Aims and objectives: To investigate the incidence of urinary tract infection and analyse its risk factors among hospitalised patients with spinal cord injury. Background: While the incidence of urinary tract infection varies widely according to the healthcare setting and patients’ clinical characteristics, formal reports are limited in quantity. There has been no consensus regarding the risk factors for urinary tract infection. Design: A retrospective descriptive study. Methods: Electronic medical records of 964 subjects between 2010–2017 were reviewed. Urinary tract infection status was examined to identify newly occurred cases. Data included demographic and clinical characteristics, hydration status and length of hospitalisation. The reporting of the study followed the EQUATOR Network's STROBE checklist. Results: Of the sample, 31.7% had urinary tract infection (95% confidence interval: 1.288 to 1.347, p <.001). Sex, completeness of injury, type of bladder emptying, detrusor function and urethral pressure were significant factors affecting urinary tract infection. Patients who were male and those with injury classifications A, B and C had higher risk of urinary tract infection. Patients with urinary or suprapubic indwelling catheters, as well as those with areflexic detrusor combined with normotonic urethral pressure or overactive detrusor combined with normotonic urethral pressure, showed higher risk. Length of hospitalisation in patients with urinary tract infection was greater than that in uninfected patients, which implies the importance of prevention of urinary tract infection. Conclusions: Nurses should carefully assess risk factors to prevent urinary tract infection in patients with spinal cord injury in the acute and sub-acute stages of the disease trajectory and provide individualised nursing care. Relevance to clinical practice: This study contributes evidence for up-to-date clinical nursing practice for the comprehensive management of urinary tract infection. This can lead to improvements in nursing care quality and patient outcomes, including length of hospitalisation.
Funding Information:
Special thanks to Dr. Ji Cheol Shin for his excellent suggestions, Dr. Chung Mo Nam for statistical support and all staffs in the Committee of Research, Division of Nursing, Severance Hospital.
Publisher Copyright:
© 2021 John Wiley & Sons Ltd
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Robert M. Kliegman MD, in Nelson Textbook of Pediatrics, 2020 Immediately following SCI there is typically a period ofspinal shock
with low tone and absent reflexes. Eventually signs of anupper motor neuron lesion may emerge, including spasticity and involuntary muscle spasms. However, if there is a substantial segment of spinal cord infarction present, patients may have persistent flaccid paralysis. Children with neurologic levels of injury at T6 or above are at particular risk for interruption and decentralization of the autonomic nervous system. The most common
manifestations include bradycardia, hypotension, temperature dysregulation, and, once spinal shock has resolved,autonomic dysreflexia (AD). AD is a sustained sympathetic response as a result of a noxious stimulusbelow the level of injury. Symptoms resulting from AD typically include hypertension, bradycardia, headache, and flushing of the skin above the level of injury, although vague symptoms such as fatigue, irritability, or crying may be the presenting
symptoms in younger patients. Noxious stimuli are most often localized to bladder or rectal distention, but may include a number of other causes (Table 729.1). Children and adolescents with cervical and upper thoracic level SCI have lower baseline blood pressures compared with the general population. Therefore caution should be used when referencing age appropriate blood pressures, since blood pressure elevations of even 20-40 mm Hg above this lower baseline may be suggestive of
AD.Identification and treatment of the noxious stimulus are typically associated with resolution of symptoms without the use of antihypertensive medication. If necessary, antihypertensive agents with a rapid onset and short duration, such as nifedipine and nitropaste, are advocated to treat elevated blood pressure while the underlying cause is identified (Fig. 729.2). Emergent management of AD is necessary due to the risk of stroke and additional organ damage resulting from
sustained hypertension. Consideration of a medical alert bracelet, education of supervising adults, and carrying of an AD emergency reference card is recommended (Fig. 729.3). Patients with SCI are particularly vulnerable todeep venous thrombosis andpulmonary embolism because of immobilization of their affected limbs. In children and youth, deep venous thromboses are more common in postpubertal children.
Prophylactic treatment is recommended as soon as possible after an SCI (unless contraindicated because of the risk of bleeding or prior allergic response), including low-molecular-weight heparin, graduated compression stockings, and sequential calf compression devices for older children and adolescents. Late-occurring deep venous thrombosis most commonly occurs with prolonged immobilization related to illness or surgery, and prophylactic measures should be continued during these situations as
well. Consequent of SCI, patients often present with varying degrees of bowel and bladder incontinence. Following a SCI, the bladder can be areflexic or hyperreflexic and detrusor sphincter dyssynergia may occur. Clean intermittent catheterization (CIC) of the bladder is typically performed up to 4-6 times/day to prevent urinary retention and vesicoureteral reflux. Constipation can negatively impact the success of a CIC program. Anticholinergic
medications may improve bladder storage capacity and prevent urinary incontinence between bladder catheterizations. Antibiotics are recommended for symptomatic urinary tract infections; asymptomatic bacteriuria, without vesicoureteral reflux, is generally due to colonization and typically not treated. Functional independence with bladder and bowel management should be promoted when developmentally appropriate.Spinal Cord Injury and Autonomic Dysreflexia Management
Clinical Manifestations
Autonomic Hyperreflexia
C. Lee Parmley, Steven J. Allen, in Complications in Anesthesia (Second Edition), 2007
PROBLEM ANALYSIS
Definition
Autonomic hyperreflexia is a disturbance arising in patients with chronic spinal cord injury. It is also termed autonomic dysreflexia, hypertensive autonomic crisis, and mass reflex. Autonomic hyperreflexia is characterized by massive sympathetic activity set off by reflex stimulation from a variety of triggers (Table 114-1). It has been reported in 85% of patients within 2 to 3 weeks of spinal cord injury. Because it requires viable spinal cord below the level of injury or transaction, the disturbance does not occur in patients with paraplegia due to spinal cord infarction.
Autonomic hyperreflexia occurs when the hypothalamus and brainstem can no longer modulate segmental spinal sympathetic nerves and thereby inhibit their output. In the acute phase following spinal cord injury, there is low sympathetic activity. However, sympathetic activity returning to viable cord below the lesion is isolated from upper inhibitory control. This can result in an uncontrolled sympathetic response to a stimulus. The sympathetic activity causes vasoconstriction in the vasculature below the spinal cord lesion, leading to systemic hypertension. The hypertension stimulates the baroreceptors in the aortic arch and carotid sinus, inducing bradycardia and vasodilatation above the spinal cord defect. The vasodilatation is thought to be the cause of headaches and flushing. The severity of autonomic hyperreflexia is dependent on the amount of cord below the lesion that is involved with sympathetic outflow. Thus, higher cord lesions have a more profound response than do lower lesions.
Recognition
Autonomic hyperreflexia should be suspected when headache or hypertension develops in any patient with paraparesis of greater than 2 weeks' duration. Autonomic hyperreflexia's onset is variable among patients, and some may exhibit signs as early as the fourth postinjury day. Clinical findings are related to the level of intact innervation. Evidence of sympathetic stimulation below the level of the lesion may include skin pallor, pilomotor erection, spastic muscle contraction, and increased muscle tone. Above the lesion, one may find flushing of the face and neck, diaphoresis, mydriasis, and lid retraction. Awake patients frequently complain of headache, dyspnea, blurred vision, chest pain, nausea, and a sense of ill ease.
Risk Assessment
The severity of autonomic hyperreflexia is dependent on the amount of cord below the lesion that is involved with sympathetic outflow. Thus, lesions below T10 generally are not associated with autonomic hyperreflexia, because there are few sympathetic spinal synapses to disinhibit. Conversely, lesions above T5 tend to be associated with the worst autonomic hyperreflexia–related problems, because the majority of spinal sympathetic efferents arise below this level.
The site and nature of the planned procedure may also play a role. The majority of patients come to the operating room for urologic procedures, all of which are likely to produce autonomic hyperreflexia. One group of at-risk patients that has been the subject of increased interest in recent years is spinal cord–injured parturients. Because uterine contractions may result in strong sympathetic outflow, these patients pose a unique challenge during labor. The literature suggests that the incidence of autonomic hyperreflexia is as high as 75% in this population. In addition, it may be difficult to distinguish autonomic hyperreflexia from preeclampsia. Accordingly, some clinicians advise epidural anesthesia for all spinal cord–injured women in labor to prevent autonomic hyperreflexia.
Implications
If untreated, autonomic hyperreflexia can lead to serious complications and even death. Cardiovascular complications include left ventricular failure, myocardial ischemia, and possibly arrhythmias, all related to increased demands related to severe hypertension or central nervous system complications. Central nervous system complications are typically those associated with hypertensive encephalopathy, such as confusion, seizures, and stroke. Autonomic hyperreflexia may also increase surgical blood loss.
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Neuromuscular Dysfunction of the Lower Urinary Tract
Alan W. Partin MD, PhD, in Campbell-Walsh-Wein Urology, 2021
Autonomic Dysreflexia
First described byGuttmann and Whitteridge in 1947, autonomic hyperreflexia (autonomic dysreflexia) is a potentially fatal emergency unique to the SCI patient. Excellent source materials include the reviews byTrop and Bennett (1991),Vaidyanathan et al. (1998), andKarlsson (1999).Autonomic hyperreflexia represents an acute massive disordered autonomic (primarily sympathetic) response to specific stimuli in patients with SCI above the cord level of T6 to T8 (the sympathetic outflow). It is more common in cervical (60%) than thoracic (20%) SCI. Onset after injury is variable—usually soon after spinal shock, but it may occur up to years after injury, and distal spinal cord viability is a prerequisite.
Symptomatically, autonomic hyperreflexia is asyndrome of exaggerated sympathetic activity in response to stimuli below the level of the lesion. The symptoms include pounding headache, hypertension, and flushing and sweating of the face and body above the level of the lesion. Bradycardia is a typical accompaniment, although tachycardia or arrhythmia may occur. Hypertension may vary in severity from causing a mild headache before voiding to life-threatening cerebral hemorrhage or seizure.
The stimuli for this exaggerated response commonly arise from the bladder or rectum and typically involve distention. Precipitation may be the result of simple LUT instrumentation, tube change, catheter obstruction, or clot retention, and in such cases the symptoms resolve quickly if the stimulus is withdrawn. Additional causes or exacerbating factors may include other upper urinary tract or LUT pathology (e.g., calculi), gastrointestinal pathology, long bone fracture, sexual activity, electrocoagulation, and decubitus ulcers. Risk factors for autonomic dysreflexia during urodynamic evaluation include complete injury, cervical-level of injury, presence of detrusor sphincter dyssynergia, poor bladder compliance, and more than 2 years since injury (Liu et al., 2017).In addition, with more SCI patients participating in athletic pursuits, the instigation of this condition related to sports activities is also being increasingly recognized (Krassioukov, 2012).
DSD invariably occurs, and, at least in males, smooth sphincter dyssynergia is also usually a part of the syndrome. The pathophysiology is that of nociceptive stimulation via afferent impulses that ascend through the cord and elicit reflex motor outflow, causing arteriolar, pilomotor, and pelvic visceral spasm and sweating. Normally, the reflexes would be inhibited by secondary output from the medulla, but because of the SCI this does not occur below the lesion level.Vaidyanathan et al. (1998) emphasized that the SCI disrupts control of the sympathetic preganglionic neurons because bulbospinal input has been lost, and the remaining regulation is accomplished by spinal circuits consisting of dorsal root afferent and spinal interneurons.Karlsson (1999), however, points out that the underlying pathogenic mechanisms may not be as simple as they first appear. The amplitude of the blood pressure reaction indicates involvement of a large vascular bed, perhaps larger than that of the skin and skeletal muscle. It may be that the splanchnic vascular bed is involved as well, either from the standpoint of active vasoconstriction or simply from a lack of the ability to exhibit compensatory vasodilatation. Afferent and efferent plasticity in the sympathetic nervous system (SNS) may also be involved.
Autonomic Dysreflexia
David L. McDonagh, in Complications in Anesthesia (Second Edition), 2007
PROBLEM ANALYSIS
Definition
Autonomic dysreflexia or hyperreflexia (see also Chapter 114) is a syndrome of episodic autonomic hyperactivity in the setting of spinal cord injury. The syndrome is more common in complete spinal cord injuries, with no sensation or motor function below the level of the lesion. Lesions at or above T6 (above the splanchnic sympathetic outflow) put a patient at risk for this problem; lesions below T6 rarely cause the syndrome. A variety of noxious stimuli below the level of the spinal cord lesion can result in an afferent volley of neural input to the spinal cord and unchecked reflex efferent sympathetic outflow. This sympathetic outflow would normally be suppressed by supraspinal, descending inhibition, but connection to the brain no longer exists. The result is an unchecked vasopressor response that results in hypertension (sometimes severe), along with other symptoms described below.
Recognition
In 1860 Hilton first described a quadriplegic patient with episodes of autonomic dysreflexia. Symptoms include anxiety, throbbing headache, facial flushing, blurred vision, nausea, and nasal congestion. Muscle spasms can also occur. On physical examination, signs include hypertension and usually, but not always, reflex bradycardia (Table 213-1). Below the level of the spinal cord injury, where sympathetic outflow predominates, the skin is typically cool, and there is piloerection. Above the level of the injury, where a parasympathetic counterregulatory response predominates, the skin is warm, flushed, and diaphoretic. Hypertension is invariably present but is not necessarily extreme. These patients may have low normal blood pressure (≤120/80 mm Hg) at rest,1 but with stimulation, they may become symptomatic. Blood pressure may increase into what is typically considered the high normal range (>120/80 mm Hg) or stage 1 hypertension (>140/90 but <160/110 mm Hg), although severe (stage 2) hypertension (≥160/110 mm Hg) can be present.
Risk Assessment
All patients with spinal cord injury at or above T6 should be considered at risk for autonomic dysreflexia. The overall incidence is greater than 50%, and men are more commonly affected than women. Those with complete spinal cord injuries are at the highest risk. The syndrome can be seen following the initial injury, after spinal shock resolves. Patients with a history of previously diagnosed autonomic dysreflexia or a history of compatible symptoms should be managed with vigilance. Recent symptoms should prompt a search for any inciting causes (Table 213-2). The most common causes are bladder distention, urinary retention, and fecal impaction. A variety of noxious stimuli below the level of the spinal cord lesion (i.e., in the area of sensory loss) can provoke autonomic dysreflexia. Keep in mind that any surgical procedures or other stimulation below the spinal cord lesion may provoke autonomic dysreflexia, even though the patient may not have sensation in that body part.
Implications
Severe hypertension is the primary insult in autonomic dysreflexia. If it is uncontrolled, sustained hypertension can result in end-organ injury—a hypertensive emergency.2 The main concerns are seizure, hemorrhagic stroke, subarachnoid hemorrhage from aneurysmal rupture, intraocular hemorrhage, arrhythmia, and myocardial strain leading to myocardial ischemia or infarction. The syndrome of autonomic hyperreflexia can be fatal on rare occasions.
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Spinal Cord Trauma
Joseph Jankovic MD, in Bradley and Daroff's Neurology in Clinical Practice, 2022
Autonomic Dysreflexia
Acute episodes of AD are characterized by acute elevations in blood pressure coupled with bradycardia, although tachycardia has been known to occur. They usually occur with injury at T6 and above. Systolic blood pressure elevations of 20–30 mm Hg signify a dysreflexic episode. Cervical or high thoracic injuries can place a baseline systolic blood pressure 15–20 mm Hg lower; thus dysreflexic episodes can typically mimic healthy or slightly elevated blood pressure readings. Sympathetic discharge is the source behind these episodes. The symptoms of a rise in blood pressure have varied consequences, from being asymptomatic (mild discomfort, headache, blurred vision) to being life threatening (seizures, intracranial or subarachnoid hemorrhage, death, retinal detachment). Vasoconstriction occurs from sympathetic activation, so dry, pale skin is often observed below the lesion. Above the lesion, intact baroreceptor reflexes initiate a parasympathetic response responsible for bradycardia, as well as sweating, piloerection, and flushing above the level of injury. Once an episode has occurred, the risk for another episode occurring in the next 24–72 hours is increased. A higher percentage of cases exists in high injuries and complete SCIs. In SCI, supraspinal input in the form of inhibitory and excitatory vasomotor pathways to the sympathetic preganglionic neurons are disrupted, and thus unstable blood pressures are found to occur. Stimulation of the urinary bladder or colon has been known to trigger these events. Symptoms are usually brief, either from termination of the episode by treatment or the self-limiting nature of the episode. Alterations have been suspected to occur in the spinal and peripheral autonomic circuits.
The clinical guidelines used for treating a patient with acute episodes of AD focus on an algorithm, with monitoring of blood pressure and heart rate after each step. The first step in caring for a patient suffering from an acute episode of AD should be to place the patient in a sitting position. Second, the patient needs to be inspected for areas of constriction (including clothing). Third, an indwelling catheter should be placed to relieve bladder distention. If a Foley catheter is in place, potential regions of kinks or obstruction should be investigated. Systolic blood pressure is measured after this step, and if the value is greater than 150 mm Hg, a fast-acting short-duration antihypertensive agent is considered. Usually, nifedipine, nitrates, and captopril have been shown to be beneficial in the acute setting. To date, only nifedipine has been studied in controlled trials for AD. Once blood pressure is within an acceptable range (<150 mm Hg), fecal disimpaction can begin. If neither indwelling catheterization nor bowel disimpaction alleviate symptoms, other potential causes should be sought after, but an admission to the hospital is likely needed first to stabilize thepatient’s blood pressure. After control of symptoms, the patient should be observed for 2 hours to make sure another episode does not recur.
Autonomic Dysreflexia
R.K. Khurana, in Encyclopedia of the Neurological Sciences (Second Edition), 2014
Pathophysiology
Autonomic dysreflexia occurs in 48–90% of patients with spinal cord injury (SCI) above the splanchnic sympathetic outflow. It usually manifests 3–4 months after SCI, but it may occur as early as the fourth day and as late as 12 years postinjury. A lesion at or above the T6 level disconnects the caudal spinal region, including splanchnic sympathetic outflow, from supraspinal control. Experimental and clinical studies demonstrate morphological and physiological changes above and below the injury. There is remodeling of synapses and increased reactivity rostral to the lesion. The vagus nerve is usually unaffected. Caudally, there is degeneration of descending tracts, sprouting of ascending sensory fibers, a decrease in inhibitory neurotransmission, an increase in calcitonin gene-related peptide and substance P, and reduction of γ-amino-butyric acid. Peripherally, potentiation of neurovascular transmission may be due to decentralization, adrenoceptor supersensitivity, altered adrenoceptor density, increased smooth muscle reactivity, increased norepinephrine release, and decreased synaptic norepinephrine uptake. The muscle and skin sympathetic activity is markedly reduced at rest; on stimulation, it shows parallel instead of sequential activation. Visceral or somatic, noxious or innocuous stimulation below the lesion is carried by pelvic parasympathetic, pudendal somatic, and hypogastric sympathetic (T9 or higher) afferents to the spinal cord. During its ascent in the dorsal and spinothalamic tracts to the lesion level, collateral branches activate the intermediolateral column neurons. An increased norepinephrine ‘spillover,’ coupled with target organ hyper-responsiveness, causes hypertension. The blood pressure elevation activates baroreflexes (cartoid sinus and aortic body→glossopharyngeal and vagus nerves→medulla→heart and blood vessels) to produce vagally induced bradycardia and vasodilation.
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Autonomic Dysreflexia
Ramesh Khurana, in Encyclopedia of the Neurological Sciences, 2003
Treatment
Treatment for autonomic dysreflexia needs to be individualized since it may occur in minor episodes that do not require treatment or it may be severe and life threatening. An acute episode with a markedly elevated blood pressure constitutes an emergency, and recurrent attacks of autonomic dysreflexia, if unrecognized and inconsistently treated, can lead to serious neurological, cardiac, and renal complications.
Primary pharmacological prophylaxis is usually not indicated, but appropriate care of bowel, bladder, and skin is essential. Premedication before urological procedures with sublingual nifedipine or oral mecamylamine is recommended in patients with suspected or documented autonomic dysreflexia. Nifedipine is the currently favored agent. It inhibits voltage-dependent Ca2+ channels in vascular smooth muscle and selectively dilates arterial resistance vessels. The contents of a 10-mg capsule are squeezed under the tongue. Mecamylamine, a ganglionic blocking agent, is given in a dosage of 2.5 or 5 mg three times a day to reduce sympathetic and parasympathetic responses.
A systematic approach is indicated when a patient presents with symptoms of autonomic dysreflexia. Blood pressure should be checked. If blood pressure in not elevated, monitoring of symptoms and blood pressure should be continued for 2 hr. If blood pressure is elevated but does not exceed 150/100 mmHg, the patient should be made to sit up to lower blood pressure and all clothing should be loosened. The catheter tubing should be checked to determine whether urine is flowing out from the bladder and to ensure that there are no kinks, or the patient should be catheterized after instilling 2% lidocaine jelly into the urethra. The bowels should be emptied if no cause is found in the urinary tract. Also, a search for pressure sores and ingrown toe nails should be made.
Blood pressure should be reassessed if no cause is found. If blood pressure elevation does not exceed 150/100 mmHg, the patient should continue to be observed. If hypertension exceeds 150/100 mmHg and a cause is either not found or found but not feasible to eradicate quickly, pharmacological treatment should be initiated.
If blood pressure elevation is between 150/100 and 180/120 mmHg, the patient should be treated with sublingual nifedipine, oral mecamylamine, or oral clonidine. Clonidine reduces sympathetic drive by activating α2 adrenoreceptors in the lower brainstem.
If blood pressure exceeds 180/120 mmHg, drugs that directly relax smooth muscle are used. They are administered intravenously for a quick response. These include hydralazine, nitroprusside, and diazoxide. Hydralazine, which directly relaxes the arteriolar smooth muscle, is administered as a 10- to 20-mg dose by slow intravenous push. Nitroprusside dilates arterioles and venules and its dose can be adjusted from 0.25 to 1.5 μg/kg/min. Diazoxide acts by hyperpolarizing arterial smooth muscle cells. Its dosage ranges from 50 to 300 mg.
In patients with recurrent life-threatening autonomic dysreflexia in whom no cause is found, radical measures may be necessary, including pudendal and sacral nerve blocks, pelvic or pudendal nerve section, sacral posterior rhizotomy, sympathectomy, subarachnoid block with alcohol or phenol, dosal root ganglionectomy, and even cordectomy.
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Sports Medicine and Adaptive Sports
Joseph E. Herrera, in Braddom's Rehabilitation Care: A Clinical Handbook, 2018
Autonomic Dysreflexia
Autonomic dysreflexia (AD) is a condition resulting from excessive sympathetic outflow in response to a noxious stimulus; the outflow is unregulated because of interruption of neural pathways after spinal cord injury. People with spinal cord injuries at the level of T6 and above are at risk for AD. The most common noxious stimuli that lead to AD include tight clothing, urinary or fecal retention, renal or bladder stones, pressure ulcers, infections, or intraabdominal pathology. In addition, “boosting” is the practice of intentionally inducing AD by athletes for the purpose of improving athletic performance.
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Cardiac Patients Requiring Emergent Noncardiac Surgery
Lev Deriy MD, ... Brian Starr MD, in Essentials of Cardiac Anesthesia for Noncardiac Surgery, 2019
Autonomic Dysreflexia
Autonomic dysreflexia (AD) occurs in patients with SCIs typically of T6 or higher and is characterized by acute hypertension and bradycardia. Typically, a noxious stimulus below the level of the cord lesion triggers AD (e.g., surgery, bladder catheter manipulation) (Fig. 16.7). AD results from unopposed sympathetic efferent outflow (extreme vasoconstriction; cool, pale skin; and severe hypertension) as a result of noxious stimuli below the spinal cord lesion, leading to reflex activation of parasympathetic outflow (bradycardia, cutaneous flushing) above the spinal cord lesion. Unopposed vasoconstriction persists because of blocked inhibitory responses at the spinal cord lesion. AD typically occurs 1 to 6 months after injury, but it can occur acutely after SCI. Regarding cardiac patients, severe hypertension is a major concern. It can lead to worsening myocardial ischemia, congestive heart failure, and occasionally cerebral hemorrhage. Prevention of AD can be accomplished with a deep regional block (spinal or PNB for lower extremity surgery; epidural block may be less effective due to sacral nerve sparing) or deep inhalation anesthesia. Treatment involves cessation of the noxious stimulus, deepening the anesthetic, and using antihypertensives. For cardiac patients and any patient in whom the index of suspicion is high for AD occurring, invasive arterial blood pressure management should be used with immediate treatment plans in place.
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Nursing Care and Education for Patients with Spinal Cord Injury
Joan P. Alverzo RN, CRRN, PhD, ... Sandra Shultz DeLeon CRRN, CCM, MS, BSN, in Spinal Cord Injuries: Management and Rehabilitation, 2009
Autonomic Dysreflexia
AD is defined as a syndrome of massively uncontrolled sympathetic nervous system discharge that is unique to patients who have sustained an SCI (Figure 3-1). It is characterized by a sudden and exaggerated reflex and with an increase in blood pressure. The mechanism of this syndrome begins with patient exposure to noxious stimuli such as pain or pressure below the level of injury. A signal is sent through a sympathetic pathway, which triggers an exaggerated reflex (e.g., vasoconstriction and a subsequent increase in blood pressure). Baroreceptors in the aorta sense this increase in blood pressure and send a signal to the brainstem, which in normal physiologic conditions responds by transmitting a signal for vasodilatation and a slowing of the heart rate. These signals are interrupted by the spinal cord lesion and, as a result, no compensatory action occurs. The blood pressure remains elevated and the cycle continues until noxious stimuli are removed.
AD occurs in patients with injuries at T6 or above, but rarely occurs during the acute phase after SCI. In general, the onset of AD begins after the resolution of spinal shock. Prevalence estimates vary from 66% to 85% of patients with lesions at or above T6.12 Symptoms of AD include the following (see Box 2-4):
•Hypertension (systolic pressure possibly as high as 300 mm Hg)
•Headache: severe or pounding
•Perspiration: above the level of injury
•Flushing: above the level of injury
•Piloerection: below the level of injury
•Vision: blurred; dilated pupils
•Nasal congestion
•Anxiety
•Bradycardia
Because AD is typically seen only in patients with SCI, clinicians who do not regularly work with these individuals may fail to recognize symptoms, delaying critical treatment. There are many causes of AD (Box 3-1). Determining the cause is essential so the reflex can be stopped by removing the stimuli at the source.
Treatment of AD involves a number of interventions (Box 3-2). The administration of nitroglycerin as a topical paste is typically the first step, followed by having the patient bite and swallow nifedipine to reduce the blood pressure. Xylocaine 2% jelly is used if the nurse is checking for fecal impaction or changing or inserting a urinary catheter. In addition, note that problems with temperature regulation may follow an incidence of AD because the dysreflexia can result in the patient sweating with heat loss and then being unable to compensate with resultant shivering. Interventions to correct the hypothermia may be required.
Preventive measures for AD are critical and reduce the chance that noxious stimuli will occur. Ensuring that clothing is loose, the bladder is nondistended, the bowel program is effective, linen under the patient is smooth, and podiatric care is regularly performed (to prevent ingrown toe nails) all help limit the possibility that AD will develop. The patient and family must be taught to recognize the symptoms of AD and to either take action or instruct care providers to take action. In addition, patient and family education needs to focus on reducing the risk of AD by using the prevention strategies discussed above.
A number of complications can result if AD goes untreated. The patient may have retinal hemorrhages. A more serious complication may be a subarachnoid or intracranial hemorrhage, potentially resulting in a cerebrovascular accident. Myocardial infarction is also a potential complication and, in some cases, AD may be fatal.
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