FIZIOPATHOLOGY I

 The main types of forces that cause cranio-cerebral injuries:

- Sudden acceleration
- Sudden deceleration
- Rotation, these types of forces can be combined - aggravated injury

 Sudden deceleration leads to:

- Polar lesions - the frontal lobes, temporal lobes
- Rupture of the veins that drain blood communicating dural sinuses

 Traumatized brain survival depends on the irrigation quality

 Adequate oxygenated blood perfusion depends on:

- Cerebral perfusion pressure (CPP)
- Intracranial pressure (ICP)
- Respiratory efficiency

 Cerebral perfusion pressure CPP is the difference between mean

arterial pressure (MAP) and intracranial pressure (ICP)
 FIZIOPATHOLOGY II

 Normal values ​of CPP are about 100 mmHg

CPP is basically determined by blood pressure, with low ICP

 Cerebral mass expansion due to cerebral edema or cerebral replacement

process is limited due to inextensible space (volume) of skull

 Increase of a cerebral volume is pushing distally the Cefalorachidian liquid

and can cause compression of dural sinuses (compensatory mechanisms)

 Overpassing these compensatory mechanisms cause increased intracranial

pressure

 Politraumatized patients with cranio-cerebral component of a CPP are

usually the result of a decrease in MAP associated with an increase in ICP -
edema
 MORFOPATHOLOGY I

 Cranio-cerebral anatomical lesions can be divided into three categories:

- Soft tissue lesions
- Skull lesions
- Lesions of the nervous and vascular elements

1. Soft tissue injuries

- Bruising, scratches (echimosis)
- Epicranial hematoma
- Scalp wounds

2. Skull lesions
- Fractures of the vault (skull cap)
- Fractures of the skull base
 MORFOPATHOLOGY II

 Fractures of the cranial vault:

- simple
- With clogging ( depression ) - no dural lesions
- with duro-cortical lesions
- with vascular lesions
Fractures of the skull base:
a. anterior cerebral fossa fractures
- monocular echimosis
- Bilateral periorbital echimosis (Raccoon's eyes)
- rhinolicvoreea
- rhinoragia
- anosmia
- Visual disturbances
 MORFOPATHOLOGY III

B. Fracture of the middle and posterior cerebral fossa :

- retro- mastoidian echimosis (Battle sign)
- otorhagia
- otolicvorea
- Peripheral facial paralysis

3. Lesionsof the nerve elements

A - primary brain lesions (produced in the moment
of trauma) - cerebral concussion
- cerebral contusion
- cerebral laceration

b. - secondary brain injury - Cerebral edema

- Epidural hematoma
- Subdural hematoma
- Intraparenchimal hematoma
 MORFOPATHOLOGY IV
CEREBRAL CONCUSSION

 Short-term abolition of consciousness

 It is due to shock waves that affected the upward activator

reticulated system

 There is NO lesion of the nervous elements, it is only a functional alteration

 It is completely reversible

 On regaining consciousness, the patient may present anterograde

and retrograde amnesia.

 No neurological deficits are interfering

 It is recommended patient’s admission and observation
 MORFOPATHOLOGY V

Brain Contusion

 Result from rupture of intracranial capillaries and oedema

 Involve major neurological damage

 Neurological deficits are usually installed immediately

 In relation to the degree of neuronal damage and neurological

deficit severity of contusion may be small, medium and severe
 Minor contusion treatment with corticosteroids (dexamethasone8-
16 mg / day), moderate sedation, analgesia, has a favorable evolution
 Severe contusion presents severe neurovegetative
disturbances, require hospitalization in intensive care service
monitoring, adequate ventilation (intubation) to maintain vital functions
 MORFOPATHOLOGY VI

 BRAIN LACERATION

Solution of continuity in the cortical tissue

Involves both nervous and vascular elements

Has serious complications, frequently severe evolution


 MORFOPATHOLOGY VII

Epidural Hematoma
Accumulation of blood between duramater and internal board of skull dome
Source of bleeding may be arterial ( meningeal medium artery frequently), venous or from
fracture’s site

 Folowing an important CCT, clinically with a short loss of consciousness there is an

interval of minutes or hours of regaining the consciousness, followed by a progressive installation of
neurological deficits and alteration of consciousness

 Clinic: anizocoria with nonreactive ipsilateral mydriasis and contralateral motor

deficit (hemiparesis, hemiplegia)

 Skull radiography reveales fractures

 Investigation of choice is CT scan :

Shows track of fracture and location of haematoma. Accurately determines the
location, lesion volume and associated lesions

Treatment - neurosurgical for evacuation of blood collection and haemostasis

 MORFOPATHOLOGY VIII
Subdural Hematoma

 Accumulation of blood in the subdural space caused by traumatic rupture of

the cortex surface’s arteries, veins, or of a drainage vein in major dural sinuses.

 Hematoma can be supraacute (growing in a few minutes), acute(hours), sub-

acute (days), chronic (growing in a few weeks)

 Clinically, after an initial episode of loss of consciousness follows a free

interval followed by signs of lateralisation: anizocoria, ipsilateral and non reactive
mydriasis and motor contralateral deficit .

 If the lesions are bilateral or in advanced phases, there is an installation of

vegetative modifications(respiratory arrhythmia, cardiac changes and TA
modifications)

 Skull fracture is revealed by radiography.

 Investigation of choice is cranial-cerebral CT: it Show track of the

fracture,subdural location and size of collection , the existence of associated injuries

 Neurosurgical treatment - for collection evacuation and for haemostasis

 MORFOPATHOLOGY IX

• Intraparenchymal Hematoma

Traumatic rupture of blood vessels in brain parenchyma

By it’s increasing of the volume it leads to increasing of the ICP,
moving laterally the midline structures

Loss of consciousness occurs quickly, followed by an important neurological

damage

Investigation of choice is cranio cerebral CT, showing fracture’s

tract, hematoma location, volume and the presence of associated injuries

The treatment is neurosurgical

 MORFOPATHOLOGY X

 Etiology CCT:
- aggression
- Accidents
- falls
- Accidents at work

 Unfavorable prognostic elements CCT:

- Cardiopulmonary arrest
- Age
- Acute respiratory failure
- shock
- Associated Lesions
- seizures
- Associated disease
- Period of time to first aid
 THE MANAGEMENT TO THE SITE OF ACCIDENT I

 The main goal is keeping the patient alive and prevent

neurological damage due - hypoxia
- systemic hypotension
- seizures

To the accident place:

- To keep the head-neck-trunk in the same plane
- Oxygen (by face mask or orotraheal intubation)
- Install a venous i.v. line
- Assessment of ventilatory efficiency
- ECG monitoring and blood gas
- Cropping seizures - Diazepam I. V.
- Monitor BP, pulse, respiratory rate

 THE MANAGEMENT TO THE SITE OF ACCIDENT II

 To Avoid:

- Administration of sedatives before neurological examination

- Administration of high doses of sedatives before to ensure good
ventilation of the patient
- Nasotracheal Intubation
- Introduction by nasal way the gastric tube drainage
- Search oculocefalic reflexes in patients with cervical spine injuries
- Hyperhydration by I.V Line if there is craniocerebral injury
 THE MANAGEMENT TO THE SITE OF ACCIDENT III

 Transport of the patient to the hospital:

- With a suitable vehicle

- Patient's head elevated to 30 °
- Cervical collar
- Monitoring of consciousness using the GCS
- Listen to your repeated cardiopulmonary
- Evaluating the respiratory or ventilatory efficiency
- Monitoring of mechanical ventilation parameters (volume,f requency,
pressure)
 THERAPEUTICA L ATTITUDE I

 Objectives:
- Check airway
- Check breathing and ventilation efficiency
-evaluation of cardiocirculatory status (pulse, BP), making hemostasis,
put one or more IV lines
- Rx for thoraco-pulmonary pneumothorax and / or hemothorax
- Skull and cervical spine Rx + / - cervical collar
- Other urgent therapeutic measures (if necessary): chest drainage, blood
transfusion

 Neurological examination - stages:

1. external examination
- Scalp - wounds, fractures
- Nose - epistaxis, rinolicvorea
- Ears - otoragia, otolicvorea
- Periorbital and retromastoidian echimosis- Battle sign
- Eyes - pupil diameter, fotomotor reflex , cornea, anizocoria

 THERAPEUTICA L ATTITUDE II

 2. Signs of intracranial hypertension

- Alteration of consciousness
- Pain
- Papillary oedema
- anizocoria
- bradycardia
- Central type of Vomiting
3. Glasgow score
4. reflexes
5. Sensorial and / or motor defficits
6. Examination of limbs
7. Coordination
8. Higher cortical functions of speech and analysis
9. Neuro-vegetative Examination (respiratory rate, heart rate,
temperature)

 THERAPEUTICA L ATTITUDE III

 10. Laboratory examinations:

- Rx examinations, CT, MRI, ultrasound

- Blood gas
- Blood group, Hb, Ht, creatinine, glucose, urea, electrolytes, bleeding
and clotting time, alcohoolemy
 THERAPEUTICA L ATTITUDE IV

 To be Noted:

- Any patient with CCT must be hospitalized and treated within a

specialized service - neurosurgery clinic - even if his neurological
condition is good
- Till demonstrate the contrary any CCT will automatically be
considered as accompanied by lesions of the cervical spine with cervical
collar immobilization
- Bradycardia is a sign of increased ICP
- Hypotenesion / tachycardia association - is usually an extracerebral
injury
- Free range to install state of coma may be represented not only by a
normal level of consciousness but also dizziness or stuporous condition
- Non-reactive Mydriasis - direct ocular trauma
- Injury to the optic nerve
- Use of mydriatic drugs

 THERAPEUTICA L ATTITUDE V

 To be Noted:
- Vascular collapse in a patient with CCT may be due to:
- Major fractures
- Severe thoracic trauma
- Severe abdominal trauma
- Major arterial trauma
- Any patient with CCT presents risk of vomiting and aspiration
- Agitation of a patient with CCT may be due to brain damage but not
only by this, but also:
- Ingestion of alcohool
- hypoxia
- Bladder distension
- Administration of opioids, sedatives, muscular relaxants, hypnotics to a
patient with CCT before a complete clinical neurologic examination can
mask the clinical signs and symptoms
 THERAPEUTICA L ATTITUDE VI
 Objectives:
1. Maintaining adequate brain oxygenation
2. Maintaining adequate cerebral perfusion pressure
3. Prevention and reduction of neuroprotective cerebral edema
4. Neuroprotection

General measures:
1. Respiratory system:
- Maintaining Pa CO2 level to 30 mmHg
- Tracheobronchial aspiration
- Mechanical ventilation - when oxygen decreases by reducing
their respiratory effort
- If mechanical ventilation is required over seven days - is required
tracheostomy
- Monitoring of blood gases - important ellement in patient
assessment and treatment planning

 THERAPEUTICA L ATTITUDE VII

 2. Cardio-vascular System
- Avoid hyperhydration to CCT patients
- A moderate degree of hypertension is beneficial for nerve
structures and proper irrigation , so it will not be corrected
- Elevated BP can be avoided by appropriate treatment of pain, urinary
bladder distension, hypoxia, hypoglycemia
- The basic objective remains to maintain a proper CPP to avoid ischemia

 3. Urinary Bladder catheterization:

- Avoiding urinary retention
- Allows monitoring of urine output
- To assess the patient's fluid status and avoiding hyper or hypohidration

 4. Early treatment of seizures:

- With diazepam or phenytoin
 THERAPEUTICA L ATTITUDE VIII

 5. Maintaining normal constants:

- Hb, glucose, urea, creatinine, electrolytes

6. Restoration of intestinal motility

7. Prevention of stress ulcers

8. Avoiding corneal dehydration

9. Preventing decubital lesions

 THERAPEUTICA L ATTITUDE IX

 Specific therapeutic measures aimed for nerve structures:

1. Reduction of cerebral edema
- hyperventilation
- Diuretics (furosemide)
- 20% mannitol
- Corticosteroids: Dexamethasone
-Hyperbarric Oxygeno therapy

2. Neuroprotection:
- Oxygen and maintain an appropriate CerebralPerfusionPressure
- Steroids - role of membrane stabilization
- Neurotropic substances: Piracetam, Meclofenoxat
- Vitamin C - role of free radicals fixative
- Vitamin B1 and B6 - important cofactors in neuronal energy
metabolism

 THERAPEUTICA L ATTITUDE X

 Clinical signs of intracranial lesion complications:

- Are secondary to cerebral edema, intracranial hematoma,
cerebral herniation
- Clinical signs - Glasgow score lower
- bradycardia
- Hypotension
- Respiratory rhythm disturbances / bradycardia
- seizures
- Signs of lateralization - focal neurological deficits
- Changes in pupillary reactivity
- Modification of reflexes
- Impairment of eye movements
- These clinical evidences are critical and urgent . They must be treated
with priority.

 THERAPEUTICA L ATTITUDE XI

 Types (patterns) of disorders of consciousness

-Loss of consciousness (less than 5 minutes) + + regaining

consciousness + amnesia = concussion

-Loss of consciousness + free lap of consciousness + altered level of

consciousness + signs of neurological distress = subdural / cerebral hematoma /
contusion

-Loss of consciousness without free interval + progressive altered level of

consciousness + progressive neurological deficit signs = severe
cerebral contusion
 THERAPEUTICA L ATTITUDE XII

 Contra indications for neurosurgical intervention in CCT

-Bilateral severe cerebral contusion

-Severe brain stem injury

-Small subdural hematomas (under 3-5 mm)

-Intra-parenchimal small volume hematoma

 THERAPEUTICA L ATTITUDE XIII
Treatment by priorities:
1. First operatory phase: Intensive treatment- prevent
hypoxia and arterial hypotension
2. Stabilizing and multidisiplinary re-evaluation phase
3. Second operatory phase( lesions not solved in the
first phase)