Neurotrauma Review Series Part 4: Autonomic Dysreflexia

Objectives:

• Describe the functions of the sympathetic and parasympathetic nervous systems.
• Explain what anatomic levels of spinal injury put patients at risk for autonomic dysreflexia and why.
• List four stimuli that commonly elicit autonomic dysreflexia.
• List four signs and symptoms of autonomic dysreflexia.
• Describe correct treatment for autonomic dysreflexia.

We usually think of our spinal neurotrauma patients as presenting to us just after their injuries, still positioned in the environment of their accident. In this, the last in a series of four CME articles on neurological injuries, we will consider our other kind of spinal trauma patient, the one we see long after the day of their injury.

It’s a brisk afternoon in Your Town, and you’re called to a 36-year-old male with “high blood pressure.” You arrive to find a single-level house with a wheelchair ramp out front. At the door you’re greeted by a visiting nurse who guides you to a young-appearing man in a hospital bed. “I’m not sure what’s wrong with him,” she tells you. “I took over from the night nurse and he was fine, but then he woke up late this morning with a headache. Now the headache is worse, he has blurred vision, and he’s not acting right.”

She explains that your patient has had T1 quadriplegia, also known as tetraplegia (see sidebar), since a rollover car accident several years ago. Today is her first day caring for him, so she is unable to give you a detailed history, but she does supply you with his vital signs. His heart rate is 100, blood pressure is 226/114, respirations are 20, SpO₂ is 100% on room air, and temperature is 98.9ºF. You talk to the patient and find that he opens his eyes to verbal stimuli and is oriented to name only. Your physical exam finds that heart sounds are loud, but there are no extra sounds or murmurs. His lung sounds are clear. His abdomen is soft and non-tender. His upper extremities have some shoulder shrug and elbow extension to your commands, but his fingers are weak and clumsy. His lower extremities are atrophied and flaccid. He has strong peripheral pulses. His skin is intact and warm and dry.

He has a Foley catheter in place, but there is not much urine in the bag. “Did you just change the catheter bag recently?” you ask.

“No” she tells you. “It’s the same one from last night.”

“Are you qualified to change his Foley catheter?”

She says she is and agrees to change it before you transport the patient to the hospital. While she does, you place an IV and think about your options for treating hypertensive emergency, just in case your hunch does not play out. The visiting nurse swiftly replaces the catheter, and the patient immediately puts out nearly 1,500 ml of urine. You smile hopefully and take his blood pressure again: 170/90—already trending down. Several minutes later the patient’s confusion begins to clear. You smile about your better-than-average start to the day, pull out your phone and call your medical control physician to discuss whether you should transport to the ED or make arrangements for the patient to see his own physician later in the day.

The Storm After the Storm              

Many of the spinal cord injury patients we care for as EMS providers were injured minutes to hours before we treat them, but others were injured years before intersecting with our care. The patients in this subset have often endured long admissions and extensive courses of rehabilitation therapy and have been sent home to try to live as normally as they can. This is obviously not an easy road.

Paralysis presents constant logistical and mental obstacles but also stresses the body in more subtle, insidious ways. In this article we will talk about autonomic dysreflexia, one of the most dangerous syndromes that challenge patients with spinal cord damage. Autonomic dysreflexia can cause hypertensive crisis and stroke. It most commonly affects patients with severe spinal injuries at T6 or above and is the result of interruption of communication between the brain and sympathetic nerves.

The Sympathetic Nervous System

The sympathetic nerves start in the brain and proceed down the spinal cord. They exit the spinal cord just below each vertebra from T1 to L2 and go out into the body to innervate the heart, blood vessels, bronchi, skin and other organs. The sympathetic nerves go to work when the brain senses a stimulus or stressor acting upon the body that is interpreted as fear, anger or pain. Examples of these stressors are increased oxygen demand from exercise, injury or infection; decreased blood pressure from trauma or sepsis; and irritating stimuli from sources such as a urinary tract infection, an overfull bladder, a full rectum, an unrelenting itch or an object exerting constant pressure against the skin.

When the sympathetic nervous system is activated, the sympathetic nerves act upon the heart to increase the heart rate, upon the lungs to dilate the bronchi, upon the blood vessels to promote vasoconstriction and upon the skin to stimulate sweat. This is part of the “fight or flight” response that makes the body ready to combat whatever stimulus or stressor has presented itself.

In uninjured persons an activated sympathetic nervous system is not allowed to just run wild without supervision. In the normal body, whenever the sympathetic nervous system is activated, the brain also activates parasympathetic nerves (which decrease the heart rate, constrict the bronchi and promote vasodilation and mucosal drying when stimulated) to keep the sympathetic nervous system in check. If the sympathetic nervous system were permitted to function without controls, it would cause dangerously high heart rates and blood pressures and could even lead to stroke instead of helping the body by increasing the heart rate and blood pressure just a little bit.

Spinal Injury: What Happens?

In persons who have a severe spinal injury above L2, communication between the brain and the sympathetic nervous system is stopped. The significance of this halt in communication depends on how high in the spinal cord the injury lies. Because the sympathetic nerves diverge from the spinal cord at T1–L2, if the spinal cord injury is at the T11, T12 or L1 vertebra (T12 is an easy vertebra to landmark because it is connected to the lowest rib; L1 lies immediately below T12, and T11 lies immediately above), then very few of the sympathetic nervous system nerves are unsupervised by the brain, and so few, if any, problems occur. In fact, amazingly few problems occur until the injury is at T6 or above. Once at or above T6, however, too many of the sympathetic nerves are uninhibited, and autonomic dysreflexia becomes a risk.

But if there is spinal cord interruption, then how do the sympathetic nerves get stimulated? In severe spinal injury, sensory nerves still exist; however, with a damaged spinal cord, their pathway to the brain is interrupted. Therefore, they can sense touch, pain, itch, hot, cold, etc., but they cannot transmit sensation to the brain. Some of these sensory nerves are involved in reflex arcs. Reflex arcs are why we can, for example, hit the patellar tendon with a reflex hammer and make the leg move, even when a patient is para- or quadriplegic. The sensory nerve, in the case of a reflex arc, goes to the spinal cord and connects to an intermediate neuron called an interneuron. That interneuron connects directly to a motor neuron, which goes back out of the spinal cord and moves the leg…all without interaction from the brain.

Reflex arcs are not just for motor nerves. There are reflex arcs for the sympathetic nerves too. Some sensory nerves connect with interneurons in the spinal cord, which connect with sympathetic neurons. This means that if the sensory neurons are stimulated, there is an “automatic” sympathetic response.¹

A True Crisis

In patients with injuries at T6 or higher, the action of these reflex arcs can cause autonomic dysreflexia. Also known as autonomic hyperreflexia, the syndrome is defined by sympathetic prompting of dangerously high heart rates and blood pressures. If uninterrupted, autonomic dysreflexia occasionally moderates on its own, but it often leads to hypertensive crisis and even to vasospastic or hemorrhagic stroke.

The most common stimuli that activate the sympathetic reflex arc and cause autonomic dysreflexia concern the bladder. They are urinary tract infections, kidney stones and even just a full bladder. Unfortunately, because many spinal cord injury patients use urine catheters, they are particularly at risk for these problems.

The second-most common dysreflexia triggers are stimuli from the rectum, such as fecal impaction or stool-filled rectum. Many spinal cord injury patients cannot have spontaneous bowel movements (caregivers must activate the rectum digitally to cause defecation), so they are especially at risk for these problems as well. Other common problem stimuli are post-operative pain,² objects such as cushions or tightly wrapped sheets or wheelchair arms exerting prolonged pressure against the skin, tight-fitting clothing, sunburn, ingrown toenails, pregnancy, appendicitis, gallstones and any other irritating stimuli occurring below the level of injury.

Autonomic dysreflexia patients look sick from the door, and they are. Along with acute onset of tachycardia and hypertension, signs and symptoms of autonomic dysreflexia include headache, vision changes, anxiety, piloerection (goose bumps), diaphoresis and flushing above the level of injury with pallor below.¹

How Do I Fix It?

First and foremost try to find the source of the irritation. If there is a caregiver on scene, such as a visiting nurse or home health aide or domestic partner or spouse, they can be of great help. So can your medical control physician. Consider the most common causes first, then call medical control, if needed, for guidance on how to proceed to eliminate them.

This means observing the urinary catheter if it is indwelling. Clean-looking catheter tubing and lots of clear, light-colored urine in the bag are good signs. Sparse, cloudy, dark urine is not. Ask whether the patient has had a normal amount of urine output over the last 24–48 hours and whether there has been a change in color or clarity. If there is any suspicion of catheter obstruction or infection, ask your medical control physician whether they want the patient or their care assistant (or you, if you are so trained) to remove and/or replace the catheter using sterile procedure. If the patient does not have an indwelling catheter but instead “straight catheterizes” to get urine out of their bladder, it is again to the patient’s advantage to empty their bladder immediately.³

Ask about the patient’s recent bowel movements. Remember, if you think a full rectum is the source of the problem, caregivers for quadriplegic patients are usually qualified to help the patient empty their rectum. Asking them to do so in situ might alleviate dysreflexic symptoms before they get worse. Look for skin ulcerations, burns, tight clothing and other trauma and irritants, and ask about recent surgery, illness, trauma, chills, fevers, cough, vomiting, diarrhea and the possibility of pregnancy.

If malignant tachycardia and/or hypertension persist once you have tried to eliminate the source of the irritation, establish IV access and transport with the head of the cot raised to 30–35 degrees (to minimize intracranial pressure). Then call your medical control physician promptly and ask how they want you to proceed. Depending on circumstances, the doctor may have you continue relatively noninvasive care or move on to administration of an alpha 2 agonist, beta-blocking medication, calcium channel-blocking medication or vasodilator.⁴

Regardless of the choice of treatment, the most important job for us as EMS providers is to recognize the situation, make the right diagnosis and find and remove the cause of the problem. Being good, diligent detectives and using the resources at hand can make the difference for our patients between rapid recovery at the scene and prolonged hospital stay, and can sometimes avoid the devastating outcomes of stroke or MI. And that’s worth our while.

Footnotes

1. Tintinalli JE, et al. Adults With Physical Disabilities, Spinal Cord Injury. In: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 6^th ed. New York: McGraw Hill, 2004.

2. James JJ, Svircev JN, Buhrer R, Heard L, Burns SP. The use of a protocol for the management of autonomic dysreflexia in an inpatient spinal cord injury unit. Arch Phys Med Rehab, 2006 Nov; 87(11): e45.

3. Breault G, Altaweel W, Corcos J. Management of autonomic dysreflexia. Current Bladder Dysfunction Reports, 2008 Mar; 3(1): 13–6.

4. Abrams GM, Wakasa M. Chronic complications of spinal cord injury. UpToDate.com, www.uptodate.com/contents/chronic-complications-of-spinal-cord-injury.

References

• Adults With Physical Disabilities, Spinal Cord Injury. In: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 6^th ed. New York: McGraw Hill, 2004.

• Santajuliana D, Zukowska-Grojec Z, Osborn JW. Contribution of alpha- and beta- adrenoceptors and neuropeptide-Y to autonomic dysreflexia. Clin Auton Res, 1995 Apr; 5(2): 91–7.

• Breault G, Altaweel W, Corcos J. Management of autonomic dysreflexia. Current Bladder Dysfunction Reports, 2008 Mar; 3(1): 13–6.

• Krassioukov A, Warburton DE, Teasell R, Eng JJ; Spinal Cord Injury Rehabilitation Evidence Research Team. A systematic review of the management of autonomic dysreflexia after spinal cord injury. Arch Phys Med Rehabil, 2009 Apr; 90(4): 682–95.

• James JJ, Svircev JN, Buhrer R, Heard L, Burns SP. The use of a protocol for the management of autonomic dysreflexia in an inpatient spinal cord injury unit. Arch Phys Med Rehab, 2006 Nov; 87(11): e45.

Tiffany Bombard, NREMT-P, MD, has been an EMS provider, firefighter and paramedic for many years in Vermont, Utah, New York, New Hampshire and Maine. She is currently a resident emergency physician at Albany Medical Center and a paramedic for the Albany County Sheriff’s Office in New York. She loves mail. Write to her with questions or suggestions at bombieskifast@yahoo.com.