TBI and the Neurosurgical Patient

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.

Mannitol is used to maintain ICPs below 20 mmHg, with early use being acceptable, but late use having limited data supporting its efficacy.

TBI is often overshadowed by the ABCs (Airway, Breathing, Circulation) during initial assessments, and it presents few overt symptoms, leading to underdiagnosis, especially when there are other life-threatening injuries.

TBI falls under the Disability category in the ATLS (Airway, Breathing, Circulation, Disability, Exposure) protocol, indicating its critical importance in trauma assessment.

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

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

'Second hits' refer to additional injuries that occur after the initial injury. These can worsen outcomes and survival rates by compounding the effects of the initial cellular damage, leading to more severe dysfunction or death of the affected cells.

Oxidative stress can lead to cellular damage, apoptosis, and metabolic disturbances, compounding the injury sustained during TBI and affecting recovery.

The mechanisms that worsen TBI include:

1. Hypoperfusion - Reduced blood flow to the brain, leading to inadequate oxygen and nutrient delivery.
2. Hypoxia - Insufficient oxygen supply to the brain, which can cause cell death and worsen injury.
3. Hypoglycemia - Low blood sugar levels, which can impair brain function and recovery.

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).

When a mass increases within the cranial space, it reduces the volume available for cerebrospinal fluid (CSF), which can lead to elevated intracranial pressure (ICP) if the compensatory mechanisms are overwhelmed.

Cerebral Blood Flow (CBF) is crucial for delivering oxygen and nutrients to the brain, which are essential for its proper functioning.

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

Mean Arterial Pressure (MAP) represents the average blood pressure in the arteries throughout the body, which is important for maintaining adequate blood flow to organs.

Intracranial Pressure (ICP) is the pressure within the skull, maintained by the balance of arterial inflow, venous outflow, and cerebrospinal fluid (CSF) dynamics.

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

• A CPP of <50 mmHg indicates cerebral ischemia.
• A CPP of <30 mmHg indicates brain death.
  MAP serves as the driving force, while ICP acts as the resistance affecting cerebral blood flow.

An increase in ICP can lead to a cascade of events:

1. Tissue edema occurs.
2. ICP rises further, compressing blood vessels.
3. This results in decreased cerebral blood flow.
4. Oxygen deprivation leads to the death of brain cells.
5. Edema forms around necrotic tissue, further increasing ICP.
6. Compression of the brainstem and respiratory center occurs, leading to accumulation of CO2.
7. Vasodilation happens, increasing blood volume and ICP, ultimately resulting in death.

Autoregulation of cerebral blood flow is limited by the body's ability to respond to changes in blood pressure (BP) and ICP.

• Autoregulation fails when BP falls or ICP rises, which can lead to inadequate cerebral perfusion and potential brain injury.

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.

The infarct core is the area of irreversible damage due to bleeding and injury, while the penumbra is the surrounding 'in-danger' tissue that is at risk but may still be salvaged. The goal after an injury is to preserve the penumbra to prevent further loss of brain tissue.

Seizures after TBI can lead to hypoxia, which exacerbates the damage to the penumbra and can result in further infarction. This worsens the overall outcome by increasing the area of brain tissue that is lost.

Oligemia areas overlap with the penumbra and are functionally similar, indicating that they are at risk of further damage. Overlapping penumbra regions have a high likelihood of progressing to irreversible injury, increasing the risk of brain tissue death.

• Cerebral Edema: Swelling of the brain tissue.
• Midline Shift: Displacement of brain structures due to increased pressure.
• Compression of Ventricles: Impairs cerebrospinal fluid (CSF) flow.
• New/Developing Infarcts: Areas of tissue death that can bleed into infarcts.

After TBI, if the brain tissue survives, 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.

A coup injury occurs when the brain impacts the inside of the skull at the site of the initial impact, typically resulting from a direct blow to the head.

A contrecoup injury is characterized by the brain bouncing off the inside of the skull on the opposite side of the initial impact, leading to injury at that site due to the brain's continued motion.

Rapid rotation of the brain cortex can exacerbate brain trauma by causing additional shear forces and damage to brain tissue, potentially leading to more severe outcomes such as diffuse axonal injury (DAI).

The types of intracranial hemorrhages include:

1. Epidural Hematoma - Blood collection between the skull and the dura mater.
2. Subdural Hematoma - Blood between the dura and arachnoid layers.
3. Subarachnoid Hemorrhage - Bleeding around the surface of the brain.
4. Intracerebral Hemorrhage - Blood within the brain tissue.
5. Intraventricular Hemorrhage - Blood within the brain ventricles.

Intracranial bleeding is usually diagnosed on non-contrast CT scans.

• Usually occurs with sudden rotation of the head
• Shearing forces 'stretch' axons
• Occurs at the grey/white matter differentiation zone (between body and axon of neurons)
• If axon is injured but not severed, it may recover without secondary injury
• Presents with impulsivity and confusion

The long-term consequences of TBI include:

• Tau/P-Tau Accumulation
• Beta Amyloid Accumulation
• Cerebrovascular Damage & Clearance Impairment
• Increased Cerebrovascular Damage
• Cognitive Impairment AD-like Pathology

Contributing factors to these consequences include:

• APOE4ε
• Hypertension
• Atherosclerosis
• Diabetes

Additionally, there is Increased Abeta & Tau Accumulation and Perivascular Damage involving JPs, MMPs, EC Death, and BBB Permeability.

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

Overstimulation can lead to a decline in brain capacity, aggravating symptoms such as headaches and dizziness, and increasing neuroinflammation. This can trigger post-concussion syndrome and result in permanent brain injury if the brain is overloaded.

The 'Safe Zone' indicates that if activity levels are kept below 25% capacity, there will be minimal headaches and no dizziness, allowing the brain to heal effectively without setbacks.

Exceeding brain capacity can lead to increased symptoms, such as headaches and dizziness, and can worsen the concussion, making recovery more difficult and potentially leading to permanent injury.

The ATLS Neuro Exam includes the following components:

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

The ATLS Neuro Exam serves as a baseline for changes in a patient's condition, allowing for effective monitoring and documentation of neurological status during trauma resuscitation.

The results of the ATLS Neuro Exam are documented in the patient's medical chart, ensuring that there is a record of the neurological assessment for future reference and monitoring.

The goals of a neuro exam in the perioperative period include:

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

The basic components of a neuro exam in the perioperative setting include:

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)

Cushing's Triad is a clinical syndrome characterized by:

• 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 in infants include:

• Irritability
• Developmental delay
• Poor feeding

The physical signs of increased intracranial pressure in infants include:

• Bulging fontanelle
• Macrocephaly
• Prominent veins
• Sunset eye sign
• Enlarged ventricles

Key symptoms to watch for during the inspection of a patient for increased intracranial pressure include:

• Vomiting
• Headache
• Seizures
• Posturing

Decorticate posturing indicates an injury above the brain stem, characterized by flexed arms and extended legs. In contrast, decerebrate posturing signifies an injury at the brain stem, with rigidly extended arms and legs.

Typical presentations include:

• Bleeding
• Edema/Mass Effect on surrounding tissue
• Symptoms such as:
  • Headache
  • Nausea
  • Vomiting
  • Confusion
• Possible after effects of anesthesia
• Possible effects of concurrent injury

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

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

The short-term management principles for TBI symptoms include:

1. Brain rest
2. Reversal of coagulopathy in cases of bleeding if concerned
3. Control systolic blood pressure (SBP) to be less than 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 (e.g., 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 when systolic blood pressure (SBP) is greater than 160 mmHg.

If coagulopathy is indicated, it is important to reverse the coagulopathy 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.

An adequate MAP for maintaining appropriate cerebral perfusion 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.

Maintaining SBP <160 is crucial for ensuring adequate cerebral perfusion pressure (CPP), which can be challenging in TBI management.

Earlier intervention is associated with better outcomes in patients with concerns about CPP.

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

CPP increases from 0 to 30 degrees of head elevation and then remains relatively stable at higher elevations, while ICP also increases with higher elevations.

Repeat CT scans are beneficial in the setting of neurological deterioration.

The use of repeat CT scans is debated for patients with normal or stable clinical exams.

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

Patients need serial labs for Osmolality and Sodium (Na) levels.

Hypertonic saline decreases CPP while lowering ICP, with good evidence supporting the use of boluses of 3% saline, and ongoing research into 23% bolus use.

Mannitol is considered inferior overall to the use of 3% saline for managing ICP.

Both can lead to a rapid increase in plasma sodium concentration, resulting in osmotic demyelination. This condition can cause significant brain damage, particularly affecting areas such as the extrapontine and pontine regions.

These conditions can lead to a rapid decrease in plasma sodium concentration, which may result in cerebral edema. This is particularly concerning in children, as it can lead to severe complications such as uncal herniation.

Sodium goals are set between 140-150 mEq/L to prevent the complications associated with rapid changes in plasma sodium concentration, such as osmotic demyelination and cerebral edema. Maintaining sodium levels within this range helps to ensure brain health and prevent damage.

Antiepileptic prophylaxis aims to decrease the incidence of early seizures (occurring within the first 7 days) using medications such as 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 (TBI).

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

Patients with TBI 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.

Treat hyponatremia and monitor serial sodium and osmolarity to direct therapy.

1. Stat head CT
2. Cerebrospinal fluid: Drain if appropriate and consult Neurosurgery if considering ventriculostomy or lumbar drain, if not already in place.

The maximum rate for continuous infusion of propofol is 80 mcg/kg/min.

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

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

The maximum volume of hypertonic saline (3%) that can be administered is 500 mL.

The recommended loading dose for inducing pentobarbital coma is 5-15 mg/kg.

Consider surgical decompression if the patient is a surgical candidate.

The criteria for considering medically induced coma include:

1. Refractory intracranial hypertension
2. Sodium levels between 145-155 (but less than 160)
3. Osmolality levels between 320-330
4. Repeat Head CT shows no surgically treatable lesion
5. Neurosurgical evaluation recommends non-surgical treatment

• ICP 21-35 for more than 4 hours
• ICP 36-40 for 1 hour
• ICP > 40 for 5 minutes
• ICP not less than 20 in 7 days without pentobarbital
• Evidence of brain death or herniation
• Side effects requiring discontinuation (e.g., hypotension, sepsis, hypercarbia)

The interventions include prevention of hypoxia and hypotension with frequent exams.

Typically, the Neurosurgeon places:

1. CSF to gravity
2. Blood (JP) to suction

Clear expectations need to be obtained with at least q1h neurochecks and GCS assessments.

The common sites for burr hole placement are:

The primary indication for decompressive craniectomy is elevated intracranial pressure (ICP) that is refractory to medical management.

The aims of decompressive craniectomy include:

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

Decompressive craniectomy involves removing a portion of the skull to relieve pressure, while decompressive craniotomy typically refers to creating an opening in the skull without removing a bone flap. Both procedures aim to manage elevated ICP, but craniectomy is more definitive for emergent decompression.

Diffuse swelling may herniate out of the craniectomy site, leading to complications.

Patients need to wear a helmet to protect the head until the edema has resolved and the flap can be restored.

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

The indications for using an external ventricular drain (EVD) include:

1. Monitoring ICP
2. Treating hydrocephalus, including negative-pressure hydrocephalus, where pressure level is set below zero, correcting intracranial hypertension (drainage for elevated ICP)
   • Watch for over and under drainage
   • Monitor for blood, accidental removal, kinks
3. Administering medication for intraventricular hemorrhage or ventriculitis
4. Diverting infected or bloodstained cerebrospinal fluid, preventing its absorption by the arachnoid villi
5. Treating hydrocephalus secondary to aneurysmal subarachnoid hemorrhage or a tumor

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

A CSF leak can result in a spinal headache, which is a common complication following spinal surgery.

The management of a spinal drain is similar to that of an external ventricular drain (EVD), as both are used to monitor and manage cerebrospinal fluid (CSF) drainage.

Early prophylactic hypothermia did not improve neurologic outcomes at 6 months compared to normothermia.

The findings do not support the use of early prophylactic hypothermia for patients with severe traumatic brain injury.