Head injury Flashcards

1
Q

What is the definition of Traumatic Brain Injury (TBI)?

A

TBI refers to a non-degenerative, non-congenital brain injury caused by an external mechanical force, which may result in temporary or permanent impairment of cognitive, physical, and psychosocial functions, often with altered consciousness.

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2
Q

What are the mechanisms of injury in TBI?

A

TBI mechanisms include blunt trauma (e.g., motor vehicle accidents) and penetrating trauma. Alcohol is often a major contributing factor in many TBIs​

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3
Q

How is TBI classified based on the Glasgow Coma Scale (GCS)?

A

Mild TBI: GCS 13-15
Moderate TBI: GCS 9-12
Severe TBI: GCS 3-8

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4
Q

What is the Monroe-Kellie Doctrine?

A

The doctrine states that the cranial cavity is non-distensible and is filled to capacity with non-compressible components (CSF, blood, brain tissue). An increase in one component must result in a decrease in another or lead to an overall increase in intracranial pressure (ICP

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5
Q

What is cerebral perfusion pressure (CPP) and how is it calculated?

A

CPP is the net pressure gradient that drives oxygen delivery to cerebral tissue. It is calculated as CPP = MAP - ICP (or CVP), where MAP is mean arterial pressure and ICP is intracranial pressure​

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6
Q

What are the primary injuries associated with TBI?

A

Primary injuries include skull fractures, intracranial hematomas, brain contusion, axonal injury, and blood-brain barrier disruption

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7
Q

What are the causes of secondary brain injury in TBI?

A

Secondary injuries result from cerebral ischemia, cerebral edema, intracerebral hypertension, excitotoxic processes (e.g., glutamate release), inflammatory processes, and hypoxia

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8
Q

What is the significance of increased intracranial pressure (ICP) in TBI?

A

Raised ICP, when above 20 mmHg, can lead to cerebral ischemia, hydrocephalus, herniation, and is considered a medical emergency requiring prompt treatment

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9
Q

What are the signs of raised intracranial pressure (RICP)?

A

Signs of RICP include Cushing’s triad (hypertension, bradycardia, irregular respiration), headache, vomiting, and visual disturbances​

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10
Q

What are the management strategies for traumatic brain injury (TBI)?

A

Prevention of secondary injury by avoiding hypoxia, hyper/hypoglycemia, hyperthermia, and raised ICP
Maintaining adequate cerebral perfusion pressure (CPP)
Surgical evacuation of hematomas when necessary
Use of osmotherapy (e.g., mannitol) to reduce ICP​

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11
Q

What are the common types of intracranial bleeds associated with TBI?

A

Epidural hematoma: Caused by impact loading to the skull, often involving dural artery/vein laceration.
Subdural hematoma: Due to injury to cortical veins or pial arteries, associated with high mortality.
Subarachnoid hemorrhage: Bleeding into the space around the brain.
Intracerebral hemorrhage: Occurs within the brain parenchyma, often

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12
Q

What is cerebral edema and how does it develop in TBI?

A

Cerebral edema can be either:

Cytotoxic edema: Due to disruption of the cell membrane and failure of sodium-potassium pumps.
Vasogenic edema: Caused by disruption of the blood-brain barrier, leading to fluid extravasation into the brain tissue​

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13
Q

What are the components of the Cushing’s triad?

A

Cushing’s triad consists of hypertension, bradycardia, and irregular respirations

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14
Q

What are the types of cerebral edema in TBI?

A

Cytotoxic edema: Results from cell membrane disruption and sodium-potassium pump failure, leading to intracellular fluid accumulation.
Vasogenic edema: Caused by blood-brain barrier (BBB) disruption, allowing fluid to leak into the brain parenchyma​

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15
Q

What is the primary cause of secondary brain injury after TBI?

A

The key cause of secondary brain injury is cerebral ischemia, often due to brain edema, microvascular pathology, or cerebral vasospasm​

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16
Q

What role does cerebral autoregulation play in TBI?

A

Cerebral autoregulation allows the brain to maintain a constant blood flow despite fluctuations in blood pressure. This helps prevent both hyperperfusion and ischemia in the brain

17
Q

What is the treatment goal for raised intracranial pressure (ICP)?

A

The goal is to prevent secondary injury by reducing ICP, maintaining adequate cerebral perfusion pressure (CPP), and ensuring sufficient oxygenation and venous drainage from the brain​

18
Q

What are the indications for using anti-convulsant therapy in TBI patients?

A

Anti-convulsant therapy is indicated to reduce the incidence of early post-traumatic seizures, especially in patients with severe TBI, depressed skull fractures, intracranial hematomas, or contusions​

19
Q

How does mannitol reduce intracranial pressure (ICP) in TBI management?

A

Mannitol increases plasma osmolality, drawing water out of the brain across the blood-brain barrier, thereby reducing ICP​

20
Q

What are the risks associated with the use of mannitol in TBI management?

A

Risks include acute kidney injury, hyponatremia, hypokalemia, and osmotic nephropathy

21
Q

What is the significance of maintaining normocapnia in TBI patients?

A

PaCO2 is a powerful determinant of cerebral blood flow (CBF), and hypercapnia can lead to increased cerebral blood flow and raised ICP. Therefore, normocapnia helps prevent secondary brain injury​

22
Q

What are the extracranial causes of secondary brain injury?

A

Extracranial causes include hypoxia, hypotension, hypercarbia, hyponatremia, acidosis, hyperglycemia, and hyperthermia​

23
Q

the formula for CPP

A

CPP = MAP -ICP-central venous pressure