Abstract 3942: Mild Controlled Hypothermia Induction is Safe and Feasible for the Treatment of Intracranial Hypertension in Patients with Aneurysmal Subarachnoid Hemorrhage.

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Mohammad Ibrahim ◽  
Mohammad Moussavi ◽  
Elzbieta Wirkowski ◽  
Adel Hanna ◽  
Cecilia Carlowicz ◽  
...  

Introduction Hypothermia has been increasingly used for cerebral resuscitation in comatose survivors of cardiac arrest. A large number of studies have been undertaken in patients with traumatic brain injury to asses the efficacy of hypothermia for reduction of intracranial hypertension. Hypothermia has also been shown to reduce mortality and increase functional outcome if used for longer duration in patients with severe traumatic brain injury. Due to the risk of rebound cerebral edema during re-warming, medical complications and other factors, hypothermia has not been widely utilized for other neurologic catastrophes. To determine the safety and feasibility of hypothermia to treat intracranial hypertension in patients with aneurysmal subarachnoid hemorrhage (SAH), we performed this study. Methods Retrospective analysis was performed on 11 consecutive patients with poor grade (Hunt and Hess IV and V) SAH who had high intracranial pressure that was either non responsive or poorly responsive to conventional methods (head of bed at 30 degrees, sedation, CSF drainage and osmotherapy). All patients had intracranial pressure (ICP) monitoring via an external ventriculostomy drain (EVD) catheter. Hypothermia was induced non-invasively via surface cooling pads (Artic Sun Temperature Management System). Intravenous sedation and paralysis was used via intravenous infusion to control shivering. Hypothermia (target temperature of 32 to 34 degree C) was maintained until ICP normalized. Results Duration of hypothermia ranged from 79 hours to 190 hours. One patient required re-induction due to rebound increase in ICP during re-warming. Modified rankin scale was recorded at 3 month after the ictus. Eight patients (72%) survived with good recovery, one patient (9%) survived with severe disability and two patients (18%) died. The most common side effect was electrolyte imbalance seen in seven patients (63%), thrombocytopenia in three patients (27%), and pneumonia in four patients(36%). All complications were successfully treated and major consequences of complications (bleeding diathesis, septic shock syndrome and death) were not observed in any of these patients. Two patients had decompressive hemicraniectomy prior to hypothermia induction. Out of nine patients who did not undergo hemi-craniectomy, two died and seven did not require surgical intervention after induction of hypothermia. Conclusions Mild hypothermia induction for 72 hours or more for the treatment of intracranial hypertension refractory to other conventional methods in patients with SAH appears safe and feasible. Hypothermia may potentially be an earlier treatment option than currently recommended. This study serves as a template for future efficacy trials.

2017 ◽  
Vol 43 (5) ◽  
pp. E13 ◽  
Author(s):  
Naif M. Alotaibi ◽  
Justin Z. Wang ◽  
Christopher R. Pasarikovski ◽  
Daipayan Guha ◽  
Fawaz Al-Mufti ◽  
...  

Elevated intracranial pressure (ICP) is a well-recognized phenomenon in aneurysmal subarachnoid hemorrhage (aSAH) that has been demonstrated to lead to poor outcomes. Despite significant advances in clinical research into aSAH, there are no consensus guidelines devoted specifically to the management of elevated ICP in the setting of aSAH. To treat high ICP in aSAH, most centers extrapolate their treatment algorithms from studies and published guidelines for traumatic brain injury. Herein, the authors review the current management strategies for treating raised ICP within the aSAH population, emphasize key differences from the traumatic brain injury population, and highlight potential directions for future research in this controversial topic.


2013 ◽  
Vol 71 (10) ◽  
pp. 802-806 ◽  
Author(s):  
Almir Ferreira de Andrade ◽  
Matheus Schmidt Soares ◽  
Gustavo Cartaxo Patriota ◽  
Alessandro Rodrigo Belon ◽  
Wellingson Silva Paiva ◽  
...  

Objective Intracranial hypertension (IH) develops in approximately 50% of all patients with severe traumatic brain injury (TBI). Therefore, it is very important to identify a suitable animal model to study and understand the pathophysiology of refractory IH to develop effective treatments. Methods We describe a new experimental porcine model designed to simulate expansive brain hematoma causing IH. Under anesthesia, IH was simulated with a balloon insufflation. The IH variables were measured with intracranial pressure (ICP) parenchymal monitoring, epidural, cerebral oximetry, and transcranial Doppler (TCD). Results None of the animals died during the experiment. The ICP epidural showed a slower rise compared with parenchymal ICP. We found a correlation between ICP and cerebral oximetry. Conclusion The model described here seems useful to understand some of the pathophysiological characteristics of acute IH.


2020 ◽  
Vol 10 (3) ◽  
pp. 208-216
Author(s):  
David P. Lerner ◽  
Starane A. Shepherd ◽  
Ayush Batra

Hyponatremia is a well-known disorder commonly faced by clinicians managing neurologically ill patients. Neurological disorders are often associated with hyponatremia during their acute presentation and can be associated with specific neurologic etiologies and symptoms. Patients may present with hyponatremia with traumatic brain injury, develop hyponatremia subacutely following aneurysmal subarachnoid hemorrhage, or may manifest with seizures due to hyponatremia itself. Clinicians caring for the neurologically ill patient should be well versed in identifying these early signs, symptoms, and etiologies of hyponatremia. Early diagnosis and treatment can potentially avoid neurologic and systemic complications in these patients and improve outcomes. This review focuses on the causes and findings of hyponatremia in the neurologically ill patient and discusses the pathophysiology, diagnoses, and treatment strategies for commonly encountered etiologies.


2012 ◽  
Vol 117 (4) ◽  
pp. 729-734 ◽  
Author(s):  
Arash Farahvar ◽  
Linda M. Gerber ◽  
Ya-Lin Chiu ◽  
Nancy Carney ◽  
Roger Härtl ◽  
...  

Object Evidence-based guidelines recommend intracranial pressure (ICP) monitoring for patients with severe traumatic brain injury (TBI), but there is limited evidence that monitoring and treating intracranial hypertension reduces mortality. This study uses a large, prospectively collected database to examine the effect on 2-week mortality of ICP reduction therapies administered to patients with severe TBI treated either with or without an ICP monitor. Methods From a population of 2134 patients with severe TBI (Glasgow Coma Scale [GCS] Score <9), 1446 patients were treated with ICP-lowering therapies. Of those, 1202 had an ICP monitor inserted and 244 were treated without monitoring. Patients were admitted to one of 20 Level I and two Level II trauma centers, part of a New York State quality improvement program administered by the Brain Trauma Foundation between 2000 and 2009. This database also contains information on known independent early prognostic indicators of mortality, including age, admission GCS score, pupillary status, CT scanning findings, and hypotension. Results Age, initial GCS score, hypotension, and CT scan findings were associated with 2-week mortality. In addition, patients of all ages treated with an ICP monitor in place had lower mortality at 2 weeks (p = 0.02) than those treated without an ICP monitor, after adjusting for parameters that independently affect mortality. Conclusions In patients with severe TBI treated for intracranial hypertension, the use of an ICP monitor is associated with significantly lower mortality when compared with patients treated without an ICP monitor. Based on these findings, the authors conclude that ICP-directed therapy in patients with severe TBI should be guided by ICP monitoring.


2020 ◽  
Vol 162 (11) ◽  
pp. 2715-2724
Author(s):  
Teemu Luostarinen ◽  
Jyri Virta ◽  
Jarno Satopää ◽  
Minna Bäcklund ◽  
Riku Kivisaari ◽  
...  

Abstract Background To ensure adequate intensive care unit (ICU) capacity for SARS-CoV-2 patients, elective neurosurgery and neurosurgical ICU capacity were reduced. Further, the Finnish government enforced strict restrictions to reduce the spread. Our objective was to assess changes in ICU admissions and prognosis of traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (SAH) during the Covid-19 pandemic. Methods Retrospective review of all consecutive patients with TBI and aneurysmal SAH admitted to the neurosurgical ICU in Helsinki from January to May of 2019 and the same months of 2020. The pre-pandemic time was defined as weeks 1–11, and the pandemic time was defined as weeks 12–22. The number of admissions and standardized mortality rates (SMRs) were compared to assess the effect of the Covid-19 pandemic on these. Standardized mortality rates were adjusted for case mix. Results Two hundred twenty-four patients were included (TBI n = 123, SAH n = 101). There were no notable differences in case mix between TBI and SAH patients admitted during the Covid-19 pandemic compared with before the pandemic. No notable difference in TBI or SAH ICU admissions during the pandemic was noted in comparison with early 2020 or 2019. SMRs were no higher during the pandemic than before. Conclusion In the area of Helsinki, Finland, there were no changes in the number of ICU admissions or in prognosis of patients with TBI or SAH during the Covid-19 pandemic.


2009 ◽  
Vol 4 (1) ◽  
pp. 40-46 ◽  
Author(s):  
Gad Bar-Joseph ◽  
Yoav Guilburd ◽  
Ada Tamir ◽  
Joseph N. Guilburd

Object Deepening sedation is often needed in patients with intracranial hypertension. All widely used sedative and anesthetic agents (opioids, benzodiazepines, propofol, and barbiturates) decrease blood pressure and may therefore decrease cerebral perfusion pressure (CPP). Ketamine is a potent, safe, rapid-onset anesthetic agent that does not decrease blood pressure. However, ketamine's use in patients with traumatic brain injury and intracranial hypertension is precluded because it is widely stated that it increases intracranial pressure (ICP). Based on anecdotal clinical experience, the authors hypothesized that ketamine does not increase—but may rather decrease—ICP. Methods The authors conducted a prospective, controlled, clinical trial of data obtained in a pediatric intensive care unit of a regional trauma center. All patients were sedated and mechanically ventilated prior to inclusion in the study. Children with sustained, elevated ICP (> 18 mm Hg) resistant to first-tier therapies received a single ketamine dose (1–1.5 mg/kg) either to prevent further ICP increase during a potentially distressing intervention (Group 1) or as an additional measure to lower ICP (Group 2). Hemodynamic, ICP, and CPP values were recorded before ketamine administration, and repeated-measures analysis of variance was used to compare these values with those recorded every minute for 10 minutes following ketamine administration. Results The results of 82 ketamine administrations in 30 patients were analyzed. Overall, following ketamine administration, ICP decreased by 30% (from 25.8 ± 8.4 to 18.0 ± 8.5 mm Hg) (p < 0.001) and CPP increased from 54.4 ± 11.7 to 58.3 ± 13.4 mm Hg (p < 0.005). In Group 1, ICP decreased significantly following ketamine administration and increased by > 2 mm Hg during the distressing intervention in only 1 of 17 events. In Group 2, when ketamine was administered to lower persistent intracranial hypertension, ICP decreased by 33% (from 26.0 ± 9.1 to 17.5 ± 9.1 mm Hg) (p < 0.0001) following ketamine administration. Conclusions In ventilation-treated patients with intracranial hypertension, ketamine effectively decreased ICP and prevented untoward ICP elevations during potentially distressing interventions, without lowering blood pressure and CPP. These results refute the notion that ketamine increases ICP. Ketamine is a safe and effective drug for patients with traumatic brain injury and intracranial hypertension, and it can possibly be used safely in trauma emergency situations.


2020 ◽  
Vol 25 (4) ◽  
pp. 375-383 ◽  
Author(s):  
Fartein Velle ◽  
Anders Lewén ◽  
Timothy Howells ◽  
Per Enblad ◽  
Pelle Nilsson

OBJECTIVERefractory intracranial pressure (ICP) hypertension following traumatic brain injury (TBI) is a severe condition that requires potentially harmful treatment strategies such as barbiturate coma. However, the use of barbiturates may be restricted due to concerns about inducing multiorgan system complications related to the therapy. The purpose of this study was to evaluate the outcome and occurrence of treatment-related complications to barbiturate coma treatment in children with refractory intracranial hypertension (RICH) due to TBI in a modern multimodality neurointensive care unit (NICU).METHODSThe authors conducted a retrospective cohort study of 21 children ≤ 16 years old who were treated in their NICU between 2005 and 2015 with barbiturate coma for RICH following TBI. Demographic and clinical data were acquired from patient records and physiological data from digital monitoring system files.RESULTSThe median age of these 21 children was 14 years (range 2–16 years) and at admission the median Glasgow Coma Scale score was 7 (range 4–8). Barbiturate coma treatment was added due to RICH at a median of 46 hours from trauma and had a median duration of 107 hours. The onset of barbiturate coma resulted in lower ICP values, lower pulse amplitudes on the ICP curve, and decreased amount of A-waves. No major disturbances in blood gases, liver and kidney function, or secondary insults were observed during this period. Outcome 1 year later revealed a median Glasgow Outcome Scale score of 5 (good recovery), however on the King’s Outcome Scale for Childhood Head Injury, the median was 4a (moderate disability).CONCLUSIONSThe results of this study indicate that barbiturate coma, when used in a modern NICU, is an effective means of lowering ICP without causing concomitant severe side effects in children with RICH and was compatible with good long-term outcome.


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