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.

     You're about to complete your first year as a medic when you're dispatched to a diabetic emergency. You arrive to find a 20-year-old male, who admits to being noncompliant with his desmopressin and claims he is now dehydrated. He says he tried to explain to the 9-1-1 operator that he doesn't have sugar diabetes; he has diabetes insipidus.

     Diabetes insipidus (DI) is a completely different disease than diabetes mellitus (aka sugar diabetes), with completely different causes and treatments. The only similarities between the two are increased thirst (polydipsia) and increased urination (polyuria).

     Thirst associated with DI may be intense and uncontrollable and may specifically manifest as a craving for ice water. Urination is frequent, even at night, disrupting sleep and possibly resulting in bedwetting.

     DI, sometimes referred to as "water" diabetes, is a disorder characterized by excretion of excessive amounts of extremely diluted urine. The frequency and concentration of urine are regulated by an anti-diuretic hormone (ADH), also known as vasopressin. ADH is produced in the hypothalamus region of the brain, then stored and secreted by the pituitary gland.

     DI can result from either insufficient production of ADH, known as central diabetes insipidus (most common), or by the kidneys' failure to respond to ADH, referred to as nephrogenic diabetes insipidus.

     With central DI, the patient is prescribed desmopressin, a synthetic replacement for vasopressin, which may be injected, but is typically administered by an intranasal spray called DDAVP. Treatment for nephrogenic DI is high fluid intake to keep pace with the amount being lost. Hydrochlorothiazide may also be prescribed. Although a diuretic, in some cases, it may help regulate urinary output.

     Unlike the urine of diabetes mellitus patients, which contains excessive glucose, urine of diabetes insipidus patients is very dilute, appearing colorless or watery. In the days before laboratory testing was readily available, diabetes mellitus and diabetes insipidus were diagnosed by the doctor dipping his finger into a urine specimen and tasting it. If it was very sweet, the diagnosis was diabetes mellitus; if it had no taste, it was diagnosed as diabetes insipidus.

     The major issue for patients with diabetes insipidus is dehydration. Symptoms include: tachycardia; weak peripheral pulses; delayed capillary refill; cool, pale skin; dry tongue and buccal membranes; and hypotension.

     Fortunately, onset of dehydration from DI is over a prolonged period of time—typically weeks, not days; however, once a patient becomes dehydrated, recovery is slow, due to electrolyte derangement. Treatment for dehydration from DI is the same as any other cause and includes fluid resuscitation, keeping the patient warm, O₂, if necessary, continued monitoring and transport.

     You're dispatched for a syncope and find a 45-year-old female sitting in a chair with Ace-like bandages on her arms and legs. The skin on her face looks tight and stiff; she is conscious, but is emotionally upset. She admits to passing out and requests transport to the hospital, but refuses an IV because she has scleroderma.

     Scleroderma is a Latin word meaning "hard skin." Scleroderma is both a rheumatic (inflammatory) and autoimmune disease. Autoimmune diseases occur when the body's tissues are attacked by its own immune system. Scleroderma is characterized by the formation of scar tissue (fibrosis) of the body's skin and organs, which leads to thickness and firmness of involved areas. Scleroderma affects females 7 to 12 times more often than males. The most frequent time of onset is during the middle to late childbearing years (30–55).

     Scleroderma can be localized and affect only one area of skin, or be systemic and affect the skin of the entire body. Areas most commonly affected are the fingers, toes and face. It begins with pain and swelling. As inflammation continues, subcutaneous circulation is reduced due to compression and constriction of the capillaries, calcium deposits develop beneath the skin, and, over time, the skin becomes thick, tight and hard.

     In addition to widespread skin involvement, systemic scleroderma may also affect internal organs. GI tract involvement can result in gastric reflux, difficulty swallowing, diarrhea, constipation and gas. Damage to the intestines will result in malabsorbtion of nutrients and malnutrition. The lungs are the most commonly affected internal organ. Pulmonary involvement results in pulmonary fibrosis and pulmonary hypertension, both of which will manifest as respiratory distress. Cardiac involvement causes inflammation of the heart muscle (myocarditis) and eventual scarring and weakening of the heart (cardiomyopathy), resulting in congestive heart failure and arrhythmia. Kidney involvement causes hypertension and kidney failure. Most severe organ problems occur within the first three years of disease onset.

     EMS intervention is generally limited to understanding, empathy and compassion for a very difficult and debilitating disease. IV access may be difficult due to brittle, constricted peripheral vasculature. Respiratory distress secondary to pulmonary fibrosis and hypertension will be limited to O₂. Nebulized breathing treatments and low-dose steroid usage may be indicated in some EMS systems. Treatment for congestive heart failure in the scleroderma patient is with O₂ and nitroglycerin. Lasix may be administered if IV access is possible, and CPAP or BiPAP may additionally be warranted in cases of severe respiratory distress. ACE inhibitors may be more effective for kidney involvement of scleroderma.

     www.emedicine.com/pmr/topic217.htm

     www.apparelyzed.com/autonomic.html

     www.spinalcord.org/news.php?dep=17&page=94&list=1178

     www.nlm.nih.gov/medlineplus/diabetesinsipidus.html

     https://familydoctor.org/online/famdocen/home/articles/048.html

     www.diabetesinsipidus.org/whatisdi.htm

     www.medicinenet.com/scleroderma/article.htm

     www.emedicine.com/MED/topic2076.htm

     www.rheumatology.org/public/factsheets/scler_new.asp

     Joe Hayes, NREMT-P, is deputy chief of the Bucks County Rescue Squad in Bristol, PA. Joe has 27 years' experience in EMS. Contact him at jhayes763@yahoo.com.