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Management of patients with traumatic : 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

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 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 (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 .

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 .

• 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 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

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 , 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), (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 in intracranial volume will produce a big increase in ICP, which, clinically, will be accompanied by a rapid decline in a patient’s neurological status. With continued increases in ICP, may result, therefore clinical signs are not a good monitoring tool for ICP as their appearance is at the end stage of the process when brain herniation has occurred and therapy will be of limited benefit. The only way ICP can be modified in volume is by reducing oedema (for example, by using mannitol) and altering CBV. CBV only represents a small component of the total intracranial volume, but small increases in CBV will result in big increases in ICP when compensatory mechanisms to control ICP have been exhausted (Figure 5).

Cushing

When volume buffering mechanisms and autoregulatory adjustments are exhausted in response to raised ICP, CBF will fall, resulting in cerebral ischaemia and reduced removal of CO2. Increased local CO2 concentration affects the vasomotor centres in the brainstem stimulating the release of catecholamines and a sympathetic discharge to increase mean arterial blood pressure in an attempt to maintain CBF. This systemic hypertension is sensed by the in the general circulation and they initiate a reflex via vagal centres in the brainstem.

The catecholamine release may also result in cardiac arrhythmias due to myocardial ischaemia. This is termed the brain heart syndrome. The is life-threatening so identification of systemic hypertension and bradycardia should indicate elevated ICP and result in a rapid treatment response.

What can we control in TBI?

5 / 16 There are very few specific treatments that will actively improve the underlying abnormalities and, therefore, neurological function. However, there are several factors related to basic management that can make things dramatically worse if inappropriate monitoring or interventions are undertaken.

Much of TBI management is aimed at the control of ICP by influencing CBV and CBF. A certain CBV and CBF flow are necessary to maintain normal brain function; however, a large or rapid increase in CBV will result in raised ICP and subsequent neurological deterioration.

We can control mean arterial blood pressure

Clinical assessment of CBF is difficult and so the term cerebral pressure (CPP) is used and applied. CPP is a variable that is more easily ascertained and is a clinical correlate of CBF. It can be used to predict a patient’s risk of cerebral ischaemia:

CPP = mean arterial blood pressure (MABP) - ICP.

Systemic blood pressure must therefore increase to prevent a decrease in cerebral perfusion pressure and a resultant decrease in CBF. Autoregulation ensures a constant CBF occurs between a MABP of 50mmHg to 150mmHg as described above (Figure 4). Outside of this range, blood flow to the brain is dependent on systemic MABP; however, an intact blood brain barrier is required for autoregulation to function. Loss of autoregulation is therefore possible following head trauma and this means CPP passively follows MABP. Because of this, mild decreases in MABP – that may otherwise be considered safe in a healthy patient – may result in markedly decreased CBF. Therapy should be aimed at maintaining MABP in an appropriate range (50mmHg to 150mmHg). The increased dependency between CBF and MABP has been suggested to be a reason for the poorer prognosis observed in patients with hypotension following TBI.

We can control the arterial concentration of carbon dioxide

The arterial concentration of carbon dioxide (PaCO2) is the most potent factor controlling CBF/CBV. Hypercapnia (more than 45mmHg) causes vasodilation and increases CBF and ICP. Hypocapnia (less than 25mmHg) causes vasoconstriction and decreases CBF leading to ischaemia.

Controlling the arterial concentration of oxygen

An arterial concentration of oxygen (PaO2) of less than 60mmHg will increase both CBF and ICP; therefore, any reduction in O2 concentration (for example, due to haemodilution or anaemia) will also increase CBF and ICP.

Controlling cerebral metabolic rate

6 / 16 Cerebral metabolic rate (CMR) and CBF are coupled, so increased CMR will lead to increased CBF. CMR will, therefore, increase in the presence of seizures, fever, excitement or pain.

Diligent use of drugs

Inhalant anaesthetics cause cerebral vasodilation and subsequently increase ICP.

Barbiturates act in two ways:

• lowering CMR and, therefore, decreasing ICP, but also decreasing CBV – resulting in decreased CPP; and

• reducing , which increases PaCO2 and increases CBV – resulting in raised ICP.

Summary

Management of TBI can at first seem daunting, but it is important to maintain a practical and logical approach to assess each patient. The initial approach should all be about stabilising the patient with the basic equipment at hand. This predominantly involves oxygenation, management of MAPB by judicial use of fluid therapy and assisted ventilation in comatose patients. This management will be further discussed in a future article with indications on when ventilation may be appropriate.

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Figure 1. The spherical shape of the skull means the forces impacting on the brain are propagated into the deeper tissues of the brain. As a result the deeper structures of the brain, such as the brainstem and thalamus, become the focus for the injury.

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Figure 2. MRI pictures from a shih-tzu that presented having been kicked over the right side of the head by a horse. The sagittal T2-weighted image is shown for localisation purposes. Transverse images B and C are T2-weighted (B) and fluid-attenuated inversion recovery (C) sequences taken at the level of the white line shown in A. A small intraparenchymal hyperintensity is seen, indicated by the white arrowheads, indicative of a contusion resulting from a contre-coup injury. Transverse images D and E are T2-weighted (D) and fluid-attenuated inversion recovery (E) sequences taken at the level of the white line shown in A. A large hyperintense signal is seen in the cerebellum as shown by the asterisk – again indicative of contusion. This dog recovered uneventfully without the need for surgery or intensive care. L denotes left side of patient.

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Figure 3. Cross-sectional imaging pictures to demonstrate the three main types of intracranial haemorrhage: intraparenchymal (A and B); subdural (C); and subarachnoid (D to F) haemorrhage. Images A and B are T2-weighted (A) and T2* gradient-echo (B) transverse MRI showing the characteristics of an intraparenchymal haemorrhage. The images reveal a well-defined mixed signal intraparenchymal lesion of the right temporal lobe (white block arrows). The lesion is predominantly hyperintense (to grey matter) on the T2-weighted image with a hypointensity (to grey matter) on the T2* gradient-echo image. Image C is a transverse CT image showing a crescent- shaped hyper-attenuating mass in the subdural space (white arrow heads). This is characteristic of a subdural haemorrhage. Images D to F, in contrast, show a subarachnoid haemorrhage on MRI. Images D to F are T2-weighted (D), fluid-attenuated inversion recovery (E) and T1-weighted (F) transverse MRI showing the characteristics of a subarachnoid haemorrhage. The lesion (shown by the arrow heads) is limited by the arachnoid trabeculae that connect the arachnoid mater to the pia mater and, therefore, the haemorrhage in this location has not expanded the subarachnoid space as it does in a subdural location. L denotes left side of patient.

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Figure 4. A graph to show the relationship between cerebral blood flow, arterial partial pressure of oxygen (PaO2), carbon dioxide (PaCO2) and mean arterial blood pressure. Note a constant cerebral blood flow occurs between a mean arterial blood pressure of 50mmHg to 150mmHg.

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Figure 5. This graph shows how changes in intracranial volume minimally impact on the intracranial pressure during the compensatory phase. However, once the compensatory mechanisms have been exhausted, a small increase in intracranial volume will lead to an exponential increase in intracranial pressure (the decompensatory phase).

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