team-based home blood pressure control

July 10th, 2013

I was reading the July 3, 2013 edition of JAMA and came across an article and an editorial on better ways to manage elevated blood pressure (BP). The basic concept stems from data reviewed by the CDC in a 2012 online publication: high BP, AKA hypertension, is a major risk factor for both stroke and cardiovascular disease which jointly are the number one causes of preventable death in the United States.

Check your blood pressure and let your healthcare team know the reading

Check your blood pressure and let your healthcare team know the reading

Do you know what your BP is? Let's start from scratch with the kind of numbers you might hear about when you see your doctor or have your BP checked in other settings (e.g., the grocery store we usually shop at has a free automated system for BP measurement).

My BP usually runs about 116/ 68, but, similar to yours and everyone else's, my BP varies from those numbers from minute to minute. The top number, called my systolic pressure is always higher than the lower (diastolic pressure) It measures pressure in my arteries when my heart contracts (beats) while the bottom number measures it between heart beats when that muscular organ is resting and refilling with blood about to be pumped out to the rest of my body. The American Heart Association has a nice webpage explaining BP.

I'd like to see BPs under 120/80 and that seems to be a reasonable consensus figure in articles I read. Hypertension (HTN) is conventionally defined as a BP higher than 140/90 and the National Heart, Lung and Blood Institute's website calls any BP between 120/80 and 140/90 prehypertension. That's new to me, as the designation used to be applied to those with BPs between 130 and 139 for the upper number and 85 to 90 for the lower one. But I retired in 1998 and the BP goals changed in 2003.

My 2006 copy of Kaplan's Clinical Hypertension, the ninth edition of this amazing, mostly one-person work by a senior professor in Dallas (I just ordered a used copy of the 2010 tenth edition), mentions that 120-129/80-84 used to be considered normal  and 130-139/85-89 was thought to be borderline. But the 2003 report of the Seventh Joint National Committee  put BPs anywhere over 120/80 into the new category saying it wasn't a disease, but a designation to identify those at high risk of developing hypertension.

So what if one of your numbers is in this range, but not the other? The Harvard Medical School's Family Health Guide article on prehypertension notes that BPs vary from time to time and from arm to arm. If you have BP numbers over 120/80, the classification will depend on your average/usual readings, not the extremes. They suggest you always use the systolic or diastolic number that puts you in a higher category (normal, prehypertension, hypertension).  So, for example, if your average is 124/76 or 118/83, you're in the prehypertensive group

The CDC paper and others say the overall prevalence (i.e., the proportion of a population having a disease) of HTN in America is ~30%, but that increases with age with many estimates stating it's 70% in those of us 65 and older. That group is more prone to systolic HTN with only the upper number being elevated. That's still high BP and dangerous.

Treatment of HTN with diet, weight control and meds is associated with considerable decreases in the dire consequences of uncontrolled HTN: strokes, heart attacks and congestive heart failure (a condition where your heart can't pump out enough blood to keep up with the needs of your body).

All of us should be screened for HTN, even if our BP is less than 120/80. Screening intervals should be at least every two years for those with normal BP and every year for people with prehypertension. Your physician will also consider your other risk factors (weight, age, gender, your blood lipid levels {e.g., total cholesterol, HDL and LDL levels} presence or absence of diabetes, heart disease or chronic kidney disease, exercise patterns) and may, in some case recommend drug therapy even if your BP is <140/80. That's especially likely for those with any of the three chronic diseases I just mentioned.

So do we all need to be on medications if our BP is >140/80 (no, your physician may start with non-pharmacologic modalities such as cutting our salt intake) and if we do start on BP meds how often do we need to see our doc? After all, they're really busy these days and we may not be able to get an appointment for several months.

Let me start with my own experience (in the "Dark Ages") and then come up to the present.

When I was in my first Air Force assignment at Langley AFB, VA from 1970 to 1972, I set up a HTN clinic run by a public health nurse, an RN with extras training who didn't want to be a ward nurse. My immediate boss was a cardiologist and, after I set up protocols (e.g., which meds to start with, appropriate followup intervals for various levels of BP, when to call for help), our nurse felt quite comfortable running the BP clinic.

She didn't see other kinds of patients, got very savvy about HTN, read a lot of the current medical literature on the subject, was entirely at ease with calling either of her two consultants whenever she had a question and our HTN patient population could easily get appointments in her clinic.

Fast forward ~forty years.

In 2011 a Veterans Administration group from Durham (coincidentally a place I worked when I was a resident and nephrology fellow at Duke) published an article in the Archives of Internal Medicine (now called JAMA Internal Medicine). Its title was "Home Blood Pressure Management and Improved Blood Pressure Control: Results From A Randomized Controlled Trial."

In brief they followed nearly 600 HTN patients who were randomized into one of four groups. The first had usual care, i.e., being seen in a primary care clinic at intervals. The other three groups involved nurses who administered behavioral management concepts, worked with docs on medication management or did both. The patients had their BPs monitored at home with data transmitted to the researchers. Incidentally 48% of the patients involved were African American.

Overall the research group felt the intervention effects were moderate, but those patients who started with the worst BP control had much better resultant effects.

there are a number of options for HTN meds

there are a number of options for HTN meds

Now there's the new JAMA article, "Effect of Home Blood pressure Telemonitoring and Pharmacist Management on Blood pressure Control: A Cluster Randomized Clinical Trial." Researchers associated with an integrated health system in Minnesota using electronic medical records, noting that typically only half of HTN patients have adequately controlled BPs, followed 450 patients, roughly half of whom got usual care. The other half got home BP telemonitoring and had PhD pharmacologists following their data and making changes in their BP meds by a protocol worked out with physicians.

BP control was better in the latter group at 6 and 12 months and was even better 6 months after the year-long study ended.

Lesson one: other healthcare professionals can manage HTN. Lesson: doing this via home BP measurements may be the path of the future.

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Posted in home BP monitoring, Hypertension, prehypertension, systolic and diastolic blood pressure, telemedicine | No Comments »

Typo and autocompletion error

July 7th, 2013

I just looked at my last post and found one typo (agreement on subject and verb) of minor consequence and one instance where my MacBook Pro's autocompletion feature changed the meaning of a sentence.

I get frustrated when the latter happens. In this case it was referring to the Harvard Health Publications editor's review of several articles. I clearly did not mean for the word "artless to be substituted for articles.

Sorry.

 

 

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Marijuana and Schizophrenia: What's the association?

July 6th, 2013

My wife called my attention to an editorial page piece in the July 2, 2013 edition of The Wall Street Journal linking marijuana use to schizophrenia. I at first wondered who the paper had chosen as a distinguished medical figure to write on his or her research study of the association between use of this drug and the most severe mental illness, but read the commentary and realized it was written, not by a professor, but by a Yale psychiatry resident in training.

Having been a Duke resident more than 45 years ago, I was aware that young physicians at major teaching centers might, as I did, see a particular spectrum of the general patient population, in many cases the most ill portion of it.  Therefore I was less than certain of the strength of the basis for his viewpoint, but felt it was a highly significant topic and it was well worth perusing the literature pro and con.

Does this cause mental illness?

Does this cause mental illness?

In 2010 Time magazine published a well-balanced article titled "The Link between Marijuana and Schizophrenia." That led me to several medical research reports, but the lay press article itself was interesting.

It commented that studies showed those who were diagnosed with schizophrenia were approximately twice as likely to be marijuana smokers than groups who didn't have this dire diagnosis. Some studies, viewing things prospectively, suggested (note the word, please) that pot smokers were at double the risk of developing schizophrenia as those who never smoked the drug.

But, as the Time article noted  the portion of our US population diagnosed with this debilitating illness has remained constant at roughly 1%, and the current National Institute of Mental Health (NIMH) web-based discussion of schizophrenia agrees with this figure. It mentions that some drug abusers exhibit symptoms like those of patents with schizophrenia, but NIMH states that most researchers do not think that drug abuse is the cause of this mental illness.

A short piece from the CDC on childhood mental disorders in JAMA  for July 3, 2013, confirmed that schizophrenia is way down the list of mental disorders in US children. On the other hand, ADHD, behavioral/conduct disorders, anxiety, depression, use of illicit drugs or alcohol or cigarette, autism spectrum disorders and even Tourette syndrome (a neurologic disorder characterized by tics {repetitive involuntary movements and vocalizations} are listed as affecting multitudes of our youth.

In any given year, according to the CDC article, up to one fifth of our kids and adolescents have a mental disorder, while inpatient admissions have sharply increased for both mental health and substance abuse problems, especially for "mood disorders," e.g., anxiety and depression.

But there may be a subset of marijuana-using/abusing youngsters that merits special attention.

A 2011 Harvard Health Publications (HHP) blog piece by the then editor of the series, a woman whose bachelors degree was not in a medical field, but had a brother who developed schizophrenia, is titled "Teens who smoke pot at risk for later schizophrenia, psychosis."

I was concerned that she might have a biased slant on the disease, but impressed, as I read her blog piece by the articles she cited.

But then I went back to the articles themselves, as I routinely do. The first was in the British Medical Journal in 20111 and was a population based cohort study, a comparison of two different groups. The outcome was the "incidence and persistence of sub-threshold psychotic symptoms after adolescence." The verbiage used was that the use (and especially the continued use) of cannabis was a risk factor for developing severe mental illness.

I'd read the study as showing kids who end up psychotic often have smoked (or otherwise used) marijuana.

The second article cited was from the Archives of General Psychiatry, again a 2011 publication and was a meta-analysis (a study of a number of articles). The authors reviewed a large number of published research studies, picked 83 of them which met their standards for inclusion and pooled the results for statistical purposes.

That's a common way to look at data in order to have enough of it to reach a significant conclusion, which in this case was that the age of onset of psychosis was 2.7 years younger in the group who used cannabis.

Once again, that's only an association, but not a proof of causation.

The third article came from Lancet (in 1987) and was the result of  long-term followup of 45,550 Swedish military conscripts. Those who had smoked pot more than fifty times had a much higher rate of developing serious mental illness.

I want to go back to the blog in Harvard Health Publication, because here's where I have to differ with the author. Her statement that, "So far, this research shows only an association between smoking pot and developing psychosis or schizophrenia later on" makes sense; she admits the data don't prove marijuana causes psychosis.

But in the very next paragraph, she compares this research to that on cigarette smoking first being noted to be associated with lung cancer and later found to be a major cause of that disease.

Do troubled youngsters choice to smoke pot or does smoking it cause later troubles?

Do troubled youngsters choice to smoke pot or does smoking it cause later troubles?

Don't get me wrong; today's marijuana is reputed to be much stronger than that which was around when I was a young research fellow and volunteered time at the Long Beach Free Clinic. And some of the studies I've read in the last week would certainly make me want to caution a teenager with a family history of schizophrenia that pot smoking is really risky for them.

Maybe we're going to see an epidemic of the disease in those of our younger generation who smoke marijuana and don't any family history of schizophrenia or other major mental illness.

But I sure haven't see any data yet that convinces me that's going to happen.

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Lyme disease: the battle continues

July 3rd, 2013
Stay away from ticks

Stay away from ticks

In April of 2012 I wrote a series of posts on tick-borne diseases. This is my 315th post so when the subject of chronic Lyme disease (called post-treatment Lyme Disease syndrome {PTLDS} by the CDC) came up in a well-balanced article in The New Yorker I needed to revisit what I had written 14+ months ago before I could determine if there was anything new on the subject.

It delineates the ongoing controversy which basically comes down to whether chronic Lyme disease actually occurs. Most academic physicians and organizations deny that this exists, but a large group of patents with a multitude of long-term symptoms have interacted with physicians who are willing to treat such an entity. They've formed an International Lyme and Associated Diseases Society who "argue that the traditional approach to diagnosis and treatment, put forth by most American physicians, all but guarantees failure."

A pamphlet from a group formed to fund-raise and increase awareness, the Lyme Action Network, is titled "It Might Be Lyme." The multitude of symptoms under this rubric is astounding as is the conclusion that years of (often intravenous and horrendously expensive) antibiotic therapy is needed to ensure a cure of the ailment.

The author of the New Yorker article was recently interviewed by Terry Gross on NPR. He comments that our current state of knowledge of the illness is incomplete, but notes that the symptoms of many of those who are said to have "chronic Lyme" are vague, commonplace and difficult to attribute to this disease when there are no positive tests and/or they don't live in region of the country known to have Lyme disease.

Let's start with a comment. I found only one medical article that shifted my point of view even a tad bit.

A research group headed by a Johns Hopkins-associated physician with infectious disease training published a study of patients with PTLDS symptoms in a journal I've never heard of before: Quality of Life Research.

His group enrolled 63 patients with the skin manifestation of Lyme disease and systemic symptoms (therefore people with pretty clear-cut diagnoses to fit the ailment) in a prospective cohort study. They followed this group and the control subjects for six months and saw each of them five times. After conventional treatment with a three week course of the antibiotic doxycycline all signs of Lyme disease went away, but after six months slightly over a third of the patents had new-onset fatigue, one fifth had widespread pain and 45% had neurocognitive problems (thinking issues that relate to a particular part of the brain).

This is the first article I've seen that prospectively followed patients with Lyme disease, but my caveats are: it was a small group (63 patients) with obvious Lyme disease and the followup period is relatively short.

I'd like to see a considerably longer prospective study of a much larger group.

Don't wait until the tick has finished its meal

Don't wait until the tick has finished its meal

The introduction to the article mentions that Lyme disease is caused by a spirochete bacteria (therefore a long, coiled member of the same family as the syphilis, but there hasn't been human to human spread that I'm aware of and of course, Lyme is not  a venereal disease). It is  the most common vector-borne (transmitted by a blood-sucking insect or arachnid (mites or ticks) infectious disease in North America. In 2009 nearly 40,000 cases were reported in this country, but most feel that there are likely at least 100,000 cases a year.

There are four other, less prevalent, illnesses that the deer tick vector can transmit, but funding for control of ticks is regarded as low especially when compared to that in Massachusetts for mosquito control in an effort to prevent other ailments, especially West Nile virus and eastern equine encephalitis.

Many academic physicians with infectious disease training feel strongly that Lyme disease should be treated with antibiotics for a month or less in most cases with an exception made for those who develop Lyme arthritis (who may require up to three months of treatment).

After realizing I hadn't done my due diligence, it was time to read lots of background material, including the article in The New Yorker. I downloaded the Kindle edition of Lyme Disease: The Ecology of a Complex System, a 2010 book written by Richard Ostfield, a Ph.D. field biologist.

This is a fascinating opus written from a different point of view, one of a scientist working at the Cary Institute of Ecosystem Studies, a private, not-for-profit in New York state with research focusing on the interactions among organisms that influence the risk of human exposure to vector-borne diseases.

Dr. Ostfeld outlines the natural history and ecology of LD and shows it is a much more convoluted ailment than I had realized. I had thought that the bacterium, the vector and the host were those I had read about, namely Borrelia burgdorferi, the black-legged tick and the white-footed mouse. But just focusing on the potential host species, chipmunks and shrews may carry the microorganism and the tick bites or tries to bite other animals, some of which are "less-efficient/competent reservoirs." So white-tailed deer and robins, depending on their abundance or lack thereof, may play a role in the likelihood of your catching LD, as may the terrain (e.g., densely forested versus subdivided into patches).

We had dinner recently with friends and one of the number was a physician who works for the CDC and has lectured extensively on Lyme disease. He feels quite strongly that the viewpoint of many of those who espouse long-term antibiotic therapy for LD is influenced by financial reward and that data is lacking to prove that this entity exists.

Allen Steele, the doctor who first discovered Lyme disease, now a rheumatologist at Massachusetts General Hospital, is the country's foremost Lyme disease researcher. These days he finds himself distrusted and sometimes harassed by those who feel Lyme disease often has chronic manifestations. A June 2, 2013 article in the Boston Globe highlighted the issue with its title "Drawing the lines in the Lyme disease battle."

I certainly don't agree with a fringe view  I found claiming that the LD bacterium was weaponized for bio-warfare.

At the end of my reading I side with the more traditional, academic view of Lyme disease. I think the other group has yet to prove its case.

 

 

 

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A valid comment on aspirin withdrawal

July 3rd, 2013

I get tons of comments that come from for=profit websites or email addresses  that bounce.

But last month I received one that made sense, asked for links to medical sites and got those in a subsequent email.

Thanks, Rosey.

Peter

 

Hi Peter,
so far these are the papers I've found on the subject of withdrawing from aspirin:

http://www.ncbi.nlm.nih.gov/pubmed/16087761

and I've cut&pasted a quote below from

"There appears to be a rebound from reversing the “blood thinning” effects of aspirin when it is stopped suddenly. Over three times the expected risk of stroke occurs in patients with a previous history of heart disease when they suddenly stop taking aspirin.13 A similar increase in risk of heart attack has been reported when aspirin was stopped.

No one has determined a safe regime for discontinuing this therapy. I suggest that people needing to stop long-term use of aspirin should do so slowly. Since as little as 30 mg (1/3 of a baby aspirin) will deactivate all of the body’s platelets, slow withdrawal should begin at about this level. Cut a baby aspirin into quarters (now 20 mg). Take 20 mg then wait for 4 days to take the next 20 mg dose. Increase the interval between 20 mg doses by one day until a 10-day interval between doses is reached, and then stop taking the aspirin. This is not an easy task since the tablets are so small. Reduction or discontinuation should be done after obtaining a doctor’s advice on the risks and benefits for each individual patient. Even before reducing the aspirin, patients should change to the McDougall Diet in order to most effectively reduce their risk of strokes and heart attacks."

"13) Maulaz AB, Bezerra DC, Michel P, Bogousslavsky J.† Effect of discontinuing aspirin therapy on the risk of brain ischemic stroke.† Arch Neurol. 2005 Aug;62(8):1217-20."

 
 
 
(This reference is the first link above)
I haven't been able to find any other advice from doctors and scientists on how to safely get off aspirin without these risks.
Thanks for your interest,
Rosemary Faire

 

 

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Treating strokes in time: an update

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.

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

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.

 

 

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

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 Degeneration, part 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.

 

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The Eyes have it: part one: Anatomy and Physiology

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.

 

 

 

 

 

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Inflight medical emergencies

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.

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