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Approach to
Head-Injured Patient

ผศ.ดร.กรองได อุณหสูต
คณะพยาบาลศาสตร์ มหาวิทยาลัยมหิดล
Cerebral Blood Flow (CBF)
O2 concentration 

 CO2

 CO2

vasodilator

vasoconstriction

dilation of
cerebral vessels
 CBF

 BF

 BF

 Blood volume

 Blood volume

ผศ.ดร.กรองได อุณหสูต
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
ผศ.ดร.กรองได อุณหสูต
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
ผศ.ดร.กรองได อุณหสูต
Mechanism of injury
Injury to the head
Sudden deceleration
Impact pressure wave
Shearing, tensile,
compressive stresses
Coup injury

Contrecoup injury

Hemorrhage,
hematomas, contusions
ผศ.ดร.กรองได อุณหสูต
Pathophysiology
Injury
Primary injury

Hypercarbia,
cerebral edema,
 ICP,
hypotension,
hypoxemia,

Fracture, hematoma

Initial damage

Autoregulation 

Secondary injury

ผศ.ดร.กรองได อุณหสูต

Compensatory
mechanism
Pathophysiology of head injury
Secondary injury
Primary injury

to days following the

• Directly by the

primary injury

external force

• Cellular damage;

• Injury evident
on P/E and CT
scan

• Occurs in the hours

• Lack of oxygen
delivery
• Increased ICP

ผศ.ดร.กรองได อุณหสูต
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
ผศ.ดร.กรองได อุณหสูต
Cerebral ischemia
CPP 
Autoregulation

Failure of autoregulation

Vasoconstriction / Vasodilation

• cerebral vasodilation,
•  blood brain volume,
• cerebral engorgement

 ICP & CPP
Maintain CPP

• cerebral edema,
•  blood brain volume,
•  ICP, CPP
Cerebral ischemia
ผศ.ดร.กรองได อุณหสูต
Cerebral ischemia
Cerebral ischemia

 CO2 concentration /  O2 concentration
CO2 dilates cerebral blood vessels
 blood brain volume
•
•
•
•
•

Headache
Nausea, vomiting
Amnesia
Altered LOC
Restless, change
in speech, loss of
judgment

•

 ICP

Early signs & symptoms
Late signs
ผศ.ดร.กรองได อุณหสูต

•
•
•
•
•
•

Dilate,
nonreactive pupil
Unresponse to
V/P
Abnormal motor
Change in RR
 SBP
Widened PP
 PR
Categories of
traumatic brain injury
Focal brain

Diffuse brain

injury

injury

• Cerebral
contusion,
epidural,

• concussion,
• Diffuse
axonal injury

subdural,

Skull fractures
• Linear,
depressed,
comminuted,
basilar

intracerebral
hematoma
ผศ.ดร.กรองได อุณหสูต
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.
ผศ.ดร.กรองได อุณหสูต
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.

ผศ.ดร.กรองได อุณหสูต
Subdural hematoma
Acute SDH
• Occurs within 48
hrs of initial injury
• Present with loss

Sub acute SDH
• Develops 2-24

Chronic SDH
• Apearent several

days after initial

weeks to months

injury

after initial injury

of consciousness

• Headache,

and deteriorating

confusion,

GCS

speech deficits
be developed if

• Required

hematoma

emergent

enlarges

craniotomy for
evacuate of the
thick, coagulated
blood
ผศ.ดร.กรองได อุณหสูต
Category of head injury
Mild

Moderate

Severe

head injury

head injury

head injury

• GCS = 13-15

• GCS = 9-12

• associated with

• associated with

• GCS less than
or equal to 8

loss of

a loss of

consciousness

consciousness

loss of

or amnesia for

for up to a day

consciousness

less

• associated with

for more than
24 hours

• than 1 hour

ผศ.ดร.กรองได อุณหสูต
1survey to head-injured patient
Step 1

Step 2

ABCDE

Immobilize

Step 3 Brief
neurological exam
2survey to head-injured patient
Step 1
Inspect
entire head

Step 6
Document

Step 2

Step 5

Palpate

Examine

entire head

cervical spine

Step 3

Step 4

Inspect

Determine

all scalp

GCS

Step 7
Reassess
& observe
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.

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Approach to head injured patient

  • 1. Approach to Head-Injured Patient ผศ.ดร.กรองได อุณหสูต คณะพยาบาลศาสตร์ มหาวิทยาลัยมหิดล
  • 2. Cerebral Blood Flow (CBF) O2 concentration   CO2  CO2 vasodilator vasoconstriction dilation of cerebral vessels  CBF  BF  BF  Blood volume  Blood volume ผศ.ดร.กรองได อุณหสูต
  • 3. 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 ผศ.ดร.กรองได อุณหสูต
  • 4. 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 ผศ.ดร.กรองได อุณหสูต
  • 5. Mechanism of injury Injury to the head Sudden deceleration Impact pressure wave Shearing, tensile, compressive stresses Coup injury Contrecoup injury Hemorrhage, hematomas, contusions ผศ.ดร.กรองได อุณหสูต
  • 6. Pathophysiology Injury Primary injury Hypercarbia, cerebral edema,  ICP, hypotension, hypoxemia, Fracture, hematoma Initial damage Autoregulation  Secondary injury ผศ.ดร.กรองได อุณหสูต Compensatory mechanism
  • 7. Pathophysiology of head injury Secondary injury Primary injury to days following the • Directly by the primary injury external force • Cellular damage; • Injury evident on P/E and CT scan • Occurs in the hours • Lack of oxygen delivery • Increased ICP ผศ.ดร.กรองได อุณหสูต
  • 8. 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 ผศ.ดร.กรองได อุณหสูต
  • 9. Cerebral ischemia CPP  Autoregulation Failure of autoregulation Vasoconstriction / Vasodilation • cerebral vasodilation, •  blood brain volume, • cerebral engorgement  ICP & CPP Maintain CPP • cerebral edema, •  blood brain volume, •  ICP, CPP Cerebral ischemia ผศ.ดร.กรองได อุณหสูต
  • 10. Cerebral ischemia Cerebral ischemia  CO2 concentration /  O2 concentration CO2 dilates cerebral blood vessels  blood brain volume • • • • • Headache Nausea, vomiting Amnesia Altered LOC Restless, change in speech, loss of judgment •  ICP Early signs & symptoms Late signs ผศ.ดร.กรองได อุณหสูต • • • • • • Dilate, nonreactive pupil Unresponse to V/P Abnormal motor Change in RR  SBP Widened PP  PR
  • 11. Categories of traumatic brain injury Focal brain Diffuse brain injury injury • Cerebral contusion, epidural, • concussion, • Diffuse axonal injury subdural, Skull fractures • Linear, depressed, comminuted, basilar intracerebral hematoma ผศ.ดร.กรองได อุณหสูต
  • 12. 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. ผศ.ดร.กรองได อุณหสูต
  • 13. 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. ผศ.ดร.กรองได อุณหสูต
  • 14. Subdural hematoma Acute SDH • Occurs within 48 hrs of initial injury • Present with loss Sub acute SDH • Develops 2-24 Chronic SDH • Apearent several days after initial weeks to months injury after initial injury of consciousness • Headache, and deteriorating confusion, GCS speech deficits be developed if • Required hematoma emergent enlarges craniotomy for evacuate of the thick, coagulated blood ผศ.ดร.กรองได อุณหสูต
  • 15. Category of head injury Mild Moderate Severe head injury head injury head injury • GCS = 13-15 • GCS = 9-12 • associated with • associated with • GCS less than or equal to 8 loss of a loss of consciousness consciousness loss of or amnesia for for up to a day consciousness less • associated with for more than 24 hours • than 1 hour ผศ.ดร.กรองได อุณหสูต
  • 16. 1survey to head-injured patient Step 1 Step 2 ABCDE Immobilize Step 3 Brief neurological exam
  • 17. 2survey to head-injured patient Step 1 Inspect entire head Step 6 Document Step 2 Step 5 Palpate Examine entire head cervical spine Step 3 Step 4 Inspect Determine all scalp GCS Step 7 Reassess & observe
  • 18. 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.