The Glasgow Coma Scale Health And Social Care Essay

The Glasgow lethargy Scale Health And Social C atomic number 18 EssayThere atomic number 18 three types of heap syndromes related to spinal cord spot. These are the primeval cord syndrome, anterior cord syndrome, and brown-sequard syndrome or the lateral cord syndrome. The substitution cord syndrome is ca apply by reproach or edema in the substitution cord usualy in the cervical area due to hyper character injuries. This dissolvers to push back failing of the upper extremities than the lower extremities. The anterior cord syndrome is caused by disk hernia or compression of the artery that runs along the front of the spinal cord. This causes way out of sensory, way out of incommode and temperature but sensitivity to position and vibrations are preserved. The brown-sequard syndrome or lateral cord syndrome may be a result of discriminating blot in the spine or hemisection of the cord. This causes ipsilateral hemiplegia with loss of touch, pressure and vibration als o contralateral pain and temperature sensation deficits. wrangle how the Glasgow Coma Scale is utilized in determining neurological office.The Glasgow coma scale is used widely in hospitals to give a reliable, target area way of recoding the level of instinct of a tolerant. The GCS has three elements, the center of attention rejoinder, verbal response and motor response. Each has their own grades. For the eye response 4pts for promiscuous spontaneously, 3pts to open to non-verbal command, 2pts on open in response to pain and 1pt to no response. For verbal response 5pts for talking/oriented, 4pts for confused speech/disoriented, 3pts on inappropriate words, 2pts for incomprehensible sounds and 1pt for no response. Last for motor response 6pts for conform commands, 5pts to localizes to pain, 4pts for flexion/ withdrawal from painful stimuli, 3pts to flexion in response to pain, 2pts for extension in response to pain and 1pt to no response. 15pts is the perfect score and 3 as t he lowest score which indicates that the patient is in deep coma. talk about breast feeding interventions related to prevention of injury in the head-injured patient.To prevent injury for patient that has headland injury the patient must be assessed to guarantee adequate oxygenation and that the bladder is non distended. Dressings and casts mast be check for constriction. The side path must be raised and padded to avoid falling. The sock must also be lowered. Reducing environmental stimuli and to stimulate an adequate lighting. smear disturbances during sleep to provide adequate rest for the patient. Medications rouse be accustomed as prescribed to prevent restlessness. For incontinence catheter rear be used. written assignmentIdentify risk performers for spinal cord injury.Spinal cord injury is an injury due to an unexpected accident. In short everyone can have a spinal cord injury. Still thither are some risk factors. One risk factor is if you are busy in active spo rts or into jobs that requires lifting heavy loads. Another risk factor is for the sight who are in the 16-30yrs of age because in these years people are active and many people at these age support is now driving and one of the leading cause of spinal cord injury is vehicular accidents. And if you have bone disorder like osteoporosis, this can cause spinal cord injury.List three clinical features of the patient with neurogenic shock.Neurogenic shock is caused by injury in the central nervous system that causes vasodilation as a result of loss of parallelism between the human and parasympathetic stimulation. This causes low blood pressure (hypotension), descend heart rate (bradycardia), and reduce venous return which gives a dry, speedy skin.Why is autonomic dysreflexia an acute emergency situation?Autonomic dysreflexia is the all over activity of the autonomic nervous system. The nerve impulses that are being pull to the brain are blocked by a lesion in the spinal cord (at t he t-5 level or supra) which causes the brain to change magnitude activity of the sympathetic system that results to a rise in blood pressure. The heart hence sends impulse to the brain that causes the heart to slow down and the blood vessels above the spinal injury to dilate. But the brain cannot send impulse at a lower place the level of injury due to the lesion therefore blood pressure cannot be regulated. This is an acute emergency situation because if not treated immediately this may lead to seizures, stroke and even death.Develop a matrix identifying concussion, contusion, and dish out axonal injury. Identify clinical verbalisms and associated diagnostic testing.DefinitionClinical manifestationDiagnostic testingConcussion wound to the brain that is a result from an impact to the head. Ranges from mild to pure(a) concussionMild concussion middling dazedBrief loss of consciousnessSevere concussionyearner loss of consciousnessLonger recovery timeOther manifestations malady and vomitingBlurred visionConfusionFatigueShort-term store lossNeurological function testsCT scanContusiontraumatic brain injury or bruising of the brain because of sever acceleration-deceleration strong point or blunt traumaLoss of consciousnessLack of motor coordinationMemory problemsCT scanMRIDiffuse axonal injuryThis is a diffuse brain injury cause by gruelling head traumas. As interweave slides over tissue, a shearing injury occurs. This causes the lesions that are responsible for unconsciousness, as well as the vegetative invoke that occurs after a severe head injuryLack of consciousnessNo lucid intervalImmediate comaMRICT scanEEG electroencephalogram dispute the long-term replenishment unavoidably of the spinal cord injured patient. Within a group, ask questions regarding fright for care in the rehabilitative phase.For patients who suffered spinal cord injury rehabilitation is needed to restore as much function to the patient. The patient must understand his conditio n and reduce assistance with activities and let the patient be independent to improve motor function and also to extend the patients self-esteem.Discuss nursing have it offment for the head-injured patient related to nursing applicable nursing diagnoses.Ineffective airway clearanceAssess the respiratory status burst the patency of the airwayEnsure airway clearanceIneffective tissue perfusion ( noetic)Assess the visual, sensory and motor functionsNote for headache, dizziness, altered mental status and personality changesElevate HOB (10 degrees) and proceed head/neck in midline or neutral position to promote circulation and venous drainpipeDecrease intracranial adaptive capabilityMonitor patients neurological racy signs (GCS)Monitor ICPAssess the patients reflexesDecrease environmental stimuliRisk for injury go out safe environmentRaise side railsLower bedWeb outputNURSING MANAGEMENT OF ADULTS WITH SEVERE TRAUMATIC originator INJURYhttp//www.dvbic.org/images/pdfs/AANN08_TBIGuide _2-13-09_update.aspxBase on the get wind that I have read, the neuroscience concord is the one who intervenes to swan and manage intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in patience with traumatic brain injury (TBI). The prevention of complications comm entirely associated with TBI is also involved in the management of care for TBI patients such as deep vein thrombosis (DVT), hyperglycemia, and excessive protein loss.In maintaining or change magnitude of ICP, this study recommended guidelines. First, an uncontrolled intracranial high blood pressure leads to an absence of cerebral perfusion and results in brain death thus, the recommended ICP according to the original Guidelines for the management of Severe head Injury should be at less than 20mmHg (Bullock, Chestnut, Clifton, 1995), as stated in the study. Second, the tiring of cerebrospinal fluid (CSF) -this descends ICP. As stated in the study, according to the encephalon scathe Foundation, Ame rican Association of Neurological Surgeons, the Joint Section on Neurotrauma and Critical Care (2000), the front step to reduce intracranial hypertension is through ventricular drainage. As early as 1960, Lund demonstrated that remotion of CSF via ventriculostomy temporarily decreases ICP (Lund, 1960). Draining as little as 3ml of CSF was found to decrease ICP by 10.1% relative to the baseline value of 10 minutes in 58 patients with severe TBI (Kerr, Weber, Sereika, Wilberger, Marion, 2001). Protocols for CSF diversion range from time- dependent (leave drainage open for 5 minutes, then close), CSF-volume-dependent (drain 5cc then close), to straight drainage (open all the time, closed(a) at intervals to obtain an accurate ICP reading). This is supported by Monroe- Kellie hypothesis stating that a normal ICP can be maintained as one segment in the cranial compartment (brain, blood and CSF) increases as long as there is a corresponding decrease of another function- therefore, d ecrease of one component decreases ICP. Third is not inducing hyperventilation to decrease ICP. Hyperventilation was routinely used to manage severe TBI. Studies done in the 1990s demonstrated the vasoconstriction associated with hyperventilation also resulted in decrease cerebral blood flow (CBF), thus, it is recommended to maintain normocapnia in close patients with severe TBI ( psyche Trauma Foundation et al., 2007). after part is administering sedation- it prevents ICP increases. A study of 17 patients with severe TBI found ICP was fundamentally higher and there was a important decrease in CPP with endotracheal suctioning among patients who were inadequately sedated compared to those patients who were well- sedated with proforol (Gemma et al., 2002) According to the study, a randomized controlled ladder of 42 patients with TBI found the use of Proforol (rather than morphine) resulted in significantly lower ICPs by federal agency- injury day 3, with less use of neuromuscula r blockers, benzodiazepines, and barbiturates and less CSF drainage was required ( Kelly et al., 1999). Fifth is administration of Mannitol is effective in decreasing ICP. Guidelines for Management of Severe TBI, 3rd Edition states, mannitol is effectice for control of raised ICP at doses of 0.25 gms/kg to 1.0 gm/kg body weight (Brain Trauma Foundation et al., 2007). The diuretic effect of mannitol can cause increase Na+ and serum osmolarity levels, this should be monitored at regular intervals. Mannitol is infused via IV bolus through a filter. Mannitol 20% contains 20g of mannitol in 100cc. 80% of 100g dose appears in the urine within 3 hrs. of infusion. Sixth is to name head of bed (HOB) 30 degrees to maintain or decrease ICP- this is image to promote intracranial venous return and increase CSF drainage from the head, resulting in decreased ICP (Fan, 2004). Four controlled studies with sample sizes ranging from 5- 38 patients with severe TBI found significant decreases in ICP w ith HOB elevations of 30 degrees (Moraine, Berr, and Mlot, 2000 Ng, Lim, Wong, 2004 Schulz- Subner Thiex, 2006 Winkleman, 2000). Seventh is removing or easiness rigid cervical collars- according to the study, it may decrease ICP. These collars may back up back venous blood flow and cause pain and discomfort, elevating ICP. 8 is administering intensive insulin therapy- it may reduce ICP. Hyperglycemia is common in severe TBI and has a negative effect on outcome. A study was conducted with a result of lower mean and minimal ICPs to those treated with intensive insulin therapy to maintain glucose levels lower than 110 mg/dl than in subjects treated with insulin only when their glucose levels exceeded 220 mg/dl. The ninth is maintenance of normothermia- it may prevent ICP increases. Hyperthermia is predominant in the TBI population, as high as 68% within 72 hours of injury (Rumana, Gopinath, Uzura, Valadka, Robertson, 1998). There have been no long- term outcome studies in the eff ect of normothermia in TBI, but a study found an increase in brain temperature was associated with significant increase in ICP as febrility ebbed, there was significant decrease in ICP.In controversial handlings for unconquerable intracranial hypertension, first is the inducing of moderate hypothermia- it may decrease ICP in refractory intracranial hypertension. There are multiple human studies that have demonstrated decreased ICP with the induction of moderate hypothermia (33-36 degrees Celsius) in patients with severe TBI (Clifton, miller et al., 2001 Marion, Obrist, carlier, Penrod, Darby, 1993 Polderman, Tjong Tjin, Peerdeman, Vandertop Girbes 2002 Tokutomi, Miyagi, Morimoto, karukay, Shigemori, 2004 Tokutomi et al., 2003). Second is admistering hypertonic saline. Third is the administration of high- dose barbiturates- are intellection to suppress cerebral metabolism, reducing cerebral metabolic demand and cerebral blood volume.In maintaining adequate CPP or increasing CP P, first is maintaining CP b/w 50- 70mmHg- optimized cerebral perfusion (Brain Trauma Foundation et al., 2007). Second is administering norepinephrine, it may maintain adequate CPP or increase CPP. Third is elevating HOB 30 degrees- not only it increases venous drainage from head, it also can decrease perfusion. Fourth is CSF drainage- the decreasing volume of CSF decreases total intracranial volume.In preventing DVT, pharmacologic treatment may be safe for DVT prophylaxis. Agency for healthcare Research and property recommends use of prophylaxis to prevent venous thromboembolism for at- risk patients.In adequate nutrition, first initiating nutrition within 72 hours of injury- according to the study, it may improve outcomes. It is recommended that patients be fed so that full caloric requirements are met by get off injury day 7 (Brain Trauma Foundation et al., 2007). Second is providing continuous intragastric feeding- it may improve tolerance. According to the study, continuous f eeding was better tolerated and achieved 75% of nutritional goals faster than bolus feeding in 152 consecutive patients admitted to neurosurgical intensive care units (20% of whom had sustained severe TBI Rhoney, Parker, Formean, yap, Coplin, 2002).In preventing seizures, administering antiepileptic drugs decreases incidence of early posttraumatic seizures. Guidelines for the Management of Severe TBI, 3rd Edition recommends the use of anticonvulsants to decrease the incidence of post traumatic seizure within the fisrt 7 days of injury when the brain is particularly vulnerable to secondary injury- involves multiple metabolic mechanisms that result from flutter of blood flow and oxygen to undamaged cells, producing anaerobic metabolism, inadequate synthesis of ATP, or cellular acidosis. Then continuous EEG monitoring has been used to identify a 20% seizure incidence with 50% of patients identify as non-convulsive (Vespa Nuwer, 2000)Reference Nursing Management of Adults with Sever e Traumatic Brain Injury, AANN Clinical Practice Guidelines Series