Traumatic Brain Injury/Closed Head Injury

True or False: Traumatic brain injury (TBI) or closed head injuries risks mirror those for spinal cord injury

True

Risk Factors for traumatic brain injury (TBI) or closed head injuries

-Males

-Ages 15-24

-Recidivism of high risk behavior

-Elderly, Children

Why are children and the elderly at risk for traumatic brain injury (TBI) or closed head injuries?

They tend to fall

Etiology of traumatic brain injury (TBI) or closed head injuries

-Extrinsic (trauma)

-Intrinsic (subarachnoid hemorrhage (SAH)) or hemorrhagic CVA

Name an example of a penetrating trauma

Gun shot

Name an example of a blunt trauma

Car accident

Injury that occurs at the time of the insult

Primary injury

Injury caused by further physiological deterioration after the primary injury, caused by hypoxia, hypercapnea, hypotension, cerebral edema, hypertension, all of which increase intracranial pressure (ICP)

Secondary Injury

True or False: All causes of secondary injury cause an increase in ICP and impact how much oxygen gets to brain tissue

True

Name primary trauma-related injuries

-Scalp laceration

-Skull fractures

-Concussion

-Contusion

-Hematoma

-Diffuse Axonal Injury (DAI)

True or False: Scalp lacerations tend to bleed profusely

True

How would a scalp laceration be treated?

Stapled, stitched, glued shut

What is important to keep in mind with scalp laceration?

Must think if anything happened under the skull

Skull fractures can be

-Open

-Closed

-Vault

-Basilar

Open skull fracture

Dura is torn

Why are open skull fractures considered better?

There is somewhere for brain to escape

Closed skull fracture

Dura is intact

Skull fracture commonly in the parietal and temporal

Vault

True or False: Basilar fractures are seen on conventional films

False

What diagnostic is used to identify a basilar fracture?

CAT scan

Signs & symptoms of basilar fractures

-Battle's sign

-Raccoon eye's

-CSF leak from nares/ears

-CN damage

Ecchymosis overlying mastoid process

Battle's sign

Ecchymosis in sub-conjunctively or periorbital region

Raccoon's eyes

CSF leak from nares

Rhinorrhea

CSF leak from ears

Otorrhea

How can nasal drainage of CSF be differentiated from mucus?

-Test for glucose

-Halo effect

Transient injury/no necrosis

Concussion

Signs & symptoms of concussion

-Brief LOC

-Confusion, disorientation, some amnesia

-Fatigue

-Sensitivity to noise

-N/V

-Headache

Diagnostics for concussion

-Skull films

-CT of head

True or False: Skull films and CT of the head for concussions show bleeding and necrosis

False

If there is lengthy LOC with a concussion what would be done?

Patient would be admitted & observed

True or False: It is important to check patients with a concussion for an increase in ICP

True

Treatment for concussion

-Observation

-Rest the brain (no TV, screen time, phone)

If someone who had a concussion were to continue activities that put them at risk for concussions before healed what would happen?

If they were to be hit again the exicted cells would die

Brain bruise (superficial parenchyma) usually secondary to acceleration/deceleration injury

Contusion

Impact against the object

Coup

The rebound

Contrecoup

Diagnostic for contusions

CAT scan

How long do contusion usually take to evolve

Over 2-3 days

True or False: Contusion can cause significant increase in ICP

True

A bleeding bruise

Hematoma

Blood between skull and dura

Epidural hematoma

Injury pattern of epidural hematoma

Skull fracture with middle meningeal artery laceration, from direct blow (MVC, fall)

Clinical manifestations of an epidural hematoma

-Brief LOC

-Lucid interval

-LOC with rapid deterioration (Ipsilateral pupil dilation

-Decorticate/decerebrate posturing)

Diagnostics for an epidural hematoma

CT of head

Treatment for epidural hematoma

Surgery to cauterize the vessel and evacuate the blood

What is the concern if we do not do surgery for a epidural hematoma?

The artery will bleed to the point there is so much pressure that the only place for it to escape is the foramen ovale. If this occurs, you instantly die because the brainstem is destroyed

Blood between dura and arachnoid, commonly from rupture of veins that connect brain and dura

Subdural hematoma

Clinical Manifestations of a subdural hematoma

Can be acute, where symptoms occur within hours of injury, to chronic, where onset of symptoms are insidious & progress over 1-2 months

Diagnostic for a subdural hematoma

CT of head

Treatment for subdural hematoma

-Craniotomy

-Burr hole

-Craniectomy

Surgical opening of the skull

Craniotomy

Drilling into the skull to relieve pressure

Burr hole

Procedure to removing part of the skull to allow for swelling

Carniectomy

Where is part of the skull stored from a craniectomy?

Stored in the abdomen or freezer

Widespread stretching and tearing of axons secondary to acceleration/deceleration or rotational injury resulting in diffuse microscopic changes

Diffuse Axonal Injury (DAI)

True or False: A CT is not helpful to diagnose diffuse axonal injury (DAI)

True

Diagnostic's for diffuse axonal injury (DAI)

Rely on clinical history and PE findings

Clinical Manifestations for Diffuse Axonal Injury (DAI)

Variable

A state lacking wakefulness and awareness

Coma

Treatment for diffuse axonal injury (DAI)

None

Name an example of primary non-trauma related injury

Subarachnoid Hemorrhage (SAH)

A type of hemorrhagic CVA that results in subararchnoid bleeding

Subarachnoid Hemorrhage (SAH)

Where subararchnoid space ?

Between arachnoid and the pia mater

Etiology of a subarachnoid hemorrhage (SAH)

-Cerebral aneurysm

-Arteriovenous

Where do cerebral aneurysm mist likely occur?

Circle of Willis

What is an arteriovenous malformation (AVM)?

No capillary beds are present so arteries go directly to veins

Risks for subarachnoid hemorrhage (SAH)

-30-60 years of age

-Family history

-Female

Clinical manifestations of subarachnoid hemorrhage (SAH)

-Sudden severe headache

-Nausea and vomiting

-Photophobia

-Nuchal rigidity

-Kernig's sign

-Brudzinski's sign

Why are there meningeal symptoms present for subarachnoid hemorrhage (SAH)?

Bleeding occurs in between arachnoid and pia where the meninges are

Diagnostics of subarachnoid hemorrhage (SAH)

CT of head

2 major complications of Subarachnoid Hemorrhage (SAH)

-Rebleeding

-Vasospasm

Why do vasospasm occur?

From blood surrounding the vessels which prevents blood from getting to where it needs to be

Why does re-bleeding occur?

The clots that form will naturally breakdown on their own

Clinical manifestations of rebleeding subarachnoid Hemorrhage (SAH)

-Deterioration on Hunt & Hess scale

-More profound symptoms of SAH

Treatment for rebleeding in subarachnoid hemorrhage (SAH)

-Prevent!

-Bedrest

-Quiet, dark room

-Limit visitors

-Stool softeners

-Control BP with meds (nitroprusside, metoprolol, hydralazine)

-Prevent seizures (phenytoin)

-Surgical repair

Clinical manifestations of subarachnoid hemorrhage (SAH) vasospasm

Same as for re-bleed, but not as acute

Treatment for subarachnoid hemorrhage (SAH) vasospasm

-Prevent!

-Nimodipine (calcium channel antagonist) x's 21 days

-Surgery

-Triple-H Therapy

Triple-H Therapy

-Arterial hypertension (If surgically clipped: SBP 160-200 mm Hg, If not clipped: SBP 120-150 mm Hg)

-Hypervolemia (LR & albumin boluses to maintain CVP 10-12 mm Hg)

-Hemodiltuion (Hct 33-36%)

Why do we give nimodipine for vasospasm prevention?

Prevent calcium being free moving causing increase in ICP

Overview of ICP principles

-Monroe-Kellie Hypothesis/Doctrine

-Autoregulation

-Cerebral Perfusion Pressure (CPP)

Monroe-Kellie Hypothesis/Doctrine

-Intracranial pressure comprised by brain (80%), CSF (10%), & blood (10%)

-Normal ICP < 15 mm Hg

-Increase in volume in one compartment must by compensated by a decrease in other(s)

To maintain constant cerebral blood flow through vasoconstriction, dilation, and production of CSF

Autoregulation

Cerebral Perfusion Pressure (CPP) is equal to

Cerebral blood flow (CBF)

How do you calculate cerebral perfusion pressure (CPP)

MAP-ICP

CPP range

70-100 mm Hg

Manifestations of increased ICP

-Altered LOC

-Headache

-Nausea and vomiting (to projectile vomiting)

-Papilledema

-Unequal pupil size

-Cushing's triad

-Decorticate/decerebrate posturing

-Return of Babinski

Cushing Triad

-Bradycardia

-Systolic hypertension

-Bradypnea (irregular respiratory rate)

Which posturing is worse decorticate or decrerebrate?

Decreebrate

What happens if decrebrate posturing is left untreated?

Brain herniation

True or False: Decorticate posturing is an indication of increase in ICP

True

Ways to monitor ICP

-Ventriculostomy

-Subarachnoid bolt

-Epidural monitor

An accurate way to monitor ICP via catheter into a ventricle

Ventriculostomy

What is a benefit of a ventriculosotomy

Can drain CSF

What is the main goal of secondary head injury?

Control ICP (< 20)

Management for an increase in ICP

-Positioning (HOB 30-34 degrees, Neck midline)

-Hyperventilation (Maintain PaCO2 35 +/- 2 mm Hg)

-FiO2 to maintain PaO2 > 70 mm Hg

-Minimize suctioning (administer lidocaine prior to necessary suctioning)

-Minimize PEEP, Sedate as needed

Why does positioning matter?

It prevents venous drainage

Why do we hyperventilate?

Keep CO2 down and prevent hypercapnia

If a patient is medically paralyzed what other treatments will we do?

They will be vented and sedated

If a patient with ICP has a temp too high what happens?

Increases cerebral metabolism