The World Health Organization (2013) estimated that some 250 000–500 000 people sustain a spinal cord injury every year, and Aspire (2019) estimated that 2500 of these cases occur in the UK. As many as 90% of patients with injuries above the 6th thoracic vertebrae, are susceptible to autonomic dysreflexia (AD) (Allen and Leslie, 2019). These patients live in the community with varying levels of independence and support. Most will have contact with community nurses due to potential issues with bladder and bowel management and, therefore, community nurses may come into contact with patients in a dysreflexia crisis, which is an acute medical emergency requiring prompt treatment or emergency transfer to secondary care. The aim of this paper is to develop and enhance community nurses' understanding of the care and management of autonomic dysreflexia.
Jordan et al (2016) defined AD as an episodic uncontrolled elevation of systolic blood pressure of more than 20 mmHg, accompanied sometimes by a resulting bradycardia. If hypertension is not managed in individuals affected by AD, it can lead to cerebral and spinal haemorrhage, seizures and pulmonary oedema (Alexander et al, 2011). AD often presents itself in the chronic phase of spinal cord injury, most often 3–6 months after the initial injury (Lindan et al, 1980). AD is a medical emergency that community nurses need to identify and react to quickly to prevent further complications.
Pathophysiology of autonomic dysreflexia
When a person sustains a spinal cord injury (Figure 1), all autonomic nerve function below the injury stops (Norris, 2020). Essentially, AD is caused by a disruption to the autonomic nervous system at T6 or above (Figure 2). The higher the level of injury, the more intense are the effects on circulation and thermoregulation, and individuals with an injury at this level also have difficulties in regulating vasomotor tone due to the loss of central nervous system control of spinal reflexes (Norris, 2020). The autonomic nervous system (ANS) enables the body to maintain homeostasis by monitoring and regulating the body's internal environment (Pete and Nair, 2017). The ANS regulates cardiac and smooth muscle activity as well as endocrine secretions, ensuring a homeostatic environment is maintained, often via a negative feedback system (Montague et al, 2005). The ANS is divided into two branches: the sympathetic and parasympathetic nervous systems (Waugh and Grant, 2014). Sympathetic stimulation prepares the body to deal with stressful situations, which in turn causes the adrenal glands to secrete the hormones adrenalin and norepinephrine (Waugh and Grant, 2014), which sustains the effect of sympathetic stimulation. However, parasympathetic activation has a tendency to slow down cardiac and respiratory activity (Pete and Nair, 2017). In healthy individuals, the systems function together to maintain a physiological balance of heart rate, blood pressure and respiration rate.
Figure 1. Dorsal and lateral views of the human spinal cord 
Figure 2. Spinal cord injury
As its name suggests, AD is a condition resulting from autonomic dysfunction (Essat, 2003). Spinal reflexes remain intact despite the spinal cord damage, but noxious stimuli below the level of injury cause a generalised sympathetic response and the release of noradrenaline and dopamine (Bauman et al, 2012). This results in vasoconstriction below the level of injury (Essat, 2003). Bauman (2012) showed how lesions above T6 cause constriction of critical mass blood vessels, including those of the splanchnic vascular bed, causing hypertension.
In normal physiology, descending brain stem inhibitory pathways would respond to a rise in blood pressure, but, in patients with spinal cord injuries, such signals are prevented from descending into the sympathetic chain (Blackmer, 2003). As a consequence, peripheral and splanchnic vasoconstriction occurs, causing the classical hypertension seen in AD. The disruption to the sympathetic activity on the cardiovascular system leads to a consistently low resting blood pressure and orthostatic hypotension in such patients (Sachdeva et al, 2019); a resting systolic blood pressure of 90 mmHg is normal for a patient with a high spinal cord injury (Walters et al, 2013), and a reading of 120/80 mmHg that is seemingly normal in the adult population is considered elevated in patients with spinal cord injury (Blackmer, 2003). The only parasympathetic response in AD is baroreceptor activation of the vagus nerve, causing bradycardia and vasodilation above the level of injury (Bhatt et al, 2016). This is thought to cause the classical head and neck flushing and sweating alongside nasal congestion seen in AD (Bycroft et al, 2005). In spinal cord injury, the two branches of the sympathetic nervous system and their complex feedback loops are interrupted, resulting in the potentially serious episodes of AD (Blackmer, 2003). Box 1 lists the main symptoms of AD.
Box 1.Symptoms of AD
- Elevated blood pressure
- Pounding headache
- Bradycardia
- Profuse sweating above the level of injury
- Goose bumps above or possibly below the level of injury
- Cardiac arrhythmias
- Flushing of the skin Blurred vision
- Nasal congestion
(adapted from Spinal Cord Medicine, 2011)
Causes of autonomic dysreflexia
AD is triggered by a noxious stimulus below the level of injury (Squair et al, 2016). From the viewpoint of community nurses, the most common causes of AD are urinary triggers (Royal National Orthopaedic Hospital NHS Trust, 2013), such as blocked or full catheter drainage bags. Krassioukov (2009) reported that one of the main cause of AD is bladder distention. Blocked or kinked catheters and lack of frequent self-catheterisation in patients (Squair et al, 2016) can result in AD episodes. Other urinary causes could be testicular torsion or renal calculi and abdominal distention from faecal loading (Rabchevsky and Kitzman, 2011). Thus, vigorous monitoring of patients' bowel habits is imperative. Patients living in the community who require bowel care will often need the support and intervention of community nursing teams, and indeed may be well known to them. It is important, therefore, that bowel management regimes are clearly documented within patient's notes. Other common causes of AD are fractured bones, pressure ulcers, ingrowing toe nails and menstruation (Brown et al, 2017).
Nurses working within community settings should also be alert to pregnant women with spinal cord injury presenting with symptoms of AD, as some clinical features make the distinction between pre-eclampsia and AD difficult. However, pre-eclampsia usually does not manifest until after 24 weeks of gestation (Spinal Cord Medicine, 2001). If the trigger for the episode of AD is not identified quickly, then the patient should be immediately transferred to hospital, due to the severity of the condition if left untreated.
As AD is an acute medical emergency, rapid patient assessment is required in order to safely manage and treat the deteriorating patient. This lends itself to the ABCDE assessment advocated by the Resuscitation Council (2012). ABCDE is a quick assessment tool that can be used within the community to assess rapidly deteriorating patients, such as those with AD.
Airway
Although it is unlikely that a patient in a dysreflexic crisis will present initially with an airway compromise, untreated airway problems may lead to hypoxia and eventually cardiac arrest if untreated (Resuscitation Council, 2012). In most cases, simple airway manoeuvres, such as head tilt or chin lift, are sufficient. Any patient presenting with potential airway compromise in the community should be transferred to secondary care without delay.
Breathing
A look, listen and feel approach should be adopted regarding breathing. The rate, rhythm and depth of respiration along with oxygen saturations should also be noted and documented on NEWS2 charts (Royal College of General Physicians, 2012). At this point, it should be noted that patients with high spinal cord injuries may have altered patterns of breathing due to the spinal injury. It is, therefore, imperative that comprehensive assessments are made for such patients when taken onto the community nursing teams case load. Calder et al (2009) identified pulmonary oedema as a recognised complication of AD, and patients also present with dyspnoea and hypoxia.
Circulation
This will be the most commonly identified symptom of an AD crisis in patients. Physical signs manifested in acute episodes of AD include hypertension (a sustained increase in systolic blood pressure of 20 mmHg) and reflex bradycardia, which is common, although tachycardia has also been reported (Eldahan and Rabchevsky, 2018). Patients experiencing acute attacks of AD will often complain of a pounding headache alongside the previously mentioned neck and head flushing above the level of injury; some patients also report blurred vision (Blackmer, 2003). The rapid rise in blood pressure can lead to an increase in intracranial pressure, causing seizures and intracranial haemorrhage (Essat, 2003; Agency for Clinical Innovation (ACI), 2014). Less common symptoms are aphasia, convulsions, dyspnoea and potentially coma (Cowan, 2015). Again, it is important to identify patients' normal blood pressure values. Often, patients in AD crisis will not score on NEWS2 as their blood pressure is around 20 mmHg lower than the general population (Popa, 2010). As previously mentioned, a systolic blood pressure of 90 mmHg is normal for patients with spinal lesions at T6 and above (Walters et al, 2013). Community nurses will be familiar with patients on their case load and should be alerted to a raise in systolic blood pressure of more than 20 mmHg compared with their usual reading in patients predisposed to AD or new patients with an existing injury above T6.
Disability
Tools such as Alert, Voice, Pain, Unresponsive (AVPU) and Glasgow Coma Scale (GCS) should be used to assess the patients' responsiveness (Soar et al, 2015). If untreated, AD can lead to an increase in systolic blood pressure to above 180 mmHg (Phillips and Krassioukov, 2015), which can lead to a rise in intracranial pressure causing seizures and intracranial haemorrhage (Essat, 2003; ACI, 2014). In this instance, community nurses need to ensure rapid transfer to definitive care.
Exposure
This final stage in the patient assessment may help to identify the noxious stimulus causing the episode of AD. A head-to-toe examination of the patient should be undertaken, and their temperature should be checked. A distended abdomen may indicate constipation or a blocked catheter (Ozisler et al, 2015), both of which are common causes of AD; pressure ulcers and ingrowing toe nails may also be noted at this point as potential AD triggers. Skin temperature changes may also be noted; as previously discussed, persistent hypertension and vasoconstriction cause the skin below the injury to become cold and mottled, while vasodilation causes flushing above the level of injury. A systematic assessment approach aims to identify a cause for AD and enable the community nurse to act swiftly to identify and manage AD symptoms or arrange transfer to secondary care as required.
Treatment of AD
As with most medical conditions, early detection and treatment by the community nurse is imperative, and, in most cases, will avoid hospital admission. Failure to treat promptly can lead to sever hypotension leading to cerebral or subarachnoid haemorrhage (Blackmer, 2003). It is imperative that any assessment takes place rapidly, and, if the noxious stimulus is not identified by the community nurse, an immediate 999 transfer to hospital should be arranged. Due to the nature of AD, patients may experience repeated episodes (Jordan et al, 2016) and may be well known to community teams.
Management of AD may require both pharmacological and non-pharmacological interventions (Rabchevsky and Kitzman, 2011; Squair et al, 2016). The taking of a comprehensive history from the patient or carer by the community nurse is imperative to elicit a clinical history and ascertain the patient's risk and likely cause of AD. In many cases, non-pharmacological interventions in the community setting will resolve the AD attack, especially if the hypertension is not severe (Jackson and Acland, 2010). Initial emergency management should include sitting the patient up (Rabchevsky and Kitzman, 2011; Squair et al, 2016), which initiates an orthostatic drop in blood pressure (Cowan, 2015). This can, in itself, be quite stressful for individuals with spinal cord injury due to a disrupted supraspinal regulation of blood vessel tone (Jordan, 2016). Any tight or restrictive clothing should be removed (ACI, 2014). Often, the removal of the noxious stimuli is enough to eliminate the AD response. Rabchevsky and Kitzman (2011) report that, when the bladder is drained, symptomatic hypertension is often alleviated in patients with AD. Identifying and removing the noxious stimuli should be a priority. The catheter drainage bag should be checked, and if it is empty, the patient should be asked as to when it was last emptied. In many cases, draining urinary catheter bags resolves the AD crisis. The catheters should be checked for kinks and blockages, and any bladder or abdominal distention should be checked for. The patient should be questioned about their bowel care and when the bowels were last emptied. If necessary, bowel care should be administered. Other causes previously discussed are ingrowing toe nails, pressure ulcers and lacerations; therefore, a general inspection of the patient's skin should also be undertaken (Squair et al, 2016). If pressure damage is detected, a swab sample should be taken and underlying infection, if any, should be addressed. Vital signs should be monitored frequently at this stage, as, if blood pressure continues to rise, medical management may be required (Rabchevsky and Kitzman, 2011), and the appropriate secondary care will, therefore, be necessary.
Blackmer (2003) suggested that a systolic blood pressure of 150 mmHg should prompt pharmacological management. Pharmacological management is vital in patients with profound hypertension. Nitrates are commonly administered for AD, causing smooth muscle relaxation due to the release of nitric oxide (Eldahan and Rabchevsky, 2017); 2% nitro-glycerine paste can be applied to the skin above the level of the spinal cord injury, or sublingual and transdermal patches can also be used. ACI (2014) advocated a single spray of glyceryl trinitrate 400 μg from a nitrolingual pump. Blood pressure should be monitored and, if there is little or no effect in 5–10 minutes, a second spray should be administered. Up to three doses can be administered in 30 minutes, but if the blood pressure remains elevated, intravenous medication should be considered (ACI, 2014). Again, patients requiring repeated doses of glyceryl trinitrate should be transferred into secondary care for ongoing management. Blackmer (2003) highlighted that many male patients with spinal cord injury are also prescribed sildenafil for erectile dysfunction, and the use of nitrates is contraindicated in such patients. This highlights the need for robust history-taking.
Nifedipine is another common treatment for AD, and 5–10 mg is recommended by the National Spinal injuries centre (2013). Reduction in blood pressure is achieved with calcium channel blockers, which reduces peripheral resistance by preventing the influx of calcium into the smooth muscles of the vascular system. If glyceryl trinitrate is contraindicated or medication for erectile dysfunction has been taken within 24 hours, alternative medication such as 25 mg sublingual captopril can also be used (ACI, 2014).
Other pharmacological interventions may include botulinum toxin injections to prevent bladder spasms (Krassioukov et al, 2009) and intrathecal baclofen, which reduces muscle spasm (Kolfer et al, 2009). It is advisable that any patient requiring medication to reverse their AD crisis is assessed in secondary care.
Patients known to community teams with recurrent AD attacks may have an emergency treatment box to allow community teams to treat AD symptoms pharmacologically at home and reduce the need for hospital admissions. It should be noted that this should only be done in conjunction with regional spinal injury centres.
Patient with recurrent AD should also be taught self-management techniques so that their symptoms can be alleviated promptly without the need for medical intervention. Patients should be taught how to manage their bladder and bowel care and when community nursing teams should be called to offer further support and management, thus alleviating some of the common causes of AD. Further, their skin should be regularly checked for pressure damage and broken areas. Patients should also be encouraged to carry medical alert cards, making rapid diagnosis possible for community nurses. Patient education is a vital component of long-term management of this condition (Essat, 2003), as they are then empowered to act proactively to avoid complications. Community nurses caring for patients with spinal cord injuries should be actively encourage to liaise with their local spinal injuries centre, which are an extremely useful resource for nurses to access support in order develop confidence and competence in caring for these patients.
Conclusion
AD is a poorly understood condition affecting many patients with both complete and incomplete spinal cord transection above the level of T6. Because of the normal physiological functioning of patients with spinal cord injuries, a rise in blood pressure and pulse will often not trigger a response on NEWS2 charts. If AD is suspected in community care settings, close monitoring of vital signs should be initiated, along with identifying and eliminating the cause of the noxious stimuli. Non-pharmacological measures have been universally identified as the first-line treatment in patients who are not displaying severe hypertension. If the patient fails to respond to these interventions, pharmacological treatment should be initiated, and the community nurse needs to consider urgent referral to emergency care. In many cases, AD episodes are resolved with non-pharmacological management, and the patient can be safely managed in the community setting.
KEY POINTS
- Autonomic dysreflexia affects spinal cord injured patients above the level of T6
- Autonomic dysreflexia results from a noxious stimulus, such as bladder distension, kinks in catheters and pressure ulcers
- A sustained rise in systolic blood pressure above 20 mmHg could be indicative of an dysreflexive episode
- Non-pharmacological interventions of removing noxious stimuli usually resolve the dysreflexive episode
CPD REFLECTIVE QUESTIONS
- Name the most common noxious stimuli that cause autonomic dysreflexia in people with spinal cord injury above the T6 level
- How can autonomic dysreflexia episodes be manage within a community setting?
- Reflecting on your own practice, how can the ABCDE assessment tool be used to identify deteriorating patients?