Intracranial pressure (ICP) monitoring should be initiated in patients with a GCS of ≤8 and evidence of structural brain dam- age. For patients with a GCS >8 with structural brain damage and at high risk for progression, ICP monitoring should also be considered. Similarly, it may be reasonable to consider ICP monitoring for patients with a GCS of <8 without a mass lesion if there is a clinical suspicion for DAI. If urgent surgery is con- sidered for extra-cranial injuries within the first 72 h of trauma, placement of an ICP monitor should be considered to guide intraoperative anesthesia management [3]. Additionally, ICP monitoring should be considered if neuroimaging demonstrates progression of pathology, or the patient is clinically deteriorat- ing. A tiered approach to ICP management adapted from the ACS TQIP TBI Management Best Practice Statement is detailed in Table 10.4.
Historically, the method of ICP monitoring was not strictly prescribed. Parenchymal monitors were favoured as cerebral Table 10.3 Goals of treatment
Pulse oximetry
≥95%
ICP 20–25 mmHg Serum sodium 135–145 PaO2≥100 mmHg PbtO2≥15 mmHg INR ≤1.4
PaCO2 35–45 mmHg CPP ≥60 mmHg Platelets ≥75 × 103/mm3 SBP ≥100 mmHg Temperature
36.0–38 °C
Hemoglobin ≥7 g/dl PH 7.35–7.45 Glucose 80–180 mg/dL
Table 10.4 Tiered approach to the management of intracranial pressure
Tier Management
Tier 1 Head of bed elevated at 30°
Short-acting sedation and analgesia Intermittent ventricular drainage Repeat CT imaging and neurological
examination to rule out the
development of a surgical mass lesion and guide treatment
If ICP remains ≥20–25 mmHg proceed to Tier 2
Tier 2 If parenchymal monitor is indicated, EVD should be considered
Intermittent (not routine) hyperosmolar therapy as needed for ICP elevation In the absence of cerebral autoregulation,
CPP goal should be lowered
PaCO2 goal 30–35 mmHg, as long as brain hypoxia is not encountered
Additional neuromonitoring may help determine optimal PaCO2 and CPP Repeat CT imaging and neurological
examination
Neuromuscular paralysis should be considered if test dose lowers ICP If ICP remains ≥20–25 mmHg proceed to
Tier 3 Tier 3 (includes potential
salvage therapies)
Decompressive hemi-craniectomy or bilateral craniectomy
Neuromuscular paralysis via continuous infusion titrated to train of four Barbituate or propofol (anesthesia dosage)
coma may be induced
Hypothermia (<36 °C) is not currently recommended as an initial TBI treatment
edema often complicated placement of external ventricular devices (EVDs). These devices are catheters attached to an external drain-gauge transducers and are the gold standard for ICP monitoring as they can serve as a diagnostic tool to measure ICP as well as therapeutic modality to treat elevated ICP via cerebral spinal fluid (CSF) drainage. In the current iteration of the TQIP Guidelines, EVD placement is recommended in lieu of parenchymal monitors for these reasons.
While invasive monitoring of ICP is considered the stan- dard of care [2, 3, 7], it has not been shown to improve out- come. The Benchmark Evidence from South American Trials:
Treatment of Intracranial Pressure (BEST TRIP trial) multi- centre randomized controlled trial failed to demonstrate a dif- ference in outcome between treatments guided by clinical examination and use of an ICP monitor. These study findings may not be generalizable to developed countries where use of invasive monitors is the current practice standard; future trials conducted in developed countries will provide direction of best practice [8].
Cerebral perfusion pressure (CPP) is the driving pressure for cerebral blood delivery. Given its relationship to mean arterial pressure (MAP) and ICP (CPP = MAP – ICP), CPP is easily calculated in patients with an ICP monitor. The CPP provides a surrogate estimate of cerebral blood flow (CBF), or the delivery of blood flow to a certain volume of brain tissue. Targeting CBF may allow determination of judicious blood pressure goals and may minimize ischemia (compromised blood flow) and hyper- emia (excessive blood flow).
Maintaining adequate brain tissue oxygenation is pivotal in the care of TBI patients. Preventing secondary cerebral injury, which evolves over hours to days following the initial insult, begins with the initial pre-hospital assessment and remains the focus of care throughout the hospital stay. Secondary injury involves cellular and molecular cascades that promote cell death; secondary injury is clinical manifest by cerebral edema,
ischemia, hemorrhage and seizure. Injured cells are more vul- nerable to further physiologic insult. ICP monitoring remains the gold standard of neuro monitoring however it is not sensi- tive in detecting regional and focal cerebral ischemia. Other forms of advanced neuro-monitoring include, but are not limited to, continuous electroencephalography, transcranial Doppler ultrasound, jugular bulb oxygen saturation (SjvO2), CBF monitoring, near-infrared spectroscopy, and cerebral microdialysis [7–12].
Recommendations for surgical management of mass lesions are detailed in Table 10.5 [2, 13–17]. Hyper-metabolic and catabolic states exist with TBI, thus increasing systemic and cerebral energy requirements. Early nutrition, as defined by starting within 24–48 h of injury and achieving full nutritional supplementation within 7 days of injury, should be the goal and is associated with fewer infections and lower mortality rates. Enteral nutrition is preferred over the use of parenteral nutrition [18].
Although there have been a few trials of neuroprotective agents for patients with TBI, none have been proved effective.
In the National Acute Brain Injury Study: Hypothermia II (NABISH II) multi-center randomized controlled trial, thera- peutic hypothermia was not associated with improved outcome, although it may have been associated with reduced ICP in the treatment arm [19]. The Progesterone for Traumatic Brain Injury, Experimental Clinical Treatment (PROTECT III) was a randomized, multicentre trial that did not demonstrate utility of progesterone in improving the outcome of patients with acute TBI over the placebo [20].
Table 10.5 Recommendations for surgical management of TBI Lesion Treatment recommendations
Subdural hematoma [13] (SDH)
Acute lesion >10 mm or >5 mm MLS should be evacuated
Comatose patients with SDH <10 mm or MLS
<5 mm should undergo evacuation if GCS decreases by ≥2 (if indicated, should be performed via craniotomy)
All patients with GCS <9 should have ICP monitoring
Epidural hematoma [14] (EDH)
EDH ≥30 cm3 should be evacuated regardless of GCS
EDH <30 cm3, <15 mm or <5 mm MLS may be managed non-operatively with close serial neurosurgical evaluation
EDH in coma with anisocoria should undergo evacuation
Parenchymal hematoma [15]
Mass lesions with related neurological deterioration, refractory intracranial hypertension, or radiographic signs of mass effect should be treated operatively GCS 6–8, frontotemporal contusions >20 cm3
and MLS ≥5 mm and/or cisternal compression should be treated operatively Any lesion >50 cm3 should be treated operatively Parenchymal lesions without neurological
compromise, with controlled ICP, and no mass effect may be monitored
Bifrontal decompressive craniectomy within 48 h of injury is an option for patients with diffuse, refractory posttraumatic cerebral edema and resultant intracranial hypertension [15]
(continued)
Table 10.5 (continued)
Lesion Treatment recommendations Posterior fossa
hematoma
Patients with radiographic mass effect or with neurological dysfunction referable to the lesion should undergo intervention
Mass effect on the fourth ventricle; compression of the basal cisterns, or the presence of obstructive hydrocephalus
Patients with lesions but no significant mass effect on CT scan and without signs of dysfunction may be managed expectantly In patients with indications for surgical
intervention, evacuation should be performed as soon as possible
Depressed skull fractures
Compound cranial fractures depressed > the thickness of the cranium should undergo operative intervention
Compound depressed fractures may be treated non-operatively in the absence of dural penetration, ICH, depression <1 cm, frontal sinus involvement, gross cosmetic deformity, wound infection, pneumocephalus, or gross wound contamination
Simple depressed fractures may be expectantly managed
Early operation is recommended to reduce infection
Primary bone fragment replacement is a surgical option in the absence of wound infection at the time of surgery
All management strategies for open (compound) depressed fractures should include
antibiotics [7]