A nurse is caring for a client with a spinal cord injury. what are possible causes of autonomic

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The autonomic nervous system is the division of the peripheral nervous system that carries motor information to the visceral organs and glands. It is made up of the sympathetic and parasympathetic autonomic nervous systems. The sympathetic fibers are responsible for the fight-or-flight response and divert blood flow away from the gastrointestinal tract and skin through the process of vasoconstriction. As a result, blood flow to skeletal muscles and lungs is significantly enhanced (by as much as 1200% in the case of skeletal muscles). [6] This also causes bronchiolar dilatation of the lung, which allows for greater alveolar oxygen exchange and increases the heart rate and contractility of cardiac myocytes.

The parasympathetic fibers typically act in opposition of the sympathetic autonomic nervous system through negative feedback control. This action is a complementary response, causing a balance of sympathetic and parasympathetic responses. Overall, the parasympathetic outflow results in conservation and restoration of energy, reduction in heart rate and blood pressure, facilitation of digestion and absorption of nutrients, and excretion of waste products. This parasympathetic response is primarily mediated through cranial nerve X, the vagus nerve, and the S2, S3, and S4 spinal nerves.

In individuals with intact central and peripheral nervous systems, a noxious stimulus results initially in a sympathetic response, leading to elevation in heart rate and blood pressure primarily through spinal reflexes. This response is modulated by the central nervous system and peripheral baroreceptors through the parasympathetic nervous system; this results in heart rate and blood pressure control both through direct responses by the vagus nerve and through inhibitory spinal cord signals. An appropriate balance of sympathetic and parasympathetic outflow is attained and modulated by both the central and peripheral nervous systems.

In those with an SCI at the level of T6 and above, a noxious (or otherwise strong) stimulus below the level of injury results in an unbalanced physiologic response. The strong stimulus causes a peripheral sympathetic response through spinal reflexes, resulting in vasoconstriction below the level of injury. This reflex response ascends and descends the spinal cord and paraspinal sympathetic ganglia, causing both direct vasoconstriction through activation of perivascular receptors and systemic/indirect vasoconstriction through stimulation of the adrenal medulla, resulting in epinephrine and norepinephrine release into the systemic circulation. This therefore results in hypertension, primarily through splanchnic and peripheral vasoconstriction.

The baroreceptors in the carotid sinus and aortic arch convey appropriate responses to hypertension through the petrosal ganglion to the nucleus ambiguous and result in strong vagal (CN X) outflow, bradycardia, and vasodilatation above the level of injury. The central nervous system cannot directly detect the strong or noxious signal below the level of injury (owing to the lack continuity of the ascending sensory fibers from the underlying SCI), and, therefore, responds to hypertension by sending a strong inhibitory response through the spinal cord aimed at reducing the sympathetic response. However, because of the lack of spinal cord continuity, the descending inhibitory response only travels as far as the level of neurologic injury and does not cause the desired response in the sympathetic fibers below the injury; therefore, the hypertension remains uncontrolled.

As a result, there is flushing and sweating only above the level of injury, bradycardia, pupillary constriction, and nasal congestion (unopposed parasympathetic responses); and below the level of injury, there is pale, cool skin and piloerection due to sympathetic tone and lack of the descending inhibitory parasympathetic modulation. [7]  (However, a study by Solinsky et al of 78 male patients with SCI who had incidents of autonomic dysfunction found that out of 445 episodes, relative tachycardia occurred in 68.0%, far more frequently than relative bradycardia [0.3%]. [8] )

T6 is of particular importance in the pathogenesis of autonomic dysreflexia. The splanchnic vascular bed is one of the body’s largest reserves of circulatory volume and is controlled primarily by the greater splanchnic nerve. This important nerve derives its innervation from T5-T9. Lesions to the spinal cord at or above T6 allow the strong and uninhibited sympathetic tone to constrict the splanchnic vascular bed, causing systemic hypertension. Lesions below T6 generally allow enough descending inhibitory parasympathetic control to modulate the splanchnic tone and prevent hypertension.

The underlying pathophysiological changes that occur in the spinal cord and in the periphery that cause autonomic dysreflexia have not been fully elucidated in a human model. It has been postulated that peripheral alpha-adrenergic receptors associated with blood vessels become hyperresponsive below the level of the spinal cord lesion. This hyperresponsiveness is secondary to a low resting catecholamine state associated with SCI. The orphaned receptors have a decreased threshold to react to adrenergic stimuli and react with an increased responsiveness. [9, 10, 11]

Another possible mechanism includes loss of supraspinal inhibitory control from the medulla oblongata–bulbospinal pathways; this loss of supraspinal control may cause a loss of the bulbospinal pathway’s inhibitory effect over serotonin in the intermediolateral nucleus of the spinal cord. The unabated serotonin then causes strong vasoconstriction. [12]

A study by Phillips et al suggested that the brain may buffer moderate instances of autonomic dysreflexia. During spontaneous episodes of autonomic dysreflexia in four patients with motor-complete cervical SCI, the report found that although the mean arterial blood pressure rose from 66 to 83 mm Hg, the cerebral blood flow and end-tidal partial pressure of carbon dioxide remained approximately the same. [13]

Autonomic dysreflexia (AD) is a life-threatening medical emergency. It most often happens to people with a spinal cord injury (SCI).

Any person with an injury in the cervical spine, thoracic spine, or above T6 is at risk of developing AD. Patients with these spinal cord injuries should be familiar with autonomic dysreflexia. Less often, people without SCI develop this condition.

Doctors define AD as an odd reaction of the autonomic nervous system, also known as the involuntary nervous system. This system controls bodily functions without you thinking about them or being able to control them. For instance, it controls your heart beating.

AD is often due to an issue with your bodily functions below the level of your spinal cord injury. The nerves in this part of the body attempt to signal your brain that something is wrong.

However, having an SCI stops these signals from reaching your brain. So, special nerves automatically constrict the blood vessels below your level of injury. This narrowing results in a rapid increase in your blood pressure.

Your brain detects the increase in blood pressure and tries to decrease it by slowing your heart rate. This slowing causes the blood vessels above the level of injury to relax and open wider. This opening may cause your face and neck to become red and blotchy.

Your brain attempts to send messages telling your body to stop squeezing your blood vessels closed. Because the messages do not travel correctly through the spinal cord, your blood pressure may continue to rise. Left untreated, AD may lead to stroke, seizure, or death.

As many as 90% of people with a cervical spine or high-thoracic SCI are at risk for AD.

What causes Autonomic Dysreflexia?

Anything that would typically be a painful or uncomfortable issue below the level of your injury could trigger AD.

About 85% of the time, the cause of AD is urological, including:

• An overfull bladder.
• A urinary tract infection.
• Bladder spasms.
• Kidney or bladder stones.

Other conditions that may cause AD in people with SCI include:

• Overfull bowel.
• Stomach issues like ulcers.
• Appendicitis.
• Gallstones.
• Sexual activity.
• Skin conditions, such as pressure ulcers or burns.
• Injuries to legs and feet, such as ingrown toenails.
• Blood clots.
• Broken bones.
• External factors, like extreme temperatures or too-tight clothing, belts, or shoes.

In people without spinal cord injuries, AD can form as a result of:

• Head trauma and brain injuries, including brain hemorrhages.
• Guillain-Barré syndrome.
• Side effects of some medications.
• Taking illegal stimulants like amphetamines or cocaine.

How do I prevent Autonomic Dysreflexia?

AD is a life-threatening emergency that patients with an SCI have little control over. You can reduce your risk of developing AD by:

• Making sure your bladder doesn't get too full.
• Asking your doctor how you can help prevent bladder infections.
• Making sure you are controlling your pain.
• Practicing good skin hygiene to help prevent infections or bedsores.
• Practicing good bowel care.

If a medicine you're taking is causing AD, talk to your doctor about changing it. Avoiding illegal stimulants is also important.

The most common symptoms associated with AD include:

• Your blood pressure increases by 20 to 40 points from your baseline.
• Your heart rate slows.
• A pounding headache (often the first symptom).
• Sweating above the level of your injury.
• Bladder or bowel problems.
• Red, blotchy skin above the level of your injury.
• Chills without fever or goosebumps.
• Blurry vision, feeling lightheaded and dizzy.
• Stuffy nose.
• Feeling anxious or jittery.
• Chest tightness and trouble breathing.
• Muscle spasms in the jaw.

How do you Diagnose Autonomic Dysreflexia?

When you start having symptoms of AD, your doctor will likely:

• Take your medical history. They'll ask about your SCI, medications, and previous AD episodes. Many patients have AD more than once.
• Do a physical examination.
• Examine your nervous system.
• Take blood or urine tests.
• Do imaging tests, like X-ray or MRI.

They may also perform additional testing. Including:

• Toxicology screening to see what medicines or drugs are in your bloodstream.
• An electrocardiogram (ECG) to study the heart's electrical activity.
• A lumbar puncture to look at the fluid around your spine.

AD is a life-threatening event. At the moment, it's crucial to reduce your high blood pressure. If your systolic blood pressure goes above 150 and stays there, get help.

The most severe complication of AD is a stroke. The first goal of treatment is to reduce that risk by treating high blood pressure. Once they've addressed the symptoms, doctors will work to treat the underlying cause of the AD.

A doctor can bring your blood pressure down safely with medicine. Dropping your pressure too low too fast can be dangerous, so your doctor will keep a close eye on you.

If medication is causing AD, treatment involves stopping that medication. If it's a blocked urinary catheter, your doctor will treat it and check for proper bladder drainage. They'll treat you with antibiotics if it's a urinary tract infection.

If bladder or bowel issues aren't the cause, your doctor will search for what else may be causing the AD and work to treat it. Other causes can include anything from ingrown toenails to latent fractures.

If you are experiencing an episode of Autonomic Dysreflexia

If you experience an episode of AD, there are a few things you need to do immediately. First, you should get into a sitting position or elevate your head as much as possible. Changing position can drop your blood pressure.

Since bladder issues are the most common cause of AD, you or a caregiver should check your bladder. Catheterize your bladder if you manage it through intermittent catheterization. If you have an indwelling catheter, check for kinks or blockage, and make sure your drainage bag is not too full. Irrigate your catheter to clear any blockage.

Next, check for bowel issues. You or your caregiver should perform digital stimulation to empty your bowel. Loosen any tight or restrictive clothing, such as belts or abdominal binder, untie shoes, and if you wear support hose, remove them.

Check your bed or wheelchair to make sure you are not sitting on anything that may be causing pressure. If none of these things resolve the issue, talk to your doctor. They can reduce your blood pressure and help uncover what may be causing AD.