PAT 401 - Wk3: TBI

What Cerebral Perfusion Pressure is Required for Brain Cells?

70-90mmHg required to perfuse cells of brain

What causes Intracranial Pressure Increases

Edema

Excess Cerebrospinal Fluid

Hemorrhage

Tumors

What happens ICP approaches Arterial Pressure?

Hypoxia

Hypercapnia (increased CO2 base)

Leads to Brain Damage

Main Causes of Cerebral Hemodynamic Injury?

Blood Flow Issues

Intracranial Pressure Increases

Decreased O2 delivery

What are the 4 Stages of Increased ICP?

1. Vasoconstriction & External Compression

2. Compromised Oxygenation; system arterial cxn

3. Brain Hypoxia & Hypercapnia

4. Brain Herniates

Manifestation of Stage 1 Increased ICP

Alert, PERRLA, Eupnea, Normal BP/HR

Manifestation of Stage 2 Increased ICP

Episodic Confusion

otherwise normal

Surgical Intervention best here

Manifestations for Stage 3 Increased ICP

Hard to Stay Awake w/ Small reactive pupils

Slow Breathing, HTN, Full & Bounding Heart Beat

Surgery NEEDED HERE

Manifestations for Stage 4 Increased ICP

Comatose, Ipsilateral-Bilateral Dilatation & Fixation of Pupils

Cheyne-Stokes Breathing, Neurogenic Hypervents

Ataxic or Apneustic Breathing w/ HTN, Irreg Pulse

Surgery is Useless now

Most common causes for TBI

Blunt Trauma

Motor Vehicle Accidents

Primary TBI

Direct impact or Injury to brain

Focal Primary TBI

One Area Impacted —> open/close trauma, contusion, hematomas

Diffuse Primary TBI

Multiple Areas —> DAIs, Subarachnoid Hemorrhage, Concussion

Open Trauma

Breaks the Dura Mater —> exposure of cranial contents

Closed Trauma

Dura remains intact leading to focal or diffuse injuries

More common vs Open Wounds

Secondary Brain Injuries

Indirect result of Primary Injury that result hours to days later —> Hypoperfusion or Ischemia

What is Cerebral Perfusion Pressure

Difference btw Mean Arterial Pressure and Intracranial Pressure —> Crucial for O2 to Brain

What is the goal of 2ndary Brain Injury Management?

Prevent Hypoxia

Maintain Cerebral Perfusion Pressure

Coup Injury?

Brain is injured at site of impact

Contrecoup injury?

Injury from brain rebounding and hitting opposite side of skull

Contusion

Blood leak from injured vessel + LOC

Smaller Area of Impact = Higher Severity injury

Epidural Hematoma

Bleeding btw Dura & Skull causing Arterial Bleed & Fracture

Most Common Site for Epidural Hematoma?

Temporal Fossa

Manifestations of Epidural Hematoma

LOC at time of injury

Lucid Period (hours-days) 

Severe H/A, Vomiting, Drowsy, Confusion, Hemiparesis

Subdural Hematoma

Bleeding btw Dura & Brain —> venous bleed

Acute Subdural Hematoma

in Hours —> Expanding clots compress brain

Manifestations of Acute Subdural Hematoma

H/A, Drowsy, Restless, Agitation, Slowed Cognition + Confusion

Treatment for Acute Subdural Hematoma

Burr Hole to remove clot

Subacute SH?

Occurs 48h-2w after injury

Chronic SH?

Occurs Weeks to Months post-injury

Manifestations of Chronic SH?

Chronic H/A & Tenderness at site

Treatment for Chronic SH?

Craniotomy or Percutaneous Drainage

Intracerebral Hematoma

Bleeding inside brain —> Increased ICP & Compression as Edema & Ischemia worsens

Occurs 3-10d after injurys

Manifestations of Intracerebral Hematoma

Decreasing LOC

Diffuse Brain Injury

Many regions of brain affected d/t rotational / twisting movements or acceleration/deceleration forces

Diffuse AXONAL Injury

Whiplash like injury that shear/stretch axonal fibers & White matter tracts

Manifestations of DAIs

Behavioral, Cognitive & Physical Changes

Not visible on CT Imaging

CTE or Alzheimer’s in Long-Term Cases

Subarachnoid Hemorrhage

Bleeding disrupts nerve roots & arachnoid granulations impairing CSF reabsorption & vasospasm

Vasospasms w/ Microthrombosis in Subarachnoid Hemorrhage

Delayed Cerebral Ischemia in 3-14 days

Manifestation of Leaking Vessels in Subarachnoid Hemorrhage

Episodic H/A

Transient MS Changes

Visual//Speech Disturbances

Manifestation of Ruptured Vessels in Subarachnoid Hemorrhage

SUDDEN Throbbing

Explosive H/A w/ N/V

Visual Disturbance

Motor Deficits and LOC

Other Findings with Subarachnoid Hemorrhage

Meningeal Irritation & Inflammation

Nuchal Rigidity —> Stiff Neck

Kernig Sign —> Painful knee flexion

Brudzinski Signs —> Neck cause Hip to Flex

Treatment of Subarachnoid Hemorrahge

1. Control BP, ICP, Vasospasm & Fluids

2. Improve CPP

3. Prevent Ischemia & Hypoxia

4. Avoid Rebleeding

5. Surgery

Concussions

LOC lasting <30 minutes

Post-Trauma Amnesia for <24h

GCS of 13-15

Mild TBI

Attention & Memory Deficits, LOC for 30m

Initial Confusion for Several Minutes w/ Possible Retrograde amnesia

GCS: 13-15

Moderate TBI

Often confused, LOC 30m-6h

Anterograde Amnesia >24h

Decerebation —> rigid extended extrems

Decortication —> arms flexed to chest, legs rigid

LOC for days-weeks

Abnormal Brain Imaging

GCS: 9-12

Severe TBI

Brainstem Damage, LOC >6hours

Permanent Neurological Deficits: mov’t, verbal/written, comms, inability to learn and reason

GCS: 3-8

Cerebral Edema (TBI)

1. Vasogenic: increased permeability of BBB that cause fluid to enter brain

2. Cytotoxic: ischemia/hypoxia cause failure of transport systems

3. Interstitial: increased CSF volume + mov’t from ventricles in to ECF of brain tissue

Post-Concussion Syndrome

occurs with Mild-TBI, weeks-months after

H/A, Dizzy, Fatigue, Nervous, Anxiety, Irritable

Depression, Insomnia, Inability to Focus

Txn = Reassure & S/S Relief and 24h close obs

Posttraumatic Seizures (TBI)

Can occur within Days, upto 2-5 years after

Treat with Phenytoin & Neuromodulation

CTE (TBI)

Violent Behaviors

Loss of control

Suicide

Memory Loss & Cognition Decline for at least 12 Months

Confusion

Impaired Decision Making

Disoriented to Memory, Self and Location

Lethargic

Obtunded

Reduced Arousal w/ Limited Stimuli Response

Otherwise asleep unless stimulated

Stupor

Deep Unresponsiveness, requires vigorous stimuli to arouse

Withdrawn responses or Grabbing

Light Coma

Purposeful mov’t on stimulation only

Coma

No response, only deep pain yields motor mov’t

Deep Coma

Unresponsive to any stimulus

Cheyne-Stokes

Hyperventilation & Apneic Periods d/t midbrain, pons / medulla injury

Central Neurogenic Hyperventilation

Sustained Hyperventilation

midbrain, pons/medulla

Apneustic Respirations

Prolonged inhalation/exhalation

Cluster Respirations

Rapid respirations of near equal depth but irregular frequency

Ataxic Respirations

Irregular respirations w/ Prolonged periods of Apnea

GCS of 13-15

Suggest Mild Concussion

GCS of 9-12

Hemorrhage or Contusion

GCS of 3-8

Cognitive/Physical Disability / Death

Brain Death

No Potential for Recovery & No Homeostasis

Brain is Autolyzing / Autolyzed

Cerebral Death

Brainstem or Cerebellum intact, can continue homeostasis but no behavioral / environmental responses

Total Brain Death Criteria

1. All appropriate procedures done

2. Unresponsive Coma —> no motor and reflex responses

3. Apnea

4. No Brainstem function

5. Isoelectric EEG for 6-12 hours

Kinetic Mutism

Eye opening w/ Visual Tracking + Little to no Speech

Minimal Conscious

Evidence of self or environmental awareness

Locked-In Syndrome

Cannot communicate but is FULLY conscious with intact cognitive functioning

Mannitol Indications

reduce ICP post-head trauma, prevent/treat AKI, lowers intraocular pressure in acute glaucoma

Mannitol Mechanism

1. Increase osmolality of blood → water out of tissues into bloodstream

   1. Pulls water into nephron & caused decreased H2O and Na reabsorption → rapid peeing

Mannitol Desired

draw water out of brain into intravascular compartment → decreased cerebral edema & ICP

Mannitol Adverse

Fluid and electrolyte imbalances (Na,Cl,K), HF, Pulmonary edema, peripheral edema, hypovolemia, dehydration, tachycardia