Pressure ulcers are one of the most common problems, both in the acute care and in long-term care for people with spinal cord injury. There's a 33% incidence of people developing pressure injuries during acute care. This is in part, as we talked about earlier, in the acute management phase when there are life-threatening complications of hypotension and trauma and hypoventilation that require significant care. And pressure ulcer prevention is put on a lower priority. But the use of prevention is the best treatment for pressure ulcers. Pressure reduction mattress or overlay, frequent skin inspection, regular turning, and proper positioning are the mainstays throughout life. When a pressure ulcer develops, we assess it using a number of different tools. We want to stage the ulcer, which is a measure of severity. And on the next slide, we'll talk in detail about the staging. The location of the pressure ulcer, which is usually described as the bony prominence over which the pressure ulcer is present, helps determine the causative factors due to positioning and posture. And whenever we're looking at how to prevent the pressure ulcer from coming back, understanding why it formed in the first place is critical. And location is one of the most important pieces of that. The tissue at the base of the wound bed, whether there is healthy granulation tissue, whether there is pale, non-granulating chronic tissue, whether there is yellow slough, whether it might be necrotic tissue and needing debridement, all of these things need to be assessed and described. And in the picture to the right, you have a large pressure ulcer, and you can see that the majority of the pressure ulcer has a pale pink and what I would call a stagnant or non-granulating bed. There are a few buds of granulation tissue that might be present, but overall, the wound bed appears to be not progressing. There is also slough and necrotic tissue on the side. And then as you look to the periphery of the wound, you can see there's damage as well to the surrounding skin. All of this is important information as we decide how to approach the wound. Measuring the wound in basically length, north to south, head to toe is length, crosswise is width and depth perpendicular can help us monitor the healing rate. And if a pressure ulcer is not healing, then we need to go back and look for the underlying causes and why is it not healing. The degree of exudate and the quality of that exudate helps us determine choices. And finally, the surrounding tissue monitoring for additional injury, infection or trauma. This is a very useful state or assessment, stage, location, wound bed, dimensions, exudate and surrounding tissue. The pressure ulcer staging system has been developed and refined over the years and is used not just in spinal cord injury, but in all pressure ulcers. A deep tissue injury is defined as intact skin with bruising, blistering or subcutaneous edema. A deep tissue injury, we cannot yet tell if this is going to turn into a pressure ulcer or if this pressure injury will heal without further treatment as long as we protect that area and minimize any further trauma. The stage one pressure ulcer is intact skin with non-blanching erythema. So when we push on the skin, it doesn't blanch, it doesn't turn white and it doesn't, it's continuing red. Differentiating a stage one and a deep tissue injury can often be difficult, but a deep tissue injury often has more evidence of this bruising and tissue edema surrounding it. And the deep tissue injury is more likely to develop into a deep wound than evolve into a stage one pressure ulcer. A stage two pressure ulcer is a partial thickness skin loss. It can look like a burst blister or partial thickness skin loss, often due to a maceration and friction or shear forces. A stage three is a full thickness skin loss with subcutaneous tissue visible. And a stage four is full thickness skin loss with bone, tendon or muscle visible. Whenever there is a full thickness injury, but the base is covered with eschar or slough, the wound is considered unstageable, but it is likely a stage three or a stage four. But until it is debrided, we cannot tell just how deep it goes. The staging of a pressure ulcer is basically the assessment of severity. This is a picture of an unfortunate individual with quadriplegia who has pressure injuries on every bony surface that you can imagine. And if we talk about positioning and what causes a pressure ulcer, the location of the pressure ulcer is key. As I mentioned, a pressure ulcer is named for the bony prominence that it overlies. And starting with the sacrum, when a person is lying flat on their back, the sacral prominence bears significant amount of weight and a sacral wound will develop. If a person is sitting in bed or in a chair in a semi-reclined position, they can often get what is either a coccygeal right on the tip of the coccyx or a sacral coccygeal, kind of a combined sacral and coccygeal wound that is over the tip of the coccyx. When the wound is over an ischium, it is called an ischial pressure ulcer. And when it is over the trochanter, remembering that when a person is side-lying, the skin that overlies the trochanter falls with gravity. And often this wound feels like it is between the bony trochanter, which you can feel up here, and the bony ischium, which is down here, but there is nothing but a sacral notch in here. This pressure ulcer was caused by pressure on the posterior aspect of the trochanter during sitting, probably with a pelvic obliquity. You can also see trochanteric ulcers that are more lateral due to side-lying in an unprotected position, or side-lying for an excessive length of time. The bony prominence will tell you what caused the pressure injury. And as we talk about pressure ulcer principles of management, the first is to correct the underlying problems. We're talking about posture, pressure, shear forces, as well as the protoplasm of the individual, their nutritional status, especially do they have adequate protein intake, which is recommended at one and a half to two grams of protein per kilogram per day, and then whether they have adequate vascular supply. If they've got anemia, if they're smokers, if they've got severe peripheral vascular disease, these are reasons for a pressure ulcer to not heal and make a pressure ulcer more likely to recur. Second principle is adequate debridement. And there are basically four types of debridement. There can be sharp or surgical debridement, which can be either at the bedside or in the operating room, depending on the need for hemostasis and anesthesia. Sharp debridement is basically with a knife and or scissors removing as much of the dead tissue as possible. Mechanical debridement, typically a wet to dry dressing, different types of lavage and hydrotherapy, mechanically try to remove the debris. Enzymatic using commercially available ointments to dissolve the slough. This is often slow, but is more specific than the sharp and the mechanical, which can damage both healthy and unhealthy tissue. Finally, the use of otolytic debridement can be used when an impervious dressing is placed over a pressure ulcer and the accumulation of fluids underneath that results in the enzymes separating the healthy tissue from the unhealthy tissue, which then allows an easier and cleaner sharp debridement. You cannot use otolytic debridement when there is evidence of infection, however. Once we have a clean wound bed, the third goal is moist wound care. The control of the moisture of the wound bed is to maintain a moist but not wet wound bed and protect the surrounding tissues. And the choice of tissues is determined based on the amount of exudate in the wound depth. And there are 101 different dressings out there. And once the wound heals, we then have to go back to the first place and look for those risk factors for the pressure ulcer. If the wound is not healing, we need to go back to the underlying causes and figure out why it's not healing. Does it need further debridement? Does a person need better circulation or better protein intake? Osteoporosis and osteopenia is a significant problem long-term for people with spinal cord injury. It begins immediately after spinal cord injury and plateaus somewhere between six months and two years after injury. There is a progression of loss of bone due to immobilization. This is due to both a neurogenic component and a loss of weight bearing mechanical component. But due to continued immobility and disuse, this can worsen more than simply due to the neurologic injury. With women, it'll worsen at menopause with loss of estrogen and with men in the presence of hypogonadism and loss of testosterone, their osteoporosis can worsen as well. And with inadequate calcium or vitamin D intake, we can see more osteopenia. It's important to look at the reversible causes of osteoporosis and osteopenia in spinal cord injury because the estrogen or testosterone replacement, calcium, adequate calcium intake, vitamin D replacement, because most of our people don't spend enough time outside in adequate sun to get vitamin D. Also hypothyroidism and other diseases can be reversible, which may not fix all of the osteopenia associated with spinal cord injury, but can prevent it from becoming bad enough to cause pathologic fractures. The incidence of pathologic fracture in chronic spinal cord injury is 40% and can be caused by relatively minor trauma. The fracture rate is higher in paraplegics and in those with complete spinal cord injury, probably because paraplegic are more active and more likely to be doing things that can cause trauma to their legs. And those with complete spinal cord injury are more likely to have severe osteoporosis because of loss of any weight bearing or muscle tension on the bone. Symptoms and signs of a pathologic fracture, soft tissue swelling, increased limb girth, warmth, increased spasticity, limb deformity, and dysreflexia. Note pain may not be a symptom. The most common site of pathological fractures are around the knee with either the distal femur, supracondylar fractures, or tibial plateau fractures. This is a tibial plateau fracture, which is often a compression fracture. The hip is the second most common, either the femoral neck or either intratrochanteric or subtrochanter. The femoral shaft and the tibial shaft are also common. With tibial shaft fractures, you often get a combination of tibial and fibular fractures as seen in this case. The lower extremity fractures in people with chronic SCI typically and historically have been managed non-operatively with well-padded splints and frequent inspections. Avoid the circumferential hard cast that cannot be removed because severe pressure ulcers can occur. And until the rotting flesh can be smelled outside of the cast, people don't know that there's a problem. So either bivalving a cast or using a well-padded splint that can be removed and examined is beneficial for many fractures, especially those around the knee. However, any displaced fracture of the hip and any tibial or femoral shaft fractures ought to have operative treatment. This is in part because the ability to truly stabilize these long bone fractures requires a significant immobilization period and one must immobilize both the joint above and the joint below. So for a tibial shaft fracture, both the ankle and the knee need to be immobilized. And with a femoral shaft fracture, both the knee and the hip need to be immobilized in order for that to heal conservatively. When in doubt, operative intervention is preferred because it prevents the complications of a long-time cast, it prevents complications of long-term immobility and immobilization, and it prevents long-time complications of potential osteomyelitis in a non-union resulting in amputation. Generally, upper extremity fractures follow the general orthopedic principles for able-bodied people. It's the lower body fractures that are unique in our population. Heterotopic ossification is reported in anywhere between 10 and 53% of people with spinal cord injury. It's clinically significant, however, in a quarter to maybe a third of people. And those clinical significance is due to restriction of joint range of motion, typically around the hip or around the knee. In a small percentage of people, that joint can be completely ankylosed. The onset is typically seen between four and 12 weeks post-injury, and early signs are a loss of range of motion, swelling with redness and warmth, making the question, is there a possible DVT, cellulitis, or fracture that need to be evaluated as an exclusion? The most common sites are the hips, knees, and shoulder. HO only presents below the level of injury. Typically, the diagnosis is made with a combination of monitoring elevations of serum alkaline phosphatase. An early elevation is often seen. It may not be abnormal for a couple of weeks, even though it's been trending up the entire time. Creatinine kinase elevation may also predict the severity of HO, and a C-reactive protein elevation has been demonstrated in people with total hip arthroplasty who develop heterotopic ossification, although that may or may not be useful specifically in spinal cord injury. Typically, when there is a clinical finding of loss of range of motion, plain films are done of the site. However, these findings may be late because the heterotopic matrix needs to ossify before the HO is evident and can be seen on plain X-rays. So if the X-ray is normal, although the range of motion is restricted, a three-phase bone scan can be very helpful early on. Typically, the first and second phases, the blood flow and blood pool phases, are positive in the first couple of weeks, but the bone phase, the phase three, is often significantly delayed and may be positive for once the HO has matured. So if we are trying to treat this early on, we need to be looking at the early phases. MRI and ultrasound can also be helpful and may be more sensitive than plain X-ray. Currently, prophylaxis is not recommended, but if treatment is indicated, then either standard nonsteroidal anti-inflammatory drugs like indomethacin or COX-2 NSAIDs can be used. Etidrinate, which is a biphosphonate, prevents mineralization of the osteoid matrix and therefore slows down the evolution of the heterotopic ossification. However, when we stop the etidrinate, there may be a rebound ossification. Typically, this is a regimen of 12 weeks at 10 to 20 milligrams per kilogram per day. The biggest side effect is GI. Radiation can be used to reduce the recurrence and is often used in combination with surgical resection. Most surgeons will not touch this until there's evidence that the bone has been mature because operating on immature HO leads to a high incidence rate of recurrence with a vengeance. The goal of surgical resection is to restore functional range in that ankylose joint and prophylaxis following the resection with a bisphosphonate and radiation is often used. Spasticity is a common problem faced by people with spinal cord injury, defined classically as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes or muscle tone with exaggerated tendon jerks resulting from hyperexcitability of the stretch reflex as one component of the upper motor neuron syndrome. Complications of spasticity include poor posture, poor positioning, pain, contractions, and an increased burden of care. Treatment of spasticity typically follows the standard pyramid approach. The base of the pyramid revolves around removing noxious stimuli and routine range of motion and stretching. For the majority of people with spinal cord injury, with a low degree of spasticity, this may be enough. The addition of oral medications, including most commonly baclofen, diazepam, tizanidine, gabapentin, and dantrium sodium, all of which have slightly different mechanisms of action, can be used either independently or in combination for those with more severe spasticity. And if these are not effective, then motor point blocks and botulinum toxin can be effective for very focal spasticity problems. Simply spastic biceps in a person with a C6 level of injury, and they need to be able to extend that using gravity. Maybe a motor point block, because it is a focal problem, could be used. But if the person has a systemic problem with spasticity, motor point blocks and Botox aren't going to fix this, and intrathecal baclofen may be your best option. The oral medications are important to understand. And briefly, baclofen is a GABA-B analog, and GABA is a central nervous system acting relaxant for overactivity in the nerves. Diazepam facilitates GABA-A, and gabapentin appears to affect GABA-C. So these three work through different mechanisms to stimulate the GABA mechanism in the central nervous system to allow a decrease in neuroexcitability. Tizanidine works differently through centrally acting alpha-2 receptors when stimulated, again, causes a decrease in overactivity in the central nervous system. Dantrolene sodium works completely in the peripheral muscle. It has no effect on the nerves, only on the muscle. It blocks the calcium influx into the sarcoplasmic reticulum, thereby weakening muscle contraction, and thereby decreasing the severity of the spasticity. So for people who have cognitive problems or side effects with some of the centrally acting medications, the dantrolene sodium may be helpful, but this can also weaken neurologically intact muscles, and you also have to monitor liver enzymes. For people on baclofen, one very dangerous problem is baclofen withdrawal. Like alcohol withdrawal, baclofen withdrawal can be fatal. Its early signs are increased spasticity, some itching, hypotension, maybe some paracesias, but it can look just like sepsis with alternmental status, fever, excessive spasticity, rigidity, and even seizures. Baclofen must be tapered slowly and cannot be withdrawn suddenly without the risk of these life-threatening symptoms. The treatment is to restore the baclofen delivery. If the person has a baclofen pump, getting the pump refilled and restarted is essential. If they don't, then using a high dose of baclofen or benzodiazepines and supportive care, including ventilator and pressors, can be necessary. Untreated withdrawal leads to rhabdomyolysis, which then leads to renal failure. There can be multiple organ failure and death.

pressure ulcers

spinal cord injuries

wound assessment

osteoporosis

pathological fractures

spasticity