TBI and the Neurosurgical Patient

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p.1

What is the consensus definition of traumatic brain injury (TBI)?

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p.1

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.

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p.1
Definition and Consensus on TBI

What is the consensus definition of traumatic brain injury (TBI)?

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.

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Management Principles for TBI

How does mannitol function in the context of managing ICP?

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

p.2
Symptoms and Underdiagnosis of TBI

What are the common challenges in diagnosing TBI in trauma patients?

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.

p.2
Management Principles for TBI

What classification does TBI fall under in the ATLS protocol?

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

p.3
Symptoms and Underdiagnosis of TBI

What percentage of individuals are estimated to experience sleep disturbances after a TBI?

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

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Pathophysiology of TBI

What is the relationship between microscopic injury and macroscopic manifestations in pathophysiology?

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.

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Pathophysiology of TBI

How do 'second hits' affect outcomes in cellular injury?

'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.

p.5
Pathophysiology of TBI

What is the difference between primary and secondary injury in the context of TBI?

Type of InjuryDescription/Features
Primary InjuryDirect trauma and damage to neural tissue; irreversible
Secondary InjuryInjury to adjacent tissue due to decreased perfusion, lipid peroxidation, free radicals, cytokines, cell apoptosis; mechanisms similar to stroke (impaired blood flow, compression, local injury)
p.6
Pathophysiology of TBI

What are the potential effects of oxidative stress in TBI?

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

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Mechanisms that Worsen TBI

What are the mechanisms that worsen Traumatic Brain Injury (TBI)?

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.
p.8
Monro-Kellie Doctrine and Intracranial Pressure

What does the Monro-Kellie Doctrine state about the relationship between the brain, cerebrospinal fluid (CSF), and blood volume within the skull?

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).

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Monro-Kellie Doctrine and Intracranial Pressure

What happens to intracranial pressure (ICP) when a mass increases within the cranial space according to the Monro-Kellie Doctrine?

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.

p.10
Pathophysiology of TBI

What is the significance of Cerebral Blood Flow (CBF) in brain function?

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

p.10
Pathophysiology of TBI

What does Cerebral Perfusion Pressure (CPP) indicate in relation to brain health?

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.

p.10
Pathophysiology of TBI

What does Mean Arterial Pressure (MAP) represent in the cardiovascular system?

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.

p.10
Monro-Kellie Doctrine and Intracranial Pressure

What is Intracranial Pressure (ICP) and how is it maintained?

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

p.11
Monro-Kellie Doctrine and Intracranial Pressure

What is the relationship between Mean Arterial Pressure (MAP), Intracranial Pressure (ICP), and Cerebral Perfusion Pressure (CPP)?

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.
p.11
Pathophysiology of TBI

What happens when Intracranial Pressure (ICP) increases due to a cranial insult?

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.
p.11
Mechanisms that Worsen TBI

What are the implications of limited autoregulation in the context of Intracranial Pressure (ICP)?

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.
p.12
Mechanisms that Worsen TBI

How does hypoventilation affect cerebral blood flow and intracranial pressure?

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).

p.12
Mechanisms that Worsen TBI

What is the effect of hyperventilation on cerebral blood flow and intracranial pressure?

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

p.12
Mechanisms that Worsen TBI

What is the relationship between arterial hypoxemia and cerebral blood flow?

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

p.12
Mechanisms that Worsen TBI

How does an increase in PaCO2 affect cerebral blood vessels?

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

p.13
Pathophysiology of TBI

What is the significance of the infarct core and penumbra in the context of local brain injury?

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.

p.13
Pathophysiology of TBI

How do seizures after traumatic brain injury (TBI) affect the penumbra?

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.

p.13
Pathophysiology of TBI

What is the relationship between oligemia and the penumbra in brain injury?

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.

p.14
Pathophysiology of TBI

What are the manifestations of pressure and poor blood flow in the brain?

  • 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.
p.15
Pathophysiology of TBI

What happens to brain tissue after a Traumatic Brain Injury (TBI)?

After TBI, if the brain tissue survives, it can partially heal, but there will always be some residual damage.

p.15
Long-term Sequelae of TBI

How does a young brain respond to deficits caused by Traumatic Brain Injury (TBI)?

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

p.16
Mechanisms that Worsen TBI

What is a coup injury in the context of brain trauma?

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.

p.16
Mechanisms that Worsen TBI

What characterizes a contrecoup injury in brain trauma?

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.

p.16
Mechanisms that Worsen TBI

How does rapid rotation of the brain cortex affect brain trauma?

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).

p.17
Pathophysiology of TBI

What are the different types of intracranial hemorrhages indicated in the illustration?

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.
p.17
Role of Imaging in TBI Assessment

How is intracranial bleeding usually diagnosed?

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

p.18
Pathophysiology of TBI

What are the common characteristics of Diffuse Axonal Injury (DAI)?

  • 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
p.19
Long-term Sequelae of TBI

What are the long-term consequences of Traumatic Brain Injury (TBI) as illustrated in the diagram?

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.

p.20
Management Principles for TBI

What is a leading cause of early deterioration in patients with acute hemorrhage?

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

p.21
Pathophysiology of TBI

What are the consequences of overstimulation on brain capacity after a concussion?

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.

p.21
Management Principles for TBI

What is the significance of the 'Safe Zone' in relation to brain recovery after a concussion?

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.

p.21
Symptoms and Underdiagnosis of TBI

What happens if a person exceeds their brain capacity after a concussion?

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.

p.22
Management Principles for TBI

What components are included in the ATLS Neuro Exam as part of trauma resuscitation?

The ATLS Neuro Exam includes the following components:

  1. Level of Consciousness
  2. Pupil size/reactivity
  3. Motor function
  4. Glasgow Coma Scale (GCS)
p.22
Management Principles for TBI

Why is the ATLS Neuro Exam important in trauma management?

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.

p.22
Management Principles for TBI

How is the ATLS Neuro Exam documented in patient care?

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.

p.23
Management Principles for TBI

What are the goals of a neuro exam during the perioperative period?

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)
p.23
Management Principles for TBI

What are the components of a basic neuro exam in the perioperative setting?

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)
p.24
Symptoms and Underdiagnosis of TBI

What are the key vital sign changes associated with elevated Intracranial Pressure (ICP)?

Vital SignChange
Systolic Blood PressureIncreases (⬆)
PulseDecreases (⬇)
RespirationsDecrease (⬇)
p.24
Symptoms and Underdiagnosis of TBI

What are the key vital sign changes associated with Shock?

Vital SignChange
Systolic Blood PressureDecreases (⬇)
PulseIncreases (⬆)
RespirationsIncreases (⬆)
p.24
Symptoms and Underdiagnosis of TBI

What is Cushing's Triad and why is it significant in the context of elevated ICP?

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.
p.25
Symptoms and Underdiagnosis of TBI

What are some behavioral changes that can indicate increased intracranial pressure in infants?

Behavioral changes that can indicate increased intracranial pressure in infants include:

  • Irritability
  • Developmental delay
  • Poor feeding
p.25
Symptoms and Underdiagnosis of TBI

What are the physical signs of increased intracranial pressure in infants?

The physical signs of increased intracranial pressure in infants include:

  • Bulging fontanelle
  • Macrocephaly
  • Prominent veins
  • Sunset eye sign
  • Enlarged ventricles
p.25
Symptoms and Underdiagnosis of TBI

What are the key symptoms to watch for during the inspection of a patient for increased intracranial pressure?

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

  • Vomiting
  • Headache
  • Seizures
  • Posturing
p.26
Symptoms and Underdiagnosis of TBI

What is the difference between decorticate and decerebrate posturing in terms of brain injury location?

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.

p.28
Symptoms and Underdiagnosis of TBI

What are the typical presentations of TBI following trauma and post-operative neurosurgery?

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
p.29
Management Principles for TBI

What are the immediate interventions in the management of TBI?

  • Prevent hypoxia and hypotension
  • Treat symptoms and provide supportive care
  • Implement brain rest for 72 hours until returning to baseline
p.29
Management Principles for TBI

What should be done if there are changes in the examination of a TBI patient?

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

p.30
Management Principles for TBI

What are the short-term management principles for TBI symptoms?

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)
p.31
Management Principles for TBI

What factors can exacerbate intracranial hemorrhage?

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.
p.31
Management Principles for TBI

What should be done if coagulopathy is indicated in a patient with intracranial hemorrhage?

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.

p.31
Pathophysiology of TBI

What are the common causes of intracranial hemorrhage?

Intracranial hemorrhage is usually caused by:

  1. Trauma
  2. Hypertensive stroke
  3. Mass lesions
p.32
Management Principles for TBI

What is the formula for calculating Cerebral Perfusion Pressure (CPP)?

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

p.32
Management Principles for TBI

What is considered an adequate Mean Arterial Pressure (MAP) for maintaining appropriate cerebral perfusion?

An adequate MAP for maintaining appropriate cerebral perfusion is greater than 65 mmHg.

p.32
Management Principles for TBI

What are the consequences of inadequate cerebral perfusion pressure (CPP)?

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

p.32
Management Principles for TBI

What are the two main factors that should be prevented to protect brain tissue perfusion?

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

p.32
Management Principles for TBI

What is the increased mortality risk associated with Anoxia and Hypotension individually and combined?

FactorMortality Increase
Anoxia25%
Hypotension25%
Both Combined75%
p.33
Management Principles for TBI

What is the significance of maintaining systolic blood pressure (SBP) below 160 in TBI management?

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

p.34
Management Principles for TBI

What is the significance of early intervention in managing Cerebral Perfusion Pressure (CPP)?

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

p.34
Management Principles for TBI

What are the recommended initial assessments and interventions for a patient worried 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

p.34
Monro-Kellie Doctrine and Intracranial Pressure

How does head elevation affect Cerebral Perfusion Pressure (CPP) and Intracranial Pressure (ICP)?

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.

p.35
Role of Imaging in TBI Assessment

When are repeat CT scans considered beneficial in the context of traumatic brain injury?

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

p.35
Role of Imaging in TBI Assessment

What is debated regarding repeat CT scans for patients with traumatic brain injury?

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

p.36
Management Principles for TBI

What is the primary goal of hyperosmolar therapy in patients with elevated intracranial pressure (ICP)?

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

p.36
Management Principles for TBI

What are the key laboratory tests required for patients undergoing hyperosmolar therapy?

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

p.36
Management Principles for TBI

How does hypertonic saline affect cerebral perfusion pressure (CPP) and ICP?

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.

p.36
Management Principles for TBI

What is the comparative effectiveness of mannitol versus 3% saline in managing ICP?

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

p.37
Pathophysiology of TBI

What are the consequences of rapid onset of acute hypernatremia and rapid correction of chronic hyponatremia?

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.

p.37
Pathophysiology of TBI

What complications arise from rapid onset of acute hyponatremia and rapid correction of chronic hypernatremia?

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.

p.37
Management Principles for TBI

Why are sodium goals set between 140-150 mEq/L?

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.

p.38
Management Principles for TBI

What is the role of antiepileptic prophylaxis in TBI management?

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).

p.38
Management Principles for TBI

What is the effectiveness of steroids in TBI management?

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

p.38
Management Principles for TBI

What are the limitations of hyperventilation in TBI management?

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.

p.38
Management Principles for TBI

What nutritional considerations should be taken into account for TBI patients?

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.

p.39
Indications for Surgical Intervention in TBI

What are the absolute indications for ICP monitoring in patients with severe head injury?

IndicationCriteria
Severe head injury + abnormal CTGCS ≤ 8 AND abnormal CT
Severe head injury + normal CTGCS ≤ 8 AND at least 2 of the following:
- Age ≥ 40 years
- Motor posturing
- Systolic BP ≤ 90 mm Hg
p.39
Indications for Surgical Intervention in TBI

What are the relative indications for ICP monitoring?

Indication CategorySpecific Situations
Impossible serial neurological examIntubation, deep sedation, or paralysis
Immediate non-neurosurgical procedure
Large cerebral infarctionHigh risk of cerebral edema
Subarachnoid hemorrhage (SAH)With hydrocephalus
CNS tumor
CNS infection
p.41
Management Principles for TBI

What should be done if a patient with increased intracranial pressure has hyponatremia?

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

p.41
Management Principles for TBI

What are the first two steps in the stepwise treatment for increased intracranial pressure?

  1. Stat head CT
  2. Cerebrospinal fluid: Drain if appropriate and consult Neurosurgery if considering ventriculostomy or lumbar drain, if not already in place.
p.41
Management Principles for TBI

What is the maximum rate for continuous infusion of propofol in the management of increased intracranial pressure?

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

p.41
Management Principles for TBI

What is the target PaCO2 level for hyperventilation in the management of increased intracranial pressure?

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

p.41
Management Principles for TBI

What should be considered if the osmolar gap is greater than or equal to 20 mOsm/kg when administering Mannitol?

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

p.41
Management Principles for TBI

What is the maximum volume of hypertonic saline (3%) that can be administered for increased intracranial pressure?

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

p.41
Management Principles for TBI

What is the recommended loading dose for inducing pentobarbital coma in the management of increased intracranial pressure?

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

p.41
Indications for Surgical Intervention in TBI

What should be done if a patient with increased intracranial pressure is a surgical candidate?

Consider surgical decompression if the patient is a surgical candidate.

p.42
Indications for Surgical Intervention in TBI

What are the surgical indications for an epidural hematoma?

IndicationCriteria
GCS with anisocoria<9
Hematoma volume>30 cm³
p.42
Indications for Surgical Intervention in TBI

What are the surgical indications for a subdural hematoma?

IndicationCriteria
SDH thickness>10 mm
Midline shift>5 mm (regardless of GCS)
GCS decline>2
PupilsFixed and dilated or asymmetric
ICP>20 mm Hg
p.42
Indications for Surgical Intervention in TBI

What are the surgical indications for a parenchymal lesion?

IndicationCriteria
Lesion volume≥50 cm³
GCS with mass effect6-8 with midline shift ≥5 mm, cistern compression, or frontal/temporal contusion ≥20 cm³
Clinical courseContinued neurologic decline, refractory intracranial hypertension, or mass effect on CT due to lesion
p.42
Indications for Surgical Intervention in TBI

What are the surgical indications for a posterior fossa lesion?

IndicationCriteria
Mass effect on CTPresent
Neurologic declineDue to lesion
p.42
Indications for Surgical Intervention in TBI

What are the surgical indications for a depressed skull fracture?

IndicationCriteria
Open fractureGreater than cranium thickness
Open fracture with dural penetrationPresent
Associated intracranial hematomaSignificant
Depression>1 cm
Frontal sinus involvementPresent
Gross deformityPresent
Wound infectionPresent
PneumocephalusPresent
Gross wound contaminationPresent
p.43
Management Principles for TBI

What are the criteria for considering medically induced coma in patients with refractory elevated intracranial pressure (ICP)?

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
p.44
Management Principles for TBI

What are the criteria for failure of pentobarbital coma 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)
p.45
Management Principles for TBI

What interventions should be prioritized for every postop patient with TBI or suspected TBI?

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

p.45
Management Principles for TBI

What types of drains are typically placed by the Neurosurgeon for postop patients?

Typically, the Neurosurgeon places:

  1. CSF to gravity
  2. Blood (JP) to suction
p.45
Management Principles for TBI

What is the frequency of neurochecks and GCS assessments required for patients in recovery or TNU?

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

p.46
Indications for Surgical Intervention in TBI

What are the common sites for burr hole placement in the skull?

The common sites for burr hole placement are:

SiteLocation
Parietal burr holeParietal region
Frontal burr holeFrontal region
Temporal burr holeTemporal region
p.47
Indications for Surgical Intervention in TBI

What are the indications for performing a decompressive craniectomy?

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

p.47
Management Principles for TBI

What are the aims of decompressive craniectomy?

The aims of decompressive craniectomy include:

  1. Decrease ICP
  2. Increase perfusion
  3. Open a closed system, allowing room for swelling
p.47
Indications for Surgical Intervention in TBI

What is the difference between decompressive craniectomy and decompressive craniotomy?

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.

p.48
Mechanisms that Worsen TBI

What is a potential consequence of diffuse swelling in the context of craniectomy?

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

p.48
Management Principles for TBI

What precaution must patients take until the edema resolves and the flap can be restored after a craniectomy?

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

p.49
Management Principles for TBI

What is the primary function of external ventricular drains?

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

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Indications for Surgical Intervention in TBI

What are the indications for using an external ventricular drain (EVD)?

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
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Management Principles for TBI

What is the purpose of placing a spinal drain?

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

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Management Principles for TBI

What are the potential complications of a CSF leak after spinal surgery?

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

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Management Principles for TBI

How does the management of a spinal drain compare to that of an external ventricular drain (EVD)?

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.

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Management Principles for TBI

What was the primary finding regarding early prophylactic hypothermia in patients with severe traumatic brain injury?

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

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Management Principles for TBI

What was the conclusion regarding the use of early prophylactic hypothermia for severe traumatic brain injury patients?

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

Study Smarter, Not Harder
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