In Praise of EMTs and Paramedics

Until recently, my experience with ambulances was limited to thinking: I’m glad it’s not me in there, please let it not be carrying anyone I love, godspeed you to help whoever you are, and, if driving, I hope that ambulance isn’t coming up behind me.

But since my recent medical  emergency, I’ve looked into who these people are who arrive in a flash, save lives, and then are gone. They don’t leave a calling card, you never know their names, and if you are in as bad a shape as I was, you might have heard their voices, but likely never saw their faces. They could be standing next to you in line at the store, sitting beside you in the theater, and you’d never know it.

I’m convinced in my case (and I expect it many others), that the Emergency Medical Services [EMS] team saved my life; the emergency room doctor then fixed the problem. But he wouldn’t have had a patient to work on were it not for the EMS. This is why I was so surprised to find no mention of the EMS’s work in my hospital records. Is this common, that their work is ignored, I wonder.

I’ve learned a little about these professionals since then. It’s more complex than you might think. There are First Responders, Emergency Medical Technicians [EMT] (and several levels of these), and Paramedics, and the requirements for these vary somewhat from state to state. Firefighters are also often cross-trained as EMTs, in case you are wondering why firetrucks accompany ambulances.  I’m sure their physical strength comes in handy, too.

Then there are different categories of emergencies: BLS and ALS. BLS refers to “basic life support” and ALS to “advanced life support.” I learned a lot from browsing the forums at and A question about the difference between BLS and ALS brought this answer from Michigan but the responses that follow show there are some state-to-state variations:

Basic Life Support Units that are designed for inter-facility transportation and pre-hospital response to ill or injured patients. Each unit is staffed with 2 licensed emergency medical technicians. …

The ALS units have a minimum of one paramedic and one EMT, can administer certain medications, and have advanced airway equipment, cardiac monitors, advanced cardiac life support equipment and blood glucose testing equipment.

What I found astounding is how poorly EMS workers are paid. All I can think of as an explanation is that in a lot of rural America, first responders are often volunteers, so somehow the idea got embedded that if there are people who will do this for free, why pay anyone well? It’s an absurd and stupid answer, but how else can the salaries of these people who deal with a range of dangerous and to most of us disgusting situations be justified?

Consider these facts from EMS Workforce for the 21st Century: A National Assessment [2008]:

…at $12.54, EMTs/paramedics are among the lowest paid of several comparable allied healthcare professions. Medical assistants, at $12.19, make somewhat less than EMTs/paramedics. L.P.N.s/L.V.N.s, at $16.94, have a median hourly wage of $4.40 more than that of EMTs/paramedics although the program length for L.P.N.s/L.V.N.s is quite similar to those for paramedics. …

EMTs/paramedics are among the bottom three categories in wages, making slightly more than nursing aids/orderlies/attendants, nearly $1 less per hour than medical assistants, and about $4 less than L.P.N.s/L.V.N.s.

…Medical assistants have a broad range of direct patient care responsibilities and work under the supervision of a physician, but have no training, certification, or licensure requirements. Low wage medical assistants (at the 10th percentile) make higher wages than EMTs/paramedics.

How can this be? Does this make sense to anyone? Am I missing something?

According to, where I live, EMTs make between $24,000 and $31,000 a year, while medical assistants, who “assist in examination and treatment of patients under the direction of a physician” make $26 – 31,000, and medical billing clerks, $27-32,000. These are all lousy salaries, but is it not astounding that people who are out in the field, making life-saving decisions without anyone there to consult, never knowing what they may encounter, make about the same as those who follow routine orders and less than those who send out the bills?

And as if this weren’t bad enough, if my experience is the norm, they don’t get any credit for their work by the ER departments to which they deliver their stabilized patients, and I could provide numerous examples of belittling depictions of their demeanor as insensitive tough guys, but this  New York Times review of the novel Black Flies by Shannon Burke (who worked in the field for five years) about “a rookie, Ollie Cross, who becomes a paramedic after failing to get into medical school” will suffice:

As Cross begins to break free of his borrowed role, Burke offers up one of the book’s most disturbing images, a tragedy of the everyday variety that produces headlines but quickly fades from the news. Five medics, smoking and arguing, stand at the closed door of an elevator that has plummeted down a shaft. As the door squawks open, the men quit bickering and jump up, reacting to “a tangled mess of limbs in contorted, grotesque shapes, tossed grocery bags, blood and eggs and a bag of Cheese Doodles covering the writhing bodies.” They are so desensitized that it takes a scene of sickening destruction to jar them into cooperative action [emphasis added].

Note that it is the reviewer, Liesl Schillinger, safe in her office, who deems the medics as “desensitized,” even as she notes that when it is time to act, they do so immediately. What’s her problem? Are EMTs and paramedics supposed to stand around solemnly and silently all shift long except for when they are saving lives? Would she be as snarky about surgeons in the hospital locker room bickering before going into the OR?

I’ll end with this summary from EMS Workforce for the 21st Century: A National Assessment [2008]:

Research into the EMS workforce in the United States reveals a complicated picture of a workforce that bridges two distinct environments: healthcare and public safety. This is only one of several reasons why the EMS workforce is a unique group of workers.

The EMS workforce comprises both employed and volunteer workers, a feature unique in the healthcare sector although common in fire fighting. Unlike other healthcare providers, EMTs and paramedics are visible and interact with the public primarily outside of healthcare facilities. However, the nature of their work and extent of their skills are often not well understood by public.

Despite their low pay and benefits relative to other healthcare and public safety professions, EMTs and paramedics are in many ways devoted to their field. There is a strong desire among leaders in the field to advance the EMS workforce.

I can attest to the devotion of the team in HEMSI Vehicle 64 to its mission. I wish I could do more.

091114-G-0000X-001 Coast Guard Station Humbolt Bay assist
SAMOA, Calif. – Station Humboldt Bay crewmembers and Eureka City paramedics remove an injured mariner from a 21-foot pleasure craft at the Coast Guard small boat station, Nov. 14, 2009. The man was injured while crossing the Humboldt Bay bar when a large swell threw him against the side of the vessel’s cockpit. U.S. Coast Guard photo by Petty Officer 2nd Class Gregory Brush.
Air Station Los Angeles medevac (FOR RELEASE)
LOS ANGELES – A paramedic from the Los Angeles County Fire Department records a patient’s information inside a Coast Guard rescue helicopter Oct. 3. The patient was medically evacuated from the cruise ship Osterdam 30 miles off Point Conception after it was suspected that he was suffering internal bleeding. (Coast Guard photo/Petty Officer 2nd Class Ken Fuerstinger)
KODIAK, Alaska (Aug. 5, 2004)–Petty Officer 2nd Class Mark Capra, Petty Officer 2nd Class Dave Southwick and Petty Officer 2nd Class Kathy Hayes assist Kodiak paramedics as they remove a litter bearing Wilmer Anderovich from an HH-60 Jayhawk helicopter here. Anderovich was medevaced from Old Harbor suffering from gastrointestinal bleeding. Anderovich was transported by ambulance to Providence Medical Center here. USCG photo by PA1 Paul Roszkowski


“She became dizzy and came to the emergency room for further evaluation”

Remember my post before last, Melena, Hematemesis, Hypovolemic Shock — and A Lot of Love? You know, the one about vomiting up great tarry mounds of clotted blood, losing consciousness, and getting oxygen and IVs in the ambulance before it left my driveway?

Well, today I went to hospital to get my medical records from my latest stay.  And here is what my History & Physical report said:

Sunday night the patient found the blood in her stool. The patient had hematemesis this a.m. Patient came to the emergency room.

Now the Consultation Report. It has the same time inaccuracy: my melena [and if I can use the correct terminology, why can’t they?] didn’t occur Sunday night but just a few hours at most prior to my hematemesis. The report goes on to say:

She became dizzy and came to the emergency room for further evaluation.

And now the Discharge Summary, same misinformation regarding melena, then:

On the day of admission, she vomited coffee-ground materials, got dizzy, and came to the emergency room.

Three reports prepared by three different doctors, each wrong about the timeline, and not a whisper in any of the three about what happened before I arrived in the ER.

There are other annoying things, like under General Impressions in the History & Physical, there’s this observation:

 a  trace of blood around the mouth

but not a word about the globs of dried blood in my hair. Never mind.

The biggie, obviously, is where are the narrative and the record of my vitals for the 20 minutes prior to my arrival? Even if it is not the hospital’s responsibility to incorporate these into the record of my stay under their roof, shouldn’t there be some mention of my means of arrival? Isn’t it downright deceptive to write:

She became dizzy and came to the emergency room for further evaluation …

… got dizzy, and came to the emergency room.

These statements are not untrue: I was dizzy before I started vomiting blood and lost consciousness. And I did come to the ER for evaluation. Not untrue, but  nonetheless false.

When I told the Records Clerk something was wrong, she called in a person who I will call the Conciliator. She’s the one who says, oh I’m so sorry this happened dear, but I haven’t a clue why it did, who is responsible, or what can be done. By the way, why did you come to get copies of your records, anyway?

Because they are mine, I replied. Silence. Because they are mine and no one cares about my health more than I do. And I like to know what is going on.

We left it with the Concilitator promising to get back with me in a few days, when she learned something about anything.

We’ll see.

At Risk for Esophageal Varices and I Nearly Bleed Out from a Gastric Ulcer: How Weird Is That?

Update: The current (November 2014) hypothesis among my doctors is that whatever they were called in my past posts — Dieulafoy lesions, Cameron’s erosions, or bleeding ulcers — all these bleeds have their source in the portal hypertension which comes from cirrhosis which is caused by my auto immune system attacking my bile ducts, that is, my primary biliary cirrhosis.

If you’ve read any of my posts on primary biliary cirrhosis (PBC), you were probably surprised by yesterday’s post that there wasn’t some sort of medical muddle involved. Wonder no longer: there was. It’s just that my emphasis was different so I left it for today.

I’ve written about being at risk for esophageal varices as a result of having PBC. These are swollen veins (like varicose veins), caused by portal hypertension (itself caused by cirrhosis [in the case of PBC — there are others. Click through to a site devoted to patients’ experiences with it]) in the esophagus. Left untreated these could “burst and bleed into the gut.”

But I had an endoscopy just this past January that showed only a trace of varices, and in such cases, 96% of people are trouble-free for at least 1-2 years (then they do another scope).

Of course, that means 4% of people aren’t.

So as soon as I regained consciousness in the ambulance, I alerted the chief EMT to tell the folks in the emergency room about this. And when I got there, I told them myself.

I will refrain from elaborating on how it feels while being transfused to have to repeatedly explain primary biliary cirrhosis and spell Urso Forte [the drug I take for it] to the ER nurses, and later my floor nurse and abdominal ultrasound technician.

However, following the endoscopy performed there in the ER trauma room, the GI who did the procedure reported that I lost enough blood to require four transfusions not because any esophageal varices burst, but because of a “gastric ulcer spurting blood.” He repaired it with three hemostatic clips and put me on pantoprazole.

But how weird is that? To be at risk of burst esophageal varices and have a gastric ulcer burst instead?

I reviewed my endoscopy report (high marks to the GI, who actually gave me a copy of my own medical report!) and found the location of the ulcer to be the cardia. Googled that, and discovered it is right where the esophagus becomes the stomach, and, in fact, for many years there was debate as to which organ it belonged to.

Now then, there is a new kid on the block at the hospital: the hospitalist. This person is sort of in charge of patients who come in through the ER and whose regular doctor doesn’t admit or have any role in their care. Like me. It took me two days to get someone to tell me who was really in charge of my case: the GI who did the procedure, or the hospitalist.

When the hospitalist visited me, I explained about my surprise that my bleed was gastric and not related to portal hypertension [PBC]. I told him that I didn’t have a local GI, but that I was under the care of a hepatologist at the UAB med center.

So the next day he returns, and says, “Good news: you don’t have to have a liver transplant.” I thought yeah, duh, but let him continue. He told me he had set up an appointment with the hepatologist who would do another endoscopy. And I said that sounds great, but what about this report from the GI deeming the cause of the bleed to be a gastric ulcer? The poor guy looked confused. I suggested he go back and have another (an initial) read of  my endoscopy findings.

But the hepatologist’s office and I agree that I should be seen by him. I have so many questions: can a burst esophageal varice adjacent to the cardia be mistaken for a spurting gastric ulcer? Is it really possible to have such an awful gastric ulcer and no abdominal pain? Can portal hypertension cause a gastric ulcer? Will this happen again? And will I have no warning other than feeling steam-rollered before it does?

And just how weird is it, if it was a garden variety gastric ulcer, for this to happen to a person who has to worry about bursting varices?

Stay tuned.

Melena, Hematemesis, Hypovolemic Shock — and A Lot of Love

Gore alert: Medical terms in title refer to situations involving blood, blood, and more blood.

Were mine a glass house, what you would ordinarily see are four people: Mom, Dad, 14-year old Daughter, and 20-year old Son sitting in separate rooms, staring at separate screens. Even holidays aren’t so different; each year they come chugging along with annoying regularity — and I still can’t figure out how to get on board. Orchestrating Hallmark Moments, creating those Special Memories your family will cherish for a lifetime, all that is beyond me. No surprise then that Mother’s Day barely registers on our screens.  But I’ve something better than a lifetime’s stack of cards (and why do people give greeting cards to people they live with, anyway?): my fractured memory of this past Monday afternoon.

Last Saturday night we returned from a 3200-mile+ roadtrip out west, so Sunday I wasn’t surprised to be really tired. Monday wasn’t any better, and I had no appetite but no stomach pains, ate a banana and some soup.  I wasn’t even that surprised when I had the most horrible black diarrhea. I put this down to culinary karma — what did I expect after eating a sausage pizza at a truckstop in rural Arkansas? But Husband was concerned and called to get me a doctor’s appointment. The nurse said I needed to get to the ER, asap. I learned later that this was blood I’d passed, blood mixed with stomach acids: melena.

I resisted. I’d just have to sit there for hours. Besides, I couldn’t even get to the refrigerator and back without having to lie on the floor to rest. Looking back I see how odd it was to think that a reason not to go to the ER. I relented, but told my husband, who needs a total hip replacement, that Son would have to help me to the car.

We hadn’t reached the door when I said I needed to rest, so Husband went to get the air going in the car.

And then I started vomiting up huge black clots of blood. I wasn’t seeing what was going on at this stage, but I was hearing it. Husband called 911 for an ambulance. Dispatcher heard collie barking, said to get him secured. Rascal wouldn’t leave my side, but Daughter and Son together pulled and pushed him out to the backyard. Then both returned and as Husband talked with dispatcher the two of them followed her instructions, keeping me on my side as I continued vomiting up this foul black matter (hematemesis). They told me later I was flailing around, maybe convulsing or seizing, with my eyes wide open but my pupils not right. I certainly wasn’t seeing anything. I remember their stroking me, kissing me, telling me they loved me.

The EMTs and fire truck arrived in minutes. The kids say that the first guys in backed away, until the woman in charge came in and told them it wasn’t trauma (did they think I’d been shot?). Because of the position of our door, deck, and steps, getting a stretcher in wasn’t an option, so they had to haul me out to a gurney placed on the sidewalk. I remember being rolled into a blanket or something. And that’s it, for a while.

Although they worked on me outside, I remember nothing til I was loaded into the ambulance. My guess is I’d lost consciousness, but they started oxygen as soon as they got me out the door so by the time I was in the ambulance I was aware of talk about my blood pressure, getting needles in both arms, hearing the sirens when after 15 minutes or so I was stabilized and we got moving, and I have a few visual memories of the Head EMT and inside the vehicle. I think at some point I must have been between stages 3 and 4 of hypovolemic shock.

In the ER I soon was given two transfusions; later I was to receive two more. I remember the Head EMT telling the nurses they had a very anxious husband pacing in the waiting room who need to be allowed back as soon as possible. Then she was gone.

I became alert enough to be interested in the trauma room. There are posters on the walls telling RN 1, RN 2, RN 3 — up to 6 or 7, I think, exactly what to do and even where to stand relative to the patient’s bed. Someone cut my housedress off, just like on TV ER shows. I complained about the pain the large IV needles were causing me, about being thirsty, about needing to get the blood out of my hair. That was really gross. Even though I couldn’t move my arms I could feel that blood was stuck in my hair, and when I looked at my pillowcase, it was totally red. Not a priority, however.

I ended up having a spurting gastric ulcer repaired via endoscopy, and was home less than 48 hours after the ordeal began.

And what was going on while I was in the ER? Son was cleaning blood off the carpet and Daughter was cleaning everything else in sight.

When I came home, my collie was waiting on the deck in the 102° heat, somehow knowing I was on my way. My bed was made with fresh linens, and Daughter had imposed order on the clutter of the bedside table. She spent a good hour getting all remains of adhesive off my badly bruised arms.

Ever since I got out of the hospital and home with my family, I’ve been uncharacteristically cheerful, bouncing off the walls buoyant.

Of course.

PBC: No Varices for Me. Well, Just a Trace.

As I noted in my first post on primary biliary cirrhosis, during my annual routine appointment I was advised to have an endoscopy procedure to determine whether I had varices in my esophagus as a result of portal hypertension as a result of cirrhosis as a result of the autoimmune destruction of my bile ducts, that is, primary biliary cirrhosis.

I was surprised by this recommendation, since my blood enzyme levels had normalized and in 2007 an MRI of my liver did not reveal damage, but things can change, and the extent of damage my liver has suffered is unknown. There are four stages of PBC, with cirrhosis being stage four, but my case had not been staged, as they put it, because I have never had a liver biopsy.

When I first visited the hepatologist, we discussed whether a biopsy was warranted. He had enough other information to feel confident about the diagnosis, and the treatment he would start me on would be the same regardless of stage. So we concluded that while the biopsy would provide more information, it wouldn’t necessarily be useful enough information to warrant the hassle.’s comprehensive article on PBC notes that whether a biopsy is optional

usually depends on the level of confidence in establishing the diagnosis of PBC using the liver tests, autoantibodies, and ultrasound. In the presence of cholestatic liver tests, high levels of AMA, and an ultrasound showing no bile duct obstruction in a middle-aged woman, the diagnosis of PBC can be made rather confidently without a biopsy.

Even had I had a biopsy three years ago when I was diagnosed, there still would have been only one way to know whether or not it was time to start worrying about varices. And that was to look.

Before we began, the doctor told me that there were four levels of varices. Levels 3 and 4 require treatment, starting with medication.

I asked whether even if I did not now have varices, was it not the case that sooner or later I would?

He quickly responded yes, then caught himself and backtracked, with the typical doctor’s abhorrence of an unqualified answer, noting that 60% to 80% of people with cirrhosis have varices, and in 1 of 6 cases, within a year’s time, if left untreated, the varices would burst and bleed into the esophagus.

The worst part of the endoscopy — really the only bad bit — had nothing to do with the endoscopy itself. I knew I was in for it when the tech responsible for starting the IV began complaining that I had no veins, and sure enough, the IV entry was and remained painful and I have the bruise to prove it.

A not-as-nasty as I was warned to expect spray was squirted in the back of my throat, Demerol was added to the IV port (there was no other use of it in my case), and that was that, until I woke up.

I had no sore throat and began eating and drinking immediately, although I’d nearly fall asleep between bites of cracker.

And the verdict was just a trace of varices, no need to do anything, just repeat in a year or two.

Varicose Veins in my Esophagus?

“And if the dam breaks open many years too soon…”

I was doing a pretty good job of cultivating indifference toward my bad luck at having somehow acquired primary biliary cirrhosis [PBC], taking my 1000 mg of  Ursodiol most days (sometimes I forget), and not scouring the internet hourly looking for the article that would tell me my future, confining that process to just the week before what had become an annual appointment at the University of Alabama at Birmingham liver clinic.

After all, my alkaline phosphatase levels had dropped from the high 400s to the upper limit of normal, 117,  indicating the Ursodiol is doing its job, increasing bile flow from the damaged bile ducts, thereby theoretically slowing the progression of liver damage caused by backed-up toxic bile.

Typically it would make sense to judge a treatment’s effectiveness  not quite so objectively, but in this situation, I’ve only the numbers to rely on.

Do I feel better than I did in December 2006 when I started on the Urso Forte (my favorite brand name for a drug, roughly translatable, or so I claim, as Strength of the Bears)?

Not dramatically. The only symptoms of PBC before the liver is damaged significantly are fatigue and itching, and I never experienced the itching and who among us doesn’t complain of fatigue?

This week the only bad marks on my blood tests were for ones I’ve scored poorly on for at least four years: low white blood cell count and low platelet counts. In the past, these scores were considered not bad enough for alarm, just an anomaly, perhaps.

So I was surprised to be told I should have an upper GI endoscopy to detect whether large varices, or swollen veins (like varicose veins), caused by portal hypertension (itself caused by cirrhosis) are in my esophagus. Left untreated these could “burst and bleed into the gut.

But I gather that an association has recently been made, or at least suggested, between portal hypertension and low white blood cell count (leucopenia), and/or low platelet count (thrombocytopenia). Moreover, in 2006, on the long and wearying road to the PBC diagnosis, an ultrasound showed a very much enlarged spleen, and hypersplenism is another red flag.

My first impulse was to say no to this test based on a strong and irrational desire not to submit to another test, a resistance that I couldn’t explain and thus ignored.

Afterwards, after I started processing this new information, that impulse seemed less irrational: if I do have varicose veins in my esophagus, it probably means that I can no longer tell myself that my mostly normal blood test numbers  mean the PBC was diagnosed  and treatment begun in time to escape cirrhosis, at least for a while. It will mean that  my liver is already dying.

Or so it seems to me. Surprises during doctor appointments frustrate me: I need time to think to know what questions to ask.


Resources for the curious or those in a similar fix:

A simple intro to PBC is at PBC Foundation

A much more thorough one is at

The “bad luck” link in the first sentence of this post refers to the rarity of the disease. In “Food for Thought about Primary Biliary Cirrhosis in 2006,” an essay on the website of the UC-Davis Immunology Lab, there’s this statement:

PBC is thought to be more commonly found in specific areas of the world. In particular, disease frequency varies between 10 and 400 cases per million population. It has been suggested that PBC is more common in northern countries, including England, Sweden, and Northern American states.

MedicineNet says:

Studies indicate that the number of people with PBC at a given time (referred to as the prevalence of disease) ranges from 19 to 251 per million population in various countries.