CONTENTS
- Rapid Reference 🚀
- Epidemiology
- Primary vs. secondary injury
- Glasgow Coma Scale (GCS)
- Initial evaluation
- Specific types of injury
- Management
- Neuroworsening s/p traumatic brain injury
- Podcast
- Questions & discussion
- Pitfalls
TBI – Initial management ✅
rapid diagnostics
- 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. 📖
coagulation optimization
- Aggressive reversal of therapeutic anticoagulants. 📖
- Consider tranexamic acid if <3 hours and moderate/severe TBI.
blood pressure control 📖
- 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.
- If hypotensive, start norepinephrine infusion immediately.
recognizing & treating ICP crisis shortly after admission 📖
- Suggested by neuroworsening, anisocoria, or posturing.
- Empiric hypertonic tx is reasonable while awaiting STAT CT scan.
seizure prophylaxis & diagnosis 📖
- Prophylactic levetiracetam (consider 2,000 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 scheduled acetaminophen and escalation to physical cooling if needed.
- Avoid hyponatremia.
- 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.
- Assault.
- 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 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
- 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.
- Hypoxemia.
- Hypercapnia.
- Seizures.
- Fever.
- Vasospasm.
- 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.
- 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 is more meaningful than the total score.
- Further discussion of the motor response to pain: 📖
labs
- Basic labs (glucose, electrolytes, Mg/Phos, CBC).
- Coagulation studies (including INR, PTT, fibrinogen, +/- TEG if available).
noncontrast CT of the head and C-spine
- 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).
- Even for isolated TBI, a C-spine CT scan is generally advisable.
- Repeat CT scanning should often be considered after 6-24 hours, based on initial CT scan, clinical evolution, and presence of anticoagulants.
indications for vascular imaging
- CT angiography (CTA) may be needed to evaluate 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).
- Basilar skull fracture with involvement of the carotid canal (e.g., petrous bone).
- Diffuse axonal injury with GCS ≤6.
- CT venography (CTV) may be indicated to evaluate for trauma-related cerebral venous thrombosis (CVT):
- Mechanism of cerebral venous thrombosis 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.
additional CT scans
- Polytraumatized patients often require CT scans of numerous body areas (the trauma pan-scan).
basics
- 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).
- DAI often causes autonomic dysfunction (e.g., hypertension, hyperpyrexia), possibly related to brainstem or hypothalamic injury.(Louis 2021) Some patients may develop paroxysmal sympathetic hyperactivity. 📖
imaging – CT scan
- Overall, CT scan may have only a ~50% sensitivity for diffuse axonal injury.(31731899)
- 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.
imaging – MRI
- Overall performance:
- MRI is more sensitive than CT scan, revealing both hemorrhagic and nonhemorrhagic lesions.
- 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.
- Findings include both:
- (#1) Nonhemorrhagic lesions: (~80%)
- DWI may be particularly sensitive for nonhemorrhagic lesions showing diffusion restriction (including some lesions that may not be detectable as hyperintensities on T2/FLAIR sequences).(31485117)
- Larger lesions may be hypodense on CT scan.
- (#2) Hemorrhagic lesions: (~20%)
- Can be well visualized using GRE/SWI sequences (which reveal microbleeds nicely). On T2/FLAIR sequences, these lesions may be seen as being hypointense.
- Larger lesions may be hyperdense on CT scan.
- Differential diagnosis of microhemorrhages: 📖
- (#1) Nonhemorrhagic lesions: (~80%)
- Commonly affected areas include the gray-white matter interface, corpus callosum, dorsolateral midbrain, and upper pons. (Tang 2015; 28865528)
management
- 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 dorsal pons and midbrain, thereby inhibiting the reticular activating system).
basics
- 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 anterior temporal areas.
- Over time, about a third of contusions may expand due to localized edema and/or ongoing bleeding (“blossoming” of the contusion to form intraparenchymal hematomas).
imaging
- 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)
basics
- 90% of epidural hematomas are arterial bleeds. The most common location is a parietotemporal hematoma due to laceration of the middle meningeal artery (which is usually associated with skull fracture).
- 10% of epidural hematomas are venous in origin, usually due to fractures causing laceration of venous sinuses (e.g., in the posterior fossa). Venous sinus displacement may occur, with subsequent occlusion of the venous sinus. (Tang 2015)
- 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.
imaging
- 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. Some clues which may help:
- (1) Epidural hematomas do not cross suture lines, since the dura is tacked to the skull at these lines (whereas subdural hematomas may as they occur under the dura mater).
- (2) An epidural hematoma can cross the midline or cross between the supratentorial and infratentorial regions (unlike subdural hematomas).
- (3) Epidural hematomas don't extent into the interhemispheric fissure (whereas subdural hematomas may).
- Swirl sign may indicate active hemorrhage: entry of unclotted fresh blood has lower attenuation than blood that has already clotted. There isn't necessarily a distinct “swirl,” rather the key finding is blood of varying density. 🌊
management
- 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 or 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).
basics
- 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.
- Since subdural hematomas usually result from a bleeding vein, the onset is generally more gradual than epidural hematomas. However, anticoagulated patients may have rapid progression of neurological deficits.
- Acuity classified based on delay to presentation: (Naidech 2022)
- Acute subdural hematoma: presents 0-3 days after trauma.
- Subacute subdural hematoma: presents 3-14 days after trauma.
- Chronic subdural hematoma: presents 15+ days after trauma.
causes of subdural hematoma
- Trauma:
- 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. However, this must be differentiated from a chronic asymptomatic subdural hematoma.
- Subdural hematoma patients can sometimes also present with a lucid interval.
- Post-procedural (e.g, neurosurgery, lumbar puncture) due to intracranial hypotension that increases transmural pressure across bridging veins. Subdural hematoma formation is one potential complication from overdrainage of a ventricular/lumbar drain. 📖
- Rarely may result from aneurysmal rupture.
presentation(s)
- Presentation may vary substantially (depending on the acuity, associated injuries such as concurrent traumatic brain injuries, and location of the hematoma).
- Subdural hematoma can exert diffuse pressure on the brain without causing focal neurological findings. This can cause nonspecific presentations including headache, nausea/vomiting, and confusion. Of course, focal neurologic findings may occur as well (e.g., mild hemiparesis or aphasia).
- Hemiparesis and pupillary abnormalities are the most common focal neurologic signs (which may reflect uncal herniation).(Louis 2021)
- Posterior fossa subdural hematoma may cause vomiting, cranial nerve deficits, cerebellar symptoms, and headache.(Naidech 2022)
imaging
- Subdural hematomas are crescent-shaped on imaging, typically hugging the skull. 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 (transtentorial subdural hematoma).
- Subdural hematoma can occur entirely along the falx (i.e., interhemispheric parafalcine subdural), which may suggest a coagulopathy.
- Swirl sign may be seen in active bleeding: Blood becomes brighter on CT as it clots. Thus, fresh blood may appear relatively darker compared to older, clotted components of the hematoma.
- Fluid-fluid level may suggest the presence of coagulopathy (or acute-on-chronic hematoma, discussed further below).
- CT scan may reveal chronicity:
- (1) Acute blood is hyperdense (in the absence of anemia). As blood clots, it becomes even more hyperdense (within hours of hemorrhage, lasting for a few days).
- (2) Subacute subdural hematomas may become isodense on days ~4-21. This may be difficult to detect.
- (3) Chronic subdural hematomas may eventually become hypodense after three weeks. Contrast enhancement of the edges of the hematoma may be seen.
- (4) Acute-on-chronic subdural hematoma may occur due to re-bleeding:(Nelson, 2020) Hyperdense acute blood may layer on top of a isodense/hypodense chronic component. Alternatively, blood of different ages may mix and result in an isodense collection.
management of acute subdural hematoma
coagulation optimization
- Review of coagulation laboratories and recent anticoagulant use.
- Anticoagulation should generally be reversed, if possible. 📖
monitoring
- There is a high rate of expansion and deterioration in patients who are initially managed conservatively.
- Consider interval head CT about every six hours until the hematoma is stable.(Nelson, 2020)
- EVD (external ventricular drain) for monitoring of ICP may be inadvisable, since drainage might encourage ongoing bleeding from the subdural hematoma.(Naidech 2022) As discussed above, overdrainage can actually cause a subdural hematoma.
seizure prophylaxis/management
- Acute subdural hematoma associates with a fairly substantial risk of seizure, especially among patients with reduced consciousness.
- Seizure prophylaxis is generally reasonable, for up to a week.
- Among patients with impaired consciousness, EEG monitoring should be considered.
- More on seizure prophylaxis and management in TBI below. 📖
drainage of acute subdural hematoma
- Neurosurgery usually is required to remove the hematoma.
- Indications for surgical drainage may include the following (noting that this determination should always be made by a neurosurgeon):
- >1 cm thickness.
- Association with midline shift >5 mm.
- GCS ≤ 8 plus any of the following:
- GCS has decreased by two or more points since admission to the hospital.
- Asymmetric or fixed and dilated pupils.
- ICP measurements consistently >20 mm. (Severe TBI patients may develop refractory ICP elevation with small subdural hematomas; management may include drainage and simultaneous decompressive hemicraniectomy).(Nelson, 2020)
- Potential complications of surgery include hematoma recollection, reaccumulation of fluid in the subdural space, subdural empyema, and tension pneumocephalus.(Naidech 2022)
chronic subdural hematoma
- Epidemiology: (Louis 2021)
- More likely in patients >50 years old, alcoholism, anticoagulation, and overdrainage of a ventriculoperitoneal shunt.
- In about half of cases, there may be no recognized head trauma.
- Symptoms: (Louis 2021)
- Enlargement of a previously asymptomatic hematoma can result from either re-bleeding (acute-on-chronic hematoma) or osmotic-mediated swelling of the fluid.
- Symptoms may be restricted to impaired mental status (potentially mimicking dementia).
- Management:
- Chronic subdural hematoma can exert mass effect and cause symptoms, in which case it should be drained. Due to the liquefied nature of a chronic subdural hematoma, this can often be managed with burr hole drainage and insertion of a Jackson-Pratt drain. (Naidech 2022)
going further
- Tweetorial by Richard Choi 7/19/22. 🌊
basics
- Traumatic SAH is not uncommon. Overall, trauma is the most common cause of subarachnoid hemorrhage.(29262441)
- 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).
imaging
- Typically, traumatic SAH is located over the cerebral convexities, rather than the sylvian fissures and basal cisterns (locations more suggestive of aneurysmal SAH).(31731899) They are typically thin.
- Traumatic SAH may be located adjacent to fractures or cerebral contusions.
- If there is confusion about whether the SAH was caused by trauma or spontaneous aneurysmal rupture, vascular imaging is indicated (e.g., CT angiography).📖 Rarely, a spontaneous aneurysmal SAH may cause loss of consciousness, which leads to an accident that causes subsequent traumatic brain injury.
management
- 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), although the presentation and timing of onset of this is somewhat more erratic.
- Vasospasm following traumatic SAH may occur earlier than vasospasm following aneurysmal SAH (as early as post-injury day #2).
- Risk factors for vasospasm include the following: (33896528)
- Larger overall blood volume.
- Younger age.
- Admission GCS ≤8.
- Nimodopine does not appear to improve outcomes in traumatic subarachnoid hemorrhage, based on a meta-analysis of several RCTs.(17110283)
- More on the management of subarachnoid hemorrhage and vasospasm here.
- Intraventricular hemorrhage 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.
- Intraventricular hemorrhage is usually not the primary finding in a patient with TBI. Lack of other imaging abnormalities might raise a question of whether the patient had a primary intraventricular hemorrhage with subsequent trauma due to loss of consciousness. Further discussion of primary intraventricular hemorrhage here: 📖
- Cerebral venous thrombosis often occurs when skull fractures cross cerebral venous sinuses (especially among patients with multiple skull fractures, or fractures involving the skull base).
- Diagnosis is generally based on CT venography, which should be obtained in at-risk patients. Additionally, the diagnosis of cerebral venous thrombosis should be considered in patients with unexplained worsening of cerebral edema, or new intracranial hemorrhage.(34618760)
- Management is challenging, as anticoagulation is often contraindicated initially (e.g., due to coexisting hemorrhages). Patients may benefit from delayed initiation of anticoagulation, when this may be safely accomplished.
- More on cerebral venous thrombosis here. 📖
basics
- Fat embolism refers to the presence of fat emboli within the bloodstream. This is quite common in some contexts (e.g., trauma, orthopedic surgery). However, the vast majority of patients with fat emboli in their blood are asymptomatic. Fat embolism syndrome (FES) refers to clinical deterioration attributable to fat emboli, which is rather rare. These terms are often used interchangeably, but it's important to remember that the detection of fat within the bloodstream is nonspecific.
- Fat embolism syndrome typically occurs in a delayed fashion, some days after an initial traumatic event. This reveals that FES is not simply a mechanical occlusive event. The pathophysiology may involve several components, such as:(34457354)
- Serum lipase converts neutral fat into inflammatory free fatty acids.
- An excessive inflammatory response may augment tissue damage.
- Activation of the coagulation cascade may exacerbate tissue ischemia.
causes
trauma
- Long-bone fractures (tibia, especially the femur).
- Pelvic fractures.
- Massive soft tissue injury (severe beating).
orthopedic procedures
- Intramedullary nail or rod placement.(34457354)
- Hip or knee arthroplasty.
- Percutaneous vertebroplasty.(30788612)
other surgical procedures
- Bone marrow transplantation or biopsy.
- Liposuction, cosmetic augmentation, or fat grafting.
other causes
- Acute pancreatitis.
- Sickle cell crisis with bone necrosis.
- Intraosseous access/infusion.(30788612)
- Lipid infusion.(30788612)
presentation
general
- Typically, FES develops insidiously over ~24-72 hours after a triggering factor (as listed above).(34457354) This may help differentiate FES from pulmonary contusion (which typically manifests within <24 hours).(Shepard 2019)
- Fever can occur.
respiratory failure
- Respiratory failure is usually a dominant clinical manifestation.(26895808)
- Hypoxemia is the most common finding (occuring in 96% of patients).(34457354) This may progress to ARDS, with diffuse pulmonary infiltrates.
- Diffuse alveolar hemorrhage may very rarely occur.(35396056)
neurologic dysfunction
- Mental status changes are common (~60%), ranging from delirium to coma.(34457354)
- Seizures occur in ~20% of patients (including convulsive and nonconvulsive status epilepticus).(28932982; 30788612)
- Focal neurological deficits occur in ~20% (e.g., hemiplegia, aphasia, agnosia).(28932982)
- Cerebral edema can occur, rarely requiring decompressive craniectomy.
- Some patients may have predominantly neurological involvement, without significant pulmonary dysfunction (“cerebral fat embolism”).(28932982)
petechial skin rash (~40%)
- Petechiae are typically on non-dependent surfaces of the axillae, upper thorax, neck, face, oral mucosa, and conjunctiva. (34457354)
- Petechiae may lag several days behind other manifestations, reducing their utility in early diagnosis. (26895808)
cardiovascular
- Pulmonary hypertension may occur, leading to right ventricular failure and shock.
- PSH (paroxysmal sympathetic hyperactivity 📖) can eventually develop in patients with severe brain injury due to fat emboli syndrome. (28932982)
laboratory investigation
general laboratory studies
- Acute thrombocytopenia and anemia can occur.
- Elevated erythrocyte sedimentation rate is common.(35396056)
fat detection
- Urinalysis can reveal lipiduria.
- Bronchoalveolar lavage may reveal fat globules within macrophages, if stained to detect lipid (e.g., with Sudan ink or oil red-O).(34457354)
- Fat detection overall suffers from poor sensitivity and poor specificity.
- Specificity is low because fat may be detected in a variety of contexts (e.g., asymptomatic fat emboli, sepsis, severe hyperlipidemia, aspiration). (34457354; 34936743) Overall, the quest for histological evidence of fat is probably more of a pathology parlor trick than high-quality evidence based medicine.
thoracic radiology
chest X-ray
- Bilateral infiltrates tend to be nonspecific.
- Chest radiograph may appear similar to other etiologies of ARDS.
CT scan
- Patchy ground-glass opacification with smooth interlobar septal thickening is the classic appearance (a crazy-paving pattern).
- 💡 Perhaps the most useful clue on thoracic radiology is interlobar septal thickening.
- There is often lobular sparing, with sharp margination between involved and normal lung.
- Small (<1 cm) nodules may be seen, sometimes with centrilobular, ground-glass characteristics.
- Usually these are seen in the context of associated ground glass opacities.
- Occasionally, nodules may be the predominant or sole abnormality.(Walker 2019)
- If pulmonary hypertension occurs, right ventricular dilation may occur.
Several examples of thoracic imaging are available in this paper by Newbigin et al. 📄
neuroradiology
- DWI
- DWI may show a “starfield” appearance as soon as one hour after symptom onset (with small hyperintense lesions scattered over a dark background). Some of these lesions may evolve into hyperintensities on T2 sequences, but not all.
- Later on (after 5-14 days), DWI lesions may become confluent.
- T2 reveals multiple nonconfluent hyperintensities beginning ~4 hours after symptom onset.(34457354) Lesions may be preferentially distributed across white matter in border zones between major arterial territories and in the deep gray matter, basal ganglia, thalamus, and cerebellum.(28932982)
- SWI or GRE sequences may be especially sensitive for the detection of microbleeds. The characteristic distribution is a “walnut kernel pattern” that involves the subcortical white matter, internal capsule, and corpus callosum (with relative sparing of the corona radiata and non-subcortical centrum semiovale). Cerebral emboli syndrome can be somewhat unique in terms of the large number of tiny lesions that it can produce. 🌊
- The differential diagnosis of these MRI findings usually focuses on: (34457354)
- Other causes of thromboembolism (e.g., cardiogenic septic emboli).
- Diffuse axonal injury (among patients with trauma).
- Disseminated intravascular coagulation.
- Watershed infarction.
- Cerebral vasculitis.
- CT scanning is generally normal. However, in severe cases CT may reveal cerebral edema, microhemorrhages, and/or ischemic lesions.
- Further discussion & images at radiopaedia: 🌊
differential diagnostic consideration: bone cement implantation syndrome (BCIS)
- Bone cement implantation syndrome (BCIS) results from embolization of cement used in orthopedic surgeries.
- BCIS tends to occur intraoperatively, within 30 minutes of cementing (unlike fat emboli syndrome, which usually occurs ~24-72 hours after the inciting event).(25367483)
- Treatment of BCIS involves hemodynamic stabilization in the context of right ventricular failure, as discussed further here: 📖
management
There is no specific therapy, so management is generally supportive.
pulmonary
- Usual supportive therapies may be required (e.g., supplemental oxygen, high-flow nasal cannula, intubation). About 40% of patients may require intubation.(34457354)
- The use of steroid in fat emboli syndrome is controversial, with some evidence suggesting that steroid reduces the incidence of hypoxemia.(28932982, 30788612) Steroid is not generally used among patients with fat emboli syndrome, but steroid administration could be a reasonable consideration among patients developing ARDS.
cardiovascular
- Right ventricular failure may require tailored management (e.g., inhaled pulmonary vasodilators and inotropes; discussed further here: 📖).
neurological
- EEG monitoring for seizures should be considered in patients with markedly depressed consciousness. Seizure prophylaxis is generally not warranted, but could be considered if there is high concern for seizure and EEG is unavailable. If seizures or status epilepticus occur, these may be treated using standard algorithms.
- In severe cases, ICP monitoring and therapy may be required.
- Fever prevention or management may be beneficial.
- If paroxysmal sympathetic hyperactivity develops, this should be managed. 📖
prognosis
- Mortality directly attributable to fat embolism syndrome is difficult to determine, but might be roughly ~10%. (28932982)
- Patients with severe presentations can make excellent neurological and cardiovascular recovery.(34457354)
anticoagulant management
- Any medication-induced coagulopathy should be emergently reversed in the presence of bleeding. 📖
- 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 treatment with either platelets, cryoprecipitate, plasma, or adding a fibrinolytic agent such as tranexamic acid. 📖
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. 🌊 A pre-planned follow-up study that evaluated CT scan findings suggested that tranexamic acid might prevent new hemorrhage development.(33262252)
- The treatment regimen used in CRASH 3 was administration of 1 gram of tranexamic acid as a bolus, followed by 1 gram of tranexamic acid infused over 8 hours.
fluid selection
- 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)
- Albumin is contraindicated, given signals of harm in the SAFE trial (and also a lack of any particular reason to use it).(15163774)
blood pressure
- 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).
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 crisis 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 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). 📖
- 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. 🌊
- ICP monitoring is generally 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 considered. (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) However, management should also take other variables into account (e.g., clinical examination and neuroimaging).(Nelson, 2020) Additionally, transient elevation of ICP (<10-15 minutes) don't necessarily mandate intervention. 📖
- 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. 📖
decompressive craniectomy
- 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.
hypothermia
- 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 doesn't appear to be beneficial for the management of ICP elevation in TBI.(31659383) For refractory ICP elevation, treatment usually focuses on either decompressive craniectomy or barbiturate coma.
target normoxia
- 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.
target normocapnia
- 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.
- Currently, targeting a normal PaCO2 seems reasonable. The lower end of normal might be a bit more attractive; The Association of Anaesthetists guideline recommends targeting a PaCO2 of 34-38 mm.(35001375)
- 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 epidemiology
- Seizures are common among patients with TBI, occurring in up to a third of patients with severe TBI.
- Risk factors for early seizures:(LaRoche 2018)
- Hematoma (either subdural, epidural, or intracerebral).
- Cortical contusion.
- Penetrating head injury, depressed skull fracture.
- GCS ≤10, prolonged unconsciousness.
seizure prophylaxis
- 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., 20 mg/kg or ~2,000 mg) may be considered in patients at higher risk of seizures.
- Valproic acid may be a useful choice in some patients with agitation, given its mood-stabilizing properties.(33896528)
- A week's duration is recommended, but additional therapy could be considered for patients with higher risk (e.g., patients who experienced a seizure or have worrisome EEG findings).
EEG monitoring
- About half of seizures may be nonconvulsive, thereby requiring EEG monitoring for detection.
- A period of EEG monitoring should be considered in all patients with moderate or severe TBI, to exclude subclinical seizures which may worsen outcome and/or exacerbate elevated intracranial pressure.(34618760)
- EEG should especially be considered in comatose patients in whom 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 expanding hemorrhage on serial CT scans, or other coagulopathies).
- For patients with intracranial hemorrhage, initiation of chemical DVT prophylaxis should be discussed with the neurosurgical team.
- 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 leak.
- Suspected infection, with inability to safely sample CSF.
general avoidance of fever
- Fever may increase cerebral metabolic stress and intracranial pressure, so this should be avoided.
- Fever prevention 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. 📖
- 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). 📖
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. 📖
- 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) 📖
- 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. 📖
causes include:
- Intracranial hemorrhage, or hemorrhage expansion.
- Venous sinus thrombosis (especially among patients who have skull fractures near a venous sinus).
- Blunt cerebrovascular injury (BCVI), including arterial dissection or pseudoaneurysm.
- Elevation of intracranial pressure (including worsening cerebral edema).
- Seizures or nonconvulsive status epilepticus (NCSE).
- CNS infection (e.g., meningitis following penetrating trauma, CSF leak, or external ventricular drain).
- Medication-induced neurologic dysfunction (e.g., accumulation of sedation; cefepime).
- Deterioration due to systemic abnormalities, for example:
- Shock.
- Fever, infection.
- Hypoxemia, hypercapnia.
- Hyponatremia, hypernatremia.
- Paroxysmal sympathetic hyperactivity (PSH).
- Vasospasm (may occur following traumatic subarachnoid hemorrhage).
evaluation may include:
- Review of vital sign trends, laboratory data, medications, recent events/procedures.
- CT head.
- Consider CTA (CT angiography) if blunt cerebrovascular injury is possible. Indications for CT angiography are discussed above. 📖
- Consider CTV (CT venography), particularly if skull fractures occur near a venous sinus.
- video EEG to exclude seizures.
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- 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.
Guidelines
- 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)
Review of seminal studies by The Bottom Line
- 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.
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