severe head injury

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I- INTRODUCTION :

The severe head injury, real public health problem usually occurs in young people and is the leading cause of death

Progress in the initial management, understanding of the pathophysiological mechanisms have contributed to the improved prognosis.

One of the causes of motor disability

Definition :

The patient suffered a serious head injury is defined as a comatose patient with a GCS (Glasgow score) less than or equal to 8/15.

II- EPIDEMIOLOGY :

The annual incidence of all head injuries (TC) is evaluated in Europe 150 at 300/100 000 inhabitants per year, with three peaks of incidence of age-related: less of 5 years, 15-24 years and more 75 years (men are more affected than women except after 75 years).

III- INJURIES ANATOMY PATHOLOGICAL :

We distinguish between primary lesions, present immediately after the trauma easily detectable, and secondary lesions that develop in a delayed manner in hours must be sought

Injuries are described from the periphery to the endocast.

a- primary lesions :

scalp wounds :

frequent, their main risk is bleeding because the scalp bleeding heavily.

bone lesions They may concern the vault or skull base.

  • At the vault, it is most often unique linear fractures Fractures with depression (embarrures) can cause sores or dural cortical. They should almost always be operated.
  • Fractures of the skull base are classified 3 groups :
  • fractures irradiated vault at the base
  • the base isolated fractures
  • fractures of the base associated with fractures of the facial massif

the frequency of CSF fistulas One notes that are revealed by rhinorrhea or otorrhea

Extra intracranial brain damage

The traumatic subarachnoid hemorrhage is extremely common

the encephalic lesions

– the encephalic focal lesions

  1. Concussion
  2. brain contusion
  3. cerebral edema
  4. Necrosis
  5. Haemorrhage

b- secondary lesions :

Extra brain lesions secondary

  • epidural hematoma

This is the major complication. This is an absolute emergency.

  • subdural hematoma acute

The clinical picture and prognosis are very serious. They are favored by AVK

  • chronic subdural hematoma is a late complication (weeks to months) head trauma

intracerebral lesions secondary

Corresponds to the aggravation of primary lesions encephalic, focal or diffuse, favored by

Local phenomena at the initial lesions

Phenomena general intracranial hypertension, low blood pressure, infections…

IV- PATHOPHYSIOLOGY :

A- Causes :

The main causes are summarized in the table below

Causes Frequences
highway accidents 60%
falls 32%
ballistic trauma <1%

B- Mechanism :

2 major mechanisms are described :

  • with direct impact on the skull
  • no direct impact on the skull

Head injuries are kinetic trauma. The head, supported by the flexible shaft of the cervical spine, never stands still.

When trauma with impact, either the head is moving before the collision and will then be subject to a deceleration effect, or it is stationary and will be subjected to an accelerating effect.

In the absence of direct impact (belted motorist), it will be submitted to the combined effects of acceleration / deceleration. Can cause :

  • lobar focal lesions by brain impact on internal reliefs skull hemispheres.
  • stretching lesions and / or shearing of the axons and of the vessels at different density areas (white matter / gray matter), called diffuse axonal injury

C- Consequences :

1- intracranial hypertension :

to’normal state :

The total brain volume is constant itself through the brain parenchyma, the cerebrospinal fluid (L.C.R.) and cerebral blood volume (YSC) including intracranial pressure (PIC) depends on the variations of these three volumes.

  • CIP is defined as the hydrostatic pressure of L.C.R supine 10 about mmHg. It is determined by l’flow balance d’admission and exit’cranioencephalic enclosure, c’ie by the flow of L.C.R and the cerebral blood flow (DSC)
  • The PPC is defined as the difference between mean arterial pressure (PAM) and intracranial pressure (PPC = PAM – PIC).
  • DSC is under the control of the cerebral perfusion pressure (PPC) and vascular resistance (RV) : DSC = PPC/RV.

physiologically, self-regulation mitigates the WFP and remains constant between 50 and 150 mmHg of PAM. DSC is also very sensitive to variations in the PaC02. C02 (Product brain metabolism) is’one of the most active agents on cerebral vasomotricity and an increase in PaC02 s’accompanies d’an increase in DSC and vice versa.

When a head injury :

It follows incompatible intracranial hypertension with sufficient PPC. This HTIC is linked to’appearance’a new volume that will modify the’pressure balance, which may correspond to a : contusion parenchymateuse, subdural hematoma- dural, extra-dural or parenchymal, cerebral edema, an increase in the volume of L.C.R. (hydrocephalus), or an increase in VSC due to loss of’DSC self-regulation.

The PIC will change little early (stage compensation) and many a Second Time (stage of decompensation), parenchymal displacement head areas of high pressure to those of low pressure => engagement.

2- Metabolic disorder and cerebral circulatory :

There is normally a coupling between the metabolic needs linked to the’neural activity and the supply of substrates. If brain metabolism increases, the DSC s’adapted

to ensure an adequate supply of substrates. Conversely, during’a coma, Cerebral oxygen consumption (CMR02) decreases, DSC and decreases in parallel. We can observe situations where the SDC is in excess of laCMR02 (situation d’hyperhémie) and promotes’intracranial hypertension, or on the contrary, it is insufficient (low flow conditions) with a risk of’ischemia.

3- systemic consequence :

We find :

A hypertension associated with’PIC rise (reflex Cushing),

Hypoxia d’multifactorial origin (airway obstruction, disorder of the respiratory mechanics, the ventilation / perfusion, rarely neurogenic pulmonary edema),

Metabolic and Electrolyte disturbances (hyper catabolisme, diabetes insipidus).

V- CLINICAL EVALUATION OF A BRAIN traumatized :

A CRANIAL TRAUMATISE IS POTENTIALLY A POLYTRAUMATISE A CRANIAL TRAUMATISE MUST BE CONSIDERED AS A TRAUMATISE OF THE CERVICAL RACHIS UNTIL’PROOF OF THE OPPOSITE

1- Assessment of’state of consciousness : Glasgow Coma Scale

The depth and duration coma are indeed two major criteria prognosis. So that’it n’there is no disagreement between the observers, l’review of’state of consciousness uses scale d’Evaluation, Glasgow Coma Scale (GCS). This clinical scale assesses the best response the injured person can provide when’we ask him to’open the eyes (sure 4 points), to answer a question (sure 5 points), and D’execute a simple order (sure 6 points).

L’glasgow scale’advantage of’be simple and allow through repeated examinations to follow the’TC evolution.

On the other hand, determination can be difficult if not impossible in some circumstances (sedation, intubation, associated neurological deficit).

Opening Eyes (E)
4 -> spontaneous
3 -> Noise
2 -> A pain
1 -> absent

verbal response (V)
5 -> oriented
4 -> Confuse
3 -> inappropriate
2 -> Incomprehensible
1 -> Nothing

Best Motor Response(M)
6 -> Obeys’order oral
5 -> Oriented to pain
4 -> avoidance M. sup. pain
3 -> Flexion M. sup. pain
2 -> Extension M. sup. pain
1 -> Nothing

We will talk about’worsening when between two successive examinations the loss of 2 dots on’Glasgow Coma Scale

2- neurological examination :

L’neurological examination’a head trauma should be simplified It assesses motor skills, tone, and l’oculomotricité.

  • Motor skills test for’limb motor deficit, who signs a focal involvement.
  • Review tone ; hypertonic attitude of the members is a derogatory sign.

We are talking about’state of decerebration when the lower and upper limbs are extended.

– Review of pupils

We examine the pupil diameter (mydriase = diam > to 4-5mm, myosis = silent < at 2 mm) and the light reflex (contraction of the pupil to light).

any anisocoria (pupillary inequality) or mydriasis should be recorded.

Bileactive mydriasis signs l’stop cerebral circulation ; this situation is irreversible.

It must be remembered that l’use of morphine drugs necessary to maintain neurosedation s’always accompanies d’a reduction in pupil diameter (léger myosis), and D’a decrease in the photomotor reflex response.

Neurological examination is completed by the research of brainstem reflexes
– fronto-orbiculaire
– photomoteur
– eye-cardiaque
– oculo-cephalique horizontal
– oculo-cephalique certical

Apart from hemodynamic instability a general examination is still needed in search of associated trauma and especially to failures that may aggravate the existing situation and which is within the scope of secondary brain injury.

3- secondary brain insults of systemic origin (ACSOS) :

are seen in severe head injuries and are original intra or extra cranial, start early on the scene of the accident or during transport and affect prognosis.

The ACSOS therefore correspond, the various systemic disorders (cardiorespiratory, metabolic). This disturbs cerebral hemodynamic changes with T intracranial pressure (PIC). They drive, through edema, of vasoplegia and intracranial hypertension (HTIC) the constitution of "real vicious circles", whose end result is cerebral ischemia

The factors are extra cranial :
– hypoxia (SpO2 inf 90%)
– Hypercapnie -Hypocapnie
– hyperthermia (T sup 38)
– hyponatremia
– Hypotension (NOT inf 90 mmhg) -hypertension (PAS has sup 160 mmhg)
– hyperglycemia -hypoglycémie
– Anemia (Hb inf a 9g/dl )

WE- ADDITIONAL TESTS :

A- radiological assessment :

The CT scanner : The brain scan without injection of contrast medium is the’appropriate examination essential in any severe head trauma. It makes it possible to carry out a lesion diagnosis and to follow the’evolution of lesions thanks to its repetition.

The CT scan will be repeated at the request before a secondary aggravation.

Rx skull face and profile

B- assessment gauge :

Measurement of intracranial pressure : In the presence of gravity waves (Clinical and CT), cerebral monitoring should include at least the measurement of ICP and CPP.

This ventricular or intraparenchymal measurement allows’assess the initial level, to give an indication of the severity, to follow its evolution and effects resuscitation.

Results We will talk about’hypertension IC when the ICP is durably higher than 15 mmHg. Severe and threatening if it reaches or exceeds 25 mmHg.

At the same time, cerebral perfusion pressure is estimated that must remain above 60 mmHg

VII- PROGNOSIS :

Factors influencing prognosis :

  • The level of awareness with mortality 80% for a score of around 3 sure 15
  • The importance of the lesion : nature, l’extent and topography of the lesions observed undoubtedly determine the prognosis.
  • l’age
  • l’age influences prognosis, mortality increases with l’age from 15 years. Conversely, mortality decreases with l’age between 0 and 15 years.
  • intracranial pressure Mortality reached 50% in those whose pressure is higher than 20 mmHg. She is from 95% when the PIC is permanently higher than 40 mmHg.

VIII- THERAPEUTIC CARE :

A- Preventing ACSOS :

The secondary brain assaults systemic origin (ACSOS) must be found and treated early to avoid worsening mainly cerebral ischemia

  • Fighting against hypoxia : tracheal intubation and mechanical ventilation, maintain
    neighbor of PaC02 35 mmHg and a neighboring Pa02 or above 100 mmHg.

Continuous sedation is required, associating usually morphine and benzodiazepine.

  • Control the hemodialty state : fast fill (20 ml / kg 15 minutes, repeat if necessary), with isotonic saline in the first intention ; under control of the central venous pressure (PVC) and AP.

The hypotonic solution (Ringer lactate, isotonic serum glucose 5%) are cons-indicated, they promote cerebral edema.

  • Treatment of intracranial hypertension mannitol (0,25 at 1 g / kg or 1,25 at 5 ml / kg of mannitol 20 % in 20 minutes). The position : the head elevation of 30 ° facilitates the venous return of the’head end and can gain up to’at 10 mmHg on PIC.
  • Maintain normal temperature.
  • Emergency Hospitalization at a center in adequate technical support (scanner, neurosurgery and intensive care) and ask the surgical indication if it exists

B- Establish a strategy for the management of traumatic brain injury :

a préhospitalier : The initial clinical assessment should look for obvious damage and collect vital signs (respiratory rate, cardiac frequency, PA, GCS) to address without delay any distress. The control of the upper airway remains a priority. Any hypoxia strike the vital prognosis. A principle is to sedate, intubate and ventilate any patient with a GCS 8 or rapid degradation of consciousness in a patient with a deficit and a GCS 11.

Transportation, integral part of the therapeutic, must use the fastest means such as’helicopter.

A l’arrival in the emergency department :

L’clinical examination must be repeated and completed. The minimum radiographic evaluation should include any patient traumatized comatose or sedated skull radiographs, cervical spine and lungs, abdominal ultrasound and CT scan. If it was realized very early, it must be repeated after six to eight hours, d’hospitalization, to freeze the therapeutic orientations of the first days.

Transfer to a specialist center The transfer to a specialist neuro trauma center should be considered for hospitalized patients in a Hospital before :

A deterioration of consciousness (in l’absence of scanner), a suspected embarrure,a fracture of the base of the skull, un polytraumatisme, neurosurgical lesions,CT signs d’HTIC.

The search for other lesions is then more or less a priority depending on the’impact on PCP requirements and indications for transfer.

C- Monitoring a TBI :

Regular monitoring is mainly clinical and close in time :

  • conscience
  • traction
  • pupils
  • General constant (TA, pulse).

IX- CONCLUSION :

Organizational aspects and deadlines’intervention are an integral part of the management of severe CT which will be carried out by a multidisciplinary team.

Course of Dr Gouadjlia – Faculty of Constantine