LOS CABOS, B.C.S. According to data from the Revista Mexicana de Neurociencia (Mexican Journal of Neuroscience); worldwide, million. Severe Cranioencephalic Trauma: Prehospital Care, Surgical Management and Multimodal Monitoring. Article · Literature Review (PDF Available) · January. Guidelines for the Management of. Severe Traumatic Brain Injury. 4th Edition. Nancy Carney, PhD. Oregon Health & Science University, Portland, OR. Annette .
|Published (Last):||21 February 2016|
|PDF File Size:||15.35 Mb|
|ePub File Size:||12.92 Mb|
|Price:||Free* [*Free Regsitration Required]|
Traumatic brain injury is a teauma cause of death in developed countries. It is estimated that only in the United States aboutpeople die annually in parallel among the survivors there is a significant number of people with disabilities with significant costs for the health system.
Head trauma management is critical is the emergency services worldwide.
Severe Cranioencephalic Trauma: Prehospital Care, Surgical Management and Multimodal Monitoring.
We present a review of the literature regarding the prehospital care, surgical management and intensive care monitoring of the patients with severe cranioecephalic trauma.
Encephalic traumatic injury is a cranioecephalic problem around cranilencephalic globe [ 1 – 4 ]. It represents at least half of deaths related to trauma and impacts health care services with high expenses for cranloencephalic health care system, for support and treatment of patients [ 5 – 7 ].
In The United States of America, health expenses are estimated as high as billions of dollars per year, whether directly or indirectly, because of labor productivity loss [ 7 ]. Despite these efficacious advantages, there are many aspects that should be upgraded about the brain traumatic injury management. The purpose of this article is to give cranioencphalic reader basic elements about brain traumatic injury, starting with the initial evaluation in the emergency room or reanimation areas, until intracranial pressure multimodal monitoring, including strategies for the control of intracranial hypertension in intensive care units.
Thus, initial evaluation; neurologic exam and management strategies that will be presented should become key tools for treatment of patients with severe neurologic trauma.
Many of the achievements related to prognosis of patient with severe brain traumatic injury have stemmed from optimization of prehospital care and better quality attention in the emergency room and during resuscitation, as well as rapid imaging evaluation and identification of potential surgical injuries. All this efforts must be accompanied by multidisciplinary management and organization of emergency response teams, trauma room and support teams radiology, respiratory therapy, blood bank, clinical laboratory, among others.
The main objective of prehospital care is to remove the traumatized patient from the environment or danger zones and move them to areas where appropriate therapy may be started.
Thus, to avoid increase of injury or worsening of initial conditions, these efforts must be accomplished in logic and controlled way. The patient must be evaluated rapidly, immobilized with a cervical neck brace and spinal board to be forwarded to a definitive trauma center. Two clinical variables, hypoxia and hypotension have shown correlation with poor prognosis of these patients. Emergency response personnel should at least be able to identify patients who need respiratory support and to intubate those patients in the field where the traumatic event took place.
Intravenous access should be set and circulatory support with resuscitation fluids is mandatory. Once the patient has arrived to the hospital, the emergency room or resuscitation team will take over.
Organized and flow transference care should be promoted to continue with the basic principles of integral attention pointing out secondary injury evasion. A standard emergency room or resuscitation area should have the basic equipment, including access to blood, laboratory service, ventilators and radiology. During primary approach, airway, ventilation, circulation, disability and exposure are evaluated ABCDE. Airway assessment consists in determining the ability of the patient to control their ventilation and respiration.
Certain circumstances may block the airway, including an altered consciousness, obstruction by foreign body, fractures or facial edema. Maintaining a permeable airway is a need and orotracheal intubation is the preferred route when needed.
Respiration is next on the list, it is often assessed with the thorax patient, verifying if there is appropriate cranioencphalic symmetric expansion, also it is important an optimal pulmonary auscultation, as well as determining appropriate ventilation with pulse oximetry and carbon dioxide monitoring.
Injuries such as pneumothorax and tracheal injury should be assessed in that moment. Circulation assessment is performed prioritizing blood trwuma pressure. In cranioenncephalic presence of evidence of blood loss immediate treatment should be started.
At least two large peripheral lines should be obtained, at the same time as blood tests complete blood count, coagulation test. It is not yet defined to use whether crystalloid or colloid fluids for initial fluid resuscitation, however they may be used indistinctly as long as used properly. The following step is disability assessment, it usually consist of a short neurologic assessment using the Glasgow Coma Scale GCS. The primary medical team may contribute promptly with valuable information for the neurosurgeon when this scale is used.
Any altered mental status in a patient without hypotension or hypoxia is suggestive of a brain traumatic injury until proven otherwise, and CT scan is the election image study to confirm this injury. Shortly, the secondary survey starts when primary survey has been completed and the patient has been stabilized.
This secondary survey usually consists of a complete reevaluation of the patient and performance of additional tests as indicated by the condition. Detailed clinical history and physical examination, ECG, pregnancy tests, and additional radiologic studies are components of this phase. The moment the neurosurgeon is consulted to assess a trxuma patient; a detailed directed neurologic trama is needed.
Details cranoiencephalic initial injury such as time and mechanism, information provided by witnesses and taking some aspects of the initial neurologic exam would be appropriate for the diagnosis and management. Data about the initial decrease of consciousness, convulsive crisis before or after the event, seatbelt use, high or low speed impact or initial motor movements may guide to a rapid decision of management that will be applied to the hospitalized scenario.
The traumatized patients will be sedated with the goal of protecting airway or facilitating the appropriate care during initial reanimation efforts. This aspect should be accounted for by the neurosurgeon, as a basic aspect for cranioencehpalic neurologic assessments. Cranioemcephalic intubated patient in whom a brain traumatic injury is suspected cranioenxephalic be kept with normocapnia, usually in a normal-low range pCO2 mmHg to avoid hypercapnia, vascular dilation and progression of cerebral edema.
Hypotonic fluids should never be used in a patient with brain and scalp injury cranioencephslic identify any rapid blood loss due to lacerations, and compression and wound closure will be indicated. The combination of hypotension and bradycardia should crnioencephalic us think about neurogenic shock and in that case vasopressor drugs should be used to maintain appropriate arterial tension levels. Any abnormality in coagulation parameters should be corrected aggressively.
Physical exam should be performed step by step, usually from head to toe. The scalp examination, head, face, eyes, and ears should alert the neurosurgeon about the possible presence of bone fractures, open wounds, otorrhea, pupil dilation, cerebrospinal fluid fistula or ecchymosis may contribute to the diagnosis.
Classically, otorrhea, rhinorrhea, retroauricular ecchymosis, or preorbital ecchymosis may be associated with fracture of cranium base.
Severe Cranioencephalic Trauma: Prehospital Care, Surgical Management and Multimodal Monitoring
However, the best score will always be used. The possibility of pharmacologic and sedation paralysis should be considered since this drugs modify the Glasgow Coma Scale and lead to erroneous evaluations. Traditionally a score of is defined as mild cranioencephalic trauma, scores of as moderate and scores below 8 as severe.
A complete and detailed neurologic evaluation is beyond this chapter but an approach to cranial nerves, sensitive exam must be performed. There are few classic pupillary findings and herniation syndromes; at least those will be described. Unilateral pupillary dilation with a background of brain traumatic injury is strongly suggestive of an expansive injury or uncus herniation, especially when associated with hemiparesis.
Bilateral fixed and dilated pupil may suggest global hypoxia and brain death, and fixed myotic pupils suggest thalamic and brain stem hemorrhage. Head radiography, cerebral arteriography and ventriculography were the principal diagnostic tool used for trauma by surgeons and neurosurgeons to assess patients with head trauma.
CT allows quick and appropriate identification of head bones, cerebral parenchyma, intra or extra-axial bleeding, air, foreign body and cerebrospinal fluid. Once primary survey is completed and the patient is clinically stable, a head CT must be performed. After performing the head CT, evaluation by a neurosurgeon is essential.
Acute bleeding seems relatively hyperdense when compared with cerebral parenchyma in a non-contrast-enhanced head CT. Extracranial collections are generally considered surgical if they are larger than 1 cm, surgical management will be detailed further in this chapter. Epidural hematoma is seen as a hyperdense mass, biconvex and adjacent to the cranium. Subdural hematomas are usually half-moon shaped; they can extend beyond the suture lines and typically are the result of venous bleeding.
Their appearance will depend on the chronicity of the bleeding; acute bleeding is hyperdense, subacute bleeding is isodense and chronic bleeding is hypodense. Traumatic subarachnoid hemorrhage is the most common type of hemorrhage, the bleeding looks hyperdense and it is often localized over the convexity, basal cisterns and major sulci.
Intracerebral hemorrhage and contusion present with several bleeding quantity of high density inside the cerebral parenchyma and intraventricular bleeding presents as high signal inside the ventricular system.
Skull fractures are better assessed with bone window. The presence of skull fractures are associated with intracranial bleeding probability, the assessment must include carefully inspection of orbital bones, frontal bone, sphenoid, maxillary bone, etmoidal sinus and temporal bone.
Sometimes, finding air or fluid may be the only clue to discover a skull fracture. Air is typically seen black on a standard CT, it may be present in soft tissues, sinuses, intracranial spaces. Ischemia or infarction may not appear early on CT but lost of cortical-subcortical differentiation or discrete edema may lead to the primary diagnosis. Cerebral edema manifests as grooves compression, ventricle effacement and basal cistern obliteration.
Any midline deviation must be objective. In those cases with skull penetrating injuries or when a possible vascular injury is suspected, a cerebral angiography is the Gold Standard diagnostic test. Other modalities, such as angio-CT and angio-MRI are growing in popularity, due to the availability, familiarity and velocity. These are useful tools and sensibility is close to the one of conventional cerebral angiography.
MRI imaging allows better soft tissue evaluation, hematic collections and edema, but the use of it in the acute scenario is limited, mainly because of time limitation.
MRI is better designed for evaluation of the late phase. Diffuse axonal injury, ischemic injuries and long term prognosis are some of the potential applications for MRI. Spectroscopy by MRI, magnetoencephalography and tractography will show in the future the possible applications in the area. Complex cellular pathways and mechanisms implicated on cerebral traumatic injury are extended.
We provide a description of clinical and cellular basic physiopathology with the objective of breaking down the most relevant topics. Cellular events, including events related with calcium, mitochondrial alterations, apoptotic mechanisms, genetic alterations and inflammatory mediators are discussed initially.
Cellular physiopathology of cerebral traumatic injury [ 49 – 19 ]. The cellular processes, which involve neuronal injury after a cerebral traumatic injury, are traditionally classified as secondary cerebral injury, unlike the primary or spontaneous injury from the direct trauma itself.
Secondary cellular events are believed to happen within hours or days after the initial trauma and may continue for weeks. Alterations in calcium homeostasis resulting from cerebral traumatic injury have been related to several cellular eventualities. One inside the cell, calcium has been related to different processes, including phospholipases activation, leading to membrane disruption, free radical production that leads to cellular genetic material injury; down regulation of genes that control survival or apoptosis and mitochondrial disruption, leading to cellular death.
Specifically, phospholipase A2 and phospholipase C lead to cellular disruption and free fatty acid generation.
These fatty acids attached to intracellular free radicals such as nitric oxide, superoxide anion and hydrogen peroxide, represent reactive oxygen species ROS which cause DNA injury and cellular membranes and may disrupt cerebral blood flow, blood-brain barer and produce cerebral edema. Intact mitochondrial function is to regulate energetic metabolism and contribute to cellular homeostasis. Elevated intracitoplasmatic and intramitochondrial calcium alters oxidative phosphorylation and electron transport chain.
Cellular death through oxidative process alterations, mitochondrial edema and Na-K-ATP pump disruption are directly related phenomena. Genetic alterations, including overregulation of early oncogenes C-Fos and C-Jun, alter expression of pro-apoptotic and anti-apoptotic genes, their significance is not yet totally understood.
These relations incline in favor of apoptosis, cysteine-protease family, and denominatedcaspases is a call to get in action. Caspase 8 and 9, known as caspase initiators influence directly caspase 3, the final executor. Activated caspase 3 points its intracellular targets, including cytoskeleton proteins, nucleic acid repair proteins and DNA-ases. Numerous cytokines, growth factors and inflammatory mediators have been associated with cerebral traumatic injury.