approach to head injured patient

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ผศ.ดร.กรองได อุณหสูต คณะพยาบาลศาสตร์ มหาวิทยาลัยมหิดล Approach to Head-Injured Patient

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Page 1: Approach to head injured patient

ผศ.ดร.กรองได อุณหสูต

คณะพยาบาลศาสตร ์มหาวิทยาลัยมหิดล

Approach to

Head-Injured Patient

Page 2: Approach to head injured patient

Cerebral Blood Flow (CBF)

CO2 CO2

vasodilator

dilation of cerebral vessels

BF

Blood volume

vasoconstriction

BF

Blood volume

O2 concentration

CBF

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Page 3: Approach to head injured patient

Intracranial Pressure (ICP)

Cranial vault: Brain 80% + Blood 10% +

Cerebrospinal fluid 10%

Normal intracranial pressure 10 mmHg

Pressure > 20 mmHg is abnormal

ICP CBF and cerebral perfusion

“Monro-Kellie hypothesis”

one volume expands…

one or both of the other 2 volumes must decrease

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Page 4: Approach to head injured patient

Cerebral Perfusion Pressure

CPP = MAP - ICP

CPP < 70 mmHg is associated with poor

outcome brain injury.

A systemic mean arterial pressure is 60-180

mmHg

Cushing response = cerebral ischemia; SBP,

wide PP, reflex bradycardia

SBP, maintain CPP do not ICP

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Page 5: Approach to head injured patient

Mechanism of injury Injury to the head

Shearing, tensile,

compressive stresses

Hemorrhage,

hematomas, contusions

Sudden deceleration

Impact pressure wave

Coup injury Contrecoup injury

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Page 6: Approach to head injured patient

Pathophysiology Injury

Primary injury

Fracture, hematoma

Secondary injury

Autoregulation

Hypercarbia,

cerebral edema,

ICP,

hypotension,

hypoxemia,

Initial damage Compensatory

mechanism

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Page 7: Approach to head injured patient

Pathophysiology of head injury

Primary injury

• Directly by the

external force

• Injury evident

on P/E and CT

scan

Secondary injury

• Occurs in the hours

to days following the

primary injury

• Cellular damage;

• Lack of oxygen

delivery

• Increased ICP

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Page 8: Approach to head injured patient

Secondary injuries

Hypoxia

Deceased oxygen supply increased cerebral blood volume, increasing ICP

Hypercapnia

CO2 is a potent cerebrovasodilator, increase cerebral blood flow and increased ICP

Hypotension

Overall blood loss contributes cerebral hypoperfusion

Intracranial hypertension

Cerebral edema leads to increased ICP

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Page 9: Approach to head injured patient

Cerebral ischemia CPP

Autoregulation

Vasoconstriction / Vasodilation

ICP & CPP

Maintain CPP

Failure of autoregulation

• cerebral vasodilation,

• blood brain volume,

• cerebral engorgement

• cerebral edema,

• blood brain volume,

• ICP, CPP

Cerebral ischemia

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Page 10: Approach to head injured patient

Cerebral ischemia

CO2 concentration / O2 concentration

CO2 dilates cerebral blood vessels

blood brain volume

Cerebral ischemia

ICP

Early signs & symptoms

Late signs

• Headache

• Nausea, vomiting

• Amnesia

• Altered LOC

• Restless, change

in speech, loss of

judgment

• Dilate,

nonreactive pupil

• Unresponse to

V/P

• Abnormal motor

• Change in RR

• SBP

• Widened PP

• PR

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Page 11: Approach to head injured patient

Categories of traumatic brain injury

Focal brain

injury

• Cerebral

contusion,

epidural,

subdural,

intracerebral

hematoma

Diffuse brain

injury

• concussion,

• Diffuse

axonal injury

Skull fractures

• Linear,

depressed,

comminuted,

basilar

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Page 12: Approach to head injured patient

Epidural hematoma Is a focal brain injury resulting in a collection

of blood between the skull & dura mater

Require immediate surgical intervention.

Signs & symptoms:

Initial LOC followed lucid interval rapid

unconscious

Persistent LOC

Hemiparesis or hemiplegia

Unilateral fixed or dilated pupil.

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Page 13: Approach to head injured patient

Subdural hematoma

Is a focal brain injury beneath the dura mater

Signs & symptoms:

Steady decline in LOC

Hemiparesis or hemiplegia

Unilateral fixed or dilated pupil.

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Page 14: Approach to head injured patient

Subdural hematoma Acute SDH

• Occurs within 48

hrs of initial injury

• Present with loss

of consciousness

and deteriorating

GCS

• Required

emergent

craniotomy for

evacuate of the

thick, coagulated

blood

Sub acute SDH

• Develops 2-24

days after initial

injury

Chronic SDH

• Apearent several

weeks to months

after initial injury

• Headache,

confusion,

speech deficits

be developed if

hematoma

enlarges

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Page 15: Approach to head injured patient

Category of head injury

Mild

head injury

• GCS = 13-15

• associated with

loss of

consciousness

or amnesia for

less

• than 1 hour

Moderate

head injury

• GCS = 9-12

• associated with

a loss of

consciousness

for up to a day

Severe

head injury

• GCS less than

or equal to 8

• associated with

loss of

consciousness

for more than

24 hours

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Page 16: Approach to head injured patient

1survey to head-injured patient

Step 1

ABCDE

Step 2

Immobilize

Step 3 Brief

neurological exam

Page 17: Approach to head injured patient

Step 1

Inspect

entire head

Step 2

Palpate

entire head

Step 3

Inspect

all scalp

Step 4

Determine

GCS

Step 5

Examine

cervical spine

Step 6

Document

Step 7

Reassess

& observe

2survey to head-injured patient

Page 18: Approach to head injured patient

Those older than 65 years of age

• are at increased risk of bleeding from head

injury because the aging brain shrinks away

from the skull, causing the veins that bridge

from the skull to the brain surface to be more

easily torn.