1. HEAD TRAUMA
UĞUR ŞEN

2. Any injury that results in trauma to the scalp, skull, or brain can be classified as a head injury or head trauma.
A traumatic brain injury (TBI) is defined as a blow to the head or a penetrating head injury that disrupts the normal function of the brain.
Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of damage to the brain.
A brief change in mental state to coma, or even death. 

3. Epidemiology
Estimated Average Annual TBI incidance in Turkey is 200/
Male:Female-2:1
Most in <35 and >70 ages

4. Epidemiology
Statistics estimate between 50-70% of TBI accidents are the result of a motor vehicle crash.
Of those who die, 50% do so within the first two hours of their injury.
Persons age 60 and older have the highest death rate after TBI, primarily because of falls.

5. Causes Motor Vehicle Accidents(%50) Falls(%21)
Home, work and sport accidents(%17)
Violence(%12)

6. Pathophysiology V(intracranial) = V(brain) + V(CSF) + V(blood)
1500 mL and CONSTANT!
Brain %85-90, intravascular blood %10, CSF <%3

7. Cerebral Perfusion Pressure
CPP= Mean Arterial Pressure(MAP) – Intracranial Pressure(ICP)
Normal CPP: mmHg
Normal MAP:60-160mmHg
Normal ICP:
Adults= 7-15mmHg
Children= 3-7mmHg
Newborns= 1.5-6mmHg

8. Classification of TBI Clinical severity scores (GCS and FOUR score)
TBI is a heterogeneous disease. There are many different ways to categorize patients in terms of clinical severity, mechanism of injury, and pathophysiology, each of which may impact prognosis and treatment.
Clinical severity scores (GCS and FOUR score)
Neuroimaging scales (Marshall and Rotterdam)
Other considerations

10. Glasgow Coma Scale Clinical severity scores – GCS: 13-15: Mild TBI
9-12: Moderate TBI
8 and less: Severe TBI

12. Neuroimaging Scales: Skull fracture Epidural hematoma
Subdural hematoma
Subarachnoid hemorrhage
Intraparenchymal hemorrhage
Cerebral contusion
Intraventricular hemorrhage
Focal and diffuse patterns of axonal injury with cerebral edema

15. TBI
Primary TBI Secondary TBI

16. 1.Primary TBI:
Primary brain injury occurs at the time of trauma. Common mechanisms include
Direct impact
Rapid acceleration/deceleration 
Penetrating injury
Blast waves
Although these mechanisms are heterogeneous, they all result from external mechanical forces transferred to intracranial contents.

17. 2.Secondary TBI:
Secondary brain injury is usually considered as a cascade of molecular injury mechanisms that are initiated at the time of initial trauma and continue for hours or days.
Free-radical injury to cell membranes
Electrolyte imbalances
Mitochondrial dysfunction
Inflammatory responses
Apoptosis
Secondary ischemia from vasospasm, focal microvascular occlusion, vascular injury

18. TBI Outcomes Brain Tissue Injury Scalp Laceration/Avulsion
Skull Fractures
Intracranial Hemorrhages

19. Character of Trauma Blunt – Penetrating Open – Closed Focal – Diffuse
Hemorrhagic – Non-hemorrhagic

20. Brain Tissue Injury Concussion Contusion (Coup & Countercoup Inj.)
Laceration
Diffuse Axonal Injury (DAI)

21. Concussion Most common type of brain injury.
Head inj. with temporary loss of consciousness.
Normal examination and normal imaging (CT)
Patients are observed and are proposed to avoid further contact to head.
Symptoms usually resolve within three weeks.

22. Contusion Direct injury of brain tissue.
It is associated with microhemorrhages and small blood vessel leaks.
They are highly associated with edema, and frequently cause increased ICP.

23. Contusion Contusions commonly occur in coup or contre-coup injuries.
In coup injuries, brain is injured directly under the area of impact.
In contrecoup injuries the opposing site of the impact is injured.

24. Contusion
Patients are observed in the ICU and CT scan is repeated in 24 hours. Patients must be observed until they are conscious and cooperative.
A heightened ICP may cause intracranial shifts that necessitates an operation.

25. Cerebral Laceration It is the penetrating type of brain injury.
Pia and arachnoid are also pierced.
It can cause gross destruction of brain tissue and increased ICP.

26. Diffuse Axonal Injury
DAI is one of the most common and devastating type of TBI and is a major cause of unconsciousness and persistent vegetative state after severe head trauma.
Loss of concsiousness with a normal CT.

27. Skull Fractures Linear Fractures Depressed Fractures
Diastatic Fracture
Basilar Fracture
Open Skull Fracture

28. Skull Fractures
Linear Fractures: most common, overlying soft tissue swelling, usually not emergent.
Depressed Fractures: Bone segment is pushed inward and can cause brain damage. Needs surgical repair. Newborns ‘’ping-pong’’ fracture.
Diastatic Fracture: Fracture line transverses one or more sutures, causing widening of the skull. It usually occurs in infants and children; but may occur in adults (esp. the lambdoidal suture)

29. Skull Fractures
Basilar Fracture: Fracture of the base of the skull, typically involving the temporal bone, occipital bone, sphenoid bone, and/or ethmoid bone.

30. Basilar Fracture
Basilar fractures are difficult to detect on X-rays. Generally diagnosis is made clinically:
Otorrhea
Rhinorrhea
Periorbital ecchymosis (Raccoon eyes)
Ecchymosis of the mastoid processes of temporal bone(Battle’s sign )
Hemotympanum

31. Basilar Fracture
Raccoon Eye
Battle’s Sign

32. Skull Fractures Open Fractures: Cranial contents are exposed.
If possible protect the exposed tissues with a moist, clean dressing and operate as soon as possible.

33. Intracranial Hemorrhages and Hematomas
Epidural Hematomas
Subdural Hematomas
Subarachnoidal Hemorrhages
Intracerebral Hematomas

35. Epidural Hematoma Rarely crosses the suture line.
Blood accumulates between external periosteal layer of dura and skull.
Classically arterial (%70) (MMA), %30 venous (MMV or dural sinus)
70-80% occur with temporoparietal fracture & MMA rupture.
Rarely crosses the suture line.
Lens shaped homogenous density.

36. Epidural Hematoma
Transient loss of consciousness, then recovery of consciousness, followen by deterioration.(vomiting,nausea)
Amnesia
Contralateral hemiparesis
Ipsilateral pupillary dilatation (Hutchinson’s pupil)
Severe headache, vomiting, focal neurologic signs
May progress to drowsiness, coma, death
Treatment: Hematoma evacuation(craniotomy)

37. Subdural Hematoma
Most common traumatic mass- effect lesion (20-40% of severe head injuries)
Potential space between dural & arachnoidal meningeal layers
Typically is rupture of bridging veins.

38. Subdural Hematoma Acute SDH : 1-3 days Subacute SDH : 4 days - 3 weeks
Timing of SDH:
Acute SDH : 1-3 days
Subacute SDH : 4 days - 3 weeks
Chronic SDH : 3 weeks - 3 months
LOC, mental status changes, focal neurological signs
Initial diagnosis usually made by non-contrast cranial CT
MRI is best for later determining size of hematoma and its effects on the brain.

39. Subdural Hematoma Treatment: 1) Acute SDH
More than 1 cm: Emergency evacuation
Less than 1 cm: Clinical observation
2) Chronic SDH
Seizure prophylaxis
Surgical evacuation

41. Subarachnoidal Hemorrhage
30% traumatic and 70% nontraumatic SAH (e.g, berry aneurysm rupture)
Patients describe as: “Worst headache of my life”

42. Subarachnoidal Hemorrhage
Symptoms of meningeal irritation in over 75%(may take several hours to develop)
LOC and mental status changes from beginning
Blood spreads diffusely, no mass effect.
May predispose to cerebral vasospasm.
Treatment: Pain relief (paracetamol,codeine,morphine)
Other medications(anti-convulsants,bb,diuretics)
Neurosurgical clipping, endovascular coiling

43. SAH - FISHER Grading Scale

44. SAH- Yaşargil Classification

45. Intracerebral Hematoma
Usually due to laceration of brain.
Bleeding into cerebral substance.
Associated with other injuries.
Increased ICP.
Neuron deficits depend on region involved and size.

46. Assesment of TBI ABC GCS + Neurological Exam
Pupillary Reflex (Isochoric – Anisochoric) and other brainstem reflexes (gag, corneal, oculovestibular, etc.)
CT is the gold standard
MRI is not preffered in acute phases. CT is faster and has favorable imaging properties in acutely traumatized patient.

47. Assesment of TBI Control of intracranial pressure is critical
Cerebral Perfusion Pressure (CPP) must be higher than 60mmHg.
(CPP = MAP – ICP)
Respiratory patterns (Cheyne-Stokes, Central Neurogenic Hyperventilation, Apneustic, Biot, Ataxic)
Motor Responses (Normal, plegia, paresis, decerebrate, decorticate, etc.)

48. Assesment of TBI Cushing’s Triad Suggests incresed ICP Increased BP
Decreased Pulse
Irregulary respiratory pattern

49. Management of Increased ICP
Head elevation at 30 degrees while the neck maintained at neutral position
Tight control of blood pressure: a single drop in the SBP<90mmHg is associated with double risk of morbidity and mortality
Adequate oxygenation: GCS≤8 intubation is mandatory
Avoid anemia: transfuse patients with Hgb<7
Light sedation
CSF drainage
Osmotherapy (or hyperosmolar therapy): mannitol ( mg/kg) and hypertonic saline
Decompressive craniotomy

50. Operation Necessary Not Necessary Scalp lacerations
Depression fractures
Epidural Hematoma
Subdural Hematoma
Penatrating Injuries
Linear fractures
Diastatic fractures
Skull Base fractures
Concussion
Contusion

51. Mass Effect Lesions Non-Mass Effect Lesions
Immediate Surgery needed
Midline shift ≥5mm defined as significant
Vascular occlusion, edema, increased ICP can worsen the initial injury
Examples: Subdural hematoma, epidural hematoma
Managed in the ICU
Blood spreads diffusely, no mass effect
Example: Subarachnoid hemorrhage

52. Medical Management Dexamethasone: Decreases cerebral edema
Mannitol: Decreases cerebral edema
Furosemide(Lasix): Decreases cerebral edema
Diazepam: Anticonvulsant (if patient experiences seizure)
Glucose: If the patient is hypoglycemic