with phenytoin (PHT), burden of exposure to PHT predicts poor neurologic and cognitive outcome after SAH (15).

When symptomatic vasospasm or delayed cerebral ischemia is diagnosed, the initial treatment is hemodynamic augmentation and maintenance of euvolemia. While there are no randomized trials of this intervention, expert consensus is in favor (16).

Traumatic brain injury

In adults with severe diffuse traumatic brain injury, refractory intracranial hypertension is an unfortunate complication. Although early bifrontotemporoparietal decompressive craniectomy decreases intracranial pressure and ICU length of stay, it is associated with more unfavorable outcomes (17). Additionally, therapeutic hypothermia in combination with standard care does not result in better outcomes than with standard care alone (18).

Status epilepticus

A retrospective study of continuous electroencephalography (cEEG) in the medical intensive care unit (MICU) revealed that—especially in patients with sepsis—non-convulsive electrographic seizures and periodic epileptiform discharges were frequent. Both seizures and periodic discharges were associated with poor outcome (19).

For subjects in status epilepticus, intramuscular midazolam is at least as safe and effective as intravenous lorazepam for prehospital seizure cessation (20).

Cardiac arrest

Following cardiac arrest of presumed cardiac etiology, there is evidence to support improved neurological outcomes with mild hypothermia to 32–34 °C (21). However, in a more recent study, unconscious survivors of out-of-hospital cardiac arrest who underwent temperature management with a target temperature of 36 °C had similar mortality and functional outcomes as those with a target temperature of 33 °C (22).

In the era of post-cardiac arrest temperature management, prognostication can be challenging. Multimodal prognostication provides the most reliable prognostication of poor outcome, though prediction of good prognosis remains inaccurate. It is possible to achieve 100% positive predictive value of poor neurological outcome using the combination of absence of EEG reactivity, incomplete recovery of brainstem reflexes in normothermia, and elevated neuron-specific enolase (23).


In summary, the field of neurological critical care has evolved in recent years. A robust body of evidence is being developed to help guide intensivists regarding optimal management of patients. Only with further research will new therapeutic approaches emerge over time.




Conflicts of Interest: Dr. Malhotra is PI on NIH RO1 HL085188, K24 HL132105 and co-investigator on R21 HL121794, RO1 HL 119201, RO1 HL081823. As an Officer of the American Thoracic Society, Dr. Malhotra has relinquished all outside personal income since 2012. The other authors have no conflicts of interest to declare.


  1. Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med 2008;359:1317-29. [Crossref] [PubMed]
  2. Berkhemer OA, Fransen PS, Beumer D, et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med 2015;372:11-20. [Crossref] [PubMed]
  3. Goyal M, Demchuk AM, Menon BK, et al. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med 2015;372:1019-30. [Crossref] [PubMed]
  4. Saver JL, Goyal M, Bonafe A, et al. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke. N Engl J Med 2015;372:2285-95. [Crossref] [PubMed]
  5. Saver JL, Starkman S, Eckstein M, et al. Prehospital use of magnesium sulfate as neuroprotection in acute stroke. N Engl J Med 2015;372:528-36. [Crossref] [PubMed]
  6. Hofmeijer J, Kappelle LJ, Algra A, et al. Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial. Lancet Neurol 2009;8:326-33. [Crossref] [PubMed]
  7. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med 2013;368:2355-65. [Crossref] [PubMed]
  8. Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med 2016. [Epub ahead of print]. [Crossref] [PubMed]
  9. Frontera JA, Lewin JJ 3rd, Rabinstein AA, et al. Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage: A Statement for Healthcare Professionals from the Neurocritical Care Society and Society of Critical Care Medicine. Neurocrit Care 2016;24:6-46. [Crossref] [PubMed]
  10. Mendelow AD, Gregson BA, Rowan EN, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial. Lancet 2013;382:397-408. [Crossref] [PubMed]
  11. Mould WA, Carhuapoma JR, Muschelli J, et al. Minimally invasive surgery plus recombinant tissue-type plasminogen activator for intracerebral hemorrhage evacuation decreases perihematomal edema. Stroke 2013;44:627-34. [Crossref] [PubMed]
  12. Allen GS, Ahn HS, Preziosi TJ, et al. Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med 1983;308:619-24. [Crossref] [PubMed]
  13. Kramer AH, Gurka MJ, Nathan B, et al. Statin use was not associated with less vasospasm or improved outcome after subarachnoid hemorrhage. Neurosurgery 2008;62:422-7; discussion 427-30. [Crossref] [PubMed]
  14. Wong GK, Poon WS, Chan MT, et al. Intravenous magnesium sulphate for aneurysmal subarachnoid hemorrhage (IMASH): a randomized, double-blinded, placebo-controlled, multicenter phase III trial. Stroke 2010;41:921-6. [Crossref] [PubMed]
  15. Naidech AM, Kreiter KT, Janjua N, et al. Phenytoin exposure is associated with functional and cognitive disability after subarachnoid hemorrhage. Stroke 2005;36:583-7. [Crossref] [PubMed]
  16. Connolly ES Jr, 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 2012;43:1711-37. [Crossref] [PubMed]
  17. Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med 2011;364:1493-502. [Crossref] [PubMed]
  18. Andrews PJ, Sinclair HL, Rodriguez A, et al. Hypothermia for Intracranial Hypertension after Traumatic Brain Injury. N Engl J Med 2015;373:2403-12. [Crossref] [PubMed]
  19. Oddo M, Carrera E, Claassen J, et al. Continuous electroencephalography in the medical intensive care unit. Crit Care Med 2009;37:2051-6. [Crossref] [PubMed]
  20. Silbergleit R, Durkalski V, Lowenstein D, et al. Intramuscular versus intravenous therapy for prehospital status epilepticus. N Engl J Med 2012;366:591-600. [Crossref] [PubMed]
  21. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549-56. [Crossref] [PubMed]
  22. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med 2013;369:2197-206. [Crossref] [PubMed]
  23. Oddo M, Rossetti AO. Early multimodal outcome prediction after cardiac arrest in patients treated with hypothermia. Crit Care Med 2014;42:1340-7. [Crossref] [PubMed]
Cite this article as: Fiallo L, Malhotra A, LaBuzetta JN. A primer of neurologic emergencies: summary from the American Thoracic Society Meeting 2016. J Thorac Dis 2016;8(Suppl 7):S576-S578. doi: 10.21037/jtd.2016.07.25

Download Citation