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Autonomic dysreflexia

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Jennie April Walker, BSc Hons, RN, Dip CPC.

Staff Nurse, Spinal Trauma and Disorders Unit, Queen’s Medical Centre, Nottingham

Autonomic dysreflexia is a sudden and exaggerated autonomic response to stimuli in people with spinal cord injuries or dysfunction. 

The condition should be addressed immediately because it is a medical emergency that can result in death if untreated. With current estimates of people living with spinal cord injuries or spinal cord damage reaching approximately 50,000 people in Britain, with four new cases occurring each day (ASPIRE 2000), it is imperative that nurses have at least a basic understanding of what autonomic dysreflexia is and how it should be addressed.

Autonomic dysreflexia

Autonomic dysreflexia occurs when there is an unrelieved stimulation of sensory receptors below the level of the cord lesion. Frequently seen within the first year following a spinal cord injury at T6 or above (Ahrens and Prentice, 1998), it can occur at any time once the period of spinal shock has passed (Grundy and Swain, 1996). 

The disconnection of the spinal sympathetic centres from supraspinal control causes the predisposition to autonomic dysreflexia (Curt, 1997). The intact autonomic nervous system reacts to this stimulus by releasing catecholamines. This induces vasoconstriction of the blood vessels above the level of injury, and produces a reflex arteriolar spasm that increases the blood pressure, resulting in hypertension.

Baroreceptors in cerebral vessels, carotid sinus and aorta detect the hypertension and stimulate the parasympathetic nervous system by sending an inhibitor signal to the medulla. Due to the spinal cord injury, this message cannot transverse the cord and therefore vasoconstriction occurs above the cord lesion, causing headaches, flushing and nasal congestion, whereas vasodilatation is evident below the lesion. The heart rate is slowed via the vagus nerve in an attempt to control the rise in blood pressure (Alderson, 1999). However, the visceral and peripheral vessels are unable to dilate because the efferent impulses are unable to pass through the cord lesion (Ahrens and Prentice, 1998). This results in the characteristic hypertension and bradycardia.

Triggers

Any noxious stimuli below the level of injury can trigger autonomic dysreflexia (Lightner 1998) (see column, right).

These triggers may occur on a daily basis when caring for a person with spinal cord injuries. Some specialised spinal injuries units induce autonomic dysreflexia in patients with spinal cord injuries before they are discharged from rehabilitation. This enables the patient to experience and recognise the signs and symptoms at an early stage. Once these have been experienced and recognised by the patient he or she can learn how to direct their carers to find and remove the stimuli responsible for the mass reflex.

Nursing management

Autonomic dysreflexia is a life-threatening emergency and needs to be addressed immediately. The first steps should involve locating the stimulus and removing it (Alderson, 1999). This should be done in conjunction with efforts to control the increasing hypertension (Gatehouse, 1998). It should be noted that the increase in arterial pressure could be so acute that it may induce a cerebral vascular accident or myocardial infarction (Curt, 1997). It is important to remember that many individuals with lesions of T6 or above may have a lower than normal blood pressure, so a blood pressure of 120/80 may represent a substantial rise (Gatehouse, 1998). 

When trying to locate the noxious stimulus it should be remembered that anything could potentially induce this reaction including pregnancy, erections, drugs and many other stimuli. The bladder and bowels should be checked initially as these are the most common causes. If a patient has a urinary catheter it may be kinked or blocked. Loosen all clothing, check skin for pressure sores and check for toe damage and remove the stimuli wherever possible (Reffell, 2001). Sitting the patient up may induce orthostatic hypotension and may assist in counteracting hypertension; however, if this proves to difficult or unsafe then Grundy and Swain (1996) recommend the administration of one of the following drugs to relieve the hypertension:

- Phentolamine 5-10mg intravenously

- Gylceryl trinitrate 300 micrograms sublingually or

- Nifedipine 5-10mg sublingually.

Regardless of the actions being taken by the nursing staff to relieve the stimuli, medical personnel should be alerted immediately to the situation. The process of relieving the stimulus is dependent on what it is. If a urinary catheter is kinked or blocked then the appropriate action is to unkink, flush or change the catheter (Grundy and Swain, 1996). Irrigation of a catheter should be done slowly and gently (Ahrens and Prentice, 1998) to reduce the risk of sudden hypotension or inducing bladder spasms, which may aggravate the current situation. A digital rectal examination should be conducted following the application of a local anaesthetic to reduce rectal stimulation and to prevent an increase in the current symptoms. If it is thought that the onset is due to constipation/the need to defecate, then the stool should be removed gently and gradually. If symptoms persist or worsen the procedure should be stopped. If symptoms subside then the process can continue cautiously (Reffell, 2001).

Conclusion

Despite the prevalence of spinal cord injuries and the likelihood that people with these injuries will experience at least one episode of hypereflexia, there is a dearth of research or relevant literature on the subject aimed and nurses and other health-care providers.

Autonomic dysreflexia is recognised as a medical emergency and hence should be taught as such to staff and patients who may encounter it. This would result in a more effective response to and treatment of patients with autonomic dysreflexia that may possibly save lives.

TRIGGERS FOR AUTONOMIC DYSREFLEXIA

- A distended bladder or a full rectum (Ahrens and Prentice, 1998)

- Stimulation of the skin (for example by tight-fitting clothing)

- Stimulation of pain receptors (for example pressure sores, ingrowing toe nails or sunburn)

- A sudden change in environmental temperature or development of pyrexia

- Digital stimulation of the rectum during bowel evacuation

- Bladder spasms

- Intermittent catheterisation 

- Enemas

- Fractures

- Orthostatic hypotension.

SYMPTOMS

Symptoms of autonomic dysreflexia include the following (Ahrens and Prentice 1998):

- Marked hypertension

- Blurred vision

- Severe throbbing headache

- Bradycardia

- Unusual apprehension

- Nasal congestion

- Piloerection

- Nausea

- Marked diaphoresis in conjunction with flushed appearance above the level of injury with pallor below

- Pupil constriction

- Respiratory distress.

USEFUL ORGANISATIONS

Spinal Injuries Association, 76 St James Lane, London N10 3DF, tel: 0800 980050 www.spinal.co.uk

ANATOMY AND PHYSIOLOGY OF THE AUTONOMIC NERVOUS SYSTEM

- The autonomic nervous system regulates smooth muscle, cardiac muscle and glands. It is divided into the sympathetic and parasympathetic nervous systems.

- The cell bodies of the sympathetic pre-ganglionic neurons are located in the lateral grey horn of the spinal cord throughout the thoracic level and the first two lumber segments. The pre-ganglionic axons are myelinated and leave the spinal cord through the anterior root of the spinal nerves, pass through the white matter to the nearest sympathetic trunk. The sympathetic trunks are paired, and consist of 22 ganglia and are situated anteriolaterally to the spinal cord on each side. Splanchnic nerves pass through the sympathetic trunk and terminate in the solar plexus. These can be further divided into the greater splanchnic nerve that passes to the celiac ganglion, and the lesser splanchnic nerve, which passes into the mesenteric ganglion.

- The pre-ganglionic cell bodies of the parasympathetic division are located in the brain stem and the lateral grey horns of the second to fourth sacral segments of the spinal cord. These fibres emerge as part of the anterior root of the spinal nerve or as part of the cranial nerve. The cranial parasympathetic outflow leaves the brain stem via the oculomotor facial, glossopharyngeal and vagus nerves. The sacral parasympathetic outflow exits through the second and fourth sacral nerves. These both end in terminal ganglia where they synapse with post-ganglionic neurons. The vagus nerves transmit nearly 80% of the total cranio-sacral outflow (Tortora and Grabowski, 1993) thus making it the most extensive distributor of parasympathetic fibres. These enter the thoracic plexuses, abdomen, cardiac and pulmonary.

 

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