HEAD INJURIES

Mizan Kidanu
April 03/2013

OUTLINE
Introduction
Epidemiology
Anatomy
Causes
Classification
Diagnosis
Management
Complication

INTRODUCTION
A head injury is any trauma that leads to injury

of the scalp, skull, or brain

The injuries can range from a minor bump on

the skull to severe brain injury

EPIDEMIOLOGY
Number one killer in trauma
25% of all trauma deaths
50% of all deaths from MVA
200,000 people in the world live with the

disability caused by these injuries

50% in ages b/n 15 and 35

ANATOMY

Anatomy of the SCALP

Skin
firmly bound to the 3rd layer by
perpendicular fibers

Connective tissue
contain blood vessels of the scalp

Aponeurosis
fibrous sheet, found over much of
the vertex
attaches occipitalis to frontalis m

Loose connective tissue

accounts for the mobility of the scalp
blood tracks freely in this layer bilateral orbital
edema following sever head injury or cranial operation

Periosteum
adheres to the suture lines of the skull
collection of blood beneath this layer outlines the
affected bone cephalohematoma (children)

Anatomy of the meninges

Dura
endosteum and true meningeal layer
forms falx, tentorium, diaphragm

Arachinoid
vascular membrane
arachinoid granulations

Pia
highly vascular
dips into sulci and fissures
carries cortical vessels

CAUSES OF HEAD INJURY

Road traffic accident

65% of deaths following severe

head injury
Falls
Injuries at work place, during

sport, or at home
Assaults

CLASSIFICATIONS OF HEAD INJURY

1.

Blunt Vs Penetrating

2.

Primary Vs Secondary

3.

Mild, Moderate, or Severe

PRIMARY INJURY TO SCALP

Hematoma - Usually do not require Rx

- If large aspiration when it liquefies

Wounds

Abrasions - Cleaned & exposed

- Dressed - if hemorrhagic or serous
exudates
Lacerations - Cleaned & sutured( LA or GA)
- LA infiltrated into scalp
- Wound closure without tension

PRIMARY INJURY TO SKULL

Linear fractures - Do not require Rx
- At temporal area tear
MMAEDH

Depressed #s - Simple Vs Open

Surgery indicated in:
ocompression (large plate of bone)
ocosmetic area
o compound/open wound:
wound debridement
elevate the depression
suture dural laceration

 Fractures of the skull base

Diagnosis
oHistory - nasal bleeding,
oPhysical examination
Raccoon eyes
Battle sign
Rhinorrhea,......
Management:

conservative, advise on danger Sn

closure of dura - persistent CSF leak

PRIMARY BRAIN INJURY

The damage caused to the brain at the moment of

impact

Concussion
temporary neuronal dysfunction after blunt head trauma
head CT is normal, & deficits resolve over minutes to hours

Contusion/laceration
bruise of the brain
breakdown of small vessels and extravasation
of blood into the brain

Diffuse axonal injury

damage to axons throughout the brain
most frequent finding in patients who die from severe head injury

Mechanisms
Coup & counter-coup injuries
Common sites:-

undersurface of frontal lobe

tip of temporal lobe

SECONDARY BRAIN INJURY

Extracranial

hypoxia
hypotension
Intracranial

hematoma
brain edema
raised ICP
infection

DIAGNOSIS
History
Age
Loss of consciousness
Cause, circumstance and mechanism of

injury
Presence of headache & vomiting
Seizures
Anticoagulant use,.

ASSESSMENT OF NEUROLOGICAL FUNCTION

AND OF CONCIOUS LEVEL
Glasgow Coma Score
Best Eye Response (4)
No eye opening1
Eye opening to pain...2
Eye opening to verbal command....3
Eyes open spontaneously....4
Best Verbal Response (5)
No verbal response 1
Incomprehensible sounds. ..2
Inappropriate words. .3
Confused ..4
Orientated 5
Best Motor Response (6)
No motor response.....1
Extension to pain....2
Flexion to pain.....3
Withdrawal from pain.....4

Classification of head injury

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

Exclude other causes of depressed

conscious level (causes of coma)
No focal signs

drugs (alcohol, opiate)

circulatory collapse
hypothermia / hyperthermia
concussion
meningitis, encephalitis
subarachinoid hemorrhage
Focal signs present

cerebral abscess ,infarction, tumor

intracranial hemorrhage

Investigations

Skull radiograph
CXR and X-ray of cervical spines
CT-Scan - first line investigation

Indication for CT-scan

GCS<13 at any stage
GCS =13 or 14 at 2 hours following injury
Suspected open or depressed #
Any sign of basal skull #
Post-traumatic seizures
Focal neurologic deficit
Post-traumatic amnesia of >30 minutes
Persistent vomiting
Coagulopathy
Significant mechanism of injury

GENERAL MANAGEMENT OF HEAD INJURY

ABC rule

stabilization of airway, breathing and circulation

IV access - maintain normovolemia
- hypotonic/glucose containing fluids
should not be used
endotracheal intubation (e.g: GCS 8, hypoxia,)
Head end elevation - 300
Treat co-existing injuries

chest drain - tension pneumothorax

cervical collar - # of cervical spine,.

Anticonvulsants
may decrease early posttrauma seizures but

no benefit in long term epilepsy prevention

Phenytoin

Loading dose = 18 - 20 mg/kg

Maintenance dose = 100 mg q 8 hrly

Regular observation at half hourly interval:

GCS
BP, HR, RR, and Temperature
oxygen saturation
pupil size & reactivity
limb movement

EPIDURAL HEMATOMA
Usually from torn middle meningeal artery

and/or vein
Other causes:

torn dural sinuses(e.g: saggital sinus)

oozing from diploe bone & stripped dura
Uncommon but serious,1- 4% of TBI
Highest among adolescents and young adults
Skull fractures in 75-95%

Clinical presentation

lucid interval (in 1/3 of cases) associated with

headache vomiting, drowsiness, confusion,
aphasia, seizures and hemiparesis
epidural hematoma due to venous bleeding
neurologic decline is slower
posterior fossa EDH - elevated ICP

Diagnostic evaluation
CT scan - lens shaped collection
- hematoma volume
estimation

Management
craniotomy / ?burr hole

Prognosis-mortality -10%

SUBDURAL HEMATOMA
Pathophysiology

result from the tearing of bridging veins crossing the

subdural space or hemorrhage from severe cerebral
contusions
Spread more diffusely over the hemisphere

than extradural and are often associated with

diffuse swelling of the underlying hemisphere

Clinical manifestations - depends on type

ACUTE SUBDURAL HEMATOMA

1-2 days after onset

coma in (56%)
lucid interval (12-38%)
posterior fossa SDH - signs of increased ICP
Result from:

torn bridging veins

cortical lacerations
torn dural sinuses

CT SCAN FEATURES

clot is bright or mixed-density

crescent-shaped (lunate)
may have a less distinct border
does not cross the midline due to
the presence of falx
Signs of mass effect:

ventricular compression, midline

shift and reduction in the size of
the basal cisterns

SUBACUTE SUBDURAL HEMATOMA

After approximately 1-2 weeks the subdural

collection become isodense to grey matter

detection may be challenging & recognized when:

effacement of cortical sulci

deviation of lateral ventricle
midline shift
Contrast enhancement will often define cortical-

subdural interface

CHRONIC SUBDURAL HEMATOMA

after 2 weeks usually post trivial injury

due to injury of small bridging veins

headache, cognitive impairment, apathy,
seizures and focal deficits
symptoms are transient and fluctuating
proximal, painless and intermittent
paraparesis

CT features
After 2 weeks, hypodense
crescentic collections
Acute-on-chronic SDHs can
further complicate the images,
with hyperdense fresh
haemorrhage intermixed, or
layering posteriorly, within the
chronic collection
Do not cross the midline

Management
Acute SDH - Surgery for symptomatic & unstable pt

Surgery
burr hole
craniotomy
Nonoperative Mx
clinically stable
clot thickness <10mm
no clinical or CT signs of herniation
repeat CT scans 6-8 hrs after initial scan

Chronic SDH

Surgery - burr hole

signs of increased ICP
clot thickness >10mm
cognitive impairment
motor impairment

RAISED INTRACRANIAL PRESSURE

The three normal contents

of the cranial vault are brain

tissue (80%), blood (10%),
and CSF (10%)
Normal state - ICP normal

4-14 mmHg - normal

>20mmHg abnormal

The Monro-Kellie doctrine states that the cranial

vault is a rigid structure, and therefore, the total

volume of the contents determines ICP
Cerebral Perfusion Pressure (CPP) can be

determined by the following formula:

CPP = MAP ICP

Symptoms & Signs of increased ICP

Diminishing level of consciousness

Headache, vomiting, seizures

Cushings Triad:
bradycardia
hypertension
abnormal respiration

Pupillary changes

Papilledema

Effects of raised ICP:

brain herniation
1. subfalcine herniation
2. uncal herniation
3. central transtentorial
herniation
4. tonsillar herniation

reduced cerebral perfusion

Management of raised ICP

includes airway protection and adequate

ventilation (intubation may be required)

a bolus of Mannitol 0.25-1g/kg causes:
free water diuresis
increased serum osmolality and extraction
of water from the brain
require rapid neurosurgical evaluation
ventriculostomy or craniotomy may be

needed for definitive decompression

COMPLICATIONS HEAD INJURY

Meningitis & brain abscess
CSF rhinorrhea

and otorrhea
Epilepsy - about 80% arise in 2yrs
Hydrocephalus- usually due to atrophied white
matter
Amnesia (PTA)
Postconcussional Sx
Posttraumatic encephalopathy
Cranial nerve injury - in up to 30% pts

REFERENCES
Mark S. Greenberg: Hand Book of Neurosurgery;

6th ed
Bailey & Loves: Short Practice of Surgery; 24 th ed,

2004
Peter J Morris: Oxford Text Book of Surgery; 2 nd

ed, 2002
Schwartz's: Principles of Surgery; 9th ed, 2010