Living With a Traumatic Brain or Head Injury

Head injury affects hundreds of thousands of people each year.

The calculated annual incidence is 281 per 100,000 people affected, with greater predominance twice for males. For information and following data already somewhat older, accidents of public roads in France represent the leading cause of head injury (60% of hospital admissions for head trauma, and 70% of deaths from head trauma), with a peak frequency between 15 and 30 years.

The second cause identified are falls (30% of hospitalizations and 14% of deaths), with two frequency peaks one before 5 years and the other after 70 years. The wounds from firearms represent less than 1% of total admissions but 13% of deaths. Among the risk factors of accidents, we must remember the importance of acute alcoholism as a factor favoring as far as the falls of traffic accidents.

The severity of a head injury depends brain damage that causes the dissipation of physical energy put in. This is damage to the brain created by the physical phenomena acceleration-deceleration which involve forces shear and stretching within the parenchyma. The effects on neuronal function are immediate; they are transient in case of stunning of the function, or in case of definitive anatomical lesion. Less frequently, it is a penetrating injury which creates final direct brain cortical injury.

The brain is the primary organ affected intracranial because of its weight, its volume in the cranium, and its internal and external configuration. The cerebellum and brainstem are usually spared. But the brain is subjected to the same risks or hypoxic ischemic lesions secondary to circulatory and respiratory disorders suffered by the injured. It is the same for all records of consecutive cell damage in a cascade of biochemical events triggered by hypoxia or the presence of blood in the brain.

The first major and immediate consequence of a head injury is the loss of consciousness. It is the sure sign of concussion, ie a disturbance of brain structures with suspension function. It may be brief or prolonged. That is why we speak of either brief loss of consciousness or coma immediately.

It represents a measure of the severity of a brain injury by its duration and also by its depth assessed by neurological examination of injured. Over the awakening of the injured will be fast and the greater his chances of a return to normal. Among all head injuries, an estimated 90% of them do not keep any consequence, 5-8% in keep major sequelae, and 1% severe sequelae (pauci-relational condition or persistent vegetative state) . Posttraumatic epilepsy is a sequela to 3% of all trauma, reaching mostly severe head trauma. However it must be remembered that the same full and speedy recovery of the injured is not sufficient evidence to say that there was no brain damage or to say there will be no ill effects.

A- physical and pathophysiological mechanisms

1. The physical mechanism of injury
All played in the 50 to 200 milliseconds after the impact. Two contemporary and simultaneous physical mechanisms are at play here:

  • a contact effect at the head impact, observed whenever the head strikes an obstacle or is hit by an object. This shock wave propagates and spreads on a plane parallel to the surface to the depth of the brain, wave or successive waves layers. The lesions first local to the point of impact, which will mark the scalp to varying degrees by a bruise or a bruise, or a wound. A one degree more, a fracture of the skull will occur, or more, a cranio-cerebral penetrating wound. It all depends on the surface of the object, for example, can be sharp (pistol bullet), round (golf ball) or flat (boards).
  • inertia effect, observed when the head is set in motion (acceleration) or is arrested in its movement (deceleration).In most cases the acceleration and deceleration phenomena are combined. Here are diffuse and multifocal lesions.

Each of these phenomena of contact and inertia could be experimentally reproduced. It has been shown that the most dangerous phenomena were the angular acceleration-deceleration. They are at their peak during the accidents at high speed, but a fall of its height, a punch to the chin, circumstances are sufficient to produce brain damage. In practice, contact purpose and effect of inertia combine their effects in varying proportions depending on the circumstances of the accident. Here are summarized some examples:

2. Brain injuries
Whether in sports, domestic life, alcoholic brawls or accidents on public roads, the physical phenomena related to the impact and inertia forces combine their effects to generate contusion injuries to the brain surface and / or axonal deep lesions.

Contusion injuries

The brain behaves inside the skull as a passenger without a belt, glued to his seat in the event of sudden acceleration or projected on the windshield when the car brakes suddenly. These crushing injuries are initially located in the brain’s surface, and are called contusion injuries. Contusion injury in principle leaves intact arachnoid and interested tissue and microvessels underlying cortex or gray matter and white matter adjacent to their arterioles, capillaries and venules.These small vascular lesions almost always a necrotic focus, hemorrhagic and edematous.

The bleeding may even become so great as to constitute a compression intraparenchymal hematoma. These bruises are present in the impact area (direct contusion hoc) or remotely (indirect contusion against by-blow). Especially because of the irregular relief of the skull base, the contusion lesions are more common in the frontal and temporal regions.

These brain moves in the skull are also the source of a tear or a pull-out veins that pass bridge to cerebral convexity dural venous sinuses. These venous lesions are a source of bleeding in the subdural space between the brain and the dura. Details of these lesions is discussed below.

b. Diffuse axonal injury

the acceleration-deceleration phenomena causing shear or stretching lesions in the gray matter junction – white substance. This is a shearing effect between these two different density areas. At the white matter is rather the stretching effects that will apply at the level of axons exposed raisonde their uniform and parallel orientation which makes them more vulnerable. Maximized, this stretching force may also injure microvessels who walk in the white matter in the middle of the axons. A axonal injury here adds micro-vascular lesion responsible for a micro-haemorrhage. If confluence of these micro-lesions may appear hemorrhagic petechiae visible to the scanner. These shear and stretching phenomena are more pronounced around the wall of the ventricles due to the proximity of the volume of the inert LCS.

c. The suspension of neural functioning

To varying degrees, the physical mechanisms involved in the TC disrupt neuronal functioning. The first phenomenon triggered by trauma, and the most minimal, is a depolarization of the cell membrane can be linked to the mechanical deformation. This depolarization responsible for the cell operation stop is accompanied by a massive release of intracellular K +, and a release of excitatory neurotransmitters. This depolarization is limited, isolated, transient and immediately reversible. For against, the released neurotransmitters would have a toxic role. The second phenomenon at the base of functional disorders of the brain injury is axonal damage.

This impairment can range from a molecular disruption of the cellular membrane until its complete disintegration. This damage would address some axons or tens of millions. These changes also affect the organization of other neural connections remained intact. This loss of nerve impulses by functional or anatomic lesion is called deafferentation phenomenon. This shock would be responsible for the immediate expression of consciousness disorders and neurological disorders, and as it is not immediately reversible and would be responsible lasting traumatic comas and persistent deficits.

3. Evolution of lesions

There are many reasons to appear secondary pathological phenomena at least as serious consequences that primary lesions. They are linked to changes autourde primary tissue damage, or to new attacks.

to. Evolution of primary lesions

1- bleeding
Any vascular wound can lead to the formation of a hematoma. In the closed, the existence of a pressure against explains both intracranial elevation and stopping bleeding by blotting, regardless of the bleeding.

2- cerebral edema cerebral _OEdème means an increase in the brain water content with its volume, which causes increased intracranial pressure.
The cerebral edema is vasogenic origin here by mechanical disruption of the blood brain barrier. The presence of toxic factors and free radicals present contusion superadded disorders of the local microcirculation, which power leads. It all adds to create a cellular suffering with increasing water content and sodium, that is to say a cell cytotoxic edema.

These swellings are often focused and present around the lesion focus of a cranio-cerebral wound. They appear within a few hours. We scanner black or dark halo, witnessed the hypodensité by increasing water that surrounds the lesions.Sometimes these are much more diffuse edema all of a cerebral hemisphere or even the whole brain. Originate more complex, and attributed to either vasomotor puff with intracerebral blood increase, or tissue ischemia diffuse, or else to a sudden accumulation of intracellular water. This phenomenon is known by the name “brain swelling”.

b. Additional attacks

1. Systemic disorders
Respiratory and circulatory conditions of the injured can significantly affect his brain state to come add extra aggression acute brain trauma.
– At the respiratory level, the injury is mainly threatened by hypoxia and / or a thoracic pressure with venous pressure and hinders the return circulation. The risk is obvious if pO2 less than 60 mmHg (8 kPa).
– At circulatory level, is threatened by the injured hypovolemia or hypotension, or anemia. The shock, blood loss from internal or external bleeding, the use of a hypotensive, are the main sources. The risk is obvious if the blood pressure falls below 60 mmHg.

The origin of these lesions is varied:

  • The disorders can be directly linked to the aggression of the nervous system and its effects on the autonomic regulation of breathing as the traffic.
    One can attend the brutal and development of neurogenic acute pulmonary edema, myocardial ischemia, severe heart rhythm disorders. All these acute phenomena appear to be related by the presence of high levels of circulating catecholamines in response to traumatic stress and the initial shock.
  • The disorders may be related to the circumstances of the accident and associated lesions responsible hypoxia or hemorrhagic anemia.
  • The disorders can finally be related to the context of the initial management on site, or even the following days. It has been shown a high incidence of secondary episodes of hypoxia, hypotension, anemia, hypercarbia, despite the extreme vigilance of health care teams. Hazardous episodes occur for example on the occasion of the transfer of the wounded to the scanner or to another care unit. Finally, multiple organ failure, or a nosocomial infection, uncontrolled hyperthermia, can add their harmful effects. It is shown that all these events play a deleterious role on morbidity and mortality of those seriously injured.

2. Cerebral ischemia

Whether or secondary circulatory origin intracranial hypertension, cerebral ischemia is the major threat to the functional and anatomical brain become traumatized. This is a global ischemia, diffuse, or muticentrique, affecting the cerebral cortex as would have done anoxia or cardiac arrest. Ischemia affecting all of the gray matter, the one that has the highest metabolic demand for oxygen and glucose. All brain functions so threatened. The dysfunction of the cerebral cortex and brainstem maintain the vigilance disorders. The cell loss is massive, marked by a visible cerebral atrophy on CT in the first weeks after the trauma.

Ischemia can take a more local form. Microcirculation of tissue around a contusion or hemorrhage home is threatened by vasoconstriction, the effect of tissue compression, capillary microthromboses, or even cellular metabolism disorders. Energy production of the cell is compromised because its oxidative metabolism is down. Toxic products such as free radicals are released. Here, everything comes together in a series of disasters biochemical cascade. One could compare this changing focus to that of the ischemic penumbra of the stroke. He was given the name of “traumatic darkness”. Any respiratory or circulatory events may precipitate the cells located in the penumbra traumatic below the viability threshold.

All these ischemic and toxic reactions are scalable for several hours if not days (experiments 24 to 96 hours after the initial trauma). This initial diffuse threat exists regardless of the severity of head trauma, and regardless of patient age.

B – Traumatic intracranial lesions

Whatever type of accident, the severity of a head injury and its future depend on the severity of brain lesion reached. A better understanding of injury mechanisms and improved visualization of lesions are essential criteria to better understand the trauma.
A classification of these lesions is essential. One can choose, for example, to do this from the image that is given us.Indeed, the brain CT or MRI have transformed the way we identify these lesions, since it is now possible to detect the patient’s lifetime, to their initial or secondary phase. Hemorrhagic lesions and / or expansive are the most easily recognizable. They are the basis of major surgical or medical treatment decisions today. But all lesons are not visible to the scanner or MRI: no visible damage to the scanner does not mean no lesions. A spectrum of diffuse lesions of the brain parenchyma, such as axonal injury break, the original hypoxic or ischemic lesions, the edematous lesions are not immediately visible and can not yet be authenticated to date by a detailed microscopic examination . They are however all the gravity of brain trauma and are causing severe sequelae. One can choose a more theoretical mode of classification, which would be based on the time of immediate or secondary occurrence of these lesions. Other modes are also operational to us to choose the one that best suits the question we ask ourselves. We propose the following classification.

  • focal or diffuse lesion? This first simple classification of intracranial lesions on imaging posttraumatiquess’appuie and distinguishes the focal or diffuse lesions. Among the focal lesions, we rank the cortical contusions, extra-cerebral hematoma, intracerebral hemorrhage and other heterogeneous density masses, and all lesions secondary to increased intracranial pressure. We classify “diffuse lesions” everything that is not “focal lesions”, that is to say, axonal injury, ischemic or edematous. In a series of 746 severe head traumas closed, diffuse lesions represent 55.4% of all injuries and intracranial massesexpansives 41.8%.
  • primary or secondary injury? From primary lesions are all those that occur during the first 250 milliseconds. The secondary lesions are formed later and promptly in a few minutes or a few hours after the trauma. Two examples: the direct or indirect injury cerebral contusion are primary lesions, while intracranial hematomas can be considered as secondary lesions as well as cortical ischemic lesions. Among the secondary lesions, we must mention the special register of secondary cell injury constituted from metabolic and biochemical processes that follow one another in a kind of fatal cascade leading to cell death.
  • open or closed injury? Head injuries open differ from those expressed closed because the skin envelope, bone and dural is no longer intact. We describe here the cranio-cerebral wounds and penetrating wounds by projectile or foreign body.
  • lesions delayed or late? Here the lesions occur away from the initial trauma, a few days (delayed injury), or a few weeks or months (late damage). For example, the initial trauma created a gap in the dura mater with after cerebrospinal fluid, followed by a bacterial inoculation and meningeal infection. Other examples, that of chronic subdural hematoma of the convexity, or that of chronic post-traumatic hydrocephalus.

We will present these lesions in the following order:

1- diffuse lesions
2- The focal lesions
3- The open head injuries
4- delayed or late lesions
5- vascular or nerve damage

INJURY intracranial

1. diffuse brain injury

It is shown that an immediate and prolonged coma occurs in half of severe head injury with absence of any expansive intracranial mass to the scanner. In this situation, mortality represents 35% of all deaths due to severe traumas. The term diffuse brain lesions clinically used to designate this table includes several types of lesions affecting the brain tissue such as ischemia, edema, or axonal rupture. These various origins lesions may be isolated, or in any combination, or combined with other hemorrhagic lesions. They alone can be life and functional outcome of the patient.In a series of 746 severe head trauma, among 414 patients with a syndrome of diffuse brain damage, 129 (31.1%) kept major sequelae, 66 (15.9%) are in the vegetative state, and 99 (23 9%) died.

Among the main diffuse brain damage, we retain only diffuse axonal injury which form the bulk of the nerve damage, and syndromes of acute cerebral hemispheric swelling, as they are specific and complex pathogenesis was recently informed by numerous experimental facts.

The diffuse axonal damage A-
The term “diffuse axonal injury” means a clinicopathological concept that is defined by:

  • very specific microscopic lesions of axonal break followed by a retraction and degeneration,
  • a clinical picture of brain injury developed in favor of a mechanism of injury by accelerating and where the dominant clinical disease is the loss of long and lasting immediate consciousness (coma immediately).

This diagnosis is suggested by the presence of a serious trauma that often shows no intracranial expansive lesions or cerebral contusion injuries. These diffuse lesions affecting axons were initially described there are more than 25 years on the occasion of cerebral pathological examination of patients who died after a long period of post-traumatic vegetative state. Due to the very diffuse nature of the lesions in the brain as the brain stem, the term diffuse axonal injury has gradually established. More recently, similar lesions were noted in the study in patients brains microscope died in the hours following the accident, suggesting that the forces involved at the trauma could have immediately stretched axons, explaining their break and shrinkage giving them their characteristic appearance in club (retraction balls).

These macroscopic and microscopic lesions by stretching are found in areas of lesser resistance axons (transition zone between gray matter and white matter, periventricular white matter, corpus callosum). These findings in humans have received experimental confirmation in an animal model reproducing head injury by acceleration-deceleration without direct impact. This work also demonstrated that the severity of the animal’s clinical status depended as much on the location of these axonal injury than their number.

Today the pathogenesis of these axonal injury certainly appears more complex than the original hypothesis advanced of these lesions which was a primary response to trauma. Experimental and clinical evidence exists to demonstrate that, in many cases, axonal rupture stretching (primary axotomy) is not the only first and last event. Initial flow axonal changes result in a progressive and localized swelling of the axon, which would result in his second break 12-72 hours after trauma (secondary axotomy).

to. Clinical presentation
Clinical signs is characteristic of diffuse axonal injury table, apart from the initial loss of consciousness. However, a group of facts is found in patients such isolated lesions:

  • the trauma of acceleration mechanism includes a high intensity (accident of the public highway)
  • cranial bone lesions are rare
  • the immediate loss of consciousness has been extended
  • a free and lucid interval is rarely noted
  • there is little or no deficit focal neurological signs.

Clinically, the severity of diffuse axonal damage is first expressed by the duration of loss of consciousness that extends over 6 hours. It is shown that even a minor head injury or light may be accompanied by axonal damage visible in large numbers in the white matter on MRI. However, only the presence of these lesions in the corpus callosum and brain stem was significantly associated with poor prognosis.

b. Aspects neuroradiologic
The CT scan can demonstrate axonal rupture if it is accompanied by a hemorrhagic petechiae by rupture of a micro-vessel whose direction was parallel to that of the axon. These vascular lesions are often micro-confluent while taking the characteristic appearance of intracerebral hemorrhage puncture from 2 to 6 millimeters or sometimes more.Sometimes referred erroneously contusion injuries when the bleeding site than 2 cm in diameter. A single visible lesion is sufficient to suggest the diagnosis of “diffuse axonal injury”. By the superiority of its definition, the magnetic resonance imaging can better differentiate diffuse axonal injury from the initial phase of the trauma in the form of hyperintense signals, but its implementation is complex and more work does not to date justified by a change taking usual medical management of these patients.

B- acute cerebral Swelling
After a seemingly even Benin trauma, acute increase in brain volume can occur within minutes. The patient’s clinical situation worsens gradually and proportionally to the degree of severity of the vasomotor reaction. This acute reaction brain swelling (brain swelling Anglo-Saxon authors) is very serious and often fatal due to acute intracranial pressure it generates. It is noted with a greater frequency in children and adolescents. It may be the only lesion observed. It often follows a surgical àl’évacuation intracranial hematoma.

This brain swelling can be unilateral or focal hemispheric, and bilateral and diffuse. Several pathophysiological hypotheses have been advanced to explain its origin and its development as a starting point with an increase in blood volume by intracerebral brain vasomotor paralysis, or an increase in brain water content, that is to say, edema acute brain. If appropriate the term “brain swelling” has not been satisfactorily translation. Also, is it wrong to the term “diffuse cerebral edema” is often used in everyday language to designate the table.

Brain swelling occurs to the scanner in the form of an increase in volume of a hemisphere become hypodense. This swelling causes a displacement of brain structures to the opposite side, that is to say a commitment. This swelling may be interested both hemispheres with erasing the cerebral ventricles and the subarachnoid all tanks.

2. Focal Brain Lesions

A – epidural hematoma
The epidural hematoma is a collection of blood between the dura (outer meninges of the brain) and the cranial vault (inner table of the skull bones). In general, a wound of the middle meningeal artery or its branches in the course of a skull fracture is the cause of the bleeding. The importance of vascular breach and the level of systemic blood pressure determine the expansion speed of the hematoma. However, the volume and extent of the hematoma is limited by the resistance opposes the dura to be detached from the bone, and the pressure exerted against progressively increased intracranial pressure. The location of the most frequent hematoma is temporal. Its direct and immediate consequence is a side brainstem compression with acute intracranial hypertension. It is a neurosurgical emergency.

to. clinical presentation
Typically the epidural hematoma (HED) is revealed after a free interval, that is to say that compression signs occur well after the trauma and as the conscience of the injured was restored completely. We note the emergence of secondary rubles vigilance, mydriasis side of the lesion, and hemiplegia on the opposite side of the lesion. These signs appear in minutes (HED hyperacute) within hours (HED acute), or after 24 hours (HED subacute).
We will mention some particular clinical forms: delayed form where signs occur more than 48 hours the accident, the form associated with a brain contusion hematoma beneath, the shape of the infant or child that occur in time after minor trauma even in the absence of skull fracture, and finally the form not known surgery due to the low volume of the hematoma requiring still an organized surveillance.

b. appearance neuroradiologic
The brain CT examination is essential for diagnosis. It shows a hyperdense image in convex lens, repressing and distorting the brain.

c. Surgical treatment
The goal of surgery is to ensure cerebral decompression by removing the hematoma, and practice hemostasis in vascular wound. A craniotomy (bone flap) will be performed next to the hematoma. Usually we find a fracture line.Decompression takes place when the bone flap is lifted. Then suction of all clots is performed followed by coagulation of the middle meningeal artery or its branches, or the dura mater, or bone slice. Closing the craniotomy is performed on a suction drain placed in the extra-dural space. The establishment of an intracranial pressure sensor is recommended if the patient is in a coma at the time of the transaction.

The is epidural hematoma neurosurgical emergency. Operated in time, the patient should heal without sequelae. In France, the overall mortality of epidural hematoma would be 15%, but exceed 45% when associated with severe head trauma. This injury intracranial traumatic expansive retains a symbolic value in neurosurgery, because of its total curability by simple neurosurgery, but also and especially because traditionally it has demonstration value of the interest of close monitoring while even minor head injury secondary to detect any worsening cause-related curable. Yet the epidural hematoma is a rare complication of a closed head injury. Its prevalence is estimated at 3 to 4% of all head injuries. It affects mostly young TBI and became rarer after 45 years. It is associated with severe head trauma in 15% of cases. The presence of a skull fracture multiplies by 25 the risk of formation of an epidural hematoma.

B – acute subdural hematoma is called subdural hematoma any intracranial hemorrhagic collection between the external convexity of the brain and the inner surface of the dura mater. Its origin is usually a wound or tear tearing a vein in the area of the brain caused by cerebral disturbance involved in the acceleration-deceleration phenomenon.Other times, the subdural hematoma acute cerebral cortical contusion accompanies; then it is less voluminous, and then we say that it is a satellite hematoma. Bleeding in the subdural space meets a low-pressure against the brain and therefore may easily spread and grow throughout the cerebral convexity. But the vascular wound stops by tamponade as intracranial hypertension installs quickly. Direct compression of the cerebral cortex and cerebral hematoma swelling reaction and add their effects are causing severe extensive cortical ischemic lesions. It is a neurosurgical emergency.

to. Clinical presentation
There is no specific clinical presentation with acute subdural hematoma. As epidural hematoma, it may be suspected in a secondary worsening of motor deficit or vigilance disorders. Usually it comes in the form of a coma immediately with signs of intracranial hypertension.

b. neuroradiological aspects
Diagnosis is easily provided by a brain scan. The feature image is that of a hyperdense release 1 to 2 cm thick, on the entire cerebral convexity, and accompanied by a proportional movement of the midline structures of the brain. The scanner should also look for brain lesions such as cortical contusion, intracerebral hemorrhage or petechial lesions of the white matter, corpus callosum and brainstem. It is useless to try to find the vascular origin of acute subdural hematoma.

c. Treatment
The goal of neurosurgical treatment of acute subdural hematoma is the intracranial pressure because of venous bleeding stopped by tamponade. Decompression is carried out through a craniotomy (bone flap) centered on the hematoma. The aspiration of blood clots mixed with liquid sometimes mixed with blood plasma fluid or cerebrospinal fluid should be as complete as possible. Hemostasis sometimes needs to be complemented by a coagulation or swabbing a vein. This gesture is always so difficult because it involves cortical veins suspended, stretched, fragile, and to which access is not always obvious. If acute subdural hematoma satellite is a cortical contusion, it will also be cleaned and hemostasis completed. The evacuation of an intracerebral hematoma associated may also be necessary.The dura mater is resealable. The bone flap is repositioned and secured. The establishment of an intracranial pressure sensor is provided at the end of the intervention. Postoperative CT scan is justified and recommended 6-12 hours after surgery.

The hematoma acute subdural is a lesion whose frequency is at least equal to that of epidural hematoma. It can occur after an accident in the highway as after a fall from height. The average age of onset is higher than that of epidural hematoma, because the risk of hematoma acute subdural increases with the risk of falls related to age. As extradural hematoma, this lesion generator is acute or hyperacute intracranial pressure and is a neurosurgical emergency. The prognosis of this lesion is unfavorable with a high mortality (57 to 90% of patients, with a 65% myenne). This is a very severe lesion that develops quickly causing major intracranial hypertension, rarely isolated lesion, and finally a major culprit lesion secondary brain damage. Coagulation disorders may frighteningly complicate the management of the bleeding lesion.

C – brain contusions
is called brain contusions, all traumatic hemorrhagic and necrotic lesions localized in brain sulci and extendable through the cortex to the white matter.

Bruises follow a relatively large direct or indirect head trauma. They can be focused or otherwise very extended surface or depth (volume). The degree of extension marks the degree of severity of the bruise. The surface contusion term well describes the situation when the lesion is limited to the cortex and extends some depth. The term hemorrhagic contusion best described cortical lesion more or less extensive bleeding associated with a collection subcortical. The contusion foci may be multiple, and bilateral. The patient’s age and history of chronic alcoholism are serious factors of these lesions. Direct bruises are distinguished so-called “shot”, or direct, situated opposite the impact and indirect bruises called “backlash”, or indirect, located away from the impact. This is an example of the temporal lobe contusion caused by a fall back with occipital cranial impact. When contusion affects both frontal and temporal poles, it is called “quadrupole”. The prognosis of these lesions is dependent on their size, and related brain damage. These contusion injuries are the source of an evolving vasogenic cerebral edema. When the lesion is expansive and localized to a temporal or frontal lobe surgical treatment may be indicated.

to. Neuroradiological aspects
On the initial CT scan hemorrhagic contusion is easy to recognize, as we note the presence of several confluent hemorrhagic hyperdense lesions located on cerebral convexity particularly in light of the temporal or frontal pole. It is necessary to perform a CT scan control 24 to 48 hours after the first. The finding of even higher volume of hemorrhagic lesions is common, and should not be surprising. This increase in the initial lesion has not always had clinical consequences. After 48 hours of evolution, it appears a hypodensité area marking the presence of cerebral edema around the lesion.

b. Principles of surgical treatment indications of neurosurgical treatment of brain contusion is rare. When the bleeding site is focused and comprehensive, it can play the role of an evolving mass and create compressive intracranial hypertension. Dan these cases, craniotomy decompressive may be indicated. The end of surgery, it may be appropriate to set up an intracranial pressure sensor. Postoperative CT guidance is useful and recommended.

D – Other post-traumatic intracranial haemorrhage
Outside intracranial extra-cerebral hematoma (epidural hematoma or subdural acute), a hemorrhagic contusion with or without hematoma intra-parenchymal partner, CT scan Initial may reveal:

  • hemorrhage of basal ganglia
  • para-sagittal bleeding,
  • a brain stem hemorrhage,
  • a subarachnoid hemorrhage,
  • ventricular hemorrhage
  • a delayed intracerebral hemorrhage

All these hemorrhagic lesions may or may not associated with each other, each of which may have a particular degree of severity weighing proportionately on prognosis. All these lesions always express the severity of the initial head injury.They are mainly found in the context of what is referred to as “diffuse brain damage” that indiscriminately include lesions other than hematomas or bruises, that is to say, diffuse axonal injury, edema diffuse cerebral and diffuse cerebral ischemia.

3. Open Lesions

A – cranio-cerebral wounds
By definition, a cranio-cerebral wound affects the scalp, cranial vault bone, dura and the brain. The presence of brain matter in the scalp wound is pathognomonic.
The brain can be puncture wound or decaying. It is a neurosurgical emergency.

A cranio-cerebral wound may be caused either by a penetrating object (knife, needle, nail) or a blunt object (tree branch, baseball bat) or by direct violent shock during acceleration -décélération (shock against a pylon). In the first case, the head was not supposed to be moving at impact, and it is said that all the energy traumatic ran out in the traumatic home. Here the lesion is focal, and the patient does not present any major disorders of consciousness. In the latter case, diffuse brain damage are also present and their consequences can even dominate coma table immediately.

The initial CT scan provides information about bone and brain damage. It verifies the absence of other associated lesions. The dura mater breach opens the intracranial cavity, and air can enter. This is called pneumatocele.

The incidence of cranio-cerebral wounds has been seriously reduced by the obligation of helmets on the road and on exposed workplaces. The patient’s prognosis is rarely involved in the case of an isolated lesion. The functional prognosis depends on the topography and the severity of the focal brain injury. The risk of functional impairment is always present. Finally, any cranio-cerebral wound has an immediate risk of infection and risk of late lobe epilepsy.

Treatment goals for trimming the entire wound, hemostasis in cerebral wound and the closure of the dura mater and the skin surface. If bone loss persists, it can not be immediately replaced with a bone graft or acrylic because of the risk of infection, and will be the subject of a later cranioplasty. The closure of the scalp wound sometimes requires the use of the technique of rotational flap.

B- penetrating wounds by firearm
The cranio-cerebral wounds from firearms see their increasing frequency in the civil field (autolysis or violence). The severity of the injury depend on the initial velocity of the projectile which determines its penetrating power. It is a neurosurgical emergency. Military born practice the principles of cranial neurosurgical treatment of these wounds and medical complications prevention principles such as infection and late lobe epilepsy.

In order of increasing severity are distinguished:
1- wound by pressing say where only skull is reached by the projectile that comes crashing it. Bone lesion is comminuted, but no bone fragment has penetrated the dura. A cortical contusion under the impact is usual.
2- wound by said penetration, when the projectile has passed through the bone and remained in the skull. Brain injury is present at the point of penetration and along the path of the projectile which may have ricocheted on the opposite internal table or having fragmented. This injury is aggravated by the diffusion of the shock wave and dissipation of the kinetic energy of the projectile density in heterogeneous environments.
3- wound by said perforation, where the projectile has passed through the cranium from side to side .

The brain scan can examine the bullet, its path, and hemorrhagic cerebral damage. To these primary lesions, add all secondary lesions foremost among which are the intracranial hemorrhagic lesions (epidural hematoma, subdural, intraparenchymal). These lesions will progress very rapidly and cause an early death.

Here are some principles of neurosurgical treatment of surgical treatment
1- emergency surgical evacuation of a unilateral compressive hematoma is indicated if the patient is in a coma immediately.
2- trimming the entry point is an indication Elective which aims to eliminate hemorrhagic gangrene and bone debris at the cerebral wound. The closure of the dural tear and skin coating will be careful.
3- removal of the foreign body is not a formal indication.

The prognosis depends on the patient’s clinical status at the time of admission and after resuscitation. When present with a score 3 on the Glasgow Coma Scale, mortality is 99% of cases. When the score is estimated between 4 and 7, mortality was 72%. It decreases to 27% if the patient is evaluated between 8 and 12 and is only 1% if the patient GCS score of 13, 14, or 15. The presence of subarachnoid hemorrhage would be a scanner poor prognosis (68% mortality).

4. Delayed lesions

A- intracranial infectious lesions

to. Posttraumatic meningitis

1- Meningitis Early
Early meningitis can occur in the first few days after head trauma have included an externalized ostéodurale breach by rhinorrhea, otorrhea, or pneumatocele. The germ is usually a pneumococcus or other saprophyte germ upper airway and sinus cavities of the face.

2- late Meningitis
Meningitis can occur days, months, or years after head trauma. Meningitis repetition is always traumatic origin until proven otherwise.
Responsible osteo-dural tear is usually located at the floor of the anterior cranial base, that is to say, the level of the ethmoid and sphenoid. Less frequently, it is a mastoid entry point. The highlight of the breach is not always easy. Can be facilitated by a scan performed after cisternal injection of contrast medium. The treatment of neurosurgical ostéodurale breccia.

3- postoperative meningitis
A meningitis infection may follow a septic neurosurgery on an open fire cerebral attrition. The germ is usually a Gram negative. Meningitis may complicate the implementation of an intracranial pressure sensor or a ventricular drainage probe

b. Post-traumatic brain abscess

A brain abscess can complicate any open head injury, especially as penetrating bone fragments remained in situ, or a foreign body of another nature penetrated the skull, or that attrition Outbreak has not been regularized. The scanner allows easy diagnosis because the abscess does not present itself differently from a brain abscess in general. It allows for locating a sample or of a hollow puncturing stereotactic condition. Local treatment is associated with a prolonged anti-infective medical treatment.

c. Subdural empyema

Usually empyema secondary to a sinus infection or post-traumatic mastoid. The pus present in the subdural space hypodense takes a look at the scanner. A contrast medium injection shows a very abnormal cortical fixation. A magnetic resonance imaging with gadolinium would be even more demonstrative. Postoperative infection can be at its origin. Exceptionally, it can be an infection of a chronic subdural hematoma during sepsis. The subdural empyema results in focal seizures and neurological deficit. His neurosurgical treatment equipment is: drainage and thorough rinsing of the cavity allow infection control in conjunction with an anti-infective systemic therapy.

B – hematoma chronic subdural

We denote hematoma chronic subdural cerebral convexity encysted a hemorrhagic collection virtual space occupying subdural cerebral arachnoid between the inside and the inside of the dura mater outside. It is a neurosurgical emergency.

This injury should not be confused with an acute subdural hematoma immediate constitution.
In traumatic, this hematoma is special because it has a progressive evolution within days or weeks. On the side of the brain, this causes hematoma by its growing volume cerebral compression set with intracranial hypertension. The side of the dura mater, it causes an inflammatory reaction that organizes and becomes responsible for a local plasma exudation and bleeding disorders (coagulopathy hyperfibrinolysis and consumption). Repeated microbleeds contribute to the increase in volume of the hematoma. It may be unilateral or bilateral isolated lesion, do or not following an acute subdural hematoma, or complicate long-term anticoagulant therapy. Signs of discovery are headache, progressive deficit, psycho-intellectual disorders, coma. The scanner is the indispensable diagnostic examination.

Frequent late complication post-traumatic, it mostly affects patients older than 65 and is rare before age 30 in adults.The chronic subdural hematoma is usually unilateral, but bilateral in 15% of cases. The incidence of this condition would be 1 to 2 per 100,000 Reported at the age of discovery, this incidence would be 7 per 100000 in patients aged over 70 years. The infant may suffer minor head injuries whose consequences are not immediate. Head injury shook the child is one example. Before the 6th month the clinical picture is that of a progressive intracranial hypertension with psychomotor retardation, increased head circumference, anterior fontanelle distension. After the 6th month a picture of chronic subdural hematoma is always that of intracranial hypertension, but its signs are less obvious. The appearance of a motor deficit is so often the telltale sign.

The brain scan shows the presence of a detachment between the brain and the skull (cranial-cortical peeling) discreetly hyperdense compared to the underlying brain, rarely isodense or hypodense. This separation interested in a wide range of cerebral convexity, if not all. It is not always uniform, as if there were areas of abutment between cerebral cortex and the dura. In the unilateral form, the impact of mass syndrome with major displacement of the lateral ventricles and the III ventricle. The MRI is superior to CT and precise better the presence and extent of subdural hematoma, but it is rarely justified.

The treatment of chronic hematoma subdural is a neurosurgical emergency. A simple gesture drainage collection subdural obtains patient recovery within days. Several treatment modalities are possible. This procedure can be done under local anesthesia, which reduces the surgical procedure mainly in elderly patients or tired. Overall mortality of this disease is low, estimated at 2 to 3%. Early recurrence is possible but uncommon (3 to 6%).

C- posttraumatic hydrocephalus

There is talk of post-traumatic hydrocephalus obvious when ventricular dilatation is detected on a CT scan performed a few days after trauma. We distinguish two etiological varieties:
1- one called passive consecutive hydrocephalus posttraumatic cerebral atrophy compared to a contusion or traumatic brain wound. It should be distinguished from a “posttraumatic porencephaly” also atrophic origin. This term, intracerebral cystic cavity is designated contacts the outer cortex or brain ventricle.
2 another called hydrocephalus active as secondary to impaired circulation and absorption of cerebrospinal fluid (CSF) leading to an increase in intracranial pressure.

Both forms may be associated with the occasion of a severe head trauma. The etiological diagnosis is based on clinical, morphological arguments and gauge. In the case of an active hydrocephalus, CSF shunt can be proposed. Its success, sometimes spectacular, depends on the primary lesions and disease duration of hydrocephalus.

5. Vascular lesions or intracranial Nerve


Intracranial vessels (internal carotid artery, basilar artery, cortical arteries) can be directly or indirectly harmed during fracture of a bone lesion from the base, or because of excessive stretching resulting, for example, tearing of a branch of secondary division.

For the most serious of them, these vascular lesions are immediately fatal. Other times, the lesion reveals only secondarily (mechanism of arterial wound “dry”) or late (post-traumatic aneurysm or fistula). Diagnosis of vascular injury may be suspected, but is shown by angiography.

1. Lesions of the upper cervical internal carotid artery.
The internal carotid artery can be injured in her driveway at the base of the skull, in its course through the petrous bone, or its entry into the cavernous sinus. Blood wound is externalized in the form of severe epistaxis and rebellious to the posterior tamponade. Only an angiography to determine the source of bleeding with certainty. Endovascular occlusion of the internal carotid artery or branches of the external carotid artery may be required. The lesion may be an arterial dissection facing C1-C2, which may be up to complete occlusion of the carotid artery and cause a hemispheric cerebral ischemia.

2. The lesions of the internal carotid cavernous sinus in
the internal carotid artery can be stretched in its intracavernous portion. The arteriovenous fistula is exteriorized exceptionally by epistaxis or subarachnoid hemorrhage, as it is strictly limited within the cavernous sinus. It causes venous pressure which is reflected in the ophthalmic vein. The initial subjective sign can be perceived by the patient of a systolic murmur intracranial. But the sign of discovery rule is a “non-pulsatile exophthalmos axile”. Ocular protrusion is evident with eyelid edema. The eye is red with a scleral dilated veins, Maximum degree, the eye is still (ophthalmoplegia) and deflected downward. Trophic disorders of the cornea are possible.
There is, to date, no indication of direct neurosurgical first of these carotid-cavernous fistulas traumatic. Only an endovascular treatment is indicated. At best, the arteriovenous fistula is occluded directly with retention of the permeability of the carotid vascular axis. At worst, endovascular occlusion (or trapping) performs occlusion of the internal carotid artery which is determined after a clamping test. This treatment is followed by a very high rate of immediate success and distance

3. Lesions basilar
They are very rare and fatal. They occur only occasionally cross serious fracture of the skull base.


All cranial nerves are threatened in connection with head trauma. Some are threatened by a direct blow as the olfactory nerve or the optic nerve in connection with a fracture of the anterior floor of the skull base, or as the facial nerve and the auditory nerve vulnerable during a break the rock. But all are threatened with indirect injury during a trauma by accélérationdécélération responsible for a stretch or a nerve contusion against osteo-dural structures of the skull base.They can also be affected by the propagation of the shock wave, or a local post-commotionnelle oedematous reaction.
These lesions are exceptionally nerve directly demonstrated the scanner or MRI. They are unilateral principle. Their signs of clinical disease are evident and immediate. However, we must distinguish primary achieved with immediate loss of function, secondary violations whose clinical signs are delayed by hours or days. In the first case, the lesion would anatomical, with little chance of recovery. In the second case, the lesion is functional, or reaction to edema or local ischemia, and the chances of recovery would be greater. The typical example is facial paralysis secondary onset and prognosis after trauma arising from the rock.

The olfactory nerve (I) is achieved in approximately 7% of all cranial traumas. His achievement is manifested by a loss of smell and partial loss of taste. The optic nerve (II) can be reached in his bone path (the optical channel of the base of the skull) with a bone splinter from a base fracture. Oculomotor nerves (III, IV and VI) may suffer injury to the orbital level, or cisternal on their path to exit the brainstem. The facial nerve (VII) cranial nerve is the most exposed to direct injury during trauma of the rock. A transverse fracture of the rock would be accompanied by facial paralysis in 30% to 50% of cases, whereas the incidence is 10% to 25% in the longitudinal fractures. Direct damage of the auditory nerve (VIII) or cochleovestibular is exceptional. Trauma focuses on the cochlea or the labyrinth and more often on the ossicular chain in the middle ear. The only spread at the base of the skull of the shock wave can damage the cochlear and vestibular structures.

C Initial assessment of head injury

In practice, the assessment of a TBI may seem simple because we only have the evaluation of the initial clinical condition and the initial brain scan. There is still no reliable biological marker that day the severity of head trauma.Those are the only tools we have to answer the following three questions:

  • what degree of severity?
  • There he has brain damage?
  • what is the prognosis?

One can not help but notice the mixture of these three basic questions so closely related. We also mark the fragility of the initial clinical examination and first brain scan since the return of consciousness can be more or less rapidly and hemorrhagic lesions may appear secondarily. This shows how the later evidence gathered during the immediate changes will be valuable. This also implies that we need to organize the supervision of the injured to detect any worsening, and that it must remain careful and not issue a prognosis too early. A few simple rules should help us gather relevant for each patient and transmitted data whether clinical data (review of the state of consciousness, neurological examination), the neuroimaging data and gauge. To guide our assessment, we must have clinical scales easy to use, store, and generalize. Then we can have some sufficient evidence to bring a prognosis on the fate of the wounded.

1- Clinical Evaluation

a- Evaluation of the state of consciousness of the injured: Glasgow Coma Scale
We have always a valuable clinical indicator, the degree of achievement of impaired consciousness. The depth and duration of coma are indeed two major criteria prognosis. For there is no disagreement between observers, considering the state of consciousness since 1972 uses a rating scale, the Glasgow Coma Scale (GCS). This clinical scale evaluates the best answer the injured can provide when asked to open their eyes (4 points), answer a question (5 points), and run a simple order (of 6 points ). The sum of the fixed three figures obtained the degree of distress in the patient’s state of consciousness that is inversely proportional to the resulting figure. The maximum response is 15 points (4 + 5 + 6, the patient has a normal vigilance), the minimum response is 3 points (1 + 1 + 1, the patient is unresponsive in a coma).We must clarify that there is no neurophysiological or neuroanatomical relationship between eye opening, verbal response and motor response. 15 points on this scale is easy to use by all, because the three chosen parameters are easy to observe, note, and this clinical examination is easy to repeat. Note that there is no zero response. The Glasgow Coma Scale has become a universal practice.

By definition, the coma is “a state of no response, eyes constantly closed, regardless of the duration.” With the use of GCS, we speak coma when the recorded answers give a score between 3 (keep your eyes closed, does not answer, is no movement in the painful stimulation, 1 + 1 + 1) and score of 7 (not open my eyes or the call or the pain, makes no verbal response, does not obey the order but directed his hand in a manner appropriate to the painful stimulus in seeking to depart, 1 + 1 + 5). The practice will make us say for example “coma Glasgow 3”. This quantification replaces all those previously proposed which left too much room for subjective interpretation of the words as coma vigil, light coma, deep coma, coma carus, coma stage I, II or III.

The degree of achievement of the fixed realize the severity of head trauma. Also, a significance was attributed to:

  • mild head trauma if GCS is 15, 14, or 13
  • average head trauma if the GCS is 12, 11,10, 9,
  • severe head trauma if GCS is 8, 7, 6, 5, 4, or 3 Note that the severe head trauma involves a category of patients who are not really in a coma (GCS 8). An additional factor of gravity of respiratory origin and / or circulatory here adds to the neurological status of these patients and control resuscitation gesture with respiratory support (intubation rule: any head trauma GCS ≤ 8).

If the GCS provides good initial identification of impaired consciousness, it follows their evolution over time, as this clinical examination can be repeated at any time, or be subject to regular evaluation systematized. When we speak of aggravation between two successive examinations will be marked loss of 2 points on the Glasgow Coma Scale. Any worsening noted will lead to an action: check-Laboratory (pulse, BP, respiration), raise the alarm that is sought an explanatory cause such as intracranial hypertension compressive hematoma, or respiratory or circulatory failure.

2- Neurological examination
Neurological examination of a head injury needs to be simplified, but should not be forgotten. It assesses motility, tone, and eye movement.

  • Examination of motor skills
    The research examining the presence of a motor weakness of the limbs, which signs a focal involvement. This deficit is mainly facial-brachial. Attention to remember that traumatic coma may hide signs of paraplegia or, more rarely, from quadriplegia.
  • Review tone
    The hypertonic attitude of the members is a derogatory sign. There is talk of state decerebration when the upper and lower limbs are extended.
  • Examination of the pupils
    are examined pupil diameter (mydriasis diam => to 4-5mm, miosis = diameter <2 mm) and light reflex (contraction of the pupil to light). From the first examination of the injured, it is important to report the diameter of his pupils, and their state of reactivity to light. Any anisocoria (pupillary inequality) or mydriasis should be noted. The most common situation is that of anisocoria little or no reactive. Monitoring the status of the pupils must accompany each review of the state of consciousness. Indeed, the occurrence of secondary anisocoria or mydriasis sign evolutionary presence of lateral compression of the brainstem (the lesion is on the side of mydriasis and the side opposite hemiplegia). Bilateral mydriasis aréactive sign the judgment of the cerebral circulation; this situation is irreversible. Remember that the use of opiate drugs needed to maintain neurosédation is always accompanied by a reduction in pupil diameter (miosis light), and a decrease in the response of the light reflex.
  • Temporo-spatial orientation Assessing the state of orientation in time and space is part of the evaluation of the state of consciousness of all patients GCS GCS 10 to 15. A motor aphasia can be easily confused with a confusional state

2-Evaluation neuroradiologic

Early detection of intracranial compressive lesions is a priority. CT scan without contrast injection is the appropriate exam to do it. Except imperative, it is recommended not to practice this examination that from 4- 6th hour after the accident, to give weakly hemorrhagic lesions are likely to be detected. CT scan will be repeated in the application to a secondary aggravation, and consistently if the first scan was performed urgently before the 6th hour. Today a simple rule of conduct requires that a brain scan is performed at any head injury presenting with a GCS score less than or equal to 13.

3 – Evaluation gauge

The measurement of intracranial pressure (ICP) is indicated in cases of severe head trauma (GCS 3-7). This measure intraparenchymal or ventricular way assesses the initial level, to give an indication of the severity, to follow its evolution and effects of resuscitation. We will speak of intracranial hypertension when the PIC is permanently above 15 mmHg. This pressure is considered severe and threatening if it reaches or exceeds 25 mmHg. At the same time, cerebral perfusion pressure was evaluated, which must remain greater than 60 mmHg (= Perfusion Pressure Blood pressure – ICP).

4- Prognosis Rating

to. prognostic factors
Faced with this potentially dangerous disease, two questions facing us: the short-term risk to life and functional long-term risk. More trauma is considered serious, and these issues are important. In response, we have immediate data we collect by clinical examination and imaging, our past experience, and all those in databases. Exploitation of a database makes it possible to establish the fate of a global group of patients that presented themselves in conditions fairly similar to those of our wounded. Individual prognosis is fraught with too many unknowns to be delivered with certainty, except in cases of extreme situation (example of irreversible coma). All these prognostic factors are both useful and fragile. We know that the condition of the wounded initial awareness is a major component, but it is often obscured by the need to neurosédation. We know that the examination of lesions visible on CT is also a determining factor, but we know the limits of his power detection. We can also support our analysis on other issues that the general experience confirms the usefulness under indicators, such as age, sex, genetic factors, measurement of intracranial pressure.Consider some of them:

  • disorders of consciousness
    Their statistical analysis was used to establish a link between the vital and functional prognosis and the condition of the patient’s initial consciousness estimated on the GCS. Thus, for a GCS to 3, the mortality is approximately 80%, whereas it is less than 1% for a GCS 15
  • the extent of damage
    the nature, extent and topography of lesions observed unquestionably determine the prognosis. The mortality of hemorrhagic lesions such as epidural hematoma, or subdural hematoma are quite well known. It is not the same for a range of parenchymal lesions of the neuroradiological evaluation remains difficult
  • age
    age influences the prognosis, because at equal initial severity, mortality increases with age from 15 years. But conversely, the mortality decreases with the age between 0 and 15 years. The mechanism of injury and biomechanical characteristics vary greatly with age, and thus indirectly influences the prognosis of age-related.
  • Sex
    females seem disadvantaged in terms of long-term results, which overall are worse. But it should be noted that the incidence of head trauma here is two times lower than humans.
  • genetic factors
    the poor prognosis of head trauma is closely linked to the presence in the genome of a particular protein factor present in the aveC allele epsilon 4. The presence of this factor would reduce the chances of recovery.
  • intracranial pressure
    measuring intracranial pressure is only for comatose patients in serious condition. Mortality wounded including intracranial pressure remains below the 20 mmHg threshold is around 19%. Mortality reached 50% in those whose pressure is above 20 mmHg. It is 95% when intracranial pressure is sustained greater than 40 mmHg.

b. Fate Assessment Scale
For us to communicate with us about the outcome of patients, we must have the same code that easily define a particular category of injuries. Almost simultaneously GCS scale that was proposed the Glasgow Outcome Score (GOS) to systematize the classes to become in terms of mortality, functional outcome, and economic reinsertion of the wounded. This scale has been criticized, it has become essential today. It can be enriched by the use of other prognostic scales with which a match is always possible. This scale consists of five categories:

  • GOS 1: good recovery. The injured may have a particular disability, but enough and finds a social and professional life.
  • GOS 2: partial recovery with moderate disability. The injured however is independent but need help in certain areas. He can find a profession in a protected environment.
  • GOS 3: severe disability. The injured man is conscious but present large deficits that make it dependent on others. He must live in family or institutional environment adapted.
  • GOS 4: persistent vegetative state. The injured has lost any semblance of emotional or relational mental life. It is entirely dependent.
  • GOS 5: Death

c. Why make a forecast in the initial phase?
Establish an overall prognosis is to give a first indication on the risk of early or immediate mortality directly related to the severity of the initial trauma. This prognosis should however not change the immediate practical conduct that should make every effort to treat the wounded, and to avoid the influence of a too pessimistic prognosis (risk of defeatism ill), or the opposite too optimistic (risk ‘exaggerated activism). After the first ten days, the overall mortality prognosis of less interest than the functional outcome.

Establish an individual prognosis would be more relevant, but it would rely on too fragile data such as personal experience, that of the medical and nursing team, and our interpretation of epidemiological data collected by other teams. It can be taken as certain, there may not be indicative. And even if one has the family of the wounded whole truth, we can not formally be sure of the hold. Although the future seems bleak injured, we must modestly admit our uncertainty, especially avoiding to leave our about any room for hope.

Establish a prognosis is finally an important element in terms of Public Health. The study of prognostic indicators allows preventive possibly correcting adverse risks, sensitization of public opinion, improved care of the wounded from the first moments.