MVC with TBI

Patient Presentation
SG, a 19 year old male with no PMH presents to the trauma bay s/p MVC as a restrained passenger in the back seat of a small car.  Upon initial assessment, SG has very minimal lacerations & abrasions and no other serious open wounds or deformities.  VS are mostly stable and as follows:  HR: NSR 60s-80s, BP: low 100s/70s, afebrile, SpO2: low 90s.  SG is intubated for a GCS of 4 to 5 with obvious posturing and bilateral nonreactive pupils; a cough reflex and gag reflex are present.  Bilateral #16 gauge PIV's are in place.  Following lab draws and negative FAST scan (Focused Assessment with Sonography for Trauma; a rapid bedside tool used to identify intra-peritoneal hemorrhage or pericardial tamponade), pt is taken for stat head CT. 

Differential
Suspected TBI, awaiting head CT interpretation for definitive diagnosis

Test Results
Labs are unremarkable; urine drug screen:  negative, H/H stable at 14/40, coags & electrolytes WNL; ABG (post intubation):  pH 7.3, PaO2 150, PaCO2 45 (rate was slightly increased and FiO2 was slightly decreased as a result).  Head CT shows severe “tightness”/cerebral edema and possible diffuse axonal injury (DAI), however an MRI is needed for more conclusive identification.  Priority right now is transfer to ICU for ICP management and plan of care.

Treatment
Upon arrival to the surgical trauma ICU, SG had an EVD placed at the bedside and open to drain as well as a LICOX® monitor in the penumbra.  Opening pressure on EVD was 45 mmHg and pt was immediately hyper-oxygenated and both a central line and arterial line were placed.  A neo (phenylephrine) gtt was started and titrated for a CPP (MAP-ICP) of 70 mmHg, per hospital protocol.  Steroids were not administered due to recent published literature indicating no benefit for patient outcomes.  Mannitol, as well as a “hot salts” (23.4% hypertonic saline) bolus was given and a 3% hypertonic saline gtt was started with q2hr ABG, Na+, K+, and serum osmolality checks.  Regardless of aggressive treatment, SG maintained ICPs throughout the night in the 30s.  His neuro exam waxed and waned with a GCS ranging from 3 to 5.  The neurosurgeons discussed a decompressive craniectomy, however, recent TBI literature has been published via retrospective studies indicating no benefit associated with this treatment versus pharmacological management (although they are still frequently used as last line of treatment and are still seen to provide positive outcomes on case by case scenarios).  SG was kept mildly hypocapnic and acetaminophen was given for core temps >38.5, as well as previously mentioned interventions.  The first few days of admission were critical but by day 5 his neuro exam began to slowly improve.  He was eventually trached and transferred to the floor almost 3 weeks later.

Outcome
These are the patients that usually don’t do well… for numerous reasons.  DAI is one of the most devastating kinds of TBI because it causes widespread shearing of white brain matter rather than a specific focal brain injury.  It is a major cause of persistent vegetative states (PVS) after head trauma with upwards of 80 % of patients with severe DAI never regaining consciousness (those who do often remain significantly impaired).  However, SG recovered completely.  The trauma team said he had one of the worst CT & (eventually) MRI scans they had seen on someone who survived.
Case created by Shanna Got, 2011.