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Autonomic dysreflexia 2007


This is an artcile I wrote years ago, and is an updated artcile from an original one I wrote for (now defunct) in 2001. …

This is an artcile I wrote years ago, and is an updated artcile from an original one I wrote for (now defunct) in 2001.

Autonomic Dysreflexia 2007 by Robert S. Cole is licensed under a Creative Commons Attribution 4.0 International License.

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  • 1. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P “It takes a lot of time to make things go right, but they can all go to hell in a heartbeat.” -Walter Slovotsky About the Author: Steve Cole has been involved in EMS and EMS education since 1990. He has worked for a variety of EMS agencies including volunteer fire, military, hospital based, private, and third service. He is currently employed by Ada County Paramedics (Boise, Idaho),a top-tier and often besieged Third Service EMS. He has no current conflicts of interest with any portion of this article, and has not received from any commercial interest for its production. He would like to mention that he is open for some money, should a sufficiently insane commercial enterprise wish to invest in his expansive, eclectic, and somewhat haphazard quest for EMS excellence. Comments are welcome. He can be reached by email at: Introduction: Autonomic Dysreflexia (AD), sometimes known as Hyperreflexia, is a potentially life threatening condition1 almost completely unique to patients with spinal cord injuries (SCI). It is characterized by a severe sympathetic response, notably stroke- level hypertension, and related symptoms. It can be triggered by the most benign and subtle of events, and can be overlooked easily in its early stages. Fortunately, in many cases treatment is fairly simple if AD is recognized. The majority of this article assumes that EMS is called after the fact, and the symptoms are severe. However, this information is also of use to those providers who transfer SCI patients to prevent the development of AD caused by inadvertent stimulus. Incidence and epidemiology: AD typically occurs in approximately 85% of patient’s with spinal cord injuries above T- 5 (although some cases of T-10 injured patient’s with AD have been reported).2 While more men than women sustain SCI, this is mainly due to lifestyle and risk-taking behaviors. Once a cord injury occurs, there is no difference between the occurrence of AD based on gender, age, or race. Spinal Cord Injury itself was first discussed in a surgical papyrus dated over 5000 years ago.3 It described two cases of high cord injury (AKA: Quadriplegia or Tetraplegia) as an “ailment not to be treated”. Until the advent of modern medicine, however, these patients seldom survived more than a few weeks. This has changed, with a typical patient surviving his injury for many, many years. With this ever-increasing life span, more and more conditions and complications of SCI are being discovered and managed. AD is one of these conditions. 1
  • 2. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P AD was first reported in modern medical literature in 1890, and has presumably been present for as long as there have been a spinal cord injured patient, although prior to the advent of modern medicine the lifespan of these patients was probably very short.4 Fortunately, prevention, patient education, and home health care greatly reduce the field presentation of this syndrome. In fact many patients encountered may be more familiar with this condition than most health care providers. Basic Pathophysiology of Autonomic Dysreflexia AD is essentially a dysfunction between two components of the Autonomic Nervous System , the Sympathetic Autonomic Nervous System and Para-sympathetic Autonomic Nervous system, with effects across multiple body systems. In order to better understand the dysfunction, we must discuss the normal interaction of the CNS and PNS, and its components. Relevant Anatomy The two largest divisions of the nervous system are the Central Nervous System (CNS) and the Peripheral Nervous System (PNS) . The CNS is made up of the brain and the spinal cord, while the PNS is pretty much everything else. The bridge between the CNS and the PNS are the 12 cranial nerves, and numerous spinous nerves. Overview of the Nervous System While we mainly think of the PNS as sensory and somatic in nature, it also has important autonomic functions as well. The autonomic portion of the PNS is known as the Autonomic Nervous System (ANS), and is responsible for sending impulses to various important organs in the body from the CNS, but not for receiving them5 . In fact, there is very little “feed back” from these organs to the autonomic PNS, this is handled through other mechanisms. An exception to this are the baroreceptors and chemoreceptors in the carotid sinus and aortic arch. These are important in the control of heart rate, blood pressure and respiratory activity. 2 ©2007, Robert S. Cole, All rights reserved
  • 3. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P The two branches of the autonomic PNS are the Sympathetic Autonomic Nervous System (SANS) and the Parasympathetic Autonomic Nervous System (PANS). It is these two components of the PNS that are responsible for AD. The SANS, also called the adrenergic nervous system, is responsible for the “Fight or Flight” response. Simply put, it is responsible for calling on the resources of the body for survival. Important chemical agents of the SANS include Epinephrine and Nor- epinephrine, and to a lesser degree, dopamine. Everyday autonomic control of blood pressure, vasoconstriction, and heart rate come from the brain and high cord. Sympathetic response can also be triggered by noxious stimuli of the distal sensory (pain, pressure, etc) nerves, without “permission” from the rest of central nervous system. Many of the symptoms of AD are directly related to stimulation of the SANS by noxious (painful) stimuli. Most of the SANS nerve branches come directly off the spinal cord in the cervical, thoracic, and lumbar regions. KEY POINT Many of the symptoms of Autonomic Dysreflexia (AD) are directly related to stimulation of the Sympathetic Adrenergic Nervous System by noxious stimuli. The PANS is responsible for mediating and buffering the SANS. Known as the “Feed and Breed” response it is responsible for the preservation and restoration of energy. Therefore it often has an opposite effect of the SANS, and suppresses or buffers its sympathetic effects on many organs. Its primary chemical agent is acetylcholine (Ach), and thus the PANS is sometimes referred to as the cholinergic nervous system. Other important chemical agents are muscarine and nicotine. KEY POINT The Para-sympathetic Autonomic Nervous System will often mediate, suppress, or otherwise buffer the effects of the Sympathetic Autonomic Nervous System on many of the body’s systems. The PANS originates from two areas: Primary, the nerves that supply the organs of the abdomen, heart, lungs, and skin above the waist begin at the level of the brain and very high spinal cord (cranial nerves III, VII, IX and X). (The most important of these is the tenth (X) cranial nerve, the Vagus nerve. This nerve directly affects heart rate during AD, and will be discussed later.) And secondarily, the nerves that supply the reproductive organs, pelvis, and leg begin at the sacral level. 3 ©2007, Robert S. Cole, All rights reserved
  • 4. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P Table: Comparing The Sympathetic And Para-Sympathetic Autonomic Nervous Systems. Organ Sympathetic Stimulation Parasympathetic Stimulation Heart Increased heart rate beta1 (& beta2) Decreased heart rate Increased force of contraction beta1 (& beta2) Decreased force of contraction Increased conduction velocity Decreased conduction velocity Arteries Constriction (alpha1) Dilation Dilation (beta2) Veins Constriction (alpha1) Dilation (beta2) Lungs Bronchial muscle relaxation (beta2) Bronchial muscle contraction Increased bronchial gland secretions Gastro- intestinal tract Decreased motility (beta2) Increased motility Contraction of sphincters (alpha) Relaxation of sphincters Liver Glycogenolysis (beta2 & alpha) Glycogen synthesisGluconeogenesis (beta2 & alpha) Lipolysis (beta2 & alpha) Kidney Renin secretion (beta2) Bladder Detrusor relaxation (beta2) Detrusor contraction Contraction of sphincter (alpha) Relaxation of sphincter Uterus Contraction of pregnant uterus (alpha) There are very few para-sympathetic receptors in the uterusRelaxation of pregnant and non- pregnant uterus (beta2) Eye Dilates pupil (alpha) Constricts pupil Increased lacrimal gland secretions Submandibular & parotid glands Viscous salivary secretions (alpha) Watery salivary secretions 4 ©2007, Robert S. Cole, All rights reserved
  • 5. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P When one nervous system becomes two As discussed earlier, normally the SANS and the PANS work together to maintain a balance in the body, and to facilitate vital functions. However, in a cord-injured patient, this synergy no longer occurs. When a patient has a cord injury above T-6, typically the moderating effects of the PANS on the SANS are inhibited. Simply put, the impulses from the brain to the PANS to trigger a para-sympathetic response are interrupted through-out most of the PANS. Remember that the PANS originates in the brain and is controlled through a number of the cranial nerves (with the exception of some nervous function in the sacrum). After a spinal cord injury, the parasympathetic nerves that begin at the brain continue to work, even during the phase of spinal shock. When AD occurs, the parasympathetic nerves attempt to control rapidly increasing blood pressure by slowing down the heart. By contrast the SANS originates and is controlled mainly from the spinal cord (T1 through L2). While the SCI will inhibit the SANS response to everyday control of blood pressure, heart rate, and similar vegetative functions (which arise from the brain and high cord), it does not effect the SANS response to noxious stimuli (which come from distal sensory nerves). This is why the SCI patient will develop chronic hypotension, and be prone to orthostatic changes (resulting from poor autonomic control) yet can still have a significant hypertensive response (from the SANS below the point of injury) to even mild noxious stimuli. KEY POINT Normally the SCI patient lives with chronic hypotension due to lack of autonomic control. This changes with noxious stimulation, which stimulates the SANS and causes hypertension. Therefore, when a cord injury occurs, the parasympathetic response is partially inhibited while the sympathetic response largely is not. The higher the cord injury, the more SANS is affected in this way. KEY POINT When the Para-sympathetic Autonomic Nervous System is interrupted or inhibited by a cord injury, the Sympathetic Autonomic System is unopposed. 5 ©2007, Robert S. Cole, All rights reserved
  • 6. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P So What Is Autonomic Dysreflexia? AD occurs after the acute phase of the injury to the spinal chord, typically about a week. It occurs most commonly and unpredictably within the first year of the injury. As discussed in detail earlier in this article, it is the PANS and the SANS that are of most importance in AD. Simply put, the SANS causes most of the life threatening symptoms, while the PANS is responsible for many other signs. In the normal non-SCI pt, when a painful/noxious stimulus occurs, the SANS is activated and the “Fight or Flight” response is directly stimulated. The blood pressure raises, the heart rate increases, and peristalsis decreases (as a result of vasoconstriction in the gut). Norepinephrine, Epinephrine, and Dopamine are released. The PANS would ideally mediate this response, doing so with mechanisms of its own. It directly mediates the sympathetic response by slowing the heart rate (thus the associated bradycardia with AD) and vasodilatation. In the normal patient this happens every day to a variety of stimuli, and due to the constant balancing act of homeostasis we often never notice a difference. In the SCI pt however, the site of injury prohibits free movement of parasympathetic responses. Thus as the SANS is activated, the massive vasculature in the body in general and the gut in particular vasoconstict, raising the blood pressure (most of the S/S in AD are directly related to this auto transfusion of blood or to the resultant hypertension). The SANS essentially has free rein, with the parasympathetic impulses blocked at the level of SCI. KEY POINT Most of the symptoms of autonomic dysreflexia are related to sympathetic- induced vasoconstriction and related hypertension. Therefore vasodilators play an important role in treatment of refractory AD. Often the only mediating response remaining in SCI is bradycardia (secondary to stimulation of the vagus nerve) and general vasodilatation above the injury (causing the sweating, nasal stuffiness, and flushed appearance) while the SANS causes its effects below the level of SCI. These remaining PANS impulses are usually inadequate to combat the work of the SANS. 6 ©2007, Robert S. Cole, All rights reserved
  • 7. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P KEY POINT When AD occurs, the parasympathetic nerves attempt to control rapidly increasing blood pressure by slowing down the heart. This is often the only significant means remaining to the PANS to combat AD. Therefore the relative hypertension of autonomic dysreflxia is often accompanied by bradycardia instead of sympathetic induced tachycardia. Signs and Symptoms of Autonomic Dysreflexia As mentioned, most of the symptoms of AD are related to unmediated sympathetic response to noxious stimuli, specifically hypertension and vasoconstriction. It is useful to think that these s/s share much in common with hypertensive crisis and eclampsia, although similar to eclampsia, relative hypertension is as dangerous as actual hypertension. KEY POINT AD shares many common symptoms with PIH/eclampsia and hypertensive crisis, although the treatments differ. Common Presentations: • Hypertension: Significant increase in both systolic and diastolic pressures usually associated with bradycardia. Blood pressure may be much greater than 200/100, however remember that a SCI pt may normally have a systolic BP as low as 90 mm Hg, so an increase in 30-40 mm Hg above this may be a warning sign. Most clinical guidelines agree to a blood pressure threshold of 150 mm hg for severe cases requiring aggressive treatment, although s/s can occur at lower pressures. Blood pressures should be done in a sitting or simi-fowlers position when possible for an accurate assessment of AD. • Pounding headache (secondary to both sympathetic induced hypertension and para-sympathetic vasodilatation) • Flushed (reddened) face (secondary to vasodilatation) • Red blotches/flushed appearance to the skin above level of spinal injury (secondary to vasodilatation) • Sweating above level of spinal injury (secondary to vasodilatation) • Nasal stuffiness (secondary to vasodilatation) 7 ©2007, Robert S. Cole, All rights reserved
  • 8. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P • Nausea (secondary to vagal/parasympathetic stimulation) • Blurred Vision/Visual disturbances. • Bradycardia - slow pulse <60 beats per minute - (secondary to Vagal parasympathetic stimulation) • Signs of Congestive Heart Failure secondary to the hypertension. • Piloerection ("goose bumps") : These can occure above or below the level of injury. • Cold, clammy skin below level of spinal injury KEY POINT When assessing for autonomic dysreflexia, blood pressures should typically be taken in a semi-fowlers or sitting position rather than laying flat. In addition, a blood pressure threshold of 150 mm Hg systolic is typically required prior to aggressive (pharmacological) treatment. . Treatment and Care First line treatment in AD is addressing underlying causes. Simply put: remove the noxious stimuli and the sympathetic response will subside. KEY POINT First line treatment of AD is to remove the underlying noxious stimuli. This should be attempted prior to pharmacological therapy in all but the most severe cases. To understand the causes, one must understand that while SCI pts have had to adapt to serious lifestyle changes, most still try to live as much of a normal life as possible. They undergo training to have regular bowel and bladder habits using “Quick Caths” and digital removal of stool (consider the alternative to these programs before laughing), they can have sexual intercourse, and even become pregnant. They are still subject to life’s daily functions, like menstrual cycles (and cramps), ulcers, and other illness. Remember that they may not be able to “feel” the pain, but that doesn’t mean that the injury /condition is not painful at the neurological level. All of these activities and/or illness can lead to AD. KEY POINT The most common cause of AD is catheter problems and bowel/bladder issues. Pressure sores and skin related discomfort are often causes as well. 8 ©2007, Robert S. Cole, All rights reserved
  • 9. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P Any stimuli that would be uncomfortable to a non-SCI patient could cause AD. The most common causes of AD are either a catheter/bladder problem and/or a bowel impaction. These are often due to a noncompliance with a bowel/bladder program, but may be secondary to an equipment malfunction. Another common cause is skin breakdown and discomfort. In general however ANY stimuli that would potentially cause pain and discomfort to a normal person may be considered suspect. A summarized list includes: • Bladder (most common) - from overstretch or irritation of bladder wall o Urinary tract infection o Kidney Stones o Urinary retention o Blocked catheter o Overfilled collection bag o Non-compliance with intermittent catheterization (Quick Cath) program • Bowel - over distention or irritation o Constipation / impaction o Distention or discomfort during bowel program/digital stimulation. o Hemorrhoids or anal fissures o Infection or irritation (e.g. appendicitis, cellulitis) • Skin-related Disorders o Any direct irritant below the level of injury (e.g. - prolonged pressure by object in shoe or chair, cut, bruise, abrasion) o Pressure sores (decubitus ulcer) o Ingrown toenails o Burns (e.g. - sunburn, burns from using hot water) o Tight or restrictive clothing or pressure to skin from sitting on wrinkled clothing • Sexual Activity o Over stimulation during sexual activity [stimuli to the pelvic region which would ordinarily be painful if sensation were present] o Ejaculation o Menstrual cramps • Other o Heterotopic ossification ("Myositis ossificans", "Heterotopic bone") o Acute abdominal conditions (gastric ulcer, colitis, peritonitis) o Skeletal fractures o Invasive procedures o Contact against hard/sharp objects o Pulmonary Emboli 9 ©2007, Robert S. Cole, All rights reserved
  • 10. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P o Deep Vein Thrombosis Basic treatment The general concept of treatment is first to identify the cause and if possible, eliminate the noxious stimulus. This often will rapidly resolve the problem. If however the cause can either not be identified or not be treated in the field, the more aggressive measures are called for. KEY POINT Removing the cause of the noxious stimuli will often resolve the problem rapidly. Loosen all constricting/restricting clothing wherever possible. A simple bunched up or constricting belt line can precipitate AD. Identify and remove the offending stimulus whenever possible. Often, this alone is successful in allowing the syndrome to subside without need for pharmacological intervention. It is also good for the person with the symptoms to be sitting up with frequent blood pressure checks until the episode has resolved. Suspected cause = bladder? Check catheter - remove kinks if found, empty urinary collection bag, irrigate catheter. If catheter is not draining, replace it immediately. If an intermittent catheterization program is in place, a straight catheterization should be performed immediately with slow drainage to prevent bladder spasms. If this is unsuccessful, consider flushing the catheter, or outright replacement. Use an anesthetic ointment to suppress the noxious stimulus, if available. The patient, home health aids, or family are often able to assist with this. Suspected cause = bowel? Unless a provider is experienced in digital removal of feces it should not be attempted as the AD can be aggravated. If episode occurred during digital stimulation/bowel evacuation, often stopping stimulation will allow symptoms to subside. Consider use of a prescribed anesthetic ointment to suppress the noxious stimulus, if available. If the issue is impacted stool, disimpact if feasible. If it occurs while doing a bowel program in bed, try commode-based bowel evacuation. Consider use of abdominal massage instead of digital stimulation. Suspected cause = skin? Loosen clothing. Check for source of potential offending stimulus - check for pressure sores to the back, heels, sacral area, toenail problems, soles of the feet. Routine assessment and management: Repeated V/S every 5 minutes may be indicated to observe for fluctuations and rebound hypertension. Elevate head 30-45 degrees. Similar to care in CVA and hypertensive crisis, this promotes venous drainage and decreases ICP related effects. In addition placing the 10 ©2007, Robert S. Cole, All rights reserved
  • 11. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P patient in a semi-fowlers position or higher may cause small reduction in the blood pressure. Pharmacological Therapies The general concept of treatment is first to identify the cause and if possible, eliminate the noxious stimulus. This often will rapidly resolve the problem. If however the cause can either not be identified or not be treated in the field, the more aggressive measures are called for. KEY POINT If the cause can not be identified, not treated in the field, or if removing the noxious stimuli is unsuccessful, then more aggressive treatments are needed. This usually means pharmacological intervention. Current clinical guidelines recommend a blood pressure threshold of 150 mm Hg systolic prior to considering aggressive pharmacological treatment (basic measures can be initiated at anytime however). Most therapies are focused on addressing vasoconstriction and hypertension rather than blunting sympathetic response. Pre-hospital EMS usually is limited to nitrates in their available drugs to treat AD, however the patient will often have his preferred pharmacological treatment with him. Frequently, either poor motor function or rapid progression of the AD prevents the patient from self medicating without assistance. While Nitrates are effective, use of the patients own medication should be strongly considered. When possible, contact medical control for guidance. Common pharmacological interventions are discussed below: Calcium Channel Blockers: Ca Channel Blockers are potent vasodilators. One of the more common (and effective) ones is Procardia. • Procardia 10 mg sublingual, may be repeated in 10-60 minutes. 11 ©2007, Robert S. Cole, All rights reserved
  • 12. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P Nitrates: Nitrates are effective, short acting, and relatively simple vasodilators. • NTG 0.4 mg sublingual every 3-5 minutes • NTG Paste 1 inch to non-hairy area of chest. Vasodilators: Hydralazine is a potent vasodilatator with little cardiac effects. It tends to last approximately 12 hours, so its effects may last longer than the AD episode. • Hydralazine 10-20 mg PO/IV/IM Alpha-2 adrenergic blockers: The most common of these is Clonidine. Clonidine is used both acutely for AD symptoms, and chronically for prevention. • Clonidine 0.1 mg to 0.2 mg p.o. Lidocaine based Lubricant: In the event that a catheter has to be replaced, or that the patient, family, or EMS may be placing a catheter, it is recommended that a 2% Lidocaine lubricant (such as commonly used during endotracheal intubation) be used instead of the more common water based lubricants without Lidocaine. In addition if digital dis-impaction is to be performed, then a lidocaine containing lubricant may be desired as well. Lidocaine should reduce the noxious stimulation to the SANS, reducing sympathetic response to the procedure. When used the Lidocaine lubricant should be allowed to “soak” for about 5 minutes prior to the procedure to achieve maximum effect. AD and Pregnancy Quite a few SCI injured patients go on to live a relatively normal life after the initial injury. This includes holding a job, enjoying many recreational activities, and even having children. Unfortunately, there is very little research into the field of SCI and pregnancy, and even less on proper management of AD in this situation. This is complicated by the number of pregnancy induced hypertension (PIH) disorders that can occur in pregnancy. About two thirds of pregnant SCI patients will develop AD during labor and delivery. False labor, as well as other painful conditions (like abrupted placenta) can precipitate AD. Complicating this is that PIH/eclampsia may be mistaken for AD, and visa versa. This is especially troublesome since while the s/s are similar, the treatment is different. Usually, other than urine screening, angioedema and history are the most important methods to tell the difference when determine treatment, but when possible medical control should be consulted. KEY POINT AD is often difficult to discern from PIH/Eclampsia in the SCI pregnant patient. All such patients should be transported for further evaluation, regardless if symptoms and suspected causes are resolved. 12 ©2007, Robert S. Cole, All rights reserved
  • 13. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P When Has AD Resolved? The primary indicator of the resolution of AD is absence of the primary c/c, such as headache, stuffy nose, blurred vision, etc. Ideally the cause of the AD would have been identified. In addition, the blood pressure should have returned to baseline (typically 90- 110 mm/hg in a quadriplegic patient who is sitting up). Finally, the heart rate should have returned to normal (no bradycardia).As discussed earlier, the patient must maintain this for at least 2 hours. KEY POINT End points for resolution of AD are: - Asymptomatic for 2 hours - Systolic Blood pressure returned to baseline (typically 90-110 mm Hg) - No bradycardia - The cause of the noxious stimuli has been identified Occasionally, after a noxious stimuli has been resolved, or if a medication proves too effective, a symptomatic hypotension may develop. This hypotension is usually transient. If needed, this can usually be treated by simply laying the patient supine. Further treatment, such as fluid boluses or vasopressors, are unlikely to be needed. Treat and Release Considerations Often, if AD is rapidly resolved, the patient will feel comfortable in remaining at home under the care of his home health service and family. This is complicated by both the patients and the family having both experience and a stronger knowledge base in AD than many health care providers who do not routinely deal with SCI (like EMS). Currently clinical guidelines recommend that the patient who has suffered an episode of AD be observed for at least 2 hours prior to release. In addition to monitoring for rebound hypertension, a screening would be done to evaluate potential causes and complications. Most of these evaluations are beyond the capability of EMS services. KEY POINT Observation is recommended for at least two hours post AD, to observe for recurrent hypertension. Therefore transport is strongly encouraged. Still, many patients and families will want to decline transport. Assuming that the patient has the legal and mental capacity to do so, such cases should always be against medical advice (AMA) and accompanied by a tactful explanation of risks and need for further evaluation. Document thoroughly. 13 ©2007, Robert S. Cole, All rights reserved
  • 14. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P In addition, EMS should attempt to ensure that the patent is accompanied in the presence of a responsible party who can assist him if his AD should recur. EMS should also offer to contact the patient’s home health service, or otherwise facilitate his personal medical care, prior to release. Routine Transport of the SCI patient. Most of this article has focused on treatment of AD after it has begun. It is worth mentioning the importance of preventing AD during a routine patient contact. Probably the single most important consideration is simple catheter care. Laying on a narrow uncomfortable cot, covered by blankets and sheets, amid the everyday distractions of even routine transport, it is a simple thing for an SCI patient to have his catheter kinked, elevated to allow back flow of urine, or even tugged. Special care should be taken to allow the catheter to drain freely, remain secure, and not place tension on the catheter itself. If the patient routinely straight caths himself, accommodations should be made to allow the patient to do this to prevent bladder distention and/or UTIs. Patient position on the cot is also of importance. Don’t allow clothes to constrict pt. Don’t allow clothes or linen to wad up under the pt. Keep the patient off of pressure sores as much as feasible. Over long transports (30 minute to an hour) turn the pt from one side to another (use pillows) to prevent pressure sores. Summary Autonomic Dysreflexia can have devastating, even fatal, effects on the pt., ranging from stroke to death. However, when treated quickly and appropriately, the pt. may have no long-term consequences. Therefore, education of patients, caregivers, and healthcare providers is imperative. This syndrome occurs suddenly and treating it must be given a priority. AD is a medical Emergency, addressing it must be a priority. Autonomic Dysreflexia can occur anytime after spinal shock has been resolved and can occur anytime after discharge. Pt’s may seek medical help at any emergency room or through any EMS. Furthermore Pt’s may present with this disorder during routine medical transport or contact for unrelated reasons. Therefore, it is important that all healthcare professionals, not just those who work with clients with SCI, become aware of this disease process. 14 ©2007, Robert S. Cole, All rights reserved
  • 15. Autonomic Dysreflexia : An Overview for EMS personnel By Robert S. Cole, CCEMT-P References 15 ©2007, Robert S. Cole, All rights reserved
  • 16. 1 Travers, Patricia L.. "Autonomic Dysreflexia: A Clinical Rehabilitation Problem." (1999) 29 MAR 2007 <>. 2 "Other Complications Of Spinal Cord Injury: Autonomic Dysreflexia (Hyperreflexia)." RehabSite. 1998. Louis Calder Memorial Library of the University of Miami/Jackson Memorial Medical Center. 29 Mar 2007 <>. 3 Consortium for Spinal Cord Medicine, "Acute Management of Autonomic Dysreflexia: Adults with Spinal Cord Injury Presenting to Health-Care Facilities." Clinical Practice Guidelines 2nd editionJul 2001 29 MAR 2007 <>. 4 Campagnolo, Denise I. "Autonomic Dysreflexia in Spinal Cord Injury." 05 OCT 2006. 29 Mar 2007 <>. 5 Bakewell, S.. "The Autonomic Nervous System ." Update in Anesthesia Issue 5, Article 6(1995) 1-2. 29 MAR 2007 <>.