TBI and the Neurosurgical Patient

Traumatic Brain Injury (TBI) is defined as an injury to the brain caused by an external force, resulting in a range of physical, cognitive, and emotional symptoms. The prevalence of TBI varies, with millions of cases reported annually, making it a significant public health concern.

A focused evaluation of a TBI patient typically includes:

1. Initial Assessment: Glasgow Coma Scale (GCS) to assess consciousness.
2. Neurological Examination: Checking motor responses, pupil reactions, and reflexes.
3. History Taking: Gathering information about the injury mechanism and symptoms.
4. Imaging Studies: CT or MRI scans to identify structural damage.

Indications for increased monitoring and consultation for surgical intervention in TBI patients include:

• Deteriorating Neurological Status: Changes in GCS or new neurological deficits.
• Significant Intracranial Hemorrhage: Evidence of bleeding on imaging.
• Increased Intracranial Pressure: Symptoms such as severe headache or vomiting.
• Severe Edema: Swelling that may require surgical intervention.

The patient was hypotensive with a small head laceration.

The patient was taken emergently to the operating room (OR).

The spleen was shattered, necessitating its removal.

After resuscitation, the patient was brought to the recovery room pending transfer to the ICU.

Not emerging from anesthesia as expected can indicate potential complications such as respiratory issues, prolonged sedation, or neurological concerns. This situation often necessitates further evaluation and monitoring in a more intensive care setting, such as the ICU, where additional diagnostic imaging like CT scans may be performed to assess for underlying issues.

The patient had several underlying cervical spine fractures and an undiagnosed traumatic brain bleed that required urgent surgical intervention with Neurosurgery.

Dylan Chirnside advocates for seat belts and transportation safety. He is involved in a social awareness campaign called 'Belt up. Live on.'

The photo-series aims to raise social awareness about the importance of seat belts and transportation safety by depicting the injuries of trauma survivors and sharing their stories.

Traumatic brain injury (TBI) is a non-degenerative, non-congenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical, and psychosocial functions, with an associated diminished or altered state of consciousness.

TBI is termed the 'silent epidemic' because it is often underdiagnosed and can have few overt symptoms, leading to a lack of awareness and recognition in trauma patients.

In trauma patients, TBI is presumed until proven otherwise, meaning it is prioritized in assessment and management, especially in the context of the ATLS protocol.

TBI is often overshadowed by the ABCs (Airway, Breathing, Circulation) because these are immediate life-threatening concerns that require urgent attention, while TBI may present with subtle or non-specific symptoms.

The underdiagnosis of TBI in the United States, particularly when there are concomitant life-threatening injuries, can lead to inadequate treatment and management of brain injuries, potentially resulting in worse outcomes for patients.

2.8 million traumatic brain injuries occur each year in the United States.

Up to 15% of those diagnosed with a mild TBI may have long-term problems.

There are 586 hospitalizations and 190 deaths related to TBI per day in the United States.

5.3 million Americans are currently living with long-term or lifelong TBI-related disabilities.

The leading cause of traumatic brain injury during this period is Falls, accounting for 35% of cases.

Traffic incidents were responsible for 17% of traumatic brain injuries in the United States from 2002 to 2006.

Men are 3 times as likely to sustain a traumatic brain injury compared to women.

The 'Struck By or Against' category accounted for 16.5% of traumatic brain injuries during this period.

Assault accounted for 10% of traumatic brain injuries in the United States from 2002 to 2006.

The incidence of TBI varies significantly across WHO regions, with some regions experiencing much higher rates than others. For instance, the South-East Asia Region (SEAR) has the highest incidence, followed by the Western Pacific Region (WPR) and Europe (EUR). In contrast, regions like the Americas (AMR) show lower incidence rates. This indicates a disparity in TBI occurrences globally, influenced by factors such as road traffic collisions and healthcare access.

The burden of TBI is highest in the South-East Asia Region (SEAR) with approximately 18.3 million cases per year, followed by the Western Pacific Region (WPR) with 17.3 million cases. Other regions like Europe (EUR) and Africa (AFR) have lower burdens, with 9.3 million and 7.9 million cases respectively. This highlights the significant regional differences in TBI prevalence and the need for targeted interventions.

Road traffic collisions are a significant contributor to the incidence of TBI, with certain regions showing higher rates of TBI resulting from these incidents. The incidence of TBI from road traffic collisions ranges from 320.0 to 530.0 per 100,000 people, indicating that areas with higher traffic volumes and less stringent safety regulations may experience greater TBI rates. This relationship underscores the importance of road safety measures in reducing TBI incidence.

Falls are the leading cause of TBI-related deaths in older age groups (>=65 years). This indicates a critical need for preventive measures and interventions targeting fall risks in this demographic to reduce TBI incidence and mortality.

1/3 of veterans with a probable TBI also met criteria for probable Post-Traumatic Stress Disorder.

23% of outpatients with TBI reported suicide ideation.

15-61% of individuals with a TBI also suffer from depression.

30-70% of individuals are estimated to experience sleep disturbances after a TBI.

The estimated economic costs of TBI in 2010 were $76.3 billion**, which included **$64.8 billion in indirect costs and $11.5 billion in medical costs.

Traumatic Brain Injury (TBI) accounts for 51.6% of mortality among trauma patients according to the 2010 data.

The progression of Intracranial Hemorrhagic Injury (IHI) is associated with:

1. Longer hospitalizations: 14.4 days compared to 9.7 days (p < 0.01)
2. Increased mortality: 24% compared to 3% (p < 0.01)

The pathophysiology of TBI involves a complex cascade of cellular and molecular events that occur following an injury to the brain. Key aspects include:

1. Primary Injury: Immediate damage caused by the mechanical forces of the impact, leading to cell death and disruption of neural pathways.

2. Secondary Injury: Subsequent biochemical processes that can exacerbate the initial damage, including:

   • Inflammation: Activation of immune responses that can lead to further neuronal injury.
   • Excitotoxicity: Overactivation of glutamate receptors causing calcium overload and cell death.
   • Oxidative Stress: Imbalance between free radicals and antioxidants, leading to cellular damage.
   • Metabolic Dysfunction: Altered energy metabolism and mitochondrial dysfunction.

3. Cerebral Edema: Swelling of brain tissue due to fluid accumulation, which can increase intracranial pressure.

4. Neurovascular Changes: Disruption of the blood-brain barrier and altered cerebral blood flow, affecting oxygen and nutrient delivery to brain tissue.

An accumulation of microscopic injury leads to macroscopic manifestations. This means that small, often unnoticed injuries at the cellular level can accumulate and result in observable changes or damage at the organ or system level.

The two types of cell injury are:

1. Reversible Cell Injury: This type of injury can be recovered from, characterized by swelling of the endoplasmic reticulum and mitochondrion, and clumping of chromatin during recovery.

2. Irreversible Cell Injury: This leads to necrosis and is characterized by more severe changes such as loss of ribosomes, lysosome rupture, membrane blebs, and fragmentation of the cell membrane and nucleus.

'Second hits' refer to additional injuries or stressors that occur after an initial injury, which can worsen outcomes and survival rates for the affected cells or tissues. This concept highlights the cumulative nature of cellular damage.

The progression of a cell from normal to irreversible injury leading to necrosis involves the following steps:

1. Normal Cell
2. Injury: The cell experiences injury, leading to changes such as swelling.
3. Reversible Cell Injury: The cell may recover from this injury if the damage is not too severe.
4. Irreversible Cell Injury: If the injury persists, it progresses to irreversible changes, leading to necrosis.
5. Necrosis: The cell undergoes necrosis characterized by fragmentation of the cell membrane and nucleus, nuclear condensation, and other severe alterations.

Primary Injury involves direct trauma and damage to neural tissue, which is irreversible.

Secondary Injury refers to injury to adjacent tissue caused by factors such as:

• Decreased perfusion
• Lipid peroxidation
• Free radicals and cytokines
• Cell apoptosis

The mechanisms of secondary injury are similar to those seen in a stroke, including impaired blood flow, compression, and local injury.

The central process involved in TBI pathophysiology is neuroinflammation, which includes microglial activation and astrogliosis.

Excitotoxicity leads to neuronal damage and cell death by causing excessive activation of glutamate receptors, resulting in increased intracellular calcium levels and subsequent cellular injury.

Inflammatory cytokines such as IL-1B, IL-6, and TNF-α contribute to blood-brain barrier (BBB) disruption and promote neuroinflammation, exacerbating the injury process.

BBB disruption can lead to increased permeability, allowing harmful substances to enter the brain, which can exacerbate neuroinflammation and contribute to further neuronal injury.

Extracranial trauma can lead to the release of inflammatory cytokines and other factors that contribute to the systemic inflammatory response, which can worsen the effects of TBI.

The key processes include excitotoxicity, metabolic disturbance, apoptosis, ischemia, oxidative stress, and neuroinflammation.

The mechanisms that worsen TBI include:

1. Hypoperfusion - Reduced blood flow to the brain.
2. Hypoxia - Insufficient oxygen supply to the brain.
3. Hypoglycemia - Low blood sugar levels affecting brain function.

The Monro-Kellie doctrine states that the total volume of the brain, cerebrospinal fluid (CSF), and blood within the skull remains relatively constant. If the volume of one component increases, the volume of at least one of the other components must decrease to maintain stable intracranial pressure (ICP).

According to the Monro-Kellie doctrine, when there is an increase in the volume of a mass within the skull, the intracranial pressure (ICP) may become elevated if the volumes of cerebrospinal fluid (CSF) or blood do not decrease to compensate for the increased mass volume.

A 'compensated state' in the context of the Monro-Kellie doctrine indicates that the intracranial pressure (ICP) remains normal despite the presence of a mass, as the volumes of other components (CSF or blood) have adjusted to accommodate the increase in mass volume.

A 'decompensated state' in relation to the Monro-Kellie doctrine indicates that the intracranial pressure (ICP) is elevated due to an increase in mass volume that cannot be compensated for by a decrease in the volumes of cerebrospinal fluid (CSF) or blood, leading to potential clinical consequences.

Factors contributing to increased ICP include:

• Airway or intrathoracic pressure
• Jugular venous pressure
• Increased PaCO2 and decreased PaO2
• Some anesthetics
• Vasodilators
• Seizures

Increased intracranial volume leads to:

• Increased intracranial pressure (ICP)
• Potential outcomes include:
  • Herniation
  • Reduced perfusion pressure

The compartments contributing to increased intracranial volume include:

• Blood volume
• CSF volume
• Cellular compartment (including mass lesions)
• Fluid compartment (including edema)

If autoregulation is defective, medical injury or ischemia can exacerbate increases in the cellular and fluid compartments, leading to further increases in intracranial pressure and potential neurologic injury.

Increased intracranial pressure (ICP) can lead to increased blood pressure (BP) as the body attempts to maintain cerebral perfusion, but this can also result in further complications such as herniation.

Cerebral Blood Flow (CBF) is crucial for delivering oxygen and nutrients to the brain, which are essential for maintaining brain health and function.

Cerebral Perfusion Pressure (CPP) is the pressure that drives blood flow to the brain, ensuring adequate delivery of oxygen and nutrients necessary for brain function.

Mean Arterial Pressure (MAP) is defined as the average blood pressure in the arteries throughout the body. It is important because it reflects the perfusion pressure that organs receive, including the brain.

Intracranial Pressure (ICP) is the pressure within the skull. It is regulated through homeostasis maintained by arterial inflow, venous outflow, and cerebrospinal fluid (CSF) dynamics.

Cerebral Perfusion Pressure (CPP) is calculated using the formula:
CPP = MAP - ICP.

• MAP is the driving force for cerebral blood flow.
• ICP acts as the resistance against this flow.
• A CPP of less than 50 mmHg indicates cerebral ischemia, while a CPP of less than 30 mmHg can lead to brain death.

Low Cerebral Perfusion Pressure (CPP) values indicate critical conditions:

• CPP < 50 mmHg: This level suggests cerebral ischemia, which can lead to inadequate blood flow to the brain.
• CPP < 30 mmHg: This level is associated with brain death, indicating a severe lack of blood flow and oxygen to brain tissues.

Autoregulation of cerebral blood flow is a mechanism that maintains stable blood flow despite changes in blood pressure. However, this autoregulation is limited and can fail under certain conditions:

• It fails if blood pressure (BP) falls significantly.
• It also fails if intracranial pressure (ICP) rises excessively, leading to compromised cerebral perfusion.

The normal and high ranges for these parameters are as follows:

Hypoventilation leads to an increase in PaCO2, which results in an increase in cerebral blood flow (CBF) and subsequently an increase in intracranial pressure (ICP).

Hyperventilation causes a decrease in PaCO2, leading to a decrease in cerebral blood flow (CBF) and a decrease in intracranial pressure (ICP).

Arterial hypoxemia results in an increase in cerebral blood flow (CBF) and an increase in intracranial pressure (ICP).

An increase in PaCO2 leads to cerebral vasoconstriction, which can affect cerebral blood flow and intracranial pressure.

The four areas affected by local injury are: 1. Normal 2. Oligemia 3. Penumbra 4. Infarct core

Oxygen extraction fraction (OEF) increases from Normal to Infarct core, indicating that as the tissue becomes more compromised, it extracts more oxygen from the blood.

As the brain transitions from Normal to Infarct core:

• Oxygen delivery (DO₂) decreases from 50-55 ml/100g/min in Normal to <12 ml/100g/min in Infarct core.
• Cerebral blood flow (CBF) also decreases from 50-55 ml/100g/min in Normal to <12 ml/100g/min in Infarct core.

The penumbra is the surrounding 'in-danger' tissue around the infarct core. After a brain injury, preserving the penumbra is crucial because it has the potential to recover if blood flow is restored, whereas the infarct core is irreversibly damaged.

After hemorrhage, the brain clots off bleeding areas, leading to physiological changes that resemble strokes, including compromised blood flow and potential infarction of surrounding tissues.

Seizures after TBI can cause hypoxia, which worsens the condition of the penumbra and can lead to further damage or expansion of the infarct core.

Overlapping oligemia areas are functionally similar to the penumbra, and overlapping penumbra regions have a high chance of dying, indicating that these areas are at significant risk of irreversible damage.

• Cerebral Edema: Swelling of brain tissue.
• Midline Shift: Displacement of midline structures due to pressure.
• Compression of Ventricles: Blocks or impairs cerebrospinal fluid (CSF) flow.
• New/Developing Infarcts: Areas of dead tissue that can bleed into infarcts.

TBI is primarily characterized by an accumulation of microscopic brain damage that includes bleeding, shear injury, and axonal injury.

If brain tissue survives a TBI, it can partially heal, but there will always be some residual damage.

A young, plastic brain can learn to function and adapt to deficits caused by TBI, but it may not always return to baseline functioning.

Coup and contrecoup injuries occur when the brain is subjected to rapid acceleration and deceleration forces.

• Coup Injury: This occurs at the site of impact where the brain strikes the skull due to a direct blow.
• Contrecoup Injury: This occurs on the opposite side of the impact, where the brain rebounds and strikes the skull after the initial impact.

Both types of injuries can lead to significant brain damage due to the movement and rotation of the brain within the skull.

Diffuse Axonal Injury (DAI) usually occurs with sudden rotation of the head, where shearing forces stretch the axons. It primarily occurs at the grey/white matter differentiation zone, which is the area between the body and axon of neurons. If the axon is injured but not severed, it may recover without secondary injury.

Common symptoms of Diffuse Axonal Injury (DAI) include impulsivity and confusion.

Key factors contributing to cognitive impairment after TBI include:

• Tau/P-Tau Accumulation
• Beta Amyloid Accumulation
• Cerebrovascular Damage
• Clearance Impairment
• APOE4e
• Hypertension
• Atherosclerosis
• Diabetes

Increased cerebrovascular damage following TBI leads to:

• Perivascular Damage
• Increased BBB Permeability
• Impaired clearance of neurotoxic proteins These factors contribute to long-term cognitive impairments and may exacerbate conditions similar to Alzheimer's disease.

The recovery process for individuals with TBI is characterized by:

• Variability: Each person's recovery is unique.
• Length and Difficulty: Recovery can be long and arduous, with some individuals experiencing incomplete recovery.

• Mechanical effect of hematoma
• Mechanical effect of oedema

Haematoma expansion is a leading cause of early deterioration, with up to half of the expansion occurring in the first few hours.

• Osmotic effect of the clot causes movement of serum into surrounding brain tissue (early)
• Inflammation; thrombin production (later)
• Red cell lysis; toxic effects of iron (delayed)
• Disruption of the blood-brain barrier; cytotoxic oedema

Perihaematomal oedema occurs in most patients and can contribute to mass effect and increased intracranial pressure (ICP).

• Red cell lysis
• Erythrophagocytosis

The graph illustrates three potential recovery paths after a concussion:

1. Path A (Green Line): Represents full recovery if the person waits a week before resuming activities, allowing the brain to heal without setbacks.

2. Path B (Brown Line): Shows initial recovery but plateaus and declines due to exceeding brain capacity, leading to increased neuroinflammation and post concussion syndrome.

3. Path C (Brown Line): Indicates a worsening condition when the concussion gets worse, making it easier to overdo activities and further aggravate the injury.

The 'Overload Zone' and 'Safe Zone' are critical concepts in managing brain capacity after a concussion:

• Overload Zone: This area indicates when brain activity exceeds its capacity (e.g., 50% capacity), leading to symptoms like headaches and dizziness, and further injury to the brain.

• Safe Zone: This area represents the capacity level where activities can be performed without aggravating symptoms, allowing for healing and minimal discomfort. Staying within this zone is essential for recovery.

The ATLS Neuro Exam includes the following components:

1. Level of Consciousness
2. Pupil size/reactivity
3. Motor function
4. Glasgow Coma Scale (GCS)

This exam serves as a baseline for monitoring changes in the patient's condition.

The goals include:

1. Prevent episodes of hypotension and hypoxia
2. Trend neuro exam to monitor changes
3. Identify changes that are suspicious for increased intracranial pressure (ICP)

The basic neuro exam includes:

1. Inspection
2. Patient complaints/issues (if able to respond)
3. Vital Signs (BP, Pulse, RR)
4. Glasgow Coma Scale (GCS)
5. Pupil assessment (reactive/non-reactive)

Common symptoms of increased intracranial pressure include:

• Changes in Level of Consciousness (LOC)
• Eye Issues:
  • Papilledema
  • Pupillary Changes
  • Impaired Eye Movement
• Posturing:
  • Decerebrate
  • Decorticate
  • Flaccid
• Decreased Motor Function:
  • Change in Motor Ability
• Headache
• Seizures:
  • Impaired Sensory & Motor Function
• Changes in Vital Signs:
  • Cushing's Triad (Systolic B/P, Pulse, Altered Respiratory Pattern)
• Vomiting
• Changes in Speech
• Infants:
  • Bulging Fontanels
  • Cranial Suture Separation
  • Increased Head Circumference
  • High Pitched Cry

The symptoms of elevated ICP include:

• Increased SBP
• Decreased Pulse
• Decreased Respirations

In contrast, the symptoms of shock include:

• Decreased SBP
• Increased Pulse
• Increased Respirations

Cushing's Triad consists of:

• Hypertension
• Bradycardia
• Irregular Respirations

It is a vital sign of brain trauma and indicates increased intracranial pressure, serving as a red flag in neuro emergencies.

Behavioral changes that can indicate increased intracranial pressure include:

• Vomiting
• Headache
• Seizures
• Posturing

Decorticate posturing indicates an injury above the brain stem, while decerebrate posturing indicates an injury at the brain stem.

Decorticate posturing is characterized by:

1. Arms flexed and adducted
2. Fists clenched
3. Legs extended
4. Plantar flexion

Decerebrate posturing is characterized by:

1. Arms extended and pronated
2. Wrists flexed
3. Legs extended
4. Plantar flexion

• Minor Brain Injury: 13-15 points
• Moderate Brain Injury: 9-12 points
• Severe Brain Injury: 3-8 points

Typical presentations of TBI include:

• Bleeding
• Edema/Mass Effect on surrounding tissue
• Symptoms such as:
  • Headache
  • Nausea
  • Vomiting
  • Confusion
• After effects of anesthesia (may vary)
• Effects of concurrent injury (may vary)

• Prevent hypoxia and hypotension
• Treat symptoms and provide supportive care
• Implement brain rest for 72 hours until the patient returns to baseline

Act with urgency because "Time is brain". A suspicion of deterioration is sufficient reason to initiate treatment.

The short-term management strategies for symptoms of TBI include:

1. Brain rest
2. Reversal of coagulopathy in cases of bleeding if concerned
3. Control systolic blood pressure (SBP) to <160, while avoiding hypotension and hypoxia
4. Maneuvers to improve cerebral perfusion pressure by managing persistently elevated intracranial pressure (ICP)
5. Repeat imaging as necessary
6. Serum sodium goal of 140-150
7. Initiating ICP monitoring if indicated (GCS <8)

Intracranial hemorrhage can be exacerbated by:

1. Blood thinners: NSAIDs, ASA, Plavix, Coumadin, Eliquis, Xarelto, fish oil, and herbal supplements.
2. High blood pressure: Specifically, systolic blood pressure (SBP) greater than 160 mmHg.

If coagulopathy is indicated, it should be reversed based on the known agent. If the agent is unknown, specific labs should be drawn to determine the coagulopathy in all trauma cases.

Intracranial hemorrhage is usually caused by:

1. Trauma
2. Hypertensive stroke
3. Mass lesions

CPP is calculated using the formula: CPP = MAP - ICP, where MAP is Mean Arterial Pressure and ICP is Intracranial Pressure.

The minimum MAP required to ensure adequate CPP is greater than 65 mmHg.

Inadequate CPP can lead to lethargy, confusion, slow recovery, and altered mental status (AMS).

To protect brain tissue perfusion, it is essential to prevent Anoxia and Hypotension.

Anoxia and Hypotension individually increase mortality risk by 25%, while combined they increase mortality risk by 75%.

Labetalol acts as an alpha-1, beta-1, and beta-2 receptor antagonist.

Cautions for Esmolol include bradycardia, congestive heart failure, and bronchospasm.

The dosing range for Nicardipine infusion is 5 to 15 mg/h.

Potential cautions when administering Enalaprilat include variable response and a precipitous fall in blood pressure with high-renin states.

Nitroprusside is a nitrovasodilator that acts on both arterial and venous systems.

Cautions for Nitroprusside include increased intracranial pressure, myocardial ischemia, and risks of thiocyanate and cyanide toxicity.

The recommended systolic blood pressure (SBP) goal is SBP < 160 mmHg.

Notifying Trauma Surgery or Neurosurgery ASAP is crucial because earlier intervention is associated with better outcomes in managing conditions related to cerebral perfusion pressure (CPP).

Initial assessments should include:

1. Assess Pain/Sedation
2. Elevate the head of the bed to 30 degrees
3. Treat temperature >99F
4. Perform STAT ABG and BMP to check sodium and osmolarity
5. Prompt MD evaluation

Initial non-contrast CT scans are used to evaluate injury and are beneficial in cases of neurological deterioration. Repeat CT scans may be performed as needed, particularly if there are changes in the patient's neurological status.

Repeat CT scans are debated for patients with normal or stable clinical exams, as their necessity can be questioned in these cases.

The current practice is to perform repeat CT scans 6 hours after injury and after any neurological changes occur.

The primary goal of hyperosmolar therapy in TBI patients is to keep ICP below 20 mmHg.

The two main types of osmotic agents mentioned are Mannitol and Hypertonic Saline.

Patients need serial labs to monitor osmolality and sodium (Na) levels during hyperosmolar therapy.

Mannitol is considered inferior overall to 3% NS usage for managing ICP.

Hypertonic Saline decreases CPP while lowering ICP, making it effective in managing intracranial pressure.

Ongoing research is focused on the use of 23% Hypertonic Saline bolus for managing TBI patients.

HTS was found to be more effective than mannitol in lowering both the cumulative and daily ICP burdens after severe TBI, with significantly lower mean cumulative ICP burden (15.52% for HTS vs 36.5% for mannitol) and daily ICP burden (0.3 ± 0.6 hours/day for HTS vs 1.3 ± 1.3 hours/day for mannitol).

Patients in the HTS group had a significantly lower number of ICU days (8.5 ± 2.1 days) compared to those in the mannitol group (9.8 ± 0.6 days).

The 2-week mortality rates were lower in the HTS group, but the difference was not statistically significant (p = 0.56).

HTS bolus therapy was superior to mannitol in reducing the combined burden of intracranial hypertension and associated hypoperfusion in severe TBI patients, with significantly fewer hours of ICP > 25 mm Hg and lower active titration of high CPPflow.

Both rapid onset of acute hypernatremia and rapid correction of chronic hyponatremia can lead to osmotic demyelination. This occurs due to a rapid increase in plasma sodium concentration, which can cause brain damage.

Rapid onset of acute hyponatremia and rapid correction of chronic hypernatremia can lead to cerebral edema, which is a serious complication that can result in brain damage, particularly in children.

Maintaining sodium goals between 140-150 mEq/L helps to prevent the complications associated with rapid changes in plasma sodium concentration, such as osmotic demyelination and cerebral edema, which can cause significant brain damage.

Early prophylactic hypothermia did not improve neurologic outcomes at 6 months compared to normothermia, with favorable outcomes occurring in 48.8% of the hypothermia group and 49.1% of the normothermia group.

In the hypothermia group, the rate of pneumonia was 55.0% and increased intracranial bleeding was 18.1%. In the normothermia group, the rates were 51.3% for pneumonia and 15.4% for increased intracranial bleeding.

Hypothermia was initiated rapidly after injury with a median time of 1.8 hours.

The risk difference in favorable outcomes was 0.4% (95% CI, -9.4% to 8.7%), indicating no significant difference in outcomes between the two groups.

The findings do not support the use of early prophylactic hypothermia for patients with severe traumatic brain injury as it did not improve neurologic outcomes at 6 months.

To decrease the incidence of early seizures occurring within the first 7 days post-injury. Common medications include Dilantin, Keppra, and possibly Valproate. However, it does not prevent late seizures (post-traumatic seizures).

Steroids are not helpful in the management of traumatic brain injury.

Hyperventilation is not helpful for long-term management; it can only temporize for less than 30 minutes. It requires monitoring of ETCO2 and can be difficult to manage effectively.

Patients are in a hypermetabolic and hypercatabolic state, leading to an increased need for glucose. It is important to keep the patient normovolemic and provide the necessary caloric intake to support recovery.

Indications for increased monitoring in TBI patients include:

1. Glasgow Coma Scale (GCS) Score: A GCS score of 8 or less indicates severe injury requiring close monitoring.

2. Neurological Deterioration: Any signs of worsening neurological status, such as decreased responsiveness or new focal neurological deficits.

3. Intracranial Pressure (ICP): Elevated ICP (>20 mmHg) necessitates increased monitoring to prevent secondary brain injury.

4. Seizures: Patients experiencing seizures require closer observation due to the risk of further complications.

5. Coagulopathy: Patients with bleeding disorders or those on anticoagulants need careful monitoring to manage potential hemorrhagic complications.

6. Age and Comorbidities: Older patients or those with significant comorbidities may require more intensive monitoring due to increased risk of complications.

Repeat previous steps if necessary to determine responsiveness.

The goal sodium level is 140-150 mEq/L.

Administer 3% NS (hypertonic saline) directed by sodium and osmolality levels.

The maximum volume of hypertonic saline (3%) is 500 mL.

Consider holding mannitol if the osmolar gap is greater than or equal to 20 mOsm/kg.

The target serum osmolality is 300-320 mOsm/kg.

Consider propofol with a bolus dose of 0.5-1 mg/kg and a continuous infusion max rate of 80 mcg/kg/min, or possibly induce pentobarbital coma with a loading dose of 5-15 mg/kg.

The recommended PaCO2 level is 30-35 mmHg, and it should be used for no longer than 30 minutes.

Consider surgical decompression if the patient is a surgical candidate.

• GCS <9 with anisocoria
• EDH >30 cm³

• 10 mg/kg bolus over 30 minutes
• 5 mg/kg/hr continuous infusion for 3 hours
• Then decrease by 1 mg/kg/hr every 30 minutes to achieve burst suppression based on EEG (2-5 bursts/min)

Key interventions include:

• Prevention of hypoxia
• Prevention of hypotension
• Frequent neuro exams

Typically, the following drains are placed:

• CSF to gravity
• Blood (JP) to suction

Patients should have neurochecks and GCS assessments at least every hour (q1h).

The common sites for burr hole placement include:

A burr hole is used to:

1. Relieve pressure from a hematoma or blood clot.
2. Facilitate drainage of accumulated fluid.
3. Access the intracranial space for further interventions if necessary.

The indications for performing a decompressive craniectomy include elevated intracranial pressure (ICP) that is refractory to medical management.

The aims of a decompressive craniectomy are to:

1. Decrease intracranial pressure (ICP)
2. Increase perfusion
3. Open a closed system, allowing room for swelling

The purpose of performing a decompressive craniectomy in emergency situations is for emergent decompression to relieve elevated ICP and prevent further brain injury.

Diffuse swelling may herniate out of the craniectomy site, leading to complications such as increased intracranial pressure and potential damage to brain tissue.

Patients need to wear a helmet until the edema has resolved and it is appropriate to restore the flap.

The two types of flaps are autologous flaps, which use the patient's own tissue, and artificial flaps, which use synthetic materials.

External ventricular drains are primarily used to drain cerebrospinal fluid (CSF) from the ventricles in cases of hydrocephalus.

The stopcock positioning in an EVD system indicates whether the drain is 'on' or 'off':

• Stopcock pointing north (upwards): EVD is 'off'. CSF remains in the collection chamber and does not enter the drainage bag. This position should be used before any nursing intervention involving movement.
• Stopcock pointing west: EVD is 'on'. CSF drains from the collection chamber into the drainage bag. This position should be restored after the intervention is finished.

The collection system is designed to manage the drainage of cerebrospinal fluid (CSF) from the ventricles of the brain. It allows for controlled drainage based on intracranial pressure (ICP) levels, ensuring that the appropriate amount of CSF is drained per hour as directed by ICP measurements.

Spinal drains are placed to monitor cerebrospinal fluid (CSF) leaks when the spinal cord or surrounding space is entered during surgery.

Spinal drains are managed similarly to external ventricular drains (EVD), as both are types of CSF drains used to monitor and manage fluid leakage.

Leakage of cerebrospinal fluid can result in a spinal headache, which is a common complication following spinal surgery.

The GCS-P, combined with CT scan findings, helps calculate the probability of outcomes in adults with TBI. It measures the odds of 6-month mortality and the likelihood of favorable or independent recovery, defined as moderate disability or good recovery on the Glasgow Outcome Scale (GOS).

GCS-P is calculated by subtracting the number of non-reacting pupils from the GCS score. It indicates the severity of the patient's condition and helps in predicting outcomes after TBI.

CT scan findings are classified into three categories: 1. No abnormality 2. Any one abnormality 3. Two or more abnormalities, which may include the presence of an intracranial hematoma, traumatic subarachnoid hemorrhage, or absence of basal cisterns.

As the number of abnormal CT findings increases, the mortality rates generally increase across all age groups. This trend indicates that patients with more severe CT findings are at a higher risk of mortality.

The percentage of favorable outcomes decreases as the number of abnormal CT findings increases. This suggests that more abnormal findings correlate with poorer prognoses across all age groups.

For patients with two or more abnormal CT findings, mortality rates tend to increase with age, indicating that older patients with significant CT abnormalities face higher mortality risks.

The GCS-P score is used to assess the level of consciousness and neurological status in TBI patients, helping to guide treatment decisions and predict outcomes.

1. IV administration of 4-factor PCC targeting INR level <1.3:
   • INR 2.0-3.9: 25 IU/kg
   • INR 4.0-6.0: 35 IU/kg
   • INR > 6.0: 50 IU/kg
2. Simultaneous administration of vitamin K (10 mg IV)
3. Serial INR monitoring with potential repeated PCC administration if necessary.

1. IV administration of Idarucizumab (2x 2.5g) for Dabigatran.
2. IV administration of Andexanetalfa (dosing according to time-window of last intake) for Factor-Xa inhibitors.
3. Unspecific reversal with 4-factor PCC or FEIBA (50 IU/kg BW).
4. Medicinal charcoal if drug intake was <4h.
5. Drug-level testing using agent specific anti-Xa activity.

1. Intensive systolic blood pressure reduction targeting ~140 mmHg.
2. Avoid hypotension by keeping systolic blood pressure > 100-120 mmHg.
3. Assess for other co-medications, including antiplatelet agents.

Thromboelastogram (TEG) provides real-time measurement of coagulation, allowing for the assessment of clot formation and stability.

The primary objective of the study is to identify the risk of traumatic hemorrhagic complications in patients with TBI who are using DOACs.

The primary outcome was any traumatic intracranial hemorrhage (ICH) on CT. Secondary outcomes included the use of reversal agents, secondary neurological deterioration, neurosurgical intervention within 30 days, length of stay (LOS), Glasgow Outcome Scale (GOS) at discharge, and mortality.

7.6% of the included patients presented with a traumatic intracranial hematoma (ICH).

The study concluded that TBI patients using DOACs have a low risk for ICH, but hematoma progression occurred in a substantial number of patients.

The mean length of stay (LOS) for patients was 6.5 days.

Progression of existing ICH was observed in 6 out of 17 patients who did not receive reversal agents.