Archive for June, 2013

Treating strokes in time: an update

Wednesday, June 26th, 2013
If you're having stroke symptoms, call 911 and get to the ER in a hurry

If you're having stroke symptoms, call 911 and get to the ER in a hurry

I've covered this territory before in a prior post, but there's compelling new data on this crucial health issue. In the June 19, 2013 edition of JAMA is an article titled "Time to Treatment With Intravenous Tissue Plasminogen Activator and Outcome From Acute Ischemic Stroke." The basic concept is that promptly getting someone who has suffered a stroke to a hospital that has modern "clot buster" therapy available markedly improves their outcome.

But in order to understand what it is that the research paper espouses, let's go back a few notches and work up gradually to the details of the paper.

I've always wondered why a stroke is called, in lay language, a stroke (physicians call it a CVA, a cardiovascular accident). The best answer I've seen is that someone who appeared to be in generally good health could abruptly be struck with acute neurologic symptoms: sudden weakness or numbness on one side of the body; sudden confusion, difficulty speaking or understanding; sudden loss of vision in one or both eyes; sudden motor problems (difficulty with walking, balance, loss or coordination or dizziness); or sudden severe headache without any known cause.

Most people (93%) recognize the first of those symptoms, the sudden onset of unilateral weakness or numbness, as indicative of a stroke, but less than 40% know all five major signs that a CVA is in progress. When you have one of the five, the CDC says you should call 911. You need to be at the Emergency Room within a realtively brief period of time to have an optimal chance of a best-outcome recovery.

What are your risk factors for stroke?

What are your risk factors for stroke?

The major risk factors for stroke are high blood pressure, high LDL cholesterol and smoking. The Stanford online article on CVAs mentions that all the usual cardiovascular threats can play a role, e.g., diabetes, obesity, lack of exercise, diet, stress. Oral contraceptives, especially those with higher estrogen content appear to increase the risk of blood clots, including those that may cause a strokes, particularly in women over 30 and post-menopausal estrogen use may somewhat elevate stroke risk.

Of course you can't change your age (some try) and two-thirds of strokes occur in those over 65. It's also about 25% more common in males and a positive family history of CVAs may be a factor. African Americans have twice the risk of having a first stroke as do whites.

The first more detailed accounts of stroke, referred to as apoplexy from the Greek word  ποπληξία, meaning struck down with violence, were written by Hippocrates (460 to 370 BCE) describing a sudden collapse, a loss of consciousness and paralysis.

The American Stroke Association has a great visual on types of strokes, listing three kinds: ischemic (lack of blood flow to the brain), hemorrhagic (the result of bleeding in that vital area of our bodies) and TIA (transient ischemic attack, a mini-stroke or warning stroke), but I also went to the online information sheets from the Stanford Stroke Center which has a comprehensive discussion of the ailment.

A stroke is sometimes called a "brain attack," presumably to underline its importance as equivalent to a heart attack . It is a leading cause of death in the United States, killing one of us in this country every 4 minutes and costing nearly $40 billion a year between health care, medications and missed work days.

Nearly 800,000 of us will have a stroke this year and 87% of all CVAs are of the ischemic type. As I've said before, "Time is Brain." You can lose 2 million brain cells every minute after the onset of a stroke.

Although the average age in large studies of CVAs is in the early 70s (actually 72, the age I'm at now), one third of all stroke victims are under the age of 65.

Prior studies with a protein called tissue plasminogen activator, a substance that can dissolve blot clots (and therefore termed a clot buster) have shown the possibility of minimizing damage from an ischemic stroke, but have been limited in size and therefore not having results as clear-cut as I wanted to see.

Now that limitation has been overcome by a very large-scale data set, the US national "Get With The Guidelines--Stroke (GWTG-Stroke) study. This is a combined project of the American Heart Association and the American Stroke Association, started in 2003 and involving 1,656 hospitals and over 2 million patents.

The JAMA article, looking at results of clot buster therapy in over 58,000 patients who had an ischemic stroke and got treatment in less than four and a half hours, had striking conclusions.Every 15 minutes slower from onset of symptoms to treatment worsened the eventual outcome.

Let's flip that around: the quicker you get to the ER the better are your chances of having a good result.

That means fewer deaths, fewer brain hemorrhages, better likelihood of walking by yourself and better chance you'll go home instead of to a nursing home.

It didn't matter what your age, gender or race/ethnicity was, the results were similar in all groups.

So remember (or learn) the five major symptoms: sudden weakness or numbness on one side of the body; sudden confusion, difficulty speaking or understanding, sudden loss of vision in one or both eyes, sudden motor problems (difficulty with walking, balance, loss or coordination or dizziness) or sudden severe headache without any known cause.

And if you have one of them, call 911 and get your brain to an ER by ambulance.

Bring the rest of you along to keep it company.

Tetanus: it hasn't disappeared, even here..

Monday, June 24th, 2013

We were at a fiftieth wedding anniversary party on a weekend night and ate, among other things, baked beans and chocolate cupcakes. So when I saw a dark splotch on a friend's arm I thought he'd spilled something on himself.

A rusty sharp piece of metal poises several dangers

A rusty sharp piece of metal poises several dangers

He said, "No, I scratched myself this morning on a rusty piece of metal."

"When did you have your last tetanus booster?"

"You know, I don't remember"

His physician is in solo practice and my friend was unsure of his weekend coverage, so I suggested going to the Urgent Care Clinic our local hospital runs. I nudged him buy showing a 1807 painting of a men with opisothonus, the most extreme muscle spasm one can imagine. At that point he showed me his contact information for his internist and I dialed the number and handed the phone back to him.

As it turned out his doc answers his own messages and told his patient that he had had boosters, but would check his record on the following Monday morning and then call him.

So why was I concerned? After all, the number of cases of tetanus, also called lockjaw, is very small in the United States, usually less than 40 to 60 a year.

That statement holds for most developed countries, but certainly not for the rest of the globe.

Worldwide it's quite a different matter with one source noting over 14,000 cases reported in 2011 and a 5-year death toll of 81,000 reported in 2008.

Still, that's a marked improvement over past years when estimates of a million deaths a year, mostly in Africa and Asia, were the rule. In the late 1980s the World Health Organization (WHO) estimated 787,000 newborns died of neonatal tetanus (NT). That's about 6.7 per every 1,000 live births.

The WHO has an ongoing campaign to eliminate maternal and neonatal (newborn) tetanus and by 2101 the number of NT deaths was estimated at 58,000, still enough souls to fill a mid-sized community, but 93% less than slightly over 20 years previous.

Yes, but a significant number of those who do get it die and having a dirty wound is clearly a risk factor for tetanus.

The tetanus bacteria, an anaerobic (capable of living without oxygen) rod-shaped organism, is found in soil and in the gut flora (the mass of bacteria living in the intestines) of animals and humans. Overall our bowels carry 100 trillion microorganisms, ten times a many as the entire number of cells in a human, with estimates of a hundred times the number of genes as our human genome possesses.

It is not transmitted from person to person, but is present throughout the environment and is commonly found in soil contaminated with manure, and animal and human feces. The incubation period is usually 7 to 8 days, but can range from 3 days to three weeks with shorter incubation timing being associated with heavily contaminated wounds.

Tetanus often begins with muscular stiffness in the jaw, e.g., lockjaw, followed by stiffness in the neck, difficulty swallowing, rigidity of the abdominal muscles, spasms, sweating and fever. Other complications can include vocal cord and/or repsiratory muscle spasm. In especially severe cases long bone or spine fractures can occur as a result of muscle spasms.

The Mayo Clinic's article on tetanus agrees that the tetanus vaccine has made the disease quite rare in developed countries, but notes there are still somewhere about a million cases every year elsewhere in the world (that's quite different from the number I mentioned above, but may represent older figures). There is no cure for this terrible disease and fatality rates, which used to range from 48% upward, are still close to 10% even in settings where modern supportive therapy is available. That may include antibiotics, bed rest in an environment with lights dimmed, noise kept at a minimum and temperature stabilized, drugs for muscle relaxation, sedation and debridement (localized surgery to clean the wound) & possibly tetanus immune globulin.

If no treatment is given, roughly 25% of those infected die and those rates are considerably higher in newborns (typically with umbilical cord infections) and in the elderly without adequate immunization. Yet, until quite recently, most recommendations for tetanus toxoid mention re-immunizing every 10 years until age 65, with no provision for those of us who are older. Below that age, studies of armed forces personnel have shown adequate protection for up to twelve years.

Over the past few years the recommendations for immunization in older adults (age 65 and up) have gradually changed. In late 2010, although there was no formally FDA approved Tdap (Tetanus, diphtheria and pertussis (whooping cough), vaccine for those in that age range, the CDC's Advisory Committee on Immunization Practices (ACIP) suggested Tdap be given to all 65+ adults who were in close contact with infants and others in that older age range could get Tdap. By early 2012 ACIP approved the use of Tdap in all older adults, with one product (Boostrix) being preferred but the use of either of the two kinds of Tdap available in the United States being valid.

Wound management recommendations have similarly changed recently. If more than 5 years have elapsed since the last tetanus booster (which may have been Td), then anyone who is 19 and older should get Tdap.

The last time I got a dirty puncture wound I thoroughly cleaned it and hurried off to the hospital's Urgent Care Clinic, shot record in my hand.

When did you last have a tetanus booster shot?

When did you last have a tetanus booster shot?

Between tetanus bacilli, flesh-eating strep, drug-resistant staph and all their compatriots I've changed my approach to outdoor work. Although I do much less of it than in years past, I still not infrequently come home with a dirty scratch. I really scrub my hands and occasionally add a topical antibiotic ointment and a band-aid.

I think you should ask your physician when your last tetanus booster was given and see what they'd suggest for supposedly minor cuts and punctures.

You may prevent one or another of the serious bacterial complications most of us have heard about happening, even in our own communities.



The Eyes have it: Part two: diseases of the cornea and retina

Wednesday, June 19th, 2013

My own eye history is complex: I found out I was nearsighted at age eight while attending a baseball game with my folks. They mentioned the score and I asked how they knew what it was.

"Just read the scoreboard," Dad said.

My eyesight isn't perfect, but I haven't gotten to this stage yet

My eyesight isn't perfect, but I haven't gotten to this stage yet

"What scoreboard?"

Much later, after years of wearing glasses (now they're bifocals), I was diagnosed as having a corneal disease...and that was even more years before the cataracts.

In my last post I outlined the anatomy and physiology of vision so that I could focus (pun intended) on diseases of the cornea and also on age-related macular degeneration this time.

In my prior post on the eye, I translated dystrophy as "it grew incorrectly," but "dys" comes from the Latin for "bad" and "trohe" from the Greek for "food," so poorly or inadequately nourished perhaps would be a better rendering for the term. A National Eye Institute document I provided a link to previously, "Facts about the Cornea and Corneal Diseases,"  says all of these dystrophies share a number of traits. They are usually inherited, affect both eyes equally, aren't caused by diet or injury, progress gradually and aren't related to systemic diseases, those that affect the rest of the body. They define a corneal dystrophy as "a condition in which one or more parts of the cornea lose their normal clarity due to a buildup of cloudy material."

Let's start with keratoconus, an abnormality of the cornea that usually affects both eyes, most frequently occurs in those who are ages 10 to 25 and slowly progresses over roughly a decade. It results in thinning and bulging of the cornea which forms a cone shape. This is a relatively uncommon disease affecting one in 2,000 of us and in its early stages can often be corrected with glasses or soft contact lenses.

Later on other kinds of contacts or even corneal transplantation may be required. If the patent gets such a transplant, its success rate is quite high with one estimate of an 89% positive outcome lasting ten or more years. An experimental treatment called collagen cross-linking is being evaluated around the world with clinical trials in multiple centers in the United States.

Less than 10% of those who have keratoconus also have a family history of the disease. Others may have had an eye injury, have other eye diseases, or unlike most other corneal problems, their keratoconus may be associated with systemic disorders including Down Syndrome.

My mother was said to have Fuchs' dystrophy, a slowly progressive corneal problem that normally affects both eyes, rarely alters vision until those who have it are in their 50s and 60s, and causes early-morning blurring that gradually clears as the day progresses. One layer of cells in the cornea, for unknown reasons, slowly dies off. They normally help pump water out of structure and, in their absence, the cornea swells, distorting vision.

Fuchs' is a major problem and some affected by this disease require advanced treatments including corneal transplantation. The success rate for this is reasonably good (73% after ten years), but waiting for donor tissue to become available is an issue.

I have map-dot-fingerprint (MDFD) dystrophy, according to most sources the most common of over 20 conditions in which parts of the cornea lose their usual clearness as cloudy materials pile up.

MDFD usually hits adults between the ages of 40 and 70, but can develop earlier. I remember cutting my right eye with a paper towel in 1971 when I was 30. It healed slowly and I had recurring episodes of eye pain, especially when I first woke up, over a period of four or five months. I'd bet that was my first hint of MDFD which typically will have flares over a few years and then go away without any long-last effect on vision.

A 2012 Medscape article says MDFD is rarely hereditary and may better be described as a corneal degeneration. Estimates of its prevalence in the general population range widely, from 2 to 43%. Like me, up to a third of those with MDFD have repeated early morning corneal tears/rips termed corneal erosions. They happen because in MDFD the outermost of the cornea's five layers of tissue, the epithelium, doesn't stay correctly attached to the layer below.

Since your eyes naturally get dry at night, your eyelid may stick to the epithelium and when you first awake and open your eyes, the not-well-attached epithelium can tear off casing mild to even severe pain.

I'm going to move to the back of the eye and age-related macular degeneration (AMD). Remember that light from images we see passes through the lens and goes to the retina, a light-sensitive layer of cells that line the inner surface of the eye. As the light impinges on these cells, two types of them react to the stimulus with a series of chemical/electrical events that eventually trigger nerve impulses sent through the optic nerve to the visual centers of the brain.  One kind is called rods and they are most important in dim light and provide our black and white vision. The other kind are termed cones and those are useful in our color perception and in daytime vision. I'll ignore a third type of receptor cells, important in reflexive responses to bright daylight.

The macula is the dull round area slightly off-center

The macula is the dull round area slightly off-center

Near the center of a retina is a small, oval-shaped spot called the macula (Latin for "spot") that is critical for high-resolution vision. It's yellow in color, absorbs UV and blue light and is sometimes referred to as a natural sunblock protecting this highly-important area of the retina. The yellow color comes from two chemicals, lutein and zeaxanthin, which are derived from our diet. They are members of the carotenoids, a group of greater than 700 fat-soluble nutrients that provide the color in foods like carrots, pumpkins, sweet potatoes and other yellow, red, orange and deep green fruits and vegetables. Some of these, but by no means all, are converted to vitamin A or retinol, its active form, in the body.

AMD is the leading cause of major loss of vision in those of us over 50, accounting for more than half of all blindness in the United States. A major project, The Age-related Eye Disease Study (AREDS) has shown that taking some supplements can reduce the risk of progression to advanced AMD by 25% at 5 years. I've been taking a half dose of one of these for some years. Now a recent article in JAMA, "Lutein +Zeaxanthin and Omega-3 Fatty Acids for Age-Related Macular Degenerationpart of the followup study, AREDS2, looked at specific components of those formulations of antioxidant vitamins and minerals.

Their conclusion was adding the two carotenoids, lutein and zeaxanthin (L&Z), and the omega-3s  to the basic ingredients didn't seem to offer a further reduction in risk of AMD, but  L&Z might lower the risk of lung cancer in former smokers.

I'm not changing the pill I now take. I don't think ingesting the equivalent of a little extra carrot or sweet potato will hurt me.


The Eyes have it: part one: Anatomy and Physiology

Friday, June 14th, 2013

I already have an eye disease, a corneal problem called map-dot-fingerprint dystrophy (translated as "it grew incorrectly"), but I'm much more concerned about the one my father had late in life, age-related macular degeneration. I need to walk you through the anatomy of the eye (How's that for a mixed metaphor?) before I can outline what either of those ophthalmologic problems are and what can be done to correct, treat or prevent them.

The National Eye Institute has a discussion of the visual system, at a level most appropriate for kids, but very worth viewing and listening to by anyone who is visually oriented in their learning style. I think it's the one link I'd suggest clicking on if you want an elementary, but accurate audio-pictorial description of how our vision works.

I'll also give you a link to the WebMD's Eye Health Center, which has a very nice picture of the parts of the eye and links to many eye diseases, but eventually I plan only write in any detail about two of those parts, the cornea and the retina.

a cross section of the human eyeWe each have two eyes, unlike spiders which usually have eight (I wonder how many Spiderman has). Each eye sees a slightly different view of an object, so we have stereoscopic vision, important in judging distance and in fine manipulation. The front of our eyes have a pigmented part called the iris, a clear domelike structure called the cornea over the iris and an opening in the iris (the pupil) to let light through.The size of the pupil varies, as we've all noticed, with how bright the light is. You can't see the conjunctiva, which is a covering for all of the rest of the front part of the eye except for the cornea. Then a tough fibrous white membrane called the sclera surrounds most of the eyeball  posterior to the cornea.

When you're looking at something, for instance, your family dog, light representing that object enters your eyes through your pupils, passes through a lens (this is a focusing device) and through a gel-like material called the vitreous humor to the retina, the light-sensitive tissue in the back of the eyeball.

The picture of the object you're looking at is inverted by the time it gets to the retina whose cells convert the light into electrics impulses which are then carried via the optic nerve to a part of the brain called the visual cortex. That's located way in the back of your skull in the occipital lobe of the brain (if you feel the back of your head, you'll note a bump called the occiput).

Then things get very complicated, much more so than I want to delve into, but if you're really interested here's a link to a 24-page convoluted article I found. The author, a professor at Weber State University, made the statement about six years ago that if we want to fully understand what happens when the signal leaves the retina, there are two fundamental questions: "What are the discrete anatomical pathways that carry the signal?" and "What information do the signals actually carry?"

His conclusion was that the answers to these questions do not (currently) exist.

So let's go back to the two parts of the eye that I personally have been most concerned about and start with the National Eye Institute' comprehensive online discussion, Facts About The Cornea and Corneal Disease. I'd term this article "Everything you might possibly want to know about the cornea and lots more," so I'll attempt to abstract some salient points.

First the cornea, in order for us to have good vision, must be free of any cloudy or opaque areas, so unlike most parts of our bodies, it doesn't have any blood vessels. How does it get its nourishment? Both our tears and the vitreous humour (British spelling), the gel-like watery substance that fills the eyeball between the lens and the retina, play a role in keeping our corneas healthy.

The cornea is both clear and strong and has several functions: it protects the eye from dust and germs and, at the same time acts as an outer lens to help focus light. It also screens out some of the potentially damaging ultraviolet (UV) light in sunlight.

The cornea is frequently misshapen and if it is curved too much or the eye is overly long, objects at a distance don't focus on the retina. So about 25% of us, those who have this corneal issue, are nearsighted (myopic). The opposite causes farsightedness (hyperopia) and that's seen in 5 to 10% of both kids and adults.

glasses can often correct myopia, hyperopia or astigmatism

glasses can often correct myopia, hyperopia or astigmatism

Two-thirds of Americans who are myopic (and some who are hyperopic) also have a condition called astigmatism where the curvature of the cornea isn't smooth, so both near and distant objects appear blurry. This often is correctable by glasses, but special contact lenses or laser surgery are sometimes needed.

Those of us who are allergic to pollen can note corneal irritation, especially during dry, hot weather and may have tearing, corneal redness, itching or other symptoms. Most of the time those problems don't necessitate medical visits. Antihistamine decongestant eyedrops often reduce our symptoms. Some of us are allergic to animal hair (dander), cosmetics, or medications and those substances or even rubbing/touching your eyes after using soaps, chemicals or applying nail polish can cause a corneal reaction.

Minor injuries to the cornea may be self-healing, but more severe ones clearly require an eye professional's attention. Similarly corneal infections from a poke in the eye or a contaminated contact lens may necessitate professional help.

As I mentioned before, tears are important for a healthy cornea so dry eye, a condition more common in women, particularly after menopause, may require the use of artificial tears and may be helped by using humidifiers and wrap-around glasses for outdoor wear. Interestingly, people who have dry eye may sometimes have tears running down their faces.

I'll get to corneal dystrophies and macular problems in my next post.






Inflight medical emergencies

Sunday, June 9th, 2013
Could this be your last flight?

Could this be your last flight?

So here you are, 68 years old, finally retired from your forty-three year career and just starting that long-awaited trip with your spouse. The Far East beckons as your board that plane headed to Shanghai. Sure, you've never gotten around to losing that extra forty pounds, but as soon as you get back you're going to join a gym and work out three, maybe four times a week. Perhaps they can help you with a Stop Smoking program too.

Six hours later, 42,000 feet above the Pacific, you're in trouble. It started with that meal you bought at the airport and brought aboard; a strange, uncomfortable feeling in your chest and now you're sweating and it feels like an elephant is standing on you, with pain coming down your left arm as well.

So this scenario happens over and over. A passenger on a commercial airline has chest pain or, perhaps, shifting gears, is a diabetic who took his or her medicine, but, in the rush of things, didn't eat before starting on their journey and now has low blood sugar. Or someone may have a stoke or a seizure or a miscarriage.

How prepared is the plane's crew for the care needed? Do they have adequate training or supplies?

A recent article brought back memories of flying across the Pacific during my Active Duty days. On seven of eight legs, going from the United States to the Philippines or back the other way, I ended up being identified as a physician and needed to help. That's also happened on a ship cruising down the Danube.

Most of the time the person who needed medical attention wasn't critically ill. But in one instance, on my last flight back to the States, a Marine went into premature labor, I had delivered fifty babies, but none for the preceding fourteen years. That time I found well-trained help; our head nurse in Labor and Delivery saw me walking down the aisle and said she'd take over.

Another episode had a young troop with acute gastroenteritis; I made the equivalent of Gatorade from supplies on the plane, gave him the rehydration fluid and had two burly young men sit next to him right in front of a bathroom.

But the question I always wondered about in those days was what would I do if someone had a cardiac arrest while we were 3,000 miles from a hospital and eight miles above sea level. This was before the advent of AEDs, automated external defibrillators, the devices that can determine if a person's abnormal heart rhythm is one that could respond to an electrical shock.

I also flew on one Air Force aeromedical evacuation flight, from Clark AFB, north of Manila, to Bali, but in that case I knew I was there to give or supervise medical care and had a crew that included flight nurses and technicians. They were used to such flights and, in those days, rarely had a doc onboard. Many of our staff members went out from Clark on similar flight to a variety of locations in the Far East.

That was long before the days of "critical care in the air," pioneered by one of my past Air Force commanders. The USAF's 59th Medical Wing (formerly known as Wilford Hall Medical Center) now has 15 three-member teams with a critical care physician, critical care nurse and a respiratory tech equipped with all they might need to support three critically ill patients for 72 hours.

But what if you're in a civilian airplane and have a major medical emergency?

A 2oo6 Federal Aviation Administration (FAA) Advisory Circular dated January 12, 2006 mandated supplies that must be carried on commercial flights. It's directed at planes with at least 30 passengers and one or more flight attendants.  An AED, blood pressure cuff, stethoscope, CPR masks (to protect those doing CPR, not for those needing it), a few needles and syringes, protective gloves, 4 adult aspirin, 4 other non-narcotic pain pills, oral and injectable antihistamines, an asthma inhaler, 10 nitroglycerin tablets, 50 cc of a 50% dextrose (sugar) solution, 500 cc of a saline solution and a few cardiac drugs are required.

Plus one set of basic instructions on how to use the drugs in the kit.

But who is going to use that kit of emergency materials? Most of the time it would be a passenger, hopefully a physician or nurse or EMT. The FAA states "It is unrealistic to expect flight attendants to achieve the same level of proficiency as emergency medical personnel who preform medical procedures on a routine basis." The circular goes on to say, "Flight attendants should not be expected to administer medications or to start IVs."

She also knows how to use an AED

She also knows how to use an AED

Since then a number of airlines have upgraded the training of their staff and added extra supplies to those the FDA requires. I'd like to see a glucometer in the list.

A recent article which caught my attention was titled "Outcomes of Medical Emergencies on Commercial Airline Flights," printed online by the New England Journal of Medicine (NEJM) on May 30, 2013. It began by stating two and three quarters billion passengers take to the skies every year . The piece tracked nearly three years of in-flight emergency calls from both domestic and international airlines (five airlines carrying roughly 10% of all such passengers) to a medical communications center staffed by physicians.

Overall there was one medical emergency per just over 600 flights; nearly half of the instances resulted in physicians providing help in the air and only 7.3% caused an aircraft diversion, i.e., emergency landing for medical care. Out of nearly 11,000 passengers for whom followup date was available, roughly three-fourths were met by EMS on landing and 2804 were then transport to an emergency room.

Only thirty-six died and of those 30 died in the air. That's less than 1/2 of one percent of those who needed medical attention.

The ability for flight crew to communicate with physicians on the ground was invaluable, especially as physicians passengers were available less than half of the time and nurses about 20% of cases.

Shortly before the NEJM piece came out, there was an article in The Atlantic, "Medical Emergencies at 40,000 feet." This one recounted the experiences of Dr. Celine Gounder, a Baltimore-based infectious disease and public health specialist.

I read her article and noted that the 1998 Aviation Medical Assistance Act protects medical personnel providing in-flight care from legal liability except in cases of gross negligence or willful misconduct.

Flight personnel can help physician/nurse volunteers by automatically contacting medical communications centers. A number of physicians who fly may be like me, fifteen years past the last time I rendered any medical care and nearly thirty years past my last ICU experience. And even a practicing ENT doc (for example) may not be comfortable giving cardiac meds without the assistance of a ground-based expert.

But as our population ages while still enjoying travel, the issue isn't going to go away.

The ongoing war: superbugs versus humanity

Tuesday, June 4th, 2013

I saw an article that gave me some hope for our current bacterial and viral dilemmas; it involved a new strategy to prevent infections, rather than treating them after they've struck. I'm all for preventive medicine, both in the infectious disease arena and in medicine in general. I think we "play catch-up" all too often.

How this ICU staffer chooses to protect you from MRSA is crucial.

How this ICU staffer chooses to protect you from MRSA is crucial.

The piece was in The Wall Street Journal on May 30, 21013 with its headline,  "New Tack in Preventing Hospital Infections: Germ-Killing Soap-Ointment Treatment for all ICU Patients Shown to be More Effective than Isolating Some After Screening" The original article  was printed online in the New England Journal of Medicine on May 29, 2013 and its title was  "Targeted versus Universal Decolonization to Prevent ICU Infection."

We're mostly talking about MRSA (Methicillin-resistant Staphylococcus aureus), that strain of the familiar Staph bacteria that's been plaguing us for the last few decades, in large part as a result of unnecessary antibiotic use.

Even if antibiotics are used only for significant bacterial infections, a small proportion of the "bugs" may survive. The population of those germs who cannot be killed by the particular antibiotic can multiply and be spread to others. When antimicrobial drugs are used inappropriately used to "treat" viral infections (e.g., "flu" or the common cold) or given wholesale to food animals (beef, chicken, pigs) to promote growth), we're also likely to be find ourselves with bacteria that are resistant to those antibiotics we've previously been able to use successfully.

About 30% of us carry staph of our skin or in our nostrils (without being ill) and somewhere between 1% and 2.5% carry MRSA. Otherwise healthy people can develop infection with it as a painful skin boil, especially in rugby or football players and high school wrestlers, but also in those who are child care workers or live in crowded settings.

Since moving here in 1999 I'm personally aware of two people who started with what seemed to be very minor skin infections, but later were diagnosed with extremely serious progression of their initial disease. One died from what was eventually diagnosed as fleshing-eating Strep; the other survived, but spend a long time in intensive care with a Staph infection that spread from a bump on his arm up to his chest.

Hospitals often screen patients for MRSA and nine states now mandate such screening. But the study mentioned above attempted to see if there was a better way to avert serious infections in the intensive care setting where patients are the sickest.

MRSA growing on a culture plate.

MRSA growing on a culture plate.

Forty-three hospitals with 74 ICUs and nearly 75,000 patents were randomly assigned to one of three infection prevention strategies: the first group screened patents for MRSA and isolated those who tested positive; the second group added "decolonization," removing the bacteria by washing MRSA-positive patents with an antimicrobial (bacteria-killing) soap plus giving them a nasal antibiotic; the third group of hospitals did not screen patents, but treated every ICU patient as though they had MRSA, i.e., with the soap and the nasal antibiotic.

Universal decolonization cut the rate of positive blood cultures, a way to look at the most serious infections, by 44%. That included not only Staph, but other bacteria as well. Only seven of the research subjects had any form of adverse reaction and those were mild rashes of itching; all resolved after stopping the washing.

The Mayo Clinic webpage on MRSA discusses risk factors for hospital-associated MRSA infections (HA-MRSA) and for those that are community-associated (CA-MRSA). Just being hospitalized increases your risk as does having an invasive medical device (urinary catheter or IV line) and residing in a long-term care facility. Remember, carriers of MRSA can spread the germ, even if they are not sick from it. For CA-MRSA the risk factors include contact sport, living in crowded or unsanitary conditions and men who have homosexual relations.

The World Health Organization (WHO) has an online fact sheet on Antimicrobial resistance. Infections that fail to respond to conventional therapy result in higher medical care costs, greater length of illnesses and a higher risk of a fatal outcome.

MRSA is by no means the only germ that has developed drug resistance. WHO estimates over 630,000 cases of multi-drug resistant tuberculosis (MDR) requiring longer therapy with more drugs. Malaria, caused by one of five species of a parasite that are carried by mosquitos, has become increasingly difficult to treat because of this issue. Malaria cases in the United States have been relatively rare, about 1,200 per year while annually there are 300 million cases and one million deaths from the disease elsewhere in the world.

Most US cases have occurred in those who travel to sub-Saharan Africa, India, or Southeast Asia; That is likely to change as the expected average temperature increase of 0.4 degrees Celcius over the next eight years will likely increase our mosquito population by up to 30%, including the one mosquito species that carries the Plasmodium falciparum, the most deadly type that I've only seen when I was serving at the Air Force Regional Medical Center located on Clark AFB in the Philippines.

A recent online copy of The New York Times has an article titled, "Pressure Grows to Created Drugs for Superbugs." Health and Human Services (HHS) is going to pay $40 million to a pharmaceutical company to develop new antibiotics to combat drug resistance; they are concerned about biological agents that terrorists may utilize to cause widespread death.

But in the meantime, tens of thousands of our citizens die from inceptions, mostly hospital-acquired and caused by the current generation of antibiotic resistant germs. The FDA's director of the Center for Drug Evaluation and research was quoted as saying, "We are facing a huge crisis worldwide not having an antibiotic pipeline... but what is worse is the thought of where we will be five to 10 years from now."

A move to fast-track approval of new anti-infective drugs is being hotly debated. The Infectious Disease Society of America would support their labeling for use on only the very sickest patients.

Others are concerned that these restrictions are insufficient; that the new medicines will be used for those less-than critically ill without our knowing how the antibiotics will perform and what their advise effects may be. One director of the infectious disease society said, "The last thing we want is for a new drug to be overused."

The next twenty to fifty years will be a critical time for the germs versus humans war.