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Spinal cord is a bundle of nerve cells and fibers wrapped together extending down from the brain stem to the lower back with in the spinal column. The brain sends electrical signals through the spinal cord, giving instructions to the legs, arms, and other areas of the body. Each portion of the spinal cord is divided into specific neurological segments.
The cervical spinal cord is divided into eight levels. Each level contributes to different functions in the neck and the arms. Sensations from the body are similarly transported from the skin and other areas of the body from the neck, shoulders, and arms up to the brain.
In the thoracic region the nerves of the spinal cord supply muscles of the chest that help in breathing and coughing. This region also contains nerves in the sympathetic nervous system.
The lumbosacral spinal cord and nerve supply legs, pelvis, and bowel and bladder. Sensations from the feet, legs, pelvis, and lower abdomen are transmitted through the lumbosacral nerves and spinal cord to higher segments and eventually the brain.
The spinal cord segments innervate specific motor and sensory regions of the body. The sensory regions are called dermatomes which are a patch of skin that is innervated by a given spinal cord level. Each dermatome has a specific point recommended for testing.
A Spinal Cord Injury (SCI) is defined as damage or trauma to the spinal cord that in turn results in a loss or impaired function resulting in reduced mobility or feeling. Common causes of damage to the spinal cord, are trauma (car/motorcycle accident, gunshot, falls, sports injuries, etc), or disease (Transverse Myelitis, Polio, Spina Bifida, Friedreich's Ataxia, etc.).
This damage disrupts the transmission of neural signals up and down the spinal cord thus compromising the bodily function. These functional impairments include the loss of:
2) Voluntary control over movements and muscles, and/or
3) Reflex function affecting autonomic activity below the point of injury (e.g., breathing, blood pressure regulation, sexual functioning, bowel and bladder control.
The severity of impairment is largely dependent on the type and level of injury (American Spinal Injury Association, 1992). SCI can be divided into two types -complete and incomplete. With a complete injury, all motor and sensory function is lost below the level of the spinal cord lesion. With an incomplete injury, motor and/or sensory function is partially preserved below the injury site. In turn, the level of the SCI determines whether the injury results in tetraplegia or paraplegia.
Tetraplegia reflects damage to the cervical segments of the spinal cord and can result in the impairment or loss of motor and/or sensory function in the arms, trunk, legs and pelvic organs. Paraplegia reflects damage in the thoracic, lumbar or sacral segments of the spinal cord. With paraplegia, arm functioning is spared, but depending on the injury level, impairment or loss of function may occur in the trunk, legs, and pelvic organs. Thus, injuries can be either complete or incomplete and may result in either tetraplegia or paraplegia.
It is also possible for someone to suffer a vertebral fracture without becoming paralyzed. This occurs when there is a fracture or dislocation of the vertebrae, but the spinal cord has not been damaged.
Clinicians have long used a clinical scale to grade severity of neurological loss. First devised at Stokes Manville before World War II and popularized by Frankel in the 1970's, the original scoring approach segregated patients into five categories, i.e. no function (A), sensory only (B), some sensory and motor preservation (C), useful motor function (D), and normal (E). The ASIA Impairment Scale is follows the Frankel scale but differs from the older scale in several important respects. First, instead of no function below the injury level, ASIA A is defined as a person with no motor or sensory function preserved in the sacral segments S4-S5. This definition is clear and unambiguous. ASIA B is essentially identical to Frankel B but adds the requirement of preserved sacral S4-S5 function. It should be noted that ASIA A and B classification depend entirely on a single observation, i.e. the preservation of motor and sensory function of S4-5.
The ASIA scale also added quantitative criteria for C and D. The original Frankel scale asked clinicians to evaluate the usefulness of lower limb function. This not only introduced a subjective element to the scale but ignored arm and hand function in patients with cervical spinal cord injury. To get around this problem, ASIA stipulated that a patient would be an ASIA C if more than half of the muscles evaluated had a grade of less than 3/5. If not, the person was assigned to ASIA D.
ASIA E is of interest because it implies that somebody can have spinal cord injury without having any neurological deficits at least detectable on a neurological examination of this type. Also, the ASIA motor and sensory scoring may not be sensitive to subtle weakness, presence of spasticity, pain, and certain forms of dyesthesia that could be a result of spinal cord injury. Note that such a person would be categorized as an ASIA E.
These changes in the ASIA scale significantly improved the reliability and consistency of the classification. Although it was more logical, the new definition of "complete" injury does not necessarily mean that it better reflects injury severity. For example, is there any situation where a person could be an ASIA B and better off the ASIA C or even ASIA D. The new ASIA A categorization turns out to be more predictive of prognosis than the previous definition where the presence of function several segments below the injury site but the absence of function below a given level could be interpreted as an "incomplete" spinal cord injury.
The ASIA committee also classified incomplete spinal cord injuries into five types. A central cord syndrome is associated with greater loss of upper limb function compared to the lower limbs. The Brown-Sequard syndrome results from a hemisection lesion of the spinal cord. Anterior cord syndrome occurs when the injury affects the anterior spinal tracts, including the vestibulospinal tract. Conus medullaris and cauda equina syndromes occur with damage to the conus or spinal roots of the cord.
The most common complications associated with SCI include infection in which the Urinary tract infections are the leading cause of death. Respiratory infection is also an issue, especially with the higher level injuries due to ineffective use of the accessory muscles of breathing. Autonomic dysreflexia is a true medical emergency; patient and family must be prepared to handle this. It is caused by a sudden increase in blood pressure due to uncontrolled sympathetic nervous system discharge. Another complication is spasticity, which can interfere with transfers and cause falls. Other complications that must be aware of are deep venous thrombosis and orthostatic hypotension.
Pressure sores are one of the most serious complications and are eminently preventable. They are a lifelong, serious complication of spinal cord injury. They have the potential to interfere with physical, psychological, and social well-being and to impact overall quality of life. Although mostly preventable, pressure ulcers frequently disrupt rehabilitation, educational and vocational pursuits, and community reintegration after SCI.
Pressure ulcers are defined as lesions caused by unrelieved pressure resulting in damage of skin and underlying tissue (Bergstrom et al., 1992). They usually occur over bony prominences and are classified as stages by the degree of tissue damage observed.
Individuals with SCI have an altered autonomic nervous system, with the degree of alteration varying with the level of injury. In normal skin when the skin temperature reaches 32-34 degrees centigrade, visible sweating normally takes place over a wide area of the body; this is called reflex sweating (Cosman, 1971). In people with SCI above the T6 level, reflex sweating is lost. Because of the loss of this reflex, individuals with SCI must be cautious since in a hot environment the body cannot cool itself effectively and can become easily overheated.
Spinal cord injury reduces or eliminates skin sensation in dermatomes below the injury site. Pressure impedes blood flow in the skin. Due to muscle atrophy, the normal tissue padding that cushions the butt may be reduced. Absence of sensation, loss of muscle padding, and long periods of pressure can lead to skin breakdown and development of pressure sores or decubiti. Decubiti are potentially life threatening but preventable.
Spinal cord injury impairs skin blood flow responses. Normally, skin responds to pressure, mechanical stimulation, or inflammation with increased blood flow. Loss of this response not only adds to the vulnerability of the skin to pressure sores but reduces the ability of the skin to repair decubiti. Thus, great care must be taken to prevent decubiti by shifting sitting positions and frequent turning. Special seats that distribute the pressure are used in wheelchairs to prevent sacral decubiti. If a decubitus develops, all pressure must be removed or the decubitus can progress to loss of skin and tissues to the point of exposing bone. Common sites for pressure ulcer development include ear, Occiput, humerous, vertebrae, elbow, sacrum thighs, greater trochanter, knees, lower legs, and heels.
Staging is used primarily for the initial assessment of a pressure ulcer. Described and illustrated below are the stages of pressure ulcers (Cuddigan and Frantz, 1998):
An observable pressure-related alteration of intact skin whose indicators as compared to an adjacent or opposite area on the body may include changes in one or more of the following: skin temperature (warmth or coolness), tissue consistency (firm or boggy feeling), and/or sensation (pain, itching). The ulcer appears as a defined area of persistent redness in lightly pigmented skin, whereas in darker skin tones, the ulcer may appear with persistent red, blue, or purple hues.
It comprises of partial-thickness skin loss involving epidermis, dermis, or both. The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater.
It consists of full-thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia. The ulcer presents clinically as a deep crater with or without undermining of adjacent tissue.
It consist of full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (e.g., tendon, joint capsule). Undermining and sinus tracts also may be associated with stage IV pressure ulcers.
Pressure ulcers do not progress from stage I to stage II to stage III and ultimately to stage IV. Rather, they begin deep inside the tissues, close to the bone, and erupt on the surface of the skin. Conversely, healing ulcers do not progress in reverse order of the stages. Muscle tissue is more sensitive than skin to pressure-induced ischemia (Daniel et al., 1981; Nolan and Vistnes, 1980). Clinically the skin may be discolored, but the muscle underneath may be necrotic. When eschar is present, the pressure ulcer cannot be graded accurately until the eschar is removed. Stage I pressure ulcers are not always accurately assessed, especially in people with darkly pigmented skin.
The risk factors for pressure ulcer development consist of extrinsic and intrinsic factors
The extrinsic (external) factors involved in tissue damage should be removed or diminished to prevent injury. Pressure is the primary external cause of ischaemic damage and tissue necrosis. This causes compression and possible capillary occlusion, which if prolonged can cause ischemia. The intensity, duration and individual's tissue tolerance for pressure are the key factors in causing tissue damage. Friction occurs when two surfaces move across each other, which causes removal of superficial layers of skin. It often occurs as a result of poor lifting technique. Shearing occurs when the bones and deep fascia slides downwards towards gravity, while the skin and upper fascia remain in the original position. It mostly occurs when individual's head is raised to fowler's position and he slides downward or is dragged upward.
Maceration of the skin due to incontinence of urine and faeces, wound drainage and sweat can irritate the skin causing pressure damage. Sedatives and hypnotics may make an individual excessively sleepy and thus decreased mobility causing pressure sore. Non-steroidal anti-inflammatory drugs can impair inflammatory response to pressure injury. Inotropes can cause peripheral vasoconstriction and tissue hypoxia. Analgesics may reduce normal stimulus to relieve pressure.
An individual's potential to develop pressure ulcer could be influenced by the intrinsic (internal) factors, which should be considered when performing a risk assessment.
Reduced mobility or immobility: - It is a key factor in the development of pressure sore e.g. Patients with old age, spinal cord injury, long term illness such as osteoarthritis,
CVA, patients who are unconscious or patients after a prolonged operation can cause pressure ulcers easily due to less mobility.
Extremes of age: - An age less than 5 years, neonates and individuals over 65 years of age are at greater risk of developing pressure sore. Neonates and children are in risk due to the immatured skin and disproportionate head to body weight. The factors that place children and neonates at risk of developing pressure sore is same as that of adult but the site of greatest risk and nature of injury may differ, e.g. there is a greater risk of pressure damage for children are head, on ears due to repeated oxygen saturation probe placement, from repeated heel pricks for blood studies etc.
Sensory impairment: - Neurological disease result in reduced sensation and thus result in insensitivity to pain or discomfort, which cause a lacking stimulus to relieve pressure.
Level of consciousness:- A reduced level of consciousness may reduce the awareness of the need to relieve pressure, similar to an anaesthetized person who has no independence to reposition to himself.
Vascular diseases: - This makes individuals more vulnerable to pressure ulcers. E.g.: smoking.
Severe chronic terminal illness: - This places individual at risk because of for example, multi organ failure, poor perfusion and immobility.
Previous history of pressure ulcer:- The individuals with previous ulcers has a greater risk of developing further ulcer than previously pressure ulcer free individuals as Scar tissue from the previous pressure ulcer is weaker and more prone for further damage.
Malnutrition and dehydration: - Both emaciated and obese individuals are vulnerable to develop pressure sore. Loosing too much weight can cause loss of padding over bony points. Dehydration may decrease the elasticity of tissue and thus increase tissue deformity under pressure
Acute illness: - this can also cause developing pressure ulcer. (Rycroft-Malone 2001)
One of the first activities in preventing pressure ulcers is the early identification of patients who are susceptible to developing them. The earliest phase of pressure ulcer development may not show any visible sign of damage. Therefore, it is important that patients at risk are given an immediate prevention plan. Patients are assessed for their risk of developing pressure ulcers based on their clinical presentation. If a patient is considered not at risk on initial assessment, reassessment should be carried out if there is any deterioration or change in condition. All assessments nurses make should be recorded or documented in the patient file.
Risk assessment scales are used as an aide memory as they do not replace clinical judgement. Various scales have been developed to identify individuals at risk of developing pressure sore. Braden, Norton, Knoll, and Waterlow scales are all tools that can be used to assess risk. A recorded assessment scale provides an accurate record of an individual's progress and risk status and it is a key factor for accountability, responsibility, risk management and evaluation. Skin inspection provides essential information for both assessment and prevention.
A regular assessment of most vulnerable areas of the body will enable early detection of pressure damage. The frequency of skin inspection should be determined in response to the changes in patient's condition in relation to recovery and deterioration. Following education, patients who are willing and able, can be encouraged to inspect their own skin. Wheelchair users should be encouraged to use a mirror to inspect the areas that they cannot see easily or get others to inspect them. Special attention to be given for the parts of the body where there are external forces exerted by equipments and clothing. e.g.: Corners of the mouth and tip of the nose if an endo-tracheal tube is present; Tip of the nose if the nasogastric tube is inserted; Sites of Intravenous line; Pulse oximetry; Catheters; Limbs or extremities with non invasive blood pressure cuffs; Elastic clothing; Restraints. While inspecting the skin, look for,
Purplish or bluish patches on dark skinned people
Red patches on light skinned people
Cracks, calluses, wrinkles
Feel for hard areas, warm areas swollen skin over bony points.
General principles of pressure ulcer treatment comprise of,
Relief of pressure
Removal of devitalized tissue
Optimization of wound environment to promote granulation and epithelialisation
Avoidance of maceration, trauma, friction or shearing force
A search for reversible underlying conditions, which may predispose to ulcer development or impede wound healing
Skin should be cleaned as soon as it is soiled with urine, stool, excessive sweat or wound drainage. A mild detergent with warm (rather than hot) water can be used to minimize irritation and drying.
Use pads, briefs etcâ€¦ for a temporary management of incontinence and treat for the cause
Give a bath only when needed for comfort or cleanliness. Avoid using hot water or too much of soap.
Use creams or moisturizer and avoid cold or dry air to prevent dryness of skin.
Do not massage the skin over bony prominence as it may squeeze and damage the tissue under the skin.
Heat lamps and similar devices should not be used to treat pressure ulcers.
Keep the heels off from the bed if sitting on the chair.
Do not make the patient sit continuously for more than 2 hours.
Give good posture & straight position.
Use cushions & arm-support to relieve pressure & to rest hand.
Positioning of individuals who spends more time in a wheel chair should take into account of distribution of weight, postural alignment and support of feet. A good position will help the individual to move more easily and help to prevent new sores.
Patient should be taught, if possible, to shift their weight every 15 min to help to distribute body weight and promote blood flow to the tissue.
Individuals who are acutely at risk of developing pressure sore should restrict chair sitting to less than 2 hours until condition improves as sitting position creates intense pressure on the ischeal tuberosities.
Individuals should be provided with a wrinkle or crease free mattress.
If the patient needed to be lifted or shifted, do it with the draw sheet.
If patient is with endo tracheal tube, assessment should be made everyday for the corner of the mouth and or nose for any ulceration.
Decision about which pressure redistributing device to use should be based on an overall assessment of the patient and not just on the basis of score from risk assessment scale. Patients at 'Very high risk' in developing pressure sore should be placed on pressure redistributing systems. Individuals who are at risk of developing pressure ulcers should be repositioned. It could take into consideration other aspect of an individual's condition like breathing, medical condition and should fit into the overall plan of care like activities such as physiotherapy, meal time etc. Position of the patient should ensure that
Prolonged pressure on bony prominence is minimized,
Bony prominences are kept from direct contact with one another.
Friction and shear damage is diminished.
Individuals who are willing and able should be taught to redistribute their own weight.
A written repositioning schedule agreed with the individual should be established.
All patients who are unable to position themselves should be kept on draw sheets.
Manual handling devices like trapeze and side rails should be provided with individuals who are to reposition with support and to be instructed the correct use to minimize shear and friction damage.
When individual is on bed, Avoid making him lie on the pressure sore.
Use foam pads or pillow to relieve pressure on the bony prominence.
Keep on changing the position at least 2 hourly.
Give a 30-degree side lying position to avoid intense pressure on the greater trochenter and lateral malleolus.
When the individual is on the back, keep his heels off the bed by placing a thin pad or pillow under the legs from mid calf to ankle
Place pillows or small foam pads to keep knees and ankles from touching each other.
Unless indicated, the head of the bed to be placed not more than 30 degree, to avoid shear force.
Urinary catheters, I.V tubing must be fixed in such a way that the tubing will not be in direct contact with the skin to exert continuous pressure.
Change the areas of pressure applied externally on a regular basis, with the non- invasive B.P. cuff, pulse oximetry probe etc
Avoid restraining the individual by tying the finger. If unavoidable, restrain by wrist but make sure that it is adequately loose to avoid compression.
Successful postoperative management depends on two important conditions:
(1) Modifying the factors that contribute to ulcer formation, and
(2) Teaching "pressure consciousness" to the individual.
It is important that no pressure be applied to the site after surgery. The individual should be placed on an air-fluidized bed or on a static support surface when the individual can be maintained on a turn regimen that does not apply pressure to the operative site. If placed on an air-fluidized bed, the head of the bed should not be elevated by more than 15 degrees in people recovering from sacral or ischial repairs since this position increases the risk of shear on the repaired ulcer site. Complications of a prone position include confusion, boredom, airway difficulties, especially in tetraplegics, and ulnar nerve compression. Constipating medications may on occasion be administered and a low-fiber diet may be used to avoid fecal contamination of the surgical site. Prophylactic antibiotics are commonly used in postoperative care, or else antibiotics appropriate to the immediate preoperative wound cultures can be employed.
Timing and degree of postoperative mobilization after reconstruction vary according to the specific protocol in a given center. Bed rest should be maintained postoperatively to allow sufficient time for the development of adequate tensile strength to the healing wound before mobilization. Individuals are taught to shift body weight once they are bearing weight on a flap and inspecting the skin with a long-handled mirror
Education is the mechanism for translating knowledge into effective strategies for prevention and treatment. If education materials and programs are to be effective, they must be relevant to the target audience. Successful patient education motivates the individual to take responsibility. Assessing knowledge and cognitive abilities, planning short and long-term objectives and teaching strategies, using understandable language, and evaluating the extent to which the learning objectives are achieved are the elements of a therapeutic environment in which successful learning can take place. However, even under the most ideal of circumstances, compliance with recommended practices may not be assured.
Rationale of study
Contemporary approaches to pressure ulcer management emphasize prevention through education. However, most pressure ulcer prevention educational programs are designed for an inpatient general population during initial rehabilitation; rarely is there a mechanism to adequately evaluate the information that has been retained, the behaviors that are practiced, and the perceived value of the prevention strategies in the individual's daily life. The person's motivation to comply may depend on beliefs about his/her susceptibility to the problem or about the severity of the problem