The principles of EMST/ ATLS apply; taking part in these courses is highly recommended if you are involved in this area at all.
Initial management is focused on preventing secondary brain injury by preventing hypoxia and hypotension, which have been shown in the context of TBI to be the most important variables affecting outcome.
Hypotension alone increases mortality in severe TBI from 27% to 60%.
Hypoxia, in addition to hypotension, is associated with a mortality of 75%.
In the context of trauma, the principles of ATLS are followed, with a primary survey focusing on airway patency and C-Spine protection, adequate ventilation with oxygenation and addressing life threatening haemorrhage. In this case, preventing haemorrhage from the arm injury is crucial to prevent hypovolaemic shock and reduced cerebral perfusion pressure.
This is followed by the appropriate adjuncts and a complete secondary survey. Associated injuries that might result in hypotension or hypoxia must be identified early.
Evaluation for occult injuries is routine, e.g. CT of the abdomen, FAST, DPL, and chest x-ray.
Urgent CT scan, frequent neurologic revaluations, and repeat CT scans are used to identify progressive injuries.
Q2. What are the specific considerations for airway management in this case?
Endotracheal intubation with rapid sequence induction is required for airway protection if the GCS is </=8 or if it falls by >/=2 points.
Intubation may also be required for other reasons, e.g. coexistent respiratory problem or prior to operative intervention.
During intubation it is critical to avoid further elevations in ICP (EICP). This may be exacerbated by hypoxia, hypotension and drugs or various manoeuvres. To avoid this, consider the following measures:
Experienced airway doctor
Full preparation for difficult intubation available
Judicious use of sedative agents (being mindful of blood pressure and ICP)
Fluids and vasopressors e.g. metaraminol available
With good clinical or radiological evidence of EICP, a MAP of >/=80mmHg should be targeted assuming ICP is >/= 20mmHg
Hypercapnoea should be avoided as it produces cerebral vasodilatation, thereby further increasing ICP. Hypocapnoea produces cerebral vasoconstriction, decreases cerebral blood volume (and flow) and therefore temporarily reduces ICP but risks inducing ischaemia itself. Therefore normocapnoea (35-40mmHg) should be targeted initially.
After initial resuscitation the patient is taken to the operating theatre; he returns to the neuro-intensive care after a decompresive craniectomy and insertion of several monitoring devices.
NIRS is a non-invasive monitor of cerebral oxygenation. It is attracting a lot of interest currently but remains to be validated for use in guiding therapy or inferring prognosis in TBI (see references).
Q7. And what is this? It is inserted through the same bolt as the ICP monitor and the blue box shown below. What are the components shown? What does the device tell you?
With permission from CMA (http://www.microdialysis.se/)
The components of the cerebral microdialysis (MD) catheter are:
microvial for collection of microdialysate
Cerebral microdialysis is a well-established laboratory tool that is increasingly used as a bedside monitor to provide on-line analysis of brain tissue biochemistry during neurointensive care. Microdialysis has the potential to become an established part of mainstream multi-modalitymonitoring during the management of acute brain injury but at present is a research tool for use in specialist centres.
A recent review by Tisdall and Smith (2006) describes the principles of cerebral microdialysis and the rationale for its use in the clinical setting, including discussion of the most commonly used microdialysis biomarkers of acute braininjury, with potential clinical applications and future potential research applications (see references).
Q8. Here is even more multi-modal monitoring. What is it? Is it more or less useful than the rest of the devices we’ve seen?
The prevention and aggressive treatment of cerebral hypo-oxygenation and control of ICP with a PbtO(2)-directed protocol has been shown to reduced the mortality rate after TBI in major trauma, and result in improved clinical outcomes over the standard ICP/CPP-directed therapy. This was shown in two single centre studies with historically matched controls, which have inherent limitations (see references: Narotam et al 2009; Spiotta et al 2010).
However, as there have been no randomized controlled trials carried out to determine whether PbtO2 monitoring results in improved outcome after severe TBI, use of this technology has not so far been widely adopted in neurosurgical intensive care units.
A study is about to commence (see the details here at www.clinicaltrials.gov — it will be the first randomized, controlled clinical trial of PbtO2 monitoring, and is designed to obtain the data required for a definitive phase III study, such as efficacy of physiologic maneuvers aimed at treating PbtO2, and feasibility of standardizing a complex intensive care unit management protocol across multiple clinical sites:
Patients with severe TBI will be monitored with ICP monitoring and PbtO2 monitoring, and will be randomized to therapy based on ICP along (control group) or therapy based on ICP in addition to PbtO2 values (treatment group). 182 participants will be enrolled at four clinical sites in the United States. Functional outcome will be assessed at 6-months after injury.
Q9. What other complications might you expect following this event?