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The Glasgow Coma Scale Health And Social Care Essay

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Published: Mon, 5 Dec 2016

There are three types of cord syndromes related to spinal cord injury. These are the central cord syndrome, anterior cord syndrome, and brown-sequard syndrome or the lateral cord syndrome. The central cord syndrome is caused by injury or edema in the central cord usualy in the cervical area due to hyperextension injuries. This results to motor weakness of the upper extremities than the lower extremities. The anterior cord syndrome is caused by disk herniation or compression of the artery that runs along the front of the spinal cord. This causes loss of sensory, loss of pain and temperature but sensitivity to position and vibrations are preserved. The brown-sequard syndrome or lateral cord syndrome may be a result of penetrating injury in the spine or hemisection of the cord. This causes ipsilateral hemiplegia with loss of touch, pressure and vibration also contralateral pain and temperature sensation deficits.

Discuss how the Glasgow Coma Scale is utilized in determining neurological status.

The Glasgow coma scale is used widely in hospitals to give a reliable, objective way of recoding the level of consciousness of a patient. The GCS has three elements, the eye response, verbal response and motor response. Each has their own grades. For the eye response 4pts for open 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 obey 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 the lowest score which indicates that the patient is in deep coma.

Discuss nursing interventions related to prevention of injury in the brain-injured patient.

To prevent injury for patient that has brain injury the patient must be assessed to ensure adequate oxygenation and that the bladder is not distended. Dressings and casts mast be check for constriction. The side rails must be raised and padded to avoid falling. The bed must also be lowered. Reducing environmental stimuli and to have an adequate lighting. Minimize disturbances during sleep to provide adequate rest for the patient. Medications can be given as prescribed to prevent restlessness. For incontinence catheter can be used.

Written assignment

Identify risk factors 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 there are some risk factors. One risk factor is if you are engage in active sports or into jobs that requires lifting heavy loads. Another risk factor is for the people who are in the 16-30yrs of age because in these years people are active and many people at these age bracket 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 balance between the sympathetic and parasympathetic stimulation. This causes low blood pressure (hypotension), decrease heart rate (bradycardia), and reduce venous return which gives a dry, warm skin.

Why is autonomic dysreflexia an acute emergency situation?

Autonomic dysreflexia is the over activity of the autonomic nervous system. The nerve impulses that are being send to the brain are blocked by a lesion in the spinal cord (at the t-5 level or above) which causes the brain to increase activity of the sympathetic system that results to a rise in blood pressure. The heart then 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 below 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 diffuse axonal injury. Identify clinical manifestations and associated diagnostic testing.

Definition

Clinical manifestation

Diagnostic testing

Concussion

Injury to the brain that is a result from an impact to the head. Ranges from mild to severe concussion

Mild concussion

Slightly dazed

Brief loss of consciousness

Severe concussion

Longer loss of consciousness

Longer recovery time

Other manifestations

Nausea and vomiting

Blurred vision

Confusion

Fatigue

Short-term memory loss

Neurological function tests

CT scan

Contusion

Traumatic brain injury or bruising of the brain because of sever acceleration-deceleration force or blunt trauma

Loss of consciousness

Lack of motor coordination

Memory problems

CT scan

MRI

Diffuse axonal injury

This is a diffuse brain injury cause by severe head traumas. As tissue slides over tissue, a shearing injury occurs. This causes the lesions that are responsible for unconsciousness, as well as the vegetative state that occurs after a severe head injury

Lack of consciousness

No lucid interval

Immediate coma

MRI

CT scan

EEG electroencephalogram

Discuss the long-term rehabilitation needs of the spinal cord injured patient. Within a group, ask questions regarding nursing 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 condition and reduce assistance with activities and let the patient be independent to improve motor function and also to increase the patients’ self-esteem.

Discuss nursing management for the head-injured patient related to nursing applicable nursing diagnoses.

Ineffective airway clearance

Assess the respiratory status

Check the patency of the airway

Ensure airway clearance

Ineffective tissue perfusion (cerebral)

Assess the visual, sensory and motor functions

Note for headache, dizziness, altered mental status and personality changes

Elevate HOB (10 degrees) and maintain head/neck in midline or neutral position to promote circulation and venous drainage

Decrease intracranial adaptive capability

Monitor patients neurological vital signs (GCS)

Monitor ICP

Assess the patients reflexes

Decrease environmental stimuli

Risk for injury

Provide safe environment

Raise side rails

Lower bed

Web output

NURSING MANAGEMENT OF ADULTS WITH SEVERE TRAUMATIC BRAIN INJURY

http://www.dvbic.org/images/pdfs/AANN08_TBIGuide_2-13-09_update.aspx

Base on the study that I have read, the neuroscience nurse is the one who intervenes to maintain and manage intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in patience with traumatic brain injury (TBI). The prevention of complications commonly 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 decreasing of ICP, this study recommended guidelines. First, an uncontrolled intracranial hypertension 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 draining of cerebrospinal fluid (CSF) -this decreases ICP. As stated in the study, according to the Brain Trauma Foundation, American Association of Neurological Surgeons, & the Joint Section on Neurotrauma and Critical Care (2000), the first step to reduce intracranial hypertension is through ventricular drainage. As early as 1960, Lund demonstrated that removal 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 continuous drainage (open all the time, closed 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 component in the cranial compartment (brain, blood and CSF) increases as long as there is a corresponding decrease of another component- therefore, decrease 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 most patients with severe TBI (Brain Trauma Foundation et al., 2007). Fourth is administering sedation- it prevents ICP increases. A study of 17 patients with severe TBI found ICP was significantly higher and there was a significant 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 trial of 42 patients with TBI found the use of Proforol (rather than morphine) resulted in significantly lower ICPs by post- injury day 3, with less use of neuromuscular 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 elevate head of bed (HOB) 30 degrees to maintain or decrease ICP- this is thought 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 with HOB elevations of 30 degrees (Moraine, Berré, and Mélot, 2000; Ng, Lim, & Wong, 2004; Schulz- Subner & Thiex, 2006; Winkleman, 2000). Seventh is removing or loosening rigid cervical collars- according to the study, it may decrease ICP. These collars may hold back venous blood flow and cause pain and discomfort, elevating ICP. Eight 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 prevalent 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 effect of normothermia in TBI, but a study found an increase in brain temperature was associated with significant increase in ICP; as fever ebbed, there was significant decrease in ICP.

In controversial treatments for refractory 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 thought to suppress cerebral metabolism, reducing cerebral metabolic demand and cerebral blood volume.

In maintaining adequate CPP or increasing CPP, 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 Quality 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 post injury day 7 (Brain Trauma Foundation et al., 2007). Second is providing continuous intragastric feeding- it may improve tolerance. According to the study, continuous feeding 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 interruption 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 identified as non-convulsive (Vespa & Nuwer, 2000)

Reference: Nursing Management of Adults with Severe Traumatic Brain Injury, AANN Clinical Practice Guidelines Series


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