Principles in the Treatment of Brain Injury - Assignment Example

rtfоliо Аssignmеnt Name Course Lecturer Date Table of Contents Table of Contents 2 1. What are the main principles in the treatment of brain injury secondary to stroke or trauma? 3 What impact does hyperglycaemia have on outcome? 4 2. Explain the mechanisms behind haemodialysis and peritoneal dialysis treatment, 5 When they are indicated 7 The dietary restrictions, if any, imposed on the patient undergoing them? 7 3. Explain the Frank-Starling and Laplace laws in relation to the heart. 7 How do these laws explain the underlying pathology of heart failure? 8 4. Discuss what the oxygen-hemoglobin curve represents, 9 Why it has a sigmoid shape, 10 What a leftward or rightward shift of the curve signifies 10 Factors that induce such shifts 11 References 14 1. What are the main principles in the treatment of brain injury secondary to stroke or trauma? Brain injury may be traumatic, whereby an external force injures the brain or stroke, which is a rapid loss of the functioning of brains due to disturbance of blood supply in the brain. In case of traumatic brain injury it might be mild or severe, closed or penetrating or it may over widespread area or specific location. It may also include other structures such as skull and scalp. Stroke, on the other hand, is caused by blockage or a hemorrhage. The affected areas of brains fail in functioning leading to inability to understand and formulate speech, move limbs or see on one side. Brain injury may be mild, moderate and severe as manifested by symptoms. Headaches, memory problems, confusion and nausea are from mild. More pronounced and symptoms that last longer depict a moderate one. Most patients recover, though there might be persistent problems. Severe injury in most cases lead to debilitating and life-changing problems. Physical, behavioral and cognitive disabilities result. Those who fall in coma and minimally responsive state remain dependent. The treatment of brain injury, from both the causes follows the principles of recovery and rehabilitation, management and prevention of further damage (Slemmer, et al, 2008). As Xi, Keep, & Hoff (2006), argues, traumatic head injury treatment follows three main principles including recovery, prevention of further injury and rehabilitation. In acute stage, medical personnel stabilize the patient and the main focus is preventing further injury. This is because there is little that can be done in order to reverse the damage caused. This begins with the initial cardiopulmonary stabilization. Initial resuscitation is critical as it prevent hypotension and hypoxia. This is important because, patients with hypotension are twice in the mortality rate to those without hypotension. Combination of hypotension and hypoxia results in a 2.5 times mortality rate which is greater than when neither of the factors was present. The primary concerns for the patients with head injury are to ensure proper supply of oxygen, control intracranial pressure and maintain adequate blood flow in the cerebral. Rehabilitation is significant for chronic and sub acute stages of recovery. The principle behind treatment of stroke related to brain injury follows the management. With its different forms, Ischemic stroke require a therapy to remove the blockage. This involves the breaking down of the clot or thrombolysis. The clot can be mechanically removed a process known as thrombectomy. Restored blood flow to the brain reduces the number of brain cells that die. Hemorrhagic stroke is detected through neurosurgical evaluation of the cause of bleeding. This requires monitoring the level of consciousness, blood pressure, sugar and oxygenation, keeping them at an optimum level. Rehabilitation enables people with disabling strokes to be treated to return to normal life. They can also regain and re-learn the skills of living. The survivals are also helped to adapt the difficulties, educate family members on supportive roles and prevent secondary complications What impact does hyperglycaemia have on outcome? From Gray, et al, (2009) discussion, hyperglycaemia involves excessive glucose amount circulating in blood plasma. The glucose level is usually higher than 200 mg/dl. Its symptoms in most cases are noticed from 250-300 mg/dl. Sustained higher levels cause blood vessels damage and to organs they supply. Chronic levels of hyperglycaemia lead and accelerate organ damage and thus brain cells which lead to complications. The outcome of control of blood sugar for the first few hours may cause harm in stroke related head injury. Stress-induced hyperglycaemia increases the risk of mortality particularly after stroke. This can be managed through the efforts of neuropsychiatry to control clinical depression and emotional distress. Patients with diabetes mellitus increase the risks of stroke by two to three times. Intensive blood sugar control does not reduce macro vascular complications of stroke. 2. Explain the mechanisms behind haemodialysis and peritoneal dialysis treatment, Haemodialysis achieve the removal of waste products including urea, free water and creatinine from the blood if kidneys are in renal failure. The other renal replacement therapy involves peritoneal dialysis (PD), which is usually for the treatment of patients who have severe chronic kidney failure. The mechanism of the two is meant for life-supporting treatments to patients with renal failure. They are not meant for cure of chronic kidney disease, they are only life-extending treatments. Both may involve in and outpatient therapy. The fundamental functions of kidney; reabsorption, filtration, and secretion are what haemodialysis and peritoneal dialysis treatment complement. They therefore respond to the basic kidney physiological mechanisms. Urinary excretion rate depend on the rates of filtration, reabsorption and secretion (Vinsonneau, 2006). They principally enable renal ultrafication that is impossible with nephrons failure of function. Cells, large molecules, and proteins filtered out of glomerulus through ultrafiltration goes on. The ultra filtrate that is left resembles plasma which forms the urine. There are two complementary models that explain dialysis that occur across the membrane. In three pore model, membrane filter molecules; water, proteins and electrolytes and exchange across membranes based on the pore size. The distributed model emphasizes the role played by capillaries and the ability of the solution to increase the active capillaries in PD. The process is routine and frequent done at hospital or at home by specialized people, technicians or the patient with skills. The mechanism in both follows the same principle of diffusion of solutes through a semi permeable membrane. This utilizes the counter current flow and thus the dialysate flows in an opposite direction to flow of blood in extracorporeal circuit. The counter-current flow then maintains concentration gradient, at maximum across the membrane increasing the efficiency of dialysis. To achieve fluid removal or ultrafication, hydrostatic pressure of dialysate compartment is altered. Free water and dissolve solutes move across that membrane along the created pressure gradient. Urea, other waste products, phosphate and potassium diffuse into dialysis solution. The concentrations of chloride and sodium are similar to that of normal plasma. According to Jaar, et al. (2005), peritoneum for PD is placed in abdomen and acts as a membrane through which dissolved substances, small molecules and fluids are exchanged regularly from the blood. Fluids pass through a permanent tube and are flushed out automatically or through a regular exchange. The two processes replace the renal physiology which happens through the action of nephron. The nephron is a tubular structure with a single layer lining of specialized cells, surrounded by capillaries. The lining cells majorly reabsorb water and small molecules into the blood, it also enhance secretion of wastes into the urine. When they are indicated The resulting solution is produced as urine with its dissolved minerals from the blood. Ultrafiltrate that resembles plasma has the cells, other large molecules and proteins, filtered out by dialysis through ultrafiltration process. This is then secreted depending o the number of times the dialysis is carried. For peritoneal dialysis a fluid is introduced in the tube and the flushed out every night or regularly daily exchanges. The dietary restrictions, if any, imposed on the patient undergoing them? There is no diet restrictions involved with haemodialysis and peritoneal dialysis. The only side effects that occurs, is brought about by removing much fluid too rapidly and they include fatigue, low blood pressure, headaches, nausea, leg cramps and chest pains. To limit the complications and side effects, fluid intake is limited between treatments. 3. Explain the Frank-Starling and Laplace laws in relation to the heart. As Anwar, et al. (2007) argues, Starling’s law relates to the heart’s stroke volume and the volume of the blood filling it. The stroke volume increases as a response to an increased volume of blood that is filling the heart when all the other factors are constant. When the heart is filled with more blood compared to the usual one, cardiac muscular contraction force increases. This result from an increased load that each muscle fiber experience as extra blood loads enters the heart. Muscle fiber stretching augments the cardiac muscle contraction through an increased affinity of calcium and troponin C which in turn cause more actin-myosin cross-bridges form in the muscle fibres. The force generated by single cardiac muscle is proportional to initial preload. The ventricular wall is stretched by an increased blood volume which causes a more forceful contraction of the cardiac muscle. The mechanism makes its greatest contribution in increasing stroke volume during lower work rates while contractivity has the greatest influence during higher work rates. The phenomenon allows synchronization of cardiac output with venous return, humoral length and arterial blood supply without dependency of external regulation that make alterations. Further, the stroke volume may increase due to greater contractility of cardiac muscle when the body is under exercise; this is independent of end-diastolic volume. As Zhang, et al. (2011) discusses, Laplace laws on the other hand describe the difference of capillary pressure that is sustained across interface due to wall or surface tension. The Law of Laplace in heart mechanism is used in cardiovascular physiology. Arteries are cylindrical, where the heart’s left ventricle is taken as part hemisphere and part cylinder modeled by this law as T= pr/2t where T is the wall tension, p is the pressure, r is the radius and t is wall thickness. For any given pressure, increase in radius requires an increased wall thickness in order to accommodate stable wall tension. Increased pressure also requires an increased thickness in order to maintain wall stable wall tension. This explains the thickening of arteries and that of the left ventricle in order to accommodate the high blood pressure. The left ventricle is thickened and thus become stiffer than the normal thickness thus requiring elevated pressure. When the heart is pressurized with the blood, the wall tension is low and this reduces the need of thick walls to prevent bursting. How do these laws explain the underlying pathology of heart failure? Law of Laplace model the left ventricle to accommodate the wall pressure build by the Frank–Starling mechanism in which the stroke volume increase as more blood fills the heart. Heart failure results from any condition that reduces myocardium or heart muscle efficiency through overloading or damage. Hypertension increases the contraction force which is needed for blood pump. The increase in workload produce changes in the heart. The primary one in relation to these laws is the reduced force of heart contraction brought by overloading of ventricle. The Frank-Starling law states that, increased filling of ventricle results in an increased contraction force, thus cardiac output rises for a healthy heart. This mechanism fails in heart failure. This comes as the ventricle get loaded with blood to a point where the heart muscle contraction is less efficient. This is due to inability to cross-link myosin and actin filaments for an over-stretched muscle (Anwar, et al. 2007). Hypertrophy, increase the physical size of myocardium by terminally differentiated fibers increase in size so as to improve contractility. Decreased ability of the muscle to relax in diastole and increased stiffness causes heart failure. The enlargement of ventricles leads to enlarged spherical shape of the heart and the increase of ventricular volume. An increased peripheral resistance with the greater blood volume strains the heart, accelerating the damage of myocardium. 4. Discuss what the oxygen-hemoglobin curve represents, As Foreman, (2005) discusses, the oxygen-hemoglobin curve involves a graphical representation of the relationship between oxygen available and oxygen amount carried by hemoglobin. It is important for understanding the way blood carries and releases oxygen. The horizontal axis represents the amount of oxygen which is available (PaO2), while the vertical axis represents the amount of oxygen saturated hemoglobin (SaO2). This is determined by hemoglobin’s affinity for O2. When the amount of available oxygen reaches 60 mm Hg, the curve is almost flat. This indicates little change in oxygen saturation in hemoglobin above this point. The PaO2 of 60 and more is thus considered adequate while that less than 60 mm Hg makes the curve steep. Small changes in the amount of available oxygen greatly reduce the oxygen saturation in hemoglobin. The partial pressure of O2 in the blood, where hemoglobin is saturated at 50% is known as P50, which for a healthy person is typically about 26.6 mmHg. P50 is conventional measure of the hemoglobin affinity for O2. The presence of disease and other conditions which change hemoglobin’s oxygen affinity consequently shift the curve to the left and right. At the same time the P50 changes accordingly. Why it has a sigmoid shape, Its sigmoid shape sums up the changes in the level of oxygen available and its saturation in hemoglobin. The partial pressure of O2 (X axis) and O2 saturation (Y axis) has an S-shapes curve. Hemoglobin’s affinity for O2 increases when successive molecules of O2 bind. More molecules bind and O2 partial pressure increases until a maximum amount that can be bound is reached. When the limit is approached, very little binding occurs thus the curve levels out when hemoglobin becomes saturated. It starts slowly when factors are constant, rise and decline. Since there is a continuous changes in pH, temperature, DPG and amount of CO2 available it rises and falls (Inayat, et al. 2006). What a leftward or rightward shift of the curve signifies According to Inayat, et al (2006), oxygen-hemoglobin curve has the left shift at the far left, normal at the centre and right shift at the far right. The curve starts when the pH is at 7.4, temperature at 37 Centigrade and PaCO2 at 40. However, a lower P50 is an indication of leftward shift due to higher affinity. The left shift is occur when the affinity; oxygen attraction to the hemoglobin binding sites changes with variation in pH, CO2 , temperature and metabolic by-product that competes with O2 at binding sites. In a left shift, oxygen has higher affinity for hemoglobin. An increased P50 is an indication which means that larger partial pressure is required to maintain a 50% O2 saturation. This indicates decreased affinity. Factors that induce such shifts There are factors which affect the dissociation curve. The factors are viewed to effect the shifting and reshaping the standard curve of a healthy person. The right shift of the curve is brought about by variation of hydrogen ion concentration (pH) in the blood decrease, the increase shifts to the left a factor known as Bohr Effect. Effects of CO2 are experienced in two ways; it first influences intracellular pH and its accumulation also causes generation of carbamino compounds through chemical reaction. The curve shift to the right due to low level carbamino compounds while higher levels lead to leftward shift. The curve shift rightward when there is high levels of 2, 3- diphosphoglycerate (DGP), and lower levels cause a leftward shift. Temperature has less effect, but generally, hyperthermia causes rightward shift and hypothermia the leftward. In a right shift, also famously referred to as fever or acidosis, oxygen has lower affinity for hemoglobin. More oxygen is released to the cells since the blood releases it more readily, but less oxygen is carried from the lungs. Other factors include the fetal hemoglobin and the effects of Methemoglobinemia. 5. What is negative pressure pulmonary oedema and how does it develop? According to Patel, & Bersten, (2006), negative pressure pulmonary oedema, also commonly known as post obstruction pulmonary oedema is a dangerous condition with potentially fatal multifactorial pathogenesis.It is manifested as an upper airway obstruction. The principal mechanism that is involved involves generation of the large and negative intrathoracic pressure through a forced inspiration that occur against an obstructed air passage. The negative pressure leads to increase of pulmonary capillary transmural pressure and pulmonary vascular volume. This creates a risk from disruption of alveolar-capillary membrane. In NPPE, there is a fine functioning of the lungs and heart. The problem arises when a thing closes off windpipe which is above the lungs and leading to suffocation. In most cases, the normal reaction tries to suck in the air hard. With a blocked-off windpipe, it is not possible to suck in the air. This creates vacuum effect in the air pockets, thus, the fluid is pulled into those air pockets from lung tissue. This commonly happens if someone swallows something down the wrong pipe or is choked by a piece of food. It also occurs if a person has bad throat infection with the windpipe top all swollen. There are two type of the disorder, Type I and Type II. Type I NPPE immediately develops after an onset of an acute air passage obstruction. There are also some other factors that increase Type I of NPPE risks including strangulation, hanging, foreign bodies, upper airways tumors, chocking, epiglottitis , goiter among others. Type II of NPPE on the other hand, develops after a relief of a chronic upper air passage obstruction. This may occur after a relief of upper air passage obstruction which was caused by big tonsils, redundant uvula and hypertrophic adenoids. However the incidence of developing Type I is lower compared to Type II. It is a clinical issue of great relevance in intensive care and anesthesiology. It can be immediate or delayed in its presentation. This necessitates an immediate recognition followed by treatment through perioperative care given to the patient. A significant obstruction of upper airway cause inspiratory efforts meant to overcome that obstruction. This generates a highly negative alveolar and intrapleural pressures. The pressure gradient which is usually high causes the fluid out the pulmonary capillaries to the alveolar and interstitial spaces. Four major mechanisms are involved with NPPE. The disturbances of the homeostasis of pulmonary fluid lead to the increase of interstitial fluid. The hydrostatic pressure in pulmonary capillary bed increases osmotic pressure of the plasma decreases, permeability of membrane increases and the return of the fluid to circulation through lymphatic decreases. Intrathoracisc pressure, between 50 to 100 cm H2O results to an increased return of the blood to the heart via the vein. The left ventricle is exposed to after load stress increasing both the systolic and diastolic ventricular volumes. Due to the interdependence effect of ventricles, there is an excessive pressure on the left ventricle. Low intrapulmonary pressure causes a sudden increase in pulmonary microvascular pressure. This then lead to formation of pulmonary oedema. The hypoxemia resulting from airway obstruction increases the pre and post-capillary pulmonary and vascular resistance. NPPE symptoms develop immediately although in some instances, the onset is delayed for a few hours. This is due to positive pressure which results from forceful expiration against the closed glottis which opposes fluid transudation. Oxidative stress is increased by linear stretch. Its clinical presentation includes a decreased oxygen saturation, pink sputum and chest abnormalities. Acute airway obstruction manifests through retractions, urgent usage of accessory inspiration muscles and facial panic. It then development reveals occasionally wheezes and crackles. Pulmonary eodema cause an impaired oxygen ventilation and diffusion. This leads to severe hypoxemia. References Anwar, A. M., et al. (2007). Left atrial Frank–Starling law assessed by real-time, three-dimensional echocardiographic left atrial volume changes. Heart, 93(11), 1393-1397. Foreman, C. W. (2005). A comparative study of the oxygen dissociation of mammalian hemoglobin. Journal of Cellular and Comparative Physiology, 44(3), 421-429. Gray, C. S., et al, (2009). The prognostic value of stress hyperglycaemia and previously unrecognized diabetes in acute stroke. Diabetic medicine, 4(3), 237-240. Inayat, M. S., et al (2006). Oxygen carriers: a selected review. Transfusion and apheresis science, 34(1), 25-32. Jaar, B. G., et al. (2005). Comparing the risk for death with peritoneal dialysis and hemodialysis in a national cohort of patients with chronic kidney disease.Annals of internal medicine, 143(3), 174. Patel, A. R., & Bersten, A. D. (2006). Pulmonary haemorrhage associated with negative-pressure pulmonary oedema: a case report. Critical Care and Resuscitation, 8(2), 115. Slemmer, J. E., Shacka, J. J., Sweeney, M. I., & Weber, J. T. (2008). Antioxidants and free radical scavengers for the treatment of stroke, traumatic brain injury and aging. Current medicinal chemistry, 15(4), 404-414. Vinsonneau, C., et al. (2006). Continuous venovenous haemodiafiltration versus intermittent haemodialysis for acute renal failure in patients with multiple-organ dysfunction syndrome: a multicentre randomised trial. Lancet, 368(9533), 379-385. Xi, G., Keep, R. F., & Hoff, J. T. (2006). Mechanisms of brain injury after intracerebral haemorrhage. The Lancet Neurology, 5(1), 53-63. Zhang, Z., et al. (2011). Comparison of the Young-Laplace law and finite element based calculation of ventricular wall stress: implications for postinfarct and surgical ventricular remodeling. The Annals of thoracic surgery, 91(1), 150-156. . Read More