Brain in MRI and Red Blood Cells - Essay Example

?Brain in MRI Question Review the relevant properties of blood and the changing MRI appearance of hemorrhage in the brain over time Blood is a liquid body tissue made up of different types of formed cells that are suspended in an aqueous complex body fluid known as the plasma, which contains various spectrums of organic molecules. Blood is composed of Red Cells also known as erythrocytes, White Cells also known as leucocytes as well as Platelets which are also referred to as thrombocytes (Mazumdar, 1992 p 121). Plasma constitutes of organic substances and electrolytes which are mainly proteins. The White Cells carry out important functions that entail fighting diseases. They are however relatively fewer in number compared to the Red Cells. Platelets, on the other hand, are numerous in number but they are smaller in size. The small size makes platelets to be considered unimportant contributors to blood flow. Red Cells contain a very flexible membrane enclosing a concentrated solution known as hemoglobin. The Red Cells play a huge role of determining various mechanical properties of blood. Properties of Red Blood Cells make up blood properties since about 95% of blood cells are the red blood cells. A red blood cell is a disc shaped element that is bounded by a membranous tissue made up of proteins, lipids and steroid substances. The most important component of the red blood cell is the hemoglobin, which plays the role of transporting oxygen to various body tissues. Visco-elastic properties of blood have been investigated by various researchers and this was achieved by measuring significant vitro conditions in transient and periodic blood flows. These flows are important in determining properties of blood since blood acts as a shear thinning non- Newtonian fluid and also exhibit thixotropy and visco-elasticity properties (Pedrizzetti and Perktold, 2004 p 54). Blood tissue is identified as a CT that contains a liquid matrix and it plays three major roles in the body system that include transportation of carbon dioxide, oxygen, nutrients, wastes, hormones and heat as well as regulation of the body temperature, pH and content of water in body cells (Mazumdar, 1992 p 34). Blood tissue protects against loss of excessive blood by facilitating blood clotting. It also protects the body against toxins and foreign microbes through the activity of specialized plasma proteins and phagocytic white blood cells. Blood is a free flowing liquid but it is more viscous and denser than water. The red color of blood is imparted by hemoglobin. When hemoglobin gets saturated with oxygen (oxyhemoglobin), it brightens the color of blood but when oxygen is removed (deoxyhemoglobin), the color of blood darkens. This is the reason why partially deoxygenated blood that comes from a vein tends to be darker compared to oxygenated blood that comes from an artery. Red blood cells constitute approximately 45% of the total blood volume. The white blood cells and platelets are smaller in number in the blood as they constitute less than one percent of the total blood cells. Plasma is the fluid portion of the blood and it is sticky and yellowish in color. These components make contributions to the properties of blood and the functions it plays in the body system. Within the body, blood is always a fluid and has turbulent flow that ensures white blood cells, red blood cells, plasma and all blood components are homogenously mixed. When blood is lost from the body through bleeding, physiochemical changes will occur as a result of blood properties causing blood to clot. Blood clotting will prevent excessive loss of blood from the body. The blood clot contains components of microscopic strands of fibrin which is a blood protein. Blood clot prevents excessive blood loss by forming a gel in which blood cells will be entrapped. When the blood clot contracts, it will release an incoagulable fluid known as serum (Geyer and Gomez, 2008 p 178). An anticoagulant can be administered to the blood to maintain its fluid state as well as prevent formation of blood clots. Changing MRI Appearance of Hemorrhage in the Brain over time Hemorrhage usually occurs when blood flows into a part of the brain which is not classified in the normal vascular system (Creasy, 2010 p 55). This situation can occur in the brain in three different part categories which are parenchyma (intra-parenchymal hemorrhage), extra axial spaces surrounding the brain or even the ventricles (intra-ventricular hemorrhage). Extra axial hemorrhage can occur in three different spaces surrounding the brain which are the subdural space, subarachnoid space and the epidural space. Hemorrhage that occurs in the brain parenchyma has been identified to be as a result of bleeding from a vascular lesion, for instance, a malignancy, malformation or hypertension. This hemorrhage can also result from a closed head injury as this will cause internal bleeding and blood may flow into a space in the brain that is not within the normal vascular system. MRI appearance of hemorrhage in the brain is very complex and it tends to vary from time to time. Differences are also recorded depending on each pulse sequence. Appearance of images of hemorrhage on MR scanning may change on each pulse sequence over the first weeks of the occurrence of the condition. This has therefore made it difficult to state the specific images of hemorrhage without first addressing the various changes that are recorded in hemorrhage as time continues to change on the different pulse sequences. MRI appearance of hemorrhages over time greatly depends on the natural evolution of blood tissues and hemoglobin degradation within the affected body tissues and also in the strength of the magnetic field. The various stages involved in conversion of oxyhemoglobin to deoxyhemoglobin, followed by conversion of deoxyhemoglobin to methemoglobin, which is first intracellular and changes to extracellular since the erythrocytes have disappeared, and the final conversion leads to the formation of hemosiderin. These processes of conversion take place as part of a continuum that evolves over long time periods as it may take weeks to months. Hyper acute hemorrhage that has occurred in just a few hours is isointense within the brain parenchyma according to the TI-weighted spin-echo (SE) images. It is however hyperintense according to the T2- weighted SE images (Geyer and Gomez, 2008 p 169). After a few hours of the occurrence of the hemorrhage, the oxyhemoglobin will be converted into deoxyhemoglobin and this will take place within the hematoma. The latter tends to shorten T2 and this will be the reason for a low signal on T2 weighted images. After a period of about two to three days, deoxyhemoglobin will be converted methemoglobin, which is a paramagnetic substances that tends to shorten both T1 and T2. This therefore results into hematomas displaying high signals in both T1 and T2 weighted images. Over the next months, the methemoglobin that had been formed will be slowly broken down into hemichromes which produces mild T1 shortening. At this stage where the hemorrhage has existed for a few months, hematomas will have a higher signal on T2 weighted images compared to T1 weighted images. Within the periphery of hematomas, macrophage activity will lead to the degradation of methemoglobin. This effect can be clearly observed within the first two weeks of occurrence of hemorrhage. The length of time within which hemosiderin remains in the area of a hematoma can therefore be easily identified over a patient’s lifetime. MRI of Hemorrhage T1 T2 T2* Figure 1: MRI of Hemorrhage MRI appearance of hemorrhages varies within the brain parenchyma according to T1 and T2 weighted SE imaging as seen in figure 1. Appearance of the hematomas greatly depends on the type of image. Magnetic properties also tend to change over time and this allows for approximate dating (Geyer and Gomez, 2008 p 170). Question 2: Hemorrhage can occur in both intra- axial and extra-axial locations. Discuss these various sites and the anatomical structures that are used to define these locations. Intra- axial hemorrhage occurs when blood flows into the brain. In most cases, it occurs due to intra-parenchymal hemorrhage or existence of blood in the ventricular system, which is a condition known as intra-ventricular hemorrhage (Kaufman, 1998 p 256). Hemorrhagic contusions in intra- axial hemorrhage are usually in direct contact with the skull and also exhibit a shear strain deformation. Lesions are commonly located along lateral, inferior and anterior frontal and the temporal lobes. This location is seen to be above bony prominences such as petrous pyramid, orbital roof as well as the aphenoid wing. The main causes of intra-axial hemorrhages can be classified as traumatic or spontaneous. Traumatic causes may include penetrating injuries that may be as a result of gun wounds and blunt injuries which may be caused by motor vehicle collision (MVC) assault. The hemorrhagic contusions may occur due to blunt trauma especially in the cortex or white matter in the brain. Contusions are mainly located at the site where there has been the greatest impact of brain on bone including the inferior/ anterior frontal lobes as well as the temporal lobes (Creasy, 2010 p 60). Intra axial hemorrhages may be classified into intra-parenchymal or intra-ventricular hemorrhages. Intra-parenchymal hemorrhage can be defined based on the intra axial hemorrhage since it is characterized with bleeding form the brain tissue itself. Spectrums of diseases vary as they consist of large hematomas as well as small contusions. These variations therefore make intra-parenchymal hemorrhage to be associated with severe outcomes since it is more difficult to treat compared to other forms of hemorrhages. (Lucey and Soto, 2009 p 6). Figure 2: Hemorrhagic contusions of Intra axial hemorrhage Extra- axial Hemorrhage Subdural Epidural Subarachnoid Figure 3: Types of extra- axial hemorrhages. Extra- axial hemorrhage occurs when blood flows into the skull but it does not get into the brain. The most common types of extra- axial hemorrhage include epidural hematoma which is a condition in which there is bleeding between the skull and the Dura matter, subdural hematoma as well as subarachnoid hemorrhage where bleeding occurs between the pia matter and arachnoid matter (Schulthess and Zollikofer, 2008 p 68). Subarachnoid hemorrhage is seen to primarily occur due to a disruption of bridging meningeal vessels. It may also occur from an extension of intra-ventricular, subdural as well as intracerebellar hemorrhage. Large subarachnoid hemorrhages may be viewed as fluid over the cerebral convexities or as wide echogenic sylvian fissure. Outcomes of subarachnoid hemorrhages (SAH) are very severe in patients who have head trauma and traumatic SAH. MRI has been identified to be less useful in the detection of subarachnoid hemorrhage. A high tension of oxygen in the subarachnoid space tends to slow down the process of transformation of oxyhemoglobin to paramagnetic products which include methemoglobin and oxyhemoglobin. (Schulthess and Zollikofer, 2008 p 78). Subdural hematoma will occur when blood builds up between the Dura matter and the arachnoid matter. It may develop gradually over a period of time or may even occur suddenly depending on the blood vessels that have ruptured during an injury. These hematomas usually spread over large areas compared to areas covered by epidural and subarachnoid hemorrhages because there is a large space between the arachnoid matter and Dura matter therefore giving room for a lot of blood to flow before the excessive pressure causes brain damage. An epidural hematoma will occur when excessive blood flows between the Dura matter and the skull. These hematomas usually occur rapidly and may spread to maximum area within the first few minutes when an injury occurs. The epidural hematoma records a high chance of re-bleeding and this will therefore increase the size of the hematoma (Carabasi and Jarell, 2007 p 302). Physical trauma to the head has been identified as the most common cause of subarachnoid hemorrhage and epidural hematoma. The trauma may result to intense force on the brain causing blood vessels to rapture and bleed excessively (Berger and Bernstein, 2007 p 289). Subdural hematomas are classified based on the rate with which an injury is sustained. An acute subdural hematoma will occur in circumstances high speed acceleration or deceleration injuries are recorded. The subdural hematoma is the most severe form of extra axial hemorrhage since bleeding tends to increase at a high rate and the force that results into the high rate bleeding also creates other injuries. A chronic subdural hematoma usually takes a few days or weeks to develop since they are caused by minor head injuries. A physician should be careful when scanning to ensure he does not miss the important signs and symptoms of each hematoma. This will ensure that the physician administers the proper tests and also conducts appropriate follow-up exams when treating hemorrhages. Preliminary tests that can be carried out to determine the type of hemorrhage in a patient include a MRI, CT scan, complete blood count as well as platelet count (Egan and Quass, 2010 p 321). Surgery may also have to be done so as to remove the ruptured vessel that caused the bleeding. A large opening in the skull may be necessary when the hematoma has to be removed. The process is known as craniotomy (Creasy, 2010 p 402). A patient may have to take anticonvulsants as this will assist to effectively control seizures. Corticosteroids are also helpful as they reduce swelling. Hemorrhages and hematomas in intra axial and extra axial locations usually have a high risk of causing impairment as well as death. Treatment of hemorrhages should be effective to eliminate the effects that may arise if neglected. Localization of hemorrhage to either the intra axial or extra axial space is important as it will assist in assessing etiology as well as determining appropriate treatment. It is important to identify the exact location of blood in extra axial location, that is, whether it is subdural or epidural. In the case of intra axial hemorrhage it has to be identified whether blood originated from parenchyma or ventricular system. Question 3: Discuss the use of Tissue Plasminogen Activator (t-PA) in the treatment of ischemic stroke Tissue Plasminogen Activator (tPA) is a protein found in endothelial cells and it takes part in breaking down of clots of blood. This protein acts as a catalyst as it speeds up the rate of conversion of plasminogen into plasmin, which is an enzyme that breakdown blood clots that have been formed by the platelets to prevent excessive loss of blood from the human body (Lew and Zivin, 2008 p 15). This function of breaking down the clotting system has made it possible for tissue plasminogen activator to be used in clinical medicine in the treatment of ischemic stroke. The most frequent causes of ischemic stroke include arterial emboli, surgical complications, endovascular procedures or arterial thrombosis. Therapy applied in the treatment of acute ischemic stroke has to be administered effectively to avoid incidences of severe intracerebral hemorrhage from occurring. Various pilot studies and double- blind trial of the recombinant tissue plasminogen activator indicated that treatment of ischemic stroke using t-PA would be most effective when the drug was administered within three hours of the occurrence of the stroke. A trial was carried out by the National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group to identify the effectiveness of using t-PA in the treatment of ischemic stroke (New England Journal of Medicine, 1995 p 1586). Patients who had strokes caused by blood clots were enrolled to take part in the trial. In the first part of the trial, a total of 291 patients were enrolled. The main aim of this part of the trial was to identify the clinical activity of t-PA as it had been indicated in base line values in the scale of National Institutes of Health Stroke. This part also determined effectiveness of administering the drug within 24 hours of occurrence of the ischemic stroke. The second part of the trial mainly focused on assessing the clinical outcome at three months by using a global test statistic. The assessment was carried out based on scores on Glasgow outcome scale, modified ranking scale, NIHSS and Barthel index. Results obtained from the first part of the trial showed a small difference between patients given t-PA and those given placebo in the percentage of patients who recorded neurologic improvements within 24 hours. Benefits were however recorded in the patients who were given t-PA at three months for all the outcome measures. In the second part of the trial, long- term effectiveness of t-PA that had been identified in the first part was confirmed. This trial showed that patients treated using t-PA gained long- term benefits as they were less likely to develop any form of disability at three months on the assessment scales. Mortality rates within the first three months were identified to be 17 percent in patients treated with t-PA and 21 percent in the group of placebo drug. This trial therefore showed that treatment of ischemic stroke using intravenous t-PA within three hours of the occurrence of the stroke led to improved clinical outcomes at three months. (New England Journal of Medicine, 1995 p 1587). Modified Ranking Scale Score 0 and 1 2 and 3 4 and 5 6 Placebo 26 25 27 21 t-PA 39 21 23 17 Table 1: Results of the National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group According to the scores on the modified ranking scale, a score of 0 shows a normal condition and a score of 6 shows death. The use of Tissue Plasminogen Activator (tPA) in the Treatment of Ischemic Stroke has been carefully assessed to determine its effectiveness as well as issues that may be associated with the drug. Table 1 indicates the scores of the results obtained in the trial carried out by the National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group and they are indicated on a modified ranking scale. According to a modified ranking scale, patients will be rated on different scales depending on their reactions and how they respond to a drug. The ratings range from a 0 which indicates an entirely normal state through varying degrees of conditions to a 6 which indicates death. The table shows that 26 percent of patients treated using placebo drug were rated on the 0 to 1 scale 3 months after the stroke had occurred. The percentage however increased to 39 percent in patients who had been treated using t-PA. This indicates that t-PA is an effective drug as it reduces the chances of patients developing neurological abnormalities as a result of stroke. The trial provided an overall probability that treatment using t-PA was effective. An analysis of the data also shows that majority of the patients with ischemic stroke treated with tissue plasminogen activator will either be improved by the treatment or may completely recover. (New England Journal of Medicine, 1995 p 1588). Many controversies have however developed regarding the use tissue plasminogen activator in treatment of ischemic stroke. Although research proved that t-PA is an effective drug and that neurologists and physicians believe it is an effective therapy, only a small number of patients receive the drug. A survey was also carried out that revealed use of t-PA for patients suffering from ischemic stroke had been restricted as the drug was not believed to be safe because of the high risk of severe effects associated with it and lack of enough efficiency. The effectiveness and potential of tissue plasminogen activator in ischemic stroke had not been comprehended regarding symptomatic intra-cerebral hemorrhage. (Greer, 2007 p 50) Use of Tissue Plasminogen Activator in the treatment of ischemic stroke should be effective so as to eliminate clinical implications. Appropriate treatment that will effectively cure ischemic stroke is necessary and it should also ensure current and future ischemic patients benefit from a high chance of reduced mortality as well as improved quality of life. Appropriate use of tissue plasminogen activator entails proper legal implications. Number of individuals suffering from stroke continues to increase. Physicians should therefore understand their roles and ensure they provide the right information regarding the benefits and risks associated with use of t-PA as an informed consent issue. The use of t-PA will raise concerns of malpractice if it is not provided under the recommended circumstances. Provision of appropriate information should be of great concern to physicians especially due to existing limited use of t-PA for ischemic stroke patients. The use of tissue plasminogen activator for treatment of ischemic stroke is effective and has also been accepted by most physicians and neurologists. The limited number of patients who are eligible to receive the drug has reduced the number of patients who are obtaining the clinical benefits of the drug. Adequate information provided by physicians and effectiveness of t-PA will ensure effective treatment will be available as the population continues to grow old and presentation of ischemic strokes becomes more common. (Greer, 2007 p 54). Bibliography Berger, M. and Bernstein, M. Neuro-oncology: The Essentials. Thieme: NY. 2007. Carabasi, A. R. and Jarell, B. E. NMS Surgery: National Medical Series for Independent Study. Lippincott Williams & Wilkins: MD. 2007. Creasy, J. L. Dating Neurological Injury: A Forensic Guide for Radiologists, Other Expert Medical Witnesses and Attorneys. Springer: London. 2010. Egan, D. and Quaas, J. Essential Emergency Trauma. Lippincott Williams & Wilkins: PA. 2010. Field, A. S. Introduction to Neuro-imaging- BRAIN. 2007. Viewed 23 August, 2012 from https://www.radiology.wisc.edu/education/med_students/neuroradiology/Neurorad-2_Brain.pdf Geyer, D. J. and Gomez, C. R. Stroke: A Practical Approach. Lippincott Williams & Wilkins: PA. 2008. Greer, D. M. Acute Ischemic Stroke: An Evidence-based Approach. John Wiley & Sons: New York. 2007. Kaufman, H. Cerebrospinal Fluid Collections. Thieme: NY. 1998. Lew, R, Liang, A. B. and Zivin, A. J. Review of Tissue Plasminogen Activator, Ischemic Stroke, and Potential Legal Issues. 2008. Viewed 23 August, 2012 from http://anesthesia.ucsd.edu/research/faculty-research/Documents/LiangLewZivinArchNeur.pdf Lucey, B. and Soto, A. J. Emergency Radiology E-Book: The Requisites in Radiology. Elsevier Health Sciences: Philadelphia, PA. 2009. Mazumdar, J. Biofluid Mechanics. World Scientific: NJ. 1992. New England Journal of Medicine. (1995). Tissue Plasminogen Activator for Acute Ischemic Stroke. New England Journal of Medicine. 333:1581-1588 Pedrizzetti, G. and Perktold, K. (2004). Cardiovascular Fluid Mechanics. Birkhauser: MI. Schulthess, G. K. and Zollikofer, C. L. (2008). Diseases of the Brain, Head & Neck, Spine: Diagnostic Imaging and Interventional Techniques. Springer: NY. Read More

 

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