Targeted Temperature Management After Intracerebral Hemorrhage
| Status: | Recruiting |
|---|---|
| Conditions: | Hospital, Neurology |
| Therapuetic Areas: | Neurology, Other |
| Healthy: | No |
| Age Range: | 18 - Any |
| Updated: | 4/2/2016 |
| Start Date: | September 2012 |
| Contact: | Jennifer Glendening, MSN, RN |
| Email: | jennifer.glendening@jefferson.edu |
| Phone: | 215-955-7962 |
Safety and Tolerability of a Protocol of Targeted Temperature Management After Intracerebral Hemorrhage
Early hematoma growth (HG) after spontaneous intra-cerebral/intra-parenchymal hemorrhage
(IPH) is common and associated with neurological deterioration and poor clinical outcome.
Temperature modulation to hypothermia (Temperature, 32-34°C) has been associated with
reduction or improvement of physiopathologic processes associated with inflammatory
activation and degradation of blood-brain barrier after all types of brain injury. In this
sense, we believe that the initiation of an ultra-early protocol of active temperature
modulation or Targeted Temperature Management (TTM) to mild induced hypothermia (MIH,
32-34°C) may be associated with good safety and tolerability profile, less HG and cerebral
edema after IPH by modulation of systemic and local inflammatory responses, so we
hypothesize that TTM to MIH will be a safe/tolerable and effective therapy to limit HG and
cerebral edema after IPH.
(IPH) is common and associated with neurological deterioration and poor clinical outcome.
Temperature modulation to hypothermia (Temperature, 32-34°C) has been associated with
reduction or improvement of physiopathologic processes associated with inflammatory
activation and degradation of blood-brain barrier after all types of brain injury. In this
sense, we believe that the initiation of an ultra-early protocol of active temperature
modulation or Targeted Temperature Management (TTM) to mild induced hypothermia (MIH,
32-34°C) may be associated with good safety and tolerability profile, less HG and cerebral
edema after IPH by modulation of systemic and local inflammatory responses, so we
hypothesize that TTM to MIH will be a safe/tolerable and effective therapy to limit HG and
cerebral edema after IPH.
In this randomized clinical trial, patients with IPH within 6 hours of onset will be
randomized to one of two study arms. In one arm, patients will have 72 hours of TTM to MIH
(32-34 degree Celcius). In the second arm, patients will have 72 hours of TTM to Normal
Temperature (NT)(36-37 degrees Celcius). Subjects in all arms will otherwise receive
identical therapeutic interventions pre-defined by our local IPH management protocol.
Primary outcomes are examining the frequency of adverse events (AEs) that will be possibly
or probably related to treatment. AEs will be assessed up to 15-days after admission or
discharge if earlier and the frequency of severe adverse events (SAEs) that will be possibly
and probably related to treatment.
SAEs will be assessed up to 90-days.
The secondary outcome measures will be in-hospital neurological deterioration between day
0-7 (decrease in GCS10 in ≥2 points, or increase in the NIHSS11 ≥4 points), in-hospital
mortality, modified Rankin Score [mRS]12 at discharge and 90-days.
To determine whether TTM to MIH can limit HG and cerebral edema, will be examining absolute
change in hematoma between baseline and 24 hours, new or absolute change in IVH between
baseline and 24 hours, the proportion of patients with HG, absolute change in hemostatic
proteins, the absolute change in cerebral edema between baseline and 24, 48,72, and
168-hours, relative change in cerebral edema.
randomized to one of two study arms. In one arm, patients will have 72 hours of TTM to MIH
(32-34 degree Celcius). In the second arm, patients will have 72 hours of TTM to Normal
Temperature (NT)(36-37 degrees Celcius). Subjects in all arms will otherwise receive
identical therapeutic interventions pre-defined by our local IPH management protocol.
Primary outcomes are examining the frequency of adverse events (AEs) that will be possibly
or probably related to treatment. AEs will be assessed up to 15-days after admission or
discharge if earlier and the frequency of severe adverse events (SAEs) that will be possibly
and probably related to treatment.
SAEs will be assessed up to 90-days.
The secondary outcome measures will be in-hospital neurological deterioration between day
0-7 (decrease in GCS10 in ≥2 points, or increase in the NIHSS11 ≥4 points), in-hospital
mortality, modified Rankin Score [mRS]12 at discharge and 90-days.
To determine whether TTM to MIH can limit HG and cerebral edema, will be examining absolute
change in hematoma between baseline and 24 hours, new or absolute change in IVH between
baseline and 24 hours, the proportion of patients with HG, absolute change in hemostatic
proteins, the absolute change in cerebral edema between baseline and 24, 48,72, and
168-hours, relative change in cerebral edema.
Inclusion Criteria:
- spontaneous supratentorial IPH documented by CT scan within 6 hours after the onset
of symptoms and admission to the Neuro-ICU,
- baseline hematoma >15cc with or without IVH
- need for mechanical ventilation
Exclusion Criteria:
- GCS <6
- age <18 years
- pregnancy
- pre-morbid mRS>2
- Do Not Resuscitate (DNR) order "prior" to enrollment
- uncontrolled bleeding of different etiology (trauma, gastro-intestinal bleeding
[UGIB/LGIB]
- planned surgical decompression within 24 hours
- secondary causes of IPH (ischemic stroke, coagulopathy [INR>1.4, aPTT> 1.5 times
baseline, thrombocytopenia platelets <100,000/uL], trauma, AVM, aneurysm, cerebral
sinus thrombosis, or other causes)
- evidence of sepsis
- inability to obtain written informed consent
- participation in another trial
We found this trial at
1
site
Thomas Jefferson University Hospital Our hospitals in Center City Philadelphia share a 13-acre campus with...
Click here to add this to my saved trials
