- Rapid Reference 🚀
- Primary vs. secondary injury
- Clinical severity scores
- Initial evaluation
- Specific types of injury
- Questions & discussion
TBI – Initial management ✅
- Basic laboratory studies (e.g., electrolytes and blood count).
- Coagulation labs (INR, PTT, fibrinogen, TEG).
- ABG or VBG if there is concern regarding hypoventilation.
- Review of anticoagulant medications the patient is on.
- CT of head, cervical spine, and other relevant areas. Consider vascular imaging of head and neck, at the same time.
anticoagulation reversal (more)
- Aggressive reversal of therapeutic anticoagulants, e.g. warfarin (see anticoagulation reversal chapter, emcrit.org/IBCC/reverse).
- Consider tranexamic acid if <3 hours and moderate/severe TBI.
blood pressure control (more)
- Initial rough blood pressure targets:
- 18-49 YO or >70 YO: SBP >110 mm.
- 50-69 YO: SBP >100 mm.
- Resuscitate as needed with blood products (in polytrauma with hemorrhagic shock) or crystalloid (e.g., plasmalyte).
- If hypotensive, start norepinephrine infusion immediately.
recognizing & treating ICP crisis shortly after admission (more)
- Suggested by neuroworsening, anisocoria, or posturing.
- Empiric hypertonic tx reasonable while awaiting STAT CT scan.
seizure prophylaxis & diagnosis (more)
- Prophylactic levetiracetam (consider 2000 mg load in high-risk patients).
- Consider vEEG for comatose patients with possible seizures.
general neurocritical care practices
- Airway control as needed (with a Bp & ICP-stable intubation).
- Aggressive fever management, with physical cooling if needed.
- Avoid hyponatremia (with aggressive treatment if this occurs).
- Target normocapnia (check ABG/VBG & trend etCO2).
- Maintain neck in a neutral position, D/C cervical collar ASAP.
- Chemical DVT prophylaxis is initially contraindicated; use sequential compression devices upon admission.
- TBI is one of the leading causes of mortality and morbidity following trauma. Since younger patients are often involved, this causes a large person-year burden of morbidity. The precise incidence is difficult to quantify, given variable definitions of exactly what constitutes TBI.
- Causes of TBI are variable, including:
- Falls (most common cause among the elderly).
- Motor vehicle collisions.
- Penetrating injury (e.g., gunshot wound) – less common, but highly morbid.
- About a third of patients with TBI may be polytraumatized. Their management will be complicated by treatment of extracranial trauma as well as TBI.
primary and secondary injury
- Primary injury refers to neuronal damage which is directly due to trauma.
- This occurs at the time of the traumatic event.
- Primary injury is generally irreversible.
- Secondary injury refers to neuronal damage due to sequelae of the primary insult, for example:
- Edema and elevated intracranial pressure.
- Loss of cerebral autoregulation, increasing vulnerability to hypotension or hypertension.
- Paroxysmal sympathetic hyperactivity as a driver of fever and autonomic instability.
- In many cases, secondary injury may be treatable. The management of TBI focuses on avoiding or minimizing secondary brain injury.
clinical severity scores
Glasgow Coma Scale (GCS)
- GCS is the most widely accepted tool for classification and prognostication.
- GCS has numerous limitations (e.g., confounding by sedation, intoxication, paralysis, or intubation).
- Communication of the individual GCS subscores may be more helpful than a single summated GCS score.
- Basic labs (glucose, electrolytes, Mg/Phos, CBC).
- Coagulation studies (including INR, PTT, fibrinogen, +/- TEG if available).
CT head without contrast
- CT is the preferred modality due to its ability to detect bleeding or tissue shifts, its speed, and the ability to repeat the scan as needed.
- STAT head CT is indicated for any patient with significant TBI (e.g., GCS <15).
- Repeat CT scanning may be indicated, based on initial CT scan and clinical evolution.
Indications for CT angiography
- (1) Evaluation for blunt cerebrovascular injury (BCVI) involving the arteries (e.g., dissection or pseudoaneurysm). Indications may include:(33896528)
- Penetrating brain injury, especially with transverse object trajectories.
- Focal neurological deficit which is otherwise unexplained (suggestive of ischemic stroke).
- Evidence of arterial injury (e.g., neck bruit or expanding cervical hematoma).
- Le Forte II or III fracture.
- Cervical spine fracture (especially involving subluxation or rotational component).
- Petrous bone fracture.
- Diffuse axonal injury with GCS ≤6.
- (2) Evaluation for a trauma-related Cerebral Venous Sinus Thrombosis:
- Mechanism is variable, can include direct compression from surrounding hematomas, endothelial injury leading to clot formation, or extension of thrombus.
- Consider dedicated venous imaging in any patient with a skull fracture spanning a venous sinus or the jugular bulb.
- Anticoagulation is controversial and not typically started, except in a delayed fashion (due to coexisting hemorrhages).
additional CT scans
- Polytraumatized patients often require CT scans of numerous body areas (the trauma pan-scan).
- Even for isolated TBI, a C-spine CT scan is generally advisable.
diffuse axonal injury (DAI)
- DAI involves the shearing of long axonal tracts within the brain. (Imagine shaking a bowl of Jello. Even if the Jello remains in one piece, the small cracks that appear within the Jello are a fair representation of what DAI looks like.)
- This usually results from high-velocity injury (e.g., vehicular crash).
- Small hemorrhagic and nonhemorrhagic lesions may occur within the grey-white matter interface, within the corpus callosum, or in the dorsal brainstem.(28865528)
- CT scan often doesn't show substantial injury, especially early on. Repeat CT scan may show small, hemorrhagic hyperdense lesions. However, 80% of lesions are not hemorrhagic, so CT scan fails to reveal the true extent of pathology. Overall, CT scan may have only a ~50% sensitivity for diffuse axonal injury.(31731899)
- MRI is more sensitive than CT scan, revealing both hemorrhagic and nonhemorrhagic lesions.
- (1) Hemorrhagic lesions can be seen using GRE/SWI sequences (which reveal microbleeds nicely).
- (2) Lesions can also be detected as small T2/FLAIR hyperintensities. DWI may be particularly sensitive for nonhemorrhagic lesions showing diffusion restriction (including some lesions which may not be detectable on T2/FLAIR images).(31485117)
- Limitations of MRI include that the patient must be able to lie flat for a prolonged period of time, without ICP monitoring. Additionally, intraparenchymal monitors or bullet fragments are not MRI compatible.
- DAI often causes coma without elevated ICP. There is no specific management for this, aside from high-quality neurocritical supportive care.
- Prognosis is often poor, since coma is largely due to the primary injury (especially if DAI involves the brainstem and reticular activating system).
cerebral contusions & intraparenchymal hematoma
- These are due to damage to the small parenchymal and cortical pial vessels, resulting from impact and subsequent deceleration within the skull compartment (coup and contrecoup injury).
- Contusions are most often seen in basal frontal and temporal areas.
- Over time, about a third of contusions may expand due to localized edema and/or ongoing bleeding (potentially forming intraparenchymal hematomas).
- CT scan may show either:
- Hypodense regions without visible hemorrhage.
- Mixed areas with hypodense, edematous tissue that abut hemorrhagic areas.
potential indications for surgical drainage of a hematoma
- Posterior fossa hematoma:
- Brainstem compression.
- Obliteration or substantial distortion of the fourth ventricle.
- Effacement of the basal cisterns.
- Obstructive hydrocephalus.
- Cerebral hemispheric hematoma:
- >50 ml volume.
- Frontal or temporal hemorrhage >20 ml with midline shift ≥5 mm and/or cisternal compression, in the context of impaired mental status (GCS 6-8).(33395087)
- Epidural hematoma is most commonly due to laceration of the middle meningeal artery, which is usually associated with skull fracture. However, epidural hematomas may also occur at other locations due to laceration of another artery, or a dural sinus.(Nelson, 2020)
- Epidural hematomas often aren't associated with severe underlying parenchymal brain damage. They may respond very well to prompt drainage, with a favorable prognosis.
- Classically these patients may have a lucid interval after the trauma, followed by loss of consciousness as the epidural hematoma rapidly expands. However, a lucid period only occurs in ~20% of cases.
- A lenticular (lens-shaped) hematoma is seen.
- An underlying skull fracture is generally present (~85%).
- Epidural hematomas and subdural hematomas can sometimes be hard to differentiate. Epidural hematomas do not cross suture lines, as the dura is tacked to the skull at these lines, whereas subdural hematomas may as they occur under the dura mater. However, an epidural hematoma can cross the midline or cross between the supratentorial and infratentorial regions (unlike subdural hematomas).
- Indications for surgical drainage may include the following (noting that this determination should always be made by a neurosurgeon):
- >30 ml volume.
- Thickness ≥15 mm.
- Midline shift ≥5 mm.
- Acute epidural hematoma with impaired consciousness and asymmetric pupils (not caused by an alternative etiology, such as ocular trauma).
- Hematoma is causing focal neurological signs.
- Deterioration over time (e.g., enlarging hematoma on serial imaging, worsening neurological examination).
- Posterior fossa epidural hematoma is often managed more aggressively (given limited space in the posterior fossa).
- Subdural hematoma is usually due to damage to the bridging veins that lie between the cerebral veins and the dural venous sinuses. As we age, our brains atrophy, which then leads to stretched bridging veins. This stretching can increase the susceptibility of the older population to subdural hematomas.
- In younger patients, subdural hematoma is often a marker of severe TBI (e.g., occurring in combination with additional injuries, such as diffuse axonal injury, intraparenchymal contusions, and other hematomas).
- In elderly patients with coagulopathy, subdural hematoma may occur following milder trauma (with minimal underlying brain injury). In this situation, patients may present after gradual expansion of the hematoma, with a chronic subdural hematoma causing subtle symptoms (e.g., headaches, nausea/vomiting, confusion, subtle localizing features such as mild hemiparesis, seizure). However, this must be differentiated from a chronic asymptomatic subdural hematoma.
- Since subdural hematomas result from a bleeding vein, the onset is generally more subacute than epidural hematomas. However, anticoagulated patients may have rapid progression of neurological deficits.
- Subdural hematoma patients can sometimes also present with a lucid interval.
- Subdural hematomas are crescent-shaped on imaging, typically hugging the skull.
- If active bleeding is occurring, a swirl sign may be seen.
- Blood becomes brighter on CT as it clots. Thus, fresh blood may appear relatively darker compared to older, clotted components of the hematoma.
- Subdural hematomas can cross suture lines, but do not cross dural reflections (e.g., the midline or between the supratentorial and infratentorial regions). Instead, blood may extend along the falx cerebri (parafalcine subdural hematoma), and/or layer along the tentorium cerebelli (figure below)(transtentorial subdural hematoma).
- Subdural hematoma can occur entirely along the falx (i.e., interhemispheric parafalcine subdural), which may suggest a coagulopathy.
- Intensity on CT scan may reveal the chronicity of the subdural hematoma.
- (1) Acute blood is hyperdense (in the absence of anemia).
- (2) As blood clots, it becomes even more hyperdense (within hours of hemorrhage, lasting for several days).
- (3) Over the ensuing month, the density decreases.
- First blood becomes isodense, then it ultimately it becomes hypodense.
- Reduction in density begins at the edges of the hemorrhage.
- Subacute, isodense hemorrhage may be difficult to detect.
- Indications for surgical drainage may include the following (noting that this determination should always be made by a neurosurgeon):
- >10 mm thickness.
- Association with midline shift >5 mm.
- GCS ≤ 8, or GCS has decreased by two or more points since admission to the hospital.
- Asymmetric or fixed and dilated pupils.
- ICP measurements consistently >20 mm.
traumatic subarachnoid hemorrhage
- Traumatic SAH is not uncommon.
- Causes of traumatic subarachnoid hemorrhage:
- (1) Primary subarachnoid hemorrhage (due to disruption of small pial veins as they pass through the subarachnoid space).
- (2) Extension from an intraventricular hemorrhage or superficial intracerebral hemorrhage.
- FLAIR may detect small acute or subacute SAH which is missed on CT imaging.(31485117)
- ⚠️ For patients with extensive subarachnoid hemorrhage, consider whether the patient may have had a primary aneurysmal subarachnoid hemorrhage, which led to alteration of consciousness and subsequent trauma (e.g., motor vehicle collision).
- Typically, traumatic SAH is located over the peripheral cerebral convexities, rather than the sylvian fissures and basal cisterns (locations more suggestive of aneurysmal SAH).(31731899)
- Traumatic SAH may be located adjacent to fractures or cerebral contusions.
- Small traumatic SAH may not require any specific management. However, larger volumes of blood in the subarachnoid space may lead to complications similar to those from aneurysmal subarachnoid hemorrhage (e.g., vasospasm and hydrocephalus), though the presentation and timing of onset of this is somewhat more erratic.
- Risk factors for vasospasm include the following: (33896528)
- Larger overall blood volume.
- Younger age.
- Admission GCS ≤8.
- More on the management of subarachnoid hemorrhage and vasospasm here.
- More commonly occurs due to extension from adjacent intraparenchymal or subarachnoid hemorrhage, but can also occur due to a primary intraventricular hemorrhage due to tearing of subependymal veins.
- Uncommon that this is the primary finding in a patient with TBI.
- Any medication-induced coagulopathy should be emergently reversed in the presence of bleeding (more on anticoagulation reversal here).
- For thrombocytopenia, a platelet target of >100,000 may be optimal for patients with active intracranial hemorrhage or pending neurosurgical intervention.
- Patients can also present with Trauma-Induced Coagulopathy (TIC) and thromboelastography can be helpful in its identification. Management focuses on restoring the abnormalities noted on thromboelastography (TEG/ROTEM) by repleting with either platelets, cryoprecipitate, plasma, or adding a fibrinolytic agent such as tranexamic acid (more on this here).
tranexamic acid (TXA)
- This might be beneficial among patients with intracranial hemorrhage or moderate/severe TBI, if administered within three hours of injury.
- CRASH 3 trial investigated the use of tranexamic acid in TBI patients with GCS <13 or with any intracranial bleeding on CT within 3 hours of injury. There was a reduction in the risk of head injury-related death in patients treated with tranexamic acid, which almost reached statistical significance. The subgroup of patients with moderately severe TBI seemed to benefit more than patients with severe brain injury.(more on the study here)
- Normal saline is usually preferred.
- Plasmalyte may not be optimal, given that the BASICS trial detected signs of potential harm among the subgroup of patients with TBI.(34375394; more on the BASICS trial here)
- Albumin is contraindicated, given signals of harm in the SAFE trial (and also a lack of any particular reason to use it).(15163774)
- Avoiding hypotension is essential. There should be a low threshold for initiation of a vasopressor infusion (e.g., norepinephrine), even while fluid resuscitation is ongoing.
- Brain Trauma Foundation guidelines recommend the following blood pressure targets:(27654000)
- 18-49 years old: systolic Bp >110 mm.
- 50-69 years old: systolic Bp >100 mm.
- >70 years old: systolic Bp >110 mm.
- Blood pressure targets may also be adjusted based on the patient's baseline blood pressure (if known) and other clinical signs of perfusion.
- For patients with an ICP monitor, blood pressure may be titrated based on the cerebral perfusion pressure (more on this below).
intracranial pressure (ICP) management
A general discussion of ICP elevation is found here. The following details apply more specifically to ICP elevation due to TBI.
immediate, empiric management of ICP elevation
- Patients may develop an ICP crisis soon after admission with TBI (e.g., due to undrained hematoma expansion with impending or ongoing herniation).
- Empiric management for possible ICP elevation may be reasonable, if there is presumptive evidence for it, such as:
- Deteriorating neurological examination or very poor examination.
- Anisocoria, abnormalities of cranial nerves 3 and/or 6.
- Motor exam showing extensor posturing or lack of response.
- Cushing's phenomenon (hypertension, bradycardia, and irregular respiration).
- Treatments may include hypertonic therapy, hyperventilation, and emergent surgical evaluation. In this context, a bolus of hypertonic therapy is indicated (e.g., 250-500 ml of 3% saline or 30-60 ml of 23.5% saline. More on hypertonic therapy here).
- Ensure that the neck is in a neutral position and remove cervical collars, if possible.
indications for ICP monitoring
- There is no Level I evidence that ICP monitoring improves outcomes in TBI. The largest RCT found no difference between invasive ICP monitoring when compared to monitoring of the neurological examination plus serial CT scans.(23234472) However, this study had numerous limitations (as explored further here).
- ICP monitoring is recommended for patients with GCS≤8 and CT scans showing hematomas, contusions, swelling, herniation, or compressed basal cisterns.(27654000)
- An external ventricular drain is generally the preferred modality of ICP monitoring (given to its accuracy, ability to be recalibrated as needed, and its ability to therapeutically drain CSF). However, in patients with compressed ventricles this may be very challenging, so an intraparenchymal monitor may be required. (more on various types of monitors here)
ICP and cerebral perfusion pressure (CPP) targets
- An ICP goal <22 mm is generally recommended as a rough guideline.(27654000)
- Some patients with severe TBI may have dysfunctional cerebral vascular autoregulation, causing cerebral perfusion to become dependent on the cerebral perfusion pressure. Such patients may become vulnerable to cerebral hypoperfusion at lower CPPs and also cerebral hyperperfusion at higher CPPs. The usual rough goal for CPP is >60 mm. (more on cerebral perfusion pressure here).
- Types of decompressive craniectomy
- Primary or prophylactic decompressive craniectomy: This is performed simultaneously with another surgery (usually hematoma evacuation). Part of the skull is left off in anticipation of the possibility of worsening ICP over time.
- Secondary or therapeutic decompressive craniectomy: This is performed for management of ICP elevation that is refractory to less invasive management.
- Refractory ICP elevation may be a relatively common mechanism of brain death in severe TBI (figure above).
- The DECRA trial randomized patients with ICP >20 mm for fifteen minutes to medical management versus decompressive craniectomy. The study found no benefit, suggesting that early decompressive craniectomy (in response to minimal elevation of ICP) is not beneficial.(21434843)
- The RESCUEicp trial represents the largest and best study of decompressive craniectomy for patients with TBI. Patients with refractory ICP >25 mm for 1-12 hours were randomized to medical management versus decompressive craniectomy.(31563989) Surgery improved survival, but did not increase the number of patients with a good neurological outcome (figure below). Thus, craniectomy did indeed prevent death, but such patients often progressed to have severe disability.
- Decompressive craniectomy remains controversial. Decisions should be individualized to each specific patient depending on the details of their injury (e.g., presence of hematoma versus diffuse axonal injury), as well as wishes expressed by surrogate decision makers.
- The POLAR trial found that prophylactic hypothermia in severe TBI did not improve neurological outcomes after six months.
- The EUROTHERM trial found evidence of harm due to therapeutic hypothermia for management of ICP elevation due to traumatic brain injury.(31773291; further discussion of the EUROTHERM trial here).
- Hypothermia is not a preferred therapy for ICP elevation in TBI.(31659383) For refractory ICP elevation, treatment usually focuses on either decompressive craniectomy or barbiturate coma.
- Both hypoxemia and hyperoxia are potentially dangerous. Hypoxemia worsens outcomes, and also leads to increased cerebral blood flow which can exacerbate an ICP crisis.
- A normal oxygen level should be targeted. Precisely optimal targets are not known.
- Low PaCO2 causes cerebral vasoconstriction, reducing cerebral blood volume as well as cerebral blood flow. This can be helpful in an acute ICP crisis, but if sustained it will lead to worsening cerebral hypoperfusion, ischemia, and secondary injury. Hypocapnia has been shown to cause harm in a prospective RCT.(1919695)
- Elevated PaCO2 may cause cerebral vasodilation, which may theoretically increase intracranial pressure.
- An optimal PaCO2 target for a patient with intracranial hypertension might be the lower end of the normocapnic range.
- End-tidal CO2 should be used to allow for close monitoring of ventilation, while simultaneously minimizing the number of blood gas measurements.
- For patients with chronic hypercapnia, it may be impossible or dangerous to “normalize” the CO2 level (this would cause post-hypercapnic metabolic alkalosis, due to chronically elevated bicarbonate levels). Targeting the patient's baseline, chronic pCO2 level may be reasonable.
wean PEEP as able
- PEEP that improves lung recruitment may improve the pulmonary vascular resistance, improve right ventricular function, and lower the central venous pressure – and thereby reduce the ICP.
- Excessive PEEP may threaten to increase the pulmonary vascular resistance (by compressing the pulmonary microvasculature), impair right ventricular function, increase the central venous pressure – and thereby elevate the ICP.
- Thus, PEEP should be used as needed, but in a conservative fashion.
seizure prophylaxis & management
- Seizures are common among patients with TBI, occurring in up to a third of patients with severe TBI.
- Risk factors for early seizures:
- Hematoma (either subdural, epidural, or intracerebral).
- Cortical contusions.
- Penetrating head injury.
- Depressed skull fracture.
- GCS ≤10.
- Seizure prophylaxis is generally recommended for patients with moderate-severe TBI (e.g., patients with a reduced level of consciousness or abnormal CT scan).
- Levetiracetam is preferred over phenytoin, given superior functional outcomes in one RCT.(19898966) Levetiracetam also has a superior side-effect profile compared to phenytoin, as well as fewer drug-drug interactions. A moderate loading dose of levetiracetam (e.g., ~2000 mg) may be considered in patients at higher risk of seizures.
- Valproic acid may be useful in selected patients, given its mood-stabilizing properties (e.g., patients with problematic agitation).(33896528)
- A week's duration is recommended, but additional therapy could be considered for patients with higher risk.
- Seizures may be nonconvulsive, thereby requiring EEG monitoring for detection.
- EEG may be considered for comatose patients, especially if the degree of mental status impairment is disproportionately severe compared to neuroimaging findings.
intermittent pneumatic compression
- This should be started in all patients upon admission.
chemical DVT prophylaxis
- Chemical prophylaxis can generally be started within ~24-48 hours after admission (in the absence of any concerning or expanding hemorrhage, or other coagulopathies).
- For patients with intracranial hemorrhage, initiation of chemical DVT prophylaxis should be discussed with the neurosurgical team.
antibiotic prophylaxis for penetrating trauma
- Generally, prophylactic antibiotics are not recommended.
- Situations where antibiotics could be considered:(33896528)
- Significant pneumocephalus due to persistent open intracranial wounds.
- Substantial foreign bodies or bone fragments that cannot be debrided, especially if contaminated by soil.
- Ongoing CSF leaks.
- Suspected infection with inability to safely sample CSF.
avoidance of fever
general avoidance of fever
- Fever may increase cerebral metabolic stress and intracranial pressure, so this should be avoided.
- Initial management may include scheduled acetaminophen (e.g., 1 gram PO q6hr). If this fails, then physical cooling may be required (e.g., adaptive surface cooling with adhesive pads). If shivering occurs, this should be treated aggressively. (more on shivering therapy here)
- Roughly half of fevers may have an infectious etiology, so appropriate investigation should be undertaken in parallel with fever therapy (e.g., obtaining blood cultures and a chest radiograph). (more on the approach to fever in the ICU here)
paroxysmal sympathetic hyperactivity (PSH)
- Paroxysmal sympathetic hyperactivity is relatively common following severe TBI. This may cause a constellation of episodic hypertension, hyperthermia, tachypnea, tachycardia, posturing, and diaphoresis.
- PSH requires specific diagnosis and unique treatment strategies. (more on this here)
- TBI causes a catabolic state, with relatively elevated nutritional requirements. Excessive delays in nutritional support may promote caloric and protein deficits.
- As a general guideline, the following may be reasonable goals:
- (1) Enteral nutrition should ideally be started within 24-48 hours of admission. A reasonable initial prescription might be to provide 50% of the estimated caloric requirement along with 100% of the protein requirement.
- (2) Nutritional support should be escalated to provide 100% of the estimated caloric requirement, ideally at least by the fifth day.(27654000)
- More on protein and caloric requirements in the chapter on nutrition here.
- TBI patients may have a tendency towards emesis and vomiting (e.g., due to elevated intracranial pressure), which can impair gastric feeding. If problems are encountered, early transition to a post-pyloric feeding tube may be considered.(more on feeding intolerance here)
- More on nutrition in critical care here.
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questions & discussion
To keep this page small and fast, questions & discussion about this post can be found on another page here.
- Prophylactic use of hypertonic saline infusions have been demonstrated not to be effective in traumatic brain injury.
- In a polytraumatized patient, permissive hypotension should be avoided in the presence of traumatic brain injury.
Acknowledgement: Thanks to Dr. Richard Choi (@rkchoi) for thoughtful comments on this chapter.
- Brain Trauma Foundation – update on decompressive craniectomy (Hawryluk GW et al., 2020)
- Seattle International Severe TBI Consensus Conference – Management for patients with both brain oxygen and intracranial pressure monitoring (Chestnut R et al., 2020)
- Seattle International Severe TBI Consensus Conference – Management for patients with intracranial pressure monitoring (Hawryluk GWJ et al., 2019)
- Brain Trauma Foundation – Guidelines for the management of severe TBI, 4th edition (Carney N et al, 2016)
- CRASH3 (2019) – Use of tranexamic acid in traumatic brain injury
- POLAR (2018) – Early prophylactic hypothermia did not benefit patients with traumatic brain injury.
- RESCUEicp (2016) – Decompressive craniectomy for patients with traumatic brain injury improved survival, while increasing the likelihood of poor neurological outcomes.
- BEST-TRIP (2015) – ICP monitoring in traumatic brain injury didn't improve outcomes, compared to clinical and CT scan monitoring.
- Eurotherm3235 (2015) – For patients with traumatic brain injury and elevated ICP, hypothermia increased a likelihood of poor neurological outcomes.
- SAFE study (2014) – Albumin vs. crystalloid for fluid resuscitation, harm found in a subgroup of patients with brain injury.
- 21434843 Cooper DJ, Rosenfeld JV, Murray L, et al.; DECRA Trial Investigators; Australian and New Zealand Intensive Care Society Clinical Trials Group. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011 Apr 21;364(16):1493-502. doi: 10.1056/NEJMoa1102077 [PubMed]
- 27602507 Hutchinson PJ, Kolias AG, Timofeev IS, et al.; RESCUEicp Trial Collaborators. Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension. N Engl J Med. 2016 Sep 22;375(12):1119-30. doi: 10.1056/NEJMoa1605215 [PubMed]
- 27654000 Carney N, Totten AM, O'Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017 Jan 1;80(1):6-15. doi: 10.1227/NEU.0000000000001432 [PubMed]
- 28865528 Hollingsworth J, Mirabelli MM. Neurologic Emergencies on Computed Tomography of the Head. Semin Ultrasound CT MR. 2017 Aug;38(4):384-398. doi: 10.1053/j.sult.2017.02.005 [PubMed]
- 31563989 Khellaf A, Khan DZ, Helmy A. Recent advances in traumatic brain injury. J Neurol. 2019 Nov;266(11):2878-2889. doi: 10.1007/s00415-019-09541-4 [PubMed]
- 31659383 Hawryluk GWJ, Aguilera S, Buki A, et al. A management algorithm for patients with intracranial pressure monitoring: the Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC). Intensive Care Med. 2019 Dec;45(12):1783-1794. doi: 10.1007/s00134-019-05805-9 [PubMed]
- 31731899 Gadde JA, Weinberg BD, Mullins ME. Neuroimaging of Patients in the Intensive Care Unit: Pearls and Pitfalls. Radiol Clin North Am. 2020 Jan;58(1):167-185. doi: 10.1016/j.rcl.2019.08.003 [PubMed]
- Nelson, S. E., & Nyquist, P. A. (2020). Neurointensive Care Unit: Clinical Practice and Organization (Current Clinical Neurology) (1st ed. 2020 ed.). Springer.
- 33852501 McCredie VA, Chavarría J, Baker AJ. How do we identify the crashing traumatic brain injury patient – the intensivist's view. Curr Opin Crit Care. 2021 Jun 1;27(3):320-327. doi: 10.1097/MCC.0000000000000825 [PubMed]
- 33896528 Takahashi CE, Virmani D, Chung DY, Ong C, Cervantes-Arslanian AM. Blunt and Penetrating Severe Traumatic Brain Injury. Neurol Clin. 2021 May;39(2):443-469. doi: 10.1016/j.ncl.2021.02.009 [PubMed]