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Wednesday, September 19, 2012

Craniocerebral Injuries

General

Injury from car accidents are a daily phenomenon especially in young people. Sometimes they are serious and result in death and sometimes in serious injury of the brain and/or spinal column. The severely injured are hospitalized in the intensive care unit where modern methods are used to monitor vital signs and body stress, perfusion, oxygenation and temperature of the brain with special microscopic probes. In this way edema and ischemia of the brain are treated in time. The complete treatment of wounds from the moment of admission is performed by following a special protocol of instructions.





The injured also have the option to be monitored after discharge from the hospital or if necessary to be transferred to special rehabilitation centers for further treatment and social/professional reintegration.

The definition of Craniocerebral injuries (CCI)

CCI defines any trauma to the skull and brain. There are two types, closed and open. In closed craniocerebral injuries the brain is not exposed to the external environment while in the open type the brain is exposed to external environment and this is a critical surgical condition  as there is a co-existing fracture of the skull. Skull fracture can also be co-existent with the closed type.  Hematoma and / or fractures and / or swelling can be present in craniocerebral injuries. When the hematoma is created in the space between the dura and the skull  it is  characterized as epidural. When the hematoma is created in the space between the brain and the dura it is characterized as a subdural and when the hematoma is created within the brain parenchyma characterized as intracerebral.

The human brain is particularly susceptible to injury. For this reason it is surrounded by 3 meninges (membranes) and covered externally by the compact hard skull.

The nerve cells of the brain are especially  sensitive, without regenerative capacity and can easily rupture, distend or compress after trauma. A blow to the head easily cause an impact of the brain against the hard ,abnormal bone and abnormal inner surface of the skull.
The post traumatic swelling creates pressure conditions in the cells and reduces blood flow to the cells. It is clear that the nerve cells work well with specific rates of cerebral blood flow and O2 supply. Any deviation from these values causes significant damage to nerve cells.

What symptoms are caused

Closed CCI  is usually due to violent contact of the skull with another object resulting in a sudden movement of the sensitive brain  inside the skull.  This can cause either focal or diffuse brain damage. The symptoms of CCI can be mild to very heavy. A mild CCI usually occurs in reversible damage whereas severe CCI  is almost always followed by severe residual neurological damage. The location, nature and intensity of the injury  determine the nature and extent of permanent neurological damage.

A patient with mild CCI may display the following symptoms:

  • Headache
  • Vertigo –Dizziness
  • Impaired mamory with loss of consciousness of variable duration
  • Vomiting
  • Fatigue, weakness, malaise
  • Drowsiness

A patient with moderate or serious traumatic head injury, may display the following:

  • Change in level of consciousness-lethargy-stupor-coma
  • Headache that does not go away but on the contrary gets worse.
  • Headache that does not go away but on the contrary gets worse.
  • Difficulty or loss of movement coordination of the hands or feet(upper and lower extremities)
  • Repetitive vomiting and nausea.
  • Dilation of one or both pupils of the eye.
  • Spasms
  • Breathing irregularities (arrhythmia)
  • Impairment of vital signs
  • Epileptic seizures



How are Craniocerebral injuries (CCI) diagnosed

CCI is confirmed by the description of the injury mechanism as well as the presence of physical signs such as trauma, abrasion, whiplash trauma or bruising of the skull. Flow of blood or cerebrospinal fluids from the nose or ears of the patient suggest injury to the base of the skull which is confirmed by the presence of a posterior spinal or  periorbital hematoma. CCI is further identified  by the general neurological signs ie. Coma lithargy, stupor ,drowsiness, epileptic seizures or focal signs ie.weakness-paralysis of a limb, speech disorder. When the above are detected the injured person must be submitted to a full neuroimaging tests such as x-ray, computerized tomography scan(CT) and Magnetic Resonance Imaging (MRI)  and MRA. These tests can confirm the presence of lesions in need of emergency surgical intervention. Neurosurgical intervention is usually aimed at relieving the brain parenchyma from pressing phenomena but does not prevent the development of cerebral edema or possible damage to nerve cell level.


There are three forms of treatment of CCI according to the severity:

  • Simple home or hospital monitoring for negative focal neural deficits and mild symptoms.
  • With conservative treatment in Neurosurgical clinic for  moderate symptoms and brain lesions that have appeared in neuroimaging control but do not have surgical perspective.
  • With emergency  or  later neurosurgical intervention for surgical injuries which have shown on the neuroimaging tests and in those cases where the patient has severe symptoms


In these cases the patient may need to be hospitalized after surgery in Intensive Care (ICU) under sedation with simultaneous recording of specific indicators of the metabolic activity of the brain and intracranial pressure by special micro-catheters. Additional medical measures  such as hyperventilation, antiedema therapy ,hypothermia and barbiturate coma, may also be necessary after surgery  to reduce intracranial pressure .

If intracranial pressure cannot be controlled with the above measures a craniectomy will have to be performed, in other words the removal of a large part of the skull in order to decompress the swelling of the brain. Finally it is important to note that epileptic seizures can appear in every case of injury to the cortex of the brain, either early or at a later stage (after six months).The treatment of the seizures is the correct medication and only in the case of late seizures it may be necessary to remove the gliotic section of the brain parenchyma that triggers the seizures.


Definition of Primary lesions

Primary lesion is defined as any immediate trauma to the skull and the direct consequences of the trauma eg any post-traumatic hematoma. The meninges and bones of the skull act as protectors of the brain from injury. Within the skull, the space  is specific and there is a dynamic balance of the volume of blood volume and CSF volume of brain parenchyma contained in the skull.
Any space-occupying lesion  (eg hematoma) affects this dynamic balance and these volumes are changed. This creates conditions of intracranial pressure, therefore we have increased intracranial pressure and the nerve cell is exposed to damage.


Definition of Secondary lesions

Swelling of the brain and  ischemia as a result to increased intracranial pressure are defined as secondary lesions. If swelling is severe and it is impossible to reduce intracranial pressure, then the injured brain cells impair function  even more  thus creating conditions that pressure the brainstem, a particularly life threatening situation. This condition is called herniation. Herniation is not only caused by brain swelling, it is also caused by the reduction of the blood flow to the brain,ie ischemia. This means that the traumatic brain injury  is complicated by reduced blood flow due to insufficient supply of sensitive nerve cells with O2 and glucose which causes increased cerebral swelling and further reduction of cerebral blood flow.


What we define as a change in level of consciousness and why it is important assessment of the patient

CCI regardless of its severity, cause transient, progressive deterioration, or even permanent change in the patient's ability to react and respond to environmental stimuli. This is defined as a change in level of consciousness of the patient.

The level of consciousness is defined as the ability to react and respond to external stimuli either verbally or by opening the eyes or some movement of limbs or face. Today the level of consciousness of the injured is now accurately coded according to verbal response, motor response and the opening of the eyes to any external stimulus. Previously the terminology waking, drowsiness, lethargy, stupor and coma were used to describe the changes in the level of consciousness however with little success due to the subjectivity of the definition by each physician in the  evaluation of each patient. The comatose state  is the severest CCI and corresponds to the complete lack of consciousness, to the unresponsiveness to stimuli with anything more than  reflexive movements or expressions of pain. Both the degree and duration of the change in level of consciousness are indicative of the severity of CCI.

The changes due to brain injury vary from barely perceptible, moderate, serious and grave nature. Given the complex structure and function of the brain it is usually risky to predict the degree of recovery from such changes. The uncertainty is a challenge for neurosurgeons to explain, and for the family or companions of the injured to accept .


Recovery from CCI

After CCI ,patients  whether they needed surgery or only conservative management  or  had to be sedated with support of vital functions begin recovering gradually and progressively. This process may require some time depending on the severity of CCI. At this point,  gradual organization of cognitive functions and their evaluation  is possible. Stimuli of mild intensity  in speech, touch, pressure, sound or visual stimuli are more beneficial than those of long duration and intensity that can only cause confusion to the incapacitated patient.

The progress of recovery depends on idiosyncratic rhythms as well as the severity and duration of CCI. It can take days, weeks or years. Unfortunately there are severe cases with no possibility of  progress and the patient remains with open eyes  in an "awake coma," without other specific responses to external stimuli. The longer a situation like this remains the less likelihood of recovery.

During recovery, however, some permanent problems can be determined (residual damage), the type and severity, however, vary depending on the extent of brain damage.


TYPES OF NEUROLOGIAL DEFICITS-RESIDUAL DAMAGE


  • Loss of memory
  • Inability to recall and retain recent information
  • Loss of cohesion and coherence of thought
  • Inability to memorise
  • Inability of complete  direct  thought
  • Difficulty concentrating
  • Easy impaired attention and concentration
  • Competitive irritability and commitment incapacity
  • Slowness of mentality
  • Slowness of thought
  • disinhibit ion-impulsivity
  • negativis
  • Irritability
  • Consolidation of emotion
  • Emotional instability
  • Difficulty adjusting
  • flat thought
  • Impaired negative thinking, inability of  higher mental  functions to solve  problems and make decisions
  • dysphasia, paraphasia, aphasia
  • Difficulties in communication, emotional expression and comprehension
  • Changes in the senses of sight, hearing, touch, smell and taste
  • physical disabilities such as hemiparesis, hemiplegia, paraparesis, paraplegia, tetraparesi, quadriplegia (when there is also trauma of the spine)

Management Options

Patients with mild head injuries are usually sent home with clear instructions for their family to monitor them for the next 48 hours. If they display peritraumatic amnesia and/or neurological signs and/or vomiting and/or indirect signs of skull fracture( persistent, for more than 7 days, runny nose, otorroia, loss of cerebralspinal fluid (CFS)), they undergo an  emergency CT scan and are admitted to hospital for at least 24- hour monitoring. A small percentage of these patients,  have ,or have developed  head contusions and/or intracranial hematoma –the removal of which may require surgical intervention.
Patients with moderate head injuries ,following the emergency assessment and support of vital functions are submitted to a cranial CT. A large percentage of these patients,  have ,or have developed  head contusions and/or intracranial hematoma –the removal of which may require  craniotomy or drainage
Patients with severe head injuries (comatose patients), immediately after their admission to the emergency room(ER) are intubated with an endotracheal tube, sedated, and placed on mechanical ventilation and support. Then an emergency cranial  CT scan is performed. If substantial intracranial hematoma is present it must be surgically removed.
In each instance the patient is then moved to the Intensive care unit.  An important part of the treatment of patients with moderate or severe CCI  is played by continuous electronic recording of specific indicators of metabolic activity of the brain, the control of intracranial pressure and consequential timely treatment of any increase in pressure.



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