Now let's continue with management of some of the common and serious medical complications of spinal cord injury. The neurogenic bladder is one of the most important areas for us to to manage. Prior to good quality urologic care people with spinal cord injury died of urosepsis and renal failure. Today with good urologic care there is no need for these to be a source of severe morbidity or mortality, but we need to follow a careful bladder approach to to get it right. The Consortium for Spinal Cord Injury Medicine has put out an excellent clinical practice guideline on bladder management for adults with spinal cord injury and it really talks about the the approach to four major complications urinary tract infections, incontinence, stones, and renal dysfunction. The goals of bladder management are to preserve renal function. To do this we need to maintain adequate storage. The second goal is to maintain social continence and to do this we need to have complete emptying and control of that emptying. And the third is to prevent urinary tract complications, especially infections and stones. A quick review of the bladder anatomy. The detrusor is the smooth muscle that makes up the dome of the bladder. There are two types of receptors in the detrusor. There are acetylcholine muscarinic receptors which when stimulated cause contraction and then there are beta-adrenergic receptors which when stimulated cause relaxation of the bladder muscle. We also have two sphincters. There's an internal sphincter which is smooth muscle and has alpha-adrenergic receptors which when stimulated cause contraction and external striated muscle which is under voluntary control or lack thereof in spinal cord injury and may be dependent on the degree of spasticity and flaccidity that a person has in their lower extremities. The ureters and the ureteral orifices are the keys to preventing upper tract function because ureteral peristalsis stops when the bladder pressure reaches 40 centimeters of water. The ureter tunnels through the bladder wall at an angle creating a natural flap to prevent reflux but when the detrusor muscle hypertrophies many times that tunneling loses its acute angle and reflux is more available and more possible with higher pressures when you have a hypertrophied bladder. All of these things can be evaluated through urodynamic testing and the tracing on the right is just an example. We're not going to go over the details of it but everybody with a spinal cord injury who has evidence of neurogenic bladder should have an initial urodynamic study and potentially follow-up depending on the type of findings. Urodynamic diagnoses are either detrusor areflexia which is a low-pressure storage capacity but inability to empty because there is no reflux contraction and no squeeze of the detrusor. Detrusor hyperreflexia is seen in 50% of people with thoracic injuries and much higher percentage of those with cervical injuries. This is when the detrusor is overactive and there is a failure to store. The detrusor hyperactivity with detrusor sphincter dyssynergia is what kills kidneys. Most people with cervical injury and 50% of those with thoracic injuries have detrusor hyperreflexia with DSD. This is both a failure to empty because their sphincter is overactive and a failure to store because their detrusor is overactive, thus leading to high-pressure storage and incomplete emptying. With a person with detrusor sphincter dyssynergia, we cannot just let them void spontaneously or they will lose kidney function. So the strategies to manage the bladder in the first two, detrusor areflexia and detrusor hyperreflexia are really the goals are to minimize incontinence and minimize urinary tract infections. So people who are unable to empty detrusor areflexia either have a competent sphincter or an incompetent sphincter. If their sphincter is incompetent and they are leaking continually and they do not even store, then they need to have some sort of external collection device and they may be able to empty with Valsalva, but most likely intermittent catheterization is necessary. If they have a competent sphincter, then intermittent catheterization to periodically empty the bladder is all that's necessary and they remain continent during the between times, although they may have some stress incontinence during transfers simply because the increased intra-abdominal pressure is transmitted into the detrusor and pushes some urine out. Those with a detrusor hyperreflexia can operate in two different ways. If they have a sphincter that does not obstruct their emptying, then they can use an external collection device. And for men, a condom catheter is widely used. For women, there are few options for this and absorbent pads and diapers can be used, but there are worries about skin health and others problems that occur. So many times, moving toward hand function and converting the bladder to an areflexic type of bladder is most effective. With the use of anticholinergic medication, we can convert the detrusor hyperreflexia into detrusor areflexia. With fluid restriction and intermittent catheterization, a person with hand function is able to then empty their bladder periodically, minimizing incontinence, minimizing urinary tract infections, and avoiding upper tract renal complications. If they don't have hand function, then an assistant to perform intermittent catheterization may be necessary unless they are able to empty into some device in which the urine can be managed. If a person has detrusor hyperreflexia with DSD, they fail to store and they fail to empty. These are the challenging patients. Those people who have hand function, people with lower cervical level with a C7 or C8 often, or paraplegia and have adequate hand function, can convert their detrusor hyperreflexia to detrusor areflexia. With a fluid restriction and intermittent catheterization, can once again empty their bladder, maintain a low storage pressure, minimize urinary tract infections, and have no incontinence between catheterizations. However, if they have no hand function, then their challenges are to either have a sphincterotomy and an external collecting device, which releases the detrusor sphincter dysenergia by eliminating the sphincter, allowing to then have detrusor hyperreflexia without DSD and low-pressure emptying. However, sphincterotomies are not commonly done in all parts of the country, and many times there remains a failure to empty at low pressure even after a sphincterotomy. And if they do not have hand function, catheterization by another person is possible following the hand function side of the diagram, but frequency of urinary tract infections increases. The worst type of bladder management ultimately is an indwelling catheter. However, unfortunately, that becomes a matter of choice and opportunity. If a person has no reliable caregiver and they have no hand function, there may be very few choices. I'd like to talk a little bit about urinary tract infection and to be able to differentiate between bacteriuria, which is without pyuria, but just bacteria. Everybody with a neurogenic bladder who has any sort of bladder instrumentation with a catheter will have some degree of colonization and bacteriuria. But unless this develops evidence of inflammation with pyuria and the presence of bacteria, this would not be considered a urinary tract infection. The presence of bacteriuria and pyuria is considered by many to be a laboratory or asymptomatic urinary tract infection and is generally not treated because of the challenge of resistant organisms becoming more and more prevalent. And once a person really needs the antibiotic, they may already be resistant to it because of over-treating of asymptomatic urinary tract infection, which may simply be colonization with a small degree of inflammation. Now, when a person develops a symptomatic urinary tract infection, this is a combination of bacteriuria, pyuria, and symptoms. Now, because of spinal cord injury, the symptoms may not be the classic bladder urgency, bladder pain, or burning on urination. But you may find that there is an incontinence between catheterization or need for increased frequency. There may be some increased spasticity, presence of autonomic dysreflexia. Oftentimes, a patient will identify their urine as a changing character. It's cloudy or change of smell. Or they feel sick, tired, and just a sense of unease. Most people with spinal cord injury who have had urinary tract infections can tell you, Doc, this is a UTI. I know the feeling. And then if you check, that's the symptom. And then if they have bacteriuria and pyuria, typically these are then treated. Those people who have recurrent urinary tract infections, we have to look for risk factors for developing these. These can be bladder overdistension, so they're on a catheterization program, but they're not catheterizing. They may have developed vesicle ureteral reflux, have high voiding pressures, large post-void residuals. There may be stones, either in the bladder or in the upper tract, and there may be some degree of outlet obstruction, and they're not emptying as well as they were before. Recommendation is that if a person has more than two UTIs in a six-month period, they need to have evaluations, which should include urodynamics, abdominal x-ray looking for bladder stones, renal ultrasound looking for hydronephrosis and reflux and kidney stones, potentially a non-contrast CT to look for kidney stones, a nuclear medicine renal scan, or a 24-hour creatinine clearance to check on the renal function, and potentially a cystoscopy to look in the bladder to see what pathology there may be. If a person has infrequent urinary tract infections, there still is a need for periodic monitoring of this, of all of these areas, but it varies depending on the type of bladder management, the level of injury, the duration of injury, and their history of urologic complications. People with sponocular injury who have indwelling catheters have an increased risk for bladder cancer. Likewise, those who have bladder stones and recurrent UTIs have a higher risk for bladder cancer. Now, the bladder cancer that we see in sponocular injury is often a squamous cell carcinoma, which is more aggressive than the typical transitional cell that is often seen in a urethelial tumor. It's not necessarily the most common cancer in sponocular injury, but squamous cell carcinoma occurs more frequently in people with SCI who have indwelling catheters. Thus, surveillance is recommended. Cytology, random bladder biopsies, and cystoscopy are typically recommended every five years for people with indwelling catheters, as well as for people who have evidence of hematuria not explained by anything else. Let's now talk about the neurogenic bowel. Neurogenic bowel encompasses the entire GI tract, and the various complications that we see range from ileus and gastric ulcers and GE reflux to autonomic dysreflexia, abdominal pain, bowel distension, diverticulosis, hemorrhoids, nausea, appetite loss, impaction, constipation, diarrhea, delayed evacuation, and unplanned evacuation or bowel accidents. And typically, this is one of the most common problems that interferes with a person's lifestyle or activities out of the home with sponocular injury. Nobody wants to be out in public when they have a bowel accident. And so if they have frequent bowel accidents, they will restrict their life and stop participating in social activities. Thus, this is not only a physiologic problem, but a rehabilitation problem as well. A quick review of the anatomy of the colon. There is extrinsic innervation to the vagus nerve carrying parasympathetic fibers as far as to the splenic flexure. And then through the pelvic nerve, also carrying parasympathetic to the descending colon, sigmoid colon, and rectum. And parasympathetic activity slows down bowel motility. Sympathetic activity is provided via the hypogastric nerve to the anal sphincter. To the anal sphincter. And the pudendal nerve provides voluntary control of the external anal sphincter. These are the three extrinsic innervations of the colon and the anal sphincters. But after sponocular injury, it's typically the descending colon, the sigmoid, and rectum, as well as the sphincters that lose the external extrinsic innervation. But they maintain their intrinsic activity and reflex activity. And it is the reflex activity and the intrinsic activity of the Auerbach and Meissner's plexuses that allow us to maintain some degree of routine and regular bowel elimination. Our goal of a neurogenic bowel program is a predictable and effective elimination, maintaining fecal continence, and minimizing GI complaints. The management depends completely on the presence or absence of these bowel reflexes. If they have a upper motor neuron spinal cord injury with positive anal reflexes, then we can utilize the reflexes in the rectum and sphincter to create an effective evacuation. If they have a lower motor neuron injury, trying to trigger reflexes through suppositories and digital rectal stimulation does not work, we need to come up with a completely different approach to the lower motor neuron bowel. So building a bowel program is one of the most important parts of the early SCI rehabilitation. The components, diet, fluid intake, and activity are the most basic components. And for both of these, we're trying to manage the quality of the stool. For an upper motor neuron bowel, our goal is soft-formed to mushy stool. For a lower motor neuron bowel, the goal is firm stool. If the stool in a lower motor neuron bowel is too soft, then with any abdominal contraction, valsalva, you will have stress incontinence. What comes down goes out unless the stool is fairly firm. But in upper motor neuron, we have the reflex activity of the sphincter that provides us with a continence mechanism. The timing is critical because just like bowel training in children, the bowel can build a habit using the same time of day, often 30 minutes following a meal for upper motor neuron bowels to use the gastrocolic reflex in which distention of the stomach triggers a reflex contraction of the colon, especially the distal colon. And oftentimes, these bowel programs are done daily or every other day. Can be in the morning, can be in the evening, depends on the individual and their personal preference. For lower motor neuron bowel dysfunction, however, they may require multiple bowel evacuation attempts every day because, as I mentioned, what comes down will come out because there is no continence mechanism. Typically, we use medications including fiber, stool softeners, and laxatives of various combinations for upper motor neuron. The fiber is beneficial in the lower motor neuron because it helps bulk the stool, keeps it from becoming too fast moving because fiber does one of two things. It either bulks up the stool and adds more water to it, which can help move things through, or it can bulk up the fiber and absorb the water that may be moving things through too quickly and can slow things down a little bit. So again, trying to create a firm stool that can be evacuated via manual evacuation or Valsalva in a lower motor neuron bowel twice a day often, whereas the trigger for an upper motor neuron bowel, there is a mechanical trigger, which is a digital rectal stimulation. Circular movement within the anal sphincters, reaching all the way to the internal anal sphincter and performing a 30 to 60 second circular motion will both relax the sphincter and trigger a mechanical contraction from the rectum. The chemical using a suppository or mini enemas can also provide a chemical trigger by irritating the mucosa of the rectum, thereby causing it to contract in those who have intact reflexes. When a person doesn't have a good bowel program or many other things, they can develop autonomic dysreflexia. And again, there is an excellent clinical practice guideline available through the Consortium for Spinal Cord Medicine. People at level, at spinal level T6 and above are at risk for autonomic dysreflexia. The more complete they are, the more at risk they are. Because of the combination of somatic and visceral afferent input to the bladder and the bowel, any irritation below the level of injury can trigger autonomic dysreflexia. It can be a DVT, it can be a fracture, it can be a hangnail, it can be a pressure injury. Any of these things can trigger autonomic dysreflexia. But because the sympathetic outflow below the level of injury is unregulated because of the spinal cord injury, we get reflex vasoconstriction, increase in the circulating blood volume, increase in the blood pressure, and the parasympathetic outflow above the level of injury is the only way the body has to react to it. And so you end up with vasodilation above the level of injury and the potential for bradycardia due to vagal overactivity. Thus the common signs and symptoms of autonomic dysreflexia are hypertension, which is defined as a systolic blood pressure increase of 20 millimeters of mercury from baseline. Now remember, many of our people with spinal cord injury have a resting blood pressure of 100 systolic and some 90 systolic, and that's their normal. So they don't have to get to 200 systolic to be called autonomic dysreflexia. A systolic increase of 20 millimeters of mercury is by definition a sign that could mean autonomic dysreflexia. Headaches, sweating above the level of injury, bradycardia most often seen in tetraplegics, although you can often see a tachycardia in the high paraplegic because of the innervation of the segmental nerves to the heart and the intact thoracic or sympathetic nerves. Facial flushing, nasal congestion, all of these are common signs and symptoms and every person at risk for dysreflexia needs to be aware of these and needs to know how to treat them. The steps for treating dysreflexia. The first is to sit up and loosen clothing. This is using the body's natural response to orthostasis and many of our people have orthostatic hypotension that we can use to bring the blood pressure down out of a very dangerous range to a safer level while we investigate. The second and really the key to this is identifying and correcting the underlying cause of the dysreflexia. Checking for bladder distention and bladder obstruction. The most common causes of dysreflexia are bladder distention and a blocked catheter or some bladder irritation is often the trigger. If the bladder is emptied but the blood pressure remains over 150 systolic, then initiating pharmacologic treatment is indicated. Generally preferring rapid onset and short-acting agents, whether they're calcium channel blockers, nitrates or alpha-2 agonists to bring the blood pressure down to less than 150 so that we can then continue to search. The second most common is a fecal impaction but if a person has dysreflexia due to a fecal impaction, just the act of checking can make the blood pressure go higher. So instilling a topical anesthetic agent into the rectum, waiting and then gently checking for a fecal impaction can be helpful alleviating dysreflexia. If there's no bladder and no bowel source immediately identified, this person should be admitted to the hospital for observation and further management, blood pressure control and evaluation for an underlying cause. The important thing to remember about dysreflexia is that as soon as you relieve the underlying cause of the problem, the blood pressure returns to normal. It can be dangerous to have medicated a person with a long-acting blood pressure medication and then reverse the cause of dysreflexia because you will then end up with a person with hypotension and at risk for a watershed infarct of the brain if they are at risk due to cerebrovascular disease. So short-acting and chemicals that can be reversed or removed are preferable while you're identifying the source and avoiding over-treating is key. Orthostatic hypotension is caused by poor venous return from the lower part of the body due to the loss of the sympathetically mediated vasoconstriction reflexes. To combat this, we use adequate fluid and salt intake, compressive stockings and abdominal binder and typically the use of a...

spinal cord injury

neurogenic bladder

neurogenic bowel

bladder management

bowel program

autonomic dysreflexia