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Brain Injury Health

1. Abstract

The management of traumatic brain injury (TBI) has evolved dramatically in the last two decades. This is the result of a more thorough understanding of the physiological events leading to secondary neuronal injury after TBI, as well as the advances in the care of critically ill patients. The brain is sensitive to changes in substrate delivery. In neurological critically ill patients, interruption of this supply causes ischemic brain damage and thus impairs the outcome. To prevent, detect, and treat these ischemic events as soon as possible, the cerebral blood flow (CBF) is continuously monitored. Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) are two parameters that often reflect ischemic events, and thus it is mandatory to continuously measure them. This critical review discusses the physiology and pathologies relating to intracranial pressure and cerebral perfusion and analyses the technologies and techniques currently used in the management of critically ill patients. These are obtained through research and experimental studies demonstrated on animals and humans. Finally, it evaluates the current technologies, identifies the limitations and suggests further improvement and research in this field.

2. Epidemiology

Various specialists who deal with the prevention, treatment, care, and rehabilitation of head injuries have recognized for the years the magnitude if the problem. However, it was under the leadership of Dr. Murray Goldstein, Director of the National Institutes of Health, that an organized effort on a national basis was begun to give widespread attention to the head injury ‘'epidemic'' problem. Dr Goldstein's efforts resulted in the formation of intra-agency Head Injury Task Force, with its formal report published in June 1989 (Goldstein, 1990). This report gives startling figures: ‘'someone receives a head injury every fifteen seconds in the United States. A conservative estimate puts the total of head injuries at over two million per year, with 500,000 severe enough to require hospital admission. 75, 000 to 100,000 persons die each year as result brain injury. It is the leading cause of disability in children and young adults and is also the principle cause of brain damage in young adults. 5000 new cases of epilepsy caused by head trauma are reported each year. Related medical and legal bills often leave families with near or total financial ruin. The economic cost alone approaches 25 billion dollars per year'' [1]. The main cause of severe head injury in teenagers and young adults are motor vehicle related accidents. The next largest group responsible for head injuries are falls, and are more common with extremes of age. Of all cases of head injuries reported, approximately 40% are alcohol related incidences [2]. Regardless of the cause of TBI, molecular and cellular derangements occur that can lead to a neuronal cell death. TBI can be classified as mild, moderate or severe. Understanding the mechanisms of primary and secondary injury allows intensive care physicians and neurosurgeons to target therapy [3]. The majority of ICP and CBF monitoring is in head injured patients. Physiological parameters within the brain are measured and detected by monitoring techniques. With the information obtained by such devices, therapeutic measures may be used to correct abnormal values and potentially decrease patient morbidity and mortality [4].

The brain's requirements for energy in relation to its weight are high. The brain consumes and extracts more oxygen and glucose per 100g of tissue than the rest of the body systems (5-10 times more), and for this reason it needs in comparison more blood flow. In physiologic situations, the requirements, the consumption, and the cerebral blood flow are coupled. This adjustment between delivery and demand is regulated by changes in blood pressure, the arterial content of oxygen and carbon dioxide, and other different mechanisms [5].

The brain depends on oxygen and glucose to survive, therefore, cannot sustain prolonged amounts of time without it. It has no characteristic of which it can store these required elements. This leads to ischemic events occurring and hence causes damage to the brain. The pathophysiology of cerebral ischemia is complex, with multiple variables playing a role, it is not fully understood at the present time [6]

The role of the physician, based mainly in the intensive care unit (ICU) is to avoid, prevent, detect and treat as soon as possible all the derangements in the normal brain substrate delivery, to improve outcome in patients at risk of suffering ischemic brain damage [6]

Neuromonitoring techniques try to detect the multiple signs of abnormalities with different origins but with a common clinical manifestation, such as an increase in ICP, alterations in CBF, or derangements in the normal brain metabolism [6].

Therefore, in the review, technology and techniques are evaluated with the information they give, their use in clinical practice, and their downfalls.

3. Pathophysiology

The brain is the control centre of the central nervous system, responsible for behaviour. The brain is located in the head, protected by the skull and close to the primary sensory apparatus of vision, hearing, equilibrioception (balance), sense of taste, and olfaction [7]. A disruption in the workings and mechanisms of the brain can lead to high risk illness. Delay in the assessment of head injured patients can have devastating consequences in terms of survival and patient outcome. Hypoxia and hypertension double the mortality of head injured patients [8]. The purpose of monitoring the brain, either in the ICU or operating theatre, is to detect secondary insults which may cause permanent neurological damage if undetected and untreated [9]. It has been discovered that secondary injury occurs more frequently than previously assumed [10] and that secondary hypoxia and hypotension are major determinants of outcome [11].

Traumatic brain injury occurs in two stages: the primary injury that occurs at the moment of impact and results from the transfer of kinetic energy to the brain and the secondary injury that is a biochemical and cellular response to the initial trauma [12]. Prognosis depends on the severity of each phase of injury.

3.1 Primary Injury

Primary injury can be divided into two sections: focal and diffuse lesions. Focal brain injury is typically associated with blows to the head that typically produce cerebral contusions and haematomas. Focal injured impact morbidity and mortality based on their location, size, and overall progression. Diffuse axonal injury is caused by inertial forces that are commonly produced by motor vehicle accidents. In clinical practice, diffuse axonal injury and focal brain lesions frequently co-exist [13]. The following are the most occurring types of primary head injuries:

3.11 Skull Fracture

Skull fractures (figure 1) may be classified as linear, depressed or compound. Linear fracture is a closed fracture across the bone lengthwise without the separation of the two edges. If the bone appears to be pressed against the brain, depressed skull fracture has occurred. A linear vault fracture increases the chances of an intracranial haematoma developing [13]. Compound fracture is noted where the fracture is open with splintering of the bone and involvement of the surrounding tissue [14]. Depressed and compound fractures have been found to be most fatal. Skull fracture indicates that a large force has impacted on the patients head. Often, signs of a fracture appears on the opposite side of the head from the point of impact and can sometimes be misjudged as contusions or lacerations to the scalp, due to the swelling, tenderness and bleeding [15]. This occurs because when there is a blow to the head, the brain is bounced within the skull. Therefore, although focal injuries occur at the site of impact, the opposite side is often severely injured too [16].

3. 12 Epidural Haematomas

Epidural haematomas are not that common, being present in < 1% of all head injured patients in <10% of those who are comatose [13]. They occur from collections of blood located between the skull and dura (figure 2). They can cause substantial mass effect if they are left to expand [12]. They are often the result from laceration of the middle meningeal artery cause by fracture and are located in the temporal or tempororparietal region. When a patient develops an epidural haematoma, they suffer from a loss of consciousness followed by a period of lucency and often logic deterioration. Patients usually have a favourable outcome, if condition is attended to quickly [13].

3.13 Subdural Haematomas

Secondary Injury

Secondary brain injury occurs after the initial trauma and is defined as the damage to neurons due to the systemic physiological responses [6]. During the first 24hr after head injury, CBF is less than half of that of normal individuals and may approach the ischemic threshold. The reduction of CBF following trauma together with vulnerability of the traumatized brain causes the rise in ICP levels. In patients who have died from head injury, posttraumatic ischemia lesions have been reported in up to 80% of patients at autopsy [7]. Further details will be discussed within the project later.

Intracranial pressure (ICP) and Cerebral Perfusion Pressure (CPP)

The cranial vault is a fixed space that contains brain tissue, cerebrospinal fluid (CSF), extra cellular fluid, and blood. These tissues are largely incompressible. After head trauma, the volume within the intracranial compartment increases due to blood and tissue oedema. Initially, small increases in intracranial volume can be accommodated by the movement of blood and CFS out of the vault (a technique called micro dialysis). However, with further expansion of its contents, ICP increases sharply. Cerebral ischemia leads to neuronal injury and cerebral oedema, which further increases ICP, progressing to irreversible neurological damage [6].CBF in humans averages approximately 50mL/100g of brain tissue per minute for a prolonged period of time [6]. CBF is equal to CPP which is defined as the difference between the mean arterial blood pressure (MAP) and the ICP, divided by the cerebral vascular resistance:

CPP is the net pressure of blood flow to the brain. Normal human values should lie between 70 - 100 mm Hg. As CBF is difficult to measure clinically, the CPP is used as an indication to assessing the adequacy of cerebral perfusion. The brain has a system known as autoregulation which maintains an adequate CPP level. In basic terms, CBF remains relatively constant when CPP is between 40 - 140 mm Hg. To lower pressure, blood vessels in the brain dilate allowing more blood to flow, and to increase pressure the reverse occurs. ICP is measured in millimeters of mercury (mmHg) and, at rest, is normally less than 10-15 mmHg [8]. Values of 20mmHg are extremely high and are cause for concern.

Cerebral Blood Flow (CBF)

If CBF is corrected and regulated properly, patients who suffer from head injuries have a more favourable prognosis. Kety and Schmidt [1] made the first determination of CBF using nitrous oxide as a marker. It is still the gold standard technique and could be useful in assessing the changes in CBF in response to different manoeuvres. There are various different studies that show the techniques used in measuring CBF. These will be discussed in detail further in the project.

Management and treatment of TBI

Once the patient has undergone routine check ups, such as stabilizing adequate airway and adequate ventilation, which is known as primary trauma survey, the patient will then need to undergo secondary trauma survey. This consists of a neurological examination which aims to give a reliable, objective way of recording the conscious state of a person, for initial as well as continuing assessment and is based on the Glasgow Coma Scale (GCS), the scale was published in 1974 by Graham Teasdale and Bryan J. Jennett [9]

Once the GCS has been determined physicians have now an indication of the severity of the injury. Techniques and technologies now play the role of identifying the exact damage and supplying knowledge of prognosis.

There have been many new developments over the past recent years in measuring ICP, CBF and CPP. Below are naming but a few, briefly discussing their origin and objective.

Computed Tomography (CT)

Historically, imaging of head injured patient relied on the skull radiographs. With the widespread availability and advancement of head CT scanning, the CT scan has become the disgnostic procedure of choice when evaluationg acute head trauma. CT scanning is recommended in patients considered to be at high risk for intracranial injury. This includes all patients with GCS score of <15. Abnormalities noted on CT imaging associated with intracranial hypertension include subdural heamatomas, subarachnoid hemorrhage (figure 1) and generalized cerebral oedema. It should be noted however, CT scanning does not include significant intracranial hypertension [6].

Transcranial Doppler Ultrasonography (TCD)

TCD has been proposed as a non-invasive method to estimate CPP and ICP in head injured patients [3]. It evaluates cerebral hemodynamics. The middle cerebral artery is the simplest vessel to isonate; in fact, 80% of the cerebral blood flows through it. TCD measures the blood velocity not flow and therefore the CBF is only estimated if vessel diameter is constant, but it seems to reflect properly the changes in CBF. However, its disadvantage is that it is subjective and needs an expert for the job. TCD is also used to access autoregulation. Ursino et al [10], used in addition, analysis of the TCD waveform and concluded that it is possible to discriminate between alterations caused by CBF changes and those caused by CPP changes. There are many other studies conducted showing the relevance of using TCD, such as Lewis et al [11] and Schoser et al, which will be discussed further in the project.

Laser Doppler Flowmetry (LDF)

Laser Doppler Flowmetry is a newuromonitoring technique that tries to continously assess the current status of the microcirculatory flow. It is very useful in measuring CBF. It can provide more direct indication of blood flow. In the last 10-15 years LDF has evolved from a research tool into a widely used clinical instrument [12] This a technique used that measures the flow of blood not velocity. This method has proven to be a good technique to used when evaluation CBF however, its downfall is that it can only assess changes in CBF in a small volume of tissue, as the probe shifts easily. The measure in not quantitative , and artifacts could be produced by a large number of external derangements [3]

Near Infared Spectroscopy (NIRS)

NIRS is a non-invasive technique used for measuring oxygenation of tissue within the body. It can applied to various parts of the body. It enables us to measure oxygen saturation and other heamodynamic variables with brain tissue. When a patient is being cared for on the ITU, after suffering head injuries, it is desirable to be able to continously measure the oxygenation of the brain tissue. Visible light does not penetrate biological tissue to a thickness greater than approximately 1cn because it is attentuated by absorption abd scattering within the tissue. The most abundant component of tissue is water which has a strong absorption at wavelengths >900nm. This leaves us with a window of wavelengths in the near infrered region between 650 and 900nm in which photons are able to penetrate far enough to illuminate deeper structures such as the cerebral cortex [13].

The above picture demonstrates a diagram of a cranial NIRS system. A light source placed on the forehead as shown. Near-infrared light penetrates the skin, subcutaneous fat, skull and the underlying brain tissue where it is either absorbed or scattered. A detector placed on the skin surface several cm away detects the reemitted light. NIRS has been a worldly accpected technique as it has great tissue penetration. It also does not discriminate so provides a global assessment of oxygenation in all vascular compartments (arterial, venous and capillary).

Inhalation of tracer gas 133Xenon

An autraumatic technique for measuring regional CBF is a recognized need in modern clinical research. The 133Xe inhalation method, first introduced BY Mallet and Veal has the distinct advantage of being non-invasive and repeatable a number of times. A major drawback of the method, however, Is contamination of the clearance curves by radioactivity from the scalp and other extracerebral sources, which may give rise to significant measuremnt error[14]. 133Xe washout use radioactive tracers which carry an inherent risk to the patient, and requires intravenous and/or intra-arterial access. Using light to measure these quantities is much more desirable from the point of view of safety [13].

All of the above mentioned techniques used in monitoring ICP, CPP and CBF in head injured patients have had great significance in the prognosis of patients to this day. Several scientists and physicians have carried out extensive work and research to enable better developments of measuring techniques. The full report will consist of the mentioned techniques but will look further into their applications and outcomes. The measure of how benefical they are as well as their pitfalls will also be discussed. The following are also a few technologies that wil be evaluated later in the report.

Conclusion

The prevention, detection, and correction as soon as possible of ischemic brain damage are the main goals in the management of neurologically critically ill patients. For this purpose the continuous assessment of ICP, CPP and CBF are imperative. The most important conclusion is that these devices do not work on their own. It is fundamental that the physician achieve complete knowledge about what is goin on, to properly interpret the data collected and thus to order the correct prognosis. Incorrect interepretation can lead to extreme events. Inadequate prognosis may be given. Without these premises, the neuromonitoring techniques do not work and even could be harmful.

References

Jugular Venous Oximetry

When the arterial oxyhaemoglobin saturation, haemoglobin concentration, and haemoglobin dissociation curve remain constant, the continuous fibreoptic monitoring of jugular oxygen saturation (SjO2) is the result of the difference between cerebral metabolic rate of oxygen *. Measuring CBF has proven difficult; therefore the measure of SjO2 offers an indirect method. In layman's terms, a low SjO2 indicates hypopefusion and elevated SjO2 indicates hyperaemia *. Jugular venous oximetry is the most established method of estimating global cerebral oxygenation and metabolism *. This technique is widely used as it is so easy to place, and when it works is extremely useful *. It has many erroneous readings; however, it is unclear which side must be monitored. As stated previously, measuring SjO2 is an indirect measurement of CBF without being able to detect focal alterations in CBF *. Nevertheless, the use of jugular venous oximetry is accepted worldwide in the management of the neurologically critically ill patients, to optimise therapy and outcome prediction *. Normal SjO2 ranges between 55% and 85%. Cerebral hypoperfusion occurs if levels fall below 55%. The supply of oxygen is considerably lower than the demand. An increase of levels above 85% suggests relative hyperaemia. With it being a global hemispheric measurement, it still does have limitations, such that, regional ischemia cannot be detected *. Chierega et al made this evident, where jugular bulb oximetry without intracranial pressure monitoring was suboptimal for managing a patient with subarachnoid haemorrhage and raise intracranial pressure *. However, while a normal SjO2 does not rule out regional ischemia, a low SjO2 indicates that there is an increase in oxygen extraction or a reduction in oxygen delivery which may be an early warning sign of ischemia *. Cruz conducted a study to assess the benefits of this technique *. Cruz compared the two different groups of neurotrauma patients. A group of 178 patients were monitored on just their SjO2 levels and the calculation of cerebral extraction of oxygen. The other group, of 175 patients, were managed with only the control of CPP and ICP. The groups were similar in GCS score, surgical interventions, age, hypotension and papillary reactivity. The results showed that the first group had a better GCS score after 6 months than the second group *. With the results given through Cruz's study Robertson et al designed a prospective randomized clinical trail with the purpose of discovering which treatment is better in head injured patients *. There were two groups being tested, the first group, their treatment aimed to control ICP below 20mmHg and CPP over 50mmHg. In the second group the CPP would be over 70mmHg with ICP less than 20mmHg. In each group, SjO2 was monitored, which were similar in demographic and clinical issues. The results were similar in their GCS at 6 months; however, the first group had more cerebral ischemia. The second group had fivefold more cases of adult respiratory distress syndrome. The authors did not test the autoregulation, and there was a big difference in the use of vasopressors and volume, which could be dangerous *. Probably a better approach would be individual management during the ICU stay. With the use of the same group * studies were shown to prove that high SjO2 does not always mean hyperthermia and a good outcome. If there is a low cerebral metabolic rate of oxygen (CMRO2), a high level of SjO2, is associated, in this study, with a wide range of CBF levels, measured with nitrous oxide as a tracer. The results of this study agrees with other previous data * and the authors recommend the use of CMRO2 to properly know the coupling between CBF and brain demands. A case from Japan shows an arteriovenous fistula can alter results *. A study was conducted by Vigue et al where they used all three parameters: ICP, CPP and SjO2 and demonstrated that the autoregulation, and early and proper management, can avoid initial ischemic events, correcting the use of vasopressors, volume and hyperventilation with SjO2 control *. Intermittent sampling allows estimation of arteriovenous oxygen difference and lactate, which will help give an indication of global cerebral oxygenation and metabolism *. Latranico et al tried to answer the question of whether intermittent SjO2 monitoring would be useful *. They found that only 3.4% of the cases, a low SjO2 implied a modification in the treatment, mainly improvement of hypocapnia, or hypovolemia. However, there were studies carried out previous to this which implied more positive results *. In regards to this study, the measurement is not continuous, so probably the authors did not detect all the ischemic episodes *.

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