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Management of Patients with Traumatic Brain Injury: Part One

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Management of Patients with Traumatic Brain Injury: Part One Vet Times The website for the veterinary profession https://www.vettimes.co.uk Management of patients with traumatic brain injury: part one Author : MARK LOWRIE Categories : Vets Date : September 1, 2014 MARK LOWRIE MA, VetMB, MVM, DipECVN, MRCVS in the first of a three-part series, discusses the effects various head traumas have on the brain, and approaches to controlling intracranial pressure TRAUMATIC brain injury (TBI) refers to any external force that traumatically injures the brain and is probably a more accurate term to describe the contents of these articles than head trauma. Head trauma usually refers to TBI, but is a broader category because it can involve damage to structures other than the brain, such as the soft tissues of the head and the calvarium. TBI is a common presentation in the emergency clinic and can result from road traffic accidents, kicks to the head, falling from heights, gunshot wounds and animal bites. Management of animals with head trauma, although often crude, remains challenging and requires the emergency clinician to have a basic understanding of neurophysiology and neuroanatomy. This, in turn, allows for a good understanding of the indications and effects of any interventions. This is important because most animals with TBI are initially treated by general practitioners and emergency clinicians, who have the added responsibility of establishing a list of priorities for that animal, enabling life- threatening injuries to be assessed and treated immediately. This article reviews the basic pathophysiology surrounding TBI in veterinary patients and discusses some of the basic interventions that can be used to manage animals with TBI. Primary brain injury 1 / 16 There are various forces that can affect the brain following head trauma. These are divided into primary and secondary brain injury. Primary injury is due to direct trauma (or contact injury) to the brain tissue (focal processes) and the forces applied to the brain at impact (diffuse processes) – for example, acceleration, deceleration and rotational forces. In treatment terms, the primary injury is exclusively sensitive to preventive, but not therapeutic, measures and so intervention is often fruitless in preventing this damage. The spherical shape of the skull and the propagation of rotational forces after the primary injury direct these forces into the deeper tissues of the brain. As a result the forebrain is not the focus for the impact of the trauma, but the brainstem (Figure 1). This is significant because it is the brainstem that contains the vital cardiovascular and respiratory centres. Diffuse processes The brain is unable to tolerate these forces because of its composition and lack of internal support. Acceleration/deceleration forces The superficial grey matter is most susceptible to the forces of acceleration, leading to haemorrhage or contusion and tearing of neuronal tissue. Rotational forces Rotational forces have more of an impact on the deeper white matter of the brain, causing concussive injuries and diffuse axonal injury. Diffuse axonal injury is usually not visualised and can only be seen at the microscopic level. The clinical term used to describe the manifestation of diffuse axonal injury is concussion. Focal processes Focal brain damage is due to contact injuries and direct trauma to the brain, resulting in contusion, laceration and intracranial haemorrhage. These focal lesions are often located in the superficial brain structures close to the skull, but sometimes deep cerebral haematomas can occur. Contusion Contusion can occur both from the initial impact of the brain with the skull (coup) or on the opposite side of the brain as it ricochets against the skull (contre-coup; Figure 2). Skull fractures Fractures of the skull may be linear or depressed fractures, which are usually benign. However, on 2 / 16 occasion, compound or open fractures can be seen that may require neurosurgical intervention. Haemorrhage Several types of intracranial haemorrhage are relevant here (Figure 3) and include the following. • Intraparenchymal haemorrhage occurs in the brain parenchyma itself and is the most commonly observed type of haemorrhage following TBI. • Epidural haemorrhage occurs between the periosteum and dura mater, and is usually the result of bleeding from the meningeal arteries. • Subarachnoid haemorrhage occurs in the subarachnoid space. This space contains a web of blood vessels so any type of force applied to the brain will result in injury to this area and haemorrhage within this compartment. • Subdural haemorrhage is not commonly seen in dogs and cats, but occurs more commonly in humans. Secondary brain injury Secondary injury refers to the secondary damage and delayed non-mechanical damage that are initiated at the moment of the injury with delayed clinical presentation. Cerebral ischaemia and intracranial hypertension refer to secondary insults and, in treatment terms, these types of injury are sensitive to therapeutic interventions and it is these processes our management aims to reduce and prevent. The inciting cause for this is usually the vascular abnormalities associated with TBI. Vasospasm accompanies any haemorrhage due to damage to the vessel walls and this, in turn, sets up an ischaemic cascade, which involves the release of free radicals that initiate lipid peroxidation. The significance of this is that the high fat content damages the brain tissues, including myelin, causing further neurotoxic damage. Neurotransmitters are also released in this process, particularly glutamate, which is the most common excitatory neurotransmitter in the brain. This excitation causes a calcium influx into the neurons, which is neurotoxic. All of these combined processes result in decreased cerebral blood flow and ischaemia, therefore treatment should centre on reversing these secondary effects, namely hypoxaemia, hypercapnia, systemic hypotension and intracranial hypertension. Brain oedema There are three types of brain oedema, but only two are relevant to TBI. Vasogenic oedema is the more treatable of the two. This occurs when there is an increase in capillary permeability, allowing 3 / 16 fluid to escape into the extracellular space, therefore it is commonly seen in TBI in response to failure of the blood-brain barrier. Fluid accumulation occurs predominantly in the white matter of the brain where the neuronal fibres run, resulting in a diffuse characteristic pattern. Cytotoxic oedema is the more devastating of the two. This involves swelling of the neuron due to failure of the sodium pumps to control the water in and out of the cell. Therefore, sodium accumulates intracellularly, causing fluid to be imbibed to maintain an osmotic equilibrium. This type of oedema is seen predominantly in the grey matter. Pathophysiology of traumatic brain injury To limit these secondary processes resulting in hypoxaemia, hypercapnia, systemic hypotension and intracranial hypertension, we must consider maintaining adequate blood flow in the face of TBI and this involves a basic understanding of the normal physiology. There are three homeostatic responses of the brain that work to maintain intracranial pressure (ICP) in a range where the brain is functional. Autoregulation Cerebral blood flow (CBF) is primarily driven by systemic mean arterial blood pressure, but is also dependent on cerebral metabolic rates, blood oxygen (O2) and carbon dioxide (CO2) concentrations. CBF is maintained by an intrinsic homeostatic mechanism called autoregulation. Myogenic autoregulation Myogenic autoregulation is when the smooth muscle of the vessel walls contract or relax to alter the mean arterial blood pressure and maintain CBF; however, this mechanism only works for a mean arterial blood pressure between 50mmHg and 150mmHg. Outside this range, CBF is dependent on the mean arterial blood pressure (Figure 4). Chemical autoregulation Chemical autoregulation is mainly driven by the arterial concentrations of O2 and CO2. If the arterial concentration of O2 decreases, vasodilation occurs and vice versa. Conversely, if the arterial concentration of CO2 decreases, vasoconstriction occurs and vice versa, allowing maintenance of CBF (Figure 4). Neurogenic autoregulation Neurogenic autoregulation is produced by sympathetic and parasympathetic innervations of the vasculature to maintain CBF. 4 / 16 These are the mechanisms, therefore, that govern a normal brain; however, in the event of disruption of the blood brain barrier, as may be seen in TBI, autoregulation may be lost and cerebral blood flow passively follows the mean arterial blood pressure. Volume buffering The cranial vault is a fixed space (closed box) that contains brain tissue (80 per cent), cerebrospinal fluid (CSF; 10 per cent) and the cerebral blood volume (CBV; 10 per cent). ICP is defined as the pressure exerted between the skull and the intracranial tissues (namely the brain tissue, CSF and CBV). Following head trauma, the body can compensate for small increases in ICP by forcing blood (for example, increasing venous return and decreasing CBF) and CSF (for example, increasing CSF absorption and displacement of the spinal subarachnoid space) out of the cranial cavity. During this time clinical signs may not be apparent unless the trauma has injured the brain parenchyma. A critical threshold for ICP is reached when these compensatory mechanisms can no longer cope and this is the time when clinical signs are observed (decompensatory phase; Figure 5). At this critical point any further small increase
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