traumatic brain injury - ACEM Fellowship Notes

See also: [[intracerebral haemorrhage|ICH]], [[Head trauma radiology|CT brain]], [[Concussion]], [[paediatric head trauma]], [[pupil exam]] > [!references]+ > - [Rosen - TBI management](x-devonthink-item://57B55CFE-5572-4019-B857-9D5512E8D2BD?page=14) > - [Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition.](bookends://sonnysoftware.com/ref/DL/89417) > - [A management algorithm for adult patients with both brain oxygen and intracranial pressure monitoring: the Seattle International Severe Traumatic Brain Injury Consensus Conference (SIBICC).](bookends://sonnysoftware.com/ref/DL/291113) - [online link](https://link.springer.com/article/10.1007/s00134-019-05900-x) > - [Traumatic Brain Injuruy - Moore Trauma](x-devonthink-item://3673A856-E48F-44F0-83B7-25775BEEF8BF?page=406) > - [alfred TBI](https://emergencyeducation.org.au/traumatic-brain-injury-herniation-syndromes-part-one/) > - [Hypertonic Saline and Mannitol Therapy in Critical Care Neurology 2013](bookends://sonnysoftware.com/ref/DL/186787) > - Hb > 90 liberal transfusion → [TRAIN study 2024](https://pubmed.ncbi.nlm.nih.gov/39382241/) # Signs of raised intracranial pressure ( ICP ) > **Cushing triad** is ↑ SBP (increased [[pulse pressure]]), reflex bradycardia, and aponea (then coma) ; sign of [[Head trauma radiology#Brain Herniation types|terminal brain herniation]] (eg tonsillar or uncal) > - ↑ ICP → ↓ cerebral blood flow → ↑ systemic blood pressure → stimulation of baroreceptors → stimulation of vagal outflow → ↓ HR and RR **clinical** - [[Papilloedema|papilledema]] - localising neurology - *Cushing's Reflex* - [[Mydriasis|dilated pupils]] **Radiological** - sulcal effacement - obstructive hydrocephalus - ventricular effacement - brainstem compression/herniation # Management ## Blood pressure - Fluids or blood transfusion should be delivered to maintain a blood pressure as close to normal as possible, with a ==SBP of at least 110 mm Hg for those 15 to 49== and over 70 years of age, and at least 100 mm Hg for those 50 to 69 years old, MAP >80 ## Reducing ICP see [[#mannitol vs 3% saline advantages / disadvantages]] - Osmolar therapy can draw water across an intact BBB and thereby lower ICP - Prior to initiation of ICP monitoring, brain-directed osmotic therapies should be reserved for **patients with signs of transtentorial herniation or progressive neurologic deterioration not attributable to extracranial causes** ### Mannitol - Mannitol, 0.25 to 1 g/kg, is given every 6 hours up to a serum osmolality of 320 mOsm/kg ### Hypertonic saline see: [Hypertonic saline in severe traumatic brain injury: a systematic review and meta-analysis of randomized controlled trials.](bookends://sonnysoftware.com/ref/DL/169781) see also [[hyponatremia#hypertonic saline]] - Peripheral administration of ==150-250 mL of 3% sodium chloride== (which is comparable to 23.4%) has a low complication rate and may be an acceptable alternative (5mL/kg likely too high a dose for exam purposes) - HTS (23.4%), 30 to 60 mL, can be given every 6 hours, up to a maximum serum sodium level of 160 mEq/L. Treatment with 30 mL of 23.4% HTS appears to be at least as effective as mannitol at lowering ICP rapidly and reversing herniation, although a central line is necessary for safe administration Ratonalle: > **Mannitol** is the time-honored mainstay for the control of elevated ICP in acute severe TBI effectively reducing cerebral edema by producing an osmotic gradient that reduces brain volume and provides increased space for an expanding hematoma or brain swelling. The osmotic effects of mannitol **occur within minutes** and peak approximately 60 minutes after bolus administration. The ICP-lowering effects of a single bolus may last for 6 to 8 hours. It also promotes CBF by reducing blood viscosity and microcirculatory resistance. It is an effective free radical scavenger, reducing the concentration of oxygen free radicals that may promote cell membrane lipid peroxidation. > Proposed benefits of **hypertonic saline** include reducing secondary injury through effects on cellular modulation, decreasing cerebral edema, improving peripheral perfusion, decreasing ICP through vasoregulatory mechanisms, and upregulation of proinflammatory and prothrombotic mediators. > ==Because it is a potent diuretic, mannitol is preferred in cases of fluid overload, whereas HTS can be used as a resuscitative fluid.== - Mannitol can precipitate renal failure or hypotension if given in large doses. It may also induce a paradoxical effect of increased bleeding into a traumatic lesion by decompressing the tamponade effect of a hematoma. - Potential adverse events associated with HTS include renal failure, central pontine myelinolysis, and rebound ICP elevation. Few comparative data exist on brain-directed osmotic therapy. Selection of mannitol versus HTS should be made on an institutional basis, so that providers across various specialties (e.g., emergency medicine, trauma surgery, neurosurgery, anesthesiology) provide consistent care. ### mannitol vs 3% saline advantages / disadvantages *no good quality evidence of improved neuro or mortality outcomes for either drugs* | treatment | advantages | disadvantages | | ------------------------------- | ---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- | ------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------ | | **3% saline** 3mL/kg | - more sustained and significant effect of ↓ ICP - restore intravascular volume - less hypotension ; haemodynamically stable - monitor end point of therapy ( Na 144-155) | - tissue necrosis with extravasation → better via central line - hypernatremia - CHF / pulm oedema - [[DKA#cerebral oedema\|cerebral oedema]] - central pontine myelinosis - ↓ K - hypercholraemic acidosis | | **mannitol** 20% 0.5 - 1g/kg | - rapid reduction in ICP - useful in situations of fluid overload - safe in peripheral line | - hypotension 2/2 osmotic diuresis - risk of AKI - haemoconcentration | ## Ventillation ![[Pasted image 20230509220204.png| neurologic effects of hypocaponea]] ## Reverse anticoagulation ## TXA see: [Crash-3](https://www.thebottomline.org.uk/summaries/crash-3/), [[TXA]] - When given early after injury (within 3 hours), tranexamic acid (TXA) has demonstrated benefit in trauma with hemorrhage without increasing the risk of adverse events. ## normothermia ## Seizure ppx - benzodiazepines if active seizure - Keppra otherwise # Summary of neuroprotective measures *Maintaining cerebral oxygen supply:* - **Normoxia**: keep the PaO2 above 60 mmHg - **Low normocapnia:** keep the PaCO2 between 35-40 mmHg - **Normotension**: measure the MAP, and keep the systolic above 90mmHg - **Intracranial Pressure monitoring**: keep it under 20mmHg - **Cerebral perfusion pressure:** keep it 60-70mmHg - **Cerebral oxygenation monitoring**:keep the SjO2 >50%, and PbrO2 >55mmHg - **Managing increased intracranial pressure** for which there is a variety of strategies: - Draining the EVD ( about 20ml/hr, max) - Positioning the head straight - Removing the C-spine collar - Sedation : - Propofol sedation to decrease distress and thus decrease ICP - Barbiturate coma if other methods of lowering ICP have failed - Analgesia to prevent increased ICP in response to suctioning and routine care - Paralysis - Osmotherapy - Controversial measures - Decompressive craniectomy - Hypothermia - Dexamethasone *Decreasing cerebral oxygen demand:* - **Sedation** - **Propofol sedation** to decrease distress and thus decrease ICP - **Barbiturate coma** if medical and surgical methods of lowering ICP have failed - **Analgesia** - opioid selection is irrelevant, but opiate boluses increase ICP - **Seizure prophylaxis** is infrequently indicated, and the course is 7 days only *Controversial measures:* - Decompressive Craniectomy - Hypothermia - [[TXA]] - Higher transfusion thresholds # common sequelae of devastating brain injury and treatment ![[Pasted image 20240909010401.png]] # Primary vs Secondary brain injury >[!key points] Overview >**Primary brain injury** : results immediately from initial trauma eg SDH, concussion, DAI >**Secondary brain injury** : indirect from processes initiated by the trauma eg inflammation >**Secondary insults** : accelerate neurotoxic damage and worsen outcomes eg hypoxia, hypotension, ↑ glucose ## Primary brain injuries in TBI, *primary injuries* result immediately from the initial trauma: - Concussions (injuries to brain parenchyma) - hematomas (subural, epidural, intraparenchyma, intraventricular, and subarachnoid) - diffuse axonal injuries (DAI) - direct cellular damage - loss of blood-brain barrier - disruption of neurochemical homeostasis - loss of electrochemical function ## Secondary brain injuries Secondary injury is an *indirect result of the injury*. It results from processes initiated by the trauma. A wave of secondary damage is unleashed by the impact that results in a a series of deleterious cellular and sub cellular events (known as **secondary neurotoxic cascade**). This causes ongoing damage to the brain and ultimately results in a poorer neurologic outcome. Massive release of neurotransmitters, such as glutamate into presynaptic space. Ionic shifts activate enzymes, induce mitochondrial damage, and lead to cell death and necrosis. pro-inflammatory cytokines and other enzymes are released in an attempt to clean and repair the damage. Additionally, many survivable cells undergo apoptosis during secondary injury. apoptosis has been reported to occur longer than a year after injury. ## Secondary insults - hypotension - hypoxemia - hyperglycemia > Not to be confused with secondary injuries. Secondary insults accelerate neurotoxic damage and worsen outcomes.