D. Heterotopic ossification (HO) is a pathologic process during which new bone
III. FREQUENT POST-INJURY PROBLEMS
A. Agitation is defined as a set of excessive behaviors that range from motoric rest- lessness and impulsivity. Behaviors such as emotional lability to verbal and phys- ical aggression are seen, often with post-traumatic amnesia (PTA). It correlates more to a history of premorbid psychiatric illness and substance abuse than to the severity of the injury and/or the presence of hypoxemia. Agitation occurs in 11% to 42% of brain injury patients, depending on the diagnostic criteria used for evaluation. The agitated behavior scale (ABS) is a 14-item test that describes and monitors the patient’s agitation which also serves as a measure of the patient’s responsiveness to treatment plans. A score of 22 or greater suggests significant agitation.
AGITATED BEHAVIOR SCALE
At the end of the observation period indicate whether the behavior described in each item was present and, if so, to what degree: Slight, moderate, or extreme.
Use the following numerical values and criteria for your ratings.
1=absent: The behavior is not present.
2=present to a slight degree: The behavior is present but does not prevent the conduct of other, contextually appropriate behavior. (The individual may redi- rect spontaneously, or the continuation of the agitated behavior does not disrupt appropriate behavior.)
3=present to a moderate degree: The individual needs to be redirected from an agitated to an appropriate behavior, but benefits from such cueing.
4= present to an extreme degree: The individual is not able to engage in appropriate behavior due to the interference of the agitated behavior, even when external cueing or redirection is provided.
1.Short attention span, easy distractibility, inability to concentrate.
2.Impulsive, impatient, low tolerance for pain or frustration.
3.Uncooperative, resistant to care, demanding.
4.Violent or threatening violence toward people or property.
5.Explosive or unpredictable anger.
6.Rocking, rubbing, moaning, or other self-stimulating behavior.
7.Pulling at tubes, restraints, etc.
8.Wandering from treatment areas.
9.Restlessness, pacing, excessive movement.
10.Repetitive behaviors, motor or verbal.
11.Rapid, loud, or excessive talking.
12.Sudden changes of mood.
13.Easily initiated or excessive crying and/or laughter.
14.Self-abusiveness, physical and/or verbal.
Total Score
The treatment of agitation in TBI follows a stepwise progression that uses psy- chotropic medications as a last resort due to their effects on cognitive and motor performance and recovery. It begins with the exclusion of any organic or metabolic factors (infection, hypoxemia, medications, “sundowning”) that could cause or con- tribute to the behaviors. When possible, establish a normal sleep wake pattern either by promoting proper sleep hygiene (sleep logs, low light environment) or the judicious use of non-sedating/short acting sleep agents (trazodone, ramelteon, melatonin).
Non-pharmacologic methods such as environmental modifications and behavioral plans are employed next. The long-term use of antipsychotics and benzodiazepines are not recommended in favor of atypical antipsychotics, mood stabilizers, lipophilic beta blockers, and stimulants.
Many spinal-cord–injured patients, especially those with tetraplegia, will have concomitant brain injury that is often overlooked in favor of resuscitative measures and acute medical management. The diagnosis is based on the observation of cogni- tive and behavioral deficits that could impact participation and rehabilitation. It is best detected by seeking evidence from the history (loss of consciousness, PTA, hypox- emia, prolonged extraction times) coupled with the neurodeficits. Neuroimaging may show local brain contusions, petechial hemorrhages, or diffuse axonal hemorrhage.
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Avoid some common medications (H2blockers and dopaminergic blockers) which may adversely affect the recovering brain injury.
B. Autonomic dysreflexia.
Autonomic dysreflexiaoccurs in patients who have sustained an SCI with a neurologic level of T6 (8) or above. With SCI at lower levels, the intact descending sympathetic control minimizes or prevents the syndrome. It is more common in complete SCI than in incomplete classification injuries. The onset is usually delayed from the initial injury and appears between 2 weeks and up to 2 months post-injury once “spinal shock” has passed allowing for reflex activity propagation. The sequence of events to elicit this life-threatening phenomenon is as follows.
Noxious stimulus occurs below the neurologic level of injury.
Reflexive unopposed sympathetic outflow is elicited. Vasoconstriction and piloerection occurs below the neurologic level of injury. Blood pressure is elevated (>20 mm Hg) above baseline systolic pressures.
In response to elevated blood pressure, the baroreceptors of the great vessels and vagal outflow are still intact and are stimulated; associated bradycardia results.
Vasodilation and flushing above the neurologic level is also seen.
1.Causes
Most common causes include over-distended bladder, over-distended bowel, decubitus ulcer, and ingrown toenail.
Other causes include fractures, constricting clothing, wrinkles in underly- ing sheets, intra-abdominal emergencies, aggressive bowel program stimulation, dysmenorrhea, orgasm with sexual activity, and onset of labor in pregnancy.
2.Treatment
Sit those with autonomic dysreflexia upright. This takes advantage of the tendency to lower blood pressure with upright posture in the SCI patient.
Since this syndrome occurs in response to a noxious stimulus, the first and most important premise is to identify and remove the stimulus; this requires a search for an inciting stimulus. Relief of the distension of bowel or bladder is often the only treatment required, with rapid return of the blood pressure to normal.
When the cause is not readily identified and corrected, control the blood pressure pharmacologically. Nitroglycerine paste is commonly used and applied to the skin. Once the inciting stimulus has been removed, the risk of resulting hypotension is reduced. Sublingual or “bite and swallow” nifedipine (10 mg) is an alternative and can be repeated in 15 to 20 minutes if necessary. Be careful since this can also cause a precipitous drop in blood pressure or cardiac arrhythmia.
In refractory cases, intravenous apresoline, nitroprusside, or spinal anesthe- sia can be used.
3.Prevention
In cases where the daily bowel or bladder management activities produce autonomic dysreflexia, use of topical anesthetic agents (lidocaine gel or alterna- tives) limits the cutaneous stimuli and the risk of developing these symptoms.
In recurrent cases (such as with bowel routines), prazosin 1 to 2 mg at night or oral guanethidine, starting with 5 mg daily, can be used prophylactically.
Mecamylamine, starting with 2.5 mg twice daily and titrating up to a total dose of 25 mg daily, is an alternative agent. Clonidine patches have also been employed.
Use of anti-cholinergic bladder relaxing medications may also decrease nox- ious stimulus from bladder distension and aid in decreasing the risk of recurrent dysreflexia.
C. Neurogenic bladder
Neurogenic bladderis one of the most serious alterations of physiologic function following neurologic trauma. In SCI, renal failure from frequent infections combined with reflux and subsequent pyelonephritis was the leading cause of death until the last two decades. Renal failure is less common now because of aggressive management and surveillance of neurogenic bladder function.
In the uninjured, the coordinated function of sensory, reflex, and volun- tary motor pathways allows normal elimination. The pathways involved include both autonomic (sympathetic and parasympathetic) and somatic motor tracts.
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Chapter 20 rRehabilitation 209 Classification of the bladder dysfunction requires detailed knowledge of these path- ways and is beyond the scope of this chapter. Instead, a protocol of care for acute management of neurogenic bladder in SCI is presented. This protocol allows safe management of the patient while other acute problems are addressed. For defini- tive management of neurogenic bladder, further workup is necessary and must be balanced with social factors to create the optimal care for the individual.
1.Seeking potential neurogenic bladder is the single most important factor in diagno- sis and management. Any process that can affect balanced control of the bladder (TBI, SCI, lumbosacral plexus injury, stroke) may cause neurogenic bladder. The patient with neurologic injury may maintain good urine output with a bladder that is operating at a very high residual volume, which induces a high risk of infection.
Check post-void residual volumes to ensure that the bladder is emptying properly.
Recurrent post-void volumes of over 100 mL indicate bladder dysfunction. The protocol that follows will suffice in the acute phase of management with all types of trauma.
a.Discontinue Foley or suprapubic catheter unless mandated by coexisting ure- thral or bladder injury, diabetes insipidus, pharmacologic diuresis, large fluid loads, or other conditions where a high urine volume is expected. Elimination of an indwelling catheter decreases the risk of infection.
b.Institute a timed void/monitoring of urinary volumes. Toileting the patient on a timed basis (q4h or q6h initially) allows a check for appropriate urinary volumes and may achieve continence in this manner alone. If the volumes at these checks are mildly elevated (>300 to 400 cc) then the intake is appropriate;
if the patient is unable to volitionally void, intermittent catheterization will be used to empty the bladder and eliminate stasis.
c.For SCI patients, start an intermittent catheterization program as soon as pos- sible after injury unless contraindicated. Do sterile catheterization unless the patient is being taught, where a “clean technique” is used.
d.Catheter urinary volumes should not exceed 300 to 500 mL. Adjust frequency of catheterization/toileting according to the patient’s output pattern. Record all output volumes and incontinent episodes on a frequency and volume chart.
e.Restrict patient fluid intake when on intermittent catheterization so that the total urine output is 1,500 to 2,000 mL/24-hour period.
In general, a combination of imaging and sequential testing of bladder pressures is indicated for lifetime surveillance of the patient with neurogenic bladder. This workup is generally deferred to the outpatient setting and initi- ated approximately 6 months after the acute injury.
Obtain urine cultures with a suspicion of symptomatic infection. Do not administer prophylactic antibiotics or urinary antiseptics unless a complicated urinary tract infection is documented. Complicated urinary tract infection is indicated by symptoms that can include:
i. Fever not attributable to other pathology ii. Increasing spasticity
iii. Autonomic dysreflexia
iv. Urinary retention or incontinence as a deviation from established patterns v. Hematuria
vi. More than 50 white blood cells per high-power field on microscopic eval- uation
vii. Evidence of stone disease
viii. Bacteriuria—100 colonies in specimen obtained by intermittent catheter- ization, or any growth in samples obtained from indwelling catheters.
Existence of a “positive” bacterial culture alone is insufficient to prompt treat- ment in absence of any of the attendantsymptomsdescribed.
D. Neurogenic bowel
Neurogenic bowel dysfunction usually coexists in patients with a neurogenic bladder since control pathways are similar. The goal of a bowel program is controlled fecal elimination with intervening periods of continence so that the individual can participate in daily activities without concern for social inappropriateness.
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All trauma patients can have bowel dysfunction, notably constipation. Since those with SCI usually have impaired or absent rectal and perineal sensation, symp- toms of bowel dysfunction may be absent or vague. Lack of appetite or nonspecific malaise may be the only indication that the problem of retained feces exists. Estab- lishment of elimination in all cases will improve patient comfort, and ultimately decrease length of stay.
An ileus typically exists in the initial period after SCI. Once the ileus subsides, often 2 to 3 days, the bowel program (see later) should be initiated. Once the bowel program is producing predictable results, the schedule can be modified as appropri- ate. The patient’s preinjury bowel pattern is the best guide to modification of timing.
Individuals who had routine, daily bowel movements usually will continue with this pattern after injury. Individuals who had less frequent bowel movements may require a less frequent bowel program in the long term.
Frequent liquid stools can indicate that bowel motility is too great or inspis- sated feces is blocking the rectum or colon. Liquid stool from above passes around this blockage and leaks from the anus. It may be possible to detect a full colon on examination, but the most reliable method of detection is to obtain a plain abdomi- nal radiograph. If fecal obstruction is seen, evacuate the colon and institute a routine and reliable bowel program. Use of rectal bags or other external collection devices or use of diapers is strongly discouraged.
1.Classification of neurogenic bowel as either an upper motor neuron or a lower motor neuron injury is essential in appropriate management.
a.In cases of upper motor neuron injury (tetraplegia), the sacral reflex arcs are intact. Presence of these reflexes helps to initiate bowel evacuation. In some cases, the individual can initiate evacuation with digital stimulation (stretch) of the anal sphincter or use of a suppository. Use of digital stimulation in concert with suppository use is central in initiation of a consistent “on demand” bowel regimen.
b.In lower motor neuron lesions (conus medullaris or cauda equina injuries), the local reflexes are lost. This situation is more difficult to control, often requiring routine digital disimpaction. Use of stool bulking agents can prevent free leakage of stool, together in combination with consistent lower rectal vault clearance on a periodic basis, is the preferred management.
2.The following bowel program for individuals with SCI also can be applied for other clinical entities in which bowel control is a problem.
A typical bowel management protocol consists of a stool softener titrated needs and a mild, orally administered stimulant laxative coordinated with a lax- ative enema (or suppository in selected patients). Use of bulking agents can also facilitate appropriate stool consistency to improve movements. Initially, this is on a daily schedule so that evacuation occurs at a time convenient for the patient and nursing staff.
Protocol for evening evacuation is Colace (100 mg) twice daily, two tablets of Senokot (Purdue Frederick, Norwalk, Connecticut) at noon, with a Fleet (Lynch- burg, Virginia) bisacodyl enema or Dulcolax (Ciba, Woodbridge, New Jersey) suppository, in combination with digital stimulation of the rectum, in the evening.
If morning evacuation is desired, the Senokot is given at bedtime.