When the drugs make things worse in Traumatic Brain Injury....
CCCF ePoster library. Quinn A. Nov 2, 2016; 150997; 116
Dr. Aoife Quinn
Dr. Aoife Quinn
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Abstract
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#116

Topic: Clinical Case Report

When the drugs make things worse in Traumatic Brain Injury....


Quinn A1, Galvin S1.
1. Dept of Anaesthesia and Critical Care Medicine. Beaumont Hospital. Dublin. Ireland
 



Abstract:

Introduction:
Optimal treatment of the young adult patient with traumatic brain injury, sustained elevations of intracranial pressure and early signs suggestive of impending propofol infusion syndrome pose management dilemmas. Neuroprotective strategies mandate maintenance of appropriate sedation for control of intracranial pressure (ICP).  The physicochemical properties of propofol make it a first line sedative agent in the management of traumatic brain injuries (TBI). However Propofol Infusion Syndrome (PRIS) has an associated mortality.1
 
Objectives: 
We present a case illustrating that prompt recognition of suspected PRIS may be associated with a good outcome, and highlighting a potential role for dexmedetomidine as an adjunct in the management of intractable intracranial pressure elevations.
 
Methods:
Case report and review of literature.
 
Results:
A 16 year old (70 kg) male was transferred to our neurocritical care unit. He was an unrestrained passenger in a high speed single vehicle accident, with prolonged extraction time. Initial GCS was 3. Injuries included bifrontal contusions, traumatic subarachnoid haemorrhage, multiple open facial fractures with CSF leak, bilateral first rib fractures, (intact aorta), pulmonary contusion and pneumothorax.
 
An ICP monitor was inserted with an opening pressure of 29mmHg. Sedation with propofol 20mg /hour and morphine and midazolam at 10 mg/ hour respectively was commenced. Noradrenaline was titrated to maintain MAPs and CPPs.
On day five, ICPs spiked and remained greater than 30mmHg. Repeat CT brain showed evolution of contusions, but nil warranting surgical intervention. Cooling to less than 35oc, boluses of mannitol, increasing propofol to 200 mg/hr and commencing thiopentone at 250mg/hour obtained control of ICPs until day 9 when they spiked and remained at greater than 45mmHg. Additionally the electrocardiogram showed some brugada changes, potassium increased acutely to 6.5 mmol/L, both myoglobuineria, and a CK of greater than 15000 developed.
He had now been on propofol for 9 days. Although not fulfilling all criteria for PRIS, and not having breached 4mg/kg/ hour, these findings were considered a precursor to PRIS. Potassium elevation was managed medically ( 10mls 10% calcium gluconate for cardioprotectin and insulin/dextrose infusion). Propofol was discontinued.  Thiopentone, morphine and midazolam were bolused and infusion rates were increased (thiopentone at 500mg/hour and both morphine and midazolam 12mg/hour.)
Dexmedetomidine  (0.2mcg/kg/hour) was commenced as an alternate sedative agent. ICPs were controlled to 25 mmMg, sufficient to tolerate transfer to CT scan demonstrating a high pressure scan, and then to theatre for placement of an extraventricular drain. Post procedure, sedation was maintained with above agents. ICPs remained less than 20 mmHg. The remainder of the 17day ICU stay was unremarkable. He made a consistent neurological improvement to VT, E4, M5, and was transferred to his referring hospital for rehabilitation
 
Conclusion
This case demonstrates the difficulty with maintaining sedation for neuroprotection in the setting of potential PRIS. Dexmedetomidine is gaining popularity as a sedative agent in ICU, but does not yet have widespread use in neurocritical care. In this case, the substitution of  propofol for dexmedetomidine allowed for ongoing control of ICP, and thus highlights a potential role  and area for further exploration for the drug in the management of neurocritical care patients.
 
 

 


References:

1. Roberts DJ, Hall RI, Sedation for critically ill adults with severe traumatic brain injury: a systematic review of randomized controlled trials. Crit Care Med. 2011 Dec;39(12):2743-51
2. Flower O, Hellings S. Sedation in traumatic brain injury. Emerg Med Int. 2012;2012:637171
3. lodenius A, Ebberyd A, Hardemark A, Christensson E. Sedation with Dexmedetoidine or Propofol Impairs Hypoxic Control of Breathing in Healthy Male Volunteers. Anaesthesiology 2016 125:700-15



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