This document provides information on head injuries, including definitions, etiology, pathophysiology, consequences, assessment, and management. The main causes of head injury are motor vehicle crashes, falls, assaults, and firearms. Head injuries can cause scalp lacerations, skull fractures, brain contusions and hemorrhages. Assessment involves the Glasgow Coma Scale and examining for neurological deficits. Initial management consists of airway control, immobilization, and monitoring vital signs. Treatments for elevated intracranial pressure include mannitol, furosemide, and midazolam.

1. Head Injuries
Dr SajalTwanabasu
Intern
GMCTH

2. Definition
 Any injury that results in the trauma to the scalp, skull or
brain.
 Traumatic brain injury (TBI) encompasses a broad range of
pathologic injuries to the brain of varying clinical severity
that result from head trauma.
 Head injury and traumatic brain injury are often used
interchangeably

3. Etiology
 Motor Vehicle Crashes-44%
 Falls - 26%
 Other/Unknown - 13%
 Non-Firearm Assaults - 9%
 Firearms - 8%

4. Pathophysiology
 On the basis of mechanism of production, head injury can be
classified as:
 Impact injuries: It results from an object striking the head or
the head striking an object.
 It includes:
Scalpinjuries
Skullfracture
Cerebral contusion andlaceration
Epiduralhaematoma

5.  Acceleration and deceleration injuries: It results essentially
as a result of differential movement between skull and
cranialcontent.
 It includes:
Diffuse axonal injury
Sub-duralhematoma

6. Coupinjury
Contracoupinjury
Coup injury:
 It occurs at the site of the impact to the head and are
produced by compression of brain due to inward movement
of the bone
Countre-coup:
 Injury occurs directly opposite to
the point of impact and are most
common in frontal and temporal
6
lobe.
 Produced by the head in motion
impacting on a stationary object

7. Consequences of head injury
Injury to the scalp:
 There can be scalp contusion, abrasion and/or lacerations
 Tremendous vascularity of the scalp can cause profuse
bleeding
 Osteomyelitis may develop after closed injury following
infections of sub-periosteal blood clot referred as Pott’s Puffy
tumour

8. Skull Fracture
Simple linear fracture:
 It is the break in the bone that transverses the full thickness
of the skull from the outer to inner table
 No clinicalsignificance
 Fracture that transverses a suture line or involves a venous
sinus groove or vascular groove should be dealt cautiously

9. Depressed Skull Fracture
 Results from blunt trauma
 Inner table extensively affected than the outer table
 High risk of increased pressure on the brain or hemorrhage
to the brain that crushes the delicate tissue

10.  Compound depressed fracture is in contact with the outside
environment increasing the risk of contamination and infection
 Complex depressed fracture tears the duramater increasing the
risk of cortical damage and epilepsy

11. Base of skull fracture
Anterior cranial fossa fracture:
 It may lead to subconjunctival haematoma, extending to
posterior limit of sclera, epistaxis, CSF rhinorrhea
Middle cranial fossa fracture:
 It involving the petrous temporal bone presents with CSF
otorrhoea, haemotympanium, ossicular disruption, Battle
sign, 7th and 8th cranial nervepalsy.

13. Brain injury
Primary brain injury:
 Injury caused at the time of impact
Irreversible
Secondary brain injury
 Subsequent or progressive brain damage arising from events
developing as a result of primary brain injury

14. Primarybraininjury Secondary braininjury
Concussion Intracranial haematoma
Cortical laceration/contusion Cerebraloedema
Diffuse axonal injury Ischaemia
Bone fragmentation Infection
Metabolic or endocrine
disturbances

15. Diffuse Axonal Injury
 Results from mechanical shearing at grey- white interface
due to severe acceleration and deceleration force
 No obvious structural damage
 Severity may range from mild damage with confusion to
coma and even death
 Major cause of unconsciousness and persistent vegetative
state after head trauma

17. Cerebral Concussion
 It is the condition of temporary dysfunction of brain without
any structural damage following head injury
 It is manifested as:
Transient loss ofconsciousness
Transient loss ofmemory
Autonomic dysfunction like bradycardia, hypotension and
sweating

18. Cerebral Contusion
 It is more severe degree of brain injury manifested by areas
of hemorrhage in the brain parenchyma but without surface
laceration
 Neurological deficit which persists more than 24 hour
 Associated cerebral edema and defects in the blood brain
barrier

19. Cerebral laceration
 Severe degree of brain injury associated with a breach in the
surface parenchyma
 Tearing of brain surface may be due to skull fracture or due
to shearing forces
 Focal neurological defecit may be present

20. Extradural haematoma
 Collection of blood between the cranial bones and duramater
 It is associated with the fracture of temporo-parietal region
 Commonest vessel: Middle meningeal artery
 Lucid interval may be present
 Confusion, irritability, drowsiness, hemiparesis to the same side
of injury
 Hutchinson’s pupils
 Features of raised ICP: hypertension, bradycardia, vomiting

21.  CT scan: Biconvex lesion
 It is thesurgical
emergency
 Craniotomy and
evacuation of clot is
done.

22. Sub Dural Haematoma
 Collection of blood between
brain and duramater
 Common intracranial mass
lesion resulting from trauma
Acute: <3 days
Sub-acute: 4-21 days
Chronic: >21 days

23. Sub Dural Haemotama
 Results from torn bridging vein or injury to the cortical
artery
 Haematoma extensive and diffuse
 No lucid interval
 Loss of consciousness occurs immediately after trauma and
is progressive
 Features of raised ICP and focal neurological defecits
 CT Scan: Concavo-convex lesion
 T/t: surgical decompression by craniotomy
 Antibiotics

24. Cerebral Herniation
 Increased ICP or presence of
intracranial mass may
predispose to cerebral
herniation.
 Herniation of contents of
supratentorial compartment
through the tentorial hiatus
 Herniation of the contents of
the infraintentorial
compartment through the
foramen magnum

25. Brain swelling
 It follows significant head
injury
 Occurs due to active
hyperaemia and edema
Infection, Seizure, Hydrocephalus

26. Approach to Head Trauma
 Detailed history should be sought in all cases of head
trauma.
 If the patient is unconscious which is usually the condition,
history should be obtained from the attendant.
 While one care provider is taking history, resuscitation
should be carried out simultaneously by other care provider.

27. Ask about:
 Type of accident: ?RTA, ?fall from height
?acceleration/deceleration injury during driving a motor car
 Level of consciousness: ?Unconscious, ?semiconscious
 If unconscious: duration of unconsciousness, ?immediately
after trauma ?lucid interval
 Post traumatic amnesia

28. Ask about:
 Vomiting: ?blood in vomitus ?persistent vomiting ?sign of
recovery from cerebral concussion
 Epileptic fits or seizure: Its nature may give clue to localization
of the site of trauma
 Swelling and pain in the head
 Other complaints: ?bleeding or watery discharge from ear,
nose and mouth

29. Ask about:
 Past history: ?fits or similar head injury in the past
?Hypertension ?DM ?Renal diseases
 Personal history: ?unconsciousness due to other cause
(alcohol, opium poisoning, diabetic coma)
 Family history: History of diabetes, HTN, epilepsy in the
family

30. Immediate management
 Initial assessment of head injuries must follow advanced
trauma and life support. (ALTS)
 It includes:
Maintenance of airway along with cervical spinecontrol
Cervical spine immobilized in neutral position usingneck
brace, sand bags, foreheadtape
Suction of airway to clear blood,vomitus
Chin lift, jawthrust
Oropharyngealairway
ET tube, tracheostomyasnecessary

31.  Maintenance of breathing
 Assessment of circulation and control of haemorrhage
 Establish iv access with two large bore iv cannulas
IV infusion of NS (Avoid 5% Dextrose as it may
precipitate cerebral edema)
 Assessment of dysfunction of CNS
 Exposure in a controlled environment
Remove all clothes and look for any obvious external
injury

32. Physical examination
 Pulse and blood pressure:
Pulse will be rapid, thready with low BP in case of cerebral
concussion
Pulse becomes slow and bounding with high BP in case of
cerebral irritation
Rapid pulse in deeply unconscious heralds impeding death

33.  Temperature:
In cerebral concussion, contusion temperature may remain
subnormal
With appearance of cerebral compression, temperature
may rise upto 100˚F
Victor Horsley’s sign

34. Physical examination
 Head:
Patient’s head must be shaved fully
Look thoroughly for any fracture of the skull, hematoma and
assess the type of fracture
Site of injury often gives clue towards the diagnosis.
 Position of the patient
 Eyes:
Is there any evidence of haemorrhage in and around the
eyes?
The condition of pupil

35. Neurological assessment
Neurological assessment can be done by using Glasgow coma scale.

36.  Minor head injury: GCS 15 with no loss of consciousness
(LOC)
 Mild head injury: GCS 14 or 15 with LOC
 Moderate head injury: GCS 9–13
 Severe head injury: GCS 3–8.

37.  Presence of neurological deficits:
Check for power, tone, superficial and deep tendon reflexes
 Rigidity of the neck:
May be present in the case of subarachnoid hemorrhage,
fracture dislocation of cervical spine
 Cranial nerve examination
Cranial nerve should be examined one after another
Of these most important is the third nerve
 Check for any other CNS manisfestation: ?Ataxia
?nystagmus

38. General Examination
Examine
 Chest for the fracture of the ribs, surgical emphysema
 Spine, pelvis and limbs for the presence of fracture
 Exclude abdomen for rupture of any hollow viscus, internal
haemorrhage form injury to any solid viscus eg: liver, spleen

39. Management:
 Place a Nasogastric tube to decompress the stomach and
reduce the risk of vomiting as aspiration
 Avoid NG tube for the patients with facial injuries as the
tube could enter the brain through bony fracture
 Insert an dwelling urinary catheter for hourly urine output
monitoring
 Avoid insertion if urethral injury suspected

40. Treatment of raised ICP
 IV Mannitol
 IV furosemide
 Reverse Trendelenburg if no counter
indications like hypovolaemia, spine injury
 If significant agitation and if hypoxia,
hypovolaemia or pain is excluded as the
cause of agitation: give IV Midazolam
 Analgesics for the pain management
 Phenytoin or phenobarbitone for post
traumatic seizure

41. Monitor
 Blood pressure
 Heart rate
 Respiratory rate
 Spo2
 ECG
 Blood samples for serum electrolyte Arterial blood gas
hyper/ hypoglycaemia

42. Special investigations!!!!
Definitive treatment!!!!

43. Complications
 Personality Changes
 Hypopituitarism e.g. DI
 Post-Traumatic Seizures
 Infectionse.g.
Meningitis
 Vasospasm, Aneurysm
 Coma, Brain Death
Long-Termeffects
 Parkinson’s
 Alzheimer’sDementia

44. Rehabilitation
Physiotherapy
Occupational Therapy
Speech and Language Therapy
Psychologists/Psychiatrists

45. References
 SHORT PRACTICEof SURGERY Bailey & Love’s 25th Edition
 SRB Manual Of Surgery
 Death & Deduction Forensic Medicine
 A Manual On ClinicalSurgery