What you didn't learn in EMT School

     Doctors complete four years of college, four years of medical school and then three or four years of internship and residency, where they get to practice what they've learned under the watchful eye of an experienced physician. Conversely, a typical EMT-Basic course runs six months, while the average paramedic class lasts about a year and a half. Despite this cavernous gap in education, the patients we see in the prehospital environment are no less real or complicated or the stakes any less critical than those the docs see.

     One easy way to bridge this education gap is called research. If you were to start looking up every drug, disease and syndrome you encountered on a call, you would be amazed at how much medicine you can learn in just one year. As Layne Shore, a former special ops combat medic and instructor colleague of mine, likes to say: "If you spend just an extra 15 minutes a day learning your job, you will be in the upper five percent of your profession." This article introduces you to three conditions you may encounter in the field that you didn't learn about in the classroom.

     You are dispatched to an ALS emergency transport. Supplemental information advises that your patient believes he is suffering from a hypertensive crisis. You're an experienced medic who's been around long enough to remember the time when hypertensive crises were aggressively treated by emergently lowering the blood pressure with nitroglycerin, Procardia and Lasix. That practice was discontinued when studies showed it increased the risk of stroke. Upon arrival, you find an anxious 35-year-old quadriplegic male with flushed diaphoretic skin, who claims to be having an attack of autonomic dysreflexia.

     Autonomic dysreflexia (AD), also known as hyperreflexia, is a potentially life-threatening condition which frequently occurs in patients with spinal cord injuries. AD is an unopposed overreaction of the sympathetic portion of the autonomic nervous system characterized by sudden and severe hypertension, reflex bradycardia, pounding headache, and flushed skin with perfuse diaphoresis above the level of injury and pale, cool skin below the level of injury. This syndrome is most frequently seen in patients with spinal cord injuries at or above T6, which includes most quadriplegics and some paraplegics.

     Up to 90% of patients with spinal cord injury (SCI) at the T6 level or above will experience autonomic dsyreflexia, with 80% of them suffering their first episode within a year of their SCI. Many of these patients suffer frequent, repeated episodes of AD.

     Autonomic dysreflexia begins when the autonomic nervous system is stimulated by noxious stimuli below the level of spinal cord injury, such as bladder distension, fecal impaction or urinary tract infection (UTI), which are the most common causes. Pressure sores, or even tight clothing, have also been implicated. The noxious stimulus triggers the sympathetic nervous system at the lumbar level, causing spasm and narrowing of the blood vessels and resulting in a rapid rise in blood pressure. Baroreceptors in the carotid sinuses and aortic arch detect this rise in blood pressure and send a message to the brain, which sends a message to the heart to slow down. The brain also sends a message to the blood vessels to dilate, but the message cannot make it below the level of injury and therefore fails to regulate the blood pressure.

     Sitting the patient up and allowing his feet to dangle over the bed can frequently reduce the blood pressure below life-threatening levels. Many spinal cord injury patients have nifedipine (Procardia) capsules, which they bite open and absorb in their mouth to quickly reduce their blood pressure. Dysreflexia may be one of the rare instances where emergently decreasing the BP with nitroglycerin would be appropriate and possibly lifesaving. Continued monitoring and transport of the patient to the hospital is warranted, since identifying and correcting the underlying cause is critical.